title: Eliminating sleep-associated hypoxemia improves growth in infants with bronchopulmonary dysplasia.
abstract: OBJECTIVE
  Infants with bronchopulmonary dysplasia (BPD) have been previously reported to have a decrease in growth velocity after stopping supplemental oxygen (SO). SO was stopped after a short-term recording (20-30 minutes) of pulse oxygen saturation (Sao2) of 92% or greater in room air. Other studies have documented that Sao2 decreases further during feedings and sleep in infants with BPD. Two questions were asked: (1) whether short-term, awake Sao2 studies would reliably predict prolonged sleep Sao2; and (2) how Sao2 sustained at 88% to 91% vs 92% or greater in room air would impact growth velocity in infants with BPD.
  
  
  METHODS
  Short-term Sao2 studies were prospectively compared with prolonged sleep Sao2 (n = 63) and the growth velocity of infants who had SO discontinued after a prolonged sleep Sao2 recording of 88% to 91% (group 1; n = 14) versus 92% or greater (group 2; n = 34) in room air.
  
  
  RESULTS
  Failure to maintain Sao2 at predetermined levels occurred in 18 (29%) of 63 infants during their first prolonged sleep study. There was no correlation between short-term awake Sao2 and prolonged sleep Sao2 recordings (r = .02). Body weight, height, weight for height, and rate of weight gain were similar for all study infants before SO was stopped and remained constant for group 2 infants after SO was stopped. However, group 1 infants had a significant decrease in the rate of weight gain (17.3 +/- 13.1 vs 3.7 +/- 6.1 g/kg per day), and the mean z scores for weight gain and weight for height also decreased significantly for group 1 infants. Energy intake, incidence of acute infection, hematocrit values, and medication use did not differ before or after stopping SO in either group.
  
  
  CONCLUSIONS
  This study indicated that short-term, awake Sao2 measurements do not predict prolonged sleep Sao2, and overall, infants with BPD continued a positive growth trend when Sao2, remained greater than 92% during prolonged sleep.
authors.affiliation: Department of Pediatrics, University of Utah, Salt Lake City 84132, USA.
authors.forename: L J
authors.initials: LJ
authors.lastname: Moyer-Mileur
authors.forename: D W
authors.initials: DW
authors.lastname: Nielson
authors.forename: K D
authors.initials: KD
authors.lastname: Pfeffer
authors.forename: M K
authors.initials: MK
authors.lastname: Witte
authors.forename: D L
authors.initials: DL
authors.lastname: Chapman
mesh_terms: D000704:Analysis of Variance; D001997:Bronchopulmonary Dysplasia / Q000097:blood / Q000503:physiopathology / Q000628:therapy*; D006128:Growth / Q000502:physiology*; D006801:Humans; D000860:Hypoxia / Q000097:blood / Q000503:physiopathology / Q000628:therapy*; D007223:Infant; D007231:Infant, Newborn; D010100:Oxygen / Q000097:blood; D010102:Oxygen Inhalation Therapy / Q000706:statistics & numerical data; D011446:Prospective Studies; D012890:Sleep / Q000502:physiology*; D013997:Time Factors; D015430:Weight Gain / Q000502:physiology
chemical_list: D010100:Oxygen