Changes in electroencephalographic power and bicoherence spectra according to depth of dexmedetomidine sedation in patients undergoing spinal anesthesia.

Background: Assessment the depth of dexmedetomidine sedation using electroencephalographic (EEG) features can improve the quality of procedural sedation. Previous volunteer studies of dexmedetomidine-induced EEG changes need to be validated, and changes in bicoherence spectra during dexmedetomidine sedation has not been revealed yet. We aimed to investigate the dexmedetomidine-induced EEG change using power spectral and bicoherence analyses in the clinical setting. Patients and Methods: Thirty-six patients undergoing orthopedic surgery under spinal anesthesia were enrolled in this study. Dexmedetomidine sedation was conducted by the stepwise increase in target effect site concentration (Ce) while assessing sedation levels. Bispectral index (BIS) and frontal electroencephalography were recorded continuously, and the performance of BIS and changes in power and bicoherence spectra were analyzed with the data from the F3 electrode. Results: The prediction probability values for detecting different sedation levels were 0.847, 0.841, and 0.844 in BIS, 95% spectral edge frequency, and dexmedetomidine Ce, respectively. As the depth of sedation increased, δ power increased, but high ß and γ power decreased significantly (P <0.001). α and spindle power increased significantly under light and moderate sedation (P <0.001 in light vs baseline and deep sedation; P = 0.002 and P <0.001 in moderate sedation vs baseline and deep sedation, respectively). The bicoherence peaks of the δ and α-spindle regions along the diagonal line of the bicoherence matrix emerged during moderate and deep sedation. Peak bicoherence in the δ area showed sedation-dependent increases (29.93%±7.38%, 36.72%±9.70%, 44.88%±12.90%; light, moderate, and deep sedation; P = 0.008 and P <0.001 in light sedation vs moderate and deep sedation, respectively; P = 0.007 in moderate sedation vs deep sedation), whereas peak bicoherence in the α-spindle area did not change (22.92%±4.90%, 24.72%±4.96%, and 26.96%±8.42%, respectively; P=0.053). Conclusions: The increase of δ power and the decrease of high-frequency power were associated with the gradual deepening of dexmedetomidine sedation. The δ bicoherence peak increased with increasing sedation level and can serve as an indicator reflecting dexmedetomidine sedation levels.

Response surface modelling of the pharmacodynamic interaction between propofol and remifentanil in patients undergoing anaesthesia.

This study describes the pharmacodynamic interaction between propofol and remifentanil. Sixty patients who were scheduled for elective surgery under general anaesthesia (30 males/30 females) were enrolled. Patients were randomly allocated to receive one of 15 combinations of drug levels. Baseline electroencephalograms (EEGs) were recorded for 5 minutes prior to administering the drugs. Patients received a target-controlled infusion at one of four predefined doses of propofol (high, 3 µg/mL; medium, 1.5 µg/mL; low, 0.5 µg/mL; or no drug) and of remifentanil (high, 6 or 8 ng/mL; medium, 4 ng/mL; low, 2 ng/mL; or no drug). The occurrence of muscle rigidity, apnoea, and loss of consciousness (LOC) was monitored, and EEGs were recorded during the drug administration phase. Electroencephalographic approximate entropy (ApEn) and temporal linear mode complexity (TLMC) parameters at baseline and under steady state conditions were calculated off-line. Response surfaces were developed to map the interaction between propofol and remifentanil to the probability of occurrence for quantal responses (muscle rigidity, apnoea, LOC) and ApEn and TLMC measurements. Model parameters were estimated using non-linear mixed effects modelling. The response surface revealed infra-additive and synergistic effects for muscle rigidity and apnoea, respectively. The effects of the combined drugs on LOC and EEG parameters (eg, ApEn and TLMC) were additive. The C50 estimates of remifentanil (ng/mL) and propofol (µg/mL) were 9.11 and 130 000 for muscle rigidity, 8.99 and 6.26 for apnoea, 13.9 and 3.04 for LOC, 23.4 and 10.4 for ApEn, and 14.8 and 6.51 for TLMC, respectively. The probability of occurrence for muscle rigidity declined when propofol was combined with remifentanil.

The Frequency and Risk Factors of Colorectal Adenoma in Health-Check-up Subjects in South Korea: Relationship to Abdominal Obesity and Age.

BACKGROUND/AIMS: Obesity is associated with the risk of colorectal cancer. However, there is a lack of information about the relationship between obesity and colorectal adenoma. We investigated whether general and abdominal obesity are risk factors for colorectal adenoma. METHODS: Subjects who received health check-ups, including colonoscopy, from April 2006 to September 2007 in Chung-Ang University Hospital were included (n=1,316). The frequency and characteristics of colorectal adenomas were analyzed according to demographic features, past history, blood tests, body mass index, and components of metabolic syndrome. Abdominal obesity was defined as a waist circumference of >/=80 cm in women and >/=90 cm in men. RESULTS: The sex ratio of the subjects was 1.9:1 (male:female) and their age was 47.7+/-10.0 years (mean+/-SD). In univariate analysis, abdominal obesity was significantly associated with the frequency of colorectal adenoma (26.5% "yes" vs 16.9% "no"; p<0.001). The frequency of colorectal adenoma was significantly higher among males, older patients, current smokers, and subjects with fasting hyperglycemia (>/=100 mg/dL) or fatty liver (p<0.05). Multivariate analysis identified that male sex (odds ratio [OR], 1.5; 95% confidence interval [CI], 1.0-2.2), old age (age >/=60 years; OR, 6.7; 95% CI, 3.5-12.5), and abdominal obesity (OR, 1.5; 95% CI, 1.0-2.2) were independent risk factors for colorectal adenoma (p<0.05). The frequency of multiple adenomas (more than two sites) was also significantly higher in subjects with abdominal obesity. However, the effect of abdominal obesity on the development of colorectal adenoma decreased in elderly people. CONCLUSIONS: Abdominal obesity is an independent risk factor for colorectal adenoma and its multiplicity, especially in younger people in South Korea.