Abstract

To examine (1) sleep architecture of infants at varied risk for sudden infant death syndrome, (2) delays or advances in preterm infants at term postmenstrual age, (3) whether ventilatory support and gestational age alter sleep, (4) whether steroids alter sleep, (5) confounding influences of sex, small for gestational age, and maternal smoking. Overnight polysomnography. Percentage of active sleep, quiet sleep, indeterminate, and awake time per total recording time; mean and longest duration of state epochs; number of episodes > or = 10 minutes; and sleep efficiency. Collaborative Home Infant Monitoring Evaluation (CHIME). Two hundred one preterm and 198 term infants between 33 and 58 weeks postmenstrual age during polysomnography. Fifty-one term infants with an apparent life-threatening event without known etiology (apnea of infancy), 59 subsequent siblings of babies who died of sudden infant death syndrome, and 88 healthy term infants. Tracings of infants with apnea of infancy and healthy term infants were similar. Subsequent siblings of babies who died of sudden infant death syndrome spent less time in quiet sleep. Preterm infants (< or = 37 weeks postmenstrual age) exhibited immature architecture compared with infants of term postmenstrual age. The latter exhibited similar sleep except that they had a lower percentage of quiet sleep and longer mean indeterminate and longest indeterminate episodes. Preterm infants with the youngest gestational age lagged behind older preterm infants. Neither sex nor use of steroids affected sleep. Assisted ventilation was associated with a delay in maturation, small-for-gestational age status with increased active sleep, and smoking with increased awake time. With few exceptions, asymptomatic premature infants do not exhibit significant delays in sleep architecture compared with term infants at comparable postmenstrual age. The preterm infant with an early gestational age and morbidity exhibited delayed sleep architecture.

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