Cardiac rhythms and yellow petals: A rare case report on yellow oleander poisoning presenting with hypomagnaesemia

INTRODUCTION

Yellow oleander (Thevetia peruviana), also known as ‘pila kaner’ in some regions, is an ornamental plant belonging to the Apocynaceae family.^[1] It is widely cultivated in Indian gardens and subtropical regions due to its evergreen nature and attractive bell-shaped yellow flowers^[1] [Figure 1]. Despite its aesthetic appeal, all parts of the plant are poisonous, containing cardiac glycosides that can cause severe toxicity when ingested.^[1]

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Figure 1:

Yellow oleander (a) flower and (b) seeds.

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The main active toxic glycosides in yellow oleander are thevetin B, cerberin, nerifolin, thevetin A, ruvoside and peruvoside.^[1] The lethal dose is 8–10 seeds or 15–20 g of root.^[1] These compounds have a mechanism of action similar to digoxin, inhibiting the Na+/K+-ATPase pump in cardiac myocytes. This inhibition leads to increased intracellular calcium, resulting in positive inotropic effects and potential cardiac arrhythmias.^[2]

Oleander poisoning is often due to accidental ingestion or deliberate consumption with suicidal intent. The clinical presentation can vary from mild gastrointestinal symptoms to life-threatening cardiac arrhythmias, making early recognition and appropriate management crucial.^[1]

CASE REPORT

A 29-year-old female presented to our hospital with complaints of nausea, persistent vomiting, chest burning sensation, restlessness and lightheadedness. These symptoms began approximately 15 h after the deliberate consumption of three yellow oleander seeds. On examination, the patient was drowsy but arousable and oriented to time, place and person. Her vital signs showed bradycardia with a pulse of 40 beats/min, blood pressure of 130/80 mmHg, respiratory rate of 18 breaths/min and oxygen saturation of 97% on room air. The patient’s pupils were bilaterally equal, mid-dilated and reactive to light. Cardiovascular examination revealed normal heart sounds without murmurs, and respiratory examination showed bilateral equal air entry with no added sounds. The abdomen was soft and non-tender, with no palpable organomegaly.

Initial investigations revealed normal haemoglobin (12.6 g/dL), total leucocyte count (6,300/mm³) and platelet count (249,000/mm³). Serum electrolytes showed hypomagnaesemia (1.2 mEq/L), while other electrolytes were within normal limits. Renal function tests were normal. Serum digoxin levels could not be obtained due to financial constraints. The initial electrocardiogram (ECG) showed sinus bradycardia with signs of digitoxin toxicity, including a characteristic ‘reverse tick’ sign [Figure 2]. During the first 24 h of admission, the ECG rhythm alternated between sinus bradycardia and first-degree heart block, necessitating continuous cardiac monitoring.

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Figure 2:

Electrocardiogram showing sinus bradycardia and ‘reverse tick’ sign.

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Upon admission to the cardiac care unit (CCU), the patient underwent immediate gastric lavage. This was followed by the administration of activated charcoal to adsorb any toxins still present in the gastrointestinal tract. Intravenous fluid therapy was initiated to maintain hydration and support cardiovascular function. The patient’s electrolytes, particularly potassium, sodium and magnesium, were closely monitored and corrected as needed. The initial hypomagnaesemia was addressed with magnesium supplementation.

Continuous ECG monitoring was employed throughout the patient’s stay in the CCU. Symptomatic treatment was provided for nausea and vomiting, and the patient was closely observed for any sign of deterioration or development of life-threatening arrhythmias. Digoxin-specific antibody fragments (Fab) were not administered due to unavailability at our institute.

The patient’s clinical course showed gradual improvement. By day 2, sinus rhythm was restored, and the patient became symptomatically better and haemodynamically stable. Overnight urine output was adequate at 600 mL. On days 3–4, the patient remained under close observation, with no recurrence of symptoms or cardiac arrhythmias. Magnesium levels rose to 1.9 meq/L. On day 5, after a thorough psychiatric evaluation and counselling, the patient was deemed fit for discharge. Follow-up appointments were scheduled with both cardiology and psychiatry departments to ensure comprehensive care and monitoring. The progression of laboratory values over the course of hospitalisation is presented in Table 1.

DISCUSSION

Yellow oleander poisoning represents a significant health concern, particularly in regions where the plant is commonly found in gardens and public spaces. The case presented here illustrates several key aspects of oleander toxicity and its management, while also highlighting the challenges faced in resource-limited settings.

The patient’s symptoms were consistent with the typical presentation of cardiac glycoside toxicity. Gastrointestinal symptoms, including nausea and vomiting, are often the first to appear and were prominent in this case.^[1,3] The cardiovascular effects, manifested as bradycardia and ECG changes, reflect the impact of cardenolides on cardiac conduction and contractility.^[2]

It is noteworthy that the patient developed symptoms approximately 15 h after ingestion. This delayed onset is common in oleander poisoning and underscores the importance of prolonged observation, even in seemingly mild cases.^[4] The variability in symptom onset can be attributed to factors such as the amount ingested, the part of the plant consumed and individual patient characteristics.^[1,5]

The diagnosis of oleander poisoning in this case was primarily clinical, based on the patient’s history of oleander seed ingestion and the characteristic symptoms and ECG findings. While serum digoxin levels can be used as a surrogate marker for oleander poisoning, they were not obtained in this case due to financial constraints. This highlights a common challenge in resource-limited settings.

The ECG changes, particularly the sinus bradycardia and the ‘reverse tick’ sign, are hallmarks of cardiac glycoside toxicity.^[1,2] These findings, combined with the patient’s symptoms and history, were sufficient for diagnosis and guided management decisions. The dynamic nature of the ECG changes, with alternating sinus bradycardia and first-degree heart block, emphasises the need for continuous cardiac monitoring in these cases.

The management of this case followed the principles of supportive care for cardiac glycoside poisoning. The approach taken demonstrates that careful monitoring and supportive care can be sufficient for managing some cases of oleander poisoning, particularly when presentation is prompt and symptoms are not severe.

Gastrointestinal decontamination with gastric lavage and activated charcoal is a standard approach in poisoning cases. However, its efficacy in oleander poisoning may be limited if performed more than 1–2 h after ingestion.^[6] In this case, despite the delay in presentation, these measures were still implemented as a precaution. While the benefit may have been minimal given the time elapsed since ingestion, this approach is often taken in clinical practice when dealing with potentially life-threatening ingestions.

Electrolyte management, particularly the correction of hypomagnaesemia, played a vital role in the patient’s care. Magnesium has been shown to have a protective effect against cardiac arrhythmias in the context of digitalis toxicity.^[5,7] The close monitoring and correction of electrolytes, especially magnesium, likely contributed to the patient’s favourable outcome.

Hypomagnaesemia, as observed in this case, is an important finding that warrants further discussion. Magnesium is a crucial electrolyte involved in numerous physiological processes, including cardiac function. It plays a vital role in maintaining normal cardiac rhythm and is essential for the proper functioning of the Na+/K+-ATPase pump.^[7] In the context of cardiac glycoside toxicity, hypomagnaesemia can exacerbate arrhythmias and increase the risk of digitalis-induced toxicity.^[7]

The causes of hypomagnaesemia in this case could be multifactorial. Vomiting, a common symptom in oleander poisoning, can lead to magnesium loss. In addition, the cardiotoxic effects of oleander glycosides may have influenced magnesium homeostasis. The correction of hypomagnaesemia in this patient may have contributed to the stabilisation of cardiac rhythm and overall improvement in clinical status.^[7]

The decision not to administer digoxin-specific antibody fragments, despite their established efficacy in severe cases, was based on the patient’s stable condition and resource limitations. This approach is common in settings where Fab fragments are unavailable or prohibitively expensive. However, it is important to note that in more severe cases or in settings where Fab fragments are readily available, their use could be life-saving.^[8]

CONCLUSION

This case highlights the ongoing public health challenge posed by oleander plants. Despite their toxicity, these plants remain popular in many regions due to their ornamental value. Public education about the dangers of oleander ingestion and proper steps to take in case of accidental exposure is crucial for prevention and early intervention. The role of hypomagnaesemia in exacerbating cardiac arrhythmias and the potential benefit of magnesium supplementation in such cases warrant further investigation.

Studies on the long-term cardiac effects of non-fatal oleander poisoning would be valuable for guiding follow-up care and prognosis. This case report describes the successful management of acute yellow oleander poisoning in a young adult using supportive care and close monitoring. It highlights the importance of recognising the clinical features of cardiac glycoside toxicity, even in resource-limited settings where advanced diagnostic and therapeutic options may not be readily available.