Pathophysiological Response to Trauma-Induced Coagulopathy: A Comprehensive Review

Abstract

Hypercoagulability can occur after severe tissue injury, that is likely related to tissue factor exposure and impaired endothelial release of tissue plasminogen activator (tPA). In contrast, when shock and hypoperfusion occur, activation of the protein C pathway and endothelial tPA release induce a shift from a procoagulant to a hypocoagulable and hyperfibrinolytic state with a high risk of bleeding. Both thrombotic and bleeding phenotypes are associated with increased mortality and are influenced by the extent and severity of tissue injury and degree of hemorrhagic shock. Response to trauma is a complex, dynamic process in which risk can shift from bleeding to thrombosis depending on the injury pattern, hemostatic treatment, individual responses, genetic predisposition, and comorbidities. Based on this body of knowledge, we will review and consider future directions for the management of severely injured trauma patients.

Impact of a goal-directed factor-based coagulation management on thromboembolic events following major trauma

“…That finding is congruent to recently published data of 750.937 patients undergoing surgery showing an association of perioperative RBC transfusion with venous thromboembolism [31]. Major trauma patients suffer from extended soft tissue injury and subsequent inflammatory response leading to a diffuse activation of coagulation factors, which culminates in a hypercoagulable state in the post-aggression phase [32]. While this alone increases the risk of developing venous thromboembolism during hospitalization, trauma patients are further exposed to numerous additional risk factors, like prolonged immobilization and a restrictive antithrombotic prophylaxis in case of a traumatic brain injury.…”

Evaluation of coagulation parameters in dogs with gallbladder mucoceles

“…Increased activated PC activity is implicated in the pathogenesis of trauma‐induced coagulopathy and associated hemorrhage. 56 , 57 The bleeding tendencies are associated with activated PC‐induced inhibition of factors V, VIII, and plasminogen activator inhibitor. No dogs in our study had bleeding tendencies, and reports of hemorrhage in patients with GBM are rare.…”

“…The clinical relevance of these increases is unknown. Increased activated PC activity is implicated in the pathogenesis of trauma‐induced coagulopathy and associated hemorrhage 56,57 . The bleeding tendencies are associated with activated PC‐induced inhibition of factors V, VIII, and plasminogen activator inhibitor.…”

Treating the endotheliopathy of SARS‐CoV‐2 infection with plasma: Lessons learned from optimized trauma resuscitation with blood products

“…Acutely bleeding trauma patients also have periods of hypercoagulability, and hence the coagulopathy of COVID and the coagulopathy of severe hemorrhage present with patients that cycle between periods of being hyper and hypocoagulable. 72 In trauma, plasma normalizes coagulation. In terms of sepsis, there is preclinical data suggesting benefits of plasma in organ failure 73,74 and there are currently trials being run testing plasma as a resuscitation fluid in sepsis.…”

“…COVID‐19 patients exhibit pathologic thrombosis resulting in tissue ischemia or infarction and organ failure. Acutely bleeding trauma patients also have periods of hypercoagulability, and hence the coagulopathy of COVID and the coagulopathy of severe hemorrhage present with patients that cycle between periods of being hyper and hypocoagulable 72 . In trauma, plasma normalizes coagulation.…”