Organophosphorus pesticide poisoning

Introduction to organophosphorus pesticide poisoning There are many kinds of organophosphorus pesticides (organophosphoruspesticide). According to their toxicity, they are classified into three categories: high toxicity, poisoning and low toxicity. The oral lethal dose (mg/kg) of rats with organophosphorus pesticides in China is as follows: parathion (1605) is 3.5 ~ 15mg; internal phosphorus (1059) is 4 ~ 10mg; phorate (3911) is 2.1 ~ 3.7mg; ethion phosphorus is 4mg; thiotep is 5mg; phosphorus amine is 7.5mg (above) Is a high-toxic class). Dichlorvos is 50-110mg; methyl parathion (methyl 1065) is 14-42mg; methyl endogenous phosphorus (methyl 1059, 4044) is 80-130mg (above is poisoning), trichlorfon is 450~ 500mg; dimethoate is 230-450mg; malathion (4049, marathon) is 1800mg; dibromophosphorus is 430mg; and killing pine (killing thiophene) is 250mg (above is low-toxic). High-toxic organophosphorus pesticides can be poisoned by a small amount of exposure, and a large amount of low-toxicity can also cause harm. The amount of organic phosphorus poisoning and lethality varies greatly from the digestive tract to the general concentration of respiratory inhalation or skin absorption. The symptoms are acute and acute; however, if a large amount or concentration of organophosphorus pesticide is inhaled, it can be 5 Inoculation within minutes, quickly killing. basic knowledge The proportion of illness: 0.025% Susceptible people: no special people Mode of infection: non-infectious Complications: pulmonary edema, coma

Causes of organophosphorus pesticide poisoning

Organophosphorus pesticides can be poisoned by ingestion, inhalation or absorption through the skin. The causes of poisoning in children are: eating food contaminated with organophosphorus pesticides (including fruits, vegetables, dairy products, food and poisoned livestock, water) Products, etc.; misuse of toys or pesticide containers contaminated with pesticides; improper use of organophosphorus pesticides to kill mosquitoes, flies, cockroaches, cockroaches, bedbugs, cockroaches and treat skin diseases and deworming, mothers did not wash their hands seriously after using pesticides And change clothes to breastfeed the baby; use a plastic bag packed with organophosphorus pesticides to make a urine pad, or fill the "green bag" with a pad of sand with organic phosphorus pesticides instead of a pad; children can also be sprayed Inhalation poisoning occurs when playing near the field of organophosphorus pesticides.

The conduction of cholinergic nerves (including motor nerves, sympathetic, parasympathetic preganglionic fibers, parasympathetic nerves, and partially sympathetic postganglionic fibers) from the human body, relying on the acetylcholine released at the junction with the cells. Control the activity of the effector; certain parts of the central nervous system, such as the cerebral cortex sensory motor area, especially the pyramidal cells in the deep cortex, the caudate nucleus, the thalamus and other nerve cells, the transmission of impulses, also the involvement of acetylcholine, cholinergic neurotransmission It must be combined with a cholinergic receptor to produce an effect. The cholinergic receptor is classified into a muscarinic type and a nicotinic type; the former is distributed in the myocardium, smooth muscle, gland and other effector organs innervated by the fibers after the cholinergic ganglia. The latter is distributed in the motor endplates of the autonomic ganglia and skeletal muscle. Under normal circumstances, the released acetylcholine is rapidly decomposed by the acetylcholinesterase present in the tissue to complete its physiological function.

When organic phosphorus enters the human body, its phosphoryl group is tightly bound to the active part of the enzyme to form phosphoryl cholinesterase and lose the ability to decompose acetylcholine, so that acetylcholine accumulates in vivo and inhibits the activity of only acetylcholinesterase. Excessive excitation of the central nervous system and cholinergic nerves, and finally into inhibition and failure, showing a series of symptoms and signs.

Organophosphorus pesticide poisoning prevention

Relevant departments should have a sound management system for organophosphorus pesticides and explain their usage, use and toxicity to the masses;

Appliances and packaging materials contaminated with drugs must be thoroughly cleaned before they can be used for other purposes.

Personnel spraying drugs must strictly follow the precautions for medication according to regulations; lactating women should not participate in the work of exposure to organophosphorus pesticides as much as possible;

Those who have contacted should change their clothes and hats before breastfeeding, do a good job of cleaning, and then contact with the baby. The fruits sprayed with organophosphorus pesticides must be eaten after a specified period of time; fasting the birds and animals poisoned by organophosphorus pesticides , aquatic products;

There are small infants living indoors. When using indoor dichlorvos to eliminate indoor mosquitoes and flies, children and their utensils must be removed. Organic phosphorus pesticides should never be applied to children's scalp, clothes, and bedding to eliminate cockroaches and cockroaches;

Do not fill "wooden pants" and urine pads with soil that has been sprayed with organophosphorus pesticides;

Educate children not to play in the fields that are spraying or spraying pesticides;

It is necessary to explain to the masses the early symptoms of organophosphorus pesticides in order to detect patients in time and avoid delays in treatment.

Organophosphorus pesticide poisoning complications Complications pulmonary edema coma

In severe cases, tachycardia, elevated blood pressure, pupil size such as needle tip, difficulty in breathing, pulmonary edema, incontinence, respiratory depression, unconsciousness or even deep coma, blood chz vitality reduced to less than 30% of normal.

Symptoms of organophosphorus pesticide poisoning Common symptoms Limb proximal muscles and muscles Muscle beating muscarinic symptoms Whole body tightness dyspnea Breathing gas for garlic smell Gastrointestinal symptoms Nausea convulsions Dizziness

After a large amount of ingestion or inhalation of concentrated poisons, the disease occurs within a short period of 3 minutes, usually within 30 minutes to 12 hours. According to different types of nerve damage, clinical manifestations can be divided into three categories:

1. The parasympathetic nerves and the cholinergic receptors in the sympathetic ganglia fibers distributed in the sweat glands stimulate the secretion of glands, showing increased sweat, runny and bronchial secretions. The contraction of the iris sphincter causes the pupil to shrink, and the gastrointestinal smooth muscle excitement causes nausea, vomiting, diarrhea, and abdominal pain. The cardiovascular system is inhibited and the heart rate is slow, and the blood pressure is lowered. This is similar to the symptoms of poisonous poisoning and is called muscarinic.

2, motor neuromuscular junction point cholinergic receptors excitatory, showing muscle fibrillation or convulsions, in the late stage, see muscle weakness or paralysis. The sympathetic preganglionic fibers and the sympathetic cholinergic receptors that innervate the adrenal medulla exhibit symptoms such as increased blood pressure, increased heart rate, and elevated body temperature, which are similar to the symptoms of nicotine poisoning and are called nicotinic effects.

3, central nervous system interstitial cholinergic receptor excitation, it produces central nervous system dysfunction symptoms, early dizziness, speech disorder, headache, unconsciousness and paroxysmal convulsions, etc., organophosphate poisoning can be caused by breathing The central paralysis is fatal.

Inspection of organophosphorus pesticide poisoning

The diagnosis is mainly based on the results of laboratory tests.

1. Determination of blood cholinesterase activity: acetylcholinesterase activity in normal poisoning is 50% to 70% of normal; moderate is 30% to 50%; and severe is <30%. The decrease of serum cholinesterase activity is parallel with the decrease of cholinesterase activity and the degree of poisoning of synapses; the recovery of serum cholinesterase activity is parallel with the degree of toxicosis, which can be used as a dynamic monitoring index of the disease.

2, gastric juice and suspected food poison analysis analysis can confirm the diagnosis.

Other auxiliary inspection

Choose according to needs: ECG examination: 1 sinus tachycardia, sinus bradycardia, pre-contraction, conduction block and atrioventricular fibrillation. 2Q-T intermittent extension and torsade ventricular tachycardia.

Diagnosis and identification of organophosphorus pesticide poisoning

Diagnosis :

Some cases are easily overlooked, especially those with early central nervous system depression, circulation, respiration and central nervous system failure, should know the relevant medical history and do related tests to eliminate the possibility of poisoning.

1. History: Determine the history of exposure to ingested or inhaled organophosphorus pesticides.

2, symptoms of poisoning: symptoms of poisoning, including sweating, runny nose, muscle fibrillation, dilated pupils and elevated blood pressure as the main symptoms. Skin contact with pesticides caused by poisoning is slightly slow onset, and the symptoms are atypical. The medical history should be carefully asked, and the skin should be thoroughly examined for erythema blister, and the clinical evolution should be closely observed to assist diagnosis.

3, vomiting or exhaled gas has a smell of garlic.

4. Laboratory examination: The blood cholinesterase activity was determined to be significantly lower than normal.

5. Determination of Organophosphorus Compounds Gastric contents, vomit or excretions washed out by gastric lavage were analyzed as organic phosphorus.

Differential diagnosis :

If the atypical case or medical history is unclear, it should be noted that other diseases, such as other food poisoning, poisonous poisoning and Japanese encephalitis, should be excluded. Blood cholinesterase activity can be identified.

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