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IRON TOXICITY
By
M.S.Jyothirmayee,
IVth.Pharm.D,
Svcop.
OBJECTIVES:
*Introduction.
*Definition.
*Sources of iron toxicty.
*Uses.
*Toxicokinetcs.
*Clinical features.
*Mechanism of iron toxicty.
*Diagnosis.
*Treatment.
*Postmortem appearances.
*Forensic importance.
INTRODUCTION:
Iron is a chemical element with symbol Fe and atomic
number 26. It is a metal that belongs to the first transition
series and group 8 of the periodic table.
It is, by mass, the most common element on Earth, right
in front of oxygen, forming much of Earth's outer and
inner core.
PHYSICAL APPEARANCE:
DEFINITION:
*Iron toxicity is classified as corrosive or cellular.Ingested iron can cause
direct caustic injury to the gastrointestinal mucosa, resulting in nausea,
vomiting, abdominal pain, and diarrhea. Significant fluid and blood loss can
lead to hypovolemia.
SOURCES OF IRON TOXICITY:
•White flour products.
•Some in supplements, containing iron alone as the ingredients.
•Red meat, especially beef
•Pollution-Iron contamination of the air, water and social is quite
common, especially in iron-producing an.
•Occupational exposure Walders, Electrical workers who use solder,
iron and pipe worker.
•Congenital intoxicity. Most children today une bom same excess irun.
•They may still be anemic because their iron is not all bouvailable.
USES:
•Medicinal
Treatment of iron deficiency anaemia
•Industry
Tunning, tokis dyes pigment
•General
Photography
TOXICOKINETCS:
ABSORPTION:▸ Iron is absorbed in intestine.Ferrous (Fe+2) form is more
readily absorbed than ferric (Fe+3) iron.Iron is absorbed in ferrous form and
is oxidized to ferric form within cells.
DISTRIBUTION:
▸ It is transported in blood bound to a protein called transferrin.
▸ The iron binding capacity (transferrin level) is usually 300-500 ug/dl
(TIBC) & normal serum iron level is 50-150 ug/dl. So, there is usually no free
iron circulating in blood.
> Citrate & ascorbate (in citrus fruits) can form complexes with iron that ↑
absorption, while tannates in tea can ↓ absorption.
CLINICAL FEATURES:
Most cases occur in children's..there are FOUR main
stages.,
Stage-1.
Stage-2.
Stage-3.
Stage-4.
STAGE-1
30 min to 6 hr post-ingestion: Vomit ing, diarrhoea, abdominal pain,
hypotension, leth argy, anion gap metabolic acidosis, leucocytosis,
and hypoglycaemia.
STAGE-2
(6 to 24 hr): The child may appear to be feeling better, which is actually
treacherous since the III stage begins and unfolds in the form of a
relentless Greek tragedy.
STAGE-3
(24 to 48 hr): There is multiple organ failure involving the gastrointestinal,
hepatorenal, central nervous, and cardiovascular systems, with metabolic
coagulopathies, hypoglycaemia, convulsions, disorientation, coma, and
death (usu ally from hepatic failure).
STAGE-4
(After 4 weeks): Recovery is often as- tly sociated with late complications
such as gastric Ma scarring and pyloric obstruction resulting from
corrosion of GI mucosa.
MECHANISM OF ACTION:
*Iron poisoning occurs when serum iron level ex ceeds the total iron-
binding capacity (TIBC), re sulting in free circulating iron in the
bloodstream.
• Free iron causes
-Massive postarteriolar dilatation which results in venous pooling.
-Increased capillary permeability resulting indecreased plasma volume.
- Oxidation of ferrous to ferric iron releasing hydrogen ions. Subsequent
hydration of ferric iron results in metabolic acidosis.
DIAGNOSIS:
•X-ray:Like all other heavy metals, iron and its compounds are radiopaque.
However, chewable iron tablets and liquid iron formulations are usu ally
not visualised on X-ray.
•Serum iron level: Poisoning is indicated if this exceeds 150 mcg/100 mL,
and serious toxicity is usually associated with levels beyond 500 to 600
mcg/100 mL.
•Chellating challenge test:Desferrioxamine in a dose of 25 mg/kg
(maximum 1 g) is given IM. If the serum iron has exceeded iron-binding
capacity, the excess iron is chelated to desferrioxamine and the complex is
excreted as a pinkish (vin rose')* colour in the urine.But a negative result
does not rule out iron poisoning.
TREATMENT:
1. Gastric decontamination:
• Forced emesis
• Gastric lavage with 5% NaHCO3
• No activated charcoal
2. Secure good IV
3. Get initial the 4hrs levels and TBC
4. Chelate with Deferoxamine if levels> 300mg/dL
POSTMORTEM APPEARANCES:
*Hepatic and elecenis, metimes with hund tinge in vous alphate
*Hamonhuic nosis of gastric macos in fir sulphate poing, gastric tons may ap
pear thaish green is cure poisoning
FORENSIC IMPORTANCE:
*Acute iron Poisoning has assumed grave significane is recent years and
case's of accident pooning are being reported with alarming frequency in
young childres.Since most preputaties (syrups and tables) are brigh and and
pleasantly, they constitute at irresistible,fatal attractice the these innocent
victims.
*Introduction of childrat containers would he very effective in mising
inadvertim ingestion by children as demonstrated by Western experience.
REFERENCE:
https://www.slideshare.net/drasimrana/iron-
toxicity
https://www.slideshare.net/Haris_Gujjar/iron-
poisoning
https://www.slideshare.net/MohammedALZahra
ni29/iron-toxicity-61259331
VV.PILLAY TextBook of forensic medicine &
Toxicology (18th.Edition).
Iron Toxicity. fe.pptx

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Iron Toxicity. fe.pptx

  • 2. OBJECTIVES: *Introduction. *Definition. *Sources of iron toxicty. *Uses. *Toxicokinetcs. *Clinical features. *Mechanism of iron toxicty. *Diagnosis. *Treatment. *Postmortem appearances. *Forensic importance.
  • 3. INTRODUCTION: Iron is a chemical element with symbol Fe and atomic number 26. It is a metal that belongs to the first transition series and group 8 of the periodic table. It is, by mass, the most common element on Earth, right in front of oxygen, forming much of Earth's outer and inner core.
  • 5. DEFINITION: *Iron toxicity is classified as corrosive or cellular.Ingested iron can cause direct caustic injury to the gastrointestinal mucosa, resulting in nausea, vomiting, abdominal pain, and diarrhea. Significant fluid and blood loss can lead to hypovolemia.
  • 6.
  • 7. SOURCES OF IRON TOXICITY: •White flour products. •Some in supplements, containing iron alone as the ingredients. •Red meat, especially beef •Pollution-Iron contamination of the air, water and social is quite common, especially in iron-producing an. •Occupational exposure Walders, Electrical workers who use solder, iron and pipe worker. •Congenital intoxicity. Most children today une bom same excess irun. •They may still be anemic because their iron is not all bouvailable.
  • 8. USES: •Medicinal Treatment of iron deficiency anaemia •Industry Tunning, tokis dyes pigment •General Photography
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  • 10. TOXICOKINETCS: ABSORPTION:▸ Iron is absorbed in intestine.Ferrous (Fe+2) form is more readily absorbed than ferric (Fe+3) iron.Iron is absorbed in ferrous form and is oxidized to ferric form within cells. DISTRIBUTION: ▸ It is transported in blood bound to a protein called transferrin. ▸ The iron binding capacity (transferrin level) is usually 300-500 ug/dl (TIBC) & normal serum iron level is 50-150 ug/dl. So, there is usually no free iron circulating in blood. > Citrate & ascorbate (in citrus fruits) can form complexes with iron that ↑ absorption, while tannates in tea can ↓ absorption.
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  • 12. CLINICAL FEATURES: Most cases occur in children's..there are FOUR main stages., Stage-1. Stage-2. Stage-3. Stage-4.
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  • 14. STAGE-1 30 min to 6 hr post-ingestion: Vomit ing, diarrhoea, abdominal pain, hypotension, leth argy, anion gap metabolic acidosis, leucocytosis, and hypoglycaemia.
  • 15. STAGE-2 (6 to 24 hr): The child may appear to be feeling better, which is actually treacherous since the III stage begins and unfolds in the form of a relentless Greek tragedy.
  • 16. STAGE-3 (24 to 48 hr): There is multiple organ failure involving the gastrointestinal, hepatorenal, central nervous, and cardiovascular systems, with metabolic coagulopathies, hypoglycaemia, convulsions, disorientation, coma, and death (usu ally from hepatic failure).
  • 17. STAGE-4 (After 4 weeks): Recovery is often as- tly sociated with late complications such as gastric Ma scarring and pyloric obstruction resulting from corrosion of GI mucosa.
  • 18. MECHANISM OF ACTION: *Iron poisoning occurs when serum iron level ex ceeds the total iron- binding capacity (TIBC), re sulting in free circulating iron in the bloodstream. • Free iron causes -Massive postarteriolar dilatation which results in venous pooling. -Increased capillary permeability resulting indecreased plasma volume. - Oxidation of ferrous to ferric iron releasing hydrogen ions. Subsequent hydration of ferric iron results in metabolic acidosis.
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  • 20. DIAGNOSIS: •X-ray:Like all other heavy metals, iron and its compounds are radiopaque. However, chewable iron tablets and liquid iron formulations are usu ally not visualised on X-ray. •Serum iron level: Poisoning is indicated if this exceeds 150 mcg/100 mL, and serious toxicity is usually associated with levels beyond 500 to 600 mcg/100 mL. •Chellating challenge test:Desferrioxamine in a dose of 25 mg/kg (maximum 1 g) is given IM. If the serum iron has exceeded iron-binding capacity, the excess iron is chelated to desferrioxamine and the complex is excreted as a pinkish (vin rose')* colour in the urine.But a negative result does not rule out iron poisoning.
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  • 22. TREATMENT: 1. Gastric decontamination: • Forced emesis • Gastric lavage with 5% NaHCO3 • No activated charcoal 2. Secure good IV 3. Get initial the 4hrs levels and TBC 4. Chelate with Deferoxamine if levels> 300mg/dL
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  • 27. POSTMORTEM APPEARANCES: *Hepatic and elecenis, metimes with hund tinge in vous alphate *Hamonhuic nosis of gastric macos in fir sulphate poing, gastric tons may ap pear thaish green is cure poisoning
  • 28. FORENSIC IMPORTANCE: *Acute iron Poisoning has assumed grave significane is recent years and case's of accident pooning are being reported with alarming frequency in young childres.Since most preputaties (syrups and tables) are brigh and and pleasantly, they constitute at irresistible,fatal attractice the these innocent victims. *Introduction of childrat containers would he very effective in mising inadvertim ingestion by children as demonstrated by Western experience.
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