Purpose of reviewPerioperative opioid-based pain management of patients suffering from obstructive sleep apnea (OSA) may present challenges because of concerns over severe ventilatory compromise. The interaction between intermittent hypoxia, sleep fragmentation, pain, and opioid responses in OSA, is complex and warrants a special focus of perioperative outcomes research.Recent findingsLife-threatening opioid-related respiratory events are rare. Epidemiologic evidence suggests that OSA together with other serious renal and heart disease, is among those conditions predisposing patients for opioid-induced ventilatory impairment (OIVI) in the postoperative period. Both intermittent hypoxia and sleep fragmentation, two distinct components of OSA, enhance pain. Intermittent hypoxia may also potentiate opioid analgesic effects. Activation of major inflammatory pathways may be responsible for the effects of sleep disruption and intermittent hypoxia on pain and opioid analgesia. Recent experimental evidence supports that these, seemingly contrasting, phenotypes of pain-increasing and opioid-enhancing effects of intermittent hypoxia, are not mutually exclusive. Although the effect of intermittent hypoxia on OIVI has not been elucidated, opioids worsen postoperative sleep-disordered breathing in OSA patients. A subset of these patients, characterized by decreased chemoreflex responsiveness and high arousal thresholds, might be at higher risk for OIVI.SummaryOSA may complicate opioid-based perioperative management of pain by altering both pain processing and sensitivity to opioid effect.

Background: High-flow, heated, and humidified nasal oxygen therapy (HFNO) is frequently used in critical care and perioperative settings for a range of clinical applications. Much of the benefit of HFNO is attributed to generation of modest levels of positive airway pressure. Concern has been raised that this positive airway pressure may cause gastric insufflation, potentially increasing the risk of regurgitation and aspiration in an unprotected airway. Methods: A prospective, interventional, assessor-blinded study was undertaken to evaluate the effects of HFNO on gastric content and gastric distension in healthy fasted adult volunteers assessed by ultrasonography. The primary outcome was the volume of gastric secretions. The secondary outcomes were the incidence of gastric air insufflation and the distribution of gastric antral grades. Results: Sixty subjects were enrolled. No subject was found to have air gastric distension either at baseline or after treatment with HFNO. All subjects had either a Grade 0 or Grade 1 antrum, with similar distribution of antral grades and similar volume of gastric secretions before and after treatment with HFNO. Conclusions: There was no evidence that treatment with HFNO at flow rates of up to 70 L min À1 for 30 min resulted in gastric distension or an increase in gastric secretions in healthy individuals breathing spontaneously. The generalisability of these findings to subjects under anaesthesia and patients with incompetence of the lower oesophageal sphincter or impaired gastric emptying requires further investigation. Clinical trial registration: NCT03134937.