Trauma-induced coagulopathy

Uncontrolled hemorrhage is a major preventable cause of death in trauma, the latter accounting for 9% of global deaths. There is no agreed definition of trauma-induced coagulopathy (TIC), the term is used to describe abnormal coagulation attributable to trauma. Early TIC occurs within 6 hours of injury and is characterized by hypocoagulability resulting in bleeding; whereas late TIC represents a hypercoagulable state associated with thromboembolic events and multiple organ failure. Research into pathophysiological mechanisms have recognized that acute blood loss, metabolic acidosis, endothelial activation, immune system of activation, platelet activation, and traumatic brain injury account for the diverse phenotypes of TIC. Multiple haemostatic abnormalities have been described including fibrinogen depletion, inadequate thrombin
generation, platelet dysfunction, dysregulated fibrinolysis, and endothelial dysfunction resulting in various phenotypes.Diagnosis is made by detecting abnormalities in viscoelastic haemostatic assays (VHA) or coagulation screening especially prolonged prothrombin times. Management priorities are controlling blood loss and reversing shock with balanced ratios of blood products; alongside prehospital tranexamic acid in long transport or austere environments. There is no international agreement on the composition of initial blood components for presumed TIC. For those who survive, there are high rates of morbidity especially in those with traumatic brain injury, which dominates short and long term quality of life and functional outcome.