Abstract 1787

Apnea of Prematurity (AoP) is most frequent in the lowest gestational age (GA) and birth weight infants. The etiology of AoP may be brainstem immaturity. Because brainstem cardiorespiratory and auditory centers are located in proximity to each other, there is reason to suspect that the rate of maturation of each may be similar. We developed norms for ABR wave latencies in infants 28-32 weeks' GA in the first postnatal week. As infants mature, latencies decrease. We classified 5-7 d infants with wave V latency ≥ 1 SD shorter than the mean as "mature" and those with latency ≥ 1 SD longer than the mean as "immature". The number of apnea and bradycardia episodes for these infants over their hospitalization was ascertained by blinded, retrospective chart review. Ninety-seven infants were evaluated; 26 were 28-29 wk GA, 71 were 30-31 wk GA. Of these, 9 had mature and 14 had immature wave V latency. Birth weight, GA, days of respiratory support, and incidence of sepsis were the same in both groups. "Mature" infants had significantly decreased treatment with methylxanthines, number of apneas, and number of bradycardic episodes compared with "immature" infants (Table). Our data suggest that if the ABR is immature at the end of the first week, there is a higher likelihood of apnea and bradycardia, despite use of methylxanthines. The positive predictive value of an abnormal ABR for the occurrence of apnea and bradycardia is 79-92% for each of the first three postnatal weeks. Conversely, the negative predictive value of a mature ABR increases from 44 to 100% over that time period. The maturity of the ABRs at the end of the first week seems to reflect cardiorespiratory brainstem maturity in premature ≤ 32 weeks GA.

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