Apnea in the newborn is primarily a disorder of prematurity and is usually secondary to immaturity of central nervous system respiratory control. Apnea in the full term infant is less frequent and assessment for upper airway problems, seizures, meningitis and other infections frequently becomes the initial focus. In both premature and full-term infants, obstructive apneas may induce hypoxemia and cyanosis, and thus increase the incidence of Apparent Life Threatening Events(ALTE). We present a case of of sleep disordered breathing in a newborn with initial presentation of ALTE.
The patient is a 24-day-old, full term newborn who is the product of a normal pregnancy and normal spontaneous vaginal delivery. The first 9 days of life were unremarkable, however on day 10 a cyanotic episode was witnessed by the mother. The patient was brought to a hospital and two more cyanotic episodes occurred within 48 hours of admission. These episodes occurred during sleep and were associated with oxygen desaturation and bradycardia. Subsequent neurologic, GI, cardiac, metabolic and septic workups were negative. Within 72 hours of hospital discharge with a home apnea monitor, another episode prompted a second hospital admission. This episode was associated with shallow breathing and right leg kicking, thus video EEG workup for seizure was done. Sleep medicine consultation revealed expected sleep/wake cycling with 1–2 hours of wakefulness followed by approximately 3–4 hours of sleep. The parents denied a history of snoring, choking or grunting noises in the infant. Although there was a history of vomiting episodes after feedings, these did not have a temporal relationship to cyanotic episodes. The family history was devoid of ALTE, SIDS or sleep disorder breathing. There was no history of smoking in the home. The physical exam was negative for pharyngeal or craniofacial abnormalities. Video EEG monitoring was negative for evidence of epilepsy. Polysomnography(PSG) revealed 25 apneas and hypopneas per hour. One central event and one obstructive event each lasted over 10 seconds. The electrocardiogram showed bradycardia as low as 58 BPM. End-tidal C02(ETC02) levels as high as 57 mmHg were recorded. The infant was treated with caffeine, after which cyanotic events and apnea monitor alarms were abolished and repeat PSG with ETC02 yielded normal results.
Instability of the control of breathing secondary to immaturity of CNS respiratory centers is not limited to the premature infant. More specifically, the causes of respiratory instability may include immaturity of inhibition/excitation mechanisms during REM sleep, inefficient respiratory response to hypercapnia or hypoxia and inefficient response to resistive loads. Periodic breathing and short central apneas are known to occur in normal, healthy, full-term infants. Obstructive events and events lasting greater than 10 seconds however, are rare in normal infants and are considered pathologic. At least one study has shown that over 50% of infants referred for ALTE may in fact have obstructive sleep apnea or evidence of upper airway resistance syndrome.
The interesting points of this case include the utility of ETC02 and efficacy of caffeine treatment in abolition of respiratory events in the full-term newborn (this is off-label use). This case also illustrates how the addition of ETC02 to PSG adds sensitivity in ruling out pathologic breathing. It should also be noted that congenital central hypoventilation syndrome is part of the differential diagnosis in these cases and that ETC02 monitoring reveals the lack of hyperventilatory response to hypercapnic stimulus typical of these newborns.
K.R. Dixon, None.