However, caffeine does not appear to act as a central nervous system stimulant, and it has no acute effect on sleep quality. In late-preterm infants, caffeine has a clear short-term respiratory stimulant effect, and it increases the arousal frequency to hypoxia. The median spontaneous arousal count was 18 per hour at baseline, and 16 per hour during caffeine treatment ( p = 0.88). Caffeine did not affect sleep stage distribution, sleep efficiency, frequency of sleep stage transitions, appearance of REM periods, or the high number of spontaneous arousals. It also increased arousal frequency to SpO 2 desaturations of more than 5% ( p < 0.001). ResultsĬaffeine acted short term as a breathing stimulant with reduction of apneas, improved baseline SpO 2 ( p < 0.001), and decreased 95 percentile of end-tidal carbon dioxide level ( p < 0.01). Polysomnography was performed twice, at baseline on day 1 and on the day after the onset of caffeine treatment (20 mg/kg loading and 5 mg/kg morning maintenance dose). We studied 21 late-preterm infants at a median gestational age of 36 weeks. It has no effect on sleep in the only existing polysomnographic study including ten preterm infants Behavioral and polygraphic studies have conflicting results.
Caffeine is widely used in preterm infants for apnea control.
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