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AUDE 5410 > Disorders affecting the middle ear > Flashcards

Disorders affecting the middle ear Flashcards

1
Q

What is otitis media ?

A

Otitis media is an infectious inflammation of the ME that results in the accumulation of fluid (effusion) in the middle ear cavity - OME

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2
Q

what is a differential diagnosis for otitis media?

A

acute myringitis
it looks the same with a red tm but it doesnt have any effusion

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3
Q

what do you have to watch out with kids in terms of Otitis media?

A

Excessive blowing of the nose/crying especially in younger children, can also cause redness of the TM without underlying effusion/infection and maybe mistaken for OM so watch out and keep that in mind

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4
Q

who is more likely to get otitis media with effusion ?

A

infants and kids

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5
Q

what is the prevalence of otitis media with effusion in kids?

A

Age is inversely related to prevalence
-At least 1 episode by 1 year of age = 50%
-At least one episode before starting school = 60 to 70%
-Recurrent OME during the first three years of life = 35%
-Of the children who experience acute OME, 5 to 10% develop chronic OME
-Prevalence at age 6 = 5%
-Prevalence between ages 7 to 10 = 4.5%
-Prevalence between ages 11 to 14 = 3%
-Prevalence between ages 15 to 19 = 2%
-OME also may occur in adults

the younger the child, the more likely they are to get otitis media

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6
Q

what race is more likely to get otitis media ?

A

Eskimos, Native Americans, Hispanics, and Australian aborigines (indigenous people of Australia), and white people
-probably because of the anatomy of the base of the skull and the Eustachian tube

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7
Q

what race isn’t really likely to get otitis media ?

A

asians and blacks

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8
Q

what gender is more likely to get otitis media ?

A

men

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9
Q

what months is otitis media appear more ?

A

october and april and declines in summer

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10
Q

otitis media appears more in kids who have a history of what other conditions?

A

upper respiratory illness such as colds, asthma, and allergies

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11
Q

at what age does a child outgrow them being a risk to otitis media?

A

6-8 years because the kids estachian tube looks like an adults

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12
Q

why are kids more susceptible to getting otitis media ?

A

Most likely route of bacterial entry in the ME is retrograde reflux of nasopharyngeal secretions through the eustachian tube

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13
Q

what are the 3 factors that facilitate bacterial reflux in the middle ear?

A

1) (any bacteria in the nasopharynx)
2) the euschaian tube isn’t going their job ofprotecting
3)Negative pressure in the ME in relation to the nasopharynx

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14
Q

what are the types of otitis media ?

A

bacterial and viral,

cleft palate,

Craniofacial disorders,

Ciliary dysfunction,

Environmental allergies

Immune dysfunction

Eustachian tube abnormalities

Obstruction

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15
Q

what pathologies cause BACTERIAL otitis media

A

Common pathogens that cause OM also are most commonly found in upper respiratory tract infections so :
1)Streptococcus pneumoniae
2)Hemophilus influenzae

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16
Q

what pathologies cause VIRAL otitis media

A

Respiratory syncytial virus – most common
Rhinovirus
Parainfluenza virus
Influenza virus

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17
Q

what 3 criteria needs to be met before diagnosing ACUTE otitis media ?

A

Acute onset
ME inflammation
ME effusion (fluid build-up in ME – almost always follows AOM)

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18
Q

what are the characteristics of ACUTE otitis media ?

A

-Short-term (< 3 weeks), a self-limiting condition characterized by otalgia and redness of TM with effusion
-Severe AOM
-Moderate to severe otalgia and temperature > 1020F (39°C)
-Non-severe AOM
-Mild otalgia and temperature < 1020F (39°C)

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19
Q

is acute otitis media over diagnosed

A

yes

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20
Q

characteristics sub-acute otitis media are

A

condition persisting for 3 weeks to 3 months

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21
Q

characteristics of recurrent otitis media are

A

-Multiple self-limiting episodes with symptom-free periods between flare-ups
-3 or more episodes w/in a 6 months period
-or 4 or more episodes w.in a year

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22
Q

characteristics of chronic otitis media are

A

-Condition persisting for > 3 months (> 30 days-Text)
-Generally with effusion but without other signs of inflammation i.e., fever or otalgia

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23
Q

middle ear effusion always follows ?

A

ME effusion almost always follows AOM and can take 2 to 3 weeks to clear post treatment/recovery
-so you call them back 3-4 weeks to come see you again to see if the m.e is clear

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24
Q

how long does middle ear effusion last for ?

A

Effusion can persist for an average of 40 days

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25
Q

what age group is susceptible for middle ear effusion ?

A

kids, white kids get this the most out of all races

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26
Q

serious effusion can occur…

A

Serious effusion can occur without OM such as in cases of barotrauma, following an airplane trip, or seasonal allergies

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27
Q

what can fluids in the ear look like?

A

-Serous OM (SOM - clear)
-Mucoid OM (MOM - thick and colored)
-Purulent OM (POM - odorous and thick)
-“Glue ear” is a term used to describe chronic mucoiud OM

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28
Q

what are characterisitics to remember when looking at glue ear

A

-Self-limiting in most cases -
If chronic low grade ME infection persists due to chronic ET dysfunction it will lead to the ME cavity filling with gelatinous inflammatory exudate/cellular debris - the “glue” of glue ear
-This process may lead to retraction of the TM and ultimately formation of retraction pockets and bone erosion

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29
Q

OM is a dynamic process in which each classification is not a distinct entity because you can progress to one to another. SOM may progress to MOM and so on
(remember this)

A
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30
Q

what are risk factors for otitis media effusion?

A

-Age – peak incidence between 6 to 11 months of age
-ET dysfunction
-Craniofacial anomalies
-increased risk with cleft lip/palate and down syndrome
-Decreased risk for breast-fed infants; duration a factor
-Day care attendance
-Susceptibility to upper respiratory tract infections (URTI)/allergies
-Smoking in the home including second-hand smoke
-Family history of OME
-Male
-Low birth weight (< 1500 grams or 3.3 lbs)
-Socio-economic status (SES): Inverse relationship between SES and OME probably because of lack of access to health care and over crowding

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31
Q

what are symptoms of otitis media effusion

A

-Otalgia
-Fever
-otalgia and fever may be absent in older children
-Erythema (redness) of the -TM
-Effusion in the ME
-Irritability/fussiness
-May not want to eat
-Inconsistent responses to sound
-Delayed speech and language development
-Reduced attention span especially in the classroom

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32
Q

what are might you see during otoscopy with otitis media ?

A

-Discolored/red TM
-Opacification of normally lustrous TM
-Partial/complete bulging of -TM with obliteration of malleolar handle
-Retracted TM
-Perforation of TM
-Fluid line or bubbles observe in the middle ear

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33
Q

how might typms (immitance) results look like for otitis media ?

A

-Flat (Type B) tympanogram
-Negative pressure >200 daPa (Type C) tympanogram
-Flat high volume (Type B - high volume) tympanogram consistent with TM perforation
-Inability to get a hermetic seal (with perforation) in older equipment

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34
Q

how would acoustic relfexes look like in otitis media ?

A

-For unilateral OM: Typical only the ipsilateral ART will be present on the unaffected side
-For bilateral OM: Ipsilateral and contralateral ARTs will be abnormal for both ears

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35
Q

how might pure tones look like for otitis media ?

A

-Hearing sensitivity may be within normal limits thresholds (< 20 dB HL)
-But there may be an air-bone gap exceeding 10 dB
HL - conductive component
-Fluctuating hearing loss may be present
-A conductive hearing loss that generally does not exceed 60 to 65 dB HL – maximum conductive loss
-Possible rising or reverse slope configuration of the hearing loss***

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36
Q

how might speech audiometry look like in otitis media ?

A

-Generally normal supra-threshold speech tests (e.g., WRS)
-Example: Excellent WRS with a conductive hearing loss
-SRT-PTA in good agreement

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37
Q

for otitis media and it’s sequelae’s auditory look like ?

A

-Permanent/temporary conductive hearing loss
-Damage to middle ear structures
-That can lead to ossicular destruction and conductive hearing loss, common with “glue ear”
-Cholesteatoma
-with chronic/untreated otitis media with effusion or chronic negative middle ear pressure
-Permanent high frequency -SNHL
-Inner ear structures affected by passive diffusion or active transportation of toxins through round window membrane resulting in a permanent SNHL

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38
Q

how can otitis media affect our speech?

A

-Auditory deprivation, which can affect language development
-Deficits in binaural auditory processing
-Difficulty attending to auditory input – learned inattention
-Difficulty with speech sound discrimination (e.g., /ta/ vs. /da/)
-Difficulty with perception of initial and final voiced and voiceless plosives (stops) (e.g., /b/ vs. /p/)
-The /p/ and /b/ sounds are some of the earliest to appear in the speech of children (Edwards, 2003)

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39
Q

in otitis media effusion and it’s sequelae, what are some known log-term implications ?

A

-Attention deficit continuing through adulthood - learned inattention (Hunter et al, 1996)
-Speech and language delays
-Children with English as a Second Language (ESL) who also have OME are at a greater risk for delayed speech and language development
-Academic failure
-Behavioral problems
-Risk factor for (C)APD?

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40
Q

what structural changes can be seen in otitis media with effusion and its sequelae

A

Alteration of the acoustic‑immittance characteristics of the middle ear system evidenced by
-Larger than normal tympanometric width
-Shallower static admittance
-Elevated acoustic reflex thresholds (Silverman & Silman, 1995; Stephenson et al, 1997)

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41
Q

what are some societal consequences of otitis media

A

-By some estimates annual expenditure of ~ $3.5 billion in treatment costs and lost productivity
-OM is the most common reason for visit to pediatricians
-Time-off work and school (lost productivity)
Tympanostomy tube placement is the 2nd most common surgical procedure in children
-Development of multidrug-resistant bacteria, a huge societal concern due to

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42
Q

what are the symptoms of ACUTE otitis media effusion

A

-Can follow upper respiratory tract infection
-Fever
-Otalgia
-Hearing loss (temporary)
-Otorrhea
-May have associated systemic symptoms
-Nausea
-General malaise
-Lack of appetite

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43
Q

what are some symptoms of chronic otitis media with effusion

A

-Can be asymptomatic
-May have a hearing loss
-May report feeling
“plugged”
-May report “popping” of ears

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44
Q

what color would the tm be in otitis media with effusion

A

Opaque, yellowish red, red or pink

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45
Q

what would be the position of the tm in otitis media with effusion

A

Bulging or retracted TM (negative pressure tympanogram)

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46
Q

what would the mobility of the tm in otitis media look like

A

Normal, hypo-mobile, or retracted TM

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47
Q

what are other findings in otitis media with effusion in otoscopy

A

Discharge, perforations, cholesteatoma, or retraction pockets

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48
Q

what would the audiogram look like for otitis media with effusion

A

conductive hearing loss (CHL)
Mixed hearing loss
SNHL

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49
Q

what will the tymp look like for otitis media with effusion

A

-Flat (Type B or Type B -
high volume, if
perforation present)
-Negative pressure (Type C)
-Abnormal gradient/width

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50
Q

what will reflexes look like with otitis media with effusion

A

Abnormal/absent
-ARTs maybe absent with as little as a >15 dB air-bone gap

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51
Q

what is the management of ACUTE otitis media with effusion

A

-Observation (?) adults and older children
-Medication
-Antihistamine and decongestants
-antibiotics:
-Amoxicillin for 7 to 10 days (most common)
-Resolution of condition occurs in 7 to 14 days for 81% of untreated children and 94% of treated children
Effusion can typically persist for > 2-3 weeks following antibiotic therapy and after resolution of the actual infection
-Follow-up tympanograms should be scheduled 2-3 weeks post antibiotics to allow ME fluid to be absorbed
-Myringotomy (incision): Fluid-filled ME cavity and dangerously bulging TM, typically in anteroinferior section of the TM

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52
Q

what is the management of CHRONIC otitis media

A

-Prophylactic/prolonged antibiotics are contraindicated because of an increase in antibiotic resistance
-Manipulation of existing environmental to decrease risk factors
-Watchful waiting for up to 3 months for children without hearing loss or not at-risk for speech and language delays
-Myringotomy followed by pressure equalization (PE) or tympanostomy tubes (TT) typically placed in the anteroinferior and maybe posteroinferior portion of the TM
-Adenoidectomy and/or tonsillectomy, if needed
-decreases the need for repeated pe tube replacement
-Chronic OM more common after the advent of antibiotics because perforation of the TM became less prevalent
-perforations allowed for fluid drainage and prevented chronic otitis media

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53
Q

what are some complications of otitis media ?

A

-Acute mastoiditis
-Ossicular erosion resulting in a conductive hearing loss
-SNHL – generally high frequency
-positively correlated with severity and duration of otitis media
-caused by permeation of toxins thru the round window
-Facial nerve paralysis (rare – 0.16%)
-Caused by involvement of CN VII by infection through bony dehiscence, inflammatory edema causing nerve compression, etc.
-Labyrinthine fistula (an opening)
-Either because of the infection or a cholesteatoma
-Meningitis - Most common intracranial complication of OME
-By direct access through bone eroded by the inflammation or through preformed pathway via round window/cochlear aqueduct
-Brain abscess – leading cause of mortality with OME

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54
Q

what are cholesteatoma ?

A

-they act like tumors
Cholesteatoma are “pseudotumors” that can occupy the external ear canal, ME cavity, or extend through the mastoid bone into the brain cavity

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55
Q

how do cholesteatoma act like tumors?

A

-Cholesteatoma manifest highly aggressive, progressively enlarging, tumor-like characteristics
-They are highly erosive and may cause destruction of bone and other tissue
-Recently, highly invasive fibroblasts were found in cholesteatoma that are not seen in normal skin, which may explain the aggressive behavior of a cholesteatoma

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56
Q

can cholesteatoma be congenital or acquired

A

both !

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57
Q

what are some characteristics in CONGENTIAL cholesteatoma

A

-Almost always present in children
-Median age is ~ 5 years
-men get it more
-The TM can be normal without a history of perforation, otorrhea, or myringotomy
-Most common location is the anterior-superior quadrant
-Etiology is controversial

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58
Q

what are characteristics of acquired

A

-More common than congenital
-Often due to chronic or untreated otitis media with effusion or trauma leading to TM perforation
-Also occurs as a result of TM retraction in the pars flaccida or posterior-superior quadrant
-Previous ear surgery/TM perforation also may be the growth site
-Slow growing condition, initially with no symptoms
-Usually presents first with a hearing loss

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59
Q

what are characteristics of Iatrogenic cholesteatomas

A

-May result because of a blunt knife used during myringotomy
-May lead to implantation of squamous epithelium in ME cavity

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60
Q

how do cholesteatoma grow ?

A

Cholesteatoma grow by forming a keratinized epithelial layer and a fibrous subepithelial layer called matrix
-Keratin (dead skin cells and debris) builds up and gets covered by cells forming a keratoma
-A keratoma will evoke inflammatory reaction leading to formation of a cholesteatoma, mostly in the attic area of the ME cavity

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61
Q

what happens once cholesteatoma grows ?

A

They over the ossicles, tympanic cavity and mastiod, leading it to mastoiditis

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62
Q

can cholesteatoma be a secondary infection?

A

yes! it can be a secondarily infected producing otorrhea (foul smelling discharge)

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63
Q

what does otoscopy look like for cholesteatoma?

A

can be normal or show perforation and/or otorrhea

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64
Q

how do tymps look like in cholesteatoma

A

-Normal if cholesteatoma has not damaged the TM or ossicles
-If cholesteatoma is filling the ME cavity; a stiffness dominated system, Type As tympanogram is possible
-If ossicular disarticulation has occurred then a Type Ad tympanogram may be seen
-If it has caused TM peroration and is filling up the ME cavity, a Type B (flat) with low volume can be seen
-If the cholesteatoma is not big enough to fill up the ME cavity and TM perforation is present, a Type B high volume tympanogram is possible

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65
Q

how does auditory sensitivity vary in cholesteatoma?

A

Auditory sensitivity varies depending on underlying damage (it just varies)
-Hearing is normal if the ossicular chain is intact and the cholesteatoma only caused TM perforation or no perforation
-Conductive hearing loss if ossicular disarticulation occurred
-Mixed hearing loss also is reported

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66
Q

how do different size perforations of the tm have different levels of HL

A

10 to 30% of the TM absent
~ 10 to 12 dB HL hearing loss
60% of the TM absent
~ 30 dB HL hearing loss
100% of the TM absent
~ 40 to 50 dB HL hearing loss

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67
Q

how do we diagnosis cholesteatoma ?

A

Usually diagnosis is not difficult because it can be visualized on a microscopic exam of the ear in the physician’s office

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68
Q

what do patients complain about in cholesteatoma ?

A

-Foul smelling discharge and often bleeding
-Hearing loss verified by an audiologic evaluation
-Otalgia, headache, or occasionally mild dizziness

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69
Q

how do ct scans appear like in cholesteatoma?

A

-To identify potential damage caused by the cholesteatoma, including facial nerve dehiscence and ossicular damage, for better patient counseling
-But many otologists do not order a CT scan because it does not change the management

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70
Q

how do we take care of cholesteatoma?

A

surgery is the primary treatment
but before surgery we use antibiotic steroids

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71
Q

what can be some side effects of cholesteatoma because of surgery

A

-Hearing loss because ossicles and TM may have to be removed
-A prosthesis, however, can be placed and the TM reconstructed
-Associated mastoiditis may require a mastoidectomy

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72
Q

what happens if the cholesteatoma isn’t completely removed ?

A

-If all of the cholesteatoma is not removed surgically it can lead to recurrences
-Recurrence can also occur if underlying pathology that led to the primary cholesteatoma, such as ET dysfunction or poor mastoid ventilation, is not corrected at the time of surgery

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73
Q

what are some complications of cholesteatoma surgery

A

-Patients need to be counseled that surgery can cause complications depending on the size and location of the cholesteatoma, such as
-Hearing loss (permanent CHL, mixed, or SNHL)
-Facial paralysis
-Dizziness
-Tinnitus
-Intracranial complications such as
1)meningitis
2) intracranial abscess
Recurrence of the cholesteatoma even after surgeryMAIN ONE

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74
Q

what is otosclerosis ?

A

-Otosclerosis is a focal disease, unique to the human temporal bone
-There is ankylosis (fixation) of the stapes footplate to the oval window due to abnormal bony growth
~ 70% cases are bilateral but often one ear is affected first

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75
Q

what does otosclerosis affect ?

A

It affects the otic capsule from which the inner ear develops

76
Q

what is the main site of fixation in otosclerosis?

A

-Fissula ante fenestram
-A minute slit like passage in the otic labyrinthine wall anterior to the oval window

77
Q

what tissue can cause otosclerosis

A

-The bone around it often contains fibrous tissue and immature cartilage
-Active remodeling of this bone is believed to cause otosclerosis
-The fissula ante fenestram lies in close proximity to the anterior portion of the stapes footplate
-as the boney lesion enlarges it encroaches on the stapes footplate

78
Q

in what position does otosclerosis typically fixate on ?

A

-the anterior portion of the footplate
The footplate becomes fixed in position limiting the amplitude of vibrations transmitted to the inner ear
-low freq conductive HL is the result**

79
Q

what can we see if the ENTIRE footplate is fixated in otosclerosis ?

A

a more flat conductive HL is seen

80
Q

what is obliterative otosclerosis

A

bony growth may overgrow the footplate

81
Q

can we determine between otosclerosis of the footplate and obliterative otosclerosis by audiologic testing alone ?

A

NO

82
Q

what is Obliterative otosclerosis of the round window

A

Rare cases of ostosclerosis occurring on the round window

83
Q

what is cochlear otosclerosis

A

-bony growth spreads to the cochlea, the result is a progressive irreversible SNHL worse in the high frequencies
-The bony growth is believed to affect the spiral ligament
-The spiral ligament fibrocytes function in conjunction with the stria vascularis to mediate cochlear ion homeostasis

84
Q

what is histologic otosclerosis?

A

-In this case, lesions do not happen on stapes footplate or cochlea
They remain small and asymptomatic, discovered only incidentally on histologic examination

85
Q

otosclerosis is a disturbance of?

A

physiologic factors that normally serve to inhibit remodeling of the otic capsule

86
Q

what is the pathogenesis of otosclerosis ?

A

-The actual bone changes in otosclerosis involve laying down of new bone with simultaneous absorption of old bone resulting in the formation of a spongy type of bone

  -Intermediate  stage
  -Final, inactive stage = the bone stops growing and gets mineralized
87
Q

what is the initial stage otosclerosis

A

otospongeosis

88
Q

what is the final, inactive, stage in otosclerosis

A

the bone stops growing and gets mineralized

89
Q

is fixation of the ossicles and otosclerosis the same thing ?

A

no! it’s ossicular ossification

90
Q

what is the etiology of otosclerosis?

A

unclear but new info is emerging

91
Q

what gene is mutated on otosclerosis and is it autosomal domincant or recessive

A

-It presents as an autosomal dominant genetic disorder
-Otosclerosis genes (OTSC 1-5) are isolated and associated with mutations of the collagen genes (COL1A1 and COL1A2)

92
Q

is peneternce in otosclerosis complete or incomplete?

A

incomplete
-it may skip a generation or members of the same generation
-it can have different degree of severity even if it’s in the same family

93
Q

what is the recent hypothesis in otosclerosis

A

may be related to persistent measles virus infection in the otic capsule

94
Q

what is the evidence that supports the hypothesis with measles as otosclerosis

A

-Measles viral-like particles found in the osteoblasts and pre-osteoblasts in active otosclerotic lesions
-Measles antigen and measles virus genes have been discovered within actively growing otosclerotic lesions
-Measles is a disease of humans and closely connected primates; otosclerosis occurs only in humans
-A significant decline in otosclerosis was observed with the measles vaccination program

95
Q

what gene is associated with otosclerosis

A

COL1A1 gene, which is also associated with type 1 osteogenesis imperfecta

96
Q

what are some similarities in otosclerosis and osteogenesis type 1

A

-Type 1 osteogenesis imperfecta shares some clinical and histological similarities with otosclerosis
~ 50% of all patients with type 1 osteogenesis imperfecta develop a hearing loss indistinguishable from otosclerosis
-Some patients with ostosclerosis have blue sclera, a feature found in almost all cases of type 1 osteogenesis imperfecta
-Histopathology of temporal bones is identical in both conditions

97
Q

what age pop is more common to get otosclerosis

A

-Single most common cause of hearing loss in young adulthood
-In 90% of cases, the age of onset is between 15 to 45 years
-it’s rare to see after 40 years

98
Q

what is the differential diagnosis is otosclerosis

A

osteogenesis type 1

99
Q

is otosclerosis is bilateral or unilateral?

A

bilateral

100
Q

does otosclerosis happen in men or women more

A

females

101
Q

what race is more likely to get otosclerosis

A

Most prevalent in white females; Rare in blacks
Uncommon among Asians

102
Q

what can happen with females during pregnancy with otosclerosis

A

In 50% of females, initial awareness/rapid acceleration of the hearing loss occurs during/immediately after pregnancy

103
Q

what is paracusis willis in otosclerosis

A

-People with a conductive hearing loss hear better in noise than normal hearing individuals
-This finding may be explained by the fact that in noise generally the intensity of conversation is louder, which makes it easy to hear

104
Q

what configuration see with otosclerosis

A

-Usually a bilateral conductive or mixed hearing loss with a rising configuration; can present as a unilateral hearing loss initially
-50 to 60% of patients present with roaring, hissing, or pulsatile tinnitus, which may indicate sensorineural involvement
-Rarely, there maybe vertigo, probably related to toxic enzymes released by the lesion
-paracusis willis
-bluish color to the sclera of the eye in some patient

105
Q

what does otoscopy look like in otosclerosis

A

-The TM is almost always normal-appearing
-Schwartze sign
-In some cases especially younger adults, increased vascularity of the actively growing bone near the oval window is reflected through the TM as a reddish blush discoloration or glow

106
Q

how does pure tone thresholds look like in early stages of otosclerosis

A

Normal or mild conductive hearing loss with rising configuration

107
Q

how does pure tone thresholds look like in middle stages of otosclerosis

A

Conductive/mixed hearing loss with rising or flat configuration

108
Q

how does pure tone thresholds look like in last stages of otosclerosis

A

-Flattening of the previously rising conductive or mixed hearing loss
-It is not uncommon to see a mixed hearing loss especially in older adults, due to presbycusis now accompanying the long standing otosclerosis

109
Q

how might bone thresholds look like in otosclerosis

A

-Poorer at 2000 Hz by 15 to 20 dB HL with narrowing of ABG
-rarely, this dip in bone thresholds seen at 1k and 3khz
-This dip in BC threshold is called Carhart’s notch
-Possibly due to mechanical effects of the disease itself on the auditory system, i.e., the effect of the stapes fixation on the ME resonance
-Carhart’s notch is present in only about < 40% of patients with otosclerosis so it’s not always there
-it’s not unique to otosclerosis, also seen in patients with ossicular fixation and incudostapedial joint detachment

110
Q

look at slide 65 (mine 66)

A
111
Q

what type of tymps does otosclerosis get ?

A

Generally normal (Jerger Type A) or As tympanogram, with low admittance and narrow gradient

112
Q

what reflexes do we get with otosclerosis

A

-Abnormal acoustic reflexes in most cases
-Reduced stapes mobility, which attenuates stimulus intensity and makes acoustic reflex production difficult
-will be elevated or absent**
-abnormal reflexes **
-Acoustic reflex decay often cannot be performed due to absence of acoustic reflexes

113
Q

how does tone decay look like otosclerosis

A

negative (test of retrocochlear pathology)

114
Q

how does speech audiometry look like in otosclerosis

A

-The SRT is consistent with the pure-tone average
-WRS excellent/good as test performed at suprathreshold levels

115
Q

when do you do tone decay

A

when you have retro cochlear pathology
and you do contra decay !

116
Q

what are surgical indications in otosclerosis

A

-The pre-operative bone conduction is the target for the surgeon
-A conductive component of at least 25 dB HL between 250 to 1000 Hz as determined by audiometry
-A negative Rinne’s test at 512 Hz
-The bigger the ABG gap the better the prognosis for restored hearing after surgery
-Bilateral otosclerosis
-The poorer ear is operated on first
-The second ear is operated on at least one year later if the operated ear remains stable

117
Q

how do we diagnose otosclerosis

A

case history
do allllll testing

118
Q

how does the rinne tuning fork help with surgical management in otosclerosis

A

-It compares patients’ bone-conduction sensitivity to their air-conduction sensitivity based on the assumption that hearing by air conduction is more efficient than bone conduction
-The tuning fork is vibrated and the stem is placed near the EAC
-When the patient stops hearing, the tuning fork is moved immediately to the mastoid process and determined if the patient can still hear the tone
-If the tone is heard longer by bone conduction
-Negative Rinne test, suggesting a conductive or mixed hearing loss (bone is better than air air)
-If the tone is heard longer by air conduction (more efficient)
-Positive Rinne test, suggesting normal hearing or SNHL

119
Q

what are surgical indications with SNHL for otosclerosis

A

-SNHL in the contralateral ear is not a contraindication to stapedectomy but does require thoughtful consideration
-Cases of advanced otosclerosis are an indication for surgery
-Such patients may show dramatic improvement in their speech discrimination abilities following surgery

120
Q

what are contraindications to surgery to otosclerosis (when you don’t want to do surgery and don’t touch that ear) (absolutely don’t want to do surgery)

A

-A dead contralateral ear (you don’t want to mess up your good ear when you have one dead ear on the other side)
-Active otitis externa or otitis media or TM perforation
-otitis media increases the risk of suppurative labyrinthitis and meningitis
-Large exostosis that may affect surgeons ability to access ME
-In the case of infection and exostosis, surgery can proceed after these conditions have been treated/resolved
-Rarely, otosclerosis may involve the endolymphatic duct resulting in S/S of Meniere’s disease – absolute contraindication

121
Q

what are careful considerations prior to surgery (thing to consider for a person to not get surgery) (recommended to not get surgery)

A

-Patients for whom vestibular function is critical for employment
-Otologic problems in contralateral ear that may threaten hearing over time
-Superior semicircular canal dehiscence (SSCD) syndrome

122
Q

what is stapedotomy in otosclerosis (surgical term)

A

A small hole made in the stapes footplate during surgery

123
Q

what is partial stapedectomy in otosclerosis (surgical term)

A

Half removal of the stapes footplate during surgery

124
Q

what is total stapedectomy in otosclerosis (surgical term)

A

total removal of the stapes footplate during surgery

125
Q

what is Prosthesis or implant used in stapes surgery in otosclerosis in surgical terms

A

A stainless steel, titanium, platinum, or teflon piston to replace the stapes footplate

126
Q

is there a difference in the success rate/outcome between stapedotomy vs. stapedectomy procedures

A

no

127
Q

what are some similarities in Stapedotomy and Stapedectomy

A

-Stapedotomy and stapedecetomy can be performed under local anesthesia with sedation or under general anesthesia
-The surgery typically takes about 30 to 45 mins
Laser surgery is now routinely used to vaporize parts of the stapes
-The remainder of the stapes is removed with an instrument
-Current prostheses are safe with lower power MRI scanners (< 1.5 Tesla)
-Titanium, platinum, and plastic prostheses are compatible with MRI scanners of all strengths

Failure rate of surgery is about 1 to 3% (can result in a profound SNHL)

128
Q

what are some complications of surgery in otosclerosis ?

A

1)WRS sometimes worsens (by up to 30%) if there was cochlear involvement
-Stapedectomy can change a the flat mixed hearing loss to a sloping SNHL with poorer WRS
-Decreased hearing at 4000 Hz is often observed post surgery
2) Oval window otosclerosis
Otosclerosis that obliterates the oval window cannot easily be managed or removed with a laser;
-Other cutting instruments used
-Surgery takes longer and it may be difficult to accurately assess the length of the prosthesis needed
3)Round window otosclerosis
-Can cause permanent conductive hearing loss
-Surgical removal of otosclerosis from a completely obliterated round window universally results in SNHL and should not be attempted
4)Hyperacusis
-increased sensitivity to sound: often temporary (sounds that sound soft to us sounds loud to them)
5)Facial paralysis/weakness
-Due to VII nerve damage during surgery – rare complication
-If the facial nerve is completely filling the oval window niche, surgery may have to be aborted
6)Chorda tympani nerve may have to be sacrificed
-It is a branch of the VII N to the anterior 2/3 of the tongue
-Temporary decreased taste/sensation for 3 to 6 months till compensation occurs by the opposite nerve and other taste/sense nerves and mechanisms
7)Perilymphatic fistula
-It is a pathologic communication between the inner ear and ME
-Most commonly occurs at either the round or oval window
-May occur during the early or late postoperative period
-Results in
>Fluctuating, sudden, or progressive SNHL
>Vertigo
>Other symptoms include:
-tinnitus
-disequilibrium
-aural fullness
(all these was because there was an opening in one of the windows and now there is a leak and perilymph is escaping
8) Labyrinthitis (rare but serious)
-Vertigo during or immediately after surgery is indicative of labyrinthine insult
-It may be caused by :
>Air or blood entering the vestibule
>Mechanical trauma to the utricle, which lies in close proximity to the oval window
9) Disarticulation of the incus
-Can occur during surgery
-need a prothesus if complete disarticulation occurs
10) SNHL
-attribute to surgical trauma in 1% of cases
11)Immediate conductive hearing loss
-Malfunction of prosthesis
-Failure to recognize malleus fixation
-Round window obliteration
-ME effusion
-Superior semicircular canal dehiscence (SSCD) syndrome
>The roof of the superior semicircular canal is missing
A conductive hearing loss similar to otosclerosis can be found in some patients with SSCD

12) Delayed-onset conductive hearing loss
-Occurs in ~ 5% of successful stapedectomies
-Most common cause is erosion of long process of incus with displacement of the prosthesis

129
Q

what are non surgical management for otosclerosis ?

A

-Amplification
-When surgery is not an option because of :
>age
>health issues
>patient refuses surgery for any reason
-Patients with otosclerosis do well with amplification as the hearing aid provides the amplification the ME system cannot***

130
Q

what are differential diagnosis for otosclerosis ?

A

1)Meniere’s disease
-Dizziness/vertigo (more common and of much longer duration in Meniere’s disease)
-Tinnitus, which can be roaring like otosclerosis
-Low frequency hearing loss, which is sensorineural in Meniere’s
2) Osteogenesis imperfecta (already discussed)
3)Superior semicircular canal dehiscence (SSCD) syndrome
-Thinning/absence of part of the bone of the semicircular canal is thought to predispose patients to this syndrome
-Low frequency conductive hearing loss (250 to 1000 Hz)
-but unlike otosclerosis, ARTs are normal in SSCD*****
-SSCD can be distinguished from otosclerosis by a temporal bone CT scan

131
Q

what is some examples of trauma ?

A

-Blow to the side of the head/falls
-Sports injuries such as in racquet ball, football, boxing
-Blast injuries (e.g., bombs/improvised explosive device – IEDs)
-Motor vehicular accidents
-Foreign body insertion such as Q-tips (ossicular disarticulation)

-In cases of head trauma, the inner ear may be involved too resulting in SNHL with accompanying ME damage such as:
>t.m perforation
>ossicular disarticulation
>hemotympanum (blood in the tympanic cavity)

132
Q

what is some basic information for ossicular disarticulation ? (ossicles move out of place)

A

-Trauma to the head or face
-Also seen in medical conditions such as osteoporosis
-In cases of cholesteatoma where the pseudo-tumor can destroy the ossicles
-Untreated ME infection that can destroy the ossicles

133
Q

what does incudomalleolar disarticulation in a ct scan

A

-an ice cream cone !
-The “ice cream cone” sign describes the normal appearance of the middle ear ossicles on axial CT scan
-The ball of the ice cream is formed by the head of the malleus and cone is formed by the body of the incus, with the tapering conical point formed by the short process of the incus
-Failure of this normal configuration suggests ossicular chain disruption (incudomalleolar disarticulation

134
Q

how does otoscopy look like in ossicular disarticulation

A

Otoscopy: Depending on the cause of the disarticulation
-Perforation of TM
-Bleeding in the ear canal with TM perforation
-Rarely, the TM and ear canal may appear normal

135
Q

how might immittance test look like for ossicular disarticulation ?

A

-Jerger type Ad tympanogram
-Abnormal reflexes

136
Q

what are pure tones thresholds going to look like for ossicular disarticulation ?

A

conductive/mixed HL

137
Q

if you have normal reflexes, do you know have otosclerosis or SSCD

A

you have SSCD!!!!

138
Q

what is some treatment for ossicular disarticulation ?

A

-Surgical repair
-Amplification, if surgery is not successful/not an option

139
Q

what percentage is temporal bone trauma in head trauma?

A

-Occurs in 30 to 75% of head injuries
-The dense temporal bone requires significant amount of force to sustain a fracture

140
Q

what can cause temporal bone injuries ?

A

-Majority of temporal bone injuries occur as part of multiple injuries following motor vehicular accidents (MVA)
-Also caused by
-Industrial accidents
-Recreational injuries
-Falls
-Assaults
-Gunshot wounds
-Self-inflicted injuries

141
Q

what are the types of temporal bone traumas

A

Blunt trauma with fracture
Longitudinal fractures
Transverse fractures

142
Q

what is longitudinal fractures

A

-(direct blow to temporal/parietal aspect)
-Most common fractures of the temporal bone (70 to 90%)
-Parallels long axis of the temporal bone in coronal plane
-Passes through the postero-superior aspect of the external auditory canal, TM, and roof of ME
-Disrupts the ossicles but generally spares the otic capsule – otic capsule sparing fracture

143
Q

what are transverse fractures?

A

-(commonly due to a blow to the occiput)
-Less common fractures of the temporal bone (20 to 30%)
-Extends through internal auditory canal or otic capsule – otic capsule disrupting fracture
-Can affect the oval or round window

144
Q

more information on blunt force trauma with fracture

A

Few temporal bone fracture are purely longitudinal or transverse
About 50 to 75% are mixed

Pediatric temporal bone fractures are primarily caused by
-falls from a height
-automobile pedestrian accident

145
Q

what is the most common penetrating temporal bone trauma

A

gun shots

146
Q

what wombs can a gun shot bring ?

A

-Gunshot wounds produce a wide variety of injuries including
-Trauma to major blood vessels
-Destruction of middle and inner ear
-Destruction of cranial nerves
-The facial nerve is injured ~ 50% of the time
-ensuing facial paralysis is immediately

147
Q

what is otitic barotrauma ?

A

trauma withOUT fracture
-Barotrauma refers to injury sustained from failure to equalize the pressure of an air-containing space with that of the surrounding environment such as observed in the ear, face, and lungs
-The most common examples of barotrauma occur in air travel and scuba diving
-Barotrauma most often occurs during compression (descent) or after a short, shallow dive
-Otic barotrauma causes sudden and severe negative ME pressure and trauma to the ear resulting in
> excruciating otalgia
>possible tm rupture w/ hemmorhage
>perilymphatic

148
Q

what is inner inner ear decompression sickness (IEDCS)

A

-a type of temporal trauma
-IEDCS most often occurs during decompression (ascent) or shortly after surfacing from a dive
-It is an injury that closely resembles inner ear barotrauma, however, the treatment is different
-It is more common among commercial and military divers who breathe a compressed mixture of helium and oxygen
Symptoms occur during ascent or shortly thereafter & include
>hearing loss and tinnitus
>tinnitus

149
Q

patients with Inner ear decompression sickness (IEDCS)
should …

A

betransported to be recompressed

Patients with IEDCS should be rapidly transported to a hyperbaric chamber for recompression
Significant correlation between early recompression and recovery

150
Q

What are categories of thermal injuries ?

A

Injuries sustained during welding leading to TM perforation
Lightning bolt conducted through phone or other means

151
Q

what are symptoms of thermal injuries

A

SNHL
dizziness
facial paralysis from devitalized bone and soft tissue

152
Q

what are characteristics of compressive injuries ?

A

-When slapped or struck on the side of the head
-Falling on water during water sports
-Most significant is from blast injuries
-Bomb explosions can cause
-disruption and implosion of tm
-high freq SNHL due to disruption of the inner ear

153
Q

what are characteristics in forgein objects

A

-Typically used by patients to remove cerumen can cause
-Localized laceration, hematoma, infection of EAC and TM
-Injuries can extend to the ME and inner ear resulting in hearing loss with or without vertigo

154
Q

What can we inspect with injuries for auditory stuff ?

A

-Acute or delayed conductive hearing loss
-Clotted blood, debris, and hematoma in the ear canal
-Perforated, lacerated, or completely disrupted TM
-ME filled with blood or cerebrospinal fluid (CSF)
-Bleeding from ears; common sign of temporal bone fracture
-Ossicular disarticulation
-Incudo-stapedial joint most commonly affected followed by fractures of the incus and stapes
-Fracture of the malleus is the least common
-Ossicular fixation due to fibrous adhesions
-High incidence of SNHL

155
Q

what are charcteristics for vestibular in injuries ?

A

Benign paroxysmal positional vertigo (BPPV)
Concussive injury to labyrinth resulting in vestibular symptoms
Perilymphatic fistula

156
Q

how does facial nerve tie with injuries?

A

80 to 90% of longitudinal temporal bone fractures result in facial nerve paralysis
-most common thru boney spicules hitting the nerve followed by neural construstion (brusing)

157
Q

how does hemotympanum tie with temporal brain trauma for treatment

A

-Self healing in 4 to 6 weeks
-Myringotomy to drain is not recommended; high risk of infection

158
Q

how does tm perforation tie with temporal bone trauma for treatment ?

A

-Self-healing; observe and manage conservatively
-Make sure perforated edges do not get infected, which may result in cholesteatoma
-If healthy perforation persists after several months then a myringoplasty can be performed

159
Q

how does persistent conductive HL tie with temporal bone trauma for treatment

A

-Exploration and repair of ossicles
-Amplification if surgery is not an option

160
Q

how does Irreversible SNHL and tinnitus tie with treatment of temporal bone trauma

A

Hearing aids and tinnitus management

161
Q

how does vestibular symptoms tie with treatment of temporal bone trauma

A

Mostly self-limiting resolving within 6 months

162
Q

how does Benign paroxysmal positional vertigo (BBPV)
ties with treatment to temporal bone trauma

A

-Typically self-limiting resolving within 3 months
-If not resolved then treatment needed i.e., Epley maneuver

163
Q

how does otitic meningitus ties with treatment to temporal bone trauma

A

Meningitis can complicate traumatic encephalocele or CSF leak
-occurs months or years w/ or w/out CSF leaks
Treated with antibiotics based on culture results

164
Q

what are Paraganglioma (Glomus Tumor)

A

Paragangliomas are the most common benign soft tissue tumor of the ME (rarely malignant)

165
Q

what is the most second common benign

A

Paragangliomas (glomus tumor)

166
Q

what do Paragangliomas (glumos tumor) involve

A

Glomus tympanicum
Glomus jugulare

167
Q

what is Glomus tympanicum

A

Arising along the course of the Jacobson nerve primarily in the tympanic cavity

168
Q

what is glomus juglare

A

Arise from the dome of the internal jugular vein bulb and involve jugular foramen and related structures

169
Q

look at slide 102(103 on mine)

A
170
Q

look at slide 104, 105 (105 and 106)

A
171
Q

what is the heredity of glomus tumors

A

-Sporadic or AD inheritance with 100% penetrance
-Mutation of gene SDHD mapped to 11q23 may be involved in these tumors
-Genomic imprinting may be involved
-Affected individuals inherit the disease from their father but expression of the phenotype may not be observed in off-springs of affected females until transmission through a male carrier
-Heredity cases show no sex predisposition with both sexes affected equally; sporadic mutations show a sex predisposition with females being more affected
-Reported in some cases of neurofibromatosis 1 (NF-1)

172
Q

what is the incidence of Paraganglioma (Glomus Tumor)

A

-Patients usually present after the 5th decade of life
-More common in females (males may be carriers if genetic)
-Even with modern genetic testing, the majority of paragangliomas appear to be sporadic
-However, approximately one-third to one-half are associated with an inherited syndrome including some cases of NF1
-So far 10 genes have been associated with paragangliomas with or without pheochromocytoma
-Pheochromocytoma is a tumor of the adrenal glands
-Because of the hormones secreted, symptoms include
>life threating high blood pressure
>sweating
>rapid heart beat
>and head ache

173
Q

Glomus Tympanicum arises from?

A

-the promontory of the ME
-Tympanicum tumors are smaller and cause early symptoms as they are growing with the narrow confines of the ME cavity

174
Q

what are some signs and symptoms of Glomus Tympanicum

A

-Pulsatile tinnitus because of the tumor vascularity is often the first presenting symptom
-Tympanic membrane may appear red due to increased vasculature of the ME cavity
-Lateral growth through the TM can mimic a bleeding polyp
-Growth of tumor can inhibit ossicular mobility resulting in a conductive hearing loss
-Medial growth towards the inner ear can cause SNHL, facial nerve dysfunction, and/or vertigo

175
Q

what is some treatment of Glomus Tympanicum

A

Surgery: Complete tumor removal is seen in > 90% of cases

176
Q

what are Glomus Jugulare

A

These tumors arise from the dome of the internal jugular vein or proximal portion of Arnold’s or Jacobson’s nerve

177
Q

what is the difference between Glomus Jugulare and glomus tympanicum

A

-More common and extensive than glomus tympanicum because of the space available to grow
-Tumors remain silent for years and tend to grow quite large
-They may grow through the floor of the ME and incorrectly present as glomus tympanicum tumors
-They can grow anywhere in the temporal bone and blood vessels in the neck
-Cranial nerves VII to XII can be affected depending on tumor growth

178
Q

what are symptoms of Glomus Jugulare

A

-For large glomus jugulare tumors:
Hearing loss
-Otalgia
-Aural fullness
-Vertigo, if involvement of vestibular division of VIII N
-Hoarseness and dysphagia due to involvement of the CN IX, X, and XI because of proximity to site of origin of glomus jugulare
-Involvement of XII (hypoglossal) nerve indicates more extensive disease
-because this nerve is farthest away from the tumor origin and least likely to be involved

179
Q

how does otoscopy look like on Glomus Jugulare

A

A red mass filling the ME cavity or lower portion of the ME cavity may be visible

180
Q

how might pure tone audiometry

A

-A conductive hearing loss may be present depending on the size of the tumor and involvement of ossicles
-Sometimes a mixed hearing loss may occur if neural involvement has occurred

181
Q

how might immittance test look like ?

A

-jerger type AS tymps
-if the tumor is big and pressing on the TM
-Jerger type B
-a large tumor pressing on the tm can render the tm immobile
-Tympanogram also will show jagged edges which will correspond to the patient’s pulse
-holding the breathe will not change the pattern
-Pulsating tympanogram, suspect glomus tumor

182
Q

what is the treatment of Glomus Jugulare

A

Surgery or radiation

183
Q

why is surgery hard for Glomus Jugulare

A

Surgery can be difficult and not without complications for large tumors that have invaded head/neck structures and cranial nerves

184
Q

what is the code for diseases of the ear and mastoid process

A

H60-H95

185
Q

whats the code for disease of middle ear and mastoid

A

H65-H75

186
Q

what are some tips for diagnostic codes?

A

-CPT (procedural) codes must always match ICD-10 codes
-For example, the CPT code 92550 – Tympanometry and Reflexes would be appropriate to use for a diagnosis of otosclerosis, ICD-10 diagnostic code - H71.90

-We don’t diagnose medical conditions even though we are required to use the most specific diagnostic ICD-10 codes
-If it is an obviously visible medical condition, code for that condition
-For example, ICD-10 code H92.10 - Otorrhea unspecified ear (code with more specific code for RE or LE)
-If its not an obvious medical condition then code for the auditory signs and symptoms
-For example H80.91 - Unspecified otosclerosis, right ear
-Patient history and test results may point to otosclerosis of the right ear but it’s a medical diagnosis
-Code instead for H90.11 – Conductive hearing loss unilateral right ear
-Unless a physician has already made the diagnosis of otosclerosis of the right ear, then you can use both ICD-10 codes: H90.11 (primary) and H80.91 (secondary)

AUDE 5410 (9 decks)

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