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Ferrous sulfate toxicity: a review of autopsy findings
J P Pestaner1, K G Ishak, F G Mullick
1Office of the Chief Medical Examiner, State of Maryland, Baltimore, USA.
Insights
Ferrous sulfate poisoning in children causes significant tissue damage, including gastric and intestinal necrosis and vascular iron deposition. Autopsy findings correlate with rapid clinical progression and elevated tissue iron levels.
Area of Science:
- Pediatric Toxicology
- Gastroenterology Pathology
Background:
- Ferrous sulfate is a leading cause of accidental pediatric poisoning.
- Despite child-resistant packaging, poisoning incidence is increasing.
- Pathologic findings in human tissue are not well-correlated with clinical data.
Purpose of the Study:
- To evaluate morphologic changes and iron levels in children who died from ferrous sulfate toxicity.
- To correlate autopsy findings with clinical data and determine the pathogenesis of poisoning.
Main Methods:
- Review of autopsies from 11 children with ferrous sulfate toxicity.
- Evaluation of clinical data, morphologic changes, and tissue iron levels.
- Analytical atomic absorption spectrophotometry for iron quantification.
Main Results:
- Ages of children ranged from 11 to 36 months.
- Prominent iron deposition in gastric and intestinal mucosa with associated necrosis.
- Vascular iron deposition observed in some cases, correlating with rapid clinical progression (Stage I to III).
- Increased tissue iron levels confirmed by spectrophotometry.
Conclusions:
- Morphologic and chemical data provide insight into ferrous sulfate poisoning pathogenesis.
- Vascular iron deposition may contribute to hemorrhage.
- Periportal hepatic necrosis is likely a direct effect of high iron levels in portal blood.
Abstract:
Ferrous sulfate is the leading cause of accidental pediatric poisonings. Despite the requirement for child-resistant packaging for any oral iron product with 250 mg or more per container, the incidence has continued to increase. Although the clinical presentation of iron toxicity has been well described, pathologic findings in human tissue and correlation with clinical data are scant. We reviewed autopsies from the Armed Forces Institute of Pathology of 11 children who died from ferrous sulfate toxicity. Clinical data, morphologic changes, and iron levels in tissue were evaluated. The children's ages ranged from 11 to 36 mo. Prominent iron deposition in gastric and small intestinal mucosa was associated with necrosis, with some cases demonstrating prominent vascular iron deposition. The clinical courses were rapid and progressed from Stage I to Stage III. These observations were correlated with increased levels of iron in various tissues, as determined by analytical atomic absorption spectrophotometry. The morphologic and chemical analysis data provide information on the pathogenesis of ferrous sulfate poisoning; the vascular iron deposition may be related to subsequent hemorrhage. In the liver the periportal necrosis is probably a direct cytopathic effect of the highest levels of iron carried to these cells by the portal blood flow.
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