OBJECTIVE: Skin preparations, like chlorhexidine, are toxic to the inner ear, preventing their use as a preoperative skin disinfectant in the presence of a nonintact eardrum (e.g., perforation or tube). We aimed to determine if a poloxamer gel applied over perforated eardrums could prevent chlorhexidine ototoxicity. STUDY DESIGN: Controlled, in vivo. SETTING: Academic research laboratory. SUBJECTS AND METHODS: Bilateral myringotomies were performed on 20 Sprague-Dawley rats. Half had poloxamer placed over both eardrums before treatment. All rats had chlorhexidine instilled in one ear and saline in the other. Auditory brainstem response thresholds were measured before and 2- and 4-weeks posttreatment. Cochlear hair cell damage was assessed using scanning electron microscopy. RESULTS: Ears with chlorhexidine without poloxamer had significant hearing loss, 37 to 50 dB worse than the other three ear treatments at 2 and 4 weeks posttreatment, at all tested frequencies (4, 18, 16, and 24 kHz; all p < 0.0001). No significant hearing loss was observed in ears that were treated with poloxamer and chlorhexidine (-2 to 8 dB) and the results were not different from the ears that received saline, with or without poloxamer (-2.5 to 8 dB and 5-17 dB; p > 0.05). Electron microscopy showed far more outer hair cell damage in the no poloxamer + chlorhexidine ears compared with the other three treatments. CONCLUSION: The use of a poloxamer barrier may be an effective approach to prevent ototoxicity before chlorhexidine disinfection of the ear with a nonintact tympanic membrane.
OBJECTIVE: Skin preparations, like chlorhexidine, are toxic to the inner ear, preventing their use as a preoperative skin disinfectant in the presence of a nonintact eardrum (e.g., perforation or tube). We aimed to determine if a poloxamer gel applied over perforated eardrums could prevent chlorhexidineototoxicity. STUDY DESIGN: Controlled, in vivo. SETTING: Academic research laboratory. SUBJECTS AND METHODS: Bilateral myringotomies were performed on 20 Sprague-Dawley rats. Half had poloxamer placed over both eardrums before treatment. All rats had chlorhexidine instilled in one ear and saline in the other. Auditory brainstem response thresholds were measured before and 2- and 4-weeks posttreatment. Cochlear hair cell damage was assessed using scanning electron microscopy. RESULTS: Ears with chlorhexidine without poloxamer had significant hearing loss, 37 to 50 dB worse than the other three ear treatments at 2 and 4 weeks posttreatment, at all tested frequencies (4, 18, 16, and 24 kHz; all p < 0.0001). No significant hearing loss was observed in ears that were treated with poloxamer and chlorhexidine (-2 to 8 dB) and the results were not different from the ears that received saline, with or without poloxamer (-2.5 to 8 dB and 5-17 dB; p > 0.05). Electron microscopy showed far more outer hair cell damage in the no poloxamer + chlorhexidine ears compared with the other three treatments. CONCLUSION: The use of a poloxamer barrier may be an effective approach to prevent ototoxicity before chlorhexidine disinfection of the ear with a nonintact tympanic membrane.