Acute yellow oleander (Thevetia peruviana) poisoning: cardiac arrhythmias, electrolyte disturbances, and serum cardiac glycoside concentrations on presentation to hospital

Abstract

Objective: To describe the cardiac arrhythmias, electrolyte disturbances, and serum cardiac glycoside levels seen in patients presenting to hospital with acute yellow oleander (Thevetia peruviana) poisoning and to compare these with published reports of digitalis poisoning.

Design: Case series.

Setting: Medical wards of Anuradhapura District General Hospital, Sri Lanka, and coronary care unit of the Institute of Cardiology, National Hospital of Sri Lanka, Colombo, the national tertiary referral centre for cardiology.

Patients: 351 patients with a history of oleander ingestion.

Measurements: ECG and blood sample analysis on admission.

Results: Most symptomatic patients had conduction defects affecting the sinus node, the atrioventricular (AV) node, or both. Patients showing cardiac arrhythmias that required transfer for specialised management had significantly higher mean serum cardiac glycoside and potassium but not magnesium concentrations. Although there was considerable overlap between groups, those with conduction defects affecting both sinus and AV nodes had significantly higher mean serum cardiac glycoside levels.

Conclusions: Most of these young previously healthy patients had conduction defects affecting the sinus or AV nodes. Relatively few had the atrial or ventricular tachyarrhythmias or ventricular ectopic beats that are typical of digoxin poisoning. Serious yellow oleander induced arrhythmias were associated with higher serum cardiac glycoside concentrations and hyperkalaemia but not with disturbances of magnesium.

Figure 1

Serum concentrations of cardiac glycosides, potassium, and magnesium in patients admitted to Anuradhapura General Hospital who were then either transferred to Colombo or discharged without specific treatment. There was a great deal of overlap between the two groups, particularly with potassium and magnesium, which suggests that neither of these electrolytes will be good early markers of toxicity. The patient with a potassium of 10.8 mmol/l was rapidly transferred but died en route to Colombo.

Figure 2

Relation of serum potassium and magnesium concentrations to serum cardiac glycoside concentration in the serum of patients with normal ECGs or relatively severe cardiotoxicity.

Figure 3

Relation between serum cardiac glycoside concentration and (A) potassium concentration and (B) magnesium concentration in relation to cardiac abnormality on presentation to Colombo coronary care unit.