GC214 Common Ear Diseases And Hearing Loss
Common ear diseases encompass conditions such as otitis media, otitis externa, otosclerosis, and cerumen impaction that affect the external, middle, or inner ear and can lead to conductive, sensorineural, or mixed hearing loss.
Common Ear Diseases and Hearing Loss
This lecture (GC 214) is the core otology teaching for the HKUMed Fourth Summative and covers the entire spectrum of ear pathology — from pinna to cerebellopontine angle (CPA). It maps onto three clinical pillars: (1) understanding hearing loss types, causes, and consequences, (2) diagnosing and managing external, middle, and inner ear diseases, and (3) hearing rehabilitation. The lecture is structured anatomically: external ear → middle ear → inner ear, moving from common benign conditions (wax, otitis externa) to life-threatening complications (intracranial abscess from CSOM) and neoplasms (acoustic neuroma, EAC carcinoma). [1]
Big idea: A patient with ear symptoms needs you to localise the lesion (external/middle/inner), classify the hearing loss (conductive/sensorineural/mixed), identify urgency (safe vs. unsafe CSOM, intracranial complications), and plan definitive management (medical vs. surgical vs. rehabilitation).
Learning objectives (derived from slides):
- Classify hearing loss and interpret a pure tone audiogram (PTA)
- Recognise and manage common external ear diseases
- Distinguish acute otitis media (AOM) from chronic suppurative otitis media (CSOM)
- Differentiate "safe" (central perforation) from "unsafe" (marginal/attic perforation ± cholesteatoma) CSOM
- List intracranial and extracranial complications of CSOM
- Understand otitis media with effusion (OME) and its causes
- Recognise acoustic neuroma and inner ear pathology
- Know hearing rehabilitation options including cochlear implant
Core Concepts: Types of Hearing Loss
High Yield: The lecture defines three types of deafness: Conductive (eardrum, ossicles), Sensorineural (cochlea, auditory nerve, brainstem), and Mixed. [1]
Sound reaches the cochlea by two routes:
- Air conduction (AC): sound wave → pinna → external auditory canal (EAC) → tympanic membrane (TM) → ossicular chain (malleus-incus-stapes) → oval window → cochlea. Any block along this path = conductive hearing loss (CHL).
- Bone conduction (BC): vibrations of the skull directly stimulate the cochlea, bypassing the outer/middle ear apparatus. If the cochlea and auditory nerve are intact, BC will be normal even with CHL.
Sensorineural hearing loss (SNHL): damage at cochlea (sensory) or auditory nerve/brainstem (neural) → both AC and BC are impaired because the transduction or neural transmission is broken.
Mixed: both conductive and sensorineural components co-exist (e.g., long-standing CSOM with inner ear damage from chronic infection).
| Test | Technique | Conductive Loss (affected ear) | Sensorineural Loss (affected ear) |
|---|---|---|---|
| Rinne | 512 Hz fork on mastoid then next to ear | Negative (BC > AC) — the bone route bypasses the block | Positive (AC > BC) — both reduced but AC still better than BC |
| Weber | 512 Hz fork on vertex/forehead | Lateralises to affected ear — background noise masking is lost, so sound seems louder | Lateralises to normal ear — the healthy cochlea perceives better |
High Yield: PTA measures thresholds at different frequencies. It plots Air Conduction (AC) and Bone Conduction (BC). [1]
- Normal hearing: thresholds ≤ 25 dB across frequencies
- Conductive loss: AC thresholds raised, BC normal → air-bone gap
- Sensorineural loss: both AC and BC thresholds raised, no significant air-bone gap
- Mixed: both raised, but AC worse than BC (gap exists)
| Severity | Threshold (dB HL) |
|---|---|
| Mild | 26–40 dB |
| Moderate | 41–55 dB |
| Severe | 56–70 (some say 71–90) dB |
| Profound | > 90 dB |
High Yield: The lecture slide shows the severity scale: mild → moderate → severe → profound. [1]
Causes of Hearing Loss
High Yield [1]:
- External ear canal: congenital meatal stenosis
- Middle ear problems: eardrum perforation, ossicular chain problems (infection, post-operative, otosclerosis, tumour), middle ear fluid (effusion)
Why these cause CHL: anything that impedes the mechanical transmission of sound from the EAC to the oval window (wax blocking the canal, a hole in the TM reducing its vibrating area, disrupted ossicles, fluid damping ossicular movement).
High Yield [1]:
- Children: born profoundly deaf (genetic), neonatal causes
- Adults: meningitis, ear/head trauma, noise exposure, inner ear dysplasia, drug-induced (e.g., TB drugs — aminoglycosides, streptomycin), chronic ear infection, cochlear otosclerosis, radiotherapy
Why these cause SNHL: they damage the hair cells of the organ of Corti or the auditory nerve. Once hair cells are destroyed, they do not regenerate in humans.
- Aminoglycosides are ototoxic because they accumulate in the endolymph and generate reactive oxygen species that destroy outer hair cells, starting at the base of the cochlea (high-frequency loss first).
- Noise-induced hearing loss causes mechanical shearing of stereocilia and metabolic exhaustion of hair cells, classically producing a "4 kHz notch" on audiogram.
- Meningitis → labyrinthitis ossificans (fibrosis then ossification of the cochlea) making later cochlear implantation difficult.
High Yield [1]:
- In-born: "deaf and dumb" (unable to develop speech without hearing input), educational difficulties
- Adult: communication/social problems, occupational impact, socio-economic consequences, safety issues in daily activities
This is why universal newborn hearing screening is critical — early identification allows early intervention (hearing aids, cochlear implant) before the critical period for language development closes (~3 years).
External Ear Diseases
| Condition | Key Points | Why It Matters |
|---|---|---|
| Preauricular sinus | Congenital pit anterior to tragus; can become infected/form abscess | Common exam image; if recurrent infection → excision |
| Accessory auricle | Skin tag near tragus; contains cartilage | Cosmetic concern; excision if desired |
| Bat ear (prominent ear) | Antihelical fold underdevelopment; ear projects > 2 cm from mastoid | Pinnaplasty (otoplasty) if desired |
| Microtia and meatal atresia | Congenital underdevelopment of pinna ± absent EAC | Associated with conductive hearing loss; may need bone-anchored hearing aid (BAHA) or surgical reconstruction |
| Pinna keloid | Exuberant scar tissue, especially after piercing | Common in darker skin types; steroid injection, pressure earrings, excision with adjuvant therapy |
| Perichondritis | Infection of perichondrium of pinna cartilage; Pseudomonas common | Can cause "cauliflower ear" deformity if untreated; requires IV antibiotics (anti-pseudomonal) |
| Herpes zoster oticus / Ramsay-Hunt syndrome | VZV reactivation in geniculate ganglion → vesicles on pinna/EAC + facial nerve palsy ± SNHL, vertigo | A medical emergency for facial nerve; needs antivirals (aciclovir) + steroids |
| Haematoma auris → cauliflower ear | Blunt trauma → subperichondrial blood collection | Must be drained urgently or avascular necrosis of cartilage → permanent deformity |
| Pinna carcinoma | SCC or BCC of pinna | Sun-exposed area; wide excision ± reconstruction |
High Yield: Ramsay-Hunt syndrome = herpes zoster + facial nerve palsy. The vesicles on the pinna/EAC are pathognomonic. [1]
What the pinna photo panel shows: vesicular/crusted zoster of the pinna (Ramsay–Hunt), tense swollen haematoma auris, chronic deformed cauliflower ear, and ulcerated pinna carcinoma — four diagnoses that look nothing like a simple “sore ear.” [1]
Exam Trap
Do not confuse Ramsay-Hunt syndrome (VZV reactivation, vesicles, CN VII palsy) with Bell's palsy (idiopathic, no vesicles). Both cause LMN facial palsy, but the presence of vesicles + severe otalgia points to Ramsay-Hunt. Ramsay-Hunt has a worse prognosis for facial nerve recovery than Bell's palsy.
External Auditory Canal (EAC) Conditions
High Yield: Impacted wax and foreign bodies (cotton wool, plastic, insects) in the EAC are common presentations. [1]
What the otoscopy montage shows: impacted wax, rounded FB, cotton wool, plastic, and an insect occupying the EAC — identify the material before choosing syringe vs instrument vs “kill the insect first.” [1]
- Wax: cerumen is protective; impaction causes conductive hearing loss, otalgia, tinnitus. Removal by syringing (if no perforation), suction clearance, or curetting under direct vision.
- Foreign bodies: insects → instil olive oil or lidocaine to kill the insect before removal (a live insect causes extreme distress). Non-organic FBs can be syringed; organic FBs (e.g., beans) swell with water, so syringing is contraindicated — remove with instruments.
Otitis Externa (OE)
High Yield [1]:
- Diffuse OE: skin infection of the EAC
- Furunculosis: localised infection of hair follicles in the cartilaginous (outer 1/3) part of EAC → can form abscess
Why cartilaginous part? — Hair follicles are only found in the outer cartilaginous portion of the EAC, not in the bony (inner 2/3) portion. Therefore furunculosis only occurs laterally.
High Yield: Pain, discharge, NO hearing loss (because the middle ear is unaffected unless the canal is completely blocked). [1]
High Yield: Commonest organism: Staphylococcus aureus. [1]
Key Clinical Pearl
The lecture emphasises: otorrhoea + conductive deafness → think middle ear problem, NOT external ear disease. External ear diseases seldom cause hearing loss. If a patient has discharge AND conductive hearing loss, the pathology is almost certainly in the middle ear (e.g., CSOM with perforation). [1]
High Yield [1]:
- Narrow ear canal (congenital, trauma)
- Skin disease (e.g., eczema)
- Diabetes mellitus (immunocompromise → risk of malignant/necrotising otitis externa)
- Humidity ("Singapore Ear")
- Impacted ear wax, foreign bodies
- Swimming, shower
- Scratching, pricking → abrasion of canal skin
High Yield [1]:
- Local cleansing: remove wax/foreign body, suction clearance (aural toilet)
- Keep away from moisture (avoid swimming, use ear plugs in shower)
- Local antibiotic eardrops (vs. Staphylococcus)
- Correct underlying causes: small meatus, osteoma
High Yield: Aspergillosis and Candidiasis — often caused by overuse of antibiotic eardrops. [1]
Why? — Prolonged antibiotic drops eliminate competing bacteria, allowing fungal overgrowth. Treatment: stop antibiotics, antifungal eardrops (clotrimazole), meticulous aural toilet.
Clinical appearance: Aspergillus niger → black spores on white/grey fungal mat; Candida → white cottage-cheese-like material.
High Yield: An aural polyp visible in the EAC may arise from the EAC skin, but more commonly it represents granulation tissue from the middle ear protruding through a perforation, or even a cholesteatoma presenting as a polyp. Always consider middle ear pathology when you see an aural polyp. [1]
High Yield: Squamous cell carcinoma of the EAC — rare but important. [1]
Presentation: persistent otalgia unresponsive to treatment, bloody otorrhoea, facial nerve palsy (tumour invading the facial nerve in its bony canal). Diagnosed by biopsy. Treatment: lateral temporal bone resection ± radiotherapy.
Middle Ear Diseases
High Yield: The lecture shows a normal TM and tympanosclerosis (white chalky deposits in the TM from previous inflammation/healed infection). Tympanosclerosis is usually incidental and does not typically cause significant hearing loss unless it immobilises the ossicles. [1]
Acute Otitis Media (AOM)
High Yield [1]:
- Ascending infection (from nasopharynx via Eustachian tube)
- Common in children (ET is shorter, more horizontal, more compliant)
- Organisms: Viral; Streptococcus pneumoniae, Haemophilus influenzae, Moraxella catarrhalis
High Yield [1]:
- Pain (otalgia — often severe, wakes child at night)
- Deafness (conductive — from middle ear fluid and inflamed TM)
- Constitutional symptoms (fever, irritability, poor feeding in infants)
- NO otorrhoea UNLESS eardrum perforated
Why is this important? — If there is discharge, either the TM has spontaneously perforated (common in AOM, often brings pain relief) or there is an existing perforation (suggesting CSOM, not pure AOM).
Otoscopy in AOM: TM is erythematous, bulging, loss of light reflex, may see pus behind TM. Late AOM may show a yellow/white TM about to rupture.
High Yield [1]:
- Oral antibiotics targeting Gram-positive bacteria:
- Amoxicillin (first-line)
- Erythromycin
- Co-trimoxazole
- Cefuroxime
- Duration: 1 week to 10 days
- Supportive treatment (analgesia, antipyretics)
- Myringotomy (drainage) if resistant / complications
Why amoxicillin first-line? — It covers S. pneumoniae and H. influenzae (non-beta-lactamase producing strains), is well-tolerated orally, and is inexpensive. If beta-lactamase producing H. influenzae or M. catarrhalis is suspected, use amoxicillin-clavulanate or cefuroxime.
Clinical Note
Many guidelines now advocate "watchful waiting" for uncomplicated AOM in children > 2 years with mild symptoms, reserving antibiotics for severe/persistent cases or children < 2 years. However, the GC lecture lists oral antibiotics as the primary treatment — follow the GC slide framing for exams. [1]
Chronic Suppurative Otitis Media (CSOM)
High Yield: CSOM is defined by a persistent, non-healing eardrum perforation with recurrent otorrhoea and hearing loss. [1]
High Yield [1]:
- Infection: AOM (most common cause — an AOM that perforated and never healed)
- Trauma: direct mechanical, iatrogenic (e.g., grommet), barotrauma, blast injury
High Yield [1]:
| Feature | Central Perforation ("Safe") | Marginal / Attic Perforation ("Unsafe") |
|---|---|---|
| Synonyms | Tubotympanic disease | Atticoantral disease |
| Perforation site | Centre of pars tensa — rim of TM intact all around | Margin of pars tensa or pars flaccida (attic region) — no rim of TM between perforation edge and annulus |
| Frequency | More common | Less common |
| Cholesteatoma risk | Low | High |
| Complication risk | Low ("safe") | High ("unsafe") |
| Management | Tympanoplasty (elective) | Mastoidectomy (semi-urgent to prevent complications) |
Why is marginal/attic perforation "unsafe"? A marginal perforation allows skin (keratinising squamous epithelium) from the EAC to migrate into the middle ear. This trapped skin forms a cholesteatoma — a sac of keratinising squamous epithelium that expands, produces collagenase and osteoclast-activating factors, and erodes bone. This is why it causes the serious complications listed below.
High Yield: Conductive or mixed deafness + recurrent otorrhoea. CSOM can be active (discharging) or inactive (dry perforation). [1]
High Yield [1]:
- Mixed organisms: Staphylococcus aureus, Pseudomonas aeruginosa, Escherichia coli, Bacteroides fragilis
- Fungus: Aspergillosis, Candidiasis
- Tuberculosis (rare — suspect when resistant to usual treatment)
Why are the organisms different from AOM? — CSOM is a chronic process with a non-intact TM, exposing the middle ear to external pathogens. Water exposure introduces Pseudomonas; chronic infection selects for resistant/mixed flora.
High Yield [1]:
- Otoscopic diagnosis — what type of CSOM? Central or marginal/attic?
- Active infection? → ear swab for bacterial culture
- Audiological assessment → pure tone audiogram
- Local cleansing, ear mopping + broad-spectrum antibiotic eardrops
High Yield [1]: Targets:
- Hearing improvement → tympanoplasty / hearing aid
- Prevent otorrhoea → seal the perforation → tympanoplasty
- Activity / water sports → seal the perforation → tympanoplasty
High Yield: Cholesteatoma = keratinising squamous epithelium in the middle ear. [1]
Pathogenesis: The most accepted theory is retraction pocket theory — negative middle ear pressure (ET dysfunction) causes pars flaccida or posterosuperior pars tensa to retract inward, forming a pocket that collects keratin debris. This debris cannot self-clean, accumulates, becomes infected, and expands erosively.
Exam Trap
Cholesteatoma is NOT a tumour despite its name. It is a misnomer — there is no cholesterol or "-oma" (neoplasm). It is a destructive, non-neoplastic accumulation of keratinising squamous epithelium. However, it is locally destructive and can cause fatal intracranial complications, so it is treated with urgency.
High Yield [1]:
Extracranial complications:
| Complication | Mechanism |
|---|---|
| Facial nerve paralysis | Erosion of bony fallopian canal by cholesteatoma/infection |
| Ossicular chain erosion | Direct bone erosion → worsening conductive hearing loss |
| Labyrinthitis | Infection spreading to inner ear → SNHL + vertigo |
| Lateral semicircular canal (LSCC) fistula | Cholesteatoma erodes into LSCC → vertigo with positive fistula test (pressure on tragus → nystagmus) |
| Subperiosteal / subcutaneous abscess | Erosion through mastoid cortex → postauricular swelling pushing pinna forward and outward |
Intracranial complications:
| Complication | Notes |
|---|---|
| Extradural abscess | Pus between dura and bone |
| Subdural abscess | Pus between dura and arachnoid — very dangerous |
| Sigmoid sinus thrombophlebitis | Infection of lateral/sigmoid sinus → septic thrombosis → Griesinger sign (postauricular oedema over mastoid emissary vein) |
| Meningitis | Direct spread to meninges |
| Brain abscess | Temporal lobe or cerebellum — anatomical proximity to middle ear and mastoid |
| Otitic hydrocephalus | Raised ICP without abscess, often from sigmoid sinus thrombosis impeding CSF drainage |
Why Temporal Lobe and Cerebellum?
The tegmen tympani (roof of middle ear) is a thin bone plate separating the middle ear from the middle cranial fossa (temporal lobe). The posterior wall of the mastoid is adjacent to the posterior cranial fossa (cerebellum). Infection eroding through these thin bony barriers reaches the respective brain regions.
High Yield [1]:
- Diagnosis (otoscopy, CT temporal bone)
- Assess for complications (facial nerve function, vertigo, headache, fever, neurological signs)
- Audiological assessment
- Definitive surgery: MASTOIDECTOMY — to eradicate infection and prevent complications
Types of mastoidectomy (for reference):
- Canal wall up (CWU): preserves posterior EAC wall → better cosmesis and hearing, but higher recurrence; needs second-look surgery
- Canal wall down (CWD): removes posterior EAC wall → lower recurrence, but creates a mastoid cavity that needs lifelong cleaning
High Yield: Traumatic TM perforations (e.g., slap, cotton bud, barotrauma, blast) usually heal spontaneously within 6–8 weeks. Keep the ear dry, avoid drops through the perforation (ototoxic risk), and review. If it fails to heal → tympanoplasty. [1]
High Yield [1]: Causes of OME:
- Mechanical obstruction of Eustachian tube (ET):
- Enlarged adenoid (children — most common cause)
- Tumour, e.g., NPC (adults — always exclude NPC in unilateral OME in a Chinese adult)
- Poor mucociliary clearance in ET:
- Infection (post-URTI)
- Rhinitis (allergic/non-allergic)
- Post-irradiation (radiotherapy for NPC damages ET mucosa)
- ET dysfunction:
- Cleft palate (tensor veli palatini doesn't open ET properly)
- Post-operative
- Haemotympanum (blood in middle ear — post-trauma)
Critical Exam Point
Management of OME in children: watchful waiting (most resolve spontaneously) → if persistent (> 3 months with hearing loss) → myringotomy + grommet (ventilation tube) insertion ± adenoidectomy [3]
High Yield: Glomus tumour (paraganglioma) of the middle ear — vascular tumour arising from glomus bodies along the jugular bulb or promontory. [1]
- Presents with pulsatile tinnitus, conductive hearing loss
- Otoscopy: reddish-blue mass behind an intact TM ("rising sun" sign)
- Do NOT biopsy through TM — risk of catastrophic bleeding
- Diagnosis: CT/MRI. Treatment: surgery ± embolisation or radiotherapy.
Inner Ear and Retrocochlear Pathology
High Yield [1]:
- Conductive deafness — e.g., middle ear blood (haemotympanum), ossicular disruption
- Sensorineural deafness — cochlear damage (inner ear concussion or fracture through cochlea)
- Always assess facial nerve function — is it intact?
- Immediate onset facial palsy → suggests nerve transection (may need surgical exploration)
- Delayed onset facial palsy → suggests oedema/compression (often recovers with steroids)
Temporal bone fracture types (for reference):
- Longitudinal (80%): along long axis of petrous bone → usually CHL (TM tear, ossicular disruption); facial nerve palsy in ~20%
- Transverse (20%): across petrous bone → usually SNHL (cochlear damage), facial nerve palsy in ~50%, and vertigo
High Yield: Presents with asymmetrical sensorineural hearing loss of gradual onset. Located in the cerebellopontine angle (CPA) and internal auditory meatus (IAM). [1]
Why asymmetrical SNHL? — The tumour arises from the Schwann cells of the vestibular portion of CN VIII, usually unilateral (bilateral in NF2). As it grows within the IAM, it compresses the cochlear nerve fibres, causing progressive unilateral SNHL.
Other features: unilateral tinnitus, unsteadiness (vestibular), and if large: facial numbness (CN V), facial weakness (CN VII), cerebellar signs, raised ICP (hydrocephalus from 4th ventricle compression).
Investigations: MRI with gadolinium of the IAMs/CPA is the gold standard. Auditory brainstem response (ABR) may show prolonged I-V interpeak latency.
Management: observation (small tumours in elderly), microsurgery, or stereotactic radiosurgery (gamma knife).
Exam Rule
Any patient with asymmetric SNHL must have NPC and acoustic neuroma excluded. NPC → nasoendoscopy. Acoustic neuroma → MRI IAMs/CPA. [1]
High Yield [1]:
- Reconstruction of sound-conducting mechanism:
- Middle ear surgery: eardrum perforation repair (myringoplasty/tympanoplasty)
- Ossicular chain surgery (ossiculoplasty)
- Hearing aids:
- BC (bone conduction) aids — for CHL when AC aids can't be used (e.g., chronically discharging ears, meatal atresia)
- AC (air conduction) aids — most common type
- Types: BW (body worn), BTE (behind the ear), ITC (in the canal), CIC (completely in the canal)
- Cochlear implant:
- Indications: bilateral profound SNHL + no benefit from appropriately-fitted hearing aid
- Bypasses the damaged hair cells and directly stimulates the cochlear nerve via electrodes inserted into the cochlea
- Works best when implanted early (children) before auditory cortex plasticity is lost
Cochlear Implant vs Hearing Aid
A hearing aid amplifies sound and delivers it through the normal pathway (requires some functioning hair cells). A cochlear implant converts sound to electrical signals and directly stimulates the auditory nerve (hair cells are bypassed). That is why a cochlear implant can help profoundly deaf patients for whom hearing aids provide no benefit. [1]
Key steps (from clinical skills session slides) [7]:
- Inspection: pinna deformity, scars, swelling, discharge, pre-auricular pits
- Palpation: tenderness of tragus (suggests OE), mastoid tenderness (suggests mastoiditis)
- Otoscopy: EAC (wax, FB, inflammation, polyp), TM (intact/perforated, central/marginal, retracted, bulging, colour, light reflex)
- Tuning fork tests: Rinne's and Weber's (512 Hz)
- Whispered voice test / free-field hearing: crude screening
- Cranial nerve assessment: especially CN VII (facial nerve) in any ear pathology
- Post-auricular region: swelling suggests subperiosteal abscess or mastoiditis
Integration with Related GC Lectures
- NPC is endemic in Southern Chinese populations. Any middle-aged Chinese male with epistaxis, nasal obstruction, unilateral OME, or cranial nerve palsies → nasoendoscopy + biopsy. [5]
- VZV reactivation in geniculate ganglion → LMN facial palsy + vesicles on pinna/EAC + otalgia ± SNHL ± vertigo
- Treatment: aciclovir + prednisolone within 72 hours of onset
- Prognosis worse than Bell's palsy
- Meniere's disease: episodic vertigo (hours) + fluctuating SNHL + tinnitus + aural fullness (cf. 2025 MCQ Q50) [8]
- BPPV: brief positional vertigo (seconds), no hearing loss
- Vestibular neuritis: prolonged vertigo (days), no hearing loss
- Labyrinthitis from CSOM: vertigo + SNHL (complication of unsafe CSOM)
Exam Intelligence
| Trap | How to Avoid |
|---|---|
| Confusing OE with AOM | OE: tragal tenderness, EAC inflamed, TM usually normal. AOM: bulging erythematous TM, no tragal tenderness |
| Calling cholesteatoma a tumour | It is NOT a neoplasm — it is keratinising squamous epithelium (benign but locally destructive) |
| Forgetting NPC in unilateral OME | Always think NPC in a Chinese adult with unilateral OME. Nasoendoscopy is mandatory |
| Mixing up "safe" vs "unsafe" CSOM | Safe = central perforation (tubotympanic). Unsafe = marginal/attic perforation (atticoantral) ± cholesteatoma |
| Thinking OE causes significant hearing loss | Lecture explicitly says: "External ear diseases seldom cause hearing problem." If there's discharge + CHL, think middle ear |
| Bell's palsy vs Ramsay-Hunt | Vesicles = Ramsay-Hunt (VZV). No vesicles = Bell's (idiopathic) |
| Immediate vs delayed facial palsy in temporal bone fracture | Immediate = likely nerve transection → explore. Delayed = oedema → steroids, likely recovers |
| Cochlear implant indications | Bilateral profound SNHL + no benefit from appropriately-fitted hearing aids (not just "severe" HL or unilateral) |
- "Describe the otoscopic findings" → know how to describe TM: intact/perforated, central/marginal, size, discharge, cholesteatoma
- "Perform and interpret tuning fork tests" → Rinne's and Weber's for conductive vs sensorineural
- "What complications do you look for in CSOM?" → facial nerve palsy, labyrinthitis, LSCC fistula, mastoiditis/subperiosteal abscess, intracranial complications
- "How would you manage this patient with otitis externa?" → aural toilet, keep dry, antibiotic drops, treat underlying cause
High Yield Summary
-
Types of hearing loss
- Conductive (EAC/TM/ossicles), Sensorineural (cochlea/nerve/brainstem), Mixed. PTA shows air-bone gap in CHL.
-
Otitis externa
- Pain + discharge + NO hearing loss. Organism: S. aureus. Predisposing: moisture, DM, eczema, trauma. Rx: aural toilet + keep dry + antibiotic drops. Fungal OE from antibiotic overuse.
-
AOM
- Ascending infection via ET in children. Organisms: S. pneumoniae, H. influenzae, M. catarrhalis. Pain + CHL + fever, NO discharge unless TM perforated. Rx: amoxicillin × 7–10 days; myringotomy if resistant.
-
CSOM
- Non-healing perforation + recurrent otorrhoea + CHL/mixed HL.
- Safe = central perforation (tympanoplasty).
- Unsafe = marginal/attic perforation ± cholesteatoma (mastoidectomy).
- Mixed organisms including Pseudomonas.
- Complications: facial nerve palsy, labyrinthitis, LSCC fistula, subperiosteal abscess, intracranial abscess/meningitis (temporal lobe/cerebellum).
-
OME
- Middle ear effusion without acute infection. Causes: adenoid hypertrophy (children), NPC (adults — must exclude in Chinese patients), ET dysfunction, cleft palate, post-RT.
-
Cholesteatoma
- Keratinising squamous epithelium in middle ear. NOT a tumour. Locally destructive. Requires mastoidectomy.
-
Acoustic neuroma
- Asymmetric gradual SNHL + CPA tumour. Investigate with MRI.
-
Cochlear implant
- For bilateral profound SNHL with no hearing aid benefit.
-
Temporal bone fracture
- Assess CHL vs SNHL and facial nerve function (immediate vs delayed palsy).
-
Occupational deafness
- Most prevalent occupational disease in HK.
Active Recall - Lecture Notes
[1] Lecture slides: GC 214. Common ear diseases and hearing loss.pdf [2] Senior notes: MBBS Final MB (Pediatrics) (Felix PY Lai).pdf (Otitis media section) [3] Senior notes: Adrian Lui Pediatrics Notes.pdf (Hearing Disability, p.92) [4] Lecture slides: CFB 26_Lecture Note_ENT (I).pdf [5] Lecture slides: GC 215. Common nasal conditions and nasopharyngeal carcinoma.pdf [6] Lecture slides: HKU OM lecture 2023.09.09.pdf (Occupational diseases definition, p.12) [7] Lecture slides: MBBS IV Clinical Skills Session Ear and Nose 2025 (1).pdf [8] Past papers: 2025 Fourth Summative MCQ.pdf (Q50) [9] Past papers: 2025 Fourth Summative MCQ.pdf (Q5)
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