Iron, salicylate and toxic alcohol poisoning — formative SAQs

1. Elemental-iron dose and severity

Ferrous sulphate 325 mg contains 65 mg elemental iron, so eight tablets equal 520 mg elemental. In a 12 kg child this is about 43 mg per kg of elemental iron. This is a SIGNIFICANT ingestion (over 40 mg per kg): emergency department assessment, serum iron, whole-bowel irrigation and consideration of intravenous desferrioxamine. The dose must be calculated from the elemental iron content, not the salt weight. [1] [2]

2. Investigations and timing

Take bloods BEFORE any antidote: serum iron, venous gas, electrolytes and anion gap, glucose, full blood count, coagulation, LFTs and renal function, plus a paracetamol and salicylate level to exclude co-ingestion. Draw the serum iron at 4 to 6 hours (the peak for immediate-release). For sustained-release or enteric-coated formulations, repeat the level at 8 to 12 hours because the peak is delayed. An abdominal X-ray may show radiopaque tablets and guide decontamination. [1]

3. Decontamination and antidote

The decontamination of choice is whole-bowel irrigation with polyethylene glycol via a nasogastric tube (20 to 40 mL per kg per hour, around 500 mL per hour in a young child) until the rectal effluent is clear and no tablets remain on a repeat X-ray. Activated charcoal is useless because iron is a metal and is not adsorbed. The antidote is intravenous desferrioxamine (deferoxamine) 15 mg per kg per hour, indicated for a serum iron over 500 microgram per dL, a high-anion-gap metabolic acidosis, shock, severe gastrointestinal symptoms or altered consciousness; the urine turns vin-rose as ferrioxamine is excreted. [1]

4. The latent phase

This is stage 2, the deceptive latent phase (6 to 24 hours). The child looks well precisely while absorbed iron is being sequestered by transferrin and is about to spill into tissues and trigger stage 3 systemic toxicity. Clinical appearance is a lie; only the serum iron and the acid-base status tell the truth. Discharge on clinical grounds in this window risks missing the transition to shock, hepatic failure and acidosis, which is why disposition must rest on the serum iron and the metabolic acidosis. [1]