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Toxicology – Iron Poisoning

Source

Iron poisoning most commonly occurs from ingestion of iron-containing medications or supplements, such as ferrous sulfate or ferrous gluconate. Young children are particularly vulnerable because tablets may resemble candy.

Typical Presentation

A child with significant iron ingestion may develop:

  • Repeated vomiting
  • Abdominal pain
  • Diarrhea
  • GI bleeding
  • Lethargy
  • Metabolic acidosis

Severe poisoning can progress to shock, liver injury, coma, and death.

Clinical Features

Severity depends mainly on the amount of elemental iron absorbed.

Milder toxicity commonly causes:

  • Nausea
  • Vomiting
  • Abdominal pain
  • Diarrhea

More severe toxicity may cause:

  • Hematemesis or GI bleeding
  • Dehydration and hypovolemia
  • Hypotension and shock
  • Metabolic acidosis
  • Altered mental status
  • Hepatic failure
  • Coma

Marked acidosis and very high serum iron concentrations suggest more serious poisoning.

Stages of Toxicity

  1. GI Phase – first several hours
  2. Vomiting, diarrhea, abdominal pain, and possible GI bleeding.
  3. Latent Phase – roughly 6–24 hours
  4. GI symptoms may temporarily improve even though systemic toxicity continues. Tachycardia, lethargy, and metabolic acidosis may persist.
  5. Shock Phase – about 12–24 hours
  6. Hypotension, vasodilation, impaired cardiac output, and circulatory collapse may develop.
  7. Hepatic Phase – approximately 2–3 days
  8. Severe poisoning can produce acute hepatotoxicity and liver failure.
  9. Late GI Scarring – weeks later
  10. Healing gastrointestinal injury can produce strictures and, in some cases, gastric outlet obstruction.

Mechanism of Action

Normally, iron is carried in the blood bound to transferrin. In overdose, transferrin becomes saturated and excess free iron circulates.

Free iron:

  • Directly damages the gastrointestinal mucosa
  • Disrupts mitochondrial energy production
  • Generates oxidative injury
  • Damages blood vessels and solid organs

This contributes to acidosis, shock, and hepatic injury.

Management

Treatment is primarily supportive and may include:

  • Airway and cardiovascular stabilization
  • IV fluids for dehydration or shock
  • Monitoring of serum iron, electrolytes, acid-base status, glucose, and liver function
  • Abdominal imaging in selected cases because some iron tablets are radiopaque
  • Whole bowel irrigation when substantial tablets remain in the GI tract and toxicology guidance supports it

Activated charcoal is ineffective because it does not meaningfully bind iron.

Deferoxamine is the specific iron chelator and may be used for patients with severe clinical toxicity or other findings suggesting substantial systemic iron poisoning.

Key Points

  • Think of the classic progression: GI symptoms → temporary improvement → shock → liver injury → possible late GI stricture.
  • A symptom-free interval does not guarantee recovery.
  • Activated charcoal does not work for iron.
  • Deferoxamine binds circulating free iron in severe poisoning.
  • Some iron tablets may be visible on plain abdominal radiographs.


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