Anesthesia and analgesia
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Anesthesia and analgesia · Jan 2003
Extending the skeletal muscle viability period in the malignant hyperthermia test.
The caffeine halothane contracture test (CHCT) is the only validated test for diagnosing malignant hyperthermia (MH) susceptibility (MHS) and phenotyping MHS families. Although most diagnostic laboratory tests can check intra- and interlaboratory consistency through the use of standard control samples, there has been no practical way to achieve this goal for the CHCT. The distances between diagnostic centers and time constraints of the CHCT protocol (5 h) prohibit centers from sharing tissue samples. In this study, we investigated varying storage conditions to extend the standard viability period of skeletal muscle to 24 h. Twenty MHS patients were tested according to the North America protocol. After standard CHCT, the surplus muscle samples were placed in one of the following four treatment groups. In Groups 1 and 2, muscles remained under tension and were stored in Krebs buffer (pH 7.4) at 23 degrees C-25 degrees C (clamped-warm) and 4 degrees C (clamped-cold), respectively. In Groups 3 and 4, muscle strips were dissected, and the ends were tied with silk sutures, cut from the clamp, and placed in Krebs buffer at 23 degrees C-25 degrees C (free-warm) and 4 degrees C (free-cold), respectively. The responses of the treatment groups to halothane (3%) and caffeine (0.5-32 mM) were tested at 22-26 h after excision. The clamped-warm storage group correctly diagnosed MHS in all patients. ⋯ Varying conditions for storage of muscle were investigated to extend the viability period of muscle in the malignant hyperthermia (MH) test from 5 to 24 h. Muscles stored for 24 h under tension at room temperature remained viable and correctly diagnosed MH susceptibility in all patients.
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Anesthesia and analgesia · Jan 2003
Neurologic complications of 405 consecutive continuous axillary catheters.
Continuous axillary brachial plexus block may theoretically increase the risk of neurologic complications because of catheter-induced mechanical trauma or local anesthetic toxicity. In this study, we retrospectively reviewed the frequency of complications using current techniques and applications. There were 405 continuous axillary catheters in 368 patients. A preexisting neurologic condition was present in 41 (10.1%) patients, including 30 patients with a preoperative ulnar neuropathy. In 305 (75.3%) cases, the axillary catheter was placed to facilitate rehabilitation after major elbow surgery. Catheters were typically placed postoperatively, after documentation of the patient's normal neurologic examination. The local anesthetic infusion contained bupivacaine in 355 (88.7%) patients and mepivacaine in 45 (11.1%) patients. The mean infusion rate was 10 +/- 2 mL/h. Catheters remained indwelling for 55 +/- 32 h. In 31 patients, the axillary catheter was replaced because of technical problems or inadequate analgesia. There were 9 complications in 8 patients for an overall frequency of 2.2%. Complications included one each of the following: localized infection (treated with catheter removal and antibiotics), axillary hematoma, and retained catheter fragment requiring surgical excision. In addition, two patients reported signs and symptoms of systemic (preseizure) local anesthetic toxicity. Four (1.0%) patients reported new neurologic deficits postoperatively. In two patients, the neural dysfunction was non-anesthesia related. All four had continuous catheters placed after major elbow surgery. We conclude that the risk of neurologic complications associated with continuous axillary blockade is similar to that of single-dose techniques. ⋯ We evaluated the risk of neurologic complications in 368 patients undergoing 405 consecutive continuous axillary blocks. New neurologic deficits were reported in four patients. This series suggests that the risk of neurologic complications associated with continuous axillary block is similar to that of single-dose techniques.
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Anesthesia and analgesia · Jan 2003
Case ReportsHemodynamic response to caudal epidural clonidine in a pediatric cardiac patient.
Postoperative management of sedation and analgesia in pediatric cardiac patients presents many challenges. This case report describes a child who experienced dramatic clinical improvement with the postoperative use of caudal morphine and clonidine after conventional therapy had failed.
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Anesthesia and analgesia · Jan 2003
Minimum alveolar anesthetic concentration of isoflurane with different xenon concentrations in Swine.
For patients requiring a fraction of inspired oxygen more than 0.3, the use of xenon (Xe) as the sole anesthetic is limited because of its large minimum alveolar anesthetic concentration (MAC) of 71%. This warrants investigating the combination of Xe with other inhaled anesthetics. We therefore investigated the influence of Xe on the MAC of isoflurane. The study was performed in 10 swine (weight, 28-35 kg) ventilated with Xe 0%, 15%, 30%, 40%, 50%, and 65% in oxygen. For each Xe concentration, various concentrations of isoflurane were administered in a step-wise design. For each combination, a supramaximal pain stimulus (claw-clamp) was applied, and the appearance of a withdrawal reaction was recorded. The isoflurane MAC was defined as the end-tidal concentration required to produce a 50% response rate. At each Xe concentration, the responses to the pain stimulus were categorized, and a logistic regression model was fitted to the results to determine isoflurane MAC. Isoflurane MAC was decreased by inhalation of Xe in a nonlinear manner from 1.92% (95% confidence interval, 1.70%-2.15%) with 0% Xe to 1.17% (95% confidence interval, 0.75%-1.59%) with 65% Xe. Although this indicates partial antagonism of the two anesthetics, a combination of Xe with isoflurane may prove valuable for patients requiring a fraction of inspired oxygen more than 0.3. ⋯ We investigated the influence of the anesthetic gas xenon on the minimum alveolar anesthetic concentration (MAC) for isoflurane (another anesthetic gas). The study was performed in 10 swine ventilated with fixed xenon and various concentrations of isoflurane. The isoflurane MAC is decreased by inhalation of xenon in a nonlinear relationship.
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Anesthesia and analgesia · Jan 2003
Preconditioning with isoflurane produces dose-dependent neuroprotection via activation of adenosine triphosphate-regulated potassium channels after focal cerebral ischemia in rats.
In this study, we determined whether repeated brief isoflurane (Iso) anesthesia induces ischemic tolerance to focal cerebral ischemia in a dose-response manner and whether the effect is dependent on adenosine triphosphate-regulated potassium channels. In Experiment 1, 40 rats were randomly assigned to 4 groups: control animals received 100% oxygen 1 h/d for 5 days, whereas the isoflurane (Iso)1, Iso2, and Iso3 groups received 0.75%, 1.5%, or 2.25% Iso in oxygen 1 h/d for 5 days. In Experiment 2, 36 rats were randomly assigned to 4 groups: controls received 100% oxygen 1 h/d for 5 days; animals in the Iso and I+G (Iso+glibenclamide) groups received 2% Iso in oxygen 1 h/d for 5 days, and the I+G group received glibenclamide (GLB) (5 mg/kg intraperitoneally) before each Iso pretreatment. Animals in the GLB group received GLB (5 mg/kg intraperitoneally) once a day for 5 days. Twenty-four hours after the last pretreatment, the right middle cerebral artery was occluded for 120 min. Neurologic deficit scores (NDS) and brain infarct volumes were evaluated at 24 h. The NDS and infarct volumes of Iso2 and Iso3 were less than those of the controls (P < 0.05). The infarct volume in Iso3 was smaller than in Iso2 (P < 0.05). The NDS and infarct volume in the Iso group were less than in the control and I+G groups (P < 0.05). There was no statistical difference among the control, I+G, and GLB groups. The study demonstrated that repeated Iso anesthesia induces ischemic tolerance in rats in a dose-response manner. GLB, an adenosine triphosphate-regulated potassium channel blocker, abolished the tolerance induced by Iso. ⋯ Brief isoflurane anesthesia induces ischemic tolerance in the brain. The effect was found to be dose dependent in a rat focal cerebral ischemia model. Ischemic tolerance induced by isoflurane preconditioning is dependent on activation of adenosine triphosphate-regulated potassium channels.