Anesthesia and analgesia
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Anesthesia and analgesia · Jan 2001
Awake craniotomy for removal of intracranial tumor: considerations for early discharge.
We retrospectively reviewed the anesthetic management, complications, and discharge time of 241 patients undergoing awake craniotomy for removal of intracranial tumor to determine the feasibility of early discharge. The results were analyzed by using univariate analysis of variance and multiple logistic regression. The median length of stay for inpatients was 4 days. Fifteen patients (6%) were discharged 6 h after surgery and 76 patients (31%) were discharged on the next day. Anesthesia was provided by using local infiltration supplemented with neurolept anesthesia consisting of midazolam, fentanyl, and propofol. There was no significant difference in the total amount of sedation required. Overall, anesthetic complications were minimal. One patient (0.4%) required conversion to general anesthesia and one patient developed a venous air embolus. Fifteen patients (6%) had self-limiting intraoperative seizures that were short-lived. Of the 16 patients scheduled for ambulatory surgery, there was one readmission and one unanticipated admission. It may be feasible to discharge patients on the same or the next day after awake craniotomy for removal of intracranial tumor. However, caution is advised and patient selection must be stringent with regards to the preoperative functional status of the patient, tumor depth, surrounding edema, patient support at home, and ease of access to hospital for readmission. ⋯ It may be feasible to perform awake craniotomies for removal of intracranial tumor as an ambulatory procedure; however, caution is advised. Patient selection must be stringent with respect to the patient's preoperative functional status, tumor depth, surrounding edema, patient support at home, and ease of access to hospital for readmission.
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Anesthesia and analgesia · Jan 2001
Comparative StudyThe effects of lidocaine on nitric oxide production from an activated murine macrophage cell line.
Nitric oxide (NO), overproduced by activated macrophages, is important in the pathogenesis of various diseases, including septic shock and inflammatory tissue injury, as well as antibacterial host defense mechanisms. We examined the effects of lidocaine on NO production and the expression of inducible NO synthase (iNOS) protein and messenger RNA (mRNA) in activated macrophages. Murine macrophage-like cell line RAW 264 was stimulated for 8 h with lipopolysaccharide (10 mg/mL) and interferon-gamma (50 U/mL) in the presence of various concentrations of lidocaine (0-500 mg/mL). NO production was assessed by measuring levels of the stable metabolites, nitrite and nitrate (NOx), in the culture medium with an automatic analyzer using the Griess reaction. Expression of iNOS mRNA in harvested RAW 264 was quantified by Northern blot analysis using mouse iNOS complementary DNA probe. Expression of iNOS protein in the cells was assessed by Western blot analysis using anti-iNOS antibody. Lidocaine dose-dependently attenuated the increase in NOx levels in response to the stimulants. The drug at any concentration failed to decrease iNOS mRNA expression in RAW 264. Lidocaine at 500 mg/mL decreased iNOS protein levels. These data suggest that lidocaine reduced NO production in activated macrophages at multiple levels after transcription. The inhibitory site appeared to vary with the dose of lidocaine. ⋯ Lidocaine dose-dependently inhibited nitric oxide production by activated macrophages, presumably at levels after transcription. The attenuating effect of lidocaine on organ injuries previously reported may be explained by the ability of the drug to suppress this inflammatory mediator.
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Anesthesia and analgesia · Jan 2001
Comment Letter Comparative StudyPotencies and probabilities: one-sided P values suggest a one-sided story!