Chorioamnionitis and neonatal outcomes

Abstract

Chorioamnionitis or intrauterine inflammation is a frequent cause of preterm birth. Chorioamnionitis can affect almost every organ of the developing fetus. Multiple microbes have been implicated to cause chorioamnionitis, but "sterile" inflammation appears to be more common. Eradication of microorganisms has not been shown to prevent the morbidity and mortality associated with chorioamnionitis as inflammatory mediators account for continued fetal and maternal injury. Mounting evidence now supports the concept that the ensuing neonatal immune dysfunction reflects the effects of inflammation on immune programming during critical developmental windows, leading to chronic inflammatory disorders as well as vulnerability to infection after birth. A better understanding of microbiome alterations and inflammatory dysregulation may help develop better treatment strategies for infants born to mothers with chorioamnionitis.

Fig 1:

Exposure to various microbes or sterile inflammation causing chorioamnionitis and release of various proinflammatory cytokines, which in turn causes preterm labor and/or premature rupture of membranes (PROM). These in turn lead to various short-term and long-term chorio mediated outcomes. DAMP- damage-associated molecular patterns, BPD – Bronchopulmonary dysplasia, RDS – Respiratory distress. IVH – Intraventricular hemorrhage. COPD – Chronic Obstructive pulmonary disease.

Fig 2:

Management algorithm of neonates exposed to chorioamnionitis. (Suspected Triple I” is defined as fever with one or more of the following symptoms: leukocytosis, fetal tachycardia, or purulent cervical discharge. Confirmed Triple I should be accompanied by evidence of amniotic fluid infection). Adapted from Higgins et. al (20)