Gando S
Division of Acute and Critical Care Medicine, Department of Anesthesiology and Critical Care Medicine, Hokkaido University Graduate School of Medicine, Sapporo, Japan.
Semin Thromb Hemost. 2001 Dec;27(6):585-92. doi: 10.1055/s-2001-18864.
Disseminated intravascular coagulation (DIC) is characterized by the in vivo activation of the coagulation system, which results in the intravascular deposition of fibrin and consumption bleeding. DIC is a serious hemostatic complication of trauma. It can be clearly distinguished from physiological hemostatic response to trauma by using sensitive coagulofibrinolytic molecular markers. Physiological hemostasis to injuries is similar in all kinds of trauma without exception. There is an increase in circulating proinflammatory cytokines in DIC patients after trauma. Elevated cytokines induce tissue factor-mediated activation of coagulation, suppression of the anticoagulant pathway, and plasminogen activator inhibitor-1 (PAI-1)-mediated inhibition of fibrinolysis followed by disseminated fibrin deposition in the microvasculature. In addition to the occlusive microvascular thrombosis and hypoxia, sustained systemic inflammatory response characterized by neutrophil activation and endothelial damage plays a pivotal role in the development of multiple organ dysfunction syndrome (MODS) in posttrauma DIC patients. DIC associated with sustained systemic inflammatory response syndrome (SIRS) after trauma leads to the development of MODS, which is the main determinant of patients' outcome after trauma.
弥散性血管内凝血（DIC）的特征是体内凝血系统被激活，导致纤维蛋白在血管内沉积并引发消耗性出血。DIC是创伤严重的止血并发症。通过使用敏感的凝血纤溶分子标志物，可将其与创伤的生理性止血反应明确区分开来。各种创伤的生理性止血反应毫无例外都是相似的。创伤后DIC患者循环中的促炎细胞因子会增加。升高的细胞因子会诱导组织因子介导的凝血激活、抗凝途径的抑制以及纤溶酶原激活物抑制剂-1（PAI-1）介导的纤维蛋白溶解抑制，随后在微血管中出现弥散性纤维蛋白沉积。除了闭塞性微血管血栓形成和缺氧外，以中性粒细胞激活和内皮损伤为特征的持续全身炎症反应在创伤后DIC患者多器官功能障碍综合征（MODS）的发生发展中起关键作用。创伤后与持续性全身炎症反应综合征（SIRS）相关的DIC会导致MODS的发生，而MODS是创伤患者预后的主要决定因素。
