The role of anesthesiologists' perceived self-efficacy in anesthesia-related adverse events.

BACKGROUND: Self-efficacy, as the vital determinant of behavior, influencing clinicians' situation awareness, work performance, and medical decision-making, might affect the incidence of anesthesia-related adverse events (ARAEs). This study was employed to evaluate the association between perceived self-efficacy level and ARAEs. METHODS: A cross-sectional study was performed in the form of an online self-completion questionnaire-based survey. Self-efficacy was evaluated via validated 4-point Likert scales. Internal reliability and validity of both scales were also estimated via Cronbach's alpha and validity analysis. According to the total self-efficacy score, respondents were divided into two groups: normal level group and high level group. Propensity score matching and multivariable logistic regression were employed to identify the relationship between self-efficacy level and ARAEs. RESULTS: The response rate of this study was 34%. Of the 1011 qualified respondents, 38% were women. The mean (SD) age was 35.30 (8.19) years. The Cronbach's alpha of self-efficacy was 0.92. The KMO (KMO and Bartlett's test) value of the scale was 0.92. ARAEs occurred in 178 (33.0%) of normal level self-efficacy group and 118 (25.0%) of high level self-efficacy group. Before adjustment, high level self-efficacy was associated with a decreased incidence of ARAEs (RR [relative risk], 0.76; 95% CI [confidence interval], 0.62-0.92). After adjustment, high level self-efficacy was also associated with a decreased incidence of ARAEs (aRR [adjusted relative risk], 0.63, 95% CI, 0.51-0.77). In multivariable logistic regression, when other covariates including years of experience, drinking, and the hospital ranking were controlled, self-efficacy level (OR [odds ratio], 0.62; 95% CI, 0.46-0.82; P = 0.001) was significantly correlated with ARAEs. CONCLUSIONS: Our results found a clinically meaningful and statistically significant correlation between self-efficacy and ARAEs. These findings partly support medical educators and governors in enhancing self-efficacy construction in clinical practice and training.

Correlation between Preoperative Anxiety and ABO Blood Types: Evidence from a Clinical Cross-Sectional Study.

Gene-environment interaction is identified as the determinant in anxiety. ABO blood types represent a part of the genetic phenotype. Therefore, we assume ABO blood types correlate with preoperative anxiety. This cross-sectional study enrolled 352 patients with different ABO blood types, scheduled for elective surgery between 2018 and 2019 in the First Affiliated Hospital of Shihezi University. HADS (hospital anxiety and depression scale) scores and VA (visual analogue scales for anxiety) scores were all used to assess the preoperative anxiety in the A, B, AB, and O groups. Bivariate correlation and logistic regression were performed to identify relationships between preoperative anxiety and related variables. A significant difference in VA and HADS-A (anxiety) scores was found between the AB and other groups. The ratio of preoperative anxiety was 3.73 (95% CI [confidence interval]: 2.32-6.00, P < 0.001) times in female than in male; 0.36 (95% CI: 0.21-0.63, P < 0.001) times in ASA (American Society of Anesthesiologists) grade II than in grade I; 0.41 (95% CI: 0.20-0.86, P < 0.05) times in ASA grade III than in grade I; 1.25 (95% CI: 1.1-1.41, P < 0.001) times in higher VAS (visual analogue scales for pain) scores than in lower VAS scores; and 0.28 (95% CI: 0.16-0.49, P < 0.01) times in non-AB blood type than in AB blood type. Differences in ABO blood types were found in preoperative anxiety, and the AB group displayed a high preoperative anxiety level. ABO blood types, sex, ASA grade, and VAS were associated with preoperative anxiety. This trial is registered with ChiCTR1800019390.

Estrogen and propofol combination therapy inhibits endoplasmic reticulum stress and remarkably attenuates cerebral ischemia-reperfusion injury and OGD injury in hippocampus.

AIM: Endoplasmic reticulum stress (ERS) is vital in inducing apoptosis via caspase-12 and C/EBP homologous protein (CHOP) apoptotic pathway in the hippocampus after ischemia-reperfusion injury. The study aimed to estimate the efficacy of estrogen and propofol combination therapy against ERS-induced apoptosis after cerebral ischemia-reperfusion injury and oxygen-glucose deprivation (OGD) injury in the hippocampus in vivo and in vitro. METHODS: Rat model of cerebral ischemia-reperfusion injury was generated by middle cerebral artery occlusion (MCAO) strategy with ischemic intervention for 90 min and reperfusion for 24 h. Propofol processing ischemia-reperfusion group (Propofol group) infused 50 mg/kg/h of propofol via the femoral vein at the onset of reperfusion for 30 min. Estrogen processing ischemia-reperfusion group (estrogen group) received 0.0125 mg/kg of estrogen via tail vein at 30 min prior to MCAO. Combination therapy for ischemia-reperfusion group (combination group) received simultaneous processing with propofol and estrogen. In vitro, brain slices were randomly exposed to dimethylsulfoxide (DSMO), 10 µm of propofol, 10 nm of estrogen, or propofol and estrogen. Changes in the orthodromic population spike (OPS) at the end of reoxygenation were recorded. Neurological deficit examination, Nissl staining, and 2,3,5-triphenyltetrazolium chloride (TTC) staining were employed to evaluate the level of cerebral ischemia-reperfusion injury. The expression of caspase-3, caspase-12, glucose-regulated protein 78 (GRP78), and CHOP were investigated by Western blot and immunofluorescence staining assays. Neural apoptotic rate in hippocampus was detected by the flow cytometry trial. RESULTS: Neurological deficit score, infarct volume, the expression of caspase-3 (P < 0.05), caspase-12, GRP78, CHOP, and neural apoptotic rate of I/R group increased markedly (P < 0.01). When obtaining drug treatment, neurological deficit score (P < 0.05), infarct volume, the expression levels of caspase-12 and GRP78, and neural apoptotic rate of the propofol group decreased significantly (P < 0.01). Furthermore, neurological deficit score, infarct volume, expression levels of caspase-3, caspase-12, GRP78, and CHOP (P < 0.05), and neural apoptotic rate decreased in the estrogen group (P < 0.01) and especially in the combination group (P < 0.01). Compared with the propofol group, the neurological deficit score (P < 0.05), infarct volume, caspase-3, caspase-12, GRP78, CHOP, and neural apoptotic rate of the combination group decreased (P < 0.01). Compared with the estrogen group, the infarct volume, caspase-3 (P < 0.05), GRP78, CHOP, and neural apoptotic rate (P < 0.05) of the combination group decreased (P < 0.01). Compared with the propofol group, the infarct volume, caspase-3, caspase-12 (P < 0.05), and GRP78 (P < 0.05) of the estrogen group decreased (P < 0.01). Propofol and estrogen treatment can delay the abolishing time of OPS and increase the recovery rate and amplitude of OPS, compared with OGD group (P < 0.01), especially in the combination therapy (P < 0.01). CONCLUSION: The neuroprotection of propofol and estrogen combination therapy inhibited excessive ERS-induced apoptosis against cerebral ischemia-reperfusion injury and OGD injury in the hippocampus of rats. Furthermore, the outcomes demonstrated that combination therapy yielded synergistic effects.