Digoxin overdose

Highlights
Summary Overview

Basics
Definition Epidemiology Aetiology Pathophysiology Classification

Prevention
Primary Screening Secondary

Diagnosis
History & examination Tests Differential Step-by-step Criteria Guidelines Case history

Treatment
Details Step-by-step Guidelines

Follow Up
Recommendations Complications Prognosis

Resources
References Patient leaflets Credits Email Print Feedback Share Add to Portfolio Bookmark Add notes

History & exam
Key factors
• • • • • presence of risk factors digoxin exposure GI symptoms CNS symptoms visual symptoms

Other diagnostic factors
• • suicidality cardiovascular symptoms History & exam details

Diagnostic tests
1st tests to order
• • • • • ECG digoxin serum concentration serum potassium level serum magnesium level serum creatinine and urea Diagnostic tests details

Treatment details
Acute
acute ingestion, low to moderate toxicity • • • o • o • o activated charcoal supportive care with hypokalaemia potassium replacement with hyperkalaemia observation ± correction of hyperkalaemia with hypomagnesaemia magnesium replacement chronic ingestion, low to moderate toxicity • • o • o • o supportive care with hypokalaemia potassium replacement with hyperkalaemia observation ± correction of hyperkalaemia with hypomagnesaemia magnesium replacement severe toxicity or haemodynamic compromise (acute or chronic toxicity) • • digoxin binding supportive care

• o • o • o • o • o

with hypokalaemia potassium replacement with hyperkalaemia observation ± correction of hyperkalaemia with hypomagnesaemia magnesium replacement with symptomatic bradycardia/high-degree AV block atropine with ventricular tachyarrhythmias defibrillation plus anti-arrhythmics

Ongoing
acute or chronic toxicity after initial treatment • • prescription of alternative drug and discontinuation of digoxin digoxin dose adjustment and regular monitoring Treatment details

Summary
• • • Can be acute or chronic, intentional, or accidental. Typically presents with components of GI, constitutional, and/or cardiovascular symptoms. Diagnosis is based on symptoms and laboratory data. At therapeutic digoxin doses (0.6-1.2 nanomol/L [0.5 to 0.9 nanograms/mL]), the ECG typically shows PR-interval prolongation and a scooped ST segment. In overdose, ECG also shows signs of increased automaticity (PVCs), AV nodal blockade, and slowed ventricular response. • Treatment includes digoxin-specific antibody fragments and supportive care. Lidocaine and phenytoin can be used for cardiac dysrhythmias when antibody fragments are unavailable. • There are no long-term complications of poisoning in patients treated appropriately for chronic digoxin toxicity, as long as anoxic brain injury, myocardial infarction, or terminal dysrhythmias have not occurred prior to treatment.

Definition
Digoxin is the most commonly prescribed cardioactive corticosteroid in the US. Cardioactive corticosteroids have been used for over 200 years in the treatment of dropsy, which is better understood today as oedema from CHF. [1] In therapeutic doses, they increase cardiac contractility and control the heart rate. Digoxin toxicity is a clinical diagnosis that relies in part on ECG findings such as signs of increased automaticity and AV node blockade

(PVCs, slowed ventricular response). Serum digoxin concentration (SDC) is usually over the therapeutic range of 0.6-1.2 nanomol/L (0.5 to 0.9 nanograms/mL), but may not be raised. In addition to pharmaceuticals, toxicity can also occur from exposure to a number of plants and animals that contain cardioactive corticosteroids, including dogbane, foxglove, lily of the valley, oleander, yellow oleander, red quill, and the Bufo species toad. Although these other toxins are clinically similar, this monograph specifically discusses only toxicity from digoxin.

Epidemiology
Digoxin is used in the treatment of heart failure, atrial fibrillation, atrial flutter, and paroxysmal atrial tachycardia. Digoxin usage is decreasing due to its inferiority to other anti-failure agents and digoxin toxicity has, therefore, become uncommon, but it is at risk of being overlooked. [2]In the US, approximately 0.4% of patients admitted to hospitals, 1% of outpatients on digoxin, and 10% to 18% of nursing home patients develop digoxin toxicity. In the Netherlands, digoxin toxicity has been reported in 0.04% of patients admitted as acute cases to hospital. In one study, the incidence rate for admissions due to digoxin toxicity was 48.5 per 100,000 prescriptions (1.94 admissions per 1000 treatment years). [3] Recent data on the incidence of digoxin toxicity in other countries is not widely available. Patients aged >55 years are more commonly affected, but toxicity occurs in both young and old people. [4] [5] It is also a common cause of adverse drug effects in older people. [6] A Japanese study has shown that older patients, especially those >71 years of age, may be at increased risk of toxicity despite serum digoxin concentrations within therapeutic range. It is thought that this may be due to unknown pharmacodynamic changes that may occur with increased age [7] Prevalence is comparable in men and women in the US, but women have been found to have a higher risk in a Netherlands study. [3] The American Association of Poison Control Centers reported 2828 exposures in 2005, with 32 deaths. [5] However, between 1991 and 2004, significant decline in hospitalised digoxin toxicity in the US and ambulatory digoxin toxicity in the UK has been demonstrated. [8] Young children are mainly at risk of unintentional medication overdose. Adults are mainly at risk from intentional ingestions in a suicide attempt. Dosing errors, increased bioavailability, and decreased clearance may also result in overdose.

Aetiology
Digoxin toxicity can occur through a number of different mechanisms: Acute
• • • Overdose after suicide attempt Medication dosing error Malicious intent (homicidal poisoning).

Chronic
• • • • • • Chronic digoxin over-medication Increased GI absorption (caused by anti-bacterial therapy, or by drug-induced P-glycoprotein inhibition) [9] [10] [11] Decreased renal clearance due to renal insufficiency or drugs [12] [13] [14] [15] [16] Displacement of digoxin from protein-binding sites [12] [13] [15] Conditions that increase susceptibility to digoxin (electrolyte abnormalities, e.g., hypokalaemia, hypomagnesaemia, hypercalcaemia) [17] [18] Digoxin is largely dependent on p-glycoprotein for elimination. Thus, medications that inhibit pglycoprotein may increase digoxin levels and potentially cause toxicity. These are numerous, but clinically significant ones include verapamil, diltiazem, amiodarone, quinidine, ketoconazole, itraconazole, vinblastine, doxorubicin, reserpine, 2,4-dinitrophenol, and erythromycin. These substances may also inhibit cytochrome 3A4. [19] Others include clarithromycin, ciclosporin, propafenone, quinidine, and spironolactone.

Pathophysiology
Digoxin inhibits Na+/K+ ATPase. This increases cytosolic Ca, which increases inotropy. Abnormal sodium, potassium, or magnesium levels and acidosis increase toxicity by further depressing the Na+/K+ ATPase pump. Therapeutically, digoxin increases automaticity and shortens the repolarisation intervals of the atria and ventricles. There is a concurrent decrease in depolarisation and conduction through the sinoatrial and AV nodes respectively. These changes are reflected on the ECG by a decrease in ventricular response rate PR-interval prolongation, QT-interval shortening, and ST-segment and T-wave forces opposite the direction of the major QRS forces (scooped ST segment). This results in the characteristic digitalis

effect. [20]
ECG showing digoxin effectFrom the personal collection of Dr Robert S. Hoffman

In overdose, digoxin produces two major effects that correlate with its therapeutic action:
1. 2. Slowed conduction by increasing block at the AV node Increased automatic triggered electrical activity in atrial muscle, the AV junction, the His-Purkinje system, and the ventricular muscle (increased automaticity).

Digoxin toxicity can also cause hyperkalaemia, which increases the risk of dysrhythmias. Toxicity depends on intra-cellular levels and does not correlate well with serum levels. Non-cardiac adverse effects may also be mediated by inhibition of Na+/K+ ATPase in other tissues.[21]

Classification
General Toxicity from digoxin is typically classified as acute or chronic.

Primary prevention
Patients on digoxin require periodic monitoring of their renal function and adjustment of their digoxin dose if creatinine clearance has changed. Serum digoxin concentration (SDC) is measured 2 to 3 weeks after any change in therapy or addition of a new medication. SDC levels are unreliable if obtained earlier than 6 hours after a dose of digoxin. [23] The current therapeutic SDC is 0.6 to 1.2 nanomol/L (0.5 to 0.9 nanograms/mL). [24]

Screening
Patients being treated chronically with digoxin have periodic monitoring of:

• • •

Serum digoxin concentration Serum electrolytes Renal function.

These patients are re-evaluated when any new medication is started, to identify potential interactions, and doses adjusted accordingly. Serum digoxin concentrations may be obtained 1 to 2 weeks after a new drug is started, to be reflective of steady state levels, although patients may just be reevaluated clinically (e.g., monitoring heart rate).

Secondary prevention
Alternative treatments are effective for 2 of the major clinical indications for digoxin, CHF and atrial fibrillation, and may be considered in place of digoxin, particularly in a patient who has experienced toxicity. [24] [23]

History & examination
Key diagnostic factorshide all
presence of risk factors (common) •

Risk factors include age >55 years, decreased renal clearance, hyperkalaemia, hypokalaemia, and use of specific drugs (e.g., amiodarone, clarithromycin, ciclosporin, itraconazole, propafenone, quinidine, spironolactone, verapamil, diltiazem, ketoconazole, vinblastine, doxorubicin, reserpine, 2,4-dinitrophenol, and erythromycin).

digoxin exposure (common) • History of exposure to digoxin or digitoxin should be confirmed if possible. GI symptoms (common) • Typically include nausea, vomiting, diarrhoea, abdominal pain, or anorexia. CNS symptoms (common) • Typically include lethargy, weakness, and confusion. visual symptoms (uncommon) •

Typically include disturbances of colour vision with a tendency to perceive yellow halos around objects (xanthopsia), blurred vision, and diplopia. Xanthopsia is not as common in digoxin overdose as in digitoxin overdose.

Other diagnostic factorshide all
suicidality (common) •

Patients or family members may provide the history of exposure or suicidality in acute digoxin toxicity.

cardiovascular symptoms (common) •

Risk

Typically include palpitations, syncope, arrhythmias, and dyspnoea. factorshide all

Strong

age >55 years •

Older adults (>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.

decreased renal clearance •

Patients with decreased GFR are more susceptible to digoxin toxicity because of decreased clearance of digoxin from the serum.

hyperkalaemia (>5.0 millimol/L) •

Patients with hyperkalaemia (>5.0 millimol/L [>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 hyperkalaemia. Other causes of hyperkalaemia include haemolysis, renal failure, and use of ACE inhibitors.

hypokalaemia (<3.0 to 3.5 millimol/L) •

Patients with therapeutic serum concentrations of digoxin can be symptomatic if they have hypokalaemia (<3.0 to 3.5 millimol/L [<3.0 to 3.5 mEq/L]). [22]

concomitant use of specific drugs •

Digoxin is largely dependent on p-glycoprotein for elimination. Thus, medications that inhibit pglycoprotein may increase digoxin levels and potentially cause toxicity.

These are numerous, but clinically significant ones include verapamil, diltiazem, amiodarone, quinidine, ketoconazole, itraconazole, vinblastine, doxorubicin, reserpine, 2,4-dinitrophenol, and erythromycin. [19]Others include clarithromycin, ciclosporin, 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 pre-renal state, thereby potentiating a state of decreased renal clearance. Verapamil may decrease renal clearance. Antibiotics inhibit antibacterial activity (against GI bacteria) and could increase the amount of digoxin absorbed from the GI tract.

hypomagnesaemia • Some electrolyte abnormalities increase susceptibility to digoxin. hypercalcaemia •

Some electrolyte abnormalities increase susceptibility to digoxin.

Weak hypothyroidism •

Recognised risk factor for developing digoxin toxicity.

Diagnostic tests
1st tests to orderhide all
Test

ECG Ordered on every patient who presents with suspected digoxin toxicity or exposure.

Sinus tachycardia, supraventricular tachycardia, and atrial fibrillation with rapid ventricular response are usually n seen with digoxin toxicity. The ECG shows the characteristic "dig effect" in therapeutic doses.

digoxin serum concentration

Measured for every patient suspected of digoxin exposure or toxicity, but is only truly reflective after distribution i be required, as levels drawn too early are not reflective of distributed levels. There is no exact serum digoxin concentration (SDC) that is predictive of chronic toxicity. There are a number of disease). [22]

complete (4 to 6 hours after the last dose). Levels are drawn immediately on presentation, but often a second lev

that can affect a patient's susceptibility to digoxin (e.g., hypokalaemia, volume status, co-morbidities, age, and ch

Patients not taking digoxin may have measurable digoxin levels that result from high circulating amounts of endo EDLS; however, levels rarely exceed 0.3 nanomol/L (0.2 nanograms/mL) in these patients.

digoxin-like substances (EDLS). Conditions such as pregnancy, renal failure, and hypothermia are associated wi

Also, spironolactone and non-digoxin cardioactive corticosteroids such as digitoxin and oleandrin can cause false positive elevations of digoxin levels. serum potassium level Required for every patient suspected of digoxin toxicity.

Hyperkalaemia: serum potassium concentrations are important as a marker for prognosis in acute digoxin toxicity digoxin toxicity and of dysrhythmias. However, acute digoxin toxicity can also cause hyperkalaemia by inhibiting

also reflect the severity of the toxicity. Patients with hyperkalaemia (>5.0 millimol/L [>5.0 mEq/L]) are more at risk

Na+/K+ ATPase pump. Other causes of hyperkalaemia include haemolysis, renal failure, and use of ACE inhibito

Hypokalaemia: chronic digoxin toxicity does not cause hypokalaemia, but digoxin toxicity is worsened by hypoka Patients with therapeutic serum concentrations of digoxin can develop symptoms of digoxin toxicity because hypokalaemia acts synergistically with digoxin's mechanism of action. [22] serum magnesium level Cardiac manifestations of chronic digoxin toxicity are worsened by hypomagnesaemia. [22]

serum creatinine and urea Renal function and volume status affect clearance.

Differential diagnosis
Condition Beta-blocker toxicity Differentiating signs/symptoms • Differentiating tests • •

Hypotension, possible depressed mental status.

ECG (slow ventricular rate, AV nodal blockade with as Blood glucose: hypoglycaemia.

Calcium-channel blocker toxicity

Hypotension, usually normal mental status.

• •

ECG (slow ventricular rate, AV nodal blockade with as Blood glucose: hyperglycaemia.

Clonidine toxicity

Hypotension, bradycardia, lethargy. Occasionally responsive to naloxone.

Normal or therapeutic serum digoxin concentration.

Hypothermia

Hypothermia, cool extremities, hypotension, ventricular dysrhythmias with rapid ventricular response.

Normal or therapeutic serum digoxin concentration.

Pesticide toxicity

Salivation, lacrimation, urination, and bronchorrhoea.

Normal or therapeutic serum digoxin concentration.

Ischemic heart disease

Hypotension, bradycardia, chest pain or discomfort,

Normal or therapeutic serum digoxin concentration.

history of exertional dyspnoea with angina or anginal equivalent. Acute MI

Chest discomfort and/or pain, dyspnoea, vomiting, pain characteristic of cardiac aetiology, bradycardia, hypotension.

Normal or therapeutic serum digoxin concentration.

Elevated intracranial pressure

Altered mental status, hypertension, sinus bradycardia (but could possibly have other bradycardic rhythms).

Normal or therapeutic serum digoxin concentration.

Hyperkalaemia

Patients with hyperkalaemia due to other aetiologies (e.g., diminished potassium excretion, excessive endogenous potassium load, pseudohyperkalaem ia, redistribution from within cells into plasma) are typically awake and not lethargic.

Normal or therapeutic serum digoxin concentration.

Patients with chronic renal

insufficiency may present with lethargy and with any number of other non-specific complaints. Patients with hyperkalaemia may also present as completely asymptomatic. Hypothyroidism

Cold intolerance, fatigue, depression, thinning of hair, lethargy, or abnormal menstrual cycle.

Elevated TSH and decreased T4 levels are useful in t

Step-by-step diagnostic approach
History and physical examination can provide clues towards the diagnosis of digoxin overdose. ECG, digoxin level, electrolytes, and renal function tests should be ordered in all patients who present with suspected digoxin toxicity or exposure. Digoxin toxicity should be suspected in patients with histories of heart failure or atrial fibrillation, particularly in patients with renal insufficiency. A drug history should be taken, including any supplements, herbal remedies, over the counter medications and any plant ingestions, with particular attention to the use of p-glycoprotein/cytochrome 3A4 inhibitors.

History and examination in acute toxicity
In acute digoxin toxicity, patients or family members may provide the history of exposure or suicidality. Acute digoxin toxicity is characterised by patients being asymptomatic for minutes to hours after an exposure to digoxin, followed by a rapid deterioration. The symptoms usually include nausea, vomiting, anorexia, diarrhoea, and/or abdominal pain (less common), and may include palpitations, syncope and dyspnoea. Acute digoxin toxicity may cause virtually any dysrhythmia. The two medications used most commonly in clinical practice are digoxin and digitoxin.

History and examination in chronic toxicity
Chronic digoxin toxicity is more common in elderly patients. It has a more indolent course with a less obvious presentation. It should be considered if the following symptoms are present: nausea, anorexia, abdominal pain, weakness, fatigue, palpitations, syncope, dyspnoea, disturbances of colour vision with a tendency to yellow halos (xanthopsia), blurred vision, and diplopia. Patients most often present with GI signs (anorexia and vomiting) and generalised non-specific complaints (generalised weakness and malaise), but could also present with CNS depression.

Investigations to order
ECG should be ordered on every patient who presents with suspected digoxin toxicity or exposure. Serum digoxin concentrations should be measured, but are only truly reflective after distribution is complete (4 to 6 hours after the last dose). Levels are drawn immediately on presentation, but often a second level will be required, as levels drawn too early are not reflective of distributed levels. Serum potassium concentrations are important as a marker for prognosis in acute digoxin toxicity, and also reflect the severity of the toxicity. Renal function should be assessed as this influences the rate of clearance of digoxin from the bloodstream. In addition, serum magnesium should be measured, as low levels exacerbate cardiac manifestations of digoxin toxicity.

Diagnostic findings in acute toxicity
Classically, patients with acute digoxin toxicity have:
• Dysrhythmias, which are associated with increased automaticity and decreased 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). [25] Premature ventricular contractions are the most common dysrhythmia. Bigeminy or trigeminy occur frequently. The only rhythm disturbances that are not definitively associated with digoxin toxicity are supraventricular tachyarrhythmias with a rapid ventricular response: for example, supraventricular tachycardia and sinus tachycardia. View image • • Hyperkalaemia (≥5.5 millimol/L [≥5.5 mEq/L]). Elevated digoxin serum concentration above 1.2 nanomol/L (0.9 nanograms/mL). [24]

Diagnostic findings in chronic toxicity
Chronic digoxin toxicity is most often associated with:

• • •

Bradyarrhythmias (ventricular tachyarrhythmias also occur) View image Normal or low serum potassium concentrations (they can also be high) Elevated serum digoxin concentrations (above the recommended therapeutic levels of <1.3 nanomol/L (<1 nanogram/mL).

Click to view diagnostic guideline references.

Diagnostic criteria

Serum digoxin concentration (SDC)
SDC is usually over the therapeutic range of 0.6 to 1.2 nanomol/L (0.5 to 0.9 nanograms/mL). However, some patients can be toxic at therapeutic digoxin serum concentrations.

Potassium
Acute overdose can cause hyperkalaemia.

Severity
Significant overdose, requiring treatment with digoxin-specific antibody fragments intravenously, is characterised by:
• • • • • • • Symptomatic bradyarrhythmias Ventricular dysrhythmias Any patient with acute digoxin overdose and potassium concentrations >5.0 millimol/L (>5.0 mEq/L) Acute ingestion of >4 mg in a healthy child (or 0.1 mg/kg) Acute ingestion of >10 mg in a healthy adult Serum concentration of ≥12.8 nanomol/L (≥10 nanograms/mL) 4 to 6 hours after ingestion (steady state) Serum concentration of ≥19.2 nanomol/L (≥15 nanograms/mL) at any time.

Case history #1
An 86-year-old woman presents with confusion and vomiting. She complains of weakness, nausea, and decreased appetite. Her history is significant for CHF for which she takes, among other medications, digoxin. In the hospital, she is alert and oriented in person, but not in time or place. Vital signs are normal except for a HR of 56 bpm. Her physical examination demonstrates bibasilar rales, irregular S1, S2 with an S3 gallop, and bilateral lower extremity 2+ pitting oedema up to her shins.

Case history #2
A 19-year-old woman presents after ingesting 30 of her grandmother's 0.25 mg digoxin tablets in a suicide attempt about 30 minutes prior to arrival. In the hospital, her vital signs are normal. She is in no acute distress and has no complaints; physical examination is within expected limits. About 30 minutes after arrival, she complains of non-specific abdominal pain and starts vomiting.

Treatment Options

Treatment Patient group acute ingestion, low to moderate toxicity line 1st Treatmenthide all

activated charcoal

The primary goal of activated charcoal is to decrease GI absorption of the drug; however, serum concentrations may also be decreased by facilitating gut dialysis via the enterohepatic and enteroenteric recirculation of digoxin (and other cardioactive corticosteroids). [35] [36]

• • •

Effective in first 6 to 8 hours post-ingestion. If severe toxicity, charcoal may be skipped and digoxin immune Fab given right away. Caution should be taken in patients who vomit or those with altered mental status. They are at risk of pulmonary aspiration when drinking the solution. Primary Options charcoal, activated : 1 g/kg orally as a single dose, repeat every 2-4 hours if required, maximum 4 doses total

plus [?]

supportive care

General supportive care includes attaching patients to a cardiac monitor, providing IV fluids in patients with hypotension or volume depletion (with caution for patients with CHF), supplemental oxygen, and/or repletion of electrolytes in patients with electrolyte abnormalities. Patients with hypokalaemia or hypomagnesaemia require additional potassium or magnesium with careful monitoring to restore normal serum levels.

with hypokalaemia

plus [?]

potassium replacement

Potassium should be given via cautious intravenous infusion to restore serum potassium to normal levels.

• •

Replacement should follow local hospital protocols. The serum potassium should be checked at intervals and therapy adjusted as needed.

Treatment Patient group acute ingestion, low to moderate toxicity line 1st Treatmenthide all

activated charcoal

The primary goal of activated charcoal is to decrease GI absorption of the drug; however, serum concentrations may also be decreased by facilitating gut dialysis via the enterohepatic and enteroenteric recirculation of digoxin (and other cardioactive corticosteroids). [35] [36]

• • •

Effective in first 6 to 8 hours post-ingestion. If severe toxicity, charcoal may be skipped and digoxin immune Fab given right away. Caution should be taken in patients who vomit or those with altered mental status. They are at risk of pulmonary aspiration when drinking the solution. Primary Options charcoal, activated : 1 g/kg orally as a single dose, repeat every 2-4 hours if required, maximum 4 doses total

plus [?]

supportive care

General supportive care includes attaching patients to a cardiac monitor, providing IV fluids in patients with hypotension or volume depletion (with caution for patients with CHF), supplemental oxygen, and/or repletion of electrolytes in patients with electrolyte abnormalities. Patients with hypokalaemia or hypomagnesaemia require additional potassium or magnesium with careful monitoring to restore normal serum levels.

with hypokalaemia

plus [?]

potassium replacement

Potassium should be given via cautious intravenous infusion to restore serum potassium to normal levels.

• •

Replacement should follow local hospital protocols. The serum potassium should be checked at intervals and therapy adjusted as needed.

Treatment Patient group acute ingestion, low to moderate toxicity line 1st Treatmenthide all

activated charcoal

The primary goal of activated charcoal is to decrease GI absorption of the drug; however, serum concentrations may also be decreased by facilitating gut dialysis via the enterohepatic and enteroenteric recirculation of digoxin (and other cardioactive corticosteroids). [35] [36]

• • •

Effective in first 6 to 8 hours post-ingestion. If severe toxicity, charcoal may be skipped and digoxin immune Fab given right away. Caution should be taken in patients who vomit or those with altered mental status. They are at risk of pulmonary aspiration when drinking the solution. Primary Options charcoal, activated : 1 g/kg orally as a single dose, repeat every 2-4 hours if required, maximum 4 doses total

plus [?]

supportive care

General supportive care includes attaching patients to a cardiac monitor, providing IV fluids in patients with hypotension or volume depletion (with caution for patients with CHF), supplemental oxygen, and/or repletion of electrolytes in patients with electrolyte abnormalities. Patients with hypokalaemia or hypomagnesaemia require additional potassium or magnesium with careful monitoring to restore normal serum levels.

with hypokalaemia

plus [?]

potassium replacement

Potassium should be given via cautious intravenous infusion to restore serum potassium to normal levels.

• •

Replacement should follow local hospital protocols. The serum potassium should be checked at intervals and therapy adjusted as needed.

Treatment Patient group acute ingestion, low to moderate toxicity line 1st Treatmenthide all

activated charcoal

The primary goal of activated charcoal is to decrease GI absorption of the drug; however, serum concentrations may also be decreased by facilitating gut dialysis via the enterohepatic and enteroenteric recirculation of digoxin (and other cardioactive corticosteroids). [35] [36]

• • •

Effective in first 6 to 8 hours post-ingestion. If severe toxicity, charcoal may be skipped and digoxin immune Fab given right away. Caution should be taken in patients who vomit or those with altered mental status. They are at risk of pulmonary aspiration when drinking the solution. Primary Options charcoal, activated : 1 g/kg orally as a single dose, repeat every 2-4 hours if required, maximum 4 doses total

plus [?]

supportive care

General supportive care includes attaching patients to a cardiac monitor, providing IV fluids in patients with hypotension or volume depletion (with caution for patients with CHF), supplemental oxygen, and/or repletion of electrolytes in patients with electrolyte abnormalities. Patients with hypokalaemia or hypomagnesaemia require additional potassium or magnesium with careful monitoring to restore normal serum levels.

with hypokalaemia

plus [?]

potassium replacement

Potassium should be given via cautious intravenous infusion to restore serum potassium to normal levels.

• •

Replacement should follow local hospital protocols. The serum potassium should be checked at intervals and therapy adjusted as needed.

Treatment Patient group acute ingestion, low to moderate toxicity line 1st Treatmenthide all

activated charcoal

The primary goal of activated charcoal is to decrease GI absorption of the drug; however, serum concentrations may also be decreased by facilitating gut dialysis via the enterohepatic and enteroenteric recirculation of digoxin (and other cardioactive corticosteroids). [35] [36]

• • •

Effective in first 6 to 8 hours post-ingestion. If severe toxicity, charcoal may be skipped and digoxin immune Fab given right away. Caution should be taken in patients who vomit or those with altered mental status. They are at risk of pulmonary aspiration when drinking the solution. Primary Options charcoal, activated : 1 g/kg orally as a single dose, repeat every 2-4 hours if required, maximum 4 doses total

plus [?]

supportive care

General supportive care includes attaching patients to a cardiac monitor, providing IV fluids in patients with hypotension or volume depletion (with caution for patients with CHF), supplemental oxygen, and/or repletion of electrolytes in patients with electrolyte abnormalities. Patients with hypokalaemia or hypomagnesaemia require additional potassium or magnesium with careful monitoring to restore normal serum levels.

with hypokalaemia

plus [?]

potassium replacement

Potassium should be given via cautious intravenous infusion to restore serum potassium to normal levels.

• •

Replacement should follow local hospital protocols. The serum potassium should be checked at intervals and therapy adjusted as needed.

Treatment Patient group acute ingestion, low to moderate toxicity line 1st Treatmenthide all

activated charcoal

The primary goal of activated charcoal is to decrease GI absorption of the drug; however, serum concentrations may also be decreased by facilitating gut dialysis via the enterohepatic and enteroenteric recirculation of digoxin (and other cardioactive corticosteroids). [35] [36]

• • •

Effective in first 6 to 8 hours post-ingestion. If severe toxicity, charcoal may be skipped and digoxin immune Fab given right away. Caution should be taken in patients who vomit or those with altered mental status. They are at risk of pulmonary aspiration when drinking the solution. Primary Options charcoal, activated : 1 g/kg orally as a single dose, repeat every 2-4 hours if required, maximum 4 doses total

plus [?]

supportive care

General supportive care includes attaching patients to a cardiac monitor, providing IV fluids in patients with hypotension or volume depletion (with caution for patients with CHF), supplemental oxygen, and/or repletion of electrolytes in patients with electrolyte abnormalities. Patients with hypokalaemia or hypomagnesaemia require additional potassium or magnesium with careful monitoring to restore normal serum levels.

with hypokalaemia

plus [?]

potassium replacement

Potassium should be given via cautious intravenous infusion to restore serum potassium to normal levels.

• •

Replacement should follow local hospital protocols. The serum potassium should be checked at intervals and therapy adjusted as needed.

Treatment Patient group acute ingestion, low to moderate toxicity line 1st Treatmenthide all

activated charcoal

The primary goal of activated charcoal is to decrease GI absorption of the drug; however, serum concentrations may also be decreased by facilitating gut dialysis via the enterohepatic and enteroenteric recirculation of digoxin (and other cardioactive corticosteroids). [35] [36]

• • •

Effective in first 6 to 8 hours post-ingestion. If severe toxicity, charcoal may be skipped and digoxin immune Fab given right away. Caution should be taken in patients who vomit or those with altered mental status. They are at risk of pulmonary aspiration when drinking the solution. Primary Options charcoal, activated : 1 g/kg orally as a single dose, repeat every 2-4 hours if required, maximum 4 doses total

plus [?]

supportive care

General supportive care includes attaching patients to a cardiac monitor, providing IV fluids in patients with hypotension or volume depletion (with caution for patients with CHF), supplemental oxygen, and/or repletion of electrolytes in patients with electrolyte abnormalities. Patients with hypokalaemia or hypomagnesaemia require additional potassium or magnesium with careful monitoring to restore normal serum levels.

with hypokalaemia

plus [?]

potassium replacement

Potassium should be given via cautious intravenous infusion to restore serum potassium to normal levels.

• •

Replacement should follow local hospital protocols. The serum potassium should be checked at intervals and therapy adjusted as needed.

Treatment Patient group acute ingestion, low to moderate toxicity line 1st Treatmenthide all

activated charcoal

The primary goal of activated charcoal is to decrease GI absorption of the drug; however, serum concentrations may also be decreased by facilitating gut dialysis via the enterohepatic and enteroenteric recirculation of digoxin (and other cardioactive corticosteroids). [35] [36]

• • •

Effective in first 6 to 8 hours post-ingestion. If severe toxicity, charcoal may be skipped and digoxin immune Fab given right away. Caution should be taken in patients who vomit or those with altered mental status. They are at risk of pulmonary aspiration when drinking the solution. Primary Options charcoal, activated : 1 g/kg orally as a single dose, repeat every 2-4 hours if required, maximum 4 doses total

plus [?]

supportive care

General supportive care includes attaching patients to a cardiac monitor, providing IV fluids in patients with hypotension or volume depletion (with caution for patients with CHF), supplemental oxygen, and/or repletion of electrolytes in patients with electrolyte abnormalities. Patients with hypokalaemia or hypomagnesaemia require additional potassium or magnesium with careful monitoring to restore normal serum levels.

with hypokalaemia

plus [?]

potassium replacement

Potassium should be given via cautious intravenous infusion to restore serum potassium to normal levels.

• •

Replacement should follow local hospital protocols. The serum potassium should be checked at intervals and therapy adjusted as needed.

Treatment Patient group acute ingestion, low to moderate toxicity line 1st Treatmenthide all

activated charcoal

The primary goal of activated charcoal is to decrease GI absorption of the drug; however, serum concentrations may also be decreased by facilitating gut dialysis via the enterohepatic and enteroenteric recirculation of digoxin (and other cardioactive corticosteroids). [35] [36]

• • •

Effective in first 6 to 8 hours post-ingestion. If severe toxicity, charcoal may be skipped and digoxin immune Fab given right away. Caution should be taken in patients who vomit or those with altered mental status. They are at risk of pulmonary aspiration when drinking the solution. Primary Options charcoal, activated : 1 g/kg orally as a single dose, repeat every 2-4 hours if required, maximum 4 doses total

plus [?]

supportive care

General supportive care includes attaching patients to a cardiac monitor, providing IV fluids in patients with hypotension or volume depletion (with caution for patients with CHF), supplemental oxygen, and/or repletion of electrolytes in patients with electrolyte abnormalities. Patients with hypokalaemia or hypomagnesaemia require additional potassium or magnesium with careful monitoring to restore normal serum levels.

with hypokalaemia

plus [?]

potassium replacement

Potassium should be given via cautious intravenous infusion to restore serum potassium to normal levels.

• •

Replacement should follow local hospital protocols. The serum potassium should be checked at intervals and therapy adjusted as needed.

Treatment Patient group acute ingestion, low to moderate toxicity line 1st Treatmenthide all

activated charcoal

The primary goal of activated charcoal is to decrease GI absorption of the drug; however, serum concentrations may also be decreased by facilitating gut dialysis via the enterohepatic and enteroenteric recirculation of digoxin (and other cardioactive corticosteroids). [35] [36]

• • •

Effective in first 6 to 8 hours post-ingestion. If severe toxicity, charcoal may be skipped and digoxin immune Fab given right away. Caution should be taken in patients who vomit or those with altered mental status. They are at risk of pulmonary aspiration when drinking the solution. Primary Options charcoal, activated : 1 g/kg orally as a single dose, repeat every 2-4 hours if required, maximum 4 doses total

plus [?]

supportive care

General supportive care includes attaching patients to a cardiac monitor, providing IV fluids in patients with hypotension or volume depletion (with caution for patients with CHF), supplemental oxygen, and/or repletion of electrolytes in patients with electrolyte abnormalities. Patients with hypokalaemia or hypomagnesaemia require additional potassium or magnesium with careful monitoring to restore normal serum levels.

with hypokalaemia

plus [?]

potassium replacement

Potassium should be given via cautious intravenous infusion to restore serum potassium to normal levels.

• •

Replacement should follow local hospital protocols. The serum potassium should be checked at intervals and therapy adjusted as needed.

Treatment Patient group acute ingestion, low to moderate toxicity line 1st Treatmenthide all

activated charcoal

The primary goal of activated charcoal is to decrease GI absorption of the drug; however, serum concentrations may also be decreased by facilitating gut dialysis via the enterohepatic and enteroenteric recirculation of digoxin (and other cardioactive corticosteroids). [35] [36]

• • •

Effective in first 6 to 8 hours post-ingestion. If severe toxicity, charcoal may be skipped and digoxin immune Fab given right away. Caution should be taken in patients who vomit or those with altered mental status. They are at risk of pulmonary aspiration when drinking the solution. Primary Options charcoal, activated : 1 g/kg orally as a single dose, repeat every 2-4 hours if required, maximum 4 doses total

plus [?]

supportive care

General supportive care includes attaching patients to a cardiac monitor, providing IV fluids in patients with hypotension or volume depletion (with caution for patients with CHF), supplemental oxygen, and/or repletion of electrolytes in patients with electrolyte abnormalities. Patients with hypokalaemia or hypomagnesaemia require additional potassium or magnesium with careful monitoring to restore normal serum levels.

with hypokalaemia

plus [?]

potassium replacement

Potassium should be given via cautious intravenous infusion to restore serum potassium to normal levels.

• •

Replacement should follow local hospital protocols. The serum potassium should be checked at intervals and therapy adjusted as needed.

Treatment Patient group acute ingestion, low to moderate toxicity line 1st Treatmenthide all

activated charcoal

The primary goal of activated charcoal is to decrease GI absorption of the drug; however, serum concentrations may also be decreased by facilitating gut dialysis via the enterohepatic and enteroenteric recirculation of digoxin (and other cardioactive corticosteroids). [35] [36]

• • •

Effective in first 6 to 8 hours post-ingestion. If severe toxicity, charcoal may be skipped and digoxin immune Fab given right away. Caution should be taken in patients who vomit or those with altered mental status. They are at risk of pulmonary aspiration when drinking the solution. Primary Options charcoal, activated : 1 g/kg orally as a single dose, repeat every 2-4 hours if required, maximum 4 doses total

plus [?]

supportive care

General supportive care includes attaching patients to a cardiac monitor, providing IV fluids in patients with hypotension or volume depletion (with caution for patients with CHF), supplemental oxygen, and/or repletion of electrolytes in patients with electrolyte abnormalities. Patients with hypokalaemia or hypomagnesaemia require additional potassium or magnesium with careful monitoring to restore normal serum levels.

with hypokalaemia

plus [?]

potassium replacement

Potassium should be given via cautious intravenous infusion to restore serum potassium to normal levels.

• •

Replacement should follow local hospital protocols. The serum potassium should be checked at intervals and therapy adjusted as needed.

Treatment Patient group acute ingestion, low to moderate toxicity line 1st Treatmenthide all

activated charcoal

The primary goal of activated charcoal is to decrease GI absorption of the drug; however, serum concentrations may also be decreased by facilitating gut dialysis via the enterohepatic and enteroenteric recirculation of digoxin (and other cardioactive corticosteroids). [35] [36]

• • •

Effective in first 6 to 8 hours post-ingestion. If severe toxicity, charcoal may be skipped and digoxin immune Fab given right away. Caution should be taken in patients who vomit or those with altered mental status. They are at risk of pulmonary aspiration when drinking the solution. Primary Options charcoal, activated : 1 g/kg orally as a single dose, repeat every 2-4 hours if required, maximum 4 doses total

plus [?]

supportive care

General supportive care includes attaching patients to a cardiac monitor, providing IV fluids in patients with hypotension or volume depletion (with caution for patients with CHF), supplemental oxygen, and/or repletion of electrolytes in patients with electrolyte abnormalities. Patients with hypokalaemia or hypomagnesaemia require additional potassium or magnesium with careful monitoring to restore normal serum levels.

with hypokalaemia

plus [?]

potassium replacement

Potassium should be given via cautious intravenous infusion to restore serum potassium to normal levels.

• •

Replacement should follow local hospital protocols. The serum potassium should be checked at intervals and therapy adjusted as needed.

Treatment Patient group acute ingestion, low to moderate toxicity line 1st Treatmenthide all

activated charcoal

The primary goal of activated charcoal is to decrease GI absorption of the drug; however, serum concentrations may also be decreased by facilitating gut dialysis via the enterohepatic and enteroenteric recirculation of digoxin (and other cardioactive corticosteroids). [35] [36]

• • •

Effective in first 6 to 8 hours post-ingestion. If severe toxicity, charcoal may be skipped and digoxin immune Fab given right away. Caution should be taken in patients who vomit or those with altered mental status. They are at risk of pulmonary aspiration when drinking the solution. Primary Options charcoal, activated : 1 g/kg orally as a single dose, repeat every 2-4 hours if required, maximum 4 doses total

plus [?]

supportive care

General supportive care includes attaching patients to a cardiac monitor, providing IV fluids in patients with hypotension or volume depletion (with caution for patients with CHF), supplemental oxygen, and/or repletion of electrolytes in patients with electrolyte abnormalities. Patients with hypokalaemia or hypomagnesaemia require additional potassium or magnesium with careful monitoring to restore normal serum levels.

with hypokalaemia

plus [?]

potassium replacement

Potassium should be given via cautious intravenous infusion to restore serum potassium to normal levels.

• •

Replacement should follow local hospital protocols. The serum potassium should be checked at intervals and therapy adjusted as needed.

Treatment Patient group acute ingestion, low to moderate toxicity line 1st Treatmenthide all

activated charcoal

The primary goal of activated charcoal is to decrease GI absorption of the drug; however, serum concentrations may also be decreased by facilitating gut dialysis via the enterohepatic and enteroenteric recirculation of digoxin (and other cardioactive corticosteroids). [35] [36]

• • •

Effective in first 6 to 8 hours post-ingestion. If severe toxicity, charcoal may be skipped and digoxin immune Fab given right away. Caution should be taken in patients who vomit or those with altered mental status. They are at risk of pulmonary aspiration when drinking the solution. Primary Options charcoal, activated : 1 g/kg orally as a single dose, repeat every 2-4 hours if required, maximum 4 doses total

plus [?]

supportive care

General supportive care includes attaching patients to a cardiac monitor, providing IV fluids in patients with hypotension or volume depletion (with caution for patients with CHF), supplemental oxygen, and/or repletion of electrolytes in patients with electrolyte abnormalities. Patients with hypokalaemia or hypomagnesaemia require additional potassium or magnesium with careful monitoring to restore normal serum levels.

with hypokalaemia

plus [?]

potassium replacement

Potassium should be given via cautious intravenous infusion to restore serum potassium to normal levels.

• •

Replacement should follow local hospital protocols. The serum potassium should be checked at intervals and therapy adjusted as needed.

Treatment Patient group acute ingestion, low to moderate toxicity line 1st Treatmenthide all

activated charcoal

The primary goal of activated charcoal is to decrease GI absorption of the drug; however, serum concentrations may also be decreased by facilitating gut dialysis via the enterohepatic and enteroenteric recirculation of digoxin (and other cardioactive corticosteroids). [35] [36]

• • •

Effective in first 6 to 8 hours post-ingestion. If severe toxicity, charcoal may be skipped and digoxin immune Fab given right away. Caution should be taken in patients who vomit or those with altered mental status. They are at risk of pulmonary aspiration when drinking the solution. Primary Options charcoal, activated : 1 g/kg orally as a single dose, repeat every 2-4 hours if required, maximum 4 doses total

plus [?]

supportive care

General supportive care includes attaching patients to a cardiac monitor, providing IV fluids in patients with hypotension or volume depletion (with caution for patients with CHF), supplemental oxygen, and/or repletion of electrolytes in patients with electrolyte abnormalities. Patients with hypokalaemia or hypomagnesaemia require additional potassium or magnesium with careful monitoring to restore normal serum levels.

with hypokalaemia

plus [?]

potassium replacement

Potassium should be given via cautious intravenous infusion to restore serum potassium to normal levels.

• •

Replacement should follow local hospital protocols. The serum potassium should be checked at intervals and therapy adjusted as needed.

Treatment Patient group acute ingestion, low to moderate toxicity line 1st Treatmenthide all

activated charcoal

The primary goal of activated charcoal is to decrease GI absorption of the drug; however, serum concentrations may also be decreased by facilitating gut dialysis via the enterohepatic and enteroenteric recirculation of digoxin (and other cardioactive corticosteroids). [35] [36]

• • •

Effective in first 6 to 8 hours post-ingestion. If severe toxicity, charcoal may be skipped and digoxin immune Fab given right away. Caution should be taken in patients who vomit or those with altered mental status. They are at risk of pulmonary aspiration when drinking the solution. Primary Options charcoal, activated : 1 g/kg orally as a single dose, repeat every 2-4 hours if required, maximum 4 doses total

plus [?]

supportive care

General supportive care includes attaching patients to a cardiac monitor, providing IV fluids in patients with hypotension or volume depletion (with caution for patients with CHF), supplemental oxygen, and/or repletion of electrolytes in patients with electrolyte abnormalities. Patients with hypokalaemia or hypomagnesaemia require additional potassium or magnesium with careful monitoring to restore normal serum levels.

with hypokalaemia

plus [?]

potassium replacement

Potassium should be given via cautious intravenous infusion to restore serum potassium to normal levels.

• •

Replacement should follow local hospital protocols. The serum potassium should be checked at intervals and therapy adjusted as needed.

Treatment Patient group acute ingestion, low to moderate toxicity line 1st Treatmenthide all

activated charcoal

The primary goal of activated charcoal is to decrease GI absorption of the drug; however, serum concentrations may also be decreased by facilitating gut dialysis via the enterohepatic and enteroenteric recirculation of digoxin (and other cardioactive corticosteroids). [35] [36]

• • •

Effective in first 6 to 8 hours post-ingestion. If severe toxicity, charcoal may be skipped and digoxin immune Fab given right away. Caution should be taken in patients who vomit or those with altered mental status. They are at risk of pulmonary aspiration when drinking the solution. Primary Options charcoal, activated : 1 g/kg orally as a single dose, repeat every 2-4 hours if required, maximum 4 doses total

plus [?]

supportive care

General supportive care includes attaching patients to a cardiac monitor, providing IV fluids in patients with hypotension or volume depletion (with caution for patients with CHF), supplemental oxygen, and/or repletion of electrolytes in patients with electrolyte abnormalities. Patients with hypokalaemia or hypomagnesaemia require additional potassium or magnesium with careful monitoring to restore normal serum levels.

with hypokalaemia

plus [?]

potassium replacement

Potassium should be given via cautious intravenous infusion to restore serum potassium to normal levels.

• •

Replacement should follow local hospital protocols. The serum potassium should be checked at intervals and therapy adjusted as needed.

Treatment approach
The main goal of treatment is to correct cardiac toxicity. Treatment of cardiac toxicity usually leads to resolution of CNS and GI symptoms. Initial treatment includes:
• • • • • General supportive care Discontinuation of digoxin therapy and prevention of further exposure Prevention of further GI absorption Administration of digoxin-specific antibody fragments (digoxin immune Fab) Treatment of specific complications: for example, dysrhythmias and electrolyte abnormalities.

Therapy of chronic toxicity is based on a clinical syndrome, not the serum digoxin concentration (SDC), which might be just above the therapeutic range. If an SDC cannot be obtained, patients are managed based on their presentation, ECG findings, and laboratory results. If toxicity is suspected and the patient is unstable, antidotal therapy is administered prior to confirmatory results. For patients with chronic digitalis poisoning, therapy may require only a few Fab vials. There is no change in therapy for renal failure other than to note that the elimination half-life of digoxin is prolonged in patients with renal failure.

Supportive care
General supportive care includes attaching patients to a cardiac monitor, providing IV fluids in patients with hypotension or volume depletion (with caution for patients with CHF), supplemental oxygen, and/or repletion of electrolytes in patients with electrolyte abnormalities.

Digoxin binding therapy
Digoxin binding (with digoxin immune Fab) is used in patients with the following features:
• • • Severe toxicity or haemodynamic compromise Symptomatic bradyarrhythmias Ventricular dysrhythmias

• • • • state) •

Any patient with digoxin overdose and potassium concentrations >5.0 millimol/L (>5.0 mEq/L) Acute ingestion of >4 mg in a healthy child (or 0.1 mg/kg) Acute ingestion of >10 mg in a healthy adult Serum concentration of ≥12.8 nanomol/L ( ≥10 nanograms/mL) 4 to 6 hours after ingestion (steady

Serum concentration of ≥19.2 nanomol/L (≥15 nanograms/mL) at any time.

If indicated; 15 vials of Fab is the quantity typically needed to treat one patient. [26] Patients who receive digoxin immune Fab have a drop in the serum potassium as it moves intracellularly.[27] [28] [29] Some patients who have been treated for hyperkalaemia and who have also received digoxin immune Fab develop profound hypokalaemia. Therefore, serial potassium measurements are made when patients receive both digoxin immune Fab and other therapies to decrease potassium. After administration of digoxin immune Fab, serum digoxin concentrations (SDC) are usually falsely elevated (10- to 30-fold). SDC can be measured again 3 to 4 days after dose is given,[30] [31] [32] but has been reported to be elevated for up to 10 days, especially in patients with renal insufficiency. [31]

Electrolyte abnormality management
In patients with chronic digoxin toxicity, hyperkalaemia is only corrected (e.g., with insulin/glucose) if it is considered life-threatening, because of the risk of producing hypokalaemia. One study showed that insulin interacts directly with Na(+)/K(+) ATPase pump and alters the effect of digoxin. [33] This supports the finding that for patients with diabetes, insulin has been shown to have cardioprotective effects after digoxin intoxication. Calcium is not used to treat hyperkalaemia in patients with suspected digoxin toxicity as it may induce arrhythmia or cardiac arrest. Patients with acute digoxin toxicity and serum potassium concentrations ≥5.0 millimol/L (≥5.0 mEq/L) are treated with digoxin immune Fab; those with hyperkalaemia have high mortality rates. Patients with hypokalaemia or hypomagnesaemia require additional potassium or magnesium with careful monitoring to restore normal serum levels.

Calcium is not used to treat hyperkalaemia in patients with suspected digoxin toxicity as it may induce arrhythmia or cardiac arrest.

GI decontamination
There is a role for GI decontamination with activated charcoal in patients with an acute ingestion of digoxin with low to moderate toxicity. [34] [35] [36] The primary goal of activated charcoal is to decrease GI absorption of the drug. [35] [36]

Bradycardia management
Adult patients with symptomatic bradycardia are treated with atropine. Atropine can be given every 3 to 5 minutes until there is a response or the 3 mg maximum dose is reached. Paediatric patients with symptomatic bradycardia require lower doses of atropine.

Tachyarrhythmia management
Type IB anti-arrhythmics (e.g., phenytoin, lidocaine) can be used if digoxin immune Fab is unavailable or is being prepared and patients have rapid ventricular dysrhythmias unresponsive to supportive measures. Transthoracic electrical cardioversion for atrial tachyarrhythmias is associated with the development of lethal ventricular dysrhythmias, so is not used. [37] Overdrive suppression with a trans-venous pacemaker is also avoided because of associated iatrogenic complications that have been seen in as many as 36% of patients. [38] [39] Patients with ventricular fibrillation or pulseless ventricular tachycardia require defibrillation along with immunotherapy.

Haemodynamic compromise management
In patients with signs of haemodynamic insufficiency and/or compromise (e.g., hypotension, altered consciousness), digoxin immune Fab is given as primary management. As a bridge to the administration of digoxin immune Fab, intravenous fluids and direct-acting pressors (e.g., phenylephrine, norepinephrine) are used. Cardiac contractility (inotropy) is typically preserved in patients with digoxin toxicity.

Ongoing monitoring and change of medicine

Ideally, digoxin is discontinued and a different medicine for rate control or a different inotrope prescribed (for AF, atrial flutter or CHF, respectively). If the patient has to remain on digoxin for some reason, then the dose of digoxin is adjusted for the patient's medication profile. GFR and SDC is monitored regularly (every 2 to 4 weeks).

Monitoring
After administration of digoxin immune Fab, serum digoxin concentrations (SDC) are usually falsely elevated (10- to 30-fold). SDC can be measured again 3 to 4 days after dose is given[30] [31] [32] but has been reported to be elevated for up to 10 days, especially in patients with renal insufficiency. [31]

Patient Instructions
If a patient suspects that they have overdosed on their medication, they should seek urgent medical attention. Patients should also beware inadvertent overdose of cardiac glycosides, which can result from herbal remedies or plant ingestion, and to consult their physician prior to initiating such regimens.

Complications
Complicationhide all

anaphylactoid (anaphylaxis-like) reaction to digoxin immune Fab see our comprehensive coverage of Anaphylaxis This is usually a rate-related phenomenon associated with the infusion of Fab minutes after infusion is started. A membrane filter will reduce the risk of a reaction. If reaction occurs, infusion needs to be stopped and restarted at a slower rate. recurrence of previous underlying AF or heart failure after digoxin immune Fab therapy AF occurs at a median of 7 days after therapy with Fab, affecting about 2% of treated patients in one study. [44]Patients who have been treated with Fab are monitored for development of uncontrolled AF or worsening heart failure and given additional treatment as required. cardiac arrest see our comprehensive coverage of Cardiac arrest There have been reported cases of patients who had cardiac arrest with prolonged resuscitation who received digoxin immune Fab after the arrest and recovered. [29]

Prognosis
The prognosis for patients who are treated appropriately is very good. Patients generally have no long-term adverse outcomes related to their toxicity from digoxin. [27] [43] Patients who present with acute digoxin toxicity and have serum potassium concentrations of ≥5.0 millimol/L (≥5.0 mEq/L), who remain untreated and/or undiagnosed, have a mortality of 50%. [38]Patients who present with chronic digoxin toxicity and remain undiagnosed and/or untreated have a reported mortality of 5% to 13%. [4]

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