Cholesteatoma Flashcards
What is a cholesteatoma?
Squamous epithelium in the middle ear or mastoid.
It p/w otorrhea and CHL.
Retraction of TM w/ squamous debris collection or a whitish mass behind an intact TM.
What are the types of cholesteatoma?
- Acquired (primary and secondary) – m/c
2. Congenital
Primary vs secondary acquired cholesteatoma
Primary: forms as a retraction of the TM (usu pars flaccida)
Secondary: forms 2/2 squamous epithelial migration from the TM or implantation of squamous epithelium into ME during surgery (PET, tympanoplasty)
What is a congenital cholesteatoma?
Occurs w/o TM retraction or implantation of squamous epithelial material.
Classically defined as an embryonic rest of epithelial tissue in ear w/o TM perf and w/o h/o ear infxn.
Pathogenesis of acquired cholesteatoma
A/w ETD and chronic inflammation of ME (COM).
Chronic neg ME pressure -> retraction -> nl migratory pattern of squamous epith disrupted -> accumulation of keratin debris -> chronic infxn and inflammation -> further growth and migration of squamous epith and inc OC activity -> bone resorption
Local inflam response further inhibits ET fnc, increases mucosal edema and mucous secretion, and disrupts drainage pathway of t-bone
This environment fosters growth of Pseudomonas, Strep, Staph, Proteus, Enterobacter, anaerobes -> more inflammation and continues the cycle
Pathogenesis of congenital cholesteatoma
Failure of involution of the epithelioid formation in the ME during fetal development
Other theories:
- Metaplasia of ME mucosa
- Direct microretractions of the TM near the malleus long process that are self-limited but leave squamous epith rests in the ME
How can cholesteatoma be prevented?
- Congenital: can’t
- Secondary acquired: careful surgical technique
- Primary acquired: restoring ET fnc, providing secondary ventilation to ME, control of infxn and inflam state of ME with regular debridement of cholesteatoma sac
How do pts present?
Recurrent or persistent purulent otorrhea
CHL
Tinnitus
Rarely, vertigo or dysequilibrium or facial n sx
Imaging study of choice
CT
CT findings
- Bone window axial and coronals with 1.5mm slices or less are ideal
- Esp useful in pts w/ hx suggestive of secondary acquired cholesteatoma but TM opaque and can’t visualize middle ear
- Erosion of bone (m/c scutum and ossicular chain)
- Erosion of the labyrinth is highly suggestive (although can be seen w/ neoplasia)
How is CT useful in surgical planning?
Can indicate presence of
- Low tegmen
- Ant sigmoid sinus
- Labyrinthine erosion
- Ossicular erosion
- Petrous apex involvement
All of which affect surgeon’s approach
Is CT a requirement prior to surgery?
No
Many will not get pre-op unless revision surgery, suspicion of labyrinthine fistula, or possibility of petrous apex dz
When is MRI useful?
If neoplasm or encephalocele is suspected
Typical audiogram
CHL
What if the audiogram shows SNHL?
May be due to chronic or recurrent inflammatory process but should consider possibility of labyrinthine fistula
Complications of cholesteatoma
- Chronic inflammation and infxn
- Bone erosion (ossicular chain)
- Otorrhea
- SNHL
- Dizziness
- Facial nerve injury
- Suppurative complications (acute mastoiditis, subperiosteal abscess, sigmoid sinus thrombosis, meningitis, and brain abscess)
Nonsurgical treatment options
Goal: reduce level of inflammatory and infectious activity
- Remove infected debris from EAC
- Keep all water out of ears
- Topical ABX ofloxacin or neomycin-polymyxin B
- Consider topical steroids for inflammation
What is the goal of surgery?
A “dry and safe” ear = permanent reversal of the processes causing bone erosion, chronic inflam, and infxn. To achieve, must remove or exteriorize all cholesteatoma matrices.
What is Prussak’s space?
Area b/w pars flaccida laterally and malleus neck and lower portion of head medially
Where most cholesteatomas invade
What is the m/c location of cholesteatoma in the ME
The area around the stapes superstructure and incus long process
List the areas of the middle ear where cholesteatoma may be left behind due to difficult access
- Area around stapes superstructure
- Facial recess
- Sinus tympani
- Posterior hypotympanum
How can visualization of the epitympanum be improved?
By removing the incus and malleus head
If tegmen is very inferior, may need to remove posterior and superior canal wall.
What are the various air cell tracts through which cholesteatoma can invade the petrous apex?
- Subarcuate
- Retrolabyrinthine
- Supralabyrinthine
- Retrofacial
- Infralabyrinthine
CWU or CWD?
- Surgeon training level and experience
- Anatomy of the pt’s t bone. Sometimes adequate exposure can be obtained w/ either.
- Low tegmen or anterior sigmoid sinus may prompt for CWD for exposure - Issue of recurrent or recidivistic (residual) dz
- ?Higher recurrent/residual dz w/ CWU esp if cholesteatoma arises from pars flaccida
Causes of otorrhea after CWD mastoidectomy?
- Recurrent or residual cholesteatoma
- High facial ridge
- Presence of mucosal tissue w/in mastoid cavity
Should treatment of cholesteatoma be staged?
Controversial
-2nd look surg is usu performed 8-12 months after 1st stage
Why is cholesteatoma around the oval window typically removed towards the end of the procedure?
In case a perilymph fistula occurs.
MAN can then be instituted w/ fascia or other soft tissue grafts w/o risk of compromising the repair during further dissection.
What is the rate of recurrent or residual dz at the 5 yr mark from surgery?
as high as 40%
Other 10 year series report 15-25%
What are the 4 procedure options for cholesteatoma?
- CWU mastoid
- Atticotomy
- Modified radical mastoidectomy (CWD)
- Radical mastoidectomy (CWD) (mastoid cavity and no TM)
As you go down, risk of otorrhea rises and risk of recurrence falls.
