Pathophysiology of Trauma-Induced Coagulopathy

There is no standard definition for trauma-induced coagulopathy (TIC). However, it could be defined as an abnormal hemostatic response secondary to trauma. The terms early TIC and late TIC have been recently suggested. Early TIC would refer to the inability to achieve effective hemostasis exacerbating an uncontrolled bleeding in a shocked patient with ischemia-reperfusion damage (bleeding phenotype) and takes place usually early after injury, whereas late TIC would represent a hypercoagulable state after surviving a severe tissue injury, that would contribute to thromboembolic events and multiorgan failure (MOF), (thrombotic phenotype), occurring typically hours after the trauma insult though it could be delayed for days. In addition, severe tissue injury when there is no associated shock could be followed by an early hypercoagulable state, representing an evolutionary maladaptive response of a physiologic mechanism created to increase clot formation and prevent bleeding. Therefore, TIC is not a uniform phenotype, ranging from bleeding to pro-thrombotic profiles. This current concept of TIC is mainly based on the recognition of TIC as a unique clotting disorder following trauma in which alterations in the endothelial function, fibrinolysis regulation and platelet behavior after major trauma are the main cornerstones. (c) 2021 Elsevier Inc. All rights reserved.

Automated summary

Trauma-induced coagulopathy (TIC) is an abnormal hemostatic response secondary to trauma, with early and late types defined. Early TIC refers to ineffective hemostasis leading to uncontrolled bleeding in shocked patients, while late TIC is characterized by a hypercoagulable state contributing to thromboembolic events. TIC is not a uniform phenotype, ranging from bleeding to pro-thrombotic profiles, and it is mainly based on alterations in endothelial function, fibrinolysis regulation, and platelet behavior after major trauma.