Question:
A child presents with tachypnea, vomiting, and altered sensorium after accidentally ingesting a drug used by his father. Labs show respiratory alkalosis and hyperglycemia. Which of the following is most likely the ingested drug?
A child presents with tachypnea, vomiting, and altered sensorium after accidentally ingesting a drug used by his father. Labs show respiratory alkalosis and hyperglycemia. Which of the following is most likely the ingested drug?
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Salicylate (Aspirin) poisoning key findings: Hyperventilation + Tinnitus + Mixed Respiratory Alkalosis and High Anion Gap Metabolic Acidosis. Treatment includes urinary alkalinization with IV sodium bicarbonate!
Updated On: Sep 3, 2026
- Methylxanthine
- TCA
- Iron
- Aspirin
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The Correct Option is D
Solution and Explanation
Concept:
Salicylate (aspirin) toxicity is a classic, complex poisoning presenting with a hallmark biphasic or mixed acid-base disturbance and characteristic metabolic derangements.
It directly stimulates the central respiratory center while simultaneously uncoupling oxidative phosphorylation in cellular mitochondria.
Explanation:
• Direct stimulation of the medullary respiratory center by salicylates leads to hyperventilation, causing marked tachypnea, hyperpnea, and an early primary respiratory alkalosis.
• Concurrently, salicylates uncouple mitochondrial oxidative phosphorylation and inhibit Krebs cycle dehydrogenases, resulting in cellular anaerobic metabolism, accumulation of lactic acid, and ketoacids, which drives a high anion gap metabolic acidosis.
• In older children and adults, the classic hallmark is a mixed primary respiratory alkalosis and primary metabolic acidosis. In toddlers, metabolic acidosis may dominate early.
• Metabolic derangements include hyperglycemia (early, due to catecholamine-induced glycogenolysis) or profound neuroglycopenia/hypoglycemia.
• Iron toxicity presents with severe hemorrhagic gastroenteritis, shock, and high anion gap metabolic acidosis, but not primary respiratory alkalosis.
• Tricyclic antidepressants (TCAs) cause anticholinergic toxidrome, sedation, respiratory depression (respiratory acidosis), and QRS widening on ECG.
Final Answer:
The classic clinical picture of tachypnea, vomiting, altered sensorium, primary respiratory alkalosis, and hyperglycemia following ingestion is indicative of Aspirin (salicylate) toxicity.
Salicylate (aspirin) toxicity is a classic, complex poisoning presenting with a hallmark biphasic or mixed acid-base disturbance and characteristic metabolic derangements.
It directly stimulates the central respiratory center while simultaneously uncoupling oxidative phosphorylation in cellular mitochondria.
Explanation:
• Direct stimulation of the medullary respiratory center by salicylates leads to hyperventilation, causing marked tachypnea, hyperpnea, and an early primary respiratory alkalosis.
• Concurrently, salicylates uncouple mitochondrial oxidative phosphorylation and inhibit Krebs cycle dehydrogenases, resulting in cellular anaerobic metabolism, accumulation of lactic acid, and ketoacids, which drives a high anion gap metabolic acidosis.
• In older children and adults, the classic hallmark is a mixed primary respiratory alkalosis and primary metabolic acidosis. In toddlers, metabolic acidosis may dominate early.
• Metabolic derangements include hyperglycemia (early, due to catecholamine-induced glycogenolysis) or profound neuroglycopenia/hypoglycemia.
• Iron toxicity presents with severe hemorrhagic gastroenteritis, shock, and high anion gap metabolic acidosis, but not primary respiratory alkalosis.
• Tricyclic antidepressants (TCAs) cause anticholinergic toxidrome, sedation, respiratory depression (respiratory acidosis), and QRS widening on ECG.
Final Answer:
The classic clinical picture of tachypnea, vomiting, altered sensorium, primary respiratory alkalosis, and hyperglycemia following ingestion is indicative of Aspirin (salicylate) toxicity.
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