Disseminated intravascular coagulation in trauma injuries

Physical injuries, especially road traffic injuries, are a leading cause of death and morbidity worldwide, ranking fifth among the leading causes of death in the United States. Immediate and early trauma deaths are mainly determined by primary brain injuries and/or hemorrhages, whereas late mortality is caused by secondary brain injuries, host defense failure, and superimposed complications including also disseminated intravascular coagulation (DIC). Trauma patients are particularly susceptible to the early development of coagulopathy, and the most severely injured patients are coagulopathic on hospital admission. The zenith of the problem is typically seen in patients with head injuries and in those who are massively injured and transfused. The resulting coagulopathy is characterized by nonsurgical bleeding from mucosal lesions, serosal surfaces, and wound and vascular access sites. DIC associated with traumatic injury results from multiple independent but interplaying mechanisms, involving tissue trauma, shock, and inflammation. As such, the multifaceted derangement of hemostasis occurring after massive traumatic injuries, especially those involving the brain, is mainly sustained by release of procoagulants (fats, phospholipids) and constitutive tissue factor from the injured tissue into the circulation, associated with a systemic inflammatory response that also promotes tissue factor hyperexpression on monocytes and the other cells. The excessive, non-wound-related thrombin generation is insufficiently antagonized by physiological anticoagulant pathways and amplified by impaired endogenous fibrinolysis. The resulting burst of systemic thrombin generation, coupled with platelet hyperaggregability, shock, hypothermia, and tissue hypoperfusion, further contribute to the development of DIC and microvascular bleeding.