Clinical experience with titrating doses of digoxin antibodies in acute digoxin poisoning. (ATOM-6).

Betty S Chan, Geoffrey K Isbister, Angela Chiew, Katherine Isoardi, Nicholas A Buckley

Journal: Clinical toxicology (Philadelphia, Pa.) 2022;60(4):433-439

PMID: 34424803

Abstract

INTRODUCTION

For acute digoxin poisoning, it has been recommended to give bolus doses of 10-20 vials or potentially larger than needed doses calculated from dose ingested or the measured concentration. However, a recent revision of internal Poisons Information Centre guidelines prompted a change of our recommendations, specifically instead of large boluses, to use titrating repeated low doses of digoxin antibodies(Digoxin-Fab) based on bedside assessment of cardiac toxicity.

METHODS

This is a prospective observational study of patients with acute digoxin poisoning identified through two Poisons Information Centres and three toxicology units. Patient demographics, signs and symptoms of digoxin toxicity, doses and response to Digoxin-Fab, free and bound serum digoxin concentrations. Outcomes were recorded and analysed.

RESULTS

From September 2013 to September 2020, 23 patients with 25 presentations (median age 56 years, females 56%) were recruited. Median dose ingested was 13 mg(IQR: 9.5-25). Median heart rate (HR) was 41 beats/min before treatment. Initial median digoxin and potassium concentrations were 14.5 nmol/L (IQR: 10.9-20) [11.2 µg/L(IQR: 8.4-15.4)] and 5 mmol/L (IQR: 4.5-5.4 mmol/L), respectively. Gastrointestinal symptoms and acute kidney injury were present in 22 patients (88%) and 5 patients (20%), respectively. Four patients received an initial bolus dose of Digoxin-Fab of 5-20 vials. Twenty-one patients received repeated titrated doses (1-2 vials) of Digoxin-Fab and the median total dose was 4 vials (IQR: 2-7.5). Median maximal change in HR post-Digoxin-Fab was 19 beats/min. The median potassium concentration decrease post-Digoxin-Fab was 0.3 mmol/L. Total dose used in the titration group was 25% and 35% of the predicted doses based on the amount of digoxin ingested or measured serum concentration, respectively. Twelve had free digoxin concentrations measured. Free digoxin concentrations dropped to almost zero after any dose of Digoxin-Fab. Ten patients had a rebound of digoxin >2.6 nmol/L (2 µg/L). There were no deaths from acute digoxin toxicity.

CONCLUSIONS

The new practice of using small, titrated doses of Digoxin-Fab led to a considerable reduction in total usage and major savings. The clinical response to titrated doses was safe and acceptable in acute digoxin poisoning.

Address: Clinical Toxicology Unit & Emergency Department, Prince of Wales Hospital, Sydney, New South Wales, Australia.; New South Wales Poisons Information Centre, Sydney, Australia.; Clinical Toxicology Research Group, University of Newcastle, Newcastle, Australia.; Department of Clinical Toxicology, Calvary Mater Newcastle, Newcastle, Australia.; Clinical Toxicology Unit, Princess Alexandra Hospital, Brisbane, Australia.; Queensland Poisons Information Centre, Brisbane, Australia.; Faculty of Medicine and Health, University of Sydney, Sydney, Australia.

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