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Production and use of organophosphorus pesticides.
Route of invasion
Can be absorbed through the skin, respiratory tract, digestive tract.
Introduction to Toxicology
The toxicity of each variety can be different, most of them are highly toxic and highly toxic, and a few are low-toxic. Some varieties have a synergistic effect when mixed, such as malathion and trichlorfon, trichlorfon and azinphos. Some varieties can be converted and poisoned. For example, the toxicity of 1605 is increased after oxidation, and trichlorfon is more toxic to dichlorvos in an alkaline solution.
Organophosphorus pesticides (organophosphate pesticides) form phosphorylcholinesterase with cholinesterase in vivo, and cholinesterase activity is inhibited, so that the enzyme can not decompose acetylcholine, resulting in excessive accumulation of acetylcholine in tissues. Excessive stimulation of cholinergic nerves, causing muscarinic, nicotinic and central nervous system symptoms. Phosphorylated cholinease esterase is generally "aged" after about 48 hours and is not easily replenished.
Some ester hydrocarbyl and aromatic hydrocarbyl phosphate compounds have delayed neurotoxic effects, because organophosphorus pesticides inhibit neurotransmitter target esterase (neurotoxic esterase) and cause "aging", which causes delayed onset Neuropathy. This toxic effect is not related to cholinesterase activity.
The organophosphorus pesticide of the sustained-release microcapsule dosage form can have a longer action time.
Clinical manifestation
Acute poisoning Latency: It varies according to the pesticide variety and concentration, the absorption route and the body condition. Generally, the skin is absorbed for 2 to 6 hours, and the respiratory tract is inhaled or taken orally for 10 minutes to 2 hours.
Symptoms of the disease: The symptoms of various ways of absorption and poisoning are basically similar, but the initial symptoms may vary. If the skin is mainly absorbed by the skin, sweating, hooliganism, irritability, etc.; nausea, vomiting, abdominal pain and other symptoms often occur after oral poisoning; symptoms such as blurred vision and difficulty in breathing when the respiratory tract inhalation causes poisoning may occur faster.
Symptoms caused by the site of toxicity:
a. muscarinic symptoms: loss of appetite, nausea, vomiting, abdominal pain, diarrhea, salivation, excessive sweating, blurred vision, dilated pupils, increased respiratory secretions, bronchospasm, difficulty breathing, pulmonary edema.
b. Nicotine-like symptoms: fasciculation, muscle weakness, tendon, respiratory muscle paralysis.
c. Central nervous system symptoms: headache, dizziness, burnout, fatigue, insomnia or lethargy, irritability, confusion, unclear language, convulsions, convulsions, coma, respiratory center inhibition caused by respiratory arrest.
d. Autonomic nervous system symptoms: Increased blood pressure, increased heart rate, slow heart rate, arrhythmia when the disease progresses.
Poisoning grade a. Mild poisoning: There are symptoms such as dizziness, headache, nausea, vomiting, excessive sweating, chest tightness, blurred vision, weakness, etc. The pupil may shrink. Whole blood cholinesterase activity is generally 50% to 70%.
b. Moderate poisoning: The above symptoms are aggravated, and there are still fasciculation, dilated pupils, mild dyspnea, salivation, abdominal pain, diarrhea, gait, confusion or confusion. Whole blood cholinesterase activity is generally between 30% and 50%.
d. Severe poisoning: In addition to the above symptoms, there are pulmonary edema, coma, respiratory paralysis or cerebral edema. Whole blood cholinesterase activity is generally below 30%.
Delayed sudden death: Sudden death can occur during the recovery period of severe poisoning such as dimethoate and trichlorfon. It often occurs 3 to 15 days after poisoning. More common in oral poisoning.
Intermediate syndrome: 2 to 4 days after poisoning of fenthion, dimethoate, monocrotophos, dichlorvos, methamidophos, etc., muscles and respiratory muscles that are dominated by the proximal muscles of the limbs, the flexor and the cranial nerves Inability to focus on clinical manifestations, including head lift, shoulder abduction, hip and blink difficulties, limited eye movements, diplopia, limited facial muscle movement, hoarseness, difficulty swallowing and chewing, due to respiratory muscle paralysis death.
Delayed peripheral neuropathy: methamidophos, amphetamine, propofol, parathion, malathion, ipilin, dimethoate, dichlorvos, trichlorfon, flurazepam and other poisoning conditions 4 to 45 after recovery There are limb-feeling-sports-type polyneuropathy. Not related to cholinesterase activity.
Pesticide splashing into the eye can cause the pupil to shrink, not necessarily systemic poisoning.
First aid treatment
Excessive contact immediately leaves the scene and is fresh to the air. Rinse immediately with plenty of water or soapy water when skin is contaminated. Rinse with water when the eye is contaminated. After oral administration, the gastric tube is indwelled after gastric lavage, so that the pesticide can be washed again when the pesticide is refluxed. For example, after oral administration of dimethoate, the gastric tube should be left for 2 to 3 days, and cleaned regularly. If you can't use the stomach tube to wash the stomach, you can use the stomach to make the tube for gastric lavage.
Mild muscarinic, nicotinic or central nervous system symptoms, normal blood cholinesterase activity; no obvious symptoms, whole blood cholinesterase activity of 70% or less; or exposure, It should be observed for 24 to 72 hours and treated in time.
Special antidote a. Atropine: It can remove or reduce muscarinic and central nervous system symptoms and improve respiratory central inhibition.
Principle of medication: Early, appropriate, repeated administration, quickly achieve "atropine" (pupil enlargement, facial flushing, skin without sweat, dry mouth, heart rate acceleration).
Usage: Mild poisoning, 1~2mg each time, subcutaneous or intramuscular injection, once every 4 to 6 hours, after "atropine", changed to oral 0.3 ~ 0.6mg, 2 to 3 times a day. Moderate poisoning, the first 2 ~ 5mg, intravenous injection. Severe poisoning for the first time 10 ~ 20mg, intravenous injection, such as muscarinic symptoms have not improved or did not reach "atropine", then 5 to 10 minutes after repeated half or full amount; can also be used to maintain the dose of intravenous drip, adjust the dose at any time, up to "Atropine" until the muscarinic symptoms improved significantly, use the maintenance amount. If the symptoms and signs basically subside, you can reduce the amount of observation for 12 hours. If the condition is not repeated, you can stop the medicine.
Mild poisoning can be applied to atropine alone, and atropine and cholinesterase regenerative agents can be combined with moderate and severe poisoning. The combined use of drugs has a synergistic effect and the dose should be appropriately reduced.
A small amount of pesticide splashed into the eye causes the pupil to shrink, no symptoms of systemic poisoning, do not have to treat with atropine for systemic treatment, apply 0.5% to 1% atropine eye drops.
Precautions:
(1) Prevent atropine poisoning caused by systemic overdose (pupil enlargement, tachycardia, urine retention, elevated body temperature, paralysis, convulsions, coma, respiratory paralysis, etc.). In the event of atropine poisoning, the drug should be discontinued immediately. In severe cases, the effects of atropine can be antagonized by pilocarpine or neostigmine.
(2) Long-term high-dose application of atropine can cause atropine dependence, which is manifested by the phenomenon of "anti-jumping" of organophosphorus poisoning, such as pale, dizziness, sweating, abdominal pain, vomiting, etc. when atropine is reduced or stopped. Once this happens, it should be gradually reduced to discontinuation.
Atropine 1ml containing 0.5mg of the dosage form is a hypotonic solution, which may cause intravascular hemolysis when used in large doses, which requires attention. The pharmacological effects of 654 (anisodamine) and 703 (anisodine) are similar to those of atropine, and have certain curative effects on organophosphate poisoning.
b. Cholinesterase Recombinant: Commonly used steroidal complexing agents are solution of phosphatidylcholine and chlorhexidine. The efficacy of regenerative agents for different varieties of poisoning is not the same, such as 1605, 1059, Suhua 203, 3911, etc. The effect of poisoning is obvious; the effect on trichlorfon and dichlorvos poisoning is slightly worse; the effect on dimethoate and 4049 poisoning is not obvious; it has adverse effects on poisoning of diazinon and azinphos, but may have certain impurities on other organic phosphates. Efficacy. Pesticide poisoning, which is not ideal for the efficacy of the regenerative agent, is mainly treated with atropine. However, there is currently disagreement about the different effects of the various agents on the treatment of various varieties.
The anaerobic agent should be applied as early as possible. Phosphoryl cholinesterase is "aged" 48 hours after poisoning and is not easy to reactivate. Usage: Mild poisoning can be used without regenerative agent, or mild to moderate poisoning. Use chlorophosphorus to fix 0.25~0.5g, intramuscular injection, or phosphate solution 0.5g intravenous injection, repeat if necessary after 2 hours. Severe poisoning to chlorophosphonate 0.75 ~ 1g or phosphate solution 1 ~ 1.5g dissolved in 10% glucose solution slowly intravenously, after half an hour, if the condition does not improve significantly, can be repeated once, then changed to intravenous drip, the speed is generally hourly Not more than 0.5g. After the nicotinic symptoms improved, the drug was gradually discontinued. General application 1 to 2 days.
If the medication is too fast, it may cause respiratory depression. It should be stopped immediately, and artificial respiration or tracheal intubation should be used to pressurize oxygen. Spontaneous breathing can be resumed in a short time.
c. Compound injection solution containing anticholinergic agent and regenerative agent: It works fast and has a long action time. Because of the variety of recipes, their usage is different. Intramuscular injection of compound agent consisting of benazexin (anticholinergic) and chlorhexidine, mild poisoning 1/2 to 1; moderate poisoning 1 to 2, plus chlorhexidine 0.5g; severe poisoning 2 to 3 Support, add chlorophosphorus to determine 0.75 ~ 1.0g. Half an amount can be repeated 1 hour after administration. The symptoms of poisoning basically subsided, and the whole blood cholinesterase activity was more than 60%. HI-6 compound: Contains HI-6 (amide phosphate, cholinesterase regenerative agent), atropine, stomach rehabilitation, diazepam, etc., 2ml each. Mild poisoning 1/2 to 1 branch, moderate poisoning 2 to 3, severe poisoning 3 to 5, all intramuscular injection. Oral poisoning should be properly added, supplemented with atropine if necessary.
Symptomatic, supportive treatment.
Prevention of "rebound" phenomenon and sudden onset of sudden death: oral administration of gastric lavage early; appropriate application of atropine, do not stop prematurely; avoid premature activity during recovery; continue to observe after 2 to 3 days after symptoms disappear, to prevent repeated illness . ECG monitoring during the recovery period of severe poisoning, timely treatment of arrhythmia, to prevent the occurrence of torsion ventricular tachycardia leading to death.
Morphine drugs are hanged.
Occupational diagnostic criteria for acute organophosphorus pesticide poisoning
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