Iron Overdose

Overview & Definition

Iron overdose is a high-yield topic because it brings together four classic examination themes: a stereotyped four-stage clinical course with a deceptive latent phase that catches the unwary, a specific chelating antidote (desferrioxamine/deferoxamine) with a memorable urinary sign ('vin rose' urine), a critical decontamination distinction (iron is a metal and is not adsorbed by activated charcoal — whole bowel irrigation is used instead), and a precise dose-to-toxicity relationship based on the elemental iron content of the tablet rather than the salt weight.[1]

Iron is essential but, uniquely among nutrients, the body has no physiological excretory mechanism for it. All iron balance is regulated at absorption. In overdose, this conserved, easily-absorbed metal overwhelms the iron-binding capacity of transferrin, and the surplus circulates as free (non-transferrin-bound) iron — a powerful redox catalyst. Two injuries follow. First, free iron is directly corrosive to the gastrointestinal mucosa, producing haemorrhagic gastritis, vomiting, diarrhoea and fluid loss. Second, absorbed free iron enters cells and catalyses the Fenton reaction, generating hydroxyl radicals that peroxidise mitochondrial membranes, uncouple oxidative phosphorylation, and inhibit the Krebs cycle. The metabolic consequence is a high-anion-gap lactic acidosis; the tissue consequences are centrilobular hepatic necrosis, coagulopathy (direct inhibition of thrombin), acute tubular necrosis, and shock from a combination of hypovolaemia, venodilatation and myocardial depression.[5]

Iron overdose is a leading cause of accidental poisoning death in children (adult prenatal and iron tablets look like sweets to a toddler) and a recognised method of deliberate self-harm in adults, typically young women with access to iron tablets.[8] The clinical skill the examiner is testing is whether you can stratify severity using the elemental-iron dose, the serum iron level and the acid–base status, avoid the trap of the latent phase, refuse to give charcoal, and start IV desferrioxamine early for significant toxicity.

Classification

Iron poisoning is classified along two axes that the examiner will probe: the elemental-iron dose (which predicts severity) and the clinical stage (which dictates what you do at the bedside). A third axis — the pharmaceutical formulation (immediate-release versus sustained-release/enteric-coated) — modifies the timing of both the symptoms and the serum-iron peak.[1]

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Toxic-dose thresholds (ELEMENTAL iron)

The dose that matters is the elemental iron content, not the weight of the iron salt. This is the single most common calculation error in MCQ stems.[1]

[1]

Elemental-iron content of common formulations

The salt weight on the packet is not the iron dose. Always convert to elemental iron.[1]

[1]

The four clinical stages

The four-stage course is the central teaching point of the topic. The danger of stage 2 is that the patient looks well precisely while iron is being sequestered by transferrin and about to spill into tissues.[1]

Epidemiology & Risk Factors

Iron poisoning is a global problem with a paediatric face. Before the introduction of child-resistant packaging in the late 1990s and 2000s, iron was one of the leading causes of accidental poisoning death in children under six in the United States and Western Europe; mortality has fallen dramatically since, but clusters of severe cases persist wherever adult iron or prenatal tablets are stored unsafely.[2][8] In South Asia, where ferrous sulphate and fumarate are cheap, widely-available prenatal supplements, accidental childhood poisoning remains a public-health concern and intentional self-harm with iron is a recognised pattern in young women.[8]

The risk factors for a severe outcome cluster around three questions: how much elemental iron was taken, what formulation, and how quickly treatment began.[1]

[1]

Modern series report mortality under 5 percent with prompt chelation, but historical mortality in severe untreated ingestions reached up to 45 percent.[2] The lesson the examiner wants: severity is dose-and-time dependent, and the dose is the elemental iron.

Pathophysiology

Iron injures the body in two mechanistically distinct waves: a direct corrosive effect on the gastrointestinal mucosa, and a systemic free-radical toxicity mediated by catalytic free (non-transferrin-bound) iron once the binding capacity of transferrin is exceeded. Understanding the second wave is the key to understanding every clinical and biochemical feature of stage 3.[5]

Wave 1 — gastrointestinal corrosive injury

In the stomach and duodenum, free iron in the lumen is directly caustic to the mucosa. The result is haemorrhagic gastritis (often erosive and confluent in the gastric antrum and pylorus), with vomiting that is frequently haematemetic, abdominal pain, and diarrhoea that may be frankly bloody. The fluid sequestration into the injured gut, plus overt GI bleeding, produces the hypovolaemic shock of stage 1.[1] The same corrosive injury is the substrate for the late scarring and gastric-outlet obstruction of stage 4.

Wave 2 — systemic free-radical toxicity (the Fenton reaction)

Once absorbed iron exceeds the iron-binding capacity of transferrin, the surplus circulates as free (non-transferrin-bound) iron. Free iron is taken up by cells (especially hepatocytes, via a transferrin-independent pathway) and becomes a redox catalyst in the Fenton reaction:[5]

The reaction is: Fe2+ + H2O2 -> Fe3+ + hydroxyl radical (OH•) + hydroxide ion (OH-). Iron is regenerated by reduction back to Fe2+, so a small amount of free iron catalyses a large, self-sustaining flux of hydroxyl radicals. [1]

The hydroxyl radical (OH•) is among the most reactive species in biology. It abstracts hydrogen atoms from polyunsaturated fatty acids in mitochondrial and cell membranes, initiating lipid peroxidation that propagates as a chain reaction. The membrane damage has three downstream consequences that explain the entire stage-3 phenotype:[5]

Why shock, hepatic necrosis and coagulopathy?

The cellular damage does not strike all organs equally.[5]

Shock. Free iron causes venodilatation and reduced systemic vascular resistance (peripheral vasodilatation) and depresses myocardial contractility. The shock of stage 3 is therefore a combination of hypovolaemia (residual GI losses), distributive (vasodilatation) and cardiogenic (myocardial depression) shock — one of the few poisons to produce all three patterns together.[1]

Hepatic necrosis. The liver is the preferential target because hepatocytes take up free iron avidly via a transferrin-independent pathway, and because zone 3 (centrilobular) hepatocytes — the most metabolically active, with the highest cytochrome P450 activity and oxygen demand — are the most vulnerable to oxidative injury. The result is centrilobular (zone 3) necrosis, the same pattern seen in paracetamol hepatotoxicity and ischaemic hepatitis.[5]

Coagulopathy. Free iron directly inhibits thrombin generation and the vitamin-K-dependent factors. The early, sometimes isolated, rise in PT/INR (within the first 12–24 h, before AST/ALT have peaked) is therefore an anticoagulant effect of iron itself, not yet hepatic synthetic failure. The later coagulopathy (after 24–48 h) is true hepatic synthetic failure. This distinction matters: an early INR rise does not by itself prove liver failure, but a rising INR with rising transaminases does.[1]

The basis of the latent phase

Stage 2 looks deceptively quiet because absorbed iron is being temporarily sequestered by transferrin in plasma and by the reticuloendothelial system. Once these binding sites are saturated — typically between 6 and 24 h after ingestion — free iron spills into tissues and stage 3 begins. The clinical lesson, repeated because examiners test it: in the latent window, clinical appearance is a lie; only the serum iron and the metabolic acidosis tell the truth.[1]

Clinical Presentation

The clinical presentation is the four-stage course described above, made real. The examiner will test whether you can recognise each stage, anticipate the next, and avoid being reassured by stage 2.[1]

Stage 1 (0 to 6 h) — gastrointestinal corrosive injury. Within the first one to two hours, the patient develops vomiting (often haematemetic), abdominal pain and diarrhoea (may be bloody). The abdomen may be diffusely tender. Dehydration is rapid in children. With significant doses, hypovolaemic shock is established within hours — tachycardia, delayed capillary refill, hypotension, oliguria, altered consciousness. The severity of stage 1 predicts progression: a patient who is shocked in stage 1 is at high risk of progressing to stage 3. [1]

Stage 2 (6 to 24 h) — the deceptive latent phase. The GI symptoms settle and the patient looks better. This is the dangerous window: clinicians may be falsely reassured and discharge the patient. The truth is that iron is being sequestered by transferrin and is about to saturate binding capacity. Disposition in this window must be based on the serum iron, the anion gap and the formulation, not on clinical appearance.[1]

Stage 3 (12 to 48 h) — systemic toxicity. This is the killer stage and the focus of intensive care. The patient develops, in variable combination:[1]

Stage 4 (4 to 6 weeks) — late gastric-outlet obstruction. Weeks after recovery, scarring of the gastric antrum or pylorus (the sites of maximal corrosive injury) produces gastric or pyloric outlet obstruction. The patient presents with early satiety, post-prandial vomiting (sometimes of food eaten a day earlier) and weight loss. A succussion splash may be present. Upper GI endoscopy confirms the stricture; management is endoscopic balloon dilation, repeated as needed, with surgery for refractory cases.[1]

Atypical and modified presentations

Examiners deliberately probe the corners. Three atypical patterns deserve attention.[2]

Differential Diagnosis

The differential of a patient presenting with vomiting, haematemesis, diarrhoea and a high-anion-gap metabolic acidosis is broad, and iron is only one cause. The discriminator is the history of iron-tablet ingestion, supported by radiopaque tablets on the abdominal X-ray and a serum iron level that is high, with hyperglycaemia and leucocytosis as clues.[2]

The key manoeuvre at the bedside is to send serum iron, salicylate and paracetamol levels together, and to calculate the anion gap and (if any doubt) the osmolal gap. A normal osmolal gap with radiopaque tablets and a high iron level closes the case for iron.[2]

Clinical & Bedside Assessment

The bedside assessment has three objectives: estimate the elemental-iron dose, grade the current severity, and decide whether to decontaminate and chelate now.[1]

History. Establish the time since ingestion, the number and type of tablets (and calculate the elemental iron), the formulation (immediate-release versus sustained-release), any co-ingestants, the intent (accidental versus self-harm), and — in children — the access to adult iron tablets. Ask specifically about prenatal tablets, ferrous sulphate versus fumarate versus gluconate, and any sustained-release preparation.[4]

Examination. Perform a focused ABCDE: vital signs (HR, BP, RR, temperature, SpO2, GCS), hydration and perfusion (capillary refill, mucus membranes, skin), the abdomen (tenderness, peritonism, distension — beware perforation), and a search for stage-3 features (shock, jaundice, bleeding, oliguria, altered consciousness). A succussion splash weeks later suggests the stage-4 stricture.[1]

Estimate the elemental-iron dose at the bedside. Multiply the number of tablets by the elemental-iron content per tablet (ferrous sulphate 325 mg = 65 mg; ferrous fumarate 325 mg = 106 mg; ferrous gluconate 325 mg = 38 mg) and divide by the weight in kg. Stratify immediately:[4]

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Plain abdominal X-ray. A KUB or abdominal X-ray may show radiopaque iron tablets in the stomach or small bowel. They are visible in roughly 30 to 50 percent of significant ingestions. Their presence confirms the diagnosis and guides decontamination (continue whole bowel irrigation until no tablets remain). Their absence does NOT exclude iron poisoning — tablets may have dissolved, been crushed, or be enteric-coated.[1]

Severity markers triggering desferrioxamine. Any one of: shock, metabolic acidosis, severe GI symptoms, altered consciousness, serum iron over 500 microgram/dL, or serum iron over 350 microgram/dL with symptoms.[1]

Investigations

The investigation bundle has three layers: the iron-specific tests, the severity / acid–base tests, and the rule-out co-ingestion tests.[2]

Serum-iron thresholds

The serum iron drawn at 4 to 6 h is the central laboratory number. It must be interpreted alongside the acid–base status — a borderline iron level with a high-anion-gap acidosis is still significant toxicity.[1]

Timing caveat

For immediate-release formulations, the peak serum iron is at 4 to 6 h. For sustained-release and enteric-coated formulations, absorption is delayed and the peak may not occur until 8 to 12 h or later. Always draw a level at 4 to 6 h AND repeat it at 8 to 12 h for sustained-release formulations, and treat a rising or high level.[2]

The WBC–glucose–iron triad

Three non-specific clues support the diagnosis and are favourite exam material:[1]

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The total iron-binding capacity (TIBC) — a trap

Historically a serum iron exceeding the TIBC (ratio over 1) was taken to indicate free iron. In practice, TIBC assays are unreliable in acute overdose (binding proteins are themselves affected, and the assay is slow). Do not wait for, or rely on, the TIBC ratio — treat on the iron level and the acid–base status.[1]

The desferrioxamine challenge test — abandoned

An older practice was to give 50 mg/kg intramuscular desferrioxamine (maximum 1 g) and observe for vin-rose urine ('rose test'). A positive result supposedly indicated free iron. Modern toxicology has abandoned the challenge test because it delays definitive IV chelation and is unreliable. Treat on the serum iron and acidosis.[3]

Management — Resuscitation

[1]

The resuscitation bundle is run concurrently with the investigations, not after them. The aims are to restore perfusion, secure the airway, control GI haemorrhage, prepare for decontamination and chelation, and avoid the useless and harmful interventions.[1]

ABCDE. Secure the airway (intubate early if comatose or shock is severe); give high-flow oxygen if hypoxic or in shock; establish two large-bore IV cannulae with continuous cardiac monitoring and (in severe cases) a urinary catheter to track output and the vin-rose colour.[1]

Fluid resuscitation. Give isotonic crystalloid (0.9% sodium chloride or a balanced crystalloid such as Hartmann's) in 10 to 20 mL/kg boluses, titrated to perfusion (capillary refill, blood pressure, urine output, lactate clearance). Children tolerate and may need larger relative boluses; the elderly and the anuric need caution (smaller boluses, frequent reassessment) to avoid pulmonary oedema. The shock of iron poisoning is multifactorial (hypovolaemic + distributive + cardiogenic), so vasopressors (noradrenaline) may be needed once intravascular volume is restored.[1]

Bloods before treatment. Draw the iron level, VBG, electrolytes, anion gap, glucose, FBC, PT/INR, LFTs, renal function, paracetamol and salicylate levels, and beta-hCG before starting desferrioxamine, because the chelator alters the iron assay. Cross-match if there is haematemesis.[2]

GI haemorrhage. Transfuse for significant bleeding; start a proton-pump inhibitor infusion; involve endoscopy and surgery early for uncontrolled haemorrhage or a large tablet bezoar. Iron-tablet bezoars may need endoscopic or surgical removal.[1]

The metabolic acidosis. The definitive treatment is desferrioxamine, which removes the iron generating the acid. Sodium bicarbonate has a limited adjunctive role for a pH under 7.1 to 7.2 — it improves haemodynamics and increases iron binding to transferrin — but it must not delay chelation. Do not chase the pH with bicarbonate at the expense of starting the chelator.[1]

What NOT to do. The single most important 'do not' in iron overdose: do not give activated charcoal. Iron is a metal, not an organic molecule, and charcoal does not adsorb it. Charcoal is useless here, obscures the view at endoscopy, and is not the decontamination of choice. The correct decontamination is whole bowel irrigation.[6][12]

Management — Definitive & Stepwise

The definitive management ladder runs from decontamination through chelation to organ-failure support. Each step has explicit triggers.[1]

Step 1 — Resuscitation (above)

ABCDE, crystalloid, oxygen, bloods before treatment; treat shock, acidosis and GI haemorrhage. [1]

Step 2 — Decontamination: whole bowel irrigation (NOT charcoal)

Whole bowel irrigation (WBI) is the decontamination of choice for iron. It is endorsed by the AACT/EAPCCT position statements.[11][12]

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Step 3 — Antidote: IV desferrioxamine (deferoxamine)

Desferrioxamine (deferoxamine, DFO) is a siderophore that binds free iron in a stable 1:1 complex (ferrioxamine), which is then excreted in the urine, giving it the characteristic vin-rose (pink-red) colour. It is the definitive treatment for significant iron toxicity.[1]

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Step 4 — Supportive care for organ failure

Stage-3 patients need intensive-care support for failing organs.[1]

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Escalation triggers to ICU, endoscopy and surgery

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Specific Subtypes & Scenarios

Paediatric accidental ingestion (the commonest scenario)

The typical victim is a toddler (1 to 4 years) who has found adult prenatal or iron tablets. Calculate the elemental iron mg/kg at once.[4]

[1]

Typically a young woman with access to iron tablets, often ingesting a large number of tablets, frequently sustained-release. Draw levels at 4 to 6 h AND repeat at 8 to 12 h; observe for at least 6 to 12 h (longer for sustained-release); low threshold for WBI and chelation; psychiatric assessment after medical stabilisation; secure the iron supply at discharge.[8]

Sustained-release and enteric-coated formulations

Absorption is delayed. Stage 1 may be prolonged or biphasic, the latent phase is distorted, and the serum-iron peak shifts to 8 to 12 h or beyond. Draw levels at 4 to 6 h AND repeat at 8 to 12 h, prolong WBI, and admit and observe for at least 12 to 24 h. Never discharge a sustained-release ingestion at 6 h.[2]

Pregnancy

Iron overdose in pregnancy typically involves prenatal iron. IV desferrioxamine IS indicated for severe maternal toxicity — the modern consensus is that maternal survival is the priority and deferring chelation for fear of fetal metal chelation costs maternal lives. Desferrioxamine crosses the placenta, but untreated maternal iron toxicity is far more dangerous to the fetus than chelation. Involve obstetrics, monitor the fetus, and remember that maternal outcome determines fetal outcome.[9][10]

Massive ingestion with tablet bezoar

A visible radiopaque mass on KUB that does not progress despite WBI may be a tablet bezoar. Endoscopic removal is first-line; surgical gastrotomy is reserved for unremovable bezoars causing obstruction or perforation. Continue WBI and chelation meanwhile.[1]

Co-ingestion (especially paracetamol)

Always send a paracetamol level at 4 h and apply the Rumack-Matthew nomogram. Co-ingestion worsens the hepatic prognosis (additive centrilobular necrosis) and may mask iron hepatitis. Treat both: N-acetylcysteine for the paracetamol, desferrioxamine for the iron.[2]

Complications & Pitfalls

Acute complications

Late complications

Gastric or pyloric outlet obstruction from scarring (4 to 6 weeks) is the classic late complication — early satiety, post-prandial vomiting, weight loss, succussion splash; managed by endoscopic balloon dilation or surgery. Less common: bowel stricture, intestinal perforation, chronic liver injury.[1]

Classic pitfalls

[1]

The desferrioxamine–ARDS and Yersinia pitfalls

Prolonged or very-high-dose desferrioxamine is associated with an acute lung injury picture ('desferrioxamine lung') and with an increased risk of Yersinia enterocolitica sepsis, because desferrioxamine is itself a siderophore that Yersinia uses to acquire iron. Suspect Yersinia sepsis in any febrile patient on desferrioxamine. The counter-measure is to stop chelation once the iron level is falling and the acidosis has resolved — do not chelate to zero.[7]

Prognosis & Disposition

The overall mortality of iron poisoning is under 5 percent in modern series with prompt chelation, but historically reached up to 45 percent in severe untreated ingestions. Severe poisoning — serum iron over 1000 microgram/dL, refractory acidosis, multi-organ failure — still carries significant mortality even with chelation.[2]

Predictors of poor outcome: large elemental-iron dose (over 60 mg/kg), sustained-release formulation, delay to desferrioxamine, anion-gap acidosis with pH under 7.1, hepatic failure with coagulopathy, multi-organ failure, and young age.[1]

Disposition criteria

Special Populations

[1]

Evidence, Guidelines & Regional Differences

The 2005 AACT/EAPCCT consensus (Manoguerra et al.) on out-of-hospital management of iron ingestion set the triage thresholds still in use: refer to the emergency department for any symptoms, any ingestion over 40 mg/kg elemental iron (or any sustained-release ingestion over 40 mg/kg), or any intentional ingestion; home observation is acceptable only for asymptomatic ingestions under 20 mg/kg.[4]

Whole bowel irrigation is endorsed by the AACT/EAPCCT 1997 position statement (Tenenbein) and its 2023 update, as the decontamination modality of choice for iron, sustained-release/enteric-coated drugs, and body-packers; it is powered by polyethylene-glycol electrolyte solution run until the rectal effluent is clear.[11][12]

The 2026 Clinical Toxicology Recommendations Collaborative reaffirmed that decontamination remains useful in selected poisonings, including iron, and that activated charcoal has no role in metal (iron) poisoning — WBI is the modality.[6]

Controversies

The desferrioxamine challenge test. Historically, 50 mg/kg IM desferrioxamine with observation for vin-rose urine was used to 'test' for free iron. It has been abandoned in favour of early IV chelation based on the serum iron and acidosis, because it delays definitive treatment and is unreliable.[3]

Desferrioxamine dosing. Historical high-dose protocols (15 mg/kg/h uptitrated to 90 mg/kg/h) caused more ARDS and hypotension. Current practice favours 15 mg/kg/h titrated to clinical response with earlier cessation, balancing efficacy against the pulmonary and infectious complications of prolonged chelation.[1]

Total iron-binding capacity (TIBC). A serum iron exceeding the TIBC was once a chelation trigger. TIBC is unreliable in acute overdose and is not used to guide modern therapy.[1]

Regional deltas

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Exam Pearls

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Exam application bank (NEET-PG / INICET)

One-line answer

Iron overdose is one of the leading causes of accidental poisoning death in children (adult prenatal/iron tablets look like sweets) and an occasional means of deliberate self-harm in adults. Iron is corrosive to the gastrointestinal mucosa (haemorrhagic gastritis, vomiting, diarrhoea) and, once absorbed iron exceeds transferrin binding capacity, becomes a systemic free-radical toxin via the Fenton reaction — it uncouples oxidative phosphorylation, blocks the Krebs cycle and produces lactic (high-anion-gap) acidosis, centrilobular hepatic necrosis, coagulopathy (direct thrombin inhibition), shock and multi-organ failure. Toxic dose (elemental iron): under 20 mg/kg usually asymptomatic; over 20 mg/kg mild; over 40 mg/kg significant; over 60 mg/kg severe, potentially lethal. Four clinical stages: Stage 1 (0 to 6 h) GI corrosive injury + hypovolaemic shock; Stage 2 (6 to 24 h) deceptive late [1]

Worked stems (answer without another resource)

Stem 1 — Classic presentation. Map symptoms to mechanism; name the first investigation and first treatment step with dose/route if drug therapy is standard. [1]

Stem 2 — Unstable / complicated. List red flags that force immediate resuscitation, theatre, ICU, antidote, or reperfusion — and what you do in the first 15 minutes. [1]

Stem 3 — Atypical group. Elderly, pregnancy, child, or immunocompromised: how presentation and thresholds change. [1]

Stem 4 — Differential trap. Name the three closest mimics and one discriminator for each. [1]

Stem 5 — Disposition. Who goes home with safety-netting, who is admitted, who needs HDU/ICU/theatre, and what follow-up is mandatory. [1]

Rapid viva checklist

1. Definition + classification
2. Pathophysiology chain
3. Bedside signs / criteria
4. Score with exact components (if any)
5. Emergency bundle
6. Definitive therapy with doses
7. Complications of disease and of treatment
8. Special populations
9. Guideline/trial name if classic
10. Three exam traps

Coverage self-check

If you cannot answer any stem above from this page alone, re-read the matching section — the page is intended to be self-sufficient for final-prof and NEET-PG/INICET questions on Iron Overdose.

References

1. [1]Fine JS. Iron poisoning Curr Probl Pediatr, 2000.PMID 10742921
2. [2]Chang TP, Rangan C. Iron poisoning: a literature-based review of epidemiology, diagnosis, and management Pediatr Emerg Care, 2011.PMID 21975503
3. [3]Madiwale T, Vereb S, Muzumdar H, Donn S, Rosenfeld W. Iron: not a benign therapeutic drug Curr Opin Pediatr, 2006.PMID 16601499
4. [4]Manoguerra AS, Erdman AR, Booze LL, Christianson G, Wax PM, Scharman EJ, Woolf AD, Keyes DC, Olson KR, Chyka PA, Caravati EM, Troutman WG. Iron ingestion: an evidence-based consensus guideline for out-of-hospital management Clin Toxicol (Phila), 2005.PMID 16255338
5. [5]Rafati Rahimzadeh M, Rafati Rahimzadeh M, Kazemi S, Moghadamnia AA. Iron; Benefits or threatens (with emphasis on mechanism and treatment of its poisoning) Hum Exp Toxicol, 2023.PMID 37526177
6. [6]Hoegberg LCG, Good AM, Tracy JA, Rubino MM, Höjer J, Cottrell E, Buckley NA, Thanacoody HKR, Greene SL, Cincinnati Clinical Toxicology Recommendations Collaborative. Recommendations from the Clinical Toxicology Recommendations Collaborative on the administration of activated charcoal in acute oral overdose Clin Toxicol (Phila), 2026.PMID 41906697
7. [7]Mofenson HC, Caraccio TR, Sharieff N. Iron sepsis: Yersinia enterocolitica septicemia possibly caused by an overdose of iron N Engl J Med, 1987.PMID 3561464
8. [8]Chandran J, Khanna K, Jayashree M, Gautam V, Sharma A, Singh M. Accidental iron poisoning in children - Experience from a teaching institution J Family Med Prim Care, 2023.PMID 38074262
9. [9]Tran T, Waxman B, Akgur FM, Hcl T, Tanyel FC, Turkmen MA, Buyukpamukcu N, Oudesluys-Murphy AM. Intentional iron overdose in pregnancy--management and outcome J Emerg Med, 2000.PMID 10699527
10. [10]Tran T, Waxman B, Nguyen A, Leong M, Tsueda K, Ueland K, Vohra BK, Roszler MH. Acute intentional iron overdose in pregnancy Obstet Gynecol, 1998.PMID 9764661
11. [11]Tenenbein M, Lheureux P, Position Statement Writing Group for the AACT/EAPCCT. The role of whole bowel irrigation in the treatment of toxic ingestions Br J Clin Pharmacol, 2023.PMID 36639859
12. [12]Tenenbein M. Position statement: whole bowel irrigation. American Academy of Clinical Toxicology; European Association of Poisons Centres and Clinical Toxicologists J Toxicol Clin Toxicol, 1997.PMID 9482429