CHRONIC OTITIS

MEDIA

Dr Apurvdeep Kaur
MBBS, MS ENT HNS
 Definition

Inflammation of the mucous membrane lining the middle ear cleft consisting
of the
• eustachian tube,
• tympanic cavity,
• mastoid antrum and
• mastoid air cells
 Epidemiology

• Incidence-higher in developing countries because of poor socio-

economic standards, poor nutrition and lack of health
education.
• both sexes
• All age groups.
• In India, the overall prevalence is 46 and 16 persons per thousand in
rural and urban population respectively.
• It is also the single most important cause of hearing impairment in
rural population.
TYPES OF C.S.O.M.
•Anatomical
• Tubo-tympanic- safe
• Attico-antral- unsafe
•Pathological
• Healed otitis media- adhesive otitis media
• Mucosal disease
• Inactive- permanent perforation
• Active- csom
• Squamous disease
• Inactive-retraction pocket
• Active-cholesteatoma
Differences between Tubotympanic and Attico-antral
types of CSOM
 Aetiolo
group.
gy
• The disease starts in childhood and is therefore common in that age

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
gets exposed to the environment and sensitized to dust, pollen and
other aeroallergens causing persistent otorrhoea.
2.Ascending infections via the eustachian tube. Infection from
tonsils, adenoids and infected sinuses may 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.
TUBO TYMPANIC
C.S.O.M
• Patency of Eustachian tube
• Nidus of infection in U.R.T.I.
• Immune status of patient
• Aerobic and Anaerobic
 Patholo
gylocalized to the mucosa and, that too, mostly
• The tubotympanic disease remain
to anteroinferior part of the middle ear cleft. Like any other chronic infection, the
processes of healing 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 the patient. Thus, acute exacerbations are not uncommon. The
pathological changes seen in this type of CSOM are:
1.Perforation of pars tensa- It is a central perforation and its size and
position varies.
2.Middle ear mucosa- It may be normal when disease is quiescent or inactive. It
is edematous and velvety when disease is active.
3.Polyp- A polyp is a smooth mass of edematous and inflamed mucosa which
has protruded through a perforation and presents in the external canal. It is
usually pale in contrast to pink, fleshy polyp seen in atticoantral disease.
 Patholo
4.Ossicular chain- It is gyintact and
usually mobile but may show some
degree of necrosis, particularly of the long process of incus.
5.Tympanosclerosis- It is hyalinization 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 with the mobility of
these structures and cause conductive deafness.
6.Fibrosis and adhesions- They are the result of healing process and
may further impair mobility of ossicular chain or block the eustachian tube.
 Bacteriology

• Pus culture shows both types of aerobic and anaerobic bacteria.

• Common aerobic organisms are- P. aeruginosa, Proteus, E. coli and Staph.

aureus.

• Anaerobes include Bacteroides fragilis and anerobic Streptococci.

 TUBO TYMPANIC C.S.O.M
• Hearing loss: usually conductive (25-
50 dB)

• Discharge profuse,mucopurulent,
intermittent, odourless, not blood-
stained
• Central perforation
 PERFORATION OF TYMPANIC MEMBRANE
Marginal perforation
Central perforation Perforation destroys even the
Pars flaccida
annulus and reaches sulcus
tympanicus. It may be

Anterior: Anterior to handle of

Anterior Attic perforation
malleus

Posterior: Posterior to handle of

Posterosuperior; most common
malleus

Inferior : Inferior to handle of

Inferior
malleus

Subtotal : Very large perforation of

pars
tensa where parts of pars tensa Total
and/or annulus of TM are still
preserved
TYPES OF TUBO TYMPANIC C.S.O.M.
• Active Tubo Tympanic C.S.O.M.
• Inactive Tubo Tympanic C.S.O.M.
• healed
DIAGNOSIS
TUBO TYMPANIC C.S.O.M.
• History
Long standing, unilateral, bilateral, painless otorrhoea,
• Discharge intermittent, mucoid, mucopurulent,
• Non odorous
• Follow U.R.T.I. and entry of water.
• Deafness
Examination
• Main basis to assess activity, type, extent
• Inspection, otoscopy, E.U.M.
• Mucoid
• Perforation , central
• Pale mucosa
• Rarely polyp
• Pus for Culture & Sensitivity
EXAMINATION UNDER MICROSCOPE
Audiological assessment

• Voice test

• Tuning fork test Rinne, Webers, A.B.C.

• Pure tone audiogram

RADIOLOGICAL
ASSESSMENT
• X-rays mastoid
RADIOLOGICAL
ASSESSMENT
• CT-scan temporal bone
treatme
nt
• Aural toilet
a. Cotton buds
b. Suction and cleaning
• Antibiotics
Topical antibiotics:
a) a. Antibiotics (Neomycin, Gentamycin, Ciproflox, Chlormycetin) + Steroid
3-4 times/day
b) b. Acetic acid irrigation
• Systemic antibiotics: Used only during
acture exaorbation (Amoxycillin, Ciprofloxacin)
 Surgical
treatment
Precipitating disease
 Adenoid
 DNS
 Nasal polyps
 Aural polypectomy
Surgical Treatment
 Tympanoplasty- For functional reconstruction
ATTICO ANTRAL C.S.O.M.
• Cholesteatoma
Keratinizing Squamous Epithelium.
A small sac
May involve whole middle ear
cleft
Atticoantral Type of
CSOM
• It involves posterosuperior part of middle ear cleft (attic, antrum and
posterior tympanum and mastoid) and is associated 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.
 Characteristics of Attico-antral CSOM

• Also called ‘Unsafe’ or ‘Dangerous’ type.

• Involves postero-superior part of middle ear cleft.
• Scanty, purulent, foul-smelling discharge
• Attic or marginal perforation
• Granulations common
• Red and fleshy polyp
• Cholesteotoma or retraction pocket present
• Complications common
• Conductive or mixed deafness
 Bacteriology

AEROBES ANAEROBES
• Ps.aeruginosa. • Bacteroides.
• B.proteus. • Streptococci.
• E.coli.
• Staph.aureus.
 Patholo
gy
• Atticoantral diseases is associated with the following pathological processes:
1. Cholesteatoma
2.Osteitis and granulation tissue. Osteitis involves outer attic wall and posterosuperior margin
of the tympanic ring. A mass of granulation tissue surrounds the area of osteitis and may even fill
the attic, antrum, posterior tympanum and mastoid. A fleshy red polypus may be seen filling
the meatus.
3.Ossicular necrosis. It is common in atticoantral disease. Destruction may be limited to the
long process of Incus or may also involve stapes superstructure, handle of malleus or the entire
ossicular chain. Therefore, hearing loss is always greater than that of tubotympanic disease.
Occasionally, the cholesteatoma bridges the gap caused by the destroyed ossicles, and hearing loss
is not apparent.
4.Cholesterol granuloma. It is a mass of granulation tissue with foreign body giant cells
surrounding the cholesterol crystals. It is a reaction to long-standing retention of secretions or
haemorrhage, and mayor may not co-exist with cholesteatoma. When present in the
mesotympanum, behind an intact drum, the latter appears blue.
 Sympto
msfoul smelling due to bone destruction. Discharge may
• 1. Ear discharge. Usually scanty, but always
be so scanty that the patient may not even be aware of it. Total duration of discharge from an ear
which has been active recently should be viewed seriously, as perforation in these cases might be
sealed by crusted discharge, inflamed and dry mucosa or a polyp, obstructing the free flow of
discharge. Pus, in these cases, may find its way internally and cause complications.

• 2. Hearing loss. Hearing is normal when ossicular chain is intact or when cholesteatoma, having
destroyed the ossicles, bridges the gap caused by destroyed ossicles(cholesteatoma hearer).
Hearing loss is mostly conductive but sensorineural element may be added.

• 3. Bleeding. It may occur from granulations or the polyp when cleaning the ear.
 Sig
ns
1.Perforation. It is either attic or posterosuperior marginal type. A small attic perforation may
be missed due to presence of a small amount of crusted discharge, Sometimes, the area of
perforation 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.
Features indicating complications
• Pain.
• Vertigo.
• Persistent headache.
• Facial weakness.
• restless child refuses to feed.
• Fever, nausea, vomiting.
• Irritability and neck stiffness.
• Diplopia.
• Ataxia.
• Abscess round the ear.
 Complications
EXTRA-CRANIAL INTRA-CRANIAL
• Mastoiditis. • Extradural abscess.
• Abscesses. • Subdural abscess.
• Petrositis. • Brain abscess.
• Facial paralysis. • Meningitis.
• Labyrinthitis. • Lateral sinus

thrombophlebitis.
• Otitic
hydrocephalus.
cholesteato
ma
 Keratinising squamous epithelium in the middle ear
Keratoma
 Ciliated columnar in ant & inferior part,
 Cuboidal in middle part & pavement like in the attic
Cholesteotoma
HYPOTHESIS OF ORIGIN
 Presence of congenital cell rest

 Invagination theory ( Wittmaack’s theory)

 Basal cell hyperplasia ( Ruedi’s theory)

 Epithelial invasion ( Habermann’s theory )

 Metaplasia ( Sade’s Theory )

Types of cholesteotoma
CONGENITAL ACQUIRED
• Arises from • PRIMARY: No H/O
embryonic previous otitis
epithelial cell media or
rest. perforation.
• TM intact. • SECONDARY:
• Occurs in middle H/O
ear, petrous otitis media with
apex, CP angle, perforation.
jugular
fossa.
 Congenital
cholesteatoma
• It arises from the embryonic epidermal cell and rests in the middle ear cleft
in the temporal bone. Congenital cholesteatoma occurs at three
important sites: middle ear, petrous apex and the
cerebellopontine angle, and produces symptomatology depending on
its location.
• A middle ear congenital cholesteatoma presents as a white mass behind an
intact tympanic membrane and causes conductive hearing loss. It
may sometimes be discovered on routine examination of children or at
the time of myringotomy.
• It may also spontaneously rupture through the tympanic membrane and
present with a discharging ear indistinguishable from a case of chronic
suppurative otitis media.
Basal cell hyperplasia
Epithelial invasion
Expansion of Cholesteatoma and
destruction
• of Bone
Once cholesteatoma enters the middle ear cleft, it invades the surrounding structures,
first having followed the path of least resistance, and then by enzymatic bone
destruction. An attic cholesteatoma may extend backwards into the aditus, antrum and
mastoid; downwards into the mesotympanum; medially, it may surround the incus
and/or head of maIleus.
• Cholesteatoma has the property to destroy bone.
• It may cause destruction of ear ossicles, erosion of bony labyrinth, canal of facial nerve,
sinus plate or tegmen tympani and thus cause several complications. Bone
destruction by cholesteatoma has been attributed to various enzymes such as
collagenase, acid phosphatase and proteolytic enzymes, liberated by
ostoclasts and mononuclear inflammatory cells, seen in association with
cholesteatoma. The earlier theory that cholesteatoma causes destruction of
bone by pressure necrosis is not accepted these days .
Retraction pockets
 Sade classification of pars tensa retraction

•GRADE I: Normal position of TM.

•GRADE II: TM touches long
process of incus.
•GRADE III: TM touches
promontory.
•GRADE IV: TM adheres to
promontory. 54
 TOS classification of attic retraction

• GRADE I: Minimal retraction.

• GRADE II: Pars flaccida in
contact
with neck of malleus.
• GRADE III: Limited outer attic wall
erosion.
• GRADE IV: Severe outer attic wall
erosion.
 Treatme
• 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 tontpreserve 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 exteriorized. The commonly performed operations for
atticoantral disease are atticotomy, modified radical mastoidectomy and rarely, the radical
mastoidectomy.
(b)Canal 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 per- meatally 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.
• 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 selected cases, when
cholesteatoma is small and easily accessible to suction clearance
under operating microscope. Repeated suction clearance and periodic
check ups are essential.
It can also be tried out in elderly patients above 65 and those who are
unfit for general anesthesia or those refusing surgery.
Other measures like aural toilet and dry ear precautions are also
essential.
 TUBERCULAR OTITIS
• Aetiology MEDIA
In most of the cases, infection is secondary to pulmonary tuberculosis;
infection reaches the middle ear through eustachian tube. Sometimes, it is
blood-borne from tubercular focus in the lungs, tonsils, cervical or
mesenteric lymph nodes. Disease is mostly seen in children and young
adults.
• Pathology
The process is slow and insidious. Tubercles appear in the submucosal layers
of middle ear cleft and caseate. There is painless necrosis of tympanic
membrane. Multiple perforations may form which coalesce to form a single
large perforation. Middle ear and mastoid get filled with pale granulations.
Caries of bone and ossicles may occur leading to complications. Mastoiditis,
facial paralysis, postauricular fistula, osteomyelitis with formation of bony
sequestrum and profound hearing loss are often seen in these cases.
• Clinical Features
1. Painless ear discharge. Earache is characteristically absent in cases of tubercular otitis media. Discharge is often foul-smelling
because of the underlying bone destruction.
2.Perforation. Multiple perforations, 2 or 3 in number, are seen in pars tensa and form a classical sign of disease. These may
coalesce into a single large perforation.
3.Hearing loss. There is severe hearing loss, out of proportion to symptoms. Mostly conductive, it may have
sensorineural component due to involvement of labyrinth.
4. Facial paralysis. It is a common complication and may come unexpectedly. This may be the presenting feature in a child.
• Diagnosis
In the presence of secondary pyogenic infection, tubercular otitis media may be indistinguishable from chronic suppurative otitis
media. Culture of ear discharge for tubercle bacilli, histopathological examination of granulations and X-ray chest, and other evidence
of tuberculosis in the body help to confirm the diagnosis.
• Treatment
5. Systemic antitubercular therapy as being carried for primary disease.
6. Local treatment in the form of aural toilet, and control of secondary pyogenic infection.
7.Mastoid surgery indicated for complications. Healing is delayed in tuberculous cases. Wound break down and fistula formation
are common. Reconstructive surgery of middle ear is delayed till antitubercular therapy has been completed.
 SYPHILITIC OTITIS
• Rare condition. MEDIA
• Spirochetes reach middle ear through eustachian tube when syphilitic lesions are present in the
nose or nasopharynx. Infection may also be blood-borne. Sensory end organs of the inner ear and
their nerve is soon invaded by spirochetes leading to cholesteatoma and chronic suppurative
otitis media, profound sensorineural hearing loss, tinnitus and vertigo.
• Bone necrosis and sequestrum formation are common, leading to foetid ear discharge. Secondary
pyogenic infection may occur, giving a clinical picture very much like chronic suppurative otitis
media.
• Definite diagnosis of syphilitic otitis media can only be made by specific treponemal antigen tests
such as treponemal pallidum immobilization (TPI) test and fluorescent treponemaI antibody
absorption test (ITA-ABS). VDRL and Wasserman tests are nonspecific and may give false positive
results.
• Treatment consists of antisyphilitic therapy with attention to aural toilet and control of secondary
infection. Surgery may be required for removal of sequestra.