Lung function trajectories in children with post-prematurity respiratory disease: identifying risk factors for abnormal growth

Jonathan C Levin,Catherine A Sheils,Craig P Hersh,Lawrence M Rhein,Jonathan M Gaffin,Lystra P Hayden

doi:10.1186/s12931-021-01720-0

Abstract

BackgroundSurvivors of prematurity are at risk for abnormal childhood lung function. Few studies have addressed trajectories of lung function and risk factors for abnormal growth in childhood. This study aims to describe changes in lung function in a contemporary cohort of children born preterm followed longitudinally in pulmonary clinic for post-prematurity respiratory disease and to assess maternal and neonatal risk factors associated with decreased lung function trajectories.MethodsObservational cohort of 164 children born preterm ≤ 32 weeks gestation followed in pulmonary clinic at Boston Children’s Hospital with pulmonary function testing. We collected demographics and neonatal history. We used multivariable linear regression to identify the impact of neonatal and maternal risk factors on lung function trajectories in childhood.ResultsWe identified 264 studies from 82 subjects with acceptable longitudinal FEV1 data and 138 studies from 47 subjects with acceptable longitudinal FVC and FEV1/FVC data. FEV1% predicted and FEV1/FVC were reduced compared to childhood norms. Growth in FVC outpaced FEV1, resulting in an FEV1/FVC that declined over time. In multivariable analyses, longer duration of mechanical ventilation was associated with a lower rate of rise in FEV1% predicted and greater decline in FEV1/FVC, and postnatal steroid exposure in the NICU was associated with a lower rate of rise in FEV1 and FVC % predicted. Maternal atopy and asthma were associated with a lower rate of rise in FEV1% predicted.ConclusionsChildren with post-prematurity respiratory disease demonstrate worsening obstruction in lung function throughout childhood. Neonatal risk factors including exposure to mechanical ventilation and postnatal steroids, as well as maternal atopy and asthma, were associated with diminished rate of rise in lung function. These results may have implications for lung function trajectories into adulthood.

Highlights

IntroductionPost-prematurity respiratory disease, including bronchopulmonary dysplasia (BPD), may be a progenitor to adult chronic obstructive pulmonary disease [2,3,4,5]
Survivors of prematurity are at risk for respiratory morbidity and abnormal lung function throughout life [1].Post-prematurity respiratory disease, including bronchopulmonary dysplasia (BPD), may be a progenitor to adult chronic obstructive pulmonary disease [2,3,4,5]
The plurality of subjects had moderate to severe BPD, with a high degree of respiratory and other neonatal morbidities, including need for surfactant, postnatal steroid exposure in the neonatal intensive care unit (NICU), patent ductus arteriosus (PDA) ligation, gastrostomy tube placement, and respiratory support at 36 weeks post-menstrual age (Table 1)

Summary

Introduction

Post-prematurity respiratory disease, including bronchopulmonary dysplasia (BPD), may be a progenitor to adult chronic obstructive pulmonary disease [2,3,4,5]. Pulmonary function in survivors with BPD often demonstrates an obstructive pattern, with regard to decreased forced expiratory volumes in one second (FEV1) and decreased ratio of FEV1 to Forced Vital Capacity (FVC) [8,9,10]. Few studies have addressed trajectories of lung function and risk factors for abnormal growth in childhood. This study aims to describe changes in lung function in a contemporary cohort of children born preterm followed longitudinally in pulmonary clinic for post-prematurity respiratory disease and to assess maternal and neonatal risk factors associated with decreased lung function trajectories

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