Influence of general anesthesia on the postoperative sleep cycle in patients undergoing surgery and dental treatment: a scoping review on the incidence of postoperative sleep disturbance

General anesthesia may influence the postoperative sleep cycle; however, no clinical studies have fully evaluated whether anesthesia causes sleep disturbances during the postoperative period. In this scoping review, we explored the changes in postoperative sleep cycles during surgical procedures or dental treatment under general anesthesia.We compared and evaluated the influence of general anesthesia on sleep cycles and sleep disturbances during the postoperative period in adult and pediatric patients undergoing surgery and/or dental treatment. Literature was retrieved by searching eight public databases. Randomized clinical trials, observational studies, observational case-control studies, and cohort studies were included. Primary outcomes included the incidence of sleep, circadian cycle alterations, and/or sleep disturbances. The search strategy yielded six studies after duplicates were removed. Finally, six clinical trials with 1,044 patients were included. In conclusion, general anesthesia may cause sleep disturbances based on alterations in sleep or the circadian cycle in the postoperative period in patients scheduled for elective surgery.

Comparison of the hemodynamic effects of propofol and ketamine as anesthetic induction agents during high-dose remifentanil administration: a single-center retrospective comparative study

BACKGROUND: We hypothesized that ketamine, when administered as the anesthetic induction agent, may prevent cardiovascular depression during high-dose remifentanil administration, unlike propofol. To test our hypothesis, we retrospectively compared the hemodynamic effects of ketamine, during high-dose remifentanil administration, with those of propofol. METHODS: Thirty-eight patients who underwent oral surgery at the Nagasaki University Hospital between April 2014 and June 2015 were included in this study. Anesthesia was induced by the following procedure: First, high-dose remifentanil (0.3-0.5 µg/kg/min) was administered 2-3 min before anesthesia induction; next, the anesthetic induction agent, either propofol (Group P) or ketamine (Group K), was administered. Mean arterial pressure (MAP) and the heart rate were recorded by the automated anesthesia recording system at four time points: immediately before the administration of high-dose remifentanil (T1); immediately before the administration of propofol or ketamine (T2); 2.5 min (T3), and 5 min (T4) after the administration of the anesthetic induction agent. RESULTS: In Group P, the MAP at T3 (75.7 ± 15.5 mmHg, P = 0.0015) and T4 (68.3 ± 12.5 mmHg, P < 0.001) were significantly lower than those at T1 (94.0 ± 12.4 mmHg). However, the MAP values in the K group were very similar (P = 0.133) at all time points. The heart rates in both Groups P (P = 0.254) and K (P = 0.859) remained unchanged over time. CONCLUSIONS: We showed that ketamine, when administered as the anesthetic induction agent during high-dose remifentanil administration, prevents cardiovascular depression.

Comparison of the hemodynamic effects of propofol and ketamine as anesthetic induction agents during high-dose remifentanil administration: a single-center retrospective comparative study

BACKGROUND: We hypothesized that ketamine, when administered as the anesthetic induction agent, may prevent cardiovascular depression during high-dose remifentanil administration, unlike propofol. To test our hypothesis, we retrospectively compared the hemodynamic effects of ketamine, during high-dose remifentanil administration, with those of propofol. METHODS: Thirty-eight patients who underwent oral surgery at the Nagasaki University Hospital between April 2014 and June 2015 were included in this study. Anesthesia was induced by the following procedure: First, high-dose remifentanil (0.3-0.5 µg/kg/min) was administered 2-3 min before anesthesia induction; next, the anesthetic induction agent, either propofol (Group P) or ketamine (Group K), was administered. Mean arterial pressure (MAP) and the heart rate were recorded by the automated anesthesia recording system at four time points: immediately before the administration of high-dose remifentanil (T1); immediately before the administration of propofol or ketamine (T2); 2.5 min (T3), and 5 min (T4) after the administration of the anesthetic induction agent. RESULTS: In Group P, the MAP at T3 (75.7 ± 15.5 mmHg, P = 0.0015) and T4 (68.3 ± 12.5 mmHg, P < 0.001) were significantly lower than those at T1 (94.0 ± 12.4 mmHg). However, the MAP values in the K group were very similar (P = 0.133) at all time points. The heart rates in both Groups P (P = 0.254) and K (P = 0.859) remained unchanged over time. CONCLUSIONS: We showed that ketamine, when administered as the anesthetic induction agent during high-dose remifentanil administration, prevents cardiovascular depression.