Influence of Covid-19 disease on hemostasis dynamics during extracorporeal membrane oxygenation (ECMO)1.

IF 2.1 4区 医学 Q3 HEMATOLOGY
D Rother, J Gehron, F Brenck, H Hudel, A Böning, F Wenzel
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引用次数: 0

Abstract

Introduction: 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.

Methods: 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.

Results: 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).

Conclusion: 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 疾病对体外膜氧合(ECMO)过程中止血动态的影响1。
简介COVID-19 会导致肺功能严重下降,甚至引发急性呼吸窘迫综合征(ARDS)。在病程中,肺部的气体交换能力会受损,以至于需要体外膜肺氧合(ECMO)来挽救生命。COVID-19 和 ECMO 可导致患者出现严重的凝血功能障碍,表现为微血栓和大血栓。先前的研究证实,D-二聚体是 ECMO 系统严重血栓形成的标志物,而入院时 D-二聚体的增加与 COIVD-19 患者死亡率的升高有关。因此,确定 COVID-19 是否会增加重要 ECMO 系统早期血栓形成的风险至关重要。COVID 组包括 20 名需要 ECMO 支持的 COVID-19 患者(n = 20),而 20 名没有 COVID-19 的 ECMO 患者被分配到对照组。使用局部加权散点图平滑法和 MANOVA 分析了 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:结果:对两组患者的分析表明,止血动态存在非常显著的差异。与 ECMO 系统血栓形成相关的 D-二聚体的增加在 COVID-19 患者中提前 2 天左右出现(p = 2,8115 10-11),而纤维蛋白原消耗稳定。在对照组中,纤维蛋白原水平在十天后迅速增加,并在五天左右达到稳定阶段(p = 1,407 10-3)。两组在开始使用 ECMO 支持后,AT III 均迅速增加(p = 5.96 10-15)。COVID 组的血小板计数在八天内从 210 千兆/升降至 130 千兆/升,而对照组的血小板计数在同一时间内从 180 千兆/升降至 105 千兆/升(p = 1,1 10-15)。两组患者的 LDH 都明显增加,超过 5000 U/l(p = 3,0865 10-15):结论:D-二聚体的早期增加和纤维蛋白原的减少表明,与其他使用 ECMO 治疗的疾病相比,COVID-19 患者 ECMO 系统早期血栓形成的风险增加。此外,对照组在 ECMO 开始 10 天后出现严重炎症迹象,而 COVID-19 患者则没有。
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来源期刊
CiteScore
4.30
自引率
33.30%
发文量
170
期刊介绍: Clinical Hemorheology and Microcirculation, a peer-reviewed international scientific journal, serves as an aid to understanding the flow properties of blood and the relationship to normal and abnormal physiology. The rapidly expanding science of hemorheology concerns blood, its components and the blood vessels with which blood interacts. It includes perihemorheology, i.e., the rheology of fluid and structures in the perivascular and interstitial spaces as well as the lymphatic system. The clinical aspects include pathogenesis, symptomatology and diagnostic methods, and the fields of prophylaxis and therapy in all branches of medicine and surgery, pharmacology and drug research. The endeavour of the Editors-in-Chief and publishers of Clinical Hemorheology and Microcirculation is to bring together contributions from those working in various fields related to blood flow all over the world. The editors of Clinical Hemorheology and Microcirculation are from those countries in Europe, Asia, Australia and America where appreciable work in clinical hemorheology and microcirculation is being carried out. Each editor takes responsibility to decide on the acceptance of a manuscript. He is required to have the manuscript appraised by two referees and may be one of them himself. The executive editorial office, to which the manuscripts have been submitted, is responsible for rapid handling of the reviewing process. Clinical Hemorheology and Microcirculation accepts original papers, brief communications, mini-reports and letters to the Editors-in-Chief. Review articles, providing general views and new insights into related subjects, are regularly invited by the Editors-in-Chief. Proceedings of international and national conferences on clinical hemorheology (in original form or as abstracts) complete the range of editorial features.
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