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Reversal of central nervous system and cardiac toxicity after local anesthetic intoxication by lipid emulsion injection.
Litz RJ et al
Journal: Anesth Analg 106(5):1575-1577, 2008. 17 References
Reprint: Dept of Anesthesiology and Intensive Care Medicine, University Hospital Carl Gustav Carus, University of Technology, Fetscherstr. 74, 01307 Dresden, Germany (RJ Litz, MD) LE.10 SP0830/270 ©2008
Faculty Disclosure: Abstracted by L. Easley, who has nothing to disclose.


Laboratory investigations and case reports have suggested that lipid emulsion infusion may be a treatment option for local anesthetic (LA)-induced systemic toxicity after failure of established resuscitation measures. The authors report a case of systemic LA intoxication after infraclavicular plexus block with 30 mL mepivacaine 1% and 10 mL prilocaine 1%, which was successfully treated by infusion of 200 mL of a 20% lipid solution. A 91-yr-old man with exacerbated chronic obstructive pulmo¬nary disease was admitted for olecranon bursitis surgery.

Within 5 min after injection of mepivacaine and then prilocaine, the patient complained of dizziness, nausea, and agitation, and became unresponsive to verbal commands. His heart rate increased from 76 to 92 beats/min and supraventricular extrasystoles with intermittent bigeminy appeared. LA toxicity was suspected and an IV bolus of 1 mL/kg Intralipid 20% was injected and repeated after 3 min. The patient regained consciousness within 5 min after the first lipid injection. Because extrasystoles were still apparent, lipid infusion was continued up to a total dose of 200 mL when extrasystoles disappeared. Surgery was started and performed uneventfully.

This is the first report of the clinical effect of lipid emulsion infusion on reversal of central nervous system (CNS) and cardiac toxicity with sequential LA plasma concentrations. The plasma concentration of mepivacaine was below 6 mcg/mL, generally con¬sidered a threshold for mepivacaine CNS toxicity. Notably, the plasma concentration of prilocaine 5 min after injection of only 100 mg was surprisingly high in this patient, suggesting possible intravascular injection, since peak plasma concentrations after absorption should occur 20-30 min later. Lipid infusion was immediately started after onset of symptoms, but before seizures occurred.

In this patient, CNS toxicity was reversed after injection of two boluses of 1 mL/kg each of Intralipid 20%. To reverse cardiac toxicity, a further dose of 2 mL/kg was required, given as a continuous infu¬sion, which was in accordance with the dose used in both case reports and Weinberg’s recommendations for treatment of LA related toxicity.