Yellow Oleander Poisoning
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Direct answer
Yellow oleander poisoning is toxicity from Thevetia peruviana, a plant whose cardiac glycosides act on the myocardium much as digoxin does. It is common in South India, and ingestion of the seed kernel is often deliberate self-poisoning. The toxicity causes bradyarrhythmias, heart block and hyperkalaemia, and treatment combines atropine and digoxin-specific Fab antibodies with early activated charcoal.
What you must remember
- Source: Thevetia peruviana, the yellow oleander, is a widely grown ornamental shrub, and its seed kernel is the most toxic part.
- Mechanism: the glycosides inhibit the Na+/K+-ATPase pump, raising intracellular sodium and calcium, as digoxin does.
- Arrhythmias: bradycardia, atrioventricular block and ventricular ectopics or tachycardia are the main cardiac features.
- Hyperkalaemia: a marker of severe toxicity that carries a poor prognosis, and it results from the pump blockade.
- Digoxin Fab: antibody fragments that bind the glycosides, used for life-threatening arrhythmia or severe hyperkalaemia.
- Activated charcoal: given early, when the patient is alert and the airway is protected, to bind glycosides in the gut.
- Atropine: the first drug for symptomatic bradycardia, with temporary pacing if atropine fails.
- Assay caution: glycosides may cross-react with digoxin immunoassays, so a level can mislead.
Managing the ingestion step by step
Yellow oleander poisoning is managed as a glycoside toxicity from the moment of presentation, because arrhythmias can be fatal before the diagnosis is confirmed by history. The steps below follow the usual order of care.
- Monitor the heart. Continuous ECG monitoring looks for bradycardia, heart block and ventricular ectopy from the outset.
- Check potassium early. Serum potassium is measured and repeated, because hyperkalaemia signals severe toxicity.
- Decontaminate the gut. Activated charcoal is given early, and gastric decontamination has a limited role once the ingestion is remote. The quantity and timing of the ingestion guide that decision.
- Treat the bradycardia. Atropine is given for symptomatic bradycardia, and temporary pacing is considered if it fails.
- Give digoxin Fab. Specific antibody fragments are given for life-threatening arrhythmia or severe hyperkalaemia.
- Correct and monitor. Hyperkalaemia is treated by other measures, intravenous calcium is traditionally avoided, and the patient is monitored for a prolonged period.
Where the exam tries to catch you
Examiners test whether you recognise glycoside toxicity and avoid the reflex treatments that worsen it.
- Trap: giving intravenous calcium for hyperkalaemia in glycoside poisoning Correct: calcium can precipitate arrhythmias in digitalis toxicity, so it is traditionally avoided.
- Trap: trusting a normal digoxin level to rule out yellow oleander toxicity Correct: immunoassays may cross-react, so the ECG and potassium guide the decision.
- Trap: confusing the yellow variety with pink oleander Correct: both contain cardiac glycosides, but Thevetia is the yellow plant common in South India.
Frequently asked questions
Which plant causes yellow oleander poisoning and where is it common?
Yellow oleander poisoning is caused by Thevetia peruviana, a shrub widely grown as an ornamental plant and common across South India. Its seed kernel is the most toxic part, and ingestion is often deliberate.
What are the cardiac features of yellow oleander poisoning?
Yellow oleander poisoning causes bradycardia, atrioventricular block and ventricular arrhythmias, all due to inhibition of the Na+/K+-ATPase pump. Hyperkalaemia usually accompanies severe toxicity and signals a poor prognosis.
When is digoxin Fab used in yellow oleander poisoning?
Digoxin Fab antibody fragments are used in yellow oleander poisoning for life-threatening arrhythmia, severe hyperkalaemia or haemodynamic compromise. They bind the glycosides in the circulation and are given intravenously.
Why is activated charcoal given after yellow oleander ingestion?
Activated charcoal is given early after yellow oleander ingestion to bind glycosides in the gut before they are absorbed. It is useful only when the patient is alert and the airway is protected, and it does not replace specific treatment for arrhythmia.
Why must intravenous calcium be avoided in glycoside poisoning?
Intravenous calcium is traditionally avoided in glycoside poisoning because it can worsen arrhythmias in digitalis toxicity, particularly when hyperkalaemia is present. Hyperkalaemia is instead managed with other measures chosen for the individual patient.