Iron Overdose — SAQ

Stem

A 2-year-old, 12 kg boy is brought to the emergency department two hours after his mother found him next to an open bottle of her prenatal ferrous sulphate 325 mg tablets. She estimates he swallowed about 15 tablets. On arrival he is drowsy but rousable, has vomited twice (the second vomit contains frank blood), and has passed one bloody stool. Temperature 37.1 degrees C, pulse 140/min, blood pressure 88/52 mmHg, capillary refill 4 seconds, respiratory rate 32/min. Abdomen is diffusely tender. Intravenous access is obtained and a fluid bolus is started. An abdominal X-ray shows multiple radiopaque tablets in the stomach and proximal small bowel.^[1]

Questions

a) Calculate the elemental iron dose ingested in mg/kg and state the severity stratum and its prognostic implication. (2 marks)

Ferrous sulphate is 20% elemental iron, so 325 mg salt contains 65 mg elemental iron. This child swallowed about 15 tablets: 15 × 65 = 975 mg elemental; 975 / 12 kg = 81 mg/kg elemental iron.^[3]

McGuigan: systemic toxicity may occur after at least 60 mg/kg elemental iron. Manoguerra: 40 mg/kg or more of adult ferrous salts is referred for medical evaluation; any intentional ingestion is referred immediately. Baranwal: over 60 mg/kg is high risk and an indication to start chelation when the level is unavailable. This child is therefore above the systemic-toxicity and chelation-threshold doses — resuscitate, whole bowel irrigation, and a low threshold for IV desferrioxamine. (1 mark for 81 mg/kg elemental; 1 mark for the 60 mg/kg systemic-toxicity stratum.)^[1][2][3]

b) Explain the molecular mechanism by which absorbed free iron produces the high-anion-gap metabolic acidosis, hepatic necrosis and coagulopathy of stage 3. (3 marks)

When serum iron exceeds binding capacity, free iron increases reactive oxygen species — hydroxyl radical, superoxide and hydrogen peroxide — causing lipid peroxidation and membrane damage (Baranwal; Rafati).^[3]

• Acidosis: intracellularly, iron shunts electrons away from the electron-transport chain and uncouples oxidative phosphorylation, producing anaerobic metabolism and metabolic acidosis. Post-arteriolar dilatation, capillary leak and coagulopathy compound shock. (1 mark)^[3]
• Hepatic necrosis: the cytopathic target is periportal hepatic necrosis (not the centrilobular/zone-3 pattern of paracetamol). Robertson: severe hepatotoxicity = transaminase over 1000 U/L, typically with iron well over 1000 microgram/dL. (1 mark)^[3]
• Coagulopathy: listed among Baranwal stage-III features; prothrombin index under 50 percent is a poor prognostic marker. (1 mark)^[3]

c) Outline the stepwise definitive management, with drug doses and escalation triggers. (4 marks)

1. Resuscitation (ABCDE): oxygen; two large-bore cannulae; isotonic crystalloid titrated to perfusion (this child is shocked); continuous monitoring; cross-match for haematemesis. Draw bloods before desferrioxamine (deferoxamine reduces iron recovery in the assay — Roberts): serum iron (at least 4 h post-ingestion), venous gas, electrolytes, glucose, FBC, PT/INR, LFTs, renal function, paracetamol and salicylate. (1 mark)^[3]

2. Decontamination — whole bowel irrigation (NOT charcoal): the 2026 CTRC concluded there is no role for activated charcoal in iron poisoning. Give polyethylene glycol electrolyte solution via nasogastric tube. Baranwal paediatric rate 30 to 40 mL/kg/h for 4 to 8 h; a 33-month-old safely received 44.3 L over 5 days. Continue until imaging is clear — a clear effluent is not a valid stop rule (Kaczorowski; Scharman). Radiopaque tablets now confirm the indication. (1 mark)^[4][3]

3. IV desferrioxamine (deferoxamine) — indicated here because estimated elemental dose is over 60 mg/kg and there is shock (McGuigan: serious symptoms or iron over 500 microgram/dL within 8 h). Dose 15 mg/kg/h IV in saline. Baranwal maximum: 360 mg/kg daily and a total of 6 g; a faster infusion may cause hypotension. Vin-rose urine may be helpful but is not seen consistently. Stop on clinical grounds (stable patient, acidosis resolving), not colour. Howland: prolonged IV dosing risks pulmonary, cardiovascular, ocular and auditory toxicity and may increase infection risk. (1 mark)^[3][2]

4. Supportive care + escalation: PICU for shock, coagulopathy (prothrombin index under 50 percent), severe acidosis or acute liver failure (Baranwal poor prognostic set). Endoscopy for undissolved tablets (Rafati). (1 mark)^[3]

d) State TWO factors that make the four-stage course deceptive and ONE late complication to counsel the parents about at discharge. (1 mark)

The two deceptive factors: (1) the quiet interval (Baranwal: apparent stabilization until 12 h; Morales-Cruz: 6 to 24 h) — symptoms subside while free iron is redistributed intracellularly; disposition must rest on serum iron and acid–base, not appearance. (2) A level drawn before 4 h can be falsely low (Fox); modified-release products specifically warrant WBI (Tenenbein 2023). (This child took immediate-release ferrous sulphate, so the quiet-interval pitfall is the main one.)^[3]

The late complication: gastric scarring / pyloric stricture at 2 to 4 weeks in Baranwal's table (prose 2 to 6 weeks; Morales-Cruz 2 to 8 weeks) — warn parents to return for recurrent vomiting or gastric-outlet symptoms. (0.5 marks each for the two deceptive factors, 0.5 for the late complication.)^[3]

References4ShowHide

1. [1]Manoguerra AS, Erdman AR, Booze LL, et al. Iron ingestion: an evidence-based consensus guideline for out-of-hospital management. Clin Toxicol (Phila), 2005.PMID 16255338
2. [2]McGuigan MA. Acute iron poisoning. Pediatr Ann, 1996.PMID 8775917
3. [3]Baranwal AK, Singhi SC. Acute iron poisoning: management guidelines. Indian Pediatr, 2003.PMID 12824662
4. [4]Hoegberg LCG, Gosselin S, Buckley NA, et al. Recommendations from the Clinical Toxicology Recommendations Collaborative on the administration of activated charcoal in acute oral overdose. Clin Toxicol (Phila), 2026.PMID 41906697