The recent interest in the use of uncommonly used lipid suspensions in patients with profound local anaesthetic toxicity prompted me to investigate whether a more readily available lipid emulsion (2, 6-diisopropylphenol, propofol) would be an acceptable alternative. The editorial by Picard and Meek  states that ‘propofol is not a suitable alternative because to give a sufficient dose of its carrier lipid, an overdose of propofol would be necessary’, though, unfortunately, they do not support this with references. The recent report by Litz et al.  demonstrated that a bolus of 100 ml of Intralipid 20% followed by an infusion in a patient with local anaesthetic-induced asystole restored cardiac output. Other authors have suggested similar dosing regimens [3, 4]. Propofol (Diprivan®, AstraZeneca, Macclesfield, UK) is similar to Intralipid® 10% with regards to its lipid chemistry . If it is assumed that 1% Diprivan® is similar to Intralipid® 10%, then it is easy to calculate that a patient in cardiac arrest secondary to local anaesthetic toxicity, who has not responded to conventional therapy, would need a bolus dose of around 200 ml of propofol to match the amount of Intralipid®, which appears to be effective in resuscitating these patients. This equates to a bolus dose of 2000 mg, or about 30 mg.kg−1 for a 70-kg patient; the recommended induction dose using propofol is 1.5–2.5 mg.kg−1. This is a large dose of a drug whose main side-effects are vasodilation and bradycardia, but these patients will already have supra-normal levels of adrenaline, which will have been administered as part of the ALS algorithm. The rapid distribution, and subsequent metabolism and excretion of propofol suggest the side-effects should not be overly prolonged, and its anticonvulsant properties may be beneficial.
I wonder how long it will be before a case report is published which shows that propofol was used successfully in a patient with refractory cardiac arrest following local anaesthetic toxicity because Intralipid wasn't available?