Background and objective: The common parameters of the electroencephalogram quantify a shift of its power spectrum towards lower frequencies with increasing anaesthetic drug concentrations (e.g. spectral-edge frequency 95). These ad hoc parameters are not optimized for the content of information with regard to drug effect. Using semilinear canonical correlation, different frequency ranges (bins) of the power spectrum can be weighted for sensitivity to changes of drug concentration by multiplying their power with iteratively determined coefficients, yielding a new (canonical univariate) electroencephalographic parameter.

Methods: Electroencephalographic data obtained during application of volatile anaesthetics were used: isoflurane (n = 6), desflurane (7), sevoflurane (7), desflurane during surgical stimulation (12). Volatile anaesthetic end-tidal concentrations varied between 0.5 and 1.6 minimum alveolar concentration (MAC). The canonical univariate parameter and spectral-edge frequency 95 were determined and their correlation with the volatile anaesthetic effect compartment concentration, obtained by simultaneous pharmacokinetic—pharmacodynamic modelling, were compared.

Results: The canonical univariate parameter with individually optimized coefficients, but not with mean coefficients, was superior to the spectral-edge frequency 95 as a measure of anaesthetic drug effect. No significant differences of the coefficients were found between the three volatile anaesthetics or between the data with or without surgical stimulus. The coefficients for volatile anaesthetics were similar to the coefficients for opioids, but different from coefficients for propofol and midazolam.

Conclusions: The canonical univariate parameter calculated with individually optimized coefficients, but not with mean coefficients, correlates more accurately and consistently with the effect site concentrations of volatile anaesthetics than with spectral-edge frequency 95.

Iatrogenic injury to the spinal accessory nerve following surgical procedures in the neck is well recognized in causing significant morbidity to patients, with shoulder pain and loss of function being particularly problematic. We have used a Magstim Neurosign 100 peripheral nerve monitor, that is most often used in our practice to monitor the facial nerve during middle ear and parotid surgery, to monitor the accessory nerve during neck surgery. Ten patients undergoing accessory nerve-sparing neck dissection, or excision biopsy of neck mass had their accessory nerve monitored during the procedure. No patient suffered injury of the nerve. In several cases the nerve closely adhered to the tissue being resected, and in two cases, the nerve bifurcated or gave off branches. We found that the monitor aided identification and preservation of the nerve.

The aim of specific monitoring in neuroanaesthesia is to detect, as quickly as possible, intraoperative ischaemic insults so that the brain and the spinal cord may be protected from harmful and frequently inevitable events due to the type of surgery, patient positioning, haemodynamic changes or any intercurrent event. New monitors are being introduced into the operating theatre, but only a few are considered to be an absolute standard of care in neurosurgery, e.g. facial nerve monitoring for surgery of acoustic neuromas and recording of evoked potentials during repair of scoliosis. In the past decade, new monitoring devices have moved from the experimental stage to the operating theatre and although most are still in a phase of technological development and/or definition of their field of applicability they are being used as guides for clinical practice in those instances where cerebral well-being might be impaired. The metabolic consequences of hyperventilation, pharmacological electroencephalogram burst suppression, hypothermia, etc. can now be assessed in the operating theatre. Non-invasive monitoring is being rapidly integrated into our daily work because of its lack of secondary effects. Nevertheless, each new development is regarded as an addition rather than as a substitute for existing equipment. The perfect combination of monitors to provide essential information during an individual surgical procedure to influence a better patient outcome, is still uncertain and needs extensive clinical research.

Background and objective This study investigates the interaction of sevoflurane and nitrous oxide on EEG median power frequency of 2.5 Hz during surgery.

Methods Sevoflurane concentrations required for electroencephalographic median power frequency between 2 and 3 Hz were measured in 25 patients during gynaecological laparotomies. Nitrous oxide was randomly administered at 0, 20, 40, 60 and 75 vol%, subsequently two different concentrations in each patient. The data were analysed using isobolographic analysis together with previously published data on nitrous oxide-isoflurane, -enflurane, or -desflurane interaction.

Results The interaction is described by the equation: C volatile anaesthetic/C0 volatile anaesthetic + C N2O/C0 N2O = 1 (C is the concentrations for a drug combination to achieve the desired effect; C0 is the concentration for single drug use). The parameters are C0 isoflurane = 1.11 vol% (95% CI 1.03–1.19), C0 enflurane = 1.64 (1.52–1.77), C0 desflurane = 5.31 (4.92–5.73), C0 sevoflurane = 2.12 (1.96–2.29), C0 N2O = 174 (153–202). These parameters decrease by 6% (2.5–10) for every 10 years of patients’ age > 40 years.

Conclusions The interaction is compatible with additivity. The potency of nitrous oxide to substitute the volatile anaesthetics is less than anticipated from previously reported MAC values.

We present a case of pulmonary embolism that occurred during the injection of lipiodol during transcatheter arterial chemoembolization under general anaesthesia. A 7-year-old child suffering from a large hepatoblastoma was admitted for arterial chemoembolization and carcinostatic administration. Pulmonary embolism due to lipiodol during arterial chemoembolization was evident by a sudden fall in oxyhaemoglobin saturation from 100 to 90%. This was associated with a spread of lipiodol into both lungs, particularly the middle lung zones and detected by chest fluoroscopy. Arterial blood gases returned to normal values 1 day later but pulmonary infiltration persisted for 7 days before final clearance. Pulmonary embolism caused by lipiodol during arterial chemoembolization is infrequent, but such a complication could prove fatal. Understanding the risk of pulmonary embolism in patients receiving lipiodol, during and after arterial chemoembolization, and late onset pulmonary injury is important and a close follow-up for several days after arterial chemoembolization is advisable.

Adequate relaxation of the masseter muscle is important during endotracheal intubation and for the patency of a patient’s airway during recovery from anaesthesia. We evaluated onset and recovery from cisatracurium-induced neuromuscular block at the masseter and adductor pollicis muscles. Thirty patients were randomly allocated to receive either 0.1 or 0.15 mg kg−1 cisatracurium. The evoked response was measured at both muscles using acceleromyography. Onset time was significantly shorter at the masseter muscle than at the adductor pollicis (0.1 mg kg−1 cisatracurium: 155±52 vs. 229±44 s; 0.15 mg kg−1 cisatracurium: 105±24 vs. 174±35 s). Following 0.1 mg kg−1 cisatracurium, recovery to a TOF-ratio of 0.7 was faster at the masseter compared to the adductor pollicis (P < 0.05). In the 0.15 mg kg−1 cisatracurium group recovery of T1 to 75% of control and to a TOF-ratio of 0.7 occurred sooner at the masseter (P < 0.05). We conclude that onset and recovery from cisatracurium neuromuscular block occurs more rapidly at the masseter than at the adductor pollicis. It appears unlikely that residual paralysis is present at the masseter once neuromuscular function at the adductor pollicis has completely recovered.

The concentrations of nitrous oxide, sevoflurane and oxygen in the circle system of a closed-circuit anaesthesia machine, the PhysioFlex™, were measured in seven patients. During anaesthesia, the settings for each gas were changed and their concentrations recorded. At the induction of anaesthesia, it took 80– 510s (median 190 s) for the end-tidal sevoflurane concentration to reach 2.0%, and 920–2640 s (median 1500 s) for the oxygen in the breathing circuit to reach 30%. At this time, the nitrous oxide concentration was 60±3% (mean±SD). During anaesthesia, it took 90–480 s (median 140 s) for the end-tidal sevoflurane concentration setting to decrease from 3.0 to 1.0%, and 90–400 s (median 110 s) to return from 1.0 to 3.0%. When the inspired oxygen was increased from 30 to 50%, circuit concentrations reached equilibrium in 40–60 s (median 40 s), and when decreased from 50% back to 30%, equilibrium took 310–470 s (median 450 s). During recovery from anaesthesia, inspiratory sevoflurane concentration took 40–70 s (median 50 s) to decrease to 0.2%. The PhysioFlex™ provided adequate control of sevoflurane and oxygen concentrations, but not of increasing nitrous oxide concentrations.