Paranoid Psychosis and Myoclonus: Flecainide Toxicity in Renal Failure

Abstract

Flecainide is a sodium channel blocker used mainly in the treatment of supraventricular arrhythmias. Central nervous system side effects such as dizziness, visual disturbances, headache and nausea are commonly associated with flecainide, but severe central nervous system toxicity is rare. We report the first case of flecainide toxicity in a patient with end-stage renal failure. Cessation of flecainide therapy resulted in a fall in serum flecainide levels, with associated resolution of adverse central nervous system effects. We also review the pharmacokinetics of flecainide in patients with chronic kidney disease.

Flecainide: Safety and Efficacy

“…CNS toxicity is usually mild with flecainide, but severe toxicity has been reported [3,4] similar to that reported by Ting et al [2] . However, CNS toxicity pales in comparison to the potential of life-threatening ventricular arrhythmias or conduction disturbances leading to severe bradycardia or asystole.…”

“…The study reported by Ting et al [2] in this issue of Cardiology points up another potential risk to consider in employing flecainide therapy. Flecainide is excreted in the urine, predominantly not metabolized and thus there is a potential toxicity in patients with renal dysfunction to be considered when prescribing flecainide.…”

A patient with mexiletine-related psychosis

“…Most of these side effects are dose-related and resolve with dose adjustment. Psychosis has been reported previously with quinidine2 and procainamide3 (Class IA agents), lidocaine4 (a Class IB agent), and flecainide (a Class IC agent) 5. Based on this case report, psychosis appears to be a dose-related side effect of mexiletine therapy, with a Naranjo probability score6 of 7, because the patient did not have any neuropsychiatric symptoms on a dose of 150 mg twice a day.…”

Skin biopsy–proven flecainide‐induced neuropathy

“…Our case is unique in that reversibility of pathologic changes in distal axons was demonstrated in this presumed toxic neuropathy. The mechanism of toxicity is unknown, but rare central nervous system toxicity has been observed both with normal levels8 and high levels9 of flecainide due to renal insufficiency. Flecainide is an inhibitor of voltage‐gated Kv2.1 potassium channels, which are responsible for delayed rectifier currents in dorsal root ganglion sensory neurons 10.…”