Soo Kweon Koo1, Geun Hyung Park2, Tae Kyung Koh2, Sung Hoon Jung2, Ho Byung Lee2, Chang Lok Ji2. 1. Department of Otorhinolaryngology-Head and Neck Surgery, Busan Saint Mary's Hospital, Yongho-dong, Nam-gu, Busan, 538-41, South Korea. koosookweon@naver.com. 2. Department of Otorhinolaryngology-Head and Neck Surgery, Busan Saint Mary's Hospital, Yongho-dong, Nam-gu, Busan, 538-41, South Korea.
Abstract
PURPOSE: Snoring and obstructive sleep apnoea (OSA) exhibit multifactorial aetiologies; mouth breathing increases airway obstruction and upper respiratory tract resistance. Of the many published studies, few have evaluated sleeping subjects. We explored how mouth breathing affected the upper respiratory tract anatomy and OSA during sleep. METHODS: Eighteen patients with OSA, confirmed via full-night polysomnography, were enrolled in this study. We performed drug-induced sleep endoscopy (DISE) and defined obstruction sites before and after mouth closure using commercial mouth strips. We evaluated obstruction sites in two ways, i.e. by grading obstructions using our DISE grading system and measuring the affected areas. Patients who improved by at least one DISE grade were defined as responders. Areas were measured based on DISE videos analysed using ImageJ software. The apnoea-hypopnoea index (AHI) and body mass index (BMI) were recorded. RESULTS: Based on the DISE grade, 40% (7/18) of patients showed obstruction site improvement. When assessed areally, the mean number of pixels improved significantly at both the retropalatal (p = 0.045) and retrolingual (p = 0.019) levels. However, DISE non-responders exhibited no areal improvements. Responders and non-responders did not differ significantly in terms of AHI or BMI (both p < 0.05). CONCLUSIONS: Mouth closure improves or at least does not lead to further deterioration of the upper airway. Improvements were evident at the retropalatal and especially retrolingual levels. Neither the BMI nor the AHI differed between the two groups. However, responders tended to have a higher AHI than non-responders (39.4 vs. 32.8 events/h).
PURPOSE: Snoring and obstructive sleep apnoea (OSA) exhibit multifactorial aetiologies; mouth breathing increases airway obstruction and upper respiratory tract resistance. Of the many published studies, few have evaluated sleeping subjects. We explored how mouth breathing affected the upper respiratory tract anatomy and OSA during sleep. METHODS: Eighteen patients with OSA, confirmed via full-night polysomnography, were enrolled in this study. We performed drug-induced sleep endoscopy (DISE) and defined obstruction sites before and after mouth closure using commercial mouth strips. We evaluated obstruction sites in two ways, i.e. by grading obstructions using our DISE grading system and measuring the affected areas. Patients who improved by at least one DISE grade were defined as responders. Areas were measured based on DISE videos analysed using ImageJ software. The apnoea-hypopnoea index (AHI) and body mass index (BMI) were recorded. RESULTS: Based on the DISE grade, 40% (7/18) of patients showed obstruction site improvement. When assessed areally, the mean number of pixels improved significantly at both the retropalatal (p = 0.045) and retrolingual (p = 0.019) levels. However, DISE non-responders exhibited no areal improvements. Responders and non-responders did not differ significantly in terms of AHI or BMI (both p < 0.05). CONCLUSIONS:Mouth closure improves or at least does not lead to further deterioration of the upper airway. Improvements were evident at the retropalatal and especially retrolingual levels. Neither the BMI nor the AHI differed between the two groups. However, responders tended to have a higher AHI than non-responders (39.4 vs. 32.8 events/h).
Authors: C Hernández-Gancedo; D Pestaña; N Peña; C Royo; H Pérez-Chrzanowska; A Criado Journal: Eur J Anaesthesiol Date: 2006-01-27 Impact factor: 4.330
Authors: Soo Kweon Koo; Jang Won Choi; Nam Suk Myung; Hyoung Ju Lee; Yang Jae Kim; Young Joong Kim Journal: Am J Otolaryngol Date: 2013-09-05 Impact factor: 1.808