CARBON MONOXIDE

POISONING
DR MACHARIA
MBchB (uon),Mmed Path
(uon), Dip. Forensic Path
(SA)
Objectives
• Causes of co poisoning
• Autopsy findings
• Mechanism of death
Causes
• Motor vehicle exhaust gases. Engines produce up to
5-7% co and more when it is idling. A 15cc petrol
engine idling in a closed garage would kill in 10min.
• Domestic heating appliances due to incomplete
combustion e.g jikos
• Structural fires where things like mattresses burn.
• Co from industrial processes like in iron and steel
works.
• Autopsy findings
• Adequate history may give a clue as to the cause
of death.
• Most striking is the colour of the skin especially in
areas of lividity. Cherry pink colour due to
carboxyhaemoglobin. This occurs if the co
concentration in blood is above 30%. Below 20%
no colouration is seen. In anaemic the colour may
be faint.
• Internally the blood and tissues appear cherry-
pink.
Other suggestive indications
• Add a few drops of blood to 10% NaOH on a
white tile. Normal blood will turn brownish green
due to methaemoglobin but if co is present, it
remains pink.
• Blood is analysed for co concentration using
spectrophotometry.
• Cause of death
• The oxygen carrying capacity of blood is
lowered since co displaces oxygen from
erythrocytes—Co has an affinity for HB
that is 200-300 times greater than that of
oxygen.
• Dissolved co also interferes with some vital
cellular enzymes.
AGROCHEMICAL POISONING
• Chemicals used in agriculture may cause
harm through
– accidental exposure
– self administration in suicide.
The main ones are the pesticides especially OP
compound like parathion, and herbicide like
paraquat
Herbicides (Paraquat)
• Once in contacy with soil, it is inactivated
• Toxicity occurs through ingestion though
inhalation of the aerosal may lead to toxicity.
• Only 5% is absorbed orally
• Poisonoining is through accidents, deliberate self
ingestion
• One mouthful of this herbicide is fatal.
• It is an irritant to epithelial tissues, thus the mouth,
esophagus, lips are superficially eroded.
• Of the absorbed, it causes necrosis of the liver.
• Diffuse tubular damage of the kidneys thus renal
failure within 2-3 days of ingestion.
• Progressive damage to the lungs is very
characteristic- pulmonary oedema and
haemorrhages occur.
Autopsy finding
• Ulceration around the mouth
• Reddened mouth mucosa or it may desquamate.
• Desquamation of the esophageal mucosa may be
seen.
• Erosison and patchy haemorrhages of the stomach.
• If the victim survives a week, pulmonary edema
and haemorrhages may be seen.
• Liver necrosis, tubular damage
Specimens
• Blood for herbicide levels (>0.2mg/L)
• Urine for herbicide levels – It is excreted slowly
therefore can be found in urine many days after
ingestion.
• Lung tissue for histology
• Stomach and its contents
• Liver, kidney
Organophosphates ( pesticides)
• Examples are parathion, marathion, dichlorvos.
• They inhibit cholinesterase.
• Can be absorbed through the skin, conjunctiva,
lungs, and gut.
• Due to inhibition of cholinesterase, acetylcholine
builds up at the neuromuscular junctions
rewsulting to hyperexcitability of muscles.
• Lethal ingested dose is 125-175 mg.
Autopsy
Has a kerosine base which can be detected by
smell.
Comercial cpds have a greenish colouring
agent that is seen in the stomach
Gastric mucosa may be haemorrhagic.
• History is very very important.
THE END
• Headache, D/V, sweating, salivation,
twitching, fits, wheezes, small pupils,
respiratory failure.
• Pralidoxime
• Atropine till full atropinization.( Dry
mouth, pulse >70 )