In recent years, due to the residual and resistance problems of organochlorine and organophosphorus pesticides, the use of carbamate pesticides for agricultural pest control and rodent control has increased, and its acute poisoning has become more common in clinical practice. It is odorless, tasteless, non-corrosive, insoluble in water, stable in neutral and slightly acidic solutions, and easily hydrolyzed in alkaline and strongly acidic solutions. It is a new type of high-efficiency, low-toxicity and broad-spectrum insecticide that has been applied in China in recent years. Furadan can be absorbed through the digestive tract, respiratory tract, and skin poisoning. After entering the body, the toxin directly combines with the active center of cholinesterase to form carbamoylase, which causes cholinesterase to lose the activity of hydrolyzing acetylcholine, and endogenous acetylcholine accumulation occurs, stimulating cholinergic nerve excitation and producing corresponding clinical manifestations, so the symptoms are similar to those of organophosphorus pesticide poisoning. The main signs and symptoms are: dizziness, nausea, vomiting, general weakness, narrow pupils, pale face, blurred vision, muscle tremors, sweaty skin, salivation, abdominal pain, confusion, coma, diarrhea, wet rales in the lungs, slowed or increased heart rate, respiratory failure, increased terminal blood leukocytes, etc. Those who are poisoned orally have a burning sensation in the stomach. Since the combination of carbamate pesticides and cholinesterase is reversible, the hydrolysis and metabolism in the body is fast and the half-life is short (6-12 hours), and the cholinesterase activity generally starts to recover in about 4 hours, and almost completely returns to normal in 24 hours. In general, the phenomenon of “rebound” does not occur during the treatment. Furadan is acidic and loses its toxicity when it meets alkali. Gastric lavage with soap and water, 2% sodium bicarbonate and 5% sodium bicarbonate drip can accelerate its toxic destruction. Atropine can quickly relieve muscarinic symptoms. It is difficult to have a uniform pattern for the application of atropine. The dose, dosing interval, and maintenance dosing should be based on the degree of poisoning and the patient’s responsiveness to treatment. Compared with organophosphorus pesticide poisoning, each dosage should not be too large and used until atropinization. For mild poisoning, use atropine 0.3~2.0 mg intramuscularly and repeat if necessary; for moderate-to-severe poisoning, use atropine 2~5 mg sedately, once in 15~45 minutes, generally until atropinization. The patient should be given fluids, diuretic, oxygen, high-dose vitamin C and symptomatic treatment, and be hospitalized for 1~3 days on average. 2.Paraquat poisoning It is extremely toxic to human and there is no special drug. The mortality rate of oral poisoning can be more than 90%, and it has been banned or strictly restricted by more than 20 countries, but it is still widely used in rural areas of China, and tragedies keep happening! 2.1 Introduction of toxic substance: Paraquat has been used in agriculture since 1963. Paraquat is economical, time-saving, short degradation time in soil and low residue in crops. Paraquat is easily soluble in water and a little soluble in low grade alcohols; it is pure white crystals or colorless or light yellow solid, odorless; it is stable under acidic and neutral conditions, easily degraded under alkaline conditions, ultraviolet light can accelerate the decomposition, inert clay and anionic surface activity can make it passivated; agricultural preparations are mostly 20% to 40% aqueous solution, some additives are dark blue, it is a highly toxic type pesticide. Paraquat has multi-system toxicity and mainly damages epithelial tissues, with lung as the main target organ. It has strong affinity to lung tissue. After paraquat enters the organism, the concentration in lung tissue is 10 to 90 times that of other tissues, and its damage is more serious than that of other tissues; the early manifestation is acute lung injury, and the pathological changes of lung tissue are edema and hemorrhage of tissue cells, infiltration of inflammatory cells, and even the formation of alveolar hyaline membrane; some patients, due to the damage of lung tissue, cause a large number of alveoli to rupture, resulting in interstitial emphysema of lung, and even the formation of mediastinal emphysema and Subcutaneous emphysema; pulmonary microcysts and pulmonary fibrosis are formed in the late stage of poisoning. Paraquat can cause the body to produce a large number of oxygen free radicals and indirectly produce lipid free radicals. Free radicals cause damage to type I and type II alveolar cell membranes and vascular epithelial cell membranes in the interstitium through lipid peroxidation and other damaging effects, which are the main causes of acute lung injury. The mechanism of pulmonary fibrosis caused by paraquat is complex and is currently thought to be related to multiple cytokines and genes. The mortality rate of paraquat poisoning is extremely high. Those who ingested large amount of paraquat can die within a short time, mostly due to multiple organ failure such as lung, kidney and liver caused by acute lung injury; those who ingested medium amount or small amount often die from acute respiratory distress syndrome later due to extensive pulmonary fibrosis. At present, there is no well-established prognostic assessment index. 2.2 Treatment issues: 1. On-site and emergency first aid treatment: Because of the unique nature of paraquat, clinically paraquat poisoning is different from other toxic poisoning in terms of performance and treatment characteristics. Except for some extra heavy poisoning patients who die quickly, the rest of the poisoned patients have no other special symptoms and signs in the early stage except local irritation and some non-specific gastrointestinal manifestations, and there are no special laboratory tests to help the diagnosis, so they are ignored by the patients themselves, their families, and even medical personnel without relevant experience, and when organ function abnormalities appear, especially pulmonary fibrosis, all changes are almost irreversible. Therefore, the correct treatment at the first time of poisoning is crucial. Inactivation treatment with bleaching earth gavage and adsorption treatment with activated charcoal and double octahedral montmorillonite (Bicil, Simethicone) are the only treatment methods with special efficacy at present. It is suggested that 15% bleach suspension should be given orally or by gavage immediately, 1000ml for adults and 15ml/kg for children. if there is no bleach or other effective treatment measures, patients can be given water and then induced to vomit, and then ordinary mud water can be given orally (mud can deactivate paraquat rapidly, the preparation of mud and water is 1:3, stir well and filter), which is also an effective temporary treatment measure. Although the former may aggravate mucous membrane damage, the latter also seems to be an informal treatment method, but it is a proven treatment method. Once paraquat is absorbed, the consequences will be fatal, while mucosal damage has no special effect on mortality. 2.Toxin removal treatment: Toxin removal means represented by blood perfusion can be expected to remove toxin, prevent liver and kidney function damage and improve survival rate in the early stage, but because the concentration in blood is not high after paraquat poisoning, it is absorbed and rapidly accumulates and acts on target organs such as lung, kidney and liver, and its effect is mainly concentrated on these target organs, so some authors also think that blood removal treatment is not effective. Rehydration and diuresis can promote the excretion of toxic substances. 3.Free radical scavenging antioxidant therapy: reduced glutathione has the effect of scavenging free radicals directly. It has been reported that in 2 cases of oral paraquat poisoning, the patients not only survived but also recovered normal lung function by using injection therapy combined with other methods. 4.Glucocorticoids and immunosuppressants: In recent years, a study by Taiwanese scholars concluded that the use of high-dose glucocorticoids alone or combined with immunosuppressants can successfully save some patients with paraquat poisoning, and they conducted a prospective clinical randomized trial on inpatients with moderate and severe paraquat poisoning. The results showed that the mortality rate in the study group was significantly lower than that in the control group. Two patients were reported to have survived without fatal pulmonary fibrosis despite obvious toxic manifestations and hepatic and renal impairment after high-dose methylprednisolone shock therapy with “early, adequate, and short course”, and although the survival rate was low, the outlook was encouraging, and research in this area deserves attention. 5. Symptomatic and supportive treatment: Special attention should be paid to the management of life-threatening toxic effects such as ARDS, hepatic necrosis and acute renal failure. Oxygen therapy should be very careful, never use high concentrations of oxygen, otherwise it will do more harm than good, generally should limit oxygen inhalation, only when the partial pressure of oxygen in the blood is less than 5.3kPa (40mmHg), only available concentration > 21% of oxygen inhalation. Currently, once pulmonary fibrosis develops, the disease will be irreversible and the patient will die within 1 to 2 weeks. Timely lung transplantation will be the only option. Various pharmacological treatments have a role in the prevention and control of complications and improved cure rates in patients with advanced disease, but they have not been supported by definitive evidence and need further experimental and clinical validation, which is one of the new challenges facing emergency medicine. 3 , Poisoned rat poisoning On September 14, 2002, a major breakfast food poisoning incident occurred in Nanjing, which caused great concern to our government and the whole society. This mega case of poisoned rat poisoning resulted in the death of 42 people, and after that, the whole country was focused on cleaning up the rat poison containing highly toxic rat poison. 3.1 poisonous rat poison: also known as no rat life, four two four, three steps down, smell to death, etc.; chemical name: Tetramethylene disulfotetramine, English name: Tetramine; Tetramethylene Disulfotetramine, a white crystal or light powder. Melting point 250～254℃. Solubility in water: about 0.25mg/ml almost insoluble in water; slightly soluble in acetone; insoluble in methanol and ethanol. Stable in dilute acids and bases (concentration to 0.1N). Decomposes at 255-260°C, but decomposes in continuous boiling water solution. Decomposes on heating, emitting oxide fumes of nitrogen and sulfur. Can be absorbed through the digestive and respiratory tracts. Not easily absorbed through intact skin. The original drug is white powder solid, purity 20-50%; marketed products for each kilogram of the original drug and flour (rice flour, etc.) 200-400 kg, and add attractants made, mostly white powder solid, no special smell, there are also products made of bags. The packaging is mostly labeled as “four two four”, “three steps down”, “atomic energy rodenticide”, “gas rodenticide” etc. 3.2. 3.2 Toxicology: The LD50 (lowest lethal dose) for mammals is 0.10mg/kg orally, 0.1~0.3mg/kg for rats orally, 0.2mg/kg for mice orally, and 0.1mg/kg for mice subcutaneously. It is a neurotoxic rodenticide and has a strong excitatory stimulating effect on the central nervous system, especially the brainstem, mainly causing strong convulsive effects. This product has antagonistic effect on γ-aminobutyric acid, mainly due to blocking γ-aminobutyric acid receptors, and this effect is reversible. It enters the body and mainly acts on the nervous system, digestive system and circulatory system. It should be noted that scientific experiments and rodent control practices at home and abroad have long proved that poisonous rodent is highly toxic to all warm-blooded animals, and is 3-30 times more toxic than another highly toxic rodenticide – fluorfenamide, and more than 100 times more toxic than arsenic and cyanide. In 1952, it was found that the seeds of fir grown in soil treated with poisonous rodenticide could kill rabbits after 4 years. The relevant departments of our country have issued a document in 1991 to determine that poisonous rodenticide is a prohibited product. However, cases of poisoning with rat poisoning still occur from time to time, so it is necessary to carry out strong management of the production, circulation and use of rodenticides to cut off the source of the use of prohibited rodenticides. At the same time, health education in rural areas should be strengthened to mobilize farmers to use new long-lasting rodenticides. 3.4 Clinical manifestations: tonic, paroxysmal convulsions, with loss of consciousness, foaming at the mouth, general cyanosis, similar to seizure continuity, and can be accompanied by psychiatric symptoms, severe poisoning with frequent convulsions without intermittent, and even corneal inversion. The poisoned person may die of respiratory failure due to violent tonic convulsions. The animal is excited and jumping, shrieking and spasming after poisoning. The limbs are rigid. Most cases of poisoning at present are oral poisoning. Mild poisoning manifests headache, dizziness, weakness, nausea, vomiting, numbness of the mouth and lips, and a sense of intoxication. Severe poisoning manifests sudden fainting, epileptic-like grand mal seizure, general convulsions, foaming at the mouth, urinary incontinence, and loss of consciousness during seizure. Toxicological analysis: Blood, urine and stomach contents can be picked up by thin layer folding method and gas chromatography analysis. EEG is very meaningful non-invasive monitoring, epileptiform discharges abnormal waves, extremely easy to pounce and long duration, even when the blood concentration is qualitatively negative, but still clearly visible. Myocardial enzyme profiles may be abnormally elevated. 3.5 Treatment progression: Patients with oral poisoning should be immediately induced to vomit, activated charcoal adsorption, gastric lavage, and catheterization. 3.5.1 Etiological treatment: Sodium dimercaptopropionate (Na-DMPS) 0.125-0.25g intramuscularly in the first dose may be effective after 10min. 5-8 sticks are generally used to control convulsions within 3-8h, which may be related to its competition for r-aminobutyric acid (GABA) receptors. Vit B6 is a coenzyme of amino acid decarboxylase, which catalyzes the generation of GABA from glutamate, and therefore has an anticonvulsant effect on rat poison. 3.5.2 Blood purification therapy: Because of the low plasma protein binding of toxoplasma, and the volume distribution of 1L/kg and relative molecular mass of 240.27, it is suitable for blood purification. The purification program can be selected according to the situation, and the methods include plasma replacement, blood perfusion, blood induced folding, etc., which not only effectively remove the toxin, but also remove the inflammatory mediators and reduce the damage of organ tissues. 3.5.3 How to remove residual toxins from the body: Continuous blood purification technology (CRRT) is a new technology born in the fire of war, the prototype first appeared on the battlefield in the 1960s. American doctors placed a small filter between an arterial cannula and a venous cannula to filter out the excess water in the casualty’s blood, maintain the water-electrolyte balance in the body, and solve their problems such as kidney failure without urine due to blood loss and shock. Later, this technique was gradually developed and perfected into continuous hemodialysis system, which was applied for the prevention of chemical warfare, rescue of seawater drowning and nuclear compound injury, and played a great role in the early treatment of severe trauma, serious infection, acute hemolysis, septic shock, multi-organ failure, hyperthermia, heat stroke and many unexplained serious diseases. Continuous hemodialysis can filter stress variant proteins, toxins, and pathogenic mediators from the patient’s blood to avoid serious toxic symptoms such as sepsis and multi-organ failure, and can also be used for long-term maintenance treatment of chronic and critical diseases. Unlike conventional hemodialysis, this dialysis facility can remove toxic substances by filter ultrafiltration and adsorption while feeding a large amount of replacement fluid to accelerate fluid exchange. The fluid exchange can reach 4-6L per hour and up to 144L in 24h, which is equivalent to dozens of times of human blood. In critical patients, dialysis and high-dose infusion for 3 consecutive days (72h) are used to thoroughly clean out the harmful substances in the blood along with those in the tissue interstices. The General Hospital of Nanjing Military Region applied this technique to save the lives of more than 200 patients during the rescue of the poisonous rat poisoning incident in Tangshan Town. Our experience can be used to partially replace CRRT with the long-term medically prescribed oral activated carbon method. 3.5.4 Symptomatic and supportive treatment: anticonvulsant treatment, etc. 3.5.5 Safe nursing care: Resuscitation should be based on the unique characteristics of its poisoning and the needs of the patient’s condition, close observation of changes in vital signs, and timely and effective implementation of all nursing operations to create favorable conditions for the successful treatment of patients poisoned with poisonous rodents. When convulsions occur, the patient should be appropriately protected and should be guarded to prevent bruises. At the same time, care should be taken not to bruise, but not to press the patient’s limbs forcibly, as muscle tears, fractures or joint dislocations can easily occur. The back should be padded with clothing to avoid back abrasions and vertebral fractures. To prevent biting the tongue, wrap the tongue depressor with gauze and insert it between the upper and lower teeth of the patient, but be careful not to cause the tongue to fall back, so as not to affect breathing. Carefully do psychological care , some patients are suicidal because of taking poison, after the patient is conscious, emotional instability, fussing, still insist on suicide, while pay attention to communication with the patient, through proper psychological care, so that the patient emotional stability, active cooperation with treatment, play a role in the patient’s healing. 4.Introduce a new snake-injury problem Red-necked Keelback Snake (Rhabdophis subminiatus) commonly known as Red-necked Grass Snake, the English common name Red-necked Keelback Snake, belongs to the family Colubriidae (Colubriue), subfamily (Rolubrinae). It is mainly found in Southeast Asian countries such as China, India, Myanmar, Thailand, Laos, Vietnam, Cambodia, Malaya and Indonesia. It has not been classified as a venomous snake in China. In 1992, we found the first case of red-necked snake bite poisoning causing blood loss and bleeding, and so far we have found 13 more cases. It is worth noting that in the past 2 years, we have found 4 cases of death due to bleeding of brain and other important organs, shock and acute renal failure after being bitten by red-necked snakes, all of which occurred in Guangxi! The Duvernoy’s gland is located above the palate and can produce a very potent toxic secretion. The venom mixture is not injected into the bite, but flows into the small wound caused by the teeth on the palate and can also penetrate the human skin. Changes in the concentration of AT-III and α2-PI in the blood are currently considered to be more sensitive and accurate indicators for the diagnosis of DIC. I have performed blood tests on patients admitted to the hospital regarding the diagnosis of DIC in snakebite, and found that the snakebite can cause a completely defibrinized state, with AT-III and α2-PI being significantly depleted, especially α2-PI, and a significant increase in FDP, suggesting that the coagulation system in the patient’s body is activated and the typical hematological changes of DIC secondary to hyperfibrinolysis. Despite the severity of the bleeding symptoms, the patient’s prognosis is still favorable if the bleeding is not in a vital organ such as the brain, so DIC caused by red-necked snake bite may be a special type, or DIC-like syndrome. The mechanism of hematologic alteration of DIC caused by this kind of snake bite is not fully understood. Unlike DIC, heparin therapy is almost ineffective and is generally not used. In any case, our clinical observation shows that although the clinical symptoms and bleeding of patients can be improved to a certain extent by active symptomatic treatment, the hematological changes such as blood de-coagulation and defibrinization status can last for more than a week, and even patients discharged from the hospital without conscious symptoms still maintain a dangerous state for a period of time. Antivenom is recognized as an effective treatment for snake bites, but no antivenom has been produced yet. It is imperative to study whether the other monovalent antivenoms currently in production are effective or to develop antivenom as a means of obtaining effective therapeutic drugs. In the absence of effective antivenom, symptomatic treatment is the mainstay. Clinical observation shows that small amount of blood transfusion can reduce the symptoms caused by blood loss, but the effect of hemostasis is not good. For local bleeding more than take the general pressure bandage is not effective, care must pay attention to minimize venipuncture, especially arterial puncture. In case of cerebral hemorrhage that is very dangerous, how to achieve the purpose of hemostasis is to be studied.