Department of Medicine, University College London Hospitals NHS Foundation Trust, London, UK.
Cardiometabolic Programme-NIHR UCLH/UCL BRC, London, UK.
Int J Lab Hematol. 2018 May;40 Suppl 1:15-20. doi: 10.1111/ijlh.12830.
Several clinical conditions, in particular those associated with a systemic inflammatory response, can cause some degree of activation of coagulation but when the procoagulant stimulus is sufficiently severe and overcomes the natural anticoagulant mechanisms of coagulation, disseminated intravascular coagulation (DIC) may occur. The clinical manifestations of DIC encompass multiorgan dysfunction caused by fibrin-platelet clots in the microcirculation, and bleeding caused by consumption of platelets and coagulation factors. Molecular mechanisms that play a role in inflammation-induced effects on coagulation have been recognized in much detail. Exposure of blood to tissue factor is the most common trigger, whereas the intravascular coagulation is propagated due to loss of function of physiological anticoagulants and impaired fibrinolysis. In patients with DIC, various abnormalities in routine coagulation parameters may be observed, including thrombocytopenia, prolonged global coagulation assays, or high levels of fibrin split products. In addition, more sophisticated tests for activation of individual factors or pathways of coagulation may point to specific involvement of these components in the pathogenesis of the disorder. A combination of readily available tests is usually sufficient in establishing the diagnosis of DIC, and for this purpose, several scoring algorithms have been developed. Some specific clinical situations may elicit coagulation responses that can be distinguished from DIC or may occur in combination with DIC, including dilutional coagulopathy, liver failure-related coagulation derangement, and thrombotic microangiopathies.
多种临床情况，特别是与全身性炎症反应相关的情况，可能导致一定程度的凝血激活，但当促凝刺激足够严重并克服凝血的天然抗凝机制时，可能会发生弥散性血管内凝血（DIC）。DIC 的临床表现包括由微循环中的纤维蛋白-血小板凝块引起的多器官功能障碍，以及由血小板和凝血因子消耗引起的出血。在炎症引起的凝血影响中发挥作用的分子机制已经得到了详细的认识。血液暴露于组织因子是最常见的触发因素，而由于生理抗凝剂功能丧失和纤溶受损，导致血管内凝血传播。在 DIC 患者中，常规凝血参数可能观察到各种异常，包括血小板减少症、全血凝血时间延长或纤维蛋白降解产物水平升高。此外，针对凝血个别因子或途径激活的更复杂测试可能表明这些成分在疾病发病机制中的特定参与。通常，结合使用几种易于获得的测试即可充分建立 DIC 的诊断，为此目的，已经开发了几种评分算法。某些特定的临床情况可能会引发不同于 DIC 的凝血反应，或者可能与 DIC 同时发生，包括稀释性凝血障碍、肝衰竭相关的凝血紊乱和血栓性微血管病。
