A young woman in her thirties presented to the emergency department with the complaint of palpitations. She was symptomatic for the past 2 hours. She had no previous cardiovascular illness. Her heart rate was 50 beats per minute, and the blood pressure was 110/70 mm Hg. Cardiovascular system examination was unremarkable. The patient denied intake of any medications; however, her husband suspected her to have consumed a poisonous substance after a dispute. The 12-lead ECG is shown in Figure 1. What is the diagnosis?

Figure 1. 12-Lead ECG at presentation.

Please turn the page to read the diagnosis.

The ECG shows sinus bradycardia, atrial ectopics, and features of digoxin therapy (digitalis effect), such as downsloping ST segment depression with upward concavity (reverse tick sign), flattened T waves, and short QT interval measuring 280 milliseconds (Figure 2). These changes are classically seen in patients receiving digoxin and do not imply toxicity. Another ECG obtained after admission showed runs of junctional rhythm and ectopic atrial rhythm (Figure 3).

Figure 2. 12-Lead ECG at presentation showing digitalis effect. There is sinus bradycardia. A prominent digitalis effect is noted in form of downsloping and concave ST segment depression (↓), flattening of T waves, and short QT interval. Two atrial ectopic beats with P wave morphology and PR interval different from the sinus beat are also present (arrowhead).

Figure 3. 12-Lead ECG during hospitalization. The ECG shows runs of junctional rhythm and ectopic atrial rhythm.

In a patient with suspected poisoning, who is not on digoxin therapy but has clinical and electrocardiographic features suggestive of digoxin toxicity or the digitalis effect on ECG, oleander poisoning should be considered. Two species of oleander exist, common oleander (Nerium oleander) and yellow oleander (Thevetia peruviana). Both contain several cardiac glycosides that are similar to digoxin in structure, function, and toxic manifestations. Oleander grows commonly in tropical countries and is used for intentional self-harm, with a reported mortality of 5% to 10%. All parts of the plant, including the leaves and stem, are poisonous, with the greatest concentration of toxins being in the kernels of the seeds.¹ Accidental poisoning has also been reported from herbal remedies containing oleander extract.

On counseling and questioning, the patient confirmed that she had consumed seeds of yellow oleander (Figure 4). She stated it is common knowledge in her village that the seeds are poisonous, and she had collected them from a local park where oleander grows. The patient was managed symptomatically and hemodynamic and ECG monitoring were performed. The serum potassium at presentation was 5.5 mEq/L. No serious or sustained arrhythmias were observed. Serum digoxin assay done subsequently was positive. ECG on the fourth day showed recovery of the changes, including the digitalis effect (Figure 5).

Figure 4. Yellow oleander.A, Flowers. B, Seeds. All parts of the plant are poisonous, with the highest concentration in the kernel of the seeds.

Figure 5. 12-Lead ECG after recovery. The ECG shows normal sinus rhythm with sinus arrhythmia. The initial ECG changes have resolved, and QT interval is normal.

Clinical manifestations of oleander poisoning are similar to digoxin toxicity and include gastrointestinal symptoms, neurological disturbances, and cardiac arrhythmias. Commonly reported arrhythmias are sinus bradycardia, sinus pauses because of sinus node arrest or exit block, ectopic atrial tachycardia, and first- and second-degree atrioventricular block.^2,3 In patients with severe toxicity, complete heart block and ventricular fibrillation refractory to direct current cardioversion can occur. Mobitz type II block, although rare in digoxin toxicity, is well reported in oleander poisoning.² Atrial fibrillation and ventricular tachycardias are less common compared with digoxin toxicity, because most patients have normal hearts.^2,3

Electrolyte disturbances are common in oleander poisoning. As the cardiac glycosides inhibit Na⁺/K⁺-ATPase, extracellular potassium concentration increases. Hyperkalemia correlates with serum cardiac glycoside levels and is a marker of serious toxicity with a poor prognosis.² Hypokalemia and hypomagnesemia potentiate cardiac toxicity and should be treated. Because of the structural similarity, conventional digoxin assays are positive and help to confirm the diagnosis; however, precise quantification of levels may not be possible. Multidose activated charcoal decreases absorption of cardiac glycosides and should be considered in patients presenting early. Antidigoxin antibody (Fab) cross-reacts with oleander glycosides and should be administered in patients with serious arrhythmias or hyperkalemia.¹ However, because these antibodies are not specific to oleander glycosides, twice the standard dose is recommended in oleander poisoning.

None.

Disclosures None.

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