Metallic arsenic is not poisonous, as it is insoluble in water and therefore incapable of absorption from the alimentary canal, but it oxidizes by exposure to the air, and then becomes poisonous. When rubbed on the skin in a finely powdered state it acts as a poison, as it is capable of being absorbed in the form of an oxide. When volatilized by heat, it readily unites with oxygen of the air, forming the poisonous vapor of arsenic trioxide.


Arsenious oxide or arsenic trioxide (Sankhya or somalkhar). This is commonly called as white arsenic or merely as arsenic. It occurs in 2 forms:

a. white, smooth, heavy, crystalline powder b. white and opaque solid mass similar to porcelain. It has no taste or smell.

2. Copper arsenite (Scheele’s green) and copper acetoarsenite (Paris green, Schweinfurt green or emerald’s green).

3. Arsenic acid

4. Sodium and potassium arsenate

5. Arsenic trichloride (butter of arsenic).

6. Arseniuretted hydrogen or arsine is a colorless gas with garlic-like, non-irritating odour.

7. Organic compounds e.g. acetarson, tryparsamide, salvarsan, mepharsen etc.

arsenic poison


Arsenic interferes with respiration by combining with the sulphydryl groups of mitochondrial enzymes, especially pyruvate oxidase, and certain phosphatase. Locally it causes irritation of the mucous membranes and remotely depression of the systema nervosum. Arsenic causes its toxicity by uncoupling mitochondrial oxidative phosphorylation. It interferes with glyoclysis.

FATAL DOSE:  The fatal dose of arsenic trioxide is typically within the range of 200–300 mg. In general, the pentavalent sort of arsenic (arsenate) is smaller amount toxic than the trivalent form (arsenite) because it’s less water soluble. The most toxic form is arsine gas.

FATAL PERIOD: the average fatal period is 12 -48 hours, though death has frequently occurred within 2-3 hours.


  1. Emetics are not recommended.
  2.  The stomach should be emptied and then thoroughly and repeatedly washed by the stomach tube with large amount of warm water and milk; activated charcoal does not adsorb arsenic appreciably and is not recommended in patient whom coingestants are not suspected.
  3.  Demulcents (butter or greasy substances) prevent absorption.
  4.  Whole bowel irrigation with polyethylene glycol could also be effective to stop GIT absorption of arsenic.
  5. Antidote is BAL or dimercaprol, 400-800 mg on first day, 200-400 mg on second and third days, in divided doses every four hours and 100-200 mg in 2 divided doses for 7-10 days or until urine level falls below 50 micro gram in a 24 hour specimen. Oral succimer (DMSA), or dimerval (DMPS, drug of choice for treating most heavy metal poisonings), could also  be used rather than BAL.
  6.  Alkalis should not be given by mouth as the increase the solubility of arsenic.
  7.  Purgatives (castor oil/magnesium sulphate) are given to remove unabsorbed poison from intestine.
  8.  Glucose-saline with bicarbonate  of sodium is useful to combat shock and improve alkali reserve.
  9.  Hemodialysis or exchange transfusion may be done.


  1. THE FULMINANT TYPE:  All capillaries are dilated, especially in the splanchic area with a marked fall of blood pressure. Arsenic also features a direct action on cardiac muscle. In this type, gastrointestinal symptoms are absent.
  2. The GASTROENTERIC TYPE: this is common form of acute poisoning, and resembles bacterial food poisoning. Symptoms usually appear half to at least one hour after ingestion, but may be delayed many hours when arsenic enters the system by mouth channel. There is a sweetish metallic taste.
  • G.I.T: constriction in the throat and difficulty in swallowing; burning and colicky pain in oesophagus, stomach and bowel occur. A garlicky odour of breath and faeces may be noted. The stools are expelled frequently and involuntarily. Purging ( within 1-3 hrs) is usually accompanied with pain and irritation about  the anus and anus is dark colored, stinking and bloody but watery resembling rice-water stools of cholera.
  • HEPATITIS: fatty infiltration
  • RENAL: oliguria, uraemia, urine contains albumen, red cells and casts, pain during urination.
  • C.V.S: acute circulatory collapse with vasodilation, increased vascular permeability, fibrillation.
  • C.N.S: headache, convulsions, coma, general paralysis, tremors.
  • SKIN: delayed loss of hair, skin eruption. Death is usually due to circulatory failure.

3. NAROCTIC FORM: in this form, the gastrointestinal symptoms are very slight. There is a giddiness, formication and tenderness of the muscles, delirium, coma and death.



i. The body looks emaciated due to dehydration.

ii. Rigor mortis appears early.

iii. Putrefaction is delayed due to anti-bacterial action of arsenic and partly due to dehydration.

iv. The eyeballs are sunken and therefore the skin is cyanosed.

v. Blood tinged vomitus and fecal matter could also be present on body and garments.


i. The mucous of the mouth, pharynx and esophagus may show inflammation or ulceration.

ii. Hemorrhages could also be found within the abdominal organs, mesentery and frequently within the larynx, trachea and lungs.

iii. Lungs: Congested with sub pleural ecchymosed.

iv. Heart: Subendocardial petechial hemorrhages of the ventricle could also be found, even when the stomach shows little signs of irritation.

v. Stomach: Mucosa is swollen, edematous, desquamated and red, either generally or in patches, especially in the pyloric region. Usually, groups of petechiae are seen scattered over the mucosa, but sometimes large sub mucosal and sub peritoneal hemorrhages may be seen—red velvety appearance. A mass of sticky mucus covers the mucosa during which particles of arsenic could also be seen.

Inflammation is more marked at the greater curvature, posterior part and therefore the cardiac end of the stomach.

vi. Small intestine: It contains large flakes of mucus with little or no faecal matter. The mucosa is light violet and shows signs of inflammation with sub mucous hemorrhages along its whole length.

vii. Caecum and rectum show slight inflammation.

viii. Liver, spleen and kidneys: Congested, enlarged and show cloudy swelling and infrequently fatty degeneration. Nephritis is seen.

ix. Brain:  there may be oedema of brain with patchy necrosis or hemorrhagic encephalitis. The meninges are congested.


It may occur due to:              

  • • Recovery from an acute poisoning.
  • • Accidental ingestion of repeated small doses by those working with the metal for a prolonged period or may occur after recovery from one large dose.
  • • Intake of food/drink during which there are traces of arsenic may be suicidal or homicidal in nature.


It is divided into four stages

i. GIT disturbances

ii. Catarrhal changes

iii. Skin rashes

iv. Nervous disturbances

Chronic exposure also causes vasospasm, peripheral neuropathy and peripheral vascular insufficiency.

  • GIT:  Nausea, vomiting, abdominal cramps, diarrhea, salivation.
  • Ocular: Congestion, watering of the eyes, photophobia.
  • RS: Cough, hoarseness of voice, haemoptysis, dyspnoea.
  • Skin and nails:  There may be a rash resembling fading measles rash.Speckled brown pigmentation, totally on the skin flexures, temples, shoulders, eyelids and neck (raindrop appearances with patches of leucoplakia).
  • Hyperkeratosis of the palms and soles with irregular thickening of the nails and development of transverse white lines in the fingernails (called Aldrich Mees lines).
  • CNS: Tingling, polyneuritis,    anesthesia, paraesthesia with painful swelling, encephalopathy.
  • (erythromelalgia), encephalopathy. Neuritis resembles chronic    alcoholism.
  • CVS: Cardiac failure, dependent edema.
  • Renal: Chronic nephritis.
  • Hepatic:  Hepatomegaly, jaundice, cirrhosis of the liver.
  • Hematologic: Bone marrow suppression, hypoplasia, anemia, thrombocytopenia, leukemia.

Postmortem Findings

External: Emaciation, pigmentation, keratosis, alopecia, white streaks on nails, jaundic and ulceration of septum.


i. Stomach: It’s going to be normal or may show a gastritis. Some rugae may show patchy inflammatory redness.

ii. Small intestine: Reddish with thickened mucosa.

iii. Liver: Fatty degeneration or even necrosis.10

iv. Kidneys: Tubular necrosis.

v. Heart: Myocardial necrosis may be seen.


Arsenic poisoning often homicidal, suicidal, accidental, occupational or unintentional.

i. Homicide: Arsenic was a popular homicidal poison because: Onset of symptoms is gradual, Cheap, Symptoms simulate those of Colorless cholera,  Tasteless, Small quantity is required To Odorless cause death, can be administered easily with food or drink.

ii. Suicide is rare, because it causes an excessive amount of pain.

iii. Accidental death could also be due to admixture with articles of food or from its improper medicinal use. Chronic poisoning results from drinking water containing arsenic.

iv. Arsenic exposure is often occupational in those working in metal foundry, mining, glass production or within the semiconductor industry.

v. It is often employed to produce abortion, especially in the form of ointment or paste on abortion sticks.

vi. It may be used as cattle poison.


  1. Excretion of more than 100  in 24 hrs urine.
  2. Detection by atomic absorption spectroscopy.
  3. Marsh’s test and Reinsch’s tests are absolute.

TOLERANCE: some people take arsenic daily as a tonic or as an aphrodisiac, and   that they acquire tolerance up to 0.3g, or more in one dose. Such people known as ARSENOPHAGISTS.

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