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论文范文
1. Introduction Bleeding contributes to about one-third of trauma-related deaths [1]. It is a major contributing factor to other causes of death such as head injury and multiorgan failure in trauma patients [2]. In a retrospective cohort study conducted at level I trauma center in Toronto, massive bleeding resulting from blunt pelvic injury was the leading cause of preventable death among trauma patients [3]. Coagulopathy is one component of the lethal triad of trauma, in addition to hypothermia and acidosis. In the setting of massive bleeding, trauma-related coagulopathy occurs through a myriad of mechanisms, including consumption and subsequent acute deficiency of clotting factors and platelets, concomitant acidosis, hypothermia and dysregulation of mediatory pathways leading to fibrinolysis, and systemic activation of thrombin [4]. The activation of fibrinolysis accompanying the massive generation of thrombin in the period immediately following trauma has been well described and is indicated by the elevated levels of D-dimers, fibrin split products, and plasmin-antiplasmin complexes found in the blood samples drawn from trauma patients on presentation [5]. Tranexamic Acid (TXA) is a synthetic lysine derivative that acts as a competitive inhibitor of plasminogen activation, whereas at higher concentration it acts as a noncompetitive inhibitor of plasmin. It is believed that its main action is to improve coagulation through stabilization of clot [6]. The CRASH-2 trial was an international randomized, placebo controlled trial of the early administration of TXA to bleeding trauma patients. CRASH-2 enrolled 20,211 patients from 274 hospitals in 40 countries. The investigators reported that all-cause mortality was significantly lower among patients who received TXA than in a placebo group (4.5% versus 16.0%; relative risk 0.91, 95% CI, 0.85–0.97; ), with number needed to treat (NNT) of 67, importantly, with no apparent increase in side effects [7]. Early treatment with TXA (within 1 hour of injury) significantly reduced the risk of death due to bleeding (5.3% in TXA group versus 7.7% in placebo group; RR 0.68; ). TXA given between 1 and 3 hours also reduced the risk of death due to bleeding (4.8% versus 6.1%; RR 0.79, ). TXA given after 3 hours seemed to increase the risk of death due to bleeding (4.4% versus 3.1%; RR 1.44, 0.004) [8]. Early administration of TXA may decrease mortality due to bleeding in trauma patients but late administration of TXA is less effective and could be harmful. The Military Application of Tranexamic Acid for Trauma Emergency Resuscitation (MATTERs) trial results showed an absolute reduction in mortality of 6.7% (14.4% in TXA group versus 28.1% in no TXA group; ), and number needed to treat (NNT) was 1 : 7. All patients in the MATTERs trial received blood transfusion: those who received TXA required less blood products [9]. MATTERs trial addressed some of the critiques of CRASH-2 trail including its use of civilian hospitals that lacked modern trauma systems, its lack of laboratory testing to determine coagulopathy, its inclusion of a small number of penetrating traumas, and, most importantly, its uncertainty concerning the need for an antifibrinolytic in a group in which only half required blood transfusion and an equally small amount required surgery [10]. In 2011, the US Army reviewed the evidence from the CRASH-2 trial and included TXA into its trauma treatment protocols [11]. A recent prospective cohort study of severely injured adult patients (injury severity score > 15) admitted to a civilian trauma system showed that TXA was independently associated with a reduction in multiorgan failure (odds ratio [OR] = 0.27, ) and was protective for adjusted all-cause mortality (OR = 0.16 CI: 0.03–0.86, ) among patients in shock. The authors concluded that TXA as part of a major hemorrhage protocol within a mature civilian trauma system provides outcome benefits specifically for severely injured shocked patients [12]. Tranexamic Acid (TXA) has been shown to reduce bleeding in many surgical and medical settings. Since the 1970s, its applications were expanded to dysfunctional uterine bleeding, refractory thrombocytopenia, hemophilia, and von Willebrand’s disease [13]. Tranexamic Acid (TXA) has been used effectively to reduce bleeding and the concomitant need for blood transfusions in nontrauma patients; for example, a systematic review of randomized trial showed that TXA reduced the number of patients receiving blood transfusion by third [13]. A meta-analysis of randomized controlled trials suggested that TXA might reduce the amount of blood transfusions in patients undergoing total knee replacement [14]. Two other randomized controlled trials suggested a benefit of TXA in patients undergoing liver transplantation and cesarean sections [15, 16]. Despite all the current evidence supporting its use in these settings, TXA is underutilized. We aimed to better understand why this is so by surveying the opinions of providers who deal directly with trauma patients, trauma surgeons and emergency physicians in the states of Maryland. 
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