Fig. 1

The inflammatory response to extracorporeal membrane oxygenation (ECMO). During ECMO, the complement and contact systems are activated as a result of blood-biomaterial interaction. The alternative complement pathway (AP) is primarily responsible for producing the anaphylatoxins C3a and C5a and the membrane attack complex (MAC). This occurs as the result of increased hydrolysis of C3 on the biomaterial surface. The contact system is responsible for producing activated factor XII (FXIIa), which induces the intrinsic coagulation pathway, leading to thrombin formation. Products produced by each of these systems, promote the production of pro-inflammatory cytokines and have direct effects on leukocytes, platelets and the vascular endothelium. In particular, neutrophils are activated, leading to increased neutrophilic infiltration of tissue and eventual organ damage