Acute iron poisoning results from ingestion of elemental iron, most commonly in children <6 years (accidental) and adolescents/young adults (intentional/suicidal), with toxicity driven by free radical–mediated lipid peroxidation affecting the GI tract, cardiovascular system, and liver. [1-2] Five distinct clinical phases are recognized: GI toxicity → relative stability → circulatory shock/acidosis → hepatotoxicity → GI scarring. [1]
1. History
- Determine the exact product ingested, number of tablets, formulation, and elemental iron content (ferrous sulfate = 20%, ferrous gluconate = 12%, ferrous fumarate = 33%) [3]
- Time of ingestion — critical for interpreting serum iron levels and anticipating clinical phase
- Intentional vs. accidental ingestion; co-ingestants (especially acetaminophen, alcohol) [4-5]
- Symptom timeline: onset of nausea, vomiting, diarrhea, hematemesis, melena
- Presence of a "quiescent phase" (6–24 hours post-ingestion) where GI symptoms resolve — this does NOT indicate recovery and may precede cardiovascular collapse [1]
- Access to prenatal vitamins, adult iron supplements, or pediatric multivitamins in the home
2. Alarm Features
- Hematemesis or bloody diarrhea — suggests mucosal necrosis
- Altered mental status, lethargy, or coma — associated with serum iron >500 µg/dL [6]
- Cardiovascular instability: hypotension, tachycardia, shock [7]
- Metabolic acidosis with elevated anion gap [6]
- Serum iron >500 µg/dL — associated with severe systemic toxicity [6][8]
- Coagulopathy, rising transaminases — herald hepatotoxicity, which carries high mortality [9-10]
- Ingestion of ≥60 mg/kg elemental iron — high risk for serious toxicity [3][11]
3. Medications
- Deferoxamine mesylate — the chelation antidote for acute iron poisoning: [12]
- IM (non-shock): initial 1,000 mg, then 500 mg q4–12h; max 6,000 mg/24h
- IV (shock/cardiovascular collapse): 1,000 mg at ≤15 mg/kg/hr, then 500 mg q4–12h at ≤125 mg/hr; max 6,000 mg/24h
- Produces characteristic "vin rosé" (pinkish-orange) urine when chelating free iron
- Whole bowel irrigation (WBI) with polyethylene glycol — for large ingestions or visible tablets on abdominal radiograph [3][13]
- Activated charcoal is NOT effective — does not bind iron
- Ipecac is NOT recommended
- Avoid deferoxamine in patients with severe renal disease; monitor for ARDS with high IV doses [12]
- Deferoxamine increases susceptibility to Yersinia infections [12]
4. Diet
- NPO during acute management
- No specific dietary triggers; this is an acute toxicological emergency
- Long-term: counsel families on safe storage of iron-containing supplements away from children
5. Review of Systems
- GI: nausea, vomiting, abdominal pain, diarrhea, hematemesis, melena
- Neuro: lethargy, confusion, seizures, coma
- Cardiovascular: palpitations, lightheadedness, syncope
- Hepatic: jaundice, RUQ pain (late)
- Renal: decreased urine output
- Hematologic: bleeding, bruising (coagulopathy)
6. Collateral History and Family History
- Confirm product and pill count with family, pharmacy, or pill bottle
- Assess for suicidal intent — intentional iron overdose is common in adolescent females (91% female in the 13–20 age group) [2][5]
- One-third of intentional overdoses are associated with concurrent alcohol use [5]
- Psychiatric history and access to means
- Family history is not directly relevant to acute toxicity but may reveal iron supplement use in the household (prenatal vitamins, anemia treatment)
7. Risk Factors
- Children <6 years: accidental ingestion of colorful, candy-like iron tablets [2][14]
- Adolescent females: intentional overdose, often with prenatal vitamins or iron supplements [2][5]
- Households with iron-containing supplements (prenatal vitamins, adult iron formulations)
- Co-ingestion with alcohol increases morbidity [5]
- Delayed presentation (>6 hours) worsens prognosis [15]
8. Differential Diagnosis
- Other toxic ingestions: acetaminophen, salicylates, caustic agents, other heavy metals (lead, arsenic)
- Infectious gastroenteritis — may mimic early GI phase
- Hemorrhagic gastritis from NSAIDs or caustic ingestion
- Sepsis/septic shock — in the late phase with acidosis and cardiovascular collapse
- Hepatic failure from other causes: acetaminophen, viral hepatitis, Amanita mushroom poisoning
- Diabetic ketoacidosis — anion gap metabolic acidosis mimic
- Theophylline or salicylate toxicity — GI symptoms + metabolic acidosis
9. Past Medical History
- Prior suicide attempts or psychiatric illness
- Anemia requiring iron supplementation
- Pregnancy (prenatal vitamin access)
- Liver disease (lower threshold for hepatotoxicity)
- Renal disease (affects deferoxamine use) [12]
10. Physical Exam
- Vitals: tachycardia, hypotension (shock phase), tachypnea (acidosis compensation)
- GI: abdominal tenderness, distension, hematemesis, melena, peritoneal signs (if perforation)
- Neuro: altered mental status, lethargy → coma in severe cases [6]
- Skin: pallor, diaphoresis, poor perfusion
- Hepatic: RUQ tenderness, jaundice (late finding)
- Gray/black stool from iron tablets
11. Lab Studies
- TIBC is NOT reliable in acute overdose — it rises artifactually and does not accurately predict toxicity [6][16-17]
- Serum iron levels should be drawn 4–6 hours post-ingestion for peak assessment [2]
- Serum iron concentrations do not always correlate with clinical severity; clinical assessment remains paramount [7][14]
12. Imaging
- Abdominal radiograph (KUB): first-line — iron tablets are radiopaque and may be visible as densities in the stomach/bowel [3][6]
- Useful for confirming ingestion and monitoring decontamination (WBI effectiveness)
- Absence of radiopacities does NOT exclude significant ingestion (liquid formulations, chewed/dissolved tablets)
- Repeat KUB after WBI to confirm clearance
- CT abdomen rarely needed unless concern for perforation or obstruction (late complication)
13. Special Tests
- Deferoxamine challenge test (historical): IM deferoxamine → vin rosé urine color change suggests free circulating iron; however, this test is no longer widely recommended as a diagnostic tool due to poor sensitivity [6][11]
- Poison control consultation — recommended for all significant ingestions
- EGD: may be indicated to evaluate mucosal injury and remove undissolved iron tablets in massive ingestions [13]
14. ECG
- Obtain ECG in all symptomatic patients
- Monitor for sinus tachycardia (most common), conduction delays
- Severe toxicity may cause wide QRS, arrhythmias from cardiovascular collapse and acidosis
- Continuous cardiac monitoring indicated for patients with hemodynamic instability
15. Assessment
Severity stratification based on elemental iron dose ingested: [3][11][18]
- <20 mg/kg: nontoxic, observation at home
- 20–60 mg/kg: mild-to-moderate; GI symptoms expected; home management may be appropriate if asymptomatic, but hospital referral if symptomatic
- >60 mg/kg: potentially life-threatening; requires hospital evaluation and likely chelation
- >120 mg/kg: potentially lethal
The five clinical phases: [1]
- Phase 1 (0.5–6 hrs): GI toxicity — vomiting, diarrhea, abdominal pain, GI hemorrhage
- Phase 2 (6–24 hrs): Relative stability — apparent clinical improvement (deceptive)
- Phase 3 (12–48 hrs): Circulatory shock, metabolic acidosis, cardiovascular collapse
- Phase 4 (2–4 days): Hepatotoxicity — fulminant hepatic failure, coagulopathy
- Phase 5 (2–8 weeks): GI scarring — pyloric/bowel strictures from mucosal necrosis
16. Treatment Plan
Initial stabilization
- ABCs, IV access, continuous monitoring
- Aggressive IV fluid resuscitation for shock
- Correct metabolic acidosis and coagulopathy
GI decontamination
- Whole bowel irrigation with PEG solution (GoLYTELY) at 1.5–2 L/hr (adults) or 500 mL/hr (children) until rectal effluent is clear and repeat KUB shows no remaining tablets [3][13]
- Activated charcoal is ineffective for iron
- Gastric lavage generally not effective due to tablet size
Chelation with deferoxamine — indications: [3][12]
- Serum iron ≥500 µg/dL
- Significant clinical toxicity (shock, AMS, metabolic acidosis, severe GI hemorrhage)
- Ingestion of ≥60 mg/kg elemental iron with symptoms
- Dosing: IV infusion at ≤15 mg/kg/hr; max 6,000 mg/24h
- Continue until clinical improvement, resolution of acidosis, and urine color normalizes
- Caution: prolonged infusion (>24 hours) associated with ARDS [12]
Supportive care
- Blood products for GI hemorrhage and coagulopathy
- Vasopressors if refractory shock
- N-acetylcysteine may be considered empirically if hepatotoxicity develops [9]
- Liver transplantation is the definitive treatment for iron-induced fulminant hepatic failure [10]
17. Disposition
- Admit to ICU: serum iron >500 µg/dL, hemodynamic instability, AMS, metabolic acidosis, need for deferoxamine infusion, significant GI hemorrhage [3][6]
- Admit for observation: serum iron 300–500 µg/dL, symptomatic patients, ingestion >40 mg/kg
- Discharge considerations: asymptomatic after 6-hour observation, serum iron <300 µg/dL, no metabolic acidosis, no radiopacities on KUB [3][14]
- Psychiatric evaluation mandatory before discharge for all intentional ingestions [3][5]
- Poison control should be contacted for all cases
18. Follow Up / Return Precautions
- Return immediately for: recurrent vomiting, bloody stools, abdominal pain, confusion, dizziness, or fainting
- Beware the quiescent phase — patients who appear to improve 6–24 hours post-ingestion may deteriorate into shock and hepatic failure [1]
- Follow-up LFTs at 48–72 hours if any concern for hepatotoxicity
- Late complication screening: patients with significant mucosal injury should be monitored for pyloric or bowel strictures (2–8 weeks post-ingestion) with symptoms of obstruction (vomiting, inability to tolerate feeds) [1][19]
- Counsel on safe medication storage and childproofing
- Psychiatric follow-up for intentional ingestions
References
1. Toxicokinetics and Toxicodynamics of Iron Poisoning. — Tenenbein M. Toxicology Letters. 1998.
2. Iron Overdose Epidemiology, Clinical Features and Iron Concentration-Effect Relationships: The UK Experience 2008-2017. — Bateman DN, Eagling V, Sandilands EA, et al. Clinical Toxicology. 2018.
3. Acute Medication Poisoning. — Vega IL, Griswold MK, Laskey D. American Family Physician. 2024.
4. Suicidal Iron Overdose: A Case Report and Review of Literature. — Yu D, Giffen MA. Journal of Forensic Sciences. 2021.
5. Intentional Iron Overdose: An Institutional Review. — Kroeker S, Minuk GY. CMAJ : Canadian Medical Association Journal = Journal De l'Association Medicale Canadienne. 1994.
6. Assessment of Acute Iron Poisoning by Laboratory and Clinical Observations. — Chyka PA, Butler AY. The American Journal of Emergency Medicine. 1993.
7. Serum Iron Concentrations and Symptoms of Acute Iron Poisoning in Children. — Chyka PA, Butler AY, Holley JE. Pharmacotherapy. 1996.
8. Hepatotoxicity in Acute Iron Poisoning. — Robertson A, Tenenbein M. Human & Experimental Toxicology. 2005.
9. Acute Liver Failure Due to Iron Overdose in an Adult. — Daram SR, Hayashi PH. Southern Medical Journal. 2005.
10. Liver Transplantation for Acute Liver Failure After Intentional Iron Overdose: A Case Report and Literature Review. — Kasuda K, Saito R, Nishiyama T, et al. Pediatric Transplantation. 2025.
11. Assessment of Management Guidelines. Acute Iron Ingestion. — Klein-Schwartz W, Oderda GM, Gorman RL, Favin F, Rose SR. Clinical Pediatrics. 1990.
12. FDA Drug Label. — Updated date: 2026-04-06. Food and Drug Administration.
13. Iron; Benefits or Threatens (With Emphasis on Mechanism and Treatment of Its Poisoning). — Rafati Rahimzadeh M, Rafati Rahimzadeh M, Kazemi S, et al. Human & Experimental Toxicology. 2023.
14. Unintentional Paediatric Iron Poisoning: A Retrospective Case Series. — Crofton AK, Harris K, Wylie C, Isoardi KZ. Emergency Medicine Australasia : EMA. 2021.
15. Fulminant Hepatic Failure in Woman With Iron and Non-Steroidal Anti-Inflammatory Drug Intoxication. — Magdalan J, Zawadzki M, Sozanski T. Human & Experimental Toxicology. 2011.
16. The Rise in the Total Iron-Binding Capacity After Iron Overdose. — Burkhart KK, Kulig KW, Hammond KB, et al. Annals of Emergency Medicine. 1991.
17. Performance Characteristics of Three Serum Iron and Total Iron-Binding Capacity Methods in Acute Iron Overdose. — Roberts WL, Smith PT, Martin WJ, Rainey PM. American Journal of Clinical Pathology. 1999.
18. Minimum Ingested Iron Cut-Off Triggering Serious Iron Toxicity in Children. — Halil H, Tuygun N, Polat E, Karacan CD. Pediatrics International : Official Journal of the Japan Pediatric Society. 2019.
19. Iron Poisoning. — Banner W, Tong TG. Pediatric Clinics of North America. 1986.