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In the treatment of organophosphate toxicity, cholinesterase reactivators such as Pralidoxime reactivate inhibited AChE at peripheral nicotinic receptors.Since AChE mediates effects on both nicotinic and muscarinic receptors, cholinesterase reactivators are co-administered with muscarinic antagonists, primarily atropine.
The ATNAA provides atropine and pralidoxime chloride in a single delivery system, although the two drugs are separate within the device. [1] [2] The use of the device is only to be administered in the extreme case of organophosphate poisoning.
[35] [36] Atropine is a muscarinic antagonist, and thus blocks the action of acetylcholine peripherally. [37] These antidotes are effective at preventing lethality from OP poisoning, but current treatment lack the ability to prevent post-exposure incapacitation, performance deficits, or permanent brain damage. [38]
Atropine is often used in conjunction with the oxime pralidoxime chloride. Some of the nerve agents attack and destroy acetylcholinesterase by phosphorylation, so the action of acetylcholine becomes excessive and prolonged. Pralidoxime (2-PAM) can be effective against organophosphate poisoning because it can re-cleave this phosphorylation.
Whenever symptoms of chlorethoxyfos start to reappear, atropine should be injected again. The atropinized state of the patient should always be maintained. Dosage of atropine is different among different age-groups. Children and infants have a maximum dosage of 0.05 mg/kg. When adults are severely intoxicated the dose can go up to 4 mg.
As a result of cholinergic crisis, the muscles stop responding to the high synaptic levels of ACh, leading to flaccid paralysis, respiratory failure, and other signs and symptoms reminiscent of organophosphate poisoning. Other symptoms include increased sweating, salivation, bronchial secretions along with miosis (constricted pupils).
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When patients are resistant to atropine, the patients can be treated with low doses of anisodamine, a cholinergic and alpha-1 adrenergic antagonist, to achieve a shorter recovery time. [19] Treatment with a combination of different alkaloids or synergistically with atropine is safer than using high antroponine concentrations, which can be toxic.