Abstract
AbstractApnea of prematurity (AOP) affects the majority of infants born prematurely, before 34 weeks of gestational age. AOP is a common diagnosis in the neonatal intensive care unit and one of significant clinical importance, both immediate and long term, as it is associated with reduced survival and poorer respiratory and neurodevelopmental outcomes. In this review, we provide an up-to-date summary of recent advances in the understanding of the pathophysiology of AOP, as well as the clinical questions relevant to physicians and staff treating infants with AOP. Finally, we discuss monitoring and discharge decisions, as these are areas of significant uncertainty.
Highlights
We provide an up-to-date summary of recent advances in the understanding of the pathophysiology of Apnea of prematurity (AOP), as well as the clinical questions relevant to physicians and staff treating infants with AOP
Preterm birth is defined by the World Health Organization as delivery before 37 completed weeks of gestation, with extreme prematurity defined as birth occurring at less than 28 weeks of gestational age, very preterm birth occurring between 28 and 32 wGA, and moderate-to-late preterm birth occurring from 32 through 36 wGA.[1]
It is responsible for the rapid rise in ventilation that occurs in response to hypoxia.[12]
Summary
Preterm birth is defined by the World Health Organization as delivery before 37 completed weeks of gestation, with extreme prematurity defined as birth occurring at less than 28 weeks of gestational age (wGA), very preterm birth occurring between 28 and 32 wGA, and moderate-to-late preterm birth occurring from 32 through 36 wGA.[1]. Immaturity of the brain stem chemosensitive neuronal network that responds to fluctuations in blood CO2 has a profound effect on the respiratory response and tendency for apnea in premature infants.[10] Another mechanism proposed to explain AOP is periodic breathing, which is frequent in term neonates and even more so in premature ones. The carotid body is a cluster of cells located at the bifurcation of internal and external carotid arteries, and acting as a sensor of arterial partial O2 and CO2 pressures It is responsible for the rapid rise in ventilation that occurs in response to hypoxia.[12] Decreased or increased carotid body sensitivity in response to hypoxia has been described in premature infants.[13,14] Incomplete developmental synaptogenesis, hyperoxic exposures from mechanical ventilatory support are partly responsible for the risk of reduced carotid body sensitivity, along with the effects of lipopolysaccharide and inflammatory mediators such as tumor necrosis factor α, which reduce carotid body sensitivity even further.[15] carotid body output and respiratory drive are partly modulated centrally through inhibitory adenosine receptors in the brain stem. No study to date has examined the epigenetic changes associated with AOP in premature human infants, though epigenetic regulation is central to the pathophysiology of prematurity.[30]
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