Clinically unsuspected hypoxia during sleep and feeding in infants with bronchopulmonary dysplasia.

Infants with bronchopulmonary dysplasia have a high incidence of sudden, unexplained death in the postneonatal period; yet the cause of these deaths is unknown. It was hypothesized that infants with bronchopulmonary dysplasia, thought to be well oxygenated based on awake PaO2 values, would have clinically unsuspected arterial oxygen desaturation during sleep and that these would correlate with the severity of pulmonary function abnormalities. The infants studied were 14 with bronchopulmonary dysplasia, 15 who were preterm, had no bronchopulmonary dysplasia, but did have neonatal respiratory distress syndrome, and eight who were full term and used for control at 37 to 45 weeks postconception. Continuous noninvasive monitoring of oxygenation (arterial oxygen saturation [SaO2, pulse oximetry] and transcutaneous oxygen tension was performed during sleep, wakefulness, and feeding. Greater than 80% of each recording was free of artifact for SaO2. Preterm infants with bronchopulmonary dysplasia and respiratory distress syndrome spent greater time at SaO2 less than 90% than control infants. Most desaturations occurred during feeding and to a lesser extent during wakefulness, active sleep, and quiet sleep. Episodes of desaturation (SaO2 less than 90%) lasted 15 to 20 seconds and were not associated with apnea, bradycardia, cyanosis, or changes in transcutaneous PO2. Only infants with bronchopulmonary dysplasia showed severe desaturations (SaO2 less than 80%). Total desaturation in those infants correlated with airway resistance (body pressure plethysmography). Abnormal pneumographic findings did not predict abnormal desaturations. It was concluded that clinically unsuspected oxygen desaturation occurs frequently in preterm infants with and without bronchopulmonary dysplasia, and profound hypoxemia may be responsible for sudden unexplained deaths in these infants.