Anesthesiology
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The ability of patients to walk without assistance after spinal anesthesia is a determining factor in the time to discharge following ambulatory surgery. The authors compared clinical markers of gross motor recovery with objective data of functional balance after spinal anesthesia. ⋯ The results suggest that the recovery time to unassisted ambulation is longer than has been assumed, and that the standard clinical markers of gross motor function are poor predictors of functional balance following ambulatory surgery.
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Activation of peripheral excitatory amino acid receptors decreases the duration of local anesthesia.
Postsurgical wound infiltration with the -methyl-d-aspartate receptor antagonist ketamine and bupivacaine can significantly prolong the duration of local anesthesia. One possible mechanism for this effect is that increased glutamate concentrations, caused by tissue damage, sensitize nociceptive primary afferent fibers through activation of peripheral excitatory amino acid receptors. ⋯ These results suggest that shortened lidocaine block durations observed after glutamate injection into the masseter muscle result from sensitization of afferent fibers as well as increases of peak extracellular water content and blood flow in masseter muscle. These effects of glutamate are mediated in part through activation of peripheral excitatory amino acid receptors.
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Randomized Controlled Trial Multicenter Study Comparative Study Clinical Trial
Prospective study on incidence and functional impact of transient neurologic symptoms associated with 1% versus 5% hyperbaric lidocaine in short urologic procedures.
The objectives of this study were to compare the incidence, onset, duration and pain scores of transient neurologic symptoms (TNS) with 1% versus 5% hyperbaric lidocaine in spinal anesthesia for short urological procedures in a large prospective study. This study would also evaluate patient satisfaction, and impact of TNS on functional recovery to assess the clinical significance of TNS. ⋯ There was no difference in the incidence of TNS between the 1% versus 5% spinal lidocaine groups. Pain scores were higher in patients with TNS than those who did not have TNS. During the first 48 h postop, a small proportion of patients who had TNS experienced functional impairment of walking, sitting, and sleeping.
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This investigation examined the possibility that the inhibitory effect of halothane on nonshivering thermogenesis (heat production) in brown adipocytes is not a universal effect of all anesthetic agents but related to the type of anesthetic. ⋯ There are two distinct classes of anesthetics with regard to effects on thermogenesis, thermogenesis inhibitors and thermogenesis noninhibitors. The results are important for the interpretation of studies in thermal biology in general; specifically, they indicate that conclusions concerning regulation of nonshivering thermogenesis during anesthesia depend on the type of anesthetic used. Of clinical importance is that the volatile anesthetics are inhibitory for nonshivering thermogenesis and thus for an alternative heat production when myorelaxants prevent shivering. As the distinction between thermogenesis inhibitors and thermogenesis noninhibitors corresponds to the distinction between volatile and nonvolatile anesthetics, it may be related to the mode of action of the volatile anesthetics.
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Tramadol hydrochloride (tramadol) is a synthetic opioid analgesic with a relatively weak affinity at opioid receptors. At analgesic doses, tramadol seems to cause little or no respiratory depression in humans, although there are some conflicting data. The aim of this study was to examine whether tramadol causes dose-dependent inhibitory effects on the ventilatory carbon dioxide response curve and whether these are reversible or can be prevented by naloxone. ⋯ Because naloxone completely reversed the inhibiting effects of tramadol on ventilatory control and it prevented more than 50% of the respiratory depression after a single dose of tramadol, the authors conclude that this analgesic causes respiratory depression that is mainly mediated by opioid receptors.