Short note for acute iron poisoning (pharmacology), give in proper format as per mbbs prof exam for a 6 mark question

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ACUTE IRON POISONING

[Short Note - Pharmacology/Forensic Medicine | 6 Marks]

Definition / Introduction

Acute iron poisoning occurs when excess unbound iron circulates freely in the body, disrupting physiological mechanisms. It is most common in children who accidentally ingest iron supplements or prenatal vitamins. The toxic dose is >20 mg/kg elemental iron; the fatal dose is 20-30 g; fatal period is 24-30 hours.

Mechanism of Toxicity

Free (unbound) iron that exceeds transferrin binding capacity causes:

Increased capillary permeability
Post-arteriolar dilatation
Release of hydrogen ions (causing metabolic acidosis)
Inhibition of mitochondrial function (disrupts oxidative phosphorylation)
Corrosive action on gastric mucosa leading to hemorrhagic necrosis

Under normal conditions, only 15-35% of transferrin's iron-binding capacity is used. Toxicity occurs when serum iron exceeds total iron-binding capacity (TIBC).

Clinical Features (Four Stages)

Stage	Time	Features
Stage I	0-6 hours	Nausea, vomiting, abdominal pain, hemorrhagic gastroenteritis, shock, acidosis, coma
Stage II	6-24 hours	Apparent recovery - symptom-free (latent phase)
Stage III	24-48 hours	Metabolic acidosis, jaundice, hypoglycemia, shock, hepatic and renal failure
Stage IV	1-2 weeks	Late complications: gastric stricture, pyloric stenosis

Note: Some sources list a 5th stage (CNS toxicity/coma at 24-48 hrs); Stage II is a deceptive "honeymoon period" - do not discharge the patient.

Diagnosis

Serum iron at 3-5 hours post-ingestion is the most useful test:
- < 350 µg/dL: minimal toxicity
- 350-500 µg/dL: moderate toxicity
- 500 µg/dL: severe toxicity (indication for chelation)
Abdominal X-ray: most iron tablets are radiopaque; confirms ingestion
TIBC is unreliable and not recommended for gauging severity
ABG: metabolic acidosis
LFTs, RFTs, blood glucose

Treatment

1. General/Supportive

IV fluids for early hypotension (due to GI losses)
Vasopressors for cardiovascular toxicity
Intubation if airway is compromised
Correct metabolic acidosis

2. GI Decontamination

Gastric lavage with 5% sodium bicarbonate solution
Instil desferrioxamine 5-10 g at the end of lavage
Orally administer egg and milk (form iron-protein complexes)
Whole bowel irrigation (WBI) with polyethylene glycol - method of choice when radiopaque tablets are visible on X-ray
Activated charcoal does NOT bind iron - not useful

3. Specific Antidote - Deferoxamine (Desferrioxamine)

A chelating agent - chelates free iron to form ferrioxamine, which is excreted in urine (turns urine "vin rose" / orange-pink color)
Indications: serum iron > 500 µg/dL OR severe symptoms regardless of level
Dose:
- IV infusion: 15 mg/kg/h in normal saline (preferred route in severe cases)
- IM: 1 g, followed by 500 mg every 4 hours x 2 doses, then 500 mg every 4-12 hours (max 6 g in 24 hours)
Continue until symptoms resolve and urine colour returns to normal
Oral chelating agents (e.g., deferasirox) do not replace IV deferoxamine in acute poisoning

4. Hemodialysis / Exchange Transfusion

Indicated in severe cases (hemodialysis also removes ferrioxamine complex)

Autopsy Findings

Gastric mucosa: hemorrhagic necrosis, possible perforation of gastric/jejunal wall
Liver: acute hepatic necrosis
Kidneys: degenerative tubular changes

Key Points to Remember

Stage II (6-24 hrs) is a false recovery - do not discharge
Antidote: Deferoxamine (IV preferred); urine turns orange-pink confirming active chelation
Activated charcoal is NOT useful
Serum iron at 3-5 hours guides treatment
WBI is the GI decontamination method of choice when tablets are radiopaque

Sources: Essentials of Forensic Medicine & Toxicology, 36th Ed. (2026); Rosen's Emergency Medicine, 10th Ed.

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