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 Definition
 Damage to the cochlea or vestibular apparatus from
exposure to a chemical source
 Many sources
 Mercury
 Herbs
 Streptomycin
 Dihydrostreptomycin

 Gentamicin
 Others
 Streptomycin, kanamycin, neomycin, amikacin, gentamicin, tobramycin,

sisomycin, netilmicin
 Enter into inner ear by unknown mechanism

 Secreted into the perilymph by spiral ligament or

endolymph by stria vascularis
 Diffuse through round window membrane
 Cochlear toxicity
 Amikacin, kanamycin, neomycin, netilmicin

 Vestibular toxicity
 Streptomycin, gentamicin, sisomycin
 Cochlear toxicity
 Increase of 10-20 dB in thresholds of one or more frequencies
 Incidence (6-13%), netilmicin lowest
 Risk factors
 Diuretics, renal failure, prolonged treatment, old age, preexisting SNHL
 Infants less affected, once daily dosing
 Cochlear toxicity presentation
 High frequency SNHL first, then lower frequencies to profound loss
 Not reversible
 Damage usually heralded by tinnitus
 Vestibular toxicity
 Dynamic posturography can detect
 Clinically
 Ataxic gait, lose balance when turning
 Bobbing oscillopsia
 Prevention
 Consider less ototoxic drugs (netilmicin)
 Identify “high-risk” patients
 Audiogram before and weekly after starting
 ENG prior if possible
 History and physical exam daily (Romberg, VA)
 Adjust doses or switch drugs if toxic
 Erythromycin

 Clinically
 Hearing loss with/without tinnitus– 2 days
 All frequencies, recovery after stopping
 Rarely permanent (hepatic)
 Vancomycin
 Believed to be ototoxic (no data)

 Penicillin, sulfonamides, cephalosporins
 May have topical toxicity in middle ear
 Ethacrinic acid, furosemide, bumetaside
 Clinically (6-7%)
 Usually tinnitus, temporary and reversible SNHL, rare vertigo within

minutes
 High doses can cause permanent SNHL
 Highest risk– coadministration of aminoglycosides
 Most common OTC drugs in US
 Mechanism
 Normal histology (no hair cell loss)
 Decreased blood flow, decreased enzymes

 Clinically
 Tonal, high frequency tinnitus (7-9 kHz)
 Reversible mild to moderate SNHL (usually high frequency)– rarely

permanent
 Similar clinical findings with aspirin
 Clinically
 High-pitched tinnitus
 Reversible, symmetric SNHL
 Occasional vertigo
 Mechanism
 Decreased perfusion, direct damage to outer hair
cells, biochemical alterations
 Cisplatin
 Incidence is high (62%-81%)
 Pathologically
 Outer hair cell degeneration

 Clinically
 Bilateral symmetric SNHL, usually high frequency– not reversible,

cumulative
 Risks factors– age extremes, cranial irradiation, high dose therapy, high
cumulative dose
 Polymixin B (Brummett)
 Chloramphenicol (Patterson)
 Neomycin (Brummett)
 Gentamicin (Webster)

 Ticarcillin (Jakob)
 Vasocidin (Brown)
 Ciprofloxacin (Lenarz)
Ototoxicity

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Ototoxicity

  • 1.
  • 2.  Definition  Damage to the cochlea or vestibular apparatus from exposure to a chemical source  Many sources  Mercury  Herbs  Streptomycin  Dihydrostreptomycin  Gentamicin  Others
  • 3.  Streptomycin, kanamycin, neomycin, amikacin, gentamicin, tobramycin, sisomycin, netilmicin  Enter into inner ear by unknown mechanism  Secreted into the perilymph by spiral ligament or endolymph by stria vascularis  Diffuse through round window membrane
  • 4.  Cochlear toxicity  Amikacin, kanamycin, neomycin, netilmicin  Vestibular toxicity  Streptomycin, gentamicin, sisomycin
  • 5.  Cochlear toxicity  Increase of 10-20 dB in thresholds of one or more frequencies  Incidence (6-13%), netilmicin lowest  Risk factors  Diuretics, renal failure, prolonged treatment, old age, preexisting SNHL  Infants less affected, once daily dosing
  • 6.  Cochlear toxicity presentation  High frequency SNHL first, then lower frequencies to profound loss  Not reversible  Damage usually heralded by tinnitus
  • 7.  Vestibular toxicity  Dynamic posturography can detect  Clinically  Ataxic gait, lose balance when turning  Bobbing oscillopsia
  • 8.  Prevention  Consider less ototoxic drugs (netilmicin)  Identify “high-risk” patients  Audiogram before and weekly after starting  ENG prior if possible  History and physical exam daily (Romberg, VA)  Adjust doses or switch drugs if toxic
  • 9.  Erythromycin  Clinically  Hearing loss with/without tinnitus– 2 days  All frequencies, recovery after stopping  Rarely permanent (hepatic)
  • 10.  Vancomycin  Believed to be ototoxic (no data)  Penicillin, sulfonamides, cephalosporins  May have topical toxicity in middle ear
  • 11.  Ethacrinic acid, furosemide, bumetaside  Clinically (6-7%)  Usually tinnitus, temporary and reversible SNHL, rare vertigo within minutes  High doses can cause permanent SNHL  Highest risk– coadministration of aminoglycosides
  • 12.  Most common OTC drugs in US  Mechanism  Normal histology (no hair cell loss)  Decreased blood flow, decreased enzymes  Clinically  Tonal, high frequency tinnitus (7-9 kHz)  Reversible mild to moderate SNHL (usually high frequency)– rarely permanent
  • 13.  Similar clinical findings with aspirin  Clinically  High-pitched tinnitus  Reversible, symmetric SNHL  Occasional vertigo  Mechanism  Decreased perfusion, direct damage to outer hair cells, biochemical alterations
  • 14.  Cisplatin  Incidence is high (62%-81%)  Pathologically  Outer hair cell degeneration  Clinically  Bilateral symmetric SNHL, usually high frequency– not reversible, cumulative  Risks factors– age extremes, cranial irradiation, high dose therapy, high cumulative dose
  • 15.  Polymixin B (Brummett)  Chloramphenicol (Patterson)  Neomycin (Brummett)  Gentamicin (Webster)  Ticarcillin (Jakob)  Vasocidin (Brown)  Ciprofloxacin (Lenarz)