GBZ 8-2002 Diagnostic criteria for occupational acute organophosphorus pesticide poisoning
Some standard content:
Ics13.100
National Occupational Health Standard of the People's Republic of China GBZ 8—2002
Diagnostic Criteria of Occupational Acute Organophosphorus Insecticides PoisoningPublished on April 8, 2002
Implemented on June 1, 2002
Published by the Ministry of Health of the People's Republic of China
Article 6.1 of this standard is recommended, and the rest are mandatory. This standard is formulated in accordance with the "Law of the People's Republic of China on the Prevention and Control of Occupational Diseases". From the date of implementation of this standard, if there is any inconsistency between the original standard GB7794-1987 and this standard, this standard shall prevail. Acute poisoning may occur in occupational activities involving contact with organophosphorus insecticides. In order to protect the health of the contactors and effectively prevent and treat acute organophosphorus pesticide poisoning, the revised standard GB7794-1987 was issued to comprehensively summarize the three clinical manifestations of organophosphorus pesticide toxicity on the nervous system, namely, acute cholinergic excitement or crisis caused by inhibition of acetylcholinesterase in the body, manifested as muscular weakness, nicotinic and central nervous system symptoms; intermediate myasthenic syndrome, manifested as weakening or paralysis of the flexor muscles of the neck and proximal muscles of the limbs, muscles innervated by cranial nerves, and respiratory muscles; delayed polyneuropathy, manifested as motor and sensory disorders with the most severe distal limbs. Appendix A of this standard is an informative appendix.
This standard was proposed and managed by the Ministry of Health of the People's Republic of China. This standard was drafted by the Occupational Health and Poison Control Institute of the Chinese Center for Disease Control and Prevention, and was drafted by the Occupational Disease Prevention and Control Institute of Sanonda Co., Ltd., Peking University Third Hospital, Huashan Hospital Affiliated to Fudan University, Shandong Provincial Institute of Labor Health and Occupational Disease Prevention and Control, Shanghai Center for Disease Control and Prevention, Xinxiang Occupational Disease Prevention and Control Institute and Tengzhou Central People's Hospital.
This standard is interpreted by the Ministry of Health of the People's Republic of China. 1
Diagnostic Standard for Occupational Acute Organophosphorus Pesticide Poisoning GBZ8-2002
Occupational acute organophosphorus pesticide poisoning is a systemic disease with neurological damage caused by exposure to a large amount of organophosphorus pesticides in a short period of time. Clinical manifestations include cholinergic excitement or crisis, and the three syndromes of intermediate myasthenia and delayed polyneuropathy that may occur later. 1 Scope
This standard specifies the diagnosis and treatment principles of occupational acute organophosphorus pesticide poisoning. This standard applies to acute poisoning caused by the production and use of organophosphorus pesticides. This standard can also be used for poisoning caused by organophosphorus pesticides in daily life and poisoning caused by mixing organophosphorus pesticides with other pesticides. 2 Normative References
The clauses in the following documents become the clauses of this standard through reference in this standard. For any dated referenced document, all subsequent amendments (excluding errata) or revisions are not applicable to this standard. However, parties reaching an agreement based on this standard are encouraged to study whether the latest versions of these documents can be used. For any undated referenced document, the latest version shall apply to this standard.
GB/T16180
3 Diagnostic principles
Diagnostic criteria for occupational acute chemical poisoning nervous system diseases Diagnostic criteria for occupational acute carbamate pesticide poisoning Evaluation of the degree of disability caused by work-related injuries and occupational diseases of employees Based on the occupational history of short-term exposure to large amounts of organophosphorus pesticides, clinical manifestations mainly based on symptoms of the autonomic nervous system, central nervous system and peripheral nervous system, combined with the determination of blood cholinesterase activity, and reference to the labor hygiene survey data of the working environment, a comprehensive analysis is conducted to exclude other similar diseases before diagnosis can be made. 4 Contact reaction
One of the following manifestations:
a) Blood or erythrocyte cholinesterase activity is below 70%, and there is no obvious clinical manifestation of poisoning; b) There are mild muscarinic autonomic nervous system symptoms and (or) central nervous system symptoms, and the blood or erythrocyte cholinesterase activity is above 70%.
5 Diagnosis and classification standards
5.1 Acute poisoning
5.1.1 Mild poisoning After a short period of contact with a large amount of organophosphorus pesticides, obvious muscarinic autonomic nervous system and central nervous system symptoms appear within 24 hours, such as dizziness, headache, fatigue, nausea, vomiting, sweating, chest tightness, blurred vision, pupil constriction, etc. The blood or erythrocyte cholinesterase activity is generally between 50% and 70%. 5.1.2 Moderate poisoning On the basis of mild poisoning, nicotinic manifestations such as fasciculations appear. The activity of cholinesterase in whole blood or red blood cells is generally between 30% and 50%.
5.1.3 Severe poisoning In addition to the above-mentioned manifestations of cholinergic excitement or crisis, patients with one of the following manifestations can be diagnosed as severe poisoning:
a) Pulmonary edema:
b) Coma;
) Respiratory failure;
d) Cerebral edema.
The activity of cholinesterase in whole blood or red blood cells is generally below 30%. 5.2 Intermediate myasthenic syndrome
About 1-4 days after acute poisoning, cholinergic crisis basically disappears and consciousness is clear, and clinical manifestations mainly of myasthenia appear.
5.2.1 Mild intermediate myasthenic syndrome
With one of the following myasthenia manifestations:
a) Weakness of the flexor muscles of the neck and proximal muscles of the limbs, and the tendon reflexes may be weakened: b) Weakness of muscles innervated by some cranial nerves. 5.2.2 Severe intermediate myasthenic syndrome
Patients with one of the following manifestations on the basis of mild intermediate myasthenic syndrome or directly present: a) respiratory muscle paralysis;
b) upper airway ventilation obstruction caused by bilateral paralysis of the muscles innervated by the IX and X cranial nerves. Electromyographic examination of high-frequency repetitive stimulation of peripheral nerves can induce progressive decrease in the amplitude of muscle evoked potentials. The activity of whole blood or erythrocyte cholinesterase is mostly below 30%. 5.3 Delayed polyneuropathy
About 2-4 weeks after acute severe and moderate poisoning, cholinergic symptoms disappear and sensory and motor polyneuropathy occurs. Neuro-electromyographic examination shows neurogenic damage. The activity of whole blood or erythrocyte cholinesterase may be normal. Principles of treatment
6.1 Principles of treatment
6.1.1 Acute poisoning
a) Remove the poison Immediately move the patient away from the poisoning site, take off the contaminated clothes, and thoroughly wash the contaminated skin, hair, and nails with soap or water: When the eyes are contaminated, quickly wash them with water or 2% sodium bicarbonate solution; b) Specific antidote Mild poisoning can be treated with anticholinergic drugs such as atropine alone: moderate and severe poisoning can be treated with atropine and cholinesterase reactivators (pralidoxime chloride, pralidoxime iodide, etc.). When the two drugs are used together, the dose of atropine should be reduced compared to when used alone;bzxz.net
c) Symptomatic and supportive treatment The principles of treatment are the same as those of internal medicine. Patients with moderate and severe poisoning should continue to be observed for several days after the disappearance of clinical symptoms, and avoid premature activities to prevent sudden changes in the disease. 6.1.2 Intermediate myasthenic syndrome
On the basis of the treatment of acute poisoning, mainly symptomatic and supportive treatment is given: for those with severe dyspnea, artificial airway is established in time, mechanical ventilation is performed, and complications are actively prevented. 6.1.3 Delayed polyneuropathy
The treatment principles are the same as those of neurology. Symptomatic and supportive treatments of Chinese and Western medicine and rehabilitation exercises of motor function can be given. 6.2 Other treatments
6.2.1 Contact reaction
Should be temporarily transferred away from organophosphorus operation for 1-2 weeks and recheck the whole blood or red blood cell cholinesterase activity. 6.2.2 Acute poisoning and intermediate myasthenic syndrome
After the recovery of acute mild and moderate poisoning and mild intermediate myasthenic syndrome, it is not advisable to contact organophosphorus pesticides within 1-2 months; after the recovery of severe poisoning and severe intermediate myasthenic syndrome, it is not advisable to contact organophosphorus pesticides within 3 months. 6.2.3 Delayed polyneuropathy
Should be transferred away from organophosphorus operation.
Arrange work or rest according to the recovery situation. If disability assessment is required, handle it according to GB/T16180.
Instructions for the correct use of this standard
See Appendix A (Informative Appendix).
Appendix A
(Informative Appendix)
Instructions for the correct use of this standard
A.1 Patients with acute poisoning caused by the mixture of organophosphorus pesticides and other pesticides often show the clinical manifestations of organophosphorus pesticide poisoning as the main manifestations. Their diagnosis and diagnostic classification can refer to this standard. A.2 The muscarinic manifestations of acute poisoning cholinergic crisis are loss of appetite, nausea, vomiting, abdominal pain, diarrhea, salivation, sweating, blurred vision, pupil constriction, increased respiratory secretions, bronchoconstriction, dyspnea, and pulmonary edema; nicotinic manifestations are fasciculations, muscle spasms, weakened muscle strength, and muscle paralysis; central nervous system manifestations are headaches, dizziness, insomnia or drowsiness, memory loss, fatigue, irritability, language disorders, mental confusion, convulsions, coma, and cerebral edema.
A.3 Intermediate myasthenic syndrome is common about 1 to 4 days after acute moderate or severe poisoning. It occurs after the acute cholinergic crisis disappears and before delayed polyneuropathy. It is mainly due to postsynaptic conduction block of neuromuscular junctions, and some or all of the following three groups of muscle weakness or paralysis may occur. A.3.1 Symmetrical weakness of flexor muscles and proximal muscles of the limbs: muscle strength is usually 2 to 3 levels, resulting in inability to raise the head when lying flat, and difficulty in lifting upper and lower limbs. Limb muscle tension is low or normal, tendon reflexes are weakened or absent, and there is no sensory impairment.
A.3.2 Weakness of muscles innervated by cranial nerves: It can affect some muscles innervated by the 3rd to 7th and 9th to 12th pairs of cranial nerves, resulting in eye difficulties, diplopia, chewing weakness, difficulty opening the mouth, limited facial expression, swallowing difficulties, hoarseness, neck and shoulder weakness, or difficulty in tongue extension and other movement disorders. A.3.3 Respiratory muscle paralysis: chest tightness, shortness of breath, nausea, decreased lung breath sounds, weakened respiratory muscle strength, often rapidly develop into respiratory failure.
A.3.4 Diseases that need to be differentiated from intermediate myasthenic syndrome mainly include "rebound" of acute organophosphorus poisoning, Guillain-Barré syndrome and myasthenia gravis cholinergic crisis. A.4 Delayed polyneuropathy is a central-peripheral distal axonopathy. Its occurrence is not related to the inhibition of cholinesterase. It is more common 2 to 4 weeks after acute poisoning with some organophosphorus (such as methamidophos, trichlorfon, etc.), and manifests as severe motor and sensory disorders in the distal limbs. It should be differentiated from polyneuropathy caused by other reasons (see GBZ76) and intermediate myasthenic syndrome caused by organophosphorus pesticide poisoning. A.5 The so-called "rebound" refers to the recurrence of cholinergic crisis in a small number of acute poisoning patients after they have improved after treatment, and they also develop more severe clinical manifestations of muscarinic, nicotinic and central nervous system. A.6 Acute organophosphorus pesticide poisoning, especially severe poisoning patients, often have varying degrees of cardiac damage. The main manifestations are arrhythmia, ST-T changes and QT interval prolongation. Because there are more typical clinical manifestations of cholinergic crisis before cardiac damage, and the abnormal manifestations of cardiac damage are not as specific as muscarinic, nicotinic and central nervous system symptoms, and it is difficult to exclude the effects of severe poisoning hypoxia, electrolyte disorders, etc. on the heart, cardiac damage is not listed as the basis for diagnosis and classification. In clinical practice, cardiac damage caused by organophosphorus pesticide poisoning should be taken seriously
A.7 The diagnosis and classification of acute poisoning is mainly based on clinical manifestations, with reference to the degree of decrease in whole blood or erythrocyte cholinesterase activity. The test of blood cholinesterase activity includes thioacetylcholine-dithiobisnitrobenzoic acid method (GBZ52), portable cholinesterase assay method and paper strip method. This standard does not make unified provisions for the method of cholinesterase activity determination.
A.8 Comprehensive measures should be taken for the treatment of acute poisoning, including removing pesticides and preventing continued absorption of pesticides, early and reasonable application of special antidotes, and symptomatic and supportive treatment. The three measures should not be neglected. Oral poisoning should be promptly and thoroughly gastric lavage with 2% sodium bicarbonate solution or water. Appropriate treatment can be given to those with symptomatic contact reactions.
A.9 The principle of using atropine to treat severely poisoned patients is "early, sufficient, and repeated administration" to achieve atropineization and avoid atropine poisoning. The indications of atropineization are dilated pupils, red face, dry skin, mouth, and increased heart rate. When atropine-like symptoms disappear, reduce the dosage, extend the medication interval, and maintain medication for several days.
A.10 Cholinesterase reactivators have good efficacy in poisoning with chlorpyrifos, parathion, phorate, ethion, chlorpyrifos, chlorpyrifos, phoxim, and terpene, but have poor efficacy or are ineffective in poisoning with dichlorvos, trichlorfon, dimethoate, oxydemeton, malathion, and diazinon. For poisoning with organophosphorus insecticides that are effective for reactivators, in addition to using them as soon as possible, a reasonable dosage and application time should be given according to the degree of poisoning. A.11 For poisoning caused by a mixture of organophosphorus insecticides and pyrethroids, they should be treated as organophosphorus poisoning first, and then symptomatic treatment should be given. For poisoning caused by a mixture of organophosphorus insecticides and carbamates, atropine should be the main treatment; when obvious nicotinic symptoms appear, reactivators can be used as appropriate under close observation. 1
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