Association between intraoperative hypotension and postoperative nausea and vomiting: a retrospective analysis of 247 thyroidectomy cases.

BACKGROUND: Postoperative nausea and vomiting (PONV) are major complications after general anesthesia. Although various pathways are involved in triggering PONV, hypotension plays an important role. We hypothesized that intraoperative hypotension during general anesthesia might be responsible for the incidence of PONV. METHODS: We retrospectively investigated patients who underwent thyroidectomy. The initial blood pressure measured before induction of anesthesia was used as the baseline value. The systolic blood pressure measured during the operation from the start to the end of anesthesia was extracted from anesthetic records. The time integral value when the measured systolic blood pressure fell below the baseline value was calculated as area under the curve (AUC) of s100%. RESULTS: There were 247 eligible cases. Eighty-eight patients (35.6%) had PONV. There was no difference in patient background between the patients with or without PONV. Univariate analysis showed that the total intravenous anesthesia (TIVA) (p=0.02), smoking history (p=0.02), and AUC-s100% (p=0.006) were significantly associated with PONV. Multiple logistic regression analysis revealed that TIVA (OR: 0.54, 95% CI: 0.29...0.99), smoking history (OR: 0.60, 95% CI: 0.37...0.96), and AUC-s100% (OR: 1.006, 95% CI: 1.0...1.01) were significantly associated with PONV. CONCLUSION: Intraoperative hypotension evaluated by AUC-s100% was related to PONV in thyroidectomy.

Association between intraoperative hypotension and postoperative nausea and vomiting: a retrospective analysis of 247 thyroidectomy cases

Abstract Background: Postoperative nausea and vomiting (PONV) are major complications after general anesthesia. Although various pathways are involved in triggering PONV, hypotension plays an important role. We hypothesized that intraoperative hypotension during general anesthesia might be responsible for the incidence of PONV. Methods: We retrospectively investigated patients who underwent thyroidectomy. The initial blood pressure measured before induction of anesthesia was used as the baseline value. The systolic blood pressure measured during the operation from the start to the end of anesthesia was extracted from anesthetic records. The time integral value when the measured systolic blood pressure fell below the baseline value was calculated as area under the curve (AUC) of s100%. Results: There were 247 eligible cases. Eighty-eight patients (35.6%) had PONV. There was no difference in patient background between the patients with or without PONV. Univariate analysis showed that the total intravenous anesthesia (TIVA) (p = 0.02), smoking history (p = 0.02), and AUC-s100% (p = 0.006) were significantly associated with PONV. Multiple logistic regression analysis revealed that TIVA (OR: 0.54, 95% CI: 0.29-0.99), smoking history (OR: 0.60, 95% CI: 0.37-0.96), and AUC-s100% (OR: 1.006, 95% CI: 1.0-1.01) were significantly associated with PONV. Conclusion: Intraoperative hypotension evaluated by AUC-s100% was related to PONV in thyroidectomy.

Morphine inhibits cell viability and growth via suppression of vascular endothelial growth factor in human oral cancer HSC-3 cells.

PURPOSE: Although many oral cancer patients require opioids, the effects of morphine and related drugs on oral cancer progression have not been well established. Thus, we examined the effects of morphine exposure on the viability of human oral squamous carcinoma HSC-3 cells and aimed to identify the underlying mechanism. METHODS: We exposed HSC-3 cells to the various concentrations of morphine (0, 0.1, 1, 10, 100, or 1000 µmol/L) for 48 h and, subsequently, evaluated cell viability using the 3-[4, 5-dimethylthiazol-2-yl]-2, 5-diphenyl tetrazolium bromide (MTT) assay and cytotoxicity using the lactate dehydrogenase (LDH) assay. To explore the effects of morphine on cell proliferation further, colony formation assay and cell cycle analysis were performed. Additionally, the intracellular expression of nuclear factor kappa B (NF-κB) was analyzed using flow cytometry, and vascular endothelial growth factor (VEGF)-A was evaluated using human VEGF assay. RESULTS: Morphine exposure reduced cell viability and enhanced cytotoxicity in HSC-3 cells in a concentration-dependent manner. The number of colonies in the morphine-treated groups was significantly lower than that in the control group. Consistent with these results, morphine exposure significantly reduced the concentration of VEGF in the cell culture medium in a concentration-dependent manner. However, our data show that morphine at clinical concentrations (0.1-10 µmol/L) does not affect cell cycle and apoptosis. CONCLUSIONS: Our results suggest that in human oral cancer HSC-3 cells, morphine exposure inhibits cell viability and growth via suppression of VEGF in clinical conditions.

A case of subcutaneous emphysema/mediastinal emphysema during the use of humidified high-flow nasal cannula.

BACKGROUND: Heated, humidified, high-flow nasal cannula (HHFNC) oxygen therapy allows optimal humidification of inspired gas at high flows and creates a distending pressure similar to nasal continuous positive airway pressure [1]. It has been safely used in adults with moderate hypoxemia with few complications [2, 3]. Hereby, we report serious complications occurred during HHFNC oxygen therapy. CASE PRESENTATION: A 53-year-old female with hemophagocytic lymphohistiocytosis (HLH) was admitted to the intensive care unit because of respiratory failure. After weaning from mechanical ventilation which lasted for 2 weeks, HHFNC therapy at 40 L/min with an FiO2 of 0.5 was started for hypoxemia. Four days later, dyspnea and hypoxemia occurred and chest X-ray and CT scan revealed localized pneumothorax, subcutaneous emphysema, and massive pneumomediastinum. After cessation of HHFNC, respiratory condition improved. CONCLUSION: Subcutaneous emphysema, pneumothorax, and pneumomediastinum should be notified as a serious complication during HHFNC therapy.

Effects of anesthetics on early postoperative cognitive outcome and intraoperative cerebral oxygen balance in patients undergoing lung surgery: a randomized clinical trial.

PURPOSE: One-lung ventilation (OLV) may impair cerebral oxygen balance and induce postoperative cognitive dysfunction (POCD). It is unclear whether the type of anesthetic influences the incidence of POCD in patients undergoing OLV. This prospective study compared the incidence of POCD and intraoperative cerebral oxygen desaturation in OLV patients anesthetized with propofol vs sevoflurane during lung surgery. METHODS: There were 148 participants enrolled in this study and randomized equally to either the propofol or the sevoflurane group. Anesthesia was maintained with either propofol or sevoflurane combined in both groups with fentanyl and epidural anesthesia. Regional cerebral oxygen saturation (rSO2), jugular bulb venous oxygen saturation (SjO2), and the incidence of cerebral oxygen desaturation (rSO2 or SjO2 < 50% or rSO2 < 80% of baseline) were measured during anesthesia. Cognitive function was assessed using seven neurocognitive tests two days preoperatively, five days postoperatively (primary outcome), and three months postoperatively. Bivariable and multivariable regression analyses were conducted to identify factors associated with POCD. RESULTS: Rates of POCD did not differ statistically between groups five days postoperatively (propofol, 16/72 patients; sevoflurane, 24/72 patients; RR, 0.67; 95% CI, 0.39 to 1.15; P = 0.14) or three months postoperatively (propofol, 9/60 patients; sevoflurane, 12/58 patients; RR, 0.73; 95% CI, 0.33 to 1.59; P = 0.42). Only three subjects per group showed intraoperative cerebral oxygen desaturation. Multivariable regression analysis revealed older age as an independent predictor of POCD. CONCLUSIONS: No statistically significant difference in the incidence of POCD could be detected between the sevoflurane and propofol anesthesia groups. Postoperative cognitive dysfunction was relatively frequent following OLV in both groups. ( REGISTRATION NUMBER: UMIN 000002826).

RéSUMé: OBJECTIF: La ventilation unipulmonaire (VUP) pourrait avoir un impact négatif sur l'équilibre d'oxygène cérébral et induire une dysfonction cognitive postopératoire (DCPO). Nous ne savons pas si le type d'agent anesthésique influence l'incidence de DCPO chez les patients recevant une VUP. Cette étude prospective a comparé l'incidence de DCPO et de désaturation peropératoire en oxygène cérébral chez les patients sous VUP anesthésiés avec du propofol vs du sévoflurane pendant une chirurgie pulmonaire. MéTHODE: Au total, 148 patients ont participé à cette étude et ont été randomisés en deux groupes égaux à recevoir du propofol ou du sévoflurane. L'anesthésie a été maintenue à l'aide de propofol ou de sévoflurane, et l'agent de choix a été combiné à du fentanyl et à une anesthésie péridurale dans les deux groupes. La saturation en oxygène cérébral régional (rSO2), la saturation en oxygène veineux au bulbe de la veine jugulaire (SjO2) et l'incidence de désaturation en oxygène cérébral (rSO2 ou SjO2 < 50 % ou rSO2 < 80 % par rapport aux valeurs de base) ont été mesurées pendant l'anesthésie. La fonction cognitive a été évaluée à l'aide de sept tests neurocognitifs deux jours avant l'opération, cinq jours après l'opération (critère d'évaluation principal) et trois mois après l'opération. Des analyses de régression bivariée et multivariée ont été réalisées afin d'identifier les facteurs associés à une DCPO. RéSULTATS: D'un point de vue statistique, les taux de DCPO n'étaient pas différents entre les groupes à cinq jours postopératoires (propofol, 16/72 patients; sévoflurane, 24/72 patients; RR, 0,67; IC 95 %, 0,39 à 1,15; P = 0,14) ou à trois mois postopératoires (propofol, 9/60 patients; sévoflurane, 12/58 patients; RR, 0,73, IC 95 %, 0,33 à 1,59; P = 0,42). Seuls trois patients par groupe ont manifesté une désaturation peropératoire en oxygène cérébral. L'analyse de régression multivariée a révélé qu'un âge avancé était un prédicteur indépendant de DCPO. CONCLUSION: Aucune différence significative d'un point de vue statistique n'a été observée en ce qui a trait à l'incidence de DCPO entre les groupes anesthésiés au sévoflurane ou au propofol. La dysfonction cognitive postopératoire était relativement fréquente après une VUP dans les deux groupes. (Numéro d'enregistrement: UMIN 000002826).

[Exposure to 1 % Sevoflurane for 6 Hours Enhances Proliferation of Human Colon Cancer Cells].

BACKGROUND: Sevoflurane is one of the commonly used volatile anesthetics in cancer patients. The protective effect of sevoflurane preconditioning has raised concerns about whether sevoflurane could act advantageously for survival even of cancer cells. Therefore, we investigated the effects of sevoflurane on proliferation in colon cancer cell lines. METHODS: HCT116 and HT29 cells were plated in 96-well plates at a density of 1 x 10(4) cells/well and incubated overnight. On the next day, cells were exposed to 1% or 2% sevoflurane for 6 hr. After 24 hr recovery, we performed MTT assay. The absorbance of the formazan product was measured at a wavelength of 570 nm using 650 nm as the reference. In addition, to investigate the role of adenosine triphosphate-sensitive potassium (K(ATP)) channels, we conducted the same experiment under co-administration of K(ATP) inhibitor, glibenclamide. RESULTS: Only 1% sevoflurane significantly enhanced cell proliferation compared to the control in HCT116 and HT29 cells. Enhanced proliferation by sevoflurane was completely blocked by co-administration with glibenclamide in HCT116 cells. CONCLUSIONS: We had shown that 1% sevoflurane for 6 hr potentially enhances cell proliferation via K(ATP) channels in cancer cells.

Effect of sevoflurane on human hepatocellular carcinoma HepG2 cells under conditions of high glucose and insulin.

Diabetes mellitus is associated with morbidity and progression of some cancers, such as hepatocellular carcinoma. It has been reported that sevoflurane, a volatile anesthetic agent commonly used in cancer surgery, can lead to lower overall survival rates than those observed when propofol is used to treat cancer patients, and sevoflurane increases cancer cell proliferation in in vitro studies. It has been also reported that glucose levels in rats anesthetized with sevoflurane were higher than those in rats anesthetized with propofol. We investigated the effect of sevoflurane, under conditions of high glucose and insulin, on cell proliferation in the human hepatocellular carcinoma cell line, HepG2. First, we exposed HepG2 cells to sevoflurane at 1 or 2 % concentration for 6 h in various glucose concentrations and then evaluated cell proliferation using the MTT assay. Subsequently, to mimic diabetic conditions observed during surgery, HepG2 cells were exposed to sevoflurane at 1 or 2 % concentration in high glucose concentrations at various concentrations of insulin for 6 h. One-percent sevoflurane exposure enhanced cell proliferation under conditions of high glucose, treated with 0.05 mg/l insulin. Our study implies that sevoflurane may affect cell proliferation in human hepatocellular carcinoma cells in a physiological situation mimicking that of diabetes.