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Otosclerosis Flashcards

1
Q

Define Otosclerosis

A
  • Primary metabolic endochondral bone disease of the otic capsule and ossicles (limited to the otic capsule)
  • Abnormal bone remodelling results in fixation of the ossicles (stapes predominantly) and resulting in conductive hearing loss
  • May have SNHL component if the cochlea is involved
  • Associated tinnitus (75%) and disequilibrium/vestibular symptoms (25%)
  • Bilateral in 80%
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2
Q

What is the genetics, inheritance, epidemiology, and symptoms of otosclerosis?

A

Inheritance:
- Autosomal dominant
- Incomplete (40%) penetrance

Epidemiology:
- 10% caucasians have histologic changes, only 12% of these people are symptomatic
- 2:1 Female predilection
- 1:1 F:M ratio for true Histologic changes
- Contralateral ear affected in 80% of cases
- 60% people report family history
- Typical age of onset is 3rd decade of life
- May be accelerated by hormonal changes during pregnancy

Symptoms:
- CHL with possible SNHL component
- Many have paracusis of Willis due to CHL

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3
Q

What is Paracusis of Willis?

A

Patients with CHL will say they hear better in noisy rooms due to this phenomenon “paracusis of Willis”
- Thought to occur because people speak louder in noisy surroundings, while the CHL reduces background noise, thus improving the signal to noise ratio
- In SNHL there is loss of outer hair cells and therefore greater problems hearing in noise (?)

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4
Q

Describe Carhart’s notch and provide a theory for its appearance

A

Carhart Notch = Hallmark audiologic sign of otosclerosis characterized by a decrease in bone conduction thresholds of (relative, not absolute): - seen ONLY IN THE BONY LINE
1. 5dB at 500Hz
2. 10dB at 1000Hz
3. 15dB at 2000Hz
4. 5dB at 4000Hz

This is a mechanical artifact that reverses with stapes mobilization

Theory:
- Stapes fixation disrupts the normal ossicular resonance (2000Hz)
- Possible relation to resonant frequency of the EAC (2-3kHz)
- Normal compressional mode of bone conduction is disturbed because of relative perilymph immobility caused by stapes fixation (therefore bone conduction is not completely normal either in Otosclerosis)

https://entokey.com/audiological-evaluation-of-the-patient-with-otosclerosis/

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5
Q

What anatomic locations does otosclerosis occur most often?

A
  1. Fissula Ante Fenestrum (most common) - a small connective tissue-filled cleft in the otic capsule of the temporal bone, not typically visualized on CT
  2. Round Window Niche
  3. Anterior wall of IAC
  4. Medial wall of cochlear apex
  5. Area posterior to the cochlear aqueduct
  6. Region adjacent to the semicircular canals
  7. Posterior Stapes footplate

FRICKS
Fissula ante fenestrum
Round window niche
IAC medial wall
Cochlear apex medial wall
Kockler aKqueduct (area posterior to it)
SCC adjacent area

FAF: https://anatomypubs.onlinelibrary.wiley.com/cms/asset/6b3e800a-3118-4751-9600-3de6f5941877/ar24711-fig-0009-m.jpg

Vancouver Pg 280

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6
Q

What is the fissula ante fenestram?

A

Small connective tissue-filled cleft located where the tendon of the tensor tympani muscle turns laterally toward the malleus.

Anterior to the oval window, posterior to the cohleariform process

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7
Q

What is the classic sign of cochlear otosclerosis?

A

Halo sign of otosclerosis
- Lucency aroudn the cochlea on CT imaging as the sclerotic bone that replaces the otic capsule is less dense than the original bone
- Results in “outlining” of the labyrinth
- Note: findings with Paget’s or osteogenesis imperfecta can be very similar

Mixed HL (conductive and SNHL component)
- Usually starts as conductive (where there is still stapes otosclerosis) and as you develop cochlear otosclerosis the ABG start to narrow as the sensorineural component worsens

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8
Q

What are the Histopathologic stages of otosclerosis?

A

A. Otospongiosis phase (“active phase”):
- Definition: Osteoclastic absorption of normal otic capsule bone, creating pseudovascular spaces
- Cells involved: Histiocytes, osteoclasts, and osteoblasts
- Pathophysiology: Bone around blood vessels are resorbed, the vessels dilate, and the osteocytes lay down rich amorphous ground substance (rich blue color under H&E - “Blue Mantles of Manasse”) - actually found in 20% of normal temporal bones

B. Sclerotic phase:
- Formation of dense, fibrotic, sclerotic bone in areas of previous bony resorption
- Vascular channels narrowed due to bone deposition
- Overall the bone is less dense than original petrous otic capsule, hence “halo sign” on CT imaging

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9
Q

What are the different areas (foci) of involvement of the footplate in otosclerosis? What are these terminologies? 6

A
  1. Anterior focus (most common)
  2. Posterior focus
  3. Circumferential - footplate margin only
  4. Bipolar involvement - both anterior and posterior ends of footplate involved
  5. Biscuit footplate - Involvement of the entire footplate (only) making it solid (not annular ligament)
  6. Obliterative otosclerosis - entire footplate and annular ligament involvement

Vancouver Pg 280

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10
Q

What is the pathognomonic histologic sign in otosclerosis?

A

Blue Mantles of Manasse

Vancouver PG 281

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11
Q

What are the layers of the bone involved with otosclerosis?

A
  • Always begins in endochondral bone
  • Later can involve endosteal and periosteal layers of bone

https://upload.wikimedia.org/wikipedia/commons/8/89/607_Periosteum_and_Endosteum.jpg

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12
Q

What is the Flamingo or Schwartze’s sign?

A

Reddish/Vascular tingue to Promontory seen through TM in otospongiosis phase of otosclerosis (due to high vascularity of active bony resorption)

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13
Q

What are 5 differences between Paget’s disease and otosclerosis?

A

Paget’s disease = chronic bony disorder that causes increased osteoclastic bony resorption followed by increased osteoblastic activity, but eventually leads to a stage of malignant destruction of bone.

  1. Paget’s involves all bones of the skull and often see enlarged calvaria; whereas otosclerosis only involves temporal bone
  2. Paget’s onset 6th decade, otosclerosis onset usually 3rd
  3. Paget’s initially periosteal but eventually involves endosteal and endochondral layers; otosclerosis only involves endochondral involvement
  4. Paget’s rarely involves stapes footplate or ossicles
  5. Greater degree of SNHL seen in Paget’s
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14
Q

What is the differential for patient with suspected otosclerosis? 8

A
  1. Third window lesions (Perilymph fistula, Semicircular canal dehiscence)
  2. Malleus head fixation
  3. Paget’s disease of the temporal bone
  4. Osteogenesis imperfecta (1/2 develop stapes fixation)
  5. Congenital stapes fixation (be cautious in a young male with onset of hearing loss at birth)
  6. Chronic serous otitis media
  7. Tympanosclerosis
  8. Ossicular discontinuity
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15
Q

What is the difference between middle ear pathology (ie. otosclerosis) and third window pathology in the following categories:
1. Air bone gap
2. Bone conduction thresholds
3. Acoustic refluexes
4. VeMP
5. OAEs
6. Umbo velocity on laser doppler vibrometry
7. Sound/pressure induced vertigo
8. Imaging
9. Exploratory tympanotomy

A
  1. Air bone gap
    - ME: 0-60dB, any frequencies
    - TW: 0-60dB greatest in lower frequencies
  2. Bone conduction thresholds
    - ME: Usually normal or elevated
    - TW: Can be negative (-5 to -20 or better) for frequencies below 2000Hz
  3. Acoustic refluexes
    - ME: Absent
    - TW: Present
  4. VeMP
    - ME: Absent
    - TW: Present, thresholds lower than normal, can have higher amplitude
  5. OAEs
    - ME: Absent
    - TW: May be normal
  6. Umbo velocity on laser doppler vibrometry
    - Stapes fixation = normal; malleus fixation = low; Ossicular discontinuity = high
    - TW: High-normal
  7. Sound/pressure induced vertigo
    - ME: Absent
    - TW: May be present
  8. Imaging
    - ME: May show middle ear/otosclerotic anomalies
    - TW: Third window pathology
  9. Exploratory tympanotomy
    - ME: Ossicular lesion
    - TW: Normal ossicular mobility
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16
Q

What are the audiometric and tympanometric findings of Otosclerosis? How do they change depending on stage of disease?

A

A. Conductive hearing loss with Carhart’s notch in bony line (Carhart resolves after Stapedectomy)
- Early disease: CHL mainly at low frequencies due to stiffness effect (SSCD has greater HL initially)
- Late disease: Maximal CHL with flat audiogram ~50dB due mass effect
- Later: May see involvement of cochlea with High frequency SNHL (basal turn most commonly affected)
- Primary cochlear otosclerosis: “Cooke-bite pattern” with Mixed hearing loss

B. Tympanogram:
- Early: Normal
- Late: As tympanogram (from tympanosclerosis)

C. Stapedial reflex:
- Early: Normal or Diphasic Stapedial reflex (“Negative on/off effect”) - increased compliance at the onset and cessation of sound stimulus - can even be seen before any CHL
- Intermediate: Reduced acoustic reflex amplitudes, followed by Loss of ipsilateral stapedial reflex
- Late: Elevated contralateral thresholds, which lastly leads to Loss of ipsilateral and contralateral stapedial reflexes (sound stimulus doesn’t get to inner ear due to CHL)

5 Stages: ORICD
On/off effect
Reduced ipsilateral amplitudes
Ipsilateral loss
Contralateral elevated thresholds
Disappearance of reflex altogether

Kevan Otology Pg 45

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17
Q

What are 3 etiologies of SNHL in otosclerosis?

A
  1. Toxic metabolites in endolymph causing neuroepithelial damage
  2. Vascular compromise from narrowing and sclerosis of vascular channels
  3. Direct extension of lesion into inner ear, affecting basilar membrane biomechanics and electrolyte concentrations
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18
Q

What are the 6 indications for obtaining a CT in otosclerosis?

A

Maximal CHL with concerns of round window closure
Suspicion of superior semicircular canal dehiscence
Congenital CHL (x-linked stapes gusher)
Post-op vertigo (piston malposition)
Revision Stapes
Significant SNHL component

SCLERO
- S: Significant SNHL component
- C: Congenital CHL (x-linked stapes gusher)
- L: Loss of maximal conductive hearing (ie. Maximal CHL with concerns of round window closure)
- E: Extra window (Suspicion of superior semicircular canal dehiscnece)
- R: Revision Stapes
- O: Operative issues (Post-op vertigo/piston malposition)

19
Q

What are the findings on imaging that can be seen with otosclerosis?

A

Otosclerosis is primarily a clinical diagnosis but CT temporal bones can be usedful in certain cases

Early:
- Lucency at the fissula ante fenestrum

Cochlear otosclerosis:
- Halo sign (demineralization of otic capsule bone)

Advanced cochlear otosclerosis:
- Increased density and thickening of sclerotic bone around the otic capsule

20
Q

What are the 7 criteria for diagnosis of SNHL due to cochlear otosclerosis? What is the name of this criteria?

A

Shambaugh’s Criteria (to identify patients suffering from SNHL due to otosclerosis - 7 features)

  1. Positive Schwartze’s sign in either ear
  2. Family history of surgically confirmed by stapedial otosclerosis
  3. Unilateral CHL consistent with otosclerosis and bilateral symmetric SNHL
  4. Audiogram with a flat or cookie bite curve with better than expected word discrimination for degree of SNHL
  5. Progressive pure cochlear loss beginning at the usual age of onset for otosclerosis
  6. CT scan in patient with one or more of above criteria that shows cochlear capsule demineralization (negative scan does not preclude diagnosis because mature disease resembles normal bone on CT)
  7. On-Off effect on impedance tympanometry

“HAS CUPS” HAS (clinical), CUPS (audiometric)
H: Halo Sign
A: Autosomal dominant (family history)
S: Schwartze sign
C: Cookie bite or flat audiogram with better than expected speech discrimination for degree of hearing loss
U: UNilateral CNHL consistent with OS with concomitant bilateral symmetric SNHL
P: Progressive pure cochlear loss beginning at expected age of onset for OS
S: Stapedial reflexes - diphasic on-off effect

21
Q

Discuss the overall management options of otosclerosis

A
  1. Clinical observation and serial audiometry
  2. Trial of Hearing Amplification
  3. Medial Management
    - Sodium Fluoride
    - Bisphosphonates
  4. Surgery (elective surgery, should have negative Rinne with 512 Hz fork)
    - Stapes mobilization
    - Stapedotomy (better high frequency)
    - Stapedectomy (better low frequency)
    - BAHA
22
Q

What are the indications of sodium fluoride use in otosclerosis?

A

INDICATIONS:
1. Presence of SNHL or vertigo (cochlear otosclerosis)
2. Non-surgical candidates
3. Positive Schwartze’s sign pre-op (treat for 6 months prior to surgery to achieve stability)
4. Otospongiosis type bone seen intraoperatively

“NAFL”: (Stands for Sodium Fluoride)
N: Non-surgical candidates
A: Active disease/resorption of bone (Otospongiosis type bone seen intraoperatievly)
F: Flamingo (Schwartze’s sign) pre-op (sign of active disease)
L: Loss of Hearing (SNHL or vertigo - symptoms of cochlear otosclerosis)

23
Q

Regarding Sodium fluoride for the treatment of otosclerosis, discuss:
1. Pathophysiology
2. Treatment regimen and dose
3. Side effects
4. Contraindications

A

PATHOPHYSIOLOGY:
- Thought to stabilize hearing loss associated with otosclerosis by 80%
- Replaces the usual hydroxyl ion in perosteal bone forming fluoroapatite (instead of hydroxyapatite) - fluoroapatite is less soluble than hydroxyapatite and is stronger/more resistant to demineralization/absorption (think fluoride in toothpaste)
- Effects: Reduces/slows bone resorption, encourages bone formation, clears Schwartz sign, and inactivates expanding foci of otosclerosis

TREATMENT REGIMEN/DOSE:
- Available over the counter as “Florical”
- Taken with Vitamin D and calcium gluconate
- 20-120mg daily x 1-2 years during active disease, can be used pre-operatively x6-12 months to achieve stability
- Can step down to 25mg daily maintenance dose long term
- Stopping treatment in patients whose disease has stabilized on therapy may result in reactivation in 2-3 years

SIDE EFFECTS:
1. Rash
2. Arthritis
3. Gastric distress

CONTRAINDICATIONS:
1. Pregnancy

24
Q

Discuss the use of bisphosphonates in otosclerosis treatment.
What is the mechanism of action?
What is the main risk?

A

3rd generation bisphosphonates used (Alendronate (Fosamax))
- MOA: Inhibit osteoclastic bone resorption, attaches to hydroxyapatite binding sites on bony surfaces
- Has been tried with variable results
- Some weak evidence that it might decrease progression of SNHL
- Small risk of ORN of the mandible

25
Q

What are four indications for lateral SCC fenetration in otosclerosis?

A
  1. Footplate refixation after stapedotomy
  2. Facial nerve overhang
  3. Persistent stapedial artery
  4. Absent oval window

Goal is to improve hearing by creating a new window in the labyrinth to allow perilymph to move better
- High risk of complications

26
Q

What is the difference between a Stapedotomy vs. Stapedectomy?

A

Stapedotomy: A hole made into the footplate for placement of prosthesis (e.g. with laser or microdrill)

Stapedectomy: Part or all of footplate is removed with picks or instruments, followed by placement of a graft and prosthesis

27
Q

What are the indications for stapedotomy/ectomy? 3

A
  1. Clear diagnosis of otosclerosis (other causes like SCCD ruled out)
  2. Otosclerosis with ABG ≥ 25dB at 250 to 1000Hz
  3. Negative Rinne with 512 Hz tuning fork (BC > AC)

Note: Concomitant SNHL is NOT a contraindication

28
Q

What are the 5 absolute and 7 relative contraindications for stapedotomy/ectomy?

A

Concomitant SNHL is NOT a contraindication

ABSOLUTE:
1. Otitis externa/media of chronic nature
2. Active infection or Middle ear effusion or middle ear disease (e.g. active cholesteatoma)
3. Unrepaired TM perforation (fix first)
4. Only hearing ear (unless they are candidate for CI)
5. Active Meniere’s disease or other uncompensated vestibular disorder

RELATIVE:
1. Family history of stapes footplate fixation or stapes gusher syndromes
2. Congenital x-linked deafness with stapes fixation (risk of perilymph gusher)
3. History of cholesteatoma
4. Repetitive barotraumas
5. Severe ET dysfunction
5. Employment requiring excellent balance or excellent taste (need to inform thoroughly)
6. Down sloping SNHL loss pre-op or post-op in first ear (often hearing will deteriorate post-op)
7. Extremes of age

Note: Avoid operating in otospongiosis phase of otosclerosis

29
Q

What are all the possible complications of a stapedotomy/stapedectomy?

A

PRE-OPERATIVE:
1. Anesthesia

INTRA-OPERATIVE:
1. General Anesthesia
2. Bleeding - high riding IJV, persistent stapedial argery
3. TM perforation/flap tear (repair with gelfoam or paper patch for small perf, underlay graft for large)
4. Facial nerve injury (overhanging CNVII - gently retract superiorly and proceed)
5. Chorda tympani injury (30%, results in metal taste, sore tongue, dry mouth; better to cut than stretch)
6. Perilymph gusher (< 1% - tissue graft to oval window and complete surgery, otherwise pack ear and stop, use CSF measures post-op)
7. Floating footplate/depressed footplate
8. Incus fracture (complete surgery if not completely broken off, otherwise use TORP or incus replacement prosthesis IRP)
9. Malleoincudal dislocation (remove incus and use TORP or IRP)
10. Malleus fixation (remove incus and use TORP or IRP)

EARLY POST-OPERATIVE COMPLICATIONS:
1. Infection 5% - usually subsides after a few days (Otitis media, Labyrinthitis, Meningitis, Vertigo/Dysequilirbium
2. Perilymph fistula (3-10%, rare with small fenestra, causes mixed HL, needs revision)
3. Oval window granuloma (causes HL, vertigo, and reddish mass in posterior-superior TM 1-6 weeks post op; associated with use of gelatin sponges or fat in OW; treat with prompt removal of granuloma in OR and replace implant)
4. Persistent TM perforation
5. Delayed facial palsy (onset up to 5 days post-op, treat with prednisone, usually resolves)
6. Dysgeusia (10%, most resolve by 4 months)
7. Tinnitus
8. Profound SNHL (< 1%, treat with prednisone 60mg x 5 days then taper)
9. Delayed SNHL (1%)

LATE POST-OPERATIVE COMPLICATIONS:
1. Fluctuating CHL (due to loose prosthesis or incus necrosis)
2. Persistent hearing loss/signs/symptoms

30
Q

What are reasons for failure/causes of (delayed) hearing loss following stapedotomy/ectomy for otosclerosis? (10)

A
  1. Prosthesis displacement (#1 cause)
  2. Incus tip erosion
  3. Footplate refixation
  4. Depressed footplate
  5. Prosthesis too deep in oval window
  6. Perilymph fistula
  7. Oval window reparative granuloma
  8. Otosclerotic regrowth
  9. Wrong diagnosis (e.g. SCCD, malleus head fixation)
  10. Cochlear Otosclerosis
31
Q

In stapedial surgery, how do you manage the following conditions:
1. Floating footplate
2. Depressed footplate
3. Biscuit footplate

A
  1. Floating footplate
    - Remove completely (convert to stapedectomy), Drill inferior to oval window at promontory and use pick to elevate, then place fascia graft and prosthesis; OR
    - Place shorter prosthesis over it
  2. Depressed footplate
    - Leave depressed and seal with vein graft; OR
    - Similar to floating footplate
    - DO NOT remove if fallen completely into vestibule
  3. Biscuit footplate
    - Management dependent on if using microdrill or laser, and if stapedectomy or stapedotomy
    - If drilling, saucerize widely before making stapedotomy
32
Q

What are 4 essential steps in stapes surgery?

A
  1. Confirm stapes fixation
  2. Assess other ossicles for fixation
  3. Assess facial nerve (its relation to footplate and dehiscence)
  4. Determine presence of persistent stapedial artery
33
Q

What are congenital causes that increases the risk for stapes gusher?

A
  1. Enlarged vestibular aqueduct
  2. Congenital X-linked mixed hearing loss (associated with congenital stapes fixation and perilymph gusher)
  3. Mondini malformation
34
Q

How does a reparative granuloma present post-stapedotomy/ectomy, and how is it managed?

A

Presentation:
- Early correct of ABG
- Subsequent worsening SNHL, vertigo, and tinnitus

Treatment:
- Re-explore ear
- Remove granuloma if present
- ± Replace prosthesis

35
Q

What are the most common causes of malleus head fixation?

A
  1. Otosclerosis
  2. Tympanosclerosis
  3. Congenital
  4. Post-infectious
  5. Trauma
36
Q

Differential for fixed conductive hearing loss?

A
  1. Otosclerosis
  2. Ossicular chain discontinuity
  3. Malleus head fixation
  4. TYmpanosclerosis
  5. TM perforation
  6. Congenital stapes fixation
  7. Ossicular fracture (e.g. in osteogenesis imperfect)
  8. Paget’s disease of the temporal bone
  9. Middle ear tumor
  10. COME
37
Q

Discuss the standard results/prognosis for stapedectomy, for both initial and revision surgery

A

INITIAL STAPEDECTOMY:
- 90% have closure of ABG to < 10dB
- 10% no change
- 1-2% profound SNHL

CONGENITAL:
- 40-80% improvement

REVISION STAPEDECTOMY:
- 65% have successful result
- 7x increased risk of profound SNHL

38
Q

You are doing an exploratory tympanostomy and find bilateral crural fractures. Name 4 different repair options.

A
  1. Otomimix (bone cement)
  2. TORP - Total ossicular reconstruction prosthesis
  3. Stapedotomy
  4. Close and counsel on further surgery or hearing aid
39
Q

What is a perilymph gusher vs. fistula?

A

“Gusher” is a sudden and profuse perilymphatic flow that occurs immediately after platinotomy and often fills up in the middle ear and external auditory canal

Fistula = Abnormal communication between the perilymph filled inner ear and the middle ear cavity, mastoid, or intracranial cavity

40
Q

Name 4 conditions that are associated with perilymph gusher

A
  1. X-linked stapes gusher syndrome
  2. Congenital Fixed footplate (only has stapes fixation, whereas x-linked may have other anomalies)
  3. Mondini deformity
  4. Enlarged vestibular aqueduct
41
Q

Regarding x-linked stapes gusher syndrome, discuss:
1. Genetics and Inheritance
2. Signs and symptoms. What is the main type of hearing loss?
3. Imaging abnormalities (5)

A

GENETICS:
1. DFN3 gene
2. Rare syndrome

ClLINICAL PRESENTATION:
1. Congenital progressive mixed hearing loss (to severe hearing loss)
2. Fixed stapes footplate
3. Perilymph gushing during attempted stapedectomy

IMAGING ABNORMALITIES:
1. Cochlear Modilous deficient
2. Lateral portion of IAC bulbous (with incomplete separation of basal turn of cochlea from the fundi of the IAC)
3. Labyrinthine portion of fallopian canal dilated
4. Posterior SCC dysplasia
5. Enlarged vestibular aqueduct

DICED:
D - Dilated labyrinthine portion of fallopian canal
I - IAC bulbous laterally
C - Cochlear modiolus deficient
E - EVA
D - Dysplastic pSCC

42
Q

What is the Modiolus?

A

Modiolus = part of cochlea/conical-shaped structure consisting of spongy (porous) bone located in the centre and contains the spiral ganglion

43
Q

What are the steps in the OR for a patient with a known X-linked gusher?

A
  1. Elevate HOV
  2. Tisseal placed prior to prosthesis
  3. Consider a lumbar drain

Otology & Neurotology (17 decks)

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