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Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 8e >

Chapter 198: IronStephanie H. Hernandez; Lewis S. Nelson

INTRODUCTION

Iron supplements are widely available, particularly in homes with small children and young women. Theattractiveness of the bright color and sugar coating of the tablets and their initial distribution in non–child-resistantvials made children susceptible to ingestion. The 1997 Federal requirement that all iron-containing pharmaceuticalscontaining more than 30 milligrams of elemental iron be distributed only in blister packs reduced the reported

incidence of iron ingestion and deaths in young children.1,2 This requirement was removed in 2003, but blister packsremain in common use along with child-resistant bottles, and serious iron poisonings in young children have

remained low.2 Women of childbearing age are at risk for intentional iron overdose due to the availability of iron and

increased stress during pregnancy and the postnatal period.3 Children with inadvertent overdoses4,5 and adults with

intentional overdose6 are at risk of serious toxicity or death.

PHARMACOLOGY

Total-body iron store averages about 4 grams in adults; the range is between 2 and 6 grams, with less iron in womenthan in men. About two thirds of the body's iron is incorporated into hemoglobin, and the remainder is found in otheriron-containing proteins such as myoglobin, cytochromes, and other enzymes and cofactors, or is stored as ferritin.The recommended daily intake of iron is about 8 milligrams for boys, adult men, and nonmenstruating women; 18

milligrams for menstruating women; and 27 milligrams for pregnant females.7 Because excess iron is toxic, the bodyuses several mechanisms to maintain iron homeostasis: serum protein binding, intracellular storage, and, most

importantly, regulation of GI tract absorption.8

The oral bioavailability of iron depends on the formulation ingested. Inorganic iron has <10% bioavailability, with

ferrous iron (Fe2+) better absorbed than ferric iron (Fe3+). Common ionic formulations include ferrous chloride, ferrousfumarate, ferrous gluconate, ferrous lactate, and ferrous sulfate (Table 198-1). Nonionic formulations include carbonyliron and iron polysaccharide (iron dextran). Most dietary iron is in the ferric form and chelated to the heme moiety.Following ingestion, the ferric ion is separated from heme and reduced to ferrous iron by a brush borderferrireductase. Chelated iron, such as that found in meat, is more readily absorbed than the iron in ionic preparations.Commercially available formulations of iron chelated with amino acids (e.g., glycinate) mimic the benefits of dietarymeat for iron absorption (Table 198-1).

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Example: A 325-milligram ferrous sulfate tablet is 20% elemental iron and contains 65 milligrams of elemental iron per tablet. Iron

sucrose is a 2% elemental iron solution and contains 20 milligrams of elemental iron per 1 mL.

TABLE 198-1

Iron Formulations and Elemental Iron Composition

Iron Formulation Elemental Iron Composition

Ionic Ferrous fumarate (PO) 33%

Ferrous chloride (PO) 28%

Ferrous sulfate (PO) 20%

Ferrous lactate (PO) 19%

Ferrous gluconate (PO) 12%

Ferrous gluconate (IV) 1.25%

Nonionic Carbonyl iron (PO) 98%

Iron polysaccharide (PO) 46%

Ferric hydroxide dextran (IV) 10% or 20%

Iron sucrose (IV) 2%

Chelated Ferrous bisglycinate (PO) 20%

Iron glycinate (PO) 27%

Ferrous iron is transported into enterocytes by a membrane proton-coupled metal transporter.7 Within the enterocyte,ferrous iron is oxidized to ferric iron. Transferrin, a serum protein, serves as a carrier and moves ferric iron from theenterocytes into the circulation and transports iron through the body. The serum total iron-binding capacity assayprimarily measures the amount of serum transferrin and is generally two to three times the normal serum ironconcentration (50 to 170 micrograms/dL or 9 to 30 micromol/L). Iron is stored within the body in the form of ferritin, alarge intracellular storage protein that can reversibly bind as many as 4500 molecules of iron. Ferritin can also beincorporated by phagolysosomes to form hemosiderin granules. In adults, about 0.5 to 1 gram of elemental iron isstored as ferritin and hemosiderin, primarily in the bone marrow, spleen, and liver. In iron deficiency, iron is mobilizedfrom ferritin and transported via transferrin to the hematopoietic cells in the spleen and bone marrow, where it is

incorporated into appropriate molecules.8 Under normal conditions, unbound iron, or free iron, does not exist withinthe body, and essentially all circulating plasma iron is normally bound to transferrin.

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There is no physiologic mechanism for removal of iron once it has entered the body.7 Regulation of GI iron uptake andlimitation of absorption by sloughing of mucosal cell containing surplus iron are the principal mechanisms for

maintaining physiologic iron concentrations.7

PATHOPHYSIOLOGY

Iron is a potent catalyst for the production of oxidants such as free radicals.9 Through this mechanism, iron is a directGI tract irritant and causes vomiting, diarrhea, abdominal pain, mucosal ulceration, and bleeding soon a�er asignificant ingestion. As the mucosal surface is injured, the regulatory enterocyte barrier is compromised, and free ironpasses unimpeded into the blood, becoming systemically available.

Free iron disrupts critical cellular processes and induces acidosis and widespread organ toxicity. It enters themitochondria, where it inhibits oxidative phosphorylation by disrupting the electron transport chain, which results inmetabolic acidosis with an elevated lactate. Production of toxic hydroxyl radicals, induction of membrane lipidperoxidation, liberation of hydrogen ions from reduction of ferrous iron, and hypotension all contribute to themetabolic acidosis seen with acute iron toxicity. Hepatotoxicity occurs as the portal blood supply delivers a largeamount of iron to the liver. In addition, coagulopathy unrelated to hepatotoxicity may occur through inhibition ofthrombin formation and the e�ect of thrombin on fibrinogen. Myocardial and vascular dysfunction result fromvasodilation, negative ionotropic e�ect, and direct myocardial iron deposition.

TOXICITY

The amount of ingested elemental iron correlates with the potential for toxicity (Table 198-2). Toxic e�ects arereported a�er oral doses as low as 10 or 20 milligrams/kg of elemental iron. In general, moderate toxicity occurs atdoses of 20 to 60 milligrams/kg of elemental iron, and severe toxicity can be expected following ingestion of >60

milligrams/kg of elemental iron.6 The most commonly prescribed formulation, a ferrous sulfate 325-milligram tablet,contains 65 milligrams of elemental iron, and approximately 20 to 35 tablets would be expected to produce moderatetoxicity a�er an acute ingestion in an adult. Pediatric multivitamins typically contain 10 to 18 milligrams of elementaliron per tablet, and this reduced amount is associated with a near absence of fatalities a�er ingestion of iron-

containing pediatric multivitamins in children compared with adult iron supplements.10 Ferric chloride poisoning can

occur with occupational inhalation, accidental ingestion through mislabeling, and suicidal ingestion.11 Ingestion ofcommercially available chemical hand warmers, containing 95 to 120 grams of reduced elemental iron (not an iron

salt), may cause corrosive injury of the esophagus and stomach12 and result in significant iron absorption with

potential toxicity.13

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*Elemental iron dose by history.

†Serum iron concentration obtained within 4–6 h of ingestion.

TABLE 198-2

Predicted Toxicity of Iron Ingestion

Predicted Clinical E�ectsElemental Iron

Dose* Serum Iron Concentration†

Nontoxic or mild GI symptoms <20

milligrams/kg

<300 micrograms/dL (<54

micromol/L)

Expected significant GI symptoms and potential for

systemic toxicity

20–60

milligrams/kg

300–500 micrograms/dL (54–90

micromol/L)

Moderate to severe systemic toxicity >60

milligrams/kg

>500 micrograms/dL (>90

micromol/L)

Severe systemic toxicity and increased morbidity >1000 micrograms/dL (>180

micromol/L)

Exceptions to the correlation of ingested dose and toxicity include chelated iron and carbonyl iron. Despite theirincreased iron content, chelated sources of supplemental iron are less toxic than nonchelated iron in overdose,

because the ligand sterically limits the iron from participating in redox reactions.14 Similarly, carbonyl iron is anonionic iron molecule that does not participate in redox reactions, and the limited experience with overdose of

carbonyl iron suggests a lower incidence of toxicity compared with ingestion of an equivalent amount of ionic iron.15

CLINICAL FEATURES

Five stages of clinical toxicity are traditionally described, although in more practical terms, acute iron toxicity can beconsidered to manifest in two clinical stages: local GI tract toxicity and systemic toxicity.

Stage 1 of iron poisoning is characterized by abdominal pain, vomiting, and diarrhea.16 Iron is directly irritating andcorrosive to the GI tract and typically induces vomiting within the first few hours following ingestion. Vomiting is theclinical sign most consistently associated with acute iron toxicity. Patients with symptoms of gastric irritation mayeither recover over several hours or progress to systemic toxicity. The absence of GI symptoms within 6 hours ofingestion essentially excludes a significant iron ingestion.

Stage 2, or the "latent" stage, does not always occur. If present, this stage is a 6- to 24-hour interval following ingestionduring which GI symptoms may resolve and falsely reassure the patient and physician. However, this is not a trulyquiescent phase. Patients with significant toxicity have ongoing clinical illness and progressive systemic deteriorationbecause of volume loss and worsening metabolic acidosis, despite the absence of GI symptoms. Alternatively, the

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resolution of GI findings may signal the end of mild poisoning, and in such a circumstance, the results of the patient'slaboratory studies should be normal.

Stage 3 is characterized by systemic toxicity from iron-induced disruption of cellular metabolism with resultant shockand lactic acidosis. Iron-induced coagulopathy may worsen bleeding and hypovolemia. The coagulopathy may bebiphasic, with prolonged prothrombin time and partial thromboplastin time within the first 24 hours. This initialcoagulopathy appears to be reversible with chelation therapy, because it is free iron that initially interferes with theactivity of factors in the coagulation cascade. Subsequent coagulopathy is from iron-induced hepatic injury thatreduced coagulation factor production. During stage 3, renal failure, cardiomyopathy, and failure of other criticalorgan systems may also occur.

Stage 4, the hepatic stage, develops 2 to 5 days following ingestion.6,17 It results from iron uptake by thereticuloendothelial system with local lipid peroxidation; it manifests as elevation of aminotransferase levels and mayprogress to hepatic failure.

Stage 5 refers to delayed sequelae, including gastric outlet obstruction secondary to the corrosive e�ects of iron on

the pyloric mucosa. Delayed sequelae are rare and occur 4 to 6 weeks a�er ingestion.16

DIAGNOSIS

LABORATORY TESTING

Laboratory tests should include CBC, determination of serum electrolyte levels, renal and liver function studies,coagulation function tests, serum glucose, and serum iron levels, with the understanding that these results are toassess the overall condition of the patient, because iron toxicity is largely a clinical diagnosis.

Arterial blood gas analysis and serum lactate determination are usually unnecessary in mild cases, becausedetermination of serum electrolyte levels (anion gap evaluation) usually yields all the important information.However, in patients with moderate to severe toxicity or in those with respiratory compromise, arterial blood gasresults yield useful information regarding the patient's acid-base status. With moderate to severe ingestions, the bloodbank should perform blood typing and screening in anticipation of potential need.

Interpret serum iron levels to assess toxicity and direct management with caution. In general, serum iron levelsmeasured within 4 to 6 hours a�er an acute ingestion correlate with the severity of toxicity (Table 198-2), but lowserum iron levels do not necessarily mean absence of toxicity. Serum iron levels may be low because of variable timesto peak level following ingestions of di�erent iron preparations, and treatment with deferoxamine can artificially lowerserum iron levels. Serum total iron-binding capacity has little value in the assessment of iron-poisoned patients. Itbecomes falsely elevated in the presence of elevated serum iron levels or deferoxamine, and significant organ damageoccurs despite exceeding the serum iron level.

IMAGING

Standard ferrous sulfate tablets and reduced iron are radiopaque and frequently visible on routine radiographs,12,13

and this may help guide GI decontamination when present. However, many iron preparations are not routinely

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detected, including pediatric chewable and liquid preparations, and absence of radiopaque material on radiographs

does not exclude iron ingestion.2

TREATMENT

Iron poisoning is a clinical diagnosis. Signs and symptoms consistent with iron poisoning should guide treatment,rather than serum iron concentrations alone (Figure 198-1). Patients who are asymptomatic on ED arrival, have notingested a potentially toxic amount, and have normal findings on physical examination can be observed and do notrequire specific medical treatment. Patients who vomit once or twice from the gastric irritant e�ects of iron but whoare otherwise asymptomatic can also be observed and may require no specific treatment.

FIGURE 198-1.

Algorithm for clinical management of iron ingestion.

Patients with clinical toxicity should first be stabilized with attention to airway, breathing, and circulation, a�er which

GI decontamination and chelation therapy with deferoxamine may proceed.2,18 Antiemetics such as metoclopramide

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or ondansetron should be used for repetitive vomiting. Patients with persistent vomiting and abnormal vital signvalues or other signs of poor perfusion or shock should undergo aggressive fluid resuscitation and treatment withdeferoxamine. Coagulopathy should be treated with parenteral vitamin K1 and/or fresh frozen plasma, as indicated.

Significant blood loss may require transfusion.

GI DECONTAMINATION

Do not use ipecac syrup because it may obscure the initial signs of clinical toxicity and is not proven to be more

e�ective at gastric emptying than is iron-induced vomiting.19 Do not give activated charcoal, cathartics, oral sodiumbicarbonate, or phosphosoda. Activated charcoal does not adsorb significant amounts of iron in an overdose to

prevent toxicity, and its use may complicate endoscopy if that becomes necessary.19 Cathartics should not be given.Orogastric lavage may not be e�ective if the ingested tablets are large or if several hours have elapsed since ingestion,but it may be useful in rare cases if performed shortly a�er large ingestion, prior to significant vomiting, or if a

modified-release formulation was ingested.2,20 There are no data to support the e�icacy of oral sodium bicarbonate or

phosphosoda in forming insoluble iron salts and preventing absorption.2,19

Radiopaque tablets visible on radiography indicate potential for progressive toxicity and can guide decontaminationmeasures (Figure 198-2). Whole-bowel irrigation with a polyethylene glycol solution is e�ective in children with large

iron ingestions.2,21 Administration of 250 to 500 mL/h in children or 2 L/h in adults by nasogastric tube may clear the

GI tract of iron pills before absorption can occur.21 Endoscopy can remove large iron loads or an iron-containing

gastric bezoar.22,23 Laparoscopic gastrotomy may be a rare option for removal of an iron-containing gastric bezoar in

profoundly ill patients when other measures are unsuccessful or impractical.24

FIGURE 198-2.

A 17-month-old boy came to the hospital with lethargy and hematemesis following a large ingestion of ironsupplement pills. [Reproduced with permission from Nelson LS, Lewin NA, Howland MA, Ho�man RS, Goldfrank LR,Flomenbaum NE: Goldfrank's Toxicologic Emergencies, 9th ed. © 2011 by McGraw-Hill, Inc., New York.]

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DEFEROXAMINE

Deferoxamine is chelating agent derived from Streptomyces pilosus used to treat iron toxicity. Deferoxamine bindsfree iron, iron from plasma, and iron from inside cells and mitochondria, but not iron bound to organic molecules.Upon binding, it forms the complex ferrioxamine, which is renally excreted. Deferoxamine can be safely administered

to children and pregnant women.3 Although deferoxamine binds a small amount of iron (9 milligrams of elementaliron for each 100 milligrams of deferoxamine) and thus chelates only a small fraction of the total amount of ironingested, removing this small but critical amount of iron o�en proves clinically e�ective in restoring cellular function.Deferoxamine may work by other mechanisms in addition to binding excess iron, and complete binding of ingestediron is not the goal of therapy.

Administration of deferoxamine is indicated in the iron-poisoned patient with systemic toxicity, persistent emesis,metabolic acidosis, progressive symptoms, or a serum iron level predictive of moderate to severe toxicity (Figure 198-

1).2,18 The manufacturer recommends IM administration for all patients not in shock,25 but most toxicologists adviseIV administration rather than IM administration because of the unreliability of IM absorption and enhanced iron

excretion following IV administration.2,18

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The initial deferoxamine adult dose is 1000 milligrams (children 50 milligrams/kg) IV. Begin the infusion slowly,starting at 5 milligrams/kg per hour to avoid producing a rate-related drop in blood pressure. Aggressive volumeresuscitation may be required in the volume-depleted, hypotensive, iron-toxic patient who is in need of deferoxamine.Hypotension is not a contraindication to IV deferoxamine administration.

The infusion rate of deferoxamine IV can be increased up to 15 milligrams/kg per hour as tolerated. The recommendedamount of deferoxamine for an acute iron overdose is a total of 360 milligrams/kg or 6 grams in an adult during the

first 24 hours, typically ordered as 500-milligram infusions over 4 to 8 hours a�er the initial 1000-milligram dose.18,25

Amounts larger than this are associated with complications, including mucormycosis, renal insu�iciency or failure,26

pulmonary toxicity,27 and sepsis from Yersinia enterocolitica, which may be related to duration of therapy.

As ferrioxamine is excreted, the urine color changes to what is classically called "vin rosé" but is more typically a

brown or rusty hue.28 Theoretically, the disappearance of the "vin rosé" color means that the patient no longer hassignificant toxicity because there is no more free iron available to be complexed with deferoxamine and excreted.False-negative results, color-change latency, and di�iculty in visualizing a color change can limit the utility of this

test.18

There is uncertainty regarding the duration of deferoxamine therapy.2,18,25 Recommended endpoints include clinicalrecovery and normal iron levels, measurement of normal iron-to-creatinine ratios, and clinical recovery with normaliron level in conjunction with normal urine color. Clinical recovery of the patient is probably the most important factorguiding the decision to terminate therapy because measured iron levels are artificially depressed by the presence ofdeferoxamine and urine color change can be unreliable. Continue deferoxamine therapy in patients who continue toexhibit severe iron toxicity a�er 24 hours of treatment, using a decreased rate to avoid the associated risks mentionedearlier.

OTHER THERAPIES

Oral iron chelators—deferiprone and deferasirox—reduce iron absorption when administered simultaneously or within

1 hour of iron ingestion.29 However, there is no evidence of benefit in human overdoses, and oral chelation therapywould theoretically be of use only when taken promptly a�er the iron ingestion; thus their use is limited by the time topresentation for treatment and the significant vomiting expected with clinical iron toxicity. Oral iron chelating agentsshould NOT replace intravenous deferoxamine when chelation is indicated in clinical iron toxicity.

Although hemodialysis and hemofiltration do not remove iron, such treatment may be necessary to remove the

deferoxamine–iron complex in patients with renal failure who are unable to excrete the complex in their urine.18,30,31

Severe iron poisoning can be treated with exchange transfusion in addition to deferoxamine therapy.32

DISPOSITION AND FOLLOW-UP

Patients who have not ingested a potentially toxic amount of iron, who remain asymptomatic (other than vomitingonce or twice from the gastric irritant e�ects of iron), and who have normal findings on physical examination for aperiod of 6 hours can be safely discharged or transferred for appropriate mental health evaluation. Patients whoreceive deferoxamine therapy should be admitted to the intensive care unit. The regional poison control center shouldbe contacted for both data collection purposes and assistance with management.

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