Investigations
1st investigations to order
ECG
Test
Perform a 12-lead ECG in all patients with suspected digoxin toxicity.
Acute overdose usually causes a marked bradycardia with PR and QRS prolongation.[1]
Arrhythmias are common if there is pre-existing heart disease.
Patients may have dysrhythmias, which are associated with increased automaticity and decreased atrioventricular (AV) conduction (e.g., atrial flutter and atrial fibrillation with high-degree AV block, non-paroxysmal atrial tachycardia with block, accelerated junctional rhythms, and/or bi-directional ventricular tachycardia).[26]
Premature ventricular contractions are the most common dysrhythmia.
Bigeminy or trigeminy occur frequently.
Chronic digoxin toxicity is most often associated with bradyarrhythmias (ventricular tachyarrhythmias also occur).
The only rhythm disturbances that are not definitively associated with digoxin toxicity are supraventricular tachyarrhythmias with a rapid ventricular response (e.g., paroxysmal atrial tachycardia and sinus tachycardia).
Repeat ECGs if possible, especially in symptomatic patients or in those who have ingested other cardiotoxic medications.[1]
Be aware that ventricular tachycardia and ventricular fibrillation may occur in patients with severe toxicity.[1]
Result
premature ventricular contractions, bidirectional ventricular tachycardia, atrial tachycardia with variable or slow ventricular response, accelerated junctional rhythms
serum digoxin concentration
Test
Measure serum digoxin concentrations in patients with suspected digoxin toxicity or at high risk for developing digoxin toxicity.[20]
Take the measurements at least 6 hours after ingestion.[1]
Serum digoxin concentrations are only truly reflective after distribution is complete (4-6 hours after the last dose).
Take samples more urgently if severe toxicity is suspected and treatment with digoxin-specific antibody (Fab) fragments is being considered.[1]
Interpret the serum digoxin concentration in the context of the wider clinical picture. Plasma concentrations do not correlate well with features of toxicity.[1]
Cardiac effects may take more than 12 hours to fully develop.[1]
The elimination of digoxin is slow (half-life is 30-40 hours with normal renal function and up to 100 hours in patients with impaired renal function), therefore repeated samples may not be clinically helpful.[1] Bear in mind that elevated digoxin concentrations can occur after treatment with digoxin-specific antibodies.[25] Routinely used assays measure both free digoxin and Fab-digoxin complexes and therefore report apparently high digoxin levels following treatment with digoxin-specific antibodies.[1]
Result
severe toxic effects may be seen with digoxin concentrations greater than 4.0 microgram/L (4.0 nanogram/mL; 5.2 nanomol/L)[1]
young children tend to tolerate a higher peak plasma digoxin concentration than adolescents and adults[1]
there is no exact serum digoxin concentration that is predictive of toxicity; there are a number of factors that can affect a patient's susceptibility to digoxin (e.g., hypokalaemia, volume status, comorbidities, age, and chronic disease)[24]
serum potassium level
Test
Always check serum potassium concentrations; they are important as a marker for prognosis in acute digoxin toxicity.[1] A patient with acute digoxin toxicity may have hyperkalaemia (≥5.0 mmol/L [≥5.0 mEq/L]), which is a marker of severe toxicity. Severe hyperkalaemia (≥6.5 mmol/L [≥6.5 mEq/L]) that is resistant to conventional treatments is considered an indication for digoxin-specific antibody therapy.
Result
hyperkalaemia (>5.0 mmol/L [>5.0 mEq/L]) or hypokalaemia (<3.0 to 3.5 mmol/L [<3.0 to 3.5 mEq/L])
serum magnesium level
Test
Cardiac manifestations of chronic digoxin toxicity are worsened by hypomagnesaemia.[24]
Result
may be low
serum creatinine and urea
Test
Renal function and volume status affect clearance.[1]
Result
may be elevated
Blood glucose
Test
Check capillary blood glucose.[1]
It may require monitoring as part of the management of hyperkalaemia.
Result
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