Ototoxicity is the pharmacological adverse reaction which affects the inner ear or auditory nerve and is characterized by cochlear or vestibular dysfunction. The scope and scenario of hearing loss caused due to use of drugs has expanded over last few decades. Although ototoxic medications play a vital role in current practice of medicine, they have the potential to cause harm which may cause significant morbidity. (Ganesan, 2018 Apr; 22(2)) The various drug groups that have been implicated in the ototoxicity include (but are not limited to) the following:

• Antibiotics such as Aminoglycosides and Macrolides
• Nonsteroidal anti-inflammatory drugs (NSAIDs)
• Salicylates
• Antimalarials
• Anti-neoplastic drugs
• Loop diuretics

Topical antibiotic solutions (WHO, Report of informal consultation on strategies for prevention of hearing impairment from ototoxic drugs., 1994)

The presenting symptoms of damage to auditory system may be multiple and include the following:

• Tinnitus
• Hearing loss
• Hyperacusis
• Fullness of ear
• Dizziness/vertigo (Ganesan, 2018 Apr; 22(2))

The factors that determine ototoxic effects of a drug in an individual have been described as personal and familial susceptibility, age (particularly extremes of age), daily dose of the drug, its total dose, and route of administration of a drug. (WHO, Report of informal consultation on strategies for prevention of hearing impairment from ototoxic drugs 1994) Amongst the different routes of administration of the drugs, the order of risk associated is reported to be maximum with intraspinal route, followed by intravenous, intramuscular, and then percutaneous (in case of burn patients). The oral route is considered relatively safe, while the consensus on ototoxicity due to topical agents is yet to emerge. (WHO, Report of informal consultation on strategies for prevention of hearing impairment from ototoxic drugs., 1994)

The other risk factors that have been documented are pregnancy, chronic kidney disease, hepatic failure and exposure to noise at workplace. Simultaneous administration of more than one ototoxic drug has an additive effect.

Cochlear toxic effect of aminoglycosides begins by damage to outer hair cells (OHC) in basal turn and then extends towards apex. Understandably the hearing loss involves higher frequencies initially and then lower frequencies. The inner hair cells damage occurs later. The ototoxicity due to aminoglycosides may occur even with single dose or many days after drug has been stopped. (Kahlmeter G, 2013) Cisplatin (an anti-neoplastic drug) ototoxicity also produces high-frequency sensorineural hearing loss and ototoxicity is dose related. Diuretics alter ionic ratio and thus produce changes in endocochlear potentials. Quinines also produce inner ear changes. Tinnitus may be the presenting symptom of ototoxicity caused by loop diuretics, aspirin, and quinine. The ototoxic effect may be reversible if these drugs are withdrawn at this stage. Erythromycin, a macrolide, is known to produce labyrinthitis and damage to central auditory nervous system. (Kumar, 2016) Usually there is an avoidable delay in detecting and diagnosing its ototoxic effect following administration of a drug. The resultant hearing loss is often variable and inconsistent.

A well-described history of patient’s symptoms and outcome of various investigations form the basis of diagnosis. The early diagnosis of ototoxicity may be affected by patient’s age, other co-existing medical conditions, and cognition level of the subject. Patients themselves and their health care providers if educated about possible ototoxic effects of drugs can contribute towards early detection of symptoms. (Ganesan, 2018 Apr; 22(2))

Pure tone audiometry including higher frequencies testing, otoacoustic emissions (OAE), Brainstem Evoked Response Audiometry (BERA), and Electro Cochleography (ECoG) are used to assess and monitor the ototoxic effects in patients who are being treated with drugs with potential ototoxic effects.

The use of OAEs is particularly logical. Ototoxic drugs cause damage to outer hair cells and OAE are OHC dependent. They can detect changes in high frequency thresholds before they can be detected by pure tone audiometry. Both Distortion Product OAE and Transient Evoked OAE are used to monitor ototoxicity. (Kumar, 2016) A middle ear dysfunction needs to be ruled out in order to determine that any changes noted are likely due to changes in cochlear function. If middle ear function is normal and hearing is good, OAEs are an excellent indicator of early ototoxic damage. However, abnormal middle ear function and baseline hearing loss greater than about 40 dB HL may preclude effective monitoring using OAEs. Use of BERA testing may be more appropriate in such cases. (Dawn Konrad-Martin, 2005)

A structured approach involving medical professionals, audiologists, hearing and other healthcare providers is needed to prevent this growing menace. Pre-treatment evaluation, intra-treatment monitoring, post-treatment evaluation and long-term follow-up are part of the management protocol. Awareness about ototoxic drugs both amongst health care providers and general public will go a long way in reducing incidence and prevalence of ototoxicity. (Kumar, 2016)

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