Intrauterine Inflammation, Neonatal Sepsis, and Chronic Lung Disease: A 13-Year Hospital Cohort Study

Abstract

OBJECTIVE. To determine the impact of intrauterine inflammation of maternal (chorioamnionitis) and fetal (umbilical vasculitis) origin and neonatal sepsis on the development of neonatal chronic lung disease in preterm infants. METHODS. This study was conducted at Royal Prince Alfred Hospital in Sydney, Australia. All infants born at <30 weeks' gestation, admitted to the NICU, and surviving to 36 weeks' corrected gestation during 1992–2004 were eligible. Infants with major congenital abnormalities and those without placental examination were excluded. Antenatal and perinatal data extracted from hospital databases were correlated with the independent, central neonatal database and diagnostic laboratory reports. Neonatal sepsis was categorized according to blood culture isolates into 3 groups: coagulase-negative staphylococci, other bacteria, and Candida species. RESULTS. There were 798 eligible infants born during the study period, and 761 (95.4%) had placental examination. The mean gestational age was 27.4 ± 1.5 weeks. Antenatal maternal steroids were given to 94.4%. Regression analysis showed that chorioamnionitis with umbilical vasculitis and increasing gestation were associated with reduced odds of chronic lung disease. Chorioamnionitis without umbilical vasculitis showed a trend to reduced odds of chronic lung disease. Birth weight at <3rd percentile and neonatal sepsis were associated with increased odds of chronic lung disease. CONCLUSIONS. A fetal inflammatory response is protective for chronic lung disease. Neonatal sepsis is strongly associated with chronic lung disease, and the infecting organism is important. Coagulase-negative staphylococcal infection confers a risk for chronic lung disease similar to that of other bacteremias. Candidemia confers the greatest risk of chronic lung disease.