Disseminated intravascular coagulation

Abstract

Following trauma, local hemostasis and thrombosis act to induce physiological wound healing and innate immune responses, respectively, to impede the dissemination of damage-associated molecular patterns (DAMPs) and thrombin into the systemic circulation. However, if overwhelmed by systemic inflammation caused by extensive tissue damage and tissue hypoperfusion, both of these processes cause pathologic changes, which manifest as systemic disseminated intravascular coagulation (DIC). High levels of DAMPs and inflammatory cytokines activate both extrinsic and intrinsic coagulation pathways. Impaired anticoagulation pathways induce insufficient control of coagulation, leading to systemic thrombin generation and ultimately consumption coagulopathy. Fibrin(ogen)olysis due to tissue-type plasminogen activator is highly active in the early phase of trauma due to endothelial hypoperfusion and hypoxia in DIC with the fibrinolytic phenotype, contributing to the oozing-type coagulopathic bleeding. Persistently high levels of plasminogen activator inhibitor-1 expressed in the endothelium change DIC with the fibrinolytic phenotype into the thrombotic phenotype, which is followed by microvascular thrombosis and then multiple organ dysfunction syndrome. The activation of coagulation and insufficient anticoagulation mechanisms underlie both types of DIC. DIC should be diagnosed by DIC scoring systems, and key to managing DIC is treating the trauma itself and hemorrhagic shock. The mechanisms of hemostatic changes in trauma are multifactorial; the coexistence of exogenously-iduced anemia, hypothermia, acidosis, and dilution aggravate DIC. As such, trauma-induced coagulopathy consists of a trauma itself-induced primary pathology, i.e., DIC, and exogenously induced secondary pathologies. Trauma itself-induced primary DIC is the core disease state of trauma-induced coagulopathy.