Yellow oleander poisoning

Clinical features

• Nausea and repeated vomiting
• Abdominal pain, diarrhea
• Excess salivation

• Weakness, lethargy, dizziness
• Confusion or altered sensorium in severe poisoning
• Occasionally visual disturbance, although less consistently reported than in pharmaceutical digoxin toxicity

• Sinus bradycardia
• First-degree AV block, progressing to second-degree or complete heart block
• Junctional rhythms
• Atrial tachycardia with block
• Ventricular ectopics, ventricular tachycardia, including bidirectional VT
• Ventricular fibrillation
• Hypotension, cardiogenic shock

• Hyperkalemia is an important marker of severe acute toxicity and poor prognosis.
• Check magnesium, calcium, renal function, glucose, and acid-base status.
• A digoxin assay may be positive because of cross-reactivity with plant glycosides, but the value does not reliably quantify severity or guide plant-poisoning antidote dosage.

Management

1. Immediate stabilization

• Treat as a medical emergency, preferably in an ICU or high-dependency monitored area.
• ABC approach, IV access, oxygen as required.
• Continuous ECG, pulse oximetry, frequent blood pressure measurements.
• Obtain serial 12-lead ECGs and repeat serum potassium, magnesium, creatinine, glucose, and acid-base status.
• Correct dehydration with cautious IV isotonic fluids if appropriate.

2. Gastrointestinal decontamination

• Activated charcoal is appropriate for a recent potentially toxic ingestion if the airway is protected.
• Consider multiple-dose activated charcoal in significant ingestion, especially early, because glycosides can undergo enterohepatic recirculation. Evidence for mortality benefit is mixed, so this should be guided by a toxicologist/poison center.
• Do not induce vomiting.
• Gastric lavage is not routine. Consider only a very recent, life-threatening ingestion with a protected airway and expert oversight.

3. Treat bradycardia and AV block

• Atropine IV for symptomatic bradycardia or AV block.
• If atropine fails and there is unstable bradycardia/high-grade AV block:
  • Arrange temporary transvenous pacing if necessary.
  • Avoid relying on isoprenaline because it may provoke ventricular ectopy.
• Definitive treatment should not be delayed while pacing is being arranged if Fab is indicated.

4. Digoxin-specific Fab fragments: antidote

• Hemodynamically unstable bradycardia or high-grade AV block not responding to atropine
• Ventricular tachycardia or ventricular fibrillation
• Cardiogenic shock
• Significant hyperkalemia, especially K+ >6.5 mmol/L, or a rising potassium with ECG/cardiac toxicity
• Severe progressive clinical toxicity

5. Hyperkalemia

• Continuous ECG monitoring.
• Give IV insulin with dextrose to shift potassium intracellularly while Fab is obtained.
• Nebulized salbutamol can be an adjunct where appropriate.
• Sodium bicarbonate is reserved for significant metabolic acidosis, not used routinely.
• Fab is the definitive treatment for toxin-mediated hyperkalemia.
• Dialysis does not remove the cardiac glycoside effectively, but may be used for refractory hyperkalemia or renal failure.

6. Arrhythmias and supportive measures

• Correct hypoxia, acidosis, and electrolyte abnormalities.
• IV magnesium sulfate may be useful for ventricular ectopy/ventricular arrhythmias.
• Avoid empiric antiarrhythmics that worsen conduction disturbances unless directed by a toxicologist or cardiologist.
• Do not give potassium supplements unless hypokalemia is documented and carefully monitored.
• Psychological assessment is required once medically stable in intentional ingestion.

Exam-style summary