2. CHRONIC
SUPPURATIVE
OTITIS
MEDIA
(CSOM)

3. OBJECTIVES Etiology What is CSOM Pathology Feature Investigation
Type of CSOM
Etiology
Pathology
Feature
Investigation
Treatment

4. INTRODUCTION the middle ear cleft characterized whole of
Long-standing infection of a part or
the middle ear cleft characterized
– By ear discharge
– A permanent perforation. •
whole of

6. TYPES OF CSOM Involves anteroinferior part of middle ear cleft,
Tubotympanic. Also called the safe or benign type;
Involves anteroinferior part of middle ear cleft,
i.E. Eustachian tube and mesotympanum
Associated with a central perforation.
There is no risk of serious complications. 1. • it • 2. •
Atticoantral. Also called unsafe or dangerous
Involves posterosuperior part of the cleft
(I.E. Attic, antrum and mastoid)
type; it •
Associated 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. •

8. Atticoantr al(unsafe)
Tubotympani
(safe)
Atticoantr al(unsafe)
Discharge
Profuse, mucoid,
odourless
Central
Uncommon
Pale
Absent
Rare
Scanty, purulent,
smelling
foul
Perforation
Granulations
Polyp
Cholesteatoma
Complications
Audiogram
Attic
or marginal
Common
Red and fleshy
Present
Mild to
moderate
Conductive
deafness
or mixed
conductive
deafness

9. TUBOTYMPANIC

10. ETIOLOGY The disease starts in childhood permanent and•
The disease starts in childhood
It is the sequela of acute otitis.
– The perforation central and becomes
permanent and
permits repeated infection from the external ear.
Ascending infections via the eustachian tube.
– Infection from tonsils, adenoids and infected sinuses may be responsible for persistent or recurring otorrhoea.
Persistent mucoid otorrhoea is sometimes the result of allergy to ingestants such as milk, eggs, fish, etc. • •

11. PATHOLOGY 1. Perforation of pars tensa. is active. 3.2.
Perforation of pars tensa.
Middle ear mucosa.
It is oedematous and velvety when disease
Polyp.
is active. 3.
It is usually pale in contrast to pink, fleshy polyp seen in
atticoantral disease
Ossicular chain.
It is usually intact and mobile but may show some degree necrosis, particularly of the long process of incus.
Tympanosclerosis. 4. of 5.
It is seen as white chalky deposit on the promontory, ossicles,
joints, tendons and oval and round windows and interfere with
the mobility of these structures and cause conductive deafness.
Fibrosis and adhesions. 6.

12. BACTERIOLOGY Pus culture in both types of aerobic anaerobic CSOM and•
Pus culture in both types of aerobic
anaerobic CSOM
Common aerobic organisms
and • –
Pseudomonas aeruginosa,
Proteus,
Escherichia coli
Staphylococcus aureus, •
Anaerobes include Bacteroides
anaerobic Streptococci.
fragilis and

13. Retraction Mucosal Squamosal diseases diseases Active Inactive Healed
CHRONIC OTITIS MEDIA
Mucosal
Squamosal
diseases
diseases
Active
Inactive
Healed
Active
Retract
Retract pockets
Retraction

15. CLINICAL FEATURES 1. Ear discharge.
It is nonoffensive, mucoid or mucopurulent,
intermittent.
2. Hearing loss.
constant or
It is conductive type; rarely exceeds
(round window shielding effect)
3. Perforation.
Always central
4. Middle ear mucosa. 50
dB.
It is seen when the perforation is large.

16. INVESTIGATIONS 1. Examination under microscope 2. 3. 4. Audiogram.
Culture and sensitivity of ear discharge.
Mastoid X-rays/CT scan temporal bone.

17. TREATMENT Aural toilet. Systemic antibiotics causes•
Aural toilet.
Ear drops. –
Antibiotic ear drops
polymyxin, chloromycetin,ciprofloxacin are
used. –
They are combined with steroids which
anti-inflammatory effect.
have
local •
Systemic antibiotics
Precautions
Treatment of contributory
Surgical treatment
Reconstructive surgery
causes

18. ATTICOANTRAL TYPE

19. INTRODUCTION It involves postero-superior part of middle ear cleft •
Associated with cholesteatoma (bone eroding properties)
unsafe or dangerous type. • • •

20. ETIOLOGY cholesteatoma and has been discussed earlier.
Etiology of atticoantral disease is same as of
cholesteatoma and has been discussed earlier.
It is seen in sclerotic mastoid. • •

21. PATHOLOGY 1. Cholesteatoma. hearer) 2. 3. 4.
Osteitis and granulation tissue. Ossicular necrosis (cholesteatoma Cholesterol granuloma.
hearer)

23. BACTERIOLOGY •
Same as in tubo-tympanic type.

24. Hearing is normal when ossicular chain is intact or
SYMPTOMS 1.
Ear discharge.
Usually scanty, but always foul-smelling destruction
Hearing loss.
due to bone 2.
Hearing is normal when ossicular chain is intact or
when cholesteatoma, having destroyed the ossicles,
bridges the gap caused by destroyed ossicles
(cholesteatoma hearer).
3. Bleeding.
From granulations or the polyp when cleaning the ear.

25. SIGN 1. Perforation. marginal
It is either attic or postero-superior type.
2. Retraction pocket.
marginal
An invagination of tympanic membrane is seen
the attic or posterosuperior area of pars tensa.
There are four stages of tympanic membrane
retraction.
3. Cholesteatoma. in

26. Stage I
•Tympanic membrane is retracted but does not contact the incus.
Stage II
•Tympanic membrane is retracted deep and contacts the incus.
•Middle ear mucosa is not
affected.

27. •Middle ear space is totally or partially obliterated but middle ear
Stage III
•Also called middle ear atelectasis.
on the promontory and ossicles.
•Middle ear space is totally or
partially obliterated but middle ear
mucosa is intact.
•Tympanic
membrane
comes to
lie
Stage IV
•Also called adhesive otitis media.
and wraps the promontory and ossicles.
•There is no middle ear space
•Mucosal lining of the middle ear is
absent and tympanic membrane
gets adherent to the promontory.
•Tympanic
membrane
is very
thin

28. INVESTIGATIONS 1. Examination under microscope bone.2. 3. 4.
Examination under microscope
Tuning fork tests and audiogram. X-ray mastoids/CT scan temporal
bone.
Culture and sensitivity of ear discharge.

32. FEATURES INDICATING COMPLICATIONS IN CSOM 1. 2. 3. 4. 5. Pain Vertigo
Persistent headache.
Facial weakness indicates erosion of facial canal.
A listless child refusing to take feeds and easily going to
sleep (extradural abscess). 6. 7. 8. 9.
Fever, nausea and vomiting (intracranial infection).
Irritability and neck rigidity (meningitis).
Diplopia (Gradenigo syndrome) petrositis.
Ataxia (labyrinthitis or cerebellar abscess).
10. Abscess round the ear (mastoiditis).

33. TREATMENT 1. Surgical can be
(a) Canal wall down procedures
(b) Canal wall up procedures.
2. Reconstructive surgery. Hearing
can be
restored by myringoplasty or tympanoplasty.
3. Conservative treatment.

39. CHOLESTEATOMA

41. What is cholesteatoma
Origin
Classification •

42. INTRODUCTION epithelium in different regions
Normally, middle ear cleft is lined by different types of
epithelium in different regions
It is the presence of keratinizing squamous epithelium in
the middle ear or mastoid.
“Skin in the wrong place.”
Essentially, cholesteatoma consists of two parts: • • •
(i) the matrix, which is made up of keratinizing squamous
epithelium resting on a thin stroma of fibrous tissues and
(ii) a central white mass, consisting of keratin debris
produced by the matrix . •
Also been named epidermosis or keratoma.

44. ORIGIN 3. Basal cell hyperplasia (Ruedi’s theory).
1. Presence of congenital cell rests.
2. Invagination of tympanic membrane from the attic or posterosuperior part of pars tensa in the form of retraction pockets (Wittmaack’s theory). 3. 4. 5.
Basal cell hyperplasia (Ruedi’s theory).
Epithelial invasion (Habermann’s theory).
Metaplasia (Sade’s theory).

45. CLASSIFICATION OF CHOLESTEATOMA The cholesteatoma is classified into:•
The cholesteatoma is
classified
into: 1. 2. 3.
Congenital
Acquired, primary
Acquired, secondary

46. 1. CONGENITAL CHOLESTEATOMA.•
It arises from the embryonic epidermal
3 important sites:
cell
rests –
Middle ear
Petrous apex
And the cerebellopontine angle •
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
Present with a discharging ear indistinguishable from a
case of chronic suppurative otitis media. • •

47. 2. PRIMARY ACQUIRED CHOLESTEATOMA No history of previous otitis media•
No history of previous otitis media
existing perforation.
Theories on its genesis are: or a
pre- •
(A)
(B) (C)
invagination of pars flaccida.
basal cell hyperplasia. squamous metaplasia.

48. 3. SECONDARY ACQUIRED CHOLESTEATOMA tensa.
Already a pre-existing perforation in pars
tensa.
This is often associated with posterosuperior • •
marginal perforation or sometimes
central perforation.
Theories on its genesis
(A) migration of squamous epithelium. (B) Keratinizing squamous metaplasia
large •

49. EXPANSION OF CHOLESTEATOMA AND DESTRUCTION OF BONE
It invades the surrounding structures, first 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 malleus.
Cause destruction of ear ossicles,
Erosion of bony labyrinth,
Canal of facial nerve,
Sinus plate or tegmen tympani •
Attributed to various enzymes such as
– Collagenase,
– Acid phosphatase and proteolytic enzymes,
Liberated by osteoclasts and mononuclear inflammatory cells, Seen in association with cholesteatoma. •

51. COMPLICATION OF
EAR
MIDDLE
MIDDLE
DISEASES

52. FACTORS INFLUENCING DEVELOPMENT COMPLICATIONS OF1. 2.
Age.
Poor socioeconomic group. –
overcrowding,
poor health education poor
personal hygiene,
limited access to healthcare 3.
Virulence of organisms.

53. Cont. 4. 6. cleft if preformed pathways exist, the middle ear
Immune-compromised host.
Preformed pathways.
– Infection can easily travel beyond
cleft if preformed pathways exist,
Cholesteatoma. 4. 5.
the middle ear 6.

54. PATHWAYS OF SPREAD OF INFECTION 1. Direct bone erosion
2. Venous thrombophlebitis.
3. Preformed pathways
(a) Congenital dehiscences, e.g. in bony facial canal,
floor of middle ear over the jugular bulb.
(b) Patent sutures, e.g. petrosquamous suture.
(c) Previous skull fractures. The fracture sites heal only by fibrous scar
which permits infection.
(d) Surgical defects, e.g. stapedectomy, fenestration and mastoidectomy
with exposure of dura.
(e) Oval and round windows.
(f) Infection from labyrinth can travel along internal acoustic meatus,
aqueducts of the vestibule and that of the cochlea to the meninges.

55. CLASSIFICATION (WITHIN THE B. INTRACRANIAL CONFINES OF
A. INTRATEMPORAL
(WITHIN THE B. INTRACRANIAL
TEMPORAL BONE)
CONFINES OF
1. Mastoiditis Extradural abscess
2. Petrositis Subdural abscess
3. Facial paralysis Meningitis
4. Labyrinthitis Brain abscess
5. Lateral sinus
thrombophlebitis
6. Otitic hydrocephalus

56. SEQUELAE OF OTITIS MEDIA1. 2. 3. 4. 5. 6.
Perforation of tympanic membrane
Ossicular erosion
Atelectasis and adhesive otitis media
Tympanosclerosis
Cholesteatoma formation
Conductive hearing loss due
or fixation
Sensorineural hearing loss Speech impairment Learning disabilities
to ossicular
erosion 7. 8. 9.