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Chronic Suppurative Otitis Media (CSOM) - Undergraduate Guide

Definition

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Types (Classification)

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Epidemiology & Risk Factors

• Most common in children under 2 years old; prevalent in areas with limited health resources and low socioeconomic status
• Common in Native Americans, Inuit, Native Australians, and New Zealanders (genetic predisposition)
• Risk factors:
  • Multiple episodes of acute otitis media (AOM)
  • AOM in the first few months of life
  • Chronic secretory otitis media
  • Eustachian tube (ET) dysfunction
  • Nasopharyngeal reflux
  • Tympanostomy tube or perforation with contamination from external auditory canal (EAC)

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Pathophysiology

1. ET dysfunction → decreased aeration of middle ear (ME) space
2. Nitrogen-absorbing mastoid cells → volume reduction of ME → negative middle ear pressure
3. TM retraction (pars flaccida most susceptible) and retraction pockets form
4. Bacterial infection → purulent effusion → mucosal edema and granulation tissue formation
5. Bacterial toxins and inflammatory mediators rupture the epithelial basement membrane → inflammatory cells enter ME lumen → fibroblast recruitment, neovascularization, polyp formation
6. Enzymes in granulation tissue break down collagen skeleton of TM → TM weakens and perforates
7. Deep retraction pockets + perforations → keratinocyte migration inward → cholesteatoma formation

• Highly organized networks of sessile bacteria
• Encased in oligopolysaccharide matrix; resist phagocytosis and humoral immunity
• Decreased metabolic rate and altered gene expression make them antibiotic-resistant
• Produce efflux pumps against antibiotics
• Frequently polymicrobial, harder to eradicate
• Pseudomonas aeruginosa is the most common pathogen in middle ear biofilms

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Microbiology

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Clinical Features

Symptoms

• Intermittent or persistent otorrhea - often foul-smelling (hallmark symptom)
• Hearing loss - typically low-frequency conductive, or mixed hearing loss
• Aural fullness

• Otalgia / headache - raises suspicion for intracranial involvement or malignancy
• Vertigo - raises suspicion for labyrinthitis or labyrinthine fistula
• Facial weakness - suggests facial nerve involvement

Signs (on Otoscopy)

• TM perforation (central in tubotympanic; marginal/attic in atticoantral)
• Otorrhea through the perforation
• Granulation tissue / aural polyps (may obscure landmarks)
• TM retraction pockets ± cholesteatoma
• Cholesteatoma: white, pearly/cheese-like mass with dead, desquamated keratin - "unsafe" finding
• Scutal erosion (bone erosion at attic wall) in atticoantral type

Audiometry

• Conductive hearing loss is common
• SNHL may coexist (document preoperatively)
• Conductive loss > 30 dB suggests ossicular erosion
• Note: hearing can paradoxically be preserved even with ossicular erosion if cholesteatoma directly transmits sound to oval window

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Cholesteatoma

• An aural polyp should be considered cholesteatoma until proven otherwise
• Causes progressive bone erosion via enzymes (matrix metalloproteinases)
• Can erode: ossicular chain, bony canal wall, tegmen, facial nerve canal, labyrinth, sigmoid sinus
• Cholesteatoma + medically refractory CSOM = nearly absolute indication for surgery

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Diagnosis

1. Clinical examination - otomicroscopy with pneumatic insufflation
2. Audiometry - mandatory
3. Imaging:
   • High-resolution CT temporal bones - for surgical planning, complicated CSOM (facial nerve paralysis, vertigo), known cholesteatoma, revision tympanomastoidectomy cases
   • MRI with contrast - for suspected intracranial complications
4. Biopsy of granulation tissue unresponsive to topical therapy - to rule out malignancy

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Complications

Extracranial (Non-intracranial)

• Mastoiditis (subperiosteal abscess, Bezold's abscess, Citelli's abscess)
• Labyrinthine fistula (→ vertigo, SNHL)
• Facial nerve palsy (due to bone erosion over Fallopian canal)
• Petrositis (Gradenigo syndrome: otorrhea + retro-orbital pain + diplopia from CN VI palsy)
• Conductive hearing loss, mixed hearing loss

Intracranial

• Extradural abscess
• Subdural abscess
• Meningitis (most common intracranial complication)
• Brain abscess (temporal lobe or cerebellar)
• Lateral sinus (sigmoid sinus) thrombophlebitis
• Otitic hydrocephalus

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Treatment

Primary Goal

Medical Treatment

• Aural toilet (suctioning of debris and discharge) - essential before topical therapy
• Topical antibiotics (4-6 week course after debridement):
  • Fluoroquinolones (ciprofloxacin ear drops) - first line, safe, no ototoxicity
  • Polymixin B or neomycin (± steroid) - second line; avoid if TM perforated due to ototoxicity risk
• Note: biofilms are frequently resistant to topical medication; they develop multicellular strategies to overcome high antibiotic levels

Surgical Treatment (Indications)

• Cholesteatoma (nearly absolute indication)
• Otorrhea refractory to medical treatment
• Complications of CSOM (facial palsy, vertigo, intracranial)
• Atelectatic ears with significant conductive hearing loss
• Retraction pockets that collect debris or show progression

Surgical Options

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Key Exam Points (High-Yield for UG)

1. Definition: TM perforation + otorrhea > 6 weeks
2. Safe vs. unsafe: Tubotympanic (central perforation, no cholesteatoma) vs. Atticoantral (marginal/attic perforation, cholesteatoma)
3. Most dangerous feature: Cholesteatoma - causes bone erosion
4. Most common organism: Pseudomonas aeruginosa
5. Most common intracranial complication: Meningitis
6. Hallmark symptom: Painless, foul-smelling otorrhea (pain suggests complication)
7. Topical treatment: Fluoroquinolone ear drops + aural toilet
8. Cholesteatoma = surgery
9. Gradenigo's syndrome: Petrous apicitis - otorrhea + retro-orbital pain + CN VI palsy (diplopia)
10. Aural polyp: Consider cholesteatoma until proven otherwise

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