Comparison between low flow sevoflurane anesthesia and total intravenous anesthesia during intermediate-duration surgery: effects on renal and hepatic toxicity.

BACKGROUND: Renal and hepatic dysfunction or injury might be involved by ether based anesthetic and intravenous anesthetic drug or surgical stress. The purpose of this study is to compare the effect of moderate duration low-flow sevoflurane versus total intravenous anesthesia on renal and hepatic functions. PATIENTS AND METHODS: Eighty (80) patients between the ages of 25-70 scheduled for elective lumbar disc herniotomy, with an expected operation time of 120-240 min, were enrolled in the study. Anesthesia was induced using remifentanil, propofol and atracurium. Patients were randomly divided into two groups. After intubation, Group S (n=40) received sevoflurane and Group T (n=40) received total intravenous anesthesia with propofol in oxygen and air with a fresh gas flow of 5 L min(?1). Ten minutes after induction the fresh gas flow was decreased to 1L min(?1) in both groups. Serum BUN, creatinine, ALT, AST, LDH and 24 hours excretion of glucose, protein, and creatinine in urine were measured preoperatively and the first three postoperative days. RESULTS: Serum BUN at 48 hours, creatinine at 24, 48. hours, and urine glucose at 24, and 48 hours were significantly higher from the preoperative values in Group S (p<0.05). However, serum BUN and creatinin, urine glucose were within the normal range. There were no significant differences in the renal and hepatic function tests between the groups. CONCLUSIONS: These results show that the renal and hepatic effect of moderate duration low-flow sevoflurane and total intravenous anesthesia is similar.

Effects of sedation during upper gastrointestinal endoscopy on endocrine response and cardiorespiratory function

Upper gastrointestinal endoscopy is often accompanied by tachycardia which is known to be an important pathogenic factor in the development of myocardial ischemia. The pathogenesis of tachycardia is unknown but the condition is thought to be due to the endocrine response to endoscopy. The purpose of the present study was to investigate the effects of sedation on the endocrine response and cardiorespiratory function. Forty patients scheduled for diagnostic upper gastrointestinal endoscopy were randomized into 2 groups. While the patients in the first group did not receive sedation during upper gastrointestinal endoscopy, the patients in the second group were sedated with intravenous midazolam at the dose of 5 mg for those under 65 years or 2.5 mg for those aged 65 years or more. Midazolam was administered by slow infusion. In both groups, blood pressure, ECG tracing, heart rate, and peripheral oxygen saturation (SpO2) were monitored during endoscopy. In addition, blood samples for the determination of cortisol, glucose and C-reactive protein levels were obtained from patients in both groups prior to and following endoscopy. Heart rate and systolic arterial pressure changes were within normal limits in both groups. Comparison of the two groups regarding the values of these two parameters did not reveal a significant difference, while a statistically significant reduction in SpO2 was found in the sedation group. No significant differences in serum cortisol, glucose or C-reactive protein levels were observed between the sedated and non-sedated group. Sedation with midazolam did not reduce the endocrine response and the tachycardia developing during upper gastrointestinal endoscopy, but increased the reduction in SpO2.

Effects of sedation during upper gastrointestinal endoscopy on endocrine response and cardiorespiratory function.

Upper gastrointestinal endoscopy is often accompanied by tachycardia which is known to be an important pathogenic factor in the development of myocardial ischemia. The pathogenesis of tachycardia is unknown but the condition is thought to be due to the endocrine response to endoscopy. The purpose of the present study was to investigate the effects of sedation on the endocrine response and cardiorespiratory function. Forty patients scheduled for diagnostic upper gastrointestinal endoscopy were randomized into 2 groups. While the patients in the first group did not receive sedation during upper gastrointestinal endoscopy, the patients in the second group were sedated with intravenous midazolam at the dose of 5 mg for those under 65 years or 2.5 mg for those aged 65 years or more. Midazolam was administered by slow infusion. In both groups, blood pressure, ECG tracing, heart rate, and peripheral oxygen saturation (SpO2) were monitored during endoscopy. In addition, blood samples for the determination of cortisol, glucose and C-reactive protein levels were obtained from patients in both groups prior to and following endoscopy. Heart rate and systolic arterial pressure changes were within normal limits in both groups. Comparison of the two groups regarding the values of these two parameters did not reveal a significant difference, while a statistically significant reduction in SpO2 was found in the sedation group. No significant differences in serum cortisol, glucose or C-reactive protein levels were observed between the sedated and non-sedated group. Sedation with midazolam did not reduce the endocrine response and the tachycardia developing during upper gastrointestinal endoscopy, but increased the reduction in SpO2.

Helicobacter pylori associated gastric pathology in patients with type II diabetes mellitus and its relationship with gastric emptying: the Ankara study.

Helicobacter pylori (HP) is the most common cause of nonerosive nonspecific gastritis. Gastric and duadenal ulcer both are found to be associated with HP infection. Another consequence of HP infection is that it may progress to chronic atrophic gastritis which is a well recognized risk factor for adenocarcinoma of the stomach. So by extension, HP infection can be accepted as a risk factor for gastric cancer. From this aspect, identification of risk groups is increasingly important. It is well-known that patients with diabetes mellitus are more prone to infection. Besides this, presence of gastroparesis diabeticorum may lead to bacterial overgrowth in the upper gastrointestinal (GI) tract. The present crossectional study was planned to study the presence of HP infection in diabetic patients with alterations in upper GI motility and to compare the results with healthy control group. Group I consisted of 51 patients with type II diabetes mellitus (as defined by National Data Group criteria) without any dyspeptic symptoms. Twenty-five age-matched healthy people served as a control in group II. Radionuclide-labelled solid meals were used to calculate gastric emptying time (GET). According to the results, patients in group I were divided into two groups. Patients with prolonged GET were grouped as group IA, while group IB consisted of patients with normal or shortened GET. Presence of HP gastritis is determined by histopathologic examination of endoscopic biopsy specimen. The results showed that the prevalence of HP gastritis in group I and II were 80.4% and 56% respectively and the difference was significant statistically (p: 0.03). In group IA, the prevalence of HP infection was estimated to be 88.2%, while in group IB it was 76.5% but the difference was not significant (p: 0.31). We have not found any correlation between HbA1c levels and the presence of HP infection in both group IA and IB (p values 0.26 and 0.15 respectively). We conclude that the prevalence of HP gastritis is higher in asymptomatic diabetic patients compared with healthy people. But there is no association between the alterations in GET and the presence of HP gastritis as indicated by our results. So prolonged GET may not be regarded as a specific pathogenic mechanism or a cause of HP infection in NIDDM patients.