Physical Address
304 North Cardinal St.
Dorchester Center, MA 02124
Essentials
- 1
Acute iron poisoning is a potentially life-threatening condition.
- 2
The risk of severe toxicity is determined by the dose of elemental iron ingested, not the weight of the iron salt.
- 3
Iron poisoning has both local (gastrointestinal) and systemic effects.
- 4
Early effective gastrointestinal decontamination with whole-bowel irrigation is important in the management of high-risk cases.
- 5
Chelation therapy with intravenous desferrioxamine is the definitive treatment for severe poisoning and should not be withheld awaiting an iron concentration in an unwell patient.
- 6
Generally, most patients recover, although presence of shock or coma indicates a poor prognosis.
- 7
Long-term sequelae are gastrointestinal scarring and obstruction but this is uncommon.
- 8
The approach to the pregnant patient with iron poisoning is identical.
Introduction
The majority of exposures to iron occur in preschool children, but significant iron ingestions also occur in adults as a result of deliberate self-poisoning. It is also one of the most commonly ingested agents in self-poisoning during pregnancy as a result of its ready availability to obstetric patients. Iron supplements are often considered by patients and parents to be innocuous dietary supplements, leading to careless storage and handling and delays in seeking medical care following ingestions.
Due to education, different packaging, smaller dosages and toxicovigilance by poisons centres, iron toxicity has declined in the past decade, but significant poisonings still occur.
Pathophysiology
Iron is an essential element in red blood cell production, haemoglobin and myoglobin oxygenation and cytochrome function. It must come from exogenous sources and as the body cannot directly excrete iron; body stores are finely regulated by the gastrointestinal (GI) tract. After absorption across the GI mucosa iron is reversibly bound and stored as ferritin, or transported across the cell membrane into the blood, where it binds to transferrin. Iron is extracted from transferrin in the bone marrow and used for haemoglobin synthesis. It is also removed from transferrin by the reticuloendothelial system and hepatocytes and stored as haemosiderin and ferritin. Total iron-binding capacity (TIBC) is a measurement of the total amount of iron that transferrin can bind and normally exceeds serum iron by two- to threefold.
When an iron deficit exists, iron is transported from ferritin and the GI tract. If the body’s iron requirements have been met, iron remains stored in the intestinal cell rather than bound to transferrin. Eventually, the intestinal cell dies and sloughs off into the lumen for elimination. This is the main mechanism limiting excessive iron absorption and the mechanism by which the body regulates iron balance.
Iron rarely exists as an unbound or ‘free’ element, and it is the free iron that is toxic to cellular processes.
Local effects
Iron preparations, like other metal salts, have a direct corrosive effect on the GI mucosa. In overdose, this can lead to irritation, ulceration, bleeding, ischaemia, infarction and perforation. Associated profound fluid losses can result in hypotension, shock and lactate formation leading to metabolic acidosis. The long-term sequelae of this corrosive action include GI scarring and obstruction from stricture formation. As the mucosal surface is disrupted, iron is absorbed passively and more readily down concentration gradients.
Systemic effects
When the absorbed iron exceeds the protein-binding capacity, the free iron causes cellular dysfunction and death. Free iron is an intracellular toxin localizing to the mitochondria, forming free radicals and disrupting oxidative phosphorylation. The resultant mitochondrial dysfunction and destruction lead to cell death. As a result, systemic findings of iron poisoning include cardiovascular collapse, anion-gap metabolic acidosis, coagulopathy and encephalopathy. Metabolic acidosis persisting after correction of hypovolaemia and hypoperfusion is probably a result of mitochondrial toxicity. Coagulopathy developing early in iron poisoning results from inhibition of thrombin formation and other clotting factors while, in the later stages, it is due to hepatic dysfunction.
Toxic dose
In general, the risk of developing iron toxicity can be predicted from the dose of elemental iron ingested per kilogram body weight ( Table 25.11.1 ). It is essential to calculate the dose of elemental iron rather than dose of iron salt. If the formulation of the iron salt is not known, then assume a worst-case scenario and calculate 105 mg of elemental iron per tablet.
Table 25.11.1
Risk assessment based on dose of elemental iron ingested
| Risk assessment | Dose ingested (mg/kg) |
|---|---|
| Asymptomatic | <20 |
| Local (GI) symptoms only | 20–60 |
| Risk of systemic toxicity | 60–120 |
| Potentially lethal | >120 |
GI , Gastrointestinal.
Prevention
Iron poisoning is a major cause of unintentional poisoning death in young children, making up almost one-third of all toxicological deaths in that age group in the 1980s to 1990s. However, there has been a decrease in the incidence of nonintentional ingestion by young children and decreased mortality following the introduction of unit-dose packaging. This, together with education, may further decrease the incidence of toxicity and late presentations.
Clinical features
The clinical course of iron poisoning is traditionally described as comprising five stages. These stages are used as a guide to conceptualize the clinical course but not all patients will experience all stages; they can die at any stage, can present at any stage and the time frames for each stage are imprecise and may overlap.
A more practical approach is to consider iron poisoning as comprising two clinical stages with a pathophysiological basis: GI toxicity and systemic toxicity.
You're Reading a Preview
Become a Clinical Tree membership for Full access and enjoy Unlimited articles
If you are a member. Log in here