1.

Sequelae
1.1.
Tympanosclerosis
Tympanosclerosis is thought to be a complication of otitis media in which
hyalin and calcium deposits accumulate within the tympanic membrane and the
submucosa middle ear. 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. In most patients, these plaques are clinically insignificant
and cause little or no hearing impairment.
Tympanosclerotic plaques within the tympanic membrane appear as a
semicircular crescent or horseshoe-shaped white plaque within 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 and ossicular reconstruction can be
performed in ears with tympanosclerosis
1.2.
Atelectasis
Atelectasis is thought to result mainly from long-standing eustachian tube
dysfunction. One of the main functions of the eustachian tube is ventilation. Opening
of the eustachian tube allows exchanging of gases and equalization between the
environment and middle ear.
If the atelectasis develops, the tympanic membrane becomes retracted.
Tympanic membrane comprises two parts, the pars tensa, which is the main part of the
eardrum, and the pars flaccida, which is a smaller part of the eardrum located above
the pars tensa. Either or both of these parts may become retracted. The retracted
segment of eardrum is often known as a retraction pocket. In atelectatic ears, the
middle ear space is partially or completely obliterated, but the Retraction of the
tympanic membrane may lead to erosion of the long process of the incus and the
stapes structure.
The management of atelectasis is controversial. If eustachian tube function 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
2.1.
Mastoiditis
Mastoiditis is an inflammation or infection of the mastoid bone, which is a
portion of the temporal bone. Inflammation in the mastoid itself is quite rare. It is
almost always a result of inflammation or infection in the middle ear space.
Since there is a direct communication between the mastoid and the middle ear
space, any inflammatory process occurring in the middle ear space is directly
transmitted into the mastoid. Infection can spread into the lateral sinus, causing an
infected clot to form within it (lateral sinus thrombosis). The infection can also extend
directly inferiorly, presenting as an abscess deep to a muscle that is attached to the
mastoid (sternocleidomastoid muscle). These abscesses are termed Bezolds
abscesses. Acute mastoiditis was also associated with high incidence of meningitis,

which is an extension of the bacterial infection from the mastoid into the lining
surrounding the brain. Untreated meningitis has a very high mortality rate; and those
individuals who do survive are often left with significant neurologic dysfunction.
Lastly, acute mastoid infections can also create a cerebellar abscess. Since the
cerebellum is involved in fine motor coordination and control of the central part of the
body, especially during walking, these individuals often would lose coordination or
have significant difficulties walking.
Mastoid infections can assume two different patterns. Chronic mastoiditis is a
disease process that is occurring more than three months and acute mastoiditis is
occurring less than three weeks.
a. Acute mastoiditis
Acute mastoiditis is almost always a consequence of an acute ear infection that
is not treated or is incompletely treated. In acute mastoiditis there is a direct
bacterial infection in the mastoid. Often the skin overlying the mastoid directly
behind the outer ear becomes inflamed and as a consequence is red and swollen. If
the infection continues for more than 10 to 14 days, the small, bony walls that
form the air-filled honeycomb begin to be destroyed. This bone destruction is
termed coalescent mastoiditis. If the infection continues, then there can be direct
pus accumulation under the skin behind the ear, with a resultant abscess.
b. Chronic mastoiditis
Chronic mastoiditis occurs whenever there is a chronic inflammatory process
that affects the mastoid. This is usually termed chronic otitis media, where there is
a perforation in the eardrum, with intermittent infected material draining through
the hole in the eardrum. In chronic mastoiditis there is no bone destruction as is
seen in coalescent mastoiditis. Instead the lining inside the mastoid often becomes
thickened and inflamed.
2.2. Petrositis
This rare complication of
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.
2.3.

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.
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 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.
2.4.

Labyrinthitis
Labyrinthinitis is an uncommon complication of acute otitis media and
mastoiditis. there are serous labyrinthitis, suppurative labyrinthitis, and labyrinthine
fistula.
Suppurative labyrinthitis results from bacterial invasion of the inner ear from
contiguous areas of the temporal bone or meninges. Serous labyrinthitis
is an irritation of the labyrinth caused by otitic or meningitic infection without
bacterial invasion of the inner ear. Fistulization of the labyrinth occurs most
commonly as a result of erosion of the bony covering of the lateral semicircular canal
by cholesteatoma

a. Serous labyrinthitis
Serous (or toxic) labyrinthitis results from irritation of the labyrinth by the byproducts of infection and inflammation. Toxins are thought to
enter the inner ear via the oval and round windows or through a fistula in the bony
labyrinth. Serous labyrinthitis may be a complication of acute or
chronic otitis media; meningitis, in which case the condition may be masked by the
more severe meningeal symptoms.
The patient presents with vertigo, which may be transient and recurrent over
months or years; sensorineural hearing loss may fluctuate and is less severe than
that seen in purulent labyrinthitis. It may not be distinguishable from purulent
labyrinthitis, except for retention of some audiovestibular function. The signs and
symptoms are less dramatic than those of purulent labyrinthitis, and the pathologic
consequences in the inner ear are less destructive.

Management is directed toward the infectious source. If the labyrinthitis

results from acute otitis media, myringotomy and antibiotic therapy are sufficient.
If coalescent mastoiditis or chronic otitis media with possible cholesteatoma is
present, labyrinthine fistula should be suspected and mastoidectomy should be
performed.

b. Suppurative labyrinthitis
Suppurative labyrinthitis can develop as a complication of acute and chronic
otitis media from migration of the bacteria through the preformed pathways of the
oval window, round window, and preexisting fractures of the temporal bone and
from direct invasion by erosion of the labyrinthine bone by cholesteatoma.
Bacteria may traverse the cochlear aqueduct in bacterial meningitis. Bacterial
invasion of the inner ear produces irreversible damage to the neuroepithelium,
atrophy of the stria vascularis, collapse of Reissners membrane, and
endolymphatic hydrops.
If the patient survives without surgery, healing occurs with fibrosis and
obliterative osteitis of the labyrinth and cochlea. No audiovestibular function is
retained.
The symptoms are most severe during the acute bacterial invasion of the
labyrinth. The vertigo and nystagmus result from sudden loss of the healthy
tonic neural impulses from the involved labyrinth, without any change in the input
from the healthy side. Recovery from a unilateral peripheral
vestibular lesion is attributed to the brains ability to compensate for the sensory
mismatch by adapting to the asymmetric sensory input. This occurs
gradually as the cerebellum and brainstem integrate the conflicting information
and adapt over time to a stable lesion. The severity of the symptoms
gradually lessens over the next few days, but central compensation occurs over
several weeks with complete resolution of nystagmus and vertigo.

c. Labyrinthine fistula
Fistulization of the labyrinth occurs most commonly as a result of erosion of
the bony covering of the lateral semicircular canal by cholesteatoma.
The patient will have active or inactive chronic otitis media for many years.
The mainstay of the diagnosis, the fistula test, is performed by application of
positive and negative pressure to the middle ear with a pneumatic otoscope.
A positive fistula test produces nystagmus with the fast component toward the
tested ear with application of positive pressure, and away from the tested ear with
application of negative pressure.
The nystagmus results from motion of the soft tissue over the fistula; positive
pressure causes ampullofugal movement of endolymph (away from the ampulla),

and negative pressure causes ampullopetal movement of the endolymph (toward

the ampulla. Management is mastoidectomy with eradication of cholesteatoma

3. Intracranial Complications
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.
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.
3.1.

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.

3.2.

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.
3.3.

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.

3.4.

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
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.

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
unknown.

Differetial Diagnosis of Facial Paralysis

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