Dear Editor,
I read the article titled ‘Renal failure, shock, and loss of pacemaker capture: A case of flecainide intoxication’ recently published in The Netherlands Journal of Medicine.1 Lipid emulsions have been widely used to treat systemic toxicity caused by local anaesthetics or other drugs with high lipid solubility.2 Flecainide, an antiarrhythmic drug with a high lipid solubility (Log [octanol/water partition coefficient]: [3.78]) and cardiac sodium channel blocking activity similar to the local anaesthetic bupivacaine (Log [octanol/water partition coefficient]: 3.41), is used for the treatment of atrial fibrillation and supraventricular tachycardia.3 Heldens et al. suggest lipid sink as an underlying mechanism for lipid emulsion-induced recovery from cardiogenic shock due to flecainide intoxication.1 However, other possible mechanisms should also be considered. First, scavenging effect is another recently widely accepted mechanism, in which the lipid phase of a lipid emulsion absorbs lipid-soluble drugs such as bupivacaine from vital organs such as the heart.2 These highly lipid-soluble drugs are then transported into adipose tissue and muscle for storage and to the liver for detoxification.2 Second, Intralipid® attenuates the blockade of cardiac sodium channels induced by bupivacaine.4 This may result in lipid emulsion-mediated reversal of sodium channel blockade by a toxic dose of flecainide and may contribute to recovery from flecainide intoxication. Third, flecainide has a negative inotropic effect, whereas lipid emulsion itself produces a positive inotropic effect.3,5 Thus, I believe that lipid emulsion treatment described in this case may be effective against flecainide intoxicationinduced cardiogenic shock refractory to standard treatment.
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