To determine whether extracorporeal membrane oxygenation (ECMO), like cardiopulmonary
bypass, produces systemic inflammatory responses that could potentiate organ injury
in infants with respiratory failure.
We evaluated the effects of neonatal ECMO on neutrophil surface adherence proteins,
elastase release, and cytokine levels in blood samples from 15 patients before and
during ECMO, and from banked blood and ECMO circuit blood before cannulation. Neutrophil
elastase, 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.
Primed ECMO circuit blood, in comparison with patient pre-ECMO blood, demonstrated
marked up-regulation of CD11b (mean fluorescence intensity 1660 +/- 109 vs 361 +/-
81; p < 0.001 (mean +/- SEM)), shedding of L-selectin (mean fluorescence intensity
10 +/- 2 vs 89 +/- 38; p < 0.01), and elevated elastase levels (349 +/- 76 vs 154
ng/ml +/- 38; p < 0.001), consistent with neutrophil activation. During ECMO, neutrophil
CD11b levels increased but L-selectin was not significantly shed. Concentrations of
circulating neutrophil elastase increase significantly during ECMO. Corrected circulating
quantities of interleukin-8 also rose significantly, 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 activation.
Neonates with respiratory failure have activation of the inflammatory cascade. ECMO
incites additional neutrophil and cytokine activation in association with early pulmonary
deterioration. Routine leukodepletion of blood for circuit priming to remove activated
neutrophils may be beneficial.