TIC can manifest as a spectrum of phenotypes from hypocoagulation to hypercoagulation (Fig. The term TIC was established during the Trans-Agency Consortium for Trauma Induced Coagulopathy Workshop conducted by the National Institutes of Health in April 2010 to describe the variety of phenomena that characterize this condition. Furthermore, not all patients with abnormalities in laboratory coagulation tests are bleeding 14.ĭespite the long-term fascination with changes in coagulation resulting from shock and tissue injury 15, there is no standard definition of TIC, which refers to abnormal coagulation capacity attributable to trauma. The remaining ongoing quagmire is the inability to distinguish between patients with exsanguinating injuries whose TIC is the result of metabolic failure (that is, who are bleeding because they are dying) from patients whose TIC is the cause of the ongoing blood loss (that is, who are dying because they are bleeding) 13.
#TRAUMA TRIAD OF DEATH DRIVERS#
However, early endogenous drivers of coagulopathy were not specifically investigated until 1982, when a case series of patients with major abdominal vascular injuries highlighted TIC as a common direct cause of early post-injury mortality: 89% of the deaths were bleeding-related, yet half occurred after mechanical control of bleeding sites - in other words, they were due to coagulopathy 12. Impaired coagulation following sudden death from injury has been observed for centuries 10 and, in the 1960s, the first clinical laboratory documentation of the temporal changes in coagulation following severe injury were documented 11. Consequently, there is intense interest worldwide in the pathogenesis of trauma-induced coagulopathy (TIC) to attenuate its adverse effects on the outcomes of seriously injured patients. Early preventable deaths after injury in civilian 2 and military 3 settings are primarily attributable to uncontrolled haemorrhage 2, 3, 4, 5, 6, 7, 8, whereas later preventable deaths are typically due to hypercoagulability 9.
Moreover, the burden is highest in individuals <50 years of age, among whom injury as a cause of death is second only to infectious diseases. Injury is the fourth leading cause of mortality worldwide, accounting for 9% of deaths globally (4.9 million people) in 2016 (ref. Survivors of TIC experience high rates of morbidity, which affects short-term and long-term quality of life and functional outcome. Tranexamic acid is used in pre-hospital settings selectively in the USA and more widely in Europe and other locations. Various blood products can be used in resuscitation however, there is no international agreement on the optimal composition of transfusion components. Management priorities are stopping blood loss and reversing shock by restoring circulating blood volume, to prevent or reduce the risk of worsening TIC. Laboratory diagnosis is based on coagulation abnormalities detected by conventional or viscoelastic haemostatic assays however, it does not always match the clinical condition. Haemostatic abnormalities include fibrinogen depletion, inadequate thrombin generation, impaired platelet function and dysregulated fibrinolysis. Traumatic brain injury also has a distinct role in TIC. Several pathophysiological mechanisms underlie TIC tissue injury and shock synergistically provoke endothelial, immune system, platelet and clotting activation, which are accentuated by the ‘lethal triad’ (coagulopathy, hypothermia and acidosis). In the early hours of TIC development, hypocoagulability is typically present, resulting in bleeding, whereas later TIC is characterized by a hypercoagulable state associated with venous thromboembolism and multiple organ failure. Trauma-induced coagulopathy (TIC) describes abnormal coagulation processes that are attributable to trauma.
Uncontrolled haemorrhage is a major preventable cause of death in patients with traumatic injury.
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