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.
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
Bronchoscopy
Bronchoscopy is of two types:
1. Rigid .
2. Flexible fibre optic.
RIGID BRONCHOSCOPY
Indications
A. Diagnostic
[ . To find out the cause for wheezing, haemoptysis,
or unexp lained cough persisting for more than
4 weeks.
2. When X- ray chest sho ws:
(a) Atelectasis of a segment, lobe or entire lung
(b) Opacity localised to a segment or lobe of lung
(c) Obstructive emphysema-to exclude foreign body
(d) Hilar or mediastinal shadows
3. Vocal cord palsy.
4. Collection of bronchial secretions for culture and
sensitivi ty tests, acid fas t bacilli, fun gus, malignant
cells.
8. Therapeutic
1. Removal of foreign bod ies.
2. Removal of retained secretions or mucus plug in
cases of head injuries, chest trauma, thoracic or
abdomi nal surge ry, or comatosed patients.
Anaesthesia
General anaesthesia with no endotracheal tube or with
only a small bore catheter is often preferred. It can also
be done under topical surface anaesthes ia.
Position
Same as fordirect laryngoscopy.
Technique
There are two methods to in trod uce bronc hoscope:
1. Direct method. Here bronchoscope is introduced
directly through the glottis.
2. Through laryngoscope. Here glo ttis is first exposed
with the help of a spatular type laryngoscope and
then the bronchoscope is introduced through the
laryngoscope into the trachea. Laryngoscope is then
withdrawn. This me thod is useful in infan ts and
young children, and in ad ults who have short neck
and thick tongue.
Details of Technique
l. A piece of ga uze is placed on the upper teeth for the ir
protect ion aga inst injury.
2. Proper-sized bronchoscope is lu bricated with a swab
of autoclaved liquid paraffin or gelly. It is held by the shaft
in surgeon's right hand in a pen- like fashion. Fingers of
the left hand are used to retract the upper lip and guide
the bronchoscope.
3. Now looking through the scope, tip of epiglottis is
identified first and the scope passed behind it and the
epiglottis lifted forward to expose the glottiS. Now bronchoscope
is rotated 90° clockwise so that its bevelled tip
is in the axis of glottis to ease its entry into the trachea.
Once trachea is entered, scope is rotated back to the original
position.
4. Bronchoscope is grad ually advanced and the entire
tracheobronchial tree examined. Axis of bronchoscope
should be made to correspond with axes of the trachea
and bronchi. To ac hieve this, head and neck are flexed
to the left when examining the right bronchial tree and
vice versa.
Openi ngs of all the segmental bronchi in both the
lungs are examined seriatim.
5. Direct vision, right angled and retrograde telescopes
can be used for magnification and detailed examination.
6. Biopsy of the les ion of susp icious area can be taken.
7. Secretions can be collected for exfoliative cytology,
or bacteriologic examination.
Post-operative Care
1. Keep the patient in humid atmosphere.
2. Watch for respiratory distress. This could be due to
laryngeal spasm or subglottic oedema if the proced ure
had been unduly prolonged or the bronchoscope
introduced repeatedly. Inspiratory stridor and suprasternal
retraction will ind icate need for tracheostomy.
Complications
1. Injury to teeth and li ps.
2. Haemorrhage from the biopsy site.
3. Hypox ia and cardiac arrest.
4. Laryngeal oedema.
Precautions During Bronchoscopy
l. Select proper size of bronchoscope according to
patient's age (see Table A 1).
2. Do not force bronchoscope thro ugh closed glott is.
3. Repeated removal and introduction of bronchoscope
should be avoided.
4. Procedure shou ld not be prolonged beyond 20 minutes
in infants and children, otherwise it may cause
subglottic oedema in pos t-operati ve period.
FLEXIBLE FIBRE OPTIC BRONCHOSCOPY
These days, flexible fibre optic bronchoscopy has
replaced rigid bronchoscopy for diagnostic procedures
particularly in adults. It provides magnification and better
illumination, and because of the smaller size, permits
examination of subsegmental bronchi. It is also easy to
use ll1 patients with neck or jaw abnormalities where rigid
bronchoscopy may almost be impossible technically.
This procedure can be performed under topical anaesthesia
and is very useful for bedside examination of the critically
ill patients. The suction/biopsy channel provided
in the fibrescope helps to remove secretions, inspissated
plugs of mucus or even small foreign bodies. Flexible
bronchoscope can also be easily passed through endotracheal
tube or the tracheostomy opening. However, it has
limited utiltty in children because of the problems of
ventilation.
1. Rigid .
2. Flexible fibre optic.
RIGID BRONCHOSCOPY
Indications
A. Diagnostic
[ . To find out the cause for wheezing, haemoptysis,
or unexp lained cough persisting for more than
4 weeks.
2. When X- ray chest sho ws:
(a) Atelectasis of a segment, lobe or entire lung
(b) Opacity localised to a segment or lobe of lung
(c) Obstructive emphysema-to exclude foreign body
(d) Hilar or mediastinal shadows
3. Vocal cord palsy.
4. Collection of bronchial secretions for culture and
sensitivi ty tests, acid fas t bacilli, fun gus, malignant
cells.
8. Therapeutic
1. Removal of foreign bod ies.
2. Removal of retained secretions or mucus plug in
cases of head injuries, chest trauma, thoracic or
abdomi nal surge ry, or comatosed patients.
Anaesthesia
General anaesthesia with no endotracheal tube or with
only a small bore catheter is often preferred. It can also
be done under topical surface anaesthes ia.
Position
Same as fordirect laryngoscopy.
Technique
There are two methods to in trod uce bronc hoscope:
1. Direct method. Here bronchoscope is introduced
directly through the glottis.
2. Through laryngoscope. Here glo ttis is first exposed
with the help of a spatular type laryngoscope and
then the bronchoscope is introduced through the
laryngoscope into the trachea. Laryngoscope is then
withdrawn. This me thod is useful in infan ts and
young children, and in ad ults who have short neck
and thick tongue.
Details of Technique
l. A piece of ga uze is placed on the upper teeth for the ir
protect ion aga inst injury.
2. Proper-sized bronchoscope is lu bricated with a swab
of autoclaved liquid paraffin or gelly. It is held by the shaft
in surgeon's right hand in a pen- like fashion. Fingers of
the left hand are used to retract the upper lip and guide
the bronchoscope.
3. Now looking through the scope, tip of epiglottis is
identified first and the scope passed behind it and the
epiglottis lifted forward to expose the glottiS. Now bronchoscope
is rotated 90° clockwise so that its bevelled tip
is in the axis of glottis to ease its entry into the trachea.
Once trachea is entered, scope is rotated back to the original
position.
4. Bronchoscope is grad ually advanced and the entire
tracheobronchial tree examined. Axis of bronchoscope
should be made to correspond with axes of the trachea
and bronchi. To ac hieve this, head and neck are flexed
to the left when examining the right bronchial tree and
vice versa.
Openi ngs of all the segmental bronchi in both the
lungs are examined seriatim.
5. Direct vision, right angled and retrograde telescopes
can be used for magnification and detailed examination.
6. Biopsy of the les ion of susp icious area can be taken.
7. Secretions can be collected for exfoliative cytology,
or bacteriologic examination.
Post-operative Care
1. Keep the patient in humid atmosphere.
2. Watch for respiratory distress. This could be due to
laryngeal spasm or subglottic oedema if the proced ure
had been unduly prolonged or the bronchoscope
introduced repeatedly. Inspiratory stridor and suprasternal
retraction will ind icate need for tracheostomy.
Complications
1. Injury to teeth and li ps.
2. Haemorrhage from the biopsy site.
3. Hypox ia and cardiac arrest.
4. Laryngeal oedema.
Precautions During Bronchoscopy
l. Select proper size of bronchoscope according to
patient's age (see Table A 1).
2. Do not force bronchoscope thro ugh closed glott is.
3. Repeated removal and introduction of bronchoscope
should be avoided.
4. Procedure shou ld not be prolonged beyond 20 minutes
in infants and children, otherwise it may cause
subglottic oedema in pos t-operati ve period.
FLEXIBLE FIBRE OPTIC BRONCHOSCOPY
These days, flexible fibre optic bronchoscopy has
replaced rigid bronchoscopy for diagnostic procedures
particularly in adults. It provides magnification and better
illumination, and because of the smaller size, permits
examination of subsegmental bronchi. It is also easy to
use ll1 patients with neck or jaw abnormalities where rigid
bronchoscopy may almost be impossible technically.
This procedure can be performed under topical anaesthesia
and is very useful for bedside examination of the critically
ill patients. The suction/biopsy channel provided
in the fibrescope helps to remove secretions, inspissated
plugs of mucus or even small foreign bodies. Flexible
bronchoscope can also be easily passed through endotracheal
tube or the tracheostomy opening. However, it has
limited utiltty in children because of the problems of
ventilation.
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
. 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
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.
Oesophagoscopy
Oesophagoscopy is of two types:
1. Rigid oesophagoscopy.
2. Flexible fibre-optic oesophagoscopy.
RIGID OESOPHAGOSCOPY
Indications
A. Diagnostic
1. To inves tigate cause for dysphag ia, e. g. cancer
oesophagus, cardiac achalas ia, strictures, oesophagitis,
diverticula, etc.
2. To find cause for retrosternal burning, e.g. reflux
oesophag itis or hiatus hernia.
3. To find cause for haematemesis, e.g. oesophageal
varices.
4. Secondaries neck with unknown primary (as a pan
of panendoscopy).
B. Therapeutic
1. Remova l of a foreign body.
2. Dilatation in case of oesophageal strictures or card
iac achalas ia.
3. Endoscopic removal of benign lesio ns, e. g. fibrom a,
papilloma, cysts, etc.
4. Insertion of Soutar's or Mou sseau ~B a rb in tube in
palliati ve treatment of oesophageal carcinoma.
5. Injection of oesophageal varices.
Contraindications
l.
2.
Trismus-makes the procedure technically difficult.
Disease of cervical spine, e.g. cervical trauma, spondylosis,
tu be rculous sp ine, osteophytes, kyphos is. They
make rigid oesophagoscopy technically difficult. Flexible
fibre -optic oesophagoscopy is performed in these
cases.
3. Receding mandible.
4. Aneurysm of aorta for fear of rupture and fatal haemorrhage.
5. Advanced heart, liver or kidney disease may be a
relative contraindication.
Anaesthesia
Genenll anaesthesia with oro-tracheal intubation, with
tube in the left corner of the mouth. it can be performed
under local anaesthesia in seleC(ed ind ividuals.
Position
Same as for direct laryngoscopy. Patient lies supine, head
is elevated by 10-15 cm, neck flexed on chest, and head
extended at adanto-occipital jo int. The purpose of this
positio n is to attain the axes of mouth, pharynx and
oesophagus in a straight line to pass the rigid tube easily.
This position can be achieved with the help of an ass istant
or a special head rest.
Technique
1. A piece of gauze is placed over the upper teeth to
protect teeth and lips.
2. Oesophagoscope is lubricated with a swab of autoclaved
liquid paraffin or jelly.
3. The oesophagoscope is held by its proximal end in
a pen-like fashion and introduced into the mouth
by the right side of the tongue and then towards the
midd le of its dorsum.
Now there a re 4 basic steps:
1. Identification of drytenoids. Once oesophagoscope
has been introduced to the back of tongue, it is
advanced gently by the left thumb and index finge r.
Epiglo ttis is first seen , then the endotracheal tube
and a little furth er down arytenoids can be identified.
2. Passing the cricophar)'ngeal sphincter. Keeping the tip
of oesophagoscope stric tly in the midline, behind
the larynx, it is lifted with movements of left thumb
to open the h ypopharynx. With slow but sustained
pressure, the sph incter will open and then the tip of
oesophagoscope can be guided easily into the
oesophag us. Never apply force to open the sphincter.
Sometimes, a fine bougie can be lIsed to find the
lumen. An add itional dose of muscle relaxant may
be required if sphincter does not open. Once oeso~
phagus has been entered, it is easier to advance the
scope, provided, oesophagea l lumen is kept constantly
in view.
3. Crossing the aortic arch and left bronchus. In an adult.
this natural narrowing lies about 25 cm from the
incisors. Aortic pulsa tion can be seen . When cro~sing
this area, head of the patient is slightly lowe red
so that oesophageal lumen is in line with that of the
scope.
4. Passing the cardia. Head and shoulders remain be 10\\'
the level of the table, head being slightly higher
than the shoulders and moved slightly to the right
At this stage, the oesophagoscope points to the lefr
ante rior-superior iliac spine. Cardia is identified b)
its redder and more velvety or rugose mucosa.
Never forget to inspect the oesophageal wall again
when the oesophagoscope is withdrawn.
Post-operative Care
1. Sips of plain water followed by usual diet may be
given in an uneventful oesophagoscopy.
2. Pat ient is watched for pain in the interscapular region,
surgical emphysema of neck, and ahrupt rise of temperatu
re. They indicate oesophageal perfora tion.
Complications
1. Injury to lips and teeth.
2. InJulY to ar)' tenoids.
3. Injur )' to pharyngeal mucosa. They are al l the result of
careless technique and can be avoided.
4. Perforation of oesophagus. Most often it occurs at the
site of Killian's dehiscence (near cricopharyngeal
sphincter) when undue force has been used to l'ass
the oesophagoscope. Surgical emphysema develops
within an hOLlr or so and the patient complains of
pain in the interscapular region. This may be complicated
by abscess in retropharyngeal space or
mediastinum ..
5. Compression of trachea. Oesophagoscope may press on
posterior tracheal wall, especially in child ren, causing
obstruction to respiration and cyanosis. Treatment is
immediate withdrawal of oesophagoscope.
FLEXIBLE FIBRE OPTIC OESOPHAGOSCOPY
Irs main ad va ntage over the rigid oesophagoscopy is
that it is an outdoor procedure , does not require general
anaesthes ia and can be used in patients wi th abnormalities
of spine or jaw where rigid endoscopy is technica
lly difficult. The oesophagus, stomach and duodenum
can all be examined in one sitting. Good illumination
and magni ication provided by the fibrescope helps in
the accurate diagnosis of the mucosa l disease affecting
these sites an.J permits taking of prec ision biopsies,
remova l of small fore ign bodies or benign tumours,
dila tation of webs or strictures and even injection of
bleeding varices with scleroSing agents. In ca 'es of malignant
disease, oesophrtgeal stent can be placed as a palliative
measure.
The procedure is pelfonned under local anaesthesia
with or without intravenous sed ation. The patient lies in
left lateral position and fib r>scope is pas eJ th rough a plastic
mouth prop inro the pharynx, post-cricoid area and
oesophagus, insufflating air as the endoscope is advanced,
to open tl1e lumen of oesophagus. These days flexible fibre
optic oesophagoscopy has practically replaced rigid
oesophagoscopyexc pt in some cases of foreign bodies.
1. Rigid oesophagoscopy.
2. Flexible fibre-optic oesophagoscopy.
RIGID OESOPHAGOSCOPY
Indications
A. Diagnostic
1. To inves tigate cause for dysphag ia, e. g. cancer
oesophagus, cardiac achalas ia, strictures, oesophagitis,
diverticula, etc.
2. To find cause for retrosternal burning, e.g. reflux
oesophag itis or hiatus hernia.
3. To find cause for haematemesis, e.g. oesophageal
varices.
4. Secondaries neck with unknown primary (as a pan
of panendoscopy).
B. Therapeutic
1. Remova l of a foreign body.
2. Dilatation in case of oesophageal strictures or card
iac achalas ia.
3. Endoscopic removal of benign lesio ns, e. g. fibrom a,
papilloma, cysts, etc.
4. Insertion of Soutar's or Mou sseau ~B a rb in tube in
palliati ve treatment of oesophageal carcinoma.
5. Injection of oesophageal varices.
Contraindications
l.
2.
Trismus-makes the procedure technically difficult.
Disease of cervical spine, e.g. cervical trauma, spondylosis,
tu be rculous sp ine, osteophytes, kyphos is. They
make rigid oesophagoscopy technically difficult. Flexible
fibre -optic oesophagoscopy is performed in these
cases.
3. Receding mandible.
4. Aneurysm of aorta for fear of rupture and fatal haemorrhage.
5. Advanced heart, liver or kidney disease may be a
relative contraindication.
Anaesthesia
Genenll anaesthesia with oro-tracheal intubation, with
tube in the left corner of the mouth. it can be performed
under local anaesthesia in seleC(ed ind ividuals.
Position
Same as for direct laryngoscopy. Patient lies supine, head
is elevated by 10-15 cm, neck flexed on chest, and head
extended at adanto-occipital jo int. The purpose of this
positio n is to attain the axes of mouth, pharynx and
oesophagus in a straight line to pass the rigid tube easily.
This position can be achieved with the help of an ass istant
or a special head rest.
Technique
1. A piece of gauze is placed over the upper teeth to
protect teeth and lips.
2. Oesophagoscope is lubricated with a swab of autoclaved
liquid paraffin or jelly.
3. The oesophagoscope is held by its proximal end in
a pen-like fashion and introduced into the mouth
by the right side of the tongue and then towards the
midd le of its dorsum.
Now there a re 4 basic steps:
1. Identification of drytenoids. Once oesophagoscope
has been introduced to the back of tongue, it is
advanced gently by the left thumb and index finge r.
Epiglo ttis is first seen , then the endotracheal tube
and a little furth er down arytenoids can be identified.
2. Passing the cricophar)'ngeal sphincter. Keeping the tip
of oesophagoscope stric tly in the midline, behind
the larynx, it is lifted with movements of left thumb
to open the h ypopharynx. With slow but sustained
pressure, the sph incter will open and then the tip of
oesophagoscope can be guided easily into the
oesophag us. Never apply force to open the sphincter.
Sometimes, a fine bougie can be lIsed to find the
lumen. An add itional dose of muscle relaxant may
be required if sphincter does not open. Once oeso~
phagus has been entered, it is easier to advance the
scope, provided, oesophagea l lumen is kept constantly
in view.
3. Crossing the aortic arch and left bronchus. In an adult.
this natural narrowing lies about 25 cm from the
incisors. Aortic pulsa tion can be seen . When cro~sing
this area, head of the patient is slightly lowe red
so that oesophageal lumen is in line with that of the
scope.
4. Passing the cardia. Head and shoulders remain be 10\\'
the level of the table, head being slightly higher
than the shoulders and moved slightly to the right
At this stage, the oesophagoscope points to the lefr
ante rior-superior iliac spine. Cardia is identified b)
its redder and more velvety or rugose mucosa.
Never forget to inspect the oesophageal wall again
when the oesophagoscope is withdrawn.
Post-operative Care
1. Sips of plain water followed by usual diet may be
given in an uneventful oesophagoscopy.
2. Pat ient is watched for pain in the interscapular region,
surgical emphysema of neck, and ahrupt rise of temperatu
re. They indicate oesophageal perfora tion.
Complications
1. Injury to lips and teeth.
2. InJulY to ar)' tenoids.
3. Injur )' to pharyngeal mucosa. They are al l the result of
careless technique and can be avoided.
4. Perforation of oesophagus. Most often it occurs at the
site of Killian's dehiscence (near cricopharyngeal
sphincter) when undue force has been used to l'ass
the oesophagoscope. Surgical emphysema develops
within an hOLlr or so and the patient complains of
pain in the interscapular region. This may be complicated
by abscess in retropharyngeal space or
mediastinum ..
5. Compression of trachea. Oesophagoscope may press on
posterior tracheal wall, especially in child ren, causing
obstruction to respiration and cyanosis. Treatment is
immediate withdrawal of oesophagoscope.
FLEXIBLE FIBRE OPTIC OESOPHAGOSCOPY
Irs main ad va ntage over the rigid oesophagoscopy is
that it is an outdoor procedure , does not require general
anaesthes ia and can be used in patients wi th abnormalities
of spine or jaw where rigid endoscopy is technica
lly difficult. The oesophagus, stomach and duodenum
can all be examined in one sitting. Good illumination
and magni ication provided by the fibrescope helps in
the accurate diagnosis of the mucosa l disease affecting
these sites an.J permits taking of prec ision biopsies,
remova l of small fore ign bodies or benign tumours,
dila tation of webs or strictures and even injection of
bleeding varices with scleroSing agents. In ca 'es of malignant
disease, oesophrtgeal stent can be placed as a palliative
measure.
The procedure is pelfonned under local anaesthesia
with or without intravenous sed ation. The patient lies in
left lateral position and fib r>scope is pas eJ th rough a plastic
mouth prop inro the pharynx, post-cricoid area and
oesophagus, insufflating air as the endoscope is advanced,
to open tl1e lumen of oesophagus. These days flexible fibre
optic oesophagoscopy has practically replaced rigid
oesophagoscopyexc pt in some cases of foreign bodies.
Adenoidectomy
Adenoidectomy may be indicated alone or in combination
with tonsillectomy. In the latter event, adeno ids are
removed first and the nasopharynx packed before sta rting
tonsillectomy.
Indications
1. Adeno id hypertrophy causing snor in g, mouth
breathing, sleep apnoea syndrome or speech abnormaliti
es, i.e. (rhino lalia clausa).
2. Recurrent rhinosinusitis.
3. Chronic secretory otitis media associated with adenoid
hype rplas ia.
4. Recurrent ear discharge in benign CSOM associated
with adeno iditis/adenoid hyperplasia.
5. Dental malocclusion. Adenoidectomy does not correct
dental abnormalities but will prevenr its recurrence
after orthodontic treatment.
Contraindications
1. Cleft palate or submucous palate. Removal of adenoids
causes velopharyngeal insufficiency in such cases.
2. Haemorrhagic diathesis.
3. Acute infection of upper respiratory tract.
Anaesthesia
A lways general, with ora l endocracheal intubation.
Position
Same as for tonsillectomy. Hyperextension of neck should
always be avoided.
Steps of Operation
1. Boyle-Davis mouth-gag is inserted. Before actual
removal of adenoids, nasopharynx should always be
examined by retracting the soft palate with curved
end of the tongue depressor and by digital pa lpation ,
to confirm the diagnos is, to assess the size of adenoids
mass and to push the lateral adeno id mas:es
towards the midline.
2. Proper size of "adenoid curette with guard" is introduced
into the nasopharynx till its free edge touches
the posterior border of nasal septum and is then
pressed backwards to engage the adenoids. At this
level, head shou ld be slightly flexed to avoid injury
to the odontoid process.
3. With gentle sweep ing move ment, adenoids are shaved
off (Fig. 91.1) . Late ral masses are simi larly removed
with smaller curettes; small tags of lymphoid tissue
left behind are removed with punch forceps.4. Haemostasis is achieved by packing the area for
sometime. Persistent bleeders are electrocoagulated
under vision. If bleeding is still not controlled, a
postnasal pack is left for 24 hours.
Endoscopic Adenoidectomy
These days adeno ids can be removed more precisely by
using a debrider under endoscopic concro!.
Post-operative Care
Sdme as in tonsil lectomy. There is no dysphagia and
patient is up and about early.
Complications
l. Haemorrhage, usually seen in immed ia te postoperative
period. Nose and mouth may ' be full of
blood or the only indication may be vomitus of darkcoloured
blood which the patient had been swallowing
gradually in post-operative period. Ri sing pulse
rate is another indicator. Treatment is same as for
per-operat ive haemorrhage. Postnasal pack under
general anaesthesia is often requi red.
2. Injury to eustachian tube opening.
3. Injury to pharyngeal musculature and vertebrae. This is
due to hyperex tension of neck and undue pressure of
curette. Care should be taken when operating patients
of Down's syndrome as 10-20% of them have atlantoaxial
instability.
4. Velophar)lngeal insufficienc)l.
5. Nasopharyngeal stenosis due to scarring.
6. Recurrence. This is due to regrowth of adenoid tissue
left behind.
with tonsillectomy. In the latter event, adeno ids are
removed first and the nasopharynx packed before sta rting
tonsillectomy.
Indications
1. Adeno id hypertrophy causing snor in g, mouth
breathing, sleep apnoea syndrome or speech abnormaliti
es, i.e. (rhino lalia clausa).
2. Recurrent rhinosinusitis.
3. Chronic secretory otitis media associated with adenoid
hype rplas ia.
4. Recurrent ear discharge in benign CSOM associated
with adeno iditis/adenoid hyperplasia.
5. Dental malocclusion. Adenoidectomy does not correct
dental abnormalities but will prevenr its recurrence
after orthodontic treatment.
Contraindications
1. Cleft palate or submucous palate. Removal of adenoids
causes velopharyngeal insufficiency in such cases.
2. Haemorrhagic diathesis.
3. Acute infection of upper respiratory tract.
Anaesthesia
A lways general, with ora l endocracheal intubation.
Position
Same as for tonsillectomy. Hyperextension of neck should
always be avoided.
Steps of Operation
1. Boyle-Davis mouth-gag is inserted. Before actual
removal of adenoids, nasopharynx should always be
examined by retracting the soft palate with curved
end of the tongue depressor and by digital pa lpation ,
to confirm the diagnos is, to assess the size of adenoids
mass and to push the lateral adeno id mas:es
towards the midline.
2. Proper size of "adenoid curette with guard" is introduced
into the nasopharynx till its free edge touches
the posterior border of nasal septum and is then
pressed backwards to engage the adenoids. At this
level, head shou ld be slightly flexed to avoid injury
to the odontoid process.
3. With gentle sweep ing move ment, adenoids are shaved
off (Fig. 91.1) . Late ral masses are simi larly removed
with smaller curettes; small tags of lymphoid tissue
left behind are removed with punch forceps.4. Haemostasis is achieved by packing the area for
sometime. Persistent bleeders are electrocoagulated
under vision. If bleeding is still not controlled, a
postnasal pack is left for 24 hours.
Endoscopic Adenoidectomy
These days adeno ids can be removed more precisely by
using a debrider under endoscopic concro!.
Post-operative Care
Sdme as in tonsil lectomy. There is no dysphagia and
patient is up and about early.
Complications
l. Haemorrhage, usually seen in immed ia te postoperative
period. Nose and mouth may ' be full of
blood or the only indication may be vomitus of darkcoloured
blood which the patient had been swallowing
gradually in post-operative period. Ri sing pulse
rate is another indicator. Treatment is same as for
per-operat ive haemorrhage. Postnasal pack under
general anaesthesia is often requi red.
2. Injury to eustachian tube opening.
3. Injury to pharyngeal musculature and vertebrae. This is
due to hyperex tension of neck and undue pressure of
curette. Care should be taken when operating patients
of Down's syndrome as 10-20% of them have atlantoaxial
instability.
4. Velophar)lngeal insufficienc)l.
5. Nasopharyngeal stenosis due to scarring.
6. Recurrence. This is due to regrowth of adenoid tissue
left behind.
Tonsillectomy
Indications
They are d ivided inro:
A. Absolute
1. ReculTent infections of throat. This is the most common
indication. Recurrent infections are further defi ned as:
(a) Seven or more episodes in one year, or
(b) Five episodes per year fo r 2 years, or
(c) Three ep isodes per year for 3 years, or
(d) Two weeks or more of lost sch ool or work in one
year.
2. PeritonsiliLlr absces~. In children, tonsillectomy is done
4-6 weeks after abscess has been treated. In adults,
second attack of peri tonsillar abscess forms the
ahsolute indication.
3. Tons ill itis causing febrile se izures.
4. H ypertro phy of tonsils causing
• airway obstruction (s leep apnoea)
• difficul ty in deglutition
• interfe re nce with speech.
5. Suspici.on of malignancy'. A unilaterally enlarged tonsil
may be a lymphoma in c hildren and an epidermoid
carcinoma in adults. An excisional biopsy is done.
B. Relative
1. Diphther ia carriers, who do not respond to antibiotics.
2. Streptococcal carriers , who may be the source of
infection to orhers.
3. Chronic tonsillitis with bad tas te or halitosis which
is unresportS ive to medical treatment.
4. Recurrent streptocccal tonsillitis in a patient with
valvular heart disease.
C. As a Part of Another Operation
1. Palatopharyngoplasty which is done for sleep apnoea
syndrome.
2. Glossopharyngeal neurectomy. Tonsil is removed first
and then IX nerve is severed in the bed of tonsil.
3. Removal of styloid process.
Contraindications
1. Haemoglobin level less than 10 g%
2. Presence of acute infection in upper respira tory
tract, even ac ute tonsillit is. Bleeding is more in the
presence of acute infection.
3. Children under 3 years of age. They are at poor
surgica I risks.
4. Overt or submucous cleft palate.
5. Bleeding disorders, e.g. leukaemia, purp ura, aplastic
anaemia, haemophilia.
6. At the time of epidemic of polio.
7. Uncontrolled systemic disease, e.g. diabetes, cardiac
disease, hypertension or asthma.
S. Tonsillectomy is avoided during the period of menses.
Anaesthesia
Usually done under ge neral anaesthesia with endotracheal
intubatio n. In adu lts, it may be done under loca l
anaest hesia.
Position
Rose's position, i. e. patient lies supine with head
extended by plac ing a pillow under the shoulders. A rubber
ring is placed under the head to stabilise it (Fig. 90.1).
Hyperextension shou ld always be avo ided.
Steps of Operation (Dissection and
Snare Method)
1. Boyle-Davis mouth gag is introduced and opened. It
is held 111 place by Draffin 's bipods or a string over a
pulley (Fig. 90.2).2. Tonsil is grasped with tonsil-holding forceps and
pulled medially.
3. Incision is made in the mucous membrane where it
reflects from the tonsil to anterior pillar. It may be
extended along the upper po le to mucous membrane
between the tonsil and posterior pillar.
4. A blunt curved sc issor may be used to dissect the
tonsil from the peritonsillar tissue and separate its
upper pole.
5. Now the tonsil is held at its upper pole and trac tion
applied downwards and media ll y. Dissection is continued
with tonsillar dissector or scissors until lower
pole is reached (Fig. 90.3).
6. Now wire loop of tonsillar snare is threaded \.wer the
tonsil on to its pedicle, tightened, and the pedicle
cut and the tonsil removed.
7. A gauze sponge is placed in the fossa and pressure
applied for a few minutes.
8. Bleeding points are tied with silk. Procedure is
repeated on the other side.
Post-operative Care
1. Immediate general care
(a) Keep the patient in coma position until fully recovered
from anaesthesia.
(b) Keep a watch on bleeding from the nose and mouth.
(c) Keep check on vital signs, e.g. purse, respiration and
blood pressure.
2. Diet. When patient is fully recovered he is permitted
to take liquids, e.g. cold milk or ice cream. Sucking of ice
cubes gives relief from pain. Diet is gradually built from soft
to solid food. They may take custard, jell y, soft boiled eggs
or slice of bread soaked in milk on the 2nd day. Plenty of flu ids
should be encouraged.
3. Oral hygiene. Patient is given Condy's or salt
water gargles 3-4 times a da y. A mouth wash with plain
water after every feed helps to keep the mouth clean.
4. Analgesics. Pain, locally in the throat and referred
to ear, can be relieved by analgesics like paracetamol. An
analgesic can be given half an hour before meals.
5. Antibiotics. A suitable antibiotic can be· giv en
rally or by injection for a week.Patient is usually sent home 24 hou rs after operation
unless there is some complication. Patient can resume his
normal duties within 2 weeks.
Other methods for tonsillectomy (Table 90.1)
1. Guillotine method Largely abandoned. It can be
done ani y when tonsils are mobile and tonsil bed has not
been scarred by repeated infections.
2. Electrocautery. Both unipo lar and bipolar e lectrocautery
has been used. It reduces blood loss but causes
thermal injurr to tissues.
3. Laser tonsillectomy. !t is indica ted in coagu lat ion disorde
rs. Both KTP-5 I 2 and CO2 lasers have been used but
the former is preferred. Technique is similar to one used in
dissection method.
4. Laser ronsillorom)' , Another method is laser tonsillotomy
which aims to reduce the size of tonsils. It is indicated
in patients who are unable to tolerate general
anaesthesia. Tonsils are reduced by laser ablation up to
ante rior pillars by stage repeated applications.
5. Intmcapsular tonsillectomy. With the use of powered
instruments (debrided tonsil is removed but its capsule is
preserved in the hope to reduce post-operative pain.
6. Harmonic scalpel. It uses ultrasound to cut and coagulate
tissues. It is a cold method with less tissue damage
and post-operative pain compared to electrocautery
t,echnqu e.
7. Plasma-mediated ablation technique. In this ablation
method, protons are energized to break molecular bonds
between tissues. It is a cold method and does not cause
thermal injury.
8. Coblation tonsil/ectom)'.
9. Cr)'osurgical technique. Tonsil is frozen by app lication
of cryoprobe and then allowed to thaw. Two applications,
each of 3-4 minutes, are applied. Tons illar tissue will
undergo necrosis and later fall off leav ing a granulating
surface. Bleeding is less due to thrombosis of vesse ls
caused by freezing.
Complications
A. Immediate
1. Primary haemorrhage. Occurs at the time of operation.
It can be contro lled by pressure, ligation or electrocoagulation
of the bleeding vessels.
2. Reactionary haemorrhage. Occurs within a period of 24
hours and can be controlled by simple measures such as
removal of the clot, application of pressure or vasoconstrictor.
Presence of a clot prevents the clipping action of
the superior constrictor muscle on the vessels which pass
through it (compare post-partum uterine bleeding). If
above measures fail, ligation or electrocoagulation of the
bleeding vessels can be done under general anaesthesia.
3. Injur)' to tonsillar pillars, uvula, soft palate, tongue or
superior constrictor muscle due to bad surgical technique.
4. Injury to teeth.
5. Aspiration of blood.
6. Facial oedema. Some patients get oedema of the face
particularly of the eyelids.
7. Surgical emphysema. Rarely occurs due to injury (()
superior constrictor muscle.
B. Delayed
1. Secondary haemorrhage . Usually seen between the 5rh
to 10th posr-ope rative day. It is the result of sepsis and
premature separation of the membrane. Usually, it is heralded
by bloodstained sputum but may be profuse.
Sim ple measu res like removal of clot, topical application
of dilute adrenaline or hydrogen peroxide with pressure
usually suffice. For profuse bleeding, genera l
anaesthesia is given and bleeding vessel is electrocoaglllated
or ligated. Sometimes, approximation of pillar.with
mattress sutures may be required. Sometimes, external
carotid ligation may also be required.
Transfu sion of blood or plasma, depending on blooJ
loss, is given. Systemic antibiotics are given for control or
infection.
2. Infection. Infection of tonsillar fossa may lead t(
parapharyngeal abscess or otitis med ia.
3. Lung complications. Asp irat ion of blood, mucus ,lr
tissue fragments may cause atelectasis or lung abscess.
4. Scarring in soft palate and pillars.
5. Tonsillar remnants. Tonsil tags or tissue, left due tl
inadequate surgery, may get repeated ly infected.
6. Hypertrophy of lingual tonsil. This is a late complication
and is compensatory to loss of palati ne tonsils.
Sometimes, lymphoid tissue is left in the plica triangu ,
laris near the lower pole of tonsil, which later gets hype rtrophied.
Plica triangularis should, therefore be removed
during tonsillectomy.
They are d ivided inro:
A. Absolute
1. ReculTent infections of throat. This is the most common
indication. Recurrent infections are further defi ned as:
(a) Seven or more episodes in one year, or
(b) Five episodes per year fo r 2 years, or
(c) Three ep isodes per year for 3 years, or
(d) Two weeks or more of lost sch ool or work in one
year.
2. PeritonsiliLlr absces~. In children, tonsillectomy is done
4-6 weeks after abscess has been treated. In adults,
second attack of peri tonsillar abscess forms the
ahsolute indication.
3. Tons ill itis causing febrile se izures.
4. H ypertro phy of tonsils causing
• airway obstruction (s leep apnoea)
• difficul ty in deglutition
• interfe re nce with speech.
5. Suspici.on of malignancy'. A unilaterally enlarged tonsil
may be a lymphoma in c hildren and an epidermoid
carcinoma in adults. An excisional biopsy is done.
B. Relative
1. Diphther ia carriers, who do not respond to antibiotics.
2. Streptococcal carriers , who may be the source of
infection to orhers.
3. Chronic tonsillitis with bad tas te or halitosis which
is unresportS ive to medical treatment.
4. Recurrent streptocccal tonsillitis in a patient with
valvular heart disease.
C. As a Part of Another Operation
1. Palatopharyngoplasty which is done for sleep apnoea
syndrome.
2. Glossopharyngeal neurectomy. Tonsil is removed first
and then IX nerve is severed in the bed of tonsil.
3. Removal of styloid process.
Contraindications
1. Haemoglobin level less than 10 g%
2. Presence of acute infection in upper respira tory
tract, even ac ute tonsillit is. Bleeding is more in the
presence of acute infection.
3. Children under 3 years of age. They are at poor
surgica I risks.
4. Overt or submucous cleft palate.
5. Bleeding disorders, e.g. leukaemia, purp ura, aplastic
anaemia, haemophilia.
6. At the time of epidemic of polio.
7. Uncontrolled systemic disease, e.g. diabetes, cardiac
disease, hypertension or asthma.
S. Tonsillectomy is avoided during the period of menses.
Anaesthesia
Usually done under ge neral anaesthesia with endotracheal
intubatio n. In adu lts, it may be done under loca l
anaest hesia.
Position
Rose's position, i. e. patient lies supine with head
extended by plac ing a pillow under the shoulders. A rubber
ring is placed under the head to stabilise it (Fig. 90.1).
Hyperextension shou ld always be avo ided.
Steps of Operation (Dissection and
Snare Method)
1. Boyle-Davis mouth gag is introduced and opened. It
is held 111 place by Draffin 's bipods or a string over a
pulley (Fig. 90.2).2. Tonsil is grasped with tonsil-holding forceps and
pulled medially.
3. Incision is made in the mucous membrane where it
reflects from the tonsil to anterior pillar. It may be
extended along the upper po le to mucous membrane
between the tonsil and posterior pillar.
4. A blunt curved sc issor may be used to dissect the
tonsil from the peritonsillar tissue and separate its
upper pole.
5. Now the tonsil is held at its upper pole and trac tion
applied downwards and media ll y. Dissection is continued
with tonsillar dissector or scissors until lower
pole is reached (Fig. 90.3).
6. Now wire loop of tonsillar snare is threaded \.wer the
tonsil on to its pedicle, tightened, and the pedicle
cut and the tonsil removed.
7. A gauze sponge is placed in the fossa and pressure
applied for a few minutes.
8. Bleeding points are tied with silk. Procedure is
repeated on the other side.
Post-operative Care
1. Immediate general care
(a) Keep the patient in coma position until fully recovered
from anaesthesia.
(b) Keep a watch on bleeding from the nose and mouth.
(c) Keep check on vital signs, e.g. purse, respiration and
blood pressure.
2. Diet. When patient is fully recovered he is permitted
to take liquids, e.g. cold milk or ice cream. Sucking of ice
cubes gives relief from pain. Diet is gradually built from soft
to solid food. They may take custard, jell y, soft boiled eggs
or slice of bread soaked in milk on the 2nd day. Plenty of flu ids
should be encouraged.
3. Oral hygiene. Patient is given Condy's or salt
water gargles 3-4 times a da y. A mouth wash with plain
water after every feed helps to keep the mouth clean.
4. Analgesics. Pain, locally in the throat and referred
to ear, can be relieved by analgesics like paracetamol. An
analgesic can be given half an hour before meals.
5. Antibiotics. A suitable antibiotic can be· giv en
rally or by injection for a week.Patient is usually sent home 24 hou rs after operation
unless there is some complication. Patient can resume his
normal duties within 2 weeks.
Other methods for tonsillectomy (Table 90.1)
1. Guillotine method Largely abandoned. It can be
done ani y when tonsils are mobile and tonsil bed has not
been scarred by repeated infections.
2. Electrocautery. Both unipo lar and bipolar e lectrocautery
has been used. It reduces blood loss but causes
thermal injurr to tissues.
3. Laser tonsillectomy. !t is indica ted in coagu lat ion disorde
rs. Both KTP-5 I 2 and CO2 lasers have been used but
the former is preferred. Technique is similar to one used in
dissection method.
4. Laser ronsillorom)' , Another method is laser tonsillotomy
which aims to reduce the size of tonsils. It is indicated
in patients who are unable to tolerate general
anaesthesia. Tonsils are reduced by laser ablation up to
ante rior pillars by stage repeated applications.
5. Intmcapsular tonsillectomy. With the use of powered
instruments (debrided tonsil is removed but its capsule is
preserved in the hope to reduce post-operative pain.
6. Harmonic scalpel. It uses ultrasound to cut and coagulate
tissues. It is a cold method with less tissue damage
and post-operative pain compared to electrocautery
t,echnqu e.
7. Plasma-mediated ablation technique. In this ablation
method, protons are energized to break molecular bonds
between tissues. It is a cold method and does not cause
thermal injury.
8. Coblation tonsil/ectom)'.
9. Cr)'osurgical technique. Tonsil is frozen by app lication
of cryoprobe and then allowed to thaw. Two applications,
each of 3-4 minutes, are applied. Tons illar tissue will
undergo necrosis and later fall off leav ing a granulating
surface. Bleeding is less due to thrombosis of vesse ls
caused by freezing.
Complications
A. Immediate
1. Primary haemorrhage. Occurs at the time of operation.
It can be contro lled by pressure, ligation or electrocoagulation
of the bleeding vessels.
2. Reactionary haemorrhage. Occurs within a period of 24
hours and can be controlled by simple measures such as
removal of the clot, application of pressure or vasoconstrictor.
Presence of a clot prevents the clipping action of
the superior constrictor muscle on the vessels which pass
through it (compare post-partum uterine bleeding). If
above measures fail, ligation or electrocoagulation of the
bleeding vessels can be done under general anaesthesia.
3. Injur)' to tonsillar pillars, uvula, soft palate, tongue or
superior constrictor muscle due to bad surgical technique.
4. Injury to teeth.
5. Aspiration of blood.
6. Facial oedema. Some patients get oedema of the face
particularly of the eyelids.
7. Surgical emphysema. Rarely occurs due to injury (()
superior constrictor muscle.
B. Delayed
1. Secondary haemorrhage . Usually seen between the 5rh
to 10th posr-ope rative day. It is the result of sepsis and
premature separation of the membrane. Usually, it is heralded
by bloodstained sputum but may be profuse.
Sim ple measu res like removal of clot, topical application
of dilute adrenaline or hydrogen peroxide with pressure
usually suffice. For profuse bleeding, genera l
anaesthesia is given and bleeding vessel is electrocoaglllated
or ligated. Sometimes, approximation of pillar.with
mattress sutures may be required. Sometimes, external
carotid ligation may also be required.
Transfu sion of blood or plasma, depending on blooJ
loss, is given. Systemic antibiotics are given for control or
infection.
2. Infection. Infection of tonsillar fossa may lead t(
parapharyngeal abscess or otitis med ia.
3. Lung complications. Asp irat ion of blood, mucus ,lr
tissue fragments may cause atelectasis or lung abscess.
4. Scarring in soft palate and pillars.
5. Tonsillar remnants. Tonsil tags or tissue, left due tl
inadequate surgery, may get repeated ly infected.
6. Hypertrophy of lingual tonsil. This is a late complication
and is compensatory to loss of palati ne tonsils.
Sometimes, lymphoid tissue is left in the plica triangu ,
laris near the lower pole of tonsil, which later gets hype rtrophied.
Plica triangularis should, therefore be removed
during tonsillectomy.
Direct Laryngoscopy
It is direct visualisa tion of larynx and hypopharynx.
Indications
A. Diagnostic
1. When indirect laryngoscopy is not possible as in
infants and young children, and the symptomato logy
points to larynx and/or hypopharynx, e.g. hoarseness,
dyspnoea, stridor and dysphagia.
2. When indirect laryngoscopy has not been successful,
e.g. due to excessive gag reflex or overhanging
epiglo ttis obscuring a part of the complete view of
the larynx.
J. To examine hidden areas of:
Hypo/)har)'nx: Base of tongue, va lleculae and lower
part of pyriform fossa.
Larynx: Infrahyoid epiglottis, anterior commissure,
ventricles and subglottic region .
4. To find the extent of growth and take a bio psy.
B. Therapeutic
1. Removal of benign lesions of larynx, e.g. papilloma,
fibroma, vocal nodule, polyp or cyst.
2. Remova l of foreign bodies from larynx and
hypopharynx.
J. Dilatation of laryngeal stric;tures.
Contra indications
1. Diseases or injuries of cervica l spine.
2. Moderate or marked dyspnoea unless the airway has
been provided by tracheostomy.
J. Recent coronary occlusion or cardiac decompensatio
n.
Anaesthesia
General anaesthesia is preferred though this procedure can
be performed under local anaesthesia. In infants and young
children, no anaesthesia may be required if procedure is for
diagnostic purpose.
Position
Patient lies supine. Head is elevated by 10-15 cm by
placing a pillow under the occiput or by ra ising h ead flap
of the operation table. Neck is flexed on thorax and the
head extended on adamO-OCCipital jo int (Barking-dog
position) .
Procedure
1. A piece of gauze is placed on the upper teeth to protect
them. aga inst trauma.
2. Laryngoscope is lubricated with a little autoclaved
liqu id paraffin.
J. Laryngoscope is held by the handle in the left hand .
Right hand is used, to retract the lips and guide the
laryngoscope and to handle suction and instru ments.
4. Laryngoscope is introduced by one side of the
to ngue which is pushed to the oppos ite side till posterior
third of to ngue is reached. It is then moved to
the midline and lifted forward to bring the epiglo ttis
in view.
5. Laryngoscope is now advanced behind the epiglottis
and lifted forward without levering it on the upper
tee th or jaw (Fig. 87.1). This gi ves good view of the
interior of the larynx.
6. If anterior commissure laryngoscope is being used,
its t ip can be advanced further between the ventricular
bands to examine the ventricles and anterior
commissure . It can be passed between the vocal
cords to examine the subglottic region .
7. Following struc tures are examined seria lly: Base of
tongue, right and left valleculae, epiglottis, (its tip,
lingual and laryngeal surfaces ), right and left pyriform
sinuses, aryepiglottic fo lds, arytenoids, postcricoid
region, both false cord s, anter ior and
posterior commissure, right and left ventricles, right
and left voca l cords and subglottic area. Mobility of
voca l cords sh ould also be observed.
A right-angled te lescope can be used to see the undersurface
of voca l cords and the walls of the subglottis .
After rhe procedure is completed, laryngoscope is withdrawn
and lips and teeth examined for any injury.Post-operative Care
1. Patient is kept in coma position to prevent aspiration
of blood or secretions.
2. Patient's respiration should be watched for any
laryngeal spasm and cyanosis.
3. Trauma to larynx, especially if repeated attempts
at laryngoscopy have been made. It may lead to
laryngeal oedema and respiratory distress.
4. Bleeding may occur from the operative site. Patient
may spit blood. Care should be taken to prevent
aspiration.
Complications
1. [njury to lips and tongue if they are nipped between
the teeth and the laryngoscope .
2. [njury to teeth. They may get dislodged and fall into
pharynx.
3. Bleeding.
4. Laryngeal oedema.
Indications
A. Diagnostic
1. When indirect laryngoscopy is not possible as in
infants and young children, and the symptomato logy
points to larynx and/or hypopharynx, e.g. hoarseness,
dyspnoea, stridor and dysphagia.
2. When indirect laryngoscopy has not been successful,
e.g. due to excessive gag reflex or overhanging
epiglo ttis obscuring a part of the complete view of
the larynx.
J. To examine hidden areas of:
Hypo/)har)'nx: Base of tongue, va lleculae and lower
part of pyriform fossa.
Larynx: Infrahyoid epiglottis, anterior commissure,
ventricles and subglottic region .
4. To find the extent of growth and take a bio psy.
B. Therapeutic
1. Removal of benign lesions of larynx, e.g. papilloma,
fibroma, vocal nodule, polyp or cyst.
2. Remova l of foreign bodies from larynx and
hypopharynx.
J. Dilatation of laryngeal stric;tures.
Contra indications
1. Diseases or injuries of cervica l spine.
2. Moderate or marked dyspnoea unless the airway has
been provided by tracheostomy.
J. Recent coronary occlusion or cardiac decompensatio
n.
Anaesthesia
General anaesthesia is preferred though this procedure can
be performed under local anaesthesia. In infants and young
children, no anaesthesia may be required if procedure is for
diagnostic purpose.
Position
Patient lies supine. Head is elevated by 10-15 cm by
placing a pillow under the occiput or by ra ising h ead flap
of the operation table. Neck is flexed on thorax and the
head extended on adamO-OCCipital jo int (Barking-dog
position) .
Procedure
1. A piece of gauze is placed on the upper teeth to protect
them. aga inst trauma.
2. Laryngoscope is lubricated with a little autoclaved
liqu id paraffin.
J. Laryngoscope is held by the handle in the left hand .
Right hand is used, to retract the lips and guide the
laryngoscope and to handle suction and instru ments.
4. Laryngoscope is introduced by one side of the
to ngue which is pushed to the oppos ite side till posterior
third of to ngue is reached. It is then moved to
the midline and lifted forward to bring the epiglo ttis
in view.
5. Laryngoscope is now advanced behind the epiglottis
and lifted forward without levering it on the upper
tee th or jaw (Fig. 87.1). This gi ves good view of the
interior of the larynx.
6. If anterior commissure laryngoscope is being used,
its t ip can be advanced further between the ventricular
bands to examine the ventricles and anterior
commissure . It can be passed between the vocal
cords to examine the subglottic region .
7. Following struc tures are examined seria lly: Base of
tongue, right and left valleculae, epiglottis, (its tip,
lingual and laryngeal surfaces ), right and left pyriform
sinuses, aryepiglottic fo lds, arytenoids, postcricoid
region, both false cord s, anter ior and
posterior commissure, right and left ventricles, right
and left voca l cords and subglottic area. Mobility of
voca l cords sh ould also be observed.
A right-angled te lescope can be used to see the undersurface
of voca l cords and the walls of the subglottis .
After rhe procedure is completed, laryngoscope is withdrawn
and lips and teeth examined for any injury.Post-operative Care
1. Patient is kept in coma position to prevent aspiration
of blood or secretions.
2. Patient's respiration should be watched for any
laryngeal spasm and cyanosis.
3. Trauma to larynx, especially if repeated attempts
at laryngoscopy have been made. It may lead to
laryngeal oedema and respiratory distress.
4. Bleeding may occur from the operative site. Patient
may spit blood. Care should be taken to prevent
aspiration.
Complications
1. [njury to lips and tongue if they are nipped between
the teeth and the laryngoscope .
2. [njury to teeth. They may get dislodged and fall into
pharynx.
3. Bleeding.
4. Laryngeal oedema.
Endoscopic Sinus Surgery
Endoscopic surgery has made a great contribution towards
management of sinus disease. Indications for conventional
operations like those of Caldwell-Luc, frontal sinus operations,
external ethmoidectomy have greatly reduced.
Endoscopic surgery is minimally invasive surgery and does
not require skin incisions or removal of intervening bone
to acces, the disease. In the sinuses, ventilation and
drainage of the sinuses is established preserving the nasal
and sinus mucosa and its function of mucociliary clearance.
Advances in endoscopic surgery have been possible due to;
1. Development of better optics.
2. Improved brighter illumination.
3. Development of microsurgical instruments to work
with the endoscopes and precise removal of tissue
with sharp cuts without stripping the mucosa.
4. Concomitant developments in imaging techniques
like CT and MRI to precise ly define the area of
pathology.
5. Introduction of powered instrumentation in the form
of sofr-t i ~s ue shavers also called micro-debriders (to
remove n asa l polyps, soft-tissue masses or mucosa)
help reduce bleeding to a great extent while bonecutting
drills help endoscopic surgery of frontal sinus,
hcrimal sac , etc. to remove bony obstruction.
6. The lar ' t advancement has been the computerassisted
image-guided navigational surgery in difficult
cases or revisional surgery when landmarks are
not easy to identify.
Indications
1. Chronic bacterial sinusitis unresponsive to adequate
medical treatment.
2. Recurrent acute bacterial sinusitis.
3 . Polypo id rhinosinusitis (diffuse nasal polypos is) .
4. Fungal sinusitis with fung<11 ball or nasal polypi.
5. Antrochnanal p()lyp.
6. Mucoce le 0 frontoethmo id or sph enoid sinus.
7. Con trol oi epistclx is by endoscopic cautery.
8. Remova l of foreign body from the nose or sinus.
9. Endoscopic se ptoplasty.
Advanced Nasal Endoscopic Techniques
1. Removal of benign tumours, e.g. in ert d papillomas
or angiufibromas.
2. Orbital abscess or cellulitis management.
3. Dacryocystorhinostomy.
4 Repair of CSF leak.
5. Pituitary surgery.
6. Optic nerve decompress ion.
7. Orbital decompression for Graves disease.
8. Control of posterior epistaxis (endoscopic clipping
of sphenopalatine artery).
9. Choanal atresia.
Contra i nd icati ons
1. Inexperience and lack of proper instrumentation.
2. Disease inaccess ible by endoscopic procedures, e.g.
lateral front al sinus disease and stenosis of internal
opening of frontal sinus.
3. Osteomyelitis.
4. Threatened intracranial or intraorbital complication.
Anaesthesia
General anaesthesia is preferred by most of the surgeons.
Local anaesthesia with i.v. sedation can be used in
when limited work is to be done.
Position
Patient lies flat in supine position with head rest ing ,m a
ring or head rest. Some also prefer to raise it by IS°
Techniques
Two surgical techniques are followed;
(a) Anterior to posterior (Stammberger's technique ); In
this technique surgery proceeds from uncinate
process backward to sphenoid sinus. Advantage of
this technique is to tailor the extent of surge ry to
the extent of disease.
(b) Posterior to anterior (Wigand's techniq ue ); Surgery
starts at the sphenoid sinus and proceecls anteriorly
along the base of skull and medial orbital wall. This
is mostly done in extensive polyposis or in revisional
sinus surgery.
Steps of Operation
1. Remove the pledgees of cotton kept for nasal decongestion
and topical anaesthesia.
2. Inspect the nose with 4 m.m 0° endoscope or do
complete nasal endoscopy if not a lready done.
3 . Inj ect submucosa lly 1 % lignocaine with 1:100, 00
adrenaline under endoscopic control (Fig. 861):
(a) On the lateral wall, near the upper end of midelk
turbinate.
(b) On the la teral wall, just below the first
inj ect ion.
(c) On the la teral \vall, just above the inferior
turbinate.
(d) In the middle turbinate, posterior aspec t.
(e) Posterior aspect of nasal septum.
4. Replace cotton pledgets and repe at injections on
the opposite side if bilateral FESS is to be done.Medialise the middle turbinate and identify the unc inate
process and bulla ethmoida lis. If middle turbinate is large ,
partial or total turbinectomy is performed . In case of concha
bullosa, lateral lamella is removed. Definitive surgical
steps include:
1. Uncinectomy. Uncinate process is incised with
sickle knife and remo ved with Blakesley forceps.
2. Identification and enlargement of maxillary
ostium. Maxillary ostium lies above the inferior
turbinate and posterior to lower third of uncinate
process. Once localised, it is enlarged anteriorly with
a back-biting forceps or pos teriorly with a through
cut-s tra ight forceps.
3. Bullectomy. Bulla ethmoidal is is penetrated with
curette or Blakesley forceps and removed. Avoid
injury to medial orbital wa ll, skull base or anterior
ethmoidal artery.
4. Penetration of basal lamella and removal of posterior
ethmoid cells. Basa l lame lla is the dividing thin
bony septum between anterior and posterior ethmoid
cells. It is penetrated in the lower and medial part
with a sma ll curette and then removed with Blakesley
forceps. Posterior ethmoid cells are exenterated. Optic
nerve is at risk if Onodi cell is present. Onodi ce ll is
a pos terior ethmoid cell which extends into the sphenoid
bone late ral and superior to the sphenoid sinus.
5. Clearance of frontal recess and frontal sinusotomy.
Iffrontal sinus is clear on CT scan and patient
also does not suffer from fremea I h eCldaches, nothing
need to be done. In the event of fron tal sinus disease
, front al recess is cleared and frontal sinus
drainage established.
Opening of frontal sinus is situated lateral to
attachment of middle turbinate, medial to medial
orbital wa ll, anterior to anterior ethmoidal artery
and posterior to agger nasi cell{s). Surgery in the area
of frontal recess is challenging as any d isrespect to
the mucosa in this area would lead to stenosis of
frontal sinus opening with mucocele formation o r
recurrent frontal sinusitis6. Sphenoidotomy. This step is done after clearance of
pos terior ethmo id cells or Clfter frontal sinuso tomy.
It is omitted if sinus is hea lthy. In this procedure
ante rior wall of sphe noid sinus is removed, and pus
and inspi ssa ted mat erial from wit hin the sinus
removed. There are two ways to remove the anterior
sinus wa ll:
(a ) By entering the sphenoid s inus anterior and
inferior to the ethmo id cavity created by the
above steps.
(b) By enlarging the opening of sphenoid sinus with
Bla kesley forceps or J -curette. Sinus opening is
identified after removal of the posterior-inferior
portion of superior turbinate near the nasal septum
and about 1.0 cm above the upper border of
posterior choana.
7. Nasal packs. Fina lly the nasal packs are aprlied, if
septal surge ry has also been done with FESS o r to
stop any bleed ing from the nasa l cavity.
Post-operative Care
It is individua lised according to the exten t of surgery
done.
I. Removal of nasal packs. Nasa l packs, if kept, are
removed at the time of discharge 24 hours
operation.
2. Antibiotics. An intraopera tive intravenous antibi otic
(amoxyclav, cephalosporin or quinolone) is
administered and then continued for 7-10 days by
oral ro ute.
3. Antihistaminics. For a llergic patients.
4 . Analgesics. For re lief of post-opera ti ve pa in.Nasal irrigations. Saline irrigations are started after 1
week post-operatively to remove blood clots, crusts and
secretions and continued once or twice a day for 1 week.
Steroid nasal sprays. Required in cases of nasal
allergy or those operated fo r nasa l polyps.
Endoscopic toilet. Blood clots, crusts and debris are
removed by suction and forceps from the ethmoid area lateral
to middle turbinate. Any adhesion fonl1ation in the
nose is di vided with suction. Healthy mucosa should not
be disturbed. Suction can be done from within the maxillary
sinus wirh a curved cannula. Since the endoscopic
clearance is a painful process, topical nasal anaesthetic
with a decongestant is sprayed before the procedure.
Patient pays weekly visits for inspection of the cavity
for 4 weeks and there after as required till mucosalisation
of the cavity is complete.
Complications
They are similar to conventional surgery of ethmoid complex
and can be divided into major and minor. Mostly they
involve orbit or skull base, or are of general nature
Major
1. Orbital haemorrhage
2. Loss of vision/ blindness
3. Diplopia
4. (SF leak
5. Meningitis rhinitis or sinusitis
6. Brain abscess
7. Massive haemorrhage
8. Intracranial haemorrhage
and direct brain trauma
9. Anosmia
10. Injury to internal carotid
artery in sphenoid sinus
11. Injury to nasolacrimal
duct and epiphora
12. Death
Minor:
1. Periorbital ecchymosis2. Periorbital emphysema 3. Post-operative epistaxis4. Post-operative infection:5. Adhesions6. Stenosis of maxilla ry 0r frontal sinus
requiring blood transfusion7. Exacerbation of asthma8. Hyposmia9. Dental pain
management of sinus disease. Indications for conventional
operations like those of Caldwell-Luc, frontal sinus operations,
external ethmoidectomy have greatly reduced.
Endoscopic surgery is minimally invasive surgery and does
not require skin incisions or removal of intervening bone
to acces, the disease. In the sinuses, ventilation and
drainage of the sinuses is established preserving the nasal
and sinus mucosa and its function of mucociliary clearance.
Advances in endoscopic surgery have been possible due to;
1. Development of better optics.
2. Improved brighter illumination.
3. Development of microsurgical instruments to work
with the endoscopes and precise removal of tissue
with sharp cuts without stripping the mucosa.
4. Concomitant developments in imaging techniques
like CT and MRI to precise ly define the area of
pathology.
5. Introduction of powered instrumentation in the form
of sofr-t i ~s ue shavers also called micro-debriders (to
remove n asa l polyps, soft-tissue masses or mucosa)
help reduce bleeding to a great extent while bonecutting
drills help endoscopic surgery of frontal sinus,
hcrimal sac , etc. to remove bony obstruction.
6. The lar ' t advancement has been the computerassisted
image-guided navigational surgery in difficult
cases or revisional surgery when landmarks are
not easy to identify.
Indications
1. Chronic bacterial sinusitis unresponsive to adequate
medical treatment.
2. Recurrent acute bacterial sinusitis.
3 . Polypo id rhinosinusitis (diffuse nasal polypos is) .
4. Fungal sinusitis with fung<11 ball or nasal polypi.
5. Antrochnanal p()lyp.
6. Mucoce le 0 frontoethmo id or sph enoid sinus.
7. Con trol oi epistclx is by endoscopic cautery.
8. Remova l of foreign body from the nose or sinus.
9. Endoscopic se ptoplasty.
Advanced Nasal Endoscopic Techniques
1. Removal of benign tumours, e.g. in ert d papillomas
or angiufibromas.
2. Orbital abscess or cellulitis management.
3. Dacryocystorhinostomy.
4 Repair of CSF leak.
5. Pituitary surgery.
6. Optic nerve decompress ion.
7. Orbital decompression for Graves disease.
8. Control of posterior epistaxis (endoscopic clipping
of sphenopalatine artery).
9. Choanal atresia.
Contra i nd icati ons
1. Inexperience and lack of proper instrumentation.
2. Disease inaccess ible by endoscopic procedures, e.g.
lateral front al sinus disease and stenosis of internal
opening of frontal sinus.
3. Osteomyelitis.
4. Threatened intracranial or intraorbital complication.
Anaesthesia
General anaesthesia is preferred by most of the surgeons.
Local anaesthesia with i.v. sedation can be used in
when limited work is to be done.
Position
Patient lies flat in supine position with head rest ing ,m a
ring or head rest. Some also prefer to raise it by IS°
Techniques
Two surgical techniques are followed;
(a) Anterior to posterior (Stammberger's technique ); In
this technique surgery proceeds from uncinate
process backward to sphenoid sinus. Advantage of
this technique is to tailor the extent of surge ry to
the extent of disease.
(b) Posterior to anterior (Wigand's techniq ue ); Surgery
starts at the sphenoid sinus and proceecls anteriorly
along the base of skull and medial orbital wall. This
is mostly done in extensive polyposis or in revisional
sinus surgery.
Steps of Operation
1. Remove the pledgees of cotton kept for nasal decongestion
and topical anaesthesia.
2. Inspect the nose with 4 m.m 0° endoscope or do
complete nasal endoscopy if not a lready done.
3 . Inj ect submucosa lly 1 % lignocaine with 1:100, 00
adrenaline under endoscopic control (Fig. 861):
(a) On the lateral wall, near the upper end of midelk
turbinate.
(b) On the la teral wall, just below the first
inj ect ion.
(c) On the la teral \vall, just above the inferior
turbinate.
(d) In the middle turbinate, posterior aspec t.
(e) Posterior aspect of nasal septum.
4. Replace cotton pledgets and repe at injections on
the opposite side if bilateral FESS is to be done.Medialise the middle turbinate and identify the unc inate
process and bulla ethmoida lis. If middle turbinate is large ,
partial or total turbinectomy is performed . In case of concha
bullosa, lateral lamella is removed. Definitive surgical
steps include:
1. Uncinectomy. Uncinate process is incised with
sickle knife and remo ved with Blakesley forceps.
2. Identification and enlargement of maxillary
ostium. Maxillary ostium lies above the inferior
turbinate and posterior to lower third of uncinate
process. Once localised, it is enlarged anteriorly with
a back-biting forceps or pos teriorly with a through
cut-s tra ight forceps.
3. Bullectomy. Bulla ethmoidal is is penetrated with
curette or Blakesley forceps and removed. Avoid
injury to medial orbital wa ll, skull base or anterior
ethmoidal artery.
4. Penetration of basal lamella and removal of posterior
ethmoid cells. Basa l lame lla is the dividing thin
bony septum between anterior and posterior ethmoid
cells. It is penetrated in the lower and medial part
with a sma ll curette and then removed with Blakesley
forceps. Posterior ethmoid cells are exenterated. Optic
nerve is at risk if Onodi cell is present. Onodi ce ll is
a pos terior ethmoid cell which extends into the sphenoid
bone late ral and superior to the sphenoid sinus.
5. Clearance of frontal recess and frontal sinusotomy.
Iffrontal sinus is clear on CT scan and patient
also does not suffer from fremea I h eCldaches, nothing
need to be done. In the event of fron tal sinus disease
, front al recess is cleared and frontal sinus
drainage established.
Opening of frontal sinus is situated lateral to
attachment of middle turbinate, medial to medial
orbital wa ll, anterior to anterior ethmoidal artery
and posterior to agger nasi cell{s). Surgery in the area
of frontal recess is challenging as any d isrespect to
the mucosa in this area would lead to stenosis of
frontal sinus opening with mucocele formation o r
recurrent frontal sinusitis6. Sphenoidotomy. This step is done after clearance of
pos terior ethmo id cells or Clfter frontal sinuso tomy.
It is omitted if sinus is hea lthy. In this procedure
ante rior wall of sphe noid sinus is removed, and pus
and inspi ssa ted mat erial from wit hin the sinus
removed. There are two ways to remove the anterior
sinus wa ll:
(a ) By entering the sphenoid s inus anterior and
inferior to the ethmo id cavity created by the
above steps.
(b) By enlarging the opening of sphenoid sinus with
Bla kesley forceps or J -curette. Sinus opening is
identified after removal of the posterior-inferior
portion of superior turbinate near the nasal septum
and about 1.0 cm above the upper border of
posterior choana.
7. Nasal packs. Fina lly the nasal packs are aprlied, if
septal surge ry has also been done with FESS o r to
stop any bleed ing from the nasa l cavity.
Post-operative Care
It is individua lised according to the exten t of surgery
done.
I. Removal of nasal packs. Nasa l packs, if kept, are
removed at the time of discharge 24 hours
operation.
2. Antibiotics. An intraopera tive intravenous antibi otic
(amoxyclav, cephalosporin or quinolone) is
administered and then continued for 7-10 days by
oral ro ute.
3. Antihistaminics. For a llergic patients.
4 . Analgesics. For re lief of post-opera ti ve pa in.Nasal irrigations. Saline irrigations are started after 1
week post-operatively to remove blood clots, crusts and
secretions and continued once or twice a day for 1 week.
Steroid nasal sprays. Required in cases of nasal
allergy or those operated fo r nasa l polyps.
Endoscopic toilet. Blood clots, crusts and debris are
removed by suction and forceps from the ethmoid area lateral
to middle turbinate. Any adhesion fonl1ation in the
nose is di vided with suction. Healthy mucosa should not
be disturbed. Suction can be done from within the maxillary
sinus wirh a curved cannula. Since the endoscopic
clearance is a painful process, topical nasal anaesthetic
with a decongestant is sprayed before the procedure.
Patient pays weekly visits for inspection of the cavity
for 4 weeks and there after as required till mucosalisation
of the cavity is complete.
Complications
They are similar to conventional surgery of ethmoid complex
and can be divided into major and minor. Mostly they
involve orbit or skull base, or are of general nature
Major
1. Orbital haemorrhage
2. Loss of vision/ blindness
3. Diplopia
4. (SF leak
5. Meningitis rhinitis or sinusitis
6. Brain abscess
7. Massive haemorrhage
8. Intracranial haemorrhage
and direct brain trauma
9. Anosmia
10. Injury to internal carotid
artery in sphenoid sinus
11. Injury to nasolacrimal
duct and epiphora
12. Death
Minor:
1. Periorbital ecchymosis2. Periorbital emphysema 3. Post-operative epistaxis4. Post-operative infection:5. Adhesions6. Stenosis of maxilla ry 0r frontal sinus
requiring blood transfusion7. Exacerbation of asthma8. Hyposmia9. Dental pain