GBZ 23-2002 Diagnostic criteria for occupational acute carbon monoxide poisoning

This standard applies to acute poisoning caused by inhalation of high concentrations of carbon monoxide in production activities such as the steel industry, chemical industry, gas, coal, and transportation. This standard can also be used for the diagnosis of acute carbon monoxide poisoning in daily life. Whether long-term exposure to low concentrations of carbon monoxide can cause "chronic carbon monoxide poisoning" is still controversial and does not fall within the scope of application of this standard. GBZ 23-2002 Occupational Acute Carbon Monoxide Poisoning Diagnosis Standard GBZ23-2002 Standard Download Decompression Password: www.bzxz.net

ICs13.100
National Occupational Health Standard of the People's Republic of China GBZ23-2002
Diagnostic Criteria of Occupational Acute Carbon Monoxide Poisoning2002-04-08 Issued
2002-06-01 Implementation
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 GB8781-1988 and this standard, this standard shall prevail. Carbon monoxide is a widely distributed asphyxiating gas, and jobs that are exposed to carbon monoxide exist in more than 70 industries. Inhalation of high concentrations of carbon monoxide can cause acute poisoning, and the number of cases and deaths ranks among the top in acute occupational chemical poisoning in my country. This standard is formulated to protect the health of workers and effectively prevent and control occupational acute carbon monoxide poisoning. Appendix A of this standard is an informative appendix, and Appendix B is a normative appendix. This standard is proposed and managed by the Ministry of Health of the People's Republic of China. This standard was drafted by the Institute of Occupational Health and Poison Control of the Chinese Center for Disease Control and Prevention and the Institute of Labor Hygiene of Anshan Iron and Steel Company.
This standard is interpreted by the Ministry of Health of the People's Republic of China. Diagnostic Standard for Occupational Acute Carbon Monoxide Poisoning GBZ23-2002
Acute carbon monoxide poisoning is an acute cerebral hypoxic disease caused by inhaling high concentrations of carbon monoxide (CO); a small number of patients may have delayed neuropsychiatric symptoms. Some patients may also have hypoxic changes in other organs. 1 Scope
This standard applies to acute poisoning caused by inhalation of high concentrations of carbon monoxide in production activities such as the steel industry, chemical industry, gas, coal, and transportation. This standard can also be used for the diagnosis of acute carbon monoxide poisoning in daily life. Whether long-term exposure to low concentrations of carbon monoxide can cause "chronic carbon monoxide poisoning" is still controversial and does not fall within the scope of application of this standard. 2 Normative references
The clauses in the following documents become the clauses of this standard through reference in this standard. For all references with dates, all subsequent amendments (excluding errata) or revisions are not applicable to this standard. However, the parties who reach an agreement based on this standard are encouraged to study whether the latest versions of these documents can be used. For all undated references, the latest versions are applicable to this standard.
3 Diagnostic principles
Diagnostic criteria for occupational acute chemical toxicity neurological diseases Based on the history of exposure to high concentrations of carbon monoxide and the symptoms and signs of acute central nervous system damage, combined with the results of timely determination of carboxyhemoglobin (HbCO) in the blood, on-site hygiene surveys and data on determination of carbon monoxide concentration in the air, and after excluding other causes, acute carbon monoxide poisoning can be diagnosed. 4 Contact reactions
Symptoms such as headache, dizziness, palpitations, and nausea appear, and the symptoms disappear after inhaling fresh air. 5 Diagnosis and classification standards
5.1 Mild poisoning
With any of the following symptoms:
a) Severe headache, dizziness, weakness in limbs, nausea, vomiting; b) Mild to moderate disturbance of consciousness, but no coma. The blood carboxyhemoglobin concentration may be higher than 10%. 5.2 Moderate poisoning
In addition to the above symptoms, the disturbance of consciousness is manifested as shallow to moderate coma, and recovered after rescue without obvious complications. The blood carboxyhemoglobin concentration may be higher than 30%. 5.3 Severe poisoning
Those with any of the following:
5.3.1 The degree of impaired consciousness reaches deep coma or decerebrate state5.3.2 Patients with impaired consciousness and any of the following manifestations:a)
Cerebral edema:
Shock or severe myocardial damage:
Pulmonary edema;
Respiratory failure;
Upper gastrointestinal bleeding;
Focal brain damage such as pyramidal system or extrapyramidal system damage signs. Blood carboxyhemoglobin concentration can be higher than 50%. 5.4 Delayed encephalopathy (neuropsychiatric sequelae) of acute carbon monoxide poisoning After the recovery of consciousness disorder in acute carbon monoxide poisoning, after a "false recovery period" of about 2 to 60 days, one of the following clinical manifestations appears: bzxZ.net
a) Mental and consciousness disorders are in the form of dementia, delirium or decerebrate cortex: b) Extrapyramidal nerve disorders show the manifestation of Parkinson's syndrome: Pyramidal nerve damage (such as hemiplegia, positive pathological reflexes or urinary incontinence, etc.): d) Focal functional disorders of the cerebral cortex such as aphasia, blindness, etc., or secondary epilepsy. Head CT examination can reveal pathological areas of decreased density in the brain: EEG examination can reveal moderate and severe abnormalities. Treatment principles
6.1 Treatment principles
6.1.1 Move the patient away from the poisoning site to a ventilated place quickly, loosen the collar, keep warm, and closely observe the consciousness state. 6.1.2 Provide first aid and treatment in time
For mild poisoning, oxygen inhalation and symptomatic treatment can be given a)
b) For moderate and severe poisoning, oxygen inhalation with normal pressure masks should be actively given, and hyperbaric oxygen treatment should be given if conditions permit. For severe poisoning, symptomatic and supportive treatments such as eliminating cerebral edema, promoting cerebral blood circulation, maintaining respiratory and circulatory functions, and sedation should be given according to the condition. Strengthen nursing care, actively prevent and treat complications, and prevent delayed encephalopathy. 6.1.3 For delayed encephalopathy, hyperbaric oxygen, glucocorticoids, vasodilators or anti-Parkinson's disease drugs and other symptomatic and supportive treatments can be given.
6.2 Other treatments
6.2.1 After being cured, mild poisoning patients can still engage in their original work. 6.2.2 After moderate poisoning is cured, the person should temporarily leave the carbon monoxide work and undergo regular reexamination. If there is no delayed encephalopathy after 2 months of observation, he/she can still do the original work. 6.2.3 Even if the person is cured after treatment, he/she should be transferred away from the carbon monoxide work. 6.2.4 If the person is still left with incomplete organic nerve damage after half a year of treatment for severe poisoning or delayed encephalopathy, he/she should be permanently transferred away from the work of contact with carbon monoxide and other neurotoxicants. Arrange treatment and rest according to the condition. Instructions for the correct use of this standard
See Appendix A (Informative Appendix) and Appendix B (Normative Appendix). Appendix A
(Informative Appendix)
Instructions for the correct use of this standard
A.1 The labor hygiene survey data of the poisoning site and the results of timely measurement of carbon monoxide concentration in the air are of reference significance for diagnosis.
A.2 The main clinical manifestation of this disease is central nervous system damage caused by acute cerebral hypoxia, so different degrees of consciousness disturbance are important bases for clinical diagnosis and classification (see GBZ76). A.3 Acute carbon monoxide poisoning may also cause abnormalities in other organs outside the brain, such as skin erythema and blisters, muscle swelling and pain, abnormal electrocardiogram or liver and kidney function, mononeuropathy or auditory vestibular organ damage, etc. Since these abnormalities do not appear as early as the central nervous system symptoms, are only seen in some patients, or are transient, this standard does not list them as the basis for diagnosis and classification. A.4 Acute carbon monoxide poisoning patients, such as secondary cerebral edema (worsening of consciousness disorder, convulsions or decerebrate rigidity, positive pathological reflexes, increased slow waves on the electroencephalogram or papilledema), pulmonary edema, respiratory failure, shock, severe myocardial damage or upper gastrointestinal bleeding, all indicate that the condition is serious. A.5 If the blood carboxyhemoglobin (HbCO) is higher than 10%, it may indicate a history of exposure to high concentrations of carbon monoxide, which is of reference significance for the diagnosis and differential diagnosis of this disease. However, after leaving the poisoning scene, the HbCO concentration in the blood will decrease, and sometimes it may not be parallel to the degree of clinical manifestations. Therefore, if HbCO detection is not timely, it should not be used as the basis for diagnosis and classification. For patients who stop contact with carbon monoxide for more than 8 hours, since HbCO is mostly below 10%, it is generally unnecessary to perform HbCO examination. A.6 Delayed encephalopathy and sequelae of acute carbon monoxide poisoning are different. The latter's symptoms are directly continued from the acute phase, while delayed encephalopathy refers to the sudden appearance of encephalopathy symptoms characterized by mental disorders, extrapyramidal system or pyramidal system damage after a period of false recovery (2 to 60 days) after waking up from a coma due to acute carbon monoxide poisoning. Therefore, patients with moderate and severe acute carbon monoxide poisoning should be observed for 2 months after waking up from a coma, and it is advisable to temporarily stop working with carbon monoxide during the observation period. A.7 Mild acute carbon monoxide poisoning needs to be differentiated from colds, hypertension, food poisoning, Meniere's syndrome, etc. Moderate and severe poisoning patients should pay attention to the differentiation from coma caused by other causes (such as diabetes, cerebrovascular accidents, sleeping pill poisoning, etc.). For patients with delayed encephalopathy, differential diagnosis should be made from other mental illnesses, Parkinson's disease, cerebrovascular diseases, etc. Appendix B
(Normative Appendix)
Blood carboxyhemoglobin determination method
B.1 Spectrophotometric determination of blood carboxyhemoglobin B.1.1 Principle
Blood contains reduced hemoglobin (Hb), oxygenated hemoglobin (HbO2), carboxyhemoglobin (HbCO) and trace amounts of methemoglobin (MetHb). Using the reducing agent sodium dithionite to reduce HbO2 and MetHb to Hb, the blood only contains two components: HbCO and Hb. HbCO has a maximum absorption peak at 420nm, and Hb has a maximum absorption peak at 432nm. By measuring the absorbance of the blood sample at these two wavelengths and substituting them into the formula containing the pre-measured HbCO and Hb absorption coefficients, the saturation of HbCO can be obtained.
B.1.2 Instruments and reagents
Domestic 721 or 751 spectrophotometer: carbon monoxide gas (steel cylinder or using a carbon monoxide generator as described in B.2); general oxygen in a steel cylinder;
General nitrogen in a steel cylinder;
Blood diluent (Tris solution): Weigh 1.21g of tris(hydroxymethyl)aminomethane (analytical grade) and dissolve it in 1000ml of hot distilled water:
Sodium dithionite (analytical grade).
B.1.3 Operation steps
B.1.3.1 Take two 10ml stoppered test tubes (one is the reagent blank tube, the other is the assay tube). Put two glass beads in each tube and fill it up with Tris solution (about 1315ml, the volume difference does not affect the accuracy of the measurement). Add 40mg of sodium dithionite to the blank tube and mix it upside down.
B.1.3.2 Use a hemoglobin tube to absorb 5ul of earlobe blood, put it into the assay tube, add 40mg of sodium dithionite: cover the stopper after filling up with Tris diluent (do not let in bubbles), and mix it upside down. After 10-15 minutes, colorimetry is performed. B.1.3.3 Pour the reagent blank tube and the test solution in the assay tube into 1cm of colorimetric blood respectively. Cover (do not let in bubbles). Adjust the zero point with the reagent blank solution and record the absorbance values ​​of the assay solution at 420 and 432nm (i.e. A420 and A432 for humans). B.1.4 Saturation calculation
Hbco saturation is calculated according to the following formula:
Hbco(%)=
A32·a2o-A20·am
-×100
Azoacoa）-As(acoa)
、aico
Where: a2o、a2、aco、
B.1.5 Determination of absorbance coefficient
The absorbance coefficient of Hb and HbCO solution at 420 and 432nm wavelengths B.1.5.1 Take 2ml of blood from a healthy person who does not smoke and is not exposed to carbon monoxide gas, add 1% heparin as an anticoagulant, and store for later use. B.1.5.2 Take a 5ml test tube, absorb 0.5ml of the original blood, and dilute it with 2ml Tris solution. B.1.5.3 Take 0.15-0.2ml of the above diluted blood, put it into a 100ml conical flask, add 60ml Tris solution and mix well. B.1.5.4 Preparation of HbO2 solution: oxygenate the blood dilution solution in B.1.5.3 for 20min (30ml/min). B.1.5.5 Preparation of HbCO solution: Take half of the HbO2 solution in B.1.5.4, put it into a dry 50ml conical flask, and pass carbon monoxide for 20min (30ml/min).
B.1.5.6 Take a 10ml test tube, fill it with B.1.5.5 HbCO solution, and then add 40mg of sodium dithionite. Cover the stopper (do not let in bubbles), mix well, and wait for testing.
B.1.5.7 Preparation of Hb solution: pass humidified nitrogen through the remaining half of B.1.5.4 HbO2 solution (i.e. pass nitrogen through a container containing distilled water at room temperature to saturate the water vapor). After 15 minutes, fill another 10ml test tube. Add 40mg of sodium dithionite, cover with a stopper (do not allow air bubbles to enter), mix well and wait for testing. B.1.5.8 Read the absorbance values ​​of B1.5.6 HbO solution and B1.5.7 Hb solution at wavelengths of 420 and 432nm according to the conditions of B1.3.3, which are:
amco.ahco
a420, a42,
B.1.6 Precautions
Sodium dithionite is easily ineffective in the air and should be packaged in small bottles for use. Avoid contact with air and moisture. b)
Absorbance coefficient determination must be carried out with fresh blood. Absorbance coefficient values ​​should be checked regularly.
d) The test solution containing HbCO should be kept away from air as much as possible and color comparison should be carried out in time, otherwise the result will be too low. B.2 Carbon monoxide gas generation method
Add 85% formic acid (analytical grade) to a flask equipped with a dropping funnel and a gas outlet tube. Add concentrated sulfuric acid from the dropping funnel. The generated carbon monoxide is introduced into the 2% NaOH gas washing bottle and then poured into the HbO2 solution. The operation should be carried out in a good fume hood.2 Method of generating carbon monoxide gas
Add 85% formic acid (analytical grade) to a flask equipped with a dropping funnel and a gas outlet tube. Add concentrated sulfuric acid from the dropping funnel. The generated carbon monoxide is introduced into a 2% NaOH gas washing bottle and then poured into the HbO2 solution. The operation should be carried out in a well-ventilated hood.2 Method of generating carbon monoxide gas
Add 85% formic acid (analytical grade) to a flask equipped with a dropping funnel and a gas outlet tube. Add concentrated sulfuric acid from the dropping funnel. The generated carbon monoxide is introduced into a 2% NaOH gas washing bottle and then poured into the HbO2 solution. The operation should be carried out in a well-ventilated hood.
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