Anesthesia and analgesia
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Anesthesia and analgesia · Mar 2004
Randomized Controlled Trial Comparative Study Clinical TrialPretreatment with thiopental for prevention of pain associated with propofol injection.
Propofol causes pain on IV injection in 28%-90% of patients. A number of techniques have been tried to minimize propofol-induced pain, with variable results. We compared the efficacy of pretreatment with thiopental 0.25 mg/kg and 0.5 mg/kg and lidocaine 40 mg after venous occlusion for prevention of propofol-induced pain. One-hundred-twenty-four adult patients, ASA physical status I-II, undergoing elective surgery were randomly assigned into 4 groups of 31 each. Group I received normal saline, group II received lidocaine 2% (40 mg), and groups III and IV received thiopental 0.25 mg/kg and 0.5 mg/kg, respectively. All pretreatment drugs were made in 2 mL and were accompanied by manual venous occlusion for 1 min. Propofol was administered after release of venous occlusion. Pain was assessed with a four-point scale: 0 = no pain, 1 = mild pain, 2 = moderate pain, and 3 = severe pain at the time of propofol injection. Twenty-four patients (77%) complained of pain in the group pretreated with normal saline as compared with 12 (39%), 10 (32%), and 1 (3%) in the groups pretreated with lidocaine 40 mg, thiopental 0.25 mg/kg, and thiopental 0.5 mg/kg, respectively (P < 0.05). Thiopental 0.5 mg/kg was the most effective treatment. We therefore suggest routine pretreatment with thiopental 0.5 mg/kg along with venous occlusion for 1 min for prevention of pain associated with propofol injection. ⋯ Pain associated with IV injection of propofol is seen in 28%-90% patients. Pretreatment with thiopental 0.25 mg/kg and 0.5 mg/kg after manual venous occlusion for 1 min effectively attenuated pain associated with propofol injection. Thiopental 0.5 mg/kg was the most effective in prevention of propofol pain and can be used routinely.
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Anesthesia and analgesia · Mar 2004
Randomized Controlled Trial Clinical TrialAdding dexmedetomidine to lidocaine for intravenous regional anesthesia.
Dexmedetomidine is approximately 8 times more selective toward the alpha-2-adrenoceptors than clonidine. It decreases anesthetic requirements by up to 90% and induces analgesia in patients. We designed this study to evaluate the effect of dexmedetomidine when added to lidocaine in IV regional anesthesia (IVRA). We investigated onset and duration of sensory and motor blocks, the quality of the anesthesia, intraoperative-postoperative hemodynamic variables, and intraoperative-postoperative pain and sedation. Thirty patients undergoing hand surgery were randomly assigned to 2 groups to receive IVRA. They received 40 mL of 0.5% lidocaine and either 1 mL of isotonic saline (group L, n = 15) or 0.5 microg/kg dexmedetomidine (group LD, n = 15). Sensory and motor block onset and recovery times and anesthesia quality were noted. Before and after the tourniquet application at 5, 10, 15, 20, and 40 min, hemodynamic variables, tourniquet pain and sedation, and analgesic use were recorded. After the tourniquet deflation, at 30 min, and 2, 4, 6, 12, and 24 h, hemodynamic variables, pain and sedation values, time to first analgesic requirement, analgesic use, and side effects were noted. Shortened sensory and motor block onset times, prolonged sensory and motor block recovery times, prolonged tolerance for the tourniquet, and improved quality of anesthesia were found in group LD. Visual analog scale scores were significantly less in group LD in the intraoperative period and 30 min, and 2, 4, and 6 h after tourniquet release. Intra-postoperative analgesic requirements were significantly less in group LD. Time to first analgesic requirements was significantly longer in group LD in the postoperative period. We conclude that the addition of 0.5 microg/kg dexmedetomidine to lidocaine for IVRA improves quality of anesthesia and perioperative analgesia without causing side effects. ⋯ This study was designed to evaluate the effect of dexmedetomidine when added to lidocaine for IV regional anesthesia. This is the first clinical study demonstrating that the addition of 0.5 microg/kg dexmedetomidine to lidocaine for IV regional anesthesia improves quality of anesthesia and intraoperative-postoperative analgesia without causing side effects.
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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
Clinical TrialContinuous parasacral sciatic block: a radiographic study.
Parasacral sciatic blockade results in anesthesia of the entire sacral plexus. In this study we sought to determine the spread of the local anesthetic injected through a parasacral catheter, the anatomical location of the inserted catheters, and the extent and reliability of the blockade. In this study, 87 consecutive patients undergoing major lower limb surgery were enrolled. After placement of the catheter and injection of 8 mL of radio-opaque contrast dye, radiographic images were evaluated for dispersion of the injectate. Sensory and motor evaluations were also performed. Radiographic analysis of the injectates revealed that nearly all catheters (86 catheters, 99%) were in the correct anatomical position. The mean volume of local anesthetic injection was 21 +/- 3 mL. All patients developed a full sensory block of all three major components of the sciatic plexus (tibial, common peroneal, and posterior cutaneous nerve of the thigh). We conclude that the parasacral sciatic block results in frequent success of blockade of all three major components of the sciatic plexus and it has a small risk of complications. Contrast radiography can be used to document the catheter placement. ⋯ The parasacral sciatic block results in a frequent success rate of blockade of all three major components of the sciatic plexus (tibial, common peroneal, and cutaneous nerve of thigh). A contrast radiography can be used to confirm the proper position of the catheter.
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Anesthesia and analgesia · Mar 2004
Intracellular calcium increases in growth cones exposed to tetracaine.
Neurotoxicity of local anesthetics has been reported for both matured and growing neurons. In the present study, we examined if tetracaine increases Ca(2+) concentration during growth cone collapse. Intracellular Ca(2+) concentration was measured by fura 2/AM after exposure to tetracaine. Tetracaine (1-2 mM) induced increases in intra-growth cone Ca(2+) concentration (P < 0.01). The Ca(2+) hot spot was expanded into the neurite from the periphery towards the cell body. When tetracaine was applied to growth cones in Ca(2+) free media, the increase was minor. However, tetracaine induced growth cone collapse even in the culture media, which did not contain Ca(2+). Ni(2+) (100 microM; a general Ca(2+) channel inhibitor) and BAPTA-AM (5 microM; intracellular Ca(2+) chelator) could not inhibit growth cone collapse induced by 1-2 mM tetracaine. Tetracaine (>1 mM) induces collapse and Ca(2+) increase at growth cones simultaneously; however, these two phenomena might be provoked independently. ⋯ Tetracaine induced intracellular Ca(2+) increases and growth cone collapse in dorsal root ganglion neurons. The Ca(2+) hot spot in the growth cone expanded into the neurite from periphery towards the cell body.