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group 438-448
CHAPTE R 1 CHAPTE R 3
The Technique 11
Incidence 5 Prognosis 16
Etiology 5
Pathology 6
recurrence 20
References 21
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Chapter
O T O S C L E R O S I S A N D S T A P E D E C T O M Y :
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Ear Anatomy:
The External, Middle and Inner
Ears
T
he human ear is one of the more remarkable parts of the human body, not
only because of the beauty and unlikelihood of its structure, but also
because of its remarkable sensitivity to sounds. From an anatomical point
of view, the ear is conventionally and conveniently divided into three parts:
The ear is a remarkable the outer, the middle and the inner ears.
part of the body sensing
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These bones are called the hammer (malleus), anvil (incus) and stirrup (stapes)
because of their resemblance to these objects. The hammer has a handle and a
head and the handle lies within the layers of the eardrum. The head of the hammer
sits in the upper part of the middle-ear space called the attic (epitympanum) and is
connected by a joint – just the same as any other joint in the body – to the rather
bulky body of the anvil. From the anvil, a long strut (the long process) descends
The middle ear is an air-filled
space that holds three small back into the middle ear proper and is connected to the head of the stirrup. The
bones (ossicles), which connect two arches (crura) of the stirrup join the footplate, which sits in a small (3 mm x 2
the eardrum to the inner ear.
mm) hole in the skull called the oval window (fenestra ovalis). This is the opening
into the fluid-filled space of the inner ear. Just below the oval window is another
small hole into the inner ear called the round window (fenestra rotunda). A thin
membrane closes this and, when the footplate of the stirrup moves ‘in and out’, the
round window membrane moves ‘out and in’ because the fluid in the inner ear
transmits the pressure changes.
The hammer and anvil are supported in the middle ear by several membranes and
ligaments, which minimise their weight, allow them to move easily and bring them
a blood supply. Unfortunately, this leaves only a small space for the passage of air
from the middle ear to the attic.
Running through the middle ear is the facial nerve (nerve VII or the seventh
nerve). This nerve leaves the brain and has to pass through the skull on its way to
supply the muscles of facial expression, that is, muscles for frowning, winking,
smiling, scowling, and so on. The nerve lies in a thin bony tube and runs
horizontally from the front to the back of the middle ear just above the oval
window and stirrup, before it turns downwards to leave the base of the skull. The
nerve then turns forwards to reach the face. The facial nerve is therefore relatively
vulnerable in diseases of the middle ear and, indeed, in middle-ear surgery itself. A
facial palsy results in one side of the face being paralysed, so that the face droops
and fails to move. Smiling results in a scowl and drinking in dribbling, and the eye
fails to close on blinking.
Running through the eardrum is the nerve that carries taste from the front two-
thirds of the tongue (the chorda tympani nerve). This nerve is on its way to join the
facial nerve in the middle ear where it ‘hitch-hikes’ a lift back to the brain.
Finally, there are two small muscles in the middle ear. The one at the front (tensor
tympani) is attached at the top of the handle of the hammer and tenses up the
eardrum when swallowing activates it. The function of this muscle is not clear but
it may be to make eating and swallowing a less noisy event.
The muscle at the back of the middle ear (stapedius) arises near the facial nerve, is
supplied by it and attaches to the head of the stirrup. It responds to loud sounds by
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contracting and stiffening the chain of small bones, and possibly reduces
transmission of prolonged and potentially damaging, loud sounds to the inner ear.
The portion of the inner ear that actually hears is the cochlea. This is a hollow
coiled tube set in the very dense bone called the bony labyrinth (part of the petrous
[rock-like] temporal bone). This tube is filled with fluid, which is much the same as
general body fluid (lymph) and that which surrounds the brain (cerebrospinal fluid
– CSF). This inner-ear fluid is called perilymph. Inside the perilymph is another
coiled triangular-shaped tube called the cochlear duct (scala media), which contains
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the all-important ‘hair cells’ – these convert sound into electricity. These hair cells
are arranged in two groups that follow the coils of the cochlear duct and spiral
upwards from base to apex. There is a single row of inner hair cells (IHCs), which
lie closer to the core of the cochlea (modiolus), and three or four rows of outer hair
cells (OHCs), which are further away. In a healthy young human ear there are
about 3,500 IHCs and about 12,000 OHCs. Each hair cell has a cluster of small
rigid hairs (stereocilia), which project from the thicker upper surface of the cell into
the special f luid that fills the cochlear duct. This fluid is called endolymph and is
remarkable in that it has a strongly positive electrical charge associated with it –
about 80 millivolts – and is rich in potassium, a metallic element.
The hearing nerves travel inwards, along with the balance and facial nerves,
through a canal in the inner part of the skull (variously called the internal auditory
meatus [IAM], internal auditory canal [IAC] or porus acousticus) to reach the brain
stem. About half of the hearing nerves from each ear cross over to the other side
of the brain stem and then, on both sides, the nerves pass up the brain stem
through the mid-brain, eventually to reach ‘conscious- ness’ in what is called the
cortex of the brain. For hearing, this conscious region is located in the temporal
lobe portion of the brain, which lies on each side of the head just above the ear.
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Chapter
Otosclerosis:
The Problem and How to Manage?
O
tosclerosis is a disease of the bony labrynth. It is characterized by
formation of a new vascularised spongy bone in localized foci replacing
the normal compact bone of the bony labyrinth resulting in conductive
In this undecalcified section,
a vascular focus of otosclerosis is
hearing loss which is commonly bilateral.
seen adjacent to the cochlea.
Incidence:
Sex: Females are 2 times affected than males.
Etiology:
While the etiology of otosclerosis remains unknown, there are two main theories
regarding its origin; genetic and viral.
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Pathology:
process inapproximately 35% of
cases. In this patient the focus has
extended through theendosteal layer
of bone that affords attachment otosclerosis is characterized by 2 phases:
for the spiral ligament. The most
common reaction seen in the spiral
ligament is a loss of cellularity and 1. Otospongiosis: affected bone becomes hypervascular and osteoclasts and
occasionally the deposition of a
layer of collagen adjacent to the
osteolytic osteocytes cause enlargement of the vascular spaces of the bone.
focus. Osteolytic osteocytes appear at the leading edge of the lesion, and sheets of
connective tissue can be observed replacing the bone. Formation of dense
sclerotic bone in areas of previous resorption signifies the late phase of
otosclerosis. The result is disorganized bone, increased population of
osteocytes, and enlarged marrow spaces containing vessels and other
connective tissue.
2. Otosclerosis: Spaces are later replaced by dense sclerotic bone with narrow
vasculature and few recognizable haversian systems. Pleomorphism is
largely due to normal coexistence of both stages of otosclerosis in any
single temporal bone.
Initiating lesions often neighbor the fissula ante fenestram and expand via vascular
channels. In 80-90% of patients, lesions are limited to the anterior oval window
and affect its pathology by calcification of the annular ligament or by involving the
Metabolic activity within the stapes. Both processes result in characteristic conductive hearing loss. In 8% of
otosclerotic focus varies. In the
active phase there are numerous
patients, the process involves the cochlea and parts of the labyrinth (labyrinthine
fibrovascular spaces and an otosclerosis), resulting in sensorineural hearing loss. Approximately 2% of patients
increased number of osteoblasts
and osteocytes. The overall
display both labyrinthine and ossicular chain involvement.
picture suggests active bone
turnover. Explanation of the clinical portion of sensorineural loss has been difficult, but
investigators theorize that enzymes from the inner ear lesion diffuse via the spiral
ligament to suppress neuron and hair cell activity.
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Clinical Picture:
• Otosclerosis is more common in females
• Juvenile type occurs in a younger age group and may be before puperty.
3. Schwarts sign: Flamingo red flush seen through the tympanic membrane
due to active vascular bone on the promontory. It is usually seen in the
juvenile type.
Differential Diagnosis:
1. Chronic non suppurative otitis media.
Investigations:
Audiological:
1. Pure-tone audiometry: it usually demonstrates low-frequency conductive
hearing loss. High-frequency losses begin to manifest with gradual air-bone
gap widening. If cochlear involvement is not present, otosclerosis is limited
to maximal conductive loss of 50-65 dB across all frequencies. If cochlear
involvement is present, a mixed hearing loss appears, with high frequencies
more affected. In severe cases, tinnitus may interfere with pure-tone
audiometry. Stapes fixation produces an audiometric artifact known as the
Carhart notch, which is characterized by elevation of bone conduction
thresholds of 5 dB at 500 Hz, 10 dB at 1000 Hz, 15 dB at 2000 Hz, and 5
dB at 4000 Hz. Cochlear otosclerosis is characterized by the presence of
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3. Acoustic reflexes: often are abnormal and may provide the earliest
evidence of otosclerosis. Observed abnormality depends on stage of
CT scan in the coronal disease. Almost half the healthy population may show initial increase in
plane (bone window)
reveals extensive bone
compliance at stimulus onset, but compliance increase observed at offset
resorption surrounding the occurs only in stapedial fixation and is virtually pathognomonic. Advancing
cochlea in a patient with fixation affects both ipsilateral and contralateral acoustic reflexes, even in
tosclerosis. The zone of
esorption highlights the unilateral disease.
noninvolved bone on either
side, creating a "double
Radiological:
halo" effect (arrow).
CT scanning of the temporal bone can often demonstrate foci of demineralization
in the otic capsule in cases of cochlear otosclerosis.
Treatment:
Medical treatment: Fluoride supplementation has met with variable response and
is used sporadically for labyrinthine otosclerosis. It has also been used for
postoperative medical management of obliterative otosclerosis.
Hearing aids: As with conductive hearing losses of other etiologies, hearing aids
usually are helpful. It also useful if surgery is refused or contra indicated.
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Chapter
Stapedectomy:
The technique, post-operative care
and prognosis.
S
tapedectomy is surgical removal of stapes or its supra structures and
replacement by an artificial prosthesis as Teflon piston or fat and wire. This
operation is indicated for stapedial and mixed but not cochlear otosclerosis.
Historical view:
In a stapedectomy, the stapes is The history of the treatment of otosclerosis is rich in stories of serendipity and of
removed and a prosthesis is
placed treatments forgotten and rediscovered. In 1704, Valsalva first described stapes
to transmit sound vibration fixation as a cause of hearing loss. In the mid-1800s, a young man with otosclerosis
from the the incus (anvil), to a fat
plug (fascia or vein) in the oval was noted to have hearing improvement following a skull fracture. After he died of
window of the inner ear. complications from the head injury, post-mortem examination of his temporal
bones revealed a fracture through the horizontal semicircular canal. Kessel, who
described the case, attempted to create a similar fistula in patients with otosclerosis
using a hammer and gouge. In 1876, Kessel removed the stapes and covered the
oval window with scar tissue. These early attempts at treatment failed.
Ménière first reported mobilization of the stapes in 1842, but it was not until the
late 19th century that stapes surgery became more common in Europe with
advances in asepsis, hearing testing (tuning forks) and discovery of the X-ray.
However, frequent complications, including meningitis, and transitory hearing
improvement due to refixation of the stapes and closure of the fenestration led
stapes mobilization and stapedectomy to be condemned as dangerous and useless
In the 1800s, Kessel
attempted to create a fistula in
by the end of the 19th century. Throughout the late 19th and early 20th centuries, dry
patients with otosclerosis catarrh was the term used to describe otosclerosis.
using a hammer and gouge.
In 1923, Holmgren first performed horizontal canal fenestration in the modern era,
covering the fistula with mucoperiosteum. His associate, Nylen, developed a
surgical microscope for the operation.
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deteriorated over time due to closure of the fenestrum. Even though the last
fenestrations were done in the late 1950s, audiologists and otolaryngologists still
encounter patients who had fenestration operations. Only an otolaryngologist or
otologist should perform cerumen removal and maintenance of the post-operative
mastoid cavity of these patients, due to the risk to the exposed labyrinth.
A century after it was first performed, stapes mobilization again came into vogue in
Fenestration, Temporal Bone the early 1950s after Rosen reported his results. Air-bone gap closure was superior
Section: to the results achieved by fenestration, but the limitations of mobilization were
The patent fenestra through the
bony wall of the lateral soon recognized as refixation and recurrence of conductive hearing loss in a
semicircular canal can be seen. substantial number of patients. While mobilization is still occasionally performed, it
The fenestra is closed by the
epithelial lining of the mastoid has now been replaced by stapedectomy and stapedotomy.
cavity.
In 1956, John Shea reported his early experience with stapedectomy. During his
operations, Shea removed the entire stapes and covered the oval window with a
vein graft and used a nylon prosthesis from the incus to the graft. Subsequent
refinements by Shea and others lead to the use of tragal perichondrium, fascia, and
gelfoam to seal the oval window and various alloplastic materials such as wires and
bucket-handle prostheses (that have a wire bale that loops over the incus) to
reconstruct the ossicular chain.
In the early 1970s, surgeons began creating small holes (fenestrum) in the oval
window (referred to as a 'stapedotomy') and placing a piston within the hole to
reconstruct the hearing mechanism. Since then, stapedotomy has become common
although many respected and competent surgeons continue to perform variations
of total or partial footplate removal.
A variety of tools, including a diamond microdrill or a laser, are now used to create
the fenestrum. The advantages of the microdrill include the speedy creation of a
perfectly round fenestrum created to the size of the prosthesis, and the ability to
work rapidly through thick footplates. The advantages of the laser include the
potential for reduced trauma to the vestibule and the ability to create a fenestrum in
the face of inadvertent mobilization of the footplate. In reality, both tools are well
suited to the task and equally able to achieve excellent results in qualified hands.
It is indicated for stapedial and mixed but not cochlear otosclerosis. However,
hearing results in patients with air-bone gaps less than 15 - 30dB, most surgeons,
recommend non-operative treatment in patients with ‘small’ air-bone gaps. The
primary reason for this is that unless complete closure of the air-bone gap is
achieved many patients with small air-bone gaps who have surgery will simply not
obtain enough subjective benefit to feel the surgery was worthwhile. Nonetheless,
patient selection varies from surgeon to surgeon and remains part of the doctor-
patient relationship. Also, The age of the patient alone should not be a
contraindication to performing surgery. In patients less than 16 years of age, there
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Contraindications:
• Coexistent Ménière disease increases the possibility of residual hearing
loss in the operated ear.
• Documented dilation of the vestibule or the vestibular aqueduct on CT
scanning or MRI also negatively impacts hearing outcome.
The technique:
Procedures may be performed under general or local anesthesia with sedation.
Steps:
Raise a tympanomeatal flap and identify and protect the chorda. Next, curette the
scutum and identify the pyramidal process, stapedial footplate, and the tympanic
segment of the facial nerve. Measure distance from incus to stapes footplate, and
then disarticulate the incus-stapes (IS) joint. Divide the posterior crus of the
footplate and remove the remainder of the superstructure. Perform either a partial
or complete stapedectomy or a stapedotomy. Place a soft tissue autograft, such as
fascia, perichondrium, or vein, over the defect. To reestablish the conducting
mechanism of the middle ear, interpose a prosthesis between the vestibule and
incus. Replace the tympanomeatal flap.
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The stapedial artery first appears in the tissue that forms the stapes at about the
fifth week of fetal life and normally atrophies during the third month of
A persistent stapedial artery development. The arch of the adult stapes is partly formed around the stapedial
is a congenital anomaly
reported to occur in 1 of
artery in a manner similar to the ‘lost wax’ method of jewelry casting. After
5,000 – 10,000 ears. ascending the promontory in a bony canal just lateral to the round window and
basal turn of the cochlea and passing through the obdurator foramen, it turns
anteriorly to join the facial nerve and ends by replacing the middle meningeal artery
or by branching into the supra- or infraorbital or mandibular arteries.
B. Superiorly located jugular bulb:
A superiorly located jugular bulb may come into juxtaposition with a tympanic
annulus and in this position is vulnerable to injury during elevation of the tympanic
meatal flap. For this reason, the elevation of the tympanic annulus inferiorly should
not be performed with both strobes of the elevator. Tears of the jugular bulb, of
course, result in profuse bleeding and constitute an alarming, although not serious,
complication. Elevating the head of the operating room table and packing the area
with Gelfoam may control the bleeding. If the bleeding is readily controlled, the
operation may be completed. If the tear is large and the bleeding is difficult to
control, the procedure should be terminated.
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Complications:
Will be discussed in the next chapter.
Post-operative care:
Immediately after the operation, we tell the patient and give him these advices:
Diet
In the immediate post-operative period, you may experience some vertigo,
nausea or vomiting. It is therefore preferable to stick to a liquid diet or a light
bland meal. A regular diet may be resumed the day after surgery. It is not
unusual to experience some earache on mastication and possibly, some
difficulty in fully opening the mouth.
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Wound Care
The operated ear is usually packed and full of blood. It will feel clogged and
you may hear crackling sounds. You may have a stitch or two on the earlobe
or the tragus (the little cartilage knob in front of the ear canal) . You will have
a cotton ball in the ear, change it when it gets soaked and replace it with a
clean cotton ball. It is not necessary to use a band aid or adhesive tape to hold
the cotton ball. Just use a little antibiotic ointment to make the cotton ball
stick. In very rare instances, if an incision is made behind the ear, you may
have a dressing wrapped around the head or sutured behind the ear, please
keep that dressing dry and avoid water at any cost. In general, such a dressing
is removed a couple of days after the surgery.
1. Do not allow any water to enter the operated ear. Protect the ear during
showering or washing the hair with a large cotton ball coated with Vaseline.
When finished washing, remove the coated cotton, wipe the ear with a soft
paper tissue and place a clean, dry cotton ball. A little antibiotic ointment
may help the cotton ball stick and stay in place.
We tell the patient not to allow any
water to enter the operated ear. 2. Thick, dark or bloody ear drainage is expected during the first week after
Protect the ear during showering surgery. You may clean the crusting from the outer part of the ear with
or washing the hair with a large
cotton ball coated with Vaseline. peroxide and Q-tips. Replace the cotton ball in the ear with a clean, dry piece
when the current one is soiled. Occasionally, you may see brown or dark red
pieces of packing (Gelfoam) extruding from the ear canal. Do not attempt to
replace them or to remove the remaining pieces that are still in the ear canal.
3. Do not blow your nose for at least two weeks from the day of surgery.
Blowing can build excessive pressure in the operated ear and displace the
eardrum.
4. If you have to sneeze, please do it with your mouth wide open to avoid
pressure build up in your ear.
Medications
Antibiotics are usually prescribed, please take them as directed until they are all
gone. You may take pain medication as needed.
Prognosis:
Commonly quoted statistics indicate that 90% of appropriately chosen surgical
candidates enjoy a significant hearing improvement. Eight percent experience no
significant hearing improvement. Up to 2% (including 0.2% who may experience
complete sensorineural hearing loss in the operative ear) experience additional
hearing loss. Stapedectomy, in experienced hands, is generally considered a safe
procedure.
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Chapter
Stapedectomy:
The Complications
A
S any interference with the body functions, Stapedectomy obtains some
complications. The complications may be due to anesthesia, the
procedure or recurrence of the pathology.
D. Anaphylactic Shock:
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Injury to the nerve occurs in up to 30% of cases. Symptoms include a dry mouth,
sore tongue, and a metallic taste. Symptoms usually subside in 3 – 4 months.
Stretching the chorda is more likely to result in symptoms than simply dividing the
nerve.
D. Infection:
Luckily rare, a post-operative infection after stapedotomy can lead to profound
hearing loss and, in rare cases, meningitis. The latter occurs when bacteria
transgress the vestibule to enter the CSF-containing subarachnoid space.
F. Dislodgement of incus:
Two situations that can lead to inadvertent dislodgment of the incus are:
1) during removal of the bony rim of the annulus to expose the ossicles; and,
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G. Erosion of incus:
While over-aggressive crimping of the crook of the prosthesis can fracture the
incus, more commonly the long process of the incus erodes over time, causing the
prosthesis to loosen and disarticulate, leading to conductive hearing loss. This
erosion may be due to disruption of the blood supply to the distal long process of
the incus . It may also be due to erosion by a bucket-style prosthesis or by over-
crimping a piston with a wire-crook.
H. Floating footplate:
In manipulating the stapes, the footplate may occasionally be dislodged if it is only
partially fixed. In stapedectomy, this may create a problem if the footplate becomes
depressed into the vestibule and cannot be safely removed. In laser stapedotomy,
the floating footplate can be fenestrated and a piston placed as usual.
Facial nerve affection is an
uncommon complication. I. Facial weakness:
It is usually due to the use of
local anesthesia or dehiscence Facial weakness is rare complication of stapes surgery. It is most often temporary
of the facial nerve. and due to the effects of local anesthesia. In these cases, it improves over a few
hours. In some cases, it may be delayed and may be the effect of traction on the
chorda tympani, heating of the nerve by the laser, or reactivation of herpes simplex
virus-1.
J. Postoperative granulomas:
postoperative granulomas can also be a cause of dysequilibrium, vertigo or
progressive sensorineural hearing loss. Granuloma formation is seen in
approximately 1:100 cases of revision stapedectomy. Foreign body reaction is a
suspected etiology of postoperative granuloma formation. The condition usually
manifests between the 5th and 15th postoperative day and is characterized
symptomatically by hearing loss after an initial hearing gain or a sensation of
unsteadiness. Associated with the hearing loss are loss of speech discrimination and
a sensation of fullness in the ear. Examination reveals an edematous, thickened and
hypervascular skin flap as well as dullness and reddening at the posterior part of the
tympanic membrane. High-dose steroids may decrease the inflammatory response
and its effects on the inner ear. The granuloma, including the portion within the
vestibule, must be removed in its entirety along with the prosthesis. They may also
be vaporized with laser after the prosthesis has been removed.
Post Stapedectomy Granuloma:
The oval window in this case is
filled with vascular granulation K. Cholesteatoma:
tissue. Extending medially into Cholesteatoma following stapedectomy is a rare complication. Proposed
the vestibule this tissue has
become adherent to the mechanisms for formation include prosthesis extrusion, the presence of a
saccular membrane. squamous epithelium in the fascial graft, inversion of the tympanomeatal flap and a
marginal perforation associated with a disruptive annulus.
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L. Diplacusis:
Diplacusis occurs in approximately one-third of the patients. There may be a
variation of distortion of sound, especially music and the human voice, of which
patients frequently complain. For the first few weeks after the operation most
people complain of pure tones appearing higher in pitch when compared with the
unoperated side. It is seldom problematic and usually fades by six weeks
postoperatively.
Recurrence:
However, stapedectomy may be considered as a symptomatic treatment and not
curative as we hadn't treated the causative pathology. Recurrence is usually due to
spread of the pathology towards the cochlea.
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References:
E-medicine website.
Allrefer.com website.
www.earsite.com
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