細胞科学と治療のジャーナル
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概要

The Case of Flecainide Toxicity: What to Look For and How to Treat

Joshua Newson, Bradford L Walters and Brett R Todd

Introduction: Flecainide is a class Ic antiarrhythmic agent used to prevent and treat both ventricular and supraventricular tachycardias including atrial fibrillation, AV nodal re-entrant tachycardia (AVNRT), and Wolff- Parkinson-White syndrome (WPW). Flecainide can cause serious side effects include cardiac arrest, arrhythmias, and heart failure. Despite its growing use, the presenting signs and symptoms of flecainide toxicity are not familiar to most clinicians.

Case description: This was a 58 year-old female who presented from her skilled nursing facility due to hypoxia and altered mental status. Past medical history was notable for paroxysmal atrial fibrillation for which she was on flecainide. At the nursing facility the patient was noted to be obtunded, whereas at baseline she was reportedly alert and oriented. On presentation to the Emergency Department EKG demonstrated wide-complex tachycardia. Subsequent lab results were notable for hypokalemia and an acute kidney injury (AKI). A repeat EKG was concerning for ischemia in leads II, III, aVF and cardiology was emergently consulted. They noted the EKG changes were consistent with flecainide toxicity, specifically a prolonged PR interval and QRS. She was eventually admitted to the medical intensive care unit. Her wide complex tachycardia on admission was ultimately attributed to flecainide toxicity in setting of AKI. Six days after presentation, it was found that her flecainide level was in the toxic range at 2.02 ug/mL (normal range: 0.20-1.00 ug/mL, toxic>1.50 ug/mL).

Discussion: Flecainide intoxication is rare but serious due to the potential for cardiogenic shock. Its diagnosis can be difficult as the flecainide serum level may take days to result and there are no pathognomonic clinical signs. This case demonstrates the necessity of keeping flecainide toxicity on the physician’s differential for patients who are taking the drug, as well as what ECG and laboratory findings can suggest it as the etiology. A heightened suspicion is warranted in the patient with new renal impairment. Treatment can be lifesaving if initiated promptly.