Vervloet M G, Thijs L G, Hack C E
Medical Intensive Care Unit of the University Hospital VU Amsterdam, The Netherlands.
Semin Thromb Hemost. 1998;24(1):33-44. doi: 10.1055/s-2007-995821.
In patients with sepsis and septic shock, both coagulation and fibrinolysis are activated frequently leading to the syndrome of diffuse intravascular coagulation (DIC). The different mechanisms leading to abnormalities in coagulation and fibrinolysis are discussed in detail. The coagulation and fibrinolytic system appear to be influenced by the septic process largely independently, leading to a procoagulant imbalance between these systems. Coagulation is initiated by mediator-induced expression of tissue factor and is associated with consumption of the natural coagulation inhibitors antithrombin III, protein C, and protein S. As a result, high plasma levels of thrombin-antithrombin complex (TAT) can be found. The effects on fibrinolysis are dominated by (highly) increased levels of plasminogen activator inhibitor type 1 (PAI-1), leading to inadequate fibrinolysis. Although levels of plasminogen activator antigen are increased, its activity is almost completely inhibited by PAI-1. The resulting effects predispose to a procoagulant state, with widespread fibrin deposition, which may be an important mechanism contributing to multiple organ failure. A thorough understanding of the pathophysiological mechanisms underlying the DIC-syndrome is a prerequisite for a rational approach and future therapy for this severe complication of sepsis.
在脓毒症和脓毒性休克患者中，凝血和纤溶均频繁激活，常导致弥散性血管内凝血（DIC）综合征。详细讨论了导致凝血和纤溶异常的不同机制。凝血和纤溶系统似乎在很大程度上独立地受到脓毒症过程的影响，导致这些系统之间出现促凝失衡。凝血由介质诱导的组织因子表达启动，并与天然凝血抑制剂抗凝血酶III、蛋白C和蛋白S的消耗有关。因此，可发现血浆中凝血酶 - 抗凝血酶复合物（TAT）水平升高。对纤溶的影响主要由1型纤溶酶原激活物抑制剂（PAI - 1）水平（高度）升高主导，导致纤溶不足。尽管纤溶酶原激活物抗原水平升高，但其活性几乎完全被PAI - 1抑制。由此产生的影响易导致促凝状态，伴有广泛的纤维蛋白沉积，这可能是导致多器官功能衰竭的重要机制。深入了解DIC综合征的病理生理机制是合理应对和治疗脓毒症这一严重并发症的前提。
