(a) to eliminate the poison that has not been absorbed

Cutting off the poison source quickly is an important measure to save the success or failure. Once acute poisoning is found, remove the patient from the toxic environment immediately. For patients with skin absorption poisoning, wash the skin thoroughly with plenty of warm water, wash your hair or shave your head if necessary, and don't use hot water to avoid dilating skin blood vessels and accelerating the absorption of poisons.

Poisons in the digestive tract must be removed by oral poisoning.

Vomiting: It is a field rescue method for conscious people, especially those who take poison after meals.

Gastric lavage: gastric lavage is not limited by time. No need to wash for more than 6 hours, but pyloric spasm, so wash for more than >12 hours.

Usually warm water is used for gastric lavage, and 0.2~0.5% activated carbon suspension can be used. It is suggested to use normal saline to avoid hyponatremia and water poisoning caused by gastric lavage with water. Generally, after gastric lavage with water, furosemide 20mg is given. It is also recommended to use 2~4% sodium bicarbonate, because organophosphorus is easy to decompose and fail under alkaline conditions, but excessive amount can easily cause metabolic alkalosis and hypernatremia, except trichlorfon, which can be converted into dichlorvos with more toxicity in alkaline solution.

Pour 300ml of gastric juice at a time, and never exceed > 500ml. Because too much gastric lavage fluid is poured into the intestine at one time, it will increase absorption.

Thoroughness of gastric lavage: It is reported that once gastric lavage, no matter how full, it can't be complete. Even if the eluent is colorless and tasteless, it still inhibits cholinesterase up to 12~ 180 elbow. It is required to bring the gastric tube into the ward and wash the stomach several times.

Laparotomy and gastrostomy are used for gastric lavage.

Anti-toxic while gastric lavage, and closely observe the condition.

Laxative: 20~40g sodium sulfate, dissolved in 20ml water, once injected into the stomach tube.

(2) Eliminate absorbed poisons:

Hemoperfusion is a method of purifying blood with activated carbon and directly removing poisons. From 65438 to 0979, it was used to treat drug poisoning in China. Our hospital has achieved satisfactory results since August 1997. However, the incidence of respiratory failure in AOPP, the complications during and after hemoperfusion, the timing of hemoperfusion, the adjustment of antidote dosage and the technical problems in hemoperfusion operation need to be studied.

Application of atropine

Atropine competes with acetylcholine in the M receptor part to resist the muscarinic effect of AOPP, so it is a palliative drug.

Atropine should be used in any case of AOPP. Early, sufficient and repeated medication should be done. Atropine can relieve bronchospasm, inhibit the secretion of bronchial glands, prevent the occurrence of pulmonary edema, and also antagonize the central inhibition and respiratory center inhibition caused by Ach accumulation. The dose of atropine must be enough to antagonize the symptoms caused by massive accumulation of ACh, so as to achieve atropinization, that is, the pupil is larger than before and no longer shrinks, the face is flushed, the skin is dry, the lung moist rales disappear, the heart rate is accelerated, the disturbance of consciousness is alleviated, or the coma patient begins to wake up. The dose is first large and then small, and the interval is first short and then long, until the symptoms are satisfactorily controlled or atropine is reduced to maintain it, so that it can be used during observation and observed during use.

Atropine iv 1~4 takes effect in 0~4 minutes, reaches its peak in 8 ~ 10 minutes, and is ineffective in 2 ~ 3 hours. In order to avoid cumulative poisoning, the time interval of intravenous injection is generally > 15 minutes, and high-dose intravenous injection of 50 ~ 100 mg is opposed.

It is most important to master the dose correctly in the first hour, and atropinization is needed within 3~5 hours.

Normal people are poisoned by atropine at 5~ 10mg, and the minimum lethal dose is 80~ 130mg. 60% of AOPP deaths are related to atropine overdose.

In the process of atropinization, besides routine vital signs monitoring, we should also pay attention to the following points:

1. Gland secretion, salivary glands and sweat glands are the most sensitive to atropine, so keep your skin thirsty at all times. If sweating, salivation and lung moist rales occur, it often indicates that the dosage of atropine is insufficient.

2. Pupils: If the pupils are narrowed, the dosage of atropine is insufficient; If the pupil is dilated to 5~6mm, we should pay attention to whether the dosage of atropine is too large.

3. Heart rate: often controlled at 100~ 120 beats/min. However, heart rate is easily affected by basic heart disease, hypoxia, blood volume, body temperature and other factors. If there are anomalies, it is necessary to identify whether these factors are combined.

4. Body temperature: After atropinization, keep the body temperature between 36.5~37.5℃. If it exceeds 38℃, it often indicates that there is an excess of atropine, which is a reliable indicator.

5. Consciousness: Maintain mild irritability and be full of energy. Slight excitement can be considered as a key indicator of atropinization and atropine overdose. If mania, delirium and convulsion often suggest atropine overdose, it is also a reliable indicator to judge atropine overdose. In severe cases, excitement turns to inhibition, coma and bulbar palsy occur, and death occurs.

To judge the meridian tropism of D 'atropine, we should observe it comprehensively, and we can't generalize everything unilaterally with the index of 1 ~ 2. Sometimes there is atropine poisoning, but the pupils are not dilated, which may be because the eyes are polluted by organophosphorus pesticides. When mastering the indicators of clinical manifestations of atropinization, we must pay attention to: (1) can't be perfect, and we can't just rely on one or two indicators. (2) Distinguish between moderate and excessive. (3) Not all atropinization indices are constant.

Atropine index Atropine poisoning

Sweating stops and the skin is dry.

Heart rate increased, but ≤ 120 beats/min.

High body temperature, but ≤37.5℃

The holes are widely distributed, but the diameter is ≤ 5 mm

Pulmonary rales disappear

Facial flushing, madness, delirium, convulsions and even coma.

Heart rate ≥ 120 beats/min.

High fever T≥39.0℃

Pupil > 5 mm

Cough pink foam-like sputum

12~24 hours when the condition is stable, the dose can be reduced. Before the dosage is reduced, the interval of medication can be extended. Each reduction is generally 1/3~ 1/2, and the maintenance medication is generally not less than 72 hours. For patients with moderate and severe poisoning, the dosage of atropine should be kept for 3~5 days, and it should not be reduced too quickly, otherwise it will easily rebound.

The antitoxic effect of atropine is not comprehensive;

1. has no effect on N receptor, for example, it can't resist muscle weakness, muscle paralysis and muscle tremor caused by neuromuscular junction blocking. It is also ineffective for central nervous system symptoms.

2. It has no effect on the activity of phosphorylated cholinesterase. Atropine can be gradually reduced and eliminated until a new cholinesterase appears in the body.

(4) Emphasize the role of oximes in the treatment of acute organophosphorus pesticide poisoning:

The mechanism of action of 1. oximes;

Protective effect of cholinesterase;

When the multifunctional agent is hydrolyzed by type I phosphorylase, the multifunctional agent itself is combined with the organic phosphorus in the body, and then hydrolyzed into non-toxic compounds to be discharged. In this process, cholinesterase is prevented from combining with free organophosphorus. (Protective effect)

It has been found that coke has affinity with N receptor of neuromuscular junction of respiratory muscle. It can revitalize local toxic enzymes and restore neuromuscular transmission function. Therefore, it is particularly important to prevent and treat AOPP complicated with respiratory failure.

2. To explore the dosage and application time of oximes.

The application principles are early, moderate and continuous.

The plasma concentration of oxime drugs for effective treatment is 4mg/L, which is 20-40mg/L abroad.

Methods: A. The first dose of chlorpyrifos was slightly poisoned by intramuscular injection of 0.5~0.7g.

Moderate poisoning is 0.75~ 1.5g im.

Severe poisoning 1.5~2.5g im

After that, half of the first dose was repeated every 1/2~ 1 hour until the symptoms disappeared and the cholinesterase activity stabilized at 50~60% of the normal value, and the drug was stopped after 48 hours.

Methods: B, the first day dose 10g, namely1gq1himx 3 times.

1gq2himx 3 times later

Then 1g q4h im until 24 hours later.

After 24 hours,1g4 ~ 6h im× 2 ~ 3 days is a course of treatment.

It depends on the condition in the future. It still takes q6h × 2~3 days for patients with oral poisoning to leave the ventilator. The total amount of one day shall not exceed 10~ 12g. Large doses of oximes can also inhibit cholinesterase activity and even cause respiratory depression, so it is necessary to strengthen respiratory monitoring in the application process.

In vitro tests showed that 99% of phosphocholinesterase "aged" within one day. But in the body, some organophosphorus is activated by metabolism; Intestinal and hepatic circulation of organophosphorus; Organophosphorus stored in adipose tissue and other places is slowly released into the blood, so the previous view that oxime drugs are effective only on the first day of poisoning or can be stopped after 2~3 days of use is incorrect.

Verb (abbreviation of verb) symptomatic treatment

(1) Keep the respiratory tract unobstructed and maintain the respiratory function: closely observe the patient's respiratory changes, remove respiratory secretions and give oxygen. The main cause of death of AOPP is respiratory failure, which can be caused by pulmonary edema, respiratory muscle paralysis or respiratory center failure. Therefore, early detection and timely rescue should be achieved. When there are early manifestations of respiratory failure, such as changes in the frequency, rhythm and amplitude of breathing, tracheal intubation or artificial respiration should be carried out decisively.

(2) Actively treat brain edema, shock, arrhythmia, cardiac arrest, water electrolyte and acid-base imbalance.

(3) Patients with severe poisoning can be given new blood to supplement cholinesterase.

(4) Proper use of antibiotics to prevent pulmonary infection.

Intermediate syndrome

The onset time of IMS is 2~4 days after organophosphorus poisoning, and some cases are 7 days. This is a syndrome characterized by myasthenia after AOPP is treated with acute cholinergic crisis (ACC) and before delayed peripheral neuropathy (OPIDP). Because the onset time is between the first two, it is named IMS, and some people call it delayed respiratory failure.

It is generally believed that after acetylcholinesterase activity is inhibited, a large amount of acetylcholine accumulated in synaptic space continues to act on N2 receptor on postsynaptic membrane, desensitizing it, resulting in transmission disorder at neuromuscular junction and skeletal muscle paralysis. The main electrophysiological changes of postsynaptic membrane are continuous depolarization and disappearance of endplate potential. Electromyography showed that high-frequency electrical stimulation showed that the amplitude of muscle response decreased gradually, which was similar to myasthenia gravis, and also suggested neuromuscular transmission disorder.

Muscles are mainly controlled by proximal limb muscles, cervical flexors and cranial nerves ⅲ ~ ⅶ and ⅹ. Severe cases may die of peripheral respiratory failure due to respiratory muscle paralysis. The main manifestations are ① difficulty in opening eyes or mouth, weakness in chewing, shallow forehead lines, air leakage in cheeks, difficulty in swallowing and swallowing, and hoarseness. (2) turn the neck and shrug the shoulders, look up with difficulty, and bend the neck. ③ Symptoms of respiratory muscle paralysis: breath holding, chest tightness, suffocation and severe cyanosis. The chest appearance showed that the respiratory muscles and auxiliary respiratory muscles trembled, the rate and frequency of respiratory nodules were disordered, the respiratory sounds of both lungs gradually disappeared, and finally peripheral respiratory failure appeared. Early patients were conscious, restless, nervous and afraid, showing a strong desire for survival, and soon appeared hypoxemia, causing organ failure and being in a coma.

For patients with severe organophosphorus poisoning, it is still necessary to closely observe the muscle strength and breathing situation after ACC disappears, and actively prepare for rescuing respiratory muscle paralysis. Once IMS-induced respiratory failure occurs, the key to treatment is to establish respiratory tract quickly and effectively and carry out mechanical ventilation treatment. The rejuvenation agent can directly fight respiratory muscle paralysis, and a sudden dose of chlorpyrifos can be given. After 24 hours,1g4 ~ 6h im× 2 ~ 3 days is a course of treatment. For patients with oral poisoning, it should be maintained for 2~3 days after offline.

rebound

It accounts for 7%~8% of the mortality, which may be related to toxic myocardial damage.

Reasons for rebound:

1. Poisons continue to be absorbed: ① gastric lavage is not complete; (2) Some organophosphorus pesticides (such as dimethoate and parathion) enhance their toxicity by tens to hundreds of times through liver oxidation, and are reabsorbed through intestinal-hepatic circulation; ③ Organic phosphorus stored in fat bank is continuously released into the blood.

2. Increase the accumulation of 2. Ach: ① delayed rescue opportunity, phosphorylated cholinesterase has aged; ② The oxime regenerant currently used has poor curative effect on some poisons (such as dimethoate);

3. Ignoring the principle of treating both the symptoms and root causes: not paying attention to the combined application of atropine and regenerant, and stopping using regenerant prematurely.

Rebound diagnosis basis:

1. Blood pressure changes suddenly, rises suddenly or drops suddenly;

2. Salivation, hyperhidrosis and lung moist rales reappear;

3. The dilated pupils contract again.

4. The complexion turns from red to white, even cyanosis.

5. mental disorder is aggravated;

6. Blood Che activity decreased again;

Prevention and treatment of rebound:

1. For poisons with long toxicity such as omethoate, the dosage should be reduced slowly for 7 ~ 10 days; Patients with severe AOPP should be strictly observed 1 ~ 2 days after ACC disappears. If it is dimethoate or malathion, it should be observed for 3 ~ 5 days.

2. Rapidly rebuild atropinization, and the dosage of atropine is increased several times than before rebound to prevent more Ach from accumulating in the body, but atropine poisoning should be prevented.

3. take oxygen. Continuous high-concentration oxygen inhalation, mechanical ventilation for oxygen when necessary.

4. Dehydration and hormone therapy for brain edema to enhance the curative effect.

5. Glucocorticoid can reduce stress, improve myocardial hypoxia tolerance, promote myocardial metabolism and improve myocardial damage caused by poisoning.

6. Correct water-electrolyte disorder and acid-base imbalance.

7. If there is arrhythmia, toxic myocarditis, heart failure should be dealt with accordingly.

Atropine dependence phenomenon

The rehabilitation process of a few patients with organophosphorus pesticide poisoning (repeated use of atropine for more than 10 days) is different from that of ordinary poisoners. After a long period of atropine treatment, once atropine is suddenly reduced or stopped, symptoms such as nausea, vomiting and hypotension reappear. After re-using atropine or switching to 654-2 treatment, the symptoms disappeared, and it took a long time to maintain the drug, and then stopped the drug slowly. Such patients have atropine dependence during treatment.

The main difference between atropine dependence and poisoned rebound phenomenon is that atropine dependence occurs in the recovery period, and then atropine is reduced or stopped, with mild symptoms, normal or close to normal blood ChE, and a small amount of atropine is reused (the original dose is slightly smaller than the original dose). Poisoning rebound usually occurs in the early stage of poisoning, which can be caused by many factors, such as atropine reduction, continuous absorption of poisons, enhanced toxicity of toxic metabolites and serious organ damage. The symptoms are serious, and the blood ChE is lower than normal, so it is often necessary to take large doses of atropine and re-atropinize it.

In short, the first aid of organophosphorus pesticide poisoning advocates early removal of poisons, application of effective regenerants and antagonists, active prevention and treatment of respiratory failure, maintenance of vital signs, comprehensive prevention and treatment of multiple organ failure, close observation of patients, timely detection of precursors, so that more patients with organophosphorus pesticide poisoning can be actively treated, saving lives and restoring health.

There are many kinds of organophosphorus pesticides, which can be divided into three categories according to their toxicity: high toxicity, poisoning and low toxicity. The oral LD50 (mg/kg) of common organophosphorus pesticides in China is as follows: parathion (1605) is 3.5 ~15 mg; The absorption of phosphorus in vivo (1059) is 4 ~10 mg; Phorate (39 1 1) was 2. 1 ~ 3.7 mg; 4 mg of phosphorus mixed with b; Thioprop is 5 mg; Amine phosphate 7.5mg (above is highly toxic). DDVP 50 ~ 1 10 mg; Methyl parathion (methyl 1065) is14 ~ 42mg; The phosphorus absorption capacity of methyl (methyl1059,4044) is 80 ~ 130mg (the above is toxic). Trichlorfon is 450-500mg; 230-450mg of dimethoate; Malathion (4049, Marathon)1800 mg; ; Nalaide 430mg；; The dosage of fenitrothion is 250mg (above belongs to low toxicity category). High toxic organophosphorus pesticides can be poisoned by a small amount of contact, and low toxic pesticides can also be harmful if they enter the body in large quantities. The toxic dose and lethal dose of human body to organophosphorus vary greatly. Inhale from the digestive tract or absorb through the skin into the respiratory tract at a general concentration, with severe symptoms and acute onset; However, if you inhale a large amount or high concentration of organophosphorus pesticides, you can get sick within 5 minutes and die quickly.

Treatment measures

1. Remove the poison to prevent further absorption.

First of all, keep sick children away from the poisoning scene, take off clothes, quilts, shoes and socks contaminated by poisons as soon as possible, and thoroughly clean their skin with soapy water, alkaline water or 2% ~ 5% sodium bicarbonate solution (when trichlorfon is poisoned, clean it with clear water or 1% salt solution), especially pay attention to poisons attached to hair and nails. If the eyes are polluted, rinse with 1% sodium bicarbonate solution or normal saline, and then drip 1% atropine solution. If the patient is conscious, induce vomiting immediately, and choose 1% sodium bicarbonate solution or 1: 5000 potassium permanganate solution for gastric lavage as appropriate. At the rescue site, if there is no such liquid, you can also temporarily lavage your stomach with light salt water (about 0.85%) or clear water. When trichlorfon is poisoned, it is forbidden to use alkaline solution such as sodium bicarbonate for gastric lavage, because it can make dichlorvos 10 times its toxicity. Thiophosphates, such as parathion, phosphorus absorbed in the body, phorate, malathion, dimethoate, cartap, isophos, fenthion and rice blast, should not be used for gastric lavage with oxidants such as potassium permanganate solution, because the toxicity of thiophosphate will increase after oxidation. After gastric lavage, sodium sulfate is used to promote diarrhea, and oily laxatives are prohibited. Long-term eaters can be used for high intestinal lavage. The application of activated carbon hemoperfusion can remove organophosphorus poisons from blood and has a good effect on rescuing children with severe organophosphorus poisoning.

2. Actively take symptomatic treatment.

Keep the sick child's respiratory tract unobstructed, eliminate oral secretions, and give oxygen when necessary. When spasm occurs, acupuncture or short-acting sedatives should be used immediately. Morphine and other respiratory inhibitors, as well as theophylline, aminophylline, succinylcholine, reserpine, neostigmine, physostigmine and phenothiazine sedatives should be avoided. In addition to injecting respiratory stimulants and artificial respiration, patients with respiratory failure are given positive pressure oxygen through tracheal intubation when necessary. Timely treatment of brain edema and pulmonary edema, pay attention to protect liver and kidney function. Extracorporeal cardiac compression was performed at the speed of cardiac arrest, intravenous injection of 1∶ 10000 epinephrine 0. 1ml/kg, and atropine could be injected intracardially if necessary. In order to replenish the lost water and electrolyte, appropriate infusion should be given at the same time, but attention should be paid to the amount, speed and composition of infusion. When there are signs of pulmonary edema and brain edema, infusion should be more cautious. Severe cases were treated with adrenocortical hormone. In the process of rescue, we should also pay attention to nutrition, warmth, urination, prevention of infection and other issues, and if necessary, we should import appropriate amount of fresh blood or adopt exchange transfusion therapy.

3. Application of detoxification drugs

At the same time of detoxification and symptomatic treatment, detoxification drugs must be applied. There are two kinds of special detoxification drugs commonly used:

① Cholinergic nerve inhibitor

Such as atropine and anisodamine, can antagonize the muscarinic effect of acetylcholine and improve the tolerance of the body to acetylcholine, so it can relieve smooth muscle spasm, reduce gland secretion, promote pupil dilation, prevent blood pressure from rising and arrhythmia, and also have significant curative effect on central nervous system symptoms, which is a powerful antagonist of respiratory center inhibition; But it has no effect on nicotine-like effect and no effect on reviving cholinesterase, so it can't prevent muscle tremor, spasm and paralysis. The application of atropine in rescuing organophosphorus poisoning must emphasize early, sufficient and repeated administration, and patients with moderate and severe poisoning must be given intravenous administration. In the process of using atropine, we should pay attention to reaching the "dose" index, that is, when the sick child's pupils are dilated and no longer shrinking, his face turns red, his skin is dry, his heart rate is accelerated, his pulmonary edema is improved, and his consciousness begins to recover, he can gradually reduce the dose of atropine and extend the injection interval, and stop taking the medicine when the main symptoms disappear and his condition basically recovers. You still need to continue to observe after stopping the drug. If there are signs of recurrence, the medication should be resumed immediately. The pharmacological action of 654-2 is basically the same as that of atropine, with less toxicity, greater distance between therapeutic dose and toxic dose, and its "dose" index is also the same as that of atropine. Mild organophosphorus poisoning can be cured by atropine or 654-2 alone. Moderate and severe poisoning must be treated with chlorpyrifos or pralidoxime.

② cholinesterase reactivating agent

For example, phosphoryl phosphate (PAM), phosphoryl chloride (PAM-Cl) and bisphosphonate (PMO4 _ 4) can seize the phosphoryl group of organophosphorus binding cholinesterase, restore the ability of cholinesterase to decompose acetylcholine, and can directly bind organophosphorus entering the body, so they have obvious effects on relieving nicotine-like effects and promoting patients' wakefulness, but the effect on muscarinic symptoms is poor. Although they also have atropine effects to some extent, they are not as fast as atropine in controlling some key symptoms such as central respiratory depression, pulmonary edema and bradycardia. Frixim and chlorophosphate are less toxic, so we can choose one of them, and neither of them can be mixed with alkaline drugs. It has obvious curative effect on acute poisoning such as phosphorus, parathion, phorate, ethion and Su Hua 203, but it has poor curative effect on dichlorvos and trichlorfon. Severe poisoning should be combined with atropine. The efficacy of parathion and dimethoate is questionable. Parathion and diazinon are ineffective. Therefore, atropine should be the main treatment for organophosphorus pesticide poisoning in the later stage, and bisphosphonates can also be used. Phosphorus has a strong function of reviving cholinesterase, easily penetrates the blood-brain barrier and has atropine-like effect, so it has an effect on nicotine-like, muscarinic and central nervous system symptoms caused by organophosphorus pesticide poisoning. For dichlorvos and trichlorfon poisoning, the effect is better than phosphate. This product can be injected subcutaneously, intramuscularly or intravenously, but it has many side effects, such as premature ventricular contraction, conduction block, ventricular fibrillation, and occasionally toxic hepatitis and hysteria.

Dosage and usage of specific detoxification drugs: adequate use in the early stage, and appropriate increase or decrease according to the change of illness. The activity of erythrocyte cholinesterase should be monitored during treatment, and when it is lower than 30%, it must be combined with medication. The following dosage and usage are for reference:

(1) Mild poisoning

Atropine 0.02 ~ 0.03 mg/kg each time, orally or intramuscularly; Or chlorpyrifos 65438 0.5 mg/kg each time, intramuscular injection; Or every time pralidoxime 10 ~ 15 mg/kg, add 20ml of 5% ~ 25% glucose solution and inject it slowly in the middle vein. If necessary, atropine or one of the latter two can be repeated 1 time within 2 ~ 4 hours until the symptoms disappear. Generally 1 ~ 2 times is enough.

(2) Moderate poisoning

Atropine should be used in combination with cholinesterase reactivation agent, the dosage of atropine is 0.03 ~ 0.05 mg/kg each time, and it should be injected intramuscularly or intravenously/kloc-0 every 30 ~ 60 minutes. The dose of cyclophosphamide or phosphorolysis is 15 ~ 30 mg/kg, and it is injected intravenously. It can be repeated every 2 ~ 4 hours 1 time (the dose is halved). After the symptoms get better, gradually reduce the dose and extend the interval of medication. Cholinesterase rejuvenation agent has no effect on azinphos-methyl and diazinon, but atropine is the main treatment, with the dosage of 0.03 ~ 0.05 mg/kg each time, 15 ~ 30 minutes, 1 time, and gradually decreases after the condition improves, and the interval is prolonged.

(3) Severe poisoning

Atropine 0.05 ~ 0.65438 0 mg/kg each time, intravenous injection. Especially for critically ill patients, atropine should be suddenly used in large quantities to save lives. Intravenous injection of 0. 1 ~ 0.2 mg/kg every10 ~/5 minutes is allowed for the first time, and then it is changed to 0.05 ~ 0. 1 mg/kg every time (according to the first half dose), and chlorpropropyl is injected intravenously at the same time.50000.000000006005 If the symptoms do not improve, it can be repeated 1 time after half an hour, and the dose is halved or 20 mg/kg; From now on, depending on the condition, 1 time every 2 ~ 4 hours or intravenous drip, 0.4g per hour. If the condition improves, gradually reduce the dosage of atropine and cholinesterase reactivation agent, extend the interval of medication, and consider stopping injection as appropriate (at least 6 hours after the condition improves). Observe for at least 24 hours after the symptoms basically disappear. In addition, 654-2 (instead of atropine) and bisphosphonate can also be used as appropriate for organophosphorus poisoning. Dosage and usage of 654-2: mild poisoning 0.3 ~ 0.5 mg/kg, intramuscular injection or intravenous injection; Moderate poisoning every time 1 ~ 2 mg/kg, intravenous injection; Severe poisoning 2 ~ 4 mg/kg each time, intravenous injection. If necessary, it can be administered repeatedly every 10 ~ 30 minutes. Dosage and usage of bisphosphonate: 5 ~10 mg/kg for mild and moderate poisoning; Severe poisoning every time 10 ~ 20 mg/kg. According to the illness,/kloc-0 every 30 minutes to 3 hours.

The cholinergic nerve inhibitor and cholinesterase reactivation agent mentioned above can only be used one at a time, not both at the same time.

Recently, it has been reported that adult organophosphorus poisoning can be treated with phenylphosphorus (composed of phentropine, carbamazepine and bisphosphonate). Developed by the Academy of Military Medical Sciences, it has the advantages of high curative effect, quick action and convenient use. However, we should pay close attention to the changes of the disease, adjust the medication methods accordingly, and appropriately increase related drugs.

It is also reported that hemoperfusion with activated carbon is a safe and effective treatment for severe organophosphorus poisoning in children.

etiology

Organophosphorus pesticides can be poisoned by ingestion, inhalation or skin absorption. The causes of children's poisoning are: eating food contaminated by organophosphorus pesticides by mistake (including fruits, vegetables, dairy products, grain, poisoned livestock and aquatic products, etc.). ); Misuse of toys or pesticide containers contaminated by pesticides; Improper use of organophosphorus pesticides to kill mosquitoes, flies, lice, fleas, bedbugs and cockroaches, and to treat skin diseases and repel insects. After using pesticides, the mother didn't wash her hands and change clothes carefully, and fed her baby. Use plastic bags filled with organophosphorus pesticides as urine pads, or use farmland sand sprayed with organophosphorus pesticides to fill "soil pants" instead of urine pads; Children playing near fields sprayed with organophosphorus pesticides may also lead to inhalation poisoning.

pathogenesis

The conduction of cholinergic nerves (including the preganglionic fibers of motor nerve, sympathetic nerve and parasympathetic nerve, parasympathetic nerve and some postganglionic fibers of sympathetic nerve) depends on acetylcholine released from its terminal at the junction with cells to dominate the activities of effector organs; Some parts of the central nervous system, such as the sensory motor area of the cerebral cortex, especially the transmission of impulses between nerve cells such as pyramidal cells, caudate nucleus and thalamus in the deep cortex, are also related to acetylcholine. Cholinergic neurotransmission must be combined with cholinergic receptors to have an effect. Cholinergic receptors are divided into muscarinic type and nicotine type; The former is distributed in the effector organs dominated by fibers behind cholinergic ganglia such as myocardium, smooth muscle and glands, while the latter is distributed in the motor endplate of autonomic ganglia and skeletal muscle. Under normal circumstances, the released acetylcholine is quickly decomposed by acetylcholinesterase existing in tissues and loses its function after completing its physiological function.

After organophosphorus enters the human body, its phosphoryl group closely combines with the active part of the enzyme to form phosphorylcholinesterase, which loses the ability to decompose acetylcholine, makes acetylcholine accumulate in the body, inhibits the only acetylcholinesterase activity, makes the central nervous system and cholinergic nerves excessively excited, and finally turns into inhibition and failure, showing a series of symptoms and signs:

① When cholinergic muscarinic receptors of some parasympathetic nerves and some sympathetic postganglionic fibers are excited, muscarinic symptoms such as smooth muscle contraction, increased gland secretion, pupil contraction, nausea, vomiting, abdominal pain and diarrhea appear.

② When the cholinergic nicotinic receptor at the junction of motor nerve and muscle is excited, muscle fiber tremors or convulsions (spasms) occur; Severe poisoning or late poisoning, turning into nicotine-like symptoms such as muscle weakness or muscle paralysis.

③ The excitability of cholinergic receptors in the intercellular contact process of central nervous system leads to dysfunction. At first, there were headache, dizziness, irritability, delirium and other exciting symptoms, and in severe cases, there were speech disorders, coma and respiratory center paralysis.

④ In the circulatory system, there may be muscarinic symptoms such as slow heart rate and decreased blood pressure, and nicotine-like symptoms such as increased blood pressure and increased heart rate.

clinical picture

The time and severity of organophosphorus pesticide poisoning symptoms are closely related to entry route, pesticide properties, intake and absorption, and human health. General acute poisoning generally occurs within 12 hours. If high-concentration or highly toxic organophosphorus pesticides are inhaled or taken orally, symptoms or even death can occur within a few minutes to ten minutes. The onset time of skin contact poisoning is slow, but serious symptoms may appear after absorption. Early or mild symptoms of this pesticide poisoning may include dizziness, headache, nausea, vomiting, salivation, sweating, blurred vision and fatigue. In addition to the above symptoms, severe patients also have pupil contraction, muscle tremor, tears, increased bronchial secretions, dry and wet rales and wheezing in the lungs, abdominal pain and diarrhea, confusion, stumbling, bradycardia, fever and chills. In severe cases, tachycardia, atrioventricular block, atrial fibrillation and other arrhythmia often occur. , blood pressure rise or fall, cyanosis, dyspnea, nose and mouth blistering and even blood (pulmonary edema), convulsion, coma, incontinence or urinary retention, quadriplegia, loss of reflex, etc. , and may die of respiratory paralysis or circulatory failure. Respiratory and eye symptoms appear earlier in patients with inhalation poisoning, and gastrointestinal symptoms often appear first in patients with oral poisoning, while skin contact poisoning is characterized by local sweating and contraction of adjacent muscle fibers. When dichlorvos come into contact with the skin, they often appear erythema-like changes and gradually become blisters, and children have itching and burning sensation.

The clinical manifestations of organophosphorus poisoning in children are sometimes atypical: some children mainly show nervous system symptoms such as headache, vomiting, hallucination, convulsion and coma; There are also digestive symptoms such as vomiting, abdominal pain and dehydration. Other poisoned children mainly show symptoms of circulatory system, such as slow or accelerated heart rate, decreased blood pressure and shock; Some of them mainly show respiratory symptoms, such as fever, asthma, excessive phlegm, dry and wet rales and wheezing in the lungs. Children who are occasionally poisoned mainly show single symptoms or signs, such as high fever, abdominal pain, convulsions, limb paralysis, unstable walking and so on. Therefore, it is sometimes misdiagnosed as encephalitis, meningitis, acute gastroenteritis, intestinal ascariasis, toxic dysentery, pneumonia in children or newborns, nephritis, epilepsy, acute infectious polyradiculitis, drug (such as barbiturates, opioids, chlorpromazine, chloral hydrate) poisoning, etc.

For suspicious cases, it is necessary to inquire about the contact history with organophosphorus pesticides in detail, and fully understand the food (breastfeeding), accommodation, clothing, contact objects and playgrounds of the children; Carefully check whether there are any specific signs of organophosphorus pesticide poisoning in children, such as pupillary contraction (it may not appear in the early stage of poisoning, dilated pupils in the late stage, occasional pupillary contraction in poisoned children, or transient pupillary dilation before pupillary contraction), muscle tremor, increased secretion such as sweating, salivation, tears, lung rales (acute pulmonary edema), erythema or blisters on the skin, etc. Some organophosphorus pesticides have a special smell or fragrance of garlic.

According to the laboratory conditions, the following tests are carried out appropriately:

① Examination of the patient's vomit, stomach contents and respiratory secretions for the first time during gastric lavage can prove the existence of organophosphorus compounds.

② The determination of organophosphorus decomposition products in urine can be used as an indicator of toxic exposure, some of which are helpful for early diagnosis.

③ Determination of blood cholinesterase activity, if cholinesterase activity drops below 80% of normal people, it is of diagnostic significance, and the degree of poisoning can be estimated according to this value as a reference for medication. The blood cholinesterase activity in mild patients decreased to 70% ~ 50% of normal people, 50% ~ 30% in moderate patients and below 30% in severe patients. In rural areas and rescue sites, the approximate results of cholinesterase activity can be determined within 20 minutes by using the simple and applicable bromothymol blue paper colorimetry.

prevent

Relevant departments should improve the management system of organophosphorus pesticides and explain their usage, dosage and toxicity to the masses; The utensils and packages contaminated by drugs must be thoroughly cleaned before they can be used for other purposes, and it is best to throw them away; Spraying personnel must strictly implement the precautions for drug use in accordance with regulations; Lactating women should try not to take part in the work of contacting organophosphorus pesticides; Those who have touched it should take off their clothes and hats before breastfeeding, do a good job of cleaning, and then touch the baby. Fruits sprayed with organophosphorus pesticides can only be eaten after a specified time; Fasting poultry, livestock and aquatic products poisoned by organophosphorus pesticides; If there are small baby households indoors, children and their utensils should be removed when dichlorvos is used to kill indoor mosquitoes and flies. Never smear organophosphorus pesticides on children's scalp, clothes and bedding to eliminate lice and fleas; Do not fill "soil-wrapped pants" and urine pads with field soil sprayed with organophosphorus pesticides; Educate children not to play in fields where pesticides are being sprayed or about to be sprayed; It is necessary to explain the early poisoning symptoms of organophosphorus pesticides to the masses so as to find patients in time and avoid delaying treatment.