Corrosive Poisoning

Sulphuric Acid
•Pure acid is colorless heavy liquid,
which emits no fumes when exposed to
air. It char and blackens the skin clothes
and other organic matters. Commercial
acid is darker in colour and when mixed
with water, it evolved great heat.
Mode of action
• The acid damages the tissue by dehydration , the
primary action of the acid is to produce a grey
white necrotic membrane with swelling of
affected surface, followed by a brownish or black
discoloration , The tissue appear black or brown
due to charring and conversion of hemoglobin
into haemitin.
 Symptoms and signs:
• Intense burning pain in mouth , throat, oesophagus and stomach
• Frothy eructation
• If quantity is more, whole stomach is cored and there is no vomiting.
• Intense thirst
• Lips and angle of mouth is partially burn
• Choking and dyspnoea are common
• Bowel are constipated
• Urine is scanty and supressed and micturition is painful
• Eye are wide sunken, collapse Skin is cold and clammy
• Pulse is slow
• Respiration is difficult
• Coughing may be frequent and painful.
Cause of death
• Death occurs with in few hours from shock or
spasm of glottis with in 24 hours from collapse
due to perforation of stomach and peritonitis.
• Fatal Dose=10-25ml
• Fatal period: death commonly occurs within
about 12-24 hrs.
 Treatment
• Infusion of antacid to neutralize acid- milk of magnesia is useful
antidote if not available give lime water, wood ash, soap and
water may be used.
• Morphine injection to relief pain
• Ice to suck to relief thirst
• Intravenous fluid to combat dehydration
• Corticosteroid to prevent shock and esophageal strictures
• Tracheostomy –if there is acute oedema of larynx.
• Burnt skin is wash away with plenty of water then thick paste of
magnesium sulphate is applied.
Conti…..
• If eye are involved-They should be washed at
once with a large amount of water followed by
irrigation with 1% solution of sodium
bicarbonate eye drop containing antibiotics and
steroids are helpful.
Postmortem appearances:
• Lips and also adjacent cheeks chin and neck
are likely to be stained by corrosion.
• Fingers are seldom burned.
• Changes in neighboring viscera may be seen
due to perforation.
Medicolegal points
• Suicide –It is easily available so may be used for
suicide.
• Homicidal- not possible unless victim is child or
drunken person or helpless person.
• Accidental-it has been mistaken as syrup or
glycerine, castor oil or whisky.
• Abortification: It is internally given for
abortion.
What is vitriolage (vitriol throwing)
• This mean throwing of any corrosive with the object
of injuring or disfiguring a person out of jealousy or
revenge. Sulphuric acid is the one most commonly
employed acid for this purpose and hence it is called
vitriloge. This produced sever chemical brun. This
may cause blindness , if thrown in eyes. Injury is
grievous if there is permanent disfigurement.
 Hydrochloric acid
• Hydrochloric acid is an aqueous solution of hydrogen
chloride.
• It is component of the gastric acid in the digestive
system of the most animal species, including
humans.
• IUPAC name- chlorane
• Other name- Muriatic acid, spirit of salts,
hydronium chloride, chlorhydric acid
Characteristics
• Colorless transparent liquid, having intensely irritated
fumes in air if concentrated.
• Strong inorganic acid that is used in many industrial
processes such as refining metal.
• Typically 18% conc of hcl is most commonly used as
pickling agent for the prickling of carbon steel grades rust
or iron oxide scale from iron oxide scale from iron or steel
before subsequent processing such as extrusion , rolling,
galvanizing and other techniques.
Signs and symptoms
• Salivation
• Convulsion: body muscles contract and relax rapidly
and repeatedly resulting in uncontrolled shaking
• Delirium
• Paralysis of limbs
• Croyza
• Corneal ulcer-also known as keratitis. It is an open
sore on the cornea
Conti….
• Nausea
• Vomiting
• Epigastric pain
• Inflammation of gums
• Loosing of teeth
• Fatal dose:15 to 20 ml
• Fatal period:18-30 hrs
Postmortem appearance
• Mucous membrane – ash grey or black color
interspersed with erosion.
• Stomach wall- Red - acute gastritis
• Brownish leathery mucosa (acid hematin)
 Chemical test of hydrochloric acid
• GUNZBERG’S TEST
• A few drops of gunzbergs reagent prepared by dissolving 2
gm of phloroglucinol and 1 gm of vanillin in 100 ml of 95%
alcohol) is taken in porcelain dish: evaporated to dryness
over a small flame and cooled.
• A glass rod together with the material to be tested is added
to the dried reagent. It is warmed gently.
• A purplish red color develops in the presence of free HCL.
Sliver nitrate test
• A few drops of sliver nitrate solution is added to 2 ml
of the sample.
• A curdy white precipitate is obtained which is soluble
in ammonia or potassium cyanide and insoluble is
strong nitric acid even on boiling (HCN also gives a
whit precipitate under the same condition but it is
soluble in nitric acid on heating)
 Nitric acid
• Nitric acid is also known as aqua fortis a Latin
which means “stronge water”.
• Also known as spirit of niter, Eau forte ,
hydrogen nitrate acidum nitricum , azitic acid,
engraver acid
• It is highly corrosive mineral acid.
• Most commercially available nitric acid has a
concentration of 68% in water.
• When the solution contain more than 86%
HNO3, it is referred to as fuming nitric acid.
• Depending on the amount of nitrogen dioxide
present fuming nitric acid is further
characterized as red fuming nitric acid 86% or
white fuming acid concentrations above 95%.
 Conti….
• Nitric acid is the primary reagent for nitration addition
of a nitro group, typically to an organic molecule.
• While some resulting nitro compounds are shock and
thermally sensitive explosive few are stable enough to
be used in ammunitions and demolitions, while others
are still more stable and used as pigments in inks and
dyes.
Conti…
• Commonly used as strong oxidizing agent which can
be dissolve all metals except gold and platinum.
• It is able to destroy organic matters with the formation
of Xanthoproteic acid that imparts deep yellow colour
to the affected tissues.
• HN03+ protein= Xanthoproteic acid (Benzenoid
structure )
Deep yellow coloured
Chemical formula:
• HNO3
• Molar mass: 63.012g mol
• Appearance
• Colorless, yellow or red fuming liquid odor
acrid, suffocating
• Density
• 1.51 gm cm-1.41gm cm
• Fetal dose: 20 to 30 ml
• Fetal Period : 12 to 24 hrs
Signs and symptoms
• Lips………softened + white
• Tongue………..Intensely + yellow
• Teeth yellow and enamel partially destroyed
• Skin and clothes are yellow coloured
• Blood in vomited matter+ yellowish brown
• Gaseous erection +Distension of abdomen.
(Gas + HN03 + organic matter)
Oliguria/Anuria
Lock jaw
Inhalation=Lacrimation, coughing, dysponea
Death immediately due to suffocation
• Pulmonary oedema, broncho pneumonia causes
death later
 Postmortem Appearance
• Corroded area+ skin + mucous membrane
• Mucous membrane (stomach) Green (if bile present)
• Stomach wall + soft , friable , ulcerated
• Corrosion of duodenum may be
• On inhalation----
• 1-congestion in larynx , trachea, bronchial tube
• 2-Lungs oedematous+ effusion of blood
• 3-Inflammatory change on lining membrane of right auricle
of heart.
 Examination of Nitric Acid
• Brown Ring test:
• Adding iron sulfate to a solution of a nitrate,
then slowly adding concentrated sulfuric acid
such that the acid forms a layers below the
aqueous solution. A brown ring will form at the
junction of the layers, indicating the presences of
the nitrate ion.
Devarda’s test
• Devarda’s alloy (cu+Al+zn) is a reducing
agent when reacted with nitrate in sodium
hydroxide solution, ammonia liberated.
• Diphenylamine test
• Solution of diphenylamine and ammonium chloride
in sulfuric acid is used. In the presence of nitrates,
diphenylamine oxidized , giving a blue coloration.
• Copper turning test:
• Identified by heating copper turning along with
concentrated sulfuric acid. Effervescence of a
brown(bubbles) , pungent gas is observed which
turns moist blue litmus paper red.
Medicolegal Significance
• Forensically cases of nitric acid poisoning reported are
mostly are accidental or suicidal in nature and rarely
homicidal.
• Workers in the glassblowing, engraving and
electroplating underground blasting operations,
farming, silage , fertilisers, welding, fire fighting and
industrial chemistry professions maybe exposed to
nitrogen oxides or Nitric acid
• Abortification
• Vitriolage
 Oxalic Acid
• Oxalic acid is an organic corrosive acid found in crystalling form
sparingly soluble in water.
Mode of action
• It has local and remote actions it combines with serum calcium to
form insoluble calcium oxalate thus there is hypocalcaemia.
Signs and symptoms
• Signs and symptoms depends upon the concentration and amount of
the acid ingested.
• Local action:
• It has a corrosive action on the mucous membrane of the GIT but has
the effects over skin.
• Remote action:
• There are effects after the poison has been absorbed from its primary
site of administration.
Effect on GIT
• Sour taste in mouth and burning in throat and stomach
• Persistent vomiting the vomit is blackish “Coffee ground” due to
formation of acid haematin by Hb and HCL.
• In case where death is delayed , there is pain and tenderness over the
abdomen and purging and tenesmus are to follow.
Effect on CNS and muscular system
• Numbness and twitching
• Spasmodic twitching of the muscles of the face and extremities.
• Convulsion
Nephrotoxic effect
• Nephrotoxic effects are evident in case where death is delayed.
• Urine contains blood, albumin, and calcium oxalate crystals.
• Oxaluria: The presences of calcium oxalate crystal in urine is called
oxaluria. These crystals are envelope shaped when seen
microscopically.
• Shock: Poison in larger doses when rapidly absorbed from the git may
lead to sudden death from shock.
• Fatal dose:15-20 gm
• Fatal period: 1 hour or may extend to few days
 Treatment
• Whatever to be done should be quick.
• Gastric lavage with warm water using soft levine tube . Warm water is
contraindicated as it can enhance the solubility of acid.
• Antidote is any calcium preparation that can form insoluble calcium
oxalate readily available is chalk. As suspension of 30 gms of chalk in
water or milk neutralized about 20 grms of oxalic acid.
• Soda , posh ammonium and other alkalis are contraindicated, as their
oxalates are soluble.
Conti…
• Shock: 10% , 10 ml glucose I/V or through mouth.
• Parathyroid extract , to combat low serum level of calcium can be
administered.
• Balanced fluid intake and out put are to be maintained to keep in view
the changes of kidney damages.
• Symptomatic treatment.
Test to be done:
• Sliver nitrate test
• Calcium test
• Lead test
• Permanganate test
Post mortem appearance
• Concentrated poison gives appearances similar to other corrosive.
Except corrosion of mouth and lips.
• Internally mucous membrane of tongue , mouth throat, and gullet are
white as if bleached but may be reddened due to irritation. Stomach
mucosa is corroded in patches. In stomach a dark brown gelatinous
liquid may be encountered due to the formation of acid haematin.
The blood vessels of submucosa appear as dark lines due to acid
haematin in them.
• In living: vomitus, mouth wash, blood for oxalates and urine
• In dead: stomach with contents and kidney are to preserved.
Medicolegal Importance
• Accidental poisoning may occur when poison is mistaken for sodium
bicarbonate and magnesium sulphate. It is also present in rhubarb
leaves so poisoning may occur when leave are used as vegetables
• Suicidal poisoning is rare
• Homicidal use of oxalic acid is rarely documented, the poisoning
being sour and rapid in action.(rare)
Christion’s saying
• The person mentioned worked on cause of oxalic acid poisoning and
gave verdict regarding clinical diagnosis of carbolism case.
• If a person after swelling a crystalline white substance the taste of
which is strongly acidic. It seized almost immediately by violent
vomiting , pain in stomach , feeble pulse , cold sweat and collapse and
dies within one hour or even earlier, there can scarcely be any doubt
that oxalic had been administered.
 Acetic acid

• Colourless volatile liquid with pungent odour.

• Pure acetic acid is an ice like solid below 16 degree C, hence it often
described as glacial acetic acid.
• The dilute form of acid is called as vinegar
• Fatal dose: 50-100 ml
• Fatal period-about 48 hrs
Sign and symptoms

• In concentrated form it acts as corrosive

• In dilute form it act as an irritant
• systemic absorption causes haemolysis , haemoglobinuria, renal
failure, disseminated intravascular coagulation.
• Metabolic acidosis and liver dysfunction.
Treatment
• Washed the part with water immediately after the contact
• Gastric lavage and emetics are contraindicated.
• When ingested demulcent( ghee, milk) are given
• Rest of the treatment is symptomatic.
• DIV given heparin to prevent clots.
Postmortem Appearance
• External:
• Evidence of acid corrosion and chemical burns
• Excoriation of lips
• Corrosion of mucous of mouth and tongue
• Internal:
• Massive liver necrosis
• Degeneration and swelling of renal tubular epithelium
Medicolegal Importance
• Accidental and suicidal cases may occur.
• Not used as a homicidal poison due to its peculiar smell.
 Hydrocyanic Acid
(Vegetable acid)
• It is vegetables poison in 1782, a Swedish chemish
karl sheel prepared from purssian blue. It is coloured
gas having penetrating colour like bitter almond. The
pure acid is colourless liquid and volatile in nature.
Their important source are potassium cyanide and
sodium cyanide. Its pure form is called prussic acid.
 Mode of action

• The poison combines with cytochrome oxidase which is

concerned with transfer and utilized of oxygen.
• The formation of cynide cytochrome oxidase compound
inhibits the metabolism of oxygen in the tissues.
• They cannot utilize the oxygen although oxygen is present in
abundant amount. As a result venous as well as arterial blood
remains oxygenated.
• The immediate case of death is histotoxic or cytotoxic
anoxia.
 Sign and symptoms
• These depends upon the level of cyanide in the blood
• 0.5-1mg/L
Conscious, flushed rapid pulse , headache
• 1-2.5mg/L
Spontaneous but response it stimuli, loss of muscle
power, tachycardia and tachypnoea.
• 2.5mg/L –more
Comatose, unresponsive, hypertensive, slow and
grasping respiration, dilated pupil, cyanosis and death
• Fatal dose:60 mg of pure acid or 60mdrops of crude oil
or 200 mg of potassium cyanide
• Fatal period:2-10minutes
 Treatment
• Remove the patient from the sources
• Remove the clothes and wash the clothes with plenty
of water
• Give sodium thiosulphate I/v.
• Methyl nitrate inhalator
• 0.3% sodium nitrate
Principal of treatment
• If we use nitrate then
• It is to reverse the cyanide cytochrome oxidase combination.
• This is achieved by converting haemoglobin into methaemoglobin has
grater affinity for cyanide than the cytochrome oxidase. So cyanide
combines cyanomethaemoglobin , which is non toxic and slowly
dissoluble.
Post mortem appearance
• External:
• Smell of bitter almond
• Postmortem lividly is pink in colour
• Fresh froth at the mouth
• Blood shoot eyes (with dilated pupils)
• Internal:
• Bitter almond smell in stomach
• Pink colour
• Brain and meninges are congested
• Lungs congested
• Petechial haemorrahge on pleura and pericardium
Medicolegal Appearance
• Poisoning is mainly suicidal as it is very cheap, easily
available and death is irritant.
• Homicidal is rare because it has a smell of bitter
almond.
• Accidental poisoning is common in children.
 Carbolic acid
• Carbolic acid is also known as phenol hedroxy benzene
• Formula:C6H4OH
• When it is pure it is in the form of colorless , needle like
crystal
• When exposed to atmosphere it turns pink.
• It has peculiar odor, sweat burning taste.
• Present in Dettol and Lysol like solution.
• Carbolic acid poisoning is known as carbolism.
•
 Sign and symptoms
• Local:
• It is very rapidly absorbed from all surface even intact
skin.
• It cause necrosis and sloughing of tissue because it has
remarkable penetrating property.
• GIT TRACK:
• It cause, burning pain, anesthesia
• It cause difficulty in swallowing.
• Lips and mouth mildly corroded.
• Burns are white later turn brown due to sloughing off
of tissue.
• Remote action:
• Shock: Due to its corrosive and CNS depressing
effect. It cause , giddy with cold , clammy skin, weak
pulse , contracted pupil.
• Strenuous breathing, carboluria.
• Kidney effect:
• oliguria
• Albumin, and metabolic product of carbolic acid
metabolism in urine.
• Dark smoky green urine to which coma and death
follow.
• Fata dose:3-10 gm( 20 drop aprox)
• Fatal Period:3-4 hrs
 Treatment
• Stomach wash with 20% alcohol , soap solution.
• Demulcents like milk, egg albumin, barley water, IV fluid add
NaCHo3( Sodium Bicarbonate).
• For Respiratory distress= Atropine sulphate
• For Circulatory collapse=J. V fluid and vasoconstrictor.
Postmortem Appearance
• Grayish white stains on corroded are, Characteristic odor from mouth,
nostril ect.
• Cerebral edema
• Pulmonary edema
• Green/ brownish urine
• Leathery stomach
• Liver /spleen white patch
• Swollen Glottis
Medicolegal Aspect
• Accidental
• Occupation hazard
• Suicidal etc.
 Finger print system

•Dactylograph ( Dermatoglyphics,
Dactyloscopy, Galton system, Finger –
print system)
Definition:
• Fingerprints are impressions of patterns formed by the
papillary or epidermal ridges of the finger tips.
• It is the process of taking impression of the pulp of
finger and thumbs on an unglazed white paper and
examination them with a magnifying lens. The system
was discovered by sir William J Herschel. It was
systematized in 18 92 by Sir Francis Galton.
WHAT ARE FINGERPRINTS:
• Caused by raised portion of the skin on your finger, toes, palms and
lips.
• Raised portion are arranged in connected units call dermal, or friction,
ridges.
• When these ridges press against things, they leave a
mark=
Principle:
It is based on principles that the individual peculiarities
of the patterns are absolutely constant and persistent
throughout life from infancy to old age and that the
patterns of on two hands resemble each others.
Features:
• Identification by this system is absolute.
• Fingerprints are highly individualistic even I
monozygotic twins.
• Fingerprints are formed during intra- uterine life.
• It has been estimated that the chances of two persons
having identical finger prints is about one in sixty four
thousand millions.
• The fingerprints follow Quetelet’s rule, all nature
made things have unlimited and infinite variation of
forms.
Classification of Finger print Pattern
• Sir Henry Galton (1892), classification the finger prints into four major
or primary types.
• 1-Loop (65% of population)
• 2-Whorl (25% of population)
• 3-Arch (07% of population)
• 4-Composite/compound is a mixed picture of all three patterns above
(02-03% of population).
Four primary type of fingerprints:
• Loops: Loops usually being on one side of the finger and
end on same side. When this happened from ulnar side it
is called ulnar loop end if on radial side---radial loop.
• Whorl—This could be having multiple circular /oval
ridges, one around the other , or a single ridge , round in
multiple rounds.
• Arches: Plain arch is sharp and spike like.
• Composite: It is combination of more than one pattern ,
either a combination of arch, whorl and loop . Four
primary types of finger prints
 Medicolegal Importance of Finger -print
1. Epidermal ridges in the skin of palms and sole are
developed as early as 4th month of IUL.
2. Finger print is a 100 percent accurate method in
establishing identity.
3. No finger prints of 2 individual , even in case of
monozygous identical twins are similar.
4. An estimated scientific report pronounces that chances of
resemblance of finger prints in two people is just : 1 in 64
billion which renders dingers prints as unique method of
establishing human identify..
5. Visible finger –prints: Fingers when smeared with blood,
grease etc. will leave their prints/ impression on the the
weapon used for the crime/ furniture or such other articles that
may be touch by criminal at the scene of crime unintentionally
and can give clue for identifying the criminals. Such
fingerprints constitute visible finger prints.
6. Latent finger print (invisible finger prints): Finger prints
expert can render a faint and invisible / latent finger prints
visible by special techniques using some developing agents
which are chemical powders as liquid.
7. Plastic finger prints : These are prints of the finger
left on soft materials such as wax, soap, dust etc.
8. Finger prints from dead body: Tip of the finger may
get shrivelled in a dead body and then may mask the
picture. So to avoid this , soak the finger in alkaline
solution first and then take the print. Finger print may
be even taken from putrefied body where the cuticle of
finger ball is peeled off from fermis, which will have
the ridges pattern still intact.
• 9. Finger prints are important because they can be transmitted easily
from one place to another by telegraphic message easily.
 FOOT PRINTS
• Similar to the finger prints, skin patterns of toes and heels from the
sole of the feet are distinctive and permanent can tell identify.
• Procedure Taking Foot Prints:
• It is taken by using printer’s ink and a clean paper.
• Collecting Foot print Impression
• Left in the soil or sand
1. Spray the impression in the soil or sand with 80 percent of alcohol
solution of shellac. This harden the soil or sand.
2. Next smear the hardened surface with lubricant or dust with French
Chalk.
3. Then, pour an aqueous mixture of plaster of paris and allow it to
dry and on drying remove the cast and study the impression.
4. Foot print will be larger on walking than on standing.
5. Important left on soft and loose material like sand will be always
smaller
6. Look for any deformities like---flat foot, web foot , loss of toes.
Foot print of new born infants-Usually taken in certain maternity
hospital for the simple.
 Caustic Alkalis
• AUSTIC ALKALIES
• AMMONIA, KOH, NaOH, Ca(OH)2,
• (Ammonium ,Na , K ) Carbonates
• Ammonia is a colourless gas with a very pungent
choking odour.
• House hold bleaches commonly consist of 5%
Na Hypochlorite solution and cause moderate
mucosal irritation.
Mode of Action
• Commonest cause of chemical burns
• OH‐ ion cause saponification of fats, soluble alkaline
proteinases, cellular dehydration and an exothermic
reaction
• The ion passes from molecule to molecule, denaturing
each in turn, and burrows deeply, producing soft
gelatinous, friable eschars (liquifactive necrosis).
• Effect esophagus> gastric mucosa
• So stricture formation much more common with
alkalies then with acids
Sign/Symptoms:
• Acid caustic taste + sensation of burning heat
extending from throat  stomach Vomited matter
alkaline and do not effervesce, contains dark altered
blood, shreds of mucosa.
• Purging frequent + severe pain & straining Motions
consist of mucous/ blood Skin shows greyish, soapy,
necrotic area, Abrasions, blisters and brownish
discoloration on lips, skin around mouth.
• Mucosa soft, swollen, grey slough readily detaches, lie
over the inflamed tissue , Oesophageal stricture
conti….CAUSTIC ALKALIES
• LYE ( NaOH)
• Transmural necrosis of the oesophagus only after 1 sec of contact
• Oesophageal stricture is common with occasional perforation.
• Miniature batteries(KOH): cause liquifaction necrosis following
leakage from battery, symptoms mostly limited to G.I.T.
Ammonia vapours: Inhalation causes congestion and watering of the
eyes, violent sneezing, coughing and choking. • Sudden collapse and
death may occur from suffocation and inflammation of glottis or
later from pneumonia
• FATAL DOSE:
• NaOH, KOH: 5 gm • Potassium carbonate:
18 gm • • FATAL PERIOD: Usually 24 Hrs
Treatment:
• 1) Demulcents • 2) In mild cases GL may be done, carefully.
• 3) Oxygen • 4) Symptomatic
PM Findings:
• Marks dark, parchment like Lips, mouth , throat shows
corrosion
• Inflammatory oedema with corrosion, sliminess of the tissues
of the oesophagus and stomach are prominent features
• Mucosa brownish due to formation of ??
• Oedema of glottis due to ???
• Pseudo membranous inflammation of the air passage and peri
bronchial pneumonia
• Perforation rare but may occur in ammonia
Medicolegal Asspect
• Suicidal Poisoning
• Accidental Poisoning