3. Otosclerosis is a localized hereditary disorder
affecting endochondral bone of the otic capsule that
is characterized by disordered resorption and
deposition of bone.
An otosclerotic lesion consists of areas of bone
resorption, new bone formation, vascular
proliferation and a connective tissue stroma.
DEFINITION
4. 'CLINICAL' OTOSCLEROSIS refers to a lesion that involves
the stapes bone or stapediovestibular joint and consequently is
clinically manifested by a conductive hearing impairment.
'HISTOLOGIC' OTOSCLEROSIS refers to a lesion that does
not involve the stapes bone, stapediovestibular joint or
cochlear endosteum, is consequently asymptomatic, and can
be diagnosed only by post-mortem examination of the
temporal bone.
'COCHLEAR' OTOSCLEROSIS is a term generally
reserved for the occurrence of pure sensorineural hearing
impairment due to otosclerosis in an ear without any
conductive component to the hearing impairment.
(involvement of the cochlear endosteum but without any stapes
fixation.)
TYPES
5. The bone of the otic capsule is unique that it exhibits
very little remodeling .
It contains small regions of immature cartilaginous tissue
called globuli interossei.
Otosclerotic focus easily diagnosed due to bone remodelling.
PATHOLOGY
6. BLUE MANTLES OF MANASSEH
'BLUE MANTLE'. BLUE MANTLES ARE AREAS OF
THE OTIC CAPSULE THAT STAIN MORE
BASOPHILIC THAN NORMAL
7. OTOSCLEROTIC FOCUS CONSISTS OF
BONE RESORPTION
NEW BONE FORMATION
VASCULAR PROLIFERATION
CONNECTIVE TISSUE STROMA
8. RESORPTION OF ENCHONDRAL BONE
ENLARGEMENT OF PERIVASCULAR SPACES
DEPOSITION OF IMMATURE BONE
ACTIVE RESORPTION + REMODELLING
MATURE(LAMELLAR BONE)
NEW BONE FORMATION– OSTEOBLAST
RESORPTION– OSTEOCLAST
CONNECTIVE TISSUE STROMA OF FIBROBLAST AND
HISTOCYTES
NO INFLAMMATORY CELLS SEEN
9. An otosclerotic focus may appear as
ACTIVE OR 'SPONGIOTIC', CHARACTERIZED BY
areas of increased cellularity and vascularity
bone resorption
new bone formation
INACTIVE 'SCLEROTIC' FOCUS
consisting of dense mineralized bone.
COMMON FOR AN OTOSCLEROTIC FOCUS TO CONTAIN
BOTH ACTIVE AND INACTIVE REGION
14. Most common site being the area anterior to the oval
window (80-95 percent) -- Fissula ante fenestrum (anterior to
stapes foot plate)
Round window niche (about 30 percent)
The apical medial wall of the cochlear labyrinth (about 15
percent)
The stapes footplate (about 12 percent)
Posterior to the oval window (5-10 percent)
Otosclerosis is usually bilateral, with involvement of both
ears in 70-90 percent of cases.
Foci of clinical or histologic otosclerosis can be single or
multiple within the temporal bone.
DISTRIBUTION OF OTOSCLEROTIC FOCUS
15. Conductive hearing impairment ranging from 5 to
60 dB (stapes involvement).
RECENT CONCEPT : Conductive hearing
impairment appeared to be caused primarily by
narrowing and impairment of the annular ligament
especially at the posterior stapediovestibular joint
space.
PATHOLOGY OF CONDUCTIVE DEAFNESS
16. SCHWARTZE'S SIGN
• The middle ear mucosa over
an otosclerotic focus often
shows a fibro vascular
proliferative response with
hypertrophy, deposition of
connective tissue and
increased vascularity.
• Red vascular blush seen at
otoscopy in patients with
active otosclerosis
(Schwartze's sign).
17. Complete obstruction of the
round window membrane
means that stapes surgery in
such an ear will not be
successful.
Round window closure
may be diagnosed by
Intraoperative examination
as well as by high
resolution computed
tomography (CT) scan
imaging.
COMPLETE OBSTRUCTION OF THE ROUND
WINDOW
18. The cytokines released by the remodeling bone within an
otosclerotic focus
that has reached the ligament
could diffuse into the spiral ligament
upset the normal state of cytokine control within the spiral
ligament.
alteration the fluid and ion hemostasis within cochlea
SNHL
PATHOLOGY OF SENSORINEURAL
HEARING IMPAIRMENT
19. When endosteum of cochlea involved there is
'hyalinization' of the spiral ligament.
PATHOLOGY OF SENSORINEURAL
HEARING IMPAIRMENT
20. Liberation of toxic metabolites
into fluid of inner ear
Vascular compromise and
hypoxemia of strucure of
middle ear
Alteration of the fluid and ion
hemostasis within cochlea due
to spiral ligament involvement
21. Unsteadiness or dizziness or recurrent attacks of vertigo
10-30%
The incidence of vestibular symptoms in such patients seems
to be correlated with the degree of sensorineural hearing
impairment.
Scarpa's ganglion cell counts were significantly lower in
patients who had vestibular symptoms.
Damage to the scrapa ganglion due to toxic substances liberated
from otosclerotic bone
Vertigo could be produced a result of otosclerotic focus coming
in contact with perilymph.
PATHOLOGY OF VESTIBULAR SYMPTOMS
22. GENETIC
The small histologic foci are ten-fold more common
than the larger lesions that result in clinical
manifestations
F:M = 2:1, Whites commonly affected
Age of onset. Deafness usually starts between 20 and 30
years of age and is rare before 10 and after 40 years.
AD transmission with incomplete penetration.
Sporadic > Familial
AETIOLOGY
23. Type 1 osteogenesis imperfecta shares both clinical and
histologic similarities with otosclerosis.
Approximately half of all patients with type 1 osteogenesis
imperfecta develop hearing loss that is clinically
indistinguishable from clinical otosclerosis.
Some patients with clinical otosclerosis have blue sclera, a
feature that is found in virtually all patients with type 1
osteogenesis imperfecta
DEFECTS IN EXPRESSION OF THE
COL1A1 GENE
24. Otosclerosis may be related to a persistent viral
infection of bone
Ultrastructural and immunohistochemical evidence of
measles like structure and antigenicity in active
otosclerotic lesion
Measles RNA has been found in archival and fresh
footplate specimens with otosclerosis.
Elevated levels of anti-measles antibody has also been
reported in perilymph from patients undergoing
stapedectomy for otosclerosis as compared to controls.
Low levels of anti measles antibody in patients with
otosclerosis.
MEASLES ASSOCIATION
25. Otosclerosis represents a form of autoimmune
disease with humoral autoimmunity to type II
collagen.
Elevated circulating antibodies to type II collagen
in the blood of some patients with otosclerosis
has also been reported.
Immunohistochemical analysis has shown tissue
bound igG in active areas
AUTOIMMUNE DISEASE
26. Otosclerosis occurs as a result of reactivation of
the arrested secondary remodelling process within
the cartilaginous rest areas of the otic capsule .
BIOCHEMISTRY
28. (M:F=1:2.5)
Women more commonly seek medical
attention for hearing loss secondary to
otosclerosis
histologic studies prevalence of otosclerosis
show no difference in men versus women
SEX VARIATION
29. The incidence of otosclerosis increases with
age.
The most common age group presenting with
hearing loss from otosclerosis is 15-45 years
however it has been reported to manifest as
early as 7 years and as late as the mid 50s.
AGE
30. OTOMICROSCOPY
TM appears normal in the majority of
patients
Schwartze sign (flamingo flush) is observed in
10% of patients).
Most helpful in ruling out other disorders
Middle ear effusions
Tympanosclerosis
Tympanic membrane perforations
Cholesteatoma or retraction pockets
PHYSICAL EXAMINATION
31. Rinnes –
negative
Webers –
lateralized to
more
affected ear
ABC--
normal
Stapedial
otosclerosis
Rinnes –
positive
Webers –
lateralized
to better
ear
ABC--
reduced
Cochlear
otosclerosis
TUNNING FORK TESTS
32. Early stage: a decrease in air conduction in the low
frequency, especially below 1000 Hz.
As the disease progresses, the air line flattens.
because the otosclerotic focus has a mass affect on
the entire system, carhart notch is noted.
PURE TONE AUDIOMETRY
33. CARHART’S NOTCH
• Hallmark audiologic
sign of otosclerosis
• Decrease in bone
conduction thresholds
5 dB at 500 Hz
10 dB at 1000 Hz
15 dB at 2000 Hz
5 dB at 4000 Hz
34. Mechanical artifact
Reverses with stapes mobilization
PROPOSED THEORY OF CARHART’S
NOTCH
Stapes fixation disrupts the normal ossicular
resonance (2000 Hz)
Normal compressional mode of bone conduction is
disturbed because of relative perilymph immobility
35. The reason why CARHART EFFECT occurs it that when the
skull is vibrated by bone- conduction sound, the sound is
detected by the cochlea via three routes Route
(a) is by direct vibration within the skull, route
(b) is by vibration of the ossicular chain which is suspended.
within the skull .
(c) is by vibrations emanating into the external auditory
canal as sound and being heard by the normal air-
conduction route.
Regained by successful reconstruction surgery . The reason
that there is a Carhart notch at 2 kHz before the surgery
is that the Carhart effect is greatest around that
frequency
36.
37. CT can characterize the extent
of the otosclerotic focus at the
oval window .
CT scan can determine
capsular involvement
(radiolucent) when patients
have significant mixed hearing
loss
An enlarged cochlear aqueduct
may be seen which potential
causes perilymph gusher
during footplate fenestration
or removal.
It reveal normal round window
and normal mastoid
pneumatization.
38. Ossicular discontinuity
• conductive loss of 60 db usually without sensorineural
component
• flaccid tympanic membrane on pneumatic otoscopy
• type Ad tympanogram
Malleus head fixation
• when congenital, associated with other stigmata (aural atresia)
• presence of tympanosclerosis
• almost always associated with type As tympanogram (only in
advanced otosclerosis)
DIFFERENTIAL DIAGNOSIS
39. Congenital stapes fixation
• Family history less likely (10%)
• usually detected in the first decade of life
• 25% incidence of other congenital anomalies (3% for juvenile
otosclerosis)
• non-progressive CHL
Osteogenesis imperfecta
• presence of blue sclera
• h/o of multiple bone fractures
• CT – more common involves the otic capsule
40. Paget’s disease
• - diffuse involvement of the bony skeleton
• - elevated alkaline phosphatase
• - CT - diffuse, bilateral, petrous bone involvement with
extensive de-mineralization
• - More commonly crowds the ossicles in the epitympanum,
partially fixing
42. 1704 – Valsalva first described stapes fixation
1857 – Toynbee linked stapes fixation to
hearing loss
1890 – Katz was first to find microscopic
evidence of otosclerosis
1893 – Politzer described the clinical entity of
“otosclerosis”
HISTORY OF OTOSCLEROSIS
43. 1912 – Siebenmann proposed a change of
nomenclature from otosclerosis to otospongiosis
1950– Raymond Thomas Carhart originated the term
air bone gap .
Reported notching in bone conduction in cases of
stapedial otosclerosis
44. 1878– Kessel—first successful stapes surgery
1890– Miot reported a series of 200 stapes
mobilization surgery
1900 Politzer and Siebenmann condemned stapes
surgery because of potential risk to cause meningitis
1916-- Gunnar Holmgren
Father of fenestration surgery
Single stage technique
Not successful in maintaining an open fenestra
HISTORY OF STAPES SURGERY
45. 1924– Sourdille
Tympanolabyrithopexy
Two stage procedure
Covering fistula in HSC with skin of EAC
1941– Lempert
Popularized the single staged fenestration procedure
Extraction of incus – no reduction in hearing
Extraction of incus – more space to create a wider fenestra
46. 1953– Rosen
first suggested mobilization of the stapes
Immediate improved hearing
1956– Shea
first to perform stapedectomy
Used operating microscope
Sealed the oval window
Homograft bone graft between oval window and incus
Immediate hearing gain
Over time– hearing loss due to adhesion
1960 Shea used teflon piston– STAPES SURGERY WAS
BORN
49. Cartilage persists throughout life in various
region of OTIC CAPSULE
Fissula ante fenestram
Fossula post fenestram
Intracochlear area(enchondral layer)
Cochlear area (round window)
Semicircular canal
Petrosquamous suture
Base of styloid process
ANATOMY OF OTIC CAPSULE
51. These contain area of
Cartilage cell remains + calcified cartilaginous matrix
Calcified area – capillary bud
Osteoblast
Deposit bone in lacunae
Small bony globules or globuli ossei
Globuli interossei (region of immature cartilage)
Loci of earliest otosclerosis
52. Early stage– low frequency conductive hearing loss
High frequency unaffected
AUDIOGRAM—RISING AUDIOGRAM / STIFFNESS TILT
Otosclerotic focus proliferates
Mass effect added to audiogram
low frequency conductive hearing loss- stabilizes
High frequency loss occurs
Flat pattern on AUDIOGRAM
AUDIOLOGICAL EVALUATION OF THE
PATIENT WITH OTOSCLEROSIS
53. IN COCHLEAR OTOSCLEROSIS
Air conduction worsen
Mixed or SNHL
High frequency more affected
Greatest degree hearing loss in mid frequency
Cookie bite pattern
54. Carharts notch
Hallmark audiologic sign of otosclerosis
Decrease in bone conduction thresholds
5 dB at 500 Hz
10 dB at 1000 Hz
15 dB at 2000 Hz
5 dB at 4000 Hz
BONE CONDUCTION
55. BING TEST
Meatus occluded or pressure varied
No shift of loudness
Bone conduction always abnormal
Surgery improves bone conduction and carharts
notch disappears following surgery
Animal experiments– bone conduction poorer
56. Tympanogram—normal pressure with normal volume
Static compliance
low compliance
Less than .2– footplate thick or obliterative otosclerosis
More than .6– footplate is thin
Acoustic reflex
IMPEDANCE AUDIOMETRY
57. Earliest evidence of otosclerosis
Diphasic pattern
Increase in compliance at onset and termination of
stimuli (probe in affected ear)
ACOUSTIC REFLEX
58. Ant footplate fixed
Elasticity—posterior footplate
Move independently
Onset compliance change
Elasticity returns to normal
Remains till pull of stapedius is relaxed
Offset compliance change
DIPHASIC PATTERN
60. CONTRACTION OF TENSOR TYMPANI TESTED SEPARATELY
STIMULATION OF TRIGEMINAL NERVE AND DOING AUDIOMETRY
STARTLE TYPE REFLEX
FATIGUEBLE IN NATURE
UNSTABLE
LONG LATENCY PERIOD
NON ACOUSTIC REFLEX
61. If speech discrimination score (SDS) score is poor
SNHL component to hearing loss
Prognosis poor following surgery
Pt. benefit more by hearing aid
SPEECH AUDIOMETRY
62. Transient evoked otoacoustic emission (TEOAE) have
low amplitude
OAE less role in otosclerosis
Lack specificity
Early identification of cochlear otosclerosis
OTOACOUSTIC EMISSION
64. Is a term generally reserved for the occurrence
of pure sensorineural hearing impairment due to
otosclerosis in an ear without any conductive
component to the hearing impairment.
(involvement of the cochlear endosteum but without
any stapes fixation.)
65. Dominant family history
Female>male
Hearing loss started or increased during pregnancy
or following use of ocp
Schwartzes sign positive
SNHL
Tinnitus vertigo
SIGNS SYMPTOMS
66. PTA– Cookie bite
Type 2 Tympanogram
SDS 80 to 90 %
SISI – high
Stapedial reflex – present
HEARING TESTS
67. In pure cochlear otosclerosis tinnitus is usually the presenting
symptom
Endolymphatic hydrops seen as a complication of cochlear
otosclerosis
BPPV is also commonly seen
68. 1926 SHAMBAUGH ( 3 CRITERIA )
1966 SHAMBAUGH (6 CRITERIA ) – COCHLEAR
OTOSCLEROSIS
1981 BEALES (8 CRITERIA ) COCHLEAR
OTOSCLEROSIS
1975 CAUSSE ET AL 3 TYPES OF CRITERIA
DIAGNOSIS OF COCHLEAR
OTOSCLEROSIS
69. 1. insidious onset + early adulthood
2. absence of other cause that may lead to hearing loss
3. conductive hearing loss in family member
1926 SHAMBAUGH ( 3 CRITERIA )
70. 1. + schwartzes sign
2. Family history of otosclerosis
3. SNHL in both ear
4. Flat rising , cookie bite ; good SDS for SNHL
5. SNHL early in life and other cause cannot be found out
6. fixation of stapes with SNHL
1966 SHAMBAUGH (6 CRITERIA ) –
COCHLEAR OTOSCLEROSIS
71. 1. SNHL with good SDS
2. RECRUITMENt + ; high SISI ; BEKESY TYPE 2
3. progression of SNHL
4. b/l symmetrical SNHL
5. unusual configuration in audiogram
6. successful use of hearing aid
7. paracusis willis in early adulthood
8. negative RINNE test
1981 BEALES (8 CRITERIA ) COCHLEAR
OTOSCLEROSIS
72. 1. Criteria of presumption
SNHL from childhood increase during puberty +
family history of SNHL
SNHL in female increased by PREGNANCY ;
MENSTRUATION ; MENOPAUSE ; INTAKE OF
OCP
SNHL + GOOD SDS
Criteria of probability
+ SCHWARTZES SIGN
SNHL + COOKIE BITE ON AUDIOGRAM
+ Radiological findings
1975 CAUSSE ET AL 3 TYPES OF
CRITERIA
73. Criteria of certainity
DIPHASIC impedance in case of SNHL
ABG in case of SNHL and absence of stapedial reflex
CT scan demonstartes cochlear otosclerosis
78. MECHANISM OF ACTION
Reduce bone resorption + increase bone formation
Antienzymatic action – proteolytic enzymes cytotoxic to
cochlea
NaF acts only on active focus
Reduces osteoclastic when focus is active
Inc osteoblastic activity
HYDROXYAPATITE ---------------- FLUORAPATITE
SODIUM FLOURIDE
• HARDER
• BETTER
QUALITY
• RESISTANT TO
BONE
RESORPTION
F ION
79. ACID PHENYLPHOSPHATASE
ENZYME OF BONE RESORPTION
INC IN OTOSCLEROSIS
THERAPY OF FLUORINE
ENZYME DECLINE
OPTIMAL DOSE OF NAF– 60mg daily
80. Stapedial otosclerosis + SNHL disproportionate to age
Cochlear otosclerosis + f/h of otosclerosis +early age of
onset + audiometric pattern + good SDS
Radiological signs
+ SCHWARTZES SIGN
Otosclerosis with secondary hydrops
Surgery refused by pt. And seeks an alternative form of
treatment
INDICATION OF NAF
81. Chronic nephritis with nitrogen retention – toxic build up
Rheumatoid arthritis – inc joint pain
Pregnant and lactating
Children in whom skeletal growth not achieved
Skeletal fluorosis
Allergy to fluoride
CONTRA INDICATION
82. Early fluorosis in spine
Hydroxyfluoric acid in stomach
Gastric disturbance
Prevented by enteric coating
Chronic arthritis
SIDE EFFECTS
83. MECHANISM OF ACTION
Antienzymatic action
Reduces osteoclastic activity
Stablise secondary bone formation
ETIDRONATE– Halt progression of otosclerotic activity
Newer –
Alendronate
Residronate
zolendronate
BIPHOSPHONATES
84. Reduce resorption of bone
IL 1 ANTAGONIST AND TNF BINDING PROTEIN
HALT BONE RESORPTION
Effective only in active phase
CYTOKINE INHIBITORS
85. Patient not fit for surgery
Only hearing ear
Inadequate hearing reserve / poor SDS
Congenital fixation of stapes
Surgery not elected by patient
Mild conductive deafness
HEARING AIDS
86. Unsuccessful stapes surgery in other ear
Otosclerosis + menieres
Stapedectomy done in advanced otosclerosis
89. GOOD HEALTH WITH A SOCIALLY ACCEPTABLE ABG,
A NEGATIVE RINNE TEST,
EXCELLENT DISCRIMINATION(>70%)
THE DESIRE FOR SURGERY AFTER AN APPROPRIATE PERIOD OF
TIME FOR DELIBERATION.
YOUNGER PATIENTS ARE MORE LIKELY TO DEVELOP RE-
OSSIFICATION OF THE STAPES FOOTPLATE OVER THEIR
LIFETIME.
INDICATIONS
90. Absolute contraindication
Only hearing ear
Relative contra indication
Active middle ear infection
Hydrops and tinnitus
Severe atelectasis
Unfit for surgery
Schwartzes sign – controversy
Pregnancy
Boxers, wrestlers
CONTRA INDICATIONS
92. Shape and mobility of
Incus
Malleus
Presence of otosclerosis
Fixation of stapes
Patency round window
Facial neve
Chorda tympani status
OPERATIVE NOTE
93. Less trauma to the oval window
Less possibility of damaging to the inner ear
Less complication
Better results
In addition, revision surgery, if required, is easier due to
preserved anatomy
Done with laser also
STAPEDOTOMY
94. Results probably are the best
Easy to perform
More traumatic to the inner ear
Increased post-op vestibular symptoms
Higher incidence of postoperative SNHL
The operation is unavoidable in:
Comminuted fracture of the footplate
Revision surgery
Floating footplate
Footplate removed accidently while removing the
suprastructure
STAPEDECTOMY
95. General anesthesia
Local anesthesia
2-3 cc of 1% lidocaine with
1:50,000 or 1:100,000
epinephrine
4 quadrants
Bony cartilaginous junction
PROCEDURE
97. 6 and 12 o’clock positions
6-8 mm lateral to the annulus
Annulus subluxated from groove
and middle ear cavity entered
98. Bony annulus curetted
Stapedius tendon
Pyramidal eminence
Long process incus
Chorda tympani nerve encountered
Separate the chorda from the
medial surface of the malleus
Avoid stretching the nerve
Cut the nerve rather than stretch it
100. Division of stapedial tendon
Divided near pyramidal
eminence
Incudostapedial joint
divided usually by right
angled pick
101. Control hole made
Stapes fractured towards
promontary
Causse crurotomy scissors
Too much force– floating
footplate
102. Mucosa over footplate excoriated
Prevent perilymph fistula formation
Measurement
Medial aspect of the long process of
the incus to the footplate
Average 4.5 mm
add .5mm
.25mm of prosthesis projects into
vestibule
103. Fenestra in post 1/3 to prevent
damage to the saccule and
utricle
Aspirator not to be used to avoid
aspiration of perilymph
Oval window seal
Tragal perichondrium
Vein (hand or wrist)
Temporalis fascia
Blood
Fat
104. Prosthesis types
Robinson bucket handle
prosthesis
Causse prosthesis
Fisch/Mc Gee piston
prosthesis
House wire prosthesis
Prosthesis is chosen and
length picked
Some prefer bucket handle
to incorporate the lenticular
process of the incus
105. 0.7mm diamond burr
Motion of the burr removes
bone dust
Avoids smoke production
Avoids surrounding heat
production
DRILL FENESTRATION
106. Carbon dioxide (CO2)
10,000 nm
Not in visible light range
Adv
Near ideal absorption
Penetration low
Disadv
Surgical beam only
Requires separate laser for an aiming beam (red helium-neon)
Ill defined fuzzy beam
Working distance more
LASER FENESTRATION
107. Argon and Potassium titanyl phosphate
(KTP/532)
Wave length 500 nm
Visible light
Absorbed by hemoglobin
Adv
Hand held probe
Surgical and aiming beam
Disadv
Char formation
LASER FENESTRATION
109. Vaporization of anterior crus
and mobilization of posterior
part of footplate
Preservation of the stapedius
tendon
Reduction in hyperacusis
Reduction in risk for long-term
postoperative inner ear injuries
No prosthesis complications
Very difficult technique
STAMP(STAPEDOTOMY MINUS
PROSTHESIS)
112. Proceed & then repair
Tragal perichondrium
Fascia
Gelform
TEAR IN TYMPANOMEATAL FLAP
113. Curettage around bony annulus
Separation of incudostapedial joint
Manipulation around oval window
Treatment
Subluxation– incus attachment prosthesis
Disarticulation – remove incus and put
malleus attachment prosthesis
SUBLUXATION OF INCUS
114. OVERHANGING FN
• Usually dehiscent
• If prolapsed nerve abrupts the
promontary inferor to oval window
– surgery to be aborted
• Surgery usually completed by
making a small fenestra in the
inferior aspect
• Prosthesis is usually longer to
accommodate the bend of nerve
115. Laser not sufficient to remove bone
Small fenestra to be made
Drill out the excess bone
Blue lined vestibule
Fenestra to be made
Long prosthesis
OBLITERATIVE OTOSCLEROSIS
INVOLVING OVAL
WINDOW
116. Per op finding
Leave it as it is
Complete procedure and note
it as a finding
OTOSCLEROSIS INVOLVING ROUND
WINDOW NICHE
117. Pulsatile tinnitus CHL SNHL
Bleeding during operation
Fenestration to be made in post half
PERSISTENT STAPEDIAL ARTERY
118. Pre op diagnosis
Reduced movement of manubrium
Palpation of malleus
Laser Doppler vibrometry
Small AB gap
Non acoustic reflex -- faint
Myringosclerosis
Removal of malleus head and reconstruction with
malleus attachment prosthesis
MALLEUS ANKYLOSIS
119. fundal defect of IAM – prilymph gusher
widened cochlear aqueduct – perilymph oozer
Ct scan
Treatment
Elevation oh head
Introduce spinal catheter and proceed
Small fenestra stapedotomy
Tissue seal over fenestra
Complete control required as may cause post op complications
Avoid cork bottle effect
PERILYMPH GUSHER OOZER
120. May be avoided if control holes are used
or by using laser fenestration
Laser is used
Assess movement of suprastructure before
disarticulation
Treatment
Small hole inferior to annular ligament
Elevation by small hook
Opening sealed with tissue graft
Appropriate sized prosthesis put
FLOATING OR DEPRESSED FOOTPLATE
122. • PRIMARY & SECONDARY
Prevention:
• Stapedectomy < stapedotomy
• Oval window seal
• No fat or gel-foam for seal
• Prohibit nose blowing, flying, diving, & lifting heavy
objects postoperatively
PERILYMPH FISTULA
123. DIAGNOSIS:
Fluctuation hearing Loss
Vertigo & tinnitus
Fullness of ear
Audiometry– SNHL
ENG– directional fixed positional nystagmus
Fistula test
radiology—presence of air bubble in vestibule at prosthesis end
TREATMENT:
Surgical closure
124.
125. Immediate or Delayed
<3 hrs due to anesthesia
>3 hrs due to operative procedure
ointegrity of nerve – steroids
ointegrity of nerve not sure– exploration
odelayed facial nerve palsy -- rare
FACIAL PALSY
126. Sacrificing the nerve better than stretching it
Injury leads to hypogeusia and dysgeusia
Stretching leads to metallic taste, altered taste to
various food, altered taste
CHORDA TYMPANI INJURY
127. Immediate post op period
Worrisome
Serous labyrinthitis meningitis
Treatment
Removal of pack
Admission
Broad spectrum anti biotic
ACUTE OTITIS MEDIA
128. Granulation tissue formation around a stapes prosthesis and
the oval window which may extend into the vestibule.
1-5%
Gradual deterioration 5-15 days postoperativly
Vertigo, tinnitus, nystagmus towards non op side and deafness
Otoscopy: reddish discoloration of the postero-superior TM
Mixed hearing loss reduced SDS
Many surgeons would now advocate a more conservative
policy of steroids and antibiotics initially and some would
consider delayed surgery if no improvement occurred.
REPARATIVE GRANULOMA
129. 0.2-10%
Serous labyrinthitis - high frequencies
Surgical trauma
Movement of stapes
Rupture of membranes of inner ear
Rapid loss of perilymph
hydrops
SNHL
