BLOOD ACTIVATION DURING NEONATAL EXTRACORPOREAL LIFE-SUPPORT

Cardiopulmonary bypass for heart operations is associated with a whole body inflammatory reaction. The main factors involved in this reactio n are the contact system and the complement system. The activation of the contact system is considered mainly responsible for impaired hemos tasis because it affects platelet function. The activation of the comp lement system is considered the main cause for organ dysfunction, part icularly of the lung, due to activation of leukocytes. This study in 1 0 neonates was undertaken to evaluate if there are effects of activati on of the contact and the complement systems in neonatal extracorporea l life support comparable to those during cardiopulmonary bypass for c ardiac operations. Two periods of blood activation during extracorpore al life support could be distinguished. The initial blood-material int eraction at the onset of extracorporeal life support resulted in activ ation of both the contact and the complement systems. The contact acti vation was apparent by elevated factor XIIa-Cl esterase inhibitor comp lexes, decreased kallikrein inhibitory capacity, thrombin-antithrombin III formation, and moderate generation of fibrin(ogen) degradation pr oducts. The complement activation was characterized by elevated C3a, d ecreased leukocyte count, elastase release, and tumor necrosis factor- alpha production. This initial activation pattern subsided by 24 hours . A second activation period was observed 72 hours after the onset of extracorporeal life support, which was characterized only by increased clotting and fibrinolytic activity while no activation of the complem ent system was observed. We conclude that the initial activation patte rn in extracorporeal life support is similar to that observed during c ardiopulmonary bypass for cardiac operations. The contact activation t hat affects platelets might explain the continuous platelet consumptio n observed during extracorporeal life support. In this period, as in c ardiopulmonary bypass, aprotinin given in the pump prime might be effe ctive to prevent platelet consumption and impairment of hemostasis als o in extracorporeal life support. The complement activation and leukoc yte inflammatory reaction during the initial period are able to cause a capillary leak syndrome and might therefore explain the frequently o bserved temporary compromised lung function in extracorporeal life sup port. This reaction, as in cardiopulmonary bypass, might be reduced by the use of specific drugs or heparin coating also in extracorporeal l ife support. The cause of the second period of activation during extra corporeal life support requires further studies before adequate measur es can be recommended.