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Stem
A 78-year-old woman is brought to the emergency department by her daughter with a one-week history of anorexia, nausea and vomiting, increasing confusion, and "everything looks yellow-green." Her past history includes permanent atrial fibrillation and heart failure with reduced ejection fraction, for which she takes digoxin 0.25 mg once daily, furosemide 40 mg once daily, and clarithromycin 500 mg twice daily (started five days ago for a chest infection). She had a recent episode of gastroenteritis with dehydration. [1]
On examination: pulse 42/min (irregular), blood pressure 98/60 mmHg, GCS 14, mildly dehydrated. Visual acuity reduced with colour disturbance (yellow-green halos). 12-lead ECG shows atrial tachycardia (atrial rate 180) with 2:1 AV block and frequent ventricular ectopics. Serum potassium 3.1 mmol/L, creatinine 165 micromol/L (baseline 95), serum digoxin 3.4 ng/mL. [1][5][2]
Questions
a) What is the diagnosis, and name TWO features in the stem that support it? (2 marks)
Diagnosis: digoxin toxicity. Supporting features (any two): (1) GI plus neurological plus visual (anorexia, nausea, vomiting, confusion, yellow-green halos / xanthopsia — xanthopsia is relatively specific); (2) cardiac toxicity — bradycardia, AV block, premature ventricular contractions (PVCs are the commonest arrhythmia); (3) serum digoxin 3.4 ng/mL above the traditional immunoassay range of 0.8 to 2.0 ng/mL, in the setting of deteriorating renal function (the usual chronic pattern). [1][3][5]
b) Outline the mechanism by which digoxin produces BOTH its therapeutic inotropic effect AND its toxic arrhythmias, and explain why this patient's potassium is low. (3 marks)
Digoxin inhibits the Na+/K+ ATPase. Intracellular sodium rises, sodium-calcium exchange slows, and intracellular calcium accumulates — the therapeutic inotropic effect. In toxicity, calcium overload produces triggered activity (PVCs, VT, bidirectional VT). Increased vagal tone produces AV block. Her potassium is 3.1 mmol/L in the setting of a loop diuretic plus dehydration; Andrews lists hypokalaemia, hypomagnesaemia, hypercalcaemia and dehydration as exacerbating factors, and diuretics among interacting drug classes. Named interacting classes also include calcium-channel blockers, NSAIDs and macrolides. Do not invent an unsourced "halve the dose for amiodarone" figure. [2][1]
c) Describe the stepwise management of this patient. (3 marks)
- Stop digoxin; continuous cardiac monitoring; IV access. Draw the level before Fab. [1]
- Supportive care including electrolyte management. Andrews: severe hypokalaemia under 2.5 mmol/L can be replaced, watching for rebound hyperkalaemia; this patient's 3.1 mmol/L is an exacerbating factor, not a sourced 4.0-to-5.0 target. [1]
- Arrhythmia: she has symptomatic high-degree AV block (pulse 42, BP 98/60) — an Andrews immediate-Fab criterion. If Fab is delayed, atropine for bradyarrhythmia (no milligram figure fetched). Avoid adrenaline and isoprenaline. [1]
- Digoxin-specific Fab. Chan practical chronic regimen: 40 mg (1 vial) at a time, repeat after 60 minutes if still symptomatic (sooner if unstable); 40 to 120 mg (1 to 3 vials) is generally sufficient. Do not use (level × kg)/100 as the default chronic dose. [2]
- Recheck potassium after Fab (hypokalaemia is an uncommon, under-10-per-cent adverse event). The post-Fab total immunoassay is uninterpretable. [2][1]
d) State TWO indications for digoxin Fab fragments and ONE treatment that should be AVOIDED, with the reason. (2 marks)
Indications (any two, sourced): Chan — life-threatening tachy-bradyarrhythmias; potassium over 6 mmol/L; haemodynamic instability with digoxin over 2 microg/L (2.6 nmol/L). Andrews — VT/VF; asystole or symptomatic high-degree AV block; potassium over 6.5 mmol/L; hypotension with end-organ dysfunction. AVOID dialysis as a removal technique (large Vd). Conservative exam practice also avoids IV calcium as first-line even though Levine found no 1-hour malignant dysrhythmia. Do not list potassium 5.0-5.5 mmol/L, ingested dose over 10 mg, or child 4 mg / 0.1 mg/kg as fetched Fab indications. [2][1][4]
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]Levine M, Nikkanen H, Pallin DJ. The effects of intravenous calcium in patients with digoxin toxicity J Emerg Med, 2011.PMID 19201134
- [5]Haruna Y, Kawasaki T, Kikkawa Y, et al. Xanthopsia Due to Digoxin Toxicity as a Cause of Traffic Accidents: A Case Report Am J Case Rep, 2020.PMID 32769961