Review of management in cardiotoxic overdose and efficacy of delayed intralipid use

Abstract

We present the case of a 51-year-old woman admitted to our intensive care unit following an intentional overdose of a calcium channel antagonist and a beta blocker. The resultant hypotension was reversed with glucagon, noradrenaline, calcium and high-dose insulin. Despite these interventions, she remained vasoplegic and received a delayed, standard dose of intralipid. Subsequently, the vasoplegia resolved rapidly, and the vasopressor was stopped. Here, we review the management of overdose of calcium channel and beta-adrenergic receptor blockers, concentrating on the pharmacology of lipid emulsion therapy. There remain some unanswered questions about lipid emulsion therapy: treatment with lipid therapy is usually advocated as soon as possible; this case report suggests that it remains efficacious even if its administration were delayed.

Keywords: Calcium channel blocker; beta-adrenergic blocker; insulin; lipid emulsion; toxicity.

Figure 1.

Proposed mechanisms of action of LE. LE may repartition drug (A): lipophilic substances are drawn into ‘lipid sink’; a concentration gradient develops between tissue and blood, and the toxic drug moves from tissue into aqueous phase into lipid phase. LE may affect sodium channel function (B), or calcium channel function or flux (C), with an increase in intracellular calcium and inotropy (D). Alternatively, LE may revert the cell to fatty acid metabolism or provide FA substrate (E), which may increase inotropy or reverse vasodilatation. LE may provide cytoprotection or stimulate repair after ischaemic injury (F).