Extracorporeal membrane oxygenation (ECMO) is life saving continuous cardiopulmonary bypass for cardiac and pulmonary failure. Four to five hundred infants and children require ECMO per year. A major complication of ECMO is the development of an inflammatory mediated capillary leak syndrome with activation of the contact and complement systems, and with fluid and neutrophil accumulation in the lungs and interstitial tissues resulting in multi-organ dysfunction and prolonged time on ECMO. Inflammatory mediators that may play a critical role in capillary leak syndrome on ECMO are the C1 inhibitor, which regulates the activated contact and complement systems, and chemokines which attract and activate white blood cells possilby contribyuting to lung injury and edema. There is limited information on C1 inhibitor or chemokines on bypass, and this information is mainly derived from studies on short term cardiopulmonary bypass for cardiac surgery. Our workng hypotheses are that the C1 inhibitor may be an important regulator of the generalized capillary leak that develops on ECMO and that the release of chemokines may contribute to the lung injury and edema. This pilot study will gather preliminary information to help develop specific hypotheses to design a larger clinical study. Our goal is to measure C1 inhibitor and chemokine levels, and determine if there is an association between C1 inhibitor and the capillary syndrome, and between chemokines and lung edema on ECMO. Future use of C1 inhibitor concentrate administered before and during ECMO therapy may attenuate the development of the capillary leak syndrome with a decrease in lung injury and edema, and with a subsequent decrease in ventilator, ECMO, and hospital days, in addition to the decreased cost of hospitalization.
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