Neuroscience & Medicine, 2012, 3, 270-274
http://dx.doi.org/10.4236/nm.2012.33030 Published Online September 2012 (http://www.SciRP.org/journal/nm)
Otoacoustic Emissions and Evoked Potentials in Infants
after Breast-Feeding Jaundice
——Hearing Dysfunction in Breast-Feeding Jaundice
Adrián Poblano1*, Norma Ballesteros1, Carmina Arteaga1, Blanca Flores2, Teodoro Flores2
1Laboratory of Cognitive Neurophysiology, National Institute of Rehabilitation, Mexico City, Mexico; 2Laboratory of Clinical Neu-
rophysiology, National Institute of Rehabilitation, Mexico City, Mexico.
Received November 11th, 2011; revised May 28th, 2012; accepted June 29th, 2012
We study hearing in a group of infants with Breast-feeding jaundice (BFJ) by means of Transient-evoked otoacoustic
emissions (T-EOE) and Brainstem auditory evoked potentials (BAEP) searching for relationship between bilirubin se-
rum levels and auditory dysfunction. Eleven infants born at-term with BFJ were selected for the study. We studied also
11 control age- and gender matched healthy at-term infants without signs of jaundice. T-EOAE studies were performed
between 5 - 7 days after birth, and 3 months later. BAEP studies were performed once. BFJ group infants exhibited
lower amplitudes in T-EOE than infants in the control group. These differences disappear at the 3-month evaluation. In
BAEP, we observed a significant latency delay of waves I and V in Breast-feeding jaundice group infants. All infants in
both groups demonstrated reproducible wave V response at 30 decibels. No significant correlation values were observed
between bilirubin serum levels and T-EOE and BAEP variables. Our data suggest that BFJ can result in transient pe-
ripheral and central auditory dysfunction. Dysfunction is reversible after treatment of infants with BFJ.
Keywords: Breast-Feed Jaundice; Hyperbilirubinemia; Hearing; Neonates; Transient-Evoked Otoacoustic Emissions;
Brainstem Auditory Evoked Potentials
Previous research has shown the relationship between
neonatal hyperbilirubinemia and sensorineural hearing
loss [1,2]. The majority of investigations have been per-
formed by means of Brainstem auditory evoked re-
sponses (BAEP) in High-risk newborns (HR-NB). These
infants have been followed throughout several years after
birth to confirm hearing loss [3-6]. Observations have
suggested repeatedly that hearing dysfunction is a mani-
festation of injury situated in the auditory neural pathway
along the brainstem. However, one paper had situated the
injury also in the peripheral cochlear system .
Breast-feeding jaundice (BFJ) provides a fair model to
study the peripheral and central auditory alterations after
pure neonatal hyperbilirubinemia, because this is differ-
ent from hyperbilirubinemia in HR-NB. The majority of
infants with BFJ are born at term with adequate weight
and without other risk factors for auditory damage, such
as asphyxia, intracranial hemorrhage, or others. Thus, the
aim of our study was to study hearing function in a group
of infants with BFJ by means of Transient-evoked oto-
acoustic emissions (T-EOE) and BAEP with the hypothesis
that there is a relationship between bilirubin serum levels
and peripheral and central auditory dysfunction. In order
to test our hypothesis, we employed T-EOE as an index
for cochlear toxicity, and BAEP as an index of auditory
2. Materials and Methods
Healthy infants born at General Hospital “Dr. Darío
Fernández” readmitted with jaundice to the Department
of Pediatrics during their first week of life with diagnoses
of BFJ were selected for the study. Inclusion criteria in-
cluded the following: jaundice in Kramer zone ≥ 2;
bilirubin levels > 15 mg/dL; age at birth between 37 and
41 of gestational weeks; weight > 2750 g; 5-min Apgar
score > 7, and without other risk factors for hearing
damage. All of the infants were exclusively breastfed.
Mothers of the patients noted jaundice at home, and it
was not accompanied by decreased activity or poor feed-
ing. None newborn had any laboratory evidence of
hemolytic disease as evidenced by anemia, reticulocyto-
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Otoacoustic Emissions and Evoked Potentials in Infants after Breast-Feeding Jaundice 271
sis, or another abnormality. Infants were screened for
neurological, and auditory dysfunction [8,9], and for
perinatal factors associated with an increased risk of hy-
perbilirubinemia including, maternal diabetes mellitus,
high blood pressure, administration of oxytocin during
labor, as well as central nervous system bleeding or in-
jury, or infection. At time of readmission to the hospital,
the infants were evaluated for clinical signs of acute
bilirubin encephalopathy manifested as changes in level
of consciousness, tone/movement, poor feeding, abnor-
mal cry, opisthotonus and/or seizures, and alterations in
brainstem function. Other causes of hyperbilirubinemia
including scalp bruising, dehydration and sepsis were
investigated. Laboratory studies included complete blood
counts, electrolytes, glucose, and cultures. Cranial Ultra-
sonographic studies were performed in all newborns to
rule-out other brain pathologies. Bilirubin determinations
and T-EOE were performed in the first days after jaun-
dice was recognized to identify and treat possible neuro-
development deviations; T-EOE were repeated 3 months
later. BAEP determinations were performed rapidly after
T-EOE examination once. We studied 11 infants with
BFJ (four males and seven females) and 11 control heal-
thy newborn infants who were age- and gender matched
at the time of study without signs of jaundice. Results of
each study were blinded to the researchers who revised
BAEP and T-EOE determinations for group pertinence.
The Research and Ethics Committees of the Hospital and
of the Institute approved the protocol. Informed consent
was obtained from parents of infants and is contained in
signed forms according to the principles expressed in the
Declaration of Helsinki.
2.2. Bilirubin Determinations
Samples were obtained by peripheral venipuncture. All
specimens were protected from light after they were
drawn, and these were analyzed immediately. Total
bilirubin concentration was determined spectrophotomet-
rically, and unbound bilirubin concentration was meas-
ured by the peroxidase method using a clinical analyzer
(UB analyzer, Arrows Co., Osaka, Japan). Samples with
high unbound bilirubin > 0.5 µg/dL were measured for
concentration of direct bilirubin by diazo method .
2.3. Transient-Evoked Otoacoustic Emissions
Responses were recorded with the ILO-88 (Otodynamic
Ltd, London, UK), during a sleep session. Studies were
conducted in a sound-proofed room. Prior to the Oto-
acoustic emission study, ear canals were checked with an
otoscope to confirm permeability of external auditory
channel. We use a miniature acoustic probe fitted into the
infant ear channel. The probe incorporates a small micro-
phone and ear-speaker. Stimuli consisted of 80 decibel
(dB) HL (Hearing level) click stimulation of 100 µsec
delivered at a repetition rate of 11/sec. Signal was ampli-
fied and filtered between 350 and 6400 Hz. Two hundred
fifty stimuli were averaged. Analysis time was 20 milli-
sec. Contralateral ear masking with white noise 20 dB
below stimulus intensity was administrated simultane-
ously. Adequate T-EOAE responses were identified
based on reproducibility of ≥75%. The detection thresh-
old of T-EOAE was measured by stimulating the ear with
decreasing click intensities in 20-dB steps. Each ear was
tested separately .
2.4. Brainstem Auditory Evoked Potentials
BAEP were recorded and analyzed following standard
international recommendations . BAEP determina-
tions were performed after a feeding sleep in a sound-
proof room. Each subject was tested with BAEP using an
ATI system (Buenos Aires, Argentina). Three gold-disk
electrodes were placed on the scalp, with negative elec-
trode on ipsilateral mastoid, positive on vertex, and neu-
tral on contralateral mastoid. Interelectrode impedances
were ≤2 kilo-ohms. Electrical activity among electrodes
was amplified and averaged over a 10 millisec time base.
Stimulus was administrated through a Telephonics TDH-
49 earphone (Telephonics Co., Huntington, NY, USA).
Stimuli were presented monoaurally at a rate of 11/sec.
Initial presentation intensity was 70-dB HL and decreas-
ed by 20-dB steps to determine neurophysiologic thresh-
old of response. Contralateral ear masking with white
noise 20 dB below stimulus intensity was administrated
simultaneously. Stimuli were delivered mono-aurally and
consisted of 100 µsec alternating clicks. Band pass filters
were set between 100 and 3000 Hz, and stimulus average
was 2024 clicks. The process was repeated at least once
to ensure reproducibility of response. Latencies of waves
I, III, and V were measured by manual cursor placement
at left and right ear recordings separately; I-III, III-V, and
I-V interpeak intervals were calculated automatically by
computer software; a normal hearing threshold was de-
termined if the reproducible wave V response was pre-
sent at last at 30 dB level.
2.5. Data Analysis
We calculate average and Standard deviation (SD) of
quantitative variables and percentages of qualitative
variables. We report BAEP data from the ear producing
the faster I-V conduction time as published previously
elsewhere [13,14], because in this way we avoid sub-
clinical hearing conductive alterations. Comparisons be-
tween both groups were performed by two-tailed Student
Copyright © 2012 SciRes. NM
Otoacoustic Emissions and Evoked Potentials in Infants after Breast-Feeding Jaundice
t test. We performed Pearson correlation analysis be-
tween total, indirect, and direct bilirubin serum levels
and T-EOE and BAEP variables. The level of statistical
significance a-priori chosen was p ≤ 0.05. Calculations
were performed with the SPSS 14.0 (SPSS Inc., Chicago,
IL, USA) computer program .
Clinical characteristics of infants in each group are
shown in Table 1; no significant differences in compared
variables between groups were observed. The infants age
at which mother requested attention ranged between 5
and 7 days after birth (median, 6 days). Average bilirubin
determinations in BFJ-group infants are presented in Ta-
Averages of response amplitude by ear determined by
T-EOE at birth and 3 months later are shown in Table 3 ;
in the neonatal period, there were significant differences
in both ear responses between groups, with BFJ-group
infants exhibiting lower amplitudes than infants in the
control group. However, these differences disappear at
the 3-month evaluation when hyperbilirubinemia was
Average of main waves (I, III, and V) and interwave
intervals (I-III, III-V, and I-V) in BAEP determinations
are presented in Table 4; we observed a significant la-
tency delay of waves I and V in BFJ-group infants.
However, all infants in both groups demonstrated repro-
ducible wave V response at 30 dB, suggesting adequate
hearing and thus no second BAEP study was performed
in infants. We did not observe cases of auditory neu-
ropathy. No significant correlation values were observed
between total, indirect, and direct bilirubin serum levels
and T-EOE, and BAEP variables.
Table 1. Clinical characteristics of control (n = 11) and in-
fants with Breast-feeding jaundice (BFJ) (n = 11).
Control (x ± SD) BFJ (x ± SD)
Weight at birth (g) 2897 ± 371 2863 ± 350
Age at birth (weeks) 37.9 ± 1.23 38.3 ± 0.84
1 min Apgar score 7.6 ± 1.21 8.0 ± 0.52
5 min Apgar score 9 ± 0 9 ± 0
x = average; SD = Standard deviation.
Table 2. Average of maximum bilirubin serum levels
(mg/dL) in infants with Breast-feeding jaundice (BF J).
Total bilirubin 18.00 0.64
Direct bilirubin 0.65 0.12
Indirect bilirubin 17.35 0.60
x = average; SD = Standard deviation.
Table 3. Average ± standard deviation of amplitude re-
sponses (dB) in T-EOE in control and BFJ-group infants.
group 17.96 ± 7.9319.08 ± 9.38 16.10 ± 6.02 18.60 ± 7.01
group 12.48 ± 8.7413.02 ± 7.57 16.60 ± 8.00 19.14 ± 6.25
p 0.05 0.04 ns ns
T-EOE = Transient-Evoked otoacoustic emissions; BFJ = Breast feeding
jaundice; not significant.
Table 4. Average ± standard de viation of latencies (msec) of
main waves and interval interwaves of BAEP at 80 dB in
control infants and in infants with BFJ.
Wave/Interval (msec) Controls BFJ p
I 1.70 ± 0.13 1.83 ± 0.250.04
III 4.41 ± 0.18 4.49 ± 0.23ns
V 6.64 ± 0.26 6.79 ± 0.290.05
I-III 2.71 ± 0.14 2.66 ± 0.21ns
III-V 2.23 ± 0.23 2.30 ± 0.25ns
I-V 4.94 ± 0.26 4.96 ± 0.29ns
x = average; SD = standard deviation; BAEP = Brainstem auditory evoked
potentials; dB = decibels; BFJ = Breast feeding jaundice; ns = not signifi-
In this paper, we showed that BFJ in low-risk at-term
infants results in both auditory peripheral and central
dysfunctions as reflected in T-EOE and BAEP alterations.
We also observed that these auditory and neurophysi-
ologic alterations could be reversible after rapid man-
agement and resolution of the hyperbilirubinemia. How-
ever, we could not demonstrate our hypothesis about sig-
nificant correlation between bilirubin serum levels and
peripheral and central auditory dysfunction.
Several in-vitro studies showed that bilirubin-induced
neuronal toxicity involves changes in energy metabolism,
alteration in membrane function, decreased membrane
potential, alteration in enzyme function, and inhibition of
protein synthesis [16,17]. It also appears from these pre-
viously cited in-vitro studies that immature cells are
more sensitive to bilirubin toxicity than differentiated
cells, supporting clinical experience demonstrating that
premature neonates are more susceptible to bilirubin-
induced neurotoxicity than at-term infants. However, our
data also suggest that the auditory responses of otherwise
healthy at-term infants could be injured by hyper-
Various clinical factors, such as hypothermia, hypoxia,
acidosis, hypercarbia, asphyxia, sepsis, intraventricular
hemorrhage, and hemolysis, have been postulated to ex-
Copyright © 2012 SciRes. NM
Otoacoustic Emissions and Evoked Potentials in Infants after Breast-Feeding Jaundice 273
plain the occurrence of bilirubin neurotoxicity at much
lower levels of serum total bilirubin . These factors
are thought to increase the risk of kernicterus by affect-
ing serum bilirubin-albumin binding, bilirubin entry into
the brain, or tissue uptake of bilirubin. For example, one
study identified a degree of acidosis with low serum al-
bumin levels that occurred prior to the maximum un-
bound bilirubin level and that was present in newborns
with kernicterus . On the other hand, a study of fol-
low-up of at-term or near-term infants with BFJ reported
transient neurologic abnormalities. These abnormalities
resolved following management with phototherapy and
exchange transfusions, and bilirubin level did not corre-
late with the long-term prognosis . Results from this
study are partially in agreement with our data.
One of the tools commonly utilized to investigate
bilirubin-induced neurotoxicity in neonates is BAEP test.
BAEP has been studied in high-risk pre-term newborns
as a non-invasive auditory neurophysiologic assessment
of bilirubin neurotoxicity. Many observations confirm
the higher frequency of auditory alterations in newborns
after hyperbilirubinemia, such a delay of wave I, III and
V latencies or the absence of response at higher intensi-
ties of auditory stimulation [3-6]. This is in indirect
agreement with our observations, because we observed a
wave I and V delay. Other studies have shown correla-
tion between indirect bilirubin serum levels and BAEP
alterations ; however we are unable to confirm this
correlation in our observations. Other studies have dem-
onstrated that BAEP alterations are reversible after blood
exchange . However, we were unable to confirm this
observation, because our infants with BFJ were not blood
ex-changed and all our infants in both, control and BFJ
groups presented response at 30 dB. Thus, there was no
reason for subsequent appointment 3 months later for an
additional BAEP study.
Otoacoustic emissions have been used to screen hear-
ing alterations after neonatal hyperbilirubinemia. T-EOE
has been employed as a first step in rapid screening of
infant auditory performance. Study investigators usually
carry out a BAEP examination after an abnormal T-EOE
[2,7]. Researchers have observed a decrease in the re-
sponse amplitude of T-EOE such as that which we ob-
served in our BFJ-group infants, or an increased number
in absences of response after auditory stimulation.
Recently, Jangaard et al. did not observed an increased
frequency in cerebral palsy, developmental delay, autism,
and hearing loss in a population of infants born at-term
or near-term with other neurologic risk-factors other than
hyperbilirubinemia (≥19 mg/dL) . This result is also
in indirect agreement with our observations, because we
observed no case of hearing loss. However, because we
measured T-EOE and BAEP variables quantitatively, we
were able to detect subclinical effects of transient hyper-
bilirubinemia in the peripheral and central auditory sys-
tem of infants with BFJ, that were not observed by the
other work team.
We did not observe cases of auditory neuropathy in
our sample, but this may be explained of our small sam-
ple size . An alternative explanation may be that
auditory neuropathy after neonatal hyperbilirubinemia is
a complex alteration that requires other risk-factors than
only high bilirubin serum levels for the production of
auditory alterations. However, our infants must be fol-
lowed, because language delay has been reported as a
possible complication after neonatal hyperbilirubinemia
Our research possesses some limitations; thus, our re-
sults must be considered as tendencies, not strong con-
clusions. The sample is small, despite its being highly
selected and age-gender-matched to a control group.
Therefore, in the future a greater number of at-term in-
fants with BFJ must be studied. Moreover, follow-up
time was brief, notwithstanding follow-up of these in-
fants will continue with these as out-patients in the Pedi-
atrics Department to determine whether minimal auditory
dysfunction or language alteration during child develop-
ment can be a result of the BFJ episode during the neo-
natal period of life.
Our data suggest that BFJ can result in peripheral and
central auditory dysfunction. The dysfunction is reverse-
ble; thus, early identification and treatment of infants
with BFJ is mandatory to prevent possible auditory com-
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