Organophosphorus pesticide poisoning in children
Introduction
Introduction to Pediatric Organophosphorus Pesticide Poisoning Pediatric organophosphorus pesticide poisoning refers to a series of clinical and pathological processes caused by organophosphorus pesticides entering the human body to inhibit acetylcholinesterase (AChE). Most of the poisoning comes from eating foods containing organophosphorus pesticides. In some parts of the country, organophosphorus pesticides with long residual time are used. Children are poisoned by accidentally eating vegetables and fruits contaminated with excessive concentrations of organophosphorus pesticides. Water and other contaminated foods are poisoned. The latter is occasionally seen in the poisoning event. Organic phosphorus enters the human body to inhibit AChE, and on the other hand, it produces a series of clinical pathological processes of vagus nerve hyperactivity and muscle nicotinic action (N-like action); It is a process of inhibition of the central nervous system arylesterase, which is life-threatening in the event of circulatory, respiratory, and central nervous system damage. It is severely poisoned. The mortality rate varies according to the type, dose, duration and other factors of poisoning, and the disability rate is relatively high. basic knowledge The proportion of illness: 0.002% Susceptible people: children Mode of infection: non-infectious Complications: urinary retention, coma,
Cause
Causes of organophosphorus pesticide poisoning in children
Causes:
1. Classification of pesticides in China: Organophosphorus pesticides are commonly used pesticides in agriculture and have certain toxicity to human body. At present, there are dozens of pesticides produced in China, which are classified into three categories according to their toxicity: (1) Acute poisoning: Parathion (1605), endogenous phosphorus (1059), and thimet. (2) Highly toxic species: methyl parathion, dichlorphos, rogor (moderately toxic), dipterex (moderately toxic), etc. (3) Low toxicity: karbofos, trichlorfon, dimethoate.
2. Entering the human body: Organic phosphorus can enter the human body through the digestive tract, respiratory tract or skin. It also has secondary poisoning, which can be caused by individual, family or collective poisoning. (1) Entering the body from the digestive tract: eating food contaminated with pesticides; the mother does not wash her hands after spraying the pesticide, and the baby is breast-feeding after changing clothes, causing baby poisoning; suicide or poisoning. (2) absorption through the skin: use organic phosphorus insecticide to kill cockroaches, cockroaches, and contaminate the skin or mucous membrane when spraying. (3) Inhalation route: Children play in the field where the pesticide has just been sprayed; they can be poisoned when staying in the pesticide warehouse.
Pathogenesis:
Organophosphorus pesticides enter the body from the digestive tract, respiratory tract and skin, and are distributed through blood and lymph circulation to various organs and tissues throughout the body to produce toxic effects, mainly inhibiting the activity of cholinesterase.
The cholinergic nerves of the human body include motor nerves, sympathetic preganglionic fibers and some postganglionic fibers, and parasympathetic ganglia fibers. These nerves are stimulated to release acetylcholine at the junction of their terminals and cells, and govern the movement of organs. In the case, the released acetylcholine is rapidly hydrolyzed and loses its vitality under the action of cholinesterase. When the organic phosphorus enters the body and combines with cholinesterase, it loses the ability to hydrolyze acetylcholine, resulting in the accumulation of a large amount of acetylcholine in the body. Physiological dysfunction, the main role is:
Excitatory cholinergic nerve
Contraction of smooth muscle, increase glandular secretion, dilated pupils, slowed heart rhythm, and decreased blood pressure.
2. Motor nerves are excited
Can cause muscle tremor, sputum, heavy muscle strength weakened and paralyzed, sympathetic ganglia and preganglionic fiber excitement, so that blood pressure, heart rate, and advanced circulatory failure.
3. The role of the central nervous system
The performance is first stimulated and then suppressed, and the respiratory center paralysis occurs in the late stage.
Prevention
Prevention of organophosphorus pesticide poisoning in children
1. Strengthen the management of pesticides, establish rules and regulations, and publicize the knowledge of pesticides. They must be kept by special persons. The storage in the home should be properly placed, and educate family members, especially children, not to move.
2. It is forbidden to use toxic pesticides to kill cockroaches, mosquitoes and flies. It is forbidden to spray on the human body or clothing. Pesticide personnel should wear long boots, long-sleeved clothes, wear hats and masks, use clothes to change clothes, thoroughly clean the skin. .
3. Lactating women are best not to contact pesticides.
Complication
Pediatric organophosphorus pesticide poisoning complications Complications, urinary retention, 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. Severe cases often have tachycardia, atrioventricular block, atrial fibrillation and other abnormal heart rhythms, elevated or decreased blood pressure, cyanosis, difficulty breathing, mouth, nose or even blood (pulmonary edema), convulsions, coma, large , urinary incontinence or urinary retention, quadriplegia, reflexes, etc., can die due to respiratory paralysis or with circulatory failure.
Symptom
Pediatric organophosphorus pesticide poisoning symptoms Common symptoms Abdominal pain, nausea, diarrhea, paralysis, numbness, tightness, convulsions, convulsions, unconsciousness, blood pressure drop
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, the clinical manifestations are divided into 3 categories:
1. Parasympathetic nerve and cholinergic receptor excitability of sympathetic ganglia fibers distributed in the sweat gland
Increased secretion of glands, visible hyperhidrosis, increased salivation and bronchial secretions, contraction of the iris sphincter to narrow the pupil, gastrointestinal smooth muscle excitation caused by nausea, vomiting, diarrhea, abdominal pain, inhibition of the cardiovascular system, slow heartbeat, blood pressure, This is similar to the symptoms of poisoning poisoning, so it is called muscarinic.
2. Exercise neuromuscular junction point cholinergic receptor excitability
Muscle fibrillation or convulsions, muscle weakness or paralysis in the late stage, sympathetic preganglionic fibers and sympathetic cholinergic receptors that innervate the adrenal medulla with increased blood pressure, increased heart rate, elevated body temperature, etc. The symptoms of poisoning are similar, called nicotinic effects.
3. Central nervous system interstitial cholinergic receptor excitability
It produces symptoms of central nervous system dysfunction. In the early stage of poisoning, there are dizziness, headache, speech disorder, unconsciousness and paroxysmal convulsions. Organophosphorus poisoning can be caused by paralysis of the respiratory center.
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 in time, and do related tests to eliminate the possibility of poisoning.
Examine
Examination of organophosphorus pesticide poisoning in children
The diagnosis is mainly based on the results of laboratory tests.
1. Determination of blood cholinesterase activity
Acetylcholinesterase activity in mild poisoning is 50% to 70% normal; 30% to 50% in moderate; <30% in severity, decreased serum cholinesterase activity and decreased cholinesterase activity in synapses And the degree of poisoning is parallel; the recovery of serum cholinesterase activity is parallel with the degree of toxicosis, and can be used as a dynamic monitoring indicator of the condition.
2. Toxic analysis of gastric juice and suspicious food
Toxic analysis can confirm the diagnosis.
Choose as needed: ECG check:
1 sinus tachycardia, sinus bradycardia, premature contraction, conduction block and atrioventricular fibrillation,
2Q-T intermittent extension and torsade ventricular tachycardia.
Diagnosis
Diagnosis and identification of organophosphorus pesticide poisoning in children
diagnosis
1. History has been determined to have contact, history of ingestion or inhalation of organophosphate pesticides.
2. Symptoms of poisoning appear in poisoning symptoms, including sweating, runny, muscle fibrillation, dilated pupils and elevated blood pressure.
Skin contact with pesticides causes poisoning. The onset is slightly slow, and the symptoms are atypical. The medical history should be carefully asked, and the skin should be examined for erythema and blisters. The clinical evolution should be closely observed to assist diagnosis.
3. The vomit or exhaled gas has a garlic odor.
4. Laboratory tests for blood cholinesterase activity were significantly lower than normal.
5. Determination of Organic Phosphorus Compound The stomach contents, vomit or excretion of gastric lavage were analyzed for 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.
