Which medication toxicity presents with vomiting, bradycardia, anorexia, and dysrhythmias in a child?

Which medication toxicity presents with vomiting, bradycardia, anorexia, and dysrhythmias in a child?

• A. Digoxin
• B. Nesiritide
• C. Dobutamine
• D. Spironolactone

Answer: (A)

Recognizing digoxin toxicity. The combination of vomiting and anorexia in a child is a classic early sign of digoxin-related GI upset, while bradycardia and dysrhythmias reflect its effects on the heart’s conduction system. Digoxin inhibits the Na+/K+-ATPase pump, which raises intracellular calcium in cardiac cells and enhances vagal tone. The increased calcium makes the heart more contractile, but the altered conduction and increased automaticity can set up a range of arrhythmias, and the higher vagal influence commonly slows the heart rate, producing bradycardia. In kids, these GI symptoms plus a slow pulse or abnormal rhythms signal digoxin toxicity, especially if there are factors that raise the drug’s level, like kidney issues or interactions that lower potassium (hypokalemia from diuretics can worsen toxicity). If toxicity is suspected, check the serum digoxin level and electrolytes, and treat based on severity. Life-threatening or high-level toxicity is treated with digoxin-specific antibody fragments to neutralize the drug, along with supportive care and careful electrolyte management. Calcium administration is generally avoided in acute toxicity because it can worsen toxicity and precipitate arrhythmias. In milder cases, stopping digoxin and monitoring the patient may be appropriate. This symptom pattern is most strongly associated with digoxin toxicity.

Recognizing digoxin toxicity. The combination of vomiting and anorexia in a child is a classic early sign of digoxin-related GI upset, while bradycardia and dysrhythmias reflect its effects on the heart’s conduction system. Digoxin inhibits the Na+/K+-ATPase pump, which raises intracellular calcium in cardiac cells and enhances vagal tone. The increased calcium makes the heart more contractile, but the altered conduction and increased automaticity can set up a range of arrhythmias, and the higher vagal influence commonly slows the heart rate, producing bradycardia. In kids, these GI symptoms plus a slow pulse or abnormal rhythms signal digoxin toxicity, especially if there are factors that raise the drug’s level, like kidney issues or interactions that lower potassium (hypokalemia from diuretics can worsen toxicity).

If toxicity is suspected, check the serum digoxin level and electrolytes, and treat based on severity. Life-threatening or high-level toxicity is treated with digoxin-specific antibody fragments to neutralize the drug, along with supportive care and careful electrolyte management. Calcium administration is generally avoided in acute toxicity because it can worsen toxicity and precipitate arrhythmias. In milder cases, stopping digoxin and monitoring the patient may be appropriate. This symptom pattern is most strongly associated with digoxin toxicity.