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Increased T-Wave Amplitude After Accidental Intravascular Injection of Lidocaine Plus Bupivacaine Without Epinephrine in Sevoflurane-Anesthetized Child

Tanaka, Makoto MD; Nitta, Rie MD; Nishikawa, Toshiaki MD

doi: 10.1097/00000539-200104000-00022
PEDIATRIC ANESTHESIA: Case Report
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Department of Anesthesia, Akita University School of Medicine, Akita, Japan

December 20, 2000.

Address correspondence and reprint requests to Makoto Tanaka, MD, Department of Anesthesia, Akita University School of Medicine, Hondo 1-1-1, Akita-city 010-8543, Japan. Address e-mail to mtanaka@med.akita-u.ac.jp.

IMPLICATIONS: Previous studies have shown that an increase in T-wave amplitude may occur after intravascular injection of an epinephrine-containing test dose in children under general anesthesia and have attributed its etiology to epinephrine, per se, without evidence. This case report describes a transient but marked increase in T-wave amplitude of lead II of the electrocardiogram after an accidental intravascular injection of lidocaine-bupivacaine mixture in a sevoflurane-anesthetized child.

Caudal anesthesia is often used as an adjunct to, and is most commonly initiated during, general anesthesia in children. To avoid potentially lethal central nervous system and cardiac toxicity associated with the inadvertent intravascular injection of large amounts of local anesthetic solution (1), a variety of strategies to reliably detect intravascular injection have been investigated (2–4). In addition to the aspiration test, heart rate (HR) and systolic blood pressure after an epinephrine-containing test dose injection have been commonly used as traditional indicators (2,5). More recently, several reports indicated that an increase in T-wave amplitude ≥25% in the electrocardiogram (EKG) could also be regarded as a diagnostic threshold for intravascular injection of epinephrine plus lidocaine or bupivacaine in sevoflurane-anesthetized children (4,6–10). Although it is presumed that the characteristic change in the EKG is associated with epinephrine, the exact mechanism remains undetermined.

In this report, we describe a case in which a dramatic increase in T-wave amplitude was documented during caudal administration of lidocaine-bupivacaine combination without epinephrine in a healthy infant during sevoflurane anesthesia. Changes in the EKG morphology associated with local anesthetics, without epinephrine or isoproterenol, have not been reported.

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Case Report

A 2-mo-old female infant was scheduled for left inguinal hernia repair. Her weight was 4.2 kg and her previous medical history was unremarkable.

On the day of surgery, she was allowed ad libitum breast milk 4 h before the anticipated time of general anesthesia induction and a maximum of 10 mL/kg clear liquid 2 h before the anticipated time of general anesthesia induction. No premedication, including atropine, was given. Standard monitors including automated blood pressure cuff, EKG lead II, and pulse oximeter were applied, and general anesthesia was induced via an anesthetic mask with incremental dosing of sevoflurane and nitrous oxide in oxygen using a Jackson-Rees circuit. A peripheral vein was cannulated, and lactated Ringer’s solution containing 2% dextrose was administered at a rate of 5 mL · kg−1 · h−1. Ventilation was first assisted and then controlled to maintain end-tidal CO2 tensions of 30–35 mm Hg. The patient was placed in the left lateral decubitus position, and a short-beveled 23-gauge needle was inserted into the caudal canal. After confirming that neither blood nor cerebrospinal fluid was aspirated, a mixture of 1% lidocaine 2 mL and 0.25% bupivacaine 2 mL (total 4 mL) without epinephrine was injected. Continuous record of the EKG was started immediately after injecting the local anesthetic solutions. Every 1 mL injection was preceded by gentle aspiration, and was followed by 20-s observation period for ventricular arrhythmia, and any change in rhythm or EKG morphology. When the third mL was administered, a significant increase in T-wave amplitude was noted on the oscilloscope 18 s after injection (Fig. 1). An aspiration test was positive for blood at this time, and the caudal anesthesia administration was stopped. End-tidal sevoflurane concentration and CO2 tension during this episode were 1.5% and 30 mm Hg, respectively. Noninvasive blood pressure and HR were 69/34 mm Hg and 134 bpm before, and 67/33 mm Hg and 136 bpm after caudal administration of local anesthetics, respectively. The increase in T-wave amplitude, which subsided spontaneously, was seen until 35 s after injection (Fig. 2). Because the patient was hemodynamically stable without further changes in EKG morphology and rhythm, the surgery commenced, during which anesthesia was maintained with sevoflurane and nitrous oxide in oxygen via an anesthetic mask. On emergence from anesthesia, the patient was agitated and showed active movements of the upper and lower extremities. The level of analgesia was not determined. The postoperative course of the patient was uneventful, and she was discharged the next day.

Figure 1

Figure 1

Figure 2

Figure 2

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Discussion

An increase in T-wave amplitude is a consistent phenomenon after a simulated IV test dose containing epinephrine plus lidocaine or bupivacaine (4,8–10), whereas IV injections of isoproterenol-containing test doses elicit variable responses, suggesting that changes in T-wave morphology are not simply a manifestation of β-adrenoceptor-mediated response (10). Recently, Kozek-Langenecker et al. (9) showed that the T-wave criterion (positive if ≥25% increase in T-wave amplitude in lead II) was more reliable than either HR or systolic blood pressure criteria for detecting intravascular injection, but 100% efficacy was only demonstrated in sevoflurane-anesthetized, but not halothane-anesthetized, children. In addition, pretreatment with atropine enhances T-wave changes after the IV test dose containing epinephrine (11). Furthermore, various physical and mental stresses also affect T-wave morphology (12). These results together with the present case indicate that the etiology of changes in T-wave morphology are multifactorial, influenced by types of volatile anesthetics, presence of epinephrine and/or local anesthetics, the status of preinjection autonomic nervous system, and the mood. It is not clear which local anesthetic, lidocaine, bupivacaine or both, caused the T-wave change in our case. Nyström et al. (13) demonstrated that the increased T-wave amplitude, the widened QRS complex, and the decreased R-wave amplitude preceded significant changes in blood pressure and HR, and hence, were the early signs of acute bupivacaine overdose in pigs. To determine the exact mechanism for the characteristic EKG change after the IV test dose, however, further study is warranted with a protocol that focuses on the effect of a single drug, epinephrine or a local anesthetic, on the EKG morphology, rather than studying their combined effect.

The peak increase in T-wave amplitude occurs within a circulation time, and 10 and 50 s earlier than those of HR and systolic blood pressure, respectively (4). To detect a subtle T-wave change with short duration, it has become our routine practice to make a continuous record of the EKG immediately after the test dose injection, from which the maximum and the serial changes in T-wave amplitudes are determined (Figs. 1 and 2). In our case, the absence of any change in the EKG morphology and the rhythm for 20 s after each of the first two doses (mL) of the lidocaine-bupivacaine solution suggests that the tip of the needle migrated immediately before or during the third dose injection. Thus, the significant increase in T-wave amplitude seen in our case was caused by the whole or a fractional dose of 1 mL lidocaine-bupivacaine mixture. Although the total doses of lidocaine and bupivacaine contained in each mL test dose, i.e., 1.2 mg/kg and 0.3 mg/kg, respectively, injected in our case were larger than the recommended doses of epidural test doses, i.e.,. 1 mg/kg and 0.25 mg/kg, respectively (2,3), a prominent increase in T-wave amplitude (250% of the preinjection value) seen in our case may be explained by the fact that the maximum percent increase in T-wave amplitude after simulated IV test dose with lidocaine and epinephrine correlates inversely with the patients’ age (4). More importantly, because bupivacaine alone or additive toxicity of the combined local anesthetics cannot be eliminated as an etiology of increased T-wave changes (13), standard test dosing regimen should be strictly followed to avoid potentially life-threatening cardiovascular complications in anesthetized children (1).

Epinephrine was not added to the local anesthetic solution as a result of erroneous preoperative communication between the resident and the attending anesthesiologist. However, the importance of adding the appropriate amount of epinephrine to the epidural local anesthetic solution should be strongly emphasized because the efficacy for detecting intravascular injection based on hemodynamic criteria have been established in sevoflurane-anesthetized children, and hence, an epinephrine-containing test dose should augment the detectability for its accidental intravascular injection (8,9).

In conclusion, we have experienced a clinically significant increase in T-wave amplitude in lead II of the EKG after unintentional IV test dose containing lidocaine and bupivacaine, but no epinephrine, in an infant anesthetized with sevoflurane and nitrous oxide. This case report suggests that a change in T-wave morphology, which has been presumed to be a result of IV epinephrine per se, may actually be a result of an IV local anesthetic.

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References

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© 2001 International Anesthesia Research Society