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Inflammatory Mediators in Tracheal Aspirates of Preterm Infants Participating in a Randomized Trial of Permissive

Sarah Gentner1, Mandy Laube2, Ulrike Uhlig3

  • 1Division of Vascular Surgery, University of Ulm, Ulm, Germany.

Frontiers in Pediatrics
|December 7, 2017
PubMed

Insights

Higher PCO2 targets in preterm infants did not reduce lung inflammation or injury. This strategy did not prove effective in preventing ventilator-induced lung injury compared to standard PCO2 levels.

Area of Science:

  • Neonatal Medicine
  • Pediatric Pulmonology
  • Critical Care

Background:

  • Ventilator-induced lung injury (VILI) is a key factor in bronchopulmonary dysplasia (BPD) pathogenesis.
  • Optimizing mechanical ventilation may decrease respiratory complications in premature infants.
  • Permissive hypercapnia is a strategy explored to mitigate lung injury.

Purpose of the Study:

  • To investigate if a higher PCO2 target range reduces lung injury in preterm infants compared to a control range.
  • To assess the impact of higher PCO2 targets on pro-inflammatory cytokines and acid sphingomyelinase (ASM) in tracheal aspirates.

Main Methods:

  • A multicenter trial randomized extremely low birthweight infants to high PCO2 (55-75 mmHg) or control (40-60 mmHg) target groups.
  • Tracheal aspirates were analyzed for inflammatory mediators from day 2 to 21.
  • Bronchopulmonary dysplasia (BPD) was assessed at 36 weeks postmenstrual age.

Main Results:

  • No significant differences in levels of interleukin-6, IL-8, IL-10, IL-1β, macrophage inflammatory protein 1α, albumin, neuropeptide Y, leukotriene B4, transforming growth factor-β1, nitrite, or ASM between groups.
  • Most inflammatory mediators increased with infant age.
  • BPD or death occurred in 14 of 62 infants, evenly distributed between groups.

Conclusions:

  • High PCO2 target levels did not lower pulmonary inflammatory activity in preterm infants.
  • The findings suggest that elevated PCO2 targets are not effective in reducing VILI compared to control targets.
Abstract

Keywords:
bronchopulmonary dysplasiapermissive hypercapniapreterm infantspulmonary inflammationtracheal aspirates

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