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ANESTHETIC PHARMACOLOGY

The Effect of Too Much Intravenous Lidocaine on Bispectral Index

From the Department of Anesthesiology, University of Virginia Health System, Charlottesville, Virginia.

Address correspondence and reprint requests to Marcel E. Durieux, MD, PhD, Department of Anesthesiology, University of Virginia Health System, Box 800710, Charlottesville, VA 22908. Address e-mail to durieux{at}virginia.edu.

	Abstract

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Systemic local anesthetics have beneficial perioperative properties and have an anesthetic-sparing effect. To assess depth of anesthesia during lidocaine infusion, it would be important to know the effect of systemic local anesthetics on bispectral index (BIS). However, this has not been investigated. We report an inadvertent overdose of IV lidocaine in a patient monitored with BIS. BIS decreased to 0 for approximately 15 min, indicating that lidocaine and sevoflurane interact to decrease BIS.

	Introduction

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Perioperative IV lidocaine infusion decreases postoperative pain, shortens duration of hospitalization (1), and has a general anesthetic-sparing effect. When bispectral index (BIS) is used to gauge depth of anesthesia, it is important to know if the anesthetic-sparing action of systemic local anesthetics is reflected in the BIS values. This, however, has not been investigated. We report a case where a patient undergoing BIS monitoring inadvertently received a large lidocaine bolus.

	CASE REPORT

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A 79-yr-old, 50 kg woman presented to the operating room for vaginal vault suspension, anterior colporrhaphy, and perineal rectosigmoidectomy. Her medical history included non–insulin-dependent diabetes, hypercholesterolemia, and hypothyroidism. Her preanesthetic arterial blood pressure (BP) and heart rate were 123/58 mm Hg and 82 bpm, respectively. Immediately before anesthetic induction, electrocardiography, peripheral oxygen saturation (Sao₂), and noninvasive BP monitors were applied, and a BIS sensor (A-2000 XP, with BIS Quatro adult sensor, Aspect medical systems, Newton, MA) was placed on the patient’s forehead. She had received 1 mg of midazolam, and BIS at the time was 80. Anesthesia was then induced with fentanyl 50 µg, propofol 100 mg, lidocaine 50 mg, and rocuronium 50 mg. During intubation, ST segment depressions of 2–3 mm were noted in electrocardiogram lead II. At this time her BP was 170/80 mm Hg and heart rate was 110 bpm. These changes lasted approximately 2.5–3 min, and resolved completely, without treatment. Anesthesia was then maintained with sevoflurane in N₂O/O₂. The BIS at this time was 45. Neuromuscular blockade was monitored throughout the procedure.

After full resolution of the ST segment depressions, lidocaine was infused using an 8 mg/mL lidocaine solution. The planned infusion rate was 0.25 mL · kg^–1 · h^–1, but the infusion pump was inadvertently programmed to deliver 0.25 mL · kg^–1 · min^–1, thus administering 100 mg lidocaine per minute. After 7–8 min, BIS read 0. The programming error was thereby discovered, and the pump was immediately stopped. The patient had by then received approximately 800 mg of lidocaine. At this time, the end-tidal sevoflurane concentration was 0.7, BP was 55/30 mm Hg, heart rate was 70 bpm with occasional premature atrial contractions, and her arterial oxygen saturation was 99%. Phenylephrine 100 µg was administered to correct the BP. BIS remained at 0 for approximately 10–12 min (Fig. 1), and the raw electroencephalogram was noted to be completely flat. BIS then returned to a value of 60 over the next 10 min. Her BP normalized within 5 min, to 100/70 mm Hg, and the occasional premature atrial contractions continued for approximately 30 min. BIS remained between 39 and 50 throughout the rest of the case, and the lidocaine infusion was restarted at the proper rate of 0.25 mL · kg^–1 · h^–1 when all vital signs and BIS had normalized, approximately 30 min after the erroneous bolus.

View larger version (11K): [in this window] [in a new window]   Figure 1. Bispectral index (BIS) progression after administration of approximately 800 mg of lidocaine IV over 8 min by a misprogrammed infusion pump in an anesthetized patient. BIS rapidly decreased to 0, and returned to normal values approximately 15 min later. Data were traced directly from the BIS monitor screen.

At the end of the 3-h procedure, the patient resumed spontaneous ventilation. Although she had not received any muscle relaxants, apart from the 50 mg rocuronium given at induction, she appeared clinically weak, and 5 mg neostigmine and 1 mg glycopyrrolate were administered. The patient remained weak despite this treatment, so 1 mg midazolam was administered, and the trachea was not extubated. After an hour in the postanesthesia care unit, the patient appeared stronger and was successfully extubated without further incident. Subsequent postoperative recovery was uneventful.

	DISCUSSION

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Systemic local anesthetics reduce MAC of volatile anesthetics in animals by 20%–40% (2–4). Senturk et al. (5) demonstrated that patients receiving IM injections of either lidocaine or bupivacaine during a total IV propofol anesthetic had a significantly decreased propofol requirement as compared with patients in the control group. BIS was used to assure equal depth of anesthesia in both groups. These findings suggest that systemic lidocaine affects BIS, although this question has not been formally investigated. Our case indicates that systemic lidocaine levels indeed decrease BIS, and are even able to suppress it to 0.

The mechanism by which lidocaine reduces MAC is, as yet, unknown. The possibility has been considered that IV lidocaine exerts its effects at the spinal level, and thereby decreases the motor response that is essential in MAC (6). This raises the worrisome possibility that MAC may be reduced without a concomitant increase in (cerebral) depth of anesthesia. However, the data reported by Senturk et al. using BIS monitoring, as well as our case, suggest that such is not the case, and that brain activity is indeed decreased by systemic local anesthetic levels (5).

Seizures are an expected consequence of lidocaine overdose. Because our patient was chemically paralyzed at the time, it is conceivable that a brief, unrecognized seizure occurred, followed by central nervous system depression. However, the fact that the BIS monitor did not record electroencephalographic signs of seizure, nor stopped recording altogether during the time of the lidocaine bolus, suggests that the presence of sevoflurane protected the patient against central nervous system excitation.

We do not know if the persistent neuromuscular weakness after the procedure was in any way related to the local anesthetic overdose. However, lidocaine (5 mg/kg) has been shown to increase twitch depression by d-tubocurarine by approximately 25% in cats, and in patients IV lidocaine (1–11 mg/kg, administered at 3 mg · kg^–1 · min^–1) prolonged succinylcholine apnea (7,8).

In summary, we report that during general anesthesia with sevoflurane, a large dose of IV lidocaine depresses BIS, even to 0.

	Footnotes

 
Accepted for publication September 14, 2006.

	REFERENCES

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1. Groudine SB, Fisher HA, Kaufman RP Jr, et al. Intravenous lidocaine speeds the return of bowel function, decreases postoperative pain, and shortens hospital stay in patients undergoing radical retropubic prostatectomy. Anesth Analg 1998;86: 235–9. Comment 87:1212–13.
2. Johns RA, DiFazio CA, Longnecker DE. Lidocaine constricts or dilates rat arterioles in a dose-dependent manner. Anesthesiology 1985;62:141–4.[Web of Science][Medline]
3. DiFazio CA, Neiderlehner JR, Burney RG. The anesthetic potency of lidocaine in the rat. Anesth Analg 1976;55:818–21.[Abstract/Free Full Text]
4. Pypendop BH, Ilkiw JE. The effects of intravenous lidocaine administration on the minimum alveolar concentration of isoflurane in cats. Anesth Analg 2005;100:97–101.[Abstract/Free Full Text]
5. Senturk M, Pembeci K, Menda F, et al. Effects of intramuscular administration of lidocaine or bupivacaine on induction and maintenance doses of propofol evaluated by bispectral index. Br J Anaesth 2002;89:849–52.[Abstract/Free Full Text]
6. Bach FW, Jensen TS, Kastrup J, et al. The effect of intravenous lidocaine on nociceptive processing in diabetic neuropathy. Pain 1990;40:29–34. Comment 1991;46:232–3.
7. Harrah MD, Way WL, Katzung BG. The interaction of d-tubocurarine with antiarrhythmic drugs. Anesthesiology 1970;33:406–10.[Web of Science][Medline]
8. Usubiaga JE, Wikinski JA, Morales RL, Usubiaga LE. Interaction of intravenously administered procaine, lidocaine and succinylcholine in anesthetized subjects. Anesth Analg 1967;46:39–45.[Free Full Text]

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