Paraquat, also known as mopara and paraquat, is a bipyridyl herbicide, which is moderately toxic. It is generally believed that paraquat is an electron receptor and can be absorbed into the body to produce a large number of free radicals, which can cause tissue cell damage. The oral lethal dose of paraquat is about 14mg/Kg, and the mortality rate of severe poisoning is as high as 60%-80%, and the survivors are often left with severe pulmonary fibrosis and poor prognosis. Diagnostic points】 1. Exposure history There is a clear history of paraquat exposure to skin, respiratory tract or oral exposure. 2. Clinical manifestations Skin contact can cause local inflammation, erythema, blistering, ulcerative necrosis and other manifestations. 1. Eye contact can cause irritation, conjunctival and corneal burns. 2. Poisoning caused by respiratory tract contact when spraying paraquat, there may be respiratory tract irritation symptoms or the lung damage is not significant at that time. 3. Oral poisoning may cause violent vomiting and burning sensation in the mouth, pharynx, esophagus and stomach. This is followed by redness, pain and ulceration of the mucous membrane and diarrhea, blood in the stool, etc. 4. Acute poisoning caused by mouth, skin, or inhalation has similar systemic symptoms and progression of disease. The most obvious symptoms of poisoning are pulmonary manifestations, such as chest pain, cough and shortness of breath in mild cases. In severe cases, respiratory distress, cyanosis, severe respiratory distress, pulmonary edema, until death by respiratory failure. 5. More severe patients may develop toxic hepatitis, myocarditis, or acute renal failure, and individual patients may develop methemoglobinemia. 3.Laboratory examination Peripheral blood leukocyte count is significantly elevated; paraquat can be detected in blood and urine; alveolar/pulmonary artery PaO2 difference is increased, severe hypoxemia. 4.Pulmonary X-ray examination Early 3 days-1 week of poisoning, mainly increased lung texture, interstitial inflammatory changes of lung, dotted and lamellar shadows, reduced lung translucency or hairy glass shape. In the middle stage 1-2 weeks, solid lung changes or large solid lung changes appeared, along with partial pulmonary fibrosis. In the later stage, after 2 weeks, pulmonary fibrosis and pulmonary atelectasis appear. Chest radiographs should be taken upon admission to hospital for paraquat poisoning. Although the fastest lung lesions are not shown until more than 10 hours after poisoning, early chest radiographs are very important, and even if the chest radiographs are normal, they can at least be used as a pair of photographs for later chest radiographs. There is no special treatment for this disease. Reducing the absorption of paraquat, accelerating excretion and eliminating chemical inflammatory damage are the main treatment means, and treatment should be fast. 1. Stop the continued absorption of poison Skin contamination immediately with soap and water, eye contamination with water and thorough cleaning. Those who are poisoned by mouth should immediately wash the stomach with alkaline liquid, then inject adsorbent orally or in the stomach tube, such as: 15% bleaching earth suspension, activated carbon, etc. And use 20% mannitol or magnesium sulfate orally to induce diarrhea. 2. Accelerate the discharge of toxic substances Hemodialysis HD, hemoperfusion HP, blood replacement PE, blood exchange and other therapies have certain efficacy in early application. However, paraquat is distributed to the surrounding tissues very fast, so it should be applied at the peak of blood concentration, usually within a few hours after oral administration. Because paraquat is mainly excreted by kidney in its original form, diuresis should be strengthened as early as possible, and furosemide tachyphylaxis, etc. can be applied. Therefore, it is better to emphasize a large amount of oral or intravenous rehydration diuretic to make the urine volume exceed 300ml/h under supervision. 3, anti-inflammatory, prevent the formation of pulmonary fibrosis Some reports believe that early lung lesions are mainly chemical interstitial lung inflammatory changes, adrenocorticotropic hormone has the effect of eliminating this inflammation and preventing pulmonary fibrosis, can be applied early, adequate, pulsatile, generally adult dose equivalent to methylprednisolone 0.5-1.0g/d, for 3 d, repeat application if necessary. If it is necessary to strengthen the anti-fibrotic effect, cyclophosphamide can be given at intervals with hormone, 0.5-1.0g/d for 2d, and then repeatedly applied if necessary, while paying attention to blood picture monitoring. 4.Competitive agents It has been reported that propranolol, propranolol, can compete with the toxins bound to the lung tissue, so that they are released. Vitamin B1, with the same chemical structure as paraquat, is a quaternary amine type, so it is presumed to have antagonistic effect and can be tried. 5.Free radical scavenger It is generally believed that paraquat is a kind of electron receptor, and its activation into free radicals in cells is the basis of toxic effects. Therefore, it is necessary to apply free radical scavengers early and in large quantities. Available: vitamin C, vitamin E, SOD, reduced glutathione, etc. 6, symptomatic treatment (1) reasonable oxygen therapy: oxygen administration has the effect of increasing the formation of free radicals, in principle, oxygen therapy is prohibited. In obvious hypoxia can be low concentration, low flow oxygen, only in PaO221% oxygen inhalation. If necessary, PEEP mechanical ventilation can be used. (2) Broad-spectrum, high-efficiency antimicrobial agents can be used to prevent and treat secondary bacterial infections. (3) Give appropriate protective agents for organ damage and maintain their physiological functions. (4) Strengthen supportive nutritional therapy. In case of severe gastrointestinal failure with corrosive damage to the digestive tract, fasting should be given, and deep venous high nutrition can be given. Generally speaking, the survival rate of patients with no organ function damage is 50% after 1 week, 80% after 2 weeks, 90% after 3 weeks and 100% after 4 weeks.