Step 1 of 14
Identify the At-Risk Patient
Flag every patient on an ototoxic drug — aminoglycosides, platinum, loop diuretics, vancomycin, salicylates, antimalarials
Ototoxicity begins not with a symptom but with a prescription, and the first task is to recognise that a patient is receiving — or is about to receive — a known ototoxic agent. The major classes are the aminoglycosides (gentamicin, tobramycin, amikacin, kanamycin, neomycin), platinum chemotherapy (cisplatin, and to a lesser degree carboplatin), the loop diuretics (furosemide, bumetanide), vancomycin and macrolides (erythromycin), the salicylates (high-dose aspirin), the antimalarials (quinine, chloroquine), and topical otologic preparations containing aminoglycosides (neomycin drops, especially through a non-intact tympanic membrane).
The agents differ in their target and their reversibility: aminoglycosides are both cochleotoxic and vestibulotoxic and their injury is largely permanent; cisplatin is profoundly cochleotoxic, cumulative, and permanent; while loop diuretics and salicylates are typically reversible on withdrawal. Recognising the class therefore predicts the pattern of injury and the monitoring it demands. Because the damage is so often irreversible, identifying the at-risk patient at the point of prescribing — rather than at the point of complaint — is the single most important step, since it is the only one that opens the door to prevention.
- Aminoglycosides (gentamicin, tobramycin, amikacin, kanamycin, neomycin) — cochleo- AND vestibulotoxic, permanent
- Platinum (cisplatin > carboplatin) — cumulative, high-frequency, permanent; loop diuretics & salicylates — usually reversible
- Also vancomycin, erythromycin, quinine/chloroquine, topical neomycin drops (non-intact TM)
- Recognise the class at prescribing — it predicts the injury pattern and the monitoring needed
★ High-yield pearls (chapter-wide)
- Prevention is the most effective treatment for ototoxicity — once the hair cells are gone they do not regenerate, so the whole algorithm is built around avoiding, minimising, and catching injury early rather than reversing it.
- Extended high-frequency hearing loss precedes speech-frequency loss, and tinnitus is often the earliest symptom — monitoring only the standard audiogram detects ototoxicity too late to act on.
- A baseline audiogram and vestibular assessment before the first ototoxic dose is non-negotiable — without it, every later 'change' is uninterpretable and the chance to intervene early is lost.
- The ASHA criteria define a real ototoxic shift — a ≥20 dB drop at one frequency, a ≥10 dB drop at two adjacent frequencies, or loss of response at three consecutive frequencies, each confirmed on a repeat test.
- Gentamicin is the great vestibulotoxin — it can destroy both labyrinths and leave the patient with oscillopsia and imbalance while hearing is relatively preserved, so vestibular monitoring matters as much as the audiogram.
- Cisplatin ototoxicity is cumulative, bilateral, high-frequency, and largely permanent — risk climbs with total dose, young age, renal impairment, and concurrent noise or radiation, and it is the cancer-survivorship sequela that follows the patient for life.
- Sodium thiosulfate given 6 hours after cisplatin roughly halves the incidence of hearing loss in children with localised disease — but it must not be used where it could reach and protect the tumour, because in disseminated disease it was associated with worse survival.
- DPOAEs can flag cochlear injury before the conventional audiogram changes, and they are invaluable in young children and anyone who cannot give reliable behavioural thresholds.
- The mitochondrial m.1555A>G (MT-RNR1) variant predisposes to severe, sometimes single-dose aminoglycoside deafness and is maternally inherited — a family history of aminoglycoside-induced hearing loss should change the antibiotic.
- Cochlear implantation is highly effective for severe-to-profound bilateral ototoxic deafness, and vestibular rehabilitation is the cornerstone for bilateral vestibulopathy — permanent loss is managed, not abandoned.
Evidence base
2 sources- HIGH
Lester GM, Konrad-Martin D, Dille MF · Int J Audiol · 2024Guideline reviewPMID 38062855
Reviews current ototoxicity-monitoring guidelines, including baseline-and-surveillance protocols, extended high-frequency and otoacoustic-emission testing, and the ASHA criteria for a significant ototoxic threshold shift.
- HIGH
Rutka J · Adv Otorhinolaryngol · 2019ReviewPMID 30947191
Reviews aminoglycoside vestibulotoxicity — especially gentamicin's capacity to cause bilateral vestibular loss with relatively preserved hearing — and the rehabilitation-led management of the resulting oscillopsia and imbalance.
Decision tree
A baseline before the first dose and risk stratification set the frame; ASHA-criterion surveillance detects the shift; and the offending drug, the injury pattern, and the phenotype route the patient to one of ten pathways — from prevention to rehabilitation.