High-Yield Ototoxicity (NEET PG Focus)
Cochleotoxic vs. Vestibulotoxic Agents
| Drug Class / Agent | Primary Target / Mechanism | Clinical Manifestation |
|---|---|---|
| Aminoglycosides | Destruction of outer hair cells in the Organ of Corti & crista ampullaris. Wide individual variation. | Cochleotoxic: Amikacin, Neomycin, Kanamycin. Vestibulotoxic: Gentamicin, Streptomycin. |
| Platinum Compounds (Cisplatin, Carboplatin) |
Outer hair cell degeneration starts at the basal turn of the cochlea. | Bilateral, irreversible, high-frequency SNHL; often accompanied by severe tinnitus. |
| Loop Diuretics (Furosemide, Ethacrynic acid) |
Edema and ion transport disruption in the Stria Vascularis. | Usually **reversible** hearing loss, but the risk multiplies exponentially if co-administered with aminoglycosides. |
| Salicylates / Aspirin | Inhibition of prestin (outer hair cell motor protein) & altered cochlear blood flow. | **Reversible** bilateral Tinnitus (often the first sign of toxicity) and mild-to-moderate flat SNHL. |
NEET PG “Must-Know” Pearls
- Mitochondrial Mutation (
): Individuals with the maternal A1555G mutation have extreme susceptibility to aminoglycoside-induced ototoxicity, even after a single standard dose.
- Audiometric Feature: Earliest changes manifest as high-frequency sensorineural hearing loss (
). Standard clinical pure tone audiometry (up to
) may miss early toxicity, making **Otoacoustic Emissions (OAE)** and high-frequency audiometry preferred monitoring choices.
- Thalidomide: Historically high-yield teratogen that causes external/middle ear anomalies along with phocomelia.
- Antimalarials (Quinine/Chloroquine): Cause vasoconstriction in cochlear capillaries, leading to a temporary or permanent sensorineural deficit and high-pitched tinnitus.