Anesthesia and analgesia
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Anesthesia and analgesia · Mar 2004
Randomized Controlled Trial Comparative Study Clinical TrialIntrathecal and oral clonidine as prophylaxis for postoperative alcohol withdrawal syndrome: a randomized double-blinded study.
In this study, we evaluated the effect of intrathecal and oral clonidine as supplements to spinal anesthesia with lidocaine in patients at risk of postoperative alcohol withdrawal syndrome (AWS). We hypothesized that clonidine would have a prophylactic effect on postoperative AWS. Forty-five alcohol-dependent patients (daily ethanol intake >60 g) scheduled for transurethral resection of the prostate were double-blindly randomized into three groups. All patients received hyperbaric lidocaine 100 mg intrathecally. The diazepam group (DiazG) was premedicated with diazepam 10 mg orally; the intrathecal clonidine group (Clon(i/t)G) received a placebo (saline) tablet and clonidine 150 microg intrathecally; and the oral clonidine group (Clon(p/o)G) received clonidine 150 microg orally. For patients diagnosed with AWS, the Clinical Institute Withdrawal Assessment for Alcohol, revised scale, was used. Twelve patients in the DiazG had symptoms of AWS, compared with two in the Clon(i/t)G and one in the Clon(p/o)G. The median Clinical Institute Withdrawal Assessment for Alcohol, revised scale, score was 12 in the DiazG versus 1 in the clonidine-treated groups. Two patients in the DiazG had severe delirium. Patients receiving oral clonidine had a slightly decreased mean arterial blood pressure 6-12 h after spinal anesthesia (P < 0.05); patients in the DiazG had a hyperdynamic circulatory reaction 24-72 h after surgery. In conclusion, preoperative clonidine 150 microg, intrathecally or orally, prevented significant postoperative AWS in ethanol-dependent patients. ⋯ In this randomized, double-blinded study, clonidine 150 microg both intrathecally and orally prevented postoperative alcohol-withdrawal symptoms in alcohol-dependent men. The effect was superior to that with a single dose of diazepam 10 mg orally.
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Anesthesia and analgesia · Mar 2004
Randomized Controlled Trial Clinical TrialThe influence of ambulation time on the incidence of transient neurologic symptoms after lidocaine spinal anesthesia.
The cause of transient neurologic symptoms (TNSs) after lidocaine spinal anesthesia remains unclear. It has been proposed that early ambulation after spinal anesthesia contributes to the development of TNSs. We evaluated the influence of ambulation time on the occurrence of TNSs after spinal anesthesia with 50 mg of 2% plain lidocaine for knee arthroscopy. One-hundred-twenty patients undergoing knee arthroscopy (ASA physical status 1-2) were randomized into 3 groups, i.e., early (Group E), 6-h (Group 6-h), or late ambulation (Group L) groups. In Group E, ambulation was allowed as early as possible after regression of spinal block (on average 229 +/- 21 min; range, 135-247 min). In Group 6-h, the patients remained in bed for approximately 6 h after the block and in Group L until the next morning. The patient groups were comparable with respect to demographic, anesthetic, and surgical variables. The overall incidence of TNSs was 16%. TNSs occurred in 3 patients of Group E (7.5%), in 11 patients of Group 6-h (28%), and in 5 patients of Group L (13%). No significant differences were detected between the patients with and without TNSs. Early ambulation was not found to be a risk factor for TNSs after spinal anesthesia with 50 mg of 2% lidocaine. ⋯ This study shows that early ambulation time does not increase the incidence of transient neurologic symptoms after spinal anesthesia with 50 mg of 2% lidocaine for elective knee arthroscopy.
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Anesthesia and analgesia · Mar 2004
The effects of a polymerized bovine-derived hemoglobin solution in a rabbit model of arterial thrombosis and bleeding.
Hemoglobin-based oxygen carriers (HBOCs) have been developed primarily for their oxygenating function and possible use as an alternative to red blood cells during surgery or after major trauma. However, their effect on hemostasis has not been studied extensively. We compared the effects on hemostasis of bovine-derived hemoglobin solution (HBOC-201) with gelatin solution and saline infusion in an experimental model of arterial thrombosis and bleeding. After anesthesia, the Folts model was constructed in 30 rabbits. The common carotid artery was exposed, and a 60% stenosis was induced. A compression injury of the artery was then produced, which triggered a series of cyclic episodes of thrombosis (cyclic flow reductions [CFRs]). After the number of baseline CFRs was counted, animals were assigned randomly to one of three groups (n = 10 each): saline (control), gelatin, or HBOC-201 solution. The effect of studied solutions was observed by recording the number of CFRs during another period and was compared with that of saline. Ear immersion bleeding time was recorded after each CFR period. Gelatin and HBOC-201 had similar effects, manifested by significantly decreased CFRs (from median of 7 to 1 and 6 to 1, respectively) and significantly lengthened bleeding time (from 88 to 98 s and 81 to 102 s, respectively; P < 0.05). Saline infusion had no significant effect on CFRs or bleeding time. HBOC-201 and gelatin had similar effects marked by a reduction in the arterial thrombosis rate and increased bleeding time in rabbits. ⋯ In a rabbit thrombosis and hemorrhagic model, a polymerized bovine-derived hemoglobin solution and a gelatin solution infusion decreased arterial thrombosis and lengthened bleeding time.
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Anesthesia and analgesia · Mar 2004
Case ReportsPersistent cerebrospinal fluid leak: a complication of the combined spinal-epidural technique.
Persistent cerebrospinal fluid (CSF) leak is an apparently rare complication of dural puncture from spinal or epidural anesthesia. Combined spinal-epidural techniques are increasingly popular but persistent CSF leak has not been reported. We describe three parturients with persistent fluid leak from the insertion site after epidural catheter removal following combined spinal-epidural anesthesia. Uncertainties related to the diagnosis, treatment, and the implications of this complication are discussed, including beta(2)-transferrin immunofixation assay as a diagnostic test for the presence of CSF in this situation. ⋯ Combined spinal-epidural block can be complicated by persistent fluid leak from the skin insertion site. Testing for the presence of cerebrospinal fluid may be a useful aid to management.
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Anesthesia and analgesia · Mar 2004
Attenuation of gap-junction-mediated signaling facilitated anesthetic effect of sevoflurane in the central nervous system of rats.
Accumulating evidence suggests that reduction of intrinsic excitability or synaptic excitation and/or an enhancement of synaptic inhibition underlie the general anesthetic condition. Besides chemical synapse, neurons could communicate with each other by electrical coupling via gap-junctions. We hypothesized that inhibition of cell-to-cell signaling through gap-junction in the central nervous system (CNS) is involved in the anesthetic mechanism of volatile anesthetics. The minimum alveolar concentration (MAC) of sevoflurane was measured after the intracerebroventricular (ICV) or intrathecal (IT) administration of carbenoxolone (CBX), a gap-junction inhibitor, in vivo. The spontaneous oscillation in membrane currents of locus coeruleus neurons that results from electrical coupling between neurons was also recorded from young rat pontine slices by the patch clamp method, and the effect of sevoflurane on this oscillation was examined in vitro. The ICV administration of CBX (125 and 250 micro g/rat) significantly reduced the MAC of sevoflurane dose-dependently, whereas IT injection failed to inhibit the MAC. Sevoflurane at clinically relevant concentrations (0.1-0.5 mM) suppressed the spontaneous oscillation in membrane current concentration-dependently. These suppressions were significant at 0.5 mM with both amplitude and frequency. We suggest that suppression of gap-junction-mediated signaling in the CNS is involved in the anesthetic-induced immobilization by sevoflurane. ⋯ The intracerebroventricular administration of the gap-junction inhibitor, carbenoxolone, reduced the MAC of sevoflurane, and sevoflurane suppressed the signaling through gap-junctions in the central nervous system. The inhibition of gap-junctions may be one of the mechanisms and the site of action of sevoflurane.