Regional anesthesia and pain medicine
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Reg Anesth Pain Med · Sep 2011
Review Comparative StudyIs sciatic nerve block advantageous when combined with femoral nerve block for postoperative analgesia following total knee arthroplasty? A systematic review.
Sciatic nerve block (SNB) is commonly performed in combination with femoral nerve block (FNB) for postoperative analgesia following total knee arthroplasty (TKA). This systematic review examines the effects of adding SNB to FNB for TKA compared with FNB alone on acute pain and related outcomes. Four intermediate-quality randomized and 3 observational trials, including a total of 391 patients, were identified. ⋯ Only 2 trials specifically assessed posterior knee pain. We were unable to uncover any clinically important analgesic advantages for SNB beyond 24 hours postoperatively. At present, there is inconclusive evidence in the literature to define the effect of adding SNB to FNB on acute pain and related outcomes compared with FNB alone for TKA.
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Reg Anesth Pain Med · Sep 2011
Comparative StudyMinimum effective volume of lidocaine for ultrasound-guided supraclavicular block.
The aim of this study was to determine the minimum effective volume of lidocaine 1.5% with epinephrine 5 μg/mL in 90% of patients (MEV90) for double-injection ultrasound-guided supraclavicular block (SCB). ⋯ For double-injection ultrasound-guided SCB, the MEV90 of lidocaine 1.5% with epinephrine 5 μg/mL is 32 mL. Further dose finding studies are required for other concentrations of lidocaine, other local anesthetic agents and single-injection techniques.
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Reg Anesth Pain Med · Sep 2011
Comparative StudyGlutamate release and neurologic impairment after intrathecal administration of lidocaine and bupivacaine in the rat.
Local anesthetic-induced neurotoxicity is one of the potential causes of postspinal anesthesia neurologic injury. Many experimental and clinical studies have demonstrated that lidocaine is more neurotoxic than bupivacaine. The mechanisms of local anesthetic-induced neurotoxicity remain unclear. Glutamate is an excitatory amino acid and widely exists in the central nervous system. Overstimulation of the glutamate receptors may produce neuronal toxic effect. In this study, we used in vivo microdialysis to examine the glutamate release in cerebrospinal fluid (CSF) after intrathecal lidocaine and bupivacaine injection. ⋯ Intrathecal lidocaine caused a concentration-dependent increase of the CSF glutamate release and postinjection neurologic impairment; these effects can be reversed by MK-801. However, intrathecal bupivacaine shows no influence. We suggest that glutamate may be involved in the pathogenesis of lidocaine-induced spinal neurotoxicity.
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Reg Anesth Pain Med · Sep 2011
Comparative StudyInterventional pain physicians' experiences of and attitudes toward surgical privileging.
No consensus guidelines exist on surgical privilege credentialing for nonsurgeons. We queried a group of academic interventional pain physicians about their experiences acquiring such credentials after training, how this process reflected their training, and their current attitudes toward both processes. ⋯ Experience doing implantation procedures during fellowship training and subsequent experience with hospital surgical credentialing seems to vary widely, even among interventional pain physicians associated with academic training programs.
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Reg Anesth Pain Med · Sep 2011
Comparative StudyThe influence of adjuvants used in regional anesthesia on lidocaine-induced neurotoxicity in vitro.
Neurotoxic properties of local anesthetics can rarely lead to irreversible neuronal damage as in cauda equina syndrome. Clinically, local anesthetics are often combined with adjuvants to improve or prolong the anesthetic effect, whereas the impact of such adjuvants on lidocaine-induced apoptosis is unclear. Therefore, we investigated the influence of different adjuvants on the neurotoxicity of lidocaine. ⋯ Sufentanil, clonidine, epinephrine, and neostigmine do not influence the neurotoxicity of lidocaine in vitro. Morphine may have some cytoprotective effect at concentrations greater than those seen intrathecally in humans. In contrast, ketamine and midazolam increase the neurotoxicity of lidocaine in vitro, presumably by additive induction of mitochondrial apoptosis.