OTOSCLEROSIS

ADITYA GHOSH ROY

PGT-2 M.S. E.N.T.
N.R.S.M.C.H.
 PARRT 1
ADITYA GHOSH ROY
PGT-2 M.S. E.N.T.
N.R.S.M.C.H.
 DEFINITION

 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.
 TYPES

 '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' OTOSCLEROSI S 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.)
 PATHOLOGY

 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.

 BLUE MANTLES OF MANASSEH

'BLUE MANTLE'. BLUE MANTLES ARE AREAS OF

THE OTIC CAPSULE THAT STAIN MORE BASOPHILIC
THAN NORMAL
OTOSCLEROTIC FOCUS CONSISTS OF
BONE RESORPTION

NEW BONE FORMATION

VASCULAR PROLIFERATION

CONNECTIVE TISSUE STROMA

 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
 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
NON-CLINICAL FOCI OF
OTOSCLEROSIS
ANTERIOR FOOTPLATE INVOLVEMENT
Bipolar involvement of
the footplate
ORGAN OF CORTI
DISTRIBUTION OF OTOSCLEROTIC FOCUS

 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.
 PATHOLOGY OF CONDUCTIVE DEAFNESS

 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.
 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).
COMPLETE OBSTRUCTION OF THE ROUND
WINDOW
 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.
 PATHOLOGY OF SENSORINEURAL
HEARING IMPAIRMENT
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
 When endosteum of cochlea involved there is
'hyalinization' of the spiral ligament.
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
PATHOLOGY OF VESTIBULAR SYMPTOMS

 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.
 AETIOLOGY

 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

 DEFECTS IN EXPRESSION OF THE
COL1A1 GENE

 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
 MEASLES ASSOCIATION

 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.
 AUTOIMMUNE DISEASE

 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
 BIOCHEMISTRY

 Otosclerosis occurs as a result of reactivation of

the arrested secondary remodelling process within
the cartilaginous rest areas of the otic capsule .
 EPIDEMIOLOGY

Race incidence of microscopic otosclerosis

Caucasian 10%
Asian 5%
African American 1%
Native American 0%
 SEX VARIATION

(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
 AGE

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.
 PHYSICAL EXAMINATION

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
 TUNNING FORK TESTS

Stapedial Cochlear
otosclerosis otosclerosis
Rinnes – Rinnes –
negative positive
Webers – Webers –
lateralized to lateralized
more to better
affected ear ear
ABC-- ABC--
normal reduced
 PURE TONE AUDIOMETRY

 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.
 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
 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

 Mechanical artifact
 Reverses with stapes mobilization
 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 Carhar t notch at 2 kHz before the surger y
is that the Carhart effect is greatest around that
frequency
 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.
 DIFFERENTIAL DIAGNOSIS

 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)
 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
 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
 PARRT 2

ADITYA GHOSH ROY

PGT-2 M.S. E.N.T.
N.R.S.M.C.H.
 HISTORY OF OTOSCLEROSIS

 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”
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
 HISTORY OF STAPES SURGERY

 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
 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
 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
 1960– Schuknecht
 Stainless steel wire prosthesis
 Gelform to seal window
 SYMPTOMS

 Hearing loss

 Paracusis willisii

 Tinnitus

 Vertigo

 speech
 ANATOMY OF OTIC CAPSULE

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
Otic capsule
enchondral
periosteal Globuli
interossei
endosteal

ENDOSTEAL

ENCHONDRAL

PERIOSTEAL
 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

 AUDIOLOGICAL EVALUATION OF THE
PATIENT WITH OTOSCLEROSIS
 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

 IN COCHLEAR OTOSCLEROSIS
 Air conduction worsen

 Mixed or SNHL

 High frequency more affected

 Greatest degree hearing loss in mid frequency

 Cookie bite pattern

 BONE CONDUCTION

 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
 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

 IMPEDANCE AUDIOMETRY

 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
 ACOUSTIC REFLEX

 Earliest evidence of otosclerosis

 Diphasic pattern
 Increase in compliance at onset and termination of
stimuli (probe in affected ear)
 DIPHASIC PATTERN

 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

 Stapes progressively fixed

 Ipsilateral and
contralateral affected
 NON ACOUSTIC REFLEX

 CONTRACTION OF TENSOR T YMPANI TESTED SEPARATELY

 STIMULATION OF TRIGEMINAL NERVE AND DOING AUDIOMETRY

 STARTLE TYPE REFLEX
 FATIGUEBLE IN NATURE
 UNSTABLE
 LONG LATENCY PERIOD
 SPEECH AUDIOMETRY

 If speech discrimination score (SDS) score is poor

 SNHL component to hearing loss

 Prognosis poor following surgery

 Pt. benefit more by hearing aid

 OTOACOUSTIC EMISSION

 Transient evoked otoacoustic emission (TEOAE) have

low amplitude

 OAE less role in otosclerosis

 Lack specificity

 Early identification of cochlear otosclerosis

COCHLEAR
OTOSCLEROSIS
ADITYA GHOSH ROY
PGT-2 M.S. E.N.T.
N.R.S.M.C.H.
 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.)
 SIGNS SYMPTOMS
 Dominant family history

 Female>male

 Hearing loss started or increased during pregnancy

or following use of ocp

 Schwartzes sign positive

 SNHL

 Tinnitus vertigo
 HEARING TESTS

 PTA– Cookie bite

 Type 2 Tympanogram

 SDS 80 to 90 %

 SISI – high

 Stapedial reflex – present

 In pure cochlear otosclerosis tinnitus is usually the presenting
symptom

 Endolymphatic hydrops seen as a complication of cochlear

otosclerosis

 BPPV is also commonly seen

 DIAGNOSIS OF COCHLEAR
OTOSCLEROSIS
 1926 SHAMBAUGH ( 3 CRITERIA )

 1966 SHAMBAUGH (6 CRITERIA ) – COCHLEAR

OTOSCLEROSIS

 1981 BEALES (8 CRITERIA ) COCHLEAR

OTOSCLEROSIS

 1975 CAUSSE ET AL 3 TYPES OF CRITERIA

 1926 SHAMBAUGH ( 3 CRITERIA )

1. insidious onset + early adulthood

2. absence of other cause that may lead to hearing loss

3. conductive hearing loss in family member

 1966 SHAMBAUGH (6 CRITERIA ) –
COCHLEAR OTOSCLEROSIS

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

1981 BEALES (8 CRITERIA ) COCHLEAR
OTOSCLEROSIS

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

 1975 CAUSSE ET AL 3 TYPES OF
CRITERIA
 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
 Criteria of certainity
 DIPHASIC impedance in case of SNHL
 ABG in case of SNHL and absence of stapedial reflex
 CT scan demonstartes cochlear otosclerosis
MECHANISM OF SNHL IN COCHLEAR
OTOSCLEROSIS
 PATHOLOGY OF SENSORINEURAL
HEARING IMPAIRMENT
 When endosteum of cochlea involved there is
'hyalinization' of the spiral ligament.
MEDICAL
TREATMENT OF
OTOSCLEROSIS
 DRUGS USED

 SODIUM FLOURIDE
 BIPHOSPHONATES
 CYTOKINE INHIBITORS
 SODIUM FLOURIDE

 MECHANISM OF ACTION
 Reduce bone resorption + increase bone formation
 Antienzymatic action – proteolytic enzymes cytotoxic to
cochlea
 NaF acts only on active focus • HARDER
 Reduces osteoclastic when focus is active • BETTER
QUALITY
 Inc osteoblastic activity • RESISTANT TO
F ION BONE
RESORPTION

 HYDROXYAPATITE ---------------- FLUORAPATITE

  ACID PHENYLPHOSPHATASE

 ENZYME OF BONE

RESORPTION INC IN

OTOSCLEROSIS

 THERAPY OF FLUORINE

 ENZYME DECLINE

 OPTIMAL DOSE OF NAF– 60mg daily

 INDICATION OF NAF

 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
 CONTRA INDICATION

 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
 SIDE EFFECTS

 Early fluorosis in spine

Hydroxyfluoric acid in stomach

Gastric disturbance

Prevented by enteric coating

 Chronic arthritis
 BIPHOSPHONATES

 MECHANISM OF ACTION
 Antienzymatic action
 Reduces osteoclastic activity
 Stablise secondary bone formation

 ETIDRONATE– Halt progression of otosclerotic activity

 Newer –
 Alendronate
 Residronate
 zolendronate
 CYTOKINE INHIBITORS

 Reduce resorption of bone

 IL 1 ANTAGONIST AND TNF BINDING PROTEIN

 HALT BONE RESORPTION

 Effective only in active phase

 HEARING AIDS

 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

 Unsuccessful stapes surgery in other ear

 Otosclerosis + menieres

 Stapedectomy done in advanced otosclerosis

 PARRT 3

ADITYA GHOSH ROY

PGT-2 M.S. E.N.T.
N.R.S.M.C.H.
SURGICAL
TREATMENT OF
OTOSCLEROSIS
 INDICATIONS

 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.
 CONTRA INDICATIONS

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
 CONSENT
 Procedure detail

 Risks
 Failure
 CHL
 SNHL
 Vestibular disturbances
 TM perforation
 FN injury
 Perilymph fistula
 Chorda tympani injury
 Delayed failure
 OPERATIVE NOTE

 Shape and mobility of

 Incus

 Malleus

 Presence of otosclerosis

 Fixation of stapes

 Patency round window

 Facial neve

 Chorda tympani status

 STAPEDOTOMY

 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

 STAPEDECTOMY

 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
 PROCEDURE

 General anesthesia
 Local anesthesia

 2-3 cc of 1% lidocaine with

1:50,000 or 1:100,000
epinephrine

 4 quadrants

 Bony cartilaginous junction

Permeatal Endaural
(Transcanal)
 6 and 12 o’clock positions

 6-8 mm lateral to the annulus

 Annulus subluxated from groove

and middle ear cavity entered
 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

 MIDDLE EAR CAVITY
EXAMINATION

 All ossice inspected

 Oval window

 Facial nerve

 Stapedial artery

 Round window

 Mobility of ossicle
 Division of stapedial tendon
 Divided near pyramidal
eminence

 Incudostapedial joint
divided usually by right
angled pick
 Control hole made

 Stapes fractured towards

promontary
 Causse crurotomy scissors
 Too much force– floating
footplate
 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
 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
 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
 DRILL FENESTRATION

0.7mm diamond burr

 Motion of the burr removes
bone dust
 Avoids smoke production
 Avoids surrounding heat
production
 LASER FENESTRATION

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

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
 Posteriorly
placed
fenestration
with the laser

 Causse also
recommends
following the
laser with the
diamond burr
to remove char
 STAMP(STAPEDOTOMY MINUS
PROSTHESIS)
 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

COMPLICAIONS
OF
OTOSCLEROSIS
 INTRA OPERATIVE COMPLICATIONS

 Tear in tympanomeatal flap

 Subluxation of incus
 Overhanging FN
 Obliterative otosclerosis
 Otosclerosis involving round window niche
 Persistent stapedial artery
 Malleus ankylosis
 Perilymph gusher oozer
 Floating or depressed footplate
 TEAR IN TYMPANOMEATAL FLAP

 Proceed & then repair

 Tragal perichondrium
 Fascia
 Gelform
 SUBLUXATION OF INCUS

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
 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
 OBLITERATIVE OTOSCLEROSIS
INVOLVING OVAL
WINDOW
 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
 OTOSCLEROSIS INVOLVING ROUND
WINDOW NICHE

 Per op finding

 Leave it as it is

 Complete procedure and note

it as a finding
 PERSISTENT STAPEDIAL ARTERY

 Pulsatile tinnitus CHL SNHL

 Bleeding during operation

 Fenestration to be made in post half

 MALLEUS ANKYLOSIS

 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
 PERILYMPH GUSHER OOZER

 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
 FLOATING OR DEPRESSED FOOTPLATE

 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

 POST OPERATIVE COMPLICATIONS

 Perilymph fistula

 Facial palsy

 Chorda tympani dysfunction

 Otitis media

 Reparative granuloma

 SNHL

 CHL
 PERILYMPH FISTULA

• PRIMARY & SECONDARY

Prevention:
• Stapedectomy < stapedotomy
• Oval window seal
• No fat or gel-foam for seal
• Prohibit nose blowing, flying, diving, & lifting heavy
objects postoperatively
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
 FACIAL PALSY

 Immediate or Delayed

 <3 hrs due to anesthesia

 >3 hrs due to operative procedure

o integrity of nerve – steroids

o integrity of nerve not sure– exploration

o delayed facial nerve palsy -- rare

 CHORDA TYMPANI INJURY

 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
 ACUTE OTITIS MEDIA

 Immediate post op period

 Worrisome

 Serous labyrinthitis meningitis

 Treatment
 Removal of pack
 Admission
 Broad spectrum anti biotic
 REPARATIVE GRANULOMA

 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.
 SNHL

 0.2-10%

 Serous labyrinthitis - high frequencies

 Surgical trauma

 Movement of stapes

 Rupture of membranes of inner ear

 Rapid loss of perilymph

 hydrops
 PERSISTENCE OR RECURRENCE OF CHL

 IMMEDIATE CHL
 Prosthesis malfunction
 Unrecognized malleus fixation
 Unrecognized round window otosclerosis
 Middle ear effusion
 Unrecognized SSCD

 RECURRENCE OF CHL
 Prosthesis malfunction
 Incus erosion
 Otosclerosis regrowth
 round window otosclerosis