Ear disorders Flashcards

1
Q

PE of ear?

A
  • pull auricle up, back and out
  • visualize canal as you put speculum in
  • use largest speculum canal will accommodate - avoid touching the bony walls (inne 2/3rds) with speculum - can be painful
  • stabilize examining hand against pts head
  • landmarks should be visible: umbo, handle of malleus, light reflex, TM
  • check mobility: pneumatic attachment of otoscope or valsalva maneuver - observe for motion and pain
  • color variations
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2
Q

How is CN 8 tested?

A
  • eval hearing - pt responding to questions
  • whispered voice test
  • ticking watch
  • weber/rinne
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3
Q

What is ETD (eustachian tube dysfxn)?

A
  • blockage of ET: ET doesn’t open or close properly in response to pressure changes within middle ear or outside ear, failure of system at proximal end (ET, palate, nasal cavities, and nasopharynx) to regulate the middle ear and mastoid gas cell system at its distal end
  • acute ETD may occur in setting of pressure chagnes (flying) or acute URI, or sinusitis
  • chronic ETD may lead to negative middle ear pressure, retracted TM, serous effusions, otitis media, adhesive otitis media, or cholesteatoma
  • Patulous ET (PET) - floppy, failure of ET to close. Often manifested as autophony, when individual’s own breathing and voice sounds excessively loud
  • sxs affected: auditory
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4
Q

Fxns of the ET?

A
  • ventilation/regulation of middle ear pressure
  • protection from nasopharyngeal secretions
  • drainage of middle ear fluid
  • ET is closed at rest and opens with yawning, swallowing, and sneezing
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5
Q

Pressure equalization of ET?

A
  • normally ET closed, but can open to let small amt of air through to prevent damage by equalizing pressure b/t middle ear and atm
  • pressure differences cause CHL by decreased motion of TM and ossicles of the ear
  • various methods of ear clearing such as yawning, swallowing, chewing gum or performing the valsalva meneuver may be used intentionally to open tube and equalize pressure
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6
Q

Cycle of ETD?

A

structural or fxnl obstruction of ET compromises 3 fxns:

  • negative prssure develops in middle ear
  • serous exudate is drawn from the middle ear mucosa by negative pressure or refluxed into middle ear if ET opens momentarily
  • infection of static fluid causes edema and release of inflammatory mediators, which exacerbates cycle of inflammation and obstruction
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7
Q

Epidemiology of ETD?

Considerations in peds?

A
  • most common in children under 5
  • usually decreases with age but may persist into adulthood in some

ETs more horizontal in kids - troubles with ventilation and drainage, shorter ET predisposes to reflux

  • can be associated with URI, adenoid hypertrophy, allergic rhinits, or GERD
  • refer to ENT if hearing loss or recurrent or chronic middle ear infections
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8
Q

RFs for ETD?

A

adults and peds:

  • tobacco and pollutant exposures
  • GERD
  • allergy
  • chronic sinusitis
  • sleep apnea with cont positive airway pressure use
  • adenoid hypertrophy or nasopharyngeal mass
  • neuromusc. disease
  • family hx
  • altered immunity
  • early onset of hx of ETD as child
  • Native american, inuit, australian aborigine (shorter neck)
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9
Q

Pediatric risk factors for developing ETD?

A
  • seond hand smoke
  • prematurity and low birth wt
  • young age
  • craniofacial abnormalities (cleft palate, down syndrome)
  • day care, exposure to many other kids
  • crowded living situations
  • low socioeconomic status
  • prone sleeping position
  • prolonged bottle use
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10
Q

Commonly assoc conditions with ETD?

A
  • hearing loss
  • middle ear effusion
  • cholesteatoma
  • allergic rhinitis
  • chronic sinusitis
  • URI
  • adenoid hypertrophy
  • GERD
  • cleft palate
  • down syndrome
  • obesity
  • nasopharyngeal carcinoma or other tumor
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11
Q

Tx of ETD?

A
  • initiate tx based on individual pt’s sxs and possible cause
  • decongestants: OTC, avoid prolonged use over 3 days, avoid in pts with HTN or cardiac risk factors:
    phenyledphrine (sudafed PE)
    pseudoephedrine (sudafed)
    oxymetazoline (afrin)
- nasal steroids: may be beneficial for those with allergic rhinitis
beclomethaasone (beconase, vancenase)
budesonide (rhinocort)
flunisolide (nasarel, nasalide)
fluticasone (flonase)
ciclesonide (omnaris)
  • 2nd gen H1 antihistamines (allergic rhinitis):
    claritin, clarinex, allegra, zyrtec
  • antihistamine nasal sprays:
    olotpatadine (patanase), astelin
  • abx: not used unless ETD is assoc with acute OM:
    amoxicillin 1st line, tx 10 days
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12
Q

What tx should be considered if TM perforation or ventilation tube present?

A
  • consider topical abx drops with topical steroid in setting of d/c alone
    neomycin-polymyxin-hydrocortisone suspension (cortisporin)
  • ciprofloxacin-hydrocortisone suspension (cipro HC)
  • pain control, anti-inflam: acetaminophen, NSAIDs
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13
Q

Diff categories of otitis media?

A
  • acute - AOM
  • recurrent AOM: 3 or more in 6 months or 4 or more in 1 yr
  • otitis media with effusion (OME)
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14
Q

What is otitis media?

A
  • an infection of middle ear with acute onset, presence of middle ear effusion (MEE), and signs of middle ear inflammation
  • 75% of children havehad at least one episode by 3
    peak incidence: 6-18 months
    male greater than female
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15
Q

RFs for otitis media?

A
  • bottle feeds while supine
  • day care
  • formula feeding
  • smoking in house
  • male gender
  • family hx of middle ear disease
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16
Q

Signs and sxs of otitis media?

A
  • earache (discomfort, pressure), otalgia - infection worsens and so does discomfort
  • tugging on ears
  • fever, most afebrile
  • accompanying URI sxs
  • irritability
  • difficulty sleeping
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17
Q

What will you see on otoscope exam in otitis media?

A
  • decreased visibility of landmarks
  • TM mobility decreases
  • bulging TM, opaque, red
  • pus in middle ear (bacteria in MEE)
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18
Q

Dx of AOM?

A
- note sxs in taking hx of illness:
discomfort, ache, pain
fever
tugging at ears
hearing loss
- bulging, usually erythematous TM which doesn't move on pneumatic otoscopy
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19
Q

Bacterial culprits of otitis media?

A
  • strep pneumo (30-35%)
  • H flu (20-25%): up to 50% produce beta-lactamases
  • M cat: 10-15%: 90% produce beta-lactamases
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20
Q

Expected course/prognosis of otitis media?

A
  • sxs usually spontaneously resolve in 2/3 of children by 24 hrs and 80% at 2-10 days
  • children tx immediately with abx had one less day of sxs (majority viral or small amt of bacteria)
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21
Q

Tx of otitis media?

A
- abx tx:
amoxicillin (strep pneumo)
augmentin
cephalosporins
erythromycin, azithromycin

-tx of pain and fever:
ibuprofen, tylenol, auralgan
(no aspirin in kids)

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22
Q

F/u of otitis media?

A
  • failure to improve after 48-72 hrs of abx - confirm dx, eval other causes, determine if new abx is warranted
  • resolved sxs - reexamined 14-21 days after initial presentation - resolution of infection
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23
Q

Managment guidelines of AOM?

A
  • most cases improve spontaneously
  • cases that require tx may be managed with abx and analgesics or observation alone
  • acetaminophen or ibuprofen should be rx with or w/o abx
  • abx should be rx for bilateral or unilateral AOM in children aged at least 6 m with severe signs or sxs and for nonsecure, bilateral AOM in children 6-23 months
  • in unilateral nonsevere AOM - make jt decision with parents to either give abx or close f/u
  • amoxicillin is abx of choice, unless CI
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24
Q

What is OME? Sxs?

A

-serous otitis media - glue ear, presence of MEE in absence of acute signs of infection

sxs of OME:

  • hearing loss
  • fullness in ear
  • tugging at ear or inserting finger in ear (trying to open ear)
  • delayed speech and language development or unclear speech
  • in young children, an unsteady gait may occur
  • pain rarely occurs
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25
Q

What will you see on otoscope exam if pt has an OME?

A
  • TM is dull, retracted (usually not bulging)
  • no mobility of TM
  • straw or tan color of ear drum or translucent gray
  • sterile fluid in middle ear
  • pneumatic otoscopy: single most recommended dx method to establish dx of OME
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26
Q

Tx of OME?

A
  • watchful waiting:
    no tx for 3 months after onset
    no hearing testing in first 3 months, 75-90% resolve spontanteously in 3 months, if middle ear effusion lasts longer than 3 months, 30% resolve within 12 months
  • during this period do the following:
    speak closely to child
    face child when speaking
    repeat phrases when needed, seating in front of classroom
  • meds are of no use, antihistamines, decongestants aren’t recommended, abx and steroids don’t have long term efficacy
  • hearing testing: after 3 months should be done, language testing should be conductd with children with hearing loss
  • surveillance: re-exam at 3-6 month intervals until effusion is resolved, hearing loss is ID’d, or structural abnormal of TM or middle ear are suspected
  • surgery: tympanostomy and tube
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27
Q

What is chronic suppurative otitis? Cause? risks?

A
  • a perforated TM with persistent drainage from middle ear
    chronic otorrhea (longer than 6-12 weeks) through a perforated TM
  • cause: initial episode of acute infection:
    cycle: inflammation - ulceration - infection - granulation of tissue
  • risks:
  • hx of multiple episodes of AOM
  • living in crowded conditions
  • daycare
  • being a member of large family
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28
Q

Bacterial culprits of chronic suppurative otitis?

sequela?

A
  • pseudomonas aeruginosa (50-98%)
  • staph aureaus (15-30%)
  • klebsiella and proteus

-sequela:
conductive hearing loss
intracranial complications

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29
Q

Presentation of chronic suppurative otitis?

A
  • continually draining ear (otorrhea), fever, pain, vertigo may indicate intracranial or intratemporal complications
  • external canal may/may not be edematous
  • usually not tender
  • granulation tissue often seen in medial canal of middle ear space
  • middle ear mucosa visualized thru perforated TM may be edematous, polypoid, pale or erythematous
  • d/c: fetid, purulent, cheeselike to clear and serous
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30
Q

Studies done for chronic suppurative otitis?

A
  • labs: culture for drainage for sensitivity
  • imaging: CT, MRI
    usually not done unless suspecting neoplasm, cranial complications, or unresponsive to medical tx
  • audiogram: hearing loss
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31
Q

Tx of chronic suppurative otitis?

A
  • removal of exudate from canal tissue: 50% peroxide with sterile water (w/o pressure)
  • abx otics
  • systemic abxs (reserved for failed cases): cipro PO
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32
Q

What is cholesteoma? Cause?

A
  • skin growth that occurs in middle ear behind the eardrum: takes form of cyst or pouch, sheds layers of old skin, increases in size and destroys surrounding delicate bones of the middle ear

Cause:
repeated infection
poor ET fxn

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33
Q

Presentation of cholesteoma?

A
  • otorrhea
  • feeling of fullness or pressure in ear
  • hearing loss
  • achy ear (esp at night)
  • dizziness
  • facial weakness on affected side (CN 7 involvement)
34
Q

Dx testing and tx of cholesteoma?

A
  • dx testing:
    otoscopy, audiometry, xray, and CT of mastoid may be necessary (recurrent infections - rule out mastoiditis)
    -refer to ENT
  • tx: surgical
35
Q

What is otitis externa?

Causes?

A
  • inflammation of EAC or auricle
  • causes:
    infectious
    allergic
    dermal disease
36
Q

Major risk factors for developing OE?

A
  • swimming
  • using Q tips
  • ask pts if they have been swimming lately, using q tips, been scratching at ear?
37
Q

Bacterial culprits of OE?

A
  • staph aureus
  • pseudomonas (swimmers ear)
  • proteus
38
Q

Signs and sxs of OE?

A
  • otalgia
  • pain at tragus or when auricle is pulled
  • pruritis
  • d/c
  • hearing loss
39
Q

What will you see on otoscopic exam of OE?

A
  • edematous and erythematous ear canal
  • may see yellow, brown, white, or grey debris
  • shouldnt be any middle ear fluid
  • TM should be mobile
40
Q

Tx of OE?

A
  • cleaning of ear canal:
    irrigate with 1:1 dilution of 3% hydrogen peroxide at body temp (gently)
  • protect ear canal from water (could be perforated)
  • tx of inflammation and infection (always use soln if you havent confirmed an intact TM):
    cortisporin, cipro HC, tobradex
41
Q

What is malignant external otitis necrotizing otitis externa?

A
  • invasive infection of EAC and skull base
  • typically occurs in elderly with DM
  • increasing in AIDS pts
  • immunocompromised pts
  • caused by pseudomonas aeruginosa (95%)
42
Q

Clinical manifestations, otoscopic exam and complications of malignant external otitis necrotizing otitis externa?

A
  • clinical manifestations: exquisite otalgia and otorrhea; pain is more severe than external otitis
  • otoscopic exam: granulation in inferior portion of EAC
  • complications: osteomyelitis of the base of skull, mastoiditis, TMJ osteomyelitis: cranial nerve palsies - 5,7,8
43
Q

Dx and tx of malignant OE?

A
  • elecated ESR
  • positive culture
  • imaging
  • tx:
    cipro 750 mg PO bid for 6-8 weeks, no role for topical abx (long term tx to ensure no residual infection - lead to osteomyelitis)
44
Q

Clinical manifestations of TM perforation?

A
  • clear, pus filled or bloody drainage from ear
  • sudden decrease in ear pain followed by drainage from that ear
  • hearing loss
  • tinnitus
45
Q

Causes of TM perforation?

A
  • middle ear infection
  • airplane ear (barotrauma)
  • acoustic trauma: direct injury, ear being struck
  • fbs in ear
  • loud, sudden noise: explosion or firearm
  • hearing loss may be great, tinnitus is severe
46
Q

Tx of TM perforation?

A
  • most heal on their own
  • usually no abx or topicals, but can consider cortisporin otic or cipro HC otic
  • keep ear dry
  • ear drum patch
  • tympanoplasty: if large perforation
47
Q

What is barotrauma? causes?

A
  • usually begins with ETD, either congenital of acquired mucosal edema
  • most common cause: flying - descent is worse than ascent
  • similar results from diving
48
Q

Clinical manifestations of barotrauma?

A
  • pressure in ear
  • pain due to stretching of TM
  • hearing loss
  • tinnitus
49
Q

Tx and prevention of barotrauma?

A
  • tx:
    valsalva maneuver
    decongestants
    myringotomy
  • prevention:
    avoidance,
    pre flight decongestants,
    chewing gum, yawning or swallowing during descent
50
Q

Why shouldn’t you irrigate origanic foreign bodies (beans, insects)?

A
  • because you can’t tell if TM is perforated or not
51
Q

Tx of fb in ear?

A
  • can be difficult to remove
  • attempts can push fb further in canal and lodge it
  • adequate visualization, appropriate equipment, cooperative pt, and skilled provider are keys to successful fb removal
  • otherwise referral to ENT
52
Q

Cerumen impaction removal?

A
  • most often cerumen impaction is self-induced
  • diff techniques:
    hydrogen peroxide
    debrox
    irrigation
    suction
  • irrigate water at body temp - to not induce vertigo
  • stream should be directed at ear canal wall adjacent to cerumen plug
  • irrigation should only be performed when TM is known to be intact
53
Q

What is mastoiditis?

A
  • complication of otitis media
  • evolves following several weeks of inadequately tx AOM
  • develops when middle ear inflammation spreads to mastoid air cells, resulting in infection and destruction of mastoid bone
  • characterized by:
    postauricular pain and erythema, spiking fever, and tender mass
54
Q

Dx and tx of mastoiditis?

A
  • ENT consult
  • CT scan
  • MRI if intracranial involvement is suspected
  • ENT will get myringotomy fluid for culture, acid fast and gram stain
    audiogram b/f and after tx
- pt admission for IV abx:
immed abx tx (21 days) -
-ceftriaxone (rocephin)
-piperacillin and tazobactam sodium (zoysn)
- oxacillin (bactocill)
- gentamicin (garamycin)
55
Q

What is an acoustic neuroma (vestibular schwannoma)?

A
  • usually unilateral
  • 5% assoc with neurofibromatosis type 2 (bilateral)
  • median age ate dx: 50
  • are benign lesions but grow to eventually compress the pons resulting in hydrocephalus
56
Q

RFs of developing an acoustic neuroma?

A
  • exposure to loud noise
  • neurofibromatosis type 2
  • hx of parathyroid adenoma
  • cell phones (probs not)
57
Q

Sxs of an acoustic neuroma?

A
  • sxs due to CN involvement, cerebellar compression and tumor progression
  • cochlear nerve: hearing losss and tinnitus
  • vestibular nerve: unsteadiness while walking
  • trigeminal: facial numbness, and hypesthesia and pain
  • facial nerve: facial paresis, and taste disturbances
58
Q

Dx of acoustic neuroma?

Tx?

A
  • demonstration of asymmetric SNHL or other CN deficits
  • determine this by Weber and Rinne
  • MRI or CT
  • ENT referral
  • audiometry
  • tx: surgery
59
Q

What is vertigo?

A
  • sx of illusory movement (you think you are moving but you aren’t, room is spinning)
  • appears as:
    transient spinning dizziness
    sense of swaying or tilting
    sense of falling backwards
60
Q

What is vertigo caused by?

A
  • asymmetry in vestibular system due to damage to or dysfxn of labyrinth, vestibular nerve or central vestibular structures in brainstem
61
Q

Sxs of peripheral vertigo?

A
  • sudden onset of vertigo
  • nystagmus usually horizontal with rotary component, fast phase usually beats away from diseased side
  • visual fixation inhibits nystagmus
  • blurred vision
  • fatigue, HA
  • palpitations
  • imbalance
  • inability to concentrate
  • increased risk for motion sickness
  • N/V
  • reduced cognitive fxn sensitivity to bright lights and noise
  • sweating (symp. stim)
62
Q

Sxs of central vertigo?

A
  • onset of vertigo is gradual
  • nystagmus can be in any direction, usually vertical
  • visual fixation doesn’t stop nystagmus
  • other signs of brainstem dysfxn
  • instability
  • diplopia
  • HA (may be severe)
  • impaired consciousness
  • inability to speak due to muscle impairment (dysarthria)
  • lack of coordination
  • N/V
  • weakness
63
Q

What is BPPV?

A
  • dizziness is thought to be due to debris which has collected within a part of the inner ear, this debris is called otoconia (ear rocks), these are small crystals of calcium carbonate derived from the utricle (helps determine body’s position in space)
  • the utricle may have been damaged by head injury, infeciton, or other disorder of the inner ear, or may have degenerated b/c of advanced age. Normally otoconia appear to have slow turnover
  • they are probably dissolved naturally as well as actively reabsorbed by dark cells of labyrinth
64
Q

Sxs of BPPV?

tests to determine BPPV?

A
  • recureent and brief episodes (less than 1 min)
  • predictable head movements or positions precipitate sxs
  • horizontal nystagmus
  • no neuro or auditory sxs
  • DIx-hallpike maneuver is best for determining BPPV
  • romberg
  • weber-rinne tests
65
Q

What is the Dix-hallpike maneuver?

A
  • person is brought from sitting to supine position, with head turned 45 degrees to one side and extend about 20 degrees backwards
    • dix-hallpike test consists of burst of nystagmus, the eyes jump upward as well as twist so that the top part of the eye jumps toward the down side
66
Q

Tx of BPPV?

A
  • wait it out
  • epley maneuver: particle repositioning or canalith repositioning procedure
  • involves sequential movement of head into 4 positions, staying in each position for 30 seconds
  • the recurrence rate for BPPV after these maneuvers is 30% at one year, some instances 2nd tx may be necessary
67
Q

What is labyrinthitis?

clinical course, cause?

A
  • inflammation of the inner ear
  • clinical course:
    vertigo: sensation of spinning or whirling - that may be severe enough to cause N or V
  • gradually goes away over period of several days to weeks
  • may be accompanied by hearing loss, which is usually temporary
  • cause isn’t clear, often triggered by URI (viral), less often may develop after middle ear infection
68
Q

How is labyrinthitis tx?

A
  • usually goes away on its own
  • normally takes several weeks
  • meds may also be used to control N and V caused by vertigo:
    prochlorperazine (compazine)
    meclazine (antivert)
    diazepam/lorazepam
69
Q

What is Meneire’s (endolymphatic hydrops0?

clinical presentation?

A
  • results from distension of endolymphatic compartment of inner ear
  • backed up fluid in the endolymphatic sac elads to swelling and pressure and this distorts balance and sound information
  • clinical presentation:
    episodic vertigo lasting 1-8 hrs, rotary or rocking, can be assoc with N/V
  • low frequency SNHL
  • tinnitus: low tone and blowing
  • sensation of aural pressure
70
Q

Dx criteria for Meniere’s?

A
  • 2 spontaneous episodes of rotational vertigo lasting at least 20 minutes
  • audiometric confirmation of SNHL
  • tinnitus and/or perception of aural fullness
  • literature suggests testing pt for syphilis
71
Q

Tx of meniere’s?

A
  • dietary restrictions:
    caffeine, tobacco, salt
  • meds:
    diuretics, antiemetics, anxiolytics, antihistamines, scopolamine (used for sea sickness)
72
Q

What is presbycusis?

A
  • referes to SNHL in elderly
  • involves bilateral high frequency hearing loss assoc with difficulty in speech discrimination and central auditory processiong of information
73
Q

How can presbycusis be devastating to elderly pt?

A
  • elderly pop relies on special senses to compensate for other age assoc disabilities
  • elderly may rely on hearing to overcome limitations of impaired vision, and slowed rxn time
  • age assoc decline in concentration and memory contribute to diff understanding speech, especially in noisy situations
  • arthritis and impaired dexterity may limit abilty to use hearing aids
  • hearing loss may contribute to isolation of some elderly people by restricting their use of the phone, causing them to foreit social opportunities such as social gatherings, and amplifying their sense of disability
74
Q

PP of presbycusis?

A
  • histologic changes assoc with aging occur throughout auditory system from hair cells of cochlea to auditory cortext in temporal lobe of brain
  • these changes may correlate with diff clinical findings and auditory test results, depending on severity of changes at anatomic level at which they occur
75
Q

What is sensory presbycusis?

A
  • epithelial atrophy with loss of sensory hair cells and supporting cells in organ of corti
76
Q

What is neural presbycusis?

A
  • atrophy of nerve cells in cochlea and central neural pathways
  • atrophy occurs throughout the cochlea, with basilar region only slightly more predisposed than the remainder of the cochlea
77
Q

What is metabolic (strial) presbycusis?

A
  • condition results from atrophy of stria vascularis
  • stria vascularis normally maintains the chemical and bioelectric balance and metabolic health of cochlea
  • atrophy of stria vascularis results in hearing loss represented by flat hearing curve b/c the entire cochlea is affected
78
Q

Mechanical (cochlear conductive) presbycusis?

A
  • condition results from thickening and secondary stiffening of the basilar membrane of the cochlea
  • the thickening is more severe in basal turn of the cochlea where the basilar membrane is narrow
79
Q

How common is presbycusis?

A
  • 25-30% of people aged 65-74 have impaired hearing

- people 75 and older - 40-50%

80
Q

Clinical presentation of presbycusis?

A
  • varies from pt to pt and is result of various combos of cochlear and neural changes that have occurred
  • pts typically may have more difficulty understanding rapidly spoken language, vocab that is less familiar or more complex, and speech within a noisy, distracting enviro
  • localizing sound is increasingly difficult as disease progresses
81
Q

Tx of presbycusis?

A

-amplification devices: properly fitted hearing aids may contribute to rehab of pt with presbycusis
older pts with arthritis and visual difficulties need extra help in learning to use hearing aids
pts using hearing aids may still experience difficulties with speech discrimination in noisy situations

  • lip reading: may help pts with diminished speech discrimination and may help hearing aid users who have difficulty with noisy environments
  • cochlear implants: pts with cochlear changes and relatively intact spiral ganglia and central pathways appear to be the best of candidates
  • assistive listening devices: range from simple amplification of telephone signal to device on tv that sends signal across room to headset worn by pt
  • pt can amplify sound w.o disturbing others
82
Q

F/u with pt that has presbycusis?

A
  • these pts require routine f/u care with an otolaryngologist and audiologist to monitor hearing thresholds, order changes in amplification device specifications as hearing thresholds change and monitor pt for other signs and sxs of ear disease that individuals with impaired hearing may overlook