Several studies have reported transient neurological symptoms after spinal anaesthesia with 5% lignocaine. In order to evaluate the role of concentrated solutions of local anaesthetic in the development of transient neurological symptoms, 200 ASA I or II patients undergoing minor orthopaedic or rectal surgery under spinal anaesthesia were allocated randomly to receive 4% mepivacaine 80 mg or hyperbaric 0.5% bupivacaine 10 mg. All patients were interviewed by an anaesthetist approximately 24 h after spinal anaesthesia, and after 1 week patients were asked to return a written questionnaire. The incidence of transient neurological symptoms consisting of pain in the buttocks or pain radiating symmetrically to the lower extremities differed (P < 0.001) between patients receiving mepivacaine (30%) and those receiving bupivacaine (3%). Hyperbaric 0.5% bupivacaine can be recommended for minor operations on the lower abdomen or lower extremities.

Interscalene brachial plexus block was performed on 40 patients for prophylactic pain relief after shoulder surgery. A dose of 1.25 mg/kg of 0.5% bupivacaine was injected for the block (Group 1) and continued with an infusion of 0.25% bupivacaine 0.25 mg/kg/h (Group 2). If the postoperative analgesia was insufficient, the patients received i.m. oxycodone 0.15 mg/kg. In Group 1, one patient managed without oxycodone supplementation during the 24-h observation period compared with eight patients in Group 2 (P less than 0.01). The rest of the patients received 3.8 +/- 1.6 doses (Group 1) and 2.5 +/- 1.2 doses (Group 2) of oxycodone (P less than 0.05). At 30 min, the mean bupivacaine plasma concentration was 1.0 microgram/ml in Group 1 and 0.9 microgram/ml in Group 2. The mean plasma level of bupivacaine increased from 0.7 microgram/ml after 180 min to 1.1 micrograms/ml (P less than 0.01) after 24 h of infusion, providing some evidence of accumulation during infusion. The dizziness and confusion experienced by three patients could be associated with the local anaesthetic, as they obtained relief after the infusion was stopped.

Three millilitre of plain 0.5% bupivacaine was injected intrathecally at two different levels in two groups of 20 patients. Injection at the L2/3 space produced a significantly higher spread of analgesia (mean T7 (SD 3.9)) than injection at L4/5 (T11(1.8)). The range of the cephalad spread of the block was less in the L4/5 group (P less than 0.001 at 60 min). The spread of anaesthesia continued beyond 30 min in both groups. In all patients anaesthesia sufficient for surgery of the knee and the foot was achieved. One patient had a final block level of T1 after injection at L2/3, accompanied by transient arterial hypotension.

Continuous interscalene brachial plexus block with a single dose of 0.5% bupivacaine 1.25 mg/kg, continued with an infusion of 0.25% bupivacaine 0.25 mg/kg/h, was performed on 24 patients to provide analgesia during shoulder surgery and in the postoperative period. The drugs for general anaesthesia included glycopyrrolate, thiopentone, vecuronium, enflurane and N2O/O2. All patients had signs of regional analgesia 30 min after the block without haemodynamic problems. The infusion of local anaesthetic was interrupted in six patients because of a failure in catheter function. Of the remaining 18 patients, nine needed no complementary analgesics and nine patients received, on average, 1.6 doses of oxycodone (0.15 mg/kg/dose) during a 24-h period. Displacement of the interscalene catheters could be prevented by a fixation suture to the skin. Two patients noted a metallic taste during the bupivacaine infusion. The most common complaints were numbness of the hand (n = 15) and hoarseness (n = 5). The mean (+/- s.e.mean) plasma concentrations of bupivacaine at 30, 60, 180 min and 24 h were 0.68 +/- 0.06, 0.62 +/- 0.05, 0.52 +/- 0.04 and 0.76 +/- 0.01 micrograms/ml, respectively. During the 24-h period, the alpha 1-acid glycoprotein (AAG) concentration (mean +/- s.e.mean) in plasma rose from 0.41 +/- 0.04 g/l to 0.54 +/- 0.04 g/l (P less than 0.001). The concentration of free bupivacaine was below detectable levels (less than 0.01 micrograms/ml) after the 24-h infusion. The rise in AAG probably increases binding of bupivacaine to plasma proteins, diminishing the risk of systemic toxicity.

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We have studied the effect of verapamil on the incidence of ECG changes and right ventricular pressures (RVP) in 25 male patients (aged 62 (SD 9) yr) undergoing thoracotomy in a placebo-controlled double-blind trial. Verapamil 0.01 mg kg-1 h-1 (n = 12) or saline (n = 13) i.v. was started after surgery and continued on the first day after operation with oral verapamil 80 mg or placebo, 8-hourly. Haemodynamic data were collected before operation and on three days after operation with the patients breathing air and then 60% oxygen (FIO2 0.60) for 10 min. Atrial tachyarrhythmia (AT) (4/13) and new ischaemic ECG changes (3/13) occurred only in the control group (P less than 0.05). With an FI02 of 0.21, systolic RVP increased by 54% on the first two days after operation in the control group and by 13% in the verapamil group (P less than 0.02). With an FIO2 of 0.60 for 10 min, systolic RVP decreased more in the control than in the verapamil group (P less than 0.01). In the control group, an increase in end-diastolic RVP (P less than 0.001) and central venous pressure (P less than 0.05) on the first day after operation was predictive of AT occurring on the second day.

Transient neurotoxicity of concentrated local anaesthetics has been thought to be the main reason for transient neurological symptoms after spinal anaesthesia. Profound musculoligamental relaxation by high doses of local anaesthetics may contribute to the development of postoperative musculoskeletal pain. In order to evaluate the role of the loss of strength of the supportive structures of the spine in the development of transient neurological symptoms, 60 patients (ASA I-II) undergoing minor orthopaedic, varicose vein or inguinal hernia operations were allocated randomly to receive spinal anaesthesia with hyperbaric lidocaine 50 mg ml-1 (85-100 mg) or balanced general anaesthesia with neuromuscular block. Patients were interviewed 24 h later and after 1 week they returned a written questionnaire. Transient neurological symptoms, consisting of pain in the buttocks or pain radiating symmetrically to the lower extremities, occurred in eight patients (27%) receiving spinal anaesthesia and in one patient (3%) receiving general anaesthesia (P < 0.05). We conclude that a transient neurotoxic effect of hyperbaric lidocaine 50 mg ml-1 is probably the main reason for transient neurological symptoms after spinal anaesthesia but musculoligamental relaxation may contribute to the development of low back or leg pain after both anaesthetic techniques.

Propofol is sequestered in extracorporeal circuits, but the factors responsible for the phenomenon are mostly unknown. We have compared two extracorporeal circuits (oxygenators, reservoirs and tubings) coated with heparin with two corresponding uncoated circuits for their capacity to sequester propofol in vitro. Three experiments were conducted with each circuit. The circuit was primed with a mixture of Ringer's acetate solution and whole blood, and the study conditions (pump flow, temperature, pH) were standardized. Propofol was added to the solution to achieve a concentration of 2 micrograms ml-1. These studies were followed with concentrations of 10- and 100-fold to assess possible saturation of propofol binding. Serial samples were obtained from the circulating solution for measurement of propofol concentration. Propofol concentrations decreased to 22-32% of the initial predicted concentration of 2 micrograms ml-1 in the circuits (no significant difference between circuits). With greater concentrations, the circuits did not become saturated with propofol, even with the highest predicted concentration of 200 micrograms ml-1. We conclude that propofol was sequestered in extracorporeal circuits in vitro, irrespective of coating the circuit with heparin.