A 35-year-old woman on long-term furosemide therapy develops sudden bilateral symmetric high-frequency sensorineural hearing loss. The mechanism of furosemide-induced ototoxicity is:

• A Damage to outer hair cells via reactive oxygen species
• B Inhibition of Na-K-2Cl cotransporter (NKCC1) in the stria vascularis, reducing endocochlear potential ✓
• C Direct toxicity to spiral ganglion neurons
• D Interference with neurotransmitter release at the hair cell synapse

Explanation

Loop diuretics (furosemide, ethacrynic acid) cause ototoxicity by inhibiting the Na-K-2Cl cotransporter (NKCC1) in the marginal cells of the stria vascularis. This transporter is essential for K+ secretion into the endolymph and for maintaining the +80 mV endocochlear potential. When inhibited, the endocochlear potential falls, impairing hair cell transduction. The hearing loss from loop diuretics is typically reversible if the drug is stopped early. Aminoglycosides, by contrast, cause permanent SNHL through reactive oxygen species damage to outer hair cells.

Reference: Dhingra Diseases of Ear, Nose and Throat, 7th ed.

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Written and medically reviewed by the StethoPrep medical team.