Download THE EAR

THE EAR
ANATOMY
THE EXTERNAL EAR
It consists of the PINNA or AURICLE and the EXTERNAL AUDITORY MEATUS.
THE AURICLE
:
It consists of a plate of yellow elastic cartilage, except for the lobule which is composed of
fibro fatty tissue. 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 in the adults. It is composed of two parts: an outer or lateral third,
which has a cartilaginous skeleton continuous with that of the pinna and 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 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 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 has the following structures :
1- The aditus which is an opening leading from the middle ear to the mastoid
antrum, and to mastoid air cells .
2- 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.
3- The fossa incudis lies just above the pyramid and it receives the attachment
of the short process of the incus.
4- 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).
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, while it is deficient in the upper third and is called PARS
FLACCIDA which is bounded by the anterior and posterior malleolar folds.
On examination the tympanic membrane is pearly grey in color and has a triangular
bright area called the cone of light extending from the center ( umbo) downwards
and forwards.
The tympanic membrane lies obliquely, at the inner end of the meatus and there is a
recess at the junction of the TM with the floor of the meatus.
The medial wall
It is the lateral wall of the inner ear and has the following structures:
1- The oval window which is closed by the footplate of the stapes.
2- The round window, lies below the oval window and is closed by the
secondary TM.
3- The promontory which represents the basal turn of the cochlea is situated
between and in front of the 2 windows.
4- The tympanic part of the facial nerve is enclosed in a bony canal and lies
above the oval window.
5- The horizontal or lateral semicircular canal is situated poster lateral to the
facial nerve canal.
The contents of the middle ear are:
1- Three ossicles, MALLEUS, INCUS and STAPES.
2- Two muscles: the STAPEDIUS and the TENSOR TYMPANI.
3- 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
It consists of a membranous labyrinth enclosed in a bony labyrinth. BOTH ARE
WITHIN THE PETROUS PART OF THE TEMPORAL BONE.
The bony labyrinth which surrounds the membranous 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, both bony and membranous, consist of
SUPERIOR(ANTERIOR), POSTERIOR and HORIZONTAL(LATERAL) canals.
The membranous labyrinth contains fluid known as the endolymph and it contains
the vestibular and the auditory components. The vestibular element, which is
connected to the vestibular nerve 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
nerve 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, and 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.
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 of the body is maintained by the coordination of information from three
systems:
1- Proprioception .
2- The eyes.
3- 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.
SYMPTOMS OF EAR DISEASE
1-
Hard of hearing or deafness, which can be conductive or sensorineural. Examples of
conductive deafness include: wax impaction, otitis externa, otitis media, and
otosclerosis. Examples of sensorineural hearing loss include: congenital hearing loss,
age related hearing loss and noise induced hearing loss.
2-
Discharge, this can be caused by inflammation of the external or the middle ear.
Watery discharge after head injury is caused by CSF leak.
3-
Pain, which is also called Otalgia. This can be produced by diseases of the external or
middle ear mainly inflammatory problems, or it can be referred to the ear from
other areas in the nose, pharynx, oral cavity and temporomandibular joint.
4-
Itching, which is caused by diseases of the external ear which can be due to wax,
inflammatory or allergic problems.
5-
Tinnitus is the subjective sensation of sound in the ear. It can be caused by different
problems in the ear. It also can be caused by general diseases which indirectly affect
the ear through the circulation like anemia, renal and cardiac diseases.
6-
Vertigo is illusion of motion usually rotational motion. It is symptom of ear disease
mainly of the vestibular system.
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. Positive Rinne test is present in normal ear and in mild to
moderate sensorineural hearing loss. Rinne test is negative when bone conduction is better
than air and it is present in conductive hearing loss and in severe to profound sensorineural
hearing loss and it is called false negative Rinne.
INVESTIGATINS
1- Audiological tests:audiogram and tympanometry.
2- Radiological investigations: X-ray of the temporal bone and mastoid, CT scan of the
mastoid and temporal bones and MRI scan.
3- 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. 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 situated in the outer part of the
external auditory canal may form a solid mass causing deafness and discomfort in the ear.
The skin of the external auditory meatus is migratory and does not desquamate.
Cleaning of the ear canal is therefore unnecessary—those who diligently clean their
ears, or those of their children, with cotton buds, for example, hinder the migration of
skin, predisposing to wax accumulation.
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. Usually wax solvents like olive oil or Na bicarbonate ear drops for a
few days before washing the ear.
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.
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 c anal and auricle.
Treatment:
Symptomatic relief of pain by using analgesics and local heat, together with antistaphylococcal 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 pain heat changing to 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
1- Thorough and gentle cleansing of the external meatus, keeping the ear dry.
2- Local preparations containing broad-spectrum antibiotics and corticosteroids are
prescribed like gentamycin and dexamethasone.
3- Ear wicks, packing the ear with ear gauze soaked with antibiotic-steroid cream.
4- As the condition improves, the antiseptic-steroid cream may be applied twice daily
to the external meatus, especially for the chronic cases.
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 is 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.
Treatment
1- antipseudomonal antibiotics like ticarcilin which are given at full doses.
2- Granulation tissues and necrotic tissues are removed regularly.
3- 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.
It usually starts as a viral infection of the middle ear resulting from upper respiratory
tract infection and followed by secondary bacterial infection. The causative
microorganism are:
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Streptococcus pneumonia.
Haemophilus influenzae .
Moraxella catarrhalis.
Others, like staphyloccus aureus and streptococcus pyogenes.
Predisposing factors
1-Young age, acute OM is disease of young children because the Eustachian tube is
shorter, wider and more horizontal.
2- Diseases of the nose and nasopharynx, like upper respiratory tract
infection(URTI), allergic rhinitis and adenoid hypertrophy.
Pathology and pathogenesis
It usually starts when the Eustachian tube is obstructed 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, with acute
inflammatory reaction in the middle ear cleft. Purulent secretion will follow and the
tympanic membrane will bulge with increased intratympanic pressure. The TM 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.
There is a marked hearing loss, fever usually occurs in young children.
In infant the earache is manifested with irritability, excessive crying and ear tugging.
Examination shows the eardrum to be 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 coming from
the ear. Once the TM ruptures the pain will decrease to a dull ache.
Management
1- Treatment of the existing URTI, especially nasal decongestants to hasten
drainage through the Eustachian tube.
2- Analgesia for pain, like paracetamol and non-steroidal anti-inflammatory like
mefanemic ascid.
3- If discharge is present, swab is taken for culture and sensitivity.
4- Empirical treatment with broad spectrum antibiotics. The antibiotics of choice
are amoxicillin, amoxicillin with clavulinic acid(augmentin), second generation
cephalosporin like cefprozil and cefpodoxime. If the patient is allergic to
penicillin, macrolides like (erythromycin, azithromycin, clarithromycin) and
sulpha drugs like co-trimoxazole can be given.
5- 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.
6- Sometimes aspiration of middle ear discharge through myringotomy is needed
for two reasons, the first is to get material for culture and sensitivity, and the
second is for decompression for symptomatic relief.
7- 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 appropriate investigations (like X-ray of the mastoid and CT
scan)should be done.
The role of surgery in the management of acute suppurative otitis media is limited
to:
1- 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.
2- 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)
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This condition is also known as serous or secretory otitis media. It is manifested with the
presence of non purulent middle ear fluid, which sometimes has a sticky, thick character
resembling the glue, for which is also called 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, like in allergic rhinitis or
chronic sinusitis.
Nasopharyngeal tumour, which should be suspected in unilateral serous otitis media in adults
and elderly.
Eustachian tube dysfunction which usually occurs in cases of cleft palate.
Clinical features
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Hard of hearing and deafness mainly in children, which is noticed by the parents.
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.
On examination, the characteristic features:
1- Retraction of the TM, with altered landmarks, like distortion or absence of the cone
of light.
2- There is alteration of the normal color of the TM, fluid level and even air bubbles
may be seen behind the TM.
3- Examination of the nose and sinuses may reveal chronic sinusitis or rhinitis.
4- In adults , the nasopharynx should be examined to rule out the presence of
nasopharyngeal carcinoma.
Investigations
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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.
Treatment
1- Medical treatment is indicated first with antibiotics and management of the
underlying cause like chronic rhinosinsitis.
2- 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.
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:
1- Tubotympanic otitis media( chronic otitis media without cholesteatoma)or(safe
ear).
2- Tympanomastoid otitis media( chronic otitis media with cholesteatoma)or ( the
unsafe ear)
Tubotympanic otitis media
It is also called otitis media without cholesteatoma, and 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 resulting from acute
otitis media which doesn't heal after the initial acute attack because of the persistence and
the recurrence of infection.
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.
Clinical features
The main symptom of this disease is mucopurulent discharge which may be intermittent or
persistent . There is also deafness which may vary in severity depending on the site and size
of the perforation and the status of the ossicular chain.
On examination, there may be discharge which needs to be cleaned by suction and dry
mopping. The perforation and the middle ear mucosa can be assessed. A swab from the
discharge can be submitted for culture and sensitivity test.
Examination should also include the nose and paranasal sinuses and the pharynx to find the
source of infection like adenoids or chronic rhinosinusitis.
Complications are rare and are not serious. Otitis externa may develop secondary to chronic
ear discharge. Ossicular fixation as a result of fibrosis or discontinuity as a result of necrosis
of the ossicles is a more usual complication.
Treatment
1- 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.
2- Treatment of the focus of infection, which includes elimination of the URTI by
medical treatment.
3- Surgery has a role when the focus needs surgical treatment like adenoidectomy or
sinonasal surgery.
4- 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.
5- Cortical mastoidectomy may be indicated when there is reservoir of infection in the
mastoid air cells.
Tympanomastoid otitis media
In this type of infection, the bone of the attic, antrum and the mastoid process is involved
a well as the mucosa of the middle ear, so it is called the 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).
Pathology and pathogenesis
The most prominent pathological finding in this type is cholesteatoma, which 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
1- The main symptom is discharge from the ear, which may be recurrent or persistent,
the discharge is purulent and may be scanty, and it is frequently foul smelling.
2- Deafness (hard of hearing), is usually present and may vary in severity.
3- 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. The
perforation is marginal, that is, 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.
Investigations
1- Hearing tests : tuning fork and Audiogram.
2- 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.
Treatment
1- 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.
2- Local antibiotic drops, according to the results of swab culture.
3- Most cases of cholesteatoma requires surgery. The operation needed is usually
modified radical mastoidectomy .
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 complications and intracranial
complications.
1- Extracranial complications
a- Mastoiditis: which is inflammation of the masoid bone with even mastoid
abscess formation.
b- Petrositis: which is inflammation of the petrous temporal bone .
c- Labyrinthitis : which is inflammation of the inner ear with consequent vertigo
and sensorineural deafness.
d- Facial nerve paralysis: which is due to pressure effect of the cholesteatoma on
the facial nerve, especially when it is dehiscent.
2- Intracranial complications
a- Meningitis.
b- Extradural dural abscess.
c- Subdual abscess.
d- Brain abscess.
e- Lateral sinus thrombosis.
f- Cortical thrombophlebitis.
g- Otitic hydrocephalus.
Deafness (Hearing Loss)
Subjective impairment of hearing.
I. Conductive
A. Congenital: congenital meatal atresia.
B. Aquired
1. External ear: wax and foreign bodies.
2. Middle ear:
a. Trauma: TM perforation & ossicular disconnection.
b. Inflammatory: acute & chronic supp. otitis media, secretory otitis media.
d. Tumours: glomus jugulari & sq. cell carcinoma.
3. Otic capsule: otosclerosis.
II. Sensorineural Hearing Loss
Sensory (cochlear) hearing loss= cochlear lesion.
Neural (retrocochlear) hearing loss= auditory nerve lesion.
A. Congenital:
a. Syndromes; Pendred,s & trisomy 18.
b. Intrauterine infections; rubella, syphilis & toxoplasmosis.
c. Toxins; hypoxia and kernicterus.
B. Acquired:
1.Cochlear
a. Traumatic; head injury and blast injury.
b. Infective; Labyrinthitis, measles, mumps and syphilis.
c. Metabolic; Meniere,s disease.
d. Toxins; ototoxic drugs.
e. Degenerative; presbyacusis.
2. Retrocochlear
a. Neoplastic; acoustic neuroma.
b. Meningitis.
c. Multiple sclerosis.
Otosclerosis (Otospongiosis)
It is hereditary localized disease of the otic capsule in which new spongy bone causes
ankylosis of the foot plate of stapes leading to conductive deafness. Cochlear involvement
with sensorineural hearing loss may also occur.
Aetiology
1. Hereditary factors: It is
inherited by autosomal dominant pattern with incomplete
penetration..
2. Racial distribution: white races (Caucasian) are more commonly affected.
3. Age: clinical manifestations usually begin between 15-45 years of age.
4. Sex: the disease appears more frequently in females 2:1.
5. Pregnancy: may accelerate the condition but never cause it.
Pathology
The condition is commonly bilateral (80%). The normal bone is absorbed and
replaced by vascular spongy osteoid bone. The most common site of disease is on the
promontory immediately anterior to the oval window (Fissula ante fenestram). In advanced
cases the stapes become ankylosed in position causing conductive deafness. Cochlear
involvement may also occur leading to sensorineural hearing loss.
Clinical Picture
(Deafness
Tinnitus
Vertigo)
1. Hearing loss: the predominant symptom of otosclerossis is slowly progressive hearing loss,
usually bilateral (80%) and conductive in type. Characteristically, the patient speaks in a quite
voice, very different from the loud and harsh speech of those with sensorineural hearing loss.
Not infrequently, the patient can hear better in a noisy environment (Paracusis Willisii).
Tinnitus: is present in 75% of cases. It tends to be worse in patients with cochlear
involvement and during periods of rapid progression.
2. Vertigo: is a rare symptom.
Examination
1. Otoscopy: the tympanic membrane is normal. In 10% of cases a "flamingo pink blush"
(Schwartze,s sign) may be seen through the membrane due to hyperaemia of the promontory.
2. Tuning fork tests: negative Rinne,s test and the Weber test is lateralized to the more affected
ear.
3. P.T.A: conductive deafness. In advanced cases there may be sensorineural hearing loss
which is associated with masses of otosclerotic bone involving the cochlea.
Treatment
1.
Medical: hearing aids.
2.
Surgical: stapedectomy which is total or partial removal of the foot plate of the stapes and
replacement by a prosthesis.
Sudden Sensorineural 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 lowfrequency 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 consists of hospital admission, infusion of low molecular weight dextran
and steroid treatment if there is no contraindication.
To have a reasonable chance of success this should begin within one week of the original
episode of sudden hearing loss.
Intratympanic steroids.
Presbyacusis (senile Hearing Loss)
A symmetrical Bilateral SNHL which occurs after the age of 65 years. The etiology is
degenerative changes of aging that affects the cochlea, the auditory nerve or both.
Clinical Picture
The deafness is characteristically progressive, bilateral SNHL with marked loss of speech
discrimination due to inability to hear the higher frequencies (consonant sounds).
They have difficulty in hearing in the presence of background noise.
Recruitment of hearing also adds to the distortion.
Recruitment means intolerance of loud sounds and
generally is associated with cochlear lesion.
Audiometry
Bilateral symmetrical SNHL.
Treatment
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 produces 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.
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 usually contain ototoxic antibiotiocs like neomycin, gentamycin,
polymyxin and framycetin. No convincing evidence that these topical medications can
cause sensorineural hearing loss.
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.
Aetiology
A. Central (Non-otological)
1.
CVS: severe anaemia, hypotension and DM.
2.
CNS: intracranial tumours, multiple sclerosis, vertebrobasillar ischaemia, temporal
lobe epilepsy and migraine.
B. Peripheral (vestibular, otological)
1. Infective: Labyrinthitis, and vestibular neuronitis.
2. Neoplastic: acoustic neuroma.
3. Metabolic: Meniere’s disease.
4. Toxins: vestibulotoxic drugs.
5. Trauma: head injury.
6. 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
The onset of symptoms is preceded a week or 10 days earlier by a sore throat, acute
sinusitis or other URTI.
1.
Vertigo which can last several days before a gradual recovery begins.
2.
Nausea and vomiting.
3.
Absence of aural symptoms: hearing is normal and there is no tinnitus.
Examination
Spontaneous nystagmus of the vestibular type.
Investigations
Caloric test: canal paresis on the affected side.
Treatment
1.
Reassurance and explanation while waiting for recovery to occur by compensation.
2. 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. There are no other aural symptoms.
Aetiology
1. Idiopathic.
2. Head injury.
3. Viral infection.
4. 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
1. Brief attacks of vertigo when the patient puts his head in the critical position. This vertigo
may be accompanied by a slight feeling of dizziness.
2. Absence of aural symptoms: hearing is normal and there is no tinnitus.
Examination
Dix-Hallpike test : Positional nystagmus is elicited by performing the
Hallpike manoeuvre. 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. Meniere's disease gets its name from the French physician Prosper
Meniere, who first described the illness in 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. Faulty absorption of the endolymph by the
endolymphatic sac may be an aetiology.
Dilated membranous labyrinth
Clinical picture
The disorder is usually unilateral, but the other labyrinth is eventually affected.
Remission is typical of the disease and may vary from a few weeks to several years. The
suddenness of the attacks is one of the most characteristic features, though some patients get
warning of attack by a change in their tinnitus or a fullness sensation in the ear (aura)..
1. Vertigo: is of sudden onset and the attack lasts for a few hours. The patient may fall and
injure himself but he has a normal level of consciousness.
2. Hearing loss: is of sensorineural type and may be during or just after the attack. In the
early stages of the disease the hearing returns to normal, but as the attacks become more
frequent, the hearings deteriorates and finally complete loss of hearing results in the affected
ear.
3. Tinnitus: referred to the affected ear, precedes or accompanies the vertigo.
4.
Aural fullness: Due to increase pressure in the endolymph.
1. Otoscopy: normal.
2. Tuning fork examination: sensorineural hearing loss during the attack.
Investigation
1. Audiological (pure tone audiometry): sensorineural hearing loss.
2. Vestibular (caloric test): canal paresis in the affected ear.
Treatment
I. Medical
The acute attack.
1. Complete bed rest.
2. Antihistamine labyrinthine sedatives: prochlorperazine (stemetil) and cinnarzine
(stugeron).
3. Anxiolytics: I.V.diazepam.
The long term management.
1. Vasodilator drugs: betahistine hydrochloride (serc) which increases the cochlear blood
flow. .
2. Reduction of labyrinthine hydrops: fluid and salt limitation with diuretics.
II. Surgical
a. Endolymphatic sac decompression or shunt.
b. Vestibular nerve section.
Rehabilitation of hearing impaired individuals
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 250-4000 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 is 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.