MedVellum
MedVellum
Back to Library

Iron Overdose

On This Page

Overview

Iron Overdose

Quick Reference

Critical Alerts

  • Iron poisoning can be rapidly fatal - especially in children
  • Four phases of toxicity - watch for deceptive "quiet phase"
  • Abdominal X-ray may show radiopaque tablets
  • Deferoxamine is the antidote - start early if severe
  • GI bleeding and acidosis are hallmarks of severe toxicity

Key Diagnostics

  • Serum iron level (peak at 4-6 hours)
  • TIBC (total iron binding capacity) - less useful acutely
  • ABG/VBG (metabolic acidosis)
  • CBC, coagulation panel
  • BMP (glucose, renal function)
  • Abdominal X-ray (radiopaque pills)

Emergency Treatments

  • GI decontamination: Whole bowel irrigation if intact tablets on X-ray
  • Deferoxamine: 15 mg/kg/hr IV for severe toxicity
  • IV fluids: Aggressive resuscitation for hypovolemia
  • Bicarbonate: For severe metabolic acidosis
  • Avoid charcoal: Does not bind iron

Definition

Iron overdose is a potentially life-threatening toxicity resulting from ingestion of elemental iron, typically from iron supplement tablets. It is particularly dangerous in children due to the availability of attractive-looking iron supplements. The toxic effects are mediated by free iron's corrosive action on the GI tract and cellular toxicity from oxidative damage.

Iron Content of Common Preparations

PreparationElemental Iron Content
Ferrous sulfate 325mg65mg (20%)
Ferrous gluconate 325mg38mg (12%)
Ferrous fumarate 325mg106mg (33%)
Prenatal vitamins30-65mg
Children's multivitamin10-18mg

Toxicity Thresholds

Dose (Elemental Iron)Expected Severity
<20 mg/kgNon-toxic to mild GI symptoms
20-60 mg/kgModerate toxicity
>0 mg/kgSevere toxicity, potentially fatal
>50 mg/kgUsually fatal without treatment

Epidemiology

  • Peak incidence: Children ages 1-3 years (accidental ingestion)
  • Leading cause: Pediatric poisoning death from pharmaceuticals (historically)
  • Adults: Often intentional overdose
  • Improved safety: Unit-dose packaging has reduced pediatric deaths

Pathophysiology

Mechanism of Toxicity

Phase 1: Direct GI Toxicity (0-6 hours)

  • Iron is directly corrosive to GI mucosa
  • Mucosal necrosis and hemorrhage
  • Third-spacing of fluids → hypovolemia
  • May cause GI perforation in severe cases

Phase 2: Systemic Toxicity

  • Absorbed iron exceeds binding capacity (transferrin)
  • Free iron catalyzes free radical formation (Fenton reaction)
  • Oxidative damage to mitochondria
  • Cellular dysfunction and death

Target Organs

OrganEffect
LiverPeriportal necrosis, hepatic failure
HeartCardiomyopathy, arrhythmias
KidneyAcute tubular necrosis
VasculatureVasodilation, capillary leak

Metabolic Effects

Anion Gap Metabolic Acidosis

  • Lactic acid from tissue hypoperfusion
  • Inhibition of mitochondrial function
  • Release of hydrogen ions from iron-hydroxide complexes
  • Serves as marker of severity

Clinical Presentation

Four Phases of Iron Toxicity

Phase 1: GI Phase (0-6 hours)

SymptomSeverity Correlation
Nausea, vomitingCommon, may be bloody
Abdominal painCramping, diffuse
DiarrheaOften bloody
HematemesisIndicates severe mucosal injury

Phase 2: Latent Phase (6-24 hours)

Phase 3: Systemic Toxicity Phase (12-48 hours)

FindingMechanism
ShockHypovolemia, vasodilation, cardiac toxicity
Metabolic acidosisLactic acid, cellular dysfunction
CoagulopathyHepatic failure, DIC
Hepatic failureDirect hepatotoxicity
HypoglycemiaHepatic dysfunction
Lethargy/comaShock, hepatic encephalopathy

Phase 4: Late Effects (2-6 weeks)

Clinical Severity Grading

GradeFeatures
AsymptomaticNo symptoms, low level
MildGI symptoms only, no acidosis
ModerateSignificant GI symptoms, mild acidosis
SevereShock, altered mental status, coagulopathy, hepatotoxicity

Apparent clinical improvement
Common presentation.
"Quiet phase" - DECEPTIVELY DANGEROUS
Common presentation.
During this time, intracellular damage progresses
Common presentation.
Do not be reassured by symptom resolution
Common presentation.
Red Flags (Life-Threatening)

Critical Findings

Red FlagConcernAction
Serum iron >00 mcg/dLSevere toxicityDeferoxamine
Metabolic acidosisCellular toxicityICU, deferoxamine
Altered mental statusShock or hepatic failureICU, aggressive resuscitation
HypotensionHypovolemia, cardiac toxicityFluid resuscitation, vasopressors
CoagulopathyHepatic failureFFP, ICU admission
GI bleedingSevere mucosal injuryTransfusion, consider endoscopy
Glucose <60 mg/dLHepatic failureDextrose

Prognostic Indicators

Poor Prognosis

  • Serum iron >1000 mcg/dL
  • pH <7.1
  • Shock unresponsive to fluids
  • Hepatic failure (elevated INR, transaminases)
  • Coma

Differential Diagnosis

Other Toxic Ingestions

ToxinFeatures
Caustic ingestionSimilar GI injury, no systemic iron effects
TheophyllineGI symptoms, acidosis, seizures
SalicylatesAcidosis, tinnitus, mixed acid-base
AcetaminophenHepatotoxicity but delayed 24-72h
Heavy metals (arsenic, lead)GI symptoms, specific levels

Other Causes of GI Bleeding with Shock

  • Upper GI bleed (ulcer, varices)
  • Lower GI bleed
  • Ischemic bowel
  • GI perforation

Diagnostic Approach

Initial Assessment

Key History

  • Exact product ingested
  • Number of pills taken
  • Time of ingestion
  • Intentional vs accidental
  • Co-ingestants

Calculate Elemental Iron Dose

Elemental iron (mg) = Number of tablets × Elemental iron per tablet
Dose (mg/kg) = Total elemental iron ÷ Patient weight (kg)

Laboratory Studies

TestPurposeCritical Values
Serum ironDiagnosis and severity>00 mcg/dL = severe
TIBCBinding capacityLess useful acutely
ABG/VBGAcidosispH <7.35 concerning
GlucoseHepatic functionLow = hepatic failure
CBCAnemia from bleeding
CoagulationHepatic functionPT/INR elevated
LFTsHepatotoxicityMay rise at 12-24h
LactateTissue perfusionElevated = severe

Serum Iron Interpretation

Level (mcg/dL)Interpretation
<300Unlikely significant toxicity
300-500Moderate toxicity possible
500-1000Severe toxicity likely
>000Life-threatening

Important Notes:

  • Peak level at 4-6 hours post-ingestion
  • Level drawn <4 hours may underestimate severity
  • Enteric-coated preparations delay absorption
  • Level AND clinical status both matter

Imaging

Abdominal X-ray

  • Iron tablets are radiopaque
  • Useful to confirm ingestion
  • Guide need for whole bowel irrigation
  • May show pill fragments, bezoar
  • Normal X-ray does not exclude significant ingestion (liquid iron, dissolved tablets)

Treatment

GI Decontamination

Activated Charcoal

  • Does NOT bind iron effectively
  • Not recommended for isolated iron ingestion

Whole Bowel Irrigation (WBI)

Indication: Significant ingestion with visible pills on X-ray

Solution: Polyethylene glycol electrolyte solution (GoLYTELY)
Rate: 
- Adults: 1.5-2 L/hour via NG
- Children: 25-40 mL/kg/hour

Duration: Until rectal effluent clear and no pills on repeat X-ray

Contraindications: Ileus, obstruction, GI perforation, unprotected airway

Gastric Lavage

  • Generally not recommended (pills too large)
  • May be considered very early (<1 hour) if life-threatening ingestion

Deferoxamine (Antidote)

Mechanism

  • Chelates free iron to form ferrioxamine
  • Water-soluble complex excreted in urine (vin rosé color)

Indications

  • Serum iron >500 mcg/dL
  • Severe clinical toxicity (shock, altered mental status, metabolic acidosis)
  • Significant ingestion with any systemic symptoms

Dosing

IV Infusion (preferred):
- Initial: 15 mg/kg/hour
- Maximum: 35 mg/kg/hour for life-threatening toxicity
- Daily max: 6-8 g in 24 hours (higher doses associated with ARDS)

Duration: Until clinical improvement AND serum iron &lt;300 mcg/dL AND urine no longer vin rosé colored

Adverse Effects

  • Hypotension (if infused too rapidly)
  • ARDS with prolonged high-dose therapy (>24 hours)
  • Allergic reactions
  • Vin rosé urine (expected)

Monitoring During Deferoxamine

  • Serial serum iron levels
  • ABG/VBG for acidosis
  • Urine color
  • Blood pressure

Supportive Care

Fluid Resuscitation

  • Aggressive crystalloid resuscitation
  • Blood products for bleeding (pRBCs, FFP)
  • Address third-spacing losses

Acidosis Management

  • Sodium bicarbonate for severe acidosis (pH <7.1)
  • Correcting perfusion is priority

Coagulopathy

  • Fresh frozen plasma
  • Vitamin K (hepatic synthetic dysfunction)

Glucose

  • Monitor closely
  • D50 for hypoglycemia (hepatic failure marker)

Special Circumstances

Bezoar

  • Iron concretion in GI tract
  • May require endoscopic removal
  • Gastric lavage with bicarbonate solution (debated)
  • Surgical removal rarely needed

Pregnancy

  • Deferoxamine is Category C
  • Use if maternal life at risk
  • Iron toxicity risk outweighs deferoxamine risk

Disposition

ICU Admission Criteria

  • Serum iron >500 mcg/dL
  • Any systemic symptoms (shock, altered mental status)
  • Metabolic acidosis
  • Coagulopathy or hepatotoxicity
  • Need for deferoxamine infusion
  • Significant GI bleeding

Observation Unit/Ward

  • Serum iron 300-500 mcg/dL with mild symptoms
  • Asymptomatic with borderline levels
  • Post-decontamination observation

Discharge Criteria (Low-Risk Ingestions)

  • Ingestion <20 mg/kg elemental iron
  • Asymptomatic at 6 hours
  • Serum iron <300 mcg/dL
  • Normal acid-base status
  • Psychiatric evaluation if intentional (before discharge)

Follow-up Considerations

TimeframeConcern
2-6 weeksGI stricture development
If GI symptoms persistUpper/lower GI evaluation
Hepatic injuryFollow LFTs to resolution

Patient Education

Understanding Iron Poisoning

  • Iron supplements can be very dangerous if too much is taken
  • Symptoms may appear to improve then worsen significantly
  • Treatment in hospital is essential for significant ingestions

Prevention (for Caregivers)

Child Safety

  • Store iron supplements out of reach of children
  • Use child-resistant containers
  • Supervise medication administration
  • Teach children that pills are not candy

Signs of Worsening

Return immediately if:

  • Vomiting blood
  • Bloody diarrhea
  • Increasing abdominal pain
  • Confusion or drowsiness
  • Fainting or dizziness

Special Populations

Pediatric Patients

  • More common accidental ingestion
  • Lower toxic threshold (lower weight)
  • Often more severe outcomes historically
  • Calculate dose carefully in mg/kg

Pregnancy

  • Iron supplements commonly prescribed
  • Deferoxamine crosses placenta but is life-saving
  • Treat maternal toxicity aggressively
  • Fetal outcomes dependent on maternal outcomes

Enteric-Coated Preparations

  • Delayed absorption (peak may be 8-12 hours)
  • May not show on X-ray if dissolved
  • WBI particularly important
  • Multiple serum iron levels recommended

Chronic Iron Overload States

  • Hemochromatosis, transfusion-dependent patients
  • Already have elevated iron stores
  • May be more susceptible to acute toxicity

Quality Metrics

Performance Indicators

MetricTarget
Serum iron level ordered100%
Abdominal X-ray if ingestion suspected>0%
Time to deferoxamine if indicated<2 hours
Poison control contacted100%
Psychiatric evaluation (intentional)100%

Documentation Requirements

  • Product and amount ingested
  • Elemental iron dose calculated (mg/kg)
  • Time of ingestion
  • Serial serum iron levels
  • Acid-base status
  • Deferoxamine administration details
  • Response to treatment
  • Disposition rationale

Key Clinical Pearls

Diagnostic Pearls

  1. Calculate elemental iron dose - determines expected severity
  2. "Quiet phase" is dangerous - don't be falsely reassured
  3. Peak iron level at 4-6 hours - draw level appropriately
  4. X-ray may show pills - helpful for WBI decision
  5. Acidosis correlates with severity - check ABG

Treatment Pearls

  1. Charcoal does NOT work for iron - don't use it
  2. Deferoxamine for severe toxicity - start early
  3. WBI for visible pills on X-ray
  4. Watch for hypotension with deferoxamine - infuse slowly
  5. Vin rosé urine confirms deferoxamine is working

Disposition Pearls

  1. Observe 6 hours if any GI symptoms
  2. ICU for any systemic symptoms or high iron level
  3. Psychiatric evaluation for intentional overdose
  4. Warn about late strictures (2-6 weeks)
  5. Poison control is helpful - call them

References
  1. Manoguerra AS, et al. Iron ingestion: an evidence-based consensus guideline for out-of-hospital management. Clin Toxicol. 2005;43(6):553-570.
  2. Baranwal AK, Singhi SC. Acute iron poisoning: management guidelines. Indian Pediatr. 2003;40(6):534-540.
  3. Tenenbein M. Hepatotoxicity in acute iron poisoning. J Toxicol Clin Toxicol. 2001;39(7):721-726.
  4. Mills KC, Curry SC. Acute iron poisoning. Emerg Med Clin North Am. 1994;12(2):397-413.
  5. Anderson AC. Iron Poisoning. In: Ford MD, et al., eds. Clinical Toxicology. Elsevier; 2001.
  6. Perrone J. Iron. In: Hoffman RS, et al., eds. Goldfrank's Toxicologic Emergencies. 11th ed. McGraw-Hill; 2019.

Version History
VersionDateChanges
1.02025-01-15Initial comprehensive version with 14-section template

At a Glance

EvidenceStandard
Last UpdatedRecently

Guidelines

  • NICE Guidelines
  • BTS Guidelines
  • RCUK Guidelines