Zeerleder Sacha, Hack C Erik, Wuillemin Walter A
Central Hematology Laboratory, University Hospital, Berne, Switzerland.
Chest. 2005 Oct;128(4):2864-75. doi: 10.1378/chest.128.4.2864.
Disseminated intravascular coagulation is a frequent complication of sepsis. Coagulation activation, inhibition of fibrinolysis, and consumption of coagulation inhibitors lead to a procoagulant state resulting in inadequate fibrin removal and fibrin deposition in the microvasculature. As a consequence, microvascular thrombosis contributes to promotion of organ dysfunction. Recently, three randomized, double-blind, placebo-controlled trials investigated the efficacy of antithrombin, activated protein C (APC), and tissue factor pathway inhibitor, respectively, in sepsis patients. A significant reduction in mortality was demonstrated in the APC trial. In this article, we first discuss the physiology of coagulation and fibrinolysis activation. Then, the pathophysiology of coagulation activation, consumption of coagulation inhibitors, and the inhibition of fibrinolysis leading to a procoagulant state are described in more detail. Moreover, therapeutic concepts as well as the three randomized, double-blind, placebo-controlled studies are discussed.
弥散性血管内凝血是脓毒症常见的并发症。凝血激活、纤维蛋白溶解抑制以及凝血抑制剂的消耗导致促凝状态，致使纤维蛋白清除不足并在微血管中沉积。因此，微血管血栓形成促使器官功能障碍。最近，三项随机、双盲、安慰剂对照试验分别研究了抗凝血酶、活化蛋白C（APC）和组织因子途径抑制剂在脓毒症患者中的疗效。APC试验显示死亡率显著降低。在本文中，我们首先讨论凝血和纤维蛋白溶解激活的生理学。然后，更详细地描述凝血激活的病理生理学、凝血抑制剂的消耗以及导致促凝状态的纤维蛋白溶解抑制。此外，还讨论了治疗理念以及三项随机、双盲、安慰剂对照研究。
