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 Organophosphorus poisoning is of common occurrence in agricultural countries since these insecticides are used for spraying of agricultural crops as well as for destruction of vermin’s and rodents. Often they are used for suicidal and homicidal purposes.

Organophosphorus poisoning compounds and carbmates are a family that have structural similarities. They act by inhibiting or inactivating acetylcholinestrase at the site of cholinergic transmission throughout the body, thus acting as ariticholinesterase agents (anti-AchE).

Majority of agents show some signs and symptoms of toxicity within 6 to 12 hours after exposure. Exception to this is highly fat soluble like Fenthoin  (Daif) which do not manifest toxicity for several days to weeks. The duration of symptoms of organophosphorus poisoning depend partly on the rate at which organophosphorus poisoning compound is destroyed or removed from the tissues.

These are highly lipid soluble and are absorbed rapidly through the skin and mucous membrane following contacts with the liquid or by lungs following inhalation of vapors while spraying or by ingestion accidentally.

Pharmacologically the actions of these compounds are classified as Muscarinic, Nicotinic and central nervous system effects:


These are nausea, vomiting, abdominal pain loose motions, and excessive salivation tightness in the chest. Bronchial constriction increased bronchial secretions with frothing, excessive lacrimation, frequent and involuntary micturition, Miosis, Bradycardia and Hypotension. The muscarinic effects are as a result of stimulation of end organs innervated by post ganglionic fibres of para sympathetic nerves.


Muscular weakness, fatigue, fasciculation’s, cramps general weakness including that of respiratory muscles, tachycardia and hypertension. These are as a result of accumulation of acetyl choline at the skeletal neuromuscular junctions and symptathetic pregangliomic nerve endings.

Central nervous system

These include irritability, anxiety restlessness, headache. Tremors of hands, lips, face or tongue, mental confusion passing on to stupor, convulsions, coma with absence of reflexes and Guillian-Barre syndrome like picture. These are as a result of accumulation of acetylcholine at various levels in central nervous system.

Types of insecticides. The various forms of poisonous compounds available which are responsible for toxicity include diazinon (tick 20, diazenol) Fenthoin (Dalf) Carbmates (Baygon) and organo chlorine compounds like DDT, Endrin, Chiordane etc.

Clinical features. Depending on the route of entry, the symptoms are marked. Patient initially complains of headache, nausea, vomiting abdominal pain and a sense of constriction in the chest. This usually follows in 15-20 minutes after exposure. There is photophobia, muscular twitching and fasciculation’s followed by neurologic deficit in next two to eight hours. If Organophosphorus poisoning is severe, patient may develop severe pulmonary edema, respiratory paralysis and pass on to circulatory arrest and death.

Depending on the route of ingestion, gastro intestinal system bears the brunt if it is taken orally while respiratory distress including pulmonary edema follows inhalation resulting in accumulation of secretions in air passages and cyanosis.

A patient often manifests a peculiar garlic or kerosene smell with the presence of froth round about the mouth. There is restlessness, sweating, salivation and muscular weakness. Heart may develop various cardiac irregularities as well as hypotension. Death is usually due to respiratory failure, cardiac arrest or muscular paralysis.

Pathology of organophosphorus poisoning

There is congestion of respiratory passages which are filled with frothy haemorrhagic exudate. Marked congestion is present in the various internal organs including liver, kidney brain and heart. Cerebral oedema with petechial haemorrhages as well as filling of right side of heart with dark colored blood are important features.


Estimation of CI-lE enzyme in the serum and RBCs is important. The normal value of true cholnestrase (RBC) is 160-300 units / ml and of serum (Pseudo) cholinestrase is 100-250 units! ml.

Clinical signs are absent if levels of serum CHE is above 50% of normal. Patients with clinically poisoned picture show very low levels (25% below normal) but no correlation may exist between cholinestrase levels and symptoms.

Grading of severity. Depending on the severity, clinically the condition may be classified as:

Mild: There is nausea, vomiting but normal consciousness.

Severe: Mild + impaired consciousness + copious secretion threatening – severe + pulmonary edema + unconsciousness.


It is based on history of ingestion or inhalation. There is typical picture of nausea, vomiting, bronchial constriction, muscular weakness, and pin point pupils. Estimation of serum or RBC CHE levels will be diagnostic in doubtful case.

Treatment of organophosphorus poisoning

It is both supportive and specific:


1. Stomach wash should be done immediately using 5% soda bicarbonate or 2% potassium permagnate solution to remove it from the stomach.

2. The skin should be washed with soap and water to cleanse it from there. Clothing should be removed and changed immediately.

3. Oxygen inhalation.

4. I/V fluid to maintain hydration. If there is hypotension vasopressors and corticosteroids be given. Antibiotics (mi. Amoxycillin 500 mg I/V 8 hrly) to prevent respiratory infection.

Specific treatment

Atropine is given immediately intravenously in a dose of 2.0 mg followed by I mg every half hour to keep the patient atropinised. There is no hard and fast rule about the frequency of administration of drug. Dosage has to be adjusted depending on the severity of the disease.

Atropine inhibits the action at many sites and reverses the muscarine effects though it has none on nicotine. It reduces bronchial secretions, relieves bronchial spasm and also diminishes depression of respiration.

Atropine has to be given till the features of atropinisation like dry flushed skin, dry mouth, tachycardia and dilatation of pupils appear. A small dose of atropine has to be continued for 4-7 days since relapse of symptoms may appear due to slow absorption of poison.


Since atropine does not activate the cholinestrase, it has no effect on neuro muscular block. But this action is specific for oximes which not only reactivate the inactivated acetyl cholinesterase both in blood and tissues by process of phosphorylation but also act at skeletal neuro muscular junctions. It counteracts the nicotinic effect but has no effect on muscarine like effect of poison.

Pralidoxime (PAM) is the main oxime compound which is given by immediate japid infusion (I g dissolved in 20 ml of distilled water or 5% glucose saline) intravenously and every 4-6 hourly.

To achieve better results PAM must be administered at the earliest preferably in the first 24- 36 hours but there are no restrictions to its use if more than 48 hours have passed. Along with PAM, atropine must be used as adjunct. The combination is effective. There is rapid rise of RBC levels.


When treatment has been stopped after 24-48 hrs, relapse may occur and the clinical picture now may be more worse than before. This may be due to slow release of organophosphorus poisoning as well as failure to continue the treatment for adequate periods.



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