Maternal, fetal, and neonatal effects of lidocaine with and without epinephrine for epidural anesthesia in obstetrics

The effects of epidural lidocaine with and without 1:300,000 epinephrine on uterine activity, progress of labor, fetal heart rate, maternal blood pressure and heart rate, newborn Apgar scores, neonatal acid-base status, and the Neurologic and Adaptive Capacity Scoring System were compared in 30 parturients during labor and delivery. Patients in group I (n = 16) received 1.5% lidocaine with 1:300,000 epinephrine and those in group II (n = 14) 1.5% lidocaine alone. Addition of epinephrine to lidocaine did not have any significant effects on uterine activity, duration of first or second stages of labor, fetal heart rate variability, or the incidence of abnormal fetal heart rate patterns. Maternal heart rate and the incidence of hypotensive episodes did not differ significantly between the two groups of patients. Apgar scores, neonatal acid-base status, and the NACS were equally good in the two groups. Duration of analgesia was significantly longer in group I as compared to group II patients (106.9 +/- 6.6 vs 66.2 +/- 4.4 min, P less than 0.001). Umbilical venous concentrations of lidocaine and umbilical vein to maternal vein ratios of lidocaine were significantly higher in group II patients (P less than 0.05). It is concluded that addition of epinephrine to lidocaine during epidural anesthesia in the normal parturient has no adverse effects on mother, fetus, neonate, or the progress of labor and it significantly prolongs the duration of anesthesia and limits the placental transfer of lidocaine.     

The pharmacokinetics and maternal and neonatal effects of epidural lidocaine in preeclampsia

The pharmacokinetics and maternal and neonatal effects of epidural lidocaine were compared in ten preeclamptic and five normotensive women undergoing cesarean section at 36-40 weeks of gestation. Lumbar epidural anesthesia was achieved using 15-20 ml of 2% lidocaine without epinephrine. Serial venous samples for lidocaine levels were drawn from all the mothers during the procedure and up to 6 hr after the initial injection. Umbilical venous and arterial samples were drawn at delivery for measurement of neonatal acid-base status and lidocaine levels. There were no significant differences between normotensive and preeclamptic patients in the total dose of lidocaine, peak maternal plasma concentration, volume of distribution, maternal elimination half-life and umbilical vein/maternal vein ratios. The calculated area under the concentration time curve in preeclamptic patients (18.5 +/- 4.7 micrograms X hr X ml-1) was significantly greater than in normotensive mothers (14.1 +/- 1.3 micrograms X hr X ml-1) (P less than 0.02). Total maternal body clearance in preeclamptic patients (24.5 +/- 7.1 L/hr) was significantly lower than in normotensives (31.1 +/- 4.4 L/hr) (P less than 0.05). Neonatal outcome as evaluated by Apgar scores, umbilical arterial and venous blood gas tensions, umbilical vein/maternal vein ratios, and early neonatal neurobehavior scores at 4 hr and 24 hr after birth were similar in the two groups. The results indicate that the total maternal body clearance of lidocaine is prolonged in preeclampsia, and repeated administration of lidocaine can result in higher blood levels than in normotensive parturients.     

Effects of interpleurally administered bupivacaine 0.5% on opioid analgesic requirements and endocrine response during and after cholecystectomy: a randomized double-blind controlled study

In 30 patients undergoing cholecystectomy, a randomized double-blind saline-controlled study was performed using interpleural 0.5% bupivacaine with or without epinephrine (5 micrograms.ml-1) in combination with 0.8% halothane inspired concentration in oxygen. The aim of the study was to investigate whether interpleural 0.5% bupivacaine could decrease the intraoperative opioid requirements and attenuate the metabolic endocrine response to surgical stress. Patients were randomly allocated to one of three groups: Group 1: 0.5% bupivacaine; Group 2: 0.5% bupivacaine with epinephrine (5 micrograms.ml-1); and Group 3: saline. The interpleural catheter was inserted after induction of anesthesia in the spontaneously breathing patient. The study drug was injected 30 min prior to surgery. Peak plasma bupivacaine concentrations in the respective groups were 1.30 +/- 0.78 and 1.16 +/- 0.48 micrograms.ml-1. In all patients concentrations were below suggested convulsive level. Two patients in Group 1 and two in Group 2 required intraoperative fentanyl (0.1 mg each). In contrast, eight patients in the saline group received an average of 0.21 mg (range 0.1 +/- 0.4 mg) fentanyl (P less than 0.05). Postoperatively, a second dose of the study drug was given. Subsequently, pain was assessed using a visual analog score and a verbal rating scale. Pain scores decreased significantly 30 min after the interpleural injection in both bupivacaine groups and remained unchanged in the saline group (P less than 0.05). Pain management by means of interpleural bupivacaine was successful in 17 of the 20 patients. In the saline group seven out of ten patients needed additional analgesics (P less than 0.05). Cortisol levels increased in response to surgery in all groups: maximum levels in Groups 1, 2 and 3 were: 1.09 +/- 0.29, 1.11 +/- 0.20 and 1.19 +/- 0.16 mumol.l-1, respectively. Plasma glucose concentrations increased significantly in all groups: maximum levels in Groups 1, 2 and 3 were: 7.6 +/- 1.3, 7.3 +/- 1.7 and 8.3 +/- 1.7 mmol.l-1, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)     

Concentrations of thiopentone in mature breast milk and colostrum following an induction dose

In two groups of eight patients, concentrations of thiopentone in mature breast milk and colostrum following anaesthesia induction with 5.4 and 5.0 mg kg-1 b.w. (mean), respectively, were measured in the first 36 h postoperatively. Blood concentrations were measured simultaneously. The maximal concentrations were: in mature breast milk, 3.4 +/- 0.68 mumol l-1 (mean +/- s.e. mean) (0.090 mg 100 ml-1), and in colostrum, 1.3 +/- 0.5 mumol l-1 (0.034 mg 100 ml-1). The milk/plasma ratio was less than 1.0 in both groups. The above concentrations may be regarded as negligible and therefore non-toxic for the nursing infant.     

Neonatal responses to alphaprodine administered during labor

The effect of intravenously administered alphaprodine on newborn Apgar scores, neonatal acid-base status, and the Neurologic and Adaptive Capacity Scoring System (NACS) were compared in 30 parturients. Patients in group 1 (n = 15) received 20-40 mg increments of alphaprodine, with a total dose of 39.3 +/- 3.7 mg (mean +/- SEM). Group 2 patients (n = 15) received no medication during labor. Apgar scores, neonatal acid-base status, and the NACS were equally good in the two groups. The concentrations of alphaprodine in maternal vein, umbilical vein, and umbilical artery at delivery were measured using a gas-chromographic mass spectrophotometric technique. The results showed an umbilical vein-to-maternal vein ratio of 0.52 +/- 0.09. It is concluded that when administered as in this study, alphaprodine has no adverse effects on the neonate.     

Disposition of propofol infusions for caesarean section

The disposition of propofol was studied in women undergoing elective Caesarean section. Indices of maternal recovery and neonatal assessment were correlated with venous concentrations of propofol. After induction of anaesthesia with propofol 2.0 mg.kg-1, ten patients received propofol 6 mg.kg-1.hr-1 with nitrous oxide 50 per cent in oxygen (low group) and nine were given propofol 9 mg.kg-1.hr-1 with oxygen 100 per cent (high group). Pharmacokinetic variables were similar between the groups. The mean +/- SD Vss = 2.38 +/- 1.16 L.kg-1, Cl = 39.2 +/- 9.75 ml.min-1.kg-1 and t1/2 beta = 126 +/- 68.7 min. At the time of delivery (8-16 min), the concentration of propofol ranged from 1.91-3.82 micrograms.ml-1 in the maternal vein (MV), 1.00-2.00 micrograms.ml-1 in the umbilical vein (UV) and 0.53-1.66 micrograms.ml-1 in the umbilical artery (UA). Neonates with high UV concentrations of propofol at delivery had lower neurologic and adaptive capacity scores 15 minutes later. The concentrations of propofol were similar between groups during the infusion but they declined at a faster rate in the low group postoperatively. Maternal recovery times did not depend on the total dose of propofol but the concentration of propofol at the time of eye opening was greater in the high group than the low group (1.74 +/- 0.51 vs 1.24 +/- 0.32 micrograms.ml-1, P less than 0.01). The rapid placental transfer of propofol during Caesarean section requires propofol infusions to be given cautiously, especially when induction to delivery times are long.     

Cardiovascular responses caused by the combination of lidocaine and vecuronium in the induction of general anaesthesia

Fentanyl, vecuronium and enflurane may cause bradyarrhythmias during anaesthesia. Lidocaine administered before endotracheal intubation may interact synergistically with these agents. In this randomized and double-blind study, lidocaine 1 mg kg-1 (24 patients) or saline (20 patients) was given, immediately after glycopyrrolate 5 micrograms kg-1, fentanyl 1.5 micrograms ml-1 and thiopentone 3-5 mg kg-1, together with vecuronium 0.1 mg kg-1 as a rapid i.v. injection to healthy (ASA 1) surgical patients. Enflurane 0.8% was included in the inhaled gases 10 min and enflurane 1.6% 25 min after lidocaine administration. The plasma concentrations of lidocaine rose to a mean level of 3.1 micrograms ml-1 (maximum 7.1 micrograms ml-1) which may affect the electrical conduction at various sites in the heart. There were no statistically significant differences in arterial blood pressures or heart rates during anaesthesia between the groups. The incidence of junctional rhythm was 7/24 patients in the lidocaine group and 5/20 patients in the saline group. Three patients in the lidocaine group, and two patients in the control group developed junctional rhythm immediately after intubation. The plasma concentrations of vecuronium were unaffected by lidocaine. The ratio of the unbound lidocaine to plasma protein bound lidocaine was at the expected level and did not differ significantly 2 and 10 min after the injection.     

Residual curarization in the neonate after Caesarean section

The transplacental transfer and the neonatal effects of atracurium 0.3 mg.kg-1 (ED95) were compared with those of d-tubocurarine at the usual clinical dose of 0.3 mg.kg-1 (ED90) in 46 patients undergoing elective Caesarean section. The atracurium group (25 patients) was similar to the d-tubocurarine group (21 patients) as far as age, parity and time intervals between precurarization, induction, skin incision, muscle relaxant administration, hysterotomy and birth. The transplacental transfer of atracurium was lower than that of d-tubocurarine, with a feto-maternal ratio of 9 +/- 3% for atracurium and 12 +/- 5% for d-tubocurarine (P less than 0.05). The transplacental transfer of laudanosine was low at 14 +/- 5%, with blood levels of 0.101 +/- 0.032 microM.L-1 in the umbilical vein. Newborns in the two groups were comparable in terms of Apgar scores at one, five and ten minutes, as well as for NACS scores (neurological and adaptive capacity scoring test) at two and 24 hours after birth. However, at 15 min after birth, only 55% of newborns in whom the mothers received atracurium had a normal NACS score (greater than or equal to 35/40) compared with 83% of newborns in whom the mothers received d-tubocurarine (P less than 0.05). Further analysis of the five variables related to active muscle tone revealed that the modal score for active extension of the neck of newborns from the atracurium group was lower than for newborns from the d-tubocurarine group (P less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)     

Comparison between clonidine and epinephrine admixture to lidocaine in brachial plexus block.

The admixture of clonidine or epinephrine to lidocaine for brachial plexus block was studied with regard to duration of block, postoperative analgesia, and plasma concentrations of lidocaine. Thirty-three patients of ASA physical status I and II received an admixture of either clonidine (150 micrograms; n = 15) or epinephrine (200 micrograms; n = 18) to 40 mL of 1% lidocaine in a randomized, double-blind fashion. Bone surgery predominated in those patients receiving clonidine and soft-tissue surgery in those receiving epinephrine (P less than 0.05). Onset and duration of block were not different between the groups. With the admixture of clonidine, fewer patients were completely pain free for greater than 12 h (13.3%) and pain scores (visual analogue scale 0-10) were higher 6 h after the block (median 4; range 0-6) than with epinephrine (61.1%; median 2; range 0-7, respectively; P less than 0.05). In patients who had received clonidine, peak plasma concentrations of lidocaine were higher (10.29 +/- 2.96 mumol/L) and occurred earlier (23.7 +/- 9.3 min; mean +/- SD) than in those treated with epinephrine (6.9 +/- 1.71 mumol/L; 72.5 +/- 56.2 min; P less than 0.05). This indicates the absence of a local vasoconstrictor effect of clonidine and implies a reduced margin of safety with regard to local anesthetic toxicity. Although clonidine does not offer advantages compared with epinephrine, it may be a useful adjunct to local anesthetics in those patients in whom the administration of epinephrine is contraindicated.     

Comparative maternal, fetal, and neonatal effects of chloroprocaine with and without epinephrine for epidural anesthesia in obstetrics

The effects of epidural chloroprocaine with and without 1:200,000 epinephrine during labor and delivery on uterine activity, progress of labor, fetal heart rate, maternal blood pressure, newborn Apgar scores, neonatal acid-base status, and the Neurologic and Adaptive Capacity Scoring System (NACS) were compared in 28 parturients. Patients in group I (n = 14) received 2% chloroprocaine with 1:200,000 epinephrine and patients in group II (n = 14) received 2% plain chloroprocaine. Addition of epinephrine to chloroprocaine had no significant effects on uterine activity, duration of first or second stages of labor, or fetal heart parameters. Apgar scores, neonatal acid-base status, and the NACS were equally good in the two groups. Duration of analgesia was significantly longer in group I than in group II patients (76 +/- 3.8 vs 42.9 +/- 1 min, P less than 0.001). We conclude that addition of epinephrine to chloroprocaine during epidural anesthesia in the normal parturient has no adverse effects on mother, fetus, neonate, or the progress of labor and that it significantly prolongs the duration of anesthesia.     

The antidotal action of thiosulfate following acute nitroprusside infusion in dogs

The authors previously demonstrated in dogs that a bolus dose of sodium thiosulfate maintained enhanced cyanide metabolism throughout a 1-h infusion of sodium nitroprusside (SNP). To further test this antidotal action, a bolus dose of thiosulfate (150 mg . kg-1) was given to eight dogs at the end of a 60-min near-lethal infusion of nitroprusside (3 mg . kg-1). Within 2 min of the antidote, mean plasma thiocyanate levels (70.3 mumol . l-1) were significantly higher than those of seven control dogs given nitroprusside only (45.9 mumol . l-1, P = 0.002) and plateaued at 153.8 mumol . l-1 within 60 min, while the control values only reached 79.1 mumol . l-1 (P less than 0.001). Although differences between plasma cyanide levels in the two groups only attained significance 1 h after administering the antidote (0.8 vs. 2.74 mumol . l-1, P = 0.03), red blood cell cyanide concentrations were significantly lower in the antidote group within 5 min (166 vs. 225 mumol . l-1, P = 0.004) and remained so throughout the 2-h observation period. Compared with the controls, there was an impressive reduction in mean half-lives of plasma cyanide (25.1 vs. 74.1 min) and red blood cell cyanide (22.4 vs. 203.6 min). Similarly, peak cyanide levels occurred much sooner following the antidote (mean times: plasma cyanide 2.9 vs. 5.9 min; red blood cell cyanide 0.25 vs. 11 min).(ABSTRACT TRUNCATED AT 250 WORDS)     

Indirect effect of catecholamines on development of insulin resistance in skeletal muscle from diabetic rats

The role of an increased sympathetic activation in the development of insulin resistance in diabetic skeletal muscle was investigated. Epitrochlearis muscles from rats with streptozocin-induced diabetes and from controls were incubated in vitro for 0.5-12.0 h. Diabetes decreased maximal insulin-stimulated (20 mU/ml) glucose transport capacity by 60% (P less than .001), but this decreased insulin responsiveness returned to normal on in vitro incubation (3.79 +/- 0.59 before vs. 8.92 +/- 0.64 mumol.ml-1.h-1 after 12 h of incubation). The reversal of decreased insulin responsiveness in diabetic muscles did not require the presence of insulin and was not affected by the presence of 5.0 x 10(-8) M of epinephrine. However, it was possible to partially prevent the development of insulin resistance with regard to glucose transport by treating the rats with the beta-adrenergic antagonist propranolol (0.5 mg/kg) every 12 h during the entire 72-h period in which the animals were kept diabetic (insulin responsiveness was 3.16 +/- 0.40 mumol.ml-1.h-1 for saline-injected group vs. 5.55 +/- 0.46 mumol.ml-1.h-1 for propranolol-treated group). This effect was not present after a single injection of the drug 2 h before the experiment or when propranolol treatment was withdrawn 12 h before the experiment. The beta-adrenergic blockade markedly reduced the plasma concentration of free fatty acids (0.5 +/- 0.01 mumol/ml for propranolol-treated rats vs. 1.1 +/- 0.1 mumol/ml for saline-treated rats; P less than .001).(ABSTRACT TRUNCATED AT 250 WORDS)     

Ventilation and ventilatory response to carbon dioxide during caudal anaesthesia with lidocaine or bupivacaine in sedated children

Resting ventilation, arterial blood-gas tensions and the ventilatory response to carbon dioxide were measured in sedated children before and after caudal anaesthesia using 10 mg.kg-1 of 1.5% lidocaine or 3.3 mg.kg-1 of 0.5% bupivacaine. Expired minute volume decreased slightly after both caudal blocks but end-tidal Pco2 increased slightly after caudal block with lidocaine. No clinical changes in Paco2 and Pao2 were observed in either group. The slope of the CO2 response curves increased significantly after both caudal blocks. The mean plasma levels of lidocaine and bupivacaine were 3.95 +/- 0.64 (s.d.) and 1.33 +/- 0.29 micrograms.ml-1, respectively. These results indicate that the ventilatory response to hypercapnia is markedly improved by the two caudal blocks, but resting ventilation is slightly impaired by caudal block with lidocaine, and from the aspect of pulmonary ventilation bupivacaine is better than lidocaine for caudal anaesthesia.     

Clinical evaluation of clonidine added to lidocaine solution for epidural anesthesia

The effects of clonidine added to lidocaine solution used for epidural anesthesia were assessed in 92 women scheduled for surgery and premedicated with diazepam 10 mg po. Patients received 18 ml 2% lidocaine with clonidine 5 micrograms.ml-1 (group C-5, n = 26), with clonidine 10 micrograms.ml-1 (group C-10, n = 20), with epinephrine 5 micrograms.ml-1 (group E, n = 26), or plain (group P, n = 20). No significant difference in the number of segments of analgesia was found at any observation period among the four groups of patients. The decreases in mean blood pressure (BP) observed 20 min after epidural injection in those given clonidine (5 +/- 8% for C-5, 10 +/- 11% for C-10, mean +/- SD) were similar to those given plain lidocaine (7 +/- 12%) but significantly less than those given epinephrine (18 +/- 12%, P less than 0.01 vs. C-5 or P). The response of BP to ephedrine given for restoring BP during anesthesia was not attenuated in patients who received epidural clonidine. Heart rate (HR) decreased significantly in patients given clonidine 10 micrograms.ml-1 (7 +/- 8%, P less than 0.01), but not in those given clonidine 5 micrograms.ml-1, whereas HR increased significantly in those given lidocaine plain or with epinephrine (10 +/- 8% and 28 +/- 14%, respectively, P less than 0.01). The incidence of sinus bradycardia was similar among the four groups of patients. Significant differences were also observed in sedation score between clonidine groups and groups P or E; sedation appeared approximately 10-20 min after epidural injection in both clonidine groups.(ABSTRACT TRUNCATED AT 250 WORDS)     

Interpleural administration of 1.0% and 1.5% lidocaine with epinephrine for pain relief after thoracotomy

Pain relief following thoracotomy and arterial concentration profiles after interpleural administration of lidocaine were studied in 23 adult patients. They were allocated to three groups and given interpleural injection of 20 ml each of 1.0% (group 1, N = 9, non-pneumonectomy patients), 1.5% (group 2, N = 10, non-pneumonectomy patients), and 1.5% (group 3, N = 4, pneumonectomy patients) lidocaine with epinephrine (5 micrograms.ml-1). Complete pain relief was obtained within 20 min after injection in all patients. The mean duration of analgesia was 2.8 hr, 3.1 hr, and 5.1 hr in group 1, 2, and 3, respectively. The maximum plasma concentrations of lidocaine (Cmax) were 1.7 +/- 1.0 (mean +/- SD) microgram.ml-1, 2.2 +/- 0.6 micrograms.ml-1, and 0.7 +/- 0.2 micrograms.ml-1 in group 1, 2, and 3, respectively. The mean duration of analgesia was significantly longer in group 3 than in group 2 (P less than 0.01). Cmax was significantly lower in group 3 than in group 2 (P less than 0.01). In conclusion, we consider interpleural injection of lidocaine with epinephrine to be an effective method of providing postoperative analgesia after thoracotomy. Our data also suggest that the duration of analgesia may increase and the plasma levels of lidocaine may remain quite low in total pneumonectomy patients, because local anesthetic solution is not absorbed through the visceral pleura but absorbed only through the parietal pleura alone in these patients.     

Endotracheal administration of lidocaine inhibits isofluraneinduced tachycardia

PURPOSE: Rapid increase in inspired isoflurane concentration increases heart rate and arterial blood pressure. To investigate whether the responses to isoflurane were elicited from stimulation of lower airway and/or lungs, haemodynamic responses to isoflurane administered after tracheal intubation were measured with or without endotracheal or intravenous administration of lidocaine. METHODS: Seventy-two ASA physical status 1 patients, aged 21-50 yr, were randomly allocated to one of four groups. After tracheal intubation, anaesthesia was maintained with oxygen 100% and isoflurane 1.0% with controlled ventilation. After stabilization for 15 min, the isoflurane concentration was rapidly increased to 3.0% in three groups. An endotracheal lidocaine group received pretreatment with endotracheal 0.4 ml lidocaine 8% spray, an intravenous lidocaine group received pretreatment of 32 mg lidocaine i.v., and an isoflurane 3% group received not pre- treatment. In a control group, inspired isoflurane concentration was maintained at 1.0%. Heart rate, systolic blood pressure and end-tidal isoflurane concentration were measured every minute for 10 min. RESULTS: The rapid increase in isoflurane concentration increased heart rate (25 +/- 12% increase from baseline; P < 0.05) but the increase was reduced by endotracheal lidocaine (9 +/- 9%), but not by intravenous lidocaine (22 +/- 13%). The plasma concentration of lidocaine was lower in the endotracheal lidocaine group (0.4 +/- 0.3 microgram.ml-1) than in the i.v. lidocaine group (1.5 +/- 0.2 micrograms.ml-1). CONCLUSION: The isoflurane-induced tachycardia is reduced by pre-treatment with endotracheal lidocaine.     

Safety and efficacy of epinephrine added to bupivacaine for lumbar epidural analgesia in obstetrics

The effects of epidural bupivacaine with and without 1:300,000 epinephrine on uterine activity, progress of labor, fetal heart rate, maternal blood pressure and heart rate, newborn Apgar scores, neonatal acid-base status, and Neurologic and Adaptive Capacity Scoring System (NACS) were compared in 32 parturients during labor and delivery. Patients in group I (n = 16) received 0.5% bupivacaine with 1:300,000 epinephrine and those in group II (n = 16) received 0.5% bupivacaine alone. Addition of epinephrine to bupivacaine had no significant effects on uterine activity, duration of first or second stages of labor, fetal heart rate and variability, or the incidence of abnormal fetal heart rate patterns. Maternal hypotension occurred less frequently in group I than in group II patients (P less than 0.05). Apgar scores, neonatal acid-base status, and the NACS were equally good in the two groups. Duration of analgesia was significantly longer in group I than in group II (186.8 +/- 11.6 vs 85.3 +/- 6.1 (mean +/- SEM) min, P less than 0.001). It is concluded that adding epinephrine to bupivacaine during epidural anesthesia in the normal parturient has no adverse effects on either mother, fetus, neonate, or the progress of labor; and that it significantly prolongs the duration of anesthesia and decreases the incidence of maternal hypotension.     

Prolongation of lidocaine spinal anesthesia with epinephrine and phenylephrine

The effect of vasoconstrictors on the duration of lidocaine spinal anesthesia is controversial. We conducted a double-blind study of 28 neurologically normal ASA Class I or II patients to determine the effect of vasoconstrictors (epinephrine and phenylephrine) on the duration of lidocaine spinal anesthesia. The patients were randomized into three groups. All patients received 1.2 mg lidocaine per inch body height, mixed with 0.5 ml of test solution. Group 1 patients received lidocaine plus 0.5 ml normal saline; Group 2 patients received lidocaine plus 0.3 mg epinephrine; Group 3 patients received lidocaine plus 5 mg phenylephrine. Segmental sensory blockade was assessed by pinprick at 2-min intervals for the first 20 min and then every 5 min thereafter. Mean highest level was between T-2 and T-3 for all 3 groups. Time from injection to highest sensory level was similar in Groups 1 and 3, 11.6 +/- 3.57 and 12.0 +/- 5.10 min, respectively, but was significantly prolonged in Group 2, 18.1 +/- 4.33 min. Time for regression by two sensory dermatomes were significantly prolonged in both Groups 2 and 3, 102.9 +/- 18.1 and 105.7 +/- 33.1 min, respectively, compared to 78.1 +/- 12.6 min in Group 1. Times for regression to T-12 was also significantly prolonged in both Groups 2 and 3, 153.7 +/- 27.6 and 156.8 +/- 26.7 min, respectively, compared to 117.71 +/- 10.0 min in Group 1. In the doses used in the present study, both epinephrine and phenylephrine significantly prolong the duration of lidocaine spinal anesthesia.     

Plasma concentrations of lidocaine and its principal metabolites during continuous epidural infusion of lidocaine with or without epinephrine

BACKGROUND AND OBJECTIVES: The purpose of this study was to evaluate the effect of epinephrine on the absorption of lidocaine and the accumulation of active metabolites of lidocaine during continuous epidural anesthesia. METHODS: Lidocaine was administered as an initial bolus of 5 mg/kg of 2% lidocaine solution followed by continuous infusion at 2.5 mg/kg/h. Patients in group I (n = 10) received lidocaine alone and patients in group II (n = 10) received lidocaine + epinephrine (5 pg/mL). Concentrations of lidocaine and its active metabolites, monoethylglycinexylidide (MEGX) and glycinexylidide (GX), were measured in plasma samples obtained after 15 minutes, 30 minutes, and 1, 2, and 3 hours of infusion using high-performance liquid chromatography with ultraviolet detection. RESULTS: Plasma lidocaine concentrations were higher in group I for the first 30 minutes; however, after 1 hour the levels were the same. Plasma MEGX and GX increased continuously in both groups. MEGX levels the were significantly higher in group I, but there was no significant difference in the sum of lidocaine + MEGX after 2 hours. There was no significant difference in GX levels between the two groups. CONCLUSIONS: With respect to continuous epidural administration, addition of epinephrine to lidocaine solutions is ineffective after 2 hours for reducing the potential for systemic toxicity, because the sum of the plasma concentrations of lidocaine and its principal active metabolite, MEGX, are unaffected.     

曲马多对母婴乳酸盐和新生儿神经行为的影响

目的　研究曲马多对母婴血乳酸盐和新生儿神经行为与适应能力评分 (NACS)的影响。方法　 6 0例足月妊娠剖宫产产妇随机分三组 :T0 组 ,2 0例 ,肌注 0 9%氯化钠 2ml;T1组 2 0例 ,肌注曲马多 1 5mg/kg ;T2 组 ,2 0例 ,肌注曲马多 2mg/kg。各组肌注后开始麻醉 ,三组均采用脊麻与硬膜外联合阻滞。观察指标 :新生儿生后 15min的Apgar评分及新生儿生后 15min的NACS ;胎儿娩出时采脐动、静脉血和母体动脉血各 2ml,行血乳酸值测定及血气分析。结果　三组新生儿Apgar评分无明显差异 ,T0 组NACS明显高于T1组 (P <0 0 5 )和T2 组 (P <0 0 1) ;T2 组脐动、静脉血乳酸值明显高于T1组 (P <0 0 5 )和T0 组 (P <0 0 1) ;母体乳酸值三组间无明显差异 ;T2 组母体和脐动、静脉血PaCO2 明显高于T0 组 (P <0 0 1) ,T2 组脐动、静脉血SaO2 明显低于T0 组 (P <0 0 5 )。结论　剖宫产术前肌注曲马多 1 5mg/kg对新生儿无明显不良影响。但 2mg/kg曲马多肌注具有呼吸抑制作用 ,使脐动、静脉血乳酸盐增加 ,对新生儿NACS有一过性影响