Emergency & Toxicology

Iron poisoning: stages and chelation

Clinical Overview and When to Suspect Iron Poisoning

— <20 mg/kg: usually asymptomatic

— 20–40 mg/kg: mild–moderate GI symptoms

— 40–60 mg/kg: moderate-to-severe systemic toxicity

— >60 mg/kg: potentially lethal; expect shock, metabolic acidosis, hepatic failure

— Toddler with sudden hematemesis, bloody diarrhea, lethargy after access to mom's prenatal vitamins

— Adolescent or adult with intentional overdose and unexplained anion-gap metabolic acidosis + shock + hepatic transaminitis

— Pregnant woman post-supplement overdose (intentional or accidental) — fetal toxicity tracks maternal toxicity

Board pearl: Always calculate mg/kg elemental iron, not mg of the salt. A bottle of "325 mg ferrous sulfate" = 65 mg elemental per tablet. A 12 kg toddler ingesting 10 tablets = 54 mg/kg → expect severe toxicity and prepare for deferoxamine.

Step 3 management: Asymptomatic patient at >40 mg/kg still warrants ED observation ≥6 hours with serial exams; symptom-free at 6 hours with normal labs predicts benign course.

Iron poisoning remains one of the most lethal pediatric ingestions in the US, historically a top cause of toxic ingestion death in children <6 years before unit-dose packaging mandates. Adult cases are usually intentional overdoses or chronic supplementation errors in pregnancy.

Toxicity is dose-dependent based on elemental iron (not total tablet weight):

Common culprits: ferrous sulfate (20% elemental), ferrous fumarate (33%), ferrous gluconate (12%), prenatal vitamins, pediatric chewables (lower elemental but children eat many). Carbonyl iron and polysaccharide-iron complexes are less toxic but not benign.

When to suspect:

Iron is directly corrosive to GI mucosa and acts as a mitochondrial poison: free iron catalyzes Fenton reactions → lipid peroxidation → hepatocellular necrosis (zone 1/periportal) and lactic acidosis from disrupted oxidative phosphorylation.

Radiopaque tablets on KUB may help confirm ingestion in early hours but chewables, liquids, and dissolved tablets are often not visible.

Presentation Patterns and Key History

— Vomiting (most sensitive early sign), hematemesis, abdominal pain, profuse diarrhea ± melena

— Hypovolemia from fluid losses and GI hemorrhage

— Absence of vomiting within 6 hours essentially rules out significant toxicity

— GI symptoms improve, patient looks deceptively well

— Subclinical progression: worsening acidosis, evolving end-organ injury

— Key distinction: This is the most dangerous stage for triage error. Do not discharge a symptomatic ingestion just because they "feel better."

— Distributive + hypovolemic + cardiogenic shock

— Profound anion-gap metabolic acidosis (lactate from mitochondrial dysfunction, plus iron itself contributing H⁺ via hydration: Fe³⁺ + 3H₂O → Fe(OH)₃ + 3H⁺)

— Coagulopathy (early: direct iron inhibition of thrombin; late: hepatic synthetic failure)

— Altered mental status, seizures, ARDS

— Fulminant hepatic failure with periportal/zone 1 necrosis (iron is taken up portally first)

— Marked AST/ALT elevation, hyperammonemia, hypoglycemia, INR rise

— Pyloric or proximal small-bowel strictures from healing corrosive injury → gastric outlet obstruction

— Late presentation: postprandial vomiting weeks after "recovery"

— Exact product, elemental iron content, max possible pills, time since ingestion, co-ingestants

— In pregnancy: gestational age, prenatal vitamin formulation

— In children: pill count from caregivers and pharmacy

Board pearl: A child who vomited once, looks well at hour 8, but has AG = 22 and lactate 6 is in Stage 2/3 — admit and start chelation discussion, do not send home.

Iron poisoning classically evolves through five stages, though stages overlap and patients can skip from stage 1 to stage 4 with massive ingestions.

Stage 1 — GI / corrosive (0.5–6 hours):

Stage 2 — latent / "quiescent" (6–24 hours):

Stage 3 — shock / metabolic acidosis (6–72 hours):

Stage 4 — hepatotoxicity (12–96 hours):

Stage 5 — delayed sequelae (2–8 weeks):

History essentials:

Physical Exam Findings and Hemodynamic Assessment

— Early tachycardia from GI losses → progresses to hypotension

— Tachypnea = compensation for metabolic acidosis (Kussmaul respirations)

— Hypothermia or hyperthermia possible; fever suggests aspiration or evolving sepsis-like SIRS

— Hypoglycemia in late stages (hepatic failure) — fingerstick mandatory

— Stage 1: pale, diaphoretic, actively vomiting, clutching abdomen

— Stage 2: deceptively well-appearing — trust the labs, not the look

— Stage 3–4: lethargic, obtunded, jaundiced, mottled

— Hematemesis, oropharyngeal irritation; assess airway protection given altered mental status risk

— Iron does NOT typically cause oropharyngeal burns (unlike caustic alkali) — corrosion is mucosal/gastric

— Hypotension may be refractory to fluids — early vasopressor need

— Pulmonary edema/ARDS in stage 3; crackles, hypoxemia

— Capillary refill, mottling — assess perfusion repeatedly

— Diffuse tenderness, distension; peritoneal signs raise concern for perforation or transmural injury

— Hepatomegaly with RUQ tenderness in stage 4

— GCS decline, seizures (from acidosis, hypoglycemia, shock, direct CNS effect)

— Coma is an ominous late finding

— Pallor (hemorrhage), jaundice (late), petechiae/bruising (coagulopathy)

— Place 2 large-bore IVs, continuous monitoring, foley for UOP, arterial line if shock

— Target MAP ≥65 mmHg with isotonic crystalloid bolus (20 mL/kg pediatric, 30 mL/kg adult), then norepinephrine

— Reassess lactate, base deficit, UOP q1–2h

CCS pearl: Order fingerstick glucose, ABG with lactate, type & screen, and serial vital signs q15 min in the first hour. Iron poisoning can deteriorate from "comfortable" to "intubated" within 2–3 hours during stage transitions.

Vital signs trajectory drives disposition more than any single number:

General appearance:

HEENT/airway:

Cardiopulmonary:

Abdomen:

Neurologic:

Skin:

Hemodynamic assessment for CCS-style cases:

Diagnostic Workup — Initial Labs, Imaging, and Biomarkers

— Draw at 4–6 hours post-ingestion (peak absorption window)

— Levels at 2 hours may miss peak; levels >8 hours may miss peak for enteric-coated/sustained-release

— Interpretation:

— <300 μg/dL: usually asymptomatic

— 300–500 μg/dL: mild–moderate toxicity, GI symptoms expected

— 500–1000 μg/dL: significant systemic toxicity, chelation indicated

— >1000 μg/dL: severe toxicity, high mortality risk, chelate aggressively

— Repeat level at 6–8 hours if sustained-release suspected or initial level borderline

— CBC (leukocytosis >15K and Hb drop suggest significant ingestion — historical "Lacouture criteria")

— CMP: glucose >150 historically associated with toxicity but not specific; transaminases (rise = stage 4); BUN/Cr; electrolytes

— ABG/VBG with lactate: anion-gap metabolic acidosis is a critical severity marker

— Coagulation: PT/INR, PTT, fibrinogen (early direct anti-thrombin effect, late hepatic)

— Type & screen / cross-match for GI hemorrhage

— Beta-hCG in women of reproductive age

— Acetaminophen and salicylate levels (co-ingestion screen in intentional overdose)

— Abdominal radiograph (KUB): radiopaque iron tablets visible in first 1–2 hours; useful in pediatric ingestion to estimate pill count and guide decontamination

— Negative KUB does NOT rule out toxicity — chewables, liquid iron, dissolved tablets, carbonyl iron are not radiopaque

— Repeat KUB after whole-bowel irrigation to confirm GI clearance

Board pearl: A patient with AG metabolic acidosis + hyperglycemia + leukocytosis + radiopaque pills on KUB is iron poisoning until proven otherwise — start workup and call poison control before the iron level returns.

Serum iron level — the cornerstone test:

Key distinction: TIBC is NOT useful in acute iron toxicity. Older teaching ("iron > TIBC = toxic") is unreliable because TIBC falsely rises with deferoxamine and severe acidosis — current toxicology guidelines have abandoned it.

Core labs:

Imaging:

ECG: baseline for co-ingestion screening (TCA, QT-prolonging agents)

Diagnostic Workup — Advanced and Confirmatory Studies

— Sustained-release or enteric-coated ferrous sulfate may have delayed peak at 6–8+ hours

— Concretion or bezoar formation in stomach can produce prolonged absorption — serial levels q2–4h until trending down

— After deferoxamine started: standard colorimetric iron assays falsely low because chelated iron (ferrioxamine) is not detected; use atomic absorption spectroscopy if available, or trust clinical course

— Old practice: give deferoxamine and observe for "vin rosé" urine (ferrioxamine excretion) as evidence of free iron

— Current standard: clinical and lab criteria drive chelation, not urine color

— Consider EGD in stage 1 with significant hematemesis to assess corrosive injury, identify retained pill concretions

— Endoscopic removal of pill bezoars when whole-bowel irrigation fails (rare)

— Also useful weeks later if delayed strictures/gastric outlet obstruction develop

— Trend AST/ALT, bilirubin, INR, ammonia, lactate, glucose q4–6h

— Factor V level if considering transplant referral

— Hepatic ultrasound with Doppler to exclude alternative causes

— King's College criteria for non-acetaminophen ALF guide transplant listing

— Early (<48 h): iron directly inhibits thrombin and factors → INR rise without hepatocyte injury

— Late (>48 h): true hepatic synthetic failure

— Key distinction: Early INR elevation may not respond to vitamin K or FFP fully — it's a direct biochemical inhibition, not a synthesis problem.

Board pearl: If a patient on deferoxamine has a "normalizing" iron level, do not be reassured — the assay underestimates total body burden during active chelation. Decide chelation duration by clinical resolution + acidosis correction + urine color clearing, not iron number.

Repeat serum iron levels:

Deferoxamine challenge test (historical, no longer recommended):

Endoscopy:

Liver-focused workup (stage 4):

Coagulation in two phases:

Biostatistics aside: Serum iron at 4–6 hours has good sensitivity for predicting stage 3 toxicity (~90%) but a single normal level in sustained-release ingestion has lower NPV — hence serial sampling.

Risk Stratification and First-Line Management Logic

— Home observation acceptable with poison control input

— Return precautions: vomiting, lethargy, bloody stools

— ED observation 6 hours minimum

— Serial vitals, fingerstick glucose, basic labs, KUB

— 4–6 hour serum iron level

— Discharge if asymptomatic at 6 hours with normal labs and falling/low iron

— Admit, aggressive resuscitation, prepare deferoxamine

— ICU if shock, altered mental status, severe acidosis, or iron >1000

— Activated charcoal does NOT bind iron — do not give (unless co-ingestant warrants it)

— Gastric lavage: limited role; consider only with very recent (<1 h) massive ingestion of liquid iron

— Whole-bowel irrigation (WBI) with polyethylene glycol (PEG): first-line decontamination for visible pills on KUB or large ingestion

— Dose: 500 mL/h (children 9 mo–6 yr), 1000 mL/h (6–12 yr), 1500–2000 mL/h (adolescents/adults) via NG until rectal effluent clear and repeat KUB negative

— Contraindications: ileus, obstruction, perforation, hemodynamic instability, unprotected airway

— Airway: intubate if GCS decline, severe acidosis can't compensate, or ARDS

— Breathing: supplemental O₂, monitor for ARDS

— Circulation: isotonic crystalloid, then norepinephrine; transfuse for hemorrhage

— Correct hypoglycemia, electrolyte derangements

— Bicarbonate for severe acidosis (pH <7.1) is temporizing only

CCS pearl: Order in this sequence: IV access ×2 → labs + iron level + KUB → fluid bolus → NG tube + PEG for WBI → call poison control (1-800-222-1222) → prepare deferoxamine if criteria met. Document time of ingestion and pill count meticulously.

Triage algorithm by exposure and clinical status:

Asymptomatic + <40 mg/kg elemental + reliable history:

Asymptomatic + 40–60 mg/kg, OR any symptoms:

Symptomatic (persistent vomiting, hematemesis, lethargy, acidosis) OR >60 mg/kg OR iron >500 μg/dL:

Decontamination:

Supportive care priorities (CCS rhythm):

Pharmacotherapy — Deferoxamine: The First-Line Chelator

— Serum iron >500 μg/dL at 4–6 hours

— Any iron level + systemic toxicity: shock, altered mental status, persistent vomiting, severe acidosis (lactate >5, base deficit >10)

— Severe symptoms regardless of level when level not yet available

— Iron 350–500 μg/dL + symptoms (clinical judgment)

— IV infusion preferred: start at 5 mg/kg/h, titrate up to 15 mg/kg/h as tolerated

— Maximum recommended 6–8 g/day (some sources allow more in severe poisoning)

— IM route (90 mg/kg, max 1 g) is alternative if IV unavailable; not preferred in shock (erratic absorption)

— Blood pressure q15 min during initiation — infusion-related hypotension from rapid administration or flushing/histamine release is the dose-limiting effect

— Urine color: monitor change to vin rosé and return to normal as endpoint

— Trend acidosis, lactate, end-organ function

— Stop when clinical improvement + acidosis resolved + urine color clears + symptoms resolve

— Typically 6–24 hours; avoid >24 hours if possible due to risk of ARDS, Yersinia infection, and renal toxicity

— If >24 h needed, reassess and reduce dose

— Hypotension (rate-related — slow infusion)

— ARDS with prolonged use (>24 h, especially >72 h)

— Anaphylactoid reactions

— Yersinia enterocolitica sepsis — iron-loving organism thrives in chelated state; suspect with fever/diarrhea

— Renal injury, ocular/auditory toxicity (chronic use)

Step 3 management: A pregnant patient meeting chelation criteria gets deferoxamine — it does not cross placenta in meaningful amounts; fetal risk from untreated maternal iron toxicity vastly exceeds drug risk. Do not withhold chelation in pregnancy.

Board pearl: Oral deferiprone and deferasirox are for chronic iron overload (thalassemia, transfusion); they have no role in acute poisoning.

Deferoxamine (DFO) is the antidote for systemic iron toxicity. It binds free (non-transferrin-bound) iron and ferritin/hemosiderin iron, forming ferrioxamine, excreted renally as a red-brown ("vin rosé") urine.

Indications for deferoxamine:

Dosing:

Monitoring during therapy:

Duration:

Adverse effects:

Advanced Pharmacology and Adjunctive Interventions

— Reserved for massive pediatric ingestion or iron level >1000 μg/dL unresponsive to DFO, or when DFO is contraindicated (severe renal failure with anuria — can't excrete ferrioxamine)

— Hemodialysis does not remove free iron effectively but does remove ferrioxamine — consider in anuric patients receiving DFO to clear the chelate

— CRRT can be paired with DFO infusion in unstable ICU patients

— Vasopressors: norepinephrine first line for distributive/hypovolemic shock after fluid resuscitation

— Sodium bicarbonate: for pH <7.1 as bridge; doesn't treat underlying mitochondrial poisoning

— PPI or H2 blocker: for mucosal protection in stage 1 corrosive injury

— Antiemetics: ondansetron preferred; avoid metoclopramide if obstruction concern

— Vitamin K + FFP: for coagulopathy with bleeding; may have limited response early due to direct iron-thrombin inhibition

— Blood products: transfuse for symptomatic anemia/active hemorrhage; cross-matched PRBCs

— N-acetylcysteine: not standard but some toxicologists give for stage 4 hepatic failure given antioxidant mechanism — low-quality evidence

— Activated charcoal — does not adsorb iron; risk of aspiration without benefit

— Ipecac — abandoned; risk > benefit

— Magnesium-based or phosphate-based binders historically tried, ineffective

— Oral deferoxamine — no benefit, may increase absorption

— Vitamin C (ascorbate) — chronic supplementation can increase iron absorption and toxicity; avoid during recovery phase

— Prochlorperazine — can lower seizure threshold in acidotic patients

CCS pearl: In a child with iron >1500 μg/dL, refractory shock, and oliguria — order deferoxamine IV at 15 mg/kg/h, intubate, central line, norepinephrine, consult nephrology for CRRT to clear ferrioxamine, and transfer to PICU. This is the high-acuity stem.

Combined modalities for severe iron poisoning:

Whole-bowel irrigation + chelation run concurrently when both indicated — WBI removes unabsorbed iron from gut while DFO chelates absorbed iron systemically. Protect airway if obtunded before NG-PEG.

Exchange transfusion / extracorporeal removal:

Adjuncts and supportive pharmacotherapy:

What NOT to give:

Drug-drug consideration:

Special Populations — Elderly and Renal/Hepatic Impairment

— Iron overdose less common but seen in medication errors, polypharmacy, and intentional ingestion in depression

— Baseline comorbidities (CAD, CKD, CHF) amplify shock and acidosis risk

— Aspiration risk from vomiting higher — early airway assessment

— Polypharmacy raises co-ingestion likelihood (anticoagulants amplify GI bleeding; beta-blockers blunt compensatory tachycardia and may mask early shock)

— Deferoxamine: same dosing but slower titration; watch BP closely given baseline orthostasis and antihypertensive use

— DFO is renally cleared as ferrioxamine — accumulation risk in CKD/AKI

— In anuric patients, add hemodialysis or CRRT to remove ferrioxamine

— Monitor for ototoxicity, retinal toxicity with prolonged use (less acute issue but document baseline)

— Iron poisoning itself causes AKI via shock + direct tubular injury — anticipate and dose-adjust other drugs (e.g., antibiotics if Yersinia coverage needed)

— Preexisting cirrhosis or hepatitis dramatically worsens prognosis — stage 4 onset is earlier and more severe

— Hemochromatosis/iron-overload disorders: patients already iron-loaded have higher baseline ferritin and lower threshold for systemic toxicity; phlebotomy history may be relevant

— Coagulopathy correction: prefer 4-factor PCC over FFP in volume-overloaded cirrhotic patients with bleeding

— Hypoglycemia management: dextrose infusion (D10) for hepatic failure

— Concurrent phenothiazines with DFO: risk of prolonged unconsciousness reported — caution

— Iron supplementation interferes with levothyroxine, levodopa, fluoroquinolone, tetracycline absorption — relevant in chronic dosing errors

— Hereditary hemochromatosis, transfusion-dependent thalassemia → chronic deferasirox or deferiprone, not DFO bolus

— Different topic but board distractor

Board pearl: An anuric ESRD patient with iron poisoning still gets deferoxamine — pair it with hemodialysis to clear the ferrioxamine complex. Do not withhold antidote because of renal failure.

Step 3 management: Adjust DFO infusion rate downward in CKD and confirm dialysis access early.

Elderly patients:

Renal impairment:

Hepatic impairment:

Polypharmacy and DDI checks:

Chronic iron toxicity (different mechanism):

Special Populations — Pregnancy and Pediatrics

— Iron is the most common lethal medicinal poisoning in pregnancy historically — prenatal vitamins are ubiquitous

— Maternal toxicity drives fetal outcome; fetal demise correlates with maternal severity, not direct fetal iron toxicity (iron crosses placenta poorly)

— Deferoxamine is category C but indicated when chelation criteria met — risk of withholding >> theoretical fetal risk

— Animal studies suggested skeletal anomalies at supratherapeutic doses; human data reassuring

— Management same as non-pregnant: WBI, IV DFO, supportive care

— Coordinate with OB for fetal monitoring (NST/BPP) based on gestational age and maternal stability; do not deliver solely for iron toxicity unless maternal status mandates

— Postpartum: counsel on safe storage of prenatal vitamins, screen for depression/intent

— Toddlers 1–3 years are highest-risk: mobile, oral-exploratory, attracted to candy-like chewables and shiny adult tablets (especially mom's prenatal vitamins left at bedside)

— Even one adult ferrous sulfate tablet (65 mg elemental) in a 10 kg toddler = 6.5 mg/kg — usually safe; but 10 tablets = 65 mg/kg = potentially lethal

— Pediatric chewable multivitamins typically have low elemental iron (10–18 mg/tablet) — large numbers needed for serious toxicity, but plausible

— KUB more useful in children: easier visualization, helps pill count

— WBI feasible in cooperative children with NG placement

— DFO dosing: same 5–15 mg/kg/h IV; max 6 g/day; pediatric ICU admission for any chelated child

— Document custody, ensure no neglect; involve social work and child protective services if recurrent or suspicious ingestion

— Psychiatric evaluation mandatory before discharge

— Suicide risk assessment, restrict access at home (safe storage counseling)

Board pearl: A 2-year-old who ate "candy from grandma's bottle," now vomiting blood with bloody diarrhea — think prenatal vitamins or iron tablets before random gastroenteritis. Get a KUB and iron level immediately.

Step 3 management: Every iron poisoning discharge in a child requires anticipatory guidance on medication storage, lockable cabinets, and Poison Control phone number.

Pregnancy — high-yield Step 3 scenario:

Pediatrics — the classic stem:

Adolescent intentional overdose:

Complications and Adverse Outcomes

— Hematemesis, GI hemorrhage requiring transfusion

— Gastric or duodenal perforation (rare but catastrophic)

— Pancreatitis from corrosive extension

— Aspiration pneumonitis from emesis

— Refractory distributive + cardiogenic shock; iron has direct negative inotropic effects

— Arrhythmias from acidosis, electrolyte derangements

— Capillary leak → third-spacing, pulmonary edema

— ARDS — both from iron itself and from prolonged DFO use (>24 h)

— Aspiration pneumonitis

— Pulmonary hemorrhage in severe coagulopathy

— Coagulopathy (biphasic: early direct anti-thrombin, late hepatic synthetic failure)

— DIC in fulminant cases

— Anemia from GI losses

— Fulminant hepatic failure with periportal/zone 1 necrosis

— Hepatic encephalopathy, hyperammonemia, hypoglycemia, lactic acidosis

— Need for transplant evaluation if meeting King's College criteria

— AKI from shock, direct tubular injury, pigment nephropathy if hemolysis

— May need RRT, also helps clear ferrioxamine

— Seizures, coma, cerebral edema in ALF

— Yersinia enterocolitica septicemia — iron-overloaded environment is permissive; treat with TMP-SMX, fluoroquinolone, or ceftriaxone

— Aspiration pneumonia

— Translocation sepsis from injured gut mucosa

— Pyloric and proximal small-bowel strictures → gastric outlet obstruction

— Presents with postprandial vomiting, weight loss weeks later

— Diagnosis: upper GI series or EGD; treatment: endoscopic dilation or surgical revision

— DFO-induced hypotension (rate-related)

— DFO-related ARDS, ocular/auditory toxicity, allergy

— Yersinia opportunism during chelation

Board pearl: Persistent or recurrent vomiting 2–4 weeks after an iron poisoning recovery = gastric outlet obstruction from stricture until proven otherwise. Order upper GI study and consult GI.

Step 3 management: Schedule a follow-up visit at 4 weeks specifically to screen for late strictures, even in patients who "did well."

Acute complications by stage:

GI/corrosive (stage 1):

Cardiovascular (stage 3):

Pulmonary:

Hematologic:

Hepatic (stage 4):

Renal:

CNS:

Infectious:

Delayed complication (stage 5, 2–8 weeks):

Treatment-related:

When to Escalate Care — ICU, Consult, and Inpatient Triage

— Hemodynamic instability or vasopressor requirement

— Altered mental status / GCS <13

— Severe metabolic acidosis (pH <7.2, lactate >5, bicarb <15)

— Serum iron >500 μg/dL warranting chelation

— Active GI hemorrhage with transfusion needs

— Need for intubation, ARDS

— Hepatic failure (rising INR, encephalopathy)

— Pediatric: lower threshold — admit to PICU for any chelation, any persistent symptoms, or iron >350 μg/dL

— Symptomatic but stable, iron 300–500, no chelation needed

— Observation post-WBI completion

— Asymptomatic at 6 hours, normal labs, iron <300 μg/dL, reliable home environment

— Poison control / medical toxicology — call early, ideally before labs return (1-800-222-1222 US)

— Nephrology — for RRT to clear ferrioxamine in renal failure

— GI — endoscopy for severe corrosive injury or pill bezoars; later for strictures

— Hepatology / transplant center — early referral if fulminant hepatic failure

— Psychiatry — all intentional ingestions before discharge; capacity assessment if refusing care

— Pediatrics / social work / CPS — for unsupervised pediatric ingestions, assess home safety, mandatory reporting where applicable

— OB — pregnancy with iron poisoning, fetal monitoring coordination

— Community hospital without DFO supply, PICU capability, or hepatology → transfer to tertiary center early

— Use stabilize-and-transfer model; start DFO before transfer if criteria met and resources allow

CCS pearl: In CCS-format cases, call poison control as an early action — it counts as appropriate consultation and demonstrates Step 3-level systems thinking. Document the time and recommendations received.

Step 3 management: Don't wait for the 8-hour iron level if a child has hematemesis and lactate of 7 — admit to PICU and prepare DFO empirically. Iron poisoning rewards aggression in the first hours.

ICU admission criteria:

Step-down or general medical/peds admission:

ED observation only (no admission):

Consultations:

Transfer considerations:

Key Differentials — Same-Category Causes (Other Toxic Ingestions)

— Tinnitus, hyperventilation (mixed respiratory alkalosis + metabolic acidosis), hyperthermia, altered mental status

— Lab: high AG metabolic acidosis with respiratory alkalosis

— Treatment: alkalinize urine with sodium bicarbonate, hemodialysis if severe

— Key distinction: Salicylates cause early hyperventilation and tinnitus; iron causes vomiting and hematemesis

— Often co-ingested in intentional overdose — always send APAP level

— Hepatic injury centrilobular (zone 3) vs iron's periportal (zone 1)

— Antidote: N-acetylcysteine

— Levels and Rumack-Matthew nomogram drive therapy

— AG metabolic acidosis with osmolar gap

— Methanol: visual changes ("snowstorm"); ethylene glycol: calcium oxalate crystals, AKI

— Antidote: fomepizole; dialysis

— Oropharyngeal burns prominent (iron does NOT cause oral burns typically)

— Stridor, drooling; endoscopy within 24 h

— No specific antidote

— Lead: chronic exposure, encephalopathy, basophilic stippling; chelate with succimer/EDTA/dimercaprol

— Arsenic: garlicky breath, rice-water diarrhea; chelate with dimercaprol or succimer

— Key distinction: Acute iron is GI-fulminant within hours; heavy metals typically subacute or chronic

— Tachycardia, seizures, hypokalemia, vomiting

— Treat with hemodialysis, beta-blockade

— Different mechanism, no hepatic necrosis

— GI symptoms → latent phase → hepatic failure (mimics iron's biphasic course)

— Hepatic injury centrilobular; treatment supportive + NAC, silibinin

— Board pearl: Mushroom hepatotoxicity mimics iron's latent/hepatic phases — history of foraging or ingestion timing distinguishes.

Step 3 management: In every intentional overdose, send a co-ingestion panel: APAP, salicylate, ethanol, +/− specific toxicology screens. Iron toxicity often co-occurs with these in suicide attempts.

Iron poisoning mimics other toxic ingestions with anion-gap metabolic acidosis (MUDPILES) and GI prodromes. Differentiate by history, co-ingestion screen, and specific features.

Salicylate (aspirin) toxicity:

Acetaminophen (APAP):

Methanol / ethylene glycol:

Caustic ingestion (alkali/acid):

Heavy metals (lead, arsenic, mercury):

Theophylline / caffeine:

Mushroom (Amanita phalloides):

Key Differentials — Other-Category Causes

— Viral/bacterial gastroenteritis can mimic iron stage 1

— Key distinction: Hematemesis is uncommon in viral GE; bloody diarrhea suggests bacterial (Shigella, EHEC, Salmonella, Campylobacter)

— Lack of metabolic acidosis disproportionate to dehydration, no radiopaque pills, no exposure history

— EHEC: watch for HUS — different complication pattern

— Distributive shock with acidosis can mimic iron stage 3

— Fever, infection source on exam; procalcitonin, blood cultures

— Treat empirically while ruling out toxicologic cause

— AG metabolic acidosis with vomiting and altered mental status

— Hyperglycemia (>250), ketonemia, history of T1DM or new-onset

— Key distinction: Iron can transiently elevate glucose but doesn't produce ketosis; DKA lacks GI hemorrhage

— Mimics stage 4

— Viral serologies (HAV, HBV, HCV, HEV), autoimmune markers (ANA, ASMA, IgG)

— No prodromal hematemesis, no iron exposure

— Aspirin + viral illness → encephalopathy + hepatic failure

— Now rare; consider in children with hepatic failure and salicylate use

— Hematemesis with hemodynamic compromise

— Endoscopy diagnostic

— No multisystem acidosis unless massive bleeding with shock

— Rapid onset, urticaria/wheezing, exposure history

— Treat with epinephrine

— Tachycardia, agitation, but different exam features (mydriasis, dry skin in anticholinergic; diaphoresis in sympathomimetic)

— Recurrent metabolic acidosis with vomiting in young children — consider organic acidemia, urea cycle defect, MCAD if no toxic exposure

Board pearl: A pediatric patient with vomiting, hematemesis, AG acidosis, and radiopaque tablets on KUB is iron poisoning until proven otherwise — no other differential combines all four. Key distinction: Radiopacity on KUB + biphasic GI-to-hepatic course is iron's fingerprint.

Beyond toxicologic mimics, consider non-toxicologic causes of similar presentations, especially when history is unclear (toddler, altered patient, unwitnessed event).

Acute gastroenteritis with dehydration:

Sepsis with shock:

Diabetic ketoacidosis:

Acute liver failure from viral hepatitis or autoimmune:

Reye syndrome (historical, in pediatrics):

Upper GI bleed (peptic ulcer, varices):

Anaphylaxis with shock:

Sympathomimetic/anticholinergic toxidrome:

Inborn errors of metabolism (pediatric):

Secondary Prevention, Discharge Planning, and Long-Term Outlook

— Confirm chelation completed (urine clear, acidosis resolved, iron trending down, symptoms resolved)

— Liver and renal function returning toward baseline

— Hemodynamically stable off vasopressors >24 h

— Tolerating oral intake without recurrent vomiting

— Psychiatry clearance if intentional ingestion

— PPI (omeprazole 20–40 mg daily) for 2–4 weeks to support mucosal healing from corrosive injury

— Antiemetic PRN (ondansetron ODT)

— Iron supplementation is withheld during recovery — re-evaluate need at follow-up; if iron deficiency anemia genuinely present, restart at low dose only after gut healing

— Avoid concurrent vitamin C megadoses

— Continue psychiatric medications as appropriate; ensure no overlapping toxicity

— Safe medication storage: lockable cabinets, child-resistant containers, count pills, never store with candy

— Poison Control number on refrigerator/phone (1-800-222-1222)

— Avoid storing prenatal vitamins on bedside tables in homes with toddlers

— Caregiver counseling: how iron toxicity progresses, when to return

— Home safety assessment; CPS consult if unsupervised access pattern

— Counsel on chewable vs adult tablets; never call medicine "candy"

— Encourage all family medications be reviewed and locked

— Outpatient psychiatry follow-up arranged before discharge

— Lethal-means restriction counseling (remove iron and other OTC meds from home)

— Suicide safety plan documented

— Address substance use, social supports, follow-up within 7 days

— Most patients who survive 48–72 h recover fully

— Hepatic recovery typically complete unless transplanted

— Stricture risk persists weeks out — schedule 4-week follow-up

— No chronic iron overload develops from a single acute ingestion (different pathophysiology from hemochromatosis)

Step 3 management: At discharge, ensure three things scheduled: PCP follow-up in 1–2 weeks, GI surveillance at 4–6 weeks for stricture screening, psychiatry within 7 days (if intentional). Document all in the discharge summary.

Board pearl: Iron supplementation is not required after iron poisoning — body iron stores often normal or elevated; reassess with labs at follow-up.

Inpatient pre-discharge optimization:

Discharge medications:

Anticipatory guidance:

Pediatric-specific prevention:

Adolescent/adult intentional ingestion:

Long-term outlook:

Follow-Up, Monitoring Parameters, and Counseling

— Symptom check: any recurrent vomiting, abdominal pain, melena, fatigue

— Vital signs, weight, hydration status

— Labs: CBC, CMP, INR — confirm resolution of transaminitis, anemia, coagulopathy

— Review medications, ensure safe storage at home

— Pediatric: developmental check, caregiver counseling reinforcement

— Watch for early stricture symptoms: postprandial fullness, early satiety, vomiting, weight loss

— Patient/caregiver education on red-flag symptoms warranting return

— Anyone with stage 1 corrosive injury, hematemesis, or large ingestion: upper GI series or EGD to screen for gastric outlet/duodenal strictures

— Endoscopic dilation if strictures found; surgical revision for refractory cases

— Within 7 days of discharge — outpatient mental health appointment

— Reassess suicidality, treat underlying depression/anxiety

— Family/social support engagement

— Document safety plan and means restriction

— Liver: AST/ALT, bilirubin, INR at week 1; repeat if abnormal

— Renal: creatinine, urinalysis if AKI occurred

— Hematologic: CBC; iron studies (ferritin, TIBC, saturation) at 4–6 weeks to assess true iron status before considering supplementation

— GI: clinical symptom review at every visit; imaging or endoscopy as indicated

— Iron is dangerous in overdose — most don't realize prenatal vitamins can kill

— Locked storage, original child-resistant containers, never decant into unlabeled containers

— Recognize early symptoms (vomiting, abdominal pain) and call poison control

— Safe-disposal of unused iron supplements (pharmacy take-back programs)

— Document poison control consultation in chart for medico-legal record

— Public health: unit-dose packaging laws (US, since 1997) reduced pediatric iron deaths >60% — reinforce why packaging matters

— Insurance: ensure mental health benefits coverage for outpatient follow-up

CCS pearl: Always schedule follow-up appointments at the time of discharge order entry — Step 3 cases reward proactive transition-of-care planning over reactive symptom management.

Board pearl: A patient seen 3 weeks after iron poisoning with new postprandial vomiting needs an upper GI series, not reassurance.

Post-discharge timeline:

Week 1 — PCP follow-up:

Weeks 2–4 — interim surveillance:

Week 4–6 — GI follow-up for high-risk patients:

Psychiatric follow-up (intentional ingestion):

Monitoring parameters by organ system:

Counseling content:

Health-systems context:

Ethical, Legal, and Patient Safety Considerations

— Intentional overdose patients may refuse care while still toxic/altered — assess decision-making capacity carefully; severe acidosis, hypotension, or altered mentation impairs capacity

— Treat under implied consent / emergency exception when capacity is impaired and harm is imminent

— Re-engage discussion when stabilized

— Pediatric iron poisoning from unsupervised access: assess for neglect

— In the US, healthcare providers are mandated reporters of suspected child abuse/neglect — file CPS report when home environment unsafe or repeated ingestions occur

— Document objective findings and report rationale; the report is not an accusation but a request for safety assessment

— Mandatory psychiatric evaluation prior to discharge for any intentional ingestion

— In most US states, involuntary psychiatric hold is permitted if patient remains at imminent risk and refuses voluntary care — know your state's procedure

— Means restriction counseling is evidence-based suicide prevention

— Iron poisoning's biphasic course is a classic handoff hazard — the well-appearing stage 2 patient transferred from ED to floor may decompensate on the receiving service

— Communicate expected trajectory explicitly during sign-out; specify which labs and exams to monitor and when to escalate

— Document anticipatory orders (e.g., "if iron >500 at 8-hour level, start DFO; if MAP <65, call ICU")

— Use closed-loop verbal handoffs and shared documentation

— Unit-dose blister packaging mandates (post-1997 US rule) cut pediatric iron mortality dramatically — institutional advocacy still relevant

— Pharmacy counseling at dispensing: every prenatal vitamin prescription should include storage counseling

— Joint Commission / patient safety: medication reconciliation should flag iron in homes with children <6

— Time-stamped ingestion details, pill counts, poison control case number, labs, treatments, consents, capacity assessments

— In pregnancy: document fetal monitoring discussion and shared decision-making for any management deviation

— Adolescent intentional ingestion: parental involvement usually required for safety, but balance adolescent privacy where state law allows confidential mental health care

Step 3 management: A 16-year-old refusing parental notification after intentional iron overdose still requires parental involvement because safety supersedes confidentiality in active suicide risk — document the override rationale and notify parents.

Board pearl: Failure to anticipate stage 2 latency during ED-to-floor handoff is a classic patient-safety vignette — always communicate biphasic risk.

Informed consent and capacity:

Mandatory reporting and child protection:

Suicide attempt management:

Transition-of-care risk (Step 3 hot topic):

Medication safety / system-level prevention:

Documentation and medico-legal:

Confidentiality nuances:

High-Yield Associations and Rapid-Fire Clinical Facts

— Ferrous sulfate: 20% (most common adult supplement; 325 mg tab = 65 mg elemental)

— Ferrous fumarate: 33%

— Ferrous gluconate: 12%

— Carbonyl iron: ~100% but less bioavailable, lower toxicity

— Polysaccharide-iron complex: variable, lower toxicity

— <20: asymptomatic

— 20–40: mild GI symptoms

— 40–60: moderate-severe systemic

— >60: potentially lethal

— <300: usually fine

— 300–500: mild–moderate

— 500–1000: chelate

— >1000: severe, aggressive chelation + ICU

— GI (0.5–6h) → Latent (6–24h) → Shock/acidosis (6–72h) → Hepatic failure (12–96h) → Strictures (2–8 weeks)

— Iron: periportal / zone 1 (portal blood arrives first, highest iron delivery)

— Acetaminophen: centrilobular / zone 3

— Ischemia: centrilobular / zone 3

— Deferoxamine for acute iron toxicity, IV 5–15 mg/kg/h, max 6 g/day

— Watch for hypotension, ARDS (>24 h use), Yersinia enterocolitica

— Vin rosé urine = active chelation

— Charcoal does NOT bind iron

— WBI with PEG = decontamination of choice

— TIBC is NOT useful in acute toxicity

— Toddler + hematemesis + radiopaque KUB = iron

— Pregnancy + intentional OD + AG acidosis = iron (prenatal vitamins)

— Iron OD + fever + diarrhea during chelation = Yersinia sepsis

— Iron OD + postprandial vomiting at 4 weeks = gastric outlet stricture

— Iron + early INR rise without hepatic failure = direct thrombin inhibition

— Iron OD + anuria = HD to clear ferrioxamine

— Pediatric iron deaths dropped >60% after 1997 US unit-dose packaging law

Board pearl: "Vin rosé" urine = ferrioxamine in the urine = deferoxamine is working. Color clearance is an endpoint for stopping chelation.

Key distinction: Acute iron poisoning ≠ hereditary hemochromatosis — different timeframes, different chelators (DFO acute; deferasirox/deferiprone chronic).

Elemental iron content (memorize):

Toxicity thresholds (mg/kg elemental):

Serum iron thresholds at 4–6 hours (μg/dL):

Five stages mnemonic — "GLad Surgeons Heal Strictures":

Hepatic necrosis zone:

Antidote facts:

Rapid associations:

Public-health pearl:

Board Question Stem Patterns

— 2-year-old, found with empty bottle of mother's prenatal vitamins, brought to ED. Vomits blood, bloody diarrhea, lethargic, HR 160, BP 70/40. KUB shows radiopaque pills.

— Question: Best next step? Answer: IV fluids + WBI with PEG + IV deferoxamine + admit to PICU. Send iron level at 4–6 hours.

— 16-year-old after intentional ingestion 8 hours ago. Initially vomited, now "feels better," wants to go home. Iron level 720 μg/dL, lactate 5.2, AG 22.

— Question: Disposition? Answer: Admit, start deferoxamine — patient is in stage 2/3 despite feeling well.

— 24-year-old G2P1 at 16 weeks gestation, intentional overdose of prenatal vitamins. Iron 850 μg/dL, vomiting, mild acidosis.

— Question: Is deferoxamine safe? Answer: Yes — give DFO; untreated maternal toxicity has higher fetal risk than chelation.

— Iron OD patient on DFO becomes anuric. Iron still high.

— Question: Next step? Answer: Hemodialysis to clear ferrioxamine; continue DFO at reduced rate.

— Activated charcoal — WRONG; doesn't bind iron

— TIBC ratio — outdated, don't pick it

— Oral deferasirox — for chronic overload, not acute

— Ipecac — abandoned

— Patient who survived iron OD 4 weeks ago now with postprandial vomiting and weight loss.

— Question: Diagnosis/next step? Answer: Gastric outlet obstruction from stricture → upper GI series or EGD with possible dilation.

— Patient on day 3 of DFO develops fever and bloody diarrhea.

— Question: Pathogen? Answer: Yersinia enterocolitica — treat with TMP-SMX, ciprofloxacin, or ceftriaxone.

— 36 hours post-ingestion, INR 4.2, ALT 4500, ammonia elevated, glucose 45.

— Question: Action? Answer: Transfer to transplant center, continue supportive care, D10, vitamin K/PCC, consider NAC.

Board pearl: Step 3 stems reward acting on clinical context + labs rather than waiting for a "magic number." If the patient looks sick and the gestalt is iron, chelate.

Step 3 management: Always pick the answer that includes poison control consultation alongside the clinical intervention when offered.

Stem pattern 1 — Classic pediatric:

Stem pattern 2 — Latent phase trap:

Stem pattern 3 — Pregnancy:

Stem pattern 4 — Renal failure complication:

Stem pattern 5 — Wrong-answer traps (recognize these distractors):

Stem pattern 6 — Delayed stricture:

Stem pattern 7 — Yersinia complication:

Stem pattern 8 — Hepatic failure:

One-Line Recap

— Stages: GI (0.5–6h) → Latent (6–24h, the trap) → Shock/acidosis (6–72h) → Hepatic failure with periportal/zone 1 necrosis (12–96h) → Strictures (2–8 weeks)

— Thresholds: >40 mg/kg elemental = symptomatic; iron >500 μg/dL or systemic toxicity = deferoxamine 5–15 mg/kg/h IV; vin rosé urine confirms active chelation

— Decontamination: Whole-bowel irrigation with PEG is the answer; charcoal does NOT bind iron; lavage and ipecac are obsolete

— Pitfalls: Stage 2 latent phase fools clinicians; pregnancy = still give DFO; renal failure = pair DFO with hemodialysis; >24 h DFO risks ARDS + Yersinia; late postprandial vomiting = stricture

Board pearl: When in doubt, chelate early — the cost of unnecessary deferoxamine is far lower than the cost of missed iron toxicity progressing to fulminant hepatic failure.

Iron poisoning is a biphasic, five-stage toxidrome (GI → latent → shock/acidosis → hepatic failure → late strictures) where toxicity is dose-dependent on elemental iron, diagnosed by 4–6-hour serum iron level, and treated with whole-bowel irrigation plus IV deferoxamine when iron >500 μg/dL or systemic toxicity is present — while activated charcoal, TIBC, and oral chelators have no role.

High-yield bullets to lock in:

CCS rhythm to remember: 2 large-bore IVs → labs + iron level at 4–6h + KUB → fluid resuscitation + NG-PEG for WBI → call poison control → IV deferoxamine when criteria met → ICU admit → trend acidosis, urine color, end-organ function → psychiatry and social work for intentional/pediatric cases → schedule 4-week GI follow-up for stricture screening

One-line teaching point: Treat iron poisoning aggressively in the first hours based on clinical severity plus serum iron at 4–6 hours, never trust the deceptively well-appearing stage 2 patient, and remember that deferoxamine + whole-bowel irrigation + supportive care saves lives across pediatrics, pregnancy, and adult intentional overdose.