wk 12, lec 3 Flashcards
15% of people 20-69 have some degree of
high frequency hearing loss due to noise
Outer and inner hair cells are damaged by noise, but the outer are more vulnerable
presbycusis
Presbycusis (age-induced) hearing loss is likely due to a combination of neuronal loss and hair cell loss
what substances are ototoxic (toxic to hearing) and what do they damage
Antibiotics, chemotherapeutic agents, diuretics are often implicated
- Many of these substances damage either the outer hair cells or the stria vascularis
conductive hearing loss vs sensorineural hearing loss
Conductive hearing loss is typically caused by physical blockages or abnormalities in the outer or middle ear, and is often treatable with medical or surgical interventions.
Sensorineural hearing loss is usually permanent, caused by damage to the cochlea or auditory nerve, and may require assistive devices like hearing aids or cochlear implants for management.
conductive hearing loss vs sensorineural hearing loss which frequencies are effected
conductive= all frequencies
sensorineural= higher frequencies
conductive hearing loss
impaired sound transmission in the external or middle ear, impacts all frequencies
conductive hearing loss causes
Trauma to the tympanic membrane, infection, plugging of the external auditory meatus/canal, otosclerosis, cholesteatoma
sensorineural hearing loss causes
▪ Presbycusis (age-induced), ototoxic agents, noise (most common)
▪ Problems with endolymph (Meniere’s), infections of the labyrinth or 8th CN, tumours (acoustic neuroma, brainstem tumours)
weber and rinne tests in sensorineural hearing loss
Rinne: AC > BC,
Weber: lateralizes to unaffected ear
weber and rinne tests in conductive hearing loss
Rinne: BC > AC,
Weber: lateralizes to affected ear
what frequency can humans hear? what is speech range?
- Human ear can hear from 20 – 20000 Hz
▪ We’re best at hearing 1000 – 4000, human speech ranges
from 500 – 2000 Hz
what does audiometry assess
- Audiometry assesses hearing at particular tones and is much better at characterizing hearing loss than tuning fork tests
what is the main cause of otitis externa
90% of otitis externa is bacterial
▪ Usually staphylococcal, pseudomonas
aeruginosa, or E. coli
risk factors for otitis externa
Humidity, loss of cerumen (trauma, excessive Q-tip use), heat, increased pH (the ear should be acidic for barrier immunity), obstruction of the ear canal, exposure, water with bugs
clinical features of otitis externa
otalgia
ottorhhea
itchy
▪ Edema → occlusion of the ear canal →
conductive hearing loss
▪ Severe infection can lead to cellulitis (deeper layers, skin involvement)
hearing loss in otitis externa
conductive
treatment for otitis externa
topical antibiotics
▪ Make sure not to use ototoxic antibiotics with a perforated TM
4 types of otitis externa
- furunculosis
- chronic otitis externa
- malignant/necrotizing otitis externa
- otomycosis
what is the worst form of otitis externa (medical emergency )
malignant/necrotizing otitis externa
furunculosis (type of otitis externa)? cause?
otitis externa of the outer 1/3 of the ear canal, usually staphylococcal
chronic otitis externa cause
less painful, more itchy
▪ Usually caused by repetitive trauma, chronic drainage from a
middle ear infection
malignant/necrotizing otitis externa
▪ Progressive, slowly developing infection, severe otalgia, lots of otorrhea, granulation/necrotic tissue in the auditory canal
* Can be life-threatening if the infection colonizes temporal bone, intracranial structures
* Cranial nerve palsies and systemic infection also possible
who is malignant/ necrotizing Otitis externa more common in
More common in the elderly, diabetics, immunocompromised
– usually P. aeruginosa
otomycosis (type of otitis externa)? cause?
fungal infection of the external auditory canal, up to 10% of otitis externa
▪ Usual agent is Aspergillus (80%), next most common is Candida species
▪ More likely in:
* Diabetes, elderly, past history of HEENT surger in the
mastoid
▪ Often seen in those with poor response to antibacterial antibiotics
acute otitis media symptoms
rapid onset of signs and symptoms, including fever and otalgia
recurrent acute otitis media
3 or more episodes within a 6-month period or four or more episodes within a 12-month period - complete resolution of symptoms between episodes
cause of acute Otitis media
Usually due to auditory tube dysfunction
- Up to age 7, eustachian tube is shorter, wider, and more horizontal than in adults – predisposes to upper airway/oral bacteria colonization
- Blockage of the tube – swelling of adenoid lymphatic tissue, swelling due to URTI or allergic rhinitis, inadequate tensor palatini function
- Lack of breastfeeding (breast milk has antimicrobial sustances in it)
pathogenesis of acute otitis media
▪ Obstruction of the auditory tube → air absorbed in middle ear→negative pressure→edema of mucosa with exudate and fluid accumulation→infection from nasopharyngeal secretions
bacteria and viruses causing acute otitis media
Major bacteria implicated: H. influenzae, S. pneumoniae, M. catarrhalis
▪ Major viruses implicated: RSV, influenza, parainfluenza, adenovirus
clinical features of acute otitis media - what is the triad
▪ Triad of otalgia, fever, and conductive hearing loss
* Rare to have tinnitus, vertigo, or facial nerve paralysis
▪ Otorrhea can occur if the TM is perforated
▪ Bulging, red TM (middle ear inflammation)
▪ Often the TM is opaque, bony landmarks are lost
▪ effusion can often be seen behind it, and mobility is limited (pneumatoscopy)
type of hearing loss in acute otitis media
conductive
otitis media with effusion (serous otitis media) cause
▪ Often due to untreated or unresolved AOM
- Persistent effusion in up to 40% of children 30 days after initial AOM, continued for 3 months in 10%
- Main concern in pediatric population is impact on hearing at early ages (prior to a year)
▪ Delay in language development
otitis media with effusion type of hearing loss
conductice
otitis media with effusion clinical feautres
▪ Conductive hearing loss with or without tinnitus
▪ Feeling of fullness in the ear, low-grade fever
▪ May or may not involve otalgia
otitis media with effusion on otoscope
▪ TM is translucent/gray (limited inflammation)
* Fluid behind the ear, can often see air-fluid levels or bubbles
▪ Loss of light reflex, reduced mobility on pneumatoscopy
treat otitis media?
- Most cases resolve on their own
▪ Tympanostomy tubes can improve hearing
▪ Case-by-case treatment depending on presentation
most common causes of tympanic membrane perforations
▪ Middle ear infections
▪ Trauma – can be barotrauma or physical injury to the ear
clinical features of tympanic membrane perforation
▪ Sudden onset of pain, hearing loss
▪ Can include bloody otorrhea
▪ Vertigo or tinnitus
* Usually transient
how to fix a tympanic membrane perforation
- Perforations usually heal spontaneously – advisable to wear earplugs while swimming, bathing
▪ Postero-superior damage to the TM is more likely to damage the function of ossicles – more urgent referral to the HEENT
what parts of the ear does chronic otitis media affect
both the middle ear and the mastoid cavity
tympanic membrane perforation from
recurrent or chronic ear infections
where is there a disfunction that causes chronic otitis media
Dysfunction of the Eustachian tube is a significant factor in this disease, observed in approximately 70% of patients undergoing middle ear surgery
types of chronic otitis media
- suppurative or serous chronic otitis media
- benign chronic otitis media
suppurative or serous chronic otitis media
describes
character of the drainage through the perforated TM
benign chronic otitis media
“dry” – no active infection
what is the most common cause of chronic otitis media
viral
Viruses usual cause, though bacteria are more likely to contribute in children
▪ Pathogens invade via the external canal → edema, fibrosis, perforation and persistent infection
▪ Can also be a complication of tympanostomy tubes
clinical features of chronic otitis media
▪ Otorrhea
▪ May or may not involve conductive hearing loss, tinnitus, or aural fullness
▪ Can have occasional severe intracranial complications in children
cholesteatomas
non-neoplastic, cystic lesions lined by keratinizing squamous epithelium or metaplastic mucus- secreting epithelium, and filled with debris
where do cholestetomas occur
middle ear
-cysts+ keratin
- Occur in the middle ear, mostly in the posterior-superior region (sometimes called the attic)
- Debris contains mostly keratin, other cellular debris
- Cyst is usually between 1 and 4 cm
three types of cholesteatomas
- primary congenital
- secondary acquired
- primary acquired
primary congenital cholesteatomas
keratined epithelium is “misplaced” into area that should only have bone or simple cuboidal mucosa
what type of hearing loss does cholesteatomas lead to
conductive hearing loss
secondary acquired cholesteatomas
– Traumatic “implantation” of
keratined epithelial cells from the “external-ear” side of the tympanic membrane or auditory canal
* Traumatic causes include blast damage, iatrogenic (surgical, insertion of ear tubes) – not as common as primary acquired
series impacts of cholesteatomas
Can cause serious bony destruction of the temporal bone→ infected cyst gains access to the dura and intracranial structures→meningitis and death
- Cholesteatoma should almost always be removed to avoid this
- Can also migrate and rupture into deep neck structures →another source of potentially life-threatening infection
primary acquired cholesteatomas
– Recent investigations implicate a
combination of chronic inflammation and abnormal TM cell migration
most common cause of cholesteatomas
primary acquired
mostly in adults
pathogenesis of primary acquired cholesteatoma
– Inner surface of the TM consists of respiratory epithelium (simple cuboidal ciliated epithelium with goblet cells) that migrates over its surface in postero- superior direction
– As it migrates more rapidly in response to chronic inflammation, it becomes “stuck” to the incus
* Next stage – mucous accumulates in the pouch→chronic inflammation (often pseudomonas implicated) if it gets infected
* This is followed by implantation/conversion of some of the cells in this cyst to keratinized epithelial cells
– Note that the “outer” surface of the TM is pulled into the cystic structure
* Outer surface formed from keratinized epithelium, not respiratory epithelium
- The “stuck” keratinized cells keep dividing, and continued inflammation is likely linked to:
– Growth of the cystic structure
– Activation of osteoclasts and invasion of the temporal bone
– Conductive hearing loss as the mobility of the ossicles is impaired (remember, the inner surface of the TM got stuck to the incus)
type of hearing loss in primary acquired cholesteatoma
– Conductive hearing loss as the mobility of the ossicles is impaired (remember, the inner surface of the TM got stuck to the incus)
where do primary acquired cholesteatomas develop in
Tend to see them develop in the pars flaccida (postero-superior to handle of malleus) because:
* This is the direction the inner
surface of the TM “likes” to migrate
* This part of the TM has a lot of
resident inflammatory cells
* This area is close to the incus
clinical features of cholesteatomas
-painless otorrhea
- conductive hearing loss
* Rarely vertigo or dysequilibrium may arise due to the inflammatory process within the middle ear or due to invasion of the labyrinth
* Facial nerve palsy, can also result from the inflammatory process or mechanical compression of the nerve
prognosis of choelsteatomas
surgery
will usually have hearing loss post-op
2 types of dizziness
vertiginous (vertigo) [peripheral and central]
non-vertiginous [ organic and functional]
vertigo
The environment seems to be moving
what 2 problems could cause vertigo
- Caused by inner ear or brainstem-cerebellar disorders
– Inner ear = peripheral
– Brainstem-cerebellar = central
organic non-vertiginous dizziness
a pathology that usually involves visual compromise or low blood pressure
functional non-vertiginous dizziness
common in a wide range of mood disorders
benign paroxysmal positional vertigo
Acute attacks of transient rotatory vertigo lasting seconds to minutes initiated by certain head positions
– Accompanied by rotatory nystagmus
what is the most common form of positional vertigo
benign paroxysmal positional vertigo
symptoms in benign paroxysmal positional vertigo
– Symptoms are usually brief, caused by changing head position – Typical history = worsening when getting out of bed,
extending the neck
cause of benign paroxysmal positional vertigo
Usually caused by migration of a free-floating otolith [crystals in the ear] (should not be free-floating, should be attached)
diagnosis of benign paroxysmal positional vertigo
– Dix-Hallpike Positional Testing
* Patient rapidly moved from a sitting position to a supine position with the head hanging over the end of the table, turned to one side at 45° and neck extended 20° holding the position for 20 s
– Onset of vertigo and rotatory nystagmus indicate a positive test for the dependent side
Meniere’s disease vs benign paroxysmal positional vertigo timeline vs vestibular neuronitis
menieres= min to hours
bppv= secs to mins
vn= days to weeks
meniere’s disease
Episodic attacks of tinnitus, hearing loss, and vertigo lasting minutes to hours
cause of meniere’s disease
excess endolymph
– Inadequate absorption of endolymph leads to endolymphatic over-accumulation that distorts the membranous labyrinth
– Usually begins in middle age
triggers of meniere’s disease
Triggered by high salt intake, caffeine, stress, nicotine, and alcohol
- Diagnostic Criteria for Menière’s Disease (must have all three)
– Two spontaneous episodes of
* Rotational vertigo ≥20 min
* Audiometric confirmation of Sensorineural Hearing Loss
* Tinnitus and/or aural fullness
vestibular neuronitis
- Acute onset of disabling vertigo often accompanied by nausea, vomiting, and imbalance without hearing loss that resolves over days leaving a residual imbalance that lasts days to weeks
causes of vestibular neuronitis
– Could be viral, often associated with URTI
acute and convalescent phase of vestibular neuronitis
- Acute phase
– Severe vertigo with nausea, vomiting, and imbalance lasting 1-5 days
– Nystagmus
– Patient tends to veer towards affected side - Convalescent phase
– Imbalance and motion sickness lasting days to weeks
– Spontaneous nystagmus away from affected side
– Gradual vestibular adaptation requires weeks to months
what is labyrinthitis
- Acute infection of the inner ear resulting in vertigo and hearing loss
labyrinthitis causes
- May be serous (viral) or purulent (bacterial)
– Occurs as a complication of acute and chronic otitis media, bacterial meningitis - Bacterial: S. pneumoniae, H, influenzae, M. catarrhalis, P. aeruginosa, P. mirabilis
- Viral: rubella, CMV, measles, mumps, varicella zoster
symptoms of labyrinthitis
- Sudden onset of vertigo, N/V, tinnitus, and unilateral hearing loss
with no associated fever or pain
– Meningitis is a serious complication
acoutsic neuromas effects what cell
Schwann cells that myelinate vestibular and/or cochlear nerve
acoustic neuroma
- Intracranial tumours that develop from Schwann cells that myelinate the vestibular and/or cochlear nerve
– Can take up much of the space of the cerebellopontine angle (80% of tumours in this area are acoustic neuromas)
– Most are from the vestibular component of the nerve
acoustic neuroma can impact brain and nerves?
alway vestibular and/or cochlear nerve
– There’s quite a bit of room in that area of the brain, so often do not elevate intracranial pressure until they are quite large
– Can also impinge on the nearby facial nerve and trigeminal nerve
risk factors for acoustic neuromas
– Neurofibromatosis type II (defective merlin gene)
– Ionizing radiation to the area
clinical features of acoustic neuroma
- Hearing loss by far the most common
– Can be sudden or gradual, constant or fluctuating
– Assume that all unilateral neurosensory hearing loss is due to an acoustic neuroma until proven otherwise - Vertigo is fairly uncommon, but balance difficulties are common
- Facial weakness or numbness due to CN VII or V impingement
- Headache due to elevated intracranial pressure
treatment/prognosis of acoustic neuroma
*Microsurgery or radiation used to treat, generally survival is quite good
* 30 – 80% maintain hearing
