Agrochemical Poisoning

Dr. Janaki Warushahennadi

Senior lecturer
Faculty of medicine
Karapitiya

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Why we should learn about Agro chemical
poisoning? It is a common casualty in
hospitals
• Sri Lanka is an agricultural country
• Agrochemicals are widely used
• No proper rules and regulations to sell, storage,
and usage – accidental poisoning

• Suicidal rate is high.

• people try to choose the most available and
cheapest method for self killing

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 Classification of Agro chemicals
• Insecticides
• Weedicides
• Rodenticides
• Fungicides
• Mollucides

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 Circumstances of poisoning

• Deliberate self poisoning/suicidal

• Accidental – agrochemical handlers

• Homicidal

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 How a person can get poisoned?
(Routes of entry)
• Per os

• Inhalation

• Per cutaneous

• IM/IV

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Medico Legal duty of a doctor in a case
of poisoning
• Patients with poisoning - ( if the circumstances
are suspicious, or homicidal) – notify the
police – the police will issue MLEF

• All deaths due to poisoning – inquest – post

mortem – course of death

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 Different groups of Agro chemicals
• Insecticides
• Weedicides
• Rodenticides
• Fungicides
• Mollucides

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 Different groups of Insecticides
• Organophosphates
• Carbamates
• Organochlorines
• pyrathroides

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 Organophosphate poisoning

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 Organophosphates(OP)
• Ex. Run bug, Folidol, Parathion

• Basis of many insecticides

• It is a colorless fluid which is oily and has a
kerosine smell
• Accounts for 1/3 of hospital admission with
poisoning in Sri Lanka
• OP is used as a chemical war – Syria,Japan
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 Action of organophosphate on human
• Irreversibly inhibit enzyme acetyl
cholinesterase in nerve endings

• Accumulate acetylcholine which is a

neurotransmitter both CNS, peripheral nerve
endings).

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Action of acetylcholine at nerve ending

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 Clinical features
• Are due to effect caused by excess
acetylcholine

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 question
• What are the clinical features of OP
poisoning?

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 Signs and symptoms of OP poisoning
• Starts soon after the ingestion

• Non specific signs

headache
general weakness
Nausea
Vomiting
Abdominal pain, abdominal cramps

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 Specific clinical features
• Specific clinical features due to the action of
particular poison on the body

• Are due to effect caused by excess

acetylcholine

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 Acetylcholine receptors are present

• Postganglionic parasympathetic nerve

endings,

• neuro- muscular junctions,

• central nervous system

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 Clinical features - Post-ganglionic
parasympathetic stimulation

• Begin to sweat, salivation, diarrhea,

• Increase bronchial secretion, Cough,

wheezing, pulmonary oedema, cyanosis

• Pupils- small, pin point. – blurred vision

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 Clinical feature - Action at neuro-
muscular junction

• Muscle twitching, in coordination, weakness,

paralysis

• Bradycardia, cardiac arrhythmia

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 Clinical feature - Action on CNS
• Disorientation, Confusion
• Depression of cranial nerve system
• Convulsion
• Coma
• Depression of respiratory system

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 Mechanism of death
• Respiratory depression

• Cardiac arrhythmia

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 Clinical features OP
• Inhalation – cough, wheezing, bronchitis,
pnevmonia

• Eye contact – irritation, pain, lacremation,

blurred vision

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 Late onset of clinical effects –
intermediate syndrome

• Appears 1 – 4 days after the ingestion in some

patients following OP exposure
• clinical feature – difficulty in breathing due to
Paralysis of respiratory system
• Exact mechanism is not known
• Require mechanical ventilation

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 Late complications on survivors
• Peripheral neuropathy
numbness of limbs

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Management of a patient following OP
poisoning

• Prevent further poisoning - Induce vomiting,

Clean the body, change cloths

• Maintain ABC - clear airway, suck out

secretion, give Oxygen, ventilation, IV cannula,
drips

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Management of a patient following OP
poisoning

• Specific management
• Antidote – Atropine. Atropine antaganize the
parasympathmimetic and the central effects
of Ach.

• Pralidoxime(PAM) – Breaks the irreversible

binding of acetylecholinesterase.
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 Management of OP poisoning
• symptomatic management
if pneumonia - antibiotis,
gastritis - antacides

• Supportive management
Psychiatric referral, psychological support,
neurological support

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 Death due to OP poisoning

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 Post mortem findings – no specific
features

• Kerosine smell from body, cloths

• White, fine froth around mouth and nose,

respiratory tract

• Gross pulmonary oedema – white froth oozing

from the cut surfaces of the lungs

• Poison in the stomach

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 Sample collection in OP poisoning
• Patients (homicides, suspicious) – 5 ml of
blood (After obtaining the consent from
patient)

• Deaths – 10 ml of blood , stomach contents

• Decomposed body – stomach contents, 500 g

of liver, skeletal muscle
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 Decomposed body

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 Carbamate poisoning

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 Carbamate poisoning
• Insecticide – EX. Baygon, baycarb
• Action same as OP
• Reversibly inhibits acetylcholiesterase
• Clinical features same as OP

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 Different groups of Agro chemicals
• Insecticides
• Weedicides
• Rodenticides
• Fungicides
• Mollucides

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Weedicides – Parquet poisoning

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 Availability

• Gramoxone – 20% of paraquot,

• Weedol

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 Why parquet is ideal weedicide
• It kills all the green plants on contact (inhibits
photocynthesis)

• It is a very safe agrochemical

• Gets inactivated on contact with soil
(treatment is Fullers earth)

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 Toxicity of parquet
• Parquet is very toxic substance

• Lethal dose is around 20 – 40 ml.

• Parquet is the second commonest

agrochemical poisoning in Sri Lanka

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 Paraquat in bowel

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 Parquet in bottle

• Distinct colour

• Distint bad smell

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 Circumstances of poisoning

Self ingestion – per os

accidental-
 children- can drink accidentally,
 Adult- inhalation,
 Theough skin usually occupational.

 Homicidal- with food, can inject IM, IV.

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 Metabolism of paraquet
• Absorption – only 5 % is absorbed through bowel

• Unabsorbed portion is excreted with stools.

• Tissue distribution- maximum blood level in 6

hours.

• Parquet has the affinity to tissues with high Oxygen

level
• Actively absorbed to lungs and stored in lungs.
• Damage – mainly to lung tissues

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 Metabolism
• After 24 –48 hours – not found in blood.

• Excretion- Release from lungs in 1- 2 weeks

and excreted unchanged with urine.
• Can be found only in urine for about 2
weeks.

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 Action on tissues

• Local effect - Paraquat cause local

corrosive effect

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 Ulceration of the tongue – paraquat
tongue

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 Action after absorption – after
absorption
• Exact mechanism is not known.

• Parquet combines with tissue NADPH

• Forming super oxide radicals which

• Cause cell membrane destruction and cell

death – mainly on lung tissues

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 Damage on lung tissues
• Early - Destructive phase (upto 7 days)

• Delayed – proliferative phase 1 – 2 weeks

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 Clinical features
• Non specific features

• GIT irritation – nausea, vomiting, abd. cramps

Discomfort, diarrhea, sweating

• Due to the corrosive effect - Soreness of the

mouth – dysphagia, burning sensation in GIT

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 Early Systemic effects - due to direct
toxicity in large doses
• Brain - Tremors , convulsions
• Kidneys – Acute Renal failure (acute tubular
necrosis)
• Liver – liver failure(centri lobular necrosis)
• Lungs – pulmonary haemorrhge, oedema,
(damage of epithelium, intersticium)ARDS

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 Early Systemic effects
• patient may die within few days due to multi
organ failure

• Autopsy features???

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 Ulceration of the tongue – paraquat
tongue

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 Distended lungs

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 Cut surface of lung shows congestion

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Fatty liver
 Autopsy features in destructive phase
• Ulceration in the lips, tongue or buccal
mucosa
• Ictarus
• Erosion and ulcerations in the upper GIT
• Enlarged fatty liver
• Swollen kidney
• Pulmonary congestion and oedema
• presence of greenish fluid in GIT

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 Delayed phase – proliferative phase

• Appears after 7 – 14 days

• Clinical sign – dyspnoea

• Pathology – diffuse intra-alveolar fibrosis

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 Autopsy features
External
• Ulceration of the mouth, tongue, buccal
mucosa
• Icterus

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 Internal autopsy findings
• Liver- enlarged, fatty, necrsis

• Kidney – swollen, pale cortex, congested

medulla
•

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 Delayed lung changes
• Features of lung • Heavy, rubbery, areas of
fibrosis fibrosis
• Honey comb lung

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 comparison

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 Local contact
• Ulcerations due to corrosive effect

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 Treatment of a victim following
paraquat poisoning
• Prevent further poisoning

• Maintain ABC

• Give Fullers earth to drink

• Should not give Oxygen

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 Collection of samples
• In early stage……………..

• Late stage…………………..

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 Question?

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