Abstract
Introduction
Prematurely born infants (PBI) very often present apnea during sleep. These events can still be detected at term equivalent age (TEA), with variable impact on ventilation. An immature respiratory control is responsible for these events, which disappear as the infant matures. This observational study describes polysomnographic results for a cohort of 12 PBI who were examined at TEA and again 11 weeks later.
Method
A cohort of 12 extreme preterm (average gestational age of 27 weeks) infants were followed by the HUDERF sleep unit as they received a cardio-respiratory monitor for home uses during sleep. Polysomnography 1 (PSG1) was performed at TEA for the 12 infants. 10 of these 12 infants had another PSG (PSG2) 11 weeks later.
Results
All infants presented with apnea of prematurity at TEA, which significantly decreased at PSG2. Respiratory rates and heart rates both decreased significantly, while saturation in oxygen was not significantly different when compared between PSG1 and PSG2.
Discussion
Poorly tuned chemo and mechanoreceptors together with a highly pliable thorax, immature lungs and suboptimal central respiratory control are responsible for the apnea. These respiratory events disappear as the child matures.Lower heart and respiratory rates at PSG2 reflect the maturing parasympathetic system.
Conclusion
Apnea in PBI result from suboptimal respiratory central control. They can result in a vicious cycle where hypoxia increases, thereby further destabilizing respiratory control. Further studies are necessary to investigate the feasibility of home use of respiratory support in the case of oxygen dependency in PBI.