A new understanding of coagulopathy in trauma: potential therapeutic implications

Exsanguination is the second commonest cause of death in trauma after central nervous system (CNS) injury [1]. Admission coagulopathy in trauma is associated with multiple organ failure, longer intensive care unit (ICU) stay, and mortality [2]. If this association is causative, prevention, rapid identification and appropriate management of coagulopathy may improve outcome. Until recently, the pathogenesis of the coagulopathy of trauma was thought to be a ‘triad’ of loss and dilution of procoagulant clotting factors, hypothermia and acidemia [3, 4], perhaps along with disseminated intravascular coagulation (DIC) [5]. However, there is emerging evidence that tissue hypoperfusion accompanying major trauma also causes hypo- (and later, hyper-) coagulation, as do endothelial dysfunction, inflammation, and possibly platelet dysfunction. More specific focus on these factors may be useful therapeutic targets in trauma. Here, we review evidence for and against the traditional model of traumatic coagulopathy and explore what is known of the interaction between traumatic coagulopathy and hypoperfusion, inflammation, and endothelial and platelet dysfunction. We conclude by suggesting potential therapeutic avenues to exploit these relationships