- Chronic Otitis Media-Squamous type is characterized by permanent abnormalities in the pars tensa flaccida, likely resulting from earlier Acute Otitis Media (AOM) and negative middle ear pressure with Otitis Media with Effusion (OME).
- Chronic Otitis Media often involves dominant mastoid infection along with concurrent otitis media, and the infectious process can persist longer (1-3 weeks) compared to resolving AOM in a previously healthy ear.
- The overall prevalence of active and inactive Chronic Otitis Media is 4.1%, with no significant sex differences. It is more prevalent in the age group of 41-80 years and in lower socioeconomic groups.
- Etiology of Chronic Otitis Media includes factors like Acute otitis media, genetics, race, environment, Eustachian tube dysfunction, gastroesophageal reflux disease (GORD), craniofacial abnormalities, autoimmune diseases, and immune deficiency.
- The classification of Chronic Otitis Media includes Mucosal COM (Inactive and Active), Squamous COM (Inactive and Active), and Healed COM stages.
- Retraction of the pars tensa can progress through different stages (I to IV) presenting varying degrees of retraction and adhesive otitis media.
- Cholesteatoma is a hallmark of active squamous epithelial COM and is characterized by the retention of keratin debris within the middle ear system. It can lead to complications such as impaired vibration of the tympanic membrane and erosion of the ossicles.
- Cholesteatoma can progress to more hazardous forms with accumulation of keratin producing squamous epithelium and three-dimensional non-malignant epidermoid structures.
- The biology of cholesteatoma involves stratified squamous epithelium zones, which have implications for the origin and direction of migration in the middle ear.
- Bacteriology of infected cholesteatoma includes both aerobic and anaerobic pathogens. Pathways of epithelial migration in cholesteatoma can differ based on zonal origins and factors like Ki 67 antigen expression.
- Acquired Cholesteatoma can be classified into primary, secondary, and tertiary types based on the pathophysiology and clinical grounds of its occurrence.
- Congenital Cholesteatoma arises from embryonal squamous epithelial cell rests and can present in different types categorized by the sites involved in the middle ear.
- The pathogenesis of Congenital Cholesteatoma can follow theories such as epithelial rest theory, acquired inclusion theory, and inflammation-related theories.
- The staging and classification of congenital cholesteatoma can help in determining the extent of involvement and the potential risks related to residual disease.
- Investigations for cholesteatoma include pure tone audiometry, CT scans, and MRIs to assess the extent and characteristics of the lesion.
- Primary acquired cholesteatoma can be associated with theories like invagination of the tympanic membrane, basal cell hyperplasia, migration theory, and squamous metaplasia of middle ear epithelium.- 1988: DMBA (dimethylbenzanthracene) identified as a chemical carcinogen
- Actions of DMBA: Induces advancement of keratinizing squamous epithelium (KSE), spreading to the Eustachian tube and middle ear cavity
- Basal cell hyperplasia theory: Proposed by Lange in 1925 and supported by Ruedi, suggests that epithelial cells from the pars flaccida invade sub epithelial tissue, leading to the formation of microcholesteatomas
- Mechanism of microcholesteatoma growth: Basal lamina alteration allows invasion into the lamina propria, eventually breaking through the basal lamina to form sub epithelial connective tissue cones
- Factors contributing to microcholesteatoma enlargement: Evidence suggests involvement of intercellular adhesion molecules, Langhans cells triggering immune reactions, and inflammation mediated by IL-1alpha
- Squamous Metaplasia: Sade's 1971 research notes a transformation of simple squamous or cuboidal epithelium in the middle ear cleft to keratinized squamous epithelium, which can lead to cholesteatoma formation
- Keratinizing area enlargement and inflammation contribute to the accumulation of debris, contact with the tympanic membrane, possible infection, and cholesteatoma development
- Role of Severe Vitamin A deficiency: Lack of Vitamin A may lead to the formation of keratinizing squamous epithelium within the middle ear without resulting in cholesteatoma formation, providing direct evidence supporting the role of nutrition in disease development
This marks the end of the bulleted notes based on the user's text. Would you like to know more about a specific aspect of cholesteatoma or have further questions on this topic?- The study identified the up-regulation of hsa-miR-21 and concurrent down-regulation of potent tumor suppressor proteins PTEN, which control aspects of apoptosis, proliferation, invasion, and migration.
- The results of the study were used to develop a model for cholesteatoma proliferation based on microRNA dysregulation.
- This model can serve as a template for studying potential RNA-based therapies for the treatment of cholesteatoma (Referencing David et al., 2009 study).
- The exact pathogenesis of cholesteatoma is not entirely clear, but it is important to consider anatomic considerations in its management due to the high rate of recidivism.
- Long-term follow-up is essential to maintain vigilance for complications related to cholesteatoma.
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CHRONIC OTITIS MEDIA-SQUAMOUS TYPE
Definition of Chronic Otitis Media:
Permanent abnormality of pars tensa or flaccida, most likely a result of earlier AOM, negative middle ear pressure or OME
( S& B, 7th ed)
Structural change in middle ear system associated with permanent defect in TM
( Ballenger,16th ed)
Cont…
COM often displays a dominant mastoid infection with concurrent otitis media
COM is present when an infectious process persists for longer than 1-3 wks usually necessary for resolving AOM in a previously healthy ear
( Cummings, vol 4)
COM: includes both CSOM & chronic perforation of TM
WHO definition,1996
Prevalance of COM:
Cont…
Overall prevalence of active & inactive COM- 4.1%
No sex difference in Prevalence of COM
Age group : 41-80 yrs
Lower socioeconomic group
( S& B, 7th ed)
Etiology of COM in general:
Acute otitis media & OME
Genetics & race
Environment
ET dysfunction
(Controversy)
GORD
Craniofacial abnormalities
Autoimmune disease
Immune deficiency
Classification:
(S & B , 7th ed)
Mucosal COM :
Inactive Permanent pars tensa defect , ME mucosa not inflamed
Active Permanent pars tensa defect, inflamed ME mucosa,
discharge
Squamous COM:
Inactive Retraction of pars flaccida or tensa ,potential to become active with retained debris
Active Retraction of pars flaccida or tensa , retained Squamous
epithelial debris +inflammation & production of pus
Cont…
Healed COM:
Thinning and /or generalized opacification of pars tensa without perforation or retraction, post surgery
INACTIVE SQUAMOUS EPITHELIAL COM
Retraction & Epidermization
Negative middle ear pressure Retraction (Atelectasis) of TM
Retraction pocket :
Fixed – Adherent to structure of ME
Free —Move medially and laterally
Stage I: Pars tensa slightly retracted
Stage II: Pars tensa in contact with long
process of incus
Stage III: Contact with promontory, mobility
present
Stage IV: Adhesive ottitis media: pars tensa
adherent to promontory, mobility
absent
Stage I: Pars flaccida dimpled and
retracted than normal ,
not adherent to malleus
Stage II: Retraction adherent to malleus neck
Full extent of retraction can be seen
Stage III: Part of retraction out of view
Partial erosion of bony attic wall
Stage IV: Full extent of retraction uncertain, out of view
Definite erosion of attic wall
Cont…
Epidermization:
Advanced retraction, replacement of ME
mucosa by KSE
No retention of keratin debris
Involve part or all of ME cavity
Often remain quiescent, doesn’t progress to
cholesteatoma
Progression:
Reaches size that ceases self cleansing- accumulate debris- infected – repeated episode of discharge
Loss of elasticity and mobility of TM: Impair vibration, Perforation of TM
Erosion of Ossicles: long process of incus
Resolve :
Pars tensa retraction in children with OME resolves spontaneously in 70% of cases
Static :
Some remain static and self cleansing
ACTIVE SQUAMOUS EPITHELIAL COM (CHOLESTEATOMA)
CHOLESTEATOMA
Keratoma, Epidermoid cyst, Cholesteoid Epidermoidosis
Greek: Cole: bile, Steatos: fat, Oma : tumour
Misnomer
Squamous epithelium and its exfoliated keratin debris trapped within tympanomastoid compartment
Cont…
Hallmark: Retention of keratin debris
Narrow neck and inner surface of sac continuously produce keratin .
Desquamated dead keratin collects in & sac expands
Cont…
Sac of KSE containing desquamated epithelium in the middle ear cleft ,attic,mastoid ,petrous apex with bone eroding property, which has lost self cleansing capacity.
Cont…
Accumulation of keratin producing squamous epithelium in middle ear, attic ,mastoid,petrous apex (Skin in wrong place)
Three dimensional non malignant epidermoid structure exhibiting independent growth replacing middle ear mucosa and resorption of the underlying bone, progression can be relentless & hazardous to patient
History:
Term cholesteatoma coined by Johannes Muller ( 1838)
Virchow( 1855) : Tumor from metaplasia arising from mesenchymal cells to epidermal cells, growing then as tumoral cells
Gruber, Wendt, Von Troeltsch, ( 1868 ) : Cholesteatoma to be result of metaplasia not of bone cells but of tympanic mucosa cells into malphigian epithelium
Cont…
Politzer( 1869): Cholesteatoma as glandular neoplasm of middle ear mucosa
Bezold & Habermann (1889) :Cholesteatoma - result of migration of external ear canal epidermis into tympanic cavity via a marginal perforation from acute/ chronic otitis media. Took 40 yrs to accept this theory as correct one that explained pathophysiology of cholesteatoma
Cont…
Age distribution: peak incidence second decade of life
Sex distribution: 3males for every 2 females
Histology:
Cont…
Cystic content: contains fully differentiated anucleate keratin squames
Matrix: contains keratinizing squamous epithelium lining a cyst like structure
Perimatrix: also lamina propria,contains granulation tissue and cholesterol granules & releases enzymes & cause bone destruction
Biology of Stratified Squamous Epithelium
Zone 1:
- Epithelium of TM originates from primary external canal which later covers pars flaccida
Zone 2:
- Pars tensa
- Composed of 2- 3 layers of epithelial cells deep to stratum granulosum
Zone 3:
- most of deep external canal
- 4-6 layers of nuclei
Zonal origin of Cholesteatoma:
If cholesteatoma arises from TM epithelium
- Zone 1 - likely origin
- Most vigourous zone seems to be source of whole migrating flux that extends from it over the pars tensa with the cartiliginous canal
-Studied by Ki 67 antigen
Migration is unique in showing no directional change
Cont…
Bacteriology of infected cholesteatoma
Aerobes
P. aeruginosa
P. fluorescens
Streptococcus sp.
Proteus sp.
Escherichia coli
Klebsiella- enterobacter – serratia
Achromobacter sp.
Staphylococcus epidermidis
Staph. Aureus
CBC group F
Anaerobes
Bacteroids
Peptococcus/peptostreptococccus
P. acnis
Fusobacterium
Bifidobacterium clostridium
Eubacterium
Classification:
According to pathophysiology (clinical ground)
Congenital
Acquired
- Primary
- Secondary
- Tertiary ( Implantation)
Congenital Cholesteatoma:
Embryonal Squamous epithelial cell rests fails to disappear during development
Source Persistence of epidermoid formation ( 1st branchial groove derivative)
Epidermoid formation regress by 33 wk normally
Failing regression presence & expansion Congenital cholesteatoma
Cont…
May arise anywhere in petrous temporal bone
Conveniently classified as:
- CP angle ,
- Deep within petrous apex ,
- Jugular fossa,
-Middle ear cleft
Cont…
Age of presentation: mean 4.5 yrs
M:F 3:1
More aggressive as bones in children are softer
In which quadrant can a pediatric cholesteatoma most often be found?
Anterosuperior > Posteriosuperior > Attic > Posterioinferior >
Anterior Inferior > Mastoid
Congenital Cholesteatoma
Pathogenesis - Theory
Congenital Cholesteatoma
Pathogenesis - Theory
“Acquired” inclusion theory
Tos
Clemis criteria for diagnosis:
1)White mass medial to normal TM
2)Normal pars tensa & flaccida
3)No prior h/o otorrhoea & perforation
4)No prior otological procedures
5)Prior bouts of otitis media not grounds for exclusion as congenital disease
Staging:
I- Limited to one qudrant
II - involving multiple quadrants without ossicular involvement
III- Ossicular involvement without mastoid extension
IV- Mastoid involvement
Potsic et al;2002
Stage IV carries 67% risk of residual cholesteatoma
Congenital Cholesteatoma - Type
(Nelson)
Type 1 – Confined to the middle ear and do not involve the ossicles
Type 2 – Involve the posterior superior quadrants and attic, the site of the ossicular chain
Type 3 – Involve the sites of type 1 and 2 as well as the mastoid
Presentation:
Asymptomatic
Hearing loss
Detected when complicated
White mass visible through intact TM
No prior history of Otitis media
Symptoms not present in infancy, time to grow
Vertigo/facial palsy
Cont…
Investigations:
-PTA: Usually normal
-CT scan: low attenuated area
- MRI: investigation of choice
Acquired Cholesteatoma:
Primary acquired: Occurs where there is no previous history of ear discharge
Secondary acquired: Occurs in already diseased ear
Tertiary Aquired : Trauma
Primary acquired cholesteatoma:
Acquired Cholesteatoma:
4 basic theories:
Invagination of TM (retraction pocket cholesteatoma)
Basal cell hyperplasia
Migration theory
Squamous metaplasia of middle ear epithelium
Cont…
Invagination theory:
Wittmack-1933
Primary mechanism for attic cholesteatoma
Retraction pocket deepen negative middle ear pressure & repeated inflammation
Retraction pocket deepens ,desquamated keratin not cleared from recess cholesteatoma results
Cont…
Origin ET dysfunction (OME) with resultant negative middle ear pressure-ex vacuo theory
Pars flaccida less fibrous ,less resistant to displacement
Apparent defect in posterosuperior quadrant
Appearance of marginal perforation but invagination
Retraction pockets precursors of cholesteatoma
Cont…
Biofilm formation
Infection, persistence ,resistance, recurrence
Cont…
For:
High recurrence of retraction pocket post cholesteatoma surgery
Against :
Negative ME pressure solely not enough
No documentation: Otoscopic progression of attic retraction to cholesteatoma
Retraction pocket Rx with VTI ; no influence on long term position of TM (Ars Marquet procedure)
Large cohort study needed; Progression of normal TM --retraction pocket Cholesteatoma
Controversy:
Condition of the anterior part of middle ear cleft in acquired cholesteatoma:
High rate of flogistic suffering of controlateral ear suggest correlation b/w tubal dysfunction & acquired cholesteatoma but low rate of pathological reports regarding anterior mesotympanic region exclude a eustachian tube dysfunction (EDT) at time of surgery
. Acta Otolaryngol. 2008 Jun ;128 (6):634-8
Cont…
Why pars flaccida and PSQ ?
Fibrous layer : less organized
Greater blood supply – affected by inflammatory cell infiltrate in AOM and OME—fibrous layer thinner than rest
Cont…
Epithelial invasion theory:
By Habermann-1889
Keratinizing squamous epithelium from TM migrates –middle ear from perforation in TM
Cont…
For:
Histology of epithelium of cholesteatoma and meatal skin identical
Against :
Perforation opening of retraction pocket
Cont…
Weiss et al;1958- epithelial cells will migrate along a surface by process called Contact guidance & when they meet another epithelium –stop migrating ie Contact Inhibition
Jackson et al;1978- Inner mucosal layer –damaged –inflammation-allowing outer keratinizing epithelium to migrate inwards cholesteatoma formation
Cont…
Cytokeratin,CK 10 seen in meatal epidermis & migrating epitheliumlocated in cholesteatoma matrix
Grote et al;1988
DMBA (dimethylbenzanthracene)
Chemical carcinogen
Induce KSE advancement
Spread over ET & middle ear cavity
Schmidt et al;2004
Cont…
Basal cell hyperplasia theory:
Lange -1925supported by Ruedi
Epithelial cells of pars flaccida invade sub epithelial tissue by proliferating columns of epithelial cells
Basal lamina must be altered to invade lamina propria
Basal lamina breaks invasion of epithelial cones into sub epithelial connective tissue microcholesteatomas
Cont…
Microcholesteatomas enlarge perforating TM
Evidence for support Human intercellular adhesion molecule-1 & 2 cell migration
Langhans cells may initiate immune reactionproliferation of KSE by IL-1alpha
Controversy regarding nature of fibroblasts by Parisier & Chole
Cont..
Squamous Metaplasia:
By Sade -1971
Simple sq. cuboidal epithelium of middle ear cleft metaplastic transformation into KSE
Epithelial cells are pleuripotent & stimulated by inflammation become keratinized
Cont…
Keratinizing area enlarge-accumulate debris & contact TM intercurrent infection & inflammation –cholesteatoma lysis of TM & perforation
Severe Vit A deficiency formation of KSE within middle ear
None developed cholesteatoma no direct evidence
Frush et al;1979
Recent advance:
Selective Dysventilation Syndrome:
Consists of presence of series of complete / incomplete epitympanic diaphragms & ME isthmus blockage causing negative epitympanic pressureformation of a retraction pocket or cholesteatoma associated with normal Eustachian tube function
Med Hypotheses. 2011 Jul ;77 (1):116-20
Tertiary Cholesteatoma:
Implantation of Squamous epithelium into middle ear
Accounts for small proportion of cholesteatoma
Trauma to TM
Squamous epithelium left behind tympanomeatal flap or TM graft
Cont…
Best evidence:
Cholesteatoma arise from skin of TM and EAC
Cytokeratin protein subunit : ME cholesteatoma and skin of EAC and TM similar
Natural history of active COM squamous (CHOLESTEATOMA):
Progression toward healing
No figure available
Automastoidectomy Cavity
Disease process selectively erode outer attic
wall +/_ posterior canal wall
Epithelial migration (self cleansing) resorted ,
Progression of active disease
Disease progress
Involvement of ossicular chain
Bony erosion leading ; IC and extracranial complication
Cont…
Typical terms:
Cholesteatoma post Temporal bone fractures/Blast injuries:
Pathogenesis:
-Epithelial entrapment in fracture line
-Rent in TM
-Traumatic implantation of TM skin into ME
-Trapping of epithelium medial to canal stenosis
Typical location: Epitympanum & antrum (fracture line)
Canal cholesteatoma preventable
Cont…
Sinus Cholesteatoma
Graft cholesteatoma
Pathology
Active Squamous Epithelial COM (Cholesteatoma)
Mucosal changes:
Chronic inflammation within mucosa of tympanomastoid
compartment:
Area of mucosa ulcerate—proliferation of blood vessels, fibroblast and
inflammatory cells-- Granulation tissue
Cont…
Mucosal change coalesce—Aural polyp
Ossicular chain:
Resorption of part or all of ossicular chain (Resorptive osteitis)
Long process of incus, Superstructure of Stapes, Body of incus, Head of malleus order of frequency
Incus and stapes commonly involved
Cont…
Cholesterol Granuloma
Found in active COM
Area of giant cell reaction around cholesterol crystal
Breakdown of hemorrhage, Middle ear effusion
Bone erosion in cholesteatoma:
Explained by:
-Pressure theory
-Enzymatic theory
-Pyogenic osteitis theory
Pressure necrosis:
-Clinical observation abandonment of pressure necrosis
-Chole measured pressure exerted by experimental cholesteatoma & found to be around 1.3-11.9 mm Hg
-For bone erosion pressure capillary perfusion pressure should exceed 25 mm Hg
Enzymatic theory:
Lautenschlager cholesteatoma elaborate enzymes that erode bones
Controversy: Monocytes or osteoclasts?
Chole – ultrasructural evidence bone resorption –result of action of multinucleated osteoclasts disrupt lamina limitans of bone cause resorption lacunae
Enzymes are elaborated by osteoclasts (resorbing cells)
Enzymes :
Acid phosphatase
Collagenase
Acid proteases
Metalloproteinase
Cathepsin B, Calpain I & II
Molecular factors:
Cytokines: IL-1, 6, TNF
Protein mediator: GF
Non protein mediator: Prostaglandin, Neurotransmitter, Nitric oxide
Recent views:
Morphological study of eroded auditory ossicles by cholesteatoma:
Osteogenesis is also a basic pathologic phenomena in cholesteatoma. Obvious bone destruction & remodeling coexist in cholesteatoma cases
Vestn Otorinolaringol. 2006 ;(5):53-5
Pyogenic osteitis:
Presence of antibiotic –resistant biofilms explain aggressiveness
Biofilms elaborate lipopolysaccharide & other bacterial products stimulate osteoclastogenesis
Anatomical considerations of Cholesteatoma spread:
Middle Ear Regions:
Epitympanum: superior to superior limit of EAC
Mesotympanum: bound superiorly by superior limit of EAC and inferiorly by inferior limit of EAC
Hypotympanum: inferior to inferior limit of EAC
Middle Ear Regions
Epitympanum:
Lies above the level of the short process of the malleus
Contents:
Head of the malleus
Body of the incus
Associated ligaments and mucosal folds
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
Hypotympanum:
Lies inferior and medial to the floor of the bony ear canal
Irregular bony groove that is seldom involved by cholesteatoma
Cholesteatoma spread
Cont…
1)Posterior epitympanum
2)Posterior mesotympanum
3)Anterior epitympanum
Predictably channeled along characteristic pathways by:
Ligaments
Folds
Ossicles
Cont…
Most common route - epitympanum is—
posteriorly from Prussacks space
Posterior route
Commonest route
Superior incudal space ( Posterolateral attic )— Aditus –Antrum
Inferior route
Frequent route
Inferior incudal space ( mesotympanum)
Anterior route
Rare
Thr ant pouch of von troeltsch –protympanum ( mesotympanum)
Posterior Mesotympanic cholesteatoma
Posterior mesotympanic cholesteatoma
Sinus tympani and facial recess
Medial to incus –posterior attic –aditus – antrum
Occurs via post tympanic isthmus & inferior incudal space
More common in children
Leads to residual disease
Anterior epitympanic cholesteatoma:
-Floor of Ant. epitympanum –related to horizontal portion of facial nerve & geniculate ganglion- facial nerve dysfunction is common
- Cholesteatoma reach middle ear thr- Ant pouch of Von Troeltsch
ROUTES OF SPREAD OF INFECTION IN COM
1. Natural Communication :(Normal anatomical pathway)
Between middle ear & labyrinth : oval & round window
Dehiscence: Bone over jugular bulb , Tegmen tympani, Suture line of temporal bone
2. Direct erosion of bone:
Most common pathway
Active infection ( Hyperaemic decalcification) or resorption by cholesteatoma or osteitis
Cont…
3. Abnormal preformed pathway
Congenital: Aberrant arachnoid granulation
Meningo-encephalocoele
Trauma: Accidental: Temporal bone fracture
Surgical: Stapedectomy, Fenestration in LSCC
4. Vascular channel:
Progressive thrombophlebitis of small venules
Along periarterial spaces of Virchow – Robin
Patient Evaluation
Cont…
History
Detailed otologic history
Hearing loss
Otorrhea
Otalgia
Tinnitus
Vertigo
Symptoms s/o complications
Prior surgery
Previous h/o middle ear diseases
Cont…
Symptoms of Active COM :
Symptoms Active mucosal Cholesteatoma
Hearing loss 74% 83%
Otorrhoea 69% 56%
Otalgia 37% 39%
Childhood ear disease 26% 43%
OTOMICROSCOPY:- Gold standard
Exam discharge, TM & polyp removal.
x6 – Cleaning meatus.
x10 – TM examination.
Great value in children-inspect TM closely
Cont…
Occurs in pars tensa or flaccida
Essential to record :Retraction pocket
Totally in view or part out of view
Self cleansing or not
Fixed or free
Part out of view may not be self cleansing , potential to become active with cholesteatoma
Foul smelling white or yellowish colored cheesy material +/-
discharge +/- bony erosion
Attic or posterior TM
In majority , cholesteatoma extent cant be determined otoscopically
Aural polyp obscuring attic or in PSQ
Cont…
Clean ear thoroughly of discharge & debris with cotton-tipped applicators /suction
Culture wet, infected ears and treat with topical and/or oral antibiotics
MOBILITY ASSESSMENT:
Pneumatic otoscopy
Tympanometry
Cont…
HEARING EVALUATION :
Tunning fork : 256HZ ( ***) 512 HZ
Pure tone audiometry: 4 frequencies (500,1000,2000,3000Hz)
(Committee on hearing & equilibrium of AAO-HNS.)
-Degree and type of hearing loss
FISTULA TEST
STATUS OF FACIAL NERVE
X-ray MASTOID :
- Position of dural and sinus plate
- Degree of Pneumatization
- Cavity
CT Scan:
1.5 mm section coronal and axial plane of temporal bone
Role of CT scan :
Revision cases due to altered landmarks from previous surgery
Diagnosis of COM ,TM not be visualized ,(narrowing or stenosis of EAC)
Suspected congenital abnormalities
Cases of cholesteatoma in which sensorineural hearing loss, vestibular symptoms, or other complication evidence exists
Sensitivity in fistula detection not reliable
Facial nerve dehiscence ; 66% detected
Role of CT in Routine Investigation of COM:
Debatable ; high false positive + ve & negative report
Preoperative CT can be justified, if it influences choice of surgical approach
In Canal wall up; Pneumatization knowledge imp ( plain x-ray)
No evidence that preoperative CT influence the surgical management
Controversy: Expertise in interpreting CT comes from regular assesment-all opportunities to view new scans should be taken all cholesteatoma cases should include CT investigation
CT disadvantage:
Granulation tissue vs. cholesteatoma
Specific soft tissue problems
Dural involvement
Abscess
Brain herniation
Labyrinth involvement
Sigmoid sinus thrombosis
MRI needed
MRI:
Delineates intracranial pathology that complicates COM
Cholesteatoma differentiated from other soft tissue
Assessment of lesion near the petrous apex
Diagnosing residual cholesteatoma
MRI characteristics of CT scan:
Magnetic Resonance
Dubrelle F et. al. Diffusion weighted MR imaging sequence in the detection of postoperative recurrent cholesteatoma. Radiology Feb 2006; 238 (2): 604-610.
Cont…
ENDOSCOPY: In teaching rather than diagnosis
Photograph: Comparison of retraction pocket over time
BACTERIOLOGY:
Valuable: Ear is active or in infective complication
Recent advance:
MicroRNAs- powerful regulators of protein translation implicated in many neoplastic diseases.
This study specifically identified up-regulation of hsa-miR-21 concurrent with down-regulation of potent tumor suppressor proteins PTEN and programmed cell death
They control aspects of apoptosis, proliferation, invasion, and migration.
Results were used to develop a model for cholesteatoma proliferation through microRNA dysregulation. This model can serve as a template for further study into potential RNA-based therapies for the treatment of cholesteatoma
David et al.2009
Conclusion:
Exact pathogenesis not entirely clear
Important anatomic considerations in management
High rate of recidivism with long-term F/U essential
Maintain vigilance for complications
