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Special Senses > The Ear > Flashcards

The Ear Flashcards

1
Q

what do we want to know in hx of an otological complaint?

A

otalgia, itchy ear, irritated ear, sensation of aural fullness, ear popping e.g. glue ear
otorrhoea
tinnitus
hearing loss-onset and rate of progression
vertigo

*is it 1 or both ears?-anything unilateral is more worrying!
URT symptoms
noise exposure
previous ear surgery
previous ear infections

ototoxic drugs e.g. aminoglycosides, bumetanide
FH of hearing loss
work, leisure-swimming

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2
Q

what disease of autosomal dominant inheritance is associated with the development of bilateral vestibular schwannomas?

A

neurofibromatosis 2

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3
Q

severe unilateral sensorineural hearing loss may produce what results with tuning fork tests, and how can the test be repeated to alter these results?

A

webers test: sound lateralises to functional ear as would be expected with SN hearing loss
rinnes test: normal ear is rinnes +ve as expected (AC greater than BC so sound loudest with tuning fork held in front of ear) but abnormal ear may have a false Rinne -ve with BC greater than AC as BC is heard in the normal ear by skull crossover.
therefore must mask good ear-use a noise emitter, and rpt test.

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4
Q

if a pt has a R ear SN hearing loss, what will tuning fork test results be?

A

Webers-sound lateralises to the good L ear
Rinnes-R ear Rinne +ve with AC greater than BC as both AC and BC reduced so sound heard loudest with tuning fork held in front of ear, L ear Rinne +ve

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5
Q

if a pt has a L ear conductive hearing loss, what will tuning fork test results be?

A

Webers-sound lateralises to L ear

Rinnes-L ear Rinne -ve with BC greater than AC, R ear Rinne +ve

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6
Q

which tuning fork test is more sensitive?

A

Weber test

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7
Q

how are hearing tests performed in young children?

A

up to 6months, gold standard=electric response audiometry-evoked potential in CN VIII, brainstem or auditory cortex recorded using skin electrodes following cochlea acoustic stimulation=objective test.
from 6 mnths to 18 mnths, distraction test-child turns to a noise-basic screening test for all children
from 2 yrs various conditioning or cooperation tests

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8
Q

how does the sign of nystagmus-an involuntary eye movement, differ between central and peripheral vestibular disorders?

A

peripheral=usually horizontal nystagmus

central=nystagmus in other directions

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9
Q

3 parts of the vestibule?

A

utricle
saccule
semicircular canals

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10
Q

most reliable method of assessing hearing thresholds?

A

pure tone audiograms

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11
Q

most common cause of acquired conductive hearing loss in children?

A

otitis media with effusion (glue ear):
middle ear fluid present with intact TM, related to Eustachian tube dysfunction impairing normal mechanical ventilation of middle ear.
diagnosis made when fluid present behind TM for 3 months or more

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12
Q

clinical features of otitis media with effusion?

A

in children, hearing loss-may be assoc. speech delay and problems at school, may be lack of concentration or recurrent otalgia which may be assoc. with fullness or popping.
may be hx of recurrent ear infections, URTIs or nasal obstruction.
may occasionally be balance problems
otoscopic examination: increased prominence of handle and short process of malleus due to retracted TM, and slightly yellow appearance to TM due to middle ear effusion, dull TM-loss of light reflex.

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13
Q

results of pure tone audiogram and impedance tympanometry in otitis media with effusion (glue ear)?

A

PTA: conductive hearing loss, may fluctuate down to 40dB, =air bone gap
IT: flat line-type B normal volume, high volume of EAM would indicate tympanic membrane perforation

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14
Q

complications of grommets?

A

otorrhoea due to infection-can treat with anti-inflammatory drops, oral Abx if discharge follows an URTI, grommet removal if persistent otorrhoea
chronic TM perforation
not a complication but tympanosclerosis-common to see TM white patches following grommet extrusion but this doesn’t impair hearing.

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15
Q

glue ear management in children?

A

conservative-most cases settle within 3 mnths, so reassure parents, tell them to stop smoking if smoke and ensure speak facing their child, clearly, may have to increase volume and slow speech to aid child’s hearing.
hearing aid-if bilateral glue ear and hearing loss where surgery not acceptable or contraindicated.
early r/f may be considered if significant hearing difficulties, part. if developmental, social or educational difficulties, or if assoc. high risk condition e.g. Down’s.
surgical procedures if effusion persists: grommet insertion, may remain in TM for up to 1 yr before extrusion.
may follow myringotomy-surgical TM incision to drain fluid, and fluid aspiration.
adenoidectomy-reduce incidence of recurrent effusions by preventing ET blockage, do only if recurrent URT symptoms.

both surgeries reduce time with glue ear, and improve hearing short term

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16
Q

how are neonates screened for hearing loss?

A

otoacoustic emissions-sound played into the ear-clicks, functioning cochlea should produce an echo which is picked up by microphone in ear. no echo measured if hearing loss present, but hearing threshold cannot be measured.

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17
Q

how is sensation provided to the external ear?

A

upper lateral surface-auriculotemporal nerve (CN V3)
lower lateral surface and medial surface-C3-greater auricular nerve
superior medial surface-C2/C3-lesser occipital nerve
EAM-auricular branch of vagus nerve (CN X)

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18
Q

history of a patient with otosclerosis?

A

progressive hearing loss
often tinnitus
improved hearing in noisy surroundings during early disease stages
FH of otosclerosis

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19
Q

signs on examination of pt with otosclerosis?

A

most commonly normal

on otoscopy, rarely a pink hue to tympanic membrane=schwartze’s sign

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20
Q

what sign may be found on otoscopy of a patient with otosclerosis?

A

schwartze’s sign-pink hue to tympanic membrane

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21
Q

what investigations would we like to do in suspected otosclerosis?

A

conductive hearing loss may have been confirmed with weber and rinne’s tests
impedence tympanogram-normal type A trace
pure tone audiogram-conductive hearing loss-notable difference between bone and air conduction, relatively flat line with degree of hearing loss same at varying frequencies. and Carhart notch at 2kHz-depression in bone conduction.

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22
Q

management of otosclerosis?

A

hearing aid

stapedectomy

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23
Q

how can a particular feature of vertigo be used to distinguish between BPPV, menieres disease and vestibular neuronitis?

A

BPPV-vertigo lasts seconds to minutes
menieres disease-vertigo lasting mins to hrs
vestibular neuronitis-vertigo lasts several days.

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24
Q

management of menieres disease?

A

precise aetiology of disease unknown, but disease involves increased fluid in endolymphatic compartment (which sits within membranous labyrinth).
conservatively: dietary-reduce salt, alcohol, caffeine, chocolate, Chinese food

medical: thiazide diuretics e.g. bendroflumethiazide
betahistine-antivertigo drug with MOA involving increased H1 receptor stimulation on b.vessels in inner ear to reduce endolymphatic pressure through vasodilation allowing fluid drainage by osmosis, by direct H1 agonist effect and H3 antagonist effect
vestibular sedatives e.g. prochlorperazine-only for acute attacks, anti-emetic properties.

surgical: grommet insertion
dexamethasone middle ear injection
endolymphatic sac decompression
middle ear gentamicin injection to destroy vestibule-hair cell loss to stop fluctuations altering balance, but warn pt can canuse further tinnitus difficult to control.
surgical labyrinthectomy
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25
Q

the semicircular canals detect what type of movements?

A

rotatory movements in all directions due to each all canals being at right angles to one another

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26
Q

what movements do the utricle and saccule detect?

A

linear movements-acceleration and deceleration

utricle: hair cells point up-detect linear/horizontal movement
saccule: hair cells stick out to side-detect vertical movement.

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27
Q

what are the 3 semicircular canals?

A

anterior
posterior-most common site of otoliths causing BPPV
lateral

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28
Q

diagnostic test for BPPV?

A

Dix-Hallpike test

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29
Q

treatment of BPPV?

A

Epley manoeuvre

advice to patients: can resolve by itself
Brandt-Daroff exercises can be done at home

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30
Q

presentation of menieres disease?

A

episodic vertigo-lasting mins to hrs
unilateral tinnitus
fluctuating SN hearing loss, over time becomes permanent and persists as acute vertigo starts to reduce in disease course
aural fullness

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31
Q

what investigation should be performed when presentation is of clinical features of menieres disease to rule out an important differential?

A

MRI scan of internal auditory meatus

as presentation similar to that of a vestibular schwannoma-benign schwann cell tumour on superior vestibular nerve.

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32
Q

neurological examination of patient with vestibular neuronitis will reveal what?

A

horizontal nystagmus, but otherwise normal

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33
Q

what is vestibular neuronitis?

A

a viral infection of the vestibular nerve causing inner ear inflammation

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34
Q

presenting features of vestibular neuronitis?

A

severe incapacitating vertigo lasting several DAYS
nausea, vomiting, diarrhoea
usually unilateral disease
absence of SN hearing loss and tinnitus seen with labyrinthitis as no cochlear nerve involvment
horizontal nystagmus on examination
often assoc. long term vestibular defecit after acute episode-can cause generalised unsteadiness after acute episode for a no. of weeks while brain compensates.

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35
Q

management of vestibular neuronitis?

A

supportive: keep well hydrated, IV fluids if required
self-resolving in 1-2wks
vestibular sedatives e.g. prochlorperazine-max. dose TDS for up to 2wks
vestibular rehabilitation exercises e.g. cawthorne-cooksey exercises if pt suffering from prolonged poor balance after acute episode as vestibular hypofunction.

DON’T take vestibular suppressants AFTER acute attack as delays recovery.

warn pt can recur

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36
Q

management of sudden onset SN hearing loss?

A

this is an ontological emergency: 1/3 recover, 1/3 some recovery and 1/3 no recovery
investigations: confirm conductive or SN hearing loss with tuning fork tests, SN requiring urgent tment, could also use PTA-should do this along with MRI-exclude lesion along central auditory pathway e.g. acoustic neuroma

manage:
PO steroids, but can be injected into middle ear
anti-virals
hyperbaric O2, carbogen

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37
Q

what frequency tuning fork used in hearing tests, and what assumption is made when using tuning fork tests?

A

256 or 512 Hz

assume normal hearing in other ear

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38
Q

why is a sound hear loudest in affected ear with conductive hearing loss in weber test?

A

conductive loss in that ear blocks out background noise so relative to other ear tone will sound louder in that ear.

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39
Q

what is otosclerosis?*

A

stapes fixation onto oval window

cause of conductive hearing loss

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40
Q

why do patients with SN hearing loss in 1 ear have Rinne +ve test in that ear?

A

tuning fork heard louder when held lateral to EAM as still getting benefit of amplification of external and middle ear.

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41
Q

PTA features of conductive hearing loss?

A

normal bone conduction-line above 20dB on PTA
reduced air conduction thresholds-line below 20dB on PTA
so there is an air bone gap

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42
Q

what diagnoses would a PTA showing no air bone gap, and ‘ski slope’ appearance for both ears be consistent with?

A

bilateral SN hearing loss:

presbycusis

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43
Q

what is a tympanogram?

A

simple test measuring TM compliance via probe insertion into external ear canal
TM compliance then measured with varying amounts of pressure in external ear canal which is sealed by the probe
compliance peaks when pressure in canal equals that of middle ear.

44
Q

normal tympanogram result?

A

type A tracing:
peak centered on OdaPa on x axis, so normal middle ear pressure as compliance peaks at 0 which is when pressure in canal equals that of middle ear.

45
Q

what conditions give a type B tracing on a tympanogram?

A

this is a flat tracing
suggests middle ear effusion (e.g. otitis media with effusion) or TM perforation
differentiate the 2 by reading canal volume on side of tympanogram: effusion=normal canal volume (around 1cm^3 in adults) whereas perforation-much larger vol measured as measuring middle and external ear volume.

46
Q

what does a type C tympanogram tracing suggest?

A

this is a tracing where peak of TM compliance has a negative pressure-so pressure in middle ear must be -ve as peak is when canal pressure equals that of middle ear.
so suggests ET dysfunction.

47
Q

how is chronic otitis media divided?

A

active or inactive-depending on if ear discharging
mucosal or squamous disease

cholesteatoma=active squamous disease

48
Q

what is active mucosal disease in chronic otitis media?

A

discharging middle ear chronically, through a TM perforation

49
Q

can chronic otitis media be treated medically?

A

NOT if a cholesteatoma present-this necessitates surgery often with a mastoidectomy
yes if mucosal disease-may clear up with topical Abx and aural toilet

50
Q

risks of mastoid surgery for a cholesteatoma?

A 
complete hearing loss in operated ear
vertigo
tinnitus
CSF leak
facial nerve palsy
taste loss to anterior 2/3 of tongue-chorda tympani damage
disease recurrence
perichondritis
fistula into semicircular canals
51
Q

patients susceptible to acute otitis externa?

A

older patients
hx of eczema-eczematous ear canal skin
patients who stick things into their ears e.g. cotton buds, or use of hearing aids or ear plugs
*pushing wax further into ear canal then if water enters ear, desquamated keratin expands which can trap fluid that may then cause otitis externa. wax=combination of desquamated tissue and cerumen.
immunocompromised patients and diabetics susceptible to malignant otitis externa-part. aggressive infection which spreads from ear canal soft tissue into bone.
swimmers-water exposure
working in moist humid environment e.g. outside
ear radiotherapy
previous topical tments for OE or OM

52
Q

presentation of malignant otitis externa?

A

this is a spreading osteomyelitis of temporal bone caused by pseudomonas aeruginosa
chronic ear discharge despite topical treatment
deep seated severe ear pain
sometimes cranial nerve palsies, most commonly facial
mastoiditis
marked granulations in ear canal
significant mortality rate of around 10%

53
Q

organism causes of otitis externa?

A

bacteria and fungi
bacteria (90%): pseudomonas aeruginosa-most common, staph aureus, streptococci
fungi: aspergillus (90%), candida

54
Q

presentation of otitis externa?

A

discharging ear (otorrhoea)
otalgia
hx of itchy ear
muffled hearing-conductive hearing loss, later with ear canal oedema and debris accumulation
tragus pressure or pinna movement will cause discomfort
otoscopy-red ear canal, and may be thin discharge, debris, if more severe TM may be obscured by oedematous ear canal which may be completely closed.

55
Q

investigations in otitis externa?

A

rarely useful but if tment fails or recurrent episodes, consider ear swab for bacterial and fungal microscopy and culture.

56
Q

when can TM be considered to be perforated in patients with OE (*assess in consideration of appropriate tment?)?

A

if can taste medication placed in ear or
can blow air out of their ears with nose pinched or
has had tympanostomy tube inserted in prev year and no documentation of extrusion and TM closure.

57
Q

why are swabs in otitis externa not part. useful?

A

cultured organisms maybe contaminants rather than causing the disease, espec. likely fungal overgrowth when used antibacterial drops due to normal bacterial flora suppression
and reported bacterial sensitivity may not correlate with clinical outcomes as determined for systemic tment and must higher concentrations of Abx can be achieved with topical tment.

58
Q

acute otitis externa management?

A
  • remove or treat aggravating or precipitating factor
  • analgesic e.g. paracetamol or ibuprofen for otalgia relief
  • topical 7 day treatment-consider acetic acid 2% spray for mild discomfort and/or itching with no discharge or deafness
  • if more severe or acetic acid ineffective, give topical antibiotic with/without topical corticosteroid, e.g. ciprofloxacin (often in secondary care, but unlicensed) or gentamicin-consider ototoxicity and fungal superinfection and contact dermatitis, cloquinol (also fungal cover) and neomycin are BNF recommended antibacterials.
  • severe infection with extensive ear canal swelling may need ear wick insertion (soaked gauze) by ENT which expands if topical drops applied and is impregnated with medication, keeps ear canal open.
  • topical antifungals for fungal infection
  • consider oral Abx severe infection e.g. cellulitis beyond ear canal, ear canal swelling and can’t insert ear wick, immunocompromised
  • EAC may be cleaned with gentle syringing or irrigation, dry swabbing or microsuction-often secondary care r/f, to remove debris and allow topical drops to get to infection site.
  • appropriate self-care advice-avoid ear canal damage e.g. cotton buds, keep ears clean and dry-swimmers avoid pool for 7-10 days if OE ideally, well controlled chronic skin conditions, no need to avoid flying.
  • swab any discharge in resistant cases.
59
Q

management of malignant otitis externa?

A

admit to hospital-need IV antibiotic treatment
CT and isotope scanning used to provide info. on extent of osteomyelitis
will also need topical ABx treatment for extended time-ABx treatment usually for 6-8wks, using quinolones e.g. ciprofloxacin
insert wicks impregnated with antipseudomonal
may need debridement surgery with disease progression despite tment

60
Q

most common presentation of a cholesteatoma (active squamous chronic otitis media)?

A

foul smelling-due to underlying osteitis persistent or recurrent ear discharge
conductive hearing loss
mild ear discomfort
rarely with disease progression can be vertigo, SN hearing loss, facial nerve palsy, meningitis or intracranial abscess

61
Q

how is diagnosis of a cholesteatoma made on examination?

A

otoscopy: deep retraction pocket in TM, with or without granulation tissue and skin debris
crust-like lesion in upper part of TM with/without surrounding pus and sometimes assoc. perforation of adjacent TM
pearly white mass behind an intact TM if congenital cholesteatoma present

TM must be clearly visualised. if cannot be seen e.g. due to ear canal excessive purulent discharge, treat for infection then re-examine after tment, treat for OE if ear canal inflammation or OM if onset of discharge with acute pain onset. ENT r/f if TM cannot be seen after tment.

62
Q

why are children more susceptible than adults to acute otitis media?

A

Eustachian tube shorter and more horizontal in children allowing organisms from URTI e.g. strep pneumonia and haemophilus influenza, to more readily ascend the ET into the middle ear.

63
Q

clinical features of acute otitis media?

A

otalgia, young children may pull their ear
otorrhoea
pyrexia
tachycardia
blood stained discharge along with pain relief if TM perforates
may have cold like symptoms e.g. rhinorrhoea and loss of smell-more suggestive of viral cause of acute otitis media.

otoscopy: bulging red and congested TM

64
Q

a patient presents with severe otalgia and vesicles are notes on the concha, what is the likely diagnosis and appropriate management?

A

herpes zoster oticus/ramsay hunt syndrome
VSV infection of facial nerve ganglion, producing severe pain, ear canal and concha vesicles, and often facial palsy.
need antiviral e.g. aciclovir

65
Q

important cause of referred otalgia in adults not to be missed?

A

upper GIT or RT cancer e.g. oesophageal Ca

66
Q

usual location of TM perforations in recurrent acute otitis media?

A

pars tensa

67
Q

presentation and treatment of active mucosal disease in chronic otitis media?

A

persistent or recurrent mucoid discharge
hearing loss-conductive

initial tment of discharging ear is with aural toilet-cleaning out external auditory canal using microsuction or irrigation, combined with topical steroid eardrops
may require hearing aid to overcome hearing difficulties
if recurring discharge, patient is a regular swimmer (middle ear water will increase mucoid otorrhoea occurrence) or aim to produce hearing improvement may consider surgery-graft TM using patient’s temporalis fascia.

68
Q

what rare disease may be suggested by change in character of persistent otorrhoea from mucopurulent to bloody?

A

carcinoma of the ear, part. if pt also complains of otalgia, which patient may be predisposed to if uncontrolled middle ear infection or infection of mastoid cavities.

69
Q

importance of systemic Abx in temporal bone fracture?

A

CSF otorrhoea may occur, this may allow intracranial infection e.g. meningitis to develop?

70
Q

define a cholesteatoma

A 
keratinizing epithelium (squamous disease) in the middle ear with TM retraction as part of chronic otitis media with an actively discharging ear, pressure cause bone erosion, as might peripheral lesion release of osteolytic enzymes.
3 types: congenital-squamous epithelium trapping within temporal bone during embryological development, primary acquired cholesteatoma-thought related to chronic -ve middle ear pressure due to ET dysfunction, and secondary acquired-related to TM insult e.g. perforation secondary to acute otitis media so squamous epithelium can be implanted in middle ear, or grommet insertion for otitis media with effusion or recurrent AOM.
71
Q

management of a cholesteatoma?

A

definitive tment is surgical, but initial presentation with discharging ear may be managed with aural toilet and topical Abx e.g. ciprofloxacin, and in some pts may need granulation tissue debridement.
Mastoidectomy only if mastoid involvement. surgical=open mastoidectomy procedure (tympanomastoidectomy)=more invasive but more successful-single procedure usually sufficient but enlarging auditory meatus so hearing aids difficult to fit and can be dizziness on cold and water exposure, must have annual or biannual auditory canal cleaning.
closed tympanoplasty-higher risk of persistence or recurrence, so need 2nd look operation at 6-12mnths

72
Q

what investigations can be performed for a cholesteatoma?

A

CT-can assess lesion extent and look for bony defects, and will guide surgery
MRI-where concern about soft tissue involvement e.g. sigmoid sinus thrombosis and epidural abscess.

73
Q

acquired causes of conductive hearing loss?

A 
otitis externa
wax
FB
otitis media with effusion (glue ear)
chronic otitis media including cholesteatoma and active mucosal disease (TM perforation)
otosclerosis
ossicular disruption
74
Q

acquired causes of sensorineural hearing loss?

A 
trauma-noise, head injury, surgery
degenerative-presbycusis
inflammatory-meningitis, syphilis, chronic otitis
ototoxicity-aminoglycosides, cytotoxics
neoplastic-acoustic neuroma
menieres disease
labyrinthitis
75
Q

congenital causes of hearing loss?

A

conductive-ossicular abnormalities, ear atresia
SN-genetic e.g. alport syndrome-commonly X-linked
rubella (prenatal)
perinatal: hypoxia, jaundice

76
Q

RFs in children for glue ear?

A

most follow episode of acute otitis media, part. in children under 3 years of age
most common in children aged between 1 and 6, in winter time
craniofacial malformations e.g. cleft palate
down’s syndrome, allergic rhinitis and cystic fibrosis where ciliary motility impaired
male
frequent URTIs
parents who smoke

=then occurs due to 1 or more of: ET dysfunction preventing adequate aeration of middle ear, low grade infection, chronic colonisation of adenoids, persistent inflammation, adenoid infection or hypertrophy.

77
Q

causes of ET dysfunction that can cause glue ear in adults?

A

severe NP infection e.g. sinusitis which inflames ET openings
severe or chronic allergy
anatomical blockage: severe nasal septum deviation with an obstructed airway
large tonsils and adenoids
NP tumour e.g. Chinese patients
head and neck radiation following Ca treatments
H and N surgery
secondary inflammation from allergic rhinitis
frequent upper resp infection

trauma-barotrauma e.g. post diving, flying

78
Q

how is glue ear investigated in children?

A

must note often spontaneous resolution some sometimes active observation for 3 mnths all that is required
r/f for hearing tests-pure tone audiometry in child of 4 yrs or older, usually evidence of conductive hearing loss-air bone gap, air conduction below 30dB on graph, may use distraction tests if younger than 4. rpt hearing test 3 months after 1st.

79
Q

typical symptoms of glue ear in adults?

A 
hearing loss
feeling of aural fullness
crackling or popping tinnitus
FB sensation in external auditory canal
mild, diffuse aural pain.
vague sense of unsteadiness without true vertigo
80
Q

which children does NICE recommend benefit most from glue ear surgery?

A

persisting bilateral glue ear lasting 3 mnths or more
hearing loss in best ear of 25-30dB or worse, averaged at 0.5, 1, 2 and 4 kHz
children with better hearing but social, educational or developmental difficulties.

81
Q

management of acute otitis media?

A
  • usually conservative with analgesia e.g. paracetamol or ibuprofen, reassure parents Abx often not needed as viral infection.
  • may do delayed Abx prescribing where if pt feels symptoms not improving within 4 days or significantly worsen can start Abx
  • immediate Abx if systemically unwell but don’t need admission, at high risk of serious complications or are immunocompromised, or symptoms for 4 days or more and not improving, and for children under 2 with bilateral disease or with perforation and/or ear discharge, =treat 5 day course of amoxicillin. can use erythro or clarithromycin if pen allergic.
  • may help treat recurrent disease with grommets
82
Q

presentation of acute mastoiditis?

A

severe pain behind the ear in a child following acute otitis media infection
pyrexia
tachycardia
sagging or oedematous posterior ear canal wall
pinna pushed down and outwards

83
Q

treatment of acute mastoiditis?*

A

hosp admission
high dose IV Abx for at least 1-2 days e.g. ceftriaxone
oral Abx after this and continue at least 1-2wks
analgesia/antipyretics e.g. ibuprofen
immediate mastoidectomy if subperiosteal abscess formation
may need urgent incision and drainage to avoid intracranial spread.

84
Q

complications of middle ear infections?

A

acute mastoiditis
facial paralysis
labyrinthitis-SN hearing loss, loss of balance, vertigo N+V, need high dose parenteral Abx and may need surgery.
meningitis-pt initially pyrexia with headache, later confusion, irritability and neck stiffness
intracranial abscess
temporal lobe abscess-may result from middle ear disease spread superiorly through tegmen tympani
cerebellar abscess
lateral venous sinus thrombosis-diagnosis often at mastoidectomy
sigmoid venous sinus thrombosis-spread through posterior mastoid

CT scan can show abscess development

85
Q

causes of facial nerve palsy?

A

Idiopathic-Bell’s palsy-unilateral, high dose oral steroids may improve outcomes e.g. 60mg prednisolone, r/f to ENT if complete palsy or no evidence of recovery within 6 wks.
Iatrogenic e.g. mastoidectomy, forceps delivery
Intracranial-stroke (CVA), acoustic neuroma, brainstem tumour (latter 2 would be frontal sparing due to frontalis bilateral innervation at cortical level), note cerebellar stroke-LMN-no frontal sparing
Ear-chronic otitis media, herpes zoster oticus (ramsay hunt syndrome), trauma-surgical or temporal bone fracture
Parotid tumours-tight parotid sheath so nerve compression
DM
MS
Lyme disease
Sarcoidosis
Polyneuritis

bilateral facial palsy-Parkinson’s disease, medication e.g. antipsychotics

86
Q

what clinical hx should be obtained in pt with facial nerve palsy, and how does this indicate likely causes?

A

otalgia-often occurs before facial weakness in bell’s palsy and herpes zoster oticus
chronic otorrhoea and conductive hearing loss-cholesteatoma
hx of trauma or surgery e.g. mastoidectomy in cholesteatoma or acute mastoiditis post acute otitis media?
unilateral painful parotid swelling?
dry eye-lesion at or proximal to geniculate ganglion-greater superficial petrosal nerve to lacrimal gland, but pt complaint of watering as puddle of tears in lower eyelid?*
loss of taste anterior 2/3 tongue-lesion proximal to chorda tympani
sensitivity to high intensity sound (hyperacusis due to loss of stapedius reflex)-lesion above stapedius nerve
loss of sensation over small area of concha?

87
Q

management of facial nerve palsy?

A

reassurance to patient that if can’t wrinkle forehead on affected side, not a stroke (excluding if cerebellar*) as this often their main concern
indication to prognosis may be given by electrodiagnostic tests-?neuropraxia-reversible block with usual complete recovery in 6 wks.
OPHTHALMOLOGICAL opinion-is the cornea covered by the upper lid during eye closure (Bell’s sign)-reduced risk of corneal abrasion-prophylaxis: regular eyedrops e.g. hylo-forte lubricant drops, or silicone ointment use, glasses with a side protector, surgical procedures e.g. canthoplasty, lower lid augmentation.
muscle transfer and facelifts
if complete nerve section e.g. surgery or temporal bone fracture, need end to end anastomosis or insertion of nerve graft after excision of damaged portion of nerve.

88
Q

where do we worry about a TM perforation?

A

involvement of attic (pars flaccida)*-may be underlying cholesteatoma, needs ENT investigation. unsafe TM perforations involve TM retraction that can enlarge to allow keratinisation to take place and cholesteatoma to form.
or in posterior region
or involving TM margin-less likely to heal?

89
Q

complications of a cholesteatoma?

A 
irreversible hearing loss from ossicular destruction
facial nerve palsy
lateral sinus thrombosis
labyrinthitis
meningitis
intracranial abscess
90
Q

when might anterior perforation of TM occur?

A

following grommet removal

inferior more likely with chronic middle ear infections

91
Q

what is the centre of the TM marked by?

A

the umbo=the end of the handle of the malleus

92
Q

where does blood collect in an auricular haematoma?

A

between the perichondrium and the elastic cartilage of the ear

93
Q

how are auricular haematomas treated?*

A

drainage
without tment, ear would become deformed due to avascular necrosis of the cartilage supplied by the perichondrium, leading to skin fibrosis.

94
Q

examples of wax softeners?

A

olive oil
sodium bicarbonate (most efficacious)-but *must ensure no TM perforation as ototoxic
hydrogen peroxide
glycerine and urea

needed for hard wax before syringing, which must NOT be done if TM perforation

95
Q

complications of wax removal?

A

incomplete removal
trauma to ear canal skin
TM perforation
vertigo

96
Q

what do we worry about if we see an ‘attic wax crust’ on otoscopy?

A

underlying cholesteatoma which requires surgical removal

97
Q

what can cause a red nodule/papule to appear on the TM?

A

a glomus tumour=rare slow growing soft tissue benign tumour arising within jugular foramen of temporal bone.

98
Q

why might pt with facial nerve palsy require 2ww referral and MRI scan?

A

may be parotid tumour-?concern if unilateral painful parotid swelling and facial nerve palsy
as facial nerve compressed by parotid swelling due to tight parotid sheath limiting expansion

99
Q

on patient inspection, what eye features may be apparent in facial nerve palsy?

A

wider palpebral fissure
inability to close affected eye-may see rolling of eye upwards when other eye blinks, as protective *Bell’s phenomenon?-cornea covering by upper eyelid

100
Q

if a patient has a cholesteatoma which has caused a fistula to form between the middle and inner ear causing vertigo, how can this be assessed?

A

fistula test-either compress tragus or use otoscope with a pneumatic bulb
feeling of vertigo, sometimes accompanied by nystagmus, indicates abnormal communication (+ve sign)

101
Q

why might asking about neck pain be important in presentation of a pt with ?vertigo?

A

may not be true vertigo but dizziness due to cervical spondylosis-osteophyte formation can constrict the vertebral artery, part. when neck hyperextended, causing fleeting imbalance due to cerebral ischaemia.
tx-neck physio and anti-inflammatories

102
Q

why might prolonged use of vestibular sedatives cause imbalance?

A

due to labyrinthine suppression

103
Q

how is tinnitus with SN hearing loss best treated?

A

with a hearing aid

104
Q

what might cause a pulsatile tinnitus?

A

normal CA, or carotid body tumour*?

105
Q

how can an ear polyp form?

A

can be mucosal herniation into the external ear through a perforation in the TM
can be surgically removed

106
Q

normal f/u time after presentation of a child with small AI perforation of TM?

A

4-8wks to check for adequate healing and any associated conductive hearing loss.

Special Senses (13 decks)

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