CARBOLIC ACID

PHENOL (C6H5OH)

CONTENT :-
• Physical properties
• Routes of absorption
• Action
• Metabolism and excretion
• Signs and symptoms
• Diagnosis
• Fatal dose
• Treatment
• Postmortem findings
• Medicolegal importance
 PHYSICAL PROPERTIES
• Pure form-
Colourless,
Short,
Prismatic needle shaped crystalline
form.
On exposure to air it turns pink and
liquifies.
It is soluble in fat, glycerine, ether,
alcohol, and slightly in water.
Characteristic carbolic or phenolic
smell.
Burning sweetish taste.
• Commercial form-
Dark brown liquid.
Contain several impurities.
Used as disinfectant
 ROUTES OF ABSORPTION
• Intact skin by local application or spillage.
• Gastrointestinal tract by oral ingestion.
• Reaspiratory tract by inhalation.
• Per rectum.
• Per vaginum.

ACTION
• Phenol is a protoplasmic poison.
• It enters into loose combination with proteins
and penetrates deep into the tissue.
• When applied to skin or mucosa it causes
necrosis and gangrene.
• The local nerve endings are first stimulated and
then paralysed, resulting in anesthesia.
• After absorption it causes widespread capillary
damage and clotting in superficial blood vessels.
• It also acts on the cells of central nervous
system, heart and kidneys.
METABOLISM AND EXCRETION
• Phenol is metabolized mainly by the kidneys,
wherein it gets converted into hydroquinone and
pyrocatechol and excreted in urine.
• These products turn urine olive green or brown
on standing and the phenomenon is called
carboluria.
• Complete elimination occurs in 36 hours.

SIGNS AND SYMPTOMS

• Poisoning by carbolic acid is known as carbolism.
• Headache, giddiness, tinitus.
• Vomiting, diarrhoea, and pain in abdomen.
• Muscular spasm and convulsions.
• Collapse – unconsciousness, coma.
• Clammy, cold, sweating body.
• Stertorous breathing with cyanosis.
• Pupils dilated.
• If survives for 48 hrs – carboluria followed by
anuria. Victim will pass dark, smoky urine which
soon turns olive green on standing.
• Methemoglobinaemia is a characteristic feature
in severe cases.
• Death may result from respiratory and
circulatory failure.
 Affected tongue

Grayish white discoloration of oesophagus inner

surface
 DIAGNOSIS
• Corrosions on face, around and inside the mouth
( grayish white if phenol or brownish if lysol).
• Phenolic odour ( breath / vomitus ).
• Carboluria.
• Dilated pupil.
• Stertorous breathing.

FATAL DOSE
• Fatal dose- 10 to 15 gm.
• Fatal period- 3 to 12 hrs.
• Toxicity rating- 4.

TREATMENT
It depends on route of administration.
A} In case of skin absorption :-
1] Remove the contaminated garments.
2] Cleanse the site by mopping with wet cloth
 and wash with soap and water.
3] Apply olive oil / methylated spirit / 10
percent ethyl alcohol which can prevent
further absorption.
4] Shift the victim to fresh atmosphere and
make him breath in fresh air.
5] Give normal saline + sodium bicarbonate
(I/V – drip)
B} In case of poisoning through oral route :-
1] Perform gastric lavage : Though phenol
corrodes the stomach wall, it also hardens
it unlike other corrosive poisons.
Hence gastric lavage is performed whenever
possible with plenty of luke warm water
containing animal charcoal, olive oil,
magnesium or sodium sulphate or saccharated
lime, soap solution, 10%glycerine etc.
When the lavage is completed, 30 gm of
magnesium sulphate or medicinal liquid paraffin
should be left in the stomach.
2] Give egg white : Epsom salt/ demulcents
orally.
 C} Symptomatic :-
1] Artificial respiration
2] Tracheal aspiration of froth / secretions.
3] Glucose saline to induce diuresis.

POSTMORTEM FINDINGS
• External :-
Grayish or brownish corrosions at the
angle of the mouth, chin tracks, in front of the
body, arms and hands (splashes) with
characteristic phenolic odour.
• Internal :-
Corrosions of gastrointestinal mucosa,
laryngeal and pulmonary oedema has been
observed in all orally ingested poisoning cases
However certain specific findings observed, as
1] Stomach changes :
Opening the stomach will emit the phenolic
odour. The stomach wall is usually hardened and
due to hardning, the stomach will have a leather
bottle appearance, and is called as leathery
stomach.
Gastric mucosa will present with marked
corrosions and swelling of mucosal folds with
coagulated grayish or brownish silvery mucus on
it. Intervening normal mucosal folds appear dark
red in colour.
2] Kidney will show haemorrhagic nephritis
when the victim survives for some time after
poisoning.
3] Vomitus and gastric lavage collection may
show partially detached gastric mucosa.
4] Preservatives used for sending viscera for
chemical examination : Supersaturated solution
of sodium chloride.
MEDICOLEGAL IMPORTANCE
1] Often phenol is used as a disinfectant and
preservative for vaccines and sera.
2] Fatalities due to phenol occurred more
frequently in the past than at present time.
Accidental poisoning still occurs, particularly in
homes. Cases of poisoning are usually due to
accidental consumption or spillage over the
body.
3] Phenol is rarely suicidal or homicidal due to
the strong phenolic odour.
4] Phenolic solution is used as an abortifacient
by quacks for syringing it into the uterine cavity
to induce criminal abortion even today.
5] Ochronosis is a condition associated with
alkaptonuria, an inborn error or metabolism, in
which homogentisic acid gets deposited in the
cartilages, ligaments, and fibrous tissues.
It is sometimes seen in chronic phenol
poisoning ( infrequent these days ) wherein the
phenolic metabolites pyrochatechol and
hydroquinone gets deposited in the cartilage
and ligaments causing dark pigmentation.
 OXALIC ACID
ACID OF SUGAR
(C2H2O4)

CONTENT :-
• Physical properties
• Action
• Signs and symptoms
• Diagnosis
• Fatal dose
• Treatment
• Postmortem findings
• Medicolegal importance
 PHYSICAL PROPERTIES
• Colorless
• Prismatic crystalline substance
• Similar to magnesium sulphate [MgSO4] and
zinc sulphate [ZnSO4].
• Natural oxalate: occurs in plants like spinach,
rhubard, cabbage, tomatoes.
• Excretion: 20mg of oxalic acid daily in urine.

ACTION
• Acts locally as a corrosive, on both skin and
mucosa. (more severe)
• Remotely on absorption into blood affects
several systems, the important once are :
➢Electrolyte Extracts tissue calcium
Hypocalcaemia.
➢Cardiovascular system Shock Death.
➢Renal system Tubular necrosis Uraemia
Death
 SIGNS AND SYMPTOMS
• Presenting in three forms :-
a] Fulminating
b] Acute
c] Delayed
A] FULMINATING :-
• With large doses (15 gm or more) orally can lead
to sour and acidic taste, followed by a sensation
of constriction around throat and burning pain
from mouth to epigastrium, which radiates all
over the abdomen.
• There will be tenderness in the epigastrium,
nausea followed by vomiting (coffee ground
coloured vomitus) , severe thirst, diarrhoea,
electrolyte imbalance and death.
B] ACUTE :-
• All signs and symptoms of hypocalcaemia
(tetany), characterised by tonic muscle spasms,
cramping , and accoucher’s hand. There is often
a positive Trousseau’s and Chvostek’s sign.
• Pupils are usually dilated.
• All findings are mainly due to hypocalcaemia
such as – muscle irritability, tenderness, tetany
and convulsions, tingling of extremities, coma,
collapse and death.
C] DELAYED :-
• Later there may be metabolic acidosis,
ventricular fibrillation and renal failure.
• Findings will be of uraemia. Urine will be scanty
with traces of albumin , blood and calcium
oxalate crystals (seen microscopically as
envelope- shaped crystals).

DIAGNOSIS
• Demonstration of urinary oxalate crystals which
may occur either as monohydrates (prism or
needle like), or dihydrates (tent or envelope
shaped).
• Oxalic acid can be measured in the urine by
colourimetry. The normal upper limit is 40 to 50
mg/24 hours.
• Average serum oxalate concentration is said to
be 1.4 mg/L.
 FATAL DOSE
• Fatal dose- 15 to 20 mg.
• Fatal period- 1 to 2 hrs.
• Toxicity rating- 4.

TREATMENT
• Gastric lavage with calcium lactate (2 teaspoon
per lavage).
• Antidotes - lime water, calcium lactate, calcium
gluconate, calcium chloride, chalk suspension in
water or milk etc may be given orally, acts as
specific antidotes, which form insoluble calcium
oxalate and are excreted easily.
• 10 ml calcium gluconate I/V frequently.
• Parathyroid extracts: 100 units I/M.
• Demulcent drinks.
• Bowel wash by enema and purgatives (castor
oil).
• Symptomatic measures.
 POSTMORTEM FINDINGS
• External :-
No specific findings. However burns of the
face and skin rarely seen.
• Internal :-
Mucosa of the mouth, tongue, pharynx and
oesophagus are bleached (whitened/ scald/ red)
if a strong solution is consumed.
• Stomach changes :-
- The stomach mucosa is reddened and
punctate due to erosions giving ‘velvety red’
or blackish appearance.
- Wall of the stomach is softned, but no
perforations.
- Contents : Gelatinous brown (due to acid
hematin formation)
• Kidney changes :-
- Swollen and congested. Tubules on
histopathological study reveal to be filled
with oxalate crystals.
 MEDICOLEGAL IMPORTANCE
• Usually consumed accidentally (mistaken for
magnesium sulphate).
• Suicidal or homicidal uses are rare due to taste.
• As an abortifacient : Occasionally used to induce
criminal abortion.
• Used for illegal erasure of signatures.
• It is detected in certain vegetables as oxalates
eg. Beets and in the leaves of spinach, rhubarb,
cabbage etc and many other vegetables, rarely
causing poisoning.
• Oxalic acid is used in paint, stain and varnish
removers, rust and ink stain removers, and
ceramics.
• It is also used in general metal and equipment
cleaning, wood cleaning, process engraving,
printing and dyeing, bleaching, textile finishing,
leather tanning, and photography.
 FORMIC ACID
METHANOIC ACID
FORMYLIC ACID
(HCOOH)

CONTENT :-
• Physical properties
• Action
• Signs and symptoms
• Complications
• Fatal dose
• Treatment
• Postmortem findings
• Medicolegal importance
 PHYSICAL PROPERTIES
• Colorless liquid.
• Pungent penetrating odour.
• It is used as kettle de-scales or bath cleaner.
• Generally airplane glue makers, cellulose
formate workers and tanning workers are
exposed to 60 per cent solution of formic acid.

ACTION
• Coagulative necrosis type of corrosive action on
the GI mucosa.
• Damages clotting factors and causes haemolysis
leading to acute renal failure.
• At the cellular level, it has an inhibitory action
on aerobic glycolysis with consequent
diminution of ATP synthesis.
 SIGNS AND SYMPTOMS
• On coming in contact with skin it produces
brownish discoloration, dermatitis, pustules,
vesicles and sometimes sloughing.
• Formic acid is unique for its ability in many
patients to cause death after a prolonged
(several weeks) course of classical acid induced
gastrointestinal damage.
• Certain other complications include severe
metabolic acidosis, intravascular haemolysis,
and disseminated intravascular coagulation.
• Accidental ingestion in children ordinarily does
not lead to fatalities since the pungent taste
prevents ingestion of lethal dose.
• It is nevertheless a problem when used
deliberatly for suicide.
• It causes acute tracheobronchitis, characterised
by cough, sour throat, chest pain and light-
headedness.
• Formic acid skin burns may also result in
systemic toxicity.
 • When absorbed by the body, it causes systemic
acidosis, haematuria and renal damage.
• Metabolism of methanol can also produce toxic
metabolites of formic acid.

Clinical features :-
• GIT :-
Burning pain, salivation, vomiting, mucosal
corrosion and ulceration, haematemesis.
• CNS :-
▪ Drowsiness, weakness, coma. Pupils are
dilated.
• CVS :-
▪ Tachy/ bradycardia, hyper/ hypotension.
• Blood :-
▪ Haemolysis, DIC.
• RS :-
▪ Acute respiratory distress, aspiration
pneumonitis, ‘shock lung’.
• Metabolic :-
▪ Acidosis, acute tubular necrosis, shock, and
death.
• Skin :-
▪ Erythema, blisters.

COMPLICATIONS
• Oral cavity burns.
• Metabolic acidosis.
• Septicaemia.
• Dysphagia.
• Oesophageal stricture.
• Gastro-intestinal perforation.
• Aspiration pneumonia.
• ARDS.
• Acute renal failure.
• Chemical pneumonitis.
• Shock.
 FATAL DOSE
• Fatal dose- 50 to 200 ml.
• Ingestions between 45 to 200 grams often result
in death within the first 36 hours post- ingestion.

TREATMENT
• First aid : Immediate dilution, by administering
milk.
• Induction of emesis, gastric lavage , and use of
activated charcoal are all contraindicated.
• High dose folinic acid (1 ml/kg IV bolus, followed
by 6 doses of 1mg/kg IV at 4 hourly intervals) is
recommended by some investigators, since it is
supposed to enhance formate degradation by
the liver.
• Supporting measures, with particular emphasis
on dialysis, exchange transfusion, intubation,
ventilatory support and correction of metabolic
acidosis and renal failure.
 POSTMORTEM FINDINGS
• Blackish corrosion of GI mucosa.
• Pulmonary oedema.

MEDICOLEGAL IMPORTANCE
• Accidental and suicidal poisoning with formic
acid is relatively common in those areas where
the chemical is easily available, for instance in
kerala where manufacturing rubber is a major
industry.
• In Europe also it is well known , if relatively
infrequent, vehicle for suicide.
• Used in dyeing colorfast wool, in electroplating,
coagulating latex rubber, regenerating old
rubber and dehairing and tanning leather.
• Used for the manufacture of acetic acid, airplane
dope, allyl alcohol, cellulose formate, phenolic
resins and oxalates used in laundry; and in
textile, insectiside, refrigeration and paper
industries.