Detail about Iron poisoning

1. POISONING
IR N
POKHARA UNIVERSITY
SCHOOL OF HEALTH AND ALLIED SCIENCE
Presented by:
Shristi Ojha
Shyam Shrestha
Suchita Subedi
Sujita subedi
• Roll no: 33-36
Presented to:
Nim Bahadur Dangi
POKHARA-30,KASKI

2. • Iron (Fe) forms ferrous (2+) and ferric (3+)
compounds.
• Ferrous compounds are easily oxidized to
ferric compounds.
• Ferrous sulfate, the most important of the
ferrous compounds, usually occurs as pale-
green crystals.
• The ferrous and ferric ions combine with
cyanides to form complex cyanide
compounds
INTRODUCTION

3. • Iron is an essential metal for almost all living systems, due to its involvement
in a number of Fe-containing enzymes and proteins.
• It is estimated that one third of the world's population suffers from anemia
due to iron deficiency.
• It is an important component of hemoglobin, myoglobin, and cytochrome
enzymes.
• The average adult human stores about 3.9 to 4.5 g of Fen
Cont…

4. Mechanism of Toxicity
•Generation of reactive oxygen species oxidize
membrane-bound lipids and result in the loss of
cellular integrity with subsequent tissue injury.
•Oxidative damage to the GI epithelium enhances iron
entry into the systemic circulation. Afterward, Fe
overloads have been observed to target systems with
very active mitochondria.
•In addition, Fe accumulation within the cellular
lysosomal compartment sensitizes lysosomes to
damage and rupture,
Release of lysosomal enzymes into the cytoplasm of
the cell induces autophagocytosis, apoptosis or
necrosis.

5. Clinical Features
Stage I (0.5 to 2 hours)
Includes vomiting, haematemesis, abdominal
pain, diarrhoea, haematochezia, lethargy,
shock, acidosis, and coagulopathy, Severe
gastrointestinal haemorrhagic necrosis with
large losses of fluid and blood contribute to
shock.
Stage II (after Stage I)
Includes apparent recovery and may
contribute to a false sense of security.
Observe closely.
Acute Fe poisoning has been well documented and is divided into 5clinical stages:

6. Stage III (2 to 12 hours after Stage I)
Includes profound shock, severe acidosis, cyanosis and
fever. Increased total peripheral resistance, decreased
plasma volume, haemoconcentration, decrease in total
blood volume, hypotension, CNS depression, and
metabolic acidosis have been reported.
Stage IV (2 to 4 days)
Includes possible hepatotoxicity, convulsions, and coma.
Thought to be a direct action of iron on mitochondria.
Stage V (days to weeks)
Includes GI scarring and strictures, GI obstruction
secondary to gastric or pyloric scarring may occur due to
corrosive effects of iron. Evaluate with barium contrast
studies, Sustained release preparations have resulted in
small intestinal necrosis with resultant scaring and
obstruction.

7. Management
• Stomach wash with normal saline performed gently
may be of benefit in massive ingestions.
Desferrioxamine must not be used for lavage.
• Activated charcoal is ineffective.
• Magnesium hydroxide solution (1%) administered
orally may help reduce absorption of iron by
precipitating the formation of ferrous hydroxide.
• Obtain serum iron levels, creatinine, electrolytes,
blood haemoglobin concentration, blood prothrombin
time, baseline liver function tests, and arterial blood
gases in seriously poisoned patients.
• Correction of hypovolemia, and metabolic acidosis,
• Chelation therapy: it can be done either with
desferrioxamine (parenteral) or deferiprone (oral).

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