Trauma-induced coagulopathy (TIC)

Trauma-induced coagulopathy (TIC) is a complex, multifaceted systemic response to severe injury characterized by an early impairment of the hemostatic system (Moore et al., 2021, Nature Reviews Disease Primers). It involves the depletion and dysfunction of plasma coagulation factors and platelets, driven by tissue injury and shock-induced hypoperfusion (StatPearls, 2023). A key mechanism is the activation of the Protein C pathway, which leads to the inactivation of Factors Va and VIIIa and the neutralization of plasminogen activator inhibitor-1, resulting in hyperfibrinolysis (Brohi et al., 2003, Journal of Trauma). Clinical management involves "damage control resuscitation" using blood products and antifibrinolytics like tranexamic acid, which was shown to reduce mortality in the CRASH-2 trial (Lancet, 2010). Because TIC is a systemic syndrome rather than a single molecular target, it is considered an "incorrect" target in the context of single-molecule drug discovery, representing instead a pathological state requiring multi-component therapy.

Other names

Acute traumatic coagulopathyATCTrauma-associated coagulopathyEarly coagulopathy of trauma

Therapeutic intervention involves the replacement of depleted coagulation factors and platelets, inhibition of hyperfibrinolysis via plasminogen activation blockade, and restoration of thrombin generation potential (Spahn et al., 2019, Critical Care).