• PDF / 170,944 Bytes
• 1 Pages / 595.245 x 841.846 pts (A4) Page_size
• 78 Downloads / 168 Views

DOWNLOAD

REPORT

---

1 S

Digoxin/flecainide Digoxin toxicity, hepatotoxicity and intrahepatic cholestasis of pregnancy : case report

A 21-year-old woman developed digoxin toxicity during treatment with digoxin for fetal supraventricular tachycardia (SVT) during pregnancy. Additionally, she developed hepatotoxicity and intrahepatic cholestasis of pregnancy (ICP) during treatment with flecainide for fetal supraventricular tachycardia (SVT) during pregnancy. The woman, who was in her 27 weeks of gestation, was transferred to a hospital in USA with fetal tachyarrhythmia ranging between 240–270 bpm. On admission, ultrasonogram and echocardiogram of the fetus at 27 weeks’ gestation showed fetal SVT, with abdominal ascites, pleural effusion and pericardial effusion indicating a clear picture of hydrops fetalis. She received IM betamethasone for fetal lung maturation, oral digoxin 0.25mg three times daily and oral flecainide 100mg twice daily. The treatment with digoxin and flecainide converted the fetus to sinus rhythm. After 1 day of the treatment, abdominal ascites reduced to 7mm, pericardial effusion diminished to 2.6mm and the pleural effusion was no longer visualised by ultrasonography. Resolution of ascites was noted by the 4th day of treatment with the pericardial effusion remaining at 3mm. After initiation of the treatment, the fetal heart rate (FHR) was assessed three times per week and non-stress testing and biophysical profile were performed two times per week. She was assessed periodically for evidence of digoxin toxicity via serum levels and maternal electrocardiography. After 5 weeks of the treatment (i.e. at 31 weeks of gestation), she was re-admitted due to chest pain later diagnosed as costochondritis. She also showed elevated liver enzymes (hepatoxicity) which was attributed to flecainide. Further hepatic testing at that time showed elevated bile acids of 327.6 µmol/L, consistent with severe intrahepatic cholestasis of pregnancy (ICP) and attributed to flecainide. Her digoxin level was found to be 2.3 ng/mL on day 4 of admission, suggestive of digoxin toxicity. Flecainide was discontinued at 31 weeks of gestation. Digoxin dose was reduced to 0.25mg two times per day which was maintained until delivery as the minimum therapeutic dose for appropriate control of SVT. Her liver enzymes normalised following the discontinuation of flecainide. However, bile acids remained elevated. She then received ursodeoxycholic acid [ursodiol] 300mg twice daily for ICP which reduced circulating bile acid levels prior to delivery [not all outcomes stated]. She underwent caesarean section at 37 weeks of gestation. The neonate showed no subsequent evidence of tachyarrhythmia or hydrops following delivery. Narayanan M, et al. Complete resolution of arrhythmia-induced hydrops fetalis in utero. BMJ Case Reports 13: No. 10, Oct 2020. Available from: URL: http:// doi.org/10.1136/bcr-2020-235827

0114-9954/20/1830-0001/$14.95 Adis © 2020 Springer Nature Switzerland AG. All rights reserved

803514963

Reactions 14 Nov 2020 No. 1830