Late-Onset Sepsis as a Risk Factor for Bronchopulmonary Dysplasia in Extremely Low Birth Weight Infants: A Nationwide Cohort Study

Euiseok Jung,Byong Sop Lee

doi:10.1038/s41598-019-51617-8

Euiseok Jung, Byong Sop Lee

Open Access

https://doi.org/10.1038/s41598-019-51617-8

Copy DOI

Abstract

This study aimed to determine the effect of late-onset sepsis (LOS) on the development of bronchopulmonary dysplasia (BPD) in extremely low birth weight (ELBW) infants. A prospective cohort study was performed using data collected from 64 centres registered in the Korean national registry. LOS was defined as a positive blood culture and antibiotics treatment after 72 hours of life and prior to 36 weeks postmenstrual age (PMA). Data on the causative organisms were collected and analysed for respiratory outcomes. Among the 1,434 ELBW infants who survived to 36 weeks PMA, 481 (34%) developed LOS caused by bacteria (n = 405), fungi (n = 28), or both (n = 48). The incidence of BPD was significantly associated with LOS in both the entire cohort and the propensity score-matched cohort. Two or more LOS episodes were a risk factor for BPD. The impact of multiple episodes of LOS on BPD was prominent in infants who received mechanical ventilation for two weeks or less. The estimated odds ratios for BPD and severe BPD were greater with fungal LOS than with bacterial LOS. In conclusion, LOS, particularly complicated by multiple episodes and/or fungi, was a risk factor for BPD in ELBW infants.

Highlights

Inflammation in utero and during the postnatal period is one of the key underlying mechanisms in the development of bronchopulmonary dysplasia (BPD)[1]
Analyses of data from extremely low birth weight (ELBW) infants who survived to 36 weeks postmenstrual age (PMA) revealed the following major findings
late-onset sepsis (LOS) was significantly associated with BPD and severe BPD, and the risk was further augmented by recurrent episodes of LOS

Summary

Introduction

Inflammation in utero and during the postnatal period is one of the key underlying mechanisms in the development of bronchopulmonary dysplasia (BPD)[1]. A consensus is being formed about the postnatal risk factors for BPD, which share a common mechanism that is characterised by the production of inflammatory cytokines[5]. These risk factors include respiratory distress syndrome (RDS), invasive mechanical ventilation (IMV), oxygen and sepsis[3,6]. Several retrospective studies have reported an association between LOS and BPD in preterm infants[2,10,11]; it is difficult to ascertain the causative role of LOS in the development of BPD.

Objectives

Methods

Results

Conclusion