Digitalis Toxicity Clinical Presentation
- Author: Vinod Patel, MD; Chief Editor: Jeffrey N Rottman, MD more...
History
Most cases of pediatric digitalis poisoning are unintentional ingestions; thus, a good social history with emphasis on available medications and the extent of home childproofing is necessary.
Extracardiac symptoms
CNS symptoms include the following:
- Drowsiness
- Lethargy
- Fatigue
- Neuralgia
- Headache
- Dizziness,
- Confusion or giddiness
- Hallucinations
- Seizures (rare)
- Paresthesias and neuropathic pain
Visual aberration often is an early indication of digitalis toxicity. Yellow-green distortion is most common, but red, brown, blue, and white also occur. Drug intoxication also may cause snowy vision, photophobia, photopsia, decreased visual acuity, yellow halos around lights (xanthopsia), and transient amblyopia or scotomata.
Gastrointestinal (GI) symptoms in acute or chronic toxicity include the following:
- Anorexia
- Weight loss
- Failure to thrive (in pediatric patients)
- Nausea
- Vomiting
- Abdominal pain
- Diarrhea
- Mesenteric ischemia - A rare complication of rapid IV infusion
Cardiac symptoms
Cardiac symptoms include the following:
- Palpitations
- Shortness of breath
- Syncope
- Swelling of lower extremities
- Bradycardia
- Hypotension
- Dyspnea
The recent addition of a new drug, such as verapamil, diltiazem, erythromycin, tetracycline, or paroxetine, should be noted because these drugs can elevate the digoxin level. Rifampin increases digitalis metabolism by enzymatic stimulation and thereby decreases the digoxin level.
Physical Examination
Patients can have an asymptomatic period of from several minutes to several hours after the oral administration of a single toxic dose. Clinical signs may be subtle or obvious, depending on the severity of toxicity. Acute toxicity is rarely subtle, and chronic toxicity may be difficult to diagnose. Nausea, vomiting, and drowsiness are among the most common extracardiac manifestations. Visual changes usually affect patients with chronic toxicity. Emphasis should be placed on the vital signs and the neurologic and cardiovascular findings.
General symptoms
The patient's mentation may change according to the severity of digoxin toxicity, as well as associated comorbid conditions. Visual changes occur, but the pupils are spared, and objective findings are few. Drug-induced fever does not occur.
Vital signs
The pulse may be irregular, depending on arrhythmias secondary to atrial fibrillation or arising from the digoxin toxicity itself. Hypotension may be observed if the patient has CHF or dehydration secondary to decreased oral intake.
Neck findings
Symptoms include increased jugular venous pressure.
Cardiovascular symptoms
Digoxin toxicity may cause any dysrhythmia. Classically, dysrhythmias associated with increased automaticity and decreased AV conduction occur (ie, paroxysmal atrial tachycardia with 2:1 block, accelerated junctional rhythm, or bidirectional ventricular tachycardia [torsade de pointes], depicted in the images below).
Bidirectional tachycardia in a patient with digitalis toxicity.
Bidirectional tachycardia in a patient with digitalis toxicity. Hemodynamic instability is related directly to the presence of a dysrhythmia or to acute CHF. Associated cardiomegaly may be identified. Cardiovascular findings on physical examination relate to the severity of CHF, dysrhythmias, or hemodynamic instability.
Premature ventricular contractions (PVCs) are the most common dysrhythmia. Bigeminy or trigeminy occurs frequently.
Sinus bradycardia and other bradyarrhythmias are very common. Slow atrial fibrillation with very little variation in the ventricular rate (regularization of the R-R interval) may occur. First-, second-, and third-degree heart block and complete AV dissociation are also very common, while rapid atrial fibrillation and atrial flutter are rare.
Ventricular tachycardia is an especially serious finding. Cardiac arrest from asystole or ventricular fibrillation is usually fatal.
Respiratory symptoms
The respiratory rate is sometimes increased. Basal crepitations are associated with CHF.
GI symptoms
GI symptoms are common, but the abdominal examination is usually nonspecific. An enlarged liver occurs secondary to CHF (ie, hepatic congestion). Hepatojugular reflux is present.
Neurologic symptoms
Neurologic findings are related to changes in sensorium or mental status. Lateralizing findings usually indicate another disease process.
Findings in the extremities
Pedal edema is noted if the patient has renal failure or decompensated CHF.
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