Cytokine release following recruitment maneuvers

Abstract

Background: There are reports of rigors and/or clinical deterioration following recruitment maneuvers (RMs), leading us to question whether the use of sustained high-pressure inflation could lead to release of inflammatory mediators.

Methods: Prospective cohort study of 26 patients with ARDS receiving mechanical ventilation. A single RM was performed during which the mean airway pressure was increased to 40 cm H2O and held constant for a period of 30 s. The concentration of nine cytokines (interleukin [IL]-1, IL-6, IL-8, IL-10, tumor necrosis factor [TNF]-alpha, Fas ligand, vascular endothelial growth factor, TNF receptor 1, TNF receptor 2) was measured longitudinally at three time points: prior to initiation of the RM, 5 min after the RM, and 60 min after the RM.

Results: RMs were tolerated well from a hemodynamic perspective. Oxygenation improved as reflected by an increased Pao2/fraction of inspired oxygen (Fio2) ratio from 140+/-49 at baseline to 190+/-78 (mean+/-SD) at 5 min after the RM (p=0.01). At 60 min, the increase in Pao2/Fio2 ratio, to 172+/-76, was no longer significant (p=0.1). There were no important changes in the levels of any of the measured cytokines at 5 min or 60 min following RM as compared with the baseline levels.

Conclusions: The results of our study demonstrate that recruitment maneuvers are well tolerated in patients with ARDS. Our data suggest no major hemodynamic or immunologic evidence of deterioration within the first hour of RM. In particular, cytokines, previously related to worsening lung injury and distal organ failure in patients with ARDS, are not elevated by use of an RM. Registered at: www.clinicaltrials.gov as NCT00127491.

Conflict of interest statement

The authors have no conflicts of interest to disclose.

Figures

Figure 1

Serum cytokine levels in 26 subjects at baseline and at 5 min and 60 min after RMs. Cytokine levels are presented as log concentrations. FAS-l = Fas ligand; VEGF = vascular endothelial growth factor; TNF-R1 = TNF receptor 1; TNF-R2 = TNF receptor 2.