Extracorporeal (veno-venous) membrane oxygenation (vvECMO) has been shown to have negative effects on platelet number and function. This study aimed to gain more information about the impact of vvECMO on platelet function assessed by multiple electrode aggregometry (MEA). Twenty patients with the indication for vvECMO were included. Platelet function was analyzed using MEA (Multiplate®) before (T-1), 6 h (T0), one (T1), two (T2), three (T3), and seven (T4) days after the beginning of vvECMO. Median aggregational measurements were already below the normal reference range before vvECMO initiation. Platelet aggregation was significantly reduced 6 h after vvECMO initiation compared to T-1 and spontaneously recovered with a significant increase at T2. Platelet count dropped significantly between T-1 and T0 and continuously decreased between T0 and T4. At T4, ADP-induced platelet aggregation showed an inverse correlation with the paO2 in the oxygenator. Platelet function should be assessed by MEA before the initiation of extracorporeal circulation. Although ECMO therapy led to a further decrease in platelet aggregation after 6 h, all measurements had recovered to baseline on day two. This implies that MEA as a whole blood method might not adequately reflect the changes in platelet function in the later stages of extracorporeal circulation.

Direct complications in patients receiving extracorporeal (veno-venous) membrane oxygenation (vvECMO) are mainly either due to bleeding or thromboembolism. We aimed to evaluate the course of routine coagulation parameters and the activity of different coagulation factors—with special focus on factor XIII (F XIII)—before, during and after vvECMO in acute respiratory distress syndrome (ARDS) patients. The activity of coagulation factors and rotational thrombelastometry were analyzed in 20 ECMO patients before (T-1) and 6 h (T0), one (T1), three (T3) and seven days (T7) after the implantation, as well as one and three days after the termination of ECMO. F XIII activity was already severely decreased to 37% (30/49) before ECMO. F XIII activity was the only coagulation factor continuously declining during vvECMO, being significantly decreased at T3 (31% (26/45) vs. 24% (18/42), p = 0.0079) and T7 (31% (26/45) vs. 23% (17/37), p = 0.0037) compared to T0. Three days after termination of vvECMO, platelet count and fibrinogen nearly doubled and factors II, V, XI and XIII showed spontaneous significant increases. Severe ARDS patients showed a considerably diminished factor XIII activity before vvECMO initiation and its activity continuously declined later on. Thus, incorporation of F XIII monitoring into the regular hemostaseologic routine during vvECMO therapy seems advisable. Due to the potential development of a hypercoagulatory state after the termination of vvECMO, tight hemostasiologic monitoring should persist in the initial phase after ECMO termination.