A Case of Flecainide‐Induced Hyponatremia

Abstract

We present a case of flecainide-induced hyponatremia in a 67-year-old woman who was treated for paroxysmal atrial tachycardia. She developed dizziness after starting flecainide and was found to be hyponatremic with a sodium level of 122 mmol/L (decreased from 136 mmol/L). Work-up failed to reveal other causes of hyponatremia. She was not on diuretics, laxatives, or herbal medications. After discontinuation of flecainide, her symptoms and sodium levels improved. Hyponatremia is a previously unrecognized entity as an adverse effect of flecainide. We will discuss the clinical presentation, lab findings, and a possible explanation for this patient's unusual reaction to flecainide.

A Possible Mechanism for Flecainide Induced Dizziness

“…Although we cannot prove that Flecainide was the cause of BVP, the works previously written on the EAR of this drug, the current knowledge of Amiodarone as cause of BVP, and the context in which the patient presented the symptoms led us to believe that it was probably the cause. Moreover, we are also aware that dizziness might be explained by more than one single mechanism, such as hyponatremia or a heart rhythm disturbance (36,37). Despite the fact that the patient followed a typical starting and maintenance dose (50 and 100 mg twice a day), the presence of dizziness and visual disturbance have been previously described within this range (21,24).…”

A case of flecainide-induced hyponatremia

“…[ 11 ] The sodium channels are also localized in the distal colon and in the renal tubules, suggesting antagonism of flecainide either in the distal nephron and cortical collecting duct or in the colon epithelial sodium channels, inhibiting sodium absorption and chloride secretion. [ 12 ] The current literature on the pharmacodynamics of flecainide does not establish a common pathway of the drug on the sodium channels at different sites, which is a probable cause for drug-induced hyponatremia.…”

A case of electrolyte disturbances leading to flecainide toxicity at normal serum levels and pacemaker malfunction

“…With flecainide also blocking sodium channels on the distal nephron and cortical collecting duct, sodium would not be reabsorbed and thus further potentiate flecainide's effects on the myocardium. 6 The concurrent use of a thiazide diuretic may have further augmented this outcome. In the myocardium, the hyponatremia, possibly augmented through effects on the nephron-as in the case of our patient-may have led to further sodium channel capacitance and blockade, leading to exacerbated effects of flecainide even at therapeutic serum levels.…”

“…5 There is sparse literature describing precipitating events for flecainide toxicity. 6,7 We report a case with hyponatremia as a precipitating event for flecainide toxicity manifest by severe bradycardia with normal flecainide serum levels in a patient with a pacemaker.…”