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Topical Ototoxicity

When the eardrum is perforated or totally absent, topical medications and the chemi­cals used in ear cleaners can gain access to the inner ear via the round and oval windows, resulting in neurologic ototoxicity.

The ingredients of an ear cleaner should be carefully considered before use. Many manufacturers of otic products are now putting warnings on the labels of these products stating that their use should be avoided if the eardrum is not intact. In addition to topical ototoxicity, many pharmacologic agents are ototoxic when administered parenterally.

The aminoglycosides, polymyxins, detergents, and most alcohols routinely used in the treatment of the external ear canal are known to be toxic to the nervous struc­tures of the inner ear.13 Potentially ototoxic antimicrobial pharmaceuticals are present in most topical formulations for treatment of otitis externa. Many ear-cleaning solu­tions contain a mixture of ototoxic substances that may gain access to the inner ear, resulting in alterations of vestibular and cochlear function. Of these compounds, chlorhexidine is probably the most toxic, especially in cats. Severe, prolonged vestibular signs can be caused by chlorhexidine, and its use in ears is strongly discouraged.

An assessment of the risks of topical use of a drug or ear flush solution that may cause ototoxicity versus the therapeutic benefit must be considered when using these formulations to treat otitis media. For example, the aminoglycoside tobramycin has shown to be an effective antibiotic for many multidrug resistant Pseudomonas organ­isms. Although it is an aminoglycoside with potential ototoxic side effects, it is often infused into the bulla to treat the bacterial infection because of its efficacy.

In acute otitis media, the thin, permeable membranes of the round and oval windows provide easy access into the inner ear for many compounds. Access of ototoxins to the inner ear structures may be enhanced by inflammatory damage to the round window.

Enzymes contained in otic exudates can cause maceration of the epithelium covering the round window, increasing its permeability. It is also possible for the round window to become hyperplastic and thickened after longstanding otitis media, providing a barrier to prevent these ototoxins from reaching the inner ear. Because the round and oval windows cannot be visually examined, it is difficult to know whether the membrane is thinned or thickened. By using non-ototoxic prod­ucts, this issue can be made less important. If there is thick mucus within the bulla, it may act as a barrier covering the round window, effectively shielding the toxic material from contact.

Ototoxicity results from damage to the hair cells either in the cochlea and/or in the vestibular apparatus. This results in hearing deficits, vestibular disease, or both. Overt deafness or severe clinical vestibular disease (nystagmus, head tilt, and circling) may be obvious. However, subtle changes in either hearing or balance may not be detected by the owner or the veterinarian. Many common topical antibiotics can cause ototoxicity. Gentamycin, for example, concentrates in the hair cells of the organ of Corti in the cochlea when administered parenterally. However, it may also cause vestibular signs when administered topically in the middle ear. The cell perme­ability is altered so the hair cells swell and become deformed. They are rendered rigid and are unable to respond to movements of the endolymph within the semicir­cular canals. Ataxia, head tilt, and circling can result. A similar situation occurs in the cochlea when neomycin or kanamycin concentrates there. The cochlear nerve cells are damaged and cannot respond to vibrations, leading to hearing loss.

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Source: Gotthelf Louis N.. Small Animal Ear Diseases: An Illustrated Guide. 2nd ed. — Saunders,2004. — 384 p.. 2004
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