Correct Answer: B. Deferoxamine
Ferrous sulphate (iron) overdose causes severe toxicity through free radical formation and direct cellular injury, manifesting as metabolic acidosis in the systemic phase. Deferoxamine is the specific iron chelator of choice in iron poisoning management. It binds ferric iron (Fe³⁺) with extremely high affinity, forming a stable ferrioxamine complex that is water-soluble and readily excreted in urine, preventing iron-mediated lipid peroxidation and organ damage. The presence of acidosis indicates progression to the systemic phase, where deferoxamine becomes critical. In India, deferoxamine is the standard DOC for iron toxicity as per poison control guidelines and is administered intravenously (50 mg/kg/dose) in symptomatic cases or when serum iron levels exceed the iron-binding capacity of transferrin. The drug effectively reduces free iron concentration and halts the cascade of oxidative injury affecting the liver, heart, and CNS. Activated charcoal is ineffective for iron (a metal), and other chelators like dimercaprol and penicillamine are not indicated for iron poisoning.
Why the other options are wrong
A. Dimercaprol — Dimercaprol (BAL) is a chelator used for heavy metal poisoning (arsenic, mercury, lead) but is NOT indicated for iron toxicity. It has no affinity for iron and may actually increase iron absorption in the GI tract. NBE may trap students who confuse all chelators as interchangeable agents. C. Activated charcoal — Activated charcoal is ineffective for iron poisoning because iron is a metal and does not bind to charcoal. While charcoal is useful for organic toxins (drugs, pesticides), it plays no role in iron overdose management. This is a classic NBE distractor for students who default to charcoal for 'any' poisoning. D. Penicillamine — Penicillamine is a chelator used for copper toxicity (Wilson's disease) and heavy metals like lead and mercury, but it is NOT the agent of choice for iron poisoning. Deferoxamine is far superior due to its specific high-affinity binding to iron and rapid ferrioxamine excretion.
High-Yield Facts
- Deferoxamine is the specific iron chelator; binds Fe³⁺ with extremely high affinity and forms water-soluble ferrioxamine excreted in urine.
- Metabolic acidosis in iron poisoning indicates systemic phase; deferoxamine must be started urgently to prevent multi-organ failure.
- Activated charcoal is ineffective for iron (a metal); GI decontamination relies on gastric lavage or whole-bowel irrigation with polyethylene glycol.
- Deferoxamine dose: 50 mg/kg IV in symptomatic cases or when serum iron exceeds iron-binding capacity of transferrin (TIBC).
- Ferrioxamine in urine (vin rosé or orange discoloration) is a clinical sign of adequate chelation and iron excretion.
Mnemonics
Iron Chelator = DeFeroxamine Deferoxamine for Deferring iron toxicity. Remember: 'De' = iron removal. Use when you see ferrous sulphate OD + acidosis. Chelator Match-Up BAL (Dimercaprol) → As, Hg, Pb | Penicillamine → Cu (Wilson's) | Deferoxamine → Fe | EDTA → Pb, Ca. Each has its metal.
NBE Trap
NBE pairs iron poisoning with 'activated charcoal' to trap students who memorize charcoal as a universal antidote without understanding that metals do not bind charcoal. The presence of acidosis is a red herring meant to distract from the core principle: deferoxamine is the only specific iron chelator.
Clinical Pearl
In Indian emergency departments, ferrous sulphate overdose is common in children due to easy access as an OTC iron supplement. The appearance of vin rosé (wine-colored) urine after deferoxamine administration is a reassuring sign of active iron chelation and should prompt continuation of therapy. Acidosis signals systemic toxicity—delay in deferoxamine administration increases mortality risk.
_Reference: KD Tripathi Pharmacology Ch. 61 (Antidotes & Chelating Agents); Harrison Principles of Internal Medicine Ch. 474 (Poisoning & Drug Overdose)_