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154 cases of rescue experience of organophosphorus pesticide poisoning


Should be noted that compared with the atropine poisoning Kam Rong q. Jing in the application of dehydration cases, continue to atropine therapy, the disease can be significantly improved. So when the agitation, disable atropine, application of sedatives instead made it worse. Therefore, close observation of clinical symptoms and by physical disc disease, severe disease of the commission should prevent the occurrence of brain water Chong, appropriate control inputs, and dexamethasone, mannitol, to correct hypoxia, keep the airway open, you can reduce brain edema occurred. Once the wizard cerebral edema, which should be systematically dehydration treatment, the disease can save the day. V. organophosphorus pesticide poisoning and pay attention to the anti-jumping and sudden death in clinical acute symptoms were relieved Pat recovery period, the condition can be repeated again deterioration or sudden death, a phenomenon known as rebound or a clinical death. Organophosphorus pesticide poisoning by oral dose, the clinical rebound occurs is not uncommon in this group occurred in 3 cases, mainly due to the child in the cross-mound Butterfly Table Tennis Grand ji l9 Snake 4 I ·. Early Xian stomach and catharsis is not complete, gastrointestinal absorption of residues continue to be caused by poisoning, or acute inert cholinesterase after poisoning a large number of in vivo phosphorylation state, coupled with early rehabilitation to agent application properly, the amount of toxic too large, too long and other reasons, the aging of phosphoryl cholinesterase low toxicity and high toxicity of poison into the complex oxide increased from 300 to 600 times more toxic ingredients, such as the inhibition of oxidation of dimethoate was more powerful cholinesterase activity omethoate, participation in the bile circulation, f yields bile which is stored gallbladder, when eating or reflex stimulation of the gallbladder, bile into the small intestine with the poison, thereby re-absorbed into the blood poisoning caused the emergence of rebound. We encountered a case of dimethoate poisoning in a stable condition has been able to eat normally after the first five-day rebound occurs. before the rebound of the amount of effective treatment with atropine, and sometimes even after rebounding 20 times the amount of confrontation with atropine still does not work, the cases were treated with atropine reached rebound 2100mg, also failed to save the patient's life. Another common cause of premature rebound disabled or sudden reduction of atropine, organophosphate poisoning death of more than 24 hours after onset,[link widoczny dla zalogowanych], but the illness can have 2 to 8 days or rebound sudden death, we rebound occurred in 2 cases were severe fear of poisoning the enemy, and a sudden reduction related to atropine, atropine of the re-post, and appropriately increase the dose, to be saved-f} f1, 'the fish live. Some advocates of organic phosphorus pesticide poisoning, not a lot of high-sugar liquid infusion or lost due to acetylcholine synthesis of coenzyme A, the main intermediate product of decomposition of glucose from pyruvate oxidative decarboxylation in the mitochondria. Therefore, the input glucose, the body's synthesis of acetylcholine may increase. However, this group of quality and quantity of the fluid does not increase Yan Gepei system, nor observe the infusion and recurrence or significant rebound relationship. organophosphate poisoning patients recovering from sudden death occurs, often can be seen. this group of case series sudden death due to zinc parathion poisoning. lead to the exact cause of death is unknown. acute organophosphate poisoning can directly damage cardiac cells, causing arrhythmia. Organic phosphorus compounds toxic effects on the heart can be divided into three phases, first phase brief The enhancement of sympathetic tone, = showed sinus tachycardia effort. The second great period of prolonged release of the parasympathetic, usually manifested various degrees of atrioventricular block. the third question of the Q ~ T extension and torsion of ventricular tachycardia (polymorphic ventricular tachycardia). severe arrhythmia may be the main reason for sudden death, unfortunately, in this case do the ECG. In severe organophosphorus poisoning after 4 cases of patients who did electrocardiography, showed sinus tachycardia or s ~ T segment, T wave changes, it is proposed to patients with severe organophosphorus pesticide poisoning should be doing and monitoring of ECG tracings to prevent sudden jaundice new therapies for hepatitis Armed Police Hospital Bei Lei Jilin thick application of our department more than ten years the treatment of various types of Anisodamine 420 cases of jaundice sunset inflammation patients have received satisfactory results. jaundice and the severity of reaction sunset injury. more severe jaundice, hepatitis Over the past has been difficult, step is to prevent early treatment of jaundice very important means of hepatic necrosis. (domestic Brings Forth 2 654 applications were reported treatment of severe hepatitis, liver Jin fans have a certain effect, its efficacy remains to be studied further.) revelation, I Application anisodamine treatment of various types of 420 cases of jaundice hepatitis patients, the effective rate was 98.2% or more. delivery method: anisodamine (654 ~ 2) 0.4mg/kg / day in 10% staphylococcus Sugar 5ooml the static point, the slow drip. the drug mainly to solve the drop yellow. inosine given according to different types of hepatitis, energy mixture. insert drugs Danshen blood stasis. Jiangmeiheji DDB Nuts alcohol, JiangMei spirit Schisandra powder. severe hepatitis branched-chain amino