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Department of Anesthesiology, University of Illinois College of Medicine, Chicago, IL
To the Editor:
We read with interest the case reported by Tung et al. (1) of cardiac arrest in a patient with chronic hypertension, pulmonary hypertension, and scleroderma during recovery from a brachial plexus block. The authors postulate that several factors, including preexisting cardiac disease, and prior administration of an angiotensin converting enzyme (ACE) inhibitor, a beta-blocker, and possibly metoclopramide, contributed to the fatal event. We agree that the incident was probably multifactorial in origin. However, the clinical setting and signs suggest another factor, local anesthetic toxicity, may have played a key role in this patient’s demise.
The patient received a combination of bupivacaine 100 mg and mepivacaine 300 mg approximately two hours before she developed hypertension and nausea in the recovery room. She received labetalol and metoclopramide, and shortly thereafter, developed bradycardia and hypotension leading to circulatory collapse. The patient required continued pressor support after resuscitation, exhibited prolonged, severe metabolic acidosis, and 13 hours later had a fatal episode of bradycardia.
Systemic absorption from a local anesthetic depot continues long after the injection, and several factors can augment the resulting serum concentration or its effects. Serum anesthetic concentration after injection will vary inversely with the patient’s weight (2), which was not reported, and is likely to be higher if, as in this case, the anesthetic solution did not contain epinephrine (3). The combination of bupivacaine with another amide local anesthetic can also increase cardiotoxicity (4).
Bupivacaine is highly tissue bound and prolonged elevation of serum anesthetic concentrations could have cumulative toxic effects on cardiac function, leading to delayed toxicity. The earliest sign of cardiovascular derangement in this patient was hypertension, a feature typical of early local anesthetic toxicity (5). Labetalol was used to treat the hypertension, however, beta-blockade can exacerbate bupivacaine toxicity, which typically causes bradycardia and contractile depression. The final events occurred in the setting of severe acidosis, a factor that is well known to aggravate bupivacaine cardiac toxicity.
Local anesthetic toxicity should be considered in the differential diagnosis of intractable cardiac dysfunction after bupivacaine-based regional anesthesia. Reports of fatal local anesthetic cardiac toxicity are rare. This case suggests that in the presence of confounding factors or an atypical presentation, such toxicity can go unrecognized and therefore unreported. Local anesthetic cardiac toxicity (6) and its treatment (7) have recently been reviewed elsewhere.
References
Department of Anesthesia and Critical Care, University of Chicago, Chicago, IL
In Response:
We reported our case (1) because of the unexpected interaction between two commonly used medications (labetalol and metoclopramide) in the setting of a disease infrequently encountered by anesthesiologists. We considered the possibility of local anesthetic toxicity, but felt for several reasons that such toxicity would be an unlikely factor in the postoperative arrest suffered by our patient. First, the time course of the patient’s arrest relative to the administration of local anesthetic was unusual for local anesthetic toxicity. Bupivacaine levels after brachial plexus blockade generally peak 15–20 min after injection (2), whereas our patient arrested nearly 2 h after block placement. Moreover, the rising blood bupivacaine levels necessary to produce a delayed cardiotoxic effect should have also produced symptoms of central nervous system toxicity (3). None were seen in our patient. Finally, bupivacaine commonly produces nodal and ventricular arrhythmias including ventricular fibrillation (3). Our patient developed a junctional bradycardia that progressed to asystole without fibrillation.
Although we agree that beta adrenergic blockade and acidosis increase local anesthetic toxicity, we believe the literature is equivocal regarding the enhanced toxicity of local anesthetic mixtures over bupivacaine alone. Recent data suggest both enhanced (4) and diminished (5) toxicity.
We agree with Schwartz et al. that local anesthetic toxicity should be considered in any patient who receives a regional anesthetic, but believe that the time course, lack of neurological symptoms, and pattern of arrhythmia seen in our patient suggest at most a minor role for bupivacaine.
References
This article has been cited by other articles:
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  G. Weinberg and T. VadeBoncouer Drug Interaction or Drug Overdose? Supercaine Revisited Anesth. Analg., August 1, 2007; 105(2): 544 - 545. [Full Text] [PDF]
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