Transcript Hearing loss

‫بسم هللا الرحمن الرحيم‬
Lecture Objectives
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Deafness (Hearing loss)
Hearing Aids
Otosclerosis (Otospongiosis)
Sudden Sensorineural Hearing Loss
Drug ototoxicity
Presbycusis (Senile hearing loss)
Deafness and Noise
Non-Organic Hearing Loss
Tinnitus
Deafness (Hearing loss)
Hearing loss
SNHL
Conductive
Congenital
Acquired
EAM
Otic
capsule
Congenital
ME
Acquired
Cochlear
Retrocochlear
Hearing Aids
A hearing aid is an electro-acoustic device used to
amplify sounds.
Design
The basic components of any hearing aid are:
• Receiver ( microphone)
• Amplifier
• Sound transmitter (Ear phone)
• Power supply
Types of hearing aid
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Behind-The-Ear (BTE)
In-The-Ear and In-The-Canal Aids:
Body-worn aids
Bone conduction HA: sound is transmitted
from a vibrator that fit on mastoid bone
Bone-anchored hearing aids
(BAHA)
• Cochlear implant:
• an electronic device that can provide useful
hearing for persons who have severe SNHL
who cannot benefit from HA. It is
composed of:
1- External component: which consist an
external speech processor and transmitter.
2- Internal component: is surgically implanted
and comprises the receiver / stimulator
package with an electrode array.
OTOSCLEROSIS
Is hereditary localized disease of the otic
capsule in which new spongy bone cause
ankylosis of the foot plate of stapes leading to
conductive deafness. Cochlear involvement with
SNHL may also occur.
HISTOPATHOLOGY
• Resorption of bone by
osteocytes
• Formation of new vascular
spongy bone
AREAS OF PREDILECTION
Fissula ante fenestram (80% to 90%)
COCHLEAR INVOLVEMENT
AETIOLOGY
• Hereditary factors: (50%) / autosomal dominant
pattern with incomplete penetration.
• Racial distribution:
white races (Caucasian) > coloured.
• Age: 15-45 years of age.
• Sex: females: male= 2:1.
• Pregnancy: may accelerate the condition but
NEVER cause it.
CLINICAL PRESENTATION
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Hearing loss of gradual onset at 15 - 45 years
Slowly progressive course
80% are bilateral
Accelerates with pregnancy (30-40%)
Tinnitus (75%)
Paracusis Willisii
Change of the speech pattern
PHYSICAL EXAMINATION
• Normal tympanic membrane
• Schwartze sign (Flamingo flush)
* seen through the membrane due
to hyperaemia of the promontory
* indicates rapid progression of the
disease.
• Tuning fork tests
PURE TONE AUDIOMETRY
• Conducive deafness.
• Carhart’s notch: is an increase
in bone conduction threshold
with a peak at 2,000 Hz.
Explanation is not known
Reverses following successful
surgery
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In advanced cases there may be
SNHL
Treatment
• Hearing aids
• Medical: sodium fluoride?!
• Surgical: stapedectomy which is total or
partial removal of the foot plate of the
stapes and replacement by prosthesis.
• Complication: perilymph fistula which is
characterized by sudden SNHL and vertigo.
It is liable to occur after sudden changes of
pressure, so the patient should avoid diving
and only fly in pressurized aircrafts.
Sudden Sensorineural Hearing Loss
Aetiology
1. Idiopathic: in 2/3 of cases
2. Vascular: spasm, thrombosis or haemorrhage of
the internal auditory artery.
3. Viral infection: mumps, measles, rubella or
Herpes zoster.
4. Head injury with temporal bone fracture, blast
injury, and ear surgery as stapedectomy.
5. Tumors: acoustic neuroma.
Clinical Picture
1) Hearing Loss
2) Tinnitus: 80% --a good prognostic sign and means that hair
cell still functioning.
3) Vertigo: is common in those with vascular aetiology and
caries a bad prognosis.
Examination
• The TM is usual normal.
• Tuning fork test
• PTA: hearing loss in high frequency.
Treatment
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Bed rest and sedation.
Steroids in tapering dose.
Vasodilators: Betahistine (Betaserc).
Low molecular weight dextran
Prognosis
• In 1/3 quick recovery. If there is no recovery within 3
weeks it is unlikely to occur spontaneously.
• In 1/3  partial recovery
• In 1/3 have none.
• Unfavorable prognostic features are severe HL and
vertigo
Drug ototoxicity
• Damage to the cochlear and/or vestibular part of the inner ear by
certain drugs.
Ototoxic drugs include:
1. Aminoglycosides
2. Loop diuretics
3. Salicylates.
4. Quinine.
5. Antiepileptics; phenytoin.
6. B-blockers.
7. Cytotoxic; cisplatin.
• Synergistic effect….
• The dangers are especially great if excretion is impaired as in renal
failure.
Presbycusis (Senile hearing loss)
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A symmetrical, progressive, bilateral SNHL
age > 65 years
no underlying cause.
The degenerative changes occur as a result of
aging process and vascular insufficiency
Treatment
1. Lip reading
2. Hearing aids
Deafness and Noise
Excessive sound stimulation  two types of SNHL
1. Acoustic trauma…very brief exposure…
2. Noise-induced hearing loss..excess of 85dB for 8
hours/day
PTA
Treatment
1. Preventive:
2. Therapeutic:
• Rest and avoidance of future trauma.
• Hearing aids
Non-Organic Hearing Loss
1. Psychogenic (hysterical)
2. Malingering.
Diagnosis
• History
• Examination
• Audiometry; repeated audiograms give
different results on each occasion.
Fracture base of the skul
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The longitudinal is more common than transverse.
Deafness
Tinnitus and Vertigo
Tympanic membrane.
Facial nerve palsy is seen more often in transverse
fracture
• X-ray and CT scan of the base of skull
Treatment:
Bleeding from the ear, with or without facial
nerve palsy, after head injury means
fracture base of skull until prove other wise.
• Never syringe the ear.
• No instrumentation of the ear.
• No caloric test.
• Systemic antibiotic…
• Facial nerve paralysis...
Tinnitus
• subjective sensation of noise
Aetiology
1. Central
2. Peripheral (ear):
A. External and middle ear.
B. Cochlear:
C. Retrocochlear
It is usually more noticeable in bed at night when
background noise is at its quietest.
Investigation
• CBC, FBS and lipid profile.
• CT scan, MRI (acoustic neuroma).
• MRA and angiography (glomus jugulare).
• PTA.
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Treatment
1. Treatment of underlying cause and reassurance.
Avoid smoking and caffeine.
2. Drugs: I.V. lidocaine, antidepressants and
anxiolytics like alprazolam.
Ginkgo biloba improves brain function by
increasing blood flow and oxygenation.
3. Tinnitus masking
4. Hearing aids