A 19-year-old female with a history of Atrial Septal Defect (ASD) repaired in 2015 was placed on Flecainide 50mg bid for atrial tachycardia. After 4 months of uneventful therapy, she presented with nausea, dizziness, and chest discomfort. She was significantly hypotensive and tachycardic and was emergently intubated. EKG demonstrated a wide complex tachycardia with a prolonged QRS of 146 ms and QTc of 562ms (Fig 1). Echocardiogram revealed global hypokinesis with an EF of 25%. Flecainide toxicity was suspected and labs were drawn. She was started on infusions of sodium bicarbonate, hypertonic (3%) saline, lipid emulsion and albumin. Arterial access was obtained for possible Extra Corporeal Membrane Oxygenation (ECMO) to treat cardiogenic shock. However, within 6 hours of intravenous therapy, her blood pressure improved and her QRS and QT interval narrowed on her EKG. A repeat echocardiogram demonstrated a normalized EF of 50%. Flecainide level resulted at 3.53 mcg/mL (0.2-1.0mcg/mL). The patient made a complete recovery and ECMO was never utilized.
Discussion:
Flecainide acetate is a Class Ic antiarrhythmic used for management of both supraventricular and ventricular arrhythmias. It causes rate-dependent slowing of rapid sodium channels slowing phase 0 of depolarization and in high doses inhibits the slow calcium channels. Flecainide overdose is rare and has a high mortality of 22% compared to mortality of 1% with other drug overdoses. Flecainide intoxication leads to arrhythmias, myocardial depression and conduction defects. It manifests as a 50% increase in QRS duration or 30% prolongation in PR interval. There is no specific antidote to treat flecainide intoxication. Treatment includes increasing the excretion of flecainide, with symptomatic support, and administration of sodium bicarbonate in severe cases, which reverses the effect of sodium channel blockade. Intravenous fat emulsion is a novel adjunctive therapy in patients with flecainide toxicity. Its mechanism of action is not fully understood, though creation of lipid sink for the lipid soluble drugs is considered to be the predominant effect.
Conclusions:
Flecainide intoxication is a rare cause of drug overdose and is frequently fatal. This case highlights the importance of early recognition, treatment of life threatening flecainide intoxication and subsequent dramatic improvement with intravenous hypertonic saline, sodium bicarbonate and lipid emulsion.