The comparative neurotoxicity of intrathecal lidocaine and bupivacaine in rats

There is a considerable difference in the number of reports of neurologic injury in the literature between lidocaine and other local anesthetics. Few in vivo animal studies have produced convincing results showing a difference in neurotoxicity among anesthetics. We investigated whether lidocaine and bupivacaine differ with respect to sensory impairment and histologic damage when equipotent doses of the two are administered intrathecally in rats. First, to determine relative anesthetic potency, rats intrathecally received 20 muL of saline, 0.625%, 1.25%, 2.5%, or 5% lidocaine, or 0.125%, 0.25%, 0.5%, or 1.0% bupivacaine, and were examined with the tail-flick test for 90 min. The potency ratio calculated was approximately 1:4.70 (95% confidence interval, 3.65-6.07) for lidocaine/bupivacaine. In the next experiment, 45 rats intrathecally received 20 muL of saline, 2.13% bupivacaine (approximately 1.5 mg/kg), or 10% lidocaine (approximately 6.9 mg/kg), and were examined for persistent functional impairment and morphologic damage. Rats given lidocaine developed significantly more prolonged tail-flick latencies than those in other groups 4 days after injection and incurred more morphologic damage than those given saline or bupivacaine. In conclusion, although the doses of anesthetics administered were larger than those used clinically, the present results suggest that bupivacaine is less neurotoxic than lidocaine when administered intrathecally at equipotent concentrations in the rat model. IMPLICATIONS: Bupivacaine induces less severe functional impairment and morphologic damage than lidocaine when the two anesthetics are intrathecally administered at equipotent concentrations in the rat.     

Effects of Preemptive or Postinjury Intrathecal Local Anesthesia on Persistent Nociceptive Responses in Rats: Confounding Influences of Peripheral Inflammation and the General Anesthetic Regimen

Background: Although experimental evidence indicates that preemptive intrathecal treatment with local anesthetics reduces postinjury neuronal hyperexcitability, clinical evidence indicates that preemptive treatments do not consistently reduce postoperative pain. The current study used experimental models of postinjury nociception, in which rats received subcutaneous or intraarticular injections of the irritant formalin, to evaluate the effects of peripheral inflammation, or the use of agents supplemental to anesthesia, as possible confounding influences on the effectiveness of preinjury and postinjury intrathecal local anesthetic treatments.

Methods: In experiment 1, lumbar intrathecal lidocaine (30 micro liter, 2%), given either 5 min before or 5 min after hind paw injection of 50 micro liter of varying concentrations of formalin, was compared with intrathecal cerebrospinal fluid, for their effects on nociceptive responses in the late phase of the formalin test. Furthermore, the effect of hind paw injection of 50 micro liter of 2.5, 3.75, or 5.0% formalin on peripheral inflammation was assessed by measuring plasma extravasation in the hind paws of rats given Evans Blue dye (50 mg/kg, intravenous). In experiment 2, rats received a deep tissue injury (100 micro liter of 5.0% formalin into the knee joint) while under halothane anesthesia. In addition to halothane (3-4%), rats received either saline, pentobarbital (13 mg/kg, intraperitoneal), or pentobarbital + morphine (0.5 mg/kg, intravenous), with or without preinjury or postinjury spinal anesthesia using intrathecal bupivacaine (30 micro liter, 0.75%), to assess the effects of supplemental treatments on the preemptive effects of intrathecal bupivacaine.

Results: Lumbar intrathecal lidocaine pretreatment, but not posttreatment, significantly reduced late phase nociceptive responses to hind paw injections of 2.5% formalin. The preemptive effects of lidocaine were overridden in rats that received hind paw injections of 3.75 and 5.0% formalin. Hind paw injection of 50 micro liter of 3.75 or 5.0%, but not 2.5% formalin produced an increase in plasma extravasation. Either pentobarbital or pentobarbital + morphine treatment, or a pentobarbital + morphine treatment and postinjury treatment with intrathecal bupivacaine failed to produce a significant reduction in the nociceptive response to the deep tissue injury. However, rats that received pentobarbital + morphine treatments and intrathecal bupivacaine before the injury had significantly reduced nociceptive responses to deep tissue injury when compared to the saline control group, but not to the group that received pentobarbital + morphine treatment and postinjury treatment with bupivacaine.     

Lidocaine increases the ventricular fibrillation threshold during bupivacaine-induced cardiotoxicity in pigs

Ventricular fibrillation (VF) is a cause of death in bupivacaine- induced cardiovascular toxicity. We have examined the therapeutic effects of lidocaine on the threshold for bupivacaine-induced VF in in situ beating swine hearts. Twenty-four animals were allocated to one of three groups: 0.25% bupivacaine, 1% lidocaine or 0.25% bupivacaine with 1% lidocaine were infused into the left anterior descending coronary artery in increasing doses of 0, 1, 2, 4, 8 and 16 ml h-1 for 15 min, respectively. ECG and haemodynamic variables were monitored continuously during infusion. Regional myocardial function in the area supplied by the left anterior descending coronary artery was assessed using the sonomicrometry technique. VF did not occur in the lidocaine group. VF developed at higher infusion rates in animals given bupivacaine with lidocaine (in one animal at an infusion rate of 8 ml h- 1 and in seven at 16 ml h-1) compared with animals given bupivacaine alone (in one at an infusion rate of 4 and in seven at 8 ml h-1). Although regional myocardial function decreased with increases in the infusion rate in each group, the depressant effects of the bupivacaine solution (medial inhibitory infusion rate of systolic shortening: IR50 = 2.43 (0.43) ml h-1) were significantly greater than those of the lidocaine solution (IR50 = 5.83 (0.87) ml h-1), but did not differ from those of the bupivacaine with lidocaine solution (IR50 = 3.54 (0.56) ml h-1). This study indicates that a combination of lidocaine and bupivacaine increased the threshold for bupivacaine-induced VF without further depressing myocardial contractility.      

The clinical effectiveness of epidural bupivacaine, bupivacaine with lidocaine, and bupivacaine with fentanyl for labor analgesia

STUDY OBJECTIVE: To examine the efficacy of bupivacaine alone and in combination with lidocaine or fentanyl for epidural analgesia during labor. DESIGN: Randomized, single-blind study. SETTING: Labor and delivery unit at a university medical center. PATIENTS: Forty-five primiparas requesting epidural analgesia. INTERVENTIONS: Following epidural placement at L3-4 interspace, patients received either bupivacaine 0.5% (Group 1, n = 15), bupivacaine 0.25% with lidocaine 1% (Group 2, n = 15), or bupivacaine 0.5% with fentanyl 50 micrograms in 10 ml of saline (Group 3, n = 15). Patients in Groups 1 and 2 received 6 to 10 ml of local anesthetic depending on patient height, while patients in Group 3 received 5 ml of local anesthetic plus 50 micrograms of fentanyl in 10 ml of saline. All solutions contained epinephrine 1:200,000. MEASUREMENTS AND MAIN RESULTS: Patients were assessed at regular intervals following administration of the epidural solution. Visual analog scale (VAS) scores were used to measure onset of analgesia, time to complete pain relief, duration of analgesia, and patient satisfaction with therapy. The frequency of shivering and pruritus and the extent of sensory/motor block also were evaluated. There were no intragroup differences in time to complete pain relief or patient satisfaction. However, patients in Group 3 noted the most rapid onset and longest duration of pain relief. Patients in Group 3 also experienced significantly less shivering and had the lowest degree of motor block. Two patients in Group 3 experienced mild pruritus. CONCLUSIONS: Epidurally administered fentanyl safely extended the duration of labor analgesia while reducing bupivacaine dose requirements and magnitude of motor block. In this setting, the combination of bupivacaine and lidocaine offered no clinical advantage over bupivacaine alone.     

Cardiac dysrhythmias induced by infusion of local anesthetics into the lateral cerebral ventricle of cats

The hypothesis that neurogenically mediated cardiac arrhythmias can be induced by the intracerebroventrical (ICV) infusion of local anesthetic solutions was tested in 11 chronically prepared, unmedicated cats. Test substances were bupivacaine (0.1%), lidocaine (0.4%), procaine (0.4 or 0.8%), or saline (pH 5.8). Cats received one or more of the test substances with two or more days between infusions. Four cats were also given bupivacaine intravenously at 1.1 and 1.4 mg/kg to help determine whether ECG changes after ICV injection of local anesthetic were due to direct cardiac action after systemic absorption. Total dose was 3.8-7.8 X the largest ICV dose (0.7 mg). No ventricular arrhythmias were observed after the ICV infusion of saline or with intravenous doses of bupivacaine as large as 1.4 mg/kg. Only one of six cats given lidocaine ICV developed sustained, severe ventricular arrhythmias. Five of seven cats given ICV procaine developed ventricular arrhythmias. All ten cats given ICV bupivacaine developed ventricular arrhythmias. It is concluded that local anesthetics can produce neurogenically mediated ventricular arrhythmias in cats and that, of the three local anesthetics tested, bupivacaine is the most potent and effective and lidocaine is the least potent and effective.     

Lidocaine plus ropivacaine versus lidocaine plus bupivacaine for peribulbar anesthesia by single medical injection.

This study was designed to compare the effects of ropivacaine and bupivacaine, each combined with lidocaine, during peribulbar anesthesia by single medial injection for cataract surgery. One hundred patients were included and randomly divided into two groups of 50, given a mixture of 50% bupivacaine (0.5%) and 50% lidocaine (2%) or 50% ropivacaine (1%) and 50% lidocaine (2%), and 25 U hyaluronidase per mL with each combination. After the first injection, patients given ropivacaine exhibited significantly better akinesia than those given bupivacaine, and significantly fewer were reinjected (19/50 vs 31/50). Among the patients reinjected, peroperative akinesia and analgesia proved satisfactory in both groups. We observed three cases of diplopia caused by retraction of the internal rectus muscle and two cases of moderate ptosis after superonasal reinjection. Hemodynamic profiles were similar in the two groups, and no major side effects were noted during the observation. One percent ropivacaine may be a more appropriate agent than 0.5% bupivacaine for peribulbar anesthesia by single medial injection. IMPLICATIONS: One percent ropivacaine may be a more appropriate agent than 0.5% bupivacaine for peribulbar anesthesia by single medial injection. Combined with lidocaine, it provides better akinesia and similar analgesia.     

Influence of bupivacaine as an adjuvant to epidural morphine for analgesia after cesarean section

The effect of the addition of bupivacaine to epidural morphine (EM) on postoperative analgesia was evaluated in 150 patients after cesarean section performed under epidural anesthesia with carbonated lidocaine. Fifty patients received 3 mg EM without bupivacaine, 50 received 3 mg EM with 0.125% bupivacaine, 25 received 5 mg EM without bupivacaine, and 25 patients received 5 mg EM with 0.125% bupivacaine. Patients were assessed for quality and duration of postoperative analgesia, as well as the incidence and severity of side effects. The addition of bupivacaine did not affect the quality or duration of analgesia afforded by EM and did not influence the incidence or severity of side effects. Furthermore, there was no statistically significant difference in the analgesia obtained by patients receiving 3- and 5-mg doses of EM with or without bupivacaine.     

The electrophysiologic actions of lidocaine and bupivacaine in the isolated, perfused canine heart

To discriminate between the electrophysiologic and arrhythmogenic effects of lidocaine and those of bupivacaine, isolated, perfused canine hearts were exposed to toxic concentrations of the drugs. The preparations included the sinus node and right atrium, and, in some cases, the AV node and interventricular septum as well. Action potentials were recorded from these areas, and right atrial twitch amplitude and spontaneous rate and rhythm were monitored. Heart rate was depressed in a dose-dependent manner by both drugs, as was atrial twitch amplitude. In the absence of arrhythmias, the spontaneous rate decreased less than 30% with lidocaine up to 50 micrograms/ml, and with bupivacaine up to 5 micrograms/ml. The twitch depression reflected a potency ratio for bupivacaine (mol. wt. 288) to lidocaine (mol. wt. 234) on a mass basis of 8.1:1. The most prominent arrhythmia found was sinoatrial block, which was caused by both drugs with a potency ratio for bupivacaine to lidocaine of 15.4:1 and was reversed by 0.02 microgram/ml norepinephrine. Sinus arrhythmias, block of retrograde conduction from AV node to atrium, and irregular rhythms originating within the AV node were observed with both drugs at concentrations similar to those which produced sinoatrial block. The atrial action potential revealed decreased upstroke velocity, overshoot, and height with both lidocaine and bupivacaine, with potency ratios (bupivacaine:lidocaine) ranging from 15:1 to 26:1. In septal cells, both drugs depressed upstroke velocity, and bupivacaine lengthened action potentials by up to 14%, but lidocaine did not. The major difference between bupivacaine and lidocaine in this study was the higher potency of the former agent with respect to electrophysiologic end-points.     

Nimodipine reduces the toxicity of intravenous bupivacaine in rats.

We examined nimodipine modification of bupivacaine toxicity in anesthetized male rats. Three minutes after pretreatment, group 1 (n = 11), group 3 (n = 10), and their respective control groups (n = 11 and n = 9) received intravenous bupivacaine LD50 (median lethal dose). After pretreatment, group 2 (n = 10), group 4 (n = 8), and their respective control groups (n = 10 and n = 8) received intravenous bupivacaine LD90 (90% lethal dose). Pretreatment was 200 micrograms/kg intravenous nimodipine in groups 1 and 2 and 500 micrograms/kg in groups 3 and 4. Control animals were pretreated with intravenous saline solution. Data were analyzed by chi 2-analysis and analysis of variance. Survival increased after 200 micrograms/kg nimodipine (P less than 0.05). In group 1, 9 (81%) of 11 survived compared with control animals (4 [36%] of 11). In group 2, 8 (80%) of 10 survived compared with control animals (2 [20%] of 10). Survival was not increased after 500-micrograms/kg nimodipine pretreatment. In group 3, 2 (22%) of 9 survived compared with control animals (4 [40%] of 10). In group 4, 4 (50%) of 8 survived compared with control animals (2 [25%] of 8). We conclude that nimodipine pretreatment with 200 micrograms/kg protects against fatal toxicity from LD50 and LD90 bupivacaine, but 500 micrograms/kg does not.     

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.     

Cardiovascular toxicity of local anesthetics: an alternative hypothesis

The current study examined the possibility that high local anesthetic concentrations within the central nervous system could contribute to the toxic cardiovascular effects observed clinically after an accidental intravenous injection. Equal numbers of molecules of lidocaine (1.6 microliter of a 2% solution) and bupivacaine (1.0 microliter of a 4% solution) were injected at three vasomotor and cardioactive areas in the rat medulla by means of a 28-gauge hypodermic needle and a microsyringe. These areas were the C1 region, the intermediolateral column (IML), and the nucleus tractus solitarius (NTS). Both lidocaine and bupivacaine at C1 significantly decreased mean arterial pressure and, at IML, resulted in significant bradycardia and hypotension. At NTS, both lidocaine and bupivacaine caused significant bradycardia and hypotension, which were accompanied by ventricular arrhythmias in 55% of the animals. In all animals in whom ventricular arrhythmias were associated with lidocaine, the arrhythmias spontaneously reverted to normal sinus rhythm. In 50% of animals developing ventricular arrhythmias after bupivacaine, the arrhythmias resulted in death. Using an equal number of molecules of lidocaine and bupivacaine, all three regions studied demonstrated that bupivacaine was 2-4 times more potent than lidocaine in producing cardiovascular effects. These data demonstrate that direct application of local anesthetics within the medullary region of the central nervous system can result in hypotension, bradycardia, and ventricular arrhythmias similar to what may be seen in humans after accidental intravenous injections of local anesthetics. Moreover, the sites and mechanisms of action appear to be identical for bupivacaine and lidocaine. Thus bupivacaine does not appear to be an aberrant local anesthetic, as some have suggested, but rather produces more profound effects related to its potency and physicochemical properties.     

Caudal anesthesia with lidocaine or bupivacaine: plasma local anesthetic concentration and extent of sensory spread in old and young patients

Continuous caudal peridural anesthesia with 2% lidocaine (6 mg/kg) or 0.75% bupivacaine (2.2 mg/kg), both with epinephrine 1:200,000, was studied in two groups of male patients, younger than 40 or older than 55 yr old, respectively. Patients receiving lidocaine in the younger group (n = 6) were 32 +/- 5.2 (mean +/- SD) yr old and weighed 75 +/- 12 kg, while those in the older group (n = 16) were 66 +/- 5.3 yr old and weighed 72 +/- 8.2 kg. Patients receiving bupivacaine in the respective groups were 27 +/- 7.0 yr old (n = 5), and 76 +/- 10 kg compared to 69 +/- 10 yr (n = 14) and 75 +/- 10 kg. Anesthesia was satisfactory in all patients. Extent of sensory anesthesia, peak plasma lidocaine or bupivacaine concentrations, and area under the plasma concentration-time curves were independent of age. No local anesthetic toxicity was observed and peak drug concentrations were below those commonly associated with toxicity.     

Effect of topical local anesthetic application to skin harvest sites for pain management in burn patients undergoing skin-grafting procedures.

OBJECTIVE: To determine if topical administration of local anesthesia, applied to fresh skin-harvest sites, reduces pain and analgesic requirements after surgery. SUMMARY BACKGROUND DATA: Nonopioid treatments for pain after therapeutic procedures on patients with burns have become popular because of the side effects associated with narcotics. The topical administration of local anesthesia originally offered little advantage because of poor epidermal penetration. METHODS: This study compares 2% lidocaine with 0.5% bupivacaine or saline, topically applied after skin harvest, to determine what effect this may have on pain and narcotic use. Sixty patients with partial- or full-thickness burns to approximately 10% to 15% of their body were randomly divided into three groups: group 1 received normal saline, group 2 had 0.5% bupivacaine, and group 3 had 2% lidocaine sprayed onto areas immediately after skin harvest. Blood samples were subsequently obtained to measure concentrations of the local anesthetic. Hemodynamic variables after surgery, wake-up times, emetic symptoms, pain, and narcotic use were compared. RESULTS: Higher heart rates were noted in the placebo group than in those receiving lidocaine or bupivacaine. No differences were noted in recovery from anesthesia or emetic symptoms. Pain scores were lower and 24-hour narcotic use was less in patients who received lidocaine. Plasma lidocaine levels were greater than bupivacaine at all time points measured. CONCLUSIONS: Topical lidocaine applied to skin-harvest sites produced an analgesic effect that reduced narcotic requirements compared with patients who received bupivacaine or placebo. Local anesthetic solutions aerosolized onto skin-harvest sites did not affect healing or produce toxic blood concentrations.     

Effects of intravenous administration of local anesthetics on the renal sympathetic nerve activity during nitrous oxide and nitrous oxide-halothane anesthesia in the cat

The effects of subseizure doses of lidocaine and bupivacaine administered intravenously (i.v.) on mean arterial pressure (MAP), heart rate (HR) and renal sympathetic nerve activity (RSNA) were studied in cats anesthetized with nitrous oxide (N2O)-O2 and N2O-O2-halothane (1%). In cats anesthetized with N2O-O2, MAP decreased briefly (P less than 0.01) and then returned to the initial level within a minute after the i.v. injection of lidocaine (5 mg/kg, 10 mg/kg). RSNA increased at first and then decreased slightly. In cats with denervated baroreceptors, the change in RSNA after lidocaine 5 mg/kg i.v. was similar to that in cats with intact baroreceptors. In contrast, MAP, HR and RSNA decreased significantly (P less than 0.01) after i.v. injection of lidocaine during N2O-O2-halothane anesthesia. The effects of bupivacaine on RSNA were similar to those of lidocaine. It is concluded that cardiovascular depression following intravenous local anesthetics during N2O-O2-halothane anesthesia may be caused by both a decreased sympathetic activity and a direct depressant effect on the myocardium.     

Intrathecal fentanyl-induced pruritus is more severe in combination with procaine than with lidocaine or bupivacaine

BACKGROUND AND OBJECTIVES: Fentanyl is used as an additive to prolong intrathecal anesthesia with both lidocaine and low-dose bupivacaine in the outpatient setting to minimize voiding or discharge delays. Pruritus is the most common side effect. When using procaine as a substitute for lidocaine, we perceived an increased frequency and severity of pruritus. We compared prospectively the frequency and severity of itching with combinations of fentanyl with lidocaine, bupivacaine, and procaine. METHODS: After institutional review board approval, 135 patients requesting neuraxial anesthesia were asked to evaluate the presence and severity (using a 100 point verbal pruritus score [VPS]) of itching 30 minutes after injection of their spinal anesthetic, on arrival to the postanesthesia care unit (PACU), and at the time of resolution of their block. Choice of anesthetic drug and dose and the use of intravenous sedation was left to the discretion of the attending and resident anesthesiologist. RESULTS: Thirty-three patients received lidocaine and fentanyl, 47 received bupivacaine and fentanyl, and 55 received procaine and fentanyl. In the lidocaine group, 21% of patients experienced pruritus compared with 55% of the bupivacaine group and 55% of the procaine group (P =.003). The average VPS at 30 minutes postblock was 18.4 in the procaine group compared with 0 and 5.5 in the lidocaine and bupivacaine groups (P =.06). On admission to the PACU, it was 37 compared with 16 and 20 for lidocaine and bupivacaine, respectively (P =.006). CONCLUSION: Procaine produces a higher frequency of pruritus than that seen with lidocaine-fentanyl combinations and a greater severity of pruritus than seen with lidocaine-fentanyl and bupivacaine-fentanyl spinal anesthesia. Reg Anesth Pain Med 2001;26:252-256.     

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).     

Comparison of ropivacaine with bupivacaine and lidocaine for ilioinguinal block after ambulatory inguinal hernia repair in children

BACKGROUND: We have compared ropivacaine with bupivacaine and lidocaine for ilioinguinal block in thirty children undergoing ambulatory inguinal hernia repair. METHODS: Patients were assigned randomly to receive 0.5 ml.kg(-1) of 0.2% ropivacaine (Group R, n = 10), 0.25% bupivacaine (Group B, n = 10) or 1% lidocaine (Group L, n = 10). The patients' parents, who were not informed of the type of local anaesthetic employed, evaluated the postoperative pain at 2 h and 6 h after operation using the Wong-Baker FACES Pain Rating Scale. RESULTS: There was a significant difference in the face scale score between Group R and Group L, and Group B and Group L. There was no difference in the face scale score between Group R and Group B. There were no complications or clinical evidence of local anaesthetic toxicity. CONCLUSIONS: We have confirmed that bupivacaine and ropivacaine are more effective than lidocaine in the prevention of postoperative pain after children's inguinal hernia repair. We suggest that ropivacaine 0.2% is an alternative to bupivacaine 0.25% for ilioinguinal block in ambulatory paediatric surgery.     

Neurotoxicity of intrathecally administered bupivacaine involves the posterior roots/posterior white matter and is milder than lidocaine in rats

BACKGROUND AND OBJECTIVES: Clinical and laboratory studies suggest that lidocaine is more neurotoxic than bupivacaine. However, histological evidence of their comparative neurotoxicity is sparse. We thus pathologically and functionally compared the intrathecal neurotoxicity of these agents. METHODS: Rats received 0.12 microL/g body weight lidocaine (0%, 2%, 10%, or 20%) or bupivacaine (0%, 0.5%, 2.5%, or 5%) in distilled water via an intrathecal catheter. The influence of high osmolarity was also examined using 5% bupivacaine in 20% glucose solution (5% BG) and a control 25% glucose solution. The L3 spinal cord, the posterior and anterior roots, and the cauda equina were examined by light and electron microscopy. Walking behavior and sensory threshold were investigated as neurofunctional tests. RESULTS: The posterior root and posterior white matter showed axonal degeneration in rats treated with 10% and 20% lidocaine and 5% bupivacaine in distilled water (5% BDW) and in 5% BG, but not in rats treated with 2% lidocaine, 0.5% and 2.5% bupivacaine, distilled water, or 25% glucose solution. The histological damages were more severe in 20% lidocaine-treated rats than in 5% bupivacaine-treated rats. The damage of posterior white matter was observed only when the posterior root was severely injured. No significant difference of histological findings was observed between 5% BDW and 5% BG. Functional abnormalities were found only in rats treated with 20% lidocaine. CONCLUSIONS: The neurotoxic lesions caused by bupivacaine and lidocaine were indistinguishable in the primary site and the extending pattern, such as axonal degeneration originating from the posterior roots and extending to the posterior white matter. The intrathecal neurotoxicity is greater in lidocaine than in bupivacaine.     

Focus on mobilisation after lower abdominal surgery. A double-blind randomised comparison of epidural bupivacaine with morphine vs. lidocaine with morphine for postoperative analgesia

BACKGROUND: Epidural infusion of morphine, usually with bupivacaine, for postoperative pain relief has proved to be safe and effective. Lidocaine with its short duration of action and low toxicity may be an alternative to bupivacaine. The clinical importance of the choice of local anaesthetic drug on mobilisation after lower abdominal surgery has not been studied previously. METHODS: A total of 52 patients was randomised to epidural infusion of morphine (1.6-4.4 micrograms.kg-1.h-1) with either lidocaine (0.44-0.98 mg.kg-1.h-1) or bupivacaine (0.10-0.28 mg.kg-1.h-1) in a double-blind fashion. The time to mobilisation, degree of pain relief, blood pressure, respiration and motor function were recorded at regular intervals postoperatively for 40 h. Serum concentrations of lidocaine, its main metabolite monoethylglycinexylidide (MEGX) and bupivacaine were measured at 3, 15 and 40 h. RESULTS: There were no significant differences in the clinical characteristics between the two patient groups. There were no significant differences in the time from the end of surgery to the time the patients were able to stand without support (bupivacaine: median 24 h (interquartile range (IQR): 22-31), lidocaine: median 28 h (IQR 23-40), P = 0.15) or were able to walk without support (bupivacaine: median 46 h (IQR 28-62), lidocaine: median 48 h (IQR 35-54), P = 0.78). No significant differences between the groups were recorded with respect to pain relief, blood pressure, respiration, sedation score and motor function. The plasma concentration of lidocaine and bupivacaine increased significantly during the treatment period (P < 0.01 for both drugs), but not the concentration of MEGX. The highest venous lidocaine concentration was 17.5 mumol/l and the highest bupivacaine concentration was 18.8 mumol/l. There was a significant correlation between the concentration of both lidocaine and bupivacaine and the concentration of alpha 1-acid glycoprotein (AAG) (lidocaine: r = 0.77, P < 0.001, bupivacaine: r = 0.60, P < 0.001), suggesting that the free fraction of the drugs did not increase. No patients showed serious signs of toxicity. The epidural infusion rates remained stable in both groups during the study period. CONCLUSION: There were no clinically or statistically significant differences in the postoperative course after lower abdominal surgery in patients who received an epidural infusion of morphine combined with bupivacaine as compared to patients who received morphine with lidocaine. Further clinical studies to establish the place of lidocaine in postoperative epidural analgesia should be performed.     

Local anesthetic toxicity in interscalene block: clinical series

We experienced two cases of local anesthetic toxicity by interscalene block. A 62-year-old man received interscalene block with lidocaine 1% 30 mL and bupivacaine 0.25% 20 mL under light sedation followed by general anesthesia. He was not awake at one hour after surgery with his pupils dilated. Three hours after interscalene block, he became awake with no complication. A 73-year-old female received interscalene block with lidocaine 1% 15 mL and ropivacaine 0.75% 15 mL under light sedation. After the injection, a catheter was inserted 5 cm. About 7-8 min after catheter insertion, generalized tonic seizure occurred. Seizure stopped in two min after anesthesia induction. She had no complication after surgery. These two cases showed neurological toxicity by interscalene block with lidocaine and bupivacaine or with ropivacaine without hemodynamic complication.