Iron Overdose

Meet the patient

A 22-month-old is brought from home after her mother found her beside an open bottle of prenatal ferrous sulphate, blue sugar-coated tablets scattered across the floor. She has vomited three times in the first hour — the last streaked with blood — and cries when her abdomen is pressed.^[8]

The bottle states the salt weight and the elemental iron per tablet, and she weighs ten kilograms. Two questions decide her next twelve hours: how many tablets did she swallow? — the calculation uses the ELEMENTAL iron content, because every triage threshold is set in elemental mg/kg — and what are the serum iron and the acid–base status doing? — because she will look better before she looks worse, and that is the trap this topic exists to teach.^[4]

What iron does — corrosive in the gut, a redox catalyst in the cell

Swallowed iron injures first at the mucosa, then inside the cell. In overdose it causes corrosive damage to gastrointestinal mucosa (acute haemorrhagic gastritis, fluid loss, bleeding and shock). When serum iron exceeds binding capacity, free iron increases reactive oxygen species — hydroxyl radical, superoxide and hydrogen peroxide — producing lipid peroxidation and membrane damage.^[14][5]

Intracellularly, iron shunts electrons away from the electron-transport chain and uncouples oxidative phosphorylation, driving anaerobic metabolism and metabolic acidosis. It also causes post-arteriolar dilatation, increased capillary permeability and coagulopathy, with ROS-induced myocardial injury contributing to shock.^[14]

The downstream phenotype is metabolic acidosis, periportal hepatic necrosis, coagulopathy and shock. From 1983 to 1991 iron caused over 30% of deaths from accidental ingestion of drug products by children in the United States; adult ferrous-salt and prenatal tablets remain the typical paediatric source, and intentional overdose is a recognised form of self-harm. The skill tested is fourfold: stratify by elemental dose, serum iron and acid–base; refuse the latent-phase reassurance; refuse charcoal; chelate when serious symptoms or a toxic iron concentration are present.^[4][8][29]

Two axes that decide everything — elemental dose and clinical stage

Severity is anchored on the elemental-iron dose; management is dictated by the clinical stage. A third axis — the formulation (immediate-release versus modified-release) — shifts both, and the suspected dose alone is an imperfect predictor, so the symptomatic patient is investigated whatever the estimate. Hold these three axes and the rest of the topic is mechanical.^[13][27]

Enlarge

^{[13] [4] [14] [26]}

The toxic-dose ladder — count elemental iron, never the salt

The number that matters is elemental iron, not the salt weight printed on the packet. This is the commonest calculation error in the MCQ stem — convert to elemental first, then divide by the weight in kilograms.^[4][13]

^{[13] [4] [26] [27]}

The salt is a decoy — always count ELEMENTAL iron

The same salt weight is a different iron dose depending on the product. Ferrous sulphate is 20% elemental iron; ferrous fumarate is 32%. Take the elemental content on the label and divide by kilograms. In reported ingestions, 55 tablets of ferrous gluconate 325 mg gave an estimated 130 mg/kg elemental dose in a toddler, while a 100-tablet bottle of ferrous sulphate 100 mg Fe2+ per tablet was 160 mg/kg in an adult who later died.^{[14][8][20][31]}

^{[8] [4] [31] [33] [32] [30] [3]}

The stages — and the quiet interval that kills the unwary

Published time-courses disagree on the clock but agree on the sequence: GI injury, a deceptive quiet interval, systemic toxicity, then late gastric scarring. Baranwal and Singhi tabulate four progressive stages; Morales-Cruz et al. describe five (splitting systemic and hepatic phases) and note that not every patient traverses every stage. Treat the serum iron and the acid–base, never the face, in the quiet window.^[14][26]

^{[14] [26] [34]}

Who takes iron, and who dies — the paediatric face

Iron poisoning has a child's face, and the lethal tablet is usually a maternal prenatal. From 1983 to 1991, iron caused over 30% of the deaths from accidental ingestion of drug products by children. Unit-dose packaging of iron preparations appeared to decrease exposures and deaths in the United States during the period it was used. In a South Indian PICU series, every child had consumed iron tablets from their pregnant mother.^[4][3][8]

In South Asia the paediatric problem is still live. In Chandran's South Indian PICU series every child had taken a pregnant mother's tablets; two of five died with liver failure. Intentional overdose is a recognised cause of self-harm, particularly among adolescents (Wada).^[8][29]

The risk factors for a severe outcome cluster around three questions: how much elemental iron, what formulation, and how quickly treatment began. Delayed presentation is associated with high mortality in reported case series, and coagulopathy, acute liver failure and shock mark the severe end.^[8][14]

^{[13] [4] [27] [11] [33] [15] [8] [9] [14]}

Outcome is not a single modern percentage. Chandran's five-child South Indian series had two deaths, both with liver failure (one presenting at 100 hours). Predictors there were coagulopathy, acute liver failure and delayed presentation. Manoguerra's historical figure remains the sourced population statistic: over 30% of paediatric accidental drug-ingestion deaths, 1983–1991.^[8][4]

The two waves — corrosion, then reactive oxygen species

Iron kills in two mechanistically distinct waves: corrosion in the gut, then ROS injury inside the cell. The first wave explains the vomiting, the haematemesis and the hypovolaemic shock of early toxicity; the second — free iron once binding capacity is exceeded — explains the acidosis, shock and hepatic necrosis of systemic toxicity.^[14][5]

Enlarge

Wave 1 — gastrointestinal corrosive injury

In the stomach and duodenum, luminal free iron is directly caustic to the mucosa. The lesion is haemorrhagic gastritis, erosive and confluent in the gastric antrum and pylorus — hence the haematemetic vomiting, the abdominal pain, the bloody diarrhoea, and the hypovolaemic shock of stage 1 from fluid sequestration and overt bleeding. The same burn scars over weeks into the gastric-outlet stricture of stage 4.^[2][20]

Wave 2 — reactive oxygen species, and why free iron does so much damage

Once serum iron exceeds binding capacity, free iron increases ROS (hydroxyl radical, superoxide, hydrogen peroxide) and lipid peroxidation. Baranwal locates the intracellular lesion at the mitochondrion: iron shunts electrons away from the electron-transport chain and uncouples oxidative phosphorylation, producing anaerobic metabolism and metabolic acidosis.^[14][5]

^{[14] [34]}

Three organs explain most of the death — and one coagulopathy trap

The cellular damage does not strike all organs equally. Shock, hepatic failure and coagulopathy carry the mortality of systemic toxicity.^[14]

Shock. Baranwal describes post-arteriolar dilatation, increased capillary permeability and coagulopathy producing severe acidosis and shock within the first few hours, with ROS-induced myocardial failure contributing — so the shock is hypovolaemic plus vasodilatory plus cardiogenic.^[14]

Hepatic necrosis. Autopsy and clinical reviews locate iron's cytopathic effect in the periportal area of the lobule, which is also the primary site of hepatic regeneration — hence the high mortality of iron-related acute liver failure. This is not the centrilobular (zone 3) pattern of paracetamol. Robertson defined hepatotoxicity as transaminase over 150 U/L and severe hepatotoxicity as over 1000 U/L, typically with serum iron well over 1000 microgram/dL.^[14][34]

Coagulopathy. Coagulopathy is part of early systemic toxicity (Baranwal stage III list) and a poor prognostic marker when the prothrombin index is under 50 percent. Do not wait for a named thrombin assay; treat the coagulopathy you measure.^[14]

The basis of the quiet interval

Apparent stabilization is attributed to redistribution of free circulating iron from the intravascular space into reticuloendothelial cells and the intracellular compartment. Once that buffering is exhausted, mitochondrial toxicity declares itself. In this window, clinical appearance is a lie; only the serum iron and the metabolic acidosis tell the truth.^[14]

The stages made real — recognise each, anticipate the next

Walk the sourced sequence onto the bedside: GI injury, quiet interval, mitochondrial/systemic toxicity, late scarring. Your job is to recognise where the patient is, anticipate the next, and refuse to be reassured by the quiet interval. Time windows differ between Baranwal (four stages) and Morales-Cruz (five); overlapping clocks are expected.^[14][26]

Early GI toxicity (Baranwal 0 to 3 h; Morales-Cruz 0.5 to 6 h). Vomiting (often haematemetic), abdominal pain and diarrhoea; third-spacing and bleeding produce hypovolaemic shock. In severe cases CNS depression and cardiovascular collapse occur in this first window.^[14][26]

Apparent stabilization (Baranwal until 12 h; Morales-Cruz 6 to 24 h). Gastrointestinal symptoms settle and the patient looks better — exactly when the unwary discharge. Disposition in this window rests on the serum iron, the anion gap and the formulation, never on the face.^[14][26]

Consultant confession: the toddler who looks brighter at eight hours is the one who frightens me. I trust the serum iron and the venous gas — I have never regretted keeping one, and I have regretted sending one home.^[14]

Mitochondrial / systemic toxicity (Baranwal 12 to 48 h; Morales-Cruz 6 to 72 h, with a separate hepatic window at 12 to 96 h). This is the focus of intensive care; the patient develops, in variable combination:^[14][26]

^{[14] [34] [26]}

Late gastric scarring (Baranwal 2 to 4 weeks in the table, 2 to 6 weeks in the prose; Morales-Cruz 2 to 8 weeks). After recovery, gastric scarring and pyloric strictures produce gastric-outlet obstruction — recurrent vomiting, early satiety, weight loss. Counsel survivors to return if these appear. Morales-Cruz also lists liver fibrosis in this late window.^[14][26]

Atypical presentations — the corners examiners probe

Examiners probe the corners, and three atypical patterns deserve attention.^[15][11]

^{[15] [11]}

The high-anion-gap acidosis — iron is only one cause

The discriminator is the history of iron-tablet ingestion, not the acidosis itself. Vomiting, haematemesis, diarrhoea and a high-anion-gap metabolic acidosis fit many poisons; iron is settled by the tablet history, radiopaque tablets on the abdominal X-ray, a high serum iron, and the hyperglycaemia–leucocytosis clues.^[2]

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

The bedside round — dose first, then severity, then the chelation trigger

The bedside assessment has three objectives, in order: estimate the elemental-iron dose, grade the current severity, and decide whether to decontaminate and chelate now.^[4]

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.^[13]

Estimate the elemental-iron dose at the bedside. Multiply the number of tablets by the ELEMENTAL iron content stated on the label and divide by the weight in kg — in a reported case, 55 ferrous gluconate 325 mg tablets meant an estimated 130 mg/kg in a toddler. Stratify immediately:^[4][20]

^{[4] [13] [14] [27]}

Plain abdominal X-ray. A KUB may show radiopaque iron tablets in the stomach or small bowel — their presence is one of the markers of severe toxicity and need for chelation in paediatric guidance, and it targets decontamination (whole bowel irrigation until no tablets remain). Their absence does NOT exclude iron poisoning: chewable preparations are rarely visualised on clinical radiographs despite being radiopaque in vitro.^[14][32]

Severity markers triggering desferrioxamine. McGuigan: give intravenous deferoxamine when there are serious clinical symptoms or when a serum iron over 500 microgram/dL is measured within 8 hours of ingestion. Fox restates the traditional laboratory trigger as 350 microgram/dL with symptoms, or 500 without. Baranwal additionally lists estimated ingestion over 60 mg/kg, symptoms, glucose over 150 mg/dL, leukocyte count over 15,000 per cubic millimetre, and tablets on the abdominal radiograph as indications of severe toxicity and need for chelation — those last two laboratory clues do not predict iron over 300 microgram/dL in adults (Palatnick).^{[13][15][14][18]}

Serum iron at four to six hours — the number that runs the resus

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

^{[15] [14] [19]}

Serum-iron thresholds — the number that triggers chelation

The serum iron drawn at least 4 hours after ingestion is the central laboratory number, and it is never read alone. A borderline iron with a high-anion-gap acidosis is still significant toxicity — interpret the two together, and remember that iron and symptoms overlap considerably in children.^[15][17]

^{[15] [13] [34] [29] [28]}

The sustained-release trap — the peak that comes late

The classic trap: a single early level reassures nobody. Concentrations drawn before 4 h can be falsely low — Fox's series found that a 2-to-4-hour concentration of 300 microgram/dL or less with at most minor gastrointestinal symptoms had a 100% negative predictive value for a later concentration of 350 or more. Modified-release products still warrant repeating the level while the patient remains exposed.^[15][11]

The WBC–glucose–iron triad — three non-specific clues

The WBC–glucose–iron cluster — taught everywhere, tested carefully. Paediatric management guidance lists leucocytosis and hyperglycaemia among the markers of severe toxicity, but clinical studies repeatedly show they do NOT reliably predict the serum iron — use them as clues, never as triggers.^[14][18][16]

^{[14] [18]}

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

The classic trap: historically a serum iron exceeding the TIBC was a chelation trigger. The ratio performs poorly — an iron above the TIBC did not identify serious poisoning in a paediatric series, and laboratory methods for TIBC are unreliable when free iron or deferoxamine is present. Do not wait for, or rely on, the ratio; treat on the iron level and the acid–base status.^[16][19]

The desferrioxamine challenge test — abandoned, do not use

An older practice gave intramuscular desferrioxamine and watched for vin-rose urine. Modern practice treats on the serum iron and the acidosis — the vin-rose sign is not seen consistently after chelation, and the optimal indications and dosing of deferoxamine remain unproven.^[14][24]

Resuscitation — and the one thing you must NOT do

Enlarge

^[14]

Run the resuscitation bundle concurrently with the investigations, not after them. The aims are to restore perfusion, secure the airway, control gastrointestinal haemorrhage, prepare for decontamination and chelation, and refuse the useless and harmful interventions.^[20]

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.^[20]

Fluid resuscitation. Give isotonic crystalloid boluses titrated to perfusion (capillary refill, blood pressure, urine output, lactate clearance) — crystalloid hydration is standard in reported severe cases, including in pregnancy. 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 may be needed once intravascular volume is restored.^[10][21][14]

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 reduces iron recovery in the assay. Cross-match if there is haematemesis.^[19][2]

GI haemorrhage. Transfuse for significant bleeding — reported cases needed packed red cells for necrotising gastroenteritis. Involve endoscopy early: esophagogastroduodenoscopy evaluates mucosal injury and can remove undissolved iron tablets; surgery for the uncontrolled.^[20][5]

The metabolic acidosis. The definitive treatment is desferrioxamine, which removes the iron generating the acid; severe acidosis is itself a poor prognostic marker. Adjunctive bicarbonate must not delay chelation — do not chase the pH at the expense of starting the chelator. (Consensus guidance also rejects oral bicarbonate solutions as decontamination.)^[14][4]

The classic trap — do not give activated charcoal. Iron is a metal, not an organic molecule, and charcoal does not adsorb it; the 2026 multinational charcoal recommendations conclude there is no role for charcoal in iron poisoning, and consensus guidance rejects it for out-of-hospital iron ingestions. The decontamination option is whole bowel irrigation.^[6][4]

The four-step ladder — decontaminate, chelate, support

The definitive ladder runs decontamination, then chelation, then organ-failure support — each step with explicit triggers.^[20]

Step 1 — Resuscitation (above)

ABCDE, crystalloid, oxygen, bloods before treatment; treat shock, acidosis and GI haemorrhage. ^[14]

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

Whole bowel irrigation (WBI) is the decontamination option for iron. Tenenbein (2023) restates the original and twice-reaffirmed AACT/EAPCCT position: WBI was recommended as a treatment for the ingestion of modified-release pharmaceuticals, iron salts and other substances not adsorbed by activated charcoal — a best-evidence recommendation, not a trial-proven one. The 1997 statement said there were insufficient data to support or exclude WBI for iron and that it remained a theoretical option.^[11][12]

^{[21] [22] [23] [23] [12] [21]}

Step 3 — Antidote: IV desferrioxamine (deferoxamine)

Desferrioxamine (deferoxamine, DFO) is the licensed parenteral chelator for acute iron poisoning. Each 100 mg binds 9 mg of elemental iron, producing a ferrioxamine complex excreted by the kidney. Tenenbein concluded that it remains attractive and the drug of choice for significant poisoning, but indications, dose, route and duration are unclear and efficacy is unproven (no dose–response studies; no RCTs in patients with iron over 500 microgram/dL).^[14][24]

^{[13] [15] [14] [21] [20] [24] [25] [26] [31]}

Step 4 — Supportive care for organ failure

Stage-3 patients need intensive-care support for each failing organ — preferably in a PICU.^[14]

^{[14] [8] [29] [31] [25] [16]}

Escalation triggers to ICU, endoscopy and surgery

^{[14] [5] [28] [12]}

The scenarios that bite — toddler, self-harm, pregnancy, bezoar

The toddler who found the prenatal tablets

The typical victim is a toddler (1 to 4 years) who found adult prenatal or iron tablets. Calculate the elemental iron mg/kg at once — a handful of adult tablets in a 10 kg child can cross the systemic-toxicity threshold quickly.^[4][13]

^{[4] [13] [3] [8]}

Deliberate self-harm in the young woman

Self-harm with iron is typically a young person with access to a large bottle — intentional overdose is a recognised cause of self-harm, particularly among adolescents. Consensus: refer ANY intentional ingestion to an acute care facility immediately, regardless of the amount. Draw the iron at least 4 h post-ingestion and repeat while exposed, keep a low threshold for whole bowel irrigation and chelation, secure the iron supply, and arrange psychiatric assessment after medical stabilisation.^[29][4]

Sustained-release and enteric-coated formulations

Modified-release iron delays absorption, and stage 1 may be prolonged or biphasic. Whole bowel irrigation is specifically recommended for modified-release products; a level drawn before 4 h can be falsely low, so draw at least 4 h post-ingestion, repeat while exposed, and observe longer than for immediate-release. Never discharge a modified-release ingestion on a single early level.^[11][15]

Pregnancy

In pregnancy, IV desferrioxamine IS indicated for severe maternal toxicity. The modern consensus is that maternal survival is the priority — pregnancy should not alter therapy, and deferoxamine given in the third trimester was not associated with perinatal complications and is potentially life-saving. A severely poisoned woman at 26 weeks was cured with IV deferoxamine plus whole bowel irrigation with a good fetal outcome. Use the pre-pregnancy weight for the mg/kg calculation.^{[10][9][21][4]}

Massive ingestion with tablet bezoar

A radiopaque mass on KUB that does not progress despite whole bowel irrigation may be a tablet bezoar. Endoscopy (esophagogastroduodenoscopy) evaluates the mucosa and can remove undissolved tablets; surgery is reserved for obstruction or perforation. Continue whole bowel irrigation and chelation meanwhile.^[5][20]

Co-ingestion (especially paracetamol)

Always send a paracetamol level in intentional overdose: the two poisons can coexist and both injure the liver, but they do so in different zones (paracetamol centrilobular; iron periportal). Treat both when both are present — N-acetylcysteine for paracetamol, desferrioxamine for iron.^[14][34]

How iron patients come to harm — the preventable list

• The child discharged looking well in stage 2 who returns in stage 3 shock and acidosis — the preventable death.^[13]
• Charcoal given instead of whole bowel irrigation while tablets remain in the gut.^[6][4]
• Desferrioxamine withheld or delayed for a serum iron over 500 microgram/dL, an acidosis, or shock.^[13]
• A modified-release ingestion discharged on a single early level drawn before 4 h.^[15][11]
• A co-ingested paracetamol missed at 4 hours, so the salvageable liver fails untreated.^[2]
• Desferrioxamine run past resolution, causing pulmonary toxicity or sepsis in the survivor.^[25][7]

Acute complications

Late complications

Gastric or pyloric outlet obstruction from scarring weeks after the corrosive injury 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.^[2]

Classic pitfalls

^{[6] [15] [14] [25] [7]}

The desferrioxamine–ARDS and Yersinia pitfalls

Howland reviews deferoxamine-induced cardiovascular, pulmonary, ocular and auditory toxicity and its potential to increase the risk of infection. Mofenson reported Yersinia enterocolitica septicaemia possibly caused by an iron overdose (title-only record — no mechanism in the fetched abstract). Stop chelation once the clinical picture and acidosis have resolved; do not chelate to zero.^[25][7]

Who goes home, who stays, who goes to ICU

There is no single modern mortality percentage in the fetched sources. Robertson linked clinically important hepatotoxicity to serum iron over 1000 microgram/dL; Chandran lost 2 of 5 children, both with liver failure. Severe poisoning still kills even with chelation (Galmén; Wada required emergency transplant).^{[34][8][31][29]}

Predictors of poor outcome in Baranwal's guideline: shock, coagulopathy (prothrombin index under 50 percent), severe acidosis and acute liver failure. Chandran's five-child series associated death with coagulopathy, acute liver failure and delayed presentation (one child presented at 100 hours).^[14][8]

Disposition criteria

^{[4] [15]}

Special populations — only the thresholds and cautions shift

The same four-step protocol runs across every age and context; what changes is the weight-based dose, the fluid caution, and the threshold to involve ICU.^[13]

^{[4] [13] [3] [9] [10] [21]}

The guidelines behind the protocol

The 2005 AACT/EAPCCT consensus (Manoguerra et al.) on out-of-hospital management set the triage rules still in use: refer to an acute-care facility immediately for any intentional ingestion regardless of the amount (Grade D); refer known ingestions of 40 mg/kg or more of elemental iron from adult ferrous salt formulations, or for severe or persistent symptoms, altered consciousness, haematemesis or bloody diarrhoea; observe at home for less than 40 mg/kg with mild symptoms that are not severe or persistent; unintentional ingestions of chewable vitamins, carbonyl iron and polysaccharide-iron can be observed at home; do NOT give ipecac, activated charcoal, cathartics or complexing agents out of hospital; patients asymptomatic more than 6 h after immediate-release ingestion are unlikely to develop symptoms; calculate mg/kg on the pre-pregnancy weight in pregnancy.^[4]

Whole bowel irrigation is endorsed by the AACT/EAPCCT 1997 position statement (Tenenbein) — iron data were then insufficient, so WBI remained a theoretical option — and reaffirmed for iron salts by the 2023 update. Adult reports used 2 L/h via nasogastric tube; a clear effluent is not proof the gut is empty.^[12][11][22]

The 2026 Clinical Toxicology Recommendations Collaborative concluded there is no role for activated charcoal in iron poisoning. For iron salts and other substances not adsorbed by charcoal, the AACT/EAPCCT position is whole bowel irrigation.^[6][11]

Controversies

The desferrioxamine challenge test. Historical practice gave intramuscular desferrioxamine and watched for vin-rose urine to 'test' for free iron. It is no longer used: vin-rose discolouration is not seen consistently even after chelation therapy, and deferoxamine's optimal indications, dose, route and duration remain unproven. Treat on the serum iron, the acid–base status and the clinical picture.^[14][24]

Desferrioxamine dosing. No dose–response studies exist and all efficacy data are descriptive. The guideline infusion rate is 15 mg/kg/h in saline, titrated to clinical response with early cessation to limit the pulmonary, cardiovascular, ocular, auditory and infectious complications of prolonged IV therapy.^[14][24][25]

Total iron-binding capacity (TIBC). A serum iron exceeding the TIBC was once a chelation trigger, but it did not reliably identify patients with serious poisoning, and assay methods are unreliable when free iron or deferoxamine is present. It is not used to guide modern therapy.^[16][19]

Regional deltas

^[27]

The whole topic on one page

^{[13] [4] [27] [15] [14] [11] [22] [21] [23] [10] [6]}

The mantra, and the danger list

The mantra: elemental iron, never charcoal, dry the iron out with desferrioxamine. Count the elemental dose from the label, refuse charcoal and reach for whole bowel irrigation, and chelate the moment the serum iron, the acidosis or the shock tells you to — then stop once they have resolved.^[14]

Ward-round test — three stems

Stem 1 — the toddler with prenatal iron and vomiting at four hours (answer)ShowHide

A two-year-old, ten kilograms, has vomited three times — the second haematemetic — four hours after swallowing an unknown number of maternal ferrous sulphate 325 mg tablets; the abdomen is tender. What do you do next? Model: Calculate the elemental dose (ferrous sulphate is 20% elemental iron; use the label, divide by ten kilograms) and draw the serum iron now — at least four hours post-ingestion — with a venous gas, glucose, FBC, PT/INR, LFTs, renal function, and paracetamol and salicylate levels. Send a KUB for radiopaque tablets. Do NOT give charcoal — start whole bowel irrigation with polyethylene glycol via a nasogastric tube (Baranwal paediatric rate 30 to 40 mL/kg/h; a 33-month-old safely received 44.3 L over 5 days). If the serum iron is over 500 microgram/dL, there is a metabolic acidosis, or she is shocked, start IV desferrioxamine 15 mg/kg/h. Admit and observe; never discharge on appearance alone in the quiet window.^{[4][15][6][23][14]}

Stem 2 — the young woman who looks well at twelve hours (answer)ShowHide

A 24-year-old took a bottle of sustained-release ferrous sulphate overnight. At twelve hours she looks well, the vomiting has settled, and the team wants to discharge her. What is the right call? Model: Do not discharge — this is the quiet-interval trap compounded by a modified-release formulation. A level drawn before 4 h can be falsely low, so a single early level reassures nobody. Check the serum iron AND the acid–base now, and repeat the iron while she remains exposed. Whole bowel irrigation is specifically recommended for modified-release products and iron salts. Send a paracetamol level in intentional overdose. Manoguerra: any intentional ingestion is referred immediately regardless of amount. Discharge only after psychiatric assessment, and only if asymptomatic, the iron is not in the toxic range, there is no acidosis, and no residual tablets on imaging.^[11][15][4]

Stem 3 — stage 3: shock plus acidosis plus hepatic failure (answer)ShowHide

A patient forty hours after a massive iron ingestion is hypotensive, oliguric, jaundiced, and bleeding from cannula sites. The VBG shows pH 7.1 with a high anion gap; AST and ALT are over 1000; the INR is 3. What is the priority, and what is the trap? Model: This is systemic (Baranwal stage III / Morales-Cruz hepatic window) toxicity. Resuscitate and start IV desferrioxamine 15 mg/kg/h immediately — serious symptoms, the acidosis and the shock are each an indication. Robertson defined transaminase over 1000 U/L as severe hepatotoxicity, typically with iron well over 1000 microgram/dL. The necrosis is periportal, not centrilobular. Arrange ICU and early transplant discussion. Stop desferrioxamine once the clinical picture and acidosis resolve, to limit pulmonary and infectious complications of prolonged chelation.^{[14][13][34][25]}

References33ShowHide

1. [2]Chang TP, Rangan C. Iron poisoning: a literature-based review of epidemiology, diagnosis, and management Pediatr Emerg Care, 2011.PMID 21975503
2. [3]Madiwale T, Liebelt E Iron: not a benign therapeutic drug Curr Opin Pediatr, 2006.PMID 16601499
3. [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
4. [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
5. [6]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
6. [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
7. [8]Chandran J, Sanketh R, Vyasam S, et al. Accidental iron poisoning in children - Experience from a teaching institution J Family Med Prim Care, 2023.PMID 38074262
8. [9]Tran T, Wax JR, Philput C, et al. Intentional iron overdose in pregnancy--management and outcome J Emerg Med, 2000.PMID 10699527
9. [10]Tran T, Wax JR, Steinfeld JD, et al. Acute intentional iron overdose in pregnancy Obstet Gynecol, 1998.PMID 9764661
10. [11]Tenenbein M The role of whole bowel irrigation in the treatment of toxic ingestions Br J Clin Pharmacol, 2023.PMID 36639859
11. [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
12. [13]McGuigan MA. Acute iron poisoning Pediatr Ann, 1996.PMID 8775917
13. [14]Baranwal AK, Singhi SC. Acute iron poisoning: management guidelines Indian Pediatr, 2003.PMID 12824662
14. [15]Fox H, Jansen A, Theobald J, Stanton M, Feldman R. Utility of iron concentration two to four hours post ingestion in predicting toxicity Am J Emerg Med, 2025.PMID 39509998
15. [16]Chyka PA, Butler AY. Assessment of acute iron poisoning by laboratory and clinical observations Am J Emerg Med, 1993.PMID 8476468
16. [17]Chyka PA, Butler AY, Holley JE. Serum iron concentrations and symptoms of acute iron poisoning in children Pharmacotherapy, 1996.PMID 8947978
17. [18]Palatnick W, Tenenbein M. Leukocytosis, hyperglycemia, vomiting, and positive X-rays are not indicators of severity of iron overdose in adults Am J Emerg Med, 1996.PMID 8765107
18. [19]Roberts WL, Smith PT, Martin WJ, Rainey PM. Performance characteristics of three serum iron and total iron-binding capacity methods in acute iron overdose Am J Clin Pathol, 1999.PMID 10549253
19. [20]Mann KV, Picciotti MA, Spevack TA, Durbin DR. Management of acute iron overdose Clin Pharm, 1989.PMID 2663331
20. [21]Turk J, Aks S, Ampuero F, Hryhorczuk DO. Successful therapy of iron intoxication in pregnancy with intravenous deferoxamine and whole bowel irrigation Vet Hum Toxicol, 1993.PMID 8249269
21. [22]Scharman EJ, Lembersky R, Krenzelok EP. Efficiency of whole bowel irrigation with and without metoclopramide pretreatment Am J Emerg Med, 1994.PMID 8179735
22. [23]Kaczorowski JM, Wax PM. Five days of whole-bowel irrigation in a case of pediatric iron ingestion Ann Emerg Med, 1996.PMID 8629765
23. [24]Tenenbein M. Benefits of parenteral deferoxamine for acute iron poisoning J Toxicol Clin Toxicol, 1996.PMID 8800185
24. [25]Howland MA. Risks of parenteral deferoxamine for acute iron poisoning J Toxicol Clin Toxicol, 1996.PMID 8800186
25. [26]Morales-Cruz MJ, MejiasMorales D, Hunsaker P, Butler E, Tassone M. Ingestion of Toxic Iron Dose With Benign Outcome Cureus, 2023.PMID 37425561
26. [27]Crofton AK, Harris K, Wylie C, Isoardi KZ. Unintentional paediatric iron poisoning: A retrospective case series Emerg Med Australas, 2021.PMID 34121325
27. [28]Carlsson M, Cortes D, Jepsen S, Kanstrup T. Severe iron intoxication treated with exchange transfusion Arch Dis Child, 2008.PMID 18356385
28. [29]Wada S, Uebayashi EY, Okamoto T, et al. Emergency ABO-Incompatible Living-Donor Liver Transplantation for Acute Liver Failure due to Intentional Iron Poisoning Pediatr Transplant, 2026.PMID 42136191
29. [30]Mackenzie CA, Poon J, Amiana C, Vegnaduzzo A. Polysaccharide iron complex ingestions reported to a regional poison centre: a retrospective review 2011-2023 Clin Toxicol (Phila), 2026.PMID 42480044
30. [31]Galmén K, Höjer J. Iron intoxication--poisoning with easily accessible medicines Lakartidningen, 2014.PMID 25606656
31. [32]Everson GW, Oudjhane K, Young LW, Krenzelok EP. Effectiveness of abdominal radiographs in visualizing chewable iron supplements following overdose Am J Emerg Med, 1989.PMID 2757710
32. [33]Nordt SP, Williams SR, Behling C, Richter P, Manoguerra AS, Clark RF. Comparison of the toxicities of two iron formulations in a swine model Acad Emerg Med, 1999.PMID 10569381
33. [34]Robertson A, Tenenbein M. Hepatotoxicity in acute iron poisoning Hum Exp Toxicol, 2005.PMID 16323571