Abstract
Trauma-induced coagulopathy (TIC) is present soon after injury and is associated with increased transfusion requirements and worse outcomes. The pathophysiological mechanisms, which result in the widespread derangements of hemostasis following major trauma hemorrhage, are as yet not fully defined. Profound activation of fibrinolytic pathways and fibrinogen depletion appear to be fundamental processes in the development of TIC and offer potential therapeutic targets. Collaborative and multi-disciplinary scientific study is thus a research priority in order to characterize the primary drivers of TIC and develop targeted and efficacious treatment strategies.
Highlights
Trauma-induced coagulopathy (TIC) is present soon after injury and is associated with increased transfusion requirements and worse outcomes
In the previous issue of Critical Care, Oshiro and colleagues [1] showed that changes in hemostatic competency occur early following trauma and are described by a profound derangement in coagulation, in particular massive activation of fibrinolysis and potentially fibrinogenolysis
In the context of the CRASH-2 (Clinical Randomization of an Antifibrinolytic in Significant Hemorrhage 2) trial [2], which showed a mortality benefit with the use of the antifibrinolytic tranexamic acid (TXA) in trauma hemorrhage, this work further highlights the pathophysiological importance of fibrinolysis in TIC
Summary
Trauma-induced coagulopathy (TIC) is present soon after injury and is associated with increased transfusion requirements and worse outcomes. In the previous issue of Critical Care, Oshiro and colleagues [1] showed that changes in hemostatic competency occur early following trauma and are described by a profound derangement in coagulation, in particular massive activation of fibrinolysis and potentially fibrinogenolysis. Detection of clotting deficiencies appears to have prognostic value, and the authors provide evidence for the utility of a scoring system in predicting outcome and transfusion need [1].
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