Citation

Chang R, Cardenas JC, Wade CE, Holcomb JB. Blood 2016; 128(8): 1043-1049.

Affiliation

Center for Translational Injury Research, University of Texas Health Science Center, Houston, TX, United States;

Copyright

(Copyright © 2016, American Society of Hematology)

DOI

10.1182/blood-2016-01-636423

PMID

27381903

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 if 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 continues to be correlative with causative links lacking. In particular, there is 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.

Copyright © 2016 American Society of Hematology.

Language: en