Duties of a doctor in suspected
poisoning is described under
S.39 CrPC
S.175 CrPC
S.193 IPC
S.176 IPC
S.201 IPC
S.202 IPC
201 –(punishment IPC no. if not
done)preserve articles , food, excreta ,
stomach wash , bottles , capsules , paper
packets should be collected and preserved
39 – if a private practitioner is convinced that it
is a homicidal poisoning he should inform
police officer or magistrate
If 39 not done doctor is punishable under 176
If he is sure that it is suicidal poisoning no
need to inform police since 309 is not included
in the section
But under 175 if asked by police officer Dr
should give all information
If conceals liable to get punished under 202
False information – section 193
He will be punished
Gastric lavage
Within 3 hrs
For salycylates,phenothiazenes,antihistaminics,TCA, -- lavage
can be done upto 12 – 18 hours
Ewald’s / Baos tube
First 250 ml then 500 ml
CI – corrosive poisoning except for phenol
Complications –
1.Laryngeal spasm
2.Aspiration pneumonitis
3.Perforation of the stomach
4.Sinus Bradycardia
Organophosphate poisoning
Mixed in a solvent called Aromax – kerosine
like smell in the body cavity,stomach contents ,
vomitus , froth, etc
Inactivation of Che becomes irriversible after 24 –
36 hrs
Sign & symptoms – when activity drops to 30% of
normal activity
Death – paralysis of the respiratory muscles
Choline esterase test
5 ml of heparinised blood
average normal values
77 – 142 in red cells
41 – 140 in plasma
Diagnosis can be confirmed by giving 2 mg of
atropine in normal signs of atropinisation and
in poisoned releives the symptoms
Post Mortem appearance
Signs of Asphyxia
Congestion – face,all internal organs
Cyanosis of lips,fingers , nose
Blood stained froth--Respiratory path ,
mouth and nose
Stomach content with smell of
kerosene
Organophosphorous can be detected in
putrified bodies
Oxims
DAM – Di Acetyl Monoxime
Praldioxime Iodide
Pralidoxime chloride
Endrin –Plant penicillin
Zinc Phosphide
Fatal dose 5g
Fatal period 24
hrs
Aluminium Phosphide
Release
phosphine
MOA – inhibition
of cytochrome
oxidase
Fatal dose -1-3
tab
Fatal period – 1
hour to 4 days
Sulphuric acid Poisoning
Treatment of Sulphuric acid
poisoning
Avoid gastric lavage
250 ml of water / milk / milk of magnesia /
lime water – within 30min
Demulcents
Prednisolone 60 mg / day - to prevent
esophageal stricture and shock
If stricture develops – 4cm diameter Hg filled
bougie should be passed daily
Give nothing by mouth
Topica l paste of Magnesium oxide / sodium
bicarbonate
PM change
Stomach – soft , spongy , black mass ,
when readily disintegrates when
touched
Treatment of vitriolage
Wash with plenty of water
Soap of Sodium or Potassium carbonate
Thick paste of magnesium oxide / carbonate
is applied
Eyes – irrigated with Dilute Sodium
bicarbonate solution
Later a few drops of olive oil or castor oil is
applied to the eyes
Nitric acid
Sign and symptoms
Greater abdominal distension due to gas
formation
Tissues are stained yellow
In esophagu and stomach …the corrosion of
the mucus membrane may not be associated
with yellow colour –Brown or Brown black due
to acid hemetin
HCl
Corrosion is less severe
Stomach contains brownish fluid
The folds of the whole stomach mucosa are
brownish
Perforation is rare
Acute inflammation and edema of the
respiratory passage are common
Oxalic acid
10%
Rarely damage the skin
Corrodes mucus membrane
Vomitus – coffee ground appearance- altered
blood and mucus
Hypocalcemia
Treatment of Oxalic Acid poisoning
Stomach wash – Calcium lactate or gluconate
Antidote – preparation of Calcium
Lime water , Calcium gluconate ,Calcium
chloride
Parathyroid extracts bowel may be evacuated
by enema or castor oil
Carbolic acid
Carboluria – further oxidation of
hydroquinone and pyrocatechol in the
urine cause green colouration
Chronic Poisoning – Phenolic
Marasmus-Anorexia , headache ,wt
loss ,headache ,darkurine , and
oochronosis
Oochronosis – pigmentation of skin
and sclera
Post Mortem findings in carbolic acid poisoning
i) Esophagus - Mucosa is tough, corrugated,
arranged
in longitudinal folds.
ii)Stomach - Mucosal folds are swollen covered
by opaque,
coagulated mucous membrane which is
thickened and leathery. Partial separation of
necrotic mucosa.
iii)Duodenum, - Similar to stomach
upper SI
iv)Liver, Spleen- Whitish, hardened patch where
stomach has
been in contact.
v) Kidneys - Haemorrhagic nephritis
vi)Brain- Congested, edematous
vii)Blood- Dark, semifluid, only partially coagulated.
Formic acid
Action – corrosive actioo on GI mucosa
Causes hemolysis leading to acute renal
failure
ATP synthesis is diminished
T/T –Milk –Folinic acid 1mg /Kg 4
th
hourly
Arsenic Poisoning
Metallic arsenic is not poisonous as it is
not absorbed from the alimentary canal
Arsenic trioxide / white Arsenic
MOA – binds and inhibits Pyruvate
oxidase which is a mitochondrial enz
Affects vascular endothelium –
increased permiabilityesp in the
intestinal canal
Irritation of the mucucs membrane
Depression of the NS
Interfers with glycolysis
Signs & symptoms
1.Fulminant type
2.Gatro enteric type
3.Narcotic
Fulminent tyoe
Massive doses – 3 -5 gm Arsenic death in 1 –
3hrs – due to shock & peripheral vascular
failure
Gastro enteric type
Common form of acute poisoning
Mostly half an hour after ingestion
Sweetish metallic taste
Constriction of the throat and difficulty in
swallowing
Burning and colicky pain in the esophagus,
stomach and bowel
Purging
Stools – frequently and involuntary first
Dark coloured stinking and bloody
resembles rice water stools
Garlicky odour in breath and feces may be
noted
Death is usually due to circulatory failure
Narcotic Form
Giddiness
Formication and tenderness of the muscle
Delerium coma and death
Arseniurated hydrogen direct poison to Hb
hemolysis ,hemoglobinuria , renal failure
Death is almost instantaneous
Treatment of Arsenic Poisoning
Emetics should not be used
Alkalis should not be used
Wash with large amount of warm water /
milk
Ferric oxide
BAL
DMPS
DMSA
Penicillamine
Demulscents
Glucose saline with Sodium bicarbonate
Hemodyalisis and exchange transfusion
PM appearance – acute
PM appearance- chronic
Mercury
Mercuric
Egg white
Ca – EDTA should not be used as it is
nephrotoxic with mercury
PM – if the patient survives forfew days
..LI shows necrosis due to the reexcretion
of mercury into the large bowel
Chronic poisoning – Hydrargyrism
PRESENCE OF TISSUE DEPOSITS OF Cu
-CHALCOSIS
INORGANIC POISONING
Phosphorus
Preservation for viscera in case of
suspected poisoning
Stomach and its contents
Upper part of small intestine and its contents
30 m
Liver 200 300 g
Kidney – half of each
Blood 30 ml
Urine 30 ml
Preservatives
Saturated sodium chloride- all except
Corrosives
Rectified spirit
KF