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Updated: Aug 1, 2026

Continuous Manual Exchange Transfusion for Patients with Sickle Cell Disease: An Efficient Method to Avoid Iron Overload
Published on: March 14, 2017
Survival after a severe iron poisoning treated with intermittent infusions of deferoxamine
K Cheney1, C Gumbiner, B Benson
1University of Nebraska Medical Center, Omaha.
Insights
A child survived a massive iron overdose with extremely high iron levels, previously considered unsurvivable. This case highlights the potential for survival with intensive care and a unique deferoxamine treatment regimen.
Area of Science:
- Pediatric Toxicology
- Emergency Medicine
- Critical Care
Background:
- Iron poisoning is a leading cause of fatal overdose in young children.
- Survival is rare with serum iron levels exceeding 2687 mumol/L.
Observation:
- A 22-month-old male ingested a massive dose of ferrous sulfate tablets.
- He presented with severe symptoms including coma, metabolic acidosis, shock, liver failure, and respiratory distress.
- Serum iron levels reached 2992 mumol/L.
Findings:
- The patient received intensive care including mechanical ventilation and a unique deferoxamine dosage schedule.
- Management was guided by Swan-Ganz catheter monitoring.
- Despite complications like gastric outlet obstruction, the child recovered and was neurologically intact upon discharge.
Implications:
- This case expands the known range for survival after severe iron overdose.
- Further research is needed to optimize deferoxamine dosing protocols.
- Highlights the importance of aggressive management in pediatric iron poisoning.
Abstract:
Iron poisoning is the most common cause of overdose mortality in children under six years of age and there are no reports of survival with iron levels > 2687 mumol/L (> 15,000 micrograms/dL). A 22-month-old male was brought to the emergency department by his parents after ingesting an estimated 50 ferrous sulfate tablets (60 mg elemental iron/tablet) several hours earlier. Despite spontaneous emesis and gastric lavage his condition deteriorated and he was found to have a serum iron of 2992 mumol/L (16,706 micrograms/dL). During the first four days in the intensive care unit, he developed coma, metabolic acidosis, hypovolemic and cardiogenic shock, liver failure, coagulopathy and adult respiratory distress syndrome. He was treated with a unique deferoxamine dosage schedule (25 mg/kg/h for 12 h/d x 3 d), mechanical ventilation, Swan-Ganz catheter monitoring, dopamine/nitroprusside therapy, blood product, bicarbonate, electrolyte and volume replacement. After a prolonged hospital course complicated primarily by gastric outlet obstruction he was dismissed on full oral feedings, gaining weight, and neurologically intact. Swan-Ganz catheter monitoring guided the management of this patient's shock, iron-induced cardiac failure, and deferoxamine mesylate induced adult respiratory distress syndrome. Further experience and research is required to determine the most appropriate deferoxamine mesylate dosing schedule and our experience expands the range for possible survival after massive iron overdose.
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