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Luke Thomson

    Luke Thomson

    Background and objectiveUpper airway surgery for obstructive sleep apnoea (OSA) is an alternative treatment for patients who are intolerant of continuous positive airway pressure (CPAP). However, upper airway surgery has variable... more
    Background and objectiveUpper airway surgery for obstructive sleep apnoea (OSA) is an alternative treatment for patients who are intolerant of continuous positive airway pressure (CPAP). However, upper airway surgery has variable treatment efficacy with no reliable predictors of response. While we now know that there are several endotypes contributing to OSA (i.e., upper airway collapsibility, airway muscle response/compensation, respiratory arousal threshold and loop gain), no study to date has examined: (i) how upper airway surgery affects all four OSA endotypes, (ii) whether knowledge of baseline OSA endotypes predicts response to surgery and (iii) whether there are any differences when OSA endotypes are measured using the CPAP dial‐down or clinical polysomnographic (PSG) methods.MethodsWe prospectively studied 23 OSA patients before and ≥3 months after multilevel upper airway surgery. Participants underwent clinical and research PSG to measure OSA severity (apnoea–hypopnoea inde...
    STUDY OBJECTIVES We aimed to determine if patients diagnosed with obstructive sleep apnea (OSA) who fail to respond to upper airway surgery may be successfully treated with supplemental oxygen and if we could identify baseline... more
    STUDY OBJECTIVES We aimed to determine if patients diagnosed with obstructive sleep apnea (OSA) who fail to respond to upper airway surgery may be successfully treated with supplemental oxygen and if we could identify baseline physiological endotypes (i.e. collapsibility, loop gain, arousal threshold and muscle compensation) that predict response to oxygen therapy. METHODS We conducted a single night, randomized double blinded cross over trial in which OSA patients who failed to respond to upper airway surgery were treated on separate nights with oxygen therapy (4 L/min) or placebo (medical air). Effect of oxygen/air on OSA on key polysomnography (PSG) outcomes were assessed: apnea-hypopnea index (AHI), AHI without desaturation (i.e. flow-based AHI [AHIfb]), arousal index and morning blood pressure. OSA endotypes were estimated from the PSG signals to determine whether baseline OSA physiology could be used to predict response to oxygen therapy. RESULTS There was a statistically significant reduction in AHI and AHIfb on oxygen versus placebo (AHIfb: 42.4±21.5 vs. 30.5±17.1 events/h, p = 0.008). Arousal index was also reduced on oxygen versus placebo (41.1±19.5 versus 33.0±15.3 events/h, p = 0.006). There was no significant difference in morning blood pressure between oxygen and placebo. While 7/20 subjects experienced a 50% reduction or greater in AHIfb on oxygen (responders), there was no difference in the baseline OSA endotypes (or clinical characteristics) between responders and non-responders. CONCLUSIONS Our findings demonstrate that a proportion of patients who fail to respond to upper airway surgery for OSA respond acutely to treatment with supplemental oxygen. CLINICAL TRIAL REGISTRATION Registry: Australian New Zealand Clinical Trials Registry; title: Oxygen therapy for treating patients with residual obstructive sleep apnoea following upper airway surgery; identifier: ACTRN12617001361392; URL: https://www.anzctr.org.au/Trial/Registration/TrialReview.aspx?id=373566.