Anesthesia and analgesia
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Malignant hyperthermia has rarely been reported in China. We report the first case of malignant hyperthermia, verified by caffeine-halothane contracture test and genetic testing, in a Chinese patient.
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Anesthesia and analgesia · Oct 2006
Dexmedetomidine does not increase the incidence of intracarotid shunting in patients undergoing awake carotid endarterectomy.
Systemic administration of dexmedetomidine (DEX) decreases cerebral bloodflow (CBF) via direct alpha-2-mediated constriction of cerebral blood vessels and indirectly via its effect on the intrinsic neural pathway modulating vascular smooth muscle. Reduction in CBF without a concomitant decrease in cerebral metabolic rate has raised concerns that DEX may limit adequate cerebral oxygenation of brain tissue in patients with already compromised cerebral circulation (e.g., carotid endarterectomy [CEA]). In this study, we established the incidence of intraarterial shunting used as a sign of inadequate oxygen delivery in a consecutive series of 123 awake CEA performed in our institution using DEX as a primary sedative. ⋯ The incidence of shunting in patient undergoing awake CEA in our institution is 10% (historical control). No patients developed a stroke or other serious complications. It appears that the use of DEX as a primary sedative drug for CEA does not increase the incidence of intraarterial shunts.
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Anesthesia and analgesia · Oct 2006
Comparative StudyCerebral metabolism assessed with microdialysis in uncontrolled hemorrhagic shock after penetrating liver trauma.
In a porcine model of uncontrolled hemorrhagic shock, we evaluated the effects of fluid resuscitation versus arginine vasopressin (AVP) combined with hypertonic-hyperoncotic hydroxyethyl starch solution (HHS) on cerebral perfusion pressure (CPP) and on cerebral metabolism using intracerebral microdialysis. Sixteen anesthetized pigs were subjected to uncontrolled liver bleeding until hemodynamic decompensation, followed by resuscitation using either fluid (n = 8) or AVP/HHS (n = 8). Thirty minutes after drug administration, bleeding was controlled by manual compression, and colloid and crystalloid solutions were administered in both groups. ⋯ Mean (+/- sem) cerebral venous partial pressure of oxygen was significantly decreased (P < 0.01) 5 min after fluid compared with 5 min after AVP/HHS administration (36 +/- 3 vs 64 +/- 4 torr). Cerebral metabolism was comparable in both groups. In conclusion, AVP/HHS proved to be superior to fluid in the initial phase of therapy with respect to CPP and cerebral oxygenation, but was comparable to fluid regarding cerebral metabolism and secondary cell damage in surviving animals.
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Anesthesia and analgesia · Oct 2006
Epidural lidocaine induces dose-dependent neurologic injury in rats.
Although epidural lidocaine administered as a bolus has been shown to cause little neurotoxicity, local anesthetics are often administered repetitively or continuously into the epidural space, and in high doses may induce neurologic injury. We investigated whether epidural lidocaine is neurotoxic when a large dose is continuously administered in rats, and whether the functional impairment and histologic damage is dose dependent. In Experiment 1, 13 rats received a 120-min epidural infusion (at 5 microL/min) of saline or 2% lidocaine. ⋯ Nerve injury scores for rats given 5% lidocaine for 30, 60, and 120 min were significantly higher than those for rats given saline. Significant difference in damage in nerve roots was also observed among rats given the anesthetic for different durations of time; nerve injury scores with 120-min infusion were higher than with 15- and 30-min infusions, and injury with 60-min infusion was greater than with 15-min infusion. In conclusion, these results suggest that epidural lidocaine causes dose-dependent neurotoxicity after continuous infusion in rats.