Current management of apnea in premature infants: Is caffeine the magic bullet?

Abstract

Apnea of prematurity is one of the most common problems observed in premature infants and it is associated with other morbidities including worse neurodevelopmental outcome. The incidence is higher in the more immature infants and it occurs in up to 90% of infants born under 28 weeks of gestation. The pathogenesis of apnea is due to immaturity of the respiratory control systems characterized by an abnormal ventilatory response to carbon dioxide and hypoxia combined with immature reflex responses. Upper airway obstruction due to airway instability is also a frequent component in apnea of prematurity. These abnormalities frequently persist until the infants reach 32–36 weeks corrected age or longer in the more immature infants. Severe apneic episodes are frequently associated with hypoxia and bradycardia and because of this they can lead to increased risk of CNS damage and neurological sequelae [1]. Infants who are mechanically ventilated also present frequently with episodes of hypoxemia but the mechanisms for these episodes differ from those of apnea of prematurity. The management of the infant with apnea episodes should start by identifying and correcting known conditions that can increase their incidence. These include metabolic abnormalities such as hypoglycemia, hypocalcemia and metabolic alkalosis, anemia and arterial hypotension, and any condition that increases the work of breathing. Medications that depress CNS activity also favor apnea and should be avoided. The level of arterial oxygenation plays a critical role in control of breathing in premature infants and low arterial oxygen tension increases the incidence of periodic breathing and apnea episodes [2].