This study aimed to assess pharyngeal function between no bolus and bolus propofol induced sedation during gastric endoscopic submucosal dissection. A retrospective study was conducted involving consecutive gastric cancer patients. Patients in the no bolus group received a 3？mg/kg/h maintenance dose of propofol after the initiation of sedation without bolus injection. All patients in the bolus group received the same maintenance dose of propofol with bolus 0.5？mg/kg propofol injection. Pharyngeal functions were evaluated endoscopically for the first 5？min following the initial administration of propofol. Fourteen patients received no bolus propofol induction and 13 received bolus propofol induction. Motionless vocal cords were observed in 2 patients (14%) in the no bolus group and 3 (23%) in the bolus group. Trachea cartilage was not observed in the no bolus group but was apparent in 6 patients (46%) in the bolus group ( ). Scope stimulated pharyngeal reflex was observed in 11 patients (79%) in the no bolus group and in 3 (23%) in the bolus group ( ). Propofol induced sedation without bolus administration preserves pharyngeal function and may constitute a safer sedation method than with bolus. 1. Introduction Early detection and diagnosis may improve outcome and survival in patients with gastric cancer. The endoscopic submucosal dissection (ESD) technique was developed to resect large neoplasms en bloc and to reduce the risk of recurrence [1]. However, ESD generally takes longer than conventional endoscopic mucosal resection (EMR) [2], so adequate moderate and deep sedations are necessary [3]. Recently, propofol sedation administered by anaesthesiologists or gastroenterologists has gained popularity in endoscopic procedures [4–7]. Propofol is a short-acting sedative, that is, an agonist of the γ-aminobutyricacid receptor in the central nervous system [8]. Effectiveness of propofol induced sedation during endoscopic procedures is under evaluation. It has been reported that monitored propofol sedation is safer than sedation with midazolam [3, 9, 10]; however, cases of respiratory depression including reduced oxygen saturation during propofol sedation have been reported [11–13]. Bolus administration of propofol is often performed at the initial stage of sedation; however, bolus induction might be regarded as one of the causes of respiratory depression. Although the relationship between propofol and respiratory depression has been reported [14], the direct association with propofol and pharyngeal function is thus far not known. Therefore, we evaluated this
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