To assess early bilirubin toxicity, a study was made of auditory brainstem responses in relation to total bilirubin levels as well as unbound bilirubin levels in 56 hyperbilirubinemic infants (total bilirubin ≥15.0 mg/dL) and 24 infants who did not have jaundice. The latencies of wave I at 85 dB HL (hearing level) in hyperbilirubinemic infants were significantly greater than those in the control group. The latencies of wave I and V in hyperbilirubinemic infants with unbound bilirubin levels ≥1.0 μg/dL (group C) were greater than those in the control group and in the hyperbilirubinemic infants with unbound bilirubin levels <0.5 μg/dL (group A) and with unbound bilirubin levels <1.0 μg/dL (group B). There were no significant differences of the wave I-V interpeak latency between the control infants and the hyperbilirubinemic infants. Thirty of the 80 infants showed prolonged peak latencies (greater than the mean ± 2 SD for the control infants) of wave I and/or V in one or both ears. The incidences of the prolonged peak latencies in group B (42%) and group C (89%) were significantly greater than that in the control group (12%). The serial determinations of auditory brainstem responses in infants treated with exchange transfusions revealed that the prolonged peak latencies before exchange transfusion improved at 48 and 96 hours after the procedure for wave I, and at 24, 48, and 96 hours after the procedure for wave V. The interpeak latency of wave I-V did not change with exchange transfusion. These results suggest that the auditory nerve is reversibly damaged in the infants with hyperbilirubinemia, and, in particular, the abnormal auditory brainstem response recordings are more closely related to the unbound bilirubin level than the total bilirubin level.
|Original language||American English|
|Number of pages||6|
|State||Published - 24 Jul 1985|