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Digoxin Toxicity

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💡 Key Point: Hyperkalaemia is a hallmark of severe Digoxin toxicity and correlates with mortality. Consult the National Poisons Information Service (NPIS) early. Digoxin-specific antibody fragments (Digoxin immune Fab / Digibind) are expensive and may be stocked only in tertiary centres.

💊 About

Origin: Digoxin is derived from the Digitalis purpurea (foxglove) plant and is also present in oleander and lily of the valley.
Therapeutic use: Rate control in atrial fibrillation and for symptomatic heart failure in selected patients.
Therapeutic index: Very narrow — small changes in dose or renal function can cause toxicity.

⚙️ Mechanism & Pathophysiology

Digoxin inhibits the Na⁺/K⁺-ATPase pump in cardiac myocytes → ↑ intracellular Na⁺ → reduced Na⁺/Ca²⁺ exchange → ↑ intracellular Ca²⁺ → enhanced contractility.
It also ↑ vagal tone → slowed AV nodal conduction and bradycardia.
Excess inhibition causes electrical instability and automaticity → arrhythmias of any type.
Lethal dose: ≈10× daily dose (≈10 mg in adults, ≈4 mg in children).
T½: 30–40 h (longer if renal impairment). Toxicity peaks at ~6 h post-ingestion; death may occur within 6–12 h.

⚠️ Factors Increasing Toxicity

Electrolytes: ↓ K⁺, ↓ Mg²⁺, ↑ Ca²⁺ enhance binding to Na/K-ATPase.
Renal impairment: Reduces clearance → accumulation.
Drug interactions: Amiodarone, verapamil, macrolides, quinidine increase serum levels.
Age/frailty: Lower volume of distribution → toxicity at “therapeutic” levels.

🩺 Clinical Presentation

Gastrointestinal: Anorexia, nausea, vomiting, abdominal pain (early clues).
Visual: Blurred or yellow vision (xanthopsia), “halo” effect.
Cardiac: Bradycardia, AV block, sinus arrest, SVT with AV block, VT, or VF.
Neurological: Confusion, weakness, delirium, lethargy.
Electrolyte: Hyperkalaemia in acute toxicity (poor prognostic sign).

🧪 Investigations

FBC, U&E, Mg, Ca, renal function.
Serum digoxin level (≥ 4 h post ingestion for accuracy).
ECG: “Reverse tick” ST depression, prolonged PR, frequent ectopics, AV block, or bidirectional VT.
Continuous cardiac monitoring (CCU/HDU).

🚫 Management Principles

❗ Do NOT give IV calcium unless under senior/NPIS guidance — may precipitate fatal “stone heart” contraction.

Management Step	Key Actions & Rationale
1️⃣ Stop Digoxin & Decontaminate	Discontinue digoxin immediately. If ingestion < 1 h: consider gastric lavage and/or activated charcoal (single or multiple doses for sustained release). Monitor airway if vomiting or reduced GCS.
2️⃣ Assess & Correct Electrolytes	Check K⁺, Mg²⁺, Ca²⁺. • Correct hypokalaemia and hypomagnesaemia. • Treat hyperkalaemia (K⁺ > 6 mmol/L) with insulin-glucose ± sodium bicarbonate. Avoid calcium unless absolutely indicated.
3️⃣ Cardiac Monitoring & Arrhythmia Control	Bradyarrhythmia: IV Atropine 0.6–1.2 mg; consider temporary pacing if refractory. Tachyarrhythmia (VT/VF): Lidocaine or Phenytoin IV. Avoid Amiodarone or Procainamide (exacerbate toxicity). Defibrillation: use low-energy shocks (≈25 J) if needed.
4️⃣ Antidote – Digoxin Immune Fab (Digibind® / DigiFab®)	Indications (per BNF/NPIS): Life-threatening arrhythmia or cardiac arrest. Serum digoxin > 15 nmol/L (acute ingestion) or > 10 nmol/L (delayed). Ingested dose > 10 mg (adult) or > 4 mg (child). Hyperkalaemia (K⁺ > 5 mmol/L). Dose: Each vial binds ≈ 0.5 mg digoxin; large overdoses may need 10–20 vials. Monitor for rebound heart failure once digoxin effect reversed.
5️⃣ Supportive Care	High-flow O₂, IV fluids (avoid overload), antiemetics, and correction of precipitating factors (renal impairment, drug interactions).
6️⃣ Monitoring & Follow-up	Repeat electrolytes and ECG frequently. Digoxin level becomes unreliable after Fab therapy (immunoassay interference). Observe ≥ 24 h post-antidote for recurrent bradyarrhythmia or hypokalaemia.

📈 Prognosis

With early Fab administration, survival exceeds 90% even in severe overdose.
Mortality correlates with initial serum potassium and delay to antidote therapy.
Chronic low-level toxicity (in elderly or renally impaired) often presents subtly with GI upset, confusion, or visual change.

📚 References

ToxBase: Digoxin poisoning
BNF: Digoxin-specific antibody fragments
Antman EM et al. Treatment of 150 cases of life-threatening digitalis intoxication with digoxin-specific Fab fragments. JACC 1990;15:73-83.
British Toxicology Society Guidelines 2022.

Summary: Digoxin toxicity produces a distinctive triad — gastrointestinal upset, visual changes, and any arrhythmia. Hyperkalaemia marks severe poisoning. Management centres on stopping the drug, correcting electrolytes, controlling arrhythmias, and giving Digoxin Immune Fab early in life-threatening cases.

PLEASE NOTE LEGAL ADVICE: The contents are under continuing development and improvements and may contain errors of omission or fact. Feedback vital and always welcome at drokane at gmail.com. This is not to be used for the assessment, diagnosis or management of patients. It should not be regarded as medical advice. It is only for educational purposes. Please adhere to your local protocols. If you are unwell please seek healthcare advice from your doctor. This does not replace senior or specialist advice. If you do not accept this then please do not use the website. If you need medical advice, please consult a doctor or other appropriate medical professional. If you are a medical professional and you need advice then speak to your senior or colleagues.

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