Iron Toxicity

Etiology and Pathophysiology

• Iron poisoning is a potentially fatal pediatric emergency, with severity directly related to the amount of elemental iron ingested.
• Adult iron preparations and prenatal vitamins are the most toxic sources, whereas children's vitamins, multivitamin preparations, and nonionic forms (carbonyl iron, iron polysaccharide) rarely contain enough elemental iron to cause significant toxicity.
• Patients ingesting $>40$ mg/kg of elemental iron require medical evaluation, while moderate to severe toxicity is typically seen with ingestions $>60$ mg/kg.
• Iron has a direct corrosive effect on the gastrointestinal mucosa, leading to hematemesis, melena, ulceration, and potential perforation.
• The presence of free iron causes massive volume losses, increased capillary membrane permeability, and vasodilation, which collectively precipitate early hypotension.
• Iron accumulates in target tissues, notably the Kupffer cells of the liver and myocardial cells, causing hepatotoxicity, coagulopathy, and cardiac dysfunction.
• Profound metabolic acidosis occurs due to a combination of hypovolemia, hypotension, and iron's direct interference with oxidative phosphorylation and the Krebs cycle.

Clinical Manifestations

• The clinical progression of acute iron toxicity is classically described in five overlapping stages.
• Patients who remain completely asymptomatic without gastrointestinal symptoms within $6$ hours of ingestion are highly unlikely to develop serious toxicity.

Diagnostic and Laboratory Evaluation

• Serum iron levels should be drawn $4-6$ hours post-ingestion in symptomatic patients or those with a history of a massive exposure.
• A serum iron concentration $<350$ $\mu$g/dL at $4-8$ hours suggests a low risk for significant toxicity.
• A serum iron concentration of $350-500$ $\mu$g/dL indicates moderate toxicity.
• A serum iron concentration $>500$ $\mu$g/dL signifies that significant, life-threatening toxicity is likely.
• Routine laboratory evaluation must include an arterial or venous blood gas, lactate, complete blood count, serum glucose, liver transaminases, and coagulation parameters.
• Iron poisoning classically presents with an elevated anion gap metabolic acidosis (part of the MUDPILES mnemonic).
• An abdominal radiograph (KUB) should be obtained as it may reveal radiopaque iron tablets (part of the CHIPPED mnemonic), although the absence of radiopacities does not rule out iron ingestion.

Emergency Management

Gastrointestinal Decontamination

• Activated charcoal does not bind to elemental iron and is entirely ineffective for gastrointestinal decontamination in this setting.
• Whole-bowel irrigation (WBI) is the definitive decontamination strategy of choice for iron ingestion, serving to mechanically flush unabsorbed iron pills from the gastrointestinal tract.
• Hemofiltration may be considered as an adjunctive method to remove iron from the systemic circulation.

Antidotal Therapy

• Deferoxamine is the specific chelating antidote utilized for moderate to severe iron intoxication.
• The deferoxamine-iron complex is excreted in the urine, classically imparting a reddish ("vin rosé") discoloration, though the intensity of this color should not be used to guide or terminate therapy.
• Therapy is maintained until clinical symptoms resolve and the metabolic acidosis is fully corrected.