Abstract

Coagulopathy commonly arises in patients following traumatic injury and is a major clinical burden [1]. Trauma-induced coagulopathy (TIC) is a multi-factorial condition associated with increased thrombin generation, coagulation factor consumption and activation of fibrinolytic pathways, leading to increased generation of plasmin, fibrin and fibrin degradation products, including D-dimers [1-3]. TIC also affects platelet function, where trauma patients can present with a hypofunctional platelet phenotype even with normal platelet count, which predicts mortality and poor patient outcome [4-7]. This article is protected by copyright. All rights reserved.

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