Characteristics and treatment of coagulopathy associated with COVID-19

P. Miljić
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Abstract

Coagulopathy in COVID-19 represents a thrombo-inflammatory condition, and it is one of the most important causes of morbidity and mortality in this disease. The occurrence of coagulopathy correlates with the intensity of the inflammatory response to SARS-Cov-2 virus infection, and its presence is characterized by laboratory markers of blood hypercoagulability and clinically pronounced prothrombotic condition. Although the mechanism of coagulopathy is not fully elucidated, dysregulated and overemphasized immune responses mediated by inflammatory cytokines, complement activation, leukocyte activation with release of free nucleic acids and histones into the circulation, hypoxia and endothelial damage play a very important role in its development. Thrombosis can occur in all parts of the circulatory system and is most often localized in the microcirculation and venous part of the vasculature. A number of studies have shown that the presence of thrombotic pulmonary embolism can be demonstrated by objective methods in approximately 15% of COVID-19 patients treated in intensive care units, while the incidence of total venous thromboembolism in this group of patients is over 20% despite antithrombotic prophylaxis. Although much less common than venous thrombosis, arterial thrombosis may also occur in COVID-19 patients, most often in the form of myocardial infarction, ischemic stroke and peripheral artery occlusion. Damage to the endothelium under the influence of virus or inflammatory response, activation of platelets and coagulation system with fibrin deposition leads to extensive thrombosis in the microcirculation of lungs and other tissues and directly contributes to respiratory failure, ARDS or multiorgan failure. Therefore, coagulopathy in COVID-19 is an integral part of the pathophysiological mechanism of the disease and contributes to its clinical manifestation and progression. Main laboratory characteristics of COVID-19 coagulopathy are elevated values of D-dimer in the blood, which occurs in the process of decomposition of precipitated fibrin under the action of fibrinolytic enzymes in the microcirculation of the lungs and other organs. Therefore, D-dimer values reflect the intensity of the inflammation in the lungs and have prognostic significance in recognizing patients at risk of serious complications and unfavorable course of the disease. In contrast to disseminated intravascular coagulation in sepsis, severe thrombocytopenia and hypofibrinogenemia as well as bleeding tendencies are rare in COVID-19 coagulopathy. Due to the high frequency and important role of coagulopathy in morbidity and mortality, the use of anticoagulant therapy is recommended in all hospitalized patients. However, the optimal way of treating coagulopathy and the intensity of antithrombotic prophylaxis are not known, and represent the subject of intensive research.
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COVID-19相关凝血功能障碍的特点及治疗
COVID-19的凝血功能障碍是一种血栓炎性疾病,是该病发病和死亡的最重要原因之一。凝血功能障碍的发生与SARS-Cov-2病毒感染的炎症反应强度相关,其存在的特征是血液高凝性的实验室标志物和临床明显的血栓前状态。虽然凝血病的发病机制尚未完全阐明,但炎性细胞因子、补体活化、白细胞活化并释放游离核酸和组蛋白进入循环、缺氧和内皮损伤介导的免疫反应失调和过度强调在凝血病的发展中起着非常重要的作用。血栓形成可发生在循环系统的所有部位,最常局限于微循环和静脉部分的血管系统。多项研究表明,在重症监护病房治疗的约15%的COVID-19患者中,可以通过客观方法证明血栓性肺栓塞的存在,而尽管进行了抗血栓预防,但这组患者的总静脉血栓栓塞发生率仍超过20%。尽管动脉血栓形成比静脉血栓少得多,但在COVID-19患者中也可能发生动脉血栓形成,最常见的形式是心肌梗死、缺血性卒中和外周动脉闭塞。在病毒或炎症反应的影响下,内皮细胞受损,血小板和凝血系统被激活,纤维蛋白沉积导致肺等组织微循环广泛血栓形成,直接导致呼吸衰竭、ARDS或多器官衰竭。因此,COVID-19的凝血功能障碍是疾病病理生理机制的重要组成部分,是其临床表现和进展的重要组成部分。COVID-19凝血病的主要实验室特征是血液中d -二聚体的升高,这发生在肺等器官微循环中纤维蛋白沉淀在纤溶酶的作用下分解的过程中。因此,d -二聚体值反映了肺部炎症的强度,对识别有严重并发症风险和病程不利的患者具有预后意义。与脓毒症中的弥散性血管内凝血相反,严重的血小板减少症和低纤维蛋白原血症以及出血倾向在COVID-19凝血病中很少见。由于凝血病在发病率和死亡率中的高频率和重要作用,建议所有住院患者使用抗凝治疗。然而,治疗凝血功能障碍的最佳方法和抗血栓预防的强度尚不清楚,并代表了深入研究的主题。
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