Paraquat, the chemical name of 1,1′-dimethyl-4,4′-bipyridine cationic salt, is a crop herbicide. With the widespread use of paraquat in recent years, the number of poisoning cases has been increasing. The prominent manifestation of human poisoning is multi-organ damage or failure, mainly acute chemical interstitial lung lesions and rapidly developing interstitial lung fibrosis. The amount of oral poisoning in humans is about 10-15ml (20% paraquat solution) or 2-6g of pure product [1]. The mortality rate of severe poisoning is as high as 60%-80% [2]. The clinical treatment of 57 cases of severe paraquat poisoning admitted to our hospital in the past 6 years is reported as follows 1. Clinical data 1.1 General data The 57 cases in this group, including 22 males and 35 females, were aged 65 years old at the maximum and 10 years old at the minimum, with an average age of 29.4 years. All of them were poisoned by oral intake of 20% paraquat original solution, the oral amount was 10.5-140ml, among which 28 cases were below 20ml, 20 cases were 20ml-50ml, 9 cases were above 50ml, the average was 26.5ml (all patients were asked to simulate the oral amount with water to measure it). According to the oral dose of 10-50ml or multiple organ function damage (FODS) as severe poisoning, more than 50ml or multiple organ function failure (MOF) as very severe poisoning (outbreak type), 57 cases in this group, 35 cases of severe poisoning, 22 cases of very severe poisoning. 1.2 Clinical manifestations The consultation time of this group of cases was 1.5h-96h, with an average of 26.7h. The early symptoms of severe poisoning cases were nausea, vomiting, pain in the oropharynx, posterior sternum and epigastrium, acute upper gastrointestinal corrosive inflammatory manifestations such as oral mucosa congestion, edema, erosion and bleeding. Among them, 22 cases were accompanied by gastrointestinal bleeding manifestations. The manifestations of lung, liver, kidney, heart and gastrointestinal tract damage such as chest tightness, breath-holding, shortness of breath, panic, abdominal distension, inability to eat, jaundice, tarry stools and oliguria began to appear after the second to third day. Six of the cases showed pancreatic damage. The above symptoms reached their peak on day 5-7. 13 cases developed MOF, mainly respiratory failure, followed by combined liver and kidney failure. All but two cases died of MOF within one week. 1.3 Laboratory examination WBC 8.4×109/L – 41.8×109/L, neutrophil percentage 78%-95%, among which 24 cases were stained with neutrophil alkaline phosphatase (NAA), positive rate 72%-100%, with a score of 216-600 points. Chest radiograph: The chest radiograph of patients with severe poisoning generally showed no significant changes in 1-2 d of onset, and 3-5 d showed increased lung texture, decreased translucency, and scattered speckled or patchy shadows in the whole lung. Some of the severe and very severe patients mostly showed hairy glass-like changes in both lungs with full-blown large shadows or white lung, and appeared early. Three of them had combined pneumothorax, two had combined mediastinal emphysema, one had combined pneumothorax with mediastinal emphysema, and two had combined pleural effusion. Oxygen saturation (SPaO2) and partial pressure of oxygen (PaO2) became proportional to the lung disease, with SPaO2 in the range of 80%-15% and PaO2 in the range of 64.7 mm Hg-24.8 mm Hg. All cases showed elevated cardiac enzyme profiles and sinus tachycardia. Five cases were accompanied by a small amount of pericardial effusion. All cases showed varying degrees of impairment of liver and kidney function, and six cases showed elevated blood glucose and elevated blood and urine pancreatic amylase. 1.4 Clinical treatment (1) Gastrointestinal decontamination: early, fast and thorough. For those admitted within 24 hours of onset or those who still need gastric lavage, 15% bleach suspension (or activated charcoal) was given for gastric lavage. All cases were given 15% bleach suspension 300ml plus 20% mannitol 250ml (or 20% magnesium sulfate 100ml) for diarrhea, once every 3-6 hours, or alternatively, until there was no blue paraquat in the stool, to be completed within a few hours. For those who cannot eat due to oropharyngeal pain, nasal feeding with gastric tube should be inserted carefully. (2) Blood purification: All cases were given semi-quantitative determination of paraquat in urine (using paraquat test kit produced by Syngenta (China) Investment Co. Hemodialysis (HD) was given to 18 cases, hemodialysis (HP) to 21 cases, bedside hemofiltration (CRRT) to 9 cases, and plasma exchange (PE) to 16 cases, of which: HD+HP to 10 cases and PE+CRRT to 6 cases. 24 h was administered until the urine was negative for paraquat. If the blood concentration is still high and the body can still tolerate it, it can also be administered once every 12 hours. The principle is to remove toxins from blood as early as possible to reduce the transfer of toxins to tissues. (3) Drug therapy: All cases were given larger doses of glucocorticoids, methylprednisolone 0.3-0.5g/day according to the kilogram of body weight, for 3 d, gradually in descending steps to reduce the dose until the disease is controlled. For those with good general condition, no important organ failure and uncontrolled pulmonary lesions, cyclophosphamide 0.2-0.5g was added once daily for 3 d. The application could be repeated if necessary. Also high doses of free radical scavengers, antioxidants, as well as antagonists and competitive agents were given in all cases. The drugs applied were: reduced glutathione (guladin or atomorelin 1.8g-2.4g iv drip qd), vitC 3.0g iv drip qd, vitE 0.1 tid, take-home 10mg tid, vitB 1200mgim qd, etc. Add ustekin 0.1-0.2MIU q12-q8h for 5-7 days during the severe phase of inflammatory response of the organism. In the recovery phase add high doses of drugs that improve microcirculation: Chuanxiong, compound Danshen injection, etc. [3]. As well as supporting nutrition, symptomatic treatment, and controlling infection. (4) Rational oxygen therapy, assisted breathing if necessary. In principle, oxygen is prohibited in the absence of obvious hypoxia, and is only given when SPaO2 is below 90% or PaO2 is below 60 mmHg. In case of ARDS or obvious respiratory failure, non-invasive or invasive ventilator-assisted respiration is given [1], and synchronous mode (SIMV) plus positive end-expiratory pressure (PEEP) of 3-5 cmH20 is applied. 2. Results The end of clinical treatment without medical dependence and survival was considered as cure. There were 57 cases in this group, 23 cases were cured, 27 cases died, and 7 cases were discharged automatically (5 cases died and 2 cases survived after the follow-up in January), and the cure rate was 40.35%. All cured cases were discharged with chest X-ray, lung CT and pulmonary function examination: chest X-ray was normalized in all cases; lung CT: 11 cases had mild pulmonary fibrosis; pulmonary function examination: 16 cases had mild diffusion dysfunction. At the return visit after one month, all 23 cases took care of themselves and regained certain working ability. Paraquat is a bipyridine herbicide, its poisoning mechanism is: in addition to its direct stimulating and corrosive effect, it also causes a series of redox reactions in tissue cells, generates many kinds of peroxides and inhibits energy synthesis, interferes with cell metabolism, and causes tissue cell damage and failure directly and indirectly. Because of the active uptake and accumulation of paraquat by alveolar cells, lung damage is the most prominent, and interstitial pulmonary edema, ARDS, hypoxemia and respiratory failure are likely to occur. There is no special antidote for paraquat at present. Through the clinical treatment of this group of cases, I have learned that the treatment of paraquat poisoning should be done every second, and it is very important to take comprehensive measures such as gastrointestinal decontamination, blood purification and drug treatment before the transfer of paraquat ions to tissue cells reaches lethal concentration. Gastrointestinal purification is the key to stop the continued absorption of paraquat. These measures include emetic, gastric lavage, diarrhea and enema, and the faster, earlier and more thorough, the better. According to clinical observation, for those who cannot do gastrointestinal decontamination in time and thoroughly after taking large amount of oral dose (more than 20ml), blue paraquat can still be observed in the stool after one week. Blood decontamination is the key to stop the transfer of paraquat to tissues. The best time for blood decontamination should be seized within 12h, but blood decontamination should be carried out as long as the urinary paraquat is positive in characterization. From the comparison of plasma purification effect of this group of cases, PE+CRRT has the best effect. Generally, only two plasma volumes need to be replaced (usually 5000ml, divided into two times, about 2500ml each time), and the urine test may be weakly positive or negative, and most of them need to be replaced 3-4 times, which can be completely negative. In combination with CRRT, the AV600 hemofilter is more effective in removing inflammatory mediators and relieving symptoms. The rest of the blood purification measures are not effective, and urine tests are still positive for more than 3-5 times [4]. MOF is the main cause of death in this disease, generally respiratory failure is the most prominent, followed by liver and kidney. Liver and kidney failure, the application of artificial liver or artificial kidney, liver and kidney function can be restored in some patients, but once the lung damage reaches severe respiratory failure (chest X-ray or CT lung lesion shadow of more than 50%) death will be difficult to avoid. Therefore, reducing lung injury, eliminating acute chemical interstitial pneumonia and inhibiting acute interstitial lung fibrosis are the keys to reducing mortality. Therefore, early, adequate and rational application of glucocorticoids and, if necessary, immunosuppressive agents are recommended for treatment. Free radical scavengers and antioxidants have certain auxiliary therapeutic effects and should be actively applied. Whether the so-called competitive antagonists, such as vitamin B1 and insulin, have a role to be further verified, but since there are no obvious side effects, they are used for the time being. In addition, symptomatic treatment, nutritional support, to maintain the restoration of important organ function, is also quite important. Ventilator-assisted breathing can really prolong the survival time of patients. In conclusion, the treatment of paraquat poisoning should be highly valued, and every second should be taken into consideration, and comprehensive treatment and proper measures should be taken to improve the cure rate.