Toxicology – A comprehensive study

Dr  Sanil Kumar BHMS MD(Hom)
Department of Forensic Medicine & Toxicology
Govt Homeopathic Medical College. Calicut

General considerations
DEFINITIONS
Toxicology: is the branch of medicine that deals with properties, actions, lethal dose, toxicity, detection or estimation of, and treatment poisons.
Forensic toxicology:
Forensic toxicology deals medical and legal aspects of the harmful effects of chemicals on human body.
Poison:
Poison is a substance, which may be liquid, solid or gas, which when administered in small quantity into the living body or brought into contact with any part of it, leads to injury or ill-health by its constitutional or local effects or both.
Clinical toxicology deals with human diseases, caused by, or associated with abnormal exposure to chemical substances.

Characteristics of Ideal suicidal and Homicidal poisons
Characteristics Suicidal Homicidal
1. Signs and symptoms nil/few Resemble diseases
2. Death Painless Definite
3. Physical quality Tasteless or of pleasant taste
Colourless, Odourless, Tasteless Highly toxic
4. Examples Opium, Barbiturates, Organo-phosphorus compounds, Endrin Organic fluorine compound, Thallium, Arsenic, Aconite

Section under Cr.P.C / IPC relevant to poisoning
1. Section under Cr PC — section 39, 40, 175
2. Section under IPC — section 176, 193, 202, 284, 299, 300, 304A, 324, 326, 328.

The law on poisons:
1. Poison’s act, 1919: It was passed to regulate the importation, possession and sale o poisons.
2. The drug and cosmetics act, 1940: It regulates the import, manufacture, distribution, and sale of all kinds of drugs. One of its main features is the control of the quality, purity and strength of drugs.
3. The drugs and cosmetic rules, 1945: They are framed under the Drugs Act, 1940, to regulate the importation of drugs, the functions and procedures of the Central Drugs Laboratory, the appointment of licensing authorities, and the manufacture, distribution and sale of drugs.
4. The pharmacy act, 1948: It was passed in order to regulate the profession of pharmacy and to constitute Central Council of Pharmacy and State Councils of Pharmacy. The object of this act is to allow only registered pharmacists to compound, prepare, mix or dispense any medicine on the prescription of a medical practitioner.
5. The drugs control act, 1950: It provides for the control of sale, supply and distribution of drugs, the issue of cash memo for sale, marking of prices, and exhibiting list of prices and stocks.
6. The drugs and magic remedies (objectionable advertisement) act, 1954: The object of this act is to ban advertisements which offend decency or morality, and to prevent self-medication and treatment which cause harmful effects.
7. Narcotic drugs and Psychotropic substances act, 1985: It repeals 3 acts; (1) The opium act, 1957 (2) The opium act, 1978 (3) The dangerous drugs act, 1930.
8. Prevention of illicit traffic in narcotic drugs and psychotropic substances act, 1988.

A love philter is a drug, which is supposed to increase the love between the giver and taker. Examples are all aphrodisiacs, such as Arsenic, Cantharides, Alcohol, Opium, Cocaine and Cannabis.

Classifications: Poisons may be classified according to the chief symptoms they produce:
I. Corrosives:
1. Strong acids
(a) Inorganic acids—Sulphuric, nitric, hydrochloric.
(b) Organic acids—Carbolic, oxalic, acetic, salicylic.
2. Strong alkalies— Hydrates & carbonates of sodium, pota¬ssium & ammonia.
3. Metallic salts—Zinc chloride, ferric chloride, potassium cyanide, chromates.

II. Irritants:
1. Inorganic
(a) Non-metallic—Phosphorus, chlorine, bromine, iodine.
(b) Metallic—Arsenic, antimony, mercury, copper, lead, zinc, silver etc.
2. Organic
(a) Vegetables—Abrus precatorius, castor, croton, calotro-pis, aloes.
(b) Animal— Snake & insect bites, cantharides, ptomaines.
3. Mechanical—Powdered glass, diamond dust, hair etc.

III. Systemic
1. Cerebral—
(a) Somniferous—Opium, barbiturates.
(b) Inebriant—Acoho, ether, chloroform.
(c) Deliriant— Dhatura, belladona, hyocyamus, cannabis etc.
2. Spinal—Nux vomica, gelsemium.
3. Peripheral—Conium, curare.
4. Cardiovascular—Aconite, digitalis, quinine, oleander, tobacco, hydrocyanic acid.
5. Asphyxiants—CO, CO2, hydrogen sulphide.

IV. Miscellaneous
Food poisoning, Botulism.

Fate of Poisons in the body
Some inorganic poisons like arsenic and antimony are retained in nails, hair, bones etc. for a considerable time. Certain poisons like chloroform, phosphorus, nitrates, aconite and acetic acid are destroyed in the body and no trace of them can be detected in the viscera or tissues if post-mortem is delayed.

Action of poisons:
1. Local
— By direct contact.
— Chemical destruction – > by corrosives.
— Congestion & inflammation by irritants.
— Tingling of skin and tongue by aconite.
— Dilatation of pupils by belladonna or dhatura.
2. Remote
— By shock caused by corrosives.
— Cantharides acting on kidneys produce nephritis.
— Nux vomica on spinal cord produces convulsions.
3. Combined
— Both local & remote, e.g. oxalic acid, phosphorus etc.

Toxicity of poisons:
(1) Extremely toxic = 1 mg/kg or less
(2) Highly toxic = 1 to 50 mg/kg
(3) Moderately toxic = 50 to 500 mg/kg
(4) Slightly toxic = 0.5 to 5 gm/kg
(5) Practically non-toxic = 5 to 11 gm/kg
(6) Relatively harmless = > 15 gm/kg

Acute poisoning: Is caused by an excessively single dose, or several smaller doses of a poison taken over a short interval of time.
Chronic poisoning :It is caused by smaller doses over a period of time resulting in gradual worsening e.g. arsenic, phosphorus, antimony and opium.

Self poisoning (attempted suicide, parasuicide, or pseudocide)
It is a conscious, often impulsive, manipulative act, undertaker to rectify an intolerable situation.

Collection:
1. Stomach wash (entire quantity).
2. 10 ml. blood.
3. Urine, as much as possible.
10 mg of sodium fluoride for 10 ml of blood acts bo¬as a preservative and as an anticoagulant.

Diagnosis of Poison in the Dead

I. Post-mortem appearances
(a) External
1. The colour changes in the corroded skin and mucous membrane: Sulphuric and Hydrochloric acid: grey, becoming black; nitric acid: brown; hydrofluoric acid: reddish-brown; carbolic acid: greyish-white; oxalic acid: grey, blackened by blood; cresols: brown, leathery; caustic alkalies: greyish-white; mercuric chloride: bluish-white; zinc chloride: whitish; chromic acid and potassium chromate: orange, leathery.
2. Colour of post-mortem staining—the skin may be dark-brown or yellow in phosphorus and acute copper poisoning. Cherry red in carbon-monoxide. Chocolate coloured in cases of death from poison¬ing by nitrites, aniline, nitrobenzene, acetanilide and chlorate of potash owing to the formation of methaemoglobin.
3. Smell about the mouth and nose — Substances which may be recognised by their odour are cyanides, phenol, cresol, opium, alcohol, ether, chloroform, camphor, paraldehyde etc.

(b) Internal
1. Smell—The skull should be opened first to detect unusual odours in the brain tissues. This is useful in cyanide, alcohol, phenol, cresol, ether, chloroform and camphor poisoning.
2. Oesophagus—Corrosive alkalies produce marked softening and desquamation of the mucous membrane. In acute cantharidin poisoning —>mucous membrane is swollen, congested and may show patches of ulceration.
3. Upper respiratory tract—Corrosive alkali or acid poi¬soning —> oedema of glottis, congestion & desquama¬tion of the mucous membrane of the trachea & bronchi.
4. Stomach:
(i) Hyperemia—Irritant poison.
(ii) Softening—Corrosive & irritant poisons,
(iii) Ulcers—Corrosive & irritant poisons,
(iv) Perforation—Seen in strong mineral acid, espe¬cially sulphuric acid.
5. Duodenum and Intestines—In intestine, characteristic change seen is mercury poisoning. It is a colitis, which may resemble enteritis of acute bacillary dysentery.
6. Liver:
Liver necrosis—Substances such as arsphenamine, chloroform, trinitrotoluene, carbon tetrachloride and senecio.
Fatty liver— Arsenic, carbon tetrachloride, amanita phylloides, yellow phosphorus, iodine, rarely ferrous sulphate.
7. Kidney—Parenchymatous degenerative changes found in irritant metal poisoning and in cantharidine poisoning. Extensive necrosis of proximal convoluted tubules may be found in deaths from poisoning by mercuric chlorides, phenol, lysol and carbon tetrachloride.
8. Heart—Subendocardial hemorrhage in left ventricle-acute arsenical poisoning.

II.  CHEMICAL ANALYSIS.
III. EXPERIMENTS ON ANIMALS.
IV.  MORAL AND CIRCUMSTANTIAL EVIDENCES.

Duties of Medical practitioner in a case of suspected poisoning
I. Medical
Care and treatment of the patient.

II. Legal
Assist the police to determine manner of death.
1. In case of suspected homicidal poisoning—Doctor has to confirm his suspicion before opinion. For this he must:-
(a) Collect vomit and urine and submit for analysis.
(b) Observe and record the symptoms in relation to food; other persons affected at the same time.
(c) Consult senior practitioner.
(d) Remove the patient to hospital or appoint nurses of his confidence.
(e) If suspicion of homicide is confirmed, shift the patient to hospital.
2. Suspected articles preserved.
3. If a private practitioner is convinced of homicidal poisoning, he is bound to inform the police officer or magistrate.
4. In suicidal poisoning—not bound to inform police.
5. If practitioner is summoned by investigating police officer, he is bound to give all information (Sec. 175 I.P.C.)
6. Govt. Medical officer has to report the police all cases of suspected poisoning.
7. If the condition of patient is serious, arrange to record dying declaration.
8. If the patient dies he should not issue death certificate, but inform police.

Differential diagnosis of Poisoning based on Vital signs and CNS activity
A. STIMULANT POISONING
1. Sympathomimetic syndromes:
(a) Amphetamines (b) Caffeine (c) Cocaine (d) Ergot alkaloid (e) MAO inhibitors (f) Theophylline.
2. Anticholinergic syndromes:
(a) Antidepressants (tricyclic) (b) Antihistamines (c) Belladonna alkaloids (d) Mydriatics (topical) (e) Plant / mushrooms.
3. Hallucinogenic syndromes.
(a) LSD & synthetic analogue (b) Marijhuana (c) Mescaline (d) Phencyclidine.
4. Withdrawal syndromes.
(a) Alcohol (b) Antidepressants (c) Beta-blockers (d) Clonidine (e) Narcotics (f) Sedative hypnotics.

B. DEPRESSANT POISONING:
1. Sympatholytic syndromes:
(a) Adrenergic blockers (b) Calcium channel blockers (c) Digoxin.
2. Cholinergic syndromes:
(a) Bethanecol (b) Carbamate insecticides (c) Organophosphate insecticides (d) Myasthenia gravis drugs (e.g. Pyridostigmine) (e) Physostigmine.
3. Narcotic syndromes:
(a) Analgesics (b) Antispasmodics (Gl).
4. Sedative-hypnotic syndromes:
(a) Alcohol (b) Anti epileptics (c) Barbiturates (d) Benzodiazepines (e) Hydrocarbons.

An anion metabolic acidosis is characteristic of methanol, ethylene glycol and salicylate intoxication. An increased anion gap metabolic acidosis with respiratory alkalosis, ketosis and tinnitus suggests salicylate poisoning. An increased osmolal gap accompanied by visual symptoms suggests methanol poisoning. Pulmonary edema (ARDS) can occur with carbon monoxide, cyanide, narcotic, paraquat, phencyclidine, sedative-hypnotics, salicylate poisoning, irritant gas. Aspiration pneumonia is common in patients with coma, seizures and petroleum distillate poisoning. Radio-opaque densities may be visible in abdominal X-rays, followed by ingestion of calcium salts, chloral hydrate, enteric coated tablets, heavy metals, lithium, phenothiazine, salicylates etc. Bradycardia and AV block may occur in patients poisoned by anti-arrhythmic agents, beta blockers, cholinergic agents (carbamate and organophosphorus insecticides), digitalis, lithium.

Treatment of Poisoning
The treatment of patient consists of
I. Removal of unabsorbed poison from the body.
II. Administration of antidotes.
III. Elimination of poison by elimination.
IV. Symptomatic treatment.

I. REMOVAL OF UNABSORBED POISON FROM THE BODY
1. Inhaled poison— Patient must be removed into fresh air; artificial respiration and oxygen (6 to 8 litres per minute) should be given. Air-passages should be kept free from mucus by postural drainage or by aspiration.
2. Injected poisons—If the poison has been injected subcutaneously by a bite or injection, a tight ligature is applied immediately above wound; wound should be excised & poison sucked out.
3. Contact poisons—Removed by washing with water or should be neutralised by specific chemical.
4. Ingested poisons—

Gastric lavage is useful within three hours after ingestion of a poison.
Contraindications:
(i) The only absolute contraindication is corrosive poisoning (except carbolic acid)
due to danger of perforation,
(ii) Stomach wash is done with proper precautions in
(a) Convulsant poisons, as it may lead to convulsions.
(b) Comatose patients, because of the risk of aspiration of fluid into the air-passages.
(c) Volatile poison, which may be inhaled.
(d) Upper alimentary disease e.g. oesophageal varices
(e) In patient with marked hypothermia.

Emetics: When difficulty in obtaining or using stomach tube.
Household emetics:
(i) Large amount of warm water.
(ii) Mustard powder in warm water.
(iii) Common salt in warm water.
(iv) Vomiting can also be produced by tickling the back of the throat with a
finger, leaf twig or, wooden tongue depressor. It is the best method.
Contraindications:
(i) Same as stomach wash
(ii) Severe heart & lung diseases
(iii) Advanced pregnancy.

II. ADMINISTRATION OF ANTIDOTES
Antidotes are substances which counteract or neutralise the effect of poison.

1. Mechanical or Physical antidotes:
They neutralise poisons by mechanical action or prevent their absorption.
(a) Animal charcoal.
(b) Demulcents are substances which form a protective coating on the gastric mucous membrane and thus do not permit the poisons to cause any damage e.g. milk, starch, egg white, mineral oil, milk of magnesia, aluminium-hydroxide gel etc. Fats and oils should not be used for oil soluble poisons as kerosene, phosphorus, organo-phosphorus com¬pound, DDT, phenol, carbon tetra- chloride etc.
(c) Bulky food acts as a mechanical antidote to glass powder.

2. Chemical antidotes
They counteract the action of poison by forming harmless or insoluble compound or by oxidising poison.
(i) Common salt decomposes silver nitrate.
(ii) Albumen precipitates mercuric chloride.
(iii) Dialysed iron is used to neutralise arsenic.
(iv) Copper sulphate is used to precipitate phosphorus.
(v) Alkalies neutralise acids by direct chemical action. It is safer to give a little weak solution of an alkaline hydroxide, magnesia or ammonia. Bicarbonates should not be given because of the possible risk of rupturing the stomach due to liberated CO2
(vi) Acids neutralise alkalies by direct chemical action: Only harmless substances should be given e.g. vinegar, lemon juice, canned fruit juice.
(vii) Potassium permanganate has oxidising property. 1: 5000 solution is used in poisoning for opium, stry¬chnine, phosphorus, cyanide, barbiturate, atropine and other alkalies.
(viii) A solution of tincture iodine or Lugol’s iodine precipi¬tates most alkaloids, lead, mercury, silver, quinine, strychnine etc.
(ix) Tannic acid tends to precipitate apomorphine, cinchona, strychnine, nicotine, cocaine, aconite, pilocarpine, lead, silver, aluminium, cobalt, copper, mercury, nickel and zinc.

Universal antidote:
When the exact poison is not known, or when a combination of two or more poisons had been taken, universal antidote is given. It consists of powdered animal charcoal 2 parts; magnesium oxide 1 part; tannic acid (strong tea) 1 part. Charcoal absorbs alkaloids; tannic acid precipitates alkaloids, glucosides and many of the metals. Magnesia neutralises acids without gas formations. It is combination of physical and chemical antidotes.

3. Physiological antidotes
They act on the tissues of the body and proc exactly opposite to those caused by the poison. Atropine and physostigmine are two real physiological antidotes. Other examples are barbiturate & picrotoxin or amphetamine; strychnine and barbiturates; cyanides and amyl nitrite.

Chelating agents:
(a) B.A.L (British anti-lewisite; dimercaprol) — It is used as physiological antidote in arsenic, bismuth, mercury, copper, gold and other heavy metals. Dimercaprol has two unsaturated sulphydryl group and thus prevents union of Arsenic with the – SH group of the respiratory enzyme system.
(b) E.D.T.A. (Ethylenediaminetetra-acetic acid; calcium disodium versenate): It is a chelating agent and is effective in lead, mercury, copper, cobalt, cadmium, iron and nickel poisoning.
(c) Penicillamine (cuprimine)—It is a hydrolysis product of penicillin, having stable – SH group. It is the chelating agent of maximum efficiency for the heavy metals. Penicillamine is commonly used for the management of heavy metal poisoning of copper, lead, mercury.
(d) Desferroxamine: Useful in acute iron poisoning.

III. ELIMINATION OF POISON BY EXCRETION
1. Renal excretion:
Salicylates and phenobarbitone can be easily excreted in alkaline urine. Alkalinisation is usually carried out with sodium bicarbonate. Amphetamine, quinine and quinidine can be excreted in acid urine. Acidification can be achieved with ammonium chloride, arginine or lysine.
2. Purging:
30 gm of sodium sulphate with large amount of water hastens the elimination of poison in the stool. Magnesium sulphate should be avoided as it may produce CNS depression in cases of renal failure.
3. Diaphoretics:
Agent increases perspiration. Agents are pilocarpine nitrate, alcohol, salicylates, and antipyretics.
4. Peritoneal dialysis
Alcohols, long acting barbiturates, chloral hydrate, lithium, salicyiate & sodium chlorate are effectively removed by peritoneal dialysis.
5. Hemodialysis or Hemoperfusion
Hemoperfusion -» Many substances that cannot be removed effectively by aquous dialysis can be removed by hemoperfusion through specially designed coated charcoal columns. It has same indications as for dialysis.
Hemodialysis may be used for following poisons: BLAST
B—Barbiturates, L—Lithium, A—Alcohol-Methanol, S—Salicylates, T—Theophylline.

IV. SYMPTOMATIC TREATMENT.

Contra-indications
1. Phosphorus —» Demulcents because, they increase absorption.
2. Sulphuric acid —» Sodium bicarbonate reacts with acid and liberates CO2 gas, which may cause per¬foration.
3. Carbaryl poisoning —» Pralidoxime.
4. Oxalic acid —» Large amounts of water.
5. In Liver damage —» BAL is contraindicated. –

Preservation of Organs
1. Rectified spirit is used as preservative for many poisons except alcohol, kerosene, phosphorus, paraldehyde, carbolic .acid, acetic acid because the organic acids and paraldehyde are soluble in alcohol and the phosphorescence of phosphorus is diminished by alcohol.
2. Saturated Sodium chloride is used for preservation of organs in poisoning with—(a) Alcohol, (b) Acetic acid, (c) Carbolic acid, (d) Paraldehyde, (e) Phosphorus poisoning, (f) Corrosive poisoning, (g) Organophosphorus poisoning, (h) Lead poisoning.
3. In alcoholic poisoning—Store blood in sodium flouride + oxalate. Store urine in phenyl mercuric nitrite.
4. Never use formalin as a preservative for chemical analysis because extraction of poison, especially non-volatile organic compounds becomes difficult.
5. Minimum quantity of blood required to be preserved for chemical analysis is 10 ml.
6. Brain is preserved in Normal saline, Rectified spirit.
7. Uterus, Brain, Heart are preserved in Rectified spirit.

Organs to be preserved
1) Nails & Hairs—In chronic arsenic poisoning.
2) Skin—In gun shot injuries and when injectable poison is used
3) Heart—In strychnine poisoning, cardiac poisons, arsenic.
4) Brain—In Barbiturate, anaesthetic gas, strychnine, organophosphorus & volatile organic acid poisoning.
5) Lung—In gas poisoning (CO-poisoning), HCN, alcohol. chloroform poisoning.
6) Bone—In Arsenic, Thallium, Antimony, Lead and Radium poisoning.
7) Hair about 20 gms—In Aconite and Arsenic poisoning.
8) CSF—Alcohol poisoning & Sodium fluoride.
9) No preservatives are required—In Lungs, Long bones, Hairs & Nails.
10) Urine should be preserved in—Opium, Barbiturate, Alcohol poisoning.

Peculiar odour (smell) emitted on opening the abdomen at autopsy:
1. Fruity Ethyl alcohol
2. Kerosene like odour Kerosene, organophosphorus compounds
3. Phenolic odour Carbolic acid, lysol
4. Rotten eggs Hydrogen sulphide
5. Garlic odour Arsenic, phosphorus, thallium
6. Fishy (mushy) Zinc phosphide
7. Bitter almonds odour Cyanide
8. Burnt rope Cannabis (marijuana)

Colour changes observed with post mortem lividity (post mortem stains)
1. Purple —> In Hypoxia (due to reduced hemoglobin).
2. Chocolate colour -> In Sodium nitrite, Quinine, Potassium chlorate.
3. Cherry red —> In CO, Hydrocyanic acid poisoning.
4. Bluish green —> Hydrogen sulphide.
5. Blue —> Copper sulphate.
6. Yellow / brownish —> Phosphorus.

CORROSIVE POISONS
A corrosive poison fixes, destroys and erodes the surface with which it comes in contact. They act by extracting water from the tissues, and coagulate cellular proteins and convert haemoglobin into haemin.

MINERAL ACIDS
They produce coagulation necrosis. They have no remote action. Nitric acid produces a yellowish stain. Sulphuric acid and caustic alkalis reddish-brown stains; hydrochloric acid and carbolic acid whitish or greyish-yellow stains on the skin and mucous membranes.

SULPHURIC ACID
Sulphuric acid is the strongest corrosive poison. Pure sulphuric acid (H2SO4) is a heavy, odourless, colourless, non-fuming, hygroscopic, oily liquid and has tendency to carbonise organic substances.

Signs and symptoms:
Burns of the mouth result in excess salivation, pain, dysphonia and dysphagia. Oesophageal symptoms and signs include drooling, painful swallowing, retrostemal pain and neck-tenderness. Vomiting of blood & mucous may occur. In sulphuric acid poisoning, stomach mucosa is stained black. It is like blotting paper. The vomit is brown or black, mucoid, strongly acid, and may contain shreds of charred wall of the stomach. Teeth are chalky-white. Constipation is severe and there is tenesmus. Edema, erythema and ulceration of the oesophagus may be followed by fibrosis with stricture formation and obstruction of the gastric outlet.
Fatal dose—5 to 10 ml.
Fatal period—24 hours.

Causes of death:
(i) Circulatory collapse, (ii) Spasm or oedema of glottis, (iii) Collapse due to perforation of stomach, (iv) Toxaemia (v) Delayed death may occur due to hypostatic, pneumonia, secondary infection, renal failure or starvation due to stricture of oesophagus.

Treatment:
Gastric lavage or emetics are contraindicated. The acid should be immediately diluted and neutralised by giving 250 ml of water or milk mixed with 4 tsf. of calcium or magnesium oxide (antidote), aluminium hydroxide gel or calcined magnesia or soap water may be used. Alkaline carbonates and bicarbonates which liberate carbon dioxide should not be used as they cause gastric dilatation and sometimes rupture. Prednisolone may be given to prevent oesophageal stricture and for shock.

Post-mortem appearances:
Corrosion of the mucous membranes of lips, mouth and throat and of the skin over the chin, angles of mouth and hands is seen. The necrotic areas are at first greyish-white but soon become brown or black and leathery.
Internal
The greater part of stomach may be converted into a soft spongy black mass which disintegrates when touched. The stomach wall has a brown or black colour. Perforation may occur in sulphuric acid poisoning with the escape of the gastric contents into the peritoneal cavity. Chemical peritonitis & corrosion of organs is seen.

VITRIOLAGE (Vitriol throwing)
Throwing of sulphuric acid on another individual is known as vitriolage. Most common agent used as vitriolage is sulphuric acid. Jealous or disgruntled persons may throw a corrosive to disfigure and harm their enemies. Blindness may occur. Death may result from shock or toxaemia. The burns are painless, penetrating and the acid devitalises the tissues and predispose to infection. Sometimes, corrosive alkali or juice of marking nut or calotropis is used to disfigure the face.
Treatment:
The affected part is washed with plenty of water and soap or sodium or potassium carbonate. Later, a thick paste of magnesium oxide or carbonate is applied.

NITRIC ACID (HNO3)
Nitric acid (aqua fortis) is a clear, colourless, fuming, heavy liquid and has a peculiar and choking odour. In concentrated form, it combines with organic matter and produces an yellow discolouration of tissue due to the production of picric acid (xanthoproteic reaction).

Signs & Symptoms:
They are those of poisoning by sulphuric acid. It causes yellow discolouration of the tissues including the crowns of the teeth and yellow stains on the clothing. Inhalation of fumes causes lacrimation, photophobia, irritation of air passages and lungs producing sneezing, coughing, dyspnoea & asphyxia. Brown colour of urine is seen in Nitric acid poisoning.
Fatal dose — 10 to 15 ml.
Fatal period — 12 to 24 hours.
Post-mortem appearance:
They are those of sulphuric acid but the tissues are stained yellow, except stomach. The stomach is soft, friable and ulcerated & greenish in colour.
Treatment : Same as for Sulphuric acid.

HYDROCHLORIC ACID (HCI)
It is a pungent, colourless, fuming liquid. It is a natural constituent of the fluid of the stomach and bowels.
Signs and Symptoms:
The mucous membrane is at first grey or grey white, and later becomes brown or black, due to production of acid haematin.
Fatal dose—15 to 20 ml. Fatal period—18 to 24 hours.

OXALIC ACID
It occurs in the form of colourless, transparent, prismatic crystals, and resembles in appearance the crystals of magne¬sium sulfate & zinc sulphate. It is used as ink-remover solution in forgeries.
Action:
(i) Local— Corrosive poison. Corrodes mucous membrane of the digestive tract.
(ii) Systemic—(a) Shock, (b) Hypocalcemia, (c) Renal damage: oxalates produce tubular nephrosis or necrosis and cause death from uremia in 2 to 14 days.
Fatal dose—15 to 20 gms. Fatal period—One to two hours.
Signs and Symptoms
(a) Fulminant poisoning: There is a burning, sour, bitter taste in the mouth with a sense of constriction around the throat and burning pain from the mouth to stomach. Vomit usually contains altered blood and mucus and has a ‘coffee ground’ appearance. Thirst may be present. In oxalic acid poisoning, pulse is feeble and rapid. If life is prolonged, diarrhoea will occur.
(b) Acute poisoning: If the patient survives for a few hours, hypocalcaemia and digestive upset occurs. There is muscle irritability and tenderness, tetany usually convulsions, numbness & tingling of the fin tips & legs. Cardiovascular collapse, stupor or coma.
(c) Delayed poisoning: Symptoms of uraemia are seen. The urine may be scanty or suppressed and may contain traces of blood, albumin and calcium oxalate crystals
Treatment:
The stomach is washed out carefully using calcium lactate or gluconate. The antidote for oxalate poisoning is calcium gluconate 10%, 10 ml i.v. at frequent intervals.
Post-mortem appearances:
Mucous membrane of the tongue, mouth, pharynx a oesophagus will be whitened, as if bleached. Stomach is reddened or, eroded or, almost black. The stomach contents are gelatinous and brownish due acid haematin formation. The kidneys are swollen by oedema, congested and the tubules are filled with oxalate crystals.

CARBOLIC ACID (Phenol)
When pure, the acid consists of short, colourless, prismatic needle-like crystals, which have a burning sweetish taste, which turn pink and liquefy when exposed to air. It has a characteristic carbolic or phenolic smell. Commercial carbolic acid is dark brown liquid. It is readily absorbed from the alimentary tract, respiratory tract, rectum, vagina, serous cavities, wounds and through the skin. Phenol is converted into hydroquinone and pyrocatechoi in the body before being excreted in the urine.
Fatal dose—One to two gm.
Fatal period—3 to 4 hours.

Signs & Symptoms: —Poisoning by carbolic acid is known as carbolism.
1. Local
(a) Skin: It causes burning and numbness. It precipitates protein and coagulates cell contents. Produces white opaque eschar.
(b) Digestive tract: Hot burning pain extends from the mouth to the stomach followed by tingling and later anaesthesia.
(c) Respiratory tract: Pulmonary & laryngeal oedema develop due to irritation.
2. Systemic effects
Depressant of nervous system, especially the respi¬ratory centre. Headache, giddiness, tinnitus, muscular spasm and later collapse, unconsciousness and coma occur. The temperature is subnormal. In phenol poisoning, pupils are contracted. Breathing is stertorous. Pulse is rapid, feeble and irregular in carbolic acid poisoning. Face is covered with cold sweat, dusky cyanosis. There is strong odour of phenol in breath.
Urine is scanty and contains albumin & free hemoglobin; suppression may follow. In carboluria, the urine may be colourless or slightly green at first, but turns green or even black on exposure to air.
In the body, phenol is partly oxidised to hydroquinone and pyrocatechol, which with unchanged phenol are excreted in the urine. The further oxidation of hydroquinone and pyrocatechol in the urine is the cause of green colouration. This is known as Carboluria. The hydroquinone and pyrocatechol may cause pigmen¬tation in the cornea and various cartilages—a condition called ochronosis.

Treatment
The stomach should be washed with plenty of lukewarm water containing animal charcoal, olive oil, castor oil, magnesium or sodium sulphate or, saccharated lime with which phenol combines and forms harmless products. Magnesium sulphate or medicinal liquid paraffins should be left in the stomach.
Post-mortem appearances
Corrosion of the skin, especially in tracks from the angles of the mouth on to chin, has a greyish or brown colour. The tongue is usually white and swollen and there is smell of phenol about the mouth. The stomach mucosal folds are swollen and covered by opaque, coagulated, grey or brown thickening and looks leathery. Kidneys show hemorrhagic nephritis.

NON-METALLIC POISONS

PHOSPHORUS
There are two varieties: (1) White or crystalline, (2) Red or amorphous.
It is a protoplasmic poison, which affects cellular oxidation.

Difference between White and Red phosphorus

	Trait	White Phosphorus	Red Phosphorus
1	Colour	White or yellow	Reddish-brown.
2.	Appearance	Translucent, waxy cylinders	Amorphous, solid mass
3	Smell	Garlic like	Odourless.
4	Taste	Garlic like	Tasteless.
5.	Luminosity	Luminous in dark	Non-luminous.
6.	Exposure to air	Oxidises   &    emits   white fumes; ignites at 34°C and as such is kept under water	Non-oxidised, Non-fuming, Non-inflammable.
7.	Toxicity	Highly toxic	Non-toxic

Signs and Symptoms:
1. Fulminating poisoning
This is seen when more than 1 gm. is taken. Death usually occurs within 12 hours due to shock.

2. Acute poisoning
(A): First stage: Symptoms occur within a few minutes to a few hours & lasts 8 hours to 3 days. Ingestion produces burning pain in the throat and abdomen with intense thirst, nausea, vomiting, diarrhoea & severe abdominal pain. Breath & excreta have garlic like odour. Luminescent vomit and faeces are diagnostic. Skin contact produces painful penetrating second & third degree burns.
(B) Second stage: This is a symptom-free period lasting for 2 to 3 days.
(C) Third stage: Symptoms of systemic toxicity. There is nausea, vomiting, diarrhoea, haema-temesis. Liver tenderness and enlargement. Jaundice and pruritis. Hemorrhages occur into skin, mucous membrane & viscera, due to injury of blood vessels and inhibition of blood clotting. Renal damage results in oliguria, haematuria, casts, albuminuria. Convulsions, delirium and coma occurs. Death may result from shock, hepatic failure, central nervous system damage, hematemesis or, renal insufficiency.
Fatal dose — 60 to 120 mg.
Fatal period — 2 to 8 days.

Treatment:
1. Gastric lavage using 1: 5000 solution of potassium permanganate oxidises phosphorus into phosphoric acid and phosphates, which are harmless.
2. Antidote—copper sulphate: It coats the particles of phosphorus with a_ film of copper phosphide which is relatively harmless.
3. Vitamin K.
4. Peritoneal or hemodialysis.

Post-mortem appearances:
In acute poisoning jaundice is produced. The gastric and intestinal contents may smell of garlic and may be luminous. The mucous membranes of the stomach and intestine are yellowish or greyish white in colour. The liver becomes swollen, yellow, soft, fatty and is es ruptured. After a week, acute yellow atrophy appears.

Chronic Poisoning:
The frequent inhalation of fumes over a period of ye causes necrosis of the lower jaw in the region of a decay tooth. This condition is known as ‘Phossy Jaw’, in osteomyelitis and necrosis of the jaw occurs, with mull sinuses discharging foul smelling pus.
Poisoning:
Phosphorus is known as Diwali poison. Accidental poisoning in children may occur due to chewing of fireworks or by eating rat poison.

IODINE
It occurs as bluish-black, soft, scaly crystals and has a metallic lustre and an unpleasant taste.
Action: It is a protoplasmic poison fixing protein and causes necrosis.
Signs & Symptoms:
It acts as acid corrosive poison. There is intense thirst, vomiting and lips are stained brown. Vomiting matter -> dark yellow or blue in colour wifi peculiar odour of Iodine. Urine -» scanty, red-brown in colour.
Fatal dose: 2 to 4 gm (30 to 60 ml of tincture). Fatal period: Several days.
Chronic poisoning (lodism):
The symptoms are pain over the frontal sinus, running of nose, conjunctivitis, bronchial catarrh, salivating nausea vomiting, purging, emaciation, wasting of breasts, testes etc. and acne & erythematous patch on the skin.

INSECTICIDES AND WEED KILLERS
Insecticide poisoning is most common form of suicide.

ZINC PHOSPHIDE
It reacts with acid in the stomach and liberates phosphine. The symptoms are vomiting, diarrhoea, cyanosis, respiratory distress, fever and death.
Fatal dose: 5 gm. Fatal period: 24 hours.
It has a garlic odour in stomach contents. Blood is cherry red.

ORGANOPHOSPHORUS POISONS
They are derived from phosphoric acid and form two series of compounds
(1) Alkyl phosphates—
(i)HETP (hexaethyltetraphosphate) (ii) TEPP (tetraethyl-pyrophosphate) (iii) OMPA (octamethylpyrophosphoramide) (iv) Malathion (kill bug).
(2) Aryl phosphates—
(i) Parathion (follidol) (ii) Diazinon (tik-20).

Action: Organophosphorus insecticides irreversibly inhibit acetyl cholinesterase and cause accumulation of acetyl choline at muscarinic and nicotinic synapses.

They have three distinct toxic effects :
1. A muscarinic-like effect—Nausea, vomiting, abdominal cramps, urinary and fecal incontinence, increased bronchial secretions, sweating, salivation, urinary frequency and incontinence. Porphyrinaemia, resulting in chromolachyorrhoea (shedding of red tears) due to accumulation of prophyrin in the lacrymal gland. Contracted pin point pupils (miosis), blurring of vision may occur. In severe poisoning, bradycardia, hypotension, pulmonary edema.
2. Nicotinic sign include—twitching, fasciculations, weaness, hypertension, respiratory rate decreased with respira¬tory failure.
3. CNS effects—anxiety, restlessness, tremor, convulsic confusion, weakness and coma.
Fatal dose:
TEPP, HETP, OMPA, Parathion—80 mg i.m. or, 175 orally.
Malathion and diazinon one gram orally.
Fatal period — Usually within 24 hours.

Cause of Death:
Death is caused by paralysis of respiratory muscles, respiratory arrest due to failure of respiratory centre or intense broncho constriction.
Diagnosis is by giving atropine. Symptoms are relieved without atropinizing.

Treatment:
1. Atropine, a muscarinic receptor antagonist, should be administered for muscarinic effect upto drying of bronchial and mucous membrane secretions.
2. Pralidoxime (2-PAM), an oxime that reactivates cholineterase, is indicated for nicotinic symptoms in organophosphorus poisoning.
3. Gastric lavage and contaminated skin is washed with 2g and water.
Post-mortem appearances:
Blood stained froth is seen at the mouth and nose. The stomach content may smell of kerosene. Suicide is very common.

CARBAMATES
Carbamate insecticides include carbaryl, aldicarb, baygon, ficam and propoxur. Carbamates reversibly inhibits acetyl cholinesterase enzyme. Atropine is the antidote.

ENDRIN
It is a polycyclic, polychlorinated hydrocarbon. It is also called plant penicillin.

METALLIC POISONS

ARSENIC
Arsenic poisoning causes premalignant condition. Metallic arsenic is not poisonous, as it is not absorbed from the alimentary canal. When volatilised by heat, arsenic unites and forms poisonous vapour of arsenic trioxide.

Poisonous compounds:
1. Arsenious oxide or, Arsenic trioxide (sankhya or, somal-khar)—It is known as white arsenic or arsenic. A pinch of Arsenic trioxide can kill as many as 5 persons.
2. Copper acetoarsenate (paris green)—It combines with sulphydryl enzymes and interferes with cell metabolism.
Signs and Symptoms:
1. The Fulminant type—Large doses of arsenic can cause death in one to 3 hours from shock.
2. The Gastroenteric type —This is acute poisoning, resem¬bling bacterial food poisoning or, cholera. The stools are expelled frequently and involuntarily, are dark coloured, stinking and bloody, but later becomes colourless, odourless and water resembling rice-water stools of cholera. Dehydration with muscular cramps, cyanosis, feeble pulses, syncope, coma, exhaustion, convulsion, general paralysis and death, skin eruptions.
3. Narcotic form—Tenderness of the muscle, delirium, coma and death.
Fatal dose: 0.1 to 0.2 gm or, 100 to 200 mg. Fatal period: One to two days.

Difference between Arsenic poisoning and Cholera:

Treatment:
Freshly prepared precipitated hydrated ferric oxide (arsenic antidote) is given. In arsenic poisoning BAL is an antidote. Calcium disodium versenate. Penicillamine.
Post-mortem appearance:
Red-Velvety appearance of the stomach mucosa.
Chronic poisoning:
1. CNS—Polyneuritic, optic neuritis.
2. Skin—finely mottled brown change mostly on the temples eyelids and neck (rain drop type).
Chronic arsenic poisoning causes (i) Basal cell carcinoma. (ii) Cirrhosis of liver.
here may be a rash resembling fading measles rashes. Hyperkeratosis & Hyperpigmentation of the part and soles with irregular thickening of the nails is seen. Development of bands of opacity in the finger nails are called Aldrich-Mess lines. Arsenophagists are people who take arsenic daily as tonic or as an aphrodisiac and they acquire a tolerance of ia 0.3 gm or more in one dose.
Poisoning : Homicidal
Arsenic is the most popular homicidal poison. It delays putrefaction. It can be detected in completely decomposed body. It can be found in bones, hair and nails for a long time. It can be detected in charred bone and ashes. It is sometimes used in abortion sticks.
Tests for detection: Marsh’s test and Reinsch’s test.

MERCURY
Most poisonous salt of Hg is mercuric chloride (corrosive sublimate), occurs as colourless masses of prismatic crystals.
Symptoms — Acrid metallic taste, hoarse voice, greyish white coating of tongue, blood-stained stool, circulatory collapse, necrosis of jaw, membranous colitis, proximal renal tubular necrosis.
Fatal dose: 1 to 4 gm. Fatal period: 3 to 5 days.
Treatment:
Gastric lavage with sodium formaldehyde sulphoxylate. BAL (BALMIER) is chelator of choice. Penicillamine. 10 gm of sulphoxylate in 100 – 200 cc of distilled water by slow i.v. injection is repeated after 4 – 6 hours acts as an antidote.
Chronic Poisoning:
The symptoms are salivation, a blue line on gum, sore mouth & throat, fine tremors of the tongue, hands, arms, anaemia. Shaking palsy is associated c Hg poisoning. Mercurial tremors are also called hatter’s shakes or glass blower’s shake. Mercurial erethism is seen in persons working with mercury in mirror manufacturing firms. Erethism is characterised by shyness, timidity, irritability, loss of confidence, mental depression, loss of memory & insomnia. Mercurialentis is a peculiar eye change due to brownish deposit of mercury through the cornea on the anterior lens capsule. It is bilateral and has no effect on visual acuity.

LEAD
Acute poisoning —The symptoms are metallic taste, dry throat, peripheral circulatory collapse, paraesthesias, depression, coma and death.
Fatal dose—Lead acetate 20 gm; lead carbonate 4 gm. Fatal period—One to two days.
Treatment:
The combination of BAL and calcium disodium versenate is effective.
Chronic poisoning (plumbism)—causes:
Inhalation of lead dust and fumes by makers of white lead, smelters, plumbers, glass-polishers. Chronic poisoning results from a daily intake of one to two mg. of lead.

Signs and Symptoms:
LAPEC : L -» Lead line; A -» Anemia; P -» Palsy, Pallor, Punctate basophilia, E -» Encephalopathy; C —> Colic, consti¬pation.
Facial pallor—The facial pallor about the mouth is one of the earliest and most consistent sign. Anemia—In early stage polycythemia but later there is anaemia which is associated with punctuate basophilia, polychromasia, nucleated RBC, and an increase in mononuclear cells of microcytic hypochromic anaemia. Punctate basophilia or basophilic stippling means the presence of many dark-blue coloured pinhead sized spots in the cytoplasm of red blood cells due to toxic action of lead on porphyrin metabolism. Lead line—A stippled blue line, called Burtonian line, is seen on the gums in 50 to 70% of cases. A similar blue line is seen in cases of poisoning by mercury, copper, bismuth, iron and silver. Abdominal colic and constipation—later symptoms. Lead palsy—wrist drop, peripheral neuropathy, foot drop. Encephalopathy—Lead encephalopathy is most common in children. The symptoms are vomiting, headache, insomnia, visual disturbances, delirium, hallucinations, convulsions, coma and death. In adult, encephalopathy is rare. Menstrual irregularity—amenorrhoea, dysmenofrhoea. Renal dysfunction. Sterility.
Diagnosis:
In poisoning, the concentration of lead in blood is usually between 0.1 to 0.6 mg. per 100 ml. X-ray evidence of increased radio-opaque bands of lines at the metaphyses of long bones is seen in children.
Treatment:
Most effective treatment of plumbism is calcium-disodium versenate. BAL Penicillamine.

COPPER
Copper as a metal is not poisonous. Copper compounds are powerful inhibitors of enzymes. Ptysalism is seen in copper poisoning.
Fatal dose—15 gm. Fatal period—1 to 3 days.
Treatment: (i) Stomach wash c solution of potassium ferrocyanide. (ii) N-penicillamine.
(iii) EDTA. (iv) BAL.

ORGANIC IRRITANT POISONS

RICINUS COMMUNIS
The castor plant (arandi) grows all over India. Seeds are smooth, flattened-oval, mottled, light and dark brown. Entire plant is poisonous, containing toxalbumen RICIN, a water-soluble glycoprotein and a powerful allergen (CBA). A toxalbumen or phytotoxin is a toxic protein, which resembles a bacterial toxin in action and causes agglutination of red cells with some hemolysis and is antigenic.
Signs and Symptoms—Symptoms include salivation, bloody diarrhoea, impaired sight, delirium, convulsions, uremia and jaundice. The powder of seeds when applied to the eye causes conjunctivitis.
Fatal dose—Ten seeds; ricin 6 mg.
Fatal period—Two to several days.
P.M. appearances—Ricin produces haemorrhagic inflamma¬tion of the G.I. tract.

CROTON TIGLIUM
Croton tiglium (Jamalgota or naepala) seeds contain toxalbumen CROTIN and CROTONOSIDE, a glycoside, which is not expressed with the oil. Seeds are oval, dark-brown with longitudinal lines.
Signs and Symptoms —There is hot burning pain from mouth to stomach, salivation, vomiting, purging, vertigo, prostration, collapse and death.
Fatal dose — 4 seeds; 1.5 cc. of oil.
Fatal period — 6 hours to 3 days.
Treatment: Stomach wash, demulcent drink and symptomatic treatment.

ABRUS PRECATORIUS
It is also known as Jequirity or Indian liquorice (gunchi or, rati). The seeds are egg-shaped, bright scarlet colour with a large black spot at one end. The seeds contain an active principle abrin, a toxalbumen, which is similar to viperine snake venom.
In seeds also present is abrine, an amino acid, haemoglutinin in the cotyledons, a lipolytic enzyme, and abralin, a glycoside.
Signs and Symptoms:
After ingestion, symptoms include abdominal pain, diarrhoea, weakness, cold perspiration, trembling of the hands, weak rapid pulse and rectal bleeding. When an extract of seeds is injected under the skin of the animal, inflammation, oedema, oozing of hemorrhagic fluid from the site of puncture, necrosis. The animal drops down after 3 to 4 days. Tetanic convulsions occur.
Fatal dose — 90 to 120 mg. by injection, 10 gm. orally. Fatal period — 3 to 5 days.
Poisoning — The seeds are used for killing cattle, small sharp-pointed spikes on needles or ‘suis’ are prepared which are then dried in the sun.
Treatment: Injection with antiabrin.

ERGOT
Ergot is the dried sclerotinum of the fungus Calviceps purpurea, which grows on cereals like rye, barley, wheat, oats etc. It contains alkaloids, ergotoxin, erqotamine. and ergometrine.
Signs and Symptoms:
In acute cases, there is nausea, vomiting, diarrhoea, giddiness, tightness in the chest, difficulty, in breathing, marked muscular weakness and exhaustion. There may be tingling and numbness in the hands and feet, paraesthesias, followed by twitchings or cramps in the muscles Bleeding from nose and other mucous surface is common.
Chronic poisoning:
There is tingling and numbness of the skin, vasomotor disturbances leading to dry gangrene of the fingers. There is a sensation of insects creeping under the skin (tactile hallucination).
Fatal dose—One to two gm. Fatal period—One to several days.
Poisoning: The consumption of bread made with contaminated rye is the chief cause of ergotism. Ergot is commonly used as an abortifacient.

SEMECARPUS ANACARDIUM
Marking nuts (bhilawa) are black, heart-shaped with rough projections at the base. Their pericarp contains an irritant juice which is brownish, oily and acrid but turns black on exposure to air.
The active principles are semecarpol and bhilawanol.
Signs and Symptoms:
The lesion resembles a bruise. The juice, when applied externally causes irritation and a painful blister, which contains acrid serum.
Fatal dose — 5 to 10 gm.
Fatal period — 12 to 24 hours.

CALOTROPIS
The juice is taken by mouth or introduced into uterus on an abortion stick for criminal abortion and as a cattle poison. Also used as arrow poison. To produce artificial bruise. The juice produces an acrid bitter taste, salivation, dilated pupils, tetanic convulsions, collapse and death.
Treatment: Stomach wash, demulcents and symptomatic.

SNAKES
The Poisonous snakes may be divided into five families—
1. Cortalidae — Pit viper, Rattle snake, Bush master.
2. Viperidae (true viper) — Russel’s viper, Saw-scaled viper.
3. Elapldae — Cobra and Krait
4. Hydrophidae — Sea snakes
5. Colubridae — Boom slangs, Bird snakes.
In India, out of 200 species of poisonous snakes, five are dangerously poisonous to man. — King cobra, cobra, common krait, Russell’s viper and saw-scaled viper.
The most common poisonous snake is Common krait. Rat-snake is a non-poisonous snake.

Difference between Poisonous and Non-poisonous snakes

Snake venom:
1) The venom of the Indian cobra (Naja-Naja) contains a neurotoxin, a hemolysin, a cardiotoxin, a cholinesterase, phosphatidase.
2) Venom of pit viper contains hyaluronidase and proteolytic enzyme.
3) Venom of elapids {cobra, krait) are neurotoxic. Death occurs from respiratory paralysis.
4) The viperine venom is mainly hemolytic, causes intra-vascular hemolysis and depression of coagulation mechanism.
5) The sea snake venom is myotoxic.

Clinical manifestations—The most common manifestation following snake bite (poisonous or non-poisonous) is fright.
Cobra:
Local symptoms start within 6 to 8 minutes. The bitten area is tender with slight burning pain. The patient feels sleepy, slightly intoxicated, weakness of legs and is unable to stand or move. There may be extra-ocular muscle weakness, ptosis and strabismus. Coma sets in and finally the respiration stops with or without convulsions and the heart stops.

Krait:
There is no swelling and burning pain at the site of the bite.
True viper (Russel viper):
When venom is injected, the spot develops severe pain, the swelling starts within 15 minutes. Tingling and numbness over the tongue and mouth or scalp and paraesthesia around the wound occur. The main feature is persisting shock. A hemorrhagic syndrome with blood stained sputum, hemorrhages from gums, rectum, the site of bite etc. occur due to increased coagulation time. Intravascular hemolysis may lead to hemoglobinuria and renal failure.

Sea-snakes:
After half to one hour, the patient develops pain, stiffness, and weakness of the skeletal muscles.
Fatal dose: — Cobra 12 mg; Russell’s viper 15 mg; Echis 8 mg; Krait 6 mg, of dried venom.
Fatal period: — Cobra half to six hours; viper one to two days.
Treatment: Polyvalent antisnake venom serum should be given to neutralise the poison.

CANTHARIDES
The powder of dried body of Spanish fly (blister beetle) is used externally as an irritant.

SOMNIFEROUS POISONS

OPIUM
Opium (afim) is also known as Kasoomba or, Madak or, Chandu. Opium is the dried juice of the poppy (papaver somniferum).
Opium contains two chemically different groups of alkaloids—
(a) The phenanthrenes—morphine 10%, codeine 0.5% and thebaine 0.3%, which are narcotic.
(b) The isoquinolines—papaverine 10% and narcotine 6%, no narcotic property.
The artificial derivatives are heroin, dihydromorphine.
Opiates exert their effects because of their chemical similarity to natural substances called endorphins. Opioid drugs are capable of producing physical addiction, and also psychological and euphoria.
Fatal dose — opium 2 gm.; morphine 0.2 gm. Fatal period — 6 to 12 hours.

Signs and Symptoms:
The contact of morphine with the skin of sensitive persons may cause erythema, urticaria and itching dermatitis. It first stimulates, then depresses and finally paralyses the nerve centres.
I. Stage of excitement—There is a sense of well being, increased mental activity, freedom from anxiety, talka¬tiveness, restlessness, hallucinations, flushing of face, maniacal condition.
II. Stage of stupor—The symptoms are headache, incapacity for exertion, a sense of weight in the limbs, giddiness, drowsiness and stupor.
III. Stage of coma—The patient passes into deep coma from which he cannot be aroused. The pupils are contracted to pinpoint size and do not-react to light, but in late stage they may be found to be dilated. — An overdose of narcotics cause hypotension, depressed reflexes and coma (except — dilated pupils).
Differential diagnosis of Opiate poisoning:
1) Opium poisoning—The odour of breath, bradycardia, pinpoint immobile pupils, stertorous respiration, slow pulse, moist perspiring skin are prominent features.
2) Acute alcoholic poisoning—Pupils are dilated and reacting.
3) Barbiturate poisoning—Shallow respiration, deep coma, no response to painful stimuli, deep reflexes are depressed, low blood pressure, dilated pupils.
4) CO poisoning—Intermittent convulsions, cherry red colour of skin and carboxy-hemoglobin in blood.
5) Uraemic coma—Cheyne-Stokes respirations, ammoniacal odour.
6) Diabetic coma—Deep respirations with air, hunger, odour of acetone in heart, sugar and acetone in the urine.

Treatment:
Naloxone hydrochloride is a specific opioid antagonist. Atropine is not recommended. N-allyl normorphine (lethidrone or nalorphine) is a specific antidote for morphine codeine, pethidine and methadone. Naltrexone is 17 times more potent than naloxone. When coma is deep -» artificial respiration and oxygen. Substitution with oral methadone, followed by gradual withdrawal of methadone.
Post-mortem appearances:
Signs of asphyxia are prominent. Froth is seen at the mouth and nostrils. The brain, meninges and abdominal organs are congested.
Chronic poisoning (morphinism; morphinomania):
The patient becomes restless, irritable, disturbed by dreams or insomnia. Loss of memory, mental fatigue, gradual intellectual, and moral deterioration occur. Constipation, contracted pupils, impotence are frequent.
Withdrawal symptoms of opioids tend to be opposite to the acute effects of the drug and include nausea and diarrhoea, coughing, lacrimation, rhinnorrhea, profuse sweating, twitching muscles, and piloerection or, goose bumps (except—miosis).
In addition, sensations of diffuse body pain, insomnia and yawning occur with intense drug craving.
Test for detection: Marquis test.

INEBRIANT POISONS

ETHYL ALCOHOL
Absolute alcohol contains 99.95% alcohol; rectified spirit contains 90% alcohol.
The approximate percentage of alcohol in beverages is— Rum and liquors—50 to 60%; Whisky, gin, brandy 40 to 45%; Port, Sherry 20%; Wine 10 to 15%; Beers 4 to 8%.
Arrack—It is a liquor distilled from palm, rice, sugar or jaggery etc. and has a strength of 40 to 50%. It may be mixed with chloral hydrates and potassium bromide for getting a greater kick.
Absorption—About 20% of alcohol is absorbed from the stomach and 80% through small intestines.
Action:
Alcohol is a well known stimulant, but is a selective depressant, especially of the higher nervous centres which it inhibits. It is a hypnotic and diaphoretic.
Symptoms:
1. Stage of excitement—There is increased confidence and a lack of self control. When jerking movement is in the direction of the gaze and independent of the position of the head, it is known as alcohol gaze nystagmus and appears at blood levels of 40 to 100 mg/100 ml. Mental concentration is poor and judgement impaired. These effects are usual between 50 to 150 mg/100 ml of blood alcohol.
2. Stage of incoordination—When alcohol content of the blood attains a level of 150-250 mg/100 ml.
3.Stage of coma—The person passes into a state of coma with stertorous breathing. The pupils are contracted, but stimulation of the person e.g., by pinching or slapping, causes them to dilate with slow return (Mc Evan sign).

Death occurs from asphyxia due to respiratory paralysis, but it may occur from shock.
‘Legal intoxication’ requires a blood alcohol concentra¬tion of atleast 80-100 mg/dl.
Fatal dose — 150 to 200 ml of absolute alcohol consumed in 1 hour.
Fatal period — 12 to 24 hours.
Treatment — Hemodialysis and peritoneal dialysis is performed.

Chronic poisoning:
Alcohol addicts are people, who cannot stop drinking for long, or who experience withdrawal symptoms. Chronic alcoholics are those who have reached a state of irreversible somatic or brain changes caused by alcohol.
Treatment:
Antabuse (disulfiram) is given in a single daily dose. Antabuse inhibits the enzyme aldehyde dehydroqenase. Antabuse leads to accumulation of acetaldehyde (aldshyde syndrome) in the blood and tissues and causes unpleasant symptoms, such as flushing, palpitation, anxiety, sweating, headache, abdominal cramps, nausea and vomiting due to which the patient dislikes alcohol.

DRUNKENNESS
A person is held responsible for crime committed in the voluntary drunkenness condition.
‘Widmark’s formula‘ is used to calculate the quantity of ethyl alcohol in the body. The widmark formula is a = prc, where (a) is the weight of alcohol in gm in the body (p) is the body weight in kg (c) is the concentration of alcohol in blood in mg/kg and (r) is a constant (0.6) for men and (0.5) for women.
Widmark’s formula for urine analysis, is a = ¾ prq, where (q) is the alcohol concentration in mg/kg.
Delirium tremens occur in chronic alcoholics due to (1) temporary excess (2) sudden withdrawal of alcohol (3) shock after receiving an injury, such as fracture of a bone, or (4) from acute infection, such as pneumonia, influenza, erysipelas etc.

All individuals with a blood alcohol level of 140 mg % are intoxicated to the point where they cannot deal with unusual, emergency or non-customary problems. Law in some countries have made it an offence to driye a motor vehicle above a specified blood alcohol level; e.g. England — 80 mq %, and USA — 150. mg %

Below 10 mg% = Sober, 20 – 70mg% = Drinking, 80 – 100 mg% = Under the influence, 150 – 300 mg% = Drunk, 400 mg% and above = Coma and death.
Saturday night paralysis occurs in the stage of coma and due to pressure on the radial nerve.
Breath analysis machines operate on the principle that alcohol absorbs radiation in the infra-red region of the spectrum and that the amount of infra-red light absorbed by a vapour is proportional to the concentration of alcohol in that vapour. 60 to 100 ml of breath received into a dry baloon and analysed by drunkotester, intoximeter, alcometer, alcotest or breathalyser.

The person is asked to blow into a plastic balloon through a glass tube, containing a crystalline bichromate-sulphuric acid mixture. If blood alcohol is 80 mg% or more, the crystals will become green to a predetermined distance. The test may be false positive because alcohol may remain in the mouth even after a small drink. The residual alcohol in the mouth disappears in 20 minutes. As such, the test should be repeated after 20 minutes.

METHYLALCOHOL
Mineralised methylated spirit consists of 90% of ethyl alcohol, 9.5% of wood naphtha and 0.5% of crude pyridine.
Signs and Symptoms:
There may be delirium and coma. Urine is strongly acid and may contain acetone and a trace of albumin. Acidosis is caused. The pupils are dilated and fixed. Visual disturbances like photophobia and blurred vision, concentric diminution of visual fields for colour and form, followed by sudden loss of vision or complete blindness occur due to optic neuritis and atrophy..
Fatal dose — 60 to 240 ml. Fatal period — 24 to 36 hours.
Treatment:
(i) Gastric lavage with 5% bicarbonate solution. (ii) Ethyl alcohol. (iii) Hemodialysis is the treatment of choice in severe poisoning.
The most effective treatment of withdrawal of ethyl alcohol including delirium tremens is Benzodiazepines.

BARBITURATES
Barbiturate administration is contraindicated in Porphyria, Anaphylaxis and Asthma. They have a depressant action on the central nervous system. Large doses directly depress the medullary respiratory centre. Involuntary suicide is accidental barbiturate poisoning.

Signs and Symptoms:
The first symptom is usually drowsiness. A short period of confusion, excitement, delirium and hallucination is common. Hypothermia, cyanosis, hypotension, weak rapid pulse and cold clammy skin occurs. The pupils are usually slightly contracted but react to light; they may dilate during terminal asphyxia. Respiration becomes irregular, sometimes Cheyne-Stokes in character and finally stop (respiratory depression). The finding of blisters on the skin, often at the area of erythema, strongly suggests barbiturate poisoning. Death may occur from respiratory failure or ventricular fibrillation in early stage and bronchopneumonia and irreversible anoxia in later stage (flaccid coma).

The combination of alcohol and barbiturate causes rapid death.
Fatal dose: Short acting—1 to 2 gm. Medium acting— 2 to 3 gm. Long acting—3 to 5 gm.
Fatal period: 1 to 2 days.
Treatment:
— No specific antidote.
1. Gastric lavage, with warm water mixed with potassium permanganate and a suspension of animal charcoal or tannic acid.
2. Supportive measures (i.e. ABC) (i.e. Airway, Breathing, Circulation).
3. Forced alkaline diuresis – it is helpful only in long acting barbiturates which are eliminated primarily by renal excretion.
4. Hemodialysis & Hemoperfusion (through a column of activated charcoal) – is highly effective in removing long acting as well as short acting agents. Therefore it is better than forced alkaline diuresis.
Scandinavian method uses anti-shock measures, maintenance of airway and adequate respiratory support.
Chronic poisoning:
Dependence is both psychic and physical.

CHLORAL HYDRATE
It is colourless, crystalline substance having peculiar pungent odour and a pungent bitter taste. It depresses CNS.
Fatal dose — 5 to 10 gm.
Fatal period — 8 to 12 hours.
Poisoning:
Accidental poisoning results by taking large doses as hypnotic. It is given in food or drink to render a person suddenly helpless for the purpose of robbery or rape. Its action is so rapid that it has been given the name ‘knockout drops’.
A combination of alcohol and chloral hydrate is commonly known as ‘Mickey Finn’

PETROLEUM DISTILLATES KEROSENE
Signs and Symptoms:
If the fumes are inhaled, there is feeling of dizziness, headache, nausea and vomiting. There may be pneumonitis, intense excitement, hallucina¬tions and convulsions, the person becomes unconscious & passes into coma. After ingestion, there is usually burning pain in throat nausea, vomiting, colicky pain and diarrhoea. There is giddiness, heaviness in the head, dyspnoea, cyanosis, drowsiness and coma.
Fatal dose — 15 to 30 c.c. of kerosene. Fatal period — Within 24 hours.

DELIRIANT POISONS

DATURA FASTUOSA
There are two varieties:
(i) Datura alba—white flowered plant.
(ii) Datura niger—a deep purple flowered plant.
The fruits are spherical and have sharp spines (thorn-apple). Datura stramonium is known as thorn apple. They contain 0.2 to 1.4% of hyoscine (scopolamine), hyoscyamine, and atropine.
Signs and Symptoms:
A bitter taste, dryness of mouth and throat, dysphagia, voice hoarse, Fever. The face becomes flushed, conjunctivae congested, widely non-reacting dilated pupils, temporary blindness, photophobia and diplopia. Restlessness, agitation. Delirium is restless and purposeless; in earlier stage indicated by excitement, talkativeness and unintelligent speech. Hallucinations of sight and hearing and delusion occurs.
Fatal dose — 1 gm (100 to 125 seeds).
Fatal period —. 24 hours.
Treatment:
Physostigmine is specific in Datura poisoning. Pilocarpine nitrate.
Poisoning: —Crushed or powdered seeds or an extract is used by criminals for stupefying a victim prior to robbery, rape or kidnapping.
Mydriatic test—The pupil dilates within half an hour, if datura is present.

CANNABIS SATIVA OR INDICA
It is also known as Indian hemp, hashish or marihuana. The principal constituent of resin of marijuana is tetrahydro cannabinol. It is a CNS stimulant.
It is used in the following forms:
1. Bhang—It is prepared from the dried leaves and fruit shoots.
2. Majoon—It is a sweet prepared with bhang. It increases appetite and sexual desire.
3. Ganja—It is prepared from the flower tops of female plant.
4. Charas or hashish—It is the resin exuding from the leaves and stems of the plant.
Signs and Symptoms
Large doses cause –
1. Inebriation—The person becomes dreamy or semi¬conscious and he has realistic vision, usually of sexual nature e.g. he sees nude beautiful women dancing before him, playing music, singing sexual love song. It causes psychological high, raises heart rate, delays psychomotor skills.
2. Narcosis—There is giddiness and ataxia, tingling and numbness of the skin, general anaesthesia.
Fatal dose—Charas 2 gm; ganja 8 gm; bhang 10 gm/kilo body weight.
Fatal period—Several days.
Chronic poisoning:
Used in excess, it causes degeneration of CNS. There is loss of appetite, weakness, wasting, tremors, vacant look, red eyes, impotence, mental deterioration. Rarely, they become insane, and may suffer from hallucinations and delusions of persecution. There may be an impulse to kill. The person may run amok i.e. he develops a psychiatric disturbance marked by a-period of depression followed by violent attempt to kill people. He first kills a person against whom he may have real or imaginary enemitv. and then kills anyone that comes in his way until homicidal tendency lasts. Then he may commit suicide or surrender himself.
Poisoning—Majoon and charas are sometimes used by road poisoners to stupefy person to facilitate robbery.

COCAINE
It is obtained from leaves of Erythroxylum coca. It is colourless, odourless, crystalline substance with bitter taste. It is used as a local anaesthetic, acts as a vaso constrictor. The usual route of intake is snorting and skin popping.
Signs and Symptoms:
(i) Stage of excitement—There is bitter taste, dryness of mouth, fatigue, black teeth and tongue & visual hallucination (ii) Stage of depression—Within an hour, respirations become feeble, collapse, convulsions and death occurs. Death is due to respiratory failure or vascular collapse.
Fatal dose — 1 to 1.5 gm orally.
Fatal period — Few hours.
Treatment — Amyl nitrite is antidote and given by inhalation.
Cocaine habit—The patient may surfer from hallucinations, convulsions, delirium and insanity.
Magnan’s symptoms or cocaine bug is characteristic, in which there is feeling as if grains of sand are lying under the skin or some small insects are creeping on the skin (tactile hallucinations).

DRUG DEPENDENCE
Drug addiction—The most important drugs of addiction are alcohol, opium, pethidine, heroin, barbiturates, cannabis and amphetamine.
Drug habituation (habits) -There is psychological or emotional dependence on the drug.
Drug dependence—It includes both the term addiction and habituation.
Addiction consists of physical and psychological dependence.

Withdrawal symptoms:
May begin within 6 to 8 hours following stoppage of drug. It includes chilliness, yawning and rhinorrhoea, goose skin, lacrimation. gross tremors, and dilatation of pupils are seen. Narcotic addicts may be killed by a hot shot i.e. a dose of narcotic with a poison as strychnine in it.
Psychoactive Drug classification:
1. Sedatives—Barbiturates, minor tranguilisers, alcohol.
2. Stimulants—Amphetamines, cocaine.
3. Opiates—Heroin, methadone, morphine.
4. Marihuana.
5. Major tranquilisers—Chlorpromazine.
6. Anti depressants—Tricyclics, MAO Inhibitors. (Mono Amino Oxidases)
MAO – A inhibitors — Clorgiline Moclobemide
MAO – B inhibitor — Selegeline (Depremyl).

Cocaine and LSD do not produce physical dependence. Street heroin is known as smack, junk or dope. Amphetamines cause paranoid, psychosis and psychic dependence. Hallucinogenic drugs—LSD, phencyclidine (angel dust).

FOOD POISONING
BACTERIAL FOOD POISONING
In the infection type, organisms belong mainly to salmonella, proteus, coli, streptococcus, shigella. In the toxic type, is due to ingestion of preformed toxin in prepared food.
—Exotoxins e.g. enterotoxin of staphylococci and the botulinum toxin, produce intoxication.
Incubation period of staphylococcal food poisoning is 1-6 hours.

BOTULISM
There are no symptoms of gastroenteritis (i.e. no diarrhoea) It is caused by neurotoxjn, an exotoxin of clostridium botulinum multiplied in the food e.g. tinned meat| fish, fruits etc.
The fatal dose, for an adult is 0.01 mg, The toxin paralyses the nerve ending.
Signs and Symptoms:
The incubation period is 12 to 30 hours. There is nausea, vomiting, constipation, ocular pharyngeal paralysis, salivation, sometimes aphonia. Excessive fatigue, diplopia. marked muscular weakness. The patient is conscious till death, which is preceded by coma or-delirium. Bulbar palsy and descending paralysis is seen.
Differential diagnosis of botulism includes Tetanus, Epilepsy and Acute gastroenteritis.

LATHYRUS SATIVUS (Khesari dal)
Consumptjon exceeding 30% of the total diet for more than 6 months; produces lathyrism. The active neurotoxic principle is B(N)-oxalyl aminoalanine -> BOAA.
The continuous use of L. sativus produces neurolathvrism, characterised by progressive spastic paraplegia, sphincters, sensation and mental faculties are preserved.

ARGEMONE MEXICANA
The Argemone oil contains two alkaloids -> sanguinarine and dihydro sanguinarine. Causes epidemic dropsy.
Hypersecretory glaucoma, Diarrhoea, CCF are seen iq —> Epidemic dropsy (But no convulsions). Sanguinarine interferes with the oxidation of pyruvic acid, which accumulates in blood.
The symptoms of epidemic dropsy consists of sudden non¬-inflammatory, bilateral swelling of legs.
Tests for detection of Argemone oil are
(i) Nitric acid test: The colour becomes brown to orange-red shows presence of Argemone oil, positive when concentration is 0.25 percent.
(ii) Paper chromatography test: This is the most sensitive test. It can detect argemone oil up to 0.0001 percent in all edible oils and fats.-

SPINAL POISONS
STRYCHNOS NUX VOMICA
Mechanism of action of strychnine poisoning is post synaptic block. Strychnine (kuchila) is a powerful alkaloid obtained from the seeds of the strychnos nux vomica. The seeds contain two principal alkaloids -> strychnine 1.5% and brucine 1 55%. Strychnine poisoning resembles tetanus poisoning. The action is particularly noted in anterior horn cells. In strychnine poisoning convulsions affect all muscles at a time. The mouth is covered with froth, frequently blood stained. The convulsions are most marked in antigravity muscles, so that the body typically arches in hyperextension opisthotonus. Sometimes spasm of abdominal muscle may bend the body forward (emprosthotonus), or to the side (pleurosthotonus). Consciousness is not lost.
Fatal dose — 30 to 100 mg; one crushed seed.
Fatal period — One to two hours.
Treatment:
(i) Short acting barbiturates, (ii) Diazepam, (iii) Stomach wash with potassium permanganate.
Post-mortem appearance — In strychnine poisoning, brain is required to be preserved.
Post-mortem caloricity is seen in strychnine poisoning.

CARDIAC POISONS
Cardiac poisons are
(i) Nicotiana tabacum (ii) Digitalis purpurea (iii) Nerium odurum (iv) Yellow oleander (v) Cerbera odallam (vi) Quinine
(vii) Aconite — Fatal period : 1 – 8 hours, antidote : atropine. (viii)Hydrocyanic acid.

DIGITALIS (D. purpurea, D.lanata, Strophathus gratus)
Entire plant is toxic, containing over 30 cardiac and steroidal toxins. The roots, leaves and seeds of digitalis contain digitoxin, digitonin and digitalin.
Action: By inhibiting the Na+K+ATPase. Digitalis prolongs the diastolic period of the heart. In therapeutic doses, it depresses both excitability and conductivity. But in toxc dose, excitability is increased with extrasystole.
Signs and symptoms:
Nausea, vomiting, abdominal pain, nervous irritability, tingling and coldness in extremities, increased heart rate, varying degrees of AV block, ectopic beats, coupled rhythm, Atrial Fibrillation and Ventricular Fibrillation. Patient becomes drowsy, coma sets in and death occurs.
Fatal dose: 15 to 30 mg of digitalin, 4 mg of digitoxin,
Fatal period: 1 to 24 hours.

Treatment:
(1) Stomach wash with tannic acid
(2) Bowels should be evacuated
(3) Specific antidotes (i) 100 mg lignocaine i.v / dilantin / propranalol
(4) Trisodium EDTA to lower serum Ca level.
(5) Potassium salts to reduce extrasystoles and arrythmias.
(6) Bradycardia is treated with atropine sulphate 0.6 mg i.v repeated for 4 days.
(7) Symptomatic.

NERIUM ODORUM (White oleander)
Grow wild in India.
All parts of plant are poisonous, containing several cardiac glycosides, primarily oleandroside (oleandrin), and nerioside (nerin), which resembles digitalis in action.
Signs and symptoms:
It produces contact dermatitis. Ingestion causes difficulty in swallowing and articulation, abdominal pain, vomiting, profuse frothy salivation, and diarrhoea. Pulse is at first slow, then later rapid and weak, BP falls, respiratory rate increased, pupils dilated, muscular twitchings, tetanic spasm, lock-jaw, drowsiness, coma, respiratory paralysis and death occurs.
Fatal dose: 15 gm of root.
Fatal period: 24 to 36 hours.

CERBERA THEVETIA (Yellow oleander)
All parts are poisonous. Seeds contain 3.5 to 4% of the cardiac glycoside thevetin. which is similar to digitalis in action, others are thevetoxin, nerifoliun, peruvoside and ruvoside and cerebrin.
Signs and symptoms:
Pulse is rapid, weak and irregular, BP low. Heart block, collapse and death from peripheral circulatory failure.
Treatment:
(1) Stomach wash
(2) Sodium molar lactate transfusion with glucose and 1 mg. atropine, 2 cc adrenaline and 2 mg noradrenaline.
(3) Symptomatic.

CERBERA ODALLUM (Pilikirbir)
Active principles: Cerberin, cerebroside, odollin, odolotoxin, thevetin and cerapain.
Signs and symptoms:
Initial symptoms are gastro-intestinal. Cardiac toxicity within 3 hours of ingestion. There is bitter taste, nausea, severe retching, vomiting, abdominal pain and in few cases diarrhoea, general weakness, blurring of vision, sinus bradycardia, irregular respiration, collapse and death from heart failure.
Chief bio-chemical changes are Hyperkalemia, and depression of transaminase activity.
Fatal dose: Kernel of one fruit.
Fatal period: 1 or 2 days or more.
Treatment:
(1) Stomach wash
(2) Atropine 0.5 mg i.v and repeated every 15 to 30 min to keep heart rate above 50 per minute
(3) Correct hyperkalemia.

QUININE
It is a strong protoplasmic poison with anaesthetic and sclerosing action. It stimulates and then depresses central nervous system.
Signs and symptoms:
Headache, giddiness, ringing in the ears, partial deafness, disorders of vision, pupils are fixed and dilated. Mental confusion, pain in the abdomen, nausea and vomiting, confusion of thought, muscular weakness, itching, erythematous or urticarial rash on the skin, methaemoglobinemia, tachycardia, hypotension, cyanosis, delirium and coma.
Fatal dose: 8 to 10 gm.
Fatal period: Few minutes to 2 days.
Treatment:
(1) Gastric lavage
(2) i.v. fluids to promote diuresis
(3) Bilateral stellate ganglion blocks causes return of vision.
(4) Symptomatic.

HYDROCYANIC ACID
It is also called prussic acid or cyanogen. The pure acid is a colourless, transparent volatile liquid with an odour like bitter.almonds. Cyanides are white powders. More than 5% carboxyhemoglobin is seen in cyanide poisoning. Cyanide inhibits the action of cytochrome oxidase and carbonic anhydrase. It kills by creating histotoxic or cvtotoxic anoxia. Cyanide acts by reducing the oxygen carrying capacity of the blood, and by combining with the ferric iron atom of intra-cellular cytochrome oxidase, prevents the uptake of oxygen for cellular respiration.
Signs and Symptoms:
Massive doses may produce sudden loss of consciousness and prompt death from respiratory arrest. People suffering from achlorhydria may not suffer from toxic effect of oral ingestion of potassium cyanide. The mouth is covered with foam which is sometimes blood-stained. Death occurs from respiratory failure.
Fatal Dose -50 to 60 mg of pure acid; 200 to 300 mg of potassium cyanide.
Fatal period—2 to 10 minutes.
Treatment:
(i) Amyl nitrite is used by inhalation. (ii) Sodium nitrite is given i.v. (iii) Sodium thiosulphate in 50% solution i.v. converts cyanide to non-toxic thiocyanates.
(iv) Methylene blue i.v. (v) Cobalt EDTA. (vi) Para amino prophenone (PAPP) acts by forming meth.Hb. (vii) Qxygen.
P. M. appearance:
The blood is bright cherry red due to formation of cyan-met-haemoglobin. The post mortem staining may be cherry-red or brick red.

ASPHYXIANTS
CARBON MONOXIDE
It is a colourless, tasteless, non-irritant gas which is produced due to incomplete combustion of carbon. It is insoluble in water. It burns with a blue flame.
Upper limit of safety of carbon monoxide in air is 0.01%.
50% COHb produces symptoms like alcoholic intoxication. 50%-60% produces syncope or coma with intermittent convulsions. Exposure of atmosphere containing 0.2% of gas will cause death in about 4 hours, 0.4% in one hour, and 10% in 20 to 30 minutes.
Symptoms of CO poisoning:

Carboxyhaemoglobin (COHb)%

Symptoms

0 to 10% 10 to 20% 20 to 30% 30 to 40% 40 to 50% 50 to 60% 60 to 70% 70 to 80% Above 80%

= No appreciable symptoms= Breathlessness on moderate exertion, mild headache= Throbbing headache, irritability, emotional instability, disturbed judgment, defective memory and rapid fatigue= Severe headache, nausea, vomiting, dizziness, dimness of vision, confusion. = Increased confusion, sometimes hallucinations, severe ataxia, rapid respirations and collapse with attempts at exertion = Syncope or coma with intermittent convulsions, rapid respirations, tachycardia with a weak pulse and pink or red discoloration of the skin. = Increasing depth of coma with incontinence of urine and faeces. = Profound coma with depressed or absent reflexes, a weak thready pulse, shallow and irregular perspiration. = Rapid death from respiratory arrest

P. M appearance: Death by CO poisoning is called Conflagration.
A cherry – red colouration of the skin, mucous membranes, areas of hypostasis. Fine froth may be seen at mouth and nose. Bilateral symmetrical necrosis of the lenticular nuclei and punctiform hemorrhages in the white matter of brain.

HYDROGEN SULPHIDE
It is found in large quantity in sewer –> sewer gas. It has a smell of rotten eggs.

WAR GASES
(i) Vesicant—Mustard gas, lewisites.–
(ii) Asphyxiant—Chlorine, phosgene.
(iii) Tear gases—Chlor acetophenone (CAP), ethyloidoaretate (K.S.K), bromobenzyl cyanide (B.B.C.).
(iv) Nerve gases—They are compounds related to phosphate easters in action and toxicity.

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