Tubercular (tuberculous) otitis media

• Through the Eustachian tube, for example by swallowed or aspirated sputum.
• Directly through an existing tympanic membrane (TM) perforation, as in pre-existing chronic otitis media.
• By blood or lymphatic spread from a distant focus, usually pulmonary. Up to 50% of childhood cases are secondary to another focus.

• Painless otorrhoea.
• Multiple TM perforations.
• Pale granulation tissue.
• Early, severe hearing loss, often out of proportion to the otoscopic findings.
• Bone necrosis.
• Facial palsy in 10 to 20% of patients, appearing early. Complications are commoner and more severe in children.
• Non-tender cervical or high jugular lymphadenopathy.

Stages (pathological phases)

1. Acute (exudative) phase.
   • The TM and mucosa become congested, then thickened, with loss of landmarks.
   • Tubercles appear, followed by perforations.
   • There is middle ear effusion, and the hearing loss is conductive.
2. Chronic (granulation) phase.
   • The course is slow and painless.
   • Perforations persist, and pale pink granulation tissue fills the middle ear.
   • Polyps may appear in the canal.
3. Necrotic or caseous phase.
   • Caseation destroys bone and forms sequestra.
   • Ossicles, mastoid cortex and otic capsule are destroyed.
   • Complications include facial nerve palsy, labyrinthitis with sensorineural loss, and a "cold" Bezold abscess from mastoid tip destruction (Cummings).

Why does the TM perforate?

• Granuloma formation in the TM. Bacilli reach the middle ear mucosa and the inner mucosal and fibrous layers of the TM. Tubercles form there. The TM first becomes thickened and congested, and Cummings shows it greatly thickened by granulation tissue containing epithelioid and multinucleated giant cells.
• Caseous necrosis and ischaemia. Caseation destroys the TM tissue. Endarteritis of the small vessels cuts off its blood supply. The TM is thin and has a limited blood supply, so it breaks down easily.
• Multiple small perforations that coalesce. Necrosis happens at several foci at once, so many small perforations appear, often with seropurulent discharge. Cummings notes they "quickly coalesce to cause loss of the tympanic membrane". Scott-Brown adds that multiple perforations are now reported less often than once thought, and a single large perforation is common.
• Painless course. Pain is minimal because the process is chronic, granulomatous and non-suppurative. It is not the acute pyogenic inflammation of ordinary acute otitis media.
• Perforations enlarge, not heal. Ongoing necrosis keeps enlarging them. A myringotomy site in an intact TM can also enlarge rapidly (Cummings).

Diagnosis and treatment

• Culture of ear discharge is positive in under 20% of cases.
• Histology of a biopsy of granulation tissue or polyp is the most definitive test. It shows caseating granulomas with epithelioid and Langerhans cells. PCR can also be used.
• Chest X-ray is needed, because pulmonary TB is present in 14 to 93% of patients.
• HRCT temporal bone is the imaging of choice.
• Treatment is standard anti-tubercular therapy. Surgery is reserved for complications or for obtaining tissue.

Posterosuperior quadrant disease in CSOM

Why this quadrant is affected (retraction first, then perforation)

1. Eustachian tube dysfunction causes negative pressure. Retraction pockets form where negative pressure, over time, pulls the TM into the middle ear and attic. The membrane is drawn in and then thinned (Cummings Otolaryngology, Ch. 137).
2. The posterosuperior area is mechanically weaker or less supported. This is standard teaching rather than something stated in the passages I found:
   • The attic and posterior mesotympanum are ventilated through the narrow tympanic isthmus. Folds, the ossicles and the tensor tympani tendon can block it, so pressure equalisation fails here first.
   • The TM near the pars flaccida and its adjoining region is less rigid. Cummings notes the pars flaccida is less rigid than the rest of the TM, which is held to the bony canal by the tympanic annular ligament.
   • The posterior-superior part is relatively thin and poorly supported, so it is the first to invaginate under persistent negative pressure.
3. Retraction turns into perforation. The thinned, atelectatic membrane can adhere to the incus or stapes and erode. Infection and keratin debris accumulating in the pocket also break it down, so the pocket becomes a marginal perforation. These perforations involve the annulus, so they have no rim of TM on one side. Cummings notes that perforations and pockets involving the annulus are more likely to trap debris and lead to cholesteatoma.
4. Bone erosion follows. Squamous epithelium trapped in the pocket produces keratin and spreads. It erodes the scutum, ossicles and posterior canal wall by enzymatic and pressure effects. This is why this site gives unsafe disease with complications.

Contrast with the central perforation