After poisoning, organophosphorus will combine with cholinesterase in the body, thus forming phosphorylated cholinesterase, which loses the ability of cholinesterase to hydrolyze acetylcholine. This results in the accumulation of excessive acetylcholine in the body, causing cholinergic nerve excitation followed by inhibition, resulting in clinical muscarinic and nicotinic-like symptoms. After the cholinergic nerve excitation, it will excite the cholinergic M receptors, causing the pupillary sphincter to contract, resulting in pupil narrowing. Early poisoning may result in loss of appetite, nausea, vomiting, abdominal pain, diarrhea, blurred vision, narrow pupils, increased respiratory secretion, and in severe cases, muscarinic-like symptoms such as pulmonary edema.