Predictably, disorders of hemostasis exacerbate hemorrhage and significantly complicate resuscitation. Dilution of platelets and coagulation factors during resuscitation was previously considered to be the major cause of hemorrhage-associated coagulopathy (technically, resuscitation-associated coagulopathy). With the exception of transfusions exceeding one blood volume (approximately 10–12 units), however, and in the absence of hypothermia and acidosis, the effect of resuscitation-induced hemodilution on coagulation is inconsequential. Clotting factors do decline in the bleeding patient, but this decline is often out of proportion to the reduction that can be attributed to dilution alone. In trauma patients, several specific hemostatic defects have been identified that are detectable in approximately 25%–56% of patients prior to resuscitation. These bleeding diatheses are collectively referred to as trauma-induced coagulopathy, acute coagulopathy of trauma, acute traumatic coagulopathy, or trauma-associated coagulopathy. Trauma-associated coagulopathy (TAC) is an independent predictor of adverse outcomes such as prolongation of I.C.U. and hospital lengths of stay, as well as a four-fold increase in mortality. The recognition of coagulopathy at admission is crucial in that this abnormality predicts a subsequent transfusion requirement and informs the decision to proceed with DCR