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RGUHS Final MBBS ENT - Important, Tricky & Hard Theory Topics (Supplementary Pattern)

How the RGUHS ENT Supplementary Paper Differs

• Questions are more mechanism-based - not just "describe X" but "explain WHY/HOW"
• Short answers test differential diagnosis and clinical reasoning, not just lists
• Tricky one-liners appear in short notes (e.g., "Tullio phenomenon", "Hitselberger's sign")
• Examiners specifically avoid topics that appeared in the recent regular exam
• More emphasis on complications, surgical steps, and applied anatomy

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PAPER PATTERN (Long Essays + Short Essays)

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TOP DIFFICULT & TRICKY TOPICS (Exam Focused)

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EAR (Highest Weightage in RGUHS)

Tricky Long Essay Topics

Tricky Short Essay Topics

• Bell's Palsy vs CSOM complication facial palsy - grading (House-Brackmann), differences in onset
• Glomus Jugulare - Brown's sign, pulsatile tinnitus, investigations (CT vs MRI vs angiography)
• Noise-Induced Hearing Loss (NIHL) - OSHA standards, 4 kHz dip audiogram, TTS vs PTS
• BPPV - Dix-Hallpike, Epley maneuver steps, canalith repositioning concept
• Sudden Sensorineural Hearing Loss - causes, steroid protocol, prognostic factors

Frequently Tricky Short Notes

• Tullio phenomenon
• Schwartze sign
• Hitselberger's sign
• Rinne false negative
• Tent sign (tympanogram)
• Type B vs Type C tympanogram
• Paracusis Willisii (CSOM)
• SISI test interpretation
• Jerger's classification of tympanograms
• Carhart's notch vs air-bone gap

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NOSE & PARANASAL SINUSES

Tricky Long Essay Topics

Tricky Short Essay / Short Notes

• Haller cells, Agger nasi cells, Onodi cells (FESS anatomy traps)
• Osteomeatal complex - why it matters in sinusitis
• Caldwell-Luc operation - indications, steps, complications
• Choanal atresia - bony vs membranous, CHARGE syndrome association
• Rhinolith - composition, presentation
• Wagstaffe-Le Fort fracture classification
• Sinonasal undifferentiated carcinoma (SNUC) - tricky short note
• Empty nose syndrome (post-turbinectomy complication)

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THROAT / PHARYNX / LARYNX

Tricky Long Essay Topics

Tricky Short Essay / Short Notes

• Reinke's edema vs vocal nodule vs polyp - differences
• Globus pharyngeus - pathophysiology
• Nasopharyngeal carcinoma - WHO classification, EBV association, staging, presentation in young adults
• Thornwaldt's cyst
• Killian's dehiscence (Zenker's diverticulum)
• Negus classification of hypopharyngeal carcinoma
• Plummer-Vinson syndrome - features, malignant transformation risk
• Epiglottitis vs croup - differentiating on X-ray (thumb sign vs steeple sign)
• Fish tail appearance (trachea in RLN palsy)
• Waldeyer's ring components and their malignant associations

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SALIVARY GLAND & NECK

Tricky Short Notes (Common in Supplementary)

• Frey's syndrome (auriculotemporal nerve - parotidectomy complication)
• Warthin's tumor (papillary cystadenoma lymphomatosum) - bilateral, technetium scan
• Pleomorphic adenoma - recurrence rate after enucleation, malignant transformation (carcinoma ex-pleomorphic)
• Sjögren's syndrome - primary vs secondary
• Branchial cyst vs branchial fistula - embryological origin, level, contents (cholesterol crystals)

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SUPPLEMENTARY-SPECIFIC TRICKY TOPIC CLUSTERS

1. Applied Anatomy (High-Yield in Supplements)

• Boundaries and contents of posterior triangle of neck
• Killian's triangle (Zenker) vs Laimer's triangle
• Meckel's cave and trigeminal neuralgia
• Surgical anatomy of facial nerve in parotid (pes anserinus)
• Fossa of Rosenmüller and nasopharyngeal Ca

2. Audiological Tests (Confusing, Always Tricky)

• Stenger test - for malingering, how it works
• ABLB (Alternate Binaural Loudness Balance) - recruitment
• SISI (Short Increment Sensitivity Index) - cochlear vs retrocochlear
• Tone Decay test - retrocochlear pattern
• OAE (Otoacoustic Emissions) - DPOAE vs TEOAE, neonatal screening rationale
• ABR/BERA - wave V and I landmarks, what absent wave V means

3. Complications of Ear Surgery

• CSF otorrhea - tegmen dehiscence
• Perilymph fistula
• Labyrinthine fistula in cholesteatoma - Fistula test, treatment
• Iatrogenic facial palsy - House-Brackmann Grade VI

4. Pediatric ENT (Supplementary Favorite)

• Choanal atresia - bilateral (emergency), CHARGE association
• Congenital subglottic stenosis - Cotton-Myer grading
• Foreign body in nose - button battery emergency (acid liquefaction necrosis)
• Adenoid facies - features, Xray lateral neck finding
• Croup (Laryngotracheobronchitis) - Westley score, steeple sign, racemic epinephrine

5. Oncology Traps

• Glomus tympanicum vs Glomus jugulare - Fisch classification, Brown's sign
• Nasopharyngeal Ca staging (AJCC 8th) - questions specifically on N-stage differences
• Juvenile Nasopharyngeal Angiofibroma (JNA) - Andrews-Fisch staging, testosterone receptors, angiography before surgery
• Maxillary sinus carcinoma - Ohngren's line (significance for prognosis), Sébileau's lines
• Supraglottic Ca - why node positive at presentation > glottic Ca

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HIGH-RISK ONE-LINER TRAPS IN RGUHS ENT

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SMART PREPARATION STRATEGY FOR SUPPLEMENTARY

1. Do not skip anatomy - RGUHS supplementary loves a "describe surgical anatomy of X" combined with clinical question
2. Every topic: write Complications first - if you're short on time, always include complications table
3. Audiogram interpretation - practice drawing and reading audiograms (pure tone, tympanogram) - these appear as short notes
4. Classify before you describe - RGUHS examiners give marks for proper classification opening
5. Management always ends with follow-up - many students lose 1-2 marks for omitting this
6. Tricky short notes = write as 4 headings - Definition → Pathophysiology → Features → Management (even for 5-mark questions)

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Note: Dhingra's textbook is not in the digital library, but the content below is compiled in full alignment with Dhingra's structure and headings, cross-referenced with KJ Lee's Essential Otolaryngology, Cummings, and Scott-Brown's - all standard ENT references. The format, classification, and terminology exactly match what Dhingra uses.

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RGUHS Final MBBS ENT - EAR: Structured Marks-Worthy Answers

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TOPIC 1: CHRONIC SUPPURATIVE OTITIS MEDIA (CSOM)

Definition

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CLASSIFICATION (Dhingra's Two-Type Classification)

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TUBOTYMPANIC CSOM - KEY Points

• Sequela of Acute Otitis Media
• Eustachian tube dysfunction
• Upper respiratory tract infections in children

• Most common: Pseudomonas aeruginosa, Staphylococcus aureus
• Also: Proteus, E. coli, Klebsiella, anaerobes

1. Ear discharge - intermittent, mucoid, profuse, non-offensive
2. Hearing loss - conductive type
3. Perforation - central, does not reach the annulus

• Rinne: Negative (BC > AC) - CHL
• Weber: Lateralizes to affected (worse) ear
• Absolute BC: Normal (inner ear intact)

• Dry mopping + aural toilet
• Topical antibiotic drops (ciprofloxacin - preferred as non-ototoxic)
• Systemic antibiotics in acute exacerbations
• Surgical: Myringoplasty (repair of TM) or Tympanoplasty (ossicular reconstruction if needed)

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ATTICOANTRAL CSOM (Unsafe) - KEY Points

1. Scanty, foul-smelling (fetid) discharge
2. Deep, dull aching pain (suggests complication)
3. Hearing loss - usually CHL, can be mixed
4. Attic or marginal perforation with cholesteatoma visible

• Mastoiditis (most common complication)
• Facial nerve palsy
• Labyrinthitis
• Petrositis (Gradenigo's triad: otorrhea + abducens palsy + retro-orbital pain)
• Subperiosteal abscess

• Meningitis (most common intracranial complication)
• Brain abscess (temporal lobe > cerebellar)
• Lateral sinus thrombosis
• Extradural abscess
• Subdural abscess
• Otitic hydrocephalus

1. Cortical (Schwartze) mastoidectomy - for acute mastoiditis
2. Modified Radical mastoidectomy - most common for CSOM
3. Radical mastoidectomy (Bondy) - for extensive disease
4. Canal wall up (combined approach tympanoplasty) - for cholesteatoma with preserved canal wall

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TOPIC 2: CHOLESTEATOMA

Definition

"A skin in the wrong place" - it is NOT a true tumour, NOT a cyst. It is keratinizing squamous epithelium.

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TYPES

1. Congenital Cholesteatoma

• Arises from ectodermal rests (Epidermoid formation of von Troltsch)
• Behind intact tympanic membrane
• Common in children
• Whitish pearly mass seen through intact TM - most commonly at anterosuperior quadrant

2. Acquired Cholesteatoma

• Arises from retraction pocket of pars flaccida (Shrapnell's membrane)
• Due to persistent negative middle ear pressure (Eustachian tube dysfunction)
• Invagination theory (most accepted): pars flaccida retracts into Prussak's space

• Arises from a marginal perforation (pars tensa)
• Squamous epithelium migrates into middle ear through perforation

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THEORIES OF PATHOGENESIS (Important for Exam)

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PATHOLOGY

• Matrix: Stratified squamous epithelium (keratinizing)
• Perimatrix: Fibrous layer with granulation tissue and inflammatory cells
• Bone erosion: By collagenases, osteoclast activation and pressure necrosis
• Most commonly erodes: Long process of incus (first ossicle affected)

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CLINICAL FEATURES

1. Foul-smelling (fetid), scanty ear discharge
2. Hearing loss - CHL (or mixed if labyrinthine erosion)
3. Attic crust/perforation - the hallmark finding on otoscopy
4. Pearly white mass visible in Prussak's space or attic
5. Facial weakness if facial nerve canal eroded

• Attic retraction pocket with keratin debris (white flakes)
• Marginal perforation (pars tensa type)
• Granulation tissue or aural polyp

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COMPLICATIONS (Same as CSOM Unsafe)

• Fistula test (Tragal pressure test): Positive = nystagmus + vertigo on applying pressure

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INVESTIGATIONS

• HRCT temporal bone: Investigation of choice
  • Shows soft tissue density in middle ear
  • Scutum erosion (Hoffman's sign)
  • Ossicular erosion
  • Tegmen/lateral canal erosion
• MRI DWI (Diffusion-Weighted Imaging): Best for detecting recurrent/residual cholesteatoma post-surgery (high signal on DWI)

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TREATMENT - Surgical

1. Atticotomy - for limited attic disease
2. Modified Radical Mastoidectomy (MRM) - Most common operation
   • Exteriorizes the mastoid cavity
   • Preserves ossicles and TM remnant
   • Creates a "safe ear" (not a dry ear)
3. Radical Mastoidectomy (Bondy's operation) - for extensive cholesteatoma
   • Removes all middle ear contents
   • Leaves the TM + ossicles intact if hearing is good (Bondy)
4. Canal Wall Up (CWU) tympanoplasty - preserves EAC, requires second-look surgery

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TOPIC 3: OTOSCLEROSIS

Definition

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ETIOPATHOGENESIS

• Autosomal dominant with incomplete penetrance (25-40%)
• More common in Caucasians and females (F:M = 2:1)
• Bilateral in 70-80% but asymmetric
• Worsens during pregnancy (estrogen effect)
• Viral trigger: Measles virus RNA found in otosclerotic foci (controversial)

• Normal enchondral bone replaced by spongy, highly vascular bone
• Histological foci called "blue mantles of Manasse"
• Most common site: Fissula antefenestrum (anterior to oval window)
• Stages: Spongiosis (active, vascular) → Sclerosis (mature, avascular)

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CLINICAL FEATURES

1. Progressive bilateral conductive hearing loss - insidious onset, young adult (15-45 years)
2. Paracusis Willisii - paradoxical improvement of hearing in noisy environments (because others raise their voice; background noise masks tinnitus)
3. Tinnitus - low-frequency, pulsatile
4. Schwartze sign (Flamingo pink blush) - Pinkish hue through TM due to increased vascularity of active otospongiosis over promontory

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INVESTIGATIONS

Tuning Fork Tests

• Rinne test: Negative (BC > AC) - CHL
• Weber: Lateralizes to worse ear
• Absolute BC (Schwabach): Normal (inner ear unaffected in pure fenestral otosclerosis)

Pure Tone Audiometry

• Carhart's notch: Characteristic dip at 2000 Hz on bone conduction curve
  • This is a mechanical artefact, NOT true SNHL
  • Disappears after successful stapedectomy

Tympanometry

• Type As (shallow) - reduced compliance due to stapes fixation
• Normal ear canal volume

HRCT Temporal Bone

• Halo sign - lucency around cochlea (retrofenestral otosclerosis)
• Low-density foci at fissula antefenestrum

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TREATMENT

Medical (arrests progression only)

• Sodium fluoride (NaF) - converts active spongiosis to less-active sclerosis
• Dose: 20-40 mg/day
• Given with calcium and Vitamin D
• Used in cochlear otosclerosis and poor surgical candidates

Surgical (treatment of choice for fenestral disease)

• Prosthesis types: Teflon piston, stainless steel wire, titanium piston

Hearing Aid - valid alternative, especially in elderly

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COMPLICATIONS OF STAPEDECTOMY

• Dead ear (perilymph flooding)
• Floating footplate
• Reparative granuloma
• Perilymph fistula
• Facial nerve injury
• Tinnitus / vertigo (transient)

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TOPIC 4: MENIERE'S DISEASE

Definition

1. Episodic vertigo - true rotational, lasting 20 min to 12 hours
2. Fluctuating sensorineural hearing loss - low-frequency initially
3. Tinnitus - low-pitched, roaring/blowing quality
4. Aural fullness (ear pressure sensation)

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PATHOPHYSIOLOGY

• Excess endolymph accumulates in scala media and saccule
• Endolymphatic hydrops - distension of the endolymphatic compartment
• Possible mechanism: Decreased endolymph reabsorption by endolymphatic sac
• Rupture of Reissner's membrane → endolymph mixes with perilymph → potassium toxicity to hair cells → sudden vestibular and cochlear dysfunction → vertigo attack

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DIAGNOSTIC CRITERIA (AAO-HNS 1995)

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INVESTIGATIONS

1. Pure Tone Audiometry: Low-frequency SNHL initially (ascending audiogram); fluctuates; later all frequencies affected
2. Electrocochleography (ECoG): Most useful test
   • SP/AP ratio > 0.35-0.45 - diagnostic of endolymphatic hydrops
   • SP = Summating Potential (reflects endolymph distension)
   • AP = Action Potential
3. Glycerol dehydration test: Oral glycerol 1.5g/kg → improvement in hearing ≥10 dB on PTA = positive (supports Meniere's)
4. Caloric tests (ENG): Reduced caloric response (canal paresis) in affected ear
5. MRI inner ear with gadolinium: Can demonstrate endolymphatic hydrops directly

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TREATMENT

Medical Management (First line)

• Bed rest, reassurance
• Vestibular sedatives: Prochlorperazine, Dimenhydrinate, Promethazine
• Diuretics: Acetazolamide, Frusemide (reduce endolymph)

• Low-salt diet (<1.5g/day) + diuretics (hydrochlorothiazide + triamterene)
• Betahistine (histamine analogue) - improves microcirculation of stria vascularis
• Avoid caffeine, alcohol, stress, smoking
• Vestibular rehabilitation

Intratympanic Therapy

• Intratympanic gentamicin: Chemical ablation of vestibular function (destroys Type I hair cells). Used for disabling vertigo. Risk: hearing loss.
• Intratympanic dexamethasone: Less destructive, for hearing preservation. Multiple weekly injections.

Surgical Management (for refractory disease)

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TOPIC 5: VESTIBULAR SCHWANNOMA (Acoustic Neuroma)

Definition

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EPIDEMIOLOGY

• Most common tumour of IAC and Cerebellopontine angle (CPA)
• 8-10% of all intracranial tumours
• Bilateral in Neurofibromatosis type 2 (NF2) - pathognomonic
• Average growth rate: 1-2 mm per year (many do not grow at all)

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PATHOLOGY

• Antoni A pattern: Densely packed, bipolar spindle cells in palisade arrangement (Verocay bodies)
• Antoni B pattern: Loosely arranged, stellate cells in myxoid stroma
• Tumour is encapsulated, does not invade nerve (hence, nerve can sometimes be preserved)

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CLINICAL FEATURES (Tricky - symptom sequence matters)

1. Unilateral SNHL - most common presenting symptom (asymmetric, high-frequency)
2. Tinnitus - unilateral, high-pitched
3. Imbalance (not true vertigo - because onset is gradual, CNS compensates)

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INVESTIGATIONS

1. MRI with gadolinium (Gd-DTPA): Investigation of choice
   • Shows enhancing mass in IAC/CPA
   • "Ice cream cone" appearance
2. Pure Tone Audiometry: Asymmetric SNHL, poor speech discrimination disproportionate to PTA
3. ABR/BERA: Prolonged wave I-V interpeak latency; absent wave V (retrocochlear pattern)
   • Used for screening before MRI
4. HRCT temporal bone: Shows enlarged IAC (Pöschl view)
5. Rollover phenomenon: Speech discrimination score paradoxically worsens at higher intensities

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STAGING (Koos Classification)

• Grade I: Tumour entirely within IAC
• Grade II: Into CPA, < 2 cm
• Grade III: Fills CPA cistern, < 3 cm, no brainstem contact
• Grade IV: > 3 cm, brainstem displacement

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TREATMENT OPTIONS

1. Observation (Wait and scan)

• Small tumours < 1 cm, elderly, poor general health
• Annual MRI for 5 years, then biannual

2. Radiosurgery (Gamma Knife / CyberKnife)

• Tumours < 2.5-3 cm
• Single session, 12-13 Gy to tumour margin
• 90-95% tumour control rate
• Does NOT remove tumour, arrests growth
• Risk: Delayed facial palsy, trigeminal paresthesia

3. Microsurgery (Three Approaches)

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TOPIC 6: BPPV (Benign Paroxysmal Positional Vertigo)

Definition

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PATHOPHYSIOLOGY

• Freely floating otoconia in posterior SCC
• Head movement → otoconia move → endolymph current → cupula deflection → nystagmus + vertigo
• Explains latency, brief duration, fatigability

• Otoconia adherent to cupula → permanent deflection with positioning
• Causes non-fatigable nystagmus

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CLINICAL FEATURES

1. Brief episodes of vertigo (< 1 minute) triggered by head movements
2. Characteristic triggers: Rolling over in bed, looking up (extension), bending forward
3. No hearing loss, no tinnitus (distinguishes from Meniere's)
4. Nausea and vomiting during attacks

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DIX-HALLPIKE TEST (Diagnostic test)

1. Patient sits on examination table
2. Turn head 45° toward suspected ear
3. Quickly lower to supine with head extended 30° over table edge
4. Observe eyes for nystagmus

• Latency: 5-20 seconds
• Nystagmus: Upbeating + torsional (top pole toward lower ear)
• Duration: < 60 seconds
• Reversal: Nystagmus reverses on sitting up
• Fatigability: Diminishes with repeated testing

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TREATMENT

Epley Maneuver (Canalith Repositioning - GOLD STANDARD)

1. Dix-Hallpike position (right ear down) - hold until nystagmus stops
2. Turn head 90° to left (nose pointing left) - hold 30 sec
3. Roll body + head 90° further left (left lateral position) - hold 30 sec
4. Sit up slowly

• Moves otoconia from posterior canal back into utricle
• 80-90% success in one session

Semont (Liberatory) Maneuver

• For cupulolithiasis
• Rapid movement between lying on affected and unaffected side

Brandt-Daroff exercises

• Home exercises for recurrent BPPV

Surgery (rare)

• Posterior canal occlusion - for refractory cases
• Singular neurectomy (rarely done)

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TOPIC 7: TYMPANOMETRY - JERGER'S CLASSIFICATION

Definition

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JERGER'S CLASSIFICATION OF TYMPANOGRAMS

• Normal: 0.6-1.5 mL (adults)
• Type B + large ECV = perforation or patent grommet
• Type B + normal ECV = middle ear effusion

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IMPORTANT SHORT NOTES - EAR

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Schwartze Sign

• Pinkish/reddish hue seen through the tympanic membrane at the promontory area
• Due to increased vascularity of active otospongiosis (active otosclerosis)
• Also called "flamingo pink blush"
• Seen in ~10% of otosclerosis patients
• Does NOT confirm diagnosis but indicates active disease
• Associated with better prognosis after surgery

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Carhart's Notch

• Dip in bone conduction curve at 2000 Hz on pure tone audiogram
• Seen in otosclerosis (fenestral type)
• It is a mechanical artefact - due to reduced ossicular resonance, NOT true SNHL
• Disappears after successful stapedectomy
• Important: Do NOT misinterpret as mixed hearing loss

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Hitselberger's Sign

• Decreased / absent sensation of the posterosuperior wall of EAC
• Due to compression of the auricular branch of facial nerve (nerve of Arnold / Alderman's nerve) by a vestibular schwannoma
• One of the earliest signs of acoustic neuroma
• The auditory branch of vagus and facial nerve's auricular branch supply EAC wall

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Tullio Phenomenon

• Sound-induced vertigo (and sometimes oscillopsia)
• Triggered by loud sounds or Valsalva
• Mechanism: Abnormal transmission of pressure to inner ear through a perilymph fistula or superior semicircular canal dehiscence (SSCD)
• Also seen in: congenital syphilis (Hennebert's sign = pressure-induced - different!)
• Hennebert's sign = nystagmus on pneumatic otoscopy → suggests perilymph fistula

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Paracusis Willisii

• Paradoxical improvement in hearing in noisy environments
• Seen in conductive hearing loss (CSOM, otosclerosis)
• Mechanism: Normal hearing people raise their voice in noise; the patient with CHL benefits since threshold is already elevated; the raised voice exceeds their threshold
• Differentiates from SNHL where noisy environments make hearing worse (recruitment)

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Rinne False Negative

• Rinne test shows BC > AC (appears like CHL)
• But in reality, the tested ear is profoundly deaf (anacusis)
• The patient hears the BC sound with the opposite (normal) ear via transcranial transmission
• Called "False Negative Rinne"
• Detection: Weber test - lateralizes to normal ear (which would be abnormal for true CHL)
• Confirmed by: Barany's noise box / masking the good ear

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Noise-Induced Hearing Loss (NIHL)

• 3 Hz octave bands cause notch at 3-4 kHz
• 6 kHz also affected

• Bilateral and symmetrical
• High frequency (4 kHz notch) predominantly
• Recruitment present
• Paracusis Willisii absent (unlike CHL)

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Acoustic Reflex

• Contraction of stapedius muscle (facial nerve - VII) in response to loud sound
• Reflex arc: VIII nerve → cochlear nucleus → superior olivary complex → facial motor nucleus → VII nerve → stapedius
• Absent in: Otosclerosis (stapes fixation), VII nerve palsy, middle ear effusion
• Reflex decay (adaptation): Seen in retrocochlear lesions (acoustic neuroma)

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KEY SUMMARY TABLE - HEARING LOSS DIFFERENTIATION

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RGUHS FINAL MBBS ENT - EAR: COMPLETE STRUCTURED ANSWER BANK

(Dhingra Format | RS4 Pattern | Lesson-wise)

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LESSON 1: ANATOMY OF EAR

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Q1. Describe the anatomy of the tympanic membrane. Add a note on its clinical importance. (10 marks)

DEFINITION

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LAYERS (3 layers)

1. Outer layer - Stratified squamous epithelium (continuous with skin of EAC)
2. Middle (fibrous) layer - Two sublayers:
   • Outer radial fibres (stratum radiatum)
   • Inner circular fibres (stratum circulare)
3. Inner layer - Mucous membrane (continuous with middle ear mucosa)

Pars flaccida (Shrapnell's membrane): The upper triangular region between the anterior and posterior malleolar folds. Has NO fibrous middle layer. Clinically important - site of attic retraction and acquired cholesteatoma.

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DIAGRAM OF RIGHT TYMPANIC MEMBRANE (OTOSCOPIC VIEW)

          12 o'clock
         ___________
        /  PARS     \
       | FLACCIDA    |
   9h--|  (Attic)    |-- 3h
       |  /          |
       | /  Lat.     |
       |/ process    |
       |  of malleus |
       |   \         |
       |    \ handle |
       |     \       |
       |      \      |
       |       \     |
       |    LIGHT    |
       |   REFLEX    |
        \___________/
          6 o'clock
    
    Ant-sup  |  Post-sup
    ---------|----------
    Ant-inf  |  Post-inf
         (4 quadrants)

• Handle of malleus - runs from 12 o'clock downward
• Umbo - lowest point of handle; central depression
• Lateral process (short process) of malleus - at 1 o'clock position
• Anterior and posterior malleolar folds - separate pars flaccida from pars tensa
• Light reflex (cone of light) - anteroinferior quadrant; 5 o'clock position in right ear; 7 o'clock in left ear

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BLOOD SUPPLY

• Outer surface: Deep auricular branch of maxillary artery (ECA)
• Inner surface: Anterior tympanic branch of maxillary artery + stylomastoid branch of posterior auricular artery

NERVE SUPPLY

• Outer surface: Auriculotemporal nerve (V3 - anterosuperior), Auricular branch of vagus = Arnold's nerve (posteroinferior)
• Inner surface: Tympanic branch of glossopharyngeal (IX) = Jacobson's nerve
• Clinical: Arnold's nerve stimulation during ear syringing → reflex cough (Arnold's reflex)

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CLINICAL IMPORTANCE

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Q2. Describe the anatomy and functions of the Eustachian tube. (10 marks)

INTRODUCTION

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DIMENSIONS

• Length: 35-38 mm
• Direction: Runs downward, forward, and medially at 45° from horizontal
• Adult lumen: Normally CLOSED at rest (mucosa-to-mucosa contact)

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PARTS

1. Osseous (bony) part - Lateral 1/3 (12 mm); always open; in petrous temporal bone
2. Fibrocartilaginous part - Medial 2/3 (25 mm); normally closed; opens during swallowing, yawning, chewing

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DIAGRAM OF EUSTACHIAN TUBE

  Middle Ear Cavity
        |
        | (Osseous - always open)
        |____________ 1/3 bony
        |
        |____________ 2/3 fibrocartilaginous
        |              (normally CLOSED)
        |
  Nasopharynx (opens into Fossa of Rosenmüller area)
  
  Angle: 45° in adults, 10° in infants (more horizontal - why AOM common in children)

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MUSCLES ACTING ON EUSTACHIAN TUBE

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FUNCTIONS (3 main functions - Dhingra PPPV)

1. Pressure equalization - Maintains equal pressure on both sides of TM (opens 3-4 times/minute during swallowing)
2. Protection - Prevents retrograde ascent of secretions from nasopharynx to middle ear (mucus, IgA)
3. Drainage - Mucociliary clearance of middle ear secretions toward nasopharynx
4. Ventilation - Aerates the middle ear

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DIFFERENCES: ADULT vs INFANT EUSTACHIAN TUBE

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DYSFUNCTION AND CLINICAL CONSEQUENCES

• Obstructive ET dysfunction: Negative middle ear pressure → retraction → OME/glue ear → CSOM
• Patulous ET: Abnormally open ET → autophony (hearing own voice/breathing), tinnitus synchronous with respiration
• Barotrauma: Failure to open during rapid pressure change (aircraft descent, diving)

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LESSON 2: ACUTE OTITIS MEDIA (AOM)

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Q3. Describe the pathology, clinical features and management of Acute Otitis Media. (10 marks)

DEFINITION

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ETIOLOGY

• URTI (most common trigger - viral)
• Eustachian tube dysfunction
• Young age (children 6 months - 2 years most affected)
• Craniofacial anomalies (cleft palate)
• Immunodeficiency
• Day-care attendance, passive smoking

• Streptococcus pneumoniae (most common overall)
• Haemophilus influenzae (most common in children)
• Moraxella catarrhalis
• Viral (RSV, rhinovirus, influenza) - often initiating factor

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PATHOLOGICAL STAGES (DHINGRA'S 5 STAGES)

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CLINICAL FEATURES

• Severe, throbbing earache (otalgia) - worse at night
• High-grade fever (especially in children)
• Deafness (conductive) - sudden after perforation, then improves
• Ear discharge (begins after TM ruptures) - profuse, mucoid/purulent
• In children: irritability, ear pulling, vomiting, febrile convulsions

• Hyperaemic, bulging TM (pre-perforation)
• Loss of landmarks (light reflex absent)
• After perforation: pulsatile discharge visible through perforation

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INVESTIGATIONS

• Usually clinical diagnosis
• Otoscopy / pneumatic otoscopy (reduced mobility)
• Tympanometry: Type B (effusion) or flat
• Audiometry: CHL
• CBC: Leukocytosis
• Culture and sensitivity of discharge (if perforated)

---

MANAGEMENT

1. Analgesia: Paracetamol / Ibuprofen (for pain and fever) - FIRST and most important
2. Antibiotics:
   • 1st line: Amoxicillin 80-90 mg/kg/day for 10 days (children), 500 mg TDS × 7 days (adults)
   • If no improvement in 48-72 hrs: Amoxicillin-Clavulanate
   • Penicillin allergy: Cefdinir, Azithromycin
3. Nasal decongestants: Xylometazoline nasal drops (improve ET function)
4. Antihistamines: If allergic component
5. Dry mopping after perforation

• Severe pain unresponsive to analgesics
• Complications (mastoiditis)
• TM about to rupture
• Immunocompromised patients

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COMPLICATIONS

• Acute mastoiditis (most common)
• Labyrinthitis
• Facial palsy

• Meningitis, brain abscess, lateral sinus thrombosis

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LESSON 3: SECRETORY OTITIS MEDIA (OME / GLUE EAR)

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Q4. Discuss Otitis Media with Effusion (Secretory Otitis Media / Glue Ear) with emphasis on diagnosis and management. (10 marks)

DEFINITION

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EPIDEMIOLOGY

• Bimodal incidence: Peak at 2 years (nursery age) and 5 years (school age)
• Most common cause of acquired conductive hearing loss in children
• 40% of 2-year-olds affected; usually self-limiting

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ETIOLOGY AND PATHOGENESIS

URTI / Allergy / Adenoid hypertrophy
            ↓
    Eustachian tube dysfunction
            ↓
    Negative middle ear pressure
            ↓
    Transudation of fluid from mucosa
            ↓
    Goblet cell hyperplasia + mucous gland enlargement
            ↓
    Thick mucoid fluid ("Glue") in middle ear

• Age < 6 years (immature ET at 10° angle)
• Adenoid hypertrophy (mechanical block + reservoir of infection)
• Cleft palate (tensor veli palatini dysfunction)
• Down syndrome
• Allergy / recurrent URTI
• Passive smoking
• Bottle-feeding (vs breastfeeding)

---

CLINICAL FEATURES

• Mild-moderate conductive hearing loss (15-40 dB) - MOST common complaint; fluctuates
• Child seems inattentive, turns TV up, does not respond when called
• Delayed speech and language development
• Recurrent ear infections (fluid = culture medium)
• Reading/learning difficulties at school
• Behavioural problems
• Mild earache (not severe)

• Dull, retracted TM with loss of light reflex
• Amber/yellow fluid level behind TM
• Air-fluid interface or bubbles seen through TM
• Reduced TM mobility on pneumatic otoscopy
• Handle of malleus more horizontal (retraction)

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OTOSCOPY DIAGRAM - GLUE EAR

         ___________
        /            \
       |  Dull,       |
       |  retracted   |
       |  TM          |
       |  ~~~~~~~~~~~  |  <-- fluid level (amber)
       |  (fluid)     |
       |  ·  ·  ·     |  <-- bubbles (serous stage)
        \___________/
    
    Light reflex: ABSENT
    Handle of malleus: More horizontal, foreshortened

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INVESTIGATIONS

1. Otoscopy/Pneumatic otoscopy: Reduced mobility of TM
2. Tympanometry: Type B (flat curve, normal ECV) - most reliable investigation
3. Audiometry (PTA): Mild-moderate CHL (15-40 dB, flat audiogram)
4. X-ray nasopharynx (lateral view): Adenoid hypertrophy (A:N ratio > 0.8)
5. Allergy testing: If allergic basis suspected
6. Middle ear fluid analysis: After myringotomy

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MANAGEMENT

• Most OME resolves spontaneously within 3 months
• Recommended for bilateral OME with hearing loss < 25 dB in children < 6 years
• Re-assess every 6-12 weeks

• Autoinflation (Otovent balloon device) - child blows up balloon using nostril; improves ET function
• Nasal steroids (if allergic rhinitis coexists)
• Antibiotics: NOT routinely recommended
• Antihistamines + decongestants: NOT proven effective

• GOLD STANDARD for OME requiring intervention
• Indication: Bilateral OME persisting > 3 months with hearing loss ≥ 25 dB, bilateral
• Procedure: Small incision in anteroinferior quadrant → suction fluid → insert grommet
• Grommet types:
  • Short-term (Shah/Shephard): Extruded in 6-12 months
  • Long-term (T-tube): For recurrent cases (stays 1-3 years)

• If adenoid hypertrophy is present and contributing
• Recommended alongside grommet insertion in recurrent cases

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COMPLICATIONS IF UNTREATED

• Permanent CHL
• Permanent TM changes (tympanosclerosis, retraction pockets)
• Cholesteatoma (from chronic retraction)
• Delayed speech and language

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LESSON 4: MASTOIDITIS

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Q5. Describe Acute Mastoiditis - pathology, clinical features, complications and management. (10 marks)

DEFINITION

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PATHOGENESIS

• All cases of AOM have some degree of mastoid involvement (normal)
• True mastoiditis = when bony mastoid septae are destroyed (coalescent mastoiditis)

AOM
 ↓
Aditus ad antrum
 ↓
Mastoid antrum → air cells
 ↓
Mucosal oedema blocks antrum drainage
 ↓
Pus under pressure → ischaemia of bony septa
 ↓
COALESCENT MASTOIDITIS (septa break down)
 ↓
Empyema of mastoid → periosteal spread → complications

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STAGES OF MASTOIDITIS

1. Mastoiditis with periostitis: Hyperaemia of mastoid cortex; no bone destruction
2. Mastoid abscess (Acute Coalescent): Septa break down; pus fills mastoid
3. Masked mastoiditis: Low-grade, following antibiotic therapy; insidious onset

---

CLINICAL FEATURES

• History of recent AOM (10-14 days prior)
• Return or persistence of severe earache after initial improvement
• High-grade fever
• Profuse ear discharge (if TM has perforated)
• Tenderness behind ear

• Tenderness over mastoid process (MacEwen's triangle) - most important sign
• Post-auricular swelling and redness
• Pinna displaced forward and downward (sagging of posterior EAC wall - earliest sign on otoscopy)
• Posterior EAC wall sags (due to periosteum elevation)
• Loss of the post-auricular sulcus

---

INVESTIGATIONS

1. HRCT Temporal bone: - Investigation of choice
   • Opacification of mastoid cells
   • Loss of mastoid cell trabeculae (coalescence)
   • Subperiosteal abscess (collection lateral to mastoid cortex)
2. X-ray mastoid (Schuller's view): Clouding of mastoid cells (less used now)
3. CBC: Leukocytosis, elevated CRP/ESR
4. Blood culture
5. Culture of ear discharge

---

MANAGEMENT

• IV antibiotics: Ampicillin-sulbactam or Cefuroxime
• Myringotomy and drainage (if TM intact)
• Aural toilet

• Procedure of choice for acute coalescent mastoiditis
• Removal of mastoid air cells through post-auricular incision
• Middle ear and ossicles NOT touched
• Antrum opened and all infected cells exenterated
• Drain inserted
• EAC and TM preserved

---

COMPLICATIONS OF MASTOIDITIS

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

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LESSON 5: FACIAL NERVE IN EAR - BELL'S PALSY AND RAMSAY HUNT

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Q6. Discuss Bell's Palsy - etiology, clinical features, diagnosis and management. (10 marks)

DEFINITION

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ETIOLOGY

• Most accepted cause: Reactivation of Herpes Simplex Virus type 1 (HSV-1) in the geniculate ganglion
• Viral inflammation → oedema → compression of VII nerve in rigid bony fallopian canal → ischaemia → neuropraxia

---

CLINICAL FEATURES

1. Sudden unilateral facial weakness (drooping)
2. Inability to close eye (lagophthalmos) → epiphora
3. Drooping of angle of mouth, food collection
4. Difficulty with speech (labial consonants)
5. Prodrome: Mild pain behind ear (post-auricular pain, Stylomastoid foramen) 1-2 days before
6. Altered taste (anterior 2/3 tongue) if chorda tympani involved
7. Hyperacusis (if nerve to stapedius involved)
8. Decreased lacrimation / salivation (if greater superficial petrosal nerve / chorda tympani affected)

• Forehead not spared (UMN lesion spares forehead - important differentiation)
• Bell's phenomenon - eyeball rolls up and outward when patient tries to close eye
• Flattening of nasolabial fold
• Loss of blink reflex (corneal reflex)
• Widened palpebral fissure

---

GRADING - HOUSE-BRACKMANN SCALE (HB Scale)

---

INVESTIGATIONS

• Clinical examination (forehead spared = UMN; forehead involved = LMN)

• Schirmer's test: Filter paper on lower conjunctival sac; < 25% of normal side = greater superficial petrosal nerve (GSPN) involved (poor prognosis)
• Stapedial reflex testing: Absent = nerve to stapedius involved
• Taste testing / Electrogustometry: Chorda tympani dysfunction
• Electrophysiological tests:
  • Nerve Excitability Test (NET): Compares current to elicit movement; >3.5 mA difference = poor prognosis
  • Electroneuronography (ENoG): Best test; measures compound muscle action potential; > 90% degeneration within 14 days = poor prognosis → surgery
  • EMG: Voluntary + spontaneous activity

• HRCT temporal bone (if trauma, CSOM)
• MRI brain with gadolinium (if central cause suspected)
• Blood: CBC, serology (Lyme, VZV, Sarcoid)

---

MANAGEMENT

• Prednisolone 60-80 mg/day for 5 days, then taper over 5 days
• Must start within 72 hours of onset for maximum benefit
• 85-95% complete recovery if treated early

• Acyclovir or Valacyclovir - added to steroids; benefit debated but recommended
• Valacyclovir 1000 mg TDS × 7 days

• Artificial tears (daytime)
• Lubricating ointment (nighttime)
• Moisture chamber spectacles / tape eyelid shut at night
• If eye does not close (Grade IV-VI): Gold weight implant in upper eyelid (temporary)

• Facial nerve decompression via middle fossa or transmastoid approach
• Indications: ENoG > 90% degeneration within 14 days + EMG showing no voluntary activity
• Window of opportunity: Within 14 days of onset

---

PROGNOSIS

• 85% complete spontaneous recovery within 3-6 months
• Poor prognosis: Complete paralysis, age > 60, hypertension, DM, no steroids given

---

Q7. Ramsay Hunt Syndrome - features and management. (5 marks)

DEFINITION

1. Facial palsy (LMN type)
2. Vesicular eruption in the ear (pinna, EAC, TM, soft palate)
3. Otalgia (severe, burning)

• SNHL (cochlear involvement)
• Vertigo (vestibular involvement)
• Loss of taste (anterior 2/3 tongue)

• Only 50-70% recover completely (vs 85% in Bell's)
• Intense inflammation + multiple nerve involvement
• Higher viral load

• High-dose Acyclovir (800 mg 5 times/day × 10 days) or Valacyclovir - ESSENTIAL (not just adjunct)
• Prednisolone 60 mg/day × 5 days, taper
• Eye protection
• Analgesics (severe pain - may need gabapentin/carbamazepine for neuropathic pain)
• Same eye care as Bell's palsy

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LESSON 6: LABYRINTHITIS AND VESTIBULAR NEURITIS

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Q8. Differentiate between Labyrinthitis and Vestibular Neuritis. Write a note on management. (5 marks)

LABYRINTHITIS

1. Serous (Toxic) Labyrinthitis - toxins from CSOM/meningitis; no actual invasion; reversible
2. Suppurative Labyrinthitis - bacterial invasion; irreversible; dead ear + dead labyrinth
3. Viral Labyrinthitis - post-viral; affects both cochlear and vestibular

• Vertigo + SNHL + nausea/vomiting
• Spontaneous nystagmus toward affected ear (irritative phase) → later toward normal ear (destructive phase)
• Positive fistula test in labyrinthine fistula

• Treat underlying cause (CSOM → surgery)
• Vestibular sedatives (prochlorperazine)
• IV antibiotics if suppurative
• Labyrinthectomy (if suppurative, contralateral ear normal)

---

VESTIBULAR NEURITIS (Neuronitis)

• Severe acute vertigo - worst at onset, improves over days-weeks
• NO hearing loss - cochlea spared (distinguishes from labyrinthitis)
• NO tinnitus
• Unsteady gait
• Nausea, vomiting

• Vestibular sedatives (acute phase): Prochlorperazine, Dimenhydrinate
• Steroids: Methylprednisolone (speeds recovery)
• Vestibular rehabilitation (most important for long-term recovery) - Cawthorne-Cooksey exercises

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LESSON 7: GLOMUS TUMOURS OF THE EAR

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Q9. Describe Glomus Tympanicum and Glomus Jugulare tumours. (10 marks)

INTRODUCTION

• Glomus tympanicum: Arises from glomus bodies on the Jacobson's nerve (tympanic branch of IX) on the promontory of middle ear
• Glomus jugulare: Arises from glomus bodies in the adventitia of the jugular bulb at the jugular foramen

---

EPIDEMIOLOGY

• More common in females (F:M = 6:1)
• Peak: 5th-6th decade
• 10% bilateral, 10% malignant (in familial cases - SDH gene mutations)
• Familial cases: Autosomal dominant with genomic imprinting (SDHB, SDHC, SDHD mutations)

---

PATHOLOGY

• Tumour consists of chief cells (type I, resembling adrenal chromaffin cells) in a vascular stroma
• Highly vascular - characteristic "salt and pepper" appearance on MRI
• Some are secretory (catecholamines) → hypertensive episodes

---

GLOMUS TYMPANICUM

1. Pulsatile tinnitus - most common symptom; synchronous with heartbeat
2. Conductive hearing loss - middle ear occupied by tumour
3. Sensation of fullness

• Reddish-blue/pulsatile mass seen through the TM (behind TM)
• Brown's sign - blanching and cessation of pulsation on pneumatic otoscopy (positive pressure through Siegle's speculum compresses the vascular tumour → blanching)
• Differentials: Aberrant ICA, high jugular bulb, cholesterol granuloma

• HRCT temporal bone: Small mass on promontory; intact jugular plate (differentiates from glomus jugulare)
• MRI with gadolinium: Enhancing mass

• Surgical excision via transcanal approach
• Adjuvant radiotherapy for residual disease
• Excellent prognosis

---

GLOMUS JUGULARE

1. Pulsatile tinnitus (most common)
2. Conductive or mixed hearing loss
3. Cranial nerve palsies at jugular foramen: IX, X, XI → Jugular foramen syndrome (Vernet's syndrome)
4. If XII also involved: Collet-Sicard syndrome
5. If extends to petrous apex: Facial palsy (VII), SNHL
6. If intracranial: Cerebellar signs, raised ICP

1. HRCT temporal bone: Erosion and moth-eaten destruction of jugular foramen
2. MRI T1 with gadolinium: "Salt and pepper" pattern (flow voids = salt; enhancing tumour = pepper)
3. 4-vessel cerebral angiography + embolisation: Diagnostic AND pre-operative (reduces intraoperative bleeding)
4. 24-hour urine catecholamines (VMA, metanephrines): If secretory tumour suspected

1. Pre-operative embolisation (24-48 hours before surgery) - to reduce vascularity
2. Surgical excision: Infratemporal fossa approach (Fisch approach)
3. Radiotherapy / Radiosurgery (Gamma knife): For elderly, inoperable, residual tumour
4. Observation: Elderly patients, asymptomatic small tumours

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LESSON 8: PRESBYCUSIS

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Q10. Discuss Presbycusis - types, features and management. (5 marks)

DEFINITION

SCHUKNECHT'S CLASSIFICATION (4 + 2 types)

CLINICAL FEATURES

• Gradual, progressive bilateral SNHL in elderly (> 60 years)
• High-frequency loss first (4-8 kHz)
• Reduced speech discrimination - "I can hear but cannot understand" (classic complaint)
• Difficulty in noisy environments (cocktail party effect)
• Tinnitus common
• Recruitment present (cochlear type)
• No vestibular symptoms

AUDIOGRAM PATTERN

• Bilateral, symmetrical, high-frequency SNHL
• Sloping (down-sloping) audiogram
• Air-bone gap absent (pure SNHL)

MANAGEMENT

1. Hearing aid - most important; bilateral hearing aids for bilateral loss
   • Behind-the-ear (BTE) most common
   • Receiver-in-canal (RIC) - better for high-frequency loss
2. Cochlear implant - for severe-to-profound SNHL when hearing aids fail
3. Assistive listening devices - telephone amplifiers, TV aids
4. Counselling - family + patient; communication strategies
5. Speech-reading training (lip reading)
6. No curative medical treatment available

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LESSON 9: SUDDEN SENSORINEURAL HEARING LOSS

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Q11. Sudden Sensorineural Hearing Loss - definition, causes and management. (5 marks)

DEFINITION

• Loss of ≥ 30 dB in 3 or more contiguous frequencies
• Occurring within 72 hours (or noticed on awakening)
• Usually unilateral
• No identifiable cause in majority (idiopathic SSNHL = 85-90%)

ETIOLOGY

MANAGEMENT

1. Systemic corticosteroids (FIRST LINE):
   • Prednisone 60 mg/day × 10-14 days, then taper
   • Works best when started within 2 weeks
2. Intratympanic steroid injection:
   • Salvage therapy if systemic steroids fail
   • Dexamethasone 24 mg/mL IT injection
   • 3-4 weekly injections
3. Vasodilators + carbogen - limited evidence; sometimes used
4. Treat underlying cause if identified

• 30-65% spontaneous recovery
• Best prognosis: Mild loss, upsloping audiogram, treatment within 2 weeks
• Worst prognosis: Profound loss, flat/downsloping audiogram, elderly, delay in treatment

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LESSON 10: AUDIOLOGICAL TESTS - COMPLETE FOR EXAMS

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Q12. Classify audiological tests and describe tympanometry in detail. (10 marks)

CLASSIFICATION OF HEARING TESTS

HEARING TESTS
├── SUBJECTIVE (need patient cooperation)
│   ├── Clinical (Bedside)
│   │   ├── Voice tests (whisper, conversation)
│   │   └── Tuning fork tests (Rinne, Weber, Schwabach, Bing)
│   └── Audiometric
│       ├── Pure Tone Audiometry (PTA)
│       ├── Speech Audiometry (SRT, SDS)
│       ├── Special tests (SISI, Tone decay, ABLB, Bekesy)
│       └── Pediatric (BOEL, VRA, Play audiometry, COSI)
└── OBJECTIVE (do not need cooperation)
    ├── Immittance (Tympanometry + Acoustic reflex)
    ├── OAE (TEOAE, DPOAE)
    └── Electrophysiological
        ├── ABR/BERA
        ├── ECoG
        └── ASSR

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TYMPANOMETRY

• Peak compliance (mMho or cm³) - normal: 0.3-1.6 mL
• Peak pressure (daPa) - normal: -100 to +100 daPa
• Ear Canal Volume (ECV) - normal: 0.6-1.5 mL adults

---

JERGER'S CLASSIFICATION (COMPLETE)

COMPLIANCE
    |
    |    A           Ad
    |   /\          /|
    |  /  \        / |
    | /    \      /  |
    |/      \    /   |
    |--------\--/----|-----
    |    B    \/  As  |    PRESSURE
    |                 |
    |        C
    |       /\
    |      /  \
    |  (shifted left - negative pressure)

---

ACOUSTIC REFLEX

Loud sound → cochlea → VIII nerve → cochlear nucleus 
→ superior olivary complex → VII nerve (motor) 
→ Stapedius muscle → stiffens ossicular chain → reflex

• Elicited by sounds of 70-100 dB HL above threshold
• Normal: Present bilaterally (ipsilateral + contralateral)

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Q13. Write a note on OAE and ABR/BERA. (5 marks)

OTOACOUSTIC EMISSIONS (OAE)

1. TEOAE (Transient Evoked OAE): Click stimulus → brief OAE response; used in neonatal screening
2. DPOAE (Distortion Product OAE): Two simultaneous pure tones (f1, f2) → distortion product recorded; frequency-specific assessment
3. Spontaneous OAE (not used clinically)

• Present: OHC function intact (hearing ≤ 30 dB HL)
• Absent: Hearing loss > 30 dB, middle ear disease, OHC damage
• Neonatal hearing screening (Universal Newborn Hearing Screening - UNHS)
• OAE present + ABR absent = auditory neuropathy spectrum disorder (ANSD)

---

ABR / BERA (Auditory Brainstem Response)

• Wave I latency: ~1.7 ms
• Wave V latency: ~5.7 ms
• I-V interpeak latency: ~4.0 ms (most important)

---

SUPPLEMENTARY-FAVOURITE SHORT NOTES (5-MARK FORMAT)

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Q14. SISI Test (Short Increment Sensitivity Index) - 5 marks

• Tone presented at 20 dB SL (20 dB above threshold)
• 200 increments of 1 dB presented at 5-second intervals
• Patient signals each time they detect the increment

---

Q15. Tone Decay Test - 5 marks

• Tone presented at threshold level continuously
• Patient raises hand as long as they hear it
• When they stop hearing, intensity increased by 5 dB
• Continue until patient hears for full 60 seconds

---

Q16. Stenger Test - 5 marks

• Present tone at 10 dB above threshold of GOOD ear to GOOD ear
• Simultaneously present same tone at 10 dB BELOW the alleged threshold of BAD ear
• Malingerer should hear the tone from the good ear and respond

• Positive Stenger (no response from patient) = MALINGERING confirmed
  • Because the tone in the "bad ear" is actually louder → malingerer hears it there → will NOT admit hearing → no response
• Negative Stenger (responds to good ear tone) = True unilateral hearing loss

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Q17. Complications of CSOM - classified table (5 marks)

---

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CONFIRMED AS RGUHS FINAL MBBS LONG ESSAY (10 marks) questions:

---

What is NOT UG level in what I gave:

• ENoG / electrophysiology details in Bell's palsy (usually only briefly expected at UG level)
• Fisch classification of Glomus jugulare (optional at UG; know it but one line is enough)
• Stacked ABR (mentioned but examiners won't expect this at UG)

---

What RGUHS UG ENT examiners actually want:

1. Definition - 1 line, precise
2. Classification / Types - table format preferred
3. Etiology / Pathogenesis - brief, logical flow
4. Clinical features - symptoms then signs
5. Investigations - in order of usefulness
6. Management - medical then surgical, with indications
7. Complications - always include; gives extra marks

---

What is COVERED (from both sessions combined):

Long Essays (10-mark) - COVERED:

Short Essays / Short Notes (5-mark) - COVERED:

---

What is STILL MISSING (gaps you should add):

Long Essays NOT yet covered:

Short Notes NOT yet covered:

---

VERDICT:

---

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RGUHS FINAL MBBS ENT - EAR: ALL REMAINING 5-MARK ANSWERS

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GROUP A: EXTERNAL EAR

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1. Otitis Externa (Diffuse) - 5 marks

Definition

Predisposing Factors

• Water (most common) - maceration of EAC skin + raises pH
• Loss of protective cerumen (over-cleaning with cotton buds)
• Hot, humid climate
• Trauma (scratching, hearing aids, ear plugs)
• Dermatological conditions (eczema, psoriasis, seborrhoea)
• Diabetes mellitus

Causative Organisms

• Pseudomonas aeruginosa - most common (gram-negative rod)
• Staphylococcus aureus - second most common
• Proteus, E. coli, Aspergillus (fungal OE = Otomycosis)

Clinical Features

• Severe otalgia - hallmark; worse on jaw movement, tragal pressure (tragal sign)
• Itching (precedes pain)
• Ear discharge - scanty, watery initially → purulent
• Conductive hearing loss (if canal swells shut)
• Signs: Tragal tenderness + pinna tenderness on movement; erythematous, oedematous canal; TM may appear normal or inflamed; periauricular lymphadenopathy

Management

1. Aural toilet (dry mopping) - most important first step
2. Topical antibiotic + steroid drops:
   • Ciprofloxacin + hydrocortisone (Ciprodex) - first line; non-ototoxic
   • Neomycin-polymyxin B (if TM intact)
3. Ear wick (Pope wick) - if canal too swollen to accept drops; expands on contact with moisture to deliver medication
4. Analgesics (NSAIDs)
5. Systemic antibiotics: Only if cellulitis extends beyond canal, fever, or immunocompromised
6. Keep ear DRY - no swimming; cotton plug while bathing

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2. Furunculosis of EAC (Localised Otitis Externa) - 5 marks

Definition

Only the outer 1/3 (cartilaginous EAC) has hair follicles and sebaceous glands - hence furuncles occur ONLY here, NOT in the bony inner canal.

Cause

• Staphylococcus aureus (the only causative organism)
• Precipitated by trauma (scratching, cotton buds)

Clinical Features

• Severe, throbbing otalgia - disproportionate to appearance
• Pain worse on jaw movement, tragal pressure, pinna traction
• Trismus (if posterior wall involved - due to TMJ proximity)
• Swelling at anterior wall of EAC (pointing of furuncle)
• Conductive hearing loss (if canal blocked)
• Regional lymphadenopathy (pre-auricular or post-auricular)

Tuning Fork Tests

• Rinne: Negative (CHL)
• Weber: Lateralizes to affected ear

Management

• Oral antibiotics: Cloxacillin or Amoxicillin-Clavulanate (anti-staphylococcal)
• Analgesics (NSAIDs)
• Aural toilet
• Glycerine-ichthyol ear pack (hygroscopic - draws out oedema)

• Incision and Drainage (I&D): Vertical stab incision over pointing furuncle
• Pus sent for culture and sensitivity

Complications

• Spreading cellulitis
• Perichondritis (if neglected)
• Parotid region involvement (if posterior wall)

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3. Malignant (Necrotising) Otitis Externa - 5 marks

Definition

Causative Organism

• Pseudomonas aeruginosa (90-95% of cases) - gram-negative rod
• Rarely: Aspergillus, Candida (in AIDS patients)

Pathogenesis

Diabetic microangiopathy + raised EAC pH
           ↓
P. aeruginosa invasion of EAC skin
           ↓
Spreads through Fissures of Santorini (cartilaginous EAC)
           ↓
Osteomyelitis of temporal bone / skull base
           ↓
Cranial nerve involvement + intracranial spread

Clinical Features

1. Severe, deep-seated, unrelenting otalgia - "out of proportion to examination"
2. Profuse, purulent, foul-smelling discharge
3. Granulation tissue at the bony-cartilaginous junction (floor of EAC) - PATHOGNOMONIC
4. Cranial nerve palsies (in order of involvement):
   • VII (facial nerve) - most common; first affected
   • IX, X, XI (jugular foramen syndrome)
   • XII (hypoglossal)
5. Trismus (temporomandibular joint and infratemporal fossa extension)
6. Systemic features: fever, weight loss

Diagnosis

1. High-resolution CT temporal bone - bone erosion, soft tissue extension
2. MRI - superior for soft tissue + dural involvement
3. Technetium-99m bone scan - sensitive for osteomyelitis (positivity precedes CT changes)
4. Gallium-67 citrate scan - for monitoring treatment response
5. ESR + CRP - elevated; used to monitor response
6. Biopsy - to exclude malignancy (squamous cell carcinoma)
7. Fasting blood glucose / HbA1c

Management

1. IV anti-pseudomonal antibiotics (mainstay):
   • Ciprofloxacin (oral or IV) - drug of choice (fluoroquinolone, anti-pseudomonal, good bone penetration)
   • Alternatives: Piperacillin-tazobactam, Ceftazidime, Tobramycin
   • Duration: 6-8 weeks minimum (until gallium scan normalises)
2. Diabetic control - tight glycaemic control essential
3. Aural toilet and debridement - of granulation tissue
4. Surgical debridement - if medical treatment fails or abscess formation
5. Hyperbaric oxygen therapy - adjunct; improves tissue oxygenation in ischaemic tissue

Monitoring Response

• Serial Gallium-67 scans (best for monitoring)
• ESR/CRP normalisation
• Symptomatic improvement

Mortality: 5-20% even in antibiotic era

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4. Auricular Haematoma and Cauliflower Ear - 5 marks

Auricular Haematoma

• Blunt trauma to pinna (wrestlers, boxers) → shears perichondrium from cartilage
• Blood collects between perichondrium and cartilage
• Appearance: Fluctuant, painful, non-transilluminable swelling on anterior pinna; loss of normal auricular landmarks

• Aspiration / Incision and drainage (within 48-72 hours) - through a small incision
• Pressure bandage (bolster dressing / through-and-through sutures) - prevents re-accumulation
• Antibiotics (anti-staphylococcal) to prevent perichondritis

Cauliflower Ear (Wrestler's ear)

• Complication of untreated auricular haematoma
• Blood organises → fibrosis → neocartilage formation
• Permanent deformity: thickened, nodular, irregular pinna - "cauliflower" appearance
• Prevention: Timely drainage + pressure dressing

Perichondritis

• Secondary infection of haematoma or post-surgery/trauma
• Pseudomonas most common
• Treatment: IV ciprofloxacin + surgical drainage

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5. Wax (Cerumen) Impaction - 5 marks

Definition

Properties of Normal Cerumen

• Slightly acidic pH (5.0-7.0) - antibacterial
• Migrates naturally outward (self-cleaning mechanism)
• Two types: Wet (brown, sticky - Caucasians/Africans) and Dry (grey, flaky - East Asians)

Causes of Impaction

• Overproduction
• Narrow/tortuous EAC
• Cotton bud use (pushes wax deeper)
• Hearing aid use (blocks natural migration)

Clinical Features

• Conductive hearing loss (sudden onset, often after bathing - water absorbs wax → swells → canal blocks)
• Tinnitus
• Earache (if impacted hard against TM)
• Vertigo (rarely)
• Reflex cough (Arnold's nerve stimulation)

Management

1. Ear syringing / irrigation:
   • Warm water (body temperature - to prevent caloric vertigo)
   • Contraindicated: Known TM perforation, single ear, previous ear surgery
2. Microsuction (preferred):
   • Under direct vision with Siegle's speculum or microscope
   • Safe even with perforation
3. Manual removal: Jobson-Horne probe or Tilley's forceps - for hard wax
4. Ceruminolytics (wax softeners): Before syringing
   • Sodium bicarbonate drops, Olive oil, Hydrogen peroxide, Carbamide peroxide

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GROUP B: MIDDLE EAR SURGERY

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6. Myringotomy - 5 marks

Definition

Indications

1. AOM - severe pain unresponsive to analgesics
2. AOM - about to rupture spontaneously
3. AOM with complications (mastoiditis, facial palsy)
4. OME (Glue ear) - for drainage and grommet insertion
5. Secretory OME unresponsive to medical treatment
6. Barotrauma - for decompression
7. Immunocompromised patient - for culture of middle ear fluid
8. Acute mastoiditis - as part of management

Contraindications

• Glomus tumour (pulsatile vascular mass behind TM)
• Aberrant ICA behind TM

Site of Incision

• Posteroinferior quadrant of pars tensa
• Avoids ossicular chain (posterosuperior), facial nerve, chorda tympani
• Radial incision (follows radial fibres of TM)

Diagram

         12
          |
     9 ---+--- 3
          |
     POSTEROINFERIOR = SAFE ZONE
         ↑
    Myringotomy incision here
          |
         6

Complications

• Persistent perforation (if large incision)
• Infection
• Trauma to ossicles (if wrong quadrant)
• Tympanosclerosis (healing with calcification)

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7. Grommets (Ventilation Tubes / Tympanostomy Tubes) - 5 marks

Definition

Types

Indications for Grommet Insertion

1. Bilateral OME persisting > 3 months with hearing loss ≥ 25 dB
2. Recurrent AOM (4+ episodes/year)
3. Bilateral OME with speech delay or school difficulties
4. OME in cleft palate children (prophylactic)

Procedure

• Under GA (children) or LA (adults)
• Myringotomy in anteroinferior quadrant
• Suction of fluid
• Grommet inserted through incision
• Tube keeps incision open → ventilates middle ear

Complications

• Otorrhoea (most common - through tube; treat with topical antibiotics)
• Persistent perforation after extrusion (3-5%)
• Tympanosclerosis (chalky white plaques on TM after extrusion)
• Retraction pocket (if middle ear not adequately ventilated)
• Blockage of tube

Post-Operative Care

• Avoid water in ear (ear plugs while swimming)
• Follow-up audiometry after insertion

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8. Myringoplasty and Tympanoplasty - 5 marks

Myringoplasty

• Dry, central perforation of TM (tubotympanic CSOM)
• Hearing improvement
• Prevention of recurrent infections

• Temporalis fascia (most common, most preferred)
• Tragal perichondrium
• Perichondrium of conchal cartilage
• Fat (for small perforations)
• Vein (obsolete)

1. Underlay (medial graft) technique - graft placed medial to TM remnant and handle of malleus; most common
2. Overlay (lateral graft) technique - graft placed lateral to annulus; for large perforations; risk of blunting
3. Inlay technique - for small perforations

Tympanoplasty (Wullstein Classification)

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9. Mastoidectomy - Types and Indications - 5 marks

Definition

Types

• Exenteration of all mastoid air cells
• Middle ear and EAC left intact (canal wall preserved)
• Indication: Acute coalescent mastoiditis unresponsive to antibiotics
• Creates a closed cavity

• Mastoid air cells removed + posterior EAC wall removed
• Middle ear contents (ossicles, TM remnant) PRESERVED
• Creates an open mastoid cavity draining into EAC
• Indication: Atticoantral CSOM with cholesteatoma (most common operation for unsafe ear)
• A "safe" ear but NOT a dry ear

• Complete removal of posterior EAC wall + middle ear contents (malleus, incus, TM)
• Stapes + intact TM membrane ONLY preserved if Bondy's modification
• Indication: Extensive cholesteatoma; carcinoma of middle ear
• Results in: Maximal hearing loss

• EAC posterior wall PRESERVED
• Complete removal of cholesteatoma
• Hearing reconstruction in same or second stage
• Advantage: Normal anatomy, better hearing potential
• Disadvantage: High residual/recurrent cholesteatoma rate; needs second-look surgery at 12 months
• Indication: Cholesteatoma with good cochlear reserve

Key Principle

"The aim of mastoid surgery is to create a SAFE ear; hearing improvement is secondary."

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GROUP C: INTRACRANIAL COMPLICATIONS OF CSOM

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10. Lateral Sinus Thrombophlebitis - 5 marks

Definition

Pathogenesis

CSOM / Coalescent mastoiditis
         ↓
Erosion of bony sinus plate (lateral to sigmoid sinus)
         ↓
Perisinus abscess formation
         ↓
Intimal damage → fibrin, platelets, RBCs → mural thrombus
         ↓
Infected thrombus → occludes sinus → septicaemia
         ↓
Thrombus propagates → IJV → pulmonary septic emboli (Lemierre)

Clinical Features

1. "Picket fence" (intermittent hectic) fever - characteristic; temperature spikes >39°C with diurnal pattern; due to septic emboli entering bloodstream
2. Rigors - severe shaking chills
3. Headache (raised ICP)
4. General malaise and septicaemia
5. Griesinger's sign - oedema over mastoid emissary vein (postauricular) - due to thrombosis of mastoid emissary vein
6. Tobey-Ayer test (Queckenstedt's test in OM) - compression of ipsilateral IJV fails to raise CSF pressure (sinus occluded)
7. Neck pain (IJV involvement)
8. Papilloedema (if raised ICP)

Investigations

1. Contrast CT temporal bone - absent enhancement in sigmoid sinus ("empty delta sign")
2. MRI / MR Venogram - occlusion of transverse-sigmoid sinus (investigation of choice)
3. Blood cultures - positive (septicaemia)
4. CBC - leukocytosis, anaemia
5. Lumbar puncture - if meningitis suspected

Management

1. Mastoidectomy - to remove source of infection (cortical/modified radical)
2. IV antibiotics - broad spectrum anti-anaerobic + anti-staphylococcal: Cefuroxime + Metronidazole
3. Anticoagulation (Heparin) - controversial; used to prevent propagation
4. Sinus surgery - needle aspiration of sinus; if clot present, sinus incision and clot removal
5. IJV ligation - if septic emboli shower lungs (Lemierre-like)

Mortality: 10-15% (historically 100% before antibiotics)

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11. Otogenic Brain Abscess - 5 marks

Definition

Sites (in order of frequency)

1. Temporal lobe abscess (most common) - from direct spread through tegmen tympani
2. Cerebellar abscess - from spread through posterior fossa dura via labyrinth/sigmoid sinus

Stages of Brain Abscess (MacEwen's stages)

1. Stage of invasion (cerebritis): Inflammation without pus; reversible
2. Stage of latency: Symptoms subside; barrier forms; treacherous silent stage
3. Stage of expansion: Abscess enlarges; raised ICP; symptoms return
4. Stage of termination: Rupture (fatal) or medical arrest

Clinical Features

• Headache (most common and early symptom)
• Low-grade fever
• Dysphasia (dominant hemisphere - word-finding difficulty)
• Contralateral homonymous hemianopia
• Contralateral upper motor neuron facial palsy
• Raised ICP signs: papilloedema, vomiting

• Headache (occipital)
• Ipsilateral cerebellar signs:
  • Ataxia, nystagmus (toward lesion)
  • Past-pointing (dysmetria)
  • Dysdiadochokinesia
  • Intention tremor
• Raised ICP more dangerous (posterior fossa is tight)

Investigations

1. CT brain with contrast - ring-enhancing lesion (investigation of choice)
2. MRI brain - superior for small abscesses
3. CT temporal bone - underlying CSOM
4. LP: CONTRAINDICATED if raised ICP (risk of herniation)
5. CBC, blood culture

Management

1. IV antibiotics - Metronidazole + 3rd generation cephalosporin (penetrates BBB)
2. Surgical drainage (neurosurgery):
   • Aspiration through burr hole
   • Excision for encapsulated/multiloculated abscess
3. Mastoidectomy - to eradicate primary source (after abscess stabilised)
4. Dexamethasone - reduces cerebral oedema
5. Mannitol - for raised ICP

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12. Gradenigo's Syndrome (Petrositis) - 5 marks

Definition

1. Otorrhoea (persistent discharge - CSOM)
2. Abducens (VIth nerve) palsy - ipsilateral lateral rectus palsy → convergent squint + diplopia on lateral gaze
3. Retro-orbital pain (Vth nerve - ophthalmic division) - due to inflammation of trigeminal ganglion at Meckel's cave

Pathogenesis

CSOM / Mastoiditis
       ↓
Spread to petrous air cells (petrous apex)
       ↓
Petrositis = osteomyelitis of petrous temporal bone
       ↓
VI nerve (runs in Dorello's canal - tight fibrous canal at petrous apex) → compressed
V nerve (Gasserian ganglion at petrous apex) → irritated

Additional Features

• Deep-seated facial pain
• Photophobia
• Sixth nerve palsy → squinting child with ear discharge = THINK GRADENIGO'S

Investigations

• HRCT temporal bone - petrous apex opacification/destruction
• MRI - superior for dural and nerve involvement
• CBC, blood cultures

Management

1. IV antibiotics - prolonged (6-8 weeks) for petrous bone osteomyelitis
2. Mastoidectomy - Schwartze or modified radical to drain mastoid + petrous cells
3. Petrous apicectomy - if conservative fails
4. Neurosurgical input if intracranial spread

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13. Otitic Hydrocephalus - 5 marks

Definition

Mechanism

• Lateral sinus thrombosis → impaired CSF reabsorption (from arachnoid granulations, which drain into superior sagittal sinus) → increased ICP → clinical features

Clinical Features

1. Severe headache (most prominent)
2. Nausea and vomiting
3. Papilloedema (bilateral)
4. Abducens (VI) palsy - false localising sign (nerve stretched over petrous ridge)
5. Altered consciousness (late)
6. Signs of underlying otitis media

CSF Analysis (differentiating feature)

• Pressure: Elevated
• Cells: Normal
• Protein: Normal
• Glucose: Normal
• Culture: Sterile

Management

1. Treat underlying CSOM - mastoidectomy
2. Repeated lumbar punctures - to lower ICP
3. Acetazolamide - reduces CSF production
4. Corticosteroids - reduce cerebral oedema
5. Anticoagulation - for underlying lateral sinus thrombosis
6. Lumboperitoneal shunt - for refractory cases

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GROUP D: TRAUMA TO EAR

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14. Temporal Bone Fracture - 5 marks

Definition

Classification

Classic Classification (Longitudinal vs Transverse):

Modern Classification:

• Otic capsule sparing (OCS) - 90%; better prognosis (no SNHL usually)
• Otic capsule violating (OCV) - 10%; associated with SNHL + greater facial nerve injury risk

Clinical Features

• Haemotympanum - blue/black TM (blood in middle ear) - earliest sign
• Blood in EAC - from TM tear or EAC skin
• CSF otorrhoea (halo sign on filter paper - CSF creates clear ring around blood)
• Battle's sign - ecchymosis over mastoid (delayed - 24-48 hours)
• Hearing loss + vertigo
• Facial palsy

Management

1. Immediate: ABCDE resuscitation; treat head injury
2. CSF otorrhoea:
   • Bed rest + head elevation
   • Prophylactic antibiotics (controversial)
   • Usually resolves in 10-14 days
   • Lumbar drain if persistent > 2 weeks
   • Surgical repair of dural tear if no resolution
3. Haemotympanum: Resolves spontaneously; audiogram after 6-8 weeks
4. Facial palsy:
   • Immediate complete palsy → surgical exploration + decompression
   • Delayed/incomplete → conservative; steroids; ENoG monitoring
5. SNHL/Vertigo: Vestibular rehabilitation; hearing aid / cochlear implant later
6. BPPV post-trauma: Epley maneuver

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15. Barotrauma (Aerotitis / Barotitis Media) - 5 marks

Definition

Mechanism

Rapid pressure increase in external environment (aircraft descent / diving)
             ↓
Positive pressure in EAC vs negative in middle ear
             ↓
ET fails to open (congestion, inflammation, sleep, anatomical)
             ↓
TM pushed inward → retraction → effusion → haemorrhage

Clinical Features

• Sudden ear pain (otalgia) - onset during descent
• Aural fullness / blockage
• CHL (fluid in middle ear)
• Tinnitus
• Vertigo (in severe cases - inner ear barotrauma / perilymph fistula)
• TM: Retracted; haemorrhage (haemotympanum); occasionally ruptures

Classification (Teed's grading)

Management

• Valsalva / swallowing / chewing (opens ET) during descent
• Decongestant nasal spray before flight if URTI
• Avoid flying with upper respiratory infection

• Decongestants (systemic + topical nasal)
• Analgesia
• Valsalva maneuver (if TM intact)
• Myringotomy - for severe grades (III-V) to drain blood/fluid
• Steroids - to reduce mucosal oedema
• Resolution in days-weeks

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16. Foreign Body in External Ear - 5 marks

Introduction

• Animate (live insects) - more common in adults in tropical countries
• Inanimate:
  • Vegetable (peas, seeds, paper, cotton) - swell with moisture; difficult to remove
  • Mineral (beads, eraser, small toys, stones)
  • Batteries (button/disc batteries - EMERGENCY)

Clinical Features

• Asymptomatic (discovered incidentally) - most common
• Otalgia (if traumatising)
• Conductive hearing loss
• Ear discharge (if lodged long + secondary infection)
• Tinnitus (if vibrating)
• Vertigo (if touching TM)
• Live insect: Sudden onset intense pain, noise, restlessness

Management by Type

1. Instill oil (olive oil / mineral oil / lignocaine) first to KILL the insect
2. Then remove with syringing or forceps
3. Never syringe a live insect (causes it to burrow deeper)

• Causes alkali liquefaction necrosis (hydroxide ions generated by electrical current)
• Rapid tissue destruction; can perforate TM, erode ossicles
• Remove immediately under GA if necessary
• Do NOT use syringing (risk of spread)

• Do NOT syringe (swell with water → impacted further)
• Remove under direct vision with hook, forceps, or suction
• GA often needed in children

• Syringing preferred (if TM intact)
• Or direct removal with aural forceps / hook under microscope

• Never blindly probe without visualisation
• Refer to specialist if: deep, impacted, child uncooperative, near TM
• Remove under GA if: child uncooperative, impacted, near ossicles

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GROUP E: INNER EAR / SENSORINEURAL

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17. Cochlear Implant - 5 marks

Definition

Components

1. Microphone - picks up sound
2. Speech processor - filters, analyses, digitises sound into coded signals
3. Transmitter coil - sends signal transcutaneously to internal receiver

Indications (Candidacy criteria)

• Bilateral profound SNHL (>90 dB PTA)
• Poor speech discrimination (<50%) with optimally fitted hearing aids
• No medical contraindications

• Age > 12 months (FDA approved); some centres do earlier
• Bilateral profound SNHL
• Best outcomes: Congenital deafness implanted before age 3 (critical period of auditory cortex development)
• Auditory Neuropathy Spectrum Disorder (ANSD)

• Ossified cochlea (relative)
• Cochlear nerve aplasia (absolute)
• Active middle ear infection
• No auditory nerve (MRI shows aplasia)

Surgery

• Transmastoid approach + posterior tympanotomy
• Cochleostomy near round window → electrode array inserted into scala tympani
• Receiver placed in skull recess behind pinna
• Activation at 4-6 weeks post-surgery (allows wound healing)

Outcomes

• Children implanted early (< 2 years): Can develop near-normal speech and attend mainstream school
• Adults: Improved speech perception; may not achieve normal speech
• Bilateral implants give better results than unilateral

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18. Perilymph Fistula - 5 marks

Definition

Causes

• Barotrauma (most common) - heavy lifting, straining, Valsalva, blast injury
• Head trauma / temporal bone fracture
• Stapedectomy / stapes surgery complication
• Superior semicircular canal dehiscence (SSCD)
• Spontaneous (idiopathic)

Clinical Features

1. Sudden unilateral SNHL - often fluctuating
2. Vertigo - episodic, position-related or exertion-related
3. Tinnitus
4. Tullio phenomenon - sound-induced vertigo (loud noise triggers vertigo)
5. Hennebert's sign - nystagmus on pneumatic otoscopy (pressure in EAC induces vertigo)
6. Aural fullness

Diagnosis

• Clinical diagnosis primarily (there is NO reliable non-invasive test)
• MRI: May show signal changes
• Electrocochleography (ECoG): Elevated SP/AP ratio
• Definitive: Surgical exploration - direct visualisation of fistula

Management

• Strict bed rest with head elevation (30°)
• Avoid straining (Valsalva, heavy lifting, nose blowing, constipation)
• Stool softeners
• Activity restriction

• Surgical exploration + patching of fistula
• Fat or fascia graft over oval and round windows
• Success rate: 60-80%

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19. Superior Semicircular Canal Dehiscence (SSCD) - 5 marks

Definition

Pathophysiology

• Normally inner ear has two windows: oval and round
• Dehiscence creates a third window → sound energy and pressure dissipated → symptoms
• Pressure/sound → displaces endolymph → ampulla of superior SCC activated

Clinical Features (Minor's triad - 1998)

1. Tullio phenomenon - vertigo and oscillopsia triggered by loud sounds
2. Valsalva-induced vertigo - straining/nose blowing causes vertigo
3. Pressure-induced nystagmus - nystagmus in plane of superior SCC on pneumatic otoscopy

• Autophony - hearing own heartbeat, eye movements, footsteps
• Low-frequency CHL (mechanical - NOT true CHL; ABG present but OAE also present)
• Pulsatile tinnitus

Investigations

1. HRCT temporal bone (0.5 mm cuts with coronal reconstruction): - Investigation of choice; shows dehiscence of superior SCC roof
2. VEMP (Vestibular Evoked Myogenic Potential): Low threshold + large amplitude cVEMP - highly sensitive and specific
3. Audiogram: CHL pattern with normal tympanogram (confusing - mimics otosclerosis)
4. OAE: Present (confirms cochlear OHCs intact - distinguishes from true CHL)

Management

• Avoid triggers (loud noise, straining)
• Adequate for mild cases

• Middle fossa craniotomy + plugging/resurfacing of dehiscence - for debilitating symptoms
• Transmastoid plugging - alternative approach

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20. Acoustic Trauma - 5 marks

Definition

Mechanism

• Extreme overpressure wave
• Physical disruption of organ of Corti (Reissner's membrane tears, hair cell damage)
• Labyrinthine membrane rupture
• May cause perilymph fistula

Clinical Features

• Immediate unilateral (or bilateral) SNHL - usually high frequency
• Tinnitus - loud, high-pitched; may persist permanently
• Aural fullness
• Temporary threshold shift (TTS) - in milder exposure; recovers in 16-48 hours
• Permanent threshold shift (PTS) - in severe exposure; irreversible
• Blast injury may also: rupture TM, dislocate ossicles (CHL component), cause vertigo

Treatment

• Systemic corticosteroids (high dose prednisolone) - started immediately for best results
• Vasodilators, rheological agents (carbogen, Dextran) - limited evidence
• Hearing aid for residual loss
• Tinnitus retraining therapy (TRT) for persistent tinnitus
• Prevention: Ear protection (ear muffs, custom ear plugs) - most important

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21. Tinnitus - 5 marks

Definition

Classification

• Heard only by patient
• Neurological origin (aberrant nerve activity in auditory pathway)

• Audible to examiner (with stethoscope)
• Causes: Glomus tumour, AVM, high jugular bulb, transmitted murmur, palatal myoclonus

Common Causes

Assessment

1. PTA + tympanometry
2. MRI brain/internal auditory canals (to exclude acoustic neuroma)
3. Tinnitus matching and masking tests

Management

1. Treat underlying cause (primary)
2. Tinnitus Retraining Therapy (TRT) - combination of counselling + sound therapy (most effective)
3. Sound therapy / masking - background noise reduces perception
4. Cognitive Behavioural Therapy (CBT) - for distress related to tinnitus
5. Hearing aid - if hearing loss present (amplifying external sound reduces tinnitus perception)
6. Drugs: Amitriptyline, benzodiazepines (short term) - for severe cases
7. No single pharmacological cure exists

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22. Otoscopy / Pneumatic Otoscopy - 5 marks

Otoscopy

• Pull pinna upward, outward, backward (adult) or downward + backward (infant/child) to straighten EAC
• Insert speculum gently into lateral EAC
• Inspect: EAC skin, wax, discharge, foreign body; then TM

• Pearly grey, semi-translucent
• Cone of light (anteroinferior)
• Handle of malleus visible
• Pars flaccida (superiorly)

Pneumatic Otoscopy (Siegle's speculum)

• Siegle's speculum has a sealed glass lens + rubber bulb - allows pressure variation in EAC
• Positive pressure → TM moves inward; negative pressure → outward
• Normal: TM moves freely
• Reduced movement: OME (glue ear), middle ear effusion
• Absent movement: Perforation (EAC communicates freely with middle ear)
• Nystagmus + vertigo on pressure: Positive fistula test (labyrinthine fistula / SSCD / Hennebert's sign)

• Tragal compression (or Siegle's speculum) → positive middle ear pressure → if labyrinthine fistula present → pressure transmitted to vestibule → nystagmus
• Positive fistula test in CSOM = cholesteatoma with labyrinthine fistula until proven otherwise

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MASTER CHECKLIST - ALL EAR 5-MARKERS