Iron Overdose — Viva

Q1: Mechanism and recognition (3 min)

Examiner: A 2-year-old is brought in after swallowing her mother's prenatal ferrous sulphate 325 mg tablets, with haematemesis and a high-anion-gap metabolic acidosis. Walk me through the mechanism and why this is iron poisoning.^[1][2]

Expected answer:

• Iron injures the body in two waves: (1) direct corrosive injury to the GI mucosa (haemorrhagic gastritis, third-spacing, bleeding, shock), and (2) systemic ROS toxicity once serum iron exceeds binding capacity.
• Free iron increases hydroxyl radical, superoxide and hydrogen peroxide, causing lipid peroxidation. Intracellularly it uncouples oxidative phosphorylation, producing metabolic acidosis. Post-arteriolar dilatation, capillary leak, coagulopathy and ROS myocardial injury contribute to shock (Baranwal).
• Hepatic injury is periportal necrosis, not the centrilobular pattern of paracetamol.
• Recognition: tablet history, radiopaque tablets when present (chewable forms are rarely visible clinically — Everson), glucose over 150 mg/dL and WBC over 15,000 as paediatric clues only (they do not predict iron over 300 microgram/dL in adults — Palatnick), and serum iron over 500 microgram/dL within 8 h or 350 with symptoms (McGuigan/Fox).^[2][3]

Follow-up: Why is the hepatic injury periportal? Baranwal: iron's cytopathic effect is on the periportal area of the lobule, the primary site of hepatic regeneration — hence the high mortality of iron-related acute liver failure.^[2]

Q2: The dose calculation and the four-stage course (3 min)

Examiner: How do you quantify the toxic dose, and what is the four-stage course?^[1][2]

Expected answer:

• The dose that matters is ELEMENTAL iron: ferrous sulphate is 20% elemental (325 mg salt = 65 mg elemental); ferrous fumarate is 32% elemental. Always use the label.
• Thresholds: McGuigan — GI effects from about 20 mg/kg, systemic toxicity may occur from at least 60 mg/kg. Manoguerra — refer 40 mg/kg or more of adult ferrous salts, or severe/persistent symptoms; observe at home if less than 40 mg/kg with mild symptoms; any intentional ingestion is referred immediately.
• Course (Baranwal four stages): I 0–3 h GI toxicity; II until 12 h apparent stabilization; III 12–48 h mitochondrial toxicity (hepatic necrosis after 48 h); IV 2–4 weeks gastric scarring (prose 2–6 weeks). Morales-Cruz publishes a five-stage variant. A child may skip the quiet interval.^[1][2][3]

Follow-up: What is the dangerous teaching point of the quiet interval? Never discharge on appearance — disposition rests on the serum iron and the acid–base status.^[2]

Q3: Management ladder with doses (3 min)

Examiner: Take me through the definitive management, with doses and triggers.^[1][2]

Expected answer — stepwise:

1. ABCDE + crystalloid titrated to perfusion; draw iron, VBG, electrolytes, glucose, FBC, PT/INR, LFTs, renal function, paracetamol/salicylate before desferrioxamine (the chelator reduces iron recovery in the assay).
2. Decontamination: WHOLE BOWEL IRRIGATION (NOT charcoal). PEG via NG: adult 2 L/h in reported series; Baranwal child 30–40 mL/kg/h for 4–8 h. Image until clear — effluent is not a stop rule. 2026 CTRC: no role for activated charcoal in iron poisoning.^[1]
3. IV DESFERRIOXAMINE 15 mg/kg/h for serious symptoms or serum iron over 500 microgram/dL within 8 h (McGuigan); traditional alternative 350 with symptoms (Fox). Baranwal max 360 mg/kg/day and total 6 g; faster infusion may cause hypotension. Vin-rose is inconsistent.^[2][3]
4. Supportive / PICU for shock, coagulopathy (PI under 50 percent), severe acidosis or acute liver failure.^[2][2]

Follow-up — when to stop desferrioxamine and why: stop on clinical grounds (stable patient, acidosis resolving). Howland: prolonged IV dosing risks pulmonary, cardiovascular, ocular and auditory toxicity and may increase infection risk. Mofenson reported Yersinia septicaemia possibly related to iron overdose (title only).^[2]

Q4: Pitfalls and sustained-release formulations (2 min)

Examiner: What are the classic pitfalls, and how does a sustained-release formulation change your approach?^[1][2]

Expected answer:

• Pitfalls: (1) being reassured by the quiet interval; (2) giving activated charcoal (2026 CTRC: no role); (3) relying on a single level drawn before 4 h; (4) delaying desferrioxamine when serious symptoms or iron over 500 are present; (5) using vin-rose colour as the sole end-point; (6) over-prolonged desferrioxamine (Howland toxicities); (7) missing co-ingested paracetamol.
• Sustained-release/enteric-coated iron: WBI is specifically recommended (Tenenbein 2023). A level drawn before 4 h can be falsely low (Fox) — draw at least 4 h post-ingestion and repeat while exposed. Never discharge on a single early level.^[1]

Follow-up — pregnancy: IV desferrioxamine IS indicated for severe maternal toxicity. Tran: pregnancy should not alter therapy; third-trimester deferoxamine was not associated with perinatal complications and is potentially life-saving. Turk: 10.2 g IV over 14 h plus WBI 2 L/h for 12 h at 26 weeks with good outcome. Calculate mg/kg on the pre-pregnancy weight (Manoguerra).^[1]

Q5: Prognosis and disposition (2 min)

Examiner: What determines outcome, and who goes home?^[1][2]

Expected answer:

• Population statistic: from 1983 to 1991 iron caused over 30% of deaths from accidental ingestion of drug products by children (Manoguerra). Chandran: 2 of 5 children died, both with liver failure.^[1]
• Poor prognostic markers (Baranwal): shock, coagulopathy (prothrombin index under 50 percent), severe acidosis, acute liver failure. Delayed presentation associated with death (Chandran).^[2]
• Discharge (Manoguerra): asymptomatic more than 6 h after immediate-release ingestion, unlikely to develop symptoms; peak iron not in the toxic range; no acidosis; no residual tablets; psychiatric clearance after intentional ingestion.^[1]
• ICU / PICU for shock, coagulopathy, severe acidosis or acute liver failure.

Follow-up — late follow-up: warn about gastric scarring / pyloric stricture at 2 to 6 weeks (Baranwal; Morales-Cruz 2 to 8 weeks).^[2]

References3ShowHide

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]Baranwal AK, Singhi SC. Acute iron poisoning: management guidelines. Indian Pediatr, 2003.PMID 12824662
3. [3]McGuigan MA. Acute iron poisoning. Pediatr Ann, 1996.PMID 8775917