What about paraquat poisoning?

What is paraquat poisoning like? What should I do after paraquat poisoning? Also ask netizens to help guide the principle of paraquat poisoning: paraquat can be absorbed through the gastrointestinal tract, skin and respiratory tract, because it is not volatile, it is generally not easy to be poisoned by inhalation. If the skin is exposed to paraquat for a long time, or short-term exposure to high concentration of paraquat, especially the damaged skin or scrotum, perineal contamination can lead to systemic poisoning. Oral poisoning is the main way of poisoning. The oral absorption rate was 515%, reached the plasma concentration peak 2 hours after absorption, and quickly distributed to the lung, kidney, liver, muscle, thyroid and so on, in which the lung content was higher and the retention time was longer. Paraquat can be partially degraded in the body, and most of it is excreted with urine through the kidney within 2 days, and a small amount can also be excreted from feces. Paraquat is moderately toxic. Paraquat is highly toxic to humans and has a high fatality rate after poisoning. The oral lethal dose was about 2g and 1g was also reported. The mechanism of paraquat poisoning is not fully understood. It is generally believed that it is an electron receptor, acting on the redox reaction in cells, producing a large number of active free radicals, causing lipid peroxidation of cell membrane and causing oxidative damage to tissues and cells. because alveolar cells have the characteristics of active uptake and accumulation of paraquat, lung injury is the most prominent manifestation. Symptoms after paraquat poisoning: symptom 1, oral poisoning patients have oral burning sensation, lip, tongue, pharyngeal mucosal erosion, ulcers, dysphagia, nausea, vomiting, abdominal pain, diarrhea, and even hematemesis, hematochezia, stomach perforation. Some patients developed toxic liver disease 2 ~ 3 days after poisoning, showing pain in the liver area, hepatomegaly, jaundice and abnormal liver function. Symptom 2: cough, expectoration, chest tightness, chest pain, dyspnea, cyanosis, lung smell and dry and wet rales. Patients with high dose may develop pulmonary edema and bleeding within 24 to 48 hours, and often die of acute respiratory distress syndrome (ARDS) within 1 to 3 days. After rescuing the survivors, pulmonary interstitial fibrosis occurred after 1-2 weeks, showing progressive dyspnea, resulting in respiratory failure and death. In patients with non-massive absorption, the pulmonary symptoms were not obvious at first, but they gradually developed pulmonary symptoms due to pulmonary fibrosis within 1-2 weeks, and pulmonary dysfunction led to intractable hypoxemia. Symptom 3. Urine protein, tube type, hematuria, oliguria, serum creatinine and urea nitrogen increased 2-3 days after poisoning, and acute renal failure occurred in severe cases. Symptom 4: dizziness, headache, hallucination, coma, convulsion. Symptom 5, after skin contact with paraquat, erythema, blisters, ulcers can occur. After contacting the nails with high concentration of paraquat liquid, the nails can be decolorized, broken, and even fall off. Eye contact can cause conjunctival and corneal edema, burns, ulcers. Symptoms 6, including fever, myocardial damage, mediastinal and subcutaneous emphysema, epistaxis, anemia and so on. Treatment after paraquat poisoning: methods 1. There is no specific antidote for paraquat poisoning, but all effective measures must be taken in the early stage of paraquat poisoning to control the development of the disease and prevent the occurrence of pulmonary fibrosis. Second, prevent the body from continuing to absorb poisons: remove contaminated clothes as soon as possible, and thoroughly wash contaminated skin and hair with soapy water. When the eyes are contaminated, rinse immediately with running water for not less than 15 minutes. Patients with oral poisoning should be given vomiting, thorough gastric lavage, and adsorbents (activated carbon or 15% bleached soil) should be added to reduce the body's absorption of poison, followed by mannitol or magnesium sulfate catharsis. Because paraquat is corrosive, be careful when gastric lavage, so as not to cause esophageal or gastric perforation and bleeding. Method 3. Accelerate the excretion of poisons from the body: in addition to routine infusion and the use of diuretics, it is best to carry out hemodialysis or hemoperfusion within 24 hours after taking poisons. the clearance rate of hemoperfusion is 5-7 times higher than that of hemodialysis. Method 4. Early administration of free radical scavengers, such as vitamin C, E, SOD, etc., to prevent pulmonary fibrosis. It has been reported that glutathione and tea polyphenols can improve the antioxidant capacity of the body and improve paraquat poisoning. High concentration oxygen inhalation should be avoided, which can increase the formation of reactive oxygen species and aggravate the damage of lung tissue. Only inhale oxygen at a concentration of 21% partial pressure of oxygen, or use positive end-expiratory pressure to breathe oxygen. In addition, the early use of corticosteroids and immunosuppressants (cyclophosphamide, azathioprine) may be effective for patients. However, once the lung injury occurs, it has no significant effect. Method 5. Symptomatic and supportive therapy: protect liver, kidney and heart function, prevent and treat pulmonary edema, strengthen nursing care of oral ulcer and inflammation, and actively control infection. In patients with paraquat poisoning, if there is lung damage, the prognosis is often poor and the mortality rate is high. Therefore, the patients with paraquat poisoning should be closely observed for pulmonary symptoms and signs, dynamic observation of chest X-ray and blood gas analysis, so as to help to determine the pulmonary lesions in the early stage. Click to get more herbicide application techniques