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MRCS (ENT) > Ear > Flashcards

Ear Flashcards

1
Q

Type of hearing loss associated with cholesteatoma:

A

Conductive

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2
Q

Complications of cholesteatoma and cholesteatoma surgery

A

**Intra-temporal: **
bleeding infection
facial nerve damage
deafness
tinnitus
perilymph fistula.

Extracranial:
cellulitis
neck abscesses (Bezold, Citelle, Luc).

Intracranial:
Meningitis
brain abscess
CSF otorrhoea
sigmoid sinus thrombosis.

complications of cholesteatoma are
similar to the complications associated with acute otitis media.

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3
Q

Symptoms of cholesteatoma (4 min)

A

Discharge (ottorhoea)
Hearing loss
Vertigo
Tinnitus
Facial weakness

Those associated with infection > Meningitis / Cerebral abscess / Mastoiditis / Petrositis

NOT Pain usually

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4
Q

Treatment for cholesteatoma

A

Mastoid exploration > Mastoidectomy

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5
Q

Complications of untreated cholesteatoma (min 5)

A

Deafness (CHL > SNHL > dead ear)
Vertigo
Tinnitus
Facial weakness
Meningitis
Intracranial abscess
Sigmoid sinus thrombosis
Taste disturbance

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6
Q

Specific complications of mastoid surgery (min 4)

A

Hearing loss
Vertigo
Tinnitus
Facial Nerve Injury

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7
Q

Surgery for cholesteatoma

A
  1. Atticotomy. Used when the disease is limited to the attic region i.e. is relatively small
  2. Modified radical mastoidectomy. Used when the disease extends backwards into the mastoid system. It is a more traditional procedure and is being replaced, by many surgeons, with…
  3. Combined approach tympanotomy (CAT). Increasingly performed for larger diseases.
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8
Q

How is the diagnosis of cholesteatoma made?

A

Clinical examination, usually plus audiogram showing CHL (although it may not)

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9
Q

Imaging for cholesteatoma

A

CT

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10
Q

Signs of cholesteatoma

A

Attic crust
Attic retraction
Keratin / aural polyp in the attic region

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11
Q

Audiogram key

A

O = Right, air conduction masked if necessary
X = Left, air conduction masked if necessary (X = bad lefties)
[ = Right, bone, masked
] = Left, bone, masked
Triangle = bone, not masked
B thing - sound field testing - not ear specific

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12
Q

Describe how you would do an audiogram:

A

Describe how you would do an audiogram:

  • Examine ear to ensure clear canal +/- clear of wax
  • Start with air conduction in better ear at 1000Hz at 60dB, Reduce by 10dB until no response, Increase by 5dB until response 2/2, 3/4 (>50%)

Threshold is the lowest level at which responses at least 50% time

  • Repeat for other frequencies, Repeat for bone conduction
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13
Q

Conductive hearing loss audiogram with narrowing of the air bone gap at 2kHz?

A

Carhart notch (basically bone conduction is improved at 2kHz)
= Otosclerosis

Fixation of the stapes within the oval window.

At 2K there is a downward depression in bone conduction and narrowing of the air bone gap.

OLD, doesn’t make sense:

2 kHz is the resonant frequency of the ossicular chain, the largest increase in bone-conduction threshold (improves, narrowing air bone gap)

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14
Q

Treatment options for otosclerosis (min 4)

A

Observation
Fluoride supplementation for labrythine disease
Coventional hearing aid
Stapes surgery (only option for restoring natural acoustic hearing levels)
Bone conduction implant / device
Cochlear implant in advanced cases

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15
Q

Audiometric investigations for otosclerosis?

A

Audiometry (audiogram)
Tympanometry - shows a As curve (shallow peaks at 0daPa)

Stapedial/Acoustic reflexes (Absent stapedial reflex)
A speech audiogram (poor speech discrimina reflects likely cochlea involvement)

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16
Q

What is associated with otosclerosis ?

A

Osetogenesis imperfecta

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17
Q

Method of inheritamce of otosclerosis

A

AD (incomplete penetrance)

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18
Q

How are acoustic reflex measured

A

Generally by tympanometry to see if the stapes stiffens the TM and therefore decreasig middle ear admittance in response to sound

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19
Q

Otosclerosis - epidemiology, diagnosis, investigations

A

Commonest cause of hearing loss in young adults in UK

Genetic predisposition

Can affect one or both ears

Diagnosis
- Clinical: adult presenting with progressive CHL / mixed hearing loss with normal otoscope

Investigations
- Tuning fork tests
- Audiometry (PTA)
- Typanometry
- Speech audiometry
- Stapedial/Acoustic reflexes (Absent stapedial reflex)
- CT scan to rule out other pathology if

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20
Q

Stapes surgery
- What is it
- Risks / Cautions

A

Only option for restoring natural acoustic hearing levels

Fitting of a prosthesis between incus and stapes footplate

0.5-1% SNHL
Infection is a containdication
Caution for this surgery in an only hearing ear

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21
Q

Pathophysiology of otosclerosis

A

Portions of the dense enchondral layer of the bony labyrinth remodel into one or more lesions of irregularly-laid spongy bone.

Lesions reach the stapes then harden (sclerosis), limiting movement = hearing loss, tinnitus, vertigo

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22
Q

Complications of otitis externa

A

Spread to temporal bone - osteomyeltis (malignant otitis externa)
Spread of the infection to
the petrous apex - Petrositis
> Gradenigo’s syndrome
Facial cellulitis

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23
Q

Name for fungal otitis externa

A

Otomycosis

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24
Q

Microorganisms that cause otitis externa (5)

A

Staphylococcus aureus
Pseudomonas aeruginosa
Proteus
Aspergillus niger
Candida Albicans

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25
Q

RFs for Otitis Externa

A

Similiar to otomycosis

Water exposure
Canal trauma (E.g. cotton buds)
Diabetes / immunosuppression
Humidity (e.g. hot countries)
Eczema
Inherited e.g. narrow ear canals, non atopic eczema

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26
Q

Otitis externa - Management

A

Assuming simple

Micro swab
Aural toilet
Topical abx + steroids drops
+/- pope wick

Water precauations

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27
Q

Causative organism of otomycosis

A

Aspergillus Niger (90%)
Candida Albicans (10%)
Actinomyces

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28
Q

Risk factors for otomycosis

A

Water exposure (E.g. swimmers - repeated exposure removes cerumen)
Canal trauma (E.g. cotton buds)
Antibiotics
Diabetes / immunosuppression
Humidity (e.g. hot countries)
Eczema
Abscence of cerumen

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29
Q

Symptoms otomycosis

A

Pruritis (more marked usually then other OE)
Pain
Ottorhoea
Conductive hearing loss

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30
Q

Management of otomycosis

A

Aural toilet
Water precautions
Topical antifungals (E.g. clotrimazole)
Analgesia

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31
Q

Causes UMN facial nerve palsy

A

Stroke
MS
MG
GBS
Gliomas
Sarcoid
Drugs

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32
Q

Causes of LMN facial palsy

A

Trauma - Temporal bone fracture
Malignant - E.g. Parotid malignancy, facial nerve schwannoma)
Infective - Herpes Zoster (Varicella Zoster Virus - Ramsey Hunt Syndrome), CMV, EBV, AOM, cholesteatoma
Autoimmune - ? Sarcoid ? MS
Idiopathic - Bell’s palsy
Iatrogenic - Parotid surgery, middle ear surgery, mastoid surgery

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33
Q

Grading of LMN facial palsy, name of scale and details:

A

House-Brackmann Scale

I - Normal

Normal facial function in all areas.

II - Mild Dysfunction

Slight weakness noticeable on close inspection; may have very slight synkinesis.

III - Moderate Dysfunction

Obvious, but not disfiguring, differences between 2 sides. Noticeable, but not severe, synkinesis or hemifacial spasm.
Complete eye closure with effort.

IV - Moderately Severe Dysfunction:

Obvious weakness of disfiguring asymmetry, normal symmetry and tone at rest but,

unable to complete eye closure.

V - Severe Dysfunction

Only barely perceptible facial muscle motion, asymmetry at rest.

VI - Complete paralysis

No movement

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34
Q

Symptoms of Ramsey Hunt Syndrome (Herpes Zoster Oticus) (min 6)

A

Otalgia
Hearing loss (SNHL)
Pharyngeal / palate ulceration / vesicles
Facial weakness (LMN facial palsy)
Other cranial neuropathies
Altered taste / metallic taste
Tinnitus
Vesicular rash (pinna and outer ear canal)
Vertigo
Nausea / vomiting
Hyperacusis (stapedius muscle)

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35
Q

Where does Herpes Zoster Virus remain dormant in Ramsey Hunt Syndrome?

A

Geniculate ganglion of the facial nerve

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36
Q

Complications or Ramsey Hunt Syndrome:

A

SNHL

Change in taste perception,

Loss of vision caused by eye damage from corneal ulcers

Synkinesis: Abnormal reactions to facial movements caused by nerves growing back to the wrong muscles

Persistent pain (postherpetic neuralgia)

Facial weakness.

Immunocompromised patients:
Meningitis
Encephalitis
Disseminated spread of infection across multiple der- matomes
Atypical pneumonia.

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37
Q

Treatment options for Ramsey Hunt syndrome (min 4) … bonus 5th

A

APE AS (Analgesia, Pope wick (+steroid drop), Eye protection, Aciclovir, Steroids)

Anaglesia
Corticoteroids (prednisolone)
Antivirals (Aciclovir)
Eye protection (taping / patch / artificial tears)
Can splint ear canal with pope wick + abx / steroid drops to reduce otalgia

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38
Q

Investigations for LMN facial nerve palsy

A

High Resolution Computed Tomography or Magnetic Resonance Imaging to cinlude petrous temporal bone to exclude Cerebellopontine angle tumours

Evoked Electroymyogram (EEMG) - checks nerve response

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39
Q

Audiometric tests for Ramsey Hunt syndrome (min 3):

A

Pure-tone audiogram
Acoustic reflexes
Electroneurography
?Tympanometry

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40
Q

Serological test for Ramsey Hunt Syndrome?

A

Varicella Zoster IgG

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41
Q

Prognosis of RHS vs Bell’s palsy?

A

Prognosis is poor in comparison

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42
Q

Parts of the temporal bone

A

Squamous
Petrous
Mastoid

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43
Q

Temporal bone fractures classification

A

Classified by orientation to long axis of petrous temporal bone (long axis is across / horizontal across head > ear to ear

  • Transverse (e.g. forehead to occiput across temporal bone, 20% usually hit to front/back of head, higher energy, otic capsule more likely involved)
  • Longitudinal (80% - hits to side of head, usually to squamous part)
  • Mixed
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44
Q

Symptoms of temporal bone fracture (6)

A
  • Hearing loss, generally (SNHL if transverse # CHL if longitudinal #)
  • Vertigo (transerse)
  • Facial palsy (transerse)
  • Tinnitus
  • CSF leak (longitudinal > transverse)
  • Nystagmus to unaffected ear
  • Focal neurological deficit
  • CN 9-12 palsy
  • Ottorhagia (bleeding from ear)
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45
Q

Signs of temporal bone # (5)

A
  • Ruptured tympanic membrane
  • Haemotympanum
  • Damage to the canal in keeping with longitudinal #
  • Battle’s sign - ecchymosis post auricular skin (squamous part # (longitudinal #)
  • Nystagmus (to unaffected ear)
  • CSF Rhinorhoea or ottorhoea
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46
Q

Management of temporal bone fractures (specifically facial nerve palsy - delayed vs immediate)

A

ATLS Assessment and head injury management

Immediate Grade VI facial nerve palsy may require surgical repair/decompression

Incomplete / delayed palsies - Rx with steroids

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47
Q

Pathophysiology of otitis media with effusion (glue ear)

+ Contributing factors

A

Eustachian tube dysfunction = chronic reduction middle ear pressure = inflammatory response middle ear = glue (mucus rich in mucoproteins)

Adenoids recognised as important contributer due to it being source pathological bacteria (not due to size)

Contributing factors:
- Parental smoking
- Allergy
- Recurrent URTIs
- Reduced nasopharyngeal dimensions

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48
Q

Symptoms of glue ear

A

Generally just hearing impairment (noticed by parents, teachers etc.)

Recurrent infections and otalgia UNCOMMON

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49
Q

Signs of glue ear (Min 3)

A

Middle ear effusion - can be dull red / amber / grey coloured

Retraction or Tympanic bulge

AIr bubbles / fluid level

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50
Q

Investigations for otitis media with effusion

A

Pure-tone audiogram (CHL)
Typanometry (impedance audiometry) - (Flat trace - helps disting. from otosclerosis)

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51
Q

Three alternative diagnosis to a cerebellopontine angle lesion

A

Meningioma
Cholesterol granuloma
Facial schwannoma
Arachnoid cyst
Epidermid cyst
Cerebellar tumour
Aneurysm of basilar or verteberal arteries

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52
Q

Three treatments for vestibular schwannoma

A

Conservative (watch and wait)
Surgery
Stereotactic radiotherapy

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53
Q

Symptoms of vestibular schwannoma
(3)

Extra - otological phase, neurological phase symptoms

A

Unilateral hearing loss
Unilateral tinnitus
Other cranial neuropathies E.g. sensory changes to V

Otological phase symptoms (as lesoon compresses structures in meatus)
- Unilateral deafness (90%)
- Unilateral Tinnitus (70%)
- Sudden onset deafness (10%)
- Vertigo is UNUSUAL as compensation of vestibular nerve gen. keeps pace with damage

Neurological phase (as expands into cerebellopontine angle)
- Trigeminal nerve symptoms (sensory changes - pain/numbness)
- Headache
- Late symptoms: Ataxia / unsteadniess / diplopia (VI) / hoarsness & dysphagia (IX & X)

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54
Q

Investigations for vestibular schwannoma?

A

Magnetic resonance imaging with gadolinium enhancement

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55
Q

vestibular schwannoma - epidemiology and pathophysiology

% of intracranial tumours
% cerebellopontine angle tumours
Onset age
% bilateral
Imminent origin site
Cells of origin

A

8% of all intracranial tumours
80% of cerebellopontine angle lessions
M=F
Usually onset between 40-50 yrs age
Generally unilateral
Bilateral (5%) due to neurofibromatosis type 2 (Autosommal dominant)
1:100,000 annual incidence

Commonest origin is superior vestibular nerve
Arise from Schwann (neurolemmal) cells

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56
Q

Reddish blue mass behind the tympanic membrane - what’s the sign and what’s the pathology?

A

Glomus tympanicum (paraganglioma)

Ear drum has appearance of a setting or rising sun

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57
Q

What are paragangliomas?

A

Rare neuroendocrine tumour that forms from chromaffin cells.

Form tumours of the middle ear and skull base in head and neck. But e.g. when found in adrenal gland they are phaeochromocytomas.

Can effectively form where there is any chemoreceptor tissue associated with the autonomic nervous system e.g. tympanic plexus, carotid body etc.

Most are not secretory enough to be synptomatic though.

58
Q

Name the four paragngliomas that form in the head and neck and which is most common?

What artery are they all supplied by?

A

Globus tympanicum
Globus jugulare
Globus vagale
Carotid body tumours (Most common)

Ascending pharyngeal artery

59
Q

Presenting symptoms globus tympanicum?

A

CHL
Pulsatile tinnitus
Mass in ear or neck (if not tympanicum)

Destruictive lesions can cause lower cranial nerve palsies (e.g. 5 / 7) and Horner’s syndrome

60
Q

What is the classification system for paagangliomas?

A

Fisch classification

61
Q

Management of paragangliomas

A

Observation with repeat scanning
Sterotactic radiosurgery
Surgical resection

62
Q

Invesitigations / diagnostic workup for suspected paraganglioma

A

MRI
CT
PET
Skull base MDT

63
Q

What is (approx) maximum conductive hearing loss and why?

A

Maximum conductive hearing loss = 60dB

At 60 dB SPL the bones of the skull begin to vibrate, bypassing the middle ear system. This direct vibration of the skull can cause the cochlea to vibrate and, thus, the hair cells to shear and to start the process of hearing.

64
Q

Describe the classic noise induced hearing loss audiogram?

A

A bilateral SNHL with a bilateral tick / dip at 4kHz

65
Q

Describe the classic Ménèires audiogram and what else should you do if you get this audiogram?

A

Generally unilateral (can be bilateral) SNHL - Menieres typically affects the lower frequencies first and hearing loss fluctuates.

However as it is often a unilaterasl hearing loss must rule out acoustive neuroma (MRI IAM with gadolinum enhancement)

66
Q

Causes of Bilateral SNHL? (3)

A

mOtotoxicity e.g. AMinoglycosides, Furosemide (loop diuretics), Aspirin Overdose;
Trauma
Bilateral acoiutsiuc neuromas if have NF Type 2

67
Q

What is the DB definition of hearing loss?

Bonus: what are the ranges?

A

Hearing loss is an inability to hear sounds of greater than 20DB.

Based on British Society of Audiology definitions of hearing loss, this is the decibel hearing level range each of these terms refer to:

mild (21–40 dB)
moderate (41–70 dB)
severe (71–95 dB)
profound (95 dB)

68
Q

What Hz does a dead ear still usually respond to and why?

A

Dead ear - will still typically show a small response at 80Hz due to the vibrotactile response ( pt feels the vibrations and thinks they hear them)

69
Q

What is interaural attentuation?

What is it (approx) for A-C vs B-C?

A

Is the amount of sound lost via transmission across the skull (cross hearing) from the test ear to the non test ear.

In air conduction it is between 40-60dB
In bone conduction is is approximately none, i.e. all the sound is conducted across the skull to the non-test ear without loss.

70
Q

What is the definition of masking in audiometry?

A

Masking is the phenomenon by which one sound impairs the perception of another

In pure tone audiometry masking is used to raise the threshold in the non-test ear using air conducted sound. This therefore overcomes cross hearing.

(From video …Masking = the process by which the threshold of audibilty of one sound is raised by the presence of another (masking) sounds)

71
Q

What are the rules of masking?

A

Must use masking when:

1) when the best A-C is =>40dB better than the unmasked A-C in the worse ear

2) when the unmasked B-C is=>10dB than the worse A-C (of either ear)

3) When rule 1 not used, where B-C is =>40dB than the worse unmasked A-C (in the other ear)

Explanation:
1) Accounts for A-C cross hearing (Interaural attenuation 40dB)
2) Accounts for B-C cross hearing (IAT 10dB)
3) Accounts for the NON-TEST ear having a conductive problem meaning the NON-TEST cochlea may be picking up the A-C during the test, despite A-C testing of that ear not picking much up due to CHL.

72
Q

Button battery in EAM - 2 consequences

A

Chemical burns to external auditory canal
Deafness

73
Q

Surfer’s ear is…

Caused by…

A

Boney exostosis of the external ear canal

Periostyeal reaction to repeated exposure to cold (swimming/surfing)

74
Q

Differential (2) for ?boney exostosis of the external ear canal and how to delineate them

A

Soft tissue fibrosis
Osteomas (uncommon)- generally singular and pendunculated along suture lines

Exostosis usually multiple and bilateral, broad based

75
Q

Symptoms of surfer’s ear

A

Deafness
Wax impaction
Recurrent infections
Otalgia

76
Q

Treatment options for boney exostosis and how to prevent progression

A

None if asymptomatic
Surgical boney meatoplasty
Earplugs when swimming/surfing

77
Q

Acute suppurative otitis media aetiology
- Organisms (3-5)
- How does it occur
- Which age groups most affected

A

Organisms
- Streptococcus pneumoniae (40%)
- Haemophilus influenzae (30%)
- Moraxella catarrhalis (10%)

NON SUPPORATIVE: Adenovirus, respiratory syncytial virus

Other: Streptococcus pyogenes Staphylococcus aureus

Occurs either primarily or secondary to viral AOM infection.

Generally bacteria enter middle ear cleft via eustachian tube.

Infants have shorter, wider, more horizontal tubes allowing contamination from food, vomiting etc.

Children aged 3-7 highest incidence

78
Q

Acute supputative otitis media
RFs (4)

A

RACE:

Recurrent / chronic rhinosinusitis
Adnoiditis
Chest disease
Eustachian tube dysfunction (caused by e.g. adenoidal hypertrophy, abnormal tube patency, cleft or submucous cleft, nasopharyangeal malignancy)

79
Q

ASOM symptoms (4)
How may a child present (5)?

A

Otalgia (throbbing)
Pyrexia
Deafness
Ottorhoea and resolution of pain if perforation

Children present as:
systemic upset
excessive crying
irritability
poor feeding
ear pulling

80
Q

ASOM signs (6 - but 3-4 related)

A

Dull TM initially (oedema)
Red/Hyperaemic TM (next)
Middle ear effusion
Bulging TM
Perforated TM
Mucopus in EAC

81
Q

ASOM Management (4)

A

Rest
Analgesia
Antibiotics (PO e.g. Amoxicillin if no allergy)

82
Q

Complications of ASOM (9)

A

Mucositis progressing to osteomyelitis (Mastoiditis)
Meningitis
Citelli’s abscess / Bezold’s abscess
Extra or subdural abscess
Cerebellar, temporal lobe, perisinus abscess
Sigmoid sinus thrombosis
LMN facial nerve paralysis
Labrynthitis
Otitis hydrocephalus

83
Q

Possible sequelae (not complications) from ASOM

A

Non-suppurative middle ear effusion

Tympanic membane perforation
Tympanosclerosis

Errosions of ossicular chain
Adhesions between ossicles and TM

High-tone SNHL (possibly from toxins migrating into cochlaear)

Sequelae of ASOM complication….

84
Q

What is Gradenigo’s syndrome?

A

Petrositis (mastoiditis spreading to petrous apex) or Meningitis or Extradural abscess at petrous apex - compresses below CNs (as the are separated fropm petrous apex by Dura only.

Resulting in:
- ASOM
- Ipsilateral CN6 abducens nerve palsy (paralysis of lateral rectus)
- Pain in ipsilateral trigmeninal nerve distribution

85
Q

What is? And what’s the cause?

  • ASOM
  • Ipsilateral CN6 lateral rectus palsy
  • Pain in ipsilateral trigmeninal nerve distribution
A

Gradenigo’s syndrome

Petrositis or Meningitis or Extradural abscess at petrous apex

86
Q

What is a Citelli’s abscess?

A

Subperiosteal abscess which has spread through medial aspect of mastoid into digastric fossa

87
Q

Subperiosteal abscess which has spread through medial aspect of mastoid into digastric fossa is a ?

A

Citelli’s abscess

88
Q

What is a Bezold’s abscess?

A

Abscess which has tracked inferiorly within the SCM sheathto form a fluctuant mass along it’s anterior border

89
Q

Abscess which has tracked inferiorly within the SCM sheath to form a fluctuant mass along it’s anterior border is a?

A

Bezold’s abscess

90
Q

Acute mastoiditis

Symptoms (3)

Signs (3)

A

Fever
Otalgia
Ottorhoea
Other signs from compolications e.g. meningism, neurological deficit, facial nerve palsy etc

Pinna protrusion
Loss of post auricualr skin crease
Post-aural erythema
Tenderness or fluctuance post aurally
Red bulging TM

91
Q

Complications of acute mastoiditis

A

Same as ASOM really:

Meningitis
Citelli’s abscess / Bezold’s abscess
Extra or subdural abscess
Cerebellar, temporal lobe, perisinus abscess
Sigmoid sinus thrombosis
LMN facial nerve paralysis
Labrynthitis
Otitis hydrocephalus

92
Q

Management of acute mastoiditis

A

IV antibiotics
Analgesia
Antipyretics

Surgery (cortical mastoidectomy+ grommet insertion) if signs of complications, systemic toxicity, failure of medical RX

CT mandatory prior to surgery to exclude intracranial sepsis (e.g. intrcranial abscess) prior

93
Q

Bugs commonly causing acute mastoiditis

A

streptococcus pneumoniae,
haemophilus influenzae
moraxella catarrhalis
Group A beta haemolytic streptococcus (Strep Pyogenes)

94
Q

Choice of Abx in Mastoidits and why

A

Co-amoxiclav (25mg/kg) because one of the 3 common bacteria responsible for this condition (haemophilus influenza) is resistant to amoxicillin

Pen allergy??

95
Q

Differentials for acute mastoiditis?

A

Post auricular lymphadenoapthy

96
Q

Post auricular lymphadenoapthy - condition which commonly causes ion childhood?

A

Rubella
Or other localised infection

97
Q

What is Chronic Otitis Media (COM)

How can it be further defined?

A

Inflammatory disorder of the middle ear.

Characterised by persistent or recurrent ear discharge

Mucosal / Chronic Suppuratuve Otitis Media
- due to tympanic membrane perforation and subsequent inflammation of the middle ear mucosa

Squamous
- due to retraction of the tympanic membrane and is associated with the formation of cholesteatoma

98
Q

Aeitiology of COM / Chronic Suppurative (Mucosal) Otitis Media

RISK FACTORS (4)

A

Recurrent acute otitis media

Other RFs
Previous traumatic perforation, Insertion of grommets
Craniofacial abnormalities

99
Q

How does COM / Chronic Mucosal / Suppurative Otitis Media present (and findings on examination)

A

Chronically discharging ear >6 weeks IN ABSCENCE of
- fever
- otalgia.

If above present consider:, mastoiditis, or intracranial involvement.

O/E
Perforation

Patients will often have a history of recurrent AOM, previous ear surgery, or trauma to the ear.

100
Q

Investigations and Rx of COM (Mucosal/Suppurative)

A

Otoscopy
Audiogram (Pure Tone)
Tympanometry
Microbiology swabs of discharge

CT Temporal bones if any concern re. cholesteatoma

Medical
Aural toileting
topical antibiotic or steroid treatments

Surgical
Myringoplasty
Tympanoplasty

101
Q

Myringoplasty vs Tympanoplasty?

A

Myringoplasty
– closure of perforation in pars tensa
The closure is achieved by patching on an autologous graft, usually harvested from the tragal cartilage or temporalis fascia

**Tympanoplasty **
– a myringoplasty combined with reconstruction of the ossicular chain

102
Q

Classification systems for TM retractions? (2)

A

Sade’s classification for pars tensa Tos’s classification for pars flaccida

Tense Sade (Stiff Sade)
Flaccid Tos

103
Q

Type and dB range of hearing loss associatd with COM (mucosal)?

A

Conductive hearing loss (20-60dB).

104
Q

Squamous Chronic Otitis Media

What is it?

Forms?

A

Active squamous COM = a cholesteatoma

Inactive squamous COM = retraction pocket (with potential to become active.

Acquired disease = pathophysiology unknown, thought to result from chronic negative middle ear pressure from Eustachian tube dysfunction > retractioin pocket

Congenital disease is seen in patients with no history of ear surgery, and no perforation or retraction of the tympanic membrane; indeed congenital cholesteatomas represent epidermoid cysts within the middle ear cavity

105
Q

Squamous Chronic Otitis Media

Investigations (3) & Management (1)

A

Pure tone audiometry
Tympanometry

CT Petrous Temporal Bone to assess for cholesteatoma

Rx
Essentially all cholesteatoma is surgery of the mastoid as per prev notes

106
Q

When is a stapes prosthesis used?

A

Any condition of stapes fixation e.g. otosclerosis

Generally inserted during any stapedectomy

107
Q

How does a stapes prosthesis work?

A

It hooks around the long process of the incus and is inserted into the stapes footplate, recreating the joined ossicualr chain, transmitting sound vibrations into the inner

108
Q

Risks of stapes prosthesis surgery? (Min 5)

A

Dead ear
Worsening or failure to improve hearing
Dizzyness
Tinnitus
Altered taste (chorda tympani damage)
Facial palsy
Perilymph leak
Prosthesis failure
Tympanic membrane perforation
Bleeding
Infection

109
Q

When would you use a T-Tube over a Shah’s grommet

A

When you want it to remain in the tympanic membrane longer. To permanently ventilate the middle ear space to prevent effusion / progressive retraction.

Usually used in adults, or some children who have needed repeated grommets due to chronic disease.

Note: Adults eustachian tube has matured and therefore will not resolve the negative middle ear pressure with growth.

110
Q

Disadvantage of T-tubes over e.g. Shah’s Grommet

A

Higher risk of residual tympanic perforation

111
Q

Risks of grommet insertion (3)

A

Residual perforation
Tympanosclerosis
Infections

112
Q

Treatment of post grommet insertion infection

A

Aural toilet
Antiobiotic / steroid ear drops
Grommet removal if conditon fails to settle / becomes severe

113
Q

Grommet insertion aftercare instructions to patients

A

Can swim afterwards
Ear plugs should be worn when shampooing
Hearing test post insertion to check hearing improved
Generally extrude at 9-12months
FU once extrude to check ears and hearing again
25% children will require furthr insertion

114
Q

What is the smallest part of a BAHA made of and why?

A

Titanium - osseointegrates

115
Q

When is a BAHA more appropriate than a conventional hearing aid?

A

Unfavourable anatomy (e.g. microtia, congenital malformations or middle / external ear)
Chronic / recurrent infection
Patient preference
Any patient failing / unable to benefit from conventional hearing aid with sufficient cochlear reserve to benefit from sound amplification
Profound single sided deafness (to conduct sound to contralateral ear via bone conduction)

116
Q

Types of BAHA

A

Aids (worn on headband)

Implants
- Percutaneous (skin piercing)
- Transcutaneous (magnetic processor)

Further subdivided into
- Active powered component under skin)
- Passive (powered component external to skin)

117
Q

What type of nystagmus does BPPV generally present with?

What other unique characteristics are there of BPPV nystagmus?

A

**Rotatory/torsional ** (often Geotropic towards ground) TOWARDS the affected ear

…or if lateral canal involvement the nystagmus beats in either a geotropic (toward the ground) or ageotropic (away from the ground) fashion

Latency of onset: there is a 5–10 second delay prior to onset of nystagmus (central causes instant!)

Limited duration: Nystagmus lasts for 5–60 seconds

**Positional: **the nystagmus occurs only in certain positions

**Fatiguable **- Repeated stimulation, including via Dix–Hallpike maneuvers, cause the nystagmus to fatigue or disappear temporarily

Visual fixation suppresses nystagmus due to BPPV

Reverses upon return to upright position

118
Q

When might you see pendular (see-saw) nystagmus?

A

Congentially blind person

119
Q

Describe the components that make up vestibular nystagmus?

What determines the direction (right/left)?

A

Fast (corrective) phase (Saccadic movement)
Slow phase (Smooth pursuit)

The fast phase

120
Q

What determines the fast phase / slow phase in nystagmus

A

Fast phase towards ear which is being stimulated more e.g. BPPV or the non- damaged ear

Slow phase towards less stimulated ear e.g. the deads ear or normal ear in e.g. BPPV

121
Q

Describe why you get a slow and fast phase in horizontal nystagmus?

A

Slow / drift phase is always in the same direction as that canal which is inhibited (and which therefore sends a reduced afferent response to the brain),

Fast phase is in the direction of the stronger canal / more stimulated canal (sends increased afferent response to brain)

122
Q

What is caloric testing, what does it test?

How do you interpret the results

A

Involves putting cold and wamt water into thr ear canal of the patient to tst the vestibulo-ocular reflex

COWS for direction of nystagmus which is normal on caloric testing
- Cold Opposite
- Warm Sam

Warm water = endolymph in the ipsilateral horizontal canal rises, causing an increased rate of firing in the vestibular afferent nerve.

Cold = endolymph falls = decreased firing of the nerve

123
Q

How do you classify horizonatal nystamgus?

A

1st degree - nystagmus only on gaze in direction of the fast phase

2nd degree - nystagmus on looking straight ahead and in the direction of the fast phase

3rd - the most serious, nystagmus on gazing in all 3 directions (left, right and straight ahead.

124
Q

Type of nystagmus most associated with BPPV? And why?

A

Geotropic rotatational nystagmus towards affected ear
Latency of onset (5-10 seconds)
Fatiguable (repeating test will result in less nystagmus)
Reversible (will eventually subside)

Posterior SCC’s are the most likely to be involved

125
Q

Which area of the vestibualr system is generally involved in BPPV?

A

Posterior semicircular canal

126
Q

Patients right ear damaged in surgery resulting in a dead cochlea - describe the type of nsytagmus?

A

Left horizontal nystagmus

Paralysis / destruction of right lateral SCC (eg after right lateral semicircular fistula leak or iatrogenic right dead ear would result in a relatively higher afferent activity from left lateral SCC

127
Q

Where is the pathology in horizontal nystagmus?

A

Lateral SCC

128
Q

Tympanograms:
Horizontal (x) is unit and the normal range (adults and children)?
Vertical (y) axis unit and what is the normal range?

A

**daPa **(basically middle ear pressure)
- -50 - +50 daPa (decapascals) in adults (down to - 200in children)

ml per equivalent air volume (cubic cm)
(basically middle ear/ TM compliance) (

Admittance / compliance: 0.3-1.6ml - Adult canal vol 0.6-1.5, Children 0.4-0.9, 0.2 ok if under 6, and older than 6months

ECV
0.6-2.5cm in adults
0.4-1cm in children

129
Q

Tympanograms:

Intensity of sound used in 3m old child vs 3yr old child

A

1000Hz
226Hz

130
Q

What produces a bifid tympanogram and why?

A

A healed perforation with monomeric segment of tympanic membrane may give rise to a bifid tympanogram

131
Q

Flat line type trace on tympanogram. What type and what pathology could it be?

A

Type B

If high Y axis due to canal volume increase due perforation

If low volume canal vol then likely OME /Glue ear (fluid or infection)

132
Q

What type of tympanogram is normal

A

Type A

133
Q

Tymapnogram, normal morphology of peak but much lower volume. Type and possible pathology?

A

Type As.
Less compliant middle ear system (therefore less volume) e.g. otosclerosis

134
Q

Tympanogram, normal morphology of peak but much higher volume. Type and pathology?

A

Type Ad.
More compliant middle ear system (therefore greater volume) e.g. ossicular chain discontinuity

135
Q

Typanogram still shaped like a teepee, but are shifted negatively on the graph.

Type and pathology

A

Type C tympanogram indicates a significantly negative peak pressure, which is possibly caused by Eustachian tube dysfunction or a developing or resolving middle ear infection

136
Q

Differentials for unilateral SNHL in adult?

A

Traumatic
Noise induced hearing loss
Presbycusis
Meniere’s disease
Acousticneuroma
Infective causes such as meningitis.

137
Q

Causes unilateral SNHL in child?

A

Congenital: Waardenburg’s syndrome
CHARGE syndrome

Intrauterine infections: TORCHS (Toxoplasmosis, Rubella, CMV, Herpes simplex, Syphillis)

Neonatal/childhood infection eg meningitis

Maternal drug/alcohol abuse during pregnancy
Ototoxic drugs during childhood.

138
Q

Management of Menière’s disease

A

Management
- Strong psychological suppotand reassurance

Dietary changes
Eating and drinking water at even intervals are specific measures patients can implement to reduce fluid retention.
- limit salt and monosodium glutamate
- Avoid caffeine
Lifestyle changes
- stopping smoking
- managing stress
**Medical - **
- Betahistine
- Thiazide diuretics
- Acute attackes - Prochlorperazine / cinarizine
- Vestibular rehabilitation
- Hearing aids

**Surgical **
- Grommet insertion
- steroid injection,
- intratympanic gentamicin,
- endolymphatic sac surgery,
- vestibular nerve section.

Bilateral profound hearing losses secondary to Meniere’s
disease may be rehabilitated with cochlear implants, if air conduction hearing aids are inadequate.

139
Q

Episodic vertigo, fluctuating hearing loss & tinnitus?

A

Menière’s disease

140
Q

Menière’s disease symptoms & presentation

A

Episodic vertigo
SNHL (often fluctuating but stepwise decline)
Tinnitus
Aural fullness

Attacks often last 1-24hrs
N&V common
Nystagmus common

141
Q

Menieres investigations

A

PUre tone audiometry
Need to rule out other causes so if unilateral MRI to rule out acousti

MRCS (ENT) (14 decks)

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