Authors: NEVRESTE DİDEM SONBAY YILMAZ, CEM SAKA, BURCU ARSLAN, NURDAN AYGENER YEŞİLYURT, DİLEK SAKA, SADIK ARDIÇ, İSTEMİHAN AKIN
Abstract: Background/aim: This study was conducted to determine the critical partial oxygen pressure (pO2) value that would impair hearing function by evaluating the effects of hypoxia on hearing function in subjects diagnosed with chronic obstructive pulmonary disease (CPOD).Materials and methods: The study included 25 male and 5 female patients referred to our clinic who were diagnosed with COPD, according to spirometry and PaO2 values, and who did not show pathology upon autoscopic examination. The control group consisted of 14 female and 16 male patients who had no lung disease and were in the same age range as the COPD group. Results: A statistically significant difference was found between the two groups for distortion-product otoacoustic emission (DPOAE) (P < 0.001). The COPD group was divided into two groups according to pO2 levels (pO2 ? 70 and pO2 > 70) in order to find a critical pO2 level which might cause significant change at a certain audiological extent. Conclusion: Hypoxia causes long-term decline in hearing thresholds, deterioration of DPOAE results, and prolongation of I?V interpeak latency in auditory brainstem response. However, the critical oxygen level that disrupts hearing function could not be determined.
Keywords: Chronic obstructive pulmonary disease, auditory brainstem response, distortion-product otoacoustic emission, hearing loss
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