She was initiated on HD for worsening acute gastrointestinal, neurologic signs of toxicity, and severe anion gap metabolic acidosis despite gastrointestinal decontamination and DFO infusion. Hyperkalemia was associated with electrocardiographic (ECG) changes (tall, peaked T-waves with a shortened QT interval). Approximately 6 h after ingestion, arterial blood gas (ABG) showed PaO 2 122 mm Hg, PCO 2 20 mm Hg, pH 7.16, bicarbonate 6.9 mmol/L, and base excess –21.5 mmol/L, potassium 2.3 mmol/L, sodium 150 mmol/L, chloride 97 mmol/L (partially compensated non-respiratory severe metabolic acidosis). Her initial liver function and renal function tests were normal. Investigations revealed hemoglobin 10.5 gm/dL, white cell count 15,300/cmm, and platelet 150 × 10 Citation 3. She was transferred to our hospital for HD in view of severe symptoms (persistent vomiting, abdominal pain, and acute gastrointestinal signs of toxicity, lethargy, altered mental status, and neurologic manifestations of toxicity), severe anion gap metabolic acidosis, and history of ingestion of significant number of ferrous sulfate pills.

Gastric lavage with a large-bore orogastric tube and whole bowel irrigation was used for gastrointestinal decontamination. The treatment was initiated with gastric lavage and DFO at a local hospital. She was afebrile and had no cyanosis/jaundice and oliguria. Her pulse rate was 124/min, regular, and blood pressure was 120/80 mm Hg. On examination, she was conscious but lethargic. An 18-year-old female with no past medical or psychiatric illness was brought by her husband with a history of accidental ingestion of 50 tablets of ferrous sulfate (100 mg of elemental iron per 335 mg tablet), 100 mg/kg of elemental iron, approximately 8 h after ingestion.

Iron toxicity antidote