Mechanisms of early trauma-induced coagulopathy

Abstract

Traumatic-induced coagulopathy (TIC) is a hemostatic disorder that is associated with significant bleeding, transfusion requirements, morbidity and mortality. A disorder similar or analogous to TIC was reported around 70 years ago in patients with shock, hemorrhage, burns, cardiac arrest or undergoing major surgery, and the condition was referred to as a "severe bleeding tendency," "defibrination syndrome," "consumptive disorder," and later by surgeons treating US Vietnam combat casualties as a "diffuse oozing coagulopathy." In 1982, Moore's group termed it the "bloody vicious cycle," others "the lethal triad," and in 2003 Brohi and colleagues introduced "acute traumatic coagulopathy" (ATC). Since that time, early TIC has been cloaked in many names and acronyms, including a "fibrinolytic form of disseminated intravascular coagulopathy (DIC)." A global consensus on naming is urgently required to avoid confusion. In our view, TIC is a dynamic entity that evolves over time and no single hypothesis adequately explains the different manifestations of the coagulopathy. However, early TIC is not DIC because an increased thrombin-generating potential in vitro does not imply a clinically relevant thrombotic state in vivo as early TIC is characterized by excessive bleeding, not thrombosis. DIC with its diffuse anatomopathologic fibrin deposition appears to be a latter phase progression of TIC associated with unchecked inflammation and multiple organ dysfunction.

Acute traumatic coagulopathy and trauma-induced coagulopathy: an overview

“…Therefore, the pathophysiologic mechanism of ATC has been emphasized as being different from that of DIC [13,27,41,54]. However, thrombin generation with marked decrease in fibrinogen and D-dimer elevation was observed [13,27,41,54], suggested to be consistent with the pathophysiology of DIC.…”

“…Almost all severely traumatized patients, especially those with ATC, are diagnosed as having DIC according to the scoring systems of the ISTH and Japanese Association for Acute Medicine [48,52,53]. However, no anatomopathologic evidence, e.g., intravascular formation of fibrin and thrombotic occlusion of vessels, has been demonstrated, and consumption coagulopathy leading to platelet and coagulation factor deficiency is not a common finding in patients with ATC [27].…”

“…Some researchers suggested that ATC is not a DIC because there is no clear evidence of diffuse anatomopathologic intravascular fibrin deposition and also because the "DIC hypothesis with a fibrinolytic phenotype" is a confusion of terms and should be abandoned. They suggested that a state in which fibrinolytic activity exceeds the capacity of the hemostatic system to make stable clots, resulting in excess or uncontrolled hemorrhage, should be termed systemic activation of fibrinolysis with poor hemostasis [27]. However, they misunderstand the concept of DIC, leading to inappropriate conclusion.…”

“…ATC that is caused by trauma-induced tissue injury and/or traumatic shock (generalized tissue hypoperfusion) presents as systemic activation of coagulation responses associated with increased fibrinolysis [19,26,27]. The clinical features of ATC can be summarized as follows [11,18,[28][29][30]:…”

Diverse coagulopathies in a rabbit model with different abdominal injuries

“…[6] Current studies have revealed that neurohormonal activation, systemic inflammation and widespread endothelial damage may similarly have an important influential role, and the etiology of traumarelated coagulopathy is multifactorial. [7,8] Much mystery still surrounds changes in coagulation taking place in the period after injury. This study developed a rabbit model of traumatic shock with abdominal injuries to characterize…”