ENT

6 symptoms of ear disease ;- pain, discharge, hearing loss, tinnitus, vertigo and
facial palsy
If external ear canal and tympanic membrane are de nitely normal, then pain
cannot arise from ear (Generally)

Acute Otitis Externa - swimmers ear

Originates in external auditory canal.

2 Common initiating events - trapped moisture after swimming or hot humid
weather, and trauma to ear canal allowing invasion of bacteria to skin.
Most common pathogen is Pseudomonas aeruginosa, followed by S.aureus
Irritation
Pinna tender to movement (Not in acute otitis media)
Discharge - thick and scanty (Mucoid copious discharge in middle ear infection)
Fever
Mild conductive hearing loss
O/E - meatus is narrowed and oedematous with debris

Di erentiate from pinna cellulitis/pinna perichondritis (ear lobe is spare) - infection

classically following trauma - piercing, acupuncture, burn
Can occur as a complication of acute otitis externa, psoriasis and eczema

Necrotising (Malignant) OE is a complication occurring in patients who are immune

compromised or in those who have received radiotherapy to skull base. In
addition, this may lead to osteomyelitis.

Tx -
Topical antibiotic +/- steroid drops
If tympanic membrane is perforated aminoglycosides are not to be used
Remove canal debris. If extensively swollen ear wick is used

Second line - PO antibiotics if infection spreading (Flucloxacillin), take swab,

empirical use of anti fungal and consider contact dermatitis secondary to
neomycin
*Malignant otitis externa is common in elderly diabetics

Acute Otitis Media -

Common following URTI and common in children. Di erent subtypes. Oedema

and congestion in middle ear secondary to infection. If perforates —> Acute
suppurative otitis media. Residual Fluid in middle ear cavity after infection is
known as Otitis Media with E usion (Glue ear)

Although viral URTICARIA typically precede otitis media, most infections are
secondary to bacteria, especially S,pneumonia, H.in uenza and Moraxella
catarrhalis
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 Otitis Media is self limiting, can be cause by viruses/bacteria, symptoms for about
3 days but can last one week. Most get better within 3 days without antibiotics
Fever, otalgia, hearing loss
Otoscope - Bulging tympanic membrane, loss of light re ex, limited mobility
of TM, in amed appearance with injected vessels (Erythema)
May see perforation with purple not otorrhea

3 criteria
Acute onset of symptoms - otalgia/ear tugging , presence of middle ear e usion
(Bulging of TM or otorrhea) and in ammation of TM (Erythema)

Management
Self limiting and usually conservative management - Paracetamol/Ibuprofen for
pain
However, prescribe antibiotics if :
Symptoms >4 days or not improving, systemically unwell but not requiring
admission, immune compromised/high complication risk (Co-morbidities), Age <2
with bilateral otitis media and lastly, otitis media with perforation and/or discharge
in canal

Abx of choice is Amoxicillin (5-7 day course). If pen allergic —> erythromycin or
clarithromycin
Common sequelae - Perforation of TM (Otorrhea) and hence develop into chronic
supppurative otitis media (De ned as perforation of TM with otorrhea for >6W),
Hearing loss and Labrynthitis.
Complications - Mastoidits, meningitis, brain abscess and facial nerve paralysis

Acute suppurative Otitis Media - PERFORATION OF TM

Characterised by ear discharge
Pain, impaired hearing, systemic illness with fever
Blocked ear feeling, then discharge when TM perforates, then pain
Pressure over mastoid elicits pain as entire middle ear is a ected
Bacteria - S.pneumonia , H.in uenza in kids, Moraxella catarrhalis
Diagnosis inspection
Tx- systemic antibiotics - Amoxicillin. Analgesia.Warm olive oil drops
If recurrent acute otitis media then myringotomy with insertion of grommet may be
advised

Otitis Media with e usion - Glue ear

Most common cause of conductive hearing loss and elective surgery in
childhood
Fluid lled in middle ear without acute infection
More common in younger children as Eustachian tube is positioned more
horizontally
Child is well and afebrile
Hearing loss for sometime - conductive
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Otoscope - E usion of any colour, air uid levels/bubbles and Injection with visible
radial vessels, normal TM landmarks
Altered mobility of TM (Reduced)

Tx - Re-assure and active observation for 3 months. Generally resolves

spontaneously with watchful waiting. However, if persistent, grommet can be
inserted (Myringotomy with tympanostomy tube insertion) - Usually stay in for one
year
Can swim - use silicone ear plugs
Re-assess after 3 months with audiology to assess hearing loss
monitoring and support, auto-in ation, hearing aids, grommets
Adenoidectomy - even with normal tonsils

Acute mastoiditis
Typically develops when an infection spreads from middle to mastoid air spaces of
temporal bone
Suspect in any patient with continuous discharge from perforated drum for >10
days, especially if unwell
Due to breakdown of trabecular (thin bony partitions) between mastoid air cells
which then coalesce and are lled with pus and granulation tissue
PERSISTENT Pain behind ear, DISCHARGE, fever, conductive hearing loss,
perforation of TM
Diagnosis is typically clinical although CT can be ordered if suspected of
complications
Tx - IV antibiotics
Complications - Meningitis, hearing loss and facial nerve palsy

Malignant Otitis Externa

Rare but serious form of infection by Pseudomonas aeuroginosa usually in elderly
diabetics and immune compromised individuals
Invades bony base of skull and adjacent soft tissue - rst in soft tissues of
external auditory meatus, then progresses to involve soft tissues and into bony ear
canal
Progresses to temporal bone osteomyelitis
Fever, severe pain, purulent otorrhea, temporal headaches and cranial nerve
palsies (Facial), granulation tissue in ear canal
CT scan is usually done
Several weeks of IV antibiotics (covering pseudomonas)

Bullous myringitis - Bullae or vesicles on TM without a ecting external or middle

ear
Hemorrhagic blistering of ear drum and external ear canal due to viral infection
Moderate to severe pain
Bloody otorrhea can occur when bulla ruptures and is known as bullous
hemorrhagic myringitis
Analgesia
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Acute Otitis Externa: commonly develops after swimming on
holiday, redness, edematous ear canal which is narrowed and
obscured by debris, conductive hearing loss, and discharge.
Initial TTT ?7 days of a topical antibiotic (aminoglycosides) with or
without a topical steroid.
If failed, empirical use antifungal agent.
If Extensive otitis externa ? Flucloxacillin (erythromycin if penicillin-
allergic)
Otitis externa in diabetics ?cipro oxacin to cover Pseudomonas
Recurrent otitis externa following numerous antibiotic treatments
should raise suspicion of Candida infection. Treatment is with
topical clotrimazole, which should be continued for 2 weeks
following resolution of the infection. These patients require ENT
referral for aural toilet. Persistent otitis externa with discharge ?
swabbed for MC+S.
*Malignant Otitis Externa: occurs in immunocompromised such as
diabetes. This is essentially osteomyelitis of the temporal bone.
History of multiple courses of antibiotic drops and symptoms have
not resolved.
Management: ENT for CT scan of the temporal bones and a
prolonged course of IV antibiotics (not topical)

Pain in ear may be referred.

Perforated TM - due to infection, barotrauma or direct trauma. Can lead to hearing

loss depending on size and also increase risk of otitis media. No treatment is
needed in most cases as TM will heal itself in 6-8 weeks. If perforation occurs
following episode of AOM then antibiotics are indicated. Myringoplasty if TM
doesn’t heal by itself.

Cholesteatoma - non-cancerous growth of squamous epithelium that is ‘trapped’

within skull base - most common in patients aged 10-20 years. Being born with
Cleft palate increases risk by x100
CF - Foul-smelling non resolving discharge
Features of local invasion - vertigo, facial nerve palsy and cerebellopontine angle
syndrome
Otoscopy - ‘attic crust’ - in uppermost part of ear drum
Refer to ENT for consideration of removal

Hearing impairment and Tinnitus

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 The two main types of defect are conductive and sensorineural. Hearing defects
are described as conductive when there is impediment to the passage of sound
waves between the external ear and the footplate of the stapes, or sensorineural if
there is a fault in the cochlea (sensory), or the cochlear nerve (neural)

Conductive deafness
Obstruction of external ear canal - Wax, Foreign body in ear canal, otitis externa/
media/OME
Tympanic membrane perforation - Infection (most common), Trauma or
Barotrauma
Otosclerosis - AD
Eustachian tube dysfunction - glue ear
Cholesteatoma
Exostosis
Tumours

Sensorineural deafnesss
Bilateral - Degenerative ageing changes of cochlea - Presbyacusis. Drug
ototoxicity (Furosemide, Aminoglycosides, Cisplatin) and noise damage (Acoustic
trauma) often occupational
Unilateral - Ménière’s disease or acoustic neuroma or Labrynthitis

Presbycusis
Presbycusis is a type of sensorineural hearing loss that a ects elderly individuals.
Typically, high-frequency hearing is a ected bilaterally, which can lead to
conversational di culties, particularly in noisy environments.
‘Old man struggling to hear his wife’
Presbycusis progresses slowly, as sensory hair cells and neurons in the cochlea
atrophy over time. Although certain factors are associated with presbycusis, it is
distinct from noise-related hearing loss.
Cause - unknown. Theories - arteriosclerosis, DM, noise exposure, stress, genetic
and drug exposure
Patients typically present with a chronic, slowly progressing history of: Speech
becoming di cult to understand, Need for increased volume on the television or
radio, Di culty using the telephone, Loss of directionality of sound, Worsening of
symptoms in noisy environments

Investigations
Otoscopy - To rule out otosclerosis, cholesteatoma and conductive hearing loss
Tympanometry - normal middle ear function with hearing loss, Audiometry - B/L
sensorineural hearing loss pattern

Address risk factors

Hearing aids
Cochlear implants

Otosclerosis
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Otosclerosis describes the replacement of normal bone by vascular spongy bone.
It causes a progressive conductive deafness due to xation of the stapes at the
oval window. Otosclerosis is autosomal dominant and typically a ects young
adults

Onset is usually at 20-40 years - features include:

conductive deafness, tinnitus, tympanic membrane - the majority of patients will
have a normal tympanic membrane, 10% of patients may have a ' amingo tinge',
caused by hyperaemia. Positive family history
Management - hearing aid, Stapedectomy

Sudden sensorineural deafness = <72 hours - SSNHL - Unilateral - mostly

idiopathic, needs MRI to exclude vestibular schwanomma
*High dose oral corticosteroids are used by ENT for all cases of SSNHL
Other - meningitis and neurological conditions

Wax removal - syringe

Rinne Test
Positive Rinne Test is normal i.e AC>BC
Conductive Hearing loss - BC>AC in a ected ear and AC>BC in una ected ear
Sensorineural hearing loss - AC>BC Bilaterally

Weber result - normal is midline

Conductive - Lateralises to a ected ear
Sensorineural - Lateralises to una ected ear

Quantitative measures of the loss, and accurate determination of its site and
cause, depend on audiometric tests.
The most familiar is pure tone threshold audiometry

Audio gram interpretation -

Anything above 20dB is normal
Conductive loss - only air conduction is impaired
Sensorineural loss - air and bone conduction is impaired
Mixed - both impaired, air conduction being worse than bone

Tinnitus - TRT Tinnitus retraining therapy

Causes of tinnitus
Idiopathic
Wax, Otosclerosis, Drugs (loop diuretics, aminoglycosides, chemo-cisplatin and
quinine), Ménière’s disease, Acoustic neuroma, SSNHL, Noise exposure
Systemic - Anemia, Thyroid, MS
Pulsatile - CV causes (aneurysms/malformation)
pulsatile tinnitus generally requires imaging as there may be an underlying vascular
cause. Magnetic resonance angiography (MRA) is often used to investigate
pulsatile tinnitus
Needs audiology assesment
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Management - Treat underlying cause, application device (Hearing aid), TRT, CBT

CPA and acoustic neuroma

With the diversity of structures in the CPA (Acoustic and vestibular nerve bundle
CN8, Facial nerve, arteries - anterior inferior cerebellar artery as well as other
cranial nerves) it is not surprising that many di erent tumours can grow there.
Fortunately, most of them are benign and by far the most common is the doubly
misnamed acoustic neuroma.
Develop on superior vestibular nerve, and are also tumours of nerve sheath cells -
schwann cells - which makes the myelin sheet surrounding nerve bres, hence
should be called vestibular schwannomas. Rarely become malignant but with
continued growth can lead to raised ICP and brain stem compression

*A particularly unpleasant manifestation of the acoustic neuroma is as a part of the

syndrome called neuro bromatosis type 2 (NF2). This is an autosomal dominant
condition, classically present- ing in youth, with bilateral acoustic neuromas, other
neuromas (especially spinal), meningiomas and even gliomas.

Variable growth - some grow rapidly whilst 50% do not grow over a 10 year period

CF - Many asymptomatic.
- Unilateral sensorineural hearing loss, vertigo, tinnitus (CN VIII) and absent
corneal re ex (CN V) and Facial palsy (CN 7)

MRI of the cerebellopontine angle is the investigation of choice. Audiometry is also

important as only 5% of patients will have a normal audiogram.

Management - surgery, radiotherapy or watchful observation

Vertigo

Mismatch between sensory inputs - vision , proprioception and signals from your
vestibular system (Inner ear - semicircular canals with endolymph uid that are
detected by stereocilia in ampulla)
Vestibular nerves carry information to vestibular nuclei in brain stem and
cerebellum which then sends signals to CN (Oculomotor, Trochlea, Abducens) for
eye movement, cerebellum, Thalamus and spinal chord
Hence vestibular nervous system help CNS co-ordinate eye movement and
movement throughout body

Causes - Vestibular causes (BPPV, Ménière’s disease, Vestibular Neuronitis) and

central

BPPV
Triggered by movement
Hallpike diagnostic
Epley’s helpful
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 Ménière’s disease
Excessive build up of endolymph in semi circular canals leading to attacks of
vertigo
Vertigo is usually the prominent symptom
Middle aged
Not associcated with movement
Recurrent episodes of sensorineural Hearing loss, tinnitus, vertigo and sensation
of fullness
nystagmus and positive rombergs
Episodes last from minutes to hours
ENT assessment to con rm diagnosis
• patients should inform the DVLA. The current advice is to cease driving until
satisfactory control of symptoms is achieved
• acute attacks: buccal or intramuscular prochlorperazine. Admission is
sometimes required
• prevention: betahistine and vestibular rehabilitation exercises may be of
bene t

Vestibular neuronitis is a cause of vertigo that often develops following a viral

infection
• recurrent vertigo attacks lasting hours or days
• nausea and vomiting may be present
• horizontal nystagmus is usually present
• no hearing loss or tinnitus

Di erential diagnosis
• viral labyrinthitis -Labyrinthitis should be distinguished from vestibular neuritis
as there are important di erences: vestibular neuritis is used to de ne cases
in which only the vestibular nerve is involved, hence there is no hearing
impairment; Labyrinthitis is used when both the vestibular nerve and the
labyrinth are involved, usually resulting in both vertigo and hearing
impairment. Features - Vertigo: not triggered by movement but exacerbated
by movement, nausea and vomiting, hearing loss: may be unilateral or
bilateral, with varying severity, tinnitus, preceding or concurrent symptoms of
upper respiratory tract infection
• Episodes are usually self-limiting. Prochlorperazine or antihistamines may
help reduce the sensation of dizziness
• posterior circulation stroke: the HiNTs exam can be used to distinguish
vestibular neuronitis from posterior circulation stroke
• Vertebrobasilar Ischemia - Elderly patient , dizziness on extension of neck

Management

• buccal or intramuscular prochlorperazine is often used to provide rapid relief

for severe cases
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 • a short oral course of prochlorperazine, or an antihistamine (cinnarizine,
cyclizine, or promethazine) may be used to alleviate less severe cases
• vestibular rehabilitation exercises are the preferred treatment for patients who
experience chronic symptoms

Other causes - MS, Vestibular migraines

Facial palsy

IAM with CN 8 initially (See pics for anatomy) and runs

5 motor branches
Motor, lacrimation and salivation, Taste in anterior 2/3 of mouth

Bell’s palsy - idiopathic lower motor neurone palsy. May have associated
hyperacusis and altered taste

Herpes zoster oticus - Ramsay Hunt syndrome

reactivation of the varicella zoster virus in the geniculate ganglion of the seventh
cranial nerve.
Auricular pain, Facial nerve palsy, Vesicular Rash around ear
Oral aciclovir and corticosteroids

Facial palsy can also occur with Stroke, trauma, Lyme disease and neoplasms as
well as MS

Paranasal sinus diseases and infections

Acute Sinusitis

Paranasal sinuses are - Frontal, Maxillary, Ethmoid and sphenoid - normally

produce mucus which drains via ostea into nasal cavity. Blockage can then lead to
sinusitis.

Acute Sinusitis describes an in ammation of the mucous membranes of the

paranasal sinuses for <12 weeks. The sinuses are usually sterile - the most
common infectious agents seen in acute sinusitis are Streptococcus pneumoniae,
Haemophilus in uenzae and rhinoviruses

Predisposing factors - NAsal obstruction (Deviation/polyp), Recent local infection

(rhinitis or dental extraction), Swimming/diving and smoking

Features - Pain - typically frontal pressure pain which is worse when bending
forward, Nasal discharge - usually thick and purulent and nasal obstruction
Fever and pain on palpation of sinuses
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 Management of acute sinusitis
Analgesia
Intranasal decongestant
Nasal irrigation with warm saline
Fluids and rest
Antibiotics are not needed normally unless prolonged (>10 days), worsening
symptoms >5 days or severe presentation - Phenoxymethylpenicillin is rst line
and co-amoxiclav if systemically unwell or at high risk of complications
If symptoms > 10 days - can also have steroid nasal spray

Chronic Rhinosinusitis >12 weeks

Predisposing factors - as previous
CF - as previous, nasal discharge is clear if allergic or vasomotor. Thicker, purulent
discharge suggests secondary infection, post-nasal drip
Tx- avoid allergen, intranasal corticosteroids and nasal irrigation with saline

Red ags - persistent symptoms for 3 months despite treatment, unilateral

symptoms and epistaxis

Allergic Rhinitis - Hay fever

Type I Hypersensitivity reaction
Allergic rhinitis is an in ammatory disorder of the nose where the nose become
sensitized to allergens such as house dust mites and grass, tree and weed pollens.
It may be classi ed as follows, although the clinical usefulness of such
classi cations remains doubtful:
• seasonal: symptoms occur around the same time every year. Seasonal
rhinitis which occurs secondary to pollens is known as hay fever
• perennial: symptoms occur throughout the year
• occupational: symptoms follow exposure to particular allergens within the
work place
CF - Sneezing, bilateral nasal congestion, clear nasal discharge, post nasal drip
Ix - skin prick testing. Bloods will show Eosinophilia
Management - Allergy avoidance, oral/intranasal antihistamines
Short course of oral corticosteroids are occasionally needed to cover important life
events

Post nasal drip - Occurs as a result of excessive mucus production by the nasal
mucosa. This excess mucus accumulates in the throat or in back of nose causing
chronic cough and bad breath

Nasal Polyps
2-4x more common in men
Associations - Asthma, infective sinusitis, Aspirin sensitivity, cystic brosis,
Kartagener’s syndrome (Primary ciliary dyskinesia - Triad of situs inversus, chronic
sinusitis and Bronchiectasis) and Churg Strauss syndrome
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Most polyps are bilateral and a unilateral polyp should be assumed neoplastic until
proven otherwise

The association of asthma, aspirin sensitivity and nasal polyposis is known as

Samter's triad.

Features - nasal obstruction, rhinorrhea, sneezing and poor sense of taste and
smell
Refer to ENT
Topical corticosteroids shrink polyp size in 80% of patients - If fails then requires
surgery

Sore Throat

Commonly due to viral infections

Most common bacterial cause is Group A Strep - Streptococcus pyogenes
followed by S.pneumonia, H. In uenza
Clinical Knowledge Summaries recommend:
• throat swabs and rapid antigen tests should not be carried out routinely in
patients with a sore throat
Management
• paracetamol or ibuprofen for pain relief
• antibiotics are not routinely indicated
NICE indications for antibiotics
• features of marked systemic upset secondary to the acute sore throat
• unilateral peritonsillitis
• a history of rheumatic fever
• an increased risk from acute infection (such as a child with diabetes mellitus
or immunode ciency)
• patients with acute sore throat/acute pharyngitis/acute tonsillitis when 3 or
more Centor criteria (40-60% Estimate probability that it is due to a bacterial
cause rather than viral) are present (1 point each - Presence of tonsillar
exudate, tender anterior cervical lymphadenopathy/lymphadenitis, history of
fever and absence of cough)
• Alternative to Centor score is the fever pain score

Abx of choice- Pen V (Phenoxymethylpenicillin) or clarithromycin if pen allergic for

7-10 days

Complications of bacterial tonsillitis - Peritonsillar abscess - Quinsy, otitis media

and rheumatic fever/glomerulonephritis (rare), Scarlet fever

Only consider surgery if person meets all of the following criteria -

• sore throats are due to tonsillitis (i.e. not recurrent upper respiratory tract
infections)
• the person has ve or more episodes of sore throat per year
• symptoms have been occurring for at least a year
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 • the episodes of sore throat are disabling and prevent normal functioning

Other Indications include -

• recurrent febrile convulsions secondary to episodes of tonsillitis
• obstructive sleep apnoea, stridor or dysphagia secondary to enlarged tonsils
• peritonsillar abscess (quinsy) if unresponsive to standard treatment
Complications of tonsillectomy - Pain, Haemorrhage - secondary hemorrhage may
occur 5-10 days after surgery and is often associated with a wound infection

Peritonsillar abscess
Streptococcus pyogenes is usually the causative organism.
CF - Severe sore throat, Trismus (almost always), fever, hot potato voice, foul
breath, drooling
Unilateral bulging above and lateral to one of the tonsils - pushes uvula to opposite
side
Immediate referral to ENT
IV uids, IV antibiotics, Analgesia
Needle aspiration - remove pus and con rm diagnosis
Complete aspiration can then be attempted or I/D (Which may be superior
If background of chronic or recurrent tonsillitis - Interval tonsillectomy

Complications - Abscess can spread to deeper neck tissues and cause necrotising
fasciitis. Other - Meidastinitis, Pericarditis, pleural e usions

Stridor

Paediatric Stridor
Acute - Epiglottitis, Laryngotracheobronchitis, acute retropharyngeal and
Peritonsillar abscess, foreign body, anaphylaxis
Chronic - Laryngomalacia, subglottic stenosis, vocals chord paralysis

Adult Stridor
Bilateral vocal chord paralysis - Idiopathic, Thyroid surgery
Malignancy
Intubation trauma
Laryngeal trauma
Angioedema

Causes of hoarseness
Voice overuse, smoking, viral illness, hypothyroidism, GERD, laryngeal cancer, lung
cancer
Suspected laryngeal cancer pathway -
If > 45 years old with either persistent unexplained hoarseness or unexplained
lump in neck
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 Epistaxis

Epistaxis (nose bleeds) is split into anterior and posterior bleeds, whereby the
former often has a visible source of bleeding and usually occurs due to an insult to
the network of capillaries that form Kiesselbach’s plexus - Little’s area. Posterior
haemorrhages, on the other hand, tend to be more profuse and originate from
deeper structures. They occur more frequently in older patients and confer a higher
risk of aspiration and airway compromise.

Mostly benign and self limiting - exacerbated by nose picking/blowing

Causes -
Trauma, foreign body insertion, bleeding disorders, cocaine use, Hereditary
hemorrhagic telangectasia, granulomatosis with polyangitis and juvenile
angio broma

Management

If haemodynamically stable - Sit up, torso forward and open mouth + breath
through mouth, pinch soft area of nose rmly
Avoid lying down
If successful - consider topical antiseptic - nauseating to reduce crusting and risk
of vestibulitis (Caution in those with peanut, soy or neomycin allergies). Advise to
avoid, picking, blowing, heavy lifting,exercise, lying at, alcohol or hot drinks.

Consider admission if - <2 years old or co-morbidity where underlying cause is

suspected (Hypertension, CAD)

If bleeding does not stop after 10-15 minutes of continuous pressure on the nose
consider cautery ( rst choice if source is visible) or packing (if source not visible) -
patients should be admitted to hospital for observation and review, and to ENT if
available

If all else fails - may require sphenopalatine ligation in theatre

Nasal septal hepatoma

Nasal septal haematoma is an important complication of nasal trauma that should
always be looked for. It describes the development of a haematoma between the
septal cartilage and the overlying perichondrium
Can be precipitated by minor trauma, sensation of nasal obstruction, pain,
rhinorrhea
Examination - classically - bilateral red swelling arising from nasal septum - which
may be di erentiated from a deviated septum by gently probing the swelling. Nasal
septal haematomas are typically boggy whereas septums will be rm
Tx - surgical drainage and IV Antibiotics
If untreated irreversible septal necrosis may develop within 3-4 days. This is
thought to be due to pressure-related ischaemia of cartilage resulting in necrosis -
can result in saddle nose deformity
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Neck Lumps

Mostly benign in children

Haemangioma/lymphangioma
Haemangioma - Bluish, compressible and resolve spontaneously within 1st
decade whereas lymphangioma persist into adulthood, are doughy and ill de ned

Branchial cyst - More lateral - Painless, Oval, mobile, smooth mass between SCM
and pharynx. Usually present in early adulthood. Intermittent swelling during URTI
may occur

Reactive Lymphadenopathy - By far the most common cause of neck swellings.

There may be a history of local infection or a generalised viral illness

Thyroglossal cyst - more common in <20, midline, between isthmus of thyroid and
hyoid bone, moves upwards with tongue protrusion and may be painful if infected

Cystic hygroma - classically on left and often in posterior triangle. Is a congenital

lymphangioma. Most evident at birth around 90% before 2 years of age

Lymphoma - systemic - night sweats, splenomegaly. Rubbery , painless

lymphadenopathy. May have pain while drinking alcohol

Thyroid swelling - moves up on swallowing

Dermiod cyst - Young children, near lateral aspect of the eye brow.
cystic teratoma containing developmentally mature skin complete with hair follicles
and sweat glands and often pockets of sebum,blood,fat,bone,nails,teeth. Almost
always benign.

Sebaceous cyst - lining resembles uppermost part of hair follicle and lls with
sebum. Punctum. Occurs anywhere on body except palms and soles. Can become
infected needing I/D and Abx

Pharyngeal pouch - older men. Dysphasia, regurgitation, aspiration , chronic cough

Carotid aneurysm - pulsatile, doesn’t move on swallowing

Cervical rib - more common in females. 10% develop thoracic outlet syndrome

Salivary glands
Parotid , submandibular and sublingual
Most tumours are parotid and most of these are pleomorphic adenomas (middle
aged, slow growing painless lump)
malignant are rare - short hx, painful, hard, CN VII involvement
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Warthins tumour - benign adenolymphoma
Stones - recurrent unilateral pain —> if becomes infected : Ludwig’s angina. Most
are submandibular. Ix - XR and Sialography. Surgical removal

Other causes of enlargement - mumps, bacterial infection, sicca syndrome and

sjögrens, RA

Black hairy tongue - predisposing factors - poor oral hygeine, antibiotics, HIV,
IVDU, head and neck radiation
Tongue should be swabbed to exclude candida
Tx - tongue scraping, topical anti-fungal if candida

Geographic tongue - benign, chronic condition of unknown cause. Erythematous

area with grey white border

Head and neck cancer

Head and neck cancer is an umbrella term. It typically includes:

• Oral cavity cancers
• Cancers of the pharynx (including the oropharynx, hypopharynx and
nasopharynx)
• Cancers of the larynx

Features
• neck lump
• hoarseness
• persistent sore throat
• persistent mouth ulcer

NICE suspected cancer pathway referral criteria (for an appointment within 2

weeks)

Laryngeal cancer
• Consider a suspected cancer pathway referral (for an appointment within 2
weeks) for laryngeal cancer in people aged 45 and over with:
◦ persistent unexplained hoarseness or
◦ an unexplained lump in the neck

Oral cancer
• Consider a suspected cancer pathway referral (for an appointment within 2
weeks) for oral cancer in people with either:
◦ unexplained ulceration in the oral cavity lasting for more than 3 weeks
or
 ◦ a persistent and unexplained lump in the neck.
• Consider an urgent referral (for an appointment within 2 weeks) for
assessment for possible oral cancer by a dentist in people who have either:
◦ a lump on the lip or in the oral cavity or
◦ a red or red and white patch in the oral cavity consistent with
erythroplakia or erythroleukoplakia.

Thyroid cancer
• Consider a suspected cancer pathway referral (for an appointment within 2
weeks) for thyroid cancer in people with an unexplained thyroid lump.

Miscellaneous
Complications following Thyroid surgery
• Anatomical such as recurrent laryngeal nerve damage.
• Bleeding. Owing to the con ned space haematoma's may rapidly lead to
respiratory compromise owing to laryngeal oedema.
• Damage to the parathyroid glands resulting in hypocalcaemia.
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