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Otology | Flashcards

1
Q

What are the 3 interpretations of dizziness?

A
  1. Presyncopal
  2. Dysequilibrium
  3. Vertigo
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2
Q

What are the clinical features of presyncopal dizziness (3)?

A
  1. Light-headedness
  2. Faintness
  3. Weak at the knees
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3
Q

Where should patients with presyncopal dizziness be referred to?

A

Cardiology, falls and funny turns clinic

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4
Q

What is dysequilibrium?

A

A feeling of unsteadiness, especially in elderly

  • momentary feelings of unsteadiness
  • veering to the side
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5
Q

What is the pathophysiology of dysequilibrium?

A

Small vessel disease in brain related to aging.

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6
Q

What is the prognosis and management of dysequilibrium

A

Self-limiting

no treatment

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7
Q

What are the clinical features of vertigo (5)?

A
  1. Feeling like they are rotating, or surroundings are
  2. Usually in horizontal plane but can be vertical plane (floor comes up)
  3. Nausea + vomiting
  4. May have diarrhoea
  5. Palor
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8
Q

What are important features in the clinical history of vertigo (6)?

A
  1. Details of first attack - important as it can give clues to pathology
  2. Duration of rotational attacks (not the nausea etc after)
  3. Temporal pattern - frequency of attacks
  4. Precipitating factors e.g. movement in positional vertigo, discharge, preceded by infection
  5. Other symptoms e.g. migraine, tinnitus, hearing loss
  6. Drugs - especially sedatives affecting NS/CVS
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9
Q

What is important in the examination for vertigo?
Ear (1)
Neuro (3)
Special tests (4)

A

Ear
1. Otoscopy

Neuro

  1. Cranial nerves
    - nystagmus
    - Past-pointing
  2. Disdidokynesis (cerebellar ataxia)
  3. Heel-toe walking

Special tests

  1. Dix-hallpike (BPPV)
  2. Head thrust/impulse test (peripheral vestibular system for vestibular ocular reflex)
  3. Unterberger’s gait (labyrinth pathology)
  4. Romberg test - useful (proprioception)
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10
Q

What could be a finding on otoscopy in a patient with vertigo?

A

Middle ear infection - can spread to the inner ear and affect the vestibular system causing vertigo

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11
Q

What would the degree of nystamus in a patient with vertigo show?

A

1st degree - present only when looking in the direction of the quick component
-happens over a longer period of time

2nd degree - if it is also present when looking straight ahead
-slightly longer duration insult

3rd degree - present when looking in the direction of the quick component, when looking straight ahead and when looking in the direction of the slow component
-acute insult

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12
Q

Which cranial nerves in particular should be examined in a patient with tinnitus and what could lesions of the nerve indicate?

A

Trigeminal V - lesions of the vestibulocochlear (CNVIII) nerve such as acoustic neuromas can extend up and compress the trigeminal nerve

Facial VII - in close proximity to the vestibulocochlear (CNVIII)

Accessory XI and Hypoglossal XII - Large acoustic neurones or glomus jugulari tumours may extend down and affect the bulba nerves

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13
Q

What would a Romberg test in a patient with vertigo show?

A

Patients with vestibular, peripheral lesions, when they close their eyes in the Romberg test will either sway which is noticible or gets worse when the eyes open

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14
Q

What does the Dix-Hallpike test diagnose?

A

Benign paroxysmal positional vertigo (BPPV)

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15
Q

How does the Dix-Hallpike test work?

A

Patients are lowered quickly to a supine position with the neck extended and turned to affected side by the clinician performing the maneuver. A positive test is indicated by patient report of a reproduction of vertigo and clinician observation of nystagmus (rotational and down towards floor).

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16
Q

What is benign paroxysmal positional vertigo (BPPV)? What is it caused by?
(3)

A
  1. The most common diagnosable from of vertigo
  2. Typically characterised by patients complaining of positional vertigo when the look up, down, or turn in bed, lasting secs/mins
  3. Occurs spontaneously or occasionally after head injury
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17
Q

Some ENT causes of dizziness (6)?

A
  1. BPPV
  2. Meniere’s disease
  3. Benign vestibulopathy
  4. Acute labrinthine failure e.g. due to acute otitis media or cholesteatoma
  5. Vestibular neuronitis
  6. Migrainous vertigo
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18
Q

What is Menieres disease? What is its pathophysiology?

A

Condition of the inner ear that causes sudden attacks of vertigo, tinnitus, (ear pressure) and hearing loss.

Thought to be due to fluid imbalance in the inner ear but exact mechanism is uncertain

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19
Q

What are the presenting features (triad) of Menieres disease?

A

1st: Rotational vertigo lasting from 15 mins to 24 hours
2nd: During or prior to the attack: Onset of tinnitus in infected ear/if tinnitus is already present, it gets louder
3rd: During or following the attack, the patient notices a deterioration of hearing in the infected ear

(Patients can also have a feeling of pressure/fullness in the ear)

Features 1-3 are critical ones for diagnosis

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20
Q

How often does Menieres disease present and what are the changes over time?

A

Attacks come in clusters or can be spaced apart by weeks, months and occasionally years

The period of time it takes for the hearing to recover becomes shorter and the hearing thresholds in the affected ear drop, giving an asymmetrical sensoneural hearing loss

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21
Q

What is Unterberger’s gait? How is it tested?

A

Means of identifying which labyrinth may be dysfunctional in a peripheral vertigo.

Procedure: ask the patient to undertake stationary stepping for one minute with their eyes closed. A positive test is indicated by rotational movement of the patient towards the side of the lesion

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22
Q

What is Romberg’s test? How is it tested?

A

The patient is asked to stand with the feet together. If the patient is steady with eyes open but unsteady with eyes closed then Romberg’s sign is positive.

Positive in patients with sensory ataxia and negative in cerebellar ataxia (in cerebellar disease they are unsteady eyes open or closed)

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23
Q

What does the head thrust/impulse test show and how is it tested?

A

Detects unilateral hypofunction of the peripheral vestibular system caused mainly by acute vestibulopathy - normally,a functional vestibular system will identify any movement of the head position and rapidly correct eye movement accordingly so that the centre of the vision remains on a target. A corrective saccade indicates a positive test and a diagnosis of vestibular as opposed to brainstem disease can be made

Procedure:

  1. Examiner holds patients head and asks them to stare at a fixed point, e.g. examiners nose
  2. When the head is turned towards the normal side the vestibular ocular reflex remains intact and eyes continue to fixate on the visual target
  3. When the head is turned towards the affected side, the vestibular ocular reflex fails and the eyes make a corrective saccade to re-fixate on the visual target
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24
Q

What are the broad systematic categories of causes of dizziness (4)?

A
  1. ENT or peripheral i.e. vertigo
  2. CVD i.e. presyncopal
  3. Central i.e. disequilibrium
  4. (Drug-induced)
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25
Q

What is vertigo almost always associated with?

A

Nausea and/or vomiting

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26
Q

What are peripheral vestibular problems characterised by?

A

Vertigo

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27
Q

What area involvement does hearing loss and tinnitus point to?

A

Cochlear involvement

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28
Q

What are the investigations of BPPV (3)?

A
  1. ENT exam
  2. Neuro exam
  3. Dix-Hallpike test
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29
Q

What is the management of BPPV (2)?

A
  1. Reassurance

2. Positional manoeuvre exercises: Epley, Semont, Cawthorne-Cooksey and Brant-Daroff exercises

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30
Q

What is the prognosis of BPPV?

A

Usually gets better spontaneously over 12-18 months

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31
Q

How is meniere’s disease investigated (4)?

A
  1. ENT exam
  2. Neuro exam
    - horizontal nystagmus
    - Tuning forks shows SNHL on affected side
  3. Pure tone audiometry - SNHL on affected side
  4. MRI in all cases to exclude acoustic neuroma
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32
Q

What is the treatment of meniere’s disease (4)?

A
  1. Sponaneously resolves so reassurance
  2. During acute phase - Bucastem (anti-sickness) and bed rest
3. Prophylaxis - salt restriction and bendroflumethiazide (thiazide diuretic) in morning
OR if fails:
Cinnarize (antihistamine)
OR if fails:
Betahistine (histamine agonist)
OR if fails:
Prochlorperazine (Bucastem)
OR if fails:
Refer to ENT
  1. Surgery for resistant cases
    - Intratympanic gentamicin (chemical neurectomy - vestibular ablation)
    - OR Vestibular nerve section
    - OR Labyrinthectomy
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33
Q

What ddx must you consider in all patients with unilateral inner ear symptoms?

A

Acoustic neuroma

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34
Q

What is benign vestibulopathy and its cause? What are its clinical features?

A

Unknown cause

Clusters of attacks of vertigo, similar to Meniere’s but without otological symptoms of hearing loss/tinnitus. Usually in middle aged people.

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35
Q

What is the prognosis of benign vestibulopathy (2)?

A

Usually resolves in about 2 years

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36
Q

What is the treatment of benign vestibulopathy (2)?

A
  1. Reassurance

2. Cawthorne-Cooksey exercises

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37
Q

What is acute labyrinthine failure?

A

Sudden loss of labyrinth function

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38
Q

What are some causes of acute labyrinthine failure (6)?

A
  1. Idiopathic
  2. Viral
  3. Local vascular occlusion
  4. Fracture of the temporal bone through labyrinth
  5. Occasionally post-surgery
  6. Rarely due to bacterial labyrinthitis secondary to acute otitis media or cholesteatoma
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39
Q

What is the typical history of acute labyrinthine failure (4)?

A
  1. Person of any age
  2. Sudden attack of deafness and severe vertigo, nausea and vomiting
  3. The vertigo is usually prostrating and the patient is confined to bed, afraid to move
  4. Moderate-profound hearing loss
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40
Q

What investigations are done for acute labyrinthine failure (4)?

A
  1. ENT exam
  2. Tuning fork test - SNHL on affected side
  3. Audiogram - Moderate to profound SNHL
  4. Neuro exam
    - Nystagmus
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41
Q

How long does an attack of acute labyrinthine failure last?

What is its course of disease?

(3)

A
  1. Attack usually lasts 10 days to 3 weeks
  2. There is gradual improvement of vertigo
  3. SNHL often does not recover
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42
Q

What is the treatment of acute labyrinthine failure (6)?

A
  1. Admit for symptomatic treatment of vertigo
  2. IV fluids
  3. Anti-emetics
  4. Vestibular sedatives
  5. i.v. plasma expanders and inhaled carbogen given to try improve blood supply to labryrinth
  6. Steroids if possible autoimmune aetiology
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43
Q

What is vestibular neuronitis? What is it caused by?

A

Infection of the vestibular nerve in the inner ear

Usually viral in aetiology

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44
Q

What is the typical history of vestibular neuronitis (2)?

A
  1. Sudden onset of vertigo with nausea, vomiting and nystagmus BUT without hearing loss/tinnitus
  2. Often bed ridden for 3-4 days
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45
Q

Where does vestibular neuronitis need to be managed?

How long does it usually last?

A

Can be managed at home, by GP
Admission is rarely needed

Usually spontenously resolves in 6 months

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46
Q

What is the epidemiology of vestibular neuronitis?

A

Occurs in small epidemics

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47
Q

What is the treatment of vestibular neuronitis?

A

Symptomatic - vestibular sedatives/antiemetics

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48
Q

What is migrainous vertigo?

A

Patients with vertigo who don’t satisfy the conditions of vestibular neuronitis and have a history of migraines

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49
Q

How is migrainous vertigo treated?

A

Amitriptyline nocte

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50
Q

What should be prescribed for vomiting? what should not be prescribed?

A

Bucastem, not prochlorperazine

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51
Q

Which drug is best for controlling vertigous symptoms?

A

Cinnarizine 30mg tds

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52
Q

What is labyrinthitis? How long does it last?

A

Infection of the inner ear

Usually spontaneously resolves in 6 months

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53
Q

Where would you refer an elderly patient to presenting with multiple pathologies?

A

ENT

Falls and funny turns clinic

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54
Q

When would you consider referring a vertigo patient to ENT?

A

After trying to manage in the community medically for 6 months

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55
Q

What are the broad categories of some central causes of dizziness (3)?

A
  1. CNS origin
  2. Basilar migraine
  3. Presbystasis
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56
Q

What causes arising from the CNS present with dizziness (5)?

A
  1. Space occupying lesion e.g. infratentorial tumours (cerebellar)
  2. Degenerative disease e.g. MS, cerebrellar degeneration (due to ageing)
  3. Head injury
  4. Intoxication
    - Alcohol
    - Barbiturates
  5. Vascular processes
    - vertebro-basilar ischaemia
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57
Q

What is a cause of basilar migraine?

A

Transient ischaemic attack (TIA)

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58
Q

How does a TIA present (5)?

A
  1. Widely varied
  2. Ataxia
  3. Gradual onset of unsteadiness
  4. Central vertigo - mild and NOT ASSOCIATED with nausea or vomiting, hearing loss or tinnitus
  5. OTher symptoms and signs of cerebellar or brainstem lesions
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59
Q

What is Presbystasis? What are its clinical features?

How is it treated?

A

Occurs in the elderly, an episode of unsteadiness lasting a few seconds, worse on movement.
No LOC, nausea or vomiting

Usually improves spontaneously so no treatment needed

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60
Q

What are some presyncopal/cardiovascular causes of dizziness (6)?

A
  1. Postural hypotension
  2. Hypertension
  3. Cardiac arrythmias
  4. Vasovagal
  5. Drugs
  6. Hyperventilation
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61
Q

How does presyncopal/cardiovascular causes of dizziness present (4)?

A
  1. Syncope, light-headedness
  2. Vague unsteadiness
  3. Faints
  4. Symptoms of gloal ischaemia
    - Blackouts with LOC
    - Fainting or feeling of light headedness on long standing
    - carotid sinus syndrome
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62
Q

What are the different types of hearing loss (3)?

A
  1. Conductive
  2. Sensorineural hearing loss
  3. Central hearing loss
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63
Q

What is conductive hearing loss?

A

The prevention or partial prevention of the sound pressure waves in the air reaching the inner ear

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64
Q

What is Sensori neural hearing loss?

A

A problem with the reception and transmission of the information from the cochlear, the hair cells convert the mechanical energy of the sound pressure waves into the electrical energy and transmits them into the CNS

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65
Q

What is central hearing loss?

A

Pathology of the higher centres

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66
Q 
What are causes of conductive hearing loss?
Outer ear (2)
Middle ear (9)
A

Outer ear:

  1. Ear wax
  2. Otitis externa (but oedema has to be so great that the pus fills the canal. Suspect otitis media)
Middle ear disease:
1.  Acute supprative otitis media
2. Chronic supprative otitis
3. Glue ear/otitis media with effusion
4. Cholesteatoma
5. Tympanosclerosis/
myringosclerosis
6. Otosclerosis
7. Tympanic membrane perforation
8. Trauma
9. Tumours
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67
Q

What is otitis media with effusion (glue ear)?

non-suppurative otitis media

A

A sterile collection of fluid in the middle ear cleft resulting in conductive deafness. The viscous properties are due to mucus glycoproteins, mucins, non-purulent

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68
Q

What would OME show on audiometry/tympanometry?

A

Audiometry: a conductive deafness of 10-40 DB

A flat tympanogram

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69
Q

What is the course of OME?

A

Usually resolves spontaneously in a few weeks

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70
Q

What are risk factors for developing OME (4)?

A
  1. Large adenoids
  2. Previous acute suppurative otitis media
  3. Cleft palate
  4. May follow an URTI
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71
Q

How often is a child followed up at ENT clinic for glue ear?

A

If glue ear confirmed at first attendance at the ENT clinic, the child is re-evaluated at 3/12

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72
Q

Which children get grommet insertion?

A

Those who are re-evaluated at 3/12 and their glue ear has not spontaneously resolved

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73
Q

What is the function of the grommet?

A

To aerate the middle ear, not to drain it

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74
Q

Can children swim with grommets?

A

Yes - no evidence to suggest they can’t

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75
Q

How long do grommets stay in?

A

They extrude spontaneously around 9 months after insertion, but can stay up to 2 years.

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76
Q

What are the complications of persistent OME (2)?

A

Thinning of the tympanic membrane giving rise to:

  1. Retraction pockets
  2. Collapse of the tympanic membrane
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77
Q

What do you need to exclude when an adult presents with unilateral glue ear?

A

Carcinoma of the postnasal space obstructing the Eustachian tube orifice

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78
Q

What is acute otitis media?

A

Inflammation of the middle ear, can be viral (50%) or bacterial in origin

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79
Q

What is the pathophysiology that occurs with an acute suppurative otitis media (3)?

A
  1. Pus forms and the inflamed tympanic membrane bulges outwards - very painful
  2. The drum ruptures and the pus, accompanied by blood drains intp the external auditory meatus
  3. The ear drum heals within 4-5 days
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80
Q

What is acute suppurative otitis media?

A

Otitis media that has purulent effusions, caused by a bacterial infection

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81
Q

What is the treatment of ASOM (2)?

A
  1. First line is amoxicillin + clavulanic acid (Augementin)

2. Myringotomy (incision in tympanic membrane) if condition fails to resolve/facial nerve palsy occurs

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82
Q

What is a life-threatening complication of inadequate treatment of ASOM?

A

Brain abscess

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83
Q

What is a cholesteatoma?

A

A bag of deep meatal skin that protrudes into the middle ear. It continues to produce keratin which fills the bag. Anaerobic bacteria breed there and produce a purulent foul smelling discharge

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84
Q

What is the treatment of cholesteatoma (3)?

A
  1. First: medical management with topical Abx and microsuction of debris from retraction pocket

But frequently needed for established disease:
2. Surgical removal with mastoidectomy under GA

  1. Regular follow up with toileting of any mastoid cavity created
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85
Q

How do complications of cholesteatoma occur?

A

The cholesteatoma erodes through to different areas, causing complications

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86
Q

What are the complications of cholesteatoma and how do they occur (6)?

A
  1. Bag erodes through ossicles causing conductive deafness of >50 dB
  2. Erodes through lateral semicircular canal causing vertigo
  3. Erodes into the 7th (facial) nerve canal causing facial palsy
  4. Erodes into the cochlear causing a SNHL which can be partial or total
  5. Erodes through the roof (tegment) into the brain causing an intracranial abscess or sepsis
  6. Erodes into the signoid sinus and causes thrombosis
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87
Q

What is a retraction pocket and when does it become a cholesteatoma?

A

Indrawing of the tympanic membrane and is self-cleansing. When debris accumulates it is a cholesteatoma

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88
Q

Where are retraction pocket patients followed up?

A

ENT out-patients

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89
Q

What is tympanosclerosis/

myringosclerosis?

A

Calcification of collagenous scar tissue on tympanic membrane originating from previous infection or trauma

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90
Q

What are the possible outcomes of tympanosclerosis/

myringosclerosis (2)?

A
  1. May just appear as a chalky patch on the drum causing no symptoms
    OR
  2. May totally obliterate the middle ear resulting in a 50 dB plus deafness - at this point it is beyond surgery
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91
Q

What is otosclerosis?

How does it present (5)?

A

Spongy bone formation around the oval window in the middle ear - it grows and fuses with the stapes causing a conductive deafness

  1. 3rd decade
  2. Slowly progressive, bilateral conductive deafness
  3. Tinnitus
  4. Sometimes, mild vertigo
  5. Later, can affect cochlear leading to mixed SNHL
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92
Q

What is the genetic inheritance of otosclerosis?

A

A familial condition which is Mendelian dominant with incomplete penetration

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93
Q

What is the treatment of otosclerosis?

A

A stapedectomy (replacing the stapes with a prosthesis) or hearing aid can restore hearing to normal

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94
Q

What is chronic suppurative otitis media (CSOM)?

A

Disease of the middle ear mucosa which gets repeatedly infected. It is often hypersecretory and hypertrophic forming micro abscesses and inflammatory cell infiltrates. Perforation may or may not be present

95
Q

What are the clinical features of CSOM (3)?

A
  1. Odourless chronic discharge if a perforation is present
  2. Discharge ranges from clear mucus to mucopus
  3. Conductive deafness
96
Q

What is the treatment of CSOM if:

  1. Disease confined to middle ear
  2. If mastoid is involved (CT evidence)
A

Confined to middle ear:

  1. Medical: topical Abx, topical steroids, microsuction
  2. Grafting the drum (myringoplasty) if TM damaged

If mastoid is involved:
A cortical mastoidectomy and myringoplasty

97
Q

What is a fatal complication of CSOM?

A

Intracranial sepsis

98
Q

What are chronic dry perforations of the ear drum caused by?

A

A result of viral infections in childhood

99
Q

What are the indications for treatment of chronic dry perforations of the eardrum (2)?

A
  1. Causing significant deafness
  2. Preventing someone’s admission to a profession/sport e.g. swimming

Otherwise, can be left alone

100
Q

What is the treatment of chronic dry perforations?

A

Myringoplasty

101
Q

What signs would lead you to suspect a tumour in the mastoid cavity (2)?

A
  1. Usually occur where previous mastoid surgery has been performed
  2. Suspect if patient with previously stable mastoid cavity complains of discharge, which may be blood stained and associated with pain
102
Q

What type of trauma would affect the ears?

A

Skull base fractures

103
Q

What are the 2 consequences of skull base fractures leading to ENT problems?

A
  1. Haemotympanum

2. Ossicular fracture or disruption

104
Q

What is haemotympanum? What are the clinical features?

3

A

Blood in middle ear

  1. The drum looks dark red or blue, it may be lacerated
  2. Conductive loss of 30 dB or less present
  3. A CSF leak may be present
105
Q

How is a haemotympanum treated?

A

Do not intervene - blood wil be reabsorbed spontaneously and tympanic membrane will heal

CSF leak will seal spontaneously

Treat to prevent 2o infection

106
Q

What does a unilateral rhinitis indicate?

A

CSF leak

107
Q

What are the clinical features of ossicular fracture/ disruption (4)?

A
  1. Blood in middle ear
  2. May be a perforated tympanic membrane
  3. May have CSF leak
  4. Hearing loss of around 50dB
108
Q

How is ossicular fracture/ disruption managed?

A

Wait for blood to be reabsorbed then put things right as it does not resolve spontaneously

109
Q

Conditions causing sensorineural deafness (9)?

A
  1. Presbyacusis
  2. Acoustic neuroma
  3. Sudden sensorineural hearing loss
  4. Noise-induced hearing loss
  5. Non-organic hearing loss
  6. Meniere’s disease
  7. Barotrauma and perilymph fistula
  8. Trauma to ear and skull base
  9. Ototoxicity
110
Q

What is presbyacusis?

A

Hearing loss due to aging, that is wear and tear on the outer hair cells.
Most common cause of sensorineural deafness

111
Q

What are the clinical features of presbyacusis (2)?

A
  1. Bilateral and symmetrical

2. Usually have a high frequency loss i.e. difficulty with consonants

112
Q

At what age is the lower limit of presbyacusis?

A

50

113
Q

What does audiometry show for presbyacusis?

A

Loss of high frequency hearing

114
Q

Are vowels or consonants lost in presbyacusis?

A

Consonants

115
Q

What problems do patients with presbyacusis often describe (3)?

A
  1. The words merge together and speech is muffled
  2. Can function well on a ‘one to one’ basis but have difficulty with group conversation and when there is background noise
  3. The major problem is speech discrimination rather than the perception of loudness
116
Q

What is the treatment of presbyacusis (4)?

A
  1. Reassurance - most are worried about becoming deaf
  2. Emphasis their good low and mid frequency hearing - good for morale
  3. Explain to family the special problems caused by high frequency loss as this makes everyone more tolerant
  4. Hearing aids
117
Q

What is an acoustic neuroma?

A

Benign, slow-growing tumours that arise from the Schwann cells surrounding the vestibular division of the vestibulocochlear nerve (CNVIII)

118
Q

What is the earliest symptom of an acoustic neuroma?

A

Unilateral hearing loss or tinnitus

119
Q

Why is early detection and removal of an acoustic neuroma important?

A

Mortality and morbidity from surgery is directly related to tumour size

Removal of large tumours can compromise the blood supply to the brain stem and preservation of the facial nerve is rarely possible

120
Q

What investigations should be done for an acoustic neuroma (2)?

A
  1. Pure tone audiometry

2. MRI or CT

121
Q

What is the treatment of an acoustic neuroma?

A

Gamma-knife - a sophisticated x-ray gun

122
Q

What should patients with unilateral or asymmetrical SNHL always be screened for?

A

Acoustic neuroma

123
Q

What is the urgency of a sudden SNHL?

A

A medical emergency, patients need urgent ENT treatment

124
Q

What is a sudden SNHL defined as?

A

Defined as a loss greater than 30dB in three contiguous frequencies, occurring over a period of less than three days

125
Q

What is the prognosis of sudden SNHL?

A

Low frequency losses recover better than high frequency deficits

126
Q

What symptom is an unfavourable factor in the prognosis of sudden SNHL?

A

Severe vertigo

127
Q

What is the early (3) and late (1) management of sudden SNHL?

A

Early:

  1. Bed rest
  2. Vasodilators
  3. Steroids** - prednisolone 40mg for 5 days

Late:
1. Exclude an acoustic neuroma or other disease in auditory system

128
Q

What is noise-induced hearing loss?

A

Inner ear damage caused by sudden acoustic trauma e.g. gunfire or by prolonged exposure to excessive noise.

129
Q

What does the audiogram typically show for noise-induced hearing loss?

A

A notch at 4, 6 and less commonly 3KHz with gradual involvement of the lower frequencies with continued exposure

130
Q

What are the protection benefits of cotton wool plugs?

A

Keep dust out the ear canals

Do not protect from noise

131
Q

What is non-organic hearing loss?

How is it diagnosed?

A

People pretending to have hearing loss usually for compensation purposes following head injury or alleged injurious exposure to noise

Audiometry

132
Q

Which groups of drugs are ototoxic (4)?

A
  1. Aminoglycosides
  2. Diuretics e.g. frusemide
  3. Salicylates
  4. Chemotherapeutic agents
133
Q

What is ototoxicity?

A

Exposure to drugs or chemicals that damage the inner ear or the vestibulo-cochlear nerve

134
Q

What is the treatment of ototoxicity?

A

Prevention - it is irreversible

135
Q

What are the symptoms of ototoxicity (3)?

A
  1. Partial or profound hearing loss
  2. Vertigo
  3. Tinnitus
136
Q

What is barotrauma and perilymph fistula?

A

Sudden pressure changes e.g. during diving, can rupture the membranes causing leakage or perilymph into the middle ear cavity or mixing of the biochemically different fluids in the inner ear, resulting in SNHL, tinnitus and vertigo

137
Q

What does sudden hearing loss, tinnitus and vertigo following barotrauma indicate?

A

Perilymph fistula

138
Q

What types of temporal bone fractures can occur?

A

Longitudinal - 80%

Transverse - 20%

139
Q

What are the complications of a transverse temporal bone fracture?

A

Damage to inner ear and facial nerve

140
Q

What are the 2 types of tinnitus?

A
  1. Subjective (intrinsic)

2. Objective (extrinsic)

141
Q

What is subjective (intrinsic) tinnitus?

A

Hallucination of noises in the head or ears

142
Q

What does a short burst of tinnitus <15 minutes indicate?

A

This is physiological and is a result of outer hair cell activation. This is normal. If longer than 15 mins it is pathological

143
Q

What is objective (extrinsic) tinnitus?

A

A noise in the head or ears that can be heard by another individual

144
Q

What is the management of tinnitus that is:

  1. Bilateral (8)
  2. Unilateral (1)
A

Bilateral:

  1. Reassurance
  2. Referral to tinnitus clinic to help them cope if severe
  3. Coping strategies e.g. masking tinnitus with background noise i.e. with music
  4. Counselling
  5. Hearing aid for those with hearing impairment - by hearing better, they ignore the tinnitus
  6. Night time sedation
  7. Tinnitus maskers e.g. white noise
  8. Support groups

Unilateral:
1. Needs to be investigated

145
Q

What does a tinnitus that is synchronous with the pulse indicate?

A

A carotid body tumour

146
Q

What are the symptoms of a carotid body tumour (4)?

A
  1. Pulsatile tinnitus
  2. Hearing loss (conductive or SNHL)
  3. Facial paralysis
  4. Paralysis of cranial nerves IX to XII
147
Q

What do you find in the examination of someone with a carotid body tumour (4)?

A
  1. Pulsatile red mass behind ear drum
  2. Audible bruit over the temporal bone
  3. Facial paralysis
  4. Paralysis of cranial nerves IX to XII
148
Q

What is the treatment of a carotid body tumour (2)?

A
  1. Surgery
  2. Radiation therapy
    or
    Combination
149
Q

What must you investigate for if a patient presents with a discharging ear and a VII nerve palsy?

A

Cholesteatoma

150
Q

What is otitis externa?

A

Inflammation of the external ear canal (external auditory meatus)

151
Q

What are the 3 main types of otitis externa?

A
  1. Diffuse
  2. Furuncle
  3. Malignant
152
Q

What is diffuse otitis externa?

A

Generalised inflammation of ear canal

  • Can be part of a generalised skin condition e.g. eczema
  • Can be localised due to trauma e.g. from cotton buds
153
Q

What are the 2 broad causes of diffuse otitis externa?

A
  1. Generalised skin condition e.g. eczema

2. Localised due to trauma from cotton buds etc

154
Q

What are the 3 groups of infective causes that can cause diffuse otitis externa?

A
  1. Bacteria
  2. Fungal
  3. Virus
155
Q

Which 2 types of bacteria can cause diffuse otitis externa?

A
  1. Pseudomonas (2o colonisation)

2. Staph. aureus

156
Q

Which 2 types of fungi can cause diffuse otitis externa?

A
  1. Candida

2. Aspergillus

157
Q

Which type of viruses can cause diffuse otitis externa?

A

Herpes zoster

158
Q

What are 2 non-infective causes of diffuse otitis externa?

A
  1. Allergic/irritant e.g. shampoos

2. Neurodermatitis as part of anxiety disorders

159
Q

What are 5 symptoms of diffuse otitis externa?

A
  1. Itchiness
  2. Irritation
  3. Pain and swelling
  4. Otorrhoea
  5. Deafness due to occlusion of EAM
160
Q

What are 3 signs of diffuse otitis externa?

A
  1. Pain on moving pinna or inserting speculum
  2. Otorrhoea
    - Bacterial: pus and debris in EAM
    - Fungal: Dry/wet debris or yellow/black spores
    - Viral: Vesicles around EAM introitus, soft palate or haemorrhagic vesicles on TM, thin watery blood-stained discharge
  3. Enlarged pre and post-auricular and upper deep cervical lymph nodes may be present
161
Q

What does the presence of mucus in EAM indicate?

A

That the infection is coming from the middle ear and there is perforation of the TM as the EAM does not contain any mucus secreting glands

162
Q

What is the treatment of diffuse otitis externa?
Necessary (3)
Optional (3)

A

Necessary:

  1. Analgesia
  2. Aural toilet - MUST remove debris by dry mopping or suction clearance
  3. Topical medication
    - Abx/steroid ear drops i.e. gentamicin+hydrocortisone 2 weeks
    - OR Astringents i.e. aluminium acetate
    - OR anti-infective drops i.e. Locorten-Vioform for 1 week

Optional:

  1. Ribbon gauze wick/Pope otowick can help drops reach deeper aspects of EAM
  2. Abx/steroid ointment can be injected or applied on a dressing in the EAM
  3. Systemic abx for gross cellulitis
163
Q

What are the possible outcomes of diffuse otitis externa after treatment (3)?

A
  1. Most cases respond to simple treatment
  2. Infection can spread to the whole of the pinna (cellulitis) requiring systemic Abx
  3. Some patients are ‘prone’ to recurrent infections
164
Q

Why is aural toilet/topical medication necessary for treating diffuse otitis media?

A

Systemic abx given without aural toilet and/or topical medication can lead to recurrence as infected debris may remain in the EAM when skin inflammation has settled

165
Q

Why should Abx/steroid ear drops i.e. gentamicin+hydrocortisone only be used for 2 weeks in diffuse otitis media?
What checks need to be done

A

Possibility of ototoxicity

Baseline audiometry

166
Q

Why should anti-infective drops i.e. Locorten-Vioform only be used for 1 week in diffuse otitis media?

A

Risk of fungal infections

167
Q

How would you tell a patient to use ear drops?

A

Tell them to put drops in and lie down with the treated ear facing upwards for 10 mins

168
Q

What is furuncle otitis externa?

A

A painful infection of one of the hair follicles of the outer 1/3 of the EAM usually due to Staphylococcus

169
Q

What usually precipitates a furuncle otitis externa (2)?

A
  1. After one of the hairs have been plucked

2. After the EAM has been scratched

170
Q

What is the main sign of a furuncule otitis externa?

A

Red swelling arising from one aspect of the outer wall of the EAM bulging into the meatus

171
Q

How is furuncle otitis externa treated (3)?

A
  1. Analgesia
  2. Astringents i.e. glycerin and ichthammol
  3. Abx in severe infections when there is lymphadenitis
172
Q

What is malignant otitis externa?

A

An aggressive form of otitis externa, involving the temporal and adjacent bones. It is not a cancerous condition but can be lethal.

173
Q

What is the main causative agent of malignant otitis externa?

A

Pseudomonas aeruginosa

174
Q

What are risk factors for malignant otitis externa (2)?

A
  1. Diabetics

2. Immunocompromised

175
Q

What are the pathophysiological consequences of malignant otitis externa?

A

Spreads from EAM to bone causing an osteitis, severe pain and the VII, IX, X and XI cranial nerve palsies as it spreads across the skull base

176
Q

What is the treatment of malignant otitis externa?

A

High dose iv Abx

177
Q

What are main bacteria that cause acute otitis media (3)?

A
  1. Streptococcus pneumoniae
  2. Haemophilus influenzae
  3. Moraxella catarrhalis
178
Q

What commonly precedes acute otitis media?

A

URTI

179
Q

Which group of patients are most commonly affected by acute otitis media?

A

Children

180
Q

What are the symptoms of acute otitis media (5)?

A
  1. Hearing loss
  2. Pain
  3. Otorrhoea (when the TM bursts)
  4. Pyrexia
  5. Systemic upset
181
Q

What is a sign on examination in acute otitis media?

A

Red bulging TM

182
Q

What is the cause of pain in acute otitis media?

A

The inflamed eardrum bulges outwards due to the formation of pus under pressure causing pain

183
Q

When does the pain get relieved in acute otitis media?

A

The drum frequently ruptures and the pus, often accompanied by blood, enters the outside world with relief of the pain

184
Q

How long does the ear drum take to heal in acute otitis media?

A

4-5 days

185
Q

What is the treatment of acute otitis media (3)?

A
  1. First line is amoxicillin
  2. Myringotomy required if:
    - condition fails to resolve
    - facial nerve palsy
    - other dire neuro-otological complication
  3. Analgesia
186
Q

What is a fatal condition that occurs with neglect/inadequate treatment of acute otitis media?

A

Brain abscess

187
Q

What is a complication of AOM?

A

Acute mastoiditis

188
Q

What is the pathophysiology of acute mastoiditis?

A
  • Infection spreads from the middle ear cavity and pus forms in the mastoid air cells, causing bony erosion.
  • Pus may spread through the bone either subperiosteally or into the subcuticular region in the postauricular region
189
Q

What is the typical history of acute mastoiditis (5)?

A
  1. AOM that fails to settle plus:
  2. Persistent otalgia
  3. Otorrhoea
  4. Hearing loss
  5. Systemically unwell
190
Q

What does the presence of a unilateral headache indicate?

A

Sign of intracranial complication = emergency

191
Q

What signs may be found in acute mastoiditis (6)?

A
  1. Systemically unwell
  2. Canal full of pus
  3. Polyp may be seen through a perforated TM
  4. Sagging of the postero-superior canal wall
  5. Tenderness over the bone immediately above the ear canal (McEwen’s triangle)
  6. Pinna pushed forwardd if pus breaks through posteriorly and the skin becomes oedematous and erythematous
192
Q

What is the treatment of acute mastoiditis at:

  1. Early stages
  2. After 48 hours/if complicated
A

Early stages:
1. High dose iv abx in hospital

If does not settle after 48h or if complications arise:
1. Cortical mastoidectomy

193
Q

What are the complications that can occur with acute mastoiditis (5)?

A
  1. Subperiosteal abscess
  2. Facial nerve palsy
  3. Labyrinthitis
  4. Petrositis (spread medially into petrous bone causing V and VIth cranial nerve palsies)
  5. Spread outside to temporal bone
194
Q

Which complications of ear infections require urgent ENT referral (3)?

A
  1. Acute mastoiditis
  2. Intracranial sepsis/abscess
  3. Malignant/necrotising otitis externa
195
Q

What are the functions of the facial nerve (4)?

A
  1. Motor to muscles of facial expression
  2. To convey taste fibres from the tongue
  3. To convey taste from the palate
  4. To convey cutaneous sensation from an area of the external auditory meatus mediated in fibres carried by way of the vagus - these nerves are carried in a separate trunk (nervus intermedius) in the subarachnoid space and run with the VIIIth nerve
196
Q

Which gland does the facial nerve run through?

A

Parotid gland

197
Q

What are the main branches of the facial nerve (7)?

A
  1. Greater petrosal nerve
  2. Branch from the ganglion
  3. Branch to stapedius muscle
  4. Chorda tympani
  5. Postauricular nerve
  6. Main trunk supplying muscles of facial expression
  7. Cutaneous branches
198
Q

Function of the greater petrosal nerve?

A

Conveys taste fibres from palate

199
Q

Function of the branch from ganglion?

A

Joins the lesser petrosal nerve and auriculotemporal nerve to convey secretomotor fibres to parotid gland

200
Q

Function of the branch to stapedius muscle?

A

Restricts excessive movement of the stapes due to loud noise

201
Q

Function of the chorda tympani?

A

Conveys taste fibres from the taste buds to the brain via the lingual nerve

202
Q

Function of the postauricular nerve?

A

Motor to muscles of the ear and occipital belly of occipitofrontalis

203
Q

What are the 5 branches of the main trunk of the facial nerve which supply muscles of facial expression?

A
  1. Temporal
  2. Zygomatic
  3. Buccal
  4. Marginal mandibular
  5. Cervical
204
Q

Function of the cutaneous branches?

A

Supplies both sides of the pinna

205
Q

How do you distinguish if the facial nerve palsy is due to an upper or lower motor neurone lesion (2)?

A
  1. LMN lesion - forehead (eyebrow raise) is affected

2. UMN - Lower face involved with preservation of bilateral eyebrow raise

206
Q

What questions should you ask in the history of a facial nerve palsy (9)?

A
  1. Whether forehead is affected
  2. Onset - congenital/rapid/slowly progressive
  3. Severity - complete/incomplete
  4. Symptoms related to VII palsy - eye closure/drooling/hyperacusis
  5. Otological symptoms? - deafness/otorrhoea/otalgia/vertigo/tinnitus
  6. Other neuro symptoms? - CVA/MS/Guillain-bare
  7. Parotid disease? - Masses/pain
  8. Systemic illness? - Symptoms of infection/sarcoid
  9. Head/facial trauma? - Skull base fracture/stab injuries
207
Q

What would you examine in facial nerve palsy (4)?

A
  1. CNS: VII in particular
  2. Ear
  3. Parotid
  4. Oral cavity
208
Q

What facial movements would you ask the patient to do to check for VII nerve (3)?

A
  1. Raise eyebrow
  2. Closure of eyes
  3. Smile
209
Q

What scale can be used to grade facial nerve function?

A

House-Brackman scale

210
Q

What 4nerves would you also test for in the CNS exam other than VII in someone with facial nerve palsy?

A
  1. Vth
  2. VIIIth
  3. Lower cranial nerves
  4. Cerebellar function
211
Q

What would you check for in the ears of a patient with facial nerve palsy?

A

Signs of infection or tumour

212
Q

What would you check for in the parotid gland in a patient with facial nerve palsy?

A

Mass - malignant until proven otherwise

213
Q

What would you check for in the oral cavity in a patient with facial nerve palsy (3)?

A
  1. Vesicles
  2. Palatal weakness
  3. Oropharynx: displaced
214
Q

What can an oropharyngeal mass displacing the tonsil medially indicate?

A

A tumour of the deep lobe of the parotid gland

215
Q

How do you differentiate a tumour of the deep lobe of the parotid gland from a peritonsillar abscess?

A

The tumour is not associated with other signs of infection

216
Q

What are the grades in the House Brackmann scale?

A

I: Normal
II: Slight weakness noticeable only on close inspection
III: Obvious weakness but not disfiguring
IV: Severe reduction in movement - incomplete eye closure
V: Asymmetry at rest - motion barely perceptible
VI: Asymmetry at rest - no facial movement

217
Q

What investigations would be done for a patient with facial nerve palsy (4)?

A
  1. Pure tone audiogram
  2. Stapedial reflexes
  3. Electroneuronography - guide to progress and prognosis. Tests the facial nerve
  4. MRI/CT in some cases
218
Q

What are the main congenital causes of facial nerve palsy in children (2)?

A
  1. Moebius syndrome - genetic disorder associated with bilateral VII nerve palsy, can also affect VI and XII
  2. Hemifacial microsomia - congenital disorder affecting development of the lower half of the face, usually the ears, the mouth and the mandible. Usually one-sided
219
Q

What are the main acquired causes of facial nerve palsy in children (3)?

A
  1. Forceps delivery
  2. Chicken pox (herpes zoster)
  3. Acute OM
220
Q

What are the 5 broad locations of where causes of facial nerve palsy in adults (and children) occur?

A
  1. Peripheral
  2. Middle ear
  3. Petrous temporal bone
  4. Intracranial
  5. Causes where site is variable
221
Q

What are the 4 peripheral causes of facial nerve palsy in adults?

A
  1. Trauma - forceps delivery as facial nerve is more superficial in early life
  2. Iatrogenic - damage from parotid/submandibular gland surgery
  3. Tumours - malignant parotid tumours including lymphoma
  4. Inflammatory conditions of the parotid e.g. sarcoidosis
222
Q

What are the middle ear causes of facial nerve palsy in adults (3)?

A
  1. Iatrogenic - Mastoid surgery of any kind
  2. Infection
    - Discharging ear and facial nerve palsy is an emergency
    - Cholesteatoma
    - AOM
    - Mastoiditis
    - Herpes zoster
  3. Tumours
    - SCC, rhabdomyosarcoma (children)
    - glomus jugulare (rare, slow-growing, hypervascular tumors that arise within the jugular foramen of the temporal bone) or glomud tympanicum (benign tumour of the middle ear)
223
Q

What are the petrous temporal bone causes of facial nerve palsy in adults (2)?

A
  1. Trauma - transverse fractures of the skull
  2. Tumour
    - Squamous cell, metastases
    - Petrous apex cysts/cholesteatoma
224
Q

What are the intracranial causes of facial nerve palsy in adults (4)?

A
  1. Tumour
    - Acoustic neuromas
    - Facial nerve neuromas
    - Meningioma
    - Carcinomatous meningitis
  2. Iatrogenic - skull base surgery
  3. Vascular - stroke
  4. Neurological e.g. MS
225
Q

What are the site variable causes of facial nerve palsy in adults (3)?

A
  1. Bell’s palsy - idiopathic lower motor palsy of VII nerve (diagnosis of exclusion)
  2. Infection - Ramsay-Hunt syndrome caused by herpes zoster virus
  3. Guillain-Barre syndrome
226
Q

What is the Tavener’s criteria for Bell’s palsy (4)?

A
  1. Acute onset
  2. Hemi-facial
  3. no CNS pathology
  4. No ear pathology
227
Q

What is the outcome and the treatment for Bell’s palsy?

A

Signs recovery begin within 2 months and 90% of patients have a satisfactory return of facial function

Oral steroids can help speed recovery if given early

228
Q

What are the clinical features of Ramsay-Hunt syndrome (5)?

A
  1. Facial palsy (often severe and irreversible)
  2. Facial pain
  3. Vesicles in the ear canal, pinna (and soft palate)
  4. +/- Sensorineural deafness
  5. +/- Vertigo
229
Q

What are the treatment principles of facial nerve palsy (2)?

A
  1. Eye care - reduced eye closure means the eye is more prone to drying and corneal abrasions which can lead to blindness
  2. General
230
Q

What are the eye care treatment options of facial nerve palsy (3)?

A
  1. Artificial tears - hypormellose drops and Lacrilube ointment
  2. Eye patch used at night
  3. Opthalmology opinion - temporal lateral tarsorrhaphy (lateral eyelid sutures) or gold weight in the eye may help eye closure
231
Q

What are the general treatment options for facial nerve palsy (3)?

A
  1. Oral steroids in Bell’s palsy and Ramsay Hunt syndrome if there are no contraindications
  2. Acyclovir can also be given if facial weakness is severe
  3. Facial slings for restoring facial symmetry in permanent weakness
232
Q

What does a progressive facial nerve palsy indicate?

A

Tumour

233
Q

What is the management of Bell’s palsy (5)?

A
  1. Reassurance - signs of recovery usually begin within 2 months and 90% of patients have a satisfactory return of facial function
  2. Oral steroids
  3. Acyclovir if facial weakness severe
  4. Eye care:
    - Artificial tears
    - Eye patch at night
    - Opthalm opinion
  5. If facial weakness does not resolve, facial slings can be inserted to restore facial symmetry
234
Q

What factors are associated with poor prognosis in the recovery of Bell’s palsy (4)?

A
  1. Increasing age
  2. Associated pain
  3. Complete palsy
  4. Increased latency to onset of recovery

ENT (4 decks)

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