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Published on: November 20, 2015
Exposure to intrauterine inflammation and late-onset sepsis in very preterm infants
Marle B van Doorn1, J Patrick van der Voorn2, Helen L Tanger1
1Department of Neonatology, Emma Children's Hospital, Amsterdam UMC, Vrije Universiteit Amsterdam, Amsterdam, the Netherlands.
Insights
Intrauterine inflammation does not appear to protect very preterm infants from late-onset sepsis. This study investigated the link between prenatal inflammation and sepsis outcomes in premature infants.
Area of Science:
- Neonatal Medicine
- Infectious Diseases
- Immunology
Background:
- Late-onset sepsis (LOS) is a significant cause of mortality and morbidity in preterm infants.
- Preterm infants primarily rely on their innate immune system, making immune enhancement a potential preventive strategy.
- The role of intrauterine inflammation as a potential immune stimulus remains unclear.
Purpose of the Study:
- To investigate the influence of intrauterine inflammation on the development of late-onset sepsis in very preterm infants.
- To determine if intrauterine inflammation acts as a protective factor against LOS in this vulnerable population.
Main Methods:
- Retrospective cohort study including 1014 infants with gestational age ≤32 weeks or birth weight ≤1500g.
- Intrauterine inflammation was categorized into histological chorioamnionitis, fetal inflammatory response, and funisitis.
- Logistic and Cox regression analyses were used to assess the association between intrauterine inflammation and LOS.
Main Results:
- 36% of infants developed late-onset sepsis, and 24% of placentas showed signs of intrauterine inflammation.
- No significant difference in LOS incidence was observed between infants exposed and unexposed to intrauterine inflammation, even after adjusting for gestational age.
- Specific markers of intrauterine inflammation (chorioamnionitis, fetal inflammatory response, funisitis) were not significantly associated with altered LOS risk.
Conclusions:
- Intrauterine inflammation does not appear to be protective against late-onset sepsis in very preterm infants.
- Findings suggest that intrauterine inflammation is not a reliable stimulus for enhancing neonatal immunity against LOS.
- Further research is needed to identify effective stimuli for improving immune defense in premature infants.
Background:
Late-onset sepsis is an important cause of mortality and morbidity in preterm infants. As these infants rely mostly on their innate immune system to fight off infection, enhancing this immune system by appropriate stimuli may prevent late-onset sepsis. However, it remains unclear which stimuli can enhance the neonatal immune system. This study aims to investigate the influence of intrauterine inflammation on late-onset sepsis.
Methods:
This is a retrospective cohort study in a Neonatal Intensive Care Unit in the Netherlands. Between 2005 and 2016, 1014 infants with ≤32 weeks gestational age and/or with a birth weight ≤1500 g were included. Intrauterine inflammation was subdivided into histological chorioamnionitis, fetal inflammatory response, and funisitis. Logistic and Cox regression analyses were performed to investigate the influence of intrauterine inflammation on late-onset sepsis.
Results:
Thirty-six percent of the included infants developed late-onset sepsis; 24% of placentas showed intrauterine inflammation. Late-onset sepsis incidence did not differ between infants with or without exposure to intrauterine inflammation after adjustment for gestational age (histological chorioamnionitis aHR 0.928 [CI: 0.727-1.185], p = 0.551; fetal inflammatory response aHR 1.011 [CI: 0.793-1.288], p = 0.930); funisitis aHR 0.965 [CI: 0.738-1.263], p = 0.797).
Conclusions:
Late-onset sepsis in very preterm infants seems not to be associated with intrauterine inflammation.
Impact:
Intrauterine inflammation is not protective of developing late-onset sepsis in premature infants. A large cohort study on the effect of intrauterine inflammation on neonatal outcome. This study adds to existing knowledge on finding appropriate stimuli to enhance the immune system of premature infants to improve neonatal outcome.
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