Division of Acute and Critical Care Medicine, Department of Anesthesiology and Critical Care Medicine, Hokkaido University Graduate School of Medicine, Kita-ku, Sapporo, Japan.
Ann Surg. 2011 Jul;254(1):10-9. doi: 10.1097/SLA.0b013e31821221b1.
A trauma patient's survival depends on the ability to control 2 opposing conditions, bleeding at the early phase and thrombosis at a late phase of trauma. The mixed existence of physiological responses for hemostasis and wound healing and pathological hemostatic responses makes it difficult to understand the mechanisms of the 2 stages of coagulopathy after trauma. Traumatic coagulopathy is multifactorial but disseminated intravascular coagulation (DIC) with the fibrinolytic phenotype is the predominant and initiative pathogenesis of coagulopathy at the early stage of trauma. High levels of inflammatory cytokines and severe tissue injuries activate the tissue-factor-dependent coagulation pathway followed by massive thrombin generation and its activation. Low levels of protein C and antithrombin induce insufficient coagulation control and the inhibition of the anticoagulation pathway. Primary and secondary fibrin(ogen)olysis is highly activated by the shock-induced tissue hypoxia and disseminated fibrin formation, respectively. Consumption coagulopathy and severe bleeding are subsequently observed in trauma patients. Persistently high levels of plasminogen activator inhibitor-1 expressed in the platelets and endothelium then change the DIC with the fibrinolytic phenotype into the thrombotic phenotype at approximately 24 to 48 hours after the onset of trauma. All of these changes coincide with the definition of DIC, which can be clearly distinguished from normal responses for hemostasis and wound healing by using sensitive molecular markers and DIC diagnostic criteria such as those outlined by the Japanese Association for Acute Medicine and the International Society on Thrombosis and Haemostasis. Treatments of DIC with the fibrinolytic phenotype involve the surgical repair of the trauma, improvement of shock, and the rapid and sufficient replacement of platelet concentrate, fresh frozen plasma, and depleted coagulation factors. The administration of an antifibrinolytic agent (tranexamic acid) may reduce the risk of death in bleeding trauma patients associated with this type of DIC.
创伤患者的生存取决于控制 2 种对立条件的能力，即在创伤早期控制出血，在晚期控制血栓形成。止血和伤口愈合的生理反应与病理性止血反应的混合存在，使得理解创伤后 2 个阶段的凝血障碍机制变得困难。创伤性凝血病是多因素的，但弥散性血管内凝血（DIC）伴纤维蛋白溶解表型是创伤早期凝血障碍的主要和起始发病机制。高水平的炎症细胞因子和严重的组织损伤激活组织因子依赖性凝血途径，随后大量生成凝血酶并激活。蛋白 C 和抗凝血酶水平降低导致凝血控制不足和抗凝途径抑制。休克引起的组织缺氧和弥散性纤维蛋白形成分别高度激活原发性和继发性纤维蛋白（原）溶解。随后在创伤患者中观察到消耗性凝血病和严重出血。持续高水平的纤溶酶原激活物抑制剂-1在血小板和内皮细胞中表达，然后在创伤发作后约 24 至 48 小时将 DIC 从纤维蛋白溶解表型转变为血栓形成表型。所有这些变化都与 DIC 的定义一致，可以通过使用敏感的分子标志物和 DIC 诊断标准（如日本急性医学协会和国际血栓形成和止血学会概述的标准）将其与止血和伤口愈合的正常反应清楚地区分开来。DIC 伴纤维蛋白溶解表型的治疗包括创伤的手术修复、休克的改善以及血小板浓缩物、新鲜冷冻血浆和消耗性凝血因子的快速和充分替代。使用抗纤维蛋白溶解剂（氨甲环酸）治疗可能会降低与这种 DIC 相关的出血性创伤患者的死亡风险。
