Abstract
This study aimed to evaluate jaundice outcomes of low-birthweight premature infants commenced on earlier versus later nutrient supplementation (80 mL/kg/day vs. 160 mL/kg/day; total fluid intake, F80 vs. F160). Demographics, feeding regimens, and clinical outcomes data were collected. Infant and maternal characteristics were similar. Earlier nutrient supplementation was associated with multiple improved jaundice outcomes: total (TSBR), unconjugated and conjugated (CSBR) serum bilirubin values (196 ± 46 vs. 228 ± 52, 184 ± 44 vs. 212 ± 50, 12 ± 4 vs. 16 ± 5, respectively, all p < 0.001); phototherapy (39% vs. 64%, p < 0.0001). % CSBR/TSBR ratio was similar between groups. For those on phototherapy, duration and median irradiance were similar. F80 infants experienced reduced: feeding intolerance (26.0% vs. 45.2%, p = 0.007); length of stay (16.0 ± 0.64 vs. 18.8 ± 0.74 days, p = 0.03), maximum weight loss as % birth weight (5% vs. 6%, p = 0.03); decrease in weight Z-score at 10 days (−0.70 ± 0.03 vs. −0.79 ± 0.03, p = 0.01). F80 infants regained birthweight earlier (10.0 ± 0.3 days vs. 11.5 ± 0.3 days, p < 0.0001) and had no differences in adverse clinical outcomes. We speculate that earlier nutrient supplementation improved jaundice outcomes due to enhanced excretion/elimination of bilirubin.
Highlights
The basic etiology of neonatal hyperbilirubinemia is well understood
The key finding of our study is that earlier nutrient supplementation of predominantly breastmilk fed babies was associated with multiple beneficial jaundice outcomes such as lower these outcomes serum bilirubin (TSBR), USBR and conjugatedsignificantly bilirubin included (CSBR) and lower phototherapy rates and less exposure irradiation
As we have previously reported in some detail [11], the nutrition requirements of moderate and late preterm infants is not well understood, earlier nutrition in the form of breastmilk fortification is well tolerated and not associated with any negative outcomes
Summary
The basic etiology of neonatal hyperbilirubinemia is well understood. Factors include: bilirubin formation from the breakdown of heme present in normal red blood cells; conjugation in the liver with glucuronic acid to form a water-soluble form; excretion in the bile [1]; some hydrolysis of bilirubin glucuronide in the small intestine with resultant reabsorption of bilirubin; final removal via faeces [2]. In the near term to term infant, risk factors for developing severe unconjugated hyperbilirubinemia include: haemolytic disease; gestational age 35–36 weeks; cephalohematoma; exclusive breastfeeding, if nursing is problematic and weight loss significant; East Asian race; macrosomic infants of a diabetic mothers; male gender [3]. A decreased risk of significant jaundice has been associated with: gestational age of 41 weeks; discharge from hospital after 72 h; exclusive bottle feeding [3]
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