Iron toxicity: Difference between revisions
 
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==Background==
==Background==
*Iron is the 4th most abundant atomic element in the earth's crust
*Iron is the 4th most abundant atomic element in the earth's crust
*biologically a component of hemoglobin, myoglobin, catalase, xanthine oxidase, etc
*Biologically a component of hemoglobin, myoglobin, catalase, xanthine oxidase, etc
*uptake highly regulated
*Uptake highly regulated
==Toxicity==
*Amount of elemental iron ingested determines the risk, not the amount of iron salt<ref>The Royal Children's Hospital Melbourne Clinical Practice Guidelines. 2020. https://www.rch.org.au/clinicalguide/guideline_index/Iron_poisoning/</ref>
*Toxicity determined by mg/kg of elemental iron
 
*Total amount of elemental iron ingested can calculated by multiplying the estimated number of tablets by the percentages of iron in the tablet preparation
{{Iron percentages table}}
*Clinical severity is based approximated by elemental dose per kilograms:<ref name="ironoverview">Robotham JL, Lietman PS: Acute iron poisoning. A review. Am J Dis Child 1980; 134:875-879.</ref>
 
===Toxicity===
''Toxicity determined by mg/kg of elemental iron ingested<ref name="ironoverview">Robotham JL, Lietman PS: Acute iron poisoning. A review. Am J Dis Child 1980; 134:875-879.</ref>''
{| {{table}}
{| {{table}}
| align="center" style="background:*f0f0f0;"|'''Severity'''
| align="center" style="background:*f0f0f0;"|'''Severity'''
| align="center" style="background:*f0f0f0;"|'''Dose (mg/kg)'''
| align="center" style="background:*f0f0f0;"|'''Elemental Iron Dose (mg/kg)^'''
|-
|-
|Mild||10-20
|Mild||10-20
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| Severe||>60
| Severe||>60
|}
|}
*Absence of GI symptoms within 6hr of ingestion excludes significant iron ingestion (exception: enteric coated tablets)
^Total amount of elemental iron ingested calculated by multiplying estimated number of tablets by the percentages of iron in the tablet preparation (see above)
*Significant iron toxicity can result in a severe lactic acidosis from hypoperfusion due to volume loss, vasodilation and negative inotropin effects.
 
===Elemental Iron Percentages===
{{Iron percentages table}}


===Pathophysiology===
===Pathophysiology===
*Direct caustic injury to gastric mucosa<ref>Robotham JL, Lietman PS. Acute iron poisoning. A review. Am J Dis Child 1980; 134:875-879.</ref>
*Direct caustic injury to gastric mucosa<ref>Robotham JL, Lietman PS. Acute iron poisoning. A review. Am J Dis Child 1980; 134:875-879.</ref>
*occurs early, usually within several hours
*Occurs early, usually within several hours
**Causing vomiting, diarrhea, abdominal pain, and GI bleeding
**Causing vomiting, diarrhea, abdominal pain, and GI bleeding
**usually affects, the stomach, duodenum, colon rarely affected
**Usually affects, the stomach, duodenum, colon rarely affected
**can lead to formation of gastric strictures 2-8 weeks post-ingestion
**Can lead to formation of gastric strictures 2-8 weeks post-ingestion
*Impaired cellular metabolism
*Impaired cellular metabolism
**Inhibiting the electron transport chain causes lactic acidosis
**Inhibiting the electron transport chain causes lactic acidosis
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**Hypotension
**Hypotension
**Venodilation
**Venodilation
**hypovolemic shock
**Hypovolemic shock
*Portal vein iron delivery to liver
*Portal vein iron delivery to liver
**overwhelm storage capatcity of Ferritin
**Overwhelm storage capacity of Ferritin
**Hepatotoxicity (cloudy swelling, periportal hepatic necrosis, elevated transaminases)
**Hepatotoxicity (cloudy swelling, periportal hepatic necrosis, elevated transaminases)
**destroys hepatic mitochondria, disrupts oxidative phosphorylation → worsening metabolic acidosis
**Destroys hepatic mitochondria, disrupts oxidative phosphorylation → worsening metabolic acidosis
*Thrombin formation inhibition
*Thrombin formation inhibition
**Coagulopathy - direct effect on vitamin K clotting factors
**Coagulopathy - direct effect on vitamin K clotting factors


==Clinical Features==
==Clinical Features==
*Absence of GI symptoms within 6hr of ingestion excludes significant iron ingestion (exception: enteric coated tablets)
*Significant iron toxicity can result in a severe [[lactic acidosis]] from hypoperfusion due to volume loss, vasodilation and negative inotropin effects.
{| class="wikitable"
{| class="wikitable"
|+ Iron Toxicity Stages
|+ Iron Toxicity Stages
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! scope="col" | '''Time Frame'''
! scope="col" | '''Time Frame'''
|-
|-
| Stage 1||GI irritation: nausea and vomiting, abdominal pain, diarrhea||30-60 mins
| Stage 1||GI irritation: Nausea, vomiting, diarrhea, abdominal pain, hematemesis, hematochezia||30 mins-6 hours
|-
|-
| Stage 2: latent||reduced GI symptoms||6-24 hours
| Stage 2: Latent||GI symptoms may improve or resolve||6-24 hours
|-
|-
| Stage 3: shock and metabolic acidosis||metabolic acidosis, lactic acidosis, dehydration, coags, renal failure||6-72 hours
| Stage 3: Shock and metabolic acidosis||Metabolic acidosis, lactic acidosis, dehydration||6-72 hours
|-
|-
| Stage 4: hepatotox||hepatic failure||12-96 hours
| Stage 4: Hepatotoxicity/Hepatic necrosis||Hepatic failure with jaundice||12-96 hours
|-
|-
| Stage 5: bowel obstruction||GI bowel scarring/healing||2-8 weeks
| Stage 5: Bowel obstruction||GI mucosa healing leads to scarring||2-8 weeks
|}
|}


*Stage I: GI toxicity: nausea, vomiting, diarrhea, GI bleeding from local corrosive effects of iron on the gastric and intestinal mucosa
*Stage I: GI toxicity: nausea, vomiting, diarrhea, GI bleeding from local corrosive effects of iron on the gastric and intestinal mucosa
*Stage II: quiescent phase with resolution of GI symptoms and apparent clinical improvement  
*Stage II: Quiescent phase with resolution of GI symptoms and apparent clinical improvement  
**controversy between toxicologists whether this stage exists in significant poisonings
**controversy between toxicologists whether this stage exists in significant poisonings
*Stage III: systemic toxicity: shock and hypoperfusion
*Stage III: Systemic toxicity: shock and hypoperfusion
**Primarily hypovolemic shock and acidosis, myocardial dysfunction also contributes
**Primarily hypovolemic shock and acidosis, myocardial dysfunction also contributes
**GI fluid losses, increase capillary permeability, decreased venous tone
**GI fluid losses, increase capillary permeability, decreased venous tone
**severe anion gap acidosis
**Severe anion gap acidosis
**free radical damage to mitochondria disrupt oxidative phosphorylation which leads to lactic acidosis
**Free radical damage to mitochondria disrupt oxidative phosphorylation which leads to lactic acidosis
**hepatotoxicity from iron delivery via portal blood flow
**Hepatotoxicity from iron delivery via portal blood flow
*Stage IV: clinical recovery, resolution of shock and acidosis usually by days 3-4
*Stage IV: Clinical recovery, resolution of shock and acidosis usually by days 3-4
*Stage V: late onset of gastric and pyloric strictures (2-8 week later) <ref> Fine, J. Iron Poisoning. Curr Probl Pediatr, Vol 30, Iss 3, p 71-90, March 2000 </ref>
*Stage V: Late onset of gastric and pyloric strictures (2-8 week later) <ref> Fine, J. Iron Poisoning. Curr Probl Pediatr, Vol 30, Iss 3, p 71-90, March 2000 </ref>


==Differential Diagnosis==
==Differential Diagnosis==
{{Heavy metals list}}
{{Heavy metals list}}
{{CAT MUDPILERS}}
{{CAT MUDPILERS}}
{{Hyperglycemia DDX}}


==Evaluation==
==Evaluation==
===Work-Up===
===Work-Up===
[[File:vin_rose.JPG|thumb|Urine changes from rusty colored vin rose to clear.]]
*Two large-bore peripheral IVs
*CBC
*CBC
*Chemistry - '''notice that this can appear like [[DKA]]'''
*Chemistry - '''notice that this can appear like [[DKA]]'''
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**Used to follow efficacy of Fe chelation
**Used to follow efficacy of Fe chelation
**Urine changes from rusty colored vin rose to clear
**Urine changes from rusty colored vin rose to clear
*Urine pregnancy test
*Type and Screen
*Type and Screen
*Xr KUB
*XR KUB
**In ambiguous cases consider abdominal xray as most Fe tabs are radioopaque
**In ambiguous cases consider abdominal xray as most Fe tabletss are radioopaque<ref>The Royal Children's Hospital Melbourne Clinical Practice Guidelines. 2020. https://www.rch.org.au/clinicalguide/guideline_index/Iron_poisoning/</ref>
[[File:vin_rose.JPG|thumbnail]]
**However, a normal XR KUB does not rule out significant ingestion, particularly if liquid iron or chewable vitamins with iron were ingested <ref>Everson GW, Oudjhane K, Young LW, Krenzelok EP. Effectiveness of abdominal radiographs in visualizing chewable iron supplements following overdose. Am J Emerg Med. 1989 Sep;7(5):459-63. doi: 10.1016/0735-6757(89)90245-3. PMID: 2757710.</ref>
*EKG
*A serum glucose > 150mg/dL and leukocyte count above 15,000 is 100% Sp and 50% Sn in predicting Fe levels > 300mcg/mL, but the absence cannot exclude iron toxicity <ref>Lacouture PG et al. Emergency assessment of severity in iron overdose by clinical and laboratory methods. J Pediatr 1981; 99:89-91.</ref>


===Diagnosis===
''Serum iron concentration can guide treatment, but is not absolute in predicting or excluding toxicity.''


===Serum Iron Concentration===
{| {{table}}
''Serum iron concentration can guide treatment but are not absolute in predicting or excluding toxicity''
| align="center" style="background:#f0f0f0;"|'''Peak Serum Iron Level (mcg/dL)^'''
| align="center" style="background:#f0f0f0;"|'''Category'''
|-
| <300||Nontoxic or mild
|-
| 300-500 ||Significant GI symptoms and potential for systemic toxicity
|-
| >500||Moderate to severe systemic toxicity
|-
| >1000||Severe systemic toxicity and increased morbidity
|}
^usually around 4hrs post ingestion although very high doses may lead to delayed peak


Peak serum iron level (usually around 4hrs post ingestion although very high doses may lead to delayed peak):
==Management==
*<300 mcg/dL: nontoxic or mild
===Observation===
*300-500 mcg/dL: Significant GI symptoms and potential for systemic toxicity
*Patients with asymptomatic ingestion of < 20mg/kg of elemental iron may only require observation for 6 hours
*>500 mcg/dL: Moderate to severe systemic toxicity
*Volume resuscitation
*>1000 mcg/dL: severe systemic toxicity and increased morbidity


If unable to obtain a serum iron level a glucose > 150mg/dL and leukocyte count above 15000 is 100% specific and 50% sensitive in predicint=g levels > 300mcg/mL<ref>Lacouture PG et al. Emergency assessment of severity in iron overdose by clinical and laboratory methods. J Pediatr 1981; 99:89-91.</ref>
===Orogastric Lavage===
*Unclear benefit. Risk of aspiration, perforation, laryngospasm
*Intubate prior to procedure if patient not protecting airway
*Indication: Normal saline via large orogastric tube for moderate to severe iron poisoning if there are still many iron tablets (20-30) in abdominal radiograph may be beneficial


==Management==
===Observation x 6 hrs===
*Patients with asymptomatic ingestion of <20mg/kg only require observation x 6hr
*Volume resuscitation
===[[Whole bowel irrigation]]===
===[[Whole bowel irrigation]]===
*Consider only for large overdose with visible pills in the stomach on x-ray
*Indicated for large ingestion
*Administer polyethylene glycol solution at 2 L/hr in adults and 250-500 mL/hr in children
*Do not base only on radioopaque evidence of iron pills as not all formulations are readily visible on XR
*Orogastric lavage only is not likely to be successful after iron tablets have moved past the pylorus
*Supported by case reports and uncontrolled case series, but rationale behind it makes it largely supported by toxicologists<ref>Hoffman RS et al. Goldfrank's Toxicologic Emergencies. 10th Ed. Pg 618-219. McGraw Hill, 2015.</ref>
*Promotes increased gastric emptying and avoids large bezoar formation<ref>Position paper: Whole bowel irrigation. J Toxicol Clin Toxicol 2004; 42:843-854.</ref>
*Promotes increased gastric emptying and avoids large bezoar formation<ref>Position paper: Whole bowel irrigation. J Toxicol Clin Toxicol 2004; 42:843-854.</ref>


===[[Deferoxamine]]===
===[[Deferoxamine]]===
{{Deferoxamine indications}}
*Indications
*large #of pills on KUB
**Pregnancy
*estimated dose > 60mg/kg Fe2+
**Systemic toxicity and iron level > 350 mcg/dL
*Administered IV or IM because of poor oral absorption
**Iron level >500mcg/dL
*one mole of Deferoxamine (100mg) bind one mole of iron (9mg) to form ferrioxamine
**Metabolic acidosis
**vin-rose urine (ferrioxamine is a reddish compound)
** Altered Mental Status
*15mg/kg/hr (determined empirically and never clinically tested), max 35mg/kg/hr
**Progressive symptoms, including shock, coma, seizures, refractory GI symptoms
**can start slower at 8mg/kg/hr if concern for hypotension and uptitrate
**Large number of pills on KUB
*can give 90mg/kg IM if unable to obtain IV however IVF is critical so IV access should be established ASAP
**Estimated dose > 60mg/kg Fe2+
*can cause hypotension
*Administered IV due to poor oral absorption
*may cause flushing (anaphylactoid reaction)
**One mole of Deferoxamine (100mg) binds one mole of iron (9mg) to form ferrioxamine
*rarely causes ARDS - associated with prolonged use
**Results in vin-rose urine (ferrioxamine is a reddish compound)
*probably safe to use in pregnancy (give if obvious signs of shock/toxicity)
*Dose
**5-15 mg/kg/hr, max of 35 mg/kg/hr or 6g total per day
**Start slower at 5-8 mg/kg/hr if hypotensive and uptitrate as tolerated
**Titrate up for worsening metabolic acidosis, progressive organ failure, persistent vin rosé urine (ongoing choleation)
**Can give 90 mg/kg IM if unable to obtain IV, but must establish IV ASAP given patient will need fluid resuscitation
*Adverse reactions
**Hypotension
**May cause flushing (anaphylactoid reaction)
**Rarely causes ARDS - associated with prolonged use
**Safe in pregnancy (give if obvious signs of shock/toxicity)


===Hemodialysis===
===Hemodialysis===
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===Not Indicated===
===Not Indicated===
====Orogastric lavage====
*Does not remove large numbers of pills and may have serious adverse events
====[[Activated charcoal]]====
====[[Activated charcoal]]====
*Does not bind iron
*Does not absorb significant amounts if iron and is not recommended


====Poison Control====
===Poison Control===
1-800-222-1222 (United States)
*1-800-222-1222 (United States)


==Disposition==
==Disposition==
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==See Also==
==See Also==
[[Toxidromes]]
*[[Toxidromes]]
*[[Hemochromatosis]]
 
==External Links==
*Example clinical practice guideline: https://www.rch.org.au/clinicalguide/guideline_index/Iron_poisoning/


==References==
==References==
<references/>
<references/>
[[Category:Toxicology]]
[[Category:Toxicology]]

Latest revision as of 18:50, 8 August 2023

Background

  • Iron is the 4th most abundant atomic element in the earth's crust
  • Biologically a component of hemoglobin, myoglobin, catalase, xanthine oxidase, etc
  • Uptake highly regulated
  • Amount of elemental iron ingested determines the risk, not the amount of iron salt[1]

Elemental Iron Percentages

Iron Preparation % of Elemental Iron
Ferrous Fumarate 33%
Ferrous Sulfate 20%
Ferrous Gluconate 12%
Ferric pyrophosphate 30%
Ferroglycine sulfate 16%
Ferrous carbonate (anhydrous) 38%

Toxicity

Toxicity determined by mg/kg of elemental iron ingested[2]

Severity Elemental Iron Dose (mg/kg)^
Mild 10-20
Moderate 20-60
Severe >60

^Total amount of elemental iron ingested calculated by multiplying estimated number of tablets by the percentages of iron in the tablet preparation (see above)

Pathophysiology

  • Direct caustic injury to gastric mucosa[3]
  • Occurs early, usually within several hours
    • Causing vomiting, diarrhea, abdominal pain, and GI bleeding
    • Usually affects, the stomach, duodenum, colon rarely affected
    • Can lead to formation of gastric strictures 2-8 weeks post-ingestion
  • Impaired cellular metabolism
    • Inhibiting the electron transport chain causes lactic acidosis
    • Direct hepatic, CNS, and cardiac toxicity (decreased CO and myocardial contractility)
    • Cell membrane injury from lipid peroxidation[4]
  • Increased capillary permeability
    • Hypotension
    • Venodilation
    • Hypovolemic shock
  • Portal vein iron delivery to liver
    • Overwhelm storage capacity of Ferritin
    • Hepatotoxicity (cloudy swelling, periportal hepatic necrosis, elevated transaminases)
    • Destroys hepatic mitochondria, disrupts oxidative phosphorylation → worsening metabolic acidosis
  • Thrombin formation inhibition
    • Coagulopathy - direct effect on vitamin K clotting factors

Clinical Features

  • Absence of GI symptoms within 6hr of ingestion excludes significant iron ingestion (exception: enteric coated tablets)
  • Significant iron toxicity can result in a severe lactic acidosis from hypoperfusion due to volume loss, vasodilation and negative inotropin effects.
Iron Toxicity Stages
Staging Clinical Effect Time Frame
Stage 1 GI irritation: Nausea, vomiting, diarrhea, abdominal pain, hematemesis, hematochezia 30 mins-6 hours
Stage 2: Latent GI symptoms may improve or resolve 6-24 hours
Stage 3: Shock and metabolic acidosis Metabolic acidosis, lactic acidosis, dehydration 6-72 hours
Stage 4: Hepatotoxicity/Hepatic necrosis Hepatic failure with jaundice 12-96 hours
Stage 5: Bowel obstruction GI mucosa healing leads to scarring 2-8 weeks
  • Stage I: GI toxicity: nausea, vomiting, diarrhea, GI bleeding from local corrosive effects of iron on the gastric and intestinal mucosa
  • Stage II: Quiescent phase with resolution of GI symptoms and apparent clinical improvement
    • controversy between toxicologists whether this stage exists in significant poisonings
  • Stage III: Systemic toxicity: shock and hypoperfusion
    • Primarily hypovolemic shock and acidosis, myocardial dysfunction also contributes
    • GI fluid losses, increase capillary permeability, decreased venous tone
    • Severe anion gap acidosis
    • Free radical damage to mitochondria disrupt oxidative phosphorylation which leads to lactic acidosis
    • Hepatotoxicity from iron delivery via portal blood flow
  • Stage IV: Clinical recovery, resolution of shock and acidosis usually by days 3-4
  • Stage V: Late onset of gastric and pyloric strictures (2-8 week later) [5]

Differential Diagnosis

Background

Heavy metal toxicity results from exposure to metals like lead, mercury, arsenic, or cadmium, which interfere with cellular function. Exposure may occur occupationally, environmentally, through ingestion, or from alternative medicines. Chronic toxicity can present insidiously, while acute toxicity may mimic sepsis or encephalopathy. Diagnosis is often delayed due to nonspecific symptoms.

Clinical Features

Symptoms depend on the metal and exposure duration but may include:

Neurologic: Peripheral neuropathy, confusion, tremor, encephalopathy

GI: Abdominal pain, nausea, vomiting, diarrhea, anorexia

Heme: Anemia (especially microcytic or hemolytic), basophilic stippling (lead)

Renal: Tubular dysfunction, proteinuria, Fanconi syndrome

Dermatologic: Mees’ lines (arsenic), hyperpigmentation, hair loss

Others: Fatigue, weight loss, hypertension (cadmium), immunosuppression

Differential Diagnosis

Sepsis or systemic inflammatory response

Drug toxicity or overdose

Metabolic disorders (e.g., porphyria, uremia)

Psychiatric illness (if symptoms are vague or bizarre)

Neurologic diseases (e.g., Guillain-Barré, MS, Parkinson’s)

Vitamin deficiencies (e.g., B12, thiamine)

Evaluation

Workup

History: Occupational exposures, home remedies, hobbies (e.g., jewelry making, battery recycling), diet, water source, imported goods

Labs:

  • CBC, CMP, urinalysis
  • Blood lead level, serum/urine arsenic, mercury, or cadmium (based on suspicion)
  • Urine heavy metal screen (note: spot testing may require creatinine correction)

Imaging: Abdominal X-ray (radiopaque material in GI tract, especially with lead)

EKG: Evaluate for QT prolongation or arrhythmias in severe cases

Diagnosis

Confirmed by elevated blood or urine levels of the specific metal in the context of clinical findings. Hair and nail testing are unreliable for acute toxicity. Interpret results with toxicologist input if possible.

Management

Remove the source of exposure (e.g., occupational control, GI decontamination if recent ingestion)

Supportive care: IV fluids, seizure control, electrolyte repletion

Chelation therapy (in consultation with toxicology or Poison Control):

Lead: EDTA, dimercaprol (BAL), succimer

Mercury/arsenic: Dimercaprol or DMSA

Cadmium: No effective chelation—focus on supportive care

Notify local public health authorities if exposure source is environmental or occupational

Disposition

Admit if symptomatic, unstable, or requiring chelation

Discharge may be appropriate for asymptomatic patients with low-level exposure and outpatient follow-up

Arrange toxicology or environmental medicine follow-up for source control and serial testing

See Also

CAT MUDPILERS

Hyperglycemia

Evaluation

Work-Up

Urine changes from rusty colored vin rose to clear.
  • Two large-bore peripheral IVs
  • CBC
  • Chemistry - notice that this can appear like DKA
    • Anion gap metabolic acidosis
    • Hyperglycemia
  • Coags
  • LFTs
  • Iron levels
  • Urinalysis
    • Used to follow efficacy of Fe chelation
    • Urine changes from rusty colored vin rose to clear
  • Urine pregnancy test
  • Type and Screen
  • XR KUB
    • In ambiguous cases consider abdominal xray as most Fe tabletss are radioopaque[6]
    • However, a normal XR KUB does not rule out significant ingestion, particularly if liquid iron or chewable vitamins with iron were ingested [7]
  • EKG
  • A serum glucose > 150mg/dL and leukocyte count above 15,000 is 100% Sp and 50% Sn in predicting Fe levels > 300mcg/mL, but the absence cannot exclude iron toxicity [8]

Diagnosis

Serum iron concentration can guide treatment, but is not absolute in predicting or excluding toxicity.

Peak Serum Iron Level (mcg/dL)^ Category
<300 Nontoxic or mild
300-500 Significant GI symptoms and potential for systemic toxicity
>500 Moderate to severe systemic toxicity
>1000 Severe systemic toxicity and increased morbidity

^usually around 4hrs post ingestion although very high doses may lead to delayed peak

Management

Observation

  • Patients with asymptomatic ingestion of < 20mg/kg of elemental iron may only require observation for 6 hours
  • Volume resuscitation

Orogastric Lavage

  • Unclear benefit. Risk of aspiration, perforation, laryngospasm
  • Intubate prior to procedure if patient not protecting airway
  • Indication: Normal saline via large orogastric tube for moderate to severe iron poisoning if there are still many iron tablets (20-30) in abdominal radiograph may be beneficial

Whole bowel irrigation

  • Indicated for large ingestion
  • Administer polyethylene glycol solution at 2 L/hr in adults and 250-500 mL/hr in children
  • Do not base only on radioopaque evidence of iron pills as not all formulations are readily visible on XR
  • Orogastric lavage only is not likely to be successful after iron tablets have moved past the pylorus
  • Supported by case reports and uncontrolled case series, but rationale behind it makes it largely supported by toxicologists[9]
  • Promotes increased gastric emptying and avoids large bezoar formation[10]

Deferoxamine

  • Indications
    • Pregnancy
    • Systemic toxicity and iron level > 350 mcg/dL
    • Iron level >500mcg/dL
    • Metabolic acidosis
    • Altered Mental Status
    • Progressive symptoms, including shock, coma, seizures, refractory GI symptoms
    • Large number of pills on KUB
    • Estimated dose > 60mg/kg Fe2+
  • Administered IV due to poor oral absorption
    • One mole of Deferoxamine (100mg) binds one mole of iron (9mg) to form ferrioxamine
    • Results in vin-rose urine (ferrioxamine is a reddish compound)
  • Dose
    • 5-15 mg/kg/hr, max of 35 mg/kg/hr or 6g total per day
    • Start slower at 5-8 mg/kg/hr if hypotensive and uptitrate as tolerated
    • Titrate up for worsening metabolic acidosis, progressive organ failure, persistent vin rosé urine (ongoing choleation)
    • Can give 90 mg/kg IM if unable to obtain IV, but must establish IV ASAP given patient will need fluid resuscitation
  • Adverse reactions
    • Hypotension
    • May cause flushing (anaphylactoid reaction)
    • Rarely causes ARDS - associated with prolonged use
    • Safe in pregnancy (give if obvious signs of shock/toxicity)

Hemodialysis

  • Not effective in removing iron due to large volumes of distribution
  • Dialysis can removes deferoxamine-iron complex in renal failure patients

Exchange transfusion

  • Minimal evidence but has been described in larger overdoses[11]

Not Indicated

Activated charcoal

  • Does not absorb significant amounts if iron and is not recommended

Poison Control

  • 1-800-222-1222 (United States)

Disposition

  • Discharge after 6hr observation for asymptomatic (or only vomited 1-2x) AND ingestion <20mg/kg
  • Admit to ICU if deferoxamine required
  • Psychiatric evaluation if intentional ingestion

See Also

External Links

References

  1. ↑ The Royal Children's Hospital Melbourne Clinical Practice Guidelines. 2020. https://www.rch.org.au/clinicalguide/guideline_index/Iron_poisoning/
  2. ↑ Robotham JL, Lietman PS: Acute iron poisoning. A review. Am J Dis Child 1980; 134:875-879.
  3. ↑ Robotham JL, Lietman PS. Acute iron poisoning. A review. Am J Dis Child 1980; 134:875-879.
  4. ↑ Aisen P et al. Iron toxicosis. Int Rev Exp Pathol 1990. 31:1-46.
  5. ↑ Fine, J. Iron Poisoning. Curr Probl Pediatr, Vol 30, Iss 3, p 71-90, March 2000
  6. ↑ The Royal Children's Hospital Melbourne Clinical Practice Guidelines. 2020. https://www.rch.org.au/clinicalguide/guideline_index/Iron_poisoning/
  7. ↑ Everson GW, Oudjhane K, Young LW, Krenzelok EP. Effectiveness of abdominal radiographs in visualizing chewable iron supplements following overdose. Am J Emerg Med. 1989 Sep;7(5):459-63. doi: 10.1016/0735-6757(89)90245-3. PMID: 2757710.
  8. ↑ Lacouture PG et al. Emergency assessment of severity in iron overdose by clinical and laboratory methods. J Pediatr 1981; 99:89-91.
  9. ↑ Hoffman RS et al. Goldfrank's Toxicologic Emergencies. 10th Ed. Pg 618-219. McGraw Hill, 2015.
  10. ↑ Position paper: Whole bowel irrigation. J Toxicol Clin Toxicol 2004; 42:843-854.
  11. ↑ Movassaghi N. et al. Comparison of exchange transfusion and deferoxamine in the treatment of acute iron poisoning. J Pediatr 1969; 75:604-608.
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