CASE DISCUSSION

ACUTE OTITIS MEDIA

Supervisor
dr. H. Oscar Djauhari, Sp. THT-KL

Presentants
Michael (2014-061-107)
Paulus Stephen (2014-061-110)

Clinical Rotation
Otolaryngology, Head and Neck Department
Medical Faculty of Unika Atma JayaSyamsudin, S.H. Regional General
Hospital, Sukabumi
Period of 30 November 2015 28th December 2015
th

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 CASE DISCUSSION

A 7-years-old boy came to ENT clinic with a complaint of right earache since 2 past days. He
was also having cold, runny nose and fever since 2 weeks days.

A. PATIENTS IDENTITY
Name : Boy. K
Gender : Male
Age : 7 years old
Occupation : Primary school student
Address : Sukabumi

B. HISTORY
Chief Complaint : right earache since 2 past days
Additional Complaint : cold, runny nose, and fever since 2 weeks past
History of Present Illness
A 7-years-old boy came to ENT clinic with right earache since 2 past days.
The earache was felt insidiously and continuously all day. The pain was increasing in
severity, from mild pain at the beginning until severe pain at the time of presentation.
The boy also felt a sensation of fullness at the right ear, and hearing loss since 4 day
prior to admission. There was a high-grade fever following this earache. History of ear
discharge, foul-smell discharge, facial pain was denied.
Two weeks before admission, the child suffered from runny nose, cold, and
fever. The nasal discharge was clear, watery, and massive in amount. The boy also had
low-grade fever.
History of previous treatment was denied.

History of Past Illness

History of previous illness was denied

History of Family Illness

History of family illness was denied

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C. PHYSICAL EXAMINATION
General condition : Appear ill
Body weight : 21 kg
Height : 120 cm
Blood pressure : 110/60 mmHg
Pulse : 120 beat per minute
Respiratory rate : 24 times per minute
Temperature : 38, 8oC

ENT Examination
Ear
Right ear
- Auricle : normal
- External auditory canal:
hyperemic (-), edema (-), mass (-), laceration (-) secretion (-) , cerumen (+)
- Tymphanic membrane:
Intact, hyperemic (+), bulging (-), light reflex

Left ear
- Auricle : normal
- External auditory canal:
hyperemic (-), edema (-), mass (-), laceration (-) secretion (-) , cerumen (+)
- Tymphanic membrane:
Intact, bulging (-), light reflex (+)

Nose
Right nose
- Mucous membrane:
hyperemic (+), edema (+), yellowish mucoid secretion (+), mass (-), laceration (-
), crust (-)
- Inferior conchae : eurtrophy
- Septum : no deviation

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 - Air passage : normal
Left nose
- Mucous membrane:
hyperemic (+), edema (+), yellowish mucoid secretion (+), mass (-), laceration (-
), crust (-)
- Inferior conchae : eurtrophy
- Septum : no deviation
- Air passage : normal

Oropharynx
- Posterior pharynx : hyperemic (-)
- Palatine tonsils : T1 / T1, hyperemic (-), detritus (-)
- Uvula : symmetrical
- Dental : no abnormatlities

Maxillofacial : symmetrical

Neck : mass (-), lymphadenopathy (-)

D. WORKING DIAGNOSIS
Acute otitis media dextra, hyperemic stage

E. DIFFERENTIAL DIAGNOSIS
-

F. WORK-UP
-

G. TREATMENT
Outpatient care
Antibiotic : Amoxicilin 3 x 500 mg PO for 7 days
Antipyretic and analgetic : Paracetamol 3 x 250 mg PO for 3 5 days
Topical anticholinergic : Oxymetazoline HCL nasal spray 2 x 3 sprays per
nostril for 3 days

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 ACUTE OTITIS MEDIA

An estimated 85% of all children experience at least one episode of acute otitis media,
making it the most common bacterial infection of childhood.3 Predisposing factors include
being of a young age or themale sex, receiving bottle feedings, and being exposed to a
daycare environment, crowded livingconditions, or smoking within the home. Medical
Condition`s such as cleft palate, Down syndrome, and mucous membrane abnormalities such
as cystic fibrosis, ciliary dyskinesia, and immunodeficiency states also predispose individuals
to otitis media.
Definitions and Terminology
Otitis media represents an inflammatory condition of the middle ear and mastoid
space, without reference to etiology or pathogenesis. Numerous terms and classifications
have been used to define the various inflammatory processes related to OM. The current
terminology is based on knowledge of the pathogenesis of OM as well as on the etiology and
clinical course. The presence or absence of middle-ear effusion (MEE) and its duration help
further to define the process. Effusion is the liquid resulting from infection and mucosal
inflammation and can occur in all areas of the pneumatized temporal bone. Effusion may be
serous (thin, watery), mucoid (thick, viscous), or purulent (pus). The temporal sequence of
the process may be described as acute (0 to 3 weeks in duration), subacute (3 to 12 weeks in
duration), or chronic (longer than 12 weeks in duration). However, the duration of the disease
can be very difficult to determine unless the patient's previous middle-ear status is known to
the examiner. Tympanograms and audiograms obtained previously can often help to define
the duration further.
The term recurrent AOM indicates four or more episodes of acute OM in 1 year or
three or more episodes in a 6-month period. Medically refractory AOM has persistent signs
and symptoms of AOM despite appropriate medical therapy. Otitis media with effusion
(OME) can occur as a postinflammatory response to AOM, from a viral infection, or because
of Eustachian-tube dysfunction. When OME is a persistent fluid collection, it can cause
decreased mobility of the tympanic membrane, serving as a barrier to sound conduction.
Many children with OME are asymptomatic. Chronic suppurative otitis media (CSOM) is
characterized by persistence of purulent otorrhea through a tympanic membrane (TM)
perforation or tympanostomy tube (TT) that is unresponsive to medical therapy. Further

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description of the TM (intact, perforated, TT present, retracted, atelectatic, or presence of
tympanosclerosis) will help more clearly define the examination.

Epidemiology
The epidemiology of OM has been well studied. The onset of AOM during the first
year of life is important because the majority of children with multiple recurrences of AOM
have their first episode before the age of 12 months . If a child has not had OM before the age
of 3 years, he is statistically unlikely to develop severe or recurrent OM. In a study by Bondy
et al., the proportion of children with a diagnosis of OM was highest (42% to 60%) in the 7-
to 36-month age range. Other studies have shown the highest incidence of AOM for both
sexes was in the 6- to 11-month age group.
More than 50% of children experience OME in thefirst year of life. Although many
episodes resolve spontaneously, 30% to 40% persist, and 5% to 10% of episodes last 1 year
or longer. OME is diagnosed 2.2 million times annually. Investigations involving healthy
children have revealed a high incidence of asymptomatic OME. The incidence of OME
appears to peak during the second year of life, is most prevalent during the winter months,
and is associated with upper respiratory infections (URIs). Most children have resolution of
asymptomatic MEE within a few months without medical or surgical intervention.
Spontaneously, 30% to 40% persist, and 5% to 10% of episodes last 1 year or longer. OME is
diagnosed 2.2 million times annually. Investigations involving healthy children have revealed
a high incidence of asymptomatic OME. The incidence of OME appears to peak during the
second year of life, is most prevalent during the winter months, and is associated with upper
respiratory infections (URIs). Most children have resolution of asymptomatic MEE within a
few months without medical or surgical intervention. In some studies, the incidence of AOM
is similar between boys and girls. However, several other studies have shown a higher
incidence in boys than in girls. Although some studies have shown an increased incidence of
OM in American white and Hispanic children in comparison to American black children,
Casselbrant and colleagues and Paradise et al found that black children had at least as much
middle-ear disease as did white children who had received equivalent care. A very high
incidence of middle-ear infections has been reported in Native Americans and Eskimos,
despite excellent access to medical care.
Casselbrant and colleagues showed a strong genetic predisposition to OM, with a
higher incidence of OM in children who have siblings or parents with a significant history of
OM. Children who live in crowded households or low socioeconomic conditions or who have
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poor medical care or both also have been found to have an increased incidence in both acute
and chronic OM. These factors are not definitive in all studies, however, and may simply
reflect increased exposure to many other children with URIs. In addition, the relation
between attending day care and an increased incidence of OM in children younger than 3
years is well established. Contributing factors for this increased incidence include exposure to
large numbers of other children (often with URIs), decreased breast-feeding, and exposure to
second-hand smoke. Seasonal variation in the incidence of OM also has been reported, most
commonly in winter, fall, and spring. All studies have shown a correlation between the
frequency of URIs and incidence of OM, and MEE that is associated with URI in the winter
months lasts longer than in the summer.

Risk Factors for Middle-Ear Disease

Many medical and or anatomic abnormalities have been noted to increase the risk of
middle-ear disease. Craniofacial anomalies affecting Eustachian tube (ET) function often
increase the risk of OM. Children with a cleft palate or deformity of the midface, skull base,
or nose/paranasal sinuses have a statistically higher incidence of OM at all ages, especially
during the first 2 years of life. Although some studies have shown that the incidence of
middle-ear disease decreases after surgical repair of the cleft palate, many children with a
cleft palate continue to have middle-ear problems. Other craniofacial disorders associated
with an increased risk of OM include Down syndrome, Apert syndrome, and the
mucopolysaccharidoses.
Children with congenital or acquired immunodeficiency are at a higher risk of many
types of infection, including middle-ear disease. Children with conditions such as
hypogammaglobulinemia, immunoglobulin (IgA) deficiency, DiGeorge syndrome, human
immunodeficiency virus (HIV) disease, and drug-induced immunodeficiency (chemotherapy,
steroids) often have difficulty fighting and clearing infections. Infants and young children
have immature immune systems, which appear to make them more susceptible to OM.
Other conditions associated with an increased incidence of OM include allergy, nasal
obstruction (sinusitis, adenoid hypertrophy, nasal or nasopharyngeal tumors), ciliary
dysfunction, and prolonged nasal intubation or nasogastric tube placement, and possibly
gastroesophageal reflux. A role for allergy in the etiology of OM has long been postulated
(Fig. 91.2). The first OME guideline found no data supporting antihistamine-decongestant
combinations in treating OME. Meta-analysis of four randomized trials showed no significant

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benefit for antihistamines or decongestants versus placebo. The second OME guideline found
that no additional studies have been published since 1994 to change this recommendation.
Most children with recurrent or persistent OM have intact immune systems. However,
if the middle-ear infections are especially severe or are associated with recurrent sinusitis,
bronchitis, or gastrointestinal problems, immunologic abnormalities may be present. The
middle-ear mucosa has a secretory immune system similar to the rest of the respiratory tract.
Middle-ear effusions that result from acute or chronic infection contain immunoglobulins
IgA, IgG, IgM, IgD), immune complexes, and chemical mediators involved in the
inflammatory response. Possible humoral immune deficiencies in children with OM include
IgA, IgG (especially of IgG subclasses 2 and 3), and complement deficiency. Otitis media
also may be one of the multiple infectious complications seen in the presence of neutropenia
or HIV disease. Defects in immune cell function such as problems with chemotaxis,
phagocytosis, and killing can predispose to OM. In comparing otitis-prone children with
those who have only occasional episodes of OM, Prellner and Kalm noted a decreased ability
of the OM-prone children to produce antibodies against AOM-associated antigens, and these
children also may have delayed B-cell maturation.

Pathophysiology
Abnormal function of the ET is the cornerstone of the pathogenesis of OM. The ET in
infants and children is shorter, more horizontal, and functionally less mature compared with
that in adults. Conditions such as URIs lead to edema and congestion of respiratory mucosa
of the ET and middle ear, causing narrowing of the ET lumen. This leads to an increase in
negative middle-ear pressure, causing an influx of bacteria and viruses from the nasopharynx

8
when the ET opens. The bacteria and viruses in the middle ear then elicit an inflammatory
response. The acute inflammatory response includes mucosal edema, capillary engorgement,
and infiltration of polymorphonuclear leukocytes into the middle-ear space. As the
inflammatory response becomes chronic, infiltration of lymphocytes, proliferation of the
mucosal lamina propria, enzymatic destruction of bone, and granulation tissue formation
occur, which worsens the obstruction and ventilation of the middle ear and ET.
Other confounding variables affecting ET function include patulous or
functionally/anatomically obstructed tubes, and abnormalities of the respiratory mucosa,
including allergy, immunocompromise, and ciliary dysfunction (see Fig. 91.2). Allergy has
long been implicated in the etiology of OM, but the exact mechanism remains elusive.
Possibilities include inflammatory swelling of the middle ear mastoid ET mucosa or allergic
nasal obstruction. However, because large numbers of highly allergic children do not have
significant otitis, and many children with significant otitis do not have documented allergy,
the relation between allergy and OME is clearly not a straightforward one. Speculation has
long occurred regarding food allergy and OME. Although no consensus has been reached, a
study by Aydogan et al. found food allergy in 44% of patients diagnosed with OME.
Conversely, in patients with known food allergy, 25% were found to have OME. In the
control group, 18% were diagnosed with food allergy, and 3% were diagnosed with OME.
Children with congenital or acquired immunocompromise require special
consideration, because they are often more susceptible to infections, including OM, and to
unusual organisms. Congenital immune abnormalities include B-cell deficiencies, such as
hypogammaglobulinemia and IgA deficiency; T-cell deficiencies, such as DiGeorge
syndrome; combined T- and B-cell deficiencies, including ataxia telangiectasia; phagocyte
defects, including Chediak-Hagashi syndrome; and complement deficiencies. Acquired
abnormalities include those secondary to neoplasms and inflammatory processes such as
acute or chronic infections. Drugs causing immune deficiencies include steroids,
chemotherapeutic agents, and antirejection agents used in transplantation patients. Although
severe forms of immune deficiency are uncommon in children, many of the otherwise normal
otitis-prone children may have immature immune systems, as documented by poor response
to polysaccharide antigen vaccines, including Haemophilus influenzae type B (HIB), tetanus,
and pneumococcal vaccine.
Abnormalities, either physiologic or anatomic, of the palate-associated musculature
(especially the tensor veli palatini) may cause or worsen ET dysfunction. For example, many
craniofacial abnormalities, including cleft palate, Crouzon syndrome, Apert syndrome, and
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Down syndrome, are associated with abnormal skull base or palate musculature with resultant
ET dysfunction.

Microbiology
The most commonly identified aerobic pathogens associated with AOM are
Streptococcus pneumoniae (30% to 50%), nontypable Haemophilus influenzae (20% to
30%), Moraxella catarrhalis (10% to 20%), and group A streptococci (1% to 5%). Other
bacteria, such as Staphylococcus aureus and gram-negative enteric organisms, including
Escherichia coli, Klebsiella species, and Pseudomonas aeruginosa, are consistently isolated in
a small proportion of patients. In neonates and young infants, S. pneumoniae and H.
influenzae are still the most commonly isolated pathogens; however, S. aureus, group B
streptococci, gram-negative enteric pathogens, and other organisms are found up to 20% of
the time. In immunocompromised children or those requiring prolonged hospitalization,
unusual organisms (i.e., Mycobacterium tuberculosis, Mycoplasma pneumoniae, and
Chlamydia trachomatis) have been isolated. M. pneumoniae is an important upper respiratory
pathogen in children and adults. Although it has been infrequently isolated from middle-ear
fluid in immunocompetent children, it is not considered a major pathogen for OM.
Chlamydia trachomatis is associated with pneumonitis in infants and has occasionally been
isolated from the middle ear of infants younger than 6 months.
-Lactamase producing bacteria are increasingly causing middle-ear disease. Up to
34% of the H. influenzae and 100% of M. catarrhalis are -lactamase positive. Although S.
pneumoniae does not make beta-lactamase, other resistance factors, including chromosomal
alterations, lead to a decrease in penicillin-binding proteins and an increase in resistance to
sulfa, chloramphenicol, tetracycline, and trimethoprim. The exact percentage of bacterial
resistance for any particular organism varies with the geographic area and the population
studied. Possible clinical factors in the development of bacterial resistance to antimicrobials
include multiple and prolonged courses (including prophylaxis), not taking the entire
prescribed course, and inappropriate administration.
In patients with medically refractory AOM who exhibit signs of toxicity despite
second-phase antibiotics, middle-ear cultures at the time of urgent myringotomy show
primarily gram-positive bacteria (coagulase negative staphylococci, Staphylococcus aureus,
and Streptococcus pneumoniae, in decreasing order of incidence). Block et al. looked at
children aged 7 to 24 months who were vaccinated with heptavalent pneumococcal vaccine

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and who had severe or refractory AOM and found them to have twofold more gram-negative
bacteria than S. pneumoniae.
In the past, chronic MEE was often thought to be sterile. However, several studies
have isolated S. pneumoniae, H. influenzae, M. catarrhalis, and group A streptococci in 30%
to 50% of children with chronic MEE. In 1995, Post et al. reported on the usefulness of the
polymerase chain reaction (PCR) in the detection of bacterial DNA in pediatric MEE samples
that were sterile by standard culture techniques. In this study, 77.3% of patients tested PCR
positive for one or more of the standard organisms (M. catarrhalis, S. pneumoniae, H.
influenzae), whereas only 28.9% were both PCR and culture positive for one or more of these
organisms. No samples were culture positive and PCR negative. Although these results are
not proof of an active bacterial infections process, they suggest that bacteria may be present
in a higher percentage of OME specimens than was previously thought. A positive PCR
result may indicate the presence of viable, although nonculturable, bacteria. The role of
anaerobic bacteria in chronic MEE remains unclear; they have been isolated in up to 10% of
chronic MEE samples. Anaerobic bacteria play a minor role in the pathogenesis of AOM. In
chronic OME, anaerobic organisms such as Peptostreptococcus spp., Prevotella spp., and
Propionibacterium acnes have been isolated.
The role of viruses as primary or copathogenic organisms in OM has gained
increasing attention. Viruses such as respiratory syncytial virus, rhinovirus, influenza virus,
adenovirus, enterovirus, and parainfluenza viruses have been isolated from middle-ear fluid.
Cytomegalovirus and herpes simplex viruses also have been isolated in a smaller number of
cases. Respiratory viruses may potentiate the possibility of nasopharyngeal colonization with
bacteria, further increasing the incidence of OM. OM also is known to accompany viral
exanthems, including measles and the Epstein Barr virus.

Evaluation
History
The diagnosis of OM is based on history and physical examination. AOM is
characterized by acute onset of signs and symptoms of middle-ear inflammation with MEE
seen on physical examination. Symptoms are variable but commonly include fever,
irritability, otalgia, and hearing loss. Other symptoms include anorexia, nausea, vomiting, and
headache.
Children themselves may complain of hearing loss, dizziness, and tinnitus. Fever is
present in up to two-thirds of children with AOM, but fever over 40C is uncommon and may
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represent bacteremia or other complications. Other symptoms associated with AOM include
anorexia, nausea, vomiting, and headache. Children may complain of hearing loss, dizziness,
and tinnitus. Parents and caretakers of infants and younger children may notice hearing loss
or loss of balance. Because the ET is less functional when the child is lying down, symptoms
often appear worse at night or during naps. In children with OME, hearing loss may be the
only symptom. Children with draining ears (especially if chronic) may have little or no pain
and may sleep well, but may still complain of hearing loss and occasional low-grade fevers.
Children with dry TM perforations are usually asymptomatic except for hearing loss.
Children with TM perforations who get water in their ears may experience significant
discomfort. Finally, children with atelectasis of the TM also are usually asymptomatic,
although many of these children experience hearing loss as well. Physical

Examination
Although pneumatic otoscopy is the most important part of the physical examination
for OM, complete evaluation of the head and neck is essential. The pinnae, external auditory
canal, TM, and middle-ear landmarks should be evaluated. If the ear is rotated forward with
edema or erythema of the posterior auricular sulcus, acute mastoiditis may be present.
Pneumatic otoscopy requires the child to be immobile but not uncomfortable. If the child is
extremely uncooperative or cannot be immobilized safely, sedation or general anesthesia may
be needed if the examination is thought to be very important for the diagnosis and treatment
of the ear disease.
The normal TM is gray and translucent with normal mobility on pneumatic otoscopy.
Middle-ear landmarks that may be seen through a normal TM include the short process of the
malleus, the incudostapedial joint, and occasionally the chorda tympani. The position of the
TM can be neutral, bulging, retracted, or full. The color of an abnormal TM is frequently
opaque and may appear yellow or blue (indicating MEE), dark red (trauma, hemorrhage), or
red (AOM or hyperemia due to crying or coughing). The mobility of the TM should be
assessed on both positive and negative pressure. Decreased mobility of the TM on both
positive and negative pressure often indicates MEE, whereas movement only with negative
pressure suggests ET dysfunction. In the case of a patent TT or TM perforation, no mobility
of the TM is found. Middle-ear effusion can be described as serous (thin, watery), mucoid
(thick, viscous), purulent, or clear (which may indicate inflammation or a cerebrospinal fluid
leak). Air-fluid levels or bubbles may be seen, indicating intermittent aeration of the middle
ear through the ET.
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 The location and size of a TM perforation should be noted; it can be of any size, and
occasionally more than one may be seen. An acutely perforated TM is often erythematous
and thickened, with otorrhea discharging through the perforation. Perforations in the posterior
superior quadrant can be difficult to visualize and are often associated with cholesteatoma.
Evaluation of the TM may reveal other pathology, including tympanosclerosis, retraction
pockets, or areas of atelectasis. Tympanosclerosis appears as white and thickened areas of the
TM that must be distinguished from cholesteatoma. Retraction pockets can be located
anywhere in the TM and may represent areas of atelectasis, healed TT or perforation sites, or
the effect of persistent negative middle-ear pressure. Retraction pockets, especially if filled
with debris or associated with otorrhea, may indicate a cholesteatoma.

Hearing Evaluation
Evaluation of hearing is an essential part of the workup in every patient with a history
of middle-ear disease. The method of audiologic workup can be divided into two groups: (a)
audiometric evaluation, to test the peripheral hearing; and (b) immitance audiometry to
evaluate the stiffness of the TM and middle-ear system. Conductive hearing loss is the most
common finding with a history of OM. The type of audiometric evaluation varies based on
the age of the patient, level of cooperation, and maturity. Otoacoustic emissions are one of
the techniques of choice for hearing screening in the newborn nursery. Middle-ear effusion is
one of the main causes of otoacoustic emission (OAE) failure; therefore OAE should not be
used for evaluation of hearing related to middle-ear disease. Auditory brainstem response is
the method of choice to distinguish conductive from sensorineural hearing loss in infants
younger than 6 months. Auditory brainstem response also is recommended in children who
are unable to participate in other audiometric evaluations because of lack of cooperation or
maturity regardless of the age, or if ear-specific information is needed. Behavioral
observation audiometry (BOA) is recommended for infants aged 6 months to 1 year, and
visual reinforcement audiometry (VRA) is used for toddlers aged 1 to 2 years. The accuracy
of BOA and VRA relies on the level of experience of the audiologist and the developmental
level of the child. BOA and VRA do not accurately differentiate between conductive hearing
loss and sensorineural hearing loss and do not generally provide ear-specific information.
Play audiometry is recommended in a cooperative child older than 2 years and is not only ear
specific but also distinguishes the type of hearing loss (conductive or sensorineural).
Conventional audiometry can be used in a cooperative child older than 5 years.

13
 Tympanometry is a measure of sound reflected by the TM and middle-ear structures.
This provides a graphic representation of compliance changes as the ear-canal pressure is
varied. Different tympanometric patterns are associated with middle-ear and TM pathology.
Measurement of ear-canal volume can be undertaken to assess further the status of the middle
ear and specifically the TM. Children with a perforated TM or patent TT will have a larger
ear-canal volume. Different immitance audiometry techniques are available to evaluate the
middle ear further if needed.
Acoustic reflectometry is used to measure the total level of the reflected and
transmitted sound. A hand-held instrument is placed in the external auditory canal to provide
an 80-dB sound source that varies from 2,000 to 4,500 Hz in a 100-ms period. The sensitivity
and specificity of this method is operator dependent and varies from fair to excellent.
Although acoustic reflectometry is not widely used for the diagnosis of middle-ear disease, it
can be a useful adjunct to otoscopy and impedance audiometry.

Treatment and Prevention

The rationale for treating OM includes avoidance of complications and treatment of
symptomatic disease. Secondary reasons include buying time until the child's ET function
and immune system have matured, and in many cases, waiting for the end of the URI season.
Management is usually medical, with surgical intervention reserved for failures of medical
therapy (Tables 91.3 and 91.4). AOM has a spontaneous resolution rate of 60% within 24
hours and 80% within 2 to 3 days. Reasons for spontaneous resolution may include drainage
of MEE down the ET or through a perforated TM, efficacy of local or systemic immunity, or
AOM that has resulted from a virus or some noninfectious process. Sometimes the diagnosis
is in error, especially in a crying child with red eardrums. The most recent guidelines
regarding diagnosis and management of AOM come from an evidence-based clinical practice
guideline for children aged 2 months through 12 years with uncomplicated AOM. The
American Academy of Pediatrics and American Academy of Family Physicians convened a
committee composed of primary care physicians and experts in the fields of otolaryngology,
epidemiology, and infectious disease to review the literature and make the guidelines. These
are guidelines only, and each patient should be managed by taking into account the age and
illness severity in the child, as well as any underlying illness or disease process that may
make the OM more difficult to manage or less likely to resolve spontaneously.

AOM Diagnosis and Management Guidelines

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The following recommendations were made in the AOM guidelines:

1. Confirm a history of acute onset, identify signs of middle-ear effusion (MEE), and
evaluate for the presence of signs and symptoms of middle-ear inflammation.
2. An assessment for pain should be completed and, if pain is present, the clinician
should recommend treatment to reduce pain.
3. Observation without use of antibacterial agents in a child with uncomplicated AOM is
an option for selected children based on diagnostic certainty, age, illness severity, and
assurance of follow-up.
4. If a decision is made to treat with an antibacterial agent, the clinician should prescribe
amoxicillin for most children. When amoxicillin is used, the dose should be 80 to 90
mg/kg/day.
5. If the patient fails to respond to the initial management option within 48 to 72 hours,
the clinician must reassess the patient to confirm AOM and exclude other causes of
illness. If AOM is confirmed in the patient initially managed with observation, the
clinician should begin antibacterial therapy. If the patient was initially managed with
an antibacterial agent, the clinician should change the antibacterial agent.
A definite diagnosis of AOM should meet the following criteria: rapid onset,
presence of MEE, and signs and symptoms of ME inflammation. The position of the
TM can be neutral, bulging, retracted, or full. The color of an abnormal TM is
frequently opaque and may appear yellow or blue (indicating MEE), dark red (trauma,
hemorrhage), or red (AOM or hyperemia due to crying or coughing). When combined
with color and mobility, bulging is the best predictor of AOM. If pain is not
adequately managed with appropriate doses of acetaminophen or ibuprofen or topical
otic analgesics, or if significant pain lasts longer than 24 hours, further medical
evaluation should be undertaken. If the child has a TT or suspected or confirmed TM
perforation, topical analgesics should be avoided. If otorrhea is seen through a TT or
TM perforation, the use of topical antimicrobial otic drops that have been approved
for use in the presence of a nonintact TM can be considered. Because no particular
pain-management strategy has been well studied in this setting, the clinician should
use his or her judgment in choosing medication for otalgia.
The observation option includes watchful waiting for 48 to 72 hours in
selected children, with pain management only. Appropriate patients for this option
may include healthy children aged 6 months to 2 years with nonsevere symptoms and

15
 an uncertain diagnosis of AOM or children aged 2 to 12 years who have nonsevere
symptoms or an uncertain diagnosis. If this option is chosen, the patient and family
should have reliable access to a clinician if reevaluation or medication is needed. If
complications are present, if the child has an underlying medical condition that would
make this option potentially problematic, if the family does not have ready access to
follow-up medical care, or if the clinician or family is not comfortable with the
option, then this may not be an appropriate management strategy for the child.
The recommendation for amoxicillin use was made because of its safety and
general efficacy profile. However, if the child is immunocompromised, if unusual or
resistant organisms are suspected, or if the patient is allergic to amoxicillin, other
antibacterial agents should be considered. The AOM guidelines further state: When
antibacterial agents are prescribed for AOM, the time course of clinical response
should be 48 to 72 hours. When observation has been the chosen management and
spontaneous improvement has not been noted by 48 to 72 hours, antibacterial therapy
is indicated to limit the duration of further illness. They recommend amoxicillin
clavulanate for patients with severe illness, if additional coverage for beta-lactamase
positive H. influenzae and M. catarrhalis is indicated and if those patients initially
treated with amoxicillin did not improve. As always, the clinician should use his or
her judgment for each patient, based on the physical examination, prior or recent use
of antibacterial agents, severity of illness, and medication allergy profile.
6. During infancy and early childhood, reducing the incidence of respiratory tract
infections by altering child-care-center attendance patterns can reduce the incidence
of recurrent AOM significantly. The implementation of breastfeeding for at least the
first 6 months also seems to be helpful against the development of early episodes of
AOM.
7. No recommendations were made regarding the use of complementary or alternative
medicine. This was based on the lack of evidence of the efficacy or effectiveness of
any complementary and alternative medicine (CAM) therapy in comparison to the
natural history of AOM.

Prevention
Several measures have been suggested to prevent OM, including antimicrobial
prophylaxis, allergy control, tonsillectomy or adenoidectomy or both, vaccination, the
administration of immunoglobulins, and changing possible environmental contributors.

16
Allergy management may help if a specific allergen can be identified. Intravenous -globulin
may occasionally be recommended for proven or suspected immunoglobulin deficiency.
However, as in the case of allergies, specific medical or surgical management of the otitis
may be needed while waiting for the allergies to become more controlled and for the immune
system to mature. Changes in environmental factors that may help decrease OM include
removing possible allergens, prolonging breastfeeding, removing the child from day care (or
moving the child from a large day-care situation to a small home-care situation), and
preventing exposure to second-hand cigarette smoke.
Vaccines directed against the bacteria and viruses that are associated with OM
provide an intriguing method for possible prevention. Most of the vaccine research has been
aimed at S. pneumoniae and nontypable H. influenzae, which is important now that these
bacteria have developed significant antimicrobial resistance patterns. The older 23-valent S.
pneumoniae vaccine has not proven very immunogenic in children younger than 6 years.
However, the new heptavalent S. pneumoniae appears to be very effective against invasive
pneumococcal disease. Use of the heptavalent pneumococcal conjugate vaccine has led to a
major decline in the prevalence of invasive pneumococcal disease (bacteremia, meningitis)
and a more modest decrease in respiratory tract infections (AOM, pneumonia). Recent studies
looking at vaccinated children revealed an increase of infections with serotypes not included
in the vaccine. Several studies have shown only a small effect on prevention of AOM with
pneumococcal conjugate vaccination in children younger than 2 years.
Vaccination against the viruses that are associated with OM has potential for great
benefit. Clements et al. reported that children aged 6 to 30 months who had received the
influenza vaccine had 32% fewer episodes of AOM than did those who did not. In a
randomized controlled trial, Hoberman et al found influenza vaccination to be no more
effective than placebo in children aged 6 to 24 months. No consensus exists regarding
influenza vaccination and prevention of AOM in children younger than 2 years. Children
younger than 2 years continue to experience the greatest number of AOM episodes but do not
appear to develop the strong immune response from vaccinations that older children display.

Surgical Therapy: Myringotomy and Tube Insertion

The use of ventilation tubes has become the treatment of choice for (a) recurrent
AOM unresponsive to medical therapy, (b) chronic OM with persistent effusion for 3 months
and conductive hearing loss, (c) negative middle-ear pressure with impending cholesteatoma,
and (d) intervention in the presence of complications of OM. Insertion of ventilation tubes
17
not only normalizes the middle-ear pressure, but it also decreases the frequency and severity
of AOM and generally resolves the conductive hearing loss associated with persistent
effusion. For children with very severe recurrent AOM, both ventilation tubes and
prophylactic antibiotics may be necessary. Children requiring both tubes and antibiotics to
manage their otitis effectively often have mild immune dysfunction that improves with time.
The average time that TTs remain in place and functional is 6 to 12 months after insertion.
Complications of ear tubes include otorrhea, persistent TM perforation when the tube
has extruded, scarring or tympanosclerosis involving the TM, plugging of the tube, formation
of granulation tissue around the tube, atrophic or thinned areas of the TM (where the tube
was), early extrusion or extrusion into the middle ear, and cholesteatoma. Otorrhea is
relatively common, occurring 12% to 30% of the time right after tube insertion, especially if
the MEE was purulent or mucoid, and in up to 50% of children at some point during the time
the tubes are in place. Otorrhea often occur secondary to a URI. Tympanic membrane
perforations that do not close spontaneously occur in up to 2% to 3% of ears with TTs,
although this number is higher (17%) with long-term tubes. Factors that may be related to a
higher persistent perforation rate include tube retention beyond 36 months and multiple sets
of tubes.

Adenoidectomy and Tonsillectomy

Historically, adenoidectomy has been recommended as an adjunctive treatment in the
management of chronic OM. The results of studies evaluating the efficacy of adenoidectomy
in preventing or decreasing middle-ear disease vary widely. Some fundamental differences
are found in these studies with regard to (a) definition of OM, (b) presence or absence of
environmental allergy, (c) adenoid size, (d) status of the ET, and (e) concurrent surgeries (i.e.,
tonsillectomy). Several studies have shown that time to recurrence of effusion, duration of
effusion, and the need for further surgery were reduced in the adenoidectomy group. Paradise
and colleagues also evaluated the usefulness of adenoidectomy in the management of
recurrent AOM and determined that the number of episodes of AOM was 35% in the
adenoidectomy group versus 28% in the control group (TTs without adenoidectomy); see
reference 30a. Gates and colleagues evaluated various combinations of myringotomy,
adenoidectomy, and TT placement for OME. They found that time with recurrent MEE was
decreased by 29% (tube only), 38% (adenoidectomy and myringotomy), and 47%
(adenoidectomy and tubes). Infor-mation about adenoidectomy in children younger than 4
years remains limited. Approximately eight adenoidectomies are needed to avoid a single
18
instance of tube reinsertion (however, this probably represents a larger reduction of
AOM/OME, including those that did not require additional surgery).
Although anecdotal evidence suggests that tonsillectomy is helpful, no study
demonstrates significant efficacy of tonsillectomy and adenoidectomy over adenoidectomy
alone in prevention of OM.

Complications
Since the introduction of antimicrobials, the incidence of both suppurative
intratemporal and intracranial complications associated with OM has plummeted. However,
complications still occur, and vigilance is needed to prevent the potential morbidity and
mortality that can be associated with them. Complications can be divided into intratemporal
and intracranial groups (Table 91.5). By far the most common complication is conductive
hearing loss (CHL), usually due to the presence of MEE. Within the past decade, significant
interest has been expressed in the long-term effect of persistent MEE on speech, language,
and cognitive development of the child. Although many studies have been done, the results
remain controversial. Possible reasons for discrepancies in these types of studies include (a)
proper documentation of history of OM, (b) timing of audiologic workup, (c) otologic status
at the time of cognitive evaluation, and (d) varying study populations. Roberts et al. showed
that the care-giving environment is more strongly related to school outcome than was OME
or hearing loss. This is a difficult problem to study well because of many confounding
factors; however, the current recommendation remains for surgical intervention when
children have hearing loss, speech delay, poor performance in school (or a combination of
these) in the setting of OME for longer than 3 months.
Fortunately, given the high incidence of OM, infrequent emergency situations occur.
Table 91.6 briefly outlines some of the warning signs for potentially complicated OM. If the
patient continues to be febrile, to have severe pain, or to exhibit any of the complications
listed in Table 91.5, immediate intervention should be considered. A high index of suspicion
should be used in evaluating neonates and immunocompromised hosts because of the
presence of possible unusual organisms. Initial studies include physical examination and
tympanocentesis to obtain an organism for culture and susceptibility testing; wide-field
myringotomy with insertion of a TT should also be considered at this time. Computed
tomographic (CT) scanning and magnetic resonance imaging can help to identify intracranial
and intratemporal complications. If the patient does not respond promptly to intravenous
antimicrobials and tympanocentesis/myringotomy, tympanomastoidectomy should be
19
considered. If intracranial complications are suspected or confirmed, neurosurgical
consultation should be obtained.

EUSTACHIAN TUBE SYSTEM

Anatomy and Physiology of the Eustachian Tube System

An understanding of the anatomy and physiology of the Eustachian tube is important
for all who are involved in the management of patients who have diseases and disorders of
the middle-ear cleft and its adjacent anatomic structures. This chapter describes not only the
anatomy and physiology of the tube but also information about how dysfunction of the

20
Eustachian tube and related structures might result in abnormalities of the middle ear and
mastoid.
The Eustachian tube should not be thought of as a separate entity from the structures
that surround it. The Eustachian tube is part of a system of contiguous organs that includes
the nose, palate, and nasopharynx proximal to the Eustachian tube, and the middle ear and
mastoid at its distal end. In reality, the Eustachian tube is not a tube but an organ consisting
of a lumen with its mucosa, cartilage, surrounding soft tissue, peritubal muscles (i.e., tensor
veli palatini, levator veli palatini, salpingopharyngeus, and tensor tympani), and its superior
bony support, the sphenoid sulcus.

Anatomy of the Eustachian Tube System

The Eustachian tube lumen is wider at both the proximal (nasopharyngeal) and distal
(middle ear) ends than in the midportion. The isthmus is the narrowest. A recent three-
dimensional study of nine human temporal bone specimens by Sudo and associates (3)
demonstrated the isthmus portion of the lumen to be near the distal end of the cartilaginous
portion and not at the junction of the cartilaginous and osseous portions. They named the
segment where the cartilaginous and osseous portions connect the junctional portion, which
was determined to be 3 mm in length in the adult. On the lateral wall of the nasopharynx, a

21
prominence, the torus tubarius, protrudes into the nasopharynx. This prominence is formed
by the abundant soft tissue overlying the cartilage of the Eustachian tube. Anterior to this is
the triangular nasopharyngeal orifice of the tube. From the torus, a raised ridge of mucous
membrane, the salpingopharyngeal fold, descends vertically. On the posterior wall of the
nasopharynx lie the adenoids, or pharyngeal tonsil, composed of abundant lymphoid tissue.
Above the tonsil is a variable depression within the mucous membrane called the pharyngeal
bursa. Behind the torus lies a deep pocket, extending to the nasopharynx posteriorly along the
medial border of the Eustachian tube. This pocket, the fossa of Rosenmller, varies in
height from 8 to 10 mm and in depth from 3 to 10 mm. Adenoid tissue usually extends into
this pocket, giving soft-tissue support to the tube.
In the adult, the Eustachian tube is longer than that in the infant and young child.
Most of the increase in length takes place before age 6 years. The Eustachian tube has been
reported to be as short as 30 mm and as long as 40 mm, but the usual range of length reported
in the literature is 31 to 38 mm. It is generally accepted that the posterior third (11 to 14 mm)
of the adult tube is osseous, and the anterior two-thirds (20 to 25 mm) is composed of
membrane and cartilage. In adults, the Eustachian tube lies at an angle of 45 degrees in
relation to the horizontal plane. In infants, this inclination is only 10 degrees. The anatomy of
the cranial base may be related to the length of the Eustachian tube, which may be related to
susceptibility for middle-ear disease. The anatomic configuration of the Eustachian tube and
its relation to other structures are presented in Figure 90.2A. The osseous Eustachian tube
(protympanum) lies completely within the petrous portion of the temporal bone and is
directly continuous with the anterior wall of the superior portion of the middle ear. The
juncture of the osseous tube and the epitympanum lies 4 mm above the floor of the tympanic
cavity. This relation, although valid, is misrepresented in the more popular descriptions and
depictions of the Eustachian tube middle ear juncture and is of some importance in the
functional clearance of middle-ear liquids.

The osseous (protympanic or middle-ear) portion of the tube has a course that is linear
anteromedially, following the petrous apex and deviating little from the horizontal plane. The
lumen is roughly triangular, measuring 2 to 3 mm vertically and 3 to 4 mm along the
horizontal base. The healthy osseous portion is open at all times, in contrast to the
fibrocartilaginous portion, which is closed at rest and opens during swallowing or when
forced open, such as during the Valsalva maneuver. The osseous and cartilaginous portions of
the Eustachian tube meet at an irregular bony surface and form an angle of about 160 degrees

22
with each other. The medial wall of the bony portion of the Eustachian tube consists of two
partsposterolateral (labyrinthine) and anteromedial (carotid) whose size, shape, and
relation depend on the position of the internal carotid artery. The average thickness of the
anteromedial portion is 1.5 to 3 mm, and in 2% of persons, the wall is absent, exposing the
carotid artery.
The cartilaginous tube then courses anteromedially and inferiorly, angled in most
cases 30 to 40 degrees to the transverse plane and 45 degrees to the sagittal plane (8). The
tube is applied closely to the basal aspect of the skull and fitted to the sulcus tubae between
the greater wing of the sphenoid bone and the petrous portion of the temporal bone. The
cartilaginous tube is attached firmly at its posterior end to the osseous orifice by fibrous
bands and usually extends some distance (3 mm) into the osseous portion of the tube. At its
inferomedial end, it is attached to a tubercle on the posterior edge of the medial pterygoid
lamina.
The tube in its cartilaginous portion has a crook-shaped mediolateral superior wall
(Fig. 90.2B). It is completed laterally and inferiorly by a veiled membrane that serves as the
site of attachment of the fibers of the dilator tubae, or tensor veli palatini muscle. The tubal
lumen is shaped like two cones joined at their apexes. The juncture of the cones is the
narrowest point of the lumen and has been called the isthmus. Its position is usually described
as at or near the juncture of the osseous and cartilaginous portions of the tube. The lumen at
this point is about 2 mm high and 1 mm wide. From the isthmus, the lumen expands to about
8 to 10 mm in height and 1 to 2 mm in diameter at the pharyngeal orifice. Tubal cartilage
increases in mass from birth to puberty, and this development has physiologic implications.
The cartilaginous Eustachian tube does not follow a straight course in the adult but extends
along a curve from the junction of the osseous and cartilaginous portions to the medial
pterygoid plate, approximating the cranial base for the greater part of its course. The
Eustachian tube crosses the superior border of the superior constrictor muscle immediately
posterior to its terminus within the nasopharynx. The thickened anterior fibrous investment of
the medial cartilage of the tube presses against the pharyngeal wall to form a prominent fold,
the torus tubarius, which measures 10 to 15 mm thick. The torus is the site of origin of the
salpingopalatine muscle and is the point of origin of the salpingopharyngeal muscle, which
lies within the inferoposteriorly directed salpingopharyngeal fold.

The mucosal lining of the Eustachian tube is conti-nuous with that of the nasopharynx
and middle ear andis characterized as respiratory epithelium. Structural dif-ferentiation of this

23
mucosal lining is evident: mucousglands predominate at the nasopharyngeal orifice, and
graded change occurs to a mixture of goblet, columnar, and ciliated cells near the tympanum .
The lining is folded, which provides greater surface area. Mucosa-associated lymphoid tissue
also is present.

Infant versus Adult Anatomy

It is likely that differences in the anatomy of the infant compared with the adult are
related, in part, to the increased incidence of otitis media in the pediatric age group. These
anatomic differences have been described only recently. The Eustachian tube in the infant is
about 50% as long as that in the adult; its length averages about 18 mm. The cartilaginous
tube represents somewhat less than two thirds of this distance, whereas the osseous portion is
relatively longer and wider in diameter than that in the adult. The height of the pharyngeal
orifice of the infant Eustachian tube is about half that of the adult, but the width is similar.
The ostium of the tube is more exposed in the infant than it is in the adult because it lies
lower in the shallower nasopharyngeal vault. The direction of the tube varies from horizontal
to an angle of about 10 degrees to the horizontal, and the tube is not angulated at the isthmus
but merely narrows. Holborow demonstrated that in infants, the medial cartilaginous lamina
is relatively shorter because less tubal mass and stiffness is found in the infant tube than in
that of the older child and adult. The tensor veli palatini muscle is less efficient in the infant.
The Eustachian tube lengthens rapidly during early childhood, essentially reaching its
adult size by age 7 years. Ishijima and colleagues found the length of the lumen of the infant
tube to be 21 mm compared with the 37 mm average length in an adult. The effect of these
changes on efficiency of Eustachian-tube function has yet to be determined, but age-related
changes in Eustachian-tube function suggest more efficient muscular activity and a system
that is less likely to act as a passive conduit for nasal secretions. Cartilage mass increases
from birth to puberty. The density of elastin in the cartilage is less in the infant, but the
cartilage cell density is greater. The volume of the Ostmann fat pad is less in the infant, but
the width is similar in the two age groups. The angular relation between the tensor veli
palatini muscle and the cartilage varies in the infant but is relatively stable in the adult.
Table 90.1 summarizes the differences between the anatomy of the Eustachian tube in the
infant and that of the adult.
Some or possibly all these developmental differences between the infant and the adult
are related to the relatively less efficient active tubal-opening mechanism in the infant and
young child, which would make this age group susceptible to middle-ear disease. Because the
24
infant (and young child) has a shorter Eustachian tube than the older child and adult,
nasopharyngeal secretions can reflux more readily into the middle ear through the shorter
tube and result in otitis media.

Physiology of the Eustachian Tube

The Eustachian tube has at least three physiologic functions with respect to the middle ear
(Fig. 90.4): (a) pressure regulation (ventilation) of the middle ear to equilibrate gas pressure
in the middle ear with atmospheric pressure; (b) protection from nasopharyngeal sound
pressure and secretions; and (c) clearance of secretions produced within the middle ear into
the nasopharynx. Even though the pressure-regulation function is the most important of these
functions, the protective, drainage, and clearance functions are reviewed so that the reader
will be better able to visualize and understand the pressure-regulation function. The term
pressure regulation is more accurate than ventilation, because the middle ear is a pressure-
regulated cavity and not continuously ventilated. In the following discussion, fluid flow
through the tube includes both gas (airflow) and liquid flow.
Clearance of secretions from the middle ear is provided by the mucociliary system of the
Eustachian tube and some of the middle-ear mucous membrane. In ideal tubal function,
intermittent active opening of the Eustachian tube, which results only from contraction of the
tensor veli palatini muscle during swallowing, maintains nearly ambient pressures in the

25
middle ear. Assessment of these functions has been helpful in understanding the physiology
and pathophysiology of Eustachian-tube function as well as in the diagnosis and management
of patients with middle-ear disease.

Protective and Clearance Functions

In the past, clearance and drainage functions of the Eustachian tube have been
assessed by a variety of methods. Radiographic techniques have been used to assess
the flow of contrast media from the middle ear (tympanic membrane not intact) into
the nasopharynx. Bauer assessed clearance by observing methylene blue in the
pharynx after it had been instilled into the middle ear. Elbrond and Larsen assessed
middle ear Eustachian-tube mucociliary flow by determining the time that elapsed
after saccharin had been placed on the mucous membrane of the middle ear until the
subject reported tasting it. Unfortunately, all these methods are qualitative and
actually test Eustachian-tube patency rather than measuring the clearance function of
the tube quantitatively. Even though abnormalities of the protective function are
directly related to the pathogenesis of otitis media, this function has been assessed
only by radiographic techniques with a test that was a modification of a tubal patency
test described by Wittenborg and Neuhauser.

Pressure-Regulation Function
From studies in children, the function of the Eustachian tube has been postulated (49).
The normal Eustachian tube is functionally obstructed or collapsed at rest; probably a
slight negative pressure develops in the middle ear. When the Eustachian tube

26
functions ideally, intermittent active dilatation (opening) of the tube maintains near-
ambient pressures in the middle ear. Under physiologic conditions, the fluctuations in
ambient pressure are bidirectional (i.e., either to or from the middle ear), relatively
small in magnitude, and not readily appreciated. These fluctuations reflect the
increase and decrease in barometric pressures associated with changing weather
conditions and elevation or both. However, the changes in middle-ear pressure show
mass directionality, can achieve appreciable magnitudes, and can result in pathologic
changes. A major reason for these conditions is that the middle ear is a relatively rigid
(noncollapsible) gas pocket surrounded by mucous membrane in which gases are
exchanged between the middle-ear space and the mucosa. Differential pressure
exceeds 54 mm Hg between the middle-ear space at atmospheric pressure and the
microcirculation in the mucous membrane. This represents a diffusion-driven gradient
from the middle-ear cavity to the mucosa that can produce an underpressure (relative
to ambient pressure) in the middle ear of more than 600 mm H2O during equilibration.
Doyle and co-workers , in experiments in primates, demonstrated that oxygen (O2)
and carbon dioxide (CO2) exchange is diffusion limited, whereas nitrogen (N2) is
perfusion limited. Some investigators have postulated that gases can pass to and from
the middle ear through the tympanic membrane, but Doyle and co-investigators
showed in animal experiments that no O2 and CO2 transtympanic membrane exchange
exists from the external ear canal into the middle ear; exchange of N2 occurs, but not
at physiologic rates.
Children have less efficient Eustachian-tube ventila-tory function than do
adults. Bylander comparedthe Eustachian-tube function of 53 children with that of55
adults, all of whom had intact tympanic membranes and who were apparently
otologically healthy. By using a pressure chamber, Bylander and Tjernstrom reported
that 35.8% of the children could not equilibrate applied negative intratympanic
pressure (-100 mm H2O) by swallowing, whereas only 5% of the adults were unable
to perform this function. Children aged 3 to 6 years had worse function than those
aged 7 to 12 years. In this study and a subsequent one conducted by the same research
group, children who had tympanometric evidence of negative pressure within the
middle ear had poor Eustachian-tube function. From these two studies, it can be
concluded that even in apparently otologically normal children, Eustachian-tube
function is not as good as that in adults; therefore the higher incidence of middle-ear
disease in children can be attributed to this finding.
27
 Many children without apparent middle-ear disease have high negative
middle-ear pressure. In children, however, Eustachian-tube function does improve
with advancing age, which is consistent with the decreasing incidence of otitis media
from infancy to adolescence. Another explanation for the finding of high negative
middle-ear pressure in children is the possibility that some people who are habitual
actually create underpressure within the middle ear by this act. This mechanism is
uncommon in children, however.

Anatomy and Physiology of the Nose and Paranasal Sinuses : Snow JB, Ballanger JJ.
Ballengers Otorhinolaryngology Head and Neck Surgery 6th. Ontario; 2003.
Effendi H, editor. Boies: Buku Ajar Penyakit THT. Ed ke-6. Jakarta: Penerbit Buku
Kedokteran EGC; 1997.
Lalwani AK, editor. Current Diagnosis & Treatment in Otolaryngology - Head &
Neck Surgery. USA: McGraw-Hill; 2008.
Cummings et al, editor. Otolaryngology - Head and Neck Surgery. Ed ke-3. USA:
Mosby-Year Book; 1998.

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