2. Physical Appearance:
Metallic iron is silvery white in colour
In fact it is an essential element and
deficiency results in anaemia.
Even if there is more than the required
intake daily, the excess is excreted.
3. Iron poisoning is related in most
instances to overdose of salts.
One of the commonest is ferrous
sulfate which occurs as bluish
green crystals
4. Sources:
Dietary Sources:
The required daily amount of iron of 10–
20 mg for adults is supplied through
average diet. The required intake
increases to 25–30 mg in pregnancy.
The average daily intake for adults is
15 mg.
Environmental Sources:
Iron is found in 5.1% of the earth’s crust. It
is the second most abundant metal, and
the fourth most abundant element. It is
believed that the earth’s core consists
7. Commonly used iron salts in therapeutics
along with respective iron content are
mentioned in Table 9.8. in Ref.
The amount of iron in a particular iron salt
(e.g. sulfate, gluconate, fumarate, etc.)
is not the same.
8. The usual fatal dose corresponds to
about 200 to 250 mg of elemental iron
per kg of body weight.
This can be calculated from the
percentage of elemental iron in a
particular preparation, e.g. a single 150
mg tablet of anhydrous ferrous sulfate
which contains 37% of elemental iron
will contain a total of 55 mg of elemental
iron.
9. In practice, this can be as low as 60
mg of elemental iron/kg. Hence just a
handful of these tablets (15 to 20 in
number), can be lethal
10. Toxicokinetics:
Iron poisoning occurs when serum
iron level exceeds the total iron-
binding capacity (TIBC), resulting in
free circulating iron in the bloodstream
12. Free iron causes:
Increased capillary permeability
resulting in decreased plasma volume.
Oxidation of ferrous to ferric iron
releasing hydrogen ions. Subsequent
hydration of ferric iron results in
metabolic acidosis.
13. A. Inhibits mitochondrial function
leading to hepatic damage,
hypoglycaemia, and
hypoprothrombinaemia.
B. Inhibits thrombin-induced
conversion of fibrinogen into
fibrin.
C. Has a direct corrosive action on the
GI mucosa.
14.
15. Stages of iron poisoning:
• Gastrointestinal 30m to 6
hrsStage I
• Latent phase 2 to 4 hrsStage II
• Shock / multiorgan failure
/ acidosis 2 to 24 hrs
Stage
III
16. • Hepatotoxicity
12 to 24 hrs
Stage
IV
• Gastrointestinal
obstruction 1 to
7 wks
Stage
V
17. 1ST Stage:
Develops within the first few hours after
the ingestion.
The direct irritative effects of iron on the
gastrointestinal (GI) tract produce
abdominal pain, vomiting,diarrhea. And
hematemesis is not unusual.
Severe gastrointestinal haemorrhagic
necrosis with large losses of fluid and
blood contribute to shock
18. Vomiting is the clinical sign most
consistently associated with acute iron
toxicity.
The absence of these symptoms
within 6 hours of ingestion essentially
excludes a diagnosis of significant iron
toxicity.
19. 2nd Stage (Latent Stage)
which may continue for up to 24 hours
after ingestion.
the patient’s GI symptoms may
resolve, thereby producing a false
sense of security despite toxic
amounts of iron being absorbed into
the body.
20. Watch Out Latent Phase !!!
A period where there is a deceptive
apparent improvement in the patient’s
gastrointestinal condition. It is often
tempting to discharge such patients.
However, in the seriously poisoned, a
metabolic acidosis is evolving. This
may be compounded by a lack of
adequate fluid resuscitation
21. 3rd Stage
may appear early or develop hours after
the second stage.
Loss of adequate tissue perfusion and
multi-organ failure:
Shock occurs secondary to
gastrointestinal haemorrhage, vomiting,
vasodilatation, and reduced cardiac
output (due to myocardial toxicity).
– most deaths occur during this
stage.
22. Multi-organ failure related to
inadequate perfusion and direct
toxicity ensues and results in:
– Altered mental status / coma
– Seizure
– Acute renal failure
– Metabolic Acidosis
– Pulmonary oedema
23. 4th Stage
develops 2 to 5 days after ingestion. It
manifests as elevation of
aminotransferase and may progress to
hepatic failure.
Patients may suffer from:
– Hypoglycaemia
– Coagulopathy and haemorrhage
– Jaundice
– Hepatic encephalopathy / coma
24. 5th Stage:
which occurs 4 to 6 weeks after
Ingestion, involves gastric outlet
obstruction secondary to the corrosive
effects of iron on the pyloric mucosa.
However Actual obstruction is,, rare.
26. Take history of ingestion and
decide:
– Ingestions of 40 to 60 mg/kg should
be medically assessed, those above
60 mg/kg should be decontaminated.
Investigation
– Abdominal x-ray
– Serum iron concentration at 2 to 4
hours post-ingestion
27. Investigations
Laboratory work should be sent for
– Serum electrolytes, blood urea
nitrogen
– Serum glucose, coagulation studies
– Complete blood count
– Hepatic enzymes & serum iron level.
It is crucial to note that the
determination of a single serum iron
level does not reflect.
28. Remember !
A single low serum level does not
exclude the diagnosis of iron toxicity
because
There are variable times to peak level
after ingestion of different iron
preparations.
Serum iron levels have limited use in
directing management because
excess iron is toxic intracellularly
and not in the blood.
29.
30. 1.Stomach wash with normal saline
performed gently may be of benefit in
massive ingestions. Desferrioxamine
must not be used for lavage.
2. Activated charcoal is ineffective.
3. Magnesium hydroxide solution
(1%) administered orally may help
reduce absorption of iron by
precipitating the formation of ferrous
hydroxide
31. Magnesium hydroxide and calcium
carbonate containing antacids may
safely be used in therapeutic doses to
help reduce iron absorption.
4. Correction of hypovolaemia, and
metabolic acidosis.
32. 6. Chelation therapy:
a. This is indicated in any of the following
situations:
More than one episode of vomiting or
diarrhoea.
Significant abdominal pain, hypovolaemia, or
acidosis.
Multiple radiopacities on abdominal radiograph.
Serum iron level greater than 350 mcg/100 ml.
33. b. Chelation can be done either with
desferrioxamine (parenteral) or
deferiprone (oral).
– Dose (desferrioxamine):
Liver transplantation is the only
therapeutic avenue open in the
presence of fulminant hepatic failure.
34. Adverse Effects:
Sepsis: The use of desferrioxamine
in iron-overdosed children has been
associated with Yersinia enterocolitica
septicaemia and mucormycosis.
In such circumstances desferrioxamine
may have provided the iron
siderophore complex growth factor
needed by the bacteria to induce
overgrowth.
35. Visual Toxicity: Continuous intravenous
administration of desferrioxamine, often
in the presence of low iron stores, has
produced visual toxicity (decreased
visual acuity, night blindness, colour
blindness, retinal pigmentary
abnormalities).
Visual toxicity has also been associated
in patients with rheumatoid arthritis and
chronic renal failure. The mechanism
remains unclear.
36. Ototoxicity: In one study, some patients
receiving desferrioxamine had
abnormal audiograms, with a few
requiring hearing aids.
Risk factors include desferrioxamine
dose, duration of therapy and the
presence of a low serum ferritin.
37. Pulmonary Toxicity: A “pulmonary
syndrome” has been associated with
high dose IV (10 to 25 mg/kg/hr)
desferrioxamine therapy for several
days for acute and chronic iron
overload patients.
Features include severe tachypnoea,
hypoxaemia, fever, eosinophilia,
preceding urticaria, and pulmonary
infiltrates
