ETIOLOGY OF HEARING LOSS IN CHILDREN
Nongenetic Causes
HEARING LOSS IN CHILDREN
Nancy J. Roizen MD
Department of Pediatrics, University of Chicago Pritzker School of Medicine, and Section of
Developmental and Behavioral Pediatrics, Chicago, Illinois
Address reprint requests to
Nancy J. Roizen, MD
Department of Pediatrics, MC 900
5841 South Maryland Avenue
Chicago, IL 60637
The identification of a specific cause of hearing loss in children facilitates
optimal management. When a specific cause of a child's hearing loss is
identified, parents are usually relieved. In many of the disorders associated with
hearing loss, other organ systems are involved, and frequently hereditary
factors are present. [61] In the article by Grundfast on the genetic causes of
hearing loss, identification of the various hereditary causes and genetic
counseling are discussed. Grundfast notes that a specific diagnosis (e.g., Usher
syndrome) can allow the anticipation of associated complications and their
appropriate management. Occasionally, medical or surgical intervention may be
needed (e.g., syphilis). Therefore, knowledge of a specific cause facilitates
habilitation planning and family planning.
The frequency of the various causes of hearing loss in children has changed
over the past 30 years and will probably continue to change as newborn hearing
screening becomes available to all children and as we develop more ways to
prevent hearing loss. The greatest victories in the arena of prevention of
hearing loss in children have been in the infectious diseases. Congenital rubella
has become almost nonexistent in the United States with the introduction of the
vaccine. With the introduction of the Haemophilus influenzae B vaccine, the
bacterial meningitis that has been responsible for most meningitis-induced
hearing loss has been enormously decreased. These advances have resulted in
hereditary causes and neonatal intensive care unit (NICU) graduates
contributing most children with hearing loss. In addition, cytomegalovirus
(CMV) remains a common cause of hearing loss in children. [42]
In this article, the many nongenetic causes of hearing loss are discussed. The
article focuses on the most common causes of nongenetic hearing loss in
50
children and attempts to place them in the context of the changes in the major
causes of hearing loss over the past few decades.
NEONATAL INTENSIVE CARE UNIT GRADUATES
Over the past 25 years, NICU graduates have increased in percentage of infants with
hearing loss. In the 1960s and early 1970s, the proliferation of NICUs had not
occurred, and low birth weight and perinatal factors accounted for perhaps 2% of the
children with hearing loss [42] ; however, with the introduction of effective ventilation for
respiratory distress syndrome in the early 1970s, a whole group of medically complex,
at-risk children who had hearing loss were surviving. In the next decade, approximately
13% of children with hearing loss had been of low birth weight, whereas 4% had
perinatal causes, thereby increasing the percentage of children with hearing loss who
were NICU graduates to 17%. In the next decade (1983-1992), the percentage of
children with hearing loss identified by NICU admission increased further, with 19% of
children being of low birth weight and 8% having perinatal factors. How much of the
increase in the percentage of children with hearing loss being identified with a NICU stay
is related to the increased survival in infants of lower and lower birth weights, and how
much is caused by the decrease during this 25-year period of rubella and meningitis as
major causes of hearing loss in infants remains unclear.
The category of NICU graduates easily identifies a group of children who are at risk for
hearing loss for a variety of reasons. Of the 10 indicators repeatedly stated by the Joint
Committee on Infant Hearing [37] as associated with the category of sensorineural or
conductive hearing loss at birth through age 28 days, four specifically relate to NICU
graduates' experience. These include (1) birth weight less than 1500 g; (2)
hyperbilirubinemia at a serum level, requiring exchange transfusion; (3) Apgar scores of
0 to 4 at 1 minute or 0 to 6 at 5 minutes; and (4) mechanical ventilation lasting 5 days or
longer. In addition, two more indicators are related to risks frequently found in NICU
graduates: (1) ototoxic medications including, but not limited to, the aminoglycosides,
used in multiple courses or in combination with loop diuretics and (2) bacterial
meningitis. Also, children with in utero infections, such as CMV, rubella, herpes, syphilis,
and toxoplasmosis; craniofacial anomalies, including those with morphologic
abnormalities of the pinna and ear canal; or syndromes known to be associated with
sensorineural or conductive hearing loss, such as children with Down syndrome, are
frequently admitted to NICUs for associated health problems.
NICU graduates have been exposed to unique health experiences: those medical
conditions for which they required intensive care; the NICU experience, with the
necessary, but potentially ototoxic, interventions and complications thereof; and the
possible potentiating effects that these factors together may produce on the inner ear. In
addition, children with sensorineural hearing loss who are NICU graduates have
complex neurologic and other health problems. The lower the birth weight, the more
likely a child will have neurosequelae, hearing loss or visual impairment, asthma, and
cognitive impairment. [56]
Most studies designed to determine the cause of hearing loss in NICU graduates have
found that the main associated factors include hypoxia, hyperbilirubinemia, exposure to
ototoxic medications, and illness. The significance of the various causes in the
pathogenesis of sensorineural hearing loss is not fully understood, and controversy
remains regarding their respective roles. Studies that have tried to identify specific causes
for hearing loss found with increased
51
frequency in NICU graduates have been complicated by multiple factors. Frequently,
studies have identified their subjects by starting with what is determined to be a high-risk
group, such as children with a gestational age of less than 36 weeks. Many of the studies
have been retrospective in design and of small numbers of children. Frequently, the
definition of hearing loss has varied from study to study, making comparisons difficult.
Many of the studies have not included all of the children admitted to the NICU.
Hypoxia
Most studies of the cause of hearing loss in NICU graduates have identified hypoxia to
be a factor. In different studies, hypoxia has been defined differently. Hypoxia might be
defined as apnea, [1] [4] a difficult delivery, [71] a history of duration of ventilation, [5] a
lower Apgar score at 5 minutes, or a more frequently documented P O2 of less than 50
mm Hg. Bergman and colleagues [5] identified 36 children with a sensorineural hearing
loss of less than 55 dB bilaterally in their NICU follow-up program, which included all
infants of less than 1500 g birth weight or with neonatal seizures. Significant neonatal
predictors of hearing loss in high-risk premature infants were prolonged respirator care,
high serum bilirubin concentration, and hyponatremia. Eavey and colleagues [20]
compared 23 patients identified between 1974 and 1986 with a sensorineural hearing
loss of greater then 35 dB bilaterally and believed to include all patients identified during
these years from the NICU population, with 17 infants serving as normal hearing
controls. They performed univariate and multivariate analysis, examining 65 prenatal,
perinatal, and NICU factors considered related to possible hearing loss. They found that
a history of ventilation was the only factor associated with hearing loss ( p = 0.0023).
Salamy and colleagues [68] studied prospectively 12 infants with sensorineural hearing
loss from a group of 224 very low birth weight ( 1500 g) infants requiring NICU
care. Salamy and colleagues [68] found that the infants with hearing loss had a P O2 less
than 50 mm Hg more frequently than the control infants ( p < 0.01). They concluded that
reliance on risk factors was an inadequate clinical method to select a patient for a hearing
test, and that each NICU survivor deserved audiometric evaluation. In a study of risk
factors of sensorineural hearing loss, Borradori and colleagues [7] compared eight
children with sensorineural hearing loss with a control group retrospectively matched for
similar birth weight and gestation to identify clinical risk factors. The study group all
presented with severe respiratory distress syndrome, required prolonged mechanical
ventilation (11-55 d), and all had none or several pneumothoraces. No significant
differences were found in the incidence of perinatal asphyxia, hyperbilirubinemia, hyaline
membrane disease, or persistent fetal circulation. The children with hearing loss were
more likely to have pneumothoraces ( p = 0.0001), bronchopulmonary dysplasia ( p =
0.002), and renal failure ( p < 0.002). Borradori and colleagues [7] went on to identify a
second control group with similar major perinatal complications, including respiratory
distress syndrome, need for ventilation, and pneumothorax. The analyses of arterial
blood gases and blood pressure did not reveal any statistical differences; however, the
duration of mechanical ventilation ( p = 0.0001) and the length of NICU stay ( p =
0.005) were higher in the study group. Simmons [71] found that the NICU graduates with
hearing loss had a higher incidence of certain factors than controls, including a difficult
delivery by a factor of 3.8 and an Apgar score of 6 or less at 5 minutes by a factor of
7.9. Simmons' [71] findings are supported by an analysis of 290,737 births in Utah, [22]
where they found that
52
the cutoffs of an Apgar score of 0 to 4 at 1 minute and 0 to 6 at 5 minutes were better
indicators of possible hearing loss than were the previous criteria of a 5-minute Apgar
score of 0 to 3.
Persistent Pulmonary Hypertension and Extracorporeal Membrane
Oxygenation
In relation to the problem of hypoxia and associated sensorineural hearing loss (SNHL),
two situations deserve special attention: persistent pulmonary hypertension (PPHN) and
extracorporeal membrane oxygenation (ECMO). Persistent pulmonary hypertension or
persistent fetal circulation occurs as a result of failure of the circulatory adaptation at
birth with the high pulmonary vascular resistance present in utero continuing and causing
right-to-left shunting at the levels of both the foramen ovale and ductus arteriosus.
Persistent pulmonary hypertension is primarily a disorder of full-term infants and
associated with severe hypoxemia. Although a recent follow-up study by Marron and
colleagues [55] found none of 27 children with PPHN to have SNHL, most follow-up
studies of this population have found an increased prevalence of SNHL of 20% to 53%.
[30] [41] [70] In infants with PPHN, Hendricks-Munoz and Walton [30] found that infants
with hearing loss were more likely to have alkalosis, a longer duration of ventilation, and
to use furosemide, whereas Sell and colleagues [70] found a correlation between PPHN
and maternal insulin-dependent diabetes. Of interest is a report by Kawashiro and
colleagues [41] that 8 of 10 children who developed hearing loss after discharge from the
NICU had PPHN, and 6 of the 8 had required ECMO. During that period, a total of 25
cases of PPHN had been treated, and 32% exhibited SNHL on follow-up. Desai and
colleagues [14] found SNHL in 12 (15%) of 80 ECMO-treated children. The children
with hearing loss did not differ with regard to neonatal clinical variables from those
without hearing loss, but 7 of the 12 with hearing loss had normal initial neonatal brain
stem auditory evoked potentials (BAEPs). These findings suggest that children who have
been treated with ECMO and children with PPHN are at increased risk for late-onset
hearing loss and need special monitoring.
Hyperbilirubinemia
Along with hypoxia, hyperbilirubinemia is the factor most frequently associated with
sensorineural hearing loss in NICU graduates. In the presence of hyperbilirubinemia,
specific aberrations appear in brain stem responses (ABRs). These aberrations
disappear after exchange transfusion and the establishment of a normal bilirubin level. [45]
[64] Most studies of NICU graduates include mainly low birth weight children and sick
children; consequently, the level of bilirubinemia that is likely to be associated with a
sensorineural hearing loss would be lower than with a preterm infant. Although a bilirubin
level of 14 mg/dL is frequently cited as a level that places NICU graduates at increased
risk for hearing loss, a specific toxic level of bilirubin elevation in premature infants
cannot be defined because so many variables affect the dynamics of bilirubin binding to
albumin and the degree of entry into the central nervous system. Acidosis, hypothermia,
hypoxia, and low serum albumin concentration may increase the "neurotoxicity" of
bilirubin, either by increasing the unbound portion of bilirubin or by increasing its access
to the brain. DeVries and colleagues [15] found that in children with hyperbilirubinemia,
adverse perinatal factors, such
53
as acidosis, a longer mean duration of hyperbilirubinemia (48 h versus 24 h), and lower
birth weight, were associated with an increased risk for SNHL. Anagnostakis and
colleagues [4] found hyperbilirubinemia (> 14 mg/dL) and apneic spells with bradycardia
and cyanosis and hypothermia (temperature < 34.5°C) to be associated with hearing
loss ( p < 0.001). In a study of 56 children of less than 1000 g birth weight, Doyle and
colleagues [18] found that four children with SNHL had significantly higher maximum
concentrations of bilirubin in the newborn period and required more intensive care. In his
study of a group of NICU graduates with a birth weight of up to 1500 g or neonatal
seizures, Bergman and colleagues [5] found that maximum serum bilirubin levels were one
of several independent predictors of hearing loss and that a negative correlation was
found with the number of exchange transfusions. Simmons [71] found that the incidence of
hyperbilirubinemia was 2.5 times greater in children with SNHL.
Ototoxic Medications
The NICU population is more likely to be exposed to ototoxic medications than possibly
any other group of children. The medications frequently used in the NICU and
associated with SNHL include aminoglycosides, such as gentamycin and kanamycin, and
diuretics, such as furosemide. The degree to which ototoxic medications used in the
NICU contribute to the increased incidence of SNHL in this population is unclear.
Several studies of the factors associated with SNHL in NICU graduates have not found
the use of aminoglycosides in the NICU to be a significant predictor of SNHL. [5] [23] [68]
Borradori and colleagues [7] found ototoxicity closely related to a prolonged
administration and higher total doses of ototoxic drugs, particularly aminoglycosides and
furosemide. Studies of furosemide in the neonatal period, especially with greater amounts
of administration for longer durations and in combination with aminoglycosides, are
associated with an increased risk for hearing loss. [68]
MENINGITIS
Between 1966 and 1992, meningitis was the cause of hearing loss in 6% to 13% of the
children who had hearing loss. From 1966 to 1972, meningitis accounted for 6% of the
cases of hearing loss, and from 1973 to 1982, meningitis increased to the point that it
accounted for 13% of the cases of hearing loss in children. This was probably not
necessarily caused by an increase in the number of cases of meningitis but probably by
the extraordinary decrease in cases of rubella with the introduction of the rubella vaccine.
Introduction of the first vaccine for H. influenzae type B (HIB) in 1985 resulted in a
dramatic decrease in the incidence of invasive bacterial disease, including meningitis. The
incidence of hospital admissions for meningitis decreased from 34 per 100,000 in 1982
to 1 per 100,000 children birth to 4 years of age in 1992. [51] During 1983 to 1992, the
incidence of meningitis decreased and accounted for 7% of cases of hearing loss. [42]
Bacterial meningitis has been the leading cause of acquired SNHL in children. Serial
recordings of BAEP beginning within 48 hours of admission have shown the early
occurrence of hearing loss, with a possible recovery or worsening occurring during the
first 2 weeks with no cases of "late" deafness or "late" recovery. [40] [81] The number of
days of illness before hospitalization and institution of antibacterial treatment has not been
shown to correlate with the development of SNHL. [16] Some studies have indicated that
the SNHL that complicates menin
54
gitis tends to be a defect isolated from other neurologic sequelae of meningitis, [24]
whereas other studies have shown a high correlation with severe neurologic deficits. [16]
Clinical and experimental research indicates that the hearing loss after meningitis is
caused by cochlear damage by ototoxic drugs used to treat the meningitis or to direct
damage to the cochlea by the meningitis. [26]
By the 1970s, advances in antibiotic therapy resulted in decreased mortality rates from
bacterial meningitis. Presently, for all types of bacterial meningitis, the mortality rate is
5% to 10%. [13] Significant morbidity, which was most frequently SNHL, has continued
to be a problem. In a study of 185 cases of bacterial meningitis in children, Dodge and
colleagues [16] found that overall 10.3% of the patients had persistent bilateral or
unilateral SNHL, with Streptococcus pneumoniae having the highest incidence (31%),
followed by Neisseria meningitidis (10.5%) and H. influenzae (6%). Introduction of
cephalosporins, which have better access to the central nervous system, has improved
outcomes. In addition, specifically in H. influenzae, studies of treatment early in the
course of the meningitis with dexamethasone have demonstrated decreased hearing loss
and neurologic sequelae. [13] The efficacy of dexamethasone in the treatment of
pneumococcal or meningococcal meningitis has not been demonstrated [83] ; however,
the Red Book [13] states that dexamethasone should be considered.
In the past, H. influenzae was the infecting organism in most cases of bacterial
meningitis in children and has therefore been studied the most. H. influenzae meningitis
was complicated by SNHL in 9% to 18% of cases of H. influenzae meningitis [50] [78]
with additional neurologic morbidity (e.g., blindness, seizures, cerebral palsy, or mental
retardation) in 4% to 9%. S. pneumoniae not only has had the highest frequencies of
SNHL but also has high mortality rates (17%-42%) [29] [31] [82] and neurologic morbidity
in 12% to 13% [29] [82] of children. In one study of 80 children with meningitis caused by
N. meningitidis, 8% of infections were fatal, and 9% developed an SNHL. [21] Little is
reported about hearing loss in children with fungal infections, but Nadol [59] reported 3
children out of 7 children with fungal meningitis developed SNHL. There have been no
studies of the sequelae of viral meningitis that have reported SNHL. [87] Clearly, all
children with bacterial or fungal meningitis need to be evaluated for hearing loss;
however, Fortnum and Hull [24] found in a survey of pediatricians in the United Kingdom
that 10.6% did not routinely refer all children with meningitis for an evaluation of their
hearing.
Although gram-negative enteric bacillary meningitis accounts for only 3.6% of bacterial
meningitis, the organisms are associated with a high mortality rate and devastating
neurologic sequelae. In a survey of gram-negative enteric bacillary meningitis from 1969
to 1989 at Parkland Hospital, [79] the most frequent organism causing gram-negative
enteric bacillary meningitis was Escherichia coli, accounting for 53% of cases, with the
remainder being caused by Klebsiella enterobacter (16%), Citrobacter diversus
(9%), Salmonella sp. (9%), and other gram-negative enteric bacilli less frequently
encountered (13%). Most frequently, the infected children were neonates, with 50% ( n
= 49) being term and 24% ( n = 23) being preterm, whereas 18% ( n = 18) were 1 to 3
months of age, and 8% ( n = 8) were more than 3 months of age. Predisposing
problems included surgical problems, especially neural tube defects and urinary tract
anomalies. The mortality rate was high (17%), and central nervous system sequelae,
such as cerebral palsy, hydrocephalus, seizures, severe mental and neurologic damage
requiring constant care, developmental delay with most being in the range of severe
mental retardation, and hearing loss, were found in 61% of survivors. Seventeen percent
of children had an SNHL.
The literature on tuberculous meningitis comes from the early 1960s, when treatment
included intramuscular and intrathecal streptomycin. The reported
55
incidence of SNHL in children who had tuberculous meningitis varied between 5% [52]
and 37%, [49] with some researchers reporting an additional 15% incidence of
high-frequency loss. Ototoxic treatment may have contributed to the high incidence of
SNHL.
CONGENITAL INFECTIONS
Cytomegalovirus
Cytomegalovirus infection occurs in 0.2% to 2.2% of all newborns, making it the most
common intrauterine infection in humans. One third of pregnant women are seronegative
for CMV; 2.5% to 6.8% of these women become infected during pregnancy, and 24%
transmit the infection to their fetuses. [73] Of the women who are seropositive, 3.4%
transmit CMV to their fetuses. [74] [92] Up to 10% of children with congenital CMV
infection exhibit systemic and neurologic symptoms at birth, and 61% of these children
develop SNHL. [65] Fowler [25] prospectively evaluated 307 children with documented
asymptomatic congenital CMV infection and found that 22 (7.2%) had SNHL. Among
the children with hearing loss, further deterioration of hearing occurred in 50.5%, and
delayed-onset SNHL was observed in 18.2% of children with a median age of 27
months but as old as 60 months of age. In addition, fluctuating SNHL was documented
in 22.7% of children with hearing loss. Eleven of the children had unilateral losses, and
12 of the ears had a severe to profound hearing loss. The authors speculated that more
children with asymptomatic CMV would probably develop late-onset hearing loss and
recommend that children with congenital CMV have continued monitoring of their
hearing status. A prospective study of 108 children with congenital CMV infection
indicated that children with congenital CMV represented approximately 12% of all
children with congenital SNHL. [62]
Herpes Simplex Infection
Neonatal herpes simplex virus (HSV) infection is a rare but potentially fatal disease that
occurs in 1 in 2500 to 1 in 10,000 pregnancies. [74] Infections are usually caused by
exposure to the HSV type 2 (HSV-2) during delivery and rarely caused by in utero
exposure to HSV-2 by maternal viremia. [86] Ninety-seven percent of children with
HSV-2 present in the first 3 weeks of life with disseminated infection, encephalitis, or
localized infection. The children with disseminated infection or encephalitis have high
mortality rates (85% and 32%, respectively). [27] The neurologic impairment, including
hearing loss, is found in most children with the disseminated presentation, 40% of the
children with encephalitic presentation, and 25% of children with infection confined to
the skin, mouth, or eyes. [85] Hutto and colleagues [33] reported on 13 infants who had
clinical manifestations of intrauterine HSV infection, including skin lesions and scars,
chorioretinitis, microcephaly, hydranencephaly, and microphthalmia. Two infants died,
whereas 6 of the remaining 12 children had severe neurologic sequelae, including mental
retardation, seizures, and three were blind and hard of hearing.
Congenital Rubella
The classic triad of congenital rubella includes congenital heart disease, vision problems,
and SNHL. Before the development of the rubella vaccine, 0.1%
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to 0.4% of children were born with congenital rubella, but since the introduction of the
vaccine, congenital rubella has become rare. Sixty percent of newborns with congenital
rubella have subclinical infections in the neonatal period, but 71% of these children go on
to develop manifestations of infection within the next 5 years. Hearing loss is the most
common permanent manifestation and affects 68% to 93% of children with congenital
rubella. The SNHL is most frequently profound and bilateral, effects all frequencies
equally, and is progressive in some cases. Central auditory imperception (an inability to
respond to sound on a cortical basis) can complicate the evaluation and remediation of
hearing loss. [3] Children with congenital rubella also have psychomotor retardation
(17-63%, depending on how it is defined), cerebral palsy (50%), cataracts (50%) and
other visual disorders, and seizures (6%). [66]
Congenital Syphilis
Since 1986, the prevalence of congenital syphilis, which is approximately 0.005% of live
births, or 0.4% of the children of mothers with syphilis, has increased in parallel with an
increased incidence of primary and secondary syphilis in the adult population. [34] One
third to two thirds of newborns with congenital syphilis are asymptomatic. Hearing loss is
one of the late manifestations of congenital syphilis and occurs after 2 years of age. The
hearing loss results from persistent, active disease with ongoing inflammation and
scarring. In 3% of children with congenital syphilis, SNHL develops in the first to fourth
decades in association with vertigo and beginning in the high frequencies and
progressing. [66]
Congenital Toxoplasmosis
A mass screening of 330,000 pregnant women revealed a seroconversion rate of 1 in
10,000. The overall rate of transmission of Toxoplasma to the fetus is 33%. At birth,
90% of the babies with congenital toxoplasmosis are asymptomatic. Educationally
significant hearing loss has been reported in 10% to 15% of children with congenital
toxoplasmosis. [58] In a group of 30 children with congenital toxoplasmosis treated at
birth with pyrimethamine and sulfonamide preparations, McGee and colleagues [58]
reported no development of hearing loss.
Prenatal Toxic Syndromes
Hearing loss has been described in association with prenatal exposure to alcohol,
trimethadione, and methyl mercury, as well as prenatal iodine deficiency. Fetal alcohol
syndrome includes growth retardation, dysmorphic facial features, and developmental
and behavioral disorders, including mental retardation, attention deficit hyperactivity
disorder, and language delays. Although not reported to be a common feature of fetal
alcohol syndrome, 14 children with fetal alcohol syndrome unselected for hearing loss
and referred for otolaryngology evaluation were found to have a high prevalence of
conductive and sensorineural hearing loss. Thirteen of the children (93%) had clinically
significant histories of bilateral recurrent serous otitis media, and four (29%) had bilateral
sensorineural hearing loss. [10] Abnormalities have been found in the offspring of children
57
whose mothers have had seizures treated with trimethadione. The children have been
reported to have mental deficiency, prenatal onset growth deficiency, facial
dysmorphology, septal defects of the heart and tetralogy of Fallot, and occasionally
hearing deficits. [39] The sources of methyl mercury exposure during pregnancy can
include fish from contaminated water, flour made from methyl mercury-treated seed
grain, or meat eaten from animals reared on such seed grain. Prenatal exposure usually
leaves permanent sequelae of all gradations. The fetus may exhibit poor growth,
microcephaly, aberrant muscle tone, hearing loss, and blindness. [39] Severe iodine
deficiency during gestation has been shown to result in fetal iodine deficiency, which is
characterized by mental deficiency, SNHL, spastic diplegia, strabismus, and nystagmus.
OTITIS MEDIA, HEARING LOSS, AND DEVELOPMENTAL
SEQUELAE
Otitis media has its peak incidence in children who are 6 months to 18 months of age.
After every episode, fluid persists in the middle ear for weeks to months. Conductive
hearing loss usually accompanies the fluid, with a median loss of 25 dB. [43] The
conductive hearing loss is reversed with the resolution of the middle ear effusion.
Although not common, permanent SNHL has been described in association with otitis
media. There continues to be concern but no resolution about the sequelae of the
fluctuating hearing loss associated with otitis media. Hubbard and colleagues [32] studied
24 children with cleft palate and aggressive treatment to maintain ventilation in the middle
ear with controls who presumably had had continuous middle ear effusion for the first
few years of life. He found mean verbal, performance, and full-scale IQs were normal in
both groups and not significantly different. On the other hand, the Greater Boston Otitis
Media Study Group evaluated 207 children followed prospectively from birth until age 7
years. They found that the more time spent with middle ear effusion during the first 3
years of life, the lower the full-scale, performance, and verbal Wechsler Intelligence
Scale for Children-Revised (WISC-R) IQ scores and the lower the scores in
mathematics and reading on the Metropolitan Achievement Test. [77]
OTOTOXIC MEDICATIONS AND SUBSTANCES
Hearing loss from ototoxic medications, such as gentamycin, and toxic substances, such
as lead, are an infrequent and preventable cause of SNHL in children. These substances
may permanently injure or destroy the hair cells of the cochlea, resulting in an SNHL.
Exposure to some drugs causes irreversible SNHL, whereas other drugs cause hearing
loss that is reversible once the drug is stopped. In some instances, the ototoxic effects
may not develop for up to 6 months after exposure. [90] With drugs excreted by the
kidney, increase of drug levels to the ototoxic range is more likely to be complicated by
hearing loss. [9] There appears to be both idiosyncratic and genetic susceptibility to
ototoxic drugs. [36] The hearing impairment caused by drugs is usually bilateral,
symmetric, and of varying severity. Hearing loss is usually progressive, with the high
frequencies affected first.
The ingestion of ototoxic drugs by pregnant women can result in hearing loss of prenatal
origin. The period in gestation when the use of ototoxic medications is most likely to
cause damage to the auditory system is in the first trimester, especially in the sixth and
seventh weeks. In hearing loss secondary
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to exposure to ototoxic drugs, otologic anomalies have included aplasia of the inner ear,
outer and inner hair cell damage, middle ear anomalies, absence of the VIIth and VIIIth
nerves, dysplasia of the organ of Corti, and a decreased number of ganglion cells.
Prenatal use of ototoxic medications has been believed to cause conductive hearing loss
as a result of ossicular malformation of the middle ear.
NOISE-INDUCED HEARING LOSS
Although the phenomenon of noise-induced hearing loss (NIHL) has been appreciated
for more than 100 years, most of the interest has focused on hazardous noise in the
occupational environment. NIHL accounts for a small percentage of the hearing loss in
children but is a preventable cause of hearing loss. The audiometric configuration
classified as NIHL has a decreased sensitivity of at least 15 dB at any or all of the
frequencies 3000, 4000, or 6000 Hz, as well as an improved threshold of at least 10 dB
at 8000 Hz. With continued exposure to loud sounds, the classic notch-type
configuration has been observed [2] to evolve into a nonspecific high-frequency hearing
loss with gradual disappearance of the characteristic audiometric notch with continued
exposure to loud sounds. Exposure to potentially injurious sounds may result in a
temporary threshold shift (TTS), acoustic trauma, or NIHL. Moderate exposure to
potentially damaging sounds may initially cause a TTS with associated subtle anatomic
changes, such as swelling of hair cells and the afferent fibers under the inner hair cells,
vascular spasm, and metabolic exhaustion. [48] What may begin as a TTS can gradually
become an NIHL with repeated exposure. A period of exposure to an intense,
short-duration noise greater than 140 dB peak sound pressure level, such as an
explosion may produce an immediate, severe, and permanent hearing loss exemplifying
acoustic trauma. With acoustic trauma, the organ of Corti may actually be displaced
from the basilar membrane, and swollen degenerating hair cells and swollen nerve fibers
and endings may be seen at the edges of the lesion. [8]
The evidence that fetuses and newborns exposed to excessive noise may suffer SNHL is
unclear. In a retrospective study of children 4 to 10 years of age, the children born to
women who were exposed consistently to occupational noise in the range of 85 to 95
dB during pregnancy were more likely to have a high-frequency hearing loss. [47] Other
studies have been inconsistent in relation to exposure to excessive noise and congenital
malformations. [38] [46] [93] Several studies have shown an increased risk of shortened
gestation in women exposed to noise. [53] [54] [57] [69] In one study, women exposed to 80
dB for an 8-hour shift were at increased risk for preterm delivery (relative risk, 1.6). [54]
Other studies have found no increase in preterm births or were inconclusive. [28] [60] [63]
[93] Studies of decreased birth weight and an association with noise exposure have also
been inconsistent.
Many studies have documented the continuous noise exposure associated with NICUs
varies from 60 dB to 80 dB, [8] with intense short duration noise from such things as the
closing of the metal cabinet doors (90 dB) and dropping the head of the mattress (120
dB). [12] Of the many studies that have documented hearing loss in NICU graduates,
three have investigated the synergism of aminoglycosides and noise exposure with
conflicting results. [4] [18] [75] [89] Winkel and colleagues [89] found that all five cases of
children with moderate to severe sensorineural hearing loss had been exposed to
kanamycin and kept in an incubator. Stennert and colleagues [75] found that 52% of 56
incubator-treated children with
59
normal hearing had minor changes on their audiograms, suggestive of noise-induced
cochlear lesions. Conversely, Anagnostakis and colleagues [4] assessed the hearing of 98
preterm NICU graduates when they were 6.5 years of age and found no association
with duration of incubator care or exposure to aminoglycosides of conventional
ventilation.
Children and adolescents have many opportunities for exposure to loud noises and the
development of noise-induced hearing loss. Riding for 2 hours on a snowmobile with
exposure to sound pressure levels of 105 dB to 136 dB [6] or being present at a rock
concert, where sound levels of 105 dB to 115 dBA are quite common [11] have been
observed to cause a TTS. Adolescents actively involved in farm work or children
exposed for extended periods of time to noisy machinery, such as tractors, which
produce sound levels of 95 dBA or greater at full throttle, are at risk. Impulse noises,
such as gunfire or firecrackers, are characterized by very high sound intensity levels and
short duration. The initial acoustic pulse of a gun discharge may have a peak sound level
from 132 dB to 179 dB, with the potential for immediate and permanent NIHL. [84]
A study by Brookhauser and colleagues [8] described a population of 114 children and
adolescents with NIHL, which provides information of the probable exposures that
caused the hearing loss and the types of hearing loss seen. His study group had a striking
preponderance of males over females (90.3% to 9.7%) compared with 58.6% males in
the entire data base of the Boys Town National Research Hospital. Twenty-six percent
of the losses were identified before 10 years of age, and 75% before 16 years of age.
Hearing losses were asymmetric (having a difference in thresholds between ears of 15
dB or greater in one or more of the frequencies between 3000 and 8000 Hz) in 71% of
the population, including 86% of the children exposed to high levels of pulse noise from
fireworks and firearms. Losses attributed to high levels of continuous noise, such as
music, recreational vehicles, and power tools or equipment showed less of a tendency
toward asymmetry (55%). Of the 94 children, 24 children had an unspecified noise
source, with the remaining sources being fireworks or firearms (29), music (11), power
tools or equipment (7), recreational vehicles (4), and multiple sources (19).
HEAD TRAUMA
Although conductive, sensorineural, and mixed hearing losses have been reported as a
complication of head trauma in children, few prospective studies have shown hearing
loss in children who suffered head injuries. Zimmerman and colleagues [94] studied 50
children 2 to 17 years of age admitted to the neurosurgical service of a children's hospital
for head trauma following a fall (52%), an automobile accident (22%), being struck by
an automobile (16%), and assault (10%). Audiologic evaluations generally performed
within 24 to 48 hours of admission revealed hearing loss in 50% of the children, with
32% being conductive, 16% high-frequency sensory, and 2% mild mid-frequency loss.
All of the patients with temporal bone fractures had conductive hearing losses, but the
presence of skull fault fracture did not correlate with the presence, type, or degree of
hearing loss. In addition, no correlation was found between either cause of injury, loss of
consciousness, or Glasgow Coma Scale scores, and the presence, type, or degree of
hearing loss. By the 6- to 8-month follow-up, all eight children with conductive hearing
loss and temporal bone fractures had regained their hearing. The children with
conductive hearing loss without temporal bone fractures were lost to follow-up, and of
the six children with the
60
high-frequency SNHL who came for follow-up, five showed complete resolution. The
one patient with the mild mid-frequency hearing loss had no change in hearing loss but
originally had a pattern typical of congenital abnormalities. Dorman [17] studied 40
patients aged 6 to 16 years who had minor head injuries defined by a loss of
consciousness from head injury. SNHL was sustained in 25%, with half in the lower
frequencies and half in the high frequencies but none greater than 30 dB. At follow-up 6
months later, none of the hearing losses persisted.
OTHER CAUSES OF HEARING LOSS
Mumps
Mumps is a systemic disease characterized by swelling of the salivary gland.
Approximately one third of infections, however, do not cause clinically apparent salivary
gland swelling. Encephalitis occurs rarely, and permanent sequelae are uncommon.
Complications include orchitis, which rarely results in sterility, arthritis, renal involvement,
thyroiditis, mastitis, pancreatitis, and hearing loss.
With the introduction of the measles, mumps, and rubella (MMR) vaccine, the incidence
of mumps infections has decreased to 1500 cases per year, with the highest rates being
in 5- to 9-year-olds. [13] Hearing loss from mumps is rare. In a group of 40,000 students
enrolled in special education programs for children with hearing loss, only 0.6% of the
cases were caused by mumps. [35] Yanagita and Murahashi [91] reviewed 95 cases (98
ears) of mumps deafness. The age of onset of deafness was less than 9 years in most
patients, and no cases of hearing improvement were observed.
Other diseases in which the complication of SNHL has been reported include infectious
mononucleosis, [88] Kawasaki disease, [76] pertussis, [9] and scarlet fever. Hearing loss
from tuberculosis may be a complication of tuberculous middle ear and mastoid disease
[72] or meningitis. Measles (rubeola) complicated by acute encephalomyelitis may result in
SNHL. [44]
Hypothyroidism
Congenital hypothyroidism increases the risk for hearing loss in children. Rovet and
colleagues [67] retrospectively studied 101 children followed longitudinally to evaluate
newborn screening for hypothyroidism. Of seventy-five children who had previously had
their hearing tested, 15 (20%) had hearing loss: 5 were conductive, 2 unilateral, and 3
bilateral; 9 sensorineural (1 unilateral, 8 bilateral; 1 child had bilateral sensorineural and
conductive losses). The hearing loss was mild (21-40 dB) in 10 cases, moderate (41-55
dB) in 2 cases, and moderately severe (56-70 dB) in 3 cases. The children with hearing
loss differed from the children without hearing loss in age of treatment onset (22 vs 14
days) but not in disease severity or duration.
EVALUATION OF THE ETIOLOGY OF HEARING LOSS
Every child with hearing loss is entitled to an evaluation to determine the cause of the
hearing loss. The medical evaluation includes the basics of a good pregnancy, labor,
delivery history, medical history, family history, and physical
61
examination followed by indicated laboratory tests. A history of meningitis, a NICU
experience, or family members with hearing loss are helpful in pointing to a cause but are
not always present. If the medical evaluation is negative, the most likely cause may be
genetic or perhaps a congenital infection, and further evaluation in these directions is
warranted. The identification of a cause is important for planning a habilitation plan, for
knowing the prognosis, for medical monitoring because so many syndromes have
associated disorders, and for family planning.
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