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GBZ8-2002 English PDF

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GBZ8-2002: Diagnostic Criteria of Occupational Acute Organophosphorus Insecticides Poisoning
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Standard ID	Contents [version]	USD	STEP2	[PDF] delivered in	Standard Title (Description)	Status	PDF
GBZ 8-2002	English	189	Add to Cart	3 days [Need to translate]	Diagnostic Criteria of Occupational Acute Organophosphorus Insecticides Poisoning	Valid	GBZ 8-2002

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Basic data

Standard ID	GBZ 8-2002 (GBZ8-2002)
Description (Translated English)	Diagnostic Criteria of Occupational Acute Organophosphorus Insecticides Poisoning
Sector / Industry	National Standard
Classification of Chinese Standard	C60
Classification of International Standard	13.1
Word Count Estimation	7,755
Date of Issue	4/8/2002
Date of Implementation	6/1/2002
Quoted Standard	GBZ 76; GBZ 52; GB/T 16180
Summary	This standard specifies the principles of diagnosis and treatment of occupational acute organophosphorus pesticide poisoning. This standard applies to acute intoxication due to the production and use of organophosphorus insecticides occurred life of organophosphorus pesticide poisoning and organophosphorus pesticides poisoning can also be mixed with other pesticides used in this standard reference.

GBZ8-2002: Diagnostic Criteria of Occupational Acute Organophosphorus Insecticides Poisoning

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Diagnostic Criteria of Occupational Acute Organophosphorus Insecticides ICS 13.100 C60 GBZ People's Republic of China National Occupational Health Standards Diagnostic criteria for occupational acute organophosphorus pesticide poisoning Released in.2002-04-08 2002-06-01 Implementation Issued by the Ministry of Health of the People's Republic of China

Foreword

Article 6.1 of this standard is recommended and the remainder is mandatory. According to the "People's Republic of China Occupational Disease Prevention Law" to develop this standard. Since the implementation of the standard date, the original standard GB 7794-1987 inconsistent with this standard, subject to this standard. Acute poisoning can occur in occupational activities that are exposed to organophosphorus pesticides. To protect the health of the contact person, it is effective To control acute organophosphorus pesticide poisoning, has released GB 7794-1987. The revised standard comprehensively summarizes the three clinical manifestations of the effects of organophosphorus pesticides on neurological toxicity, namely, inhibitors Acetylcholinesterase-induced acute cholinergic excitability or crisis, manifested as muscarinic, nicotine-like and central nervous system Symptoms; intermediate myasthenia gravis, manifested as the neck muscle and limb proximal muscles, the innervation of the muscles of the brain, and call Muscle strength weakened or paralysis; delayed multiple neuropathy, the performance of the distal limb for the heavy exercise and sensory disturbances. Appendix A to this standard is an informative appendix. This standard is proposed and centralized by the Ministry of Health of the People's Republic of China. This standard is drafted by Occupational Health and Poison Control Center of China Center for Disease Control and Prevention. Hospital of Disease Control, Third Hospital of Peking University, Huashan Hospital Affiliated to Fudan University, Shandong Province, Labor and Occupational Disease Prevention and Control Research Institute, Shanghai Center for Disease Control and Prevention, Xinxiang City Institute of Occupational Disease Prevention and Control and Tengzhou City People's Hospital grass. This standard is interpreted by the Ministry of Health of the People's Republic of China. Diagnostic criteria for occupational acute organophosphorus pesticide poisoning Occupational acute organophosphorus pesticide poisoning is a short period of time after exposure to a large number of organophosphorus pesticides, causing the nervous system Systemic damage-based systemic disease. Clinical manifestations include cholinergic excitability or crisis, and subsequent possible intermediate muscle Weakness and delayed multiple neuropathy.

1 Scope

This standard specifies the principles of diagnosis and treatment of occupational acute organophosphorus pesticide poisoning. This standard applies to the production and use of organic phosphorus insecticide and the occurrence of acute poisoning, life of organic phosphorus insecticide Toxic and organic phosphorus insecticide and other pesticide poisoning can also be used in this standard.

2 normative reference documents

The terms of the following documents are hereby incorporated by reference into this standard. Any reference to the date of the document, All subsequent amendments (excluding corrigenda) or revisions do not apply to this standard, however, The parties to the standard agreement have studied whether the latest versions of these documents can be used. Whichever is not the date of the reference file, its The latest version applies to this standard. GBZ 76 Occupational acute chemical poisoning Nervous system disease diagnostic criteria Standard Test Method for Occupational Acute Carbamate Insecticide Poisoning Identification of Occupational Injury and Occupational Disease Disability in Staff and Workers GB/T 16180

3 diagnostic principles

According to a short period of exposure to a large number of organic phosphorus pesticide occupational history, to autonomic nerve, central nervous system and peripheral nervous system Symptoms of the main clinical manifestations, combined with the determination of blood cholinesterase activity, reference to the working environment of the labor hygiene survey Information, a comprehensive analysis, excluding other similar diseases, can be diagnosed.

4 contact reaction

Has one of the following manifestations. a) whole blood or erythrocyte cholinesterase activity below 70%, there is no obvious clinical manifestations of poisoning; b) have mild muscarinic-like autonomic symptoms and/or central nervous system symptoms, whereas whole blood or erythrocyte choline Esterase activity is above 70%.

5 Diagnostic and grading standards

5.1 acute poisoning 5.1.1 mild poisoning exposure to a large number of organic phosphorus insecticide within a short time, within 24 hours of more obvious muscarinic Like autonomic and central nervous system symptoms such as dizziness, headache, fatigue, nausea, vomiting, sweating, chest tightness, Blurred, and so on. Whole blood or erythrocyte cholinesterase activity is generally 50% -70%. 5.1.2 moderate poisoning on the basis of mild poisoning, muscle beam tremor and other nicotine-like performance. Whole blood or erythrocyte cholinester Enzyme activity is generally between 30% and 50%. 5.1.3 Severe poisoning In addition to the above-mentioned cholinergic excitement or crisis performance, one of the following manifestations can be diagnosed as heavy Poisoning. a) pulmonary edema; b) coma; c) respiratory failure; d) brain edema. Whole blood or erythrocyte cholinesterase activity is generally below 30%. 5.2 Interventricular myasthenia syndrome In the acute poisoning after about 1-4 days, cholines can basically disappear and clear consciousness, the emergence of muscle weakness of the clinical table Present. 5.2.1 Mild intermediate myasthenia syndrome One of the following weaknesses. a) flexor muscle and limb proximal muscle weakness, tendon reflex can be weakened; b) Part of the innervation of the brain. 5.2.2 Heavy-term myasthenia gravis On the basis of either mild primary myasthenia gravis or one of the following manifestations. a) respiratory muscle paralysis; b) Bilateral IX and X on the innervation of the brain caused by muscle paralysis caused by upper airway obstruction. High frequency repeated stimulation of peripheral nerve EMG examination, can lead to muscle evoked potential amplitude was progressive decline. Whole blood or Erythrocyte cholinesterase activity more than 30%. Delayed multiple neuropathy About 4 to 4 weeks after acute severe and moderate poisoning, cholinergic symptoms disappeared, feeling, motorized multiple nerves disease. Neuro-electromyography shows neurogenic damage. Whole blood or erythrocyte cholinesterase activity can be normal.

6 Principles of handling

6.1 Principles of treatment 6.1.1 acute poisoning a) remove the poison immediately remove the patient from the poisoning scene, take off contaminated clothing, with soap or water thoroughly clean the sewage Dyed skin, hair, finger (toe) A; eye contaminated, quickly washed with water or 2% sodium bicarbonate solution; b) effects of antidote mild poisoning can be used alone with atropine and other anti-choline drugs; moderate and severe poisoning, combined with Atto And cholinesterase complexing agent (chlorpheniramine, iodized phosphorus, etc.). When the two drugs are used together, the dose of atropine should be compared Reduce when used alone; c) symptomatic and supportive treatment principles with internal medicine. Moderate and severe poisoning in patients with clinical manifestations should continue after the disappearance Observe the number of days, and avoid premature activity, to prevent the disease mutation. 6.1.2 Interventricular myasthenia syndrome In the treatment of acute poisoning on the basis of the main given symptomatic and supportive treatment; severe dyspnea, the timely establishment of people Work airway, for mechanical ventilation, while actively preventing complications. 6.1.3 Delayed multiple neuropathy Treatment principles and neurological principles, can be given in Western medicine and symptomatic and supportive care and motor function rehabilitation exercise. 6.2 Other treatments 6.2.1 Contact reaction Should be temporarily removed from the organic phosphorus 1-2 weeks and review the whole blood or erythrocyte cholinesterase activity. 6.2.2 acute poisoning and intermediate myasthenia syndrome Acute mild and moderate poisoning and mild intermediate myasthenia gravis after cure, 1-2 months should not be exposed to organic phosphorus Pesticides; severe poisoning and severe intermediate myasthenia gravis after cure, 3 months should not be exposed to organic phosphorus insecticide. 6.2.3 Delayed multiple neuropathy Should be transferred from organic phosphorus operation. According to the recovery situation, arrange work or rest. For disability identification, press GB/T 16180 treatment.

7 Correctly use the instructions in this standard

See Appendix A (informative).

Appendix A

(Informative) Correctly use the instructions in this standard A.1 acute organophosphorus pesticides and other pesticide poisoning, often with organic phosphorus pesticide poisoning clinical Performance-based, the diagnosis and diagnosis of grading can refer to this standard. A.2 acute poisoning cholinergic canine-like muscarinic-like manifestations of loss of appetite, nausea, vomiting, abdominal pain, abdominal Diarrhea, salivation, sweating, blurred vision, miosis, increased respiratory secretions, bronchial spasm, dyspnea Difficult, pulmonary edema; nicotine-like performance for muscle bundle tremor, muscle spasms, muscle weakness, muscle paralysis; central nervous system System performance for headache, dizziness, insomnia or drowsiness, memory loss, fatigue, irritability, language barriers, mental Trance, convulsions, coma, brain edema. A.3 intermediate myasthenia syndrome more common in acute moderate or severe poisoning after 1 to 4 days or so, occurred in acute Cholestatic crisis and delayed onset of multiple neuropathy, mainly due to neuromuscular junction postsynaptic resistance Stagnation, there may be some or all of the following three groups of muscle weakness or paralysis. A.3.1 flexor muscle and limb proximal muscle symmetry muscle strength weakened. muscle strength is often 2 to 3, caused by supine Rise, upper limbs and lower limbs difficult to lift. Limb muscle tension is low or normal, tendon reflexes weakened or disappeared, not feeling Feel obstacle. A.3.2 Nerve-dominated muscle weakness. can be involved in the first 3 to 7 and 9 to 12 on the innervation of the part of the brain Meat, eyes open difficulties, diplopia, chewing weakness, mouth difficulties, facial expression activities limited, swallowing difficulties, Hoarseness, tightening of the neck and shrug, or difficulties in stretching. A.3.3 Respiratory muscle paralysis. chest tightness, shortness of breath, cyanosis, reduced respiratory tone, decreased muscle strength, Often developed rapidly for respiratory failure. A.3.4 need to diagnose the disease with intermediate myasthenia gravis syndrome mainly acute organophosphate poisoning Jump ", Green - Bally syndrome and myasthenia gravis cholinergic crisis and so on. A.4 Delayed multiple neuropathy is central - peripheral peripheral axonal disease, its occurrence and inhibition of cholinesterase Unrelated, more common in some organic phosphorus (such as methamidophos, trichlorfon, etc.) acute poisoning after 2 to 4 weeks, the performance of limbs Distal for heavy exercise and sensory disturbances. Should be associated with other causes of multiple neuropathy (see GBZ 76) and yes Identification of Phase I Myasthenia Gravis Syndrome in Phosphorus Insecticide. A.5 The so-called "rebound" refers to a small number of acute poisoning patients after treatment improved, the cholinergic crisis to reproduce, and produce Heavier muscarinic, nicotinic and central nervous system clinical manifestations. A.6 acute organophosphorus pesticide poisoning, especially in patients with severe poisoning, often can occur in varying degrees of cardiac damage harm. Mainly manifested as arrhythmia, ST-T changes and prolonged QT interval. Due to before the heart damage has been compared Typical cholinergic crisis of clinical manifestations, and abnormal cardiac performance is not as muscarinic, nicotine and Central nervous system symptoms specific, coupled with the difficulty of excluding severe poisoning hypoxia, electrolyte imbalance on the heart of the shadow Sound, so the heart damage is not included in the diagnosis and classification basis. In clinical practice, the introduction of organic phosphorus insecticide poisoning From the heart damage should be taken seriously. A.7 acute poisoning diagnosis and classification of clinical manifestations as the main basis, reference to whole blood or erythrocyte cholinesterase activity The degree of decline. Blood cholinesterase activity test with thioacetyl-dithiobisobenzoic acid method (GBZ 52), portable cholinesterase assay and paper method, the standard of cholinesterase activity determination of the side Law is not unified. A.8 The treatment of acute poisoning should take comprehensive measures, including the removal of pesticides and prevent the absorption of pesticides, early Rational use of special effects detoxification drugs and to give symptomatic and supportive care, three measures can not be neglected. Oral poisoning Should be promptly and thoroughly with 2% sodium bicarbonate solution or water gastric lavage. For symptomatic contact reactors may be given appropriate treatment Treatment. A.9 The principle of treatment of severe poisoning with atropine is "early, adequate, repeated administration" to reach Atto To prevent atropine poisoning. Atropine indications are pupil enlargement, facial redness, dry skin, mouth Dry, heart rate faster. When reaching atropine or muscarinic-like symptoms disappeared when appropriate, to extend the medication interval And maintain medication for several days. A.10 cholinesterase complex agent on the phosphorus, parathion, phorate, ethionophos, borer, chlorpyrifos, Thiophosphate, phoxim, tep and other poisoning effect is better, against dichlorvos, trichlorfon, dimethoate, omethoate, horse Thiophosphate, diazepine and other poisoning efficacy is poor or ineffective. Toxicity of organic phosphorus insecticide effective for complexing agent, except to do Early application, should be based on the degree of poisoning, to give a reasonable dose and application time. A.11 for organic phosphorus insecticide and pyrethroid mixed poisoning, should first be treated with organic phosphorus poisoning, and then Given symptomatic treatment. The organophosphorus pesticide and carbamate mixed poisoning, should be based on atropine treatment; When the obvious nicotine-like symptoms, in close observation, the appropriate use of oxime complex agent.

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