Professional Documents
Culture Documents
Supervised by :
dr. H. Oscar Djauhari, Sp. THT
Presented by :
Hambiah Hari Oki
2012.061.068
Sardito
2012.061.069
Steven Yoe
2012.061.074
Elsa Aprillia S
2013.061.012
Jovita Olivia
2013.061.017
Clinical Rotation
Medical Faculty of Unika Atma Jaya Jakarta
Syamsudin, S.H. Regional General Hospital, Sukabumi
Period June 2nd 2014 June 28th 2014
PATIENTS IDENTITY
Name
: Mr. X
Age
: 55 years old
Sex
: Male
Occupation
: Labor
Race
: Sundanese
Address
: Sukabumi
Weight
: 72 kg
Height
: 165cm
ANAMNESIS
Chief complaint
:
o Difficulty smiling and drop of the right corner of the mouth since 5 days
ago.
Additional complaint
: History of present illness :
o Patient had secretion coming out of his right ear. It comes out
intermittently since 4 months ago and the latest was 1 month ago.
Secretion was yellowish in color, slightly thick in consistency and has foul
smell. Patient went to general practitioner before but with no
improvement.
o 5 days ago, patient noticed a drop of his right mouth corner and difficulty
in smiling. Patient felt this symptom became worse along with time.
Earache was absent. Fever and pain on other places were absent. Hearing
loss (+). Tinnitus (+). History of trauma (-).
History of past illness
:
History of yellowish purulent discharge from the right ear 4 months ago
He went to the community health centre 2 months ago and was given oral
medication but the discharge still came out.
No history of allergic
No history of diabetes mellitus, hypertension
Physical Examination
1. General status
General appearance
Awakeness
Blood Pressure
Pulse rate
: moderately ill
: compos mentis (E4M6V5)
: 110/70 mmHg
: 80 beat per minute
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Respiration rate
Temperature
2. ENT Status
Auris
o Auricle
: normal/normal
o CAE
:
hyperemis -/-, edema -/-, discharge + yellowish and purulent
(minimal) /-, , cholesteatoma -/- odorous smell +/-, laceration
Working diagnosis
Chronic Supurative Otitis Media auris dextra with complication dextra facial nerve
paralysis
Differential Diagnosis
- Cholesteatoma
- Chronic granulomatous
- Necrotizing otitis media
Workup
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Therapy
Medication :
i. Topical Antibiotic : ofloxacin 3mg/ml, 2x10 drops, AD
ii. Oral Antibiotic : amoxicillin-clavulanat acid, 2x500mg/125mg, PO
iii. Steroid : Prednisone, 4 X 20 mg per day p.o.
iv. Nerve decompression
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.
CLINICAL FINDING
a. Symptomps and Signs
History of otorrhea, intermittent or continuous
Hearing loss
Discharge mucopurulent or bloodstained otorrhea ( which lead to polyp or
b. Special Test
DIFFERENTIAL DIAGNOSIS
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
diagnosis.
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,
TREATMENT
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
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.
COMPLICATION
1. Sequelae
Tympanosclerosis
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.
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Atelectasis
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
Mastoiditis
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
Petrositis
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.
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
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Meningitis
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
puncture.
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
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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
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
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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.
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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
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nerve). At the lower end of the canal, the facial nerve exits the skull through the stylomastoid
foramen.
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.
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