Predictor of respiratory disturbances during gastric endoscopic submucosal dissection under deep sedation

BACKGROUND Sedation is commonly performed for the endoscopic submucosal dissection(ESD)of early gastric cancer.Severe hypoxemia occasionally occurs due to the respiratory depression during sedation.AIM To establish predictive models for respiratory depression during sedation for ESD.METHODS Thirty-five adult patients undergoing sedation using propofol and pentazocine for gastric ESDs participated in this prospective observational study.Preoperatively,a portable sleep monitor and STOP questionnaires,which are the established screening tools for sleep apnea syndrome,were utilized.Respiration during sedation was assessed by a standard polysomnography technique including the pulse oximeter,nasal pressure sensor,nasal thermistor sensor,and chest and abdominal respiratory motion sensors.The apnea-hypopnea index(AHI)was obtained using a preoperative portable sleep monitor and polysomnography during ESD.A predictive model for the AHI during sedation was developed using either the preoperative AHI or STOP questionnaire score.RESULTS All ESDs were completed successfully and without complications.Seventeen patients(49%)had a preoperative AHI greater than 5/h.The intraoperative AHI was significantly greater than the preoperative AHI(12.8±7.6 events/h vs 9.35±11.0 events/h,P=0.049).Among the potential predictive variables,age,body mass index,STOP questionnaire score,and preoperative AHI were significantly correlated with AHI during sedation.Multiple linear regression analysis determined either STOP questionnaire score or preoperative AHI as independent predictors for intraoperative AHI≥30/h(area under the curve[AUC]:0.707 and 0.833,respectively)and AHI between 15 and 30/h(AUC:0.761 and 0.778,respectively).CONCLUSION The cost-effective STOP questionnaire shows performance for predicting abnormal breathing during sedation for ESD that was equivalent to that of preoperative portable sleep monitoring.

Carbon dioxide accumulation during analgosedated colonoscopy: Comparison of propofol and midazolam

AIM: To characterize the profiles of alveolar hypoventilation during colonoscopies performed under sedoanalgesia with a combination of alfentanil and either midazolam or propofol. METHODS: Consecutive patients undergoing routine colonoscopy were randomly assigned to sedation with either propofol or midazolam in an open-labeled design using a titration scheme. All patients received 4 μg/kg per body weight alfentanil for analgesia and 3 L of supplemental oxygen. Oxygen saturation (SpO 2 ) was measured by pulse oximetry (POX), and capnography (PcCO 2 ) was continuously measured using a combined dedicated sensor at the ear lobe. Instances of apnea resulting in measures such as stimulation of the patient, a chin lift, a mask maneuver, or withholding of sedation were recorded. PcCO 2 values (as a parameter of sedation-induced hypoventilation) were compared between groups at the following distinct time points: baseline, maximal rise, termination of the procedure and 5 min after termination of the procedure. The number of patients in both study groups who regained baseline PcCO 2 values (± 1.5 mmHg) five minutes after the procedure was determined.RESULTS: A total of 97 patients entered this study. The data from 14 patients were subsequently excluded for clinical procedure-related reasons or for technical problems. Therefore, 83 patients (mean age 62 ± 13 years) were successfully randomized to receive propofol (n = 42) or midazolam (n = 41) for sedation. Most of the patients were classified as American Society of Anesthesiologists (ASA) Ⅱ [16 (38%) in the midazolam group and 15 (32%) in the propofol group] and ASA Ⅲ [14 (33%) and 13 (32%) in the midazolam and propofol groups, respectively]. A mean dose of 5 (4-7) mg of Ⅳ midazolam and 131 (70-260) mg of Ⅳ propofol was used during the procedure in the corresponding study arms. The mean SpO 2 at baseline (%) was 99 ± 1 for the midazolam group and 99 ± 1 for the propofol group. No cases of hypoxemia (SpO 2 < 85%) or apnea were recorded. However, an increase in PcCO 2 that indicated alveolar hypoventilation occurred in both groups after administration of the first drug and was not detected with pulse oximetry alone. The mean interval between the initiation of sedation and the time when the PcCO 2 value increased to more than 2 mmHg was 2.8 ± 1.3 min for midazolam and 2.8 ± 1.1 min for propofol. The mean maximal rise was similar for both drugs: 8.6 ± 3.7 mmHg for midazolam and 7.4 ± 3.2 mmHg for propofol. Five minutes after the end of the procedure, the mean difference from the baseline values was significantly lower for the propofol treatment compared with midazolam (0.9 ± 3.0 mmHg vs 4.3 ± 3.7 mmHg, P = 0.0000169), and significantly more patients in the propofol group had regained their baseline value ± 1.5 mmHg (32 of 41vs 12 of 42,P = 0.0004). CONCLUSION: A significantly higher number of patients sedated with propofol had normalized PcCO 2 values five minutes after sedation when compared with patients sedated with midazolam.