A randomized double-blinded study consisting of 107 patients was conducted to compare the effect on post-operative pain relief of intra-articular fentanyl and intra-articular bupivacaine after knee arthroscopy. The results showed that intra-articular bupivacaine produced superior analgesia in the immediate post-operative period. At 2 h post-operatively, the intra-articular bupivacaine group had a mean pain score of 2.0 (standard deviation 2.1, P <0.05) compared with the intra-articular fentanyl group which had a mean pain score of 3.2 (standard deviation 2.3, P <0.05) After 2 h post-operatively, intra-articular bupivacaine and intra-articular fentanyl had a similar effect on pain scores. The mean pain score 18 h post-operatively was 2.7 for the intra-articular bupivacaine group (standard deviation 2.2, P value 0.6) compared with the intra-articular fentanyl group which had a mean pain score of 2.8 (standard deviation 1.9, P value 0.6).

Lignocaine added to the anaesthetic preparation Diprivan® reduces propofol induced pain on injection. This effect is due to a drop in pH which decreases the content of propofol in the aqueous phase of the soya bean emulsion. This in turn changes the electrostatic forces in the emulsion and destabilization occurs. The effect of lignocaine on the anaesthetic potency of propofol was validated in a randomized blind study in the rat. The induction dose of 1% propofol mixed with 1% lignocaine (10+1) was significantly higher when compared with the induction dose of propofol 1% given after a separate injection of 1% lignocaine (9.4±5.5 vs. 5.6±5.2 mg; P<0.05). The duration of sleep was shorter in rats injected with propofol 1% mixed with lignocaine 1% (10+1) compared with those given 1% lignocaine and 1% propofol in separate injections (160±181 vs. 375±202 s; P<0.05). The anaesthetic potency of propofol was not significantly changed by the addition of either saline or hydrochloric acid. The anaesthesia inducing effect was not time-dependent. A similar lower potency was observed for a solution stored for 4 h compared with one freshly prepared, although sleeping time was longer (9.2±6.8 mg; 428±110 s) as compared with the 4 h mixture. The results indicate that lignocaine altered the propofol preparation. The reduced anaesthetic potency of propofol after addition of lignocaine is not due to the resultant drop in pH, which is known to occur.

In a prospective randomized study in children, we compared caudal bupivacaine–clonidine with bupivacaine–morphine to evaluate whether clonidine can be used as an alternative to morphine in caudal anaesthesia. Caudal anaesthesia was administered in 36 children undergoing orchidopexy, hernia repair or circumcision, using 1.5 mL kg−1 bupivacaine 0.18% with either 1 μg kg−1 clonidine (group 1) or 30 μg kg−1 morphine (group 2). Haemodynamic and respiratory parameters, anaesthetic requirements, recovery time and pain score were monitored for 24 h. Eleven children in group 1 and nine children in group 2 did not need any supplementary systemic analgesics throughout the 24-h observation period. Mean (±SD) duration of analgesia in the remaining patients was 6.3 h (±3.3 h) in group 1 and 7.1 h (±3.4 h) in group 2 (P=0.43). Recovery time after anaesthesia was significantly longer in group 1 (16.6±8.8 min) than in group 2 (11.5±4.7 min) (P< 0.05). We conclude that analgesia provided by 1 μg kg−1 clonidine added to caudal bupivacaine is comparable with that provided by 30 μg kg−1 caudal morphine with bupivacaine. Clonidine at this low dose did not cause respiratory depression.

Local anaesthetics injected into the epidural space may deform the dural sac to a variable degree, thereby contributing to variability in the extent of the block. We investigated deformation of the lumbar dural sac after injection into the lumbar epidural space. The subjects were 26 patients with low-back pain who underwent lumbar epidurography and computed tomographic (CT) epidurography, of whom seven also underwent myelography and computed tomographic myelography. The epidural space was entered via the sacral hiatus in 24 patients and through the L5/S1 interspace in two patients. Ten millilitres of local anaesthetic was then injected into the epidural space followed by 20 mL of contrast medium. Computed tomographic epidurography was undertaken approximately 30 min after the epidural injection at the mid-vertebral and mid-discal levels from the first lumbar through to the first sacral vertebrae. The dural sac usually showed an oval or hexagonal shape on the transverse views at the first and second lumbar vertebral levels, and the shape of an inverted triangle below the level of the third lumbar vertebra. A median line of translucency was also observed on the postero-anterior epidurographic view in 25 of the 26 patients. This line was thought to be a manifestation of the dural deformation to the inverted triangle. Dural sac deformation usually shows a specific pattern, although there are individual variations. Dural deformability is an important consideration in any analysis of the spread of epidural block or of the changes of epidural pressure after epidural injection of local anaesthetics.

An increase of more than 50% in cerebral blood flow velocity in the middle cerebral artery was recently reported in hypocapnic volunteers, while inhaling 50% nitrous oxide. We measured cerebral blood flow velocity in the middle cerebral artery in 10 anaesthetized hypocapnic (ETCO2=25 mmHg) patients with brain tumours while administering increasing concentrations of nitrous oxide. At an end-tidal concentration of 50% and 70% nitrous oxide in oxygen, neither mean arterial pressure (base-line: 84±8 mmHg vs. (50% nitrous oxide): 82±9 mmHg and (70% nitrous oxide): 80±8 mmHg) nor cerebral blood flow velocity in the middle cerebral artery (base-line: 32±7 cm s−1 vs. (50% nitrous oxide): 34±8 cm s−1 and (70% nitrous oxide): 34±9 cm s−1) changed significantly. The data from our clinical investigation indicate that administration of increasing concentrations of nitrous oxide to already anaesthetized and hypocapnic patients does not change cerebral blood flow velocity in the middle cerebral artery.

A patient with acute intermittent porphyria was anaesthetized with propofol as part of general an-aesthesia for cholecystectomy. Post-operatively, no clinical sequelae resulted and urinary porphyrins did not exceed pre-operative values.

A prospective, double-blind, randomized, controlled study was undertaken to compare the perioperative analgesic and recovery characteristics of equipotent doses of tramadol, pethidine and nalbuphine (3.0 mg kg−1, 1.5 mg kg−1 and 0.3 mg kg−1 respectively) with placebo (saline 0.02 ml kg−1) given at induction of anaesthesia in 152 ASA I children and young adults undergoing tonsillo-adenoidectomy. Premedication (temazepam and diclofenac), induction and maintenance of anaesthesia (thiopentone, atracurium, nitrous oxide and isoflurane), with controlled ventilation, were standardized. Variables monitored were heart rate (HR) and systolic arterial pressure (SAP) during surgery, time to recovery of spontaneous respiration at the termination of anaesthesia and restlessness, time to awakening, sedation and emesis in the recovery unit. Increases in HR or SAP >33% of baseline during surgery were treated with esmolol 2.0 mg kg−1 intravenously (i.v.) and restlessness during recovery was treated with the same opioid i.v. given with anaesthesia, or pethidine i.v. in the placebo group. With placebo, there was a high requirement for esmolol during surgery and for pethidine in the recovery ward. Tramadol did not reduce the rate of intra-operative treatment with esmolol, but reduced the tramadol requirement during recovery (P<0.05). Pethidine and nalbuphine reduced the intra-operative esmolol requirement more significantly (P<0.025 and P<0.005 respectively) and the need for treatment during recovery with opioids (P<0.005 each). The time to recovery of spontaneous respiration at the end of anaesthesia was only delayed by pethidine. Other recovery variables were similar, except that restlessness–pain scores were reduced by tramadol (P<0.02), pethidine (P<0.005) and nalbuphine (P<0.005). These results suggest that pethidine 1.5 mg kg−1 and nalbuphine 0.3 mg kg−1 given with induction of anaesthesia provide better analgesia during and after tonsillo-adenoidectomy than does tramadol 3.0 mg kg−1. The delay to recovery of spontaneous respiration with pethidine suggests a greater safety profile of nalbuphine and tramadol.

Intrinsic positive end-expiratory pressure can occur when the sternum is closed following cardiac surgery, causing anaesthetic and surgical problems. We measured intrinsic positive end-expiratory pressure after sternal closure in two studies of patients undergoing coronary artery bypass grafting with the same anaesthetic regime. In one, patients were ventilated at 10 breaths min−1, in the other they were randomized to be ventilated at 10 or 20 breaths min=1. After sternal closure, intrinsic positive end-expiratory pressure increased significantly, especially in patients in whom it had been present before sternotomy. Multiple linear regressions with the pooled data from the studies showed that intrinsic positive end-expiratory pressure was positively correlated with ventilatory rate (P<0.005), age (P<0.005) and Body Mass Index (P<0.0005), and negatively with FEV1, as percentage of predicted (P<0.01). There was no correlation between intrinsic positive end-expiratory pressure and a history of smoking. As there was no difference in expiratory resistance between patients ventilated at the two different rates, any effect on intrinsic positive end-expiratory pressure of the higher ventilatory rates could have been due only to the shorter expiratory time.

Hypnotic endpoints and/or EEG variables, e.g. bispectral index, 95% spectral edge frequency and median frequency, have been studied to monitor anaesthetic (hypnotic) depth during total intravenous anaesthesia. In this study, the relation between the hypnotic endpoints of unresponsiveness to verbal commands, loss of eyelash reflex and body movement response to mechanical nasal membrane stimulation vs. bispectral index, 95% spectral edge frequency and median frequency during propofol anaesthesia with or without fentanyl is presented. Forty-two patients were randomly assigned to receive either propofol infusion, 30 mg kg−1 h−1 (n=22), or propofol infusion, 30 mg kg−1 h−1+fentanyl bolus, 2 μg kg−1 i.v. (n=20). Bispectral index, 95% spectral edge frequency and median frequency and propofol doses were monitored and recorded at unresponsiveness to verbal commands, loss of eyelash reflex and inhibition of nasal body movement response. The bispectral index values were significantly higher in the propofol+fentanyl compared with the propofol group, i.e. 74.7±10.9, 73.1±10.5 and 47.1±9.2 vs. 65.8±9.8, 59.6±10 and 33.8±5.7 at unresponsiveness to verbal commands, loss of eyelash reflex and inhibition of nasal body movement response respectively. Doses of propofol for achieving the hypnotic endpoints were significantly lower in the propofol+fentanyl compared with the propofol group. Plasma propofol concentrations at inhibition of nasal body movement response were lower in the propofol+fentanyl compared with the propofol group (9.2±2.0 μg mL−1 vs. 14.1± 4.2 μg mL−1). Our results suggest that fentanyl pretreatment potentiates the effects of propofol and achieves the hypnotic endpoints at higher bispectral index values and lower propofol doses and concentrations (measured at inhibition of nasal body movement response).

In the management of adult respiratory distress syndrome pressure limited mechanical ventilation may protect the lungs from overdistention injury. Unacceptable hypoxia may be avoided by adding nitric oxide to the inspiratory gas, and thus make pressure limited ventilation easier to perform. There exists no consensus about an acceptable lower limit of SaO2, and in the present case we gave preference to pressure limitation at the cost of oxygenation. A young woman with severe adult respiratory distress syndrome was set on pressure limited mechanical ventilation with peak pressures of 35–38 cm H2O, PEEP of 10–12 cm H2O, and FiO2 of 0.95 with 20 ppm nitric oxide. SaO2 varied between 75 and 85%, and cardiac output ranged between 5.2 and 7.5 L min−1. Oxygen consumption was in the upper normal range, and she did not became acidotic. After 3 days, she started to improve. In conclusion, it seems that hypoxia might be well tolerated as long as the circulation is not compromised. It might prove benefical to accept some hypoxia to avoid ventilator induced lung damage.

The post-operative period is particularly dangerous for obese patients. The aim of this study was to compare the immediate post-operative course after either laparoscopic or open gastroplasty. We studied retrospectively 20 and 14 consecutive patients who underwent laparoscopic or open adjustable silicone gastric banding, respectively. After the laparoscopic procedure, patients had a significantly shorter stay in the post-anaesthesia care unit (0.3±0.4 and 1.1±1 days), reduced analgesic requirements, a shorter period of intravenous catheter use (2.3±1.9 and 4.8±1.4 days), were able to walk sooner (1±0.4 and 2.1±1.6 days) and had a significantly shorter duration of in-hospital stay (5.4±2.3 and 15.8±4.5 days) than after an open procedure. This report suggests that the use of laparoscopy for gastroplasty in morbidly obese patients may significantly improve the immediate post-operative course.

A case of recurarization in the recovery room is reported. Accumulation of atracurium in the intravenous line led to recurarization after flushing the line in the recovery room. A respiratory arrest with severe desaturation and bradycardia occurred. Circumstances leading to this event and the mechanisms enabling a neuromuscular blockade to occur, following the administration of a small dose of relaxant, are discussed.

A 42-year-old man presented as an emergency to the ENT department with sore throat and complete dysphagia, having undergone an umbilical hernia repair under general anaesthesia with tracheal intubation 3 weeks previously at another institution. One course of antibiotics from his general practitioner improved the symptoms but, on discontinuation of the antibiotics, symptoms flared up leading to complete dysphagia. Indirect laryngoscopy showed a bulging of the retropharyngeal wall, which was confirmed as a widening of the retropharyngeal space on a lateral soft-tissue X-ray film of the neck. Surgical exploration confirmed a retropharyngeal abscess, which probably occurred as a complication of the original tracheal intubation.

Monocytes play a very important part in humoral as well as in cell-mediated immunity. At present, however, the knowledge of the influence of anaesthetic agents on the functions of monocytes is limited. In the present study, the effects of thiopentone, methohexitone, ketamine, midazolam, droperidol, propofol, etomidate, and fentanyl on monocyte chemotaxis were examined in vitro using a 48-well microchemotaxis chamber. Clinically relevant concentrations of ketamine, midazolam, and droperidol significantly (P≤0.05) inhibited chemotaxis. For that reason, it is possible that these anaesthetics impair the immunological system in vivo. This possibility should be further examined.

In this study the effects of γ-hydroxybutyrate/fentanyl on cerebral blood flow velocity (CBFV) (as measured in the middle cerebral artery by transcranial Doppler ultrasonography) and on cerebrovascular carbon dioxide reactivity were investigated. Mean CBFV (̇Vmean) and haemodynamic responses were recorded in 12 non-neurosurgical patients before, during and after induction of general anaesthesia with γ-hydroxybutyrate (GHB) (20 min constant rate infusion of 100 mg kg−1). Two patients were excluded, one because of bradycardia and the other because of severe myoclonia. During the infusion of GHB, normocapnia was maintained by manually assisting ventilation as necessary. The infusion of GHB did not affect ̇Vmean [awake: 57±12 cm s−1 (mean±SD); 22.5 min: 62±15 cm s−1, NS difference] or mean arterial blood pressure (MAP) (awake: 97±12 mmHg; 22.5 min: 89±10 mmHg, NS). This suggests that cerebral blood flow velocity is unaltered by an anaesthetic dose of GHB. Twenty-five minutes after the start of GHB, fentanyl 3 μg kg−1 and vecuronium 0.1 mg kg−1 were given, the trachea was intubated and the lungs were mechanically ventilated to maintain end-tidal Pco2 of 4.6±0.4 kPa (30 min). At 30 min after the start of the GHB infusion, ̇Vmean and MAP decreased to 38±10 cm s−1 and 76±12 mmHg (both P<0.05 vs 22.5 min) respectively. After adjusting the ventilation to achieve hypocapnia (40 min: end-tidal Pco2 3.5±0.2 mmHg), ̇Vmean decreased to 29±7 cm s−1, while MAP did not change. This allowed the relative vasoreactivity (percentage change in ̇Vmean/0.133 kPa change in the end-tidal Pco2 from normocapnia to hypocapnia) to be estimated as 2.7±1.6% 0.133 kPa−1. This suggests that cerebrovascular response to CO2 during γ-hydroxybutyrate/fentanyl anaesthesia is maintained.

We have studied the apnoea time after induction with two successful drug intubating regimes, both containing remifentanil. Group 1 (n=20); propofol 2 mg kg−1 and remifentanil 2 μg kg−1 and group 2 (n=20); propofol 2 mg kg−1, remifentanil 1 μg kg−1 and lignocaine 1 mg kg−1. Intubation was possible in all 40 patients, and regarded as acceptable in 90% and 85% of patients, respectively. The median time to the return of spontaneous respiration was 487 s in group 1 and 270 s in group 2 (P < 0.05). Median end-tidal CO2 concentration at the time of the first spontaneous respiration was 7.37 kPa in group 1 and 6.3 kPa in group 2 (P < 0.05). Both groups had a decrease in heart rate after induction, but this failed to reach either clinical or statistical significance, and no patient required atropine. Similarly, there was a decrease in arterial pressure after induction in both groups (P < 0.05), but this was not deemed to be clinically significant. Only two patients in each group required ephedrine 6 mg before arterial pressure was restored to within 25% of the base-line. Intubating conditions were similar in both groups, but group 2 provided a significantly shorter apnoea time.

We report the successful use of the intubating laryngeal mask airway in a patient with maxillo-facial trauma for whom the facemask and laryngoscope were relatively contraindicated and the fibreoptic scope potentially difficult to use.

Aprotinin has been reported to influence positively or negatively the process of ischaemia-reperfusion. However, it is a complex drug acting on platelets, neutrophils and coagulation, which may also have a direct effect by inhibiting intracellular proteases and free radical generation. The goal of this study was to determine the direct effects of aprotinin on the myocardial performances of an isolated blood perfused rabbit heart preparation after normothermic global ischaemia. Two groups of 10 hearts were studied. The control group (ischaemia) underwent 30 min of global normothermic ischaemia. In the aprotinin group, (aprotinin) 200 KUI mL−1 of aprotinin was added to the perfusate before ischaemia. Measurements were obtained at base-line, 10, 30 and 60 min after reperfusion. Normothermic ischaemia significantly decreased myocardial performance in both groups. After 60 min reperfusion, myocardial contractility significantly recovered in the aprotinin group compared with the ischaemia group. Aprotinin contributes significantly by limiting the consequences of ischaemia on myocardial performances. This effect may be due to a direct action of the drug because leucocytes and plasma proteins were removed in this preparation.

We evaluated the relation between dose and response for the neuroprotective effect of propofol in a rat model with incomplete cerebral ischaemia. For clarification of the mechanism of neuroprotection, plasma catecholamines and tumour necrosis factor-α levels were measured. Three doses (low, moderate and high-dose) of propofol were tested. These produced, respectively, a low amplitude, slowing and a burst-suppression pattern of electroencephalographic activity. Incomplete cerebral ischaemia was produced by right carotid artery occlusion combined with haemorrhagic hypotension (35 mmHg) for 30 min. Neurological outcome at 72 h post-ischaemia in the high-dose group was significantly better than that in both low-dose and moderate-dose groups. Propofol exhibited a trend in the dose-related attenuation of the increases in plasma adrenaline and noradrenaline during ischaemia. Tumour necrosis factor-α increased during and after ischaemia in all groups with no intergroup differences. The results indicate that a burst-suppression dose of propofol provides neuroprotection. The protective effect can not be completely explained by the attenuating effect on circulating catecholamines.