Fatal Oleander Cardenolide Toxicity Presenting With Bradyarrhythmia And Hyperkalemia: A Case Report
DOI:
https://doi.org/10.64252/z8ra5y22Keywords:
Oleander poisoning, Cardiac glycoside toxicity, Atrioventricular block, Hyperkalemia, Digoxin-specific antibody fragmentsAbstract
Oleander (Nerium oleander) contains cardenolide cardiac glycosides that produce a digoxin-like toxidrome. We report a fatal ingestion presenting to a tertiary emergency department. A 54-year-old woman arrived two hours after ingesting crushed oleander leaves mixed with food. She complained of vomiting and breathlessness and was drowsy but arousable. Initial examination showed tachypnoea (34/min) with bilateral crepitations, blood pressure 100/60 mmHg, bradycardia 48/min, and oxygen saturation 97% on room air. ABG revealed pH 7.35, HCO₃⁻ 13 mmol/L, and K⁺ 5.39 mmol/L. ECG demonstrated sinus bradycardia with PR prolongation, intermittent non-conducted P waves suggestive of second-degree AV block, and frequent premature ventricular complexes. Management comprised atropine 1 mg IV (heart rate to 74/min), intravenous fluids, insulin 10 units IV, and 50 g activated charcoal via nasogastric tube. She underwent rapid-sequence intubation and was prepared for temporary pacing. Repeat ABG showed worsening acidemia and hyperkalemia (K⁺ 5.72 mmol/L); additional insulin and 100 mEq sodium bicarbonate were administered. She developed cardiac arrest, achieved ROSC after four minutes, received temporary pacing, lignocaine infusion, dual vasopressors, and CRRT, but suffered recurrent arrests and died nine hours after ingestion. The case underscores the rapid progression of oleander cardiotoxicity and the value of early ECG and potassium-guided escalation.




