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Capillary leak syndrome is a complication of extracorporeal membrane oxygenation(ECMO) which results in prolonged time on bypass. The etiology of capillary leak syndrome is likely multifactorial involving blood-surface activation of inflammatory mediators, including C3a and C1 inhibitor of the complement system and the chemokine IL-8 from leukocytes. Our hypothesis is that complement system activation(C3a), complement system regulation(C1 inhibitor), and chemokine levels(IL-8) contribute to the pulmonary edema and capillary leak during ECMO. We studied 9 neonatal and 4 pediatric patients requiring ECMO for respiratory failure. Causes for respiratory failure included congenital diaphragmatic hernia, meconium aspiration syndrome, persistent pulmonary hypertension of the newborn, respiratory distress syndrome, pneumonia (influenza A and respiratory syncytial virus), and acute respiratory distress syndrome. We measured plasma levels of C3a by ELISA (Quidel, San Diego), C1 inhibitor antigen by radial immunodiffusion (The Binding Site, San Diego), and total IL-8 by ELISA (Genzyme,CA) before and during ECMO. Pulmonary edema was assessed by blinded radiographic scoring (Radiology 161:347,1986). The relationships of C3a, C1 inhibitor, and IL-8 to radiographic scores across time were analysed by repeated measures of variance. (Table)
Kaufman, D., Kilpatrick, L., Harty, M. et al. Capillary Leak, C3a, C1 Inhibitor, and IL-8 Levels on ECMO.
Pediatr Res45, 263 (1999). https://doi.org/10.1203/00006450-199904020-01565
