Iron accumulation causes toxicity in tissues and organs due to excessive saturation of iron in the body.
Iron overload caused due to excess intake or chronic accumulation.
It is an historically significant medical concern in children also affects individuals with frequent iron supplements or blood transfusions cases.
Forms of iron poisoning are:
Acute Iron Poisoning
Chronic Iron Poisoning
Acute poisoning occurs due to rapid ingestion of high doses of iron. Excessive iron levels exceed storage capacity to cause toxicity and free iron circulation.
Chronic poisoning develops gradually over time due to frequent blood transfusions. The body controls iron absorption that stores excess ferritin and transferrin proteins for safe transportation.
Iron poisoning overloads regulatory system and releases free iron to promote free radicals, oxidative stress, and tissue damage.
Epidemiology
Iron poisoning rates declined in high-income countries due to childproof packaging and parental education efforts.
Iron supplements distributed in developing countries with high nutritional deficiencies increase risk of overdose in rural areas.
Common in Northern Europeans while hereditary hemochromatosis affects 1 within 200 to 300 individuals.
Children under 6 years old and pregnant women are most at risk for accidental or intentional iron overdose from tablets that resemble candy.
Symptoms of hereditary hemochromatosis arises between 40 to 60 years old due to gradual iron buildup.
Anatomy
Pathophysiology
Excess iron is toxic to various body systems due to interference with enzymatic processes and oxidative phosphorylation.
Iron cause free radical formation and contributes to metabolic acidosis. Coagulopathies occur early due to coagulation cascade disruption and later due to liver injury.
Iron in Fenton reactions form free radicals that damage cells and DNA. Iron impairs mitochondria and reduces ATP production to cause metabolic acidosis from lactic acid buildup.
Excess iron disrupts blood vessel function that shows low blood pressure and cardiovascular collapse.
Etiology
The causes of iron poisoning are:
Therapeutic Overdose
Hereditary Hemochromatosis
Accidental Ingestion
Repeated Blood Transfusions
Genetics
Prognostic Factors
Prompt treatment of acute poisoning can lead to full recovery or permanent damage.
Metabolic acidosis from mitochondrial dysfunction and lactic acid worsens prognosis.
Intestinal complication patients face poor prognosis. Bleeding raises hypovolemia and cardiovascular collapse risk.
Administer deferoxamine early to bind and remove iron for better outcomes.
Clinical History
Clinical History:
Collect details including transfusion, social, and environmental history to understand clinical history of patient.
Intervention therapies for iron poisoning includes decontamination with gastric lavage and whole bowel irrigation along with chelation therapy with deferoxamine and supportive care.
use-of-phases-in-managing-iron-poisoning
In the initial treatment phase, evaluation of patient history, physical examination and laboratory testing to confirm diagnosis.
Pharmacologic therapy is effective in the treatment phase as it includes use of chelating agents, antidotes, and GI decontaminants.
In supportive care and management phase, patients should receive required attention such as lifestyle modification and intervention therapies.
The regular follow-up visits with the physician are scheduled to check the improvement of patients along with treatment response.
Iron accumulation causes toxicity in tissues and organs due to excessive saturation of iron in the body.
Iron overload caused due to excess intake or chronic accumulation.
It is an historically significant medical concern in children also affects individuals with frequent iron supplements or blood transfusions cases.
Forms of iron poisoning are:
Acute Iron Poisoning
Chronic Iron Poisoning
Acute poisoning occurs due to rapid ingestion of high doses of iron. Excessive iron levels exceed storage capacity to cause toxicity and free iron circulation.
Chronic poisoning develops gradually over time due to frequent blood transfusions. The body controls iron absorption that stores excess ferritin and transferrin proteins for safe transportation.
Iron poisoning overloads regulatory system and releases free iron to promote free radicals, oxidative stress, and tissue damage.
Iron poisoning rates declined in high-income countries due to childproof packaging and parental education efforts.
Iron supplements distributed in developing countries with high nutritional deficiencies increase risk of overdose in rural areas.
Common in Northern Europeans while hereditary hemochromatosis affects 1 within 200 to 300 individuals.
Children under 6 years old and pregnant women are most at risk for accidental or intentional iron overdose from tablets that resemble candy.
Symptoms of hereditary hemochromatosis arises between 40 to 60 years old due to gradual iron buildup.
Excess iron is toxic to various body systems due to interference with enzymatic processes and oxidative phosphorylation.
Iron cause free radical formation and contributes to metabolic acidosis. Coagulopathies occur early due to coagulation cascade disruption and later due to liver injury.
Iron in Fenton reactions form free radicals that damage cells and DNA. Iron impairs mitochondria and reduces ATP production to cause metabolic acidosis from lactic acid buildup.
Excess iron disrupts blood vessel function that shows low blood pressure and cardiovascular collapse.
The causes of iron poisoning are:
Therapeutic Overdose
Hereditary Hemochromatosis
Accidental Ingestion
Repeated Blood Transfusions
Prompt treatment of acute poisoning can lead to full recovery or permanent damage.
Metabolic acidosis from mitochondrial dysfunction and lactic acid worsens prognosis.
Intestinal complication patients face poor prognosis. Bleeding raises hypovolemia and cardiovascular collapse risk.
Administer deferoxamine early to bind and remove iron for better outcomes.
Clinical History:
Collect details including transfusion, social, and environmental history to understand clinical history of patient.
Fatigue, cardiomyopathy, cirrhosis, acute heart or liver failure, and endocrine issues.
Gastroenteritis
Diabetic Ketoacidosis
Hypoglycemia
Peptic Ulcer Disease
Lead Poisoning
Consider iron poisoning in mixed ingestions and small children with iron access and unexplained symptoms.
Abdominal x-ray confirms ingestion, but misses chewed or dissolved iron tablets, liquid iron, and iron in multivitamins.
Test serum iron, electrolytes, and pH post-ingestion in 3 to 4 hours.
Iron binding capacity test is unreliable and not recommended for poisoning diagnosis.
Sequentially measure serum iron, bicarbonate, and pH levels, then evaluate together and correlate with patient’s clinical status for accuracy.
Nasogastric tube used to deliver large volumes while protecting airway during administration.
Emergency Medicine
Promote policies with clear labelling of iron supplements and require warnings about toxicity.
Stock deferoxamine in emergency departments and intensive care units.
Monitor patients in controlled environment to prevent harm. Avoid iron-rich foods and alcohol for chronic iron overload patients.
Evaluate and manage suicide attempt patients in safe psychiatric settings to establish follow-up care for prevention.
Proper awareness about iron poisoning should be provided and its related causes with management strategies.
Appointments with a physician and preventing recurrence of disorder is an ongoing life-long effort.
Emergency Medicine
Deferoxamine:
It binds as free iron in the bloodstream to form a non-toxic complex.
Emergency Medicine
Activated charcoal:
It absorbs toxins in the gastrointestinal tract to prevent absorption into the bloodstream.
Emergency Medicine
Polyethylene Glycol:
It promotes bowel movements and the expulsion of unabsorbed iron/toxins.
Emergency Medicine
Intervention therapies for iron poisoning includes decontamination with gastric lavage and whole bowel irrigation along with chelation therapy with deferoxamine and supportive care.
Emergency Medicine
In the initial treatment phase, evaluation of patient history, physical examination and laboratory testing to confirm diagnosis.
Pharmacologic therapy is effective in the treatment phase as it includes use of chelating agents, antidotes, and GI decontaminants.
In supportive care and management phase, patients should receive required attention such as lifestyle modification and intervention therapies.
The regular follow-up visits with the physician are scheduled to check the improvement of patients along with treatment response.
Iron accumulation causes toxicity in tissues and organs due to excessive saturation of iron in the body.
Iron overload caused due to excess intake or chronic accumulation.
It is an historically significant medical concern in children also affects individuals with frequent iron supplements or blood transfusions cases.
Forms of iron poisoning are:
Acute Iron Poisoning
Chronic Iron Poisoning
Acute poisoning occurs due to rapid ingestion of high doses of iron. Excessive iron levels exceed storage capacity to cause toxicity and free iron circulation.
Chronic poisoning develops gradually over time due to frequent blood transfusions. The body controls iron absorption that stores excess ferritin and transferrin proteins for safe transportation.
Iron poisoning overloads regulatory system and releases free iron to promote free radicals, oxidative stress, and tissue damage.
Iron poisoning rates declined in high-income countries due to childproof packaging and parental education efforts.
Iron supplements distributed in developing countries with high nutritional deficiencies increase risk of overdose in rural areas.
Common in Northern Europeans while hereditary hemochromatosis affects 1 within 200 to 300 individuals.
Children under 6 years old and pregnant women are most at risk for accidental or intentional iron overdose from tablets that resemble candy.
Symptoms of hereditary hemochromatosis arises between 40 to 60 years old due to gradual iron buildup.
Excess iron is toxic to various body systems due to interference with enzymatic processes and oxidative phosphorylation.
Iron cause free radical formation and contributes to metabolic acidosis. Coagulopathies occur early due to coagulation cascade disruption and later due to liver injury.
Iron in Fenton reactions form free radicals that damage cells and DNA. Iron impairs mitochondria and reduces ATP production to cause metabolic acidosis from lactic acid buildup.
Excess iron disrupts blood vessel function that shows low blood pressure and cardiovascular collapse.
The causes of iron poisoning are:
Therapeutic Overdose
Hereditary Hemochromatosis
Accidental Ingestion
Repeated Blood Transfusions
Prompt treatment of acute poisoning can lead to full recovery or permanent damage.
Metabolic acidosis from mitochondrial dysfunction and lactic acid worsens prognosis.
Intestinal complication patients face poor prognosis. Bleeding raises hypovolemia and cardiovascular collapse risk.
Administer deferoxamine early to bind and remove iron for better outcomes.
Clinical History:
Collect details including transfusion, social, and environmental history to understand clinical history of patient.
Fatigue, cardiomyopathy, cirrhosis, acute heart or liver failure, and endocrine issues.
Gastroenteritis
Diabetic Ketoacidosis
Hypoglycemia
Peptic Ulcer Disease
Lead Poisoning
Consider iron poisoning in mixed ingestions and small children with iron access and unexplained symptoms.
Abdominal x-ray confirms ingestion, but misses chewed or dissolved iron tablets, liquid iron, and iron in multivitamins.
Test serum iron, electrolytes, and pH post-ingestion in 3 to 4 hours.
Iron binding capacity test is unreliable and not recommended for poisoning diagnosis.
Sequentially measure serum iron, bicarbonate, and pH levels, then evaluate together and correlate with patient’s clinical status for accuracy.
Nasogastric tube used to deliver large volumes while protecting airway during administration.
Emergency Medicine
Promote policies with clear labelling of iron supplements and require warnings about toxicity.
Stock deferoxamine in emergency departments and intensive care units.
Monitor patients in controlled environment to prevent harm. Avoid iron-rich foods and alcohol for chronic iron overload patients.
Evaluate and manage suicide attempt patients in safe psychiatric settings to establish follow-up care for prevention.
Proper awareness about iron poisoning should be provided and its related causes with management strategies.
Appointments with a physician and preventing recurrence of disorder is an ongoing life-long effort.
Emergency Medicine
Deferoxamine:
It binds as free iron in the bloodstream to form a non-toxic complex.
Emergency Medicine
Activated charcoal:
It absorbs toxins in the gastrointestinal tract to prevent absorption into the bloodstream.
Emergency Medicine
Polyethylene Glycol:
It promotes bowel movements and the expulsion of unabsorbed iron/toxins.
Emergency Medicine
Intervention therapies for iron poisoning includes decontamination with gastric lavage and whole bowel irrigation along with chelation therapy with deferoxamine and supportive care.
Emergency Medicine
In the initial treatment phase, evaluation of patient history, physical examination and laboratory testing to confirm diagnosis.
Pharmacologic therapy is effective in the treatment phase as it includes use of chelating agents, antidotes, and GI decontaminants.
In supportive care and management phase, patients should receive required attention such as lifestyle modification and intervention therapies.
The regular follow-up visits with the physician are scheduled to check the improvement of patients along with treatment response.
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