Abstract

In developing nations like India, organophosphate (OP) chemicals are among the most often utilized substances for intentional self-harm. Acetylcholinesterase, an enzyme that hydrolyses the neurotransmitter acetylcholine in the central and peripheral nervous systems (PNS), is inhibited by OP chemicals. In the case of insecticides, these anticholinesterase substances are thought to produce a delayed intermediate syndrome that need extended breathing, as well as an acute cholinergic syndrome characterized by diminished consciousness and respiratory failure.(2)Most of the time, acute respiratory failure caused by both central and peripheral mechanisms is the main cause of death. Preclinical and clinical research conducted over the past 20 years, however, has revealed a more nuanced picture of the respiratory complications following OP insecticide poisoning. These complications include the involvement of solvents in OP toxicity, the onset of delayed neuromuscular junction dysfunction during the cholinergic syndrome, and aspiration leading to pneumonia and acute respiratory distress syndrome.