History and exam
Key diagnostic factors
common
digoxin exposure
History of exposure to digoxin or digitoxin should be confirmed if possible.
gastrointestinal symptoms
Typically include nausea, vomiting, diarrhea, abdominal pain, or anorexia.
central nervous system symptoms
Typically include lethargy, weakness, and confusion.
uncommon
visual symptoms
Typically include disturbances of color vision with a tendency to perceive yellow halos around objects (xanthopsia), blurred vision, and diplopia. Xanthopsia is not as common in digoxin overdose as it is in digitoxin overdose.
Other diagnostic factors
common
suicidality
Patients or family members may provide the history of exposure or suicidality in acute digoxin toxicity.
cardiovascular symptoms
Typically include palpitations, syncope, arrhythmias, and dyspnea.
Risk factors
strong
age >55 years
Older adults (aged >55 years) are at risk for toxicity from a number of mechanisms, such as dosing error, chronic medical conditions, decreased clearance, increased bioavailability, and interaction with other chronic medications.[5]
decreased renal clearance
Patients with decreased glomerular filtration rate are more susceptible to digoxin toxicity because of decreased clearance of digoxin from the serum.
hyperkalemia (>5.0 mEq/L)
Patients with hyperkalemia (>5.0 mEq/L) are more at risk of digoxin toxicity and of dysrhythmias, leading to a worse prognosis. However, acute digoxin toxicity can also cause hyperkalemia. Other causes of hyperkalemia include hemolysis, renal failure, and use of ACE inhibitors.
hypokalemia (<3.0 to 3.5 mEq/L)
Patients with therapeutic serum concentrations of digoxin can be symptomatic if they have hypokalemia.[22]
concomitant use of specific drugs
Digoxin is largely dependent on p-glycoprotein for elimination. Thus, medications that inhibit p-glycoprotein may increase digoxin levels and potentially cause toxicity.
These are numerous, but clinically significant ones include verapamil, diltiazem, amiodarone, quinidine, ketoconazole, itraconazole, vinblastine, doxorubicin, 2,4-dinitrophenol, and erythromycin.[19] Others include clarithromycin, cyclosporine, propafenone, quinidine, and spironolactone.
Other mechanisms may also affect digoxin levels. Amiodarone decreases renal clearance and displaces digoxin from its protein-binding sites. Quinidine is also able to displace digoxin from its protein-binding sites. Spironolactone may increase prerenal state, thereby potentiating a state of decreased renal clearance. Verapamil may decrease renal clearance. Antibiotics inhibit antibacterial activity (against gastrointestinal bacteria) and could increase the amount of digoxin absorbed from the gastrointestinal tract.
hypomagnesemia
Some electrolyte abnormalities increase susceptibility to digoxin.
hypercalcemia
Some electrolyte abnormalities increase susceptibility to digoxin.
weak
hypothyroidism
Recognized risk factor for developing digoxin toxicity.
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