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Supervised by :
dr. H. Oscar Djauhari, Sp. THT
Presented by :
Didi Suryana

Clinical Rotation
Medical Faculty of Muhammadiyah Jakarta University - Syamsudin, S.H.
Regional General Hospital, Sukabumi
Period Jully 25th agust 27th 2016



: Mr. X


: 22 years old


: Male


: Student


: Javanese


: Jl. Koperasi, Sukabumi


: 55 kg


: 165cm

Chief complaint

o ottorheae since 3 month ago.

Additional complaint

: difficult of speaking, opening mouth and Drop of the

right corner of the mouth since 5 days ago

History of present illness :
Patient, 22 years old, male, comes to the ENT clinic with chief complaint
ottorheae since 3 month ago and difficult of speaking, opening mouth and Drop of
the right corner of the mouth since 5 days ago. He also complaints about slurred
speech due to unable to lift up the right corner of the mouth. Patient felt this
symptom became worse along with time. Pain on the face (-), numbness (-),
difficulty in swallowing (-). Cough and cold was present too.
The patient had yellowish, purulent secretion from the right ear with foul
smelling which comes out intermittent since 4 months ago. He went to the
community health center 2 months ago and he was given some oral medication
but he felt the discharge still came out. Fever (-), earache (-), hearing loss (+),
tinnitus (-), hystory of trauma (-).
History of past illness
Since 3 month ago, patient felt waters coming out the right ear.

Physical Examination
1. General status
General appearance
Blood Pressure
Pulse rate
Respiration rate

: Mild ilness
: compos mentis
: 120/80 mmHg
: 80 beat per minute
: 20 times per minute
: 37,7 oC

2. ENT Status
Right ear
o Auricle
o Canalis Acousticus Externa

: hyperemia (-), oedema (-)

: hyperemic (-), mass (-), Secretion (+)

minimal, yellowish green in color, cholesteatoma (-), Odorous smell

o Tymphanic membrane
: marginal perforation
o Rinne test (-), Weber lateralitation to the right, prolonged

Left ear
o Auricle
: hyperemia (-), oedema (-)
o Canalis Acousticus Externa : hyperemic (-), mass (-)
o Tymphanic membrane
: intact, bulging (-), light reflex (+)
o Secretion (-)
o Rinne test (+), Schwabach test same with the examiner.

o Mucosa

: hyperemis -/-, edema -/-

o Tonsil

: T1/T1

o Arcus anterior : uvula in the middle, massa -/

Maxillofacial : Asymmetrical


: lymphadenopathy -/-

3. Facial Nerve Examination (right / left)

Facial expression
: asymmetrical, right side of face slightly dropped
Raising eyebrow
: difficult / normal
Closing eyes
: left behind / normal
Opening mouth
: left behind / normal

Working diagnosis
Chronic Supurative Otitis Media auris dextra with complication dextra facial nerve

Differential Diagnosis
Primary tumor in the middle of right ear

: Complete Blood Count including differential count of white blood cells

Culture of pus from the right ear and bacterial resistance test
Audiometry test
Polimiksin B drops 0.3%, 3 x 4 drops per day
Ciprofloxacin, 2 X 500 mg p.o.
Prednisone, 4 X 20 mg per day p.o.
Mecobalamin 3 x 500 mcg p.o

Chronic Suppurative Otitis Media

Chronic suppurative otitis media (CSOM) is defined as a persistent or intermittent
infected discharge through a nonintact tympanic membrane (ie, perforation or tympanostomy
tube). Chronic perforation of the tympanic membrane can occur without suppuration and is
often referred to as inactive CSOM.
Chronic suppurative otitis media is particularly prevalent in developing countries and
is more common in lower socioeconomic groups in the developed world.

There are a number of mechanisms by which a persistent tympanic membrane
perforation may develop. In most cases, CSOM occurs as a consequence of an episode of
AOM with perforation, with subsequent failure of the perforation to heal. There is also an
association between OME and chronic perforation. The continued presence of a middle ear
effusion leads, in some cases, to degeneration of the fibrous layer of the tympanic membrane.
This weakness of the tympanic membrane both predisposes to perforation and reduces the
likelihood of spontaneous healing. Although most tympanic membranes heal spontaneously
after the extrusion of ventilation tubes, a small percentage do not. Traumatic perforations,
particularly if large, may fail to heal.
There are two main mechanisms by which a chronic perforation can lead to
continuous or repeated middle ear infections:
1. Bacteria can contaminate the middle ear cleft directly from the external ear because
the protective physical barrier of the tympanic membrane is lost.
2. The intact tympanic membrane normally results in a middle ear gas cushion, which
helps to prevent the reflux of nasopharyngeal secretions into the middle ear via the
eustachian tube. The loss of this protective mechanism results in the increased
exposure of the middle ear to pathogenic bacteria from the nasopharynx.
The most commonly isolated bacteria responsible for CSOM are P aeruginosa, S aureus, and
the Proteus species.
a. Symptomps and Signs

History of otorrhea, intermittent or continuous

Hearing loss

Discharge mucopurulent or bloodstained otorrhea ( which lead to polyp or

granulation tissue formation )

Edematous on middle ear mucosa

Large preforation identify the presence of ossicular discontinuity due to

necrosis of the long process of the incus

b. Special Test

A swab of the discharge ( before beginning antimicrobial therapy ) for

culture and sensitivity test

An audiologic evaluation

Computed tomographic (CT) scans : demonstrating bony anatomy and are

essential if an intracranial extension of the infection is suspected.

1. Cholesteatoma.
Both pathologies present with a very similar clinical course, and the presence
of severe inflammation or granulation tissue can cause difficulty with the diagnosis.
Reexamination after a course of medical treatment usually provides an accurate
2. Chronic Granulomatous
If granulations are severe and unresponsive to antimicrobial therapy, then
chronic granulomatous conditions such as Wegener granulomatosis, mycobacterial
infection, histiocytosis X, and sarcoidosis should be considered. Biopsy of the
granulation or polyp in these circumstances is recommended.
3. Necrotizing Otitis Externa
Pain is not usually a prominent feature of CSOM, and its presence should raise
the possibility of necrotizing otitis externa (particularly in the immunocompromised,
eg, AIDS patients or elderly diabetics) or a malignant neoplasm of the eternal canal or
middle ear.
The treatment goals of uncomplicated CSOM are to eliminate infection, prevent
further infection, and restore normal functioning to the middle ear. Both medical and surgical
interventions play a role in achieving these aim.
A. Nonsurgical Measures
1. Aural toilet
Aural toilet is important for the successful treatment of CSOM,
particularly when topical medication is used. Clearing the discharge from the
external auditory canal allows the topical agent to reach the middle ear in an
adequate concentration.
2. Topical antibiotics

Although topical antibiotics are more effective than systemic

antibiotics in the treatment of CSOM, many contain aminoglycosides, which
are potentiall ototoxic. However, sensorineural hearing loss as a result of the
use of topical aminoglycosides in CSOM is rarely reported. This circumstance
is probably due to a combination of the relatively low concentration of
aminoglycoside reaching the middle ear and edema of the middle ear mucosa,
which prevents the direct absorption of the drug through the round window.
Despite the risk of ototoxicity, topical aminoglycosides are widely prescribed
by otolaryngologists for the treatment of CSOM because the benefits of
effective treatment outweigh the risks. The recent availability of topical
ofloxacin preparations may prove to be as effective as topical aminoglycosides
without the ototoxic potential.
3. Systemic antibiotics
Systemic antibiotics tend to have a poor penetration of the middle ear
and are therefore less effective than topical antibiotics. Because P aeruginosa
is the primary pathogen responsible for CSOM, the choice of oral systemic
antibiotics is limited. Both ciprofloxacin and ofloxacin have good
antipseudomonal activity. Unfortunately, these quinolone antibiotics are not
recommended in children owing to the possibility of causing arthropathies.
This circumstance limits the choice of systemic antibiotics in children to
broad-spectrum penicillins, such as piperacillin and cephalosporins, which
must be administered parenterally.
B. Surgical Measures
Some cases of CSOM resolve with medical treatment, and if the patient is
asymptomatic, then no further intervention is required. However, if otorrhea recurs or
persists despite medical treatment or if the patient feels handicapped by a residual
conductive hearing loss, surgical therapy should be considered.
1. Tympanoplasty
Ideally, surgery should be carried out when the infection has been
adequately treated and the middle ear mucosa is healthy, since the chance of a
successful outcome is increased. In this situation, a tympanoplasty, with repair
of the tympanic membrane and ossicular chain (if required), is recommended.
2. Tympanomastoid surgery

In cases that are refractory to medical treatment, it is necessary to

perform tympanomastoid surgery (tympanoplasty combined with a cortical
mastoidectomy). The aims of this procedure are to aerate the middle ear and
mastoid, remove chronically inflamed tissue, repair the tympanic defect, and
reconstruct the ossicular chain. The achievement of all of these goals often
requires more than one procedure.
1. Sequelae

Tympanosclerosis is characterized by hyalinization and the deposition
of calcium in the tympanic membrane, middle ear, or both. It often occurs as a
result of inflammation or trauma and is therefore commonly seen after
recurrent episodes of AOM and OME and after ventilation tube insertion. The
typical clinical appearance is of white plaques in the tympanic membrane. If
the process is limited to the tympanic membrane (ie, myringosclerosis), then
hearing is usually unaffected. However, if the middle ear is involved, then the
ossicular chain can become immobilized, resulting in a conductive hearing
loss. Attempts at surgical correction by tympanoplasty may initially be
successful, but refixation of the ossicles is not uncommon.

Atelectasis refers to the presence of a grossly retracted or collapsed
tympanic membrane. It probably occurs as a result of prolonged negative
middle ear pressure secondary to chronic eustachian tube dysfunction. The
whole of the tympanic membrane can be affected, but if collapse is only
partial, then a localized retraction pocket is formed. The presence of an
atelectatic tympanic membrane may not produce any symptoms, but more
commonly results in a mild conductive hearing loss. Prolonged contact
between the tympanic membrane and the ossicles can result in ossicular
erosion, particularly of the long process of the incus; consequently, a more
significant hearing loss results. Another consequence of persistent atelectasis
is that the normal migration pattern of squamous epithelium from the
tympanic membrane may be disrupted, leading to the accumulation of

squamous debris and cholesteatoma formation. This situation is a particular

risk if the retraction pocket is located in the pars flaccida or the
posterosuperior pars tensa.
The management of atelectasis is controversial. If eustachian tube
dysfunction is still considered to be present, the insertion of ventilation tubes
could potentially reverse the changes in the tympanic membrane by
normalizing the pressure in the middle ear space. If no improvement is
observed and the location of the retraction raises the concern of subsequent
cholesteatoma formation, then excision and grafting of the affected portion of
the tympanic membrane are recommended. The recurrence of tympanic
membrane retraction after this procedure is not uncommon; therefore,
prolonged observation is advised.
2. Intratemporal Complications

The fact that the mastoid air cell system is part of the middle ear cleft
means that some degree of mastoid inflammation occurs whenever there is
infection in the middle ear. In most cases, this infection does not progress to
clinically apparent acute mastoiditis. However, if pus collects in the mastoid
air cells under pressure, necrosis of the bony trabeculae occurs, resulting in the
formation of an abscess cavity. The infection may then progress to periostitis
and subperiosteal abscess, or to a more serious intracranial infection.
a. Acute mastoiditis
Typically, acute mastoiditis presents as a complication of AOM
in a child. Pain and tenderness over the mastoid process are the initial
indicators of mastoiditis. As the infection progresses, edema and
erythema of the postauricular soft tissues with loss of the postauricular
crease develop. These changes result in anteroinferior displacement of
the pinna. Fullness of the posterior wall of the external auditory canal
is frequently seen on otoscopy as a result of the underlying osteitis. If a
subperiosteal abscess has developed, fluctuance may be elicited in the
postauricular area.
Once the diagnosis of acute mastoiditis is suspected, the
radiologic investigation of choice is a CT scan, which provides

information about the extent of the opacification of the mastoid air

cells, the formation of subperiosteal abscess, and the presence of
intracranial complications. In some cases, acute mastoiditis can be
successfully managed by antibiotic therapy alone, but some patients
require surgical intervention. When there is no clinical or radiologic
indication of a subperiosteal abscess or an intracranial extension of
disease, then high-dose broadspectrum intravenous antibiotics should
be commenced.
If, after 24 hours of treatment, there is no evidence of
resolution or if symptoms progress, a cortical mastoidectomy should be
performed, along with myringotomy if spontaneous perforation of the
tympanic membrane has not occurred. If a subperiosteal abscess or an
intracranial extension of disease is suspected, surgery in combination
with high-dose intravenous antibiotics should be the first-line therapy.
b. Subacute mastoiditis
Subacute or masked mastoiditis may occur when inadequate
treatment of AOM results in a low-grade infection of the mastoid air
cells. The symptoms and signs are equivalent to those of acute
mastoiditis, but are less severe and more persistent. Most cases resolve
with ventilation of the middle ear combined with appropriate antibiotic
therapy. If this treatment fails to resolve the infection, cortical
mastoidectomy is indicated.

This rare complication of suppurative OM occurs in both acute and
chronic forms. In the acute form, there is extension of acute mastoiditis into a
pneumatized petrous apex. The chronic form of petrositis usually occurs as a
result of mucosal or cholesteatomatous CSOM; pneumatization of the petrous
apex is not a prerequisite as the infection spreads by thrombophlebitis,
hematogenous dissemination, or direct extension. Because of the close
relationship of the ophthalmic division of the trigeminal nerve and the
abducens nerve to the petrous apex, the classic features of petrositis are
otorrhea associated with retroorbital pain and lateral rectus palsy (Gradenigo


syndrome). Because of the high incidence of an intracranial extension of

infection from petrositis, a combination of antibiotics and surgical drainage of
the petrous apex is the management of choice.

Facial Nerve Paralysis

Facial nerve palsy can occur as a result of either acute or chronic OM.
There are two mechanisms by which OM can result in facial nerve paralysis:
1. as a result of the locally produced bacterial toxins
2. from direct pressure applied to the nerve by cholesteatoma or
granulation tissue.
If there is a congenital dehiscence of the bony canal of the facial nerve
in the middle ear, then an episode of AOM can lead to inflammatory edema of
the nerve and a subsequent paresis. This situation should be managed by
myringotomy with aspiration of pus from the middle ear along with antibiotic
therapy, which will mostly result in the rapid resolution of paralysis. Further
surgical exploration of the facial nerve is not indicated unless the paralysis
fails to resolve. If facial nerve paralysis occurs as a result CSOM, urgent
surgical exploration, with decompression of the facial nerve, is indicated.
Facial paralysis from otitis media is rare but can occur in acute or
chronic cases. In a recent series, otitis media accounted for only 3.1% of acute
facial palsies. Of these 50 cases, only 5 were children with acute otitis media.
The remaining adult cases were divided equally between chronic purulent
otitis media and cholesteatomas. Three additional cases were from tuberculous
otitis. Most paralyses were incomplete. Nearly all patients explored surgically
had a dehiscence of the bony canal of the facial nerve, usually in the tympanic
segment, which presumably allowed spread of the inflammation from the
middle ear to the nerve. Facial paralysis associated with acute otitis media,
especially in infants and children, should be managed with parenteral
antibiotics and a wide myringotomy for drainage. Surgical manipulation of the
facial nerve in acute otitis media is not recommended. Adour also
recommended the addition of a 10-day course of corticosteroids in conjunction
with myringotomy and antibiotics.
Facial paralysis associated with chronic otitis media suggests a high
probability of cholesteatoma, and surgical intervention is appropriate. The


mechanism of facial paralysis associated with cholesteatoma could be

compression or inflammation. Djeric studied autopsy specimens from patients
who had chronic otitis media but no antemortem evidence of facial paralysis.
Two of 20 facial nerves had focal areas of demyelination, suggesting that
adjacent inflammation may be more important than pressure.

Suppurative Labyrinthitis
Infection of the middle ear can lead to direct bacterial invasion of the
inner ear, usually via the round window, resulting in acute suppurative
labyrinthitis. Erosion of the bony capsule of the inner ear by a cholesteatoma
(most commonly the lateral semicircular canal) provides an alternative route
of entry to the inner ear. Suppurative labyrinthitis presents with sudden
sensorineural hearing loss, severe vertigo, nystagmus, and nausea and
vomiting. The cochlear aqueduct provides a direct communication between the
perilymph and the cerebrospinal fluid; therefore, there is a significant risk of
developing meningitis. The aim of treatment is to eradicate infection, thereby
preventing meningitis. Surgical intervention is often required for underlying
chronic middle ear disease, although the timing of surgery is controversial.
Cochlear and vestibular functions are invariably permanently lost and, as
healing occurs, obliterative osteitis of the inner ear commonly develops.

3. Intracranial Complications
The incidence of intracranial complications has been considerably reduced
since the introduction of antibiotics. Despite this fact, once an intracranial
complication develops, it carries a significant risk to life. Therefore, early recognition
and treatment are vital to
improve the prognosis. It is not uncommon for more than one intracranial
complication to occur simultaneously.
The most common early symptoms of intracranial extension of infection are
persistent headache and fever. Other features include lethargy, irritability, and neck
stiffness. A decreasing level of consciousness and seizures are late signs associated
with a poor prognosis.
Once suspicion of an intracranial infection is raised, an MRI of the brain is the
investigation of choice, along with lumbar puncture if meningitis is suspected. The
causative organism depends on whether the complication has developed as a

consequence of acute or chronic OM; the initial antibiotic therapy should be

prescribed accordingly until the results of bacterial cultures and sensitivity are

Acute otitis media is the most common cause of bacterial meningitis. It
can occur as a result of hematogenous spread, of direct extension from the
middle ear through a bony dehiscence, or through the cochlear aqueduct via
the inner ear.
The most common organisms responsible for otic meningitis are S
pneumoniae and H influenzae type B.
The classic presentation is with headaches,photophobia, neck stiffness,
and fluctuating levels of consciousness. The evaluation should include an MRI
of the brain to rule out other intracranial complications as well as a lumbar
If meningitis is secondary to AOM, then a myringotomy should be
performed once antibiotic therapy has been initiated. In the case of CSOM
resulting in meningitis, the patient should be fully stabilized before
considering surgical management of the chronic ear disease.

Intracranial Abscess
Brain, subdural, and extradural abscesses can all arise as a
complication of middle ear infections (commonly associated with chronic
disease). Intracranial abscesses are usually caused by multiple aerobic and
anaerobic bacteria. Commonly cultured organisms include streptococci, S
aureus, S pneumoniae, H influenzae, P aeruginosa, Bacteroides fragilis, and
Proteus species.
a. Brain Abscess
Most otogenic brain abscesses develop within the temporal lobe
or cerebellum. The progression of symptoms from a brain abscess can
be gradual, occurring over days or even weeks. In addition to the
generalized symptoms, focal neurologic signs can develop depending
on the anatomic location of the abscess within the brain. As the abscess
enlarges, features typical of raised intracranial pressure develop. Once

a brain abscess has been diagnosed, urgent neurosurgical intervention

is indicated to drain the abscess. Surgery for the associated ear disease
is less urgent and should be planned when the patients condition is
more stable.
b. Subdural Abscess
A subdural abscess forms between the dura mater and the
arachnoid mater. Symptoms and signs tend to progress much more
rapidly than those seen with a brain abscess. Drainage of the abscess is
the mainstay of treatment.
c. Extradural Abscess
Extradural abscesses are typically formed in the middle fossa
between the dura mater and the thin bony plate of the tegmen. They
can also occur in the posterior fossa, where they are commonly
associated with lateral sinus thrombosis. The clinical features are often
nonspecific and may fluctuate if a dehiscence in the tegmen is present,
allowing the abscess to partially drain into the mastoid cavity. As with
other intracranial complications, headache and fever are the most
common features. Because of its location, an extradural abscess can
usually be drained through a mastoidectomy approach while treating
the underlying middle ear disease.

Lateral Sinus Thrombosis

Because of its close proximity to the mastoid air cells, the lateral, or
sigmoid, sinus is prone to involvement in middle ear infections, which may
lead to thrombosis. Once an infected thrombus has formed in the lateral sinus,
it may propagate both distally and proximally and may give rise to infected
emboli. Typically, there are intermittent episodes of high pyrexia associated
with rigors.
If the thrombus propagates into the neck, there will be neck tenderness
along the internal jugular vein and neck stiffness or torticollis. Proximal
extension of the thrombus to the sagittal sinus can result in symptoms and
signs of raised intracranial pressure.


MRI most reliably makes the diagnosis of lateral sinus thrombosis. The
management of lateral sinus thrombosis requires broad-spectrum antibiotics
and surgery. A complete mastoidectomy should be performed, with exposure
of the lateral sinus. Once the diagnosis has been confirmed by needle
aspiration, the sinus is opened and the infected thrombus evacuated. If
symptoms persist after this procedure, consideration should be given to
ligation of the ipsilateral internal jugular vein, once the possibility of other
intracranial complications has been excluded.

Otic Hydrocephalus
Otic hydrocephalus is a rare complication in which raised intracranial
pressure develops as a result of a middle ear infection, but its pathophysiology
is poorly understood.
The usual features are headache, vomiting, disturbed mental state,
visual disturbance, and papilledema associated with a middle ear infection.
Imaging of the brain reveals the ventricular size to be normal, but lumbar
puncture confirms raised cerebrospinal fluid pressure.
Management is aimed at resolving the middle ear infection while
normalizing intracranial pressure with the use of steroids, diuretics (eg,
mannitol), and, if required, intermittent drainage of cerebrospinal fluid.

Facial Nerve
Motor Component of Facial Nerve
The nucleus of the motor component of the facial nerve is located in the ventrolateral
portion of the pontine tegmentum. The neurons of this motor nucleus are analogous to the
anterior horn cells of the spinal cord, but are embryologically derived from the second
branchial arch. The root fibers of this nucleus take a complicated course.
Within the brainstem, they wind around the abducens nucleus (forming the so-called
internal genu of the facial nerve), thereby creating a small bump on the floor of the fourth
ventricle (facial colliculus). They then form a compact bundle, which travels ventrolaterally
to the caudal end of the pons and then exits the brainstem, crosses the subarachnoid space in
the cerebellopontine angle, and enters the internal acoustic meatus together with the nervus
intermedius and the eighth cranial nerve (the vestibulocochlear nerve).
Within the meatus, the facial nerve and nervus intermedius separate from the eighth
nerve and travel laterally in the facial canal toward the geniculate ganglion. At the level of
the ganglion, th e facial canal takes a sharp downward turn (external genu of the facial

nerve). At the lower end of the canal, the facial nerve exits the skull through the stylomastoid
Its individual motor fibers are then distributed to all regions of the face (some of them
first traveling through the parotid gland). They innervate all of the muscles of facial
expression that are derived fromthe second branchial arch, i.e., the orbicularis oris and oculi,
buccinator, occipitalis, and frontalis muscles and the smaller muscles in these areas, as well
as the stapedius, platysma, stylohyoid muscle, and posterior belly of the digastric muscle.


Motor lesions involving the distribution of the facial nerve.

The muscles of the forehead derive their supranuclear innervation from both cerebral
hemispheres, but the remaining muscles of facial expression are innervated only unilaterally,
i.e., by the contralateral precentral cortex. If the descending supranuclear pathways are
interrupted on one side only, e. g., by a cerebral infarct, the resulting facial palsy spares the
forehead muscles: the patient can still raise his or her eyebrows and close the eyes forcefully.
This type of facial palsy is called central facial palsy.
In a nuclear or peripheral lesion, however, all of the muscles of facial expression on
the side of the lesion are weak. One can thus distinguish central from nuclear or peripheral
facial palsy by their different clinical appearances. The motor nuclei of the facial nerve are
innervated not only by the facial cortex but also by the diencephalon, which plays a major
role in emotion-related facial expressions. Further input is derived from the basal ganglia; in
basal ganglia disorders (e. g., Parkinson disease), hypomimia or amimia can be seen. There
are also various dyskinetic syndromes affecting the muscles of facial expression with

different types of abnormal movement: hemifacial spasm, facial dyskinesias, and

blepharospasm, among others. The site of the causative lesion in these syndromes remains

Differetial Diagnosis of Facial Paralysis

- 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.

Baehr M, Frotscher M. Duus Topical Diagnosis in Neurology. Ed ke-4. Germany:

Georg Thieme Verlag; 2005.

Putz R, Pabst R. Sobotta: Atlas Anatomi Manusia. Ed ke-22. Jilid 1. Jakarta: Penerbit
Buku Kedokteran EGC; 2006.

-Effendi H, editor. Boies: Buku Ajar Penyakit THT. Ed ke-6. Jakarta: Penerbit Buku

Kedokteran EGC; 1997.