Corosive Poison

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CORROSIVE POISON

K.Ashika Rizwana
CORROSIVE POISON
ACTION : Destruction of the tissue on local applications.
Act by

01 02 03

Extracting Coagulate Haemoglobin to


water from cellular haematin
tissues. proteins. convert.
CORROSIVE POISON
ACTION :Destruction of the tissue on local applications.
Act by

01 02 03

Extracting Coagulate Haemoglobin to


water from cellular haematin
tissues. proteins. convert.
CORROSIVE POISON
ACTION :Destruction of the tissue on local applications.
Act by

01 02 03

Extracting Coagulate Conversion of


water from cellular Haemoglobin to
tissues. proteins. haematin.

Also known as caustics.


Classification
Corrosive poison

Acid Alkali
( Coagulative necrosis ) ( liquefactive necrosis )

Inorganic acids Organic acids


1. Ammonia
 Carbolic acid 2. Potassium hydroxide
 Sulphuric acid 3. Potassium carbonate
 Nitric acid  Oxalic acid
4. Sodium hydroxide
 Hydrochloric acid  Formic acid 5. Sodium carbonate
 Acetic acid

Exception : Hydrofluoric acid


(inorganic acid)
CARBOLIC ACID ( phenol C6H4OH )
USES
PHYSICAL CHARACTERS : : ANTISEPTIC
DISINFECTANT

 Needle like crystal


 Colourless
 Prismatic
 PHENOL
solubility PHENOL
CRYSTAL

Exposure to air
CARBOLIC ACID ( phenol C6H4OH )
USES
: ANTISEPTIC
DISINFECTANT
PHYSICAL CHARACTERS :

 Needle like crystal


 Colourless
 Prismatic
Freely soluble: glycerine, Ether, alcohol, benzene
 solubility

Slightly soluble: water


PREPARATIONS
Absorption: Alimentary canal, Respiratory Tract, Serous cavity, rectum,
 Lysol vagina.

 Dettol Metabolite: Hydroquinone, Pyrocatechol.


 Resorcinol
Detoxified: Liver.
 Cresol
 Thymol Excretion: Kidney (urine).

 Tannic acid
FATAL DOSE : 10 to 15 gm / 25 to 50 ml
 menthol FATAL PERIOD : 3 to 4 hrs
ACTION
Poisoning by carbolic acid is carbolism

LOCAL

SKIN Respiratory tract Digestive tract


 Burning and Numbness  Pulmonary and laryngeal oedema.  Hot burning pain.
 Damage to the Nerve ending  Bronchitis.  Deglutition And Speech.
 White opaque Eschar  Bronchopneumonia.  Leathery stomach mucosa.
 Respiratory failure.  Lips, mouth, tongue corroded.
 Nausea and vomiting.
SYSTEMIC

 Respiratory failure.
 CNS depression.
 Convulsion.
 Constriction of pupils.
 Respiratory alkalosis.
 Metabolic acidosis.
 Dusky cyanosis.
 Methemoglobinemia.
 Haemolysis.
 Liver damage.
Urine:
 Contains Albumin & Free Haemoglobin.
 Colourless / slightly green in colour.
 CARBOLURIA – ( acute poisoning ).

Chronic poisoning : PHENOL MARAMUS

 Anorexia.
 Weight loss.
 Headache.
 Vertigo.
 Dark urine.
 Pigmentation in the cornea & various cartilages.
Urine:
 Contains Albumin & Free Haemoglobin.
 Colourless / slightly green in colour.
 CARBOLURIA – ( acute poisoning ).

Chronic poisoning : PHENOL MARASMUS

 Anorexia.
 Weight loss.
 Headache.
 Vertigo.
 Dark urine.

 Pigmentation in the cornea & various cartilages. oochronosis


Cause of death

1. Syncope
2. Asphyxia
Treatment

1. No emetics.
Cause of death 2. Gastric lavage.
3. 10% glycerine.
4. Administration of olive oil &
1. Syncope paraffin.
2. Asphyxia 5. Saline with 7g of sodium
bicarbonate in (iv).
6. Haemodialysis.
7. Methylene blue (iv).
POSTMORTEM APPEARANCE

External Internal
 Mucosa of oesophagus is tough.
 Corrosion of the skin, angle of mouth on to  Stomach mucosal folds are swollen, opaque,
chin. coagulated.
 Tongue ( become white and swollen ).  Mucous membrane is thickened and looks
 Smell of phenol about the mouth. leathery.
 Mucous membrane of lips, mouth and the  Stomach may contain reddish fluid.
throat is corrugated, sodden, whitened / ash  Liver and spleen usually show a whitish and
grey. hardened patch.
 Numerous small submucous haemorrhages.  Kidneys haemorrhagic nephritis.
 Brain is congested and oedematous.
 Blood is dark, semifluid & partially coagulated.
 Laryngeal & pulmonary oedema.
TEST

10% ferric chloride solution to one ml of urine.

BLUE colour

Circumstances of poisoning :

• Suicidal purposes.
• Accidental poisoning.
• ( Rarely ) homicide.
• Injected into vagina & uterus to produce abortion.
FORMIC ACID

Characteristics :

 Colourless liquid
 Penetrating odour
Action:

 coagulation necrosis
Uses:  Haemolysis
 ATP Synthesis is diminished
 Electroplating
 Tanning
 Rubber
 Textile
 Paper industry
 Stain remover
FATAL DOSE: 50 to 200ml
SIGNS AND SYMPTOMS

GIT CNS RS

 Drowsiness Acute respiratory


 Burning pain.
 Coma distress
 Salivation.
 Vomiting.  Dilated pupils
 Mucosal ulceration.
 Corrosion.
 Haematemesis.

Blood
CVS
 Tachycardia / Bradycardia  Shock and death.
 Hypertension / Hypotension  Haemdysis

SKIN Blisters
SIGNS AND SYMPTOMS

GIT CNS RS

 Drowsiness Acute respiratory


 Burning pain.
 Coma distress
 Salivation.
 Vomiting.  Dilated pupils
 Mucosal ulceration.
 Corrosion.
 Haematemesis.

Blood
CVS
 Tachycardia / Bradycardia  Shock and death.
 Hypertension / Hypotension  Haemdysis

SKIN Blisters
SIGNS AND SYMPTOMS

GIT CNS RS

 Drowsiness Acute respiratory distress.


 Burning pain.
 Salivation.  Coma
 Vomiting.  Dilated pupils
 Mucosal ulceration.
 Corrosion.
 Haematemesis.

Blood
CVS
 Tachycardia / Bradycardia  Shock and death.
 Hypertension / Hypotension  Haemdysis

SKIN Blisters
SIGNS AND SYMPTOMS

GIT CNS RS

 Drowsiness Acute respiratory


 Burning pain.
 Coma distress.
 Salivation.
 Vomiting.  Dilated pupils
 Mucosal ulceration.
 Corrosion.
 Haematemesis.

Blood
CVS
 Tachycardia / Bradycardia  Shock and death.
 Hypertension / Hypotension  Haemdysis

SKIN Blisters
SIGNS AND SYMPTOMS

GIT CNS RS

 Drowsiness Acute respiratory


 Burning pain.
 Coma distress.
 Salivation.
 Vomiting.  Dilated pupils
 Mucosal ulceration.
 Corrosion.
 Shock
 Haematemesis. Shock andand
death
death.

CVS Blood
 Tachycardia / Bradycardia  Haemolysis
 Hypertension / Hypotension

SKIN Blisters Metabolic acidosis : shock and death


SIGNS AND SYMPTOMS

GIT CNS RS

 Drowsiness Acute respiratory


 Burning pain.
 Coma distress.
 Salivation.
 Vomiting.  Dilated pupils
 Mucosal ulceration.
 Corrosion.
 Haematemesis.

Blood
CVS
 Tachycardia / Bradycardia  Haemolysis
 Hypertension / Hypotension

SKIN : Blisters Metabolic acidosis : shock and death


SIGNS AND SYMPTOMS

GIT CNS RS

 Drowsiness Acute respiratory


 Burning pain.
 Coma distress.
 Salivation.
 Vomiting.  Dilated pupils
 Mucosal ulceration.
 Corrosion.
 Haematemesis.

Blood
CVS
 Tachycardia / Bradycardia  Haemolysis
 Hypertension / Hypotension

SKIN :Blisters Metabolic acidosis , shock and death.


Treatment
 MILK is given for dilution of acid.
 Gastric lavage and emetics are contraindicated.
 Folinic acid 1mg/kg (iv).
 Dialysis (or) exchange transfusion.

Postmortem appearance
 Corrosion.
 Blackening of gastric mucosa.
 Pulmonary oedema.

Poisoning is suicidal (or) accidental.


BORIC ACID

Used as Detergent

Antiseptic and insecticide. To produce hydrogen sulphide gas


in car
Closet and enclosed spaces.
Fatal: 15 to 20gm

Symptoms
Chemical suicide
Boiled lobster Boiled lobster appearance.
appearance Generalised Erythema. Committing suicide.
Desquamation of massive area.
OXALIC ACID (C2H2O4)

( Acid of sugar; salt of sorrel )

Characteristics About 20mg is excreted in urine daily

 Colourless
 Transparent
 Prismatic crystals
 It resembles the crystals of MAGNESIUM SULPHATE & ZINC SULPHATE

Source Uses

 Spinach.  Remove stain


 Rhubarb.  To clean brass or copper articles
 Cabbage.  Calico printing
Action:

LOCAL
Crystal of the acid and concentrated solution of more than 10% of oxalates are corrosive
poisons.
Rarely : skin
Readily : mucous membrane of the digestive tract.

SYSTEMIC
Shock: Large dose cause rapid death.
Hypocalcaemia : Feature of tetany.
Oxalic acid + calcium ions

Calcium oxalate crystals Hypocalcaemia

OXALURIA
Feature of tetany

Needle shape / envelope shaped casts

Comes out in urine Blocks tubules

Renal damage lead to renal failure

Tubular necrosis Tubular nephrosis


FATAL dose : 15 to 30 gm
FATAL period : 1 to 2 hours

Fulminating poisoning Acute poisoning


 Occurs by large dose
 Large concentrated dose of 15 gm  Hypocalcaemia
 Sense of constriction  Digestive upset
 Burning pain ( from mouth to stomach )  Muscle irritability
 Vomit usually coffee ground appearance  Convulsions
 Signs of cardiovascular collapse
 Coma, stupor.

Delayed poisoning
 Uraemia
 Urine contain blood, albumin, calcium oxalate crystals.
 Ventricular fibrillation
Treatment
 The stomach is washed out carefully by Calcium lactate (or)
gluconate.
 Antidote: any preparation of calcium.
 Calcium gluconate 10%, 10 ml i.v. at frequent intervals.
 Dialysis (or) exchange transfusion.
 Parathyroid extract 100 units in i.v. severe cases.
 Demulcent drinks.
 Symptomatic.
 Evacuated by an enema or by caster oil.
POSTMORTEM APPEARANCE

 Tongue, mouth, pharynx and oesophagus is corrugated.


 Softened in patches but perforations is rare.
 Stomach content are gelatinous and brownish.
 Stomach will become corroded.
 Intestine escapes usually.
 Duodenum may affected.
 Kidneys are swollen and tubules are filled with oxalate crystals.
 Congestion of lungs, liver, kidney and brain.

Circumstances of poisoning

 Accidental poisoning.
 Suicidal poisoning is rare.
 Homicidal poisoning is rare.
 Rarely, used to procure abortion by vaginal injection.
CAUSTIC ALKALIS
Physical characters:
 Used in commerce.
 Occurs as white powder.
 Ammonia is colourless gas.
 Ammonium hydroxide is a liquid.

Action :
 Chemical burns.
 Hydroxide ion produces saponification of fat.
 Cellular dehydration.
 Exothermic reaction.

Liquefaction necrosis
Stricture formation is much more common with alkalis than with acids.
Sign and symptoms

 Vomited matters are alkaline & do not effervesce on contact with the ground.
 Purging is a frequent symptom.
 Contact with skin causes the greyish, soapy, Necrotic area.
 Mucosa of digestive tract is swollen, soft and detached.
 In oesophagus – transmural necrosis (NaOH) LYE .
 Oesophagus stricture is a major long term complication.
Properties of agents
 Household bleaches
 Detergents
 Drain cleaners
 Ammonium hydroxide 3% usually causes minor irritations but
at higher concentration can cause severe injury to oesophagus
and stomach
 Miniature ( button ) Batteries – potassium hydroxide
Fatal period: usually 24 hours.

Fatal dose:
 Potassium (or) sodium hydroxide 5 gm
 Potassium carbonate 18 gm
 Sodium carbonate 30 gm
 Ammonia 15 to 20 ml
Treatment

 Demulcents.
 In mild cases the stomach can be washed carefully.
 In poisoning by ammonia vapour, oxygen inhalation.
 Keep the airway patent.
 Tracheostomy may be necessary.
 Give adequate parenteral analgesics.
 Antibiotics to prevent infection.

• Caustic alkalis produce a brown precipitate with silver nitrate.


Test : • Caustic carbonate produce a white-yellow precipitate.
Circumstances of poisoning
 Poisoning by alkali is rare.
 Accidental cases (mistake for medicine)
 Homicidal poisoning is rare.
 Few suicidal cases.
Acids Alkali

1. Causes coagulative necrosis. 1. Causes liquefactive necrosis.


2. Eschar formation due to precipitation of proteins. 2. No Eschar formation.
3. Prevents further lateral spread of acid.
4. Superficial injury. 3. unrestricted lateral spread of alkali.
5. Less dangerous. 4. Deeper damage.
6. Mucosal Involved: gastric > oesophageal 5. More dangerous.
Inorganic acid organic acid 6. Mucosal involved: gastric < oesophageal
Only local effects local + systemic effects
7. Strong acids (PH< 2 ) causes tissues damage.
7. Strong alkali ( PH>11.5 ) causes tissues damage.
THANK YOU

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