Chapter 110. Iron

Iron toxicity from an intentional or accidental ingestion is a common poisoning. Based on clinical findings, iron poisoning can be divided into 5 stages.

The first stage develops within the first few hours of ingestion. Direct irritative effects of iron on the gastrointestinal (GI) tract produce abdominal pain, vomiting, and diarrhea. Vomiting is the clinical sign most consistently associated with acute iron toxicity. The absence of these symptoms within 6 hours of ingestion essentially excludes a diagnosis of significant iron toxicity.

During the second stage, which may continue for up to 24 hours following ingestion, the patient's GI symptoms may resolve, providing a false sense of security despite toxic amounts of iron absorption. While patients may be asymptomatic, they often appear ill, and may have abnormal vital signs reflecting hypovolemia and metabolic acidosis.

The third stage may appear early or develop hours after the second stage as shock and a metabolic acidosis evolve. Iron-induced coagulopathy may cause bleeding and worsen hypovolemia. Hepatic dysfunction, cardiomyopathy, and renal failure may also develop.

The fourth stage develops 2 to 5 days after ingestion and is characterized by elevation of aminotransferase levels and possible progression to hepatic failure.

The fifth stage, which occurs 4 to 6 weeks after ingestion, reflects the corrosive affects of iron on the pyloric mucosa and may cause gastric outlet obstruction.

The diagnosis of iron poisoning is based on the clinical picture and the history provided by the patient, significant others, or EMS providers. When determining a patient's potential for toxicity, the total amount of elemental iron must be used in calculations. Table 110-1 reviews the predicted clinical effects based on the amount of iron ingested.

Laboratory evaluation includes serum electrolytes, renal studies, serum glucose, coagulation studies, complete blood count, hepatic enzymes, and a serum iron level. It is crucial to note that a single serum iron level does not reflect what iron levels have been previously, what direction they are going, or the degree of iron toxicity in tissues; a single low serum level does not exclude the diagnosis of iron poisoning since there are variable times to peak level following ingestion of different iron preparations. Serum iron levels have limited use in directing management since toxicity is primarily intracellular rather than in the blood. The total iron binding capacity (TIBC) becomes falsely elevated in the presence of elevated serum iron levels or deferoxamine, and is of no clinical value.

Plain radiographs may reveal iron in the GI tract; however, many iron preparations are not radiopaque so normal radiographs do not exclude iron ingestion.

Patients who have remained asymptomatic for 6 hours after ingestion of iron, have not ingested a potentially toxic amount, and who have a normal physical examination do not require medical treatment for iron toxicity. Patients whose symptoms resolve after a short period of time, and who have normal vital signs, usually have mild toxicity and require only supportive care. This subset of patients still requires an observation period. Figure 110-1 is an algorithm for the clinical management of patients after an acute iron ingestion.

Patients who are symptomatic or demonstrate signs of hemodynamic instability after iron ingestion require aggressive management in the ED.

1. Place the patient on supplemental oxygen and a cardiac monitor, and establish 2 large-bore IVs.

2. Administer vigorous intravenous (IV) crystalloid infusion to help correct hypovolemia and hypoperfusion.

3. Perform gastric lavage in patients who present within 60 min of ingestion. Activated charcoal is not recommended.

4. Whole-bowel irrigation with a polyethylene glycol solution is efficacious. Administration of 250 to 500 mL/h in children or 2 L/h in adults via nasogastric tube may clear the GI tract of iron pills before absorption occurs.

5. Administer antiemetics such as ondansetron (4 milligrams IV in adults; 0.1 milligrams/kilogram to a maximum dose of 4 milligrams in pediatric patients) or promethazine 25 milligrams IV in adults.

6. Correct coagulopathy with vitamin K1 (5 to 10 milligrams SC) and fresh frozen plasma (10 to 25 mL/kg in adults; 10 mL/kg in pediatric patients). Order blood for type and screen or crossmatch as necessary.

7. Deferoxamine is a chelating agent that can remove iron from tissues and free iron from plasma. Deferoxamine is safe to administer to children and pregnant women. Deferoxamine therapy is indicated in patients with systemic toxicity, metabolic acidosis, worsening symptoms, or a serum iron level predictive of moderate or severe toxicity.

   Intravenous infusion is the preferred route of deferoxamine administration because IM absorption is unpredictable in the hypovolemic patient. The recommended initial dose is 1000 milligrams IV. Since hypotension is the rate-limiting factor for IV infusion, it is recommended to begin with a slow IV infusion at 5 milligrams/kilogram/hour. The deferoxamine infusion rate can be increased to 15 milligrams/kilogram/h, as tolerated, within the first hour of treatment. The recommended total amount of deferoxamine is 360 milligrams/kilogram or 6 grams during the first 24 hours. Initiate deferoxamine therapy without waiting for the serum iron level in any clinically ill patient with a known iron ingestion.

   Evaluate the efficacy of deferoxamine treatment through serial urine samples. As ferrioxamine is excreted, urine changes to a classic vin rose appearance. Clinical recovery is the most important factor guiding the termination of deferoxamine therapy.

8. Patients who remain asymptomatic after 6 hours of observation, have a normal physical examination, and have a reliable history of an insignificant ingestion may be considered for discharge. Patients initially symptomatic who become asymptomatic should be admitted for further evaluation since this may represent the second stage of iron toxicity. Admit all patients who receive deferoxamine therapy to an intensive care setting. Assess all patients for suicide risk. Consider child abuse or neglect in pediatric cases.