Cholesteatoma is a benign, keratinizing squamous epithelium sac in the middle ear cleft with bone-eroding properties and a loss of self-cleaning capacity, posing significant clinical and examination challenges in ENT.
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Hey guys.
Welcome back to my channel,
The ENT resident.
Today I'll be discussing a very big topic
in ENT, and that is Cholesteatoma.
This is a very important topic.
Not only from the perspective
of seeing your patients, you get a lot
of cases of cholesteatoma.
And even from the perspective of appearing
for your VIVA exams, in your
practical cases and even in your theory
papers, it can come as a long question.
So, you can also purchase my notes
now.
I have added the links in the description.
Now let's get started with it.
So what is cholesteatoma?
This is the first question you
are asked in any practical exam.
The cholesteatoma is basically
defined as a benign sac of
keratinizing squamous epithelium in
the middle ear cleft and it has a
bone eroding property and it has
also which has also lost its self
cleaning capacity.
So this is how you define cholesteatoma.
Now why is the presence of keratinizing
squamous epithelium in the middle
ear cleft being termed as abnormal?
That's because first we have to know what
epithelium does the middle ear cleft has?
So normally the middle ear cleft
is lined by different types
of epithelium in different areas.
Like in the anterior and inferior part
there is ciliated columnar epithelium,
in the middle part there is
cuboidal epithelium, and in the attic
there is pavement like epithelium.
So basically middle ear is nowhere lined
by keratinizing squamous epithelium.
So the very presence of keratinizing
squamous epithelium in middle ear or
the mastoid is called as cholesteatoma.
Therefore it is also,
a term that is used for
this is skin in the wrong place
because skin is basically
keratinizing squamous epithelium.
There are two other synonyms
or alternative names by which
cholesteatoma can be known as.
One is keratoma, which is
basically signifying the keratin
filled nature of the lesion.
And second is epidermosis which describes
its origin from squamous epithelium.
So that is about cholesteatoma.
Second thing we need to know is
why is the term cholesteatoma a misnomer?
There are two reasons for it.
One is the fact that it actually does
not contain cholesterol crystals.
Even though the word cholesteatoma
includes the cholesterol word in it.
And secondly, it is ending
with the suffix "oma".
We know that usually anything ending with
a suffix "oma", it ends up being a tumor.
But cholesteatoma is not a tumor.
So having the suffix "oma" is
actually quite contradictory.
Hence the term cholesteatoma
has been termed as a misnomer.
Next, let's discuss about
what is the structure of a cholesteatoma.
So cholesteatoma basically
consists of two parts.
If you see in the image over here,
the first part is the matrix.
This is the matrix, the red
colored portion that you see.
This matrix is made up
of keratinizing squamous epithelium.
And the matrix is resting on a very
thin layer of fibrous stroma around.
And the second part is this white
central mass that you are seeing
which consists of keratin debris.
And this keratin debris are
being produced by the matrix.
So if you had to describe the structure of
cholesteatoma, there's a thin stroma of
fibrous tissue on which lies the matrix.
And the matrix is made up
of keratinizing squamous epithelium.
And inside the matrix is a central white
mass which is produced by the matrix.
And this consists of keratin debris.
Next, let's talk about, how does
a cholesteatoma originate and what
are the theories behind it?
So there are a lot of theories behind it.
We'll first start with number one,
which explains,
how a congenital cholesteatoma forms.
And that is because of the presence of
embryonic epidermal cell rests,
which are basically keratinizing
epithelium entrapped in the middle
ear cleft or the temporal bone.
Usually these embryonic epidermal
cell rests disappear over
time, but if it ends up persisting,
it can lead to the development
of congenital cholesteatoma.
Now we'll discuss four different
theories which will describe
acquired cholesteatoma.
And I'll also talk about what
are the different types
of cholesteatoma right after this.
So first let's talk about the theories.
The first one is Wittmack's theory, also
known as the invagination theory.
Here what happens is, there is
an invagination of the tympanic membrane
from either the attic or the postero
superior part of pars tensa.
And this occurs in the form
of a retraction pocket.
If you see in the image over here,
you can see
this is forming
a retraction pocket over here.
And why does this begin?
This begins because of any kind
of eustachian tube dysfunction.
So whenever there is an eustachian tube
dysfunction, it leads to the formation
of negative middle ear pressure.
And when there is negative middle
ear pressure, it leads to invagination
of the tympanic membrane leading
to a retraction pocket.
Now once the retraction pocket forms,
the outer surface
of the tympanic membrane is lined with
stratified squamous epithelium.
So this layer, after invagination,
it starts to form the matrix layer
of the cholesteatoma and it starts
laying down keratin in the pocket.
So that's how it starts to form
the retraction pocket.
Now as the retraction pocket keeps
deepening because of the negative,
persistent negative middle ear
pressure and repeated inflammation,
now desquamated keratin cannot be
cleared anymore from the recess.
So basically this retraction pocket
loses its self cleaning capacity.
And the moment they loses its self
cleaning capacity, it lays down a layer
of keratin inside and leads
to the formation of cholesteatoma.
Now bacteria can end up infecting
the keratin matrix and form biofilms
resulting in chronic infection
and epithelial proliferation.
So this is basically Wittmack's
invagination theory, which starts from
the fact that there is a eustachian tube
dysfunction, which leads to a negative
middle ear pressure, which leads to the
formation of a retraction pocket either
in the attic or in the posterior superior
part of pars tensa.
Now the outer layer of the tympanic
membrane, which is lined
by keratinizing squamous epithelium.
It starts, forming the Matrix
of the cholesteatoma and lays down
the keratin in the pocket.
Now as the negative pressure
continues, to persist, it leads to
formation of more desquamated
keratin inside and the retraction
pocket ends up losing its self
cleaning capacity leading to the
formation of cholesteatoma.
Okay, that's all about this.
Next is Ruedi's theory, which is also known
as the basal cell hyperplasia theory.
Here what happens is under the influence
of an infection, the basal cells
of the germinal layer of skin
can proliferate and start laying down
keratinizing squamous epithelium.
See in the image over here, there is an
epithelial cone being formed which
starts to lay down keratinizing
squamous epithelium. now the prickle
epithelial cells of Pars flaccida can
end up invading the subepithelial
tissue by means of proliferating
columns of epithelial cells.
This will lead to basal lamina disruption,
ultimately leading
to epithelial cone invasion into the sub
epithelial connective tissue.
And this will result in the formation
of microcholesteatoma.
These microcholesteatoma will now
enlarge and proliferate and sorry,
enlarge and perforate an intact
tympanic membrane leading
to the formation of a cholesteatoma.
So this is basically starting from
an infection which leads
to hyperplasia of the basal cells
of the germinal layer of skin.
This is about Ruedi's theory.
Next theory is Habermann's theory,
also known as epithelial invasion
theory or migration theory.
Now here the starting point is
there is already a pre existing tympanic
membrane perforation
and usually this is of the marginal type.
Now what is marginal type?
The marginal type is where
basically the annulus tympanicus
has been destroyed.
So what happens here is the keratinizing
squamous epithelium, which is
the outer layer of the tympanic membrane
or even the external auditory canal.
It starts to migrate into the middle ear
through this pre existing perforation.
If you see in the image over here,
there is a pre existing
perforation right here in the attic.
Now through this attic either the outer
layer of the tympanic membrane or
the lining of the external auditory canal
starts to migrate towards the middle ear.
And damaged inner mucosal lining
of the tympanic membrane allows this
keratinizing squamous epithelium
to migrate inward and leading
to the development of cholesteatoma.
We have seen that cholesteatoma which
arise after temporal bone fracture
more commonly follow this theory.
So this is known as the epithelial
invasion theory where we already
have a pre existing perforation.
Now the last theory is Sade's theory, also
known as the squamous metaplasia theory.
Here basically we have come across a lot
of times where we have seen that
respiratory epithelium, it can
undergo a lot of metaplastic changes
in different other parts of the body.
In the lungs that same thing can
happen here where the middle ear
mucosa, like respiratory mucosa
elsewhere it also starts to undergo
metaplasia due to repeated infections
and it starts transforming into
squamous epithelium.
So these are all the theories behind,
the origin of cholesteatoma.
Now, it might be a little difficult
for you to remember sometimes.
What are the names
of the cholesteatoma theories
exactly.
So I have a small mnemonic
that can help you with it.
So the mnemonic is
Real Big Ears Make Echoes.
So the first letter of each
of the five words will make
you remember the theories.
So with R comes retraction pocket,
which is the Wittmack's theory.
B is for basal cell hyperplasia,
which is Ruedi's theory.
E is for epithelial migration, which is
Habermann's theory.
And M is for metaplasia,
which is Sade's theory.
And last is embryonic cell rests,
which is basically the cause
behind congenital cholestioma.
So this is a mnemonic that will
help you remember all the theories
behind origin of cholesteroma.
Now, let's talk about the classification.
What are the different
types of cholestioma?
Cholesteatoma can be classified
into two types, two major types, which is
congenital and acquired, and acquired
in itself can be further classified
into primary and secondary types.
I'll discuss each one of them separately.
So I'll first begin with
congenital cholesteatoma.
So what is congenital cholesteatoma?
Congenital cholesteatoma is an expanding
cystic mass with keratinizing squamous
epithelium, which is located medially
to an intact tympanic membrane.
This part is very important.
It has an intact tympanic membrane, and
this is usually assumed to be present at
birth, but usually it gets diagnosed
either during infancy or in early
childhood in patients with no prior
history of otorrhea, perforation or
previous ear surgery.
Now, the cause behind congenital
cholesteatoma, as I've already
mentioned, is a persistent persistence
of embryonic cell rests, which
are found in the epitympanum.
Usually they regress in a normal
individual, but if in the in case
they do end up persisting and
growing, the squamous epithelium
accumulates in the middle ear space,
leading to formation of the
congenital cholesteatoma.
Now, you have to know the three common
sites where the congenital
cholesteatoma is commonly seen, because
the symptomology of the patient will
depend on where it has come from.
The three types, the three sites are
middle ear, petrous apex
and cerebellopontine angle.
The most common out of them,
Is from the middle ear.
Now, there's a criteria that has been
mentioned, which is Levenson's criteria,
which came out in 1989, which basically
gives the diagnostic criteria
to label a cholesteatoma as congenital.
Now, for that there are four, criteria
and all of them have to be met for it to
be diagnosed as congenital cholesteroma.
Number one is you have to be able
to see a pearly white mass medial
to an intact tympanic membrane.
Secondly, there will be
no history of otorrhea.
Third, there is no history
of previous ear surgery.
And fourth, there will be no prior
tympanic membrane perforation.
These four criteria together make
up the Levenson's criteria, and all
of them have to be fulfilled in order to
diagnose a cholesteatoma as congenital.
Now coming to clinical features
of congenital cholesteatoma.
Usually, as I have already mentioned,
it is seen as a pearly white mass
behind an intact tympanic membrane.
You can see in the image over here
that the tympanic membrane is intact.
But you can see this pearly white mass,
medial to the intact tympanic membrane.
Patient will also have
conductive hearing loss.
Sometimes this is discovered
on routine examination or
at the time of myringotomy.
And this also has the capacity
to spontaneously rupture, sometimes
through the tympanic membrane
and present with a discharging ear.
Then it can actually get difficult to
distinguish from a typical case of csom.
Now, congenital cholesteatoma
also has a staging system.
And, the staging system
has been described by Potsic and it is
a four point staging system.
Stage one is when there is a single,
it involves in a single quadrant
and there is no ossicular
involvement or mastoid extension.
Stage 2 is multiple quadrant involvement
with still no ossicular
involvement or mastoid extension.
Stage three is there is
ossicular involvement but without
any mastoid extension.
And stage four is when there is
mastoid extension regardless
of any other finding elsewhere.
So this is all about
congenital cholesteroma.
Next we'll discuss
primary acquired cholesteatoma.
Now, why is it called primary?
It is called primary because here
there is no previous history
of any otitis media of a pre existing
perforation or otorrhea.
The theories that can be used to explain
primary acquired cholesteatoma are
the invagination theory, basal cell
hyperplasia theory and metaplasia theory.
So I have drawn a diagram over
here which will show you
the genesis of the the origin
of primary acquired cholesteatoma.
So you can see, one theory is where
there is a eustachian tube obstruction leading
to persistent negative pressure in the
middle ear, leading to attic or
posterior superior retraction pocket
and that will lead to primary acquired
cholesteatoma.
Or on the other hand, when there's
repeated subclinical infections
of middle ear, on one side it can
undergo metaplasia of the middle ear
mucosa leading to cholesteatoma.
On the other side there can be
a proliferation of basal layer leading
to primary acquired cholesteatoma.
So that's all about primary
acquired cholesteatoma.
Next, let's talk about secondary
acquired cholesteatoma here.
This usually occurs in case of a pre
existing perforation of pars tensa, which
is usually postero superior marginal
perforation, or sometimes it can
even be a large central perforation.
The theories which can be used
to explain this are the migration
theory and the metaplasia theory.
So if you had to talk about the genesis,
first of all, it can start from repeated
infections through perforation leading
to metaplasia of middle ear mucosa
leading to cholesteatoma formation.
On the other hand, it can start from an
acute necrotizing otitis media leading to
the development of a large central
or marginal perforation, which leads to
epithelial migration through the
perforation leading to the formation of
cholesteatoma.
So these are all the three
different types of cholesteatoma
that you need to know about.
Now let's talk about the bone
destruction property of
the cholesteatoma and how does it work?
How does bone destruction occur?
So cholesteatoma has this
capability of destroying the bones
which comes in its way.
It can be the ossicles, bony
labyrinth, facial nerve canal, sinus
plate or tegmen tympani. Depending on
which bone has been eroded,
it can lead to different types
of serious complications.
Now, there are two theories
behind bone destruction.
The first theory is the pressure theory,
which Today it is no longer,
accepted as a proper theory.
It has been outdated.
But this was the first theory
that explained bone destruction
in cholesteatoma.
So what was thought that earlier
Bone destruction was thought
to be a result of pressure necrosis.
But why was it discarded?
This theory got discarded because
clinically observing the cases, it led
to abandonment of this theory because
it was thought that it is highly
unlikely that cholesteidoma could,
exert a pressure which exceeds
capillary perfusion pressure, which is
approximately 25mmHg.
That is why it was thought that
pressure theory is not the right way
to explain the bone destruction
caused by cholesteotoma.
So the current theory that, explains
the bone destruction which is caused
by cholesteatoma is the enzymatic theory.
So basically there are enzymes which
get liberated by the osteoclasts
and mononuclear inflammatory cells which
are associated with cholesteatoma.
And these enzymes include collagenase,
acid phosphatase, acid protease,
cathepsin like proteolytic enzymes,
PGE2, interleukin 1 alpha, 1 beta, tumor
necrosis factor alpha and beta.
So these are the two theories
behind bone destruction.
Now, since we are talking about bone
destruction, what is the most
common bone that is destroyed here
in order of decreasing frequency?
The first one is the long
process of incus.
Second is stapes crura,
and third is body of incus.
Now the next question you are asked is why
is long process of incus the most common
bone to be destroyed by cholesteatoma?
That is because the long process of incus
has basically presence
of a single nutrient vessel and absence
of any other collateral circulation
makes it very susceptible to necrosis.
And that is why long process
of incus is the most common bone
to undergo necrosis and cholesteatoma.
Next, let's talk about the growth pattern
and how it spreads in the middle ear.
So there are three common sites
of origin of acquired cholesteatoma.
In terms of the frequency
of occurrence, the most common one is
posterior epitympanum, second is
posterior mesotympanum and,
and third is anterior epitympanum.
Now each of these three different
sites, when cholesteatoma arise,
in all of them it has different,
different, spread pathways.
So first we'll talk about
posterior epitympanum
Cholesteatoma.
This is basically cholesteatoma
in the Prussak's space, there are three
modes of spread over here one is
through anterior pouch of Von Troeltsch
and it from there it goes to anterior
epitympanum and from there to the
supratubal recess and anterior
epitympanic sinus.
Second pathway is through
posterior pouch of Von Troeltsch.
From here it goes into the posterior
mesotympanum and from here it can
involve the sinus tympani, round
window area and the facial recess.
Third pathway is through lateral
malleal fold and lateral incudal fold.
From here it goes to the superior
incudal space or lateral attic
to then to the aditus, then antrum
and then the whole of mastoid.
These are the three pathways
of spread if the cholesteatoma is present
in the posterior epitympanum.
Next is if it is present
in posterior mesotympanum which is
the inferior incudal space.
Again it has three modes of spread.
First is it can directly spread
to sinus tympani and facial recess.
And this is the most common pathway.
Second is through the posterior
tympanic isthmus.
It can spread and occupy the medial attic
which is basically
epitympanum medial to the body of incus.
Third is it can spread through
the posterior pouch of Von Troeltsch via
the prussak space leading
into the superior incudal space, then
into the aditus, antrum and then mastoid.
So these are the three pathways
of spread for a posterior
mesotympanum cholesteatoma.
The third type is when it arises
in anterior epitympanum, a portion
of which is known as supratubal recess.
So from here superiorly it can grow to
the tegman or dural middle cranial fossa.
Anteriorly it can spread
to involves the zygomatic root cells,
it can also involve the geniculate
ganglion and the facial canal.
And very long standing cases can
lead to labyrinthine fistula.
So these are the three different
growth patterns and spread
of cholesteatoma that you can observe.
Now next is what are the different
microorganisms which have been isolated
in cases of cholesteatoma.
These include Pseudomonas aeruginosa,
Streptococcus, Proteus, E.
Coli, Bacteroides,
Peptococcus and Fusobacterium.
Next let's discuss a little about
how is pediatric cholesteatoma different
from adult cholesteatoma.
There are seven points over here.
First is congenital cholesteatoma.
More commonly arises from anterior middle
ear and it completely fills up the middle
ear cleft including the eustachian
tube orifice before spreading
to involve the attic and mastoid.
Second, pediatric cholesteatoma spreads
more extensively through temporal bone
than in adults with more involvement
of perilabyrinthine cells and petrous apex.
Third, pediatric cholesteatoma is more
aggressive than adult cholesteatoma
because this happens because of a reason
because pediatric temporal bone is
usually more pneumatized than adults so
the pathways through which a
cholesteatoma spreads is more open and
the process of spread is easier.
Therefore it can lead to more
extensive disease at presentation.
Fourth is there is a greater
inflammatory response seen in pediatric
cholesteatoma than in adults
with an increased expression of a lot
of markers which includes
metalloproteinases and antibodies.
This leads to more bone erosion
and spread of squamous epithelium.
Fifth is as compared to adult
cholesteatoma, pediatric ones do not seem
to invade the petrous labyrinth.
Sixth, lateral semicircular canal
fistula and erosion of fallopian
canal is less common in pediatric
cholesteatoma and lastly ossicular
erosion is seen to be more common
in pediatric cholesteatoma.
Next, let's talk about what are
the clinical features you see in a case
of cholesteatoma, which is basically
the atticoantral disease or the squamosal
type of chronic otitis media.
Now, coming to, discussing symptoms first.
First is the patient comes
to you with ear discharge.
Now the characteristics
of the ear discharge is it is
persistently foul smelling.
Why foul smelling?
Because two reasons.
One is because of the extensive
bone erosion and second is because
of infection by saprophytic
bacteria and anaerobes.
The ear discharge can be blood
stained, which is a typical feature
of atticoantral disease.
And this blood stained is due
to the presence of granulation tissue
and ostitis and a purulent discharge.
The discharge is scanty
in amount, so scanty that sometimes
patient is not aware of it.
A very important thing to remember is
whenever, a patient who has had a
continuously discharging ear but comes
to you with a sudden cessation of the
discharge, that suddenly the discharge
has completely stopped, do not take it
as a good sign, but rather it is
actually a very ominous sign because
what can happen here is sometimes a
perforation may get sealed with crusted
discharge, mucosa or polyp.
So basically there is an obstruction
to the free flow
of the discharge being formed.
Now as a result of this, discharge
starts accumulating in the middle ear.
And now this has the potential
to result in a lot of complications.
And the discharge is also seen
to be continuous due to the presence
of osteitis in these cases.
So this is about the ear discharge that
you see in a case of cholesteatoma.
The patient will also complain
to you about hearing loss.
And hearing loss.
There is a term over here that is very
important known as cholesteatoma hearer.
Here basically what happens is
the patient, even though
the ossicles have been damaged by
cholesteatoma, will actually not present
with much of a hearing loss.
That's because the damaged ossicles, the
gap that, leads to, the gap that forms
after there is damaged ossicles, gets
bridged by cholesteatoma sometimes and
hence the hearing appears to be normal,
even though the ossicles have been
damaged.
That is known as cholesteatoma hearer.
In cholesteatoma, the hearing loss is
mostly conductive, but sometimes you
can even see a sensorineural element.
Next you can see bleeding from the ear.
This can be because
of granulation tissue or polyp.
When you try to clean the ear, patient
can have tinnitus and any, a lot of other
symptoms which can signify some kind
of complication of chronic otitis media.
Coming to signs.
First of all there will be
a perforation of tympanic membrane
which is either attic or
posterior superior marginal type.
If you see in the image over
here, the first image shows
an attic perforation and the second
image shows a posterosuperior marginal perforation.
Sometimes a small attic perforation
can get easily missed because of presence
of either some crusted discharge or
some small granuloma present
which is obscured securing it.
First sign is the perforation
of tympanic membrane.
Second we see a retraction pocket.
Retraction pocket is basically
invagination of the tympanic membrane
seen in attic or
posterosuperior area of pars tensa.
And degree of retraction
pocket can varies.
And in early stages this
retraction pockets are usually
shallow and self cleansing.
But later as the pocket keeps getting
deeper, it starts accumulating
keratin mass and it loses its
self cleaning capacity
and then it starts getting infected.
There are two classifications
of retraction pockets
in pars flaccida and pars tensa.
That is the TOS and the Sade's
classification which I have separate
videos about and you can check it out
in my video over there.
Next, what does cholesteatoma look like?
If you see in the image over here
you can see some pearly
white flakes of cholesteatoma
in the retraction pocket.
And most common site for this
to develop is usually the attic
and the posterosuperior margin.
And I have already mentioned if it
is a congenital cholesteatoma,
it will appear like a pearl like mass
behind an intact tympanic membrane.
You'll also be able to see
osteitis and granulation tissue.
In the image over here you can see that
there is a granulation tissue present.
Over here there can be ossicular necrosis
and even cholesterol granuloma formation.
So these are all the signs you
will be noticing when you
examine the patient and when you
perform the tuning fork tests.
Rinne's test will be negative,
Weber's will be lateralized
to the diseased ear and absolute bone
conduction test will be normal.
Next, let's talk about what are
the investigations you'll do
in a case of cholesteidoma.
First of all, all cases on a priority
basis, you should definitely
examine the patient under microscope.
This is what is the reason behind this.
First of all this will help you in
confirming the diagnosis and look for
things that can be very easily missed
because, sometimes you need to suction
clear the ear before you are able to see
all your findings.
So you will try to see the presence
of cholesteatoma.
Where is it present?
What is the extent of it?
Is there any evidence of bone destruction?
Is there any granuloma or any
granulation tissue formation?
What is the condition of the ossicles?
Are they damaged or are they intact?
All kinds of information
can be found in this test.
Second, we'll definitely be
performing a pure tone audiometry.
This will help you in finding out what is
the type and the degree of hearing loss.
And this will also help you in having
a conversation, with your patient
to explain to them what would be
the outcomes of surgery for them.
Usually we see a conductive type
of hearing loss, but there can be
a sensorineural element as well.
Third, if the, if it is a continuously
discharging ear, we can perform
we can perform a culture
and sensitivity of the ear discharge.
Fourth, we can do an X ray mastoid.
And what will the X ray mastoid reveal?
Usually what we see here we'll see.
We'll look for the presence
of cholesteatoma and any bony erosions.
We look for what is the type of mastoid,
is it sclerotic or is there clouding?
What is the extent of pneumatization?
And if there is any presence of
anatomical variations like a low
lying dura or an anteriorly placed
sigmoid sinus, this will make you
more conscious when you are
performing the surgery as to not,
not injure the structures.
So the basic findings that you see
here are there will be an area of bone
destruction in the attic or mastoid
antrum associated with sclerosis.
Around the bone destruction, mastoid
process will be usually sclerotic.
The first evidence of bone
destruction is usually noticing
the osseous pattern of the attic.
We can also see widening of aditus.
This is best seen in the Stenver's view.
In the image over here you can see
that there is opacification
and a large mastoid cavity present.
This is about XRay mastoid.
And the best, radiological investigation
is to do a CT scan of the temporal bone.
Now this will indicate the extent
of bone destruction and the degree
of mastoid pneumatization.
Again, it can help you in finding
any anatomical variations.
And, cholesteatoma is seen as a soft
tissue mass with homogeneous opacity.
If you see in the image over here
in the left side you can see the yellow
arrow is pointing towards cholesteatoma.
You are able to see it as a soft
tissue mass with homogeneous opacity.
Cholesteatoma will also lead
to destruction
in the attic and antrum areas.
The earliest sign you'll see
on CT scan is that of blunting of scutum.
If you see the right sided image over
here on the left side you can see that
the scutum is very pointed, sharp edge
of a bone, whereas on the right side
where the yellow arrow is pointed, you
can see that the scutum has been
eroded.
There can also be erosion of other
structures like ossicles, lateral wall
of attic, tegmen, sigmoid, sinus plate,
posterosuperior canal wall,
facial canal and even labyrinth.
Mastoid is usually sclerotic
in these cases.
So that's all about the investigations.
In a case of cholesteatoma.
Last part is we'll discuss about
the treatment in case of a cholesteatoma.
Now, in cases of cholesteatoma, there
is no role of conservative management
mostly, unless in some specific cases,
which I'll mention in the end.
But the mainstay of treatment
over here is surgery.
And there are two aims to my surgical
treatment in a case of cholesteoderma.
First of all, I have to eradicate
disease and make the ear safe.
And second, I will reconstruct
the hearing mechanism.
So these are the two aims of surgery
in case of a cholesteatoma.
Now, the cholesteatoma surgeries
can be divided into two types.
One is the canal wall down procedures
and canal wall up procedures.
Canal wall down procedures are
the procedures where you leave
the mastoid cavity open into
the external auditory canal.
So basically you are exteriorizing the,
the diseased area completely.
Now, the common canal wall down procedures
are atticotomy and atticoantrostomy,
MRM and radical mastoidectomy.
Atticotomy is done when cholesteotoma
Is limited into the tympanic
epitympanic or the attic region.
Atticoantrostomy is a type of modified
radical mastoidectomy which is done only
for cases of primary acquired
cholesteatoma with perforation of pars
flaccida and an intact pars tensa.
Disease in this case is usually limited
to the attic and antrum and does
not involve the middle ear space.
Next comes modified radical
Mastoidectomy, which is basically a
modification of radical mastoidectomy
where you try to, preserve much of the
hearing mechanism as possible, that is
the remnants of tympanic membrane
ossicles and disease process, often
localized to attic,
antrum is removed and whole
area is exteriorized into the EAC
by removing the posterior
meatal and lateral attic walls.
The last option is radical mastoidectomy,
which is rarely performed nowadays.
Here what you do is, it is an operation
to eradicate disease
from the middle ear and mastoid without
reconstructing the hearing mechanism.
Where the posterior meatal wall is
removed, an entire area of middle ear
and mastoid, it is converted into a single
cavity and any remnants of tympanic
membrane ossicles except for stapes, foot
plate and periosteal lining is all
removed and you even end up obliterating
the eustachian tube opening with a piece
of muscle or cartilage.
So these are the, common canal wall down
Procedures that are usually done.
next coming to canal wall up procedures.
Here, disease is usually removed through
a combined approach through either,
through EAC as well as the mastoid.
So you are not trying to convert it into
single cavity like in canal wall down
procedure, but you try to approach
both, both ends of the, you try to
approach the ear through both sides,
which is the meatus and the mastoid,
and you keep the posterior medial bony
wall intact.
And hence you end up avoiding all
the problems of an open mastoid cavity.
So in a combined approach or intact canal
wall mastoidectomy, disease is removed,
both permeately and through cortical
mastoidectomy and posterior tympanotomy
approach in which a window is created
between the mastoid and middle ear
through facial recess to reach the sinus
tympani.
So this was all about
the primary surgical treatment.
Second is the reconstructive surgery where
you try to restore the hearing mechanism.
But different types of tympanoplasty
depending on the findings of the disease.
You perform tympanoplasty here,
you can either do it at the time
of the surgery or you can do it
as a second stage procedure.
This, you can take a, decision
yourself, depending on the case that you
are seeing, whether the patient
also will be compliant about coming back
for a second stage procedure.
There are a lot of other variations that
the lot of other, things you need to
consider before you make that decision.
Last of all, we'll discuss a little about
the conservative role, of conservative
management in cholesteatoma.
It has a very limited role.
You can only do for very few cases,
maybe when the cholesteatoma is very
small and easily accessible
for suction clearance under microscope.
So in these cases, you routinely do,
repeated suction clearance and keep
periodic checkups of the patient.
You can also do this in elderly patients
above the age of 65 years who are
generally a little unfit for surgery,
patients who are, unfit for general
anesthesia, and for patients who refuse
to do surgery.
So in these patients you can
try conservative management.
And if there's any polyp and granulation
tissue, you can even try
to surgically remove them with the help
of cup forceps or cauterized
by chemical agents like silver nitrate.
So this completes everything
you need to know about cholesteatoma.
This is a very important discussion
for your theory, for your
viva, your practicals.
This basically forms a major
chunk of knowing ent.
If you have any other questions,
please note them down in the comment
section and I'll get back to you.
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