Histologic chorioamnionitis concomitant placental abruption and its effects on pregnancy outcome

Two possible causative pathways have been suggested to participate in the development of placental abruption (PA), an acute inflammatory pathway and placental vascular derived, a chronic pathway. We aimed to study the impact of the inflammatory pathway on maternal and neonatal outcome.

The computerized medical files and placental reports of all pregnancies diagnosed with PA, between 11/2008-1/2019, at 24-42 weeks, were reviewed. Placental lesions were classified according to "Amsterdam" criteria into maternal and fetal vascular malperfusion lesions, acute inflammatory responses and chronic villitis. Composite neonatal morbidity included ≥1 of the following: seizures, intra-ventricular hemorrhage (IVH), hypoxic-ischemic encephalopathy, periventricular leukomalacia (PVL), blood transfusion, necrotizing enterocolitis (NEC), neonatal sepsis, respiratory distress syndrome, or neonatal death. Maternal and neonatal outcome were compared between PA with and without histologic chorioamnionitis (HC).

As compared to the PA without HC group (n = 267), the PA with HC group (n = 77) was characterized by lower gestational age (GA) at delivery (32.9 ± 5.5 vs. 35.6 ± 4.1 weeks, p < 0.001), higher rates of oligohydramnios (p < 0.001), bloody amniotic fluid at labor (p < 0.001), maternal postpartum fever (p < 0.001), longer maternal hospitalization (<0.001), and increased composite adverse neonatal morbidity (41.6% vs. 22.8%, p = 0.002). By multivariate analysis, GA and HC were found to be independently associated with adverse neonatal outcome, aOR 0.63 95% CI 0.43-0.78, p < 0.001, and aOR1.12, 95% CI 1.02-3.87, p = 0.04, respectively.

The involvement of the inflammatory causative pathway in the development of placental abruption, is associated with increased maternal and neonatal morbidity.