Background Although the use of volatile sedatives in the intensive care unit (ICU) is increasing in Europe, it remains infrequent in Asia. Therefore, there are no clinical guidelines available. This study investigates the proper initial concentration of sevoflurane, a volatile sedative that induces a Richmond agitation-sedation scale (RASS) score of –2 to –3, in patients who underwent head and neck surgery with tracheostomy. We also compared the amount of postoperative opioid consumption between volatile and intravenous (IV) sedation.
Methods We planned a prospective study to determine the proper initial sevoflurane concentration and a retrospective analysis to compare postoperative opioid consumption between volatile sedation and propofol sedation. Patients scheduled for head and neck surgery with tracheostomy and subsequent postoperative sedation in the ICU were enrolled.
Results In this prospective study, the effective dose 50 (ED50) of initial end-tidal sevoflurane concentration was 0.36% (95% confidence interval [CI], 0.20 to 0.60%), while the ED 95 was 0.69% (95% CI, 0.60 to 0.75%) based on isotonic regression methods. In this retrospective study, remifentanil consumption during postoperative sedation was significantly lower in the sevoflurane group (2.52±1.00 µg/kg/hr, P=0.001) than it was in the IV propofol group (3.66±1.30 µg/kg/hr).
Conclusions We determined the proper initial end-tidal concentration setting of sevoflurane for patients with tracheostomy who underwent head and neck surgery. Postoperative sedation with sevoflurane appears to be a valid and safe alternative to IV sedation with propofol.
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Malignant hyperthermia is a potentially fatal genetic and metabolic myopathy that presents with high fever, and muscle rigidity, and it often occurs after administering anesthetic medication. Most cases of malignant hyperthermia occur during anesthesia or surgery, but delayed malignant hyperthermia is very rare, and if it is detected late, it has a high mortality rate. A 39-year-old male with an acute subdural hematoma underwent decompressive craniectomy without any intraoperative medical problems, but a high fever above 40degrees C occurred after 8 hours and he was dead in spite of aggressive management after 48 hours postoperatively. We present here a case of delayed malignant hyperthermia along with a review of the related literature.
BACKGROUND Cerebral hyperperfusion syndrome is a recognized complication of carotid endarterectomy, with a reported incidence of 0.3 to 1.2%. Monitoring of regional cerebral blood flow (rCBF) may limit neurological damage. This study was planned to investigate the changes of rCBF according to inhalational anesthetic agents. METHODS: 2.40+/-0.04 kg weighed New Zealand White Rabbits were undergone transient brain ischemia by bilateral carotid artery ligation for 20 minutes. The rCBF was measured by Bowman Perfusion Monitor. RESULTS The value of rCBF in pre-ligation state was not significantly different among the three groups. rCBF in sevoflurane group was decreased to 46% of baseline value during ischemia and increased to 143% just after reperfusion. rCBFs in isoflurane and enflurane groups were abruptly increased instead of decrease like sevoflurane group. The values of rCBF was more increasing after reperfusion in isoflurane and enflurane groups. rCBFs in all groups were return to baseline value 10 minutes after reperfusion. CONCLUSIONS: This results was suggested that sevoflurane might be contributed to create a neurologic damage during ischemia and the hyperperfusion was seen in all three anesthetic agents. The clinical investigation may be needed to establish the value of this experiment.
BACKGROUND It is a well-known phenomenon that alveolar and peritoneal macrophages exposed to bacterial lipopolysaccharide (LPS) induce a large output of nitric oxide (NO) and an inducible nitric oxide synthase (iNOS) mRNA expression. The purpose of this study is actually how much NO production and iNOS mRAN expression are effected by anesthetics (sevoflurane and propofol) on endotoxemic rats. METHODS To examine the production of NO in peritoneal macrophages, NO concentration were measured from the rats following 2 hours exposure to LPS and 2 hours administration of sevoflurane and propofol, respectively. Culture supernatants were collected 24 hours after exposure to LPS and anesthetics and assayed by ELISA (Enzyme Linked Immunosorbent Assay) for production of NO. The iNOS mRNA expression was measured using PCR (Polymerase Chain Reaction) techniques and autoradiography. RESULTS: In the control group, the NO concentration was measured at 2 hours after infusion of LPS to rats, and showed 12 4micrometer.
After insufflations of anesthetics to experimental animals, NO concentration increased in the sevoflurane and propofol groups, 37 13 (p<0.05) and 29 12micrometer (p<0.05) respectively. The size and brightness of the iNOS mRAN bands were distinct in sevoflurane and propofol in order. CONCLUSIONS There were no different in regard of NO production and hemodynamic changes but iNOS mRNA expression between sevoflurane and propofol group in endotoxemic rats.
The mechanism is not clear, but it is related to the strong stimulating effects on the respiratory tract of inhalation anesthetics.
BACKGROUND Spinal cord injury occurring as the result of surgical repair of thoracic and thoracoabdominal aortic disease remains a devastating complication. Anesthetic and ischemic preconditioning have been known to prevent ischemic injury. The purpose of this study was to elucidate the effects of sevoflurane and ischemic preconditioning (IPC) on neurologic outcome, DNA fragmentation and Bcl-2 protein gene expression in transient spinal ischemia. METHODS: Rats were anesthetized with enflurane or sevoflurane, divided by 5 groups: Sevoflurane group and enflurane group (13 minutes of ischemia), Control group, Rapid group, Delayed group (15 minutes of ischemia). Spinal ischemia was produced by both induced hypotension and thoracic aortic cross clamping.
Neurologic scores were assessed at the time of recovery and 1, 2, 3, 24 hours after transient spinal ischemia. After 24 hours, rats were euthenized and spinal cords were removed for the assay of DNA fragmentation. Other groups of rats received 5 minutes of ischemia, and after 1, 6, 24, 48 and 72 hours, spinal cords were removed for the assay of Bcl-2 family protein mRNA and DNA fragmentation. RESULTS: The neurologic injury and DNA fragmentation of sevoflurane group were significantly lesser than enflurane group. 5 minutes of IPC caused increase in Bcl-xl protein mRNA transcription at 48 and 72 hours reperfusion. There were no significant changes in neurologic injury, Bcl-2 family mRNA transcription and DNA fragmentation between control group, rapid group, and delayed group. CONCLUSIONS: Sevoflurane was effective in preventing neurologic injury after 13 minutes of transient spinal ischemia. However, rapid and delayed ischemic preconditioning did not potentiated neuroprotective action of sevoflurane during 15 minutes of spinal ischemia.