Background: Trauma-induced coagulopathy (TIC) progresses to disseminated intravascular coagulation (DIC), as consequences of dysregulated inflammatory and coagulofibrinolytic responses to the trauma.

Aims:
We hypothesized that both DIC and TIC patients elicit same coagulofibrinolytic changes characterized by pathomechanisms of DIC, leading to massive transfusion.

Methods: Severely injured trauma patients with injury severity score>16 were prospectively included and 276 patients were eligible for the analyses. Platelet counts, global markers of coagulation and fibrinolysis as well as specific markers of thrombin and plasmin generation, anticoagulation, endothelial injury, and inhibition of fibrinolysis were measured immediately at the presentation to the emergency department (0h) and 3h later the arrival. The patients were subdivided into those with and without DIC or those with and without TIC using 0h data. Time courses of these markers and association of various variables with development of DIC and prevalence of massive transfusion were evaluated.

Results: Severity of injury and thrombin generation were associated with the development of DIC. DIC patients showed increased thrombin generation, insufficient anticoagulation controls, endothelial injury, increased fibrinolysis followed by elevation of plasminogen activator inhibitor-1, leading to consumption coagulopathy. These changes were associated with critical bleeding, resulting in more massive transfusion and poorer outcome than non-DIC patients. Same changes in measured specific markers both at 0h and 3h were observed in TIC patient.

Conclusions: DIC and TIC evoked same coagulofibrinolytic responses in severely injured trauma patients immediately after trauma and were associated with massive transfusion.

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ISTH Congress Abstracts - https://abstracts.isth.org/abstract/a-multicenter-prospective-validation-study-on-disseminated-intravascular-coagulation-in-trauma-induced-coagulopathy/