iron-toxicity Prepublication-and-ExpertPeerReviewAtomic number 26 toxicity is determined by the amount of elemental iron (Fe) ingested. Examples of Fe formulations and the corporeality of elemental Iron independent in each conception are listed in the tabular array below (adapted from 1 ).

Contents Elemental Iron (%)
Ferrous chloride 28
Ferrous fumarate 33
Ferrous gluconate 12
Ferrous lactate 19
Ferrous sulfate twenty

Computing amount of elemental Fe ingested

Multiply the full Atomic number 26 content in each tablet by the per centum of elemental Atomic number 26 for the product conception. For example, the elemental iron equivalent calculation for 80 tablets of Ferrous Sulfate is: 325 mg Atomic number 26/tablet ten 20% elemental Iron/tablet = 65 mg elemental Fe/tablet. The total elemental Iron ingested is: (65 mg/tab ten 80 tablets) /50 kg = 104 mg/kg. Notable levels for elemental Iron include:

  • >20 mg/kg Gastrointestinal symptoms start
  • ≥40 mg/kg Current level recommended for ED referral afterwards ingestion ii

Pharmacology and Toxicology

Humans do not synthesize or secrete Fe. Total trunk Fe is regulated via assimilation from the gastrointestinal tract. Absorption occurs in the duodenum, where Iron is stored equally ferritin in the intestinal cells. It is then tending of via epithelial jail cell shedding or, depending on the body's need, can be released to transferrin, a serum Atomic number 26-binding poly peptide. In Fe overdoses, the corrosive effects of Atomic number 26 on the GI tract mucosa permit passive assimilation of Iron. Once transferrin is saturated, "gratis" Fe is available to cause toxicity. Iron causes toxicity thru several mechanisms, including three :

  • Engages in redox reactions with the formation of free radicals and oxidative damage
  • Alters cellular energy and metabolism
  • Uncouples oxidative phosphorylation
  • Ultimately results in cellular death

Iron Toxicity: Presentation

Classically, 5 stages of atomic number 26 toxicity are described (adjusted from four ):

Stage Timing post-ingestion Symptoms of Iron Toxicity
1 0.5-6 hours Local toxicity: Nausea, vomiting, diarrhea; intestinal pain, gastrointestinal bleeding
2 6-24 hours Latent toxicity: Resolution of local toxicity with ongoing cellular toxicity, hypovolemia, poor tissue perfusion (metabolic acidosis, ↑ lactate levels)
3 12-24 hours Shock, acidosis, coagulopathy, blackout, multisystem organ failure
iv 2-3 days Hepatic failure (periportal)
five 3-6 weeks Sequelae: Gastric outlet obstacle, pocket-sized bowel obstacle

The lack of airsickness early on later an ingestion (during phase I) has important clinical significance. If no vomiting has occurred within vi hours after ingestion, then the patient probable did not ingest a toxic dose. This patient can be medically cleared. ii

Laboratory Testing

For most preparations,a peak Fe level occurs two–6 hours mail service-ingestion. The peak level predicts severity of atomic number 26 toxicity and guides management decisions (meet tabular array below). Subsequently 6 hours, Fe distributes out of the intravascular compartment, and levels are less useful for predicting toxicity. 1 Boosted lab tests to consider obtaining include:

  • Basic metabolic panel
  • Lactate
  • Complete blood count (CBC)
  • Coagulation tests (PT/INR/PTT)
  • Liver part tests (LFT)

Total iron binding capacity (TIBC), glucose, and WBC counts are unreliable in predicting iron toxicity. 4  The radiopacity of Fe varies with the grooming, time since ingestion, and amount of ingestion. If pill fragments are visualized on the KUB, and then administration of whole bowel irrigation (WBI) may limit farther absorption of Fe. However, a normal KUB does not exclude ingestion.

Serum Iron Level (mcg/dL) Clinical Symptoms of Iron Toxicity
<300 Lacks pregnant clinical effect
300-499 Mild – moderate: nausea, vomiting, diarrhea; mild systemic symptoms; serious toxicity unlikely
500-yard Moderate – Severe systemic toxicity
>1000 Significant morbidity and mortality

Initial Treatment

The handling of Iron overdose starts with attending to supportive intendance and acceptable fluid resuscitation.

  1. Isotonic fluids: Numerous reasons account for hypovolemia and poor perfusion. Starting time fluid resuscitation with isotonic fluid boluses to restore hypovolemia.
  2. Activated charcoal (or other oral complexing agents): This is INEFFECTIVE at binding Atomic number 26 to limit absorption. 2,5
  3. Whole bowel irrigation: This may be considered when Fe tablets are visualized on the KUB motion picture. However, no controlled studies support the efficacy of WBI and and then individual risks and benefits should be considered. WBI is achieved by assistants of polyethylene glycol (PEG) solution via NG tube at recommended rates of 500 mL/hour in children and i.5 – ii 50/hr in adolescents and adults. half dozen
  4. Gastric lavage: Generally Not recommended 7

Antidote: Deferoxamine (DFO)

DFO is a chelator with high analogousness and specificity for Fe. Subsequently chelation with Iron, it forms a stable chemical compound ferrioxamine that is excreted in the urine. Indications for employ in acute Atomic number 26 toxicity are non well defined, or based on controlled studies, and are expert consensus derived. General indications for intravenous DFO administration includeANY of the following:

  • Atomic number 26 level > 500 mcg/dl
  • Presence of metabolic acidosis
  • Languor/coma
  • Shock
  • Toxic appearance

Unfortunately, no study has determined the optimal dosing regimen, maximum dose, or length of administration. As such, consultation with a toxicologist for dosing assistants and duration is recommended. Side effects from DFO:

  • Acute, rate related side effects of DFO includeurticaria and hypotension. Thus adequate fluid resuscitation prior to initiation of DFO is of import.
  • A late side effect is Yersiniasepsis. DFO is a siderophore that fosters the growth ofYersinia, accounting for sepsis.
  • ARDS has been noted with prolonged DFO infusions > 24 hours.

Outdated Practice Regarding Deferoxamine

Ferrioxamine is a brick-orange color (AKAvin rose). 2 antiquated recommendations guiding the administration of DFO relate to visualizingvin rose in the urine. The first is to administer a DFO challenge (IM shot); ifvin roseis present in urine, so continue with farther DFO treatment. The second is to continue DFO untilvin rose in the urine clears. Both practices have been abandoned secondary to lack of reliability. 1,4

Madiwale T, Liebelt Eastward. Iron: not a benign therapeutic drug. Curr Opin Pediatr. 2006;eighteen(2):174-179. [PubMed]
Manoguerra A, Erdman A, Booze L, et al. Atomic number 26 ingestion: an show-based consensus guideline for out-of-hospital management. Clin Toxicol (Phila). 2005;43(6):553-570. [PubMed]
Mills K, Curry S. Acute iron poisoning. Emerg Med Clin Northward Am. 1994;12(2):397-413. [PubMed]
Chang T, Rangan C. Fe poisoning: a literature-based review of epidemiology, diagnosis, and management. Pediatr Emerg Care. 2011;27(10):978-985. [PubMed]
Matteucci K, Habibe K, Robson K, Baldassano A, Riffenburgh R, Tanen D. Effect of oral calcium disodium EDTA on iron assimilation in a human model of iron overdose. Clin Toxicol (Phila). 2006;44(1):39-43. [PubMed]
Position newspaper: whole bowel irrigation. J Toxicol Clin Toxicol. 2004;42(half-dozen):843-854. [PubMed]
Benson B, Hoppu K, Troutman W, et al. Position paper update: gastric lavage for gastrointestinal decontamination. Clin Toxicol (Phila). 2013;51(three):140-146. [PubMed]
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