EAR,

NOSE & THROAT

NOTES

Written by: Amierah Nabillah Haji Othman

Sources:
UCC 4th Year ENT Lecture Notes
Oxford Handbook of Clinical Specialties (9th Edition)


EAR

1.

-

2.
-

3.
-

4.

-

5.

INTRODUCTION:

Wash hands
Introduce yourself
Confirm patient details
Explain examination (Today Id like to examine your ears,
this will involve me having a look inside your ears using a
special piece of equipment known as an otoscope. In
addition Ill also be assessing your hearing using a number
of different tests)
Gain consent (Are you happy for me to go ahead)

GROSS HEARING ASSESSMENT:

Ask the patient if they have noticed any change in their
hearing recently.
Explain that youre going to say a word or number and
youd like them to repeat it back to you.
To test:
o With your mouth approximately 15cm from the ear,
whisper a number or word (e.g: 41 or chicken)
o Mask the ear not being tested by rubbing the tragus
o Ask the patient to repeat the number or word back
to you
o If the patient repeats the correct word or number,
repeat the test at an arms length from the ear
(normal hearing whisper heard at 60cm)
o Assess the other ear in the same way

RINNES TEST:

Air conduction (AC):
o Tap a 512HZ tuning fork & place at the external
auditory meatus
o Ask: Can you hear it?
Bone conduction (BC):
o Move the tuning fork (whilst still vibrating), placing
its base onto the mastoid process
o Ask: Where is the sound louder? - In front of the ear
(EAM) or behind it (mastoid process)
Findings:
o Normal = AC > BC (Rinnes positive)
o SNHL = AC > BC (both air & bone conduction
equally)
o Conductive deafness = BC > AC (Rinnes negative)
WEBERS TEST:

Tap a 512HZ tuning fork & place in the midline of the

forehead
Ask the patient: Where do you hear the sound?
Findings:
o Normal = sound is heard equally on both ears
o SNHL = sound is heard louder on the side of the
normal ear
o Conductive deafness = sound is heard louder on the
side of the affected ear

To recap


Rinnes
Webers
Normal
AC > BC
Equal on both ears
(Rinnes positive)
SNHL
AC > BC
Louder on normal ear
(both equally)
Conductive
BC > AC
Louder on affected
(Rinnes negative)
ear

6.

OTOSCOPY:

Ask the patient if they have any ear discomfort (if so,
examine the non-painful side first)
Pinnae:
o Scars:
! Postauricular: Mastoidectomy
! Endaural: Middle ear surgery
o Abnormalities:
! Perichondritis -> Cauliflower ear
Ear canal / tympanic membrane:
o Ensure the light is working on the otoscope
o Apply a sterile speculum (the largest that will
comfortably fit in the external auditory meatus)
o To straighten the external auditory meatus, pull the
pinna:
! Up & back (3 y/o and older)
! Down & back (< 3 y/o)
o Position otoscope at the external auditory meatus:
! Otoscope should be held in your right hand for
the patients right ear and vice versa
! Hold the otoscope like a pencil and rest your
hand against the patients cheek for stability
! Advance the otoscope under direct supervision
o Look for:
! Wax
! Swelling
! Erythema
! Discharge
! Foreign bodies
o Examine the tympanic membrane:
! Colour?: Pearly grey & translucent (normal) /
erythematous (inflammation)
! Erythema or bulging of the membrane?: Inspect
for a fluid level (e.g. otitis media)
! Perforation of the membrane?: Note the size and
site
! Light reflex (cone of light) present?: Absence /
distortion may indicate inner ear pressure (e.g.
otitis media)
! Scarring of the membrane?: Tympanosclerosis
(can result in significant hearing loss)
o Withdraw the otoscope carefully
o Discard the otoscope speculum in a clinical bin
TO COMPLETE EXAMINATION:

Thank patient
Wash hands
Summarise findings
Suggest further investigations (e.g. audiometry)

Source:

Hearing/Ear
examination
(http://geekymedics.com/2015/03/28/hearing-ear-
examination-osce-guide/)

2) OTALGIA

1. OTITIS EXTERNA (OE)

Definition:
Inflammation of the outer ear and ear canal
Sometimes known as swimmers ear

Risk factors/aetiology
Trauma (fingernails/cotton bud/keys)
Moisture (humid weather/swimming/bathing)
Skin conditions (eczema/psoriasis)
Absence of wax

Organism:
Bacterial: Pseudomonas (chief), Staph
Fungal: Aspergillus, Candida
Viral: Herpes zoster/simplex

Presentation:
Minimal ear discharge
Itch
Pain
Swelling
Tragal tenderness
Dulled hearing

Complications:
Hearing loss
Canal stenosis

Investigation:
Swab for C&S

Management:
Aural toilet (microsuction)
Aural drops (antibiotics +/- corticosteroid) *pg 543 OHCS
Pope wick (if canal narrowed)
Analgesia

Look out for:
Persistent unilateral OE in diabetics/immunosuppressed
patients/elderly (at risk of malignant/necrotizing otitis
externa)
Treatment resistant OE (sign of malignancy)

2. MALIGNANT/NECROTIZING OTITIS EXTERNA

Definition:
An aggressive life threatening extension of OE leading to
temporal bone destruction and base of skull osteomyelitis
This is not a type of cancer!

Risk factors/aetiology:
Middle aged diabetics (90%)
Immunosuppression
Aural irrigation

Organism:
Pseudomonas (chief)
Proteus
Kiebsella

Presentation:
Similar to OE but more severe
Pain deep in ear (may be worse when moving head)
Ongoing purulent discharge
Cranial nerve palsy (trouble swallowing/facial weakness)

Investigations:
Swab for C&S
Cranial nerve examination
CT/MRI

Management:
IV antibiotics (8 weeks)
Surgical debridement

3. PERICHONDRIAL HAEMATOMA

Pathophysiology:
Blunt trauma causes haematoma between cartilage and
perichondrium (which supplies nutrients)
Cartilage loses blood supply and becomes fibrosis
As a result, the cartilage regenerates in a haphazard
manner giving characteristic deformity/redundant skin
(cauliflower ear)
The ear may also become slightly pale due to reduced
blood flow
Also known as: pinna/auricular haematoma

Management:
Urgent referral after ear trauma
Drainage of haematoma
Pressure dressing with splints
Antibiotics

4. CHONDRODERMATITIS NODULARIS HELICIS (CNH)

Definition:
Benign tender cartilaginous inflamed nodule dwelling on
the upper helix or antihelix
Also known as: Winklers disease

Risk factors/aetiology:
Poor blood flow from pressure (headphone users)
Vasoconstriction (from cold)

Management:
Pressure-relieving methods/prosthesis
Avoid excessive exposure to the cold
Wide excision or deep shave (if not resolved)

5. TEMPOROMANDIBULAR (TMJ) DYSFUNCTION

Definition:
Pain and dysfunction of muscles of mastication and the
TMJ joints
A form of referred otalgia

Risk factors/aetiology:
F>M (oestrogen-related?)
Malocclusion
Bruxism (teeth-grinding)
Stress

Presentation:
Earache
Facial pain
Joint clicking/popping
Joint derangement
Joint tenderness (exacerbated by lateral movements of
the open jaw or trigger points in the pterygoid)

Management:
Analgesia
Occlusal splints
CBT
Physiotherapy
Acupuncture
Reconstructive surgery


*Other causes of otalgia:
Furunculosis/Bullous myringitis/Barotrauma/Referred pain
*Auricular skin tumours:
Benign: Keratoacanthoma/CNH
Malignant: BCC/SCC/Melanoma

3) DISCHARGING EARS & OTITIS MEDIA

Lets look at the character of the discharge (otorrhoea)

External ear:
o Scanty watery discharge (no mucinous gland!)
o Blood (if theres trauma)
o Liquid wax (if it leaks out)
Middle ear:
o Serosanguinous discharge (chronic granulation OM)
o Offensive discharge (cholesteatoma)
CSF otorrhoea (think of trauma!):
o Halo sign on filter paper
o Glucose or B2 (tau) transferrin present

1. OTITIS MEDIA WITH EFFUSION (OME)

Definition:
Fluid in middle ear
Also known as: serous otitis media (SOM)/ secretory
otitis media (SOM)/ glue ear

Risk factors/aetiology:
Cleft palate
Downs syndrome
Cystic fibrosis
Primary ciliary dyskinesia
Children of smokers
Atopy
URTI
Oversized adenoids
Narrow nasopharyngeal dimensions
Post radiotherapy, e.g. nasopharyngeal carcinoma

Pathophysiology:
Dysfunction of the Eustachian tube (due to any of the
above)
Middle ear (connected with the nasopharynx via ET)
which normally absorbs air, creates a negative pressure if
ET blocked, thus interstitial fluid pulled in

Presentation:
Hx:
o Poor listening
o Poor speech/language delay
o Hearing fluctuation (Ossicle function disrupted)
o Ear infections/ URTI
o Balance problems (LSCC exposed)
Examination:
o Variable (retracted/bulging drum)
o Dull, grey or yellow
o Superficial radial vessels
o Decreased drum mobility

Investigations:
Audiogram (Conductive defects)
Tympanometry (Flat tympanogram- Type B)

Management:
Usually resolves over time
Topical/systemic methods are NOT recommended!
Hearing aids: Bilateral OME and hearing loss if surgery
contraindicated
Surgery
o Indication:
! Persistent bilateral OME (>3 months)
! Hearing level in better ear <25dBHL
! Speech/language/developmental problems
! Age > 3 years
o Grommets
(complication:
tympanosclerosis/
infection) preferred over T-tubes (complication:
residual perforation)
o +/- Adenoidectomy

2. ACUTE OTITIS MEDIA (AOM)

Definition:
Middle ear inflammation (commonly after URTI)

Organism:
Bacterial: Pneumococcus/Haemophilus/Moraxella
Viral: Rhinovirus

Presentation:
Acute onset
Presence of fluid (otorrhoea)
Middle ear inflammation
Local symptoms (otalgia)
Systemic signs (fever/vomiting)
Age (6 months to 3 years)

Management:
Analgesia
Antibiotics
o Not routinely prescribed as initial treatment, but if
prescribed, a short course ~5 days (e.g. amoxicillin)
o Consider age and severity
Decongestants/antihistamines NOT recommended!

Complications (if discharge persists): *slide 24 (Middle ear part 1)
Mastoiditis
o Definition: Middle ear inflammation leading to
destruction of air cells in mastoid bone +/- abscess
o RF: Withholding antibiotics in otitis media
o Presentation: temperature, tender mastoid,
protruding auricle
o Investigation: CT
o Management: IV antibiotics (e.g. ceftriaxone),
myringotomy, grommet, mastoidectomy
Facial nerve palsy
Labyrinthitis
Petrositis
Meningitis
Intracranial abscess

ENT referral if:
> 4 episodes in 6 months
Complications arise

Management:
Surgery (grommets +/- adenoidectomy)
Specific
treatment
for
complications
GROMMETS

Function:
o Ventilates & maintains pressure of middle ear
(reduces risk of fluid build up)
o Helps pus flow out if infection occurs
Indications:
o Recurrent otitis media (4-6 x per year)
o OME > 3 months with hearing loss/speech delay
o Complicated AOM
o Eustachian tube dysfunction
o Adenoidectomy on the second set of grommets if
adenoids enlarged
Procedure:
o Placed in antero-inferior quadrant
o Lasts ~ 6-12 months and falls out on its own
Complications:
o Bleeding
o Perforated tympanic membrane
o Otorrhoea
o Infections
o Further grommets


3. CHRONIC OTITIS MEDIA (COM)

Types:
Without cholesteatoma (mucosal)
o Mucosa of middle ear is chronically inflamed and
infected
Cholesteatoma (squamous)
o Squamous epithelium trapped within the temporal
bone

Presentation:
Hx:
o Hearing loss
o Otorrhoea
o Otalgia
o Tinnitus
o Vertigo
o Nasal obstruction
o Previous history of COM, tympanic membrane
perforation or otologic surgery
o *Urgent referral if theres progressive unilateral
hearing loss with chronic foul-smelling
otorrhoea (suspect cholesteatoma)
Examination:
o Otomicroscopy
o Posterosuperior retraction pocket with squamous
epithelium
o Granulation from diseased bone
o Aural polyps
o Pneumatic
otoscopy
(positive:
suggests
perilymphatic fistula)
o Remember to take cultures!

Investigations:
Audiology (usually conductive loss & may vary greatly,
confirm with tuning forks)
Imaging (CT temporal bone to evaluate extent of
cholesteatoma

Management:
Mucosal:
o Topical treatment (steroid/antibiotic drops)
o Aural toilet
o +/- Mastoid exploration
Cholesteatoma:
o Mastoid exploration
o Removal of cholesteatoma

CHOLESTEATOMA

Pathophysiology:
o Stratified squamous epithelium (skin cyst)
trapped in middle ear
o Locally destructive around and beyond pars
flaccida (places pressure on bone and secretes
enzymes)
Classification: *slide 4 (Middle ear part 2)
o Congenital
o Primary acquired
o Secondary acquired
Aetiology:
o Peak age: 5-15 y/o
Complications:
o Hearing loss (CHL, SNHL)
o Tinnitus
o Perilymphatic fistula
o Facial paralysis
o Meningitis/brain abscess

TYMPANIC MEMBRANE PERFORATION

Mostly occur with AOM
Risk factors/aetiology:
o Infection (fluid in middle ear)
o Iatrogenic (grommets)
o Trauma (explosion, instrumentation)
Presentation:
o Pain (usually transient)
o Hearing loss
o Bleeding
o Tinnitus
o Vertigo (rare)
Management:
o Leave alone (small usually heals, large dont, if in
between, just wait and see!)
o Waterproof
o No antibiotics/drops
o OPD in 8-12 weeks (if not healed, tympanoplasty)

TYMPANOSCLEROSIS

Definition:
o Calcification of tissues of the tympanic membrane
and middle ear
Aetiology:
o Recurrent AOM
o OME
o Post grommet insertion

4) HEARING LOSS

AUDIOMETRY

Pure Tone Audiometry

Function:
o Quantifies hearing loss and determines nature
o Subjective
Standard measure
> 4 years can be tested
Procedure:
o Headphones deliver electronically generated tones
at different strengths over frequencies of 250-
8000 Hz in a sound-proofed room
o The patient says when he hears sounds
o The intensity is recorded in decibels (dB) by the
tester as the AC threshold
o BC threshold is obtained by using a transducer
over the mastoid process
o Masking (narrowband noise to the untested ear)
prevents cross stimulation of the non-test ear
Results:

ACOUSTIC IMPEDENCE AUDIOMETRY (TYMPANOMETRY)

Function:
o To test the condition of the middle ear by
measuring the compliance of tympanic membrane
o Objective
Procedure:
o The tympanometer is fitted into the ear
o As the tympanometer continuously changes the
pressure in the ear canal, a transmitter sends a
sound to the drum
o The wave that is reflected back is picked up by the
microphone in the probe
o The tympanometer measures the energy of the
reflected sound
Results:

Type A
Type B
Type C
Sensorineural Hearing Loss

Conductive Hearing Loss

Mixed Hearing Loss

*Extra info: http://www.dilworth.co.nz/clinical-information-articles/guide-to-tympanometry-1

Speech audiometry

Function:
o Examines speech discrimination above threshold
o Assesses disability
o Predicts whether hearing aids would help
Procedure:
o Patient is asked to repeat words presented via
headphones

: Normal
: Fluid in ear or perforation
: Negative middle air pressure

1) CONDUCTIVE HEARING LOSS

Aetiology:
External canal obstruction
o
Wax
o
OE
o
Atresia
Tympanic membrane perforation
o
Trauma
o
Barotrauma
o
Infection
Problems with ossicular chain
o
Otosclerosis
o
Infection
o
Trauma
Inadequate ET ventilation
o
OME
o
Tumour in middle ear (glomus)

Management:
Find out cause and treat


OTOSCLEROSIS

Definition:
o Fixation of stapes footplate by immature new bone
Prevalence:
o 0.5%-2% clinically
o 10% subclinically
Risk factors/aetiology:
o Autosomal dominant
o F> M
o Pregnancy
o Age 20-30 y/o
Presentation:
o Initially conductive HL, but may later affect cochlea
causing SNHL
o Initially unilateral, but may later become bilateral
o Tinnitus
o Mild, transient vertigo
o Schwartz sign (pink tinge to TM)
o Carharts notch (dip at 2kHz) at masked bone
conduction

Left sided otosclerosis

Management:
o Hearing aid
o Surgery (risk of dead ear):
Stapedectomy (removing)
Stapedotomy (drilling)
Cochlear implant if severe

2) SENSORINEURAL HEARING LOSS

A) Sudden SNHL

Definition:
> 30 dbHL in 3 contiguous pure tone frequencies over <
72 hours

Aetiology:
Infection (mumps/measles/meningitis/TB/syphilis)
Trauma (skull base fracture/ear surgery)
Tumour (Acoustic neuroma)
Autoimmune (Wegeners granulomatosis)
Multiple sclerosis
Idiopathic

Investigations:
MRI to rule out tumour
Blood tests
o FBC
o ESR
o Glucose
o ACE
o ANCA
o Auto-antibodies
o Syphilis serology

Management:
Controversial! (Oral steroids/ vasodilator/ antivirals)

Prognosis:
Better if early presentation
Negative prognostic factors:
o Age <15 or >65 y/o
o ESR
o Vertigo
o Hearing loss in the opposite ear
o Severe hearing loss
o Long history

B) Gradual SNHL

Site:
Bilateral:
o Presbyacusis (age)
o Noise-induced
o Drug-induced (ototoxicity)
Unilateral:
o Idiopathic/presbyacusis
o Acoustic neuroma
o Menieres disease
o Late otosclerosis

Management:
Hearing aids
o Audio-amplification system
o Types
!
Behind ear
!
In ear
!
In canal
!
BAHA (Bone anchored hearing aids)
Indications: conductive HL/ unilateral
HL/ intolerance to ear level hearing
aids/congenital
malformations/single-
sided deafness
Contraindications:
average
bone
threshold <45 dB/ non compliance/ poor
hygiene/ lack bone volume
Advantage: Presence not felt

PRESBYACUSIS

Definition:
o Age-related hearing loss from accumulated
environmental noise toxicity
Presentation:
o Loss of high frequency sounds before 30 y/o
o Progressive
o Hearing most affected in the presence of
background noise

Management:
o Hearing aids

C) SNHL in children

Aetiology:
Congenital
o AD
o AR
o X-linked
Acquired
o Antenatal:
! TORCH infections
! Drugs
o Perinatal:
! Hypoxia
! Trauma
o Neonatal:
! Congenital abnormalities
! Meningitis
! Convulsions
! Kernicterus
! Low birth weight
! Ototoxic drugs

Management:
Auditory rehabilitation
o Lip reading
o Sign language
o Environmental aids (special units in school/ visits
from teachers of the deaf)
o Hearing aids (if cochlear hair cells present)
o Cochlear implants (if cochlear hair cells absent)
! Infants
Profound bilateral SNHL
No benefit from hearing aids
No contraindications
High
motivation
and
appropriate
expectations from family
Earlier implantation if SNHL secondary to
meningitis
! Children (and adults)
Severe to profound bilateral SNHL
No benefit from hearing aids
Poor speech discrimination

5) TINNITUS

Definition:
Perception of sound in the absence of auditory
stimulation (usually age 50-60 y/o)

Subjective tinnitus:
Local:
o Hearing loss
o Presbyacusis
o Noise-induced
o Head injury
o Otosclerosis/post-stapedectomy
o Menieres disease
o Acoustic neuroma
o TMJ problems
o Meningitis
o Syphillis
General:
o Cardiovascular (HTN/anemia/heart failure
Drugs:
o Anti-inflammatory
o Antibiotics
o Antidepressants
o Aspirin
o Loop diuretics
o Aminoglycosides
o Quinine
o Alcohol
Psychological:
o Divorce/retirement/etc

Objective (pulsatile) tinnitus:
AV malformations
Venous hum
Atherosclerosis
Ectopic carotid artery
Carotid stenosis
Carotid body tumours
Glomus tumours
Aneurysm
High CO states
o Pagets disease
o Hyperthyroidism
o Pregnancy
o Anemia)

Investigations:
Hx:
o Character (Constant? Pulsatile?)
o Alleviating/exacerbating factors
o Otalgia
o Hearing loss
o Worse if isolated or depressed
o Disturbs sleep
o Drugs
Examination/tests:
o Otoscopy (patulous ET/myoclonus of tensor
tympani)
o Hearing/tuning fork test
o BP & pulse
o Audiometry
o Tympanogram
o MRI (to exclude acoustic neuroma)
o Hb/ lipids

Management:
Treat underlying cause
Removal of cerumen
Masking devices
Hearing aids
Medication (Alprazolam/TCA)
Tinnitus retraining therapy (TRT)

6) VERTIGO (VESTIBULAR)

Definition:
Subjective sensation of self-motion when no-self motion
is occurring/ the sensation of distorted self-motion
during an otherwise normal head movement

Vestibular causes of vertigo:
Peripheral
o Benign positional vertigo (seconds-minutes)
o Menieres disease (hours)
o Vestibular neuronitis (days)
o Labirinthitis
Central
o Acoustic neuroma

Other causes of vertigo:
Multiple sclerosis
Head injury
Malignancy
Verterbral-basilar insufficiency
Arrhythmias
Hypotension
IHD
Migraine
Diabetes
Medications
o Gentamicin (neuronitis)
o Antihypertensives
o Diuretics
o Metronidazole
o Sedatives
o Alcohol

Presentation (Focusing on vestibular vertigo):
More severe compared to central vertigo
May be described as swaying, tilting, bobbing, bouncing,
sliding
Accompanied by
o Nausea
o Vomiting
o Hearing loss
o Tinnitus
o Nystagmus (usually horizontal)

Examination:
ENT/Head and neck
Cranial nerves (Rinne & Weber)
Nystagmus
Rhombergs
Unterbergers
Hallpike manoeuvre

Investigations:
Audiogram
Electronystagmography
Brainstem auditory evoked responses
Calorimetry (COWS)
CT/MRI

1) BENIGN POSITIONAL VERTIGO

Presentation:
Attacks of sudden rotational vertigo lasting >30 sec
provoked by head turning
Symptom free interval
+/- minor head injury

Pathogenesis:
Displacement of otoconia in semicircular canals

Diagnosis:
No persistent vertigo

No speech/visual/motor/sensory problems
No tinnitus/headache/ataxia/facial numbness/dysphagia
Hallpike manoeuvre
o Latency (a few seconds)
o Rotatary nystagmus (Geotropic)
o Reversal upon return to upright position

Management:
Reassurance (usually self-limiting in months)
Precaution against heights (dangerous!)
Vestibular rehabituation exercises
Reduce alcohol intake
Epleys manoeuvre
Drugs:
o Histamine analogues (betahistine)
o Vestibular sedatives (prochlorperazine)
o Antidepressants
Posterior semicircular canal denervation (last resort!)

2) MENIERES DISEASE

Definition:
Dilatation of endolymphatic spaces of the membranous
labyrinth
F>M
Age 35 y/o (peak)

Presentation:
Vertigo for ~12h with prostration
Nausea/vomiting
Aural fullness
Uni/bilateral tinnitus
+/- SNHL (fluctuating)
Occurs in clusters (<20/month)

Diagnosis:
Electrocochleography/ electonystagmography
Calorimetry
Endolymphatic space MRI

Management:
Prochlorperazine, Betahistine
Endolymphatic shunts
Labyrinthectomy (stops vertigo but causes total
ipsilateral deafness)
o Chemical (gentamicin)/ Surgical
Vestibular neurectomy (spares hearing)

3) VESTIBULAR NEURONITIS

Definition:
Inflammation of the vestibular nerves

Synonyms:
Vestibular neuritis (acute and chronic)
Acute/viral labyrinthitis
Vestibular paralysis
Epidemic vertigo
Vestibular neuropathy

Presentation:
Previous URTI (Herpes simplex?)
Severe sudden vertigo
Vomiting
Prostration are exacerbated by head movement
No auditory or CNS manifestations

Management:
Audiometry
CT
Vestibular testing
Vestibular sedative
Cyclizine
Reassure (improve in days/full 2-3 wks/elderly longer)

4) LABIRINTHITIS

Definition:
Inflammatory disease of inner ear of labyrinth

Aetiology:
Viral: Rubella, CMV, Herpes zoster, mumps, measles
Bacterial: Secondary to meningitis, OM
Autoimmune: Wegener Granulomatosis, polyarteritis
nodosa (uncommon)


5) ACOUSTIC NEUROMA

Definition:
Tumours arising from schwann cells around vestibular or
cochlear nerves that behave as space-occupying lesions
Also known as: Vestibular schwannoma

Presentation:
Progressive unilateral tinnitus +/- SNHL
Headaches
Facial numbness (trigeminal compression)
Ipsilateral cerebellar signs/ Increased ICP signs
Vertigo (rare)

Investigations:
Audiogram
MRI (especially in those with unilateral tinnitus/
deafness)

Differential:
Meningioma

Management:
Watch and wait
Surgery (difficult & often not needed, esp elderly)
Gamma knife surgery (to reduce neuroma volume)

Follow up:
MRI (to detect expansion)

NOSE

1)

2)

3)
-

HISTORY:

Facial pain/ pressure
Obstruction/ snoring
Rhinorrhoea
Epistaxis
Itchy/sneezing
Taste/smell dysfunction
Eye symptoms
EXAMINATION:

External abnormality
Anterior rhinoscopy
Septal deviation/ haematoma
Rigid nasendoscopy
Flexible nasendoscopy
INVESTIGATIONS:

RAST (IgE)
Sweat test if appropriate
Photographs (for rhinoplasty)
CT sinues (for sinusitis/ nasal polyps/ orbital cellulitis)
MRI sinus/brain (tumour/ intracranial lesion)

1) RHINITIS

Definition:
Inflammation in the nose and paranasal sinuses with
more than two symptoms:
o Cardinal symptoms
! Nasal congestion
! Nasal discharge
o Other symptoms
! Facial pain
! Facial pressure
! Decreased olfaction
! Endoscopic signs of nasal polyps/mucus & pus
discharged primarily from the sinus
! CT showing mucosal changes within the sinuses

Epidemiology:
Very common presentation to GP
10-25% of certain populations (40% children)
Allergic and infective causes are most common
QoL impairment

Other causes of NASAL CONGESTION:
Child:
o Big adenoids
o Choanal atresia
o Postnasal space tumour
o Foreign body
*Refer urgently if:

Unilateral obstruction

+/- Foul bloody discharge

Adult:
o Deflected nasal septum
o Granuloma (TB/syphilis/granulomatosis
with
polyangiitis/leprosy)
o Topical vasoconstrictors
o Tricyclics
*Refer urgently if:

Unilateral obstruction

Numbness

Tooth loss

Bleeding

1) ALLERGIC RHINITIS

Definition:
Inflammation to the mucosal lining of the nose caused by
inappropriate hypersensitivity reaction to an
aeroallergen

Aetiology:
Seasonal (outdoor allergens)
o Tree pollen
o Grass pollen
o Weed pollen
Perennial (indoor allergens)
o House dust mite faeces
o Pets (dog/ cat/ horse)
o Cockroaches
o Moulds

Symptoms:
Nasal pruritus
Sneezing
Rhinorrhoea
Stuffiness/ nasal congestion
+/- hyposmia, altered taste

Signs:
Swollen turbinates
Mucosa pale or mauve
Nasal polyps

Pathophysiology:
IgE mediated inflammation to nasal mucosa from allergen
exposure, causing inflammatory mediator release from
mast cells

Classification:
Intermittent: <4 days a week or <4weeks
Persistent: >4 days a week or >4 weeks
If mild, none of the below, but if moderate-severe, more
than one of:
o Sleep disturbance
o Impaire work of school
o Impaired daily activities
o Troublesome symptoms

Investigations:
Skin prick test: look for wheal
Radio-allergoabsorbent test (RAST), if skin prick test C/I:
measures antigen specific IgE
Intradermal testing

Management:
Nasal saline irrigation
Nasal steroids (beclomethasone)
Antihistamines (loratadine)
Systemic decongestants (pseudoephedrine) *C/I in: HTN/
hyperthyroidism/ heart disease/ MAOI use
Anti-leukotriene agents (zafirlukast)
Immunotherapy *when medical treatment fails

2) NON-ALLERGIC RHINITIS

Definition:
Rhinitis in the absence of an identifiable allergy,
structural abnormality or sinus disease

Occupational rhinitis:
Aetiology:
o
Cigarette smoke
o
Chemicals/solvents
o
Metal salts
o
Latex
o
Glues
o
Wood dusts

Medication induced rhinitis:

Aetiology:

Rhinitis Medicamentosa:
Definition:
o A condition of rebound nasal congestion brought on
by extended use of topical decongestant (e.g.
phenylephrine) & certain oral medications (e.g.
sympathomimetic amines) that constrict blood
vessels in the lining of the nose
Pathophysiology:
o Nasal mucosa innervated by sympathetics mainly
o NA stimulates Alpha 1 and 2 leading to
vasoconstriction
o Sympathomimetics produce vasoconstriction by
endogenous release of NA
o Prolonged use will lead to reduced presynaptic NA
which in turn reduces alpha receptor sensitivity
Treatment:
o Dont take the meds longer than recommended
o Gradual stopping of decongestant (introduce
corticosteroid spray)
o Warn of temporary worsening of symptoms!

Non-allergic rhinitis with eosinophilia syndrome (NARES):
Definition:
o A condition comprising of symptoms consistent with
allergic rhinitis in which an absence of allergy has
been demonstrated by allergen skin testing, and
nasal cytology analysis demonstrates >25%
eosinophils
Associated with Samters triad:
o Asthma
o Aspirin and NSAID sensitivity
o Nasal/ethmoidal polyposis

Hormonal:
Aetiology:
o Pregnancy
o Puberty
o Menstruation
o ? Hypothyroidism

Vasomotor rhinitis (Idiopathic rhinitis)
A diagnosis of exclusion! Exclude:
o Positive allergy test
o Smoking
o Nasal polyps
o Pregnancy
o Medications affecting nasal functions
o Beneficial effects of nasal corticosteroid sprays
Consider also:
o Structural abnormalities
o Immunologic conditions
Wegeners granulomatosis
Sarcoidosis
Polychondritis
Rheumatoid arthritis
o Infections (bacterial (TB)/HIV)
o Foreign body
o CSF (after head injury, + glucose)
o Cystic fibrosis
o Kartageners syndrome

2) SINUSITIS

Definition:
Infection/inflammation of the nasal cavity and paranasal
sinuses

Differential diagnosis:
Migraine
TMJ dysfunction
Neuralgia
Cervical spine disease
Temporal arteritis
Herpes zoster

Anatomy:
4 sinuses: maxillary, frontal, ethmoid and sphenoid
Drain into the nasal cavity (lateral to the middle
turbinate)
Lined by respiratory mucosa, with goblet cells and cilia
Osteomeatal complex (OMC) obstruction is critical in the
development of sinusitis

Classification:
Acute: <4 weeks
Subacute: 4-12 weeks
Chronic: >12 weeks

Signs & symptoms:
Major:
o Facial pain /pressure
Maxillary: at cheek or teeth
Ethmoidal: between eyes
Worse on bending
*Percussion tenderness
o Nasal obstruction/congestion
o Purulent rhinorrhea/post nasal drip
Minor:
o Halitosis
o Ear pain / pressure / fullness
o Anosmia/hyposmia
o Headache
o Fever

Viral sinusitis:
How to recognise:
o < 10 days post URTI
Pathophysiology:
o Virus causes mucosal oedema & decreased ciliary
action, leading to mucous retention and secondary
bacterial infection

Bacterial sinusitis:
How to recognise:
o >10 days post URTI
o Responds to antibiotics
Aetiology:
o Direct spread (dental root infection/swimming in
infected water)
o Odd anatomy (septal deviation/large ethmoidal
bulla/ polyps/ large uncinate process)
o ITU causes (mechanical ventilation/ recumbency/
use of nasogastric tube)
o Systemic causes (Kartageners/ immunodeficiency)
o Biofilms
Organisms:
o Staph aureus
o Pseudomonas
o Strep pneumonia
o Haemophilus influenza
o Moraxella catarrhalis
o Fungi

Investigations:
CT
o Excellent visualisation
o Consider for complicated acute sinusitis or chronic
sinusitis preoperatively
MRI
o Rule out intracranial complication
Plain x-ray/USS are useless!

Management:
Analgesia (if painful)
Antipyretic (if feverish)
Decongestants (Antihistamines are NOT routinely used as
they may thicken secretion & complicate drainage))
Nasal saline irrigation
Antibiotics (amoxicillin/co-amoxiclav)

Complications:
Acute local:
o Frontal (subperiosteal abscess)
o Ethmoidal (orbital cellulitis/abscess/cavernous
sinus thrombosis)
o Maxillary (swollen cheek)
o Sphenoidal (cavernous sinus thrombosis)
Acute distal:
o Intracranial (meningitis/ extradural or subdural
abscess/ intracerebral abscess)
o Septicemia
o Toxic shock syndrome
Chronic:
o Mucocoele (chronic slowly expanding lesions of the
sinuses that may erode bone)
o Dental problems
Orbital:
o Orbital cellulitis *below

ORBITAL CELLULITIS *A medical emergency!

Pathophysiology:
o Lamina papyracea (paper thin bone) separates the
ethmoid sinus from the orbit, allowing pus to track
through it, causing:
Proptosis (exophthalmos)
Chemosis
Periorbital oedema/ abscess
Raised IOP leading to ischaemia of the optic
nerve (colour vision goes first)
Management:
o Urgent ophthalmology and E NT opinion
o CT sinus
o MRI brain (if concerned about intracranial
collection)
o Broad spectrum antibiotics IV (e.g. cephalosporin,
metronidazole
o Topical decongestants (e.g. otrivine)
o Surgical:
Aim to drain pus and ventilate sinuses
Internal (endoscopic) or external approach

3) NASAL POLYPS

Definition:
Polypoidal mass arising from the mucous membrane of
the nose and paranasal sinuses

Associations:
Asthma
Cystic fibrosis
Allergic rhinitis
Rhinosinusitis
Aspirin sensitivity
Primary ciliary dyskinesia

Typical patient:
Male >40 y/o

Sites:
Middle turbinates
Middle meatus
Ethmoids
Maxillary (If the polyp here prolapses and fills in
nasopharynx, it is called: antrochoanal polyps)
*Refer urgently if: Polyp causing unilateral obstruction
(esp with pain or bleeding), and do biopsy! (Look at the
ddx below)

Differential diagnosis:
Juvenile nasopharyngeal angiofibroma
Nasopharyngeal carcinoma
Lymphoma
Inverting papilloma
Glioma
Neuroblastoma
Encephalocoele

Symptoms: *depends on size of polyps
Nasal obstruction
Anosmia
Facial pain/ pressure
Rhinorrhoea
Snoring

Signs: *upon anterior rhinoscopy/rigid nasendoscopy
Pale
Mobile
Insensitive to gentle palpation

Investigations:
Allergy testing
Sweat test (Polyp in a child have to outrule CF)
RAST (IgE)
CT (Before the surgery)
MRI (If concerned about intracranial lesion extending into
the nose)

Management:
Corticosteroids
o Nasal drops (betamethasone)
o Nasal sprays (beclomethasone)
o Oral medication (presdnisolone)
Surgical (If failed medical management)
o Endoscopic sinus surgery
o Risks:
! Bleeding (anterior ethmoid)
! Infection
! Orbital injury (medial rectus, globe, optic
nerve)
! Intracranial injury (CSF leak)
o Post-op:
! Watch for bleeding
! Beclomethasone drops
! 0.9% saline douched/sniffed to relieve
crusting

4) NASAL OBSTRUCTION

Aetiology:
Anatomical
o Adenoid hypertrophy
o Septal deviation/ haematoma/ perforation
o Turbinate hypertrophy
o Choanal atresia
Mucosal
o Allergic rhinitis
o Non-allergic rhinitis
o Sinusitis
o Rhinitis medicamentosa
o Nasal polyps
o Neoplasms


CHOANAL ATRESIA

Definition:
o A congenital disorder where the back of the nasal
passage (choana) is blocked, usually by abnormal
bony or soft tissue due to failed recanalization of
the nasal fossae during fetal development
Presentation:
o Unilateral
Usually not detected until much later in life
because baby manages to get along with only
one nostril available for breathing
o Bilateral
Life-threatening
Neonates are obligate nasal breathers (they
mainly use their nose to breathe)
Management (of bilateral choanal atresia)
o Airway maintenance
o Nutrition (orogastric tube f eeding)
o Associated anomalies (ECG, renal USS)
o Surgery (endoscopic/transpalatal approach)
Associated conditions (CHARGE syndrome):
o Coloboma
o Heart defects
o Atresia of the choanae
o Retarded growth or development
o Genitourinary abnormalities
o Ear abnormalities

Management:
Refer to ENT OPD 7 days post trauma
Reduce nasal bones if displaced (LA/GA) within 2 weeks
post trauma as complete settling occurs at 3 weeks
*Refer urgently if:
Septal haematoma
Anterior ethmoidal artery bleed

SEPTAL HAEMATOMA

Definition:
o Blood collection between cartilage and
perichondrium and may form abscess (Mid-face is
danger area as it has valve-less veins
communicating intracranially)
Presentation:
o Soft, fluctuant & tender on palpation
Treatment:
o Drainage and packing
o Antibiotics (to prevent septal abscess)
Complications:
o Septal perforation
o Nasal collapse

SEPTAL PERFORATION

Aetiology:
o Post septal surgery
o Trauma
o Nose picking
o Body piercings
o Nasal prongs (O2 delivery)
o Sniffing chrome salts/cocaine
o Malignancies (e.g. BCC)
o Nasal steroid/decongestant spray
o Chronic mucosal inflammation/granuloma
Presentation:
o Irritates
o Whistles
o Crusts
o Bleeds
Treatment:
o Rhinoplasty (as closure is usually hard)
o Saline douche (for crust)
o Silastic buttons to occlude the hole

5) NASAL TRAUMA

Considerations:
Nasal bones
Nasal septum
Facial bones

Examination:
GCS
Vital signs
Inspect
o Anterior rhinoscopy (for septal deviation/ abscess)
o Eye movements
Palpate
o Nasal bones
o Facial bones

Complications:
Cosmetic concerns
Functional concerns
Epistaxis
Septal haematoma/ abscess
Head injury/ LOC
Trapped inferior rectus muscle

CSF RHINORRHOEA

Pathophysiology:
o Ethmoid fractures disrupting dura and arachnoid
can result in CSF leaks
o If not associated with trauma, ask if its a tumour
Investigations:
o Lab glucose (+ for glucose)
o Immunoelectrophoresis (B tau transferrin)
Management:
o Lumbar drain
o Bedrest
o Surgery often not needed
o Antibiotics (for traumatic leaks)

6) EPISTAXIS (NOSEBLEED)

History:
How long?
How much blood? (Quantity)
Ear/ nose/ throat symptoms?
Risk factors?
o Anticoagulation (warfarin/ aspirin/ Plavix)
o Hypertension
o Trauma
o Neoplasia
! Benign (e.g. angiofibroma)
! Malignant (e.g. SCC)
o Thrombocytopenia
o Dyscrasia/ haemophilia

Anatomy:
Blood supply to the nose
o Sphenopalatine artery (80%)
o Anterior ethmoid artery (10%)
o Posterior ethmoid artery (5%)
Kiesselbachs plexus (Littles area)
o Arterial anastomosis
o Source of most bleeding!

Surgery:
o SPA ligation (through the nose)
o AEA ligation (facial incision)
o IMA ligation (through maxillary sinus)
o ECA ligation (identify two branches first)
Radiological embolization:
o Can be lifesaving for bleeding not responding to
surgical measures, but can cause stroke!

JUVENILE NASAL ANGIOFIBROMAS

Epidemiology:
o Young adolescent males
Presentation:
o Recurring epistaxis
o Nasal obstruction
Investigation:
o Rigid nasendoscopy (To see mass in nose)
Management:
o Surgical incision

MANAGEMENT

First Aid:
Pinch nose (Littles area) for 15 minutes
Head forward (dont swallow blood)
Ice pack to the nape of the neck

Hospital:
Resus: ABC
o Wide bore IV access
o Bloods/ group and hold
o Fluids
o Control BP (? Address anti-coagulant effects)

Examination:
Anterior rhinoscopy (? Anterior bleed)
Oral cavity (? Posterior bleed)
Otoscopy (? OME indicating nasopharyngeal mass)
Head and neck (? Metastatic neck node)
Nasendoscopy (? Source, tumour)

Managing the epistaxis
Topical lignocaine/adrenaline
Silver nitrate (AgNO3) cautery to Littles area
Nasal packing
o Merocel tampon
o BIPP (bismuth iodoform paraffin paste)
o Posterior balloon (if posterior bleed)
* Packing a nose:
Go PARALLEL to the palate, NOT up towards the
brain!
Pack BIPP in layers standing along the floor of
the nasal cavity
Same as for passing an NG tube

THROAT

1)

2)
-

3)

HISTORY:

Sore throat
Hoarseness
Dysphagia/ odynophagia
Stridor
Haemoptysis/ hematemesis
Cough
Oral ulceration
Neck lump
EXAMINATION:

Entire oral cavity
o Lips
o Buccal mucosa
o Gingivo-alveolar sulcus
o Dentition
o Tongue
o Floor of mouth
o Palate
o Uvula
o Tonsils
Waldeyers ring of lymphoid tissue
o Pharyngeal tonsils (Adenoids) - Top
o Palatine tonsils Sides
o Lingual tonsils - Bottom
Ulcer?/ Mass?
Palpate (bimanual for submandibular gland and parotid)
Lymph nodes
o Submental
o Submandibular
o Jugulo-digastric
o Anterior/ posterior cervical
o Pre- post auricular
o Posterior triangle
o Supraclavicular
INVESTIGATIONS:

RAST (IgE)
Sweat test if appropriate
Photographs (for rhinoplasty)
CT sinues (for sinusitis/ nasal polyps/ orbital cellulitis)
MRI sinus/brain (tumour/ intracranial lesion)

1) TONSILS & ADENOIDS

1) OBSTRUCTIVE SLEEP APNOEA (OSA)

Definition:
Apnoea = Cessation of airflow for 10 seconds
Hypopnoea = Continued breathing over 10 seconds but
ventilation reduced by 50% during sleep

Apnoea Hypopnoea Index (AHI):
Number of events of apnoea and hypopnoea per hour
Severity of OSA
o Mild: 5-14
o Moderate: 15-30
o Severe: >30

Complications:
Hypertension
CCF/Cor Pulmonale
Cardiac arrhythmias
Myocardial infarction
CVA
Diabetes
Depression
Road Traffic Accidents!!

Aetiology:
Central
o The nervous system fails to adequately control
breathing, thus leading to irregular sleep patterns
and decreased oxygen levels
Peripheral
o Negative thoracic pressure during inspiration causes
collapse of upper airway structures leading to
decreased oxygen levels
















Presentation:
Excessive daytime sleepiness
Impaired concentration
Snoring
Choking episodes during sleep
Witnessed apnoea
Restless sleep
Nocturia
Reduced libido

Examination:
BMI
Neck circumference
Nasal obstruction
Small jaw
Large tongue
Large tonsils/ adenoids
Craniofacial abnormalities

Investigations:
CXR (cardiomegaly)
ECH (arrythmias)
Polysomnography

Management:
Behavioral
o Weight loss
o Stop smoking
o Reduce alcohol
Non-surgical
o CPAP
Surgical
o Adenotonsillectomy (cures 90% children)
o Nasal surgery
o Uvulopalatopharyngoplasty (UPPP)
o Tracheostomy

2) TONSILLITIS

Definition:
Infection of palatine tonsils (but may involve adenoids
and lingual tonsils) +/- preceding URTI

Presentation:
Sore throat
Lymphadenopathy

Organisms:
Viral
Bacterial
o Group A or B Strep
o Strep viridans
o Staph aureus
o Haemophilus influenza
o Strep pneumonia
o Moraxella catarrhalis
o E. Coli

Differential diagnosis:
Epstein Barr virus
Agranulocytosis
Leukaemia
Scarlett fever, diphtheria

Management:
Swab (OHCS mentions that swabbing is irrelevant and can
lead to overdiagnosis)
Analgesia
o Paracetamol
o Ibuprofen
o Diclofenac if severe
Antibiotics
o Benzylpenicillin
o Amoxicillin*
o Coamoxyclavulinic acid*
o Erythromycin
*Not in mononucleosis
Hospital referral if
o Not eating/ drinking
o Airway concerns
o Peritonsillar abscess (Quinsy)
Tonsillectomy if recurrent problem

3) PERITONSILLAR ABSCESS (QUINSY)

Definition:
Tonsillitis that suppurates (collection of pus that forms
around the tonsil)
If untreated, can spread through neck fascia, causing
airway obstruction and aspiration of pus

Presentation:
Trismus (unable to open mouth completely)
Severe sore throat
Hot potato voice (muffled voice)

Examination:
Swelling of soft palate around tonsil
Uvular deviation
Tender cervical lymphadenopathy

Management:
Analgesia
Antibiotics
Fluids
Aspiration and drainage under LA (Be careful as the
carotid artery is nearby)

4) MONONUCLEOSIS (GLANDULAR FEVER)

Epidemiology and Aetiology:
Young adults
Epstein Barr virus

Presentation:
Sore throat
Generalised malaise
Altered voice

Examination:
Membranous tonsillitis
Extensive lymphadenopathy
Hepatosplenomegaly

Investigations:
FBC
Monospot (heterophil) test
LFT

Management:
Benzyl penicillin +/- metronidazole
AVOID ampicillin/ amoxicillin antibiotics (leads to diffuse
non-allergic rash)
Paracetamol (if LFTs are normal

TONSILLECTOMY

Indications:
o Absolute
OSA
Malignancy
o Relative
Tonsillitis (5 or more episodes per year, for at
least 2 years)
Quinsy (2 episodes)
Snoring
Halitosis (food debris collecting within the
crypts of the tonsils)
Post transplant lymphoproliferative disorder
Complications:
o Bleeding
Reactionary (if clot displaced/ligature slipped)
Primary (within the first 24 hours)
Secondary (after the first 24 hours)
o Pain (adults > kids)
NSAIDS, PCM, +/- codeine
o Pulmonary oedema (tonsillectomy f or OSA)
o Regrowth of lymphoid tissue
o Death (1 in 20000)
Management (of post tonsillectomy haemorrhage):
o ABC
o IV access
o Bloods including GXM (cross matching)
o Resuscitate with f luids (+/- bloods)
o Cauterise tonsil f ossa if possible
o Cauterise under GA otherwise
o IV antibiotics: Co-amoxiclav (if pyrexic/
neutrophilic/ elevated CRP)
Blood volume recap
o 1-6 years: 80 mls/kg
o 10 years: 75 mls/kg
o Adult: 70 mls/kg
*So for a 20 kg 4 year old who bleeds, his total blood
volume is approximately 1.6 litres

3) DEEP NECK SPACE INFECTIONS

4) UPPER AERODIGESTIVE TRACT

CONDITIONS

Key Points:
Infection within the head and neck may suppurate
Pus can track along defined planes (between fascial
sheaths)
Some planes extend down to diaphragm (danger space)
Swelling: airway compromise possible
Involvement of vessels: septic emboli

Presentation:
Sore throat
Dysphagia / odynophagia
Neck pain / swelling
Otalgia (referred pain)
Respiratory distress / voice change
Fever / reduced PO intake / malaise (paediatric)

Signs:
Trismus
Stridor / obstructive breathing
Reduced range of neck movement / torticollis
Neck mass (red, fluctuant, tender, hot)

Aetiology:
Pharyngitis / tonsillitis
Odontogenic infection
Suppurative lymph node (esp. paeds)
IVDU (Intravenous drug user)
Trauma
Sialoadenitis
Microorganisms (Strep/ Staph/ Klebsiella/ Neisseria/
Bacteroides

Management:
ABC
Secure airway if necessary (tracheostomy)
CT
IV antibiotics (augmentin / clindamycin)
Incision and drainage of pus (transoral or external)

Complications:
Airway obstruction
Aspiration of pus
Sepsis
Mediastinitis (from retropharyngeal and danger spaces)
Carotid artery rupture

1) PHARYNGEAL POUCH (ZENKERS DIVERTICULUM)

Presentation:
Dysphagia with gurgling
Regurgitation
Choking on swallowing
Halitosis

Investigations:
Barium swallow
Endoscopy (can cause perforation when a pouch is
unsuspected)

Management:
Endoscopic stapling of pouch
o
15-20 minutes
o
Minimal morbidity
o
Can be repeated
External division of pouch (Cricopharyngeal myotomy/
Transcervical diverticulectomy)
o
2-3 hours
o
Significant morbidity
o
Not undertaken as often as stapling
o
Risk of mediastinitis

2) FOREIGN BODIES (RESPIRATORY TRACT)

Epidemiology:
Peak incidence: 1-3 years
Most common cause of accidental death at home
Peanuts most common
Delays in diagnosis is common

Types of foreign body:
Inorganic FB
o Usually plastic/ metals
o Examples: Small parts from toys/ beads etc
o Little reaction
o Obstructive only
o However, button batteries are corrosive!
Organic FB
o Examples: Food/ rubber/ wood/ sponge
o Can induce marked inflammatory reaction
o Granulations
o Abscess
o Haemoptysis

Presentation:
Silent period (delay)
Choking
Coughing (paroxysmal)
Wheezing
Pyrexia
o Unexplained
o Persistent
o Lobar pneumonia

Examination:
Reduced air entry (may be unilateral)
Atypical BS (audible click/ fluttering)
Wheeze (may be unilateral)
Atelectasis of lung & midline shift of mediastinum

Management:
Airway assessment
Microlaryngoscopy &Bronchoscopy
Surgical airway (emergency only, and its rare!)
o Cricothyroudotomy
o Tracheostomy

3) FOREIGN BODIES (OESOPHAGEAL)

Common FB:
Meat bolus
Coins
Bones
Batteries (corrosive!)
o Risk of oesophageal perforation
! Mediastinitis >50% mortality

Management:
Soft food bolus
o Try muscle relaxant
o Buscopan IM
o Endoscopy
Bone/ battery
o Urgent oesophagoscopy (rigid/ flexible)

4) ANGIOEDEMA

Pathophysiology:
Inflammation of venules in layers below the dermis
Vascular leakage mediated by histamine, serotonin &
kinins

Classification:
Allergy (shellfish/ nuts/ animal dander)
Drugs (contrast/ opiates/ ACE-I/ aspirin/ NSAIDS)
Hereditary (C1 esterase deficient or dysfunctional)

Treatment:
Dexamethasone IC (8mg)
Piriton IV
SC adrenaline may be necessary
Anaesthetic intubation
Tracheostomy if airway occluded

5) LARYNGEAL PAPILLOMATOSIS

Aetiology:
Benign tumours form on the larynx
Caused by HPV 6& 11
Commonly found in children
o Direct transmission during vaginal delivery
o C-secs in mothers with genital warts

Presentation:
Adults:
o Hoarseness
o Strained/breathy voice
o Breathing difficulties more common in children
Babies and small children:
o Weak cry
o Trouble swallowing
o Noisy breathing (may be a stridor)
o Chronic cough

Management:
Surgical debulking
Intralesional cidofovir

Prognosis:
Most resolve with repeated surgery
Can be fatal if disseminates to lungs

VOCAL CORD LESIONS

Benign:
o Papilloma (90%)/ Polyps/ Reinkes oedema/
Adenoma/ Chondroma/ Hemangioma/ Lipoma/
Neurofibroma
Malignant:
o SCC (90%)/ Adenocarcinoma/ Adenoid cystic/
Muco-epidermoid

5) UPPER AIRWAY OBSTRUCTION

1) STRIDOR

Definition:
Turbulent air flow through a narrowed airway
(supraglottis/ glottis/ subglottis/ trachea)
Differentiate from STERTO = Low pitched snoring noise,
generated at nasopharynx, oropharynx

Classification:
Inspiratory: supraglottic
Expiratory: trachea
Biphasic: glottis/ subglottic

History (Paediatric):
Onset/ duration
Pallor/cyanosis
Impact of position and feeding
Abnormal cry/ voice
Feeding difficulty/ failure to thrive
Perinatal hx (NICU/ traumatic birth)
Developmental hx

Examination (Paediatric):
Vitals (sepsis?)
Altered level of consciousness
Accessory muscle use
Nasal flaring
Tracheal tug
Drooling
Altered cry or speech
Cutaneous haemangioma at beard area (capable of
growing into the airway)
Neck mass
Auscultation of neck and chest

Aetiology (Paediatric):
Congenital (laryngomalacia/ web stenosis/ vascular
rings)
Inflammation
(laryngitis/
epiglottitis/
laryngotracheobronchitis/ anaphylaxis)
Tumours (haemangiomas/ papillomas)
Trauma (thermal/ chemical/ intubation)
Misc (airway/ oesophageal foreign body/ vocal cord
prolapse)

2) CROUP (LARYNGOTRACHEOBRONCHITIS)

Definition:
Infection of the upper airway, generally in children, which
obstructs breathing and causes characteristic barking
cough

Epidemiology:
Winter months
Parainfluenza virus (95%)
Peak 6-18 months old

Presentation:
Gradual onset hoarseness
Barking cough
Biphasic stridor
Fever
+/- Cyanosis
CXR may show steeple sign of tapering trachea

Management:
May require admission
Humidification
Oxygen
Steroids
Nebulised adrenaline
Intubate if deteriorate

3) RETROPHARYNGEAL ABSCESS

Definition:
Lymph nodes suppurate in the retropharynx

Epidemiology:
Rare
Typical patient: child (1-3 years)

Presentation:
Stiff, extended neck/ torticollis
Fails to eat or drink

Investigation:
CT (diagnostic)
Lateral neck x-ray (soft tissue swelling)

Management:
IV antibiotics
Surgical drainage (under GA and head down to prevent
aspiration)

4) EPIGLOTTITIS

Definition:
Infection of the epiglottitis and/ or supraglottic structures
with potential for airway obstruction

Epidemiology:
Rarer than croup but high mortality (Its an emergency as
respiratory arrest can occur)

Organisms:
Haemophilus influenza
Strep pyogenes

Presentation:
History is often short
Septicemia is rapid
Cough is ABSENT
Others:
o Sore throat
o Fever
o Dyspnoea
o Voice change
o Dysphagia
o Tender anterior neck +/- cellulitis
o Hoarseness
o Pharyngitis
o Anterior neck nodes
o Drooling (head forward, tongue out)
o Prefers to sit

Management:
Take to ITU
Minimal handling- dont examine throat! (May cause
respiratory arrest)
Caution with:
o Fibreoptic examination
o Throat swab
o Radiology
Anaesthetic and ENT opinion
Secure airway in a controlled manner
Treat with IV (e.g. ceftriaxone, analgesia)
May require tracheostomy

Differential diagnosis:
Laryngomalacia
Subglottic stenosis
Vocal cord palsy
Laryngeal papilloma

5) LARYNGOMALACIA

Definition:
A main congenital anomaly of the larynx (60%) appearing
within hours of birth (or up to a few months)

Pathophysiology:
Soft laryngeal cartilages prolapse into airway on
inspiration

Presentation:
Stridor
o Onset after 6 weeks
o More noticeable in certain positions, sleep, or if
excited/ upset
+/- Cyanosis
+/- Feeding difficulties

Management:
Usually observe + reflux medications (in 85%, no
treatment is needed and symptoms usually improve by 2
years old)
Aryepiglottoplasty/pexy (if failure to thrive)

6) SUBGLOTTIC STENOSIS (SGS)

Definition:
Narrowing of the subglottic airway

Types:
Congenital (if there is problems in the formation of the
cartilage ring that make up the trachea)
Acquired (post intubation/ gastro-oesophageal reflux)

Presentation:
Stridor
Dyspnoea
Difficulty feeding
Failure to thrive
Recurrent episodes of croup

Management:
Dilatation
Laser division
Cricoid split/ laryngotracheal reconstruction
May need tracheostomy to secure airway at least
temporarily

7) LARYNGEAL PARALYSIS

Epidemiology:
10% of all laryngeal lesions

Aetiology:
Cardiovascular anomalies (including PDA ligation)
Birth trauma
Neurological (e.g. Arnold Chiari malformation)
Idiopathic

Presentation/ Management:
Unilateral
o May manifest during the 1st few weeks of life with
hoarse, breathy cry aggravated by agitation, feeding
difficulties +/- aspiration
o Supportive (most recover by 2-3 years)
Bilateral
o Inspiratory stridor at rest that worsens upon
agitation +/- significant respiratory distress
o May need urgent airway intervention (intubation,
tracheotomy) +/- surgery

6) HOARSENESS (DYSPHONIA)
ACUTE AIRWAY OBSTRUCTION MANAGEMENT IN
ADULTS

Sit patient up
Oxygen
IV steroids
Nebulised adrenaline
Note O2 sats, RR, pulse, BP
Call anaesthetist, E NT doctor
If no relief, obtain an emergency airway
o Cricothyroidotomy
Good quick access
Neck extended
Midline through cricothyroid membrane
Kits available
Limitations for long term use
o Tracheostomy
Airway obstruction
Pulmonary toilet
Prolonged intubation
Part of a head and neck procedure
If the tube comes out
Anaesthesia to reintubate
Reintroduce the trachea (Stay sutures)
Cricothyroidotomy
Take brief hx from relatives, keeping in view common
causes of stridor
o Inflammatory
o Infective
o Neoplastic
o Autoimmune
o Anaphylactic
Do ABG if possible without causing delay or stress
When stridor improves, do a flexible nasendoscopy
(ENT doctor) to visualise the airway to get an idea of
the cause of the stridor
Get AP + lateral x -rays of neck and chest

WHY IS THIS CHILD DROOLING?

<3 y/o: Teething
Decreased cerebral control of oral function
Hypersalivation
Obstruction to swallowing
Angioedema/ anaphylaxis
Rabies
Epiglottitis
Neurodisability decreased oromotor function
(CP/bulbar palsy)
Muscle problems (oesophageal dysmotility/
cricopharyngeal achalasia)
Ingestion of foreign body, heavy metals, lithium or
caustic substances
Head and neck trauma to swallowing strictures
Enlarged tonsils or adenoids +/- nasal polyps/
rhinosinusitis/ severe tonsillitis
Congenital lesions/ nasal masses (e.g. encephalocoele/
glioma)

Definition:
Difficulty producing sound with change in voice pitch or
quality (breathy, scratchy, husky)

History (Ask about):
Gastro-oesophageal reflux (GORD)
Dysphagia
Smoking (Hoarseness lasting >3 weeks in smoker, suspect
larygngeal carcinoma- may be the only presentation!)
Stress
Singing/ shouting

1) REFLUX LARYNGITIS

Definition:
Chronic laryngeal sign associated with GORD

Management:
PPI (BDS) for 2-4 months
+/- Surgical fundoplication

2) LARYNGITIS

Definition:
Inflammation of the larynx
Usually viral and self-limiting, but there may be
secondary infection with streps or staphs
Can be secondary to GORD or autoimmune disease

Presentation:
Pain (hypopharyngeal/ dysphagia/ pain on phonation)
Hoarseness
Fever

Management:
Supportive
If necessary, give penicillin (PO) for 1 week
Steam inhalation may help

3) REINKES OEDEMA

Definition:
The swelling of the vocal cords due to oedema

Aetiology:
Smoking
GORD
Hormonal changes (hypothyroidism)
Chronic voice abuse

Management:
Laser therapy (if conservative management fails)

4) SINGERS NODULE

Definition:
Fibrous nodules (often bilateral) at the junction of the
anterior 1/3rd and posterior 2/3rd of the cords caused by
vocal abuse
The junction is the middle of the membranous vocal folds
(the posterior portion of the vocal fold is cartilage) and it
may receive most contact injury during speech

Presentation:
Hoarseness
Painful phonation
Frequent vocal breaks
Reduced vocal range

Management:
Speech therapy (if used early)
Excision

5) LARYNGEAL NERVE PALSY

Anatomy/ pathophysiology:
The recurrent laryngeal nerve supplies the intrinsic
muscles of the larynx (apart from the cricothyroideus,
external branch of the superior laryngeal nerve)
It is responsible for the abduction and adduction of the
vocal cord
It originates from the vagus nerve. It runs
o Left under the ligamentum arteriosum
o Right under the subclavian artery
o Turns back in a cephalic direction to run in the
trachea-oesophageal groove
In its passage between the cricoid and thyroid cartilages,
it is vulnerable to compression from the cuff on an
overinflated ET tube

Presentation:
Hoarseness with a breathy voice & weak cough
Repeated coughing/ aspiration
Exertional dyspnoea

Causes:
Cancer (30%)
o Laryngeal
o Thyroid (Reversible in 35%)
o Oesophageal
o Hypopharynx
o Bronchus
o Malignant node
Iatrogenic (25%), usually after
o Parathyroidectomy
o Oesophageal surgery
o Pharyngeal pouch surgery
Others:
o CNS disease (polio/ syringomelia)
o TB
o Aortic aneurysm
o Idiopathic (e.g. neurotropic virus)

Investigations:
CXR
Barium swallow
MRI
Panendoscopy

Management:
The nerve may recover on its own
Voice therapy may be useful
If surgery is needed, the goal is to change the position of
the paralyzed vocal cord to improve the voice, which can
be done through
o Arytenoid adduction (stitches to move the vocal cord
towards the middle of the airway)
o Injections of collagen, Gelform, or another substance
o Thyroplasty
If both the left and right nerves are damaged, a
tracheotomy may be needed to allow breathing, followed
by another surgery later

6) OTHERS

*OHCS Pg 568
Functional disorders of speech articulation
Spasmodic dysphonia

DIFFERENTIAL DIAGNOSIS OF HOARSENESS

Consider generalised infiltrating entities:
Hyperkeratosis (smoking/ alcohol abuse/ pollution)
Leukoplakia
Granulomata
Papilloma
Polyps
Cysts

Less common causes:
Intrinsic (decreased lubrication/ laryngocoele/
Wegeners granulomatosis/ sarcoidosis/ TB/ syphilis)
Extrinsic (goitre/ carotid body tumours)
Neoplasia (Pancoast/ larynx or thymus cancer/
lymphoma/ glomus tympanicum tumour)
Toxic (vomit/ fumes)
Injury (arytenoid subluxation/ CVP lines)
Bacterial (Epiglottitis/ diphtheria/ abscess/ aortitis)
CNS (vagus lesion/ Gullian-Barre/ MG)
Endocrine (acromegaly/ addisons/ myxodema)

Rarer causes:
Mycotic aneurysm
Subclavian aneurysm
Malformations
Mucormycosis/ fungi in HIV
Mucosal leishmaniasis
Hamartoma/ hemangioma
Angioneurotic oedema
Gouty cricoarytenoiditis
Behcets vasculitis
Chondrosarcoma
Relapsing polychondritis

Emergency presentation:
Epiglottitis
Aortic dissection
Anaphylaxis
Acid/alkali ingestion
Trauma/ foreign body

HOW SHOULD YOU TAKE CARE OF YOUR VOICE?

Dont whisper and dont shout!
Drink plenty of fluids (8 cups/day, but not tea, coffee,
alcohol or cola)
Get plenty of Zzz
Avoid irritants (spicy food/ tobacco/ smoke/ dust/
alcohol/ aspirin gargles)
Avoid eating before sleeping (to prevent indigestion)
Humidify living area
Dont suck on medicated lozenges (numbs the throat
and menthol is drying) *Chew gum instead
Steam inhalations when ill

7) NECK LUMPS

History:
Onset/ duration
Systemic/ local symptoms
Rapid growth (? Malignant)
Maternal hx if infection
Trauma
Radiation (thyroid malignancy)
Family hx of neck masses
Cats, animals at home
Travel
Smoking/ drinking hx

Examination:
Mass
o Site
o Size
o Shape
o Surface
o Edge
o Consistency
o Mobility
o Tenderness
o Skin changes
Full ENT/ Head and Neck examination

Differential diagnosis:
V : Vascular
I
: Inflammatory
T : Traumatic
A : Autoimmune
M : Medication
I
: Infective
N : Neoplastic
C : Congenital

Neck masses more likely to be malignant if:
Supraclavicular/ posterior triangle
Fixed
Increased age
Generalised lymphadenopathy
>3cm in side
Hepatosplenomegaly

Management:
Bloods
o FBC
o ESR
o Rapid strep test
o LDH (lymphoma)
o PPD (mycobacterial lymphadenitis)
o Serology (EBV/ Toxo/ Bartonella/ CMV/ HIV/
Borellia)
CXR (TB)
USS
CT/ MRI
ECG/ ECHO (Kawasaki)

1) PAEDIATRIC NECK LUMPS

Epidemiology:
90% children 4-8 years
Acute usually infective

Differential Diagnosis (Elaboration in OHCS Pg 572):
Congenital:
o Midline
! Thyroglossal duct cyst
! Lymph node
! Thyroid
! Dermoid cyst
! Ranula

Lateral
! Lymph node
! Branchial cyst
! Salivary gland
! Sebaceous cyst
! Hemangioma
! Lymphatic malformation
! Torticollis
Acquired:
o Infective
! Bacterial (strep/ staph/ TB/ Cat scratch/ Lyme
disease/ Toxoplasmosis/ Brucellosis)
! Viral (EBV/ CMV/ Coxsackie/ Adenovirus)
! Fungal (Coccidiomycosis)
o Inflammatory
! Kawasaki/ Langerhans cell/ histiocytosis
o Medications
! Dilantin/ INH/ Immunisations (MMR/DTP)
o Vascular
! Lymphatic malformation/ hemangioma
o

2) ADULT NECK LUMPS

Differential diagnosis:
The ddx mnemonic used for paediatric neck lumps can
also be used for adults
The big difference is that neck lumps in adults are overall
more likely to be neoplastic!
Benign:
o Lipoma
o Sebaceous cyst
o Hemangioma
o Fibroma
Malignant (primary or metastatic):
o Upper aerodigestive tract cancer
o Thyroid cancer
o Salivary gland cancer
o Skin cancer
o Lymphoma

THYROGLOSSAL DUCT CYST

Definition:
A fibrous cyst that forms in the neck from persistence of
the portion of embryonic thyroglossal duct
Most common congenital abnormality of the neck
Classically at or below the hyoid

Presentation:
Moves with tongue protrusion and swallowing
Some may have neck/throat pain/dysphagia

Management:
Sistrunk procedure (Surgical resection of the duct to the
base of the tongue and removal of the central portion of
the hyoid bone)


BRANCHIAL CYST

Definition:
An epithelial cyst arising f rom the lateral part of the
neck from a failure of obliteration of the second
branchial cleft in embryonic development
Divided into 4 types (90% is Type II along the anterior
border of SCM)

Management:
Conservative (no treatment)
Surgical excision

8) HEAD & NECK SQUAMOUS CANCER (HNSCC)

HNSCC in general

Epidemiology:
5-6% of all cancers
Overall 50% 5 year survival

Aetiology:
Alcohol
Smoking/ chewing tobacco
Family hx
HPV 15-60% (oropharyngeal cancer)
Wood dust exposure
Betel nut
Nitrosamines
EBV (nasopharyngeal cancer)
Immunosuppression

Investigations:
Panendoscopy and biopsy
FNA of neck node
Bloods: FBC/ U&E/ LFT/ Albumin/ Ca
CT with contrast (neck and chest)
MRI (neck)
PET scan

Management:
MDT
Surgery
o Remove tumour
o Neck dissection
o Reconstruction
Radiotherapy
o Neck treatment
Chemotherapy
o Cisplatin, 5-FU

Surgical complications:
Breathing
o Stoma
o Tracheostomy tube
Swallowing
o Aspiration
o PEG feeding
Cosmetic deformity
o Scars
o Radiation burns
Speech
o Post-laryngectomy (TOF valve, oesophageal speech,
electrolarynx)
Chyle leak
Fistulae

Radiotherapy complications:
Skin burn
Mucositis
o Dry mouth
o Odynophagia
o Weight loss
Osteroradionecrosis
Carcinogenesis
Secondary tumour
o Leukaemia
Injury to vital structures
o Brain
o Eyes
o Spinal cord

Chemotherapy complications:
Nephrotoxicity
Ototoxicity
Exacerbates the complications of radiotherapy
Cautious use in elderly, frail or very ill

Subdivisions of the head and neck (figure):
Nasopharynx
o Skull base to lower border of soft palate
Oral cavity
o Lips to circumvallate papillae
Oropharynx
o Lower border of soft palate to posterior tip of
epiglottis
o Posterior to circumvallate papillae
Larynx
o Supraglottis
o Glottis
o Subglottis
Hypopharynx
o Piriform fossae
o Post cricoid region
Cervical oesophagus















Lymph nodes levels in the neck (figure):
I
: Midline to posterior digastric
II : Along IJV, skull base to hyoid
III : Along IJV, hyoid to cricoid
IV : Along IJV, cricoid to clavicle
V : Posterior SCM to anterior trapezius
VI : Between medial borders of carotid sheaths

Lymph nodes in the neck:
I
: Submental/ submandibular triangles, nodes
II : Jugulodigastric nodes
III : Nodes around carotid bifurcation
IV : Lower cerivical nodes
V : Supraclavicular and posterior triangle nodes

Importance of lymph node levels in the neck:
Staging of SCC
Metastatic disease
Some tumours present with an enlarged node only

1) NASOPHARYNGEAL CARCINOMA

Epidemiology:
25% of all cancers in China

Aetiology/ Associations:
HLA A2 Allele
EBV
Tobacco, formaldehyde, wood dust exposure
Weaning on to salted fish (nitrosamines)

Staging:
T1: Nasopharynx, oropharynx, nasal cavity
T2: Parapharyngeal extension
T3: Bony structures of skull base/ paranasal sinuses
T4: Intracranial, cranial nerves, hypopharynx, orbit,
infratemporal fossa/ masticator space
N1: Unilateral cervical, unilateral or bilateral
retropharyngeal nodes, above supraclavicular fossa,
6cm in the greatest dimension
N2: Bilateral cervical above supraclavicular fossa 6cm
N3: >6cm / N3b: Supraclavicular fossa

Presentation:
Neck nodes (painless)
Nasal obstruction, bleeding
OME (Conductive deafness as Eustachian tube is affected)
Headaches
Cranial nerve palsies (not I, VII, VII)

Investigations:
Endoscopy/biopsy
PCR (for EBV)
MRI staging

Treatment:
Chemoradiation

2) ORAL CAVITY CANCER

Aetiology/ Associations:
Tobacco
Alcohol
Betel nut chewing
Poor oral hygiene
Irritation by ill-fitting dentures
HPV

Presentation:
Ulcer
Pain
Bleeding
Mass
Neck node
Leukoplakia/erythroplakia (take biopsy)

Treatment:
Surgery:
o Maxillectomy
o Mandibulectomy
o Glosstectomy
o Radical neck dissection
o Mohs surgery
o Combinational (e.g. glossectomy + laryngectomy)
Radiotherapy +/- Chemotherapy

3) OROPHARYNGEAL CARCINOMA

Epidemiology:
Male > Female = 5:1
Typical older patient: Smoker
Typical younger patient: HPV

Presentation:
Sore throat
Voice change
Dysphagia/ odynophagia
Neck lump
Referred otalgia

Treatment:
Surgery:
o Jejunal flaps
o Tubed skin flaps
o Gastric pull ups
o Transoral laser
o Robotic surgery
o Partial laryngeal surgery
Radiotherapy:
o May be 1st line is T1 (<2cm) or T2 (>2cm but <4cm)

4) LARYNGEAL CARCINOMA

Epidemiology:
Typical older patient: Smoker
Typical younger patient: HPV

Sites:
Supraglottic
Glottic (Best prognosis as hoarseness occurs earlier)
Subglottic

Presentation:
Hoarseness (occurs early if glottis tumour)
Stridor
Dysphagia/ odynophagia
Sore throat
Haemoptysis/ haematemesis
Otalgia (if pharynx involved)

Investigations:
Laryngoscopy + biopsy
HPV status
MRI staging

Treatment:
Organ preservation
Chemoradiotherapy
Laryngectomy
Treat the neck

5) HYPOPHARYNGEAL CARCINOMA

Epidemiology:
Rare
Disease of the elderly
Often presents at advanced stage

Aetiology/Associations:
Previous irradiation
Smoking
Alcohol
*However, not as clearly as laryngeal carcinoma

Presentation:
Dysphagia/ odynophagia
Neck nodes
Hoarseness
Stridor
Weight loss

Treatment (similar to laryngeal carcinoma):
Organ preservation
Chemoradiotherapy
Laryngectomy
Treat the neck

9) THYROID

1) GOITRE

Definition:
Generalised enlargement of the thyroid gland

Aetiology:
Sporadic (diffuse/ multinodular)
Physiological (pregnancy)
Autoimmune (Graves/ Hashimotos/ postpartum)
Thyroid cancer
Endemic goitre (iodine deficiency)
Dyshormonogenesis
Drug-induced
Inflammatory (de Quervains Riedels)

Sporadic goitre:
Females > males
Pathogenesis:
o Early: Diffuse hypertrophy of follicular cells with
colloid depletion
o Late: Involution of epithelium with colloid
accumulation
o Focal hyperplasia/ variable involution (+/-
haemorrhage, fibrosis, calcification) resulting in
multinodular goitre (MNG)
o MNG: nodules are demarcated but not encapsulated
o Hyperplastic nodule: adenomatous, not neoplastic

2) ADENOMA

Definition:
Benign neoplasm of follicular cells which is encapsulated
and solitary (it is NOT premalignant and is difficult to
distinguish adenoma from carcinoma on FNA)


3) THYROID NODULES

Epidemiology:
Affects 10% of the population especially:
o Females
o Elderly
o Pregnancy
o 50% are by the age of 50 y/o
Overall:
o 80% benign hyperplastic nodules
o 15% benign adenomas
o 5% carcinoma

Risk factors for MALIGNANT thyroid nodules:
Children
Male
Hx of prior neck irradiation*
Family hx of thyroid cancer*
Clinical features* (rapid growth/ RLN palsy/ fixed)
Solitary
Size > 4cm
Suspicious ultrasound features
Radioactive iodine (RAI) uptake: cold >> hot scans
(functioning or hot nodules are rarely from cancer)
PET scans: FDG avid (FDG is an analogue of glucose, so
anything that is metabolically active will have an uptake)
*Very important questions to ask about in the history!

Investigations:
Bloods: TFT (decreased TSH may indicate toxic nodule)
FNA:
o For all nodules >1 to 1.5 cm
o Can diagnose malignancy
o Cannot differentiate between follicular/ Hurthle cell
adenomas from carcinomas (Thus need thyroid
lobectomy)

Ultrasound (FNA under ultrasound more accurate)

CT
o Retrosternal goitre
o Noncontrast always for thyroid malignancy (iodine
in contrast prevents use of radioactive iodine
treatment as cancer treatment for 3 to 6 months!)
MRI (alternative to CT)

Indications for thyroid surgery:
FNA positive or suspicious for malignancy
FNA inconclusive (follicular adenoma)
High risk (elderly males/ children/ radiotherapy/ family
hx)
Clinical suspicion
Compressive symptoms
Cosmetic concerns
Graves (failed medical treatment/ RAI contraindicated)

4) THYROID CANCER

Epidemiology:
Differentiated (85-90%)
o Papillary carcinoma
o Follicular carcinoma
o Hurthle cell carcinoma
Poorly differentiated (<10%)
Anaplastic
Medullary

DIFFERENTIATED THYROID CANCER

Papillary carcinoma:
80-90% of thyroid cancers
20-40 years
F >> M
Indolent disease
Risk factors (radiation esposure)
Histology (orphan Annie, psammoma bodies)
Often multicentric and bilateral
Lymph node involvement often wont affect prognosis if
age <45 y/o
Good prognosis overall

Follicular carcinoma:
15% of thyroid cancers
Cant diagnose on FNA alone
Usually not multicentric or bilateral
Slightly worse prognosis that papillary

Poor prognostic factors: *(GAMES, AGES or AMES criteria)
Age > 45 years
Male sex
Distant metastases
Size of primary tumour
Extrathyroid extension

Treatment:
Surgery:
o Thyroid lobectomy (low risk patients)
o Total thyroidectomy (higher risk patients)
! Risk of recurrence
! Complications from revision thyroid surgery
! Thyroglobulin as a tumour marker
! RAI use
o Neck dissection
! If pre/paratracheal nodes involved, may require
more extensive neck dissection
Radioactive iodine ablation:
o Used to treat/ diagnose differentiated thyroid cancer
o Smaller dose of radiation
o For high risk patients/ those with local or distant
mets
o Not good for poorly differentiated malignancies

TSH suppression is very important post-op

Thyroglobulin may be monitored
Repeat RAI uptake scan as necessary

POORLY DIFFERENTIATED THYROID CANCER

Malignancy of follicular cell origin
Features between differentiated and anaplastic
carcinoma
Contrast CT and PET best investigations
Not well detected or treated by RAI
Treat with external beam radiotherapy

ANAPLASTIC THYROID CANCER

Poor prognosis (Most die within 6 months)
Stages as T4
Rapid growth, local invasion
Avoid pre-emptive tracheostomy if possible

MEDULLARY THYROID CANCER (MTC)

From parafollicular C-cells
RET proto-oncogene mutation
Sporadic (75%)
Familial (25%): MEN/ non-MEN
MEN IIa
o MTC
o Primary hyperparathyroidism
o Phaeochromocytoma
MEN IIb
o MTC (aggressive)
o Phaeochromocytoma
o Marfanoid features
o Mucosal neuromas
Treatment:
o Genetic analysis
o Urinary/plasma catecholamines
o Calcitonin
o Total thyroidectomy and neck dissection
o Prophylactic thyroidectomy for MEN
! Before 5 years MEN IIa
! Before 5 months MEN IIb

THYROIDECTOMY

Complications:
Scar
Infection
Haematoma*
Hypocalcemia*
Recurrent laryngeal nerve palsy (bilateral if total
thyroidectomy)

Management of haematoma post thyroidectomy:
Presentation:
o Neck swelling
o Airway obstruction
Call f or help (ENT doctor/ anaesthesist)
Management (if the patient cant breathe):
o Open skin clips/ skin sutures
o Open 2-3 layers of sutures which close the subcut
tissues (first layer) and muscles (second layer)
together
o Stay in midline until you reach the clot or see the
trachea, remove the clot
o Bring to theatre (all the above done in ward)

Continued

Management of hypocalcaemia post thyroidectomy:

Presentation:
o Pins/needles
o Muscle cramps
o Arrythmias
Management:
o Check Ca and albumin, ECG
o To calculate corrected Ca:
Ca + {(40-albumin)x0.02}
o If corrected Ca <1.8:
10 mls of 10% Ca gluconate over 10 mins IV
o If corrected Ca > 1.8 but < 2.1:
If symptomatic, 10 mls of 10% Ca gluconate
over 10 mins IV
o If corrected Ca >2.1
No treatment
o If patient is very symptomatic give Ca gluconate
without waiting on the bloods
o Repeat until symptoms abate

10) SALIVARY GLANDS

Major salivary glands:
Parotid
Submandibular
Sublingual

Minor salivary glands situated in:
Oral cavity
Oropharynx
Nasopharynx

Parotid gland:
Serous
Produce 20% saliva
Extent: External auditory canal to angle of mandible
Divided into: superficial and deep lobes
Separated by CNVII (facial)
Tail of gland
Surrounded by fascia capsule
Stensons (parotid) duct pierces buccinators at 2nd molar

Submandibular gland (SMG):
Serous + Mucous
Produce 65-70% saliva (eventhough its smaller than the
parotid!)
Extent: Superior to digastric muscles
Whartons duct
o Exits medial surface
o Between mylohyoid & hyoglossus
o 5 cm in length
o Lingual nerve and CNXII (hypoglossal)

Sublingual gland (SL):
Mucous
Produce 5% saliva
Extent:
Between
mylohyoid
muscle
and
geniohyoid/genioglossus
The ductal system do not have intercalated ducts and
usually do not have striated ducts either so they exit
directly from 8-20 excretory glands

Minor salivary glands:
600-1000
Simple ducts
Buccal, labial, palatal, lingual
Tumour sites: Palate, upper lip, check
Lingual & palatine nerves

Functions of saliva:
Moistens oral mucosa
Moistens & cools food
Medium for dissolved food
Buffer (HCO3)
Digestion (Amylase/ Lipase)
Antibacterial (Lysozyme, IgA, Peroxidase, FLOW)
Mineralization
Protective Pellicle

Important considerations in the examination:
Parotid swelling:
o CNVII document
o Look in the oral cavity (Tonsil displaced medially
from a deep lobe of parotid tumour?_
o Always examine the lymph nodes throughout the
neck

DISORDERS OF SALIVARY GLANDS

1) SIALADENITIS

Definition:
Inflammation of the salivary gland

Organisms
Viral
o Paramyxovirus (mumps)
Bacterial
o Staph aureus
! Acute suppurative parotitis
! Acute sialadenitis

Risk factors:
Dehydration
Diabetes mellitus
Sialolithiasis

Presentation:
Pain/ tenderness
Temperature/ Fever
Facial swelling
Mass

Management:
Medical
o IV antibiotics
o Rehydration
o Analgesics
o Oral hygiene
o Sialogogues
Surgical
o Incision and drainage

2) MUMPS

Definition:
Epidemic parotitis, a viral disease caused by the mumps
virus (paramyxovirus)
2-3 weeks incubation period

Presentation:
Prodrome
o Fever
o Malaise
Painful swelling in one or both glands

Complications:
SNHL
Encephalitis
Sterility

Treatment:
Empirical

Prevention:
Vaccination

CHRONIC INFLAMMATION OF SALIVARY GLANDS

1) SJOGRENS SYNDROME

Definition:
A chronic systemic inflammatory disorder characterized
by lymphocytic infiltrates in exocrine glands

Presentation:
Oral symptoms:
o Dry mouth secondary candidiasis
o Stomatitis
o Glossitis
o Dental caries
Eye symptoms:
o Keratoconjunctivitis sicca
Salivary gland:
o Subjective enlargement 40%
o Clinical enlargement 20%

Findings:
Raised ESR
Rheumatoid factor (75-95%)
Antinuclear factor (68%)
Antithyroglobulin factor
10-20% risk developing non-hodgkins lymphoma

2) SIALOLOTHIASIS

Definition:
Salivary calculi

Common site (Submandibular gland)
Mucoid, thick secretions
Duct orientated superiorly at orifice
Precipitation of salivary minerals
Alteration of salivary components Stasis of salivary flow

Presentation:
Intermittent painful swelling
Associated with eating
+/- Secondary infection

Examination:
Bimanual palpation
Stone visible?
Thick salivary secretions

Investigations:
Radiology (Plain films, CT)
Bloods (Ca2+, PTH)

Management:
Conservative:
o Sialogogues
o Milking
Surgical:
o Dilatation of duct orifice
o Excision of duct papillae
o Exploration of duct and removal of stone
o Excision of gland

SALIVARY GLAND NEOPLASMS

Epidemiology:
Account for only 6% of head and neck cancers
Only 0.3% of all cancers
Proportion of malignant and benign varies with the gland
of origin

Presentation/ What to look out for:
Painless neck mass (parotid/ SMG/SL)
Oral cavity mass (minor salivary gland)
CNVII palsy (more likely malignant)
Pain
Growth rate
Fixation

Examination:
Full ENT/ head and neck examination
Neck nodes present?
Flexible nasopharyngoscopy (very important for minor
salivary gland lesions that may present innocuously, e.g.
globus, throat pain)

Investigations:
Fine needle aspirate:
o Accuracy = 84-97%
o Sensitivity = 54-95%
o Specificity = 86-100%
o Safe, well tolerated
Ultrasound (neck mass)
CT
MRI

BENIGN NEOPLASMS

1) PLEOMORPHIC ADENOMA

Aetiology:
Most common of all salivary gland neoplasms
o 70% of parotid tumours
o 50% of submandibular tumours
o 45% of minor salivary gland tumours
o 6% of sublingual tumours
Age 40-60 y/o
F>M = 3-4:1
Long-term risk of developing SCC!

Presentation:
Slow growing painless mass
o Parotid: 90% in superficial lobe, most in tail of gland
o Minor salivary gland: lateral palate, submucosal
mass

Gross pathology:
Smooth
Well-demarcated
Solid
Cystic changes
Myxoid stroma

Treatment:
Complete surgical excision
Parotidectomy with facial nerve preservation
Submandibular gland excision
Wide local excision of minor salivary gland
Avoid enucleation and tumour spill

2) WARTHINS TUMOUR (PAPILLARY CYSTADENOMA
LYMPHOMATOSUM)

Aetiology:
6-10% of parotid neoplasms
Older, Caucasian, males
10% bilateral or multicentric
3% with associated neoplasms

Presentation:
Slow growing painless mass

Gross pathology:
Encapsulated
Smooth/lobulated surface
Cystic spaces of variable size, with viscous fluid, shaggy
epithelium
Solid areas with white nodules representing lymphoid
follicles

Treatment:
Surgical excision

MALIGNANT NEOPLASMS

1) PLEOMORPHIC ADENOMA

Aetiology:
Most common salivary gland malignancy
5-9% salivary neoplasms
Parotid 45-70% of cases
Palate 18%
Age 30-80 y/o, peak around 50 y/o
F>M

Presentation:
Low-grade: slow growing painless mass
High-grade: rapidly enlarging, +/- pain

Minor salivary glands: may be mistaken for being benign

or inflammatory process:
o Hemangioma
o Papilloma
o Tori

Treatment:
Influenced by site, stage, grade
Stage 1 & II
o Wide local excision
Stage III & IV
o Radical excision
o +/- Neck dissection
o +/- Postoperative radiation therapy

2) ADENOID CYSTIC CARCINOMA

Aetiology:
Overall 2nd most common malignancy
Most common in submandibular, sublingual and minor
salivary glands
M>F

Presentation:
Asymptomatic enlarging mass
Pain, paraesthesia, facial weakness, paralysis

Treatment:
Complete local excision
Tendency for perineural invasion: facial nerve sacrifice
Postoperative radiotherapy

Prognosis:
Local recurrence: 42%
Distant metastasis: lung
Indolent course:
o 5 year survival 75%
o 20 year survival 13%

3) ACINIC CELL CARCINOMA

Aetiology:
2nd most common parotid and paediatric malignancy
5th decade
F>M
Bilateral parotid disease in 3%

Presentation:
Solitary, slow growing, often painless mass

Treatment:
Complete local excision
Postoperative radiotherapy

Prognosis:
5 year survival 82%
10 year survival 68%
25 year survival 50%

4) CARCINOMA (EX: PLEOMORPHIC ADENOMA)

Aetiology:
2-4% of all salivary gland neoplasms
4-6% of mixed tumours
Age 60-80 y/o
Parotid > submandibular > palate
Risk of malignant degeneration:
o 1.5% in first 5 years
o 9.5% after 15 years

Presentation:
Long standing painless mass that undergoes sudden
enlargement

Treatment:
Radical excision
Neck dissection (25% with lymph node involvement at
presentation)
Postoperative XRT

Prognosis:
Dependent upon stage and histology

5) SQUAMOUS CELL CARCINOMA

Aetiology:
1.6% of salivary gland neoplasms
Age 70-80 y/o
M>F = 2:1
Must rule out:
o High-grade mucoepidermoid carcinoma
o Metastatic SCC of intraglandular nodes
o Direct extension of SCC

Treatment:
Radical excision
Neck dissection
Postoperative radiotherapy

Prognosis:
5-year survival 24%
10-year survival 18%
COMPLICATIONS OF SALVARY SURGERY:

Parotidectomy:
o Scar (modified Blair incision)
o Infection
o Haematoma
o Freys syndrome
o Parasthesia of lobule
o CNVII injury (transient up to 15%/ permanent
<1%)
Submandibular gland:
o Scar
o Haematoma
o Infection
o Hypoglossal nerve
o Marginal mandibular nerve
o Lingual nerve

11) THE FACIAL NERVE

Facial nerve distribution:
Motor root:
o Muscles of facial expression
Sensory root:
o External ear
Secremotor:
o Submandibular gland
o Lacrimal gland
Special taste:
o Taste (chorda tympani)

FACIAL NERVE PALSY

Lesion:
Upper motor neuron:
o Upper facial muscles are partially spared Upper
spares upper (e.g. patient can wrinkle their
forehead unless there is bilateral lesion, and the
sagging of the face seen with LMN is not as
prominent)
o Source:
! Brain/ brainstem
Lower motor neuron:
o Patient cant wrinkle forehead
o Source:
! Cerebello-pontine angle
! Labyrinthine segment
! Geniculate segment
! Tympanomastoid segment
! Extracranial

Examination:
Ear (AOM?/ Cholesteatoma?)
Oral cavity (Ramsay Hunt?/ deep lobe mass?)
Head and neck (parotid mass?)
Muscles of facial expression
CN II and XII especially Rinne/Weber tests

House-Brackmann Grading of CNVII Palsy:

I
: Normal movement
II : Slight asymmetry
III : Weak at rest, complete eye closure, synkinesis
IV : Incomplete eye closure, synkinesis
V : Flicker of movement
VI : No movement
*Synkinesis = the development of linked or unwanted facial
movements

Investigations:
Audiogram
Electroneuronography (ENoG) and Electromyography
(EMG) to aid in prognosis
+/- CT or MRI is not settling or recurring

Aetiology:
Idiopathic:
o Bells Palsy (60-75%)
Infective/ Inflammatory:
o Chronic suppurative otitis media
o HZV, HSV
o Sarcoidosis
o Lyme Disease (Borrelia)
o TB
o HIV
o Botulinism
Trauma:
o Temporal bone fracture, surgery, forceps delivery
Tumour:
o Acoustic neuroma, glomus, parotid
Other:
o Metabolic (DM/ pregnancy)
o Congenital (Mobius syndrome)
o Neurological (Guillain-Barre syndrome)

Treatment:
Identify and treat specific cause:
o E.g. AOM, cholesteatoma, parotid mass
Bells Palsy:
o Protect Eye e.g. tape closed at night, sunglasses,
lubricants
o Steroids
Temporal Bone trauma:
o Decompress VII only if dead ear and complete palsy
at time of trauma
Post trauma / surgery:
o Gold weights
o Tarsorraphy
o Slings
Recurrent palsy/failure to improve:
o Low threshold for MRI

1) BELLS PALSY

Definition:
A disorder affecting the facial nerves causing weakness of
the muscles usually on one side of the face
Viral prodrome
Diagnosis of exclusion!

Presentation:
Rapid onset
Numbness/ pain in face, ear, neck
HSV in geniculate oedema > pressure

Prognosis:
Recovery 3-6 weeks
15% residual weakness
Recurrence 12%

2) RAMSEY HUNT SYNDROME

Definition:
A herpes zoster virus infection of the geniculate ganglion
of the facial nerve

Presentation:
Painful vesicles

Complications:
SNHL
Vertigo
Encephalitis

Treatment:
Acyclovir
Strong analgesics

3) OTHER CAUSES

Acute Otitis Media:
o Children in particular
o Facial nerve has no bony covering as it crosses
middle ear in 25% people (Thus, inflammatory
mediators irritate it!)
o Treatment:
! Myringotomy
! Drainage of middle ear
! Grommets
Chronic Otitis Media:
o Cholesteatoma
o Pressure, superimposed Infection
o Treatment:
! Surgical removal of cholesteatoma
Parotid Tumour:
o Usually malignant if CNVII paralysis
o Facial skin malignancy metastasising to intraparotid
LNs
o Following parotidectomy
Facial trauma:
o Injure branch directly
Temporal bone fracture:
o Longitudinal or transverse
o Exploration if immediate & complete
o CT Scan
Surgical injury:
o Acoustic neuroma surgery
o Mastoid surgery, parotidectomy

THE END!