Iron poisoning

Last updated

Iron poisoning typically occurs from ingestion of excess iron that results in acute toxicity. Mild symptoms which occur within hours include vomiting, diarrhea, abdominal pain, and drowsiness. [1] In more severe cases, symptoms can include tachypnea, low blood pressure, seizures, or coma. [2] If left untreated, acute iron poisoning can lead to multi-organ failure resulting in permanent organ damage or death. [1]

Contents

Iron is available over the counter as a single entity supplement in an iron salt form or in combination with vitamin supplements and is commonly used in the treatment of anemias. [1] [2] Overdoses on iron can be categorized as unintentional ingestion which is predominantly associated with children or intentional ingestion involving suicide attempts in adults. [3] Unintentional ingestion of iron containing drug products are a major cause of mortality in children under the age of 6 years old in the United States. [3] As a response, in 1997 the US Food and Drug Administration (FDA) implemented a regulation requiring warning labels and unit dose packaging for products containing more than 30 mg of elemental iron per dose. [4]

The diagnosis of iron poisoning is based on clinical presentation including laboratory tests for serum iron concentrations and metabolic acidosis along with physical examination. Treatment for iron poisoning involves providing fluid replacement, gastrointestinal decontamination, administering deferoxamine intravenously, liver transplants, and monitoring the patient's condition. [4] The degree of intervention required depends on whether the patient is at risk for serious toxicity.

Signs and symptoms

Manifestation of iron poisoning may vary depending on the amount of iron ingested by the individual and is further classified by five stages based on timing of signs and symptoms. In mild to moderate cases, individuals may be asymptomatic or only experience mild gastrointestinal symptoms that resolve within six hours. [5] In serious cases, individuals may present with systemic signs and symptoms and require treatment. Clinical presentation of iron poisoning in the absence of treatment progresses in five stages: the gastrointestinal phase, latent phase, metabolic acidosis and shock phase, hepatotoxicity phase, and bowel obstruction due to scarring. [2]

Stages of Iron Toxicity [4]
StagePhaseTime Post-IngestionClinical Presentation
1Gastrointestinal30 minutes to 6 hoursAbdominal pain, diarrhea, vomiting, black stool
2Latent6 to 24 hoursNone
3Metabolic Acidosis and Shock6 to 72 hours Hypovolemic shock, low blood pressure, rapid breathing, shortness of breath, tachycardia
4Hepatotoxicity12 to 96 hoursAcute liver failure
5Bowel Obstruction2 to 8 weeksVomiting, obstruction of small intestine preventing passage of food (due to scarring)

The first indication of iron poisoning occurs within the first six hours post-ingestion and involves gastrointestinal symptoms including abdominal pain accompanied by nausea and vomiting with or without blood. Due to the disintegration of iron tablets, the stool may appear as black or dark green or gray. [4] After the first stage, gastrointestinal symptoms appear to resolve in the latent phase and individuals may show signs of improvement. [2] Following this stage, the iron begins to affect the cells of the body's organs which manifests as numerous systemic signs and symptoms developing after 6 to 72 hours, in the metabolic acidosis phase. Individuals may present with signs of cardiogenic shock indicated by low blood pressure, rapid heart rate and severe shortness of breath. [5] Hypovolemic shock occurs due to loss of blood from the gastrointestinal bleeding caused by the iron. During this phase, metabolic acidosis may also develop damaging internal organs such as the brain and liver. [4] In the fourth stage taking place 12 to 96 hours after ingestion, liver toxicity and failure occurs as the cells begin to die. In the last stage of iron poisoning following 2 to 8 weeks after ingestion, scarring of the gastrointestinal mucosal lining resulting in bowel obstruction. [3]

Cause

Pathophysiology

Iron is essential for the production of hemoglobin in red blood cells which is responsible for transporting oxygen throughout the body. In normal physiologic conditions, nonionic forms of iron (Fe°) are converted into ferrous iron (Fe2+) by gastric acid in the stomach. Ferrous iron is then absorbed in the small intestine where it is oxidized into its ferric iron (Fe3+) form before being released into the bloodstream. [4] Free iron in the blood is toxic to the body as it disrupts normal cell function, damaging organs such as the liver, stomach, and cardiovascular system. [4] The human body has protective mechanisms in place to prevent excess free ferric iron from circulating the body. When being transported throughout the body, iron is bound to an iron transporting protein called transferrin to prevent iron from being absorbed into different cells. [6] Any excess iron is stored as ferritin in the liver. [6] In the event of iron overdose, iron stores become oversaturated and the body's protective mechanisms fail resulting in excess free circulating iron. [6]

Toxic Dose

Iron poisoning can occur when doses of 20 to 60 mg/kg or more of elemental iron is ingested with most cases reporting primarily gastrointestinal symptoms. [4] Systemic signs and symptoms shown in serious toxicity occur at higher doses exceeding 60 mg/kg. [5] Ingesting above 120 mg/kg may be fatal. [4] The therapeutic dose for iron deficiency anemia is 3–6 mg/kg/day. Individuals who have ingested less than 20 mg/kg of elemental iron typically do not exhibit symptoms. [4] It is unlikely to get iron poisoning from diet alone with iron supplements being the cause of overdose. The amount of elemental iron in an iron supplement can be calculate based on the percentage it constitutes for per tablet. For example, a 300 mg tablet of ferrous fumarate will contain 100 mg of elemental iron or 33%.

Diagnosis

Iron toxicity is primarily a clinical diagnosis that involves getting a detailed patient history and physical examination of the individuals signs and symptoms. Information such as how much iron was ingested and the timing should be gathered to assess the level of toxicity. Signs for severe iron poisoning should be evaluated such as any confusion or extreme lethargy, increased heart rates, low blood pressure for adults. [4] In children, signs of shock can be noted with behavioral changes such as decreased responsiveness, crying, and inability to focus. [7] Persistent vomiting is often associated with iron poisoning and also used to determine severity of iron poisoning. Laboratory tests such as measuring the peak serum iron level after 4 to 6 hours of ingestion can be useful in determining the severity of iron toxicity. [4] In general, levels below 350mcg/dL are associated with more mild iron poisoning while upper levels above 500mcg/dL are associated with more severe iron poisoning. [3] Measuring electrolyte levels, kidney function, serum glucose, liver function tests (enzymes and bilirubin), complete blood count, clotting time via prothrombin and partial thromboplastin time, anion gap for metabolic acidosis, should be conducted for clinical monitoring and confirmation of iron poisoning. [3] [1] [4]

The deferoxamine challenge test is a diagnostic test for confirming iron poisoning, however it is no longer recommended for diagnostic purposes due to concerns regarding the accuracy. [3] Deferoxamine can be administered intramuscularly as a single dose where it then binds to free iron in the blood and is excreted into the urine turning it to a "brick orange" or pink/red/orange color. [4] [8] Radiographs are no longer used for diagnosis due to the lack of connection between severity of iron toxicity and the presence of radiopaque iron tablets in the stomach on X-rays. [3] This method also requires that the ingested tablet to be radiopaque which most iron preparations are not. [3]

Treatment

Management of acute iron poisoning involves providing a patient with respiratory support and intravenous deferoxamine. Patients exhibiting severe symptoms in the gastrointestinal phase should receive volume resuscitation to prevent hypovolemic shock from the loss of blood volume. [4] Normal saline is administered intravenously to maintain adequate volume of fluid in the body. Deferoxamine is a drug that is used in cases of serious iron poisoning. It is a chelating agent and binds to free iron in the body in order to be eliminated by the kidneys into urine. [8] Dosing of deferoxamine should be determined through consultation with a toxicologist but is typically continuously infused at 15 mg/kg to 35 mg/kg per hour and not exceeding the maximum daily dose of 6 grams for adults. [3] In pediatric patients, doses should not exceed 15 mg/kg per hour. [4] recommended duration of treatment is until symptoms have resolved which is usually 24 hours. [3] In non-fatal cases of iron poisoning where there is liver failure, liver transplantation may be necessary. [4]

Treatment of iron poisoning should be based on clinical presentation, peak serum iron levels and other laboratory results. As a general guideline, patients who have ingested lower doses of elemental iron, have a peak serum iron level less than 500mcg/dL and are asymptomatic or only exhibit mild gastrointestinal symptoms typically do not require treatment and should be monitored for 6 hours after ingestion. [1] [4] In cases where high doses of elemental iron have been ingested and the patient is exhibiting signs and symptoms of severe systemic iron poisoning, supportive care measures like volume resuscitation and deferoxamine should be initiated immediately. [4] A quick response to iron poisoning can significantly improve clinical outcomes.

See also

Related Research Articles

<span class="mw-page-title-main">Uremia</span> Excess urea in the blood due to kidney dysfunction

Uremia is the term for high levels of urea in the blood. Urea is one of the primary components of urine. It can be defined as an excess in the blood of amino acid and protein metabolism end products, such as urea and creatinine, which would be normally excreted in the urine. Uremic syndrome can be defined as the terminal clinical manifestation of kidney failure. It is the signs, symptoms and results from laboratory tests which result from inadequate excretory, regulatory, and endocrine function of the kidneys. Both uremia and uremic syndrome have been used interchangeably to denote a very high plasma urea concentration that is the result of renal failure. The former denotation will be used for the rest of the article.

<span class="mw-page-title-main">Metabolic acidosis</span> Imbalance in the bodys acid-base equilibrium

Metabolic acidosis is a serious electrolyte disorder characterized by an imbalance in the body's acid-base balance. Metabolic acidosis has three main root causes: increased acid production, loss of bicarbonate, and a reduced ability of the kidneys to excrete excess acids. Metabolic acidosis can lead to acidemia, which is defined as arterial blood pH that is lower than 7.35. Acidemia and acidosis are not mutually exclusive – pH and hydrogen ion concentrations also depend on the coexistence of other acid-base disorders; therefore, pH levels in people with metabolic acidosis can range from low to high.

<span class="mw-page-title-main">Glycogen storage disease type I</span> Medical condition

Glycogen storage disease type I is an inherited disease that prevents the liver from properly breaking down stored glycogen, which is necessary to maintain adequate blood sugar levels. GSD I is divided into two main types, GSD Ia and GSD Ib, which differ in cause, presentation, and treatment. There are also possibly rarer subtypes, the translocases for inorganic phosphate or glucose ; however, a recent study suggests that the biochemical assays used to differentiate GSD Ic and GSD Id from GSD Ib are not reliable, and are therefore GSD Ib.

<span class="mw-page-title-main">Nicotine poisoning</span> Medical condition

Nicotine poisoning describes the symptoms of the toxic effects of nicotine following ingestion, inhalation, or skin contact. Nicotine poisoning can potentially be deadly, though serious or fatal overdoses are rare. Historically, most cases of nicotine poisoning have been the result of use of nicotine as an insecticide. More recent cases of poisoning typically appear to be in the form of Green Tobacco Sickness, or due to unintended ingestion of tobacco or tobacco products or consumption of nicotine-containing plants.

<span class="mw-page-title-main">Abrin</span> Chemical compound

Abrin is an extremely toxic toxalbumin found in the seeds of the rosary pea, Abrus precatorius. It has a median lethal dose of 0.7 micrograms per kilogram of body mass when given to mice intravenously. The median toxic dose for humans ranges from 10 to 1000 micrograms per kilogram when ingested and is 3.3 micrograms per kilogram when inhaled.

<span class="mw-page-title-main">Fomepizole</span> Medication

Fomepizole, also known as 4-methylpyrazole, is a medication used to treat methanol and ethylene glycol poisoning. It may be used alone or together with hemodialysis. It is given by injection into a vein.

In clinical chemistry, the osmol gap is the difference between measured blood serum osmolality and calculated serum osmolality.

Iron(II) gluconate, or ferrous gluconate, is a black compound often used as an iron supplement. It is the iron(II) salt of gluconic acid. It is marketed under brand names such as Fergon, Ferralet and Simron.

<span class="mw-page-title-main">Iron supplement</span> Iron formulation used to prevent or treat iron deficiency anemia

Iron supplements, also known as iron salts and iron pills, are a number of iron formulations used to treat and prevent iron deficiency including iron deficiency anemia. For prevention they are only recommended in those with poor absorption, heavy menstrual periods, pregnancy, hemodialysis, or a diet low in iron. Prevention may also be used in low birth weight babies. They are taken by mouth, injection into a vein, or injection into a muscle. While benefits may be seen in days, up to two months may be required until iron levels return to normal.

Ethylene glycol poisoning is poisoning caused by drinking ethylene glycol. Early symptoms include intoxication, vomiting and abdominal pain. Later symptoms may include a decreased level of consciousness, headache, and seizures. Long term outcomes may include kidney failure and brain damage. Toxicity and death may occur after drinking even in a small amount as ethylene glycol is more toxic than other diols.

<span class="mw-page-title-main">Oleandrin</span> Chemical compound

Oleandrin is a cardiac glycoside found in the poisonous plant oleander. As a main phytochemical of oleander, oleandrin is associated with the toxicity of oleander sap, and has similar properties to digoxin.

<span class="mw-page-title-main">Paracetamol poisoning</span> Toxicity due to paracetamol overdose

Paracetamol poisoning, also known as acetaminophen poisoning, is caused by excessive use of the medication paracetamol (acetaminophen). Most people have few or non-specific symptoms in the first 24 hours following overdose. These symptoms include feeling tired, abdominal pain, or nausea. This is typically followed by absence of symptoms for a couple of days, after which yellowish skin, blood clotting problems, and confusion occurs as a result of liver failure. Additional complications may include kidney failure, pancreatitis, low blood sugar, and lactic acidosis. If death does not occur, people tend to recover fully over a couple of weeks. Without treatment, death from toxicity occurs 4 to 18 days later.

<span class="mw-page-title-main">High anion gap metabolic acidosis</span> Medical condition

High anion gap metabolic acidosis is a form of metabolic acidosis characterized by a high anion gap. Metabolic acidosis occurs when the body produces too much acid, or when the kidneys are not removing enough acid from the body. Several types of metabolic acidosis occur, grouped by their influence on the anion gap.

<span class="mw-page-title-main">Tricyclic antidepressant overdose</span> Medical condition

Tricyclic antidepressant overdose is poisoning caused by excessive medication of the tricyclic antidepressant (TCA) type. Symptoms may include elevated body temperature, blurred vision, dilated pupils, sleepiness, confusion, seizures, rapid heart rate, and cardiac arrest. If symptoms have not occurred within six hours of exposure they are unlikely to occur.

<span class="mw-page-title-main">Salicylate poisoning</span> Medical condition

Salicylate poisoning, also known as aspirin poisoning, is the acute or chronic poisoning with a salicylate such as aspirin. The classic symptoms are ringing in the ears, nausea, abdominal pain, and a fast breathing rate. Early on, these may be subtle, while larger doses may result in fever. Complications can include swelling of the brain or lungs, seizures, low blood sugar, or cardiac arrest.

Treatment of the inherited blood disorder thalassemia depends upon the level of severity. For mild forms of the condition, advice and counseling are often all that are necessary. For more severe forms, treatment may consist in blood transfusion; chelation therapy to reverse iron overload, using drugs such as deferoxamine, deferiprone, or deferasirox; medication with the antioxidant indicaxanthin to prevent the breakdown of hemoglobin; or a bone marrow transplant using material from a compatible donor, or from the patient's mother. Removal of the spleen (splenectomy) could theoretically help to reduce the need for blood transfusions in people with thalassaemia major or intermedia but there is currently no reliable evidence from clinical trials about its effects. Population screening has had some success as a preventive measure.

<span class="mw-page-title-main">Methanol toxicity</span> Medical condition

Methanol toxicity is poisoning from methanol, characteristically via ingestion. Symptoms may include a decreased level of consciousness, poor or no coordination, vomiting, abdominal pain, and a specific smell on the breath. Decreased vision may start as early as twelve hours after exposure. Long-term outcomes may include blindness and kidney failure. Blindness may occur after drinking as little as 10 mL; death may occur after drinking quantities over 15 mL.

<span class="mw-page-title-main">Taxine alkaloids</span> Chemical compound

Taxine alkaloids, which are often named under the collective title of taxines, are the toxic chemicals that can be isolated from the yew tree. The amount of taxine alkaloids depends on the species of yew, with Taxus baccata and Taxus cuspidata containing the most. The major taxine alkaloids are taxine A and taxine B although there are at least 10 different alkaloids. Until 1956, it was believed that all the taxine alkaloids were one single compound named taxine.

<span class="mw-page-title-main">Lithium toxicity</span> Medical condition

Lithium toxicity, also known as lithium overdose, is the condition of having too much lithium. Symptoms may include a tremor, increased reflexes, trouble walking, kidney problems, and an altered level of consciousness. Some symptoms may last for a year after levels return to normal. Complications may include serotonin syndrome.

Iron preparation is the formulation for iron supplements indicated in prophylaxis and treatment of iron-deficiency anemia. Examples of iron preparation include ferrous sulfate, ferrous gluconate, and ferrous fumarate. It can be administered orally, and by intravenous injection, or intramuscular injection.

References

  1. 1 2 3 4 5 Manoguerra, Anthony S.; Erdman, Andrew R.; Booze, Lisa L.; Christianson, Gwenn; Wax, Paul M.; Scharman, Elizabeth J.; Woolf, Alan D.; Chyka, Peter A.; Keyes, Daniel C.; Olson, Kent R.; Caravati, E. Martin (2005-01-01). "Iron Ingestion: an Evidence-Based Consensus Guideline for Out-of-Hospital Management". Clinical Toxicology. 43 (6): 553–570. doi: 10.1081/CLT-200068842 . ISSN   1556-3650. PMID   16255338.
  2. 1 2 3 4 "Iron Poisoning - Injuries and Poisoning". MSD Manual Consumer Version. Retrieved 2020-12-30.
  3. 1 2 3 4 5 6 7 8 9 10 Yuen, Ho-Wang; Becker, Wenxia (2020), "Iron Toxicity", StatPearls, Treasure Island (FL): StatPearls Publishing, PMID   29083637 , retrieved 2020-12-30
  4. 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 UpToDate. "Acute Iron Poisoning". www.uptodate.com. Retrieved 2020-12-31.
  5. 1 2 3 Chang, Todd Pou-Yen; Rangan, Cyrus (October 2011). "Iron poisoning: a literature-based review of epidemiology, diagnosis, and management". Pediatric Emergency Care. 27 (10): 978–985. doi:10.1097/PEC.0b013e3182302604. ISSN   1535-1815. PMID   21975503. S2CID   29833860.
  6. 1 2 3 Robotham, James L. (September 1980). "Acute Iron Poisoning: A Review". JAMA Pediatrics. 134 (9): 875–879. doi:10.1001/archpedi.1980.02130210059016. PMID   6998282.
  7. ↑ Waltzman, Mark. "Initial Evaluation of Shock in Children". www.uptodate.com. Retrieved 2021-04-27.
  8. 1 2 Lexicomp. "Deferoxamine: Drug Information". www.uptodate.com. Retrieved 2021-04-27.
This page is based on this Wikipedia article
Text is available under the CC BY-SA 4.0 license; additional terms may apply.
Images, videos and audio are available under their respective licenses.