• Organo phosphorous compounds are a large group of compounds having the potential to irreversibly inhibit cholinesterase enzymes like Acetyl Cholinesterase & Neuropathy Target Esterase (NTE).

• They are not only used as insecticides & pesticides but also as Chemical Warfare Agents, Petroleum Additives & Industrial Plasticizers. • Serious human exposure leads to muscarinic (cholinergic) hyper stimulation as well as nicotinic receptor stimulation.

ORGANO . VE Diethyl Compounds: • Chlorpyrifos • Diazinon • Parathion .ethyl • Quinalphos • Phenthoate • Phorate • Phosphamidon • Profenofos INSECTICIDES Dimethyl Compounds: • Dichlorvos • Fenthion • Malathion • Methamidophos OTHERS • Acephate • Dimethoate • Ethion • Fentrothion • Moncrotofos . Soman •V Agents: VX.PHOSPHOROUS COMPOUNDS NERVE AGENTS •G Agents: Sarin. Tabun.

sarin. Lange in Berlin & Schrader. OPs were reintroduced worldwide as pesticides as were originally intended. During World War II. a chemist at Bayer AG. Germany. 1854 – Philip de Clermont described the synthesis of Tetra Ethyl Pyro Phosphate at a meeting of the French Academy of Sciences. soman). investigated the use of Organophosphates as insecticides. in 1941. Eighty years later. However the German Military prevented the use of OPs as insecticides & instead developed an arsenal of chemical warfare agents (tabun. • • • • • . A fourth agent VX was developed a decade later in England.HISTORY • First synthesized in the early 1800s when Lassaigne reacted alcohol with phosphoric acid.

• In 1995 . Trichlorfon.used Sarin to poison people on a Tokyo subway. . • Worldwide mortality rates currently range from 3 – 25% • The compounds most commonly involved are circumvent prohibition laws – led to massive OP intoxication.a religious sect . • Agricultural pesticides accounted for 12.HISTORY • Jamaican Ginger Palsy incident (1930) .8% of all cases of poisoning in India.Aum Shinrikyo . Dichlorvos.

Risk Factors for Poisoning • Young age • Low Socio – economic strata • Unemployment • Unstable emotional relationships • Psychiatric disorders • Alcohol abuse .

Nicotinic receptors – in skeletal neuromuscular junctions and autonomic ganglia 3. This leads to accumulation of acetylcholine at: 1. • The principal effect is inhibition of cholinesterase cholinergic receptor cells 2.PATHOLOGY • Organophosphate are absorbed through the skin lungs & GI tract and distributed widely in tissues and are slowly eliminated in hepatic metabolism. CNS . Muscarinic receptors. particularly acetyl cholinesterase (AChE).


MOA of OP Compounds .

CLINICAL FEATURES • Acute Cholinergic Crisis • Intermediate Syndrome (IMS) • OPIDN • EPS. CNS • DIPPERS’ FLU .

depression Circulatory collapse Respiratory Rhinorrhea Bronchorrhea/spasm Cough Musculoskeletal Weakness Fasciculations Cramps Paralysis Gastrointestinal Increased salivation Nausea/vomiting Abdominal pain Diarrhoea Fecal incontinence Genitourinary Urinary incontinence Ocular Blurred vision/miosis Increased lacrimation .ACUTE CHOLINERGIC CRISIS Muscarinic Cardiovascular Bradycardia Hypotension Nicotinic Cardiovascular Tachycardia Hypertension Central receptors Anxiety Restlessness Ataxia Convulsions Insomnia Dysarthria Tremors Coma Absent reflexes CS respiration Resp.

information processing & memory  Depression.COPIND & EPS • Chronic OP Induced Neuropsychiatric Disorder (COPIND):  Behavioural changes  Impaired vigilance. anxiety. irritability • EPS:  Resting tremor  Rigidity  Hypokinesia  Dystonia  Chorea NOTE: • Dose – dependent effects: Muscarinic < Nicotinic < CNS • Tachycardia / Hypertension – s/o severe poisoning .

PARALYSIS • Type I: Acute Paralysis – due to continued depolarization at the NMJ • Type II: IMS – develops 24 . neck muscles & cranial nerves. neck & trunk with sparing of distal muscles. may require mech. weakness of proximal muscle groups.96 hrs after resolution of acute OPP symptoms. cranial nerve palsies. Ventilation & may be complicated by infections or cardiac arrhythmias. Persists for 4 – 18 days . • Type III: OPIDN – occurs 2-3 weeks after exposure to large doses & is due to inhibition of NTE. distress. . Distal muscle weakness with relative sparing of proximal muscle groups. Paralysis & resp. Recovery may take upto 12 months.

OTHERS • Neuro-ophthalmic manifestations: o Optic neuropathy o Retinal degeneration • Rarer manifestations: o GBS o Ototoxicity o Sphincter involvement .

EVALUATE PULMONARY OEDEMA • ECG .MANAGEMENT • DIAGNOSIS: Mainly based on the characteristic clinical features and history of exposure to a known OP compound. • INVESTIGATIONS: Estimation of serum or RBC cholinesterase levels & electro diagnostic tests (not routinely used) • Clinical features of OP poisoning appear when RBC cholinesterase activity is < 75% of normal & in clinically overt poisoning it is usually < 10% • No definite relationship between plasma levels of cholinesterase & severity of symptoms and prognosis • OTHERS: • CXR .CARDIAC ARRHYTHMIAS • ELECTROLYTES • UREA .

PRINCIPLES • • • • • • Airway Breathing Circulation Decontamination Gastric lavage Activated charcoal through ryles tube 4th hourly • Atropine & Oxime therapy .TREATMENT .

to prevent further absorption. .consider oxygenation Remove soiled clothes Wash contaminated skin. with soap & running water.TREATMENT MILD CASES: • • No specific treatment Clearing the Airway • • • Adequate ventilation .

repeat dose very 5-15 minutes till atropinised – CHILDREN: 0.05 mg/kg – S/O Atropinisation: » » » » Heart rate about 100/min Pupils mid position / dilated Bowel sounds just heard Clear lung fields Reduces .PATIENTS WITH SYSTEMIC FEATURES i) ATROPINE:  Initiate as soon as the diagnosis is suspected – ADULTS: 2 mg IV bolus .05 mg/kg initially then 0.02-0.muscarinic agent. .Bronchorrhoea & Rhinorrhoea & wheezing It is an anti .

.Prevents permanent binding of the organophosphate to cholinesterase. . 1-2gms IV . Pralidoxime • Dose – Slow IV injection 30mg/kg every 4-6 hours i. 200-400mgs/h MOA .Reactivates phosphorylated acetyl cholinesterase. vii) Consider ICU care if in coma or unconscious.or infusion 8-10mg/kg/h i.ii) Add an OXIME: prevent dermal absorption vi) Monitor patient 2 hourly in left lateral position.e.e. iii) Gastric lavage within an hour followed by activated Charcoal administered via nasogastric tube iv) Remove soiled clothes v) Wash the exposed areas of skin with soap & running water .g.

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