Ear Pain/hearing
Ear pain (otalgia) and hearing impairment are symptoms arising from conditions affecting the external, middle, or inner ear—such as infections, cerumen impaction, or eustachian tube dysfunction—that disrupt normal sound conduction or auditory perception.
Ear Pain (Otalgia) and Hearing Loss
Ear pain (otalgia) refers to pain perceived in or around the ear. It is one of the most common presenting complaints in primary care and ENT clinics. The term derives from the Greek roots: oto- = ear, -algia = pain.
Hearing loss (hypoacusis) is a partial or complete inability to hear sounds in one or both ears. From Greek: hypo- = under/reduced, akousis = hearing.
Otalgia is broadly divided into two categories:
- Primary otalgia: pain originating from pathology within the ear itself (external ear, middle ear, or inner ear).
- Secondary (referred) otalgia: pain perceived in the ear but originating from a distant site. This is possible because the ear has one of the richest and most complex sensory nerve supplies of any organ, receiving branches from five cranial nerves (CN V, VII, IX, X) and two cervical nerves (C2, C3). Any pathology along the distribution of these nerves can "refer" pain to the ear.
Why is referred otalgia so important? Because in up to 50% of adults presenting with ear pain but a normal otoscopic exam, the cause is referred pain from the teeth, TMJ, cervical spine, throat, or other structures [1].
Clinical Pearl
If an adult presents with ear pain but normal auroscopy, examine possible referral sites, namely TMJ, mouth, throat, teeth and cervical spine. [1]
Hearing loss is classified into:
- Conductive hearing loss (CHL): impaired sound transmission through the external ear canal, tympanic membrane, or ossicular chain to the oval window.
- Sensorineural hearing loss (SNHL): damage to the cochlea (sensory) or the cochlear nerve/central auditory pathways (neural).
- Mixed hearing loss: a combination of both.
2. Epidemiology
- Otalgia is one of the most frequent reasons for GP/paediatric consultations.
- Acute otitis media (AOM) is the single most common cause of otalgia in children: by age 3, approximately 80% of children will have had at least one episode.
- Otitis externa is extremely common, particularly in tropical/subtropical climates like Hong Kong (hot, humid summers) and in swimmers ("swimmer's ear").
- In adults, referred otalgia accounts for a significant proportion — studies report 30–50% of adult otalgia is secondary/referred.
- Global burden: WHO estimates >1.5 billion people live with some degree of hearing loss (2021 World Report on Hearing).
- Age-related hearing loss (presbycusis) is the most common cause of SNHL and the third most common chronic condition in older adults. By age 65, approximately 30% have disabling hearing loss; by age 75, this rises to ~50%.
- In Hong Kong, noise-induced hearing loss (NIHL) is a significant occupational hazard, and the ageing population means presbycusis is increasingly prevalent.
- Congenital SNHL occurs in approximately 1–3 per 1,000 live births.
- Nasopharyngeal carcinoma (NPC), which is endemic in Southern China including Hong Kong [2], can present with unilateral conductive hearing loss due to Eustachian tube obstruction — a critical "do not miss" diagnosis.
| Category | Ear Pain | Hearing Loss |
|---|---|---|
| Age | AOM peaks in children 6–24 months | Presbycusis: progressive >50 years |
| Environment | Humid/tropical climate (HK), swimming, water exposure | Occupational noise, recreational noise (concerts, earbuds) |
| Anatomical | Narrow ear canals, craniofacial abnormalities, cleft palate | Eustachian tube dysfunction, chronic OM |
| Infections | URTI (precedes AOM), immunosuppression | Congenital TORCH, meningitis, chronic OM |
| Habits | Use of cotton buds to clean the ear [1], ear piercing | Prolonged earphone use at high volume |
| Genetic | — | Alport syndrome, Pendred syndrome, connexin 26 mutations, otosclerosis (family history) |
| Drugs (ototoxicity) | — | Aminoglycosides, loop diuretics, cisplatin, high-dose aspirin |
| Other | Depression, spinal dysfunction (cervical) [1]; dental pathology, TMJ dysfunction | NPC (HK-endemic), cholesteatoma, Ménière's disease, acoustic neuroma |
Hong Kong High Yield
In any Hong Kong patient with unilateral serous otitis media (especially an adult male), you MUST exclude nasopharyngeal carcinoma with a post-nasal space examination ± nasopharyngoscopy. NPC is endemic here and classically presents late because the nasopharynx is a "clinically occult site" [2].
3. Anatomy and Physiology of the Ear
Understanding ear anatomy is essential because it directly explains:
- Why certain pathologies cause pain vs. hearing loss vs. both
- Why referred pain patterns exist
- How to localise a lesion based on clinical features
Structure:
- Pinna (auricle): elastic cartilage covered by skin. Functions as a sound-collecting funnel. The lobule (earlobe) contains no cartilage — just fat and connective tissue.
- External auditory canal (EAC): ~2.5 cm long in adults. The lateral one-third is cartilaginous (contains ceruminous glands that produce wax, and hair follicles); the medial two-thirds is bony (thin skin directly on periosteum — very sensitive to pain, which is why even minor infections here are exquisitely painful).
- Tympanic membrane (TM): a thin, semi-translucent membrane separating the EAC from the middle ear. It has three layers: outer squamous epithelium, middle fibrous layer, and inner mucosal layer.
Nerve Supply of the External Ear — this is the key to understanding referred otalgia:
| Nerve | Origin | Area Supplied | Referred Pain Source |
|---|---|---|---|
| Auriculotemporal nerve (V3) | Mandibular division of trigeminal | Anterior EAC, anterosuperior pinna, TM (outer) | Teeth, TMJ, parotid, oral cavity |
| Greater auricular nerve (C2, C3) | Cervical plexus | Posterior pinna, lobule, skin over mastoid | Cervical spine pathology |
| Arnold's nerve (CN X, vagus) | Vagus nerve (auricular branch) | Posterior EAC, concha, posterior TM | Larynx, pharynx, oesophagus, lung |
| Nerve of Jacobson (CN IX) | Glossopharyngeal | TM (medial surface), middle ear mucosa | Oropharynx, tonsils, tongue base |
| Sensory branch of CN VII | Facial nerve | Concha, posterior EAC (zone of Ramsay Hunt) | — |
Why does throat cancer cause ear pain? Because the glossopharyngeal nerve (CN IX) supplies both the tonsillar fossa/base of tongue AND the medial surface of the TM. Cancers of the oropharynx or hypopharynx irritate CN IX, and the brain "misinterprets" the signal as coming from the ear.
Why does coughing sometimes occur during ear syringing? Arnold's nerve (vagus) in the posterior EAC can trigger a vagal reflex (Arnold's reflex) causing coughing, and rarely bradycardia or syncope.
Structure:
- An air-filled cavity (tympanic cavity) within the temporal bone, containing the three ossicles: malleus, incus, and stapes — the smallest bones in the body.
- The ossicular chain amplifies sound ~22× from TM to oval window (area ratio amplification + lever effect).
- Eustachian tube (pharyngotympanic tube): connects the middle ear to the nasopharynx. In adults, it is ~36 mm long, running inferomedially. Functions: pressure equalization, mucociliary clearance, protection from nasopharyngeal secretions.
- In children, the Eustachian tube is shorter, more horizontal, and floppier → easier for pathogens from the nasopharynx to ascend → explains why AOM is so common in children.
- Mastoid air cells: communicate with the middle ear via the aditus ad antrum. Infection can spread here → mastoiditis.
Important relations:
- Roof (tegmen tympani) → middle cranial fossa (infection can cause intracranial complications)
- Floor → jugular bulb
- Posterior wall → mastoid air cells
- Medial wall → inner ear (promontory overlying cochlear basal turn; oval window; round window)
- Anterior wall → carotid canal, Eustachian tube
Nerve running through the middle ear:
- Chorda tympani (branch of CN VII): runs across the medial surface of the TM, between the malleus and incus. Carries taste from the anterior 2/3 of the tongue and parasympathetic fibres to submandibular/sublingual glands. Can be damaged in middle ear surgery or chronic otitis media → loss of taste on ipsilateral anterior tongue.
The inner ear sits within the petrous part of the temporal bone and contains two functional divisions:
a) Cochlea (Hearing)
- A spiral, snail-shaped structure (~2.5 turns) containing the Organ of Corti — the sensory transducer for hearing.
- Sound waves transmitted via the stapes to the oval window → perilymph vibrations in the scala vestibuli → endolymph vibrations in the scala media (cochlear duct) → movement of the basilar membrane → shearing of stereocilia on inner and outer hair cells against the tectorial membrane → mechano-electrical transduction → nerve impulses via the cochlear nerve (CN VIII).
- Tonotopic organization: high-frequency sounds are detected at the base of the cochlea; low-frequency sounds at the apex. This is why noise-induced hearing loss and presbycusis (which damage basal hair cells first) initially affect high frequencies.
- The Organ of Corti is connected to the basilar membrane via type IV collagen (α3-4-5 network). In Alport syndrome, mutations in COL4A3-5 lead to bilateral sensorineural hearing loss, beginning in high frequency range and progress to affect lower frequencies due to decreased adhesion of Organ of Corti to basilar membrane via defective α-3-4-5 collagen IV fibres [3].
b) Vestibular apparatus (Balance)
- 3 semicircular canals (superior, posterior, lateral): detect angular/rotational acceleration.
- Utricle and saccule (otolith organs): detect linear acceleration and gravity.
- Vestibular dysfunction causes vertigo, nausea, and nystagmus — which can co-exist with hearing loss and ear pain in certain conditions (e.g., Ménière's disease, labyrinthitis).
External ear → TM → ossicles → oval window → cochlea (inner ear) → cochlear nerve (CN VIII) → cochlear nuclei (pons) → superior olivary complex → lateral lemniscus → inferior colliculus → medial geniculate body (thalamus) → auditory cortex (Heschl's gyrus, superior temporal gyrus).
Understanding this pathway explains why:
- External/middle ear pathology → conductive hearing loss
- Cochlear pathology → sensorineural hearing loss (sensory type)
- CN VIII / central pathway pathology → sensorineural hearing loss (neural/retrocochlear type)
4. Etiology (Focus on Hong Kong)
4.1 Primary Otalgia — Causes Organized by Anatomical Site
| Condition | Key Features | Pathophysiology |
|---|---|---|
| Otitis externa (OE) | Most common cause of primary otalgia in adults; pain worse with tragal pressure/pinna traction; ear canal erythema, oedema, discharge | Infection of EAC skin (usually Pseudomonas aeruginosa or S. aureus); disruption of protective cerumen/epithelial barrier (water exposure, trauma from cotton buds, eczema) → bacterial invasion of skin/soft tissue |
| Malignant (necrotizing) otitis externa | Severe OE in elderly diabetics or immunocompromised; granulation tissue at bone-cartilage junction of EAC floor; can involve skull base → CN palsies (VII most common, then IX, X, XI, XII) | Pseudomonas aeruginosa invades from soft tissue into periosteum and bone → osteomyelitis of temporal bone and skull base; immunocompromise + microangiopathy in diabetes allows rapid spread |
| Furunculosis | Very painful, localized swelling in lateral (cartilaginous) EAC | Infection of a hair follicle (usually S. aureus); only occurs in lateral EAC because that is where hair follicles are |
| Herpes zoster oticus (Ramsay Hunt syndrome) | Vesicular eruption on pinna/EAC + ipsilateral facial nerve palsy ± SNHL, vertigo, tinnitus | VZV reactivation in the geniculate ganglion of CN VII → inflammation and damage to facial nerve; can spread to CN VIII → cochleovestibular symptoms |
| Perichondritis | Painful, red, swollen pinna (spares the lobule, which has no cartilage); can progress to abscess and "cauliflower ear" | Infection of perichondrium (usually Pseudomonas or S. aureus) after trauma, ear piercing through cartilage, or burns → compromised blood supply to cartilage (avascular, depends on perichondrium) → necrosis |
| Chondrodermatitis nodularis helicis [1] | Painful, small nodule on the helix or antihelix; exquisitely tender; worsens with pressure (sleeping on that side) | Pressure-induced ischaemic necrosis of cartilage with secondary inflammation and perichondritis; common in older males |
| Foreign body | Pain, discharge, hearing loss; common in children | Mechanical irritation, impaction, secondary infection of surrounding skin |
| Impacted cerumen | Dull ache, fullness, conductive hearing loss | Excessive/impacted wax presses on sensitive bony EAC skin; complete occlusion blocks sound conduction |
| Trauma | Pain after direct blow, barotrauma (diving, flying), or instrumentation (cotton buds) | Direct tissue damage; barotrauma → inability to equalize pressure → TM stretching/rupture |
| Neoplasia | SCC of EAC/pinna (most common malignancy); persistent otalgia, bleeding, granulation tissue | Malignant invasion of periosteum and bone → pain via periosteal nociceptors |
| Condition | Key Features | Pathophysiology |
|---|---|---|
| Acute otitis media (AOM) | Most common cause of otalgia in children; severe, deep ear pain; fever; bulging, erythematous TM; the pain of otitis media may be masked by fever in babies and young children [1] | URTI → Eustachian tube inflammation and oedema → negative middle ear pressure → fluid accumulation → secondary bacterial infection (S. pneumoniae, H. influenzae, M. catarrhalis) → pus under pressure → stretching of TM (highly innervated) → pain |
| Otitis media with effusion (OME / "glue ear") | Usually painless or mild discomfort; conductive hearing loss; retracted or dull TM with fluid level/bubbles | Eustachian tube dysfunction → negative middle ear pressure → transudation of fluid into middle ear → "glue-like" mucoid effusion impedes TM and ossicular vibration |
| Chronic suppurative otitis media (CSOM) | Chronic (>6 weeks) ear discharge through a persistent TM perforation; usually painless unless complications arise | Chronic mucosal infection/inflammation; pain suggests complication (mastoiditis, cholesteatoma, intracranial extension) |
| Cholesteatoma | Foul-smelling discharge, hearing loss, may be painless; retraction pocket or marginal perforation with keratinous debris | Abnormal keratinizing squamous epithelium in middle ear/mastoid; produces collagenases and other enzymes → erosion of ossicles, tegmen, lateral semicircular canal; can erode facial nerve canal → facial palsy |
| Acute mastoiditis | Post-auricular swelling, erythema, tenderness; pinna pushed forward and outward; deep ear pain; fever | Spread of AOM to mastoid air cells → suppuration → destruction of bony septae → coalescent mastoiditis; can form subperiosteal abscess; can extend intracranially |
| Barotrauma | Sharp ear pain during descent in flying/diving; hearing loss, vertigo | Failure to equalize middle ear pressure via Eustachian tube → relative negative pressure in middle ear → TM retraction → haemotympanum → possible TM rupture |
Inner ear pathology rarely presents with pain alone — it typically causes hearing loss ± vestibular symptoms. However, when acute, there may be a sense of "deep" ear discomfort.
| Condition | Key Features | Pathophysiology |
|---|---|---|
| Ménière's disease | Classic triad: episodic vertigo + fluctuating SNHL + tinnitus (± aural fullness) | Endolymphatic hydrops → distension of the membranous labyrinth → mechanical distortion of hair cells; episodes may be triggered by pressure changes in endolymph |
| Labyrinthitis | Acute vertigo + SNHL ± otalgia; follows viral URTI or AOM | Viral or bacterial infection spreading to labyrinth → inflammation of cochlea AND vestibular apparatus |
| Sudden SNHL | Sudden unilateral hearing loss (≥30 dB over ≥3 contiguous frequencies within 72 hours); ± tinnitus, aural fullness | Vascular (cochlear artery thrombosis), viral (cochlear neuritis), autoimmune, or idiopathic; treated as a medical emergency |
This is the critical concept: if an adult presents with ear pain but normal auroscopy, examine possible referral sites, namely TMJ, mouth, throat, teeth and cervical spine [1].
| Nerve Pathway | Source of Referred Pain | Examples |
|---|---|---|
| CN V (Trigeminal) — via auriculotemporal nerve (V3) | Teeth, TMJ, oral cavity, parotid | Dental caries, dental abscess, impacted wisdom teeth, TMJ dysfunction, parotid glands [1] pathology |
| CN VII (Facial) — sensory fibres via nervus intermedius | Geniculate ganglion, facial nerve | Ramsay Hunt syndrome (primary), Bell's palsy |
| CN IX (Glossopharyngeal) — via Jacobson's nerve | Oropharynx, tonsils, base of tongue | Tonsillitis, peritonsillar abscess (quinsy), tonsillar/base-of-tongue carcinoma, post-tonsillectomy pain, Eagle syndrome (elongated styloid process) |
| CN X (Vagus) — via Arnold's nerve | Larynx, hypopharynx, oesophagus, thyroid | Laryngeal carcinoma [4], hypopharyngeal carcinoma, oesophageal pathology, thyroiditis (subacute thyroiditis pain may radiate to angle of jaw and ears [5]), GORD |
| C2, C3 — via greater auricular nerve and lesser occipital nerve | Cervical spine, posterior neck | Cervical spinal dysfunction [1], cervical spondylosis, cervical disc disease, occipital neuralgia |
Must-Know Referred Otalgia Sources
The classic exam trap: an adult (especially a male smoker/drinker in Hong Kong > 40 years old) presents with persistent unilateral otalgia but a completely normal ear examination. You must think of:
- NPC (endemic in HK — Eustachian tube obstruction → OME; CN involvement → referred pain) [2]
- Oropharyngeal/hypopharyngeal/laryngeal carcinoma (via CN IX, X)
- Dental pathology / TMJ (via CN V3) — the most common cause of referred otalgia overall
- Cervical spine (via C2/C3)
Missing a head and neck malignancy in an otalgia presentation is a serious clinical error.
The Murtagh's masquerades checklist for ear pain includes: [1]
- Depression — chronic pain syndromes can manifest as otalgia
- Spinal dysfunction (cervical) — C2/C3 referred pain
- "Is the patient trying to tell me something?" — consider factitious pain, particularly in children; more likely in children; consider psychogenic/functional pain [1]
5. Classification
| Type | Site of Lesion | Examples |
|---|---|---|
| Conductive | External ear or middle ear | Cerumen impaction, OE, foreign body, TM perforation, OME, AOM, otosclerosis, cholesteatoma, ossicular discontinuity |
| Sensorineural (Sensory) | Cochlea | Presbycusis, NIHL, Ménière's, ototoxicity, sudden SNHL, congenital (connexin 26, CMV) |
| Sensorineural (Neural / Retrocochlear) | CN VIII or central pathways | Vestibular schwannoma (acoustic neuroma), CPA tumours, auditory neuropathy, MS, brainstem lesion |
| Mixed | Combined | Chronic otitis media with labyrinthine involvement, otosclerosis with cochlear extension, temporal bone fracture |
- Congenital: present at birth (genetic syndromes, TORCH infections, prematurity, hyperbilirubinaemia)
- Acquired: develops after birth
- Sudden (< 72 hours): sudden SNHL — medical emergency
- Gradual/Progressive: presbycusis, NIHL, otosclerosis, Ménière's, cholesteatoma
| Grade | Hearing Threshold (better ear) |
|---|---|
| Normal | ≤ 20 dB |
| Mild | 21–34 dB |
| Moderate | 35–49 dB |
| Moderately Severe | 50–64 dB |
| Severe | 65–79 dB |
| Profound | 80–94 dB |
| Complete/Total | ≥ 95 dB |
6. Pathophysiology — Mechanisms of Pain and Hearing Loss
Pain in the ear arises from stimulation of nociceptors in:
- Skin of the EAC (especially the medial bony portion — very thin skin directly on periosteum → extremely sensitive)
- Tympanic membrane (richly innervated by CN V3, IX, X)
- Periosteum (inflammation, infection, or tumour eroding bone)
- Perichondrium (infection or pressure on cartilage)
The middle ear mucosa and inner ear structures have limited direct pain innervation — pain from middle ear disease arises mainly from:
- Stretching of the TM by positive pressure (pus in AOM)
- Mucosal inflammation stimulating CN IX fibres (Jacobson's nerve on promontory)
- Extension to periosteum or dura
Conductive mechanisms:
- Anything that blocks the passage of sound waves: cerumen, foreign body, EAC oedema (OE), TM perforation (reduces surface area for sound collection), middle ear effusion (dampens ossicular vibration), ossicular erosion (cholesteatoma), ossicular fixation (otosclerosis).
Sensorineural mechanisms:
- Hair cell damage: these cells do not regenerate in humans. Noise, ototoxins, ageing, and ischaemia preferentially damage outer hair cells (which amplify sound) before inner hair cells (which transduce sound).
- Presbycusis: progressive loss of hair cells beginning at the cochlear base → high-frequency loss first.
- NIHL: damage at the 4 kHz region of the basilar membrane (due to resonance properties of the EAC and middle ear transfer function).
- Ototoxicity: aminoglycosides preferentially destroy outer hair cells at the base; cisplatin also targets cochlear hair cells.
- Endolymphatic hydrops (Ménière's): distension of endolymphatic space → mechanical disruption of stereocilia and potassium homeostasis → fluctuating SNHL.
- Vascular compromise: cochlea supplied by the labyrinthine artery (a branch of AICA, occasionally basilar artery directly) — an end artery with no collateral supply. Occlusion → sudden SNHL (analogous to a "cochlear stroke").
- Neural damage: compression of CN VIII (e.g., vestibular schwannoma) → retrocochlear SNHL; characteristically shows poor speech discrimination out of proportion to pure-tone loss.
6.3 Pathophysiology of Specific Conditions
- Disruption of protective cerumen barrier (water, trauma, cotton buds) → maceration of EAC skin → bacterial colonization → infection → oedema and inflammation of EAC → pain (tragal pressure compresses inflamed canal tissue against bone) → conductive hearing loss if canal swollen shut.
- URTI → mucosal oedema of Eustachian tube → obstruction → negative middle ear pressure → aspiration of nasopharyngeal flora into middle ear → bacterial proliferation → purulent effusion → positive pressure on TM → severe pain; bulging, erythematous TM.
- Acute otitis media due to Eustachian tube dysfunction and bacterial translocation from upper respiratory tract [6].
- Abnormal bone remodelling at the fissula ante fenestram (anterior to the oval window) → fixation of stapes footplate → impaired sound transmission → progressive conductive hearing loss.
- Often bilateral; typically presents in young adults (20–40), more common in females, worsened by pregnancy (oestrogen effect).
- Can extend to involve the cochlea ("cochlear otosclerosis") → mixed hearing loss.
- Carhart's notch: characteristic dip in bone conduction at 2 kHz on audiometry — an artefact of stapes fixation changing middle ear resonance, not true sensorineural loss.
- Retraction pocket (usually pars flaccida/attic region) → trapped keratinizing squamous epithelium → accumulation of keratin debris → enzymatic bone erosion (collagenases, osteoclast activation) → progressive destruction of ossicles, tegmen, lateral semicircular canal, facial nerve canal.
- Complications: conductive hearing loss (ossicular erosion), vertigo (lateral SCC fistula), facial palsy (CN VII erosion), intracranial complications (meningitis, brain abscess, sigmoid sinus thrombosis).
- Multi-factorial: loss of hair cells (sensory type), atrophy of stria vascularis (metabolic type, causes flat audiogram), loss of cochlear neurons (neural type), stiffening of basilar membrane (mechanical type).
- Begins with high-frequency loss → difficulty understanding speech, especially in noisy environments ("cocktail party deafness").
- NPC typically arises in the fossa of Rosenmüller (pharyngeal recess) [2] → local invasion or extrinsic compression of the Eustachian tube orifice in the nasopharynx → Eustachian tube obstruction → negative middle ear pressure → OME → unilateral conductive hearing loss.
- Can also cause referred otalgia via CN IX/X involvement.
7. Clinical Features
Assess the site of pain and radiation, details of the onset of pain, nature of the pain, aggravating or relieving factors and associated features such as vertigo, tinnitus, sore throat and irritation of the external ear. Ask about trauma, especially the use of a cotton bud to clean the ear. [1]
| History Element | What to Ask | Clinical Significance |
|---|---|---|
| Site | Where exactly is the pain? Point to it. In the ear? Around it? Deep? Superficial? | External ear pathology = superficial; middle ear = deep; referred = may be poorly localised |
| Onset | Sudden? Gradual? Duration? | Sudden severe pain → AOM, TM perforation, barotrauma; gradual → OE, OME, referred |
| Character | Sharp? Dull? Throbbing? Burning? | Sharp/stabbing → AOM, barotrauma; dull/aching → OME, referred (TMJ, dental); burning → herpes zoster |
| Radiation | Does pain spread to jaw, teeth, throat, neck? | Radiation to jaw/teeth → TMJ/dental; to throat → pharyngeal pathology; to neck/occiput → cervical spine |
| Aggravating factors | Chewing? Swallowing? Lying down? Head movement? Pressure? | Chewing → TMJ, OE (movement of jaw via EAC anterior wall); swallowing → pharyngeal/Eustachian tube; pressure → chondrodermatitis nodularis helicis |
| Relieving factors | — | — |
| Associated features | Vertigo, tinnitus, sore throat, irritation of the external ear [1], hearing loss, discharge, fever, facial weakness | Vertigo → inner ear involvement; discharge → OE, CSOM; facial weakness → cholesteatoma, Ramsay Hunt, malignant OE |
| Hearing loss | Uni/bilateral? Sudden/gradual? Fluctuating? | Unilateral sudden → sudden SNHL or AOM; gradual bilateral → presbycusis; fluctuating → Ménière's |
| Trauma | Especially the use of a cotton bud to clean the ear [1]; instrumentation, slap to ear, barotrauma (diving, flying), noise exposure | Cotton bud → EAC abrasion → OE, TM perforation; noise → NIHL; barotrauma → haemotympanum, TM rupture |
| PMH | Diabetes (malignant OE), immunosuppression, atopy/eczema (OE), previous ear surgery, recurrent OM | Diabetes + severe OE = think necrotizing OE; eczema → OE |
| Drug history | Aminoglycosides, cisplatin, loop diuretics, aspirin, ear drops | Ototoxicity → SNHL |
| Social history | Smoking, alcohol (risk for H&N malignancy), occupation (noise), swimming | Smoking + alcohol + otalgia = exclude H&N cancer [4]; swimming → OE |
| Family history | Otosclerosis, NPC, Alport syndrome, hereditary hearing loss | Otosclerosis = autosomal dominant with variable penetrance |
7.2 Symptoms — With Pathophysiological Basis
| Symptom | Pathophysiological Basis |
|---|---|
| Deep, severe, throbbing ear pain (AOM) | Pus under positive pressure stretching the richly innervated TM (CN V3, IX, X fibres) |
| Pain worse with tragal pressure / pinna traction (OE) | Manipulation compresses inflamed EAC skin against underlying bone/cartilage, stimulating nociceptors |
| Pain on chewing | Movement of the mandibular condyle transmits force to the anterior wall of the EAC (cartilaginous portion shares anterior wall with TMJ); also seen in TMJ dysfunction and parotitis |
| Burning pain with vesicles on pinna (Ramsay Hunt) | VZV reactivation causes neuroinflammation of the geniculate ganglion and sensory fibres of CN VII → neuropathic (burning) pain |
| Pain radiating to jaw/teeth | Shared CN V3 innervation between ear and dental/TMJ structures |
| Pain on swallowing (odynophagia with otalgia) | Shared CN IX/X innervation between pharynx and ear; also seen in Eustachian tube inflammation, peritonsillar abscess |
| Nocturnal pain, relieved by sitting up | Recumbent position increases venous congestion and middle ear pressure; seen in AOM |
| Exquisite tenderness of a small nodule on the helix | Chondrodermatitis nodularis helicis [1]: pressure ischaemia of cartilage → localized necrosis and inflammation |
| Post-auricular pain and tenderness | Mastoiditis: inflammation/suppuration of mastoid air cells → periosteal inflammation |
| Symptom | Pathophysiological Basis |
|---|---|
| Gradual bilateral high-frequency hearing loss (presbycusis) | Progressive loss of cochlear hair cells and neurons, starting at the base (high frequency end) of the cochlea |
| Unilateral conductive hearing loss with effusion in adult | OME — must exclude NPC in Hong Kong (Eustachian tube obstruction by tumour) [2] |
| Sudden unilateral hearing loss | Sudden SNHL: vascular occlusion of labyrinthine artery (end artery), viral cochleitis, autoimmune inner ear disease |
| Fluctuating hearing loss with episodic vertigo and tinnitus | Ménière's disease: episodic endolymphatic hydrops → variable cochlear distortion |
| Progressive conductive hearing loss, young female, worsened in pregnancy | Otosclerosis: oestrogen accelerates abnormal bone remodelling at the oval window → stapes fixation |
| Hearing loss with foul-smelling discharge | Cholesteatoma: enzymatic erosion of ossicles by keratinous debris |
| Bilateral SNHL beginning at high frequencies in a young person with haematuria | Alport syndrome: bilateral sensorineural hearing loss beginning in high frequency range, due to decreased adhesion of Organ of Corti to basilar membrane via defective α-3-4-5 collagen IV fibres [3] |
| Autophony (hearing own voice louder) | Patulous Eustachian tube (tube stays abnormally open) or SOM/OME (change in middle ear impedance) |
| Symptom | Pathophysiological Basis |
|---|---|
| Continuous high-pitched tinnitus | Usually accompanies cochlear SNHL; damaged hair cells generate spontaneous neural activity interpreted as sound |
| Pulsatile tinnitus | Vascular origin: glomus tumour (glomus tympanicum/jugulare), carotid stenosis, AV malformation, IIH (pulsatile tinnitus) [7]; the patient hears their own pulse transmitted through vascular structures near the ear |
| Low-pitched roaring tinnitus | Ménière's disease: low-frequency cochlear distortion from endolymphatic hydrops |
| Type | Significance |
|---|---|
| Watery, clear | CSF otorrhoea (temporal bone fracture, post-surgical); early OE |
| Purulent (yellow/green) | Bacterial OE, AOM with perforated TM, CSOM |
| Foul-smelling | Cholesteatoma, chronic infection with anaerobes |
| Bloody (sanguinous) | Trauma (TM perforation, skull base fracture), granulation tissue (malignant OE, carcinoma), bullous myringitis |
| Mucoid ("glue") | OME (if TM perforated or grommet in situ) |
| Symptom | Pathophysiological Basis |
|---|---|
| Episodic rotatory vertigo lasting 20 min to hours | Ménière's disease: episodic endolymphatic hydrops distorts vestibular hair cells |
| Brief positional vertigo < 1 min | BPPV: displaced otoconia in semicircular canal (usually posterior) trigger inappropriate cupula deflection during head position changes |
| Prolonged vertigo with hearing loss after URTI | Labyrinthitis: viral/bacterial inflammation of both cochlear and vestibular structures |
| Vertigo + facial palsy + vesicles | Ramsay Hunt: VZV in CN VII geniculate ganglion spreading to CN VIII |
7.3 Signs — With Pathophysiological Basis
Key examination: The external ear with manipulation of the ear. Check helix for chondrodermatitis nodularis helicis. Palpate the face and neck to include the parotid glands, regional lymph nodes and skin and temporomandibular joint (TMJ). Inspect both empty ear canals and tympanic membrane (TM) with the auroscope using the largest possible earpiece. Look for causes of referred pain: cervical spine, nose, postnasal space and mouth including teeth. [1]
| Sign | What It Means | Pathophysiology |
|---|---|---|
| Tragal tenderness / Pinna traction pain | Otitis externa | Inflamed EAC skin compressed against bone/cartilage |
| Red, swollen, tender pinna (sparing lobule) | Perichondritis | Cartilage infection → perichondrial inflammation; lobule spared because it has no cartilage |
| Red, warm, fluctuant pinna pushed forward | Mastoid subperiosteal abscess | Mastoiditis → pus breaks through mastoid cortex → subperiosteal collection → displaces pinna anteroinferiorly |
| Vesicles in concha/EAC | Herpes zoster oticus (Ramsay Hunt syndrome) | VZV eruption in CN VII sensory distribution (zone of Ramsay Hunt) |
| Small, tender nodule on helix | Chondrodermatitis nodularis helicis [1] | Pressure-induced cartilage ischaemia and necrosis |
| Tophi on helix | Gout | Monosodium urate crystal deposition in avascular cartilage |
| Sign | Condition | Pathophysiology |
|---|---|---|
| Erythematous, oedematous EAC with debris | Otitis externa | Infection and inflammation of canal skin |
| Granulation tissue at bone-cartilage junction | Malignant (necrotizing) OE | Osteomyelitis progressing from soft tissue; granulation = attempted healing at bone margin |
| Bulging, erythematous TM | Acute otitis media | Positive middle ear pressure from pus → TM pushed outward |
| Retracted TM with fluid level/bubbles | Otitis media with effusion | Negative middle ear pressure → TM sucked inward; fluid visible behind TM |
| TM perforation | Acute (trauma, AOM rupture) or chronic (CSOM) | Acute: pressure rupture or direct trauma; chronic: persistent inflammation preventing healing |
| Retraction pocket (attic) with keratin/debris | Cholesteatoma | Persistent negative pressure → pars flaccida retraction → trapping of squamous epithelium |
| White mass behind intact TM (chalk-like patches) | Tympanosclerosis | Hyaline degeneration and calcification of TM fibrous layer from previous inflammation/infection |
| Blue/dark TM | Haemotympanum | Blood in middle ear (temporal bone fracture, barotrauma) |
| Vesicles/bullae on TM | Bullous myringitis | Viral (or Mycoplasma) infection → haemorrhagic blistering of TM |
These are bedside tests using a 512 Hz tuning fork to differentiate conductive from sensorineural hearing loss. (256 Hz is too low — gives tactile sensation rather than true hearing; 1024 Hz decays too quickly.)
Rinne Test:
- Technique: Place vibrating tuning fork on mastoid process (bone conduction, BC). When patient can no longer hear it, move it to beside the ear canal (air conduction, AC). Ask which is louder, or whether they can still hear after it stops on the mastoid.
- Normal / SNHL: AC > BC ("Rinne positive") — because the normal ossicular amplification makes air conduction louder. In SNHL, both are reduced proportionally, so AC > BC still holds.
- Conductive HL: BC > AC ("Rinne negative") — because the conductive apparatus is impaired, air-conducted sound is attenuated, but bone conduction bypasses the middle ear and stimulates the cochlea directly.
Weber Test:
- Technique: Place vibrating tuning fork on the vertex (midline forehead or top of skull).
- Normal: sound perceived equally in both ears (midline).
- Conductive HL: lateralises to the affected (worse) ear — because background masking noise is reduced on that side AND bone-conducted sound is trapped (Carhart effect).
- SNHL: lateralises to the better (unaffected) ear — because the cochlea on the damaged side cannot transduce the sound as effectively.
| Test | Conductive HL | SNHL |
|---|---|---|
| Rinne | Negative (BC > AC) on affected side | Positive (AC > BC) bilaterally |
| Weber | Lateralises to affected ear | Lateralises to unaffected (better) ear |
Exam Pitfall — False Negative Rinne
In severe unilateral SNHL (dead ear), a Rinne test on the affected side may appear "negative" because the bone conduction is being heard by the contralateral (good) cochlea via cross-conduction through the skull, not by the ipsilateral cochlea. This is a "false negative Rinne." You can confirm this with the Weber test (which will lateralise to the normal ear, confirming SNHL, not conductive loss).
| Sign | Condition | Pathophysiology |
|---|---|---|
| Facial nerve palsy (LMN pattern) | Cholesteatoma, malignant OE, Ramsay Hunt, temporal bone fracture, Bell's palsy | CN VII runs through the middle ear (horizontal/tympanic segment) and mastoid (vertical segment); erosion, infection, or inflammation damages the nerve |
| Cranial nerve palsies (VII, IX, X, XI, XII) | Malignant OE (skull base osteomyelitis) | Pseudomonas spreads along skull base → sequential CN involvement |
| Post-nasal space mass | NPC | Frequently originates from pharyngeal recess (fossa of Rosenmüller) [2]; visible on nasopharyngoscopy |
| TMJ tenderness, clicking on palpation [1] | TMJ dysfunction | Disc displacement or arthritis → referred otalgia via CN V3 |
| Lymphadenopathy (regional) [1] | Infection, malignancy | Reactive in infection; hard, fixed nodes suggest malignancy (H&N cancer, NPC) |
| Parotid swelling and tenderness | Parotitis [8] | Infection of parotid gland → swelling → pain referred to ear via CN V3 (auriculotemporal nerve runs through/near parotid) |
Key investigations: Seldom necessary. Consider hearing tests, audiometry. Any ear discharge for MC [microscopy and culture] but swabs of no value if the TM is intact. [1]
| Investigation | When to Use | What It Shows |
|---|---|---|
| Otoscopy | All patients | Visualisation of EAC and TM — the single most important examination |
| Tuning fork tests (512 Hz) | Bedside assessment of hearing loss | Differentiates CHL from SNHL (see above) |
| Pure-tone audiometry (PTA) | Any patient with hearing loss | Gold standard for hearing assessment; plots air and bone conduction thresholds; air-bone gap = conductive component |
| Tympanometry | Suspected middle ear pathology | Measures TM compliance; Type A = normal; Type B (flat) = effusion; Type C (negative peak) = Eustachian tube dysfunction; Type As (shallow peak) = otosclerosis/tympanosclerosis |
| Ear swab MC&S | Ear discharge present | Identifies causative organism; of no value if TM is intact [1] (skin commensals confound results) |
| CT temporal bone | Cholesteatoma, mastoiditis, malignant OE, trauma, tumours | Bony detail: erosion, opacification, fractures |
| MRI (with gadolinium) | Vestibular schwannoma, retrocochlear pathology, intracranial complications | Soft tissue detail; schwannoma enhances with gadolinium |
| Nasopharyngoscopy | Unilateral OME in adult (HK: exclude NPC) | Direct visualization of nasopharynx |
| EBV serology / plasma EBV DNA | Suspected NPC | EBV VCA IgA and EBV DNA [2] — screening and monitoring for NPC |
| Blood tests | Malignant OE (ESR/CRP, glucose), autoimmune SNHL (ANA, ESR), syphilis (VDRL/RPR) | Guided by clinical suspicion |
| OAE / ABR | Neonatal hearing screening, retrocochlear pathology | OAE (otoacoustic emissions) tests outer hair cell function; ABR (auditory brainstem response) tests neural pathway |
High Yield Summary
-
Otalgia = primary (pathology in the ear) or secondary/referred (pathology elsewhere, perceived in the ear due to shared sensory innervation from CN V, VII, IX, X, C2/C3).
-
If an adult presents with ear pain but normal auroscopy, examine possible referral sites: TMJ, mouth, throat, teeth, cervical spine. [1]
-
Most common causes by age: Children = AOM; Adults = OE, TMJ dysfunction, dental pathology, referred pain.
-
Hong Kong critical "do-not-miss": Unilateral OME/conductive hearing loss in an adult → exclude NPC with nasopharyngoscopy. NPC arises in the fossa of Rosenmüller and obstructs the ipsilateral Eustachian tube.
-
Hearing loss types: Conductive (external/middle ear) vs. Sensorineural (cochlea/CN VIII/central). Differentiate at bedside with Rinne and Weber tests.
-
Weber lateralises to: the affected ear in CHL (reduced masking + trapped bone conduction); the better ear in SNHL (damaged cochlea cannot transduce).
-
Malignant OE: elderly diabetic + severe OE + granulation tissue at bone-cartilage junction + CN palsies → Pseudomonas skull base osteomyelitis. Not a neoplasm despite the name.
-
Cholesteatoma: not a tumour — it's trapped keratinizing squamous epithelium that erodes bone. Foul-smelling discharge + retraction pocket + ossicular erosion → CHL.
-
Sudden SNHL (≥30 dB in ≥3 frequencies within 72 hours) is an ENT emergency — analogous to a "cochlear stroke." Treat with systemic (± intratympanic) corticosteroids.
-
Key investigations are seldom necessary. Consider hearing tests, audiometry. Ear discharge for MC but swabs of no value if TM is intact. [1]
-
Masquerades checklist: depression, cervical spinal dysfunction, factitious pain (especially in children). [1]
Active Recall - Ear Pain and Hearing
[1] Lecture slides: murtagh merge.pdf (p44, "Ear pain") [2] Senior notes: felixlai.md (Nasopharyngeal cancer section) [3] Senior notes: Ryan Ho Urogenital.pdf (p60, Alport Syndrome) [4] Senior notes: felixlai.md (Laryngeal carcinoma section) [5] Senior notes: Ryan Ho Endocrine.pdf (p31, Subacute Thyroiditis) [6] Senior notes: Ryan Ho Respiratory.pdf (p49, Acute Coryza — complications) [7] Senior notes: Ryan Ho Neurology.pdf (p158, Idiopathic intracranial hypertension) [8] Senior notes: felixlai.md (Parotitis section)
Differential Diagnosis of Ear Pain and Hearing Loss
The differential diagnosis of ear pain (otalgia) and hearing loss is best approached using a structured framework. Murtagh's diagnostic strategy organises differentials into probability diagnoses (common things seen commonly), serious disorders not to be missed (the ones that kill or maim), pitfalls (often missed), and the masquerades checklist [1]. This is a superb framework for clinical practice and exams because it forces you to think about both the likely and the dangerous.
1. Murtagh's Diagnostic Strategy for Ear Pain [1]
These are the diagnoses you will see day in, day out. When a patient walks in with ear pain, one of these is the answer the vast majority of the time.
| Diagnosis | Why It's Common | Key Distinguishing Feature |
|---|---|---|
| Otitis media (viral or bacterial) [1] | URTI is ubiquitous; Eustachian tube dysfunction is extremely common in children (short, horizontal tube) → middle ear infection/effusion | Deep ear pain, fever, bulging erythematous TM on otoscopy; pain may be masked by fever in babies and young children [1] |
| Otitis externa [1] | Warm humid climate (Hong Kong), swimming, cotton bud use → disruption of cerumen barrier → bacterial colonisation of EAC | Pain worse with tragal pressure / pinna traction; swollen, erythematous EAC with debris |
| Boils and furuncles of canal [1] | Hair follicle infection (S. aureus) in the lateral (cartilaginous) EAC — the only part of the canal with hair follicles | Localised, exquisitely tender swelling in the lateral EAC; tragal tenderness |
| TMJ arthralgia [1] | Extremely common (bruxism, dental malocclusion, stress); anterior wall of EAC is shared with the TMJ → chewing/jaw movement exacerbates pain | Pain on chewing, clicking/crepitus on jaw opening, tenderness over TMJ; normal otoscopy (referred pain via CN V3) |
| Eustachian tube dysfunction [1] | Follows URTI, allergic rhinitis, or anatomical obstruction; negative middle ear pressure → retracted TM, aural fullness, mild pain | Popping/crackling sensation, fullness, mild conductive hearing loss; retracted TM on otoscopy |
Why is TMJ arthralgia in the "probability" category? Because the temporomandibular joint shares its nerve supply (auriculotemporal nerve, CN V3) with the external ear, and the anterior wall of the bony EAC is literally the posterior wall of the TMJ fossa. Jaw clenching/bruxism is extremely prevalent — many patients have referred otalgia from the TMJ without realising it.
These are the diagnoses that, if delayed, lead to serious morbidity or death. You must actively exclude these.
| Diagnosis | Why It's Serious | Key Features |
|---|---|---|
| Neoplasia of external ear [1] | SCC of pinna/EAC — can invade temporal bone, parotid, skull base | Non-healing ulcer or mass on pinna/EAC; chronic bloody discharge; pain out of proportion |
| Cancer of other sites (e.g. tongue, throat) [1] | Head and neck cancers (especially NPC in Hong Kong [2], oropharyngeal, hypopharyngeal, laryngeal carcinoma [4]) cause referred otalgia via CN IX/X; delayed diagnosis = late-stage presentation | Persistent unilateral otalgia with normal otoscopy in a smoker/drinker; dysphagia, hoarseness, neck mass; unilateral OME in adult → must exclude NPC |
| Herpes zoster — Ramsay Hunt syndrome [1] | VZV reactivation in geniculate ganglion → CN VII palsy (may be permanent), CN VIII involvement → SNHL, vertigo | Vesicles in concha/EAC (zone of Ramsay Hunt) + ipsilateral LMN facial palsy + severe otalgia ± SNHL/vertigo |
| Acute mastoiditis [1] | Complication of AOM; can lead to intracranial abscess, meningitis, sigmoid sinus thrombosis | Post-auricular swelling/erythema/tenderness, pinna pushed forward; fever, deep pain; often follows inadequately treated AOM |
| Cholesteatoma [1] | Erosive — destroys ossicles, erodes into lateral SCC (vertigo), facial nerve canal (palsy), tegmen (intracranial complications) | Foul-smelling discharge, progressive conductive HL, retraction pocket with keratin on otoscopy; NOT a tumour but behaves like one locally |
| Necrotising otitis externa [1] | Skull base osteomyelitis from Pseudomonas in diabetics/immunocompromised; can involve CN VII, IX, X, XI, XII; mortality up to 20% if delayed | Severe disproportionate pain, granulation tissue at bone-cartilage junction, cranial nerve palsies, raised ESR/CRP; not "malignant" in the neoplastic sense — the name refers to aggressive destructive behaviour |
Do Not Miss in Hong Kong
Cancer of other sites (e.g. tongue, throat) [1] — in the Hong Kong context, nasopharyngeal carcinoma is the critical "do-not-miss." Any adult with unilateral OME, persistent unilateral otalgia, or conductive hearing loss with a normal EAC must have a nasopharyngoscopy to visualise the post-nasal space. NPC is endemic in Southern China including Hong Kong [2] and frequently presents late because the fossa of Rosenmüller is a clinically occult site.
These are the diagnoses that clinicians frequently overlook — leading to unnecessary investigations, repeated consultations, and patient frustration.
| Diagnosis | Why It's Missed | Key Features |
|---|---|---|
| Foreign bodies in ear [1] | Children don't volunteer history; small objects may not be visible without careful otoscopy | History from child/parent; visible on otoscopy if you look carefully; unilateral discharge |
| Hard ear wax [1] | Dismissed as trivial, but impacted cerumen causes real pain and hearing loss | Dull ache, fullness, conductive hearing loss; wax visible on otoscopy — simple to treat |
| Trauma including barotrauma [1] | Patient may not connect recent flight/dive with ear symptoms; cotton bud use not volunteered | History of flying, diving, slap to ear, cotton bud use [1]; haemotympanum, TM perforation |
| Dental abscess [1] | Ear pain may be the presenting symptom with no dental complaint initially | Normal otoscopy; dental tenderness on percussion; pain on chewing; jaw/face swelling |
| Referred pain: neck, throat (e.g. tonsillitis) [1] | Clinician focuses on the ear and forgets to examine the throat and neck | Sore throat, cervical spine tenderness; look for causes of referred pain: cervical spine, nose, postnasal space and mouth including teeth [1] |
| Unerupted wisdom tooth and other dental causes [1] | Impacted 3rd molar irritates CN V3 → referred ear pain; patient presents to GP not dentist | Young adult; trismus; tender posterior mandible; normal otoscopy |
| TMJ arthralgia [1] (also a probability diagnosis) | Listed twice because it is so commonly missed — clinicians forget to palpate the TMJ [1] | Pain on chewing, clicking, crepitus; tenderness on TMJ palpation; normal otoscopy |
| Chondrodermatitis nodularis helicis [1] | Small nodule easily overlooked unless you check helix for chondrodermatitis nodularis helicis [1] | Exquisitely tender small nodule on helix/antihelix; worsened by pressure (sleeping on that ear) |
| Facial neuralgias, esp. glossopharyngeal [1] | Paroxysmal lancinating pain in ear/throat triggered by swallowing → mistaken for throat/ear pathology | Brief electric-shock-like pain in ear/throat/tonsillar fossa; triggered by swallowing, talking, yawning |
| Post-tonsillectomy [1]: from the wound [1] and from TMJ due to mouth gag [1] | Post-operative referred otalgia is expected but can alarm patients; also the mouth gag used in surgery stresses the TMJ → TMJ-related otalgia | Otalgia after tonsillectomy; no ear pathology on exam; pain from raw tonsillar bed referred via CN IX; TMJ strain from prolonged mouth opening |
| Masquerade | Mechanism |
|---|---|
| Depression [1] | Chronic pain syndromes, somatisation — patients with depression can present with persistent otalgia without organic cause; pain perception is amplified by central sensitisation |
| Spinal dysfunction (cervical) [1] | C2/C3 cervical nerve roots supply the ear via the greater auricular and lesser occipital nerves; cervical spondylosis, disc disease, or facet joint dysfunction → referred otalgia |
| "Is the patient trying to tell me something?" [1] — Unlikely, but always possible with pain. More likely in children. Consider factitious pain. [1] | Psychogenic/factitious otalgia; children may use ear pain to express distress or gain attention; in adults, consider secondary gain |
2. Differential Diagnosis of Hearing Loss
Hearing loss differentials are best organised by type (conductive vs. sensorineural) and then by site of lesion within each type, because this mirrors the clinical reasoning you'll use when you have audiometry results.
| Site | Condition | Key Feature |
|---|---|---|
| External ear | Cerumen impaction | Most common benign cause; easily seen on otoscopy |
| Otitis externa (severe, with canal oedema) | Canal swollen shut → sound cannot reach TM | |
| Foreign body | Common in children | |
| Exostoses / osteomata | Bony narrowing of EAC in cold-water swimmers ("surfer's ear") | |
| EAC atresia/stenosis | Congenital (Treacher Collins, etc.) or acquired (post-inflammatory) | |
| Tympanic membrane | TM perforation | Trauma, AOM, CSOM; degree of HL depends on size and location |
| Tympanosclerosis | Calcified patches on TM from prior inflammation; usually minimal HL | |
| Middle ear | AOM / OME | Fluid/pus dampens ossicular vibration |
| CSOM | Chronic inflammation, possible ossicular erosion | |
| Cholesteatoma | Ossicular erosion (incus long process most vulnerable) | |
| Otosclerosis | Stapes footplate fixation at oval window; progressive CHL; Carhart's notch at 2 kHz | |
| Ossicular discontinuity | Trauma, cholesteatoma; large air-bone gap (~60 dB max) | |
| Haemotympanum | Temporal bone fracture → blood in middle ear | |
| NPC causing OME | Unilateral OME in adult → exclude NPC [2] |
| Category | Condition | Key Feature |
|---|---|---|
| Cochlear (sensory) | Noise-induced hearing loss [9] | 4 kHz notch on audiogram; occupational/recreational noise exposure |
| Presbycusis (ageing) [9] | Bilateral, symmetrical, high-frequency loss; most common cause of SNHL globally | |
| Ménière's disease/syndrome [9] | Fluctuating low-frequency SNHL + episodic vertigo + tinnitus + aural fullness | |
| Ototoxicity | Aminoglycosides (irreversible), cisplatin, loop diuretics (usually reversible), high-dose aspirin | |
| Sudden SNHL | ENT emergency; ≥30 dB in ≥3 frequencies within 72 hours; vascular, viral, autoimmune, or idiopathic | |
| Viral cochleitis / ear infection [9] | Post-viral SNHL; may follow mumps, measles, VZV, CMV | |
| Congenital SNHL | Genetic (connexin 26 mutation, Pendred syndrome, Alport syndrome [3]); TORCH infections | |
| Autoimmune inner ear disease | Bilateral, rapidly progressive SNHL; may be associated with systemic autoimmune disease | |
| Retrocochlear (neural) | Acoustic neuroma (vestibular schwannoma) [9] — unilateral | Unilateral progressive SNHL with poor speech discrimination; tinnitus; can cause CN V/VII involvement if large |
| CPA tumours (meningioma, epidermoid) | Similar presentation to vestibular schwannoma | |
| Auditory neuropathy spectrum disorder | OAE present but ABR absent/abnormal; speech perception disproportionately poor | |
| Central | MS, brainstem stroke, tumour | Central auditory processing affected; rare |
| Condition | Mechanism |
|---|---|
| CSOM with labyrinthine involvement | Chronic infection erodes into inner ear → combined CHL + SNHL |
| Cholesteatoma with inner ear fistula | Erosion into lateral SCC → CHL (ossicular) + SNHL (labyrinthine) |
| Otosclerosis with cochlear extension | "Far-advanced otosclerosis" — spongiotic bone involves cochlear capsule → mixed loss |
| Temporal bone fracture | Ossicular disruption (CHL) + cochlear/CN VIII damage (SNHL) |
| Paget's disease of bone [10] | Skull involvement → hearing loss due to cochlear involvement [10]; combined ossicular fixation + cochlear bone changes |
3. Differential Diagnosis of Tinnitus [9]
Since tinnitus commonly co-exists with ear pain and hearing loss, it is worth considering its differential separately.
| Condition | Mechanism |
|---|---|
| Ear wax or debris [9] | Physical contact with TM or altered resonance → perceived sound |
| Sensorineural hearing loss (esp. noise-induced) [9] | Damaged cochlear hair cells generate spontaneous aberrant neural activity → phantom sound |
| Otosclerosis [9] | Altered middle ear mechanics + possible cochlear involvement → tinnitus |
| Ageing [9] | Presbycusis → deafferentation of auditory cortex → central tinnitus generation |
| Ear infection (e.g. viral cochleitis) [9] | Cochlear inflammation → aberrant neural discharge |
| Ménière syndrome [9] | Endolymphatic hydrops → cochlear distortion → low-frequency roaring tinnitus |
| Category | Condition | Key Feature |
|---|---|---|
| Vascular [9] | Arteriovenous malformation, carotidovenous fistula, arterial bruits (esp. carotid), venous hum (jugular) [9] | Pulsatile tinnitus — synchronous with heartbeat; objective (can be heard by examiner with stethoscope over ear/mastoid) |
| Infection [9] | Suppurative otitis media [9] | Middle ear infection → mucosal inflammation near cochlear promontory → tinnitus |
| Cancer/tumour [9] | Acoustic neuroma — unilateral [9] | Unilateral tinnitus + progressive unilateral SNHL + poor speech discrimination → MRI with gadolinium |
| Other [9] | Head injury [9] | Temporal bone fracture, concussion → cochlear damage or central auditory pathway injury |
| Condition | Mechanism |
|---|---|
| Impacted wisdom tooth [9] | CN V3 irritation → referred perception of tinnitus (somatosensory tinnitus) |
| Temporomandibular injury/dysfunction [9] | Tensor tympani is innervated by CN V3; TMJ dysfunction can cause reflex tensor tympani spasm → tinnitus |
| Alcoholism [9] | Direct ototoxic effect of chronic alcohol; also causes peripheral neuropathy and cerebellar degeneration → balance + auditory dysfunction |
Pulsatile vs Non-Pulsatile Tinnitus
Non-pulsatile tinnitus is overwhelmingly associated with cochlear/sensorineural pathology (NIHL, presbycusis, Ménière's, ototoxicity). The mechanism is deafferentation: damaged hair cells → reduced input to auditory cortex → cortex "turns up the gain" → perceives phantom sound.
Pulsatile tinnitus is a vascular symptom and should prompt investigation for: glomus tumour (tympanicum/jugulare), carotid stenosis/bruit, AV malformation, dural AV fistula, idiopathic intracranial hypertension [7] (young obese female, headache, papilloedema), or benign venous hum (abolished by ipsilateral IJV compression or head turning).
The clinical approach to differentiating ear pain and hearing loss can be distilled into a logical algorithm:
| Presentation | Top Differentials | Key Distinguishing Investigation/Feature |
|---|---|---|
| Child + acute ear pain + fever + bulging TM | AOM | Otoscopy diagnostic; pain may be masked by fever in babies [1] |
| Swimmer + itchy painful ear + tragal tenderness | Otitis externa | Otoscopy: oedematous EAC, debris; tragal/pinna tenderness |
| Elderly diabetic + severe otalgia + granulation tissue + CN palsy | Necrotising OE | CT temporal bone, Tc-99m/Ga-67 bone scan; ESR/CRP markedly raised |
| Adult + unilateral ear pain + normal otoscopy | Referred otalgia (TMJ, dental, throat, cervical spine, NPC) | Examine TMJ, mouth, throat, teeth, cervical spine; nasopharyngoscopy [1] |
| Adult HK male + unilateral OME | NPC until proven otherwise | Nasopharyngoscopy + biopsy; EBV DNA/VCA IgA [2] |
| Young female + progressive bilateral CHL + family history | Otosclerosis | Audiometry: CHL with Carhart's notch at 2 kHz; tympanometry: Type As (reduced compliance) |
| Sudden unilateral hearing loss | Sudden SNHL (emergency) | Audiometry confirms ≥30 dB SNHL in ≥3 frequencies; MRI to exclude acoustic neuroma |
| Unilateral progressive SNHL + tinnitus | Vestibular schwannoma (acoustic neuroma) | MRI with gadolinium: enhancing CPA mass; ABR: prolonged I-V interpeak latency |
| Episodic vertigo + fluctuating SNHL + tinnitus + aural fullness | Ménière's disease | Clinical diagnosis; audiometry shows low-frequency SNHL during attack |
| Vesicles on pinna + facial palsy + ear pain | Ramsay Hunt syndrome (herpes zoster oticus) | Clinical diagnosis; vesicles in concha/EAC; can send VZV PCR of vesicle fluid |
| Foul-smelling discharge + CHL + retraction pocket | Cholesteatoma | Otoscopy + CT temporal bone (soft tissue mass with bony erosion) |
| Bilateral high-frequency SNHL in young person + haematuria | Alport syndrome | Family history, urinalysis (haematuria/proteinuria), renal biopsy (basket-weave GBM), genetic testing [3] |
These warrant urgent evaluation:
| Red Flag | Concern |
|---|---|
| Unilateral OME in adult (especially in HK) | NPC [2] |
| Sudden hearing loss (hours to days) | Sudden SNHL — cochlear stroke; ENT emergency |
| Cranial nerve palsies with ear pain/discharge | Necrotising OE (skull base osteomyelitis), cholesteatoma, NPC, malignancy |
| Facial palsy with ear vesicles | Ramsay Hunt — needs urgent antiviral + steroid |
| Post-auricular swelling pushing pinna forward | Acute mastoiditis — risk of intracranial complication |
| Blood-stained discharge from ear after head trauma | Temporal bone fracture → CSF otorrhoea risk |
| Progressive unilateral SNHL with poor speech discrimination | Acoustic neuroma — needs MRI |
| Persistent otalgia with normal otoscopy in a smoker/drinker | H&N malignancy — needs full ENT/H&N examination including nasopharyngoscopy [1][2] |
High Yield Summary
-
Murtagh's framework for ear pain [1]: Probability = AOM, OE, furunculosis, TMJ arthralgia, Eustachian tube dysfunction. Serious = neoplasia (ear, tongue, throat, NPC), Ramsay Hunt, mastoiditis, cholesteatoma, necrotising OE. Pitfalls = foreign body, wax, barotrauma, dental abscess, referred pain, unerupted wisdom tooth, chondrodermatitis nodularis helicis, glossopharyngeal neuralgia, post-tonsillectomy pain. Masquerades = depression, cervical spine dysfunction, factitious pain.
-
Normal otoscopy + ear pain in adult = REFERRED OTALGIA — systematically examine TMJ (CN V3), teeth (CN V3), throat/tonsils (CN IX), larynx/hypopharynx (CN X), cervical spine (C2/C3), nasopharynx (NPC).
-
Unilateral OME in adult in HK = NPC until proven otherwise.
-
Hearing loss DDx: CHL → external/middle ear (wax, OE, OME, AOM, otosclerosis, cholesteatoma); SNHL → cochlear (presbycusis, NIHL, Ménière's, ototoxicity, sudden SNHL) or retrocochlear (acoustic neuroma); Mixed → CSOM with labyrinthine extension, cholesteatoma, otosclerosis with cochlear involvement.
-
Tinnitus DDx [9]: Non-pulsatile = cochlear/SNHL pathology. Pulsatile = vascular (glomus tumour, AVM, carotid stenosis) or raised ICP (IIH).
-
Acoustic neuroma = unilateral progressive SNHL + tinnitus + poor speech discrimination → MRI with gadolinium.
-
Sudden SNHL = ENT emergency → urgent audiometry and steroids; MRI to exclude retrocochlear lesion.
Active Recall - Differential Diagnosis of Ear Pain and Hearing Loss
References
[1] Lecture slides: murtagh merge.pdf (p43–44, "Ear pain") [2] Senior notes: felixlai.md (Nasopharyngeal cancer section) [3] Senior notes: Ryan Ho Urogenital.pdf (p60, Alport Syndrome) [4] Senior notes: felixlai.md (Laryngeal carcinoma section) [7] Senior notes: Ryan Ho Neurology.pdf (p158, Idiopathic intracranial hypertension) [9] Lecture slides: murtagh merge.pdf (p96, "Tinnitus") [10] Senior notes: Ryan Ho Endocrine.pdf (p53, Paget's Disease of Bone)
Diagnostic Criteria, Algorithm and Investigations for Ear Pain and Hearing Loss
Most ear diagnoses are clinical — made by careful history and otoscopy. Formal "diagnostic criteria" exist only for select conditions. The key principle is: investigations are seldom necessary [1]. However, when they are needed, you must know exactly what to order and how to interpret the results.
1. Diagnostic Criteria for Key Conditions
AOM is a clinical diagnosis. There is no blood test or imaging that confirms it. The diagnosis rests on three pillars:
Definite AOM requires ALL of:
- Acute onset of symptoms (ear pain, irritability in infants, fever)
- Middle ear effusion — evidenced by any of:
- Bulging TM (best single predictor)
- Limited or absent TM mobility (pneumatic otoscopy)
- Air-fluid level or bubbles behind TM
- Otorrhoea not due to otitis externa
- Signs of middle ear inflammation — evidenced by any of:
- Distinct erythema of the TM
- Otalgia (ear pain that interferes with normal activity or sleep)
Why does the TM bulge? Because bacterial infection in the middle ear produces purulent exudate → positive pressure builds up in a closed space (Eustachian tube is already oedematous and blocked) → TM is pushed outward.
Diagnostic Tip
The pain of otitis media may be masked by fever in babies and young children [1]. In pre-verbal children, look for irritability, pulling at the ear, and feeding difficulty rather than relying on a pain history. Otoscopy is essential.
Distinguishing AOM from Otitis Media with Effusion (OME):
| Feature | AOM | OME |
|---|---|---|
| Acute symptoms (pain, fever) | Present | Absent or minimal |
| TM appearance | Bulging, erythematous, opaque | Retracted or neutral, dull, amber/grey; air-fluid level or bubbles |
| TM mobility | Reduced or absent | Reduced |
| Middle ear effusion | Yes (purulent) | Yes (serous/mucoid) |
| Treatment | ± Antibiotics | Watchful waiting; exclude NPC in adults |
No formal criteria exist. Diagnosis is clinical based on:
- Rapid onset (generally within 48 hours) of:
- Ear canal pain (otalgia), tenderness, fullness
- Tragal tenderness and/or pinna traction pain (distinguishes OE from middle ear pathology — in AOM, tragal pressure does NOT worsen pain because the inflammation is behind the TM, not in the canal)
- Otoscopic findings: diffuse EAC oedema, erythema, debris/discharge; TM may be obscured but is normal if visualised
- ± Hearing loss (if canal is significantly oedematous or occluded by debris)
Why is tragal tenderness specific to OE? Pressing the tragus compresses the anterior cartilaginous EAC wall inward against inflamed canal skin. In AOM, the canal skin is normal — it is the TM and middle ear mucosa that are inflamed, which are not affected by tragal pressure.
Suspect when:
- Severe, disproportionate otalgia in an elderly diabetic or immunocompromised patient
- Granulation tissue at the bone-cartilage junction of the EAC floor on otoscopy
- Failure to respond to standard OE treatment (topical antibiotics for >1–2 weeks)
- Cranial nerve involvement (CN VII earliest and most common, then IX, X, XI, XII — progressive skull base osteomyelitis)
- Elevated inflammatory markers: ESR > 70 mm/h, raised CRP
- Imaging confirmation: CT temporal bone (bony erosion); Tc-99m bone scan or Ga-67 scan (uptake at skull base); MRI for soft tissue extension
Why granulation tissue at the bone-cartilage junction? This is the fissures of Santorini — natural clefts in the cartilaginous floor of the EAC where soft tissue is in direct contact with the periosteum. Pseudomonas aeruginosa uses these gaps to spread from the soft tissue directly into the temporal bone periosteum, initiating osteomyelitis. The granulation tissue represents the body's attempt to wall off this advancing infection.
| Feature | Finding |
|---|---|
| Otoscopy | Retraction pocket (usually posterosuperior pars flaccida / attic region) filled with white keratinous debris; marginal or attic perforation; foul-smelling discharge |
| Audiometry | Conductive hearing loss (ossicular erosion); mixed loss if labyrinthine involvement |
| CT temporal bone | Soft tissue mass in middle ear/epitympanum/mastoid with bony erosion (scutum erosion is classic); look for tegmen erosion, lateral SCC fistula, facial canal dehiscence |
| MRI (DWI) | Non-echo-planar DWI distinguishes cholesteatoma (restricts diffusion — bright on DWI) from granulation tissue/inflammatory tissue; increasingly used for surgical planning and post-operative surveillance to detect residual/recurrent disease |
"Ménière" comes from Prosper Ménière, who first attributed vertigo to the inner ear rather than the brain.
Definite Ménière's disease:
- Two or more spontaneous episodes of vertigo, each lasting 20 minutes to 12 hours
- Audiometrically documented low-to-medium frequency sensorineural hearing loss in the affected ear on at least one occasion before, during, or after one of the episodes of vertigo
- Fluctuating aural symptoms (hearing loss, tinnitus, aural fullness) in the affected ear
- Not better accounted for by another vestibular diagnosis
Probable Ménière's disease:
- Two or more episodes of vertigo/dizziness lasting 20 min to 24 hours
- Fluctuating aural symptoms in the affected ear
- Not better accounted for by another diagnosis
Why low-to-medium frequency SNHL initially? Endolymphatic hydrops preferentially distorts the apical cochlea (which transduces low frequencies) because the membranous labyrinth is most distensible there. As disease progresses, higher frequencies are also affected.
- ≥30 dB sensorineural hearing loss in ≥3 contiguous audiometric frequencies within 72 hours
- This is a clinical definition used internationally (AAO-HNS 2019 guideline)
- Treated as an ENT emergency — analogous to a "cochlear stroke" because the labyrinthine artery is an end artery
No formal criteria set, but the diagnosis is made by the constellation of:
- Progressive conductive hearing loss (usually bilateral but asymmetric), young adult (20–40 years), more common in females
- Family history (autosomal dominant with variable penetrance)
- Normal otoscopy (TM and EAC look normal — the pathology is at the stapes footplate, invisible on otoscopy)
- Audiometry: conductive hearing loss with characteristic Carhart's notch (dip in bone conduction at 2 kHz)
- Tympanometry: Type As (reduced peak compliance / shallow peak) — because the stapes is fixed, the entire ossicular chain is stiffened, reducing TM compliance
- Absent stapedial reflex (the stapes cannot move, so no reflex contraction is recorded)
Why Carhart's notch at 2 kHz? It is NOT true sensorineural loss. The middle ear has a natural resonance around 2 kHz. Stapes fixation disrupts this resonance, causing an artefactual dip in bone conduction thresholds at that frequency. After successful stapes surgery, the notch disappears — confirming it was mechanical, not cochlear.
- MRI with gadolinium is the gold standard — shows an enhancing mass at the cerebellopontine angle (CPA) centred on the internal auditory meatus (IAM)
- Suspected when: unilateral progressive SNHL, unilateral tinnitus, disproportionately poor speech discrimination relative to pure-tone thresholds
- ABR: prolonged wave I–V interpeak latency (because the tumour compresses CN VIII, slowing neural conduction); sensitivity ~90% for tumours > 1 cm but misses small tumours → MRI preferred
The following algorithm systematises the clinical approach from presentation to diagnosis:
3. Investigation Modalities — Key Findings and Interpretations
3.1 Bedside Investigations
Inspect both empty ear canals and tympanic membrane (TM) with the auroscope using the largest possible earpiece [1]
Why the largest earpiece? A larger speculum provides a wider field of view for examining the EAC and TM. It also creates a better seal, which matters if you are using a pneumatic otoscope to assess TM mobility (essential for distinguishing AOM from OME).
| Finding | Interpretation | Underlying Pathophysiology |
|---|---|---|
| Erythematous, oedematous EAC with debris | Otitis externa | Infection/inflammation of canal skin; debris = desquamated epithelium + exudate |
| Granulation tissue at bone-cartilage junction | Necrotising OE | Osteomyelitis at fissures of Santorini; attempted healing with granulation |
| Bulging, erythematous, opaque TM | AOM | Purulent effusion under positive pressure pushing TM outward |
| Retracted TM with fluid level / bubbles behind | OME | Negative middle ear pressure (Eustachian tube dysfunction) → transudation |
| Central perforation with mucopurulent discharge | CSOM (tubotympanic / safe type) | Chronic infection through non-marginal perforation; "safe" because less risk of cholesteatoma |
| Marginal/attic perforation with keratin debris | Cholesteatoma (atticoantral / unsafe type) | Keratinising squamous epithelium in retraction pocket; "unsafe" because erodes bone |
| Vesicles on TM / concha | Ramsay Hunt or bullous myringitis | VZV reactivation (Ramsay Hunt) or viral/Mycoplasma infection (bullous myringitis) |
| Blue/dark TM | Haemotympanum | Blood in middle ear — trauma, basal skull fracture |
| White patches (tympanosclerosis) | Previous inflammation / healed AOM | Hyaline degeneration and calcification of the fibrous layer of TM |
| Normal TM | Does NOT exclude pathology — consider referred otalgia, otosclerosis, inner ear disease, retrocochlear pathology | The TM and EAC are normal in otosclerosis, SNHL, and all causes of referred otalgia |
- A sealed otoscope with a rubber bulb allows the examiner to apply positive and negative pressure against the TM
- Normal: TM moves freely with applied pressure
- Effusion (AOM/OME): TM mobility is reduced or absent because fluid behind the TM dampens movement
- Perforation: no seal can be maintained; air escapes through the hole
- Considered the most accurate bedside method for detecting middle ear effusion (sensitivity ~94% when performed correctly)
Already covered in prior sections but critical to include in the diagnostic algorithm:
| Test | Technique | Normal | CHL | SNHL |
|---|---|---|---|---|
| Rinne | Fork on mastoid then beside ear | AC > BC (positive) | BC > AC on affected side (negative) | AC > BC bilaterally (positive) |
| Weber | Fork on vertex | Midline | Lateralises to affected ear | Lateralises to better ear |
False negative Rinne: In severe unilateral SNHL ("dead ear"), bone conduction of the affected side is heard by the contralateral (good) cochlea via transcranial transmission → appears as BC > AC (falsely suggesting CHL). Weber test resolves this: lateralisation to the normal ear confirms SNHL, not CHL.
- Stand at arm's length (~60 cm) behind the patient, occlude and mask the non-test ear by rubbing the tragus
- Whisper a combination of numbers and letters; ask patient to repeat
- Normal: can repeat whispered voice at 60 cm (roughly equivalent to ~20–30 dB hearing threshold)
- Sensitivity ~80–90% for detecting moderate hearing loss; limited for mild loss
- Useful as a quick screening tool but NOT a substitute for formal audiometry
3.2 Audiological Investigations
Consider hearing tests, audiometry [1]
This is the gold standard for quantifying hearing loss and classifying it as conductive, sensorineural, or mixed.
Principle:
- Tones of specific frequencies (typically 250 Hz to 8000 Hz) are presented at increasing intensity
- Air conduction (AC): tested with headphones/earphones — sound travels through the whole pathway (external ear → middle ear → cochlea → CN VIII)
- Bone conduction (BC): tested with a bone vibrator on the mastoid process — sound bypasses the external and middle ear, directly stimulating the cochlea through skull bone vibration
Interpretation:
| Audiometric Pattern | Diagnosis | Explanation |
|---|---|---|
| Air-bone gap (AC thresholds worse than BC) | Conductive hearing loss | The conductive apparatus (EAC/middle ear) is impaired; the cochlea works normally, so BC is normal but AC is elevated |
| BC and AC both elevated, no air-bone gap | Sensorineural hearing loss | The cochlea or CN VIII is damaged; both routes deliver sound to the same damaged cochlea |
| Air-bone gap + elevated BC | Mixed hearing loss | Both conductive and sensorineural components present |
| 4 kHz notch (dip at 4 kHz, recovery at 8 kHz) | Noise-induced hearing loss | 4 kHz is the most vulnerable frequency due to EAC resonance amplification (~2.5 kHz) + middle ear transfer function pushing peak energy to 3–4 kHz; hair cells at this tonotopic region are preferentially destroyed |
| Carhart's notch (dip in BC at 2 kHz) | Otosclerosis | Artefactual — stapes fixation disrupts middle ear resonance at ~2 kHz; disappears after successful stapes surgery |
| Low-frequency SNHL | Ménière's disease (early) | Endolymphatic hydrops distorts the apical cochlea (low-frequency region) first |
| Bilateral symmetric high-frequency SNHL with gradual down-sloping | Presbycusis | Progressive loss of basal cochlear hair cells (high-frequency end) |
| Flat SNHL | Metabolic presbycusis (stria vascularis atrophy), autoimmune inner ear disease | Uniform cochlear damage |
| Asymmetric SNHL + poor speech discrimination | Retrocochlear (vestibular schwannoma) | Neural compression → disproportionate impairment of speech processing (which requires fine temporal coding) |
Speech Audiometry:
- Tests the ability to understand words at comfortable listening levels
- Speech discrimination score (SDS) / word recognition score: percentage of correctly repeated words
- Key interpretation: a disproportionately low SDS relative to the pure-tone average strongly suggests retrocochlear pathology (e.g., vestibular schwannoma) — because the tumour disrupts the neural coding needed for speech, beyond what pure-tone loss would predict
Principle: Measures the compliance (mobility) of the TM and middle ear system by varying air pressure in the sealed EAC and measuring sound reflected back from the TM. A compliant TM absorbs more sound (less reflection); a stiff TM reflects more.
| Tympanogram Type | Appearance | Interpretation | Pathology |
|---|---|---|---|
| Type A | Normal-shaped peak centred at 0 daPa | Normal middle ear function | Normal |
| Type As | Shallow/reduced peak height at 0 daPa | Reduced TM/ossicular compliance → stiff system | Otosclerosis, tympanosclerosis |
| Type Ad | Very tall/sharp peak at 0 daPa | Excessive TM/ossicular compliance → hypermobile system | Ossicular discontinuity, healed TM (thin scar) |
| Type B | Flat tracing, no identifiable peak | No TM mobility at any pressure | Middle ear effusion (OME, AOM), cerumen against probe, TM perforation (if high canal volume) |
| Type C | Peak shifted to negative pressure (< -100 daPa) | Negative middle ear pressure | Eustachian tube dysfunction (early OME, retracted TM) |
Why does effusion cause a flat (Type B) tympanogram? Fluid in the middle ear essentially eliminates the air space behind the TM. Without compressible air, the TM cannot vibrate regardless of the pressure applied — hence no compliance peak.
How to distinguish perforation from effusion on Type B? Look at the ear canal volume. If the TM is perforated, the probe "sees" the entire middle ear space → abnormally large canal volume. If the TM is intact with fluid behind it → normal or small canal volume.
Principle: Loud sound (70–100 dB above hearing threshold) triggers a bilateral contraction of the stapedius muscle (innervated by CN VII), stiffening the ossicular chain. This reflex is measured as a sudden change in TM impedance.
| Finding | Interpretation |
|---|---|
| Normal reflex thresholds | Normal middle ear and CN VII/VIII function |
| Absent reflexes ipsilaterally | Otosclerosis (stapes fixed → cannot move), severe CHL, severe SNHL |
| Elevated reflex thresholds | Retrocochlear pathology (acoustic neuroma — reflex decay test shows abnormal adaptation) |
| Reflex decay (reflex amplitude drops > 50% within 10 seconds) | Retrocochlear lesion — nerve fatigue from CN VIII compression; highly suggestive of acoustic neuroma |
Principle: Healthy outer hair cells (OHC) actively amplify sounds within the cochlea. As a byproduct, they generate tiny sounds that travel backward through the middle ear and can be detected by a sensitive microphone in the EAC. These are otoacoustic emissions.
| Type | Method | Clinical Use |
|---|---|---|
| Transient evoked OAE (TEOAE) | Brief click stimulus → records OHC response | Neonatal hearing screening (universal newborn screening); quick pass/fail |
| Distortion product OAE (DPOAE) | Two tones → records distortion product from OHC nonlinearity | Frequency-specific assessment of OHC function; monitoring ototoxicity |
| Finding | Interpretation |
|---|---|
| OAE present | Outer hair cells functional → cochlea likely normal (hearing loss, if present, is conductive or retrocochlear) |
| OAE absent | Outer hair cell dysfunction → cochlear SNHL; OR significant conductive loss blocking the emission from reaching the microphone |
| OAE present + abnormal ABR | Auditory neuropathy spectrum disorder — cochlea works (OHC intact) but neural transmission is disrupted |
Why are OAEs used for neonatal screening? Neonates cannot cooperate for behavioural audiometry. OAEs are objective, fast (~2 minutes), and non-invasive. If OAEs are absent, the baby is referred for ABR to confirm and characterise the hearing loss.
Principle: Clicks or tone bursts are delivered via earphones while surface electrodes on the scalp record electrical activity from the auditory pathway. Five characteristic waves (I–V) are generated from different anatomical stations:
| Wave | Anatomical Generator |
|---|---|
| I | Distal cochlear nerve (near cochlea) |
| II | Proximal cochlear nerve (near brainstem) |
| III | Cochlear nucleus (pons) |
| IV | Superior olivary complex (pons) |
| V | Lateral lemniscus / inferior colliculus (midbrain) |
| Finding | Interpretation |
|---|---|
| Normal ABR | Normal auditory pathway from cochlea to midbrain |
| Prolonged I–III interpeak latency | Lesion between distal nerve and pons → CN VIII pathology (acoustic neuroma) |
| Prolonged I–V interpeak latency | Retrocochlear pathology (acoustic neuroma, demyelination) |
| Absent waves | Severe SNHL, auditory neuropathy, brainstem death |
| Normal OAE + absent/abnormal ABR | Auditory neuropathy spectrum disorder (synaptopathy/neuropathy) |
Why is ABR used to screen for acoustic neuroma? The tumour compresses CN VIII → slows neural conduction → prolonged interpeak latencies. However, MRI is more sensitive for small tumours, so ABR is now primarily used for threshold estimation in infants and for detecting auditory neuropathy, rather than as the primary screening tool for acoustic neuroma.
3.3 Imaging
Indication: Cholesteatoma, mastoiditis, necrotising OE, temporal bone fracture, congenital anomalies, pre-operative planning
| Finding | Diagnosis |
|---|---|
| Soft tissue mass in epitympanum/mastoid with bony erosion (scutum blunting, ossicular erosion) | Cholesteatoma |
| Opacified mastoid air cells with loss of bony septae (coalescence) | Coalescent mastoiditis |
| Bony erosion of EAC floor / skull base | Necrotising OE |
| Fracture line through temporal bone | Temporal bone fracture (longitudinal vs. transverse vs. mixed) |
| Lucency around oval window (halo sign) | Otosclerosis (fenestral type) |
Longitudinal vs. transverse temporal bone fracture — why it matters:
- Longitudinal (~80%): fracture along the long axis of the petrous bone; typically spares the otic capsule → CHL (ossicular disruption, haemotympanum), EAC laceration, possible facial palsy (10–20%, often delayed/incomplete)
- Transverse (~20%): fracture across the petrous bone through the otic capsule → SNHL (cochlear damage), vertigo, facial palsy (50%, often immediate/complete), CSF otorrhoea
Indication: Suspected retrocochlear pathology (acoustic neuroma), intracranial complications of ear disease, cholesteatoma surveillance
| Sequence | Finding | Diagnosis |
|---|---|---|
| T1 + gadolinium | Enhancing CPA mass in IAM | Vestibular schwannoma |
| T1 + gadolinium | Enhancing middle cranial fossa / mastoid mass | Intracranial complication of cholesteatoma/mastoiditis |
| Non-echo-planar DWI | Restricted diffusion (bright) in middle ear/mastoid | Cholesteatoma (keratin restricts diffusion); distinguishes from granulation tissue |
| T2 / CISS sequence | High-resolution image of IAM and labyrinth; fluid-filled spaces appear bright | Endolymphatic hydrops (dilated endolymphatic space with gadolinium-enhanced MRI in Ménière's); labyrinthine anatomy |
| Scan | Indication | Finding |
|---|---|---|
| Tc-99m bone scan | Necrotising OE | Increased uptake at skull base — sensitive for osteomyelitis but not specific |
| Ga-67 scan | Necrotising OE — monitoring treatment response | Normalises with successful treatment (unlike Tc-99m which may remain positive due to ongoing bone remodelling); useful to determine when to stop antibiotics |
3.4 Other Investigations
Any ear discharge for MC but swabs of no value if the TM is intact [1]
Why are swabs useless with an intact TM? If the TM is intact, any swab from the EAC will only culture normal skin commensals (coagulase-negative staphylococci, diphtheroids, etc.) — not the causative organism in the middle ear. Swabs are only valuable when there is discharge, i.e., the TM is perforated or there is active OE.
| Scenario | Likely Organisms |
|---|---|
| Otitis externa | Pseudomonas aeruginosa (most common), S. aureus, fungi (Aspergillus, Candida) |
| AOM with perforated TM | S. pneumoniae, H. influenzae, M. catarrhalis |
| CSOM | Mixed flora: Pseudomonas, Proteus, S. aureus, anaerobes (Bacteroides, Peptostreptococcus) |
| Fungal OE (otomycosis) | Aspergillus niger (black spores), Candida (white/creamy) |
Indication: Unilateral OME in an adult (especially in Hong Kong) → must exclude NPC [2]
- Flexible nasopharyngolaryngoscopy: passed through the nose to visualise the nasopharynx, including the fossa of Rosenmüller, Eustachian tube orifices, and posterior choanae
- Any suspicious mass → biopsy for histology; send EBV VCA IgA and plasma EBV DNA [2]
| Test | When to Order | Interpretation |
|---|---|---|
| FBG / HbA1c | Severe OE or suspected necrotising OE | Undiagnosed diabetes; poor glycaemic control predisposes to necrotising OE |
| ESR / CRP | Necrotising OE, suspected malignancy, vasculitis | Markedly elevated in necrotising OE and GCA |
| EBV VCA IgA, plasma EBV DNA | Suspected NPC [2] | Elevated in NPC; used for screening and monitoring |
| Syphilis serology (VDRL/RPR, TPHA) | Unexplained SNHL, especially bilateral | Syphilis (congenital or acquired) can cause SNHL |
| TFTs | Unexplained SNHL, especially with goitre | Pendred syndrome (genetic SNHL + goitre due to defective pendrin/iodide transport) |
| Autoimmune panel (ANA, ESR, anti-68kD Ab) | Bilateral rapidly progressive SNHL in young patient | Autoimmune inner ear disease |
| Pure tone audiometry [3] | Alport syndrome suspected | Screen for SNHL; bilateral high-frequency SNHL [3] |
| Genetic testing | Family history of SNHL, Alport syndrome features | COL4A3-5 mutations [3]; connexin 26 (GJB2) for congenital SNHL |
- Universal newborn hearing screening (UNHS) is recommended for all neonates before 1 month of age
- Two-stage protocol: OAE screening → if fail, repeat → if fail again, diagnostic ABR by 3 months
- Goal: early identification → hearing aid fitting by 6 months → optimise speech/language development during the critical period
- High-risk factors for congenital SNHL: family history, NICU stay > 5 days, TORCH infections (especially CMV), hyperbilirubinaemia requiring exchange transfusion, craniofacial anomalies, ototoxic drug exposure
| Clinical Scenario | First-Line Investigation | Additional Investigations |
|---|---|---|
| Suspected AOM | Otoscopy (clinical diagnosis) | None routinely; investigations seldom necessary [1] |
| Otitis externa | Otoscopy (clinical diagnosis) | Swab MC&S if severe/refractory; FBG if suspect necrotising OE |
| Suspected necrotising OE | CT temporal bone + ESR/CRP + FBG | Tc-99m/Ga-67 bone scan; MRI for soft tissue |
| Unilateral OME in adult | Nasopharyngoscopy | EBV DNA/VCA IgA [2]; audiometry; CT nasopharynx |
| Hearing loss — any type | PTA + tympanometry | Guided by type (see algorithm above) |
| Suspected otosclerosis | PTA (CHL, Carhart's notch) + tympanometry (Type As) | CT temporal bone (fenestral lucency); stapedial reflex (absent) |
| Sudden SNHL | Urgent PTA | MRI with gadolinium (r/o acoustic neuroma); blood tests (FBC, ESR, glucose, syphilis, autoimmune) |
| Suspected acoustic neuroma | MRI with gadolinium | ABR; PTA with speech audiometry |
| Cholesteatoma | CT temporal bone | MRI DWI (residual/recurrent); audiometry |
| Ménière's disease | PTA (low-frequency SNHL) | Gadolinium-enhanced MRI (endolymphatic hydrops); electrocochleography |
| Congenital SNHL | OAE → ABR | Genetic testing (connexin 26, Pendred); TORCH serology; CT/MRI temporal bone |
High Yield Summary
-
Most ear diagnoses are clinical — made by history + otoscopy. Investigations are seldom necessary [1].
-
AOM diagnostic pillars: acute onset + middle ear effusion (bulging TM, reduced mobility) + middle ear inflammation (erythema, otalgia). Pneumatic otoscopy is the most accurate bedside tool for detecting effusion.
-
Audiometry interpretation: Air-bone gap = CHL; elevated AC and BC without gap = SNHL; both = mixed. Key patterns: 4 kHz notch (NIHL), Carhart's notch at 2 kHz (otosclerosis), low-frequency SNHL (early Ménière's), asymmetric SNHL with poor speech discrimination (acoustic neuroma).
-
Tympanometry types: A = normal; As = stiff (otosclerosis); Ad = hypermobile (ossicular discontinuity); B = flat (effusion or perforation — check canal volume to distinguish); C = negative pressure (Eustachian tube dysfunction).
-
Swabs: only useful if there is discharge — swabs of no value if the TM is intact [1].
-
Unilateral OME in Hong Kong adult → nasopharyngoscopy + EBV DNA to exclude NPC [2].
-
Sudden SNHL: defined as ≥30 dB in ≥3 frequencies within 72 hours. ENT emergency. Urgent PTA + MRI with gadolinium.
-
Acoustic neuroma workup: MRI with gadolinium (gold standard); ABR shows prolonged I–V interpeak latency; PTA shows asymmetric SNHL with disproportionately poor speech discrimination.
-
Necrotising OE: CT temporal bone (bony erosion) + Tc-99m/Ga-67 scan + ESR/CRP + blood glucose. Ga-67 scan is used to monitor treatment response.
-
Neonatal screening: OAE (outer hair cell function) → if fail → ABR (objective threshold estimation). Goal: identify by 1 month, diagnose by 3 months, intervene by 6 months.
Active Recall - Diagnosis of Ear Pain and Hearing Loss
References
[1] Lecture slides: murtagh merge.pdf (p43–44, "Ear pain") [2] Senior notes: felixlai.md (Nasopharyngeal cancer section) [3] Senior notes: Ryan Ho Urogenital.pdf (p57–60, Alport Syndrome)
Management of Ear Pain and Hearing Loss
The overarching management principle is: treat the underlying cause. Ear pain and hearing loss are symptoms, not diagnoses. Once you have identified the aetiology through history, otoscopy, and targeted investigations, treatment follows logically. This section systematically covers management of each major condition, organised from the most common to the most serious.
- Analgesia first — a patient in pain needs relief regardless of the underlying diagnosis. Simple analgesics (paracetamol, NSAIDs) while working up the cause [6].
- Treat the cause — antibiotics for bacterial infection, surgery for cholesteatoma, steroids for sudden SNHL, etc.
- Prevent complications — e.g., protecting the cornea in facial nerve palsy [11], early intervention for hearing loss in children.
- Rehabilitate hearing — hearing aids, cochlear implants, and communication support where hearing cannot be restored.
- Investigations are seldom necessary [1] for straightforward cases — avoid over-investigation.
3. Condition-Specific Management
3.1 External Ear Conditions
OE is one of the probability diagnoses [1] — you will see this constantly.
Principles of management:
| Step | Treatment | Rationale |
|---|---|---|
| 1. Analgesia | Paracetamol ± NSAIDs (e.g., ibuprofen) | Pain relief while treating the infection; NSAIDs also reduce canal inflammation |
| 2. Aural toilet | Microsuction or gentle dry mopping under direct vision (microscope or otoscope) | Removes debris, discharge, and desquamated epithelium → allows topical drops to contact infected skin; debris acts as a biofilm reservoir for bacteria |
| 3. Topical antibiotic ± steroid drops (1st-line) | Ciprofloxacin 0.3% + dexamethasone 0.1% (e.g., Ciprodex); OR neomycin + polymyxin B + hydrocortisone (e.g., Otosporin) | Topical route delivers high local drug concentration directly to the infection with minimal systemic side effects; steroid component ↓inflammation and oedema → ↓pain and restores canal patency |
| 4. Ear wick (if canal severely oedematous) | Pope wick or ribbon gauze wick inserted into the swollen EAC | The canal is too swollen for drops to penetrate → the wick draws topical medication deep into the canal by capillary action; removed/replaced after 48–72 hours when oedema subsides |
| 5. Oral antibiotics (only if spreading cellulitis) | Flucloxacillin (anti-staphylococcal) or ciprofloxacin (anti-pseudomonal) | Systemic antibiotics are NOT routinely needed for uncomplicated OE — the infection is localised to the canal skin; only indicated if there is periauricular cellulitis, fever, or immunocompromise |
Contraindications and cautions:
- Aminoglycoside-containing drops (e.g., gentamicin, neomycin): contraindicated if TM perforation is present or suspected → aminoglycosides are ototoxic and can damage cochlear hair cells if they enter the middle ear through a perforation. Use fluoroquinolone drops (ciprofloxacin/ofloxacin) instead, which are non-ototoxic.
- Avoid oral antibiotics routinely — promotes resistance without benefit in uncomplicated OE.
- Water precautions: advise patient to keep ears dry (cotton ball with petroleum jelly during showering, avoid swimming until resolved). Why? Water re-maceration of the canal skin perpetuates the infection cycle.
Otomycosis
If the discharge looks like wet newspaper with black spores (Aspergillus niger) or creamy white debris (Candida), the cause is fungal. Treat with topical antifungal: clotrimazole 1% solution or acetic acid 2% drops (acidifies the canal, creating a hostile environment for fungi). Antibacterial drops are ineffective and may worsen fungal OE by eliminating competing bacterial flora.
This is a serious disorder not to be missed [1]. Management is aggressive and prolonged.
| Step | Treatment | Rationale |
|---|---|---|
| 1. Admit to hospital | — | Life-threatening skull base osteomyelitis requiring IV therapy and monitoring |
| 2. Glycaemic control | Optimise blood glucose (insulin sliding scale if needed) | Hyperglycaemia impairs neutrophil function (chemotaxis, phagocytosis, oxidative killing); poor glycaemic control = poor outcomes |
| 3. Prolonged IV anti-pseudomonal antibiotics | IV ciprofloxacin OR IV piperacillin-tazobactam OR IV ceftazidime + IV ciprofloxacin; minimum 6–8 weeks total (IV → oral step-down with ciprofloxacin) | Pseudomonas aeruginosa is the causative organism in >95% cases; prolonged course needed because osteomyelitis requires weeks of antibiotic penetration into avascular bone |
| 4. Aural toilet | Regular microsuction under microscope | Removes granulation tissue and debris; improves local drug delivery |
| 5. Monitoring | Serial ESR/CRP; Ga-67 scan to assess treatment response | ESR normalisation indicates resolution; Ga-67 normalises with successful treatment (unlike Tc-99m which remains positive) → guides duration of therapy |
| 6. Surgical debridement | Rarely needed; reserved for extensive bony sequestration | Surgery in skull base is hazardous (CN VII, major vessels); prefer medical management |
Why NOT just oral ciprofloxacin alone? While ciprofloxacin has excellent oral bioavailability (~70–80%) and good bone penetration, the severity of skull base osteomyelitis with risk of CN palsies and death warrants initial IV therapy to ensure maximum drug levels. Oral step-down can follow once clinically improving.
Prognosis: Mortality ~10–20% even with treatment; CN VII palsy recovery is poor once established.
Boils and furuncles of canal [1] — a probability diagnosis.
| Treatment | Details |
|---|---|
| Oral antibiotics | Flucloxacillin 500 mg QDS for 7 days (targets S. aureus) |
| Analgesia | Paracetamol ± NSAIDs |
| Incision and drainage | If fluctuant/pointing abscess — relieves pressure immediately |
| Topical antibiotic drops | Adjunctive; same as for OE |
Why do furuncles only occur in the lateral EAC? Because hair follicles are present ONLY in the lateral (cartilaginous) third of the EAC. The medial (bony) two-thirds has no hair follicles and no ceruminous glands → furuncles cannot form there.
Herpes zoster — Ramsay Hunt syndrome [1] — a serious disorder not to be missed.
| Treatment | Details | Rationale |
|---|---|---|
| Oral antiviral | Valaciclovir 1g TDS for 7 days (or aciclovir 800 mg 5x/day for 7 days) | VZV reactivation in geniculate ganglion → antiviral limits viral replication and reduces nerve damage; valaciclovir preferred for better bioavailability |
| Oral corticosteroid | Prednisolone 1 mg/kg/day (max 60 mg) for 5 days, then taper | Reduces perineural inflammation and oedema within the bony fallopian canal → reduces compression of CN VII → improves chance of facial nerve recovery |
| Eye care [11] | Artificial tears, lubricating ointment at night, protective glasses/taping eyelid shut | Cornea is at risk due to poor eyelid closure and reduced tearing which may result in drying and abrasions [11]; CN VII palsy → lagophthalmos (inability to close eye) → corneal exposure |
| Analgesia | Paracetamol, NSAIDs; consider gabapentin/pregabalin for neuropathic pain | VZV causes neuropathic pain that may persist as post-herpetic neuralgia (PHN) |
Why is Ramsay Hunt worse than Bell's palsy? VZV directly destroys neural tissue (unlike Bell's palsy where inflammation causes conduction block without axonal destruction in most cases). Ramsay Hunt has a lower rate of complete facial nerve recovery (~50–70%) compared to Bell's palsy (~85–95%).
Contraindication: Do NOT give antivirals or steroids as monotherapy — combined treatment is superior. Steroids alone without antiviral cover may theoretically worsen viral replication (though this is debated).
Hard ear wax [1] — a pitfall often missed.
| Method | Details | Contraindications |
|---|---|---|
| Cerumenolytics (softening agents) | Olive oil drops, sodium bicarbonate drops, or commercial preparations (e.g., Cerumol) for 3–5 days before removal | None significant; avoid hydrogen peroxide if TM perforation suspected (fizzing in middle ear) |
| Ear syringing / irrigation | Warm water (~37°C) irrigated against the posterosuperior canal wall to flush wax out | Contraindicated if: (1) known/suspected TM perforation (water enters middle ear → infection), (2) previous ear surgery, (3) only hearing ear (risk of rare complication), (4) grommets in situ |
| Microsuction (preferred) | Suction under direct microscopic or otoscopic vision | Safest method; suitable even with perforation; requires equipment and training |
| Instrumentation | Jobson-Horne probe, wax hook — manual removal under direct vision | Requires skill; risk of canal trauma if patient moves |
Why warm water at body temperature for syringing? Cold or hot water stimulates the vestibular apparatus via caloric effect (cold water → inhibitory nystagmus toward that ear → vertigo/nausea; hot water → excitatory nystagmus). Water at ~37°C avoids this caloric stimulation.
Foreign bodies in ear [1] — a pitfall often missed, especially in children.
| Method | Details |
|---|---|
| Direct removal | Under otoscopic vision with wax hook, crocodile forceps, or suction. In children, may require general anaesthesia for cooperation |
| Syringing | Can be used for non-organic, non-hygroscopic objects. Avoid for organic material (e.g., seeds, peas) — they swell with water and become more impacted |
| Superglue technique | Blunt probe with cyanoacrylate glue touched to the object, allowed to set, then withdrawn — useful for smooth round objects (beads) |
| ENT referral | If impacted, unsuccessful attempts, or button battery (EMERGENCY — tissue necrosis within hours from alkaline leakage) |
Button Battery in Ear — Emergency!
A button battery in the EAC is a time-critical emergency. The battery generates an electrical current between its poles, creating an alkaline (NaOH) environment → liquefactive necrosis of surrounding tissue within 2 hours. Must be removed immediately. Do NOT irrigate (worsens alkaline injury). Do NOT delay for imaging.
3.2 Middle Ear Conditions
Otitis media (viral or bacterial) [1] — the most common probability diagnosis.
Key management principle: AOM is often self-limiting (viral or bacterial with spontaneous resolution). The question is: who needs antibiotics?
Step 1: Analgesia (ALL patients)
| Drug | Dose (paediatric example) | Notes |
|---|---|---|
| Paracetamol | 15 mg/kg/dose Q4–6H | First-line; safe and effective [6] |
| Ibuprofen | 10 mg/kg/dose Q6–8H | More effective for inflammatory pain; avoid if dehydrated (renal risk), GI issues, or aspirin-sensitive asthma [6] |
The pain of otitis media may be masked by fever in babies and young children [1] — so always consider AOM in a febrile, irritable child even without obvious ear-pulling.
Step 2: Antibiotics — Immediate vs. Watchful Waiting
| Scenario | Management | Rationale |
|---|---|---|
| Age < 6 months | Immediate antibiotics | Immature immune system; higher risk of complications |
| Age 6 months – 2 years with bilateral AOM | Immediate antibiotics | Bilateral disease = higher bacterial burden; poor spontaneous resolution |
| Age 6 months – 2 years with unilateral AOM, mild symptoms | Watchful waiting for 48–72 hours (safety-net prescription) | ~80% resolve spontaneously; avoid unnecessary antibiotic exposure |
| Age ≥ 2 years with non-severe symptoms | Watchful waiting for 48–72 hours | NNT for antibiotics = 20 (i.e., need to treat 20 children to benefit 1); self-resolution is the rule |
| Any age with severe symptoms (moderate-severe otalgia, fever ≥39°C, toxic-looking) | Immediate antibiotics | High risk of complications; unacceptable to wait |
| AOM with TM perforation (otorrhoea) | Immediate antibiotics (oral ± topical) | Perforation indicates significant middle ear pressure and infection |
| Recurrent AOM (≥3 episodes in 6 months or ≥4 in 12 months) | Consider prophylactic measures | Grommets (ventilation tubes); avoid antibiotic prophylaxis (promotes resistance) |
Antibiotic choices:
| Line | Drug | Dose | Duration | Notes |
|---|---|---|---|---|
| 1st-line | Amoxicillin | 80–90 mg/kg/day divided BD (high dose) | 5–10 days | Covers S. pneumoniae (most important pathogen); high dose overcomes intermediate penicillin resistance |
| 2nd-line (if no response in 48–72h or recent amoxicillin use) | Amoxicillin-clavulanate (Augmentin) | 90 mg/kg/day (amoxicillin component) divided BD | 10 days | Adds β-lactamase inhibitor → covers β-lactamase-producing H. influenzae and M. catarrhalis |
| Penicillin allergy (non-anaphylactic) | Cefuroxime axetil | 30 mg/kg/day divided BD | 10 days | 2nd-generation cephalosporin; ~1–2% cross-reactivity with penicillin allergy |
| Penicillin anaphylaxis | Azithromycin | 10 mg/kg day 1, then 5 mg/kg days 2–5 | 5 days | Macrolide; inferior coverage of S. pneumoniae but acceptable alternative |
Why high-dose amoxicillin? S. pneumoniae with intermediate penicillin resistance (MIC 2–4 μg/mL) can still be overcome by achieving high drug concentrations at the infection site. Standard-dose amoxicillin may not reach these levels in the middle ear fluid, but 80–90 mg/kg/day does. This is NOT full resistance — truly penicillin-resistant pneumococci (MIC ≥ 8) require different agents.
Eustachian tube dysfunction [1] is a related probability diagnosis.
| Step | Treatment | Rationale |
|---|---|---|
| 1. Watchful waiting (3 months) | Observation with serial audiometry | ~90% of OME resolves spontaneously within 3 months; intervention is only needed for persistent effusion with clinically significant hearing loss |
| 2. Autoinflation | Otovent balloon (blow up a balloon through the nose) | Actively opens the Eustachian tube by generating positive nasopharyngeal pressure; evidence supports modest benefit |
| 3. Grommet insertion (ventilation tubes / tympanostomy tubes) | Under GA (usually); small tube placed through myringotomy incision in anteroinferior TM quadrant | Bypasses the dysfunctional Eustachian tube → equalises middle ear pressure → allows fluid to drain → restores hearing. Grommets typically extrude spontaneously in 6–12 months |
| 4. Adenoidectomy (if recurrent OME with adenoid hypertrophy) | Removal of enlarged adenoid pad | Adenoid hypertrophy can mechanically obstruct the Eustachian tube orifice in the nasopharynx AND act as a bacterial reservoir; adenoidectomy reduces OME recurrence |
| NOT recommended | Antibiotics, oral/nasal steroids, antihistamines, decongestants | No sustained benefit for OME; antibiotics promote resistance without meaningful long-term resolution |
OME in Adults — Exclude NPC
In children, OME is overwhelmingly due to Eustachian tube immaturity and adenoid hypertrophy — benign and self-limiting. In adults, especially in Hong Kong, unilateral OME must prompt nasopharyngoscopy to exclude nasopharyngeal carcinoma [2]. NPC obstructs the Eustachian tube from the nasopharyngeal end. Never just "watch and wait" without examining the post-nasal space in an adult with unilateral effusion.
Grommet complications:
- Otorrhoea (~15–25%) — topical antibiotic drops (non-ototoxic, e.g., ciprofloxacin); NOT oral antibiotics
- Premature extrusion or blockage
- Residual perforation after extrusion (~2%)
- Tympanosclerosis (cosmetic, rarely affects hearing)
- Water precautions: surface swimming usually fine; diving and submerging the ear should be avoided (water through the grommet → middle ear infection)
| Step | Treatment | Rationale |
|---|---|---|
| 1. Aural toilet | Regular microsuction | Removes purulent discharge and biofilm; prerequisite for topical drops to work |
| 2. Topical antibiotic drops (non-ototoxic) | Ciprofloxacin 0.3% drops ± dexamethasone | Fluoroquinolone ear drops are first-line; safe with TM perforation (non-ototoxic); covers Pseudomonas and Gram-negatives common in CSOM |
| 3. Water precautions | Keep ear dry | Water carrying bacteria enters middle ear through the perforation → perpetuates infection |
| 4. Surgery (if refractory or complications) | Myringoplasty (TM repair) if dry and safe; Tympanoplasty (TM + ossicular reconstruction); Mastoidectomy if mastoid involved | Myringoplasty closes the perforation → restores middle ear seal → reduces infection risk and improves hearing |
Contraindication: Aminoglycoside drops (gentamicin, neomycin) are contraindicated in the presence of TM perforation due to ototoxicity risk — the drops can pass through the perforation → round window membrane → cochlea → hair cell destruction → SNHL.
Cholesteatoma [1] — a serious disorder not to be missed. Surgery is the definitive treatment — there is no medical cure.
| Treatment | Details | Rationale |
|---|---|---|
| Surgical excision (mainstay) | Mastoidectomy (canal wall up or canal wall down) ± tympanoplasty | Complete removal of keratinising squamous epithelium is essential; cholesteatoma is locally destructive and will erode bone if left untreated → CN VII palsy, labyrinthine fistula, intracranial complications |
| Canal wall up (CWU) mastoidectomy | Posterior canal wall preserved; better cosmesis; requires second-look surgery at 9–12 months | Higher recurrence/residual disease rate (~20–30%) because disease in the attic/posterior tympanum is harder to visualise with canal wall intact |
| Canal wall down (CWD) mastoidectomy | Posterior canal wall removed → open mastoid cavity (mastoid bowl) | Lower recurrence (~5–10%); easier surveillance; but requires lifelong aural toilet of the cavity; cannot get ear wet (swimming, bathing) |
| Ossicular reconstruction | Prosthesis or autograft (incus interposition) | Cholesteatoma typically erodes the incus long process first → ossicular discontinuity → CHL; reconstruction improves hearing |
| MRI DWI surveillance | Non-echo-planar DWI at 12 months post-op (especially after CWU) | Detects residual/recurrent cholesteatoma (restricts diffusion → bright on DWI) without need for re-exploration surgery |
Why is surgery mandatory? Cholesteatoma is not a tumour, but it behaves like one locally. The trapped keratinising squamous epithelium produces collagenases and cytokines that activate osteoclasts → progressive bone erosion. Without surgical removal, it will inevitably erode the ossicles, lateral SCC, facial nerve canal, or tegmen tympani → deafness, vertigo, facial palsy, or intracranial sepsis.
Acute mastoiditis [1] — a serious disorder not to be missed.
| Step | Treatment | Rationale |
|---|---|---|
| 1. Admit to hospital | — | Risk of intracranial complications (meningitis, brain abscess, sigmoid sinus thrombosis) |
| 2. IV antibiotics | IV amoxicillin-clavulanate or IV ceftriaxone ± metronidazole | Must cover S. pneumoniae, H. influenzae, S. pyogenes, and anaerobes; higher doses and IV route needed for bone/deep infection |
| 3. Myringotomy | Incision in TM to drain middle ear pus; send for MC&S | Relieves pressure; identifies causative organism for targeted therapy |
| 4. Cortical mastoidectomy | If subperiosteal abscess, intracranial complication, or failure to improve on IV antibiotics within 48 hours | Drains infected mastoid air cells; removes necrotic bone (coalescent mastoiditis); may be life-saving |
| 5. CT temporal bone | Pre-operative if complication suspected | Identifies abscess, bone destruction, intracranial extension |
3.3 Inner Ear and Sensorineural Conditions
This is a medical emergency. Think of it as a "cochlear stroke."
| Step | Treatment | Evidence / Rationale |
|---|---|---|
| 1. Urgent ENT referral + audiometry | Within 24–72 hours of onset | Delays > 2 weeks → significantly worse outcomes; time = hearing |
| 2. Systemic corticosteroids (1st-line) | Oral prednisolone 1 mg/kg/day (max 60 mg) for 10–14 days with taper; OR IV methylprednisolone if severe | Reduces cochlear inflammation and oedema; presumed mechanism: anti-inflammatory + immunomodulatory effect on inner ear; evidence from 2011 SSNHL trial supports steroids vs. placebo |
| 3. Intratympanic steroid injection | Dexamethasone 10–24 mg/mL injected through TM into middle ear → diffuses through round window membrane into cochlea | Achieves much higher perilymphatic steroid concentrations than systemic route; used as salvage therapy if systemic steroids fail (within 2–6 weeks), or as primary therapy if systemic steroids are contraindicated (e.g., diabetes, peptic ulcer, glaucoma) |
| 4. MRI with gadolinium | To exclude vestibular schwannoma | ~1–3% of sudden SNHL is caused by an acoustic neuroma; must be excluded |
| 5. Address modifiable factors | Blood glucose optimisation, cardiovascular risk factor management | Vascular aetiology (cochlear artery thrombosis) is one proposed mechanism |
What NOT to do:
- Do NOT prescribe antivirals (no proven benefit in idiopathic sudden SNHL despite viral aetiology being suspected)
- Do NOT delay treatment to await investigation results — start steroids immediately
- Hyperbaric oxygen therapy: some evidence supports it as adjunctive therapy within the first 2 weeks, but not widely available
Contraindications to systemic steroids: active infection (TB, untreated bacterial infection), uncontrolled diabetes (relative — can use with insulin cover), peptic ulcer disease, psychosis. In these cases → intratympanic steroids as primary therapy.
Ménière syndrome [9] — a probability diagnosis for tinnitus and important cause of episodic vertigo.
Management is stepwise — "escalation ladder":
| Step | Treatment | Mechanism / Rationale |
|---|---|---|
| 1. Lifestyle modification | Low-salt diet (< 1.5–2 g sodium/day); avoid caffeine, alcohol, stress; adequate hydration | Reducing sodium intake reduces endolymphatic fluid retention → ↓endolymphatic hydrops; caffeine/alcohol may worsen vestibular symptoms |
| 2. Betahistine (1st-line pharmacotherapy) | 16–48 mg TDS | Histamine H1 agonist and H3 antagonist → improves inner ear microcirculation → reduces endolymphatic hydrops; reduces frequency and severity of vertigo attacks |
| 3. Thiazide diuretics | Hydrochlorothiazide 25–50 mg daily | Reduces total body fluid volume → reduces endolymph production; evidence is modest |
| 4. Acute attack management | Prochlorperazine (vestibular sedative) or dimenhydrinate; short course only | Suppresses vestibular nucleus firing → reduces vertigo and nausea acutely; NOT for chronic use (delays vestibular compensation) |
| 5. Intratympanic corticosteroids | Dexamethasone injected through TM | Anti-inflammatory effect on inner ear; for refractory cases; preserves hearing |
| 6. Intratympanic gentamicin (chemical labyrinthectomy) | Low-dose gentamicin injected through TM → selectively destroys vestibular hair cells | Gentamicin is preferentially vestibulotoxic (more toxic to vestibular hair cells than cochlear); ablates vestibular function on that side → eliminates vertigo attacks; risk of SNHL (~20–30%) |
| 7. Endolymphatic sac decompression | Surgical decompression of endolymphatic sac | Aims to improve endolymph drainage; variable outcomes; hearing-preserving |
| 8. Labyrinthectomy (last resort) | Surgical destruction of entire labyrinth | Eliminates vertigo but causes total ipsilateral hearing loss → only if hearing already very poor |
| 9. Vestibular neurectomy | Selective section of vestibular portion of CN VIII | Eliminates vertigo while preserving hearing; major neurosurgical procedure |
Why betahistine? The name breaks down as "beta-histine" — it is a structural analogue of histamine. It acts as an H1 agonist (vasodilation of inner ear blood vessels → improved cochlear blood flow) and an H3 antagonist (H3 receptors are presynaptic autoreceptors on histaminergic neurons; blocking them ↑histamine release → further vasodilation). The net effect is improved inner ear microcirculation and reduced endolymphatic pressure.
Acoustic neuroma (unilateral) [9] — a serious disorder not to be missed for tinnitus.
| Option | Indication | Details |
|---|---|---|
| Observation ("watch, wait, and scan") | Small tumours (< 1–1.5 cm), elderly patients, minimal symptoms | Serial MRI every 6–12 months; ~50% of small tumours show no significant growth over 5 years |
| Microsurgery | Large tumours (> 2.5–3 cm), brainstem compression, young patients, serviceable hearing | Approaches: translabyrinthine (sacrifices hearing), retrosigmoid/suboccipital (hearing preservation possible), middle fossa (small tumours with good hearing). Risk: CN VII injury (~10–30% depending on tumour size) |
| Stereotactic radiosurgery (SRS) | Small-medium tumours (< 2.5–3 cm), elderly/comorbid patients, patient preference | Gamma Knife or CyberKnife; single-fraction high-dose radiation → stops tumour growth in ~90–95%; hearing preservation ~50–70% at 5 years; lower CN VII risk than surgery |
Sensorineural hearing loss (esp. noise induced) [9] — a probability diagnosis for tinnitus.
| Step | Management | Rationale |
|---|---|---|
| Prevention (most important) | Hearing protection (earplugs, earmuffs), noise exposure limits (< 85 dB for 8 hours), regular audiometric screening for at-risk workers | Damaged cochlear hair cells do NOT regenerate in humans; prevention is the ONLY way to avoid permanent NIHL |
| Hearing aids | For established NIHL with communication difficulty | Amplifies sound to compensate for hair cell loss; modern digital aids can target the 4 kHz region specifically |
| Occupational health | Noise surveys, workplace modifications, legal compensation | Hong Kong: employees with NIHL may claim compensation under the Employees' Compensation Ordinance |
Ageing [9] — a probability diagnosis for tinnitus and the most common cause of SNHL.
| Step | Management | Rationale |
|---|---|---|
| Hearing aids (mainstay) | Behind-the-ear (BTE), receiver-in-canal (RIC), or completely-in-canal (CIC) aids | Amplification compensates for hair cell loss; digital aids can be programmed to the patient's audiogram; evidence links untreated hearing loss to cognitive decline, social isolation, and depression |
| Communication strategies | Face the speaker, reduce background noise, lip-reading, assistive listening devices | Complements hearing aid use; patients with presbycusis struggle most in noisy environments |
| Cochlear implant | If bilateral severe-to-profound SNHL with limited benefit from hearing aids (speech discrimination < 50%) | Bypasses damaged hair cells entirely → directly stimulates spiral ganglion neurons; highly effective even in elderly patients |
| Aural rehabilitation | Audiology follow-up, hearing aid adjustment, counselling | Ensures optimal device use; addresses psychosocial impact |
| Step | Management | Details |
|---|---|---|
| 1. Observation | If mild, asymptomatic CHL | Not all patients require intervention |
| 2. Hearing aid | Non-surgical option for CHL | Amplification overcomes the conductive deficit; appropriate for patients who decline surgery or have surgical contraindications |
| 3. Stapedotomy / Stapedectomy (definitive) | Stapedotomy (preferred): laser fenestration of stapes footplate + prosthesis from incus to oval window; Stapedectomy: removal of stapes superstructure + prosthesis | Bypasses the fixed stapes → restores sound transmission to the cochlea; success rate ~90–95% for closing air-bone gap; stapedotomy has lower complication rate than full stapedectomy |
| 4. Sodium fluoride (controversial) | May slow otosclerotic bone remodelling | Promotes mineralisation of spongiotic bone → may prevent progression; limited evidence; not widely used |
Surgical complications:
- SNHL (< 1% — most feared; damage to inner ear during footplate manipulation)
- Vertigo (transient, common; persistent if perilymph fistula)
- Tinnitus (may improve or worsen)
- Facial nerve injury (rare; nerve dehiscence over oval window in some patients)
- Reparative granuloma
- Prosthesis displacement
Contraindications to surgery:
- Only hearing ear (relative — risk of total deafness is unacceptable)
- Active middle ear infection
- Patient unable to tolerate general/local anaesthesia
Since referred otalgia accounts for a substantial proportion of adult otalgia [1], management targets the underlying cause:
| Source | Management |
|---|---|
| TMJ arthralgia [1] | Occlusal splint (bite guard) worn at night → reduces bruxism-related TMJ stress; jaw physiotherapy; soft diet; NSAIDs; referral to oral and maxillofacial surgery if refractory |
| Dental abscess / unerupted wisdom tooth [1] | Dental referral → extraction, root canal treatment, or incision and drainage as appropriate |
| Tonsillitis [1] | Penicillin V or amoxicillin for bacterial tonsillitis (Group A Strep); paracetamol/NSAIDs; tonsillectomy if recurrent (≥7 episodes/year, or ≥5/year for 2 years, or ≥3/year for 3 years) |
| Nasopharyngeal carcinoma [2] | Concurrent chemoradiotherapy (cisplatin-based) — NPC is highly radiosensitive; staging with PET-CT; EBV DNA monitoring; surgical salvage for recurrence |
| Laryngeal carcinoma [4] | Depends on stage: early glottic (T1–T2) → radiotherapy or laser cordectomy; advanced → surgery (laryngectomy) + adjuvant chemoradiotherapy |
| Cervical spine dysfunction [1] | Physiotherapy (mobilisation, exercises); NSAIDs; cervical collar (short-term); referral to musculoskeletal specialist if persistent |
| Glossopharyngeal neuralgia [1] | Carbamazepine or oxcarbazepine (same approach as trigeminal neuralgia — membrane-stabilising antiepileptic drugs that ↓neuronal firing); microvascular decompression if refractory |
| Post-tonsillectomy pain [1] | Expected; regular paracetamol ± NSAIDs (note: some surgeons avoid NSAIDs post-tonsillectomy due to bleeding risk — this is debated); reassurance |
| Depression [1] | Antidepressants (SSRIs), CBT, psychological support; address underlying pain amplification |
| Hearing Loss Type | Mild–Moderate | Severe–Profound |
|---|---|---|
| CHL | Hearing aid; treat underlying cause (e.g., grommet for OME, surgery for otosclerosis) | Bone-anchored hearing aid (BAHA) if conventional aid inadequate or canal/ear unsuitable |
| SNHL | Hearing aid (standard) | Cochlear implant (CI) — bypasses damaged hair cells; directly stimulates spiral ganglion neurons |
| Mixed | Address conductive component first (surgery if possible), then hearing aid for residual SNHL | CI ± middle ear surgery |
| Unilateral total deafness | CROS hearing aid (contralateral routing of signal) or BAHA on deaf side → routes sound to the hearing ear | — |
| Children | Early intervention: hearing aid fitting by 6 months of age; speech therapy; educational support; cochlear implant by 12 months if profound bilateral SNHL | CI ideally before age 2 (during critical period for auditory cortex development) |
| Condition | Key Management | Critical Points |
|---|---|---|
| OE | Aural toilet + topical abx/steroid drops | No aminoglycoside drops if perforation; ear wick if swollen; water precautions |
| Necrotising OE | Prolonged IV anti-pseudomonal antibiotics + glycaemic control | Minimum 6–8 weeks; Ga-67 scan for treatment monitoring |
| AOM | Analgesia ± antibiotics (amoxicillin 80–90 mg/kg/day) | Watchful waiting in >2y with mild symptoms; immediate abx if < 6m, bilateral, severe, or perforated |
| OME | Watchful waiting → grommets if persistent > 3 months with hearing impact | Exclude NPC in adults with unilateral OME [2] |
| CSOM | Aural toilet + topical ciprofloxacin drops; surgery if refractory | No aminoglycoside drops (ototoxic through perforation) |
| Cholesteatoma | Surgery (mastoidectomy ± tympanoplasty) — no medical cure | Mandatory surgical removal; MRI DWI for surveillance |
| Mastoiditis | IV antibiotics ± cortical mastoidectomy | Myringotomy for drainage and culture |
| Ramsay Hunt | Valaciclovir + prednisolone + eye care [11] | Worse prognosis than Bell's palsy for facial nerve recovery |
| Sudden SNHL | URGENT systemic steroids ± intratympanic salvage; MRI to r/o acoustic neuroma | ENT emergency; do not delay treatment |
| Ménière's | Stepwise: low-salt diet → betahistine → diuretics → intratympanic therapy → surgery | Betahistine is 1st-line pharmacotherapy; intratympanic gentamicin for refractory cases |
| Acoustic neuroma | Observation / microsurgery / stereotactic radiosurgery | Based on tumour size, patient age, hearing status |
| Otosclerosis | Hearing aid or stapedotomy | Stapedotomy: ~90–95% success; risk of SNHL < 1% |
| Presbycusis / NIHL | Hearing aids; prevention for NIHL | Hair cells do not regenerate; untreated hearing loss → cognitive decline |
High Yield Summary
-
OE management: aural toilet + topical antibiotic-steroid drops (ciprofloxacin/dexamethasone). Use an ear wick if canal is too swollen. NEVER use aminoglycoside drops if TM perforation is present or suspected — ototoxic.
-
AOM antibiotics: not always needed. Watchful waiting for ≥2 years with mild symptoms. When indicated → high-dose amoxicillin (80–90 mg/kg/day) to overcome intermediate pneumococcal resistance. Augmentin if no response in 48–72h.
-
Cholesteatoma requires surgery — no medical cure. Mastoidectomy (CWU vs CWD) ± tympanoplasty. MRI DWI for post-op surveillance.
-
Sudden SNHL is an ENT emergency: oral prednisolone 1 mg/kg immediately; intratympanic dexamethasone as salvage; MRI to exclude acoustic neuroma. Do not delay for investigations.
-
Ménière's disease: stepwise escalation — diet → betahistine → diuretics → intratympanic steroids → intratympanic gentamicin → surgery.
-
Betahistine: H1 agonist + H3 antagonist → improves inner ear microcirculation → reduces endolymphatic hydrops.
-
Ramsay Hunt: combined valaciclovir + prednisolone + eye care. Worse prognosis than Bell's palsy (~50–70% vs ~85–95% recovery).
-
Grommets for OME: only if persistent > 3 months with hearing impact. In adults, exclude NPC before attributing unilateral OME to benign Eustachian tube dysfunction [2].
-
Hearing rehabilitation: hearing aids for mild-severe SNHL; cochlear implant for bilateral profound SNHL (ideally before age 2 in children). BAHA for unilateral deafness or unsuitable ears.
-
Button battery in ear = emergency removal — liquefactive necrosis within 2 hours. Do NOT irrigate.
Active Recall - Management of Ear Pain and Hearing Loss
References
[1] Lecture slides: murtagh merge.pdf (p43–44, "Ear pain") [2] Senior notes: felixlai.md (Nasopharyngeal cancer section) [4] Senior notes: felixlai.md (Laryngeal carcinoma section) [6] Senior notes: Ryan Ho Respiratory.pdf (p49, Acute Coryza — management of symptomatic treatment) [9] Lecture slides: murtagh merge.pdf (p96, "Tinnitus") [11] Senior notes: felixlai.md (Bell's palsy / facial nerve palsy — treatment section)
Complications of Ear Pain and Hearing Loss Conditions
Complications in otology are best understood by following the anatomical paths of spread — infection and disease propagate along paths of least resistance: through natural bony dehiscences, along blood vessels, through the Eustachian tube, across the tegmen tympani into the middle cranial fossa, or posteriorly into the mastoid and sigmoid sinus. Understanding the anatomy explains every complication from first principles.
1. Complications of Otitis Externa
Most OE resolves with topical treatment without significant complications. However:
| Complication | Mechanism | Clinical Features |
|---|---|---|
| Chronic/recurrent OE | Inadequate treatment, persistent moisture exposure, underlying eczema/psoriasis → chronic inflammation → EAC skin thickening and stenosis | Persistent pruritus, discharge; narrowed EAC on otoscopy; hearing loss if severe stenosis |
| EAC stenosis | Chronic inflammation → fibrosis and cicatricial narrowing of the canal | Progressive CHL; difficulty fitting hearing aids; requires surgical canalplasty if severe |
| Myringitis (TM involvement) | Direct spread of infection from EAC skin to the outer squamous layer of the TM | Pain, bullae on TM (bullous myringitis); bloody discharge if bullae rupture |
| Perichondritis → auricular cartilage necrosis | Infection spreads from EAC skin to adjacent auricular perichondrium; cartilage is avascular (relies on perichondrium for blood supply) → compromised perichondrium → cartilage ischaemia → necrosis | Red, swollen, tender pinna (sparing lobule); if untreated → "cauliflower ear" deformity from cartilage destruction and fibrosis |
This is where OE becomes life-threatening. Necrotising otitis externa [1] is a serious disorder for a reason — it spreads along the skull base.
| Complication | Mechanism | Clinical Features |
|---|---|---|
| Skull base osteomyelitis | Pseudomonas invades from the EAC soft tissue through the fissures of Santorini → temporal bone periosteum → progressive osteomyelitis spreading along the skull base | Severe deep pain disproportionate to exam findings; elevated ESR > 70; CT shows bony erosion |
| Facial nerve palsy (CN VII) — most common CN involved | CN VII runs through the stylomastoid foramen adjacent to the inferior EAC; infection at the skull base reaches the nerve early | Ipsilateral LMN facial palsy; inability to close eye, droop of mouth. Poor prognostic indicator |
| Other cranial nerve palsies (IX, X, XI, XII) | Progressive skull base osteomyelitis extends medially to the jugular foramen (CN IX, X, XI) and hypoglossal canal (CN XII) | Dysphagia and dysphonia (IX, X); shoulder weakness (XI); tongue deviation (XII); multiple CN palsies = very poor prognosis |
| Contralateral spread | Infection crosses the midline via the clivus or petrous apex | Bilateral CN palsies; extremely rare but devastating |
| Meningitis / intracranial abscess | Osteomyelitis erodes through the skull base into the posterior or middle cranial fossa | Headache, fever, meningism, altered consciousness; CT/MRI shows meningeal enhancement or abscess |
| Sigmoid sinus thrombosis | Infection adjacent to the sigmoid sinus → venous wall inflammation → thrombosis | Severe headache, fever, raised ICP signs; MRV demonstrates non-filling of sigmoid sinus |
| Death | Multi-organ sepsis or intracranial complications | Mortality ~10–20% even with aggressive treatment; higher if cranial nerves are involved at presentation |
Why is CN VII affected first? The facial nerve exits the skull through the stylomastoid foramen, which is located just posterior to the tympanic bone — very close to the floor of the EAC and the fissures of Santorini where Pseudomonas first invades bone. Geographically, it is the nearest cranial nerve to the primary infection site.
2. Complications of Acute Otitis Media (AOM)
AOM is the commonest cause of ear pain in children [1] [6]. While most episodes are self-limiting, complications arise when infection is uncontrolled and spreads beyond the middle ear cavity.
| Complication | Mechanism | Clinical Features |
|---|---|---|
| TM perforation | Purulent middle ear effusion under positive pressure → ischaemic necrosis of the TM → spontaneous rupture | Sudden pain relief (pressure released) + purulent otorrhoea; most acute perforations heal spontaneously within weeks |
| Acute mastoiditis [1] | Infection spreads from the middle ear through the aditus ad antrum to the mastoid air cells → suppuration → destruction of bony septae between air cells (coalescent mastoiditis) | Post-auricular erythema, swelling, tenderness; pinna displaced anteroinferiorly; a serious disorder not to be missed [1] |
| Subperiosteal abscess | Coalescent mastoiditis → pus erodes through the mastoid cortex (usually the lateral cortex) → accumulates between bone and periosteum | Fluctuant, tender post-auricular mass; pinna pushed forward and outward; requires surgical drainage |
| Petrous apicitis (Gradenigo syndrome) | Infection extends from mastoid to petrous apex → inflammation near Dorello's canal (CN VI) and trigeminal ganglion (CN V) | Classic triad: (1) retro-orbital pain (CN V1), (2) CN VI palsy (lateral rectus palsy → diplopia with abduction deficit), (3) otorrhoea/middle ear infection. Rare but important for exams |
| Facial nerve palsy | CN VII runs through the middle ear in its tympanic (horizontal) segment, often with bony dehiscence in ~30% of the population; AOM → oedema and inflammation compress the nerve within its bony canal | Ipsilateral LMN facial weakness during or after an episode of AOM; usually resolves with adequate treatment of the infection (antibiotics + myringotomy) |
| Labyrinthitis | Infection spreads from the middle ear into the inner ear via the round window membrane or through a labyrinthine fistula | Severe vertigo, nystagmus, SNHL, nausea/vomiting during or after AOM; the triad of middle ear infection + vertigo + hearing loss |
| Bezold's abscess | Pus tracks from the mastoid tip inferiorly, breaking through the medial surface of the tip along the insertion of the sternocleidomastoid and posterior belly of digastric → deep neck space infection | Neck mass below and behind the ear along the SCM; torticollis (head tilted toward the abscess); fever; deep neck tenderness |
Why does mastoiditis cause the pinna to be pushed forward? The subperiosteal abscess forms on the lateral cortex of the mastoid process, which sits BEHIND the pinna. The expanding collection pushes the overlying pinna anteriorly, inferiorly, and laterally. This is a classic clinical sign.
These are the most feared complications of AOM/mastoiditis. They arise because the middle ear and mastoid are separated from the middle and posterior cranial fossae by only thin bone (tegmen tympani) — and in some individuals this bone has natural dehiscences.
| Complication | Mechanism | Clinical Features |
|---|---|---|
| Meningitis | Most common intracranial complication; infection spreads through the tegmen tympani or through pre-formed pathways (eg. labyrinthine windows, bony dehiscences, or haematogenous) → subarachnoid space infection | Headache, fever, neck stiffness, photophobia, positive Kernig's/Brudzinski's signs; LP: ↑WCC, ↑protein, ↓glucose, positive Gram stain/culture |
| Epidural abscess | Infection erodes through the tegmen → pus accumulates between dura and bone | May be clinically silent (discovered incidentally on CT); or headache, low-grade fever; usually found during mastoidectomy |
| Subdural empyema | Infection penetrates the dura → pus in the subdural space | Rapidly progressive: high fever, headache, altered consciousness, seizures, focal neurological deficits; neurosurgical emergency |
| Brain abscess | Haematogenous spread or direct extension → parenchymal infection, most commonly in the temporal lobe (adjacent to tegmen) or cerebellum (adjacent to posterior fossa/sigmoid sinus area) | Headache, fever, focal neurological signs (depending on location), raised ICP; CT/MRI: ring-enhancing lesion with surrounding oedema |
| Sigmoid/lateral sinus thrombosis | Infection from the mastoid (which abuts the sigmoid sinus plate) → venous wall inflammation → thrombophlebitis → thrombosis of the sigmoid or lateral sinus | "Picket fence" fever (spiking, swinging); headache; raised ICP (impaired venous drainage); Griesinger's sign (oedema over the mastoid emissary vein); papilloedema; MRV: non-filling of sinus |
| Otitic hydrocephalus | Sigmoid/lateral sinus thrombosis → impaired CSF absorption (CSF drains via the arachnoid granulations into the venous sinuses, mainly the superior sagittal sinus; major lateral/sigmoid sinus thrombosis, especially if on the dominant side, impairs overall venous outflow → raised ICP) | Headache, papilloedema, CN VI palsy (false localising sign from raised ICP stretching CN VI over petrous apex); normal brain parenchyma on imaging |
Why temporal lobe abscess from ear disease? The tegmen tympani — the thin bony plate forming the roof of the middle ear — is also the floor of the middle cranial fossa. The temporal lobe sits directly above it. Infection eroding through the tegmen has immediate access to the temporal lobe.
Why cerebellar abscess from ear disease? The posterior wall of the mastoid is the anterior wall of the posterior fossa. The sigmoid sinus plate separates the mastoid from the cerebellum. Erosion through this bone or septic emboli from sigmoid sinus thrombophlebitis can seed the cerebellum.
Classic Exam Question — Route of Intracranial Spread
Middle ear infection → intracranial complication routes:
- Upward through tegmen tympani → middle cranial fossa → epidural abscess / temporal lobe abscess / meningitis
- Posteriorly through sigmoid sinus plate → posterior fossa → cerebellar abscess / sigmoid sinus thrombosis
- Medially through labyrinthine windows → labyrinthitis → meningitis (via IAM and cochlear aqueduct)
- Haematogenous via diploic or emissary veins → brain abscess at any location
CSOM can produce all the same intracranial complications as AOM, but typically more insidiously. The key distinction is that CSOM is divided into:
- Safe (tubotympanic) type: central perforation, mucosal disease → lower complication rate
- Unsafe (atticoantral) type: marginal/attic perforation, often with cholesteatoma [1] → higher complication rate
| Complication | Mechanism |
|---|---|
| Conductive hearing loss | Persistent TM perforation (↓surface area for sound collection) + chronic mucosal inflammation → ossicular erosion (incus long process most vulnerable) |
| Tympanosclerosis | Chronic inflammation → hyaline degeneration and calcification of TM fibrous layer and middle ear mucosa; may fix ossicles → CHL |
| Cholesterol granuloma | Chronic OME → haemorrhage → cholesterol crystals released from lysed RBCs → foreign body giant cell reaction → granuloma; appears as blue/dark mass behind TM |
| All intracranial complications (as above) | Same pathways as AOM but with a more chronic, smouldering course |
Cholesteatoma [1] is essentially a complication factory. The keratinising squamous epithelium produces collagenases and activates osteoclasts, causing relentless bone erosion in all directions.
| Structure Eroded | Complication | Clinical Features |
|---|---|---|
| Ossicles (incus long process first, then stapes superstructure, then malleus) | Progressive conductive hearing loss | Worsening CHL over months/years; audiometry shows increasing air-bone gap |
| Lateral semicircular canal | Labyrinthine fistula → vertigo | Episodic or positional vertigo; positive fistula test (pressure applied to EAC via pneumatic otoscope → vertigo and nystagmus); Hennebert sign. SNHL may co-occur if cochlea is involved → mixed hearing loss |
| Facial nerve canal (tympanic or mastoid segment) | Facial nerve palsy | Gradual onset LMN facial palsy; cholesteatoma is the most common cause of facial palsy in chronic ear disease. Urgent surgical exploration required |
| Tegmen tympani (roof of middle ear/mastoid) | Meningitis, epidural abscess, temporal lobe abscess | As described above for AOM intracranial complications; more insidious onset |
| Sigmoid sinus plate | Sigmoid sinus thrombosis, cerebellar abscess | As above |
| Cochlea | Sensorineural hearing loss | Irreversible damage to cochlear structures; combined with ossicular CHL → mixed HL |
| Dural plate | CSF leak (otorrhoea) | Clear, watery discharge; β2-transferrin positive in CSF [12]; risk of ascending meningitis |
Why is the incus eroded first? The incus long process is the thinnest, most vulnerable part of the ossicular chain and it sits in the direct path of cholesteatoma expansion in the posterosuperior retraction pocket/attic. It also has a tenuous blood supply — the lenticular process (tip connecting to stapes) is supplied by a single end artery.
Mastoiditis is itself a complication of AOM, but it can further complicate into:
| Complication | Mechanism |
|---|---|
| Subperiosteal abscess | Pus erodes through lateral mastoid cortex → collection between bone and periosteum |
| Bezold's abscess | Pus tracks through mastoid tip → deep to SCM into the neck |
| Citelli's abscess | Pus tracks through the digastric groove → posterior triangle of neck |
| Luc's abscess | Pus tracks superiorly through the zygomatic root → temporal fossa |
| All intracranial complications | As described above — meningitis, brain abscess, sigmoid sinus thrombosis, epidural/subdural collections |
Herpes zoster — Ramsay Hunt syndrome [1].
| Complication | Mechanism | Prognosis |
|---|---|---|
| Permanent facial nerve palsy | VZV causes axonal degeneration (not just oedema/conduction block as in Bell's palsy) within the bony fallopian canal → wallerian degeneration → incomplete reinnervation | Complete recovery in only ~50–70% (vs ~85–95% in Bell's palsy); worse if treatment delayed > 72 hours |
| Sensorineural hearing loss | VZV spreads from geniculate ganglion of CN VII to CN VIII (cochlear component) in the IAM — the two nerves run together | May be permanent; high-frequency loss most common |
| Vestibular dysfunction | VZV involves the vestibular component of CN VIII | Acute vertigo; most patients compensate centrally over weeks–months |
| Post-herpetic neuralgia (PHN) | Chronic neuropathic pain from damaged sensory neurons in the geniculate ganglion; aberrant neural remodelling after acute inflammation | Burning, lancinating ear pain persisting > 3 months after acute episode; more common in elderly |
| Synkinesis (aberrant reinnervation) | Following severe axonal damage, regenerating fibres may take wrong paths → involuntary movements accompanying voluntary ones | Eg. mouth twitches when blinking (ocular-oral synkinesis); "crocodile tears" (gustatory lacrimation) — salivatory fibres regenerate into lacrimal pathways |
| Corneal complications | CN VII palsy → lagophthalmos → corneal exposure → corneal drying and abrasions [11] → ulceration → perforation if severe | Requires aggressive eye care: artificial tears, lubricant ointment, taping eyelid shut at night; gold weight implant if chronic [11] |
Hearing loss itself — regardless of aetiology — has profound secondary consequences. These are frequently underappreciated.
| Complication | Mechanism | Population Most Affected |
|---|---|---|
| Speech and language delay | Hearing is essential for auditory feedback during speech development; the critical period for language acquisition is 0–3 years; deprivation during this window causes irreversible deficits | Children with congenital or early-onset SNHL; this is why neonatal hearing screening and early intervention by 6 months are so critical |
| Cognitive decline and dementia | Lancet Commission on Dementia (2024): hearing loss is the largest modifiable risk factor for dementia (accounting for ~8% of cases). Mechanisms: (1) increased cognitive load from effortful listening, (2) reduced auditory input → cortical atrophy, (3) social isolation | Elderly with presbycusis; correctable with hearing aids — evidence suggests hearing aids reduce cognitive decline |
| Social isolation and depression | Inability to participate in conversation, especially in noisy environments ("cocktail party" difficulty) → withdrawal from social activities → loneliness → depression | All ages, particularly elderly and adolescents |
| Reduced educational attainment | Children with untreated hearing loss struggle in classrooms → poor academic performance | Children with OME (glue ear) or undiagnosed SNHL |
| Safety hazards | Cannot hear alarms, sirens, traffic, warning shouts | All age groups |
| Tinnitus and psychological distress | Cochlear damage commonly produces tinnitus; chronic tinnitus causes anxiety, insomnia, difficulty concentrating, depression; in severe cases, suicidal ideation | Patients with NIHL, presbycusis, Ménière's disease |
Hearing Loss and Dementia — High Yield
The Lancet Commission on Dementia Prevention (2024) identifies mid-life hearing loss as the single largest potentially modifiable risk factor for dementia, ahead of hypertension, obesity, depression, and smoking. The proposed mechanisms include cognitive load hypothesis (brain diverts resources from memory and executive function to decoding degraded auditory input), sensory deprivation (reduced input → temporal lobe atrophy), and social isolation. Treating hearing loss with hearing aids may delay or prevent cognitive decline — a powerful argument for early audiological intervention.
| Complication | Mechanism |
|---|---|
| Progressive SNHL | Repeated endolymphatic hydrops episodes → cumulative hair cell damage → hearing worsens with each attack; initially low-frequency, eventually all frequencies ("burnt-out" Ménière's with flat SNHL) |
| Drop attacks (Tumarkin's crises) | Sudden otolith-mediated vestibular stimulation → sudden fall without loss of consciousness; extremely dangerous — risk of fractures, head injury |
| Chronic imbalance | Progressive bilateral vestibular hypofunction → difficulty maintaining balance, especially in the dark (when visual compensation is absent) |
| Psychological morbidity | Unpredictable attacks of severe vertigo, nausea, hearing loss → anxiety, agoraphobia (fear of attacks in public), depression; significant impact on quality of life and employment |
| Bilateral disease | ~15–40% develop contralateral involvement over time → bilateral fluctuating SNHL and vestibular dysfunction; further limits rehabilitation options |
| Complication | Mechanism |
|---|---|
| Progressive conductive hearing loss | Continued spongiotic bone remodelling at oval window → increasing stapes fixation |
| Mixed/sensorineural hearing loss (cochlear otosclerosis) | Spongiotic foci extend from the anterior oval window to the cochlear capsule → disruption of the spiral ligament and stria vascularis → cochlear damage → SNHL component ("far-advanced otosclerosis") |
| Complications of stapedotomy (surgical treatment complications) | SNHL (< 1% — most feared; inner ear trauma during footplate manipulation), perilymph fistula → vertigo, tinnitus worsening, prosthesis displacement, reparative granuloma, taste disturbance (chorda tympani injury during surgical approach) |
Acoustic neuroma (unilateral) [9] — a serious disorder not to be missed [9].
| Complication | Mechanism |
|---|---|
| Progressive SNHL | Tumour compresses cochlear fibres of CN VIII → progressive neural hearing loss with disproportionately poor speech discrimination |
| Vestibular dysfunction | Vestibular fibres gradually compressed → chronic imbalance (NOT typically acute vertigo — the slow growth allows central compensation) [13] |
| CN V involvement | Large tumours in the CPA compress the trigeminal nerve → facial numbness, hyperesthesia, pain [13]; absent corneal reflex (ophthalmic division) |
| CN VII involvement | Despite CN VII being directly stretched over the tumour surface, facial nerve involvement is rare due to the nerve's resilience — facial nerve bundle is thick and resilient, usually only stretched over the slowly growing tumour [13]. Palsy occurs mainly after surgical removal, not from the tumour itself |
| Brainstem compression | Very large tumours (> 3–4 cm) compress the pons and cerebellum → ataxia, long tract signs (hemiparesis), hydrocephalus (compression of 4th ventricle → obstructive hydrocephalus) |
| Hydrocephalus | As above — obstruction of CSF flow at the 4th ventricle → ↑ICP → headache, papilloedema, N/V, CN VI palsy (false localising sign) |
| Post-surgical complications | CN VII injury (most common and most feared surgical complication — CN VII is draped over the tumour and must be carefully dissected off), CSF leak, meningitis, SNHL (if not already present) |
Temporal bone fractures are relevant because they can produce sudden otalgia, hearing loss, and multiple cranial neuropathies simultaneously.
| Fracture Type | Complications | Mechanism |
|---|---|---|
| Longitudinal (~80%) | Conductive hearing loss (ossicular disruption, haemotympanum); EAC laceration with bleeding; CN VII palsy (~10–20%, usually delayed and incomplete → oedema/contusion of nerve, not transection); TM perforation; CSF otorrhoea (if dura torn) | Fracture runs along the long axis of the petrous bone → through EAC and middle ear, usually sparing the otic capsule |
| Transverse (~20%) | Sensorineural hearing loss (often profound and permanent); severe vertigo (labyrinthine damage); CN VII palsy (~50%, often immediate and complete → transection of the nerve in the labyrinthine segment); CSF otorrhoea/rhinorrhoea | Fracture runs perpendicular to the petrous axis → through the otic capsule (cochlea + vestibule) and internal auditory canal → devastating inner ear and neural damage [12] |
| Both types | CSF leakage + meningitis [12]; CN palsy [12]; traumatic aneurysm [12]; traumatic carotid-cavernous fistula (CCF) [12] | Basal skull fracture complications from damage to structures at the skull base |
Since NPC commonly presents with ear symptoms in Hong Kong [2]:
| Complication | Mechanism |
|---|---|
| Persistent conductive hearing loss | Eustachian tube obstruction → chronic OME → conductive hearing loss; may not resolve until tumour is treated |
| Cranial nerve palsies (III–XII) | Local invasion into the skull base, cavernous sinus, jugular foramen → sequential CN involvement; CN V (numbness), CN VI (diplopia), CN IX–XII (lower CN palsy syndrome) |
| Distant metastases | NPC has a high propensity for early metastasis; common sites: bone (75%), liver, lung, distant lymph nodes [2] |
| Treatment-related complications (radiotherapy) | Xerostomia (salivary gland damage), osteoradionecrosis of mandible/skull base, radiation-induced SNHL (cochlear damage), trismus (fibrosis of pterygoid muscles), hypothyroidism (thyroid in radiation field), second malignancy |
| Condition | Key Complications | Most Feared |
|---|---|---|
| OE | Chronic OE, EAC stenosis, perichondritis | Necrotising OE → skull base osteomyelitis → CN palsies → death |
| AOM | TM perforation, mastoiditis, labyrinthitis | Intracranial: meningitis, brain abscess, sigmoid sinus thrombosis |
| CSOM/Cholesteatoma | CHL (ossicular erosion), facial palsy, labyrinthine fistula | Intracranial complications; cholesteatoma = relentless bone erosion |
| Ramsay Hunt | Permanent facial palsy, SNHL, PHN | Poor facial nerve recovery (~50–70%); corneal complications |
| Hearing loss | Speech delay (children), cognitive decline (elderly), social isolation, tinnitus | Dementia (mid-life hearing loss = largest modifiable risk factor) |
| Ménière's | Progressive SNHL, drop attacks, bilateral disease, psychological impact | Tumarkin's crises (sudden falls) |
| Acoustic neuroma | Progressive SNHL, CN V involvement, brainstem compression, hydrocephalus | Post-surgical CN VII injury |
| Temporal bone fracture | CHL or SNHL, CN VII palsy, CSF leak, meningitis | Transverse: permanent profound SNHL + immediate CN VII transection |
| NPC | CHL from OME, CN palsies, distant metastases, treatment toxicity | Late presentation → advanced stage at diagnosis |
High Yield Summary
-
Intracranial complications of middle ear disease spread via: (a) tegmen tympani → middle cranial fossa (temporal lobe abscess, epidural abscess, meningitis), (b) sigmoid sinus plate → posterior fossa (cerebellar abscess, sigmoid sinus thrombosis), (c) labyrinthine windows → meningitis via cochlear aqueduct.
-
Cholesteatoma erodes everything: ossicles (CHL) → lateral SCC (vertigo, fistula sign) → facial nerve canal (CN VII palsy) → tegmen (intracranial complications). Surgery is mandatory — there is no medical cure [1].
-
Necrotising OE complications escalate by anatomical proximity: CN VII first (stylomastoid foramen) → CN IX, X, XI (jugular foramen) → CN XII (hypoglossal canal). Multiple CN palsies = very poor prognosis.
-
Gradenigo syndrome (petrous apicitis): retro-orbital pain (CN V1) + CN VI palsy (abduction deficit) + otorrhoea. Classic triad for exams.
-
Ramsay Hunt has worse facial nerve prognosis than Bell's palsy (~50–70% vs ~85–95% complete recovery) because VZV causes axonal degeneration, not just conduction block.
-
Hearing loss complications beyond the ear: speech/language delay in children (intervene by 6 months), cognitive decline and dementia in elderly (largest modifiable risk factor per Lancet Commission 2024), social isolation, depression, safety hazards.
-
Temporal bone fractures: longitudinal → CHL, delayed CN VII palsy; transverse → SNHL, immediate CN VII palsy, severe vertigo. CSF otorrhoea in both → meningitis risk [12].
-
Acoustic neuroma: CN VII is usually spared by the tumour itself (nerve is resilient and slowly stretched) but is at high risk during surgical removal [13].
Active Recall - Complications of Ear Conditions
References
[1] Lecture slides: murtagh merge.pdf (p43–44, "Ear pain") [2] Senior notes: felixlai.md (Nasopharyngeal cancer section) [6] Senior notes: Ryan Ho Respiratory.pdf (p49, Acute Coryza — complications including AOM) [9] Lecture slides: murtagh merge.pdf (p96, "Tinnitus") [11] Senior notes: felixlai.md (Bell's palsy / facial nerve palsy — treatment and eye care section) [12] Senior notes: felixlai.md (Skull fractures — complications, basal skull fracture section) [13] Senior notes: Ryan Ho Neurology.pdf (p167, Acoustic neuroma / vestibular schwannoma)
High Yield Summary
-
Otalgia = primary (pathology in the ear) or secondary/referred (pathology elsewhere, perceived in the ear due to shared sensory innervation from CN V, VII, IX, X, C2/C3).
-
If an adult presents with ear pain but normal auroscopy, examine possible referral sites: TMJ, mouth, throat, teeth, cervical spine. [1]
-
Most common causes by age: Children = AOM; Adults = OE, TMJ dysfunction, dental pathology, referred pain.
-
Hong Kong critical "do-not-miss": Unilateral OME/conductive hearing loss in an adult → exclude NPC with nasopharyngoscopy. NPC arises in the fossa of Rosenmüller and obstructs the ipsilateral Eustachian tube.
-
Hearing loss types: Conductive (external/middle ear) vs. Sensorineural (cochlea/CN VIII/central). Differentiate at bedside with Rinne and Weber tests.
-
Weber lateralises to: the affected ear in CHL (reduced masking + trapped bone conduction); the better ear in SNHL (damaged cochlea cannot transduce).
-
Malignant OE: elderly diabetic + severe OE + granulation tissue at bone-cartilage junction + CN palsies → Pseudomonas skull base osteomyelitis. Not a neoplasm despite the name.
-
Cholesteatoma: not a tumour — it's trapped keratinizing squamous epithelium that erodes bone. Foul-smelling discharge + retraction pocket + ossicular erosion → CHL.
-
Sudden SNHL (≥30 dB in ≥3 frequencies within 72 hours) is an ENT emergency — analogous to a "cochlear stroke." Treat with systemic (± intratympanic) corticosteroids.
-
Key investigations are seldom necessary. Consider hearing tests, audiometry. Ear discharge for MC but swabs of no value if TM is intact. [1]
-
Masquerades checklist: depression, cervical spinal dysfunction, factitious pain (especially in children). [1]
High Yield Summary
-
Murtagh's framework for ear pain [1]: Probability = AOM, OE, furunculosis, TMJ arthralgia, Eustachian tube dysfunction. Serious = neoplasia (ear, tongue, throat, NPC), Ramsay Hunt, mastoiditis, cholesteatoma, necrotising OE. Pitfalls = foreign body, wax, barotrauma, dental abscess, referred pain, unerupted wisdom tooth, chondrodermatitis nodularis helicis, glossopharyngeal neuralgia, post-tonsillectomy pain. Masquerades = depression, cervical spine dysfunction, factitious pain.
-
Normal otoscopy + ear pain in adult = REFERRED OTALGIA — systematically examine TMJ (CN V3), teeth (CN V3), throat/tonsils (CN IX), larynx/hypopharynx (CN X), cervical spine (C2/C3), nasopharynx (NPC).
-
Unilateral OME in adult in HK = NPC until proven otherwise.
-
Hearing loss DDx: CHL → external/middle ear (wax, OE, OME, AOM, otosclerosis, cholesteatoma); SNHL → cochlear (presbycusis, NIHL, Ménière's, ototoxicity, sudden SNHL) or retrocochlear (acoustic neuroma); Mixed → CSOM with labyrinthine extension, cholesteatoma, otosclerosis with cochlear involvement.
-
Tinnitus DDx [9]: Non-pulsatile = cochlear/SNHL pathology. Pulsatile = vascular (glomus tumour, AVM, carotid stenosis) or raised ICP (IIH).
-
Acoustic neuroma = unilateral progressive SNHL + tinnitus + poor speech discrimination → MRI with gadolinium.
-
Sudden SNHL = ENT emergency → urgent audiometry and steroids; MRI to exclude retrocochlear lesion.
High Yield Summary
-
Most ear diagnoses are clinical — made by history + otoscopy. Investigations are seldom necessary [1].
-
AOM diagnostic pillars: acute onset + middle ear effusion (bulging TM, reduced mobility) + middle ear inflammation (erythema, otalgia). Pneumatic otoscopy is the most accurate bedside tool for detecting effusion.
-
Audiometry interpretation: Air-bone gap = CHL; elevated AC and BC without gap = SNHL; both = mixed. Key patterns: 4 kHz notch (NIHL), Carhart's notch at 2 kHz (otosclerosis), low-frequency SNHL (early Ménière's), asymmetric SNHL with poor speech discrimination (acoustic neuroma).
-
Tympanometry types: A = normal; As = stiff (otosclerosis); Ad = hypermobile (ossicular discontinuity); B = flat (effusion or perforation — check canal volume to distinguish); C = negative pressure (Eustachian tube dysfunction).
-
Swabs: only useful if there is discharge — swabs of no value if the TM is intact [1].
-
Unilateral OME in Hong Kong adult → nasopharyngoscopy + EBV DNA to exclude NPC [2].
-
Sudden SNHL: defined as ≥30 dB in ≥3 frequencies within 72 hours. ENT emergency. Urgent PTA + MRI with gadolinium.
-
Acoustic neuroma workup: MRI with gadolinium (gold standard); ABR shows prolonged I–V interpeak latency; PTA shows asymmetric SNHL with disproportionately poor speech discrimination.
-
Necrotising OE: CT temporal bone (bony erosion) + Tc-99m/Ga-67 scan + ESR/CRP + blood glucose. Ga-67 scan is used to monitor treatment response.
-
Neonatal screening: OAE (outer hair cell function) → if fail → ABR (objective threshold estimation). Goal: identify by 1 month, diagnose by 3 months, intervene by 6 months.
High Yield Summary
-
OE management: aural toilet + topical antibiotic-steroid drops (ciprofloxacin/dexamethasone). Use an ear wick if canal is too swollen. NEVER use aminoglycoside drops if TM perforation is present or suspected — ototoxic.
-
AOM antibiotics: not always needed. Watchful waiting for ≥2 years with mild symptoms. When indicated → high-dose amoxicillin (80–90 mg/kg/day) to overcome intermediate pneumococcal resistance. Augmentin if no response in 48–72h.
-
Cholesteatoma requires surgery — no medical cure. Mastoidectomy (CWU vs CWD) ± tympanoplasty. MRI DWI for post-op surveillance.
-
Sudden SNHL is an ENT emergency: oral prednisolone 1 mg/kg immediately; intratympanic dexamethasone as salvage; MRI to exclude acoustic neuroma. Do not delay for investigations.
-
Ménière's disease: stepwise escalation — diet → betahistine → diuretics → intratympanic steroids → intratympanic gentamicin → surgery.
-
Betahistine: H1 agonist + H3 antagonist → improves inner ear microcirculation → reduces endolymphatic hydrops.
-
Ramsay Hunt: combined valaciclovir + prednisolone + eye care. Worse prognosis than Bell's palsy (~50–70% vs ~85–95% recovery).
-
Grommets for OME: only if persistent > 3 months with hearing impact. In adults, exclude NPC before attributing unilateral OME to benign Eustachian tube dysfunction [2].
-
Hearing rehabilitation: hearing aids for mild-severe SNHL; cochlear implant for bilateral profound SNHL (ideally before age 2 in children). BAHA for unilateral deafness or unsuitable ears.
-
Button battery in ear = emergency removal — liquefactive necrosis within 2 hours. Do NOT irrigate.
High Yield Summary
-
Intracranial complications of middle ear disease spread via: (a) tegmen tympani → middle cranial fossa (temporal lobe abscess, epidural abscess, meningitis), (b) sigmoid sinus plate → posterior fossa (cerebellar abscess, sigmoid sinus thrombosis), (c) labyrinthine windows → meningitis via cochlear aqueduct.
-
Cholesteatoma erodes everything: ossicles (CHL) → lateral SCC (vertigo, fistula sign) → facial nerve canal (CN VII palsy) → tegmen (intracranial complications). Surgery is mandatory — there is no medical cure [1].
-
Necrotising OE complications escalate by anatomical proximity: CN VII first (stylomastoid foramen) → CN IX, X, XI (jugular foramen) → CN XII (hypoglossal canal). Multiple CN palsies = very poor prognosis.
-
Gradenigo syndrome (petrous apicitis): retro-orbital pain (CN V1) + CN VI palsy (abduction deficit) + otorrhoea. Classic triad for exams.
-
Ramsay Hunt has worse facial nerve prognosis than Bell's palsy (~50–70% vs ~85–95% complete recovery) because VZV causes axonal degeneration, not just conduction block.
-
Hearing loss complications beyond the ear: speech/language delay in children (intervene by 6 months), cognitive decline and dementia in elderly (largest modifiable risk factor per Lancet Commission 2024), social isolation, depression, safety hazards.
-
Temporal bone fractures: longitudinal → CHL, delayed CN VII palsy; transverse → SNHL, immediate CN VII palsy, severe vertigo. CSF otorrhoea in both → meningitis risk [12].
-
Acoustic neuroma: CN VII is usually spared by the tumour itself (nerve is resilient and slowly stretched) but is at high risk during surgical removal [13].
Dysuria, Urinary Frequency
Dysuria is painful or burning sensation during urination, and urinary frequency is the need to urinate more often than normal, both commonly indicating lower urinary tract irritation or infection.
Fever/chills
Fever is an elevation of body temperature above the normal set point, often accompanied by chills (rigors), typically resulting from the release of pyrogenic cytokines in response to infection, inflammation, or other pathological processes.