Regional anesthesia and pain medicine
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Reg Anesth Pain Med · Nov 2000
Randomized Controlled Trial Comparative Study Clinical Trial Controlled Clinical TrialPain on intramuscular injection of bupivacaine, ropivacaine, with and without dexamethasone.
We wished to determine which long-acting local anesthetic would produce the least pain on injection for treatment of myofascial pain disorders. We compared the pain on intramuscular injection of bupivacaine, ropivacaine, bupivacaine with dexamethasone, ropivacaine with dexamethasone, and needle placement alone. ⋯ The pain on intramuscular injection of bupivacaine is significantly more intense than with ropivacaine. The difference in the intensity of the pain on injection between bupivacaine and ropivacaine does not appear to be related to differences in pH. The results of our study have implications on the choice of the local anesthetic used in trigger point injections.
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Reg Anesth Pain Med · Nov 2000
Randomized Controlled Trial Clinical Trial Controlled Clinical TrialA low dose of plain or hyperbaric bupivacaine for unilateral spinal anesthesia.
Unilateral spinal anesthesia may be advantageous, especially in the outpatient setting. A low dose of anesthetic solution, pencil-point needle, low speed of intrathecal injection, and a lateral position have been reported to facilitate the production of unilateral distribution of spinal anesthesia. We compared the effects of plain and hyperbaric bupivacaine in attempting to obtain a unilateral spinal anesthesia for patients undergoing outpatient knee arthroscopy. ⋯ In conclusion, the spinal anesthesia in both groups are suitable alternatives for adult outpatient knee arthroscopies, but hyperbaric bupivacaine provides us with a more unilateral spinal block.
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Reg Anesth Pain Med · Nov 2000
Randomized Controlled Trial Clinical TrialEfficacy of simulated epinephrine-containing epidural test dose after intravenous atropine during isoflurane anesthesia in children.
A double-blind, randomized study was performed to investigate heart rate (HR) and blood pressure responses to 2 doses of intravenous (IV) epinephrine (0.5 and 0.75 microg/kg) in 61 children, ages 3 months to 12 years. ⋯ A simulated epidural test dose containing lidocaine 1 mg/kg with epinephrine 0.75 microg/kg, administered IV following atropine, may reliably increase HR to indicate unintentional injection into epidural vessels of children anesthetized with 1 MAC isoflurane.
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Reg Anesth Pain Med · Nov 2000
Randomized Controlled Trial Clinical TrialSkin blood flow changes in response to intradermal injection of bupivacaine and levobupivacaine, assessed by laser Doppler imaging.
The vascular effects of local anesthetics are important determinants of their therapeutic activity. Drugs that vasoconstrict have the potential clinical advantages of limited systemic uptake and prolonged duration of effect. The aim of this study was to assess quantitatively the cutaneous vasoactivity of racemic bupivacaine and one of its enantiomers, levobupivacaine. ⋯ Bupivacaine and levobupivacaine both have a biphasic effect on skin microvessels. The vasoconstriction observed after 40 minutes may occur when the quantity of drug remaining at the administration site has decreased to a lower level. The continued vasodilatation caused by bupivacaine is more difficult to interpret. The results suggest that these local anesthetics cause vasodilatation at high doses and vasoconstriction at lower, subclinical doses. This hypothesis and the clinical relevance of these effects warrant further investigation.
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Reg Anesth Pain Med · Nov 2000
Conduction block by clonidine is not mediated by alpha2-adrenergic receptors in rat sciatic nerve fibers.
Clonidine, an alpha(2)-adrenergic agonist, has been shown to prolong local anesthesia. It appears that clonidine by itself produces conduction block by acting on peripheral nerves. However, whether clonidine-induced conduction block is mediated through alpha(2)-adrenergic receptors remains unclear. The purpose of this study was to see if clonidine's nerve-blocking action was through alpha(2)-adrenergic receptors by examining clonidine's action in the presence of alpha(2)-adrenergic antagonists. ⋯ The results indicated that the mixture of clonidine and yohimbine, in which either drug inhibited impulse conduction, produced conduction block in an additive manner, and that clonidine-induced conduction block was not reversed by coapplication with a specific alpha(2)-adrenergic antagonist idazoxan. These data suggest that clonidine's effects likely depend on mechanisms not mediated by alpha(2)-adrenergic receptors.