University of science& technology

IBB-branch , Medical Science Faculty

Bachelor of Pharmacy Students
Level-4

Toxicology- Lecture NO-(5)

 CORROSIVE POISONS
Definition: any substance that in contact with living tissue will cause destruction
by its chemical action

Classification

A. Inorganic acids B. Caustic alkali C. Organic acids D. Metal (mineral salts)

1. Sulfuric acid 1. Na hydroxide 1. Oxalic acid 1. Mercuric chloride
2. Nitric acid 2. K-hydroxide 2. Carbolic acid 2. Antimony chloride
3. HCl acid 3. NH4OH 3. Acetic acids.
Examples of Common Acids and Alkalis:
A. Acids:
1. Hydrochloric acid: used in:
− Swimming pool cleaners.
− Toilet bowl cleaners ( Flash or Harbic).
− Dye manufacturing
Examples of Common Acids and Alkalis
2. Sulfuric acid: used in
− Battery acid
− Toilet bowl cleaners.
− Wine fermentation.
3. Nitric acid: used in
− In electroplating.
− Fertilizer manufacturing.
Examples of Common Acids and Alkalis
B. Alkalis:
1. Na and potassium hydroxide used in:
− Oven cleaners
− Detergents.
− Paint removers
− Washing powders
2. Ammonium hydroxide: used in:
− Detergents
− Bleaching agents
− Jewelry cleaners
C. Others:
1. Clorox liquid (Na hypochlorite- NaClO)
2. Swimming pool sanitizers (Na hypochlorite- NaClO)
3. Tide (Na silicate- Na2SiO3).
I. Inorganic acids (Mineral acids):
Examples:
1. Sulfuric acid,
2. Hydrochloric acid
3. Nitric acid.
Common sources:
Industry, laboratories, domestic use, agriculture and explosives
manufacturing.
Appearance:
− H2SO4:
1. Colorless
2. Odorless
3. Hygroscopic liquid. i.e. it has a great affinity to absorb water, causing
charring of any organic matter when it comes in contact with it.
− HCl:
1. Colorless or yellow volatile liquid.
− HNO3:
1. Colorless
2. Highly volatile (fuming)

3. More liable to produce respiratory symptoms and edema glottis.

Mechanism of action of Corrosives
Mode of poisoning:
1. Accidental: /
2. Homicidal: /
3. Suicidal: X
Clinical features:
1. Corrosion of the skin and mucus membranes.
2. Severe burning pain from the mouth down the stomach.
3. Vomiting.
4. Clothes may show streaks of charting.
5. Pulmonary complications e.g. pneumonia, edema glottis.
6. Corneal corrosions.
Fatal dose:
− Conc H2SO4 : 5-10 ml
− Conc HNO3: 10-15ml
− Conc HCL: 15 -20ml

Postmortem Picture (P.M.P):

1. Sulfuric acid:
Corrosions with brown or black discoloration of tissues & mucous
membrane .
2. Hydrochloric acid:
Corrosions with grey or red -white color
3. Nitric acid:
Yellow coloration of affected tissues
2. Corrosive alkalis
Examples:
1. NaOH (caustic soda)
2. KOH (caustic potash).
3. Sodium carbonate (washing soda)
Common sources:
Industry, soap manufacturers and laboratories.
Appearance:
Usually milky or white solids.
Mode of poisoning:
Usually accidental: in case of children as they resemble milk and during their
industrial use.
Clinical picture:
1. Severe burning pain from the mouth down the stomach,
abdomen and chest.
2. Vomiting: the vomit is soapy or bloody and alkaline
3. Diarrhea: soapy diarrhea or bloody with mucus.
4. Respiratory edema: cough, cyanosis, dyspnea.
5. Shock: leads to death.
Fatal dose: About 10 to 15 gm for most alkalis.
P.M.P: (post mortem picture)
1. White eschars on the lips.
2. Corrosions of esophagus and stomach
3. Gastric perforation.
4. Alkaline stomach contents
3) Ammonium hydroxide (NH4OH )
Appearance
 It is highly volatile corrosive, has penetrating odor.
 It produces symptoms other corrosives beside respiratory
manifestations leading to respiratory distress and sense of
suffocation and lacrimation.
Fatal dose: 8 ml by oral route.
Cause of death: shock, asphyxia and pulmonary edema.
Location of injury Alkaline agents tends to affect the esophagus
while acidic agents cause their greater damage to the stomach and

pylorus.
 3-Others Corrosive
A. Chlorox:
 Bleaching agent.
 Contains Na hypochlorite upto 10%.
 It has a corrosive action partly due to the formation of
hypochlorous acid and liberation of free chlorine when
hypochlorite reacts with gastric acid. The chlorine may in turn
be inhaled and causes respiratory symptoms.
 HCL + NaClO → NaCL + HClO
 HCL + HCLO → H2O + CL2
Mode of poisoning of Chlorox:
1. Accidental in children mainly under 5 years of age.
2. Suicidal by girls

Treatment of Chlorox poisoning :

1. In small ingested doses only anti-acid or milk should be given
with immediate water gargling.
2. If big doses are ingested, sodium thiosulfate( Na₂S₂O₃ )should
be given to reduce the remaining hypochlorite in the stomach.
3. Corticosteroids to decrease laryngeal edema.
B. Flash or Harbic :
 Contains concentrated HCL
 Used as toilet and bowl cleaner. It's effect is that of HCL.
C. shampoos:
Have very low toxicity apart from slight irritation of mucosal
surfaces but those containing anti-dandruff may have more
effects particularly those containing selenium.
 Complications of corrosive toxicity:
Sulfuric acid may be thrown on the face of persons for vengeance
causing
1. Burns of skin
2. And/or eye destruction and loss of vision (permanent infirmity).
3. Scars of eye or mouth which remain open and expose to
inflammations or dribbling of saliva.
4. Scar in neck, twisted to one or other side.
5. Scar in limbs causing limitation of j joint
movements.
6. Keloid may have malignancy transformation
Other acids and alkalis complications:
I. Acute complications:
1. Upper air way obstruction.
2. G.I.T hemorrhage.
3. Esophageal and gastric perforation (mediastinitis, pericarditis, pleuritis).
4. Sepsis.
II. Chronic complications:
1. Esophageal obstruction
2. Pyloric stenosis.
3. squamous cell carcinoma of esophagus

4. sepsis.
 General Management Of Corrosive Poisoning
1. Contraindications:
i. Neutralizing agents : They cause exothermic reaction causing
more tissue destruction beside carbonates lead to CO2 production
causing distension and perforation.
ii. Gastric lavage : may cause perforation.
iii.Emesis : because it may lead to additional esophageal injury and
increases the risk of perforation and aspiration.
iv.Cathartics : they enhance the movement of corrosive substances
through G.I.T which leads to increase in tissue damage.
v. Charcoal : It poorly adsorbs corrosives, blocks the visual field of
endoscopy
2. Eye and skin decontamination.
3. Dilution by water or milk .
4. Treatment of shock and pain: 5-10 mg morphine i.v. or strong analgesic.
5. Treatment of dehydration : I.V drip using 5% dextrose in saline.
6. Steroids: l -2 mg/kg/day may be given to relief laryngeal edema and to delay
esophageal stenosis
7. Antibiotics for pneumonia
8. Nutrition by i.v. fluids or by soft RyIe's tube
9. Surgical intervention: As follows:
− Tracheostomy for suffocation by edema of larynx or glottis.
− Partial gastrostomy for gastric perforation.
− esophageal dilatation or transplant for stenosis
10. Diagnostic procedure: Esophagoscopy to determine the extent of injury.
IV.Organic Acid : Carbolic, Acetic and Oxalic acids
A. Carbolic Acid (phenol):
Phenolic compounds:
1. Phenol (pure carbolic acid).
2. Phenolic disinfectants: e.g.
Cresol
I. Cresol (methyl phenol)
II. Lysol (cresol and soap solution)
III. Dettol (chloroxy lenol).

Dettol
IV. Organic Acid
A. Phenolic compounds

 Common sources:
 Domestic use as household disinfectants.
 Industry
 Ink and plastic manufacturing

 Characters:
 The pure acid is colorless, crystalline
 The commercial is a brown liquid
 Has a characteristic odor

 Uses:
 as antiseptics, Disinfectants, caustics germicides, surface anesthetic and

preservatives.
Absorption:
It is ingested, inhaled and absorbed through skin, per rectum/per vaginum.
Metabolism and Excretion
„
Phenol is metabolized mainly through the kidneys, wherein it gets converted into
hydroquinone and pyrocatechol and excreted in the urine, partly free and partly
in an unstable combination with glucoronic acid. Further oxidation of
hydroquinone and pyrocatechol cause a dark smoky green coloration of the
urine known as carboluria
It may also cause pigmentation in the cornea and various cartilages, a condition
called ochronosis
Action of Phenolic compounds:
It is a general protoplasmic poison, it has a double actions:
1. Local action:
− Mild local anesthesia
− Coagulative necrosis: induces clotting in superficial blood
vessels→ Gangrene of the tip of fingers and thickening of the
wall of esophagus and stomach with Shallow ulcers.
2. Systemic:
− CNS: initial stimulation followed by depression
− Kidney: acute tubular necrosis
Clinical picture of Phenolic compounds:
A. Local Clinical picture :
It produces Coagulative necrosis of the tissue with which it
comes in contact.
Blanching and corrosion of the skin.
Necrosis of skin or mucus membrane → eschars are white then
become brown due to oxidation with smell of phenol.
B. Systemic Clinical picture :
C.N.S:
– Stimulation: headache, convulsions, followed by
– Depression and coma.
C.V.S:
• Depression of the myocardium (rapid pulse, decrease B.P).
Renal:
‾ Albuminuria, Haematuria, oliguria and anuria followed by
depression of respiration, coma and death.
 Mode of poisoning of Phenolic compounds
1. Suicidal: common because:
a. Phenol is easily obtained.
b. Painless.
c. Rapidly fatal.
2. Accidental: In children and during its use. in industry or for house
disinfection.
3. Homicidal: Phenol cannot be used as a homicidal poison because
of its distinct odor.
 Fatal dose:

 1–2 g of phenol, or 25–50 ml of house-hold phenol.

 Fatal period: 3–4 h.

 Diagnosis:

Add 1 ml of 10% ferric chloride to 10 ml of urine; a purple

or blue color is formed which persists even on heating.

Cresol gives green color

  Phenolic compounds
 Laboratory findings:
1. urine + few drops of ferric chloride → a violet or blue color.
2. Urine shows red blood cells, protein and casts.
3. Blood CO2 content may be below 20 mEq/L.
Methaemoglobinaemia may be present.
 Prevention:
Phenol and its derivatives must be stored safely, and should not
be used over a large areas of the body.
Treatment of Phenolic compounds
1. Stomach wash is allowed because of thick wall and shallow ulcers
using :
a. 60 ml of castor oil.
b. 10-25% alcohol or glycerin to dissolve phenol and should be
rapidly removed to avoid re-absorption.
c. Magnesium sulfate (MgSO4) solution (15-30 gm) to precipitate
phenol as magnesium sulphocarbolate.
Gastric wash is essential if the patient is seen within 3 hours and
if he is conscious, but if he is in coma an endotracheal tube with
inflammable cuff must be inserted before lavage.
2. Symptomatic treatment of Phenolic compounds:

a. Demulcents (egg white, milk or olive oil).

b. Control convulsions using diazepam, 0.1 mg/kg I.V slowly.

c. Treat haemoglobinaemia ( methaemoglobinemia).

IV. Organic Acid
B. Oxalic acid :(COOH - COOH)
Common sources:
Shoemakers, brass polishers and book binders, and stain
removal from cloths particularly ink.
Properties: Colorless, transparent, prismatic crystals and
resembles MgSO4 and ZnSO4 Its a naturally occurring
component of plants and is found in relatively high levels in
dark-green leafy foods, e.g. Beet leaves, purslane, spinach,
rhubarb and parsley.
IV. Organic Acid
B. Oxalic acid :(COOH - COOH)
Action:
1. Local corrosive action on mucus membranes.
2. Systemic action after absorption:
Mode of poisoning:
1. Accidental; during its use in industry, or its use in house.
2. Suicidal: is less commonly used.
Fatal dose: 5-15 grams.
Fatal period: usually within 1/2 an hour and may be rapid as l0-15
minutes.
Clinical Pictures:
i. Locally: it produces hot burning pain (mouth and epigastrium)
vomiting. If taken as a dilute solution will not produce these local
effect.
ii. Systemic action: produces:
− Numbness and tingling.
− Hypocalcaemia
− Haematuria, oliguria or anuria.
− Weak irregular pulse.
− Coma and death.
Laboratory findings:

 Ca oxalate crystals, red blood cells, and protein in urine.

 Stomach contents + solution of calcium salt → a white ppt.

insoluble in ammonia and soluble in HCL and sulfuric acid.

 Stomach contents + lead acetate, → a white ppt.

insoluble in acetic acid and soluble in nitric acid

Oxalic acid Treatment:
1. Antidotes: Limewater, calcium lactate, calcium gluconate or calcium chloride
when given orally (150mg/kg) act as specific antidotes and form insoluble calcium
oxalate, and are excreted.
2. Calcium gluconate:10 ml of 10% solution IV frequently.
3. Parathyroid extracts:100 units IM
4. Milk: is one of the oral antidotes because it is rich is Ca, demulcent and 1s a buffer.
5. Stomach wash using plane treated water or chalky or plaster treated water (if
Calcium is not available)
6. Symptomatic treatment: analgesics, sedatives.
7. Alkaline I.V fluids, if kidney function is good using 1.26% sodium Bicarbonate to
wash out crystals in the renal tubules.
8. If renal function is impaired, haemodialysis is to be done.
IV. Organic Acid
C. Acetic acid (Glacial acetic acid)
 Characters: is colorless liquid, having strong corrosive effect and
characteristic odor.
 Uses: In industry for synthesis and manufacture of dyes.
 Mode of poisoning: Accidentally in mistake of vinegar (vinegar
contains 5% acetic acid)
 Fatal dose: 5 gm or ml
Clinical picture of Acetic acid :
1. Ingestion:
a) severe burning pain in the mouth, pharynx and abdomen
following vomiting and diarrhea of dark precipitated blood.
b) Sharp drop of B.P.
c) Asphyxia from glottis edema.
2. Inhalation: Fumes or irritating gases causes: Coughing, choking,
pulmonary edema with tightness in chest, dizziness, cyanosis.
3. Skin contact: Severe pain, burns penetrate the full thickness of the
skin, have sharply defined edges and heal with scar.
4. Eye contact: Conjunctival edema and corneal destruction.
Chemical Test of Acetic acid :
1. Characteristic odor.
2. Stomach contents is warmed with alcohol and a drop of sulfuric
acid gives a characteristic fruity smell of ethyl acetate.
Treatment of Acetic acid :
 Administration of milk of magnesia, lime Water Ca(OH)2 or soap
to dilute the acid.
 Gastric lavage or emesis is contraindicated.
 Morphine sulfate 5-10 mg every 4 hours to relieve pain
 Care of respiration, due to asphyxia caused by the and
P.M.P of Acetic acid :
 Characteristic smell of the acid.
 Corrosion and sloughing with hemorrhage of the mucous
membranes of the mouth and stomach.
 Inflamed and swollen mucus membranes of the throat and larynx.
Thank you