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Complications and Sequelae:
Intratemporal
OUTLINE
Hearing Loss
Conductive hearing loss
Sensorineural hearing loss
Studies of hearing loss with AOM
Studies of hearing loss with otitis media with effusion
Effects of Otitis Media on the Development of the Child
Studies
Factors of importance in analysis of Studies of otitis
media and development of speech, language, and
cognitive abilities
Parents also suffer
Recurrent and persistent otitis media as a chronic
disease
Critical ages for effects of otitis media
Auditory deprivation
Unilateral hearing loss
Effects of group day care
Child behavior and quality of life outcomes
Other variables that may relate to early childhood
language development
Test results and functional significance
Summary: role of otitis media in infant development
Vestibular, Balance, and Motor Dysfunctions
Perforation of the Tympanic Membrane
Acute perforation
Classification
Acute perforation without otitis media
Acute perforation with otitis media
Pathogenesis
Microbiology
Management
Prevention
Chronic perforation
Classification
Chronic perforation without otitis media
Epidemiology
Management
Tympanoplasty
Chronic perforation with otitis media
Classification
Chronic perforation with AOM
Chronic perforation with chronic otitis media
(chronic suppurative otitis media)
Terminology
Epidemiology
Pathogenesis
Microbiology
Pathology
Diagnosis
Management
Ototopical medications
Oral antimicrobial agents
Parenteral antimicrobial agents
Surgery
Prevention of recurrence
Complications and sequelae
Role of the primary care physician
Mastoiditis
Anatomy, pathogenesis, and pathology
Mastoiditis without periosteitis or osteitis
Diagnosis
Management and outcome
Acute mastoiditis with periosteitis
Epidemiology
Pathogenesis
Clinical presentation and diagnosis
Differential diagnosis
Microbiology
Management
Outcome
Acute mastoiditis with osteitis (with and without
subperiosteal abscess)
Epidemiology
Pathogenesis and pathology
Clinical presentation
Diagnosis
Microbiology
Management
Summary of recommended treatment plan related to
the stage of acute mastoiditis
327
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OTITIS MEDIA IN INFANTS AND CHILDREN
Subacute mastoiditis (masked mastoiditis, occult mastoiditis)
Chronic mastoiditis (with and without chronic suppurative otitis media or cholesteatoma)
Diagnosis
Management
Petrositis
Microbiology
Diagnosis
Management
Labyrinthitis
Acute labyrinthitis
Acute serous labyrinthitis (with or without perilymphatic fistula)
Clinical presentation
Diagnosis
Management
Conclusion
Acute suppurative labyrinthitis
Epidemiology and pathogenesis
Clinical presentation and diagnosis
Management
Chronic labyrinthitis
Clinical presentation and diagnosis
Management
Labyrinthitis ossificans (labyrinthine sclerosis)
Facial Paralysis
Management
External Otitis
Diagnosis
Microbiology
Management
Atelectasis of the Middle Ear (with and without a
Retraction Pocket)
Pathogenesis
Diagnosis and classification
Management
Tympanoplasty
Adhesive Otitis Media
Pathology and pathogenesis
Management
Cholesteatoma
Classification
Staging of acquired cholesteatoma
Epidemiology, complications, and sequelae
Pathogenesis
Microbiology
Pathology
Diagnosis
Management
Cholesterol Granuloma
Management
Tympanosclerosis
Epidemiology and pathogenesis
Management
Ossicular Discontinuity and Fixation
Pathology and pathogenesis
Diagnosis
Management
Even though the intracranial suppurative complications of otitis media, such as meningitis and
brain abscess, are relatively uncommon today in
developed countries of the world, clinicians everywhere still frequently encounter the intratemporal
(extracranial) complications and sequelae of otitis
media—those that occur within the aural cavity
and adjacent structures of the temporal bone.
These complications can develop from an antecedent acute otitis media (AOM) or complications
or sequelae from acute or chronic middle-ear
infections.1–3 The intratemporal complications of
otitis media are hearing loss; vestibular, balance,
and motor dysfunctions; acute perforation of the
tympanic membrane; mastoiditis; petrositis; labyrinthitis; facial paralysis; and external otitis.4 The
intratemporal sequelae of otitis media are chronic
suppurative otitis media, atelectasis of the middle
ear, adhesive otitis media, cholesteatoma, cholesterol granuloma, tympanosclerosis, and ossicular
discontinuity and fixation (Figure 1). Hearing loss
can be either a complication or a sequela of otitis
media.5 Almost all children who have a middle-ear
effusion have some degree of hearing loss, but
hearing loss can also occur when another
suppurative complication (eg, perforation of the
tympanic membrane or labyrinthitis) or sequela of
otitis media develops, such as perforation of the
tympanic membrane, adhesive otitis media, cholesteatoma, tympanosclerosis, or ossicular discontinuity or fixation. Even though there have been
some recent clinical trials to the contrary, other
studies have suggested that children who have had
recurrent episodes of otitis media or persistent
middle-ear effusion in early childhood perform less
well on tests of speech and language than do their
disease-free peers. These data suggest that delay in
or impairment of development may be an important sequela of otitis media. Also, there are some
reports that otitis media in infants may predispose
children to later disturbances of balance and ultrahigh-frequency hearing. Recently, Landis and col-
Complications and Sequelae: Intratemporal
329
illiterate. Necrotizing otitis media leading to
permanent perforation of the tympanic membrane and other complications of otitis media are
discussed in Chapter 4.
Surgery is indicated for many of the aural and
intratemporal complications and sequelae of otitis
media. Many of the concepts of the surgical procedures are described in Pediatric Otolaryngology,8
and the surgical techniques are described in the
Surgical Atlas of Pediatric Otolaryngology.9
HEARING LOSS
Figure 1. Intratemporal complications and sequelae of otitis media
include infectious eczematoid dermatitis (A); cholesteatoma (B);
retraction pocket of the tympanic membrane (C); tympanosclerosis
(D); perforation of the tympanic membrane (E); chronic suppurative
otitis media (F); cholesterol granuloma (G); ossicular discontinuity
(H); facial paralysis (I); adhesive otitis media with fixation of the
ossicles (J); hearing loss (K); petrositis (L); labyrinthitis (M); and
mastoiditis with extension into the neck (Bezold’s abscess) (N).
Reproduced with permission of Pediatrics from Teele DW et al.62
leagues reported an unusual and apparently not
recognized disorder associated with otitis media,
significantly lower taste function on the tongue;
the more severe the middle-ear inflammation, the
greater impairment in gustatory function.6
In this chapter, we discuss the epidemiology,
pathogenesis, microbiology, and management of
intratemporal complications and sequelae of otitis
media. In the next chapter, we present similar
information for intracranial complications. and
sequelae.
The burden of otitis media is particularly
heavy for children in areas of the world in which
access to medical care is limited. Untreated otitis
media may lead to persistent perforation of the
tympanic membrane and dysarticulation of
ossicles, causing permanent conductive hearing
loss. Berman reviewed reports from developing
countries indicating high rates of tympanic
membrane perforation, persistent otorrhea (consistent with chronic suppurative otitis media),
and mastoiditis.7 Hearing loss associated with
otitis media is a particular concern in developing
countries because of the importance of comprehension of normal speech for those who are
Fluctuating or persistent hearing loss is present
in most infants and children with middleear effusion; hearing impairment is the most
prevalent complication of otitis media.10 The
hearing loss is most frequently conductive, but
sensorineural hearing loss can also be a consequence.5 Even though the hearing loss is
characterized as ‘‘mild’’ and self-limited when
otitis media is present, the loss can be substantial
in some children, especially when it is associated
with a complication or sequela of otitis media.
Conductive Hearing Loss
Audiograms of children with middle-ear effusion usually reveal a mild to moderate conductive
loss averaging between 20 and 30 dB, but the
range is 0 to 60 dB. Even with mild deficits, the
softer speech sounds and voiceless consonants
may be missed. The frequency distribution of
thresholds for speech stimuli associated with
otitis media with effusion, obtained by Fria
and colleagues, is shown in Figure 2.11 The
average hearing loss in that study was 27 dB at
500, 1,000, and 4,000 Hz; at 2,000 Hz, the loss
was only 24.5 dB, which probably accounts for a
three-frequency (500, 1,000, 2,000 Hz) pure-tone
average better than it truly is. Other studies have
reported similar losses, although with differing
criteria.12,13 The hearing loss is not influenced by
the quality of fluid in the middle ear; ears with
thin fluid are impaired to the same degree as are
those with fluid of a glue-like consistency.14,15
Ears that are partially filled with fluid (identified
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OTITIS MEDIA IN INFANTS AND CHILDREN
Figure 2. Frequency distribution of
thresholds for speech stimuli associated with otitis media with effusion.
Left, Speech reception threshold
(SRT) of 540 children. Right,
Speech awareness threshold (SAT)
of 222 infants. HL 5 hearing level.
Reproduced with permission from
Fria TJ et al. 11 Copyright 1985,
American Medical Association.
otoscopically by the presence of bubbles or an
air-fluid level) have less hearing impairment than
do ears that are completely filled with fluid.11
The hearing impairment is usually reversed with
resolution of the effusion.16,17 On occasion,
permanent conductive hearing loss is due to
irreversible changes resulting from recurrent
acute or chronic inflammation (eg, adhesive
otitis media or ossicular discontinuity). High
negative pressure in the ear, or atelectasis, in the
absence of effusion is another cause of conductive loss.18
Hearing in children with chronic suppurative
otitis media is usually worse than that reported
when otitis media with effusion is present. One
study from Sierra Leone evaluated the hearing in
children who had perforation with and without
suppuration. Of the 37 ears that had dry
perforations, 33 (89%) had a pure-tone average
of 26 dB or greater, and of the 100 ears that had
chronic suppurative otitis media, 96 (96%) also
had this degree of hearing loss.19
Sensorineural Hearing Loss
Sensorineural hearing loss may also result from
AOM or otitis media with effusion.20 A reversible hearing impairment is generally attributed
to the effect of increased tension and stiffness of
the round window membrane. A permanent
sensorineural loss may occur, presumably as a
result of the spread of infection or products of
inflammation through the round window membrane,21–26 the development of a perilymphatic
fistula in the oval round window,27–29 or a
suppurative complication, such as labyrinthitis.9
Chronic suppurative otitis media, cholesteatoma, or both can be associated with sensorineural hearing loss.30 Sensorineural hearing loss
and middle-ear disease frequently coexist.
Brookhouser and colleagues evaluated 437 children with bilateral sensorineural hearing loss and
found a sufficient degree of otitis media to
warrant tympanostomy tubes in 35%.31 In
Finland, Rahko and colleagues tested 359
individuals who had a known history of otitis
media and failed to detect sensorineural hearing
loss.32 However, Mutlu and colleagues reviewed
the audiograms of 71 children (119 ears) who had
otitis media with effusion and found that 9% had
either temporary sensorineural involvement
(temporary threshold shift), which improved
when the effusion resolved, or possibly permanent sensorineural loss, which they attributed to
the effusion.33 Ultra-high-frequency hearing
(9,000–20,000 Hz) can also be affected in children with otitis media, which would not be
detected in routine audiometric testing,34,35 and
it may be affected for the long term.36 It is most
likely that otitis media with the presence of
bacteria, viruses, inflammatory mediators,
enzymes, and possibly even a neurotoxin, such
as quinolinic acid,37 can affect the inner ear in
some children.
Complications and Sequelae: Intratemporal
Studies of Hearing Loss with AOM
Few studies of hearing have been performed
during acute episodes of otitis media. Olmstead
and colleagues studied children 2 to 12 years of
age with a diagnosis of AOM who were seen in the
Outpatient Department of St. Christopher’s
Hospital in Philadelphia.38 Of 82 children enrolled
in the study, 33% had no loss of hearing on the
initial audiometric test after acute infection; 40%
had loss of hearing (up to 15 dB) initially, which
disappeared in 1 to 6 months; 12% had loss of
hearing throughout the 6-month period of observation; and 15% had loss of hearing initially but
were lost to the study between 1 and 4 months
after the acute episode of otitis media. The
children had no history of hearing difficulty or
chronic ear infection. Otoscopic examinations
were not performed after the initial diagnosis,
and data were not presented concerning the
duration of fluid in the middle ear. These data
indicate that after a single episode of AOM, many
children have prolonged hearing impairment.
Hearing loss has also been identified in
children who have apparently recovered from
AOM. A longitudinal study of Alaskan Eskimo
children showed a statistically significant association between the frequency of episodes of otitis
media and hearing loss of greater than 26 dB. Of
children who had one or more attacks of otitis
media per year, 49% had hearing loss; hearing loss
was evident in 15% of children with no diagnosed
episodes of otitis media.39 Other studies with
differing criteria have found the incidence of
hearing loss associated with AOM to vary
between 6 and 30%.40,41
Ryding and colleagues assessed hearing
thresholds in children who had had recurrent
AOM in the past, compared with those without
middle-ear disease, and found no difference in
hearing at the traditional levels (ie, 125–8,000 Hz)
between the two groups, but children in the otitis
media group had hearing levels at high frequencies
(8,000–16,000 Hz) and the acoustic middle-ear
reflex thresholds were elevated; also middle-ear
compliance was higher, and click-evoked otoacoustic emission response levels and middle-ear
331
pressures were lower.42 They concluded that
children with a history of middle-ear disease not
only had disturbances of middle-ear mechanics
but also cochlear function may have been
abnormal as a sequela of the midddle-ear disease.
Studies of Hearing Loss with Otitis Media
with Effusion
Hearing loss frequently accompanies persistent
middle-ear effusion (documented at the time of
surgery).43,44 Fria and colleagues evaluated hearing in 222 infants (aged 7–24 months) and 540
older children (aged 2–12 years).11 Both the
younger and older children had, on average,
thresholds for speech reception and speech awareness of 24.6 and 22.7 dB, respectively (see Figure
2). Not all children with middle-ear effusion have
apparent hearing impairment. About one-third of
the children had air conduction thresholds of 15
dB, but approximately 25% of children with
middle-ear effusion had thresholds of up to 30
dB. The cumulative frequency curves were similar
for children of various ages and for the duration of
effusion. This large study provides a complete
picture of the number of children affected and the
extent of the hearing loss when middle-ear effusion
is present. Audiometric techniques for children of
various ages are discussed in Chapter 7.
In a recent report, Gravel and colleagues
found that otitis media with effusion in early
childhood, compared with those children without
a past experience with otitis media, was associated
with disturbances of auditory processing when the
children were age 8 years; also, the study revealed
hearing sensitivities to be significantly poorer in
the children who had had the middle-ear disease.45
EFFECTS OF OTITIS MEDIA ON THE
DEVELOPMENT OF THE CHILD
The results of many studies of the association of
otitis media and development of speech, language, and cognitive abilities have been reviewed
by the Agency for Health Care Policy and
Research,46 by Vernon-Feagans,47 and most
recently by the American Academy of
332
OTITIS MEDIA IN INFANTS AND CHILDREN
Pediatrics.48 Some studies have identified associations of recurrent otitis media with effusion and
lower scores on tests of vocabulary, auditory
comprehension, and language skills. Other studies
failed to find significant differences among children with and without a history of prolonged time
spent with middle-ear effusion. The variables in
these studies are many, including documentation
of the ear disease, the type of test administered, the
socioeconomic class of the parents, the quality and
quantity of language in the home and in out-ofhome day care, the child’s temperament, and the
child’s and the parents’ IQ. The variability of the
results of these many studies suggests that the
effects of otitis media may be more substantial in
some children than in others. The focus of current
studies is on the development of criteria for those
children who are most likely to be affected by the
hearing loss accompanying otitis media.
Sensorineural hearing loss has been associated with impairment in the cognitive, language, and emotional development of children.
Children with sensorineural hearing impairment,
compared with peers who have normal hearing,
are significantly retarded in the development of
vocabulary,49 are placed below their grade level
in school,50 have poorer articulation and auditory discriminatory abilities,51 and have a high
rate of maladjusted behavior patterns52 and
disturbances in psychosocial adjustment.53
The first months of life are important in
language acquisition. The infant is capable of
speech sound discrimination as early as 1 month of
age. By the age of 6 weeks, the infant is attracted to
human voices more than to environmental sounds
and to female more than to male voices. At 5 to 6
months, the infant enters the babble phase and
plays with sound-making. The child is putting
words together in sentences by the age of 18
months, and by 4 years, the child produces all of
the basic syntactic structures that he or she will
ever use.54 Because so much progress in language
acquisition is made during infancy, any problems
in receiving or interpreting sound signals might
have a significant effect on speech and language
development. Softer speech sounds and voiceless
consonants, in particular, may be missed or
confused when effusion is present in the middle
ear (Figure 3).55 Important differences have been
identified in the early patterns of vocalization of
the hearing-impaired infant compared with hearing infants. It is unknown how these data about
differences in infant babble relate to the ultimate
development of speech and language when the
hearing impairment is mild and fluctuating.
The current hypothesis for the effects of otitis
media on the child’s development is presented in
Figure 4. Children with severe or recurrent otitis
media spend prolonged time with middle-ear
effusion. Hearing impairment (average loss
approximately 25 dB) accompanies the effusion
in most children, and if the hearing impairment
occurs at a time of rapid intellectual growth, the
result may be impaired development of speech,
language, and cognitive abilities.
Studies
Many investigators have studied the effects of
otitis media on the development of the child.
Figure 3. Range of speech energy related to a standard
audiogram. The shaded area shows the range of sound energy
present in normal speech, and the dashed line indicates the average
of speech energy. The line connected by solid circles shows the
mean of hearing losses from otitis media. It can be seen that softer
speech sounds may not be heard when otitis media is present.
Adapted from Skinner MW. The hearing of speech during language
acquisition. Otolaryngol Clin North Am 1978;11:631–50.
Complications and Sequelae: Intratemporal
333
Figure 4. Long-term sequelae of middle-ear effusion.
Although most studies indicate that children with
a history of recurrent episodes of acute otitis
media score lower on tests of speech and
language than do their disease-free peers, some
important recent studies fail to show a difference
in long-term developmental outcomes. A brief
resume of the results of selected studies follows:
1. One of the earliest and most widely cited
studies is that of Holm and Kunze of Seattle.56
Children aged 5 to 9 years who had a history
of chronic otitis media with onset before the
age of 2 years were compared with children in
a control group matched for age, sex, and
socioeconomic background. Children with a
history of ear disease were delayed in all
language skills requiring the receiving or
processing of auditory stimuli, but the groups
were similar in tests measuring visual and
motor skills (Figure 5). The diagnosis of otitis
media was made on the basis of history;
otoscopic and audiometric examinations were
not performed, and the sample size was small
(16 children in each group).
2. Eskimo children were observed prospectively
during the first 4 years of life and had tests of
hearing, intelligence, and assessment of
school performance at age 10 years.57
Children with recurrent episodes of otitis
media (defined as the presence of a draining
ear) during the first 2 years of life and with
loss of hearing of 26 dB or more had lower
scores in tests of reading, mathematics, and
language than did children who had little or
no disease in infancy. Otorrhea was the sole
Figure 5. The results of language tests in children with and without
otitis media (standard score mean and standard deviation). Reproduced
by permission of Pediatrics from Holm VA and Kunze LH.56
criterion for otitis media; data were not
available about the presence or duration of
middle-ear effusions or episodes of AOM
that did not result in otorrhea.
3. Lewis studied Aboriginal children from
Brisbane, Australia. Children aged 7 to 9
years who ‘‘failed otoscopic examinations’’
and had hearing deficits measured by audiometry or tympanometry during a 4-year
period were compared with age-matched
control children who had consistently passed
the audiometric tests and were assumed to be
disease free.58 Children with ear disease had
mean scores for speech and language development that were significantly lower than
those of the children without ear disease. The
sample size was small: 14 children with
disease and 18 control subjects.
4. Needleman evaluated 20 children aged 3 to 8
years with a history of recurrent otitis media
and a first episode before the age of 18
months.59 Twenty control subjects who had
no history of hearing problems or recurrent
334
OTITIS MEDIA IN INFANTS AND CHILDREN
ear infections were matched with the patients
for age, grade, and socioeconomic status. The
children were evaluated for their ability to use
speech sounds expressively and receptively.
Children with a history of ear disease had
poorer phonologic abilities than did the
control children. The diagnosis of ear disease
was based on the history alone.
5. Sak and Ruben used a sibling control for
children with a history of otitis media.60
Children received tests of speech and language between the ages of 8 and 11 years.
One sibling of each pair had a documented
history of persistent otitis media beginning before the age of 5 years, whereas the
other sibling had had no middle-ear problem. The children who had had otitis media
had a lower verbal IQ, poorer auditory
reception, and lower spelling achievement than their matched sibling controls.
More of the siblings with otitis media were
boys, and more minor middle-ear abnormalities identified by audiometry or tympanometry were prevalent among the otitis media
siblings than among the control siblings,
suggesting the possibility that deficits were
associated with recent, rather than earlier,
middle-ear disease.
6. Friel-Patti and colleagues examined the
association of otitis media early in life with
language development at 12, 18, and 24
months.61 The infants had been selected from
intensive care units of low birth weight
nurseries and were predominantly from low
socioeconomic groups. Frequent episodes of
otitis media were correlated with a higher
prevalence of language delay, but no correlation was found between hearing impairment
measured by auditory brainstem response
testing and language delay.
7. Teele and colleagues studied 190 white
children of varying socioeconomic strata
from greater Boston to determine the association between time spent with middle-ear
effusion and development of speech, language, and cognitive abilities.62 The children
were selected from a cohort of children in five
health centers who were observed from birth
with regular examinations of the middle ear
at each visit to the office or clinic, whether for
illness or for routine care. The study was
prospective, used uniform criteria to diagnose
otitis media and middle-ear effusion, and
tested children from all socioeconomic strata.
Tests of speech and language administered at
the third birthday included the Peabody
Picture Vocabulary Test (a test of both early
receptive and expressive language), the
Fisher-Logemann and Goldman-Fristoe tests
of articulation (tests of production of speech
sound), and other measurements of language
structure complexity and estimates of intelligibility.
Children who had spent fewer than 30 days
with middle-ear effusion during the first 3 years
of life were compared with those who had spent
30 to 129 days with middle-ear effusion during
the first 3 years of life and with those who had
spent 130 or more days with middle-ear effusion
from birth to age 3 years. A summary of the
results indicated the following:
N
Test scores were lower for the total number of
children tested, but significant differences were
present only in the test scores of children from
the high socioeconomic group. No significant
differences were found for children from low
socioeconomic groups (Tables 1 and 2). The
basis for the difference in the results for
Table 1. COGNITIVE ABILITY AT AGE 7 YEARS BY
ESTIMATED DAYS WITH MIDDLE-EAR EFFUSION DURING
THE FIRST 3 YEARS OF LIFE
Estimated Days with MEE
IQ Test
Full scale
Verbal
Performance
, 30
{
113.1*
111.5{
112.2{||
30–129
. 130
107.5*
106.5{
108.3||
105.4{
105.81
104.1{
Adapted from Teele DW et al.63
MEE 5 middle-ear effusion.
Cognitive ability is expressed as mean IQ by the Wechsler Intelligence Scale
for Children-Revised after adjusting for socioeconomic status and gender
(general linear model procedure SAS-GLM). Time spent with MEE is a natural
log of time with effusion (days, 1). Intervals with MEE were selected to produce
three groups of about equal size.
p 5 *.007, {.001, {.026, 1.008, ||not significant (.07).
Complications and Sequelae: Intratemporal
Table 2. ACUTE OTITIS MEDIA AND DEVELOPMENTAL
OUTCOME AT AGE 1 YEAR
Mental and motor development of children with AOM
No differences from disease-free controls in Bayley mental or
motor scores
Behavior of children with AOM
Less attentive and persistent (rated by examiner)
More irregular in sleeping and eating (rated by parents)
Less response in structural interaction with parent
Behavior of parents of children with AOM
Less skillful at providing effective teaching
Adapted from Chase C.66
AOM 5 acute otitis media.
N
children in lower and upper socioeconomic
strata is unclear but might be accounted for by
the lower scores of children in the low socioeconomic group. The tests used may have been
insensitive to differences in performance by
these children at age 3 years.
Increased time with middle-ear effusion during
the first year of life was most significantly
associated with lower scores in children tested
at age 3 years. Confounding variables, such as
race and birth order, were either controlled for
or excluded.
The authors followed up 207 children randomly selected from the same cohort who were
observed from birth to the age of 7 years and
administered tests of intellectual ability, school
achievement, speech, and language.63 After
confounding variables were controlled for, estimated time spent with middle-ear effusion during
the first 3 years of life was significantly associated
with lower scores on tests of cognitive ability,
speech and language, and school performance at
age 7 years. The adjusted mean full-scale
Wechsler Intelligence Scale for ChildrenRevised (WISC-R) score was 113.1 for those
with the least time with middle-ear effusion and
105.4 for those with the most time (see Table 1).
Similar significant differences were found for
verbal and performance IQ scores. For the
Metropolitan Achievement Test, we found that
middle-ear disease in the first 3 years of life was
associated with significantly lower scores in
mathematics and reading. Similar differences
were found for articulation and use of morpho-
335
logic markers. After time spent with middle-ear
effusion during the first 3 years of life was
considered, time spent after the first 3 years was
not a significant predictor of scores on any of the
tests administered.
8. Hubbard and colleagues in Pittsburgh evaluated two matched pairs of children with
repaired palatal clefts.64 The treatment of the
children had been equivalent, with the exception that one group had undergone early
myringotomy with tympanostomy tube placement (mean age 3 months) and the other
group had undergone initial myringotomy
later (mean age 30.8 months) or not at all.
Hearing acuity and consonant articulation
were significantly less impaired in the group
having undergone early myringotomy. Mean
verbal performance and full-scale IQs and
scores on psychosocial indices were normal in
both groups and did not differ significantly
between the groups.
9. Watanabe and colleagues studied total speaking time in infants and children with and
without middle-ear effusion.65 To support the
premise that improvements in the child’s
performance
occurred
when
hearing
improved with the resolution of middle-ear
effusion, the authors developed a technique
to identify the time of vibration of the vocal
cords. The duration of speaking time was
measured in children with otitis media with
effusion before and after tympanostomy tube
placement. Preoperative speaking time was
found to be 8 minutes and 2 seconds per
measured hour when middle-ear effusion was
present and 10 minutes per hour when the
effusion cleared after tympanostomy tube
placement. The implications of this innovative study are uncertain but suggest that
hearing improvement increases speaking time
and causes the child’s ordinary behavior to be
more animate.
10. Chase studied the early development of
children with and without experience with
otitis media in the first year of life (one episode
within 6 months or two episodes in the first
336
OTITIS MEDIA IN INFANTS AND CHILDREN
year) (see Table 2).66 There were no differences
in overall mental and motor development.
There were, however, clear behavioral differences between 1-year-old children who experienced recurrent otitis media in the first year
and those who did not. Children who experienced otitis media were rated by their parents
as less attentive and less persistent by the
examiner during testing and more irregular in
their patterns of sleeping, eating, and elimination. In addition, children who had experienced otitis media were less responsive and less
attentive in working with their mothers in a
learning situation. These findings suggest that
a child who has experienced ear infection and
mild hearing loss may show signs of attentional difficulty early in life.
11. The Pittsburgh studies by Paradise and colleagues reported on an extensive, prospective
study, 6,350 infants followed from soon after
birth to the age of 3 years were systematically
examined for the presence or absence of
middle-ear disease. The design of the study
included randomization of subjects who developed sufficient otitis media to warrant myringotomy and tympanostomy tube placement.
To determine the effect of a relatively short
period of middle-ear effusion versus a more
prolonged course, the children were randomly
assigned to either early (prompt) or delayed
insertion of the tubes, and then the two groups
had assessment of developmental outcomes at
3 years of age and later at age 6 months of age.
The investigators concluded in the first report
that ‘‘in children younger than three years of
age who have persistent otitis media, prompt
insertion of tympanotomy tubes does not
measurably improve outcomes at age three
years.’’67 This conclusion was challenged by
Rosenfeld, who asked for more details,68
which was responded to by Paradise and
colleagues.69 Then Paradise and colleagues
concluded in the later assessment that ‘‘in
otherwise healthy children younger than three
years of age who have persistent middle-ear
effusion within the duration that we studied,
prompt insertion of tympanostomy tubes does
not improve developmental outcomes at age
six years of age.’’70 Even though the relatively
short difference in the period between the
‘‘early’’ tube insertion versus the ‘‘delayed’’
placement was a substantial design flaw. These
fesults are an important contribution to the
discussion of the effects of otitis media on the
development of the child.
Other studies of otitis media and language
performance demonstrated the following results:
N
N
N
N
N
N
A study of children in Montreal, aged 3 to 5
years, identified significant differences among
the children with a history of otitis media and
matched control children.71
A study of Danish children aged 3 to 9 years
did not show an effect of otitis media with
effusion early in life on reading achievement.72
A study by Lous demonstrated a small but
significant correlation between flat tympanograms (type B) in first-grade children and
silent work reading at the beginning of the
second grade.73
An evaluation of Apache Indian children aged
6 to 8 years with a contrasting history of otitis
media showed no significant difference in
language performance.74
A retrospective study suggested that middleear disease in school-aged children was associated with hyperactivity or inattention, independent of learning ability.75 Also, a recent
brief report by Rinkel and colleagues found
that early-life otitis media with effusion
negatively influenced the development of
speech-in-noise understanding, which was
postulated to subsequently affect speech,
language, and learning development.76
Roberts and colleagues prospectively followed
83 black children, primarily from low-income
families, who were examined periodically from
6 months to 4 years of age for the presence of
middle-ear effusion, and then assessed the
children’s later academic skills in reading and
word recognition during the early years of
elementary school.77 The children who had
had otitis media and hearing loss scored lower
in mathematics and expressive language at
Complications and Sequelae: Intratemporal
younger ages but caught up in math on
entering school and in expressive language by
the second grade. The investigators concluded
that the child’s home environment was more
related to these outcomes than the presence of
a past experience with otitis media with
effusion but cautioned about interpreting these
findings when generalizing to other populations. In a follow-up study with a similar
design and methodology that included children
from New York, outcomes were comparable
to those of the first report.78
These reports are disturbing, but many have
one or more flaws in study design: reliance on
a retrospective history of AOM; uncertain
validity of the diagnosis of otitis media; a lack
of information or documentation about middleear effusion; the presence of significant hearing
impairment in subjects at the time of tests of
speech and language; small numbers of subjects;
special populations tested (eg, Australian
Aborigines, Alaskan Eskimos, children with a
cleft palate); and inadequate criteria for selection of children without disease used for comparison.
Hignett summarized the study design issues
and evaluated the effectiveness of 10 early studies
of otitis media and speech, language, and
behavior.79 The studies of Teele and colleagues
and Hubbard and colleagues represent significant advances in study design compared with
previous investigations,62,64 but both of these
studies have been subject to criticism because
of perceived limitations and deficiencies.80,81
Roberts and colleagues conducted a meta-analysis of the studies reported on the effect of otitis
media on speech and language and found a small
effect but also that the evidence was neither
combinable nor generalizable.82 Vernon-Feagans
and colleagues, in a similar review, arrived at a
similar conclusion.83 These inadequacies of study
design limit general application of these results to
planning care for young children, but they do not
prevent concern that many children may suffer
from the sequelae of otitis media with persistent
middle-ear effusion in infancy.
337
Factors of Importance in Analysis of Studies
of Otitis Media and Development of Speech,
Language, and Cognitive Abilities
Parents Also Suffer
The working parent who has spent a sleepless
night attending to a child who is fretful because
of ear pain may have work- and home-related
stress. Chase noted that parents of 1-year-old
children who had experienced otitis media were
less effective teachers in structured interactive
tasks.66 They were less effective in gaining the
child’s attention, less able to respond effectively
when the child was distracted from the task, and
less able to help the child understand and
perform the task. The parent must contend with
the child’s acute pain, persistent irritability and
inattentiveness, and the expense and inconvenience of frequent visits to the physician. Although
some families can accept and cope with the stress
of a child’s recurrent illnesses, other families
cannot. A constellation of disturbances in
psychosocial development may result. Paradise
and colleagues noted that stress ratings were
highest among those parents whose baseline
stress scores were the highest.84
Focus groups of parents described chronic
otitis media as a condition that affects not only
the child who is ill but the entire family. These
findings were reported by the Functional
Outcomes Project of the American Academy of
Pediatrics, whose goals were to assess various
aspects of the physical, social, and emotional
well-being of children with chronic illnesses and
their families.85 Parents reported the influence of
the disease on the child’s behavior, such as
aggressiveness, whining, or excessive clinging.
Parents worried about the cost of visits to the
physician, prescription medication, and tests and
expressed frustration over inconsistently effective
medications. Siblings often demanded more
attention when another was ill, and parents
expressed feelings of guilt over spending so much
time with one child to the exclusion of siblings.
The implications for the practitioner include
providing support groups and teaching materials
or information sessions for parents and encoura-
338
OTITIS MEDIA IN INFANTS AND CHILDREN
ging office-based research in the area of child and
family well-being to better understand the impact
of chronic illnesses, such as otitis media, on the
family.
Recurrent and Persistent Otitis Media as a
Chronic Disease
The systemic effects of illness, including irritability, malaise, lethargy, and local or generalized
pain, may be sufficiently distracting to affect
development. These effects of a chronic illness
must be distinguished from the specific effects of
otitis media (ie, hearing loss) in the interpretation
of the sequelae of the disease. Is the child treated
differently by the parents, siblings, peers, or
teachers because of the recurrent illnesses? Is the
child vulnerable to effects unassociated with the
specific morbidity of the disease (kept indoors,
away from peers, or out of exercise and athletic
programs)?
Critical Ages for Effects of Otitis Media
Otitis media of a similar duration may affect
children differently at different ages. There may
be critical periods of perception of language
when the child is most vulnerable to mild,
fluctuating, or persistent hearing loss. The results
of the Boston study suggested that the children
were most affected by middle-ear effusion when
disease occurred during the first year of life.62
During early stages of language development, the
child learns the sounds of the language; different
or changing auditory signals resulting from
persistent or fluctuating hearing deficits may
impede the child’s abilities to form linguistic
categories.86
Auditory Deprivation
Studies in birds and rodents indicate that
deprivation of sound early in life leads to
identifiable changes in auditory sectors of the
brain. A decrease in the size and number of
neurons in the auditory nuclei of mice occurred
when the animals were deprived of auditory
stimuli during early development.87 In the
normal postnatal development of the mouse,
the neurons of the auditory brainstem reach
adult size by the age of 12 days, the time of onset
of hearing. Mice that underwent auditory deprivation by experimentally produced conductive
hearing loss 4 to 45 days after birth had auditory
brainstem neurons that were significantly smaller
than normal. If the mice that underwent induced
hearing loss early in life were returned to normal
hearing after 45 days, the smaller-than-normal
neurons were retained. The size of the neurons
was not altered in mice raised in a normal sound
environment until 45 days and then deprived of
sound until 90 days of age.
These data demonstrate that a period exists
in the development of mice during which
adequate sound stimulation is needed to establish
the normal size of neuronal cells in the auditory
brainstem. These experimental data in animals
raise concerns about irreparable damage from
temporary conductive hearing loss in infants.
Webster pointed out, however, that the factors in
the experimental model differ from the mild to
moderate hearing losses of otitis media with
effusion in humans; in the experimental model,
the conductive loss is approximately 50 dB,
greater than the loss in most cases of otitis media
with effusion.87 The loss is persistent rather than
fluctuating, and the impairment starts at the
inception of hearing in the mouse, whereas
inception of sound occurs prenatally in the
human. The author concluded that although
the restrictions of the animal model must be kept
in mind, ‘‘the fact that early auditory restriction
has a profound effect on the central nervous
system in one mammal must arouse concern
about possible related effects in humans.’’
Unilateral Hearing Loss
Unilateral hearing loss has not been considered a
handicap for children. Data indicate, however,
that children with unilateral hearing impairment
score less well on auditory, linguistic, and
behavioral tests than do children without hearing
impairment.88 Although the children studied had
sensorineural hearing deficits, the data suggest
that we should no longer accept a unilateral
hearing loss as benign. Children with unilateral
conductive loss may also suffer during critical
Complications and Sequelae: Intratemporal
periods of language perception because of confused speech signals.
Effects of Group Day Care
Respiratory infections are readily spread among
children in day care, and children in day care are
likely to have more episodes of otitis media than
will children in home care. In relation to
development of language, the quantity and
quality of the speech sounds around the infants
in group care differ from those presented to the
child in home care. The factors of increased
number of infections and differences in the
speech environment in group day care will need
to be considered in future studies.
Child Behavior and Quality of Life
Outcomes
Disturbances in children’s behavior associated
with otitis media have been reported to include
restlessness, frequent disobedience, impaired task
orientation in the classroom, inattention, short
attention span and distractibility, and restricted
social interaction. Only selected children may be
most affected. Paradise and colleagues found
that parent-child stress and behavior problems
were highest among children from the most
socioeconomically disadvantaged homes.84 Gray
suggested that inconsistencies in the child’s
ability to hear may have a lasting effect on the
child’s motivation to achieve and may cause
strained relationships with teachers and parents.89 A review of the various studies of the
impact of otitis media on the quality of life of
the child’s behavior was recently prepared by
Haggard and colleagues.90 They concluded that
limitations of study design hampered interpretation of the results of the studies.
Other Variables that May Relate to Early
Childhood Language Development
Future study designs must also consider these
factors: quality of the diagnosis of ear disease;
visual status; physical and motor development;
intellectual, social, and emotional development;
nutritional status; history of medications; dialect
exposure; birth order; and number of siblings.
339
Other factors to be considered are the social and
economic class of the parents and the quality and
quantity of language in the home and day-care
center.
Test Results and Functional Significance
Do a few percentage points of one or more
standard tests of speech, language, or cognitive
abilities affect the child’s capability to function
in the school, play, and home settings? Some
investigators question whether these are statistical differences of limited importance to the
child’s development, but there are reasons for
concern. Because the data are expressed here in
terms of mean differences, some children will be
close to or better than the norm, whereas others
will have scores that are much lower. Otitis
media is so common in early childhood that
even if a small percentage of children are
adversely affected in terms of development, the
number of children who suffer is large. Of the
3.7 million children born in the United States
each year, more than one-third will have
recurrent episodes of otitis media (three or more)
by the age of 3 years. If only 10% of the children
with recurrent episodes are affected adversely,
the national impact is greater: more than 100,000
of each year’s newborn infants would be
involved.
Because the tests measure the child’s potential for achievement, it is possible that the loss
suffered by the child with frequent and recurrent
episodes of otitis media accompanied by hearing
loss in early infancy is never perceived by the
parents, teachers, or physicians. The child is not
obviously slow or behind his or her peers. The
failure of the child to reach his or her potential is
a loss for the child and the family, and because
the number of these children is large each year, it
must be considered a national concern.
Summary: Role of Otitis Media in Infant
Development
The accumulated results of the various studies of
otitis media and development of speech, language,
and cognitive abilities suggest that children do
340
OTITIS MEDIA IN INFANTS AND CHILDREN
suffer long-term effects from otitis media early in
life. The scientific evidence, however, remains
incomplete. As recently concluded by Roberts,
‘‘the issue of whether recurrent otitis media with
effusion affects later acquisition of speech, language, and academic skills continues to be
controversial.’’91 Some experts are skeptical about
available data.92,93 Ventry concluded that no
causal link had been established (by 1982) between
early recurrent middle-ear effusion and language
delay or learning problems.93 Rapin noted that no
studies published by 1977 ‘‘met the standards of
rigor needed to provide a definitive answer to this
question, although the burden of the evidence is
that a persistent and mild hearing loss, especially if
present since infancy, probably has a measurably
deleterious effect on the language of most, but not
all, children.’’94 Rapin’s statement is as applicable
today as it was in 1977.
The difficulties in study design needed to
resolve the issues and account for many of the
variables are formidable. The optimal design will
need to include frequent otoscopic observations
beginning soon after birth to develop a chronology of time spent with middle-ear effusion.
Hearing assessments will need to be performed
in infants when they have effusion and are free of
effusion to measure the duration and severity
of hearing deficits. All of this will need to be
done in the first years of life, when hearing
assessments are more difficult and less precise
than in the older child. The study will need to be
cross-sectional and prospective from birth and
should be performed by validated otoscopists.
Tests of speech, language, and cognitive abilities
will need to be selected that are accurate and
standardized for the populations to be tested.
The tests should be performed at least annually
to define the time of onset or the effect of otitis
media on development. The previous section
identified the other variables that will need to be
considered, including the quality of parenting,
the effect of siblings, and the time spent in group
day care.
Concern about the association of middle-ear
disease and development of speech and language
was expressed in a policy statement of the
American Academy of Pediatrics.95 Although
recognizing the validity of criticism of published
studies, the Committee on Early Childhood,
Adoption and Dependent Care concluded that
‘‘there is growing evidence demonstrating a
correlation between middle-ear disease with
hearing impairment and delays in the development of speech, language, and cognitive skills...
When a child has frequently recurring AOM and/
or middle-ear effusion persisting for longer than
3 months, hearing should be assessed and the
development of communicative skills must be
monitored.’’ Until definitive answers are available from studies of appropriate design to
evaluate the sequelae of otitis media in early
infancy, the physician must decide, for each child
in his or her care, the optimal management of
persistent middle-ear effusion. Chapter 8 provides guidelines for such care.
VESTIBULAR, BALANCE, AND MOTOR
DYSFUNCTIONS
The most common cause of vestibular disturbance in children is otitis media.96 Many parents
of infants and children report balance problems,
such as clumsiness, when a middle-ear effusion is
present.97 We now have evidence from studies of
labyrinthine function in children with and without middle-ear effusion to confirm that the
vestibular system is adversely affected, and after
tympanostomy tube placement, these dysfunctions return to normal.98–101 Test results of
motor proficiency have also been demonstrated
to be abnormal in children when middle-ear
effusion is present.102–104 Most recently, a study
revealed that children who had a history of otitis
media but no middle-ear effusion at the time of
the vestibular testing also had abnormal function, which indicates that there may be some
residual effect of otitis media on the labyrinth.105
Also, a recent case report described a child who
had otitis media with effusion and vestibular
neuritis.106 Disturbances in balance associated
with otitis media may also be due to labyrinthitis,
as described later in this chapter.107 Furman and
Casselbrant have provided a detailed description
Complications and Sequelae: Intratemporal
of the methods to evaluate children with vestibular disorders.108
PERFORATION OF THE TYMPANIC
MEMBRANE
Perforation of the tympanic membrane secondary to otitis media (and certain related conditions, such as atelectasis of the tympanic
membrane) can be either acute or chronic; otitis
media may or may not be present; and when
otitis media is present, otorrhea may or may not
be evident.1,10 The perforation can be classified
according to the following:
Site: pars tensa (anterosuperior, anteroinferior, posterosuperior, or posteroinferior quadrants) or pars flaccida
Extent: limited to one quadrant (less than
25%); involving two or more quadrants, but
not total; or total perforation (all quadrants).
341
perforation extends to the annulus, it is termed
marginal.
A defect in the pars flaccida has commonly
been called an attic perforation. The so-called
marginal perforation of the pars tensa, which
usually occurs in the posterosuperior portion,
and the ‘‘perforation’’ are, in reality, either a
deep retraction pocket or a cholesteatoma, which
are described later in this chapter (Figure 6). For
the attic perforation and marginal perforation,
there is usually no continuity between the defect
in the membrane and the middle ear until late in
the disease process, when infection erodes the
membrane of the pocket or the matrix of the
cholesteatoma. Therefore, the terms marginal
perforation and attic perforation are misnomers;
they were applied on the basis of observations
made before the availability of the otomicroscope, modern middle-ear surgery, advances in
temporal bone histopathologic techniques, the
use of immittance testing, and a better under-
Duration: acute or chronic
A perforation may also be due to a complication of a surgical procedure for management of
otitis media, such as myringotomy, tympanostomy tube insertion, or tympanoplasty (ie, an
iatrogenic complication). An acute perforation is
most frequently secondary to an episode of
AOM; if it persists for more than 3 months, it
is considered chronic. The defect may involve
almost the entire pars tensa or be so small as to
be detectable only with the otomicroscope or
when the immittance testing measures a volume
larger than the expected ear canal volume (see
Chapter 7). Otitis media (with or without
discharge) may be present or absent; when
chronic otitis media is present, the condition is
called chronic suppurative otitis media, which is
described in detail in a later section. Likewise, a
perforation may be associated with some of the
other complications and sequelae described in
this chapter. In the past, perforations have been
classified into central and marginal types.
Regardless of size, if there is a rim of tympanic
membrane remaining at all borders, the perforation is classified as central. When any part of the
Figure 6. Examples of defects in the tympanic membrane. A, A
small ‘‘central’’ perforation in the anteroinferior portion of the pars
tensa of the tympanic membrane. B, A ‘‘central’’ perforation that
involves approximately half of the pars tensa. C, A deep retraction
pocket in the posterosuperior portion of the pars tensa that has been
incorrectly called a marginal perforation. D, A deep retraction pocket
in the pars flaccida that has been inappropriately called an attic
perforation.
342
OTITIS MEDIA IN INFANTS AND CHILDREN
standing of the pathogenesis of a retraction
pocket and cholesteatoma.
Acute Perforation
An acute perforation of the tympanic membrane
is usually caused by an episode of AOM that is
complicated by rupture of the eardrum.109
However, an acute perforation can be present
in which otitis media is absent, such as when the
perforation is secondary to trauma or occurs as a
complication of ear surgery (eg, after tympanostomy tube insertion).
Classification
Acute perforations can be classified (see Chapter
1) as acute perforation without otitis media and
acute perforation with otitis media, with or
without otorrhea (AOM with perforation).110
Acute Perforation without Otitis Media
When an acute perforation is not a complication
of otitis media, otitis media may be absent, such
as after spontaneous extrusion or removal of a
tympanostomy tube or secondary to trauma.
Management of such perforations is ‘‘watchful
waiting’’ because most will heal within 2 to 3
months. In the two clinical trials conducted in
Pittsburgh that evaluated the efficacy of tympanostomy tube placement for chronic otitis media
with effusion in 215 children who were observed
for 2 to 3 years after the tubes were inserted,
32 (14.8%) had a perforation at the tube site
after extrusion, but only 3 children (1.4%)
developed a chronic perforation requiring tympanoplasty.111,112 Not only can an acute perforation persist into a chronic perforation, but a child
with an acute perforation may develop an AOM;
both are discussed in the following.
Acute Perforation with Otitis Media
An acute perforation (not due to trauma) is
usually secondary to AOM but may also occur
during the course of chronic otitis media with
effusion. Boswell and Nienhuys described spontaneous perforations developing in Australian
Aborigines who had chronic middle-ear effu-
sions.113 Because a spontaneous perforation
commonly accompanies an episode of acute
middle-ear infection, it may be considered part
of
the
disease
process
rather
than
114
a complication.
Because such a perforation
allows purulent material to drain into the
external canal and enhances drainage of pus
down the eustachian tube (owing to the effects of
an opening in the eardrum), a perforation of the
eardrum may prevent further spread of infection
within the temporal bone or, more important,
into the intracranial cavity. Infants and children
of certain racial groups, such as Alaskan natives
(Eskimos) and some Native American tribes,
have a high incidence of spontaneous perforation
with discharge; the eardrum is perforated spontaneously with almost every episode of AOM.115
In 711 Australian Aboriginal children 6 to 30
months of age, 7% had an AOM with perforation.116 The disease runs a similar course in
certain other children not belonging to these
high-risk
populations
(see
‘‘Chronic
Perforation’’).
Pathogenesis. Because of the presence of a
patulous or semipatulous eustachian tube, the
perforation may occur in high-risk populations,
such as the White River Apache American
Indian tribe.117 A eustachian tube with low
resistance would permit a larger bolus of
bacteria-laden purulent material from the nasopharynx to enter (by reflux, aspiration, or
insufflation) the middle ear, causing a more
fulminating infection than would occur if the
eustachian tube had either normal or high
resistance. An alternative explanation of why
some children seem to suffer a perforated
eardrum with each episode of AOM whereas
others do not could be that there are differences
in the virulence of the bacteria or decreased
resistance of the host. Factors that predispose
children to acute perforation are most likely
similar to those described later for chronic
perforation, especially in high-risk populations.
The possible outcomes of an acute perforation associated with an attack of AOM are as
follows:
Complications and Sequelae: Intratemporal
N
N
N
N
The otitis media and otorrhea completely
resolve, and the tympanic membrane perforation heals.
The otitis media and otorrhea completely
resolve, but the perforation persists and
becomes chronic.
Otitis media and perforation persist into the
chronic stage, which is termed chronic suppurative otitis media.
A suppurative complication develops.
Microbiology. The organisms most frequently cultured from an aural discharge when
AOM is present are the same as those that have
been cultured from acute middle-ear effusions
when a tympanocentesis has been performed (eg,
Streptococcus pneumoniae, Haemophilus influenzae, and Moraxella catarrhalis). Streptococcus
pyogenes, when present and untreated, has been
associated with acute perforation of the tympanic
membrane. These organisms have also been
cultured from children who have tympanostomy
tubes in place and have an episode of acute
otorrhea. Pseudomonas aeruginosa can also be
cultured from children.118 More recently, methicillin-resistant Staphylococcus aureus (MRSA)
has been isolated from discharging ears,119 which
emphasizes the importance of obtaining a culture
and studies for susceptibility, especially when the
infection does not respond to the more traditional, routine antimicrobial treatment. A report
from Australia described the development of a
perforation of the tympanic membrane in 22
patients who had fungal external otitis, but most
perforations closed following successful treatment of the external otitis.120 Also, tuberculosis
may be involved in acute and chronic middle-ear
infections with perforation and otorrhea.121
Management. Antimicrobial therapy for
children with acutely perforated eardrums should
be the same as or similar to that recommended
for those with AOM when a perforation is not
present (see Chapter 8).122,123 The current trend
toward not actively treating AOM with an
antibiotic agent is not acceptable when the attack
343
is complicated by rupture of the tympanic
membrane with otorrhea because the episode
can be characterized as severe; thus, active
treatment is indicated. When an aural discharge
is present, it is desirable to culture the drainage.
The antimicrobial regimen can then be adjusted
according to the results of the Gram stain,
culture, and susceptibility testing.124 The most
effective method for obtaining a sample of the
discharge is to remove as much of the purulent
material as possible from the external canal by
suction or a cotton-tipped applicator and then
aspirate pus directly at or through the perforation, using a spinal needle attached to a
tuberculin syringe or an Alden-Senturia trap
and suction. Some experts would argue against
using ototopical medication when a perforation
is present because of the potential danger of
ototoxicity. Some children, however, benefit
when otic drops are instilled into the external
canal.
In addition to the systemic antibiotic therapy,
it is advisable to add an ototopical medication,
which will not only aid in eliminating the
organisms from the external auditory canal, but
if the ear drops are pumped into the canal by
gently applying pressure on the tragus (eg, four
to five times), the medication can enter the
middle ear through the perforation and potentially aid in curing the middle-ear infection.125
Also, it is important to treat the initial canal
infection to prevent potentially pathogenic bacteria from the external ear canal entering the
middle ear, such as Pseudomonas and S. aureus,
causing a secondary infection of the middle
ear.115 If the suppurative process in the external
canal and middle ear is not effectively treated in
the acute stage, the infection can progress into
chronic suppurative otitis media; chronic infection is prevented by effective treatment of acute
infection.126,127 The most common bacterium
cultured from the middle ear in chronic suppurative otitis media that develops after an acute
otorrhea is P. aeruginosa and not the common
bacteria isolated initially (eg, S. pneumoniae and
H. influenzae) from AOM with or without
perforation. Many clinicians advocate applica-
344
OTITIS MEDIA IN INFANTS AND CHILDREN
tion of an antibiotic-cortisone otic medication
whenever a discharge is present despite the
possibility of ototoxicity because the topical
medication may treat or prevent an external
canal infection and hasten the resolution of the
middle-ear infection. Even though the new
ototopical antimicrobial agent ofloxacin (Floxin
Otic, Daiichi Pharmaceutical Corp, Montvale,
NJ) is approved for treatment of AOM and
otorrhea in children only when a tympanostomy
tube is in place, this medication should be equally
effective when a perforation is present.128,129 This
agent is currently the only ototopical medication
that has been demonstrated to be safe and
effective and is approved for use when a tympanostomy tube is present.128 A recent clinical
trial has shown that topical ciprofloxacin-dexamethosone otic solution (Ciprodex, Alcon, Inc,
Fort Worth, TX) may be superior to ofloxacin
for post-tympanostomy tube otorrhea, which is
probably due to the addition of the corticosteroid; also, ciprofloxacin-dexamethasone is effective when granulation tissue on the tympanic
membrane is present.130,131 Some have advocated
the use of other ototopical agents, but only these
two agents cited above are approved for use
when the tympanic membrane is not intact. Thus,
ototopical agents such as Burow’s solution
(aluminum acetate, 13%), even though relatively
inexpensive and shown to be effective for the
offending bacteria,132 are not currently indicated
when the middle ear is exposed to the external
canal. Likewise, the other agents listed in Table 3
are also not indicated, such as the still commonly
prescribed combination of neomycin, polymyxin
B sulfate, and hydrocortisone otic suspension
(Pediotic Suspension, Monarch Pharmaceutics,
Bristol, TN), owing to their potential ototoxicity.133,134 Therefore, it is likely that applying an
ototopical antibiotic medication during the acute
episode would prevent the secondary chronic
infection.
The discharge, especially when it is profuse,
should be prevented from draining onto the
pinna and adjacent areas because this usually
results in dermatitis (see the section on external
otitis). The parent should be instructed to keep
Table 3. OTOTOPICAL AGENTS USED IN THE
TREATMENT OF CHRONIC SUPPURATIVE OTITIS MEDIA
AND OTORRHEA*
Generic Name
Acetic acid (2%) otic solution
Acetic acid (2%) and
hydrocortisone (1%) otic
solution
Acetic acid 2% in aqueous
aluminum acetate otic solution
Ciprofloxacin hydrochloride
and hydrocortisone otic
suspension
Colistin sulfate–neomycin
sulfate–thonzonium bromide–
hydrocortisone acetate otic
suspension
Neomycin, polymyxin B
sulfate, and hydrocortisone
otic suspension
Ofloxacin otic solution 0.3%
Ciprofloxacin-dexamethasone
otic suspension
Trade Name (Company)
VōSol (Wallace Laboratories,
Cranbury, NJ)
VōSol HC (Wallace
Laboratories, Cranbury, NJ)
Otic Domeboro (Bayer
Corporation, West Haven, CT)
Ciprofloxin HC Suspension
(Alcon, Humacao, PR)
Cortisone-TC Otic Suspension
(Monarch Pharmaceuticals,
Bristol, TN)
Pediotic Suspension (Monarch
Pharmaceuticals, Bristol, TN)
Floxin Otic (Daiichi
Pharmaceutical Corp.,
Montvale, NJ)
Ciprodex (Alcon Laboratories,
Fort Worth, TX)
*Agents listed are commonly used in children and adults; only Floxin Otic and
Ciprodex have US Food and Drug Administration approval for this indication,
but only for adults.
cotton in the external auditory meatus and
change it as often as necessary to keep the canal
dry. Cotton-tipped applicators should not be
used by the child or parent. Prevention of water
entering the ear canal is advisable; swimming is
not recommended until the infection is cured and
the tympanic membrane is healed.
The tympanic membrane will frequently heal
after the suppurative process in the middle ear
ends. The defect usually closes within a week
after onset of infection. When persistent discharge lasts longer than the initial 10-day course
of antibiotic treatment, the child requires more
intensive evaluation and aggressive management.
In addition to obtaining a culture of the purulent
material from the middle ear and adjusting
antimicrobial agents, frequent cleaning of the
canal, followed by instillation of ototopical
drops, may also be required.
The presence of acute mastoiditis with
periosteitis or acute mastoid osteitis should be
suspected if the child has persistent otalgia,
tenderness of the ear to touch, erythema, and
Complications and Sequelae: Intratemporal
swelling in the postauricular area. Computed
tomography (CT) of the mastoids may be helpful
but is not always diagnostic of mastoid osteitis
(see the section on mastoiditis). CT scans can
also help diagnose spread of infection outside the
middle ear and mastoid. Even if an intratemporal
(or intracranial) complication is not readily
apparent, if the aural discharge persists 2 or 3
weeks after onset of AOM that has been treated
with appropriately administered oral antibiotics,
the patient may require hospitalization. The
child should be evaluated again thoroughly in a
search for an underlying illness that would
interfere with resolution of the infection. The
otologic assessment should include an examination of the entire external canal and tympanic
membrane, with use of the otomicroscope to
determine whether another otologic condition,
such as a cholesteatoma or neoplasm, is
present. If an adequate examination cannot be
performed with the child awake, it should be
carried out under general anesthesia, at which
time a culture can be obtained directly from the
middle ear. If no condition other than the
perforation and subAOM is found, parenteral
antimicrobial agents should be administered. The
selection of both the systemic and topical
antimicrobial agents should be based on the
results of cultures. A gram-negative organism
(eg, P. aeruginosa) is frequently present at this
stage, and management is essentially as recommended later under ‘‘Chronic Perforation with
Chronic Otitis Media (Chronic Suppurative
Otitis Media).’’
With this method of management, the infection will usually subside. If the discharge persists,
an exploratory tympanostomy and complete
simple mastoidectomy are indicated even if no
signs and symptoms of mastoid osteitis are
present and the CT scans fail to show osteitis
(ie, coalescence). During surgery on the middle
ear and mastoid, a thorough search for another
cause of the persistent infection must be made.
On occasion, a cholesteatoma that could not be
visualized through the otomicroscope will be
found. Resolution of infection in the middle ear
and mastoid will invariably follow the surgery
345
because mastoid osteitis is the usual cause of this
complication of AOM.
Fortunately, the occurrence of such cases is
now uncommon, and the perforation usually
heals rapidly. However, the defect will frequently
remain open without evidence of otitis media
(with or without discharge). If the perforation
remains free of infection, it will frequently close
in a few months. At this stage, no attempt at
surgical closure of an uncomplicated perforation
is indicated. If there is no sign of progressive
healing after 3 months or more, management
should be as described later (see ‘‘Chronic
Perforation’’), such as tympanoplasty.
Prevention. In patients who are prone to
recurrent AOM and who perforate their tympanic membrane, prevention is desirable (described
in detail in Chapter 8). In certain populations at
high risk of AOM and perforation, which
subsequently progresses to chronic suppurative
otitis media, the most effective method of
prevention of the chronic infection is to prevent
development of an acute perforated tympanic
membrane during an attack of AOM.116 This is
most effectively accomplished by treating the
child early, appropriately, and adequately with
an antimicrobial agent at the onset of the episode
of AOM (see ‘‘Chronic Perforation’’).
Chronic Perforation
A perforation of the tympanic membrane may
remain open after an episode of AOM or after
spontaneous extrusion (or removal) of a tympanostomy tube. When an acute perforation is
present with no signs of healing and there are no
signs of otitis media for 3 months or longer, the
perforation is considered chronic and possibly
permanent. If chronic suppurative otitis media is
present, the perforation may close spontaneously
after appropriate treatment if the infection
resolves. However, healing of the perforation
may not occur for the same reason that chronic
perforations, without chronic infection, fail to
heal: the presence of squamous epithelium at the
edges of the perforation prevents spontaneous
346
OTITIS MEDIA IN INFANTS AND CHILDREN
repair. The effect on hearing of a small chronic
perforation is not significant, regardless of its
location and in the absence of other middle-ear
abnormalities. A large perforation, however, can
be associated with an appreciable conductive
hearing loss (eg, 20–30 dB).
Classification
Chronic perforation of the tympanic membrane
can be classified as chronic perforation without
otitis media and chronic perforation with otitis
media.110 Chronic perforation with otitis media
can be further classified into chronic perforation
with AOM, with or without otorrhea, and
chronic perforation with chronic otitis media
(chronic suppurative otitis media), with or without otorrhea. The last disease stage is invariably
associated with chronic mastoiditis (see Chapter
1).
Chronic Perforation without Otitis Media
Chronic perforation without otitis media has
been inappropriately termed chronic otitis media
inactive. This terminology is confusing and
incorrect in many instances. The patient may
never have an attack of AOM—other than
possibly the one that originated the perforation—or an episode of chronic suppurative otitis
media (see Chapter 1).
Epidemiology. The incidence of chronic
perforation in the pediatric population has not
been formally studied, but chronic perforation is
a frequent reason for referral to an otolaryngologist. In a study of tympanoplasty for chronic
perforation—not associated with infection, cholesteatoma, or ossicular involvement—in children from Finland, Vartiainen and Vartiainen
operated on 60 children during a 15-year
period.135 Caylan and colleagues described a
similar number of children who had surgical
repair of a chronic perforation in an Italian
center during a 10-year period.136 They also
reviewed the literature from 1974 to 1991 and
found that 640 children had tympanoplasty as
reported in 12 studies. Another review of the
literature from 1979 to 1995 reported that 870
had tympanoplasty,137 and still another review
found 1,741 cases reported between 1985 and
1998.138 However, many reports combine children and adults in the study, which often
prevents assessment of the number of children
included. Many reports in the literature also
combine children who have chronic perforation
without active infection with those patients who
have chronic suppurative otitis media (see later,
‘‘Chronic Perforation with Chronic Otitis Media
[Chronic Suppurative Otitis Media]’’). In addition, the incidence of tympanoplasties performed
in children would not accurately reflect the true
incidence of chronic perforation because many
physicians elect to withhold surgery until later in
the child’s life. More important, most otolaryngologists do not report their results of tympanoplasty in children. Thus, the number of
children being operated on for repair of a chronic
perforation is a great deal larger than is reported
in the literature. Next to myringotomy, with or
without tympanostomy tube insertion, tympanoplasty is the most common ear operation
performed in children.139
Chronic perforation, as a complication of
otitis media, is more prevalent in certain racial
groups that also have a high prevalence and
incidence of perforations associated with acute
middle-ear infection. In 1970, new cases of
chronic perforation (with or without chronic
suppurative otitis media) were reported in 8% of
the native population of Alaska, although this
rate appears to be dropping.140 Similar rates have
been reported in Native American populations.
Zonis reported that of 207 Apache Indian
children examined in Canyon Day, Arizona, 17
(8%) had chronic perforations as their only sign
of otitis media,141 whereas Todd and Bowman
returned to the same village 16 years later in
1983, examined 145 Indian children living there
at the time, and found only 1 child who had a
perforation of the tympanic membrane but 12
(8%) children who had other evidence of otitis
media.142 Even though chronic perforation with
chronic suppurative otitis media is common in
young Australian Aboriginal children, chronic
perforation without otitis media is less common.
Complications and Sequelae: Intratemporal
Indeed, Morris and colleagues reported that 15%
of 711 of these children, aged 6 to 30 months, had
chronic suppurative otitis media, but only 2%
had a perforation, without otitis media.116
Because many of these chronic perforations are
associated with chronic middle-ear and mastoid
infection, the epidemiology of this complication
of otitis media is presented in more detail under
‘‘Chronic Perforation with Chronic Otitis Media
(Chronic Suppurative Otitis Media).’’
Chronic perforation of the tympanic membrane is a recognized complication of tympanostomy tube insertion.143 Of 1,062 ears of
children who received tympanostomy tubes in
one study reported from West Germany, 26 ears
(2.5%) had a persistent perforation.144 This
figure, however, depends on the site of the tube
placement and the type of tube used. The rate of
chronic perforation as a complication of tube
placement has been reported to be as low as 0.5%
and as high as 25%. The conventional tubes are
associated with the lowest rate and the permanent tubes with the highest rate. Of the 215
children prospectively observed for at least 2 to 3
years in the three clinical trials of efficacy and
safety of tympanostomy tube insertion conducted in Pittsburgh, 2.4% had to eventually
have tympanoplasty for chronic perforation (see
‘‘Myringotomy and Tympanostomy Tube
Placement’’ in Chapter 8).111,112,145
Management. The management of so-called
dry chronic perforation (more appropriately
termed chronic perforation without otitis media)
in children is both difficult and controversial. On
the one hand, the perforation provides ventilation and drainage of the middle ear. On the other
hand, the physiologic protective function of the
eustachian tube–middle-ear system is impaired;
the middle ear is too open. The middle ear and
mastoid gas cells no longer have a gas cushion to
prevent nasopharyngeal secretions from entering
the ear, which can then result in reflux otitis
media (Figures 7 and 8).127 In addition, the open
tympanic membrane can permit contaminated
water to enter the middle ear during bathing and
swimming. Therefore, the dilemma of when to
347
Figure 7. A perforation of the tympanic membrane may promote
the reflux of secretions into the middle ear from the nasopharynx
because the middle-ear air cushion is not present (see also Figure 8).
Figure 8. Flask model showing how a perforation of the tympanic
membrane may result in reflux of nasopharyngeal secretions into the
middle ear. The nasopharynx–eustachian tube–middle-ear–mastoid
air cell system is likened to a flask with a narrow neck. When the
system is intact, liquid is prevented from entering the body of the
flask, but when the body of the flask is not intact (ie, a perforation is
present), liquid can readily flow through the system.
348
OTITIS MEDIA IN INFANTS AND CHILDREN
close such a perforation is comparable to
that regarding the most appropriate time to
remove a tympanostomy tube: a small, uncomplicated chronic perforation and a tympanostomy tube have similar benefits and risks. Like a
tympanostomy tube, a perforation may be
beneficial for a child who had had recurrent
AOM or chronic otitis media with effusion
before the perforation developed, but recurrent
acute reflux otitis media with discharge, which
can progress into chronic suppurative otitis
media, may become a problem, making repair
of the eardrum defect a consideration. However,
recurrent AOM that results in otorrhea through
a chronic perforation can be effectively treated
and even prevented without repair of the
tympanic membrane (or removal of a tympanostomy tube).
When the episodes are infrequent, the treatment of each bout should be the same as
recommended for an acute perforation associated with AOM. If the episodes of acute
infection are frequent and the interval between
bouts is short, preventive measures are recommended. The options appropriate today are the
same as those recommended for infants and
children whose tympanic membranes are intact
but who have frequently recurrent AOM (see
Chapter 8). Reducing the risk of exposure to viral
infections (eg, eliminating day care or choosing a
day-care setting with as few children as possible)
may prove helpful. The currently available
pneumococcal vaccine (after the age of 2 years)
and the influenza vaccine can be administered. A
search for an underlying problem, such as an
immune disorder, adenoid hypertrophy, paranasal sinusitis, or allergy, may also help. If none of
these recommendations prove beneficial and an
underlying problem is not uncovered, prophylaxis with an antimicrobial agent during the risk
months for upper respiratory tract infections
(late fall, winter, and spring) can be initiated.
This method was demonstrated to be effective in
reducing recurrent otorrhea in Alaskan
natives.146 A prolonged course of a prophylactic
antimicrobial agent (eg, amoxicillin, 20 mg/kg,
given in one dose before bedtime) may be
considered to prevent recurrent middle-ear infection and discharge. The selection of the agent
should be based on the results of the cultures
obtained from previous episodes of discharge.
The dosage and duration of treatment should be
the same as those recommended for children who
have had frequently recurrent AOM without a
perforation. Today, however, with the everincreasing rate of antibiotic-resistant otogenic
bacteria that has been attributed to the overuse
of antibiotics for treatment and prolonged lowdose prophylaxis, other preventive measures
should be attempted before systemic antimicrobial prophylaxis is recommended. One method
that can be helpful is to give the child a course of
an ototopical ofloxacin during the duration of an
upper respiratory tract infection. This method is
more appealing than systemic administration of
an antimicrobial agent because drug-resistant
bacteria apparently do not develop during
topical treatment. Also, consideration should be
given to repairing the perforation. Children in
whom an attack of acute middle-ear infection
and discharge persists despite adequate medical
treatment and in whom the infection is thought
to be chronic should be evaluated and managed
as described in the section on chronic suppurative otitis media.
Most children who have a defect in the
eardrum that is thought to be preventing otitis
media can be watched until the risk of recurrence of infection is low enough to consider
surgical closure of the perforation. A perforation, such as a tympanostomy tube, may prevent
development of a retraction pocket and, subsequently, a cholesteatoma. If the eustachian tube
function is poor, it is desirable to delay such
surgery as long as possible to prevent such
complications. Surgery for a chronic perforation
should not necessarily be withheld in children
because of recurrent episodes of otitis media and
discharge; the perforation may be causing the
middle-ear infection (as a result of reflux from
the nasopharynx) rather than preventing disease.127 Also, perforation of the tympanic membrane is associated with some degree of hearing
loss.147
Complications and Sequelae: Intratemporal
Tympanoplasty. Tympanoplasty is not as
successful in children as it is in adults.148–150
These results may be due to the higher incidence
of upper respiratory tract infection leading to
otitis media in children and the unpredictability
of their eustachian tube function. However, the
success rate of tympanoplasty is still high, as
shown in Table 4. The study by Bluestone and
colleagues had the lowest success rate compared
with later studies because a medial graft technique was used initially and the criteria for success
versus failure were rigid during a prolonged
follow-up period.151 Since then, a variety of
surgical techniques have been used, with success
rates comparable to those reported in the recent
literature.152
Optimal ages at which to perform tympanoplastic surgery have variously been stated to be
from 3 years to puberty.150,153–155 Lau and Tos
reviewed the outcome of 124 tympanoplasties
performed on 116 children between the ages of 2
and 14 years and found a 92% success rate of
grafts; these authors recommend tympanoplasty
in children of all ages,156 as do Paparella,157
Table 4. OUTCOME OF TYMPANOPLASTY, TYPE I
(MYRINGOPLASTY), IN CHILDREN WHO HAD CHRONIC
PERFORATION OF THE TYMPANIC MEMBRANE AS
REPORTED FROM 20 CENTERS FROM 1979 TO 2005
Study (Year)
Bluestone et al (1979)151
Cohn et al (1979)552
Raine and Singh (1983)553
Adkins and White (1984)554
François et al (1985)555
Lau and Tos (1986)156
Ophir et al (1987)556
Koch et al (1990)161
Prescott and Robartes (1991)557
Kessler et al (1994)558
Black and Wormald (1995)559
Chandrasekhar et al (1995)560
Mitchell et al (1997)561
Vartiainen and Vartiainen (1997)135
Caylan et al (1998)136
Bajaj et al (1998)137
Denoyelle et al (1999)138
Carr et al (2001)562
Collins et al (2003)172
Couloigner et al (2005)175
Number
of Ears
Success
Rate (%)
51
21
114
30
150
155
172
64
114
209
100
268
342
60
51
45
231
89
72
29
35
81
81
87
81
92
79
73
84
92
75
81
80
90
82
91
83
75
82
71
349
Vartiainen and Vartiainen,135 Bajaj and colleagues,137 and Denoyelle and colleagues.138 In the
Lau and Tos study, however, the initial 92%
success rate of the procedure fell to 64% over
time; 14% required tympanostomy tubes, 5% had
persistent middle-ear effusion, and 9% had postoperative atelectasis.156 Tos updated these outcomes in the young child.158 Similar outcomes
were reported by Manning and colleagues in a
study of 56 children (63 ears).159 Even though
78% of the grafts healed, only 52% of the
children had a healed graft and adequate
middle-ear function during the postoperative
period. Sheehy and Anderson do not recommend
elective tympanic membrane grafting for children
who are younger than 7 years because of the
possibility of postoperative otitis media.160 Other
surgeons reported tympanoplasty outcomes that
agree with the recommendation of Sheehy and
Anderson and not with Tos and Lau.160–164 In
general, infants and children younger than 7
years have less favorable outcomes after tympanoplasty than do older children and adults. The
controversy over which age is most appropriate is
due to definitions of failure and the duration of
follow-up, as well as the intervals between
observations. Graft take should not be the only
outcome measure. Additional outcomes should
be recurrence of middle-ear effusion, high
negative middle-ear pressure, atelectasis, subsequent reperforation, the need for tympanostomy
tube placement, and serial assessment of hearing
during a long period. When children aged 7 years
and older are operated on, their outcomes are
relatively good.165 A meta-analysis of tympanoplasty in children from 1966 to 1997 by Vrabec
and colleagues revealed that the success rate
increased with advancing age and that none of
the other parameters studied were shown to be
significant predictors of success.166
The level of experience of the surgeon has also
been called into question.164 Whereas a teaching
institution has a responsibility to train young
surgeons, that is not the case with the private
practitioner or in areas where only the attending
surgeon performs the surgery. These factors are
also probably related to the variation in post-
350
OTITIS MEDIA IN INFANTS AND CHILDREN
operative outcomes reported in the literature.
Persistent perforation is a problem in some
patients even in the best of circumstances.167
Some surgeons advocate removing the adenoids before repairing a chronic tympanic
membrane perforation, but Vartiainen and
Vartiainen reported that their graft failures
occurred in patients who had had a previous
adenoidectomy.135 They suggest that children
who had had adenoidectomy in the past most
likely had more middle-ear disease and were
more likely to have failure of tympanoplasty.
Indications for adenoidectomy in children who
have a chronic perforation should be similar to
the indications for children in whom the tympanic membrane is intact (see Chapter 8). Also, on
occasion, a tympanostomy tube has been recommended as part of the procedure.168
The addition of a mastoidectomy to the
tympanoplasty, when a chronic perforation without otitis media is present, has been advocated by
some,169 but the evidence that the benefits of
mastoidectomy outweigh the potential risks (eg,
facial paralysis, injury to the inner ear, increased
time of general anesthesia) has not been demonstrated, and we do not advocate this additional
surgical procedure.9
Studying eustachian tube function before the
patient with a chronic perforation of the tympanic
membrane is operated on may be helpful in
determining the potential results of tympanoplastic surgery because the function of the tube can
affect outcome.170 Bluestone and colleagues, in a
study of 45 children with chronic perforation,
found that the assessment of eustachian tube
function was an aid in preoperative assessment.151
In a subsequent study at the same institution,
Manning and colleagues evaluated eustachian tube
function preoperatively in 56 children and found
that normal function was associated with a good
outcome, whereas poor function did not predict a
poor outcome.159 Kumazawa and colleagues
reported that they consider preoperative evaluation with eustachian tube function tests to be
helpful in prognosis.171 An alternative method to
assess eustachian tube function when actual testing
is unavailable is to observe the contralateral ear, if
the tympanic membrane is intact, for four or more
seasons to determine if middle-ear disease recurs,
for example, otitis media, atelectasis, and symptoms of eustachian tube dysfunction. This predictor of outcome has not been formally tested,
but it does not make sense to repair the tympanic
membrane perforation in the face of recurrent
middle-ear disease in the opposite ear; in children,
eustachian tube function is usually similar in both
ears. Collins and colleagues agree that the status of
the contralateral ear is an important factor related
to outcome.172
Thus, children, especially those who are
younger than 7 years, are uncertain candidates
for tympanoplastic surgery because as a group,
their eustachian tube function is not as good as
that of adults. Improvement may occur in some
children, indifferent results are obtained in
others, and there are more problems with
middle-ear infections in a third group. The
problem for the clinician is deciding which child
should have the perforation repaired. The development of an improved method of testing the
eustachian tube, a method more indicative of the
actual function available for clinical use, could
possibly help in this decision-making process.
Currently, we recommend tympanoplasty for
children after the age of 6 years because the
incidence of middle-ear disease declines after that
age, probably owing to maturation of the
structure (length) and function of the eustachian
tube and maturation of the child’s immunity. In
general, the indications for repairing a perforation are similar to the indications for removing a
retained tympanostomy tube; both procedures
attempt to restore an intact tympanic membrane.
The indications for removing a tympanostomy
tube are listed in the section ‘‘Myringotomy and
Tympanostomy Tube Placement’’ in Chapter 8.
There have been many surgical techniques
proposed to repair the defect in the eardrum.173–175 The surgical techniques performed
by us are described in detail in Bluestone.9
Chronic Perforation with Otitis Media
When an acute perforation of the tympanic
membrane is associated with AOM, the infection
Complications and Sequelae: Intratemporal
can progress into a chronic perforation and
chronic suppurative otitis media.176 This is
termed chronic suppurative otitis media.110 A
chronic perforation may also be present with
no middle-ear infection but is susceptible to an
episode of otitis media. This is initially AOM,
which can progress to the chronic stage (ie,
chronic suppurative otitis media).
Classification. Chronic perforation with
otitis media can be classified as follows:
N
N
Chronic perforation with AOM, with or without otorrhea
Chronic perforation with chronic otitis media,
with or without otorrhea
The term chronic suppurative otitis media
implies that a chronic perforation of the tympanic membrane is present, as in chronic mastoiditis, but otorrhea may or may not be present.
Chronic Perforation with AOM. A chronic
perforation of the tympanic membrane can
develop AOM, which can then have the following possible outcomes115:
N
N
N
N
The AOM and otorrhea completely resolve,
and the chronic perforation heals.
The AOM and otorrhea completely resolve,
but the chronic perforation persists.
AOM persists into the chronic stage, that is,
chronic suppurative otitis media.
A suppurative complication, such as acute
mastoiditis, develops.
The presumed reason that a chronic perforation occasionally heals after an episode of AOM
is that the rim (margins) of the perforation is
denuded of the epithelium by the infection; the
epithelium at the margins prevented healing
before the infection.
When an episode of AOM develops in a child
who has a chronic perforation of the tympanic
membrane, initial management should be similar
to that described earlier when an acute perforation develops during an attack of AOM. If the
AOM resolves but the chronic perforation
persists, the decision-making process to close
351
the perforation, or not to close it, is the same as
described before for a chronic perforation without otitis media.
Chronic Perforation with Chronic Otitis
Media (Chronic Suppurative Otitis Media).
Chronic suppurative otitis media is the stage of
ear disease in which there is chronic inflammation of the middle ear and mastoid and in which
a nonintact tympanic membrane (chronic perforation or tympanostomy tube) is present.
Otorrhea may or may not be evident; a discharge may be present in the middle ear,
mastoid, or both, but otorrhea is not evident
through the perforation—or tympanostomy
tube—or in the external auditory canal. There
is no consensus regarding the duration of otitis
media to be designated chronic suppurative otitis
media. Even though 3 months or longer appears
to be appropriate, some clinicians consider a
shorter duration of otitis media to be chronic,
especially when the causative organism is
Pseudomonas.
Terminology. Chronic suppurative otitis
media is the term commonly used when a chronic
perforation is associated with chronic otitis
media. Mastoiditis is invariably part of the
pathologic process.115 The condition has also
commonly been called chronic otitis media, but
this term can be confused with chronic otitis
media with effusion, which is not a complication
of otitis media and in which no perforation of the
tympanic membrane is present. Chronic otitis
media is also an inappropriate term when a
chronic perforation of the tympanic membrane is
present but the middle ear and mastoid are free
of infection. The proper term for this condition is
chronic perforation without otitis media or, more
simply, chronic perforation. Some clinicians also
inappropriately use the terms chronic otitis media
inactive and chronic otitis media active; chronic
perforation associated with infection is active,
and when infection is absent, it is inactive.177
Other terms for chronic suppurative otitis media
are chronic suppurative otitis media and mastoiditis, chronic purulent otitis media, and chronic
352
OTITIS MEDIA IN INFANTS AND CHILDREN
otomastoiditis. The most descriptive term is
chronic otitis media with perforation, discharge,
and mastoiditis,178 but this is not commonly used.
When a cholesteatoma is also present, the term
cholesteatoma with chronic suppurative otitis
media is appropriately used. However, because
an acquired aural cholesteatoma does not have to
be associated with chronic suppurative otitis
media, cholesteatoma is not part of the pathologic features of the type of ear disease described in
this section and is presented as a separate entity
in this chapter.176,179
Despite the strict definition of chronic
suppurative otitis media presented here, a
review of the literature reveals that many
reports describing various aspects of chronic
suppurative otitis media, such as epidemiology
and pathogenesis, improperly include chronic
perforation without otitis media in this disease
entity.
Epidemiology. Chronic suppurative otitis
media is a major health problem in many
populations around the world, affecting diverse
racial and cultural groups living not only in
temperate climates but in climate extremes
ranging from the Arctic Circle to the equator.
From a review of approximately 50 reports
published during the past 30 years, the disease
appears to be prevalent in four groups of
populations (Table 5).115 The prevalence of
chronic otitis media (defined here as chronic
perforation with and without suppuration) has
been reported to be the highest in the Inuits
of Alaska (30–46%), Canada (7–31%), and
Greenland (7–12%); Australian Aborigines (12–
25%); and certain Native Americans, such as
Apache and Navajo tribes (4–8%). Apparently,
these North American Indian tribes have higher
rates than others.180 One study from the Eastern
Canadian Arctic compared the rates in Cree
Table 5. PREVALENCE OF CHRONIC SUPPURATIVE OTITIS MEDIA*
Highest
Population
Prevalence (%)
References
Inuits
Alaska
Canada
30–46
7–31
Brody et al,563 Kaplan et al,57 Tschopp564
Ling et al,565 Schaefer,189 Baxter and Ling,566 Timmermans and Gerson,567 Baxter,568
Baxter et al181,569
Pederson and Zachau-Christiansen,570 Homoe and Bretlau,571 Homoe et al572
Stuart et al,573 McCafferty et al,412 Lewis et al,574 Moran et al,575 Dugdale et al,576
Hudson and Rockette,577 McCafferty et al,578 Foreman,579 Leach et al,188 Boswell
and Nienhuys,113 Morris et al116
Greenland
Australian
Aborigines
High
Low
Lowest
Native
Americans
Apache, Navajo
South Pacific
Islands
Solomon Islands
New Zealand
Maori
Malaysia
Micronesia
Africa
Sierra Leone
Gambia
Kenya
Nigeria
Tanzania
Korea
India
Saudi Arabia
United States
United Kingdom
Denmark
Finland
7–12
12–25
4–8
Johnson,580 Zonis,141 Jaffe,462 Mortimer,581 Wiet,463 Todd and Bowman142
4–6
4
Eason et al582
Tonkin,583 Giles and O’Brien584
4
4
Elango et al585
Dever et al,586,587 Chan et al588
6
4
4
4
2–3
2
2
1.4
,1
,1
,1
,1
Seeley et al19
McPherson and Holborow589
Hatcher et al590
Miller et al,183 Okeowa184
Manni and Lema,591 Bastos et al,592 Minja and Machemba593
Kim et al594
Kapur595
Muhaimeid et al596
Casselbrant et al,597,598 Zeisel et al,599 Paradise et al600
Mawson and Ludman,150 Williamson et al601
Fiellau-Nikolajsen602
Marttila603
*Some reports included patients who had chronic perforation but without otitis media.
Complications and Sequelae: Intratemporal
Indian schoolchildren with the rates in Inuit
children living in the same area and found the
rate to be 22% in the Inuit but only 1% in the
Cree.181 In a recently reported prevalence study
of 711 Aboriginal children from 29 remote
communities in Australia, 118 (15%) had chronic
suppurative otitis media, which verifies that this
stage of middle-ear disease is still a major health
problem in this special population.116
Populations with moderately high rates are
certain natives of the South Pacific islands, such as
natives of the Solomon Islands (4–6%), New
Zealand Maori (4%), natives of Malaysia (4%),
and natives of Micronesia (4%) (in contrast to
these high rates in some islands of the South
Pacific, natives of Melanesia have an extremely
low rate, less than 1%182); and some African
populations, such as those of Sierra Leone (6%),
Gambia (4%), Kenya (4%), and Tanzania (2–3%).
However, not all reports from Africa have
documented these relatively high rates. One study
from Nigeria reported less than 1% with the
disease183; another study found a 4% rate.184 One
study of South African rural blacks also found a
rate of less than 1%.185 A study from south India
found the rate to be 6% in rural children.186
Populations with relatively low rates of
chronic otitis media are those of Korea (2%),
India (2%), and Saudi Arabia (1.4%). Studies
from highly industrialized nations have reported
the lowest rates (none or less than 1%), such as
the United States, Finland, the United Kingdom
(in one adult population, the rate has been
reported to be 3.1%177), and Denmark. However, with the widespread use of tympanostomy
tubes in these countries, chronic suppurative
otitis media occurs as a not uncommon complication in infants and children in whom these
tubes have been inserted.187
Risk factors that have been attributed to the
high rates of chronic suppurative otitis media in
these populations are a lack of breast-feeding,
overcrowding, poor hygiene, poor nutrition,
passive smoking, high rates of nasopharyngeal
colonization with potentially pathogenic bacteria, and inadequate and unavailable health
care.140,181,188,189
353
Pathogenesis. The etiology and pathogenesis of chronic suppurative otitis media are
multifactorial, involving one or more of the risk
factors noted before, but chronic suppurative
otitis media begins with an episode of AOM.
Thus, the factors that have been associated with
AOM may initially be involved, such as upper
respiratory tract infection; anatomic factors,
such as eustachian tube dysfunction; host factors,
such as young age; immature or impaired
immunologic status; the presence of an upper
respiratory allergy; familial predisposition; the
presence of older siblings in the household; male
sex; race; method of feeding (bottle versus
breast); and environmental (eg, smoking in the
household) and social factors. Probably the most
important factors related to the onset of AOM in
infants and young children are immaturity of the
structure and function of the eustachian tube and
immaturity of the immune system.127
AOM with perforation (or when a tympanostomy tube is present) usually precedes chronic
suppurative otitis media, but in certain high-risk
populations, such as the Australian Aborigines,
chronic otitis media with effusion is initially
present.113 Factors most likely related to the
progression of AOM into the chronic stage have
been noted before, but most likely the process, if it is
long-standing, results in a chronic osteitis of the
middle-ear cleft.190 Figure 9 shows the possible
outcomes of an episode of AOM that may result in
chronic suppurative otitis media. Because a spontaneous perforation commonly accompanies an
episode of AOM that is untreated with an
antimicrobial agent, and less commonly despite
adequate treatment, it may be part of the natural
history of the disease process rather than a
complication. Figure 10 also shows the sequence
of events after an attack of AOM that can lead to a
chronic perforation or chronic suppurative otitis
media.
When a chronic perforation or tympanostomy
tube is present and there is no evidence of infection,
reinfection probably occurs in one of two ways:
1. Bacteria from the nasopharynx gain access to
the middle ear by reflux or insufflation of
354
OTITIS MEDIA IN INFANTS AND CHILDREN
Figure 9. Possible outcomes of acute otitis media. CSOM 5
chronic suppurative otitis media; OME 5 otitis media with effusion.
nasopharyngeal secretions (owing to the
infant crying, nose blowing, or swallowing
when a nasal obstruction is present, that is,
the Toynbee phenomenon191) through the
eustachian tube because the middle-ear air
cushion is lost; an episode usually occurs with
an upper respiratory tract infection. In most
instances, these bacteria are initially the same
as those isolated when AOM occurs behind
an intact tympanic membrane, such as S.
pneumoniae and H. influenzae.118 After the
acute otorrhea, P. aeruginosa, S. aureus, and
other organisms from the external ear canal
enter the middle ear through the nonintact
tympanic membrane, which results in secondary infection and acute otorrhea and chronic
suppurative otitis media (Figure 11). Bacteria
commonly isolated from ears with chronic
suppurative otitis media (eg, P. aeruginosa, S.
aureus) are isolated as normal flora from the
Figure 10. One possible sequence of events after an episode of acute otitis media that can result in a chronic perforation of the tympanic
membrane or chronic suppurative otitis media in a right ear (1). During an upper respiratory tract infection (URI), nasopharyngeal secretions with
viruses and bacteria can gain entrance into the middle ear (2), causing acute otitis media, perforation of the tympanic membrane, and otorrhea
(3), after which bacteria from the ear canal can enter the middle ear (4), resulting in chronic suppurative otitis media (5). The infection resolves,
but the perforation persists and becomes chronic (5a), or there is both resolution and healing of the perforation (5b).
Complications and Sequelae: Intratemporal
355
Figure 11. One of two proposed
sequences of events in the pathogenesis of recurrence of otorrhea when
the tympanic membrane is not intact
and active infection is absent in a
right ear (1). After an upper respiratory tract infection (URI), nasopharyngeal organisms are refluxed or
insufflated into the middle ear (2),
which results in an acute otitis media
and otorrhea (3). Organisms from the
external canal can then enter the
middle ear (4), which can result in
chronic suppurative otitis media (5).
TVP 5 tensor veli palatini muscle
(see Figure 12).
external auditory canal192 and thus can be
readily available as secondary invaders into
the middle ear.
2. Chronic suppurative otitis media also occurs
when the middle-ear cleft is contaminated by
organisms (eg, P. aeruginosa) present in water
that enters the nonintact eardrum during
bathing and swimming (Figure 12).193
As described before, certain populations are
at high risk of development of chronic perforation of the tympanic membrane with and without
chronic suppurative otitis media. From this
review, it appears that there are special populations who are at highest risk of development of
chronic suppurative otitis media who live in
diverse geographic regions in the world (see
Table 5), which would make climate an unlikely
explanation for their disease. In these racial
groups, it is likely that the pathogenesis of their
disease is due to genetic differences in their
eustachian tube function. The tube is most likely
hyperpatent, which may be due to a semipatulous
or patulous lumen, the tube is too short, or both.
(Histopathologic temporal bone specimens of
young individuals who had cleft palate and those
who had Down syndrome—both conditions of
high risk of otitis media—had statistically shorter
eustachian tubes than age-matched specimens
from individuals without these disorders.194)
Nevertheless, environmental and behavioral factors and the availability of adequate health care
are also important in these racial groups. Thus,
these other factors (ie, other than abnormalities
of the eustachian tube) would make other
populations also at risk. What other host factors
contribute to their high rate of disease? One
important possible explanation is that these
groups have eustachian tubes that make them
more prone than others to middle-ear infection.
Indeed, a study identified anatomic differences in
the bony segment of the eustachian tube in the
356
OTITIS MEDIA IN INFANTS AND CHILDREN
Figure 12. One of two proposed
sequences of events in the pathogenesis of recurrence of otorrhea when
the tympanic membrane is not intact
and active infection is absent in a
right ear (1). The middle ear is
contaminated by organisms in water
that enter the middle ear through the
perforation (2), which can result in
acute otitis media and otorrhea (3)
and, if persistent, chronic suppurative
otitis media (4). TVP 5 tensor veli
palatini muscle (see Figure 11).
craniofacial structures of Eskimo, American
Indian, white, and black crania.195 In a clinical
study, White Mountain Apache Indians were
also found to have eustachian tubes that were
semipatulous (of low resistance) compared with
those of a group of white subjects.117 Similar
findings have been reported in Canadian Inuits.
Ratnesar calibrated the eustachian tube with
ureteric catheters in Canadian Inuits and white
individuals and found the tube to be larger in
Inuits than in whites.196
One study reported that environment plays a
role in a high-risk population but that genetic
differences are probably more important in those
who are at high risk. Adopted Apache children
had more episodes of AOM than did their nonApache siblings and had an illness rate similar to
that of Apache children who remained on the
reservation.197 In a study from Greenland of 591
children aged 3, 4, 5, and 8 years, 9% had chronic
perforation, with and without chronic suppurative otitis media, which was statistically most
common in children whose parents were both
native Greenlanders.198
It is likely that eustachian tube dysfunction is
involved in the process even in individuals who
are not members of high-risk populations or who
have an obvious craniofacial abnormality. In a
study of eustachian tube function in the ears of
Japanese children and adults who had chronic
perforations, Iwano and colleagues found
impaired active opening function of the tube.199
They concluded that the tube was functionally
obstructed; however, organic (ie, mechanical or
anatomic) obstruction was also considered to be
involved in the pathogenesis in adults.
One possible mechanism that can cause
chronic suppurative middle-ear infection is an
allergic reaction from a tympanostomy tube, as
described in one child by Dohar.200 But this is an
extremely unusual case. Most presumed similar
cases are not truly an allergic reaction to the
components of a tympanostomy tube but acute
and chronic infection owing to the middle ear
Complications and Sequelae: Intratemporal
being nonintact and bacterial contamination
from the external canal or reflux of nasopharyngeal secretions into the middle ear.127
Microbiology. The bacteria that cause the
initial episode of AOM and perforation or acute
otorrhea through a tympanostomy tube are
usually not those that are isolated from chronic
suppurative otitis media.118 The most common
organism isolated from around the world is P.
aeruginosa; S. aureus is also found, but less
commonly.201–206 Table 6 shows the frequency of
bacteria isolated from children with chronic
suppurative otitis media at the Children’s
Hospital of Pittsburgh.207 More recently,
MRSA has been isolated from draining ears.119
Anaerobic bacteria were isolated infrequently in
this study. Anaerobic bacteria have been isolated
from ears with chronic suppurative otitis media,
but whether they are true pathogens remains to
be demonstrated. Brook isolated Bacteroides
melaninogenicus in 40% and Peptococcus species
Table 6. BACTERIOLOGY OF OTORRHEA IN 51
CHILDREN (80 EARS) WITH CHRONIC SUPPURATIVE
OTITIS MEDIA
Bacteria Isolated
Pseudomonas aeruginosa
Staphylococcus aureus
Diphtheroids
Streptococcus pneumoniae
Haemophilus influenzae
(nontypeable)
Bacteroides species
Candida albicans
Candida parapsilosis
Enterococcus
Acinetobacter
Staphylococcus epidermidis
Morganella morganii
Providencia stuartii
Klebsiella species
Proteus species
Serratia marcescens
Moraxella
Pseudomonas cepacia
Providencia rettgeri
Pseudomonas maltophilia
Achromobacter xylosoxidans
Eikenella
Number of Isolates*
(N 5 118)
56
18
8
7
6
3
2
2
2
2
1
1
1
1
1
1
1
1
1
1
1
1
Adapted from Kenna MA et al.207
*Number exceeds 80 because more than 1 organism was isolated in 38 ears.
357
in 35% of middle-ear exudates; the collection of
exudate was performed through the perforation
in the tympanic membrane with use of an 18gauge needle covered by a plastic cannula.208
There have also been reports of isolation
of unusual organisms, such as Mycobacterium
tuberculosis, Mycobacterium chelonae, Mycobacterium avium-intracellulare, Blastomyces dermatitidis, Actinomyces, Alcaligenes piechaudii,
and Candida species.120,121,209–216
Pathology. It is important to understand the
pathologic process of chronic suppurative otitis
media because the decision for or against surgical
intervention may depend on the pathologic
changes in the middle ear and mastoid. These
include edema, submucosal fibrosis, and infiltration with chronic inflammatory cells, which
together cause thickening of the mucous membrane.217 Polyps may result from excessive
mucosal edema; in the more advanced stage,
there may be polypoid tissue and granulation
tissue and osteitis of the mastoid bone, ossicles,
and labyrinth. Adhesive otitis media and sclerosis of bone may occur with healing.
Tympanosclerosis may also be present and is
commonly associated with this disease in
Alaskan (Eskimo) natives.140 If intensive medical
treatment is instituted early, these pathologic
changes may be reversible without surgery. When
long-standing chronic disease has led to irreversible changes, however, middle-ear and mastoid
surgery is usually indicated to eradicate the
infection.
Diagnosis. A purulent, mucoid, or serous
discharge through a ‘‘central’’ perforation of the
tympanic membrane for at least 2 or 3 months is
evidence of chronic suppurative otitis media. A
polyp will frequently be seen emerging through
the perforation or tympanostomy tube (Figure
13), which must be distinguished from a tumor in
the external canal.218 The size of the perforation
has no relation to the duration or severity of the
disease, but the defect frequently involves most
of the pars tensa. There is no otalgia, mastoid or
pinna tenderness, vertigo, or fever. When any of
358
OTITIS MEDIA IN INFANTS AND CHILDREN
Figure 13. Aural polyp in external auditory meatus. The polyp came
through a large perforation of an ear with chronic suppurative otitis
media.
these signs or symptoms are present, the examiner should look for a possible suppurative
intratemporal complication, such as mastoiditis
or labyrinthitis, or an intracranial complication
(see Chapter 10).219 A search for the underlying
cause of the infection may reveal paranasal
sinusitis, which must be actively treated because
the ear infection may not respond to medical
treatment until the sinusitis resolves. An upper
respiratory tract allergy or a nasopharyngeal
tumor may also contribute to the pathogenesis of
chronic suppurative otitis media and will need to
be managed appropriately.
The discharge should be appropriately examined by a Gram-stained smear and cultured as
described earlier (see ‘‘Acute Perforation with
Otitis Media’’).
One of the most important parts of the
evaluation is a complete examination of the ear
canal, the tympanic membrane, and, if the
perforation is large enough, the middle ear.
This should be done with the aid of the
otomicroscope. If a satisfactory examination
cannot be performed with the child awake, an
examination under general anesthesia will be
necessary. At this time, the discharge can be
aspirated and a specimen for culture can be
obtained from the middle ear. A search for a
polyp or unsuspected cholesteatoma or neoplasm
should also be conducted.
A conductive hearing loss usually accompanies chronic suppurative otitis media. If a hearing
loss greater than 20 to 30 dB is found, the ossicles
may be involved. However, the patient may also
have a sensorineural component, which is most
likely due to a serous labyrinthitis.26 Impedance
testing may be helpful if purulent material in the
ear canal prevents adequate visualization of the
eardrum to identify a possible perforation. If a
perforation is present, the measured volume of
the external canal will be larger than expected.
However, the tympanometric pattern may be
flat, despite the presence of a perforation, if the
volume of air in the middle ear and mastoid is
small. When this is suspected, the pressure on the
pump-manometer of the impedance audiometer
can be increased in an attempt to force open the
eustachian tube. If the tube can be opened with
positive air pressure from the pump-manometer,
a perforation must be present.
CT scans of the middle ear and mastoid
should be obtained when intensive medical
treatment (including intravenous antimicrobial
therapy) fails, the child has an early recurrence,
or cholesteatoma is suspected initially. In the
typical case, the sclerotic or undeveloped mastoid
appears ‘‘cloudy.’’ If a defect in the bone owing
to osteitis is present, however, the area will
appear on the CT scans. Discontinuity of the
ossicular chain, if present, may be visualized on
the CT scans.
Unusual causes of a chronic draining ear,
including neoplasms and eosinophilic granuloma, must be considered in the differential
diagnosis of chronic suppurative otitis media,
and in such cases, CT scans should be obtained
initially. Erosion of portions of the temporal
bone, especially the labyrinth, on the CT scan is
suggestive of tumor.
Management. Treatment of chronic suppurative otitis media is initially medical and
directed toward eliminating the infection from
Complications and Sequelae: Intratemporal
the middle ear and mastoid. Because the bacteria
most frequently cultured are gram-negative,
antimicrobial agents should be selected to be
effective against these organisms.122
Ototopical Medications. Ototopical medications can be safe and effective, but not all still
being prescribed are.125 A suspension containing
polymyxin B, neomycin sulfates, and hydrocortisone (Pediotic) and one that has neomycin,
polymyxin E, and hydrocortisone (Coly-Mycin)
have been used in the past but are no longer in
use in the United States. Caution is also advised
owing to the concern over the potential ototoxicity of these agents.220–223 In addition, an in vitro
susceptibility study showed that only 18% of
middle-ear isolates were sensitive to topical
neomycin.187 Some clinicians use topical tobramycin (with dexamethasone) (TobraDex)224 or
gentamicin (Garamycin) ophthalmic drops
instilled into the ear when Pseudomonas is
isolated, but, again, these agents are aminoglycosides and may therefore be ototoxic.134,225–229 A
recently convened consensus panel concluded
that there is relatively no indication to use these
potentially ototoxic agents today.230 More
important, none of these popular medications
are approved for use when there is a nonintact
tympanic membrane.129 Nevertheless, these ototopical agents are used widely and appear to be
effective for treating chronic suppurative otitis
media.231 Clinicians who have employed them
with apparent success think that if the infection is
not eliminated, it, too, may cause damage to the
inner ear. The bacteria, or their by-products, may
enter the inner ear through the round window
during a middle-ear infection.22,24
The US Food and Drug Administration
(FDA) has approved ofloxacin otic solution
(Floxin Otic), an ototopical agent, for use in
children when AOM with otorrhea occurs when
a tympanostomy tube is in place. At present, it is
the only topical antimicrobial agent that has been
demonstrated to be safe and effective126,128,232,233
and approved for this indication in children. It is
also approved for adults who have chronic
suppurative otitis media, but it is currently not
359
approved for this indication in children,234 even
though it has been reported to be effective in this
age group.235 Topical ofloxacin has been shown
to be more effective than the combination of
neomycin–polymyxin B–hydrocortisone otic
drops in adults with chronic suppurative otitis
media.236
Even though ciprofloxacin is not approved, it
appears to be effective for chronic suppurative
otitis media.237–241 One study showed that topical
ciprofloxacin was more effective than topical
gentamicin for chronic suppurative otitis media
in adults,242 and another showed that this
antibiotic and tobramycin are equally effective
in adults with this infection.243 No apparent
ototoxicity has occurred after use of this ototopical agent in patients with chronic suppurative
otitis media.244 In addition, topical ciprofloxacin
did not cause ototoxicity in the monkey model of
chronic suppurative otitis media.245 There is still
no consensus about the potential efficacy of
adding a corticosteroid component to the antimicrobial agent, but the addition of a steroid
may hasten resolution of the inflammation.246
Recently, the combination of ciprofloxacindexamethasone otic suspension (Ciprodex) has
become available for treatment of otorrhea.
Roland and colleagues reported success in
treating children who had AOM with otorrhea
through a tympanostomy tube,130 and it is
effective when granulation tissue is present on
the eardrum and around the tube.131 The
consensus panel concluded that these two new
fluoroquinolone agents that are now available
provide a safe and effective alternative to the
older, potentially ototoxic agents.133 Thus, the
lack of reported clinical trials in children with
chronic suppurative otitis media notwithstanding, it seems reasonable today to use ofloxacin or
ciprofloxacin-dexamethasone initially in children
who have uncomplicated chronic suppurative
otitis media, especially since they are not ototoxic
and are effective when the tympanic membrane is
not intact (ie, following insertion of a tympanostomy tube).125
Other ototopical agents have been used for
treatment of chronic suppurative otitis media
360
OTITIS MEDIA IN INFANTS AND CHILDREN
although not approved for this use by the Food
and Drug Administration. Ciprofloxacin with
hydrocortisone (Cipro HC) has been used for
treatment of external otitis in both children and
adults but is not indicated when the tympanic
membrane is not intact. As an alternative to an
antibiotic topical agent, some clinicians recommend antiseptic drops. An antiseptic ototopical
agent (aluminum acetate) was found to be as
effective as topical gentamicin sulfate for otorrhea in a randomized clinical trial reported from
the United Kingdom.247 Thorp and colleagues
evaluated the in vitro activity of acetic acid and
aluminum subacetate (Burow’s solution) and
found both to be effective against the major
pathogens causing chronic suppurative otitis
media.248 More recently, Kashiwamura and
colleagues also found Burow’s solution to be
effective.132 Burow’s solution was somewhat
more effective than acetic acid. Antiseptic drops
(eg, acetic acid) are commonly used in underdeveloped countries and are reputed to be
effective. Because of cost and availability, antibiotic ototopical agents are used when antiseptic
drops are ineffective. But, again, these agents are
currently not recommended in the face of an
open eardrum.133
Table 3 provides a list of ototopical agents
currently (2006) approved by the FDA for ear
infections. As stated before, only ofloxacin otic
solution and ciprofloxacin-dexamethasone otic
suspension solution are approved for children
when the tympanic membrane is nonintact and
then only when a tympanostomy tube is present.
Nevertheless, other agents, such as ciprofloxacin
with hydrocortisone, may be beneficial for use in
children with this middle-ear and mastoid infection. The advantage of quinolone topical agents
is that there is no evidence of ototoxicity in
animal models, which had been reported with use
of the aminoglycosides. With the growing concern regarding the emergence of multidrugresistant bacterial otic pathogens, an ototopical
agent is desirable because it is hoped that the use
of a high concentration of the drug directed at
the site of infection will prevent emergence of
resistant organisms; to date, we have not seen
resistance developing following use of these new
quinolone ototopical agents.133
If topical antibiotic medication is elected, the
child should ideally return to the outpatient
facility daily to have the discharge thoroughly
aspirated or swabbed (ie, aural toilet, ear mopping) and to have the ototopical medication
directly instilled into the middle ear through the
perforation or tympanostomy tube by use of an
otoscope or otomicroscope. Frequently, the
discharge rapidly improves within a week with
this type of treatment, after which the eardrops
may be administered at home until there is
complete resolution of the middle-ear–mastoid
inflammation. When daily administration by the
physician is not feasible, the parent or caregiver
can administer the drops.
Oral Antimicrobial Agents. Oral antibiotics
that are approved for treatment of AOM may be
effective if the bacterium is susceptible, but
because the organism is usually P. aeruginosa,
agents that are currently approved for children
will usually not be effective; approximately 40%
of Pseudomonas is susceptible in vitro to
trimethoprim-sulfamethoxazole.249 Despite these
potential drawbacks, many clinicians administer
a broad-spectrum oral antibiotic in the hope that
the underlying infection is caused by the usual
bacteria that are isolated from ears with
AOM.123 In a report of a randomized clinical
trial conducted in Kenya, Smith and colleagues
compared (1) oral amoxicillin-clavulanate, dry
mopping of the ear, and ototopical antibioticcortisone drops; (2) dry mopping alone; and (3)
no treatment.231 They found the combination of
oral antibiotic and topical agents to be statistically more effective than dry mopping alone or
no treatment. However, a randomized clinical
trial found that topical ofloxacin was more
effective than systemic amoxicillin-clavulanate
(without eardrops) in adults with chronic suppurative otitis media.250 At present, we recommend for initial treatment an approved
ototopical quinolone and an oral agent if the
bacteria are susceptible.
Complications and Sequelae: Intratemporal
Orally administered ciprofloxacin has been
shown to be effective in adults and Israeli
children who had chronic suppurative otitis
media, but this agent is currently not approved
for patients younger than 17 years in the United
States.204,251–253 In addition to aural toilet,
topical ciprofloxacin was effective management
in Australian Aboriginal children.241 Some clinicians advocate a course of an oral quinolone for
chronic suppurative otitis media when the
causative organism is Pseudomonas and obtain
oral consent from the parent or guardian. Safety
concerns are of less concern today given the lack
of serious side effects in children who have cystic
fibrosis and who have taken these drugs for
many years.
When ototopical agents, oral antimicrobial
agents, or both are used, the child should be
reexamined in about 1 week, when any adjustments can be made in the medications after the
results of the microbiologic studies are available.
After approximately 1 week, there should be
cessation of the discharge or marked improvement. If, indeed, the otorrhea is improving, the
child is reexamined periodically thereafter until
resolution occurs. If there is no improvement
after 1 to 2 weeks, other treatment options
should be considered, such as parenteral antimicrobial therapy. As noted above, a systemic
course of a quinolone (with appropriate parental
consent) may be preferable to initiating parenteral treatment when Pseudomonas is the offending bacterium.
Parenteral Antimicrobial Agents. If treatment
of the child with the administration of ototopical
agents, with or without an oral antimicrobial
agent, has failed, the patient should receive a
parenteral b-lactam antipseudomonal drug, such
as ticarcillin, piperacillin, or ceftazidime; empirically, ticarcillin-clavulanate is usually selected
because Pseudomonas, with and without S.
aureus, is frequently isolated; the results of the
culture and susceptibility studies dictate the
antimicrobial agent ultimately chosen (see
Chapter 8).203,207,254 Dagan and colleagues in
Israel and Arguedas and colleagues in Costa Rica
361
reported excellent results with the use of ceftazidime.255,256 In Finland, Vartiainen and
Kansanen also recommended a trial of intravenous antimicrobial therapy before considering
mastoid surgery.257 The regimen can be altered
when the results of culture and susceptibility tests
are available. Also, the external canal purulent
material and debris (and middle ear, if possible)
are aspirated and the ototopical medication is
instilled daily. This method of treatment is
usually performed with the child hospitalized,
but it can be carried out on an ambulatory
basis.255 The intravenous line can be inserted as
an operative procedure or in the radiology suite.
In about 90% of children, the middle ear will
be free of discharge and the signs of chronic
suppurative otitis media will be greatly improved
or absent within 5 to 7 days. Kenna and
colleagues conducted a study of 36 pediatric
patients with chronic suppurative otitis media in
which all received parenteral antimicrobial therapy and daily aural toilet.203 Medical therapy
alone resolved the infection in 32 patients (89%);
4 children required tympanomastoidectomy. The
investigators later increased the study group to
66 children and reported similar short-term
results; 89% had dry ears after intravenous
antibiotic therapy.190 In a follow-up of that
study, 51 of the original 66 were evaluated for
their long-term outcomes.207 Of these 51 children, 40 (78%) had resolution of their initial or
recurrent infection after medical treatment and
11 (22%) had to eventually have mastoid surgery.
Failure was associated with older children and an
early recurrence. Englender and colleagues did
serotyping and pyocin typing of P. aeruginosa of
142 patients, including children, and found that if
the patient had a recurrence with a different type,
medical treatment was frequently successful.258 If
the patient had recurrence of the otorrhea with
the same type, medical therapy usually failed and
the patient required mastoid surgery. Leiberman
and colleagues found that when children had an
early recurrence, they were less likely to benefit
from either medical treatment, including intravenous antibiotics, or surgical management.259
(For details of the surgical technique of mastoi-
362
OTITIS MEDIA IN INFANTS AND CHILDREN
dectomy for chronic suppurative otitis media, see
Bluestone.152)
If resolution occurs during hospitalization,
the child can be discharged and receive the
parenteral antibiotic and eardrops (by the parent
or caregiver) for a period of 10 to 14 days at
home. The patient should be observed at periodic
intervals to watch for signs of spontaneous
closure of the perforation, which frequently
happens after the middle ear and mastoid are
no longer infected. Appropriate intensive medical
treatment should be attempted before major ear
surgery is recommended because the outcome of
surgery is not as favorable when medical treatment is withheld.205
Surgery. When chronic suppurative otitis
media fails to respond to intensive medical
therapy (ie, intravenous antibiotics, aural toilet,
and ototopical medications) within several days,
surgery on the middle ear and mastoid (ie,
tympanomastoidectomy) may be required to
eradicate the infection. A CT scan should be
obtained (see earlier). Failures usually occur
when there is an underlying blockage of the
communication between the middle ear and
mastoid (ie, aditus ad antrum), irreversible chronic
osteitis, cholesteatoma (or tumor), or early recurrence with the same causative organism.207
Insertion of a tympanostomy tube can be
helpful if the chronic suppurative otitis media is
associated with a perforation that is too small to
permit adequate drainage or if the perforation
frequently closes, only to reopen with episodic
drainage. On the other hand, if the chronic
infection is related to a tympanostomy tube (ie,
the middle-ear air cushion is absent), some
clinicians advocate removal of the tube, hoping
that the infection will subsequently subside.
However, the recurrent and chronic ear infections for which the tube was originally inserted
frequently recur. There may be some merit in
attempting this approach in a child who has had
a long-standing retained tube.
Prevention of Recurrence. With an understanding of the pathogenesis of chronic suppura-
tive otitis media (ie, chronic otorrhea is preceded
by acute otorrhea), the most effective way to
prevent recurrence of otorrhea when the tympanic membrane is intact and an attack of AOM
occurs is to promptly, appropriately, and adequately treat the infection with the usual oral
antimicrobial agents recommended for AOM. If
the tympanic membrane is not intact (ie,
perforation or a tympanostomy tube is present
without evidence of infection), early treatment of
acute otorrhea (ie, AOM) should likewise be
effective. Treatment with an oral antimicrobial
agent may be enhanced by adding an ototopical
agent to prevent a secondary infection with
external ear canal organisms, such as
Pseudomonas.
When a perforation (or tympanostomy tube)
is present, in the absence of middle-ear–mastoid
infection, and it is desirable to maintain middleear ventilation through a nonintact eardrum,
recurrent episodes of otorrhea can usually be
prevented with antimicrobial prophylaxis (eg,
amoxicillin).146 If a tympanostomy tube is present and the middle ear is now disease free, its
removal may restore middle-ear–eustachian tube
physiology (ie, prevent reflux or insufflation of
nasopharyngeal secretions). Yet removal of
tympanostomy tubes may not be desirable,
especially in infants and young children, and in
these cases, antimicrobial prophylaxis should
also be considered until the tubes spontaneously
extrude. As an alternative to long-term, low-dose
systemic antimicrobial prophylaxis, with its
potential for development of antibiotic-resistant
bacteria, prevention may be effective by the
instillation of one of the new and approved
quinolone ototopical agents (ie, ofloxacin otic
solution or ciprofloxacin-dexamethasone suspension) into the ear canal at the onset of an upper
respiratory tract infection and maintained for the
duration of the viral infection.
If the child has a chronic perforation that is
now dry, tympanoplastic surgery should be
considered. The same factors should be considered in deciding to repair an eardrum perforation
in children as described before in relation to
removing a tympanostomy tube.9
Complications and Sequelae: Intratemporal
Complications and Sequelae. The most
common sequela of chronic suppurative otitis
media is chronic hearing loss, with the potential
deficits related to this disability. The chronic
infection may result in permanent conductive
hearing loss because of damage to the ossicles,
and sensorineural loss may also occur. Chronic
suppurative otitis media can also progress into
one or more of the intratemporal (extracranial)
suppurative complications (acute mastoiditis,
acute labyrinthitis, facial paralysis) or an intracranial suppurative complication, which will
require
immediate
surgical
intervention.
Intracranial complications caused by chronic
suppurative otitis media occur with a frequency
equal to or greater than that of those due to
cholesteatoma. Not only is this finding important
in underdeveloped countries where chronic suppurative otitis media is common, it has also been
reported from industrialized nations (see Chapter
10).260
A child who has a chronic suppurative
aural discharge and who develops one or more
of the intratemporal suppurative complications
(such as acute mastoid osteitis, labyrinthitis, and
facial paralysis) or an intracranial suppurative
complication requires immediate surgical intervention.261 It is not uncommon for a cholesteatoma to be present when an ear with chronic
suppurative otitis media fails to respond to
intensive medical treatment, even though no
preoperative evidence for the presence of cholesteatoma was identified by otomicroscopy or
imaging. The cholesteatoma is usually found in
the middle ear (and mastoid) following migration
of the squamous epithelium through the perforation in the tympanic membrane. When a
cholesteatoma is found, surgical removal is
indicated as outlined later in this chapter.
Role of the Primary Care Physician. Many
children who have chronic suppurative otitis
media can be effectively managed by the primary
health care provider with ototopical antimicrobial medications, oral antibiotic agents, or both.
When these measures fail, the child requires
parenteral administration of an antimicrobial
363
agent. Referral to an otolaryngologist is advisable in the following situations:
N
N
N
N
N
A suppurative complication, cholesteatoma, or
tumor is present or suspected.
An otomicroscope is necessary to completely
examine the ear.
An examination under general anesthesia is
required to completely evaluate the ear (and
child, eg, the nose and pharynx).
A child does not respond to intensive medical
therapy because tympanomastoidectomy is
usually required.
Prevention of recurrence involves possible
adenoidectomy, surgery for chronic or recurrent paranasal sinusitis, surgical repair of a
tympanic membrane perforation (ie, tympanoplasty), or removal of a tympanostomy tube.
MASTOIDITIS
Mastoiditis is a potential complication of acute
and chronic middle-ear infections.1,115 In the
preantibiotic era, acute mastoiditis was the most
common infection for which infants and children
were hospitalized. Since the widespread use of
antimicrobial agents, the incidence has fallen
dramatically, but the clinician should always be
aware that acute mastoiditis remains the most
common suppurative complication of acute otitis
media.262 In addition, there is some evidence that
the incidence of acute mastoiditis has increased
in certain geographic areas263–265 and may be
related to withholding antimicrobial agents in
children who have AOM.266,267 But some studies
report that acute mastoiditis may be the first
evidence of ear infection and that initial treatment with an antimicrobial agent would not have
prevented the mastoiditis.268,269 Also, some
reports concluded that there has been no increase
in the incidence of acute mastoiditis during the
recent past.270,271 The incidence of acute mastoiditis appears to be greater in southern Israel than
the rates reported elsewhere and was related to
S. pyogenes as a common causative bacterium
but not penicillin-nonsusceptible S. pneumoniae.272 But in Dallas, a recent report implicated
364
OTITIS MEDIA IN INFANTS AND CHILDREN
resistant S. pneumoniae as the cause of an
increase in suppurative complications of
AOM.273
Chronic mastoiditis that develops after an
episode of acute mastoiditis has also decreased
during the past 50 years for similar reasons.
However, chronic mastoiditis is still a major
problem when chronic suppurative otitis media is
present, especially in racial groups and geographic areas in which this disease is common.115
Both acute and chronic mastoiditis can occur in
the presence of cholesteatoma.274 Thus, both
acute and chronic mastoiditis still occur and may
be responsible for significant morbidity and lifethreatening infection, especially from intracranial
extension of the disease.275–279
Anatomy, Pathogenesis, and Pathology
At birth, the mastoid consists of a single cell, the
antrum, connected to the middle ear by a small
channel, the aditus ad antrum. Pneumatization
of the mastoid bone takes place soon after birth
and is usually extensive by the age of 2 years. The
process may continue throughout life. The
clinical importance of the mastoid is related to
contiguous structures, including the posterior
cranial fossa, the middle cranial fossa, the
sigmoid and lateral sinuses, the canal of the
facial nerve, the semicircular canals, and the
petrous tip of the temporal bone. The mastoid air
cells are lined with modified respiratory mucosa,
and all are interconnected with the antrum
(Figure 14A).
Infection in the mastoid proceeds after
middle-ear infection through the following
stages:
N
N
N
Hyperemia and edema of the mucosal lining of
the pneumatized cells
Accumulation of serous and then purulent
exudates in the cells
Demineralization of the cellular walls and
necrosis of bone owing to pressure of the
purulent exudate on the thin bony septa and
ischemia of the septa, caused by a decrease in
blood flow
Figure 14. Schematic depiction of the right eustachian tube, middle
ear, and mastoid air cell anatomy. The middle ear is normally
connected to the mastoid air cells through the narrow aditus ad
antrum (A). When the middle ear and mastoid are infected, the aditus
ad antrum can become obstructed by mucosal edema and
granulation tissue, which has been termed aditus block or the
bottleneck (B).
N
N
Formation of abscess cavities owing to coalescence of adjacent cells after destruction of cell
walls
Escape of pus into contiguous areas
This process may halt at any stage with
subsequent resolution. However, when infection
persists for more than a week or 10 days,
inflammatory granulation tissue forms in the
pneumatic cavity. A hypertrophic osteitis develops that results in thickening and sclerosis of
cellular walls and a reduction in the size of the
cellular space. There may be repeated cycles of
absorption and deposition of bone. If the
infection remains chronic but low grade, there
is thickening of the mucosa caused by a fibrinous
exudate, which may become organized and lead
to permanent adhesions. Columnar metaplasia
Complications and Sequelae: Intratemporal
365
with new gland formation may result in extensive
production of mucus in the former cells.
Mastoiditis can be classified into acute and
chronic types.10 Acute mastoiditis is further
subdivided according to the pathologic stage
present, which has clinical significance because
management depends on the stage of the
disease.280 Unfortunately, because of failure to
appreciate the natural history and pathologic
features of acute mastoiditis, there is confusion in
the minds of clinicians, as well as in the current
literature, regarding the most appropriate management of each stage.
Mastoiditis without Periosteitis or Osteitis
Because the mastoid gas cell system is connected
to the distal end of the middle ear, most likely all
episodes of otitis media are associated with some
inflammation of the mastoid. Thus, mastoiditis
can be a natural extension and part of the
pathologic process of middle-ear inflammation;
the mastoid may be involved in AOM or otitis
media with effusion (of any duration).
Diagnosis
The diagnosis is commonly made after CT scans
or magnetic resonance imaging (MRI) studies are
obtained for another problem (eg, sinusitis, head
trauma) in a child who has no signs or symptoms
referable to the ears, in which case, it is an
incidental finding.281 No specific signs or symptoms of mastoid infection (eg, protrusion of the
pinna, postauricular swelling, tenderness, pain,
and erythema) are present in this most common
stage of mastoiditis. Imaging of the mastoid area
frequently reveals cloudy mastoids, which indicates inflammation, but no mastoid osteitis (ie,
bony erosion of the mastoid air cells) is evident
(Figure 15).
Management and Outcome
The process is usually reversible as the middleear–mastoid infection resolves, either as a natural
process or as a result of medical management (eg,
antimicrobial therapy). Thus, with no periosteal
involvement of the postauricular region, osteitis
Figure 15. Mastoiditis without periosteitis or osteitis. Computed
tomogram of the left temporal bone of a child with acute otitis media
in which the mastoid air cells show signs of inflammation without
osteitis; the pinna was not displaced, and no periosteal involvement
was present. The diagnosis was acute mastoiditis without periosteitis
or osteitis, which commonly occurs during an episode of acute otitis
media and usually resolves when the middle-ear infection is
eliminated.
of the mastoid, or subperiosteal abscess, this
stage of mastoiditis is not a suppurative complication of otitis media.
When this stage of mastoiditis is diagnosed,
such as by CT scan, in a child who has an episode
of AOM, the management is the same as
recommended for AOM because the involvement
of the mastoid is a natural extension of the
middle-ear infection (see Chapter 8). Indications
for tympanocentesis (diagnostic aspiration of the
middle ear) are the same as when AOM is
diagnosed and the status of the mastoid is
undetermined (by CT or MRI), such as when
the patient is severely ill or toxic, fails to improve
rapidly while receiving appropriate and adequate
antibiotic treatment, develops otitis media while
receiving antimicrobial agents, develops otitis
media in the newborn period, is immunologically
deficient, or has a suppurative complication.
Myringotomy is indicated when drainage of the
middle ear is desirable, such as when the child
366
OTITIS MEDIA IN INFANTS AND CHILDREN
has severe otalgia or when a suppurative
complication is suspected or is present (see
Chapter 7).
When acute infection in the mastoid (and
usually middle ear) does not resolve at this stage,
the disease can rapidly progress to acute mastoiditis with periosteitis. The next stage is acute
mastoid osteitis, which can occur with or without
the presence of a subperiosteal abscess.
When imaging of the head reveals the
incidental finding of inflammation of the mastoid
gas cells in a child who has an episode of otitis
media with effusion (regardless of the duration of
the effusion), management is the same as
recommended for this middle-ear inflammation
when the status of the mastoid is unknown, that
is, CT or MRI is not obtained (see Chapter 8).
Acute Mastoiditis with Periosteitis
When infection within the mastoid spreads to the
periosteum covering the mastoid process, periosteitis can develop. The route of infection from the
mastoid cells to the periosteum is by venous
channels, usually the mastoid emissary vein. The
condition should not be confused with a subperiosteal abscess, the management of which
usually requires a mastoidectomy. Periosteitis
frequently responds to medical treatment and
tympanocentesis or myringotomy.
Epidemiology
Before the antibiotic era, the incidence of acute
mastoiditis as a complication of AOM was high.
In 1938, the rate was 20%, whereas it was 2.8% 10
years later (with an almost 90% reduction in the
mortality rate during that period), and in some
studies, it dropped almost to zero.282–284 At the
Children’s Hospital of Pittsburgh between 1980
and 1995, there were 72 infants and children with
acute mastoiditis, but only 18 (25%) required a
mastoidectomy; the remaining 54 (75%) did not
have a mastoidectomy.262 The majority of
children who develop acute mastoiditis today
most likely have acute mastoiditis with periosteitis. The growing enthusiasm for withholding
antimicrobial therapy today in some countries
will most likely result in an increase in this
suppurative complication.
Pathogenesis
Infection in the mastoid air cells, which is
frequently part of an episode of AOM, usually
resolves spontaneously or after effective antimicrobial treatment. The effusion within the
mastoid air cells drains into the middle ear,
which, in turn, drains down the eustachian tube
(ie, the clearance function of the tube). The
narrow communication between the middle ear
and the mastoid air cells is the aditus ad antrum
(see Figure 9–14A). Physiologically, the mastoid
air cell system is most likely a reservoir of gas for
the middle ear, and this narrow passage makes it
more difficult for middle-ear infection to enter
the mastoid. When infection is in the mastoid,
however, the aditus ad antrum can become
obstructed by edema and granulation tissue
(Figure 9–14B). This obstruction has been called
the bottleneck and has been implicated in the
pathogenesis of acute mastoiditis. If the obstruction persists, acute mastoiditis with periosteitis
can develop, which can then progress into acute
mastoid osteitis (with and without subperiosteal
abscess) and further progress into another
suppurative complication in the temporal bone
or the intracranial cavity.
Clinical Presentation and Diagnosis
The child has the classic signs and symptoms of
AOM, such as fever and otalgia, but also
postauricular erythema; mild tenderness and
some edema may also be present in the postauricular area. The pinna may or may not be
displaced inferiorly and anteriorly, with loss of
the postauricular crease.285 Subperiosteal abscess
is absent. Examination of the eardrum typically
reveals evidence of AOM. However, the middle
ear may be effusion free in the presence of acute
mastoiditis if there is an obstruction of the aditus
ad antrum. The middle-ear effusion drains down
the eustachian tube, but the infection in the
mastoid cannot drain into the middle ear. Table 7
shows the age and frequency of the presenting
signs and symptoms of 72 infants and children
Complications and Sequelae: Intratemporal
Table 7. AGE, PRESENTING SYMPTOMS, AND SIGNS OF
Table 8. HEARING STATUS IN 41 INFANTS AND
72 INFANTS AND CHILDREN WITH ACUTE MASTOIDITIS
CHILDREN WITH ACUTE MASTOIDITIS
Patients (%)
Age (yr)
0–3
4–6
7–12
13–18
Symptoms
Otalgia
Postauricular pain
Fever
Otorrhea
Upper respiratory infection
Irritability
Hearing loss
Signs
Postauricular tenderness
Pinna protrusion
Postauricular erythema
Middle-ear effusion
Tympanic membrane erythema
Contralateral middle-ear abnormalities
Middle-ear effusion
Tympanic membrane bulging
Tympanic membrane erythema
Tympanic membrane perforation
Tympanic membrane bulging
Otorrhea
Fever $ 38.3uC
Tympanic membrane perforation
Postauricular mass
Cervical adenopathy
Postauricular abscess
Sagging of posterior auditory canal wall
35
12
17
7
(50.0)
(16.7)
(23.6)
(9.7)
62
58
51
29
17
16
6
(86.1)
(80.6)
(70.8)
(40.3)
(23.6)
(22.2)
(8.3)
58
51
51
48
42
35
20
8
6
1
34
24
24
13
13
12
9
2
(80.6)
(70.8)
(70.8)
(66.7)
(58.3)
(48.6)
(27.8)
(11.1)
(8.3)
(1.4)
(47.2)
(33.3)
(33.3)
(18.1)
(18.1)
(16.7)
(12.5)
(2.8)
Adapted from Goldstein NA et al.262
who had acute mastoiditis at the Children’s
Hospital of Pittsburgh from 1980 to 1995 (some
of these patients had acute mastoid osteitis with
and without subperiosteal abscess). In this series,
half were 3 years of age or younger; two-thirds
were younger than 7 years. Also, only 28% of
these children were diagnosed as having a
middle-ear effusion, which is clinically important
because this finding emphasizes the point made
earlier that mastoiditis can be present despite the
lack of otitis media; the middle-ear effusion
resolves, but the infection in the mastoid persists.
Table 8 shows the hearing status of 41 of
these patients who received an audiometric
test.262 About half of these 41 children had
hearing in the normal range and half had
abnormal hearing levels, but most of the severely
ill children did not have an evaluation of hearing
Audiologic Findings
Patients (%)
Normal range
Abnormal
Conductive loss (dB)
30–39
40–49
50–59
Mixed loss (dB)
60–69
80–99
Sensorineural (dB)
40–49
Profound
21 (51)
20 (49)
367
4 (10)
8 (20)
2 (5)
2 (5)
2 (5)
1 (2)
1 (2)
Adapted from Goldstein NA et al.262
before management, which usually included
mastoidectomy.
For this stage of acute mastoiditis, a CT scan
of the temporal bones (and intracranial cavity)
should be obtained to determine whether osteitis
of the mastoid is present. A CT scan is not
mandatory if the infection is limited to the
middle ear and mastoid, the child is not severely
ill or toxic, and improvement is rapid after
tympanocentesis-myringotomy and parenterally
administered antimicrobial therapy.
Differential Diagnosis
The differential diagnosis of a child who has a
suspect acute mastoiditis with periosteitis
includes perichondritis of the pinna and external
otitis. The typical presentation of a child who has
a perichondritis of the pinna is swelling and
erythema of the outer ear, which may spread to
the periosteum of the postauricular area, but the
postauricular crease is usually obliterated and
external otitis and middle-ear effusion are absent
unless a concurrent, unrelated otitis media is
present. External otitis can also spread to the
postauricular area; like perichondritis, it will
obliterate the postauricular crease. In contrast to
these two infections, the postauricular crease is
still evident when the perichondritis is an
extension of acute mastoiditis, and middle-ear
effusion is usually—but not always—present.
When the acute mastoiditis has progressed to
a subperiosteal abscess, the postauricular swel-
368
OTITIS MEDIA IN INFANTS AND CHILDREN
ling may be misdiagnosed as an enlarged lymph
node. Lymph node enlargement in the postauricular area is typically due to a scalp infection,
dermatitis, or an insect bite above the affected
ear, and middle-ear effusion is absent. The lymph
node is well circumscribed, usually freely movable in all four directions, and most often not
tender to touch. On the other hand, a subperiosteal abscess, secondary to acute mastoiditis,
does not move readily, is not well circumscribed,
and is tender to touch (Table 9).
Microbiology
Middle-ear aspirates reveal bacterial pathogens
similar to those isolated from children’s ears that
have uncomplicated acute middle-ear infection,
such as S. pneumoniae, S. pyogenes, or H.
influenzae, but there may be an unusual organism, such as P. aeruginosa, if there has been
otorrhea.286,287 Indeed, the leading pathogen in
Israel today is Pseudomonas when the child has
had recurrent episodes of AOM.288 Also, tuberculosis has been reported to be the causative
bacterium in mastoiditis, not only in Korea,289
but also in Chicago.290 Table 10 shows the type
and frequency of bacteria isolated from 65
infants and children who had acute mastoiditis
(acute mastoiditis with periosteitis and acute
mastoid osteitis) diagnosed at the Children’s
Hospital of Pittsburgh between 1980 and
1995.262 Cultures were obtained from one or
more of the following sites: the external auditory
canal when otorrhea was present, the middle ear
Table 10. BACTERIOLOGY OF EFFUSIONS, OTORRHEA,
AND MASTOIDS IN 65 INFANTS AND CHILDREN WITH
ACUTE MASTOIDITIS
Organism
Number of isolates (%)
Streptococcus pneumoniae
Pseudomonas aeruginosa
Streptococcus pyogenes
Diphtheroids
Anaerobes
Others*
No growth
Total{
21
19
12
9
7
39
6
113
(32.3)
(29.2)
(18.5)
(13.9)
(10.8)
(60.0)
(9.2)
Adapted from Goldstein NA et al.262
*Coagulase-negative staphylococcus (23), b-hemolytic streptococcus (4),
Haemophilus influenzae (3), Micrococcus species (2), Moraxella catarrhalis
(1), Staphylococcus aureus (1), Staphylococcus species (1), Enterobacter
cloacae (1), Neisseria species (1), Enterococcus species (1), Citrobacter
diversus (1).
{
Total of isolates is greater than 100% because some cultures were
polymicrobial.
by tympanocentesis, or the middle ear, mastoid,
or both at the time of mastoidectomy. The most
common pathogenic bacteria were S. pneumoniae, P. aeruginosa, and S. pyogenes.
Management
The patient may be managed on an ambulatory
basis if the infection is not severe. However,
hospitalization is usually necessary because
parenteral antimicrobial therapy is frequently
needed, and most patients require an immediate
tympanocentesis (for aspiration and microbiologic assessment of the middle-ear–mastoid effusion) and myringotomy to drain the middle ear.
In the absence of an aditus ad antrum ‘‘block,’’
this should also drain the mastoid. If the child
Table 9. DIFFERENTIAL DIAGNOSIS OF POSTAURICULAR INVOLVEMENT OF ACUTE MASTOIDITIS WITH PERIOSTEITIS OR
ABSCESS
Postauricular Signs and Symptoms
Disease
Acute mastoiditis with
periosteitis
Acute mastoiditis with
subperiosteal abscess
Periosteitis of pinna with
postauricular extension
External otitis with postauricular
extension
Postauricular lymphadenitis
External
Canal
Middle-Ear
Crease*
Erythema
Mass
Tenderness
Infection
Effusion
May be absent
Yes
No
Usually
No
Usually
Absent
Maybe
Yes
Yes
No
Usually
Intact
Yes
No
Usually
No
No
Intact
Yes
No
Usually
Yes
No
Intact
No
Yes
(circumscribed)
Maybe
No
No
*Postauricular crease (fold) between pinna and postauricular area.
Complications and Sequelae: Intratemporal
has had recurrent attacks of AOM or has the
current episode of AOM superimposed on
chronic otitis media with effusion, insertion of a
tympanostomy tube is indicated. Insertion of a
tympanostomy tube is desirable and will enhance
drainage for a longer time than myringotomy
alone.193 Even though there have been reports
revealing that antibiotic treatment was successful
in curing some children, without the benefit of
tympanocentesis or myringotomy, aspiration of
the middle ear is an important diagnostic (and
therapeutic) procedure today. An antibiotic-resistant bacterial pathogen, such as multidrugresistant S. pneumoniae, may be the causative
organism, which may require an antimicrobial
agent not frequently used for AOM–mastoiditis,
such as vancomycin.262,286,287,291,292
Cultures for bacteria from the middle ear are
required to identify the causative organism. Antimicrobial susceptibility studies are important
for selecting the most effective antibiotic agent.
For empiric parenteral antimicrobial therapy,
cefuroxime sodium, ticarcillin disodium with
clavulanate potassium, or ampicillin-sulbactam
can be initiated until the results of Gram stain,
culture, and susceptibility studies of the middleear aspirates are available. If penicillin-resistant
S. pneumoniae is the possible pathogen, some
clinicians today also add vancomycin while
awaiting the culture and susceptibility report.
The periosteal involvement should resolve
within 24 to 48 hours after the tympanic
membrane has been opened for drainage and
adequate and appropriate antimicrobial therapy
has begun. Some recent reports indicate that
needle aspiration of the subperiosteal abscess, in
conjunction with intravenous antibiotic therapy
and myringotomy, is effective and thus avoids
mastoidectomy.293–295 A mastoidectomy should
be performed if the symptoms of the acute
infection (such as fever and otalgia) persist, the
postauricular involvement does not progressively
improve, or a subperiosteal abscess develops.
A CT scan can be helpful in the decision to
surgically intervene.296 A mastoidectomy is also
indicated if another intratemporal (extracranial)
suppurative complication (facial paralysis, labyr-
369
inthitis, petrous apicitis) or intracranial complication (meningitis, lateral sinus thrombosis, or
abscess of the epidural or subdural space or
brain) of otitis media is present.
Outcome
In the review by Goldstein and colleagues of the
72 infants and children with acute mastoiditis at
the Children’s Hospital of Pittsburgh, 54 (75%)
were managed conservatively with broadspectrum intravenous antibiotics and myringotomy, with and without tympanostomy tube
insertion.262 The other 18 (25%) required mastoidectomy. Of these 18 children, 14 (78%) had
one or more of the following: mastoid osteitis,
subperiosteal abscess, cholesteatoma, or another
suppurative complication (eg, facial paralysis). A
review from Australia by Harley and colleagues
related approximately the same experience as in
Pittsburgh.286 Between 1982 and 1993, 58 infants
and children were admitted to the Royal
Children’s Hospital of Melbourne, and of these,
45 (78%) were treated conservatively with intravenous antimicrobial therapy, with and without
tympanostomy tube insertion. The remaining 13
patients required mastoidectomy. Others have
also reported that the majority of children with
acute mastoiditis can be managed conservatively,
but other centers have reported that most of their
patients required a mastoidectomy.287,297–302 The
reasons for these conflicting reports are most
likely the lack of a uniform definition of the
disease, dissimilarity in the presentation of cases,
and variation in management. Our opinion is
that most patients with acute mastoiditis with
only periosteitis recover without the need for
mastoidectomy.
Immediate treatment at this stage of acute
mastoiditis is mandatory. Failure to provide
immediate treatment may result in development
of acute mastoid osteitis (with or without a
subperiosteal abscess) or, potentially more lifethreatening to the child, a suppurative complication such as meningitis or brain abscess.
In the absence of mastoid osteitis (with or
without subperiosteal abscess), the primary care
physician or pediatric infectious disease specialist
370
OTITIS MEDIA IN INFANTS AND CHILDREN
can provide the initial medical care for patients
with acute mastoiditis with periosteitis. However,
tympanocentesis-myringotomy is required, and
an otolaryngologist will be needed if the medical
specialists are untrained in this procedure.
Referral to an otolaryngologist is appropriate if
a mastoidectomy is indicated. Immediate referral
for surgical evaluation and management is
indicated when acute mastoid infection develops
in a child with chronic suppurative otitis media,
cholesteatoma, or both.
N
N
N
Lateral to the surface of the mastoid process,
resulting in a postauricular subperiosteal
abscess (Figure 16)
Anterior into the zygomatic cells, with development into an abscess in the anterior and
superior portion of the pinna and preauricular
area306
Inferior through the tip of the mastoid,
burrowing beneath the skin to form a soft
tissue abscess below the pinna or behind the
attachment of the sternocleidomastoid muscle
in the neck, which is known as Bezold’s
abscess307–309 (Figures 17 and 18)
Acute Mastoiditis with Osteitis (with and
without Subperiosteal Abscess)
Acute mastoiditis with osteitis has also been
called acute coalescent mastoiditis or acute
surgical mastoiditis, but the pathologic process
is really acute mastoid osteitis.193 A subperiosteal
abscess may or may not be present.303
Epidemiology
A review during a 20-year period (1977–1996) in
one Danish county revealed that 79 children had
a mastoidectomy performed for acute mastoiditis; a subperiosteal abscess was present in 66%.304
In the review during a 15-year period (1980–
1995) of 72 children who had acute mastoiditis
by Goldstein and colleagues, 31% had either a
postauricular mass or subperiosteal abscess.262 In
a report from Rome, Italy, in which 39 children
had mastoidectomy for acute mastoiditis, all had
a subperiosteal abscess.305
Pathogenesis and Pathology
When infection within the mastoid progresses,
rarefying osteitis can cause destruction of the
bony trabeculae that separate the mastoid cells so
that there is a ‘‘coalescence’’ of the cells. At this
stage, a mastoid empyema is present. The pus
may spread in one or more of the following
directions:
N
Anterior to the middle ear through the aditus
ad antrum, in which case spontaneous resolution usually occurs
Figure 16. An example of a subperiosteal abscess in a child who
had acute mastoid osteitis. Note that the pinna is displaced inferiorly
and anteriorly, with obliteration of the postauricular crease owing to
the abscess.
Complications and Sequelae: Intratemporal
Figure 17. An abscess in the neck (Bezold’s abscess) can be seen
in this child who has a draining ear owing to acute otitis media. The
pus has extended from acute mastoid osteitis and empyema into the
neck.
N
N
Medial to the petrous air cells, resulting in
petrositis
Posterior to the occipital bone, which can
result in osteomyelitis of the calvarium, or
Citelli’s abscess
The acute mastoid infection may be associated with an episode of AOM, cholesteatoma,
or chronic suppurative otitis media. In the review
of 39 Italian children who had this complication,
23 (59%) had AOM, and most of the remaining
16 had an associated cholesteatoma.305
Infection may also spread medial to the
labyrinth, involve the facial nerve,262 or extend
into the intracranial cavity, causing one or more
suppurative complications, such as dural sinus
thrombosis.310,311
371
Clinical Presentation
The child usually has the same signs and
symptoms as those associated with AOM, such
as fever and otalgia, although the fever may be
low grade, with occasional temperature spikes.
Some patients may have toxic symptoms. The
signs and symptoms referable to the mastoid
infection are swelling, erythema, and tenderness
to touch over the mastoid bone; displacement of
the pinna outward and downward (Figure 19);
and swelling or sagging of the posterosuperior
external auditory canal wall (see Table 9). A
fluctuant subperiosteal abscess or even a draining
fistula from the mastoid to the postauricular area
may be present (Figure 20). The subperiosteal
abscess can be in any of the anatomic sites
described.
Examination of the tympanic membrane
usually reveals middle-ear effusion, or there
may be a purulent discharge and a perforation.
In the 20-year review of 79 Danish children
who developed acute mastoiditis and had a
mastoidectomy, 92% had a purulent middle-ear
effusion.304 Conversely, the tympanic membrane
and middle ear may appear almost normal for
the reasons described when mastoiditis with
periosteitis occurs. Acute mastoid osteitis (without otitis media) may also be the focus of
infection when a child has a fever of unknown
origin, in which case the disease in the mastoid is
occult; as described later, the term subacute or
masked mastoiditis has been used to describe this
entity.
Diagnosis
The diagnosis should be suspected on the basis of
clinical signs and symptoms. CT scans of the
mastoid area usually reveal one or more of the
following: haziness, distortion, or destruction of
the mastoid outline; loss of sharpness of the
shadows of cellular walls owing to demineralization, atrophy, and ischemia of the bony septa
(Figure 21); and a decrease in density and
cloudiness of the areas of pneumatization owing
to inflammatory swelling of the air cells. In longstanding cases, a chronic osteoblastic inflammatory reaction may obliterate the cellular struc-
372
OTITIS MEDIA IN INFANTS AND CHILDREN
Figure 18. Computed tomogram of
a child with acute mastoiditis and a
Bezold’s abscess. A, Erosion of the
mastoid apex is evident (arrow). B,
Abscess in the neck is noted by the
ring-enhancing defect on the scan
(arrow).
ture. Small abscess cavities in sclerotic bone may
be confused with pneumatic cells.
Antonelli and colleagues reviewed CT scans
of 21 patients with acute coalescent mastoiditis
(with osteitis) or acute noncoalescent mastoiditis
(without osteitis) and 12 patients with chronic
mastoiditis.312 They found that erosion of the
cortical plate overlying the sigmoid sinus was the
most sensitive and specific CT finding to distinguish osteitis from nonosteitis acute disease.
As part of the diagnostic workup, cultures to
determine the causative bacterial organisms
should be obtained, either before or at the time
of mastoid surgery. When otorrhea is present,
cultures for bacteria from the ear drainage must
be taken with care to discern fresh drainage from
debris in the external canal. As described in detail
earlier (see ‘‘Chronic Perforation with Chronic
Otitis Media [Chronic Suppurative Otitis
Media]’’), the canal must be initially cleaned.
Then, if fresh pus is exuding through a perforation in the tympanic membrane, the discharge is
cultured at the point of exit from the tympanic
membrane with a cotton-tipped wire swab or,
preferably, a needle and syringe under direct
view. A Gram stain of the pus provides
Complications and Sequelae: Intratemporal
Figure 19. Acute mastoid osteitis in an infant, showing the outward
displacement of the pinna.
immediate information about the responsible
organisms. When the mastoidectomy is performed, portions of mucosa and bone of the
mastoid should be sent for Gram stain, culture,
and antibiotic susceptibility testing.
The differential diagnosis between this stage
of mastoiditis and other disease entities (eg, acute
external otitis with postauricular periosteitis or
postauricular lymphadenitis) that involve the
postauricular area is described in the section
‘‘Acute Mastoiditis with Periosteitis’’ (see Table
9).
Microbiology
The microbiology of mastoid osteitis is the same
as that of acute mastoiditis with periosteitis, as
described before (see Table 10). In the review by
373
Figure 20. An example of a postauricular fistula with purulent
discharge in a child who had acute mastoid osteitis.
Petersen and colleagues of children who had a
mastoidectomy for acute mastoiditis, S. pneumoniae, S. pyogenes, and H. influenzae were the
most common organisms isolated.304 Unusual
organisms, such as M. avium313 and M. chelonae,314 have been reported.
Management
An otolaryngologist should be consulted if a
child has a diagnosis of acute mastoid osteitis.
Parenteral antimicrobial therapy should be instituted as described before for acute mastoiditis
with periosteitis. To ensure that drainage of the
middle ear and mastoid is adequate, in the
absence of a large perforation and otorrhea, a
wide-field large myringotomy should be done
immediately. Insertion of a tympanostomy tube,
374
OTITIS MEDIA IN INFANTS AND CHILDREN
Figure 21. Computed tomogram of temporal bones showing left
acute osteitis with loss of septa between the mastoid air cells, which
has been termed acute coalescent mastoiditis; the right mastoid is
normal. Mastoid surgery was performed in this case.
in addition to a large myringotomy incision,
can provide more prolonged drainage from the
middle-ear–mastoid than myringotomy alone.
The tympanostomy tube placement will also
help prevent AOM (and mastoiditis) from
recurring.
A cortical (simple) mastoidectomy is usually
required when there is evidence of acute mastoid
osteitis, especially when the mastoid empyema
has extended outside the mastoid bone and a
subperiosteal abscess is present.315 The procedure should be considered an emergency, but the
timing of the operation depends on the status of
the child. Ideally, sepsis should be under control,
and the patient must be able to tolerate a general
anesthetic. The principle is to clean out the
mastoid infection, to drain the mastoid air cell
system into the middle ear by eliminating any
obstruction caused by edema or granulation
tissue in the aditus ad antrum, and to provide
external drainage (Figure 22).152 If another
suppurative intratemporal or intracranial complication is also present, surgical intervention for
these conditions may also be required.
Figure 22. Schematic depiction of aditus ad antrum ‘‘block’’ (A) and
the principles of a cortical (simple) mastoidectomy (B) in a right ear.
The infected mastoid air cell walls are removed with the use of a
surgical drill to form one large mastoid cavity, and the granulation
tissue in the aditus ad antrum is excised to promote drainage from
the mastoid to the middle ear.
Summary of Recommended Treatment Plan
Related to the Stage of Acute Mastoiditis
Table 11 shows the clinical features of acute
mastoiditis and findings on a CT scan on
presentation to the physician related to our
recommended management. From this summary,
it is apparent that we recommend consultation
with an otolaryngologist for possible tympanocentesis and myringotomy (and tympanostomy
tube insertion) whenever the primary physician
lacks the expertise (or qualifications for tympanostomy tube placement) to perform these
procedures. Consultation with the otolaryngologist is also indicated for possible mastoidectomy
whenever a child has the diagnosis of acute
mastoiditis with subperiosteal abscess, regardless
of the findings on a CT scan, and the CT scan
No
Yes
No{
Yes
Yes
Yes
Yes
Optional*
Yes
Yes
Yes
Yes
Yes
Yes
375
reveals osteitis, regardless of the other clinical
features. Surgical procedures for mastoidectomy
have been described in detail elsewhere.9
An otolaryngologist should be immediately
consulted whenever acute mastoiditis is associated with another possible suppurative complication of otitis media and mastoiditis and when
acute mastoiditis develops in a child who has
chronic suppurative otitis media, cholesteatoma,
or both.
Subacute Mastoiditis (Masked Mastoiditis,
Occult Mastoiditis)
*Indications are the same as for acute otitis media because disease in the mastoid is mastoiditis without periosteitis or osteitis.
{
Yes, if there is treatment failure after myringotomy and parenteral antibiotics.
Mastoidectomy
Myringotomy
Parenteral
No
Yes
Yes
Yes
Yes
Yes
Yes
Yes
No
No
No
No
No
No
Oral
(on CT)
No
Yes
No
Yes
Yes
No
Yes
No
No
No
No
No
Yes
Yes
Abscess
Periosteitis
Protrusion
No
No
Yes
Yes
No
Yes
Yes
Osteitis
Subperiosteal
Postauricular
Pinna
No
No
Yes
Yes
Yes
Yes
Yes
Tympanocentesis
with or without Myringotomy
Antibiotics
Management
Features
Table 11. FEATURES OF ACUTE MASTOIDITIS RELATED TO RECOMMENDED MANAGEMENT
Complications and Sequelae: Intratemporal
A condition has been described called masked
mastoiditis, for which a complete simple mastoidectomy has been advocated.150 The disease
appears to be a subacute stage of otitis media
and mastoiditis (without osteitis) characterized
by the same signs and symptoms as AOM (such
as fever and ear pain), except that they are
persistent and less severe. The progression to this
stage is attributed to failure of the initial antimicrobial agent to resolve the middle-ear and
mastoid infection within a short period.
Persistence of otalgia and fever in a patient
receiving an antimicrobial agent is an indication
for tympanocentesis and myringotomy to identify the causative organism and promote drainage. In selected children, especially those who
have had frequently recurrent episodes of AOM,
insertion of a tympanostomy tube (in addition to
the appropriate antimicrobial therapy) will
resolve the problem. Mastoid surgery is not
indicated unless insertion of the tympanostomy
tube and intravenous antimicrobial therapy are
ineffective.193
Denoyelle and colleagues described 165
children, identified during 2 years, with subacute
mastoiditis, which was defined as an attack of
AOM that did not resolve with 10 days of
antibiotic treatment, despite intravenous therapy.316 Middle-ear aspiration (or cultures of
otorrhea) revealed H. influenzae (28%), P.
aeruginosa (23%), and S. pneumoniae (16%). Of
these 165 children, 31 (19%) had mastoidectomy.
It is likely that tympanostomy tube insertion in
376
OTITIS MEDIA IN INFANTS AND CHILDREN
these children would have prevented mastoidectomy in most if not all.
In contrast to this condition, which is usually
a failure of initial antimicrobial treatment that
frequently resolves after adequate middle-ear
drainage and identification of the causative
organism followed by administration of a
culture-directed antibiotic, infants and children
may have a suppurative process in the mastoid
that is not clinically obvious (ie, occult). This
mastoid infection may even result in an intratemporal or intracranial complication, in which
the middle ear may not appear to be diseased and
the patient lacks the classic signs and symptoms
of otitis media and mastoiditis. This condition
can be called masked mastoiditis. The diagnosis is
usually made by CT scan or by obtaining a bone
scan.317 Children who have intracranial suppurative disease or disease of the temporal bone that
could possibly be due to mastoid infection should
have CT of the temporal bones included in the
workup, even though there is no evidence of
middle-ear disease on otoscopy. Although rare,
children who have fever of unknown origin may
have masked mastoiditis.
On occasion, older children or adolescents
will complain of persistent or recurrent postauricular pain, but the middle ear appears to be
free of disease. The communication between the
middle ear and the mastoid air cells (ie, aditus ad
antrum) may be blocked, causing mastoiditis.
These children usually have had a history of
recurrent AOM, recurrent or chronic otitis media
with effusion, or chronic suppurative otitis
media, and when a CT scan is obtained, mastoiditis is diagnosed. Medical treatment (eg, antimicrobial therapy) is indicated, but if the
symptoms are severe or a trial of medical
management fails, a mastoidectomy is indicated
to relieve the aditus ad antrum blockage and
eliminate the infected cells. More rarely, a child
with these symptoms may have relatively normal
mastoid cellular architecture on a CT scan, in
which case, the patient could have negative
pressure within the mastoid because of an aditus
ad antrum obstruction. Again, mastoidectomy
may be the only method of eliminating the
blockage and relieving the symptoms.
Chronic Mastoiditis (with and without
Chronic Suppurative Otitis Media or
Cholesteatoma)
Today, chronic mastoiditis is most commonly
associated with chronic suppurative otitis media
(see earlier).318 Also, chronic mastoiditis can be
involved in a child’s ear that has a cholesteatoma
that extends to the mastoid gas (air) cells, which
is associated with chronic suppurative otitis
media.179 However, an occasional child will
develop acute mastoiditis that is either untreated
or inappropriately treated, or the child is
neglected, and the infection progresses to a
chronic stage in which no perforation (or
tympanostomy tube) is present in the tympanic membrane; no chronic suppurative otitis
media, with or without otorrhea, is present.
Nevertheless, the disease in the mastoid progresses to the chronic stage, and otitis media may
or may not be present.193 These children can
present with a fever of unknown origin or
chronic or recurrent otalgia and tenderness over
the mastoid process. Like the child who has
subacute or masked mastoiditis, the patient
with chronic mastoiditis may have another
intratemporal or intracranial complication. A
child with an intracranial infectious process, such
as a brain abscess, who has no clinical evidence
of otitis media or mastoiditis, may have chronic
mastoiditis as the focus of the intracranial
infection.193
Diagnosis
Examination of the tympanic membrane shows
evidence of middle-ear effusion, but the eardrum
may appear normal if the chronic infection is
localized only to the mastoid. The diagnosis that
the mastoid is affected is made by CT. The
mastoid may be poorly pneumatized or sclerotic,
or it may show evidence of bone destruction,
with opacification of the mastoid.
Complications and Sequelae: Intratemporal
Management
The chronic infection, if it is reversible, may be
brought under control by medical treatment with
antimicrobial agents (similar to those recommended for acute mastoiditis without periosteitis
or osteitis). A tympanocentesis (for Gram stain,
culture, and susceptibility studies) and myringotomy (for drainage) should be performed. When
there are extensive amounts of granulation tissue
and osteitis in the mastoid (ie, irreversible
mastoid disease) or the child fails to improve
with medical therapy, referral to an otolaryngologist is needed because a tympanomastoidectomy is required to eliminate the chronic mastoid
osteitis.9 When another suppurative complication is present in addition to the chronic
mastoiditis, such as brain abscess, dural sinus
thrombosis, or otitic hydrocephalus, mastoidectomy is indicated.277
Chronic mastoiditis can also be caused by a
cholesteatoma, which is usually manifested by
chronic otorrhea through a defect in the tympanic membrane.274 A cholesteatoma requires
definitive surgical treatment.
PETROSITIS
Petrositis is a relatively rare suppurative complication secondary to an extension of infection
from the middle ear and mastoid into the petrous
portion of the temporal bone.10 All of the
inflammatory and cellular changes described in
the mastoid can also occur in the pneumatized
petrous pyramid. Only about 30% of individuals
have well-pneumatized petrous bones.319 Petrositis may be more frequent than is appreciated by
clinical and radiographic signs because there is
communication of the petrosal air cells with the
mastoid–middle-ear system. Pneumatization
usually does not occur before the age of 3 years.
For a more complete and detailed discussion of
petrositis, the reader is referred to Bluestone.320
Petrositis may be either acute or chronic. It
has also been found to be recurrent.321 In the
acute form, there is extension of AOM and
mastoiditis into the pneumatized petrous air cells.
The condition, like acute mastoiditis, is usually
377
self-limited, with resolution of the acute middleear and mastoid infection, but the infection in the
petrous portion of the temporal bone occasionally
does not drain owing to mucosal swelling or
because granulation is obstructing the passage
from the petrous air cells to the mastoid and
middle ear. This results in acute petrous osteomyelitis.322 The widespread use of antimicrobial
agents has made this a rare complication. Chronic
petrous osteomyelitis, however, can be a complication of chronic suppurative otitis media or
cholesteatoma, and it is much more common than
the acute type. Pneumatization of the petrous
portion of the temporal bone does not have to be
present because the infection can invade the area
by thrombophlebitis, by osteitis, or along fascial
planes.323 The infection may persist for months or
years with mild and intermittent signs and
symptoms, or it may spread to the intracranial
cavity and result in one or more of the suppurative
complications of ear disease, such as an extradural
abscess or meningitis.
At the Children’s Hospital of Pittsburgh
during the 15-year period from 1980 to 1995,
only four children were admitted with this
diagnosis, and three of these patients had
simultaneous intracranial suppurative complications, such as dural sinus thrombosis.262 All of
these children had this complication as a result of
spread of an attack of AOM.
Microbiology
The organisms that cause acute petrositis are the
same as those that cause acute mastoid osteitis:
S. pneumoniae, H. influenzae, and group A
streptococci. Chronic petrous osteomyelitis,
however, may be caused by the bacteria associated with chronic suppurative otitis media and
cholesteatoma, such as P. aeruginosa or Proteus
species. Tuberculosis has also been isolated from
these ears.324
Diagnosis
The disease is characterized by pain behind the
eye, deep ear pain, persistent ear discharge, and
378
OTITIS MEDIA IN INFANTS AND CHILDREN
sixth nerve palsy. However, in the four patients
who were admitted to Children’s Hospital of
Pittsburgh during a 15-year period with this
complication of otitis media, eye pain, deep ear
pain, and persistent otorrhea were not consistently present,262 which has been the experience
in other reviews. Eye pain is due to irritation of
the ophthalmic branch of the fifth cranial nerve.
On occasion, the maxillary and mandibular
divisions of the fifth nerve are involved, and
pain occurs in the teeth and jaw. A discharge
from the ear is common with acute petrositis but
may not be present with chronic disease.
Paralysis of the sixth cranial nerve leading to
diplopia is a late complication.325 Acute petrous
osteomyelitis should be suspected when persistent purulent discharge follows a complete simple
mastoidectomy for mastoid osteitis. The triad of
pain behind the eye, aural discharge, and sixth
nerve palsy is known as Gradenigo’s syndrome.
The diagnosis of acute petrous osteomyelitis
is suggested by the unique clinical signs.
Standard radiographs of the temporal bones
may show clouding with loss of trabeculation
of the petrous bone. The visualization is uncertain, however, because of normal variation in
pneumatization (including asymmetry) and the
obscuring of the petrous pyramids by superimposed shadows of other portions of the skull.
CT scans of the temporal bones can lead to
diagnosis and should be obtained if there might
be a possibility of an extension of infection into
the cranial cavity. This complication must be
distinguished from destructive lesions of the
petrous apex owing to such conditions as
cholesteatoma, cholesterol granuloma, and arachnoid cysts; CT and MRI can be diagnostic in
distinguishing these diseases.326,327
Management
Management of acute petrositis is similar to that
described for acute mastoiditis with osteitis; at
this stage, it can be considered further spread of
the mastoid infection into the pneumatized
petrous portions of the temporal bone. All four
of the patients who had this diagnosis at the
Children’s Hospital of Pittsburgh (see earlier)
were successfully treated with high-dose broadspectrum intravenous antibiotic therapy and
cortical (simple) mastoidectomy without entering
the petrous apex; the petrous apex disease most
likely drained into the mastoid cavity during the
postoperative period.262 The three patients with
intracranial complications also had specific
management of that complication. In more
severe cases of acute petrous osteomyelitis and
acute mastoid osteitis, a more aggressive surgical
approach to management may be required. A
transcanal approach to the petrous apex has been
reported,328 but the more traditional approaches
have been described by Coker and Jenkins.329
LABYRINTHITIS
This complication of otitis media occurs when
infection spreads into the cochlear and vestibular
apparatus. The usual portal of entry is the round
window or, less commonly, the oval window, but
invasion may take place from an infectious focus
in an adjacent area, such as the mastoid antrum,
the petrous bone, or the meninges, and as a result
of bacteremia.330 Schuknecht classified labyrinthitis into three types217:
1. Serous (toxic) labyrinthitis, in which there
may be bacterial toxins or biochemical
involvement, but no bacteria are present
2. Suppurative (acute and chronic otogenic
suppurative) labyrinthitis, in which bacteria
have invaded the otic capsule
3. Meningogenic suppurative labyrinthitis,
which is the result of invasion of bacteria
from the subarachnoid space into the labyrinth. Labyrinthitis ossificans (labyrinthine
sclerosis), in which there is replacement of
the normal labyrinthine structures by fibrous
tissue and bone, is the end stage of this
complication if it is arrested.
An acceptable classification of labyrinthitis
today is acute labyrinthitis, subacute labyrinthitis, chronic labyrinthitis, and labyrinthitis ossificans.
Complications and Sequelae: Intratemporal
Acute Labyrinthitis
Acute labyrinthitis can be classified as serous or
suppurative, and each of these entities can be
either localized or generalized.10
Acute Serous Labyrinthitis (with or without
Perilymphatic Fistula)
The acute serous (toxic) type of labyrinthitis is
considered to be one of the most common
suppurative complications of otitis media.
Paparella and colleagues described the histopathologic evidence of serous labyrinthitis in
most of the temporal bone specimens from
patients who had otitis media.26 Bacterial toxins
from the infection in the middle ear may enter the
inner ear, primarily through an intact round
window or through a congenital defect between
the middle ear and inner ear. The portal of entry
may also be through an acquired defect of the
labyrinth, such as from head trauma or previous
middle-ear or mastoid surgery. Biochemical
changes within the labyrinth have also been
found. The cochlea is usually more severely
involved than the vestibular system. Paparella
and colleagues reviewed the audiograms of 232
patients who had surgery for chronic otitis media
and found a significant degree of bone conduction loss in the younger age groups.331 In
addition, there was a marked difference in the
presence and degree of sensorineural hearing loss
in the affected ear, compared with the normal
ear, in patients of all age groups who had
unilateral disease. They postulated that the
high-frequency sensorineural hearing loss frequently accompanying this disease is due to a
pathologic insult to the basal turn of the cochlea.
In the review of intratemporal complications of
otitis media from the Children’s Hospital of
Pittsburgh between 1980 and 1995, three children
were admitted with a diagnosis of acute serous
labyrinthitis that was a complication of an attack
of AOM.262
Fluctuating sensorineural hearing loss has
been described in patients with otitis media and
has been thought to be due to either endolymphatic hydrops332 or a perilymphatic fistula.27–29,333
379
However, fluctuating or progressive sensorineural
hearing loss can be due to a variety of other
hereditary and acquired causes.334
Clinical Presentation
The signs and symptoms of serous labyrinthitis
(especially when a perilymphatic fistula is present) are sudden, progressive, or fluctuating
sensorineural hearing loss and vertigo in association with otitis media or one or more of its
complications or sequelae, such as mastoid
osteitis. The loss of hearing is usually mixed,
that is, there are both conductive and sensorineural components, when serous labyrinthitis is
a complication of otitis media. In some children
who have recurrent middle-ear infections, the
hearing may be normal between episodes. In
other children, only a mild or moderate sensorineural hearing loss will be present at all times.
The presence of vertigo may not be obvious in
children, especially infants. Older children may
describe a feeling of spinning or turning; younger
children may not be able to verbalize the
symptoms but manifest the dysequilibrium by
falling, stumbling, or being clumsy. The vertigo
may be mild and momentary, and it may tend to
recur during a period of months or years. Onset
of vertigo, progressive sensorineural hearing loss,
or both in a patient who has a preexisting hearing
loss is frequently due to a fistula.335 Spontaneous
nystagmus may also be present, but the signs and
symptoms of acute suppurative labyrinthitis,
such as nausea, vomiting, and deep-seated pain,
are usually absent. Fever, if present, is usually
due to a concurrent upper respiratory tract
infection or AOM.
If congenital perilymphatic fistula is present,
nystagmus may be present during the course of
the episode of AOM, in addition to the
mixed hearing loss. In a review of 47 infants
and children who had exploratory tympanotomy for possible fistula at the Children’s
Hospital of Pittsburgh, 30 children (64%) had a
history of otitis media, and of these 30 patients,
28 (93%) had a fistula diagnosed at surgery
(Table 12).336
380
OTITIS MEDIA IN INFANTS AND CHILDREN
Table 12. NUMBER AND PERCENTAGE OF 47 INFANTS AND CHILDREN WHO DID AND DID
NOT HAVE CONGENITAL PERILYMPHATIC FISTULA CONFIRMED AT SURGERY
(TYMPANOTOMY) RELATED TO HISTORY OF OTITIS MEDIA
Perilymphatic Fistula Present, n (%)
Presence of
Otitis Media in Past
Yes
No
Total patients
Yes
No
Total Patients
28 (76)
9 (24)
37
2 (20)
8 (80)
10
30
17
47
Adapted from Bluestone CD.336
Diagnosis
A labyrinthine fistula may be identified by
performing a fistula test with a Siegle pneumatic
otoscope or by applying positive and negative
external canal pressure with use of the pumpmanometer system of an impedance audiometer.
The fistula test result is considered positive if
nystagmus or vertigo is produced by the application of the pressures. Electronystagmography is
an objective way of documenting the presence or
absence of the nystagmus; the findings of the
fistula test may be misleading because there can
be false-positive and false-negative results. The
test can be done in the presence of a perforation
of the tympanic membrane or tympanostomy
tube. Fistulae are frequently associated with
congenital or acquired defects in the temporal
bone, such as the Mondini malformation. CT
scans may be helpful in identifying such defects,
such as a dilated vestibular aqueduct, as shown in
Figure 23. Weissman and colleagues assessed the
CT scans of 10 children (15 ears) with fistula,
Figure 23. Computed tomogram of a left temporal bone showing a
dilated vestibular aqueduct (arrow).
confirmed at surgery, and were able to identify
an abnormality of the inner ear, middle ear, or
both in 53% of the ears.337 Electrocochleography
has also been advocated for diagnosis of a
fistula,338 but this method has not proved to be
as sensitive and specific as desired. Currently, the
most effective method for diagnosis of a perilymphatic fistula is exploratory middle-ear surgery.339
Weber and colleagues proposed a relatively
new test for the presence of perilymph in the
middle ear as a way to confirm the presence of a
perilymphatic fistula.340,341 A sample of the
suspect fluid in the middle ear must be obtained
at the time of exploratory surgery, and then it is
assessed by an immunopathologic assay. The test
appears to be specific but not sensitive.342 A
study by Buchman and colleagues found that the
test did not identify perilymph, but the result was
positive when cerebrospinal fluid was present.343
Thus, when the test result is positive, it most
likely confirms a cerebrospinal fluid leak from
the inner to the middle ear. A more appropriate
term for these malformations of labyrinthine
windows is congenital perilymphatic/cerebrospinal
fistula because the fluid emanating from the
defect may be cerebrospinal fluid.344
Management
When this complication occurs during an attack
of AOM, a tympanocentesis and myringotomy should be performed for microbiologic
assessment of the middle-ear effusion and drainage. If possible, a tympanostomy tube should
also be inserted for more prolonged drainage and
in an attempt to ventilate the middle ear.
Antimicrobial agents with efficacy against S.
Complications and Sequelae: Intratemporal
pneumoniae, H. influenzae, and M. catarrhalis,
such as parenteral amoxicillin-sulbactam, should
be administered; other organisms, such as S.
aureus and Pseudomonas, have also been isolated
from the middle ears of children who have acute
labyrinthitis.262 After resolution of the otitis
media with effusion, the signs and symptoms of
the labyrinthitis should rapidly disappear; however, sensorineural hearing loss may persist. If
the diagnostic assessment indicates a possible
congenital or acquired defect of the labyrinth, an
exploratory tympanotomy should be performed
as soon as the middle ear is free of infection. The
most common malformations are an abnormal
round window and niche (such as a laterally
facing round window), deformities of the stapes
superstructure and footplate, deformed long
process of the incus, or some combination of
these congenital defects. More rarely, a congenital fissure between the round and oval windows is
present.28,29 If a perilymphatic fistula is found, it
should be repaired by use of temporalis muscle
grafts. Even when no defect of the oval or round
window is identified but a fistula is still
suspected, the stapes footplate and round window should be covered with connective tissue
because a leak may not be present at the time
of the tympanotomy but may recur.27,28,333 A
tympanostomy tube should be reinserted if
recurrent otitis media persists.
When acute mastoid osteitis, chronic suppurative otitis media, or cholesteatoma is present, definitive medical and surgical management
of these conditions is essential in eliminating the
labyrinthine involvement. A careful search for a
labyrinthine fistula must be performed when
mastoid surgery is indicated. However, a labyrinthectomy is not indicated for serous labyrinthitis. The surgical procedure to repair a
perilymphatic or cerebrospinal fluid fistula is
described in detail by Bluestone.152
Conclusion
Any child with sensorineural hearing loss (with
or without vertigo) who also has recurrent acute
or chronic otitis media with effusion should be
carefully evaluated for the possible existence of
381
serous labyrinthitis, which can be secondary to
a perilymphatic fistula.333 This combination
appears to be common, and failure to identify
this complication can result in irreversible severe
to profound hearing loss, making early diagnosis
and prevention imperative. Because prevention
of sensorineural hearing loss owing to other
causes (such as congenital and viral) is not yet
possible, our goal should be to prevent this loss
of function in those children in whom it can be
prevented. In addition, serous labyrinthitis may
develop into acute suppurative labyrinthitis.
Acute Suppurative Labyrinthitis
Suppurative (purulent) labyrinthitis may develop
as a complication of otitis media or be one of
its complications and sequelae when bacteria
migrate from the middle ear into the perilymphatic fluid through the oval or round window, a
preexisting temporal bone fracture, an area
where bone has been eroded by cholesteatoma
or chronic infection, or a congenital defect, such
as a congenital perilymphatic (cerebrospinal)
fistula, as described before. The most common
way that bacteria enter the labyrinth is from the
meninges, but migration by this route is usually
not a complication of otitis media.
Epidemiology and Pathogenesis. The
incidence of suppurative labyrinthitis as a complication of otitis media is unknown, but it is rare
because of the widespread use of antibiotics. In a
series of 96 cases of suppurative intratemporal
and intracranial complications of acute and
chronic otitis media that were treated from
1956 to 1971, there were only 5 cases of
suppurative labyrinthitis, and all were secondary
to cholesteatoma that had caused a labyrinthine
fistula.345 Nonetheless, suppurative labyrinthitis
still occurs. When it occurs in children who have
an episode of AOM and who are apparently
treated appropriately and adequately, a congenital (or acquired) perilymphatic fistula must be
ruled out to prevent further hearing loss and
recurrence, which can be life-threatening because
of meningitis. Conversely, when a child develops
bacterial meningitis, especially recurrent epi-
382
OTITIS MEDIA IN INFANTS AND CHILDREN
sodes, a congenital defect of the inner and middle
ear must be ruled out. A congenital or acquired
defect between the paranasal sinuses and the
anterior cranial cavity can also cause meningitis.
In a review of children who had intratemporal
complications of otitis media, Goldstein and
colleagues found two patients who had a
suppurative labyrinthitis during a recent 15-year
period; one child had a congenital defect of the
labyrinthine windows, which was considered to
be a perilymphatic or cerebrospinal fluid fistula
(Figure 24).262
Meningitis that has even resulted in death
was reported to be caused by otitis media
progressing to labyrinthitis in children who have
had cochlear implants (one offending implant
has been removed from the market), but in most
cases, the pathogenesis is most likely due to a
congenital defect between the middle and inner
ears. The appropriate vaccines have been recommended for prevention, and prompt treatment of
AOM in children who have congenital malformations of the ear, and repair of the defect is
desirable.9
Clinical Presentation and Diagnosis. The
sudden onset of vertigo, dysequilibrium, deepseated pain, nausea and vomiting, and sensorineural hearing loss during an episode of AOM
or an exacerbation of chronic suppurative otitis
media indicates that labyrinthitis has developed.
The hearing loss is severe, and there is loss of the
child’s ability to repeat words shouted in the
affected ear, with masking of sound in the
opposite ear. Spontaneous nystagmus and pastpointing can often be observed. Initially, the
quick component of the nystagmus is toward the
involved ear, and there is a tendency to fall
toward the opposite side. However, when there is
complete loss of vestibular function, the quick
component is toward the normal ear.
Today, radiographic imaging can be an
invaluable diagnostic aid. MRI can be diagnostic
of the labyrinthitis, and CT can identify congenital or acquired defects of the inner and
middle ear that may have predisposed the child
to spread of the infection from the middle ear to
Figure 24. Magnetic resonance image (axial view) of left acute
suppurative (generalized) labyrinthitis (arrow) as a complication of
the first attack of acute otitis media in an 18-month-old boy who had a
preexisting congenital perilymphatic or cerebrospinal fluid fistula of
the labyrinthine windows. The child presented with left otorrhea,
fever, vertigo, and dehydration 5 days after the onset of the acute
otitis media; the causative organism was Pseudomonas aeruginosa.
Labyrinthectomy on the left ear as an emergency procedure was
performed, with no further progression of the infection. Because the
contralateral (right) ear was found to have a mild sensorineural
hearing loss, an exploratory tympanotomy was performed at a later
date, at which time an identical middle-ear malformation was
diagnosed; the b2-transferrin test result was positive in this ear.
The middle-ear defects were patched at the time of each of the
surgical procedures with grafts from the temporalis muscle. The child
had no further hearing loss or suppurative complication during the
ensuing 3-year follow-up period.
the labyrinth (and subarachnoid space). In the
absence of associated meningitis, the cerebrospinal fluid pressure and cell count are normal.
The onset of suppurative labyrinthitis may
frequently be followed by facial paralysis,
meningitis, or both. In later stages, cerebellar
abscess can develop. Thus, suppurative labyrinthitis is a serious complication of otitis media.
The development of purulent labyrinthitis means
that infection has spread to the fluid of the inner
Complications and Sequelae: Intratemporal
ear, and infection can then spread to the subarachnoid space through the cochlear aqueduct,
the vestibular aqueduct, or the internal auditory
canal. Figure 25 shows the radiographic image of a
child in whom acute suppurative labyrinthitis
owing to otitis media spread to the labyrinth
through a congenital perilymphatic fistula and
spread to the meninges, resulting in death.
Management. The management of suppurative labyrinthitis in the absence of meningitis
consists of otologic surgery combined with
intensive antimicrobial therapy. A congenital
defect between the middle and inner ears should
be investigated using imaging. If this complication is due to AOM, immediate tympanocentesis
and myringotomy with tympanostomy tube
insertion are indicated, as described when serous
labyrinthitis is present. If acute mastoid osteitis is
present, a cortical (simple) mastoidectomy
should be performed. However, because this
complication can be secondary to cholesteatoma,
383
a radical mastoidectomy or modified radical
mastoidectomy may be required. A modified
radical mastoidectomy may also be required
when chronic suppurative otitis media is present
without cholesteatoma.
If meningitis has also occurred in association with suppurative labyrinthitis, otologic
surgery other than a diagnostic and therapeutic
tympanocentesis-myringotomy may have to be
delayed until the meningitis is under control and
the child is able to tolerate a general anesthetic,
but it is important to control the source of the
infection in the middle ear and labyrinth as soon
as possible. A labyrinthectomy should be performed only if there is complete loss of labyrinthine function or if the infection has spread to
the meninges in spite of adequate antimicrobial
therapy. Parenteral antimicrobial agents appropriate for management of the primary middle-ear
and mastoid disease should be administered
initially. However, because cholesteatoma and
chronic suppurative otitis media are frequent
causes of suppurative labyrinthitis, antimicrobials
effective for the gram-negative organisms (P.
aeruginosa and Proteus) are frequently required.
The results of culture of the middle-ear effusion,
the purulent discharge, or the cerebrospinal fluid
may alter the selection of the antibiotics.
Chronic Labyrinthitis
Figure 25. Computed tomogram of temporal bones (postmortem)
showing bilateral Mondini malformation of the inner ears (arrows),
cochlear implant in the left ear (arrowheads), and effusion in the right
middle ear and mastoid of a 6-year-old boy. The child had
progressively severe headache, photophobia, vomiting, and seizures
during a 24-hour period and died of pneumococcal meningitis
secondary to otitis media and suppurative labyrinthitis, which, in
turn, spread to the meninges. The infection spread from the middle
ear to the labyrinth through a congenital perilymphatic fistula.
Reproduced with permission from Suzuki C, Sando I, Fagan JJ, et
al. Histopathological features of a cochlear implant and otogenic
meningitis in Mondini dysplasia. Arch Otolaryngol Head Neck Surg
1998;124:462–6.
The most common cause of chronic labyrinthitis
as a complication of middle-ear disease is a
cholesteatoma that has eroded the labyrinth,
resulting in a fistula.346 Osteitis may also cause
bone erosion of the otic capsule. The fistula most
commonly occurs in the lateral semicircular canal
and is filled by squamous epithelium of a
cholesteatoma, granulation tissue, or fibrous
tissue entering the labyrinth. The middle ear
and mastoid are usually separated from the inner
ear by the soft tissue at the site of the fistula,
but when there is continuity, acute suppurative
labyrinthitis may develop. However, chronic
labyrinthitis may be caused by chronic suppurative otitis media or even chronic otitis media with
effusion, especially if the child has a congenital
384
OTITIS MEDIA IN INFANTS AND CHILDREN
defect between the middle and inner ear (congenital perilymphatic fistula).
Clinical Presentation and Diagnosis
The signs and symptoms of chronic labyrinthitis
are similar to those of the acute forms of the
disease (eg, sensorineural hearing loss and
vertigo), except that their onset is more subtle.
The disease is characterized by slowly progressive
loss of cochlear and vestibular function during a
prolonged period. The fistula test may be helpful
in diagnosis of a labyrinthine fistula, MRI may
reveal labyrinthitis, and CT may reveal a bony
defect. When there is complete loss of function,
there may be no signs or symptoms of labyrinthine dysfunction.
Management
Because a cholesteatoma is the most common
cause of this type of labyrinthitis, middle-ear and
mastoid surgery must be performed. For children
with a labyrinthine fistula owing to a cholesteatoma, a modified radical mastoidectomy may be
required. When labyrinthine function is still
present, the cholesteatoma matrix overlying the
fistula should be left undisturbed because
removal can result in total loss of function.
Even though there are advocates of performing
an intact canal wall procedure and surgeons who
prefer to remove the cholesteatoma matrix, either
during the initial surgery or in a second-stage
procedure, the approach that is the safest is
recommended when a cholesteatoma has caused
a labyrinthine fistula in a child.
Failure to diagnose this complication and perform the surgery as soon as possible may result in
complete loss of cochlear and vestibular function
with possible development of labyrinthine sclerosis
or an acute suppurative labyrinthitis. Suppurative
labyrinthitis can cause a life-threatening intracranial
complication, such as meningitis.
ossificans) in part or all of the labyrinth, with
resulting loss of labyrinthine function. Today,
this end stage of labyrinthitis is most commonly
the result of meningitis, not of otitis media. As
found in the review of CT scans by Weber and
colleagues, however, one child had labyrinthitis
ossificans in association with a congenital perilymphatic fistula, presumably secondary to otitis
media because meningitis had not occurred.29
This condition is the end stage of healing after
acute or chronic labyrinthitis, and prevention of
disease of the middle ear is the most effective way
to avoid this complication.
FACIAL PARALYSIS
Facial paralysis, as a complication of otitis media
and related diseases, is still a common problem in
infants and children.10 Facial paralysis most
commonly occurs in children during an episode
of AOM because of exposure of the facial nerve
from a congenital bony dehiscence in its tympanic portion within the middle ear (Figures 26 and
27).347 It can also be a complication of acute
mastoiditis with osteitis262 or chronic suppurative otitis media.348 When it occurs as a
complication of chronic suppurative otitis media,
Labyrinthitis Ossificans (Labyrinthine
Sclerosis)
Labyrinthitis ossificans is caused by fibrous
replacement or new bone formation (labyrinthitis
Figure 26. The course of the facial nerve in the middle ear and
mastoid. The nerve can be involved by infection in these areas, which
can result in facial paralysis.
Complications and Sequelae: Intratemporal
385
Table 13. AGE, PRESENTING SYMPTOMS, AND SIGNS IN
22 INFANTS AND CHILDREN WHO DEVELOPED ACUTE
FACIAL PARALYSIS AS A COMPLICATION OF OTITIS
MEDIA OR RELATED INFECTION: CHILDREN’S HOSPITAL
OF PITTSBURGH, 1980–1995
Characteristic
Figure 27. Infant in whom a right facial paralysis developed within a
few days after the onset of acute otitis media.
a cholesteatoma is also frequently present. On
rare occasions, it can occur in children as a
complication of otitis media with effusion.349
Also, on rare occasions, it can be bilateral after
the onset of AOM350,351 or as a complication of
acute mastoiditis.352 Not infrequently, when
facial paralysis develops during an attack of
otitis media, an underlying disease, such as
leukemia, may be present.262,353 It is not uncommon for a child who has an acute facial paralysis
to be examined in an emergency center and to be
misdiagnosed as having Bell’s palsy. All infants
and children who have an acute onset of a facial
paralysis should have a complete ear, nose, and
throat examination, which should include pneumatic otoscopy to rule out an otogenic cause of
the paralysis.354
Facial paralysis is a relatively frequent
complication of AOM in infants and children.
In the preantibiotic era, facial paralysis was
estimated to occur in 0.5% of patients with
AOM, whereas the current rate is 0.005%, as
reported in a study from Denmark.355 A review
by Goldstein and colleagues of 22 infants and
children who had facial paralysis in association
with otitis media or related infections at the
Children’s Hospital of Pittsburgh between 1980
and 1995 revealed that paralysis occurred most
frequently in children aged 6 years and younger;
50% were younger than 4 years (Table 13).262
Age (yr)
0–3
4–6
7–12
13–18
Signs and symptoms
Facial weakness
Middle-ear effusion
Otalgia
Otorrhea
Perforation of tympanic membrane
Upper respiratory tract infection
Fever
Hearing loss
Irritability
Postauricular cellulitis/mass
Number of
Patients (%)
11
6
3
2
(50)
(27)
(14)
(9)
22
16
15
8
8
8
7
2
2
2
(100)
(73)
(62)
(36)
(36)
(36)
(32)
(9)
(9)
(9)
Adapted from Goldstein NA et al.262
Facial weakness, otalgia, otorrhea, concomitant
upper respiratory tract symptoms of infection,
and fever were the most common symptoms. The
mean duration of ear symptoms and of facial
weakness on presentation to the hospital was 6
and 4 days, respectively. Two children had acute
mastoiditis with periosteitis, and one patient had
acute mastoiditis with osteitis and subperiosteal
abscess. In 18 patients (80%), initial treatment
consisted of antimicrobial therapy, and in all but
1 of these children, a myringotomy, with or
without tympanostomy tube placement, was also
performed. However, of these 22 children, 4
patients (18%) had further surgery: 2 patients
had a cortical (simple) mastoidectomy for acute
mastoiditis; 1 child who had lymphoblastic
leukemia underwent facial nerve decompression,
radical mastoidectomy, and a labyrinthectomy;
and 1 child who had had a previous mastoidectomy for cholesteatoma later developed an acute
mastoiditis with subperiosteal abscess and a
facial paralysis and had a revision tympanomastoidectomy.
In a smaller series of 10 patients who
developed facial paralysis after the onset of
AOM in Washington, DC, Elliott and colleagues
386
OTITIS MEDIA IN INFANTS AND CHILDREN
reported that 8 had an incomplete paralysis,
which resolved with only myringotomy and
intravenous administration of an antibiotic.356
Two children who had complete paralysis and
persistent fever and otorrhea despite antibiotic
treatment had a mastoidectomy. None required
decompression of the facial nerve.
Most children who have facial paralysis that
is not associated with acute mastoiditis or a
concomitant underlying disease can be treated
successfully with parenteral antimicrobial therapy, tympanocentesis, and myringotomy with or
without tympanostomy tube insertion. When it
occurs as an isolated complication, tympanocentesis and a myringotomy should be performed,
and parenteral antibiotics effective for S. pneumoniae and H. influenzae should be administered.
Insertion of a tympanostomy tube is indicated
when the child has had recurrent episodes of
AOM, when the attack AOM is superimposed on
preexisting chronic otitis media with effusion,
and whenever prolonged drainage of the middle
ear and mastoid is desirable. The paralysis will
usually improve rapidly without requiring
further surgery (eg, mastoidectomy or facial
nerve decompression).357 Mastoidectomy is not
indicated unless acute mastoiditis with osteitis
(acute ‘‘coalescent’’ mastoiditis), chronic suppurative otitis media, or cholesteatoma is present. However, if there is complete loss of facial
function and electrophysiologic testing indicates
the presence of degeneration or progressive
deterioration of the nerve, facial nerve decompression may be necessary to achieve complete
return of function.
Immediate surgical intervention is indicated
when a facial paralysis develops in a child who
has chronic suppurative otitis media, cholesteatoma, or both.
EXTERNAL OTITIS
Otitis media with perforation (also a patent
tympanostomy tube) can be associated with an
infection of the external auditory canal secondary to a discharge from the middle ear and
mastoid.358 This is external otitis; the terms acute
diffuse external otitis and acute infectious eczematoid dermatitis are also used.110 The infection
can be acute or chronic. When acute, it usually
follows an episode of AOM in which the
tympanic membrane perforates, or a chronic
perforation (without otitis media) is present and
an episode of AOM occurs. The otorrhea that
follows is then complicated by acute infection of
the external auditory canal. Similarly, when a
tympanostomy tube is in place, an attack of
AOM develops with otorrhea followed by infection of the external canal. An infection in the
mastoid may also erode the bone of the ear canal
or the postauricular area, resulting in a dermatitis.
Diagnosis
The ear canal skin is erythematous, edematous,
and filled with purulent drainage and yellowcrusted plaques, and a perforation of the eardrum (or tympanostomy tube) is present. It is
frequently difficult for the clinician to distinguish
between external otitis caused by otitis media
with otorrhea secondary to a perforation or
tympanostomy tube and acute diffuse external
otitis in which middle-ear disease is absent.
However, severe inflammatory stenosis of the
external auditory meatus owing to middle-ear
infection and otorrhea is uncommon; therefore,
it can be differentiated from the extreme tenderness and pain that are so commonly present in
acute external otitis not secondary to middle-ear
infection. When the differential diagnosis is in
doubt, the most effective way in which to make
the distinction is to clean the products of the
infection from the external auditory canal with a
suction or cotton-tipped applicator to determine
the status of the tympanic membrane. However,
the external auditory canal may be too edematous and tender to be cleaned adequately for
visualization of the entire drum. In such a
circumstance, the immediate history (eg, recent
episode of AOM) may be valuable. If a
significant hearing loss is present, in the absence
of extreme canal stenosis, it is also likely that the
patient has otitis media in association with the
Complications and Sequelae: Intratemporal
external otitis. A tympanogram can be helpful if
the canal is not too tender for insertion of the
probe tip of the instrument because a large
volume indicates a nonintact tympanic membrane. The presence of a tympanometric peak in
the normal pressure zone, even though somewhat
lower than normal, suggests a normal middle ear;
a flat pattern (with normal canal volume)
suggests the presence of a middle-ear effusion
without a perforation or patent tympanostomy
tube. Also included in the differential diagnosis
are impetigo contagiosa and a secondary infection associated with contact, or seborrheic,
dermatitis.
The external canal infection may be associated with a mass in the canal, on the tympanic
membrane, or both that is difficult to distinguish
between an aural polyp, which may be due to a
middle-ear cholesteatoma, versus a true tumor of
the ear canal.218 When a canal mass is present,
thorough cleaning of the canal and elimination
of the external canal otorrhea are critical in
confirming the diagnosis. When this procedure is
difficult in the young child or one who is
uncooperative, the patient may have to be taken
to the operating room for an examination under
general anesthesia (see Chapter 7). Appropriate
imaging of the temporal bone, biopsy, or both
may be required for a definitive diagnosis.
When the external otitis owing to otitis media
involves the pinna and postauricular area, the
condition may be misdiagnosed as acute mastoiditis with periosteitis.285,359 As described in Table
9, however, the postauricular crease is commonly
obliterated when the swelling is secondary to
external otitis, whereas the crease is maintained
when acute mastoiditis with periosteitis is present.
Microbiology
The organisms involved are usually the same as
those found in the middle-ear–mastoid infection,
but the flora of the external canal may contribute
to the infectious process. P. aeruginosa, S. aureus,
and Proteus are frequently present.192 Also,
MRSA may be the causative organism.208
387
Fungi may also be found in chronic cases—most
commonly, Aspergillus niger or Aspergillus alba.
These are bacteria similar to those isolated from
the external canals of individuals who have acute
external otitis in which the tympanic membrane
is intact.360,361
A culture of the external auditory canal
should be obtained and the results compared
with those of a needle aspiration of the middleear discharge through the tympanic membrane
perforation or the tympanostomy tube. This will
aid in determining the offending organisms.
Antimicrobial therapy can then be selected by
the results of the culture and susceptibility
testing. The infection may spread to the auricle,
periauricular area, or other parts of the body,
possibly as a result of direct implantation of the
organisms or as an autosensitivity phenomenon.
Coagulase-positive S. aureus is the most frequently involved bacterium in this type of
reaction.362
Management
Management should be directed toward resolving the middle-ear–mastoid infection. This may
require medical treatment, surgery, or both. But
the principles of treatment for otitis externa
should be followed if the skin of the ear canal
and the tympanic membrane are involved,358,363
but it should be remembered that the tympanic
membrane is not intact when this complication
occurs secondary to a middle-ear infection. The
ototopical medications listed in Table 3 can be
beneficial, but ofloxacin otic solution (Floxin)
and ciprofloxacin-dexamethasone suspension
(Ciprodex) are currently the only ototopical
agents approved by the FDA for use in children
who have a tympanostomy tube in place and
develop otorrhea.125,130 The other ototopical
drops used in the past, such as the aminoglycosides, are potentially toxic to the inner ear when
the tympanic membrane is not intact and are not
indicated.129,133,134 Ofloxacin is safe and effective, and it is approved for children (and adults)
who have external otitis.364 These topical eardrops are usually equally effective when a
388
OTITIS MEDIA IN INFANTS AND CHILDREN
perforation is present and an episode of acute
otitis occurs. It is also approved for use in adults
who have chronic suppurative otitis media. Other
combinations of an antibiotic with hydrocortisone otic drops, such as ciprofloxacin hydrochloride with hydrocortisone, may be effective
when external otitis is present and are approved
for children when the tympanic membrane is
intact and external otitis is present.365
Analgesics are usually required to control the
otalgia until the infection is under control. When
canal stenosis is present and too severe to permit
adequate application of ototopical medications,
a cotton or Mericel Pope Ear Wick may have to
be inserted into the ear canal to enhance
treatment. When the infection is severe, such as
when the patient has a high fever or is toxic, or
when the infection spreads to the pinna, periauricular areas, or cervical lymph nodes, intravenous antimicrobial therapy effective against
the offending bacterial organism is required.
Even though the oral quinolones would be a
reasonable initial treatment alternative to parenteral antibiotics at this stage, these agents are
not approved for children younger than 18 years.
Since the orally administered quinolones, such as
ciprofloxacin, have been used for many years in
children who have cystic fibrosis and appear to
be safe, these agents are a reasonable alternative
to parenteral therapy, but appropriate informed
consent should be obtained from the parent or
guardian prior to being given. But intravenous
antimicrobial therapy may have to be instituted,
which can be administered on an outpatient
basis.254
If a fungal infection is present, m-cresyl
acetate eardrops (Cresylate) may need to be
prescribed. Irrigation of the ear canal with 2%
acetic acid or frequent suctioning of the ear canal
may also hasten the resolution of the external ear
canal infection, but, again, acetic acid is not
approved for use when the tympanic membrane
is not intact. Likewise, other topical antifungal
agents, such as terbinafin hydrochloride, are not
approved when the eardrum is open. An alternative is to paint the external auditory canal with
gentian violet, being careful not to contaminate
the middle ear with this medication, but this
method is also problematic owing to a lack of
approval for use for this ear infection.
When the skin adjacent to the auricle or on
other parts of the body is involved, the skin
should be cleaned with saline solution or
aluminum acetate and treated with a local
antibiotic-corticosteroid cream. The child should
be cautioned about spread of the infection from
the ear canal to other parts of the body and
should refrain from putting his or her finger in
the ear or scratching the infected skin. Cotton in
the external ear canal can be helpful if profuse
drainage is present but should be changed as
frequently as necessary. One recently reported
randomized trial found that medicated ribbon
gauze inserted into the external canal facilitates
cure more effectively and less costly than the
customary insertion of ear wicks, but this study
was conducted in patients with external otitis and
presumably an intact eardrum.366
The acute infection can become chronic,
which requires a thorough investigation of the
pathogenesis and etiology to rule out chronic
middle ear and mastoid disease.122
Strategies to prevent recurrence of this
complication of otitis media are similar to those
described for when AOM or chronic suppurative
otitis media occurs in the presence of a perforation of the eardrum or tympanostomy tube (see
‘‘Perforation of the Tympanic Membrane’’).
ATELECTASIS OF THE MIDDLE EAR (WITH
AND WITHOUT A RETRACTION POCKET)
Atelectasis of the middle ear—which includes the
tympanic membrane—is a sequela of eustachian
tube dysfunction. The condition, as the term
implies, occurs when there is recurrent or chronic
underpressure in the middle ear, which results in
retraction or collapse of the tympanic membrane.
Retraction of the tympanic membrane may be
attributed to the presence of high negative
middle-ear pressure; retraction of the tympanic
membrane can also occur in the absence of
middle-ear negative pressure. A flaccid, atelectatic tympanic membrane may or may not be
Complications and Sequelae: Intratemporal
associated with high negative intratympanic
pressure; the abnormal negative pressure may
have been the original cause of such a condition
of the membrane but may no longer be present.
Also, a middle-ear effusion may or may not be
present. The term atelectasis has been borrowed
from the pulmonary disorder atelectasis of the
lung.
Unfortunately, there have been no reports
of studies of the incidence of atelectasis and
retraction pockets. However, a retraction pocket
is a common sequela of atelectasis of the
tympanic membrane with or without otitis media
with effusion.367 As a sequela of tympanostomy
tube insertion, retraction pockets at the site of
the extruded tube are common and are more
prevalent in older children, adolescents, and
adults as a long-term aftermath of tubes than in
young children.368 The incidence in individuals
with cleft palates must be greater than that of
cholesteatoma in this population (7.1%) because
a retraction pocket precedes the development of
a cholesteatoma in children with cleft palate.369
Pathogenesis
Atelectasis of the middle ear is the result of
transient or chronic underpressure within the
middle ear, which, in turn, is caused by
eustachian tube dysfunction. The dysfunction is
most commonly failure of opening of the
eustachian tube, anatomic obstruction, or both;
in some individuals, it may be secondary to
habitual sniffing in the presence of a tube that
fails to close.370 Because the eustachian tubes of
individuals with chronic atelectatic middle ears
can be successfully inflated, the tube is not
anatomically obstructed.371 Thus, the tube is
more likely to be functionally obstructed, that is,
there is a failure of the opening mechanism.369,372
An alternative but less convincing hypothesis for
the pathogenesis is related to the persistence of
mesenchyme or an inflammatory reaction, secondary to otitis media, in the middle ear,
especially in the posterosuperior quadrant of
the pars tensa and the pars flaccida, two sites that
commonly develop partial atelectasis with a
389
retraction pocket.373 However, these two portions of the tympanic membrane are the most
compliant areas of the eardrum374 and thus most
likely to retract when there is significant underpressure within the middle ear. In some children,
these deformations of the tympanic membrane
are seen when chronic otitis media with effusion
is present.375 Retraction pockets are also not an
uncommon sequela after extrusion of tympanostomy tubes. The pocket occurs when the
tympanic membrane has a dimeric membrane at
the tube site, and if eustachian tube dysfunction
persists, the membrane retracts because it is more
compliant than before the tube was inserted.
Thus, retraction pockets occur at naturally
floppy portions of the tympanic membrane
(posterosuperior quadrant and pars flaccida) or
at the site of an acquired defect, such as a dimeric
membrane from a previously inserted tube or the
site of a healed spontaneous perforation.
In studies of children who have retraction
pockets, the eustachian tube was determined to
have a failure of the opening mechanism, that is,
functional obstruction (see Chapter 3).376 This
sequela of eustachian tube dysfunction or otitis
media increases with advancing age.368,377 If the
atelectasis is persistent and progressive, it can
lead to sequelae such as hearing loss, ossicular
chain discontinuity, and cholesteatoma. All are
described in this chapter.
Also, an atelectatic middle ear can have
positive pressure in the middle ear,378 but this
phenomenon may be due to insufflation of gas
from the nasopharynx during closed-nose swallowing (ie, Toynbee phenomenon) or from forced
inflation (eg, Valsalva’s maneuver) of the eustachian tube–middle ear in an effort to improve
hearing and treat middle-ear pressure sensation;
even though positive pressure is within the
middle ear, dysfunction of the eustachian tube
is still the underlying pathogenic mechanism.
Diagnosis and Classification
The diagnosis of atelectasis is only by visual
inspection with the aid of either an otoscope or
otomicroscope; tympanometry is not diagnostic.
390
OTITIS MEDIA IN INFANTS AND CHILDREN
The tympanic membrane is deformed. Atelectasis
of the middle ear can be acute or chronic; partial
(localized), which may or may not be a retraction
pocket, or total (generalized); and mild, moderate, or severe. Partial atelectasis, with or without
a retraction pocket, may also be visualized in an
area of a healed perforation or at the site where a
tympanostomy tube had been inserted (‘‘atrophic
scar’’ or dimeric membrane).10 A retraction
pocket in the posterosuperior quadrant of the
pars tensa or a pars flaccida retraction pocket is
more frequently associated with the development
of more serious sequelae (ossicular discontinuity,
cholesteatoma, or both) than is a retraction
pocket in other areas of the tympanic membrane.
As described later, these variations should be
kept in mind in deciding how to manage
atelectasis.
It is appropriate to classify, grade, and stage
atelectasis of the middle ear, as visualized by the
clinician, according to its extent, severity, and
duration because these factors are related to
management decisions. The following is a proposed classification:
Partial atelectasis is a localized area of the
tympanic membrane that is atelectatic, which
may or may not be a retraction pocket because
the depth of the retraction can be mild,
moderate, or severe. When partial, in the
absence of a retraction pocket, it may be in
one or more of the four quadrants of the pars
tensa (ie, anterosuperior, anteroinferior, posterosuperior, posteroinferior), in the pars
flaccida, or in both the pars tensa and the
pars flaccida.
A retraction pocket is characterized by a
partial area of atelectasis of the tympanic
membrane in which there is indrawing of the
membrane forming borders (ie, an edge or
margin), most frequently at the site of an
osseous anatomic structure (eg, notch of
Rivinus or scutum) or the malleus.379 A
retraction pocket can be in one or more of
the four quadrants of the pars tensa, in the
pars flaccida, or both and can be acute or
chronic or reversible or irreversible. Sadé
proposed a classification of a posterosuperior
retraction pocket that is helpful but does not
include duration, the presence or absence of
adhesive changes (which relates to reversibility), or other sites.380 Tos and Poulsen
classified attic retraction pockets in relation
to their extent and severity.377
The stages of retraction pockets are
divided into acute (less than 3 months in
duration) and chronic (3 months or longer in
duration). Key factors that affect the progression
of a retraction pocket from stage 1 to stage 4 are
the following:
1. Relation to middle-ear structures: The pocket
does or does not approximate (touch) or is
not adherent (ie, adhesive otitis media) to an
ossicle (ie, incus, incudostapedial joint,
stapes, head of malleus, or incudomallear
joint) or other middle-ear structure, such as
the promontory of the cochlea.
2. Expands with pressure: The entire pocket does
or does not easily expand to the normal
position when negative pressure is applied
with a pneumatic otoscope or with the
Bruening otoscope with a nonmagnifying
lens under the otomicroscope, or when
positive pressure is applied when the patient
is anesthetized with nitrous oxide.
3. Extent visualized: The entire pocket is visualized or parts are not seen even after pressure
is applied. This is because the pocket extends
beyond the visible portion of the middle-ear
space (eg, sinus tympani, facial recess, epitympanum, or medial to other parts of the
tympanic membrane).
4. Self-cleansing and free of infection: Epithelial
debris, crusting, or purulent material is or is
not within the pocket.
Total atelectasis can be acute (less than 3
months in duration) or chronic (3 months or
longer in duration). It involves all four quadrants
of the pars tensa, with or without involvement of
the pars flaccida, and can be staged as follows:
Stage 1a, acute total mild atelectasis: middle
ear aerated
Complications and Sequelae: Intratemporal
Stage 1c, chronic total mild atelectasis: same as
stage 1a but chronic
Stage 2a, acute total severe atelectasis: middle
ear not aerated (ie, no apparent middle-ear
space)
Stage 2c, chronic total severe atelectasis: same
as stage 2a but chronic
Management
When atelectasis of the tympanic membrane is of
relatively recent onset, a middle-ear effusion may
or may not be present, and a retraction pocket is
absent, current management options are of
uncertain benefit and are controversial.381
There have been no clinical trials reported that
have addressed the efficacy of the various
treatments compared with no treatment. (The
decisions related to actively treat or not to treat
and the treatment options when an effusion of
short duration is present are discussed in detail in
Chapter 8.) Total atelectasis, or even a partial
area that is retracted for only a short time (acute
retraction), is usually caused by transient high
negative middle-ear pressure associated with an
acute upper respiratory tract infection or barotrauma. This condition is common in children
and adolescents and is usually self-limited. No
specific treatment should be directed toward the
middle ear unless the child complains of severe
otalgia, hearing loss, tinnitus, or vertigo. The
atelectasis (and high negative intratympanic
pressure) and associated symptoms, if present,
will usually subside when the acute upper respiratory tract infection disappears. Treatment
at this time should be directed toward relief of
the nasal symptoms. Topical or systemic nasal
decongestants may provide relief of these symptoms and may also relieve congestion of the
eustachian tube, although their effectiveness in
this latter area has not been demonstrated. If the
symptoms become severe, myringotomy may be
necessary to provide relief by returning middleear pressure to ambient levels, such as when
the atelectasis is secondary to barotrauma (see
391
Chapter 8). Middle-ear inflation through the
eustachian tube has been advocated, but as
described later, when atelectasis progresses to
the chronic stage, this method of management is
of uncertain benefit. Thus, watchful waiting is
appropriate.
When the atelectasis is chronic (with or
without the presence of chronic otitis media with
effusion) and there is no evidence of a deep
retraction pocket in the posterosuperior quadrant or pars flaccida, a thorough search should
be made for an underlying origin, such as
hypertrophied adenoids, nasal allergy, or paranasal sinusitis. If none is found, the management
options are either watchful waiting or active
treatment. (See also Chapter 8, when chronic
otitis media with effusion is present.) The
decision for or against treatment should rest on
the presence or absence of other associated
symptoms and whether there is abnormal negative pressure within the middle ear. The presence
of persistent or transient otalgia, hearing loss,
vertigo, or tinnitus that is troublesome to the
patient warrants active treatment. For chronic
atelectasis in this case, a trial with a topical or
systemic nasal decongestant with or without an
antihistamine may be helpful. However, this type
of treatment is often disappointing.
Inflation of the eustachian tube–middle-ear
system by use of the Valsalva or Politzer method
has been advocated when middle-ear effusion is
present.382 However, studies in animals indicate
that these methods will not return the middle-ear
pressure to normal for a sustained period when
the eustachian tube is functionally obstructed.245
A clinical trial conducted by Chan and Bluestone
also failed to show efficacy of middle-ear
inflation in 41 children who had chronic
middle-ear effusion with use of a specially
designed inflation device.383,384 Kaneko and
colleagues also failed to show consistent and
sustained improvement after inflation in children
who had middle-ear effusion.385
Inflation of the eustachian tube and middle ear
may provide temporary relief of atelectasis, in
which no effusion is present, but must usually be
repeated for permanent control of the symptoms
392
OTITIS MEDIA IN INFANTS AND CHILDREN
and to maintain the tympanic membrane in a more
normal position. However, Luntz and Sadé
inflated the middle ears of individuals with chronic
atelectasis with either air or nitrogen for up to 5
consecutive days and found that the eardrum
returned to its former atelectatic position within 15
minutes to 5 hours after the inflation.386 Yung
used nasal continuous positive airway pressure in
patients with atelectasis and reported a short-term
benefit but did not study the long-term effect.387
Doyle and Alper explained this phenomenon using
a mathematical model.388
When a chronic retraction pocket or total
atelectasis is present and nonsurgical methods
of management have failed, myringotomy and
insertion of a tympanostomy tube should be
performed to prevent possible irreversible
changes in the middle ear. After insertion of a
tympanostomy tube, the tympanic membrane in
the area of the retraction pocket should return to
a more neutral position within several weeks or
months. If the retraction area remains adherent
to the ossicles, middle ear, or both (Figure 28),
adhesive otitis media is present (see ‘‘Adhesive
Otitis Media’’), and tympanoplasty should be
considered to prevent further progression of the
disease process (such as ossicular discontinuity,
cholesteatoma formation, or both). To prevent a
recurrence of the retraction pocket (or total
atelectasis), in addition to tympanostomy tube
insertion, a portion of cartilage (from the pinna)
placed over the affected area is effective. Even
though this method of management has not been
tested in appropriately controlled clinical trials
and the natural history of retraction pockets in
these areas has not been adequately studied, this
method of management appears to be reasonable.152,376
When a flaccid tympanic membrane is
passively collapsed on the ossicles and middle
ear and high negative middle-ear pressure is not
present, the nonsurgical and surgical management options described before may not be
effective in restoring the tympanic membrane to
a more normal position. Fortunately, symptoms
of high negative middle-ear pressure and eustachian tube obstruction are frequently absent, so
Figure 28. When a retraction pocket is in the posterosuperior
portion of the pars tensa of the tympanic membrane and adhesive
otitis media is not present between the eardrum and ossicles, the
insertion of a tympanostomy tube may return the tympanic
membrane to the neutral position. If adhesive otitis media is present,
however, the retraction pocket will persist in spite of the presence of
a tympanostomy tube and middle-ear ventilation.
no treatment may be necessary. Even myringotomy and tympanostomy tube insertion may not
be beneficial because the tympanic membrane is
no longer actively being retracted by high
negative middle-ear pressure. In addition, at this
stage, adhesive otitis media may also be present,
and portions of the tympanic membrane may be
adherent to the middle ear. The posterior or
epitympanic (attic) portions of the middle ear
may become separated from the anterior portion
by adhesions, and, subsequently, ventilation
from the eustachian tube or a tympanostomy
tube does not aerate the affected area. In such
cases, there are two management options: tympanoplasty or periodic observation (once or
twice a year).
Tympanoplasty
In selected cases in which severe atelectasis is
present, a tympanoplastic procedure may be
indicated. The surgical procedures recommended
Complications and Sequelae: Intratemporal
are described in detail elsewhere.9 The most
compelling indication for such a procedure is the
presence of a deep retraction pocket in the
posterosuperior portion of the pars tensa that is
unresponsive to nonsurgical and other surgical
methods of management previously described for
this defect. For example, if a tympanostomy tube
had been inserted previously but the retraction
pocket did not return to the neutral position after
several months of equalization of the intratympanic pressure, tympanoplasty should be considered because adhesive otitis media is most
likely binding the drum to the ossicles and
surrounding structures within the middle ear.
Even though the natural history of such deep
retraction pockets has not been formally studied,
the risk of erosion necrosis of the incus,
formation of a cholesteatoma, or both appears
to be high. It is frequently difficult to determine
whether there is only a retraction pocket present
or if a cholesteatoma has already developed;
therefore, a thorough examination of the entire
external canal and tympanic membrane should
be performed with the otomicroscope. An
examination under general anesthesia will be
required for all infants and children in whom the
examination is unsatisfactory without general
anesthesia. At the time of the examination under
anesthesia, a thorough examination of the
retraction pocket, employing a curved, blunt
probe, should be performed to determine the
extent of the pocket. In addition, the continuity
of the incus and stapes should be assessed
because erosion of the long process of the incus
may require surgical correction. When nitrous
oxide is employed as one of the anesthetic agents,
the retraction pocket can frequently be seen to
balloon laterally, as visualized through the
otomicroscope. When this occurs, insertion of
the tympanostomy tube will usually be sufficient
to prevent recurrence of the retraction pocket.
Reinsertion of the tube may be needed, however,
if the retraction pocket recurs after spontaneous
extubation.
Many techniques are advocated for repair of
a severely atelectatic tympanic membrane, many
of which have been shown to be successful.389,390
393
The surgeon should be cautioned, however, that
even though the graft ‘‘takes,’’ the child will most
likely have persistent eustachian tube dysfunction with sustained fluctuating or negative
intratympanic pressure after the procedure,
which could result in recurrence of the retraction
pocket months or years later. Therefore, a
tympanostomy tube should be inserted at the
time of the tympanoplastic surgery and reinserted if atelectasis begins to recur after the
tympanostomy tube is spontaneously extruded.
Some surgeons prefer use of tragal or conchal
cartilage attached to its perichondrium to cover
the area of the retraction pocket so that
recurrence of an attic or posterosuperior retraction pocket can be prevented.152,391,392
All children who require tympanoplasty for
severe atelectasis must be observed at relatively
frequent intervals for the first year after the
procedure and at appropriate intervals for
several succeeding years. Recurrence of the
atelectasis should always be anticipated.
ADHESIVE OTITIS MEDIA
Adhesive otitis media is a sequela of recurrent
and chronic inflammation of the middle ear and
mastoid and is a result of the healing process.
The mucous membrane is thickened by proliferation of fibrous tissue, which frequently impairs
(binds) the movement of the ossicles, resulting in
a conductive hearing loss.393
Adhesive otitis media can be classified
according to three stages related to the severity,
extent, and presence or absence of functional
impairment10:
Stage 1: adhesive otitis media within the
middle ear, mastoid, or both, with no functional deficit secondary to the adhesive
changes (ie, hearing loss). The middle ear
remains aerated.
Stage 2: adhesive otitis media within the
middle ear (with or without mastoid involvement) with mild hearing loss secondary to an
adhesive pathologic process, such as involvement of the ossicular chain (fixation, disconti-
394
OTITIS MEDIA IN INFANTS AND CHILDREN
nuity, or both; see ‘‘Ossicular Discontinuity
and Fixation’’), limitation of tympanic membrane compliance, or both. The middle ear
remains aerated.
Stage 3: similar to Stage 2 but with maximal
conductive hearing loss secondary to an
ossicular pathologic process. No middle-ear
space is present. Both conditions are due to
extensive adhesive otitis media.
Pathology and Pathogenesis
Schuknecht has described the pathologic process
as a proliferation of fibrous tissue within the
middle ear and mastoid and has termed the
condition fibrous sclerosis.217 When cystic spaces
are present, it is called fibrocystic sclerosis; when
there is new bone growth in the mastoid, he has
classified it as fibro-osseous sclerosis.
The etiology and pathogenesis have not been
extensively studied in the past. Caye-Thomasen
and colleagues, in experiments in animals,
proposed that adhesive otitis media is a pathologic phenomenon caused by infection in six
pathogenic stages394:
1. Localized epithelial rupture
2. Prolapse of subepithelial tissue
3. Epithelialization of the prolapse, resulting in
a polypoid, fold-like prominence
4. Growth and elongation of the prominence
5. Fusion of the end tip of the prominence with
another part of the mucosa
6. Formation of an adhesion
Management
No data are currently available on the prevalence
of adhesive otitis media in children, but the
condition is commonly encountered in the pediatric
age group when recurrent or chronic middle-ear
disease has been a long-standing problem. Unfortunately, we likewise have no data from which to
establish the probability with which a child who
has recurrent or chronic disease of the middle ear
might develop adhesive otitis media. However, the
possible occurrence of adhesive changes when
recurrent or chronic inflammation—including
atelectasis of the middle ear—is present in the
middle ear and mastoid must be seriously considered in selecting the most appropriate medical or
surgical treatment of children who have recurrent
acute and chronic middle-ear disease.
In addition to fixation of the ossicles, adhesive otitis media may result in ossicular discontinuity and conductive hearing loss owing to
rarefying osteitis, especially of the long process
of the incus. When there is a retraction pocket
(severe partial atelectasis) in the posterosuperior
portion of the pars tensa of the tympanic
membrane, adhesive changes may bind the eardrum to the incus, stapes, and other surrounding
middle-ear structures and cause resorption of the
ossicles. Once adhesive changes bind the tympanic
membrane in this area, a cholesteatoma may also
develop. Timely ventilation of the middle ear and
mastoid before the adhesive changes may return
the tympanic membrane to the normal position,
thus preventing ossicular damage. If medical
treatment fails, a myringotomy should be performed, and a tympanostomy tube should be
inserted in an attempt to reverse the potentially
progressive pathologic condition (see Figure 28).
If the tympanic membrane is still attached to the
ossicles after tympanostomy tube insertion,
adhesive otitis media is present. In children,
tympanoplasty should be considered to prevent
further structural damage; the process may progress because of persistent eustachian tube
obstruction.
When ossicular fixation occurs, ossiculoplasty may be performed to restore function,
but, unfortunately, this procedure is not always
successful. When the middle ear and mastoid are
bound by adhesive otitis media, the results of
ossiculoplasty are frequently not permanent
because the adhesive process recurs. However,
surgery should be considered.
The best method of management for adhesive
otitis media is prevention. This involves treating
its precursors: recurrent AOM, chronic otitis
media with effusion (see Chapter 8), and atelectasis (see earlier).
Complications and Sequelae: Intratemporal
CHOLESTEATOMA
Cholesteatoma is keratinizing stratified squamous epithelium and an accumulation of desquamating epithelium of keratin within the
middle ear or other pneumatized portions of
the temporal bone. This disease has also been
called a keratoma, but cholesteatoma is the more
commonly used term.395 Cholesteatoma is histologically similar to epithelium of the skin of the
external auditory canal.
Classification
Aural cholesteatoma can be classified as congenital and acquired. Cholesteatomas can be
acquired as a sequela of middle-ear disease or
from implantation, which can be due to either
trauma or related surgery of the middle ear
(including the tympanic membrane), external
auditory canal, or mastoid (ie, iatrogenic).
A congenital cholesteatoma has been defined
as a congenital rest of epithelial tissue and
appears as a white, cyst-like structure within
the middle ear (intratympanic) or temporal bone.
The tympanic membrane is intact, and it is
apparently not a sequela of otitis media or
eustachian tube dysfunction.396,397 Rosenfeld
and colleagues reviewed the records of 232
children in Pittsburgh who had cholesteatoma
and identified 43 (18%) patients in whom the
cholesteatoma was thought to be congenital in
origin.398 Possibly more would have been diagnosed as congenital, but in 46% of the children,
the distinction between acquired and congenital
origin could not be made owing to the advanced
stage of the disease.
Acquired cholesteatoma may be secondary to
implantation, or it may be a sequela of otitis
media or a retraction pocket. Implantation
cholesteatoma may develop from epithelium that
has migrated through a traumatic perforation of
the tympanic membrane (or the site of a
tympanostomy tube) or that has inadvertently
been overlooked in the middle ear or mastoid
during surgery of the ear (iatrogenic).399
Iatrogenic cholesteatoma can develop in the ear
395
canal after middle-ear and mastoid surgery at the
site of the incisions made in the canal and can
occur after any of the various incisions.
The most common cholesteatoma is the
acquired type, which is a sequela of middle-ear
disease. In a study of 1,024 patients (adults
and children), a cholesteatoma was found in 42%
in the attic, in 31% in the posterosuperior
quadrant, in 18% when there was a ‘‘total’’
perforation, in 6% when there was a ‘‘central’’
perforation, and in 3% when there was no
perforation.400 However, it is possible that the
patients in whom the cholesteatoma was associated with a total perforation originally had
involvement of the posterosuperior portion of
the pars tensa. In children, the most common
defect in the tympanic membrane begins developing in the posterosuperior quadrant of the pars
tensa or, somewhat less commonly, in the pars
flaccida. The term marginal perforation has been
used to describe the defect in the posterosuperior
quadrant, and the defect in the pars flaccida has
been called an attic perforation, but in reality,
these are most frequently not perforations but
are either retraction pockets or cholesteatomas
that appear otoscopically to be perforations
(Figure 29). No continuity between the defect
and the middle ear occurs until later in the
disease process.
Staging of Acquired Cholesteatoma
It is appropriate to stage cholesteatomas for
management, reporting, and research. Staging
can be extremely helpful in determining the
outcomes of surgery, such as residual and
recurrence rates, from center to center around
the world.401,402 In staging of cholesteatoma, the
presence or absence of infection should be noted
and, if present, the duration of the otitis media as
follows10,320:
Cholesteatoma without infection is a cholesteatoma that is not associated with infection,
either within the cholesteatoma itself or in any
other portion of the middle-ear cleft
396
OTITIS MEDIA IN INFANTS AND CHILDREN
Figure 29. Evolution of acquired
attic cholesteatoma. A, Attic retraction pocket, which appears on otoscopic examination to be a
perforation. B, Narrow neck sac
developing. C, Enlargement of the
sac with erosion of the ossicles. D,
Large cholesteatoma sac, a portion of
which can be seen through the eardrum.
Cholesteatoma with infection is a cholesteatoma that is associated with infection, which
can be either acute infection (with or without
otorrhea) or chronic. The most common
infection associated with cholesteatoma is
chronic suppurative otitis media.
Cholesteatoma can be further classified by its
site and extent:
Stage 1: Cholesteatoma is confined to the
middle ear (hypoepitympanum and mesoepitympanum), without erosion of the ossicular
chain
Stage 2: Same as stage 1 but with erosion of
one or more ossicles
Stage 3: Middle ear and mastoid gas cell
system are involved without erosion of the
ossicles
Stage 4: Same as stage 3 but with erosion of
one or more ossicles
Stage 5: Extensive cholesteatoma of the middle
ear, mastoid, and other portions of the
temporal bone, the extent of which is not
totally accessible to surgical removal (eg,
medial to labyrinth), with one or more ossicles
involved. Fistula of the labyrinth may or may
not be present.
Stage 6: Same as Stage 5, but cholesteatoma
extends beyond the temporal bone
Epidemiology, Complications, and Sequelae
Cholesteatoma has persisted as a sequela of
middle-ear disease in adults and children despite
the advent of the widespread use of antimicrobial
agents and tympanostomy tubes during the past
half-century. However, the mortality associated
with cholesteatoma has fallen dramatically during this period in the developed countries of the
world.
In an epidemiologic study from Michigan,
Ritter compared 152 adults and children who
had cholesteatoma identified during the period
from 1965 to 1970 with 303 cases from a similar
study in Massachusetts that were identified
during a period before the use of antimicrobial
agents (1925–1936).403 He found in both series
that about 45% of cases of cholesteatoma were
operated on before the patient was 20 years old;
that in approximately 65% of the patients, the
aural discharge had begun by the age of 11 years;
and that the distribution of sites on the tympanic
membrane where the defect was located was
about the same. He concluded that antimicrobial
agents had not altered the incidence and natural
Complications and Sequelae: Intratemporal
history of cholesteatoma during the 40 years
between the two studies. However, Rigner and
colleagues concluded that in the Gothenburg
area of Sweden, the incidence declined during a
10-year period between 1977 and 1986; they
attributed the fall in cases to better accessibility
to specialists and improved methods to diagnose
middle-ear disease earlier in that community
compared with other parts of their country.404
The epidemiology of cholesteatoma in children has been reported by several investigators
during the past several decades. Harker and
Koontz, in a study of the general population in
Iowa, reported the overall incidence of cholesteatoma to be 6 per 100,000; in children up to 9
years of age, the incidence was 4.7 per 100,000,
whereas in children 10 to 19 years old, the
incidence of 9.2 per 100,000 was the highest for
all age groups.405 Karma and colleagues in
Finland and Tos in Denmark estimated the
annual incidence of cholesteatoma to be 4.5
and 15 per 100,000 children, respectively.406,407
In a more recent report from Finland, the mean
annual incidence of cholesteatoma during the
period from 1982 to 1991 in one region for all age
groups was 9.2 per 100,000 inhabitants (range
3.7–13.9).408
Cholesteatoma is a common sequela in
children with a cleft palate. Severeid reviewed
the records of 160 children and young adults with
a cleft palate (70% were aged 10 to 16 years), all
of whom had had a history of ear disease, and
found the incidence of cholesteatoma to be
7.1%.409 The posterosuperior portion of the pars
tensa was the most common site. A later review
from the same institution reported that almost
10% of children with a cleft palate developed
cholesteatoma.410 During a recent 10-year period
in Finland, of 500 patients who had cholesteatoma, 8% had a cleft palate.408
In contrast to this high incidence of cholesteatoma in the cleft palate population is the rare
occurrence of cholesteatoma in Alaskan
(Eskimo) natives, American Indians,411 and
Australian Aboriginal children,412 in whom other
middle-ear disease is common. This remarkable
difference in the incidence of cholesteatoma in
397
children with a cleft palate and in certain racial
groups, both of which have a high prevalence
and incidence of otitis media, is most probably
related to differences in the pathogenesis and
natural history of the respective middle-ear
disease processes (see Chapter 3).
Before the widespread use of antimicrobial
agents and modern otologic surgery, complications of cholesteatoma were common. For many
children, the result was death when infection
involved the intracranial cavity. Now, serious
complications of cholesteatoma in children are
uncommon in the developed countries of the
world. In a study of 181 children who had
cholesteatoma, 8 (4.4%) developed a labyrinthine
fistula and 1 suffered facial paralysis, but none
had intracranial complications.400 However, in
the same study, which also included 843 adults,
the incidence of both intratemporal and intracranial complications increased the longer the
cholesteatoma was present. Because most of the
adults could date the onset of their disease to
childhood and because the best way of preventing serious complications of cholesteatoma is by
diagnosis and surgery, physicians dealing with
ear problems in children should treat suspected cholesteatoma early and aggressively.
Nevertheless, intratemporal complications and
sequelae are still a problem in even the highly
industrialized nations of the world.
The rate of cholesteatoma, and especially its
complications, in developing countries is relatively high compared with that in industrialized
nations. Prescott reported his experience in
treating 81 children who had cholesteatoma from
1988 to 1996; 24 (30%) presented with mastoiditis, and 7 (9%) had an intracranial complication.413 In that study, 56 (70%) of the
cholesteatomas were from a retraction pocket,
and 21 (25%) were from a central perforation or
total atelectasis; 3 were congenital (see Chapter
10).
Sequelae, such as ossicular involvement,
which not only contribute to the associated
conductive hearing loss but are related to the
residual and recurrence rates, are common.398
Cholesteatoma with chronic suppurative otitis
398
OTITIS MEDIA IN INFANTS AND CHILDREN
media has also been shown to be associated with
sensorineural hearing loss.414
Pathogenesis
The pathogenesis of acquired middle-ear cholesteatoma is a subject of continuing controversy,
but most likely there is more than one pathogenetic mechanism. Of the many hypotheses
proposed to explain the pathogenesis of cholesteatoma, the most popular are (1) metaplasia of
the middle ear and attic owing to infection415,416;
(2) invasive hyperplasia of the basal layers of the
meatal skin adjoining the upper margin of the
tympanic membrane417–421; (3) invasive hyperkeratosis of the deep external auditory canal422;
and (4) retraction or collapse of the tympanic
membrane with invagination secondary to eustachian tube dysfunction.423–425 In addition, there
are those who consider the condition not to be
acquired but to be an embryonic epidermal rest
occurring in the attic.426–428 Thus, it is apparent
that there are probably several ways in which
cholesteatoma can develop.429
In a study from Pittsburgh, varying degrees of
functional rather than mechanical (anatomic)
obstruction of the eustachian tube were found in
13 children and adults who had a retraction
pocket or an acquired cholesteatoma.376 Subsequently, from the same center, the findings in
12 children with acquired cholesteatoma, all of
whom had functional obstruction of the eustachian tube, were also reported by the same
group.430 Children were specifically studied
because the development of an acquired cholesteatoma with its attendant irreversible changes
was thought to occur early in life and because the
function of the eustachian tube might improve
with growth and development. In these children,
the function of the eustachian tube was assessed by
the modified inflation-deflation technique (after
Ingelstedt and colleagues431). Bluestone and colleagues and Chan and colleagues performed two
other studies to further clarify the cause of this
functional obstruction by employing a new test of
eustachian tube function, the forced-response
test,433 and to evaluate a larger group of children
who had either a cholesteatoma or a retraction
pocket.369,372 In addition, children with an apparent congenital cholesteatoma were also studied,
and the results obtained in both groups were then
compared with the results of testing children who
had traumatic perforation of the tympanic membrane but who were otherwise considered otologically normal. Another goal of these studies was to
determine whether there were any differences in
eustachian tube function among ears with a
posterosuperior or pars flaccida retraction pocket
or cholesteatoma, ears with a central perforation
and a cholesteatoma, and ears with congenital
cholesteatoma.
In a study from Sweden, Lindeman and
Holmquist showed similar findings in adults with
acquired cholesteatoma.433 Compared with
adults with traumatic perforations (ie, control
subjects), 20 adults with cholesteatoma had poor
eustachian tube test results and smaller mastoid
air cell areas as measured on radiographs.
It appears from these studies that the basic
problem in children with acquired cholesteatoma
is a failure of the opening mechanism of the
eustachian tube. This results in a functional
obstruction of the tube during swallowing
rather than normal dilation of the tube. (This
type of functional obstruction of the eustachian
tube was present in subjects with a retraction
pocket or cholesteatoma irrespective of the site.)
In the absence of obstruction of the middle-ear
end of the tube by cholesteatoma, anatomic
(mechanical) obstruction is not involved in the
pathogenesis. Abnormal functioning of the tube
then results in impaired ventilation of the
middle-ear–mastoid air cell system, which, in
turn, results in fluctuating or sustained high
negative middle-ear pressure. Periodic, rather
than regular, ventilation could result in wide
variations in middle-ear pressure that would
produce greater than normal excursions of the
tympanic membrane. The membrane would then
lose elasticity and would become flaccid and,
eventually, atelectatic. The most flaccid parts of
the tympanic membrane are the posterosuperior
and pars flaccida areas.374 When the atelectasis
becomes severe and localized in these sites, a
Complications and Sequelae: Intratemporal
retraction pocket forms. Inflammation between
the medial portion of the retracted or collapsed
tympanic membrane could then result in adhesive changes and could fix the pocket to the
ossicles, surrounding structures, or both. The
next stage in this series of events would be
discontinuity of the ossicles, cholesteatoma formation, or both. Figure 30 shows the progression
from the stage of a retraction pocket with
atelectasis to adhesive otitis media and, finally,
to cholesteatoma in the posterosuperior quadrant of the pars tensa and pars flaccida.
Even with the aid of the otomicroscope, it
is frequently difficult to make the distinction
between a deep retraction pocket and a cholesteatoma in either the posterosuperior quadrant
of the pars tensa or the pars flaccida (Figure 31).
The transition between the two conditions
usually follows a progressive change from a
retraction pocket to cholesteatoma; however, the
factors involved in this transition are currently
obscure, although infection within the retraction
pocket–sac appears to be important.
A cholesteatoma can also develop at the site
of a central perforation. Most likely this is due
to migration of epithelium from the tympanic
membrane through the perforation and into the
middle ear. However, it must be stressed that in
children, this type of acquired cholesteatoma is
less common than the posterosuperior or attic
type.
Congenital cholesteatoma is classically differentiated from acquired when the tympanic
membrane is intact and the child does not have
a history of otorrhea or has had middle-ear
surgery.434,435 But it is often difficult to distinguish between acquired and congenital choleateatoma, especially when the cholesteatoma is
extensive and the tympanic membrane is
involved.398,436 There is some uncertainty as to
the origin of congenital cholesteatomas. Some
authorities consider them to be truly congenital
in origin because there is epidermoid formation
in the fetus middle ear, which then presumably
disappears prior to birth.437 But children who
have an intratympanic cholesteatoma may have
had otitis media. On the one hand, it could be
399
Figure 30. Chain of events in the pathogenesis of acquired aural
cholesteatoma in the posterosuperior portion of the pars tensa of the
tympanic membrane.
argued that intratympanic cholesteatoma is the
result of metaplasia secondary to middle-ear
inflammation and that it is not congenital.438,439
Also, a cholesteatoma behind an intact tympanic
membrane could have been due to a retraction
pocket that subsequently resolved, leaving the
tympanic membrane without evidence of the
400
OTITIS MEDIA IN INFANTS AND CHILDREN
Figure 31. Sequence of events leading from a localized area
of atelectasis (retraction pocket) in the posterosuperior portion of
the pars tensa of the tympanic membrane to a cholesteatoma
and ossicular discontinuity. Adhesive otitis media in this area is
shown as the stage between atelectasis and the development of a
cholesteatoma.
pocket.440 On the other hand, otitis media, when
present, may be unrelated to a congenital rest.
The fact that children who have congenital
cholesteatomas tend to be younger than those
who present with a retraction pocket or acquired
cholesteatoma would support the congenital
origin of a cholesteatoma medial to an intact
tympanic membrane.398 In any event, most
acquired cholesteatomas not due to implantation
are secondary to otitis media. a retraction
pocket, or both, and some children who have
an apparently congenital cholesteatoma may
have developed the disease in the same way.441
Levenson and colleagues believe that the pathogenesis of congenital cholesteatoma is an epithelial rest, which is stimulated to grow by otitis
media.442 Some surgeons believe that since
congenital cholesteatomas commonly occur in
two different sites (ie, anterosuperior and posterosuperior mesotympanum), they have a different
pathogenesis.443
Studies reveal that inflammatory factors,
such as cytokines, adhesion molecules, tumor
necrosis factor a, and the nuclear phosphoprotein TP53 tumor suppressor gene, may play a
role in invasion, migration, and proliferation of
congenital and acquired cholesteatoma.444–448
Also, erbB-2 protein, nitric oxide, bone morphogenetic protein 2 messenger ribonucleic acid,
telomerase activity, angiogenesis and angiogenic
growth factors, and changes in noncollagenous
protein content in the mastoid bone may play
roles in the pathogenesis.449–455
A common sequela of middle-ear disease
in patients with a cleft palate is cholesteatoma.409,410 It has been shown that all infants
with an unrepaired cleft palate have otitis media
with effusion456,457 and that they have functional
obstruction of the eustachian tube because of impairment of the tubal opening mechanism.458–460
Studies of infants, children, and adolescents with
a cleft palate demonstrate constriction of the
eustachian tube during the forced-response
test.461 Cholesteatoma is a common sequela of
middle-ear disease in patients with a cleft
palate.409 Therefore, the child with a cleft palate
represents an in vivo model of the type of
functional eustachian tube obstruction that can
result in an acquired cholesteatoma. Because this
type of dysfunction also occurs commonly in
whites who have otitis media or atelectasis but
who do not have a cleft palate,432 they are also at
risk of development of cholesteatoma.
In contrast to the frequency of cholesteatoma
in the cleft palate population, cholesteatoma is
uncommon in American Indian populations.140
Jaffe reported that attic perforations are rarely
found in Navajo children; in more than 200
Complications and Sequelae: Intratemporal
tympanoplasties performed to repair central
perforations, no cholesteatoma was found.462
Wiet, in a study of 600 White Mountain
Apache Indians, also reported a low incidence
of cholesteatoma; the few cases he found were
mostly of the attic type.463 In a subsequent study
by Beery and colleagues, otoscopic examination
of 25 Apache Indians revealed no cholesteatomas.117 The eustachian tube function was tested
in these Indians by the inflation-deflation and
forced-response tests, which revealed a eustachian tube that had low resistance to airflow (was
semipatulous) but active muscle function. This
type of tube probably precludes the development
of high negative middle-ear pressure, a retraction
pocket, or cholesteatoma. The Apache Indian
appears to have a eustachian tube that allows
easier passage of gas and liquid than does that of
the white subject with or without a cleft palate.
The middle ear of the Apache individual is easily
ventilated and, consequently, is not protected
from unwanted secretions from the nasopharynx.
It appears that the structure of the eustachian
tube of the Apache Indian of the White
Mountain Reservation is conducive to the development of reflux otitis media, perforation, and
discharge.
Some American Indian tribes appear to be
in vivo models of the semipatulous eustachian
tube that actively dilates during swallowing.
Cholesteatoma formation is rarely seen in such
ears because the middle ear is aerated either by
the eustachian tube, a central perforation, or
both. By studying these in vivo models, we can
gain a clearer perspective of the whole spectrum
of eustachian tube dysfunction (see Chapter 3).
Microbiology
Cholesteatomas may or may not be associated
with infection, and when infection is present, it
can be either acute or chronic.122 An acute
infection can also be superimposed on a preexisting chronic infection. A cholesteatoma is
frequently present in the middle ear (and
mastoid) without any signs of acute or chronic
infection; but when infection is present, it can
401
involve the entire middle-ear cleft (ie, eustachian
tube, middle ear, and mastoid), or only the
cholesteatoma is infected and the rest of the
middle-ear cleft is apparently free of infection.
When infection is present, the organisms
cultured from the discharge are similar to those
identified from ears with chronic suppurative
otitis media; P. aeruginosa and Proteus are the
most commonly identified aerobic bacteria, and
Bacteroides and Peptococcus-Peptostreptococcus
are the most commonly seen anaerobic organisms. Multiple bacteria were cultured from the
discharges of more than half of 30 patients with
cholesteatomas studied by Harker and Koontz
(Table 14).405 Karma and colleagues reported
that when they cultured 18 infected cholesteatomas, they found both aerobic and anaerobic
bacteria in half of the cultures.464 From the
results of these studies, it seems that the most
appropriate ototopical medication126 and systemic antimicrobial therapy for patients who
have an infected cholesteatoma are agents
effective against gram-negative organisms and
anaerobic bacteria; however, the results of
culture of the discharge will aid in selecting the
proper antimicrobial therapy. A recent study
found microbial biofilms in human and experiTable 14. BACTERIOLOGIC FINDINGS IN INFECTED
CHOLESTEATOMAS IN 30 CHILDREN AND ADULTS
Organism
Aerobes
Pseudomonas aeruginosa
Pseudomonas fluorescens
Proteus species
Escherichia coli
Klebsiella, Enterobacter, and Serratia species
Streptococcus species
Alcaligenes and Achromobacter species
Staphylococcus aureus
Staphylococcus epidermidis
Anaerobes
Bacteroides species
Peptococcus and Peptostreptococcus species
Propionibacterium acnes
Fusobacterium species
Bifidobacterium species
Clostridium species
Eubacterium species
Adapted from Harker LA, and Koontz FP.405
Number of
Cases
11
2
4
4
4
8
3
1
2
13
11
8
4
3
3
2
402
OTITIS MEDIA IN INFANTS AND CHILDREN
mental cholesteatoma, which could explain the
persistent infection in many patients who have
cholesteatoma despite apparently appropriate
and adequate medical treatment.465 These considerations may be lifesaving when an intratemporal or intracranial complication of
cholesteatoma is present. In addition, preoperative and postoperative antimicrobial therapy for
patients with profuse otorrhea may also be
necessary to prevent a postoperative infection
from developing.
Pathology
Cholesteatoma is characterized by keratinizing
stratified squamous epithelium, with accumulation of desquamating epithelium or keratin
within the middle-ear cleft or other pneumatized
portions of the temporal bone. A cyst-like
structure is usually produced by the keratinizing
squamous epithelium. Laminated keratin from
its inverted surface accumulates within the
cavity, which may also contain necrotic tissue
and purulent material. If the pocket is dry, the
rate of exfoliation may be slow.217 A cholesteatoma may or may not be infected or associated
with chronic suppurative otitis media. Sheehy
and colleagues reported that of 1,024 children
and adults with cholesteatoma, 26% had no
history of aural discharge in the past; in 53%, it
had been intermittent, and in only 21% of the
patients was discharge reported as being continuous.400 When these patients had surgery, almost
half had no evidence of discharge.
Cholesteatoma usually causes bone resorption, which is thought to be secondary to
pressure erosion as the mass enlarges or
possibly due to the activity of collagenase.466
Erosion can occur anywhere in the temporal
bone, although the ossicles are commonly
involved.398,467,468 Ossicular erosion can result
in discontinuity (usually erosion of the long
process of the incus) and a conductive hearing
loss or fistulization of the labyrinth. (The lateral
semicircular canal is the most common site of
erosion.)
Alternatively, the epidermis may invade the
aerated space of the temporal bone and form
an incomplete surface lining into which the
desquamated keratin debris overflows. This
process may give the impression that the mucous
membrane is converted by metaplasia to keratinizing squamous epithelium.438 However, there
apparently is no histopathologic support for this
hypothesis.469
In children, cholesteatoma is considered to be
more aggressive (invasive) than the disease that
occurs in adults217,470,471 for two reasons: (1)
extensive disease is found at the time of surgery
more frequently in children than in adults and (2)
higher rates of residual (persistent) and recurrent
cholesteatoma after surgery have been found in
children compared with the rates in adults.472
Palva and colleagues compared 65 children with
cholesteatomas with 65 adults with the same
disease and found that whereas 22% of the
children had extensive disease that filled the
middle ear and mastoid, only 6% of adults had
such extensive disease.473 In children, in contrast
to adults, cholesteatoma frequently extends into
the cell tracts of the temporal bone because
pneumatization is usually more extensive in
children than in adults.217 However, despite the
finding that cholesteatomas in children tend to be
more extensive than those occurring in adults,
childhood cholesteatoma may still be confined to
the mesotympanum or epitympanum. Schuring
and colleagues compared the extent of and
outcomes after surgery for cholesteatoma in 228
adults and teenagers with those in 38 children
and concluded that children had more recurrent
disease, greater ossicular necrosis, and poorer
hearing postoperatively.474
Diagnosis
Because there may be a lack of signs and
symptoms of ear disease, cholesteatoma may go
undetected for many years in children and adults.
In children, this is an even greater problem
because they are frequently unaware of slowly
developing ear problems. Most adults have a
history of hearing loss, which is usually progres-
Complications and Sequelae: Intratemporal
sive and associated with recurrent ear discharge.
However, children rarely complain of hearing
loss, especially if the disease is unilateral. There is
frequently no discharge, and otalgia may be
absent in most children and adults. In addition,
children are usually unaware of the more subtle
symptoms associated with the disease, such as
fullness in the ear, tinnitus, mild vertigo, and the
foul smell of the discharge when it is present.
Fever is not a sign of cholesteatoma; when it
accompanies this disease, and especially when
otalgia is also present, a search for an intratemporal or intracranial complication must be made.
Other signs and symptoms, such as facial
paralysis, severe vertigo, vomiting, and headache,
should also alert the physician to the presence of
a suppurative complication. In children, the attic
type of cholesteatoma appears to be less symptomatic than a cholesteatoma in the posterosuperior quadrant; in the posterosuperior quadrant,
cholesteatoma is frequently preceded by symptomatic recurrent or chronic otitis media with
effusion and an early onset of ossicular discontinuity with a significant hearing loss. However, in
both types, the preceding atelectasis and retraction pocket may not be associated with significant symptoms in children. The intratympanic
congenital cholesteatoma, which may be secondary to otitis media, is even more obscure because
hearing loss may be a late sequela and discharge
is not present.
The diagnosis of cholesteatoma is most
effectively made with an otoscope or, more
accurately, with the otomicroscope. However,
otoscopic findings may be equivocal, otoscopy
may be difficult to adequately perform if infection is present in the ear canal, or the child may
be uncooperative. If otoscopy is not successful
and a cholesteatoma is suspected, the child may
have to be examined with use of a general
anesthetic. A CT scan may be diagnostic.
Recurrent or chronic otorrhea that is unresponsive to medical management can be a sign that
a cholesteatoma is the underlying pathologic
process.
In a defect in the posterosuperior portion of
the pars tensa or the attic or through a large
403
perforation, otoscopy will usually reveal the
presence of white, shiny, greasy flakes of debris,
which may or may not be associated with a foulsmelling discharge. A polyp may be seen coming
through the defect, which, like a crust, can
prevent adequate visualization of the tympanic
membrane. A crust overlying the area of the
posterosuperior quadrant or the pars flaccida
must be removed because a retraction pocket or
cholesteatoma may be present. The size of the
defect in the tympanic membrane may not
indicate the extent of the cholesteatoma because
a small defect, especially in the attic, may be
associated with extensive cholesteatoma. On the
other hand, the cholesteatoma may be confined
only to the attic or middle ear despite the
presence of a large defect. If an adequate
examination of the child’s ear is not possible
with the child awake, an examination with the
patient under anesthesia is indicated. Every child
who must be given a general anesthetic for
myringotomy (with or without a tympanostomy
tube insertion) should have the entire tympanic
membrane examined to identify a possible
cholesteatoma or its precursor, a retraction
pocket. In addition, an intratympanic cholesteatoma may be visualized through the tympanic
membrane or through the incision after a
myringotomy.
It is frequently difficult to determine whether
the defect is a retraction pocket or a ‘‘dry’’
cholesteatoma. However, even though this distinction cannot be made, the management of the
defect is usually the same (see ‘‘Atelectasis of the
Middle Ear’’).
Unfortunately, there is no tympanometric
pattern for diagnosis of a cholesteatoma. An
abnormal tympanogram should alert the clinician to the presence of middle-ear disease, but
the tympanogram may be normal even when a
cholesteatoma is present. Impedance testing may
reveal a perforation of the tympanic membrane,
but this occurs less commonly in children than in
adults. Likewise, audiometric testing may reveal
a conductive hearing impairment or possibly a
mixed conductive and sensorineural deficit, but a
cholesteatoma may be present without a loss of
404
OTITIS MEDIA IN INFANTS AND CHILDREN
hearing. A sensorineural hearing loss is presumably due to serous labyrinthitis26 or possibly a
labyrinthine fistula.
CT scans of the temporal bone are helpful in
diagnosis and management when a cholesteatoma is suspected.475,476 The CT scans should be
studied carefully to identify the extent of the
cholesteatoma, possible ossicular involvement,
and any complication that might be present, such
as a labyrinthine fistula. The CT scans should be
restudied preoperatively in planning the surgical
procedure; decisions concerning the surgical
approach and the extent of surgery can be aided
by CT scans.477
When aural discharge associated with a
cholesteatoma is profuse, microbiologic assessment of the discharge is indicated so that the
infection can be controlled by administering the
most appropriate antimicrobial agent preoperatively and, when indicated, intraoperatively and
postoperatively.
Management
Medical management of cholesteatoma is indicated only when infection is coexistent and
should be directed at the organisms listed above
(see ‘‘Microbiology’’). Otherwise, the primary
method of management is surgical. Aural toilet,
obtaining a Gram stain, and culture and susceptibility studies are key to culture-directed antibiotic treatment. Ototopical agents that are
nontoxic to the inner ear are recommended.133
As discussed above for chronic suppurative otitis
media, there are ototopical agents that are
potentially ototoxic and not indicated today
with the availability of the two new fluoroquinolone options, ofloxacin otic drops and
ciprofloxacin-dexamethasone. Systemic antibiotics may also be beneficial but should be culture
directed. Pseudomonas is the most common; thus,
orally administered quinolones are restricted in
children, but with appropriate parental informed
consent, oral administration of a quinolone,
such ciprofloxin, is more feasible than intravenous potentially toxic agents, such as the
aminoglycosides.
Surgical management of cholesteatoma and
conditions that may be causally related to this
disease should be based on an understanding of
its pathogenesis.478,479 A deep retraction pocket
in the posterosuperior or pars flaccida area of the
tympanic membrane, if persistent, should be
managed promptly by insertion of a tympanostomy tube in an effort to return the tympanic
membrane to the neutral position and to prevent
adhesions from forming between the tympanic
membrane and the middle-ear structures (see
Figure 28).480 If the pocket is not treated, a
cholesteatoma may develop. In children, the
retraction pocket may be seen (through the
otomicroscope) to distend during inhalation
anesthesia; this is a promising sign that the
tympanic membrane will return to the normal
position after the insertion of a tympanostomy
tube. On the other hand, if the retraction pocket
does not distend during anesthesia, the surgeon
should carefully examine the depth and extent of
the pocket, probing gently with a blunt rightangled hook. Mirrors may also help visualize the
extent of the pocket. We prefer a Hopkins rodlens telescope to determine the exact borders of
the pocket.481 Also, we have found the telescope
to be invaluable in removing cholesteatoma at
the time of middle-ear (and mastoid) surgery.9
Others have also now advocated its use in
reducing postoperative residual disease.482,483
A retraction pocket can extend into any area
of the middle ear, but it is found most frequently
extending into the epitympanum, facial recess,
and sinus tympani. If the retraction pocket
persists after the middle ear has been ventilated
by a tympanostomy tube that has been in place
for several weeks, a tympanoplasty procedure to
prevent ossicular discontinuity, the development
of a cholesteatoma, or both should be recommended.152 Heermann and colleagues advocate
the use of cartilage to support the tympanic
membrane graft to prevent recurrence of the
retraction pocket.392 Other surgeons have
reported good results using cartilage to prevent
postoperative retraction.484–489 Simple excision
of the retraction pocket has also been advocated,490 but this technique is not as effective as
Complications and Sequelae: Intratemporal
reconstruction of the defect and reinforcing the
tympanic membrane with cartilage. In children, a
tympanostomy tube should be inserted into the
tympanic membrane remnant because eustachian
tube function will most probably remain poor
postoperatively.
Tympanotomy is a surgical procedure that
opens the middle-ear space. In an exploratory
tympanotomy, a tympanomeatal flap is elevated
so that the middle ear and its structures can be
viewed directly. An exploratory tympanotomy is
indicated when it is suspected that there is an
abnormality, such as intratympanic cholesteatoma or ossicular chain abnormality, or it is a
planned second-stage procedure after tympanoplasty with or without mastoidectomy has been
performed to manage cholesteatoma.
Myringoplasty is the surgical repair of a
defect in the tympanic membrane with no
attempt made to explore the middle ear. A
perforation (or retraction pocket) is commonly
repaired by use of an autogenous connective
tissue graft (temporalis fascia or compressed
adipose tissue from the earlobe) as a lattice onto
which epithelial cells can migrate from the edges
of the existing perforation. The procedure is
employed to manage a simple uncomplicated
tympanic membrane perforation without cholesteatoma.
Tympanoplasty is the surgical reconstruction
of the tympanic membrane–ossicle transformer
mechanism. If a perforation is present, it is
repaired with a connective tissue graft, but unlike
in a myringoplasty, the middle ear is explored.
Ossicles can be repositioned (ossiculoplasty) to
restore ossicular chain continuity. Traditionally,
tympanoplasty operations are characterized
according to the degree to which the reconstructed ossicular chain approximates the anatomic juxtaposition of ossicles in the normal
middle ear (see ‘‘Perforation of the Tympanic
Membrane’’ and ‘‘Ossicular Discontinuity and
Fixation’’).
Mastoidectomy involves the surgical exposure
and removal of mastoid air cells. There are
several types of mastoidectomy (Figure 32). In a
complete simple (cortical) mastoidectomy (see
405
Figure 32A), the mastoid air cell system is
exenterated, including the epitympanum, but
the canal wall is left intact. The operation is
performed when acute or chronic mastoid osteitis
is present and is frequently part of the surgical
procedure advocated by some surgeons for
cholesteatoma. A posterior tympanotomy or
facial recess tympanotomy (see Figure 32B)
involves exenteration of mastoid air cells followed by formation of an opening between the
mastoid and middle ear created in the posterior
wall of the middle ear lateral to the facial nerve
and medial to the chorda tympani. This procedure is an extension of the complete simple
mastoidectomy that allows better visualization of
the facial recess without removal of the canal
wall and is primarily advocated for ears in which
a cholesteatoma is present. A modified radical
mastoidectomy (see Figure 32C) is an operation
in which a portion of the posterior ear canal wall
is removed and a permanent mastoidectomy
cavity is created, but the tympanic membrane
and some or all of the ossicles are left. The
procedure is usually performed when a cholesteatoma cannot be removed without removal of
the canal wall; some function may be preserved.491 Radical mastoidectomy (see Figure
32D) involves exenteration of all mastoid air
cells, opening of the epitympanum, and removal
of the posterior ear canal wall along with the
tympanic membrane, the malleus, and the incus.
Only the stapes, or the footplate of the stapes,
remains. No attempt is made to preserve or
improve function. By the removal of the posterior ear canal wall, the exenterated mastoid
cellular area, middle ear, and external auditory
canal communicate, forming a common single
cavity. The procedure is indicated when there is
extensive cholesteatoma in the middle ear and
mastoid that cannot be removed by a less radical
procedure. In addition, the operation may be
indicated when a suppurative complication of
otitis media is present.
Tympanomastoidectomy with tympanoplasty
is the term used when a tympanoplasty operation
is performed in conjunction with a mastoidectomy. Mastoidectomy operations that leave the
406
OTITIS MEDIA IN INFANTS AND CHILDREN
Figure 32. Examples of four types
of mastoid surgery. A, Complete
simple (cortical) mastoidectomy in
which the canal wall has been left
intact. The exposure of the epitympanum is an important part of the
surgical procedure. B, A posterior
tympanotomy–facial recess access
to the middle ear has been added to
the complete simple mastoidectomy.
C, Modified radical mastoidectomy.
D, Radical mastoidectomy.
posterior ear canal wall intact are termed closed
cavity, canal wall up, or intact canal wall
procedures, whereas those in which the posterior
canal is partially removed are called open cavity
or canal wall down procedures. For more
complete details of the surgical procedures, the
reader is referred to Bluestone and Bluestone and
Stool.9,492
The type of surgery chosen for management
of cholesteatoma in children should be selected
on the basis of the site and extent of the
cholesteatoma and other factors, such as the
patient’s age, presence or absence of otitis media,
eustachian tube function, and availability of
health care.478,493,494 The operation must be
tailored for each child. Today, every effort
should be made to maintain the posterior ear
canal in children as opposed to performing canal
wall down procedures, that is, modified or
radical mastoidectomy.495 However, when the
tympanic membrane is preserved or recon-
structed (tympanoplasty), a second operative
procedure is indicated in most children, usually
6 months later, to determine whether there is
residual cholesteatoma.398,468 Unfortunately, CT
and MRI are not sensitive enough to replace
exploratory surgery; the disease must be far
advanced for these scans to be an effective
diagnostic tool.496 Some have advocated use of
a telescope to detect residual cholesteatoma in
an effort to avoid the traditional exploratory
tympanotomy (and possible mastoidotomy).497
We advocate exploratory tympanotomy (ie,
‘‘second look’’) and possible mastoidotomy in
children in approximately 6 months in a search
for possible residual disease from the initial
procedure.9,398 Other surgeons also recommend
a second-stage procedure.498
Preventing the recurrence of cholesteatoma
in these children is important because the same
underlying pathogenetic conditions may still be
present. Thus, effective management of medical
Complications and Sequelae: Intratemporal
conditions that may interfere with adequate
eustachian tube function, such as adenoids,
allergy, or chronic sinusitis, may prove to be
beneficial. However, because many of these
children have a basic eustachian tube dysfunction, placement of cartilage grafts, tympanostomy tubes, or both is usually required to prevent
a new cholesteatoma. Long-term follow-up
(eg, 5–7 years) after initial control of cholesteatoma in children is required because recurrence
has been reported to be as high as 50 to
70%.398,549–501
CHOLESTEROL GRANULOMA
Cholesterol granuloma is a sequela of chronic
otitis media with effusion. It has been described
as idiopathic hemotympanum because, clinically,
the tympanic membrane appears to be dark blue,
a so-called blue eardrum.502 However, this term
is a misnomer because there is no evidence that
bleeding within the middle ear or the presence
of fresh blood or microscopic amounts of old
blood is related to the etiology of this disease.10,503 The condition is rare in all age groups
but does occur in children and is most likely due
to long-standing changes associated with chronic
otitis media with effusion.504,505 In a series of 17
cases of cholesterol granuloma of the petrous
apex reported by Brodkey and colleagues, 3
(18%) occurred in adolescents and the rest in
adults.506
The blue color of the tympanic membrane as
visualized through the otoscope is probably due
to the reflection of light from the thick liquid
(granuloma) within the middle ear. The condition must be differentiated from an uncovered
high jugular bulb and a glomus tumor, either
tympanicum or jugulare,507 and more commonly
chronic otitis media with effusion or barotitis.
Because cholesterol granuloma is relatively rare
in children, the presence of a blue color of the
tympanic membrane, as visualized by otoscopy
or otomicroscopy, is most commonly middle-ear
effusion, and the blue appearance is related to
how the light is reflected off the drum.
407
Chronic granulations, with foreign body
giant cells and foam cells within the middle ear,
mastoid, or both are characteristic of the tissue.
Cholesterol crystals are usually present. The
condition is similar to a chronic middle-ear
effusion except that a soft brownish material
that contains shining golden-yellow specks is
present. The pathologic process present with
cholesterol granuloma should not be confused
with that of a cholesteatoma.217 Similar granulomas have been described in other parts of the
body: atheromatous and dermoid cysts, periapical and follicular cysts of the jaw, old infarcts,
and hematomas.508 When the granulomas are
stained, prominent iron deposits or hemosiderin
may be found,509,510 but not in quantities
sufficient to account for the otoscopic appearance of the blue tympanic membrane.
The condition has been reproduced in experimental animals by injection of foreign material
into the middle ears of guinea pigs511 and
rabbits,512 by obstruction of the long bones of
birds,513–515 and after chronic obstruction of the
eustachian tube in monkeys.516 The pathogenesis
described in the last experimental model is
similar to that known to occur in humans when
the eustachian tube was obstructed by a muscle
pedicle flap517 or by a tumor. In addition to
occurring as an isolated pathologic entity,
cholesterol granuloma can be associated with
chronic suppurative otitis media with or without
cholesteatoma, any inflammation that may
obstruct portions of the middle ear or mastoid,
or both.
CT may be helpful in diagnosis and in
determining the extent of the disease, but MRI
is probably more specific as a diagnostic aid.518
Management
Cholesterol granuloma will not respond to
medical treatment, middle-ear inflation, or myringotomy with tympanostomy tube insertion.
However, when a child is observed to have a
tympanic membrane that has a dark blue
appearance and is unresponsive to nonsurgical
management, a myringotomy under general
408
OTITIS MEDIA IN INFANTS AND CHILDREN
anesthesia should be performed because, on
occasion, chronic otitis media with effusion
may also be associated with a blue tympanic
membrane (again, probably as the result of the
way light from the otoscope is reflected from the
middle-ear effusion). However, if a thick, brown
liquid is found during the procedure, successful
aspiration of the material will not be possible,
and if a tympanostomy tube is inserted, it will
become occluded immediately. Takahashi and
colleagues reported success in treating five
patients, aged 6 to 19 years, with a short course
of oral prednisone for a 10- to 14-day period and
tympanostomy tube insertion.519 Despite the
small number of patients evaluated, this method
of treatment may be helpful because the traditional method of management has been middleear and mastoid surgery.
When tympanostomy tube insertion and
possibly a trial of cortisone fail, the treatment
is middle-ear and mastoid surgery.520 The granuloma in the mastoid can be removed by
performing a complete simple mastoidectomy,
and the middle-ear portion can be removed by
use of a tympanomeatal approach. There is no
reason to remove the canal wall unless a
cholesteatoma is present. A tympanostomy tube
should be inserted into the tympanic membrane
at the time of the procedure and reinserted as
often as needed, that is, until the middle ear
remains normally aerated after spontaneous
extubation.
When cholesterol granuloma involves the
petrous apex, conservative management is
recommended unless the patient has severe
symptoms, such as vertigo and otalgia. When
surgery is indicated, a transmastoid drainage
procedure is recommended, as opposed to resection of the petrous apex.506 However, recurrence
after a drainage procedure has a rate as high as
60% and requires an extended middle fossa
approach or petrosal approach.521
It appears from what is known of the
pathogenesis and pathology of cholesterol granuloma that the best management is prevention,
which should consist of active treatment and
prevention of chronic otitis media with effusion.
TYMPANOSCLEROSIS
Tympanosclerosis may be a sequela of chronic
middle-ear inflammation or the result of trauma.
It is characterized by whitish plaques in the
tympanic membrane and nodular deposits in the
submucosal layers of the middle ear.522,523 When
the disease is limited to the tympanic membrane,
the term myringosclerosis is applied. Conductive
hearing loss may occur if the ossicles become
embedded in the deposits.
Tympanosclerosis was first described by von
Troltsch, who called it sclerosis,524 but it was
Zollner who called the disorder tympanosclerosis
and differentiated it from otosclerosis.525
Schuknecht preferred the term hyalinization to
tympanosclerosis because the histopathologic
condition is that of hyalin degeneration, which
is the result of a healing reaction characterized by
fibroblastic invasion of the submucosa, followed
by thickening and fusion of collagenous fibers
into a homogeneous mass.217 He also described
the hyalinized collagen around the ossicles. The
pathologic condition in the tympanic membrane
occurs in the lamina propria, whereas the
pathologic condition within the middle ear is in
the basement membrane; in both sites, there is
hyalinization followed by deposition of calcium
and phosphate crystals.
Epidemiology and Pathogenesis
Tympanosclerosis (myringosclerosis) of the tympanic membrane is a common sequela in children
who have or have had recurrent AOM or chronic
otitis media with effusion. It is also common at
the site of a healed, spontaneous perforation or
after myringotomy and tympanostomy tube
placement. In children who have had tympanostomy tube insertion for otitis media, tympanosclerosis increases with advancing age as the
incidence of otitis media with effusion
declines.368,526 The middle ear may have tympanosclerosis without the presence of clinically
evident myringosclerosis.527 It is not commonly
a sequela of myringotomy, and when due to the
Complications and Sequelae: Intratemporal
aftermath of tympanostomy tube insertion, it is
not linked to hearing loss.528 The chalky patch
seen in the tympanic membrane of children may
be due to inflammation, trauma, or both. In the
pediatric age group as a whole, however, the
condition is not common in the middle ear,
especially in infants and young children. In
particular, ossicular involvement is rare in very
young children. Of 311 cases of tympanosclerosis
studied by Kinney, only 20% occurred in
individuals 30 years of age or younger.529 This
implies that the condition in the middle ear takes
many years to develop. An expression of macrophages is an early event.530 Mattsson and
colleagues, in experiments in rats, reported that
the formation of oxygen free radicals contributes
significantly to the development of myringosclerosis.531 This finding supported their hypothesis that the condition is secondary to a
hyperoxic condition of the middle ear, such as
when the tympanic membrane is not intact (eg,
perforation or tympanostomy tube). In experiments in rats, nitrous oxide was found to be
involved in this pathologic condition.532 A
classification-related site, severity, and middleear involvement have been proposed by
Bluestone and colleagues.10
Schiff and colleagues hypothesized that tympanosclerosis has an immune component that
occurs in the middle ear after an insult or
mucosal disruption.533 They also proposed that
there is a genetic component, which would
explain the low incidence of the condition in
children who have such a high prevalence and
incidence of middle-ear inflammation.
This hypothesis may be the explanation for
the relatively high rate of tympanosclerosis
among children who are Alaskan natives
(Eskimos) and American Indians.462,463,534
Other factors may predispose these children to
the disease, such as differences in eustachian tube
function. Wiet and colleagues reported that
tympanosclerosis affected a higher percentage
of Alaskan native children than children of a
similar age in his New Hampshire private
practice; tympanosclerosis of the tympanic membrane, the ossicles, or both was found in 78 (68%)
409
of 114 Alaskan native children who had tympanoplasty surgery, whereas only 7 such cases were
diagnosed in 377 consecutive tympanoplasties
performed on children in his practice.140 In
addition, they also found that far-advanced
tympanosclerosis that resulted in fixation of the
ossicular chain occurred at an early age in the
Alaskan native children but not in children in his
practice.
Inflammatory mediators have been uncovered as being involved in the pathogenesis in
humans535,536 and in animal models.537
Management
Currently, no surgical correction, such as tympanoplasty, is indicated when tympanosclerosis
of the tympanic membrane (ie, myringosclerosis),
even though extensive, is the only abnormality of
the middle ear. Medical treatment and prevention are still in the laboratory stage of
research.538 However, surgical intervention can
be indicated on an individualized basis.523 If a
middle-ear effusion is present and a myringotomy, with or without tympanostomy tube insertion, is indicated, the incision should be placed, if
possible, in an area without involvement, leaving
the affected area untouched. Removal of large
tympanosclerotic plaques may result in a permanent perforation of the tympanic membrane.
When an incision must be made in an area of
tympanosclerosis, only the amount necessary to
perform the procedure should be removed. When
a tympanoplasty is being performed to repair a
perforation of the tympanic membrane and
tympanosclerosis is present in the drum remnant,
removal of the plaque is optional; the plaque may
remain if the area of tympanosclerosis does not
interfere with the surgical procedure and is not
impeding function. When tympanosclerosis is the
cause of ossicular fixation and a tympanoplasty
procedure is elected, the methods of removing
the plaques and ossiculoplasty described by
Glasscock and Shambaugh539 are appropriate
for the rare child with this advanced stage of
tympanosclerosis. A two-stage stapedectomy has
410
OTITIS MEDIA IN INFANTS AND CHILDREN
been advocated to correct the conductive hearing
loss with some success.540 However, refixation of
the ossicles is not uncommon even after apparently adequate surgical removal of the plaques
and ossiculoplasty. A hearing aid should be
considered if surgery is not performed or is not
successful in restoring the hearing loss.
Nevertheless, long-term hearing success was
reported after ossicular reconsruction in older
children and adults.541
Even though the pathogenesis of tympanosclerosis is not completely understood, it seems
most probable that appropriate management of
recurrent and chronic middle-ear inflammation
in infants and children is the best method of
prevention. Because it also occurs after trauma to
the tympanic membrane, myringotomy with
tympanostomy tube placement should be performed with tympanosclerosis in mind as one of
the potential complications and sequelae. In
general, tympanosclerosis involving the tympanic
membrane does not appreciably affect function,
although when the ossicles are involved, the
patient may have a significant conductive hearing
loss. Thus, tympanostomy tubes may increase the
incidence of tympanosclerosis of the tympanic
membrane, but their placement may decrease the
frequency of ossicular fixation owing to this
disease later in life.
Some clinicians believe that tympanosclerosis, as a sequela of tympanostomy tube insertion,
causes conductive hearing loss.542 For most
children who have tympanosclerosis that affects
the tympanic membrane secondary to recurrent
or chronic otitis media, tympanostomy tube
placement, or both, the condition is cosmetic
and does not affect hearing. Stenstrom and
Ingvarsson observed 88 otitis-prone children for
up to 8 years and concluded that the level of
hearing, as assessed by audiometry, was a poor
indicator of tympanic membrane disease.543 Of
course, the more ear disease and the more
surgical procedures the child has can eventually
involve the conductive hearing mechanism (see
also ‘‘Myringotomy and Tympanostomy Tube
Placement’’ in Chapter 8).
OSSICULAR DISCONTINUITY AND
FIXATION
Discontinuity and fixation of the ossicles are
possible sequelae of recurrent acute and chronic
middle-ear disease and, in rare instances, complications of surgery.544 A staging system related
to site and pathology has been proposed by
Bluestone and colleagues,10 and Dornhoffer and
Gardner have provided a statistical staging
system related to prognostic factors in ossiculoplasty to correct the defects.545 Staging that is
agreed on by consensus is important when
reporting the outcome of ossiculoplasty.546
Pathology and Pathogenesis
Ossicular interruption is the result of rarefying
osteitis secondary to chronic inflammation of the
middle ear. A retraction pocket or cholesteatoma
may also cause resorption of the ossicles. The
long process of the incus is most commonly
involved, which results in incudostapedial disarticulation. The commonly accepted reason for
erosion of this portion of the incus is its poor
blood supply. However, because the tympanic
membrane frequently becomes attached to this
part of the incus when a posterosuperior retraction pocket is present, adhesive otitis media may
be the cause of the osteitis and subsequent
erosion. Cholesteatoma is also commonly found
in the same area.376 The stapes (or, more
specifically, its crural arches) is the second most
commonly involved ossicle. Erosion of the stapes
is more likely to be associated with a retraction
pocket or cholesteatoma than with decreased
vascular supply. Less commonly, the body of the
incus and the manubrium of the malleus may
also be eroded. The ossicles may become fixed
by fibrous tissue secondary to adhesive otitis
media or, more rarely in children, secondary to
tympanosclerosis. Neither the incidence of ossicular discontinuity and fixation nor the natural
history of the pathologic conditions that precede
these abnormalities has been formally studied in
children. However, ossicular discontinuity is
commonly associated with a deep retraction
Complications and Sequelae: Intratemporal
pocket or cholesteatoma in the posterosuperior
portion of the tympanic membrane. Disarticulation or fixation of the ossicles may also occur
when there is a central perforation of the
tympanic membrane with or without chronic
suppurative otitis media and, more rarely, when
the tympanic membrane is intact.
Diagnosis
Ossicular chain abnormalities that are secondary
to otitis media and its related conditions can
frequently be diagnosed by visualization of the
defect through the otoscope or, more accurately,
the otomicroscope. Erosion of the long process
of the incus can usually be seen when a deep
posterosuperior retraction pocket is present. A
significant conductive hearing loss (eg, . 30 dB)
when a perforation of the tympanic membrane is
present is evidence of ossicular involvement.
When the tympanic membrane is normal, a
significant conductive loss may be due to
inflammatory ossicular involvement that has
occurred in the past. However, congenital
ossicular abnormalities and otosclerosis must be
part of the differential diagnosis.
In addition to the history, otoscopic examination, and conventional audiometric testing,
immittance audiometry may aid in the diagnosis.
A tympanogram showing high compliance is
evidence of ossicular chain discontinuity when
there is a significant conductive hearing loss. If
the compliance is low, ossicular fixation is more
probable. However, the accuracy with which
tympanometry can differentiate between ossicular discontinuity and fixation is not high because
several other parameters in the middle ear affect
the shape of the tympanogram, such as the
mobility of the tympanic membrane. CT may
also aid in identifying ossicular discontinuity but
is usually of diagnostic benefit only when a large
defect is present. The most accurate way to
diagnose these defects is exploration of the
middle ear, either during exploratory tympanotomy, when the tympanic membrane is intact, or
by inspecting the entire ossicular chain when
411
surgery of the middle ear and mastoid is
indicated, such as tympanoplasty.
Conductive hearing loss is usually present
when the ossicular chain is affected, and the
degree depends on the site and the degree of
involvement of the ossicles and on the presence
or absence of associated conditions, such as a
perforation of the tympanic membrane.547 When
there is a discontinuity of the incudostapedial
joint and the tympanic membrane is intact, a
maximal conductive hearing loss may be present,
that is, 50 to 60 dB. However, when the same
ossicular pathologic condition is present and a
perforation is also present, the hearing loss may
be less severe. Erosion of the manubrium of the
malleus is usually associated with a perforation
of the tympanic membrane but does not contribute to the hearing loss. However, erosion of
the ossicles may not be associated with any
significant degree of hearing loss if the defect is
partial and the continuity of the ossicular chain is
present or the tympanic membrane, retraction
pocket, or cholesteatoma connects a disarticulation. When a cholesteatoma creates this artificial
connection, this phenomenon is commonly
termed hearing through cholesteatoma.
Management
Ossicular deformities in children can be managed
like those in adults, with some notable exceptions. Most adults who have ossicular discontinuity or fixation are no longer at risk of
development of otitis media with effusion or
high negative pressure within the middle ear
owing to eustachian tube dysfunction, but many
children still have or will have these conditions.
These conditions could interfere with the success
of reconstructive middle-ear surgery generally
and ossiculoplasty specifically. Therefore, the
indications for timing and the type of middleear surgery may be different for children.548
When an ossicular deformity is suspected and
the tympanic membrane is intact, such as when
the child has a conductive hearing loss, and there
is no evidence of otitis media or any of its other
complications or sequelae (eg, retraction pocket
412
OTITIS MEDIA IN INFANTS AND CHILDREN
or cholesteatoma), the decision to perform an
exploratory tympanotomy to diagnose and possibly repair the ossicular deformity depends on
several considerations. First, and most important, is the child still at risk of developing a
middle-ear effusion, atelectasis (retraction
pocket), or both? As a general rule, if neither
condition has occurred in either ear for 1 year or
longer, the risk is low. However, the younger the
child, the higher the risk. If further middle-ear
disease may still occur, the operation should be
delayed. The second consideration is the degree
of hearing loss and whether the defect is
unilateral or bilateral. A child who has a
maximal conductive hearing loss in both ears is
a probable candidate for surgical intervention,
whereas the child who has only a unilateral mild
conductive loss should not be operated on.
Another important consideration is the need for
general anesthesia to perform the surgery in all
children. The benefit of surgery must be weighed
against the risk of general anesthesia. For the
child who has a bilateral maximal conductive
hearing loss, the benefit of hearing improvement
may outweigh the risk of general anesthesia,
whereas the risk of anesthesia may not override
the potential chance of improving the hearing in
a child with only a unilateral mild to moderate
hearing loss. Withholding the reconstructive
surgery until the child is able to tolerate a local
anesthetic (adolescence) is a preferred option
when the hearing loss is unilateral and mild to
moderate in degree. Whenever surgical intervention is not planned or the operation is delayed
until the child is older, a hearing aid evaluation
should be considered, even when the hearing loss
is unilateral.
When surgery of the middle ear is indicated
because a perforation of the tympanic membrane
is present, with or without chronic suppurative
otitis media, a cholesteatoma, or a retraction
pocket, the very fact that the patient is a child
still affects the decision to perform an ossiculoplasty. This is because children are at increased
risk of suffering future episodes of otitis media
and of developing atelectasis or adhesive otitis
media. When these conditions are a possibility,
the surgeon should consider staging the surgery
and performing the ossiculoplasty when the child
is older. If the patient has a cholesteatoma, and a
canal wall up procedure followed by a planned
‘‘second-look’’ tympanotomy is elected to determine whether residual cholesteatoma is present,
the ossiculoplasty can be performed when the
middle-ear cleft is free of disease.
There are various ways in which ossicles that
are either eroded or fixed may be reconstructed.
However, the type of ossiculoplasty chosen for a
child may be different from that performed in an
adult. We believe, and most experts agree, that
middle-ear ossicular implants should, in general,
be used only in selected children who have
ossicular defects as a result of middle-ear disease
because neither the long-term safety nor the
efficacy of these prostheses has been proved.
However, if the child’s middle ear is free of
disease and the patient is unlikely to have future
middle-ear problems, insertion of a prosthesis is
an option.549
Some surgeons advocate the use of homograft ossicles in children. Whenever possible,
only the child’s own tissue should be used to
reconstruct the ossicular chain. For the most
common discontinuity encountered, that of the
incudostapedial joint, an incus transposition or
insertion of a fitted incus is the ideal procedure.
When the stapes crura are missing, the shaped
incus can usually be inserted between the mobile
footplate of the stapes and the malleus handle.
For all age groups, whenever the stapes is fixed, a
stapedectomy should not be performed unless the
tympanic membrane is intact; and in children
who have had otitis media in the recent past,
stapedectomy should rarely, if ever, be performed, even when the tympanic membrane is
intact because a recurrence of otitis media with
suppurative labyrinthitis as a complication is an
ever-present risk. Freeing other fixed ossicles can
be attempted in children, but refixation often
occurs because adhesive otitis media, which is the
most frequent cause of fixation, commonly leads
to further fibrosis. There are surgical procedures
in which no prosthesis is used,550 but for some
defects, a prosthesis is necessary, the placement
Complications and Sequelae: Intratemporal
of which should be as optimal as possible to
optimize the chance of as good a hearing result as
possible.551 For further details of surgical techniques for children, see Batti and Bluestone.548
The most effective method of managing
ossicular discontinuity and fixation is preventing
the diseases that cause these ossicular abnormalities. Of special note is the early diagnosis and
management, usually by insertion of a tympanostomy tube, of a posterosuperior retraction
pocket in which the tympanic membrane is lying
on the incus and stapes (see the section on
atelectasis of the middle ear).
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