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

Iron is the only nutrient the human body has no way to excrete. All iron balance is regulated at absorption, so a toxic swallowed dose has no renal or biliary escape — the metal must go somewhere, and that somewhere is the gut wall and the cell. This is why a child who looks well at three hours can be in shock and acidosis by twelve.[5]

Free iron injures the body in two waves. In the gut lumen it is directly corrosive — haemorrhagic gastritis, vomiting, diarrhoea, fluid loss. Once absorbed iron exceeds the binding capacity of transferrin, the surplus circulates as free iron and catalyses the Fenton reaction: hydroxyl radicals that peroxidise mitochondrial membranes, uncouple oxidative phosphorylation and stall the Krebs cycle.[5][20]

The downstream phenotype is the high-anion-gap lactic acidosis, centrilobular hepatic necrosis, coagulopathy and shock of stage 3. Iron remains a leading cause of accidental poisoning death in young children — prenatal tablets look like sweets — and a recognised method of self-harm in young women. The skill tested is fourfold: stratify by elemental dose, serum iron and acid–base; refuse the latent-phase reassurance; refuse charcoal; chelate early with IV desferrioxamine.[8][4]

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]

[13] [4]

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] [14]

The salt is a decoy — always count ELEMENTAL iron

The same salt weight is a different iron dose depending on the product. Every triage threshold is defined in ELEMENTAL iron, so take the elemental content stated on the label and divide by the weight in kilograms — never trust the salt weight. 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.[4][20][31]

[8] [4] [31] [33] [32] [30] [3]

The four stages — and the latent phase that kills the unwary

The four-stage course is the spine of the topic, and stage 2 is the trap. The patient looks well in the latent phase precisely while iron is being mopped up by transferrin and is about to saturate it and spill into the tissues — so you treat the serum iron and the acid–base, never the face.[9][17]

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. Before child-resistant packaging in the late 1990s, iron was among the leading causes of accidental poisoning death in children under six in the United States and Western Europe; mortality has fallen sharply since, but clusters persist wherever prenatal tablets are stored unsafely.[2][8]

In South Asia the paediatric problem is still live. Cheap ferrous sulphate and fumarate prenatal supplements keep accidental childhood poisoning common, 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, 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]

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

The two waves — corrosion, then the Fenton reaction

Iron kills in two mechanistically distinct waves: corrosion in the gut, then free-radical catalysis inside the cell. The first wave explains the vomiting, the haematemesis and the hypovolaemic shock of stage 1; the second — catalytic free iron once transferrin is saturated — explains every biochemical and clinical feature of stage 3.[5]

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 — the Fenton reaction, and why a little free iron does so much damage

Once absorbed iron exceeds transferrin's binding capacity, the surplus circulates as free iron and becomes a redox catalyst. Hepatocytes take it up avidly through a transferrin-independent route, which is why the liver bears the brunt of stage 3.[5]

Etymology for viva gold: the Fenton reaction is named for Henry Fenton, who described it in 1894. Ferrous iron (Fe2+) plus hydrogen peroxide yields ferric iron (Fe3+) plus the hydroxyl radical (OH•) — and the iron is then regenerated, so a catalytic trace of free iron sustains a runaway flux of the most reactive radical in biology.[5]

The hydroxyl radical abstracts hydrogen from polyunsaturated fatty acids in mitochondrial membranes, igniting lipid peroxidation as a chain reaction. Three downstream consequences together build the entire stage-3 phenotype:[5]

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 are the three that carry the stage-3 mortality.[5]

Shock. Free iron venodilates (dropping systemic resistance) and simultaneously depresses myocardial contractility, so the stage-3 shock is hypovolaemic plus distributive plus cardiogenic at once — one of the few poisons to produce all three patterns together.[13][14]

Hepatic necrosis. The liver is the preferential target because hepatocytes take up free iron avidly, 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 as paracetamol hepatotoxicity and ischaemic hepatitis.[5]

Coagulopathy. Free iron directly inhibits thrombin generation and the vitamin-K-dependent factors. The classic trap: the early, sometimes isolated PT rise — before AST and ALT have peaked — is the anticoagulant effect of iron itself, not yet liver failure. A rising INR with rising transaminases IS hepatic failure; an isolated early INR is not.[16][14]

The basis of the latent phase

Stage 2 looks quiet because transferrin and the reticuloendothelial system are still sequestering the absorbed iron. Once those binding sites saturate, free iron spills into the tissues and stage 3 begins. Examiners test this relentlessly: in the latent window, clinical appearance is a lie; only the serum iron and the metabolic acidosis tell the truth.[9][13]

The four stages made real — recognise each, anticipate the next

The clinical course is the four-stage framework walked onto the bedside. Your job at each hour is to recognise the current stage, anticipate the next, and refuse to be reassured by stage 2.[9]

Stage 1 (0 to 6 h) — corrosive gastrointestinal injury. Within the first hours the patient vomits (often haematemetic), with abdominal pain and diarrhoea that may be bloody; the abdomen is diffusely tender. Dehydration is rapid in children, and with a significant dose hypovolaemic shock — tachycardia, delayed capillary refill, hypotension, oliguria, altered consciousness — is established within hours. A patient shocked in stage 1 is heading for stage 3: severity here predicts progression.[9][14]

Stage 2 (6 to 24 h) — the deceptive latent phase, and the classic trap of the topic. The gastrointestinal symptoms settle and the patient looks better — exactly when the unwary discharge. Iron is being sequestered by transferrin and is about to saturate it. Disposition in this window rests on the serum iron, the anion gap and the formulation, never on the face.[9][13]

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.[13]

Stage 3 (12 to 48 h) — systemic toxicity, the killer. This is the focus of intensive care; the patient develops, in variable combination:[9][14]

Stage 4 (4 to 6 weeks) — late gastric-outlet obstruction. Weeks after recovery, the corrosively burned antrum or pylorus scars and strictures, producing gastric or pyloric outlet obstruction — early satiety, post-prandial vomiting (sometimes of food eaten a day earlier), weight loss, a succussion splash. Upper GI endoscopy confirms the stricture; management is endoscopic balloon dilation, repeated as needed, with surgery for the refractory.[2]

Atypical presentations — the corners examiners probe

Examiners probe the corners, and three atypical patterns deserve attention.[2]

[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. Give IV desferrioxamine for serious clinical symptoms (shock, metabolic acidosis, severe GI symptoms, altered consciousness) or a serum iron over 500 microgram/dL measured within 8 hours of ingestion; a concentration of 350 microgram/dL or more WITH symptoms is also considered toxic and likely to need treatment.[13][15]

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] [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, and modified-release formulations delay absorption further — draw at least 4 h post-ingestion, repeat while the patient remains exposed, and treat a rising or high level.[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

[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. The AACT/EAPCCT position (original 1997, twice reaffirmed — most recently 2023) recommends WBI for iron salts, modified-release products and substances not adsorbed by charcoal; the 1997 statement regarded the iron evidence as insufficient, with WBI a theoretical option, so the endorsement is best-evidence rather than trial-proven.[11][12]

[21] [22] [23] [23] [12] [21]

Step 3 — Antidote: IV desferrioxamine (deferoxamine)

Desferrioxamine (deferoxamine, DFO) is a siderophore — a molecule bacteria evolved to scavenge iron — repurposed as our antidote. It binds free iron in a stable 1:1 complex, ferrioxamine, which is excreted in the urine as the characteristic vin-rose (pink-red) flow. Etymology for viva gold: des-ferri-oxamine literally means 'remove iron', and siderophore comes from the Greek sideros, iron, and phorein, to carry. It remains the drug of choice for significant iron poisoning, though its optimal use is unproven.[24]

[13] [15] [14] [21] [20] [24] [25]

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

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

Prolonged high-dose desferrioxamine causes ocular, auditory and pulmonary toxicity, and predisposes to infection — including Yersinia enterocolitica sepsis — because deferoxamine is itself a siderophore that siderophore-dependent organisms can exploit for iron. Suspect such infection in any febrile patient on desferrioxamine, and stop chelation once the iron is falling and the acidosis has resolved — do not chelate to zero.[25][7]

Who goes home, who stays, who goes to ICU

Modern mortality is under 5 percent with prompt chelation; historical mortality in severe untreated ingestions reached 45 percent. Severe poisoning — serum iron over 1000 microgram/dL, refractory acidosis, multi-organ failure — still kills even with chelation.[2]

Predictors of poor outcome: shock, coagulopathy (prothrombin index under 50 percent), severe acidosis and acute liver failure — the four markers associated with death in a 12-year paediatric series; delayed hospitalisation likewise proved fatal, and cardiovascular instability tracked the highest iron concentrations in children.[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) — which listed iron among the toxic indicators for WBI (theoretical basis only — iron data were then insufficient) — and reaffirmed for iron salts by the 2023 update: polyethylene-glycol electrolyte solution run until the rectal effluent is clear, at rates such as 1.5 to 2 L per hour in adults.[12][11][22]

The 2026 Clinical Toxicology Recommendations Collaborative concluded there is no role for activated charcoal in iron (metal) poisoning — for substances not adsorbed by charcoal, whole bowel irrigation remains the modality.[6]

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)

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 (the label's elemental iron per tablet, divided by ten kilograms) and draw the serum iron now — four hours post-ingestion is the minimum meaningful sampling time — 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, run at a rate she tolerates (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 latent window.[4][15][6][23][14]

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

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 latent-phase trap compounded by a modified-release formulation. Absorption is delayed, and a level drawn before 4 h can be falsely low, so a single early level reassures nobody. Check the serum iron AND the anion gap now, repeat the iron level, and observe longer than for an immediate-release ingestion. Whole bowel irrigation is specifically recommended for modified-release products. Send a paracetamol level, because co-ingestion is common in self-harm. Discharge only if asymptomatic, the peak iron is under 350 microgram/dL, there is no acidosis and no residual tablets on imaging, and after psychiatric assessment.[11][15][2]

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

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 stage 3 systemic toxicity — the killer. Resuscitate (airway, two large-bore cannulae, isotonic crystalloid boluses, vasopressors for the multifactorial shock) and start IV desferrioxamine 15 mg/kg/h immediately — serious symptoms, the acidosis and the shock are each an indication. Give blood products for the bleeding coagulopathy, and arrange ICU for organ-failure support (ventilation, renal replacement therapy). The trap: do not attribute the early INR to liver failure alone, because it is also iron's direct anticoagulant effect — but a rising INR with transaminases over 1000 here IS hepatic failure. Stop desferrioxamine once the iron is falling and the acidosis resolves, to avoid the pulmonary and infectious complications of prolonged chelation.[14][13][28]

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