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Extracorporeal life support is an increasingly used technique for respiratory and cardiocirculatory support. Besides primary organ dysfunction, an excessive systemic hyperinflammatory response can be the underlying cause for acute organ failure necessitating extracorporeal life support therapy, or it may be associated with the extracorporeal life support itself. Controlling this overwhelming inflammatory response using CytoSorbIn this retrospective case series, we describe 23 patients undergoing extracorporeal life support therapy and CytoSorb hemoadsorption. Cytokine levels were monitored, hemodynamic and metabolic variables were recorded, and outcome measures such as duration of organ support, intensive care unit mortality, and hospital mortality were noted.CytoSorb treatment was associated with a trend toward a reduction in plasma cytokine levels (first treatment median interleukin-6 pre 595 vs post 350 pg/mL (n.s.); second treatment median interleukin-6 317 vs 108 pg/mL, p 0.05), a reduced vasoplegic response resulting in a reduction in vasopressor requirements (first treatment median norepinephrine pre 0.15 vs post 0.02 µg/kg/min (n.s.); second treatment median norepinephrine 0.1 vs 0.02 µg/kg/min, p 0.05) as well as rebalancing of deranged metabolic parameters (first treatment median lactate pre-treatment 6 vs post-treatment median lactate 2 mmol/L, p 0.05). The hemoperfusion treatment was well tolerated and safe, without the occurrence of any CytoSorb device-related adverse events.Hemoadsorption may offer a potentially promising therapeutic option for critically ill patients undergoing extracorporeal life support therapy, with cytokine reduction and a consecutively mitigated inflammatory response, decreased vasoplegia, and improved organ function as seen in our patients.

A 46-year-old woman on oral contraceptives developed an intrahepatic hematoma due to a benign hepatic tumor. As an incidental finding, a computed tomography showed a pulmonary embolism. Unfractionated heparin was given in a prophylactic dosing in an attempt to balance the risk of further intrahepatic bleeding with that of thrombosis. Ten days later, the patient developed a second pulmonary embolism along with acute right heart failure requiring cardiopulmonary resuscitation. As a sufficient circulation and oxygenation could not be reestablished, a veno-arterial extracorporeal membrane oxygenation (ECMO) was installed. An ELISA-Test, detecting PF4-Heparin associated antibodies, resulted in a positive result for a type II heparin induced thrombocytopenia even in the absence of thrombocytopenia. After hemodynamic and pulmonary stabilization, six days after ECMO-support the cannula was scheduled to be removed. On removal of the venous cannula the patient developed another massive pulmonary embolism with cardiac arrest which led to immediate reinstallation of va-ECMO. Under therapeutic anticoagulation using argatroban the ECMO support continued until the patient was on day 17 successfully weaned.Bei einer 46-jährigen Patientin zeigt sich neben einem neu aufgetretenen Leberhämatom zusätzlich noch eine Lungenarterienembolie, so dass eine Antikoagulation mit Heparin begonnen wird. Daraufhin kommt es zu einer heparininduzierten Thrombozytopenie Typ II mit fulminanter Lungenarterienembolie, die eine Therapie mit einer venoarteriellen extrakorporalen Membranoxygenierung (va-ECMO) notwendig macht.