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Organophosphate poisoning and its management
The document discusses organophosphate poisoning, detailing the types of compounds involved, mechanisms of toxicity, and clinical features such as cholinergic symptoms and intermediate syndrome. Management includes supportive care, decontamination, and the use of antidotes like atropine and pralidoxime. It emphasizes the importance of airway maintenance and addresses potential complications following exposure.
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Organophosphate poisoning and its management
- 1.
- 2. Organophosphorus compounds • Nerveagents: • G agents: sarin, tabun, soman V agents: VX,VE • Insecticides: Dimethyl compounds Diethyl compounds • Dichlorvos • Fenthion • Malathion • Methamidophos Diethyl compounds • Chlorpyrifos • Diazinon • Parathion-ethyl • Quinalphos Intoxication may follow ingestion, inhalation or dermal absorption.
- 3. Mechanism of toxicity Inhibitacetyl cholinesterase causing accumulation of acetylcholine at central and peripheral cholinergic nerve endings, including neuromuscular junctions
- 4. Clinical features • onset,severity and duration of poisoning depend on the route of exposure and agent involved • causes an acute cholinergic phase, which may occasionally be followed by the intermediate syndrome or organophosphate-induced delayed polyneuropathy (OPIDN
- 5. • muscarinic featuressuch as nausea, vomiting, abdominal colic, diarrhoea, sweating, hypersalivation, miosis, bronchospasm, bronchorrhea, bradycardia, urinary incontinence • Nicotinic features such as muscle fasciculation and flaccid paresis of limb, respiratory, and occasionally, extraocular muscles • CNS features is characterized by anxiety, slurred speech, mental status changes (e.g., delirium, coma, and seizures), and respiratory depression
- 7. Intermediate syndrome • Occurin 20% case of OP poisoning • Development of weakness of muscle rapidly • Spreading from ocular muscle to head and neck, proximal limbs and muscle of respiration may leads of ventilatory failure • May appear after 1-4 days after exposure when symptomps/signs of acute cholinergic syndrome are no longer obvious • May last 2-3 weeks • no specific treatment but supportive care, including maintenance of airway and ventilation,
- 8. Organophosphate-induced delayed polyneuropathy •Rare complication • Occur 2-3 weeks after exposure • Mixed sensory/motor polyneuropathy • C/F :muscle cramps followed by • numbness and paraesthesis flaccid paralysis of lower limbs and subsequently upper limbs
- 9. General management • Maintenanceof ABC ◦ Airway should be cleared of secretion ◦ High flow O2 ◦ IV access • Decontamination of skin ◦ To prevent further absorption ◦ Contaminated clothing and contact lenses removed ◦ Skin washed with soap and water and eye irrigated • Gastric lavage and activated charcoal if within 1hours
- 10. Antidotes - Atropine •2mg IV,repeated every 10-25 minutes until atropinization (as manifested by drying of secretions, tachycardia, flushing,dry mouth, and dilated pupils) occurs
- 11. Pralidoxime • Dose:1-2 gfor adults and 20-40 mg up to 1 g in children ,infused in NS over 5-10 minutes • reactivates the cholinesterase and counteracts weakness, muscle fasciculations, and respiratory depression
- 12. • Treat seizureswith a benzodiazepine and phenytoin; if severe seizures require muscle relaxants
- 13. References • Davidson's Principlesand Practice of Medicine 21 Edition • Kumar and Clark 7th Edition (2009) • Emergency Medicine,Tintinalli
- 14.
Editor's Notes
- #4 Mechanism of toxicity OP compounds phosphonylate the active site of acetylcholinesterase (AChE), inactivating the enzyme and leading to the accumulation of acetylcholine (ACh) in cholinergic synapses (Fig. 9.5). Spontaneous hydrolysis of the OP–enzyme complex allows reactivation of the enzyme. However, loss of a chemical group from the OP–enzyme complex prevents further enzyme reactivation, a process termed ‘ageing’. After ageing has taken place, new enzyme needs to be synthesised before function can be restored. The rate of ageing is an important determinant of toxicity and is more rapid with dimethyl compounds (3.7 hours) than diethyl (31 hours), and especially rapid after exposure to nerve agents (soman in particular), which cause ageing within minutes.
- #10 Organophosphate-induced delayed polyneuropathy (OPIDN) is a rare complication that usually occurs 2–3 weeks after acute exposure. It is a mixed sensory/ motor polyneuropathy, especially affecting long myelinated neurons, and appears to result from inhibition of enzymes other than AChE. It is a feature of poisoning with some OPs such as trichlorocresylphosphate, but is less common with nerve agents,. Early clinical features are muscle cramps followed by numbness and paraesthesiae, proceeding to flaccid paralysis of the lower and subsequently the upper limbs. Paralysis of the lower limbs is associated with foot drop and a high-stepping gait, progressing to paraplegia. Paralysis of the arms leads to wrist drop. Sensory loss may also be present but is variable. Initially, tendon reflexes are reduced or lost but mild spasticity may develop later. Paralysis of the lower limbs is associated with foot drop and a high-stepping gait, progressing to paraplegia. Paralysis of the arms leads to wrist drop. Sensory loss may also be present but is variable. Initially, tendon reflexes are reduced or lost but mild spasticity may develop later. There is no specific therapy for OPIDN. Regular physiotherapy may limit deformity caused by musclewasting. Recovery is often incomplete and may be limited to the hands and feet, although substantial functional recovery after 1–2 years may occur, especially in younger patients.