Sevoflurane may be more beneficial than propofol in patients receiving endoscopic variceal ligation and endoscopic variceal sclerotherapy: A randomized, double-blind study

Abstract

Abstract. The aim of the present study was to evaluate the safety and efficacy of various general anesthesia regimens during endoscopic variceal ligation (EVL) and endoscopic variceal sclerotherapy (EVS). A total of 123 patients with American Society of Anesthesiologists physical status III and IV, aged 40-70 years, undergoing general anesthesia for EVL and EVS were randomly divided into two groups: Sevoflurane anesthesia (group S; n=60) and propofol anesthesia (group P; n=60). Vital signs, particularly heart rate (HR) and mean arterial pressure (MAP), were monitored. The designated time points were as follows: 5 min before induction (T0), and 1, 5, 10, 15, 20, 25 and 30 min after intubation (T1, T2, T3, T4, T5, T6 and T7, respectively). Time intervals were recorded, including recovery time and extubation time. Following surgery, the observer recorded the Ramsay sedation scale (RSS) score and the visual analogue scale (VAS) score. Adverse reactions were noted. Results demonstrated that there were significant differences in MAP between the two groups at T2, T3, T5, T6 and T7 (P<0.05). There was a significant difference in HR between the two groups at T2, T3 and T4 (P<0.05). Recovery time and extubation time in group P were significantly longer than those in group S (P<0.05; 18.38±2.25 min vs. 14.57±1.04 min and 21.70±2.70 min vs. 15.83±0.88 min, respectively). The rate of ephedrine injected was 58.3% (35/60 patients) in group P vs. 28.3% (17/60 patients) in group S (P<0.05). There was a significant difference in the RSS score between the two groups 5 min after extubation (P<0.05). VRS scores demonstrated that anesthetists and patients were significantly more satisfied with the procedure in group S than in group P (P<0.01). In conclusion, the superiority and special clinical value of inhalational anesthesia has been demonstrated during EVL and EVS attributed to stable hemodynamics and high quality of anesthesia recovery in the present study.

A novel balanced anesthesia shortens time to emergence in patients undergoing modified radical mastectomy: a randomized prospective trial

“…Furthermore, compared with sevoflurane, propofol is metabolized dependent of liver and renal function; therefore, it is less controllable. Tang et al reported that patients receiving propofol-based intravenous anesthesia experienced a delay in the decided extubation time compared with the sevoflurane group (19), which is in accordance with our results. In contrast, of all currently used anesthetics, the pharmacokinetic properties of sevoflurane come closest to that of the ideal anesthetic.…”

Anesthetic effect of propofol combined with remifentanil or sevoflurane anesthesia on patients undergoing radical gastrectomy

“…It was found that patients' sedation score in group A was lower than that in group B, and the incidence of pain in group A was higher than that in group B, indicating that patients had a high acceptance of propofol combined with sevoflurane anesthesia and a low incidence of adverse reactions. Cancer patients were prone to restlessness and other adverse reactions in general anesthesia due to pain, so sedation and analgesia effect were the main indicators to evaluate the anesthetic effect (21,26). In addition to produce general anesthesia, sevoflurane also had vasodilator and analgesic effects, so it is more suitable for elderly patients and patients with cardiovascular insufficiency (27).…”

Dexmedetomidine suppresses sevoflurane anesthesia-induced neuroinflammation through activation of the PI3K/Akt/mTOR pathway

“…In recent years the inhalational anesthetic sevoflurane has replaced other volatile anesthetics due to its quick induction, stable maintenance, rapid revival and because the irritation it causes is mild [1]. However, recent evidence has shown that sevoflurane can lead to pathophysiological alterations of the brain during the recovery period, such as neuronal apoptosis, tau aggresomes, abnormal discharge of neurons, and neuroinflammation, which cause neurodegenerative changes in the development of the mammalian brain [2–6].…”