Currently, there is still ambiguity in the recognition and even confusion in the treatment of acute organophosphorus pesticide poisoning (AOPP). As China is a large agricultural country, pesticide poisoning is also a common disease at the grassroots level, and has been ranked among the top causes of death from various diseases in China, which is more harmful. This paper addresses several misconceptions that often exist in the clinical diagnosis and treatment of AOPP among primary care workers, hoping that primary care clinicians will change their concepts, get out of the misconceptions and improve the success rate of treatment. Myth 1: Overemphasis on the use of anticholinergic drugs and neglect of the application of reenergizing agents In the treatment of AOPP, the use of reenergizing agents, such as chlorophosphamide and iodophosphamide, is the “primary” drug, while atropine is the “primary” drug, and the priorities of the two should not be reversed. The priorities should not be reversed. In the past, the textbooks overemphasized the use of atropine, which resulted in the death of more patients from atropine poisoning than from poisoning itself, a lesson worth learning. The current emphasis on the use of reenergizers and the use of reenergizers first during treatment can reduce the dose of atropine and also protect respiratory muscles and prevent the occurrence of respiratory muscle paralysis. When patients with severe AOPP poisoning are seen, it is recommended that: clofibrate be administered intramuscularly, 2-3 g for the first time, 1 g after 1 hour, 1 hourly, for 3 times, then 1 g, administered once in 4-6 hours for maintenance for 3 days, and the total amount should not exceed 10 g/day. Iodine can also be used in hospitals where pharmacies do not have clofibrate. It is recommended to use clofentezine because it is easy to use, can reach the effective blood concentration in a short time, and has a fast action time. Atropine is given after the first dose of the reenergizer (first 2-3 g intramuscular injection) has been executed. Myth 2: Blindly believe in textbooks and stop using reenergizers and anticholinergics too early According to the clinical cases I have encountered in the past, the phenomenon of “rebound” due to premature discontinuation of reenergizers has occurred, which should be taken as a warning. A typical example is the case described in this teaching visit. The time of discontinuation of reenergizer is not necessarily 3 days, but should follow the scientific basis, and should not emphasize the view that poisoned enzymes are not easily revived after 3 days of poisoning. Studies have shown that ChE viability is steadily restored at 50% or more and generally does not rebound. Therefore, it is ensured that the drug should be stopped only when the blood cholinesterase (ChE) activity is steadily restored to more than 50%. The rationale is that further absorption of residual toxicity (including hepatic-intestinal circulation pathway) will inactivate new enzymes at any time, which still need to be reenergized; secondly, the new enzymes are protected by the fourth pharmacological effect of the reenergizer to inactivate the toxicity. Atropine discontinuation time should be discontinued along with the reenergizer. Myth 3: As long as the pupils are not dilated, it means that the amount of atropine is insufficient Atropine insufficiency and atropine overdose are sometimes not easily distinguished clinically and easily confused, which can cause difficulties in treatment and lead to the aggravation of the disease caused by human factors. The atropinization effect can be easily masked in the following cases: (1) atropine “reversal effect”; (2) concurrent cerebral edema; (3) acidosis. (See the article “Identification and treatment of three special cases of acute organophosphorus pesticide poisoning” for specific descriptions) After being diagnosed with AOPP, standardized treatment, attention to the treatment of cerebral edema and electrolyte disorders, and careful observation of changes in the condition and vital signs can avoid the “reverse effect” of atropine. The “reverse effect” of atropine and the occurrence of artificial factors such as atropine overdose can be avoided. Myth 4: Atropine is routinely implemented and used regularly and quantitatively There are roughly four methods of atropine maintenance after atropinization: ① intermittent dosing method (regular and quantitative dosing method); ② intravenous drip dosing method; ③ intravenous drip and intravenous injection combination method; ④ dosing method with symptom observation. Since there is no unified opinion on the exact comparative efficacy observation among the four methods, there is a controversy. Because the interval time (δt) and the single dose (m) of the regular intermittent dosing method are not easy to grasp, or too mechanical application, it is difficult to match the 24-h dosing amount (m×24/δt) with the actual amount needed, and the advantages of its efficacy are often not given full play when it is not used skillfully, which can easily lead to insufficient and excessive use of the drug. Regardless of what kind of drug delivery program, we must adhere to the general principle of “observation in the use of drugs, in the observation of drugs”, the purpose is not to cause atropine deficiency, and no atropine overdose, not a uniform, mechanical rigid application. The author in the clinical experience, atropine and other anticholinergic drugs, to be given temporarily in conjunction with the condition, pay attention to the electrocardiographic monitoring, atropinization if the heart rate < 90 beats / min, then give 2 to 3 mg each time, it is not necessary to emphasize too many indicators, such measures are relatively safe. Myth 5: Not understanding the pharmacological characteristics of the drug, the use of iodine dephosphoridine initially on the static drip Because iodine dephosphoridine (1.53 g of iodine dephosphoridine is equivalent to 1 g of chlorine dephosphoridine) can only be used intravenously, and the effectiveness of the drug is not strong, foreign countries have been eliminated. Although it is recommended to use chlorophosphamide, some primary hospitals in China are still using iodophosphamide. As a "curative" drug, the use of reenergizers should be emphasized. If the drug is administered intravenously at the beginning, it will take a long time to reach the effective blood concentration, which will result in excessive use of atropine during this period, leading to an increased incidence of atropine poisoning, and may also cause the occurrence of peripheral respiratory muscle paralysis (RMP), because the occurrence of RMP is related to the insufficient dosage of reenergizer in the early stage of poisoning. The correct protocol for the treatment of severe AOPP with iodophosphatidine: first, an intravenous loading dose of 1.0 g (dilution or half an hour and then intravenous injection of 0.5 to 1.0 g) at a rate of 5 to 8 minutes, and then added to the liquid in a sedative drip at a rate of 0.5 g/hour to maintain effective blood concentrations, with a total dose of <10 g/day. Myth 6: To increase the efficacy, clinical anticholinergics such as atropine and scopolamine are used together. Atropine, scopolamine and camptothecin are anticholinergics with strong peripheral effects. The central and peripheral effects of the four anticholinergics are in the following order: scopolamine > atropine > camptothecin > scopolamine, and so is the strength of the anti-AOPP effect. However, because there are fewer camptothecin products and scopolamine has greater central adverse effects, atropine is still the typical representative of this class of drugs used in AOPP clinics. If atropine is not available in a particular situation, it can be replaced by three other drugs, except that scopolamine alone is less effective. Atropine usage and dosage have accumulated a lot of experience, so it is appropriate to be the preferred anticholinergic. It is not advisable to mix atropine and scopolamine because it is not easy to grasp the dose. Myth 7: Atropine is given to counteract myalgia when patients develop myalgia. Myalgia is one of the typical nicotine-like symptoms of organophosphorus pesticide poisoning and is seen in patients with moderate or above poisoning. The peripheral effect of atropine is mainly to block muscarinic cholinergic receptors on the postganglionic cholinergic innervation effectors, thus it can counteract the muscarinic-like symptoms of acetylcholine and various choline-like drugs, but not the effect of counteracting nicotinic-like poisoning symptoms. Therefore, atropine cannot counteract the myofibrillation caused by AOPP, while reenergizers have a direct counteracting effect on myofibrillation, muscle weakness and muscle paralysis caused by AOPP. It should be noted that myofibrillation and respiratory depression can also occur with an overdose of restorative agents, but a large dose is required, or the rate of sedation is too fast, e.g. >500 mg/min. In moderately poisoned patients with myofibrillation, it is necessary to identify whether it is a lack of reenergizer or an overdose. Myth 8: It is not advisable to eat prematurely after poisoning AOPP After effective anti-toxic treatment, the patient is awake and the symptoms are relieved, and after several hours of observation, the patient can eat if he has appetite. At this time to eat, not only to play a nutritional and potassium role, more importantly, food in the gastrointestinal tract in the full peristaltic digestion process can be not absorbed in the gastrointestinal tract of pesticides mixed in food, later can be excreted with food residues. The principle of feeding is the first liquid food, followed by semi-fluid, fully recovered before you can enter the general diet; first light carbohydrate-based food, and then to high protein and moderate fat food. The reason is that whether the organophosphorus pesticide itself or atropine-based anti-toxic drugs, will have a certain impact on the body’s digestive system function, prematurely given to eat or into high-protein, high-fat food, will certainly cause adverse consequences. After feeding patients with oral organophosphorus poisoning treated by gastric lavage, attention should be paid to the observation of the patient’s condition, because in addition to the effects of the poison and drugs on the function of the digestive system, the local chemical irritation caused by the poison and the mechanical irritation of gastric lavage may cause potential gastric bleeding, etc. Myth 9: The dosage of rescue drugs is the same for poisoning by any route Compared with oral organophosphorus pesticide poisoning, the dosage of atropine and reenergizer is generally small for organophosphorus pesticide poisoning via skin and respiratory tract (OPPSRT) for patients with the same disease classification. For patients with mild OPPSRT poisoning, it is not necessary to routinely maintain atropinization on the basis of adequate anti-toxic drugs, and temporary symptomatic treatment and attention to skin washing can be provided.