Pediatric Iron Toxicity Clinical Presentation

Most pediatric poisonings are unintentional. Specifically, in relation to iron toxicity, children may ingest the iron administered to mothers as prenatal vitamins or as postpartum supplements. Other iron exposures include ingestion of iron-fortified children's vitamins, although these tend to be less toxic. A recent study examined the effects of iron supplements in breastfed infants.^[3] Parents may not immediately be aware of the ingestion or the specific amount of the iron tablets ingested.

• If possible, determining the number of pills ingested, how much iron was in each pill, and the formulation of iron in the supplement is important.
• Different formulations of iron contain varying amounts of elemental iron, as follows:

  • Ferrous sulfate - 20% elemental iron
  • Ferrous gluconate- 12% elemental iron
  • Ferrous fumarate - 33% elemental iron
  • Ferrous lactate - 19% elemental iron
  • Ferrous chloride - 28% elemental iron
• The following is a formula used to calculate the amount of ingested iron for a 10-kg child who consumed ten 320-mg tablets of ferrous gluconate (12% elemental iron per tablet): 10 tablets X 38.4 mg elemental iron per tablet = 384 mg/10 kg = 38.4 mg/kg
• Carbonyl iron and iron polysaccharide complex are nonionic forms of iron that have less toxicity than ferrous salts.
• Attempt to determine the time of ingestion. This is important in determining observation periods and timing of serum levels.

As stated in Pathophysiology, iron toxicity is typically described in 5 sequential phases. Universal agreement does not exist as to the number of phases or the times assigned to those phases. Patients may not always demonstrate each of the phases.

Few, if any, physical examination findings are specific to iron toxicity.

• Phase 1 usually occurs within the first 6 hours postingestion. This phase is associated with hemorrhagic vomiting, diarrhea, and abdominal pain due to mucosal injury. The hemorrhagic GI symptoms are due to the direct effects of iron on the GI mucosa. A patient is unlikely to develop significant systemic toxicity without first having GI symptoms. In severe cases, the GI losses of blood and fluid may be massive and lead to shock and coma.
• Phase 2 usually occurs 6-12 hours postingestion and may be associated with an improvement in symptoms, especially when supportive care has been provided during phase 1. This period of apparent recovery may be confusing. In mild cases, this recovery may represent true recovery. However, in serious ingestions, it may represent only a temporary respite or may not occur at all; the patient may progress directly to phase 3. The etiology of phase 2 is unclear, but it may represent the time it takes for iron to distribute throughout the body and for systemic injury to occur. The only findings on examination may be lethargy, mild tachycardia, or tachypnea.
• Phase 3 begins after 12-24 hours postingestion and consists of multisystem damage. This may include marked metabolic acidosis, coagulopathy, shock, seizures, and altered mental status due to mitochondrial damage and hepatocellular injury.
• Phase 4 occurs 2-3 days postingestion and is characterized by hepatic injury.
• Phase 5 occurs 2-6 weeks postingestion and is characterized by late scarring of the GI tract, which causes pyloric obstruction or hepatic cirrhosis. However, these complications are rare, even in severe cases.

• As with any ingestion, the risk of ingestion increases as the availability of the medication increases.
• Childproof containers for multivitamins and prenatal vitamins may be of some assistance in decreasing exposure. In addition, some consideration has been given to changing the appearance of prenatal vitamins to make them look less like candy.
• One study found an association between iron poisoning in young children and recent birth of a sibling.^[4]