2. It is the common environmental toxicant and is found in
soil, water, and air.
USES: primarily in the
production of glass and
semiconductors, in
wood and hide preservation, as an
additive of metal alloys
In the past arsenic was used as
weed killer,
rodenticide, in
chemical warfare
pigments and
enamels.
3.
4.
5. Arsenious oxide (As2o3): most toxic form white arsenic/arsenious
acid/ arsenic trioxide/ sankhya/ somalkar.
It occurs in two forms white
Crystalline powder or
Opaque mass.
No taste or smell and sparingly soluble in water
It is widely used in a) –
Calico printing ,
Taxidermy (preparing mounting skin of animals),
Artificial flowers,
Wall papers preparation,
Preservation of timber against ants ,
For treatment of
Rheumatic arthritis,
Impotence,
Syphilis.
6. Rat poisons Calico print Fruit sprays Sheep-dips
Weed-killer Taxidermy Fly papers preserving timber
against white
ants
7. Sulphides of Arsenic: colouring agent, depilatory, fly paper
Arsenic trisulphide (As2S3)/ yellow orpiment/ hartal
Arsenic disulphide (As2S2)/ red realgar/ manseel
Copper compounds of Arsenic: colouring agent
Scheels green/ copper arsenite
Paris green / copper acetoarsenite
Organic compounds:
Cacodylates,
Atoxyl,
Salvarson,
Arsenobentine (trimethylated arsenic)
Arsine gas
8. • It is cheap
• Easily obtained
• Colourless
• No smell
• No taste
• Small quantity is required to cause death.
• Can be easily administered with food or drink.
• Onset of symptoms is gradual
• Symptoms simulate those of Cholera.
9. Disadvantages Of Arsenic:
• It delays putrefaction
• Can be detected in completely decomposed bodies.
• Can be found in bones, hairs and nails for several
years.
• Can be detected in charred bones or ashes.
10. Interferes with cellular respiration: It combines with sulphydryl groups of
mitochondrial membrane especially pyruvate dehydrogenase
It is a capillary poison: increased permeability, causes tissue oedema and
hemorrhage
Hyperaemia and haemorrhage in the intestine.
Interferes with glucose uptake, gluconeogenesis, fatty acid oxidation: Fatty
degeneration of liver
Renal tubular necrosis
Peripheral nerves show axonal neuropathy: depression of nervous system.
Arsenolysis is a major form of toxicity in which the arsenic anions can substitute
for phosphate in many reactions.
11.
12. It can be inhaled and absorbed through the skin or through GIT after
ingestion.
Once absorbed arsenic rapidly combines with the globins portion of haemoglobin
and therefore localize in the blood, within 24 hours it redistribute to liver, kidney,
spleen, lung and GI tract, with lesser accumulation in the muscle and nervous
tissue.
Excreted mainly through kidneys as methylated arsenic and some part by
faeces, sweat, bile.
It is excreted in stomach and intestine even when given by other routes
(enterohepatic circulation ).
It becomes fixed in cancellous tissue or bones. Replaces phosphorous.
It is a known carcinogen: skin, liver, bladder
13. Fatal dose-
Arsenic trioxide: 180 mg,
But it varies on ingestion,
Inherent tolerance of the patient.
Fatal period:-
12-48 hours.
But can be fatal within 2-3 hours.
14. Patient experience a
Metallic taste,
Garlicky odour in the breath
Xerostomia
Dysphagia.
Increased salivation
Excessive thirst.
Severe nausea
Vomiting.
Colicky abdominal pain and
Profuse diarrhoea.
The stool are dark coloured and bloody and
Later on
Colourless,
Odourless, and
Watery resembling rice watery
Due to vasodilatation with transudation of fluid into the bowel lumen in addition to
mucosal vesicle formation and sloughing leading to increased peristalsis.
15. Vomiting is
Projectile ,
Dark brown or yellow colour and
Contain stomach contents,
Blood and mucus
Purging, tenesmus , pain and irritation around anus.
Severe headache, vertigo, periorbtal odema, skeletal muscles cramps.
Renal damage manifested as
Oligurea,
Proteinurea, and
Haematuria.
Fatty infilteration of liver
Delayed loss of hair, skin eruptions
16. Trait Arsenic poisoning Cholera
1.Pain in throat Before vomiting After vomiting
2.Purging Follows vomiting Precedes vomiting
3.StoolsLike Bloody
later rice-water in early stage,
Rice-watery and pass in
continuous involuntary jet
4.Tenesmus Present Absent
5.Vomited matter Contains mucous, bile and blood Watery without mucou
s, bile and blood
17.
18. When massive dose (> 3-5 mg) is rapidly absorbed.
Gastric sign are usually absent
Cyanosis, cold clammy skin,
Hypoxic encephalopathy, convulsion,
Acute tubular necrosis and renal failure
Hyperpyrexia and acute haemolysis
Acute hepatic failure, cirrhosis, ascitis,
Cardiomyopathy, subendocardial haemorrhages,
Decreased cardiac output due to hypovolemia by vasodilatation.
Death d/t shock and peripheral vascular failure
19. It produces mainly CNS symptoms:
Giddiness
Precordial distress.
Tenderness of muscles.
Delirium.
Dilated pupils and complete paralysis of the muscles at times
Usual symptoms can also be produced such as
Convulsion,
Lockjaw,
Raised temperature,
Loss of speech and
Memory ,
Joint pain
20. Arsine gas act as a poison to haemoglobin and causes
haemolysis.
It most commonly produces haemoglobinuria and anaemia.
The other symptoms produced as a result of poisoning are
Jaundice,
Dark red urine,
Renal failure,
Heart failure,
Delirium and
Coma.
Death usually instantaneous.
21. Urine: proteinuria, cast and albuminuria are there.
Arsenic poisoning is usually diagnosed with the urine test for
arsenic as arsenic ions are present very shortly after ingestion.
A urinary excretion of arsenic >100mg/24 hours is regarded as
indicative of exposure to a potentially toxic amount of arsenic
Monomethylarsine and dimethylarsine are present in the urine
24 hours after ingestion. acute poisoning).
22. Blood: 0.9 µg/dl, monocytic hypochromic anaemia, leukocytosis
and mild eosinophilia.
Liver function test: serum alkaline phosphatase and bilirubin is
raised and there is excretion of urobilinogen in the urine.
Hair and nails samples containing >300 ppm or 100 mg of arsenic
per 100 gm of specimen are diagnostic of arsenic poisoning
Radiopaque sign on abdominal x-ray
Effective methods for arsenic detection.
Colorimetry,
Atomic absorption spectroscopy and
Neutron activation analysis
23. Stomach wash should be done with milk and warm water.
For Gastric Lavage 1% sodium thiosulphate in water is
helpful
Demulcent such as ghee and barley water are given.
Purgatives like Castor oil and magnesium sulphate is
administered to diminish intestinal absorption of arsenic
24. British anti lewisite (B.A.L.) Is administered
4 hourly for 2 days,
6 hourly for 1 day and
Total dose 12 hourly after wards,
Total dose is 2.5-3 mg/kg body wt.
To know when the chelation is to be stopped, 24 hour urine
sample is to be collected and if arsenic level is fall below
50mg/24 hours,
It should be stopped for 5 days and then started again so that
the tissue arsenic is mobilized and ready for chelation.
25. Oral Penicillamine
100mg/kg. Body wt.
In 4 divide doses in 24 hours for 4-8 days after initial
12-48 hours of B.A.L therapy.
Morphine is given to relieve pain.
Saline is administered i.v. for dehydration and enuresis.
To relieve cramps , massage employed, body temperature to be
maintained.
26. ◦ Patient to be taken to fresh air.
◦ Oxygen inhalation to be started .
◦ Exchange transfusion should be undertaken.
◦ Haemodialysis is ensued.
◦ Alkaline drinks are given.
◦ All of the methods help to eliminate arsine gas from the blood.
◦ B.A.L. is not effective in arsine gas poisoning.
27. ◦ Emaciated body d/t dehydration
◦ Rigor mortis lasts longer
◦ Blood tinged vomitus and faecal matter
◦ Mucus membrane of small intestine are inflamed
◦ Stomach red velvety appearance
◦ Liver, heart and kidney: congested, enlarged, swelling and
fatty degeneration may be seen
28. Chronic arsenic poisoning result from chronic repetitive
ingestion or inhalation of arsine gas by:
Arsenic Extraction
Extraction of metals from ore by melting .
Refining of the ores.
Manufacture of
The weed killers,
Insecticides,
Paints,
Dyes and
Cosmetics
29. Person who ingest it as medicine for long periods may follow
the acute poisoning after recovery.
When the dose is not large enough to kill the patient, a number
of secondary effects can be seen 2-4 weeks after ingestion of
the poison
30.
31. FIRST STAGE: GIT disturbances
◦ Loss of weight .
◦ Loss of appetite and salivation.
◦ Colicky pain and constipation.
◦ Vomiting and diarrhoea.
◦ Gums are red and soft.
◦ Tongue is coated, is thin white salivary furred.
◦ Oedema of eyelids and ankles
◦ Temperature and pulse is raised
32. Second Stage: Cattarhal Stage
Dryness and etching of the skin.
Voice is hoarse and husky,
Runing nose,
Cough
Bronchial coryza .
Photophobia and conjunctivitis
Liver is enlarged and cirrhotic,
Chronic nephritis.
33. Erythematous flushing caused by cutaneous capillary
dilation, generalised and localised.
RAIN DROP TYPE of pigmentation of the skin involving
the covered part of the body such as flexors, nipples,
lower abdomen, temples and eye lids.
Epithelial hyperplasia, discrete multiple wart like keratosis
on the palms and sole, head and trunk.
Hyperkeratosis then occurs with desquamation of the palm
and soles
34.
35.
36.
37. ◦ Nails are brittles with linear pigmentation, Aldrich Mee`s
Line ( white transverse line seen on the nail plate up to a
year after arsenic intoxication).
◦ Hair are dry patchy and diffuse alopecia.
◦ Painless perforation in the nasal septum.
38. that look much like
traumatic injuries are found
on the fingernails.
39. ◦ Peripheral neuritis with glove and stocking type of anaesthesia
resembling alcoholism.
◦ Encephalopathy may be seen in some cases, presenting in
severe headache, personality disturbance, convulsion or coma.
◦ The predominant clinical feature of neuropathy are
parasthesia, numbness, pain on particularly on the soles of the
feet.
◦ It is usually a symmetrical sensorimotor polyneuropathy often
resembling Gullian- Barre Syndrome
◦ Eventually muscular atrophy resulting in wrist drop and Foot
drop.
40.
41. Muscular weakness, ataxia, cramps tremors and general emaciation and
death is due to failure of heart muscles.
Oedema of the face, periorbital region or ankle from localised transudation
of intravascular fluid, knee jerk is usually lost.
Impotence is commonly present.
There is evidence of
◦ Bone marrow depression
◦ Aplastic anaemia
◦ Normochromic normocytic anaemia
◦ Leucopenia, thrombocytopenia and mild eosinophilia.
◦ Megaloblastic anaemia
42. Differential Diagnosis:
◦ Chronic arsenic poisoning is to be differentiated from alcoholic
neuritis.
◦ In chronic arsenic poisoning the symptoms and signs are
developed rapidly , are widespread.
◦ There is no glycosuria in as poisoning whereas in alcoholic
neuritis glycosuria is positive.
43.
44. ◦ Remove the patient from the source of poison.
◦ B.A.L is to be given 6 hourly for 2-3 days.
◦ once daily Vitamin B1 injection for peripheral neuritis.
◦ Improve general health.
45. ◦ Emaciation, pigmentation, keratosis, Aldrich Mees lines,
jaundice , wasting of muscles and ulceration of nasal septum
◦ Internally stomach shows patchy inflammation, fatty
degeneration of liver, tubular necrosis of kidney, and
myocardial necrosis
◦ Preserve hair, nail and bone(lower end of femur)
46. It is ideal homicidal poisoning that is used frequently in India.
It is used as a cattle poison.
It is used for suicidal purpose.
Poisoning can result accidentally due to its improper medicinal use
when it is applied locally as a cure for impotence.
Poisoning can result from its application on the abraded skin, when it
is used as vaginal pessaries or when it is mistaken for baking powder
or soda.
Arsenophagist: Use the drug as a habit as aphrodisiac and can acquire
tolerance upto .03gm or more in one dose
47. Accidental cases of poisoning sometimes occur from its admixture with
drink or articles of food.
White arsenic has been mistaken for baking powder, soda, salt or flour and
has caused mass accidental poisoning.
The mountaineers of Styriaand Tyrol used it daily with a view to becoming
hardier tocarry weights and climb mountains.
The greatest concentration of arsenic is found in hair and nails. Its
deposition in hair may begin in 15 days after administration.
48. Exhumed body: Arsenic cannot percolate in the
cadaver from the soil, as it is an insoluble form ofsalt.
The nails and hair will have a higher concentrationfrom
the soil. The soil is to be kept forchemical analysis.
49. Napoleon Bonaparte (Emperor of France from 1804 to 1815)
has been the source of attention of the historians because of his
flamboyance and daring exploits, and perhaps also because of his
tragic demise. On being defeated in legendary Battle of Waterloo
in 1815, he was exiled to the very remote island of St. Helena (a
British colony in the Atlantic),where he died a mysterious death.
His death remained speculative until the scientific authenticity
was finally established.
Some hair from the scalp were procured by Ben Wielder(a
Napoleonic scholar) submitted to neutron activation analysis,
revealing fluctuating levels of arsenic throughout the length of
the hair, ranging from 4.4 to 23.0 parts per million.