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AUDE 5410 - Acquired Auditory-Vestibular Disorders > Disorders Affecting the Middle Ear > Flashcards

Disorders Affecting the Middle Ear Flashcards

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Preparativo Vestibular e ENEM flashcards
1
Q

What is otitis media with effusion?

A

An infectious inflammation of the ME that results in the accumulation of the fluid (effusion) in the middle ear cavity
Primarily child disorder

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2
Q

What is often misdiagnosed as acute OM?

A

Acute myringitis
Redness of the TM without effusion
Excessive blowing the nose/crying can also cause redness of TM

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3
Q

Is OME a historical disorder?

A

Yes
TM perfs and mastoid bone destruction reported in Egyptian mummies

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4
Q

Can you just base diagnosis of OME on otoscopic exam?

A

No

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5
Q

Who does OME affect?

A

Primarily children and infants
World wide

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6
Q

Is OME the second common reason for visits to pediatrician?

A

Yes
First is viral infections

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7
Q

What is the incidence for OM in urban areas?

A

90% within the first 2 years of life

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8
Q

Is age inversely related to prevalence of OME?

A

Yes

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9
Q

What percentage of kids will have at least one episode of OME by 1 year of age?

A

50%

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10
Q

What percentage of kids will have at least one incidence of OME before starting school?

A

60 to 70%

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11
Q

What percentage of kids will have recurrent OME during the first 3 years of life?

A

35%
Of these children, 5-10% will develop chronic OME

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12
Q

What percentage of kids will have prevalence of OME at age 6?

A

5%

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13
Q

Can OME occur in adults?

A

Yes
Rare, but possible
Could be a symptom, not the actual problem
Must look to see if there is other problem

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14
Q

What racial groups have the greatest incidence of OME?

A

Eskimos, native americans, hispanics, and australian aborigines

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15
Q

Is OME more common in caucasians and less common in asians and blacks?

A

Yes

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16
Q

Is there a slightly higher incidence in males than females?

A

Yes

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17
Q

What are the peak incidence months of OME?

A

Between October and April
Declines in summer months

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18
Q

Is there a greater incidence in children with a history of upper respiratory illnesses such as colds, asthma, and allergies?

A

Yes

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19
Q

Why is there a greater incidence in eskimos, native americans, hispanics, and australian aborigines?

A

Due to their anatomy of the skull base and ET
Flat face, bigger nose

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20
Q

When do children generally outgrow susceptibility to OM?

A

By 6 to 8 years of age
As ET assumes adult proportions

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21
Q

What are the anatomical differences between adult and children’s ET?

A

Child has a short and horizontal ET composed of flaccid cartilage
10 degrees vs 45 degrees

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22
Q

Is the ET the most likely route of bacterial entry in the ME?

A

Yes
Through retrograde reflux of nasopharynx secretions

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23
Q

What are three factors that can facilitate bacterial reflux in the ME?

A

Bacterial colonization of the nasopharynx
Incompetence of the protective function of the ET
Negative pressure in the ME in relation to the nasopharynx

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24
Q

Is it presumed that during acute OM, ciliary function of the ET and ME are impaired?

A

Yes
It affects the clearance of secretions

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25
Q

Are common pathogens that cause OM also commonly found in upper respiratory tract infections?

A

Yes

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26
Q

What are some bacterial infections that can result in OM?

A

Streptococcus pneumoniae
Hemophilus influenzae

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27
Q

What are some common viral infections that can cause OM?

A

Respiratory syncytial virus (most common)
Rhinovirus
Parainfluenza virus
Influenza virus

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28
Q

Can cleft palate cause OME?

A

Yes
But incidence decreases after repair

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29
Q

Can some craniofacial disorders result in OME?

A

Yes
Treacher Collins
Down’s syndrome

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30
Q

Can ciliary dysfunction result in OM?

A

Yes
Disorders of mucociliary clearance such as kartagener’s syndrome and cystic fibrosis

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31
Q

Can environmental allergies result in OM?

A

Yes

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32
Q

Can immune dysfunction result in OM?

A

Yes
AIDS, steroid therapy, and chemotherapy

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33
Q

Can eustachian tube abnormalities result in OM?

A

Yes
Impaired opening
Shorter tube

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34
Q

Can obstruction result in OM?

A

Yes
Nasogastric tubes
Adenoids/tonsils
Tumors

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35
Q

What three criteria does acute otitis media need to meet for diagnosis?

A

Acute onset
ME inflammation
ME effusion (fluid build-up of ME)

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36
Q

Who set the criteria for acute otitis media?

A

American Academy of Pediatrics and The American Academy of Family Physicians

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37
Q

Is AOM short term (3 weeks or shorter)?

A

Yes

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38
Q

Is AOM characterized by otalgia and redness of the TM with effusion?

A

Yes

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39
Q

Are there two categories of AOM?

A

Yes
Severe
Non-severe

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40
Q

What is severe AOM?

A

Moderate to severe otalgia and temp > 102 degrees F

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41
Q

What is non-severe AOM?

A

Mild otalgia and temp < 102 degrees F

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42
Q

Is AOM often over-diagnosed?

A

Yes

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43
Q

What characterizes a sub-acute OM?

A

Persisting for 3 weeks to 3 months

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44
Q

What characterizes recurrent OM?

A

Multiple self-limiting episodes with symptom-free periods between flare-ups
3 or more episodes within a 6 month period
4 or more episodes within a year

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45
Q

What characterizes chronic OM?

A

Condition persisting of >3 months
Generally with effusion but without other signs of inflammation (fever or otalgia)

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46
Q

Does middle ear effusion almost always follow AOM?

A

Yes
Can take up to 2 to 3 weeks to clear post treatment

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47
Q

What is persistent middle ear effusion?

A

Effusion can persist for an average of 40 days
High incidence in children (children <2 years more likely to have persistent MEE)
Higher incidence for caucasian children

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48
Q

Can serious effusion occur without OM?

A

Yes
In barotrauma, following an airplane trip, or seasonal allergies

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49
Q

What is another way to classify OM?

A

Fluid composition

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50
Q

What are the different kinds of fluid composition?

A

Serous OM
Mucoid OM
Purulent OM
Chronic mucoid OM

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51
Q

What is serous OM?

A

SOM
Clear

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52
Q

What is mucoid OM?

A

MOM
Thick and colored

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53
Q

What is purulent OM?

A

POM
Odorous and thick

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54
Q

What is another term for chronic mucoid OM?

A

Glue ear

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55
Q

What is chronic mucoid OM?

A

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

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56
Q

Is OM dynamic?

A

Yes
Classification is not a distinct entity
SOM may progress to MOM and so on

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57
Q

What are some risk factors for OME?

A

Age (peak incidence between 6-11 months of age)
ET dysfunction
Craniofacial anomalies (increased risk with cleft lip/palate and Downs)
Decreased risk for breast fed infants (stronger immune systems due to antibodies in breast milk)
Day care attendance
Susceptibility to upper respiratory tract infections/allergies
Smoking in the home including second-hand smoke
Family history of OME
Male
Low birth weight
Socio-economic status (inverse relationship between SES and OME)

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58
Q

Why is SES a factor for OME?

A

Due to lack of access to healthcare, poor diet, and overcrowding

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59
Q

What are some signs and symptoms of OME?

A

Otalgia
Fever
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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60
Q

Do older children have otalgia and fever associated with OME?

A

They may not

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61
Q

Why do children have inconsistent responses to sound?

A

They may have fluctuating or mold hearing loss

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62
Q

What may you find in an otoscopic exam of OME?

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 observed in the ME

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63
Q

What are some tymp results that might be seen for OME?

A

Flat (type B)
Neg pressure >200 daPa (type C)
Flat high volume (type B) - PE tube or perforation
Inability to get a hermetic seal with perf in older equipment

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64
Q

What ARTs will you see for unilateral OM?

A

Typically only the ipsilateral ART will be present on the unaffected side

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65
Q

What ARTs will you see for bilateral OM?

A

Ipsilateral and contralateral abnormal for both ears

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66
Q

What are some possible pure tone test results for OM?

A

May be within normal limits (but their may be a ABG exceeding 10 dB HL)
Fluctuating loss may be present
Conductive hearing loss that does not exceed 60-65 dB HL
Possible rising or reverse slope

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67
Q

What speech audiometry results do you expect for OM?

A

Normal WRS
SRT and PTA in good agreement

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68
Q

If OM is not treated, what can result?

A

Permanent/temporary CHL
Damage to ME structures (release of enzymes that result in collagen and tissue destruction - can lead to ossicular destruction and glue ear)
Cholesteatoma
Permanent high freq SNHL (toxins can go into inner ear)

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69
Q

What is a cholesteatoma?

A

Pseudo-tumor
Fast growing and invasive
Can result in a dead ear

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70
Q

What is the treatment for cholesteatoma?

A

Surgery
If any is left, it can grow back

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71
Q

Can untreated OM lead to auditory deprivation?

A

Yes
Can effect language development

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72
Q

Can untreated OM lead to deficits in binaural auditory processing?

A

Yes
Important for sound localization and hearing in noise

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73
Q

Can untreated OM lead to learned inattention?

A

Yes
They have difficult attending to auditory input

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74
Q

Can untreated OM lead to difficulty with sound discrimination?

A

Yes

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75
Q

Can untreated OM lead to difficulty with perception of initial and final voiced and voiceless stops (/b/ vs /p/)?

A

Yes

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76
Q

Are /b/ and /p/ sounds some of the earliest to appear in the speech of children?

A

Yes

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77
Q

What are some societal consequences of OM?

A

Loss of money in treatments and productivity
Most common reason for pediatrician visit
Time off work and school
Tympanostomy tube placement is the 2nd most common surgical procedure in children
Development to multi-drug resistant bacteria due to over-prescription of antibiotics and not taking the entire dose of antibiotics

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78
Q

What are some signs and symptoms for acute OME?

A

Follows upper respiratory tract infection
Fever
Otalgia
Hearing loss
Otorrhea
Systemic symptoms (nausea, general malaise (feeling blah), and lack of appetite)

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79
Q

What are some signs and symptoms for chronic OME?

A

Can be asymptomatic
May have hearing loss
May report feeling plugged
May report popping of ears

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80
Q

What does TM color with standard otoscopy look like for OME?

A

Opaque, yellowish red, red, or pink

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81
Q

What is the position of the TM with standard otoscopy look like for OME?

A

Bulging or retracted TM

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82
Q

What is the mobility of the TM with standard otoscopy look like for OME?

A

Normal, hypo-mobile, or retracted

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83
Q

What are some other otoscopy findings with OME?

A

Discharge, perforations, cholesteatoma, or retraction prockets

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84
Q

What type of otoscopy is the gold standard for OME?

A

Pneumatic

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85
Q

What could an audiogram look like for OME?

A

Conductive component or CHL
Mixed HL
SNHL

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86
Q

What could a tympanogram look like for OME?

A

Flat (Type B or Type B high volume)
Negative pressure (Type C)
Abnormal gradient/width

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87
Q

What do acoustic reflexes look like for OME?

A

Abnormal or absent
Cannot raise level to overcome conductive hearing loss

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88
Q

How is OME managed?

A

Observation (if no symptoms)
Medication
Myringotomy (incision) - done with fluid-filled ME cavity and dangerously bulging TM

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89
Q

What medications do they prescribe for OME?

A

Antihistamine/decongestants
Antibiotics (Amoxicillin)

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90
Q

How long is an amoxicillin dose?

A

7 to 10 days

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91
Q

What percentage of OME will clear up in 7-14 days without treatment?

A

81%

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92
Q

What percentage of OME will clear up in 7-14 days with treatment?

A

94%

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93
Q

How long can effusion persist following antibiotic therapy and after infection resolution?

A

2-3 weeks

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94
Q

How long should you wait to follow up with a tymp after OME treatment?

A

2-3 weeks post antibiotics

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95
Q

Why are prophylactic (prevention) and prolonged antibiotics contraindicated for management of chronic OM?

A

Due to an increased risk of antibiotic resistance

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96
Q

Can manipulation of existing environment decrease risk for chronic OME?

A

Yes

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97
Q

Is there typically watchful waiting for up to 3 months for children without hearing loss or not at-risk for speech and language delays?

A

Yes

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98
Q

What quadrants are PE tubes placed in?

A

Anteroinferior and maybe posteroinferior

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99
Q

Are adenoidectomy and/or tonsillectomy needed for management of chronic OME?

A

Maybe
It decreases the need for repeated PE tube replacement

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100
Q

Is chronic OM more common after the advent of antibiotics because perforation of the TM became less prevalent?

A

Yes
Perf allowed for drainage of fluid
Prevented chronic OM

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101
Q

What are some complications with OME?

A

Acute mastoiditis
Ossicular erosion resulting in CHL
SNHL (high freq)
Facial nerve paralysis
Labyrinthine fistula
Meningitis
Brain abscess

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102
Q

How does SNHL occur due to OME?

A

Caused by permeation of toxins through the round window
Positively correlated with severity and duration of OME

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103
Q

Why does OME cause facial nerve paralysis?

A

Caused by involvement of CN VII by infection through bony dehiscence, inflammatory edema causing nerve compression, etc.

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104
Q

What is a labyrinthine fistula?

A

Opening to labyrinth

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105
Q

What causes a labyrinthine fistula in OME?

A

Infection or cholesteatoma

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106
Q

What is a cholesteatoma?

A

A pseudotumor that can occupy the external ear canal, ME cavity, or extend through the mastoid bone into the brain cavity

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107
Q

Are cholesteatomas highly aggressive?

A

Yes
They are also very fast growing

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108
Q

Are cholesteatomas highly erosive?

A

Yes
They eat through everything

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109
Q

What could explain the highly aggressive behavior of cholesteatomas?

A

Invasive fibroblasts
Not found in normal skin

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110
Q

Can cholesteatomas be congenital and acquired?

A

Yes

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111
Q

What is congenital cholesteatoma?

A

Almost always present in children
Median age is 5 years
3:1 male to female
TM can be normal without history of perf, otorrhea, or myringotomy
Anterior-superior most common area
Etiology is controversial

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112
Q

What is acquired cholesteatoma?

A

More common
Due to chronic or untreated OME or trauma leading to TM perf
Also could be a result of TM retraction in the pars flaccida
Previous ear surgery/TM perf may be growth site
Slow growing
Usually present first with a hearing loss

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113
Q

What are latrogenic cholesteatoma?

A

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

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114
Q

How do cholesteatomas grow?

A

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
This will evoke inflammatory reaction leading to formation of cholesteatoma

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115
Q

From the growth spot, where can cholesteatomas grow and engulf?

A

Ossicles
Mastoid (resulting in mastoiditis)

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116
Q

If the cholesteatoma is large enough, can it exert pressure on CN VII and cause facial palsy?

A

Yes

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117
Q

Can a cholesteatoma become secondarily infected and produce otorrhea?

A

Yes

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118
Q

What are the otoscopic findings of a cholesteatoma?

A

Variable
Can be normal or show perfs and/or otorrhea

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119
Q

What are the tympanogram findings of a cholesteatoma if the TM and ossicles are not damaged?

A

Normal

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120
Q

What are the tympanogram findings of a cholesteatoma if it is filling the ME cavity

A

As
Stiffness dominated system

121
Q

What are the tympanogram findings of a cholesteatoma if there is ossicular disarticulation?

A

Ad

122
Q

What are the tympanogram findings of a cholesteatoma if there is a perf and is filling the ME cavity?

A

B with low volume

123
Q

What are the tympanogram findings of a cholesteatoma if it is not big enough to fill the ME cavity and perf?

A

Type B high volume

124
Q

Does auditory sensitivity vary for cholesteatomas?

A

Yes
Depending on underlying damage

125
Q

When is normal hearing present for cholesteatomas?

A

Is the ossicular chain is intact and the cholesteatoma is only caused TM perf or no perf

126
Q

When is CHL present for cholesteatomas?

A

If ossicular disarticulation occurred

127
Q

Is mixed hearing loss also reported for cholesteatomas?

A

Yes

128
Q

Will different sized perfs cause different levels of hearing loss?

A

Yes

129
Q

What type of hearing loss presents if 10-30% of the TM is absent?

A

10 to 12 dB HL of hearing loss

130
Q

What type of hearing loss presents if 60% of the TM is absent?

A

30 dB HL of hearing loss

131
Q

What type of hearing loss presents if 100% of the TM is absent?

A

40 to 50 dB HL of hearing loss

132
Q

Is diagnosis difficult for cholesteatomas?

A

No
It can be visualized on a microscopic exam of the ear in physician’s office

133
Q

What do patients complain of with cholesteatomas?

A

Foul smelling discharge and bleeding
Hearing loss
Otalgia, headache, or occasionally mild dizziness

134
Q

What is a CT scan used for in cholesteatomas?

A

To identify bone damage done by cholesteatomas and the facial nerve
Many do not refer for this because it doesn’t change management

135
Q

What is the management of a cholesteatoma?

A

Surgical removal is the primary treatment
Antibiotic steroid drops may be prescribed prior to surgery to decrease inflammation and granulation tissue (decreases bleeding during surgery)

136
Q

What can cholesteatoma surgery result in?

A

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

137
Q

Can cholesteatomas recur if it is not removed?

A

Yes
Recurrence can occur if underlying pathology that led to the primary cholesteatoma is not corrected at the time of surgery

138
Q

What are some of the complications that can result from cholesteatoma surgery?

A

Hearing loss (permanent - CHL, SNHL, or mixed)
Facial paralysis
Dizziness
Tinnitus
Intracranial complications (meningitis and intracranial abscess)
Recurrence after surgery

139
Q

What is otosclerosis?

A

Focal and unique to humans
Disease of the temporal bone
Affects the otic capsule from which the inner ear develops

140
Q

Is otosclerosis insidious and progressive?

A

Yes

141
Q

What is the etiology of otosclerosis?

A

Not known
But it is primarily an active remodeling process of the endochondral (cartilage) layer of the temporal bone
Normally no remodeling of the otic capsule occurs following embryonic development

142
Q

What is required to call it otosclerosis?

A

Fixation of the stapes footplate to the oval window due to abnormal bony growth

143
Q

Is otosclerosis often bilateral?

A

Yes, 70%
But often one ear is affected first

144
Q

What is the main site of fixation for otosclerosis?

A

Fissula ante fenestram
Bone around it often contains fibrous tissue and immature cartilage
Active remodeling of this bone is believed to cause it
Encroaches the stapes footplate

145
Q

What is fissula ante fenestram?

A

It is a minute slit in the otic labyrinthine will anterior to the oval window
Lies close to the anterior portion of the stapes footplate

146
Q

Is the degree of footplate involvement variable for otosclerosis?

A

Yes, highly

147
Q

In the majority of otosclerosis cases, is involvement limited to the anterior portion of the footplate?

A

Yes
The footplate becomes fixed in position limiting the amplitude of vibrations transmitted to the inner ear

148
Q

What type of hearing loss is the result of otosclerosis?

A

Low frequency CHL
Might end up flat as it progresses

149
Q

What type of hearing loss is present when there is fixation of the entire footplate?

A

Flat

150
Q

What happens if the bony growth overgrows the footplate?

A

Obliterative otosclerosis

151
Q

Is management different for obliterative otosclerosis?

A

Yes

152
Q

Is an audiogram enough alone to distinguish between otosclerosis and obliterative otosclerosis?

A

No

153
Q

Does the actual bone change during otosclerosis?

A

Yes
Laying down new bone with simultaneous absorption of old bone
Results in spongy bone

154
Q

What are the stages of otosclerosis?

A

Initial (otospongeneosis)
Intermediate
Final, inactive - bone stops growing and gets mineralized

155
Q

Is the fixation of other ossicles otosclerosis?

A

No

156
Q

Is the etiology of otosclerosis clear?

A

No
New information is emergine

157
Q

Is there a genetic basis for otosclerosis?

A

Yes
It presents as an AD condition

158
Q

Are otosclerosis genes isolated?

A

Yes
And they are associated with mutations of the collagen genes

159
Q

What type of penetrance does otosclerosis have?

A

Incomplete

160
Q

What type of expressivity does otosclerosis have?

A

Varying

161
Q

What is a hypothesis with the relation of otosclerosis to measles?

A

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

162
Q

What is some of the evidence that supports the hypothesis for otosclerosis and measles?

A

Measles virus-like particles found in the osteoblasts and preosteoblasts in active osteosclerotic lesions
Measles antigen and measles virus genes have been discovered with actively growing osteosclerotic lesions
Measles is a disease of humans and close primates
A significant decline of otosclerosis has been observed with measles vaccine

163
Q

Are some cases of otosclerosis associated with type 1 osteogenesis imperfecta?

A

Yes
They share some clinical and histological similarities

164
Q

Is hearing loss from osteogenesis imperfecta distinguishable from otosclerosis?

A

No

165
Q

Do some patients with otosclerosis also have blue sclera (feature found in osteogenesis imperfecta)?

A

Yes

166
Q

Is the histopathology of the temporal bones the same in both otosclerosis and osteogenesis imperfecta?

A

Yes

167
Q

Is osteogenesis imperfecta an AD condition?

A

Yes

168
Q

What is the single most common cause of hearing loss in young adulthood?

A

Otosclerosis

169
Q

What is the age of onset for 90% of cases of otosclerosis?

A

15 to 45 years
Mean incidence is 20-30 years

170
Q

Is otosclerosis onset rare after 40 years of age?

A

Yes

171
Q

Are most cases of otosclerosis bilateral?

A

Yes, 70%

172
Q

What is the gender ratio of otosclerosis?

A

2:1 female to male

173
Q

What ethnicity is otosclerosis common in?

A

Most prevalent in white females, rare in blacks
Uncommon in Asians

174
Q

Does initial awareness or rapid acceleration of otosclerosis occur during or immediately after pregnancy?

A

Yes
Hormones surging and accelerates gene expression
Can also worsen at menopause

175
Q

What are some signs and symptoms of otosclerosis?

A

Bilateral conductive or mixed hearing loss with a rising configuration
Can present as a unilateral hearing loss initially
50-60% will experience roaring, hissing, or pulsatile tinnitus (may indicate sensorineural involvement)
Rarely vertigo
Paracusis willis (CHL and hearing better in noise)
Blue sclera

176
Q

Why do people with CHL hear better in noise?

A

Because the intensity of conversation is louder, which is easier for them to hear

177
Q

What does an otoscopic exam look like for otosclerosis?

A

Almost always normal
Schwartze sign (vascularization of the actively growing bony growth which is reflected through the TM as a reddish discoloration) in the early stages

178
Q

What will pure tone audiometry look like in the early stages of otosclerosis?

A

Normal or mild conductive loss with rising configuration

179
Q

What will pure tone audiometry look like in the middle stages of otosclerosis?

A

Conductive/mixed hearing loss with rising or flat configuration

180
Q

What will pure tone audiometry look like in the later stages of otosclerosis?

A

Flattening of the previously rising conductive or mixed hearing loss

181
Q

Is it uncommon to see a mixed hearing loss with otosclerosis?

A

No, especially in older adults
Due to presbycusis accompanying the long standing otosclerosis

182
Q

If the loss is purely conductive, will it exceed 60 to 65 dB HL?

A

No

183
Q

What is the bone conduction thresholds for otosclerosis?

A

Poorer at 2000 Hz by 15 to 20 dB HL with narrowing of ABG (carhart’s notch)
Only present in < 40% of patients

184
Q

Why does carhart’s notch occur?

A

Possibly due to the mechanical effects of the disease itself
The effect of the stapes fixation on the ME resonance
Changes on how the stapes moves

185
Q

Is carhart’s notch unique to otosclerosis?

A

No, it is also seen in patients with ossicular fixation and incudostapedial joint detachment
Also seen in osteogenesis imperfecta

186
Q

What tymps can you get with otosclerosis?

A

You can have A or As (low admittance and narrow gradient)

187
Q

Is otosclerosis the only ME condition that can give you normal tymps?

A

Yes

188
Q

What do the acoustic reflexes look like for otosclerosis?

A

Abnormal
Reduced stapes mobility which attenuates stimulus intensity and makes acoustic reflex production difficult
Cannot do reflex decay

189
Q

What is the tone decay (retrocochlear sign) result for otosclerosis?

A

Negative

190
Q

What will speech audiometry look like for otosclerosis?

A

SRT is consistent with the PTA
WRS is good

191
Q

Is surgical management used for otosclerosis?

A

Yes
A conductive component of at least 25 dB HL between 250 to 1000 Hz (pre-op)
A negative rinne at 512 Hz

192
Q

For otosclerosis, do bigger ABG have a better prognosis after surgery?

A

Yes

193
Q

For bilateral otosclerosis, are the ears operated on at the same time?

A

No
The poorer ear is operated on first and the second ear is operated on at least one year later if the operated ear remains stable

194
Q

What are surgical indications?

A

These are signs that you need surgery

195
Q

Is SNHL in the contralateral ear a contraindication to a stapedectomy?

A

No, but it does require thoughtful consideration because the otosclerosis ear will have SNHL if unsuccessful

196
Q

What are some contraindications to surgery for otosclerosis?

A

A dead contralateral ear
Active otitis externa or media or TM perf
Large exostosis that may affect access to ME
Rarely, otosclerosis may involve the endolymphatic duct and present as menieres (which is an absolute contraindication of surgery)

197
Q

What are some things that consider careful consideration before otosclerosis surgery?

A

Patients for whom vestibular function is critical for employment
otologic problems in contralateral ear that may threaten hearing overtime
SSCD syndrome

198
Q

What is a stapedotomy?

A

A small hole made in the stapes footplate during surgery

199
Q

What is a partial stapedectomy?

A

Half removal of the stapes footplate during surgery

200
Q

What is a total stapedectomy?

A

Total removal of stapes footplate during surgery

201
Q

What is a prothesis or implant used in stapes surgery?

A

A stainless steel, titanium, platinum, or teflon piston to replace the stapes footplate
Don’t cause problem with MRI

202
Q

Is there a difference in the success rate/outcome between stapedotomy and stapedectomy procedures?

A

No

203
Q

Can stapedotomy and stapedectomy be performed under local anesthesia or general anesthesia?

A

Yes

204
Q

How long does the surgery take?

A

About 30 to 45 minutes
Laser surgery now used to vaporize parts of the stapes
The remainder is removed with an instrument

205
Q

Are current prosthesis for stapes safe for MRI?

A

Yes
Up to 1.5 tesla
Titanium, platinum, and plastic are compatible at all strengths

206
Q

What is the failure rate of the surgery?

A

About 1 to 3%
Can result in a profound SNHL

207
Q

What are some complications for surgery?

A

WRS sometimes worsens (up to 30%) if there was cochlear involvement (decreased hearing sensitivity at 4000 Hz)
Oval window otosclerosis - cannot be easily managed with a laser and surgery takes longer
Round window otosclerosis - can cause permanent CHL (removal results in SNHL)

208
Q

Is hyperacusis also a complication of surgery?

A

Yes
Often temporary

209
Q

Is facial paralysis/weakness also a complication?

A

Yes
Due to VII N damage during surgery (rare)
If the facial nerve is completely filling the oval window niche, surgery may have to be aborted

210
Q

May the chorda tympani nerve have to be sacrificedin stapes surgery?

A

Yes
It is the branch of the VII N to the anterior 2/3 of the tongue
Temporary decreased taste/sensation for 3 to 6 months but then other nerves take over

211
Q

Is a perilympatic fistula surgery also a complication?

A

Yes
It is a pathologic communication between the inner ear and the ME
Most commonly occurs at either the oval or round window
May occur during the early or late postop period

212
Q

What does perilymphatic fistulas result in?

A

Results in fluctuating, sudden, and progressive SNHL, vertigo, as well as others (tinnitus, disequilibrium, and aural fullness)

213
Q

Is labyrinthitis also a complication for stapes surgery?

A

Yes, rare but serious
Vertigo during or immediately after surgery is indicative of labyrinthine insult
may be caused by air or blood entering the vestibule or mechanical trauma to the utricle (lies close to oval window)

214
Q

Is disarticulation of the incus also a for stapes surgery complicaiton?

A

Yes
Can occur during surgery
May require a prothesis if complete disarticulation occurs

215
Q

Is SNHL also a complciation?

A

Yes
Attributed to surgical trauma in 1% of cases

216
Q

Is immediate CHL also a complication for stapes surgery?

A

Yes
Malfunction of prothesis
Failure to recognize malleus fixation
Round window obliteration
ME effusion
SSCD (conductive hearing loss can be found)

217
Q

Can a delayed onset CHL be a complication?

A

Yes
Occurs in 5% of patients of successful stapedectomy
Most common cause of erosion of the long process of the incus and displacement of the prothesis

218
Q

What is a non-surgical option?

A

Amplification

219
Q

Why might surgery not be an option?

A

Age
Health issues
Patient refuses surgery for any reason

220
Q

Do patients with otosclerosis do well with amplification as the hearing aid provides the amplification the ME system cannot?

A

Yes
Need to counsel them on this

221
Q

What is the differential diagnosis for otosclerosis?

A

Meniere’s disease (dizziness/vertigo, tinnitus, low frequency hearing loss SNHL in meniere’s)
Osteogenesis imperfecta
SSCD (thinning/absence of part of bone in SSC, low freq CHL (250 to 1000 Hz), unlike otosclerosis ARTs are normal in SSCD, can be distinguished by CT scan)

222
Q

What is the etiology of trauma?

A

Blow to the side of the head/falls
Sports injuries
Blast injuries
Motor vehicle accidents
Foreign body insertion such as q-tips (ossicular disarticulation can occur, can result in dead ear if punctures inner ear)

223
Q

Can the inner ear be involved in trauma too?

A

Yes
Can result in SNHL with accompanying ME damage like TM perf, ossicular disarticulation, and hemotympanum (blood in the tympanic cavity)

224
Q

What is the etiology of ossicular disarticulation?

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 ossicles
Untreated ME infection that can destroy ossicles

225
Q

What does the ice cream cone sign mean?

A

Normal ossicles
Ball of the ice cream is the head of the malleus and the bone is the body of the incus

226
Q

What does ossicular disarticulation look like on a CT?

A

Like the ice cream fell off the cone

227
Q

What does otoscopy look like for ossicular disarticulation?

A

Otoscopy depends on the cause of the disarticulation
Perf
Bleeding in the ear canal with perf
Rarely, the TM and the canal will appear normal

228
Q

What are the audiologic findings for ossicular disarticulation?

A

Ad tymp
Abnormal reflexes
Conductive/mixed loss

229
Q

What is the treatment for ossicular disarticulation?

A

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

230
Q

How common is temporal bone trauma in head injuries?

A

30 to 75%

231
Q

Does the temporal bone require a significant amount of force to sustain a fracture?

A

Yes, it is very dense

232
Q

How do the majority of temporal bone injuries occur?

A

Occur as part of multiple injuries following a motor vehicle accident

233
Q

Besides motor vehicle accidents, what else causes temporal bone trauma?

A

Industrial accidents (anything related to industry)
Recreational injury
Falls
Assaults
Gunshot wounds
Self-inflicted injuries

234
Q

What are the two types of temporal bone trauma?

A

Trauma with fracture and trauma without fracture

235
Q

What are the kinds of traumas with fractures?

A

Blunt trauma with fracture
Longitudinal fractures
Transverse fractures
Penetrating temporal bone trauma

236
Q

What are longitudinal fractures?

A

Direct blow to the temporal/parietal aspect
Most common
Parallels long axis of the temporal bone in coronal plane
Passes through the postero-superior aspect of the EAC, TM, and roof of ME
Disrupts ossicles but generally spare otic capsule

237
Q

What is a transverse fracture?

A

Commonly due to a blow to the occiput
Less common
Extends through internal auditory canal or otic capsule
Can affect oval or round window

238
Q

Are most temporal bone fractures longitudinal or transverse?

A

No, most are mixed (50 to 75%)

239
Q

What are pediatric temporal bone fractures caused by?

A

Falls from a height
Automobile-pedestrian accidents

240
Q

What is the most common cause of penetrating temporal bone trauma?

A

Gunshot wounds

241
Q

What are some of the injuries that result from gunshot wounds?

A

Trauma to major blood vessels
Destruction of middle and inner ear
Destruction of cranial nerves
Facial nerve injured 50% of the time (facial paralysis immediate)

242
Q

What are the kinds of trauma without fracture?

A

Otitic barotrauma
Inner ear decompression sickness
Thermal injuries
Compressive injuries
Foreign objects

243
Q

What is otitic barotrauma?

A

Injury sustained from failure to equalize pressure
Air travel and scuba diving
Often occurs during compression (decent)
Causes sudden and severe negative ME pressure and trauma

244
Q

What is inner ear decompression sickness?

A

Occurs during decompression (ascent) and shortly after surfacing from dive
Closely resembles barotrauma
More common among commercial and military divers who breathe compressed oxygen

245
Q

What are some symptoms of inner ear decompression sickness?

A

Hearing loss
Tinnitus
Dizziness

246
Q

Should patients with inner ear decompression sickness be transported to a hyperbaric chamber for recompression?

A

Yes
Significant correlation between early recompression and recovery

247
Q

What are thermal injuries?

A

Injuries sustained during welding leading to TM perf
Another means is a lightning bolt through phone

248
Q

What are some symptoms of thermal injuries?

A

SNHL
Dizziness
Facial paralysis from devitalized bone and soft tissue

249
Q

What are 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

250
Q

What can bomb explosions cause?

A

Disruption and implosion of TM
High freq SNHL due to disruption of inner ear

251
Q

What are foreign objects?

A

Caused by patients trying to remove cerumen

252
Q

What can result from foreign objects?

A

Localized laceration, hemotoma, infection of EAC and TM
Injuries can extend to the ME and inner ear resulting in hearing loss

253
Q

What are the auditory signs of injury?

A

Acute or delayed CHL
Clotted blood, debris, and hemotoma in canal
Perforated, lacerated, or completely disrupted TM
ME filled with blood or CSF
Ossicular disarticulation
Ossicular fixation due to fibrous adhesions
High incidence of SNHL

254
Q

What are the vestibular symptoms of injury?

A

BPPV
Concussive injury to labyrinth resulting in vestibular symptoms
Perilymphatic fistula

255
Q

What are the facial nerve symptoms of injury?

A

80 to 90% of longitudinal fractures result in facial nerve paralysis
Bony spicules hitting the nerve and bruising

256
Q

What is the treatment for hemotympanum?

A

Self-healing in 4 to 6 weeks
Myringotomy to drain is not recommended
Risk of infection

257
Q

What is the treatment for TM perf?

A

Self-healing
Observe
Make sure edges don’t get infected (may result in cholesteatoma)
If healthy perf persists, myringoplasty can be performed

258
Q

What is the treatment for persistent CHL?

A

Exploration and repair of ossicles
Amplification if surgery not an option

259
Q

What is the treatment for irreversible SNHL and tinnitus?

A

Hearing aids and tinnitus management

260
Q

What is the the treatment for vestibular symptoms?

A

Mostly self-limiting resolving within 6 months

261
Q

What is the treatment for BPPV?

A

Typically self-limiting resolving within 3 months
If not resolved, treatment needed

262
Q

What is the treatment for otitic meningitis?

A

Always a concern for an open structure
Can complicate things
May occur within months or years
Treated with antibiotics based on culture results

263
Q

What are paragangliomas (glomus tumors)?

A

The most common benign soft tissue tumor of the ME
Rarely malignant
2nd most common benign tumor of the temporal bone

264
Q

What are the two categories of glomus tumors?

A

Glomus tympanicum and glomus jugulare

265
Q

Are glomus tumors inherited?

A

They can be sporadic or AD with 100% penetrance

266
Q

Is genomic imprinting involved in glomus tumors?

A

May be
Affected individuals inherit the disease from their father but expression of the phenotype may not be observed in off-springs of affected females

267
Q

If glomus tumors are inherited, is there a sex predisposition?

A

No

268
Q

If glomus tumors are sporadic, is there a sex predisposition?

A

Yes
More females affected

269
Q

Are glomus tumors reported in some cases of NF1?

A

Yes

270
Q

Do patients usually present with glomus tumors after the 5th decade of life?

A

Yes

271
Q

Do the majority of glomus tumors appear to be sporadic?

A

Yes

272
Q

Are approximately 1/3 to 1/2 of cases associated with an inherited syndrome (like NF1)?

A

Yes

273
Q

How many genes have been proven to have association with glomus tumors?

A

10 with or without pheochromocytoma

274
Q

What is pheochromocytoma?

A

Tumor of adrenal glands
Because of hormones secreted, the symptoms are life threatening HBP, sweating, rapid heartbeat, and headache

275
Q

What is a globus tympanicum?

A

Arise from promontory of ME
Smaller and cause early symptoms as they are growing with narrow confines

276
Q

What are the signs and symptoms of globus tympanicum?

A

Pulsatile tinnitus because of the tumor vascularity is often the first symptom
Tympanic membrane may appear red
Lateral growth through TM can mimic a bleeding polyp
Growth of tumor can inhibit ossicular mobility (CHL)
Medal growth towards inner ear can cause SNHL, facial nerve dysfunction, and vertigo

277
Q

What is the treatment for glomus tympanicum?

A

Surgery
Complete tumor removal is seen in over 90% of cases

278
Q

What are glomus jugulare?

A

Tumors that arise from the dome of the internal jugular vein or proximal portion of arnold’s or jacobson’s nerve

279
Q

Are glomus jugulare more common and extensive than glomus tympanicum?

A

Yes
More space to grow

280
Q

How do glomus jugulare grow?

A

They remain silent for years and tend to grow quite large
Grow through the floor of the ME and incorrectly present as glomus tympanicum
Grow anywhere in the temporal bone and blood vessels in the neck

281
Q

Which cranial nerves are affected by glomus jugulare?

A

VII and XII

282
Q

How do you get a definitive diagnosis of glomus jugulare?

A

MRI

283
Q

What are some symptoms of large glomus jugulare?

A

Hearing loss
Otalgia
Aural fullness
Vertigo (if involvement of vestibular division of VIII N)
Hoarseness and dysphasia due to involvement of CN IX, X, and XI (proximal to site)
Involvement of VII N indicates more extensive disease (farthest away)

284
Q

What are otoscopy findings of glomus jugulare?

A

Red mass filling ME cavity or lower portion of ME cavity may be visible

285
Q

What are the pure-tone audiometry findings of glomus jugulare?

A

CHL may be present depending on size of tumor and ossicle involvement
Sometimes mixed HL if neural involvement has occurred

286
Q

What are the immattance findings of glomus jugulare?

A

As tymps if tumor is big and pressing on TM
B tymps if large tumor on TM renders TM immobile
Can show jagged edges that correspond with pulse

287
Q

Should a pulsating tymp suspect a glomus tumor?

A

Yes

288
Q

What is the treatment for glomus jugulare?

A

Surgery or radiation
Surgery can be difficult and have complications
Radiation can reduce tumor size and delay occurrence of nerve deficits prior to surgery

289
Q

Where do glomus tympanicums arise?

A

Along the course of jacobson nerve primarily in the tympanic cavity

290
Q

Where do glomus jugulare arise?

A

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

291
Q

Do both glomus tympanicums and jugulare show slow progressive growth spreading through path of least resistance such as temporal bone air cells and ET?

A

Yes

292
Q

When does diagnosis usually occur after initial occurrence of glomus tumors?

A

4 to 10 years
Can grow to large proportions

293
Q

Are glomus tumors unilateral usually?

A

Yes

294
Q

What are other characteristics of glomus tumors?

A

Reddish-purple
Highly vascular
Lobulated

295
Q

Do glomus tumors arise from paraganglia cells?

A

Yes

296
Q

What are paraganglia cells?

A

Small groups of flat, oval, vascular paraganglionic bodies connected with the ganglia of the sympathetic nervous system
Exist throughout temporal bone

297
Q

Were these tumors originally believed to be from the glomus complexes?

A

Yes, hence the name

298
Q

Jacobson’s nerve

A

One of the places that a glomus tumor can arise
Glomus tympanicum

299
Q

Arnold’s nerve

A

Branch of the vagus nerve
Causes the cough reflex
Can also be a site for golmus tumors

AUDE 5410 - Acquired Auditory-Vestibular Disorders (11 decks)

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