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ARSENIC POISONING
BY S.G YADUNAND
HISTORY OF ARSENIC
 Word meaning Arsenic is ‘STRONG POISON’
 Used in ancient times as poison for Political Assasinations.
 There are romours that Nepoleon was killed by Arsenic Poisoning.
Some hairs from scalp were analysed revealing fluctuating levels of
arsenic.
INTRODUCTION
 Categorized under irritant poisoning
Sub- Metallic poisoning.
 Metallic arsenic is not poisonous.
 When volatilised by heat unites with O2 and forms poisonous
vapour of As2O3.
 Common environmental toxicant, found in soil, water and air.
 Abundance : Earth’s crust- 20th, Sea water-14th, Human body-12th.
COMPOUNDS
1. Arsenious oxide or Arsenic trioxide (Sankhya / Somalkhar/ Gouripashana):
Commonest form used, White Arsenic, No taste or Smell, Low Solubility.
2. Copper Compounds: Colouring Agent
Copper arsenite (Scheele’s Green) & Copper acetoarsenite (Paris Green).
3. Arsenic acid.
4. Sodium and Potassium Arsenate.
5. Arsenic Sulphide (Manashila As2S2 & Haratala As2S3): Colouring Agent.
6. Organic Compounds.
7. Arsine Gas (colourless gas with garlic like non-irritating odour)
8. Environmental sources like contaminated drinking water (as in Bangladesh),
mineral species, marine animals.
USES
Rat Killer Calico printing Fruit spray Sheep dips
Weed killer Taxidermy Fly papers Preserving timber
ACTIONS
 Interferes with cellular respiration, Glycolysis (by combining with
Sulphydryl groups of mitochondrial enzymes)
 Pyruvate to acetyl CoA reduced, decreased ATP production
 Particularly targets vascular endothelium leading to increased
permeability, tissue oedema and haemorrhage especially in intestinal
canal.
 Local action – Irritation to mucous membrane
 Remote action – Depression of Nervous system.
ABSORPTION
Orally (pentavalent arsenic)
Dermally (Arsenite)
Inhalation (Arsine)
Parenterally
DISTRIBUTION
Once absorbed Arsenic rapidly combines with Globin of Hb and then localize in
blood, within 24hours it redistribute to liver, kidney, spleen, lungs and GI tract, lesser
accumulation in muscle and nervous tissue (including brain)
Replaces phosphorous in bone and remains for years, found in keratin tissues of
hair, nail and skin for years
ELIMINATION
Excreted mainly by kidney in the form of methylated arsenic
Also by feaces, bile, sweat and other secretions
CIRCUMSTANCES
Arsenic is a Popular Homicidal Poison
 Cheap
 Easy availability
 Colourless
 Odourless
 Tasteless
 Small quantity can be fatal
 Can be easily administered with food or drinks
 Gradual onset of symptoms
 Symptoms of Gastro-enteric type stimulate those of Cholera
Disadvantages of As
 Delays Putrefaction.
 Can be detected in completely decomposed bodies.
 Can be found in Hair, bones and nails for several years.
 Can be detected in charred bones or ashes.
TYPES
I. FULMINANT TYPE
II. GASTRO-ENTERIC TYPE
III. NARCOTIC FORM
IV. CHRONIC ARSENIC POISONING
FULMINENT TYPE
 Massive dose (3–5g) causes rapid or delayed death
 Rapid death: when rapidly absorbed causes death in 1-3 hours, due to shock
and peripheral vascular failure.
 Delayed death: due to Hepato-renal failure, death can be prolonged to few
days.
 Capillaries are markedly dilated with a marked fall of blood pressure.
 Cyanosis, cold clammy skin.
 Gastric signs are usually absent.
GASTROENTERIC TYPE
 Common form of acute poisoning, resembles bacterial food poisoning.
 Symptoms usually appear half to one hour after ingestion but may be delayed
many hours especially when taken with food.
 Symptoms:
1. GIT : Burning and colicky pain in oesophagus, stomach and bowel.
Intense thirst, nausea and severe projectile vomiting.
Constriction in throat & difficulty in swallowing.
Purging accompanied with tenesmus, pain and irritation in anus.
Stools are expelled involuntarily, dark coloured, stinking and bloody
later resembles rice water stools of cholera.
Garlicky odour of breath and faeces maybe noted
DIFFERENCES:
TRAIT ARSENIC POISON CHOLERA
1. PAIN IN THROAT BEFORE VOMITING AFTER VOMITING
2. PURGING FOLLOWS VOMITING PRECEDS VOMITING
3. STOOLS BLOODY, DARK
COLOURED, LATER RICE
WATERY
RICE WATERY STOOLS,
NOT BLOODY,
INVOLUNTARY
4. TENESMUS PRESENT ABSENT
5. VOMITED MATTER CONTAINS MUCOUS,
BILE AND BLOOD
WATERY AND WITHOUT
MUCUS, BLOOD, BILE
2. Hepatic : Fatty infiltration, Hepatomegaly.
3. Renal: Oliguria, uraemia, albuminuria, hematuria, pain in micturition.
4. C.V.S: acute circulatory collapse with vasodilation, increased vascular
permeability, ventricular fibrillation, ventricular tachycardia.
Death is usually due to circulatory failure.
NARCOTIC FORM
 Can be due to improper medicinal use or use of As as an aphrodisiac, etc.
 It produces mainly CNS symptoms
 Giddiness, formication and tenderness of the muscles
 Delirium, coma, death
 Rarely paralysis
 Loss of memory and speech
 Convulsions
 Stocking glove pattern
ARSINE GAS
 Arsine gas acts as poison to haemoglobin and cause haemolysis.
 It mostly produces haemoglobinuria, anaemia, and renal failure.
 Death is almost instantaneous.
FATAL DOSE
0.1 – 0.3 g As2O3
FATAL PERIOD
1 – 2 days (sometimes few hours is enough)
CHRONIC POISONING
CAUSE
SYMPTOMS
 Accidental ingestion of repeated small doses (workers).
 Repeated intake of food or drink in which there are traces of drug.
 Polyneuritis, Anaesthesias, Paraesthesia, Encephalopathy.
 Photophobia, Congestion and watering of eyes.
 Hepatomegaly, jaundice, cirrhosis.
 Pigmentation : Rain drop type of pigmentation, Hyperkaratosis, Epithelial
hyperplasia, Leucomelanosis, Arsenicosis
 Aldrich-Mees Lines: Development of white transverse lines in finger nails.
 Chronic nephritis, bone marrow suppression, thrombocytopenia.
HYPERKARASTOSIS
DEW DROP PIGMENTATION
ALDRICH-MEES LINES
DIAGNOSIS
 Acute poisoning: findings in blood Sample
 Chronic poisoning: findings in hair, nail and bones
 Some tests like Marsh test, Reinsch test
TREATMENT
 Stomach wash with large amount of warm water and milk.
 Freshly precipitated, hydrated, ferric oxide in small doses (converts toxic arsenic
to non toxic ferric arsenite)
 B.A.L (British Anti Lewisite), chelation therapy is administered
 Penicillamine can be used with B.A.L
 Demulcents (ghee/barley) lessen irritation
 Castor oil or MgSO4 to prevent intestinal absorption
 In case of Renal failure Haemodyalisis or exchange transfusion may be given
POSTMORTEM FINDINGS
IN ACUTE POISONING
EXTERNAL FINDINGS
 Sunken eyeballs
 Cyanosed skin
 Shrunken body due to dehydration
INTERNAL
 In some cases mouth, pharynx and oesophagus maybe inflamed or ulcerated.
 Lesions are found in the stomach
 Swollen, oedematous and red mucosa especially in the pyloric region
 Stomach mucosa resembles red velvet
 Small intestinal mucosa is pale violet and inflamed
 Liver, Spleen and Kidney are congested, enlarged, swollen and shows fatty
degeneration
 Maybe oedema of brain with patchy necrosis or haemorrhagic encephalitis
 Meninges are congested
POSTMORTEM FINDINGS
IN CHRONIC POISONING
 Stomach may show chronic gastritis, patchy inflammatory redness in rugae
 Fatty degeneration of liver maybe with severe necrosis
 Tubular necrosis of kidneys
 Myocardial necrosis
 Pigmentation, Hyperkeratosis, Aldrich-Mees lines, ulceration of mucosa.
Thank you

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Arsenic poisoning

  • 2. HISTORY OF ARSENIC  Word meaning Arsenic is ‘STRONG POISON’  Used in ancient times as poison for Political Assasinations.  There are romours that Nepoleon was killed by Arsenic Poisoning. Some hairs from scalp were analysed revealing fluctuating levels of arsenic.
  • 3. INTRODUCTION  Categorized under irritant poisoning Sub- Metallic poisoning.  Metallic arsenic is not poisonous.  When volatilised by heat unites with O2 and forms poisonous vapour of As2O3.  Common environmental toxicant, found in soil, water and air.  Abundance : Earth’s crust- 20th, Sea water-14th, Human body-12th.
  • 4. COMPOUNDS 1. Arsenious oxide or Arsenic trioxide (Sankhya / Somalkhar/ Gouripashana): Commonest form used, White Arsenic, No taste or Smell, Low Solubility. 2. Copper Compounds: Colouring Agent Copper arsenite (Scheele’s Green) & Copper acetoarsenite (Paris Green). 3. Arsenic acid. 4. Sodium and Potassium Arsenate. 5. Arsenic Sulphide (Manashila As2S2 & Haratala As2S3): Colouring Agent. 6. Organic Compounds. 7. Arsine Gas (colourless gas with garlic like non-irritating odour) 8. Environmental sources like contaminated drinking water (as in Bangladesh), mineral species, marine animals.
  • 5. USES Rat Killer Calico printing Fruit spray Sheep dips Weed killer Taxidermy Fly papers Preserving timber
  • 6. ACTIONS  Interferes with cellular respiration, Glycolysis (by combining with Sulphydryl groups of mitochondrial enzymes)  Pyruvate to acetyl CoA reduced, decreased ATP production  Particularly targets vascular endothelium leading to increased permeability, tissue oedema and haemorrhage especially in intestinal canal.  Local action – Irritation to mucous membrane  Remote action – Depression of Nervous system.
  • 7. ABSORPTION Orally (pentavalent arsenic) Dermally (Arsenite) Inhalation (Arsine) Parenterally DISTRIBUTION Once absorbed Arsenic rapidly combines with Globin of Hb and then localize in blood, within 24hours it redistribute to liver, kidney, spleen, lungs and GI tract, lesser accumulation in muscle and nervous tissue (including brain) Replaces phosphorous in bone and remains for years, found in keratin tissues of hair, nail and skin for years ELIMINATION Excreted mainly by kidney in the form of methylated arsenic Also by feaces, bile, sweat and other secretions
  • 8. CIRCUMSTANCES Arsenic is a Popular Homicidal Poison  Cheap  Easy availability  Colourless  Odourless  Tasteless  Small quantity can be fatal  Can be easily administered with food or drinks  Gradual onset of symptoms  Symptoms of Gastro-enteric type stimulate those of Cholera
  • 9. Disadvantages of As  Delays Putrefaction.  Can be detected in completely decomposed bodies.  Can be found in Hair, bones and nails for several years.  Can be detected in charred bones or ashes.
  • 10. TYPES I. FULMINANT TYPE II. GASTRO-ENTERIC TYPE III. NARCOTIC FORM IV. CHRONIC ARSENIC POISONING
  • 11. FULMINENT TYPE  Massive dose (3–5g) causes rapid or delayed death  Rapid death: when rapidly absorbed causes death in 1-3 hours, due to shock and peripheral vascular failure.  Delayed death: due to Hepato-renal failure, death can be prolonged to few days.  Capillaries are markedly dilated with a marked fall of blood pressure.  Cyanosis, cold clammy skin.  Gastric signs are usually absent.
  • 12. GASTROENTERIC TYPE  Common form of acute poisoning, resembles bacterial food poisoning.  Symptoms usually appear half to one hour after ingestion but may be delayed many hours especially when taken with food.  Symptoms: 1. GIT : Burning and colicky pain in oesophagus, stomach and bowel. Intense thirst, nausea and severe projectile vomiting. Constriction in throat & difficulty in swallowing. Purging accompanied with tenesmus, pain and irritation in anus. Stools are expelled involuntarily, dark coloured, stinking and bloody later resembles rice water stools of cholera. Garlicky odour of breath and faeces maybe noted
  • 13. DIFFERENCES: TRAIT ARSENIC POISON CHOLERA 1. PAIN IN THROAT BEFORE VOMITING AFTER VOMITING 2. PURGING FOLLOWS VOMITING PRECEDS VOMITING 3. STOOLS BLOODY, DARK COLOURED, LATER RICE WATERY RICE WATERY STOOLS, NOT BLOODY, INVOLUNTARY 4. TENESMUS PRESENT ABSENT 5. VOMITED MATTER CONTAINS MUCOUS, BILE AND BLOOD WATERY AND WITHOUT MUCUS, BLOOD, BILE
  • 14. 2. Hepatic : Fatty infiltration, Hepatomegaly. 3. Renal: Oliguria, uraemia, albuminuria, hematuria, pain in micturition. 4. C.V.S: acute circulatory collapse with vasodilation, increased vascular permeability, ventricular fibrillation, ventricular tachycardia. Death is usually due to circulatory failure.
  • 15. NARCOTIC FORM  Can be due to improper medicinal use or use of As as an aphrodisiac, etc.  It produces mainly CNS symptoms  Giddiness, formication and tenderness of the muscles  Delirium, coma, death  Rarely paralysis  Loss of memory and speech  Convulsions  Stocking glove pattern
  • 16. ARSINE GAS  Arsine gas acts as poison to haemoglobin and cause haemolysis.  It mostly produces haemoglobinuria, anaemia, and renal failure.  Death is almost instantaneous.
  • 17. FATAL DOSE 0.1 – 0.3 g As2O3 FATAL PERIOD 1 – 2 days (sometimes few hours is enough)
  • 18. CHRONIC POISONING CAUSE SYMPTOMS  Accidental ingestion of repeated small doses (workers).  Repeated intake of food or drink in which there are traces of drug.  Polyneuritis, Anaesthesias, Paraesthesia, Encephalopathy.  Photophobia, Congestion and watering of eyes.  Hepatomegaly, jaundice, cirrhosis.  Pigmentation : Rain drop type of pigmentation, Hyperkaratosis, Epithelial hyperplasia, Leucomelanosis, Arsenicosis  Aldrich-Mees Lines: Development of white transverse lines in finger nails.  Chronic nephritis, bone marrow suppression, thrombocytopenia.
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  • 23. DIAGNOSIS  Acute poisoning: findings in blood Sample  Chronic poisoning: findings in hair, nail and bones  Some tests like Marsh test, Reinsch test
  • 24. TREATMENT  Stomach wash with large amount of warm water and milk.  Freshly precipitated, hydrated, ferric oxide in small doses (converts toxic arsenic to non toxic ferric arsenite)  B.A.L (British Anti Lewisite), chelation therapy is administered  Penicillamine can be used with B.A.L  Demulcents (ghee/barley) lessen irritation  Castor oil or MgSO4 to prevent intestinal absorption  In case of Renal failure Haemodyalisis or exchange transfusion may be given
  • 25. POSTMORTEM FINDINGS IN ACUTE POISONING EXTERNAL FINDINGS  Sunken eyeballs  Cyanosed skin  Shrunken body due to dehydration
  • 26. INTERNAL  In some cases mouth, pharynx and oesophagus maybe inflamed or ulcerated.  Lesions are found in the stomach  Swollen, oedematous and red mucosa especially in the pyloric region  Stomach mucosa resembles red velvet  Small intestinal mucosa is pale violet and inflamed  Liver, Spleen and Kidney are congested, enlarged, swollen and shows fatty degeneration  Maybe oedema of brain with patchy necrosis or haemorrhagic encephalitis  Meninges are congested
  • 27. POSTMORTEM FINDINGS IN CHRONIC POISONING  Stomach may show chronic gastritis, patchy inflammatory redness in rugae  Fatty degeneration of liver maybe with severe necrosis  Tubular necrosis of kidneys  Myocardial necrosis  Pigmentation, Hyperkeratosis, Aldrich-Mees lines, ulceration of mucosa.
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