The newest progress of research on acute trauma-induced coagulopathy

Traumatic injury remains the leading cause of death with bleeding in the world, representing the main cause of preventable death. But if immediate management could be applied, the outcomes will be dramatically improved. Trauma-induced coagulopathy (TIC) as an early endogenous process in many traumatic patients is driven by the multi-tissue injury and shock, and is associated with increased mortality and bad outcomes in the multi-trauma patients. The understanding of the mechanisms of TIC and its effect on the outcomes of severely injured patients has been developed over the past few years. Here, we aim to review the current understanding and recent findings in the pathobiology of coagulopathy. The principal causes of TIC are hypoperfusion, inflammation response and the activation of the neurohumoral system. Hypoperfusion causes the activation of many biomarkers, like protein C, syndecan-1, plasminogen, and so on. The elevation of these markers indicates the damage of the endothelium, which will lead to autoheparinization in body. When accompanied with acidosis, hypothermia, and hemodilution, the mortality of trauma patients will rise significantly. This article aims to focus on our updated acknowledges on the principal mechanisms and causes of the TIC.