Chronic suppurative otitis media (CSOM) is a longstanding
infection of a part or whole of the middle ear cleft
characterised by ear discharge and a permanent perforation.
A perforation becomes permanent when its edges are
covered by squamous epithelium and it dews not hea l
spontaneously. A permanent perforation can be likened [0
an epithelium-lined fistulous track.
Epidemiology
Incidence of CSOM is higher in developing countries
because of poor socio-economic standards, poor nutritionand lack of health education. It affects both sexes and all
age groups. In India, the overall prevalence mte is 46 and
16 persons pcr thousand in rural and urban population
respectively. It is also the singlemost imporranc cause of
hearing impairment in rural population.
Types of CSOM
Clinically, it is divided into two types:
1. Tubotympanic. Also called the safe or benign type;
it in volves anteroinferior part of middle ear cleft and is
assoc iated with a central perforation. There is no risk of
serious complications.
2. Atticoantral. Also ca lled unsafe or danaerou5 type;
it involves posterosuperior part of the cleft (i.e. attic,
antrum and mastoid) and is assoc ia ted with an attic or a
marginal perforation. The disease is often associated with
a bone-eroding process such as cholesteatoma, granulations
or osteitis. Risk of complications is high in this
variety.A. Tubotympanic Type
Aetiology
The disease starts in childhood and is therefore common
in that age group.
1. It is the seque la of acute otitis media usually following
exanthematous fever and leaving behind a large
central perforation.
The perforation becomes permanent and permits
repeated infection from the external ear. Also the
middle ear mucosa ge ts exposed to the environment
and sensitised to dust, pollen and other aeroallergens
causing persistent otorrhoea.
2. Ascending infec tions via the eustachian tube. Infection
from tonsils, adenoids and infected sinuses Lllay
be responsible for persistent or recurring otorrhoea.
3. Persistent mucoid otorrhoea is sometimes the result
of allergy to ingestants such as milk, eggs, fish, etc.
Pathology
T he tubotympanic disease remain localised to the mucosa
and, that toO, mostly to anteroinferior part of the middle
ear cleft. Like any other chronic infection, the processes
of heal ing and destruction go hand in hand and either of
them may take advantage over the other, depending on
the virulence of organism and resistance of [he patient.
Thus, acute exacerbmions are not uncommon. The
pathological changes seen in this type of CSOM are:
1. Perforation of pars tensa. It is a central petforation
and its size and position varies.
2. Middle ear mucosa. It may be normal when disea~
e is quiescent or inactive. It is oedematous and velvety
when disea e is active.
3 . Polyp. A polyp is a smooth mass of oedemarous
and inflamed mucosa which has protruded through a perfot'arion
and presents in the external canal. It is usually
pale in contrast to pink, fleshy polyp seen in att icoa ntral
disease (Fig. 11.4).4. Ossicular chain. It is usually intact and mobile
but may show some degree of necrosis, particularly of the
long process of incus.
5. Tympanosclerosis. It is hyalinisation and subsequent
calcification of subepithelial connective tissue. It
is seen in remnants of tympanic membrane or under the
mucosa of middle ear. It is seen as white chalky deposit
on the promontory, ossicles, joints, tendons and oval and
round windows. Tympanosclerotic masses may interfere
\\'ith the mobility of these structures and cause conductive
deafness.
6. Fibrosis and adhesions. They are the result of
bealing process and may' further impair mobility of ossicular
chain or block the eustachian tube.
Bacteriology
Pus culture in both types of aerobic and anaerobic
CSOM may show multiple organisms. Common aerobic
organisms are Ps aeruginosa, Proteus, Esch. coli and Staph.
aureUS, while anaerobes include Bacteroides fragilis and
anaerobic Streptococci.
Clinical Features
1. Ear discharge. It is non-offensive, mucoid or
ucopurulent, constant or intermittent. The discharge
pears mostly at time of upper respiratory tract infection
- on accidental entry of water into the ear.
2. Hearing loss. It is conductive type; severity varies
t rarely exceeds 50 dB. Sometimes, the patient reports
. a paradoxical effect, i.e. hears better in the presence of
, harge than when the ear is dry. This is due to "round
:Jow shielding effect" produced by discharge which
l\-; to maintain phase differential. In the dry ear with
_rforation, sound waves strike both the oval and round
windows simultaneously, thus cancelling each other's
effect (see Physiology of hearing).
In long standing cases, cochlea may suffer damage due
to absorption of toxins from the oval and round windows
and hearing loss becomes mixed type.
3. Perforation. Always central, it may lie anterior,
posterior or inferior to the handle of malleus. It may be
small, medium or large or extending up to the annulus,
i.e. subtotal (Fig. 11.5).
4. Middle ear mucosa. It is seen when the rLltuwtion
is large. Normally, it is pale pink and moist; when
inflamed it looks red, oedematous and swollen.
Occasionally, a polyp may be seen.
Investigations
1. Examination under microscope is essential in every
case and provides useful information regarding presence
of granulations, in-growth of squamous epithelium from
the edges of perforation, status of ossicular chain, tympanosclerosis
and adhesions. An ear which appears dry
may show hidden discharge under the microscope. Rarely,
cholesteatoma may co-exist with a central pelforation and
can be seen under a microscope.
2. Audiogram. It gives an assessment of degree of
hearing loss and its type. Usually, the loss is conductive
but a sensorineural element may be present.
3. Culture and sensitivity of ear discharge. It helps
to select proper antibiotic ear drops .
4. Mastoid X-rays. Mastoid is usually sclerotic but
may be pneumatised with clouding of air cells. There is
no evidence of destruction. Presence of bone destruction
is a feature of atticoantral disease.Treatment
The aim is to control infection and eliminate ear discharge
and at a later stage, to correct the hearing loss
by surgical means.
1. Aural toilet. Remove all discharge and debris
from the ear. It can be done by dry mopping with
absorbent cotton buds, suction clearance under microscope
or irrigation (not forceful syringing) with sterile
normal saline. Ear must be dried after irrigation.
2. Ear drops. Antibiotic ear drops containing
neomycin, polymyxin, chloromycetin or gentamicin are
used. They are combined with steroids which have local
anti-inflammatory effect. To use ear drops, patient lies
down with the diseased ear up, antibiotic drops are
instilled and then intermittent pressure applied on the
tragus for antibiotic solution to reach the middle ear.
This should be done three or four times a day. Acid pH
helps to eliminate pseudomonas infection, and irrigations
with 1.5% acetic acid are useful.
Care should be taken as ear drops are likely to cause
maceration of canal skin, local allergy, growth of fungus
or resistance of organisms. Some ear drops are potentially
ototox ic.
3. Systemic antibiotics. They are useful in acute
exacerbation of chronically infected ear, otherwise, role
of systemic antibiotics in the treatment of CSOM is
limited.
4. Precautions. Patients are instructed to keep water
out of the ear during bathing, swimming and hair wash.
Rubber inserts can be used. Hard nose-blowing can al
push the infection from nasopharynx to middle ear an
should be avoided.
5. Treatment of contributory causes. Attenri
should be paid to treat concomitantly infected ton ii,
adeno ids, maxillary antra, and nasa l allergy.
6. Surgical treatment. Aural polyp or granulati mif
present, should be removed before local treatment wiantibiotics.
It will facilitate ear toilet and permit eClr
drops to be used effectively. An aural polyp should never be
avulsed as it may be arising fr~m the stapes, facial nerve
or horizontal canal and thus lead to facial paralysis or
labyrinthitis.
7. Reconstructive surgery. Once ear is dry,
myringoplasty with or without ossicular reconstruction
can be done to resto re hearing. Closure of perforation
will also check repeated infec tion from the external
canal.
B. Atticoantral Type
It involves posterosuperior part of middle ear cleft (att ic,
antrum and posterior tympanum and mas toid) and is
assoc iated with cholesteatoma, which, because of its
bone eroding properties, causes risk of serious complications.
For this reason, the disease is also called unsafe or
dangerous type.
Aetiology
Aetiology of atticoantral disease is same as of cholesteatoma
and has been discussed earlier. It is seen in scleroticmastoid, and whether the latter is the cause or effect of
dISease is not yet clear.
Pathology
-\ tticoantral diseases is associated with the following
rarhological processes:
1. Cholesteatoma
2. Osteitis and granulation tissue. Osteitis involves
uter attic wall and posterosuperior margin of the tym"
CIn ic ring. A mass of granulation tissue surrounds the
ea of osteitis and may even fill the attic, antrum, pos'
erior tympanum and mastoid. A fleshy red polypus may
e seen filling the meatus.
3. Ossicular necrosis. It is common in atticoantral
disease. Destruction may be limited to the long process of
malleus or may also involve stapes superstructure, handle of
malleus or the entire ossicular chain. Therefore, hearing
s is always greater than in disease of tubotympanic
type. OccaSionally, the cholesteatoma bridges the gap
u-ed by the destroyed ossicles, and hearing loss is not
apparent.
4. Cholesterol granuloma. It is a mass of granulation
ue with foreign body giant cells surrounding the choterol
crystals. It is a reaction to long-standing retention
:"ecretions or haemorrhage, and mayor may not co-exist
lth cholesteatoma. When present in the mesotympanum,
~.h ind an intact drum, the latter appears blue.
Bacteriology
- me as in tubotympanic·type.
Symptoms
1. Ear discharge. Usually scanty, but always foul'
1lelling due to bone destruction. Discharge may be so
-anty that the patient may not even be aware of it. Total
c: 'ation of discharge from an ear which has been active
I recently should be viewed seriously, as perforation in
, e-e cases might be sealed by crusted discharge, inflam.."
w ry mucosa or a polyp, obstructing the free flow of
:; harge. Pus, in these cases, may find its way internally
nd cause complications.
2. Hearing loss. Hearing is normal when ossicular
chain is intact or when cholesteatoma, having destroyed
'he ossicles, bridges the gap caused by destroyed ossicles
cholesteatoma hearer). Hearing loss is mostly conducti ve
[ enso rineural element may be added.
3. Bleeding. It may occur from granulations or the
)lyp when cleaning the ear.
Signs
1. Perforation. It is either attic or posterosuperior
marginal type. A small attic perforation may be missed
due t0 presence of a small amount of crusted discharge.
Sometimes, the area of perf~ration is masked by a small
granuloma.
2. Retraction pocket. An invagination of tympanic
membrane is seen in the attic or posterosuperior area of
pars tensa. Degree of retraction and invagination varies.
In early stages, pocket is shallow and self-cleansing but
later when pocket is deep, it accumulates keratin mass
and gets infected.
3. Cholesteatoma. Pearly-white flakes of cholesteatoma
can be sucked from the retraction pockets. Suction
clearance and examination under operating microscope
forms an important part of the clinical examination and
assessment of any type of CSOM.
Investigations
1. Tuning fork tests and audiogram. They are
essential for pre-operative assessment and to confirm the
degree and type of hearing loss.
2. X-ray mastoids. They indicate extent of bone
destruction and degree of mastoid pneumatisation. They
are useful to indicate a low-lying dura or an ante posed sigmoid
sinus when operation is being contemplated on a
sclerotic mastoid. Cholesteatoma causes destruction in the
area of attic and antrum (key area), better seen in lateral
view. CT scan of temporal bone gives more information.
3. Culture and sensitivity of ear discharge. It helps
to select proper antibiotic for local or systemic use .
Features Indicating Complications in CSOM
1. Pain. Pain is uncommon in uncomplicated
CSOM. Its presence is considered serious as it may indicate
extradural, perisinus or brain abscess. Sometimes, it
is due to otitis externa associated with a discharging ear.
2. Vertigo. It indicates erosion of lateral semicircular
canal which may progress to labyrinthitis or meningitis.
Fistula test should be performed in all cases.
3. Persistent headache. It is suggestive of an
intracranial complication.
4. Facial weakness indicates erosion of facial canal.
5. A listless child refusing to take feeds and easily
going to sleep (extradural abscess).
6. Fever, nausea and vomiting (intracranial infection.).
7. Irritability and neck rigidity (meningitis).
8. Diplopia (Gradenigo's syndrome).
10. Abscess round the ear (mastoiditis).It is not uncommon for a patient of CSOM, residing
in a fad1ung village, where medical facilities are poor, to
go to a doctor for the first time, presenting with complications.
It then demands urgent attention and emergency
medical or surgical treatment.
Treatment
1. Surgical. It is the mainstay of treatment. Primary
aim is to remove the disease and render the ear safe,
and second in priority is to preserve or reconstruct the
hearing but never at the cost of the primary aim. Two
types of surgical procedures are done to deal with
cholesteatoma:
(a) Canal wall down procedures. They leave the mastoid
cavity open into the external auditory canal so that
the diseased area is fully exteriorised. The commonly
performed operations for atticoantral disease
are atticotomy, mod ified radical mastoidectomy and
rarely, the radical mastoidectomy (see operative
surgery) .
(b) Cand wall up procedures. Here disease is removed by
combined approach through the meatus and mastoid
but retaining the posterior bony meatal wall intact,
thereby avoiding an open mastoid cavity. It gives dry
ear and permits easy reconstruction of hearing mechanism.
However, there is danger of leaving some
cholesteatoma behind. Incidence of residual or recurrent
cholesteatoma in these cases is very high and
therefore long-term follow-up is essential. Some even
advise routine re-exploration in all cases after 6
months or so. Canal wall up procedures are advised
only in selected cases. In combined-approach or
intact canal wall mastoidectomy, disease is removed
both permeatally and through cortical mastoidectomy
and posterior tympanotomy, in which a window
is created between the mastoid and middle ear,
through the facial recess, to reach sinus tympani (see
page 6).
2. Reconstructive surgery. Hearing can be restored
by myringoplasty or tympanoplasty. It can be done at the
time of primary surgery or as a second stage procedure.
Conservative treatment. It has a limited role in the
management of cholesteatoma but can be tried in
se lected cases, when cholesteatoma is small and easily
accessible to suction clearance under operating microscope.
Repeated suction clearance and periodic check
ups are essen tial. It can also be tried out in elderly patients
above 65 and those who are unfit for general anaesthesia
or those refusing surgery. Polyps and granulations can
also be surgically removed by cup forceps or cauterised by
chemical agents like silver nitrate or trichloroacetic acid.
Other measures like aural toilet and dry ear precautions
are also essential.
Showing posts with label ear. Show all posts
Showing posts with label ear. Show all posts
Tuesday, December 28, 2010
Serous Otitis Media, Secretory Otitis Media, Mucoid Otitis Media, "Glue Ear"
Serous Otitis Media (Syn. Secretory Otitis
Media, Mucoid Otitis Media, "Glue Ear")
This is an insidious condition characterised by accumution
of non-purulent effusion in the middle ear cleft.
ften the effusion is thick and viscid but sometimes it
Illay be thin and serous. The fluid is nearly sterile. T he
c llndition is commonly seen in school-going children.
Pathogenesis
Two main mechanisms are thought to be responsible:
1. Malfunctioning of eustachian tube. Eustachian
' ube fails to aerate the midd le ear and is also unable to
J rain the fluid.
2. Increased secretory activity of middle ear mucosa.
Biopsies of middle ear mucosa in these cases have confirmed
n crease in number of mucus or serous-secreting cells.
Aetiology
1. Malfunctioning of eustachian tube. The causes are:
I') Adenoid hyperplasia .
Ii) Chronic rhinitis and sinusiti s.
DISORDERS OF MIDDLE EAR
(iii) Chronic tonsillitis. Enlarged tonsils mechanically
obstruct the movements of soft palate and interfere
with the physiologica l opening of eustachian tube.
(iv) Benign and malignant tumours of nasopharynx.
This cause should always be excluded in unilate ral
serous otitis media in an adu lt.
(v) Palatal defects, e.g. cleft palate, palatal paralys is.
2. Allergy. Seasonal or perennial a lle rgy to inha lants
or foodstuff is common in children. This not only obstructs
eustachi
in such cases.
3. U nresolved otitis media. Inadequate antibiotic
therapy in acute suppurative otitis media may inactivate
infection but fail to resolve it completely. Low grade infection
lingers on. This acts as stimulus for mucosa to secrete
more fluid. T he number of goblet cells and mucous glands
also increase. Recent increase in the incid ence of this
disease seems to be due to this factor.
4. Vi ral infections . Various adeno- and rhinoviruses
of upper respiratory tract may invade middle ear
mucosa and stimulate it to increased secretory activ ity.
Clinical Features
Symptoms. T he disease affects children of 5-8 years of
age. The symptoms include:
(1) Hearing loss. T his is the presenting and sometimes
the only symptom. It is insidious in onset and rare ly
exceeds 40 dB. Deafness may pass unnoticed by the parents
and may be acc iden tally discovered during a udiometric
sc reen ing tests.
(ii) Delayed and defective speech. Because of hearing lo 's,
development of speech is delayed or defective.
(iii) Mild earaches. There may be history of upper respiratory
tract infections with mild earaches.
Otoscopic findings. Tympanic membrane is often dull
and opaque with loss of light reflex. It may appear yellow,
grey or bluish in colour.
Thin leash of blood vessels may be seen along the
handle of malleus or at the periphery of tympanic membrane
and differs from marked congestion of acute suppurative
otitis med ia.
Tympanic membrane may show varying degree of
retraction. Sometimes, it may appear full or slightly
bu lging in its posterior part due to effusion.
Fluid level and air bubbles may be seen when fluid is
thin and tympanic membrane transparent (Fig. 10. 2).
Mobility of the tympanic membrane is restricted.
Hearing Tests
(i) Tuning fori< tests show conductive hearing loss
(1i) Audiometry. There is conductive hearing loss of
20-40dB. Sometimes, there is assoc iated sensorineural
hearing loss due to fluid pressing on the round window
membrane. This disappears with evacllation of fluid .(iii) Impedance audiometry. It is an objective test useful
in infants and children. Presence of fluid is indicated
hy reduced compliance and flat curve with a shift to
negative side.
(iv) X-ray maswids. There is clouding of air cells due to
fluid.
Treatment
The aim of treatment is removal of fluid and prevention
of its recurrence.
A. Medical
1. Decongestants. Topical decongestants in the
form of nasal drops, sprays or systemic decongestants
help co relieve oedema of eustachian tube.
2. Antiallergic measures. Antihistaminics or sometimes
sceroids may be used in cases of allergy. If possible,
allergen should be found and desensitisation done.
3. Antibiotics. They are useful in cases of upper respiratory
tract infections or unresolved acute suppurative
otitis media.
4. Middle ear aeration. Patient should repeatedly
perform Valsalva manoeuvre. Sometimes, politzerisation
or eustachian tuhe catheterisation has to be done. This
helps to ventilate middle ear and promote drainage of
fluid. Children can be given chewing gum to encourage
repeated swallowing which opens the tube.
B. Surgical
When fluid is thick and medical treatment alone does
not help, fluid must be surgically removed.
1. Myringotomy and aspiration of fluid. An incision
is made in tympanic membrane and fluid aspirated
with suction. Thick mucus may require installation of
saline or a mucolytic agent like chymotrypsin solution to
liquify mucus before it can be aspirated. , umetimes, two
incisions are made in the tympanic membrane, one in
the antero-inferior and the other in antero-superior
quadrant, to aspirate thick, glue-like secretions (Fig.
10.3) on "beer-can" principle.2. Grommet insertion. If myringotomy and aspiration
combined with medical measures has not helped
and fluid recurs, a grommet is inserted to provide continued
aeration of middle ear (Fig. 10.4). It is left in place
for weeks or months or till it is spontaneously extruded.
3. Tympanotomy or cortical mastoidectomy. It is
sometimes required for removal of loculated chick fluid or
other associated pathology such as cholesterol granuloma.
4. Surgical treatment of causative factor. Adenoidectomy,
tonsillectomy and/or wash-out of maxillary
antra, may be required. This is usually done at the time
of myringotomy.
Sequelae of Chronic Secretory Otitis Media
1. Atrophic tympanic membrane and atelectasis of
the middle ear. In prolonged effusions, there is dissolution
of fibrous layer of tympanic membrane. It becomes
thin and atrophic and retracts into the middle ear.
2. Ossicular necrosis. Most commonly, long process
of incus gets necrosed. Sometimes, stapes superstructure
also gees necrosed. This increases the conductive hearing
loss to more than 50 dB.
3. Tympanosclerosis. Hya linised collagen with chalky deposits
may be seen in tympanic membrane, around the
ossicles or their joints, leading to their fixation.
4. Retraction pockets and cholesteatoma. Thin
atrophic part of parS tensa may get invaginated to form
retraction pockets or cholesteatoma. Sim dar pockets
may be seen in the a ttic region.
5. Cholesterol granuloma. This is due to stasis of
secre tions in middle ear and mastoid.
Media, Mucoid Otitis Media, "Glue Ear")
This is an insidious condition characterised by accumution
of non-purulent effusion in the middle ear cleft.
ften the effusion is thick and viscid but sometimes it
Illay be thin and serous. The fluid is nearly sterile. T he
c llndition is commonly seen in school-going children.
Pathogenesis
Two main mechanisms are thought to be responsible:
1. Malfunctioning of eustachian tube. Eustachian
' ube fails to aerate the midd le ear and is also unable to
J rain the fluid.
2. Increased secretory activity of middle ear mucosa.
Biopsies of middle ear mucosa in these cases have confirmed
n crease in number of mucus or serous-secreting cells.
Aetiology
1. Malfunctioning of eustachian tube. The causes are:
I') Adenoid hyperplasia .
Ii) Chronic rhinitis and sinusiti s.
DISORDERS OF MIDDLE EAR
(iii) Chronic tonsillitis. Enlarged tonsils mechanically
obstruct the movements of soft palate and interfere
with the physiologica l opening of eustachian tube.
(iv) Benign and malignant tumours of nasopharynx.
This cause should always be excluded in unilate ral
serous otitis media in an adu lt.
(v) Palatal defects, e.g. cleft palate, palatal paralys is.
2. Allergy. Seasonal or perennial a lle rgy to inha lants
or foodstuff is common in children. This not only obstructs
eustachi
in such cases.
3. U nresolved otitis media. Inadequate antibiotic
therapy in acute suppurative otitis media may inactivate
infection but fail to resolve it completely. Low grade infection
lingers on. This acts as stimulus for mucosa to secrete
more fluid. T he number of goblet cells and mucous glands
also increase. Recent increase in the incid ence of this
disease seems to be due to this factor.
4. Vi ral infections . Various adeno- and rhinoviruses
of upper respiratory tract may invade middle ear
mucosa and stimulate it to increased secretory activ ity.
Clinical Features
Symptoms. T he disease affects children of 5-8 years of
age. The symptoms include:
(1) Hearing loss. T his is the presenting and sometimes
the only symptom. It is insidious in onset and rare ly
exceeds 40 dB. Deafness may pass unnoticed by the parents
and may be acc iden tally discovered during a udiometric
sc reen ing tests.
(ii) Delayed and defective speech. Because of hearing lo 's,
development of speech is delayed or defective.
(iii) Mild earaches. There may be history of upper respiratory
tract infections with mild earaches.
Otoscopic findings. Tympanic membrane is often dull
and opaque with loss of light reflex. It may appear yellow,
grey or bluish in colour.
Thin leash of blood vessels may be seen along the
handle of malleus or at the periphery of tympanic membrane
and differs from marked congestion of acute suppurative
otitis med ia.
Tympanic membrane may show varying degree of
retraction. Sometimes, it may appear full or slightly
bu lging in its posterior part due to effusion.
Fluid level and air bubbles may be seen when fluid is
thin and tympanic membrane transparent (Fig. 10. 2).
Mobility of the tympanic membrane is restricted.
Hearing Tests
(i) Tuning fori< tests show conductive hearing loss
(1i) Audiometry. There is conductive hearing loss of
20-40dB. Sometimes, there is assoc iated sensorineural
hearing loss due to fluid pressing on the round window
membrane. This disappears with evacllation of fluid .(iii) Impedance audiometry. It is an objective test useful
in infants and children. Presence of fluid is indicated
hy reduced compliance and flat curve with a shift to
negative side.
(iv) X-ray maswids. There is clouding of air cells due to
fluid.
Treatment
The aim of treatment is removal of fluid and prevention
of its recurrence.
A. Medical
1. Decongestants. Topical decongestants in the
form of nasal drops, sprays or systemic decongestants
help co relieve oedema of eustachian tube.
2. Antiallergic measures. Antihistaminics or sometimes
sceroids may be used in cases of allergy. If possible,
allergen should be found and desensitisation done.
3. Antibiotics. They are useful in cases of upper respiratory
tract infections or unresolved acute suppurative
otitis media.
4. Middle ear aeration. Patient should repeatedly
perform Valsalva manoeuvre. Sometimes, politzerisation
or eustachian tuhe catheterisation has to be done. This
helps to ventilate middle ear and promote drainage of
fluid. Children can be given chewing gum to encourage
repeated swallowing which opens the tube.
B. Surgical
When fluid is thick and medical treatment alone does
not help, fluid must be surgically removed.
1. Myringotomy and aspiration of fluid. An incision
is made in tympanic membrane and fluid aspirated
with suction. Thick mucus may require installation of
saline or a mucolytic agent like chymotrypsin solution to
liquify mucus before it can be aspirated. , umetimes, two
incisions are made in the tympanic membrane, one in
the antero-inferior and the other in antero-superior
quadrant, to aspirate thick, glue-like secretions (Fig.
10.3) on "beer-can" principle.2. Grommet insertion. If myringotomy and aspiration
combined with medical measures has not helped
and fluid recurs, a grommet is inserted to provide continued
aeration of middle ear (Fig. 10.4). It is left in place
for weeks or months or till it is spontaneously extruded.
3. Tympanotomy or cortical mastoidectomy. It is
sometimes required for removal of loculated chick fluid or
other associated pathology such as cholesterol granuloma.
4. Surgical treatment of causative factor. Adenoidectomy,
tonsillectomy and/or wash-out of maxillary
antra, may be required. This is usually done at the time
of myringotomy.
Sequelae of Chronic Secretory Otitis Media
1. Atrophic tympanic membrane and atelectasis of
the middle ear. In prolonged effusions, there is dissolution
of fibrous layer of tympanic membrane. It becomes
thin and atrophic and retracts into the middle ear.
2. Ossicular necrosis. Most commonly, long process
of incus gets necrosed. Sometimes, stapes superstructure
also gees necrosed. This increases the conductive hearing
loss to more than 50 dB.
3. Tympanosclerosis. Hya linised collagen with chalky deposits
may be seen in tympanic membrane, around the
ossicles or their joints, leading to their fixation.
4. Retraction pockets and cholesteatoma. Thin
atrophic part of parS tensa may get invaginated to form
retraction pockets or cholesteatoma. Sim dar pockets
may be seen in the a ttic region.
5. Cholesterol granuloma. This is due to stasis of
secre tions in middle ear and mastoid.
ACUTE NECROTISING OTITIS MEDIA
It is a variety of acute suppurative otitis media, often
seen in children suffering from measles, scarlet fever or
influenza. Causative organism is b -haemolytic streptococcus.
There is rapid destruction of whole of tympanic
membrane with its annulus, mucosa of promontory, ossicular
chain and even mastoid air cells. There is profuse
otorrhoea. In these cases, healing is followed by fibrosi ~
or ingrowth of squamous epithelium from the meatu:;
(secondary acquired cholesteatoma).
Treatment is early institution of antibac terial therapy.
It is continued for at least 7-10 days, even if response i
seen early. Cortical mastoidectomy may be indicated ('
medical treatment fails to control or the condition g rcomplicated
by acute mastoiditis.
seen in children suffering from measles, scarlet fever or
influenza. Causative organism is b -haemolytic streptococcus.
There is rapid destruction of whole of tympanic
membrane with its annulus, mucosa of promontory, ossicular
chain and even mastoid air cells. There is profuse
otorrhoea. In these cases, healing is followed by fibrosi ~
or ingrowth of squamous epithelium from the meatu:;
(secondary acquired cholesteatoma).
Treatment is early institution of antibac terial therapy.
It is continued for at least 7-10 days, even if response i
seen early. Cortical mastoidectomy may be indicated ('
medical treatment fails to control or the condition g rcomplicated
by acute mastoiditis.
ACUTE SUPPURATIVE OTITIS MEDIA
It is an acute inflammation of middle ear by pyogenic
organisms. Here, middle ear implies middle ear cleft, i.e.
eustachian tube, middle ear, attic, aditus, antrum and
mastoid air cells.
Aetiology
It is more common especially in infants and children of
lower socio-economic group. Typically, the disease follows
viral infection of upper respiratory tract but soon the
pyogenic organisms invade the middle ear.
Routes of Infection
1. Via eustachian tube. It is the most common route.
Infection travels via the lumen of the tube or along subepith
elial peritubal lymphatics. Eustachian tube in infants
and young children is shorter, wider and more horizontal
and thus may account for higher incidence of infections
n this age group. Breast or bottle feeding in a young
infant in horizontal position may force fluids through the
tube into the middle ear and hence the need to keep the
infant propped up with head a little higher. Swimming
nd diving can also force water through the tube into the
middle ear.
2. Via external ear. Traumatic perforations of tymp
anic membrane due to any cause open a route to middle
ill infection.
3. Blood-borne. This is an uncommon route.
Predisposing Factors
Anything that interferes with normal functioning of eusta-
chian tube predisposes to middle ear infection. It could be:
1.Recurrent attacks of common cold, upper respiratory
tract infections, and exanthematous fevers like
measles, diphtheria, whooping cough.
2.Infections of tonsils and adenoids.
3.Chronic rhinitis and sinusitis.
4.Nasal allergy.
5. Tumours of nasopharynx, packing of nose or
nasopharynx for epistaxis.
6 Cleft palate.
Bacteriology. Most common organisms in infants and
young children are Streptococcus pneumoniae (30%),
Haemophilus influenzae (20%) and Moraxella catarrhalis
U 2%). Other organisms include Streptococcus pyogenes,
Staphylococcus aureus and sometimes Pseudomonas aerugnosa.
In about 18-20%, no growth is seen. Many of
[he strains of H. inJluenzae and MoraxelLa cawrrhalis are
b -lactamase producing.
Pathology and Clinical Features
The disease runs through the follOWing stages:
1. Stage of tubal occlusion
2. Stage: of pre-suppuration
3. Stage of suppuration
4. Stage of resolution or complication
1. Stage of tubal occlusion. Oedema and hyperaemia
of nasopharyngeal end of eustachian tube blocks the tube,
leading to absorption of air and negative intratympanic
pressure. There is retraction of tympanic membrane with
some degree of effusion in the middle ear but fluid may not
be clinically apprC'ciable.
Symptoms. Deafness and earache are the two symptoms
but they are not marked. There is generally no fever.
Signs. Tympanic membrane is relracted with handle of
malleus assuming a more horizontal position, prominence
of lateral process of malleus and loss of light reflex.
Tuning fork tests show conductive deClfness.
2. Stage of pre-suppuration. If tubal occlusion is prolonged,
py0genic organisms invade tympanic cavity causing
hyperaemia of its lining. Inflammatory exudate appearS in
the middle ear. Tympanic membrane becomes congested.
Symptoms. Th re is marked earache which my disturb
sleep and is of throbbing n ature. Deafness and tinnitus
are a L~ o present, but complained only by adults.
Usually, ch ild runs high degree of fever and is restl ess.
Signs. To begin with, there is congestion of pars tensa.
Leash of blood vessels appear along the handle of malleus
and at the periphery of tympanic membrane imparting It
a cart-wheel appearance. Later, whole of tympanic membrane
incl uding pars flaccida becomes uniformly red.
Tuning fork tests will again show conductive type of
hearing loss.
3. Stage of suppuratio n. This is marked by formation
of p us in the middle ear and to some extent in mastoid
air cells. Tympanic membrane starts bulging to the
point of ruptu re.
Symptoms. Earache becomes excruciating. Deafne".increases,
child may run fever of 102-103°F. This may be
accompanied by vomiting and even convulsions.
Signs. Tympanic membrane appears red and bulging
with loss of landmarks. Handle of malleus may be engulfed
by the swollen and protruding tympanic memhrane and
may not he discernible. A yellow spot may be seen on the
tympanic membrane where rupture is imminent. In preantibiotic
era, one could see a nipple-like protrusion of
tympanic membrane with a yellow spot on its summit.
Tenderness may he eli cited over the mastoid antrum.
X-rays of mastoid will show clouding of air cells
because of exudate.
4. Stage of resolution. The tympanic membrane
rupture, with release of pus and subsidence of symptoms.
Inflammatory process begins to resol ve. If proper treatment
is started early or if the infection was mild, reso lution
may start even without rupture of tympanic membrane.
Symptoms. With evacuation of pus, earache is
relieved, fever comes down and ch ild feels better.
Signs . External auditory canal may contain blood tinged
discharge which later becomes mucopurulent. Usually, a
small perforation is seen in antero-inferior quadrant of
pars tensa. Hyperaemia of tympanic membrane begins to
subside with return to normal colour and landmarks.
5. Stage of complication. If virulence of organism is
high or resistance of patient poor, resolution may not take
place and disease spreads beyond the confines of middle ear.
It may lead to acute mastoiditis, subperiosteal abscess, facial
paralysis, labyrinth itis, petrositis, extradural abscess, meningitis,
brain absces or lateral sinus thromboph lebitis.
Treatment
1. Antibacterial therapy : It is indicated
in all cases with fever and severe earache. As the most common
organisms are Strert. pneumoniae and H. inj7uenzae,
the drugs which are effective in acute otitis media are
ampic illin (50 mg/kg/day in 4 divided doses), amoxicillin(40 mg/kg/day in 3 divided duses). Those allergic to these
penicillins can be given cefaclor, co-trimoxazole or
erythromycin. In cases where b-lactamase-producing H.
inj7uenzae or Moraxella cararrhalis are isolated, antibiotics
like amoxicillin-clavulanate, augmentin, cefuroxime axetil
or cefixime may be used. Antibacteria l therapy must
be continued for a minimum of 10 days, till tympanic
membrane regains normal appearance and hearing returns
to normaL Early discontinuance of therapy with relief of
earache and fever, or therapy given in inadequate doses
may lead to secretory otitis media and residual hearing loss.
2. Decongestant nasal drops. Ephedrine nose drops
(1 % in adults and 0.5% in children) or oxymetazoline
(Nasivion) or xylometazoline (Otrivin) should be used to
relieve eustachian tube oedema and promo te ventilation
of middle ear.
3. Oral nasal decongestants. Pseudoephedrine
(Sudafed) 30 mg twice daily or a combination of decongestant
and antihistaminic (Triominic) may achieve the
same result without resort to nasal drops which are difficult
to administer in children.
4. Analgesics and antipyretics. Paracetamol helps to
relieve pain and bring down temperature.
5. Ear toilet. If there is discharge in the ear, it is drymopped
with sterile cotton buds and a wick moistened
with antibiotic may be inserted.
6. Dry local heat. It helps to relieve pain.
7. Myringotomy. It is incising the drum to evacuate
pus and is indicated when (a) drum is bulging and there is
acute pain, (b) there is an incomplete resolution despite
antibiotics when drum remains full with persistent conductive
deafness, (C) there is persistent effusion beyond
12 weeks.
All cases of acute suppurative otitis media shou ld be
carefully followed till drum membrane returns to its normal
appearance and conductive deafness disappears
organisms. Here, middle ear implies middle ear cleft, i.e.
eustachian tube, middle ear, attic, aditus, antrum and
mastoid air cells.
Aetiology
It is more common especially in infants and children of
lower socio-economic group. Typically, the disease follows
viral infection of upper respiratory tract but soon the
pyogenic organisms invade the middle ear.
Routes of Infection
1. Via eustachian tube. It is the most common route.
Infection travels via the lumen of the tube or along subepith
elial peritubal lymphatics. Eustachian tube in infants
and young children is shorter, wider and more horizontal
and thus may account for higher incidence of infections
n this age group. Breast or bottle feeding in a young
infant in horizontal position may force fluids through the
tube into the middle ear and hence the need to keep the
infant propped up with head a little higher. Swimming
nd diving can also force water through the tube into the
middle ear.
2. Via external ear. Traumatic perforations of tymp
anic membrane due to any cause open a route to middle
ill infection.
3. Blood-borne. This is an uncommon route.
Predisposing Factors
Anything that interferes with normal functioning of eusta-
chian tube predisposes to middle ear infection. It could be:
1.Recurrent attacks of common cold, upper respiratory
tract infections, and exanthematous fevers like
measles, diphtheria, whooping cough.
2.Infections of tonsils and adenoids.
3.Chronic rhinitis and sinusitis.
4.Nasal allergy.
5. Tumours of nasopharynx, packing of nose or
nasopharynx for epistaxis.
6 Cleft palate.
Bacteriology. Most common organisms in infants and
young children are Streptococcus pneumoniae (30%),
Haemophilus influenzae (20%) and Moraxella catarrhalis
U 2%). Other organisms include Streptococcus pyogenes,
Staphylococcus aureus and sometimes Pseudomonas aerugnosa.
In about 18-20%, no growth is seen. Many of
[he strains of H. inJluenzae and MoraxelLa cawrrhalis are
b -lactamase producing.
Pathology and Clinical Features
The disease runs through the follOWing stages:
1. Stage of tubal occlusion
2. Stage: of pre-suppuration
3. Stage of suppuration
4. Stage of resolution or complication
1. Stage of tubal occlusion. Oedema and hyperaemia
of nasopharyngeal end of eustachian tube blocks the tube,
leading to absorption of air and negative intratympanic
pressure. There is retraction of tympanic membrane with
some degree of effusion in the middle ear but fluid may not
be clinically apprC'ciable.
Symptoms. Deafness and earache are the two symptoms
but they are not marked. There is generally no fever.
Signs. Tympanic membrane is relracted with handle of
malleus assuming a more horizontal position, prominence
of lateral process of malleus and loss of light reflex.
Tuning fork tests show conductive deClfness.
2. Stage of pre-suppuration. If tubal occlusion is prolonged,
py0genic organisms invade tympanic cavity causing
hyperaemia of its lining. Inflammatory exudate appearS in
the middle ear. Tympanic membrane becomes congested.
Symptoms. Th re is marked earache which my disturb
sleep and is of throbbing n ature. Deafness and tinnitus
are a L~ o present, but complained only by adults.
Usually, ch ild runs high degree of fever and is restl ess.
Signs. To begin with, there is congestion of pars tensa.
Leash of blood vessels appear along the handle of malleus
and at the periphery of tympanic membrane imparting It
a cart-wheel appearance. Later, whole of tympanic membrane
incl uding pars flaccida becomes uniformly red.
Tuning fork tests will again show conductive type of
hearing loss.
3. Stage of suppuratio n. This is marked by formation
of p us in the middle ear and to some extent in mastoid
air cells. Tympanic membrane starts bulging to the
point of ruptu re.
Symptoms. Earache becomes excruciating. Deafne".increases,
child may run fever of 102-103°F. This may be
accompanied by vomiting and even convulsions.
Signs. Tympanic membrane appears red and bulging
with loss of landmarks. Handle of malleus may be engulfed
by the swollen and protruding tympanic memhrane and
may not he discernible. A yellow spot may be seen on the
tympanic membrane where rupture is imminent. In preantibiotic
era, one could see a nipple-like protrusion of
tympanic membrane with a yellow spot on its summit.
Tenderness may he eli cited over the mastoid antrum.
X-rays of mastoid will show clouding of air cells
because of exudate.
4. Stage of resolution. The tympanic membrane
rupture, with release of pus and subsidence of symptoms.
Inflammatory process begins to resol ve. If proper treatment
is started early or if the infection was mild, reso lution
may start even without rupture of tympanic membrane.
Symptoms. With evacuation of pus, earache is
relieved, fever comes down and ch ild feels better.
Signs . External auditory canal may contain blood tinged
discharge which later becomes mucopurulent. Usually, a
small perforation is seen in antero-inferior quadrant of
pars tensa. Hyperaemia of tympanic membrane begins to
subside with return to normal colour and landmarks.
5. Stage of complication. If virulence of organism is
high or resistance of patient poor, resolution may not take
place and disease spreads beyond the confines of middle ear.
It may lead to acute mastoiditis, subperiosteal abscess, facial
paralysis, labyrinth itis, petrositis, extradural abscess, meningitis,
brain absces or lateral sinus thromboph lebitis.
Treatment
1. Antibacterial therapy : It is indicated
in all cases with fever and severe earache. As the most common
organisms are Strert. pneumoniae and H. inj7uenzae,
the drugs which are effective in acute otitis media are
ampic illin (50 mg/kg/day in 4 divided doses), amoxicillin(40 mg/kg/day in 3 divided duses). Those allergic to these
penicillins can be given cefaclor, co-trimoxazole or
erythromycin. In cases where b-lactamase-producing H.
inj7uenzae or Moraxella cararrhalis are isolated, antibiotics
like amoxicillin-clavulanate, augmentin, cefuroxime axetil
or cefixime may be used. Antibacteria l therapy must
be continued for a minimum of 10 days, till tympanic
membrane regains normal appearance and hearing returns
to normaL Early discontinuance of therapy with relief of
earache and fever, or therapy given in inadequate doses
may lead to secretory otitis media and residual hearing loss.
2. Decongestant nasal drops. Ephedrine nose drops
(1 % in adults and 0.5% in children) or oxymetazoline
(Nasivion) or xylometazoline (Otrivin) should be used to
relieve eustachian tube oedema and promo te ventilation
of middle ear.
3. Oral nasal decongestants. Pseudoephedrine
(Sudafed) 30 mg twice daily or a combination of decongestant
and antihistaminic (Triominic) may achieve the
same result without resort to nasal drops which are difficult
to administer in children.
4. Analgesics and antipyretics. Paracetamol helps to
relieve pain and bring down temperature.
5. Ear toilet. If there is discharge in the ear, it is drymopped
with sterile cotton buds and a wick moistened
with antibiotic may be inserted.
6. Dry local heat. It helps to relieve pain.
7. Myringotomy. It is incising the drum to evacuate
pus and is indicated when (a) drum is bulging and there is
acute pain, (b) there is an incomplete resolution despite
antibiotics when drum remains full with persistent conductive
deafness, (C) there is persistent effusion beyond
12 weeks.
All cases of acute suppurative otitis media shou ld be
carefully followed till drum membrane returns to its normal
appearance and conductive deafness disappears
Tympanoplasty
Tympanoplasty
It is an operation to (I) emdicme disease in the middle car
and ( ii) to rec.on stnict heming mechanism. It may be combmcd
wirh mastOldectomy if disease proce~s so nen1~li n s .
TYr€'". of minnie ear reconstructi.on dcpcnJs on r.he d(lm(lge
present in the ea r. The procedure m(lY be limited only to
repair of tympanic memhrane (myringoplast),), or to reconstruc
tion of oss icular chain (ossicuioplaslY), or both (l)'m-
1}{1T1lJl)U1.~t),). Reconsffilcrive surgery of the car has heen
gready facihcared by development of opcrating microscope,
microsurgical instruments and hi(Kompatible implant
materials.
Front the ph)'1'iiology uf hearing mech anism, the follow~
ing principles can be ded uced Lo reslOre hearing surgicillly:(i) An intact tympanic memhrane, to provide large
hydraulic ralio between the rympanic membrane
and stapes f(.:x) tplate.
(ii) Ossicular chain , to conduct sound from tympa nic
membrane ro (he oval window.
( iii) Two funcCluning windows, one 011 the scala veslibuli
([0 receJve sound vibrations) ~nd lhe other on the
scala rympani (to act as <.I re lief window). If it is only
one Window, as in smpes fixation or closurc of round
Window, (here will he no movement uf cochlem
fluids re::.ultin~ in conductivt: he;)[lng loss.
(Lv) Acou.~ tic separation of twO wirnlool.l's, so that sound
does not" reach bo th the 'windows simultaneo usly.
It can be achie ved by providlllg an inrac t tympanic
membrane, prefe re ntia l I,athway to o ne window
(usually the uvcd.) by providing o~::;icu lar c hain and
by the prese nc.e of air in thc miJdle e~r.
(v) Functioning cus wchian tube) to provide J,er
(v i) A functioning sensorineum/ apparatus, I.e. t he
cochlca and Vllltb ncrv e.
Types of tympanoplasty. Wullstein c l ~ssi fied l ympano~
pl"sry into five types (Fig. S.2).
Type I De fcCl is perforation of tympanic membrane
which i1'i repaired with a graCe It i~ also cill l~rI
myringoplasLY.
Type II Defect is perforation of tymparuc: mc: mhl~lte
with ero~iO n of m~lIel..1s. Uraft is placed un the
incus o r rt:rnn~nt of malleus.
Type III M""eu, and incus are ahscnt. Gra(t is placed
di recd y on the stapes head . it is als() called
mY"ingostapcdiopcX)' flf" columella tympano·
plasty.
T ype IV Only the (ootplutc of stapes is present. Ir is
exposcJ LO the eXTernal ear, and grafr is placed
between the oval and round wiuJows. A narrowmiddle e-al (cClvum minor) is rhus ereattn , to
h~V(' ~n nir pocket around rhe round willdow. A
mlK'( )Sn~ l iTleJ SI);)CC cx(ends from the eustachian
(Ube ro [he round window. Sound wa vc~ in this
case ::let di recrly on the footp late whil ~ the
rou nd window h as been shielded.
Type V Stapes footplate is fix ed hllr round wLndow i::;
iunctioning. In such ('8~CS, another window is
crerlteJ un hOfl2ontal semlC ircular canal and
covered with rt graft. A lso catted fenestration
operation .
Several modificat ions h", ve rJPpeared in the above
classificarion and they mainly perta in [U lhe types of
ossiculnr reconstruction.
My ringoplasty. It is tepair
It is an operation to (I) emdicme disease in the middle car
and ( ii) to rec.on stnict heming mechanism. It may be combmcd
wirh mastOldectomy if disease proce~s so nen1~li n s .
TYr€'". of minnie ear reconstructi.on dcpcnJs on r.he d(lm(lge
present in the ea r. The procedure m(lY be limited only to
repair of tympanic memhrane (myringoplast),), or to reconstruc
tion of oss icular chain (ossicuioplaslY), or both (l)'m-
1}{1T1lJl)U1.~t),). Reconsffilcrive surgery of the car has heen
gready facihcared by development of opcrating microscope,
microsurgical instruments and hi(Kompatible implant
materials.
Front the ph)'1'iiology uf hearing mech anism, the follow~
ing principles can be ded uced Lo reslOre hearing surgicillly:(i) An intact tympanic memhrane, to provide large
hydraulic ralio between the rympanic membrane
and stapes f(.:x) tplate.
(ii) Ossicular chain , to conduct sound from tympa nic
membrane ro (he oval window.
( iii) Two funcCluning windows, one 011 the scala veslibuli
([0 receJve sound vibrations) ~nd lhe other on the
scala rympani (to act as <.I re lief window). If it is only
one Window, as in smpes fixation or closurc of round
Window, (here will he no movement uf cochlem
fluids re::.ultin~ in conductivt: he;)[lng loss.
(Lv) Acou.~ tic separation of twO wirnlool.l's, so that sound
does not" reach bo th the 'windows simultaneo usly.
It can be achie ved by providlllg an inrac t tympanic
membrane, prefe re ntia l I,athway to o ne window
(usually the uvcd.) by providing o~::;icu lar c hain and
by the prese nc.e of air in thc miJdle e~r.
(v) Functioning cus wchian tube) to provide J,er
(v i) A functioning sensorineum/ apparatus, I.e. t he
cochlca and Vllltb ncrv e.
Types of tympanoplasty. Wullstein c l ~ssi fied l ympano~
pl"sry into five types (Fig. S.2).
Type I De fcCl is perforation of tympanic membrane
which i1'i repaired with a graCe It i~ also cill l~rI
myringoplasLY.
Type II Defect is perforation of tymparuc: mc: mhl~lte
with ero~iO n of m~lIel..1s. Uraft is placed un the
incus o r rt:rnn~nt of malleus.
Type III M""eu, and incus are ahscnt. Gra(t is placed
di recd y on the stapes head . it is als() called
mY"ingostapcdiopcX)' flf" columella tympano·
plasty.
T ype IV Only the (ootplutc of stapes is present. Ir is
exposcJ LO the eXTernal ear, and grafr is placed
between the oval and round wiuJows. A narrowmiddle e-al (cClvum minor) is rhus ereattn , to
h~V(' ~n nir pocket around rhe round willdow. A
mlK'( )Sn~ l iTleJ SI);)CC cx(ends from the eustachian
(Ube ro [he round window. Sound wa vc~ in this
case ::let di recrly on the footp late whil ~ the
rou nd window h as been shielded.
Type V Stapes footplate is fix ed hllr round wLndow i::;
iunctioning. In such ('8~CS, another window is
crerlteJ un hOfl2ontal semlC ircular canal and
covered with rt graft. A lso catted fenestration
operation .
Several modificat ions h", ve rJPpeared in the above
classificarion and they mainly perta in [U lhe types of
ossiculnr reconstruction.
My ringoplasty. It is tepair
Sudden Hearing loss
Sudden Hearing loss
Ir is deft ned <.I~ st'nsorinemal hearing \o::;s that has devel,
oped over a period of hours or a few d8Y::i. Loss may he
parrh)1 or co mplete:. Mos rly ir is unilateral. It may be
accompani_ed by tinnitus or remporary spell of ve rtigo.
Aetiology. Most ofren the cause of sudden deafness
remains obscure, in which Ci.-'lSC it is called rhe idiopathic
vari e ty. In such cases, three aetiological fac((Jr~ are
consitkrccl- viral, vascular or the rupture of cochlear
membranes. SponG.H H':ouS perilymph fistu lae may /()rm
in the oval or round winJow. Other aetiological factors
which C(luse sudden deafness rind lIllist be excluded 8re
listed b~ low. Remember [he mnf':monic "In The Very Em
Too No Mfljor Patho logy)).
1.
2.
3.
Infections. Mumps, herpes zoster, meningitis,
enc~phalitis) <;yphilis, otitis media.
Trauma. Heacf injury, ear operations, no ise trauma,
ba rotr~uma, spontaneous ruprure of cochlear
me mbran<::~.
Vascu1ar. Hacmonha~~e (leuk8e rnia) , embo lism Or
rhrombos is of l<.Iby rinthinc or coc hlr.,u artery or rh~ i r
vrlsospasm. They may be a::.~ciJ.ted with dmhr:tcs,
hypencnsion, polyeythaemi8, macroglobinacmia or
sickle edl (fair.
4. Ear (otologic). Menicr~'s disease, Cogan's syndrome.
large vesnhular aquecfuct.
5. Toxic. Ototoxic drugs, inscct1cldes.
6. N eoplastic. Acoustic neuroma. Ml"t
7. Miscellaneous. Multiple sclerosis, h ypothyroidlsm,
sarcoidosis.
8. Psychogenic.
Managemex1t. As far as possible, the aetio loJ;.:Y or."Iud,
den hearing loss shollid be Ji, covered by del " .Jed histO ry,
physical examinnrion and laboratory In vcstigatiLlP:". The
invesrigations l11r1y include ()udiomeuy, vestibular tes rs,
imaging studies of tL'mporal bonc:s , sedilDentation r8te,
rests for syphilis, di(lbe tc:s, h ypothyroidism , blood disor·
dets and lipid ptofiles. Some cases m
pecreJ . Where the cause stH! remains obsc ure, treatment
lS empirical and conslsts of:
1. n ed rcst.
2. Steroid therapy. Prednisolone 40--60 mg in " single
mo rning dose for one wet!k anJ then raileJ off in
II period of 3 weeks. Stero ids ate anti,inflamlDatory
and re lieve ceduna. They have been found usef,J!
in iJiopathic sllJJcn hearing loss of moderate
Jegree .
3. Inhalation of carbogen (5% CO2 + 95% 0,) .
It increases cochlear hlood flow and improves
oxygenation.
4. Vasodilator drugs.
5. Low molecular weight dextran. It decrea,es blood
viscosiTY. Ir is conrra,indlCatecl in cardiac failure and
bleedlng disorders.
6. Hyperbaric oxygen therapy. G iven in the firs(
month of o nset of hearing loss, some benefits h~ve
he en claimed.
Prognosis. Fortuna tely, ahout half rhe pa(iems of idiopathic
sen~orineura l hearing loss recover spomaneously
within 15 cla)ls. Chances of recovery
tigo ha v(~ poor prognosis. Younger patient'S- below 40 and
those with mcx1erate losses have better prugnosis.
Ir is deft ned <.I~ st'nsorinemal hearing \o::;s that has devel,
oped over a period of hours or a few d8Y::i. Loss may he
parrh)1 or co mplete:. Mos rly ir is unilateral. It may be
accompani_ed by tinnitus or remporary spell of ve rtigo.
Aetiology. Most ofren the cause of sudden deafness
remains obscure, in which Ci.-'lSC it is called rhe idiopathic
vari e ty. In such cases, three aetiological fac((Jr~ are
consitkrccl- viral, vascular or the rupture of cochlear
membranes. SponG.H H':ouS perilymph fistu lae may /()rm
in the oval or round winJow. Other aetiological factors
which C(luse sudden deafness rind lIllist be excluded 8re
listed b~ low. Remember [he mnf':monic "In The Very Em
Too No Mfljor Patho logy)).
1.
2.
3.
Infections. Mumps, herpes zoster, meningitis,
enc~phalitis) <;yphilis, otitis media.
Trauma. Heacf injury, ear operations, no ise trauma,
ba rotr~uma, spontaneous ruprure of cochlear
me mbran<::~.
Vascu1ar. Hacmonha~~e (leuk8e rnia) , embo lism Or
rhrombos is of l<.Iby rinthinc or coc hlr.,u artery or rh~ i r
vrlsospasm. They may be a::.~ciJ.ted with dmhr:tcs,
hypencnsion, polyeythaemi8, macroglobinacmia or
sickle edl (fair.
4. Ear (otologic). Menicr~'s disease, Cogan's syndrome.
large vesnhular aquecfuct.
5. Toxic. Ototoxic drugs, inscct1cldes.
6. N eoplastic. Acoustic neuroma. Ml"t
7. Miscellaneous. Multiple sclerosis, h ypothyroidlsm,
sarcoidosis.
8. Psychogenic.
Managemex1t. As far as possible, the aetio loJ;.:Y or."Iud,
den hearing loss shollid be Ji, covered by del " .Jed histO ry,
physical examinnrion and laboratory In vcstigatiLlP:". The
invesrigations l11r1y include ()udiomeuy, vestibular tes rs,
imaging studies of tL'mporal bonc:s , sedilDentation r8te,
rests for syphilis, di(lbe tc:s, h ypothyroidism , blood disor·
dets and lipid ptofiles. Some cases m
pecreJ . Where the cause stH! remains obsc ure, treatment
lS empirical and conslsts of:
1. n ed rcst.
2. Steroid therapy. Prednisolone 40--60 mg in " single
mo rning dose for one wet!k anJ then raileJ off in
II period of 3 weeks. Stero ids ate anti,inflamlDatory
and re lieve ceduna. They have been found usef,J!
in iJiopathic sllJJcn hearing loss of moderate
Jegree .
3. Inhalation of carbogen (5% CO2 + 95% 0,) .
It increases cochlear hlood flow and improves
oxygenation.
4. Vasodilator drugs.
5. Low molecular weight dextran. It decrea,es blood
viscosiTY. Ir is conrra,indlCatecl in cardiac failure and
bleedlng disorders.
6. Hyperbaric oxygen therapy. G iven in the firs(
month of o nset of hearing loss, some benefits h~ve
he en claimed.
Prognosis. Fortuna tely, ahout half rhe pa(iems of idiopathic
sen~orineura l hearing loss recover spomaneously
within 15 cla)ls. Chances of recovery
tigo ha v(~ poor prognosis. Younger patient'S- below 40 and
those with mcx1erate losses have better prugnosis.
Presbycusis
SensorLneural hcaring loss assoc iareci wirh phys iological
aging process in rhe ear is called presbycusls. It usually
lIlani(esls at: the age of 65 years bur may do so e.a.rly if
there is hereditary pred isposition) chronic noise exposure
or generalised vascu lar disease.
r our pathological types of presbyclls is ha ve been
identified.
1. Sensory. 'Ihis is characteri sed hy degeneration of
the organ of coni, starting at the hasal coil and progressing
gr aci lJ ~~ lly to the apex. Higher frequencies are affeCTed
bur speech discrimination remains good.
2. Neural. This i,s characterised by degeneration of
the ceLis of spiral ganglion. staning at the hl1.'i
ways may al::.o he tl ffecr.ed. Thi$ manifests Wilh high wnc
loss bllt speech di sc rimir'Hl1'joll is poor and Ollt of propor~
tion to the pure mne loss,
3. Strial or metj)bolie. This is charac terised byatro,
phy of stria vascularis tIl ali Lufns of coch lea. In this, t.he
physical ann chemiC-II processes of energy produc tion are
atfl~i.:ted. It runs in famili es. Audiogram ls flat hut speech
discrimin,nion is goud.
4. Cochlear conduct ive. This is due ro stiffening uf
the basilar memhrnne thus affecting its movements.
Audiogram is sloping Lype.
Pat ients of prcsbycusis hiJve great difficulty in hea ring
in thc presence of background noi se though (hey may
hear well in quiet surroundings. They may complain of
speech being heard but not understood. RecrLlinnent phe~
llomenon is pOSit ive and all the sounds suddenly become
iOLOierablc when volume is raised. Tinnitus is another
horhersome rrob lem and in some it is rhe only complaint.
Patients of presbycusis can be helped by a hearing aid.
They should also have lessons in speech reading through
visual cues. C unaitmenr. uf smoking and sriln lll nn(s like
tea and coffee Ulay help to decrease tinnitus.
aging process in rhe ear is called presbycusls. It usually
lIlani(esls at: the age of 65 years bur may do so e.a.rly if
there is hereditary pred isposition) chronic noise exposure
or generalised vascu lar disease.
r our pathological types of presbyclls is ha ve been
identified.
1. Sensory. 'Ihis is characteri sed hy degeneration of
the organ of coni, starting at the hasal coil and progressing
gr aci lJ ~~ lly to the apex. Higher frequencies are affeCTed
bur speech discrimination remains good.
2. Neural. This i,s characterised by degeneration of
the ceLis of spiral ganglion. staning at the hl1.'i
ways may al::.o he tl ffecr.ed. Thi$ manifests Wilh high wnc
loss bllt speech di sc rimir'Hl1'joll is poor and Ollt of propor~
tion to the pure mne loss,
3. Strial or metj)bolie. This is charac terised byatro,
phy of stria vascularis tIl ali Lufns of coch lea. In this, t.he
physical ann chemiC-II processes of energy produc tion are
atfl~i.:ted. It runs in famili es. Audiogram ls flat hut speech
discrimin,nion is goud.
4. Cochlear conduct ive. This is due ro stiffening uf
the basilar memhrnne thus affecting its movements.
Audiogram is sloping Lype.
Pat ients of prcsbycusis hiJve great difficulty in hea ring
in thc presence of background noi se though (hey may
hear well in quiet surroundings. They may complain of
speech being heard but not understood. RecrLlinnent phe~
llomenon is pOSit ive and all the sounds suddenly become
iOLOierablc when volume is raised. Tinnitus is another
horhersome rrob lem and in some it is rhe only complaint.
Patients of presbycusis can be helped by a hearing aid.
They should also have lessons in speech reading through
visual cues. C unaitmenr. uf smoking and sriln lll nn(s like
tea and coffee Ulay help to decrease tinnitus.
Vertigo
Disorders of vestibular system cause vertigo and are
divided into:
A. Peripheral, which involve vestibu lar end organs
and the ir first order neurons (i.e. the vesti bu lar nerve).
The cause lies in the internal ear or the Vlllth nerve.
They are responsib le for 85% of all cases of vertigo.
B. Central, which involve central nervous system
after the entrance of vestibular nerve in the brainstem
and involve vestibulo-ocular, vestibulo-spinal and other
central nervous system pathways.
Table 7.1 lists the common causes of vertigo of peripheral
and central origin.
A. PERIPHERAL VESTIBULAR DISORDERS
1. Meniere's disease (endolymphatic hydrops). It is
characterised by vertigo, f1uctuating hearing loss, tinnitus
and sense of pressure in the involved ear. Vertigo is of
sudden onset, las ts for a few minutes to 24 hours or so.
(The disease has been discussed on page 99).
2. Benign paroxysmal positional vertigo (BPPV). It
is characterised by vertigo when the head is placed in a
certain critical posi tion . There is no hearing loss or oth er
neurologic symptoms. Positional testing establishes the
diagnosis and helps to differentiate it from positional vertigo
of central origin (Table 7.1). Disease is caused by a disorder
of posterior semicircular canal though many patients
have history of head trauma and ear infection.
I t has been demonstrated that otoconial debris, consisting
of crystals of calcium carbonate, is released from the
degenerating macula of the utricle and f10ats freely in the
endolymph. When it se ttles on the cupula of posterior
Table 7.1 Vestibular disorders
Peripheral
(Lesions of end organs
vestibular nerve)
• Meniere's disease
• Benign paroxysmal
positiona l veliigo
• Vestibular neuron itis
• Labyrinthit is
• Vestibu lotoxic drugs
• Head trauma
• Perilymph fistula
• Syphilis
• Acoustic neuroma
Central
(Lesions of brainstem
and central connections)
• Veriebrobas ilar insuffi ciency
• Posterior inferior
cerebellar ariery syndrome
• Basilar mig raine
• Cerebellar disease
• Multiple sclerosis
• Tumours of brainstem and
fou rih ventricle
• Epilepsy
• Cervical veriigo
semicirc ular canal in a cr itical head position, it causes
displacement of the cupu la and vertigo. The vertigo is
fat iguable on assurning the same position repeatedly due
to dispersal of the otoconia but can be induced again
after a period of rest. Thus, typica l history and Hallpike
manoeuvre es tablishes the diagnosis.
The condition can be treated by performing Epley's
manoeuvre. The principle of this manoeuvre is to reposition
the otoconial debris from the posterior se micircular canal
back into the utricle. The doctor stands behind the patient
and the assistant on the side. The patient is made to sit on
the table so that when he is made to lie down, his head
is beyond the edge of the table as is done in Dix-Hallpike
manoeuvre. His face is turned 45° to the affected side.
The manoeuvre consis ts of five positions.
Position 1. With the head turned 45°, the patient is made
to lie down in head-hanging posi tion (DixHallpike
manoeuvre). It will cause vertigo and
nystagmus. Wait till vertigo and nys tagmus
subside.
Position 2. Head is now turned so that affec ted ear is up.
Position 3. The who'le body and head are now rorated
away from the affected ear to a la teral recumbent
posi tion in a face-down position.
Position 4. Patient is now brought to a Sitting pO,,'ition
with head st ill turned to the unaffected side::
hy 45°
Position 5. The head is now turned forward and chin
brought down 20°.
There should be a pause at each position till there is
no nystagmus or there is slowing of nystagmus, before
changing to the next posi tion. After manoeuvre is complete,
patient should maintain an upright posture for 48
hours. Eighty percent of the patients will he cured by
a single manoeuvre. If the patient remains symptomati c,
the manoeuvre can be repeated. A bone vibrator placed
on the mastoid bone helps to loosen the debris.
3. Vestibular neuronitis. It is charac terised by
severe vertigo of sudden onset with no cochlear symptoms.
Attacks may last from a few days to 2 or 3 weeks. It is
thought to occur due to a virus that attacks ves tibular
ganglion. Management of acute attack is similar to th at
in Meniere's disease. The disease is usually self-limiting.
4. Labvr inthitis. It has been discussed in detail on
page 79.
Circumscribed labyrinthitis is seen in cases of unsafe
type of CSOM, and fistu la test is positive.
Serous labyrinthitis is caused by trauma or infection
(viral or hacterial) adjacent to inner ear but without
45
DISEASES OF EAR
actual in vasion. There is severe vertigo and sensorineural
h earing loss. A partial or full recovery of inner ear functions
is possible if trcated early.
PLLndent labpinthitis is a complication of CSUM. There
is actual bacte rial in vr\sion of inner ear with total loss of
cochlear and vesl ibuLlr func tions. Vertigo in this condition
is due to acu te vestibular fa ilure. There is severe nausea
and vomiting. Ny~ ragnlll ~ is seen to the opposite side due
to destruction of the affected labyrinth .
5. Vestibulotoxic drugs. Several drugs cause otOtox icity
by dclll1:1ging the hair cells of the inner ear. Some primarily
affect the cochlear while others affect the vestibular
labyrinth. A minoglycoside antib iotic" p,m icularly strep tomycin,
gentamicin, kanamycin have he n shown to affect
hair cells of the crista <1mpullaris and to some extent those
of the maculae. Certain oth er drugs which cause dizziness
or unsteadiness are antihy pertens ives, labyrinthine sedatives,
oestrogen preparations, diuretics, antimicrobia ls
(nalidixic ac id, metronidazo le) and antima lar ia ls.
HoweVt'f, their mode of action may be diffe rent.
6. Head trauma. Head injury may cause concus:;ion
of labyrimh, complet' ly disrupt the bony labyrinth or
VIllth nerve, or cause a perilymph fistula. Severe
acoustic trauma, slich a:i th'lt caused by an explosion can
also disturh the vestibular end organ (oro liths) and result
in vertigo.
7. Perilymph fistula. In this condition, perilymph
leaks into the middle ear through the oval or round window.
It can follow as a complication of stapedectomy, or ear
surgery when siapes is accidenta lly dislocated. It can also
result from sudden prc:- ure changes in the middle ear (t- .cz
barotrau ma, diving, forceful Valsalva) or raised intracranial
prellsure (weightlifting or vigorous coughing). A perilymph
fistula causes intermittent verLigo 8nd fluctuating
sensorineural hearing loss, sometimes wi th tinnit us and
sense of fulln ess in the ear (compare Meniere's disease ).
8. Sypbilis. Syphilis of inner ear, both acquired and
congenital, causes dizzines in addition tn .ensorineural
hearing loss. Late congenital syphilis uSllally manifesting
between 8 and 20 years, mimics Meniere's disease with
episodes of acute vertigo, sensorineural hearing loss and
tinnitus. Hennebe rt 's ign, i.e. a positive fistula test in the
presence of an intact tympanic memhrane, is present in
congenital syphilis. Neurosyphilis (tertiary acquired) can
cause central type of vestibular dysfunctiun.
9. Acoustic neuroma. It has been cia-sified in peripheral
vestibu lar disorders as it arises from CN VIII within
internal acoll stic meatus. It causes only unstead iness or
vague sensation of motion. Severe episod ic vertigo, as s n
in the end organ disease, is usually miss in g. (For details
refer Chapter 18) .
Other tumours of temporal bone (e. g. glomus tumour,
carcinoma of external or midd le ear and secondaries) ,
destroy the labyrinth directly and cau. e vertigo.
B. CENTRAL VESTIBULAR DISORDERS
1. Vertebrobasilar insufficiency. It is a common cause
of central vertigo in patients over the age of 50 years.
There is transient decrease in cerebral blood flow. Common
cause is atherosclerosis. Ischaemia in these patients may
also be preCipitated by hypotension or neck movements
when cervical os teophytes press on the vertebral a rte ries
during rotat ion and extension of head.
Vertigo is a brupt in onset, lasts several minutes and is
assoc iated with n ausea and vomiting. Other ne urological
symptoms like visual disturbances, drop attacks, diplopia,
hemianopia, dysphagia, hemiparesis resulting from ischaemia
to other areas of brain may also accompany ve rtigo.
Some patients only compla in of intermittent attacks
of d izzine s or vertigo on lateral rotation and extension of
head .
2. Posterior inferior cerebellar artery syndrome
(Wall('nberg's syndrome). Thrombos is of the posterior
in fe rior cerebellar artery cuts off blood supply to late ral
medullary area. There is violent vertigo along with diplopia,
dysphagia, hoarseness of voice, Horner's syndrome, sensory
loss on ipsilateral side of face and contralateral side of the
body, and ataxia. There may be horizontal or ro tatory
nys tagmus to the side of the les ion.
3. Basilar migraine. Migraine is a vascular syndrome,
producing recurrent headaches with symptom-free intervals.
Headache is usually unilateral and of the throbbing
type. Basilar artery migra ine produces occipital headache,
visua l disturbances, diplopia and severe vertigo which
is abrupt and may last for 5- 60 minutes. Basilar migraine
is common in adolescent girls with strong menstrual
relationship and positive family history.
4. Cerebellar disease. Cerebellum may be affected
by haemorrhage (hypertension), infarction (occlusion of
arterial supply) , infection (otogenic cerebellar abscess ) or
tumours (glioma, teratoma or haemangioma). Acute cerebellar
disease may cause severe vertigo, vomitin,g and atax ia
Simulating an ac ute periphera l laby rinthine diso rd er.
Tumours are slow grow ing and produce classical features
of ce rebellar disease, i. e. incoordination, past-pointing,
adiadokokinesia, rebound phenomenon, wide-based gait.
5. Multiple sclerosis. It is a demyelinating disease
affecting young adults. Vertigo and dizziness are common
complaints. There are other multiple neurological signs
and symptoms, e.g. blurring or loss of vision, diplopia,
dysarthria, paraestheSia and ataxia. Spontaneous n ystagmus
may be seen. AcqU ired pendular n ystagmus, dissuciated
nys tagmus and vertical upbeat nystagmus are
important features in diagnosis.
6. Tumours of brainstem and floor of IVth ventricle.
Gliomas, astrocytomas may arise from pons and midbrain;
medulloblastoma, ep idymomas, epidermoid cysts or teratomas
may arise from floor of IVth ventricle. These
. g
h
\e
al
or
:e(
ia
er.
res
l.g,
lit.
ase
,on
:lns
) ia ,
.agiSOare
de.
a in;
terlese
tumours cause other neurological signs and symptoms in
addition to vertigo and dizziness. Positional vertigo and
nystagmus may also be the presenting features. cr scan and
magnetic resonance imaging are useful in their diagnosis.
7. Epilepsy. Vertigo may occur as an aura in temporal
lobe epilepsy. The history of seizure and/or unconscioLlsness
following the aura may help in the diagnos is.
Sometimes, vertigo is the only symptom of epilepsy and
that may pose a difficult diagnostic problem. E.E.G. may
show abnormalities during the attack.
8. Cervical vertigo. Vertigo may follow injuries of neck
7-10 days after the accident. It is usually provoked with
movements of neck to the side of injury. Examination shows
tenderness of neck, spasrns of cervical muscles and limi tation
of neck movements. X-rays show loss of cervical
lordosis. Exact mechanism of cervical ve rtigo is not known.
It may be due to disturbed vertebrobasil ar circulation ,
DISORDERS OF VESTI BULAR SYSTEM
involvement of sympathetic vertebral plexLls or alteration
of tonic neck reflexes.
Other Causes of Vertigo
Ocular vertigo. N orma lly, balance is mai ntained by
integrated information received from the eyes , labyrinths
and somatose nsory system. A mismatch of information
from any of these organs causes vertigo and in this case
from the eyes. Ocular vertigo may occur in case of acute
extraocular muscle paresis or high errors of refraction.
Psych genic vertigo. This diagnosis is suspected in
patients suffering from emotional tension and anxiety.
Often other symptoms of neurosis, e.g. palpitation, breathlessness,
fatigue, insomnia, profuse sweating and tremors are
also present. Symptom of vertigo is often vague in the form
of floating or swim.ming sensation or light-h eadedness.
The re is no nystagmus or hearing loss. Caloric test shows
an exaggerated response .
47
divided into:
A. Peripheral, which involve vestibu lar end organs
and the ir first order neurons (i.e. the vesti bu lar nerve).
The cause lies in the internal ear or the Vlllth nerve.
They are responsib le for 85% of all cases of vertigo.
B. Central, which involve central nervous system
after the entrance of vestibular nerve in the brainstem
and involve vestibulo-ocular, vestibulo-spinal and other
central nervous system pathways.
Table 7.1 lists the common causes of vertigo of peripheral
and central origin.
A. PERIPHERAL VESTIBULAR DISORDERS
1. Meniere's disease (endolymphatic hydrops). It is
characterised by vertigo, f1uctuating hearing loss, tinnitus
and sense of pressure in the involved ear. Vertigo is of
sudden onset, las ts for a few minutes to 24 hours or so.
(The disease has been discussed on page 99).
2. Benign paroxysmal positional vertigo (BPPV). It
is characterised by vertigo when the head is placed in a
certain critical posi tion . There is no hearing loss or oth er
neurologic symptoms. Positional testing establishes the
diagnosis and helps to differentiate it from positional vertigo
of central origin (Table 7.1). Disease is caused by a disorder
of posterior semicircular canal though many patients
have history of head trauma and ear infection.
I t has been demonstrated that otoconial debris, consisting
of crystals of calcium carbonate, is released from the
degenerating macula of the utricle and f10ats freely in the
endolymph. When it se ttles on the cupula of posterior
Table 7.1 Vestibular disorders
Peripheral
(Lesions of end organs
vestibular nerve)
• Meniere's disease
• Benign paroxysmal
positiona l veliigo
• Vestibular neuron itis
• Labyrinthit is
• Vestibu lotoxic drugs
• Head trauma
• Perilymph fistula
• Syphilis
• Acoustic neuroma
Central
(Lesions of brainstem
and central connections)
• Veriebrobas ilar insuffi ciency
• Posterior inferior
cerebellar ariery syndrome
• Basilar mig raine
• Cerebellar disease
• Multiple sclerosis
• Tumours of brainstem and
fou rih ventricle
• Epilepsy
• Cervical veriigo
semicirc ular canal in a cr itical head position, it causes
displacement of the cupu la and vertigo. The vertigo is
fat iguable on assurning the same position repeatedly due
to dispersal of the otoconia but can be induced again
after a period of rest. Thus, typica l history and Hallpike
manoeuvre es tablishes the diagnosis.
The condition can be treated by performing Epley's
manoeuvre. The principle of this manoeuvre is to reposition
the otoconial debris from the posterior se micircular canal
back into the utricle. The doctor stands behind the patient
and the assistant on the side. The patient is made to sit on
the table so that when he is made to lie down, his head
is beyond the edge of the table as is done in Dix-Hallpike
manoeuvre. His face is turned 45° to the affected side.
The manoeuvre consis ts of five positions.
Position 1. With the head turned 45°, the patient is made
to lie down in head-hanging posi tion (DixHallpike
manoeuvre). It will cause vertigo and
nystagmus. Wait till vertigo and nys tagmus
subside.
Position 2. Head is now turned so that affec ted ear is up.
Position 3. The who'le body and head are now rorated
away from the affected ear to a la teral recumbent
posi tion in a face-down position.
Position 4. Patient is now brought to a Sitting pO,,'ition
with head st ill turned to the unaffected side::
hy 45°
Position 5. The head is now turned forward and chin
brought down 20°.
There should be a pause at each position till there is
no nystagmus or there is slowing of nystagmus, before
changing to the next posi tion. After manoeuvre is complete,
patient should maintain an upright posture for 48
hours. Eighty percent of the patients will he cured by
a single manoeuvre. If the patient remains symptomati c,
the manoeuvre can be repeated. A bone vibrator placed
on the mastoid bone helps to loosen the debris.
3. Vestibular neuronitis. It is charac terised by
severe vertigo of sudden onset with no cochlear symptoms.
Attacks may last from a few days to 2 or 3 weeks. It is
thought to occur due to a virus that attacks ves tibular
ganglion. Management of acute attack is similar to th at
in Meniere's disease. The disease is usually self-limiting.
4. Labvr inthitis. It has been discussed in detail on
page 79.
Circumscribed labyrinthitis is seen in cases of unsafe
type of CSOM, and fistu la test is positive.
Serous labyrinthitis is caused by trauma or infection
(viral or hacterial) adjacent to inner ear but without
45
DISEASES OF EAR
actual in vasion. There is severe vertigo and sensorineural
h earing loss. A partial or full recovery of inner ear functions
is possible if trcated early.
PLLndent labpinthitis is a complication of CSUM. There
is actual bacte rial in vr\sion of inner ear with total loss of
cochlear and vesl ibuLlr func tions. Vertigo in this condition
is due to acu te vestibular fa ilure. There is severe nausea
and vomiting. Ny~ ragnlll ~ is seen to the opposite side due
to destruction of the affected labyrinth .
5. Vestibulotoxic drugs. Several drugs cause otOtox icity
by dclll1:1ging the hair cells of the inner ear. Some primarily
affect the cochlear while others affect the vestibular
labyrinth. A minoglycoside antib iotic" p,m icularly strep tomycin,
gentamicin, kanamycin have he n shown to affect
hair cells of the crista <1mpullaris and to some extent those
of the maculae. Certain oth er drugs which cause dizziness
or unsteadiness are antihy pertens ives, labyrinthine sedatives,
oestrogen preparations, diuretics, antimicrobia ls
(nalidixic ac id, metronidazo le) and antima lar ia ls.
HoweVt'f, their mode of action may be diffe rent.
6. Head trauma. Head injury may cause concus:;ion
of labyrimh, complet' ly disrupt the bony labyrinth or
VIllth nerve, or cause a perilymph fistula. Severe
acoustic trauma, slich a:i th'lt caused by an explosion can
also disturh the vestibular end organ (oro liths) and result
in vertigo.
7. Perilymph fistula. In this condition, perilymph
leaks into the middle ear through the oval or round window.
It can follow as a complication of stapedectomy, or ear
surgery when siapes is accidenta lly dislocated. It can also
result from sudden prc:- ure changes in the middle ear (t- .cz
barotrau ma, diving, forceful Valsalva) or raised intracranial
prellsure (weightlifting or vigorous coughing). A perilymph
fistula causes intermittent verLigo 8nd fluctuating
sensorineural hearing loss, sometimes wi th tinnit us and
sense of fulln ess in the ear (compare Meniere's disease ).
8. Sypbilis. Syphilis of inner ear, both acquired and
congenital, causes dizzines in addition tn .ensorineural
hearing loss. Late congenital syphilis uSllally manifesting
between 8 and 20 years, mimics Meniere's disease with
episodes of acute vertigo, sensorineural hearing loss and
tinnitus. Hennebe rt 's ign, i.e. a positive fistula test in the
presence of an intact tympanic memhrane, is present in
congenital syphilis. Neurosyphilis (tertiary acquired) can
cause central type of vestibular dysfunctiun.
9. Acoustic neuroma. It has been cia-sified in peripheral
vestibu lar disorders as it arises from CN VIII within
internal acoll stic meatus. It causes only unstead iness or
vague sensation of motion. Severe episod ic vertigo, as s n
in the end organ disease, is usually miss in g. (For details
refer Chapter 18) .
Other tumours of temporal bone (e. g. glomus tumour,
carcinoma of external or midd le ear and secondaries) ,
destroy the labyrinth directly and cau. e vertigo.
B. CENTRAL VESTIBULAR DISORDERS
1. Vertebrobasilar insufficiency. It is a common cause
of central vertigo in patients over the age of 50 years.
There is transient decrease in cerebral blood flow. Common
cause is atherosclerosis. Ischaemia in these patients may
also be preCipitated by hypotension or neck movements
when cervical os teophytes press on the vertebral a rte ries
during rotat ion and extension of head.
Vertigo is a brupt in onset, lasts several minutes and is
assoc iated with n ausea and vomiting. Other ne urological
symptoms like visual disturbances, drop attacks, diplopia,
hemianopia, dysphagia, hemiparesis resulting from ischaemia
to other areas of brain may also accompany ve rtigo.
Some patients only compla in of intermittent attacks
of d izzine s or vertigo on lateral rotation and extension of
head .
2. Posterior inferior cerebellar artery syndrome
(Wall('nberg's syndrome). Thrombos is of the posterior
in fe rior cerebellar artery cuts off blood supply to late ral
medullary area. There is violent vertigo along with diplopia,
dysphagia, hoarseness of voice, Horner's syndrome, sensory
loss on ipsilateral side of face and contralateral side of the
body, and ataxia. There may be horizontal or ro tatory
nys tagmus to the side of the les ion.
3. Basilar migraine. Migraine is a vascular syndrome,
producing recurrent headaches with symptom-free intervals.
Headache is usually unilateral and of the throbbing
type. Basilar artery migra ine produces occipital headache,
visua l disturbances, diplopia and severe vertigo which
is abrupt and may last for 5- 60 minutes. Basilar migraine
is common in adolescent girls with strong menstrual
relationship and positive family history.
4. Cerebellar disease. Cerebellum may be affected
by haemorrhage (hypertension), infarction (occlusion of
arterial supply) , infection (otogenic cerebellar abscess ) or
tumours (glioma, teratoma or haemangioma). Acute cerebellar
disease may cause severe vertigo, vomitin,g and atax ia
Simulating an ac ute periphera l laby rinthine diso rd er.
Tumours are slow grow ing and produce classical features
of ce rebellar disease, i. e. incoordination, past-pointing,
adiadokokinesia, rebound phenomenon, wide-based gait.
5. Multiple sclerosis. It is a demyelinating disease
affecting young adults. Vertigo and dizziness are common
complaints. There are other multiple neurological signs
and symptoms, e.g. blurring or loss of vision, diplopia,
dysarthria, paraestheSia and ataxia. Spontaneous n ystagmus
may be seen. AcqU ired pendular n ystagmus, dissuciated
nys tagmus and vertical upbeat nystagmus are
important features in diagnosis.
6. Tumours of brainstem and floor of IVth ventricle.
Gliomas, astrocytomas may arise from pons and midbrain;
medulloblastoma, ep idymomas, epidermoid cysts or teratomas
may arise from floor of IVth ventricle. These
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tumours cause other neurological signs and symptoms in
addition to vertigo and dizziness. Positional vertigo and
nystagmus may also be the presenting features. cr scan and
magnetic resonance imaging are useful in their diagnosis.
7. Epilepsy. Vertigo may occur as an aura in temporal
lobe epilepsy. The history of seizure and/or unconscioLlsness
following the aura may help in the diagnos is.
Sometimes, vertigo is the only symptom of epilepsy and
that may pose a difficult diagnostic problem. E.E.G. may
show abnormalities during the attack.
8. Cervical vertigo. Vertigo may follow injuries of neck
7-10 days after the accident. It is usually provoked with
movements of neck to the side of injury. Examination shows
tenderness of neck, spasrns of cervical muscles and limi tation
of neck movements. X-rays show loss of cervical
lordosis. Exact mechanism of cervical ve rtigo is not known.
It may be due to disturbed vertebrobasil ar circulation ,
DISORDERS OF VESTI BULAR SYSTEM
involvement of sympathetic vertebral plexLls or alteration
of tonic neck reflexes.
Other Causes of Vertigo
Ocular vertigo. N orma lly, balance is mai ntained by
integrated information received from the eyes , labyrinths
and somatose nsory system. A mismatch of information
from any of these organs causes vertigo and in this case
from the eyes. Ocular vertigo may occur in case of acute
extraocular muscle paresis or high errors of refraction.
Psych genic vertigo. This diagnosis is suspected in
patients suffering from emotional tension and anxiety.
Often other symptoms of neurosis, e.g. palpitation, breathlessness,
fatigue, insomnia, profuse sweating and tremors are
also present. Symptom of vertigo is often vague in the form
of floating or swim.ming sensation or light-h eadedness.
The re is no nystagmus or hearing loss. Caloric test shows
an exaggerated response .
47
Otosclerosis
Anatomy
It may be pertinent to re view the anatomy of the
labyrinth and introduce the terminology often used in
describing the labyrinth.
(i) Otic labyrinth. Also called membranous labyrinth
or endolymphatic labyrinth. It consists of utricle,
saccule, cochlea, semicircular ducts, endolymphatic
duct and sac It is filled with endolymph.
(ij) Periotic labyrinth or perilymphatic labyrinth (or
space). It surrounds the otic labyrinth and is filled
with perilymph. It includes vestibule, scala tympani,
sca la vestibuli, perilymphatic space of semicircular
canals and the periotic duct, which surrounds the
erlclolymphatic duct of otic labyrinth.
(iii) Otic capsule. It is the bony labyrinth. It has three
laye rs.
Endos ~e(ll. The innermost layer. It lines the bony
labyrinth.
Enchondral. Deve lops from the cartilage ancllater oss ifies
into bone. It is in this layer that some islands of cartilage
are left unoss ified that later give rise to otosclerosis.
Periosteal. Covers the bony labyrinth.
Otic capsule or the bony labyrinth oss ifies from 14
centres, the first one appears in the region of cochlea at
16 weeks and the last one appears in the postero lateral
part of posterior semicircular canal at 20th week.
Otosclerosis, more aptly called otospongws is, is a
primary disease of the bony labyrinth. In this, one or
more foci of irregularly laid spongy bone replace part of
normally dense enchondral layer of bony otic capsule.
Most often, otosc le rotic focus involves the stapes region
leading to stapes fixation and conductive deafness.
However, it may involve certain other areas of the bony
labyrinth whe re it may cause neurosensory loss, or no
symptoms at all.
Aetiology
The exact cause of otosclerosis is not known; however the
following facts have been documented.
Anatomical basis. Bony labyrinth is made of enchondral
bone which is subject to little change in life. But
sometimes, in this hard bone there are areas of cartilage
rests which, due to certain non-specific factors, are act ivated
to form new spongy bone. One such area is the fissula.
ante fene stram lying in front of the oval window- the
site of predilection for stapedial type of otospongiosis.
Heredity. About 50% of otoscl erotics have positive
family history; rest are sporadic Genetic studies reveal
that it is an autosomal dominant trait with incomplete
penetrance and variable express ivity.
Race. White races are affected more than Negros. It is
common in Indians but rare among Chinese and Japanese.
Sex. Females are affected twice as often as males but in
our country, otosclerosis seems to predominate in males.
Age of onset. Deafness usually starts between 20 and
30 yea rs of age and is rare before 10 and after 40 years.
Effect of other factors . Deafness due to otoscle rosis may
be initiated or made worse by pregnancy. Similarly, deafness
may increase during menopause, after an accident or
a major operation.
The disease may be associated with os teogenesis imperfecta
with histo ry of multiple fracture s. The triad of
symptoms of osteogenesis imperfecta, otoscleros is and
blue sclera, is called van der Hoeve s),ndrome. Lesions of
otic capsule seen in osteogenesis impelfecta are histologically
indistinguishable from those of otosclerosis and
both are due to genes encoding type I collagen.
Viral infection. Electron microscop ic and immunohistochemical
studies have shown RNA related to measle
virus. It is likely that otosclerosis is a viral disease as has
been suggested for Page t's disease.
Types of Otosclerosis
1. Stapedial otosclerosis. Stapedial otosc lerosis
causing stapes fixation and conductive deafness is the
most common variety. Here lesion starts just in front of
the oval window in an area called 'fissu la ante fenestram'.
This is the site of predilection (anterior focus).
Lesion may start behind the oval window (p os terior
focus), around the margin of the stapes foo tplate (circumferential),
in the footpl ate but annular ligament being
free (biscuit type). Sometimes, it may completely obliterate
the oval window niche (obliterative type) (Fig. 13.1).
2. Cochlear otosclerosis. Cochlear o tosclerosis
invo lves region of round windo~' or other areas in the
otic capsule, and may cause sensorineural hearing loss
probably due to liberation of toxic materials into the
inner ear fluid.
3. Histologic otosclerosis. This type of otosclerosis
remains asymptoma tic and causes neither conductive
nor se nsorineural hearing loss .
Pathology
Grossi)., otosclerotic Lesion appears chalky white, greyish
or yellow. Sometimes, it is red in colour due to increased
vascularity, in which case, the otosclerotic focus is active
and rapidly progress ive.
Microscopicall)" spongy bone appears in th.e normally
dense enchon.dral layer of otic capsule. In immature;1ctive lesions, there are numerous marrow and vascular
paces with plenty of osteoblasts and osteoclasts and a lot
of cement substance which stains blue (blue mantles)
vith haematoxylin-eosin stain. Mature foci show less
\'ascu larity and laying of more bone and more of fibrillar
,ubstance than cementum, and is stained red.
Symptoms
1. Hearing loss. This is the presenting symptom and
usually starts in twenties. It is painless and progressive with
Isidious onset. Often it is bilateral conductive type .
2. Paracusis willisii. An otosclerotic patient hears
better in noisy than quiet surroundings. This is because a
normal person will raise his voice in noisy surroundings.
3. Tinnitus. It is more commonly seen in cochlear
toscleros is and in active lesions.
4. Vertigo. It is an uncommon symptom.
5. Speech. Patient has a monotonous, well moduted
soft speech.
Signs
Tympanic membrane is quite normal and mobile.
Sometimes, a reddish hue may be seen on the promontory
through the tympanic membrane (Schwartze
sign). This is indicative of active focus with
increased vascularity.
Eustachian tube function is normal.
Tuning fork tests show negative Rinne (i.e.
BC > AC) first for 256 Hz and then 512 Hz and
still later, when stapes fixat ion is complete, for
1026 Hz. Weber test will be lateralised to the ear with
greater conductive loss. Absolute bone conductionmay be normal. It is decreased in cochlear otosclerosis
with sensorineural loss.
Pure tone audiometry shows loss of air conduction,
more for lower frequencies.
Bone conduction is normal. In some cases, there is a
dip in bone conduction curve. It is different at different
frequencies but maximum at 2000 Hz and is called the
Carhart's notch. (5 dB at 500 Hz, 10dB at 1000Hz, 15 dB
at 2000 Hz and 5 dB at 4000 Hz) (Fig. 13.2). Carhart's
notch disappears after successful stapedectomy.
Mixed hearing loss is not uncommon in otosclerosis.
There is loss in bone conduction with air-bone gap.
Speech audiometry reveals normal discrimination
score except in those with cochlear involvement.Tympanometry may be normal in early cases but later
shows as curve due to oss icular stiffness. Stapedial reflex
becomes absent when stapes is fixed.
Differential Diagnosis
Orosclerosis should be differenti ated from other causes of
conductive deafness particularly serous oti tis media,
adhesive otitis media, tympanosclerosis, attic fixation of
head of malleus, oss icular discontinuity or congenital
stapes fixation.
Treatment
Medical. There is no medical treatment that cures
otosclerosis. Sodium fluoride has been tried to hasten the
maturity of act ive focus and arrest further cochlear loss,
but controve rsies exist and this tre atment is not recommended
generally.
Surgical. Stapedectomy with prosthesis replacement
is the treatment of choice. Here the fixed otosclerotic
stapes is removed and a prosthesis inserted between
the incus and oval window (Fig. 13.3). Prosthesis employed
may be a teflon piston, stainless steel piston, platinum
teflon or titanium teflon piston (Fig. 13.4). In 90%
of patients, there is good improvement in hearing after
stapedectomy.
Selection of patients for stapes surgery. Hearing
threshold should be 30dB or worse (It is this level wnen
patient sta rts feeling socially handicapped).
Average air-bone gap should be at least 15 dB with
Rinne negat ive for 256 and 512 Hz.
Speech discrimination score should be 60% or more.
Contraindications to stapes surgery
(i) The only hearing ear.
(ii) Associated Meniere 's disease. When there is histo ry of
vert igo with clinical evidence of Meniere's d isease
in an otosclerotic patient, there are more chances of
sensorineural hearing loss after stapedectomy.(iii) Young children . Recurrent eustachian tube dysfunction
is common in children. It can displace the prosthesis
or cause acute otit is media. Also the growth of otoscle
rotic focus is faster in children leading to reclosure
of oval window.
(iv) Professional athletes, high construction workers, divers,
and frequent air-travellers. Stapes surgery has the risk
to cause post-operati ve ve rtigo and/or dizziness and
thus interfere with their profess ion; or frequent air
pressure changes may damage the hearing or cause
severe vertigo.
(v) Those who work in noisy surroundings . After stapedectomy,
they would be more vulnerable to get sensorineural
hearing loss due to noise trauma.
(v i) Otitis externa, tympanic membrane perforation and
exostosis are relative contra indications. Stapedectomy
can be done after they have been treated first for
above conditions. S imilarly, stapedectomy is avoided
during pregnancy.
The operation is preferably done under loca l anaesthesia.
Steps of stapedectomy (Fig. 13.5) include:
1. Meatal incision and elevation of the tympanomeatal
flap.
2. Exposure of stapes area . This may requ ire removal of
posterosuper ior bony overhang of the canaL
3. Removal of stapes superstructure.
4. Creation of a hole in the stapes footplate (stapedotomy)
or removal of a part offootplate (stapedectomy).
5. Placement of prosthesis.
6. Repositioning the tympanomeatal flap .
Two percent of patients undergoing this operation
may suffer sensorineural loss. Slowly progressive high frequency
loss is seen in long-term follow up. One in 200
patients may get a totally "dead" ear.
Stapes mobilisation is no longer done these days as it
gives temporary results; refixation being quite common.Lempert's fenestration operation is almost outdated n ow.
t-fere all. alternative window is created in the lateral
-.e micircular canal to function for the obliterated oval
" indow. It has the disadvantage of a post-operativemastoid cavity and an inherent hearing loss of 25 dB
which cannot be corrected.
Hearing aid. Patients who refuse surgery or are unfit for
surgery can use hearing a id. It is an effective alternative.
It may be pertinent to re view the anatomy of the
labyrinth and introduce the terminology often used in
describing the labyrinth.
(i) Otic labyrinth. Also called membranous labyrinth
or endolymphatic labyrinth. It consists of utricle,
saccule, cochlea, semicircular ducts, endolymphatic
duct and sac It is filled with endolymph.
(ij) Periotic labyrinth or perilymphatic labyrinth (or
space). It surrounds the otic labyrinth and is filled
with perilymph. It includes vestibule, scala tympani,
sca la vestibuli, perilymphatic space of semicircular
canals and the periotic duct, which surrounds the
erlclolymphatic duct of otic labyrinth.
(iii) Otic capsule. It is the bony labyrinth. It has three
laye rs.
Endos ~e(ll. The innermost layer. It lines the bony
labyrinth.
Enchondral. Deve lops from the cartilage ancllater oss ifies
into bone. It is in this layer that some islands of cartilage
are left unoss ified that later give rise to otosclerosis.
Periosteal. Covers the bony labyrinth.
Otic capsule or the bony labyrinth oss ifies from 14
centres, the first one appears in the region of cochlea at
16 weeks and the last one appears in the postero lateral
part of posterior semicircular canal at 20th week.
Otosclerosis, more aptly called otospongws is, is a
primary disease of the bony labyrinth. In this, one or
more foci of irregularly laid spongy bone replace part of
normally dense enchondral layer of bony otic capsule.
Most often, otosc le rotic focus involves the stapes region
leading to stapes fixation and conductive deafness.
However, it may involve certain other areas of the bony
labyrinth whe re it may cause neurosensory loss, or no
symptoms at all.
Aetiology
The exact cause of otosclerosis is not known; however the
following facts have been documented.
Anatomical basis. Bony labyrinth is made of enchondral
bone which is subject to little change in life. But
sometimes, in this hard bone there are areas of cartilage
rests which, due to certain non-specific factors, are act ivated
to form new spongy bone. One such area is the fissula.
ante fene stram lying in front of the oval window- the
site of predilection for stapedial type of otospongiosis.
Heredity. About 50% of otoscl erotics have positive
family history; rest are sporadic Genetic studies reveal
that it is an autosomal dominant trait with incomplete
penetrance and variable express ivity.
Race. White races are affected more than Negros. It is
common in Indians but rare among Chinese and Japanese.
Sex. Females are affected twice as often as males but in
our country, otosclerosis seems to predominate in males.
Age of onset. Deafness usually starts between 20 and
30 yea rs of age and is rare before 10 and after 40 years.
Effect of other factors . Deafness due to otoscle rosis may
be initiated or made worse by pregnancy. Similarly, deafness
may increase during menopause, after an accident or
a major operation.
The disease may be associated with os teogenesis imperfecta
with histo ry of multiple fracture s. The triad of
symptoms of osteogenesis imperfecta, otoscleros is and
blue sclera, is called van der Hoeve s),ndrome. Lesions of
otic capsule seen in osteogenesis impelfecta are histologically
indistinguishable from those of otosclerosis and
both are due to genes encoding type I collagen.
Viral infection. Electron microscop ic and immunohistochemical
studies have shown RNA related to measle
virus. It is likely that otosclerosis is a viral disease as has
been suggested for Page t's disease.
Types of Otosclerosis
1. Stapedial otosclerosis. Stapedial otosc lerosis
causing stapes fixation and conductive deafness is the
most common variety. Here lesion starts just in front of
the oval window in an area called 'fissu la ante fenestram'.
This is the site of predilection (anterior focus).
Lesion may start behind the oval window (p os terior
focus), around the margin of the stapes foo tplate (circumferential),
in the footpl ate but annular ligament being
free (biscuit type). Sometimes, it may completely obliterate
the oval window niche (obliterative type) (Fig. 13.1).
2. Cochlear otosclerosis. Cochlear o tosclerosis
invo lves region of round windo~' or other areas in the
otic capsule, and may cause sensorineural hearing loss
probably due to liberation of toxic materials into the
inner ear fluid.
3. Histologic otosclerosis. This type of otosclerosis
remains asymptoma tic and causes neither conductive
nor se nsorineural hearing loss .
Pathology
Grossi)., otosclerotic Lesion appears chalky white, greyish
or yellow. Sometimes, it is red in colour due to increased
vascularity, in which case, the otosclerotic focus is active
and rapidly progress ive.
Microscopicall)" spongy bone appears in th.e normally
dense enchon.dral layer of otic capsule. In immature;1ctive lesions, there are numerous marrow and vascular
paces with plenty of osteoblasts and osteoclasts and a lot
of cement substance which stains blue (blue mantles)
vith haematoxylin-eosin stain. Mature foci show less
\'ascu larity and laying of more bone and more of fibrillar
,ubstance than cementum, and is stained red.
Symptoms
1. Hearing loss. This is the presenting symptom and
usually starts in twenties. It is painless and progressive with
Isidious onset. Often it is bilateral conductive type .
2. Paracusis willisii. An otosclerotic patient hears
better in noisy than quiet surroundings. This is because a
normal person will raise his voice in noisy surroundings.
3. Tinnitus. It is more commonly seen in cochlear
toscleros is and in active lesions.
4. Vertigo. It is an uncommon symptom.
5. Speech. Patient has a monotonous, well moduted
soft speech.
Signs
Tympanic membrane is quite normal and mobile.
Sometimes, a reddish hue may be seen on the promontory
through the tympanic membrane (Schwartze
sign). This is indicative of active focus with
increased vascularity.
Eustachian tube function is normal.
Tuning fork tests show negative Rinne (i.e.
BC > AC) first for 256 Hz and then 512 Hz and
still later, when stapes fixat ion is complete, for
1026 Hz. Weber test will be lateralised to the ear with
greater conductive loss. Absolute bone conductionmay be normal. It is decreased in cochlear otosclerosis
with sensorineural loss.
Pure tone audiometry shows loss of air conduction,
more for lower frequencies.
Bone conduction is normal. In some cases, there is a
dip in bone conduction curve. It is different at different
frequencies but maximum at 2000 Hz and is called the
Carhart's notch. (5 dB at 500 Hz, 10dB at 1000Hz, 15 dB
at 2000 Hz and 5 dB at 4000 Hz) (Fig. 13.2). Carhart's
notch disappears after successful stapedectomy.
Mixed hearing loss is not uncommon in otosclerosis.
There is loss in bone conduction with air-bone gap.
Speech audiometry reveals normal discrimination
score except in those with cochlear involvement.Tympanometry may be normal in early cases but later
shows as curve due to oss icular stiffness. Stapedial reflex
becomes absent when stapes is fixed.
Differential Diagnosis
Orosclerosis should be differenti ated from other causes of
conductive deafness particularly serous oti tis media,
adhesive otitis media, tympanosclerosis, attic fixation of
head of malleus, oss icular discontinuity or congenital
stapes fixation.
Treatment
Medical. There is no medical treatment that cures
otosclerosis. Sodium fluoride has been tried to hasten the
maturity of act ive focus and arrest further cochlear loss,
but controve rsies exist and this tre atment is not recommended
generally.
Surgical. Stapedectomy with prosthesis replacement
is the treatment of choice. Here the fixed otosclerotic
stapes is removed and a prosthesis inserted between
the incus and oval window (Fig. 13.3). Prosthesis employed
may be a teflon piston, stainless steel piston, platinum
teflon or titanium teflon piston (Fig. 13.4). In 90%
of patients, there is good improvement in hearing after
stapedectomy.
Selection of patients for stapes surgery. Hearing
threshold should be 30dB or worse (It is this level wnen
patient sta rts feeling socially handicapped).
Average air-bone gap should be at least 15 dB with
Rinne negat ive for 256 and 512 Hz.
Speech discrimination score should be 60% or more.
Contraindications to stapes surgery
(i) The only hearing ear.
(ii) Associated Meniere 's disease. When there is histo ry of
vert igo with clinical evidence of Meniere's d isease
in an otosclerotic patient, there are more chances of
sensorineural hearing loss after stapedectomy.(iii) Young children . Recurrent eustachian tube dysfunction
is common in children. It can displace the prosthesis
or cause acute otit is media. Also the growth of otoscle
rotic focus is faster in children leading to reclosure
of oval window.
(iv) Professional athletes, high construction workers, divers,
and frequent air-travellers. Stapes surgery has the risk
to cause post-operati ve ve rtigo and/or dizziness and
thus interfere with their profess ion; or frequent air
pressure changes may damage the hearing or cause
severe vertigo.
(v) Those who work in noisy surroundings . After stapedectomy,
they would be more vulnerable to get sensorineural
hearing loss due to noise trauma.
(v i) Otitis externa, tympanic membrane perforation and
exostosis are relative contra indications. Stapedectomy
can be done after they have been treated first for
above conditions. S imilarly, stapedectomy is avoided
during pregnancy.
The operation is preferably done under loca l anaesthesia.
Steps of stapedectomy (Fig. 13.5) include:
1. Meatal incision and elevation of the tympanomeatal
flap.
2. Exposure of stapes area . This may requ ire removal of
posterosuper ior bony overhang of the canaL
3. Removal of stapes superstructure.
4. Creation of a hole in the stapes footplate (stapedotomy)
or removal of a part offootplate (stapedectomy).
5. Placement of prosthesis.
6. Repositioning the tympanomeatal flap .
Two percent of patients undergoing this operation
may suffer sensorineural loss. Slowly progressive high frequency
loss is seen in long-term follow up. One in 200
patients may get a totally "dead" ear.
Stapes mobilisation is no longer done these days as it
gives temporary results; refixation being quite common.Lempert's fenestration operation is almost outdated n ow.
t-fere all. alternative window is created in the lateral
-.e micircular canal to function for the obliterated oval
" indow. It has the disadvantage of a post-operativemastoid cavity and an inherent hearing loss of 25 dB
which cannot be corrected.
Hearing aid. Patients who refuse surgery or are unfit for
surgery can use hearing a id. It is an effective alternative.
Caldwell-Luc Operation
Caldwell-Luc operation is a process of opening the maxillary
antrum through canine fossa by sublabial approach
and dealing with the pathology inside the antrum.
Indications
1. Chronic maxillary sinusitis with irreversible changes
in the sinus mucosa.
2. Removal of foreign bodies or root of tooth.
3. Dental cyst.
4. Oroantral fistula.
5. Suspected neoplasm in the antrum and its biopsy.
6. Recurrent antrochoanal polyp.
7. Fracture of maxilla or blow-out fractures of the orbit.
8. As an approach to ethmoids (Horgan's transantral
ethmoidectomy) .
9. Approach to pterygopalatine fossa for ligation of
maxillary artery.
10. Vidian neurectomy.
Contra indications
Patient below 17 years of age.
Anaesthesia
General anaesthesia with cuffed endotracheal tube and a
pharyngeal pack. Can be done under local anaesthesia.
Position
Reclining with head-end of the table raised. Patient lies
supine with face turned slightly to the opposite side.
Technique
1. Incision. A horizontal incision with its ends upward
is made below the gingivolabial sulcus, from lateral incisor
A
to the 2nd molar (Fig. 82.1). It cuts through mucous
membrane and periosteum.
2. Elevation of flap. The mucoperiosteal flap is raised
from the canine fossa to the infraorbital nerve avoiding
injury to the nerve .
3. Opening the antrum. Using cutting burr or gouge
and hammer, a hole is made in the antrum. Opening is
enlarged using Kerrison's punch.
4. Dealing with pathology. Once maxillary antrum
has been opened, pathology is removed. Diseased antral
mucosa can be removed with elevators, curettes and
forceps. Cyst, benign tumour, foreign body or a polyp is
removed .
5. Making nasoantral window. A curved haemostat
is pushed into the antrum from the inferior meatus and
then this opening is enlarged with Kerrison's and sidebiting
forceps to make a window, 1.5 cm in diameter.
6. Packing the antrum. Rihhon gauze. impregnated
with liquid paraffin or Furacin ™ (Furacin ™ is 0.2% w/w
nitrofurazone) ointment can be packed in the antrum
and its end brought out from the nasoantral window into
the nose. Intrasinus packing is done if there is severe
bleeding. Pack is also kept in the nose.
7. Closure of wound. Sublabial incision is closed
with one or two catgut sutures.
Post-operative Care
1. Ice packs over the cheek in the fi rst 24 hours prevent
oedema. haematoma and discomfort to the patient.
2. Packing in the sinus and nose can be removed in
24-48 hours.3. Antibiotics are given for 5-7 days.
4. Patient should avoid blowing his nose for 2 weeks to
avoid surgical emphysema.
Complications
1. Post-operative bleeding. This can be controlled by
nasal pack.
2. Anaesthesia of the cheek due to stretching of
infraorbital nerve. It may last for a few weeks or
months.
3. Anaesthesia of teeth.
4. Injury to nasolacrimal duct.
5. Sublabial fistula .
6. Osteomyelitis of maxilla (rare).
antrum through canine fossa by sublabial approach
and dealing with the pathology inside the antrum.
Indications
1. Chronic maxillary sinusitis with irreversible changes
in the sinus mucosa.
2. Removal of foreign bodies or root of tooth.
3. Dental cyst.
4. Oroantral fistula.
5. Suspected neoplasm in the antrum and its biopsy.
6. Recurrent antrochoanal polyp.
7. Fracture of maxilla or blow-out fractures of the orbit.
8. As an approach to ethmoids (Horgan's transantral
ethmoidectomy) .
9. Approach to pterygopalatine fossa for ligation of
maxillary artery.
10. Vidian neurectomy.
Contra indications
Patient below 17 years of age.
Anaesthesia
General anaesthesia with cuffed endotracheal tube and a
pharyngeal pack. Can be done under local anaesthesia.
Position
Reclining with head-end of the table raised. Patient lies
supine with face turned slightly to the opposite side.
Technique
1. Incision. A horizontal incision with its ends upward
is made below the gingivolabial sulcus, from lateral incisor
A
to the 2nd molar (Fig. 82.1). It cuts through mucous
membrane and periosteum.
2. Elevation of flap. The mucoperiosteal flap is raised
from the canine fossa to the infraorbital nerve avoiding
injury to the nerve .
3. Opening the antrum. Using cutting burr or gouge
and hammer, a hole is made in the antrum. Opening is
enlarged using Kerrison's punch.
4. Dealing with pathology. Once maxillary antrum
has been opened, pathology is removed. Diseased antral
mucosa can be removed with elevators, curettes and
forceps. Cyst, benign tumour, foreign body or a polyp is
removed .
5. Making nasoantral window. A curved haemostat
is pushed into the antrum from the inferior meatus and
then this opening is enlarged with Kerrison's and sidebiting
forceps to make a window, 1.5 cm in diameter.
6. Packing the antrum. Rihhon gauze. impregnated
with liquid paraffin or Furacin ™ (Furacin ™ is 0.2% w/w
nitrofurazone) ointment can be packed in the antrum
and its end brought out from the nasoantral window into
the nose. Intrasinus packing is done if there is severe
bleeding. Pack is also kept in the nose.
7. Closure of wound. Sublabial incision is closed
with one or two catgut sutures.
Post-operative Care
1. Ice packs over the cheek in the fi rst 24 hours prevent
oedema. haematoma and discomfort to the patient.
2. Packing in the sinus and nose can be removed in
24-48 hours.3. Antibiotics are given for 5-7 days.
4. Patient should avoid blowing his nose for 2 weeks to
avoid surgical emphysema.
Complications
1. Post-operative bleeding. This can be controlled by
nasal pack.
2. Anaesthesia of the cheek due to stretching of
infraorbital nerve. It may last for a few weeks or
months.
3. Anaesthesia of teeth.
4. Injury to nasolacrimal duct.
5. Sublabial fistula .
6. Osteomyelitis of maxilla (rare).
Myringoplasty
Closure of perforation of pars tensa of the tympanic membrane
is called myringoplasty. It has the advantage of:
(i) restoring the hearing loss and in some cases the
tinnitus.
(ii) checking re-infection from external auditory canal
and eustachian tube (nasopharyngeal infection
ascends easily via eustachian tube in the presence
of perforation than otherwise).
(iii) checking aeroallergens reaching the exposed middle
ear mucosa, leading to persistent ear discharge.
Myringoplasty can be combined with ossicular reconstruction
when it is called tympanoplasty.
Physiologic principles for middle ear reconstruction
are discussed on page 32.
Contra indications
(i) Active discharge from the middle ear.
(ii) Nasal allergy. It should be brought under control
before surgery.
(iii) Otitis extema.
(iv) Ingrowth of squamous epithelium into the middle
ear. In such cases, excision of squamous epithelium
from the middle ear or a tympanomastoidectomy
may be required.
(v) When the other ear is dead or not suitable for
hearing aid rehabilitation.
(vi) Children below 3 years.
Anaesthesia
Local or general, the former is preferred.
Position
Supine with face turned to one side; the ear to be operated
is up.
Graft materials used are:
(i) Temporalis fascia (most common),
(ii) Perichondrium from the tragus,
(iii) Tragal cartilage,
(iv) Vein.
Incision for exposure of tympanic membrane depends
on the size of the ear canal; it may be endomeatal, endaural
or posta ural.
Technique
Underlay Technique
1. Harvesting the graft of temporal is fascia or perichondrium
from the tragus.
2. Preparing the T.M. for grafting. An incision is
made along the edge of perforation and the ring of
epithelium removed. Remove also a strip of mucosal
layer from the inner side of perforation.
3. Inspecting the middle ear. A stapes-type incision
is made and the tympanomeatal flap raised to see the
integrity and mobility of the ossicular chain and to
ensure that no squamous epithelium has grown into the
middle ear.
4. Placing the graft. Middle ear is packed with
gelfoam soaked with an antibiotic. A proper sized graft is
placed so that its edges extend under the margins of perforation
all round and a small part also extends over the
posterior canal wall. Tympanomeatal flap is replaced. An
underlay technique has the advantage that the squamous
epithelium is not buried in the middle ear.
Overlay Technique
1. Temporal fascia or perichondrial graft is harvested as
above.
2. Incision is made in the meatus as shown (Fig. 79.1)
and meatal skin raised along with all epithelium from the
outer surface of tympanic membrane remnant.
3. Graft placed on the outer surface of TM. A slit is
made in the graft to tuck it under the handle of malleus.
4. Meatal skin removed earlier is now replaced, covering
the periphery of the graft. Ear canal packed with gelfoam
and then with a small antibiotic pack.
A modification of the overlay technique is to place
the anterior edge of fascia graft under the annulus after
removing the epithelium. This prevents blunting of anterior
canal which is seen as a complication of overlay
technique .
5. Closure of endaural or postaural incision.
6. Mastoid dressing.
Post-operative Care
l. Stitches are removed after 5-6 days.
2. Ear pack is removed after 5-6 days without disturbing
the gelfoam.
3. Patient is seen at 3 and 6 weeks after operation.
4. Complete epithelialisation of graft takes 6-8 weeks.
Complications
Underlay Technique
l. Middle ear becomes narrow.
2. Graft may get adherent to the promontory.
3. Anteriorly, graft may lose contact from the remnant of
tympanic membrane leading to anterior perforation.
Overlay Technique
l. Blunting of the anterior sulcus.
2.Epithelial pearls. They are epidermal cysts, when
squamous epithelium is buried under the graft.
3.Lateralisation of graft. Graft loses contact from the
malleus handle resulting in conductive loss. It is prevented
by tucking the graft under the handle.
Other Procedures for Closure of Tympanic
Membrane Perforation
1. Splintage. It is used in fresh traumatic perforations.
The torn edges of the petforation are carefully everted
lmder the microscope and splinted with absorbable gelfoam
placed in the middle ear through the tear. Smaller tears can
be splinted on the outer surface of the tympanic membrane
with a piece of cigarette paper, gelfilm or silicon sheet.
2. Cautery-patching. This is useful in small, longstanding
central perforations where the margins, have
become epithelialised and chronic. In this procedure,
margins, of the perforation are cauterised with 50%
trichloracetic acid to remove the epithelialised edge (or
freshened with a fine pick used for myringoplasty) and
then supported with a cigarette paper moistened with
1 % phenol in glycerine. This procedure can be repeated
at two weeks interval. Instead of cigarette paper, other
material such as steristrip, gelfilm or silicone sheets have
also been used .
3. Fat-graft myringoplasty. It is also used to close
small perforations. After local anaesthesia, edges of perforation
are freshened with 1 mm stapes hook. The inside
of perforation is also scrapped. A small piece of fat harvested
from the ear lobule is plugged into the perforation
like an hour-glass. Over a time, the fat graft adheres and
closes the perforation.
is called myringoplasty. It has the advantage of:
(i) restoring the hearing loss and in some cases the
tinnitus.
(ii) checking re-infection from external auditory canal
and eustachian tube (nasopharyngeal infection
ascends easily via eustachian tube in the presence
of perforation than otherwise).
(iii) checking aeroallergens reaching the exposed middle
ear mucosa, leading to persistent ear discharge.
Myringoplasty can be combined with ossicular reconstruction
when it is called tympanoplasty.
Physiologic principles for middle ear reconstruction
are discussed on page 32.
Contra indications
(i) Active discharge from the middle ear.
(ii) Nasal allergy. It should be brought under control
before surgery.
(iii) Otitis extema.
(iv) Ingrowth of squamous epithelium into the middle
ear. In such cases, excision of squamous epithelium
from the middle ear or a tympanomastoidectomy
may be required.
(v) When the other ear is dead or not suitable for
hearing aid rehabilitation.
(vi) Children below 3 years.
Anaesthesia
Local or general, the former is preferred.
Position
Supine with face turned to one side; the ear to be operated
is up.
Graft materials used are:
(i) Temporalis fascia (most common),
(ii) Perichondrium from the tragus,
(iii) Tragal cartilage,
(iv) Vein.
Incision for exposure of tympanic membrane depends
on the size of the ear canal; it may be endomeatal, endaural
or posta ural.
Technique
Underlay Technique
1. Harvesting the graft of temporal is fascia or perichondrium
from the tragus.
2. Preparing the T.M. for grafting. An incision is
made along the edge of perforation and the ring of
epithelium removed. Remove also a strip of mucosal
layer from the inner side of perforation.
3. Inspecting the middle ear. A stapes-type incision
is made and the tympanomeatal flap raised to see the
integrity and mobility of the ossicular chain and to
ensure that no squamous epithelium has grown into the
middle ear.
4. Placing the graft. Middle ear is packed with
gelfoam soaked with an antibiotic. A proper sized graft is
placed so that its edges extend under the margins of perforation
all round and a small part also extends over the
posterior canal wall. Tympanomeatal flap is replaced. An
underlay technique has the advantage that the squamous
epithelium is not buried in the middle ear.
Overlay Technique
1. Temporal fascia or perichondrial graft is harvested as
above.
2. Incision is made in the meatus as shown (Fig. 79.1)
and meatal skin raised along with all epithelium from the
outer surface of tympanic membrane remnant.
3. Graft placed on the outer surface of TM. A slit is
made in the graft to tuck it under the handle of malleus.
4. Meatal skin removed earlier is now replaced, covering
the periphery of the graft. Ear canal packed with gelfoam
and then with a small antibiotic pack.
A modification of the overlay technique is to place
the anterior edge of fascia graft under the annulus after
removing the epithelium. This prevents blunting of anterior
canal which is seen as a complication of overlay
technique .
5. Closure of endaural or postaural incision.
6. Mastoid dressing.
Post-operative Care
l. Stitches are removed after 5-6 days.
2. Ear pack is removed after 5-6 days without disturbing
the gelfoam.
3. Patient is seen at 3 and 6 weeks after operation.
4. Complete epithelialisation of graft takes 6-8 weeks.
Complications
Underlay Technique
l. Middle ear becomes narrow.
2. Graft may get adherent to the promontory.
3. Anteriorly, graft may lose contact from the remnant of
tympanic membrane leading to anterior perforation.
Overlay Technique
l. Blunting of the anterior sulcus.
2.Epithelial pearls. They are epidermal cysts, when
squamous epithelium is buried under the graft.
3.Lateralisation of graft. Graft loses contact from the
malleus handle resulting in conductive loss. It is prevented
by tucking the graft under the handle.
Other Procedures for Closure of Tympanic
Membrane Perforation
1. Splintage. It is used in fresh traumatic perforations.
The torn edges of the petforation are carefully everted
lmder the microscope and splinted with absorbable gelfoam
placed in the middle ear through the tear. Smaller tears can
be splinted on the outer surface of the tympanic membrane
with a piece of cigarette paper, gelfilm or silicon sheet.
2. Cautery-patching. This is useful in small, longstanding
central perforations where the margins, have
become epithelialised and chronic. In this procedure,
margins, of the perforation are cauterised with 50%
trichloracetic acid to remove the epithelialised edge (or
freshened with a fine pick used for myringoplasty) and
then supported with a cigarette paper moistened with
1 % phenol in glycerine. This procedure can be repeated
at two weeks interval. Instead of cigarette paper, other
material such as steristrip, gelfilm or silicone sheets have
also been used .
3. Fat-graft myringoplasty. It is also used to close
small perforations. After local anaesthesia, edges of perforation
are freshened with 1 mm stapes hook. The inside
of perforation is also scrapped. A small piece of fat harvested
from the ear lobule is plugged into the perforation
like an hour-glass. Over a time, the fat graft adheres and
closes the perforation.
Radical Mastoidectomy
Radical Mastoidectomy is a procedure to eradicate disease
from the middle ear and mastoid without any attempt to
reconstruct hearing. Posterior meatal wall is removed and
the entire area of middle ear, attic, antrum and mastoid is
converted into a single cavity. All remnants of tympanic
membrane, ossicles (except stapes footplate) and mucoperiosteallining
are removed (Fig. 77.1). Eustachian tube is
obliterated by a piece of muscle or cartilage. Aim of the
operation is to permanently exteriorise the diseased area
for inspection and cleaning. The radical mastoidectomy is
infrequently required these days.
Indications
1. When all cholesteatoma cannot be safely removed,
e.g. that invading eustachian tube, round window
niche, perilabyrinthine or hypotympanic cells.
2. If previous attempts to eradicate chronic inflammatory
disease or cholesteatoma have failed.
3. As an approach to petrous apex.
4. Removal of glomus tumour.
5. Carcinoma middle ear. Radical mastoidectomy followed
by radiotherapy is an alternative to en bloc
removal of temporal bone in carcinoma middle ear.
Anaesthesia
Mos tly, general anaesthesia is given. Local anaesthesia
can be used in selected cases.
Position
Patient lies supine with face turned to one side and the
ear to be operated upper-most.
Steps of Operation
1. Incision. Postaural (Fig. 77.2) or endaural
(Fig. 77.3).
Horizontol
Eust. tube
opening closed
with muscle
ROIJr:vl w.i.r.I.rlnw
Fig. 77.1 Radical mastoidectomy. The entire area of
mastoid, middle ear, attic and antrum is exteriorised.
Eustachian tube is obliterated and no attempt is made to
reconstruct the hearing mechanism .
2. Retraction of soft tissues and exposure of mastoid
area. Mastoid area from posterior root of zygoma to
behind the suprameatal triangle and from temporal line
above to the lower part of mastoid tip below is exposed
by elevating the periosteum and the wound retracted.
3. Removal of bone and exposure of attic and
antrum. With the help of burr, bone is removed from
the area of suprameatal triangle, spine of Henle, root of
zygoma to just above the anterior meatal wall, upper part
of superior meatal wall is also removed. This will expose
attic and antrum. Identify the tegmen antri and lateral
semicircular canal.4. Removal of the "bridge" and the buttresses.
Deeper part of superior osseous meatal wall that bridges
over the notch of Rivinus is removed.
Anterior spine of the notch (anterior buttress) and
posterIor spIne of th.e notc.h. (posterior buttre",,) are abo
removeJ. This removes the late ral attic wall. The incus
and the malleus are also removed.
5. Lowering the facial ridge. The deeper part of posterior
meatal wall that overlies the vertical part of facial
nerve is called facial ridge. It is removed as much as possible
within the safety of VIIth nerve so that the mastoid
cavity is freely accessible from the meatus.
6. Toilet of middle ear. Remnants of tympanic
membrane with its annulus and sulcus tympanicus are
removed. Middle ear mucoperiosteum along with any
polyp or granulation tissue is removed. Malleus and incus
are removed if not already done. Stapes is left intact.
Eustachian tube opening is closed by curetting its mucosa
and plugging the opening with tensor tympani muscle or
piece of cartilage.
7. Inspection of the cavity and irrigation. It is necessary
to ensure complete exteriorisation of the attic,
antrum and middle ear and mastoid cavity into external
aud itory meatus . Any bony overhangs are removed and
cavity smoothened with polishing burr. Finally, it is irri gated
with saline to remove any blood or bone particles.
8. MeatopIasty. A flap, based laterally at the concha
is raised from posterior and superior meatal wall and
turned into the mastoid cavity to cover the area of the
facial ridge. This helps in the epithelialisation of the
mastoid cavity. A piece of conchal cartilage can be
removed to enlarge the meatus and to facilitate inspection
and access to cavity.
9. Obliteration of the cavity. If mastoid cavity is
very large, it may be obliterated with temporalis muscle
or other soft tissues, taking care that no vestige of disease
(cholesteatoma) is buried underneath .
10. Closure of wound. The cavity is packed with
ribbon gauze, impregnated with an antibiotic/antiseptic
and the wound is dosed withmterrupted suture:.
Masto id dressing is applied.
Post-operative Care
1. Dressing. First dressing is done on 3rd or 4th day
Replace the outer gauze and cotton and look for any
signs of perichondritis or infection of meatal pack.
Second dressing is done on 6th or 7th day when stittches
are removed and meatal pack is changed. Thereafter
change the pack at weekly intervals or leave the cavity
unpacked with regul ar suction and cleaning till
epithelialisation is complete.
2. Antibiotic. A suitable antibiotic is given for about
week.
3. Cavity care. Usually, cavity is fully epithelialised in
2-3 months. It shou ld be period ically checked (every
4-6 months) in the first year and then annually .
removal of any debris or infection. Any granulation tissue
which delays epithelialisation is removed or cauterized.
Complications
1. Fac ial paralysis.
2. Perichondritis of pinna.
3. Injury to dura or sigmoid sinus.
4. Labyrinthitis, if stapes gets dislocated.
5. Severe conductive deafness of 50 dB or more. This
due to removal of all ossicles and tympanic membrane.
6. Cavity problems. Twenty five percent of the cavities
do not heal and continue to discharge, require
regular after-care.
Modified Radical Mastoidectomy: It is a modification of radical mastoidectomy where as
much of the hearing mechanism as possible is preserved.
The disease process which is often localised to the attic
and antrum is removed and the whole area fully exteriorised
into the meatus by removal of the posterior meatal
and lateral attic wall (Fig. 78.1).
Indications
1. Cholesteatoma confined to the attic and antrum.
2. Localised chronic otitis media.
Irreversibly damaged tissues are removed, preserving
the rest to conserve or reconstruct hearing mechanism.
Anaesthesia
Mostly general, local anaesthesia can be used in selected
cases.
Position
Same as for cortical mastoidectomy.
Steps of Operation
1. Incision, postaural or endaural.
2. Retraction of soft tissues and exposure of mastoid
area.
3. Removal of cortical bone and exposure of antrum
and attic.
Steps 2 and 3 are the same as in radical mastoidectomy.
4. Removal of diseased tissue. Cholesteatoma, granulations
or unhealthy mucosa is removed. Incus and head
of malleus often require removal, if cholesteatoma
engulfs them or extends medial to them. They are
preserved if possible. Lateral attic wall is removed
to fully exteriorise the attic.
5. Facial ridge is lowered.
6. Mastoid cavity is smoothened with polishing burr,
removing any overhangs and then irrigated with
normal saline.
7. Reconstruction of hearing mechanism. Pars tensa of
tympanic membrane and middle ear, if healthy, are left
undisturbed. If disease extends into middle ear, only
the irreversible tissues are removed. Reconstruction
of tympanic membrane or ossicular chain, if damaged,
can also be done (mastoidectomy with tympanoplasty
operation) .
8. Meatoplasty and closure of wound is same as in
radica l mastoidectomy.
Post-operative Care and Complications
Same as in radical mastoidectomy.
from the middle ear and mastoid without any attempt to
reconstruct hearing. Posterior meatal wall is removed and
the entire area of middle ear, attic, antrum and mastoid is
converted into a single cavity. All remnants of tympanic
membrane, ossicles (except stapes footplate) and mucoperiosteallining
are removed (Fig. 77.1). Eustachian tube is
obliterated by a piece of muscle or cartilage. Aim of the
operation is to permanently exteriorise the diseased area
for inspection and cleaning. The radical mastoidectomy is
infrequently required these days.
Indications
1. When all cholesteatoma cannot be safely removed,
e.g. that invading eustachian tube, round window
niche, perilabyrinthine or hypotympanic cells.
2. If previous attempts to eradicate chronic inflammatory
disease or cholesteatoma have failed.
3. As an approach to petrous apex.
4. Removal of glomus tumour.
5. Carcinoma middle ear. Radical mastoidectomy followed
by radiotherapy is an alternative to en bloc
removal of temporal bone in carcinoma middle ear.
Anaesthesia
Mos tly, general anaesthesia is given. Local anaesthesia
can be used in selected cases.
Position
Patient lies supine with face turned to one side and the
ear to be operated upper-most.
Steps of Operation
1. Incision. Postaural (Fig. 77.2) or endaural
(Fig. 77.3).
Horizontol
Eust. tube
opening closed
with muscle
ROIJr:vl w.i.r.I.rlnw
Fig. 77.1 Radical mastoidectomy. The entire area of
mastoid, middle ear, attic and antrum is exteriorised.
Eustachian tube is obliterated and no attempt is made to
reconstruct the hearing mechanism .
2. Retraction of soft tissues and exposure of mastoid
area. Mastoid area from posterior root of zygoma to
behind the suprameatal triangle and from temporal line
above to the lower part of mastoid tip below is exposed
by elevating the periosteum and the wound retracted.
3. Removal of bone and exposure of attic and
antrum. With the help of burr, bone is removed from
the area of suprameatal triangle, spine of Henle, root of
zygoma to just above the anterior meatal wall, upper part
of superior meatal wall is also removed. This will expose
attic and antrum. Identify the tegmen antri and lateral
semicircular canal.4. Removal of the "bridge" and the buttresses.
Deeper part of superior osseous meatal wall that bridges
over the notch of Rivinus is removed.
Anterior spine of the notch (anterior buttress) and
posterIor spIne of th.e notc.h. (posterior buttre",,) are abo
removeJ. This removes the late ral attic wall. The incus
and the malleus are also removed.
5. Lowering the facial ridge. The deeper part of posterior
meatal wall that overlies the vertical part of facial
nerve is called facial ridge. It is removed as much as possible
within the safety of VIIth nerve so that the mastoid
cavity is freely accessible from the meatus.
6. Toilet of middle ear. Remnants of tympanic
membrane with its annulus and sulcus tympanicus are
removed. Middle ear mucoperiosteum along with any
polyp or granulation tissue is removed. Malleus and incus
are removed if not already done. Stapes is left intact.
Eustachian tube opening is closed by curetting its mucosa
and plugging the opening with tensor tympani muscle or
piece of cartilage.
7. Inspection of the cavity and irrigation. It is necessary
to ensure complete exteriorisation of the attic,
antrum and middle ear and mastoid cavity into external
aud itory meatus . Any bony overhangs are removed and
cavity smoothened with polishing burr. Finally, it is irri gated
with saline to remove any blood or bone particles.
8. MeatopIasty. A flap, based laterally at the concha
is raised from posterior and superior meatal wall and
turned into the mastoid cavity to cover the area of the
facial ridge. This helps in the epithelialisation of the
mastoid cavity. A piece of conchal cartilage can be
removed to enlarge the meatus and to facilitate inspection
and access to cavity.
9. Obliteration of the cavity. If mastoid cavity is
very large, it may be obliterated with temporalis muscle
or other soft tissues, taking care that no vestige of disease
(cholesteatoma) is buried underneath .
10. Closure of wound. The cavity is packed with
ribbon gauze, impregnated with an antibiotic/antiseptic
and the wound is dosed withmterrupted suture:.
Masto id dressing is applied.
Post-operative Care
1. Dressing. First dressing is done on 3rd or 4th day
Replace the outer gauze and cotton and look for any
signs of perichondritis or infection of meatal pack.
Second dressing is done on 6th or 7th day when stittches
are removed and meatal pack is changed. Thereafter
change the pack at weekly intervals or leave the cavity
unpacked with regul ar suction and cleaning till
epithelialisation is complete.
2. Antibiotic. A suitable antibiotic is given for about
week.
3. Cavity care. Usually, cavity is fully epithelialised in
2-3 months. It shou ld be period ically checked (every
4-6 months) in the first year and then annually .
removal of any debris or infection. Any granulation tissue
which delays epithelialisation is removed or cauterized.
Complications
1. Fac ial paralysis.
2. Perichondritis of pinna.
3. Injury to dura or sigmoid sinus.
4. Labyrinthitis, if stapes gets dislocated.
5. Severe conductive deafness of 50 dB or more. This
due to removal of all ossicles and tympanic membrane.
6. Cavity problems. Twenty five percent of the cavities
do not heal and continue to discharge, require
regular after-care.
Modified Radical Mastoidectomy: It is a modification of radical mastoidectomy where as
much of the hearing mechanism as possible is preserved.
The disease process which is often localised to the attic
and antrum is removed and the whole area fully exteriorised
into the meatus by removal of the posterior meatal
and lateral attic wall (Fig. 78.1).
Indications
1. Cholesteatoma confined to the attic and antrum.
2. Localised chronic otitis media.
Irreversibly damaged tissues are removed, preserving
the rest to conserve or reconstruct hearing mechanism.
Anaesthesia
Mostly general, local anaesthesia can be used in selected
cases.
Position
Same as for cortical mastoidectomy.
Steps of Operation
1. Incision, postaural or endaural.
2. Retraction of soft tissues and exposure of mastoid
area.
3. Removal of cortical bone and exposure of antrum
and attic.
Steps 2 and 3 are the same as in radical mastoidectomy.
4. Removal of diseased tissue. Cholesteatoma, granulations
or unhealthy mucosa is removed. Incus and head
of malleus often require removal, if cholesteatoma
engulfs them or extends medial to them. They are
preserved if possible. Lateral attic wall is removed
to fully exteriorise the attic.
5. Facial ridge is lowered.
6. Mastoid cavity is smoothened with polishing burr,
removing any overhangs and then irrigated with
normal saline.
7. Reconstruction of hearing mechanism. Pars tensa of
tympanic membrane and middle ear, if healthy, are left
undisturbed. If disease extends into middle ear, only
the irreversible tissues are removed. Reconstruction
of tympanic membrane or ossicular chain, if damaged,
can also be done (mastoidectomy with tympanoplasty
operation) .
8. Meatoplasty and closure of wound is same as in
radica l mastoidectomy.
Post-operative Care and Complications
Same as in radical mastoidectomy.
Mastoid Surgery
Myringoplasty
It is an operation in which reconstructive procedure is
limited to repair of tympanic membrane perforation.
Tympanoplasty without Mastoidectomy
(tympanum = middle ear)
It is an operation to eradicate disease in the middle ear
and to reconstruct the hearing mechanism without mastoid
surgery, with or without tympanic membrane grafting.
This means ossicular reconstruction only or ossicular
reconstruction with myringoplasty.
Tympanoplasty with Mastoidectomy
It is an operation to eradicate disease in both the mastoid
and middle 'ear cavity, and to reconstruct the hearing
mechanism with or without tympanic membrane grafting.
Cortical Mastoidectomy (Simple
Mastoidectomy or Schwartz Operation)
It is an exenteration of all accessible mastoid air cells preserving
the posterior meatal wall.
Modified Radical Mastoidectomy
It is an operation to eradicate disease of the attic and mastoid,
both of which are exteriorised into the external auditory
canal by removal of the posterior meatal and lateral
attic walls. Tympanic membrane remnant, functioning
ossicles and the reversible mucosa and function of the
eustachian tube are preserved. These structures are necessary
to reconstruct hearing mechanism at the time of surgery
or in a 2nd stage operation.
Radical Mastoidectomy
It is an operation to eradicate disease of the middle ear
and mastoid in which mastoid, midd le ear, attic and the
antrum are exteriorised into the external ear by removal
of posterior meatal wall. All remnants of tympanic membrane,
malleus, incus (not the stapes) chorda tympani and
the mucoperiosteal lining are removed, and the opening
of eustachian tube closed by packing a piece of muscle or
cartilage into the eustachian tube.
Meatoplasty
Meatoplasty is an operation in which a crescent of concha 1
cartilage is excised to widen the meatus. It is invariably
combined with all canal wall down procedures, i.e. modified
radical for periodic cleaning or inspection, and radical
mastoidectomies for easy access to the mastoid cavity, or it
is done as an isolated procedure in a sagging auricle seen in
older people. Sagging auricle obstructs the ear canal and
causes hearing loss and retention of wax.
Mastoid Obliteration
It is an operation to eradicate mastoid disease, when
present, and to obliterate the mastoid cavity.
Obliteration of mastoid cavity is done with pedicled temporalis
muscle or musculofascial tissue raised as flaps.
SURGICAL APPROACHES TO THE
EAR AND INCISIONS
1. Endomeatal or transcanal approach. It is used to
raise a tympanomeatal flap in order to expose the middle
ear. Rosen's incision is the most commonly used for
stapedectomy. It requires the meatus and canal to be wide
enough to work. It consists of two parts; (a) a small vertical
incision at 12 o'clock position near the annulus and (b) a
curvilinear incision starting at 6 o'clock position to meet
the 1st incision in the posterosuperior region of the canals,
5-7 mm away from the annulus (Fig. 76.1) Posterior
meatal canal skin is raised in continuity with tympanic
membrane, after dislocating the annulus from the sulcus. It
gives a good view of the middle ear and ossicles. Stapes, if
still covered by posterosuperior overhang of bony meatus,
can be exposed by removing this part of the overhang. This
incision is also used commonly for exploratory tympanotomy
to find cause for conductive hearing loss, inlay
myringoplasty or ossicular reconstruction.2. Endaural approach. It is used for:
(a) Excision of osteomas or exostosis of ear canal.
(b) Large tympanic membrane perforations.
(c) Attic cholesteatomas with limited extension into
the antrum.
(d) Modified radical mastoidectomy where disease is
limited to attic, antrum, and part of mastoid.
Endaural approach is made through Lempert's incision
(Fig. 76.2). It consists of 2 parts:
Lempert I-It is semicircular incision, made from 12
o'clock to 6 o'clock position in the posterior meatal wall
at the bony-cartilaginous junction.Lempert II-Starts from the 1st incision at 12 o'clock
and then passes upwards in a curvilinear fashion between
tragus and the crus of helix. It passes through the incisura
terminalis and thus does not cut the cartilage. Both mastoid
and external canal surgery can be done.
3. Postaural (or Wilde's) incision (Fig. 76.3). It starts
at the highest attachment of the pinna, follows the curve
of retroauricular groove, lying 1 cm behind it, and ends at
the mastoid tip. In infants and children up to 2 years of age,
the mastoid process is not developed and the facial nerve
lies exposed near its exit, and the incision therefore is slanting
posteriorly, avoiding lower part of the mastoid. Some
surgeons prefer to make the postaural incision in the sulcus
(retroauricular groove) . Postaural incision is used for:
(i) Cortical mastoidectomy.
(ii) Modified radical and radical mastoidectomy.
(iii) Tympanoplasty: when perforation extends anterior
to handle of malleus.
(iv) Exposure of CN VII in vertical segment.
(v) Surgery of endolymphatic sac.
CORTICAL MASTOIDECTOMY
Cortical mastoidectomy, known as simple or complete
mastoidectomy or Schwartz operation, is complete exenteration
of all accessible mastoid air cells and converting
them into a single cavity. Posterior meatal wall is left
intact. Middle ear structures are not disturbed.
Indications
1. Acute coalescent mastoiditis.
2. Incompletely resolved acute otitis media with reservoir
sign.
3. Masked mastoiditis.
4. As an initial step to perform:
(a) endolymphatic sac surgery
(b) decompression of facial nerve
(c) translabyrinthine or retro-Iabyrinthine procedures
for acoustic neuroma.
Figure 76.4 shows the various structures and landmarks
seen after cortical mastoidectomy.
Anaesthesia
General anaesthesia.
Position
Patient lies supine with face turned to one side and the
ear to be operated upper-most.
Steps of Operation
1. Incision. A curved postaural incision about 1 em
behind but parallel to the retroauricular sulcus, starting
at the highest attachment of pinna to the mastoid tip
(Fig. 76.3B).In infants and children up to 2 years, the incision is
short and more horizontal. This is to avoid cutting facial
nerve which is superficial in the lower part of mastoid
(Fig. 76.3C).
Incision cuts through soft tissues up to the periosteum.
Temporalis muscle is not cut in the incision.
2. Exposure of lateral surface of mastoid and
MacEwen's triangle. Periosteum is incised in the line of
first incision. A horizontal incision may be made along
the lower border of temporalis muscle for more exposure.
Periosteum is scraped from the surface of mastoid and
posterosuperior margin of osseous meatus. Tendinous
fibres of sternomastoid are sharply cut and scraped down.
A self-retaining mastoid retractor is applied.
3. Removal. of mastoid cortex and exposure of
antrum. Mastoid cortex is removed with burr, or gouge
and hammer. Mastoid antrum is exposed in the area of
suprameatal triangle (MacEwen's triangle). In an adult,
antrum lies 12-15 mm from the surface. Horizontal semicircular
canal is identified.
4. Removal of mastoid air cells. All accessible mastoid
air cells are removed leaving behind the bony plate
of tegmen tympani above, sinus plate behind and posterior
meatal wall in front.
5. Removal of mastoid tip and finishing the cavity.
Lateral wall of the mastoid tip is removed, exposing muscle
fibres of posterior belly of digastric. Zygomatic cells situated
in the root of zygoma, retrosinus cells lying between
sinus plate and cortex, behind the sinus, are removed. A
finished cavity should have bevelled edges so that soft
tissue can easily sit in and obliterate the cavity.
6. Closure of wound. MastoiJ cavity is thoroughly
irrigated with saline to remove bone dust, and the wound
is closed in two layers. A rubber drain may be left at the
lower end of incision for 24-48 hours in case of infection
or excessive bleeding. A meatal pack should be kept to
avoid stenosis of ear canal. Mastoid dressing is applied .
Post-operative Care
1. Antibiotics started pre-operatively are continued
post-operatively for at least one week. Culture swab
taken from the mastoid, during operation, may dictate
a change in the antibiotic.
2. Drain, if put, is removed in 24-48 hours and sterile
dressing done.
3. Stitches are removed on the 6th day.
Complications
1. Injury to facial nerve .
2. Dislocation of incus.
3. Injury to horizontal semicircular canal. Patient will
have post-operative giddiness and nystagmus.
4. Injury to sigmoid sinus with profuse bleeding.
5. Injury to dura of middle cranial fossa.
6. Post-operative wound infection and wound
break-down.
It is an operation in which reconstructive procedure is
limited to repair of tympanic membrane perforation.
Tympanoplasty without Mastoidectomy
(tympanum = middle ear)
It is an operation to eradicate disease in the middle ear
and to reconstruct the hearing mechanism without mastoid
surgery, with or without tympanic membrane grafting.
This means ossicular reconstruction only or ossicular
reconstruction with myringoplasty.
Tympanoplasty with Mastoidectomy
It is an operation to eradicate disease in both the mastoid
and middle 'ear cavity, and to reconstruct the hearing
mechanism with or without tympanic membrane grafting.
Cortical Mastoidectomy (Simple
Mastoidectomy or Schwartz Operation)
It is an exenteration of all accessible mastoid air cells preserving
the posterior meatal wall.
Modified Radical Mastoidectomy
It is an operation to eradicate disease of the attic and mastoid,
both of which are exteriorised into the external auditory
canal by removal of the posterior meatal and lateral
attic walls. Tympanic membrane remnant, functioning
ossicles and the reversible mucosa and function of the
eustachian tube are preserved. These structures are necessary
to reconstruct hearing mechanism at the time of surgery
or in a 2nd stage operation.
Radical Mastoidectomy
It is an operation to eradicate disease of the middle ear
and mastoid in which mastoid, midd le ear, attic and the
antrum are exteriorised into the external ear by removal
of posterior meatal wall. All remnants of tympanic membrane,
malleus, incus (not the stapes) chorda tympani and
the mucoperiosteal lining are removed, and the opening
of eustachian tube closed by packing a piece of muscle or
cartilage into the eustachian tube.
Meatoplasty
Meatoplasty is an operation in which a crescent of concha 1
cartilage is excised to widen the meatus. It is invariably
combined with all canal wall down procedures, i.e. modified
radical for periodic cleaning or inspection, and radical
mastoidectomies for easy access to the mastoid cavity, or it
is done as an isolated procedure in a sagging auricle seen in
older people. Sagging auricle obstructs the ear canal and
causes hearing loss and retention of wax.
Mastoid Obliteration
It is an operation to eradicate mastoid disease, when
present, and to obliterate the mastoid cavity.
Obliteration of mastoid cavity is done with pedicled temporalis
muscle or musculofascial tissue raised as flaps.
SURGICAL APPROACHES TO THE
EAR AND INCISIONS
1. Endomeatal or transcanal approach. It is used to
raise a tympanomeatal flap in order to expose the middle
ear. Rosen's incision is the most commonly used for
stapedectomy. It requires the meatus and canal to be wide
enough to work. It consists of two parts; (a) a small vertical
incision at 12 o'clock position near the annulus and (b) a
curvilinear incision starting at 6 o'clock position to meet
the 1st incision in the posterosuperior region of the canals,
5-7 mm away from the annulus (Fig. 76.1) Posterior
meatal canal skin is raised in continuity with tympanic
membrane, after dislocating the annulus from the sulcus. It
gives a good view of the middle ear and ossicles. Stapes, if
still covered by posterosuperior overhang of bony meatus,
can be exposed by removing this part of the overhang. This
incision is also used commonly for exploratory tympanotomy
to find cause for conductive hearing loss, inlay
myringoplasty or ossicular reconstruction.2. Endaural approach. It is used for:
(a) Excision of osteomas or exostosis of ear canal.
(b) Large tympanic membrane perforations.
(c) Attic cholesteatomas with limited extension into
the antrum.
(d) Modified radical mastoidectomy where disease is
limited to attic, antrum, and part of mastoid.
Endaural approach is made through Lempert's incision
(Fig. 76.2). It consists of 2 parts:
Lempert I-It is semicircular incision, made from 12
o'clock to 6 o'clock position in the posterior meatal wall
at the bony-cartilaginous junction.Lempert II-Starts from the 1st incision at 12 o'clock
and then passes upwards in a curvilinear fashion between
tragus and the crus of helix. It passes through the incisura
terminalis and thus does not cut the cartilage. Both mastoid
and external canal surgery can be done.
3. Postaural (or Wilde's) incision (Fig. 76.3). It starts
at the highest attachment of the pinna, follows the curve
of retroauricular groove, lying 1 cm behind it, and ends at
the mastoid tip. In infants and children up to 2 years of age,
the mastoid process is not developed and the facial nerve
lies exposed near its exit, and the incision therefore is slanting
posteriorly, avoiding lower part of the mastoid. Some
surgeons prefer to make the postaural incision in the sulcus
(retroauricular groove) . Postaural incision is used for:
(i) Cortical mastoidectomy.
(ii) Modified radical and radical mastoidectomy.
(iii) Tympanoplasty: when perforation extends anterior
to handle of malleus.
(iv) Exposure of CN VII in vertical segment.
(v) Surgery of endolymphatic sac.
CORTICAL MASTOIDECTOMY
Cortical mastoidectomy, known as simple or complete
mastoidectomy or Schwartz operation, is complete exenteration
of all accessible mastoid air cells and converting
them into a single cavity. Posterior meatal wall is left
intact. Middle ear structures are not disturbed.
Indications
1. Acute coalescent mastoiditis.
2. Incompletely resolved acute otitis media with reservoir
sign.
3. Masked mastoiditis.
4. As an initial step to perform:
(a) endolymphatic sac surgery
(b) decompression of facial nerve
(c) translabyrinthine or retro-Iabyrinthine procedures
for acoustic neuroma.
Figure 76.4 shows the various structures and landmarks
seen after cortical mastoidectomy.
Anaesthesia
General anaesthesia.
Position
Patient lies supine with face turned to one side and the
ear to be operated upper-most.
Steps of Operation
1. Incision. A curved postaural incision about 1 em
behind but parallel to the retroauricular sulcus, starting
at the highest attachment of pinna to the mastoid tip
(Fig. 76.3B).In infants and children up to 2 years, the incision is
short and more horizontal. This is to avoid cutting facial
nerve which is superficial in the lower part of mastoid
(Fig. 76.3C).
Incision cuts through soft tissues up to the periosteum.
Temporalis muscle is not cut in the incision.
2. Exposure of lateral surface of mastoid and
MacEwen's triangle. Periosteum is incised in the line of
first incision. A horizontal incision may be made along
the lower border of temporalis muscle for more exposure.
Periosteum is scraped from the surface of mastoid and
posterosuperior margin of osseous meatus. Tendinous
fibres of sternomastoid are sharply cut and scraped down.
A self-retaining mastoid retractor is applied.
3. Removal. of mastoid cortex and exposure of
antrum. Mastoid cortex is removed with burr, or gouge
and hammer. Mastoid antrum is exposed in the area of
suprameatal triangle (MacEwen's triangle). In an adult,
antrum lies 12-15 mm from the surface. Horizontal semicircular
canal is identified.
4. Removal of mastoid air cells. All accessible mastoid
air cells are removed leaving behind the bony plate
of tegmen tympani above, sinus plate behind and posterior
meatal wall in front.
5. Removal of mastoid tip and finishing the cavity.
Lateral wall of the mastoid tip is removed, exposing muscle
fibres of posterior belly of digastric. Zygomatic cells situated
in the root of zygoma, retrosinus cells lying between
sinus plate and cortex, behind the sinus, are removed. A
finished cavity should have bevelled edges so that soft
tissue can easily sit in and obliterate the cavity.
6. Closure of wound. MastoiJ cavity is thoroughly
irrigated with saline to remove bone dust, and the wound
is closed in two layers. A rubber drain may be left at the
lower end of incision for 24-48 hours in case of infection
or excessive bleeding. A meatal pack should be kept to
avoid stenosis of ear canal. Mastoid dressing is applied .
Post-operative Care
1. Antibiotics started pre-operatively are continued
post-operatively for at least one week. Culture swab
taken from the mastoid, during operation, may dictate
a change in the antibiotic.
2. Drain, if put, is removed in 24-48 hours and sterile
dressing done.
3. Stitches are removed on the 6th day.
Complications
1. Injury to facial nerve .
2. Dislocation of incus.
3. Injury to horizontal semicircular canal. Patient will
have post-operative giddiness and nystagmus.
4. Injury to sigmoid sinus with profuse bleeding.
5. Injury to dura of middle cranial fossa.
6. Post-operative wound infection and wound
break-down.
Myringotomy
It is incision of the tympanic membrane with the purpose
to drain suppurative or nonsuppurative effusion of the
middle ear or to provide aeration in case of malfunctioning
eustachian tube. Ventilation tube (grommet) may
also be required in the latter case.
Indications
1. Acute suppurative otitis media
(a) Severe earache with bulging tympanic membrane.
(b) Incomplete resolution with opaque drum and
persistent conductive deafness.
(c) Complications of acute otitis media, e.g. facial
paralysis, labyrinthitis or meningitis with bulging
tympanic membrane.
2. Serous otitis media.
3. Aero-otitis media (to drain fluid and "unlock" the
eustachian tube).
4. Atelectatic ear (grommet is often inserted for long-term
aeration).
Contraindications
Suspected intratympanic glomus tumour. Myringotomy
in these cases can cause profuse bleeding. Tympanotomy
is preferred.
Anaesthesia
In infants and children, always use general anaesthesia. For
adults, general anaesthesia is used only when tympanic
membrane is acutely inflamed. If there is no inflammation,
myringotomy can be done under local anaesthesia or no
anaesthesia at all.
Steps of Operation
1. Ear canal is cleaned of wax and debris.
2. Operation is ideally performed under operating microscope
using a sharp myringotome and a good suction
apparatus.
3. In acute suppurative otitis media, a circumferential
incision is made in the posteroinferior quadrant of
tympanic membrane, midway between hundle uf
malleus and tympanic annulus, avoiding injury to
incudostapedial joint (Fig. 75.lA).
4. In serous otitis media, a small radial incision is given
in the posteroinferior or anteroinferior quadrant and
all the effusion sucked out (Fig. 75.1B).
When ventilation tube is to be inserted, incision should
be just enough to admit the tube (Fig. 75.2).
Pitfalls of Myringotomy
1. When tympanic membrane is thick, incision may
remain only in the superficial layers of drumhead
without cutting through its entire thickness.
2. Incision in the posterior meatal wall. This may happen
when distinction between drum-head and posterior
meatal wall is lost, when both are inflamed.
Post-operative Care
Daily mopping of ear discharge will be required in cases
of acute suppurative otitis media. In serous otitis media,
just leave a wad of cotton wool for 24-48 hours.
Drum incisions usually heal rapidly. No water should
be permitted to enter the ear canal for at least one week,
and if a grommet has been inserted, entry of water is
prevented so long as grommet is in position.
Complications
1. Injury to incudostapedial joint or stapes.
2. Injury to jugular bulb with profuse bleeding, if jugular
bulb is high and floor of the middle ear dehiscent.
3. Middle ear infection.
to drain suppurative or nonsuppurative effusion of the
middle ear or to provide aeration in case of malfunctioning
eustachian tube. Ventilation tube (grommet) may
also be required in the latter case.
Indications
1. Acute suppurative otitis media
(a) Severe earache with bulging tympanic membrane.
(b) Incomplete resolution with opaque drum and
persistent conductive deafness.
(c) Complications of acute otitis media, e.g. facial
paralysis, labyrinthitis or meningitis with bulging
tympanic membrane.
2. Serous otitis media.
3. Aero-otitis media (to drain fluid and "unlock" the
eustachian tube).
4. Atelectatic ear (grommet is often inserted for long-term
aeration).
Contraindications
Suspected intratympanic glomus tumour. Myringotomy
in these cases can cause profuse bleeding. Tympanotomy
is preferred.
Anaesthesia
In infants and children, always use general anaesthesia. For
adults, general anaesthesia is used only when tympanic
membrane is acutely inflamed. If there is no inflammation,
myringotomy can be done under local anaesthesia or no
anaesthesia at all.
Steps of Operation
1. Ear canal is cleaned of wax and debris.
2. Operation is ideally performed under operating microscope
using a sharp myringotome and a good suction
apparatus.
3. In acute suppurative otitis media, a circumferential
incision is made in the posteroinferior quadrant of
tympanic membrane, midway between hundle uf
malleus and tympanic annulus, avoiding injury to
incudostapedial joint (Fig. 75.lA).
4. In serous otitis media, a small radial incision is given
in the posteroinferior or anteroinferior quadrant and
all the effusion sucked out (Fig. 75.1B).
When ventilation tube is to be inserted, incision should
be just enough to admit the tube (Fig. 75.2).
Pitfalls of Myringotomy
1. When tympanic membrane is thick, incision may
remain only in the superficial layers of drumhead
without cutting through its entire thickness.
2. Incision in the posterior meatal wall. This may happen
when distinction between drum-head and posterior
meatal wall is lost, when both are inflamed.
Post-operative Care
Daily mopping of ear discharge will be required in cases
of acute suppurative otitis media. In serous otitis media,
just leave a wad of cotton wool for 24-48 hours.
Drum incisions usually heal rapidly. No water should
be permitted to enter the ear canal for at least one week,
and if a grommet has been inserted, entry of water is
prevented so long as grommet is in position.
Complications
1. Injury to incudostapedial joint or stapes.
2. Injury to jugular bulb with profuse bleeding, if jugular
bulb is high and floor of the middle ear dehiscent.
3. Middle ear infection.
Otomycosis
Otomycosis is a fungal infection of
the ear canal that often occurs due to Aspergillus niger,
A. fumigatus or Candida albicans.It is seen in hot and humid
climate of tropical and subtropical countries. Secondary
fungal growth is also Seen in patients using topical antibjotics
for treatment of otitis externa or middle ear suppuration.
The clinical features of otomycosis include: intense
itching, discomfort or pain in the ear, watery discharge
with a musty odour, and ear blockage. The fungal mass
may appear white, brown or black and has been likened
to a wet piece of filter paper.
Examined with an otoscope, A. niger appears as blackheaded
filamentous growth, A. fumigatus, pale blue or
green; and Candida as white or creamy deposit. Meatal
skin appears sodden, red and oedematous.
Treatment consists of thorough ear toilet to remove all
discharge and epithelial debris which are conducive to the
growth of fungus. It can be done by syringing, suction or
mopping. S pec ific antifungal agent, can be applied.
Nystatin (100,000 units/ml of propylene glycol) is ffective
aga inst Candida. Other broad spectrum antifungal
agenrs include clotrimazo le and povidone iodine. 2% sa licylic
acid in alcohol is also effec tive. It is a keratolytic
agent which removes superficial layers of epidermis, dnd
along with that, the fungal mycelia growing into them.
Antifungal treatment should be continued for a week
even after apparent cure to avoid recurrences. Ear must
be kept dry. Bacterial infections are often associated with
otomycosis, and treatment with an antibiotic/steroid preparation
helps to reduce inflammation and oedema and thus
permitting better penetration of antifungal agents.
the ear canal that often occurs due to Aspergillus niger,
A. fumigatus or Candida albicans.It is seen in hot and humid
climate of tropical and subtropical countries. Secondary
fungal growth is also Seen in patients using topical antibjotics
for treatment of otitis externa or middle ear suppuration.
The clinical features of otomycosis include: intense
itching, discomfort or pain in the ear, watery discharge
with a musty odour, and ear blockage. The fungal mass
may appear white, brown or black and has been likened
to a wet piece of filter paper.
Examined with an otoscope, A. niger appears as blackheaded
filamentous growth, A. fumigatus, pale blue or
green; and Candida as white or creamy deposit. Meatal
skin appears sodden, red and oedematous.
Treatment consists of thorough ear toilet to remove all
discharge and epithelial debris which are conducive to the
growth of fungus. It can be done by syringing, suction or
mopping. S pec ific antifungal agent, can be applied.
Nystatin (100,000 units/ml of propylene glycol) is ffective
aga inst Candida. Other broad spectrum antifungal
agenrs include clotrimazo le and povidone iodine. 2% sa licylic
acid in alcohol is also effec tive. It is a keratolytic
agent which removes superficial layers of epidermis, dnd
along with that, the fungal mycelia growing into them.
Antifungal treatment should be continued for a week
even after apparent cure to avoid recurrences. Ear must
be kept dry. Bacterial infections are often associated with
otomycosis, and treatment with an antibiotic/steroid preparation
helps to reduce inflammation and oedema and thus
permitting better penetration of antifungal agents.
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