Preface organophosphorus pesticides are commonly used in agricultural production of insecticides, toxicity to humans and animals mainly inhibit cholinesterase, causing the accumulation of acetylcholine, cholinergic nerves are subject to sustained impulses, resulting in a series of muscarinic-like, nicotinic-like and central nervous system and other symptoms of excitation followed by failure, severe cases can appear coma and respiratory failure and death. Types of organophosphorus pesticides dichlorvos, 3911 (methomyl), 1605 (parathion), 1059 (endosulfan), lewisite, oxymoron, parathion, trichlorfon, malathion, phoxim, etc. The toxicity of various organophosphorus pesticides varies greatly, and the general LD50 varies from a few milligrams per kilogram of body weight to thousands of milligrams per kilogram of body weight, such as 3911, 1605 LD50 are less than 10mg/kg, while the LD50 of malathion is 5000mg, and the LD50 of dichlorvos is about 50-60mg/kg. Performance after poisoning Oral poisoning at the earliest Clinical symptoms can appear in 10 minutes, and can be characterized by excessive sweating, lacrimation, salivation, foaming at the mouth, shortness of breath, dyspnea, narrow pupils, pulmonary edema, vesicular sounds on auscultation of both lungs, and garlic odor on exhaled gas; some patients also show incontinence, abdominal pain, and other manifestations. Observation of the face, eyelids, tongue and even limbs and whole body muscles can appear small twitches (muscle bundle tremors), and in severe cases the whole body muscles tonic spasm, the patient has a sense of pressure, tight bundle, and finally can appear muscle weakness and paralysis, and even respiratory failure. The manifestations of central nervous stimulation include headache, dizziness, irritability, delirium, unsteady walking, convulsions and coma. Reverse jumping Some patients who are poisoned and whose symptoms improve with rescue treatment suddenly revert to coma, pulmonary edema or even sudden death after several days. The mechanism is not very clear and may be related to the reabsorption of drugs remaining in the skin, hair and other parts of the organism or the premature end of treatment, which is common in those poisoned by lego and malathion. Delayed neuropathy Patients with organophosphorus poisoning generally do not have sequelae, but individual patients can develop neurological symptoms such as lower limb paralysis, limb muscle atrophy, and numbness of limb ends 2-3 weeks or even longer after the disappearance of acute poisoning symptoms, called delayed neuropathy, which may be related to the inhibition of neural target esterases by organophosphorus pesticides, and there is no special treatment yet. Intermediate syndrome After the remission of acute poisoning symptoms and before the manifestation of delayed neuropathy (mostly in 2-3 days after acute poisoning), some patients suddenly die, before death can have muscle paralysis of eyelids, face, neck, upper limbs, respiratory muscles, etc., which is related to the long-term inhibition of cholinesterase, affecting the function of the post-synaptic neuromuscular junction. Close observation for early detection and immediate application of ventilator to support respiratory function can save the lives of most patients. Skin and mucous membrane damage There are reports of causing allergic dermatitis and even blistering and peeling, and entering the eyes can result in conjunctival congestion and pupil narrowing. Principles of resuscitation Gastric lavage, catheterization, cholinesterase revival drugs (dephosphoridine, chlorophosphoridine, etc.), anticholinergics (atropine, 654-2, etc.). Observe the condition closely and treat complications such as cerebral edema, shock, cardiac arrhythmia, infection, etc. Blood transfusion therapy is available for critically ill patients.