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Chronic Suppurative Otitis Media (CSOM)

  1. Definition:
    CSOM is a long -standing infection (> 3 months) of part or whole of the middle ear cleft characterized by discharge and a permanent perforation.
    Perforation becomes permanent when its edge gets covered by squamous epithelium-
  2. Organisms:
    1. Pseudomonas aeruginosa
    2. Proteus
    3. E.Coli
    4. Bacteroides melaninogenicus
    5. Bacteroides fragilis
  3. Predisposing conditions
    1. Developing countries
    2. In rural area
    3. In poor socio-eco groups
    4. Most common cause of H. impairment in rural areas
  4. Types:
    1. Tubotympanic (safe/benign)
      1. Involves the antero-inferior part of the middle ear cleft
      2. Associated with central perforation
      3. Granulations: Uncommon
    2. Atticoantral (unsafe/dangerous)
      1. Posterosuperior part of the cleft
      2. Associated with marginal or attic perforation
      3. Granulations: are common
      4. Osteitis (+) as the essential pathology
  5. ​​Differences between tubo tympanic (safe) and attico antral (unsafe) C.S.O.M




1. Discharge

Copious, odourless

Scanty, foul-smelling

2. Perforation


Attic or marginal

3. Polyps

Pale coloured


4. Cholesteatoma



5. Complication




Recent Classification

Healed perforation

  1. Mucous
    1. Active: wet ear
    2. Inactive: central perforation
  2. Squamous
    1. Active:      cholesteatoma
  1. Features associated with C.S.O.M
    1. Perforation of pars tensa/pars flaccida
    2. Tympanosclerosis
    3. Cause: due to continuous middle ear infection
    4. Pathology: Formed as an end result of the hearing process à hyalinization
    5. Collagen of the fibrous layer hyalinizes without calcification
    6. Ossicular erosion (Incus > stapes> malleus)
    7. (Due to hyperemic decalcification) most common in incus due to poorest blood supply
    8. (Due to cholesteatoma)
    9. Fibrous sclerosis
    10. Mastoid sclerosis:
      1. Remodeling
      2. Deposition of new bone
    11. Cholesterol granuloma:
      1. It is a mucosal pathology showing giant cell reaction to cholesterol crystals formed due to
      2. breakdown of extravasated blood cells or iron deposits.
    12. Features:
      1. It is a microscopic diagnosis
      2. The tympanic membrane otoscopically may appear blue
    13. Labyrinthitis:
    14. Sensorineural hearing impairment
    15. Active mucosal disease: Polyps
    16. Active C.S.O.M with cholesteatoma
  2. Treatment of C.S.O.M.: (Tubotympanic type)
    1. Starts in childhood, common in childhood.
    2. Usually as sequel to ASOM
    3. Repeated Infection through Eustachian tube/allergy/URTI
    4. Profuse mucoid/ mucopurulent, no foul smell discharge​
  1. Aural toileting
  2. Ear drops
  3. Systemic antibiotics (if acute on chronic)
  4. Treatment of contributing factors (adenoids, sinusitis, allergy)
  5. Precautions (not to let water/any fluid in the canal)
  6. Surgical treatment
  1. Atticoantral type (unsafe type)
    1. Symptoms
      1. Discharge: scanty, foul - smelling, purulent, may be blood stained
      2. Hearing loss:
        1. Conductive
        2. Mixed
        3. Normal (Cholesteatoma hearers) or when the conductive mechanism  is normal Bleeding — granulation tissue
    2. Signs:
      1. Perforation:
        1. Marginal
        2. Total
        3. Attic
​​​Perforation Of Tympanic Membrane

Pars tensa I

Pars flaccida (Attic perforation)

1. Central perforation

1. Marginal perforation

2. Anterior: Anterior to handle of malleus

2. Perforation destroys even the annulus and
    reaches sulcus tympanicus. It may be
a.   Posterosuperior ?
b.   Anterior
c.    Inferior
d.   Total (Posterosuperior marginal perforation is the most common)

3. Posterior: Posterior to handle of malleus

4. Inferior: Inferior to handle of malleus

5. Subtotal: Very large perforation of pars

6. Tensa where parts of pars tensa

7. And /or annulus of TM is still preserved



Cholesteatoma is keratinzed squamous epithelium lined sac present abnormally within the middle ear or in the other pneumatized portion of the temporal bone (syn- Epidermosis/keratoma)

Classification of Cholesteatoma
The cholesteatoma is classified into:
  1. Congenital
  2. Acquired, Primary
  3. Acquired, Secondary
Congenital cholesteatoma m/c location anterior quadrant
Congenital cholesteatoma is squamous epithelium cyst which can arise from any site in the temporal bone (petrous pyramid, middle ear cleft, cerebellopontine angle, jugular fossa region) from embryonic epidermal rests.

  1. An intact tympanic membrane
  2. No previous history of otitis media
  3. Origin is from the embryonal inclusion of squamous epithelium
Primary acquired cholesteatoma. It is called pri­mary as there is no history of previous otitis media or a pre-existing perforation. Theories on its genesis are:
  1. Invagination of pars Placida. Persistent negative pres­sure in the attic causes a retraction pocket which accumulates keratin debris. When infected, the ker­atin mass expands towards the middle ear. Thus, attic perforation is in fact the proximal end of an expanding invaginated sac.
  2. Basal cell hyperplasia. There is proliferation of the basal layer of pars flaccida induced by subclinical childhood infections. Expanding cholesteatoma then breaks through pars flaccida forming an attic perforation.
  3. Squamous metaplasia. Normal pavement epithelium of attic undergoes metaplasia, keratinizing squamous epithelium due to subclinical infections.
  4. secondary acquired cholesteatoma. In these cases, there is already a pre-existing perforation in
  5. pars tensa. This is often associated with posterosuperior mar­ginal perforation or sometimes large central perforation. Theories on its genesis include:
  6. Migration of squamous epithelium. Keratinizing squa­mous epithelium of external auditory canal or outer surface of tympanic membrane migrates through the perforation into the middle ear. Perforations, involv­ing tympanic annulus as in acute necrotizing otitis media, are more likely to allow in-growth of squa­mous epithelium.
  7. Metaplasia. Middle ear mucosa undergoes metaplasia due to repeated infections of middle ear through the pre-existing perforation.

Fig.: Schematic structure of cholesteatoma

Genesis of cholesteatoma

Epithelial invasion through posterosuperior perforation
Genesis of primary and secondary cholesteatoma.

Origin of Cholesteatoma:

  1. Theories:
    1. Congential cell rest theory
    2. Whit Mack’s theory (for attic cholesteatoma)
      1. Negative pressure in the Epitympanum due to blockade by persistent embryonic mucoperiosteum it causes →
      2. Retraction of Shrapnell’s membrane. It leads to
      3. Accumulation of Keratin debris it leads to Cholesteatoma
    3. Ruedi’s theory:
      Basal cell hyperplasia infection  Grow into subepithelial layer  cholesteatoma
    4. Habermann’s theory
      (Epithelial invasion theory)
      Following perforation  epithelium from the external auditory  Cholesteatoma
      (esp. marginal type)              canal or from the drum surface grows inwards
    5. Sade’s theory:
      Middle ear  Metaplasia of the epithelium  Squamous  Cholesteatoma
      Mucosa      due to repeated infection                Cholesteatoma
  2. Expansion/Theories of Bone Erosion of Cholesteatoma:
    1. Pressure necrosis theory : Bone erosion by pressure necrosis not accepted
    2. Enzymatic theory: The subepithelial layer of the matrix of the Cholesteatoma have multinucleated osteoclasts and mononuclear histiocytes which produce enzymes:
      1. Acid phosphates
      2. Collagenases
      3. IL-1
      4. Proteolytic enzymes
    3. Pyogenic osteitis theory: Colonizing bacteria may release enzymes to cause bone resorption​.

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