Iron toxicity occurs when excess iron accumulates in the body, leading to harmful effects on various organs. It is most commonly seen in children who accidentally ingest large quantities of iron-containing supplements, but it can also occur in adults due to overdose or chronic iron overload conditions such as hemochromatosis. Iron is an essential mineral required for oxygen transport and cellular metabolism; however, in toxic amounts, it generates free radicals that damage cellular structures, particularly in the gastrointestinal tract, liver, heart, and central nervous system. Without timely treatment, iron toxicity can progress rapidly and become life-threatening.
Epidemiology
According to the 2015 Annual Report from the American Association of Poison Control Centers (AAPCC), there were 4,072 reported cases involving exposure to iron or iron salts. Of these, 3,211 were due to unintentional ingestion. Notably, 2,036 incidents involved children aged five years or younger, and 1,161 individuals required medical treatment at a healthcare facility. One fatality was recorded that year.
Anatomy
Pathophysiology
Iron toxicity can be categorized into two main types: corrosive and cellular. When ingested, iron may cause direct damage to the gastrointestinal (GI) lining, leading to symptoms such as nausea, vomiting, abdominal pain, and diarrhea. In severe cases, this damage can result in significant fluid and blood loss, potentially causing hypovolemic shock. Hemorrhagic necrosis of the GI tract may also occur, increasing the risk of vomiting blood, intestinal perforation, and peritonitis. On a cellular level, excess iron disrupts metabolic processes in organs like the heart, liver, and brain. Free iron accumulates inside cells, particularly in the mitochondria, where it interferes with oxidative phosphorylation, promotes lipid peroxidation, generates reactive oxygen species, and ultimately causes cell death.
Etiology
Iron toxicity typically results from excessive iron intake, either acutely or chronically. The most common cause of acute iron toxicity is accidental ingestion of iron-containing supplements, particularly in children. Even small amounts can be dangerous in pediatric patients due to their lower body weight and increased sensitivity.
Genetics
Prognostic Factors
Time to Treatment: Early medical intervention, particularly within 6 hours of ingestion, significantly improves outcomes. Delayed treatment increases the risk of systemic complications.
Clinical Presentation: Severe symptoms such as persistent vomiting, hypotension, lethargy, metabolic acidosis, or shock are associated with worse outcomes.
Response to Chelation Therapy: Patients who respond well to deferoxamine chelation therapy generally have better outcomes.
Clinical History
Iron toxicity typically follows a five-stage clinical progression, although not all patients experience every stage, and transitions between stages can occur rapidly.
Stage I (30 minutes to 6 hours post-ingestion) is marked by prominent gastrointestinal symptoms, including abdominal pain, vomiting, diarrhea, and, in more severe cases, hematemesis and hematochezia due to mucosal irritation and bleeding.
Stage II (6 to 24 hours) may appear deceptively calm, as initial GI symptoms often subside. However, this phase reflects ongoing systemic absorption of toxic iron levels despite apparent clinical improvement.
Stage III (6 to 72 hours) signals the onset of systemic toxicity. Patients may develop recurrent GI symptoms, circulatory shock, and metabolic acidosis. Complications such as coagulopathy, hepatic dysfunction, cardiomyopathy, and acute kidney injury may emerge.
Stage IV (12 to 96 hours) involves hepatic injury, evidenced by rising aminotransferase levels, with the potential progression to acute liver failure.
Stage V (2 to 8 weeks post-ingestion) reflects delayed complications related to mucosal healing. This phase may include gastrointestinal strictures or obstructions, particularly in the pyloric or proximal small bowel regions, due to scarring and fibrosis.
Age group
Iron toxicity can occur at any age but is most commonly seen in children under 5 years old, particularly due to accidental ingestion of iron-containing supplements. Young children are at higher risk because their smaller body size means even small amounts of iron can lead to severe toxicity.
Stage I (0-6 hours post-ingestion)-Gastrointestinal Phase
Nausea, vomiting, abdominal pain, and diarrhea
Hematemesis or melena in severe cases
Signs of hypovolemia (tachycardia, hypotension) may occur due to fluid and blood loss
Stage II (6-24 hours)-Latent Phase
Apparent clinical improvement
GI symptoms may resolve, but systemic absorption continues silently
Dangerous as it may delay seeking medical attention
Stage III (12-48 hours)-Systemic Toxicity
Shock, metabolic acidosis, lethargy, seizures
Multi-organ dysfunction involving liver, kidneys, and CNS
Stage IV (2-5 days)-Hepatic Failure
Hepatotoxicity becomes evident
Coagulopathy, hypoglycemia, jaundice, and hepatic encephalopathy may occur
Stage V (2-6 weeks)-GI Scarring/Obstruction
Late complications due to healing of GI mucosa
Strictures or obstruction, especially in the pyloric region
Differential Diagnoses
Several other conditions can mimic the clinical presentation of iron toxicity. These include sepsis, acetaminophen overdose, and other toxic ingestions that lead to anion gap metabolic acidosis, such as salicylate, cyanide, methanol, and ethylene glycol poisoning. Additionally, mushroom poisoning, heavy metal exposure, theophylline toxicity, and gastrointestinal bleeding from alternate causes should also be considered in the differential diagnosis.
Laboratory Studies
Imaging Studies
Procedures
Histologic Findings
Staging
Treatment Paradigm
by Stage
by Modality
Chemotherapy
Radiation Therapy
Surgical Interventions
Hormone Therapy
Immunotherapy
Hyperthermia
Photodynamic Therapy
Stem Cell Transplant
Targeted Therapy
Palliative Care
lifestyle-modifications-in-treating-iron-toxicity
Safe Storage of Medications
Keep iron supplements and multivitamins in child-resistant containers.
Store all iron-containing products out of reach and sight of children, preferably in a locked cabinet.
Avoid transferring pills into non-childproof containers like ziplock bags or daily pill organizers.
Clear Labeling and Education
Ensure all iron-containing medications are clearly labeled.
Educate caregivers and parents about the dangers of iron overdose, even from common over-the-counter supplements.
Regulation and Packaging
Support policies that require unit-dose packaging or blister packs for iron supplements to limit the amount accessible in a single accidental ingestion.
Promote use of warning labels for iron-containing products.
Reduce Unnecessary Supplementation
Avoid prescribing or recommending iron supplements unless clinically indicated.
Monitor iron therapy regularly to prevent accumulation in chronic use, especially in patients with comorbidities like anemia of chronic disease or transfusion dependence.
Clinical Settings
In hospitals or clinics, ensure that iron preparations are clearly separated from look-alike medications to prevent administration errors.
Implement medication reconciliation processes to prevent duplicate or excessive prescribing.
Role of chelating agents in treating iron toxicity
Deferoxamine
Deferoxamine is an iron-chelating agent used to bind and remove free iron from the bloodstream and tissues. It is recommended in cases of systemic toxicity, metabolic acidosis, progressive clinical deterioration, or when serum iron concentrations suggest moderate to severe poisoning. The drug is typically given as a continuous intravenous infusion at a rate of 15 mg/kg/hour for up to 24 hours.
role-of-whole-bowel-irrigation-in-treating
Whole-bowel irrigation using a polyethylene glycol electrolyte solution can be employed to eliminate unabsorbed iron tablets from the gastrointestinal tract. This is especially useful when radiopaque pills are seen on abdominal imaging. The solution is administered through a nasogastric tube at a rate of 250-500 mL per hour for children and 1.5-2 liters per hour for adults, until the rectal effluent is clear.
role-of-management-in-treating-iron-toxicity
Management of iron toxicity involves several critical phases, beginning with initial stabilization. This includes assessment and support of airway, breathing, and circulation, along with continuous monitoring of vital signs and mental status. Intravenous access should be established promptly for fluid resuscitation and medication administration. Decontamination measures may follow, with whole bowel irrigation indicated in cases of significant or sustained-release iron ingestion, especially if tablets are visible on abdominal X-ray. Activated charcoal is ineffective, as it does not bind iron.
Diagnostic evaluation is essential to guide treatment decisions. Serum iron concentration, ideally measured 4–6 hours after ingestion, helps assess severity levels above 500 µg/dL are concerning. Additional labs such as liver function tests, arterial blood gas, complete blood count, and electrolytes are also important, along with abdominal imaging when indicated.
Chelation therapy with intravenous deferoxamine is the cornerstone of treatment for moderate to severe toxicity. It is recommended for patients with high serum iron levels, significant symptoms like hypotension or altered mental status, or radiographic evidence of retained tablets. Supportive care remains crucial throughout, including fluid and electrolyte management, correction of acidosis, and intensive care monitoring in severe cases. Finally, ongoing monitoring is needed to assess treatment response and detect late complications, such as gastrointestinal scarring. Psychiatric evaluation should be considered in cases of intentional overdose.
Iron toxicity occurs when excess iron accumulates in the body, leading to harmful effects on various organs. It is most commonly seen in children who accidentally ingest large quantities of iron-containing supplements, but it can also occur in adults due to overdose or chronic iron overload conditions such as hemochromatosis. Iron is an essential mineral required for oxygen transport and cellular metabolism; however, in toxic amounts, it generates free radicals that damage cellular structures, particularly in the gastrointestinal tract, liver, heart, and central nervous system. Without timely treatment, iron toxicity can progress rapidly and become life-threatening.
According to the 2015 Annual Report from the American Association of Poison Control Centers (AAPCC), there were 4,072 reported cases involving exposure to iron or iron salts. Of these, 3,211 were due to unintentional ingestion. Notably, 2,036 incidents involved children aged five years or younger, and 1,161 individuals required medical treatment at a healthcare facility. One fatality was recorded that year.
Iron toxicity can be categorized into two main types: corrosive and cellular. When ingested, iron may cause direct damage to the gastrointestinal (GI) lining, leading to symptoms such as nausea, vomiting, abdominal pain, and diarrhea. In severe cases, this damage can result in significant fluid and blood loss, potentially causing hypovolemic shock. Hemorrhagic necrosis of the GI tract may also occur, increasing the risk of vomiting blood, intestinal perforation, and peritonitis. On a cellular level, excess iron disrupts metabolic processes in organs like the heart, liver, and brain. Free iron accumulates inside cells, particularly in the mitochondria, where it interferes with oxidative phosphorylation, promotes lipid peroxidation, generates reactive oxygen species, and ultimately causes cell death.
Iron toxicity typically results from excessive iron intake, either acutely or chronically. The most common cause of acute iron toxicity is accidental ingestion of iron-containing supplements, particularly in children. Even small amounts can be dangerous in pediatric patients due to their lower body weight and increased sensitivity.
Time to Treatment: Early medical intervention, particularly within 6 hours of ingestion, significantly improves outcomes. Delayed treatment increases the risk of systemic complications.
Clinical Presentation: Severe symptoms such as persistent vomiting, hypotension, lethargy, metabolic acidosis, or shock are associated with worse outcomes.
Response to Chelation Therapy: Patients who respond well to deferoxamine chelation therapy generally have better outcomes.
Iron toxicity typically follows a five-stage clinical progression, although not all patients experience every stage, and transitions between stages can occur rapidly.
Stage I (30 minutes to 6 hours post-ingestion) is marked by prominent gastrointestinal symptoms, including abdominal pain, vomiting, diarrhea, and, in more severe cases, hematemesis and hematochezia due to mucosal irritation and bleeding.
Stage II (6 to 24 hours) may appear deceptively calm, as initial GI symptoms often subside. However, this phase reflects ongoing systemic absorption of toxic iron levels despite apparent clinical improvement.
Stage III (6 to 72 hours) signals the onset of systemic toxicity. Patients may develop recurrent GI symptoms, circulatory shock, and metabolic acidosis. Complications such as coagulopathy, hepatic dysfunction, cardiomyopathy, and acute kidney injury may emerge.
Stage IV (12 to 96 hours) involves hepatic injury, evidenced by rising aminotransferase levels, with the potential progression to acute liver failure.
Stage V (2 to 8 weeks post-ingestion) reflects delayed complications related to mucosal healing. This phase may include gastrointestinal strictures or obstructions, particularly in the pyloric or proximal small bowel regions, due to scarring and fibrosis.
Age group
Iron toxicity can occur at any age but is most commonly seen in children under 5 years old, particularly due to accidental ingestion of iron-containing supplements. Young children are at higher risk because their smaller body size means even small amounts of iron can lead to severe toxicity.
Stage I (0-6 hours post-ingestion)-Gastrointestinal Phase
Nausea, vomiting, abdominal pain, and diarrhea
Hematemesis or melena in severe cases
Signs of hypovolemia (tachycardia, hypotension) may occur due to fluid and blood loss
Stage II (6-24 hours)-Latent Phase
Apparent clinical improvement
GI symptoms may resolve, but systemic absorption continues silently
Dangerous as it may delay seeking medical attention
Stage III (12-48 hours)-Systemic Toxicity
Shock, metabolic acidosis, lethargy, seizures
Multi-organ dysfunction involving liver, kidneys, and CNS
Stage IV (2-5 days)-Hepatic Failure
Hepatotoxicity becomes evident
Coagulopathy, hypoglycemia, jaundice, and hepatic encephalopathy may occur
Stage V (2-6 weeks)-GI Scarring/Obstruction
Late complications due to healing of GI mucosa
Strictures or obstruction, especially in the pyloric region
Several other conditions can mimic the clinical presentation of iron toxicity. These include sepsis, acetaminophen overdose, and other toxic ingestions that lead to anion gap metabolic acidosis, such as salicylate, cyanide, methanol, and ethylene glycol poisoning. Additionally, mushroom poisoning, heavy metal exposure, theophylline toxicity, and gastrointestinal bleeding from alternate causes should also be considered in the differential diagnosis.
Emergency Medicine
Safe Storage of Medications
Keep iron supplements and multivitamins in child-resistant containers.
Store all iron-containing products out of reach and sight of children, preferably in a locked cabinet.
Avoid transferring pills into non-childproof containers like ziplock bags or daily pill organizers.
Clear Labeling and Education
Ensure all iron-containing medications are clearly labeled.
Educate caregivers and parents about the dangers of iron overdose, even from common over-the-counter supplements.
Regulation and Packaging
Support policies that require unit-dose packaging or blister packs for iron supplements to limit the amount accessible in a single accidental ingestion.
Promote use of warning labels for iron-containing products.
Reduce Unnecessary Supplementation
Avoid prescribing or recommending iron supplements unless clinically indicated.
Monitor iron therapy regularly to prevent accumulation in chronic use, especially in patients with comorbidities like anemia of chronic disease or transfusion dependence.
Clinical Settings
In hospitals or clinics, ensure that iron preparations are clearly separated from look-alike medications to prevent administration errors.
Implement medication reconciliation processes to prevent duplicate or excessive prescribing.
Emergency Medicine
Deferoxamine
Deferoxamine is an iron-chelating agent used to bind and remove free iron from the bloodstream and tissues. It is recommended in cases of systemic toxicity, metabolic acidosis, progressive clinical deterioration, or when serum iron concentrations suggest moderate to severe poisoning. The drug is typically given as a continuous intravenous infusion at a rate of 15 mg/kg/hour for up to 24 hours.
Emergency Medicine
Whole-bowel irrigation using a polyethylene glycol electrolyte solution can be employed to eliminate unabsorbed iron tablets from the gastrointestinal tract. This is especially useful when radiopaque pills are seen on abdominal imaging. The solution is administered through a nasogastric tube at a rate of 250-500 mL per hour for children and 1.5-2 liters per hour for adults, until the rectal effluent is clear.
Emergency Medicine
Management of iron toxicity involves several critical phases, beginning with initial stabilization. This includes assessment and support of airway, breathing, and circulation, along with continuous monitoring of vital signs and mental status. Intravenous access should be established promptly for fluid resuscitation and medication administration. Decontamination measures may follow, with whole bowel irrigation indicated in cases of significant or sustained-release iron ingestion, especially if tablets are visible on abdominal X-ray. Activated charcoal is ineffective, as it does not bind iron.
Diagnostic evaluation is essential to guide treatment decisions. Serum iron concentration, ideally measured 4–6 hours after ingestion, helps assess severity levels above 500 µg/dL are concerning. Additional labs such as liver function tests, arterial blood gas, complete blood count, and electrolytes are also important, along with abdominal imaging when indicated.
Chelation therapy with intravenous deferoxamine is the cornerstone of treatment for moderate to severe toxicity. It is recommended for patients with high serum iron levels, significant symptoms like hypotension or altered mental status, or radiographic evidence of retained tablets. Supportive care remains crucial throughout, including fluid and electrolyte management, correction of acidosis, and intensive care monitoring in severe cases. Finally, ongoing monitoring is needed to assess treatment response and detect late complications, such as gastrointestinal scarring. Psychiatric evaluation should be considered in cases of intentional overdose.
Iron toxicity occurs when excess iron accumulates in the body, leading to harmful effects on various organs. It is most commonly seen in children who accidentally ingest large quantities of iron-containing supplements, but it can also occur in adults due to overdose or chronic iron overload conditions such as hemochromatosis. Iron is an essential mineral required for oxygen transport and cellular metabolism; however, in toxic amounts, it generates free radicals that damage cellular structures, particularly in the gastrointestinal tract, liver, heart, and central nervous system. Without timely treatment, iron toxicity can progress rapidly and become life-threatening.
According to the 2015 Annual Report from the American Association of Poison Control Centers (AAPCC), there were 4,072 reported cases involving exposure to iron or iron salts. Of these, 3,211 were due to unintentional ingestion. Notably, 2,036 incidents involved children aged five years or younger, and 1,161 individuals required medical treatment at a healthcare facility. One fatality was recorded that year.
Iron toxicity can be categorized into two main types: corrosive and cellular. When ingested, iron may cause direct damage to the gastrointestinal (GI) lining, leading to symptoms such as nausea, vomiting, abdominal pain, and diarrhea. In severe cases, this damage can result in significant fluid and blood loss, potentially causing hypovolemic shock. Hemorrhagic necrosis of the GI tract may also occur, increasing the risk of vomiting blood, intestinal perforation, and peritonitis. On a cellular level, excess iron disrupts metabolic processes in organs like the heart, liver, and brain. Free iron accumulates inside cells, particularly in the mitochondria, where it interferes with oxidative phosphorylation, promotes lipid peroxidation, generates reactive oxygen species, and ultimately causes cell death.
Iron toxicity typically results from excessive iron intake, either acutely or chronically. The most common cause of acute iron toxicity is accidental ingestion of iron-containing supplements, particularly in children. Even small amounts can be dangerous in pediatric patients due to their lower body weight and increased sensitivity.
Time to Treatment: Early medical intervention, particularly within 6 hours of ingestion, significantly improves outcomes. Delayed treatment increases the risk of systemic complications.
Clinical Presentation: Severe symptoms such as persistent vomiting, hypotension, lethargy, metabolic acidosis, or shock are associated with worse outcomes.
Response to Chelation Therapy: Patients who respond well to deferoxamine chelation therapy generally have better outcomes.
Iron toxicity typically follows a five-stage clinical progression, although not all patients experience every stage, and transitions between stages can occur rapidly.
Stage I (30 minutes to 6 hours post-ingestion) is marked by prominent gastrointestinal symptoms, including abdominal pain, vomiting, diarrhea, and, in more severe cases, hematemesis and hematochezia due to mucosal irritation and bleeding.
Stage II (6 to 24 hours) may appear deceptively calm, as initial GI symptoms often subside. However, this phase reflects ongoing systemic absorption of toxic iron levels despite apparent clinical improvement.
Stage III (6 to 72 hours) signals the onset of systemic toxicity. Patients may develop recurrent GI symptoms, circulatory shock, and metabolic acidosis. Complications such as coagulopathy, hepatic dysfunction, cardiomyopathy, and acute kidney injury may emerge.
Stage IV (12 to 96 hours) involves hepatic injury, evidenced by rising aminotransferase levels, with the potential progression to acute liver failure.
Stage V (2 to 8 weeks post-ingestion) reflects delayed complications related to mucosal healing. This phase may include gastrointestinal strictures or obstructions, particularly in the pyloric or proximal small bowel regions, due to scarring and fibrosis.
Age group
Iron toxicity can occur at any age but is most commonly seen in children under 5 years old, particularly due to accidental ingestion of iron-containing supplements. Young children are at higher risk because their smaller body size means even small amounts of iron can lead to severe toxicity.
Stage I (0-6 hours post-ingestion)-Gastrointestinal Phase
Nausea, vomiting, abdominal pain, and diarrhea
Hematemesis or melena in severe cases
Signs of hypovolemia (tachycardia, hypotension) may occur due to fluid and blood loss
Stage II (6-24 hours)-Latent Phase
Apparent clinical improvement
GI symptoms may resolve, but systemic absorption continues silently
Dangerous as it may delay seeking medical attention
Stage III (12-48 hours)-Systemic Toxicity
Shock, metabolic acidosis, lethargy, seizures
Multi-organ dysfunction involving liver, kidneys, and CNS
Stage IV (2-5 days)-Hepatic Failure
Hepatotoxicity becomes evident
Coagulopathy, hypoglycemia, jaundice, and hepatic encephalopathy may occur
Stage V (2-6 weeks)-GI Scarring/Obstruction
Late complications due to healing of GI mucosa
Strictures or obstruction, especially in the pyloric region
Several other conditions can mimic the clinical presentation of iron toxicity. These include sepsis, acetaminophen overdose, and other toxic ingestions that lead to anion gap metabolic acidosis, such as salicylate, cyanide, methanol, and ethylene glycol poisoning. Additionally, mushroom poisoning, heavy metal exposure, theophylline toxicity, and gastrointestinal bleeding from alternate causes should also be considered in the differential diagnosis.
Emergency Medicine
Safe Storage of Medications
Keep iron supplements and multivitamins in child-resistant containers.
Store all iron-containing products out of reach and sight of children, preferably in a locked cabinet.
Avoid transferring pills into non-childproof containers like ziplock bags or daily pill organizers.
Clear Labeling and Education
Ensure all iron-containing medications are clearly labeled.
Educate caregivers and parents about the dangers of iron overdose, even from common over-the-counter supplements.
Regulation and Packaging
Support policies that require unit-dose packaging or blister packs for iron supplements to limit the amount accessible in a single accidental ingestion.
Promote use of warning labels for iron-containing products.
Reduce Unnecessary Supplementation
Avoid prescribing or recommending iron supplements unless clinically indicated.
Monitor iron therapy regularly to prevent accumulation in chronic use, especially in patients with comorbidities like anemia of chronic disease or transfusion dependence.
Clinical Settings
In hospitals or clinics, ensure that iron preparations are clearly separated from look-alike medications to prevent administration errors.
Implement medication reconciliation processes to prevent duplicate or excessive prescribing.
Emergency Medicine
Deferoxamine
Deferoxamine is an iron-chelating agent used to bind and remove free iron from the bloodstream and tissues. It is recommended in cases of systemic toxicity, metabolic acidosis, progressive clinical deterioration, or when serum iron concentrations suggest moderate to severe poisoning. The drug is typically given as a continuous intravenous infusion at a rate of 15 mg/kg/hour for up to 24 hours.
Emergency Medicine
Whole-bowel irrigation using a polyethylene glycol electrolyte solution can be employed to eliminate unabsorbed iron tablets from the gastrointestinal tract. This is especially useful when radiopaque pills are seen on abdominal imaging. The solution is administered through a nasogastric tube at a rate of 250-500 mL per hour for children and 1.5-2 liters per hour for adults, until the rectal effluent is clear.
Emergency Medicine
Management of iron toxicity involves several critical phases, beginning with initial stabilization. This includes assessment and support of airway, breathing, and circulation, along with continuous monitoring of vital signs and mental status. Intravenous access should be established promptly for fluid resuscitation and medication administration. Decontamination measures may follow, with whole bowel irrigation indicated in cases of significant or sustained-release iron ingestion, especially if tablets are visible on abdominal X-ray. Activated charcoal is ineffective, as it does not bind iron.
Diagnostic evaluation is essential to guide treatment decisions. Serum iron concentration, ideally measured 4–6 hours after ingestion, helps assess severity levels above 500 µg/dL are concerning. Additional labs such as liver function tests, arterial blood gas, complete blood count, and electrolytes are also important, along with abdominal imaging when indicated.
Chelation therapy with intravenous deferoxamine is the cornerstone of treatment for moderate to severe toxicity. It is recommended for patients with high serum iron levels, significant symptoms like hypotension or altered mental status, or radiographic evidence of retained tablets. Supportive care remains crucial throughout, including fluid and electrolyte management, correction of acidosis, and intensive care monitoring in severe cases. Finally, ongoing monitoring is needed to assess treatment response and detect late complications, such as gastrointestinal scarring. Psychiatric evaluation should be considered in cases of intentional overdose.
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