Iron Overdose

Quick Reference

Critical Alerts

• Iron poisoning can be rapidly fatal - mortality up to 10% in severe cases without treatment [1]
• Toxic dose: > 20 mg/kg elemental iron - severe toxicity at > 60 mg/kg [2]
• Five phases of toxicity - beware the deceptive "latent phase" at 6-24 hours
• Deferoxamine is the chelating antidote - indicated for serum iron > 500 mcg/dL or systemic toxicity [3]
• Activated charcoal does NOT bind iron - whole bowel irrigation is the GI decontamination of choice
• Vin rose urine indicates deferoxamine efficacy - pink-red discoloration from ferrioxamine excretion

Key Diagnostics

Emergency Treatments

• GI decontamination: Whole bowel irrigation with polyethylene glycol if intact tablets on imaging
• Deferoxamine: 15 mg/kg/hr IV (max 35 mg/kg/hr critically ill), maximum 6-8 g/24 hours [4]
• IV crystalloid resuscitation: Aggressive for hypovolemia from GI losses
• Sodium bicarbonate: For severe metabolic acidosis (pH less than 7.1)
• Blood products: pRBCs for hemorrhage, FFP for coagulopathy
• DO NOT use activated charcoal: Iron is not adsorbed

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Overview

Iron poisoning represents a potentially life-threatening toxicological emergency resulting from ingestion of elemental iron, most commonly from iron supplement tablets, prenatal vitamins, or children's multivitamins. Despite implementation of unit-dose packaging regulations in many countries, iron toxicity remains a significant cause of poisoning morbidity and mortality, particularly in the pediatric population where accidental ingestion predominates, and in adults where intentional overdose is more common [1,5].

The pathophysiology of iron toxicity involves two distinct mechanisms: direct corrosive injury to the gastrointestinal mucosa from unabsorbed iron, and systemic cellular toxicity from circulating free iron that exceeds the binding capacity of transferrin. Free iron catalyzes formation of reactive oxygen species through the Fenton and Haber-Weiss reactions, leading to lipid peroxidation, mitochondrial dysfunction, and multiorgan failure affecting the liver, cardiovascular system, and kidneys [6,7].

Understanding the characteristic five phases of iron toxicity is critical for emergency physicians, as clinical improvement during the "latent phase" may provide false reassurance before the onset of devastating systemic toxicity. Early recognition of severity markers and timely initiation of deferoxamine chelation therapy can be life-saving [3,8].

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Epidemiology

Incidence and Demographics

Risk Factors

Population at Risk:

• Children aged 1-3 years (accidental ingestion of colorful tablets)
• Adults with psychiatric comorbidity (intentional self-harm)
• Pregnant women (access to prenatal iron supplements)
• Patients with chronic iron supplementation

Product-Related Factors:

• High elemental iron content preparations (ferrous fumarate)
• Non-unit-dose packaging
• Appealing appearance of tablets (colored, sugar-coated)
• Large quantity availability (90-count bottles)

Historical Context

Iron poisoning was historically a leading cause of pediatric poisoning fatalities in the United States. Following FDA implementation of unit-dose packaging requirements in 1997, pediatric iron poisoning deaths declined significantly from an average of 5.3 deaths per year (1988-1997) to 0.7 deaths per year (1998-2002) [5]. However, the regulation was challenged legally and partially reversed, underscoring the importance of continued vigilance.

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Toxicology

Elemental Iron Content of Common Preparations

Accurate calculation of ingested elemental iron is essential for risk stratification.

Toxicity Thresholds

Dose Calculation Formula:

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

Exam Detail: Clinical Pearl - Dose Uncertainty: In cases where the ingested dose is uncertain or unreliable history, clinical presentation and serum iron levels should guide management. Assume worst-case scenario for dose estimation when in doubt. Always err toward more aggressive monitoring and treatment.

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Pathophysiology

Mechanism of Iron Absorption

Under normal physiological conditions, iron absorption is tightly regulated by enterocyte ferroportin and the hepcidin-ferroportin axis. In overdose, this regulatory mechanism is overwhelmed, leading to massive unregulated absorption particularly in the duodenum and proximal jejunum [6].

Phases of Toxicity - Detailed Mechanism

Phase 1: Gastrointestinal Phase (0-6 hours)

The ferric (Fe3+) and ferrous (Fe2+) forms of iron cause direct oxidative damage to the gastrointestinal epithelium. Mucosal necrosis may extend to perforation in severe cases. Massive fluid and blood losses into the GI tract contribute to early hypovolemic shock [6,7].

Phase 2: Latent/Quiescent Phase (6-24 hours)

This phase represents the most dangerous period from a clinical decision-making perspective:

• Apparent clinical improvement
• Resolution of GI symptoms
• Patient appears stable
• DANGER: Ongoing intracellular toxicity progressing
• Free iron redistributing to tissues
• Cellular damage accelerating silently

Do not discharge patients during this phase based on symptom resolution alone. Serial monitoring and repeat serum iron levels are mandatory [8].

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

Once absorbed, free iron exceeds transferrin binding capacity (normally saturated at 300-350 mcg/dL). Unbound iron catalyzes free radical formation:

Cellular Toxicity Targets:

Metabolic Acidosis Generation:

1. Lactic acid accumulation from tissue hypoperfusion
2. Mitochondrial dysfunction impairing aerobic metabolism
3. Hydration of ferric iron releasing hydrogen ions: Fe3+ + 3H2O → Fe(OH)3 + 3H+
4. Direct inhibition of Krebs cycle enzymes [7]

Phase 4: Hepatotoxicity Phase (2-3 days)

Peak hepatic injury typically manifests 2-3 days post-ingestion:

• Massive transaminase elevation (AST/ALT may exceed 10,000 U/L)
• Coagulopathy from synthetic failure (elevated PT/INR)
• Hypoglycemia from impaired gluconeogenesis
• Hepatic encephalopathy
• May progress to fulminant hepatic failure requiring transplantation [11,12]

Phase 5: Late Gastrointestinal Phase (2-8 weeks)

Delayed complications from mucosal healing:

• Gastric outlet obstruction from pyloric stenosis
• Small bowel strictures
• Intestinal obstruction
• May require surgical intervention [6]

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Clinical Presentation

Symptoms by Phase

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

Phase 2 (Latent Phase: 6-24 hours):

• Apparent clinical improvement
• Resolution of GI symptoms
• May appear "well"
• CRITICAL: This does NOT indicate safety

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

Physical Examination Findings

General:

• Vital signs: Tachycardia, hypotension, tachypnea
• Skin: Pallor, diaphoresis, peripheral cyanosis in shock

Abdominal:

• Tenderness (diffuse or epigastric)
• Distension
• Absent/reduced bowel sounds (ileus)
• Signs of peritonitis (rare, indicates perforation)

Cardiovascular:

• Hypotension
• Tachycardia
• Weak peripheral pulses
• Delayed capillary refill

Severity Grading System

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Red Flags (Life-Threatening Features)

Immediate Recognition Required

Prognostic Indicators

Factors Predicting Poor Outcome [11,12]:

• Peak serum iron > 1000 mcg/dL
• Arterial pH less than 7.0
• Shock unresponsive to fluid resuscitation
• Coma at presentation
• White blood cell count > 15,000/mm3
• Blood glucose > 150 mg/dL (stress response)
• Coagulopathy with INR > 2.0
• Hepatic failure with AST > 1000 U/L

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Differential Diagnosis

Other Toxicological Emergencies

Non-Toxicological Differential

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Diagnostic Approach

Initial Assessment (First 30 Minutes)

Essential History:

• Exact product ingested (obtain container if possible)
• Number of tablets taken
• Elemental iron content per tablet
• Time of ingestion
• Intentional vs. accidental
• Co-ingestants (especially acetaminophen, salicylates)
• Vomiting since ingestion (may have reduced absorbed dose)
• Pregnancy status
• Medical comorbidities

Physical Examination Focus:

• Vital signs (repeated every 15-30 minutes initially)
• Mental status assessment
• Abdominal examination
• Signs of shock

Laboratory Investigations

Serum Iron Level Interpretation

Exam Detail: Important Caveats for Serum Iron Interpretation:

1. Timing matters: Peak serum iron occurs 4-6 hours post-ingestion for immediate-release preparations. Levels drawn less than 4 hours may underestimate severity.

2. Enteric-coated/sustained-release: Peak may be delayed to 8-12 hours. Multiple serial levels required.

3. Deferoxamine interference: Deferoxamine-iron complex (ferrioxamine) may falsely lower measured serum iron depending on assay method.

4. Clinical-laboratory correlation: A "normal" iron level does NOT exclude toxicity if patient is symptomatic with acidosis. Treat the patient, not the number.

5. TIBC utility: Total iron-binding capacity (TIBC) was historically used to calculate "free iron" but is no longer recommended as it is often falsely elevated in overdose and does not add to management [2,3].

Imaging Studies

Abdominal X-ray (KUB):

Limitations:

• Liquid iron preparations are not radiopaque
• Dissolved tablets may not be visible
• Chewable/children's vitamins may not be radiopaque
• Normal X-ray does NOT exclude significant ingestion [8]

CT Abdomen: Reserved for suspected perforation, unclear diagnosis, or complications.

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Management

Overview Algorithm

IRON OVERDOSE MANAGEMENT ALGORITHM
==================================

1. INITIAL STABILIZATION (ABCDE)
   |
   v
2. HISTORY: Calculate elemental iron dose (mg/kg)
   |
   +---> less than 20 mg/kg AND asymptomatic --> Observe 6 hours, discharge if well
   |
   +---> ≥20 mg/kg OR symptomatic --> Continue to step 3
   |
   v
3. INVESTIGATIONS: Serum iron, ABG, glucose, coags, X-ray
   |
   v
4. GI DECONTAMINATION (if indicated)
   |
   +---> Pills visible on X-ray --> Whole Bowel Irrigation
   |
   v
5. SEVERITY ASSESSMENT
   |
   +---> Serum iron > 500 OR systemic symptoms OR acidosis
   |          --> DEFEROXAMINE + ICU
   |
   +---> Serum iron 300-500, GI symptoms only
   |          --> Admit, monitor, supportive care
   |
   +---> Serum iron less than 300, asymptomatic
              --> 6-hour observation, likely discharge

6. ONGOING MONITORING AND SUPPORTIVE CARE
   |
   v
7. DISPOSITION BASED ON CLINICAL COURSE

GI Decontamination

Activated Charcoal:

• NOT recommended for iron ingestion
• Iron is NOT adsorbed by activated charcoal [8,13]
• May obscure subsequent imaging
• Only indicated if significant co-ingestants

Gastric Lavage:

• Generally NOT recommended
• Iron tablets typically too large to pass through lavage tube
• Risk of esophageal injury
• Consider only if:
  • Life-threatening ingestion
  • Very recent (less than 1 hour)
  • Large bore tube available
  • Protected airway [13]

Whole Bowel Irrigation (WBI):

Contraindications to WBI:

• Ileus or bowel obstruction
• GI perforation or significant hemorrhage
• Unprotected airway (unless intubated)
• Hemodynamic instability (stabilize first)
• Intractable vomiting

Exam Detail: Technique for Whole Bowel Irrigation:

1. Place NG tube (confirm position)
2. Commence PEG solution at recommended rate
3. Antiemetics PRN (ondansetron 4-8 mg IV)
4. Position patient upright if possible
5. Monitor for abdominal distension
6. Repeat abdominal X-ray after 4-6 hours
7. Continue until effluent clear and imaging clear
8. May require 12+ hours in severe cases

Other Decontamination Methods:

Deferoxamine (Chelation Therapy)

Mechanism of Action: Deferoxamine mesylate (DFO) is a hexadentate iron chelator that binds ferric (Fe3+) iron with high affinity, forming a stable, water-soluble ferrioxamine complex that is excreted renally. Each 100 mg of deferoxamine binds approximately 9 mg of elemental iron [3,4].

Indications for Deferoxamine [3,4,14]:

• Serum iron > 500 mcg/dL
• Serum iron 350-500 mcg/dL with symptoms
• Systemic toxicity (shock, altered mental status, acidosis)
• Severe GI symptoms with clinical deterioration
• Any patient with metabolic acidosis attributable to iron
• Ingestion > 60 mg/kg elemental iron with symptoms

Dosing Protocol:

Administration:

DEFEROXAMINE IV INFUSION PROTOCOL

1. Calculate initial dose: 15 mg/kg/hour
2. Dilute in 0.9% NaCl or D5W
3. Commence infusion via dedicated IV line
4. Monitor blood pressure every 15 minutes initially
5. If hypotension occurs: slow rate, fluid bolus
6. Increase to maximum 35 mg/kg/hr if life-threatening

EXAMPLE: 70 kg patient
- 15 mg/kg/hr = 1050 mg/hour = 17.5 mg/min
- Dilute 1000 mg in 100 mL --> run at 105 mL/hour

Endpoints for Deferoxamine Cessation:

1. Clinical improvement (resolution of acidosis, hemodynamic stability)
2. Serum iron less than 300 mcg/dL
3. Urine color returns to normal (loss of vin rose appearance)
4. Resolution of metabolic acidosis
5. Typically 24-48 hours of therapy

Vin Rose Urine: Ferrioxamine excretion imparts a characteristic pink-red ("vin rose" or rose wine) color to urine. This indicates:

• Deferoxamine is chelating free iron
• Therapy is working
• Continue until color normalizes

Adverse Effects of Deferoxamine:

Exam Detail: Why ARDS Occurs with Prolonged Deferoxamine:

The mechanism is not fully understood but is believed related to:

1. Free radical generation during iron mobilization
2. Pulmonary oxidative stress
3. Ferrioxamine accumulation in pulmonary tissue
4. Typically occurs after > 24 hours at high doses (> 6g/24h)

Prevention: Limit infusion to 24 hours if possible. If extending therapy, ensure clear indication and monitor closely for respiratory deterioration [4,14].

Supportive Care

Fluid Resuscitation:

• Crystalloid (0.9% NaCl or Ringer's lactate) for hypovolemia
• Initial bolus: 20 mL/kg, repeat as needed
• Target: MAP > 65 mmHg, UOP > 0.5 mL/kg/hr
• Blood products for hemorrhagic shock

Acidosis Management:

• Primary treatment: resuscitation and deferoxamine
• Sodium bicarbonate for pH less than 7.1 or HCO3 less than 8 mmol/L
• Dose: 1-2 mEq/kg IV, repeat as needed
• Target: pH > 7.2 (not complete correction)

Coagulopathy Management:

• Fresh frozen plasma (FFP) 15-20 mL/kg for INR > 2.0 and bleeding
• Vitamin K 10 mg IV (hepatic synthetic support)
• Platelet transfusion if less than 50,000/mm3 and bleeding
• Consider cryoprecipitate if fibrinogen less than 100 mg/dL

Glucose Management:

• Frequent monitoring (hourly in severe cases)
• Dextrose 10-25% infusion for hypoglycemia
• Target: blood glucose 100-180 mg/dL

Vasopressor Support:

• If hypotension refractory to fluids (30 mL/kg crystalloid)
• Norepinephrine first-line: 0.1-0.5 mcg/kg/min
• Consider vasopressin if catecholamine-resistant

Airway Management:

• Intubation for altered mental status (GCS less than 8)
• Profound shock
• Anticipated clinical deterioration
• Need for aggressive GI decontamination with aspiration risk

Special Circumstances

Iron Bezoar/Concretion:

• Retained mass of iron tablets forming gastric concretion
• Perpetuates ongoing absorption
• Management options:
  1. Prolonged WBI (may require 24+ hours)
  2. Endoscopic fragmentation and removal
  3. Gastric lavage with bicarbonate solution (controversial)
  4. Surgical gastrotomy (rare, last resort) [13]

Pregnancy:

• Iron supplements commonly prescribed; overdose possible
• Deferoxamine: Pregnancy Category C
• Maternal iron toxicity poses greater risk than deferoxamine
• Treat aggressively; maternal survival critical for fetal survival
• Fetal outcomes dependent on maternal hemodynamic stability [15]

Enteric-Coated/Sustained-Release Preparations:

• Delayed and prolonged absorption
• Peak serum iron may be 8-12 hours post-ingestion
• Extended WBI often required
• Serial serum iron levels essential (repeat at 8 and 12 hours)

Chronic Iron Overload States:

• Patients with hemochromatosis, thalassemia major
• Baseline elevated iron stores
• May have increased sensitivity to additional iron load
• Lower threshold for chelation

Hemodialysis:

• Deferoxamine-iron complex (ferrioxamine) is dialyzable
• Consider in:
  • Acute kidney injury preventing renal ferrioxamine excretion
  • Massive ingestion with very high serum iron
  • Anuric patients requiring chelation [14]

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Disposition

ICU Admission Criteria

Mandatory ICU admission for ANY of the following:

• Serum iron > 500 mcg/dL
• Metabolic acidosis (pH less than 7.3 or HCO3 less than 20)
• Shock or hemodynamic instability
• Altered mental status
• Coagulopathy (INR > 1.5)
• Hepatic dysfunction (elevated transaminases, hypoglycemia)
• Requirement for deferoxamine infusion
• Significant GI hemorrhage requiring transfusion
• Need for vasopressor support
• Airway compromise

Ward Admission Criteria

• Serum iron 300-500 mcg/dL with mild GI symptoms only
• Normal acid-base status
• Hemodynamically stable
• Normal mental status
• Post-decontamination observation
• Borderline ingestion with some uncertainty

Observation Unit (6-Hour Minimum)

Suitable for:

• Ingestion less than 20 mg/kg with initial GI symptoms now resolved
• Serum iron less than 300 mcg/dL
• Asymptomatic at 6 hours
• Normal vital signs and mental status
• Normal acid-base status

Discharge Criteria

All of the following must be met:

• Ingestion confirmed less than 20 mg/kg elemental iron
• Asymptomatic at 6 hours observation
• Serum iron less than 300 mcg/dL
• Normal ABG/VBG
• No acidosis
• Tolerating oral intake
• Reliable follow-up available
• Psychiatric evaluation completed (if intentional overdose)
• Safe home environment (especially if child - assess for neglect/safety)

Follow-up Requirements

Psychiatric Considerations (Intentional Overdose)

• Mandatory psychiatric evaluation before discharge
• Assess suicidal ideation, intent, plan
• Determine appropriate psychiatric disposition
• Secure medication access on discharge
• Involve mental health crisis team
• Consider inpatient psychiatric admission if ongoing risk

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Complications

Acute Complications

Late Complications (2-8 weeks)

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Prognosis

Outcome Predictors

Good Prognosis:

• Ingestion less than 40 mg/kg
• Serum iron less than 500 mcg/dL
• No metabolic acidosis
• Normal mental status
• Rapid presentation and treatment

Poor Prognosis [11,12]:

• Serum iron > 1000 mcg/dL (mortality ~50%)
• pH less than 7.0 (mortality approaches 50%)
• Coma at presentation
• Refractory shock
• Hepatic failure (AST > 1000, INR > 2)
• Age extremes (young children, elderly)

Survival Rates

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Prevention

Primary Prevention

Packaging Regulations:

• Unit-dose (blister) packaging for iron supplements
• Child-resistant containers
• Warning labels on iron-containing products

Safe Storage Practices:

• Store all medications out of reach of children
• Use locked medication cabinets
• Never transfer pills to non-child-resistant containers
• Dispose of unused iron supplements safely

Patient Education Points

For Caregivers of Children:

• Iron tablets are NOT candy
• Even a few tablets can be fatal in small children
• Store all vitamins/supplements locked away
• Teach children medication safety
• Call poison control immediately if ingestion suspected

For Patients with Intentional Overdose:

• Provide crisis resources (helpline numbers)
• Medication safety planning
• Remove access to large quantities of iron supplements
• Psychiatric follow-up arrangements

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Exam-Focused Content

Common Exam Questions

1. "What are the phases of iron toxicity?"
2. "How do you interpret serum iron levels?"
3. "What are the indications for deferoxamine?"
4. "Why doesn't activated charcoal work for iron?"
5. "What is vin rose urine and what does it indicate?"
6. "How do you manage the latent phase?"
7. "What are the adverse effects of deferoxamine?"

Viva Points

Viva Point: Opening Statement: "Iron overdose is a potentially life-threatening toxicological emergency characterized by direct gastrointestinal corrosive injury followed by systemic cellular toxicity from free iron exceeding transferrin binding capacity. It classically presents in five phases and is managed with supportive care, whole bowel irrigation for GI decontamination, and deferoxamine chelation therapy for significant toxicity."

Key Facts to Quote:

• Toxic dose: > 20 mg/kg elemental iron; severe toxicity > 60 mg/kg
• Serum iron > 500 mcg/dL indicates severe toxicity requiring deferoxamine
• Deferoxamine dose: 15 mg/kg/hour IV, maximum 6-8 g/24 hours
• Vin rose urine confirms deferoxamine is working
• Activated charcoal does NOT bind iron
• Latent phase (6-24 hours) is deceptively dangerous

Evidence to Cite:

• Manoguerra et al., Clinical Toxicology 2005 - AACT/AAPCC consensus guidelines
• Tenenbein, J Toxicol Clin Toxicol 2001 - hepatotoxicity in iron poisoning

Common Mistakes That Fail Candidates

• Giving activated charcoal for iron ingestion
• Discharging during the latent phase based on symptom resolution
• Failing to calculate elemental iron dose
• Not obtaining serum iron level at appropriate timing (4-6 hours)
• Delaying deferoxamine in severe cases
• Not recognizing that normal X-ray doesn't exclude significant ingestion
• Using TIBC to guide management (no longer recommended)
• Forgetting psychiatric evaluation for intentional overdose

Model Viva Answers

Q: "A 25-year-old woman presents 3 hours after ingesting 50 ferrous sulfate 325mg tablets. How would you approach this case?"

A: "This is a potentially severe iron overdose. First, I would calculate the ingested dose: 50 tablets of ferrous sulfate 325mg contains 50 x 65mg = 3,250mg elemental iron. For a 60kg woman, this is approximately 54 mg/kg, which is in the severe toxicity range above 40 mg/kg.

My immediate priorities are ABCDE stabilization, IV access, and obtaining baseline investigations including serum iron level, ABG, glucose, coagulation profile, and abdominal X-ray.

If the X-ray shows radiopaque pills, I would commence whole bowel irrigation with polyethylene glycol at 1.5-2 L/hour via NG tube.

Given the ingested dose exceeds 40 mg/kg, I would not wait for serum iron results before preparing for likely deferoxamine therapy. I would obtain the 4-6 hour serum iron level and expect it to be elevated.

If serum iron exceeds 500 mcg/dL or she develops systemic symptoms, acidosis, or altered mental status, I would commence deferoxamine at 15 mg/kg/hour IV and admit to ICU.

I would warn the team about the latent phase - apparent clinical improvement at 6-24 hours does not indicate safety.

Finally, as this appears to be an intentional overdose, psychiatric evaluation is mandatory before any consideration of discharge."

Q: "What would make you stop deferoxamine therapy?"

A: "I would discontinue deferoxamine when there is clinical improvement evidenced by resolution of acidosis and hemodynamic stability, when serum iron falls below 300 mcg/dL, and when the characteristic vin rose urine color returns to normal, indicating ferrioxamine excretion has ceased. Typically this requires 24-48 hours of therapy. I would also discontinue if the patient develops ARDS, which can occur with prolonged high-dose therapy beyond 24 hours."

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Clinical Pearls

Diagnostic Pearls

1. Always calculate elemental iron dose - this predicts expected severity better than early symptoms
2. The latent phase is a trap - never be falsely reassured by symptom resolution at 6-12 hours
3. Peak serum iron is at 4-6 hours - earlier levels may underestimate severity
4. Enteric-coated preparations delay peak - check levels at 8 and 12 hours
5. Normal X-ray doesn't exclude toxicity - liquid iron and dissolved tablets are radiolucent
6. Acidosis correlates with severity - always obtain ABG/VBG
7. TIBC is not useful - often falsely elevated, no longer recommended for management

Treatment Pearls

1. Activated charcoal is useless for iron - do not use it
2. WBI is the GI decontamination of choice - if pills visible on imaging
3. Start deferoxamine early in severe cases - don't wait for serum iron if clinically toxic
4. Vin rose urine confirms efficacy - continue until it resolves
5. Infuse deferoxamine slowly - too rapid causes hypotension
6. Limit deferoxamine duration - ARDS risk with > 24 hours at high doses
7. Prepare for hepatic failure - may manifest at 48-72 hours

Disposition Pearls

1. Observe all symptomatic patients for minimum 6 hours - preferably 24 hours
2. ICU for any systemic symptoms - shock, acidosis, altered mental status
3. Psychiatric evaluation is mandatory for intentional overdose - before discharge
4. Warn about late strictures - follow up at 2-6 weeks for GI symptoms
5. Poison control is your friend - call them for guidance (available 24/7)
6. Document calculated mg/kg dose - essential for medicolegal records

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Quality Metrics

Performance Indicators for Iron Overdose Management

Documentation Checklist

• Product ingested (brand, formulation)
• Number of tablets
• Elemental iron content per tablet
• Calculated total elemental iron (mg)
• Patient weight (kg)
• Calculated dose (mg/kg)
• Time of ingestion
• Intentional vs. accidental
• Co-ingestants
• GI decontamination performed (method, duration)
• Serial serum iron levels with times
• ABG/VBG results
• Deferoxamine: indication, dose, duration, response
• Urine color changes (vin rose)
• Complications encountered
• Disposition decision and rationale
• Psychiatric assessment (if applicable)
• Follow-up arrangements

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References

1. Manoguerra AS, Erdman AR, Booze LL, et al. Iron ingestion: an evidence-based consensus guideline for out-of-hospital management. Clin Toxicol (Phila). 2005;43(6):553-570. doi:10.1081/CLT-200068842

2. Tenenbein M. Unit-dose packaging of iron supplements and reduction of iron poisoning in young children. Arch Pediatr Adolesc Med. 2005;159(6):557-560. doi:10.1001/archpedi.159.6.557

3. Baranwal AK, Singhi SC. Acute iron poisoning: management guidelines. Indian Pediatr. 2003;40(6):534-540. doi:10.1007/BF02887769

4. Howland MA. Deferoxamine. In: Nelson LS, Howland MA, Lewin NA, et al., eds. Goldfrank's Toxicologic Emergencies. 11th ed. McGraw-Hill; 2019:633-637.

5. Madiwale T, Liebelt E. Iron: not a benign therapeutic drug. Curr Opin Pediatr. 2006;18(2):174-179. doi:10.1097/01.mop.0000193302.94355.04

6. Chang TP, Rangan C. Iron poisoning: a literature-based review of epidemiology, diagnosis, and management. Pediatr Emerg Care. 2011;27(10):978-985. doi:10.1097/PEC.0b013e3182302604

7. Tenenbein M. Hepatotoxicity in acute iron poisoning. J Toxicol Clin Toxicol. 2001;39(7):721-726. doi:10.1081/clt-100108512

8. Perrone J. Iron. In: Hoffman RS, Howland MA, Lewin NA, et al., eds. Goldfrank's Toxicologic Emergencies. 11th ed. McGraw-Hill; 2019:626-633.

9. Gummin DD, Mowry JB, Beuhler MC, et al. 2022 Annual Report of the National Poison Data System (NPDS) from America's Poison Centers. Clin Toxicol (Phila). 2023;61(12):1483-1666. doi:10.1080/15563650.2023.2286194

10. Proudfoot AT, Simpson D, Dyson EH. Management of acute iron poisoning. Med Toxicol. 1986;1(2):83-100. doi:10.1007/BF03259830

11. Mills KC, Curry SC. Acute iron poisoning. Emerg Med Clin North Am. 1994;12(2):397-413. doi:10.1016/S0733-8627(20)30433-4

12. Robotham JL, Lietman PS. Acute iron poisoning: a review. Am J Dis Child. 1980;134(9):875-879. doi:10.1001/archpedi.1980.02130210063016

13. Position paper: whole bowel irrigation. J Toxicol Clin Toxicol. 2004;42(6):843-854. doi:10.1081/CLT-200035932

14. Kontoghiorghes GJ. Advances on chelation and chelator metal complexes in medicine. Int J Mol Sci. 2020;21(7):2499. doi:10.3390/ijms21072499

15. Rayburn WF, Donn SM, Wulf ME. Iron overdose during pregnancy: successful therapy with deferoxamine. Am J Obstet Gynecol. 1983;147(6):717-718. doi:10.1016/0002-9378(83)90457-9

16. Banner W Jr, Tong TG. Iron poisoning. Pediatr Clin North Am. 1986;33(2):393-409. doi:10.1016/s0031-3955(16)35009-1

17. Cheney K, Gumbiner C, Benson B, et al. Survival after a severe iron poisoning treated with intermittent infusions of deferoxamine. J Toxicol Clin Toxicol. 1995;33(5):531-536. doi:10.3109/15563659509010610

18. McGuigan MA. Acute iron poisoning. Pediatr Ann. 1996;25(1):33-38. doi:10.3928/0090-4481-19960101-08

19. Anderson AC. Iron poisoning in children. Curr Opin Pediatr. 1994;6(3):289-294. doi:10.1097/00008480-199406000-00010

20. Ioannides AS, Panisello JM. Acute respiratory distress syndrome in children with acute iron poisoning: the role of intravenous desferrioxamine. Eur J Pediatr. 2000;159(3):158-159. doi:10.1007/s004310050040

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