ENT

Key Facts

Otitis externa is diffuse inflammation of the skin of the external auditory canal, with or without infection. It is extremely common, particularly in swimmers ('swimmer's ear'), and usually responds well to topical treatment.

Epidemiology

• Lifetime prevalence: 10%
• Accounts for 1% of GP consultations
• Peak incidence in summer months and tropical climates
• More common in swimmers, hearing aid users, and eczema sufferers
• Annual incidence: 10-20 per 1,000

Aetiology

• Bacterial (most common): Pseudomonas aeruginosa (60-70%), Staphylococcus aureus (10-20%), polymicrobial
• Fungal (otomycosis, 10%): Aspergillus niger (black spores), Candida albicans (white)
• Predisposing factors: excessive moisture (swimming), trauma (cotton buds, hearing aids), eczema/psoriasis, narrow ear canals, absence of cerumen, immunosuppression, diabetes
• Dermatological: eczema, psoriasis, contact dermatitis (nickel earrings, hearing aid material, topical antibiotic sensitivity)

Pathophysiology

• Normal protective cerumen barrier is disrupted (excessive cleaning, moisture)
• Loss of cerumen's acidic, hydrophobic, antimicrobial properties
• Canal skin becomes waterlogged, macerated, and susceptible to infection
• Bacterial colonisation triggers inflammatory response
• Oedema and debris accumulate, creating a warm, moist environment that perpetuates infection
• In malignant OE: Pseudomonas invades from canal skin into periosteum and temporal bone, causing osteomyelitis

Typical Presentation

• Ear pain (otalgia): often severe, worse on tragal pressure (tragal tenderness) and pinna manipulation
• Ear discharge: may be scanty or profuse, often offensive
• Itching (early symptom)
• Hearing loss (conductive, due to canal oedema and debris)
• Ear fullness

Examination Findings

• Erythematous, oedematous ear canal
• Debris, discharge, or crusting in canal
• Tragal tenderness (distinguishes from otitis media)
• Pinna manipulation painful
• TM may be obscured; if visible, usually normal (unless concurrent OE and OM)
• Pre- or post-auricular lymphadenopathy

Malignant (Necrotising) Otitis Externa

• Severe, unremitting ear pain (especially at night)
• Granulation tissue at bone-cartilage junction of EAC (pathognomonic)
• Cranial nerve palsies (VII most common, then IX, X, XI, XII)
• Diabetic or immunocompromised patient
• Systemically unwell

Red Flags

• Severe pain disproportionate to findings (malignant OE)
• Granulation tissue in EAC
• Cranial nerve palsy
• Diabetes/immunosuppression with worsening OE
• Not responding to 2 weeks of topical treatment
• Mastoid tenderness

Bedside

• Otoscopy: canal erythema, oedema, debris; TM often obscured but should be normal if visible
• Tragal tenderness testing
• Assessment of hearing
• Cranial nerve examination (if malignant OE suspected - especially VII)

Bloods

• Not required for uncomplicated OE
• FBC, CRP, ESR, HbA1c, blood cultures: if malignant OE suspected

Microbiology

• Ear swab: if not responding to empirical treatment or recurrent infection
• Fungal culture: if otomycosis suspected

Imaging

• CT temporal bone: if malignant OE suspected (bony erosion, skull base involvement)
• MRI: for soft tissue assessment and intracranial extension
• Technetium-99m bone scan or Gallium-67 scan: sensitive for osteomyelitis in malignant OE

Special Tests

• Biopsy of granulation tissue: to exclude malignancy (squamous cell carcinoma) and confirm diagnosis in malignant OE

Non-pharmacological

• Aural toilet: microsuction (gold standard) or dry mopping under direct vision
• Keep ear dry: use ear plugs or cotton wool with Vaseline when bathing/swimming
• Avoid cotton buds and ear instrumentation
• Pope wick insertion: if canal is too swollen for drops to penetrate (remove/replace in 48-72 hours)

Pharmacological

• First-line: topical antibiotic-steroid drops:
  • Ciprofloxacin 0.3%/dexamethasone 0.1% (Cilodex) 3 drops BD for 7 days
  • OR Sofradex (framycetin/gramicidin/dexamethasone) 3 drops TDS for 7 days
  • Avoid aminoglycoside drops (gentamicin, neomycin) if TM perforation (ototoxicity risk)
• Otomycosis: clotrimazole 1% drops/cream (antifungal), aural toilet; acetic acid 2% drops
• Second-line (not improving): ear swab and adjust antibiotics; consider acetic acid 2% spray (EarCalm)
• Analgesia: paracetamol, ibuprofen; codeine for severe pain
• Malignant otitis externa:
  • IV ciprofloxacin (400mg BD) or IV piperacillin-tazobactam (4.5g TDS) for 6-8 weeks
  • Prolonged course of oral ciprofloxacin 750mg BD following IV treatment

Surgical

• Surgical debridement: for malignant OE with extensive disease
• Rarely required for uncomplicated OE

Referral Criteria

• ENT referral: suspected malignant OE, not responding to 2 weeks of treatment, recurrent OE (>4 episodes/year), suspected cholesteatoma or canal malignancy
• Urgent ENT referral: cranial nerve palsy, granulation tissue, severe pain in diabetic patient
• Audiology referral if persistent hearing loss

• Uncomplicated OE: >95% resolve with topical treatment within 7-10 days
• Recurrence rate: 30-40% (particularly in swimmers, hearing aid users, eczema)
• Otomycosis: may require prolonged treatment (2-4 weeks) and has higher recurrence rate
• Malignant OE: mortality 10-20% (historically higher, improving with modern antibiotics)
  • Cranial nerve involvement indicates worse prognosis
  • Skull base osteomyelitis may require months of antibiotics
• Chronic OE may develop in 5-10% - requires ongoing management and triggers avoidance

Comparison: Otitis Externa vs Otitis Media

Topical Ear Drop Selection

Key Facts

Cholesteatoma is an abnormal accumulation of keratinised squamous epithelium that grows within the middle ear cleft and mastoid. Despite its benign histology, it behaves aggressively, eroding bone through enzymatic activity and pressure effects. It requires surgical management and long-term follow-up.

Epidemiology

• Incidence: 9-12 per 100,000 per year in the UK
• Peak incidence: children and young adults
• Male:female ratio 1.5:1
• More common in Caucasian populations
• Acquired cholesteatoma is far more common (98%) than congenital (2%)

Aetiology

• Acquired cholesteatoma (most common): develops from retraction pocket of tympanic membrane (usually pars flaccida/attic region)

• Also from TM perforation (marginal) with epithelial migration into middle ear
• Congenital cholesteatoma: keratinised epithelium behind intact TM, usually in children; thought to arise from embryonic epithelial rest
• Risk factors: chronic otitis media, recurrent AOM, Eustachian tube dysfunction, cleft palate, previous ear surgery

Pathophysiology

• Trapped squamous epithelium desquamates and accumulates keratin debris
• Growing mass exerts pressure on surrounding structures
• Cholesteatoma releases collagenases (MMP-2, MMP-9) and inflammatory cytokines (TNF-α, IL-1, IL-6)
• Enzymatic bone resorption erodes ossicular chain, tegmen tympani, semicircular canals, and facial nerve canal
• Secondary infection is common due to trapped debris
• Can create fistula into labyrinth or erode into middle/posterior cranial fossa

Typical Presentation

• Persistent foul-smelling ear discharge (otorrhoea) - typically unilateral and unresponsive to standard antibiotic treatment
• Conductive hearing loss (progressive)
• Ear fullness or discomfort
• Usually painless unless superinfected

Examination Findings

• Attic retraction pocket or crust (pars flaccida) on otoscopy - pathognomonic
• Keratin debris or polyp in the attic/posterior-superior TM
• Marginal perforation with squamous epithelium
• Granulation tissue
• Aural polyp arising from middle ear

Red Flags

• Facial nerve palsy (VII nerve erosion - urgent surgical indication)
• Vertigo or sensorineural hearing loss (labyrinthine fistula)
• Headache, meningism (intracranial complication)
• Mastoid abscess (post-auricular swelling)
• Bilateral cholesteatoma (rare, consider congenital)

Bedside

• Otoscopy: attic crust/retraction, keratin debris, marginal perforation, polyp
• Microsuction/aural toilet: to adequately visualise pathology
• Tuning fork tests: Rinne (negative on affected side), Weber (lateralises to affected ear in CHL)

Bloods

• Not routinely required
• FBC, CRP if acute infection or complications suspected

Imaging

• High-resolution CT temporal bones (non-contrast): gold standard for pre-operative planning
  • Soft tissue mass in middle ear/mastoid with bony erosion
  • Ossicular chain erosion (long process of incus most commonly affected)
  • Tegmen erosion, lateral semicircular canal fistula
  • Facial nerve canal dehiscence
• MRI (diffusion-weighted imaging): increasingly used to detect residual/recurrent cholesteatoma post-operatively (bright on DWI due to restricted diffusion in keratin)
  • Non-echo planar DWI (e.g. HASTE) preferred for small lesions
  • May reduce need for second-look surgery

Special Tests

• Pure tone audiometry: conductive hearing loss (air-bone gap)
• Tympanometry: often not possible if perforation
• Fistula test: positive if labyrinthine fistula present (caloric-type response to pressure changes)

Non-pharmacological

• Regular aural microsuction to keep cholesteatoma cavity clean
• Water precautions (keep ear dry)
• Surveillance audiometry

Pharmacological

• No medical cure - antibiotics and drops do not treat cholesteatoma itself
• Topical antibiotic drops (ciprofloxacin 0.3%) for secondary infection
• Systemic antibiotics (co-amoxiclav) for acute exacerbation or pre-operative infection control
• IV antibiotics if intracranial complications

Surgical

• Surgery is the definitive treatment - aim is complete disease removal and creation of a safe, dry ear
• Canal wall up mastoidectomy (combined approach tympanoplasty):
  • Preserves posterior canal wall anatomy
  • Better cosmetic result and water precaution avoidance
  • Higher recurrence rate (~30%) - requires second-look surgery at 9-12 months or DWI MRI surveillance
• Canal wall down mastoidectomy (modified radical mastoidectomy):
  • Creates open mastoid cavity (needs lifelong aural toilet)
  • Lower recurrence rate (~10%)
  • Used for extensive disease, revision surgery, or unreliable follow-up
• Ossiculoplasty: ossicular chain reconstruction for hearing rehabilitation (may be staged)
• Tympanoplasty: TM repair

Referral Criteria

• All suspected cholesteatoma requires ENT referral (2-week wait if malignancy concern)
• Urgent referral: facial nerve palsy, vertigo, suspected intracranial complication
• Long-term ENT follow-up: minimum 5 years post-surgery

• Recurrence/residual disease: 10-30% depending on surgical technique (higher with canal wall up)
• Hearing restoration: variable; ossiculoplasty can improve but rarely restores normal hearing
• Facial nerve palsy: occurs in <1% from cholesteatoma but is a surgical risk
• Labyrinthine fistula: present in 5-10% of cholesteatoma cases; may cause permanent SNHL
• Intracranial complications (meningitis, abscess): <2% in modern practice
• Lifelong follow-up recommended for canal wall down cavities
• MRI DWI surveillance increasingly used to monitor canal wall up cases and detect early recurrence

Cholesteatoma Complications by Structure Eroded

Canal Wall Up vs Canal Wall Down Mastoidectomy

Key Facts

Hearing loss is one of the most common disabilities worldwide and the third most common chronic health condition in older adults. It significantly impacts communication, social interaction, mental health, and quality of life. Early identification and management are essential.

Epidemiology

• 11 million people affected in the UK (1 in 6)
• Prevalence increases steeply with age: 40% of >50s, 70% of >70s
• Congenital hearing loss: 1-2 per 1,000 newborns
• Noise-induced hearing loss affects 17% of adults
• WHO estimates 466 million people worldwide have disabling hearing loss

Aetiology

• Conductive: cerumen impaction (most common treatable cause), otitis media with effusion, chronic otitis media, otosclerosis, TM perforation, cholesteatoma, Eustachian tube dysfunction
• Sensorineural: presbycusis (most common overall), noise-induced, ototoxic drugs (aminoglycosides, cisplatin, loop diuretics), Ménière disease, vestibular schwannoma, congenital (genetic, TORCH infections), sudden SNHL (idiopathic/viral)
• Mixed: combination, e.g. chronic otitis media with cochlear damage

Pathophysiology

• Conductive: mechanical impedance to sound transmission through external or middle ear
• Sensorineural: damage to cochlear hair cells (especially outer hair cells), stria vascularis, or cochlear nerve
• Presbycusis: progressive loss of hair cells starting at basal turn (high-frequency loss first)
• Noise-induced: mechanical damage to stereocilia from excessive sound energy
• Ototoxicity: direct damage to hair cells (aminoglycosides) or stria vascularis (loop diuretics)

Conductive Hearing Loss

• Difficulty hearing, often aware of reduced volume
• May hear better in noisy environments (paracusis of Willis, classically otosclerosis)
• History of ear infections, discharge, trauma, or surgery
• Family history (otosclerosis)

Sensorineural Hearing Loss

• Difficulty understanding speech, especially in background noise
• High-frequency loss: difficulty hearing consonants, women's/children's voices
• Tinnitus (common association)
• Vertigo (if vestibular involvement - Ménière, vestibular schwannoma)
• Gradual onset (presbycusis, noise-induced) or sudden (viral, vascular)

Red Flags - Urgent Assessment Required

• Sudden sensorineural hearing loss (<72 hours) - ENT emergency
• Unilateral hearing loss - exclude vestibular schwannoma (MRI)
• Asymmetric hearing loss - investigate for retrocochlear pathology
• Pulsatile tinnitus - vascular cause (glomus tumour, AVF)
• Associated facial nerve palsy
• Hearing loss with vertigo and progressive symptoms

Bedside

• Otoscopy: cerumen, TM abnormalities, middle ear pathology
• Tuning fork tests (512Hz):
  • Rinne test: compares air conduction (AC) and bone conduction (BC)
    • Normal/SNHL: AC > BC (Rinne positive)
    • CHL: BC > AC (Rinne negative)
  • Weber test: central placement
    • CHL: lateralises to affected ear
    • SNHL: lateralises to unaffected (better) ear
• Whispered voice test: simple screening (sensitivity ~90%)

Bloods

• Not routinely required
• Consider: FBC, ESR, TFTs, glucose, syphilis serology, autoimmune screen in unexplained SNHL

Imaging

• MRI internal auditory meatus (IAM) with gadolinium: gold standard for suspected vestibular schwannoma (unilateral/asymmetric SNHL)
• CT temporal bones: for conductive hearing loss assessment, cholesteatoma, otosclerosis, trauma

Special Tests

• Pure tone audiometry (PTA): gold standard hearing assessment
  • Air and bone conduction thresholds at 250Hz-8kHz
  • Air-bone gap >10dB indicates conductive component
• Tympanometry: middle ear compliance (types A, B, C, As, Ad)
• Speech audiometry: speech discrimination testing
• Otoacoustic emissions (OAE): tests outer hair cell function
• Auditory brainstem response (ABR): threshold estimation, retrocochlear assessment
• Newborn hearing screening: AOAE and ABR

Non-pharmacological

• Cerumen removal: microsuction, ear irrigation, olive oil drops for softening
• Hearing aids: first-line for mild-moderate SNHL (NICE NG98)
  • Behind-the-ear (BTE) most common NHS provision
  • Digital hearing aids with directional microphones
• Assistive listening devices: personal amplifiers, loop systems, subtitles
• Communication strategies: face the speaker, reduce background noise, lip reading
• Noise protection: ear defenders, custom-moulded plugs for occupational/recreational exposure

Pharmacological

• Sudden SNHL: oral prednisolone 1mg/kg (max 60mg) OD for 7-14 days, taper over 1-2 weeks
  • Intratympanic dexamethasone injection as salvage therapy if oral steroids fail
• Ménière disease: betahistine 16mg TDS (symptomatic relief)
• Ototoxic drug review: discontinue or substitute where possible

Surgical

• Grommets: for persistent OME with hearing loss in children (NICE NG233)
• Stapedectomy/stapedotomy: for otosclerosis (success rate >90% closure of air-bone gap)
• Tympanoplasty/ossiculoplasty: for chronic ear disease with conductive loss
• Cochlear implants: for severe-profound bilateral SNHL (NICE TA566)
  • Criteria: ≥80dB HL at 2 and 4kHz, inadequate benefit from hearing aids
• Bone-anchored hearing aid (BAHA): for single-sided deafness, conductive/mixed hearing loss not suitable for conventional aids

Referral Criteria

• Emergency ENT: sudden SNHL (<72 hours)
• Urgent ENT (2 weeks): unilateral/asymmetric SNHL (vestibular schwannoma exclusion)
• Routine ENT: conductive hearing loss, persistent hearing difficulty, cholesteatoma
• Audiology: all patients with hearing difficulty for PTA and hearing aid assessment

• Presbycusis: progressive; hearing aids provide significant benefit and improve quality of life
• Sudden SNHL: 30-65% spontaneous partial recovery; better with early steroid treatment
• Otosclerosis: excellent surgical prognosis; stapedectomy success rate >90%
• Noise-induced: preventable; once established, hearing loss is permanent
• Cochlear implants: significant speech perception improvement in >80% of adults and >90% of children
• Untreated hearing loss is associated with social isolation, depression, cognitive decline, and increased dementia risk (Lancet Commission 2020: hearing loss is the single largest modifiable risk factor for dementia)

Classification of Hearing Loss Severity (WHO/BSA)

Common Audiometric Patterns

Key Landmark: Lancet Commission on Dementia (2020)

Key Facts

Sensorineural hearing loss results from dysfunction of the cochlea, cochlear hair cells, or the vestibulocochlear nerve (CN VIII). It is the most common type of hearing loss overall and significantly impacts quality of life, communication, and cognitive function.

Epidemiology

• Accounts for >90% of all hearing loss
• Presbycusis affects >50% of those >70 years
• Noise-induced hearing loss: estimated 17% of adults have measurable noise damage
• Congenital SNHL: 1-2 per 1,000 live births
• Vestibular schwannoma: incidence 1-2 per 100,000 per year

Aetiology

• Congenital: genetic (Connexin 26/GJB2 most common, Pendred syndrome, Usher syndrome, Waardenburg syndrome), TORCH infections (CMV most common infectious cause), prematurity, hypoxia, kernicterus
• Acquired: presbycusis, noise-induced, ototoxic drugs (aminoglycosides, cisplatin, loop diuretics, high-dose aspirin), Ménière disease, labyrinthitis, vestibular schwannoma, autoimmune inner ear disease, head trauma, otosyphilis
• Sudden SNHL: idiopathic (most common), viral (CMV, mumps, measles), vascular (cochlear infarction), autoimmune, perilymph fistula

Pathophysiology

• Cochlear (sensory): damage to outer hair cells (OHCs) initially, then inner hair cells (IHCs)
  • OHC damage reduces cochlear amplification and frequency selectivity
  • IHC damage reduces afferent signal to auditory nerve
• Neural (retrocochlear): CN VIII compression (schwannoma), demyelination (MS), auditory neuropathy
• Presbycusis involves multiple mechanisms: sensory (hair cell loss), strial (atrophy of stria vascularis), neural (spiral ganglion degeneration)
• Hair cell loss is irreversible in mammals - no spontaneous regeneration

Symptoms

• Difficulty hearing, especially speech in background noise
• Bilateral, symmetric, gradual loss (presbycusis, noise-induced)
• Unilateral or asymmetric loss (vestibular schwannoma, sudden SNHL)
• Tinnitus (very common association)
• Recruitment: abnormally rapid growth of loudness (cochlear cause)
• Difficulty with high-pitched sounds (consonants, alarms, birdsong)

Associated Features by Cause

• Ménière disease: episodic vertigo, fluctuating low-frequency SNHL, tinnitus, aural fullness
• Vestibular schwannoma: unilateral tinnitus, imbalance, facial numbness (CN V involvement)
• Noise-induced: occupational or recreational noise exposure history, 4kHz audiometric notch
• Ototoxicity: temporal relationship with drug exposure

Red Flags

• Sudden SNHL (<72 hours) - ENT emergency
• Unilateral/asymmetric SNHL - exclude vestibular schwannoma
• Associated facial nerve palsy
• Progressive unilateral SNHL
• SNHL in a child (developmental implications)

Bedside

• Otoscopy: typically normal in SNHL
• Tuning fork tests (512Hz):
  • Rinne: positive (AC > BC) - consistent with normal or SNHL
  • Weber: lateralises to unaffected ear
• Whispered voice test

Bloods

• Guided by clinical suspicion:
  • FBC, ESR, CRP (inflammatory/autoimmune)
  • TFTs (hypothyroidism)
  • Glucose/HbA1c (diabetes)
  • Syphilis serology (RPR/VDRL, TPHA)
  • Autoimmune screen (ANA, anti-dsDNA) if autoimmune inner ear disease suspected
  • Genetic testing (Connexin 26/GJB2) for congenital SNHL

Imaging

• MRI IAM with gadolinium: gold standard for excluding vestibular schwannoma in unilateral/asymmetric SNHL
• CT temporal bones: for pre-cochlear implant assessment, congenital anomalies

Special Tests

• Pure tone audiometry: air and bone conduction; no significant air-bone gap (<10dB) in pure SNHL
• Speech audiometry: disproportionately poor speech discrimination suggests retrocochlear pathology
• Otoacoustic emissions (OAE): test OHC function; present = cochlea working
• Auditory brainstem response (ABR): threshold estimation, retrocochlear assessment
• Electrocochleography (ECoG): for Ménière disease (elevated SP/AP ratio)

Non-pharmacological

• Hearing aids: first-line for mild-moderate SNHL (NICE NG98)
• Communication strategies: lip reading, sign language, assistive devices
• Noise protection: hearing protection for occupational/recreational exposure
• Environmental modification: reduce background noise, loop systems, visual alerts

Pharmacological

• Sudden SNHL: oral prednisolone 1mg/kg (max 60mg) OD for 7-14 days (start ASAP, ideally within 72 hours)
  • Intratympanic dexamethasone (0.5-1ml of 4mg/ml): salvage therapy if oral steroids fail, or first-line if oral steroids contraindicated
• Autoimmune inner ear disease: systemic corticosteroids, steroid-sparing agents (methotrexate, azathioprine)
• Ménière disease: betahistine 16mg TDS, intratympanic gentamicin for refractory cases
• Ototoxic drug management: therapeutic drug monitoring (aminoglycosides), dose adjustment, alternative agents

Surgical

• Cochlear implants (NICE TA566):
  • Bilateral severe-profound SNHL (≥80dB at 2 and 4kHz)
  • Inadequate benefit from optimally fitted hearing aids
  • Bilateral simultaneous or sequential implantation
• Bone-anchored hearing aid (BAHA/Osia): for single-sided deafness (routes sound to contralateral cochlea)
• Vestibular schwannoma: surgical excision (translabyrinthine, retrosigmoid, middle fossa) or stereotactic radiosurgery (Gamma Knife)

Referral Criteria

• Emergency: sudden SNHL (<72 hours)
• Urgent (2-week wait): unilateral/asymmetric SNHL, suspected vestibular schwannoma
• Routine: bilateral symmetric SNHL for audiological assessment and hearing aid fitting
• Paediatric: any child with suspected hearing loss - urgent audiology referral

• Presbycusis: progressive but hearing aids significantly improve quality of life
• Sudden SNHL: 30-65% achieve some spontaneous recovery; better prognosis with early steroid treatment, younger age, mild-moderate loss, and no vertigo
• Noise-induced: preventable; once established, permanent; tinnitus often accompanies
• Cochlear implants: speech perception improves in >80% adults; children implanted before age 2 have best language outcomes
• Vestibular schwannoma: hearing preservation possible with radiosurgery or observation for small tumours
• Untreated SNHL: associated with 2-5× increased risk of cognitive decline and dementia (Lancet Commission 2020)
• Congenital SNHL: early identification and intervention (hearing aids/CI before age 3) essential for speech and language development

Causes of Congenital SNHL

Common Ototoxic Drugs

Audiometric Patterns

Key Facts

Conductive hearing loss occurs when sound waves cannot be efficiently transmitted from the external environment through the ear canal, tympanic membrane, and ossicular chain to the oval window. Unlike sensorineural hearing loss, many causes of CHL are treatable medically or surgically.

Epidemiology

• CHL accounts for approximately 10-15% of all hearing loss in adults
• OME affects virtually all children at some point; persistent bilateral OME affects 5-10% of school-age children
• Otosclerosis affects 0.3-0.4% of the population; clinical disease in 0.1%
• Chronic suppurative otitis media: prevalence 1-2% in developed countries

Aetiology

• External ear: cerumen impaction, otitis externa, foreign body, exostoses (surfer's ear), canal stenosis/atresia
• Tympanic membrane: perforation (trauma, infection), tympanosclerosis, retraction
• Middle ear: OME (most common in children), otosclerosis (most common in young adults), cholesteatoma, ossicular discontinuity/fixation, chronic suppurative otitis media, haemotympanum

Pathophysiology

• Sound waves require mechanical transmission through air in the EAC, vibration of the TM, and ossicular chain leverage to amplify sound at the oval window
• The ossicular chain provides approximately 25-30dB of amplification through the impedance-matching mechanism
• Any obstruction or disruption in this pathway causes an air-bone gap on audiometry
• Maximum CHL is approximately 60dB (the limit of bone conduction hearing)
• In otosclerosis, abnormal bone remodelling around the stapes footplate causes fixation and progressive CHL

Symptoms

• Reduced hearing, often noticed as needing to increase volume
• May hear better in background noise (paracusis of Willis - classic for otosclerosis)
• Ear fullness or pressure sensation
• History of ear discharge, infection, or surgery
• Autophony (hearing own voice louder)

Examination Findings

• Otoscopy: may reveal cerumen, effusion, perforation, retraction pocket, cholesteatoma, tympanosclerosis
• Tuning fork tests (512Hz):
  • Rinne: negative on affected side (BC > AC)
  • Weber: lateralises to affected ear
• Normal external canal appearance in otosclerosis (Schwartze sign - pink blush on promontory - rare)

Red Flags

• Unilateral CHL with foul discharge (cholesteatoma)
• Facial nerve palsy with CHL
• Blood behind tympanic membrane (haemotympanum - trauma, barotrauma, skull fracture)
• Progressive CHL in young adult (otosclerosis - family history)
• Conductive hearing loss in a child not improving (persistent OME, cholesteatoma)

Bedside

• Otoscopy (pneumatic otoscopy if OME suspected)
• Tuning fork tests (512Hz): Rinne and Weber
• Whispered voice test

Bloods

• Not routinely required

Imaging

• CT temporal bones: for cholesteatoma, otosclerosis (rarely needed), congenital anomalies, trauma
• MRI: if cholesteatoma suspected (DWI for post-operative surveillance)

Special Tests

• Pure tone audiometry: air-bone gap >10dB confirms conductive component
  • Carhart notch at 2kHz: characteristic of otosclerosis (artefact of stapes fixation)
• Tympanometry:
  • Type A: normal
  • Type B: effusion or perforation
  • Type C: negative middle ear pressure (Eustachian tube dysfunction)
  • Type As: reduced compliance (otosclerosis, tympanosclerosis)
  • Type Ad: increased compliance (ossicular discontinuity)
• Speech audiometry: typically good speech discrimination in CHL (unlike retrocochlear SNHL)
• Stapedial reflexes: absent in otosclerosis

Non-pharmacological

• Cerumen removal: microsuction (gold standard), irrigation, manual removal
• Hearing aids: option for all causes of CHL, particularly if surgery declined or unsuitable
• Watchful waiting: for OME (3 months observation, spontaneous resolution likely)

Pharmacological

• OME: no effective medical treatment (antibiotics, decongestants, antihistamines NOT recommended - NICE NG233)
• Active ear infection: topical or systemic antibiotics as appropriate
• Otosclerosis: sodium fluoride (historical; rarely used now)

Surgical

• Grommets (ventilation tubes): for bilateral OME >3 months with hearing loss ≥25dB (NICE NG233)
• Stapedectomy/stapedotomy: definitive treatment for otosclerosis; >90% success in closing air-bone gap
• Tympanoplasty: repair of TM perforation (success rate 85-95%)
• Ossiculoplasty: reconstruction of disrupted ossicular chain
• Mastoidectomy: for cholesteatoma
• Canalplasty: for exostoses or canal stenosis
• Bone-anchored hearing aid (BAHA): for CHL where conventional hearing aids or surgery not suitable

Referral Criteria

• ENT referral: persistent CHL, suspected cholesteatoma, progressive CHL in young adult (otosclerosis), bilateral OME >3 months in children
• Audiology: all patients for formal assessment
• Emergency: facial nerve palsy, suspected intracranial complication

• Cerumen: immediate restoration of hearing after removal
• OME: >90% resolve spontaneously within 12 months; grommets effective in >90%
• Otosclerosis: stapedectomy success rate >90% for closure of air-bone gap; 1% risk of dead ear
• Tympanoplasty: success rate 85-95% for perforation closure
• Cholesteatoma: requires surgery; recurrence 10-30%
• Maximum CHL: approximately 60dB (remaining hearing via bone conduction)
• Overall, CHL has a better prognosis than SNHL as many causes are surgically correctable

Comparison of Common CHL Causes

Otosclerosis Key Facts

Key Facts

Tinnitus is the conscious perception of an auditory sensation in the absence of a corresponding external stimulus. It is a symptom rather than a disease and can be associated with almost any disorder of the auditory pathway. Management focuses on reducing distress and improving coping rather than eliminating the sound.

Epidemiology

• Prevalence: 10-15% of UK adults experience tinnitus
• Bothersome tinnitus: 1-2% of the population
• Increases with age (correlates with presbycusis)
• Equal sex distribution
• Strongly associated with hearing loss, noise exposure, and ageing

Aetiology

• Otological: hearing loss (any cause), cerumen impaction, otitis media, Ménière disease, otosclerosis, vestibular schwannoma
• Noise-related: occupational, recreational, acute acoustic trauma
• Neurological: MS, head injury, migraine
• Vascular (pulsatile): glomus tumour (paraganglioma), dural arteriovenous fistula, carotid stenosis, venous hum, benign intracranial hypertension
• Drugs: aspirin (high-dose), NSAIDs, aminoglycosides, loop diuretics, quinine, cisplatin
• Other: temporomandibular joint dysfunction, cervical spine pathology, psychological stress/anxiety

Pathophysiology

• Reduced peripheral auditory input (from hearing loss) leads to maladaptive central auditory neuroplasticity
• Central gain model: the brain increases neural gain to compensate for reduced input, amplifying spontaneous neural activity perceived as tinnitus
• Involvement of limbic system and autonomic nervous system explains the emotional distress
• In pulsatile tinnitus: turbulent blood flow near temporal bone is transmitted to the cochlea

Subjective Tinnitus (Most Common)

• Ringing, buzzing, hissing, whistling, or humming sounds
• Usually bilateral; may be unilateral
• Continuous or intermittent
• Often worse in quiet environments, at night
• Frequently associated with hearing loss

Pulsatile Tinnitus

• Rhythmic sound synchronous with heartbeat
• May be objective (audible with stethoscope over ear/mastoid)
• Suggests vascular aetiology

Associated Features

• Hearing loss (most common association)
• Sleep disturbance
• Anxiety and depression
• Difficulty concentrating
• Hyperacusis (reduced tolerance to sound)

Red Flags

• Unilateral tinnitus (vestibular schwannoma until excluded)
• Pulsatile tinnitus (vascular cause)
• Associated neurological symptoms (facial weakness, numbness, vertigo)
• Sudden onset with hearing loss (sudden SNHL)
• Objective tinnitus (heard by examiner)
• Associated with head trauma

Bedside

• Otoscopy: cerumen, TM abnormalities, vascular mass behind TM (glomus)
• Auscultation over ear/mastoid: objective tinnitus (bruit)
• Tuning fork tests
• Cranial nerve examination
• TMJ assessment

Bloods

• FBC, TFTs, ESR: if systemic cause suspected
• Lipid profile, glucose: vascular risk factors (pulsatile tinnitus)

Imaging

• MRI IAM with gadolinium: for unilateral tinnitus or asymmetric hearing loss (exclude vestibular schwannoma)
• CT temporal bones: if middle ear pathology or pulsatile tinnitus
• CT/MR angiography: for pulsatile tinnitus (vascular cause)
• NICE NG155: routine imaging NOT recommended for bilateral tinnitus without red flags

Special Tests

• Pure tone audiometry: assess hearing (almost all tinnitus patients)
• Tympanometry: middle ear assessment
• Tinnitus questionnaires: Tinnitus Handicap Inventory (THI), Tinnitus Functional Index (TFI)
• Psychological assessment: PHQ-9, GAD-7 for associated depression/anxiety

Non-pharmacological

• Education and reassurance: explaining the mechanism of tinnitus reduces distress significantly
• Cognitive behavioural therapy (CBT): strongest evidence for reducing tinnitus-related distress (NICE NG155)
• Sound therapy: background sound (radio, white noise) reduces contrast between tinnitus and silence
  • White noise generators, nature sounds, tinnitus apps
• Hearing aids: if concurrent hearing loss (amplification reduces central gain and masks tinnitus)
  • Combination devices: hearing aid with integrated tinnitus sound generator
• Tinnitus retraining therapy (TRT): combines counselling with low-level broadband sound (habituation)
• Mindfulness-based interventions: emerging evidence for reducing tinnitus distress
• Sleep hygiene: for tinnitus-related insomnia

Pharmacological

• No drug is specifically licensed or recommended for tinnitus (NICE NG155)
• Antidepressants (SSRIs, e.g. sertraline 50mg OD): for associated depression/anxiety, NOT for tinnitus itself
• Betahistine 16mg TDS: if associated Ménière disease
• Short-term benzodiazepines: rarely, for acute severe distress (risk of dependence)
• Melatonin: may help tinnitus-related sleep disturbance

Surgical

• Treat underlying cause: cerumen removal, grommet insertion, stapedectomy, vestibular schwannoma management
• Cochlear implants: may reduce tinnitus in patients with severe SNHL

Referral Criteria

• ENT/audiology referral: all patients with bothersome tinnitus (NICE NG155)
• Urgent ENT referral: unilateral tinnitus, pulsatile tinnitus, associated neurological symptoms
• Psychology/CBT referral: for tinnitus-related distress, anxiety, depression
• Emergency: sudden hearing loss with tinnitus

• Most patients habituate over time (months to years); tinnitus becomes less noticeable
• 60-80% report significant improvement with CBT or structured management programmes
• 10-15% develop severe, debilitating tinnitus affecting quality of life
• Hearing aids provide significant tinnitus relief in >50% of patients with concurrent hearing loss
• Tinnitus from noise exposure: may be permanent but coping improves with management
• Suicidal ideation occurs in a small minority; screen for mental health impact
• Spontaneous resolution is uncommon in chronic tinnitus (>6 months)

Tinnitus Handicap Inventory (THI) Grading

Causes of Pulsatile Tinnitus

NICE NG155 Key Recommendations

Key Facts

Ménière disease is an idiopathic inner ear disorder characterised by episodes of vertigo, fluctuating sensorineural hearing loss, tinnitus, and aural fullness. The underlying pathology is endolymphatic hydrops - distension of the endolymphatic compartment of the inner ear.

Epidemiology

• Prevalence: 50-200 per 100,000
• Peak onset: 40-60 years
• Slight female predominance (1.3:1)
• Bilateral involvement: 25-40% over 10-20 years
• Rare in children

Aetiology

• Exact cause unknown; likely multifactorial
• Endolymphatic hydrops is the pathological hallmark
• Proposed mechanisms: impaired endolymph reabsorption by endolymphatic sac, abnormal endolymph production, altered ion homeostasis
• Possible contributing factors: viral infection, autoimmune mechanisms, genetic predisposition (familial in 5-15%), allergy, vascular insufficiency

Pathophysiology

• Excess endolymph accumulates in the scala media (cochlear duct) and vestibular labyrinth
• Distension of the membranous labyrinth (Reissner membrane bulges)
• Membrane rupture may cause mixing of endolymph (high K+) with perilymph (high Na+)
• Potassium-rich endolymph exposure to hair cells and vestibular nerve causes depolarisation block
• This results in acute vertigo, hearing loss, and tinnitus during attacks
• Membrane heals, symptoms resolve, but repeated attacks cause progressive hair cell damage
• Over time, hearing loss becomes permanent and vertigo attacks may diminish ('burn out')

Typical Attack

• Episodic rotational vertigo: lasting 20 minutes to 12 hours (usually 2-4 hours)
• Associated nausea, vomiting, pallor, sweating
• Fluctuating hearing loss: low-frequency initially; recovers between attacks initially but becomes progressive
• Tinnitus: usually low-pitched roaring, worsens during attacks
• Aural fullness: pressure sensation in affected ear
• Attacks are unpredictable; may cluster or be separated by months

Between Attacks

• May be asymptomatic initially
• Progressive hearing loss between attacks over years
• Persistent tinnitus
• Imbalance/unsteadiness

Late Disease ('Burnt Out')

• Vertigo attacks reduce in frequency and severity
• Permanent SNHL (often moderate-severe)
• Persistent tinnitus
• Chronic imbalance

Red Flags

• Persistent vertigo >24 hours (consider vestibular neuritis, stroke)
• Acute onset without fluctuation (consider labyrinthitis, stroke)
• Progressive unilateral SNHL without vertigo (exclude vestibular schwannoma)
• Neurological symptoms (diplopia, dysarthria, dysphagia) - exclude posterior circulation stroke
• Drop attacks (Tumarkin's otolithic crisis) - sudden falls without loss of consciousness

Bedside

• Otoscopy: usually normal
• Nystagmus assessment: horizontal nystagmus during acute attack (towards affected ear initially, then away)
• Head impulse test: may be positive (abnormal) on affected side
• Romberg test: positive, falling towards affected side
• Dix-Hallpike: negative (rules out BPPV)

Bloods

• FBC, TFTs, glucose, syphilis serology: to exclude other causes of SNHL
• Autoimmune screen if bilateral or atypical

Imaging

• MRI IAM with gadolinium: to exclude vestibular schwannoma (essential for unilateral SNHL)
• MRI inner ear with intratympanic gadolinium: can demonstrate endolymphatic hydrops (research/specialist centres)

Special Tests

• Pure tone audiometry: low-frequency SNHL (250Hz, 500Hz, 1kHz) during or shortly after attack; may be normal between attacks early in disease
• Caloric testing: reduced or absent vestibular response on affected side (canal paresis)
• Electrocochleography (ECoG): elevated SP/AP ratio (>0.4) supports diagnosis
• Glycerol dehydration test: temporary improvement in hearing after oral glycerol (rarely used)
• Serial audiometry: documents fluctuating hearing loss

Non-pharmacological

• Low-salt diet: <1.5g sodium/day (reduces endolymph volume; widely recommended)
• Avoid caffeine, alcohol, and tobacco (may trigger attacks)
• Vestibular rehabilitation: for chronic imbalance between attacks
• Stress management
• Driving: must inform DVLA; must not drive during attacks; Group 1 licence may continue if attacks controlled

Pharmacological

• Acute attack:
  • Prochlorperazine 5-10mg PO/IM TDS or buccal 3-6mg BD (vestibular sedative)
  • Cyclizine 50mg PO/IM TDS
  • Ondansetron 4-8mg for severe nausea/vomiting
• Prophylaxis:
  • Betahistine 16mg TDS (H1 agonist/H3 antagonist; improves inner ear microcirculation)
  • Titrate up to 48mg TDS if needed
  • BEMED trial showed no significant difference vs placebo, but widely used in UK practice

Surgical/Interventional

• Intratympanic steroid injection (dexamethasone 4mg/ml): for acute episodes or refractory disease (hearing-sparing)
• Intratympanic gentamicin: chemical labyrinthectomy; controls vertigo in >85% but risk of further hearing loss (vestibulotoxic)
• Endolymphatic sac decompression/shunt: controversial; modest evidence of benefit
• Labyrinthectomy: definitive vertigo control for unilateral Ménière with no useful hearing; destroys residual hearing
• Vestibular neurectomy: selective section of vestibular nerve; preserves hearing; major neurosurgical procedure

Referral Criteria

• ENT referral: all suspected Ménière disease for diagnosis confirmation and management
• Audiology: serial audiometry monitoring
• Urgent ENT: sudden SNHL, suspected vestibular schwannoma, disabling vertigo
• Driving advice: DVLA notification required

• 60-70% of patients achieve adequate symptom control with conservative measures
• Vertigo attacks typically burn out over 5-15 years as vestibular function declines
• 50% develop moderate-severe hearing loss in the affected ear over 10 years
• Bilateral involvement: 25-40% within 10-20 years (significant impact on quality of life)
• Tumarkin's otolithic crisis (drop attacks): occurs in 5-10%, risk of serious injury
• Quality of life significantly impacted during active disease
• With appropriate management, most patients maintain functional independence

AAO-HNS 2020 Diagnostic Criteria for Definite Ménière Disease

Management Escalation Ladder

Ménière Disease vs Vestibular Migraine

Key Facts

BPPV is a mechanical disorder of the inner ear causing brief episodes of vertigo triggered by specific head movements. It is the most common vestibular disorder and is diagnosed and treated at the bedside with specific positional manoeuvres.

Epidemiology

• Most common cause of vertigo (20-30% of all vertigo)
• Lifetime prevalence: 2.4%
• Annual incidence: 64 per 100,000
• Peak age: 50-70 years
• Female:male ratio 2:1
• Incidence increases with age

Aetiology

• Idiopathic in >50% of cases (especially elderly)
• Head trauma (15-20%)
• Vestibular neuritis (preceding viral illness)
• Ménière disease (associated)
• Prolonged bed rest or immobility
• Inner ear surgery (post-stapedectomy, post-cochlear implant)
• Osteoporosis and vitamin D deficiency (associated with recurrence)

Pathophysiology

• Otoconia (calcium carbonate crystals) normally embedded in the utricular macula become dislodged
• Free-floating otoconia enter a semicircular canal (posterior canal in 90%, horizontal in 8%, anterior in 2%)
• Canalithiasis: otoconia float freely in canal endolymph (most common mechanism)
• Cupulolithiasis: otoconia adhere to cupula (less common, causes persistent positional nystagmus)
• Head movement in the plane of the affected canal causes gravity-dependent movement of otoconia
• This creates abnormal endolymph flow, deflecting the cupula and stimulating vestibular nerve
• Results in brief intense vertigo with characteristic nystagmus pattern

Typical Presentation

• Brief episodes of intense rotational vertigo lasting <1 minute (typically 10-30 seconds)
• Triggered by specific head movements: rolling over in bed, looking up, bending forward, getting out of bed
• Often worse in the morning
• Associated nausea (vomiting less common)
• No hearing loss, no tinnitus, no neurological symptoms
• Between episodes: may have mild unsteadiness

Dix-Hallpike Test Findings (Posterior Canal BPPV)

• Latency: 2-5 seconds before nystagmus onset
• Torsional upbeat nystagmus (geotropic, towards the ground, with torsional component towards the affected ear)
• Duration: <1 minute (typically 10-30 seconds)
• Crescendo-decrescendo pattern
• Fatigable: reduces on repeated testing
• Associated with vertigo

Red Flags

• Vertigo lasting >1 minute continuously (not BPPV)
• Hearing loss or tinnitus (consider Ménière, labyrinthitis)
• Neurological symptoms (diplopia, dysarthria, dysphagia, limb weakness) - posterior stroke
• Non-fatigable, no latency nystagmus (central cause)
• Persistent vertigo not related to position
• Downbeat nystagmus (posterior fossa lesion)

Bedside

• Dix-Hallpike test: gold standard for posterior canal BPPV (positive on affected side)
• Supine roll test: for horizontal canal BPPV (geotropic or apogeotropic nystagmus)
• HINTS exam (Head Impulse, Nystagmus, Test of Skew): to differentiate peripheral from central vertigo in acute vestibular syndrome
• Romberg test, gait assessment
• Cranial nerve examination
• Otoscopy (should be normal)

Bloods

• Not routinely required
• Vitamin D levels if recurrent BPPV

Imaging

• Not routinely required for typical BPPV with positive Dix-Hallpike
• MRI brain: if atypical features, central signs, or failed treatment after multiple repositioning manoeuvres

Special Tests

• Audiometry: not routinely needed; if performed, should be normal
• Videonystagmography (VNG): may be used to confirm and characterise nystagmus

Non-pharmacological

• Epley manoeuvre (canalith repositioning procedure): first-line treatment for posterior canal BPPV
  • Single treatment effective in 80%
  • Can be repeated; >95% effective with repeated treatments
  • Can be taught as home exercise (modified Epley)
• Semont manoeuvre: alternative to Epley for posterior canal BPPV
• BBQ roll manoeuvre (Lempert/Gufoni): for horizontal canal BPPV
• Brandt-Daroff exercises: home vestibular habituation exercises for persistent symptoms
• Post-Epley: no evidence that post-manoeuvre restrictions (sleeping upright, avoiding head movement) improve outcomes

Pharmacological

• Vestibular sedatives are NOT recommended (prochlorperazine, betahistine, cinnarizine) - they delay vestibular compensation and are ineffective for BPPV
• Short-term antiemetics (cyclizine) may be used for acute severe nausea
• Vitamin D supplementation: evidence suggests reduces recurrence if deficient (serum 25-OH vitamin D <20ng/ml)

Surgical

• Posterior semicircular canal occlusion: very rarely, for intractable BPPV unresponsive to repeated repositioning manoeuvres; highly effective (>95%) but risk of SNHL
• Singular neurectomy: historical; rarely performed

Referral Criteria

• Most BPPV can be diagnosed and treated in primary care or emergency departments
• ENT/vestibular physiotherapy referral: if failed Epley after 3 attempts, atypical features, horizontal/anterior canal BPPV
• Urgent referral: if central features, neurological symptoms, diagnostic uncertainty

• Epley manoeuvre success rate: 80% after single treatment, >95% after repeated treatments
• Spontaneous resolution: 20-30% within 1 month even without treatment
• Recurrence: 30-50% within 5 years; higher in elderly, post-traumatic, and vitamin D deficient patients
• No risk of permanent hearing loss or vestibular damage
• Functional impact: risk of falls in elderly; driving and work may be temporarily affected
• Quality of life returns to normal between episodes with successful treatment
• Chronic or treatment-resistant BPPV (<5%): consider cupulolithiasis, bilateral BPPV, or central mimic

Epley Manoeuvre Steps (Right Posterior Canal)

Types of BPPV by Canal Affected

BPPV vs Central Positional Vertigo

Key Facts

Vestibular neuritis (vestibular neuronitis) is an acute unilateral vestibular loss causing prolonged rotational vertigo. It is the most common cause of acute vestibular syndrome and must be differentiated from posterior circulation stroke.

Epidemiology

• Annual incidence: 3.5 per 100,000
• Peak age: 30-60 years
• No sex predominance
• Accounts for 5-10% of all vertigo presentations
• Often preceded by viral URTI (1-2 weeks before)

Aetiology

• Viral reactivation: HSV-1 reactivation in Scarpa's (vestibular) ganglion is the leading theory
• Post-infectious inflammation of the vestibular nerve
• Superior vestibular nerve affected more commonly than inferior division
• Vascular ischaemia of the vestibular nerve is an alternative hypothesis

Pathophysiology

• Unilateral vestibular nerve inflammation causes acute loss of vestibular input from one labyrinth
• Tonic vestibular imbalance: the intact contralateral vestibular system generates relative excitation
• This imbalance is perceived as rotation (vertigo) and drives spontaneous nystagmus towards the intact ear
• Central compensation begins within hours to days via cerebellar and brainstem adaptation
• Vestibular rehabilitation accelerates central compensation
• Incomplete compensation may result in chronic dizziness/imbalance

Typical Presentation

• Acute onset severe rotational vertigo (usually developing over hours)
• Duration: 24-72 hours of intense vertigo, then gradual improvement over 1-6 weeks
• Severe nausea and vomiting
• Postural instability: difficulty standing/walking, falling towards affected side
• May have preceding viral URTI symptoms
• No hearing loss, no tinnitus (if present, consider labyrinthitis or Ménière)

Examination Findings

• Spontaneous horizontal-torsional nystagmus: beating AWAY from the affected ear
  • Follows Alexander's law: increases when looking in direction of fast phase
  • Inhibited by visual fixation (use Frenzel glasses to unmask)
• Positive head impulse test (HIT): corrective saccade when head turned towards affected side
• Negative test of skew: no vertical misalignment (skew deviation suggests central cause)
• Romberg positive: falls towards affected side
• Gait deviation towards affected side

Red Flags (Suggesting Central Cause - Stroke)

• Negative head impulse test (normal) with acute vertigo - paradoxically suggests central lesion
• Direction-changing nystagmus (changes with gaze direction)
• Skew deviation (vertical misalignment on alternate cover test)
• Acute hearing loss with vertigo (consider AICA stroke)
• New headache, especially occipital
• Truncal ataxia unable to sit unsupported
• Other neurological signs (diplopia, dysarthria, dysphagia, limb ataxia)

Bedside

• HINTS exam (most important bedside assessment):
  • Head Impulse Test (HIT): positive (abnormal) = peripheral (reassuring)
  • Nystagmus: unidirectional, inhibited by fixation = peripheral
  • Test of Skew: negative = peripheral
  • HINTS positive for peripheral cause = safe to diagnose vestibular neuritis
  • HINTS suggesting central cause = urgent MRI/neurology
• Hearing assessment (whispered voice, tuning forks): should be normal
• Blood pressure, blood glucose
• Gait assessment

Bloods

• Not routinely required
• Consider glucose, lipids, coagulation if stroke risk factors

Imaging

• Not routinely required if HINTS confidently peripheral
• MRI brain (DWI): if any central features on HINTS exam, stroke risk factors, or diagnostic uncertainty
  • DWI-negative MRI within first 48 hours does NOT fully exclude posterior fossa stroke (sensitivity ~80% in first 24 hours)

Special Tests

• Caloric testing: absent or reduced vestibular response on affected side (canal paresis >25%)
• vHIT (video Head Impulse Test): quantitative assessment of VOR; reduced gain on affected side
• Pure tone audiometry: should be normal (if abnormal, diagnose labyrinthitis)
• Vestibular evoked myogenic potentials (VEMPs): assess inferior vestibular nerve function

Non-pharmacological

• Vestibular rehabilitation exercises: most important treatment; begin as soon as acute symptoms allow (usually 3-5 days)
  • Cawthorne-Cooksey exercises: head movements, balance exercises, gait training
  • Customised vestibular physiotherapy
  • Promote central compensation
• Early mobilisation (avoid prolonged bed rest)
• Adequate hydration (especially if vomiting)

Pharmacological

• Acute phase (first 3-5 days only):
  • Prochlorperazine 5-10mg TDS PO or buccal 3-6mg BD
  • Cyclizine 50mg TDS
  • Ondansetron 4-8mg for severe vomiting
  • STOP vestibular sedatives after 3-5 days - prolonged use delays vestibular compensation
• Corticosteroids: methylprednisolone starting at 100mg OD, tapered over 3 weeks (Strupp et al., NEJM 2004 - showed improved vestibular recovery)
  • Evidence is modest; not universally adopted
  • If used, start within 72 hours of symptom onset
• Antivirals (valaciclovir): no evidence of benefit; NOT recommended

Surgical

• Not applicable for vestibular neuritis

Referral Criteria

• Emergency assessment if central features on HINTS exam (stroke)
• ENT/audiovestibular referral if: not improving after 6 weeks, recurrent episodes, hearing loss develops
• Vestibular physiotherapy referral for rehabilitation
• Neurology referral if diagnostic uncertainty or atypical features

• Most patients recover well over 1-6 weeks with vestibular rehabilitation
• 50-70% achieve complete vestibular compensation within 3 months
• 30-50% have persistent mild imbalance or dizziness at 1 year
• Caloric testing: 50% show persistent canal paresis at 1 year (asymptomatic due to central compensation)
• 10-15% develop BPPV subsequently (otoconia displaced during acute illness)
• Recurrence of vestibular neuritis is rare (<2%)
• Incomplete compensation more likely in elderly patients and those with delayed mobilisation
• Prolonged use of vestibular sedatives significantly delays recovery

HINTS Exam Interpretation

Vestibular Neuritis vs Labyrinthitis

Strupp et al. (NEJM 2004) Key Findings

Key Facts

Tonsillitis is an acute inflammatory condition of the palatine tonsils, usually caused by viral or bacterial infection. It is one of the most common reasons for GP consultation and antibiotic prescribing, making appropriate use of clinical scoring systems essential to reduce unnecessary antibiotic use.

Epidemiology

• Extremely common, particularly in children aged 5-15 years
• Less common in adults >40 and children <3
• Most cases are viral (70-80%)
• Peak incidence: winter and early spring
• Recurrent tonsillitis affects approximately 11% of children

Aetiology

• Viral (most common): EBV (glandular fever), adenovirus, rhinovirus, influenza, parainfluenza, enterovirus, coronavirus
• Bacterial: Group A Streptococcus (GAS/Streptococcus pyogenes) - 15-30% in children, 5-10% in adults
• Other bacteria: Group C/G Streptococcus, Fusobacterium necrophorum (Lemierre syndrome), Arcanobacterium haemolyticum

Pathophysiology

• Pharyngeal lymphoid tissue (Waldeyer's ring) is exposed to inhaled/ingested pathogens
• Tonsils are immunologically active, particularly in childhood, trapping and processing antigens
• Infection triggers acute inflammatory response: neutrophil infiltration, oedema, exudate
• Recurrent infections may lead to tonsillar hypertrophy and cryptic debris accumulation
• GAS produces virulence factors: M protein (adhesion, immune evasion), streptolysin O/S (tissue damage), pyrogenic exotoxins (scarlet fever)

Typical Presentation

• Sore throat (odynophagia): often severe, difficulty swallowing
• Fever (>38°C)
• Tonsillar enlargement and erythema ± exudate (white/yellow spots or membrane)
• Tender cervical lymphadenopathy (anterior chain)
• Malaise, headache
• Children: may present with abdominal pain, nausea

Viral vs Bacterial Features

• Viral: concurrent coryza, cough, conjunctivitis, hoarseness, diarrhoea
• Bacterial (GAS): acute onset, high fever, exudate, tender anterior lymph nodes, absence of cough/coryza, scarlatiniform rash (scarlet fever)

Red Flags

• Unilateral tonsillar swelling with trismus (peritonsillar abscess/quinsy)
• Drooling, muffled voice ('hot potato'), neck stiffness (parapharyngeal/retropharyngeal abscess)
• Stridor or respiratory distress (airway compromise)
• Inability to swallow fluids (severe dehydration risk)
• Persistent fever >5 days despite antibiotics (abscess, EBV, alternative diagnosis)
• Sandpaper rash (scarlet fever - notifiable disease)

Bedside

• Clinical assessment using FeverPAIN score or Centor criteria
• Throat examination: tonsillar size, erythema, exudate, asymmetry
• Temperature
• Assessment for dehydration

Bloods

• Not routinely required for uncomplicated tonsillitis
• FBC: if EBV suspected (atypical lymphocytes >20%)
• Monospot/Paul-Bunnell test: heterophile antibodies for EBV (sensitivity ~85% in second week; may be negative initially)
• EBV serology: IgM VCA (acute infection)
• LFTs: often deranged in EBV
• ASO titre/anti-DNase B: if post-streptococcal complications suspected (retrospective)

Microbiology

• Throat swab: not routinely recommended in primary care (NICE NG84) - delay in results; treat based on clinical scoring
• Rapid antigen detection test (RADT) for GAS: not widely used in UK primary care

Imaging

• Not required for uncomplicated tonsillitis
• CT neck with contrast: if peritonsillar/parapharyngeal/retropharyngeal abscess suspected

Non-pharmacological

• Adequate fluid intake
• Soft diet
• Rest
• Avoid smoking

Pharmacological

• Analgesia (mainstay for all cases): paracetamol 1g QDS and/or ibuprofen 400mg TDS
• Antibiotic prescribing (NICE NG84 - FeverPAIN score):
  • Score 0-1: no antibiotic (self-limiting viral illness >80% probability)
  • Score 2-3: delayed (back-up) prescription to use if not improving at 3-5 days
  • Score 4-5: immediate antibiotic prescription
• First-line: phenoxymethylpenicillin (penicillin V) 500mg QDS (adults) or 250mg QDS (children) for 5-10 days
• Penicillin allergy: clarithromycin 500mg BD for 5 days
• Severe/unable to swallow: IM benzylpenicillin 1.2g stat or IV amoxicillin
• AVOID amoxicillin if EBV suspected (maculopapular rash in >90%)
• Corticosteroids: single dose dexamethasone 10mg PO or IM may reduce pain severity and duration (TOAST trial); not routinely recommended in NICE

Surgical

• Tonsillectomy indications (Paradise criteria/SIGN 117):
  • ≥7 episodes in 1 year, OR
  • ≥5 episodes per year for 2 years, OR
  • ≥3 episodes per year for 3 years
  • Each episode should be documented as: sore throat + one of: fever >38.3°C, cervical lymphadenopathy, tonsillar exudate, positive GAS culture
• Also indicated for peritonsillar abscess (quinsy tonsillectomy or interval tonsillectomy)

Referral Criteria

• ENT referral: meets tonsillectomy criteria, recurrent peritonsillar abscess, suspected malignancy (unilateral enlargement in adult)
• Emergency referral: suspected quinsy, airway compromise, parapharyngeal abscess, Lemierre syndrome
• Hospital admission: unable to swallow fluids, signs of sepsis, respiratory compromise

• Most cases resolve within 7-10 days regardless of antibiotic treatment
• Antibiotics reduce symptom duration by approximately 1 day (NNT 6 for sore throat at day 3)
• Peritonsillar abscess complicates 1-3% of untreated bacterial tonsillitis
• Rheumatic fever: rare in UK but important globally (follows GAS pharyngitis by 2-4 weeks)
• Post-streptococcal glomerulonephritis: 1-3 weeks after GAS; antibiotics do NOT prevent this
• Tonsillectomy reduces episodes of sore throat for 1-2 years but benefit may diminish over time
• Post-tonsillectomy haemorrhage: primary (<24h) 0.5-2%, secondary (5-10 days) 2-4%

FeverPAIN Score (NICE NG84)

Centor Criteria (Modified)

Complications of GAS Tonsillitis

Key Facts

Peritonsillar abscess (quinsy) is a collection of pus in the peritonsillar space, forming between the tonsillar capsule and the pharyngeal constrictor muscle. It is the most common deep neck space infection and the most common complication of acute tonsillitis requiring hospital admission.

Epidemiology

• Incidence: approximately 30 per 100,000 per year
• Peak age: 20-40 years (less common in young children)
• Male = Female
• More common in smokers
• Seasonal: winter and spring (parallel to tonsillitis)

Aetiology

• Usually develops as a complication of acute bacterial tonsillitis
• Infection spreads through the tonsillar capsule to the peritonsillar space
• Polymicrobial in most cases: GAS, Fusobacterium necrophorum, Prevotella, Staphylococcus aureus
• Weber's glands (minor salivary glands in the supratonsillar fossa) may serve as the site of initial abscess formation
• Risk factors: recurrent tonsillitis, smoking, dental infections, immunocompromise

Pathophysiology

• Pus collects in the potential space between tonsillar capsule and superior constrictor
• Abscess typically forms at the upper pole of the tonsil (supratonsillar)
• Expanding abscess pushes tonsil medially and inferiorly
• Uvula is deviated away from the affected side
• Trismus results from inflammation of pterygoid muscles
• Can extend to parapharyngeal space if untreated

Typical Presentation

• Severe unilateral sore throat (progressively worsening, often despite antibiotics for tonsillitis)
• Trismus (difficulty opening mouth) - pathognomonic
• Muffled, 'hot potato' voice
• Odynophagia (pain on swallowing, often cannot swallow saliva)
• Drooling
• Referred otalgia (ipsilateral ear pain)
• High fever, malaise

Examination Findings

• Unilateral peritonsillar swelling - soft palate/anterior pillar bulging
• Uvula deviation away from the affected side
• Tonsil displaced medially, inferiorly
• Trismus (often cannot fully examine oropharynx)
• Tender, enlarged ipsilateral cervical lymph nodes
• Foetor oris (halitosis)

Red Flags

• Stridor or respiratory distress (airway compromise)
• Bilateral peritonsillar swelling
• Neck swelling extending below mandible (parapharyngeal extension)
• Torticollis (parapharyngeal/retropharyngeal abscess)
• Sepsis features (high fever, tachycardia, hypotension)
• Failure to improve after drainage (recurrence, deeper space infection)

Bedside

• Clinical diagnosis is usually sufficient (experienced clinician)
• Assessment of trismus severity
• Assessment of airway
• Temperature and observations
• Hydration status

Bloods

• FBC (raised WCC, neutrophilia)
• CRP (markedly elevated)
• U&Es (dehydration assessment)
• Blood cultures if sepsis suspected

Microbiology

• Aspirate pus for MC&S (guides antibiotic adjustment)
• Throat swab

Imaging

• Not routinely required if diagnosis is clinically clear
• CT neck with IV contrast: if diagnostic doubt, suspected deep space extension (parapharyngeal/retropharyngeal), failure to improve post-drainage
  • Shows rim-enhancing collection in peritonsillar space
• Intraoral ultrasound: emerging tool to differentiate cellulitis from abscess at bedside

Special Tests

• Needle aspiration: is both diagnostic and therapeutic (purulent aspirate confirms abscess)
• If no pus aspirated: likely peritonsillar cellulitis (treat with IV antibiotics alone)

Non-pharmacological

• IV fluid resuscitation if dehydrated
• Nil by mouth if airway concern or surgical drainage planned
• Analgesia and antipyretics
• Head elevation

Pharmacological

• IV antibiotics:
  • IV co-amoxiclav 1.2g TDS (covers GAS, anaerobes)
  • OR IV ceftriaxone 2g OD + IV metronidazole 500mg TDS
  • If penicillin allergy: IV clindamycin 600mg QDS
  • Duration: IV until improving, then oral for total 7-10 days
• Analgesia: paracetamol 1g QDS, ibuprofen 400mg TDS
• Dexamethasone 8-10mg IV stat: may reduce pain, trismus, and speed recovery (evidence supportive but not universally adopted)
• Topical anaesthetic gargle: benzydamine (Difflam) spray

Surgical/Interventional

• Needle aspiration: first-line drainage technique
  • Performed under local anaesthetic (topical + infiltration)
  • Success rate 85-95% with single or repeated aspiration
  • Aspirate sent for MC&S
• Incision and drainage: if aspiration fails or abscess re-accumulates
  • Performed under local anaesthesia in most cases
  • Break down loculations with Hilton's method (sinus forceps)
• Quinsy tonsillectomy (tonsillectomy à chaud): performed at same time as drainage
  • Definitive treatment; lower recurrence rate
  • Considered if: recurrent quinsy, meets tonsillectomy criteria
• Interval tonsillectomy: elective tonsillectomy 6-8 weeks after drainage

Referral Criteria

• All suspected quinsy requires same-day ENT assessment
• Emergency: airway compromise, deep space extension, sepsis
• Post-discharge: ENT follow-up for consideration of interval tonsillectomy

• Excellent prognosis with prompt drainage and antibiotics
• >95% resolve completely after drainage
• Recurrence: 10-15% without tonsillectomy; <1% after tonsillectomy
• Complications (rare with prompt treatment): parapharyngeal abscess (<5%), airway obstruction, aspiration pneumonia, Lemierre syndrome, internal jugular vein thrombosis, mediastinitis, sepsis
• Lemierre syndrome (septic IJV thrombophlebitis): mortality 5-18% historically; requires prolonged IV antibiotics and anticoagulation consideration
• Most patients discharged within 24-48 hours of drainage

Peritonsillar Abscess Drainage Technique

Indications for CT Neck in Quinsy

Key Facts

Rhinosinusitis is defined as inflammation of the nose and paranasal sinuses characterised by nasal obstruction, discharge, facial pain/pressure, and reduced sense of smell. It is one of the most common conditions seen in primary care.

Epidemiology

• Acute rhinosinusitis: extremely common; adults average 2-5 URTIs per year; 0.5-2% develop bacterial complication
• Chronic rhinosinusitis: prevalence 11% in UK adults
• Nasal polyps: affect 1-4% of the population; more common in males
• Significant socioeconomic burden: lost work days, healthcare costs

Aetiology

• Acute viral (most common): rhinovirus, influenza, parainfluenza, adenovirus
• Acute bacterial: Streptococcus pneumoniae, Haemophilus influenzae, Moraxella catarrhalis, Staphylococcus aureus
• Chronic: multifactorial - mucosal inflammation, impaired mucociliary clearance, bacterial biofilms, allergy, nasal polyps, anatomical factors (deviated septum, concha bullosa)
• Fungal: allergic fungal rhinosinusitis, fungal ball, invasive fungal sinusitis (immunocompromised)

Pathophysiology

• Viral infection causes mucosal oedema and inflammation at the ostiomeatal complex
• Obstruction of sinus ostia impairs ventilation and mucociliary drainage
• Retained mucus becomes secondarily infected with bacteria
• Chronic inflammation leads to mucosal remodelling, polyp formation, and biofilm development
• Aspirin-exacerbated respiratory disease (AERD/Samter's triad): nasal polyps + asthma + aspirin sensitivity

Acute Rhinosinusitis

• Nasal congestion and obstruction
• Purulent nasal discharge (anterior or posterior drip)
• Facial pain/pressure (worse on bending forward, unilateral or bilateral)
• Reduced or lost sense of smell (hyposmia/anosmia)
• Headache, malaise, fever
• Maxillary toothache

Chronic Rhinosinusitis

• Persistent nasal obstruction
• Ongoing nasal discharge (mucopurulent)
• Reduced sense of smell (often prominent)
• Facial pressure (less acute than acute sinusitis)
• Post-nasal drip
• Nasal polyps visible on examination (if present)

Red Flags

• Periorbital cellulitis/oedema (orbital complication)
• Frontal swelling (Pott's puffy tumour - frontal osteomyelitis)
• Severe headache, photophobia, neck stiffness (meningitis)
• Visual changes or proptosis (orbital abscess)
• Altered consciousness (intracranial abscess)
• Unilateral nasal mass with epistaxis in adults (malignancy)
• Blood-stained discharge (granulomatosis with polyangiitis, malignancy)

Bedside

• Anterior rhinoscopy: mucosal oedema, purulent discharge, polyps
• Nasal endoscopy (ENT): detailed examination of nasal cavity, middle meatus, and nasopharynx
• Temperature and observations

Bloods

• Not routinely required for acute rhinosinusitis
• FBC, CRP, ESR if complications suspected
• ANCA: if granulomatosis with polyangiitis suspected
• Total IgE, specific IgE: if allergic component

Imaging

• Not recommended for acute uncomplicated rhinosinusitis (NICE, EPOS)
• CT paranasal sinuses (non-contrast): gold standard for chronic rhinosinusitis assessment and pre-operative planning
  • Shows mucosal thickening, air-fluid levels, bony anatomy
  • Lund-Mackay scoring system for severity
• CT with contrast: if complications suspected (orbital, intracranial)
• MRI: if malignancy or intracranial extension suspected

Special Tests

• Nasal swab/culture: not routinely helpful (correlates poorly with sinus pathogens)
• Smell testing: olfactometry for chronic rhinosinusitis
• Allergy testing: if allergic rhinitis component

Non-pharmacological

• Steam inhalation: may provide symptom relief (no evidence of efficacy)
• Saline nasal irrigation: evidence of benefit in acute and chronic rhinosinusitis
• Adequate hydration
• Avoidance of triggers (allergens, irritants)

Pharmacological

• Acute rhinosinusitis:
  • Symptomatic relief: paracetamol/ibuprofen, saline nasal rinse
  • Intranasal decongestant: xylometazoline 0.1% spray BD for maximum 7 days (rebound congestion risk)
  • Antibiotics (NICE NG79 - only if clinically indicated):
    • Phenoxymethylpenicillin 500mg QDS for 5 days (first-line)
    • OR Amoxicillin 500mg TDS for 5 days
    • Alternative: doxycycline 200mg stat then 100mg OD for 5 days
    • Indicate: systemically very unwell, high fever, symptoms >10 days without improvement, immunocompromised, complications
• Chronic rhinosinusitis:
  • Intranasal corticosteroid: mometasone 200mcg (2 sprays) each nostril OD or fluticasone 200mcg each nostril OD - long-term
  • Saline irrigation: daily, large-volume (240ml)
  • Short course oral prednisolone: 25-30mg OD for 5-10 days for acute exacerbation or polyp reduction (before FESS)
  • Dupilumab (anti-IL4/13): for severe CRSwNP refractory to surgery and steroids (NICE TA851)

Surgical

• FESS (functional endoscopic sinus surgery): for chronic rhinosinusitis refractory to maximal medical therapy
  • Enlarges sinus ostia, removes polyps, improves drainage
  • Success rate 80-90% for symptom improvement
• Polypectomy: nasal polyp removal
• Balloon sinuplasty: minimally invasive alternative for selected cases
• Emergency surgery: drainage of orbital/intracranial abscess

Referral Criteria

• ENT referral: chronic rhinosinusitis >12 weeks not responding to medical therapy, recurrent acute sinusitis (≥4 episodes/year), nasal polyps, suspected complications
• Urgent/2-week wait: unilateral symptoms with epistaxis/obstruction in adults (exclude malignancy)
• Emergency: orbital complications, intracranial complications, facial swelling

• Acute viral rhinosinusitis: >90% resolve within 2-3 weeks without antibiotics
• Acute bacterial sinusitis: >70% resolve without antibiotics; antibiotics shorten duration by 1-2 days
• Chronic rhinosinusitis: chronic condition requiring long-term management; FESS provides significant improvement in 80-90%
• Nasal polyp recurrence after surgery: 20-40% at 5 years
• Complications of acute sinusitis (orbital, intracranial): <1% but potentially life-threatening
• Anosmia in chronic rhinosinusitis: may improve with topical steroids and surgery but often incompletely

EPOS 2020 Classification of Rhinosinusitis

Samter's Triad (AERD)

Complications of Acute Sinusitis

Key Facts

Nasal polyps are benign inflammatory growths of the nasal and paranasal sinus mucosa. They are a common manifestation of chronic rhinosinusitis and are associated with asthma, aspirin sensitivity, and cystic fibrosis. They cause nasal obstruction and anosmia and often require combined medical and surgical management.

Epidemiology

• Prevalence: 1-4% of the general population
• Male:female ratio 2:1
• Peak onset: >40 years; rare in children (if present, investigate for cystic fibrosis)
• Present in 20-50% of patients with asthma; 60-70% of patients with aspirin-exacerbated respiratory disease (AERD)

Aetiology

• Chronic eosinophilic inflammation of the sinonasal mucosa
• Associated conditions: chronic rhinosinusitis, asthma, allergic fungal rhinosinusitis, AERD (Samter's triad), cystic fibrosis, primary ciliary dyskinesia (Kartagener syndrome), Churg-Strauss syndrome (EGPA)
• Type 2 inflammation: IL-4, IL-5, IL-13 driven eosinophilic infiltration
• Not caused by allergy per se, but allergic rhinitis is a common comorbidity

Pathophysiology

• Chronic inflammation leads to oedematous thickening of the sinus mucosa
• Prolapse of oedematous mucosa through sinus ostia into the nasal cavity
• Eosinophilic infiltration predominates; driven by type 2 cytokines (IL-5, IL-13)
• Epithelial barrier dysfunction and Staphylococcus aureus superantigens contribute
• Polyps cause mechanical obstruction, impaired mucociliary clearance, and olfactory dysfunction
• Recurrence after surgical removal is common due to underlying mucosal disease

Symptoms

• Nasal obstruction (bilateral, progressive)
• Anosmia/hyposmia (often the most troublesome symptom)
• Nasal discharge (mucoid or mucopurulent)
• Post-nasal drip
• Facial pressure/fullness
• Snoring
• Headache (if sinus involvement)

Examination

• Anterior rhinoscopy/nasal endoscopy: pale, grey, smooth, glistening, insensitive, pedunculated masses
• Bilateral in most cases
• Originate from middle meatus (ethmoid sinus mucosa)
• Do NOT bleed on touch or cause pain (insensitive - distinguishes from turbinates)

Red Flags

• Unilateral polyp in adult - biopsy to exclude inverted papilloma or malignancy
• Nasal polyps in a child - investigate for cystic fibrosis (sweat test)
• Bloodstained discharge or friable tissue (malignancy)
• Facial deformity or proptosis (aggressive lesion)
• Anosmia with polyps and asthma - consider AERD/Samter's triad

Bedside

• Anterior rhinoscopy and nasal endoscopy
• Assessment of nasal airflow
• Smell testing

Bloods

• Total IgE and specific IgE (allergic component)
• Eosinophil count (type 2 inflammation marker)
• Aspergillus-specific IgE (allergic fungal rhinosinusitis)
• Sweat test: if polyps in a child (cystic fibrosis screening)
• ANCA: if vasculitis suspected (EGPA)

Imaging

• CT paranasal sinuses (non-contrast): gold standard
  • Mucosal thickening, opacification, polypoidal changes
  • Lund-Mackay score for severity grading
  • Pre-operative planning for FESS
• MRI: if complications, malignancy, or skull base involvement suspected

Special Tests

• Nasal peak inspiratory flow (NPIF): objective measure of nasal airflow
• SNOT-22 questionnaire: validated quality of life measure for rhinosinusitis
• Biopsy: for unilateral polyps (exclude malignancy/inverted papilloma)
• Skin prick testing: for allergic rhinitis assessment

Non-pharmacological

• Saline nasal irrigation (daily, large-volume - NeilMed, sterile saline)
• Allergen avoidance if allergic component identified
• Smoking cessation

Pharmacological

• First-line: intranasal corticosteroid drops or spray:
  • Mometasone 200mcg each nostril OD or fluticasone 200mcg each nostril OD
  • Betamethasone 0.1% drops (head-down position) - more effective for polyps than sprays
  • Long-term maintenance therapy
• Short course oral prednisolone: 25-30mg OD for 5-10 days
  • For significant polyp load, acute exacerbation, or pre-operatively (to shrink polyps)
  • Limit to 2-3 courses per year (steroid side effects)
• Biologics (for severe CRSwNP refractory to steroids and surgery):
  • Dupilumab (anti-IL4Rα): SC injection, NICE TA851 approved
  • Mepolizumab (anti-IL5): for severe eosinophilic CRSwNP
  • Omalizumab (anti-IgE): if concurrent allergic asthma
• Antihistamines: if concurrent allergic rhinitis
• Aspirin desensitisation: for AERD (specialist centre)

Surgical

• FESS (functional endoscopic sinus surgery) with polypectomy:
  • Indicated when polyps refractory to maximal medical therapy (≥8 weeks of intranasal steroids + at least one course of oral steroids)
  • Removes polyps and opens sinus ostia to improve drainage and topical steroid access
  • Success rate for symptom improvement: 80-90%
• Revision FESS: for recurrent polyps (recurrence rate 20-40% at 5 years)

Referral Criteria

• ENT referral: nasal polyps visible on examination, chronic rhinosinusitis not responding to 3 months of medical therapy
• Urgent/2-week wait: unilateral polyp (exclude malignancy), bloodstained discharge
• Paediatric: nasal polyps in child (cystic fibrosis investigation)

• Nasal polyps are a chronic condition with high recurrence after treatment
• Intranasal steroids: reduce polyp size and improve symptoms in >60%
• Oral steroids: rapid but temporary reduction in polyp size
• Post-FESS: 80-90% symptom improvement; 20-40% polyp recurrence at 5 years
• Biologics: significant improvement in polyp score, smell, and QoL in refractory patients
• AERD/Samter's triad: more aggressive disease, higher recurrence rates
• Anosmia: may not fully recover despite treatment
• Long-term follow-up required with serial nasal endoscopy and SNOT-22 scoring

Nasal Polyp Grading (Lildholdt Scale)

Samter's Triad (AERD)

When to Investigate for Cystic Fibrosis

Key Facts

Epistaxis is bleeding from the nasal cavity. It is one of the most common ENT emergencies. Most cases are anterior, self-limiting, and easily managed, but posterior epistaxis can be severe and life-threatening, requiring urgent intervention.

Epidemiology

• 60% of people experience epistaxis at some point in their life
• 6-10% require medical attention
• Bimodal age distribution: children (2-10 years, nose picking) and elderly (>65 years, anticoagulants, hypertension)
• More common in winter months (dry air, URTIs)
• Male predominance in adult presentations

Aetiology

• Local causes: digital trauma (nose picking - most common in children), mucosal drying, nasal fracture, nasal surgery, foreign body, septal perforation, nasal tumours, hereditary haemorrhagic telangiectasia (HHT/Osler-Weber-Rendu)
• Systemic causes: anticoagulants (warfarin, DOACs, heparin), antiplatelets (aspirin, clopidogrel), hypertension (may prolong bleeding), coagulopathies (haemophilia, von Willebrand disease, thrombocytopenia, liver disease), leukaemia
• Idiopathic: most common overall

Pathophysiology

• Little's area (Kiesselbach's plexus) on the anterior nasal septum is the most common site (90%)
  • Anastomosis of anterior ethmoidal, superior labial, greater palatine, and sphenopalatine arteries
  • Thin mucosa, exposed location, trauma-prone
• Posterior epistaxis: branches of sphenopalatine artery (posterior nasal septum and lateral nasal wall)
  • Higher flow, harder to control, more likely to require intervention
• Hypertension does not directly cause epistaxis but makes bleeding harder to control

Anterior Epistaxis

• Bleeding from one or both nostrils
• Patient can usually identify the bleeding side
• Visible bleeding point on anterior septum (Little's area)
• Usually self-limiting
• Common in children and young adults

Posterior Epistaxis

• Bleeding from back of nose, often bilateral or into throat
• Patient may swallow blood (presenting with haematemesis, melaena)
• Often profuse, continuous
• More common in elderly patients, those on anticoagulants
• May cause haemodynamic compromise

Red Flags

• Haemodynamic instability (tachycardia, hypotension)
• Signs of significant blood loss (pallor, dizziness)
• Known coagulopathy or anticoagulant use
• Bilateral epistaxis or blood in oropharynx (posterior source)
• Recurrent epistaxis requiring medical attention
• Unilateral nasal mass or obstruction (tumour)
• Multiple mucocutaneous telangiectasiae (HHT)

Bedside

• ABC assessment: if significant bleeding
• Blood pressure measurement
• Anterior rhinoscopy: identify bleeding point
• Nasendoscopy: if anterior source not identified

Bloods

• FBC: haemoglobin, platelets
• Coagulation screen: PT/INR, APTT (essential if on anticoagulants)
• Group and save / crossmatch: if significant ongoing blood loss
• U&Es: if significant blood loss

Imaging

• Not routinely required for epistaxis
• CT/MRI sinuses: if recurrent epistaxis with no identifiable source, suspected tumour
• CT angiography: if considering embolisation for refractory posterior epistaxis

Special Tests

• Von Willebrand factor assay, factor levels: if recurrent epistaxis suggesting coagulopathy
• Genetic testing: if HHT suspected (Curaçao criteria met)

Non-pharmacological

• First aid (ABCDE approach):
  1. Sit patient forward, mouth open
  2. Pinch soft part of nose continuously for 15-20 minutes
  3. Spit out blood (swallowed blood causes nausea/vomiting)
  4. Ice pack to nasal bridge (minimal evidence but widely used)
  5. Avoid nose blowing, sneezing with mouth closed, hot drinks for 24 hours

Pharmacological

• Topical vasoconstrictor: phenylephrine or xylometazoline spray before examination
• Cautery: silver nitrate (75%) applied to visible bleeding point for 5-10 seconds after topical anaesthesia (co-phenylcaine or lidocaine/phenylephrine)
  • Only cauterise ONE side of septum at a time (risk of septal perforation if bilateral)
• Naseptin cream (chlorhexidine/neomycin) or Vaseline: to anterior septum BD for 2-4 weeks after cautery or for recurrent minor epistaxis
• Tranexamic acid: 1g IV or topical (soaked gauze) as adjunct for significant bleeding
• Reverse anticoagulation: vitamin K (phytomenadione), prothrombin complex concentrate, fresh frozen plasma as indicated by INR/APTT

Surgical/Interventional (Escalation Pathway)

1. Anterior nasal packing: Rapid Rhino (inflatable) or Merocel (expandable) - leave for 24-48 hours
2. Posterior nasal packing: Foley catheter or posterior balloon tampon + anterior packing
3. Sphenopalatine artery ligation (endoscopic): definitive treatment for refractory posterior epistaxis; success rate >95%
4. Anterior ethmoidal artery ligation: for bleeding from anterior ethmoidal territory
5. Angiographic embolisation: alternative to surgical ligation in high-risk patients

Referral Criteria

• ENT assessment: all patients requiring nasal packing
• Emergency ENT: posterior epistaxis, haemodynamic compromise, failed anterior packing
• ENT follow-up: recurrent epistaxis, post-packing review
• Haematology: suspected coagulopathy

• >90% of anterior epistaxis controlled with first aid and/or cautery
• Anterior packing success rate: 70-80%
• Posterior packing success rate: 60-70%
• Sphenopalatine artery ligation: >95% success rate for posterior epistaxis
• Recurrence after cautery: 10-30% (higher in children due to nose picking)
• Posterior epistaxis in anticoagulated elderly patients carries significant morbidity
• HHT: lifelong recurrent epistaxis; may require multiple interventions
• Mortality from severe epistaxis is rare (<0.01%) with modern management

Epistaxis Management Escalation

Curaçao Criteria for HHT (≥3 = definite)

Blood Supply to Little's Area

Key Facts

Laryngitis is inflammation of the larynx affecting the vocal cords and surrounding structures. Acute laryngitis is extremely common, usually viral, and self-limiting. Chronic laryngitis (hoarseness >3 weeks) warrants investigation to exclude underlying pathology including malignancy.

Epidemiology

• Acute laryngitis: extremely common; often accompanies URTI
• Affects all age groups
• More common in winter months
• Professional voice users (teachers, singers, call centre workers) are more susceptible

Aetiology

• Acute: viral (most common - rhinovirus, influenza, parainfluenza, adenovirus), bacterial superinfection (rare), voice abuse
• Chronic: smoking (most important risk factor for malignancy), gastro-oesophageal/laryngopharyngeal reflux, chronic voice abuse/misuse, inhaled corticosteroids (candidiasis), allergic laryngitis, granulomatous disease (sarcoidosis, TB, GPA), fungal laryngitis (immunocompromised)

Pathophysiology

• Viral infection causes mucosal oedema and inflammation of the vocal cords
• Swollen, inflamed cords vibrate irregularly, producing hoarse voice
• Chronic irritation (smoke, acid, voice abuse) causes epithelial changes: oedema, keratosis, leucoplakia, dysplasia

Acute Laryngitis

• Hoarseness or voice loss (aphonia)
• Sore throat
• Dry, irritating cough
• Voice fatigue
• Associated URTI symptoms (coryza, malaise)
• Self-limiting within 7-10 days

Chronic Laryngitis

• Persistent hoarseness (>3 weeks)
• Voice change (deeper, rougher)
• Throat clearing habit
• Globus sensation (feeling of lump in throat)
• Chronic cough

Red Flags

• Hoarseness >3 weeks (exclude malignancy - NICE NG12)
• Stridor (airway obstruction)
• Dysphagia or odynophagia with hoarseness
• Haemoptysis
• Weight loss
• Smoker/ex-smoker with persistent hoarseness (high malignancy risk)
• Unilateral vocal cord palsy on laryngoscopy (recurrent laryngeal nerve - think lung/thyroid cancer, aortic aneurysm)

Bedside

• Voice assessment (perceptual - GRBAS scale: Grade, Roughness, Breathiness, Asthenia, Strain)
• Examination of neck (lymphadenopathy, thyroid)

Bloods

• Not routinely required for acute laryngitis
• TFTs if hypothyroidism suspected
• ACE level if sarcoidosis suspected

Imaging

• Not required for acute self-limiting laryngitis
• CT neck/chest: if malignancy suspected or vocal cord palsy identified
• MRI: for soft tissue detail of laryngeal lesions

Special Tests

• Fibreoptic nasendoscopy (FNL): essential for hoarseness >3 weeks
  • Visualises vocal cords, assesses mobility, identifies lesions
• Direct laryngoscopy and biopsy: under GA for suspicious lesions
• Stroboscopy: detailed assessment of vocal cord vibration
• 24-hour pH monitoring / impedance: for laryngopharyngeal reflux
• Speech and language therapy assessment: for functional voice disorders

Non-pharmacological

• Voice rest (reduce voice use, not complete silence)
• Adequate hydration
• Steam inhalation
• Humidification of environment
• Avoid irritants (smoking, alcohol, dusty environments)
• Speech and language therapy: for chronic voice disorders, vocal cord nodules, functional dysphonia

Pharmacological

• Acute viral laryngitis: NO antibiotics (self-limiting)
• Simple analgesia (paracetamol, ibuprofen)
• Laryngopharyngeal reflux: PPI trial (omeprazole 20mg BD for 2-3 months)
• Inhaled corticosteroid-related laryngitis/candidiasis: mouth rinse after inhaler use, consider spacer, dose reduction
• Fungal laryngitis: oral fluconazole 50mg OD for 2 weeks

Surgical

• Microlaryngoscopy and excision/biopsy: for vocal cord polyps, nodules (refractory to speech therapy), suspicious lesions
• Laser treatment: for papillomatosis, leucoplakia
• Laryngeal framework surgery: for vocal cord palsy (medialization thyroplasty)
• Injection laryngoplasty: hyaluronic acid injection for vocal cord palsy (temporary)

Referral Criteria

• 2-week wait ENT referral (NICE NG12): hoarseness >3 weeks, particularly smoker/ex-smoker >45 years, or neck lump >3 weeks
• Routine ENT referral: recurrent laryngitis, chronic voice change, vocal cord nodules
• Speech and language therapy: for voice rehabilitation
• Emergency: stridor, airway compromise

• Acute viral laryngitis: resolves within 7-10 days in almost all cases
• Vocal cord nodules: >80% resolve with speech therapy alone (surgery rarely needed)
• Vocal cord polyps: may require surgical excision if not responding to voice therapy
• Laryngopharyngeal reflux: often improves with 2-3 months of PPI + lifestyle modification
• Reinke oedema: improvement with smoking cessation; surgical debulking if persistent
• Laryngeal carcinoma: 5-year survival for early (T1) glottic carcinoma: >90% with radiotherapy

GRBAS Voice Assessment Scale

Causes of Vocal Cord Palsy

Key Facts

Hoarseness is one of the most common ENT symptoms, with a wide differential diagnosis ranging from benign self-limiting conditions to life-threatening malignancy. Any patient with hoarseness persisting beyond 3 weeks requires visualisation of the larynx to exclude serious pathology.

Epidemiology

• Point prevalence: approximately 1% of the population
• Lifetime prevalence: 30% experience at least one episode of significant hoarseness
• More common in professional voice users (teachers, singers)
• Laryngeal cancer: approximately 2,400 cases/year in the UK; M:F ratio 4:1

Aetiology

• Inflammatory: acute viral laryngitis (most common overall), chronic laryngitis, laryngopharyngeal reflux
• Structural: vocal cord nodules, polyps, cysts, Reinke oedema, papillomatosis, laryngeal carcinoma
• Neurological: vocal cord palsy (recurrent laryngeal nerve palsy - causes include lung cancer, thyroid surgery, aortic aneurysm, idiopathic)
• Functional: muscle tension dysphonia, psychogenic aphonia
• Systemic: hypothyroidism, RA (cricoarytenoid arthritis), amyloidosis
• Iatrogenic: post-intubation granuloma, post-thyroidectomy RLN injury, inhaled corticosteroid effect

Pathophysiology

• Normal voice production requires: adequate subglottic air pressure, regular vocal cord vibration, and normal resonance
• Any disruption to vocal cord structure, mass, tension, or mobility causes hoarseness
• Mass lesions (nodules, polyps, tumours) increase vocal cord mass and alter vibration
• Vocal cord palsy prevents full cord adduction, causing breathy voice and air escape
• Oedema (Reinke oedema, reflux) deepens the voice due to increased cord mass

History Points

• Duration and onset (acute vs chronic)
• Character of voice change (rough, breathy, strained, weak)
• Associated symptoms: sore throat, dysphagia, odynophagia, otalgia, stridor, cough, haemoptysis, weight loss
• Voice demands: professional voice user
• Smoking and alcohol history (strong risk factors for laryngeal cancer)
• Reflux symptoms: heartburn, throat clearing, globus, chronic cough
• Previous surgery: thyroidectomy, cardiac, thoracic, anterior cervical spine
• Previous intubation
• Medications: inhaled corticosteroids, ACE inhibitors (cough)

Examination

• Voice quality assessment
• Neck palpation: thyroid, lymphadenopathy
• Oral cavity and oropharynx inspection
• Indirect laryngoscopy or fibreoptic nasendoscopy

Red Flags

• Hoarseness >3 weeks (NICE NG12)
• Smoker/ex-smoker >45 years
• Dysphagia or odynophagia
• Haemoptysis
• Stridor
• Weight loss
• Neck lump
• Otalgia (referred pain from larynx via Arnold's nerve)

Bedside

• GRBAS voice assessment
• Neck examination (lymph nodes, thyroid)
• Fibreoptic nasendoscopy (FNL): essential for all hoarseness >3 weeks

Bloods

• TFTs (exclude hypothyroidism)
• FBC if anaemia/malignancy suspected

Imaging

• CT neck and chest (skull base to diaphragm): for vocal cord palsy (identify cause along nerve course)
• CT with contrast: for laryngeal masses and staging
• MRI: for soft tissue detail of laryngeal/hypopharyngeal lesions
• CXR: if vocal cord palsy (exclude left hilar mass)

Special Tests

• Stroboscopy: detailed assessment of vocal cord vibration pattern
• Direct laryngoscopy and biopsy (under GA): for suspicious lesions
• Laryngeal EMG: for vocal cord palsy (prognostication)
• 24h pH/impedance monitoring: for laryngopharyngeal reflux
• SALT assessment: for functional voice disorders

Non-pharmacological

• Voice rest and vocal hygiene: reduce voice use, avoid whispering (increases cord tension)
• Hydration
• Avoid irritants (smoking, alcohol)
• Speech and language therapy (SALT): first-line for functional dysphonia, vocal cord nodules, muscle tension dysphonia

Pharmacological

• PPI trial for suspected laryngopharyngeal reflux: omeprazole 20mg BD for 2-3 months
• Topical antifungal if inhaled corticosteroid-related candidiasis
• Levothyroxine if hypothyroidism confirmed
• Treat underlying cause (cancer, infection, reflux)

Surgical

• Microlaryngoscopy and excision: for vocal cord polyps, cysts, papillomatosis, suspicious lesions/biopsy
• Medialization thyroplasty: for permanent unilateral vocal cord palsy (implant pushes paralysed cord medially)
• Injection laryngoplasty: temporary medialization with hyaluronic acid or autologous fat for vocal cord palsy
• Laryngeal framework surgery: for bilateral cord palsy (tracheostomy may be needed if airway compromise)
• Treatment of malignancy: radiotherapy (early glottic), surgery (partial/total laryngectomy), chemoradiotherapy

Referral Criteria

• 2-week wait ENT referral: hoarseness >3 weeks (NICE NG12)
• Routine ENT: chronic voice change, globus, frequent throat clearing
• Emergency: stridor, airway compromise
• SALT referral: for voice rehabilitation

• Acute laryngitis: resolves within 7-10 days
• Vocal cord nodules: >80% resolve with speech therapy
• Vocal cord palsy: spontaneous recovery in 50-60% of idiopathic cases within 6-12 months
• Early glottic carcinoma (T1): >90% 5-year survival with radiotherapy
• Functional dysphonia: responds well to SALT; prognosis good
• Reinke oedema: improves with smoking cessation; surgery if persistent
• Post-thyroidectomy RLN palsy: temporary in 5-10%, permanent in 1-2%

Approach to Hoarseness >3 Weeks

Key Causes of Vocal Cord Palsy and Investigation

Key Facts

OSA is a condition in which the upper airway repeatedly collapses during sleep, causing intermittent hypoxia, sleep fragmentation, and excessive daytime somnolence. It has significant cardiovascular, metabolic, and neurocognitive consequences and is a major cause of preventable road traffic accidents.

Epidemiology

• Prevalence: 2-4% of middle-aged adults (estimated >1.5 million in UK)
• Significantly underdiagnosed - 80-90% of cases unrecognised
• Male:female ratio 2-3:1 (narrows after menopause)
• Prevalence increases with obesity (>20% in BMI >30 men)
• More common with increasing age

Aetiology

• Obesity: most important modifiable risk factor; fat deposition around pharynx narrows airway
• Anatomical: retrognathia/micrognathia, large tonsils/adenoids, macroglossia, deviated septum, nasal polyps
• Male sex: different fat distribution, hormonal factors
• Age: loss of muscle tone, weight gain
• Alcohol and sedatives: relax pharyngeal muscles
• Hypothyroidism: myxoedematous tissue, obesity
• Acromegaly: macroglossia, soft tissue overgrowth
• Down syndrome: midface hypoplasia, macroglossia, obesity

Pathophysiology

• During sleep, pharyngeal dilator muscle tone decreases
• In predisposed individuals, the airway narrows or collapses completely
• Apnoea (cessation of airflow ≥10 seconds) or hypopnoea (≥30% reduction in airflow with ≥3% desaturation or arousal)
• Results in intermittent hypoxia, hypercapnia, and repeated arousals from sleep
• Sympathetic nervous system activation → hypertension, cardiovascular disease
• Sleep fragmentation → excessive daytime somnolence, cognitive impairment

Nocturnal Symptoms

• Loud snoring (often reported by bed partner)
• Witnessed apnoeas (bed partner observes breathing cessation)
• Gasping/choking episodes during sleep
• Restless sleep
• Nocturia

Daytime Symptoms

• Excessive daytime somnolence (falling asleep during activities)
• Non-refreshing sleep
• Morning headaches
• Poor concentration and memory
• Irritability and mood changes
• Reduced libido

Examination

• BMI (usually >30)
• Neck circumference (>43cm/17 inches in males)
• Mallampati score (III or IV - limited oropharyngeal view)
• Retrognathia/micrognathia
• Tonsillar hypertrophy
• Nasal obstruction
• Blood pressure (often hypertensive)

Red Flags

• Falling asleep while driving (immediate driving cessation, DVLA notification)
• Severe hypoxia (SpO2 <80%) on sleep study
• Coexisting COPD (overlap syndrome - worse hypoxia)
• Cor pulmonale (right heart failure)
• Occupational risk (HGV driver, pilot, machine operator)

Bedside

• Epworth Sleepiness Scale (ESS): validated self-report questionnaire (score 0-24; ≥11 abnormal)
• STOP-BANG questionnaire: screening tool (≥3 = high risk for OSA)
• BMI, neck circumference
• Mallampati score
• Blood pressure
• Pulse oximetry (may show desaturations)

Bloods

• TFTs (exclude hypothyroidism)
• HbA1c (diabetes screening)
• FBC (polycythaemia from chronic hypoxia)
• ABG if obesity hypoventilation syndrome suspected

Sleep Study

• Home sleep study (limited polygraphy): first-line
  • Measures airflow (nasal cannula), respiratory effort (chest/abdominal bands), SpO2, snoring, body position
  • AHI (apnoea-hypopnoea index): mild 5-14, moderate 15-29, severe ≥30 events/hour
  • ODI (oxygen desaturation index): number of ≥4% desaturations per hour
• Polysomnography (PSG): gold standard (in-lab); includes EEG, EMG, EOG; used if diagnostic uncertainty

Imaging

• Not routinely required
• Lateral cephalometry: if surgical planning (mandibular advancement)
• CT/MRI upper airway: if structural cause suspected

Special Tests

• Drug-induced sleep endoscopy (DISE): identifies site of upper airway collapse under sedation (guides surgical planning)

Non-pharmacological

• Weight loss: target 10% body weight reduction (can significantly reduce AHI)
• Positional therapy: avoid supine sleeping (use positional device) for positional OSA
• Alcohol and sedative avoidance (especially before bed)
• Sleep hygiene: regular sleep schedule, avoid caffeine

Pharmacological

• No first-line drug treatment for OSA
• Modafinil: may be considered for residual daytime sleepiness despite adequate CPAP use (specialist use only)
• Treat contributing conditions: hypothyroidism, nasal congestion

CPAP (Continuous Positive Airway Pressure)

• First-line treatment for moderate-severe OSA (AHI ≥15) (NICE TA139)
• Also offered for mild OSA (AHI 5-14) with significant symptoms
• Pneumatic splint holds airway open during sleep
• Reduces AHI to <5 in most patients
• Improves daytime sleepiness, blood pressure, cardiovascular risk, quality of life
• Compliance: critical; minimum 4 hours/night for benefit; long-term adherence 60-70%

Surgical

• Mandibular advancement device (MAD): oral appliance; alternative to CPAP for mild-moderate OSA or CPAP intolerance (NICE TA139)
• Tonsillectomy/adenoidectomy: first-line in children with OSA due to adenotonsillar hypertrophy
• Uvulopalatopharyngoplasty (UPPP): limited evidence; reserved for selected patients
• Maxillomandibular advancement: effective but major surgery
• Hypoglossal nerve stimulation (Inspire device): for moderate-severe OSA intolerant of CPAP
• Bariatric surgery: for morbid obesity with OSA

Referral Criteria

• Sleep clinic/respiratory referral: suspected OSA (ESS ≥11, witnessed apnoeas, excessive sleepiness)
• ENT referral: if upper airway structural cause (nasal obstruction, tonsillar hypertrophy)
• DVLA notification: mandatory if excessive daytime sleepiness affecting driving

• Untreated moderate-severe OSA associated with:
  • 3-6× increased risk of road traffic accidents
  • 2-3× increased risk of hypertension, cardiovascular events, and stroke
  • Increased risk of type 2 diabetes, AF, heart failure
  • Increased all-cause mortality
• CPAP treatment: reduces excessive daytime sleepiness, normalises AHI, reduces BP by 2-3mmHg, reduces cardiovascular events
• Weight loss of 10% can reduce AHI by 26-50%
• Compliance with CPAP is the key determinant of long-term outcomes
• OSA in children: tonsillectomy/adenoidectomy curative in >80%

OSA Severity Classification

STOP-BANG Screening Questionnaire

DVLA and OSA

Key Facts

Head and neck cancers are a heterogeneous group of malignancies arising from the mucosal lining of the upper aerodigestive tract. They are predominantly squamous cell carcinomas and are strongly associated with smoking, alcohol use, and increasingly HPV infection. Early detection and multidisciplinary management are essential.

Epidemiology

• Approximately 12,000 new cases/year in the UK
• 8th most common cancer in UK males
• Male:female ratio 2-3:1 (narrowing due to changing smoking and HPV patterns)
• Incidence increasing, particularly HPV-related oropharyngeal cancer
• Peak age: >50 years for smoking/alcohol-related; 40-60 years for HPV-related

Aetiology

• Smoking: strongest risk factor; dose-dependent (pack-years)
• Alcohol: independent and synergistic risk with smoking (15× combined risk)
• HPV (particularly HPV-16): major cause of oropharyngeal cancer (tonsil, base of tongue)
• Betel nut chewing: oral cavity cancer (South Asian populations)
• EBV: nasopharyngeal carcinoma (Southern Chinese populations)
• Other: occupational exposure (hardwood dust - sinonasal adenocarcinoma), radiation, immunosuppression

Pathophysiology

• 90% are squamous cell carcinomas arising from mucosal epithelium

• Field cancerisation: entire mucosal field exposed to carcinogens, predisposing to multiple primary tumours
• HPV-positive cancers: HPV E6 and E7 oncoproteins inactivate p53 and Rb, driving carcinogenesis in lymphoid tissue (tonsils, base of tongue)
• Spread: local invasion, lymphatic (cervical lymph nodes), distant metastases (lung, liver, bone - rare at presentation)
• HPV-positive tumours have different biology: better response to treatment, better prognosis

Symptoms by Subsite

• Oral cavity: persistent ulcer, white/red patch (leucoplakia/erythroplakia), lump, pain, loose tooth, difficulty with dentures
• Oropharynx: sore throat, dysphagia, referred otalgia, neck lump (often the presenting complaint in HPV-related disease)
• Larynx: hoarseness (glottic), stridor (subglottic), dysphagia (supraglottic)
• Hypopharynx: dysphagia, odynophagia, weight loss, referred otalgia, neck lump (often late presentation)
• Nasopharynx: nasal obstruction, epistaxis, OME (unilateral), cranial nerve palsies

Red Flags (2-Week Wait - NICE NG12)

• Unexplained neck lump >3 weeks
• Hoarseness >3 weeks
• Persistent oral ulcer >3 weeks
• Unexplained unilateral otalgia with normal otoscopy
• Persistent unexplained dysphagia
• White or red patch in oral cavity
• Cranial nerve palsy with neck lump

Examination

• Full head and neck examination including oral cavity, oropharynx
• Flexible nasendoscopy (visualise nasopharynx, hypopharynx, larynx)
• Neck palpation: cervical lymphadenopathy (levels I-VI)
• Cranial nerve assessment

Bedside

• Flexible nasendoscopy: visualise primary tumour
• Oral cavity examination
• Fine needle aspiration (FNA) of neck lump (USS-guided)

Bloods

• FBC, U&Es, LFTs: baseline and nutritional status
• EBV serology: if nasopharyngeal carcinoma suspected
• TFTs: baseline before neck radiotherapy

Imaging

• CT neck and chest with contrast: staging of primary and regional disease, lung metastases
• MRI: superior soft tissue detail for oral cavity, oropharynx, nasopharynx
• PET-CT: for staging, detection of occult primary, assessment of treatment response, surveillance
• Orthopantomogram (OPG): dental assessment before radiotherapy

Special Tests

• Panendoscopy (EUA): examination under anaesthesia with biopsy - definitive histological diagnosis
• p16 immunohistochemistry: surrogate marker for HPV status in oropharyngeal SCC
• HPV DNA testing: confirmatory for HPV-related cancer
• TNM staging: guides treatment and prognosis

Non-pharmacological

• MDT discussion: all head and neck cancers managed via MDT (surgeon, oncologist, radiologist, pathologist, CNS, SALT, dietitian)
• Nutritional support: dietitian input; PEG/RIG tube if unable to swallow
• Speech and language therapy: pre- and post-treatment swallow and voice rehabilitation
• Dental assessment: prior to radiotherapy (extractions before RT to prevent osteoradionecrosis)
• Smoking cessation: essential
• Psychological support: CNS, psychologist, support groups

Pharmacological

• Chemotherapy: cisplatin 100mg/m² 3-weekly (radiosensitiser) with concurrent radiotherapy
• Cetuximab (anti-EGFR): alternative to cisplatin in patients unfit for chemotherapy
• Immunotherapy: pembrolizumab/nivolumab (anti-PD-1) for recurrent/metastatic disease (NICE TA661)

Surgical

• Primary surgery: resection of tumour with adequate margins
  • Oral cavity: glossectomy, mandibulectomy, maxillectomy
  • Larynx: partial or total laryngectomy
  • Reconstructive surgery: free flap (radial forearm, fibula, anterolateral thigh)
• Neck dissection: for regional lymph node management (selective, modified radical, or radical)
• Transoral robotic surgery (TORS): for oropharyngeal tumours (minimally invasive)
• Transoral laser microsurgery (TLM): for early glottic and supraglottic cancers

Radiotherapy

• Primary radiotherapy: for early laryngeal cancer (T1-T2 glottic - voice preservation), nasopharyngeal cancer
• Adjuvant radiotherapy: post-operative for advanced disease, positive margins, extranodal extension
• Concurrent chemoradiotherapy: standard for locally advanced disease (organ preservation protocols)
• Intensity-modulated radiotherapy (IMRT): reduces parotid gland dose, minimising xerostomia

Referral Criteria

• 2-week wait ENT referral: as per NICE NG12 criteria (above)
• MDT discussion: all confirmed head and neck cancers
• Palliative care: for advanced/incurable disease

• Overall 5-year survival: approximately 50-60%
• Early stage (T1-T2, N0): >80% 5-year survival
• HPV-positive oropharyngeal cancer: >80% 5-year survival (significantly better than HPV-negative)
• HPV-negative oropharyngeal cancer: <50% 5-year survival
• Early glottic carcinoma (T1): >90% 5-year survival with radiotherapy alone
• Hypopharyngeal cancer: worst prognosis among H&N sites; 30-35% 5-year survival (often late presentation)
• Factors affecting prognosis: stage at presentation, HPV status, comorbidities, smoking during treatment
• Second primary tumour risk: 3-5% per year (field cancerisation)

HPV-Positive vs HPV-Negative Oropharyngeal Cancer

NICE NG12 - 2-Week Wait Referrals for H&N Cancer

Key Facts

Laryngeal cancer is one of the most common head and neck malignancies. It is strongly associated with smoking and alcohol use. Early glottic tumours have an excellent prognosis due to early presentation with hoarseness and high cure rates with radiotherapy.

Epidemiology

• Approximately 2,400 new cases/year in the UK
• Male:female ratio 4:1 (narrowing with changing smoking patterns)
• Peak incidence: 60-70 years
• Incidence declining in males (reduced smoking) but increasing in females
• 7th most common cancer in UK males

Aetiology

• Smoking: most important risk factor (10-30× risk)
• Alcohol: independent and synergistic risk factor with smoking
• HPV: minor role in laryngeal cancer (unlike oropharyngeal cancer)
• Occupational: asbestos exposure, paint fumes, wood dust
• GORD/laryngopharyngeal reflux: possible risk factor
• Previous radiation to the neck

Pathophysiology

• 95% are squamous cell carcinoma arising from mucosal epithelium

• Glottic (vocal cords - 65%): presents early due to hoarseness; lymphatic drainage poor → low rate of nodal metastasis at presentation
• Supraglottic (epiglottis, aryepiglottic folds, false cords - 30%): rich lymphatic drainage → higher rate of nodal metastasis; presents later
• Subglottic (below vocal cords - 5%): rare, poor prognosis due to late presentation

• Pre-malignant lesions: dysplasia, leucoplakia, erythroplakia may precede invasive cancer

Glottic Cancer (Most Common)

• Persistent hoarseness (earliest and most common symptom)
• Voice change progressing over weeks to months
• Stridor (advanced, airway obstruction)
• Dyspnoea

Supraglottic Cancer

• Dysphagia and odynophagia
• Referred otalgia (via Arnold's nerve, CN X)
• Muffled voice ('hot potato' voice)
• Neck lump (cervical lymphadenopathy - often the presenting feature)
• Late hoarseness (when tumour involves cords)

Subglottic Cancer

• Stridor (insidious onset)
• Dyspnoea
• Hoarseness (late)
• Often advanced at presentation

Red Flags

• Hoarseness >3 weeks (NICE NG12 - 2WW referral)
• Stridor
• Dysphagia with weight loss
• Haemoptysis
• Neck lump >3 weeks
• Otalgia with normal ear examination

Bedside

• Flexible nasendoscopy: visualise larynx, assess vocal cord mobility, identify mass
• Neck palpation for lymphadenopathy
• Voice assessment

Bloods

• FBC, U&Es, LFTs: baseline
• TFTs: baseline before neck radiotherapy

Imaging

• CT neck and chest with contrast: assess primary tumour extent, cervical lymph nodes, lung metastases
• MRI larynx: superior soft tissue detail, assess cartilage invasion and pre-epiglottic space
• PET-CT: for staging, detection of distant metastases, surveillance

Special Tests

• Panendoscopy with biopsy (EUA): definitive diagnosis - microlaryngoscopy with biopsy under GA
• TNM staging: critical for treatment planning
• Dental assessment: before radiotherapy (extract diseased teeth to prevent osteoradionecrosis)
• SALT assessment: swallow and voice assessment pre-treatment

Non-pharmacological

• MDT discussion: all cases
• Smoking and alcohol cessation: critical
• Nutritional support: dietitian, PEG/RIG if needed
• SALT: voice and swallow rehabilitation
• Psychological support: significant impact of diagnosis and treatment on quality of life

Radiotherapy

• Primary radiotherapy: first-line for early glottic cancer (T1-T2)
  • T1 glottic: 5-year cure rate >90% with voice preservation
  • T2 glottic: 5-year cure rate 70-80%
  • Typically 55-70Gy in 20-35 fractions
• Concurrent chemoradiotherapy: for T3-T4 laryngeal cancer (organ preservation)
  • Cisplatin 100mg/m² on days 1, 22, 43 with concurrent radiotherapy
  • RTOG 91-11 trial: chemoRT superior to induction chemo for larynx preservation

Surgical

• Transoral laser microsurgery (TLM): for early glottic cancers (T1-T2) - alternative to radiotherapy
• Partial laryngectomy: supraglottic laryngectomy, vertical partial laryngectomy
• Total laryngectomy: for advanced disease (T4), recurrence after radiotherapy
  • Permanent tracheostomy (end stoma)
  • Voice rehabilitation: tracheoesophageal puncture (TEP) + voice prosthesis (most common), oesophageal speech, electrolarynx
• Neck dissection: for cervical lymph node disease

Pharmacological

• Cisplatin: concurrent with radiotherapy for organ preservation
• Cetuximab: alternative to cisplatin if unfit for chemotherapy (NICE)
• Immunotherapy (pembrolizumab/nivolumab): for recurrent/metastatic disease (NICE TA661)

Referral Criteria

• 2-week wait ENT referral: hoarseness >3 weeks, neck lump >3 weeks (NICE NG12)
• MDT discussion: all confirmed laryngeal cancers
• Palliative care: for advanced/incurable disease

• T1 glottic: >90% 5-year survival (excellent)
• T2 glottic: 70-80% 5-year survival
• T3 glottic (organ preservation): 50-60% 5-year survival
• T4 laryngeal: 30-40% 5-year survival
• Supraglottic cancer: 50-60% 5-year survival (higher nodal metastasis rate)
• HPV status: less relevant in laryngeal cancer than oropharyngeal
• Continued smoking during radiotherapy reduces cure rates by 50%
• Voice preservation achieved in >60% with organ preservation protocols
• Total laryngectomy: significant impact on quality of life but excellent local control
• Second primary tumour risk: 3-5% per year

TNM Staging - Glottic Cancer (AJCC 8th Edition)

Landmark Trials in Laryngeal Cancer

Voice Rehabilitation After Total Laryngectomy

Key Facts

Salivary gland tumours are a heterogeneous group of neoplasms arising from the major (parotid, submandibular, sublingual) or minor salivary glands. The parotid gland is the most commonly affected, and the majority of parotid tumours are benign.

Epidemiology

• Account for 3-6% of all head and neck tumours
• Annual incidence: approximately 2-3 per 100,000
• Peak age: 40-60 years for benign; 60-70 years for malignant
• Equal sex distribution (Warthin tumour: male predominance)

Aetiology

• Mostly unknown aetiology
• Radiation exposure (prior radiotherapy) increases risk of salivary malignancy
• Smoking: associated with Warthin tumour
• EBV: associated with lymphoepithelial carcinoma
• Genetic: PLAG1 rearrangement in pleomorphic adenoma; MAML2 fusion in mucoepidermoid carcinoma

Pathophysiology

• Salivary glands contain diverse cell types (serous, mucous, myoepithelial, ductal) giving rise to varied tumour histology
• Benign tumours: well-encapsulated but may have pseudopod extensions (pleomorphic adenoma)
• Malignant tumours: may invade surrounding structures including facial nerve
• The facial nerve (CN VII) divides the parotid into superficial and deep lobes; most tumours arise in the superficial lobe
• Pleomorphic adenomas have a 5-10% risk of malignant transformation (carcinoma ex pleomorphic adenoma) if left untreated >10-15 years

Benign Tumours

• Slow-growing, painless, firm, mobile lump in the parotid, submandibular, or palatal region
• Intact facial nerve function
• May have been present for months to years

Malignant Tumours

• Rapid growth
• Pain (nerve invasion)
• Facial nerve palsy (highly suspicious for malignancy in parotid mass)
• Fixation to skin or deep structures
• Cervical lymphadenopathy
• Trismus (deep lobe extension)

Red Flags

• Facial nerve palsy with parotid mass
• Rapidly enlarging salivary gland mass
• Hard, fixed mass
• Skin invasion or ulceration
• Cervical lymphadenopathy
• Pain/paraesthesia

Bedside

• Thorough head and neck examination
• Facial nerve function assessment (House-Brackmann grading)
• Bimanual palpation (submandibular, floor of mouth)

Bloods

• Not routinely diagnostic
• FBC, LDH if lymphoma suspected

Imaging

• USS: first-line imaging; assesses size, solid/cystic nature, guides FNA
• MRI: superior for deep lobe parotid tumours, perineural spread, and malignancy assessment
• CT neck with contrast: for suspected malignancy staging, bony invasion
• PET-CT: for staging of high-grade malignancy

Special Tests

• FNA cytology (USS-guided): first-line tissue diagnosis; sensitivity 80-90% for distinguishing benign from malignant
• Core biopsy: if FNA non-diagnostic
• Incisional biopsy is AVOIDED for parotid tumours (risk of tumour seeding, facial nerve damage)
• Histopathology of excised specimen: definitive diagnosis

Non-pharmacological

• All salivary gland tumours require surgical excision for definitive diagnosis and treatment
• MDT discussion for malignant tumours

Surgical

• Superficial parotidectomy: for benign parotid tumours in superficial lobe
  • Careful identification and preservation of facial nerve
  • Recurrence rate: <5% for pleomorphic adenoma
• Total conservative parotidectomy: for deep lobe tumours or malignancy (nerve preserved if not invaded)
• Radical parotidectomy: sacrifice of facial nerve if invaded by tumour
• Submandibular gland excision: for submandibular tumours
• Neck dissection: for confirmed cervical lymph node metastasis
• Nerve grafting: if facial nerve sacrificed (great auricular or sural nerve graft)

Adjuvant Treatment

• Radiotherapy: for high-grade malignancy, positive margins, perineural invasion, adenoid cystic carcinoma, recurrence
• Neutron therapy: historically for adenoid cystic carcinoma
• Chemotherapy has limited role in salivary gland malignancy

Referral Criteria

• 2-week wait referral: any unexplained salivary gland mass >3 weeks
• Urgent ENT: facial nerve palsy with salivary gland mass
• MDT: all malignant salivary gland tumours

• Pleomorphic adenoma: excellent prognosis; recurrence <5% after adequate excision; 5-10% risk of malignant transformation if untreated >10-15 years
• Warthin tumour: excellent; rarely recurs; bilateral in 10%
• Mucoepidermoid carcinoma: variable; low-grade >90% 5-year survival; high-grade 30-50%
• Adenoid cystic carcinoma: tendency for perineural invasion and late distant metastases (lung); 5-year survival 60-70% but 15-year survival 20-30%
• Acinic cell carcinoma: generally favourable; >80% 5-year survival
• Complications of parotid surgery: temporary facial nerve weakness (10-20%), permanent palsy (<3%), Frey syndrome (gustatory sweating, 30-50%), salivary fistula

The 80% Rule of Salivary Gland Tumours

Classification of Salivary Gland Tumours

Complications of Parotid Surgery

Key Facts

Foreign bodies in the ear, nose, and throat are among the most common ENT emergencies, particularly in the paediatric population. Most can be managed in the emergency department or primary care, but certain foreign bodies (button batteries, airway FBs) constitute true emergencies requiring immediate intervention.

Epidemiology

• Nasal FB: peak age 2-5 years; accounts for up to 25% of paediatric ENT emergencies
• Ear FB: common across all ages; children (beads, small toys), adults (cotton buds, insects)
• Inhaled (airway) FB: peak 1-3 years; significant cause of paediatric mortality (NICE)
• Ingested FB (throat): common in adults (fish bones) and children (coins)

Aetiology

• Nasal: beads, buttons, peas, tissue paper, button batteries, magnets
• Ear: beads, insects, cotton bud tips, stones, hearing aid parts, button batteries
• Throat/oesophagus: fish bones, coins, food bolus, dentures
• Airway (laryngotracheal/bronchial): peanuts (most common), small toy parts, food items

Pathophysiology

• Nasal FB: causes unilateral mucopurulent rhinorrhoea, mucosal irritation, infection
• Button batteries: generate electric current causing alkaline burns, tissue necrosis, septal perforation within 2 hours
• Ear FB: may impact against TM, cause otitis externa, or be asymptomatic
• Airway FB: partial or complete airway obstruction; ball-valve effect may cause unilateral hyperinflation, atelectasis, or pneumonia
• Oesophageal FB: may cause dysphagia, pain; perforation risk with sharp or button battery objects

Nasal Foreign Body

• Unilateral foul-smelling nasal discharge (most common presenting feature)
• Nasal obstruction
• Epistaxis
• Child may be unaware or deny insertion

Ear Foreign Body

• Ear pain or discomfort
• Hearing loss (if EAC obstructed)
• Buzzing (if insect - live insect causes extreme distress)
• Otorrhoea
• May be asymptomatic (incidental finding)

Inhaled (Airway) Foreign Body

• Acute: choking episode, coughing, stridor, wheeze, respiratory distress
• Chronic (missed aspiration): recurrent pneumonia, persistent cough, unilateral wheeze
• Witnessed choking event (often not reported by the time of presentation)

Throat/Oesophageal Foreign Body

• Sensation of something stuck in the throat
• Odynophagia
• Drooling (complete obstruction)
• Sharp pain localised to neck

Red Flags

• Stridor or respiratory distress (airway FB - emergency)
• Button battery in nose or oesophagus (tissue necrosis emergency)
• Complete airway obstruction (back blows, abdominal thrusts)
• Drooling with inability to swallow (oesophageal obstruction)
• Sharp object (perforation risk)

Bedside

• Anterior rhinoscopy or otoscopy: direct visualisation of FB
• Flexible nasendoscopy: for posterior nasal or pharyngeal FB
• Oropharyngeal examination with tongue depressor and headlight
• Respiratory assessment (chest auscultation for inhaled FB: unilateral reduced air entry, wheeze)

Imaging

• X-ray (AP and lateral): for radio-opaque objects (coins, batteries, metallic items)
  • Lateral neck X-ray: for oesophageal or pharyngeal FB (disc battery appears as 'double ring' sign)
  • Chest X-ray: inhaled FB - unilateral hyperinflation, mediastinal shift, atelectasis
  • Inspiratory/expiratory CXR or lateral decubitus films: air trapping on affected side
• CT: if FB location unclear or complications suspected

Special Tests

• Rigid bronchoscopy: diagnostic and therapeutic for inhaled FB
• Rigid oesophagoscopy: for oesophageal FB removal
• Flexible nasendoscopy: to visualise pharyngeal/laryngeal FB

Nasal Foreign Body

• Positive pressure technique ('mother's kiss'): parent occludes unaffected nostril, delivers sharp puff of air into child's mouth - may dislodge FB
• Instrumented removal: Jobson-Horne probe, crocodile forceps, suction, balloon catheter (Fogarty) passed behind FB
• Button battery: remove IMMEDIATELY under direct vision; do NOT irrigate; apply honey to anterior nares if delay anticipated (shown to reduce tissue damage)
• ENT referral if failed removal after 1-2 attempts; removal under GA if needed

Ear Foreign Body

• Insects: kill first with olive oil or 2% lidocaine drops, then remove
• Removal with Jobson-Horne probe, crocodile forceps, or suction
• Irrigation: effective for smooth, non-organic objects with intact TM; AVOID for organic material (swells), button batteries, or perforated TM
• ENT referral: impacted objects, failed removal, uncooperative child, suspected TM damage

Inhaled (Airway) Foreign Body

• Complete obstruction: back blows (infant <1 year), abdominal thrusts (Heimlich, >1 year and adults) - BLS protocol
• Partial obstruction, stable: do NOT intervene; keep calm, allow coughing, transport to hospital
• Definitive: rigid bronchoscopy under GA for removal (paediatric/ENT surgeon)
• Flexible bronchoscopy may be used in adults

Throat/Oesophageal Foreign Body

• Visible fish bone: remove with Magill forceps or Tilley forceps under direct vision
• If not visible: flexible nasendoscopy to locate
• Oesophageal FB: rigid or flexible oesophagoscopy under GA
• Button battery in oesophagus: EMERGENCY removal (risk of aorto-oesophageal fistula)

Referral Criteria

• Emergency: airway FB, button battery (nose or oesophagus), sharp object, respiratory distress
• Urgent ENT: failed removal, impacted FB, suspected complications
• All children with suspected inhaled FB: paediatric ENT/respiratory for bronchoscopy

• Most FBs in ear and nose: excellent prognosis with appropriate removal
• Button battery: if removed within 2 hours, minimal damage; delayed removal causes septal perforation (nose) or oesophageal perforation/fistula (oesophagus)
• Inhaled FB: prompt bronchoscopic removal: excellent outcome; delayed diagnosis increases risk of pneumonia, bronchiectasis, lung abscess
• Oesophageal FB: risk of perforation (sharp objects, batteries); mediastinitis if perforated
• Complications of removal: mucosal trauma, bleeding, TM perforation (ear), laryngospasm (airway)
• Prevention: parental education about choking hazards in young children is essential

Button Battery Emergency Protocol

Foreign Body Removal Techniques

Key Facts

A tracheostomy is an artificial opening created in the anterior wall of the trachea to provide a secure airway. It may be temporary or permanent. Safe tracheostomy care is a core competency for healthcare professionals in acute and community settings.

Epidemiology

• Approximately 15,000 temporary tracheostomies performed annually in the UK
• Approximately 5,000 patients with permanent tracheostomies (post-laryngectomy)
• ICU: 10-24% of ventilated patients require tracheostomy

Aetiology/Indications

• Prolonged mechanical ventilation: failed weaning from endotracheal tube (most common ICU indication)
• Upper airway obstruction: tumour, angioedema, bilateral vocal cord palsy, facial trauma, burns
• Airway protection: aspiration risk (bulbar palsy, severe neurological injury)
• Secretion management: inability to clear secretions (neuromuscular disease, spinal cord injury)
• Post-surgical: total laryngectomy (permanent), major head and neck surgery

Types

• Surgical tracheostomy: open procedure, horizontal incision between 2nd-4th tracheal rings, performed in theatre
• Percutaneous dilatational tracheostomy (PDT): Seldinger technique (Ciaglia), performed at bedside in ICU under bronchoscopic guidance
• Temporary: cuffed or uncuffed tube; plan for decannulation
• Permanent: total laryngectomy (no connection between trachea and pharynx - cannot be ventilated via mouth/nose)

Normal Tracheostomy

• Patent, well-positioned tube
• Clean stoma site without erythema, swelling, or discharge
• Effective cough and secretion clearance
• Inner cannula clean
• Appropriate cuff management

Complications

• Early (<7 days): haemorrhage, tube displacement (DANGEROUS before tract matures), subcutaneous emphysema, pneumothorax, tube occlusion
• Late (>7 days): tube occlusion (secretions), granulation tissue, tracheal stenosis (most common long-term complication), tracheo-innominate fistula (life-threatening haemorrhage), tracheo-oesophageal fistula, stomal infection

Red Flags - Tracheostomy Emergency

• Unable to ventilate through tracheostomy tube
• Tube displacement or dislodgement
• Massive haemorrhage from stoma (tracheo-innominate fistula)
• Increasing respiratory distress, desaturation
• Subcutaneous emphysema
• Inability to pass suction catheter (tube obstruction)