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Q1: Mechanism and clinical recognition (3 min)
Examiner: A patient on digoxin presents with nausea, confusion and yellow-green halos. Walk me through the mechanism of digoxin and why this is toxicity. [1][2]
Expected answer:
- Digoxin inhibits the Na+/K+ ATPase — Chan: narrow therapeutic index; bioavailability 60 to 80 per cent; mean half-life 40 hours; Vd 5 to 10 L/kg; protein binding 20 per cent. [2]
- Toxicity: calcium-overload automaticity plus vagal AV block.
- Clinical: gastrointestinal (loss of appetite, nausea, vomiting, diarrhoea), neurological (headache, confusion, lethargy), visual (blurring, halos, colour change), cardiac. Xanthopsia is relatively specific. [1]
- Toxicity is a clinical diagnosis — levels do not correlate consistently; toxicity can occur within the traditional immunoassay range 0.8 to 2.0 ng/mL. [1]
Follow-up: Why does hypokalaemia matter? Andrews: hypokalaemia, hypomagnesaemia and hypercalcaemia exacerbate toxicity. Do not invent a competition-binding millimole target. [1]
Q2: The cardiac arrhythmias (3 min)
Examiner: What arrhythmias would you expect, and which is pathognomonic? [1][3]
Expected answer:
- Andrews: bradycardia, all degrees of AV block, premature ventricular contractions and ventricular tachycardia, hypotension and cardiogenic shock. [1]
- StatPearls: PVCs are the commonest; bidirectional VT is pathognomonic. [3]
- Atrial tachycardia with AV block is a recognised digitalis pattern, not the pathognomonic rhythm.
- Distinguish digoxin EFFECT (scooped or reverse-tick ST, T flattening, U waves — can occur without toxicity) from digoxin TOXICITY (arrhythmias plus symptoms). [1]
Q3: Management ladder (3 min)
Examiner: How do you manage digoxin toxicity? Give sourced regimens, not invented milligrams. [1][2]
Expected answer — stepwise:
- Stop digoxin; continuous cardiac monitoring. [1]
- Electrolytes: Andrews 5.5 to 6.5 mmol/L hyperkalaemia should resolve with Fab; severe hypokalaemia under 2.5 mmol/L can be replaced. [1]
- If Fab is delayed: lidocaine or magnesium sulfate for VT; atropine for bradyarrhythmia; avoid adrenaline and isoprenaline. No fetched milligram doses. [1]
- Digoxin Fab for life-threatening features (see Q4).
- Activated charcoal: Chyka — not routine; may consider if a potentially toxic amount up to 1 hour, at least 50 g, protected airway. Andrews — may consider within 2 hours of acute overdose after Fab. [1]
Follow-up — what to AVOID and why:
- Dialysis/haemoperfusion as removal (large Vd). [1][2]
- IV calcium as first-line remains conservative exam practice; Levine: 0 life-threatening dysrhythmias within 1 hour of calcium in 23 patients. [5]
Q4: Fab fragments — indications and dosing (2 min)
Examiner: When do you give Fab, and how do you dose it? [2][1]
Indications:
- Chan: life-threatening tachy-bradyarrhythmias; K over 6 mmol/L; haemodynamic instability with digoxin over 2 microg/L (2.6 nmol/L). [2]
- Andrews: VT/VF; asystole or symptomatic high-degree AV block; K over 6.5 mmol/L; hypotension with end-organ dysfunction. [1]
- Do not quote K 5.0-5.5 mmol/L, adult ingestion over 10 mg, or child 4 mg / 0.1 mg/kg as fetched indications.
Dosing:
- 40 mg DigiFab binds 0.5 mg digoxin; Fab half-life 19 to 30 hours. [2]
- Acute (Chan): 80 mg bolus, repeat to clinical response; most need less than half a calculated full-neutralising dose.
- Chronic (Chan): 40 mg (1 vial), repeat 60 minutes; 1 to 3 vials generally sufficient.
- Arrest (Andrews): five 40-mg vials immediately, a further five if no response at 30 minutes.
- Non-life-threatening selected cases (Andrews): half-neutralisation = SDC (ng/mL) × kg × 0.005, rounded up to a vial — not the crashing-patient default.
- Antman: 150 patients; 80 per cent resolved; median 19 minutes; 54 per cent of arrest-as-manifestation survived hospitalisation. [4]
Pearl: after Fab the total immunoassay is uninterpretable (does not distinguish free versus bound). Free concentration falls to almost zero within minutes. Recrudescence is infrequent. [1][2]
Q5: Special scenarios and pitfalls (2 min)
Expected answer:
- Chronic elderly/renal: the usual pattern. Traditional range 0.8 to 2.0 ng/mL; HF favoured 0.5 to 0.8 ng/mL. [1]
- Acute overdose: hyperkalaemia is a Fab trigger (Chan over 6; Andrews over 6.5).
- Yellow oleander: anti-digoxin Fab reversed serious arrhythmias in a Sri Lankan RCT (1200 mg).
- Pitfalls: treating effect as toxicity; chasing the post-Fab total level; relying on dialysis; missing plant glycoside exposure.
References5ShowHide
- [1]Andrews P, Anseeuw K, Kotecha D, et al. Diagnosis and practical management of digoxin toxicity: a narrative review and consensus Eur J Emerg Med, 2023.PMID 37650725
- [2]Chan BS, Buckley NA. Digoxin-specific antibody fragments in the treatment of digoxin toxicity Clin Toxicol (Phila), 2014.PMID 25089630
- [3]Regina AC, Hai O. Cardiac Glycoside and Digoxin Toxicity StatPearls, 2026.PMID 29083729
- [4]Antman EM, Wenger TL, Butler VP Jr, et al. Treatment of 150 cases of life-threatening digitalis intoxication with digoxin-specific Fab antibody fragments. Final report of a multicenter study Circulation, 1990.PMID 2188752
- [5]Levine M, Nikkanen H, Pallin DJ. The effects of intravenous calcium in patients with digoxin toxicity J Emerg Med, 2011.PMID 19201134