Oleander Seed Poisoning: Management

Overview

Clinical Features

Diagnostic Workup

• ECG immediately: look for bradycardia, AV block, ventricular ectopy, ST scooping
• Serum electrolytes: K⁺ is critical — hyperkalemia (>5.0 mEq/L) = severe toxicity
• Serum digoxin level: cross-reacts variably with plant glycosides; useful to confirm exposure but does not reliably correlate with severity of plant glycoside toxicity
  • Levels are most meaningful ≥6 hours post-ingestion (distribution phase complete)
• Renal function, glucose, magnesium
• Continuous cardiac monitoring from the outset

Management

1. Immediate Stabilization

• IV access, continuous cardiac monitoring, 12-lead ECG
• Correct hypoxia, hypoglycemia, hypovolemia

2. GI Decontamination

• Activated charcoal (AC) 1 g/kg PO — give in awake, alert, cooperative patients presenting within 1 hour of ingestion
  • Yellow oleander: AC has been studied in large randomized trials with mixed results; still reasonable to administer early
• Gastric lavage is not recommended (vagal stimulation risk → asystole)
• No role for cathartics, forced diuresis, hemodialysis, or hemoperfusion (large volume of distribution precludes elimination enhancement)

3. Antidote: Digoxin-Specific Antibody Fragments (Digoxin-Fab)

Indications (Box 142.4, Rosen's)

1. Ventricular dysrhythmias (beyond isolated PVCs)
2. Symptomatic bradydysrhythmias / AV block unresponsive to atropine
3. Serum K⁺ >5.0 mEq/L (hyperkalemia = marker of severity; treat with Fab, not insulin/bicarb)
4. Rapidly progressive rhythm disturbances or rising potassium
5. Co-ingestion of other cardiotoxic drugs
6. Ingestion of a known cardioactive steroid plant + severe symptoms

Dosing for Plant Glycoside Poisoning

Key caveat: Yellow oleander glycosides have poor cross-reactivity with digoxin-Fab at standard doses — higher doses are required than for pharmaceutical digoxin toxicity.

• Re-evaluate every 30–60 min; repeat dosing if response is inadequate
• Median time to initial response: ~19 minutes after infusion completion
• Success rate approaches 90%; non-responders typically received Fab too late or have comorbidities

Adverse Effects of Fab

• Allergic reactions <1% (urticaria, erythema, facial edema → treat with diphenhydramine, steroids, epinephrine)
• Hypokalemia (rebound after Fab binds glycosides and Na/K-ATPase normalizes)
• Exacerbation of heart failure (if patient had underlying HF on digoxin)
• Increased ventricular rate in atrial fibrillation

4. Managing Bradydysrhythmias

• Atropine 0.5–1 mg IV as a temporizing bridge while Fab is prepared
• Transcutaneous pacing if atropine fails — use as bridge to Fab, not as primary therapy (transvenous pacing carries higher risk of provoking ventricular dysrhythmia in glycoside toxicity)
• IV magnesium may reduce ventricular irritability

5. Managing Hyperkalemia

• Digoxin-Fab is the definitive treatment for hyperkalemia in this setting
• Insulin/dextrose, sodium bicarbonate, exchange resins: do not reduce mortality; avoid relying on these
• Calcium is controversial — traditionally avoided due to concern for "stone heart" (tetanic cardiac contraction), though recent limited data suggest no increased harm. Given the uncertainty, avoid IV calcium in confirmed cardiac glycoside toxicity unless hyperkalemia is immediately life-threatening and Fab is unavailable

6. Chronic Toxicity / Hypokalemia

• In chronic poisoning, correct hypokalemia and hypomagnesemia promptly — both markedly potentiate cardiac glycoside toxicity

7. Cardiac Arrest

• Standard ACLS; prolonged CPR is appropriate given reversibility with Fab
• Give Fab immediately as IV bolus (10–20 vials); late administration has resuscitated ~54% of arrest patients

Drugs to Avoid

• Calcium (relative contraindication)
• Class IA/IC antiarrhythmics (may worsen conduction)
• Electrical cardioversion — if absolutely needed, use lowest effective energy (can precipitate VF); should only be used after Fab

Disposition

• Any symptomatic patient or significant ingestion → ICU monitoring
• Asymptomatic patients with potential toxic ingestion → minimum 6–8 hours observation with continuous cardiac monitoring
• Serial ECGs and potassium levels