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The health effects associated with organophosphate poisoning are a result of excess acetylcholine (ACh) present at different nerve synapses and neuromuscular junctions across the body. Specifically, acetylcholinesterase (AChE), the enzyme that normally and constantly breaks down acetylcholine, is inhibited by the organophosphate substance.
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.
Atropine, which is choice of drug to antagonise the muscarinic effects of organophosphates, is administered even before pralidoxime during the treatment of organophosphate poisoning. While the efficacy of atropine has been well-established, clinical experience with pralidoxime has led to widespread doubt about its efficacy in treatment of ...
Organophosphate-induced delayed neuropathy (OPIDN), also called organophosphate-induced delayed polyneuropathy (OPIDP), is a neuropathy caused by killing of neurons in the central nervous system, especially in the spinal cord, as a result of acute or chronic organophosphate poisoning.
As a result of cholinergic crisis, the muscles stop responding to the high synaptic levels of acetylcholine, 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).
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.
Atropine, however, is difficult to administer safely, because its effective dose for nerve agent poisoning is close to the dose at which patients suffer severe side effects, such as changes in heart rate and thickening of the bronchial secretions, which fill the lungs of someone suffering nerve agent poisoning so that suctioning of these ...
When adults are severely intoxicated the dose can go up to 4 mg. In mild cases 1 or 2 mg will be required. In total, during the first 24 hours 20 or 30 mg might be required. [11] Next to atropine, chlorethoxyfos intoxication can be treated with pralidoxime chloride, also known as 2-PAM chloride. 2-PAM may be used as an effective antidote in ...