Advances in the understanding of trauma-induced coagulopathy

Abstract

Ten percent of deaths worldwide are due to trauma, and it is the third most common cause of death in the United States. Despite a profound upregulation in procoagulant mechanisms, one-quarter of trauma patients present with laboratory-based evidence of trauma-induced coagulopathy (TIC), which is associated with poorer outcomes including increased mortality. The most common causes of death after trauma are hemorrhage and traumatic brain injury (TBI). The management of TIC has significant implications in both because many hemorrhagic deaths could be preventable, and TIC is associated with progression of intracranial injury after TBI. This review covers the most recent evidence and advances in our understanding of TIC, including the role of platelet dysfunction, endothelial activation, and fibrinolysis. Trauma induces a plethora of biochemical and physiologic changes, and despite numerous studies reporting differences in coagulation parameters between trauma patients and uninjured controls, it is unclear whether some of these differences may be "normal" after trauma. Comparisons between trauma patients with differing outcomes and use of animal studies have shed some light on this issue, but much of the data continue to be correlative with causative links lacking. In particular, there are little data linking the laboratory-based abnormalities with true clinically evident coagulopathic bleeding. For these reasons, TIC continues to be a significant diagnostic and therapeutic challenge.

Figure 1

Schematic overview of TIC. Trauma induces a laboratory-evident coagulopathy through a variety of different pathways, which is likely modulated by baseline patient factors such as genetics and comorbidities. Unfortunately, few causative relationships are currently known. TIC is a separate entity from iatrogenic causes of coagulopathy including hemodilution and preinjury anticoagulant therapy. Currently, the literature only identifies TIC based on laboratory abnormalities, and its relationship to true clinical coagulopathic bleeding is unknown.