Respiration/Mechanical VentilationA single recruitment maneuver in ventilated critically ill children can translocate pulmonary cytokines into the circulation
Introduction
Mechanical ventilation with low tidal volumes (Vt) reduces patient mortality in acute respiratory distress syndrome (ARDS) and acute lung injury (ALI) [1], [2]. However, small Vt (<6 mL/kg) may result in loss of aerated lung tissue and decreased oxygenation. To augment the number of aerated alveoli, various lung recruitment maneuvers (RM) have been developed and are commonly used [3]. Although several experimental studies have shown a positive effect of RM on oxygenation, clinical studies thus far show controversial results [4]. In patients ventilated with sufficient positive end expiratory pressure (PEEP) and low Vt, RM appear to improve oxygenation in only a few patients, which generally lasts only for a short period, and several authors have pointed at adverse effects of RM and questioned its use in ARDS [4], [5], [6], [7], [8].
Because RMs require a transient increase in ventilation pressure, the biological sequelae such as cytokine up-regulation and translocation may have clinical importance. Both animal and clinical studies have shown that high airway pressures during mechanical ventilation are associated with increased cytokine up-regulation and lung injury. Translocation of such inflammatory mediators and bacteria from the alveolar space into the systemic circulation after a high-pressure RM has been demonstrated in several experimental models, and these elevations are associated with lung injury and multiorgan failure and adverse outcome [9], [10], [11], [12], [13]. Increase of ventilation pressures augments the levels of inflammatory markers within 1 hour in adult patients with ALI [14]. These observations illustrate possible deleterious effects of RM.
Of the limited number of studies on lung recruitment studies that exist in children, all are performed in healthy children during anesthesia, none in critically ill children [4]. Although the general principles of recruitment and derecruitment in the adult patient probably also apply to small children, lungs and chest wall are essentially different: increased chest wall compliance, development of Kohn pores necessary to limit over inflation, a maturing anti-inflammatory response to stress [4], [15], [16], [17]. This may imply children might be more sensitive to high-pressure RM than adults, and thus, observations in adult intensive care unit (ICU) patients cannot directly be extrapolated to critically ill children.
In this study, we determined the effect of a single RM in children on the pulmonary and systemic inflammatory response.
Section snippets
Methods
Both the hospital- and the national ethical committee approved the study. Written informed consent was obtained from both parents before inclusion.
Results
After the inclusion of 5 patients, the interim analysis was performed, during which 2 additional patients were included. When the cytokine data became available, indicating the possibility of adverse effects in the absence of beneficial effects on pulmonary gas exchange, we decided together with the ethical committee to terminate the study.
Median age was 6 (0.5-45) months, and admission diagnosis was meningococcal sepsis (n = 2), respiratory syncitial virus bronchiolitis (n = 2), influenza A
Discussion
Our study shows that a commonly used method to recruit alveoli [3] can result in a transient increase in circulating cytokines in ventilated critically ill children. The rapid and transient increase indicates that increased up-regulation of cytokine production is not the primary responsible mechanism because this would take far longer than the 15 minutes to reach the observed peak levels. From these data, we assume that the RM increased circulating cytokines by translocation of pulmonary
Acknowledgments
We would like to thank our Research Nurses Leen van t Sant, Tijn Bouw, and Olof Moesker and laboratory assistant Trees Jansen for their contributions to conduct this study.
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