Thevetia peruviana (yellow oleander) is an ornamental shrub found in tropical and subtropical regions, including tropical America. All parts of the plant are toxic due to cardiac glycosides, which can cause severe cardiotoxicity and arrhythmias. Poisoning is associated with significant mortality, often due to deliberate self-harm. This report describes a case of accidental ingestion of Thevetia peruviana seeds by a patient who believed that they could treat benign prostatic hyperplasia (BPH). The patient presented to the emergency department within 30 minutes of ingesting yellow oleander seeds with nausea, vomiting, and abdominal cramps. Although initial vital signs were stable, he developed sinus bradycardia and symptoms of cardiac glycoside toxicity, including dizziness, tachypnea, and visual disturbances. Lab results later showed a serum digoxin level of 4.04 ng/mL, and the poison control center recommended digoxin immune fab (DigiFab). He received a total of 15 vials intravenously, resulting in marked clinical improvement. He was monitored on continuous telemetry in the cardiac unit and discharged in stable condition after four days. Although DigiFab is not approved by the U.S. Food and Drug Administration for oleander poisoning, it remains the most effective reported antidote, and timely administration is crucial for successful management. Given the limited reports of oleander toxicity in the United States, this case highlights the risks of unregulated herbal remedies and the clinical presentation and management of oleander toxicity, underscoring the need for public education about oleander toxicity and the dangers of unregulated herbal remedies.

Digoxin, a cardiac glycoside and sodium-potassium adenosine triphosphatase inhibitor, has a narrow therapeutic index and is primarily prescribed for conditions such as systolic heart failure and atrial fibrillation. This narrow window increases the risk of toxicity, especially among susceptible populations. Although digoxin use has declined in recent decades and cases of toxicity have become less frequent, clinicians must remain vigilant, particularly with geriatric patients, who are more susceptible due to polypharmacy and reduced renal function. Here, we present a case of a 77-year-old woman with dementia who exhibited elevated digoxin levels and was successfully treated with digoxin immune Fab. While the use of immune Fab in chronic toxicity cases remains uncertain, our retrospective review of similar cases, managed both with and without immune Fab, provides insights into its role and limitations. We further underscore the importance of regular digoxin monitoring rather than checking the levels only during toxic episodes, as consistent monitoring can prevent fatal cases and reduce overall mortality.

Yellow oleander contains digoxin-like cardiac glycosides that frequently cause intoxications in Sri Lanka and India. To date, though, no exposure has been analytically confirmed and quantitative determination of the plant specific glycosides in human biological fluids was never performed. We report an unusual case of self-poisoning in a young female in Italy who ingested 9 crushed seeds of Cascabela thevetia and was admitted to the emergency room with a 2nd degree atrio-ventricular block at the ECG. The case was managed with activated charcoal, repeated doses of anti-digoxin immune Fab and supportive care. A transient thrombocytopenia developed and resolved within a few days. Ultra-high performance liquid chromatography coupled with tandem mass spectrometry was used for the determination and quantification of thevetin A, thevetin B and peruvoside in plasma and urine. Thevetin A and thevetin B, two of the primary glycosides in the seeds, were not present in any of the samples, while detectable levels of the metabolite peruvoside were found in all biological samples on day 1 and 3. Digitoxigenin, the aglycone of thevetin B, was also identified using a semi-untargeted analysis. This is the first report of a quantitative determination of cardiac glycosides of yellow oleander in blood and urine. The finding may support very early administration of activated charcoal to possibly prevent further formation of secondary, and possibly more potent, glycosides and limit toxicity.

Acute digoxin poisoning is increasingly uncommon in emergency medicine. Furthermore, controversy exists regarding indications for antidotal digoxin immune fab in acute poisoning. In healthy adults, the fab prescribing information recommends administration based on "known consumption of fatal doses of digoxin: ≥10mg," while many emergency medicine textbooks suggest fab administration be driven by clinical features or potassium concentration. A 54 kg adult, not on digoxin, presented one hour after ingesting 12.5 mg. Electrocardiogram revealed only ST depression and first degree heart block. Initial pulse was 102 beats/min, systolic blood pressure was 170 mmHg. The patient was otherwise asymptomatic. Poison center recommended immediately obtaining serum potassium and digoxin concentrations; call-back was planned for two hours. The emergency physician was instructed to have ≥10 fab vials bedside and to administer if instability ensued. Thirty-five minutes later (≈90 min post-ingestion) ventricular fibrillation cardiac arrest occurred; initial serum potassium resulted at this time at 3.3 mEq/L. Bicarbonate, insulin and glucose, amiodarone, magnesium, calcium, and 10 fab vials were administered. Cardioversion resulted in wide-complex tachycardia which became ventricular fibrillation then asystole and the patient died. Serum digoxin concentration drawn on hospital arrival resulted after death at 44 ng/mL. In this fatal case of acute digoxin poisoning, fab was not empirically recommended because the patient initially did not have significant signs or symptoms that accompanied the history of ingesting ≥10 mg digoxin. While the bedside team was given clear anticipatory guidance by the regional poison center, the patient died despite fab administration once instability occurred.

No information is available on the clinical use of digoxin immune fab (ovine) during breastfeeding. Because it is a large protein molecule with a molecular weight of about 46,000 Da, the amount in milk is likely to be very low and absorption is unlikely because it is probably destroyed in the infant's gastrointestinal tract.

While there has been a decline in the use of digoxin in patients with heart failure and atrial fibrillation, acute and chronic digoxin toxicity remains a significant clinical problem. Digoxin's narrow therapeutic window and nonspecific signs and symptoms of toxicity create clinical challenges and uncertainty around the diagnostic criteria of toxicity and responsive treatment choices for the bedside clinician. A systematic review of published literature on digoxin toxicity (34,587 publications over 6 decades, with 114 meeting inclusion criteria) was performed to develop 33 consensus statements on diagnostic and therapeutic approaches which were then evaluated through a modified Delphi process involving a panel of experts in cardiology, nursing, emergency medicine, and medical toxicology. The results demonstrate agreement about the need to consider time of ingestion and nature of the exposure (ie, acute, acute-on-chronic, chronic) and the use of digoxin immune Fab for life-threatening exposure to decrease risk of death. While several areas of continued uncertainty were identified, this work offers formalized guidance that may help providers better manage this persistent clinical challenge.

Digoxin immune fab is a medication used in the management and treatment of digoxin toxicity. Most toxicity cases are seen in patients with a past medical history of atrial fibrillation and underlying heart failure. It is also indicated in the treatment of pre-eclampsia, eclampsia, and other plant-derived cardiac glycoside poisonings. It is in the antidote class of medications. This activity will highlight the indications, contraindications, mechanism of action, adverse profile, and other key factors of digoxin immune Fab therapy. These clinical details are pertinent for interprofessional team members managing patients with digoxin overdose and other indicated treatable conditions.