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Comparison between sevoflurane/remifentanil and propofol/remifentanil anaesthesia in providing conditions for somatosensory evoked potential monitoring during scoliosis corrective surgery.

Electrophysiological monitoring is an important tool in spinal corrective surgery. Studies have shown that continuous and intermittent undisruptive intraoperative monitoring provides safer conditions for spinal manipulation and reduces neurological deficit after scoliosis surgery (1-3). Somatosensory evoked potentials (SSEP) represent the reproducible electrical activity of cortical and subcortical structures time-locked to a peripheral nerve stimulus (4). Intraoperative SSEP changes may result from surgical injury or ischaemia to the spinal cord. Unfortunately, the signal is also affected by anaesthetic drugs and certain physiological variables (blood pressure, [P.sub.a]C[O.sub.2], Pa[O.sub.2] and haemoglobin concentration). Increasing anaesthetic dose will attenuate the amplitude of the SSEP signal. This effect is reversible and is time- and dose-dependent. An anaesthetic technique that has the least effect on SSEP monitoring and allows quick return of consciousness for immediate neurological assessment ('wake-up' test) is advantageous.

The aims of this study were to compare inhalational sevoflurane/remifentanil infusion anaesthesia with intravenous target-controlled infusion propofol/ remifentanil infusion anaesthesia during idiopathic scoliosis spinal corrective surgery in terms of 1) the effect on SSEP signals and 2) the clinical wake-up profiles.

METHODS

After local institutional ethics committee approval, 20 patients with adolescent idiopathic scoliosis scheduled to undergo spinal fusion and instrumentation at Duchess of Kent Children's Hospital were recruited (Figure 1). All patients were American Society of Anesthesiologists (ASA) PS I or II. Those with congenital musculoskeletal disease, mental retardation, cerebral palsy or known allergy to sevoflurane, propofol or remifentanil were excluded. Informed consent was obtained from all patients and their parents.

[FIGURE 1 OMITTED]

Patients were randomly allocated to one of two groups (S or P). This was a randomised, single-blinded trial. Randomisation was done by drawing lots from 20 envelopes containing pieces of paper, 10 marked with "S" and the other 10 marked with "P". Complete blinding was not possible in this study. EMLA[R] (eutectic mixture of local anaesthetics--lignocaine and prilocaine, AstraZeneca) cream was applied for insertion of an intra-venous cannula but pharmacologic premedication was not used. group S (lots marked S) patients received sevoflurane anaesthesia. These patients were induced by a gradual increase in sevoflurane concentration in 100% oxygen and anaesthesia was subsequently maintained with sevoflurane 0 to 3% (<1.5 minimum alveolar concentration) titrated to clinical requirement. group P (lots marked P) patients were induced and maintained by a target-controlled infusion of propofol at a plasma effect-site concentration of 2 to 5 [micro]g/ml using the Marsh pharmacokinetic model (5) titrated to clinical requirement. Both groups of patients were ventilated with 35% [O.sub.2] mixed with air. Intra-operative analgesia was provided by a remifentanil infusion in a dose range of 0.2 to 0.5 [micro]g/kg/minute with 1 [micro]g/kg boluses given as required in both groups. Atracurium 0.5 mg/kg was given after induction of anaesthesia to facilitate intubation and intraoperative paraspinal muscle dissection. No other opioids were given until completion of the study. Patients were kept normothermic with a warm air blanket (Bair Hugger[R] Temperature Management, Arizant Heatlthcare Inc., USA) and a fluid warmer (Biegler Bw385-L, E. Biegler gmbH, Austria).

Intraoperative monitoring consisted of intra-radial and non-invasive blood pressure, body temperature with a rectal or oesophageal temperature probe, end-tidal C[O.sub.2] and agent monitoring, [O.sub.2] monitoring, pulse oximetry, central venous pressure and peripheral nerve stimulation (AS/3, Datex-Ohmeda Inc, Madison, WI, USA).

The SSEP signals were collected over Cz (2 cm posterior to Cz, 10 to 20 international system of EEg electrode placement) and Cv (on the cervical spine over the spinous process of C2) versus the Fz of the 10 to 20 system. To elicit SSEP, a pair of stimulating electrodes were applied over the posterior tibial nerve behind the medial malleoli. The stimulation current used ranged from 10 to 30 mA and was kept constant once selected for a particular patient. Pulse stimulations with a frequency between 5.1 and 5.7 Hz and duration of 300 [micro]s were applied. An intraoperative spinal cord monitoring system (Nicolet Viking IV, Nicolet Biomedical Inc, Madison, wI, USA) was utilised to record the responses with a 20 to 3000 Hz band pass filter. Continuous averaging was used with 100 times averaging. Averaging times up to 500 times could be taken if the SSEP signal showed poor quality measurement of the latency and amplitude. However, this situation did not occur in the series of cases in this study.

The P37-N46 waveform in the Cz SSEP tracings and the initial negative and following positive in the Cv SSEP were identified so that the latency and the peak-to-peak amplitude could be measured. The mean value and standard deviation of these variables were calculated for each patient at five time-points during surgery, including pre-incision and after anaesthesia induction, spine exposure, instrumentation loading, deformity correction and wound closure. within-patient variability was used as it reflects the reproducibility and reliability of intraoperative SSEP monitoring (6). The within-patient variability was calculated from the ratio of standard deviation to mean value of those SSEP latency/ amplitude measurements:

Variability = SD/mean x 100%

After the baseline SSEP was measured at the time of pre-incision after anaesthesia induction and during the period of spine exposure, SSEP changes were observed in relation to anaesthetic dose increase. In this period, SSEPs were continually recorded and measured, until the amplitude changes had decreased to below 5% of the baseline value. Subsequently SSEP changes in relation to anaesthetic dose decrease were observed, while SSEPs were continually recorded and measured until its amplitude returned to 90% of original baseline. The changes in SSEP amplitude in response to adjustments of anaesthetic dose were analysed with a scatter chart in relation to time. These trend lines of SSEP amplitude with anaesthetic dose change were plotted with a best-fit polynomial function (Microsoft Excel 2000). The change point of the fitting curve was visually measured when the time-point of the best fit polynomial line reached a plateau. For the sevoflurane group, fresh gas flow was increased (6 l/minute) during the dose change in order to allow rapid titration of the end-tidal concentrations.

After surgery, the patients were turned to the supine position. A peripheral nerve stimulator was used to detect any residual muscle relaxation and reversal (atropine 20 [micro]g/kg and neostigmine 50 [micro]g/kg) was given. Anaesthetic agents were stopped and the fresh gas flow increased when the train-of-four ratio was greater than 75%. The recovery period was utilised as a simulated wake-up test. The time intervals from stopping the anaesthetic to eye-opening and toe movement (on command) and extubation were then recorded. At that time, a behavioural score was determined by the physician using a simple classification of level of consciousness in order to decrease observer bias: 1=calm/ cooperative/good, 2=confused/restless/disorientated and 3=drowsy/unable to obey commands. Subsequently, analgesia was administered using incremental boluses of intravenous morphine followed by patient-controlled morphine analgesia.

Data were analysed using the unpaired t test for normally distributed data and Mann-Whitney U test for non-parametric data. For categorical data, the chi-square test was used. SAS system for windows version 8.02 was used for statistical analysis.

RESULTS

Twenty patients completed the study, 10 in each group. Table 1 shows the demographic data. There were no significant differences in age, height, body weight, body mass index, ASA grading or average dose of remifentanil ([micro]g/kg/minute). Table 2 displays the within-patient variability of SSEP in each group of patients. SSEP amplitude varied by 20.1% [+ or -] 7.3% in cortical recording and 18.0% [+ or -] 3.5% in subcortical recording in the propofol group. The corresponding variation in the sevoflurane group was 28.7% [+ or -] 5.9% and 22.2% [+ or -] 5.8% respectively. SSEP latencies varied very little in both groups (1.3% [+ or -] 0.4% to 2.6% [+ or -] 1.2%). There were significant differences in Cz amplitude and Cz latency (Table 2), suggesting that cortical SSEP was affected more by sevoflurane anaesthesia.

[FIGURE 2 OMITTED]

[FIGURE 3 OMITTED]

As the anaesthetic dose increased, the SSEP waveform amplitude decreased with time. Conversely, the amplitude increased when the anaesthetic dose return to baseline. Figure 2 illustrates an example of SSEP recording during this study period. when changes in SSEP amplitude in response to changes in anaesthetic dose were analysed with a scatter chart corresponding to time (Figure 3), there were two clear delay periods in relation to changes in anaesthetic dose. The dose-increase delay period was the decrease in SSEP amplitude in response to an increase in anaesthetic dose. It was measured from the time that the anaesthetic concentration started to increase to the time that the consequent reduction in SSEP amplitude reached a plateau. The dose-decrease delay period was the increase in SSEP amplitude occurring when the anaesthetic dose was decreased. It was measured as the time taken for the SSEP amplitude to increase back to 90% of its baseline value after the anaesthetic concentration had reverted back to the baseline value. The data on dose-increase and dose-decrease delay periods for the two groups are shown in Table 3. Both dose-increase and dose-decrease delay periods were significantly shorter with sevoflurane compared with propofol.

The recovery time intervals in minutes (time from stopping the anaesthetic agent to eye-opening, toe movement and extubation) were significantly shorter in the sevoflurane group (Table 4). Table 5 is a contingency table depicting the behavioural scores. Patients in the sevoflurane group were more calm and cooperative.

DISCUSSION

Observation of SSEP signals has become very important in spinal surgery since it can determine the integrity of the spinal cord during the most critical periods of the procedure. It is reliable not only in idiopathic scoliosis spinal surgery, but also in neuromuscular scoliosis spinal surgery (7). Unfortunately, anaesthetic drugs can affect SSEP signals. All volatile agents produce a dose-dependent increase in SSEP latency and a decrease in amplitude. Sevoflurane is associated with less amplitude reduction than older drugs (8). The effect of propofol on SSEP is still controversial. In some studies, it has attenuated SSEP (9,10), whereas one recent study showed propofol to have little effect (11). Recently, studies showed that propofol anaesthesia caused less suppression, better preservation of cortical SSEP amplitude and less variability (12,13) compared with isoflurane. Opioid drugs cause minimal depression of SSEP (14-16) and opioid-based general anaesthesia should improve the quality of SSEP monitoring intraoperatively. However, when using large doses of opioids for anaesthesia, the pharmacokinetics of conventional drugs would make wake-up testing difficult and may lead to slow recovery and postoperative respiratory depression. Remifentanil is a powerful opioid with a very short context-sensitive half-time that is independent of the duration of infusion and the total dose used. Concurrent administration of remifentanil allows much lower concentrations of propofol or volatile anaesthetics while maintaining stable anaesthesia and producing a faster recovery (17,18).

We have previously shown that sevoflurane/nitrous oxide ([N.sub.2]O)/alfentanil and target-controlled infusion of propofol/alfentanil have comparable effects on SSEP monitoring, whereas sevoflurane/[N.sub.2]O provides a slightly better recovery profile (19). However, recovery was still not particularly fast and [N.sub.2]O has a number of undesirable side-effects, including inhibition of the enzyme methionine synthetase (20). Also, [N.sub.2]O alone or in combination with volatile agent further suppresses the SSEP signal (21,22). Therefore, we feel that using remifentanil to provide opioid-based anaesthesia and avoiding [N.sub.2]O will better preserve intraoperative SSEP signals and produce a better and more predictable patient recovery profile.

In our study, we showed that both agents influence SSEP signals but propofol has significantly less effect than sevoflurane in cortical SSEP. A large number of synaptic transmissions are involved in cortical SSEP. Both intravenous and volatile anaesthetics will suppress interneuronal activity in the cerebral cortex (23), but an animal study showed that volatile anaesthetics modulate synaptic transmission through gABA(A), NMDA and non-NMDA receptors while propofol affects synaptic transmission through gABA(A) receptors alone (24). This would explain the observation that sevoflurane influences cortical SSEP more than propofol. However, there were no significant differences between propofol and sevoflurane anaesthesia in subcortical SSEP signals. The lesser number of synaptic transmissions involved in subcortical SSEP than cortical SSEP is one possible explanation.

The 'wake-up' test, wherein the patient is temporarily allowed to recover consciousness for neurological assessment, has been largely superseded by SSEP monitoring but may still occasionally be necessary and is possibly the gold standard for detection of injury during and after spinal surgery (25). To facilitate this test, an anaesthetic agent that can facilitate rapid and compliant recovery of consciousness will obviously be an advantage. An anaesthetic agent with a short dose-decrease delay period will be better in the event of signal suppression as the anaesthetist will be able to quickly decrease the dose to see if the change is related to anaesthesia. We found that sevoflurane had a significantly shorter time interval from cessation of administration to eye-opening and toe movement and a significantly shorter dose-decrease delay period than propofol. Extubation time was also shorter (P=0.05). The smaller standard deviation with the sevoflurane group (Table 4) suggests that the time required for recovery is more predictable than that with propofol. Although there have been reports of postoperative agitation after sevoflurane anaesthesia (26), in our study patients receiving sevoflurane anaesthesia tended to wake up in a more calm and cooperative state.

Remifentanil consumption was similar between groups so this disparity is unlikely to be related to different doses of propofol compared to sevoflurane. We feel that remifentanil is beneficial during this surgery because it is easily titratable, can significantly reduce MAC, allows analgesia in the event of a wake-up test and has a consistently short context-sensitive half-time. Recent research suggests that there is no increase in postoperative analgesic requirements when used as a substitute for nitrous oxide (27).

Previous studies in Chinese patients in our institution have calculated the [EC.sub.50] for propofol (28) and this data was used, along with clinical signs and drug titration at induction to attempt to maintain equivalent depths of anaesthesia during the monitoring period and also at the end of surgery. Muscle relaxation was used sparingly to assist in the detection of inadequate anaesthesia. It was not possible to measure the actual plasma concentration of propofol in real time and, therefore, difficult to make a direct comparison between sevoflurane MAC and the median effective concentration of propofol ([EC.sub.50]). However, even if we could, there is considerable population variability in these parameters. Processed EEG, such as the bispectral index and the middle latency auditory evoked potential, can be helpful in monitoring anaesthetic depth, but neither has the required sensitivity and specificity to assist us for this purpose and may give different values at equivalent depth of anaesthesia with different drugs and between different patients. Despite our efforts, however, it is not possible to be sure that the doses of sevoflurane and propofol were equipotent between patients and this must be borne in mind as a potential limitation of this study.

In conclusion, this study showed that both sevoflurane and propofol affect the SSEP signal. Sevoflurane has a more pronounced SSEP depressant effect than propofol but a faster onset and offset of this effect with possibly a better recovery profile. Since we believe that better preservation of SSEP signal is more important than faster wake-up, we recommend propofol-based anaesthesia in this setting.

REFERENCES

(1.) Nuwer MR, Dawson EG, Carlson LG, Kanim LE, Sherman JE. Somatosensory evoked potential spinal cord monitoring reduces neurologic deficits after scoliosis surgery: results of a large multicenter survey. Electroencephalogr Clin Neurophysiol 1995; 96:6-11.

(2.) Meyer PR Jr, Cotler HB, Gireesan gT. Operative neurological complications resulting from thoracic and lumbar spine internal fixation. Clin Orthop Relat Res 1988; 237:125-131.

(3.) Epstein NE, Danto J, Nardi D. Evaluation of intraoperative somatosensory-evoked potential monitoring during 100 cervical operations. Spine 1993; 18:737-747.

(4.) Banoub M, Tetzlaff JE, Schubert A. Pharmacologic and physiologic influences affecting sensory evoked potentials. Anesthesiology 2003; 99:716-737.

(5.) Marsh B, white M, Morton N, Kenny GN. Pharmacokinetic model driven infusion of propofol in children. Br J Anaesth 1991; 67:41-48.

(6.) Luk KD, Hu Y, wong YW, Leong JC. Variability of somatosensory-evoked potentials in different stages of scoliosis surgery. Spine 1999; 24:1799-1804.

(7.) Hermanns H, Lipfert P, Meier S, Jetzek-Zader M, Krauspe R, Stevens MF. Cortical somatosensory-evoked potentials during spine surgery in patients with neuromuscular and idiopathic scoliosis under propofol-remifentanil anaesthesia. Br J Anaesth 2007; 98:362-365.

(8.) Rehberg B, Ruschner R, Fischer M, Ebeling BJ, Hoeft A. [Concentration-dependent changes in the latency and amplitude of somatosensory-evoked potentials by desflurane, isoflurane and sevoflurane]. Anasthesiol Intensivmed Notfallmed Schmerzther 1998; 33:425-429.

(9.) Borrissov B, Langeron O, Lille F, Gomola A, Saillant G, Riou B et al. Combination of propofol-sulfentanil on somatosensory evoked potentials in surgery of the spine. Ann Fr Anesth Reanim 1995; 14:326-330.

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(11.) Boisseau N, Madany M, Staccini P, Armando g, Martin F, grimaud D et al. Comparison of the effects of sevoflurane and propofol on cortical somatosensory evoked potentials. Br J Anaesth 2002; 88:785-789.

(12.) Clapcich AJ, Emerson RG, Roye DP Jr, Xie H, Gallo EJ, Dowling KC et al. The effects of propofol, small-dose isoflurane, and nitrous oxide on cortical somatosensory evoked potential and bispectral index monitoring in adolescents undergoing spinal fusion. Anesth Analg 2004; 99:1334-1340.

(13.) Liu EH, wong HK, Chia CP, Lim HJ, Chen ZY, Lee TL. Effects of isoflurane and propofol on cortical somatosensory evoked potentials during comparable depth of anaesthesia as guided by bispectral index. Br J Anaesth 2005; 94:193-197.

(14.) Pathak KS, Brown RH, Cascorbi HF, Nash CL Jr. Effects of fentanyl and morphine on intraoperative somatosensory cortical-evoked potentials. Anesth Analg 1984; 63:833-837.

(15.) Schubert A, Drummond JC, Peterson DO, Saidman LJ. The effect of high-dose fentanyl on human median nerve somatosensory-evoked responses. Can J Anaesth 1987; 34:35-40.

(16.) Kimovec MA, Koht A, Sloan TB. Effects of sulfentanil on median nerve somatosensory evoked potentials. Br J Anaesth 1990; 65:169-172.

(17.) O'Hare RA, Mirakhur RK, Reid JE, Breslin DS, Hayes A. Recovery from propofol anaesthesia supplemented with remifentanil. Br J Anaesth 2001; 86:361-365.

(18.) Samra SK, Dy EA, welch KB, Lovely LK, Graziano GP. Remifentanil- and fentanyl-based anesthesia for intraoperative monitoring of somatosensory evoked potentials. Anesth Analg 2001; 92:1510-1515.

(19.) Ku AS, Hu Y, Irwin Mg, Chow B, Gunawardene S, Tan EE et al. Effect of sevoflurane/nitrous oxide versus propofol anaesthesia on somatosensory evoked potential monitoring of the spinal cord during surgery to correct scoliosis. Br J Anaesth 2002; 88:502-507.

(20.) Brodsky JB, Cohen EN. Adverse effects of nitrous oxide. Med Toxicol 1986; 1:362-374.

(21.) da Costa VV, Saraiva RA, de Almeida AC, Rodrigues MR, Nunes LG, Ferreira JC. The effect of nitrous oxide on the inhibition of somatosensory evoked potentials by sevoflurane in children. Anaesthesia 2001; 56:202-207.

(22.) wolfe DE, Drummond JC. Differential effects of isoflurane/ nitrous oxide on posterior tibial somatosensory evoked responses of cortical and subcortical origin. Anesth Analg 1988; 67:852-859.

(23.) Woodforth IJ, Hicks RG, Crawford MR, Stephen JP, Burke D. Depression of I waves in corticospinal volleys by sevoflurane, thiopental and propofol. Anesth Analg 1999; 89:1182-1187.

(24.) Wakasugi M, Hirota K, Roth SH, Ito Y. The effects of general anesthetics on excitatory and inhibitory synaptic transmission in area CA1 of the rat hippocampus in vitro. Anesth Analg 1999; 88:676-680.

(25.) Vauzelle C, Stagnara P, Jouvinroux P. Functional monitoring of spinal cord activity during spinal cord activity during spinal surgery. Clin Orthop Relat Res 1973; 93:173-178.

(26.) Uezono S, Goto T, Terui K, Ichinose F, Ishguro Y, Nakata Y et al. Emergence agitation after sevoflurane versus propofol in pediatric patients. Anesth Analg. 2000; 91:563-566.

(27.) Lee LH, Irwin Mg, Lui SK. Intraoperative remifentanil infusion does not increase postoperative opioid consumption compared with 70% nitrous oxide. Anesthesiology 2005; 102:398-402.

(28.) Irwin Mg, Hui TW, Milne SE, Kenny GN. Propofol effective concentration 50 and its relationship to bispectral index. Anaesthesia 2002; 57:242-248.

N. Y. FUNG *, Y. HU [[dagger]], M. G. IRWIN [[double dagger]], B. F. M. CHOW [[section]], M. Y. YUEN **

Departments of Anaesthesiology and Orthopaedic and Tramatology, Duchess of Kent Children's Hospital, Hong Kong

* F.H.K.C.A., M.B., B.S., Resident Specialist, Department of Anaesthesiology.

[[dagger]] Ph.D., Research Assistant Professor, Department of Orthopaedics and Traumatology.

[[double dagger]] M.B., Ch.B., M.D., D.A., F.R.C.A., F.H.K.C.A., F.H.K.A.M., Professor and Head, Department of Anaesthesiology, The University of Hong Kong.

[[section]] M.B., Ch.B., D.A., F.R.C.A., F.H.K.C.A., F.H.K.A.M., Consultant, Department of Anaesthesiology.

** M.B., B.S., F.A.N.Z.C.A., F.H.K.A.M., Associate Consultant, Department of Anaesthesiology, Queen Mary Hospital.

Address for reprints: Dr Nga Yin Fung, Department of Anaesthesiology, The University of Hong Kong, Room 424, Block K, Queen Mary Hospital, Pokfulam Road, Hong Kong.

Accepted for publication on June 25, 2008.
TABLE 1
Demographic data

 Propofol Sevoflurane P

Age (y) 15.9 [+ or -] 2.7 15.7 [+ or -] 6.3 0.93
Height (cm) 159 [+ or -] 10.2 155 [+ or -] 5.4 0.28
Body weight (kg) 44 [+ or -] 8.1 44.3 [+ or -] 5.7 0.92
Body Mass Index 17.4 [+ or -] 3.3 18.5 [+ or -] 2.8 0.42

ASA 1:11 4:6 4:6 1.00

Blood loss (ml) 475 (350-1500) 500 (200-1200) 0.73
Remifentanil 0.23 [+ or -] 0.05 0.26 [+ or -] 0.07 0.20
([micro]g/kg/min)

Values are mean [+ or -] SD or median (range).

TABLE 2
Within patient variability of SSEP latency and amplitude in
sevoflurane and propofol groups

 Propofol Sevoflurane P
 (n = 10) (n = 10)

SSEP Cz latency 1.3 (0.4) 2.6 (1.2) 0.006
SSEP Cz amplitude 20.1 (7.3) 28.7 (5.9) 0.01
SSEP Cu latency 1.9 (0.6) 2.0 (0.7) 0.83
SSEP Cu amplitude 18.0 (3.5) 22.2 (5.8) 0.07

Values are mean percentage (SD).

TABLE 3
Dose-increase and dose-decrease delay periods in minutes

 Sevoflurane Propofol p

Dose-increase period of Cz 13.5 (3.3) 18 (12) <0.01
Dose-decrease period of Cz 20.3 (6.6) 31.5 (10.6) 0.03
Dose-increase period of Cu 11.5 (2) 21 (14) <0.01
Dose-decrease period of Cv 17 (6) 29.5 (10.2) 0.01

Values are mean (SD).

TABLE 4
Time from stopping the administration of anaesthetic to eye opening,
toe movement and extubation in minutes

 Sevoflurane Propofol P

Eyes open 5.2 (5.8) 16.5 (14.8) 0.04
Toe movement 5.4 (2.3) 17.4 (14.8) 0.03
Extubation 8.4 (4.0) 18.2 (13.9) 0.05

Values are mean (SD).

TABLE 5
Contingency table for the behavioural score between sevoflurane
and propofol groups (P = 0.07)

Score Sevoflurane Propofol

1 8 3
2 1 7
3 1 0
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Article Details
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Title Annotation:Original Papers
Author:Fung, N.Y.; Hu, Y.; Irwin, M.G.; Chow, B.F.M.; Yuen, M.Y.
Publication:Anaesthesia and Intensive Care
Article Type:Clinical report
Geographic Code:9CHIN
Date:Nov 1, 2008
Words:3889
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