Utility of thromboelastography in traumatic brain injury and the neuroscience intensive care unit

Introduction Hemorrhage in trauma patients, despite damage control surgery, is responsible for up to 40% of trauma-related deaths and increased morbidity in traumatic brain injury (TBI). Current theory proposes that the initial tissue injury, hypoperfusion, accelerated fibrinolysis, and inflammatory mediated responses are the most likely culprits in trauma-induced coagulopathy. Interactions between thrombin, fibrinogen, platelets, protein clotting factors, calcium ions, inflammatory mediators, and endothelium contribute to systemic coagulopathy present in the trauma population. In addition, coagulopathy in the setting of hypothermia, acidosis, clotting factor depletion, and dilutional effects of trauma resuscitation compromise the body's ability to achieve homeostasis and place the trauma patient at significant risk for thromboembolic events (Gonzalez, Pieracci, Moore, & Kashuk, 2010). Coagulopathy is associated with an estimatedfivefold increase in mortality, and 25% of trauma patients are coagulopathic on admission (Toker, Hak, & Morgan, 2011). Coagulopathy is an independent predictor of morbidity and mortality in isolated TBI (Davis et al., 2013). Over the years, coagulopathy in TBI has been consistently identified by derangements in the standard coagulation studies of prothrombin time, international normalized ratio, activated partial thromboplastin time, and platelet counts, but these tests were not developed to adequately assess the coagulopathy (Davis et al., 2013). Thromboelastography (TEG) is more precise in identifying the exact derangements of hemostasis compared to conventional methods, especially when they fail to detect the coagulopathy. TEG is superior to prothrombin time, international normalized ratio, activated partial thromboplastin time, and other conventional coagulation laboratory tests in identifying coagulopathy and thrombin activity, and TEG has the ability to differentiate between enzymatic and platelet coagulopathy (Gonzalez, Kashuk, Moore, & Silliman, 2010). It provides information on clot initiation, clot growth, final clot strength, and presence of fibrinolytic clot breakdown, giving a global evaluation of all phases of the coagulation cascade (Schochl et al., 2011).