Awareness
LSTN Editorial Team · Editorially overseen by Dan McCoy
Ototoxicity is the property of certain medications to damage the inner ear, specifically the cochlea and vestibular system. The damage can be permanent. Knowing which drug classes carry risk, and what to ask your prescriber, is a reasonable precaution.
Ototoxic medications damage the hair cells of the cochlea, the stria vascularis (the cochlear structure responsible for maintaining the ionic environment hair cells need), or the vestibular hair cells that govern balance. The damage is sometimes dose-dependent; for other agents it can be idiosyncratic and unpredictable.
Because cochlear hair cells don't regenerate in humans, ototoxicity-related hearing loss is often permanent. The vestibular effects (dizziness, imbalance) can sometimes partially recover, but cochlear damage typically does not.
Ototoxicity monitoring (baseline and serial audiological testing before and during treatment with known high-risk drugs) is standard of care in oncology but considerably underutilized in other clinical settings.
Aminoglycoside antibiotics (gentamicin, tobramycin, streptomycin, amikacin) are used for serious bacterial infections, particularly in hospitalized patients. Cochlear toxicity is cumulative and often permanent. Applied as ear drops with an intact eardrum, they're generally safe; the risk is with systemic (intravenous) administration. Genetic variants (particularly in the MT-RNR1 mitochondrial gene) dramatically increase individual susceptibility.
Platinum-based chemotherapy, cisplatin in particular, causes permanent sensorineural hearing loss in a significant proportion of patients. High-frequency loss is typical and often occurs during treatment. Carboplatin is less ototoxic. Sodium thiosulfate is being studied as a protective agent in some pediatric protocols.
Loop diuretics (furosemide, ethacrynic acid), high-dose salicylates (aspirin above ~3g/day), and some antimalarials (quinine, chloroquine) round out the most commonly implicated classes. Loop diuretics typically produce reversible effects at standard doses; the risk increases significantly when combined with aminoglycosides. Aspirin at standard cardiovascular doses (81–325 mg/day) poses minimal ototoxic risk.
If you are being prescribed an aminoglycoside antibiotic or cisplatin-based chemotherapy, ask: 'Is baseline audiological testing planned? How will my hearing be monitored during treatment? What are the early signs of ototoxicity I should report?'
If you already have documented hearing loss, mention it. Some prescribers will prefer less ototoxic alternatives when a patient has pre-existing auditory vulnerability, particularly if the clinical indication allows flexibility.
If you develop new tinnitus, muffled hearing, or a sense of fullness in the ears during any medication, report it promptly, even if it's not a listed side effect. Earlier dose adjustment or drug substitution can sometimes limit the extent of permanent damage.
Formal monitoring involves audiograms at baseline, at regular intervals during treatment, and after treatment ends. Extended high-frequency audiometry (testing frequencies above the standard 8,000 Hz range) detects early cochlear changes before they appear in speech frequencies.
Clinically significant change is typically defined as a 20 dB shift at any single test frequency, a 10 dB shift at two or more consecutive frequencies, or a new loss of response at two or more consecutive frequencies. When these thresholds are crossed, the clinical team adjusts the treatment protocol.
If you are receiving a drug with known ototoxic potential and monitoring has not been offered, it is reasonable to ask your oncologist or infectious disease physician why, and whether audiological monitoring is indicated in your case.
Common Questions