Medication Ototoxicity Checker

Cisplatin is one of the most ototoxic drugs in clinical use. It damages the outer hair cells of the cochlea, particularly affecting high-frequency hearing first. Hearing loss is dose-dependent and cumulative, meaning it worsens with each treatment cycle. Audiological monitoring before and during treatment is strongly recommended. There is now an FDA-approved protective option: sodium thiosulfate (Pedmark), approved in 2022 to reduce the risk of hearing loss in patients 1 month of age and older receiving cisplatin for localized, non-metastatic solid tumors — ask your oncology team whether it applies to your treatment plan.

We have moved carboplatin down from high risk, because it is meaningfully less ototoxic than cisplatin at standard doses — its label reports clinical ototoxicity in about 1% as a single agent and 12% in combination, against 33% for cisplatin in a head-to-head trial. For an adult on standard AUC-based dosing for lung, ovarian or bladder cancer, filing it identically to cisplatin overstated the risk. Two escalations matter though: in higher-than-recommended or transplant-conditioning regimens, and in infants and young children, risk rises sharply — one paediatric series found children under about two and a half years had roughly twelve times the odds. Reviews put paediatric incidence in the 10-30% range. If a child is on carboplatin, ask about audiological monitoring.

Gentamicin is an aminoglycoside antibiotic that is particularly toxic to the vestibular system, causing balance problems, dizziness, and vertigo. It can also damage the cochlea, leading to hearing loss. Risk increases with higher doses, longer treatment, and impaired kidney function. Serum levels should be monitored closely.

Tobramycin is an aminoglycoside antibiotic that can cause permanent damage to the hair cells of the inner ear. Both cochlear (hearing) and vestibular (balance) systems may be affected. Monitoring kidney function and drug levels helps reduce risk.

Amikacin primarily affects cochlear hair cells, with hearing loss typically starting at high frequencies. It is considered one of the more cochleotoxic aminoglycosides. Patients with kidney impairment or those receiving prolonged courses are at greatest risk.

Streptomycin was one of the first antibiotics recognized as ototoxic. It has a strong tendency to damage the vestibular system, causing problems with balance and spatial orientation. Cochlear damage and hearing loss can also occur, especially with prolonged use.

Neomycin is among the most cochleotoxic aminoglycosides, and the practical warning for our readers is specific: neomycin-containing ear drops can damage hearing directly if your eardrum is perforated or you have a ventilation tube, because the drug reaches the inner ear rather than staying in the ear canal. If you have a perforation or a grommet, do not use neomycin drops without an ENT explicitly clearing them — ask for an alternative. Oral neomycin is poorly absorbed in a healthy gut, but absorption rises with damaged bowel or kidney failure. Irrigating wounds or body cavities with it can also produce systemic exposure.

Vancomycin's reputation here is bigger than its evidence. Its FDA label quantifies the entire signal as "a few dozen cases of hearing loss" — across six decades of very heavy worldwide use — and reports them mostly in people given excessive doses, who already had hearing loss, who had kidney impairment, or who were also receiving another ototoxic drug. No study has established that vancomycin on its own damages hearing. Where it clearly does matter is as an amplifier: in children receiving cisplatin, concurrent vancomycin raised the odds of hearing loss by about 60%. Kidney toxicity, not hearing, is what vancomycin gets a dedicated monitoring protocol for. The label does state ototoxicity has occurred and may be transient or permanent, so this is not a zero — but if you are on vancomycin without another ototoxic drug, this is not the thing to worry about.

If you take furosemide as a daily tablet for heart failure or blood pressure, the ototoxicity warnings you find online almost certainly do not describe your situation. The label ties hearing effects specifically to rapid intravenous injection, doses above those recommended, severe kidney impairment, low blood protein, and combination with other ototoxic drugs. Professional guidance classes loop diuretic effects as usually temporary. Two things genuinely worth knowing: furosemide meaningfully amplifies aminoglycoside risk — in children on cisplatin it raised the odds of hearing loss by around 60% — and the label says not to use it alongside ethacrynic acid. Report new tinnitus to your prescriber, but do not stop a heart failure medication over it.

Ethacrynic acid is the most ototoxic of the loop diuretics, and we have kept it at high risk while lowering furosemide. That difference is deliberate: ethacrynic acid has documented permanent deafness, its label explicitly warns against combining it with aminoglycosides, and it is prescribed to a much smaller group — typically people with sulfonamide allergy or significant kidney impairment, who are already higher risk. Most hearing effects are brief, lasting from an hour to a day, but permanent loss has happened. If you have been switched to this because you could not tolerate other diuretics, that is a reasonable trade — just report any hearing change promptly.

Teprotumumab (Tepezza) is an infusion medication for thyroid eye disease. Its prescribing information warns that it may cause severe hearing impairment including hearing loss, which in some cases may be permanent. Clinicians are advised to assess hearing before, during, and after treatment and weigh the benefits and risks with each patient. If you are receiving Tepezza, ask about baseline and follow-up hearing tests.

High-dose aspirin (typically more than 6-8 tablets per day) can cause tinnitus and temporary hearing loss. This is one of the most well-known and predictable ototoxic effects in medicine. The good news is that these effects almost always resolve completely once the dose is reduced or the medication is stopped.

This is better documented than most people realise. Prescription ibuprofen labels list tinnitus as an adverse reaction occurring in more than 1% of patients, with a probable causal relationship assigned, and hearing loss in under 1% on the same basis — so this is a labelled effect, not just a statistical association. Separately, large cohort studies link frequent long-term use to a modest increase in hearing loss risk. Two things keep this in proportion: effects are usually reversible once you stop, and the occasional tablet for a headache is not the pattern implicated. Worth knowing for consistency: the same cohort research implicates regular acetaminophen (paracetamol) at least as strongly as NSAIDs, so switching painkillers is not automatically a fix. If you take ibuprofen most days and notice ringing, that is worth raising with your doctor.

Naproxen labels list tinnitus, visual disturbances and hearing disturbances together at an incidence of 1% to 10%, with hearing impairment additionally reported after marketing at under 1% — a somewhat stronger labelled signal than ibuprofen carries. As with other NSAIDs, effects are usually reversible once you stop, and the risk described relates to regular long-term use rather than occasional doses. If you already have hearing loss and take naproxen most days, it is reasonable to ask your doctor whether something else would do the job.

Quinine is well-known for causing a collection of symptoms called "cinchonism" which includes tinnitus, hearing loss, dizziness, and headache. These effects are dose-dependent and typically reversible after discontinuation. Quinine is found not only in antimalarial drugs but also in tonic water, though in much smaller amounts.

Chloroquine is often described as causing irreversible hearing loss, in contrast to quinine. We have softened that here because the claim rests on a teaching reference rather than primary evidence, and a 2026 systematic review of antimalarial hearing toxicity found the overall evidence limited and did not separate chloroquine from hydroxychloroquine in its conclusions. So: hearing loss has been reported, the mechanism is plausible, and the honest position is that severity and reversibility are not well established. Notably, that same review concluded routine standardised hearing monitoring is not supported by the evidence — so report symptoms rather than expecting scheduled tests.

Hydroxychloroquine keeps lupus and rheumatoid arthritis under control for very large numbers of people, and stopping it triggers flares — so proportionality matters here more than most entries. A 2026 systematic review of antimalarial hearing toxicity found the available evidence limited and inconclusive, and concluded that routine standardised hearing monitoring is not supported. Tinnitus and hearing changes have been reported with long-term use, so mention them to your rheumatologist if they appear. But this is not a reason to stop a medication that is holding your disease steady.

Erythromycin can cause hearing loss when given at high doses intravenously, particularly in patients with kidney or liver impairment. The hearing loss is typically reversible once the drug is discontinued or the dose is reduced. Oral doses at standard levels carry much lower risk.

Hearing appears on the azithromycin label only under postmarketing experience, with the label itself noting that such reports cannot reliably establish frequency or causation. It is absent from the warnings and from clinical-trial adverse reactions. That is a much weaker signal than erythromycin, which quantifies risk at high intravenous doses. A standard Z-Pack is not a meaningful ototoxicity concern. Prolonged high-dose use is a different matter and worth monitoring.

Bumetanide is a loop diuretic similar to furosemide. It can cause temporary hearing changes, especially at high intravenous doses. The risk increases when combined with other ototoxic medications such as aminoglycosides. Hearing changes are usually reversible when the dose is adjusted.

Torsemide is often described as the gentler loop diuretic for hearing, and it may well be — but we looked for the evidence and it is not there. That claim traces to review articles asserting it without comparative data, and no head-to-head study has measured hearing outcomes against furosemide. A large analysis of adverse-event reports found no ototoxicity signal for torsemide, but it found none for furosemide or bumetanide either, so it cannot separate them. We have kept torsemide level with the rest of the class rather than implying a safety advantage nobody has demonstrated.

We have moved methotrexate out of the risk tiers because the claim did not hold up. Its FDA labelling contains no hearing-related adverse reactions, and the large analysis of drugs that worsen cisplatin hearing loss did not even examine it. A 2026 paper describes ototoxicity from adalimumab combined with methotrexate, but that implicates the combination, not methotrexate alone. It stays listed so searches still find it, with the honest answer. If you or your child are on a chemotherapy protocol containing methotrexate, the drug to ask about is any platinum agent in the regimen.

Like methotrexate, 5-FU is listed so searches find it rather than because it carries established ototoxicity — its labelling lists no hearing-related adverse reactions. One real source of confusion: 5-FU and capecitabine can cause an acute cerebellar syndrome with unsteadiness and abnormal eye movements. That is neurological, not ear damage, and gets misfiled as ototoxicity. Report those symptoms urgently, but they are a different problem with a different cause.

This entry needs splitting, because averaging it into one number loses both halves of the truth. Taken as prescribed for short-term pain, hearing loss is not an expected effect — the FDA label attributes reported cases predominantly to chronic overdose. But in high-dose long-term misuse, the documented pattern is rapid and sometimes profound permanent hearing loss, occasionally severe enough that a cochlear implant becomes the only option. So the usual advice on this page — never stop a prescribed medication over hearing worries — comes with a companion here: never escalate beyond your prescribed dose, and if your hearing drops suddenly while taking opioids, treat that as urgent and seek care the same day.

We no longer assign these a risk tier. Some labels list tinnitus among "special senses" reactions at well under 1%, with no causality assigned and no quantified incidence — that is not evidence of ototoxicity, and giving it a tier implied a risk nobody has established. Blood pressure medication is also exactly the category where a scary-looking label could cost someone far more than their hearing. If tinnitus starts after beginning a new blood pressure drug, mention it to your doctor, who can consider alternatives — but there is no ototoxicity reason to avoid this class.

Same reasoning as ACE inhibitors: some beta blocker labels do list tinnitus, but as an unquantified low-frequency entry with no causality assigned. That does not establish ototoxicity, and giving it a risk tier overstated it. These are drugs people take to prevent heart attacks and strokes. Raise new tinnitus with your doctor rather than stopping anything.