Cardiac glycoside poisoning following suicidal ingestion of Cerbera manghas

Cardiac glycoside poisoning following suicidal ingestion of Cerbera manghas

To the Editor:

Many plants, such as woolly foxglove (Digitalis lanata), common oleander (Nerium oleander), yellow oleander (Thevetia peruviana), and ouabain (Strophanthus gratus) contain cardiac glycosides (1,2). We recently managed a man who presented with digoxin-like toxicity after intentional ingestion of the seeds of Cerbera manghas (sea-mango). Although sea-mango is known to contain cardiac glycosides (1–3), poisonings by Cerbera manghas and related plants are rarely reported in English medical literature.

A 50-year-old man experienced numbness of the face, throat, and upper extremities after ingesting three seeds of Cerbera manghas in a suicidal attempt. Nausea and vomiting ensued one hour later, followed by light-headedness, chest tightness, palpitation, and dyspnea. He presented to the emergency department two hours post-ingestion.

On arrival, his heart rate was 90 beats/minute and blood pressure was 142/72 mmHg. Examination ten minutes later revealed a slow, regular heart rate of 22 beats/minute which was documented to be complete atrioventricular block (Fig. 1). Other physical examination and routine laboratory data were unremarkable except serum potassium of 5.4 mmol/L; serum digoxin concentration was 1.03 ng/ml.

Fig. 1.

The patient was placed on oxygen, intravenous fluids, and other supportive measures. Atropine and temporary pacing were not given because his hemodynamic status was stable despite the presence of bradycardia with a heart rate ranging between 30 and 50 beats/minute. Twenty hours post-ingestion, his blood pressure was 132/76 mmHg and a follow-up electrocardiogram revealed first-degree atrioventricular block with non-specific ST-T change at a rate of 30 beats/minute. Serum potassium level was 5.9 mmol/L and serum digoxin concentration was 0.65 ng/ml. Because of increasing serum potassium level, treatment with glucose, insulin, sodium bicarbonate, and calcium gluconate was commenced. Single-lead rhythm strip showed sinus bradycardia after the above treatment.

Twenty-six hours post-ingestion, his clinical condition remained stable, yet serum potassium level increased to 6.5 mmol/L. Glucose, insulin, sodium bicarbonate, and sodium polystyrene sulfonate were administered, which ameliorated both hyperkalemia and the clinical manifestations. Repeat electrocardiogram showed normal sinus rhythm at a rate of 60 beats/minute. Serum digoxin concentration was undetectable on day four and the patient was discharged without sequellae.

Cerbera manghas is an evergreen tree with a mango-like fruit. It belongs to the Apocynaceae family, which also includes the yellow and common oleanders (4). Cerbera manghas and other plants in the Cerbera genus are distributed throughout the world's tropical coasts: South East Asia, India, Sri Lanka, Australia, and Madgascar (1,4,5). The plant's kernel is the most toxic part and is attributable to various cardiac glycosides, with cerberin being the major component (5). Toxic manifestations of Cerbera manghas and related species are similar to cardiac glycosides found in other plants or cardiac genins in toad venom (1–4,6). Cerbera odollam (sometimes misclassified as Cerbera manghas) and Cerbera venenifera have been implicated in many fatalities in certain parts of South Asia and Madagascar (3,4). No definitive case reports of Cerbera manghas poisonings have been published.

The diagnosis of Cerbera manghas poisoning can be made by the exposure history and digoxin-like clinical manifestations. A positive digoxin level by fluorescence polarization immunoassay, as seen in our patient, further supports the diagnosis. Both plant cardiac glycosides and toad venom can cross-react with various digoxin immunoassays (1,6,7). The magnitude of cross-reactivity, however, is unknown. Moreover, there is no correlation between serum digoxin levels and cardiac glycoside concentrations or clinical toxicity (6).

Management of patients with Cerbera manghas toxicity is similar to that in patients with digoxin poisoning, and includes gastric decontamination and supportive treatments such as atropine, cardiac pacing, and antiarrhythmic agents. Life-threatening hyperkalemia is treated by intravenous glucose, insulin, and sodium bicarbonate and oral use of potassium-binding resins.

Calcium salts are generally avoided because it is widely believed that calcium administration may enhance myocardial calcium load and ultimately lead to arrhythmia or cardiac arrest. Hyperkalemia in our patient was initially treated with calcium gluconate and the patient did not develop any arrhythmia. Although we agree that calcium salts should better be avoided in digoxin or similar poisonings, the dangers of calcium therapy might have been overstated (8,9).

Digoxin-specific Fab fragments are generally considered the first-line therapy for patients with severe digoxin toxicities (3,10). For plant cardiac glycoside or toad venom poisonings, the antidote has also been shown to be effective in treating severe cardiac dysrhythmias and hyperkalemia (3,6). Although our patient did not receive antidotal therapy, he may have had a smoother hospital course had he received the antidote.