Abstract: TH-PO164
A Case of Pilsicainide Hydrochloride Toxicity That Relapsed After Discontinuation of Hemodialysis
Session Information
- Drug Events Trainee Case Reports
November 07, 2019 | Location: Exhibit Hall, Walter E. Washington Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Trainee Case Report
- 1800 Pharmacology (PharmacoKinetics, -Dynamics, -Genomics)
Authors
- Yamada, Takayuki, Mount Sinai Beth Israel, New York, United States
- Wakui, Hiromichi, Yokohama City University, Yokohama, Japan
- Tamura, Kouichi, Yokohama City University, Yokohama, Japan
- Takahashi, Toshiya, Hadano Red Cross Hospital, Hadano, Kanagawa, Japan
- Miura, Takahiko, Yokohama Sakae Kyosai Hospital, Kanagawa-ken, Japan
- Takizawa, Toshikazu, Hadano Red Cross Hospital, Hadano, Kanagawa, Japan
- Burger, Alfred, Mount Sinai Beth Israel, New York, New York, United States
- Charen, Elliot M., Mount Sinai Beth Israel, New York, New York, United States
Introduction
Pilsicainide is a class I C sodium channel blocker known to be effective in treating atrial fibrillation (Afib). However, the high plasma concentration of pilsicainide can trigger ventricular tachycardia (VT) and ventricular fibrillation. We present a case of pilsicainide induced VT, which relapsed after discontinuation of hemodialysis (HD).
Case Description
An 84-year-old male with a history of hypertension, paroxysmal Afib on pilsicainide, and Parkinson’s disease developed a cough and fever three days before admission. One day prior, he became lethargic and was brought to a local hospital. A 12-lead electrocardiography (ECG) showed VT. He was transferred to our hospital due to pilsicainide toxicity. His creatinine increased to 6.2mg/dL secondary to sepsis (baseline 0.9 mg/dL). We initiated emergent HD, which narrowed the QRS instantly (Figure). We performed 3 hours of HD. Two hours after ending HD his QRS prolonged again; we resumed HD followed by direct hemoperfusion. The QRS remained narrow after the 2nd HD session. He remained hemodynamically stable and was transferred to the initial hospital. Serum pilsicainide levels were: at previous hospital 3.47 µg/mL, on admission 2.61 µg/mL, after 1st HD 2.31 µg/mL, after 2nd HD 1.1 µg/mL, and after hemoperfusion 0.76 µg/mL.
Discussion
Pilsicainide is excreted by the kidney; therefore, elimination is prolonged in patients with chronic kidney disease (CKD). The mean clearance of this drug by HD is 32 %. Interestingly, the QRS was narrow during HD even though the serum pilsicainide level was high. The volume of distribution of this medication is 1.7 L/kg in CKD patients; most of the drug is distributed in the tissue. We infer that the drug in the tissue was re-distributed after HD. In conclusion, pilsicainide should be administered cautiously to elderly patients even if the serum creatinine is normal. Serum pilsicainide level may not correlate with EKG findings.