CASE REPORT

ACUTE OTITIS MEDIA

Moderator :
dr. Kenny
Presenter
:
GROUP 14205
Decky Abraham T
Qurani Hemas N
Wan Gustika R
Vegha Nedya
Raymond Nesan
Bima Prasetya
Eva Aguswulandari

KU/16732
KU/16839
KU/16838
KU/16867
KU/16763
KU/16860
KU/16759

Department of Otorhinolaryngology Head and Neck Surgery

Faculty of Medicine
Gadjah Mada University
dr. Sardjito General Hospital
Yogyakarta
2012

CHAPTER I
PREFACE

Otitis media, according to, is generally defined as an inflammation of the

middle ear, regardless of etiology or pathogenesis.1 Otitis media is then classified
into several classifications, by its duration (acute and chronic), presence of
discharge (suppurative and non-suppurative), causative organisms (e.g. nonspecific bacterial and specific bacterial infection, such as tubercular and syphilitic)
and unto otitis media with effusion or aero-otitis media.2
Acute otitis media (AOM) is the rapid onset of signs and symptoms, such
as otalgia and fever, because of a present infection in the middle ear. Otitis media
effusion is an inflammation of the middle ear with the collection of sterile liquid
in the middle ear, without the witnessed sign and symptom of an acute infection
and perforation of tympanic membrane.3
The risk factors of AOM are low socio-economic level, pediatric patient,
genetic predisposition, premature birth, male gender, native American and Inuit
ethnicity, family history of recurrent otitis media, presence of siblings in the
household, cigarette smoke and allergen exposure.4
The signs and symptoms of AOM are otalgia and conductive hearing loss,
usually accompanied with pyrexia but without concurring otorrhea. In pediatric
patients, usually the fever will reach 39,50 C, restless, sleep disturbance, diarrhea,
and convulsion. But in the event of tympanic membrane rupture, a sudden
purulent discharge will be complained by the patient.4
AOM have several outcomes, such as spontaneous resolution, acute
perforation of tympanic membrane that will continue to persistent perforation,
glue ear or otitis media with effusion, recurrent episodes of AOM and acute
mastoiditis.3
Diagnosis of AOM may be achieved through several founding, such as
mastoid tenderness on palpation; opaque, thickened, erythematous, or bulging
tympanic membrane; and immobility of tympanic membrane on pneumatic
otoscopy.

CHAPTER II
LITERATURE REVIEW

A. Anatomical Review and Ear Physiology

Anatomically, the ear is divided into three parts, external, middle and
internal part. The external part of the ear consists of the auricle, external auditory
meatus, external auditory canal and tympanic membrane. The outer ear is called
the auricle and is made of ridged cartilage covered by skin. Sound wave tunnels
through the auricle into the external auditory canal, which is a short tube that ends
at the tympanic membrane. One third of the external part of the auditory canal is
made of cartilage and the last two third of this canal is made of bone. This canal is
covered by skin. Ceruminous glands and hair follicles can be found on the first
one third part of the canal while sweat glands could be found throughout the
length of the canal.6

Tympanic membrane is round and concaved in shape, when is seen from

the outer part of the canal and is oblique with respect to the canal axis. Tympanic

membrane forms the major part of the lateral wall of the middle ear. It is thin,
resistant, semi-transparent, has a pearly grey color and is cone like. The apex of
the membrane lies at the umbo, which corresponds to the lowest part of the handle
of the malleus. The tympanic membrane is divided into four quadrants, the anterosuperior, antero-inferior, postero-superior and postero-inferior. This division
facilitates the description of the different pathologic affections of the tympanic
membrane. The membrane forms an acute angle with the anterior wall of the canal,
this angulation is important in the myringoplasty operation. The external surface
of the tympanic membrane is innervated by the auriculotemporal nerve and the
auricular branch of the vagus nerve whereas, the inner surface is supplied by the
branch of the glossopharyngeal nerve. The blood supply is derived from the deep
auricular and anterior tympanic arteries, both are branches of the maxillary
artery.6,7

Middle ear is a small air filled cavity in the petrous portion of the temporal
bone and lined by epithelium. It is separated from the external ear by the tympanic
membrane and the internal ear by a thin bony partition that contains two small
membrane-covered opening, the oval window and the round window. Across the

middle ear, the auditory ossicles are three bones that are connected by synovial
joints, and are attached to the middle ear by ligaments. The bones are the malleus,
incus and stapes, which are articulating with each other, respective to their
positions. The base of the stapes fits into the oval window, which locates directly
above the round window, which is enclosed by a membrane called the secondary
tympanic membrane. Besides the ligaments, two tiny skeletal muscles also attach
to the ossicles, the tensor tympani muscle, which is innervated by the mandibular
branch of the trigeminal nerve, limits movement and increases tension on the ear
drum to prevent damage to inner ear from loud noises. The stapedius muscle is
innervated by the facial nerve. It takes a fraction of a second for the tensor
tympani and stapedius muscles to contract. They can protect the inner ear from
prolonged loud noises but not from a brief one, such as a gunshot. The anterior
wall of the middle ear contains an opening that leads directly into the Eustachian
tube, connecting the middle ear to the nasopharynx. It is normally closed at its
medial end (pharyngeal end) and opens during swallowing and yawning to allow
air to enter or leave the middle ear until the pressure of the middle ear is equal
with the atmospheric pressure. When the pressures are balanced, the tympanic
membrane vibrates freely as sound waves strike it. If the pressure is not equalized,
intense pain, hearing impairment, tinnitus and vertigo could develop. The auditory
tube is also a route for pathogens.6
Internal ear is also called the labyrinth, it consists of mainly two divisions;
the outer bony labyrinth that encloses an inner membranous labyrinth. The bony
labyrinth is lined with periosteum and contains perilymph and it is divided into
three areas; the outer semicircular canal, the vestibules, and the cochlea. The
labyrinth in the vestibules consists of two sacs, called utricle and saccules, which
are connected by a small duct. Projecting superiorly and posteriorly from the
vestibules are the three semicircular canals, each of which lies at approximately
right angles to the other two. Based on their positions, they are named the anterior,
posterior and lateral semi-circular canal. At the end of each canal is a swollen
enlargement called the ampula. The portions of the membranous labyrinth that lie
inside the bony semi-circular canals are called the semi-circular ducts, which are

connected with the utricle of the vestibule. The vestibular branch of the
vestibulochochlear nerve consists of ampullary, utricular, and saccular nerve.
These nerves contain both first order sensory neuron and motor neuron that
synapses with receptor for equilibrium. The first order sensory neurons carry
sensory information from the receptor and the motor neurons carry feedback
signals from the receptor, apparently to modify their sensitivity. The cell bodies of
the sensory neuron lie in the vestibular ganglia.
Cochlea is a bony spiral canal and makes almost three turns around a
central bony core, called the modulus. It is divided into three channels; cochlear
duct, vestibule scale and tympanic scale. The cochlear duct is a continuation of
the membranous labyrinth into the cochlea and filled with endolymph. The
channel above the cochlear duct is the vestibule scale, which ends at the oval
window. The channel below is the tympanic scale. Both the vestibule and the
tympanic scale are part of the bony labyrinth of the cochlea. Therefore, these
chambers are filled with perilymph. The vestibule and tympanic scales are
completely separated by the cochlear duct, except for an opening at the apex of
the cochlea, called the helicotrema. The vestibular membrane separates the
cochlear duct from the vestibule scale, meanwhile the basilar membrane separates
the cochlear duct from the tympanic scale. Resting on the basilar membrane is the
Organ of Corti. The Organ of Corti is a coiled sheet of epithelial cells, including
supporting cells at about 16,000 hair cells, which are the receptors of hearing.
There are two groups of hair cells, the inner hair cells which are arranged in a
single row and the outer hair cells which are arranged in three rows. At the apical
tip of each hair cell is forty to eighty stereocilia that extend into the endolymph of
the cochlear duct. Stereocilia are long, hair-like microvilli, arranged in several
rows of graded height. At their basal ends, inner and outer hair cells synapse both
with first-order sensory neurons and with motor neurons from the cochlear branch
of the VIII nerve. Cell bodies of the sensory neurons are located in the spiral
ganglion. Although the outer hair cell outnumber the inner hair cell by three to
one, the inner hair cells synapse with 90-95% of the first-order sensory neurons in
the cochlear nerve that relay auditory information to the brain. By contrast, 90%

of the motor neurons in the cochlear nerve synapse with outer hair cells. The
tectorial membrane, a flexible gelatinous membrane, covers the hair cells of the
spiral organ. In fact, the ends of these stereocilia of the hair cells, are embedded in
the tectorial membrane, while the bodies of the hair cells rest on the basilar
membrane.
The hearing process starts at the auricle. It directs sound waves into the
external auditory canal then, when the sound waves strike the tympanic membrane,
the alternating high and low pressure of the air causes the tympanic membrane to
vibrate back and forth. The distance it moves, which is very small, depends on the
intensity and frequency of the sound waves. The ear drum vibrates slowly in
response to low frequency (low pitched) sounds and rapidly in response to high
frequency (high pitched) sounds. The central area of the ear drum connects to the
malleus, which also starts to vibrate. The vibration is transmitted from the malleus
to the incus and then to the stapes. As the stapes moves back and forth, it pushes
the membrane of the oval window in and out. The oval window vibrates about
twenty times more vigorously than the ear drum, because the ossicles efficiently
transmit small vibrations spread over a large surface area (ear drum) into larger
vibration of a smaller surface (oval window), thus amplifying the sound caught by
the ear. The movement of the oval window sets up fluid pressure waves in the
perilymph of the cochlea. As the oval window bulges inward, it pushes on the
perilymph of the vestibule scale. Pressure waves are transmitted from the
vestibule scale to the tympanic scale and eventually to the round window, causing
it to bulge outward into the middle ear. As the pressure waves deform the walls of
the vestibule scale and the tympanic scale, they also push the vestibular
membrane back and forth, creating pressure waves in the endolymph inside the
cochlear duct. The pressure waves in the endolymph cause the basilar membrane
to vibrate, which moves the hair cells of the Organ of Corti against the tectorial
membrane. This leads to bending of the hair cells stereocilia, which produces
receptor potentials that ultimately lead to the generation of nerve impulses. The
membrane at the at the base of the cochlea is responsible for high pitched (high
frequency) sounds, near 20,000 Hz, while the membrane at the apex of the

cochlea, near the helicotrema is responsible for low frequency sounds, near 20 Hz.
6,7

Most of the external ear gets its blood supply from the external carotid
artery branches, while posterior auricular artery and superficial temporal artery,
both branches of the external carotid artery, gives blood supply to the auricle and
the lateral aspect of the external auditory canal. Auricle branch of the maxillary
artery gives vascularization to the medial aspect of the external auditory canal and
the external surface of the tympanic membrane. The middle ear is supplied by
mastoid branch of the occipital or posterior auricular arteries, tympanic branch of
the maxillary artery and some branches from different arteries, including the
middle meningeal artery, ascending pharyngeal artery, internal carotid artery and
the artery of pterygoid canal. The inner ear is supplied by the anterior tympanic
branch of the maxillary artery, stylomastoid branch of the posterior auricular
artery, petrosal branch of middle meningeal artery and the labyrinthine artery
arising from either the anteroinferior cerebellar artery or the basilar artery. The
blood from the external ear is drained into posterior auricle vein and superficial
temporal artery.9,10

The innervation of the external ear is derived from the auriculotemporal

branch of the trigeminal nerve and some contributions from the other cranial
nerve, such as the facial, glossopharyngeus, and vagus nerve, also from the great

auricular nerve, which is a branch of the cervical plexus, composed mainly of the
branches of the C2 and C3 spinal nerves. The middle ear gets its sensory
innervation from auriculotemporal nerve, and tympanic nerve, which is a branch
of the n. IX, and from the auricular branch of the vagus nerve.9,11

Lymphatic drainage of the ear is important to calculate the direction of

how an infection in the ear will spread. The anterior wall and superior part of the
external auditory canal and the tragus are drained towards the pre-auricle lymph
nodes. The infra auricular lymph nodes are responsible of the lymphatic drainage

from the helix and inferior wall of the external auditory canal, while the concha
and the antihelix are drained to the mastoid lymph nodes. The external acoustic
meatus is drained with the auricle via the superior deep cervical nodes, while the
middle and innermost ear are drained into the superior deep cervical nodes or the
parotid node, from where they reach the jugular trunk.9

B. Acute Otitis Media

1. Definition
Acute otitis media is defined as the presence of inflammation in the middle
ear accompanied by the rapid onset of signs and symptoms of an ear infection.
Acute otitis media involves the middle ear, which causes the tympanic membrane
to become inflamed and opaque. Due to inflammation processes, blood vessels to
the area dilate. Fluid accumulates in the middle ear space. The causative
pathogens may be viruses or bacteria, although in some cases the causative
pathogens are unidentified.15

2. Etiology
AOM is usually associated with either bacterial or viral infections. Global
reports show that H. influenza and Streptococcus pneumonia are the most
prevalent organisms responsible for AOM. AOM is usually a complication of
Eustachian tube dysfunction experienced during an acute viral upper respiratory
infection. Some viruses such as respiratory syncytial virus, adenovirus, and
human metapnemovirus are associated with high rate of AOM. Bacteria are
isolated from middle ear fluid cultures in 50-90% of cases of AOM and OME.
Strepcoccus pneumonia, haemophilus influenza (non-typable) and Moraxella
catarrhalis are the most common organisms isolated from middle ear fluid. A
variety of bacteria, including group A strep and Staphylococcal aureus are isolated
from approximately 10% of ears. Approximately 5% of ears have multiple
pathogens. Gram negative bacilli were identified in 10,5% of infants under six
weeks of age.11

3. Risk factors
Age. Infants and toddlers are more severely affected, may take longer to
response to treatment and can be more difficult to diagnose accurately. 11
Additional risk factors. Exposure to group day care with subsequent
increase in respiratory infections put a child at high risk of getting AOM.
Environmental smoke or other respiratory irritants and allergens may
interfere with Eustachian tube function and dysfunction of Eustachian tube
may result in AOM. Lack of breastfeeding, supine feeding position, use of
pacifiers by toddlers and older children are the risk factors of AOM.
History of recurrent AOM in a family will add to the risk of AOM. An
individual with clinical conditions such as craniofacial abnormalities,
immune deficiency and GERD, has a higher chance of acquiring AOM.11

4. Clinical features
The clinical mode of presentation is usually systemic (generalized) and
local (ear) symptoms and signs. The typical picture is a child with high
grade fever (40-410C), refusal of feeds, incessant cries and irritability.
There is associated ear pain (otalgia) and sometimes noise in the ear
(tinnitus) with difficulty in hearing (conductive hearing loss). Ear
discharge is seen in well above 90% of cases in some parts of the
developing world, whereas it is only about 10% among the developed
nations. Delay of presentation to the clinician most probably accounts for
this disparity2.
Specifics clinical features are found in each stage of AOM. The stages are:
1.

Eustachian tube occlusion. On otoscopy, the tympanic membrane is

seen retracted due to the negative pressure in the middle ear space.
However, it might appear normal or pale.

2.

Hyperemic (pre-suppurative) stage. In this stage, dilated blood

vessels of the tympanic membrane can be seen. Hence, the tympanic
membrane may appear hyperemic and even oedematous.

3.

Suppurative stage. Purulent exudate accumulates in the middle ear

space and pushes the tympanic membrane towards the external
auditory canal (bulging eardrum). Otalgia and body temperature of the
patients intensify. The exudates will eventually exert pressure on one
spot of the tympanic membrane and appear yellow. This point will be
the rupture point of the tympanic membrane.

4.

Perforated stage. The tympanic membrane ruptures and pus flows

from the middle ear space to the external ear. All symptoms disappear,
patients feel relieved.

5.

Resolution stage. If the tympanic membrane is intact, its conditions

gradually improve and eventually become normal. If perforation has
occurred, the secret reduces until it is dry. 6

- Diagnosis

To diagnose acute otitis media, the clinician should 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. However, clinical
history alone is poorly predictive of the presence of AOM, especially in younger
children. The presence of MEE is indicated by any of the following: a. Bulging of
the tympanic membrane, b. limited or absent mobility of the tympanic membrane ,
c. air fluid level behind the tympanic membrane, d. otorrhea. Fullness or bulging
of the tympanic membrane has the highest predictive value for the presence of
MEE. When combined with color and mobility, bulging is also the best predictor
of AOM.

The presence of MEE is commonly confirmed with the use of

pneumatic otoscopy, tympanometry and/or acoustic reflectometry. MEE also can

be demonstrated directly by tympanocentesis or by the presence of fluid in the
external auditory canal as a result of tympanic membrane perforation. The
diagnosis of AOM, particularly in infants and young children, is often made with
a degree of uncertainty. When the presence of middle-ear fluid is questionable or
uncertain, a diagnosis of AOM may be considered but cannot be confirmed. A
certain diagnosis of AOM meets all 3 of the criteria: rapid onset, presence of MEE,
and signs and symptoms of middle-ear inflammation. 12

- Treatment

Ear swab for discharging ears are taken for microcopy, culture and
sensitivity test prior to commencement of broad spectrum oral and or topical
antibiotics. This is usually guided by the knowledge and behavior of predominant
causative agents within a given environment. A daily aural toileting of the ear is
mandatory for the discharging ear. Myringotomy to evacuate the exudates in
bulging tympanic membrane is encouraged prior to antibiotics management.

Adequate analgesia to reduce otalgia is valuable in the management of AOM.

Imaging may be necessary especially in suspected cases of complications2.

Many episodes of AOM are associated with pain. The management of pain,
especially during the first 24 hours of an episode of AOM, should be addressed,
regardless of the use of antibacterial agents.12

Empiric antibiotics that are suggested are vancomycin and third generation
cephalosporin, second generation amoxicillin, amoxicillin or clavulanat acid, and
azithromycin. Amoxicillin 80mg-90mg/kg/24 hours in three divided doses , for 10
days, remains the first-line therapy for AOM, although with increasing numbers
of resistant strains of bacteria, it may be necessary to use more broad-spectrum
antibiotics in the future. In resistant cases, amoxicillin should be given in
combination with clavulanate.13

Complication and Prognosis

Without antibiotic, AOM can cause subperiosteal abscess, even meningitis
and cerebral abscess. If antibiotics are administered, COSM might be a
complication from OMA. Some cases are self-limited which resolve within 24 to
48 hours. However, when antibiotis are needed, full recovery depends on the
patients compliance. Disruption in antibiotic therapy may result in recurrence of
the infection.14

CHAPTER III
CASE REPORT

1.1 Identity
Name

: OR

Age

: 37 years old

Gender

: Female

Address

: Kalikalong RT1/2, Purworejo

Occupation

: Housewife

1.2 Anamnesis
Chief complaint: Low-key tinnitus at auricular dextra.
History of present illness:
Patient came to hospital on 08 September 2014.
The low-key tinnitus is felt since mid July, continuously. Patient also felt pain at
mastoid process, however there was no complaint of discharge coming out from
the right ear. Fullness in the right ear was present. She suffered from coughing,
and runny nose at that time. And she felt discomfort in her throat. She denied
having dizziness.

History of past illness:

- History of the same complaints (+). On treatment
- History of allergy

(-)

- History of trauma

(-)

- Hypertension

(-)

- Diabetes Mellitus

(-)

- Chronic Faringitis

(+)

History of illness in family members:

- History of the same complaints (-)

- History of allergy (-)

Resume Anamnesis
Tinnitus (+), Pain at mastoid process (+)

3.3 Physical Examination

General status : CM, adequately nourished

Otorhinolarygology examination:
1. Ear
Inspection:
Auricula AD/S within normal limit
External auditory canal AD was hyperemic
External auditory canal AS within normal limit with minimal cerumen
Tympanic membrane AD hyperemic (+), bulging (-), cone of light (-) , AS
within normal limit
Palpation
Tragus pain AD/S (-)
Auricular pain AD/S (-)
Retroauricular pain AD (+) AS (-)
Preauricular lymph nodes enlargement AD/S (-)

2. Nose
Inspection
Deformity (-)
Nasal septum deviation (-)
Concha inferior D/S were hyperemic
Discharge D/S (+)

Palpation
Tenderness (-)

Crepitation (-)

3. Throat
Inspection
Cavum oris within normal limit
Uvula in the middle, edema (-)
Arcus pharynx simetris
Tonsils hypertrophy (-)
Pharyngeal wall hyperemic (+), granulation (-)
Palpation : lymph node enlargement (-)

Diagnosis
Based on the result from anamnesis and physical examinations, this patient was
diagnosed as acute otitis media in hyperemic stage auricular dextra.

3.5 Treatment
- Clavamox tab. 500 mg No XV . S 3 dd Tab 1
- Fexofed tab no X. S 2dd Tab 1
- Na Diclofenac tab 50mg no X. S 2dd Tab 1 pc
- Ambroxol tab 30 mg no XV S 3dd Tab 1

Problem
No improvement on the first treatment

Planning
Follow-up again after 5 days of treatment to evaluate the disease.

CHAPTER IV
DISCUSSION

The chief complaint felt by the patient was low-key tinnitus. Tinnitus is
associated with sensoryneural hearing loss, conductive hearing loss, and negative
pressure in the middle ear space. Tinnitus, which is caused by conduction
disturbance, is commonly low-key tinnitus. A simple tool like tunning fork is used
to test for sensoryneural hearing loss or conductive hearing loss. Tunning fork test,
consisting of Rinne, Weber, and Swabach tests, was performed on the patient and
the result for Rinne test of both ears were positive, lateralisation to the left ear on
Weber test, and prolonged Swabach test was obtained. From the results, it can be
concluded that the patient suffered from SNHL. However, it does not fit into the
diagnosis established based on the physical examinations and clinical history. The
presence of chronic pharyngitis should be considered as one of the causes of
AOM in this patient. Patient was also present with rhinitis. Upper respiratory
infections such as pharyngitis and rhinitis may be the predisposition factors in this
case.
In this patient, after doing a basic examination in the ear, nose and throat,
the examiner found an hyperemic state in the external auditory canal of the right
ear and in the tympanic membrane, without concurrent bulge, meanwhile there
was no cone of light found in the right ear, probably due to the cellular changes
caused by the inflammation of the tympanic membrane. Retroauricular pain on
palpation was found, this is caused by the spread of the infection to the mastoid
process, thus creating an inflammation in the process and will cause patient some
discomfort on touch.
According to the results of physical examinations by otoscopy and clinical
presentations, the patients condition was diagnosed as acute otitis media of the
right ear. The therapy given was as the following:
- Clavamox tab. 500 mg No XV . S 3 dd Tab 1
- Fexofed tab no X. S 2dd Tab 1
- Na Diclofenac tab 50mg no X. S 2dd Tab 1 pc

- Ambroxol tab 30 mg no XV S 3dd Tab 1

The patient was advised to be complient in taking the medicine, avoid
food or drink of extreme temperatures, have plenty of rest, and see the doctor
again for a control after completing the therapy.
On the next visit, there was no improvement. In this case, there are some
probabilities to her unimproved condition, lack of compliance or inadequate
therapy. 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(s), the clinician should change the
antibacterial agent(s).12

Once the patient has shown clinical improvement, follow-up is based on the usual
clinical course of AOM. Persistent MEE after resolution of acute symptoms is

common and should not be viewed as a need for active therapy. Two weeks after
an episode of AOM, 60% to 70% of children have MEE, decreasing to 40% at 1
month and 10% to 25% after 3 months.12

CHAPTER V
SUMMARY

It has been reported that a female patient, aged 37 years old, has been
diagnosed with acute otitis media in hyperemic state at the right ear. It has been
reported that a male patient, 4 years old , has been diagnosed with acute otitis
media in hyperemic stage at the left ear. The initial treatment of this patient is
Clavamox tab. 500 mg No XV . S 3 dd Tab 1, Fexofed tab no X. S 2dd Tab 1, Na
Diclofenac tab 50mg no X. S 2dd Tab 1 pc, Ambroxol tab 30 mg no XV S 3dd
Tab 1, follow-up after 5 days, also education. The patient was educated to return
for follow-up after 5 days, to take the medicine according to instructions, and to
avoid food or drink of extreme temperatures.

REFERENCES
1. Rosenfeld RM, Bluesone CD. Evidence - Based Otitis Media. 2nd ed. Canada:
BC Decker Inc. 2003
2. Ibekwe

TS.

Otitis

media

focusing on

the

developing world.

http://ptolemy.library.utoronto.ca/members/archives/2009/Otitis/Otitis%20me
dia.pdf
3. Bailey BJ, Johnson JT. Head and Neck Surgery Otolaryngology. 4th ed.
Lippincott Williams & Wilkins. 2006
4. Lanphear BP, Byrd RS, Auinger P, Hall CB. Increasing Prevalence of
Recurrent Otitis Media Among Children in the United States. Pediatrics.
1997 Mar; 99(3): E1
5. Djaafar ZA. Kelainan Telinga Tengah Dalam: Buku Ajar Ilmu Penyakit
Telinga Hidung Tenggorok. Ed 6. FKUI. Jakarta. 2007.P: 64-76
6. Tortora GJ, Derrickson BH. Principles of Anatomy and Physiology. 12th ed.
Wiley. 2009
7. Guyton, Hall. Guyton and Hall Textbook of Medical Physiology. 12th ed.
Saunders Elsevier. 2010
8. Lalwani AK. Disease of the External Ear, Chapter 47 In: Current Diagnosis &
treatment otolaryngology Head & Neck Surgery. 2nd ed. New York:
McGrawhill Lange. 2008
9. Healy GB, Rosbe KW.

Otitis Media and Middle Ear Effusions. In

Ballengers Manual of Otorhinolaryngology Head and Neck Surgery. London:

BC Decker.2002. P: 34-42.
10. Adams GL, Boies LR, Higler PA. Boies Buku Ajar Penyakit THT edisi 6.
Jakarta: EGC. 2012.
11. Blackwood RA, Cooke JM, Van Harrison R, Harnes KM, Passamani PP.
Otitis

Media.

http://www.experts.umich.edu/expertPubs.asp?n=Heather+L+Burrows&u_id
=2992&oe_id=1&o_id=29
12. Lieberthal AS, et al. Clinical Practice Guideline Diagnosis and Management
of Acoustic Otitis Media. American Academy of Family Physicians.

13. Clinical Practice Guideline for the Management of Acute Otitis Media in
Children

months

12

years.

Cited

from:

http://www.mahealthcare.com/assets/pdf/Practice_guidelines/Otitis_Media.pd
f
14. http://www.mdguidelines.com/otitis-media/prognosis
15. Linsk R et al. Otitis Media. Guidelines for Clinical Care. University Michigan
Guideline Time. 2002.