Chronic Suppurative Otitis Media (CSOM) - Complete Viva Q&A

PART 1: CONCEPTUAL FRAMEWORK (Read This First)

PART 2: VIVA QUESTIONS WITH ANSWERS

SECTION A: DEFINITION, CLASSIFICATION & EPIDEMIOLOGY

• Tubotympanic disease (safe/benign type) - involves the tubotympanic recess derived from the 1st branchial pouch, lined by respiratory epithelium. Perforation confined to pars tensa.
• Atticoantral disease (unsafe/dangerous type) - involves the attic and antrum derived from the 1st branchial groove (ectodermal). Associated with cholesteatoma.

SECTION B: ETIOLOGY & PATHOGENESIS

1. Persistent negative middle ear pressure
2. Middle ear effusion (serous or purulent)
3. Mucosal edema and granulation tissue formation
4. Bacterial infection perpetuates the cycle
5. Chemical mediators cause chronic mucosal changes - mucosa develops submucosal glands converting to secretory type, perpetuating effusion
6. Enzymes in granulation tissue and chronic effusion weaken the TM collagen skeleton, leading to perforation or retraction pockets

1. Invagination theory (Wittmaack): Negative pressure from ET dysfunction causes retraction of pars flaccida forming a retraction pocket that accumulates keratin debris - the most widely accepted theory
2. Squamous metaplasia theory (Sade): Middle ear respiratory epithelium undergoes metaplastic change to keratinizing squamous epithelium under inflammatory stimuli
3. Immigration/Basal cell hyperplasia theory (Ruedi): Basal cells proliferate and migrate inward through a marginal perforation
4. Congenital rest theory (Teed): Squamous epithelial cell rests left behind during embryological development - explains congenital cholesteatoma

• Anaerobes are found in up to 67% of cholesteatomas at surgery (Harker and Koontz)
• Fungal overgrowth (Candida spp.) occurs especially after topical antibiotic use - in up to 35% of ears treated with topical ciprofloxacin for 3 weeks
• Biofilm formation is common in CSOM - contributes to antibiotic resistance

SECTION C: CLINICAL FEATURES & DIAGNOSIS

1. Chronic/intermittent otorrhea - the cardinal symptom
2. Hearing loss (conductive, occasionally mixed)
3. Tympanic membrane perforation (or retraction pocket in atticoantral type)

• Otalgia/headache - uncommon in uncomplicated CSOM; suggests intracranial involvement or malignancy
• Vertigo - suggests labyrinthitis or perilymph fistula (labyrinthine fistula)
• Facial weakness - Fallopian canal erosion with facial nerve involvement
• Fever + meningism - intracranial complications
• New-onset SNHL - inner ear involvement
• Postauricular swelling/erythema - subperiosteal abscess, coalescent mastoiditis

1. Full head and neck exam
2. Otomicroscopic examination (gold standard) - otorrhea often obscures TM
3. Note EAC: edema, polyps, cholesteatoma
4. Evaluate TM: perforation site and size, retraction, atelectasis, cholesteatoma (white pearly mass)
5. Look through perforation: middle ear mucosa, granulation tissue, scutal erosion, ossicular erosion
6. Tuning fork tests (Rinne, Weber) to assess type of hearing loss
7. Full audiometry - conductive loss >30 dB suggests ossicular erosion

• Tubotympanic: Mild conductive hearing loss (CHL) - typically 20-30 dB
• Atticoantral: Larger CHL; note that sound can be transmitted directly to the oval window via a cholesteatoma mass even when ossicular chain is eroded - this gives falsely preserved hearing ("columella effect")
• Conductive loss >30 dB suggests ossicular erosion (Shambaugh Surgery)
• Mixed hearing loss occurs when the labyrinth is involved (labyrinthine fistula)
• SNHL range of 5-33 dB found in several studies even without overt labyrinthine involvement

SECTION D: PATHOLOGY - CHOLESTEATOMA

1. Congenital cholesteatoma: Arising from embryological squamous epithelial rests. Presents behind an intact TM, typically in anterior-superior quadrant, without prior ear disease. More common in children.
2. Acquired cholesteatoma:
   • Primary acquired: From invagination of pars flaccida (most common, ~98%) - starts in Prussak's space
   • Secondary acquired: Squamous epithelium migrates through a marginal perforation of pars tensa into middle ear

• Pars flaccida cholesteatoma: Scutum erosion, medialization of ossicular chain, soft tissue in Prussak's space
• Pars tensa cholesteatoma: Erosion of posterior-superior EAC wall, lateralization of ossicular chain, haziness medial to ossicular chain, possible erosion of lateral semicircular canal - scutum is NOT eroded
• CT cannot distinguish cholesteatoma from granulation tissue, cholesterol granuloma, or other soft tissue masses
• MRI with diffusion-weighted imaging (DWI) is used to detect residual/recurrent cholesteatoma

SECTION E: COMPLICATIONS

1. Acute coalescent mastoiditis
2. Subperiosteal abscess (behind the ear)
3. Bezold's abscess (tracking along sternocleidomastoid into the neck)
4. Citelli's abscess (tracking into digastric triangle)
5. Temporal root abscess (zygomatic root abscess)
6. Facial nerve palsy (VII nerve)
7. Labyrinthitis (serous, suppurative)
8. Labyrinthine fistula (lateral semicircular canal most commonly)
9. Petrous apicitis (Gradenigo's syndrome)

1. Meningitis (most common intracranial complication)
2. Extradural (epidural) abscess
3. Subdural abscess/empyema
4. Brain abscess (temporal lobe or cerebellar)
5. Lateral (sigmoid) sinus thrombosis
6. Otitic hydrocephalus

1. Otorrhea (chronic ear disease)
2. Retrobulbar/periorbital pain (trigeminal neuralgia - V nerve involvement, especially ophthalmic division)
3. Ipsilateral lateral rectus palsy (VI nerve palsy = diplopia)

1. Direct extension: Through bone - via tegmen, posterior fossa plate, or emissary veins (thin bone of Trautmann's triangle)
2. Hematogenous spread: Via emissary veins to dural sinuses, cerebral veins, or meninges

SECTION F: MEDICAL MANAGEMENT

1. Aural toilet (dry mopping, microsuction) - removes debris and discharge, essential first step
2. Topical antibiotic eardrops:
   • Fluoroquinolone drops (ciprofloxacin, ofloxacin) - first-line, safe for middle ear
   • Combined antibiotic-steroid preparations
   • Acetic acid drops (for Pseudomonas)
3. Systemic antibiotics: For acute exacerbations or systemic signs; guided by culture and sensitivity
4. Avoid water entry into ear (cotton wool with petroleum jelly while bathing)
5. Treat underlying nasal/Eustachian tube dysfunction: Decongestants, nasal steroids
6. Goal: Dry the ear, reduce inflammation, prepare for possible surgery

1. Failure of repeated medical treatment (persistent otorrhea despite adequate conservative therapy)
2. Symptoms suspicious for complications: Vertigo, facial weakness, headache
3. Large or marginal perforation unlikely to heal spontaneously
4. Patient preference (to achieve dry ear, improve hearing)
5. Tympanoplasty (myringoplasty ± ossiculoplasty) is the surgical option

SECTION G: SURGICAL MANAGEMENT

1. Eradication of disease (primary goal)
2. Prevention of recurrence
3. Preservation or restoration of hearing

• Type I (Myringoplasty): Repair of TM perforation only; ossicular chain intact and mobile
• Type II: TM repair with malleus erosion - graft placed on remaining ossicles or incus
• Type III (Columella): Malleus + incus absent; graft placed on head of stapes; natural columella effect
• Type IV: All ossicles except stapes footplate absent; sound protection for round window
• Type V: Fenestration of horizontal semicircular canal (now rarely done)

• Temporalis fascia - most commonly used; strong, easily harvested
• Tragal cartilage - more rigid, good for retraction-prone patients and revision cases
• Perichondrium - from tragus or pinna
• Vein graft - thin, used for small perforations historically
• Fat graft - for pinhole perforations

1. Underlay technique: Graft placed medial to the TM remnant and handle of malleus - most commonly used
2. Overlay (onlay) technique: Graft placed lateral to the TM; risk of blunting of anterior sulcus
3. Approaches: Endaural, postauricular, or transcanal (depends on exposure needed)

1. Simple (cortical) mastoidectomy (Schwartze operation): Exenteration of mastoid air cells; posterior meatal wall preserved; no access to epitympanum
2. Modified radical mastoidectomy (Bondy operation): Posterior EAC wall removed; epitympanum exenterated; middle ear hearing mechanism preserved; designed for localized attic cholesteatoma
3. Radical mastoidectomy (Schwartze-Stacke operation): Posterior EAC wall + tympanic membrane + middle ear contents removed except stapes and ET; creates a common meatomastoid cavity; no hearing reconstruction
4. Canal wall up (CWU) mastoidectomy: Posterior canal wall preserved; better cosmesis, less care needed; higher recurrence rate
5. Canal wall down (CWD) mastoidectomy: Posterior canal wall removed; better access; open cavity requires lifelong cleaning; lower recurrence

SECTION H: SPECIAL TOPICS

1. Mild retraction of pars flaccida/pars tensa
2. Progressive retraction - TM touches the incus/stapes
3. TM lies on promontory (adhesive otitis media)
4. Deep retraction pocket loses self-cleansing ability → accumulates keratin debris → cholesteatoma

• If ear is dry at time of implantation - single-stage CI can be done
• Staged approach for active CSOM: Stage 1 - mastoidectomy + ET obliteration ± cavity obliteration; Stage 2 - CI after ear is dry (usually 2-6 months later)
• Cholesteatoma must be fully eradicated before implantation
• Biofilm eradication is essential before inserting CI hardware
• Risk of recurrent cholesteatoma in obliterated cavity must be monitored; DWI-MRI difficult to interpret due to CI artifact

1. High-resolution CT temporal bone (HRCT): First-line; shows bony erosions (scutum, ossicles, tegmen, semicircular canals, Fallopian canal), soft tissue density, mastoid pneumatization. Cannot differentiate cholesteatoma from other soft tissue.
2. MRI (DWI sequences): Detects cholesteatoma by restricted diffusion (bright on DWI). Used for:
   • Pre-operative extent assessment
   • Post-operative detection of residual/recurrent cholesteatoma
   • Replacing second-look surgery
3. Normal CT has extremely high NPV for absence of cholesteatoma

• Removes discharge and debris that provide a medium for bacterial growth
• Allows topical antibiotics to reach the middle ear mucosa
• Helps assess the TM and middle ear cavity
• Regular microsuction by an ENT specialist is essential for cholesteatoma patients to debride keratin debris and monitor disease progression
• Inadequate aural toilet reduces efficacy of topical antibiotics

• Pain/headache
• Vertigo
• Facial weakness
• Fundal changes (papilledema) Must be treated as having unsafe disease until proven otherwise.

1. Eradication of cholesteatoma (most important)
2. Eradication of irreversible mucosal disease in the mastoid unresponsive to medical treatment
3. Approach for cholesteatoma removal
4. Establishment of aeration (less important, per Shambaugh)
5. Some surgeons also use it for persistent suppurative drainage after failed tympanoplasty

• Dry ear for at least 6 weeks (ideally 3 months)
• Good Eustachian tube function
• No active cholesteatoma or irreversible middle ear disease
• Contralateral ear assessment
• Patient cooperation and understanding

• Central, dry perforation
• Good ET function
• Young age (once nasal disease resolved)
• Smaller perforation
• Experienced surgeon
• Temporalis fascia or cartilage graft

• Marginal perforations
• Poor ET function
• Active infection at time of surgery
• Revision surgery
• Atrophic drum remnant
• Anterior perforations (difficult visualization)

• Myringoplasty: Repair of TM perforation only (= Wullstein Type I tympanoplasty)
• Tympanoplasty: Broader term encompassing TM repair plus any work on the ossicular chain (ossiculoplasty), middle ear mucosa, or mastoid

SECTION I: RAPID-FIRE VIVA

• Safe: Central pars tensa perforation (rim of TM all around, no squamous epithelium lining)
• Unsafe: Marginal or attic perforation (squamous epithelium can migrate in, risk of cholesteatoma)

SUMMARY TABLE: Key High-Yield Points

Pertinent Negative History in CSOM - What You Ask & What It Rules Out

1. PAIN (Otalgia / Headache)

Viva key point: Uncomplicated CSOM is painless. Onset of pain = red flag = complication until proven otherwise.

2. VERTIGO / DIZZINESS

• Labyrinthine fistula (lateral SCC erosion by cholesteatoma) - episodic vertigo triggered by pressure changes
• Suppurative labyrinthitis - severe vertigo + SNHL + nausea/vomiting
• Serous labyrinthitis - mild vertigo from toxin spread without direct bacterial invasion
• Cerebellar abscess - unsteady gait, past-pointing (not spinning)

Absence of vertigo in CSOM = inner ear and labyrinth not yet involved.

3. FACIAL WEAKNESS

• Facial nerve palsy - VII nerve runs through the Fallopian canal in the middle ear; cholesteatoma or granulation tissue can erode the canal and compress/invade the nerve
• This is an absolute surgical emergency in CSOM - requires urgent mastoidectomy

Absence of facial weakness = VII nerve intact so far.

4. CHANGE IN HEARING / TINNITUS

• Sudden SNHL - suggests labyrinthine involvement (labyrinthitis or perilymph fistula)
• Ossicular chain erosion - gradual worsening CHL
• Tinnitus can indicate labyrinthine irritation

Stable mild CHL = reassuring. Sudden worsening = inner ear threatened.

5. FEVER / SYSTEMIC SYMPTOMS

• Acute exacerbation / coalescent mastoiditis - fever + otalgia + postauricular tenderness
• Lateral sinus thrombosis - "picket fence" (intermittent spiking) fever with rigors = Griesinger's pattern
• Meningitis - high fever + neck stiffness
• Septicemia - from lateral sinus thrombosis or brain abscess

Absence of fever = no systemic sepsis at present.

6. NECK STIFFNESS / PHOTOPHOBIA / ALTERED SENSORIUM

• Meningitis (most common intracranial complication of CSOM) - neck stiffness, photophobia, Kernig's sign
• Brain abscess - altered sensorium, focal neurological deficits, raised ICP signs
• Subdural empyema - rapid neurological deterioration

These are life-threatening - absence is essential to document clearly in notes/viva.

7. DIPLOPIA / VISUAL DISTURBANCE

• Gradenigo's syndrome - VI nerve palsy = lateral rectus palsy = diplopia (petrous apicitis)
• Otitic hydrocephalus - raised ICP → VI nerve palsy as false localizing sign + papilledema
• Cavernous sinus thrombosis (rare) - multiple cranial nerve palsies

8. NECK SWELLING

• Bezold's abscess - pus tracking along SCM from mastoid tip
• Citelli's abscess - tracking into digastric triangle
• Zygomatic (temporal root) abscess - swelling in temporal/zygomatic region

9. NASAL / NASOPHARYNGEAL SYMPTOMS

• Chronic rhinosinusitis - perpetuates ET dysfunction, maintains CSOM
• Adenoid hypertrophy (especially in children) - blocks ET orifice in nasopharynx
• Nasopharyngeal carcinoma - must be excluded in adult with unilateral CSOM + cervical lymphadenopathy (NPC can obstruct ET, present exactly like CSOM - a critical differential)

Viva trap: Unilateral middle ear effusion/CSOM in an adult = always examine postnasal space / do nasopharyngoscopy to exclude NPC.

10. BLOOD IN DISCHARGE

• Malignancy (squamous cell carcinoma of temporal bone) - can arise in longstanding CSOM; presents with blood-stained otorrhea, pain, facial palsy
• Granulation tissue - bleeds on touch but discharge is usually mucopurulent, not frankly bloody
• Vascular anomaly (e.g., aberrant carotid, jugular bulb dehiscence)
• Glomus tumor - pulsatile blood-stained discharge

11. PREVIOUS TREATMENT HISTORY

• Residual/recurrent cholesteatoma after previous mastoidectomy
• Resistant organisms due to repeated antibiotic use
• Fungal otitis media - after prolonged topical antibiotic use (Candida overgrowth in 35% after 3 weeks of ciprofloxacin drops)
• Iatrogenic causes of symptoms

12. TRAUMA HISTORY

• Traumatic TM perforation - different management (often heals spontaneously)
• CSF otorrhea - clear watery discharge after head injury = tegmen fracture
• Traumatic cholesteatoma (implantation cholesteatoma) - from squamous epithelium implanted into middle ear during trauma

13. DIABETES / IMMUNOCOMPROMISED STATE

• Malignant (necrotizing) otitis externa - in diabetics/immunocompromised, Pseudomonas invades temporal bone; can mimic severe CSOM clinically - granulation tissue at bony-cartilaginous junction, severe bone destruction, cranial nerve palsies
• Immunocompromise worsens prognosis of any CSOM complication
• Fungal infections more likely

QUICK SUMMARY TABLE FOR VIVA

HOW TO SAY IT IN VIVA (Template)

"On history, there was no pain, no headache, no vertigo, no facial weakness, no diplopia, no fever or rigors, no neck stiffness, no neck swelling, no blood in the discharge, and no nasal symptoms - thus ruling out complications including labyrinthine fistula, facial nerve palsy, meningitis, brain abscess, lateral sinus thrombosis, Bezold's abscess, Gradenigo's syndrome, and associated nasopharyngeal pathology."

Complications of CSOM - Quick Table

EXTRACRANIAL COMPLICATIONS

INTRACRANIAL COMPLICATIONS

EPONYMS AT A GLANCE

ONE-LINE MEMORY AID

"My Big Cat Zaps Five Lions In My Bloody Skull" Mastoiditis → Bezold → Citelli → Zygomatic → Facial palsy → Labyrinthitis/fistula → Intracranial (Meningitis, Brain abscess, Sinus thrombosis, Hydrocephalus)