How does intraamniotic infection (chorioamnionitis) during pregnancy affect the fetus and newborn?

Updated: May 08, 2018
  • Author: Fayez M Bany-Mohammed, MD; Chief Editor: Ted Rosenkrantz, MD  more...
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Answer

Maternal fever during labor, and perhaps other signs and symptoms of chorioamnionitis, often results in a call to the family practitioner, pediatrician, or neonatologist related to concern for the neonate. This communication often causes an evaluation to rule out early-onset neonatal sepsis. [15] Because of a concern for early-onset sepsis (EOS) when signs and symptoms of maternal chorioamnionitis occur, 18-38 newborns are evaluated and treated with antibiotics for every infant with proven bacteremia. The reason for this clinical phenomenon is that newborns who develop EOS, defined as proven infection (positive culture from a normally sterile site like blood, tracheal aspirate, cerebrospinal fluid) at less than 72 hours of life, have a high mortality rate. A strong association is observed between very preterm infants dying when younger than 24 hours and chorioamnionitis. [16, 17]

Heightened clinical evaluations for EOS began in the 1970s because group B streptococcal (GBS) infections resulted in a neonatal mortality of about 50%. [18] Over the past 50 years, awareness of GBS-related neonatal morbidity and mortality resulted in the widespread implementation of intrapartum chemoprophylaxis with antibiotics to reduce the risk of GBS disease, which led to an 85% reduction in the rate of culture-proven early-onset GBS sepsis, from approximately1.8 per 1000 live births in the early 1990s to fewer than 0.26 per 1000 live births in 2010. [19]

Early-onset bacterial infections in the newborn may occur when the mother has abnormal bacterial colonization of the urogenital tract, an ascending but silent amniotic fluid infection, or symptomatic chorioamnionitis. Thus, the physician cannot assume that maternal signs and symptoms alone will identify all infected infants.

GBS infections continues to be the major cause of EOS in term neonates; however, Escherichia coli has surpassed GBS as the most significant pathogen in preterm infants for over 10 years. [20] Intrapartum ampicillin exposure (as part of GBS prophylaxis as used at some institutions) was identified as an independent risk factor for ampicillin-resistant E coli EOS, as well as for a significant increase in E coli late-onset sepsis. [21]

Additionally, methicillin-resistant Staphylococcus aureus (MRSA), already a common cause of nosocomial infection in maternity and neonatal units, looms as a potential cause of EOS. [22] So far, maternal colonization during pregnancy with MRSA has not translated into an increase in MRSA-associated EOS, but close monitoring for this infection is warranted. [23]

This article discusses intraamniotic infection during pregnancy and its effects on the fetus and newborn, as well as summarizes the history, physical examination, and laboratory findings in both mother and infant to provide appropriate decision-making tools for cost-effective management of the neonate. The subject is expansive in scope, and readers are encouraged to seek more information from other sources. Other Medscape Drugs and Diseases articles of interest include Congenital PneumoniaMeningitis, Bacterial; and Neonatal Sepsis.

An entire 2016 issue of the Journal of Perinatal Medicine was devoted to clinical chorioamnionitis. [24]  Several chapters in the monograph by Romero et al contain information on the intraamniotic inflammatory response in women with clinical chorioamnionitis, molecular mechanisms to identify infecting microorganisms, and the cytokine profiles of the mother and the newborn infant. [25, 26, 27, 28, 29]

Readers are also referred to the 2017 Committee Opinion Number 712 by the American College of Obstetrics and Gynecology (ACOG) on intrapartum management of intraamniotic infection, [30] as well as an excellent 2016 review article about clinical chorioamnionitis by Kim et al in the American Journal of Obstetrics and Gynecology that discusses the definition, pathogenesis, grading, staging, and clinical significance of the most common lesions in placental disease, accompanied by illustrations of the lesions as well as diagrams. [31]


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