Pathophysiology of Trauma-Induced Coagulopathy

•Trauma-induced coagulopathy (TIC) is not a uniform phenotype, ranging from bleeding to pro-thrombotic profiles.•Endotheliopathy occurs after major trauma in a state of shock and ischemia.•Shock and hypoperfusion lead to hypocoagulability and hyperfibrinolysis.•Fibrinolysis dysregulation after sever...

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Bibliographic Details
Published in:Transfusion medicine reviews 2021-10, Vol.35 (4), p.80-86
Main Authors: Duque, Patricia, Calvo, Alberto, Lockie, Christopher, Schöchl, Herbert
Format: Article
Language:English
Subjects:
Blood Coagulation Disorders - etiology
Blood Platelets
Fibrinolysis
Hemorrhage - etiology
Hemorrhagic shock
Hemostasis
Humans
Multiple trauma
Thrombosis
Wounds and Injuries - complications
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Summary:•Trauma-induced coagulopathy (TIC) is not a uniform phenotype, ranging from bleeding to pro-thrombotic profiles.•Endotheliopathy occurs after major trauma in a state of shock and ischemia.•Shock and hypoperfusion lead to hypocoagulability and hyperfibrinolysis.•Fibrinolysis dysregulation after severe trauma is linked to worse outcomes.•Platelet hypofunction occurs early and is common after severe trauma. 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.
ISSN:0887-7963
1532-9496
DOI:10.1016/j.tmrv.2021.07.004