Comparison of the Analgesic Duration of 0.5% Bupivacaine With 1:200,000 Epinephrine Versus 0.5% Ropivacaine Versus 1% Ropivacaine for Low-Volume Ultrasound-Guided Interscalene Brachial Plexus Block: A Randomized Controlled Trial
Ben SafaBrendan P. FlynnPaul McHardyAlex KissLynn Haslam‐LarmerPatrick HenryLilia KaustovStephen Choi
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BACKGROUND: Bupivacaine and ropivacaine are the preferred long-acting local anesthetics for peripheral nerve blocks as they provide prolonged analgesia in the postoperative period. No studies have directly compared the analgesic duration of these commonly used local anesthetics in the setting of low-volume ultrasound-guided interscalene block (US-ISB). This study was designed to determine which local anesthetic and concentration provides superior analgesia (duration and quality) for low-volume US-ISB. METHODS: Sixty eligible patients scheduled for arthroscopic shoulder surgery were randomized (1:1:1) to receive US-ISB (5 mL) with 0.5% bupivacaine with 1:200,000 epinephrine, 0.5% ropivacaine, or 1% ropivacaine. All individuals were blinded including study participants, anesthesiologists, surgeons, research personnel, and statistician. All participants received a standardized general anesthetic and multimodal analgesia. The primary outcome was duration of analgesia defined as the time from the end of injection to the time that the patients reported a significant increase in pain (>3 numeric rating scale [NRS]) at the surgical site. RESULTS: The mean duration of analgesia for 0.5% bupivacaine with 1:200,000 epinephrine, 0.5% ropivacaine, or 1% ropivacaine was 14.1 ± 7.4, 13.8 ± 4.5, and 15.8 ± 6.3 hours, respectively (analysis of variance [ANOVA], P = .51). There were no observed differences in analgesic duration or other secondary outcomes between the 3 groups with the exception of a difference in cumulative opioid consumption up to 20h00 on the day of surgery in favor of ropivacaine 0.5% over bupivacaine of minimal clinical significance. CONCLUSIONS: In the context of single-injection low-volume US-ISB, we have demonstrated a similar efficacy between equal concentrations of ropivacaine and bupivacaine. In addition, increasing the concentration of ropivacaine from 0.5% to 1% did not prolong the duration of US-ISB.Keywords:
Ropivacaine
The effects of age, operative site (penoscrotal or inguinal), and the addition of epinephrine 1:200,000 to bupivacaine on duration of postoperative analgesia after caudal block were prospectively and blindly evaluated in 341 children aged 13 months to 17 yrs. At the conclusion of the surgical procedures under halothane/N2O/O2 anesthetics (n = 419), caudal blocks were performed with 0.5 ml/kg of either 0.25% bupivacaine or 0.25% bupivacaine with 1:200,000 epinephrine injected at a rate of 0.5 ml/sec. The duration of analgesia was noted by parents or nurses who had been instructed how to identify, in a standard manner, the onset of postoperative pain. The mean duration of analgesia was significantly longer in young children (P < 0.001), in children having penoscrotal operations (P < 0.001), and when epinephrine was added to bupivacaine (P < 0.001). There were no major complications. The authors conclude that duration of analgesia is significantly influenced by age, operative site, and the addition of epinephrine 1:200,000 to bupivacaine.
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Since bupivacaine and epinephrine may both precipitate dysrhythmias, circulating bupivacaine during regional anesthesia could potentiate dysrhythmogenic effects of epinephrine.We therefore examined whether bupivacaine alters the dysrhythmogenicity of subsequent administration of epinephrine in conscious, healthy dogs and in anesthetized dogs with myocardial infarction. Forty-one conscious dogs received 10 micro gram centered dot kg-1 centered dot min-1 epinephrine. Seventeen animals responded with ventricular tachycardia (VT) within 3 min. After 3 h, these responders randomly received 1 or 2 mg/kg bupivacaine or saline over 5 min, followed by 10 micro gram centered dot kg-1 centered dot min-1 epinephrine. In the bupivacaine groups, epinephrine caused fewer prodysrhythmic effects than without bupivacaine. VT appeared in fewer dogs and at a later time, and there were more sinoatrial beats and less ectopies. Epinephrine shortened QT less after bupivacaine than in control animals. One day after experimental myocardial infarction, six additional halothane-anesthetized dogs received 4 micro gram centered dot kg-1 centered dot min-1 epinephrine until VT appeared. After 45 min, 1 mg/kg bupivacaine was injected over 5 min, again followed by 4 micro gram centered dot kg-1 centered dot min-1 epinephrine. In these dogs, the prodysrhythmic response to epinephrine was also mitigated by preceding bupivacaine. Bupivacaine antagonizes epinephrine dysrhythmogenicity in conscious dogs susceptible to VT and in anesthetized dogs with spontaneous postinfarct dysrhythmias. There is no evidence that systemic subtoxic bupivacaine administration enhances the dysrhythmogenicity of subsequent epinephrine. (Anesth Analg 1996;83:62-7)
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To determine what effect the addition of epinephrine has on bupivacaine toxicity, toxic doses of bupivacaine were administered to awake spontaneously breathing pigs. Twenty animals were randomized to one of two groups. One group received an infusion of bupivacaine with epinephrine (5 micrograms/ml) at a rate of 2 mg.kg-1.min-1; the other received an infusion of plain bupivacaine at the same rate. Bupivacaine infusion was continued until cardiovascular collapse. Following cardiovascular collapse we attempted to resuscitate the animals via open chest cardiac massage and a standardized resuscitation protocol. The addition of epinephrine to bupivacaine significantly increased blood pressure and systemic vascular resistance but not heart rate or cardiac output early in the bupivacaine infusion. Epinephrine had no effect on the dose of bupivacaine that caused cardiovascular collapse (P = 0.1), on the plasma concentration of bupivacaine at collapse (P = 0.9), or on the ability to resuscitate animals following cardiovascular collapse. The addition of epinephrine decreased the dose of bupivacaine required to initiate cardiac dysrhythmias (P = 0.003). The first dysrhythmia experienced by the epinephrine group was second degree heart block, which contrasts with the premature ventricular and atrial dysrhythmias experienced by the plain group. The dose of bupivacaine that produced seizures was also reduced by the addition of epinephrine (P = 0.006). The addition of epinephrine to bupivacaine did not alter the dose of bupivacaine that caused cardiovascular collapse in awake spontaneously breathing pigs but did decrease the dose of bupivacaine that caused seizures and dysrhythmias.
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BACKGROUND: Ropivacaine, a derivative of mepivacaine like its older counterpart Bupivacaine, has recently been introduced in Indian pharmacopeia. Ropivacaine is an amide local anaesthetic but less cardiotoxic than bupivacaine.OBJECTIVE: To compare the clinical effectiveness of ropivacaine versus bupivacaine in patients undergoing lower extremity and lower abdominal surgeriesMETHODS: 50 patients were randomized to receive 20ml of 0.5% ropivacaine or 0.5% bupivacaine through epidural catheter. Sensory (pinprick) and motor (bromage) measurements were made while the block was in effect, haemodynamic changes; use of additional analgesics and sedatives was noted.RESULTS: The quality and extent of sensory and motor blockade between the two groups was comparable, although bupivacaine was found to be slightly longer acting. Both had similar motor blocking characteristics, with the exception that bupivacaine had a blockade of slightly longer duration but statistically not significant(p>0.05).CONCLUSION: Ropivacaine being lesser cardio toxic is the preferred agent for clinical epidural anaesthesia. JMS 2011;14(1):15-18
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Reports on the analgesic and hemodynamic effects of epinephrine added to bupivacaine for epidural use in obstetrics are conflicting. In this study, healthy parturients received in a random manner either 10 ml of 0.25% bupivacaine (n = 50) or 10 ml of 0.25% bupivacaine with 1:300,000 epinephrine (n = 50) epidurally. Epinephrine enhanced the analgesia produced by bupivacaine: onset was hastened (5.8 ± 0.6 vs 8.7 ± 0.8 min, mean ± SEM, P < 0.05), duration prolonged (123 ± 7.0 vs 92 ± 5.0 min, P < 0.05), and the number of women requiring additional local anesthetic for analgesia decreased (9 vs 18, P < 0.05) compared to the group receiving plain bupivacaine. The incidence of hypotension did not differ between groups. Maternal heart rate increased only after injection of the epinephrine-containing solution. The authors conclude that epinephrine 1:300,000 modestly but statistically significantly improves the analgesic efficacy of epidurally administered 0.25% bupivacaine during labor.
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Since bupivacaine and epinephrine may both precipitate dysrhythmias, circulating bupivacaine during regional anesthesia could potentiate dysrhythmogenic effects of epinephrine.We therefore examined whether bupivacaine alters the dysrhythmogenicity of subsequent administration of epinephrine in conscious, healthy dogs and in anesthetized dogs with myocardial infarction. Forty-one conscious dogs received 10 micro gram centered dot kg-1 centered dot min-1 epinephrine. Seventeen animals responded with ventricular tachycardia (VT) within 3 min. After 3 h, these responders randomly received 1 or 2 mg/kg bupivacaine or saline over 5 min, followed by 10 micro gram centered dot kg-1 centered dot min-1 epinephrine. In the bupivacaine groups, epinephrine caused fewer prodysrhythmic effects than without bupivacaine. VT appeared in fewer dogs and at a later time, and there were more sinoatrial beats and less ectopies. Epinephrine shortened QT less after bupivacaine than in control animals. One day after experimental myocardial infarction, six additional halothane-anesthetized dogs received 4 micro gram centered dot kg-1 centered dot min-1 epinephrine until VT appeared. After 45 min, 1 mg/kg bupivacaine was injected over 5 min, again followed by 4 micro gram centered dot kg-1 centered dot min-1 epinephrine. In these dogs, the prodysrhythmic response to epinephrine was also mitigated by preceding bupivacaine. Bupivacaine antagonizes epinephrine dysrhythmogenicity in conscious dogs susceptible to VT and in anesthetized dogs with spontaneous postinfarct dysrhythmias. There is no evidence that systemic subtoxic bupivacaine administration enhances the dysrhythmogenicity of subsequent epinephrine. (Anesth Analg 1996;83:62-7)
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We compared analgesic efficacy and degree of motor block induced by ropivacaine 0.1% (R 0.1) and 0.2% (R 0.2) vs. bupivacaine 0.2% (B 0.2) after caudal anaesthesia in children. Total and free plasma concentrations were measured after caudal injection. Duration of caudal analgesia (median/range) was significantly shorter in group R 0.1 (1.7 h/0.2–6 h) than in group R 0.2 (4.5 h/1.7–6 h) or group B 0.2 (4 h/1–6 h) ( P < 0.05). Motor block in the first 2 h postoperatively was significantly less for both ropivacaine groups compared with bupivacaine ( P < 0.05). Peak plasma concentrations after ropivacaine 0.2% were higher and protein binding lower than after bupivacaine 0.2% ( P < 0.05). We conclude that caudal analgesia with ropivacaine 0.1% is less effective and of shorter duration than that of ropivacaine 0.2%, whereas ropivacaine 0.2% provides pain relief similar to bupivacaine 0.2%. Motor block in the early postoperative period is less with ropivacaine than with bupivacaine.
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Background: Ropivacaine is the first S‐enantiomer aminoamide local anaesthetic in clinical use, and has been found to be less toxic than bupivacaine. Caudal ropivacine has been shown to cause less motor blockade and longer duration of analgesia in the postoperative period than bupivacaine in children. Plasma levels of ropivacaine and bupivacaine have not been previously compared in children. This study was undertaken to compare the total venous plasma concentrations of similar doses of ropivacaine and bupivacaine following caudal administration. Methods: Blood samples were obtained to determine the total venous plasma levels of the used local anaesthetic in 30 children, aged 2.3–8.7 years, ASA I, given 1 ml · kg −1 of either 0.2% ropivacaine or 0.2% bupivacaine in a prospective, randomised manner. Results: There were no differences in the individual peak plasma concentrations achieved. Time to the measured peak plasma concentration was significantly shorter in the bupivacaine group. The plasma concentrations of bupivacaine were significantly lower than for ropivacaine at 60, 90 and 120 min after the block. Conclusion: Absorption and tissue distribution of ropivacaine is slower than for bupivacaine following caudal administration in children.
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Intercostal blockade produces the highest serum local anesthetic concentrations of all regional anesthetic techniques. The purpose of this study was to determine the pharmacokinetic properties of ropivacaine and bupivacaine after bilateral intercostal blockade.The pharmacokinetics of ropivacaine (n = 7) and bupivacaine (n = 7) were determined in adult human volunteers from venous samples drawn over 24 h after bilateral intercostal blockade of T5-T11 with 140 mg of either drug (0.25% plain solutions, 56 ml). Sensory (pinprick, temperature, and touch) and motor blockade (RAM-test and integrated electromyography) were assessed every 2 h.There was no significant difference between the maximum plasma concentrations (Cmax) obtained for either drug (ropivacaine 1.1 +/- 0.4 microgram/ml, bupivacaine 0.9 +/- 0.2 microgram/ml, P = 0.39), and there were no toxic signs observed in the obtained plasma concentration ranges. Plasma concentrations tended to peak (tmax) earlier with ropivacaine (21 +/- 9 versus 30 +/- 8 min, P = 0.09). The terminal half-life (t1/2 beta) of ropivacaine (2.3 +/- 0.8 h) was significantly less than that for bupivacaine (4.6 +/- 2.6 h, P = 0.04). Sensory blockade measured by pinprick was of shorter duration with ropivacaine (6.0 +/- 2.5 h versus bupivacaine 10.0 +/- 3.0 h; P < 0.001). Likewise, motor blockade was less intense and of shorter duration for ropivacaine by RAM-test (P = 0.02).The results of this pharmacokinetic study indicate that 0.25% ropivacaine and 0.25% bupivacaine (56 ml, 140 mg) produce peak plasma levels less than those considered toxic when used in bilateral intercostal blockade. Studies of ropivacaine for intercostal blockade in surgical patients are necessary before the optimum concentration for efficacy and anesthetic/analgesic duration is identified.
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The transpleural passage of lidocaine, bupivacaine-lidocaine mixtures, and of bupivacaine, with and without epinephrine, was studied in vitro using pleural from piglets. Our objective was to ascertain whether changing physical parameters of local anesthetics such as pH, concentration, and addition of epinephrine might influence the transfer. Rate of transfer is linearly related to concentration at a given pH, but raising the pH increases the rate for bupivacaine. No change in rate was detectable when the pH of lidocaine was increased or in the rate of transfer of bupivacaine when bupivacaine and lidocaine were mixed. The mixture did however facilitate lidocaine flux. Epinephrine [1:200,000] lowers the pH of the solution dramatically but does not statistically change the transpleural passage of bupivacaine. We conclude that the onset of interpleural blockade may be shortened by using more concentrated solutions of bupivacaine whose pH have been modified by the addition of alkali, by using the higher concentrations of lidocaine or by mixing lidocaine with bupivacaine.
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