Purpose To identify the effectiveness of remimazolam at the end of tonsillectomy and adenoidectomy for preventing emergence delirium in children under sevoflurane anesthesia. Patients and Methods One hundred and four patients aged 3–7 years scheduled for tonsillectomy and adenoidectomy under sevoflurane anesthesia were recruited. Patients were randomly assigned to receive either remimazolam 0.2 mg kg –1 (intervention, n=52) or 0.9% normal saline (control, n=52) at the end of the procedure. The primary outcome was the incidence of emergence delirium, defined as a Pediatric Anesthesia Emergence Delirium (PAED) score ≥10. Secondary outcomes were peak PAED score, emergence time, postoperative pain intensity, length of postanesthesia care unit (PACU) stay, parental satisfaction, and postoperative behavior changes three days postoperatively. Results Emergence delirium occurred in 6 of 51 (12%) patients receiving remimazolam versus 22 of 50 (44%) patients receiving saline (risk difference 32% [95% confidence interval, 16% to 49%], relative risk 0.27 [95% confidence interval, 0.12 to 0.60]; P <0.001). The peak PAED scores (median [interquartile range]) were lower in the remimazolam group than in the saline group (7 [6–8] versus 9 [8–11], P <0.001). Likewise, parental satisfaction was improved in the remimazolam group compared with the saline group (9 [8–10] versus 8 [7–8], P <0.001). There was no difference between groups concerning postoperative pain scores, length of PACU stay, or postoperative behavior changes. Conclusion In children undergoing tonsillectomy and adenoidectomy, administration of remimazolam 0.2 mg kg –1 at the end of the surgery, compared with 0.9% saline, resulted in a significantly lower likelihood of emergence delirium after sevoflurane anesthesia.

Background: Postoperative cognitive dysfunction (POCD) is the progressive deterioration of cognitive function after surgery. The mechanism underlying the development of POCD is unclear. Previous studies have suggested that neuroinflammation is a major contributor to the development of POCD. The purpose of this study was to observe the effects of preoperative pain on inflammatory factors and neuronal apoptosis in the hippocampus. Methods: Cognitive function was evaluated by the Morris water maze (MWM), and the expression levels of pro-inflammatory cytokines (IL-6, IL-1β, and TNF-α) were measured on the 1st, 3rd and 7th days after surgery. The levels of Ach, cAMP, PKA, and GABAA in the hippocampus were measured at the same time points. Results: Our results showed that the rats that experienced preoperative pain exhibited impaired learning and memory after surgery (P< 0.001). Moreover, rats in the preoperative pain+surgery group exhibited increased neuronal apoptosis compared to that of rats in the surgery group. On the 1st, 3rd and 7th days after surgery, the expression of IL-1β, IL-6 and TNF-α in the pain+surgery group was increased compared to that in the surgery group (P<0.001). Furthermore, the expression of key proteins, including ACh, cAMP, PKA and GABAA, was decreased in the pain+ surgery group compared to the surgery group. Conclusions: Preoperative pain may be a key risk factor for the development of POCD by inhibiting the cholinergic anti-inflammatory pathway (ACh-cAMP-PKA signalling pathway) and decreasing the expression of GABAA in the CNS.

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