title: Enhanced feeding in very-low-birth-weight infants may cause electrolyte disturbances and septicemia--a randomized, controlled trial.
abstract: OBJECTIVE
  High supply of protein and energy has been introduced to very-low-birth-weight infants to improve growth and cognitive development. The aim of this study was to compare two different feeding strategies on postnatal growth and clinical outcome during neonatal hospitalization.
  
  
  METHODS
  Fifty very-low-birth-weight infants were randomized to either an enhanced or a standard feeding protocol within 24 h after birth. Chi-square and T-tests were applied.
  
  
  RESULTS
  First week protein, fat and energy supply was significantly higher in the intervention group compared to the control group (all P < 0.001). After inclusion of 50 patients we observed a higher occurrence of septicemia in the intervention group, 63% vs. 29% (P = 0.02), and no more patients were included. The infants in the intervention group demonstrated improved postnatal growth, but they also disclosed significant electrolyte deviations during the first week of life with hypophosphatemia, hypokalemia and hypercalcemia. First week phosphate nadir was lower in the infants experiencing septicemia (1.23 (0.50) mmol/L) as compared to the infants without (1.61 (0.61) mmol/L) (P = 0.03).
  
  
  CONCLUSIONS
  Our study implies that enhanced feeding may induce electrolyte imbalances in VLBW infants, and that deleterious side effects similar to those seen in refeeding syndrome may occur. ClinicalTrials.gov, number NCT01103219 and the EudraCT number is 2010-020464-38.
authors.affiliation: Oslo University Hospital HF, Ullevål, Oslo, Norway. sissel.moltu@medisin.uio.no
authors.forename: Sissel J
authors.initials: SJ
authors.lastname: Moltu
authors.forename: Kenneth
authors.initials: K
authors.lastname: Strømmen
authors.forename: Elin W
authors.initials: EW
authors.lastname: Blakstad
authors.forename: Astrid N
authors.initials: AN
authors.lastname: Almaas
authors.forename: Ane C
authors.initials: AC
authors.lastname: Westerberg
authors.forename: Kristin
authors.initials: K
authors.lastname: Brække
authors.forename: Arild
authors.initials: A
authors.lastname: Rønnestad
authors.forename: Britt
authors.initials: B
authors.lastname: Nakstad
authors.forename: Jens P
authors.initials: JP
authors.lastname: Berg
authors.forename: Marit B
authors.initials: MB
authors.lastname: Veierød
authors.forename: Kirsti
authors.initials: K
authors.lastname: Haaland
authors.forename: Per O
authors.initials: PO
authors.lastname: Iversen
authors.forename: Christian A
authors.initials: CA
authors.lastname: Drevon
mesh_terms: D002118:Calcium / Q000097:blood / Q000652:urine; D005260:Female; D006801:Humans; D007008:Hypokalemia / Q000097:blood / Q000175:diagnosis / Q000178:diet therapy; D017674:Hypophosphatemia / Q000097:blood / Q000175:diagnosis / Q000178:diet therapy; D007227:Infant Nutritional Physiological Phenomena; D007231:Infant, Newborn; D007235:Infant, Premature, Diseases / Q000097:blood / Q000175:diagnosis / Q000178:diet therapy; D019102:Infant, Very Low Birth Weight / Q000254:growth & development*; D016014:Linear Models; D008274:Magnesium / Q000097:blood; D008297:Male; D008895:Milk, Human / Q000737:chemistry; D010288:Parenteral Nutrition; D010710:Phosphates / Q000097:blood / Q000652:urine; D011188:Potassium / Q000097:blood; D018805:Sepsis / Q000097:blood / Q000178:diet therapy*; D012964:Sodium / Q000097:blood; D014882:Water-Electrolyte Balance
chemical_list: D010710:Phosphates; D012964:Sodium; D008274:Magnesium; D011188:Potassium; D002118:Calcium