Download THE EAR

THE EAR
Dr. Basil M.N. Saeed
Assistant professor
ENT Department
College of Medicine
Mosul University
Embryology
Auricle : a series of six tubercles which form around the margins of the
first visceral cleft about 6 weeks of gestation.
External Auditory Canal : Ectoderm of the first visceral cleft.
Tympanic Membrane
1. An outer epithelial layer; the ectoderm of the first visceral cleft.
2. A middle fibrous layer; the mesoderm between the first visceral cleft
and the tubotympanic recess.
3. An inner mucosal layer; the entoderm of the tubotympanic recess.
Eustachian Tube and Tympanic Cavity
The dorsal recess of the first and second entodermal pouches fuse
to form the tubotympanic recess.
The recess expands around the ossicles forming the Eustachian tube
and tympanic cavity.
ANATOMY
THE EXTERNAL EAR
It consists of the PINNA or AURICLE and the
EXTERNAL AUDITORY MEATUS.
THE AURICLE :
Plate of yellow elastic cartilage, except for the
lobule.
The skin of the lateral surface is closely adherent
to the perichondrium.
The auricle is attached to the side of the head by
ligaments and rudimentary auricular muscles.
Parts of the auricle include:
Helix, Antihelix, Tragus, Antitragus, Concha and
Lobule
THE EXTERNAL ACOUSTIC MEATUS
It measures about 2.5 cm.
It is composed of two parts: an outer or lateral
third, which has a cartilaginous skeleton directed
medially upwards and backwards; and an inner
two thirds which has a bony skeleton and is
directed medially, slightly downwards and
forwards.
The meatus can be partly straightened in adults by
pulling the auricle upwards, outwards and
backwards.
The external canal ends medially at the tympanic
membrane
THE EXTERNAL ACOUSTIC MEATUS
The skin of the cartilaginous canal is closely
adherent to the underlying tissues and
contains sebaceous glands, ceruminous
glands and hair follicles.
These structures are absent in the bony canal.
The blood supply: superficial temporal and
posterior auricular branches of the external
carotid artery.
Nerve supply: fifth, ninth, tenth cranial nerves,
greater auricular and lesser occipital nerves
of the cervical plexus.
THE MIDDLE EAR
It is an air filled cavity within the petrous part
of the temporal bone.
The temporal bone has four parts: tympanic,
squamous, petrous and mastoid.
It is called the tympanic cavity and lies between
the tympanic membrane TM laterally and the
cochlea (inner ear)medially.
It is a six-sided box with its vertical length
greater than its breadth.
THE MIDDLE EAR
The roof of the middle ear is formed by a thin plate
of bone called the tegmen tympani which separates
the the middle ear cavity and the mastoid antrum
from the middle cranial fossa.
The floor is formed by a thin plate of bone which
separates the middle ear cavity from the bulb of
the internal jugular vein.
The anterior wall
In its lower portion is formed by a thin plate of bone
separating the cavity from the internal carotid
artery. The upper part has two openings, the lower
one being the auditory( eustachiuan) tube and above
it lies the canal for the tensor tympani muscle.
The posterior wall
The aditus which is an opening leading from the
middle ear to the mastoid antrum, and to mastoid air
cells .
 The pyramid, which is a conical bony projection
bellow the aditus. The stapedius tendon comes out of
the pyramid and is inserted to the stapes.
 The fossa incudis lies just above the pyramid and it
receives the attachment of the short process of the
incus.
 The facial nerve bends downwards at the level of
the fossa incudis and lies close to the posterior wall(
the mastoid segment of the facial nerve).
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The lateral wall
It is formed by the tympanic membrane which
separates the external canal from the middle ear.
The membrane has an outer layer of squamous
epithelium continuous with the skin of the
meatus, a middle fibrous tissue layer and an inner
layer of mucus membrane continuous with the
lining of the middle ear cavity.
It is about 0.9 cm in diameter.
The fibrous middle layer is found in the lower 2
thirds of the tympanic membrane and is called
PARS TENSA, and deficient in the upper third
and is called PARS FLACCIDA which is bounded
by the anterior and posterior malleolar folds.
The medial wall
It is the lateral wall of the inner ear. Has the followings
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The oval window which is closed by the footplate of
the stapes.
The round window, lies below the oval window and is
closed by the secondary TM.
The promontory which represents the basal turn of
the cochlea is situated between and in front of the 2
windows.
The tympanic part of the facial nerve is enclosed in a
bony canal and lies above the oval window.
The horizontal or lateral semicircular canal is situated
postero lateral to the facial nerve canal.
The contents of the middle ear
Three ossicles, MALLEUS, INCUS and STAPES.
Two muscles: the STAPEDIUS and the TENSOR
TYMPANI.
Two nerves: the FACIAL and the CHORDA TYMPANI.
The mucosal lining of the middle ear is ciliated
columnar epithelium.
The mastoid air cells are peumatizations of the
mastoid bone , the biggest air cell being the mastoid
antrum which is always present. Other cells are
variable in existence.
THE INNER( INTERNAL) EAR
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It consists of a membranous labyrinth
enclosed in a bony labyrinth.
BOTH ARE WITHIN THE PETROUS PART
OF THE TEMPORAL BONE.
The bony labyrinth consists of the
VESTIBULE which is the central portion, the
BONY SEMICIRCULAR CANALS which
are situated posterior to the vestibule and the
BONY COCHLEA which is anterior to the
vestibule.
The semicircular canals, consist of
SUPERIOR(ANTERIOR), POSTERIOR
(VERTICAL)and HORIZONTAL(LATERAL) canals.
The membranous labyrinth
Contains fluid known as the endolymph.
 It contains the vestibular and the auditory
components.
 The vestibular element, which is connected
to the vestibular part of the 8th cranial nerve,
consists of three semicircular canals, the
utricle and the saccule.
 The auditory element consists of the cochlear
duct and is connected to the cochlear part of
the 8th cranial nerve.

PHYSIOLOGY OF HEARING
The basic function of the ear is to convert the sound
energy from mechanical vibrations in the air to
mechanical vibrations in the inner ear fluids (cochlear
duct) and then to electrical energy in the hair cells that
is transmitted to the brain via the auditory nerve.
 The auricle collects the sound waves.
 They pass through the external meatus to the TM
which is set in motion.
 The vibrations are transmitted to the ossicles, malleus ,
incus and the stapes.
 The stapes footplate is attached to the oval window,
and from it vibrations are transmitted to the inner ear
fluids.

PHYSIOLOGY OF HEARING
Two factors are important to magnify the vibrations
to overcome the resistance of the inner ear fluids.
The first is the ratio between the surface area of
the TM to that of the oval window.
 The second is the lever ratio in the ossicular chain.
 In the inner ear, fluid displacement caused by the
transmitted waves stimulates the hair cells and the
nerve terminals in the ORGAN OF CORTI.
 These nerve impulses are transmitted to the higher
centers of hearing via the cochlear( auditory) nerve.

PHYSIOLOGY OF THE VESTIBULAR
APPARATUS
The balance is maintained by the coordination of information
from three systems:
 Proprioception .
 The eyes.
 The vestibular system.
 The vestibular system consists of three semicircular canals,
the utricle and the saccule.
 The UTRICLE and the SACCULE respond to linear
acceleration.
 The SEMICIRCULAR CANALS respond to angular
acceleration.
These nerve impulses are transmitted via the
vestibular nerve to the higher vestibular centers in
the brain where are interpreted with other
information from other systems to keep balance
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SYMPTOMS OF EAR DISEASE
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Hard of hearing or deafness, conductive or sensorineural.
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Discharge, this can be caused by inflammation of the external
or the middle ear. Watery discharge after head injury is
caused by CSF leak.
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Pain, which is also called Otalgia. It can be referred.
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Itching, which is caused by diseases of the external ear.
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Tinnitus is the subjective sensation of sound in the ear.
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Vertigo is illusion of motion usually rotational motion.
PHYSICAL EXAMINATION
It is usually done with the aid of head
mirror and light source or headlight, and
ear speculum.
Otoscope(auroscope), is also used in the
examination of the ear.
Sometimes, microscope is used for ear
examination.
HEARING TESTS
These tests are done with the aid of a tuning fork
512 Hz.
 Two main tests are done, Rinne and the Weber
tests.
 Rinne test is done for each ear separately and
compares the air and bone conductions of a single
ear( the RT and LT) ears separately.
 Rinne test is called positive when air conduction is
better than bone conduction.
 Rinne test is negative when bone conduction is
better than air.

Weber test is the test of lateralization.
Central weber occurs in normal hearing or
in cases of bilateral symmetrical hearing
loss.
Weber is lateralized:
To the side of conductive hearing loss
Away from the side of sensorineural
hearing loss
INVESTIGATINS
Audiological tests:audiogram and
tympanometry.
Radiological investigations: X-ray of the
temporal bone and mastoid, CT scan of the
mastoid and temporal bones and MRI scan.
Bacteriological investigations, like swab for
culture and sensitivity.
DISEASES OF THE EXTERNAL EAR
Congenital malformations of the external ear, like
MICROTIA and ATRESIA of the external auditory
meatus.
Microtia. Absence of the pinna or gross deformity
is often associated with meatal atresia and ossicular
abnormalities.
Treatment: either surgical reconstruction or
prosthesis.
Hematoma of the auricle
It is accumulation of blood beneath the perichondrium
of the auricle.
It generally results from trauma to the auricle like in
wrestlers.
Treatment : aspiration or drainage of the blood with
full aseptic technique and application of a firm
bandage to the ear to prevent re collection of the
blood.
Surgical evacuation with quilting sutures
If it is not treated properly, infection of the cartilage
may occur or thickening of the cartilage leading to
auricular deformity
PERICHONDRITIS OF THE AURICLE
It is inflammation of the perichondrium and the
cartilage of the auricle.
 It may follow hematoma, or result from extension
of infection from a boil on the posterior meatal wall
or be a complication of a surgical procedure or
external trauma.
 The causative micro-organism is Pseudomonas
pyocyanea.
 It is manifested with severe pain in the ear with
fever, the auricle is swollen, dusky colour and loses
normal shape.

Treatment
Anti- Pseudomonas antibiotics are given with incision and
drainage of any collection of pus.
The External Auditory Meatus
Impacted wax
The accumulated secretion of the ceruminous glands
May form a solid mass causing deafness and
discomfort in the ear.
Diagnosis is simple by clinical examination with wax
having a brown or yellowish colour, but sometimes
it is black or grayish.
Treatment is either by instrumental manipulation of
the wax which must be careful and gentle, or by ear
wash.
Wax solvents like olive oil.
Keratosis obturans
It is a hard mass of wax, desquamated epithelium and
cholesterol that is found in the deep part of the bony canal.
It can be unilateral or bilateral.
The cause is unknown, and there is an association with
bronchieactasis and chronic bronchitis in young patients.
The clinical picture in manifested with pain and deafness.
As the mass increases in size, erosion of the deep bony
canal can occur with facial nerve exposure and even paralysis
in severe cases.
Treatment is removal which is usually done under general
anesthesia. Wax solvents are given prior to removal to soften
the wax.
Foreign bodies in the ear
They can be in the form of objects that are
deliberately inserted into the ear, usually in young
children.
 These can be organic or non organic.
 Foreign bodies can be small insects that enter the
canal by accident.
 Treatment is removal mainly by ear wash for the
non organic objects.
 Instrumental manipulation of the foreign bodies is
also done for their removal, and general anesthesia
is needed in young uncooperative children.
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Otitis Externa
It is inflammation of the skin of the external ear , it
can be a localized form or more generalized
inflammation.
 A boil or furuncle is a localized form of infection
and inflammation of a hair follicle of the external
cartilaginous part of the meatus.
 It is caused by staphylococcus aureus and clinically
is characterized by severe pain and tenderness in
the external canal and auricle.
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Treatment:
Symptomatic relief of pain by using analgesics and
local heat, together with anti-staphylococcal
antibiotics like cloxacillin. Topical application of local
antibiotic ointment or cream will help to hasten
resolution. Incision of the boil is done when it is
clearly pointing to the skin surface.
Diffuse otitis externa
This condition occurs in acute or chronic forms.
 The acute form of otitis externa presents as feeling
of heat, pain which is often severe and is increased
by jaw movements. Thin serous discharge is
accompanied by easing of the pain. The discharge
later becomes thicker and purulent. Conductive
deafness is usually present due to accumulation of
the discharge.
 The chronic form is manifested by discharge and
constant irritation or inching.

Treatment
Thorough and gentle cleansing of the external
meatus, keeping the ear dry.
 Local preparations containing broad-spectrum
antibiotics and corticosteroids are prescribed like
gentamycin and dexamethasone.
 Ear wicks, packing the ear with ear gauze soaked
with antibiotic-steroid cream.
 As the condition improves, the antiseptic-steroid
cream may be applied twice daily to the external
meatus, especially for the chronic cases.
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Otomycosis
It is mycotic ( fungal )infection of the external canal.
 Predisposing factors include excessive humidity like
in tropical and subtropical climates and the use of
antibiotic drops in the ear.
 Two types of fungi are responsible for otomycosis,
candida albicans and aspergillus niger.
 Clinically the situation is characterized by irritation
and itching in the ear and failure to respond to the
usual management of otitis externa.
 On examination, a mass of fungal debris is usually
seen in the ear canal .

Treatment
thorough cleansing of the meatus and dry mopping.
Application of local antifungal preparations like
clotrimazole lotion. Regular cleansing may be
needed every few days till the subsidence of the
condition.
Eczematous otitis externa.
It is characterized by intense itching causing considerable
distress.
 Secondary infection due to scratching of the ear usually
produces a diffuse reaction.
 Treatment is by treating the secondary bacterial infection
and application of local steroids to the ear.

Otitis externa hemorrhagica
It is infection of the deep external canal and the
tympanic membrane, caused by streptococcus
combined with a virus . it is characterized with
intense pain and tinnitus.
On examination, blood blisters may be seen in the
deep meatal wall and the tympanic membrane
which are prone to spontaneous rupture.
Treatment:
A course of antibiotics, like penicillin is given together
with analgesia for pain.
Malignant Otitis Externa
It is uncommon disease mainly seen in elderly diabetics.
 It is characterized by increasing severe pain in the ear
with purulent discharge.
 The responsible organism is pseudomonas pyocyanea.
 It is characterized by granulation tissue in the floor of
the meatus at the junction of the cartilaginous and the
bony parts.
 Infection can spread to the parotid gland and the
structures at the base of the skull causing wide spread
osteomylitis, intracranial complications and even death.
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Treatment
Antipseudomonal antibiotics like ticarcilin
which are given at full doses.
 Granulation tissues and necrotic tissues
are removed regularly.
 Treatment of the associated medical
problem ( control of diabetes).

Acute Suppurative Otitis Media
It is an acute infection and inflammation of the
middle ear cleft.
 usually starts as a viral infection of the middle ear
resulting from URTI, followed by secondary
bacterial infection.
 The causative microorganism are:
 Streptococcus pneumonia.
 Haemophilus influenzae .
 Moraxella catarrhalis.
 Others, like staphyloccus aureus and streptococcus
pyogenes.
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Predisposing factors
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1-Young age, acute OM is disease of young children
because the Eustachian tube is shorter, wider and
more horizontal. Higher incidence of URTI.
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2- Diseases of the nose and nasopharynx, like upper
respiratory tract infection(URTI), allergic rhinitis
and adenoid hypertrophy.
Pathology and pathogenesis
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Eustachian tube obstruction as a result of edema from
the URTI.
Decreased ventilation of the middle ear occurs with
consequent effusion in the ear .
This effusion becomes secondarily infected with
bacteria.
Tympanic membrane will bulge with increased
intratympanic pressure and may finally rupture causing
ear discharge.
Resolution of the inflammatory reaction will end in
healing of the ear.
In severe infections,There is destruction of the
bony trabeculae of the mastoid air cells with
consequent mastoiditis and abscess formation.
Clinical picture
The first symptom is a dull ache inside the ear which
may become more severe.
 Marked hearing loss, fever usually occurs in young
children.
 In infant : irritability, excessive crying and ear tugging.
 Examination: TM very red and in severe cases there will
be marked bulging of the membrane with loss of the
surface markings.
 If there is a perforation in the TM, there will be a
copious mucopurulent discharge.
 Once the TM ruptures the pain will decrease to a
dull ache.
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Management
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Treatment of the existing URTI.
Analgesia for pain.
If discharge is present, swab is taken for culture and
sensitivity.
Empirical treatment with broad spectrum antibiotics.
Amoxicillin, amoxicillin with clavulinic acid(augmentin),
second generation cephalosporin.
If the patient is allergic to penicillin, macrolides and
sulpha drugs like co-trimoxazole can be given.
When the response to treatment is unsatisfactory, it
may be that the antibiotic has to be changed according
to the result of culture if present.
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Sometimes aspiration of middle ear discharge through
myringotomy is needed.
If discharge and pain persist, despite the patient having
been given the appropriate doses of the correct
antibiotics, a mastoid reservoir of infection may be
present and needs appropriate investigations.
The role of surgery in the management of acute
suppurative otitis media is limited to:
Myringotomy, which is perforation of the tympanic
membrane to aspirate pus to relieve the pain and to
get a sample for C&S. It is also the first treatment of
acute mastoiditis.
Cortical mastoidectomy for acute mastoiditis if the
medical management and myringotomy fail. It is also
needed for mastoid reservoir
Otitis media with effusion( chronic middle ear
effusion)
Serous or secretory otitis media.
Non purulent middle ear fluid, sometimes has a sticky,
thick character resembling the glue, Glue ears.
 The basic cause is long standing or chronic Eustachian
tube dysfunction or obstruction.
 Causes of tube obstruction are :
 Mass lesion in the nasopharynx, which is mainly
adenoid tissue in children.
 Edematous swelling of the mucus membrane of the
nasopharynx, Allergic rhinitis or Chronic sinusitis.
 Nasopharyngeal tumour, suspected in unilateral serous
otitis media in adults and elderly.
Eustachian tube dysfunction which usually occurs
in cases of cleft palate.
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Clinical features
Hard of hearing and deafness mainly in children.
 In adults, there is blocked feeling in the ear.
 Discomfort, occasional tinnitus or mild vertigo can
be features of the disease.
 Symptoms of the causative etiology, like snoring due
to adenoids in children and features of rhinosinusitis
in adults and children.
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On examination
Retraction of the TM, with altered landmarks.
 There is alteration of the normal color of the TM.
 Fluid level and even air bubbles may be seen behind
the TM.
 Examination of the nose and sinuses may reveal
chronic sinusitis or rhinitis.
 In adults , the nasopharynx should be examined to
rule out the presence of nasopharyngeal carcinoma.

Investigations
Audiogram which usually shows conductive hearing loss.
 Tympanometry shows flat curve(typeB).
 X-Ray of the postnasal space which may show enlarged
adenoids in young children.
 Radiography of the sinuses is indicated when sinus disease
is suspected.
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Treatment
Medical treatment is indicated first with antibiotics
and management of the underlying cause like
chronic rhinosinsitis.
 Surgery is indicated if the condition persists despite
the conservative measures.
 Surgical treatment includes myringotomy and
aspiration of the middle ear fluid, usually combined
with insertion of ventilation tubes(grommets).
 Surgery may also be needed for the causative
etiology like adenoidectomy and nasal and sinus
surgery.
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Chronic suppurative otitis media
It is a chronic infection and inflammation of the
middle ear and may be the mastoid air cells.
 It can be classified into 2 types:
 Tubotympanic otitis media( chronic otitis
media without cholesteatoma)or(safe ear).
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Tympanomastoid otitis media( chronic otitis
media with cholesteatoma)or ( the unsafe ear)
•
Tubotympanic otitis media
It is also called otitis media without cholesteatoma.
Tends to follow a benign course and considered to
be safe.
It is a complication of acute otitis media where
there is persistent perforation in the TM and
persisting or recurring infection of the middle ear
resulting from spread of infection via the Eustachian
tube or through the perforation itself.
It rarely gives rise to any serious complications.
The main pathological condition in this type is a
perforation of the TM.
 A patient with such a perforation is liable to
persistent or recurrent discharge secondary to
URTI, or from bacteria entering the middle ear
through the perforation from the external canal.
 The perforation is always a central one, that is, it is
surrounded by part of the pars tensa throughout its
circumference.
 The perforation may be anterior, posterior, or
subtotal, but always surrounded by TM remnant.
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Clinical features
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Mucopurulent discharge which may be intermittent or
persistent .
Deafness which may vary in severity depending on the site
and size of the perforation and the status of the ossicular
chain.
O/E: Suction and dry mopping. A swab from the discharge can
be submitted for culture and sensitivity test.
The perforation and the middle ear mucosa can be assessed.
Nose and paranasal sinuses and the pharynx: adenoids or
chronic rhinosinusitis.
Complications are rare and are not serious.
Otitis externa: secondary to chronic ear discharge.
Ossicular fixation / discontinuity.
Treatment
Local measures which include dry mopping and
local antibiotic drops instilled into the ear.
 Instructions are given to the patient to avoid getting
water into the ear when washing or swimming, and
to avoid nose blowing when he or she gets a cold
to avoid movement of the infected material up the
Eustachian tube to the middle ear cavity.
 Treatment of the focus of infection, which includes
elimination of the URTI by medical treatment.
 Surgery has a role when the focus needs surgical
treatment like adenoidectomy or sinonasal surgery.
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The surgical management of TM perforation is
tympanoplasty.
The simplest form is myrigoplasty which is
repair of the perforation of the TM using fascial or
cartilage graft.
 The operation may be more complex with
ossicular reconstruction in addition to TM
repair.
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 Cortical
mastoidectomy may be indicated
when there is reservoir of infection in the mastoid
air cells.
Tympanomastoid otitis media
The bone of the attic, antrum and the mastoid
process is involved a well as the mucosa of the
middle ear, atticoantral disease.
 The main pathology of this disease is the presence
of cholesteatoma, so it is also called chronic otitis
media with cholesteatoma.
 As erosion of bone may extend to adjacent vital
structures, there is always a danger of serious
complications (unsafe ear).
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Pathology and pathogenesis
The most pathological finding is cholesteatoma.
 It consists of a sac of keratinizing squamous
epithelium surrounded by granulation tissues.
 The surface layers of the epithelium( which is
inside) keep producing keratin causing gradual
expansion of the sac.
 The granulation tissues on the outside of the sac
produce lysozymes and this gradually erodes the
ossicles, the ear drum and the mastoid bone.

The most accepted theory of the origin
of cholesteatoma is the retraction pocket
theory.
When the Eustachian tube is blocked, the
TM tends to retract in the thin pars flaccid
in to the attic region.
With gradual increase in the size of the sac,
it passes to the mastoid antrum and the
mastoid bone.
Clinical features
Ear discharge: recurrent or persistent, the discharge is
purulent and may be scanty, and it is frequently foul
smelling.
 Hard of hearing, may vary in severity.
 Bleeding from the ear may occur when there is
granulation or polyps.
On examination
 The perforation is usually marginal, in the attic or
posterosuperior segment of the TM. It extends to the
bony margin of the drum.
 Polyps or granulation tissues may be seen .
Cholesteatoma may be seen as a grayish( typically 
pearly white)substance, projecting from or filling
an attic or a marginal perforation.
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Investigations

Hearing tests : tuning fork and Audiogram.
Radiography :
 X-Ray of the temporal bone and mastoid.
 Now CT scan of the temporal bone is widely use to
investigate mastoid disease as it shows the details of
the disease and detailed anatomy of the temporal
bone.

Soft tissue opacity
Scutum erosion
Ossicles eroded
Tegmen intact
Erosion into HSCC
Cholesteatoma with fistula
Treatment
Local measures which involve cleaning the ear of
discharge and the assessment of the status of the
TM. This is usually done with the aid of the
microscope and involves removal of polyps and
granulations. This procedure is called SUCTION
CLEARANCE.
 Local antibiotic drops, according to the results of
swab culture.
 Most cases of cholesteatoma requires surgery. The
operation needed is usually modified radical

mastoidectomy .
Skin flap
Periosteal flap
Complication of otitis media
These complications can follow either acute or
chronic otitis media.
 With the advent of antibiotic therapy, these
complications are now rare with the acute otitis
media.
 Nowadays these complication are mostly associated
with chronic otitis media with cholesteatoma (
unsafe ear).
 These complications can be classified into
extracranial and intracranial complications.

Extracranial complications
Mastoiditis: which is inflammation of the mastoid
bone with even mastoid abscess formation.
 Petrositis: which is inflammation of the petrous
temporal bone .
 Labyrinthitis : which is inflammation of the inner ear
with consequent vertigo and sensorineural
deafness.
 Facial nerve paralysis: which is due to pressure
effect of the cholesteatoma on the facial nerve,
especially when it is dehiscent.

Mastoiditis
It can be acute or chronic.
Infection involves the bony walls of the cells
of the mastoid process.
The acute form usually follows AOM and
inflammatory reaction can be severe to
cause break down of the trabeculae of air
cells resulting in mastoid abscess.
Clinical picture
Increasing or recurring pain and tenderness over
the area of the mastoid antrum, tip or posterior
border.
Fever and rising pulse rate in children.
Deafness.
Edema and displacement of the auricle forwards
and downwards.
Stenosis and Sagging of the posterosuperior canal
wall.
If abscess is present fluctuant swelling is present.
Treatment
Antibiotic treatment, C&S.
Drainage of pus.
Cortical mastoidectomy
When medical treatment fails, increasing fever and
pulse rate, sagging of the meatal wall, labyrinthine
or intracranial complicstions, onset of facial
paralysis, persistent OM, and ptrogressive
deafness.
Intracranial complications
Meningitis.
 Extradural dural abscess.
 Subdual abscess.
 Brain abscess.
 Lateral sinus thrombosis.
 Cortical thrombophlebitis.
 Otitic hydrocephalus

Otosclerosis
It is a common disease 1:200 of general
population.
It usually affects the age from 18-30.
Etiology
Sex: it affects females more than males.
There is a marked hereditary tendency.
There is association between the onset of the
disease with the onset of puberty and
pregnancy( possible hormonal effect).
Pathology
First the normal bone is absorbed and replaced by
a vascular spongy osteoid bone.
Later the new bone becomes thicker and less
vascular.
The most common site is the region of the
anterior margin of the oval window which is the
site of the ( fissula ante fenestram) which could
be the region of anastomosis of vessels between
the middle ear and the inner ear, or it could be
the site of vestigial cartilaginous remnant which
is prone to otosclerotic changes.
Symptoms and Signs
Gradually increasing deafness.
There may be tinnitus especially in rapidly
progressing disease.
Paracusis Willisii: means the patient states that he
can hear better in noisy environment.
Vertigo is a rare symptom of the disease.
The patient usually speaks in a low, well modulated
voice.
The TM is usually normal, yet in 10% of cases there
is a flamingo-pink blush may be seen behind the
TM on the promontory which is due to hyperemia
and indicates an active phase of otosclerosis
Note: Otosclerosis may coexist with other middle
ear problems like TM perforation.
Tuning fork test:
It shows negative Rinne test, and Weber is
lateralized to the affected ear.
Investigations:
Audiogram usually shows conductive hearing loss
with Cahart notch.
Tympanometry typically shows low compliance
impedance curve.
Treatment
Treatment Is usually with a hearing aid or
surgery.
The surgery is stapedectomy.
SENSORINEURAL DEAFNESS
The cause of this deafness is in the cochlea or in the
auditory nerve.
Sensory deafness refers to cochlear origin
Neural or retrocochlear deafness refers to nerve origin.
The disability of the sensorineural deafness is greater
than that of conductive deafness.
A patient with a sensorineural deafness hears with more
difficulty in the presence of background noise.
Tinnitus is present in many patients.
Recruitment means intolerance of loud sounds and
generally is associated with cochlear lesion.
Lesion in either site will reduce the discrimination for
speech, but it is more marked in neural lesions.
Causes of sensorineual deafness
Infection
Viral deafness:
Mumps sudden sensorineural deafness which is usually
unilateral. The hearing loss is usually severe to profound and
is usually permanent.
Measles, is a less common cause than mumps, and can cause
bilateral high frequency hearing loss and is usually severe and
permanent.
Herpes zoster oticus( Ramsay Hunt syndrome): is a reactivation
of herpes zoster virus in the geniculate ganglion. It is
manifested by a lower motor neuron facial palsy, herpetic
vesicles on the external canal and the inside of the cheek,
vertigo, and severe sensorineural hearing loss.
Bacterial infections
Suppurative labyrinthitis, it is usually a complication of
chronic otitis media with cholesteatoma.
It can be serous( non purulent) labyrinthitis which can be
treated by prompt antibiotic therapy together with surgery(
mastoid surgery).
In purulent labyrinthitis there is suppuration within the
labyrinth, and is associated with irreversible severe to
profound hearing loss and vertigo.
The treatment consists of proper antibiotic therapy and
surgery to eradicate the source of infection and to prevent its
spread.
Syphilis
Can cause deafness both in its congenital and acquired forms.
The hearing loss is bilateral and progressive, and diagnosis is
aided by serological tests.
Treatment is both antibiotic treatment, and steroids.
Presbyacusis
It is hearing loss resulting from degenerative changes of
aging that affects the cochlea, the auditory nerve or
both.
The hearing loss is symmetrical in both ears and
progression is usually slow.
The onset can start after the third decade.
Characteristically old people complain of difficulty in
understating speech because of the inability to hear
high frequencies ((consonant sounds)).
They have difficulty in hearing in the presence of
background noise.
Recruitment of hearing also adds to the distortion.
Treatment is by hearing aids.
Noise induced hearing loss
Exposure to loud noise can lead to SNHL.
It usually starts as temporary loss of hearing in the
region 4-6 kHz, which is often accompanied by
tinnitus.
This is known as temporary threshold shift, and is
usually reversible. If the exposure is repeated and
prolonged, a permanent threshold shift may occur.
The loss usually starts in the region of 4-6 kHz and
typically produce the acoustic dip or notch in the
audiogram.
Later on the damage progress and the lower as well
as the higher frequencies are affected.
The hearing loss is roughly symmetrical in both ears,
except in certain circumstances in which one ear is
receiving the injurious noise more than the other as
in shooting.
In occupational cases, the workers should be
instructed to have ear protection like the use of
earmuffs, together with routine audiometry.
In blast injury, there is usually perforation of the TM with
consequent conductive HL.
frequently inner ear injury with consequent SNHL which
may be severe and permanent and is mostly marked in
the higher frequencies.
Surgical trauma
Injury to the inner ear resulting in SNHL is a risk in
every ear surgery.
Ototoxicity
Drugs can cause sensrineural hearing loss
Aminoglycosides and Chemotherapeutic agents.
Loop diuretics (ethacrinic acid and frusemisde).
Beta blockers and Antiepileptics.
Quinine and salicylates.
Topical ear drops containing ototoxic antibiotiocs like
neomycin, gentamycin, polymyxin and framycetin.
No convincing evidence that these topical
medications can cause sensorineural hearing loss.
Sudden idiopathic hearing loss
Sudden HL that the patient is aware of the onset.
It is associated with tinnitus.
Any pattern of hearing loss can be found on
audiometry.
Patients with greater loss at high frequency have a
poorer prognosis than those of low- frequency loss.
In most cases there is quick recovery from deafness
within hours, days or weeks.
If there is no recovery within 3 weeks it is unlikely to
occur spontaneously.
The exact etiology is unknown, presumed vascular
causes and immune process are implicated.
Causes like acoustic neuroma, viral causes,
perilymphatic fistula should be excluded.
The treatment consist of hospital admission, infusion
of low molecular weight dextran and steroid
treatment if there is no contraindications.
To have a reasonable chance of success this should
begin within one week of the original episode of
sudden hearing loss.
Intratympanic steroids.
Hearing aids
They are electroacoustic devices used to amplify sounds.
The basic component of a hearing aid are: a receiver( a
microphone), an amplifier, a sound transmitter, and a power
source.
Most current aids amplify sounds in the frequency range 2504000 Hz.
They can be of several types:
Postaural HA, also called behind the ear, which are the most
common in use.
In the ear HA, these aids sits in the concha, or canal.
Body worn aids.
Spectacle aids.
Osseointegrated HA,also called bone anchored HA, which
transmit sounds directly into the bones of the skull.
Cochlear Implants
A cochlear implant is a device used to stimulate residual neural
tissue in patients with a profound hearing loss.
Their major benefit are as aids to lip reading and in the
recognition of some environmental sounds.
It consists of 2 parts: an external part, and an implanted part.
The external part consists of a power source, microphone
sound receiver and a microprocessor which filters, analyses,
and codes the sound and then passes it to an external
transmitter.
The implanted part consists of a receiver with a stimulating
and ground electrodes.
The connection between the two is through the skin of the
scalp, more often by transcutaneous induction method.
Rehabilitation is of paramount importance for the success of
CI.
Tinnitus
It is the sensation of sound not brought about by
simultaneously externally applied mechanoacoustic or
electrical signals.
This definition excludes vascular sounds.
Almost every ear disease and cause of deafness can be
associated with tinnitus.
Tinnitus can be the major annoyance and the presenting
symptom.
In some patients it may lead to depression and
occasionally to suicide.
The first essential in the treatment is to make an
accurate diagnosis.
The diagnosis can be easy and its treatment can solve the
problem, like wax removal, treatment of otitis media or
externa, and Eustachian tube obstruction
If the cause is not obvious on examination, audiological
tests are done to find the cause.
When the tinnitus is associated with sensorineual hearing
loss, the choice treatment is between hearing aid or
tinnitus masker or a combination of the two.
Medical treatment for tinnitus is not always rewarding,
labyrinthine sedatives like betahistin hydrochloride and
cinnarizine are used in the treatment.
Even antidepressants may be used in cases of depression
due to tinnitus
Vertigo( Dizziness, giddiness)
It is illusion of movement of the patient’s body or the
patient’s environment. It can be the sensation of linear
motion as in tending to stagger to one side.
Physiology of vestibular system
Normal balance is maintained by input from the
visual, vestibular and proprioceptive system in
muscles and joints. These are integrated and
modulated in the brain stem, cerebellum and higher
cortical centres.
Central (Non-otological)
CVS, CNS.
Peripheral (vestibular, otological)
Infective: Labyrinthitis, and vestibular neuronitis.
Neoplastic: acoustic neuroma.
Metabolic: Meniere’s disease.
Toxins: vestibulotoxic drugs.
Trauma: head injury.
Miscellaneous: benign paroxysmal positional vertigo.
Vestibular neuronitis
This condition is characterized by a severe vertigo of
sudden onset without deafness or signs of neurological
involvement.
Aetiology
The condition is thought to result from a selective
inflammation of the vestibular nerve, presumably of
viral origin following a vague URTI.
Clinical picture
Preceded a week or 10 days earlier by an URTI.
Vertigo which can last several days before a gradual
recovery begins ,,Nausea and vomiting.
Absence of aural symptoms.
Examination; Spontaneous nystagmus of the
vestibular type.
Investigations
Caloric test: canal paresis on the affected side.
Treatment
Reassurance and explanation while waiting
for recovery to occur by compensation.
Antivertigo drugs: prochlorperazine
(stemetil), cinnarzine (stugeron) and
betahistine (betaserc).
Prognosis
Vestibular neuronitis has no
complications and recovery is usual in a few
weeks.
Benign Paroxysmal Positional Vertigo
Recurring paroxysmal short lived attacks of vertigo
provoked by certain critical positions of the head.
Aetiology: Idiopathic, Head injury, Viral infection,
Aging process.
Pathology The disease is thought to be due to
displacement of otoliths (calcium carbonate particles)
from the utricle and saccule to the cupula of the
posterior semicircular canal.
Clinical picture
Brief attacks of vertigo when the patient puts his head
in the critical position.
Examination
Dix-Hallpike test: The patient sits on a coach and the
head is turned 45 towards the examiner and taken
backwards into the provokating position 30 below the
horizontal. The patient is instructed to keep the eyes
open and focused on examiner’s eyes or forehead.
Treatment
Medical: Antivertigo drugs:
prochlorperazine (stemetil),
cinnarzine (stugeron) and
betahistine (betaserc).
Repositioning maneuver:
Epley maneuver
Meniere’s Disease
This disease is characterized by paroxysmal attacks of
vertigo associated with deafness and tinnitus.
French physician Prosper Meniere, 1861.
Pathology
There is dilatation of the endolymphatic
compartment of the inner ear.
The aetiology of this endolymphatic hydrops is
unclear, but it's presence infers an abnormality of
endolymph formation or absorption.
Clinical picture
Usually unilateral, other labyrinth is eventually
affected.
Vertigo: is of sudden onset and the attack lasts for a
few hours.
Hearing loss: sensorineural.
Tinnitus: referred to the affected ear, precedes or
accompanies the vertigo.
Aural fullness
Otoscopy: normal.
Investigations
Audiological (pure tone audiometry):
sensorineural hearing loss.
Vestibular (caloric test): canal paresis in the affected
ear.
Treatment
The acute attack.
Bed rest.
Antihistamine labyrinthine sedatives: prochlorperazine
(stemetil) and cinnarzine (stugeron).
Anxiolytics: I.V.diazepam.
The long term management.
Vasodilator drugs: betahistine hydrochloride
(serc) which increases the cochlear blood
flow.
Reduction of labyrinthine hydrops: fluid and
salt limitation with diuretics.
II. Surgical
Endolymphatic sac decompression or shunt.
Vestibular nerve section.