Purpose of review
Hemorrhage is the leading cause of potentially preventable death following injury. Excessive and uncontrolled bleeding, commonly referred to as trauma-induced coagulopathy (TIC), affects a quarter of all trauma patients and is associated with substantial injuries, increased transfusion requirements, and poor outcomes. Recent data have contributed to our current understanding of the molecular mechanisms driving TIC.
The current literature offers evidence supporting proposed mechanisms that induce TIC, such as platelet dysfunction, endogenous anticoagulation, endothelial activation, fibrinogen modifications, and hyperfibrinolysis. However, the majority of these data are mere associations; causative data are slowly unfolding through the utilization of animal models of hemorrhagic shock coupled with prospective observational clinical studies.
As both clinical and basic science research expands our understanding of TIC, trauma patient care is improving substantially. Future studies should focus on the interplay between the coagulation pathways whose simultaneous or codependent dysregulation could offer the most advantageous points for intervention.