Tuesday, December 28, 2010

Chronic Suppurative Otitis Media

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.
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
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.
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
6. Fibrosis and adhesions. They are the result of
bealing process and may' further impair mobility of ossicular
chain or block the eustachian tube.
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.
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
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
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
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 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.
-\ 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
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.
- me as in tubotympanic·type.
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.
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
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.
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.
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
(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.

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.
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.
1. Malfunctioning of eustachian tube. The causes are:
I') Adenoid hyperplasia .
Ii) Chronic rhinitis and sinusiti s.
(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
eustachisecre tory activity as middle ear mucosa acts as a shock organ
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
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.


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.


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.
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.
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


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
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,erthe lUlddle eat.
(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
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·
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 is of two types:
1. Rigid .
2. Flexible fibre optic.
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
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.
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.
Same as fordirect laryngoscopy.
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
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.
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.
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

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)).
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:ingle, carcino mllrolls ncuropal hy.
7. Miscellaneous. Multiple sclerosis, h ypothyroidlsm,
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(yrnpanotomy whcre perilymph fistula is st rongly sus'
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
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 L month. Severe heming loss ;:Jnn rhal associated with vcr ~
tigo ha v(~ poor prognosis. Younger patient'S- below 40 and
those with mcx1erate losses have better prugnosis.