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Presentation on

ORGANOPHOSPHORUS
POISONING
• Organophosphates are used world wide
• Common cause of poisoning in the
developing world

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Types of organophosphate insecticides

Diazinon - phosphorothioic acid


Chlorpyrifos
Malathion
Parathion
Fenthion
Sarin

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Absorption route;
CUTENEOUSLY

INGESTION(ACCIDENTAL OR
SUICIDAL)

INHALATION

INJECTION

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Pathology
• Organophosphate are absorbed through the skin
lungs & GI tract and distributed widely in tissues
and are slowly eliminated in hepatic metabolism.
• The principal effect is inhibition of cholinesterase
enzymes, particularly acetylcholinesterase (AChE).
This leads to accumulation of acetylcholine at;
1. Muscarinic receptors- in cholinergic receptor
cell.
2. Nicotinic receptors – in skeletal
neuromuscular junction and autonomic
ganglia
3. CNS.
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Clinical Features
1. History of
– Ingestion
– Inhalation
– Dermal absorption

2. Features of intoxication are delayed i.e.


because it requires biotransformation to
become active

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3.Muscarinic effects of • Nausea,
Poisoning are • Urinary and fecal
characterized by; incontinence,
– Anxiety • Lacrimation
– Restless
• Miosis,
– Tiredness
– Vomiting • Wheeze
– Abdominal colic, cramps
– Diarrhea
– Tenesmus
– Sweating
– Rhinorrhoea
– Bronchorrhoea
– Dyspnoea due to
bronchoconstiction
– Chest tightness

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5. Nicotinic effects
• Muscle fasciculation
• Flaccid paralysis
– Limbs muscles
– Respiratory muscles
– Extra ocular muscles
• Weakness
• Fatigue
• Tremor

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6. Respiratory system
• Respiratory failure – worsened/exacerbated by
development of rhinorrhoea and pulmonary
Oedema.
7. CNS – occur in severe poisoning
– Coma
– Convulsions
– Headache
– Loss of memory
– Anxiety
– Drowsiness

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8. Organophosphate induced neuropathy
• Starts two weeks or more after exposure
• Occurs due to degeneration of
mylenated motor & sensory fibres

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DIAGNOSIS
1. Erythrocyte cholinesterase activity.
• Plasma cholinesterase is less specific
i.e. it may be depressed.

Others

• CXR - EVALUATE PULMONARY OEDEMA


• ECG - CARDIAC ARRHYTHMIAS
• ELECTROLYTES
• UREA 10
Treatment
1. Mild
• No specific treatment
• Clearing the Airway,
• Adequate ventilation-consider
oxygenation
• Remove soiled clothes
• Wash contaminated skin to prevent
further absorption.
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2. Patients with systemic features
i) IV atropine 2mgs every 15 minutes till signs of atropinization are seen (DRY SKIN,
DILATED PUPILS)
MOA
- Reduces - Bronchorrhoea & Rhinorrhoea & wheezing
- It is a beta adrenoceptor blocking drug.

ii) Add an OXIME e.g. Pralidoxime


• Dose – Slow IV injection 30mg/kg every 4-6 hours i.e. 1-2gms IV
- or infusion 8-10mg/kg/h i.e. 200-400mgs/h
MOA
- Reactivates phophorylated acetyl cholinesterase.
- Prevents permanent binding of the organophosphate to cholinesterase.

iii) Gastric lavage within an hour followed by activated


Charcoal administered via nasogastric tube
iv) Wash the patient – to prevent dermal absorption
v) Wash soiled clothes

vi) Monitor patient 2 hourly in left lateral position

Vii) Consider ICU care if in coma or unconscious


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Complications
1. Respiratory failure – this is due to respiratory muscle
paralysis, bronchial constriction and copious
respiratory secretions
2. Hyperglycaemia, complete heart block and
arrhythmias occurs in severely poisoned patients
3. Intermediate syndrome. Consists of cranial nerve
and brain stem lesions, and proximal neuropathy.
• Commence 1-4 days after acute poisoning
• Lasts for appro. 3 weeks
• Unresponsive to atropine and Oximes

4. Organophosphate induced delayed Neuropathy


– Starts 2 weeks or more after exposure
– It is as a result of degeneration of large myelinated motor and
sensory fibres.
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NOTE
1. Initial flaccidity and muscle weakness in the arms
and legs give rise to a clumsy shuffling gait and
are followed later by spasticity, Hypertonicity,
Hyperreflexia, and clonus.
2. Patients with damage to lower exteremities such
as foot drop is permanent.
3. Haemoperfusion and haemodialysis are of no
benefit in patients with organophosphate
poisoning.
4. OXIMES. Are cholinesterase reactivators.
Examples include, Pralidoxime (P2S) and
Obidoxime (toxogonin). This drugs are helpful if
given before the organophosphorus-cholinestrase
enzymes complex ‘ages’.
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THE END
Presented by:
Dr. Amani Alshara’abi

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