Tracheal and arterial CO2 partial pressures were measured simultaneously in 27 laryngectomized patients both while they were awake and during high-frequency jet ventilation. Tracheal gas was sampled during brief interruptions of high-frequency jet ventilation. Agreement between tracheal and arterial CO2 partial pressures was assessed using the Bland–Altman method. The tracheal–arterial CO2 partial pressures gradient during spontaneous breathing was significantly lower (P<0.0002) than during high-frequency jet ventilation. During spontaneous ventilation, the bias was −0.77 kPa (95% CI= −0.99 to −0.55 kPa), and the upper and lower limits of agreement were 0.29 kPa (95% CI= −0.11 to −0.7 kPa) and −1.83 kPa (95% CI= −2.24 to −1.43 kPa). During high-frequency jet ventilation, the bias was −1.61 kPa (95% CI= −1.76 to −1.46 kPa), and the limits of agreement were −0.48 kPa (95% CI= −0.75 to −0.21 kPa) and −2.74 kPa (95% CI= −3.01 to −2.47 kPa). Despite the poor agreement between tracheal CO2 partial pressure and arterial CO2 partial pressure, it is sufficient to allow for adjustment of ventilator settings during jet ventilation.

Major knee surgery is associated with moderate or severe post-operative pain. Intrathecal morphine and continuous femoral 3-in-1 block were compared prospectively in 40 patients for pain after major knee surgery under spinal anaesthesia, with 4 mL isobaric 0.5% bupivacaine. In a random order, 20 patients received preservative free morphine 0.3 mg mixed with spinal bupivacaine. In 20 patients, following spinal anaesthesia with only bupivacaine, femoral 3-in-1 block was performed post-operatively with 0.5% bupivacaine 2 mg kg−1. The block was continued via a catheter with 0.25% bupivacaine 0.1 mL h−1 kg−1 until the next morning (24 h after induction of spinal anaesthesia). Intramuscular oxycodone was given as a rescue analgesic in all patients. Two patients from the femoral group were excluded due to technical failure. Three patients in the morphine group and one patient in the femoral group did not need any additional oxycodone. In the morphine group on average 2.8 (range 0–7) and in the femoral group 3.2 (0–5) additional doses of oxycodone were needed during the 24 h observation period. The mean pain scores were significantly lower in the morphine group at 9 and 12 h into the 24-h trial. Itching was seen only in the morphine group (40% of the patients). Other side effects were similar in the two groups. All patients were satisfied with their pain therapy. Both intrathecal morphine and femoral 3-in-1 block alone were insufficient for the treatment of severe pain after major knee surgery.

One hundred and three patients ASA grades I–II, 16–80 years of age scheduled for arthroscopic meniscectomy were prospectively studied, and randomly allocated to one of four groups: group 1 (n=25): 0.25% bupivacaine (50 mg) intra-articular (IA), group 2 (n=27): 1 mg of 0.1% preservative free morphine chloride in saline, group 3 (n=26): 1 mg of 0.1% preservative free morphine chloride in 0.25% bupivacaine and group 4 (n=25): normal saline (0.9%). The volume given was always 20 mL. Ketorolac [Toradol®, 30 mg intramuscularly (i.m.)] was used as rescue medication; analgesia was assessed using a visual analogue scale (VAS), a verbal rating scale (VRS), supplemental analgesic consumption post-operatively (SAC) and the presence of side effects. Verbal rating scale and visual analogue scale scores showed better pain control in group 1, 20 min after surgery, and in groups 1 and 2 at 4 h and 10 h as well as in the global VAS. In multi-factorial analysis no significant differences among groups or side effects was found. pH analysis of the substances used showed no alterations in the basal pH range. The analgesic efficacy of 20 mL of bupivacaine 0.25% is similar to that of 1 mg of morphine in 20 mL of saline 0.9%. The morphine–bupivacaine mixture was no more efficacious than bupivacaine or morphine alone.

The objective of this prospective study was to determine the nocturnal/diurnal distribution of peri-operative cardiac dysrhythmias in patients with coronary artery disease undergoing major vascular surgery. Eight patients with significant coronary artery disease undergoing major vascular surgery were studied. Continuous Holter monitoring was performed on each patient from approximately 1 h pre-operatively until 2–5 days post-operatively. Frequencies of isolated supraventricular and ventricular premature beats, and runs of supraventricular and ventricular premature beats were calculated for 6-h periods (00.00–06.00; 06.00–12.00; 12.00–18.00; 18.00–24.00 hours). Supraventricular tachycardia occurred significantly more frequently between 00.00 and 06.00 hours than during the other 6-h periods studied in the post-operative period following major vascular surgery.

The influence of acute moderate haemodilution on the relation between dose and response for rocuronium was evaluated in 60 adult patients, ASA grade I, undergoing elective plastic surgery. The patients were randomly allocated to either the control or the haemodilution group. Following the induction of general anaesthesia, the status of acute moderate haemodilution in the haemodilution group was achieved by draining venous blood, and intravenous infusion of lactated Ringer's solution, 6% dextran or gelofusine, during which the levels of haemoatocrit and haemoglobin dropped from 44% to 27.5% and from 148.3 to 91.3 g L−1, respectively. Neuromuscular function was assessed mechanomyographically with train-of-four stimulation at the wrist every 12 s and the percentage depression of T1 response was used as the study parameter. The relation between dose and response for rocuronium in the two groups was determined by the cumulative dose–response technique. The results showed that the dose–response curve for rocuronium during acute moderate haemodilution was shifted in a parallel fashion to the left and the potency of rocuronium was increased. There were significant differences in ED50, ED90 and ED95 between the two groups. The ED50, ED90 and ED95 of rocuronium in the haemodilution group was decreased by 28.2%, 35.4% and 38.8%, respectively, compared with the control group.

The effects of adding midazolam and bupivacaine to human cerebrospinal fluid in glass test tubes were examined by looking for changes in pH and a reduction in the transparency of the solution. Midazolam (n=6), 0.25% bupivacaine (n=6), 5 mg of midazolam in 6 mL of 0.25% bupivacaine (n=6) and 5 mg of midazolam in 10 mL of saline (n=6) were added to 1.5-mL samples (n=24) of cerebrospinal fluid taken at the time spinal anaesthesia was begun. Transparency and pH were checked after each increment. Cerebrospinal pH was decreased to below 7.0 by adding more than 3 mg of midazolam, more than 1.9 mL of 0.25% bupivacaine or 1.3 mL of the mixture. Cerebrospinal transparency was decreased by adding more than 0.7 mg of midazolam, 1.1 mL of 0.25% bupivacaine or 0.6 mL of the mixture. Midazolam in saline neither decreased the pH below 7.0 nor reduced transparency. These results do not suggest that clinically useful doses of intrathecal or epidural midazolam are neurotoxic.

Lignocaine is a suitable and safe agent for intravenous regional anaesthesia (IVRA) with rapid onset of good surgical anaesthesia. The onset time of the local anaesthetic action of lignocaine was 11.2±5.1 min. Satisfactory surgical conditions, evidenced by good sensory blockade were achieved within 20 min, and no additional analgesics were required. There was no trend towards a fixed sequence, radial, median and ulnar in the development of sensory blockade. No patient exhibited objective symptoms of toxicity, either local or systemic, after release of the tourniquet, nor were there any subjective complaints. No changes in blood pressure, heart rate or oxygen saturation were observed at any time during the procedure, or after deflation of the tourniquet. After releasing the tourniquet lignocaine is rapidly and biexponentially eliminated, with a t1/2a of 4.3±2.1 min and a t1/2β of 79.1±31.2 min. Total body clearance was 0.86 ± 0.39L min−1. Eight patients showed rapid release of lignocaine from the exsanguinated area. In two patients the systemic plasma concentration of lignocaine increased more slowly than in the remaining eight. This can be explained by a greater degree of lignocaine absorbtion in the tissues of the arm. Pharmacokinetic constants after rapid and slow absorption were calculated.

The aim of the present study was to evaluate the effects of neostigmine as a final anaesthetic manoeuvre on colonic anastomoses. A colonic anastomosis was constructed in 40 Sprague-Dawley rats. The animals were divided into two groups: (1) rats receiving intravenous saline solution (placebo); and (2) rats receiving an intravenous injection of neostigmine. The size of the caecum, and the diameters of the pre-anastomotic and post-anastomotic colon were measured during the operation and 4 days after surgery, when all the animals were sacrificed. At this time, the presence of adhesions was also investigated. Each segment containing an anastomosis was removed, and the bursting pressure and bursting wall tension were determined. Loss of caecum diameter was significantly greater in group 2 than in group 1 (P=0.03). Dilatation and obstruction of the colon were significantly more frequent in group 1 (dilatation, P=0.01; obstruction, P=0.047). Also, consumption of water by group 2 was greater than that by group 1 (P=0.049). No statistically significant differences were found between the diameters of the colon (pre- and post-anastomosis), or with respect to general adhesions and adhesions to the anastomotic line. No significant differences were found between anastomotic resistance (determined in terms of bursting pressure and bursting wall tension) in the two groups. The inclusion of neostigmine in an anaesthetic protocol under experimental setting did not reduce the resistance of colonic anastomoses and did not compromise normal healing. Moreover, obstruction caused by peristaltic weakness might be prevented by the expulsion of stool that is induced by the strong contraction of the colonic smooth muscle.

Pulmonary impairment is more frequent after cardiac surgery than after other major surgical procedures. The present study investigates whether, by using standard respiratory monitoring, i.e. side-stream spirometry and blood gas analysis, it is possible to detect changes in pulmonary function secondary to cardiopulmonary bypass. We investigated 18 patients undergoing elective coronary bypass surgery or aortic valve replacement. Cardiopulmonary bypass resulted in a nonsignificant increase in alveolar-arterial oxygen difference from 33.0 ± 10.6 kPa to 36.1 ± 12.5 kPa and arterial to end-tidal CO2 tension difference from 0.67±0.39 kPa to 0.79±0.54 kPa. Respiratory system resistance was unaltered. In contrast, dynamic compliance decreased significantly after cardiopulmonary bypass from 78.6 ± 22.9 to 65.4 ± 22.4 mL cmH2O−1 with open chest and from 61.0 ± 10.2 to 51.1 ± 17.2 mL cmH2O−1 with closed chest, compared with corresponding values before cardiopulmonary bypass. In conclusion, pulmonary gas exchange was not compromised after cardiopulmonary bypass, but a diminished respiratory compliance was a consistent finding, even in uncomplicated cardiac surgery using routine respiratory monitoring.

A transoesophageal Doppler cardiac output monitor was used to study the cardiovascular changes occurring during laparoscopic cholecystectomy in patients without (group A) or with (group B) a history of cardiovascular disease, i.e. hypertension, ischaemic heart disease or heart failure. Insufflation of the abdomen with carbon dioxide caused significant (P<0.01) falls in mean cardiac index (17.9% in group A, 25.1% in group B) and mean stroke volume index (15.3% in group A, 21.2% in group B). Simultaneously, there was a significant (P<0.05) increase in mean systolic blood pressure (19.4%) in group A. There were no other differences in the cardiovascular responses of the two groups. There was no correlation between systolic blood pressure and either cardiac index or stroke volume index. No significant complications or morbidity were associated with the use of the transoesophageal Doppler monitor. We conclude that the cardiovascular changes associated with insufflation are neither predictable by clinical assessment nor adequately determined by routine monitoring. We recommend the transoesophageal Doppler monitor for use in this situation.

The cause of hearing loss after spinal anaesthesia is unknown. Up until now, the only factor studied has been the effect of the diameter of the spinal needle on post-operative sensorineural hearing loss. The aim of this study was to describe this hearing loss and to investigate other factors influencing the degree of hearing loss. Two groups of 22 similar patients were studied: one group received 6 mL prilocaine 2%; and the other received 3 mL bupivacaine 0.5%. Patients given prilocaine were more likely to develop hearing loss (10 out of 22) than those given bupivacaine (4 out of 22) (P<0.05). The average hearing loss for speech frequencies was about 10 dB after prilocaine and 15 dB after bupivacaine. None of the patients complained of subjective hearing loss. Long-term follow-up of the patients was not possible.

Tramadol is a centrally acting opioid with a low affinity resfor μ-opioid receptors, which has been claimed not to depress respiration as do the classic opioids. The respiratory effects of intravenous (i.v.) pethidine (0.6 mg kg−1) and tramadol (0.6 mg kg−1) were compared in 36 ASA Grade I–II patients in a placebo-controlled double-blind study. After induction of anaesthesia with propofol followed by suxamethonium-facilitated endotracheal intubation, the patients spontaneously breathed halothane in 70% nitrous oxide and oxygen via a non-rebreathing valve. Inspiratory and expiratory oxygen, and end-tidal carbon dioxide concentrations (PetCO2), tidal volume (VT), minute volume of ventilation (MV) and respiratory rate were monitored by a side-stream spirometry at an end-tidal halothane of 0.3%. The recordings were collected before surgery. Pethidine caused significant respiratory depression seen as an increase in fractional inspiratory–expiratory oxygen difference and PetCO2 and as a decrease in MV and respiratory rate. However, the effects of tramadol were similar to those of a placebo. Tidal volume was not affected by any study drug. In conclusion, tramadol 0.6 mg kg−1 was shown not to be associated with respiratory depression, unlike equipotent dose of pethidine in this setting.

Ondansetron 4 mg was compared with metoclopramide 10 mg for prevention of post-operative nausea and emesis in in-patients undergoing major gynaecological surgery in this double-blind, randomized, placebo-controlled, multicentre study. A total of 1044 patients received a single intravenous (i.v.) injection of study medication immediately before induction of anaesthesia. Nausea and emesis were assessed over the 24 h post-operative period. Significantly more patients who received ondansetron experienced no emetic episodes (44%) compared with those who received metoclopramide (37%, P=0.049) or placebo (25%, P<0.001). No nausea was experienced by significantly more patients who received ondansetron (32%) than with patients who received metoclopramide (24%, P=0.009) or placebo (16%, P<0.001). In addition, fewer emetic episodes, less severe nausea and a reduced need for rescue antiemetics were also observed with ondansetron (P<0.05 vs. metoclopramide and placebo). Metoclopramide and placebo-treated patients were also 1.5 times (95% CI 1.5–4.2) and 2.5 times (95% CI 1.1–2.0) more likely, respectively, to experience nausea post-operatively. Overall, ondansetron was the most effective antiemetic in this patient population.

Besides the fast tetrodotoxin-sensitive Na+ current, small dorsal root ganglion neurones of rats also possess a slower tetrodotoxin-resistant Na+ current. The blocking effect of commonly used local anaesthetics upon the tetrodotoxin-resistant Na+ current was investigated in the present paper. Dorsal root ganglia were dissected from adult rats and cells were enzymatically isolated. The whole-cell patch clamp technique was then used to measure inward Na+ currents of small dorsal root ganglion neurones. Externally applied local anaesthetics reversibly blocked the tetrodotoxin-resistant Na+ current in a dose-dependent manner. Half-maximal blocking concentrations for tonic block were: lignocaine, 326 μm; prilocaine, 253 μm; mepivacaine, 166 μm; etidocaine, 196 μm bupivacaine, 57 μm procaine, 518 μm benzocaine, 489 μm; tetracaine, 21 μm; and dibucaine, 23 μm. Blocking of the current by lignocaine was independent of temperature. The quaternary lignocaine derivative QX-314 did not have any effect upon the tetrodotoxin-resistant Na+ current when applied externally. High concentrations of tetrodotoxin also blocked the tetrodotoxin-resistant Na+ current with a half-maximal blocking concentration of 115 μm. The block by high tetrodotoxin concentrations did not compete with the lignocaine block, suggesting that there were two independent blocking mechanisms for the two substances. The tetrodotoxin-resistant Na+ currents also showed a marked sensitivity to phasic (use-dependent) block by local anaesthetics.

The molecular effects of droperidol (C22H22FN3O2) on single sodium channels from the human brain were investigated using the electrophysiological planar lipid-bilayer technique. Droperidol (0.05–0.8 mm) induced a concentration dependent and voltage independent reduction in the time averaged single channel conductance by two mechanisms: a reduction in the fractional channel open time (major effect, approximately 90%) and a decrease in the channel amplitude (minor effect). The weighted computer fit of the concentration response for the combined effect curve yielded an EC50 of 0.68 mm droperidol and a maximal conductance block of 77%. These blocking effects of droperidol on CNS sodium channels occurred at a concentration range comparable with other specific anaesthetic compounds but far beyond clinical serum levels (up to 0.002 mm). Therefore in contrast with animal preparations (frog peripheral nerve, sodium channel) the human brain sodium channel is not a major target site for droperidol during clinical anaesthesia.

Calcium-channel blockers reduce the in vitro effects of hypothermia and benzodiazepines have been reported to reduce inward calcium flow through L-type cardiac-calcium channels. Thus, this study was designed to determine if diazepam could reduce hypothermia-induced changes in ventricular papillary muscle electromechanical activity. Conventional microelectrode techniques were used while force was recorded using a miniature force transducer. Six experimental groups of electrically paced papillary muscles were formed (n=6 per group). One was exposed to one μm nisoldipine and four were exposed to one of four diazepam concentrations (0.1, 1.0, 10 or 100 μm). A final group had no drug and provided a time-matched control. The effects were determined at 37°C and then at 27°C. At 37°C, diazepam initially increased and then reduced inotropy and APD90. Nisoldipine reduced both APD90 and inotropy. At 27°C, 100 μm diazepam and nisoldipine (1.0 μm) reduced the hyhypothermia-induced lengthening of APD and the increase in force. Although diazepam reduced the hypothermia-induced alterations, the concentration required to do so (100 μm) suggests that this effect has little role in clinical use.

The medical literature sometimes reports neurological complications after spinal or epidural anaesthesia. In a few cases, the onset of symptoms can be a sign of a pre-existing disease without a primary connection with regional anaesthesia. In the following case report, the patient complained of paraesthesias in both legs after a failed spinal anaesthesia, even though the needle had been placed intrathecally. Only neurological examination and nuclear magnetic resonance imaging revealed the presence of syringomyelia.

A 36-year-old female presented with seizures and transient dysphasia in her 31 week of pregnancy. Neuro-radiological investigations revealed a large falx meningioma. A decision was taken to deliver the infant and excise the tumour before term because of the risk of an increase in the size of the tumour and the risk of sinus thrombosis. Therefore, she underwent in her 32 week of pregnancy an elective Caesarean section followed by a craniotomy to remove the meningioma. There were no neonatal complications and she made an uneventful recovery. The final pathology report confirmed the diagnosis of meningioma with progesterone positive receptors.

While Horner's syndrome is a rare and occasionally reported complication of epidural ‘top-ups’ administered for labour and Caesarean delivery, the case reported here followed a low-dose epidural infusion of bupivacaine. Low-dose epidural infusions have generally been regarded as a safer alternative to bolus doses in labour. It is also the case that close supervision is deemed unnecessary in some centres where the mother is receiving such an epidural infusion. This case is reported in order to highlight the potential dangers of a low-dose regime which in spite of the lack of early warning signs may be associated with a high block.

We describe a case of transient neurological deficit that occurred after unilateral spinal anaesthesia with 8 mg of 1% hyperbaric bupivacaine slowly injected through a 25-gauge pencil-point spinal needle. The surgery and anaesthesia were uneventful, but 3 days after surgery, the patient reported an area of hypoaesthesia over L3–L4 dermatomes of the leg which had been operated on (loss of pinprick sensation) without reduction in muscular strength. Sensation in this area returned to normal over the following 2 weeks. Prospective multicentre studies with a large population and a long follow-up should be performed in order to evaluate the incidence of this unusual side effect. However, we suggest that a low solution concentration should be preferred for unilateral spinal anaesthesia with a hyperbaric anaesthetic solution (if pencil-point needle and slow injection rate are employed), in order to minimize the risk of a localized high peak anaesthetic concentration, which might lead to a transient neurological deficit.