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Errors in medical practice are not uncommon and may contribute significantly to health care costs and result in harm to patients 1. The risk of serious drug errors in anaesthesia may be higher than other specialties 2. This is hardly surprising, considering that the average anaesthetist administers at least a quarter of a million drugs during a practice lifetime 3. The reported incidence of drug error during anaesthesia varies considerably from 1:133 (0.75%) to 1:5475 (0.02%) 4-7. Differences in study design and data collection may account for some of this discrepancy. Limited data exist for South Africa 8,9. This prospective study was undertaken to determine the incidence of drug administration errors and near-misses at three tertiary-care hospitals in South Africa. Hospitals A and C had predominantly adult patients and Hospital B was a specialist paediatric hospital. MATERIALS AND METHODS The study was approved by the Ethics Committees of the universities to which the hospitals were affiliated. Anaesthetists were asked to complete a study form for every anaesthetic performed during a six-month period. They were asked to indicate whether a drug administration error or near-miss (an incident with * M.B., Ch.B.

Tracheal intubation, performed routinely during general anaesthesia in patients undergoing intraocular surgery, may have adverse effects on cardiovascular function and intraocular pressure. This study assessed the suitability of the laryngeal mask airway (LMA) as a substitute for tracheal intubation. Intraocular and systemic pressor effects, heart rate changes and catecholamine concentrations were measured in two groups of 10 patients receiving standardized anaesthesia with either a tracheal tube (TT) or a LMA. There were significantly smaller changes in the pressor responses to insertion and in concentrations of catecholamines at critical times in the anaesthetic sequence in the LMA group. Mean (SEM) rate-pressure product was significantly smaller in the LMA group compared with the TT group after both insertion (8276 (730) vs 13307 (1348), P < 0.01) and removal (10152 (595) vs 14137 (1044), P < 0.01) of the airway device. The change in intraocular pressure was significantly less in the LMA group at all time points after airway instrumentation than that in the TT group, with the greatest difference after extubation (-2.3 (2.4) mm Hg vs 14.5 (3.4) mm Hg, P < 0.01).

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The effects of increasing concentrations of halothane and enflurane on selected components of the auditory evoked response were studied in 12 patients; six received halothane and six enflurane. After the induction of anaesthesia with thiopentone, anaesthesia was maintained with 70% nitrous oxide in oxygen. Ventilation was controlled. The inspired concentration of the inhalation agent was increased incrementally, halothane in steps of 0.5% up to 2.5%, and enflurane in steps of 1% up to 5%. With both agents, linear dose-related increases were seen in the latencies of waves III, V, Pa and Nb and the interpeak intervals I-V and III-V, with decreases in the amplitudes of Pa and Nb. In five of the patients the inhalation agent was discontinued at the end of the test period, resulting in reversal of the changes in some or all of these waves. End-tidal carbon dioxide tension was controlled and variations of temperature and arterial pressure were insufficient to produce the observed changes. The results show that halothane and enflurane delay neural transmission along the brainstem and cortical sections of the auditory pathway and that the effects of these agents are approximately related to their known anaesthetic potencies.

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We have studied the effect of propofol on the enzymatic degradation of alfentanil and sufentanil utilizing isolated liver microsomes obtained from pig and human liver. Propofol inhibited dose-dependently the oxidative metabolic degradation of alfentanil and sufentanil by both microsomal preparations. The calculated concentration of propofol causing 50% inhibition of metabolic degradation (IC50) was 32.6 mumol litre-1 for alfentanil and 22.1 mumol litre-1 for sufentanil in pig liver microsomes. Similar values of inhibitory activity of propofol (IC50 values 62.8 and 52.9 mumol litre-1, respectively) were observed using human microsomes prepared from liver taken from an organ transplant donor. We suggest that propofol in clinically relevant concentrations interferes with oxidative metabolic degradation of alfentanil and sufentanil in the microsomal fraction of pig and human liver.