4. At the end of the topic the student will
be able to
• Classify corrosive poisons
• Describe the signs , symptoms, diagnoses,
treatment and postmortem appearances due
to sulphuric acid, Nitric acid, Carbolic acid,
oxalic acid and alkalies
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5. Definition of a corrosive
• A corrosive is a substance which erodes and
destroys any surface it comes in contact with
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6. Phases seen in caustic exposure
• Acute inflammatory phase ( upto 7 days) :
vascular thrombosis and cellular necrosis
• Latent granulation phase ( 1 to 2 weeks):
sloughed mucosa shows fibroplasia and
granulation tissue. Collagen replaces G.tissue
• Chronic cicatrisation phase( after 2 weeks):
excessive scar tissue resulting in contractures
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8. Classification
1. Strong acids
(A) Mineral / Inorganic acids
(B) Organic acids
2. Strong alkalis
hydroxides & carbonates of Na, K, Ca,
ammonia
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9. Mineral/ Inorganic acids
1. Severe local actions
2. No remote or systemic actions
3. Desiccation & Coagulation necrosis
• Sulphuric acid (oil of vitriol)
• Nitric acid (aqua fortis)
• Hydrochloric acid (muriatic acid)
• Hydrofluoric acid
• Boric acid Dr Varun Pai AIMST university 9
10. Organic acid
1. Severe systemic actions
2. Less severe local actions
• Carbolic acid (phenol)
• Oxalic acid (salt of sorrel)
• Formic acid
• Salicylic acid
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11. Sulphuric acid
• Oil of vitriol . Oleum, battery acid
• Heavy, colourless, odourless, non-fuming,
hygroscopic,
oily liquid
Uses
• Storage batteries
• Pipe and drain cleaners
• Laboratory
• Industry Dr Varun Pai AIMST university 11
12. • Fatal dose: 20 to 30 ml of Conc H2 SO4
• Mode of action: produces coagulation
necrosis of tissue on contact
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13. Clinical features
• Burning pain, intense thirst
• Teeth –chalky white, brittle
• Vomiting- brown/black material ( coffee
ground vomitus )
• Respiratory manifestations
• Burnt skin ( blackish eschar formatin )
• Acidemia
• Generalised shock
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14. • Lips are swollen and excoriated with blackish
streaks present running down the angles of
the mouth.
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16. Complications
a) Perforation of GIT
b) Secondary infection
c) Stricture formation
d) Carcinoma
e) Renal failure
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17. Diagnosis
• Litmus test
• Sodium bicarbonate drops (cloths) -bubbles
• Addition of barium chloride
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18. Treatment
• Oral feeds, stomach wash or induction of
emesis is contraindicated.
• Wash and the irrigate the skin copiously
with saline
• Demulcents
• Respiratory distress – 100% oxygen
• Morphine & crushed ice
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19. • Antibiotics & corticosteroids
• Fiber optic endoscopy
• Emergency laprotomy
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20. Pm appearances
• Corroded areas appear brownish or blackish
• Stomach mucosa- wet blotting paper ( Black
in color)
• Acids act on the columnar epithelium of the
stomach
• The mucosal ridges are more damaged then
the furrows
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26. Medicolegal importance
-Vitriolage- example of grevious hurt.
• Jealous or disgruntled persons may use to
disfigure enemies. blindness may occur.
• Death may result from shock or toxemia.
• The penetrating burns devitalises the tissues
and predispose to infection.
• Scar tissue may lead to contracture
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28. Treatment
• - washing skin with water & soap
- raw surface covered with some antibiotic
cream
-eyes should be washed with water and
irrigated with1% sodium bicarbonate
solution
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30. Nitric acid (Syn: Aqua Fortis , engraver’s acid )
• Colourless or yellow, Fuming liquid, pungent
odour
Uses
✓Engraving
✓Electroplating
✓Fertilizers
✓Metal refineries
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31. • Xanthoproteic reaction
-Yellow stains on
clothing and tissues and crowns of teeth
Reacts with organic acid to produce
trinitrophenol
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32. Signs and symptoms
• Inhalation of fumes can produce lacrimation ,
coughing & dysnoea
• Abdominal distension
• Perforation of the GIT is less common
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33. • PM appearance- corroded areas of skin and
mucous membrane appear yellowish
• Perforation is not as common as in cases of
H2SO4
• Treatment is same as in cases of H2SO4.
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34. Organic acids
• weaker in corrosive action
• Absorbed in to circulation- both systemic &
local actions
• Carbolic acid (Phenol)
• Oxalic acid
• Salicylic acid
• Formic acid
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35. Carbolic acid (Phenol)
• Colorless, needlelike crystals turns pink &
liquefy
• Commercial phenol- brownish liquid with
several impurities with hospital odour
• Derivatives- cresol, coal tar, thymol, tannic
acid Dr Varun Pai AIMST university 35
36. Uses
• Antiseptic and disinfectants
• Preservative in injectable medications
• Face peel in plastic surgery
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37. Signs and symptoms
• Acute poisoning ( carbolism )
Local: skin or mucosal contact: hardening and
whitish discoloration with burning pain,
tingling, numbness,
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39. • Metabolic : hypothermia, with metabolic
acidosis
• Hepatorenal: oliguria with scanty urine which
turns greenish or brownish on exposure to air
this is due to metabolities hydroquinone and
pyracatechol
Also called as carboluria
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40. Pm appearance
• Distinct odour of phenol at mouth and
stomach contents
• Corroded area –brownish or whitish
• Stomach mucosa – pale, hardened, leathery
• Cerebral & pulmonary oedema
• Congestion of internal organs
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41. Treatment
• Stomach wash – thick, hard & leathery
consistency
• Demulcents
• Sodium bicarbonate IV
• Methylene blue IV
• Haemodialysis
• Supportive measures
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43. Oxalic acid ( Syn: salt of sorrel, acid
of sugar)
• Prismatic crystals similar to magnesium & zinc
sulphates
• Uses – ink & rust remover
- Bleaching agent & industry
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44. Mechanism of action
• local- do not lose poisonous properties when
diluted
• Combines with serum calcium & produce
features of tetany
• Forms calcium oxalate and it is precipitated
and accumulated in the liver, kidneys, heart,
lungs and is excreted in urine
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45. Clinical features
Local: whitish or yellowish corrosion of the skin
The mucosa is referred to as “ scalded”
appearance
Systemic: vomiting and diarrhoea
Signs and symptoms of tetany
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46. Diagnosis
• Demonstration of urinary oxalate crystals
Monohydrates( prism or needle like)
Dihydrates ( tent or envelope shaped)
• Measurement of oxalic acid in urine by
colorimetry
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47. Treatment
• Stomach wash – lime water, chalk
suspension, ca gluconate solution.
• Calcium gluconate- IV (10ml of a 10%
solution)
• Demulcents
• Parathyroid extract-100 units IM
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48. PM APPEARANCE
• Corrosion of mucosa- whitish or yellowish
• Scalded mucosa of the GI tract, especially
stomach
• Kidney- necrosis & hyaline degeneration of
tubules
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50. Alkalies
• Ammonium hydroxide: paint, oil and dirt
remover
• Sodium hydroxide: drain cleaner, oven cleaner
• Potassium hydroxide: drain cleaners, hearing
aid batteries
• Sodium hypochlorite: household bleach
• Sodium carbonate: washing soda
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51. Mode of action
• Produce liquefaction necrosis
• Extensive penetrating damage because of
saponification of fats and solubility of proteins
• Oesophogus more affected
• Alkalis are more prone to cause perforation
than acids
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52. Clinical features
• Corrosion of the GI mucosa with
pseudomembrane formation
• Oesophagus is commonly affectes resulting in
dysphagia, vomiting, drooling and stridor
• Abdominal pain, diarrhea, tenesmus
• Greyish soapy necrotic areas on the skin
• Eye involvement
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53. Diagnosis
• In stomach contents
✓White slimy lumps, flakes and granules
✓Turns litmus paper blue
✓Soapy and slimy feeling when touched
✓ sharp penetrating odour in case of ammonia
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