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Diffuse Otitis Externa

Presented by:

1. Cynthia Tejasaputra 10/296652/KU/13652

2. Danang Setia Budi 10/296964/KU/13720
3. Valentina Tjandra Dewi 10/296636/KU/13647
4. Rosinta Pratiwi 10/304677/KU/14096
5. Wiwid Santiko 10/304804/KU/14171
6. Primadhy Rahardian Wijaya 10/297192/KU/13772
7. Sarah Mardhiah 10/304643/KU/14062


dr. Danu Yudhistira

Department of Otorhinolaryngology Head and Neck Surgery

Faculty of Medicine Gadjah Mada University

Dr. Sardjito General Hospital




Otitis externa (OE) is an inflammation or infection of the external auditory canal

(EAC), the auricle, or both. It is a common disease that can be found in all age groups. OE
usually represents an acute bacterial infection of the skin of the ear canal (most commonly
attributable to Pseudomonas aeruginosa or Staphylococcus aureus but can also be caused by
other bacteria, viruses, or a fungal infection.

Several factors can contribute to EAC infection and the development of OE, including the
following :

Absence of cerumen
High humidity
Retained water in ear canal
Increased temperature
Local trauma (eg, use of cotton swabs or hearing aids)

Aquatic athletes are particularly prone to the development of OE because repeated

exposure to water results in removal of cerumen and drying of the EAC. Retained water in
the ear canal can cause maceration of the skin and a milieu conducive to bacterial or fungal
proliferation. OE occurs more often in the summer months, when swimming is more
common, and it is also common in tropical areas.[9] Individuals with allergic conditions (eg,
eczema, allergic rhinitis, and asthma) are also at significantly higher risk for OE.

Although OE rarely causes prolonged problems or serious complications, the infection is

responsible for significant pain and acute morbidity. Prompt diagnosis and appropriate
therapy cure the majority of cases without complications; however, patients who are diabetic,
immunocompromised, or untreated may develop necrotizing (malignant) OE, a potentially
life-threatening infection.

OE may be classified as follows:

Acute diffuse OE - Most common form of OE, typically seen in swimmers

Acute localized OE (furunculosis) - Associated with infection of a hair follicle
Chronic OE - Same as acute diffuse OE but is of longer duration (>6 weeks)
Eczematous (eczematoid) OE - Encompasses various dermatologic conditions (eg,
atopic dermatitis, psoriasis, systemic lupus erythematosus, and eczema) that may
infect the EAC and cause OE

Necrotizing (malignant) OE - Infection that extends into the deeper tissues adjacent to
the EAC; occurs primarily in immunocompromised adults (eg, diabetics, patients with
Otomycosis - Infection of the ear canal from a fungal species (eg, Candida,


Although the infection can affect all age groups, OE appears to be most prevalent in
the older pediatric and young adult population, with a peak incidence in children aged 7-12
years. A single epidemiologic study from the United Kingdom found a similar 12-month
prevalence for individuals aged 5-64 years and a slight increase in prevalence for those older
than 65 years.This was postulated to occur secondary to an increase in comorbidities, as well
as an increase in the use of hearing aids, which may cause trauma to the EAC.

OE affects both sexes equally. No racial predilection has been established, though
people in some racial groups have small ear canals, which may predispose them to
obstruction and infection.

The disease is often found in areas that hot and humid and rarely on cool and dry
climate. The incidence of otitis externa occurs in 4 out of 1,000 children and adults per year.
The first report of the CDC (Center for Disease Control and Prevention) that describes the
overall epidemiology of otitis externa in the United States, it is estimated that 2.4 million
visits per year that diagnosed at the health center is a case of acute otitis externa (8.1 visits
per 1,000 population ).



The ear consists of external, middle, and internal parts. The tympanic membrane separates the
external ear from the middle ear. The pharyngotympanic tube joins the middle ear to the
nasopharynx. The external ear is composed of the shell-like auricle (pinna), which collects
sound, and the external acoustic meatus (canal), which conducts sound to the tympanic
membrane. The arterial supply to the auricle is derived mainly from the posterior auricular

and superficial temporal arteries, The main nerves to the skin of the auricle are the great
auricular and auriculotemporal nerves. The auriculotemporal nerve, a branch of CN V3,
supplies the skin of the auricle anterior to the external acoustic meatus. Minor contributions
of embryological significance are made to the skin of the concha and its eminence by the
vagus and facial nerves. The external acoustic meatus is a canal that leads inward through the
tympanic part of the temporal bone from the auricle to the tympanic membrane, a distance of
2-3 cm in adults.

The auricle has several depressions and elevations. The concha is the deepest depression. The
elevated margin of the auricle is the helix. The other depressions and elevations are identified
in. The non-cartilaginous lobule (earlobe) consists of fibrous tissue, fat, and blood vessels. It
is easily pierced for taking small blood samples and inserting earrings. The tragus (G. tragos,
goat; alluding to the hairs that tend to grow from this formation, like a goat's beard) is a
tongue-like projection overlapping the opening of the external acoustic meatus.

The arterial supply to the auricle is derived mainly from the posterior auricular and
superficial temporal arteries. The main nerves to the skin of the auricle are the great auricular
and auriculotemporal nerves. The great auricular nerve supplies the cranial (medial) surface
(commonly called the back of the ear and the posterior part (helix, antihelix, and lobule) of
the lateral surface front. The auriculotemporal nerve, a branch of CN V3, supplies the skin of
the auricle anterior to the external acoustic meatus. Minor contributions of embryological
significance are made to the skin of the concha and its eminence by the vagus and facial
nerves. The lymphatic drainage of the auricle is as follows: the lateral surface of the superior
half of the auricle drains to the superficial parotid lymph nodes; the cranial surface of the
superior half of the auricle drains to the mastoid nodes and deep cervical lymph nodes; and
the remainder of the auricle, including the lobule, drains into the superficial cervical lymph

The ceruminous and sebaceous glands in the subcutaneous tissue of the cartilaginous part of
the meatus produce cerumen (earwax). The external surface of the tympanic membrane is
supplied mainly by the auriculotemporal nerve a branch of CN V3. Some innervation is
supplied by a small auricular branch of the vagus (CN X). The internal surface of the
tympanic membrane is supplied by the glossopharyngeal nerve (CN IX).

The tympanic membrane, approximately 1 cm in diameter, is a thin, oval semitransparent

membrane at the medial end of the external acoustic meatus. It forms a partition between the
meatus and the tympanic cavity of the middle ear. The tympanic membrane is covered with
thin skin externally and mucous membrane of the middle ear internally. Viewed through an
otoscope, the tympanic membrane has a concavity toward the external acoustic meatus with a
shallow, cone-like central depression, the peak of which is the umbo. The central axis of the
tympanic membrane passes perpendicularly through the umbo like the handle of an umbrella,
running anteriorly and inferiorly as it runs laterally. Thus the tympanic membrane is oriented

like a mini radar or satellite dish positioned to receive signals coming from the ground in
front and to the side of the head.

Superior to the lateral process of the malleus (one of the small ear bones, or auditory ossicles,
of the middle ear), the membrane is thin and is called the flaccid part (L. pars flaccida). It
lacks the radial and circular fibers present in the remainder of the membrane, called the tense
part (L. pars tensa). The flaccid part forms the lateral wall of the superior recess of the
tympanic cavity.

The tympanic membrane moves in response to air vibrations that pass to it through the
external acoustic meatus. Movements of the membrane are transmitted by the auditory
ossicles through the middle ear to the internal ear. The external surface of the tympanic
membrane is supplied mainly by the auriculotemporal nerve, a branch of CN V3. Some
innervation is supplied by a small auricular branch of the vagus (CN X). The internal surface
of the tympanic membrane is supplied by the glossopharyngeal nerve (CN IX).

Otoscopic Examination

The tympanic membrane is normally translucent and pearly gray. The handle of the
malleus is usually visible near the center of the membrane (the umbo). From the inferior end
of the handle, a bright cone of light is reflected from the otoscope's illuminator. This light
reflex is visible radiating anteroinferiorly in the healthy ear.

Middle Ears

The cavity of the middle ear or tympanic cavity is the narrow air-filled chamber in the
petrous part of the temporal bone. The cavity has two parts: the tympanic cavity proper, the
space directly internal to the tympanic membrane, and the epitympanic recess, the space
superior to the membrane. The tympanic cavity is connected anteromedially with the
nasopharynx by the pharyngotympanic tube and posterosuperiorly with the mastoid cells
through the mastoid antrum. The tympanic cavity is lined with mucous membrane that is
continuous with the lining of the pharyngotympanic tube, mastoid cells, and mastoid antrum.
The contents of the middle ear are the:

Auditory ossicles (malleus, incus, and stapes).

Stapedius and tensor tympani muscles.

Chorda tympani nerve, a branch of CN VII.

Tympanic plexus of nerves.

Walls of the Tympanic Cavity:

1. The tegmental wall (tegmental roof) is formed by a thin plate of bone, the tegmen
tympani, which separates the tympanic cavity from the dura mater on the floor of the
middle cranial fossa.

2. The jugular wall (floor) is formed by a layer of bone that separates the tympanic
cavity from the superior bulb of the internal jugular vein.

3. The membranous wall (lateral wall) is formed almost entirely by the peaked
convexity of the tympanic membrane; superiorly it is formed by the lateral bony wall
of the epitympanic recess. The handle of the malleus is attached to the tympanic
membrane, and its head extends into the epitympanic recess.

4. The labyrinthine wall (medial wall) separates the tympanic cavity from the internal
ear. It also features the promontory of the labyrinthine wall, formed by the initial part
(basal turn) of the cochlea, and the oval and round windows, which, in a dry cranium,
communicate with the inner ear.

5. The anterior carotid wall separates the tympanic cavity from the carotid canal;
superiorly, it has the opening of the pharyngotympanic tube and the canal for the
tensor tympani.

6. The mastoid wall (posterior wall) features an opening in its superior part, the aditus
(L. access) to the mastoid antrum, connecting the tympanic cavity to the mastoid
cells; the canal for the facial nerve descends between the posterior wall and the
antrum, medial to the aditus.

The mastoid antrum is a cavity in the mastoid process of the temporal bone. The antrum (L.
from G., cave), like the tympanic cavity, is separated from the middle cranial fossa by a thin
plate of the temporal bone, called the tegmen tympani. This structure forms the tegmental
wall (roof) for the ear cavities and is also part of the floor of the lateral part of the middle
cranial fossa. The antrum is the common cavity into which the mastoid cells open. The
antrum and mastoid cells are lined by mucous membrane that is continuous with the lining of
the middle ear. Anteroinferiorly, the antrum is related to the canal for the facial nerve.

Pharyngotympanic Tube

The pharyngotympanic tube connects the tympanic cavity to the nasopharynx, where it opens
posterior to the inferior nasal meatus. The function of the pharyngotympanic tube is to
equalize pressure in the middle ear with the atmospheric pressure, thereby allowing free
movement of the tympanic membrane. By allowing air to enter and leave the tympanic cavity,
this tube balances the pressure on both sides of the membrane. The arteries of the
pharyngotympanic tube are derived from the ascending pharyngeal artery, a branch of the
external carotid artery, and the middle meningeal artery and artery of the pterygoid canal,
branches of the maxillary artery. The nerves of the pharyngotympanic tube arise from the
tympanic plexus, which is formed by fibers of the glossopharyngeal nerve (CN IX).
Anteriorly, the tube also receives fibers from the pterygopalatine ganglion

Auditory Ossicles

The auditory ossicles form a mobile chain of small bones across the tympanic cavity from the
tympanic membrane to the oval window (L. fenestra vestibuli), an oval opening on the
labyrinthine wall of the tympanic cavity leading to the vestibule of the bony labyrinth. Its
consist : Maleus, incus, stapes

1. Malleus

The malleus (L. a hammer) attaches to the tympanic membrane. The rounded superior head
of the malleus lies in the epitympanic recess. The neck of the malleus lies against the flaccid
part of the tympanic membrane, and the handle of the malleus is embedded in the tympanic
membrane, with its tip at the umbo; thus the malleus moves with the membrane. The head of
the malleus articulates with the incus; the tendon of the tensor tympani inserts into its handle
near the neck. The chorda tympani nerve crosses the medial surface of the neck of the
malleus. The malleus functions as a lever, with the longer of its two processes and its handle
attached to the tympanic membrane.

2. Incus

The incus (L. an anvil) is located between the malleus and the stapes and articulates with
them. It has a body and two limbs. Its large body lies in the epitympanic recess, where it
articulates with the head of the malleus. The long limb lies parallel to the handle of the
malleus, and its interior end articulates with the stapes by way of the lenticular process, a

medially directed projection. The short limb is connected by a ligament to the posterior wall
of the tympanic cavity.

3. Stapes

The stapes (L. a stirrup) is the smallest ossicle. It has a head, two limbs (crura), and a base. Its
head, directed laterally, articulates with the incus. The base (footplate) of the stapes fits into
the oval window on the medial wall of the tympanic cavity. The oval base is attached to the
margins of the oval window. The base is considerably smaller than the tympanic membrane;
as a result, the vibratory force of the stapes is increased approximately 10 times over that of
the tympanic membrane. Consequently, the auditory ossicles increase the force but decrease
the amplitude of the vibrations transmitted from the tympanic membrane.

Muscles Associated with the Auditory Ossicles

Two muscles dampen or resist movements of the auditory ossicles; one also dampens
movements (vibration) of the tympanic membrane. The tensor tympani is a short muscle that
arises from the superior surface of the cartilaginous part of the pharyngotympanic tube, the
greater wing of the sphenoid, and the petrous part of the temporal bone. The muscle inserts
into the handle of the malleus. The tensor tympani pulls the handle medially, tensing the
tympanic membrane and reducing the amplitude of its oscillations. This action tends to
prevent damage to the internal ear when one is exposed to loud sounds. The tensor tympani is
supplied by the mandibular nerve (CN V3).

The stapedius is a tiny muscle inside the pyramidal eminence (pyramid), a hollow, cone-
shaped prominence on the posterior wall of the tympanic cavity. Its tendon enters the
tympanic cavity by emerging from a pinpoint foramen in the apex of the eminence and inserts
on the neck of the stapes. The stapedius pulls the stapes posteriorly and tilts its base in the
oval window, thereby tightening the anular ligament and reducing the oscillatory range. It
also prevents excessive movement of the stapes. The nerve to the stapedius arises from the
facial nerve (CN VII).

Internal Ear

The internal ear contains the vestibulocochlear organ concerned with the reception of sound
and the maintenance of balance. Buried in the petrous part of the temporal bone the internal
ear consists of the sacs and ducts of the membranous labyrinth. The membranous labyrinth,
containing endolymph, is suspended within the perilymph-filled bony labyrinth, either by
delicate filaments similar to the filaments of arachnoid mater that traverse the subarachnoid
space or by the substantial spiral ligament. It does not float. These fluids are involved in
stimulating the end organs for balance and hearing, respectively

Cochlea Structure

Hearing Nerve Pathway

Physiology Of Hearing

Hearing is a response to vibrating air molecules and equilibrium is the sense of motion and
balance. These senses reside in the inner ear, a maze of fluid-filled passages and sensory
cells. This section explains how the fluid is set in motion and how the sensory cells convert
this motion into an informative pattern of action potentials.

Pitch is our sense of whether a sound is high (treble) or low (bass). It is determined by
the frequency at which the sound source, eardrum, and other parts of the ear vibrate. One
movement of a vibrating object back and forth is called a cycle, and the number of cycles per
second (cps or hertz, Hz) is called frequency. The lowest note on a piano, for example, is
27.5 Hz, middle C is 261 Hz, and the highest note is 4,176 Hz. The most sensitive human
ears can hear frequencies from 20 to 20,000 Hz. The infrasonic frequencies below 20 Hz are
not detected by the ear, but we sense them through vibrations of the skull and skin, and they
play a significant role in our appreciation of music. The inaudible vibrations above 20,000 Hz
are ultrasonic. Human ears are most sensitive to frequencies ranging from 1,500 to 4,000 Hz.
In this range, we can hear sounds of relatively low energy (volume), whereas sounds above or
below this range must be louder to be audible (fig. 16.8). Normal speech falls within this
frequency range. Most of the hearing loss suffered with age is in the range of 250 to 2,050

The auditory ossicles provide no amplification; vibrations of the stapes against the inner ear
normally have the same amplitude as vibrations of the eardrum against the malleus. Why
have auditory ossicles, then? There are two answers to this. One is that the eardrum, which
moves in air, vibrates easily, whereas the stapes footplate must vibrate against the fluid of the
inner ear. This fluid puts up a much greater resistance to motion than air does. If airborne
sound waves struck the footplate directly, they would not have enough energy to overcome
this resistance and move the stapes. The eardrum, however, has 18 times the area of the oval
window. By concentrating the energy of the vibrating eardrum on an area 1/18 that size, the
ossicles create a greater force per unit area at the oval window and overcome the resistance of
the endolymph. The ossicles and their muscles also have a protective function. In response to
a loud noise, the tensor tympani pulls the eardrum inward and tenses it, while the stapedius
reduces mobility of the stapes.

This tympanic reflex muffles the transfer of vibrations from the eardrum to the oval window.
The reflex probably evolved in part for protection from loud but slowly building noises such
as thunder. It has a latency of about 40 msec, which is not quick enough to protect the inner
ear from sudden noises such as gunshots. The tympanic reflex also does not adequately
protect the ears from sustained loud noises such as factory noise or loud music. Such noises
can irreversibly damage the hair cells of the inner ear by fracturing their stereocilia. It is
therefore imperative to wear ear protection when using firearms or working in noisy
environments. The middle-ear muscles also help to coordinate speech with hearing. Without
them, the sound of your own speech would be so loud it could damage your inner ear, and it
would drown out soft or high-pitched sounds from other sources. Just as you are about to
speak, however, the brain signals these muscles to contract. This dampens the sense of
hearing in phase with the inflections of your own voice and makes it possible to hear other
people while you are speaking.

Stimulation of Cochlear Hair Cells

To produce a sensation of sound, vibration of the auditory ossicles leads to vibration of the
basilar membrane on which the hair cells rest. A simple mechanical model of the ear makes it
easy to see how this happens. The stapes pushes on the perilymph of the scala vestibuli; the
perilymph pushes the vestibular membrane down; the vestibular membrane pushes on the
endolymph of the cochlear duct; and the endolymph pushes the basilar membrane down. (The
vestibular membrane is omitted from the diagram for simplicity; it has no significant effect
on the mechanics of the cochlea.)

The basilar membrane puts pressure on the perilymph of the scala tympani below it, and the
secondary tympanic membrane bulges outward to relieve this pressure. In short, as the stapes
goes in-out-in, the secondary tympanic membrane goes out-in-out, and the basilar membrane
goes down-up-down. It is not difficult to see how this happens the only thing hard to
imagine is that it can happen as often as 20,000 times per second! The vestibular membrane
separates the perilymph of the scala vestibuli from the endolymph of the cochlear duct. In
order for the hair cells to function properly, the tips of their stereocilia must be bathed in

Endolymph has an exceptionally high K_ concentration, which creates a strong

electrochemical gradient from the tip to the base of a hair cell. This gradient provides the
potential energy that ultimately enables a hair cell to work. The tectorial membrane is
especially important in cochlear mechanics. Remember that the stereocilia of the outer hair
cells have their tips embedded in it, and those of the inner hair cells come very close to it. The
tectorial membrane is anchored to the modiolus, which holds it relatively still as the basilar
membrane and hair cells vibrate up and down. Movement of the basilar membrane thus bends
the hair cell stereocilia back and forth. At the tip of each stereocilium of the inner hair cells is
a single transmembrane protein that functions as a mechanically gated ion channel. A fine,
stretchy protein filament called a tip link extends like a spring from the ion channel of one
stereocilium to the side of the stereocilium next to it.

The stereocilia increase in height progressively, so that all but the tallest ones have tip links
leading to talle stereocilia beside them. When a taller stereocilium bends away from a shorter
one, it pulls on the tip link and opens the ion channel of the shorter stereocilium. The channel
is nonselective, but since the predominant ion of the endolymph is K_, the primary effect of
this gating is to allow a quick burst of K_ to flow into each hair cell. This depolarizes the hair
cell while the channel is open, and when the stereocilium bends the other way its channel
closes and the cell becomes briefly hyperpolarized. During the moments of depolarization, a
hair cell releases a neurotransmitter that stimulates the sensory dendrites synapsing with its
base. Each depolarization thus generates action potentials in the cochlear nerve.

Sensory Coding

Our ability to distinguish loudness and pitch depends on the ability of the cochlea to respond
differently to vibrations of different amplitude and frequency. Loud sounds produce more
vigorous vibrations of the organ of Corti. This excites a greater number of hair cells over a
broader area of basilar membrane and triggers a higher frequency of action potentials in the
cochlear nerve fibers. If the brain detects intense activity in nerve fibers from a broad region
of the organ of Corti, it interprets this as a loud sound. Frequency discrimination requires a
more sophisticated mechanism. The basilar membrane is spanned by short, stiff collagen
fibers of various lengths. At its proximal (basal) end, the basilar membrane is attached,
narrow, and stiff. At its distal (apical) end, it is unattached, five times wider than at the base,
and more flexible.

Think of the basilar membrane as analogous to a rope stretched tightly between two posts. If
you pluck the rope at one end, a wave of vibration travels down its length and back. This
produces a standing wave, with some regions of the rope vertically displaced more than
others. Similarly, a sound causes a standing wave in the basilar membrane. The peak
amplitude of this wave is near the distal end in the case of low-frequency sounds and nearer
the proximal (attached) end with sounds of higher frequencies. When the brain receives
signals mainly from inner hair cells at the distal end, it interprets the sound as low-pitched;
when signals come mainly from the proximal end, it interprets the sound as high-pitched.
Speech, music, and other everyday sounds, of course, are not pure tonesthey create
complex patterns of vibration in the basilar membrane that must be decoded by the brain.

Cochlear Tuning

Just as we tune a radio to receive a certain frequency, we also tune our cochlea to receive
some frequencies better than others. The outer hair cells (OHCs) are supplied with a few
sensory fibers (5%10% of those in the cochlear nerve), but more importantly, they receive
motor fibers from the brain. In response to sound, the OHCs trigger nerve signals to the
medulla by way of the sensory neurons, and the pons sends signals immediately to the OHCs
by way of the motor neurons. In response, the hair cells contract by about 10% to 15%.
Because an OHC is anchored to the basilar membrane below and its stereocilia are embedded
in the tectorial membrane above, contraction of an OHC reduces the basilar membranes
freedom to vibrate.

This results in some regions of the organ of Corti sending fewer signals to the brain than
neighboring regions, so the brain can better distinguish between the more active and less
active hair cells and sound frequencies. When OHCs are experimentally incapacitated, the
inner hair cells (IHCs) respond much less precisely to differences in pitch. There is another
mechanism of cochlear tuning involving the inner hair cells. The pons sends efferent fibers to
the cochlea that synapse with the sensory nerve fibers near the base of the IHCs. The efferent
fibers can inhibit the sensory fibers from firing in some areas of the cochlea, and thus
enhance the contrast between signals from the more responsive and less responsive regions.

Combined with the previously described role of the OHCs, this sharpens the tuning of the
cochlea and our ability to discriminate sounds of different pitch.

The Auditory Projection Pathway

A spiral ganglion, wound around the modiolus, is composed of bipolar sensory neurons.
Their dendrites originate at the hair cells and their axons form the cochlear nerve. The
cochlear nerve joins the vestibular nerve, discussed later, and the two together become the
vestibulocochlear nerve (cranial nerve VIII).

The cochlear nerve fibers from each ear lead to cochlear nuclei on both sides of the pons.
There, they synapse with second-order neurons that ascend to the nearby superior olivary
nucleus of the pons. By way of cranial nerve VIII, the superior olivary nucleus. issues the
efferent fibers back to the cochlea that are involved in cochlear tuning. By way of cranial
nerves V3 and VII, it issues motor fibers to the tensor tympani and stapedius muscles,
respectively. The superior olivary nucleus also functions in binaural31 hearingcomparing
signals from the right and left ears to identify the direction from which a sound is coming.
Other fibers from the cochlear nuclei ascend to the inferior colliculi of the midbrain. The
inferior colliculi help to locate the origin of a sound in space, process fluctuations in pitch
that are important for such purposes as understanding another persons speech, and mediate
the startle response and rapid head turning that occur in reaction to loud or sudden noises.

Third-order neurons begin in the inferior colliculi and lead to the thalamus. Fourth-order
neurons begin here and complete the pathway to the primary auditory cortex, which is in the
superior margin of the temporal lobe deep within the lateral sulcus. The temporal lobe is the
site of conscious perception of sound, and it completes the information processing essential to
binaural hearing. Because of extensive decussation in the auditory pathway, damage to the
right or left auditory cortex does not cause a unilateral loss of hearing.


1. External Ear

The auricle (pinna) consists of an irregularly shaped plate of elastic cartilage covered by
tightly adherent skin on all sides. The external auditory meatus is a somewhat flattened
canal extending from the surface into the temporal bone. Its internal limit is the tympanic
membrane. A stratified squamous epithelium continuous with the skin lines the canal. Hair
follicles, sebaceous glands, and the ceruminous glands (a type of modified sweat gland) are
found in the submucosa. Ceruminous glands are coiled tubular glands that produce the
cerumen or earwax a brownish, semisolid mixture of fats and waxes. Hairs and cerumen
probably have a protective function. The wall of the external auditory meatus is supported by

elastic cartilage in its outer third, whereas the temporal bone provides support for the inner
part of the canal.

Across the deep end of the external auditory meatus lies an oval membrane, the tympanic
membrane (eardrum). Its external surface is covered with a thin layer of epidermis, and its
inner surface is covered with simple cuboidal epithelium continuous with the lining of the
tympanic cavity (see below). Between the two epithelial coverings is a tough connective
tissue layer composed of collagen and elastic fibers and fibroblasts. The tympanic membrane
is the structure that transmits sound waves to the ossicles of the middle ear

2. Middle Ear

The middle ear, or tympanic cavity, is an irregular space that lies in the interior of the
temporal bone between the tympanic membrane and the bony surface of the internal ear. It
communicates anteriorly with the pharynx via the auditory tube (eustachian tube) and
posteriorly with the air-filled cavities of the mastoid process of the temporal bone. The
middle ear is lined with simple squamous epithelium resting on a thin lamina propria that is
strongly adherent to the subjacent periosteum. Near the auditory tube and in its interior, the
simple epithelium that lines the middle ear is gradually transformed into ciliated
pseudostratified columnar epithelium.

Although the walls of the tube are usually collapsed, the tube opens during the process of
swallowing, balancing the pressure of the air in the middle ear with atmospheric pressure. In
the medial bony wall of the middle ear are two membrane-covered oblong regions devoid of
bone; these are the oval and round windows.

The tympanic membrane is connected to the oval window by a series of three small bones,
the auditory ossicles the malleus, incus, and stapes that transmit the mechanical vibrations
generated in the tympanic membrane to the internal ear. The malleus inserts itself into the
tympanic membrane and the stapes into the membrane of the oval window. These bones are
articulated by synovial joints and, like all structures of this cavity, are covered with simple
squamous epithelium. In the middle ear are two small muscles that insert themselves into the
malleus and stapes. They have a function in regulating sound conduction.

3. Internal Ear

The internal ear is composed of two labyrinths. The bony labyrinth consists of a series of
spaces within the petrous portion of the temporal bone that houses the membranous

labyrinth. The membranous labyrinth is a continuous epithelium-lined series of cavities of
ectodermal origin. It derives from the auditory vesicle that is developed from the ectoderm of
the lateral part of the embryo's head. During embryonic development, this vesicle invaginates
into the subjacent connective tissue, loses contact with the cephalic ectoderm, and moves
deeply into the rudiments of the future temporal bone. During this process, it undergoes a
complex series of changes in form, giving rise to two specialized regions of the membranous
labyrinth: the utricle and the saccule. The semicircular ducts originate from the utricle,
whereas the elaborate cochlear duct is formed from the saccule. In each of these areas, the
epithelial lining becomes specialized to form sensory structures such as the maculae of the
utricle and saccule, the cristae of the semicircular ducts, and the organ of Corti of the
cochlear duct.

The bony labyrinth consists of spaces in the temporal bone. There is an irregular central
cavity, the vestibule, housing the saccule and the utricle. Behind this, three semicircular
canals enclose the semicircular ducts; the anterolateral cochlea contains the cochlear duct.

The cochlea, about 35 mm in total length, makes two-and-one-half turns around a bony core
known as the modiolus. The modiolus has spaces containing blood vessels and the cell
bodies and processes of the acoustic branch of the eighth cranial nerve (spiral ganglion).
Extending laterally from the modiolus is a thin bony ridge, the osseous spiral lamina. This
structure extends across the cochlea farther in the basal region than it does at the apex

The bony labyrinth is filled with perilymph, which is similar in ionic composition to
extracellular fluids elsewhere but has a very low protein content. The membranous labyrinth
contains endolymph, which is characterized by its low sodium and high potassium content.
The protein concentration in endolymph is low.

Cochlear Duct

The cochlear duct, a diverticulum of the saccule, is highly specialized as a sound receptor. It
is about 35 mm long and is surrounded by specialized perilymphatic spaces. When observed
in histological sections, the cochlea (in the bony labyrinth) appears to be divided into three
spaces: the scala vestibuli (above), the scala media (cochlear duct) in the middle, and the
scala tympani The cochlear duct, which contains endolymph, ends at the apex of the cochlea.
The other two scalae contain perilymph and are, in reality, one long tube, beginning at the
oval window and terminating at the round window. They communicate at the apex of the
cochlea via an opening known as the helicotrema.

The cochlear duct has the following histological structure. The vestibular (Reissner's)
membrane consists of two layers of squamous epithelium, one derived from the scala media
and the other from the lining of the scala vestibuli. Cells of both layers are joined by means
of extensive tight junctions that help preserve the very high ionic gradients across this
membrane. The stria vascularis is an unusual vascularized epithelium located in the lateral
wall of the cochlear duct. It consists of cells that have many deep infoldings of their basal
plasma membranes, where numerous mitochondria are located. These characteristics indicate
that they are ion- and water-transporting cells, and it is generally believed that they are
responsible for the characteristic ionic composition of endolymph.

The structure of the internal ear that contains special auditory receptors is called the organ of
Corti; it contains hair cells that respond to different sound frequencies. It rests on a thick
layer of ground substancethe basilar membrane. Supporting cells and two types of hair
cells can be distinguished. Three to five rows of outer hair cells can be seen, depending on
the distance from the base of the organ, and there is a single row of inner hair cells. The
most characteristic feature of these cells is the W-shaped (outer hair cells) or linear (inner hair
cells) array of stereocilia. A basal body is found in the cytoplasm adjacent to the tallest
stereocilia. In contrast to vestibular receptors, no kinocilium is present. This absence of a
kinocilium imparts symmetry to the hair cell that is important in sensory transduction.


Otitis externa (OE) is an inflammation or infection of the external auditory canal
(EAC), the auricle, or both. Otitis externa, also called swimmers ear, involves diffuse
inflammation of the external ear canal that may extend distally to the pinna and proximally to
the tympanic membrane. The acute form has an annual incidence of approximately 1 percent
and a lifetime prevalence of 10 percent. On rare occasions, the infection invades the
surrounding soft tissue and bone; this is known as malignant (necrotizing) otitis externa, and
is a medical emergency that occurs primarily in older patients with diabetes mellitus. Otitis
externa lasting three months or longer, known as chronic otitis externa. This condition can be
found in all age groups.


Acute localized OE (furunculosis) - Associated with infection of a hair follicle. It
affect the outer third ear canal, there were abundant hair follicle, sebaceous and
cerumen glands. In term, infection take place at the pilosebaceous gland which turn to
Acute diffuse OE - Most common form of OE, typically seen in swimmers. Affecting
the inner 2/3 of outer ear canal.
Chronic OE - Same as acute diffuse OE but is of longer duration (>6 weeks). Chronic
otitis externa is often caused by allergies or underlying inflammatory dermatologic
Eczematous (eczematoid) OE - Encompasses various dermatologic conditions (eg,
atopic dermatitis, psoriasis, systemic lupus erythematosus, and eczema) that may
infect the EAC and cause OE
Necrotizing (malignant) OE - Infection that extends into the deeper tissues adjacent to
the EAC; occurs primarily in immunocompromised adults (eg, diabetics, patients with
Otomycosis - Infection of the ear canal from a fungal species (eg, Candida,

The external auditory canal is warm and humid, and exfoliated skin provides an ideal
growth medium for bacterial and fungi. The canal skin is unique in that it is continually
migrating laterally, carrying debris with it. Cerumen is protective as it is acidic (pH 6.1-6.4)
and hydrophobic, produced by pilosebaceous glands. In addition, it contains lysozymes that
inhibit bacterial growth. Too little or too much cerumen predisposes to otitis externa. Hair
helps prevent entry of foreign bodies. However, too much prevents migration and can
predispose to cerumen impaction.
The process of OE can be divided into four categories :
1. Obstruction (eg, cerumen buildup, surfers exostosis, or a narrow or tortuous canal),
resulting in water retention
2. Absence of cerumen, which may occur as a result of repeated water exposure or
overcleaning the ear canal
3. Trauma
4. Alteration of the pH of the ear canal
If moisture is trapped in the EAC, it may cause maceration of the skin and provide a good
breeding ground for bacteria. This may occur after swimming (especially in contaminated
water) or bathinghence the common lay term swimmers ear. It may also occur in hot
humid weather. Obstruction of the EAC by excessive cerumen, debris, surfers exostosis, or a

narrow and tortuous canal may also lead to infection by means of moisture retention.Trauma
to the EAC allows invasion of bacteria into the damaged skin. This often occurs after
attempts at cleaning the ear with a cotton swab, paper clip, or any other utensil that can fit
into the ear.
Cerumen creates a slightly acidic pH that inhibits infection (especially by P aeruginosa)
but can be altered by water exposure, aggressive cleaning soapy deposits, or alkaline
eardrops. The alteration of pH from normal or acidic pH into alkaline cause decreasing in
protective function and facilitate the infection to occur. Necrotizing (malignant) OE is a rare
complication that occurs in patients who are immunocompromised or in those who have
received radiotherapy to the skull base. In this condition, bacteria invade the deeper
underlying structures of the soft tissues and cause osteomyelitis of the temporal bone. This is
a life-threatening disorder with an overall mortality that historically has approached 50%.
Once infection is established, an inflammatory response occurs with skin edema. Exudate and
pus often appear in the EAC as well. If severe, the infection may spread and cause a cellulitis
of the face or neck.
OE is most often caused by a bacterial pathogen;(91%), the most common causative
bacteria are Pseudomonas (38%), staphylococcus species and anaerobes and gram negative
organisms. Fungal OE (otomycosis), in one study, Fungal OE may result from overtreatment
with topical antibiotics or may arise de novo from moisture trapped in the EAC. It is caused
by Aspergillus 80-90% of the time; Candida and other organisms have also been isolated.
Eczematoid (psoriatic) OE is associated with the following conditions, eczema, seborrhea,
neurodermatitis, contact dermatitis from earrings or hearing aid use and sensitivity to topical
Elements of the diagnosis of diffuse acute otitis externa, 1) Rapid onset (generally
within 48 hours) in the past three weeks, AND 2) Symptoms of ear canal inflammation,
including, otalgia (often severe), itching or fullness, WITH or WITHOUT hearing loss or jaw
pain (pain in the ear canal and temporomandibular joint region intensified by jaw motion),
AND 3) Signs of ear canal inflammation, including, tenderness of the tragus, pinna, or both,
OR diffuse ear canal edema, erythema, or both WITH or WITHOUT ottorhea, regional
lymphadenitis, tympanic membrane erythema, or cellulitis of the pinna and adjacent skin.
Topical therapy for canal disease was described more than 3,000 years ago;
astringents and alcohols were common. Two percent acetic acid (Vosol), sometimes diluted in
half by 90% to 95% alcohol, is effective for prophylaxis against acute OE and, with or

without the addition of a steroid, for the treatment of mild disease. The caveat is that these
solutions can cause stinging and irritation if applied to highly inflamed skin4.
More advanced disease warrants the use of an ototopical that includes an
antimicrobial agent. Regardless of the ototopical selected, penetration to the epithelium is
mandatory; any obstruction should be cleared. Warming the ototopical to body temperature
(e.g., by placing it in a shirt pocket or a warm room) before application helps the patient
avoid the dizziness from caloric stimulation that cold liquid can incite. Instructing the patient
to lie on his or her side with the affected ear up for a few minutes after the administration of
ear drops aids migration to the medial canal. Having the patient or someone else pump the
tragus a few times improves this process. There is wide variability in the self-administered
dosing of ear drops, and relying on another person to place the drops or to perform the pump
maneuver better standardizes the process4.
A cotton ball temporarily placed in the external os before the patient reassumes an
erect position will absorb excess liquid. If the canal is narrowed at least 50 percent by edema,
placement of a wick (which can be anything from gauze to a preformed cellulose sponge)
ensures ototopical access to the medial canal. When indicated, a return visit in two to three
days for removal of the wick is necessary. Ototopical therapy usually should continue for five
to 10 days depending on disease severity, or for three days after the last symptoms 4.


A. Identitiy
Name : Mr. SK
Age : 20 year-old
Sex : Male
Address : Purworejo
M. R. : 10345XX
B. Anamnesis
Main complaint : Pain of the right ear
History of present illness :

Patient came to the ENT Polyclinic, with pain on the right ear, since 3 days ago.
Together with pain, there were also itchiness, sensation of aural fullness, and decrease on
hearing of the right ear. There were no blood nor fluid coming out from the right ear. Patient
admitted to using cotton bud frequently to clean the ears. Patient denied the entrance of
water or any other foreign objects into the ear. Other complaints such as, tinnitus, dizziness,
cold, flu, sore throat or fever were also denied. There were also no complaints of the left ear.

History of past illness :

Patient never had similar complaint in the ear previously. There are no history of
asthma, allergy, hypertension, diabetes mellitus, and surgery. Patient have not consulted a
doctor nor taken any medication for the current complaint.

History of family illness

There is no history of similar complaints, asthma, allergy, hypertension, and diabetes


Anamnesis Summary
Pain in the right ear.
Itchiness of right ear.
Sensation of aural fullness of the right ear.
Decrease hearing of the right ear
C. Physical Examination
General status : Good, compos mentis
Vital sign:
BP :120/80 mmHg
Pulse : 78x/minute
RR :20x/minute
T : 36,6 oC

ENT status
Right ear Left ear
Outer ear Hyperemic(-), edema(-), no lesion, no hyperemic,
tragus pain on palpation no mass, no edema
and retraction(+)
Ear canal no discharge, no discharge, no
hyperemic(+), edema (+) hyperemic, no mass, no
Tympanic Unable to asses Intact, cone of light (+)

Nose and Paranasal Sinuses
Right Left
Inspection Within normal limit Within normal limit
Palpation no tenderness no tenderness
Anterior discharge (-), edematous conchae(-),septal deviation (-)
rhinoscopy , mass (-)
Posterior discharge (-), edematous conchae(-),septal deviation (-)
rhinoscopy , mass (-)

Mouth and Throat

Lips Within normal limit
Gum & teeth Within normal limit
Tongue Within normal limit
Palate Within normal limit
Uvula Within normal limit
Tonsil T1-T1, hyperemic (-), widenedcrypt
Posterior oropharynx Within normal limit
Indirect laryngoscopy Within normal limit

D. Diagnosis
Diffuse Acute Otitis Externa of the right ear

E. Management & Treatment

Placement of Sofra-tulle (Daryant Tulle-Framycetin Sulphate 1%) in left ear canal
for two days.

R. Tab. Diclofenac Potassium mg 50 No. XVIII

S. 2 dd Tab I p.c


The patient should meet the doctor for follow-up to know the progress of the
Take care of the ear hygiene, keep the ear dry and prevent the entrance of
water or any foreign objects into the ear.
Prevent frequent cleaning and scratching with cotton buds.

E. Planning
Follow up after 2 days to remove tampon and evaluate ear condition.

F. Follow Up
On follow up, tampon was removed from patients right ear canal and the ear
canal was evaluated (pain and edema of the ear canal has improved)
Treament is then continued with Otilon (polymyxin B sulfate, neomycin
sulfate, fludrocotrisone acetate, lidocaine) ear drops (3 drops each time, 3
times per day).

G. Prognosis
Dubia ad bonam

H. Problem


III. Discussion
Based on anamnesis, patient came complaining with pain on the right ear, since 3
days ago. Together with pain, there were also itchiness, sensation of aural fullness, and
decrease on hearing of the right ear. Inspection of the right ear showed that the outer ear
canal was hyperemic with diffuse oedem . Palpation of tragus results in pain. Diagnosed as
Diffuse Acute Otitis Externa of AD because of the rapid onset in the past 3 days (less than
3 weeks) with sign and symptoms of canal inflammation in which the margin is undefined.

Acute otitis externa is diagnosed clinically based on 1) a rapid onset (generally

within 48 hours) in the past 3 weeks with 2) signs and 3) symptoms of ear canal
inflammation2 The clinical course of external otitis may be divided into the following
stages: preinflammatory; acute inflammatory, which can be mild, moderate, or severe; and
chronic inflammatory8
The main findings of our patient through history taking were itchiness, sensation of
aural fullness, and decrease on hearing of the right ear; in physical examination, there was
tenderness and pain of the tragus on palpation and when retracted; while in otoscopic
examination, we found that the ear canal of the right ear was hyperemic and edema.
Tympanic membrane of the right ear was unable to asses. Our patient was diagnosed with
diffuse acute otitis externa of the right ear.
The four fundamental principles in the treatment of otitis externa in all stages are 1)
frequent and thorough cleaning, 2) judicious use of appropriate antibiotics, 3) treatment of
associated inflammation and pain, and 4) recommendations regarding the prevention of
future infections. In any stage of infection, thorough cleaning is a priority. Meticulous
debridement of exfoliated debris, purulence, and cerumen will do as much if not more than
simply placing the patient on ear drops8
In the preinflammatory stage, a complete cleaning may be all that is required. In the
absence of purulence, a brief course of an acidifying drop such as aluminium sulfate-
calcium sulfate (Domeboro) is efficacious in discouraging bacterial or fungal growth8
Treatment of the acute inflammatory stage varies with the extent of disease. In the
mildest form, cleaning as above is indicated. An antibiotic otic drop is recommended to
cover what is probably a Pseudomonas infection. At this stage, edema of the EAC should
not be severe, and the patient should be able to instill drops into the ear by tilting the head to
the side or by lying down with the involved ear upright8
In the moderate stage of inflammation, edema of the canal may interfere with the
instillation of drops. When there is marked canal edema, a wick of compressed cellulose or

ribbon gauze may be placed in the canal and instill drop on it to facilitate antimicrobial or
antibiotic administration. Wick placement permits antibiotic drops to reach portions of the
external auditory canal that are inaccessible because of canal swelling. Often the canal may
accommodate two or even three wick. As the wick expands, it presses the soft tissues and
periosteum toward the nondistracted position; this alone may relieve pain. As the canal
responds to treatment and patency returns to the ear canal, the wick often falls out.15
All instrumentation of the ear is best done under the microscope. The wick is
removed by the physician at the time of re-examination. If the edema has not been
significantly reduced, repacking is indicated. Antibiotic drops should be continued for at
least 2 to 3 days after the cessation of pain, itching, and drainage so that complete
eradication of infection may be ensured. Also in this stage, an oral analgesic is often
prescribed because pain can be pronounced. If the infection has not spread beyond the
boundaries of the external canal, the use of oral antibiotics will be of little if any value8
In the severe stage, infection usually extends beyond the limits of the canal. In
addition to the cleaning, packing, and use of antibiotic drops as discussed previously,
attends to any soft tissue involvement by using an oral antibiotic with broad-spectrum
coverage. Successive generations of the cephalosporins widen gram-negative coverage at
the expense of gram-positive coverage. In addition to anti-Pseudomonas ear drops, common
choices of oral antibiotics are one of the antipseudomonal fluoroquinolones such as
ciprofloxacin or levofloxacin, antistaphylococcal penicillins, or cephalosporins. The
fluoroquinolone antibiotics are effective against Pseudomonas species. In children under 12
years old, one should check with the pediatrician prior to starting oral fluoroquinolones.
Warm soaks (normal saline or a mild aluminum sulfate- calcium acetate solution) are also
useful in the treatment of the crusting and edema involving the auricle and surrounding skin.
Culture of the canal for aerobic bacteria and/ or fungi is indicated only for the severe stage
or for patients who have previously been treated without resolution. Treatment is generally
continued for 10 to 14 days if there is a good response. In rare patients who do not respond
to this regimen, hospitalization and vigorous daily local care, repeat culturing, and
intravenous antibiotics are indicated.8
The chronic stage of external otitis is manifested by marked thickening of the skin of
the EAC due to long-standing infection. Examination reveals flakes of dry scaly skin in the
canal. Although removal of debris isrecommended, this may be difficult due to the
narrowing of the lumen of the canal. Repeated cleaning and instillation of antibiotics and
steroids are indicated. Triamcinolone acetonide 0.25% cream or ointment (Kenalog),

fluocinolone 0.01% oil (DermOtic), or dexamethasone sodium phosphate 0.1% ophthalmic
drops (Decadron, Pred Forte 1%) may be used.8
In all cases of acute or chronic external otitis, instruct the patient to avoid future
infections by not instrumenting the ear. Foreign objects such as Q-tips often excoriate the
canal skin and push debris further into the canal rather than remove it. Swimmers should be
taught to towel dry the concha and lateral canal, to shake water out of the canal, or to instill
an acidifying drop after swimming, Also, patients who have repeated infections despite
adhering to these measures are best advised to use an acidifying drop composed of equal
measures of vinegar and water, or ethyl alcohol and water, when exposed to high humidity.
One should suspect otomycosis if all other reasonable measures have failed and should treat
with drying agents, especially powders. Custom-made ear molds are useful for these
patients. A final office visit is important to ensure that the infection has completely resolved
and the canal is back to its normal state.8
In our case, a medicated gauze Sofra-Tulle (Daryant Tulle-Framycetin Sulphate 1%)
was used as an ear tampon (substitution for ear wick) and placed in the right ear of our
patient for 2 days; also the patient was given oral analgesic diclofenac potassium (1 tablet
each time, 2 times per day) to reduce the pain. Later in the next visit, the tampon was
removed and the condition of the ear was evaluated (pain and edema of the ear canal has
improved). Treatment was then continued with topical ear drop Otopain (polymyxin B
sulfate, neomycin sulfate, fludrocotrisone acetate, lidocaine) 3 drops each time, 3 times per
day; Patient is advised to take care of his ear hygiene, keep the ear dry and prevent the
entrance of water or any foreign objects into the ear and avoid cleaning or scratching the ear
with cotton buds.
Topical preparations are recommended as initial therapy for diffuse, uncomplicated
AOE because of safety, efficacy over placebo in randomized trials, and excellent clinical
and bacteriologic outcomes in comparative studies. There are no data on the efficacy of
systemic therapy with the use of appropriate antibacterials and stratified by severity of the
infection. Moreover, orally administered antibiotics have significant adverse effects that
include rashes, vomiting, diarrhea, allergic reactions, altered nasopharyngeal flora, and
development of bacterial resistance.2
An advantage of topical therapy is the very high concentration of antimicrobial that
can be delivered to infected tissue, often 100 to 1000 times higher than can be achieved
with systemic therapy. For example a 0.3% solution of antibiotic (a typical concentration in
commercial otic drops) has a concentration of 3000 mcg/mL. Any organisms known to
cause AOE, even those considered resistant, will be unlikely to survive contact with this

antibiotic concentration. Because there are between 10 to 20 drops/ mL, depending on the
nature of the liquid (solution vs suspension, viscosity, etc), each dose of 3 to 5 drops
contains about 0.5 to 1.5 mg of antibiotic. Topical therapy avoids prolonged exposure of
bacteria to subtherapeutic concentrations of antibiotic, and may therefore be less likely than
systemic therapy to result in selective pressure for resistant organisms. The avoidance of
antibiotic exposure of host bacteria resident outside the ear canal, as occurs with systemic
therapy, provides a further advantage to the reduction of the selection of resistant
microorganisms. Restrictive use of oral antibiotics for AOE is important because of the
increased resistance among common AOE pathogens, especially S. Aureus and P.

IV. Conclusion

A 20 year-old male patient diagnosed with diffuse acute otitis externa of the right ear.
The patient was first treated with placement of an ear tampon Sofra-Tulle (Daryant Tulle-
Framycetin Sulphate 1%) in his right ear canal for two days with an oral analgesics
diclofenac potassium and then continued with a topical ear drop Otopain after the tampon
was removed. Patient was advised to take care of his ear hygiene, keep the ear dry and
prevent the entrance of water or any foreign objects into the ear and avoid cleaning or
scratching the ear with cotton buds.