Department of Haemostaseology and Hemophilia Center, Medical Clinic 2, Institute of Transfusion Medicine, University Hospital Frankfurt, Germany.
Department of Infection, Immunity and Cardiovascular Disease, University of Sheffield, United Kingdom.
Clin Appl Thromb Hemost. 2020 Jan-Dec;26:1076029620938149. doi: 10.1177/1076029620938149.
The novel coronavirus infection (COVID-19) is caused by the new coronavirus SARS-CoV-2 and is characterized by an exaggerated inflammatory response that can lead to severe manifestations such as adult respiratory syndrome, sepsis, coagulopathy, and death in a proportion of patients. Among other factors and direct viral effects, the increase in the vasoconstrictor angiotensin II, the decrease in the vasodilator angiotensin, and the sepsis-induced release of cytokines can trigger a coagulopathy in COVID-19. A coagulopathy has been reported in up to 50% of patients with severe COVID-19 manifestations. An increase in d-dimer is the most significant change in coagulation parameters in severe COVID-19 patients, and progressively increasing values can be used as a prognostic parameter indicating a worse outcome. Limited data suggest a high incidence of deep vein thrombosis and pulmonary embolism in up to 40% of patients, despite the use of a standard dose of low-molecular-weight heparin (LMWH) in most cases. In addition, pulmonary microvascular thrombosis has been reported and may play a role in progressive lung failure. Prophylactic LMWH has been recommended by the International Society on Thrombosis and Haemostasis (ISTH) and the American Society of Hematology (ASH), but the best effective dosage is uncertain. Adapted to the individual risk of thrombosis and the d-dimer value, higher doses can be considered, especially since bleeding events in COVID-19 are rare. Besides the anticoagulant effect of LMWH, nonanticoagulant properties such as the reduction in interleukin 6 release have been shown to improve the complex picture of coagulopathy in patients with COVID-19.
新型冠状病毒感染（COVID-19）由新型冠状病毒 SARS-CoV-2 引起，其特征为炎症反应过度，可导致部分患者出现成人呼吸窘迫综合征、败血症、凝血功能障碍和死亡等严重表现。除其他因素和直接病毒作用外，血管收缩素血管紧张素 II 增加、血管扩张素血管紧张素减少以及败血症引起的细胞因子释放，可引发 COVID-19 的凝血功能障碍。高达 50%的重症 COVID-19 患者出现凝血功能障碍。重症 COVID-19 患者凝血参数中最显著的变化是 D-二聚体增加，且逐渐升高的值可用作预后参数，提示预后不良。有限的数据表明，尽管大多数情况下使用标准剂量的低分子肝素（LMWH），但仍有高达 40%的患者发生深静脉血栓形成和肺栓塞的发病率较高。此外，据报道存在肺微血管血栓形成，这可能在进行性肺衰竭中发挥作用。国际血栓形成与止血学会（ISTH）和美国血液学会（ASH）建议预防性使用 LMWH，但最佳有效剂量尚不确定。根据血栓形成的个体风险和 D-二聚体值，可考虑使用较高剂量，尤其是因为 COVID-19 中的出血事件罕见。除了 LMWH 的抗凝作用外，还显示其非抗凝特性，如减少白细胞介素 6 的释放，可改善 COVID-19 患者凝血功能障碍的复杂情况。
