The Pathophysiology and Management of Acute Traumatic Coagulopathy

Abstract

Acute traumatic coagulopathy (ATC) is commonly seen among patients with severe injury and will lead to uncontrolled bleeding diathesis, which is an important contributor to trauma death. During the past 10 years, the understanding of the mechanism causing ATC has changed rapidly. The mechanisms for ATC are complicated. To date, the possible mechanisms include activation of protein C, shedding of endothelial glycocalyx, catecholamine release, platelet dysfunction, primary, and secondary fibrinolysis, with tissue injury and hypoperfusion as the triggers. Classic factors such as dilution, acidosis, and hypothermia can further aggravate the coagulopathy. Inflammation may have a potential effect on the onset and prognosis of ATC. With the aid of diagnostic device, the outcome can be improved through early and customized treatment. Antifibrinolytics such as tranexamic acid has some benefits in patients with bleeding trauma, especially in the early time. This review presents the current understanding of ATC mechanisms and management.