Dr Kaleem Khan

Assistant Professor
JNMCH
 It is the common environmental toxicant and is found in
soil, water, and air.

 USES: primarily in the

 Production of glass
 Semiconductors,
 Wood and hide preservation,
 Additive of metal alloys
 In the past arsenic was used as

 Weed killer,
 Rodenticide,
 Chemical warfare
 Pigments and
 Enamels.
 The most common reason for long-term exposure is

◦ Contaminated drinking water

(Recommended levels in water are less than 10–50 µg/L (10–50 parts per billion)
◦ Traditional medicines.
 Arsenious oxide (As2 o3): 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 ) –
 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.
 Rat poisons Calico print Fruit sprays Sheep-dips

Weed-killer Taxidermy Fly papers preserving timber against

white ants
 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
• 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.
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.
 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.
It can be inhaled and absorbed through the skin

Or through GIT after ingestion.

Combines with the globins portion of haemoglobin

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

 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.
 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 stools are dark coloured and bloody
 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.
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

Trait Arsenic poisoning Cholera

1.Pain in throat Before vomiting After vomiting

2.Purging Follows vomiting Precedes vomiting

3.StoolsLike Bloody Rice-watery and pass in
later rice-water in early stage, continuous involuntary jet

4.Tenesmus Present Absent

5.Vomited matter Contains mucous, bile and blood Watery without mucou
s, bile and blood
 When massive dose (> 3-5 mg) is rapidly absorbed.

 Gastric sign are usually absent

 Cyanosis, cold clammy skin,

 Hypoxic encephalopathy, convulsions,

 Acute tubular necrosis and renal failure

 Hyperpyrexia and acute haemolysis

 Acute hepatic failure, cirrhosis, ascitis,

 Cardiomyopathy, subendocardial haemorrhages, hypovolemia by

vasodilatation.

 Death d/t shock and peripheral vascular failure

 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
 Arsine gas 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.

 Urine:
 Proteinuria, cast and albuminuria are there.

 A urinary excretion of arsenic >100mg/24 hours(

diagnostic )

 Monomethylarsine and dimethylarsine are present in

the urine 24 hours after ingestion in acute poisoning).
 Blood:
 0.9 µg/dl,
 Monocytic hypochromic anaemia,
 Leukocytosis and
 Mild eosinophilia.

 Liver function test:

 Serum alkaline phosphatase and bilirubin is raised
 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
 Stomach wash with milk and warm water.

 Gastric Lavage 1% sodium thiosulphate in water

 Demulcent such as ghee and barley water,

 Purgatives like Castor oil and magnesium sulphate

 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.

 24 hour urine sample is to be collected and if arsenic level is

fall below 50mg/24 hours, ( chelation therapy to be stopped)

 It should be stopped for 5 days and then started again so that

the tissue arsenic is mobilized and ready for chelation.
 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.
◦ 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.
◦ 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
 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
 As medicine

 Person who ingest it as medicine for long periods

 When the dose is not large enough to kill the patient.

 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
 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.
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
◦ 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.

 that look much like
traumatic injuries are found
on the fingernails.
◦ Peripheral neuritis with glove and stocking type of anaesthesia

◦ Encephalopathy- severe headache, personality disturbance,

convulsion or coma.

◦ Neuropathy- parasthesia, numbness, pain on particularly on the

soles of the feet.

◦ Symmetrical sensorimotor polyneuropathy , resembling

Gullian- Barre Syndrome

◦ Muscular atrophy resulting in Wrist drop and Foot drop.

 ◦ Muscular weakness, ataxia, cramps tremors
◦ Oedema of the face, periorbital region
◦ Impotence is commonly present.

 There is evidence of
 Bone marrow depression
 Aplastic anaemia
 Normochromic normocytic anaemia
 Leucopenia, thrombocytopenia and mild eosinophilia.
 Megaloblastic anaemia
Differential Diagnosis(chronic arsenic poisoning )

◦ To be differentiated from alcoholic neuritis.

◦ the symptoms and signs are developed rapidly , are

widespread.

◦ No glycosuria whereas in alcoholic neuritis glycosuria is

positive.
◦ 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.

◦ 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)

 It is ideal homicidal poisoning
 It is used as a cattle poison.
 It is used for suicidal purpose.
 Accidentally , when it is applied locally as a cure for
impotence.
 Application on the abraded skin ( criminal abortion )
 Arsenophagist: used as aphrodisiac and can acquire
tolerance upto .03gm or more in one dose
◦ Accidental cases, from its admixture with drink or articles of
food.

◦ White arsenic has been mistaken for baking powder, soda,

salt or flour.

◦ The mountaineers of Styria and Tyrol used for becoming

hardier to carry weights and climb mountains.

◦ Its deposition in hair may begin in 15 days after

administration.
 Exhumed body:

 Arsenic cannot percolate in the cadaver from the

soil, as it is an insoluble form of salt.
 The nails and hair will have a higher concentration
from the soil.
 The soil is to be kept for chemical analysis.
 Napoleon Bonaparte (Emperor of France from 1804 to
1815) was exiled to the very remote island of St. Helena
(a British colony in the Atlantic),where he died a
mysterious death.

 Ben Wielder(a Napoleonic scholar) submitted hair to

Neutron Activation Analysis, revealing fluctuating levels
of arsenic throughout the length, ranging from 4.4 to
23.0 parts per million.
thanks