The document outlines the effects and management of various corrosive substances, including sulphuric acid, nitric acid, hydrochloric acid, oxalic acid, and carbolic acid, highlighting their physical properties, clinical features of poisoning, diagnostic tests, and treatment protocols. It details the injuries caused by these acids, such as burns, gastrointestinal perforations, respiratory complications, and long-term sequelae, along with forensic issues related to their misuse. The document also emphasizes the fatal doses, management strategies, postmortem appearances, and the legal implications of corrosive poisoning.

1. CORROSIVES

2. CORROSIVE POISON
• Fixes, destroys and erodes the surface with
which it comes in contact.
• Extract water from tissues
• Coagulate cellular proteins
• Convert haemoglobin to haematin

3. ACID vs ALKALI
• Alkalis are more dangerous
• Causes liquefaction necrosis
• Results in deeper penetration
• Acids cause coagulative necrosis
• Results in hard eschar
• Prevents deeper penetration

4. SULPHURIC ACID (Oil of Vitriol)
Battery acid, Oleum
• Identification : colourless, odourless, heavy,
oily, nonfuming, hygroscopic liquid.
• It has great affinity for water with which it
reacts violently, giving off intense heat.

5. Sulphuric acid is used in two forms :
Commercial concentrated sulphuric acid – 93-
98% solution in water.
Fuming sulphuric acid is a solution of sulphur
trioxide in sulphuric acid
Commercial sulphuric acid is brown or dark in
colour
Causes superficial burn after one second of
contact and full thickness burn after 30 seconds
of contact

6. USES
• Probably the most widely used industrial chemical
• Manufacture of a number of chemicals e.g. acetic
acid, hydrochloric acid, phosphoric acid,
ammonium sulphate, barium sulphate, copper
sulphate, phenol, fertilizers, dyes,
pharmaceuticals, detergents, paints,etc.
• Storage batteries – electrolytes
• Industries- leather, fur, food processing, wool,
uranium and as a laboratory reagent

7. CLINICAL FEATURES
• Burning pain from mouth to stomach; severe abdominal
pain
• Odynophagia (painful swallowing)
• Pharyngeal pain – most common presenting symptom
• Intense thirst; attempts at drinking water usually invoke
retching;
• Eructations, nausea, vomiting
• Vomitus is brownish or blackish in colour due to altered
blood (coffee grounds vomit), may contain shreds of the
charred wall of the stomach

8. Clinical Features (contd.)
• Dysphonia - voice hoarse and husky (if there is coincidental
damage to the larynx during swallowing or due to regurgitation)
dysphagia and dyspnoea
• Tongue swollen, blackish or brownish in colour
• Teeth chalky white
• Drooling of saliva – indicative of oesophageal injury
• Acid spillage while swallowing with consequent corrosion of
the skin of the face( especially around the mouth), neck and chest.
Burnt skin appears dark brown or black.
• Abdomen – distended and tender, tenesmus
• constipation

9. Clinical features(contd.)
• Generalised shock
• Renal failure, decreased urinary output – after
several hours of uncorrected circulatory
collapse
• Metabolic acidosis, - due to severe tissue
burns, shock and absorption of acid.
• Leucocytosis – common after exposure to
strong mineral acids

10. Clinical features(contd.)
• Perforation of stomach – severe form of chemical peritonitis result.
(rarely perforation of the duodenum, or even further down the
small intestine can occur).
• Mind remains clear till death
• If the patient recovers,long term sequelae e.g. stricture formation
which may lead to pyloric obstruction, antral stenosis, or hour glass
deformity of the stomach; oesophageal stenosis; increased
propensity for carcinomas
• Contact with eyes- severe injury, conjunctivitis, periorbital oedema,
coneal oedema and ulceration, necrotizing keratitis, iridocyclitis

11. CAUSE OF DEATH
IMMEDIATE
• Circulatory collapse
• Edema glottis - asphyxia
• Perforation of stomach
DELAYED
• Hypostatic pneumonia
• Renal failure
• Secondary infection
• Starvation (due to oesophageal strictures)

12. CHRONIC EXPOSURE
• Occupational exposure to sulphuric acid mist
can cause erosion of teeth and increased
incidence of upper respiratory infections
• Sulphuric acid can react with other substances
to form mutagenic and possibly carcinogenic
products(alkyl sulphates). Carcinoma of vocal
cords, nasopharyngeal and laryngeal cancer.

13. DIAGNOSIS
• Litmus test: the pH of saliva can be tested with a
litmus paper to determine whether the chemical
ingested is an acid or alkali
• Fresh stains in clothing may be tested by adding a
few drops of sodium carbonate. Production of
effervescence (bubbles) is indicative of an acid
stain.
• If vomitus or stomach contents are available, add
10% barium chloride. A heavy white precipitate
forms which is insoluble on adding 1ml nitric acid.

14. TREATMENT
• Respiratory distress due to laryngeal oedema-
100% oxygen and cricothyroidotomy
• Some recommend water or milk if the patient is
seen within 30 minutes of ingestion. NO ALKALIS(it
results in exothermic reaction). Even
administration of buffering agents e.g. antacids can
produce significant exothermic reaction

15. Remove all contaminated clothing
Irrigate exposed skin copiously with saline; Non-adherent
gauze may be used
Topical silver sulphadiazine – for second degree burns
Eye injury –
Retraction of eyelids and prolonged irrigation with normal
saline, Ringer lactate solution or tap water
Continue irrigation till normal pH of ocular secretions is
restored (which can be tested by litmus paper
Slit lamp examination is mandatory to assess the extent of
corneal damage

16. The following measures are contraindicated
• Induction of vomiting
• Stomach wash
• Activated charcoal
• Oral feeds
• Administration of steroids – controversial
• Shown to delay stricture formation when given within 48 hours
of acid ingestion (in animals);
• The practice is generally not recommended because of
increased risk of perforation.
• Administer antibiotics- if infection. Prophylactic antibiotic has
no role unless corticosteroid therapy is being undertaken.
• Powerful analgesics e.g. morphine for severe pain

17. • Flexible fibreoptic endoscopy in the first 24 – 48 hours of
ingestion to assess the extent of oesophageal and gastric
damage
• If there are circumferential 2nd
or 3rd
degree burns,
exploratory laparotomy is indicated.
• If gastric necrosis is present an oesophagogastrectomy may
have to be done.
• Emergency laparotomy – if perforation or peritonitis
• Long-term sequelae – stenosis or stricture formation; follow
up to look for signs of obstruction – anorexia, nausea,
vomiting, weight loss; surgical procedures – dilatation,
oesophagogastrostomy

18. AUTOPSY FEATURES
• Corroded areas of skin and mucous
membrane appear brownish or blackish; teeth
– chalky white
• Stomach mucosa has the consistency of wet
blotting paper
• Inflammation, necrosis or perforation of the
GIT

19. MEDICOLEGAL ISSUES
• Accidental poisoning due to mistaken
identity as sulphuric acid resembles
glycerine and castor oil.
• Rare choice for suicide and homicide
• Abortifacient
• Disposal of dead bodies – after murder
• Blinding an enemy or to extort confession
• Self-defence

20. VITRIOLAGE
• Throwing of H2SO4 on the body of a person to
cause bodily injury. The term is used in general
for throwing any corrosive (acid, alkali, salt,
irritant juice of a plant – calotropis, marking nut)
to cause disfiguration of the face, destruction of
eyes, contractures with or without restricted
movement of joints.
• Motive – jealousy, hatred, rivalry, revenge
Section 326A IPC - Voluntarily causing grievous hurt by the use of acid; Imprisonment not less
than 10 years, may extend to life and fine
Section 326B IPC - Voluntarily throwing or attempting to throw acid; Imprisonment not less
than 5 years and fine

21. SAMPLES PRESERVED IN AUTOPSY
In addition to routine viscera and body fluids, a
portion of corroded skin should be cut out and
preserved in rectified spirit and sent for
chemical analysis. Stained clothing must also be
sent.

22. NITRIC ACID (Aqua fortis, azotic
acid,Engraver’s acid)
• PHYSICAL APPEARANCE: Colourless or yellowish
fuming liquid with an acrid, penetrating odour
• Occupational hazard; workers in the following
professions may be exposed to nitrogen oxides
or nitric acid: chemical industry, metal refinery,
glassblowing, engraving and electroplating,
underground blasting operations, manufacturing
fertilizers, nitroglycerine,welding, fire fighting.

23. FATAL DOSE – 10-15ml
FATAL PERIOD - 12-24 hours
MODE OF ACTION: Nitric acid is a powerful oxidising agent
and reacts with organic matter, producing yellow
discoloration of tissue due to production of picric acid
(xanthoproteic reaction).
Corrosion is less severe when compared to sulphuric acid.

24. CLINICAL FEATURES
• The general picture is the same as in the case of
sulphuric acid, with the following differences:
• Corroded areas appear yellowish due to xanthoproteic
reaction. Stains on clothing and teeth also appear
yellowish
• More severe eructation and abdominal distension due
to gas formation.
• Perforation of GI tract is less common.
• Inhalation of fumes produce coughing, rhinorrhoea,
lacrimation, dyspnoea and pulmonary oedema

25. DIAGNOSIS
• Litmus test
• Drop a small piece of copper in the stomach contents
and heat it. Pungent, dark brown heavy fumes will
emanate if nitric acid is present in sufficient
concentration
• Brown ring test: a mixture of strong ferrous sulphate
and sulphuric acid is taken in a test tube. The side of
the tube adds nitric acid. Formation of brown ring in
between the layers indicate positive reaction.

26. TREATMENT
• Same as that for sulphuric acid
• Respiratory distress is present more often and
requires special attention.

27. AUTOPSY FEATURES
• Corroded areas of skin, teeth and mucous
membranes appear yellowish. Stains on clothing
show yellowish discolouration. (to differentiate this
from stains produced by iodine, apply ammonia solution. Iodine
stains will be decolourised, while those due to nitric acid will
deepen in intensity and turn to orange).
• Gastrointestinal perforation is less common.

28. FORENSIC ISSUES
• Same as for sulphuric acid.
• Mistaking it for glycerine or castor oil is rare
because it is a fuming liquid.

29. HYDROCHLORIC ACID (Muriatic acid, Spirit of
salts)
• PHYSICAL APPEARANCE: Colourless, fuming liquid
which may acquire a yellowish tinge on exposure to
air.
• USES : Bleaching agent (less than 10%)
• dyeing industry
• metal refinery
• soldering
• metal cleaner, drain cleaner
• laboratories and pharmacies

30. DIAGNOSIS
• Litmus test
• If an open bottle of concentrated ammonia solution
is placed near the stomach contents or vomitus,
copious white fumes of ammonium chloride will
emanate.
• Addition of AgNO3 to the sample produces a heavy,
white, curdy precipitate of silver chloride, insoluble
in excess of HNO3 but soluble in NH4OH. The white
precipitate turns grey on exposure to sunlight.

31. CLINICAL FEATURES
• Same as for H2SO4 except that symptoms are less severe.
• Respiratory manifestations are more pronounced; acute
inflammation and oedema of respiratory passages and
lung tissue are common
• Inhalation of fumes cause intense irritation of throat and
lungs – suffocation, coughing, dyspnoea, cyanosis
• Corrosion is less severe; Corroded areas are more likely to
be greyish, later becomes brown or black due to acid
haematin
• Perforation is rare

32. Constant exposure to fumes produces chronic
poisoning:
Coryza, conjunctivitis, corneal ulcer, pharyngitis,
bronchitis, inflammation of gums, loosening of
teeth

33. POSTMORTEM APPEARANCE
• Same as that for sulphuric acid
• Corrosion is less severe
• Stomach contains brownish fluid
• Folds of the stomach mucosa are brownish
• Acute inflammation and oedema of
respiratory passages and lung tissue are
common

34. FATAL DOSE – 15-20ml
FATAL PERIOD – 18-36hours

35. FORENSIC ISSUES
• Same as H2SO4
• Forgery – erasing writings from documents

40. OXALIC ACID
• C2H2O4
• Acid of sugar/ salt of sorrel
• Colourless, transparent, prismatic
crystals
• In the form of oxalates, exists as
natural constituents of many plants –
spinach, cabbage
• Daily excretion in urine – 20mg

41. USES
• Bleach to remove stains
• Clean brass or copper articles, leather
• Calico printing
• Removing writing and signatures
illegally

43. ACTION
• LOCAL – crystals and concentrated
solution(more than 10%)- act as corrosive
poisons
• Rarely damage the skin but readily corrode
the mucous membrane of the digestive tract
• Less than 10%- strong irritant; causes
serious systemic effects when absorbed

44. SYSTEMIC
• Shock - large doses cause rapid death
• Hypocalcaemia – reacts with calcium in plasma-
forms calcium oxalate. Precipitation of calcium
oxalate crystals in liver, kidney, heart, lungs;
excretion of calcium oxalate crystals in urine
• Renal damage – oxalates produce tubular necrosis-
uraemia- death in 2 to 14 days

45. SIGNS AND SYMPTOMS
LOCAL :
• Acts as corrosive
• Skin- rarely damaged; maybe discoloured
with underlying congestion
• Mucosa – corroded (yellowish/whitish) –
referred to as ‘scalded appearance’.
Production of acid haematin can turn the

46. INGESTION
• Burning , sour or bitter taste in the mouth which goes up to the
stomach
• Sense of constriction around the throat
• Intense thirst
• Mouth - scalded or sometimes black
• Severe pain - begins in the epigastrium, soon radiates all over the
abdomen
• Abdomen tender
• Persistent vomiting, eructations and diarrhoea (vomitus contains
altered blood and mucus)
• Stupor and coma - rarely

47. Signs and symptoms of hypocalcaemia
–
Tetany
Tingling and numbness of
fingertips

48. DELAYED:
If patient survives initial poisoning
episode, delayed symptoms may be due
to renal failure (calcium oxalate crystals
in kidneys)
Urine – scanty or suppressed. Contains
traces of blood, albumin and calcium

49. MANAGEMENT
• Gastric lavage – if patient seen early, perform gastric lavage carefully with
calcium salts (chloride, gluconate, lactate, chalk powder, lime water, milk) 1.5 g of
chalk neutralizes 1g of acid.
Converts acid to insoluble calcium oxalate
• Antidote – calcium preparations orally
• Calcium gluconate IV (10%)
• Parathyroid extract- 100 units IM in severe cases. Mobilizes calcium from bones
• Dialysis or exchange transfusion – for renal failure
• Demulscents, evacuation of bowels by enema or castor oil
• Symptomatic

50. POSTMORTEM APPEARANCE
• Mucous membrane of tongue, mouth, pharynx,oesophagus; In concentrated
solution- whitened, ‘bleached’(scalded appearance), sometimes brown or black
(due to acid haematin) & in weaker solution- reddened because of irritation
• Oesophagus – mucosa corrugated with longitudinal erosions
• Stomach – mucosa – soft and reddened, shows punctate erosions, may be black
(acid haematin), numerous dark brown or black streaks seen running
longitudinally along the length of the stomach, often with intercommunicating
branches. Often entire mucosa is corroded
Contents – gelatinous and brownish(acid haematin)
• Perforation is rare

51. • INTESTINE – Upper part of duodenum shows
corrosion
• LIVER – Centrilobular necrosis
• KIDNEY – Congested and swollen (Histologically –
glomeruli – swelling , renal tubules – full of
oxalate crystals; PCT-necrosed
• URINARY BLADDER – Urine with calcium oxalate
crystals. Looks like envelope under the
microscope
• All internal organs – congested

52. TEST
• Suspected solution + BaNO3 --
White precipitate of barium
oxalate, which is soluble in HCl or
HNO3

53. MLI
• Accidental poisoning – due to mistaken
identity with Epsom salt or ZnSO4.
• Homicide – rare due to acrid sour taste
• Suicide – rare
• Abortifacient

54. Carbolic acid
• Sir Joseph Lister used it for its antiseptic
properties for the first time.
• Smell
• Not a true acid
• Prismatic crystals
• Converted to catechol and quinol
• Excreted as green-coloured urine known as
carboluria
• FD – 10-15 gm
• Fatal Period – 3-4 hours

56. Acute CA Poisoning
• Local –
Numbness
Burns – eschar formation
Necrosis and gangrene greenish-white in colour
Nausea vomiting
Lips and mouth corroded
Deglutition and speech difficult

57. • Systemic –
General – phenol odour in breath, pupils-
variable
CNS – initially stimulatory followed by
depressant symptoms
Laboured breathing
Liver – hepatotoxicity
Methaemoglobinaemia
Urine – scanty and contains albumin

58. Management
• Remove clothing
• Irrigation of contact area with polyethylene glycol
(water worsens the injury) or ethylene glycol/ olive
oil.
• Gastric Lavage – lukewarm water with castor oil/olive
oil/glycerine/soap solution.
• After completing lavage leave medical liquid paraffin
in the stomach.
• Normal saline with Sod. Bicarb.
• Dialysis
• Methylene Blue IV

59. PM Appearance
• External –
1. Smell of phenol
2. Trickling and corrosion around mouth.
3. Tongue white gardened
4. Lips, throat - corrugated

60. PM Appearance
• Internal
1. Stomach – reddish fluid with mucous, thick and
leathery, necrosed mucosa, furrows.
2. Intestines – same as stomach.
3. Resp. tract – coag. Necrosis, congestion, laryngeal
edema.
4. Liver, spleen – whitish hardened patch.
5. Kidney – hemorrhagic nephritis

62. Chronic Poisoning
• Phenol Marasmus
• Yellowish discoloration of cartilage,
sclera and skin – Ochronosis
• D/D - Alkaptonuria

63. MLI
• Suicide
• Accidental – carelessness in storage and
application in raw wounds
• Criminal abortion
• Homicidal - rare