Haemorrhage and its effects
Control of minor haemorrhage is predominantly via the primary and secondary methods of haemostasis, however, following massive or significant trauma a systemic failure of the coagulation system results in ATC (Acute Traumatic Coagulopathy). Current research has categorised ATC as a clinical syndrome that includes hypoperfusion caused by hypovolaemic shock, activation of protein C (APC), platelet dysfunction, and endothelial glycocalyx disruption. The activation of protein C (APC) and its subsequent binding with thrombin appears to play a significant role in the disruption of the intrinsic, extrinsic and common coagulation pathway. Such disruption causes significant depletion of fibrinogen due to the inactivation of factors Va and VIIIa.
Fibrinogen depletion is further compounded by increased fibrinolysis due to APC’s ability to inhibit the effects of plasminogen activator inhibitor (PAI). APC’s link to ATC has been confirmed via various studies and with elevated APC levels being consistent with ATC and crucially elevated APC results being associated with a higher mortality rate than patients who had suffered trauma without high APC levels.