Summary

Background and objective: In previous studies we have demonstrated that it is possible and safe to identify the lumbar epidural space by an acoustic and visible signal. The use of an experimental set-up constructed for this purpose, the acoustic puncture assist device, the lumbar epidural puncture procedure became both audible and visible. In the present study we have extended the use of the device to localize the thoracic epidural space. We have also evaluated whether the device can be used as a practical tool to confirm correct catheter placement.

Methods: In 100 consecutive patients a prototype of the acoustic puncture assist device was connected to the epidural needle in order to localize the epidural space. The device translates the pressure encountered by the needle tip into a corresponding acoustic and visible signal and enables the anaesthesiologist to detect the epidural space by means of the acoustic signal. After catheter insertion, local anaesthetic was administered. Subsequently the epidural block was tested. In 10 patients the device was also connected to the epidural catheter after its insertion into the epidural space.

Results: In all 100 patients included in the study the epidural space was successfully located by means of the acoustic signal. The only recorded complication was intravascular catheter placement in two patients.

Conclusions: It is possible to localize the thoracic epidural space guided by an acoustic signal. The method was shown to be safe, reliable and simple. Potential implications of this technique include better needle control, improved monitoring for training purposes and for clinical documentation of the thoracic epidural puncture as well as identifying correct catheter placement.

Summary

Background and objective: Target-controlled infusions (TCIs) of remifentanil and fentanyl in conscious sedation regimes for extra-corporeal shock-wave lithotripsy have not been reported. We estimated the effect site concentrations of remifentanil and fentanyl needed to obtain adequate analgesia in 50% of patients (EC50) and compared both drugs in terms of intra- and post-procedure complications.

Methods: Forty-four adult patients were randomly distributed into two groups: Group R received remifentanil and Group F received fentanyl TCI with initial effect site concentrations of 1.5 and 2 ng mL−1, respectively. Pain was assessed using a 10-point verbal analogue scale and <3 was considered adequate analgesia. Increments or decrements of 0.5 ng mL−1 were then introduced for subsequent patients according to Dixon's up and down method. During the rest of the procedure, TCI was adjusted to maintain verbal analogue scale <3.

Results: Remifentanil and fentanyl EC50 were 2.8 ng mL−1 (95% confidence interval (CI): 1.8–3.7 ng mL−1) and 2.9 ng mL−1 (95% CI: 1.7–4.1 ng mL−1), respectively (n.s.). At EC50, the probability of having a respiratory rate <10 was 4% (95% CI: 0–57%) for remifentanil and 56% (95% CI: 13–92%) for fentanyl. Hypoxaemia, vomiting and sedation were more frequent in Group F during and after the procedure (P < 0.05).

Conclusions: A similar EC50 but more respiratory depression, sedation and PONV were found with fentanyl TCI than with remifentanil TCI.

To evaluate the effects of adding low-dose fentanyl to 0.75% ropivacaine during peripheral nerve blocks, 30 ASA physical status I–II patients undergoing hallux valgus repair under combined sciatic–femoral nerve block were randomly allocated in a double-blind fashion to receive nerve block placement with 30 mL of either 0.75% ropivacaine alone (group: ropivacaine, n=15) or 0.75% ropivacaine plus fentanyl 1 μg kg−1 (group: ropivacaine–fentanyl, n=15). A blinded observer recorded haemodynamic variables and sedation, as well as the time required to achieve surgical block and the first request for analgesia. Readiness to surgery required 10 min (5–20 min) with 0.75% ropivacaine and 10 min (3–20 min) with the ropivacaine–fentanyl mixture. No differences in the degree of sedation, peripheral oxygen saturation, and haemodynamic variables were observed between the two groups. The degree of pain measured at first analgesic request, and the consumption of postoperative analgesics, was similar in the two groups, while the mean time from block placement to the first request for pain medication was 13.7 h (25–75th percentiles: 11.8–14.5 h) in the ropivacaine group and 13.9 h (25–75th percentiles: 10.5–14.5 h) in the ropivacaine–fentanyl group (P=not significant). We conclude that adding fentanyl 1 μg kg−1 to 0.75% ropivacaine did not provide clinically relevant advantages in terms of onset time, quality and duration of combined sciatic–femoral nerve block in patients undergoing elective hallux valgus repair.

Summary

Background and objective: Magnesium administered before anaesthesia induction results in a significant reduction in intravenous anaesthetic consumption. The purpose of this study was to evaluate whether the dose of intravenous magnesium sulphate reduces the minimum alveolar anaesthetic concentration of sevoflurane for endotracheal intubation (MACEI) and skin incision (MAC), and attenuates haemodynamic responses. Methods: We studied 60 patients who were scheduled for elective surgery. Patients were not premedicated before induction of anaesthesia and were randomly assigned to receive intravenous saline 0.9% (Group I, n = 20) or magnesium sulphate 30 mg kg−1 bolus + 10 mg kg−1 h−1 continuous infusion (Group II, n = 20) or 50 mg kg−1 bolus + 10 mg kg−1 h−1 continuous infusion (Group III, n = 20). Results: Median and 95% confidence limits for sevoflurane MACEI were 2.68 (2.48–2.85), 2.88 (2.70–3.06) and 2.96 (2.70–3.16), and for sevoflurane MAC were 2.08 (1.76–2.40), 2.26 (2.08–2.47) and 2.40 (2.19–2.68) in Groups I, II and III, respectively. The differences in MACEI and MAC among groups were not statistically significant, except Group III in MAC study (P < 0.05). Mean arterial pressures and heart rate did not increase in Groups II and III after endotracheal intubation and skin incision. Conclusions: Magnesium sulphate administered before induction of anaesthesia increases MAC of sevoflurane and reduces cardiovascular responses to intubation.

Summary

Background and objective: The tunnelling phase of ventriculoperitoneal shunt insertion is the most painful part but patients are often given inadequate opioid analgesic for fear of post operative delayed recovery and/or respiratory depression. This may result in an increase in intracranial pressure. Methods: Twenty adults scheduled to undergo ventriculoperitoneal shunt insertion were administered standard anaesthesia. Monitoring included heart rate, electrocardiogram, end-tidal carbon dioxide, invasive blood pressure, and oxygen saturation. Intracranial pressure was monitored by placing the ventricular end of shunt catheter in the dilated lateral ventricle. Five minutes before tunnelling, fentanyl 1 μg kg−1 was administered. Mean arterial pressure, heart rate and intracranial pressure were recorded during tunnelling and subsequently at 1-min interval for 5 min. Data were analysed using t-test and repeated measured test. Results: Tunnelling caused significant increase in mean arterial pressure (from 81.4 ± 11.0 to 110.9 ± 15.3 mmHg, P < 0.05), intracranial pressure (from 21.4 ± 8.1 to 29.2 ± 12.5 mmHg, P < 0.05) and heart rate (from 74.4 ± 13.8 to 94.1 ± 17.8 beats min−1, P < 0.05). Whereas, the increase in haemodynamic parameters persisted for 3 min post-tunnelling, elevated intracranial pressure lasted for 2 min. Conclusion: Tunnelling significantly increases intracranial pressure and blood pressure despite prior fentanyl administration. This may be deleterious in the presence of intracranial pathology.

Background and objective: In this randomized, double-blind study, we aimed to investigate the effect of aminophylline on recovery from sevoflurane.

Methods: One-hundred ASA I–II patients scheduled for elective surgery were randomly divided into two groups receiving either NaCl 0.9% (Group 1, n = 50) or aminophylline 5 mg kg−1 (Group 2, n = 50). All patients were premedicated with atropine 0.01 mg kg−1 and midazolam 0.06 mg kg−1 intramuscularly. Anaesthesia was induced with propofol 2 mg kg−1 for muscle relaxation, and atracurium 0.5 mg kg−1 was maintained with sevoflurane 2% in 50% oxygen and nitrous oxide. Further atracurium (0.1 mg kg−1 was given when needed. Aminophylline or saline was given after sevoflurane was discontinued. Heart rate, mean arterial pressure, peripheral oxygen saturation, the duration of anaesthesia and recovery times (eye opening, verbal response, extubation and successful performance of arithmetical calculations) were recorded.

Results: There were no statistically significant differences in mean arterial pressure, peripheral oxygen saturation and anaesthesia time between the two groups. Heart rate increased significantly (P < 0.05) after aminophylline and was also higher than in the placebo group. Recovery times were significantly shorter (P < 0.001) in the patients receiving aminophylline.

Conclusions: Aminophylline speeded recovery after sevoflurane anaesthesia and it may have some advantage in anaesthesia practice for patients.

Sudden accidental loss of the airway during surgery is potentially hazardous especially when the patient is lying in any position which prevents easy intubation of the trachea. We describe two patients lying in the lateral position who required urgent airway management and endotracheal intubation. In both cases endotracheal intubation was achieved successfully using a light–guided technique – with a prototype illuminated flexible catheter – through an intubating laryngeal mask airway.

Cardiac and major abdominal surgery are associated with granulocytosis in peripheral blood. The purpose of the present study was to describe the granulocyte and monocyte oxidative burst and the expression of adhesion molecules following cardiac surgery with cardiopulmonary bypass and abdominal surgery. The ability to respond with an oxidative burst was measured by means of flow cytometry using 123-dihydrorhodamine. The adhesion molecules CD11a/CD18, CD11c/CD18, CD44 were measured using monoclonal antibodies. Blood samples from eight patients undergoing open-heart surgery were taken before surgery, 1, 5, 10 and 20 min after aortic clamping, and then 1, 5, 10 and 20 min and 1, 2 and 3 h after declamping. Samples from eight patients undergoing abdominal surgery were taken before surgery, at the end of surgery, and 2 and 3 h post-operatively. A decrease in number of granulocytes and monocytes during cardiopulmonary bypass was observed. The percentage of CD11a-positive granulocytes increased from 30% preoperatively to 75% following cardiopulmonary bypass, while CD44-positive granulocytes increased from 5% to 13%. Despite the extent of the changes, these were not significant. The oxidative burst of the granulocytes and monocytes decreased after declamping to 15% and 27% of initial values in vitro. Several hours after surgery, there was no significant difference between the two groups. These results can be explained by a granulocyte and monocyte refractory response developing subsequent to an increased per-operative oxidative burst activity, and the induction of adhesion molecules on granulocytes associated with the cardiopulmonary bypass and surgery. In conclusion, open-heart surgery with cardiopulmonary bypass was associated with a rapid and pronounced activation of leukocytes which may play a role in reperfusion injury.

Background and objective: The aim was to determine if the intravenous administration of sufentanil or clonidine before the induction of anaesthesia could obtund the increase of intraocular pressure associated with rapid-sequence induction.

Methods: Thirty-two ASA I—II patients with no history of eye illness scheduled for elective non-ophthalmic surgery were randomly assigned to receive either sufentanil 0.05 µg kg−1 i.v. (Group A, n = 15) or clonidine 2 µg kg−1 i.v. (Group B, n = 17) prior to induction. General anaesthesia was induced with thiopental (5 mg kg−1) followed by succinylcholine 1 mg kg−1 to facilitate tracheal intubation. The general anaesthetic technique was standardized in both groups. Intraocular pressure was measured using the Schioetz tonometer just before the succinylcholine administration (t0), just before tracheal intubation (t1) and immediately after intubation (t2). Mean arterial pressure and heart rate were recorded at the same time intervals.

Results: Intraocular pressures were similar in both groups at t0, but the sufentanil group had significantly lower values compared with the clonidine group just before (t1) and immediately after tracheal intubation (t2).

Conclusions: Sufentanil is effective in blunting the increase in intraocular pressure caused by rapid-sequence induction with succinylcholine, while clonidine did not seem to have any effect in intraocular pressures just before (t1) and just after (t2) intubation.

Summary

Background and objective: We examined the efficacy of intraoperative propofol administration to prevent pruritus induced by epidural morphine. Methods: Seventy patients ASA I–II undergoing combined epidural and general anaesthesia for hysterectomy were randomly assigned to two groups, Group P where anaesthesia was induced with propofol and fentanyl and maintained with propofol-nitrous oxide and Group S in which anaesthesia was induced with thiopental and fentanyl and maintained with sevoflurane-nitrous oxide. All patients received a ropivacaine epidural bolus with 3 mg morphine 1 h before the end of surgery. The incidence and severity of pruritus were evaluated every 4 h for the first 12 h postoperatively by blinded observers. Results: The total incidence of pruritus was significantly higher (P = 0.024) in Group S (65.6%) compared to Group P (29%) between 4 and 8 h postoperatively. There were also significantly more patients (P = 0.03) reporting severe pruritus in Group S (22%) compared to Group P (0). Conclusion: Propofol-based general anaesthesia compared to thiopental–sevoflurane-based anaesthesia reduces the incidence and severity of pruritus induced by a single injection of 3 mg epidural morphine with ropivacaine.

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.

Summary

Background and objective: The glutamate-nitric oxide-cyclic guanosine monophosphate pathway has been identified as a potential target for anaesthetic agents. However, mice deficient in neuronal nitric oxide synthase have a similar susceptibility to volatile anaesthetic agents to wild-type mice and are not affected by non-isoform selective inhibitors. We hypothesized that the neuronal nitric oxide synthase selective inhibitor, 7-nitroindazole, would also reduce the propofol requirements in wild-type mice but would have no effect in neuronal nitric oxide synthase knockout mice. Methods: We determined the time to loss of righting reflex, time to painful stimulus and time to regaining the righting reflex in neuronal nitric oxide synthase knockout and wild-type mice following the intraperitoneal injection of propofol in untreated, 7-nitroindazole and vehicle only treated animals (n = 6 per group). Propofol (200 mg kg−1) resulted in loss of righting reflex in the untreated and vehicle only groups but was lethal in 7-nitroindazole pre-treated mice, requiring a reduced dose of propofol (100 mg kg−1). Results: 7-nitroindazole pre-treatment significantly reduced the loss of righting reflex (P < 0.001) in both wild-type and knockout mice when compared to untreated and vehicle only pre-treated animals, but had no effect on time to painful stimulus or regaining of the righting reflex. 7-nitroindazole reduced the propofol requirements in knockout mice to the same extent as in wild-type animals. Conclusions: Propofol exerts its anaesthetic effects at least partially via the glutamate-nitric oxide-cyclic guanosine monophosphate pathway. The neuronal nitric oxide synthase knockout mice are sensitive to neuronal nitric oxide synthase selective inhibition suggesting that compensatory pathways in neuronal nitric oxide synthase knockout mice exist.