Fetal inflammatory response severity on placental histology identifies neonates at risk for meconium aspiration syndrome.

BACKGROUND

While fetal hypoxia-ischemia is a known trigger for meconium aspiration syndrome (MAS), many infants develop MAS without it, suggesting other risk factors. We examined the association between MAS and the presence and severity of fetal inflammatory response (FIR) on placental histopathology.

METHODS/STUDY

DESIGN

A single-center retrospective cohort study of term infants with meconium-stained amniotic fluid (MSAF) born at Parkland Hospital (2010-2018). Maternal and infant demographics and clinical data were recorded. Placental histopathologic evidence of FIR was classified per Amsterdam criteria. MAS was defined as respiratory distress in an infant with MSAF requiring NICU admission and ≥48 hours of respiratory support and/or radiographic findings of MAS.

RESULTS

Among 1,696 term neonates with MSAF, 118 (6.9%) developed MAS. Univariate analysis showed that MAS was associated with post-term delivery, non-reassuring fetal heart patterns, cesarean delivery, thick meconium, low Apgar scores, severe acidosis, and presence of FIR (all P < 0.001). On multivariate analysis, FIR remained significant (adjusted OR 2.50, 95% CI 1.41-4.82). Moderate to severe FIR conferred 5-times higher odds for developing MAS (adjusted OR 5.43, 95% CI 2.83-10.40).

CONCLUSION

FIR, particularly its severity, is an independent predictor of MAS, highlighting intrauterine inflammation as a key mechanism alongside hypoxia-ischemia.

IMPACT: Fetal Inflammatory Response (FIR) is independently associated with Meconium Aspiration Syndrome (MAS) Increasing severity of FIR confers progressively higher risk of MAS. This is the first study to demonstrate a dose-response relationship between FIR severity on MAS. These observations highlight the role of intrauterine inflammation in MAS pathogenesis and provide new insight into its impact on term neonates.