ENT

 Sections of the ear + function

o Outer ear  Protects tympanic membrane from damage (NB: Pinna = entire outer ear)

o Middle ear  Transmits sound waves

 Auditory Ossicles
 Malleus  Attached to tympanic membrane
 Incus  Synovial joints with Malleus and Stapes
 Stapes  Piston movement transmits fluid waves to cochlea via oval window

 Muscles  Protect from loud sounds

 Stapedius
o Innervation: Facial nerve
o Function: Inhibits stapes to protect from high noise levels
o Non-functioning: Hyperacusis – hear sounds louder than you should
 E.g. this occurs with Bell’s palsy (unilateral)
 Tensor tympani
o Innervation: Trigeminal
o Function: Pull malleus medial = tense tymp mem = dampen sound

o Inner ear/Labyrinth
 Cochlea  Transduces sound waves to nerve impulses
 Semi-circular canals  Balance from rotational acceleration
TESTS IN AUDIOLOGY

 Pure Tone Audiogram

o Test the threshold at which sound can JUST be heard in each ear
 Test decibels at different frequencies (Normal = 0-20dB)
o Both air conduction AND bone conduction tested

 Tuning fork tests – 512Hz

o Webers
 Tuning fork placed in the middle of forehead
 Patient reports which ear hears better
 If both ears hear equally  Normal
 If lateralises, can either be:
o CHL on the side it lateralises to
o SNHL on the opposite side to which it lateralises

o Rinnes  Most useful w/ Webers when abnormal ear is not known

 Tuning fork vibrates – ask patient if they can hear
 Place tuning fork behind ear on mastoid process
 Which was louded? Sound when not touching or when touching mastoid process?
 If better when not touching  POSITIVE
o AC > BC  Normal/Sensorineural loss
 If better when touching  NEGAITVE
o BC > AC  Conductive/combined loss

*Weber in RIGHT means deficit must be either: conductive loss in RIGHT or sensorineural loss in LEFT as Weber
tests sensorineural function, the the response may be exaggerated in conductive loss

**Rinne test also looks at sensorineural function, but in only ONE ear. If AC>BC this means the conductive element
is better than the sensorineural element which can be NORMAL but is pathological is Webers is abnormal. If BC>AC
this is ABNORMAL and represents that sensorineural is better than conductive hence a conductive hearing loss.

***In SEVERE SN hearing loss, BC > AC in affected ear as it is heard in OTHER ear (e.g. right ear = severe = right ear
BC > AC because BC actually heard in L ear)
PURE TONE AUDIOGRAM INTERPRETATION

NORMAL HEARING – anything within 0-20dB considered NORMAL

Sensorineural hearing loss – damage of cochlea, CN8, brainstem or cortex (most common cause: Presbycusis)

Why?  Presbycusis (age-related high-frequency hearing loss); noise exposure (4kHz loss)
Meniere’s disease cause LOW-frequency SN hearing loss

BOTH air and bone conduction is decreased because neural component needed for
conductive hearing, and there is LESS than a 10dB gap between AC + BC... if gap >10dB and
both in abnormal range then this is MIXED HEARING LOSS

NB: If loss ONLY at 4kHz and jumps back to normal at 8kHz = NOISE-INDUCED HEARING LOSS

Conductive hearing loss – any outer or middle ear pathology (e.g. otitis media, otosclerosis)
 Top line represented bony conduction (NORMAL as sensorineural component intact)
 Bottom line represents air conduction (ABNORMAL as mechanical component not intact,
but gets better as frequency increased)

Otosclerosis  2kHz dip

Other Tests

 Speech Audiometry
o Speech Reception Threshold
 Method: Says 2 syllable words at different dBs, test complete when patient attains 50%
correct at particular dB

 Interpretation: Should be within 5dB of Pure Tone Audiometry

 Use: To test reliability of Pure Tone Audiometry

o Speech Discrimination
 Method: Says 1 syllable word x50 at different dBs, measures % correct

 Use: Measures degree of SNHL (NB: Normal or conductive HL = normal = >90% correct)

 Impedence Audiometry
o Tympanogram
 Method: Air pressure via 226Hz tone generated into external ear, measured by
instrument which detects reflection of sound off tympanic membrane

 Interpretation:

 Use: Test tympanic membrane ability to transmit sound through middle ear (i.e. tests
both tympanic membrane AND middle ear function)

 Pathology: Tympanic membrane disease (e.g. perforation), middle ear disease (e.g.
AOM, or OM w/ effusion)

o Static Compliance
o Acoustic Stapedial Reflexes (CN7 palsy?)

 Auditory Brainstem Response

o Method: Measure neural waves in 5 different areas to determine where sensory neural HL exists
 Measured as delays  when delay seen, lesion must be prior to that area

o Uses: Best for children (does not require participation) and malingerers, also adults

 Otoacoustic Emissions
Aural Rehabilitation/Hearing Aids

 Types:
o MILD
 Behind Ear – for mild impairment
 In Ear – for mild impairment

o MODERATE
 Bone Anchored Hearing Aid (BAHA; for bone conduction) – for CHL
 Requires surgery

 Contralateral Routing of Signals (CROS)

 *All are now “digital signal processing” rather than “analogue”

o DSP filters extraneous sound out better

o SEVERE
 Cochlear Implant
 Indication:
o Hear only 90dB at 2 and 4kHz
o 3mo external hearing aid fail
Hearing Loss

 Hearing loss
o Types
 Mechanical/Conductive  Problems with external or middle ear (to the oval window)
 Sensorineural  Problems with inner ear (from the oval window to the brain)
 Mixed  Both combined

o Measuring hearing loss

 Principles
 Air conduction
o Loudspeaker/headphones to determine whether sound can be heard
o Measures the overall conductance/function of the hearing system

 Bone conduction
o Vibrating transducer placed on skull to transmit directly to cochlea
o Measures inner ear function ONLY and therefore tests sensorineural

 Causes

Conductive Sensorineural
Congenital Atresia of ear Genetic
Ossicle abnormalities Rubella (or other TORCH)
Acquired External Degenerative – presbyacusis
Wax/cerumen (most common), noise-induced
(com cause CHL age 15-50)
Infective – meningitis, measles,
Otitis externa mumps, syphilis

Foreign body Ototoxic – aminoglycosides

Exostoses Neoplastic – acoustic neuroma

Trauma
Middle
Perforated drum Meniere’s (idiopathic)

AOM

OM w/ Effusion (glue ear)

Otosclerosis (2nd most com cause

CHL age 15-50)

Cholesteatoma
Diseases of the OUTER EAR/EAR CANAL – otitis externa + malig OE, wax impaction, for body, polyps, exostoses

 Otitis externa (“Swimmers ear”)

o Definition: Any inflammation of the outer ear (infectious + dermatological)
o Cause
 Infectious
 Bacteria (90%)  Psuedomonas aeruginosa, Staph, Strep, E coli
 Fungus (10%)  Candida, Aspergillus
 Viral (rare)  Ramsay Hunt syndrome (herpes zoster oticus)
 Skin  Eczema, psoriasis

o Associations  Swimming, Q-tips/ear buds/anything which occludes ear (e.g. headphones)

o Symptoms
 Acute:
 PAIN (esp when tragus pushed/ear pulled)
 CHL + aural fullness
 Discharge (yellow)
 Post-auricular lymphadenopathy
 Chronic:
 NO pain on auricle movement
 Itchy external ear + excoriation
 Atrophic/scaly epidermal lining ±discharge ±CHL

o Treatment
 Irrigation OR Microsuction (clean ear + send for MCS)
 Analgesia

 BACTERIAL  Antibiotic drops (antipseudomonal, e.g. gent drops) + steroid spray

 NB: Do NOT use gent drops is TM perforated (ototoxicity)
 FUNGAL  Anti-fungals (e.g. nystatin)

o Complication: Cellulitis (will require oral Abx), Malignant otitis externa (see below)

 Malignant (Necrotizing) Otitis Externa AKA Skull Base/Temporal Bone Osteomyelitis

o Definition: Rare but life threatening complication of otitis externa causing osteomyelitis of the
temporal bone

o Cause: Pseudomonas (99% of cases), typically in elderly/diabetic/immunocompromised

o Features: Pain, discharge, facial nerve palsy (sometimes) – *refractory to medical therapy*

o Complications:
 Lower cranial nerve palsies
 Systemic infection, death

o Ix: Swab discharge for MCS, HRCT, MRI w/ Gad, Technetium bone scan

o Rx: Debridement, IV Abx, Hyperbaric O2

 Wax/Cerumen (commonest conductive hearing loss in ages 15-50)
o Physiology  Shed skin cells + glandular secretions (e.g. sebum)
 Cleaning  Cells + wax move from middle of tympanic membrane, outwards
 Lubrication  Prevents dryness, itching and burning
 Antibacterial + Antifungal
o Features: Asymptomatic OR CHL
o Ix: Auroscope, Webers, Rinnes
o Treatment
 Soften + Irrigate
 First: Softener ear drops x7d  Sodium Bicarbonate, Olive Oil, “EarEx”
 Then: Irrigate  Syringe the softened wax with warm fluid
 Health promotion: Throw away cotton buds

 Foreign body  In children/developmental problems; pull out first time to avoid GA

 Polyps

 Exostoses (“Swimmers bony ear”)

o Definition: Benign, asymptomatic bony protuberance in external ear composed of lamellar bone
o Association: Swimming in cold water
o Pathology: Can lead to wax impaction or otitis externa
o Rx: NIL unless repeated infection or wax impaction
Diseases of the MIDDLE EAR – AOM, OME, CSOM, Perf TM, Tympanosclerosis, cholesteatoma, otosclerosis

 Acute otitis media

o Definition: Inflammation of the middle ear typically seen only in children (any painful ear)

o Epidemiology: 70% of children have 1 episode AOM by age 3; peak 1-6yr in winter

o Cause
 Viral
 2° Bacterial (Strep pneumo [35%], Haemophilus [25%], Branhamella catarrhalis)

o Risk:
 Eustachian tube dysfunction or obstruction (does not allow air to escape middle ear,
and air is irritant to middle ear mucosa  exudate/effusion + infection from
nasopharyngeal secretions
 URTI
 Second-hand smoke

o Symptoms  TRAID – pain, fever, conductive hearing loss

 Otorrhea (if TM perforated)
 Red, bulging TM + loss of landmarks (e.g. process of malleus not visible)

 (NB: Pain may resolve with discharge drainage from perforation)

o Treat
 Paracetamol/Calpol
 Decongestants
 Antibiotics/Amoxicillin if...
 Symptoms persist >3d
 Age <2 w/ bilateral AOM
 Age <2 w/ bulging ear drug + 4 symptoms
 Patients with comorbidity (e.g. CF, heart disease, etc)

o Complications:
 Mastoiditis
 Definition: Infection of mastoid air cells two weeks following onset of
untreated OR inadequately treated acute suppurative otitis media

 Causes: Same organisms as AOM (S pneumo, H influ, M cattarhalis, S pyo, S aur,

Pseudomonas aeruginosa)

 Features: Triad of
o DISCHARGE
o PAIN ON MASTOID PROCESS (no pain in CSOM)
o RETROAURICULAR SWELLING (+protrusion of ear)
o (+fever)

 Ix: CT scan  Opacification of mastoid air cells

 Rx: IV antibiotics; surgery (not responsive to ABx or complicated)

 Meningitis, brain abscess, facial palsy, TM perforation + chronic suppurative OM

 Otitis Media w/ Effusion (“Glue ear”) – a long-term complication of acute otitis media
o Definition: Presence of fluid in middle ear WITH OR WITHOUT signs of ear infection

o Cause: Frequently follows AOM, esp if recurrent AOM (40% cases for 1mo afterwards)

o Features:
 Conductive hearing loss ± tinnitus
 Aural fullness
 Speech delay

 Discoloured/grey TM – “Glue Ear”

 Fluid level behind TM

 NO pain, NO fever (unlike AOM)

o Ix:
 Audiogram – CHL (if >4yr)... McCormick Toy Test (if <4yr)
 Tympanogram – no compliance/immobility

o Rx: Usually self-limiting

 First: Watch and wait – 90% resolve by 3mo
 Must document hearing loss + repeat testing at 3mo period
 Abx + Decongestants have NO EVIDENCE for their use

 If refractory: Surgery – tympanostomy/grommet OR myringotomy

 Tympanostomy/grommet – allows equalisation of pressures; NOT for drainage
 Myringotomy – allows for equalisation of pressure AND drainage

 Specific Indications:
o Persistent effusion >3mo w/ no response to Abx >3mo
o Recurrent episodes (>7 in 6mo)
o Bilateral conductive hearing loss

 Consider adenoidectomy if enlarged (may be blocking Eustachian tube)

 Chronic suppurative otitis media

o Definition: Chronic inflammation of middle ear + mastoid cavity, with a perforated TM
o Cause: Recurrent AOM, TM perforation, grommet insertion
o Types:
 Safe  WITHOUT cholesteatoma
 Unsafe  WITH cholesteatoma
o Features: DISCHARGE (>2wk) with hearing loss (TM perforation)
 NO Fever, NO pain (as seen with mastoiditis)
o Ix: Audiogram, CT
o Rx:
 Topical gent or quinolone (both have risks with perforated TM, so use cautiously)
 Surgery  Myringoplasty (repair TM), mastoidectomy (if cholesteatoma present),
choclear implant (last line)
 Perforated TM  Rx: Abx (amox) + R/V in 2wk; should heal on own; if not healed then refer if still unlwee
but if doing better R/V again in 4wk; if still not healed then refer for consideration of myringoplasty
o Causes
 Infected chronic perforation (most common cause)
 Discharge (suppurative otitis media) through a chronic perforation
 Treat with topical or systemic antibiotics
 Less likely to heal

 Traumatic
 Sharp instrument/cotton bud into ear
 Little-to-no effect on hearing; Usually heals spontaneously
 Needs ENT follow-up
 Water precautions until healed

 Loud noise

 Tympanosclerosis
o Calcium deposition on tympanic membrane
o Asymptomatic; Little-to-no effect on hearing

 Cholesteatoma
o Definition: Migrating skin of ear canal begins migrating inwards within middle ear causing local
destruction and CHL

o Types + Features:
 Congenital (less common):
 Small white pearl behind TM
 CHL
 NO otitis media, NO Eustachian tube dysfunction

 Acquired (more common): consequence of OM + chronic Eustachian tube dysfunction

 Primary: TM sucked back, pockets of air form in middle ear
 Secondary: TM rupture/surgery  squamous cells enter middle ear + grow
o Features:
 Hearing loss, Pain, discharge (foul smelling), otoscopy shows “attic crust”
 Hx of otitis media OR ruptured TM OR tympanostomy tube insertion OR ear surgery
 Surgery allows cells to be displaced which triggers disease
 Complication:
 Deafness
 Vertigo
 Headache
 Facial palsy

 Rarer:
o Meningitis
o Intracranial abscess
o Lateral sinus thrombosis

o Ix: CT/MRI – determine extent + plan for surgery

o Rx: Surgery (no conservative therapy available)
 Otosclerosis (2nd most common cause of CHL in 15-50 y/o after wax impaction)
o Definition: Fusion of stapes footplate to oval window so it cannot vibrate

o Cause: Genetics

o Features: Progressive CHL (?bilateral) in teens/20’s; tinnitus

o Ix: Audiogram  2kHz dip on audiogram

o Rx:
 Hearing aid
 Surgery (stapedectomy or stapedotomy)
Diseases of the INNER EAR

 Congenital Sensorineural Hearing Loss

o Types:
 Hereditary
 Non syndromic (70%)  Hearing loss only, idiopathic
 Syndromic (30%)
o E.g. Treacher-Collins (1st + 2nd branchial cleft anomalies)
o E.g. Alport (hereditary nephritis)
 Prenatal  TORCH infections
 Perinatal  Anoxia
 Post-natal  MMM (mumps, measles, meningitis)

o Screening for hearing loss done for ALL neonates (otoacoust emissions, auditory brainstem resp)

o Rx: ?Choclear implant (may be an option)

 Acquired hearing loss

o Presbyacusis (“age-related SNHL”) – most common SNHL
 Definition: SNHL starting @ age 50-60

 Cause: Hair cell degeneration, cochlear neuron damage, ischemia of inner ear

 Features:
 Progressive, bilateral hearing loss initially at HIGH FREQUENCY, then at middle
frequencies
 Hearing worse with background noise – describe people as “mumbling”
 Recruitment phenomenon – cannot tolerate loud sounds
 Tinnitus

 Rx: Hearing aid if >30dB hearing loss

 Consider – lip reading training, auditory aids (e.g. doorbell + phone lights)

o Noise-induced SNHL
 Pathogenesis:
 High dB sound (>90dB over time OR >135dB single impulse) = cochlear damage
 Early-stage lost at 4kHz (as this is resonance frequency of temporal bone)
 Later-stage wider range lost, and speech frequency impaired to >30dB (i.e.
hearing loss is a LATE sign)

 Rx: Hearing aid + prevention (e.g. ear protections [muffs, plugs], ear rest from noise)

o Sudden sensorineural loss

 Features: Unilateral sudden SNHL
 Rx: Corticosteroids/pred x2wk (10% still have permanent hearing loss)

o Drug ototoxicity
 Aminoglycosides – days to weeks post-treatment
 Some VESTIBULOTOXIC (inc gent), some cochleotoxic
 All toxic to hair cells (first OUTER, then INNER – high frequency lost FIRST)
 Anti-malarials (quinines), Chemotherapy, Loop diuretics, glycopeptides
Vertigo and Dizziness

 “Dizziness” can be:

o Light-headedness  ASK: “Are you light-headed”?  Will NOT be vertiginous
 Cardiac related
 Rhythm problem?
 Outflow obstruction problem?  AS, MS, HOCM
o Vertigo  Physical sensation where the room is spinning around you, but they are standing still
 ASK: “Is the room spinning around you”?
 Neurological related
o Stroke  ASK: “Do you have weakness or numbness”?  Can cause CENTRAL vertigo
o Cerebellar dysfunction  Can cause CENTRAL VERTIGO
 Vertigo
o Peripheral (80%)
 Associated with:
 Hearing loss
 Tinnitus (perception of sound in the ear without true external sound)
 Nystagmus which stops on looking at something/fixation after short period
 Caused by dysfunctional CN8 AFTER it leaves the brain
 Problems inside the tympanic membrane
 Problems inside the vestibulocochlear system (most common)

 Specific types of peripheral vertigo:

 Benign Positional Vertigo  Cause = SC canal otolith; 90% posterior SC canal
o ONLY vertigo
o ALWAYS from sitting/lying to standing position
o ↓↓ Duration (seconds)
o Dix-Hallpike POSITIVE (50-80%)
o NO tinnitus
o NO hearing loss

 Vestibular Neuronitis/Labyrinthitis/Meniere’s Disease

o Meniere’s Disease  SNHL, Fluctuating Tinnitus, Recurrent episodes
of ↓ duration (1-8hrs), aural fullness, rare “drop attacks” w/ no LoC,
HL may be permanent, usually resolves after 5-10 YEARS

o Vestibular neuronitis  NO hearing loss, tinnitus, recent virus/URTI +

↑ duration (1-5 days), usually SINGLE episode, 2wk post-vertiginous
“imbalance”/motion sickness
 If hearing loss present = Labyrinthitis (+ lasting for DAYS)

 Perilymph Fistula
o DO get hearing loss (+/- tinnitus)
o Caused by TRAUMA TO THE EAR

 Acoustic Neuroma/Vestibular Schwannoma  Tumour of CN8

o Dizziness possible, vertigo rare (slow growing=time for compensation)
o DO get SNHL (+/- tinnitus), CN 5 + 7 palsy
o Associated with ATAXIA (compression of cerebellum)
o Associated w/ Neurofibramatosis Type 2 (bilateral ANs)
 o Central (20%)
 Associated with:
 (NOT associated with hearing loss or tinnitus)
 Nystagmus which DOES NOT stop  termed “non-extinguishing” nystagmus
 Caused by stroke, multiple sclerosis, trauma, drug toxicity, cerebellar tumours
 All of these disrupt the territory of CN8 in the brain
 Drug toxicity  Phenytoin
o Mild: Horizontal nystagmus  eyes move horizontally
o Severe: Vertical nystagmus  eyes move vertically

 Ix: Ear examination, Dix-Halpike, Epley, Audiogram, MRI (if acoustic neuroma)
o BPPV: Dix-Hallpike, Epley (Rx also)
o Meniere’s: Audiogram (SNHL)
o Acoustic Neuroma: MRI w/ Gad, audiogram, auditory brain stem response (5th wave delay),
delayed/absent stapedial reflex

 Treatment
o For all  Cyclizine (anti-emetic effect)

o Benign Positional Vertigo

 Reassurance – resolves spontaneously
 Head repositioning techniques (to dislodge otolith)  Epley manoeuvre (by MD)
 Brandt-Daroff exercises (by patient)
 Surgery if refractory

o Labyrinthitis/Vestibular neuronitis
 Prochlorperazine for 1-2 weeks
 Vestibular rehab
 IF labyrinthitis  IV Abx (if bacterial in cause)

o Meniere’s Disease
 Lifestyle Measures  Salt restriction
 Prophylaxis  Betahistine
 Acute attack  Diuretics (HCTZ; to decrease endolymph), Prochlorperazine
 If refractory  Surgery

o Perilymph fistula  Surgical reconstruction

o Acoustic Neuroma/Vestibular schwannoma  Observation, Radiotherapy, Surgical resection

Peripheral Vertigo Central Vertigo

Onset Sudden Gradual (except stroke?)
Hearing Loss + Tinnitus **Present** **Absent**
Nystagmus Unidirectional Bidirectional
Exhausts with fixation DOES NOT exhaust with fixation
Neighbourhood Signs (diplopia,
cortical blindness, dysarthria, Absent Present
extremity weakness/numbness) 
i.e. FOCAL SIGNS
 Notes
o All vertigo presents with nystagmus, but whether it extinguishes or not helps differentiate
THROAT

Pharyngitis (sore throat)

 Cause:
o Viral  Rhinovirus, adenovirus
o Bacteria  GABHS (S pyo)
o Fungi  Candida

 Features: Sore throat and...

o Viral  Conjunctivitis, arthralgia, cough
o Bacteria  Exudate, quinsy, NO cough

o Diagnostic Criteria for GABHS – Centor Score:

 Hx of fever (also seen in viral)
 Exudates
 Tender anterior cervical lymphadenopathy
(also seen in viral)
 NO cough (?respiratory), NO hoarseness
(?laryngitis)

 0-1 = Unlikely GABHS

 2 = Rapid antigen test/Culture (NB: 40% asymptomatic = +GABHS on culture)
 3-4 = Empiric Abx

 Rx:
o Paracetamol/ibuprofen
o Abx (Pen V QDS x10d) if:
 Centor 2 culture/rapid antigen +
 Centor 3-4
 Not resolving after few days (consider DELAYED PRESCRIPTION after 3d)
 Otherwise severe
Diseases Causing HOARSENESS (ranging from HARSH to WEAK voice)
ANY PATIENT WITH HOARSENESS FOR >3wk  CXR Immediately (prior to referral) [esp if >50 + smoker + drinker]
If CXR abnormal  Urgent referral lung cancer specialist
If CXR normal  Urgent referral ENT specialist

Acute Laryngitis

 Definition: <2wk inflammatory changes to laryngeal mucosa

 Cause:
o Viruses (influ, adeno)
o Bacteria (S pyo)
o Mechanical acute voice strain (causes vocal cord edema = hoarseness)

 Features: Hoarseness, URTI

 Rx: Self-limiting, no treatment needed; conservative (e.g. voice rest, humidified air) may help

Chronic Laryngitis

 Definition: >2wk inflammatory changes to laryngeal mucosa

 Cause:
o Chronic: irritants, voice strain, sinusitis w/ post-nasal drip, alcohol use
o GORD

 Features: Chronic dysphonia, cough

 Ix: Laryngoscopy – R/O malignany

o Chronic laryngitis – erythematous cords, thickened, normal movement

 Rx: Remove cause, treat any underlying disorder (e.g. GORD)

Vocal Cord Polyps

Vocal Cord Nodules (AKA “Singer’s nodules” – callus formation)
Laryngeal Papilloma – HPV 6, 11; Rx: Surgery

Laryngeal Carcinoma – 50% of ALL H+N cancer; M>F 10:1

 Risk: Smoking (virtually ONLY seen in smokers)

 Types: SCC most common

 Sites:
o Supraglottic (35%)
o Glottic (60%)
o Subglottic (1%)
Diseases of the SALIVARY GLANDS – inflammation, stone, neoplasia
Sialadenitis

 Definition: Inflammation of salivary glands

 Cause:
o Viral/mumps (most common)
o Bacterial – S aureus, S pneumo, H influ
o Stone

 Features: Pain + swelling of salivary gland (usually parotid, submandibular)

 Ix: USS (differentiate if obstructive cause e.g. stone/sialolithiasis)

 Ix: Viral = nil; Bacterial = Abx + abscess drainage

Sialolithiasis

 Definition: Ductal stone leading to chronic sialadenitis

o 80% submandibular (under chin)
o <20% parotid (at angle of jaw)
o 1% sublingual

 Risk: Dehydration, hypercalcaemia

 Features: Pain, swelling which increases at meal times, palpation of calculi

 Ix: Sialogram

 Rx: Encourage salivation, analgesia

o If large/does not resolve spontaneously – surgery

Salivary Gland Neoplasia (80% parotid, 10% submandibular, 1% sublingual)

 BENIGN: (80% parotid, 80% benign, 80% pleomorphic adenomas)

o Pleomorphic adenoma (80%)  Felt at angle of jaw
 Does NOT affect facial nerve, is NOT hard, NOT painful, NOT rapidly growing
 These are features of malignancy
o Warthin’s tumour (10%; parotid)
o Cysts, lymph nodes, adenomas (10%)

 MALIGNANT:
o Mucoepidermoid (40%)
o Adenoid cystic (30%)
Parotid Gland Neoplasia (benign or malignant)

 Features:
o Painless, slow-growing mass
o Salivary changes
o Bilateral = benign (Warthin’s tumour, Sjogren’s, mumps) OR possibly lymphoma

 Ix: FNA, CT/MRI

 Rx: Surgical excision (beware: FACIAL NERVE INJURY)

o NB: Pleomorphic adenomas recur if not all tissue removed, or if cells become seeded elsewhere
during operation (extremely careful removal necessary)

 Paediatric airway
o Basics
 Larynx + treachea small therefore small pathology = big consequences
 <5month = preferential nasal breathers
 Signs of respiratory failure
 Lethargy or reduced consciousness
 Shallow breathing
 Apnea
 NB: THESE REQUIRE SUCTION, ORAL AIRWAY, MASK VENTILATION
o Intubation may be required eventually
o Diseases
 Subglottic haemangioma
 Benign vascular tumour growing rapidly until 1 year, resolves by 5 years
 Presents at 3-6 months with stridor and/or barking cough
 Diagnose  Endoscopy
 Treat  Intralesional steroids, laser, interferon alpha, embolisation
o Consider tracheostomy if airway obstructed
 Subglottic stenosis
 Diagnose  Endoscopy
 Treat  Conservative (improve with age), surgery, tracheostomy
 Laryngomalacia  Most common congenital laryngeal abnormality
 Laryngeal cartilage collapses on inspiration causing “stridor flutter”
 Diagnose  Endoscopy
 Treat  Watchful waiting; aryepiglottoplasty (opening of larynx)
 Choanal atresia
 Stenotic nasal airway
o Neonates are obligatory nasal breathers
 Emergency if bilateral
 Treat
o First: Oropharyngeal airway
o Second: Definitive surgery (stenting)
o Follow-up: Dilatations of stents
 Foreign body  2-4y/o child
 Symptoms  choking, gagging, coughing, wheezing
 Diagnose  Endoscopy + Removal
 Post-bronchoscopy  Steroids for post-removal oedema by instruments
NOSE
Rhinitis

 Definition: Inflammation of mucosal lining of nasal cavity

 Classification:
o Inflammatory – e.g. Asthma, allergies, infection, sarcoid/Wegener’s, irritants (dust, chemical)
o Non-inflammatory

 Allergic Rhinitis (Hay Fever):

o Definition: IgE mediated hypersensitivity to foreign allergens
 Allergen contacts nasal mucosa = reaction
 Quantity of allergen = degree of symptoms

o Types:
 Acute and seasonal – e.g. pollen from trees
 Chronic and persistent/perennial
 Inhaled – e.g. dust, wool, feathers, tobacco
 Ingested – e.g. wheat, eggs, milk, nuts

o Features:
 <20 onset
 Nasal obstruction w/ pruritus, sneezing
 Clear nasal discharge (contains eosinophils)
 Itching of eyes w/ tearing
 “Boggy” feeling

o Ix: Allergy testing (only necessary if refractory to initial therapy)

o Rx: Avoid allergen, oral/intranasal anti-histamine, intranasal corticosteroid, topical decongest

 If refractory consider desensitization by allergen immunotherapy
 Oral corticosteroids rarely, Oral decongestants NEVER used
Sinusitis

 Definition: Inflammation of mucosal lining of sinuses caused by any form of blockage

o NB: All sinuses drain to common area under middle meatus called osteomeatal complex

 Classification:
o Acute = <4wk
o Subacute = 4wk – 3mo
o Chronic = 3mo

 Cause: Obstruction
o Inflammation – URTI/Allergy
o Mechanical – Turbinate hypertrophy, polyps, tumour, large adenoids, foreign body
o Immune – Wegener’s, lymphoma/leukaemia

 Acute Suppurative Sinusitis:

o Definition: Acute infection + inflammation of paranasal sinuses

o Cause: Viral > Bacterial

 Viruses: Rhino, Influenza, Parainfluenza
 Bacteria: S pneumo (40%), H influ (40%), M catarrhalis

o Diagnostic Criteria: 2 major OR 1 major + 2 minor symptoms

o Other features:
 Sudden onset nasal blockage/congestion AND/OR nasal yellow/green discharge
AND/OR posterior nasal drip
 Post-nasal drip = dry cough
 Facial pain/pressure
 Maxillary sinus most affected

 Viral - <10d, non-purulent

 Bacterial – worsens >5d and/or persists >10d, purulent discharge

o Diagnose: X-Ray  CT  MRI  Sinus puncture (culture; NONE of these usually needed)

o Rx: Paracetamol, IN Decongestant, ?INCS, ?Abx, ?FESS (functional endoscopic sinus surgery)
 1st 5d, non-severe: Symptomatic management (paracetamol, decongestant)
 Moderate + >5d: Intra-nasal corticosteroid spray
 Severe + >5d OR >10d OR refractory to INCS: Abx

 Refractory to all: FESS (functional endoscopic sinus surgery)

Chronic Sinusitis

 Definition: Inflammation of paranasal sinuses for >3mo

 Cause: Inadequate treatment of acute sinusitis, untreated allergy, anatomic abnormality, chronic
inflammatory disorder (e.g. Wegener’s)
o Organisms: Same as acute

 Features:
o Chronic nasal obstruction + discharge
o Sinus pain/headache
o Chronic cough

 Rx: Abx 3-6wk, intranasal corticosteroid spray, FESS

Influenza

 Features: Headache, myalgia, joint pain, cough, sore throat

 Treat:
o <48 hours: Oseltamivir (-ivir)
o >48 hours: Supportive
*Consider vaccination
Epistaxis**

 Epidemiology:
o 90% occur in Little’s area (Kiesselbach’s Plexus) - anterior
o Consists of arteries from both external + internal carotid
 Sphenopalatine
 Posterior ethmoid
 Anterior ethmoid
 Superior labial
 Greater palatine

o Sometime can occur posterior from sphenopalatine only

 Causes:
o Local – trauma (esp nose picking), foreign body
 Also inflammation, tumours, chemical (e.g. cocaine), barometric changes, etc

o Systemic:
 Haem  Thrombocytopenia (?Malignancy [leuk/lymph], ?Isolated platelets/VWD/ITP)
 Cardiac  HTN
 Systemic  Wegener, SLE, OWRendu
 Drugs (aspirin, anticoags, cocaine)

o (Adolescent male, recurrent, unilateral – juvenile nasopharyngeal angiofibroma)

 Ix: FBC, Clotting, CT (only if SEVERE episode)

 Rx:
o First: ABCDE + Sit upright + Lean forward + pinch SOFT part of nose for 20min + ice pack on nose
 IV fluid, G+S/X-match

o Second: Insert cotton wool w/ topical lidocaine

o Third: Definitive stoppage of bleeding

 Topical vasoconstrictor (e.g. phenylephrine, xylometazoline)
 Cauterization (w/ silver nitrate)

o If all fails: Nasal packing (pressure effect can stop bleeding), Suture vessels
Adenoid Hypertrophy

 Features:
o Peak size age 5
o Nasal obstruction  Nasal voice, snoring + tired, mouth breather
o Choanal obstruction  Rhinitis, OSA
o Inflammation  Post-nasal drip + cough

 Ix: Laryngoscopy

 Complications: Otitis media (Eustachian tube obstruction); mouth breathing; OSA + cor pulmonale

 Rx: Adenoidectomy
o Indications  OSA/sleep disturbances; chronic OM or recurrent AOM; persistent rhinorrhea
Tonsillitis

 Definition: Inflammation of tonsils due to infection

o NB: pharyngitis is inflammation of back of throat, laryngitis is inflammation lower down

 Cause: S pyogenes (GABHS)

 Features: Pain in throat (±ears, ±abdo pain), red tonsils (±pus/exudate), lymphadenopathy
o Diagnostic Criteria for GABHS – Centor Score:
 Hx of fever
 Tonsillar exudates
 Tender anterior cervical lymphadenopathy
 NO cough

 0-1 = Unlikely GABHS

 2 = Rapid antigen test/Culture
 3-4 = Empiric Abx

 Rx:
o Paracetamol/ibuprofen
o Abx if Centor 3-4, not resolving after few days, otherwise severe, culture+

o Surgery:
 Indications:
 ALL 4 of the following:
o Sore throats due to tonsillitis
o 5+ episodes/yr
o Symptoms for 1+ yr
o Episodes are disabling/prevent normal functioning

 Acute airway obstruction ONLY

 Suspected malignancy (e.g. lymphoma, SCC) or TB

 Complication:
o Peritonsillar Abscess AKA Quinsy
 Definition: Cellulitis of space behind tonsillar capsule  Abscess

 Cause: GABHS (S pyo; 50%; post-tonsillitis), S aureus, H influ

 Features:
 Unilateral abscess of tonsil
 Fever + tonsillitis symptoms

 Complication:
 Aspiration pneumonia (after quinsy rupture)
 Airway obstruction
 Sepsis

 Rx: Refer to ENT for drainage + Abx

 First: Drain + Abx, then CONSIDER tonsillectomy (not all cases)
Random Notes

 Tumours
o Benign
 Papilloma
 Osteoma
 Inverted papilloma
 Unilateral, locally aggressive
 Treat  Surgery
 Follow-up  Crucial as high rate of recurrence
o Malignant (rare)
 Symptoms  Obstruction, haemorrhage, pain
 Diagnose  Histology + imaging
 Treat  Surgery and/or radiotherapy
 Infection
o Sinusitis (complications include eye problems and CNS problems  abscesses)
 Acute (<2wks)
 Predisposing factors  URTI, Blockage
 Clinical
o Symptoms: Pain, fullness, fever, paroxysmal nocturnal dyspnea
o Signs: Inflammation, pus, tenderness
 Diagnose: Clinical + Culture + X-ray + CT
 Treat: Analgesia, Antibiotics, Decongestant
 Recurrent acute (4 or more episodes in a year)
 Chronic (>8wks + metaplasia of nasal mucosa)
 Predisposing factors  Inappropriate Rx to acute; metaplasia of mucosa
 Clinical
o Symptoms  Same as acute (pain, fullness, fever, PND)
o Signs  oedema, pus
 Diagnose: Clinical + CT
 Treat: Same as acute (pain relief, Abx, decongestants) + steroids; ?surgery
 Inflammation
o Polyposis  Inflammation of nasal mucosa for unknown cause
 Symptoms: Obstruction (from oedema), runny nose (rhinorrhea)
 Diagnosis: Clinical + CT
 Treat: Steroids + ABx; ?surgery
o Rhinitis  Inflammation of nasal mucosa due to infection, allergy, vasomotor, inflammatory
 Infective  e.g. common cold
 Inflammatory  e.g. Wegeners (upper and lower respiratory)
 Foreign body  Unilateral obstruction and discharge in a child... remove with probe/forceps
HEAD + NECK
Anatomical Triangles of the Neck (2 big, 5 small)

 Anterior Triangle  Anterior SCM, anterior midline of neck, lower border of mandible
o Submental triangle
o Digastric
o Carotid

 Posterior Triangle  Posterior SCM, anterior trapezius, middle 1/3 of clavicle

o Occipital
o Subclavian

Facial Nerve

 Function: “Face, Taste, Ears, Tears”

o Muscles of facial expression
o Taste anterior 2/3 tongue (via chorda tympani nerve of facial nerve)
o Stapedius
o Lacrimation (lacrimal gland via greater petrosal nerve of facial nerve), salivation (parotid gland;
hence CN7 injury risk in surg)
 Course:
o Motor + sensory:
 Inside skull:
 Enter petrous temporal bone via internal auditory
meatus
o Very close to inner ear
 Runs through Z-shapes facial canal to emerge into face
from stylomastoid foramen

 Branches given off (in order): greater petrosal,

stapedial, chorda tympani
 Outside skull:
 Passes through parotid gland
 Gives off two branches:
o Posterior auricular (hence pain sometimes in Bell’s Palsy)
o Branch to digastrics + stylohyoid
 Then divides into 5 terminal branches  Temporal, Zygomatic, Buccal,
Mandibular, Cervical

Carotid Anatomy – external carotid branches

 Internal
 External
o Branches  “Externally, Some Attendings Like Freaking Out Potential Medical Students”
 Superior thyroid
 Ascending pharyngeal
 Lingual
 Facial
 Occipital
 Posterior auricular (terminal)
 Maxillary (terminal)
 Superficial temporal
NECK MASSES

 Midline
o Thyroglossal cyst
o Thyroid isthmus
o Thyroid goitre
 Colloid goitre
 Euthyroid multinodular goitre
 Hashimoto’s, Graves...
o Dermoid cyst
 Lateral
o Branchial cyst
o Cystic hygroma
o Cervical lymph node (e.g. lymphoma)
o Pharyngeal pouch

 Anterior Triangle (lateral masses):

o Lymph nodes (most commonly)

o Submandibular masses:
 Lymph nodes (e.g. infection [?TB], lymphoma)
 Salivary calculus
o Carotid body tumour
o SCM tumour
o Cystic hygroma
o Branchial cyst

 Posterior Triangle (lateral masses):

o Lymph nodes
o Cervical rib
o Pharyngeal pouch
o Cystic hygroma
o Branchial cyst

 Questions to ask:
o Age (>45 = risk for malignancy)
o Site, when did it start, size change, coming and going or always there
o Symptoms of mass:
 Tender? Warm? Red? Hard? Pulsatile?
o Symptoms to localise pathology:
 Pharynx  Sore throat, trouble swallowing, move on swallowing
 Larynx  Hoarse voice
o Worrying symptoms:
 Fever?
 Weight loss?
 Night sweats?
o Risk  Tobacco, alcohol use

Ix: Bloods, Imaging (USS, CT w/ contrast, ?CXR [TB]), Biopsy (FNA, core, open)
Approach to a Neck Mass According to Age

 <20:
o Congenital:
 Lateral – branchial cleft cyst, laryngocele, cystic hygroma
 Midline – thyroglossal duct cyst
o Inflammatory neck nodes (tonsillitis, glandular fever, Kawasaki’s)
o Lymphoma
 20-40:
o HIV
o Salivary gland (calculi, infection, tumour)
o Thyroid (duct cyst, goitre, infection, tumour)
o Granulomatous disease (TB, sarcoid)
 >40  Primary/Secondary cancer

 Ix:
o First: Bloods (inflammatory/infection, TFTs)
o Second: Imaging (USS, CT)
o Third: Biopsy (FNA, needle biopsy, open biopsy)
CONGENITAL NECK MASSES
Thyroglossal Duct Cyst

 Cyst occurring anywhere between back of throat (foramen caecum; superior)  ventral
to hyoid  normal thyroid location (inferior)
o Relates to embryology as thyroid starts as back of throat (superior) and decends towards normal
thyroid location on trachea
o 65% infrahyoid; 20% suprahyoid; 15% juxtahyoid
o Presents 10-40y/o  If >40 more likely to be a goitre

 Features:
o 20-40y/o, painless midline swelling which elevates w/ tongue protrusion
o Infection, rarely airway obstruction

 Ix:
o USS (to see mass, and ensure they have a thyroid [i.e. that this is not it]) – do not want to remove
their thyroid!
o I-123 radio-isotope scan (NB: I-131 for radioablation)
 Rx:
o Pre-op Abx to reduce inflammation
o Surgery ALWAYS (potential for neoplastic transformation; must remove whole tract up to FC)
 MUST avoid hypoglossal injury
Cystic Hygroma (Lymphangioma)

 Definition: Lymphatic malformation arising from vestigial lymph channels in neck

 Features: 2y/o, thin-walled cyst in posterior triangle or supraclavicular, painless + soft + compressible
o TRANS-ILLUMINATES

 Rx: Surgery if does not resolve spontaneously

Branchial Cyst/Fistula

 Definitions:
o Branchial fistula – persistent communication between skin and GI tract
o Branchial sinus – blind-ended tract opening to skin
o Branchial cyst – persistent sinus with NO external opening

 Features: Present in early adulthood

o 2nd branchial cleft (most common)
 Cyst  Smooth, painless, slowly-enlarging lateral neck mass after URTI in teens
 Fistula  Small opening anterior to SCM in infancy

o 1st branchial cleft

 Pit/sinus around/behind hear

 Rx: Surgical removal (NB: If infected, let infection settle first)

HEAD AND NECK NEOPLASIA

 Pre-malignant disease:
o Leukoplakia
o Erythroplakia
o Dysplasia
 Neck lumps
o Midline
 Thyroglossal cyst
 Dermoid cyst (occur anywhere; due to embryonic anatomical problems)
 Thyroid isthmus (normal ventral component of thyroid connecting the main lobes)
o Lateral
 Cervical lymph node
 Types
o Infective
 Bacterial  e.g. tonsillitis (GBHS); other rare
 Viral  EBV, HIV
 Protozoal  Toxoplasmosis
o Malignant
 Lymphoma
 Squamous Ca
 Symptoms
o Throat  Dysphagia, Odynophagia, Voice
changes
o Nose  Bleeds, CN palsies, Pain
 Signs: Smooth neck mass in anterior or posterior
triangle
 Diagnosis (TNM staging)
o Fine needle aspiration + cytology (FNAC)
o CT scan
 Treat  Surgery and/or radiotherapy
 Thyroid
 Bilobed
 Attached to trachea via ligament of Berry
 Posteriorly lies recurrent laryngeals and parathyroid glands
 Blood supply
o Arterial  Superior + Inferior thyroid arteries
o Venous  Superior, middle and inferior thyroid veins
 Diseases
o Goitre (sign of hyper OR hypo thyroidism)
 Types of goitre
 Multinodular
 Solitary nodule
o Cancerous
o Toxic nodule
o Dominant nodule of multinodular
 Symptoms
 Hyper: Flushing, sweating, weight loss, tremor, heart
 Hypo: weight gain, depression, hair loss
 Signs
 Neck lump moving with swallowing
 Hoarseness
 Stridor
 Diagnosis:
 Blood  TFT
 USS
 CT
 FNAC
  Treat  Surgery and/or radiotherapy
 Indication  If symptomatic (even cosmesis)
 Branchial cyst (neck lump; FNAC + Scans; treat with surgery)
 Pharyngeal pouch (dysphagia, breath, aspiration pneumonia; barium swallow; surgery)
Other

Facial Nerve Palsy

 Types:
o Supranuclear + Nucelar (MS, brain tumours, stroke)
o Infranuclear:
 Bell’s Palsy (90% of infranuclear)
 Cause: 50% idiopathic, 50% viral; risk in pregnancy + diabetes

 Features: Diagnosis of exclusion; facial nerve palsy +:

o Numb ear
o Hyperacusis
o ABSEBNCE of CNS disease

 Ix: Viral serology, EMG if palsy persists

o Other:
 Stapedial reflex ABSENT
 Audiology NORMAL
 CT/MRI

 Rx: Remits in 3wk

o Protect eye w/ patch/tape; artificial tears (hypromellose); sunglasses
o Steroids
o Antivirals (in some cases – acyclovir)

o Surgery if not recovered by 3mo

 Prognosis:
o Most patients with partial OR full paralysis recover completely
o Axonal degeneration is a complication

 Sjogren’s
 Herpes  Zoster Oticus (Ramsay-Hunt Syndrome), HSV1
 Auricular pain (often 1st symptom)
 Facial nerve palsy
 Vesicular rash around ear
 Vertigo + Tinnitus

 Rx  Oral acyclovir + corticosteroids

 Iatrogenic
 Temporal Bone Fracture

 Rx: PREDNISOLONE if >16 + present for <72hr

(acyclovir no longer used)
Aphthous Ulcer (on gums, on tongue)

 Often occurs shortly after long-term smokers stop smoking

o Consider oral squamous cell carcinoma – especially in smoker + drinker
 These present as “large aphthous ulcers” but they are not truly aphthous ulcers as
aphthous ulcer refers to a benign condition
 Rarely painful
 Refer under 2WW
o Viruses also can cause it  CMV, HBV
o Behcets, but should have genital ulceration, eye disease...

 Rx  Symptomatic
o Anaesthetic spray
o Lozenges
o Membrane coating agents (Bongella)

(Topical steroids if refractory, Oral steroids ONLY if severe disease like Pemphigus Vulgaris)

Nasal Polyps
Aspirin + asthma sensitivity + nasal polyps = Samter’s triad
CF
Kartagener’s
Churg-Strauss

NASAL POLYPS ARE MOST COMMONLY SEEN IN MALE ADULTS – not young boys
ALL NASAL POLYPS, ESP UNILATERAL, SHOULD BE REFERRED TO ENT FOR FULL EXAMINATION
Osler-Weber-Rendu

 Epistaxis
 Telangiectasia (e.g. lips, oral cavity, many other places)
 Visceral AVM  e.g. GI, pulmonary, hepatic AVMs
 FH OWR