Organophosphorus compounds are widely used as pesticides and some were developed as nerve agents. They work by inhibiting acetylcholinesterase, resulting in excess acetylcholine in synapses and stimulation of receptors. Acute poisoning causes cholinergic effects like bronchospasm, vomiting, and bradycardia. Without treatment, respiratory failure can be fatal. Pralidoxime and atropine are used as antidotes to regenerate acetylcholinesterase and block muscarinic effects, respectively. Chronic exposure may cause neuropathies or psychiatric issues.

2. ORGANOPHOSPHORUS
OP compounds are widely used as pesticides, especially in
developing countries.
 Nerve agents developed for chemical warfare are derived
from OP insecticides but are much more toxic.

3. Physical Appearance
These compounds are available as dusts, granules or
liquids.
Some products need to be diluted with water before use,
and some are burnt to make smoke that kills insects.
Toxicokinetics
Organophosphates are absorbed by any route including
transdermal, transconjunctival, inhalational, across the
GI and GU mucosa and through direct injection.

4. Nerve agents
. G agents :- Sarin,Tabun,Soman
. V agents :- VX,VE
Insecticides
Dimethyl compounds Diethyl
compounds
- Dichlorvos - Diazinon
- Fenathion - Parathion-ethyl
- Malathion

5. G agents are volatile, are absorbed by inhalation or via
skin
and dissipate rapidly after use.
 V agents are contact poisions unless aerolised, and
contaminate ground for weeks or months.
The toxicology and management of nerve agent and
pesticide Poisoning are similar.
 Organophosphates are powerful inhibitors of
acetylcholinesterase.
As a result there is accumulation of acetylcholine in
synapses with continued stimulation of local receptors and
eventual pralysis of nerve or muscle

7. Acute Poisoning
1. Cholinergic excess
Muscuranic effects like Broncho-constriction with
wheezing
and dysponea, cough, pulmonary oedema, vomiting,
diarrhoea ,abdominal cramps, increased salivation ,
lacrimation and sweating , bradycardia, hypotension,
miosis and urinary incontinence.
Nicotinic effects like fasciculations, weakness,
hypertension, tachycardia and paralysis.
CNS effects
 Restlessness, headache, tremor, drowsiness, delirium,
slurred speech, ataxia and convulsions.
Death usually results from respiratory failure
.

8.  A characteristic kerosene-like odour is often perceptible in
the vicinity of the patient since the solvent used in many
organophosphate insecticides is some petroleum derivative
such as aromax.
 There may be either tachycardia or bradycardia.
 Miosis while being a characteristic feature, may not be
apparent in the early stages. In fact, maydriasis is often
present and hence treatment should not be delayed if there
is absence of pupillary constriction.
 While respiratory failure is the commonest cause of death
other causes may contribute including hypoxia due to
seizures, hyperthermia, renal failure and hepatic failure.

9. Intermediate Syndrome :-
 Occurs one to four days after poisioning due to long lasting
Cholinesterase inhibition and muscle necrosis , main features
include paralysis characterised by motor cranial nerve palasy .
 It may be due to inadequate treatment of the acute episode
especially involving sub-therapeutic assisted ventilation.
 Intermediate Syndrome have to be managed by supportive
measures, since it does not respond to oximes or atropine.
Delayed Syndrome:-
 Occurs one to four weeks after poisioning due to nerve
demyelination and is characterized by flaccid weakness and
atrophy of distal limb muscles or spasticity and ataxia
 These Syndrome also does not respond to either oximes or
atropine.

10. Chronic poisioning:-
It is usually occurs as an occupational hazard in
agriculturists, especially those who engaged in pesticide
spraying of crops.
Route of exposure is usually inhalation or contamination
of skin. The following are the main features :-
Polyneuropathy:-Paraesthesias, muscle cramps, weakness,
gait disorders.
CNS Effects:-Drowsiness, Confusion, irritability, anxiety,
psychiatric manifestations.

11. Depression of Cholinesterase activity
If the RBC Cholinesterase level is less than 50% of
normal, it indicates organophosphate toxicity.
Disadvantages:-
A very low Cholinesterase level does not always correlate
with clinical illness.
False depression of RBC Cholinesterase level is seen in
perinicious anaemia, hemoglobinopathies, anti- Malarial
treatment.
Depression of plasma Cholinesterase level is less reliable
indicator of organophosphate toxicity , but is easier to
assay and more commonly done.

12. P-Nitrophenol Test:-
P-Nitrophenol is a metabolite of some organophosphates
and is excreted in the urine .
Procedure:-
Steam distilled 10mL of urine and collect the disitillate.
Add sodium hydroxide (2pellates) and heat on a water
bath for 10 minutes.
Production of yellow colour indicates the presence of P-
NITROPHENOL.

13. 1. Decontamination
2. Antidote administration
3. Supportive measures
4. Prevention of further exposure

14. If skin spillage has occured ,it is imperative that the
patient be stripped and washed with soap and water.
If ocular exposure has occured, copius eye irrigation
should be done with normal Saline or tap water.
In case of ingestion stomach wash can be done. Activated
charcoal is beneficial.

15. Atropine- a competitive antagonist to acetylcholine at the
muscuranic post synaptic membrane and in the CNS, will
block muscuranic manifestations of organophosphate
poisioning.
Oximes- help to regenerate acetylcholinesterase at
muscuranic, nicotinic, and CNS sites.
The commonest oxime used in India is PRALIDOXIME.

16. Administration of iv fluids to replave the losses.
Oxygenation/intubation/positive pressure ventilation.
Following drugs are contraindicated like
parasympathomimitics, phenothiazines, antihistamines,
and opiates.

17. After the patient has recovered, he should not be re-
exposed to organophosphates for atleast a few weeks since
he is likely to suffer serious harm from a dose that
normally would be harmless owing to alteration of body
chemistry.

18. External
1. Characterstic odur (garliky or kerosene-like)
2. Frothing at mouse and mouth and nose.
3. Cyanosis of extremities
4. Constricted pupils

19. Internal
1. Congestion of GI tract:garliky or kerosene-like odur of
contents.
2. Pulmonary and cerebral odema
3. Genaralised visceral congestion.