Professional Documents
Culture Documents
Supervised by :
dr. H. Oscar Djauhari, Sp. THT
Presented by :
Didi Suryana
2012730029
Clinical Rotation
Medical Faculty of Muhammadiyah Jakarta University - Syamsudin, S.H.
Regional General Hospital, Sukabumi
Period Jully 25th agust 27th 2016
PATIENTS IDENTITY
Name
: Mr. X
Age
: 22 years old
Sex
: Male
Ocupation
: Student
Race
: Javanese
Address
Weight
: 55 kg
Height
: 165cm
ANAMNESIS
Chief complaint
Physical Examination
1. General status
General appearance
Awakeness
Blood Pressure
Pulse rate
Respiration rate
Temperature
: 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
Schwabach.
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.
NPOP
o Mucosa
o Tonsil
: T1/T1
Maxillofacial : Asymmetrical
Neck
: lymphadenopathy -/-
Working diagnosis
Chronic Supurative Otitis Media auris dextra with complication dextra facial nerve
paralysis
3
Differential Diagnosis
Primary tumor in the middle of right ear
Workup
Lab
Culture of pus from the right ear and bacterial resistance test
Audiometry test
Therapy
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
PATHOGENESIS
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.
CLINICAL FINDING
a. Symptomps and Signs
Hearing loss
b. Special Test
5
An audiologic evaluation
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, AIDS patients or elderly diabetics) or a malignant neoplasm of the eternal canal or
middle ear.
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
6
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.
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
8
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
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
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
10
11
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
12
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
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
13
14
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
15
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.
16
RESOURCES:
- Lalwani AK, editor. Current Diagnosis & Treatment in Otolaryngology - Head & Neck
-
-Effendi H, editor. Boies: Buku Ajar Penyakit THT. Ed ke-6. Jakarta: Penerbit Buku
18