Abstract
Foetal hypoxia–ischaemia is a key trigger of meconium aspiration syndrome (MAS). However, many neonates develop MAS without evidence of hypoxia–ischaemia, suggesting the presence of covert but important risk variables. We evaluated the association of MAS with clinical variables, placental histopathologic findings, and inflammatory biomarkers at birth. Of 1336 symptomatic and asymptomatic term singleton neonates with meconium-stained amniotic fluid, 88 neonates (6.6%) developed MAS. Univariate analysis showed that MAS development was associated with low 1- and 5-min Apgar scores, low cord blood pH, funisitis, higher α1-acid glycoprotein levels, and higher haptoglobin levels (all p < 0.001 except for p = 0.001 for haptoglobin). Associations of MAS with caesarean delivery (p = 0.004), premature rupture of the membranes (p = 0.006), chorioamnionitis (p = 0.007), and higher C-reactive protein levels (p = 0.008) were lost when adjusted for multiple comparisons. The final multivariate model to explain MAS development comprised lower cord blood pH (odds ratio [OR] 0.58; 95% confidence interval [CI] 0.47–0.73; p < 0.001), funisitis (OR 2.45; 95% Cl 1.41–4.26; p = 0.002), and higher α1-acid glycoprotein levels (OR 1.02; 95% Cl 1.01–1.03; p = 0.001). Our data from a large cohort of neonates suggested that intrauterine inflammation is one of the key independent variables of MAS development, together with foetal hypoxia–ischaemia.
Highlights
Foetal hypoxia–ischaemia is a key trigger of meconium aspiration syndrome (MAS)
This study aimed to confirm the relationship between foetal hypoxia–ischaemia, intrauterine inflammation, and the development of MAS in a large cohort of term neonates with meconium-stained amniotic fluid
Univariate logistic regression analysis showed that the development of MAS was associated with low 1- and 5-min Apgar scores, low cord blood pH (p < 0.001) (Table 1), funisitis (p < 0.001), higher α1-acid glycoprotein (α1-AG) levels (p < 0.001), higher haptoglobin levels (p = 0.001), and higher acute-phase inflammatory reaction (APR) scores (p < 0.001) (Table 2)
Summary
Foetal hypoxia–ischaemia is a key trigger of meconium aspiration syndrome (MAS). many neonates develop MAS without evidence of hypoxia–ischaemia, suggesting the presence of covert but important risk variables. Our data from a large cohort of neonates suggested that intrauterine inflammation is one of the key independent variables of MAS development, together with foetal hypoxia–ischaemia. No evidence of foetal hypoxia and stress is noted in approximately 50% of neonates with MAS9,11 This suggests the presence of covert but important risk factors for MAS other than acute foetal hypoxia–ischaemia. The association between meconium-stained amniotic fluid and inflammation is well established, the relationship between foetal inflammation and MAS development remains unclear because most previous studies assessed the umbilical cord and placenta in only a part of the study cohort[15,16]. This study aimed to confirm the relationship between foetal hypoxia–ischaemia, intrauterine inflammation, and the development of MAS in a large cohort of term neonates with meconium-stained amniotic fluid
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