| ID | 218 |
|---|---|
| Name | Back ground: Suicidal, some are accidental, sometimes homicidal e.g diaginon, endrin, melathion. Minimum lethal dose (MLD): 0.02-Igm. |
| Cause | |
| Signs Symptoms | |
| Diagnosis | |
| Investigations | |
| Management | Management: Acute cholinergic syndrome: 1. Immediate hospitalization. 2. Gastric Lavage ( 30min) and Complete rest. 3. Remove the contaminated clothes and wash the body surface and nails thoroughly. 4. Induce vomiting or stomach wash with water or oropharyngeal suction of the drug ingested, or, activated charcoal may be considered within 1 hour of ingestion. 5. Maintain clear airway. 6. Oxygen inhalation. 7. Infuse 5% dextrose in aqua 2000c.c. and dextrose in normal saline l000c.c, in i.v drip in 24 hours. 8. Inj. Atropine (I amp. =0.6mg.) 10 amp. i.v stat and 10 amp. in the i.v drip and 2 amp. in every 10-15 minutes interval till the pupil js widely dilated (i.e full atropinisation) and then reduce the dose gradually, and this is maintained for at least 2-3 days. Dose of atropine inj. depends on the amount of poison taken and best monitored by the size of pupil. 9. If available, Pralidoxime should be given in addition to atropine in a dose of 30mg/kg i.v at a rate not exceeding 500mg (in Sc.c) per minute and repeated every 30 minutes, if necessary. More recently inj. obidoxime 3mg/kg i.m has been found more effective than “pralidoxime as it has a faster action and crosses the blood-brain barrier. When these cholinesterase reactivators take effect the dosage of atropine should be reduced to avoid atropine toxicity. 10. Antibiotics to prevent infection. 11. Take general nursing care- i. If urinary incontinence then apply condo catherer or catheterization. ii. Change the posture half-hourly, iii. Maintain intake and output chart. The intermediate syndrome: 1. No specific treatment, supportive care as above including special management for airway maintenance and ventilation. 2. Continuation of the treatment given for acute syndrome, as needed. Organophosphate-induced delayed polyneuropathy: 1. No specific treatment, supportive care as required. 2. Physiotherapy should be given regularly to limit deformity caused by muscle-wasting. |
| Introduction | |
| History | |
| Etiology | |
| Clinical Features | Clinical features: Presence of smelling of organophosphorus (OP) compounds. Clinical features appear within a few minutes to hours of exposure. OP poisoning generally causes- i. an acute cholinergic phase, occasionally may be followed by ii. an intermediate syndrome, or, iii. organophosphate-induced delayed polyneuropathy. Acute cholinergic phase starts within a few minutes and consists of headache, sweating, increased salivation, abdominal cramps, vomiting diarrhoea, muscular cramps, twitching, convulsion & blurring of vision, pulmonary congestion and finally flaccid paralysis and deep coma. Pulse and B.P are variable & pupils are constricted. An ‘intermediate syndrome’ (IMS) may develop in about 20% of patients in between 1 & 4 days of OP poisoning often after resolution of acute phase. In this, weakness spreads rapidly from the ocular muscles to the muscls of head, neck, proximal limbs & chest, resulting in ventilatory failure. This phase may last 2-3 weeks. Organophosphate-induced delayed polyneuropathy is a rare complication occurs 2-3 weeks after acute exposure. It is a mixed motor and sensory polyneuropathy, affecting particularly long myelinated neurons. These complications occur with some specific OPs, such as- trichlorocresylphosphate. |
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| Treatment | |
| Complications | Complications: 1. Aspiration pneumonia 2. Retension of urine 3. Tachycardia, heart failure 4. Pyrexia 5. Atropine toxicity |
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