Organophosphate poisoning

2. DEFINITION
• Organophosphate (OP) compounds are a group of chemicals
used in both domestic and industrial settings.
• Poisoning occurs after dermal,respiratory, or oral exposure to
organophosphate pesticides
(Eg.Chlorpyrifos,dimethoate,malathion,parathion) or nerve agent
(Tabun,Sarin) causing inhibition of Acetylcholinesterase at nerve
synapse.

3. Types
1. NERVE AGENTS :
• developed for chemical warfare, are derived from OP insecticide and are much
more toxic.
• They are commonly classified as G (originally synthesised in Germany) or V
(‘venomous’) agents.
• Tabun(GA),Sarin(GB),Soman(GD),cyclosarin (GF)
VX And VR.
2. INSECTICIDES:
DIMETHYL COMPOUND DIETHYL COMPOUND
Dichlorvos chlorpyrifos
Fenthion Diazion
malathion Parathionchlor

4. PATHOPHYSIOLOGY
• OPP acts as
• Anticholinesterase(Any sub.that inhibit Cholinesterase)Enzyme that hydrolyses
acetylcholine into Acetyl
Choline Secreted by
Nerve Cells Muscle Cells
(At Synapse) (At NM Junction)
• Anticholinesterase Disruption of muscle and Nerve function Death by
respiratory muscle paralysis.

5. Acetylcholine
Accumulate in nervous system
Overstimulation of 2 classes of receptor
Nicotinic Receptor Muscarinic Receptor

6. CLINICAL PHASES
1.Acute Cholinergic Syndrome(Crisis).
2.Intermediate phase.
3.Delayed polyneuropathy.

8. Muscarinic Effects
Bronchopulmonary Bronchospasm,Bronchorrhoea,Non Cardiogenic pulmonary oedema.
GIT Nausea,Vomitting,Diarrhoea,Abdominal pain.
Sweat glands Excessive Sweating.
Salivary glands Excessive Salivation.
Eyes Lacrimation,Miosis,Blurred vision.
Cardiovascular Bradycardia, occasionally tachycardia, arrhythmias, QT prolongation, Hypotension,rarely
hypertension.

10. 2.Intermediate Phase
• 24-96 hours after poisoning after the cholinergic phase settles.
• Excess Ach an NMJ causes down regulation of nicotinic
receptors- muscles affected.
• Characterized by proximal neck muscle leading to respiratory distress
and failure without muscarinic signs.
• Without intervention, cyanosis, coma and death occurs rapidly.
• Incidence 8-49%, lasts for few days to about 3 weeks

11. OP INDUCED DELAYED POLYNEUROPATHY
• Rare. Usually ,1-3 weeks after acute exposure.
• Due to degeneration of long myelinated nerve fibres.
• Found in Triorthocresyl phosphate (TOCP) and Tricresyl Phosphate
(TCP)..Less common with nerve agent.
• Characterized by cramps in the legs, numbness and paraesthesia in
the distal UL & LL, shuffling gait, foot and wrist drop.
• No specific therapy.
• Regular physiotherapy may limit deformity caused by muscle wasting

12. Diagnosis
• ECG-Prolonged QT interval,elevated ST segment,Inverted T wave.
• Chest X ray-May reveal pulm.oedema.
• ABG
• Other routine examination.

13. Management
• Hospitalisation/ICU
• 1)Initial Stabilization.
• 2)Reduction of exposure.
• 3)Administration of specific antidote.
• 4)Supportive treatment.

17. • Initial dose 1 mg IV, if no any adverse effect 2 mg every 15 minutes till the patient
developes atropinisation.
(Drying of secretions, tachycardia, dry mouth , dilated pupils)
• Injection:(Vial) 1 ml contains 1 mg Atropine. (Ampoule 1 ml = 0.6 mg Atropine).
• Atropine also can be used as infusion (Avg.person requires approx.40mg/day).
• Monitor the patient’s –Heart rate,pupils,fasciculations,secretions,lung
crepitations.

19. Features of Atropine toxicity.
• 1)Hypertension.
• 2)Tachycardia.
• 3)Pyrexia.
• 4)Confusion.
• 5)Urine retension.
• Some pt.suffers from unwanted tachycardia,violent behaviour (as it crosses BBB)
Give
GLYCOPYROLATE (Not crosses BBB, No altered behaviour)
Each 1 ml contains 0.2 mg.

21. • Current WHO guidelines,
• 30 mg/kg body weight as initial dose for 10-20 min followed by 8-10
mg/kg/Hr continuous maintainance dose until clinical recovery.