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Delivery: <= 3 days. True-PDF full-copy in English will be manually translated and delivered via email. GBZ23-2024: Diagnostic standard for occupational acute carbon monoxide poisoning Status: Valid GBZ23: Historical versions
Basic dataStandard ID: GBZ 23-2024 (GBZ23-2024)Description (Translated English): Diagnostic standard for occupational acute carbon monoxide poisoning Sector / Industry: National Standard Classification of Chinese Standard: C60 Classification of International Standard: 13.100 Word Count Estimation: 6,633 Date of Issue: 2024-05-09 Date of Implementation: 2025-05-01 Issuing agency(ies): State Administration for Market Regulation, China National Standardization Administration Summary: This standard specifies the diagnostic principles and diagnostic classification of occupational acute carbon monoxide poisoning. This standard applies to the diagnosis of acute poisoning caused by inhalation of high concentrations of carbon monoxide in occupational activities. GBZ23-2002: Diagnostic Criteria of Occupational Acute Carbon Monoxide Poisoning---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 Carbon Monoxide Poisoning ICS 13.100 C60 GBZ People's Republic of China National Occupational Health Standards Diagnostic criteria for occupational acute carbon monoxide poisoning Released in.2002-04-08 2002-06-01 Implementation Issued by the Ministry of Health of the People's Republic of China ForewordArticle 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 8781-1988 inconsistent with this standard, subject to this standard. Carbon monoxide is a widely distributed asphyxiating gas, and exposure to carbon monoxide is present in more than 70 industries. Inhalation High concentrations of carbon monoxide can cause acute poisoning, the number of deaths and the number of deaths in China before the acute occupational chemicals poisoning before Column. To protect the health of workers, effective prevention and treatment of occupational acute carbon monoxide poisoning, the development of this standard. Appendix A to this standard is an informative appendix and Appendix B is a normative appendix. 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 Occupational Health and Poison Control, Anshan Iron and Steel Company Labor Hygiene Research Institute Responsible for drafting. This standard is interpreted by the Ministry of Health of the People's Republic of China. Diagnostic criteria for occupational acute carbon monoxide poisoning Acute carbon monoxide poisoning is inhalation of higher concentrations of carbon monoxide (CO) caused by acute cerebral hypoxia; Patients may have delayed neuropsychiatric symptoms. Some patients may also have other organs of hypoxia changes.1 ScopeThis standard applies to the iron and steel industry, chemical industry, gas, coal, transportation and other production activities due to inhalation of high concentrations of oxygen Acute poisoning caused by carbon. Diagnosis of acute acute carbon monoxide poisoning can also be used in this standard. Long-term exposure to low concentrations Carbon monoxide can cause "chronic carbon monoxide poisoning" is still controversial, does not belong to the scope of application of this standard.2 normative reference documentsThe 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. Those who do not mind the date of the reference file, the most The new version applies to this standard. GBZ 76 Occupational acute chemical poisoning Nervous system disease diagnostic criteria3 diagnostic principlesDepending on the exposure history of high concentrations of carbon monoxide and the symptoms and signs of acute central nervous system damage, The results of timely determination of carbon oxynucleotides (HbCO) in blood, on-site hygienic investigation and determination of carbon monoxide in air Information, and exclude other causes, can be diagnosed as acute carbon monoxide poisoning.4 contact reactionHeadache, dizziness, palpitations, nausea and other symptoms, inhalation of fresh air after the symptoms can disappear.5 Diagnostic and grading standards5.1 mild poisoning Have any of the following. a) severe headache, dizziness, limb weakness, nausea, vomiting; b) mild to moderate disturbance of consciousness, but no coma. Blood carbon oxymoglobin concentration can be higher than 10%. 5.2 moderate poisoning In addition to the above symptoms, the consciousness of the performance of shallow to moderate coma, after recovery and no obvious complications. Blood carbon oxymoglobin concentration can be higher than 30%. 5.3 severe poisoning Have any of the following. 5.3.1 Consciousness disorder to deep coma or to the cerebral cortex state; 5.3.2 patients with disturbance of consciousness and concurrent with any of the following performance. a) brain edema; b) shock or severe myocardial damage; c) pulmonary edema; d) respiratory failure; e) upper gastrointestinal bleeding; f) brain focal lesions such as cones or extrapyramidal signs. Blood carbon oxymoglobin concentration can be higher than 50%. 5.4 acute carbon monoxide poisoning delayed encephalopathy (neuropsychiatric late onset) Acute carbon monoxide poisoning after the recovery of consciousness, by about 2 to 60 days of "leave period", the emergence of the following clinical manifestations One of the following. a) mental and disturbance of consciousness is dementia, delirium or to the cerebral cortex state; b) the appearance of Parkinson's syndrome in extrapyramidal neurological disorders; c) Cone nerve damage (such as hemiplegia, pathological reflex positive or urinary incontinence, etc.); d) focal cerebral cortex dysfunction such as aphasia, blindness, etc., or secondary epilepsy. Head CT examination can be found in the brain with pathological density reduction area; EEG examination can be found in moderate and high abnormalities.6 Principles of handling6.1 Principles of treatment 6.1.1 quickly remove the patient from the poisoning site to the ventilation, loosen the collar, pay attention to warm, close observation of the state of consciousness. 6.1.2 timely first aid and treatment a) mild poisoning, can be given oxygen inhalation and symptomatic treatment; b) moderate and severe poisoning should be actively given atmospheric pressure mask oxygen therapy, conditions should be given hyperbaric oxygen therapy. weight Degree of poisoning as the disease should be given to eliminate brain edema, promote cerebral blood circulation, to maintain the respiratory and circulatory function and antispasmodic Symptomatic and supportive care. Strengthen the care, active prevention and treatment of complications and the prevention of delayed encephalopathy. 6.1.3 for delayed encephalopathy, can be given hyperbaric oxygen, glucocorticoids, vasodilators or anti-Parkinson's disease drugs and other pairs Disease and supportive care. 6.2 Other treatments 6.2.1 Mild poisoning can still be engaged in the original work after being cured. 6.2.2 moderate poisoning after treatment recovery, should be temporarily out of carbon monoxide operation and regular review, observed 2 months as late Hair disease, can still engage in the original work. 6.2.3 severe poisoning and the emergence of late encephalopathy, although the treatment recovery, should be transferred from carbon monoxide operation. 6.2.4 due to severe poisoning or delayed encephalopathy treatment for half a year is still left incomplete recovery of organic nerve damage, should always be transferred from the Touch carbon monoxide and other neurotoxic operations. Depending on the condition of treatment and rest.7 Correctly use the instructions in this standardSee Appendix A (informative), Appendix B (normative).Appendix A(Informative) Correctly use the instructions in this standard A.1 poisoning site of the labor hygiene survey data and the concentration of carbon monoxide in the air to determine the results of the diagnosis of reference Righteousness A.2 The disease with acute cerebral hypoxia caused by central nervous system damage as the main clinical manifestations, so different degrees of consciousness is temporary An important basis for bed diagnosis and classification (see GBZ 76). A.3 acute carbon monoxide poisoning can also appear outside the brain other organs of the abnormal, such as skin erythema blisters, muscle swelling and pain, heart Electrogram or liver, renal dysfunction, single neuropathy or auditory vestibular organ damage. Because these abnormalities are not as central nervous system The appearance of early, only seen in some patients, or for a transient, so this standard is not included in the diagnosis and classification basis. A.4 acute carbon monoxide poisoning patients such as secondary brain edema (increased consciousness, convulsions or to the brain rigidity, pathology Reflex positive, EEG slow wave or optic nerve edema), pulmonary edema, respiratory failure, shock, severe myocardial damage Or upper gastrointestinal bleeding, are prompted in serious condition. A.5 blood carbon hemoglobin (HbCO) if higher than 10%, can suggest a higher concentration of carbon monoxide contact history, Diagnosis and differential diagnosis of this disease have reference significance. But from the poisoning scene, the blood HbCO concentration that is decreased, and with the clinical The degree of performance is sometimes not parallel. So HbCO detection if not timely, not as a basis for diagnosis and classification. Stop touch one More than 8 h carbon monoxide in patients with HbCO more than 10% in the following, generally no need for HbCO examination. A.6 acute carbon monoxide poisoning delayed encephalopathy and sequelae different. The symptoms of the latter are continually followed by the acute phase Brain disease refers to acute carbon monoxide poisoning coma awakening, after a period of time (2 to 60 days) of the holiday period, suddenly appeared Consciousness of mental disorders, extrapyramidal or apical system damage-based encephalopathy, so moderate and severe acute carbon monoxide poisoning After a coma awake, should be observed for 2 months, during the observation period should be temporarily out of carbon monoxide operation. A.7 mild acute carbon monoxide poisoning with colds, high blood pressure, food poisoning, Meniere's syndrome and other identification, moderate And severe poisoning should pay attention to and other causes (such as diabetes, cerebrovascular accident, sleeping pills poisoning) caused by coma identification, For patients with delayed encephalopathy, with other mental illness, Parkinson's disease, cerebrovascular disease and other differential diagnosis.Appendix B(Normative appendix) Determination of blood carbon oxynucleotides Determination of blood carbon - oxygen hemoglobin by spectrophotometry Principle of B.1.1 The blood contains hemoglobin (Hb), oxygen hemoglobin (HbO2), carboxyhemoglobin (HbCO) and Trace methemoglobin (MetHb). HbO2 and MetHb were reduced to Hb by the reducing agent sodium dithionite Only contains HbCO and Hb two components. HbCO has a maximum absorption peak at 420 nm, Hb has a maximum absorption peak at 432 nm, The absorbance values of the measured blood samples at this two wavelengths were measured, and in the formula containing the previously measured HbCO and Hb absorbance coefficients, The saturation of HbCO can be obtained. B.1.2 Instruments and reagents a) Domestic 721 or 751 spectrophotometer; b) carbon monoxide (cylinders or carbon monoxide generators as described in B.2); c) cylinder oxygen; d) cylinder nitrogen; e) Blood dilution (Tris solution). 1.21 g of trimethylolmethane (analytically pure) was weighed and dissolved in 1000 ml of hot In the water; f) sodium dithionite (analytical grade). B.1.3 Operating Procedures B.1.3.1 take 10ml plug test tube 2 (one for the reagent blank tube, the other for the measurement tube). Each put two pieces of glass beads And filled with Tris solution (about 13 ~ 15ml, the volume difference does not affect the determination of accuracy), blank tube by adding 40mg dithionite Sodium, upside down mix. B.1.3.2 with hemoglobin tube sucking ear blood 5μl, into the test tube, plus sodium dithionite 40mg; filled Tris dilution Liquid after the cover plug (do not enter the bubble), upside down mix. 10 ~ 15min after the color. B.1.3.3 Reagent the reagent blank tube and the measuring tube into the 1cm cuvette, respectively. Stamped (not into the bubble). To reagent Blank liquid zero, record the measured solution 420,432 nm absorbance value (ie, human A420, A432). B.1.4 Saturation calculation The HbCO saturation is calculated as follows. ) () ( (%) 420420432432432420 432420420432 × • - • = HbHbCOHbHbCO HbHb aaAaaA aAaAHbCO Where.,, - Hb and HbCO are at the wavelengths of 420 and 432 nm number. Hba420 Hba432 HbCOa420 HbCOa432 B.1.5 Determination of absorbance B.1.5.1 take no smoking, do not contact carbon monoxide gas healthy human blood 2ml, plus anticoagulant heparin 1%, save stand-by. B.1.5.2 take a 5 ml test tube, take the original blood 0.5 ml, diluted with Tris 2 ml. B.1.5.3 Take the above diluted blood 0.15 ~ 0.2ml, into the 100ml Erlenmeyer flask, add 60ml Tris liquid mixture. B.1.5.4 Preparation of HbO2 solution. 1.5.3 blood dilution oxygen 20min (30ml/min). B.1.5.5 Preparation of HbCO solution. B 1.5.4 HbO2 liquid in half, into the dry 50ml Erlenmeyer flask, through the oxidation Carbon 20 min (30 ml/min). B.1.5.6 Take a 10ml test tube, filled with B. 1.5.5 HbCO solution, then add sodium dithionite 40mg. Cover Bubbles), mix, test. B.1.5.7 Preparation of Hb solution. The remaining half of the B.1.5.4 HbO2 liquid was passed through a humidified nitrogen (i.e., nitrogen was passed through a room temperature Distilled water container to saturate the water vapor), after 15 min, filled with another 10 ml test tube. And joined 40 mg of Lian Ya Sodium sulfate, gasser (do not enter the bubble), mix to be measured. B.1.5.8 Read the B1.5.6 HbO solution and B1.5.7 Hb two liquids at the wavelength of 420,432 nm according to B1.3.3 Value is. Hba420, Hba432 HbCOa420 HbCOa432 B.1.6 Precautions a) Sodium dithionite is susceptible to failure in the air and should be used in vials. Avoid contact with air and moisture. b) Absorbance factor determination must use fresh blood. c) Absorbance values should be checked regularly. d) containing HbCO test solution should try to avoid contact with air, timely color, otherwise it will result in low results. B.2 carbon monoxide gas generation method In a flask equipped with a dropping funnel and a gas outlet tube, 85% formic acid (analytical grade) was added. Self-dropping funnel with concentrated sulfuric acid. The resulting carbon monoxide is introduced into a 2% NaOH wash gas bottle and poured into the HbO2 solution. The operation should be carried out in a good fume hood. ......Tips & Frequently Asked Questions:Question 1: How long will the true-PDF of GBZ23-2024_English be delivered?Answer: Upon your order, we will start to translate GBZ23-2024_English as soon as possible, and keep you informed of the progress. The lead time is typically 1 ~ 3 working days. The lengthier the document the longer the lead time.Question 2: Can I share the purchased PDF of GBZ23-2024_English with my colleagues?Answer: Yes. 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