Tag Archives: Sevoflurane

Modification of Renal Permeability for Proteins after General Anesthesia with Sevoflurane and Desfluran

Introduction: Sevoflurane degradation by carbon dioxide absorbents during low-flow anesthesia lead to the formation of a haloalkene called compound A, which causes nephrotoxicity.
Material and methods: We determined proteinuria by spectophotometry at 600 nm, preoperatively and postoperatively at 24 and 72 hours in 52 patients undergoing general anesthesia with sevoflurane and 25 patients undergoing general anesthesia with Desfluran. We selected patients without previous renal disease, with anesthetic risk ASA I–III who underwent major abdominal and thoracic surgery lasting more than 150 minutes and we used a 2 l/minute FGF-fresh gas flow, with a MAC-minimal alveolar concentration of 1.5 to 1.8 for Sevoflurane, and of 6–8 MAC for Desfluran.
Results: Renal permeability is impaired by general anesthesia with Sevoflurane (p ˂ 0.0001) and Desfluran (p > 0,001). The amount of filtered protein has a maximum at 24 hours after surgery with gradual decrease within 72 hours, but without reaching the normal preoperative values.
Conclusions: There is proteinuria after exposure to volatile agents like Sevoflurane and Desfluran recording a maximum in the first 24 hours and there is also a tendency to normalization within 72 hours. We noticed a marked impairment of renal permeability in association with specific groups of pathology as septic patients, diabetics, hypertensives, especially after Sevoflurane anesthesia. There was no-one case of acute renal failure in which to criminalize Sevoflurane or Desfluran.

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Myocardial Protection with Sevoflurane in Patients with Cardiac Risk Undergoing Non-cardiac Surgery

Objective: Evaluation of cardioprotective effects of sevoflurane compared with propofol in high-risk cardiac patients undergoing non-cardiac surgery.
Material and methods: Prospective study enrolling 14 patients with cardiac risk Lee’s score > 3 points, undergoing abdominal elective surgery. The patients were divided into two groups: Group S (sevoflurane) – 8 patients who received balanced anesthesia with sevoflurane; Group P (propofol) – 6 patients receiving total intravenous anesthesia – target control infusion (TIVA-TCI). All patients were monitored hemodynamically, cardiac biomarkers (troponine I – TnI, the precursor of brain natriuretic peptide – proBNP, myocardial creatine kinase – CKMB) and inflammatory tests (high sensitive C-reactive protein – CRP, fibrinogen – FBG, interleukin 6 – IL6) were registered perioperatively.
Results: All patients had a decrease of mean arterial pressure (MAP) after induction, with significant values in Group P (48.4±3.82 mmHg). There were no acute cardiac perioperative events and the concentration of TnI after surgery was significantly lower in patients with sevoflurane anesthesia ( 0.017±0.01 ng/ml vs. 0.2±0.18 ng/ml) at 12 h and 24 h respectively (p <0.05). CKMB had lower postoperative values in Group S vs. Group P. ProBNP was elevated preoperatively in all patients and it is correlated with increased cardiac risk. In postoperative period the patients have lower levels in Group S compared with Group P (p <0.05). IL6 showed a significant decrease in patients in Group P at 12–48 h after surgery.
Conclusion: Anesthesia with sevoflurane, in patients with increased cardiac risk undergoing non-cardiac surgery, was accompanied by decreased values of TnI, proBNP and CKMB postoperatively, compared with propofol anesthesia.

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Study on Changes of the Urea, Serum Creatinine and Glomerular Protein Permeability, after General Anesthesia with Sevoflurane

DOI: 10.1515/amma-2015-0053

Introduction: The widespread use of sevoflurane as an induction and maintenance volatile agent of general anesthesia demostrates an increased safety profile. Sevoflurane contact with CO2 absorbents lead to the occurrence of toxic compounds such as Compund A and Compound B . Among the side efffects of Sevoflurane remember the renal toxic effect much discussed in the literature but still unresolved. In previous research we have demonstrated the glomerular protein changes as a result of exposure to Sevoflurane. In the current study we intend to monitor the changes in blood urea nitrogen and serum creatinine after exposure to Sevoflurane.
Material and method: We included in our study 90 patients who were anesthetized in the Department of Anesthesiology of the County Mure Hospital during 01.10.2009-01.10.2014. They had normal values for blood urea nitrogen and serum creatinine and had no preoperative proteinuria. Serum and urine samples were taken preoperatively and at 24 and 72 hours postanesthetic and were analyzed in the laboratory. Proteinuria was determined by spectrophotometry.
Results: After protein quantitative determination by spectrophotometry and statistical anaysis we obtained significant differences by comparing the average preoperative/24 hours total protein (p<0.0001) and 24/72 hours (p<0.0001). There are no significant statistical differences by comparing the blood urea nitrogen at the three intervals (p<0.53) and no statistical changes for mean serum creatinine (p<0.18).
Conclusions: Changes in glomerular filtered proteins following exposure to Sevoflurane demonstrate its toxic effect on glomerular tubules. Lack of perioperative significant wich is why we recommend determining perioperative urinary protein as a marker of glomerular damage.

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