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Open Access Research article

Nutrition of preterm infants in relation to bronchopulmonary dysplasia

Andreas Wemhöner12*, Daniel Ortner1, Edda Tschirch12, Alexander Strasak3 and Mario Rüdiger12

Author Affiliations

1 Medical University Innsbruck, Department for Pediatrics, Neonatology; Austria

2 Technical University Dresden; University Hospital Dresden, Department for Pediatric Intensive Care and Neonatology, Germany

3 Medical University Innsbruck, Department of Medical Statistics, Informatics and Health Economics; Austria

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BMC Pulmonary Medicine 2011, 11:7  doi:10.1186/1471-2466-11-7

Published: 3 February 2011

Abstract

Background

The pathogenesis of bronchopulmonary dysplasia (BPD) is multifactorial. In addition to prenatal inflammation, postnatal malnutrition also affects lung development.

Methods

A retrospective study was performed to analyse during the first two weeks of life the total, enteral and parenteral nutrition of premature infants (<31 weeks, birth weight ≤1500 g) born between 08/04 and 12/06.

Results

Ninety-five premature infants were analysed: 26 with BPD (27 ± 1 weeks) and 69 without BPD (28 ± 1 weeks). There was no statistical significant difference in the total intake of fluids, calories, glucose or protein and weight gain per day in both groups. The risk of developing BPD was slightly increased in infants with cumulative caloric intake below the minimal requirement of 1230 kcal/kg and a cumulative protein intake below 43.5 g/kg. Furthermore, the risk of developing BPD was significantly higher when infants had a cumulative fluid intake above the recommended 1840 ml/kg. In infants who developed BPD, the enteral nutrition was significantly lower than in non-BPD infants [456 ml/kg (IQR 744, 235) vs. 685 (IQR 987, 511)]. Infants who did not develop BPD reached 50% of total enteral feeding significantly faster [9.6 days vs. 11.5].

Conclusions

Preterm infants developing BPD received less enteral feeding, even though it was well compensated by the parenteral nutrient supply. Data suggest that a critical minimal amount of enteral feeding is required to prevent development of BPD; however, a large prospective clinical study is needed to prove this assumption.