Trauma-induced coagulopathy (TIC) is a recently described condition which traditionally has been diagnosed by the common coagulation tests (CCTs) such as prothrombin time/international normalized ratio (PT/INR), activated partial thromboplastin time (aPTT), platelet count, and fibrinogen levels. The varying sensitivity and specificity of these CCTs have led trauma coagulation researchers and clinicians to use Viscoelastic Tests (VET) such as Thromboelastography (TEG) to provide Targeted Thromboelastographic Hemostatic and Adjunctive Therapy (TTHAT) in a goal directed fashion to those trauma patients in need of hemostatic resuscitation. This review describes the utility of VETs, in particular, TEG, to provide TTHAT in trauma and acquired non-trauma-induced coagulopathy.Keywords: Thromboelastography, point-of-care, acquired coagulopathy, blood component therapy, systemic hemostatic agents, trauma-induced coagulopathy, hemostatic resuscitation, tranexamic acid, targeted pharmacologic therapy.
TRAUMA INDUCED COAGULOPATHY AND AC-QUIRED COAGULOPATHY
IntroductionCoagulopathy is found in approximately 25% of severely injured trauma patients on admission to the emergency department (ED). Patients with Trauma-Induced Coagulopathy (TIC) are at a higher risk for increased transfusion requirements and death compared to those without TIC [1][2][3][4][5]. The etiology of TIC has been a matter of speculation. Trauma induced disturbances of compensatory activation of activated protein C (APC), hypofibrinogenemia, Tissue Factor (TF) release, coagulation factor consumption and dilution, platelet dysfunction, and fibrinolysis have been cited as possible causes of TIC [1][2][3][4][5][6][7][8][9]. In addition, it has been argued by Gando and others that TIC is a variant of disseminated intravascular coagulation [10,11]. Most recently, Dobson et al. have described the etiology of TIC in relation to four paradigms of hemostatic derangement which are: 1) the DIC/ consumption/ fibrinolysis hypothesis 2) the activated protein-C hypothesis 3) the glycocalyx hypothesis and 4) the "fibrinogencentric" hypothesis. These hypotheses are not mutually exclusive. It is necessary to refer to this theoretical aspect of