w7 Flashcards
Cochleotoxic
: results in cochlear damage and CN VIII; auditory dysfunction
Vestibulotoxic
results in damage to vestibular end organs & CNVIII; vestibular dysfunction
ototoxic Symptoms
Tinnitus (typically)- constant, high pitch
SNHL (typically)- High freq with progression to mid/low freq (most agents); mid frequency (loop diuretics); difficulties understanding speech in noise
Vestibular dysfunction: disequilibrium, imbalance, vertigo & nystagmus
- may go unnoticed by patients until a communication problem becomes apparent
2 main classes responsible for permanent otoxic damage:
- aminoglycoside antibiotics
- antineoplastic (chemotherapeutic)- may be reversable initially
aminoglycoside antibiotics
resistant bacterial infections, induced vestibulotoxcity for relief of vestibulopathy
antineoplastic medications
tumor treatment
Diuretics
management of excess body fluid
Drug administration
Systemic application (bilateral effects): affecting whole body (i.e., intramuscular, intravenous, oral
Topical (unilateral affects): skin or mucous membrane application, apply drug to specific target
Cochlea (unilateral effects) Round window: drug applied to surface of round window
Direct perfusion: invasive procedure by injecting drug directly into perilymph or endolymph
Salicylates
pain, anti-inflammatory
ototoxic incidence
Incidence varies depends on definition of ototoxity, classification of medication & drug type (loop 1-6% and antineoplastic drug cisplatinum 25-90% , dosage schedule
- ototoxic drugs can induce stress signals which initiate cell death occurring via 2 mechanisms (which interact)
necrosis and apoptosis
apoptosis HC death
apoptosis: active, programmed cell death, controlled process by which cells self-destruct
- no inflammation of neighbouring tissue
necrotic HC death
Necrosis: passive form of cell death, unregulated release of cellular debris into the intracellular space
- neighbouring phagocytes find difficulty in locating and eliminating cell by-products (immune response)
oxidative stress
when free radicals are floating around causing stress on cell until they find electron they are looking for; free radicals start to steal electrons from other cells
stress signalling in auditory haircell death
- Oxidative stress: occurs early in the damage process
- Accumulation of intracellular free radicals in the form of reactive oxygen species (ROS) and reactive nitrogen species (RNS)
- Oxidative stress results from an imbalance between ROS and antioxidants
- Excess ROS and RNS cause damage by reacting with DNA, proteins, cytosolic molecules, cell surface receptors, and breaking down membrane lipids - Expression of extracellular pro-inflammatory cytokines & other cell death signals
aminoglycosides
Damage is progressive affecting serval different cochlear structures with OHC most sensitive (then IHC then spiral ganglion, stria vascularis & support cells), base more sensitive than apex (progress from high to low frequencies)
- May be cochleotoxic or vetsibulotoxic or both
- Permanent SNHL
- Individual susceptibility may be inherited
cispaltin
used for cancer
- Highest ototoxic potential
- Earliest symptoms: tinnitus and high freq hearing loss
- Irreversible bilateral SNHL progress from high to low freq.
- OHC and stria vascularis most susceptible to damage
- Base more sensitive than apex
- Severe degeneration: support cells, collapse of Reisner’s membrane, eventual destruction of entire organ of corti replaced by epithelium
side effects of cisplatin
ototoxicity, nephrotoxicity, neuropathies, nausea, vomiting
carboplatin
similar to cisplatin but incidence of SNHL lower, mixed OHC and IHC damage
carboplatin chinchilla model
IHC most susceptible with sig. loss, ohc damage occurs with later progression (ONLY Found in chinchilla)
loop diuretics
treat fluid volume overload
Ototoxicity low incidence of HL compared to aminoglycosides and antineoplastics
- Tinnitus, usually reversable SNHL, risk of permanent loss with cumulative dose
- Known to exacerbate aminoglycoside and cisplatin ototoxicity
Anatomical changes: stria vascularis: edema, damage/swelling of hair cells
criteria for sig changes
- > 20dB pue tone threshold at 1 freq
- > 10dB shift at 2 consecutive test frequencies
- > 5 db shift at 3 adjacent test freq.
- If pre-existing profound loss: threshold shift to “no response” at 3 consecutive test frequencies
- Confirmed by re-test
audiological outcomes of ototoxicity
bilateral decline in thresholds (usually), progress from high to low frequencies, behavioural and physiological responses (OAEs, ABR) deteriorate in pattern reflecting damage to cochlea
Monitoring program baseline evaluation
no later than 24 hours after chemotherapeutic
No later 72 hours after aminoglycoside antibiotics
Ototoxicity medical examination
History; other medications, chemical and/or noise exposure
Physical exam: tinnitus, hearing loss, vestibular dysfunction: nystagmus
Additional assessment: audiology, vestibular, radiology if retrocochlear damage suspected
salicylate
(Asprin)- anti-inflammatory effects
Ototoxicity usually reversable, tinnitus, high frequency or flat SNHL, no clear affects on anatomy, temporary threshold shift and OAE temporarily altered
Possible pathophysiological effects: OHC motility, auditory synapse
acute SSNHL
- Very sudden onset of unilateral SNHL that may be accompanied by acute vertigo, aural fullness/pressure and tinnitus
- Medical emergency
criteria for ssnhl
unliateral hl of 30dB or more in 3 adjacent frequencies
- Rapid progression occurring within 72 hours of initial symptoms
SSNHL incidence
5-27/100 000 in us ; about 1% of all SSNHL
SSNHL age
40-60 year olds
sex differences
none Male=Female
etiology
unknown 90% idiopathic; identifiable causes are neoplastic, infectious (autoimmune, neurologic, ototoxicity)
idiopathic SSNHL
rapid onset
- Not explained by other identifiable cause
audiologic assessment for SSNHL
Clinical features: SNHL is usually unilateral, sudden & rapid, progressive (<3days) additional symptoms: vertigo, aural fullness, tinnitus
Comprehensive audiologic evaluation: behavioural and objective tests
- Rule out retrocochlear involvement (immittance with acoustic reflexes, OAE, ABR)
why is SSNHL an emergency
better prognosis if treatment starts early, rule out stroke
case history SSNHL
: critical to diagnosis which is based on exclusion of other known causes
Goal is to rule out: specific treatable infections (bacterial or viral), cardiovascular/stroke, labyrinthine membrane rupture (trauma or barotrauma), mass lesions (retrocochlear) autoimmune (systematic or inner ear specific), ototoxicity
imaging for SSNHL
to rule out cerebellopontine angle tumors, MS, vascular compromise, malformations
laboratory evaluations SSNHL
may be considered when specific disorder is suspected (thyroid function test, bacterial infection, autoimmune disease)
idiopathic SSNHL medical treatments
- Varies with underlying condition but majority of cases are peripheral auditory (vestibular) disorder classified as idiopathic (likely viral)
- Systemic steroids (e.g. prednisone) to reduce ear inflammation
- Intratympanic steroids
- Hyperbaric oxygen therapy
order of treatment for idopathic SSNHL
Initial is systemic prednisode then follow up treatment with corticosteroid into ME (intratympanic delivery)
- HBOT recommended as initial with steroids or as salvage treatment for SSNHL
prognosis trends
Delay in steroids=poorer prognosis
Age: younger people more favourable recovery
Mild low frequency HL recovery better than mild high frequency
Severe to profound loss=poor prognosis
audiologic monitoring of SSNHL
Monitor patients for: effect of treatment & recovery in affected ear, SNHL in contralateral ear, development of associated diseases (autoimmune)
- Aural rehab for hearing that does not improve
Following stabilization of hearing thresholds for SSNHL what do we do and when is stabilization
3-6 months)
o Consider amplification if residual SNHL
o CROS if no residual hearing
o ALDs
o Cochlear implant
