AOM, Chronic Ear, Cholesteatoma Flashcards
What is the name of TM Pars Tensa retraction staging? Describe each stage.
Sade stages (1979)
1. Type 1: Retraction only of the pars tensa
2. Type 2: Retraction pocket contacts the incudostapedial joint
3. Type 3: Atelectatic otitis - Retraction pocket contacts the promontory, but is not adherent (can only be determined intraoperatively)
4. Type 4: Adhesive otitis - retraction pocket contacts promontory and is adherent (cannot be lifted off intraoperatively)
5. TM perforation
Page 286 Vancouver
https://www.otoscape.com/eponyms/sade-classification-of-pars-tensa-retraction.html
What is the name of TM Pars Flaccida retraction staging? Describe them.
Tos and Poulsen stages (1980)
1. Type 0: Normal
2. Type 1: Attic retraction, towards but not in contact with neck of malleus
3. Type 2: Retraction contacts the neck of the malleus
4. Type 3: Retraction extends beyond bony annulus, no bony erosion (?except scutum?). Bottom of pocket can be visualized.
5. Type 4: Definite bony erosion, cannot visualize bottom of pocket
https://www.otoscape.com/eponyms/tos-poulsen-classification-of-pars-flaccida-retraction.html
Why does eustachian tube dysfunction cause negative middle ear pressure?
Middle ear mucosa is made up of respiratory epithelium. When Eustachian tube is blocked, the middle space is isolated. The middle ear absorbs trapped air (gas exchange) and therefore this creates a negative pressure in the middle ear.
Describe the 5 theories of acquired cholesteatoma formation. What is the most common theory? What are the types of acquired cholesteatoma and what theories are associated with them?
OH MIMI
Hyperplasia of basal cells: Basal cells of the tympanic membrane proliferate and move medially through the basement membrane into the middle ear
Implantation of epithelial cells (ie. iatrogenic during surgery/trauma/foreign body )
Invagination (negative pressure –> retraction pocket –> keratin trapping within pocket, and ingrowth. Occurs in the pars flaccida
Metaplasia of normal middle ear squamous(??) epithelium to keratinizing epithelium (through to be due to chronic or recurrent infection)
Migration through TM perforation (especially marginal or attic perforations)
Otitis media with effusion theory (creates retraction pockets)
Most common theory is invagination, so it is called “primary acquired cholesteatoma”.
All other theories are considered “secondary acquired cholesteatoma” (most common is migration)
Why don’t PE tubes always correct TM retraction pockets?
PE tubes may not pneumatize the area of retraction (e.g. there is a separate pocket at Prussak’s space)
Define the borders of Prussak’s space. What is it’s significance?
Most common location for acquired cholesteatoma
Boundaries:
- Lateral: TM - pars flaccida (Shrapnell membrane) and lower edge of scutum
- Medial: Malleus Neck
- Inferior/floor: Lateral process of malleus
- Superior/roof: Lateral malleolar fold
- Anterior limit: anterior malleal fold
- Posterior wall: open into the posterior pouch of von Troeltsch
Page 287 Vancouver notes
Page 37 Kevan’s notes
https://www.otoscape.com/eponyms/prussak-s-space.html
What does waxy crust in the attic likely represent?
Cholesteatoma. Crust is from the dry drainage.
What is the most common location of primary acquired cholesteatoma? What are 4 different routes of spread?
Prussak’s space, caused by invagination of the pars flaccida, invagination through the posterior pouch of von Troelsch –> prussak’s space
4 routes of spread:
1. 60-67% - Through open floor (normal aeration) of the posterior pouch of von Troeltsch (between TM laterally and posterior malleolar fold medially) –> goes to the posterior mesotympanum (sinus tympani and facial recess)
2. 30% - Posterior pouch of von Treltsch (closed floor) –> posterior tympano-malleolar fold directs expansion towards the inferior incudal space –> cholesteatoma may extend medial to the long process of the incus and then through the tympanic isthmus into the medial attic
3. Anteriorly into the anterior pouch of von Troeltsch (between pars tensa and anterior malleolar fold) through a weak or dehiscent anterior malleolar fold –> goes to protympanum and supratubal recess
4. 6% - through lateral superior malleolar fold (thin or dehiscence) and malleus neck –> into superior incudal space (superior epitympanum) –> into aditus and mastoid antrum (only direct epitympanum pattern of spread)
https://www.otoscape.com/eponyms/pouches-of-von-troeltsch.html
https://journals.uic.edu/ojs/index.php/jbc/article/download/6628/version/3393/5597/48853/jbc-40-e7-g002.jpg
https://journals.uic.edu/ojs/index.php/jbc/article/view/6628/5597
See vancouver notes pictures page 287
Most common locations for residual cholesteatoma
Top most common:
Sinus tympani
Facial recess
Anterior epitympanum (protympanum)
Others:
Hypotympanum
Aditus Ad Antrum
Sinus tympani
Facial recess
Oval window
Anterior epitympanum
Supratubal recess
What is the definition of cholesteatoma?
Keratinizing squamous epithelium within the pneumatized spaces of the temporal bone
What are three mechanisms that cholesteatoma cause bony erosion?
Mechanical: pressure necrosis
Cellular: osteoclastic activity
Biochemical: inflammatory & enzymatic mediators (e.g. TNF-alpha, Interleukins, macrophages, etc.), bacterial endotoxins, granulation tissue products, collagenase, hydrolase
*Cholesteatoma easily infected - resorbs bone at a higher rate
What are the potential complications of cholesteatoma? List 14, and their order of frequency
Extratemporal:
- Bezold’s abscess (infection erodes from mastoid through to the attachment of the SCM) OR Subperiosteal abscess due to erosion of mastoid cortex
- Chronic otorrhea
- Conductive hearing loss (ossicular chain disruption) - 30%
- Recurrent cholesteatoma
Intratemporal:
- Labyrinthine Fistula - 10%, mainly horizontal SCC, rarely cochlea
- Facial nerve paralysis (acute = infection, chronic = slow expansion)
- Ossicular erosion
- Labyrinthitis - serous or suppurative
Intracranial:
- CSF leak
- Dural/subdural or intraparenchymal abscess
- Meningitis (2o tegmen erosion)
- Extradural or perisinus abscess
- Sigmoid sinus thrombosis/phlebitis
Indications for balloon ET dilation 3
- Persistent and troublesome ETD symptoms in adults
- Recurring otitis media in adults
- Difficulty to equality pressure in the ears during rapid changes in atmospheric pressure in adults
What is the definition of congenital cholesteatoma?
Embryonic rest of epithelial tissue in the ear without tympanic membrane perforation
What are the diagnostic criteria for congenital cholesteatoma? Describe two systems.
Levenson Criteria (1989 modification of Derlacki and Clemis):
1. Presence of white mass behind an intact TM (typically seen anterior to the malleus)
2. Normal pars flaccida and pars tensa
3. No prior history of perforation or otorrhea
4. No prior history of otologic procedures
*Previous otitis media without otorrhea are not grounds for excluding congenital origin
Derlacki and Clemis:
1. An embryonic rest of epithelial tissue in the ear
2. No tympanic membrane perforation
3. No history of ear infection
What is the mean age of presentation of congenital cholesteatoma? What is the male to female preponderance?
4.5 years old
M:F preponderance of 3>1
List 5 CT features that are suggestive of cholesteatoma
- Soft tissue mass in the middle ear, especially at Prussak’s space
- Ossicular erosion
- Blunting of the scutum
- Dehiscent facial nerve
- Horizontal SCC fistula
What is the theory of congenital cholesteatoma formation?
Teed’s embryological epithelial rests theory
- Teed noted an ectodermal epithelial thickening that developed in proximity to the geniculate ganglion, at the junction of ET orifice and middle ear near anterior tympanic annulus, which then involuted to become the mature middle ear lining (derived from 1st branchial groove ectoderm)
- Normally involutes in 33rd week GA
- Failure of involution leads to congenital cholesteatoma
- Michael’s body: squamous cell tuft present from 10-33 weeks
Other theories:
1. Ectodermal implants trapped in fusion plates
2. Ectodermal migration
3. Adhesive otitis that resolves early but leaves some squamous epithelium behind
4. Squamous metaplasia of the middle ear mucosa, amniotic fluid debris
Describe the histology of a cholesteatoma
- Cystic content - desquamated keratin centre (peeled off/scales)
- Matrix - fully differentiated squamous epithelium
- Perimatrix/fibrous stoma - inflamed connective tissue, layer of granulation tissue in contact with bone
Page 287 photo Vancouver notes
Describe the histologic differences between cholesterol granuloma vs. cholesteatoma
Cholesterol granulomas have “empty” spaces contained cholesterol crystals prior to tissue processing
Cholesteatoma - higher power magnification of keratinizing stratified squamous epithelium
What are 3 cell types and their chemical mediators in cholesteatoma
Osteocytes (cell in mature bone): BMP-2, TGF-beta
Osteoclasts: Acid phosphatase, acid proteases, collagenase
Macrophages: IL-1/6/11; TNF-a, TGF-a, Prostaglandins, leukotrienes, PTHrP (related protein), CSF-1 (colony stimulating factor)
What are the boundaries of the epitympanum
Anterior: middle cranial fossa
Posterior: Cog/cochleariform process
Lateral: Tympanic bone/chorda
Floor: Horizontal facial nerve
What infectious etiology is the most commonly seen in Chronic otitis media? What about those seen in the presence of cholesteatoma?
COM:
- Pseudomonas aeruginosa
- Staphylococcus aureus
- Corynebacterium diphtheria
- Proteus species
- Klebsiella pneumoniae
In cholesteatoma: (anaerobes more common):
- B. Fragilis
- Peptococcus
- Peptostreptococcus
- Proprionibacterium
- Invasive fungal infection: aspergillus niger, fumigatis, or flavus
What is the name of the staging system for congenital cholesteatoma? Describe it and define its significance
Potsic Staging
- Stage I: Confined to one quadrant of the middle ear
- Stage II: 2 or more quadrants of the middle ear are involved
- Stage III: Ossicular involvement
- Stage IV: Mastoid involvement
Significance: strong association between stage and residual disease. 13% risk of residual disease at stage I, 67% at stage IV.
https://www.otoscape.com/eponyms/potsic-staging-system-for-congenital-cholesteatoma.html
What are 4 types of incisions that can be done for tympanomastoidectomy?
- Permeatal
- Endaural
- Postauricular
- Extended
https://otosurgeryatlas.stanford.edu/otologic-surgery-atlas/fundamentals-of-ear-surgery/endaural-incision/#iLightbox[gallery_image_1]/1
Describe McEwan’s triangle. What are the borders and what does it show?
Triangle created by:
1. Temporal line superior
2. Spine of henle (suprametal crest)
3. Tangential line that follows along the posterior EAC canal
Overlies the mastoid antrum by 1.2-1.5cm
See vancouver notes page 288
What are the main goals of mastoid surgery, in order of importance?
- Create a SAFE ear - treat and prevent disease complications
- Remove disease
- Create a dry ear (dry ear prevents otorrhea, reduces inflammation and also negative pressure that may be causing cholesteatoma formation; especially in context of CWD)
- Preserve hearing
- Preserve anatomy (debatable whether this is 4 or 5)
Define the following procedures: Simple mastoidectomy, complete, canal wall down, modified radial, Bondy modified radial, and radical mastoidectomy. Classify them further into canal wall up vs. canal wall down.
Discuss in each what structures are removed?
Canal Wall Up:
- Simple Mastoidectomy: Cortical mastoidectomy, identification of the aditus ad antrum/antrum (goal for acute mastoiditis)
- Complete mastoidectomy (canal wall up): Removal of all mastoid air cells along the tegmen, sigmoid sinus, pre-sigmoid dural plate, facial nerve, semicircular canals, and posterior wall of EAC (but wall itself is preserved)
Canal Wall Down: Complete mastoidectomy and removal of the posterior EAC, which can be further divided into:
- Radical Mastoidectomy: Complete mastoidectomy + removal of annulus, TM, ossicles (with stapes left intact), middle ear mucosa, and eustachian tube obliterated (essentially exteriorization of the entire middle ear)
- Modified radical mastoidectomy: CWD mastoidectomy but leave the pars tensa TM preserved (don’t enter middle ear), used only for epitympanic disease to exteriorize the epitympanum
- Bondy Modified Radical Mastoidectomy: Like a Modified radical (Cumming’s definition), plus removal of the scutum and a portion of the psoterior canal wall with preservation of ossicles and middle ear space. Do not remove the entire posterior canal wall (not a full CWD). option for large attic cholesteatomas
What are the two types of mastoidectomy incisions?
- Lempert (endaural)
- Postauricular
Tympanomastoid also:
1. Permeatal
2. Extended
https://otosurgeryatlas.stanford.edu/otologic-surgery-atlas/fundamentals-of-ear-surgery/endaural-incision/
List 9 indications for canal wall down mastoidectomy
- Only hearing ear
- Horizontal SCC fistula (or other complication)
- Multiple recurrent cholesteatoma (previous unsuccessful surgery)
- Unreliable patient follow up
- Extensive erosion/disease of posterior canal wall (auto-mastoidectomy)
- High risk anesthesia
- Sclerotic mastoid
- Poor eustachian tube dysfunction
- Anterior sigmoid / tight sinodural angle
Radiological indications:
1. Erosion of posterior canal wall
2. Sclerotic mastoid
3. Anterior sigmoid/tight sinodural angle
4. Horizontal SCC fistula or other complication
What’s another name for Canal wall up mastoidectomy?
Combined approach tympanoplasty:
CWU mastoidectomy + transcanal tympanoplasty
List five advantages of canal wall down mastoidectomy
- Less common residual disease (10%), single OR often complete
- Able to see recurrent disease more easily
- Less common recurrent disease overall (< 10%)
- Complete exteriorization of the facial recess
- Cost effective
List six disadvantages of canal wall down mastoidectomy
- Shallow middle ear and harder to reconstruct
- EAC and TM destroyed - TM needs to be reconstructed
- Altered anatomy
- More risk of hearing loss (with difficulty achieving hearing improvement)
- Necessity to clean mastoid bowl for rest of patient’s life
- More frequent episodes of post-operative discharge
List five advantages of canal wall up mastoidectomy
- Physiologic TM position (TM preserved)
- Preservation of anatomy (EAC preserved)
- Less risk of hearing loss, better acoustic properties
- Middle ear is deep and easier to reconstruct
- No mastoid bowl exposure
List six disadvantages of canal wall up mastoidectomy
- More common residual disease (30% - less common with endoscope) - and may be occult
- More common recurrence (up to 15%) - and may be occult
- Incomplete exteriorization of facial recess
- Delayed canal breakdown
- Second stage often required
What are the rates of residual and recurrent disease after ICW (intact canal wall) vs. CWD mastoidectomy?
Canal wall up:
a. Residual = 20-35%
b. Recurrence = 5-20%
30&15
Canal wall down:
a. Residual = 2-17%
b. Recurrence = 0-10%
10&5
Describe 12 ways to find the facial nerve in a mastoidectomy
- Identify the short process of the incus (transverse segment just medial to that - incus marks the beginning of the second genu)
- Fossa indicus (short process is in this)
- Identify the** horizontal semicircular canal** (2nd genu should be anterior and inferior to this)
- Identify the fallopian canal in the middle ear
- Identify the digastric ridge (anterior extent of ridge leads to stylomastoid foramen - slightly superior anterior)
- Drilling out the facial recess
- Stimulate along the expected course of the vertical segment
- Cochleariform process - nerve above the process
- Chorda tympani
- Oval window (nerve superior)
- Cog (nerve inferior)
- Pyramidal eminence (over nerve)
List 7 ways to obliterate the mastoid cavity following CWD mastoidectomy
- Palva flap (anteriorly based post-auricular muscoperiosteal flap)
- Hong-Kong flap (deep temporalis fascia flap that is separated from the underlying temporalis muscle and swung into the cavity. Performed through endaural incision
- Temporalis muscle flap
- Free temporalis fascia
- Pericranial flap (inferiorly based)
- Bone chips/cartilage/calcium hydroxyapetite
- Fat (rarely used)
What are the boundaries of the facial recess
- Mastoid segment of the facial nerve
- Chorda tympani
- Incus buttress
What are the boundaries of the sinus tympani
Superior: Ponticulus, Lateral SCC
Inferior: Subiculum, Jugular wall
Medial: Labyrinth, medial wall of mesotympanum
Lateral: Pyramidal eminence, facial nerve
Posterior: Posterior SCC
https://otosurgeryatlas.stanford.edu/otologic-surgery-atlas/cholesteatoma/sinus-tympani-facial-recess-in-cholesteatoma/#iLightbox[gallery_image_1]/0
Vancouver notes Page 290
What are the steps to deal with cholesteatoma over a dehiscent facial nerve, around the footplate, or over a dehiscent lateral canal?
- Be ready for it (pre-op CT review)
- Leave it for last
- Reduce suction
- High power sharp dissection
- Have graft ready
- IV steroids/intratympanic steroids
What are five things that can be done intraoperatively during modified radical mastoidectomy to ensure dry ear?
- Complete saucerization of mastoid bowl (remove all mucosa)
- Lower the facial ridge to remove any dependent spaces (Bone overlying mastoid segment of facial nerve - high facial ridge is defined as having bone overlying the facial nerve that is ≥2mm in thickness)
- Take down the mastoid tip
- Cavity obliteration with fat or muscle (palva flap or temporalis muscle)
- Wide meatoplasty removing anterior canal wall buldge
- Consider STSG for re-epithelialization
What are causes for continued draining ear post-mastoidectomy?
Surgical Factors:
- Residual cells/mucosa (mastoid tip)
- Granulation tissue
- Residual or recurrent cholesteatoma
- High facial ridge
- Inadequate meatoplasty
Patient Factors:
- Failure to adhere to water precautions
- Poor hygiene
- Infrequent debridement
- Hearing aid use
- Infection
- Perforation with Chronic suppurative otitis media
List 11 complications of mastoidectomy
General anesthesia
Bleeding
Infection
Hearing loss (CHL or SNHL)
Residual or recurrent disease
Facial nerve injury
Chorda injury (dysgeusia)
Otorrhea
Injury to tegmen, sigmoid sinus, posterior canal wall
CSF leak
Injury to inner ear/labyrinth (esp. horizontal SCC) - dizziness
List some powders/topical treatments that can be used in the mastoid cavity to dry the cavity and prevent infection within cholesteatoma/debris
Ciprofloxacin
Clotrimazole
Boric acid
Hydrocortisone or dexamethasone
1/2 white vinegar + water (doesn’t burn unless acute inflammation)
What is the Fisch procedure?
List its 5 indications
How does the procedure work
3 goals
4 complications
Fisch blind sac ear closure
Indications: “CCCGI”
- CSF leak
- Improving CPA access
- Glomus or other middle ear tumors
- Chronic ear disease
- Cholesteatoma
Procedure:
- To create a sealed ear cavity (e.g. in CSF leak)
- Cavity is filled with abdominal fat graft or muscle
- Eustachian tube is obliterated using pieces of periosteum and/or cartilage
Goal:
- Obtain a safe, dry ear
- Optimize post-operative care
- Increase long-term satisfaction of the patient
Complications:
- Hematoma
- Closure breakdown/dehiscence
- Epidermoid cyst
- Pre- or post-auricular abscess due to retained skin (rate highest in chronic mucosal disease)
https://skullbasesurgeryatlas.stanford.edu/illustrations-of-skull-base-surgery-and-neurotology/ear-canal-closure/#
A patient has cholesteatoma with erosion of the lateral SCC. What management would you recommend?
List 3 surgical approaches
- Medical management of granulation/infection
- Surgical options:
- a. Remove all matrix and cover the defect with soft tissue or bone wax
- b. Perform CWD and allow matrix to remain in place as part of the mastoid cavity lining
- c. Perform intact CW mastoid and leave the matrix in place. To be removed at a second stage when the ear is sterile - Ongoing surveillance (second-look vs. DW-MRI)
What is the best imaging to assess for recurrent/residual cholesteatoma?
Diffusion weighted MRI
What is the best imaging to diagnose labyrinthitis ossificans? What would the stages look like on MRI?
MRI
- Early labyrinthitis ossificans may not yet show ossification, so early treatment is best decided on based on MRI findings
- MRI is better at picking up early stages of fibrosis prior to ossification (absence of fluid signal in the cochlea/labyrinth on T2WI)
List as many complications of acute otitis media. What are the most common?
Can you name 20?
Extracranial
- Subperiosteal abscess
- Bezold’s (SCM) abscess
- Temporal abscess
- Otorrhea
- Chronic suppurative otitis media
- Adhesive otitis
- Tympanosclerosis
- TM Perforation
- Fixation or discontinuity of ossicular chain
Intratemporal:
- Mastoiditis (#1 extracranial complication of AOM)
- Mastoidits with or without abscess: postauricular, bezold’s zygomatic, parapharyngeal, retropharyngeal)
- Temporal bone osteomyelitis
- Sigmoid sinus thrombosis
- Lateral sinus thrombosis
- Facial nerve paralysis (suggests deschient facial nerve)
- Petrous apicitis (Gradenigo’s syndrome)
- Labyrinthine fistula
- Labyrinthitis - serous or suppurative
- Cholesteatoma
- CHL or SNHL
Intracranial:
- Meningitis (#1 intracranial complication of AOM)
- Encephalitis
- Epidural abscess
- Subdural abscess
- Cerebral abscess
- Otitic hydrocephalus
- Blindness with optic neuropathy
Discuss various abscess complications that can develop because of AOM
- Sub-periosteal mastoid abscess
- Zygomatic abscess
- Occipital abscess
- Bezold’s abscess: abscess along the medial aspect of the mastoid tip up to the sheath of SCM
- Citelli’s abscess: Along the posterior belly of digastric
- Luc’s abscess: at the root of the pneumatized zygoma
B-ZOLDS
Bezolds abscess
Zygomatic
Occipital
Luc’s abscess
Digastric (posterior belly - Citelli’s abscess)
Subperiotseal mastoid abscess
List four indications for mastoidectomy in facial nerve palsy secondary to otitis media complication
1.History of chronic otitis media
2.Onset of paralysis >2 weeks after onset of AOM
3.ENoG showing >90% degeneration after 6 days
4.Failure of paralysis to resolve after appropriate medical management
What is the most common organism causing bacterial meningitis?
Streptococcus pneumoniae
What percentage of bacterial meningitis cases will result in hearing loss?
20%
What are the signs and symptoms of mastoiditis? How is it diagnosed? Management?
Symptoms:
- Auricular proptosis/erythema
- Post-auricular tenderness
- Purulent middle ear effusion
Diagnosis is CLINICAL
Management:
1. If uncomplicated (no altered LOC, cranial nerve deficits, etc.) no imaging required
2. Admission
3. IV antibiotics - ceftriaxone with CNS dosing if concerned about potential for intracranial complications)
4. Trend CBC
5. Consider imaging ± mastoidectomy in 48-72 hours if not clinically improving
6. Consider tympanostomy tube at presentation or if not clinically improving
7. Topical antibiotics after tympanostomy tube
8. Mastoidectomy if coalescent mastoiditis
Describe the pathophysiology of coalescent mastoiditis
AKA Mastoid osteomyelitis
Pathophysiology:
- Hyperemia and edema of the mucoperiosteal lining blocks the aditus ad antrum, disrupting aeration
- Mucous membrane thickening and impaired ciliary function prevents ET drainage
- Serous exudates becomes purulent as inflammatory cells accumulate
- Continued inflammation and accumulation results in venous stasis, localized acidosis, and decalcification of bony septae
- Osteoclastic activity in the inflamed periosteum softens and decalcifies the bony partitions, causing the cells to coalesce into a larger cavity
What population is Bezold’s abscess more common in and why?
More common in older children/adults compared to younger children
Coalescent mastoiditis most commonly extends laterally through the mastoid cortex (post-auricular).. It can also erode the mastoid tip into the upper neck. More common in olden children because mastoid tip is more pneumatized and the bone is thinner
Regarding lateral sinus thrombosis as a complication of temporal bone infections, discuss:
1. What is it?
2. Pathophysiology?
3. Signs and symptoms? What is Greisinger’s sign?
4. Diagnostic features and imaging findings? Name 3 tests you can do
5. Treatment? 4
LATERAL SINUS THROMBOSIS:
- Occlusion of lateral sinus with an infected thrombus
PATHOPHYSIOLOGY:
- Propagation of infection to peri-sigmoid sinus area via direct extension or bone erosion
- Attraction of fibrin and platelets to the area leads to thrombus formation
- Thrombus can spread anterograde (IJV, petrosal sinus, cavernous sinus), or retrograde (transverse/superior saggital sinus)
- Thrombus can also result in shower emboli and septicemia
- Infection can result in meningitis and intracranial complications
- Can also result in OTIC HYDROCEPHALUS (High ICP secondary to obstructed venous outflow)
SIGNS AND SYMPTOMS: Overall similar to AOM/mastoiditis, plus:
1. Picket Fence fevers (historically described as a term for repeatedly spiking fevers, like a picket fence)
2. Greisinger’s sign: Pain and tenderness over the mastoid tip due to thrombosis of the mastoid emissary veins
3. Papilledema if there is otic hydrocephalus
DIAGNOSTIC FEATURES:
1. Delta Sign: Triangular enhancement of the sigmoid sinus wall
2. Absent flow on MR venogram
3. Toby-Ayer (Queckenstadt) test: No effect on CSF pressure with compression of ipsilateral IJV in presence of ipsilateral sigmoid sinus thrombosis. Not commonly done, as this requires LP for CSF pressure monitoring
TREATMENT:
1. Mastoidectomy for source control
2. Decompession of the sigmoid sinus:
- ± open clot evacuation
- ± IJV ligation if propagated to neck
- ± Neurosurgery involvement if intracranial involvement
- IV antimicrobials
- Anticoagulation is controversial, but should be considered if thrombus progresses beyond sigmoid sinus
- Thrombolytics not recommended due to risk of septic thrombus dislodgement
What is the petrous apex? What are its borders?
Pyramid-shaped anteromedial part of the petrous portion of the temporal bone. Articulates with the posterior aspect of the greater wing of the sphenoid and occipital bones
Lateral: inner ear
Medial: petrooccipital fissure
Anterior: petrosphenoidal fissure and petrous part of the ICA in the carotid canal
Posterior: posterior cranial fossa
Superior: Middle cranial fossa, meckel’s cave, and petrous ICA
Inferior: Jugular bulb, inferior petrosal sinus
Division between anterior and posterior petrous apex - Internal Auditory Canal (IAC)
https://d45jl3w9libvn.cloudfront.net/jaypee/static/books/9789351524632/Chapters/images/149-1.jpg
Bony landmarks
Discuss petrous apicitis as a complication of temporal bone infection.
What are the possible causes? 2
Pathophysiology?
Symptoms?
Management?
Petrous apicitis = Petrous apex syndrome = Gradenigo syndrome = osteomyelitis of the petrous apex
Causes:
- Infectious: extradural abscess involving the petrous bone
- Tumor at the petrous apex (more common) - this is not traditionally called “petrous apicitis/gradnigo syndrome” - the syndromic term traditionally only refers to infectious causes
Pathophysiology:
- Abscess results from petrositis with inflammation of Dorello’s canal between petrous tip and petroclinoid ligament
Gradenigo’s Triad: Symptoms 2o petrous apicitis
1. Otorrhea
2. Retroorbital pain (due to irritation of trigeminal ganglion in meckel’s cave (aperture in medial portion of middle cranial fossa that is a conduit for trigeminal nerve))
3. Abducen’s CNVI palsy (as it passes through Dorello’s canal)
Other symptoms:
- Fever
- Headache
- CNVII, VIII, IX involvement
- Hearing loss, tinnitus, vertigo
Management:
- Topical and prolonged systemic antibiotics
- Failure to respond to antibiotics = surgery
- Translabyrinthine approach is useful in non-hearing ears
- In hearing individuals, anatomy permitting, the transcanal infracochlear approach with stenting was the preferred approach for drainage of petrous apex
https://operativeneurosurgery.com/lib/exe/fetch.php?w=400&tok=7768f0&media=inferior_petrosal_sinus.jpg
https://encrypted-tbn0.gstatic.com/images?q=tbn:ANd9GcRswDADguK0qnRniTrb-YGtUZM4ItxEkmOl-exGAeyV5wCMH61hk2KhAGVMor9Op5eyI94&usqp=CAU
https://media.springernature.com/lw685/springer-static/image/art%3A10.1007%2Fs13244-018-0604-7/MediaObjects/13244_2018_604_Fig1_HTML.png
What is Gradenigo’s triad?
Gradenigo’s Triad: Symptoms 2o petrous apicitis
1. Otorrhea
2. Retroorbital pain (due to irritation of trigeminal ganglion in meckel’s cave (aperture in medial portion of middle cranial fossa that is a conduit for trigeminal nerve))
3. Abducen’s CNVI palsy (as it passes through Dorello’s canal)
What is the name of the canal that the abducen’s nerve passes through? What else runs in this canal?
Dorello’s canal
Contains the inferior petrosal sinus and abducens nerve (CNVI)
Both structures then merge into the cavernous sinus
What clinical features are expected from a petrous apex lesion?
- Meckel’s cave involvement –> trigeminal irritation –> retroorbital pain, numbness
- Dorello’s canal involvement –> VI palsy
- Labyrinth involvement –> Hearing loss, tinnitus, vertigo
Define Otitic Hydrocephalus. What is the treatment?
Increase ICP secondary to acute or chronic middle ear disease, with or without lateral/sigmoid sinus thrombosis, WITHOUT evidence of meningitis or abscess
Normal ICP = 5-15mmHg
Treatment:
- Immediate neurosurgical consultation
- CT Head (brain)
- Medical: Acetazolamide (diuretic) 500mg BID, Steroids, Possible lumbar drain, Furosemide & Mannitol 0.5g/kg
- If still uncontrolled –> VP shunt
- Surgical: Mastoidectomy, expose diseased dura, debride granulations, ± remove clot
What are the surgical approaches to the petrous apex? Also categorize further into anterior and posterior petrous apex approaches
Petrous apex is divided into anterior and posterior by the plane running through IAC/cochlea.
Posterior petrous apex pneumatized in 30%, anterior pneumtized in 10%.
Non-hearing/balance preserving approaches:
- Translabyrinthine
- Subtotal petrosectomy
Hearing and balance preservation to posterior petrous apex
- Subarcuate
- Retrolabyrinthine
- **Infralabyrinthine (retrofacial) **
- Sinodural
Hearing and balance preservation to anterior petrous apex
- Middle cranial fossa
- Transcanal Infracochlear (hypotympanic)
- Peritubal (glenoid fossa)
- Endoscopic trans-sphenoidal (anterior skull base approach)
https://encrypted-tbn0.gstatic.com/images?q=tbn:ANd9GcQvJSlchbbOh5PHvXOq7-rwG44uhjiiq7VwTiNRkaS0TaMV6Xi-s4ivl8EQKoewqKHECpQ&usqp=CAU
Kevan’s notes page 40 images
Vancouver notes page 292
What are the boundaries of each petrous apex approach, as well as advantages, and disadvantages.
- Subarcuate
- Boundaries: Through the arch of the semicricular canal (Following subarcuate artery)
- Structures at risk: superior semicircular canal
- Advantage: hearing and balance preservation
- Disadvantage: ?difficult access - Retrolabyrinthine
- Boundaries: Superior to the posterior and horizontal SCC, posterior to the superior SCC (medial to where the sinodural angle is)
- Structures at risk: Tegmen, Sigmoid sinus, labyrinth
- Advantage: Hearing and balance preservation - Infralabyrinthine (retrofacial)
- Boundaries: Inferior to the posterior semicircular canal, posterior to the facial nerve, superior to the jugular bulb
- Structures at risk: Facial nerve (common site of injury), jugular bulb, labyrinth
- Advantages: Direct approach that is more familiar to most ENT
- Disadvantages: Difficult with high jugular bulb; drainage into mastoid cavity is far from eustachian tube (therefore difficult to clear infection post-op) - Subcochlear/infracochlear or also named hypotympanic/Transcanal
- Boundaries: Hypotympanic air cell tract between the internal carotid artery, jugular bulb, and cochlea. (Create a superior based TM flap, open the skin, and go through the annulus bone a bit to access the hypotympanum and go through the hypotympanum that way)
- Structures at risk: carotid artery, jugular bulb, cochlea
- Advantages: Direct drainage near the opening of eustachian tube (From Petrous to middle ear via hypotympanum)
- Disadvantages: Anatomy may be challenging to surgeons not familiar with hypotympanum and major vessels of temporal bone
Peritubal (glenoid fossa): Between internal carotid artery, cochlea, and tegmen (where eustachian tube would be)
Middle cranial fossa:
- Structures at risk: Temporal lobe, cochlea, labyrinth, IAC, greater superficial petrosal nerve (GSPN)
- Advantage: Drains cut directly into bony eustachian tube
- Disadvantages: Middle fossa craniotomy poorly tolerated in elderly, drainage is not dependnet, temporal lobe may obstruct drainage pathway
Transphernoidal:
- Structures at risk: Carotid artery, optic nerve, cavernous sinus, maxillary nerve, pituitary gland
- Advantages: Direct approach to large cysts that are in contact with posterior wall of sphenoid sinus; Opening into cyst may be directly observed in clinic with endoscope
- Disadvantages: Can be used only for “giant” cysts in contact with sphenoid sinus
Translabyrinthine or Subtotal petrosectomy
- Structures at risk: Labyrinth, jugular bulb, IAC
- Advantages: Cyst and wall can be removed if desired
- Disadvantages: Profound postoperative SNHL
Vancouver notes page 293 image
Describe the Austin Classification of Middle Ear apparatus Conductive Hearing Loss
In Austin’s 1978 review, he identified 5 categories of anatomic defects in the middle ear sound conducting system and described the prototypic hearing loss associated with them.
- TM Perforation Only
- Loss of area ratio and catenary lever
- HL proportional to size of perforation - TM Perforation with ossicular interruption
- 40 dB loss - Total loss of TM and ossicular chain
- 50 dB loss
- Loss of ossicular, hydraulic, and catenary levers
- Sound transmission is by acoustic coupling - Ossicular interruption with intact TM
- 60dB loss
- Worse than with loss of TM because the intact TM reflects sound away from the middle ear - Ossicular interruption with intact TM and closure of the oval window (distinct congenital malformation)
- 60dB loss
- SImilar to #4, closure of the oval window reflects sound away from the inner ear
Discuss the Austin/Kartush Classification of Ossicular chain status
Not in Vancouvers
M = Malleus handle present (+) or absent (-)
S = Stapes Superstructure present (+) or absent (-)
Austin classification:
A –> M+S+
B –> M+S-
C –> M-S+
D –> M-S-
Kartush added:
0 –> Completely intact ossicular chain (including incus) M+I+S+
E –> Malleus head fixation / ossicular head fixation
F –> Stapes fixation
C and D types are associated with a worse hearing outcome post ossiculoplasty
https://image.slidesharecdn.com/ossiculoplasty-160608173426/85/ossiculoplasty-10-320.jpg?cb=1666079861
What is the most important criteria for success of a stapedectomy or ossicular chain reconstruction?
Intact stapes superstructure
OR
ventilated middle ear space
Debated - discuss OOPS criteria vs. Austin/Kartush Classification of Ossicular Status
What is the Middle Ear Risk Index and what is the score?
Not in Vancouvers
MERI quantifies pre-operative poor prognostic factors for ossicular chain reconstruction.
Risk factors:
- Otorrhea (Belluci)
I Dry 0
II Occasionally wet 1
III Persistently wet 2
IV Wet, cleft palate 3 - Perforation
None 0
Present 1 - Cholesteatoma
None 0
Present 1 - Ossicular status
0 M+I+S+ 0
A M+S+ 1
B M+S- 2
C M-S+ 3
D M-S- 4
E Ossicular head fixation 2
F Stapes Fixation 3 - Middle ear: granulation or effusion
No 0
yes 1 - Previous surgery
None 0
Staged 1
Revision 2
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3244584/
What is the OOPS Index?
Not in Vancouver notes
Ossiculoplasty outcome parameter staging index
Developed by Dornhoffer who found that MERI was less reliable with very low and very high indices
Findings noted that presence/absence of staples superstructure did not play a significant role in hearing outcomes, but the most important features were presence of malleus head and quality of middle ear space (e.g. fibrosis)
A: Middle ear risk factors
1. Drainage (N-0, Present >50% -1)
2. Mucosa (Normal-0, Fibrotic-2)
3. Ossicles (Normal -, Malleus+ 1, Malleus- 2)
B: Surgical risk factors
1. Type of surgery (No mastoid 0, Canal wall up 1, Canal wall down 2)
2. Revision Surgery (No 0, Yes 2)
Discuss myringitis: Definition, Causative organisms, diagnosis, treatment.
Define bullous myringitis and special treatment circumstances.
Primary Myringitis: Inflammation or infection of the TM alone
Secondary Myringitis: Inflammation or infection of the TM and adjacent middle ear or EAC
Bullous myringitis: Formation of serous/hemorrhagic bullae on the epithelial surface of the TM
Causative pathogens
- Strep pneumoniae (most common)
- Mycoplasma pneumonia
- Influenza
Diagnosis: Clinical, consider culture
Treatment: Analgesia, ciprodex, oral Clarithromycin to cover possible mycoplasma
Bullous myringitis - may puncture the bullae to relieve severe pain
See image Vancouver page 278
