Der Anaesthesist
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Randomized Controlled Trial Comparative Study Clinical Trial
[Ondansetron as prophylaxis for postoperative nausea and vomiting. A prospective randomized double-blind comparative study with droperidol].
Ondansetron, a selective 5-HT3 receptor antagonist, has recently been shown, in a dose of 8 mg, to be superior to 1.25 mg droperidol in preventing postoperative vomiting. There are indications that a dose of 4 mg of ondansetron may be just as effective in reducing postoperative nausea and vomiting as a dose of 8 mg. The aim of this study was to evaluate the efficacy and the adverse effects of 4 mg ondansetron in the prevention of postoperative nausea and vomiting compared to droperidol in patients undergoing surgery with inhalation anaesthesia supplemented with alfentanil. ⋯ CONCLUSION. Our results show that for the prevention of postoperative nausea and vomiting 4 mg of Ondansetron was inferior to 1.25 mg of droperidol. The drugs were given intravenously prior to general anaesthesia for minor gynaecological surgery with nitrous oxide and enflurane in oxygen supplemented with small boluses of alfentanil.
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Randomized Controlled Trial Clinical Trial
[The optimal administration time for neostigmine following atracurium blockade. Kinetics of antagonists].
The aims of the study were: (1) to predict reversal time from intensive atracurium blockade; and (2) to determine the optimal time of neostigmine administration during recovery from atracurium blockade, i.e., the time at which the administration of neostigmine results in the shortest total recovery time (time from administration of last supplemental dose of atracurium to train-of-four [TOF] ratio 0.70), and at the same time results in the shortest time from administration of neostigmine to TOF ratio 0.70. ⋯ Reversal time can be predicted as 27.3 min - (0.89 x prereversal time (min), and the optimal time of neostigmine administration in atracurium blockade appears to be when TH1 is 1%-10%.
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Randomized Controlled Trial Clinical Trial
[Local oxygen supply to the cerebral cortex during thiopental and propofol anesthesia. First results].
Because the brain is highly vulnerable to damage from even a brief imbalance of oxygen delivery and demand, intraoperative disturbances of local oxygen supply must be avoided. Until now, there has been no method allowing fast and reliable intraoperative measurement of the local oxygen supply in the human brain. Intraoperative investigations were therefore performed using the Erlangen micro-lightguide spectrophotometer. ⋯ In all patients receiving propofol anaesthesia higher local SO2 values were found, even if the patients first received thiopentone (values in parenthesis). The mean local SO2 amounted to 65.4% (57.3%) in the propofol group and 38.8% (45.2%) in the thiopentone group. The number of values below 25% SO2 was 5.6% (5.8%) in the propofol group and 18.7% (19.1%) in the thiopentone group.
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A 34-year-old male (190 cm/100 kg) was scheduled for surgery of the nasal septum. He had had uneventful anaesthesia for appendicectomy 14 years earlier: following 600 mg thiopentone, 180 mg suxamethonium and up to 2 vol.% halothane for 20 min had been used and no symptoms of malignant hyperthermia (MH) were recorded. Following oral premedication with 2 mg flunitrazepam at 7.00 a.m. anaesthesia was induced with a priming dose of atracurium at 8.45 a.m. followed by 0.2 mg fentanyl, 500 mg thiopentone, and 100 mg suxamethonium. Endotracheal intubation was accomplished easily, and the patient was ventilated manually in a semi-closed circle system until spontaneous ventilation resumed. Enflurane (1.5% for 5 min, 1.0% for 10 min, and 0.8% until the diagnosis of MH was suspected) was given in 33% O2/66% N2O. Seventy minutes after induction it was noted that the spontaneous respiratory rate and minute volume had risen continuously from 10/min and 6 l/min, respectively, to 20/min and 12 l/min. Attempts at deepening anaesthesia with repeated doses of fentanyl up to a total dose of 0.95 mg failed to reduce the hyperventilation. In spite of a high fresh gas flow of 6 l/min and assisted manual ventilation, the FIO2 started to fall from 0.34 to 0.28 at 10:20 a.m. The O2/N2O ratio was changed to 1:1, but the FIO2 remained at 0.3. MH was suspected, enflurane was discontinued, and an arterial blood gas analysis was done (Table 2). When marked acidosis and hypercarbia were found, dantrolene 2.5 mg/kg was given, the operation was terminated, and the patient's trachea was extubated and he was monitored closely in the intensive care unit for 24 h. Vital signs were stable (Table 3) and no further complications were observed. The patient did not mention pain or uneasiness postoperatively. About 6 months later, a muscle biopsy was done according to the European MH Protocol and the patient was found to be MHEh. ⋯ It is concluded that the hypercarbia and mixed acidosis were caused by hypermetabolism. A thorough postoperative examination by an internist did not reveal any thyroid, pulmonary, endocrine, or circulatory reason for our intra- and postoperative findings. Iatrogenic factors like superficial anaesthesia or systemic side effects of adrenaline admixture to local anaesthetics can cause hypermetabolism without striking clinical signs, but they do not cause mixed acidosis lasting longer than 6 h (Table 2). The most suitable explanation in this case is an abortive form of MH. Even patients who are MHS positive on muscle biopsy do not necessarily go through an MH crisis every time they have stress or undergo anaesthesia. The diagnosis of a fulminant MH crisis is a clinical one. Therefore, we are aware that there is no direct scientific ev