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Otology & Neurotology > √SNHL > Flashcards

√SNHL Flashcards

1
Q

xWhat are the different types of Presbycusis?

A

SCHUCKNECHT’S 6 TYPES

  1. Sensory presbycusis:
    - Loss of receptor hair cells, initially at the basal aspect of the cochlea
    - Timing: Occurs starting in middle age
    - Audio: Resulting in characteristic downsloping high-frequency hearing loss
    - Speech: Good SDS related to frequency range affected, can be abnormal depending on severity (preserved to abnormal)
  2. Neural presbycusis:
    - Atrophy of auditory neurons in the spiral ganglion cells and nerves of the spiral lamina
    - Affects all turns of the cochlear
    - Timing: Later in life
    - Audio: Flat to down sloping
    - Speech: Severe discrimination loss
  3. Strial/Metabolic/Vascular presbycusis:
    - Atrophy and degeneration of stria vascularis cells (essential for maintaining ion composition of endolymph to generate endocochlear potential for signal transduction)
    - Initially starts at apex of cochlea
    - Audio: Flat sensory loss affecting all frequencies
    - Speech: Minimal discrimination loss
  4. Mechanical/Conductive presbycusis:
    - Stiffness of basilar membrane, affecting basal and all turns of the cochlea
    - Audio: high tone gradual loss, downsloping
    - Speech: Discrimination related to steepness of slope (can be preserved to abnormal)
  5. Indeterminant Presbycusis:
    - Submicroscopic/intercellular changes, similar to strial/sensory - changes similar to above but not significant/severe
    - Audio: Can be flat or downsloping, high frequency loss
    - Speech: Depends on affect, can be preserved or mild to abnormal
  6. Mixed presbycusis: characterized by pathologic changes in more than one of the above structures.

Statpearls

Vancouver 299

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2
Q

XXRegarding presbycusis, discuss:
1. What is the incidence?
2. What are the implications?
3. Treatment?

A

Incidence: 15%

Implications:
1. Social isolation
2. Loss of independence
3. Poor communication

Treatment:
1. Improve general medical conditions
2. Hearing aid
3. Cochlear implant if severe

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3
Q

√What is the definition of asymmetric SNHL?

A

Definition from Choosing Wisely Canada:
Discrepancy of more than 20dB at 1 frequency, 15 dB at 2 frequencies, or 10dB at 3 frequencies

Saliba’s rule 3000 rule
- Asymmetric SNHL of 15dB or more at the frequency of 3000Hz
- Study by Issam Saliba showed that LR+ for this was 2.91 in identifying a VS, which was superior to other definitions

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4
Q

√What is the differential for flat SNHL hearing loss? (4)

A
  1. Presbycusis (strial aka. metabolic type)
  2. Late Meniere’s disease
  3. Otosyphillis
  4. Vascular loop

Kevan 53

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5
Q

√What is the differential for high-frequency (down-sloping) hearing loss?

A
  1. Presbycusis (sensory, cochlear types)
  2. Ototoxic medications
  3. Neurodegenerative disorders (e.g. MS, DM)
  4. Retrocochlear lesion (e.g. VS)
  5. Alexander’s dysplasia

Kevan 54

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6
Q

√What is the differential for low frequency (reverse-sloping) hearing loss?

A
  1. Early otosclerosis
  2. Meniere’s disease

Kevan 54

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7
Q

√What is the differential for cookie-bite hearing loss pattern?

A
  1. Congenital hearing loss
  2. Cochlear otosclerosis

Kevan 54

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8
Q

√What is the differential for reverse cookie bite (tenting) hearing loss pattern?

A
  1. Cogan syndrome
  2. Meniere’s (late)

Kevan 54

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9
Q

√What are 12 viruses involved in SNHL?

A
  1. CMV (#1 cause of congenital viral deafness)
  2. Mumps (#1 cause of acquired unilateral SNHL)
  3. EBV
  4. Hepatitis
  5. HSV I & II
  6. Adenovirus
  7. Polio
  8. Varicella
  9. Variola (smallpox)
  10. Influenza
  11. Rubella
  12. Measles (Rubeola) - Warthin-Finkleday cells
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10
Q

xDiscuss the workplace noise allowances

A
  1. Canada (Federal) = 87dB x 8 hours; cut hours by 1/2 every 3dB (“exchange rate”)
  2. USA = 90 dB x 8 hours; cut hours by 1/2 ever 5dB

Protection must be worn ≥ 85dB

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11
Q

xWhat is the role of a workplace hearing conservation program? 4

A
  1. Measure workplace noise
  2. Reduce or control exposures (protection)
  3. Audiometric surveillance
  4. Education
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12
Q

xWhat is the pathophysiology of Noise-induced hearing loss?

A
  1. Outer hair cells are susceptible to damage from loud noises exposure, loss of hair cells may be due to oxygen radical formation with subsequent membrane and cellular damage
  2. Worst noises - impulse < 0.2ms, 2-3kHz energy, > 140dB HL (small guns)
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13
Q

xWhat is the clinical pattern of noise induced hearing loss (NIHL)?

A
  1. Permanent SNHL with damage principally to cochlear hair cells, primarily OHCs
  2. History of long-term exposure to dangerous noise levels (ie. > 85dB for 8h/day) sufficient to cause degree and pattern of HL by their audiogram
  3. A gradual loss of hearing over the first 5-10 years of exposure (hair cells most susceptible to damage and fastest degeneration in the first 10-15 years)
  4. Hearing loss that involves initially the higher frequencies from 3-8kHz, before including < 2kHz; Greatest sensitivity of human ear is to frequencies between 1-5kHz
  5. Speech recognition scores consistent with audiometric loss
  6. Hearing loss that stabilizes (progression stops) after the noise exposure is terminated
  7. Protective effect of stapedial reflex is < 2kHz intermittent loud sounds, more protective for the lower frequencies
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14
Q

xWhy does all noise induced HL have 4000 Hz notch?

A

“Boilermakers notch”

  1. Beginning region of impairment involves the sensitive mid-frequency rage, 3-6kHz, corresponding to the 4kHz notch (small region of hair cell and nerve fiber degeneration) – Hair cells at the basal turn are most susceptible to oxidative stress
  2. Also related to the fact that 3000Hz is the natural resonance frequency of the EAC, but routine audio only tests 4000Hz; and 5000Hz is the natural resonance frequency of the concha
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15
Q

√What is a temporary threshold shift in audiology?

What is a permanent threshold shift? What dB level is at risk?

A
  • Depending on the level of sound exposure, either reversible or permanent damage can occur to the cochlea
  • Reversible loss referred to as “temporary threshold shift (TTS)”
  • Results from exposures to moderately intense sounds (e.g. loud concert, noisy power tools)

Hearing problems associated with TTS:
- Elevated thresholds, particularly higher mid-frequency region including 3-6 kHz frequencies
- Often associated with tinnitus, loudness recruitment, muffled sounds, or diplacusis

Recovery: can occur over minutes to hours or days (usually < 24 hours, up to 3 weeks)
- If threshold shifts do not fully recover, then referred to as permanent threshold shift
- Relationship between TTS and PTS is unknown, but anecdotally PTS occurs after repeated TTS - threshold shifts up to 50dB may recover spontaneously, anythiing above 50dB likely to have a degree of permanent threshold shift

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16
Q

√Describe permanent threshold shifts. What are two types of permanent threshold shifts (PTS)?

A

Permanent threshold shifts: Permanent cochlear damage, specifically to the outer hair cells.
- Occurs depending on frequency, intensity and duration of sound exposure

Two main causes:

  1. Acoustic trauma: caused by a single brief exposure to a very intense sound (e.g. explosive blast) that results in sudden, usually painful loss in hearing. Sudden violent changes in air pressure can produce direct mechanical damage to the peripheral auditory apparatus (e.g. cell injury or membrane rupture).
  2. Noise-induced hearing loss: Due to chronic exposure to less intense (but still harmful) levels of sounds - a slower, progressive destruction of cochlear components
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17
Q

√Define recruitment in audiology

A
  • An abnormal increase in the perceived loudness produced by a relatively small increase in intensity above threshold
  • Causing a compression in the dynamic range of perceived sound in patients with SNHL
  • Observed in the frequencies that are most impaired (usually high frequencies), which also carry critical information for speech understanding
  • Narrows the hearing range for loudness
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18
Q

xDefine Diplacusis in audiology

A
  • Perceptor of a single auditory stimulus as two separate sounds which may differ in pitch or in time
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19
Q

xWhy is the stapedial reflex not fully protective against acoustic trauma?

A

Stapedial reflex has a latency time of 10ms and is triggered by noise > 90dB, thus if the noise exposure is sudden onset, the noise may have reached the cochlear causing damage before acoustic reflex is activated

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20
Q

xWhat are the symptoms of noise-induced hearing loss? 7

A
  1. SNHL (usually bilateral and symmetric)
  2. Tinnitus
  3. Recruitment
  4. Non-auditory (anxiety, etc.)
  5. Diplacusis
  6. Distortion
  7. Compared to presbycusis (can get severe to profound HL), NIHL usually no more than 40dB in low frequencies and no more than 70dB in the high frequencies
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21
Q

√Describe the AAO-HNS hearing handicap

A

Since the 1950s, the federal and state courts have maintained the liability of employers to compensate employees financially for hearing handicaps incurred as a result of job related conditions. The orderly and equitable payment of compensation for hearing handicap requires a means for determining not only the existence but also the EXTENT of hearing handicap.

AAO-HNS Assumptions:
1. Hearing loss does not begin handicapping until the PTA (0.5, 1, 2, 3 kHz) exceeds 25dB
2. Handicap grows at a rate of 1.5% per dB HL beyond 25dB
3. Unilateral deafness only a mild handicap
4. 2 ears should not be equally weighed

CALCULATIONS:
1. Monoaural impairment (MI) = 1.5(PTA-25) %
2. Hearing Handicap (HH) = [5(MI better ear) + (MI worse ear)]/6
- Breaking this down, the better ear contributes = HHb = MIb/2
- The worse ear contributes HHw = (2MIb + MIw)/6

If patient had previous hearing impairment, need to calculate contribution of the new injury on the current HH

Example:
- Before injury PTA R = PTA L = 45dB
- Injury to left ear only; PTAr 45, PTAl 85dB
- Overall HH to this is 40%
- Breaking down the ears, 15% of handicap is contributed by better ear (right), and 25% of the HH is contributed by the worse ear (left)
- The left ear was the only ear that got injured, so how much of that injury contributes to the HH?
- Left ear injury was 40dB worse (85-45), which worsened the ear by (40/85)% = 47%.
- We know that the left ear is contributing 25% overall to HH, so the new injury is contributing (47%) of (25%) to the overall HH (0.47x0.25 = 0.118).
- Therefore, the injury is responsible for 11.8% hearing handicap

https://aao-hnsfjournals-onlinelibrary-wiley-com.proxy.bib.uottawa.ca/doi/epdf/10.1177/019459989010300512

https://www.asha.org/policy/rp1981-00022/

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22
Q

xHow do you counsel patients on hearing protection?

A
  1. Ear plugs: Reduce noise by 15-30dB, works bets in the 2-5kHz range
  2. Ear muffs: More effective protectors, reduces noies by 30-40dB, works best in 500-1000Hz
  3. Must be worn at all times ≥ 85dB, removal even for short periods severely reduces their effective cumulative attenuation capability
    - e.g. 30dB effective attenuation is reduced to 13-15dB if earmuffs removed for 5% of an 8 hour day
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23
Q

√What is the criteria for idiopathic progressive bilateral SNHL? (IPBSHL)

A
  1. Bilateral SNHL of at least 30dB at any frequency
  2. Significant change in discrimination score or progression in at least one ear
    - Defined as a threshold shift > 15dB at any frequency; or >10dB at 2 or more consecutive frequencies

This definition excludes patients with sudden SNHL < 24 hours, which more likely is due to microvascular or viral etiology

24
Q

√What is the differential diagnosis of autoimmune inner ear disease (AIED)?

A
  1. Relapsing polychondritis
  2. Polyarteritis nodosa
  3. Behcet’s syndrome
  4. Rheumatoid arthritis
  5. Systemic lupus erythematosus
  6. Wegener’s granulomatosis
  7. Churg-Strauss syndrome
  8. Cogan’s syndrome
  9. Meniere’s disease (AIED is continually progressive)
  10. Otosyphillis
  11. Vestibular schwannoma/retrocochlear pathology
25
Q

√What are causes associated with secondary autoimmune ear disease?

A
  1. Sjogren’s syndrome
  2. Behcet’s syndrome
  3. Rheumatoid arthritis
  4. Cogan syndrome
  5. Systemic lupus erythematosus
  6. Giant cell arteritis
  7. GPA
  8. Ulcerative colitis
  9. Systemic sclerosis
  10. Polyarteritis nodosa
  11. Antiphospholipid syndrome
  12. Takayasu’s arteritis
  13. Hashimoto’s thyroiditis
  14. Relapsing polytonicities
  15. Vogt-Koyanagi-Harada disease
  16. Mixed cryoglobinemia
26
Q

√What is the diagnostic criteria for autoimmune inner ear disease? 4

A

No official criteria exist

Classic definition:
1. Progression of deafness over weeks to months, asymmetrical bilateral, fluctuating symptoms/hearing course (but eventually overall progressive), aural fullness, tinnitus
2. Vestibular symptoms up to 79%: Ataxia, imbalance, positional or episodic vertigo, motion intolerance
2. Responsive to corticosteroids
3. Exclusion of other causes

27
Q

√What are antigen specific tests for autoimmune inner ear disease?

A

Divided into (1) Antigen non-specific, and (2) Antigen specific

ANTIGEN NON-SPECIFIC (Useful in routine screening for evidence of systemic immunologic dysfunction, non-specific for AIED):
1. Levels of circulating immune complexes
2. Complement levels (C3, C4)
3. Antinuclear antibody levels (ANA), ENA (extractable nuclear antigen), TSH
4. Rheumatoid factor
5. ESR, CRP
6. CBC with differential
7. Antineutrophil cytoplasmic antibodies (ANCA), Antidouble-stranded DNA antibodies, Anti-SSA antibodies, Anti-SSB antibodies, Antiphospholipid antibodies
8. Others: Lyme serology, HIV, HbA1c, FTA (syphillis)

ANTIGEN SPECIFIC (historic interest #1 and 2 below)
1. Lymphocyte migration inhibition assay
2. Lymphocyte transformation test
3. Western Blot analysis (Oto-blot): Anti-68-kD anticochlear antibody (but not diagnostically accurate)

Heat shock protein**

28
Q

√What are the treatment options of primary autodimmune inner ear disease?

A
  1. Corticosteroids (standard of care) - 1mg/kg/day x 4 weeks ASAP to avoid irreversible damage within 3 months; if no response then taper slowly over 4 weeks to a maintenance dose of 10-20mg/day
  2. Cyclophosphamide
  3. Methotrexate (DMARD)
  4. Etanercept (TNF antibody, inflammatory mediator)
  5. Azathioprine (DMARD)
  6. Mycophenolate Mofetil (cellcept) - inhibits T and B cell synthesis
  7. Intratympanic anti-TNF-alpha inhibitors (golimumab, infliximab)
  8. IV anti-CD20 inhibitor (Rituximab)
  9. Cochlear implantation
29
Q

√What is a proposed management algorithm for autoimmune inner ear disease/treatment pathway?

What is the prognosis with treatment?

Definition of steroid responder 4

A
  1. Prednisone 60mg PO daily x 4 weeks
  2. Add methotrexate 7.5-20mg PO qweekly with folic acid for people who relapse during steroid taper
  3. Add cyclophosphamide 1-2mg/kg/d for non-responders to steroids and methotrexate
  4. Responders continue full-dose therapy until monthly audiograms reach a plateau of recovery, then taper meds over 8 weeks to a maintenace dose of Prednisone 10-20mg q2d and continue for a variable time
  5. Non-responders are tapered off steroids in 12 days

Steroid responder definition:
1. ≥ 15 dB at one frequency; OR
2. ≥ 10 dB at two or more consecutive frequencies; OR
3. If the discrimination is significantly improved (>10dB)
4. 12% or more improvement in SDS at 40dB HL

PROGNOSIS:
- Overall steroid response rate ~60% in AIED
- Patients with treatment duration of < 6 months are at increased risk of relapse
- New evidence suggests allowing disease process to burn out, and then considering cochlear implant

Vancouver Pg 297

30
Q

√Regarding Otosyphillis, discuss:
1. What is it?
2. Classic symptoms and signs?
3. Investigations?
4. Treatment and prognosis?

A

OTOSYPHILLIS:
- Hearing loss that can be seen in congenital syphillis, or tertiary syphillis

SYMPTOMS:
1. SNHL
2. Interstitial keratitis (Ocular symptoms - Cogan’s syndrome mimics!)
3. Hennebert’s sign (positive fistula test without evidence of a fistula, also seen in Meniere’s - nystagmus associated with a change in pressure on the tympanic membrane)
4. Tulio’s phenomenon (dizziness with loud noise)
5. May have notched incisors (Hutchinson’s teeth)
6. May have mulberry molars (molars with multiple abnormal cusps)
7. Frontal bossing
8. Septal perforation or saddle nose deformity

Hutchinson’s triad (late congenital syphillis, as late as 2 years old):
1. Hutchinson’s teeth/incisors
2. Interstitial keratitis
3. SNHL

INVESTIGATIONS:
1. Non-treponemal tests (measurse antibody titres)
- Easily performed, inexpensive, but only 70% sensitive with late disease like in otosyphillis
- VDRL: Venereal disease research laboratory
- RPR: Rapid plasma reagin

  1. Treponemal tests (identifies presence of organism) - DIAGNOSTIC TEST OF CHOICE
    - More expensive but far more sensitive (95%) with late disease
    - FTA-abs: Free Treponemal Antigen Absorption
    - MHATP: Microhemagglutinin Treponemal Pallidum assay
  2. LP is NOT indicated, since it is only positive in 5% of otosyphillis

TREATMENT:
1. ID consultation
2. High dose penicillin
3. Systemic steroids

PROGNOSIS:
1. 35-50% have improvement in hearing and resolution of vestibular symptoms with treatment

Kevan Otology Page 72

31
Q

√Regarding Cogan’s syndrome, discuss:
1. What is it?
2. Epidemiology
3. Clinical Presentation
4. Diagnosis and workup
5. Treatment
6. Prognosis

A

Cogan’s Syndrome = Autoimmune (med-large vessel vasculitis) disease, characterized by non-syphillitic ocular keratitis and vestibuloauditory dysfunction

EPIDEMIOLOGY:
1. Presents ~4th decade of life
2. Patients typically have URTI within 7-10 days of initial onset

CLINICAL PRESENTATION
1. Sudden hearing loss as presenting symptom in 50%
2. Ocular symptoms and Vestibulocochlear symptoms within several months, 85% in 2 years
3. Natural course: First, a brief episode of inflammatory eye disease (interstitial keratitis most common), shortly followed by bilateral audiovestibular symptoms

Ocular:
- Interstitial keratitis (bilateral) - pain, scleral redness, photophobia, lacrimation
- Decreased visual acuity 2o corneal clouding
- Atypical symptoms: scleritis, uveitis, episcleritis, papilledema, retinal detachment

Vestibulocochlear:
- Hearing loss - sudden b/l fluctuating and progressive - mostly downsloping (like meniere’s, can be peak shaped initially)
- Sudden true Vertigo
- Tinnitus
- Ataxia
- Vegetative symptoms
- Oscillopsia (25%)

  1. Associated with Chlamydia pneumonia infection
  2. Systemic inflammatory involvement: aortitis, aortic insufficiency, pleuritis, pleural effusion, pericarditis, pericardial effusion, coronary arteritis
  3. Atypical symptoms/forms: Systemic vasculitis (glomerulonephritis, GI, polyarteritis nodosa, arthritis)

DIAGNOSIS/WORKUP
1. Urinalysis
2. CXR
3. Echocardiogram
4. Histology (temporal bone): Degeneration of vestibular and spiral ganglion, edema to membranous cochlea and SSC, often accompanied with smal//med vessel vasculitis

TREATMENT:
1. Topical steroids for ocular symptoms
2. Systemic steroids
3. Cyclophosphamide

PROGNOSIS:
- Untreated may lead to profound SNHL and loss of vestibular function
- Approximately half progress to bilateral Class D hearing
- Only a minority experience permanent visual loss

32
Q

√Regarding Susac Syndrome, discuss:
1. What is the pathophysiology?
2. Etiology
3. Epidemiology
4. Triad of symptoms
5. Pathology
6. Imaging
7. Treatment

A

Pathophysiology/Etiology:
- Not completely known, but thought to be a autoimmune vasculopathy, causing infarcations of the microvasculature of the retina and inner ear
- “Retinocochleocerebral vasculopathy”

EPIDEMIOLOGY:
1. W:M 3:1
2. Presents age 20-40 years

RED-M syndrome (Triad):
1. Retinopathy - Branch retinal artery occlusion
2. Encephalopathy
3. SNHL - Hearing loss fluctuates, asymmetric, worse in low-to-mid frequencies (arteriopathy at cochlear apex)
M = associated with microangiopathy
± Vestibular symptoms (labyrinth involvement)

Natural Course:
- Progression of symptoms can last weeks to years
- Neuropsychologic symptoms typically dominate the clinical picture
- Neurologic symptoms are self-limiting with resolution over 2-4 years; some patients follow polycyclic course with mulitple remissions
- Vestibular symptoms often resolve
- Residual hearing loss often persists

PATHOLOGY:
- Inner ear pathology results from cochlear end-arteriole occlusion

IMAGING
1. MRI T2 FLAIR - snowball white lesions in corpus callosum (MS on DDx)

TREATMENT:
1. IVIg
2. Steroids
3. Immunosuppresive regimens
4. Antiplatelet agents

33
Q

√What are five classes of ototoxic medications?

A

Note: Often present with tinnitus initially before HL

“CLAMS”
C: Cisplatin
L: Loop diuretics
A: Aminoglycosides
M: Macrolides
S: Salicylates (anti-inflammatories)

34
Q

√List the sites of ototoxic activity for cisplatin

A
  • Affects mainly the OHCs at basal turn
  • Degeneration of IHC (Carboplatin IHC > OHC), stria and ganglion cells are also noted; possibly due to oxygen free radicals

Effects:
- Bilateral symmetric high frequency SNHL & tinnitus; usually permanent
- increased risk with vincristine, age, and dose

35
Q

√List the sites of ototoxic activity for loop diuretics

A
  • Affects the stria vascularis by altering potassium ion transport and alters endocochlear potential
  • Reversible (furosemide) or Permanent (Ethacrynic acid) cochleotoxicity

Effects:
- Tinnitus and vertigo also symptoms
- Hearing loss typically flat

36
Q

√List the sites of ototoxic activity for anti-inflammatories (e.g. salicylates)

A
  • OHC main site
  • Salicylates may also affect cochlear blood flow

Effects:
- All cause REVERSIBLE high frequency tinnitus, and mild-moderate flat/high frequency hearing loss

Examples: ASA, NSAIDs, Quinine

37
Q

√List the sites of ototoxic activity for aminoglycosides. Which are vestibulo vs cochleartoxic? Association?

A
  • Affects OHCs all the way from base to apex. Initially base is affected more, hence get high frequency hearing loss first
  • Affects Type I hair cells in cristae and macula (more than Type II hair cells) - therefore can get vestibular effects
  • Hearing loss with Aminoglycosides may be associated with an 12s mitochondrial rRNA gene mutation (A1555G, or C1494T)

Effects:
- Usually IRREVERSIBLE
- Gentamycin & Streptomycin more vestibulotoxic, and tinnitus common
- Kanamycin, Amikacin, Neomycin, Tobramycin are more cochleotoxic (KANT hear)

38
Q

√List the sites of ototoxic activity for macrolides

A
  • Thought to affect strial function, but no definite mechanism known

Effects:
- Reversible, flat SNHL

Examples: Erythromycin, Azithromycin

39
Q

List the sites of ototoxic activity for vancomycin (glycopeptide)

A
  • Ototoxicity disputed, no firm mechanism
40
Q

√Name 10 pre-existing conditions which increase susceptibility to ototoxicity (from medications)

A

EARS TOOXIC

E: Elevated peak and trough drug levels (dose)
A: Advanced Age (> 65 years)
R: Renal or liver failure (decreased excre=tion)
S: SNHL pre-existing

T: Treatment course > 14 days
O: Other ototoxic medications co-administrating (e.g. loop diuretics, aminoglycosides)
O: Ototoxicity previous history
X: GenetiX - Mitochondrial 12S rRNA gene (A1555G nucleotide) mutation in Chiense population
I: Immunocompromised
C: Collagen vascular disorders

41
Q

√What is the definition of idiopathic sudden SNHL, and percentage of recovery? What is the definition of recovery 2?

A

Definition:
1. Hearing loss ≥ 30dB in 3 contiguous frequency in < 3 days, AND underlying condition cannot be identified by history and physical examination

Prognosis:
- 33-66% recovery without therapy (AAO 2019)
- Recovery: Defined as within 10dB of other ear at the same frequency, and SDS within 10% of the other ear at the same decibel level

42
Q

√What are the different suspected etiologies of idiopathic sudden SNHL? 5

A
  1. Viral infection of the labyrinth
  2. Vascular - ischemia of the supplying inner ear vasculature/labyrinthine artery
  3. Intracochlear membrane rupture or perilymph fistula
  4. Autoimmune inner ear disease (although AIED usually bilateral by definition and slower in onset, but may begin asymmetrically)
  5. Sudden expansion of a CPA lesion (bleed)
43
Q

√Per the 2019 AAO guidelines, what investigations should not be ordered for idiopathic sudden SNHL?

A
  1. No CT scan - low yield exam (strong rec against)
  2. No routine bloodwork (strong rec against)
44
Q

√What are the strong recommendations in the 2019 idiopathic SSNHL guidelines?

A
  1. Confirm SNHL with an audiogram
  2. Educate patients on treatments, workup, and amplification
  3. No routine labs
  4. If investigating with labs - CBC, ESR/CRP, syphillic, lyme serology, clotting profile, TSH, autoantibodies
45
Q

√Per the 2019 Idiopathic SSNHL guidelines, what is the percentage of patients with vestibular schwannoma report SSNHL, and what percentage of patients with SSNHL are found to have vestibular schwannomas?

A
  1. Vestibular schwannoma that have ISSNHL = 10-20%
  2. SSNHL that are found to have vestibular schwannoma = 2.7-10.2%
46
Q

√Which frequency loss is associated with vestibular schwannoma?

A

High frequency

47
Q

√Per the 2019 guidelines for idiopathic SSNHL, what are the 3 methods of evaluating patients with idiopathic SSNHL for retrocochlear pathology?

A
  1. MRI
  2. ABR
  3. Audiometric follow up (patients with residual hearing in whom aggressive treatment of pathology would be unlikely)
48
Q

√What are the two types of MRI scans that can be ordered to rule out vestibular schwannoma?

A
  1. High-resolution fast-spin echo or gradient echo MRI imaging (does not require contrast, specific protocol depends on the scanner used - e.g. FIESTA protocol for GE scanners/CISS - constructive interference in steady state)
  2. MRI with gadolinium
49
Q

√What is a rare but deadly complication of using gadolinium in patients with renal problems?

A
  • Gadolinium induced nephrogenic systemic fibrosis
  • Contraindicated when GFT < 30mL/min
50
Q

√For patients with idiopathic SSNHL, if they are being observed without treatment, what audiometric findings is required to order an MRI or ABR (based on guidelines)?

A
  1. Hearing drop of > 10dB HL in ≥ 2 frequencies
  2. Drop in SDS of ≥ 10%
51
Q

√Based on AAO guidelines, what are the 3 initial treatments for idiopathic SSNHL that have some evidence?

A
  1. Systemic Corticosteroids (option, Grade B)
    - Ideally, within 14 days; benefit reported up to 6 weeks
    - Prednisone 1mg/kg/day or Methylprednisone 48mg/d, or dexamethasone 10mg/day
    - Full dose for 7-14 days, then taper over similar time period
  2. Intra-tympanic corticosteroids (option, Grade B)
    - May offer within 3 months (2-6 weeks ideal)
    - 10mg/mL methylprednisolone
    - 0.4-0.8mL every 3-7 days for 3-4 sessions
  3. Hyperbaric oxygen (option, grade B evidence)
    - Within 2 weeks for primary treatment
    - May offer within 3 months as a secondary salvage
52
Q

√Based on AAO guidelines, what salvage therapy can be offered for patients with incomplete recovery from idiopathic SSNHL after failure of initial management?

A

Up to 3 months after initial treatment failure, patients might be offered intratympanic steroid injection (2 times per week for 2 weeks)

53
Q

√According to guidelines, when should audiometric follow up be arranged for patients with idiopathic SSNHL who have been treated (regardless of outcome)?

A

Within 3-6 months
- 97% of people achieve final hearing level at 3 months
- 99.6% achieve final hearing level within 6 months

54
Q

√What are 7 poor prognostic indicators for sudden SNHL?

A

“SAAVVED”

Severity (total deafness worse)
Audiogram shape (flat/down sloping worse)
Age (advanced = poorer)
Vertigo
Vascular risk factors (HTN, DM)
Elevated ESR
Delay in initiation of treatment

55
Q

√What are 5 good prognostic indicators for sudden SNHL?

A

“My Ears Are Loved Now”

Minimal hearing loss
Early treatment (within 3 days)
Absence of vestibular symptoms
Low frequency loss (upsloping shape)
No chances in N1 latency on ECoG

Otology & Neurotology (17 decks)

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