Auditory Nerve and Brainstem Responses in Newborn Infants With Hyperbilirubinemia

Nakamura, Hajime; Takada, Satoshi; Shimabuku, Roberto; Negishi, Hirokuni

doi:10.1203/00006450-198404001-01462

Cited by 60 publications

(84 citation statements)

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“…Since reversible ABR wave changes have been associated with hyperbilirubinemia in the human newborn (4,7,8), it is possible that ABR monitoring of the jaundiced infant may prove to be an important clinical tool for detecting early, reversible bilirubin injury. Although it is not clearly established that these bilirubin-associated ABR changes indicate a need for more aggressive treatment of the jaundice, the continued association of sensorineural hearing loss with hyperbilirubinemia, particularly in the premature infant, indicates a need for further investigation in this area (19,20).…”

Section: Discussionmentioning

confidence: 99%

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Changes in the Auditory Brainstem Response Associated with Intravenous Infusion of Unconjugated Bilirubin into Infant Rhesus Monkeys

et al. 1986

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ABSTRACT'. The auditory brainstem response (ABR) was monitored in nine infant rhesus monkeys during the intravenous infusion of 50-168 mg/kg of unconjugated bilirubin. Sulfisoxazole (200 mg/kg) was sometimes given near the end of or just before the bilirubin infusion if no obvious ABR change had yet occurred. Five of the animals were term gestation, four were preterm, and they ranged from 1 to 40 days of age at the time of study. The three oldest term animals, studied at 20,35 and 40 days of age, respectively, showed variable changes in the ABR waves during bilirubin infusion and these changes were not altered further by sulfisoxazole administration. The other two term infants, studied at 1 and 6 days of age, respectively, showed sulfisoxazole enhanced ABR wave latency increase and amplitude reduction followed by loss of the ABR. Both of these animals became apneic following ABR loss and eventually died. The ABR reappeared in one animal prior to death. Minimal gross and microscopic changes were present in the brain of the 6-day-old animal at autopsy. The four preterm animals all had a progressive wave amplitude decrease followed by loss of the ABR with bilirubin alone. These preterm animals were sacrificed shortly after the ABR loss with only one showing yellow staining of the basal ganglia at autopsy. The infant rhesus monkey may be a useful paradigm for bilirubin-induced ototoxicity as manifested by potentially reversible ABR changes. The changes are dependent on gestational and chronological age of the animal and appear to occur in the peripheral eighth nerve or cochlea as well as in brainstem pathways. (Pediatr Res 20: 51 1-515, 1986) Abbreviation ABR, auditory brainstem response Hearing loss occurs in about half of the infants surviving bilirubin encephalopathy (1), and the ABR measured months or years following the bilirubin injury is often absent or present only at increased stimulus intensity suggesting auditory nerve injury (2, 3).Recent reports have documented a variety of acute, usually reversible ABR wave latency changes, amplitude changes, and

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Section: Discussionmentioning

confidence: 99%

“…It is speculated that at least some of these changes represent reversible bilirubin toxicity, although the data are conflicting as to whether the toxicity is occurring primarily in brainstem pathways (4-7) or auditory nerve (8).…”

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confidence: 99%

Changes in the Auditory Brainstem Response Associated with Intravenous Infusion of Unconjugated Bilirubin into Infant Rhesus Monkeys

et al. 1986

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“…Table 1 lists the values of UB for consideration of exchange transfusion 18)). The other UB levels (peroxidase method) and their relations with clinical observations are taken from various reported studies and reviews (19)(20)(21)(22)(23). Given the rapid acceleration of the increase of UB as TB approaches BBC (4) and the unknown agreement of the UB assays from different places, times, and infant populations, the uniformity of threshold UB levels in Table 1 is both remarkable and comforting.…”

Section: Discussionmentioning

confidence: 99%

Neonatal bilirubin binding capacity discerns risk of neurological dysfunction

Lamola

Bhutani

et al. 2014

Pediatr Res

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Background: Bilirubin binding capacity (BBC) defines the dynamic relationship between an infant's level of unbound or "free" bilirubin and his/her ability to "tolerate" increasing bilirubin loads. BBC is not synonymous with albumin (Alb) levels because Alb binding of bilirubin is confounded by a variety of molecular, biologic, and metabolic factors. Methods: We utilized a novel modification of a previously developed hematofluorometric method to directly assay BBC in whole blood from preterm and term neonates and then combined these data with an archived database. Total bilirubin (TB) was also measured, and multiple regression modeling was used to determine whether BBC in combination with TB measurements can assess an infant's risk for developing bilirubininduced neurotoxicity. results: TB and BBC levels ranged from 0.7-22.8 to 6.3-47.5 mg/dl, respectively. Gestational age (GA) correlated with BBC (r = 0.54; P < 0.0002) with a slope of 0.93 mg/dl/wk by logistic regression. Our calculations demonstrate that recently recommended GA-modulated TB thresholds for phototherapy and exchange transfusion correspond to 45 and 67% saturation of our observed regression line, respectively. conclusion: We speculate that the spread of BBC levels around the regression line (±5.8 mg/dl) suggests that individualized BBC assays would provide a robust approach to gauge risk of bilirubin neurotoxicity compared with TB and GA.B ilirubin binding capacity (BBC) is a determinative measure of a neonate's ability to cope with an excessive bilirubin load (e.g., due to increased bilirubin production from hemolysis) that may be impacted by a variety of biologic factors, including disordered or insufficient bilirubin binding to albumin (Alb) (1,2). The long-standing belief that total serum/ plasma bilirubin (TB), by itself, does not reliably predict an infant's risk for developing bilirubin-induced neurological dysfunction (BIND) or kernicterus has been recently reconfirmed (2-5). The traditional reliance on the TB level alone as a clinical measure of both bilirubin exposure and risk for neurotoxicity may result in overuse of phototherapy or delayed phototherapy in cases where exposure risk is underestimated.It is recommended to use risk factors, including prematurity, hemolysis, sepsis, acidosis, and hypoalbuminemia, to modulate assessment of risk of neurotoxicity at TB levels adjusted for age-in-hours (2,6-8). However, neither serum Alb levels nor the molar ratio of TB to Alb has been predictive of bilirubin neurotoxicity (4,6-8). BBC, when directly measured by various methods, is generally lower than that expected from the Alb level, especially in preterm and sick infants in whom the ratio of capacity to Alb is highly variable (9,10). Thus, the Alb level is only a rough estimate of an infant's BBC. The neuroprotective role of serum Alb, the bilirubin transport protein, was demonstrated in vitro years ago (11). Seminal demonstration that the antibiotic sulfisoxazole was the cause of acute bilirubin encephalopathy even at low TB values highlig...

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“…This usually occurs when the two conditions such as pre-hepatic and hepatic source of bilirubin result in the same time [18]. The higher bilirubin amount is normal due to stress birth in newborns causing the deposition of the yellow pigment in the skin.…”

Section: Normal Jaundice In Newbornmentioning

confidence: 99%

Yellowness Is a Threat to Newborn - A Review

Jena

Mohapatra

Dash

2018

Asian J Pharm Clin Res

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Jaundice is a very well-known disease found worldwide. Jaundice comes from the French word "Jaune" -which means yellow. In medical term, jaundice is known as icterus which is a Greek word. This is a very common disease in the population, which causes the yellowish or greenish pigmentation in the skin and whiteness in the eyes. This is a condition of hyperbilirubinemia in which the amount of bilirubin increases in the blood. In this case, the high amount of bilirubin is found in blood, and the disruption of the movement of bilirubin into the liver and out of the body causes jaundice. Different symptoms seen in this case are yellow skin, yellow/white eyes, dark or reddish urine, loss of appetite, bitter taste of tongue, pale faces, nausea, itching in skin, anfd slow pulse rate. Jaundice may be mild to severe. Different types of jaundice are seen like normal jaundice in newborn, hepatic jaundice, and post-hepatic Jaundice.

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Auditory Nerve and Brainstem Responses in Newborn Infants With Hyperbilirubinemia

Cited by 60 publications

References 0 publications

Changes in the Auditory Brainstem Response Associated with Intravenous Infusion of Unconjugated Bilirubin into Infant Rhesus Monkeys

Changes in the Auditory Brainstem Response Associated with Intravenous Infusion of Unconjugated Bilirubin into Infant Rhesus Monkeys

Neonatal bilirubin binding capacity discerns risk of neurological dysfunction

Yellowness Is a Threat to Newborn - A Review

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