Fig. 4
New considerations on pathways involved in acute traumatic coagulopathy. Hemorrhage leads to fibrinogen depletion and decreases its competitive inhibition on the thrombin/thrombomodulin complex, enhancing protein C activation. In addition, shock induces a decrease in thrombin clearance, also increasing thrombin/thrombomodulin interactions and protein C activation. The result is a hyperfibrinolysis triggered by aPC. Shock also lead to an increase in endogenous epinephrine, leading to heparan sulfate exposition on endothelial cells, activating antithrombin. The repression on coagulation mediated by antithrombin and activated protein C is counteracted by increases in tissue factor and myoglobin triggered by tissular damages, explaining the preservation of thrombin generation despite the expression of a hemorrhagic phenotype due to hyperfibrinolysis.