Arsenic Poisoninig

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 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.

ARSENIC

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.

Compounds:

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.

Arsenic Is The Most Popular Homicidal Poison

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.

Action

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

Absorption and Excretion

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 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.

Acute Poisoning Arsenic

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 vomiting3.StoolsLike     Bloody

later rice-water    in   early stage,

Rice-watery and pass in continuous involuntary jet

4.Tenesmus Present Absent5.Vomited matter

Contains mucous, bile and blood

Watery    without   mucous, bile and blood

Difference between Arsenic Poisoning and Cholera

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

Fulminant type:

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

Narcotic form

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.

Arsine gas

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).

Laboratory diagnosis

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

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

Treatment:

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.

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.

TREATMENT OF POISONING BY ARSINE GAS:

◦ 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

PM Appearance

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

CHRONIC ARSENIC POISONING

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

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

Sign And Symptom

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

Third Stage: Skin Eruptions

Chronic toxicity is more insidious and may manifest as a classical dermatitis (hyperkeratosis with a classical "dew drops on a dusty road" appearance)

Hyperkeratosis

◦ 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.

Whitish lines (mees lines) that look much like

traumatic injuries are found on the fingernails.

◦ 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.

Fourth Stage: nervous disturbances

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

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.

◦ 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.

Treatment

◦ 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)

Post Mortem Appearance

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

Medico- Legal Importance:

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.

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.

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.

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