Anesthesia and analgesia
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Anesthesia and analgesia · Aug 2003
Randomized Controlled Trial Clinical TrialThe effect of mixing lidocaine with propofol on the dose of propofol required for induction of anesthesia.
Lidocaine is used to reduce pain associated with propofol injection, either mixed with propofol or preceding it as a separate injection. The addition of lidocaine to propofol causes destabilization of the emulsion and reduces anesthetic potency in rats and humans. We conducted a randomized double-blinded study on 67 patients to assess the effect of mixing lidocaine with propofol on the dose of propofol required for the induction of anesthesia. Patients in Group S (n = 32) received IV lidocaine 0.2 mg/kg followed by an infusion of propofol whereas those in Group M (n = 35) received IV normal saline (placebo) followed by an infusion of a freshly prepared mixture of propofol 1%/lidocaine 1% in 10:1 volume ratio. The infusion was stopped when the subjects lost consciousness, as detected by the syringe-drop method. There was no statistically significant difference between the two groups in the mean (95% confidence interval) doses of propofol required for loss of consciousness: 2.0 (1.8-2.2) mg/kg for Group S versus 1.9 (1.7-2.0) mg/kg for Group M (P = 0.206). Mixing 20 mg of lidocaine with 200 mg of propofol is unlikely to affect the dose of propofol required for the induction of anesthesia. ⋯ Adding lidocaine to propofol destabilizes the propofol emulsion. A randomized double-blinded trial found no statistically significant difference in the doses of propofol required for the induction of anesthesia whether administered as a freshly prepared propofol 1%/lidocaine 1% 10:1 mixture or as a separate injection after a dose of lidocaine.
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Anesthesia and analgesia · Aug 2003
Randomized Controlled Trial Clinical TrialThe effect of small dose fentanyl on the emergence characteristics of pediatric patients after sevoflurane anesthesia without surgery.
We designed this study to measure the effect of a small dose of IV fentanyl on the emergence characteristics of pediatric patients undergoing sevoflurane anesthesia without any surgical intervention. Thirty-two ASA physical status I or II pediatric outpatients receiving sevoflurane anesthesia for magnetic resonance imaging scans were enrolled and assigned in a random and double-blinded manner to receive either placebo (saline) or 1 micro g/kg IV fentanyl 10 min before discontinuation of their anesthetic. The primary outcome measure was the percentage of patients with emergence agitation. We also evaluated the duration of agitation and time to meet hospital discharge criteria. Patients who received fentanyl had a decreased incidence of agitation (12% versus 56%) when compared with placebo. There was no significant difference in time to meet hospital discharge criteria. We conclude that the addition of a small dose of fentanyl to inhaled sevoflurane anesthesia decreases the incidence of emergence agitation independent of pain control effects. ⋯ The addition of a small dose of fentanyl given to patients undergoing nonsurgical sevoflurane anesthesia resulted in a significant decrease in emergence agitation in a prospective, randomized, and controlled trial involving pediatric patients.
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Anesthesia and analgesia · Aug 2003
Randomized Controlled Trial Clinical TrialEphedrine fails to accelerate the onset of neuromuscular block by vecuronium.
The onset time of neuromuscular blocking drugs is partially determined by circulatory factors, including muscle blood flow and cardiac output. We thus tested the hypothesis that a bolus of ephedrine accelerates the onset of vecuronium neuromuscular block by increasing cardiac output. A prospective, randomized study was conducted in 53 patients scheduled for elective surgery. After the induction of anesthesia, the ulnar nerve was stimulated supramaximally every 10 s, and the evoked twitch response of the adductor pollicis was recorded with accelerometry. Patients were maintained under anesthesia with continuous infusion of propofol for 10 min and then randomly assigned to ephedrine 210 microg/kg (n = 27) or an equivalent volume of saline (n = 26). The test solution was given 1 min before the administration of 0.1 mg/kg of vecuronium. Cardiac output was monitored with impedance cardiography. Ephedrine, but not saline, increased cardiac index (17%; P = 0.003). Nonetheless, the onset of 90% neuromuscular block was virtually identical in the patients given ephedrine (183 +/- 41 s) and saline (181 +/- 47 s). There was no correlation between cardiac index and onset of the blockade. We conclude that the onset of the vecuronium-induced neuromuscular block is primarily determined by factors other than cardiac output. The combination of ephedrine and vecuronium thus cannot be substituted for rapid-acting nondepolarizing muscle relaxants. ⋯ Ephedrine increased cardiac index but failed to speed onset of neuromuscular block with vecuronium. We conclude that ephedrine administration does not shorten the onset time of vecuronium.
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Anesthesia and analgesia · Aug 2003
Randomized Controlled Trial Comparative Study Clinical TrialA comparison of three different concentrations of levobupivacaine for caudal block in children.
We investigated three different concentrations of levobupivacaine (0.125%, 0.20%, and 0.25%; n = 20 in each group) for caudal blockade in a prospective, randomized, observer-blinded fashion in children (1-7 yr) undergoing subumbilical surgery. The duration of postoperative analgesia was assessed as the time to first administration of supplemental analgesia (based on a Childrens and Infants Postoperative Pain Scale score of >or=4), and the degree of immediate postoperative motor blockade was determined by use of a 3-point scale. A dose-response relationship was observed both with regard to median duration of postoperative analgesia (0.125%, 60 min; 0.20%, 118 min; 0.25%, 158 min) and the number of patients with evidence of early postoperative motor blockade (0.125%, 0; 0.20%, 4; 0.25%, 8). The 0.125% concentration was associated with significantly less early motor blockade (P = 0.003) but was found to result in a significantly shorter duration of postoperative analgesia (P < 0.05). Based on these results, the use of 0.20% levobupivacaine might represent the best clinical option if a plain levobupivacaine solution is to be used for caudal blockade in children. ⋯ The use of 0.125% levobupivacaine for caudal blockade (1 mL/kg) in children (1-7 yr) was associated with less early postoperative motor blockade but a shorter duration of postoperative analgesia compared with 0.20% and 0.25% solutions.
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Anesthesia and analgesia · Aug 2003
Lidocaine attenuates cytokine-induced cell injury in endothelial and vascular smooth muscle cells.
Local anesthetics have been reported to attenuate the inflammatory response and ischemia/reperfusion injury. Therefore, we hypothesized that pretreatment with local anesthetics may protect endothelial and vascular smooth muscle (VSM) cells from cytokine-induced injury. Human microvascular endothelial cells and rat VSM cells were pretreated with lidocaine or tetracaine (5-100 microM for 30 min) and then exposed to the cytokines tumor necrosis factor-alpha, interferon-gamma, and interleukin-1beta for 72 h. Cell survival and integrity were evaluated by trypan blue exclusion and lactate dehydrogenase release. The role of adenosine triphosphate-sensitive potassium (KATP) channels, protein kinase C, or both in modulating local anesthetic-induced protection was evaluated with the mitochondrial KATP antagonist 5-hydroxydecanoate, the cell-surface KATP antagonist 1-[5-[2-(5-chloro-o-anisamido)ethyl]-2-methoxyphenyl]sulfonyl-3-methylthiourea (HMR-1098), and the protein kinase C inhibitor staurosporine. Lidocaine attenuated cytokine-induced cell injury in a dose-dependent manner. Lidocaine (5 microM) increased cell survival by approximately 10%, whereas lidocaine (100 microM) increased cell survival by approximately 60% and induced a threefold decrease in lactate dehydrogenase release in both cell types. In contrast, tetracaine did not attenuate cytokine-induced cell injury. 5-hydroxydecanoate abolished the protective effects of lidocaine, but staurosporine and HMR-1098 had no effect on the lidocaine-induced protection. This study showed that lidocaine, but not tetracaine, attenuates cytokine-induced injury in endothelial and VSM cells. Lidocaine-induced protection appears to be modulated by mitochondrial KATP channels. ⋯ This study demonstrates that lidocaine attenuates cytokine-induced injury of endothelial and vascular smooth muscle cells via mechanisms involving adenosine triphosphate-sensitive potassium channels. Protection of the vasculature from cytokine-induced inflammation may preserve important physiological endothelial and vascular smooth muscle functions.