A young female comes to the emergency department after consuming 100 aspirin tablets. What should be the next step in management?

Explanation

## Correct Answer: B. Give sodium bicarbonate to alkalize urine Acute aspirin overdose presents with a complex toxidrome dominated by **salicylate toxicity**. The pathophysiology involves uncoupling of oxidative phosphorylation, leading to metabolic acidosis, respiratory alkalosis, hyperthermia, and altered mental status. Salicylates are weak acids that undergo renal reabsorption in acidic urine—the key discriminator for management. Alkalizing the urine with **sodium bicarbonate** increases urinary pH to 7.5–8.5, which ionizes salicylates in the renal tubule and prevents their reabsorption, dramatically increasing renal clearance (from ~2–3 mL/min to 10–20 mL/min). This is the cornerstone of salicylate elimination in moderate-to-severe poisoning. Sodium bicarbonate also corrects the underlying metabolic acidosis, which itself worsens salicylate toxicity by promoting CNS penetration. In Indian clinical practice (per AIIMS and PGIMER protocols), urine alkalinization is the first-line pharmacological intervention for salicylate overdose, often combined with supportive care, fluid resuscitation, and monitoring of serum salicylate levels. Hemodialysis is reserved for severe cases with levels >100 mg/dL or CNS involvement. ## Why the other options are wrong **A. Pralidoxime** — Pralidoxime is an **acetylcholinesterase reactivator** used exclusively in **organophosphate and carbamate poisoning** to restore cholinesterase activity. Aspirin toxicity does not involve cholinergic mechanisms; salicylates cause uncoupling of oxidative phosphorylation and acid-base disturbances. Pralidoxime has no role in salicylate management. This is a classic NBE trap pairing antidotes with wrong toxins. **C. N-acetyl cysteine to replenish glutathione stores** — N-acetyl cysteine (NAC) is the **antidote for acetaminophen overdose**, where it replenishes hepatic glutathione depleted by toxic metabolite NAPQI. Aspirin does not deplete glutathione stores or cause the same hepatotoxic mechanism as acetaminophen. While aspirin can cause hepatotoxicity at very high doses, NAC is not indicated and does not address the primary pathophysiology of salicylate toxicity (uncoupling and acid-base disturbance). **D. Glucagon to control bradycardia and hypoglycemia** — Glucagon is used in **beta-blocker and calcium channel blocker overdoses** to increase heart rate and blood glucose. Salicylate toxicity causes **tachycardia and hyperglycemia** (from uncoupling and catecholamine release), not bradycardia or hypoglycemia. Glucagon is inappropriate and does not address the core management of salicylate elimination or acid-base correction. ## High-Yield Facts - **Salicylate toxicity** uncouples oxidative phosphorylation, causing metabolic acidosis + respiratory alkalosis + hyperthermia (classic triad). - **Urine alkalinization with sodium bicarbonate** (target pH 7.5–8.5) increases salicylate ionization and renal clearance 5–10 fold, making it the DOC for moderate-to-severe poisoning. - **Serum salicylate levels >100 mg/dL** or CNS symptoms (altered mental status, pulmonary edema) mandate **hemodialysis** as salicylates are water-soluble and dialyzable. - **Metabolic acidosis worsens salicylate toxicity** by promoting CNS penetration; bicarbonate corrects both the acid-base disorder and enhances renal elimination. - **Salicylates are weak acids** (pKa ~3) that undergo renal reabsorption in acidic urine; alkaline urine traps them as ionized salicylate anions, preventing reabsorption. ## Mnemonics **SALICYLATE TOXICITY TRIAD** **M**etabolic acidosis + **R**espiratory alkalosis + **H**yperthermia = MRH. Remember: salicylates uncouple mitochondria → heat + acid production, but respiratory drive increases → blows off CO₂ → respiratory alkalosis paradoxically coexists with metabolic acidosis. **ANTIDOTE PAIRING (Indian coaching shortcut)** **Aspirin** → Bicarb (urine alkalization) | **Acetaminophen** → NAC (glutathione) | **Organophosphate** → Pralidoxime (AChE reactivation). Use this to eliminate wrong antidotes in 3 seconds. ## NBE Trap NBE pairs salicylate overdose with unrelated antidotes (pralidoxime, NAC, glucagon) to test whether students know the specific mechanism of salicylate toxicity (uncoupling + acid-base disturbance) versus memorizing antidote names. The trap exploits confusion between aspirin, acetaminophen, and organophosphate poisonings. ## Clinical Pearl In Indian emergency departments, a young patient presenting with altered mental status, tachypnea, and hyperthermia after aspirin ingestion should trigger immediate serum salicylate level and arterial blood gas. Urine alkalinization with sodium bicarbonate (1–2 mEq/kg IV bolus, then infusion to maintain urine pH >7.5) is started empirically while awaiting levels—delays in alkalinization increase mortality risk in severe poisoning. _Reference: KD Tripathi Pharmacology Ch. 13 (Autacoids & NSAIDs); Harrison Ch. 474 (Poisoning & Drug Overdose)_