Course Content
Zambian Paediatric & Obstetrics-Gynecology (OB/GYN) Clinical Mastery

Paediatric Iron Overdose 

Lesson Objectives

By the end of this lesson, the learner should be able to:

  1. Identify the common sources and mechanisms of iron overdose in children.

  2. Describe the stages and systemic effects of acute iron toxicity.

  3. Recognize early and severe clinical manifestations.

  4. Conduct essential investigations for diagnosis and monitoring.

  5. Administer evidence-based treatment including chelation therapy.

  6. Monitor therapeutic response and recognize when to discontinue antidotal therapy.

Description

Iron overdose is a potentially life-threatening paediatric emergency commonly resulting from accidental ingestion of maternal antenatal or therapeutic iron supplements. Toxicity occurs when excess iron exceeds the binding capacity of transferrin, leading to free circulating iron that causes cellular damage, metabolic acidosis, and circulatory collapse.

Symptoms usually develop within 6 hours of ingestion; an asymptomatic child beyond this period rarely requires antidotal therapy. Early recognition and prompt management significantly reduce morbidity and mortality.

Pathophysiology

  • Iron acts as a direct corrosive agent on the gastrointestinal mucosa, causing bleeding and fluid loss.

  • Systemically, free iron catalyzes free radical formation, leading to cellular necrosis, particularly in the liver, heart, and gastrointestinal tract.

  • Iron interferes with oxidative phosphorylation, resulting in lactic acidosis and metabolic derangements.

Signs and Symptoms

Severity Clinical Features
Mild (Early phase: 0–6 hours) Nausea, vomiting, abdominal pain, diarrhea, grey/black vomitus or stools
Moderate Gastrointestinal bleeding, dehydration, hypotension, drowsiness
Severe (Systemic toxicity) Convulsions, metabolic acidosis, cardiovascular collapse, hepatic dysfunction, coma

Note: The presence of vomiting, diarrhea, or haematemesis within 6 hours strongly suggests toxicity. Absence of symptoms after 6 hours is reassuring.

Investigations

Test Purpose / Findings
Chest & Abdominal X-ray Detect radiopaque iron tablets in the gastrointestinal tract
Serum Iron Studies Assess serum iron concentration and total iron-binding capacity (TIBC)
Electrolytes and Renal Function Evaluate metabolic acidosis, dehydration, and renal compromise
Blood Glucose Hypoglycemia may occur secondary to hepatic dysfunction
Arterial Blood Gas (ABG) Determine degree of metabolic acidosis

Treatment Algorithm

Step Intervention Details / Rationale
1. Initial Resuscitation ABCs Maintain airway, breathing, and circulation. Oxygen if hypoxic. Establish IV access.
2. Fluid Resuscitation 20 ml/kg Normal Saline or Ringer’s Lactate Used for shock or hypotension to restore perfusion. May repeat as necessary.
3. Gastrointestinal Decontamination Gastric lavage Consider only if potentially toxic doses were ingested within 1 hour and airway is protected.
4. Activated Charcoal Contraindicated Ineffective because iron is not adsorbed by charcoal.
5. Chelation Therapy Deferoxamine (IV preferred) Indicated in symptomatic patients or if serum iron > 300–500 µg/dL. Dose: 15 mg/kg/hr slow IV infusion for 4–6 hours, not exceeding 80 mg/kg in 24 hours (max 6 g/day). Reduce rate once stable.
6. IM Route (if IV not possible) 50 mg/kg IM every 6 hours Avoid if patient is in shock due to poor perfusion.
7. Monitoring Stop infusion when patient improves clinically Usually within 24 hours. Observe for hypotension, allergic reaction, or reddish discoloration of urine (vin rose color) during infusion.

Monitoring and Supportive Measures

  • Vital signs: continuous monitoring of heart rate, BP, RR, O₂ saturation.

  • Urine output: ensure >1 mL/kg/hr for renal clearance of iron–deferoxamine complex.

  • Serum iron levels: repeat 4–6 hours post-treatment to confirm reduction.

  • Watch for side effects of deferoxamine (hypotension, allergic reaction, ARDS).

Complications

  • Gastrointestinal bleeding and perforation

  • Metabolic acidosis

  • Hepatic necrosis and acute liver failure

  • Hypovolemic shock

  • Seizures and coma

  • Renal failure due to tubular necrosis

Key Points Summary

  • Most paediatric iron overdoses are accidental.

  • Toxicity develops rapidly (within 6 hours).

  • Activated charcoal is ineffective.

  • Deferoxamine is the definitive antidote, given cautiously to avoid side effects.

  • Stop chelation when the patient stabilizes—usually within 24 hours.

  • Prevention involves secure storage of iron supplements in households with children.

 

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