• Marc Maegele.
• Department of Trauma and Orthopedic Surgery, Institute for Research in Operative Medicine (IFOM), University of Witten/Herdecke, Cologne-Merheim Medical Center, Cologne, Germany. Marc.Maegele@t-online.de
• Transfusion. 2013 Jan 1;53 Suppl 1:28S-37S.

AbstractCoagulopathy after traumatic brain injury (TBI) is frequent and represents a powerful predictor related to outcome and prognosis. The complex pathophysiological mechanisms of the coagulopathy of TBI are multifactorial and remain still undefined. The nature of the coagulation abnormalities differs between severe TBI and non-TBI with somatic injuries. The current hypothesis for the development of coagulopathy after TBI includes combinations of both hypo- and hypercoagulable states promoted by the magnitude and the extent of the injury resulting in a variable degree of secondary injury via subsequent ischemic and hemorrhagic lesioning. The proposed underlying mechanisms may comprise the release of tissue factor (TF), hyperfibrinolysis, shock, and hypoperfusion thus triggering the protein C pathway, disseminated intravascular coagulation, and platelet dysfunction. Hemocoagulative disorders after TBI may be amenable to treatment, and adequate and timely management may protect from secondary injury and poor outcomes. Functional assays such as viscoelastic tests may be supportive in early detection, diagnosis, and guidance of treatment. This review summarizes the current understanding with regard to frequency, pathogenesis, diagnosis, and treatment of the coagulopathy after TBI.© 2013 American Association of Blood Banks.

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