Background and objective The effect of anaesthesia induced by intrathecal injection of 6.3% MgS04 or 4% lidocaine on intracellular electrolyte homeostasis in spinal cord neurones of a rat model was investigated. Methods Intracellular Ca2+, Mg2+, Na+ and K+ concentrations were determined at different times after intrathecal administration of NaCI (saline, a control group), MgS04 or lidocaine.

Results In both thoracic and lumbar spinal cord segments, Ca2+ concentrations rose significantly 30min and 2 h after 6.3% MgSO4 injection, and after 24 h were still significantly increased compared with the values obtained from the control group which were subjected to sham ‘anaesthesia’ by saline injection (172,121 and 108ngmg−1 protein vs. control 23ngmg−1 protein, respectively, in the thoracic segment and 222, 229 and 176ngmg−1 protein vs. control 43ngmg−1 protein, respectively, in the lumbar segment). Lidocaine injection also produced a significant increase in intracellular Ca2+ in the thoracic and lumbar spinal cord segments (69, 64 and 53ngmg−1 protein vs. control 33.4 ngmg−1 protein and 26, 94 and 46ngmg−1 protein vs. 23ngmg−1 protein respectively). Only a modest rise in intracellular Mg2+ was observed after intrathecal MgS04 or lidocaine injection (27ngmg−1 protein vs. 23ngmg−1 protein). Na+ and K+ concentrations decreased 24 h after MgS04and 1h after lidocaine injection.

Conclusion Intrathecal anaesthesia by MgS04 or lidocaine alters intracellular electrolyte homeostasis in spinal cord neurones of experimental rats. A possible common mechanism of action via Ca2+ ion channels is discussed.

Background and objective The aim of the present study was to compare and assess the quality of analgesia, the safety and the side-effects after the use of a continuous, thoracic epidural infusion of sufentanil (5 μg h−1), 0.25% bupivacaine (10 mL h−1), 0.2% ropivacaine (10 mL h−1) alone or in combination in patients who had undergone major urological surgery. This prospective, randomized, double-blinded study investigated the efficacy of thoracic epidural infusions after major urological surgery.

Methods Patients received a 72-h continuous infusion␣(10 mL h−1) of 0.25% bupivacaine (B), 0.2% ropivacaine (R), 0.25% bupivacaine with 0.5 μg mL−1 sufentanil (BS), 0.2% ropivacaine with 0.5 μg mL−1 sufentanil (RS) or 0.5 μg mL−1 sufentanil only (S). The analysis included 109 patients.

Results The mean visual analogue scale (VAS) scores for pain were highest in the groups R and S (P < 0.001). The PaCO2 values were significantly higher in the groups RS and S (P = 0.003). Motor block occurred more frequently in the groups B and BS than in the other groups (P < 0.001). Sedation, nausea and pruritus were more common in the groups that received sufentanil.

Conclusions A continuous, epidural infusion with these drugs was safe and effective in our patients. The combination of 0.2% ropivacaine plus sufentanil appeared preferable because of the low incidence of motor block.

Background and aim We evaluated the costs and benefits of total intravenous anaesthesia compared with a balanced anaesthesia regimen.

Methods One-hundred and twenty-four patients undergoing cataract surgery were randomized to either a pro-pofol/remifentanil or an isoflurane/fentanyl group. In the propofol/remifentanil group, both drugs were used for induction and maintenance of anaesthesia; in the isoflurane/fentanyl group, anaesthesia was induced with etomi-date and fentanyl and maintained with isoflurane and fentanyl. All patients received mivacurium for muscle relaxation and the lungs were ventilated mechanically. The use of propofol and remifentanil resulted in a faster emergence and an overall savings per case of € 12.25 due to a reduction in personnel costs which outweighs the higher drug acquisition costs.

Results In the propofol and remifentanil group, more patients were satisfied and would accept the same anaesthetic again.

Conclusion We conclude that propofol and remifentanil is more cost-effective than isoflurane/fentanyl due to its better recovery profile, reduced total direct costs and higher patient satisfaction.

Background and objective The aim of the study was to test the peripheral analgesic action of neostigmine. Intraplantar administration of neostigmine was studied in carrageenan-injected rats.

Methods After assessing baseline values (T0) for paw circumference and the paw withdrawal threshold on both hind paws, the right hind paw was injected with 0.2mL of 1% carrageenan and the left hind paw with 0.2mL of saline (0.9% NaCl). Two hours later (T1), both hindpaws were tested for inflammation (paw circumference) and for hyperalgesia (paw withdrawal threshold) and subsequently 20 mg of neostigmine was injected in the right hind paw. The paw withdrawal threshold was tested again 10 (T2), 20 (T3) and 60 min (T4) and paw circumference 60 min (T4) after neostigmine injection.

Results Carrageenan injection in the right hindpaw was associated with a decrease in the paw withdrawal threshold reflecting mechanical hyperalgesia (P < 0.001) and an increase in paw circumference reflecting oedema (P < 0.001) in the right hind paw when compared with the left side from T1 to T4. Neostigmine had no effect on paw circumference and the paw withdrawal threshold at measuring points T2, T3 and T4 when compared with T1 in the right hindpaw. Conclusion Our results support the lack of peripheral analgesic effect of neostigmine.

Background and objective The amount of procalcitonin eliminated in the urine and the plasma disappearance rate of procalcitonin were evaluated in patients with normal and impaired renal function, because patients with sepsis are a main target group for procalcitonin measurement, and these patients often develop renal dysfunction.

Methods Elimination of procalcitonin in the urine (μg 12 h−1) was measured in 76 patients. In another 67 patients, the 50% plasma disappearance rate (t½, h) was evaluated 48 h after peak concentrations (procalcitonin >2 μg L−1). Renal function was assessed by creatinine clearance.

Results Procalcitonin elimination in the urine was significantly reduced in patients with severe renal dysfunction. However, the plasma disappearance rate correlated only weakly with renal dysfunction (Spearman's rank correlation R = −0.36, P = 0.004, regression t½ = 49.87−0.15 creatinine clearance). The 25% quartile and median were 25.2 h and 30.0 h in patients with normal renal function, and 36.3 h and 44.7 h in patients with severely impaired renal function (creatinine clearance <30 mL min−1).

Conclusions Renal elimination of procalcitonin is not a major mechanism for procalcitonin removal from the plasma. Although the plasma disappearance rate may be prolonged up to 30–50% in some patients with renal dysfunction, clinical diagnostic decisions may not be severely influenced by this moderate prolongation of procalcitonin elimination. We conclude that procalcitonin can be used diagnostically in patients with renal failure as well as in those with normal renal function.

Background and objective To test the hypothesis that magnesium sulphate reduces the amount of remifentanil needed for general anaesthesia in combination with propofol and mivacurium, we studied 50 patients undergoing elective pars plana vitrectomy in a double-blind, randomized prospective fashion.

Methods Magnesium sulphate (50 mg kg−1 body weight) or placebo (equal volume of NaCl) was given slowly intravenously after induction of anaesthesia with propofol 1–2 mg kg−1. Anaesthesia was maintained with propofol (using electroencephalographic control), mivacurium (according to train-of-four monitoring of neuromuscular blockade) and remifentanil (according to heart rate and arterial pressure).

Results We observed a significant reduction in remifentanil consumption from 0.14 to 0.09 μg kg−1> min–1 (P> < 0.01). Mivacurium consumption was also markedly reduced from 0.01 to 0.008 mg kg −1min−1 (P < 0.01), whereas propofol consumption remained unchanged. There was a trend towards lower postoperative pain scores, less pain medication requirements in 24 h after surgery and less postoperative nausea and vomiting in the magnesium group but not statistically significant. No side-effects were observed.

Conclusion We can recommend the use of magnesium sulphate as a safe and cost-effective supplement to a general anaesthetic regimen with propofol, remifentanil and mivacurium, although we cannot clearly distinguish between a mechanism as a (co)analgesic agent at the NMDA-receptor site or its properties as a sympatholytic. The effect of a single bolus dose of 50 mg kg−1 on induction lasts for about 2 h. For longer cases, either a continuous infusion or repeated bolus doses might be necessary.

Background and objective Intravenous morphine titration is used to obtain postoperative pain relief, but few studies have assessed the appropriate regimen. In a quality programme, we performed a prospective non-randomized study of morphine titration in a postanaesthesia care unit (PACU).

Methods Four regimens of morphine titration were studied: every 10 (group 1, n = 400) or 5min (group 2, n = 400) with a maximum of five intravenous boluses; every 5min, without any limitation in the number of boluses (groups 3 and 4, n = 400 each); in groups 1, 2, and 3, subcutaneous morphine was administered 4 h after titration. In group 4, administration of subcutaneous morphine was allowed only 2h after titration. A visual analogue pain scale (VAPS) > 30 mm was required to administer morphine and pain relief was defined as a VAPS ≤ 30 mm.

Results After morphine titration, VAPS was lower and the number of patients with pain relief was greater in patients from groups 3 and 4. Patients from group 4 had the lowest VAPS (26±17mm) and the highest percentage of pain relief (73%) at the end of the PACU period. The number of sedated patients increased in groups 3 (62%) and 4 (61%) compared with group 1 (27%). No significant differences in morphine-related adverse effects were observed.

Conclusion Intravenous morphine titration every 5min with an unlimited number of boluses and early subcutaneous administration provided the best analgesic regimen.

Background and objective The purpose of this study was to investigate retrospectively what factors contribute to the development of the type of hyperlactatemia which may follow cardiopulmonary bypass despite well-maintained oxygen delivery and a normal perioperative course.

Methods The medical records of 124 patients undergoing elective cardiac surgery using cardiopulmonary bypass were reviewed. The patients were divided into a hyperlactatemia group (n = 34), where the serum lactate concentration was > 5.0 mmol L−1 perioperatively, and a normal lactatemia group (n=90), which comprised the remaining patients.

Results The duration of cardiopulmonary bypass in the hyperlactatemia group was significantly longer than for the normal lactatemia group. Significant differences of lactate concentrations between the groups, and significant elevations of serum lactate had been observed after the start of cardiopulmonary bypass. Oxygen extraction rates were significantly reduced during the period of cardiopulmonary bypass but, on the contrary, increased in the hyperlactatemia group after surgery. The area under the curve of mean arterial pressure consisted of 5-min interval plots during the initial period of cardiopulmonary bypass in the hyperlactatemia group. This was significantly smaller than for the normal lactatemia group. Weakly significant correlations between maximal lactate and duration of cardiopulmonary bypass, and especially the area under the curve, were observed.

Conclusions It is suggested that the pathophysiology observed is based on impairment of tissue oxygen utilization. The duration of cardiopulmonary bypass and especially the occurrence of hypotension at the start of the bypass period appears to be related to the development of lactic acidosis.

Background and objective Laboratory stress studies found that acute psychological stresses may elicit changes in leukocyte numbers similar to those occurring in physical stresses. Both types of stress evoke – mainly by release of catecholamines – leukocytosis resulting from a release of natural killer cells (NK-cells), of CD8+ T-cells, of monocytes and of neutrophils. However, there is little proof that laboratory stress models can be applied to daily clinical routines. As a likely inductor of an immunological stress response the setting of retrobulbar anaesthesia prior to intraocular surgery permits the study of a short-term painful anaesthetic procedure under highly standardized conditions. This was examined in 16 female patients.

Methods Counts of leukocyte subsets, serum cortisol and cardiovascular variables were measured 30 min and 1 min prior to retrobulbar anaesthesia as well as 2, 15 and 45 min afterwards.

Results The setting of retrobulbar anaesthesia induced an increase in total leukocytes [+380 cells μL−1; P < 0.01 (means; significance level)] mainly due to rising counts of neutrophils (+241 cells μL−1, P < 0.01). Of all lymphocyte subpopulations, natural killer cells increased most markedly (+64 cells μL−1; P < 0.01). Furthermore, the retrobulbar block induced an increase in systolic arterial pressure (+15.2 mmHg; P < 0.01).

Conclusion These changes in immunological and cardiovascular variables are considered to be elements of a sympatho-adrenal stress reaction; catecholamines are considered to induce a demargination of leukocytes by binding to β2-adrenoceptors and by modifying the avidity state of adhesion molecules.

The purpose of this paper is to describe the impact of anaesthesia research on clinical practice. The evolution of neuromuscular blocking drugs from the laboratory to the operating room is used as an example. Particular emphasis is given to the pioneers whose vision made this possible: H. R. Griffith and G. E. Johnson; D. Savage, J. B. Stenlake and W. C. Bowman and J. Viby-Mogensen. Our challenge is to ensure the supply of clinical scientists for the future.

Background and objective The objective of this study was to determine the dose as well as the duration of exposure–dependent effects of methohexital on neutrophil [polymorphonuclear leucocyte (PMN)] free amino acid profiles and, in a parallel study, on PMN immune functions.

Methods Whole blood samples were taken from 20 volunteers and incubated with methohexital [0 (control), 3.6, 26, 130 and 260 μgmL−1] for 10, 30, 60 or 120 min. PMN amino acid profiles were documented using advanced PMN separation and highperformance liquid chromatography procedures. Superoxide anion (O2−) and hydrogen peroxide production (H2O2), and activity of released myeloperoxidase (MPO), were determined photometrically.

Results After methohexital, significant dose (≥26 μg mL−1) as well as duration of exposure–dependent (≥30 min) increases in histidine, isoleucine, leucine, valine, methionine, serine, glycine, threonine, and decreases in glutamine, glutamate, aspartate, asparagine, arginine, ornithine, citrulline, alanine and taurine were observed (P ≤0.05). Concerning PMN immune functions, methohexital significantly decreased O2−, H2O2 formation and MPO (≥26 μgmL−1, ≥30 min, P≤0.05).

Conclusions Altogether, there is significant relevance to the pharmacological regimens which enhance the supply of methohexital in whole blood. In regards to our results, we suggest that considerable changes in PMN ‘dynamic free amino acid pool’, for example induced by methohexital, may be one of the determinants in cell nutrition adversely affecting PMN metabolism. It is partially through its effect on the PMN free amino acid pool that maleficent pharmacological stress may have an unintentional influence on PMN immune functions.

Background and objective Assessment of cardiac preload is of major importance in the management of critically ill patients. Echocardiographic determined left ventricular end-diastolic area and indicator dilution derived intrathoracic blood volume are used as surrogates for cardiac preload. However, no controlled comparison studies on the relationship between induced changes in end-diastolic area and intrathoracic blood volume and concomitant changes in stroke volume index are available.

Methods The effects of a change in body position on these variables were investigated in 10 anaesthetized patients.

Results Intrathoracic blood volume and end-diastolic area decreased by 18 ± 11% and 27 ± 13% respectively. Stroke volume index concomitantly decreased by 19 ± 11%. Correlation analysis revealed a close relation between stroke volume index and intrathoracic blood volume (r = 0.75) and end-diastolic area (r = 0.76).

Conclusions Within the observed range of data, intrathoracic blood volume and end-diastolic area are equivalent indices of cardiac preload.

Background and objective Despite the fact that both general anaesthetics and hypotensive drugs influence autonomic nervous activity, no study has yet examined the heart rate variability during deliberate hypotension and general anaesthesia. The aim of this was to clarify the heart rate variability changes during deliberate hypotension under sevoflurane–nitrous oxide anaesthesia.

Methods Autonomic nervous system activity in patients (n = 45) subjected to deliberate hypotension during sevoflurane in nitrous oxide and oxygen anaesthesia was investigated by a heart rate variability measurement. Three different types of hypotensive drugs, a calcium channel antagonist (nicardipine), a nitric oxide donor (nitroglycerin) and a vasodilatory prostaglandin (alprostadil), were used to induce hypotension.

Results In all groups, low frequency power (sympathetic and parasympathetic indicator) and the ratio of low frequency to high frequency power (the LF/HF ratio, sympathetic indicator) were suppressed by induction of anaesthesia. In the control group, preanaesthesia low frequency power was 195 ± 139 ms2, the LF/HF ratio 10.3 ± 5.7, during anaesthesia 5 ± 9 ms2, 0.6 ± 0.8, respectively, P = 0.0093, 0.0034, whereas high frequency power (parasympathetic indicator) was not significantly changed. In those patients receiving nicardipine or nitroglycerin during anaesthesia, these variables did not differ significantly from those in the control group. During prostaglandin E1 infusion, high frequency power was higher compared with the values in the other groups (17 ± 12 ms2 in the prostaglandin group, 7 ± 6 ms2 in the nicardipine group, 6 ± 5 ms2 in the nitroglycerin group and 6 ± 4 ms2 in the control group, respectively, P = 0.0326, 0.0251, 0.0197).

Conclusions Sevoflurane in nitrous oxide and oxygen anaesthesia reduces sympathetic autonomic activity considerably, and the expected increases caused by hypotensive agents that occur in awake volunteers were not seen.

Background and objective To investigate whether the administration of ketamine before induction with propofol produces a smaller decrease in arterial pressure.

Methods Twenty-two patients were assigned to one of two groups to receive either propofol with ketamine (n = 11) or propofol alone (n = 11, control). Anaesthesia was induced with 2 mg kg−1 propofol and 0.5 mg kg−1 ketamine or 2 mg kg−1 propofol alone. Ketamine was administered 1 min prior to induction with propofol. Immediately after induction with propofol, vecuronium (0.15 mg kg−1) was administered. Four minutes after administration of vecuronium, tracheal intubation was performed. Anaesthesia was maintained using sevoflurane (0.5%) in 66% nitrous oxide until 3 min after intubation. Systolic, diastolic and mean arterial pressure and heart rate were recorded on arrival, directly before induction with propofol, prior to tracheal intubation, immediately after intubation and at 3 min after intubation.

Results and conclusions Administration of ketamine before induction with propofol preserved haemodynamic stability compared with induction with propofol alone.

The aim of this paper is to provide an outline of the current developments in drug discovery. However, in doing so, it is important to put these developments into an historical perspective and to acknowledge the impact that the previous research effort has had on research in progress.

Background and objective We studied the influence of systemic (aortic) blood flow velocity on changes of cerebral blood flow velocity under isoflurane or sevoflurane anaesthesia.

Methods Forty patients (age: isoflurane 24–62 years; sevoflurane 24–61 years; ASA l–lll) requiring general anaesthesia undergoing routine spinal surgery were randomly assigned to either group. Cerebral blood flow velocity was measured in the middle cerebral artery by transcranial Doppler sonography (depth: 50–60 mm). Systemic blood flow velocity was determined by transthoracic Doppler sonography at the aortic valve. Heart rate, arterial pressure, arterial oxygen saturation and body temperature were monitored. After standardized anaesthesia induction (propofol, remifentanil, vecuronium) sevoflurane or isoflurane were used as single agent anaesthetics. Cerebral blood flow velocity and systemic blood flow velocity were measured in the awake patient (baseline) and repeated 5 min after reaching a steady state of inspira-tory and end-expiratory concentrations of 0.75, 1.00, nd 1.25 mean alveolar concentrations of either anaesthetic. To calculate the influence of systemic blood flow velocity on cerebral blood flow velocity, we defined the cerebral-systemic blood flow velocity index (CSvl). CSvl of 100% indicates a 1:1 relationship of changes of cerebral blood flow velocity and systemic blood flow velocity.

Results Isoflurane and sevoflurane reduced both cerebral blood flow velocity and systemic blood flow velocity. The CSvl decreased significantly at all three concentrations vs. 100% (isoflurane/sevoflurane: 0.75 MAC: 85 ± 25%/81 ± 23%, 1.0 MAC: 79 ± 19%/74 ± 16%, 1.25 MAC: 71 ± 16%/79 ± 21%; [mean ±SD] P% 0.0001). Conclusions The reduction of the CSvl vs. 100% indicates a direct reduction of cerebral blood flow velocity caused by isoflurane/sevoflurane, independently of systemic blood flow velocity.

Background and objective To assess retrospectively the complications and morbidity of electroconvulsive therapy.

Methods Complications occurring in 75 patients during 612 electroconvulsive therapy procedures under propofol anaesthesia were reviewed by data analysis.

Results At least one complication occurred in 51 patients (68%) during the course of their treatment. Among these complications, 12 were potentially life-threatening: one patient developed angina pectoris, another aspiration pneumopathy, there were two incidences of bronchospasm, three hypoxic episodes (SpO2 < 92% with FiO2 = 1) and five severe episodes of laryngospasm which caused hypoxia. Twenty-five patients (33%) were confused for more than 2 h after the electroconvulsive therapy. Confusion recurred in 10 patients (13%) after several sessions of electroconvulsive treatment. Six patients had a traumatic complication, with one requiring surgery.

Conclusion Our results, compared with other studies, suggest that electroconvulsive therapy is not a low-risk procedure, with a particularly high rate of respiratory complications that may have been previously overlooked. Therefore, ambulatory anaesthesia may not be appropriate on a regular basis for most of these patients.

Background and objective The γ1-aminobutyric acidA receptor (GABAAR) is a target for anaesthetic agents. We investigated the interactions of sevoflurane with a recombinant GABAAR. Emphasis was on the mechanism of block, as relevant open-channel block by a volatile anaesthetic would possibly explain prolonged GABAergic postsynaptic currents.

Methods The effect of sevoflurane on GABA–induced currents through recombinant α1β1γ1 GABAAR channels was studied (patch clamp; HEK293 cells). GABA 0.01mM or 1mM was applied alone or together with sevoflurane (0.05mM to 5mM).

Results Currents elicited by GABA 0.01mM were increased by low sevoflurane concentrations to 183% and decreased by high sevoflurane concentrations (> 1mM) to 34% (P < 0.05). Ten- to 90%-rise times of the currents were reduced by sevoflurane concentration dependently. At GABA (1mM), peak currents and 10–90%-rise times decreased with increasing sevoflurane concentrations. A transient current increase was induced by discontinuation of GABA and sevoflurane. Such rebound currents indicate a reversal of an openchannel block by sevoflurane.

Conclusions Sevoflurane (a) increases the apparent affinity of GABA to the GABAAR, as suggested by the decreased current rise times. This explains the enhancement of the currents induced by low GABA concentrations (0.01mM). Additionally, sevoflurane (b) induces a picrotoxin-like open-channel block at the GABAAR. The reversal of the open-channel block elicits a delayed GABA response. These findings indicate at least two different sites of action of sevoflurane at this receptor that are both important for an enhanced GABAergic synaptic transmission.

Background and objective Insertion of the laryngeal mask airway in the anaesthetized patient can sometimes be difficult and propofol has been advocated as the anaesthetic induction agent of choice because of its depressant effect on laryngeal reflexes compared with other intravenous anaesthetics. However, when used as the sole induction agent, relatively large doses of propofol are required to achieve successful laryngeal mask insertion. This has cost implications and may produce unwanted cardiorespiratory depression.

Methods One hundred and forty-two patients were randomized to receive either: fentanyl 1 μg kg−1 and lidocaine 1.5mgkg−1 (group 1), or fentanyl 1μgkg−1 and midazolam 0.04 mg kg−1 (group 2), or fentanyl 1μg kg−1, midazolam 0.04 mg kg−1 and lidocaine 1.5mgkg−1 (group 3) or fentanyl 1 μg kg−1 (group 4) 2min before induction of anaesthesia. Anaesthesia was established with propofol infused at 33.3mgmin−1.

Results Patients who were given midazolam required significantly less propofol to achieve satisfactory laryngeal mask insertion, median propofol doses: group 1, 1.63mgkg−1; group 2, 1.16mgkg−1; group 3, 1.01 mgkg−1; group 4, 1.9mgkg−1, P < 0.0001 (analysis of variance). Patients given midazolam reported less pain on injection with propofol 13% and 3% groups (2 and 3) compared with 37.5% and 77% (groups 1 and 4) P = 0.002 (χ2).

Conclusions Midazolam reduces the dose of propofol required for induction of anaesthesia and successful insertion of the laryngeal mask airway. There was no clinical benefit to be gained from the addition of lidocaine.

Background and objective Little information exists on cerebrospinal fluid pressures in non-labouring pregnant women. The technique of spinal anaesthesia means that inadequate levels of sensory blockade are difficult to manage. If the block is found to be inadequate after surgery has commenced, then conversion to general anaesthesia may be the only option. It is important that any manoeuvre altering the spread of local anaesthetic is considered at the time of subarachnoid injection. This study investigates the feasibility of using a fine bore needle with an electronic transducer to measure cerebrospinal fluid pressure and whether this was affected by either of the two lateral positions. We also sought to measure whether the right or left lateral position affected subsequent block height and requirements for supplementary analgesia.

Methods Two groups of 17 women presenting for elective Caesarean section were allocated to receive spinal anaesthesia in either the right or left lateral position. Cerebrospinal fluid pressure was measured by use of a rapid response electronic transducer connected to the hub of the spinal needle. Anaesthetic levels to cold sensation were assessed at 5, 10 and 15 min after injection of hyperbaric bupivacaine. During surgery, requirements for supplementary analgesia were recorded.

Results There was no significant difference in cerebrospinal fluid pressure between the two positions. While there was a trend towards more rapid analgesia in the right lateral group, this did not reach statistical significance. Two blocks performed in the left lateral group were inadequate for surgery but this was not statistically significant. Overall, 39% of women required supplementary analgesia during surgery. The incidence was not significantly different between the two groups.

Conclusion Adoption of either the right or left lateral position for placement of spinal anaesthesia results in no difference in cerebrospinal fluid pressure or quality of block. The technique described gives a reliable and reproducible method of cerebrospinal fluid pressure measurement.