Dr. Rosenblatt and her Mount Sinai colleagues,1along with Doctor Weinberg and his companion editorial,2deserve the specialty's heartfelt gratitude for reporting a definitive treatment of the dreaded enigma of resuscitation from (racemic) bupivacaine–induced cardiotoxicity. It is a vexing problem that, heretofore, called for prolonged resuscitation at best and heroic measures up to, and including, cardiopulmonary bypass at worst. None of these measures ever could assure resumption of spontaneous heartbeat—let alone restoration of normal brain function. All of that may have become a nightmare of the past, now that the experimentally promising infusion of lipid emulsion3has borne fruit in reversing clinical cardiac asystole promptly and completely.1As the editorial2states, lipid infusion well may prove to be a watershed antidote for this fearsome local anesthetic complication.

The bone I have to pick here is the unfortunate inference that the undoubted success of lipid infusion in reversing cardiac arrest imputes its corresponding effectiveness in treating any and all local anesthetic–induced toxicity, starting with the editorial's seductive title (“… Resuscitation for Local Anesthetic Toxicity ”[italics mine]) and ending with the suggestion that lipid emulsion be stored routinely wherever peripheral nerve blocks are performed. The editorial's title, regrettably, restates the original report's misleading overgeneralization (“… Resuscitation for Local Anesthetic Toxicity ”[italics mine]). My comments are by no means intended to belittle the authors' contribution, but rather to constrain lipid infusion to its proven limits as a treatment option for racemic bupivacaine–induced cardiac asystole.

Lipid infusion well may prove to be the silver bullet for treating racemic bupivacaine–induced asystole, but it by no means has been demonstrated (as yet) to be effective in treating local anesthetic–induced cardiotoxicity in general, and even less so in treating local anesthetic cerebrotoxicity. Rather, lipid infusion has been shown to be effective only in reversing racemic bupivacaine–induced asystole.3That is to say, unintended cardiotoxicity caused by any local anesthetic other than racemic bupivacaine probably is better treated by conventional advanced cardiac life support resuscitation. Witness, for example, recent reports of conventional methods in restoring cardiac function after cardiotoxicity from closely related local anesthetics such as levobupivacaine4or ropivacaine.5More to the point yet: Lipid emulsion infusion hardly is a panacea for treating the noncardiac (and far more common) manifestations of local anesthetic toxicity such as convulsions from cerebrotoxicity. Moreover, restoration of normal sinus rhythm does not necessarily imply restoration of normal cerebral function. Quite the contrary, permanent brain damage (underreported because of court-imposed constraints) may be the all-too-common heartbreaking outcome.

To take the authors' words truly to heart, turn around their conclusion instead, and question whether racemic bupivacaine (and its lipid emulsion antidote) still warrant a place in “… areas in which peripheral nerve blocks are being performed.” Rather, one might just as well consider a moratorium on the use of bupivacaine and avoid this dreadful complication (and its unconventional treatment) altogether—using more heart-kind, equally long-lasting local anesthetics such as levobupivacaine or ropivacaine.

With safer monomeric alternatives to racemic bupivacaine (now irreverently dubbed “retro-bupivacaine”) available, hasn't the time arrived to retire this notoriously hazardous local anesthetic that by now has accumulated more than 30 yr of evidence of disproportionate cardiotoxicity? All that racemic bupivacaine has going for it, in truth, is the low price of a generic drug. No question but that drug cost is a substantial practice expense—still, patient safety always must be the overriding consideration.

In the flush of exciting news, it is all too convenient to ignore the dark side of this case report. The stark truth remains that, even in skilled hands, racemic bupivacaine is an unpredictably cardiotoxic local anesthetic that—perhaps—should be retired from practice altogether. It is a bit like promoting a surefire cure for lung cancer, rather than snuffing out cigarette smoking in the first instance, or not belting up because your car has the latest inflatable device.

University of South Carolina, Columbia, South Carolina. dejong@nuvox.net

Rosenblatt MA, Abel M, Fischer GW, Itzkovich CJ, Eisenkraft JB: Successful use of a 20% lipid emulsion to resuscitate a patient after a presumed bupivacaine-related cardiac arrest. Anesthesiology 2006; 105:217–8
Weinberg G: Lipid infusion resuscitation for local anesthetic toxicity: Proof of clinical efficacy. Anesthesiology 2006; 105:7–8
Weinberg GL, Ripper R, Murphy P, Edelman LB, Hoffman W, Strichartz G, Feinstein DL: Lipid infusion accelerates removal of bupivacaine and recovery from bupivacaine toxicity in the isolated rat heart. Reg Anesth Pain Med 2006; 31:293–303
Salomaki TE, Laurila PA, Ville J: Successful resuscitation after cardiovascular collapse following accidental intravenous infusion of levobupivacaine during general anesthesia. Anesthesiology 2005; 103:1095–6
Chazalon P, Tourtier JP, Villevielle T, Giraud D, Saïssy JM, Mion G, Benhamou D: Ropivacaine-induced cardiac arrest after peripheral nerve block: Successful resuscitation. Anesthesiology 2003; 99:1449–51