Emergency Medicine · Toxicology
The facts most likely to be tested
Acute iron poisoning presents in stages, starting with gastrointestinal phase symptoms including hematemesis, abdominal pain, and bloody diarrhea within 6 hours of ingestion.
The latent phase of iron toxicity may show a transient clinical improvement, which is often a false sense of recovery before the onset of systemic collapse.
Systemic toxicity manifests as anion gap metabolic acidosis, hypotension, and shock due to direct cellular injury and mitochondrial dysfunction.
Abdominal radiographs are the diagnostic test of choice because iron tablets are radiopaque and may be visualized in the stomach or small intestine.
Serum iron levels should be measured 4 to 6 hours post-ingestion to guide the decision for chelation therapy.
Deferoxamine is the specific chelating agent indicated for patients with severe symptoms, shock, or serum iron levels exceeding 500 µg/dL.
Long-term complications of iron toxicity include gastric outlet obstruction or pyloric stenosis resulting from corrosive injury to the gastric mucosa.
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A 2-year-old boy is brought to the emergency department by his parents after he was found playing with an open bottle of his mother's prenatal vitamins. The child has had three episodes of hematemesis and persistent bloody diarrhea over the last two hours. On physical exam, the child is tachycardic and hypotensive. An abdominal radiograph reveals multiple radiopaque densities in the stomach. Laboratory studies demonstrate a significant anion gap metabolic acidosis.
What is the most appropriate next step in the management of this patient?
Intravenous deferoxamine
The patient exhibits signs of severe iron toxicity (shock, metabolic acidosis, hematemesis), necessitating immediate stabilization and the administration of the chelating agent deferoxamine.
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Etiology / Epidemiology
Common in pediatric ingestions of prenatal vitamins; causes corrosive mucosal injury and systemic metabolic acidosis.
Clinical Manifestations
Presents with hematemesis, abdominal pain, and anion gap metabolic acidosis; watch for the latent phase.
Diagnosis
Diagnosis is clinical; serum iron level >500 mcg/dL is highly suggestive of severe toxicity.
Treatment
Use whole bowel irrigation for large ingestions; deferoxamine is the antidote for severe systemic toxicity.
Prognosis
Risk of pyloric stenosis or bowel obstruction due to scarring; mortality is high if shock is untreated.
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Epidemiology & Etiology
Most cases involve accidental ingestion of prenatal vitamins by children. Adult toxicity is rare but occurs in intentional overdose or chronic iron overload states like hemochromatosis.
Pertinent Anatomy
Iron is directly corrosive to the gastrointestinal mucosa, causing ulceration and hemorrhage. Systemic absorption leads to mitochondrial dysfunction in the liver and heart.
Pathophysiology
Free iron acts as a catalyst for free radical production, leading to lipid peroxidation and cellular death. This results in uncoupled oxidative phosphorylation, causing severe lactic acidosis. The systemic phase involves profound vasodilation and cardiovascular collapse.
Clinical Manifestations
Stage 1 (0-6h) features vomiting, hematemesis, and diarrhea. Stage 2 (6-24h) is the latent phase where patients appear to improve. Stage 3 (12-48h) presents with shock, metabolic acidosis, and coagulopathy. Stage 4 (2-5d) involves hepatic failure.
Diagnosis
Diagnosis is primarily clinical based on history and symptoms. Serum iron level is the gold standard; levels >500 mcg/dL correlate with severe toxicity. Obtain an abdominal X-ray to visualize radiopaque iron tablets.
Treatment
Initiate whole bowel irrigation with polyethylene glycol for large ingestions. Administer deferoxamine for patients with severe symptoms, shock, or iron levels >500 mcg/dL. Do not use activated charcoal as it does not bind iron.
Prognosis
Survivors of the acute phase are at risk for gastric outlet obstruction due to strictures. Monitor for liver failure and coagulopathy during the first 48 hours.
Differential Diagnosis
Salicylate toxicity: presents with tinnitus and respiratory alkalosis
Gastroenteritis: lacks the systemic shock and metabolic acidosis
Lead poisoning: usually chronic, presents with neuro symptoms and basophilic stippling
Corrosive ingestion: causes immediate oropharyngeal burns
Diabetic ketoacidosis: presents with hyperglycemia and ketones