351 - Severity of Fetal Inflammatory Response on Placental Histopathology is Associated with Meconium Aspiration Syndrome

Publication Number: 351.6809

Roberto Gonzalez, University of Texas Southwestern Medical School, Dallas, TX, United States; Nazia Bhat, Government Medical College Handwara, Kupwara, Jammu and Kashmir, India; Manahil Firdaus, University of Texas Southwestern Medical School, Colleyville, TX, United States; Jawahar Jagarapu, University Of Texas Southwestern Medical Center, dallas, TX, United States; Vishal Kapadia, University of Texas Southwestern Medical School, Dallas, TX, United States; Imran N. Mir, University of Texas Southwestern Medical School, Dallas, TX, United States; L. Steven Brown, Parkland Health, Dallas, TX, United States

Background: Fetal hypoxia-ischemia is a key trigger for Meconium aspiration syndrome (MAS) in term infants. However, many neonates develop MAS without evidence of hypoxia-ischemia, suggesting the presence of covert but important risk factors.

Objective: Our objective was to evaluate the association of MAS with the evidence and severity of fetal inflammatory response (FIR) on placental histopathologic analysis and perinatal clinical markers of inflammation

Design/Methods: A single-center retrospective cohort study of prospectively collected data of term infants (>/=37 weeks GA) born at Parkland Hospital between 2010-2018 with meconium-stained amniotic fluid (MSAF). Infant demographics, maternal factors during pregnancy, and clinical information during hospitalization were recorded. Placental histopathologic evidence of severity of maternal inflammatory response (MIR) and fetal inflammatory response (FIR) was defined using the Amsterdam Placental Workshop Group Consensus Statement. MAS was defined as respiratory distress in an infant born to a mother with MSAF, admitted to NICU needing respiratory support for at least 48 hours and with radiographic findings consistent with MAS.

Results: Of 2196 term singleton neonates with MSAF born Parkland Hospital Dallas, 118 (5.4%) developed MAS. Placental histopathologic analysis was performed in 1696/2196 (80%) of these infants. Univariate analysis showed that MAS development was associated with clinical variables including post-term delivery, non-reassuring fetal heart pattern, cesarean delivery, thick meconium, low 1-and 5-min APGAR scores and severe fetal acidosis (Table 1). MAS was also associated with evidence of MIR, FIR and the severity of FIR (P < 0.001) (Table 2). After controlling for 5-min APGAR scores, evidence of fetal hypoxia-asphyxia, gestational age, severe fetal acidosis on multivariate regression analysis, infants with FIR still had 2.5 times higher odds of developing MAS (P < 0.01, adjusted OR 2.50, 95% CI 1.41, 4.82), while the association with MIR was lost (P=0.32, adjusted OR 1.34, 95% CI 0.75, 2.40). Moreover, infants with moderate to severe FIR had 5 times higher odds of developing MAS (P < 0.01, adjusted OR 5.43, 95% CI 2.83, 10.40), thus indicating that severity and magnitude of FIR is associated with higher odds of developing MAS (Table 3).

Conclusion(s): Our data from a large cohort of neonates suggests that fetal inflammatory response and its severity and progression is one of the key independent variables of MAS development, together with fetal hypoxia-ischemia.

Association of meconium aspiration syndrome (MAS) and clinical variables among term neonates with meconium-stained amniotic fluid
Table 1 .pdf

Association of meconium aspiration syndrome and placental histopathologic findings of acute inflammation among neonates with meconium-stained amniotic fluid on univariate analysis
Table 2.pdf

Multivariate logistic model to explain the development of meconium aspiration syndrome
Table 3.pdf