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It is clear that in the past decade, we have come to realize that the coagulation disturbance in trauma patients is more than just the result of consumption of clotting factors at sites of injury and dilution from the infusion of intravenous (IV) fluids and red blood cells (RBCs). Hence, it is clear that the infusion of plasma alone in the management of severely injured trauma patients with coagulopathic-type http://www.selleckchem.com/products/obeticholic-acid.html bleeding is likely to be insufficient to achieve hemostasis. The known coagulation disturbances and their potential treatments in massive hemorrhage are detailed in Table?1. It is extremely likely that throughout resuscitation of the massively bleeding patient, the predominant mechanism for coagulopathy may change over time as a result of therapy and/or the hemostatic response to injury. Hence, for us to truly understand this process, we will need serial measurements throughout resuscitation to fully understand what is happening to the coagulation variables of the massively bleeding patient. It is also true that therapy will need to be individualized��patients with differing injuries and at different points in the resuscitation process will need different therapies. In 2003, Brohi and colleagues5 analyzed a cohort of 1088 trauma patients transported to hospital http://www.selleckchem.com/products/Adriamycin.html by helicopter and found that 24% had a coagulopathy (defined as a prothrombin time of >18?sec, an activated partial thromboplastin time of >60?sec, or a thrombin time of >15?sec). Patients presenting with these abnormal laboratory test results had a higher rate of death (46% vs. 11%, p? http://www.selleck.cn/products/sch772984.html factors in this process. These findings support development of coagulopathy in some patients before therapeutic intervention. Several studies have confirmed that severely injured trauma patients have activation of the protein?C pathway as shown in Fig.?1 resulting in an ��anticoagulant�� effect.6-8 A prospective cohort study of 203 major trauma patients found that patients with tissue hypoperfusion and severe injury had activation of protein?C, with subsequent inactivation of Factor (F)V and FVIII and derepression of fibrinolysis.8 Protein?C is activated by thrombin, thrombomodulin, and endothelial protein?C receptor. Hypoperfusion is believed to result in increased expression of thrombomodulin on the surface of endothelial cells. The thrombomodulin binds thrombin and the complex activates protein?C.