Ototoxicity

Ototoxicity is toxicity to the inner ear and vestibular apparatus caused by certain drugs or chemicals. It commonly presents as sensorineural hearing loss, tinnitus, or balance disturbances. The onset can be gradual or rapid, and high-frequency hearing is often affected first. The effect may be temporary or permanent and is typically related to dose and duration of exposure.

Mechanisms include damage to cochlear hair cells, the stria vascularis, or spiral ganglion neurons. Injury may arise from oxidative stress, mitochondrial dysfunction, and disruption of ionic homeostasis in the endolymph and perilymph. Vestibular toxicity can produce vertigo, disequilibrium, and nystagmus.

Key ototoxic agents include aminoglycoside antibiotics (eg, gentamicin, tobramycin, amikacin), platinum-based chemotherapies (cisplatin, carboplatin), loop diuretics (furosemide, ethacrynic acid), and glycopeptides such as vancomycin. High-dose salicylates and other drugs may contribute. Risk is higher with renal impairment, older age, preexisting hearing loss, longer therapy, and concurrent use of multiple ototoxic drugs.

Diagnosis relies on baseline audiometry before starting exposure and regular follow-up audiometry during treatment, with high-frequency testing and otoacoustic emissions when available. Vestibular testing is indicated if dizziness or imbalance develops. Management centers on minimizing exposure by dose adjustment or drug substitution, and providing rehabilitation for hearing loss (hearing aids, cochlear implants) or balance therapy as needed.

Prevention emphasizes cautious use, therapeutic drug monitoring where applicable, hydration, and avoidance of unnecessary combination exposure. Early detection improves the chance of reversibility and functional recovery, though prognosis varies by agent and individual risk factors.