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APNEA OF PREMATURITY CAUSES
Category: Child Health
Abstract : apnea of prematurity causes: A premature neonate in whom all other causes of
apnea have been excluded may be considered to have true idiopathic apnea.
Although the etiology of AOP is not fully understood, several mechanisms have
been proposed to explain this condition, including the following: • AOP is
considered the final response of incompletely organized and interconnected
re
apnea of prematurity causes: A premature neonate in whom all other causes of
apnea have been excluded may be considered to have true idiopathic apnea.
Although the etiology of AOP is not fully understood, several mechanisms have
been proposed to explain this condition, including the following:
• AOP is
considered the final response of incompletely organized and interconnected
respiratory neurons to a multitude of afferent stimuli. Abnormal control of
breathing is secondary to neuronal immaturity of the brain.
• In a
premature neonate, protective respiratory reflex activity is decreased, and
Hering-Breuer reflex activity is increased.
• Dopaminergic receptors may
have an inhibitory role in peripheral chemoreceptor responses and central neural
mechanisms elicited by hypoxia. Evidence from neonatal animal studies indicates
that endogenous endorphins may depress the central respiratory drive. Although
endogenous opiates may modulate the ventilatory response to hypoxia in newborn
animals, a competitive opiate receptor antagonist, naloxone, has no benefit in
the resuscitation of an asphyxiated human neonate. Naloxone appears to have no
therapeutic role in AOP.
• Negative luminal pressures are generated
during inspiration, and the compliant pharynx of the premature neonate is
predisposed to collapse. Genioglossus activation failure has been most widely
implicated in mixed and obstructive apnea in adults and infants. The ability of
medullary chemoreceptors to sense elevated CO2 levels is impaired; thus, an
absent, small, or delayed upper airway muscle response to hypercapnia can
possibly cause upper airway instability when accompanied by a linear increase in
chest-wall activity. This impairment may predispose the infant to obstructed
inspiratory efforts after a period of central apnea.
• Another important
factor to consider is the excitation of chemoreceptors in the larynx by acid
reflux. Laryngeal receptors send afferent fibers to the medulla and can elicit
apnea when stimulated.
• Swallowing during a respiratory pause is unique
to apnea and does not occur during PB. Accumulation of saliva in the pharynx
hypothetically could prolong apnea with a chemoreflex mechanism and also elicit
swallowing movements.
• Gastroesophageal reflux (GER) has been associated
with recurrent apnea. Menon et al observed that regurgitation of formula into
the pharynx after feeding is associated with an increased incidence of apnea in
premature infants. Gastric fluids can possibly activate laryngeal chemoreflexes,
leading to apnea. Aminophylline may also exacerbate reflux in patients with
apnea. On the other hand, findings from several studies have not demonstrated a
relationship between episodes of apnea and episodes of acid reflux into the
esophagus.
• However, Newell et al demonstrated that effective control of
GER in infants with xanthine-resistant AOP was associated with a significant
decrease in number of apneas. In 1992, Booth suggested that the reduction of
apneic episodes was due to the resolution of esophagitis because clinical
improvement of apnea occurred 1-2 days after initiation of antireflux
therapy.
• Many clinicians treat xanthine-resistant apnea with H2
blockers, metoclopramide, thickened formula, and upright positioning during
feeding. However, to the author's knowledge, no controlled trials have
demonstrated that antireflux medications are effective in preventing apnea.
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