Both remifentanil 1 microg.kg(-1) and alfentanil 15 microg.kg(-1) can be used to prevent rocuronium-associated withdrawal movement in children because they are equally effective and attenuate the increase in MAP and HR after intubation.
A 63-year-old woman with amyotrophic lateral sclerosis (ALS) was scheduled for open reduction and internal fixation of the right tibia. Total intravenous anesthesia using propofol and remifentanil without muscle relaxant was selected as the anesthetic method, in order to avoid the possible occurrence of ventilatory depression due to abnormal responses to muscle relaxants and exacerbation of the motor neuron disease. After standard and neuromuscular monitoring devices were applied, anesthesia was induced and maintained with target controlled infusion of propofol and remifentanil in the range of 2.5-5.0 microg x ml(-1) and 2.5-5.0 ng x ml(-1), respectively. To avoid delayed neuromuscular recovery, we did not use any muscle relaxant at all. Intubation was successful and there were no remarkable events during anesthesia, except for three brief hypotensive events; there was no exacerbation of ALS itself during or after the anesthesia. She was discharged on postoperative day 3, without any discomfort.
There is both in vitro and clinical evidence that high-dose propofol can inhibit mitochondrial respiration, resulting in metabolic acidosis. The purpose of this study was to evaluate the effects of propofol anesthesia on the acid-base status in neurosurgical patients with large amount of normal saline administration. Thirty patients undergoing clipping of cerebral aneurysm were randomly assigned to receive propofol (n=15) or isoflurane (n=15). Propofol dose (mean+/-standard error) infused for maintenance was 5.7+/-0.2 mg/kg/h in propofol group. Acid-base parameters such as PaCO2, pH, serum bicarbonate concentration, standard base excess, serum electrolyte concentration, total protein, albumin, lactate, and phosphate were measured before and 4 hours after the induction of anesthesia, and after surgery. The apparent strong ion difference (SIDa), the effective SID (SIDe), and the amount of weak plasma acid were calculated using the Stewart equation. There were no significant differences in pH, PaCO2, bicarbonate, and lactate between 2 groups throughout the whole investigation period. After surgery, standard base excess significantly decreased in both groups without intergroup difference. SIDa and SIDe significantly decreased in both groups, and lactate and strong ion gap significantly increased after surgery in propofol group, but there were no significant differences between 2 groups. Both propofol and isoflurane were associated with hyperchloremic metabolic acidosis in neurosurgical patients with large amount of normal saline administration. The acid-base balance between the 2 anesthetics was similar using Stewart's physicochemical approach.
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