Effects of caudal block with mepivacaine on resting ventilation and ventilatory response to carbon dioxide in sedated children

We examined the effects of caudal anaesthesia using 10 mg.kg-1 of one or two per cent mepivacaine without epinephrine on resting ventilation, arterial blood gas tensions and the ventilatory response to carbon dioxide in 27 sedated children. Expired minute volume and respiratory frequency decreased significantly after the caudal blocks in both groups. PaO2 and PaCO2 remained unchanged in both groups. The slope of the CO2 response curve increased significantly in both groups. The mean plasma mepivacaine levels were 4.6 +/- 1.6 (SD) and 4.6 +/- 1.0 micrograms.ml-1 20 minutes after the caudal blocks with one and two per cent mepivacaine, respectively. These results demonstrate that resting ventilation is impaired but the ventilatory response to carbon dioxide is improved similarly by caudal block with one or two per cent mepivacaine.     

Plasma determination of lidocaine and bupivacaine after caudal anesthesia in children

Serum concentrations of lidocaine and plasma concentrations of bupivacaine were measured so as to assess the risk of systemic toxicity following their administration by the caudal route in children, and study their pharmacokinetic profiles according to age. The serum concentrations of lidocaine were measured by immuno-enzymology in 37 children (23 +/- 13 kg) during the first hour after administration of 7 mg . kg-1. The plasma concentrations of bupivacaine were measured by high performance liquid chromatography in 40 children (18.03 +/- 8.90 kg) during the first hour after administration of 2.5 mg . kg-1. The greatest concentrations observed between 15 and 30 min after the injection were of 2.40 +/- 0.86 micrograms . ml for lidocaine and 0.93 +/- 0.44 microgram . ml-1 for bupivacaine. Higher values were observed in infants weighing less than 12 kg where they reached 2.89 +/- 0.72 and 1.52 +/- 0.68 micrograms . ml-1 respectively. These results showed that caudal anaesthesia with lidocaine (7 ml . kg-1) and bupivacaine (2.5 ml . kg-1) was a safe technique for children, giving average plasma concentrations inferior to toxic values. However, it seemed prudent not to give more than the prescribed doses in the small infant.     

Caudal block in children: analgesia and respiratory effect of the combination bupivacaine-fentanyl]

A study of the duration of analgesia and of the respiratory response to hypercapnia was carried out in 14 children who had had a caudal block with either bupivacaine alone (group B) or combined with fentanyl (Group B+F). Fourteen ASA I or II 5 to 10-year-old children undergoing genital and urinary surgery were included. They were not premedicated. At first, general anaesthesia was induced with halothane and nitrous oxide in oxygen. Thereafter, caudal anaesthesia was then carried out with 1 ml.kg-1 of 0.25% bupivacaine with adrenaline 1 in 200,000. Group B+F patients were also given 1 microgram.kg-1 of fentanyl in 1 ml of normal saline, and those in Group B 1 ml of normal saline. The level of sensory loss on leaving the operating theatre as well as the duration of motor paralysis were monitored. Postoperative pain was scored with Hannalah and Broadman's score (0 to 10) 2, 4, 8 and 24 h after the caudal block. Respiratory rate (fR), tidal volume (VT) and minute ventilation (VE) were assessed 10 min before induction of general anaesthesia, and 30, 60 and 120 min after the caudal anaesthesia. Petco2 was also measured before induction of general anaesthesia, and 60 and 120 min after caudal anaesthesia; at the same times, the ventilatory response to hypercapnia was assessed using Read's method with a Douglas bag containing 7% CO2 and 93% O2.(ABSTRACT TRUNCATED AT 250 WORDS)     

Ventilatory response to CO2 following intravenous and epidural lidocaine

The authors determined the effects of intravenous infusion and epidural administration of lidocaine on the control of ventilation in two groups of eight healthy unpremedicated subjects. In the intravenous group, an injection of 1.5 mg/kg lidocaine was followed by an infusion at a rate of 60 micrograms X kg-1 X min-1 for 30 min. The slope of the ventilatory response to CO2 was significantly increased (P less than 0.05) from its control value (2.65 +/- 1.22 1 X min-1 X mmHg-1 [mean +/- SD]) at the end of the infusion (58%), while plasma lidocaine level was at 3.14 +/- 0.82 microgram/ml. The correlation between individual plasma lidocaine levels and the changes in the slope of the ventilatory response to CO2 was significant (r = 0.58, n = 24, P less than 0.01). In the epidural group, after the administration of 5 mg/kg of lidocaine, the slope of the ventilatory response to CO2 increased significantly (P less than 0.05) from its control value (1.52 +/- 0.75 1 X min-1 X mmHg-1) at 15 (+22%) and 25 min (+42%), while plasma lidocaine levels were at 1.79 +/- 0.42 and 2.22 +/- 0.47 microgram/ml, respectively. In both groups, resting minute ventilation and end-tidal CO2 values remained unchanged. These results suggest that epidural lidocaine has a stimulating effect on the ventilatory control mechanisms that results from the systemic effect of the drug.     

Caudal block with 4 mg x kg-1 (1.6 ml x kg-1) of bupivacaine 0.25% in children undergoing surgical correction of congenital pyloric stenosis

BACKGROUND: Since 1970, bupivacaine 0.25% in a dose of 4 mg x kg-1 (1.6 ml x kg-1) has been used at the Hospital Infantil de México for caudal block in children undergoing surgical correction of congenital pyloric stenosis (CPS). Although this dose is considered unsafe, in our experience, it has been associated with a high success rate and a low incidence of adverse events. This experience has not been previously documented. METHODS: A retrospective cohort of patients undergoing surgical correction of CPS was studied. Nineteen patients received general anaesthesia while 223 received caudal block. The latter were then grouped according to the sedation technique. The rate of successful caudal blocks and complications were considered the major outcomes of the study, whereas the postsurgical fasting period and hospital stay were considered secondary outcomes. RESULTS: The rate of success of caudal block was 96%. Anaesthetic complications related to bupivacaine were present in 1.3%. Mortality occurred in the postoperatory period in one septic patient who also was suffering from gastroschisis that required general anaesthesia. Postoperatory fasting period and hospital stay tended to be higher with general anaesthesia than caudal block. However, of the 19 patients receiving general anaesthesia, five suffered serious comorbidity and nine were failed caudal blocks. CONCLUSIONS: Caudal block with bupivacaine 0.25% (4 mg x kg-1) was associated with a low rate of anaesthetic complications. Further prospective studies to clarify the risks and benefits are required.     

A randomized trial of caudal block with bupivacaine 4 mg x kg-1 (1.8 ml x kg-1) plus morphine (150 microg x kg-1) vs general anaesthesia with fentanyl for cardiac surgery

BACKGROUND: Regional anaesthesia has been used effectively in paediatric patients undergoing cardiac surgery and is thought to be safe. METHODS: Thirty patients ASA physical status II-III undergoing scheduled palliative or corrective cardiac surgery, receiving premedication with midazolam and anaesthetic induction with sevoflurane, fentanyl and pancuronium were randomly allocated to two groups. In group 1, patients received bupivacaine 0.22% 4 mg.kg-1 (1.8 ml.kg-1) and morphine 150 microg x kg-1 by the caudal route. After a 20-min period for the block to take effect, sevoflurane 0.5-1.0% and fentanyl 5 microg x kg-1 were administered for maintenance of anaesthesia. In group 2, the anaesthetic technique was the same as in group 1, without a caudal block and fentanyl 25 microg x kg-1 was administered at the moment of surgical incision. RESULTS: Cardiovascular and haemodynamic responses of patients receiving caudal block showed minor variations during the 20-min period between caudal and general anaesthesia. Fentanyl requirements during surgery were lower (P = 0.001) in patients with caudal block than patients with general anaesthesia. Extubation time was shorter (P = 0.034) in the caudal group. Two patients in the general anaesthesia group and one in the caudal group died because of postoperative complications. CONCLUSIONS: Caudal block with bupivacaine 0.22% 4 mg.kg-1 (1.8 ml.kg-1) and morphine 150 microg x kg-1 was safe and effective for paediatric patients undergoing cardiac surgery. However, patients might have a better outcome with a reduction of morphine dosage and administration of a muscle relaxant of shorter duration of action than pancuronium.     

Comparison of ropivacaine with bupivacaine for paediatric caudal block

In a double-blind, multicentre study 245 children aged 1-10 yr undergoing elective minor surgery as inpatients were randomly allocated to receive a single caudal extradural injection of 1 ml kg-1 of either 0.25% bupivacaine or 0.2% ropivacaine after induction of light general anaesthesia. The groups were comparable for age, weight, vital signs and duration of surgery. The onset time was similar for ropivacaine and bupivacaine (9.7 vs 10.4 min). Further analgesia was not required in 40% of children. The mean time to first analgesia in the remainder was 233 min in the bupivacaine group and 271 min in the ropivacaine group. No motor block was measurable in either group. Ropivacaine 2 mg kg-1 was as effective as bupivacaine 2.5 mg kg-1 for caudal analgesia in children.      

Caudal neostigmine for postoperative analgesia in paediatric surgery

BACKGROUND: This study was conducted to evaluate analgesia and side-effects of caudal neostigmine coadministered with bupivacaine in paediatric surgery. METHODS: We studied children, aged 1-5 years, undergoing elective surgery (inguinal hernia and hypospadias). After standard induction of anaesthesia, caudal anaesthesia was performed. Group 1 received 0.25% bupivacaine 0.5 ml.kg-1 and Group 2 received 0.25% bupivacaine 0.5 ml x kg-1 with 1 microg x kg-1 neostigmine via the caudal route. Heart rate, mean arterial pressure, peripheral oxygen saturation were recorded before induction, after induction but before caudal anaesthesia, and then every 5 min after caudal anaesthesia. Haemodynamic, Toddler, Preschooler, Postoperative Pain Scale (TPPPS) pain score and sedation score values were recorded 30 min after extubation and at hours 2, 4, 6, 12 and 24. A pain score >3/10 resulted in administration of rectal paracetamol. The duration of postoperative analgesia was defined as the time between caudal drug injection and the first rectal paracetamol administration. RESULTS: There were no differences between the groups in demographic and haemodynamic date, duration of surgery and anaesthesia, time to extubation or sedation scores. The duration of postoperative pain relief did not differ between the two groups; 15.40 +/- 10.97 h for group 1 vs. 15.45 +/- 10.99 h for group 2 (P > 0.05). The incidence of nausea (three patients in group 2 and one patient in group 1) was not statistically significant. No other side-effects were seen. CONCLUSIONS: We found that a single caudal injection of 1 microg x kg-1 neostigmine mixed with bupivacaine offers no significant advantage over bupivacaine alone for postoperative pain relief in children undergoing genitourinary surgery.     

Ventilatory response to CO2 following axillary blockade with bupivacaine

The systemic effect of bupivacaine on the control of ventilation was studied in eight ASA I (six male, two female) unpremedicated healthy subjects aged 30-55 yr (mean 43.5 yr) and weighing 59-82 kg (mean 69 kg) after axillary blockade with bupivacaine 0.5% without epinephrine, 3 mg/kg. The slope of the ventilatory response to CO2 was significantly increased (P less than 0.05) from its control value (1.77 +/- 1.03 l X min-1 X mmHg-1 [mean +/- SD]) 30 min (+19 +/- 32%) and 60 min (+32 +/- 37%) after axillary blockade, while plasma bupivacaine levels were 1.65 +/- 0.82 and 1.40 +/- 0.60 micrograms/ml, respectively. The correlation between individual plasma bupivacaine levels and the changes in the slope of the ventilatory response to CO2 was significant (r = 0.57, n = 16, P less than 0.05). Resting minute ventilation and end-tidal CO2 values did not change significantly. These results suggest that bupivacaine has a systemic stimulating effect on the ventilatory control mechanisms.     

Comparison of clonidine 1 microgram kg-1 with morphine 30 micrograms kg-1 for post-operative caudal analgesia in children

In a prospective randomized study in children, we compared caudal bupivacaine-clonidine with bupivacaine-morphine to evaluate whether clonidine can be used as an alternative to morphine in caudal anaesthesia. Caudal anaesthesia was administered in 36 children undergoing orchidopexy, hernia repair or circumcision, using 1.5 mL kg-1 bupivacaine 0.18% with either 1 microgram kg-1 clonidine (group 1) or 30 micrograms kg-1 morphine (group 2). Haemodynamic and respiratory parameters, anaesthetic requirements, recovery time and pain score were monitored for 24 h. Eleven children in group 1 and nine children in group 2 did not need any supplementary systemic analgesics throughout the 24-h observation period. Mean (+/- SD) duration of analgesia in the remaining patients was 6.3 h (+/- 3.3 h) in group 1 and 7.1 h (+/- 3.4 h) in group 2 (P = 0.43). Recovery time after anaesthesia was significantly longer in group 1 (16.6 +/- 8.8 min) than in group 2 (11.5 +/- 4.7 min) (P < 0.05). We conclude that analgesia provided by 1 microgram kg-1 clonidine added to caudal bupivacaine is comparable with that provided by 30 micrograms kg-1 caudal morphine with bupivacaine. Clonidine at this low dose did not cause respiratory depression.     

Measurement of respiratory effects of propofol by indirect spirometry

The effects of a continuous steady rate infusion of propofol on spontaneous ventilation were studied in eight unpremedicated ASA 1 male patients. All were non smokers, aged 29 +/- 8 years, and weighed 67 +/- 9 kg. After an initial 1 mg.kg-1 bolus, they received 10 mg.kg-1.h-1 propofol for 10 min, followed by 8 mg.kg-1.h-1 for a further 10 min, and then 6 mg.kg-1.h-1 during the whole study period. Endotracheal intubation was carried out using lidocaine for local anaesthesia. Spontaneous ventilation was assessed during three periods of five minutes: in the awake subject, using indirect spirometry (measurement of variations in chest circumference) and direct spirometry separately, and then, in the anaesthetized subject, using both methods simultaneously. This study aimed: a) to compare the results obtained with the two methods, b) to characterize the effects of propofol anaesthesia on chest wall mechanics using the partitioning of ventilation between rib cage and abdomen provided by the non-invasive method, and c) to assess abdominal compliance by means of a gastric balloon catheter. There was an increase in rib cage ventilation in the awake state, induced by the apparatus for direct spirometry (mouth piece, nose clip). This explained that the ventilatory depression induced by propofol anaesthesia was more pronounced when measured by the direct method. The major determinant of this depression was a shortened inspiratory time, and, to a lesser extent, a decreased mean inspiratory flow rate. By contrast to inhalational anaesthesia, rib cage ventilation was preserved during propofol anaesthesia. The decrease in abdominal ventilation was partly related to a lowered abdominal compliance, suggesting recruitment of the abdominal muscles.     

S(+)-ketamine for caudal block in paediatric anaesthesia

We have evaluated the intra- and postoperative analgesic efficacy of preservative-free S(+)-ketamine compared with bupivacaine for caudal block in paediatric hernia repair. After induction of general anaesthesia, 49 children undergoing hernia repair were given a caudal injection (0.75 ml kg-1) of S(+)-ketamine 0.5 mg kg-1 (group K1), S(+)- ketamine 1.0 mg kg-1 (group K2) or 0.25% bupivacaine with epinephrine 1:200,000 (group B). No additional analgesic drugs were required during operation in any of the groups. Haemodynamic and respiratory variables remained stable during the observation period. Mean duration of analgesia was significantly longer in groups B and K2 compared with group K1 (300 (SD 96) min and 273 (123) min vs 203 (117) min; P < 0.05). Groups B and K2 required less analgesics in the postoperative period compared with group K1 (30% and 33% vs 72%; P < 0.05). Postoperative sedation scores were comparable between the three groups. We conclude that S(+)-ketamine 1.0 mg kg-1 for caudal block in children produced surgical and postoperative analgesia equivalent to that of bupivacaine.      

Gastroesophageal reflux with combined caudal and halothane anesthesia in children]

Sixteen children, aged 2 to 5 years and ranked ASA 1, were included in this study assessing gastro-oesophageal reflux occurring under halothane anaesthesia, before and during, caudal anaesthesia. They were scheduled for surgery below the umbilicus lasting 1 to 5 h. After premedication with oral hydroxyzine (2 mg.kg-1) and intravenous atropine (10 micrograms.kg-1), induction was carried out with 3% halothane. A gastro-oesophageal pH probe was inserted via the nose after calibration at 37 degrees C. A neutral pH for the oesophageal electrode and an acid pH for the gastric one demonstrated the correct position of the probe. The pH was then registered every 4 s. The probe was left in situ until the patient left the recovery room. The caudal anaesthesia catheter was then inserted with the patient lying on his left side. Caudal anaesthesia was began with 2.5 mg.kg-1 of plain bupivacaine and 5 mg.kg-1 of plain lidocaine. When the patient was lying supine again, narcosis was maintained with 0.5% halothane and 50% nitrous oxide. A dose of 1.5 mg.kg-1 of bupivacaine was injected every 30 to 45 min. None of the children displayed any respiratory signs (coughing, dyspnoea, bronchospasm, cyanosis) during the combined anaesthetic. Two episodes of asymptomatic gastro-oesophageal reflux were revealed by this method, one lasting 7 minutes and occurring during insertion of the caudal catheter, and the other, lasting 4 minutes, during recovery. There were no pulmonary sequels. There was excellent respiratory and haemodynamic stability throughout. The two episodes seemed to have been triggered off by rapid displacement of the patient and too deep an anaesthetic.(ABSTRACT TRUNCATED AT 250 WORDS)     

The effect of lidocaine on neutrophil respiratory burst during induction of general anaesthesia and tracheal intubation

BACKGROUND AND OBJECTIVE: Respiratory burst is an essential component of the neutrophil's biocidal function. In vitro, sodium thiopental, isoflurane and lidocaine each inhibit neutrophil respiratory burst. The objectives of this study were (a) to determine the effect of a standard clinical induction/tracheal intubation sequence on neutrophil respiratory burst and (b) to determine the effect of intravenous lidocaine administration during induction of anaesthesia on neutrophil respiratory burst. METHODS: Twenty ASA I and II patients, aged 18-60 years, undergoing elective surgery were studied. After induction of anaesthesia [fentanyl (2 microg kg-1), thiopental (4-6 mg kg-1), isoflurane (end-tidal concentration 0.5-1.5%) in nitrous oxide (66%) and oxygen], patients randomly received either lidocaine 1.5 mg kg-1 (group L) or 0.9% saline (group S) prior to tracheal intubation. Neutrophil respiratory burst was measured immediately prior to induction of anaesthesia, immediately before and 1 and 5 min after lidocaine/saline. RESULTS: Neutrophil respiratory burst decreased significantly after induction of anaesthesia in both groups [87.4 +/- 8.2% (group L) and 88.5 +/- 13.4% (group S) of preinduction level (P < 0.01 both groups)]. After intravenous lidocaine (but not saline) administration, neutrophil respiratory burst returned towards preinduction levels, both before (97.1 +/- 23.6%) and after (94.4 +/- 16.6%) tracheal intubation. CONCLUSION: Induction of anaesthesia and tracheal intubation using thiopentone and isoflurane, inhibit neutrophil respiratory burst. This effect may be diminished by the administration of lidocaine.     

Ventilatory and circulatory responses to carbon dioxide and high level sympathectomy induced by epidural blockade in awake humans

In order to examine the effects of cervico-thoracic epidural block with 1.5% lidocaine on ventilatory and circulatory responses to carbon dioxide, the authors studied the CO2-ventilatory response curves and the changes in heart rate (HR) and blood pressure (AP) to rebreathing of exhaled gas before and after the block in healthy volunteers. Neither resting ventilation nor ventilatory response to CO2 was affected by the epidural block (mean analgesic level extended from C4 to T7); the slope of the CO2-ventilatory response curve averaged 2.38 +/- 0.81 L X min-1 X mm Hg-1 (mean +/- SD) before and 2.32 +/- 0.82 L X min-1 X mm Hg-1 after the block. Resting HR and AP decreased significantly (P less than 0.01) after the block, but responses in HR and AP to CO2 rebreathing were not significantly changed by the block. Plasma concentrations of norepinephrine and epinephrine were similar before and after the block both with and without CO2 rebreathing. These results indicate that high levels of sympathetic denervation induced by epidural block do not impair circulatory and ventilatory responses to carbon dioxide in awake, healthy humans.     

Addition of clonidine or fentanyl to local anaesthetics prolongs the duration of surgical analgesia after single shot caudal block in children

Caudal anaesthesia is indicated for surgical procedures lasting less than 90 min. Fentanyl and clonidine are known to prolong postoperative caudal analgesia, but there are no data on their effect on duration of surgical analgesia. We evaluated if the addition of clonidine or fentanyl to local anaesthetics prolonged the duration of surgical analgesia after single shot caudal block in children in a randomized, double-blind study. We studied 64 children, aged 6-108 months, undergoing bilateral correction of vesicoureteral reflux which was expected to last more than 90 min. Patients were allocated to one of four groups: group O received 1 ml kg-1 of a mixture of 0.25% bupivacaine with epinephrine and 1% lidocaine in equal parts; group F received the same mixture of local anaesthetics in addition to fentanyl 1 microgram kg-1; group C received the same mixture of local anaesthetics in addition to clonidine 1.5 micrograms kg-1; and group C + F received the same mixture of local anaesthetics in addition to fentanyl 0.5 microgram kg-1 and clonidine 0.75 microgram kg-1. Single shot caudal block was sufficient in only 57% of children in group O compared with 93% in groups C and F and 86% in group C + F (P = 0.035). Global assessment of anaesthesia, defined as the time from caudal injection to the first administration of analgesic (either during or after surgery), was significantly longer in the three groups of children who received additives compared with local anaesthetics alone (P = 0.035), but there were no differences between the three additive groups. Vomiting was observed only in children who received fentanyl. Addition of clonidine or fentanyl to local anaesthetics prolonged the duration of surgical analgesia of caudal block, allowing single shot caudal anaesthesia to be recommended for surgery lasting 90-150 minutes. Clonidine had some advantages over fentanyl as it did not produce clinically significant side effects.      

Lidocaine inhalation for local anaesthesia and attenuation of bronchial hyper-reactivity with least airway irritation. Effect of three different dose regimens

The inhalation of lidocaine attenuates bronchial hyper-reactivity but also causes airway irritation. However, how lidocaine dose and plasma concentration influence relationships are unknown. Accordingly, we evaluated the effects of three concentrations of lidocaine (1, 4, and 10%, total dose of 0.5, 2.0, and 5.0 mg kg-1, respectively) vs. placebo in 15 mild asthmatic patients, selected by their response to a histamine challenge (decrease in FEV1 > 20% to less than 18 mg mL-1 of histamine [PC20]). Baseline lung function, histamine-induced bronchoconstriction, topical anaesthesia, and lidocaine plasma concentrations were obtained. FEV1 following lidocaine inhalation showed the greatest decrease for the highest dose (from 3.79 +/- 0.15-3.60 +/- 0.15; P = 0.0012). Lidocaine inhalation increased baseline PC20 (6.1 +/- 1.3 mg mL-1) significantly (to 11.8 +/- 3.1, 16.1 +/- 3.3, and 18.3 +/- 4.5 mg mL-1, respectively) with no difference between the two highest doses. The duration of local anaesthesia was not significantly different between lidocaine concentrations of 4% and 10%. Thus, lidocaine inhalation, with increasing concentrations of the aerosolized solution, increases initial bronchoconstriction while significant attenuation of bronchial hyper-reactivity is not further enhanced with increasing concentrations from 4 to 10%. Plasma concentrations of lidocaine were always far below the toxic threshold. In conclusion, when local anaesthesia of the airways is required a lidocaine dose of 2.0 mg kg-1 as a 4% solution can be recommended for local anaesthesia and attenuation of bronchial hyper-reactivity with the least airway irritation.     

Comparative systemic toxicity of convulsant and supraconvulsant doses of intravenous ropivacaine, bupivacaine, and lidocaine in the conscious dog

This study evaluated the systemic toxicity, arrhythmogenicity, and mode of death of convulsant and supraconvulsant doses of lidocaine, bupivacaine, and ropivacaine. Experiments in awake dogs were designed to mimic the clinical situation of an accidental intravenous (IV) injection of local anesthetics. On the first experimental day, lidocaine (8 mg.kg-1.min-1), bupivacaine (2 mg.kg-1.min-1), and ropivacaine (2 mg.kg-1.min-1) were infused intravenously until seizures occurred (n = 6 for each group). The average dose and arterial plasma concentration at seizure onset was 20.8 +/- 4.0 mg/kg and 47.2 +/- 5.4 micrograms/mL for lidocaine, 4.31 +/- 0.36 mg/kg and 18.0 +/- 2.7 micrograms/mL for bupivacaine, and 4.88 +/- 0.47 mg/kg and 11.4 +/- 0.9 micrograms/mL for ropivacaine. The margin of safety between the convulsive and lethal doses was determined by administering two times the convulsive dose 24 h later. Two dogs given lidocaine died because of progressive hypotension, respiratory arrest, and finally cardiovascular collapse with an average peak plasma concentration (Cmax) of 469 micrograms/mL. No ventricular arrhythmias were observed in this group. Ventricular arrhythmias occurred in five of six dogs receiving bupivacaine. Four animals died because of hypotension, respiratory arrest, and cardiovascular collapse. One additional animal died because of ventricular fibrillation. The Cmax for bupivacaine was 70.1 +/- 14.6 micrograms/mL in nonsurvivors. In the ropivacaine group one animal died because of hypotension, respiratory arrest, and cardiovascular collapse (Cmax = 72.4 micrograms/mL). A surviving dog had transient premature ventricular contractions. Twenty-four hours later three times the convulsive dose was administered to the survivors.(ABSTRACT TRUNCATED AT 250 WORDS)     

The efficacy of pre- versus postsurgical axillary block on postoperative pain in paediatric patients

We compared the effects of pre- and postsurgical axillary block on pain after hand and forearm surgery in 55 children in a double-blind randomized study. The successful blocks are reported here (n=49). Children aged 1-11 years and ASA I or II were allocated randomly to receive axillary block with 2 mg.kg-1 of 0.25% bupivacaine, either after induction but before the surgery (presurgical group, n=25) or immediately after surgery, before the end of anaesthesia (postsurgical, n=24). In all patients, a standard general anaesthesia technique was used. The Faces Pain Scale (FPS) and analgesic requirements were recorded for 24 h at various times after operation. Eight patients (32%) in the presurgical group and 20 patients (83.33%) in the postsurgical group did not require additional analgesic within the first 24 h after operation (P< 0.05). In patients who had pain during the observation period, the pain started 13.66+/-2.61 h in the presurgical group and 13.14+/-2.34 h in the postsurgical group after performing block (P> 0.05). The FPS scores were similar in both groups during the first 8 h in the postoperative period (P> 0.05). There was a significant difference at 10 h after surgery (P< 0.05). Cumulative FPS score was higher in the presurgical group (10.50+/-1.06) than in the postsurgical group (9.45+/-1.28) (P< 0.05), but both groups had effective analgesia overall, the mean FPS score being less than 2. Additional analgesic consumption was similar in these patients in both groups. A lower isoflurane concentration was used in the presurgical group (0.68% vs 1.72%, P< 0.001). We did not demonstrate the superiority of preemptive analgesia, but our results indicate that presurgical axillary block with 0.25% bupivacaine allows the use of inhalational anaesthetics at lower concentrations while providing a reasonably painless postoperative period.     

Oral flunitrazepam in the prevention of local anaesthetic-induced convulsions in mice

The present study determined whether oral flunitrazepam was effective reducing CNS toxicity of lidocaine and bupivacaine. Pretreatment of mice with flunitrazepam, 0.065-0.25 mg X kg-1, significantly reduced or prevented convulsions and mortality induced by lidocaine 106 and 209 mg X kg-1 or bupivacaine 58 and 90 mg X kg-1 injected intraperitoneally. The doses of flunitrazepam used did not cause measurable sedation in mice. The efficacy of oral flunitrazepam in preventing local anaesthetic-induced convulsions is similar to that previously reported by intraperitoneal or intramuscular injections in mice. Flunitrazepam could be useful for oral premedication of patients before regional anaesthesia.