0071643192.pdf

TOXICOLOGY

Toxicity may be either acute or chronic:

■ Acute toxicity

■ Results from an acute ingestion (eg, children or suicidal)

■ Tends to cause severe Na+K+ATPase pump malfunction →hyperkalemia

■ Hyperkalemia in acute toxicity is a predictor of poor outcome.

■ Chronic toxicity

■ Results from an increase in dose or decrease in renal excretion of

digoxin in a patient on chronic therapy

■ Hypokalemia may enhance chronic toxicity →toxicity at lower digoxin

levels.

■ Has a higher overall mortality (sicker patient population at baseline)

SYMPTOMS/EXAM

■ Onset of symptoms is often insidious in chronic toxicity

■ Nausea/vomiting, anorexia

■ Visual disturbances (eg, scotomata, yellow halos around lights)

■ Mental status changes

■ Headaches, generalized weakness

■ Dysrhythmias: Virtuallyanydysrhythmia is possible.

■ PVCs (most common ECG finding)

■ Bradycardia

■ Atrial tachycardia with block

■ Slow atrial fibrillation

■ Bidirectional ventricular tachycardia (fairly specific).

■ Acute toxicity →more bradycardia and blocks.

■ Chronic toxicity →ventricular dysrhythmias more common.

DIAGNOSIS

■ Usually obvious from patient’s history and presentation

■ Serum digoxin levels: May not correlate with symptoms and may take

6–12 hours to reach steady state in acute ingestion

■ Potassium and renal function monitoring are essential.

TREATMENT

■ Supportive therapy

■ Activated charcoal (with airway protection, as needed)

■ Hyperkalemia: Treat in the normal manner, but calcium should be

avoided.

■ Hypokalemia in chronic toxicity: Replete if <4.0 mEq/dL.

■ Bradycardias

■ Treat with atropine and/or pacing.

■ Tachydysrhythmias

■ Cardioversion and defibrillation may induce VT/Vfib.

■ Phenytoin and lidocaine are felt to be safest drugs.

■ Phenytoin can increase AV nodal conduction.

■ Antidote = digoxin-specific antibodies (see Table 6.15 for indications).

■ Acute = 10 vials

■ Chronic = 5 vials

Angiotensin-Converting Enzyme Inhibitors and Angiotensin

Receptor Blockers

Both are prescribed for the treatment of HTN and CHF. ACE-I are also used

post-MI and for diabetic nephropathy.

Hypokalemia in a patient on

chronic digoxin therapy may

lead to toxicity at lower

digoxin levels.

Bidirectional VT is fairly

specific for cardiac glycoside

toxicity.

Calcium may precipitate fatal

cardiovascular collapse if

given in digoxin toxicity.

Hyperkalemia in acute digoxin

toxicity is a predictor of poor

outcome.