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Anesth Analg 2007;104:1613-1614
© 2007 International Anesthesia Research Society
doi: 10.1213/01.ane.0000263288.37114.39


LETTER TO THE EDITOR

Section Editor:
Lawrence Saidman

The Sedative Effect of High Dose Lidocaine

Cheryl M. Gaughen, MD, and Marcel E. Durieux, MD, PhD

Department of Anesthesiology; University of Virginia Health System; Charlottesville, VA; durieux{at}virginia.edu

In Response:

The observations of Szmuk et al. (1) are of interest, as muscle weakness after IV lidocaine has not been well investigated. It is therefore conceivable that, as Dr. Kempen (2) suggests, the postoperative weakness observed in our patients may have resulted from a high blood lidocaine level. The lidocaine infusion was restarted 30 min after the accidental bolus, which may not have been sufficient time for the blood level to decline (although BIS had recovered to normal general anesthetic values). The infusion was restarted at a rate of 2 mg/kg/hr, and was continued for approximately an hour. It was discontinued 45 min before the patient was transported, still intubated, to the PACU. In the PACU, the patient displayed signs of being weak despite receiving neostigmine. To clarify, the patient did not appear sedated, but physically weak, i.e., she was able to follow commands and did display purposeful movements (reaching for the endotracheal tube), but could not lift her head nor did she possess a strong hand squeeze. To maintain comfort, we administered IV midazolam (which of course induced some sedation), and the trachea was extubated 1 hr later when the patient was able to lift her head.

Although it has been shown that patients receiving prolonged lidocaine infusions (24 hr or more) experience an increase in the half-life of lidocaine due to impaired hepatic extraction, it is not known if this is also the case after a brief overdose of lidocaine (3). Our patient had no known hepatic disease or congestive heart failure, both of which have been shown to have a large effect on lidocaine clearance (4). It seems to us rather unlikely that a blood pressure decrease to 55 mm Hg for several minutes would induce sufficient cerebral ischemia to induce muscle weakness several hours later. It also seems unlikely that the transient hypotension would have played a major role in the dramatic BIS decrease, as such episodes occur not infrequently during clinical anesthesia and, at least in our experience, are not associated with any pronounced effect on BIS.

REFERENCES

  1. Szmuk P, Farrow-Gillespie A, Sheran P, Ezri T. The sedative effect of high dose lidocaine. Anesth Analg 2007;104:1613.[Free Full Text]
  2. Kempen PM. Weakness following an overdose of lidocaine during general anesthesia. Anesth Analg 2007;104:1613.[Free Full Text]
  3. LeLorier J, Moisan R, Gagne J, Caille G. Effect of the duration of infusion on the disposition of lidocaine in dogs. J Pharmacol Exp Ther 1977;203:507–11.[Abstract/Free Full Text]
  4. Waller ES. Pharmacokinetic principles of lidocaine dosing in relation to disease state. J Clin Pharmacol 1981;21:181–94.[Abstract]




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Lippincott, Williams & Wilkins Anesthesia & Analgesia® is published for the International Anesthesia Research Society® by Lippincott Williams & Wilkins and Stanford University Libraries' HighWire Press®. Copyright 2007 by the International Anesthesia Research Society. Online ISSN: 1526-7598   Print ISSN: 0003-2999 HighWire Press