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THALLIUM
DR RONI DUDHWALA (M.D. HOMOEOPATH)
ASSISTANT PROFESSOR, FORENSIC MEDICINE & TOXICOLOGY
S. S. AGRAWAL HOMOEOPATHIC MEDICAL COLLEGE, NAVSARI
THALLIUM
I N T R O D U C T I O N
U S E S
A C T I O N
A B S O R P T I O N A N D E X C R E T I O N
A C U T E P O I S O N I N G
 S I G N A N D S Y M P T O M S
 T R A T M E N T
 P O S T M O R T E M F I N D I N G S
THALLIUM
PHYSICAL PROPERTIES:
Thallium : soft, heavy metal
a tin-white lustrous color which tarnishes:
on exposure to air due to formation of
thallous oxide.
Currently, the toxicity is through occupational
exposure, environmental contamination
and accumulation in food , mainly
vegetables grown on contaminated soil.
THALLIUM
1. Thallium acetate:
• Colorless and almost tasteless.
• Used: as a depilatory in the treatment of ringworm of
scalp, for removing the superfluous hair, as constituent of
of some proprietary depilatory creams, in fireworks and
as a rodenticide and insecticide.
2. Thallium sulfate:
• Used: for killing rats and ants
THALLIUM
Thallium and its salts are corrosive to the GIT.
 After absorption, it replaces potassium in
numerous potassium-dependent enzyme
(similar atomic radius to thallium).
In addition, thallium damages the ribosomes,
resulting in impaired protein synthesis.
This results in failure of aerobic respiration and
cellular energy production.
THALLIUM
In the PNS, thallium causes a ‘dying-back’ or
Wallerian degenerative sensory neuropathy
due to acute myelin fragmentation and axonal
degeneration.
Motor neuropathy may occur, since it impairs
depolarization of muscle fibers.
Hair loss is caused by stunted mitosis of hair
follicle epithelial cells and by destruction of
hair shaft cells.
THALLIUM
Thallium absorbed: through the skin and mucous
membrane of the GIT and respiratory tract.
It is a cumulative poison, and is deposited in the
epididymis, liver, kidneys, muscles, hairs and bones.
Excretion: through the kidneys, and it is also excreted
through the milk.
THALLIUM
In acute poisoning, signs and symptoms start between 12–
36 hours (h) to 12 days.
The effects are the most severe in the nervous system.
Unlike exposure to most metal salts, GIT symptoms are
relatively minor, and constipation is more characteristic than
diarrhea.
SIGNS AND SYMPTOMS:
THALLIUM SYSTEM SIGNS AND SYMPTOMS
GIT Irritation, metallic taste in mouth, nausea, vomiting, hematemesis,
abdominal pain, anorexia, dryness of mouth, colic, diarrhea or
constipation.
RS Distress, running nose, respiratory depression.
OCULAR Conjunctivitis, scotoma, blindness.
MS Polyneuritis, tingling and pain sensation in hands and feet (‘pins
and needles’), ‘glove-stocking’ numbness, muscular weakness with
paralysis of some muscles (peripheral neuropathy), tremors.
CNS Confusion, nystagmus, insomnia, psychosis, ataxia, organic brain
syndrome, coma. Dysfunction of cranial nerves II, III, IV and VI,
which govern oculomotor and visual function are most common.
OTHERS Loss of scalp hair, lateral eyebrows ( Medial part of eyebrow are in
a resting phase, and not affected by THALLIUM POISONING) , body
and axillary hair (10-14 days after exposure) and deafness.
THALLIUM
In mild cases, the symptoms are joint pains in the legs and
feet, loss of appetite, stomatitis, drowsiness, and
hypochlorhydria.
These generally pass off in few days.
In sub-acute cases, there is encephalopathy with white
stripes across the nails (Mees lines).
In chronic exposure, these symptoms appear in milder
forms.
 The diagnosis may be difficult because it is often unsuspected.
The cardinal features are gastroenteritis, peripheral
neuropathy and alopecia
A symmetrical mixed peripheral neuropathy is characteristic
with distal nerves more strongly affected than proximal
nerves.
 There may be extreme sensitivity of the legs, followed by
‘burning feet’ syndrome and paresthesia.
THALLIUM
BURNING FEET
SYNDROME PARESTHESIA
THALLIUM
Causes of death :
• usually are related to the CNS, cardiac and renal
system effects.
Fatal dose :
• Adults: 200 mg–1 g (> 8 mg/kg).
• Children: 8 mg/kg body wt.
Fatal period:
• Variable, usually 24–36 h.
THALLIUM
Thallium toxicity can be monitored in blood, urine
and hair.
Eosinophilia is a common phenomenon.
Thallium > 40 µg% in blood, and > 150 µg/l in
urine (levels up to 20 µg/l is considered normal) is
significant.
Hair levels < 15 ng/g are considered normal.
Urine may be: green, with proteinuria, diminished
creatinine clearance, elevated blood urea nitrogen.
THALLIUM
GIT and polyneuritic symptoms together
with the falling of hair from head,
eyebrows and axilla should lead to
of thallium poisoning.
A brownish black pigmentation close to
the hair root is characteristic of thallium
exposure and may appear as early as 3rd–4th
day.
Opacity in the liver on X-rays has been
reported.
THALLIUM
i. Patient should be kept warm.
ii. Emesis is indicated within 4–6 h of ingestion.
iii. Multiple-dose of activated charcoal may be given, followed by
saline purgative.
iv. Whole bowel irrigation with polyethylene glycol electrolyte
lavage solution may be useful.
v. Stomach wash is performed with 1% sodium or potassium
iodide solution.
• It forms insoluble iodide salts of thallium.
• Iodide also acts as a systemic antidote.
vi. Prussian blue or Berlin blue (potassium ferric
hexacyanoferrate).
• which acts : to sequester the ions in the intestine and preventing their
absorption is given in a dose of 250 mg/kg/day in 2–4 divided doses
orally.
THALLIUM
potassium ferric hexacyanoferrate:
Potassium is exchanged preferentially for thallium entering the
enterohepatic circulation.
As Prussian blue sequesters thallium, a concentration gradient
established for the continued movement of thallium into the gut.
vii. Although chelating agents including BAL and EDTA are
contraindicated in the treatment, sodium-diethyl-dithio-
carbamate 25 mg/kg body wt in 500 ml of 5% glucose iv once
daily may be given.
viii.Pilocarpine in usual doses is also a physiological antidote.
ix. Potassium chloride promotes: renal excretion of thallium.
x. Administration of sodium polystyrene sulfonate as sodium-
exchange resin may be helpful.
xi. Hemodialysis/peritoneal dialysis may be useful within 48 h of
ingestion.
THALLIUM
•There is anemia and loss of hair.
•Stomach: Mucous membrane may be
inflamed and there may be sub mucous
petechial hemorrhages.
•Spleen: Congested.
•Liver: Congested, and shows centri-lobular
necrosis and fatty degeneration.
THALLIUM
•Kidneys: Congested, glomeruli are swollen,
convoluted tubules show cloudy swelling and
necrosis of the cells.
•Trachea and bronchi: Congested.
•Lungs: Congested with sub-pleural
hemorrhages.
•Heart: Fatty degeneration.
•Brain: Meningeal vessels may be congested.
•Cells of adrenal cortex, thyroid and hair follicles
show vacuolization and degenerative changes.
THALLIUM
Poisoning by thallium is rare in contrast to
poisoning by lead or mercury, probably due
to its infrequent use.
Thallium was used as an IDEAL
HOMICIDAL POISON in some European
countries and Australia, where it was used as
rodenticide.
It is tasteless and odorless, dissolves
completely in liquid, rapidly and completely
absorbed, and they defy detection on routine
THALLIUM
Accidental intoxication may result from its
therapeutic use as a depilatory or
or from its accidental ingestion when used as
a rodenticide.
Chronic poisoning occurs from industrial
exposure.
Suicidal cases are also seen sometimes.
THALLIUM
Thallium stress test: In clinical practice, thallium
201 is used as a radioactive tracer in heart
scintigraphy to detect myocardial ischemia.
Accidental poisoning has become rare in the
domestic setting since the 1970s, when thallium-
based rodenticides were banned in many countries.
The majority of reported cases of thallium
poisoning in the last two decades have been
caused by deliberate poisoning.
THALLIUM
Thallium may be detected in the urine 1 h after ingestion
(normal level, < 0.003 µmol/l; a level of > 0.98 µmol/l is
toxic),
but most clinical laboratories may not have the facilities to
quantitatively analyze the thallium content.
A rapid quantitative urine test can be done by mixing
urine with 0.4% sodium bismuth in 20% nitric acid and 10%
sodium iodide.
A red precipitate indicates that thallium is present
THALLIUM
Microscopic examination of hair after
application of 10% sodium hydroxide may
reveal dark bands of pigmented material
characteristic of presence of thallium.
THALLIUM
RONI DUDHWALA
ronidudhwala@Hotmail.com

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Thallium- inorganic metallic poison (Forensic Toxicology)

  • 1. THALLIUM DR RONI DUDHWALA (M.D. HOMOEOPATH) ASSISTANT PROFESSOR, FORENSIC MEDICINE & TOXICOLOGY S. S. AGRAWAL HOMOEOPATHIC MEDICAL COLLEGE, NAVSARI
  • 2. THALLIUM I N T R O D U C T I O N U S E S A C T I O N A B S O R P T I O N A N D E X C R E T I O N A C U T E P O I S O N I N G  S I G N A N D S Y M P T O M S  T R A T M E N T  P O S T M O R T E M F I N D I N G S
  • 3. THALLIUM PHYSICAL PROPERTIES: Thallium : soft, heavy metal a tin-white lustrous color which tarnishes: on exposure to air due to formation of thallous oxide. Currently, the toxicity is through occupational exposure, environmental contamination and accumulation in food , mainly vegetables grown on contaminated soil.
  • 4. THALLIUM 1. Thallium acetate: • Colorless and almost tasteless. • Used: as a depilatory in the treatment of ringworm of scalp, for removing the superfluous hair, as constituent of of some proprietary depilatory creams, in fireworks and as a rodenticide and insecticide. 2. Thallium sulfate: • Used: for killing rats and ants
  • 5. THALLIUM Thallium and its salts are corrosive to the GIT.  After absorption, it replaces potassium in numerous potassium-dependent enzyme (similar atomic radius to thallium). In addition, thallium damages the ribosomes, resulting in impaired protein synthesis. This results in failure of aerobic respiration and cellular energy production.
  • 6. THALLIUM In the PNS, thallium causes a ‘dying-back’ or Wallerian degenerative sensory neuropathy due to acute myelin fragmentation and axonal degeneration. Motor neuropathy may occur, since it impairs depolarization of muscle fibers. Hair loss is caused by stunted mitosis of hair follicle epithelial cells and by destruction of hair shaft cells.
  • 7. THALLIUM Thallium absorbed: through the skin and mucous membrane of the GIT and respiratory tract. It is a cumulative poison, and is deposited in the epididymis, liver, kidneys, muscles, hairs and bones. Excretion: through the kidneys, and it is also excreted through the milk.
  • 8. THALLIUM In acute poisoning, signs and symptoms start between 12– 36 hours (h) to 12 days. The effects are the most severe in the nervous system. Unlike exposure to most metal salts, GIT symptoms are relatively minor, and constipation is more characteristic than diarrhea. SIGNS AND SYMPTOMS:
  • 9. THALLIUM SYSTEM SIGNS AND SYMPTOMS GIT Irritation, metallic taste in mouth, nausea, vomiting, hematemesis, abdominal pain, anorexia, dryness of mouth, colic, diarrhea or constipation. RS Distress, running nose, respiratory depression. OCULAR Conjunctivitis, scotoma, blindness. MS Polyneuritis, tingling and pain sensation in hands and feet (‘pins and needles’), ‘glove-stocking’ numbness, muscular weakness with paralysis of some muscles (peripheral neuropathy), tremors. CNS Confusion, nystagmus, insomnia, psychosis, ataxia, organic brain syndrome, coma. Dysfunction of cranial nerves II, III, IV and VI, which govern oculomotor and visual function are most common. OTHERS Loss of scalp hair, lateral eyebrows ( Medial part of eyebrow are in a resting phase, and not affected by THALLIUM POISONING) , body and axillary hair (10-14 days after exposure) and deafness.
  • 10. THALLIUM In mild cases, the symptoms are joint pains in the legs and feet, loss of appetite, stomatitis, drowsiness, and hypochlorhydria. These generally pass off in few days. In sub-acute cases, there is encephalopathy with white stripes across the nails (Mees lines). In chronic exposure, these symptoms appear in milder forms.  The diagnosis may be difficult because it is often unsuspected. The cardinal features are gastroenteritis, peripheral neuropathy and alopecia A symmetrical mixed peripheral neuropathy is characteristic with distal nerves more strongly affected than proximal nerves.  There may be extreme sensitivity of the legs, followed by ‘burning feet’ syndrome and paresthesia.
  • 12. THALLIUM Causes of death : • usually are related to the CNS, cardiac and renal system effects. Fatal dose : • Adults: 200 mg–1 g (> 8 mg/kg). • Children: 8 mg/kg body wt. Fatal period: • Variable, usually 24–36 h.
  • 13. THALLIUM Thallium toxicity can be monitored in blood, urine and hair. Eosinophilia is a common phenomenon. Thallium > 40 µg% in blood, and > 150 µg/l in urine (levels up to 20 µg/l is considered normal) is significant. Hair levels < 15 ng/g are considered normal. Urine may be: green, with proteinuria, diminished creatinine clearance, elevated blood urea nitrogen.
  • 14. THALLIUM GIT and polyneuritic symptoms together with the falling of hair from head, eyebrows and axilla should lead to of thallium poisoning. A brownish black pigmentation close to the hair root is characteristic of thallium exposure and may appear as early as 3rd–4th day. Opacity in the liver on X-rays has been reported.
  • 15. THALLIUM i. Patient should be kept warm. ii. Emesis is indicated within 4–6 h of ingestion. iii. Multiple-dose of activated charcoal may be given, followed by saline purgative. iv. Whole bowel irrigation with polyethylene glycol electrolyte lavage solution may be useful. v. Stomach wash is performed with 1% sodium or potassium iodide solution. • It forms insoluble iodide salts of thallium. • Iodide also acts as a systemic antidote. vi. Prussian blue or Berlin blue (potassium ferric hexacyanoferrate). • which acts : to sequester the ions in the intestine and preventing their absorption is given in a dose of 250 mg/kg/day in 2–4 divided doses orally.
  • 16. THALLIUM potassium ferric hexacyanoferrate: Potassium is exchanged preferentially for thallium entering the enterohepatic circulation. As Prussian blue sequesters thallium, a concentration gradient established for the continued movement of thallium into the gut. vii. Although chelating agents including BAL and EDTA are contraindicated in the treatment, sodium-diethyl-dithio- carbamate 25 mg/kg body wt in 500 ml of 5% glucose iv once daily may be given. viii.Pilocarpine in usual doses is also a physiological antidote. ix. Potassium chloride promotes: renal excretion of thallium. x. Administration of sodium polystyrene sulfonate as sodium- exchange resin may be helpful. xi. Hemodialysis/peritoneal dialysis may be useful within 48 h of ingestion.
  • 17. THALLIUM •There is anemia and loss of hair. •Stomach: Mucous membrane may be inflamed and there may be sub mucous petechial hemorrhages. •Spleen: Congested. •Liver: Congested, and shows centri-lobular necrosis and fatty degeneration.
  • 18. THALLIUM •Kidneys: Congested, glomeruli are swollen, convoluted tubules show cloudy swelling and necrosis of the cells. •Trachea and bronchi: Congested. •Lungs: Congested with sub-pleural hemorrhages. •Heart: Fatty degeneration. •Brain: Meningeal vessels may be congested. •Cells of adrenal cortex, thyroid and hair follicles show vacuolization and degenerative changes.
  • 19. THALLIUM Poisoning by thallium is rare in contrast to poisoning by lead or mercury, probably due to its infrequent use. Thallium was used as an IDEAL HOMICIDAL POISON in some European countries and Australia, where it was used as rodenticide. It is tasteless and odorless, dissolves completely in liquid, rapidly and completely absorbed, and they defy detection on routine
  • 20. THALLIUM Accidental intoxication may result from its therapeutic use as a depilatory or or from its accidental ingestion when used as a rodenticide. Chronic poisoning occurs from industrial exposure. Suicidal cases are also seen sometimes.
  • 21. THALLIUM Thallium stress test: In clinical practice, thallium 201 is used as a radioactive tracer in heart scintigraphy to detect myocardial ischemia. Accidental poisoning has become rare in the domestic setting since the 1970s, when thallium- based rodenticides were banned in many countries. The majority of reported cases of thallium poisoning in the last two decades have been caused by deliberate poisoning.
  • 22. THALLIUM Thallium may be detected in the urine 1 h after ingestion (normal level, < 0.003 µmol/l; a level of > 0.98 µmol/l is toxic), but most clinical laboratories may not have the facilities to quantitatively analyze the thallium content. A rapid quantitative urine test can be done by mixing urine with 0.4% sodium bismuth in 20% nitric acid and 10% sodium iodide. A red precipitate indicates that thallium is present
  • 23. THALLIUM Microscopic examination of hair after application of 10% sodium hydroxide may reveal dark bands of pigmented material characteristic of presence of thallium.