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.

In the use of hypothermia in cardiac surgery an increased risk of bleeding is noticeable intra- and postoperatively. So far, the effects on coagulation and platelets caused by complex interactions between the extracorporeal circulation (ECC), surgical trauma and the effects of hypothermia prevent a clinical investigation of the cause of hypothermia associated bleeding in cardiac surgery. Methods: Using a Chandler-Loop blood flow model the effects of hypothermia could be studied under in-vitro conditions isolated from other competing factors. In the experimental group blood samples of three adult probands were cooled down from 37 °C to 28 °C and reheated at standardized temperature and flow conditions. During the measurements blood samples were taken at four checkpoints from the Chandler-Loops. A normothermic series of measurements served as a control group. Coagulation was examined using thrombelastometry and platelet function using impedance aggregometry. Results: Hypothermia irregularly caused a reduced coagulation; however, the platelet function seemed to be unaffected or only reversibly affected. Therefore, a decreased platelet function associated to hypothermia could not be detected via impedance aggregometry. In both groups the effects caused by the circulation in the Chandler-Loops on coagulation and platelet function were more pronounced than the effects caused by hypothermia. Discussion: The effects of hypothermia on coagulation seem to be not as pronounced and uniform as in other studies described. It is instead to assume that only specific components are impaired by cooling whereas the rotation in the Chandler-Loops always leads to measurable contact reactions. The results of the thrombelastomtry indicate that the cause for an impaired coagulation under hypothermia are reduced protein kinetics and a decreased platelet function. The reversible effects of hypothermia on platelets may account for the lack of measurable alterations in platelet function when using the Multiplate method. This being the case hypothermia caused impairment of platelet function could not be detected using the Multiplate method under clinical conditions.