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Unanswered questions in the use of blood component therapy in traumaAbstract: As outlined by Dries [1], recent advances in our approach to blood component therapy in traumatic hemorrhage have resulted in a reassessment of many of the tenants of management which were considered standards of therapy for many years. Indeed, despite the use of damage control techniques, the mortality from trauma induced coagulopathy has not changed significantly over the past 30 years [2,3]. More specifically, a resurgence of interest in postinjury hemostasis has generated controversies in three primary areas: 1) The pathogenesis of trauma induced coagulopathy 2) The optimal ratio of blood components administered via a pre-emptive schedule for patients at risk for this condition, ("damage control resuscitation"), and 3) The appropriate use of monitoring mechanisms of coagulation function during the phase of active management of trauma induced coaguopathy, which we have previously termed "goal directed therapy". Accordingly, recent experience from both military [2] and civilian centers[3] have begun to address these controversies, with certain management trends emerging which appear to significantly impact the way we approach these patients.Coagulation disturbances following trauma appear to follow a trimodal pattern, with an immediate hypercoagulable state, followed quickly by a hypocoagulable state, and ending with a return to a hypercoagulable state. An improved understanding of the early hypocoagulable state, or "trauma induced coagulopathy", has received particular attention over recent years. This state was traditionally believed to be the consequence of clotting factor depletion (via both hemorrhage and consumption), dilution (secondary to massive resuscitation), and dysfunction (due to both acidosis and hypothermia). However, recent evidence documents the presence of a coagulopathy prior to fluid resuscitation and in the absence of the aforementioned parameters [4,5]. Specifically, coagulopathy was observed only in the presence of hypoperfusion (base defic
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