Response to “Use of Lipid Emulsion in the Resuscitation of a Patient With Prolonged Cardiovascular Collapse After Overdose of Bupropion and Lamotrigine”

Abstract

We read with interest the report by Sirianni et al of the use of lipid emulsion in the resuscitation of cardiovascular collapse.1Sirianni A.J. Osterhoudt K.C. Calello D.P. et al.Use of lipid emulsion in the resuscitation of a patient with prolonged cardiovascular collapse after overdose of bupropion and lamotrigine.Ann Emerg Med. 2008; 51: 412-415Abstract Full Text Full Text PDF PubMed Scopus (224) Google Scholar However, we are concerned that readers may get the impression that the successful use of intravenous lipid emulsion in a patient with prolonged cardiac collapse from sodium channel blockade occurred only after the patient had received adequate boluses of sodium bicarbonate. In the case presented by the authors there was clear ECG evidence of sodium channel blockade (QRS 0.122 and a prominent terminal R wave in augmented ventricular lead right) in a patient that has a total of 3 cardiac arrests with a wide complex rhythm. During the first cardiac arrest, the patient appeared to respond to an intravenous bolus of sodium bicarbonate (50mEq) after a number of other options had been tried. Following return of circulation they report a QRS of 152 msec, well beyond the upper limit of normal. This would be a clear indication for further treatment with boluses of sodium bicarbonate in a poisoning suspected to be due to fast sodium channel blockade. During the second cardiac arrest it is not clear from the figure or text in the report at which point the NaHCO3 boluses were administered, particularly in relation to the administration of intralipid. It is therefore difficult to determine what contribution bicarbonate and intralipid made to the return of circulation. We are concerned that the authors attribute the return of circulation to lipid emulsion and it may in fact be due to bicarbonate therapy. Despite this, the patient receives only 150 mEq of sodium bicarbonate (2.7mEq/kg) in total and remains acidotic (pH 7.196) with a low plasma bicarbonate (12.2mEq/L). It would appear that this patient may not have received sufficient amounts of sodium bicarbonate before being administered a dose of lipid emulsion. While lipid emulsion may be familiar to intensive care unit staff, it is unlikely to be well known in the emergency department where these events are likely to occur. We would caution clinicians against the use of lipid emulsion as a first line agent in this situation and that fast sodium channel toxicity should be treated with boluses of sodium bicarbonate in a dose of 1–2 mEq per kg. In the context of cardiac arrest due to such agents, NaHCO3 should be given early and titrated toward a high normal serum pH of 7.55.2Blackman K. Brown S.G.A. Wilkes G.J. Plasma alkalinisation for tricyclics antidepressant toxicity A systemic review.Emerg Med Austral. 2001; 13: 204-210Crossref Scopus (30) Google Scholar, 3Hoffman J.R. Votey S.R. Bayer M. et al.Effect of hypertonic sodium bicarbonate in the treatment of moderate to severe cyclic antidepressant overdose.Am J Emerg Med. 1993; 11: 336-341Abstract Full Text PDF PubMed Scopus (110) Google Scholar Although most of the evidence for this treatment comes from tricyclic antidepressant overdose, it would seem reasonable to extrapolate this to other poisonings where the mechanism of toxicity also appears to be quinidine-like sodium channel blockade. Use of Lipid Emulsion in the Resuscitation of a Patient With Prolonged Cardiovascular Collapse After Overdose of Bupropion and LamotrigineAnnals of Emergency MedicineVol. 51Issue 4PreviewAnimal studies show efficacy of intravenous lipid emulsion in the treatment of severe cardiotoxicity associated with local anesthetics, clomipramine, and verapamil, possibly by trapping such lipophilic drugs in an expanded plasma lipid compartment (“lipid sink”). Recent case reports describe lipid infusion for the successful treatment of refractory cardiac arrest caused by parenteral administration of local anesthetics, but clinical evidence has been lacking for lipid’s antidotal efficacy on toxicity caused by ingested medications. Full-Text PDF In replyAnnals of Emergency MedicineVol. 51Issue 6PreviewWe are grateful to Dr. Downes et al for their correspondence, and in particular the attention they bring to the issue of optimal use of sodium bicarbonate (bicarbonate) in the treatment of toxic cardiac sodium channel blockade. Our report was not meant to suggest that intravenous lipid infusion should supplant bicarbonate as a primary treatment in most such drug overdoses, with the possible exception of parenteral local anesthetic toxicity. However, several of the questions and comments in their letter do warrant further clarification and discussion. Full-Text PDF