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)     

Quantitative and selective assessment of sensory block during lumbar epidural anaesthesia with 1% or 2% lidocaine

We have examined sensory block during lumbar epidural anaesthesia using a cutaneous current perception threshold (CPT) sensory testing device in 20 patients who received 10 ml of either 1% or 2% lidocaine (lignocaine). CPT at 2000, 250 and 5 Hz stimulation at the trigeminal (V), ninth thoracic (T9) and second lumbar (L2) dermatomes, and dermatomal levels of block to light touch, temperature and pinprick discrimination were measured before and every 5 min until 60 min after epidural lidocaine. There were significant differences between 1% and 2% epidural lidocaine in all CPT at T9 and L2, in addition to maximal cephalad spread of the three sensory modalities. After 2% lidocaine, all CPT increased significantly at T9 and L2. In contrast, only at 250 and 5 Hz for L2 did epidural block with 1% lidocaine produce significant increases in CPT. Maximal level of loss of touch sensation after 1% lidocaine was significantly lower than that of cold and pinprick sensations. We conclude that the dose of lidocaine affected intensity of sensory block during lumbar epidural anaesthesia. In addition, differential neural block resulting from epidural anaesthesia appeared to be associated with a differential effect on nerve fibres of different sizes.      

Epidural anaesthesia attenuates the catecholamine response to hypoventilation

The effect of a high epidural block on the catecholamine response to hypoventilation was studied in six unanesthetized dogs given intravenous sufentanil (15 micrograms.kg-1). Sufentanil alone resulted in a increase of norepinephrine (NE) concentration from 108 +/- 73 pg.ml-1 to 843 +/- 399 pg.ml-1 and epinephrine (E) from 279 +/- 80 pg.ml-1 to 2010 +/- 1416 pg.ml-1. At least one week later, an epidural block to T1 was achieved using 8-10 ml, two per cent lidocaine. Plasma NE and E decreased after EA to about 50 per cent of resting baseline measurements. The addition of sufentanil increased NE and E levels to reach approximately the resting base-line levels. In all dogs intravenous sufentanil resulted in bradypnoea, bradycardia, hypoxaemia, and hypercarbia. Intravenous lidocaine infusions had no significant effect on plasma catecholamine levels when plasma lidocaine levels ranged from 1.7 micrograms.ml-1 to 5.3 micrograms.ml-1. We conclude that a high two per cent lidocaine epidural block attenuates the catecholamine response to hypoventilation in dogs, but the persistence of baseline plasma levels of NE and E suggests that the efferent sympathetic block by high EA is incomplete.     

Lidocaine hydrocarbonate and lidocaine hydrochloride for cesarean section: transplacental passage and neonatal effects

Twenty-six patients, ASA physical status 1, scheduled for elective cesarean section, were divided at random into two groups and received via an epidural catheter 20 ml of 2.2% lidocaine hydrocarbonate (17.3 mg.ml-1 lidocaine base) with 5 micrograms.ml-1 epinephrine freshly added (Group CO2 = 13 patients) or 20 ml of 2% lidocaine hydrochloride (17.3 mg.ml-1 lidocaine base) also with 5 micrograms.ml-1 epinephrine freshly added. Following clampage of the umbilical cord (at 40.1 +/- 4.9 min after the injection of lidocaine for the CO2 group and at 41.0 +/- 5.4 min for the HCl group), serum concentrations of lidocaine were measured both in the mother and in the umbilical vein. All newborns were examined by the same blinded pediatrician with Apgar scores at 1, 5 and 10 min and with Neurobehavioral Adaptive Capacity Scores (NACS) at 15 min, 2 h and 24 h. The concentrations of lidocaine in the serum were comparable in both groups: in the mothers 8.61 +/- 1.48 mumol.l-1 for the CO2 group vs 8.04 +/- 2.36 mumol.l-1 for the HCl group and in the newborns 3.86 +/- 0.84 mumol.l-1 for the CO2 group vs 3.92 +/- 0.95 mumol.l-1 for the HCl group. The ratio of umbilical vein to maternal vein concentrations of lidocaine was also similar in both groups: 0.45 +/- 0.07 for the CO2 group vs 0.54 +/- 0.24 for the HCl group. The percentage of newborns with a normal NACS (score > or = 35/40) was equal in both groups, i.e. 91% at 15 min and 2 h of life and 100% at 24 h of life.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effect of thoracic epidural anesthesia combined with general anesthesia on segmental wall motion assessed by transesophageal echocardiography.

Patients scheduled for vascular surgery are considered at risk for perioperative cardiac complications. Choice of anesthetic in such patients is guided by a desire not to adversely affect myocardial function. On the basis of data from laboratory studies, thoracic epidural anesthesia (TEA) has been advocated to prevent myocardial ischemia. The aim of this study was to assess whether TEA combined with general anesthesia has any effect on segmental wall motion (SWM) monitored by transesophageal echocardiography in these patients. Patients received alfentanil, midazolam, vecuronium, and 50% N2O in oxygen, and ventilation was controlled after orotracheal intubation; 12.5 mL of 2% lidocaine HCl was injected through an epidural catheter placed at T6-7 or T7-8. Hemodynamic measurements and transesophageal echocardiographic recordings were obtained before and 10, 20, 30, 40, and 60 min after lidocaine injection. Segmental wall motion was graded a posteriori by two independent experts on a predetermined scale (from 1 = normal to 5 = dyskinesia). A decrease greater than or equal to 2 grades was considered an SWM abnormality indicative of ischemia. Thoracic epidural anesthesia induced a decrease in systemic arterial blood pressure, heart rate, and cardiac index. The SWM score decreased slightly from 1.34 +/- 0.68 to 1.27 +/- 0.64 (mean +/- SD) (at 10 and 20 min, respectively) (P less than 0.05). Patients were a posteriori analyzed according to whether they had documented coronary artery disease or not. The SWM score before TEA was significantly higher in patients with documented coronary artery disease (1.51 +/- 0.88 vs 1.17 +/- 0.51, respectively; P less than 0.05) and did not change significantly after TEA.(ABSTRACT TRUNCATED AT 250 WORDS)     

Small-dose dopamine increases epidural lidocaine requirements during peripheral vascular surgery in elderly patients

We studied 20 patients over the age of 65 yr undergoing prolonged peripheral vascular surgery under continuous lidocaine epidural anesthesia, anticipating that the increased hepatic metabolism caused by small-dose IV dopamine would lower plasma lidocaine concentrations. Subjects were assigned (random, double-blinded) to receive either a placebo IV infusion or dopamine, 2 microg. kg(-1). min(-1) during and for 5 h after surgery. Five minutes after the IV infusion was started, 20 mL of 2% lidocaine was injected through the epidural catheter. One-half hour later, a continuous epidural infusion of 2% lidocaine at 10 mL/h was begun. The epidural infusion was temporarily decreased to 5 mL/h or 5 mL boluses were added to maintain a T8 analgesic level. Arterial blood samples were analyzed for plasma lidocaine concentrations regularly during and for 5 h after surgery. Plasma lidocaine concentrations increased continuously during the epidural infusion and, despite wide individual variation, were similar for the two groups throughout the observation period. During the observation period, the mean maximal plasma lidocaine concentration was 5.8 +/- 2.3 microg/mL in the control group and 5.7 +/- 1.2 microg/mL in the dopamine group. However, the mean hourly lidocaine requirement during surgery was significantly different, 242 +/- 72 mg/h for control and 312 +/- 60 mg/h for dopamine patients (P < 0.03). At the end of Hour 4, the last period when all 20 patients were still receiving the epidural lidocaine infusion, the total lidocaine requirement was significantly different, 1088 +/- 191 mg for the control group and 1228 +/- 168 mg for the dopamine group (P < 0.05). Despite very large total doses of epidural lidocaine (1650 +/- 740 mg, control patients, and 1940 +/- 400, dopamine patients) mean maximal plasma concentrations remained below 6 microg/mL, and no patient exhibited signs or symptoms of toxicity. We conclude that small-dose IV dopamine increased epidural lidocaine requirements, presumably as a consequence of increased metabolism. IMPLICATIONS: We tested dopamine, a drug that increases liver metabolism of the local anesthetic lidocaine to determine if it would prevent excessively large amounts of lidocaine in the blood during prolonged epidural anesthesia in elderly patients. Dopamine did not alter the blood levels of lidocaine, but it did increase the lidocaine dose requirement to maintain adequate epidural anesthesia.     

Pharmacokinetics of clonidine after epidural administration in surgical patients. Lack of correlation between plasma concentration and analgesia and blood pressure changes

The pharmacokinetics of epidural clonidine 150 micrograms was studied in 13 patients who had undergone abdominal hysterectomy. Plasma clonidine concentrations were measured up to 19 h in eight patients. In another five patients frequent blood sampling was performed only during the first 20 min to define early vascular uptake better. Peak plasma clonidine concentrations of 1.08 +/- 0.35 ng ml-1 (mean +/- s.d.) were reached between 5 and 10 min after injection. Plasma elimination half-life was 829 +/- 157 min and plasma clearance was 177 +/- 28 ml min-1. There was a significant decrease in arterial blood pressure within 10 min of the injection of clonidine. The maximum decrease in systolic blood pressure, from a pre-injection value of 135 +/- 24.7 to 99 +/- 14.4 mmHg (18.0 +/- 3.3 to 13.2 +/- 1.9 kPa), occurred at 60 min. Blood pressure remained significantly lower than the pre-injection value for 4 h. There was no change in heart rate. Verbal analogue pain scores, on a scale 0-10, decreased from a median of 7.6 before clonidine to 5.0 after 30 min (P less than 0.05). The median score at 60 min was 4.3. Thereafter, pain scores were not significantly different from the control score. We conclude that epidural clonidine 150 micrograms produces only moderate and short-lived postoperative analgesia. Absorption of clonidine from the epidural space into the blood is very rapid and may contribute to the hypotension that occurs.     

Epidural Anesthesia and Acutely Increased Intracranial Pressure: Lumbar Epidural Space Hydrodynamics in a Porcine Model

Background: The effects of epidural injection on intracranial pressure (ICP), lumbar epidural pressure, cerebral blood flow (CBF), and spinal cord blood flow (SCBF) were studied after acutely increased ICP in swine.

Methods: Twenty pigs, anesthetized with isoflurane and mechanically ventilated to maintain normocarbia, had two Tuohy needles placed in the lumbar epidural space. The ICP, lumbar epidural pressure, heart rate, mean arterial pressure, and central venous pressure were monitored. All animals had a Fogarty catheter placed in the parietal epidural space. Six pigs were randomized to a normal ICP group (group N) and eight pigs to an increased ICP group by inflation of the Fogarty catheter balloon (group R). Each pig had 0.33 ml [centered dot] kg sup -1 of 2.0% carbonated lidocaine injected over 20 s via an epidural needle placed at L3. The ICP and lumbar epidural pressure were then monitored continuously for 30 min. Pressure-time data were fit to traditional compartmental models. Epidural elastance and resistance were calculated using a derivation of the Windkessel theory. An additional six pigs had ICP elevated as in group R and CBF and SCBF measured using radioactive microspheres at five time periods: baseline, 0-60 s, 100-160 s, 200-260 s, and at 30 min after epidural injection.

Results: The animals did not differ with respect to heart rate, central venous pressure, or mean arterial pressure at baseline. The ICP was 10 +/- 2 mmHg in group N, and 24 +/- 2 mmHg after balloon inflation in group R. After epidural injection, peak ICP was significantly greater in group R (76 +/- 22 vs. 54 +/- 17 mmHg) but not different by 30 min (17 +/- 5 vs. 11 +/- 1 mmHg). Epidural elastance in group N was 8.3 +/- 3.1 mmHg [centered dot] ml sup -1 and 12.8 +/- 3.0 mmHg [centered dot] ml sup -1 in group R (P = 0.045). Epidural resistance was 1,330 +/- 590 mmHg [centered dot] s [centered dot] ml sup -1 in group N and 2,220 +/- 600 mmHg [centered dot] s [centered dot] ml sup -1 in group R (P = 0.038). The CBF and SCBF were less than 10% of baseline during the 0- to 60-s time period after epidural injection. Thereafter, CBF and SCBF did not differ from baseline values.     

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.     

硬膜外局部麻醉药物中添加去氧肾上腺素对老年患者血流动力学影响的初步研究

目的 观察硬膜外局部麻醉药物中添加去氧肾上腺素对老年患者血流动力学的影响.方法 选择30例ASA分级Ⅰ、Ⅱ级,择期硬膜外麻醉下进行全髋或半髋关节置换术的老年患者,按随机数字表法分为对照组和观察组(每组15例).对照组硬膜外局部麻醉药为利多卡因(2％利多卡因17 ml+生理盐水3 ml,不添加血管活性药物),观察组硬膜外局部麻醉药为添加15 mg/L去氧肾上腺素的利多卡因(2％利多卡因17 ml+100 mg/L去氧肾上腺素3ml).记录硬膜外给药前1 min(T0)和麻醉后5 min (T1)、15 min (T2)、30 min (T3)、60 min (T4)及术毕时刻(T5)的HR、SBP、DBP、MAP、心排血量指数(cardiac output index,CI)和每搏指数(stroke volume index,SVI).记录术中麻黄碱用量. 结果 观察组患者麻醉期间麻黄素用量明显低于对照组[(1.5±3.2)mg比(6.4±8.6) mg] (P＜0.05),观察组患者T3、T4和T5时的心脏SVI明显高于T0[分别为(35±8)、(36±9)、(36±9) ml/m2比(31±8)ml/m2](P＜0.05). 结论 老年患者硬膜外局部麻醉药物中添加少量去氧肾上腺素可减少硬膜外麻醉后麻黄素的用量,并可以增加心脏SVI.     

Magnesium sulfate decreases maternal blood pressure but not uterine blood flow during epidural anesthesia in gravid ewes

The purpose of this study was to determine whether administration of magnesium sulfate decreased maternal blood pressure during epidural anesthesia in gravid ewes. Twenty-two experiments were performed in 11 chronically instrumented animals between 0.8 and 0.9 of timed gestation. The experimental sequence included: 1) T = 0: magnesium sulfate 4 g intravenously over 5 min followed by an infusion of magnesium sulfate at 4 g/h, or normal saline iv followed by an infusion of normal saline alone; 2) T = 135 min: 500 ml normal saline intravenously over 12 min; and 3) T = 150 min: epidural administration of 2% lidocaine. The initial bolus of magnesium sulfate slightly decreased maternal mean arterial pressure (MAP) but increased uterine artery blood flow (UBF). The increase in UBF was accompanied by an increase in fetal PaO2 at 145 min in the magnesium sulfate group but not in the control group. At 165 min (i.e., 15 min after the epidural injection of lidocaine), epidural lidocaine resulted in a median sensory level of T-10 in the magnesium sulfate group and T-11 in the control group. During epidural anesthesia, maternal MAP was lower (P = 0.001) in the magnesium sulfate group than in the control group. At 165 min, maternal MAP was 18 +/- 3% below baseline (P = 0.0001) in the magnesium sulfate group but did not differ significantly from baseline in the control group. Maternal cardiac output and UBF did not differ from baseline after epidural injection of lidocaine in either group.(ABSTRACT TRUNCATED AT 250 WORDS)     

Epidural lidocaine decreases sevoflurane requirement for adequate depth of anesthesia as measured by the Bispectral Index monitor

BACKGROUND: Epidural anesthesia potentiates sedative drug effects and decreases minimum alveolar concentration (MAC). The authors hypothesized that epidural anesthesia also decreases the general anesthetic requirements for adequate depth of anesthesia as measured by Bispectral Index (BIS). METHODS: After premedication with 0.02 mg/kg midazolam and 1 microg/kg fentanyl, 30 patients aged 20-65 yr were randomized in a double-blinded fashion to receive general anesthesia with either intravenous saline placebo or intravenous lidocaine control (1-mg/kg bolus dose; 25 microg x kg(-1) x min(-1)). A matched group was prospectively assigned to receive epidural lidocaine (15 ml; 2%) with intravenous saline placebo. All patients received 4 mg/kg thiopental and 1 mg/kg rocuronium for tracheal intubation. After 10 min of a predetermined end-tidal sevoflurane concentration, BIS was measured. The ED50 of sevoflurane for each group was determined by up-down methodology based on BIS less than 50 (MAC(BIS50)). Plasma lidocaine concentrations were measured. RESULTS: The MAC(BIS50) of sevoflurane (0.59% end tidal) was significantly decreased with lidocaine epidural anesthesia compared with general anesthesia alone (0.92%) or with intravenous lidocaine (1%; P < 0.0001). Plasma lidocaine concentrations in the intravenous lidocaine group (1.9 microg/ml) were similar to those in the epidural lidocaine group (2.0 microg/ml). CONCLUSIONS: Epidural anesthesia reduced by 34% the sevoflurane required for adequate depth of anesthesia. This effect was not a result of systemic lidocaine absorbtion, but may have been caused by deafferentation by epidural anesthesia or direct rostral spread of local anesthetic within the cerebrospinal fluid. Lower-than-expected concentrations of volatile agents may be sufficient during combined epidural-general anesthesia.     

Analgesic effects of epidural morphine, fentanyl and lidocaine

The analgesic effects of epidurally administered morphine 5 mg (group M, n = 15), fentanyl 100 micrograms (group F, n = 15), 2% lidocaine 60 mg (group L, n = 15) and normal saline (group S, n = 10) were investigated in 55 patients scheduled for abdominal surgery. Each drug was prepared in 3 ml solution and was injected though an epidural catheter introduced 3 cm cephalad into the epidural space at T10-11. Analgesic effects were assessed by changes in the dull pain sensation induced by electrical stimulation at 3 Hz through a pair of stainless needles which were placed subcutaneously at T7 and T10 dermatomes. In group M, analgesic effects at T10 were demonstrated in 12 of 15 subjects and the onset of analgesia was more rapid at T10 than at T7. The mean onset time of analgesia was 7.8 +/- 3.6 (mean +/- SD) min. There were 5 subjects in group F and 6 in group L who showed more rapid onset of analgesic effects at T10 than at T7, respectively. There were 2 subjects in group F and 5 in group L, with more rapid onset of analgesia at T7 than at T10. There were several subjects in group F and L with simultaneous onset of analgesia at T7 and T10. In group L, the mean distribution of analgesic area, confirmed with pinprick, was 5.2 +/- 1.9 (mean +/- SD) dermatomal segments. Hypercapnea, associated with somnolence, was frequently seen in group F. None of the subjects in group M, L or S showed such incidents. These results suggest that the main site of action of epidural morphine is located in the spinal cord while that of epidural fentanyl in the brain.     

Epidural Lidocaine Decreases Sevoflurane Requirement for Adequate Depth of Anesthesia as Measured by the Bispectral Index ® Monitor

Background: Epidural anesthesia potentiates sedative drug effects and decreases minimum alveolar concentration (MAC). The authors hypothesized that epidural anesthesia also decreases the general anesthetic requirements for adequate depth of anesthesia as measured by Bispectral Index (BIS).

Methods: After premedication with 0.02 mg/kg midazolam and 1 [mu]g/kg fentanyl, 30 patients aged 20-65 yr were randomized in a double-blinded fashion to receive general anesthesia with either intravenous saline placebo or intravenous lidocaine control (1-mg/kg bolus dose; 25 [mu]g [middle dot] kg-1 [middle dot] min-1). A matched group was prospectively assigned to receive epidural lidocaine (15 ml; 2%) with intravenous saline placebo. All patients received 4 mg/kg thiopental and 1 mg/kg rocuronium for tracheal intubation. After 10 min of a predetermined end-tidal sevoflurane concentration, BIS was measured. The ED50 of sevoflurane for each group was determined by up-down methodology based on BIS less than 50 (MACBIS50). Plasma lidocaine concentrations were measured.

Results: The MACBIS50 of sevoflurane (0.59% end tidal) was significantly decreased with lidocaine epidural anesthesia compared with general anesthesia alone (0.92%) or with intravenous lidocaine (1 %;P < 0.0001). Plasma lidocaine concentrations in the intravenous lidocaine group (1.9 [mu]g/ml) were similar to those in the epidural lidocaine group (2.0 [mu]g/ml).     

Epidural anesthesia with lidocaine reduces propofol injection pain

PURPOSE: To determine whether epidural lidocaine reduces the severity of propofol injection pain compared with iv lidocaine. METHODS: A prospective, randomized double-blind clinical study was conducted in 120 female patients scheduled for elective gynecological laparotomy. A lumbar epidural catheter and an iv catheter placed in the cephalic vein of the non-dominant hand were used in all patients. Patients of the control group (Group C) were given epidural normal saline followed by iv normal saline then iv propofol. Patients of Group E were given epidural 2% lidocaine (0.08 mL.cm(-1)) followed by iv normal saline and then propofol. Patients of Group V were given epidural normal saline followed by iv 2% lidocaine (0.05 mL.kg(-1)) then propofol. Pain was scored as no pain=0, minimal pain=1, moderate pain=2, severe pain=3. RESULTS: The pain scores, in group E; 1 (0-2) and group V; 2 (0-2), were significantly lower than in group C; 2 (1-3); median (25th-75th percentile) (P <0.001). There was no difference in pain score between groups E and V The plasma lidocaine concentration 15 min after epidural lidocaine was 2.74 +/- 0.54 microg.ml(-1), compared with 1.54 +/- 0.31 microg.mL(-1) at three minutes after iv lidocaine. CONCLUSION: Epidural and iv lidocaine equally reduced the severity of propofol injection pain despite higher lidocaine plasma concentrations in epidurally administered lidocaine.     

Blood levels of lidocaine during continuous epidural anesthesia as indicated by leg skin temperature

Arterial blood concentrations of lidocaine were measured in 7 patients undergoing pancreas operation during continuous epidural anesthesia and repeated doses of lidocaine were given according to the skin temperature of the toe. After the epidural catheter placement at the middle level of thoracic spine, 3 ml (test dose) plus 9 ml of 2% lidocaine with epinephrine (1:200,000) were injected. Additional doses of lidocaine, 6 ml, were injected when the skin temperature of the toe decreased for 0.3 degrees C. Two cases were excluded from this study because the skin temperature did not increase following additional doses of lidocaine. Lidocaine was added for 3.4 times on an average during anesthesia (duration 345 +/- 35 min, mean +/- SE). The first, second, third and fourth intervals of repeated injections from the initiation of epidural anesthesia were 119 +/- 10 min, 184 +/- 16 min, 251 +/- 20 min and 323 +/- 27 min, respectively. Arterial blood concentrations of lidocaine before each injection were 2.4 to 2.8 micrograms.ml-1 and these values showed no significant changes. These results demonstrate that the estimation of the necessity of additional injections by monitoring the skin temperature during prolonged epidural anesthesia prevents the lidocaine intoxication.     

Systemic absorption of 2% lidocaine from the lumbar epidural space

The curves of lidocaine (LDC) plasma levels versus time were evaluated in a group of 16 patients receiving single epidural injections of 2% LDC for each metamer to be anesthesized. LDC absorption from epidural space is fairly rapid (tmax = 17 +/- 4 min and t1/2a = 6.2 +/- 1.7 min). This results in very shape peak plasma levels (2.97 +/- 0.87 micrograms/ml with 2% LDC). The remaining pharmacokinetic parameters were: Ke = 0.0057 +/- 0.0022 min-1 and Vd = 1.5 +/- 0.5 l/kg. In all patients adequate levels for operation were obtained.     

Onset of spinal block is more rapid with isobaric than hyperbaric bupivacaine

PURPOSE: To compare isobaric with hyperbaric 9.75 mg bupivacaine injected intrathecally, and to evaluate the effects of subsequent injection of lidocaine 2% into the epidural space. METHODS: Patients in group 1 (n = 30) received isobaric 9.75 mg bupivacaine and in group 2 (n = 30) hyperbaric 9.75 mg bupivacaine injected into the subarachnoid space in a combined spinal-epidural technique. They were undergoing urological, gynecological, orthopedic, gastro-intestinal or vascular surgery. Using a double blind technique, the followings parameters were measured: cutaneous analgesia to pinprick, motor blockade, time for two segment regression, time for complete regression of the motor block, quality of anesthesia. In 12 patients the effect of epidural injections of 3 ml lidocaine 2% was observed. RESULTS: Motor and sensory block developed more rapidly (five minutes) in the isobaric group (P<0.05). Maximum upper level (T7+/-2), two-segment regression (52 min in both groups), motor recovery (160 vs. 157 min), and quality of anesthesia did not differ between the two groups. Thirty nine epidural injections of 3 ml lidocaine 2% were given in 12 patients 10 min after spinal injection, 28 were in the hyperbaric group (P<0.05). Twenty six of the epidural injections produced an increase in sensory block of 0 or 1 dermatome, and 13, of 2 or more. CONCLUSION: The block developed more rapidly in the isobaric group, but both isobaric and hyperbaric 9.75 mg bupivacaine produced adequate upper levels of analgesia for surgery. The effect of epidural injections of 3 ml lidocaine 2% was usually minimal.     

The addition of epinephrine increases intensity of sensory block during epidural anesthesia with lidocaine

BACKGROUND AND OBJECTIVES: Little is known about the effect of adding epinephrine to local anesthetic solutions on the intensity of sensory block during epidural anesthesia. This study examined development of sensory block during lumbar epidural anesthesia using a cutaneous current perception threshold (CPT) quantitative sensory testing device. METHODS: Twenty ASA I patients who were randomly divided to receive 10 mL 1% lidocaine with (group E) or without (group P) epinephrine 1:200,000. Current perception threshold at 2,000, 250, and 5 Hz stimulation at the trigeminal (V), ninth thoracic (T9), and second lumbar (L2) dermatomes, and the dermatomal levels of block of light touch, temperature, and pinprick discrimination were measured before and every 5 minutes, until 60 minutes after injection of epidural lidocaine. RESULTS: After epidural administration of lidocaine with epinephrine, all CPT significantly increased at T9 and L2, whereas no increase was detected after epidural plain lidocaine. Areas under the curves, calculated to express overall magnitude and duration of CPT values, were significantly larger in group E than those in group P at 2,000 and 250 Hz at T9. No differences were observed in the maximal levels of loss of cold, pinprick, and touch sensations between both groups. CONCLUSIONS: These results suggest that lumbar epidural anesthesia using 10 mL 1% lidocaine with epinephrine produces a more intense block of both large and small diameter sensory nerve fibers than that with plain lidocaine. It appears, therefore, that the addition of epinephrine improves the quality of sensory block during epidural anesthesia with lidocaine.     

Preemptive analgesia. Clinical evidence of neuroplasticity contributing to postoperative pain.

Recent evidence suggests that surgical incision and other noxious perioperative events may induce prolonged changes in central neural function that later contribute to postoperative pain. The present study tested the hypothesis that patients receiving epidural fentanyl before incision would have less pain and need fewer analgesics post-operatively than patients receiving the same dose of epidural fentanyl after incision. Thirty patients (ASA physical status 2) scheduled for elective thoracic surgery through a posterolateral thoracotomy incision were randomized to one of two groups of equal size and prospectively studied in a double-blind manner. Epidural catheters were placed via the L2-L3 or L3-L4 interspaces preoperatively, and the position was confirmed with lidocaine. Group 1 received epidural fentanyl (4 micrograms/kg, in 20 ml normal saline) before surgical incision, followed by epidural normal saline (20 ml) infused 15 min after incision. Group 2 received epidural normal saline (20 ml) before surgical incision, followed by epidural fentanyl (4 micrograms/kg, in 20 ml normal saline) infused 15 min after incision. No additional analgesics were used before or during the operation. Anesthesia was induced with thiopental (3-5 mg/kg) and maintained with N2O/O2 and isoflurane. Paralysis was achieved with pancuronium (0.1 mg/kg). Postoperative analgesia consisted of patient-controlled intravenous morphine. Visual analogue scale pain scores were significantly less in group 1 (2.6 +/- 0.44) than in group 2 (4.7 +/- 0.58) 6 h after surgery (P less than 0.05), by which time plasma fentanyl concentrations had decreased to subtherapeutic levels (less than 0.15 ng/ml) in both groups.(ABSTRACT TRUNCATED AT 250 WORDS)