Classification of Poisons (according to mode of action








Strong Acids

Strong Alkalis

Mineral Acids

Organic Acids

Vegetable Acids

• Corrode means wearing off • Chemicals that cause the destruction of tissues due to there nature of action • Mechanism of action
– Corrodes the mucus membrane of GI tract – Conversion of hemoglobin into haematin – Coagulation of cellular proteins – Extraction of water from the tissue


Strong Acids

Strong Alkalis
Caustic potash and Soda, ammonium hydroxide

Mineral Acids
(Sulphuric acid, nitric acid, hydrochloric acid)

Organic Acids
(Oxalic acid, Carbolic acid, Acetic acid, Salicylic acid)

Vegetable Acids
(Hydrocyanic acid)

Mineral Acids
Sulphuric Acid (H₂SO₄) Nitric Acid (HNO₃) Hydrochloric Acid (HCl)

Mineral Acids
• Act locally
• On GI tract • Respiratory tract

• No systemic action except
• Shock

• Mode of action
– Extraction of water from the tissue – Coagulation of cellular proteins – Conversion of hemoglobin into haematin

Steps of management (Case of mineral acid poisoning)
• • • • • • • History (accidental, suicidal) Sign / symptoms Early Investigations Differential diagnosis General treatment according to s/s Late investigations Specific treatment

• History • Usually accidental intake of poison due to
• Keeping acid in bottle of juices with juice label

General signs :• • • • • • Anxious look Dilated pupils, sunken eyes Erosion of mouth, lips or both Rapid but feeble pulse Skin cold and slight sticky Noisy respiration / dyspnoea

• Sulphuric acid: Brown or black discoloration. • Nitric acid: yellow stain • Red line of demarcation

Symptoms :Immediately after swallowing, • Burning sensation of mouth lips entire GI tract, Resp tract due to inhalation of fumes • Difficulty in swallowing due to swelling of throat • Nausea, • Vomiting, vomitus contain shredded blood stained material, dark brown and black in color. • Difficulty in breathing • Constipation / diarrhea

Early and late
– 5cc blood sample
• • • • • • • Blood complete picture (anemia) LFTs (normal) RFTs (oxalic acid poisoning deranged) Blood sugar (normal) Serum Electrolytes (K, Na, Ca++) Urine Routine examination scanty urine vomitus to forensic chemical laboratory

• Differential diagnosis a) Acid poisoning b) Alkali poisoning

EFFECT Injury Necrosis Burns Edema Scar Charring Alkali Severe Liquefaction Deep Marked Acid Less severe Coagulation 2nd degree Mild

Soft, edematous, Hard translucent Not seen Seen

The most important step in the management of a poisoned patient is, what to do? In what order to do?

What to do? It is much more important step to think, than to provide an agent to reduce absorption of poison or to counteract its effects. The fact is Patient must be treated first and then the Poison.

Once the victim is stabilised, only then try to identify the poison, its quantity involved and how much time has passed. SO THE FLOW CHART OF MANAGEMENT WILL BE,

After clinical evaluation of the patient and after saving the life of the patient, the next aim should be, 1) Removal of unabsorbed poison 2) Elimination of absorbed poison from the body 3) Treatment of general condition and symptoms

Steps of management will be, 1) Clinical evaluation 2) Non- Specific Anti-doting 3) Dilution of poison 4) Emesis 5) Adsorbents

6) Cathartics 7) Gastric Lavage 8) Forced Diuresis 9) Demulcents 10) Dialysis & Haemo- perfusion 11) Specific Anti-doting

• Stomach tube and emetics are

contraindicated • However soft stomach tube (levine tubes) can be passed within one hour to prevent serious caustic burns.

ACID POISON: Alkaline carbonates & bicarbonates - contraindicated • Weak alkalis e.g. calcium and magnesium hydroxide along with plenty of water or neutralizing agents like milk and egg albumin is given ALKALI POISON:  Neutralize poison by giving acids like acetic acid,citric acid mixed with large quantity of water

• • • • •

Morphine: to relieve pain Ice: to relieve thirst IV fluids: to compensate fluid loss Steroids: Shock To prevent esophageal strictures Keep the airway patent • Tracheostomy: Acute edema of glottis • Poisoning by ammonia vapors give oxygen

• Keep the patient NPO • Nutrient substances are given by IV route for about a week. • Try liquids,soft food and finally a regular diet. • Antibiotics to prevent infection

IMMEDIATE • Shock • Suffocation: edema/spasm of glottis • Gastric perforation DELAYED (quantity of poison small) • Hypostatic pneumonia • Esophagial stricture :(emaciation and malnutrition) • Secondary infections

Depends on: • Quantity • Strength of acid • Time the patient survives after intake of acid

• Corrosion of mucus membranes of lips, mouth, throat & skin over the chin, angles of mouth & hands. • Necrotic areas - brown or black and leathery. • More marked in cases of sulphuric acid poisoning. • Tissues poisoning. stained yellow in nitric acid

• Gastric perforation: esp with sulphuric acid • Irritation of respiratory tract: (volatile poisons like nitric acid, HCL)

Attempted Suicides: • Not seen now a days due to use of less painful substances like barbiturates, narcotics & organo-phosphorous compounds. For Homicides: • Rarely; because of taste, immediate local action & physical changes it produces in food.

Vitriolage: • Throwing of a corrosive on face out of jealously or rage. Accidental: • Severe injury or death. Abortifacient: • Sulphuric & hydrochloric acid

• Throwing of any corrosive on a person with malicious intent. • These fluids are usually thrown on face for destroying vision or causing facial disfigurement. • Results in Grievous Hurt.

(H₂SO₄) ₂SO₄

Characteristics of pure form: • Heavy • Odorless • Colorless • Non fuming,oily liquid Commercial preparation: • Brown or black in color • Fatal period 12 – 24 hrs. • Fatal dose 5 – 10 ml.

• Mode of action:The acid has great affinity for water and damages the tissue by dehydration. Acid produces a grey white necrotic membrane with swelling of the affected surface followed by brownish or black discoloration.

• Sulphuric acid - Commonly used Causes chemical burns • Burns are painless, penetrating • Acid devitalizes tissues, predisposes to infection. • Repair is slow • Scar causes contractures. • Death may result from shock, toxemia if extensive areas are involved

• Sulphuric acid: Brown or black discoloration and staining of skin and clothing. • Nitric acid: yellow stain • Trickle marks • Red line of demarcation not present

Sites likely to be effected by local contact 1- skin / face 2- mouth and throat 3- upper alimentary tract 4- respiratory tract

Early effect

1- pain and shock 2- vomiting 3- dyspnoea due to respiratory obstruction from laryngeal odema

Late effect
1- Perforation of stomach 2- Pulmonary odema / bronchopneumonia

Delayed effect
1- oesophageal or pyloric stricture 2- laryngeal stricture 3- pulmonary fibrosis

Treatment :Relief from pain. i/v morphine To prevent thirst. Ice To prevent fluid loss. i/v fluids To prevent shock and esophageal stricture. Steroid therapy • To maintain airway open • • • •
– In case of acute odema of glottis. Trecheostomy

Treatment :• Antidote :- for sulphuric acid

• Milk of Magnesia or • Mixture of soap and water
Mechanism :- Neutrilization of acid pH

• On Skin: Wash the corrosive acid with large amount of water and soap or dilute solution of sodium or potassium bicarbonate.  Thick paste of magnesium oxide is applied  Raw surface - covered with antibiotic ointment

Eyes:• Washed with large amount of water and irrigated by 1 % solution of sodium bicarbonate. • Eye drops containing steroids and

antibiotics are helpful

• If ingested:• Milk of magnesia or lime water or soap water or wood ash • Demulcent drinks like barley water, beaten eggs

Postmortem appearence
 Sign of corrosion Lips, mouth & surrounding skin, cheeks, chin  Pupils dilated  Carbonisation :- Due to extraction of water from tissue and conversion of hemoglobin into haematin. Entire GI tract appear as black, dried, swollen, charred mass.  Tongue black corroded shapeless mass.  Teeth chalky white appearance.  No systemic effect but due to gastric perforation near by organs may be partly corroded.

Medicolegal Aspects
• Accidental intake because of its color and due to keeping acid in bottles with juice label • mistaken as medical syrups, whisky • Vitriolage: Throwing of a corrosive on face out of jealously or rage.

Nitric Acid

• Characteristic features:– Yellowish liquid – Very irritating fumes

• Commercial Preparation:Light Yellow to Orange in color depends upon concentration Use in the manufacturing of nickel ornaments, coloring matters, separating gold from other metals.

• Mechanism of action:– Xanthoprotic Reaction:-

• Nitric acid reacts with organic matter to form picric acid (yellow color), tissue therefore stained yellow.

• Sign and Symptoms:– When swallowed
• Tissues are not blackened but stained yellow • Due to highly irritable fumes respiratory symptoms are also pronounced. • No charring no perforation

– Additional symptoms are lacrimation, sneezing, coughing, dyspnoea, cynosis, odema of lungs, suffocative bronchitis.

• Fatal Dose:– Adult ------------ 15- 20 ml only depends upon site and extend of damage

• Fatal Period:– Within 24 hr

• Treatment:– Same as for sulphuric acid

Postmortem Appearence
• Same as for acid burns • Mouth lips deeply stained yellow orange brown. • Stomach stained yellow • Vomitus yellowish in color with irritating fumes • Inflammation of larynx, acute pulmonary odema

Hydrochloric Acid


Hydrochloric Acid
• • • • • • • Colorless gas Irritating odor Extremely soluble in water (light yellow) In houses used as a cleaning agent Gives off fumes at temp slightly above ordinary temp Fatal dose:- 20-30ml Fatal period:- 24-30 hours

Strong Acid Sulphuric Acid Common uses

Nitric Acid

Hydrochloric Acid

Batteries, Separating Toilet / floor pipe & drain Gold from cleaner cleaner other ornaments, paint preperation corrosion, coagulation & dehydration

Mode of Action


Strong Acid Sulphuric Acid

Nitric Acid

Hydrochloric Acid

Sign / Symptoms Fatal dose

Thirst, Erosion of Tissues are Thirst, dyspnea, mouth, lips, stained Yellow, dysphagia, pain. Dyspnea lacrimation due to fumes.

5 – 10 ml

10 – 15 ml 24 hr

15 – 30 ml 30 hr

Fatal Period 12 hr

Medicolegal aspects

Accidental Abortifacient Vitriolage

Accidental Vitriolage

Accidental Vitriolage

Thank You

The Strong Acids are, a.) Mineral Acids, like Sulphuric acid, Nitric acid, Hydrochloric acid. b.) Organic acids, like Oxalic acid, carbolic acid, Acetic acid, Salicylic acid. C.) Vegetable Acids, like Hydro-cyanic acid.

Oxalic Acid

• OXALIC ACID • Synonyms: Ethanedioic acid, dihydrate; oxalic acid dihydrate • Chemical Formula: HOOCCOOH.2H2O • It occurs in the form of • colourless, • transparent, • prismatic crystals and • resembles in appearance the crystals of magnesium sulfate & zinc sulphate. • It is used as ink-remover solution in forgeries.

Commercial Uses of OXALIC ACID
• It is used in the process of rust removal because it forms a water-soluble complex ion (chelate) around each iron ion.

Oxalic acid is found in some bleaches and household cleaning products

1) It is used by those pre-treating stainless steel. 2) The most common uses of oxalic acid are in tanning leather and removing rust and ink stains. 3) The potassium and calcium salts of oxalic acid are found naturally in cabbage, spinach, and rhubarb leaves. 4) The metabolism of sugar by many species of mold results in the production of oxalic acid. Ingestion of large amounts can cause kidney damage, convulsions, and death.

• Mechanism of Action:Oxalic acid is corrosive to tissue. When ingested, oxalic acid removes calcium from the blood. Kidney damage can be expected as the calcium is removed from the blood in the form of calcium oxalate. The insoluble calcium oxalate then obstructs the kidney tubules.

• 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.

• • •

(a) Fulminant poisoning: (b) Acute poisoning: (c) Delayed poisoning:

Signs and Symptoms
• (a) Fulminant poisoning:
• 1. There is a burning, 2. sour and acidic taste 3. Sense of constriction around the throat and burning pain from the mouth to stomach. 4. Vomit usually contains altered blood and mucus and has a 'coffee ground' appearance. 5. Thirst may be present. 6. In oxalic acid poisoning, pulse is feeble and rapid. 7. 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.

• Chronic Exposure: May cause inflammation of the upper respiratory tract. Prolonged skin contact can cause dermatitis, cyanosis of the fingers and possible ulceration. May affect kidneys. • Aggravation of Pre-existing Conditions: Person with pre-existing skin disorders or eye problems, or impaired kidney or respiratory function may be more susceptible to the effects of the substance.

• First Aid Measures • Inhalation: Remove to fresh air. If not breathing, give artificial respiration. If breathing is difficult, give oxygen.

• Ingestion: DO NOT INDUCE VOMITING! Give large quantities of limewater or milk to drink. Never give anything by mouth to an unconscious person.

• Skin Contact: In case of contact, wipe off excess from skin then immediately flush skin with plenty of water for at least 15 minutes while removing contaminated clothing and shoes. • Eye Contact: Immediately flush eyes with gentle but large stream of water for at least 15 minutes, lifting lower and upper eyelids occasionally.

• •

Fire Fighting Measures Fire: Oxalic Acid is a combustible solid below 101C (215F) Explosion: Reacts explosively with strong oxidizing materials and some silver compounds. Fire Extinguishing Media: Water spray, dry chemical, alcohol foam, or carbon dioxide. Foam or water on molten oxalic acid may cause frothing. Water spray may be used to keep fire exposed containers cool.

• If material comes in contact with water, neutralize liquid with alkaline material (soda ash, lime), then absorb with an inert material (e.g. vermiculite, dry sand, earth) and place in a chemical waste container. Do not use combustible materials, such as saw dust. Do not flush to sewer.

Post-mortem appearances:
• Mucous membrane of the tongue, mouth, pharynx and 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

• 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 pyrocatechol in the body before being excreted in the urine.

• Phenol is also used in the preparation of cosmetics including sunscreens, • hair dyes, and • skin lightening preparations. • Compounds containing phenol moieties can be used to prevent ultraviolet light-induced damage to hair and skin

Fatal dose— 10-15 gm./ 20 drops. 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 scar. (b) Digestive tract: Hot burning pain extends from the mouth to the stomach followed by tingling and later anaesthic action on Stomach • (c) Respiratory tract: Pulmonary & laryngeal oedema develop due to irritation.

• 2. Systemic effects
1. Depressant of nervous system, especially the respiratory centre. 2. Headache, giddiness, tinnitus, muscular spasm and later collapse, unconsciousness and coma occur. 3. pupils are contracted. 4. Breathing is stertorous. 5. Pulse is rapid, feeble and irregular 6. Face is covered with cold sweat, dusky cyanosis. There is strong odour of phenol in breath. 7. Urine is scanty and contains albumin & free hemoglobin; suppression may follow. 8. In , the urine may be colourless or slightly green at first, but turns green or even black on exposure to air. oxidation of hydroquinone and pyrocatechol in the urine is the cause of green colouration. This is known as Carboluria. 9. The hydroquinone and pyrocatechol may cause pigmentation 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.

Vegetable acid Hydrocyanic Acid (HCN)

• It acts as portoplasmic poison • inhibit enzyme cytochrome oxidase and • prevent uptake of oxygen by the cell i.e interference with cell respiration leading to death of cell. • Oxygen is there incirculation but cell cannot utilize it. • Leading to hypoxia and death of cell.

HCN is highly volatile and corrosive.
• Occurrence:– Present in various fruits like
• Peaches, plums and bitter almonds and cherries.
– In these fruits it exists in the form of amygdalin (glucoside) which is harmless.

– In gaseous state it is use to disinfect ships and buildings as well as trees.

• HCN is colorless gas, • Highly soluble in water, • Volatile – quickly absorbs through lungs and even through skin in contact. • Odor of bitter almond

• Mode of entry:– HCN is soluble in water. Rapidly absorbs from mucous membrane, sudden death – If inhaled very toxic, victim may not even utter a cry, if survives then he may show,

• Symptoms and signs
– – – – – Bitter almond smell in breath Convulsions Dilated and fixed pupil Dysponea, loss of muscle power, nausea death

Derivatives of HCN HCN + Strong Alkalies

• Sodium cyanide and • potassium cyanide are white powder, librate HCN when comes in contact with Acid (gastric HCl).

• Use in laboratories where electroplating, coating silver, photography, • Ca++ cyanide is used as fertilizer. Mode of action:Cyanides comes in contact with HCl converted in to Hydrocyanic acid which is then absorbed from gastric mucosa. It acts as portoplasmic poison inhibit enzyme cytochrome oxidase and prevent uptake of oxygen by the cell i.e interference with cell respiration leading to death of cell.

Fetal dose = 60 drops of crude oil of bitter Almonds
Fetal Period = 2 – 10 mins

Sign and symptoms
• • • • Are mainly due to anoxia of cell Organs effected first are brain, causes dizziness, unconsciousness blood, non utilization of oxyhemoglobin result in pink coloration of arterial and venous blood • small blood vessels, dilation due to paralysis • and cardiac as well as sk muscles looses power of contraction and results in circulatory collapse , flushed skin.

Postmortem appearence
• Externally:– Mouth, lips, cheeks becomes pinkish – Nails cyanosis – Post mortem staining is pink in color

• Internally:– Characteristic bitter almond odor is present in brain, serous membrane and stomach – Mucous membrane of stomach is pink

Principle of Treatment is to reverse the
cyanide- cytochrome combination. This is achieve by convertiing hemoglobin in to methemoglobin to form non-toxic cynmethaemoglobin.

• Treatment : • without specific antidote life cannot be saved. • Amyl nitrite inhalation, sodium nitrite iv, sodium thiosulphate iv may be given at the same time. • Gastric lavage with sol of sodium thiosulphate. • 100% oxygen

• Postmortem findings: • Externally: signs of asphyxia
– cyanosed – Blue nails – PMstaining PINK in color

• Internally:
– Bitter Almond smell – Mucous mem of stomach may be pink in color

• Medicologal Aspects:– Suicidal poison of choice.
• It is cheep, readily available, death is instantaneous. • Use commonly by terrorist commit suicide when feel necessary

– Accidental poisoning:
• In labs photo studios, if cyanide sol is thrown in wash basin already containing caustic soda (washing powder) HCN liberated suddenly, fumes inhalation cause instantaneous death.

Caustic potash and soda


Strong Acids

Strong Alkalis
Caustic potash and Soda, ammonium hydroxide

Mineral Acids
(Sulphuric acid, nitric acid, hydrochloric acid)

Organic Acids
(Oxalic acid, Carbolic acid, Acetic acid, Salicylic acid)

Vegetable Acids
(Hydrocyanic acid)

• • • •

Washing powders, cleansing agents, drainpipe cleaners, paint removers.

• Toxicity is due to • rapid absorption of water from tissues • Combines with fat and protein
– Form soap and proteinates – Soft necrotic tissue.

• Corrosive symptoms like
– Burning pain from mouth to stomach – Errosion of mucous membrane – Stricture formation – Anxious look and feeble pulse.

• • • •

Strong soapy nauseating taste Vomitus is soapy, blood blood stained Fatal Dose: approx 5gm Fatal Period: 24hrs to months or even year miserable death occur due to weakness and starvation

• Treatment: • Neutralize the acid
– By giving weak acids like vinegar, lemon or orange juice.

• Postmortem Appearance:
– Tissues come in contact are soapy, soft and swollen.

• Medicolegal acpects:
– Suicide – Vitriolage – Accidental poisioning

• Thank You

Irritant group includes, a.) In-organics b.) Organics c.) Mechanical substances

In-Organics consists of, A. Metals B. Non-Metals Metals are, Arsenic, Antimony, Mercury, Lead, Copper, Zinc, etc. Non-Metals are Phosphorus, Chlorine, Iodine, Bromine



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.


• 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
White Phosphorus Trait 1 Colour White or yellow Translucent, waxy cylinders Garlic like Garlic like Luminous in dark Reddish-brown. Amorphous, solid mass Odourless. Tasteless. Non-luminous. 2. Appearance 3 4 Smell Taste Red Phosphorus

5. Luminosity 6. Exposure to air

Oxidises & emits Non-oxidised, Nonwhite fumes; ignites at fuming, Non34°C and as such is kept inflammable. under water Highly toxic Non-toxic

7. Toxicity

• 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 years 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 luster 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 respiratory 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.