Universitätsklinikum Gießen und Marburg GmbH, Klinik für Herz-, Kinderherz- und Gefäßchirurgie, Gießen, Germany.
Medical and Life Sciences, Hochschule Furtwangen, Villingen-Schwenningen, Germany.
Clin Hemorheol Microcirc. 2024;87(1):1-11. doi: 10.3233/CH-229105.
COVID-19 causes a considerable degradation of pulmonary function to the point of an acute respiratory distress syndrome (ARDS). Over the course of the disease the gas exchange capability of the lung can get impaired to such an extent that extracorporeal membrane oxygenation (ECMO) is needed as a life-saving intervention. In patients COVID-19 as well as ECMO may cause severe coagulopathies which manifest themselves in micro and macro thrombosis. Previous studies established D-dimers as a marker for critical thrombosis of the ECMO system while on admission increased D-dimers are associated with a higher mortality in COIVD-19 patients. It is therefore crucial to determine if COVID-19 poses an increased risk of early thrombosis of the vital ECMO system.
40 patients who required ECMO support were enrolled in a retrospective analysis and assigned into 2 groups. The COVID group consist of 20 COVID-19 patients who required ECMO support (n = 20), whereas 20 ECMO patients without COVID-19 were assigned to the control group. D-dimers, fibrinogen, antithrombin III (AT III), lactate dehydrogenase (LDH) and platelet count were analysed using locally weighted scatterplot smoothing and MANOVAs.
The analysis of both groups shows highly significant differences in the dynamics of hemostasis. The increase in D-dimers that is associated with thrombosis of the ECMO systems occurs in COVID-19 patients around 2 days earlier (p = 2,8115 10-11) while fibrinogen is consumed steadily. In the control group fibrinogen levels increase rapidly after ten days with a plateau phase of around five days (p = 1,407 10-3) . Both groups experience a rapid increase in AT III after start of support by ECMO (p = 5,96 10-15). In the COVID group platelet count decreased from 210 giga/l to 130 giga/l within eight days, while in the same time span in the control group platelets decreased from 180 giga/l to 105 giga/l (p = 1,1 10-15). In both groups a marked increase in LDH beyond 5000 U/l occurs (p = 3,0865 10-15).
The early increase in D-dimers and decrease in fibrinogen suggests that COVID-19 patients bear an increased risk of early thrombosis of the ECMO system compared to other diseases treated with ECMO. Additionally, the control group shows signs of severe inflammation 10 days after the start of ECMO which were absent in COVID-19 patients.
COVID-19 导致肺部功能严重下降,甚至发展为急性呼吸窘迫综合征(ARDS)。在疾病发展过程中,肺部的气体交换能力可能会严重受损,以至于需要体外膜氧合(ECMO)作为挽救生命的干预措施。在 COVID-19 患者中,ECMO 可能会导致严重的凝血障碍,表现为微血栓和大血栓。先前的研究表明 D-二聚体是 ECMO 系统严重血栓形成的标志物,而入院时 D-二聚体升高与 COVID-19 患者的死亡率升高有关。因此,确定 COVID-19 是否会增加 ECMO 系统早期血栓形成的风险至关重要。
本回顾性分析纳入了 40 名需要 ECMO 支持的患者,并将其分为两组。COVID 组包括 20 名需要 ECMO 支持的 COVID-19 患者(n=20),而对照组则包括 20 名没有 COVID-19 的 ECMO 患者。使用局部加权散点平滑和 MANOVAs 分析 D-二聚体、纤维蛋白原、抗凝血酶 III(AT III)、乳酸脱氢酶(LDH)和血小板计数。
两组的分析均显示出止血动力学的显著差异。与 ECMO 系统血栓形成相关的 D-二聚体升高在 COVID-19 患者中早出现约 2 天(p=2,8115×10-11),而纤维蛋白原则持续消耗。在对照组中,纤维蛋白原水平在 ECMO 支持后 10 天迅速升高,然后进入为期约 5 天的平台期(p=1,407×10-3)。两组在 ECMO 支持开始后 AT III 迅速增加(p=5,96×10-15)。COVID 组的血小板计数在 8 天内从 210 吉/升至 130 吉/,而对照组在同一时间内从 180 吉/降至 105 吉/(p=1,1×10-15)。两组的 LDH 均显著升高至 5000 U/l 以上(p=3,0865×10-15)。
与其他接受 ECMO 治疗的疾病相比,COVID-19 患者的 D-二聚体早期升高和纤维蛋白原降低表明其 ECMO 系统早期发生血栓形成的风险增加。此外,对照组在 ECMO 开始后 10 天出现明显的炎症迹象,而 COVID-19 患者则没有这些迹象。