Nutrition in preterm infants with bronchopulmonary dysplasia

Abstract

Bronchopulmonary dysplasia (BPD) is a common complication of preterm birth. Currently most infants developing BPD are extremely preterm infants who develop chronic lung inflammation despite being treated with antenatal steroids, early surfactant and gentle ventilation. This new form of BPD is caused mainly by premature arrest of alveolarization, and lung growth, and not predominantly by iatrogenic lung injury. Undernutrition, specifically insufficient protein intake, has been considered to play an important role in the pathogenesis of the new BPD. Infants with BPD have higher energy requirements and oxygen consumption than healthy preterm infants. Nutritional support for preterm infants with BPD includes early and aggressive parenteral nutrition, high protein and energy intakes, balancing of lipids and carbohydrates and fluid restriction. Protein intakes of 4.5 g/kg/day have been reported to be well tolerated by preterm infants. Glucose administration is limited by glucose oxidative capacity, above which glucose is converted into fat in an energy inefficient process that results in increased basal energy expenditure, oxygen consumption and CO 2 production. Lipids provide essential fatty acids, improve bioavailability of fat-soluble vitamins, provide energy, and limit conversion of carbohydrates to fat. Recent studies do not support an association between early lipid administration and BPD. Enteral feeding difficulties in infants with BPD include inability to tolerate higher volume of enteral feeds; limitations imposed by fluid restriction, gastroesophageal reflux, and importantly, delayed suck-swallow maturation, difficulties in feeding-breathing coordination, and fatigue. The current strategies for parenteral and enteral nutrition in infants with BPD are reviewed.