[Trauma-induced coagulopathy--mechanisms and state of the art treatment]

Uncontrolled bleeding is a major cause for early death in both military and civilian trauma. The process of massive bleeding which begins as "surgical bleed" from injured vessels may rapidly evolve into a complex coagulopathy that can be detected early, sometimes within minutes of injury. The magnitude of coagulopathy is directly related to the severity of the injury and its presence is also an independent predictor of early mortality. Therefore, an early "hemostatic resuscitation" is now the "state of the art" in trauma management. Combined mechanisms contribute to the complex coagulopathy as described herein: excessive consumption of coagulation factors and platelets, dilutional coagulopathy due to administration of large volumes of fluids, especially high molecular solutions such as Hydroxyethyl starch (HES); the use of multiple red blood cells (RBC) transfusion without sufficient fresh frozen plasma (FFP) and platelets; acidosis that markedly attenuates thrombin generation and platelets function; hypothermia that slows down enzymatic reactions and platelets function and hyperfibrinolysis which accelerates the degradation of fibrin and might cause platelet dysfunction. An important breakthrough was the understanding that abnormal coagulation tests early in the process of trauma are not the consequences of disseminated intravascular coagulation (DIC). Supported by these new data, an aggressive approach to hemostatic resuscitation was developed which is based on the following principles: permissive hypotension to avoid "dilutional" coagulopathy, awareness of the prevention of hypothermia and acidosis and the use of hemostatic agents such as rFVIIa, fibrinogen concentrate and tranexamic acid early in the course of trauma. Importantly, the common practice of blood component therapy was revised and it is recommended that RBC, FFP and platelets will be transfused early and preferably in 1:1:1 ratio.