Rare Hearing Loss Signal Linked to Common Antibiotic Imipenem/Cilastatin

A widely used hospital antibiotic may, in rare circumstances, be linked to sudden hearing loss, according to a new case report published in BMC Infectious Diseases. The report describes a 75-year-old patient with liver cancer and cirrhosis who developed right-sided hearing loss within 24 hours of starting imipenem/cilastatin, a carbapenem antibiotic reserved for severe infections and those caused by multidrug-resistant bacteria. When the drug was stopped, the patient’s hearing gradually improved, even though other medications, including the diuretic furosemide, were continued. The case is notable not because it proves the antibiotic caused the hearing loss, but because it adds a rare signal to a drug class whose neurological side effects are well known while its effects on the ear remain poorly documented.

Imipenem was the first carbapenem antibiotic to reach clinical use, and it is paired with cilastatin, a molecule that blocks renal degradation of imipenem and prolongs its activity in the body. Carbapenems are often described as last-line agents, deployed when other antibiotics fail or when bacteria produce enzymes that destroy common drugs. Their most recognized adverse effects are neurological: seizures, confusion, and other central nervous system disturbances, particularly at high doses or in patients with kidney impairment. Hearing loss, by contrast, has rarely been reported with this class, which is why the authors of the new report conducted a literature review alongside their case description to see whether similar events had been documented before.

The patient in the report was being treated for an abdominal infection complicating liver cancer and cirrhosis. Within a day of receiving intravenous imipenem/cilastatin, the patient reported subjective hearing loss on the right side. Importantly, the loss was never confirmed with objective audiological testing such as pure-tone audiometry or high-frequency audiometry, the standard tools for measuring hearing thresholds. This absence of objective measurement is a central limitation the authors themselves acknowledge. Subjective complaints of hearing change can arise from many causes in a critically ill, older patient, including the infection itself, other drugs, or fluctuations in attention and perception that are difficult to disentangle at the bedside.

To assess how plausible a drug-related cause was, the team applied two standard pharmacovigilance tools: the WHO-UMC causality system and the Naranjo scale. Both frameworks weigh factors such as the timing of the reaction relative to drug exposure, whether the reaction improved when the drug was stopped, whether it recurred on re-exposure, and whether alternative explanations exist. In this case, the temporal relationship was strong, with symptoms appearing within 24 hours of the first dose, and the improvement after discontinuation supported a possible link. However, the patient was never re-exposed to the antibiotic, and the concurrent use of furosemide, a loop diuretic with well-established ototoxic potential, meant that causality could not be established with certainty. The authors characterized the association as possible rather than probable, and they explicitly note that alternative explanations, particularly furosemide exposure, cannot be excluded.

Furosemide deserves particular attention in this context. Loop diuretics are among the classic ototoxic drugs in medicine, capable of damaging the stria vascularis and outer hair cells of the cochlea, especially when given intravenously at high doses or in patients with kidney dysfunction. The blood-labyrinth barrier, a specialized barrier that separates the inner ear from the bloodstream, normally shields the delicate sensory cells of the cochlea from many circulating substances, but certain drugs can cross it or disrupt it. When a patient receives both a carbapenem and a loop diuretic simultaneously, attributing a hearing change to one agent rather than the other becomes genuinely difficult. This pharmacological ambiguity is precisely why the authors stopped short of declaring imipenem/cilastatin the culprit, even though the timing pattern favored it.

The literature review accompanying the case report adds context to how rarely hearing loss has been tied to carbapenems. Most documented ototoxicity in antibiotic therapy involves aminoglycosides such as gentamicin and amikacin, which accumulate in cochlear fluid and can cause permanent, often irreversible damage to hair cells. Vancomycin, particularly when combined with aminoglycosides, has also been implicated. Carbapenems, by contrast, have a safety profile dominated by neurological and gastrointestinal effects rather than auditory ones. The rarity of prior reports means that a single case, however suggestive, cannot establish a pattern. What it can do is alert clinicians and pharmacologists to a possibility worth monitoring, especially in patients receiving multiple potentially ototoxic drugs at once.

The clinical implications of this report are practical rather than dramatic. For physicians prescribing imipenem/cilastatin, the case suggests that new hearing complaints during treatment should be taken seriously, documented carefully, and evaluated with objective audiological testing whenever feasible. For pharmacists and hospital safety committees, it reinforces the value of reviewing concomitant medications when an adverse reaction appears, since the presence of furosemide here complicated the causal picture considerably. For regulators and pharmacovigilance databases, single case reports like this one function as early signals that may prompt further investigation if similar cases accumulate. The authors emphasize that their findings warrant clinical attention and further investigation rather than any change in prescribing practice.

From a mechanistic standpoint, the report raises interesting questions about how a carbapenem could theoretically affect the inner ear. The blood-labyrinth barrier restricts drug entry into cochlear fluids, but it is not absolute, and factors such as inflammation, infection, and kidney dysfunction can alter its permeability. Patients with cirrhosis and severe abdominal infections often have altered drug metabolism and clearance, which can raise drug concentrations in ways that are difficult to predict. Whether imipenem or its metabolites can reach ototoxic concentrations in the cochlea under such conditions remains unknown, and the authors do not claim a mechanism. What they offer instead is a carefully documented temporal association, an honest accounting of confounders, and a call for systematic audiological monitoring in similar patients.

The case also illustrates a broader tension in modern pharmacovigilance. Objective testing, such as pure-tone audiometry and high-frequency audiometry, provides the gold standard for confirming hearing loss, yet it is often impractical in acutely ill patients on complex antibiotic regimens. Subjective reports, meanwhile, are common and meaningful to patients but difficult to verify. The authors of this report are transparent about this gap, noting that no objective audiological assessment was performed and that the hearing loss remained subjectively confirmed only. Their use of the WHO-UMC system and the Naranjo scale reflects an effort to bring structure to an inherently uncertain judgment, and their conclusion that causality cannot be established with certainty is a model of careful causal reasoning in a single-patient report.

For now, imipenem/cilastatin remains a critical tool against severe and drug-resistant infections, and this single case does not change that. What it does change is the level of awareness among clinicians who use it. A patient who suddenly reports hearing changes while receiving this antibiotic, particularly alongside other potentially ototoxic drugs, now has a documented precedent that clinicians can consult. The report, published open access in BMC Infectious Diseases by a team from the Department of Pharmacy and the Department of Infectious Diseases at Longyan Second Hospital in Fujian, China, adds a small but carefully reasoned data point to the pharmacological record. As the authors conclude, the association between imipenem/cilastatin exposure and subjective hearing loss remains possible but unconfirmed, and it is precisely this kind of disciplined uncertainty that allows rare adverse drug signals to be recognized without overstating the evidence behind them.

Subject of Research: Possible association between the carbapenem antibiotic imipenem/cilastatin and hearing loss reported in a single clinical case

Article Title: Hearing loss associated with imipenem/cilastatin: a case report and literature review

Article References: Zhang, S., Liao, S., Zhang, L., Huang, Q., & Liu, H. (2026). Hearing loss associated with imipenem/cilastatin: a case report and literature review. BMC Infectious Diseases. https://doi.org/10.1186/s12879-026-14657-w

Image Credits: AI Generated

DOI: 10.1186/s12879-026-14657-w

Keywords: hearing loss, ototoxicity, imipenem/cilastatin, carbapenem antibiotics, adverse drug reaction, furosemide, pharmacovigilance, blood-labyrinth barrier, BMC Infectious Diseases, case report, antimicrobial therapy, inner ear