PeerJ (May 2019)

Influence of foetal inflammation on the development of meconium aspiration syndrome in term neonates with meconium-stained amniotic fluid

  • Kyoko Yokoi,
  • Osuke Iwata,
  • Satoru Kobayashi,
  • Kanji Muramatsu,
  • Haruo Goto

DOI
https://doi.org/10.7717/peerj.7049
Journal volume & issue
Vol. 7
p. e7049

Abstract

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Background Meconium-stained amniotic fluid is observed in approximately 10–15% of all deliveries; however, only 5% of neonates with meconium-stained amniotic fluid develop meconium aspiration syndrome (MAS). Although foetal distress and subsequent sympathetic stimulation have been considered as the primary upstream events of MAS, this clinical complication sometimes occurs due to other pathologies, such as intraamniotic inflammation. The aim of this study was to investigate whether the incidence of MAS is associated with the presence of funisitis and chorioamnionitis in term neonates with meconium-stained amniotic fluid. Methods Between April 2013 and March 2015, a total of 95 term neonates with meconium-stained amniotic fluid, who were hospitalized at a neonatal intensive care unit, were enrolled in the study. The placenta and umbilical cord were histopathologically examined. Clinical variables and histopathological findings associated with the incidence of MAS were studied. Results A total of 36 neonates developed MAS. Univariate logistic regression analysis revealed that a heavier birth weight, male sex, 1-min Apgar score ≤ 7, funisitis (but not chorioamnionitis), and elevated acute-phase inflammatory reaction score were associated with increased incidence of MAS (all p < 0.05). The multivariate model comprised funisitis (OR = 5.03, 95% CI [1.63–15.5], 1-min Apgar score ≤ 7 (OR = 2.74, 95% CI [1.06–7.09], and male sex (OR = 3.4, 95% CI [1.24–9.34]. Conclusion In neonates with meconium-stained amniotic fluid, funisitis, as well as low 1-min Apgar score and male sex, was identified as an independent variable for MAS development. Intraamniotic inflammation might be involved in the pathological mechanisms of MAS.

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