Infections of the middle ear space and their sequelae

have plagued mankind from the beginning of time.

First described by Hippocrates in 450 BC, this uni-
versally observed process continues to present one
of the most perplexing medical problems of infancy
and childhood, while being the leading cause of
hearing loss in this age group. It is estimated that
70% of children will have had one or more episodes
of otitis media (OM) by their third birthday.
1
This
disease process knows no age boundaries but occurs
mainly in children from the newborn period
through approximately age 7 years, when the inci-
dence begins to decrease. It occurs equally in males
and females. A racial prevalence exists, with a higher
incidence occurring in specic groups such as Native
Americans, Alaskan and Canadian Natives, and Aus-
tralian aboriginal children. African American chil-
dren appear to have less disease than do American
white children, but this observation has yet to be
adequately explained.
Important epidemiologic factors include a
higher incidence of OM in children attending day-
care centers, a seasonal variation with more disease
being present in the fall and winter versus the
spring and summer, and a genetic predisposition to
middle ear infection. Other epidemiologic factors
include a lower incidence and duration of OM in
breast-fed children and a higher incidence in chil-
dren with altered host defenses.
2
Anatomic changes
such as cleft palate and other craniofacial anomalies
as well as congenital and acquired immune de-
ciencies are also important factors. One of the ear-
liest signs of acquired immune deciency syndrome
(AIDS) in infants is recurring episodes of OM. This
has been observed in more than 50% of neonates
with AIDS.
3
DEFINITIONS
Unfortunately, numerous terms have been used to
describe the various inammatory conditions of the
middle ear space (Table 91). This has resulted in
both confusion and a lack of uniformity in report-
ing. An attempt to standardize nomenclature was
undertaken in the early 1980s and will be used
throughout this chapter when discussing this disease
process.
4
Otitis media represents an inammatory con-
dition of the middle ear space, without reference to
cause or pathogenesis.
Middle ear effusion is the liquid resulting from
OM. An effusion may be either serous (thin, watery),
mucoid (viscid, thick), or purulent (pus). The
process may be acute (0 to 3 weeks in duration), sub-
acute (3 to 12 weeks in duration), or chronic (greater
than 12 weeks in duration).
Otitis media may occur with or without effu-
sion. In those cases without effusion, inammation
of the middle ear mucous membrane and tympanic
membrane may be the only physical nding. Occa-
249
C HA P T E R 9
Otitis Media and Middle Ear Effusions
Gerald B. Healy, MD, Kristina W. Rosbe, MD
TABLE 91. Synonyms Used in the Past for Otitis
Media
Acute Otitis Media Otitis Media with Effusion
Suppurative Serous
Purulent Secretory
Bacterial Mucoid
Glue ear
Middle ear effusion
sionally, infection may involve only the tympanic
membrane (myringitis), without involving the
mucosa of the middle ear space.
This chapter deals primarily with two disease
processes: acute otitis media (AOM) and chronic oti-
tis media with effusion (COME). Acute otitis media
represents the rapid onset of an inammatory
process of the middle ear space associated with one
or more symptoms or local or systemic signs. These
usually include otalgia, fever, irritability, anorexia,
vomiting, diarrhea, or otorrhea. Physical examina-
tion usually reveals a thickened, erythematous or
bulging tympanic membrane with limited or no
mobility to pneumatic otoscopy. Erythema of the
tympanic membrane may be an inconsistent nding
and may be absent in certain systemic illnesses such
as immune deciency, when the patient cannot
mount a sufcient inammatory response to present
this more classic nding. The acute onset of fever,
otalgia, and, on occasion, a purulent discharge is usu-
ally evidence of AOM. Following such an episode, the
patient may move into a subacute or even chronic
phase in which uid is present in the middle ear
space, although active infection may be absent.
Chronic otitis media with effusion indicates
the presence of asymptomatic middle ear uid, usu-
ally resulting in conductive hearing loss. The tym-
panic membrane may present numerous physical
ndings including thickening, opacication, and
impaired mobility. An air-uid level and/or bubbles
may be observed through a translucent tympanic
membrane. This entity is distinguished from AOM
in that the signs and symptoms of acute infection
are lacking (eg, otalgia, fever, otorrhea).
ETIOLOGY
Eustachian tube (ET) dysfunction is considered the
major etiologic factor in the development of middle
ear disease. Politzer rst proposed the ex vacuo the-
ory of OM in 1867.
5
The theory postulates that
chronic negative pressure, secondary to ET malfunc-
tion, results in the development of a transudate into
the middle ear space. Numerous experiments have
been carried out by many authors to substantiate
this theory. It is traditionally maintained that the
effusion is sterile; therefore, therapy should be aimed
chiey at relieving ET dysfunction. Most proponents
of the theory have proposed that there are essentially
two types of ET obstruction resulting in middle ear
effusion: mechanical and functional. Mechanical
obstruction may be either intrinsic or extrinsic.
Intrinsic mechanical obstruction is usually caused
by inammation of the mucous membrane of the
ET or an allergic diathesis causing edema of the
tubal mucosa. Extrinsic mechanical obstruction is
caused by obstructing masses such as adenoid tissue
or nasopharyngeal neoplasms.
Some observers believe that infants and
younger children may suffer from functional ET
obstruction as a result of either decreased tubal stiff-
ness or an inefcient active opening mechanism.
Proponents believe that either form of obstruction
results in inadequate ventilation of the middle ear
with resulting negative middle ear pressure. This
theory supports the development of a rational med-
ical or surgical approach to alleviate the obstruction
and thus overcome negative pressure.
The ET has three functions (1): ventilation of
the middle ear associated with equalization of air
pressure in the middle ear with atmospheric pres-
sure, (2) protection of the middle ear from sound
and secretions, and (3) drainage of middle ear secre-
tions into the nasopharynx with the assistance of
the mucociliary system of the ET and middle ear
mucous membrane.
The second etiologic theory was rst suggested
by Brieger in 1914 and proposes an inammatory
origin to OM.
6
Since that time, several other authors
have supported this theory. In 1958, Senturia
reported a 41% incidence of positive bacterial cul-
tures in 130 specimens taken from patients with a
diagnosis of serous otitis media.
6
Other series have
supported this nding.
7
Sades observation that the
basic histopathologic mechanism in otitis media
with effusion (OME) is an inammatory hypertro-
phy of the middle ear mucous membrane and
hyperplasia of its mucous glands also tends to sup-
port an inammatory basis.
8
Protein analysis of middle ear effusions indi-
cates a higher concentration of total protein, lactate
dehydrogenase, malate dehydrogenase, and acid
phosphatase than in serum. This nding has led to
the speculation that this material represents an exu-
date rather than a transudate, giving further evi-
dence that this is an inammatory process. Some
proponents of the inammatory theory feel, how-
250 Ballengers Otorhinolaryngology
ever, that inammation occurs secondary to ET dys-
function; thus, the inammatory response is not the
primary etiologic factor.
Numerous other factors may well contribute to
the development of middle ear disease. These include
allergy, ciliary dysfunction, nasal and/or sinus dis-
ease, and immaturity of the immune system.
In the last 10 years, the role of allergy in OME
has been extensively investigated.
9,10
Otitis media in
the pediatric population is felt to be associated with
allergy in 5 to 80% of cases. Inhalant allergies are felt
to play a greater role than food allergies. Most stud-
ies have been unable to demonstrate, however, an
increase in serum immunoglobulin E (IgE) in chil-
dren with OME.
11
Allergic rhinitis, itself, is not felt to be the cause
of OME. A viral or bacterial infection may prime the
environment, which, in response, produces inam-
matory mediators. These mediators begin the phys-
iologic cycle, creating ET dysfunction, pressure
gradients, and transudation of uid.
12
Middle ear mucosa is rarely the target organ.
The nasopharynx is felt to be the major site of action
with subsequent spread via the ET to the middle ear.
Allergy is felt to affect ET function in several ways.
Nasal obstruction can occur secondary to mast cell
degranulation with increased vascular permeability,
increased mucosal blood ow, and increased mucus
production. Retrograde extension of inammatory
mediators from the anterior nose to the nasophar-
ynx as well as allergen contact with the nasopharynx
can cause ET edema and obstruction with a second-
ary increase in the pressure gradient through nitro-
gen gas exchange and subsequent transudation of
uid.
12
Animal models have demonstrated immune-
mediated inammation as a contributing factor in
the pathogenesis of OME. The role of immune com-
plexes in experimental models has also been estab-
lished. Normal middle ear mucosa is not felt to be
immunocompetent tissue. During inammation,
however, it is transformed into a secretory epithe-
lium containing multiple goblet cells with inltra-
tion of macrophages and lymphocytes. This
immune response may result from circulating anti-
bodies that enter the middle ear through increased
vascular permeability.
Otitis mediaprone children have been shown
to have higher levels of IgG antibody and IgG-anti-
gen immune complexes in their serum and middle
ears versus a nonOM-prone cohort. Immunoglob-
ulin may be the predominant immune mechanism
in the middle ear. It is felt that bacteria may actually
cause immunosuppression of cell-mediated immu-
nity. Immunoglobulin A is thought to be a late
defense mechanism and may actually prevent bacte-
riolysis by IgG and complement, acting as a blocking
antibody. Others have proposed an IgE-mediated
hypersensitivity reaction to viral antigens.
Immune tolerance is the concept that immu-
nization through the oral or pulmonary route may
modulate the middle ear immune response. Studies
have shown that oral immunization after systemic
sensitization actually increased immune-mediated
OME. Vaccines are now becoming available, includ-
ing the recently US Food and Drug Administration
(FDA)-approved pneumococcal conjugate vaccine.
13
MICROBIOLOGY
Numerous studies have documented the microbiol-
ogy of OM.
14,15
Approximately 30% of middle ear
effusions demonstrate known pathogens for OM.
16
Although the treatment of AOM is directed toward
the elimination of the bacteria from the middle ear
space, viruses may also play an important etiologic
role in this disease process.
17
The most common bac-
terial pathogens responsible for acute infection
include Streptococcus pneumoniae and nontypable
Haemophilis inuenzae. These two microorganisms
account for approximately 60% of the cases associ-
ated with bacterial infection. Group A Streptococcus,
Branhamella catarrhalis, Staphylococcus aureus, and
gram-negative enteric bacteria are less frequent
causes of OM (Figure 91).
Because of the difculty in obtaining viral cul-
tures, fewer specic data are available regarding their
occurrence in patients with OM. However, respira-
tory syncytial virus accounts for a majority of the
viral infections of the middle ear space.
17
Otitis
media may accompany exanthematous viral infec-
tions such as infectious mononucleosis and measles.
Over the years, chronic effusions have been
thought to be sterile. However, more recent studies
have conrmed the presence of bacteria in middle
ear uid, and studies show that the bacterial spec-
trum closely resembles that found in AOM.
18
This
Otitis Media and Middle Ear Effusions 251
information becomes increasingly important when
consideration is given to the treatment of patients
with both of these disease processes (Figure 92).
DIAGNOSIS
In most cases, a careful history and physical exami-
nation will lead to the accurate diagnosis of OM.
A careful history should elicit classic symptoms
of OM. In the patient with the acute form of the dis-
ease, otalgia, fever, irritability, vomiting, and diar-
rhea may be present. Less frequently, otorrhea,
vertigo, and facial paralysis may be associated with
an acute infection of the middle ear space. In those
patients in whom infection has spread into the mas-
toid air cell system and beyond, swelling of the
postauricular area may be present.
In COME, hearing loss may be the only symp-
tom. The most denitive part of the diagnosis is an
appropriate physical examination to conrm the
presence or absence of middle ear pathology. A
complete examination of the head and neck should
be undertaken rst to identify the possibility of any
predisposing condition such as craniofacial anom-
aly, nasal obstruction, palatal defect, or adenoid
hypertrophy. In patients with unilateral OM, the
nasopharynx should be visualized to rule out the
possibility of neoplasm.
Otoscopy represents the most critical part of the
examination to establish the diagnosis of OM (Figure
93). Use of the pneumatic otoscope is essential. The
existence of chronic middle ear effusion is most eas-
ily conrmed when there is a denite air-uid level or
when bubbles are clearly visible within the middle ear
space (Figure 94). However, ndings commonly
associated with OME include a severely retracted
tympanic membrane with apparent foreshortening of
the handle of the malleus and a reduction in tym-
panic membrane mobility (Figure 95). Occasionally,
the tympanic membrane may be dull or thickened
and have an amber hue (Figure 96). In severe cases,
middle ear uid may become purplish or blue, indi-
cating hemorrhage within the tympanic cavity.
The color of the tympanic membrane is
important but is not conclusive in making a diagno-
sis. An erythematous tympanic membrane alone
252 Ballengers Otorhinolaryngology
FIGURE 92. Bacterial incidence in chronic otitis media
with effusion.
FIGURE 91. Bacterial incidence
in acute otitis media with effu-
sion.
may not be indicative of a pathologic condition
because the vasculature of the tympanic membrane
may be engorged as a result of the patients crying or
the presence of fever.
Acute otitis media usually presents with a
hyperemic tympanic membrane that is frequently
bulging and has poor mobility (Figure 97). Occa-
sionally, perforation may be present, and purulent
otorrhea is clearly visible.
The use of tympanometry has been popular-
ized to conrm the ndings of pneumatic otoscopy.
This modality provides an objective assessment of
the mobility of the tympanic membrane as well as
the ossicular chain. By measuring tympanic mem-
brane impedance, one can accurately predict condi-
tions of the middle ear space (see Chapter 5).
The ultimate diagnostic test to conrm the
presence of OM involves aspiration of middle ear
contents. In acute situations, myringotomy or tym-
panocentesis may be undertaken to confirm the
diagnosis, obtain material for culture, and relieve
pus under pressure in an effort to avoid further com-
plications. This may be necessary in patients who are
unusually ill or toxic secondary to OM or in patients
with severe suppurative complications. It may also
be necessary in those patients who are having an
unsatisfactory response to antibiotic therapy, in toxic
newborns, or in patients who are significantly
immune decient.
With the rise in bacteria resistant to initial
antibiotic therapy, tympanocentesis has been exam-
ined for its role in more specic antibiotic therapy.
19
Bluestone recommends tympanocentesis for several
indications: (1) OM in patients with severe otalgia or
toxic patients; (2) unsatisfactory response to antimi-
crobial therapy; (3) onset of OM in a patient already
receiving antibiotics; (4) OM associated with a con-
rmed or potential suppurative complication; and
(5) OM in a newborn, sick neonate, or immunosup-
pressed patient. This procedure does have signicant
risks including conductive and sensorineural hearing
losses if not done properly. Otolaryngologists and
pediatricians must be well trained in the technique to
prevent these serious complications.
The hearing loss associated with OM should be
documented whenever possible, especially in
patients in whom chronic effusion is present.
Although the presence of a conductive hearing loss
does not conrm the diagnosis of COME, its pres-
ence does contribute to the conrmation of middle
ear fluid. It is also important in documenting
response to therapy.
MANAGEMENT
ACUTE OTITIS MEDIA
Acute otitis media represents one point in a contin-
uum of the disease process known as otitis media.
The current standard of care strongly indicates that
patients diagnosed as having an acute middle ear
process should receive antimicrobial therapy for at
least 10 to 14 days. In light of the fact that culture
material is usually not readily available, therapy is
begun on an empiric basis with treatment being
aimed at the more common microorganisms found
Otitis Media and Middle Ear Effusions 253
FIGURE 93. Normal right tympanic membrane at
otoscopy.
in the acute process. Some have recommended with-
holding antimicrobial agents in certain cases.
20
How-
ever, in light of the fact that suppurative compli-
cations have markedly declined during the antibiotic
era, antibiotic therapy is still strongly recommended
in the acute process.
20
The standard initial treatment for AOM is
amoxicillin, 40 mg/kg every 24 hours in three
divided doses, or ampicillin, 50 to 100 mg/kg every
24 hours in four divided doses for 10 days. In chil-
dren allergic to penicillin, a combination of erythro-
mycin, 40 mg/kg every 24 hours, and sulsoxazole,
120 mg/kg every 24 hours in four divided doses, may
be substituted. If -lactamase-producing H. inuen-
zae or B. catarrhalis is suspected, either amoxicillin-
clavulanate, 40 mg/kg every 24 hours in three
divided doses, or trimethoprim-sulfamethoxazole,
8 mg/kg of trimethoprim and 40 mg/kg of sul-
254 Ballengers Otorhinolaryngology
FIGURE 94. Otitis media with
effusion. Note bubbles conrm-
ing the presence of uid.
FIGURE 95. Advanced otitis
media with effusion with
markedly retracted right tym-
panic membrane, with an
apparent foreshortened handle
of the malleus and thick,
mucoid effusion.
famethoxazole every 24 hours, may be used in two
divided doses. Cexime (Suprax, Lederle Laborato-
ries, Wayne, NJ), 8 mg/kg in one dose, or cefprozil
(Cefzil, Bristol-Myer-Squibb, Princeton, NJ), 15
mg/kg every 24 hours in two divided doses, may also
be used effectively. A single intramuscular injection
of ceftriaxone (Rocephin, Hoffman-Roche, Nutley,
NJ), 50 to 100 mg/kg mixed with 1% lidocaine, not
to exceed 1.5 mL, may be used in patients with vom-
iting (Table 92). Newer treatment for -lactamase-
producing microorganisms include high-dose
amoxicillin at 80 mg/kg every 24 hours.
21
Dosages of
appropriate antimicrobial agents for use in AOM are
noted in Table 92.
Most patients who are receiving antibiotic
therapy for AOM have significant improvement
within 48 hours. If the child has not improved or the
condition has worsened, tympanocentesis for cul-
ture and possibly myringotomy for drainage may be
indicated. The patient may be re-examined some
time during the course of therapy to ensure that the
treatment has been effective.
Most children will have an effusion present at
the completion of a 10- to 14-day course of antibi-
otic therapy. Such effusions may last up to 12 weeks
before spontaneous clearance can be expected.
22
Additional therapy such as analgesics, anti-
pyretics, and oral decongestants (antihistamines and
sympathomimetic amines) may be useful. Oral
decongestants may relieve nasal congestion, provid-
ing some aeration of the ET. Their efcacy has not
been proven, however.
The patient may remain in a subacute phase of
the disease process for several weeks.
Repeated episodes of AOM plague many chil-
dren, especially during the rst 3 to 4 years of life.
Several issues should be considered and evaluated in
the management of such patients. A search should
be made for a concomitant source of infection in the
upper respiratory tract such as chronic adenoiditis
or chronic sinusitis. Mild immune immaturity, espe-
cially in the IgG subclass group, may be responsible
for this relentless process. Testing of immunoglobu-
lins should be considered in relentless cases.
Such patients may be divided into two groups,
the first being children who clear their effusion
between episodes, whereas the second is made up of
patients who have a persistent effusion between
Otitis Media and Middle Ear Effusions 255
TABLE 92. Daily Dosage for Common Antibiotic
Agents in Acute Otitis Media
Agent Dosage/24 hr
Amoxicillin 40 mg/kg in 3 doses
Ampicillin 50100 mg/kg in 4 doses
Erythromycin- 40 mg/kg (E) and
Sulsoxazole 120 mg/kg (S) in 4 doses
Amoxicillin-clavulanate 40 mg/kg in 3 doses
Trimethoprim- 8 mg (TMP) and 40 mg
sulfamethoxazole (SMZ)/kg in 2 doses
Cexime 8 mg/kg in 1 dose
FIGURE 96. Chronic otitis media with effusion.
episodes. In the latter group, chronic hearing loss
becomes an additional major issue, especially as it
impacts speech and language development.
1
Several options are available for those patients
who clear their effusion between episodes. The rst
option includes antibiotic therapy for each separate
episode; a second option would be the use of antibi-
otic prophylaxis on a prolonged basis, whereas the
third would include myringotomy and ventilation
tube insertion. The administration of pneumococcal
vaccine also may be useful.
Amoxicillin, or a suitable substitute in peni-
cillin-allergic patients, may be given once daily at
bedtime as prophylaxis. This form of therapy is usu-
ally administered during the months in which OM
has its highest prevalence.
In children in whom the middle ear does not
clear between acute episodes, ventilation tubes may
be necessary to address the concomitant hearing loss
associated with the process. Their use may also be
necessary in those patients with antibiotic allergy or
intolerance.
CHRONIC OTITIS MEDIA WITH EFFUSION
Medical Therapy Chronic otitis media with effu-
sion may occur as a sequela to AOM or in patients
who have had no documented recent episodes of
acute suppurative disease. Numerous associated fac-
tors must be considered; thus, a careful history
should be taken for the possibility of underlying
allergy, sinus disease, or nasopharyngeal obstruction,
which may be secondary to hypertrophic adenoids
or even neoplasm.
Numerous methods of management have
been advocated over the years for the persistent
form of the disease. Antihistamine-sympath-
omimetic amine preparations were used frequently
to clear the effusion. However, controlled clinical
trials have demonstrated a lack of efcacy.
23
The use
of corticosteroids, either applied topically in the
nose or given systematically, has been reported to
be advantageous in clearing middle ear fluid.
24
Unfortunately, there is a paucity of data to demon-
strate efficacy; therefore, their use cannot be
strongly recommended at this time.
The most effective medical therapy used to this
point has been antibiotic administration. Numerous
trials have concluded that some patients may
respond to a 21- to 30-day course of full-dose antibi-
otic therapy.
25
The demonstration of viable bacteria
in the middle ear effusions of chronically diseased
ears has led to this recommendation. In light of the
similarity of the bacterial spectrum, the same
antibiotics recommended for AOM may be used in
this disease. This form of therapy is strongly rec-
256 Ballengers Otorhinolaryngology
FIGURE 97. Acute otitis
media showing an erythe-
matous, bulging tympanic
membrane.
ommended in any child who has not received
antibiotic treatment before consideration is given to
myringotomy and ventilation tube insertion and/or
adenoidectomy.
Historically, there was debate as to whether
OME should be treated with antibiotics since there
exists a certain spontaneous resolution rate. Physi-
cians in other countries have traditionally not
treated OM with antibiotics as frequently as is done
in the United States. Rosenfeld and Posts meta-
analysis of studies of antibiotic therapy for OME
found a statistically signicant efcacy for short-
term resolution of OME.
16
Gates stated that approx-
imately 40% of children with OME treated with
antibiotics still have an effusion after 30 days,
whereas 10% have a documented effusion 3 months
after initial therapy.
26
Another factor that has not
been studied well to date is what the impact of
COME is on language development and learning in
the child with conductive hearing loss secondary to
COME and at what time point this decit becomes
an unacceptable risk. The success of prophylactic
antibiotic therapy for OME had also not been stud-
ied in a systematic fashion.
In children with concomitant disease of the
upper respiratory tract such as chronic sinusitis or
adenoiditis, consideration must be given to the
simultaneous control of these diseases. In addition,
systemic problems such as allergy or immunode-
ciency must also be addressed if long-term reversal
of the middle ear abnormality is to be achieved.
With the emerging role of allergy in OME, the
role of corticosteroid therapy has been re-examined.
Investigators have demonstrated that a brief course
of oral corticosteroids is efcacious for the short-
term cure of OME. The proposed therapeutic mech-
anisms include stabilization of phospholipids to
prevent arachidonic acid formation and subsequent
inammatory mediator formation, possible decrease
in peritubal lymphoid tissue size, enhanced secretion
of ET surfactant, and reduced middle ear uid vis-
cosity by action on mucoproteins.
27
The risks of oral
corticosteroid therapy in children remain a concern,
however. Studies have demonstrated an increase in
the development of AOM if corticosteroids are not
prescribed with antibiotics, transient depression in
adrenal function, and the potential for disseminated
varicella infection and its complications. Because of
these risks, Rosenfeld recommends a trial of antibi-
otics and corticosteroids only if the next step would
be tympanostomy tube placement. There have been
no good randomized controlled trials to examine the
risk-to-benet ratio.
27
Relapses have been demon-
strated within several weeks after treatment. The
effects of nasal corticosteroids or immunotherapy
on OME have not been studied.
Surgery The use of ventilation tubes with or with-
out adenoidectomy has become the ultimate treat-
ment of COME. This surgical intervention
immediately corrects the conductive hearing loss
associated with the middle ear process and dimin-
ishes the patients tendency toward recurrent infec-
tion. It should be strongly considered in the
following situations:
1. Recurrent AOM
a. Unresponsive to antibiotic therapy
b. Signicant antibiotic allergy or intolerance
2. Negative middle ear pressure with impending
cholesteatoma
3. Chronic effusion of the middle ear space with a
duration of greater than 3 months
a. Conductive hearing loss of greater than 15 dB
b. Nasopharyngeal neoplasm for which treatment
such as radiation therapy may be necessary
Although some controversy exists over the use
of ventilation tubes, they do provide a safe method
for normalizing middle ear pressure and, in most
cases, restoring hearing to normal. They are usu-
ally associated with minimal morbidity, although
tympanosclerosis or persistent perforation may be
seen in a few instances. In most circumstances, it is
difcult to determine whether these ndings are a
result of the underlying middle ear pathology with
middle ear atelectasis or secondary to the ventila-
tion tube itself. Numerous types of tubes are avail-
able for ventilation of the middle ear space, but,
basically, they are all designed to provide equaliza-
tion of pressure across the tympanic membrane
(Figure 98). Some designs favor intubation of
greater duration but also carry a slight risk of an
increased incidence of persistent perforation upon
extrusion.
Depending on the age of the patient, tube
insertion may be carried out under local or general
anesthesia.
It is usually advisable to allow spontaneous
extrusion of the tubes to occur. Most tympanostomy
tubes remain in the tympanic membrane for
Otitis Media and Middle Ear Effusions 257
approximately 6 to 12 months, with some extruding
earlier and some later.
The most common complication of tube inser-
tion is otorrhea. This may be secondary to either
reux of nasopharyngeal secretions, especially dur-
ing an upper respiratory infection, or as a result of
pathogens entering the middle ear through the
lumen of the ventilation tube. It is commonly
believed that contaminated water that is allowed to
enter the middle ear through the tympanostomy
tube may result in AOM media with otorrhea. In
these instances, the external ear canal should be
carefully cleaned and a culture obtained from the
middle ear by aspirating through the tympanostomy
tube. After this has been accomplished, oral antibi-
otics should be initiated as well as topical antibiotic
therapy. The usual treatment includes the use of
antibiotic agents commonly prescribed for other
forms of AOM.
To avoid this possible complication, water
protection of the ears is usually advised when con-
tamination may be a possibility. This may be accom-
plished through the use of earplugs or cotton
covered with petrolatum jelly, both of which can be
inserted into the ear canal to provide adequate pro-
tection. In summary, tympanostomy tubes can pro-
vide a useful means of ventilating the middle ear
space, controlling hearing loss secondary to middle
ear effusion, and controlling recurrent infection.
Adenoidectomy may be useful as an adjunct to
myringotomy in the treatment of middle ear effu-
sion.
28
Removal of adenoid tissue improves the ven-
tilatory function of the ET, thus allowing for
appropriate equalization of pressure. The adenoid
has been felt to play a role in OM in two ways: when
hypertrophic, by causing mechanical obstruction of
the ET, and when small, as a bacterial reservoir.
29
The
adenoid is thought to be an important site for pri-
mary contact of inhaled microorganisms. Two stud-
ies are frequently cited regarding the use of
adenoidectomy in OME. Gates demonstrated greater
long-term efcacy in the treatment of OM in chil-
dren 4 to 6 years of age when adenoidectomy
was added to tympanostomy tube placement or
myringotomies even if this was the rst surgical
intervention in a child.
26
Paradise et al, on the other
hand, recommend adenoidectomy only if a child
fails initial tympanostomy tube placement.
30
Studies
have also shown that the recurrence rate of AOM
may be reduced by adenoidectomy.
30
In addition,
other confounding factors may warrant adenoidec-
tomy such as evidence of chronic adenoiditis, nasal
obstruction, or recurrent or chronic sinusitis sec-
ondary to nasal obstruction.
258 Ballengers Otorhinolaryngology
FIGURE 98. Ventilation tube
in place in the right tympanic
membrane.
CONCLUSION
The future solution to OM, acute or chronic, does
not lie in current therapy regimens. Manipulation
of the immune system to provide enhanced protec-
tion will probably result in a signicant decrease in
the incidence of this disease process. Vaccination
may play a signicant role in this endeavor. Both
nontypable H. inuenzae and S. pneumoniae are
leading etiologic factors in the development of bac-
terial OM and have polysaccharide capsules. Poly-
saccharide vaccines lack immunogenicity in infants
and children under 2 years. Based on the same
premise as the successful H. inuenzae type b vac-
cine, in which the capsular polysaccharide is conju-
gated with a protein, a heptavalent pneumococcal
conjugate vaccine, PCV7 (Prevanar, Wyeth-Lederle
Vaccines), has become available. PCV7 and other
pneumococcal vaccines may prove to be an impor-
tant step in the prevention of AOM. This vaccine is
recommended for universal use in children 23
months and younger. The American Academy of
Pediatrics recommends that if immunization is ini-
tiated in infants younger than 7 months, four doses
of PCV7 be given concurrently with other recom-
mended childhood immunizations at 2, 4, 7, and 12
to 15 months. If immunization is initiated in infants
who are between 7 and 23 months of age, who have
not received their prior doses of PCV7, fewer doses
are recommended. Children with congenital
immunodeficiency, chronic cardiac disease, and
infection with human immunodeficiency virus,
chronic pulmonary disease, and other serious
chronic conditions are especially vulnerable to
pneumoccocal infection.
31
Attempts are under way
to develop conjugated vaccines against nontypable
H. influenzae and B. catarralis, which also has a
polysaccharide capsule. It is too early to determine
the impact of vaccination on the incidence of AOM.
Other factors such as the role of gastroesophageal
reux or the role of such substances as surfactant
have yet to be determined.
Currently, OM represents a costly medical
problem worldwide. In some cultures, its morbidity
with associated hearing loss, learning difculties,
and secondary central nervous system complications
are almost unmeasurable. This signicant medical
problem deserves more research attention than it
receives so that signicant costs and morbidity asso-
ciated with it can be reduced. Berman et al have
developed a cost-effectiveness model for OME ther-
apy.
32
Their recommendations include a trial of cor-
ticosteroids and antibiotic therapy at the 6-week
follow-up visit if no resolution, another course of
antibiotics at the 9-week visit, and tympanostomy
tube placement if no resolution at 12 weeks. With
OM continuing to be one of the most common rea-
sons for physician visits in children today, nding
the safest, most efcacious, and cost-effective treat-
ment remains an important goal.
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