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Phase 3b > ENT > Flashcards

ENT Flashcards

1
Q

what 3 main parts is the ear anatomy decided into?

A

the external ear
the middle ear
the inner ear

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2
Q

what makes up the external ear?

A 
the Pinna  (auricle) 
the external auditory canal
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3
Q

what is cauliflower ear?

A

The cartilage derives its nutritional support from the overlying
perichondrium. Separation of the two layers (with blood, infection or
inflammation often following trauma) may result in cartilage necrosis
resulting in a cauliflower ear

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4
Q

what is the function of the middle ear?

A

to amplify and transmit sound energy

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5
Q

what structures are in the middle ear?

A

ossicles (malleus, incus and stapes)
tensor tympanic and stapedius muscles - which are attached to the ossicles to regulate their movement
chords tympani - provides taste to the anterior two thirds of the tongue
facial nerve

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6
Q

what is the function of the inner ear?

A

Cochlea - Transduction of energy from sound to electrical
impulses, which are relayed and interpreted by the brain
3 Semicircular canals (superior, lateral and posterior) – Detect
angular head acceleration
Utricle and saccule – Detects linear acceleration
forwards/backwards and up/down respectively

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7
Q

what sound range can the average human ear detect?

A

between 20 and 20,000Hz

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8
Q

what is vertigo?

A

vertigo may be defined as the false sensation that the body or environment is moving

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9
Q

what are the most common causes of vertigo?

A 
viral labyrinthitis 
vestibular neuritis 
benign paroxysmal positional vertigo 
Meniere's disease
Vertebrobasilar ischaemia 
acoustic neuroma

other causes include:

  • posterior circulation stroke
  • trauma
  • MS
  • ototoxicity e.g. gentamicin
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10
Q

once you have established that a person has true vertigo what must you do?

A

it is imperative to ascertain the duration and frequency of attacks, asthis is the key to reaching the correct diagnosis and determining if
the disorder is most likely peripheral (pertaining to the ear) or central (brain).

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11
Q

what is the symptoms and signs benign paroxysmal positional vertigo?

A

Dix hall pike test will be positive
rotatory vertigo on moving head (triggered by change in head position)
gradual onset
each epsiode last around 10-20 second

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12
Q

what is meniere’s disease?

symptoms and signs

A

Meniere’s disease is a disorder of the inner ear of unknown cause. It is characterised by excessive pressure and progressive dilation of the endolymphatic system

  • rotatory vertigo associated with fluctuating hearing loss often with low-frequency thresholds affects.
  • tinnitus usually gets worsen during an attack
  • patients classically get an aural fullness or pressure in one or both ears before the onset of vertigo

symptoms resolve in the majority of patients after 5-10 years but the majority of patients will be left with a degree of hearing loss and psychological distress is common

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13
Q

what is vestibular neuritis?what are the signs and symptoms of vestibular neuritis?

A

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

recent viral infection
rotatory vertigo that is continuous for over 24 hours
often associated with nausea and vomiting
horizontal nystagmus is usually present
classically confined to bed and takes several days weeks to recover

there will be no hearing loss or tinnitus

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14
Q

what are the signs and symptoms of vestibular migraine?

A

rotatory vertigo can last minutes to hours to days

classically associated with headaches/photophobia/visual disturbance/phonophobia

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15
Q

what is labyrinthitis?

signs and symptoms viral labyrinthitis?

A

Inflammatory condition affecting the labyrinth in the cochlea and vestibular system of the inner ear. can be viral bacterial or associated with systemic disease - viral labyrinthitis is the most common form

  • they will have had recent viral infection.
  • it will be sudden onset vertigo usually not triggered by movement but exacerbated by movement
  • nausea and vomiting
  • hearing may be affected (sensorineural hearing loss)
  • tinnitus

they may have nystagmus towards the unaffected side
they may have gait disturbances
there may be abnormality on inspection of the external ear canal and the tympanic membrane e.g. vesicles in herpes simplex infection

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16
Q

what investigations might you perform for vertigo?

A

-full neurological exam
- pure tone audiometry
- Dix-Hallpike test
- MRI of internal auditory meatus may be appropriate with asymmetrical sensorineural loss to exclude an acoustic
neuroma
- video head impulse testing

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17
Q

What are the investigations and management of benign paroxysmal positional vertigo?

A

INVESTIGATIONS: dix-hallpike manoeuvre, supine lateral head turns, audiogram, brain MRI

MANAGEMENT: BPPV has good prognosis and usually resolves spontaneously after weeks or months so patient education and reassurance is needed.
for symptomatic treatment you can do the Epley manoeuvre (particle reposition manoeuvre)
teaching the patient exercises that they can do themselves at home, termedvestibular rehabilitation e.g. Brandt-Daroff exercises

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18
Q

what are the investigations and management for Meniere’s disease?

A

INVESTIGATIONS: pure-tone air and bone conduction with masking, speech audiometry, tympanometry/immittance/stapedial reflex levels, oto-acoustic emissions

MANAGEMENT: low salt diet and diuretics
vestibular suppressants: meclozine, secondary options include prednisolone and betahistine
intratympanic injections (dexamethasone sodium phosphate)
vestibular and balance rehabilitation
if they have persistent hearing loss - hearing aids

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19
Q

what are the investigations and management of labyrinthitis?

A

INVESTIGATIONS
- audiogram
- Weber’s and RInne’s test will show sensorineural hearing loss
investigations to consider
- pure tone audiometry can be done to assess hearing loss
- full blood count and blood culture: if systemic infection suspected
- culture and sensitivity testing if any middle ear effusion
- temporal bone CT scan: indicated if suspecting mastoiditis or cholesteatoma
- MRI scan: helpful to rule out causes such as suppurative labyrinthitis or central causes of vertigo
- vestibular function testing: may be helpful in difficult cases and/or determining prognosis

MANAGEMENT 
vestibular suppressants (benzo e.g. diazepam), antiemetics and prednisolone can be added
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20
Q

Labyrinthitis vs vestibular neuritis?

A

Labyrinthitis should be distinguished from vestibular neuritis as there are important differences: vestibular neuritis is used to define 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.

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21
Q

how do you manage vestibular neuritis?

A

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

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22
Q

vertigo vs dizziness?

A

Vertigo is the hallucination of movement and is often a
manifestation of inner ear dysfunction

Dizziness is a less specific complaint that may be a
manifestation of visual , CNS, Proprioceptive, Vascular,
Cardiac or ear abnormality.

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23
Q

what are the two main types of hearing defect?

A

CONDUCTIVE: When there is impediment to the passage of sound waves between the external ear and footplate of the stapes (decreased transmission of sound to the cochlea via air conduction)

SENSORINEURAL: if there us a fault in the cochlea (sensory) or the cochlear nerve (neural) - sound is transmitted normally to the inner ear but the problem is at the level of the cochlea and nerve

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24
Q

what are some causes of conductive deafness?

A

obstruction of the external ear canal: wax, inflammatory oedema, debris, atresia, foreign bodies
perforate of the tympanic membrane
discontinuity of the ossicular (infection or trauma)
fixation of the ossicular chain (otosclerosis)

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25
Q

what are some causes of sensorineural deafness?

A

Bilateral progressive loss: Presbyacusis, drug ototoxicity, noise damage.

Unilateral progressive loss:
Meniere’s disease (endolymphatic hydrops), acoustic neuroma.

Sudden loss: Trauma, viral
infections (mumps, measles, VZ), impaired vascular flow (CVA), acoustic neuroma, barotrauma and leakage of perilymph fluid from inner ear.

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26
Q

physiology of the ear??

A

Sound waves require a medium, such as air or water. The compression in a sound wave is channelled down the ear canal to the tympanic membrane. Vibrations of the tympanic membrane are then transmitted by the ossicular chain through the oval window into the cochlea. The vibrations of the cochlea cause a fluid wave, which stimulates hair cells within the cochlea, generating an electrical impulse, which is transmitted along the cochlear nerve to the brain, where it is heard/interpreted. Mechanical energy is thereby converted to electrical energy. Anything that interferes with the movement of sound from the external ear to the middle ear to the inner ear, and then to the brain, can cause a hearing loss. The external ear and middle ear may appear normal on examination if the cause is in the inner ear or brain. It is possible for hearing loss to be permanent if not treated in a timely fashion.

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27
Q

what investigations would you perform for hearing loss?

A

clinical examination - ear exam and neurological examination - cranial nerves and cerebellar

pure tone audiogram
tympanometry

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28
Q

what is presbycusis?

A

Presbycusis describes age-related sensorineural hearing loss. Patients may describe difficulty following conversations

Audiometry shows bilateral high-frequency hearing loss

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29
Q

what is otosclerosis?

how is it managed?

A

Autosomal dominant, replacement of normal bone by vascular spongy bone. Onset is usually at 20-40 years - features include:
conductive deafness
tinnitus
tympanic membrane - 10% of patients may have a ‘flamingo tinge’, caused by hyperaemia
positive family history

management: hearing aid, stapedectomy.
flouride may inhibit sclerotic progression
if severe a cochlear implant is another option

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30
Q

what is glue ear?

A

Also known as otitis media with effusion
peaks at 2 years of age
hearing loss is usually the presenting feature
secondary problems such as speech and language delay, behavioural or balance problems may also be seen

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31
Q

what are ototoxic drugs?

A 
gentamicin 
furosemide 
aspirin 
co-trimoxazole
metronidazole
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32
Q

how is a perforated tympanic membrane managed?

A

Tympanoplasty - Cartilage or temporalis fascia is used to repair a perforation in tympanic membrane. N.B. This surgery is normally done for recurrent ear infections or to waterproof theear; hearing improvement often occurs when a perforation is
closed but cannot be guaranteed.

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33
Q

what surgical procedure if performed in otosclerosis?

A

Stapedectomy - Prosthesis used to bypass fixed
stapes/footplate in otosclerosis and allow transmission of sound
into inner ear

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34
Q

what is a bone anchored hearing aid?

A

Bone anchored hearing aid – a transcutaneous or percutaneous
device can be surgically implanted under general or local
anaesthesia for a conductive, mixed conductive /sensorineural
hearing loss or unilateral dead ear

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35
Q

what are the different types of hearing aid?

A

bone anchored hearing aid
cochlear implantation
middle ear implant - suitable for conductive and mixed hearing loss

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36
Q

how is excessive ear wax managed?

A

topical ear drops (warm olive oil, sodium bicarb) - softens impacted earwax allowing it to migrate naturally out of the canal

Microsuction - evacuates softened wax and wax tightly adherent to the ear canal

Syringing - sometimes performed in primary care setting

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37
Q

what is tinnitus?

A

Tinnitus is a term used to describe the perception of sound when no
external sound is present.

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38
Q

what are the two types of tinnitus?

A

non-pulsatile tinnitus (referred to as a false perception of sound.It is often described as a buzzing, high pitched tone or a clicking or popping. It can be associated with noise induced hearing loss, prebycusis, Meiere’s disease, head injury, otitis media and drug related causes)

Pulsatile Tinnitus - defined by a heart sound heard by an individual that is synchronous with their heartbeat and is usually caused by turbulent blood flow that reaches the cochlear. It may be associated with a treatable cause

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39
Q

what are the causes of pulsatile tinnitus?

A

vascular causes (atherosclerosis on the internal carotid, vascular malformations, glomus tumours)

non-vascular causes (page’s disease, otosclerosis, myoclonus of the middle ear muscles or palatal muscles )

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40
Q

how would you investigate tinnitus?

A

if unilateral and associated with hearing loss, MRI should be performed exclude acoustic neuroma

pulsatile tinnitus may be investigated using MR or CT angiography. Caroitd duplex scanning may also be helpful if carotid artery stenosis is suspected

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41
Q

how is tinnitus managed?

A

often patient just needs reassurance that it is common and they will adapt to it.
address any underlying causes
a hearing aid may improve tinnitus if hearing loss is preset through a masking effect.

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42
Q

what is otalgia?

A

otalgia is ear pain that can originate from the ear itself or can also be referred from elsewhere in the head or neck

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43
Q

what are some causes otalgia?

A 
acute otitis media 
otitis externalities 
Necrotising otitis externalities (malignant otitis externalities, skull base osteomyelitis)
TMJ dysfunction 
referred pain
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44
Q

what can caused referred pain in the ear?

A

any pathology involving the cranial nerves V,VII, IX, and X and the upper cervical nerves C2 and C3 can cause the sensation of referred otalgia.

Trigeminal neuralgia is the most common cranial neuralgia linked to referred otalgia.

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45
Q

what is Otorrhoea?

A

discharge from the ear

the ear can discharge wax, pus, blood, mucus and even CSF.

Discharging wax should be reassured as normal.

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46
Q

what is otitis Externa?

A

infection of the external ear
typically affects the eternal auditory canal

the skin become erythematous, swollen, tender and warm leading to debris and discharge accumulation. The narrowing of the canal, in combination with the accumulation of the debris, leads to further entrapment of pathogens and propagating the infective process.

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47
Q

what is the most common causative pathogens in otitis externa?

A

Pseudomonas Aeruginosa (around 40%), S. Epidermidis, S. Aureus, and anaerobes

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48
Q

what are risk factors for otitis externa?

A
  • frequent water contact
  • humid environments
  • presence of ear polyps or foreign bodies
  • narrow ear canals
  • ear eczema or psoriasis
  • local trauma
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49
Q

what are the clinical features of otitis externa?

A
  • progressive ear pain with purulent discharge
  • itchiness and ear fullness may also be preset

less commonly

  • hearing loss
  • tinnitus
  • swollen ear

on examination: the external ear canal will appear swollen and erythematous.

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50
Q

what types of ear discharge might suggest bacterial, fungal otitis externa infection or otitis media?

A

White-yellow – related to bacterial infection
Thick white grey with visible hyphae or spores – fungal infection
Clear grey – otitis media

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51
Q

what differential diagnosis would you want to consider for anyone presenting with ear discharge?

A

Otitis media with perforation – usually clear discharge or bloody followed by relief of pain, with an inflamed tympanic membrane with perforation.

Ramsay Hunt syndrome – may present with symptoms of otitis externa, yet has evidence of vesicular eruptions within 2 days of first onset of pain.

Furuncle – a painful ear canal due to localised abscess formation from infection of the hair follicle in the lateral third of ear canal. A visible bulge is present when examining with an otoscope.

Less common conditions include ear canal malignancy, branchial cyst, atopic dermatitis, and exostosis.

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52
Q

what investigations would you perform for otitis externa?

A

usually a clinical diagnosis based on a history and examination of the ear ring an otoscope.

if otitis externa is not resolving with antibiotics or there is signs of fungal disease on otoscope swabs of the discharge can be sent for culture.

complicated cases of otitis externa may warrant a high resolution CT (HRCT) scan to investigate the extent of the disease.

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53
Q

what risk scoring can be used to quantify the severity of otitis externa?

A

the Brighton grading system

Grade 1 - Localised canal inflammation with mild pain, no hearing loss and tympanic membrane visible

Grade 2- Debris in ear canal (not completely occluded) and erythematous ear canal, tympanic membrane may be partially obscured

Grade 3 - The ear canal is oedematous, erythematous, and occluded (often completely closed), and the tympanic membrane cannot be seen

Grade 4 - The tympanic membrane is obscured, perichondritis and pinna cellulitis, and signs of systemic involvement.

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54
Q

how do you manage otitis externa?

A

topical antibiotics combined with a steroid - ciprofloxacin/dexamethasone otic
simple analgesia
if there is canal debris then consider removal
micro suction
if infection is spreading consider oral antibiotics - flucloxacillin

if fungal give acetic acid/hydrocortisone otic

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55
Q

what is malignant otitis externa ?

A

it is an uncommon type of otitis externa that is found in immunocompromised individuals (90% of cases are found in diabetics)
where otitis externa extends into the mastiidand temporal bones

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56
Q

what is malignant otitis externa usually caused by?

A

pseudomonas aeruginosa

infection commences in the soft tissues of the external auditory meatus, then progresses to involve the soft tissues and into the bony ear canal

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57
Q

what are the key features in a history which suggest malignant otitis extra ?

A

Diabetes (90%) or immunosuppression (illness or treatment-related)
Severe, unrelenting, deep-seated otalgia
Temporal headaches
Purulent otorrhea
Possibly dysphagia, hoarseness, and/or facial nerve dysfunction

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58
Q

how is malignant otitis externa diagnosed ?

A

usually a CT scan is done

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59
Q

how is malignant otitis externa treated?

A

non-resolving otitis externa with worsening pain should be referred urgently to ENT
Intravenous antibiotics that cover pseudomonal infections

60
Q

what are some complication of otitis externa?

A

malignant otitis externa
mastoiditis
osteomyelitis
intracranial spread

61
Q

what is acute otitis media?

A

a bacterial infection of the middle ear which results from nasopharyngeal organisms migrating via the eustachian tube

more common in children because in children the eustachian tube is more horizontal

62
Q

what organisms usually cause acute otitis media?

A

Haemophilus influenzas
streptococcus pneumonia
Moraxella catarrhalis
Streptococcus pyogenes

viral causes: RSV and rhinovirus

63
Q

what are the risk factors for acute otitis media?

A 
age (6-24months) 
parental/passive smoking
previous URTI
enlarged adenoids 
bottle fed
dummy use 
GORD 
raised BMI inn adults

breast feeding is protective

64
Q

what are the clinical features of acute otitis media?

A 
pain 
malaise 
fever 
coryzal symptoms 
-usually last for a few days

on otoscopy - tympanic membrane will look erythematous and may be bulging - there may be a small tear visible with purulent discharge in the auditory canal

patients may have conductive hearing loss or a cervical lymphadenopathy

65
Q

when examining a patient with acute otitis media what is it important to do?

A

It is important to test and document the function of the facial nerve (due to its anatomical course through the middle ear). Examination should also include checking for any intracranial complications, cervical lymphadenopathy, and signs of infection in the throat and oral cavity.

66
Q

what are the differentials for acute otitis media?

A
  • chronic suppurative otitis media
  • otitis media with effusion
  • otitis externa
  • meningitis
  • mastoiditis
  • intracranial extension of infection
  • intracranial abscess
  • head and neck malignancies
67
Q

how would you investigate acute otitis media?

A

mostly diagnosed clinically
blood tests such as ESR and CRP may help confirm infective cause
discharge should be sent for fluid culture and blood cultures should be considered if patient shows signs of sepsis

68
Q

how is acute otitis media managed?

A
  • most cases will resolve spontaneously within 24 hours, nearly all within 3 days
  • simple analgesics and a wait and watch

if significant deterioration or disease progession give amoxicillin 5 day course

if allergic to penicillin give erythromycin or clarithromycin

69
Q

when should you prescribe antibiotics in otiitis media?

A
  • Antibiotics should be prescribed immediately if:
  • Symptoms lasting more than 4 days or not improving
  • Systemically unwell but not requiring admission
  • Immunocompromise or high risk of complications secondary to significant heart, lung, kidney, liver, or neuromuscular disease
  • Younger than 2 years with bilateral otitis media
  • Otitis media with perforation and/or discharge in the canal
70
Q

what are the complications of otitis media?

A 
mastoiditis 
meningitis 
facial nerve paresis 
intracranial abscess
sigmoid sinus thrombosis
chronic otitis media
71
Q

what is mastoiditis ?

A

the spread of the infection into the mastoid air cells
it presents clinically as boggy, erythematous swelling being the ear, which if left untreated progresses to push the pinna forward

any suspected cases should be admitted for IV antibiotics and investigated further via CT head if no improvement is seen after 24 hours of IV Abx

there is a higher risk of intracranial spread and meningitis, hence cases are often considered for mastoidectomy as definitive management if there is no improvement with IV Abx

72
Q

what is otitis media with effusion?

A

aka glue ear

it is a buildup of a viscous inflammatory fluid within the middle ear, resulting a conductive hearing impairment

73
Q

what is otitis media with effusion usually caused by?

A

usually caused by a combination of chronic inflammatory changes and Eustachian tube dysfunction either from infective causes or from occlusive masses

74
Q

what are the risk factors for otitis media with effusion?

A

bottle fed
paternal smoking
atopy - eczema, asthma
genetic disorders - e.g. CF or primary ciliary dyskinesia, craniofacial disorders

75
Q

what are the clinical features of otitis media with effusion?

A

difficulty hearing (conductive hearing loss) - in children you may notice difficulty with attention at school
sensation of pressure
there may be popping or crackling noises
there may be vertigo
the tympanic membrane will appear dull and the light reflex will be lost

76
Q

what investigations would you perform for otitis media with effusion?

A

usually diagnosed clinically on the basis of history and otoscopy findings

pure tone audiometry will reveal conductive hearing loss
tympaometry will show a reduced membrane compliance

In adults, a full ENT examination should be performed, including flexible nasoendoscopy (to exclude a post nasal space mass).

77
Q

how should you manage otitis media with effusion?

A

Otitis media with effusion in children can be managed in an outpatient setting. Approximately 50% of cases will resolve within 3 months; hence many cases are managed by ‘active surveillance’.

If no resolution is seen after 3 months, the management options can be divided into surgical and non-surgical:

  • Non-surgical – hearing aid insertion.
  • Surgical – myringotomy and grommet insertion.
    In the UK, NICE guidance recommends the insertion of Grommets for those with >3months of bilateral OME and hearing level in better ear <25-30dBHL.
    Any child with persistent disease and multiple grommet insertion should be considered for potential adenoidectomy
78
Q

what is chronic otitis media?

A

chronic infection of the middle ear cavity
caused by an ongoing inflammatory response within the middle ear (with granulation) and is typically associated with unresolved and resistance bacterial infections

often leads to hearing impairment

79
Q

what are the different types of chronic otitis media?

A

Mucosal COM – chronic inflammation secondary to a perforation.
The cause of the initial perforation may be infective, iatrogenic (e.g. grommet insertion), or trauma
Any associated discharge from the perforation is termed an ‘active’ mucosal COM, also known as ‘Chronic Suppurative OM’ (CSOM)
A dry perforation is referred to as ‘inactive’ mucosal COM

Squamous COM – discharge due to a cholesteatoma
Perforations deemed as ‘safe’ are those in the tubotympanic (anteroinferior) part of the tympanic membrane, as they carry a low risk of cholesteatoma
‘Unsafe’ perforations are in the atticoantral (posterosuperior) aspect of the tympanic membrane, as they are associated with high risk of cholesteatoma

80
Q

what are the risk factors for chronic otitis media?

A

recurrent acute otitis media
traumatic perforation of the TM
insertion of grommets
craniofacial abnormalities s

81
Q

what are the clinical features of chronic otitis media?

A

chronically discharging ear (>6weeks) in the absence of fever or otalgia

on examination tympanic membrane will be perforated

It is important to test facial nerve function and document this clearly. Hearing loss can occur, which is nearly always conductive hearing loss, unless the disease is extensive

82
Q

what investigations should you perform for chronic otitis media?

A

audiograms and tympanometry
swabs may be useful

if any suspicion of cholesteatoma the CT warranted

83
Q

how should you manage chronic otitis media?

A

aural toileting with micro suction
topical antibiotic/steroid treatments until symptoms reduce/resolve

surgery may improve hearing

84
Q

what is cholesteatoma?

A

A cholesteatoma refers to a pocket of ectopic epithelium which grows in the attic of the middle ear. In this condition, epithelial cells naturally shed within this pocket but cannot escape the middle ear and so the collection grows

85
Q

what are the clinical features of cholesteatoma?

A

conductive hearing loss on a background of chronic otitis media

congenital cholesteatoma are rare and difficult to detect

86
Q

how do you diagnose cholesteatoma?

A

Diagnosis is made clinically during examination whereby a pearly, keratinized, or waxy mass in the attic region is seen. These are best seen when a perforation of the TM is present, providing a window into the middle ear.

CT scan should be arranged pre operatively for surgical planning and guide clinical suspicion

87
Q

how is cholesteatoma managed?

A

surgery to remove the entire cholesteatoma or it will recur

88
Q

what is epistaxis?

A

bleeding from the nose

89
Q

what are the two types of epistaxis?

A

Anterior bleeds – originate from ruptured blood vessels in Little’s area, a highly-vascularised region formed by the anastomosis of 5 arteries, and cause around 90% of cases

Posterior bleeds – originate from the posterior nasal cavity, typically from branches of the sphenopalatine arteries of the nose, and cause around 10% of cases (more common in older patients)

90
Q

what is littles area?

A

Little’s area (also known as Kiesselbach’s plexus) is found on the anterior nasal septum and is an anastomosis of 5 arteries: anterior ethmoidal artery, posterior ethmoidal artery, sphenopalatine artery, greater palatine artery, and the septal branch of the superior labial artery.

91
Q

what are some causes of epistaxis ?

A 
trauma (e.g. nose picking)
hypertension 
iatrogenic (e.g. anticoagulants)
foreign bodies
coagulopathies
platelet disorders
vascular malformations
vasculitis 
rhino sinusitis (including allergies)
malignancies 
cocaine use
92
Q

why should every case of epistaxis be initially approached as severe?

A

a patient having a large bleed may be bleeding posteriorly and swallowing a large volume of blood, therefore showing seemingly little external bleeding

93
Q

how should a non-life threatening epistaxis be managed?

A

management should occur in a stepwise manner

  • all patients should be kept sat up and sat forward (to ensure the blood is passing out anteriorly through the nostrils and not posteriorly to the pharynx
  • compression should be applied to the anterior nose for 20 minutes without releasing pressure, ice can be applied to the bridge of the nose to stimulate further vasoconstriction
  • if unsuccessful, a thudichum can be used to inspect the septum, if an anterior bleed point is identified, the vessel can be cauterised using silver nitrate. The oropharynx should also be examined in all patients the check for features of a posterior bleed
  • if there is too much blood present to visualise the septum, adrenaline soaked gauze can be inserted into the nasal cavity to cause localised vasoconstriction and soak up any excess blood
94
Q

what is the further management for epistaxis when initial management has failed to stop the bleed?

A

if no bleeding point can be visualised anterior packing should be trialled.

ensure routine bloods (FBC, clotting, group and save) have been sent - manage any reversible underlying causes

if epistaxis persists and bleeding entering oropharynx, posterior packing with foley catheter is warranted.

if nasal packing fails to stop bleeding, then the blood vessels can either be ligated surgically or embossed radiologically

95
Q

what are some causes of nasal obstruction?

A

> Infectious (viral, bacterial or fungal infections causing rhinitis/rhinosiusitis)
allergy inflammation with or without nasal polyps
Developmental -resulting in septal deviation, bony deviation or both, cleft lip
traumatic
iatrogenic (surgery causing scar tissue)
Drugs
neoplastic
inflammatory/systemic disease e.g. granulomatosis with polyangiitis, churg-stauss, sarcoidosis, CF

96
Q

how should you manage nasal fractures?

A
  • they don’t need to be X-rayed
  • if patient well, no epistaxis and no septal haematoma they can be sent home
  • if no change in shape or no new nasal obstruction then they don’t need to be seen by ENT specialist (however if lots of bruising and swelling which may be hiding deformity review in 5-7 days in and ENT emergency clinic for assessment of the injury

they may need manipulation under anaesthesia but there are associated risks -pain, bleeding, the need to wear a splint, failure to get the nose back to its original shapee

97
Q

when is a septoplasty and a septorhinoplasty done

A

When the underlying midline cartilaginous or bony septum is deviated, a septoplasty can be undertaken to remodel and improve the functional nasal airway.

A septorhinoplasty may be indicated if the septum and bony vault are deviated.

both of these done 6-12 months after injury

98
Q

what is rhinitis?

A

inflammation of the lining (mucous membranes) of the nose, characterised by nasal congestion, a runny nose, sneezing, itching and post-nasal drip

it can be divided into allergic and non-allergic

99
Q

what is rhino sinusitis?

A

inflammation of the lining of the nose and paranasal sinuses.

it has a number of manifestations, the commonest symptoms being anterior or posterior rhinorrhea (runny nose or post-nasal drip), nasal blockage/congestion or obstruction, and facial headache or reduction in sense of smell

100
Q

what happens if a nasal septal haematoma is left untreated?

A

irreversible septal necrosis may develop within 3-4 days - this is thought to bed to pressure-related ischaemia of the cartilage resulting in necrosis and may lead to a saddle nose deformity

101
Q

what it allergic rhinitis and how is it classified?

A

inflammatory disorder of the nose where the nose become sensitised to allergens such as house dust mites and grass, tree and weed pollens.

seasonal: symptoms occur around the same time every year
perennial: symptoms occur following exposure to particular allergens within the work place

102
Q

what are the clinical features of allergic rhinitis?

A 
sneezing 
bilateral nasal obstruction 
clear nasal discharge 
post nasal drip 
nasal pruritus
103
Q

how should allergic rhinitis be managed?

A

allergen avoidance
mild/moderate intermitted or mild persistent symptoms - oral (e.g. cetirizine, loratadine, fexofenadine)or intranasal (azelastine nasal) antihistamines. 2nd line - leukotriene receptor antagonist

if more severe intranasal corticosteroid - beclometasone (beconase) nasal spray can be used
a short course of oral corticosteroids are occasionally needed to cover important life events

there may be a role for short courses of topical nasal decongestants (e.g. oxymetazoline). They should not be used for prolonged periods as increasing doses are required to achieve the same effect (tachyphylaxis) and rebound hypertrophy of the nasal mucosa (rhinitis medicamentosa) may occur upon withdrawal

104
Q

what are causes of non-allergic rhinitis?

A
  • Irritants: tobacco, pollution, cleaning products (occupational)
  • Vasomotor: temperature changes- especially cold, dry air
  • Gustatory: Spicy food
  • Pharmacological: rhinitis medicamentosa (rebound nasal
  • congestion following prolonged use of topical decongestants),
  • substance abuse- cocaine
  • Infection
  • Systemic- Granulomatosis with polyangitis (GPA), sarcoidosis.
  • Physiological- exercise, positional, hormonal
  • Atrophic rhinitis
105
Q

what are the symptoms of non-allergic rhinitis?

A
  • nasal congestion
  • rhinorrhea
  • post nasal drip
  • hyposmia (reduced ability to smell)
106
Q

what investigations might you perform for non-allergic rhinitis?

A

allergy testing to exclude allergic causes

107
Q

how do you manage non-allergic rhinitis?

A
  • avoidance of tiggers e.g. stop smoking
  • intranasal antihistamine - azelastine nasal
  • intranasal saline irrigation can also be added
  • intranasal corticosteroids

if rhinorrhoea is predominant
- intranasal ipratropium

108
Q

what is acute rhinosinusitis ?

A

it is a common condition

it is characterised by inflammation of the mucosal linings of the nasal passage and paranasal sinuses

109
Q

what are the three main types of acute rhinosinusitis?

A

> viral rhinosinusitis - most commonly caused by rhinovirus and coronavirus

> post viral rhinosiusitis - residual mucosal inflammation following a viral infection that produces ongoing symptoms

> bacterial rhinosinusitis - usually preceded by a viral infection which predisposes the mucosa to bacterial infection. the most common causative organisms are s. pneumoniae, H. influenzae, M. catarrhalis and S. aureus

110
Q

what are some risk factors for acute rhinosinusitis?

A 
smoking 
air pollution exposure
anatomical variations such as septal deviation, nasal polyps or sinus hypoplasia
anxiety or depression 
asthma or diabetes
111
Q

what are the clinical features of acute rhinosinusitis?

A

symptoms must be lasting for less than 12 weeks

sudden onset of two or more of the following symptoms:

  • nasal obstruction
  • discoloured nasal discharge
  • facial pain or pressure
  • altered sense of smell

symptoms <10 days - acute viral
symptoms >10 days to 4 weeks - acute bacterial

112
Q

what symptoms may suggest a bacterial cause of acute rhinosinusitis?

A

severe local pain
discoloured discharge
fever
worsening after initial improvement (post-viral)

113
Q

how do you manage suspected acute viral sinusitis ?

A

analgesics/antipyretics
decongestants can be used - oxymetazoline nasal or pseudoephedrine.

nice reccomends that intranasal corticosteroids may be considered if the symptoms have been present for more than 10 days or if they are worsening after 5 days. And also they may need oral antibiotics.

114
Q

how is acute bacterial sinusitis managed?

A

antibiotics - amoxicillin/clavulanate

plus analgesics/antipyretic, plus decongestant plus intranasal corticosteroid

if no improvement after 7-14 days of treatment or the presence of red-flag symptoms, referral to ENT services should be considered.

115
Q

what are the red flag symptoms in acute sinusitis?

A
  • Eye signs, including periorbital swelling or erythema, displaced globe, visual changes, ophthalmoplegia.
  • Severe unilateral headache, bilateral frontal headache, or frontal swelling.
  • Neurological signs or reduced conscious level.
116
Q

what are the complication of acute sinusitis?

A
  • preseptal cellulitis, orbital cellulitis or abscesses
  • osteomyelitis - infection invading the bone can eventually lead to penetration into the skill vault causing intracerebral complications
  • pott’s puffy tumour (osteomyelitis of the frontal sinus can result in a soft boggy swelling over the overlying tissues on the forehead)
  • intracranial abscesses
  • venous sinus thrombosis
117
Q

what is chronic sinusitis?

A

inflammation of the nasal mucosa and paranasal sinuses for >12 weeks. Its pathophysiology is complex, involving interactions between the dysfunctional nasal mucosa and environmental factors.

can be divided into chronic sinusitis with or without polyps

118
Q

what are the risk factors for chronic rhinosinusitis?

A 
asthma or atopy
aspirin sensitivity 
ciliary impairment 
smoking
immunosuppression
119
Q

what are the clinical features of chronic sinusitis?

A

it can be diagnosed if two or more of the following symptoms are present for >12 weeks

  • nasal obstruction
  • discoloured nasal discharge
  • facial pain or pressure
  • altered sense of smell
120
Q

what are the differentials for chronic sinusitis?

A

recurrent acute sinusitis
malignancy - consider in cases of unilateral nasal polyposis, the presence of blood stained discharge, or eye signs
foreign bodies

121
Q

how is chronic sinusitis investigated?

A

nasal endoscopy is required and at least on of the following should be present

  • mucosal swelling
  • mucopurulent discharge
  • mucosal occlusion of middle meatus
  • nasal polyps
122
Q

how is chronic sinusitis managed?

A

The treatment of chronic rhinosinusitis is dependant on the severity of symptoms. This can be assessed via a severity Visual Analogue Score (VAS) score, in addition to examination of the nasal cavity.

Mild disease (VAS 0-3 with no significant mucosal disease) – treated with nasal saline douching and topical steroid spray or drops.
Moderate to severe disease (VAS >3 with significant mucosal disease) – requires long term antibiotics with topical steroids and a CT imaging of the sinuses
Refractory cases should be considered for surgical intervention (FESS). After surgery, it is important that topical treatments are continued.

FESS=functional endoscopic sinus surgery

123
Q

what are the complications of chronic sinusitis?

A

mucocoele - a collection of mucus in an epithelial lined cavity.
they are rare and most commonly in the frontal sinus and usually present with a lump on the forehead - in the long term them can erode bone and invade local structures such as the orbit and the brain.

124
Q

what are the different types of nasal polyp?

A

Inflammatory/Allergic Polyps – sino-nasal polyposis, often
multiple grey, oedematous polyps associated with CRS

Antro-choanal polyp – single polyp arising from maxillary sinus
extending out towards nasopharynx causing unilateral nasal
obstruction.

125
Q

what are nasal polyps associated with?

A 
asthma* (particularly late-onset asthma)
aspirin sensitivity*
infective sinusitis
cystic fibrosis
Kartagener's syndrome
Churg-Strauss syndrome
126
Q

what are the features of nasal polyps?

A

nasal obstruction
rhinorrhoea, sneezing
poor sense of taste and smell

unusual symptoms which always require further investigation include unilateral symptoms or bleeding

127
Q

how are nasal polyps managed?

A

steroid based treatment (a short course of oral steroid followed by intra nasal drops) combined with nasal saline rinses

surgical

128
Q

what is Samter’s triad?

A

Samter’s Triad is a chronic condition defined by asthma, sinus inflammation with recurring nasal polyps, and aspirin sensitivity. It’s also called aspirin-exacerbated respiratory disease (AERD), or ASA triad

129
Q

what is cleft lip and what are the variants of it?

A

A cleft is a gap or split in the upper lip and/or roof of the mouth (palate) resulting in an abnormal connection between the oral and
nasal cavity.

commonest variants are:

  • isolated cleft lip
  • isolated cleft palate
  • combined cleft lip and palate
130
Q

what problems occur with cleft lip and palate ?

A

feeding - orthodontic devices may be helpful
speech - with speech therapy 75% of children will develop normal speech
increased risk of otitis media for cleft palate babies

131
Q

what nerve supplies muscles of mastication?

A

trigeminal nerve

132
Q

what nerve supplies muscles of facial expression?

A

facial nerve

133
Q

what are the three major salivary glands ?

A

parotid gland - large serous salivary glad anterior and inferior to the ear,

Submandibular gland - mixed serous and mucous salivary gland

Sublingual Gland - mucous glad

134
Q

what are the states of swallowing?

A
  1. Oral Stage (voluntary)
    Oral preparatory - Food bolus is formed and held in the anterior part
    of the oropharyngeal cavity. The oral cavity is closed posteriorly by
    the soft palate and tongue to prevent leakage into the pharynx
    Oral Propulsive - The dorsum of the tongue gradually propels the
    food bolus to the back of the oral cavity
  2. Pharyngeal Stage (involuntary-
    CNIX)

The soft palate elevates and closes the nasopharynx at the same
time as the bolus comes into the pharynx- this prevents bolus
regurgitation into the nasal cavity
The larynx is closed, elevated and tucked under the base of the
tongue to prevent aspiration.
The pharyngeal constrictor muscles contracts from top to the bottom,
squeezing the bolus inferiorly

  1. Oesophageal Stage
    The food bolus enters the upper oesophageal sphincter, which
    includes the cricopharyngeus muscle. This muscle relaxes at the
    arrival of the food bolus
    Peristalsis propels the food bolus at a rate of 4cm/s towards the
    lower oesophageal sphincter which also relaxes
    Gravity aids peristalsis in the upright position
135
Q

when asking about a lump in the neck what questions would you ask about the HPC?

A 
What made you notice the lump?
How many lumps have you noticed?
Where do you notice the lump?
Has the lump changed in size?
Is the lump always there or does the lump come and go?
How long have you had the lump?
136
Q

when taking a history from someone with a neck lump what associated symptoms would you ask about?

A

Has the lump been painful at all?
Any sore throat?
Have you had any difficulties swallowing?
Have you had painful swallowing?
Have you had any problems with breathing?
Any coughs or colds?
Have you noticed any blood?
Have you noticed any weight change?
Have you had any ear pain?
Have you noticed any sweating at night/ temperatures?
Has your voice changed?

137
Q

what are the red flag symptoms for a neck lump which need urgent referral ?

A
  • Hard and fixed lump
  • Associated otalgia, dysphagia, stridor, or hoarse voice
  • Epistaxis or unilateral nasal congestion
  • Unexplained weight loss, night sweats, or fever or rigors
  • Cranial nerve palsies
  • non healing ulcers
  • white or red lesion in the mouth or oropharynx
138
Q

what are the differential diagnosis for neck lumps?

A
  • Infective – Reactive lymphadenopathy, atypical mycobacterium
  • Neoplastic – Lymphoma, head and neck cancer, metastatic disease
  • Vascular – Carotid body tumour, glomus jugulare
    Inflammatory – Sarcoidosis
  • Traumatic – Haematoma
  • Autoimmune – Thyroid disease (such as Graves’ disease, Hashimoto’s disease)
  • Congenital – Cystic hygroma, thyroglossal cyst, branchial cyst, dermoid cyst, teratoma
139
Q

Cystic hygroma

A

benign fluid filled sac caused by a malformation of the lymphatic system - they can be found anywhere on the body but classically present in the axilla or posterior triangle of the neck
classically on the left side
Most are evident at birth, around 90% present before 2 years of age

140
Q

carotid body tumour

A

benign neuroendocrine tumours that arise from the paraganglion cells of the carotid body.

presents as a pulsatile painless neck lump often with a bruit present on auscultation

they are slow growing but can become large enough to compress surrounding cranial nerves leading to palsies

they may need surgical excision
radiotherapy may be an option for tumours that are unresectable

141
Q

thyroglossal cyst

A

congenital fluid filled sac, commonly presenting in younger patients (typically less than 20 years)

they present as a palpable painless midline mass that present with profusion of the tongue. when infected, they can increase in size and become painful.

removed with the sistrunk procedure

142
Q

Branchial cyst

A
  • congenital masses which are oval and mobile and arise in the lateral aspect of the neck, typically anterior to the sternocleidomastoid.
  • the cyst is filled with acellular fluid with cholesterol crystals and encapsulated by stratified squamous epithelium
  • they usually present in early adulthood
  • when infected they become painful

larger branchial cysts can result in dysphagia, dysphonia and difficulty breathing

surgical excision is the definitive treatment

Care needs to be taken when managing these patients as a common differential diagnosis is a cystic metastasis from a squamous cell carcinoma of the head and neck region. As such, an ultrasound-guided FNA is an important investigation prior to arranging for excision of the mass.

143
Q

when a patient presents with a neck lump what would be suggestive of lymphoma?

A

Rubbery, painless lymphadenopathy
The phenomenon of pain whilst drinking alcohol is very uncommon
There may be associated night sweats and splenomegaly

144
Q

when a patient presents with a neck lump what would be suggestive of reactive lymphadenopathy?

A

By far the most common cause of neck swellings. There may be a history of local infection or a generalised viral illness

145
Q

when a patient presents with a neck lump what would be suggestive of thyroid swelling?

A

May be hypo-, eu- or hyperthyroid symptomatically

Moves upwards on swallowing

146
Q

when a patient presents with a neck lump what would be suggestive of pharyngeal pouch?

A

More common in older men
Represents a posteromedial herniation between thyropharyngeus and cricopharyngeus muscles
Usually not seen but if large then a midline lump in the neck that gurgles on palpation
Typical symptoms are dysphagia, regurgitation, aspiration and chronic cough

147
Q

how would you investigate a neck lump?

A

history and examination of the lump
if suspicious will require an USS +/- fine needle aspiration (FNA)

if further imaging is needed the CT or MRI scan can be carried out - CT provides visualisation of bony anatomy, whilst MRI provides soft tissue detail and delineation of abnormalities in the oral cavity or oropharynx
CT and MRI also aid in the management of head and neck cancer, including staging disease, detecting metastases, and radiotherapy planning

Phase 3b (34 decks)

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