Op poisioning

Organophosphorus poisoning

1. ORGANOPHOSPHORUS POSIONING

2. ORGANOPHOSPHORUS COMPOUNDS 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. ORGANOPHOSPHORUS COMPOUNDS 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

6. Clinical features Acute Poisoning 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 .

7. It is important to note that:- 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.

8. 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.

9. 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.

10. Diagnosis 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.

11. 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.

12. Treatment Decontamination Antidote administration Supportive measures Prevention of further exposure

13. Decontamination 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.

14. Antidote administration 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.

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

16. Prevention of further exposure 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.

17. Postmortem appearance External Characterstic odur (garliky or kerosene-like) Frothing at mouse and mouth and nose. Cyanosis of extremities Constricted pupils

18. Internal Congestion of GI tract:garliky or kerosene-like odur of contents. Pulmonary and cerebral odema Genaralised visceral congestion.