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GBZ76-2024 English PDF

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GBZ76-2024: (Diagnostic criteria for occupational acute chemical toxicity-related nervous system diseases)
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GBZ 76-2024English259 Add to Cart 3 days [Need to translate] (Diagnostic criteria for occupational acute chemical toxicity-related nervous system diseases) Valid GBZ 76-2024
GBZ 76-2002English389 Add to Cart 3 days [Need to translate] Diagnostic Criteria of Occupational Acute Neurotoxic Disorders Caused by Chemicals Valid GBZ 76-2002

Standard similar to GBZ76-2024

GB/T 50082   GBZ 234   

Basic data

Standard ID GBZ 76-2024 (GBZ76-2024)
Description (Translated English) (Diagnostic criteria for occupational acute chemical toxicity-related nervous system diseases)
Sector / Industry National Standard
Word Count Estimation 12,138
Date of Issue 2024-03-11
Date of Implementation 2025-03-01
Issuing agency(ies) State Administration for Market Regulation, China National Standardization Administration

GBZ76-2002: Diagnostic Criteria of Occupational Acute Neurotoxic Disorders Caused by Chemicals


---This is a DRAFT version for illustration, not a final translation. Full copy of true-PDF in English version (including equations, symbols, images, flow-chart, tables, and figures etc.) will be manually/carefully translated upon your order.
Diagnostic Criteria of Occupational Acute Neurotoxic Disorders Caused by Chemicals ICS 13.100 C60 GBZ People's Republic of China National Occupational Health Standards Occupational acute chemical toxicity - Criteria for the diagnosis of neurological diseases Diagnostic Criteria of Occupational Acute Neurotoxic Diseases Caused by Chemicals 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. In a variety of professional activities, may be in a short period of time exposure to some high concentrations and high toxicity of chemicals and acute poison. Some of these chemicals, some known species; and some are poisoned after the moment is not clear pathogenic species; Of the species caused by poisoning has been included in the list of occupational diseases, and some have not yet included; some have independent diagnostic criteria, while others Has not yet developed a separate diagnostic criteria. But all acute poisoning diseases have a common incidence of the law can be developed also necessary Develop rules that should be observed when diagnosing acute poisoning. The rules set out in this series of standards relate to the diagnosis of occupational acute chemical poisoning, which are used to ensure that The diagnosis of acute chemical poisoning is unified, whether it is known or concealed by the cause, and whether it is poisoned The damage to which the target organ is caused can be diagnosed in accordance with the rules prescribed in this standard. "Occupational acute chemical poisoning Of the diagnosis "includes the following sections, each of which will be defined in the preface and the introduction to each section. Part 1. Diagnostic criteria for occupational acute chemical poisoning (general); Part 2. Diagnostic rules for occupational acute occult chemical poisoning; Part 3. Occupational acute chemical toxicity - Multiple diagnostic criteria for multiple organ dysfunction syndrome; Part 4. Diagnostic criteria for occupational acute exogenous death; Part 5. Occupational acute chemical toxicity - Criteria for the diagnosis of neurological diseases; Part 6 Occupational acute chemicals - Criteria for the diagnosis of toxic respiratory diseases; Part 7. Diagnostic criteria for occupational acute toxic liver disease; Part 8. Diagnostic criteria for occupational acute toxic nephropathy; Part 9 Occupational Acute Chemicals - Toxic Cardiac Disease Diagnostic Criteria; Part 10 Occupational Acute Chemicals Toxicity Diagnostic criteria for blood system diseases; Appendix A to this standard is an informative appendix, Appendix B, C, and D are normative appendices. This standard is proposed and centralized by the Ministry of Health of the People's Republic of China. This standard by the China Center for Disease Control and Prevention of occupational health and poisoning control is responsible for drafting, to participate in the drafting of the unit Sea Chemical Industry Occupational Disease Prevention and Control Research Institute and Sichuan University Huaxi Occupational Disease Hospital. This standard is interpreted by the Ministry of Health of the People's Republic of China. Occupational acute chemical toxicity - Criteria for the diagnosis of neurological diseases Occupational acute chemical poisoning Nervous system disease refers to the workers in the short-term occupational activities in large contact Quantitative disease caused by the nervous system damage-based systemic disease.

1 Scope

This standard specifies the diagnostic criteria and principles of occupational acute chemical toxic neurological diseases. This standard applies to the diagnosis of toxic neurological diseases caused by chemicals in occupational activities. Non - professional Acute chemical poisoning caused by the diagnosis of neurological diseases, can also refer to this standard.

2 normative reference documents

The terms of the following documents are hereby incorporated by reference into this standard. Any date that references the date of the document All subsequent amendments (excluding corrigenda) or revisions do not apply to this standard, however, The parties to the agreement are able to use the latest version of these documents. Those who do not mind the date of the reference file, its latest The version applies to this standard. GBZ 71 Occupational Acute Chemical Poisoning Diagnostic Criteria (General) Identification of Occupational Injury and Occupational Disease Disability in Staff and Workers GB/T 16180

3 diagnostic principles

According to the short-term exposure to a large number of chemical career history, the emergence of neurological damage-based clinical manifestations, combined The necessary laboratory test results and on-site labor hygiene survey data, excluding other causes of similar diseases, the only clinics Off.

4 observation object

4.1 acute toxic encephalopathy observed object Headache, dizziness, fatigue, nausea and other symptoms, in a short time subsided. 4.2 poisoning peripheral neuropathy observed object Has one of the following. a) appear distal limb numbness, pain, both lower limbs heavy feeling, fatigue, but no typical symptoms of peripheral nerve damage and Signs; b) Neuronal-electromyography shows suspicious neurogenic lesions without typical symptoms and signs of peripheral nerve damage.

5 clinical type and classification diagnosis

Occupational acute toxic nervous system damage can be caused by a variety of toxic substances, different types of clinical manifestations, common clinical Type is as follows. 5.1 acute toxic encephalopathy 5.1.1 Mild Has one of the following. a) severe headache, dizziness, insomnia, nausea, vomiting, malaise, apathetic, and gait With excitement, emotional excitement, irritability and other psychiatric symptoms; b) mild disturbance of consciousness, such as confusion, drowsiness or hazy state. 5.1.2 Moderate Has one of the following. a) Moderate disturbance of consciousness, such as delirium, turbidity; b) epilepsy seizures; c) the clinical manifestations of mild toxic encephalopathy accompanied by bilateral pyramidal tract signs. 5.1.3 Severe Has one of the following. a) severe disturbance of consciousness, such as shallow coma, moderate coma, deep coma, plant state; b) obvious psychiatric symptoms, such as orientation disorders, hallucinations, delusions, psychomotor excitement or aggressive behavior; c) status of epilepsy; d) the performance of hernia formation, e) brain focal lesions, such as cortical blindness, cerebellar ataxia, Parkinson's syndrome. EEG examination can be moderate and high abnormalities; brain evoked potential of the central segment can be extended when the latent; head computer Layer scan (CT) or magnetic resonance imaging (MRI) can show cerebral edema. 5.2 Acute toxic myelopathy 5.2.1 Mild There are bilateral lower extremity pyramidal tract signs, not associated with lower limb motor function and bladder dysfunction, and no manifestations of these encephalopathy; 5.2.2 Severe There is mild spasmodic paraplegia, may have urinary retention or urinary incontinence, but no manifestations of encephalopathy. 5.3 Toxic Peripheral Neuropathy 5.3.1 Mild In addition to the above symptoms, have one of the following. a) limb spontaneous burning pain, and pain allergy; b) limb symmetry gloves, socks-like distribution of pain, touch, tuning fork vibration disturbance, while Achilles tendon reflex Weakened c) pain, hallucinations, and corneal reflex or blink reflex abnormalities in the cranial nerve; d) Neuro-electromyography shows neurogenic damage. 5.3.2 Moderate On the basis of mild poisoning, has one of the following. a) distal limb pain, touch, tuning fork vibration disorders elbow, knee above, accompanied by Achilles tendon reflex; b) deep sensation obvious obstacle with sensory ataxia; c) multiple cranial nerve dominated muscle incomplete paralysis; d) Neuro-electromyography showed significant neurological damage. 5.3.3 severe Has one of the following. a) limb muscle strength decreased to 3 or 3 below; b) respiratory muscle paralysis; c) Neuro-electromyography showed neurogenic damage with nerve conduction velocity was slowed down. Or evoked potentials were significantly reduced.

6 Principles of handling

6.1 Principles of treatment 6.1.1 According to the principles of treatment in GBZ 71 to rescue acute poisoning. 6.1.2 Etiology of treatment. If the corresponding indications, the timely application of complexing agents, special antidote or blood purification therapy. 6.1.3 treatment of acute toxic encephalopathy a) reasonable oxygen therapy, conditional administration of hyperbaric oxygen therapy, hypoxic encephalopathy is particularly important; b) active prevention and treatment of brain edema, control the amount of liquid, given hypertonic dehydrating agent, adrenal glucocorticoid, diuretics Wait; c) control of convulsions, available antiepileptic drugs or stabilizer, if necessary, can be used short-term anesthetic; d) the use of drugs to promote the recovery of brain cell function; e) other symptomatic supportive care. 6.1.4 acute acute myelopathy, should be active symptomatic support treatment, prevention of urinary tract and other parts of the infection. 6.1.5 acute toxic peripheral neuropathy, according to the needs of short enough to apply adrenocorticotropic hormone, and can be used B Vitamins, energy mixture or with the role of blood circulation of traditional Chinese medicine treatment, supplemented by physical therapy and symptomatic, supportive treatment. 6.2 Other treatments 6.2.1 observed subjects, mildly toxic central nervous system and peripheral nervous system diseases were cured after the return to the original work Bit. 6.2.2 moderate and severe poisoning Central nervous system and peripheral nervous system diseases patients should not be engaged in the original toxic operations. should According to the recovery after treatment, arrange work or rest. For identification of labor capacity, according to GB/T 16180 treatment.

7 Correctly use the instructions in this standard

a) The correct use of this standard is described in Appendix A (informative). b) Neurological-electromyographic methods and criteria for determining neurological damage are given in Appendix B (normative). c) The strength rating criteria are given in Appendix C (normative). d) Criteria for classification and classification of awareness disorders, see Appendix D (normative appendix).

Appendix A

(Informative) Correctly use the instructions in this standard A.1 This standard applies to occupational acute chemical poisoning caused by the central nervous system diseases and peripheral nervous system diseases Diagnosis and grading. Living acute poisoning caused by the central nervous system and peripheral neurological diseases can be diagnosed Row. A.2 cause poisoning of occupational acute toxic encephalopathy A.2.1 Toxic effects of brain tissue metabolism or inhibition of enzyme activity Lead, tetraethyl lead, trialkyltin, arsenide, boron Alkane, gasoline, benzene, toluene, carbon disulfide, trichlorethylene, methanol, ethanol, chloroethanol, methyl mercaptan, methyl chloride, iodine Alkane, dichloroethane, tetrachloroethane, ethylene oxide, carbon tetrachloride, butyl acetate, organic phosphorus, carbamates Pyrethroids, insecticides, organic mercury, phosphine, methyl bromide, nereavirus, fluoroacetamide, tetramine, propylene Amide and so on; A.2.2 toxic substances that cause brain tissue hypoxia are carbon monoxide, hydrogen sulfide, cyanide, acetone cyanohydrin, acrylonitrile and so on; A.3 Occupational acute toxic encephalopathy due to a short period of time due to exposure to high doses of neurotoxicity, the general incidence of acute. But some Toxic substances such as tetra-lead, bromomethane, methyl iodide, trialkyl tin, organic mercury and other acute poisoning, can be a few hours, a few days, even To 2-3 weeks after the incubation period, in the incubation period can be no obvious symptoms, and once the symptoms, the disease progressed rapidly. Cyanide, carbon monoxide and other toxic encephalopathy caused by, can be restored in the acute phase 2-3 weeks after the loss of the bottom section and the brain Subcortical white matter caused by delayed encephalopathy. A.4 acute toxic encephalopathy pathological features of cerebral edema, so the general performance of the whole brain symptoms and increased intracranial pressure Like (such as severe headache, frequent vomiting, restlessness; or apathetic, disturbance of consciousness increased; or repeated convulsions, Bilateral pupil narrowing, blood pressure, slow pulse breathing; eyeballs associated with edema or increased eye tension; part of the eyes of patients The emergence of optic nerve papillae edema); severe cases can appear herniation (such as the formation of tentorial hernia hernia, hippocampus and hook back Down the oppression of the brain stem, unconsciousness was deep coma, eye fixed, bilateral pupil small or large, light reaction disappeared, call Suction irregular, or appear to the brain straight state; when the occurrence of occipital large hole hernia, can lead to bilateral dilation of the pupil and breathing suddenly stopped Only); few cases of focal cerebral lesions. The grading diagnosis is mainly based on the degree of disturbance of consciousness, the type of mental disorder, pumping Twitch appear, the consequences of increased intracranial pressure, and whether the brain focal damage and other comprehensive judgments. A.5 in the professional activities due to excessive air containing methane, carbon dioxide, nitrogen and other lead to suffocation, can cause hypoxic brain Disease; its pathological features are brain edema, the disease classification and treatment can refer to this standard. A.6 moderate toxic encephalopathy, the consciousness can occur in the absence of obstacles when the cone beam, often manifested as abdominal wall reflex and testis Reflexes such as shallow reflexes diminish or disappear, tendon reflexes active or hyperactivity, or ankle claws, or leads to Babinski or Chaddock Sign and other pathological reflex. A.7 Most patients with acute toxic encephalopathy, EEG abnormalities, the main manifestations of abnormal a wide range of α-rhythm disorders, α wave is reduced. When there is disturbance of consciousness or convulsions, θ wave δ amplitude activity increased, severe cases were highly unconscious or appear spines Wave, sharp wave But the degree of EEG abnormalities and clinical severity is not necessarily completely parallel relationship. A.8 The current commonly used brain evoked potentials are somatosensory evoked potential (SEP), visual evoked potential (VEP), brainstem Sensory evoked potential (BAEP). In the case of toxic encephalopathy, these brain evoked potentials often appear in the central segment abnormalities, and with consciousness The degree of obstruction can be used to assist in monitoring brain function and prognosis, but also help to predict the occurrence of delayed encephalopathy. A.9 computed tomography (CT) and cranial magnetic resonance imaging (MRⅠ) on cerebral edema, cerebral softening, cortical Lower white matter demyelinating lesions and other diagnostic value. Magnetic resonance imaging or CT examination can be shown in acute toxic encephalopathy Lateral ventricle smaller, cerebral cortex under the white matter diffuse low density changes, or see the globus pallidus and shell density decreased. MRI showed Brain edema lesions often than CT early, but the early onset of clinical disease may not be able to detect the above changes. Other functional brain imaging techniques Including positron emission scanning (PET), local cerebral blood flow (RCBF), single photon emission computed computer scanning (SPECT) And FLAIR, etc., due to expensive, in the application of toxic encephalopathy is still a lack of mature experience, it is not included in this standard. A.10 acute toxic encephalopathy focus on improving brain oxygen and prevention of brain edema. Should be given a reasonable oxygen therapy (yes Conditions can be used high-pressure oxygen), hypertonic dehydrating agent; diuretics and short-term adequate adrenal cortex hormones, the use of antiepileptic drugs or Adjuvant to control the convulsions, the application of brain cells to restore the function of drugs and other symptomatic and supportive treatment. On the emergence of status epilepsy or mental exercise excitement by antiepileptic drugs or stabilizer control effect is not good, or accompanied by central High fever and no obvious liver, kidney dysfunction, available short-term anesthetic such as thiopental sodium. Such as the merger of toxic Liver, kidney dysfunction, then choose sedation, spasmodil should be careful. Generally combined with liver dysfunction, to use chloral hydrate, Acetopitrazine, haloperidol is appropriate, combined with renal dysfunction were selected aldehyde, perphenazine, haloperidol, pentobarbital, Or the Division can be barbiturate (speed can sleep) is appropriate A.11 purely toxic myelopathy is rare, can occur in moderate acute or subacute organic mercury poisoning or some acute Organophosphate poisoning caused by delayed neuropathy. Due to spinal cord collateral damage, the main clinical manifestations of bilateral lower limbs appear pyramidal tract Levy, severe cases of spasmodic paraplegia, urinary retention or incontinence. A.12 cause occupational acute toxic to the peripheral neuropathy toxic thallium, arsenic, and certain organophosphate compounds, such as Trichlorfon, methamphetamine, dimethoate, dimethoate Ester (TOCP), etc., n-hexane, ethylene oxide and the like. Acute carbon monoxide poisoning can occur when a single neuropathy. A.13 acute toxic symptoms of peripheral neuropathy can occur in contact with poison 1 to 2 days, but arsenic and a number of organic phosphorus acute Poison, can be 2 to 3 weeks after the incubation period of delayed peripheral neuropathy. Some organophosphate poisoning in the acute phase of cholinergic crisis Elimination of 1 to 5 days after the occurrence of neuromuscular joint disease, there "intermediate muscle weakness syndrome", the performance of cranial nerve dominated muscle, The muscular muscles and the proximal limbs of the limbs, or the weakness of the respiratory muscles. A.14 neurological-electromyographic examination of the early diagnosis of toxic peripheral neuropathy is important, check the method and the results of judgment Standard see Appendix B of this standard, should be used as far as possible disposable concentric pin electrode. The nerve conduction velocity was measured for occupational groups Degree, the general use of surface electrodes, a few people use near nerve method [see Chinese Journal of Neuropsychiatry 1988, 2 (2). 87]. Limb strength rating criteria are given in Appendix C of this standard. A.15 Differential diagnosis is very important. Diagnosis of occupational acute chemicals poisoning encephalopathy, the need to be infected with the central nervous system, Cerebrovascular accident, craniocerebral trauma, metabolic disorders, epilepsy, acute drug poisoning, psychiatric disorders and other identification. week Peripheral neuropathy can be caused by other causes, such as acute infectious polyneuropathy (Guillain-Barre Syndrome), Diabetes, hereditary diseases, drug poisoning and so on. Therefore, in the diagnosis of toxic peripheral neuropathy, should exclude these diseases.

Appendix B

(Normative appendix) Neurological - electromyographic examination method and its neurological damage criteria Method of Electromyography B.1.1 Preparation before inspection B.1.1.1 First, the inspection requirements and precautions to the subjects were clearly confessed to avoid mental stress, For. B.1.1.2 Subject to take appropriate position, so that the muscles are supported and stable, both natural relaxation, but also according to the requirements of all kinds of transport move. B.1.1.3 Place the grounding electrode on the same body as the muscle. Bl1.4 local skin with 2.5% iodine and 75% alcohol disinfection. B.1.2 Check procedures Bl2.1 insertion of the electromyography activity. concentric needle electrode (needle area of 0.45mm2) quickly inserted into the muscle, scanning The speed of 50 ~ 100ms/cm, the sensitivity of 100μv/cm, observe the needle when the characteristics of electrical activity and the presence of muscle rigidity, The muscle is straight and the electrical activity is prolonged. B.1.2.2 Muscle relaxation when the electrical activity. scanning speed of 5 ~ 10ms/cm, sensitivity of 100μv/cm, observe whether the self Power generation potentials such as fibrillation potential, positive phase potential and beam potential. B.1.2.3 Electromyographic activity when small force is shrunk (lightly shrunk). condition is the same as B.1.2.2. When muscle is slightly contracted, The average time limit of the potential of the motion unit and the average voltage, and the percentage of the multiphase potential. (For the determination of the average unit time limit, If necessary, should be in the same muscle selection 2 to 3 different locations to check). To avoid the error, each wave should appear at the same time 2 ~ 3 Times, can only be included. The time limit is from the initial skew of the baseline to the last skew back to the baseline. The phase of the movement unit Whichever is higher than the baseline. B.1.2.4 Electromyographic activity when vigorously shrinks. The scanning speed is 50 ~ 100ms/cm...

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