Csom_squamosal Type Anila
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Transcript of Csom_squamosal Type Anila
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CSOM
SQUAMOSAL TYPEETIOLOGY, PATHOLOGY
CLINICAL FEATURES
MODERATOR DR.C .RAVISHANKARPRESENTER- DR. ANILA VISWANATH
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Definition of csom
Chronic inflammation of themucoperiosteal lining of the middle earcleft
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classification
Inactive mucosal com- perforation
Inactive squamosal com- retraction
Active mucosal com- Active squamosal com - cholesteatoma
Healed com
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Inactive squamosal
Negative static middle ear pressure lead toretraction of tm
Retraction pocket invagination of a partof tm into middle ear
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Retraction pocket
Fixed free
TM adherent to can move mediallyM E structures or laterally
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Epidermisation
Advanced type of retraction
Refers to replacement of middle earmucosa by keratinising squamous
epithelium without retention of keratindebris
Often remains quiescent
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Active squamosal com- cholesteatoma
History
Johannes Mller (1838) coined the termcholesteatoma
a pearly tumor of fatamong sheets of
polyhedral cells
Shucknecht coined the term keratoma.
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Definition
Cholesteatoma is a bag like cysticstructure lined by keratinizing squamousepithelium containing desquamated
epithelium having erosive properties andmostly seen in temporal bone.
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May develop anywhere within pneumatizedportions of the temporal bone
Most frequent locations:
Middle ear space
Mastoid
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Histologically made up of :
Cystic content anucleate keratin
squames Matrix keratinizing squamous epithelium
Perimatrix granulation tissue in contact
with bone (produces proteolytic enzymes)
Essential diagnostic feature presence ofkeratinising squamous epithelium
Epithelium shows maturation withoutdysplasia
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Histology
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Histology
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Cholesteatoma Classification
Congenital
Acquired
Primary
Secondary
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Congenital Cholesteatoma
Defined by Derlacki & Clemis as anembryonic rest of epithelial tissue in anear without tympanic membrane
perforation in a patient without a history ofear infection
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Criteria
Levenson, 1989
White mass medial to normal tympanicmembrane
Normal pars flaccida and pars tensa
No prior history of otorrhea or perforations
No prior otologic procedures
Prior bouts of otitis media were not groundsfor exclusion as was the case in originaldefinition
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Congenital cholesteatoma
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Pathogenesis theories
Failure of involution of ectodermal epithelialthickening called epidermoid formation that is
present during fetal development found atjunction of middle ear & ET (10 -33 wks ofgestation)
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Location -petrous pyramid,
mastoid and middle ear cleft
Male preponderanceMean age of presentation- 4.5 yrs
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Congenital Cholesteatoma
Anterosuperior > Posterosuperiorquadrant quadrant
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Congenital Cholesteatoma - TypeNelson
Type 1 Confined to the middle ear and do notinvolve the ossicles
Type 2 Involve the posterior superiorquadrants and attic, the site of the ossicular
chain Type 3 Involve the sites of type 1 and 2 as well
as the mastoid
Nelson et. al Congenital Cholesteatoma:Classification, Management and Outcome. ArchOto Head Neck Surg July 2002; 128: 810:814.
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Congenital Cholesteatoma -Stage
Stage I Limited to one quadrant
Stage II Involving multiple quadrants withoutossciular involvement
Stage III Ossicular involvement withoutmastoid extension
Stage IV Mastoid involvement (67% risk ofresidual cholesteatoma)
Potsic WP, Korman SB, Samadi DS, et al.Congenital cholesteatoma: 20 years experienceat The Childrens Hospital of Philadelphia.Otolaryngol Head Neck Surg 2002;126(4):409
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Primary Acquired Cholesteatomas
Eustachian tube dysfunction
Persistent negative pressure in middle ear
Results in poor aeration of epitympanic
space
attic or posterosuperior retraction pocket
N l i t tt f th t i
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Normal migratory pattern of the tympanicmembrane epithelium altered by retractionpocket
Enhances potential accumulation of keratin
primary acquired cholesteatoma
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Primary acquired
Pars tensa cholesteatoma
Pars flaccida cholesteatoma/ atticcholesteatoma
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Pathology of pars flaccidacholesteatoma
The epithelium of the cholesteatoma sac iscontinuous with that of pars flaccida and theaccumulation of white keratin debris is visible
Associated with osteitis, granulation tissue and
erosion of the outer attic wall Erosion of the ossicular heads occurs relatively
late in the disease process hence minordegree of hearing loss
The disease further progresses into the anteriorepitympanum and posteriorly in to the mastoidantrum and air cell system
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Pars flaccida retraction
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Pathology of para tensacholesteatoma
Retraction onto the long process of incus,incudostapedial joint and promontory
Long process involved early markedconductive deafness
Occasionally cholesteatoma hearer Invagination into facial recess, sinus tympani
and round window niche difficulty ineradication
In the region of posterior annulus there isexposed bone that can be the site of osteitisand granulation tissue
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Pars tensa retraction
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Primary acquired cholesteatoma
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Secondary Acquired
CholesteatomasRepeated infection through perforation
Metaplasia of epithelialmiddle ear mucosa Migration through
perforation
Metaplasia theory-Sade
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Metaplasia theory Sade
middle ear epithelium is transformed to keratinizedstratified squamous epithelium secondary tochronic or recurrent otitis media
Epithelial invasion theory - HabermannSquamous epithelium migrates along perforationedge medially along undersurface of tympanicmembrane
Papillary ingrowth theory- RuedisInflammatory reaction in Prussacks space with anintact pars flaccida (likely secondary to poorventilation) may cause break in basal membrane
allowing cord of epithelial cells to start inwardproliferation
Implantation theory
Squamous epithelium implanted in the middle earas a result of surgery, foreign body, blast injury,etc.
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Once cholesteatoma enters middle earcleft it invades surrounding structures firstby folllowing path of least resistance &
then by enzymatic bone destruction
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bone destruction produced by
cholesteatoma explained by
Pressure theory not accepted now
Enzymatic theory- first by Lautenslager
Acid po4ase
Collagenase
Acid protease
Pge2, IL-1a, IL-1b, TNF-a, TNF-b
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AnatomyMiddle Ear Regions
Epitympanum: superior to superior limit of EAC
Mesotympanum: bound superiorly by superior
limit of EAC and inferiorly by inferior limit ofEAC
Hypotympanum: inferior to inferior limit of
EAC
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Middle Ear Regions
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Epitympanum
Lies above the level of the short processof the malleus
Contents:
Head of the malleus
Body of the incus
Associated ligaments and mucosal folds
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Mesotympanum
Contents: Stapes Long process of the incus Handle of the malleus Oval and round windows
Eustachian tube exits from the anterior aspect Two recesses extend posteriorly that are often not visible
directly Facial recess
Lateral to facial nerve Bounded by the fossa incudis superiorly Bounded by the chorda tympani nerve laterally
Sinus tympani Lies between the facial nerve and the medial wall
of the mesotympanum
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Hypotympanum
Lies inferior and medial to the floor of thebony ear canal
Irregular bony groove that is seldominvolved by cholesteatoma
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Common Sites of CholesteatomaOrigin
Posterior epitympanum
Posterior mesotympanum
Anterior epitympanum
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Cholesteatoma Spread
Predictable in that they are channeledalong characteristic pathways by:
Ligaments
Folds
Ossicles
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B/w 3rd & 7th month 4endothelially linedsacs evaginate from
first branchial pouch.Mucosal folds and
ossicular suspensoryligaments formedwhen these sacscontact each other.
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Saccus anticus
Smallest pouch
Form anterior pouch of von TroltschContact with anterior most saccule from
saccus medius -Tensor fold. Above it isanterior compartment of attic.
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Saccus medius
Breaks into three saccules
Anterior sacculeatticMedial sacculesuperior incudal space.
Sends an offshoot between lateral mallear
and lateral incudal prussaks space. Posterior saccule pneumatise petrous
temporal
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Saccus superior
Extends b/w malleus handle and tip oflong crus of incus posterior pouch of vonTroltsch and inferior incudal space
Saccus posticus
Form round window niche , sinus tympanioval window niche
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Cholesteatoma Spread
Posterior epitympanic
cholesteatoma passing
from Prussaks space
through superior incudal
space and aditus ad
antrum
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Reaches middle ear by descendingthrough floor of prussaks space intoposterior space of von troeltsch
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Posterior mesotympanum
Extend to mastoid through
posterior tympanic isthmus
& inf. incudal space
sinus tympani and
facial recess commonlyinvolved
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Extend to mastoid viaposterior tympanic
isthmus & inf incudalspace
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Anterior epitympanum
Reach middle ear
via anterior pouch
of von Troltsch.facial n. dysfunction
common
may gain access to
supratubal recess
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Bacteriology
Pseudomonas aeruginosa
Streptococcus
Proteus
E coli
Anaerobes- Bacteroids,
peptococcus, fusobacterium
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Clinical features
Symptoms
Discharge-
foulsmelling- anaerobic infection,
Bloodstained- granulation tissue & osteitis
scanty,
purulent
Tinnitus
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Hearing loss
perforation of tympanic membrane- 10 40dB
- ossicular interruption with intact drum 54 dB
- ossicular interruption with perforation 38 dB
- closure of oval window 60 dB Sometimes , patient hears better in presence of
cholesteatoma- cholesteatoma hearer
Ear acheDizziness- labyrinth involved
Facial deviation- facial canal eroded
Signs
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Signs
Foul smelling discharge in eac
Attic perforation/ marginal perforation
Attic retraction
Cholesteatoma flakes- fishy odour
Granulation tissue
Aural polyp
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Pars tensa retraction - sade
Stage 1-mild retraction not touching longprocess of incus
Stage 2- retracted drum touching long
process of incus
Stage 3- retracted drum touchingpromontory
Stage 4- drum plastered to promontory
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Pars flaccida retraction- tos
Stage 1-Mild retraction not touching neckof malleus
Stage 2-Attic retraction touching neck of
malleus
Stage 3-limited outer attic wall erosion
Stage 4- severe attic wall erosion
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Complications of CSOM
Causes
Pathway of spread
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Classification
Intra temporal
Mastoiditis
Petrositis
Facial Paralysis
Labyrinthitis
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Intra Cranial
Extradural abscess
Subdural abscess
Meningitis
Brain abscess
Lateral sinus thrombophlebitisOtitic Hydrocephalus
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Acute Mastoiditis Infection involve bony walls of mastoid
Beta hemolytic streptococcus
CL/F Pain behind ear, fever, ear discharge
Signs:
Mastoid tenderness
Sagging of posterosuperior meatal wall
Swelling over mastoid- Ironed out mastoid
Ab i R l i id i f i
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Abscess in Relation to mastoid infection
Post auricular abscess commonest
Zygomatic abscess
Bezold abscess
Meatal / lucs abscess
Citellis abscess
Petrositis
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Petrositis
Infection of petrous part of temporal bone
2 groups of air cell tracts-Posterosup & anteroinf
Attic ,around semicircular hypotympanum
Canal to apex around ET
around cochlea
to apex
6th N & trigeminal ganglion closely related
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Gradenigo syndrome
Triad of LR palsy, deep seated retro orbitalpain, persistent ear discharge
Fever
headache
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Facial paralysis
destruction of bony canal of facial nerve
by cholesteatoma or from penetratinggranulation tissue
genu or horizontal portion
Labyrinthitis
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Labyrinthitis
Diffuse serous Labyrinthitis
Diffuse suppurative Labyrinthitis
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Diffuse serous LabyrinthitisDiffuse intralabyrinthine inflammation
without pus formation
VertigoNausea
nystagmus
High frequency SN hearing loss
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Diffuse suppurative Labyrinthitis
Diffuse infection of labyrinth withpermanent loss of vestibular & cochlearfunctions
Severe vertigo nausea vomitingspontaneous nystagmus
Loss of hearing
Extradural abscess
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Extradural abscess
b/w bone & dura
Cl/f:Persistent headache
Severe pain in ear
Malaise
Low grade fever
persistent purulent ear discharge
disappearance of headache with free flowof pus from ear
S
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Subdural abscess
b/w dura & arachnoid
Meningeal irritation- headache fever malaiseneck rigidity
Cortical venous thrombophlebitis- aphasia
hemiplegia ,hemianopia
Raised ICT-papilloedema, ptosis
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Meningitis
Inflammation of leptomeninges
With bacterial invasion of CSF insubarachnoid space
Fever, headache, neck rigidity, nausea,vomiting
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Otogenic brain abscess
Stage of invasion pass unnoticed ,headache malaise
Stage of localisation pus localised bycapsule
stage of enlargement-oedema around
abscess, ICT
Stage of termination
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Lateralsinus thrombophlebitis
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Lateralsinus thrombophlebitis
Inflammation of inner wall of lateralsinus
with thrombus formationStage of perisinus abscess
Endophlebitis & mural thrombus formation
Obliteration of sinus lumen & intrasinusabscess
Extension of thrombus
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Picket fence fever Headache
Greisingers sign- oedema over posterior part ofmastoid- thrombosis of mastoid emissary vein
Pappiloedema
Tobey ayer test -rise in csf pressure on healthyside no effect on d/s side on compression of
jugular veinCrowe Back test- engorgement of retinal veins on
healthy side on pressure on jugular vein
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Otitic hydrocephalusRaised ICT with normal csf finding
Lateral sinus thrombosis obstructs venous
return, if extending to superior sagittalsinus impede absorption of villi to absorbCSF
headache diplopia blurring of visionpapilloeedema nystagmus CSF pr. >300mmwater
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