NEUTROPHIL AND CYTOKINE ACTIVATION WITH NEONATAL EXTRACORPOREAL MEMBRANE-OXYGENATION

Objective: To determine whether extracorporeal membrane oxygenation (E CMO), like cardiopulmonary bypass, produces systemic inflammatory resp onses that could potentiate organ injury in infants with respiratory f ailure. Study design: We evaluated the effects of neonatal ECMO on neu trophil surface adherence proteins, elastase release, and cytokine lev els in blood samples from 15 patients before and during ECMO, and from banked blood and ECMO circuit blood before cannulation. Neutrophil el astase, tumor necrosis factor alpha, and interleukin types 1 beta, 6, and 8 were measured. Chest radiographs were evaluated by a radiologist using a lung injury score in blinded fashion. Results: Primed ECMO ci rcuit blood, in comparison with patient pre-ECMO blood, demonstrated m arked up-regulation of CD11b (mean fluorescence intensity 1660 +/- 109 vs 361 +/- 81; p < 0.001 (mean +/- SEM)), shedding of L-selectin (mea n fluorescence intensity 10 +/- 2 vs 89 +/- 38; p < 0.01), and elevate d elastase levels (349 +/- 76 vs 154 ng/ml +/- 38; p < 0.001), consist ent with neutrophil activation, During ECMO, neutrophil CD11b levels i ncreased but L-selectin was not significantly shed. Concentrations of circulating neutrophil elastase increased significantly during ECMO, C orrected circulating quantities of interleukin-8 also rose significant ly, but the responses of tumor necrosis factor alpha and interleukin-1 beta were minimal, Radiographic lung injury scores worsened with the initiation of ECMO (median score: 6 before ECMO vs 11 in first hour of ECMO; p = 0.012), in conjunction with indicators of neutrophil activa tion. Conclusion: Neonates with respiratory failure have activation of the inflammatory cascade, ECMO incites additional neutrophil and cyto kine activation in association with early pulmonary deterioration, Rou tine leukodepletion of blood for circuit priming to remove activated n eutrophils may be beneficial.