GBZ 66-2002 Diagnostic criteria for occupational acute organic fluoride poisoning
Some standard content:
ICS13.100
National Occupational Health Standard of the People's Republic of China GBZ 66—2002
Diagnostic Criteria of Occupational Acute Fluorohydrocarbon PoisoningPublished on April 8, 2002
Implemented on June 1, 2002
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 the original standard GB4867-1996 is inconsistent with this standard, this standard shall prevail. Acute poisoning may be caused by inhalation of organic fluorine monomers, cracking gases, residual liquid gases and pyrolysis gases of fluoropolymers during the production, processing and use of organic fluorine materials. This standard highlights the characteristics of acute organic fluorine poisoning. According to the degree of damage to the respiratory system of the main target organ of organic fluorine poisoning, the diagnostic classification has been modified, and toxic myocardial damage has been included in moderate poisoning, making the diagnosis of this standard clearer, more reasonable and easier to use. 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 is drafted by the Shanghai Chemical Occupational Disease Prevention and Control Institute. This standard is interpreted by the Ministry of Health of the People's Republic of China..com Occupational acute organic fluorine poisoning diagnostic standard GBZ66-2002
Occupational acute organic fluorine poisoning refers to a systemic disease with respiratory damage as the main cause caused by workers inhaling excessive organic fluorine monomer cracking gas, residual liquid gas or thermal decomposition gas for a short time in the production environment. 1 Scope
This standard specifies the diagnostic criteria and treatment principles for occupational acute organic fluorine poisoning. This standard applies to acute poisoning caused by inhalation of monomers such as tetrafluoroethylene and hexafluoropropylene; cracking gas and residual liquid gas such as difluoromonochloromethane; thermal decomposition gas of fluoropolymers such as polytetrafluoroethylene, polyperfluoroethylene propylene, and polytrifluorochloroethylene during the production, processing, and use of organic fluorine materials.
Acute organic fluorine pesticide poisoning and fluoroether poisoning are not within the scope of this standard. Normative referenced documents
The clauses in the following documents become clauses of this standard through reference in this standard. For all dated referenced documents, all subsequent amendments (excluding errata) or revisions are not applicable to this standard. However, parties to an agreement based on this standard are encouraged to study whether the latest versions of these documents can be used. For all undated referenced documents, the latest versions shall apply to this standard.
3 Diagnostic principles
Diagnostic criteria for pneumoconiosis
Based on a definite history of short-term, excessive inhalation of organic fluorine gas, combined with clinical manifestations, chest X-rays, electrocardiograms and other related examination results, comprehensive analysis, and exclusion of other diseases before diagnosis. 4 Observation subjects
After inhaling organic fluorine gas, symptoms of upper respiratory tract infection appear, and the symptoms gradually improve after 72 hours of observation, and there is no cardiopulmonary injury. 5 Diagnosis and grading standardsbzxz.net
5.1 Acute poisoning
5.1.1 Mild poisoning
Symptoms include headache, dizziness, cough, sore throat, nausea, chest tightness, fatigue, and scattered dry rales or a small amount of wet rales in the lungs. Chest X-rays show signs of enhanced lung texture and blurred edges in the middle and lower lung fields of both lungs, which are consistent with the clinical signs of acute bronchitis and peribronchitis.
5.1.2 Moderate poisoning
Anyone with any of the following conditions can be diagnosed as moderate poisoning: a) The clinical manifestations of mild poisoning are aggravated, with chest tightness, chest pain, palpitations, dyspnea, irritability and mild flare-ups, localized decrease in lung breath sounds, and more dry or wet rales in both lungs. The chest X-ray shows enhanced lung texture, extensive reticular shadows, and scattered small dot-like shadows, which reduce the transparency of the lung field, or widening of the horizontal fissure, bronchial cuff signs, and occasional Kerley's B line, which are consistent with the clinical signs of interstitial pulmonary edema. b) Symptoms and signs are as above, with increased lung texture in the middle and lower lung fields, patchy shadows distributed along the lung texture, mostly seen in the middle and inner bands, and can merge into pieces when they are dense, which is consistent with the clinical signs of bronchopneumonia. ..com5.1.3 Severe poisoning
Anyone with any of the following conditions can be diagnosed as severe poisoning: a) Acute alveolar pulmonary edema:
b) Acute respiratory distress syndrome (ARDS); c) Toxic myocarditis:
d) Complicated with mediastinal emphysema, subcutaneous emphysema, and pneumothorax. 5.2 Fluoropolymer fume fever
After inhaling the pyrolysis of organic fluorine polymers, metal fume fever-like symptoms such as chills, fever, chills, and muscle aches appear: accompanied by cough, chest tightness, headache, nausea, vomiting, etc., which generally subside within 24 to 48 hours. 6 Treatment principles
6.1 Treatment principles
6.1.1 Anyone with a definite history of accidental inhalation of organic fluorine gas, regardless of whether they have subjective symptoms or not, must leave the scene immediately, absolutely stay in bed, undergo necessary medical examinations and preventive treatment, and observe for 72 hours. 6.1.2 Give oxygen in the early stage, and the oxygen concentration should be generally controlled within 50% to 60%. Use pure oxygen and hyperbaric oxygen with caution. In case of acute respiratory distress syndrome, lower pressure positive end-expiratory pressure breathing (PEEPO.5kPa or so) can be used. 6.1.3 Apply glucocorticoids as soon as possible, in sufficient quantity, and for a short period of time. Emphasize that all observation subjects and poisoned patients should be given preventive treatment such as intravenous injection of glucocorticoids on the spot. For poisoned patients, the dose can be appropriately increased on the first day after poisoning according to the severity of the disease, and then sufficient short-term intravenous administration can be given. For moderate and above poisoning patients, small doses of glucocorticoids can be continued intermittently after the acute phase to prevent and treat pulmonary fibrosis. 6.1.4 To maintain airway patency, ultrasonic atomization inhalation such as bronchial spasmolytics can be given. Those who cough up a lot of foamy sputum should use defoaming agent dimethyl silicone oil (defoaming net) early. Tracheotomy can be performed after dyspnea is ineffective after medical treatment measures. 6.1.5 When toxic myocarditis and other clinical signs occur, the treatment principles are generally the same as those of internal medicine. 6.1.6 Rationally select antibiotics to prevent and treat secondary infections. 6.1.7 Fluoropolymer fume fever is generally treated symptomatically. Those with recurrent illnesses should be given treatment to prevent and treat pulmonary fibrosis. 6.2 Other treatments
6.2.1 Cure criteria
The patient is considered cured when the clinical manifestations caused by acute poisoning disappear and the results of relevant examinations such as chest X-rays basically return to normal. 6.2.2 After the poisoning patient is cured, he or she may resume his or her original work; if the patient has residual lung and heart function impairment after poisoning, he or she should be transferred from the original job and undergo regular reexamination.
7 Instructions for the correct use of this standard
See Appendix A (Informative Appendix) and Appendix B (Normative Appendix). ..comAppendix A
(Informative Appendix)
Instructions for the correct use of this standard
A.1 When using this standard, a clear history of accidental occupational inhalation of organic fluorine gas must be available. Fluorine-containing polymers themselves are non-toxic and will not cause acute poisoning, but accidental inhalation of organic fluorine monomers, cracking gases, residual liquid gases, and fluoropolymer thermal decomposition gases can all cause acute organic fluorine poisoning.
Organic fluorine monomers refer to a monomer in the component fluorine-containing polymers, such as tetrafluoroethylene, difluorochloromethane, trifluorochloroethylene, hexafluoropropylene, etc.
Cracking gas refers to the reaction by-products produced when organic fluorine monomers are prepared by high-temperature cracking. For example, the cracking gas produced when tetrafluoroethylene is prepared by high-temperature cracking of difluorochloromethane (F22), the components of which are more than 10 reaction products such as tetrachloroethylene, hexafluoropropylene, and octafluoroisobutylene.
Residual liquid gas refers to the residual liquid left after high-temperature cracking to prepare monomers. It is a gaseous compound at room temperature, including extremely toxic octafluoroisobutylene, etc.
Pyrolysis gas refers to the gaseous pyrolysis product of fluorinated polymers at high temperature. The pyrolysis product above 400°C contains highly toxic fluorophosgene and hydrogen fluoride, etc.
A.2 Certain components of organic fluorine gas, such as fluoroalkanes and olefins, have obvious myocardial damage effects. Myocardial damage and various types of arrhythmias are shown in the electrocardiogram of patients with this disease. After excluding previous organic heart diseases, even if the lesions on the chest X-ray are relatively mild, they can still be diagnosed as toxic myocarditis and should be treated as severe poisoning. A.3Organic fluorine gas is a highly toxic substance that affects the lungs, but patients with this disease may also have transient liver and kidney dysfunction, the degree of which is often mild, and generally they can recover without special treatment. The diagnostic classification should still be based on the clinical manifestations of the respiratory system and chest X-rays.
A.4. Regarding the "early, sufficient, and short" principle of using glucocorticoids, all observation subjects and poisoned patients should be given preventive medication on site. Dexamethasone 10mg + 25% glucose solution 40mL can be slowly injected intravenously. Although the observation subjects are not in the category of acute poisoning, hormone preventive treatment can still be used for 1 to 3 days during the observation period. For mild, moderate, and severe poisoning, dexamethasone 20-60mg/d or hydrocortisone 400-200mg/d can be used intravenously according to the condition within the first 1 to 5 days of poisoning. The drug can be stopped quickly after the symptoms of the acute phase of mild poisoning are controlled. After the acute phase of moderate and above poisoning patients, small doses of oral glucocorticoids can be continued for about 2 to 4 weeks to prevent pulmonary fibrosis.
A.5 Fluoropolymer fume fever usually occurs during the hot processing of polytetrafluoroethylene and polyperfluoroethylene propylene. The sintering temperature is around 350-380℃. The workers inhale the pyrolysis products, which cause a cold-like reaction. The symptoms are similar to metal fume fever. It is a special clinical type. Generally, antipyretic and analgesic treatment is given and the patient recovers within 24-48 hours. However, for patients with repeated attacks, literature reports that pulmonary fibrosis can occur, so anti-pulmonary fibrosis treatment should be given. A.6 The early symptoms of poisoning in this disease are atypical, so the occupational exposure history of organic fluorine monomers, cracks, and pyrolysis gases (products) is extremely important. For those listed as observation objects, it is emphasized that they should rest in bed, reduce oxygen consumption, and be under close medical observation. In the early stage, attention should be paid to distinguishing from the common cold, acute tonsillitis, and acute gastroenteritis. Appendix B
(Normative Appendix)
Technical requirements for bedside chest X-ray filming and notes for reading films B.1 Position: Take an anteroposterior chest film in a sitting or semi-recumbent position as much as possible. The chest radiograph must include the entire thorax and the costophrenic angles on both sides: the sternoclavicular joints on both sides are symmetrical, and the target-film distance is 100cm. B.2 Exposure: There is no breathing movement during exposure. The lungs, bones and soft tissues have good contrast and layers, and the 1st to 4th thoracic vertebrae are clearly visible. The exposure time should be as short as possible, which should be 1/10s or shorter. The center line is aligned with the 5th thoracic vertebra and is perpendicular to the dark box. B.3 Darkroom: The tissue-free area above the shoulders should be dark black, and the area below the diaphragm should be transparent. B.4 Blood distribution in the lungs: When standing in the posteroanterior position, the lung texture in the upper lung field is slender due to the gravity of the blood in the lungs, while when lying, the lung texture in the upper lung field becomes thicker.
B.5 The heart shadow increases and tends to be transverse.
a: The diaphragm is elevated, causing the heart to move upward and rotate. b When standing in the posteroanterior position, the heart is supported by the diaphragm, and when lying, it is supported by the spine, posterior mediastinum and lungs on both sides. People with weaker heart walls are more likely to change their shape.
C. When standing, a large amount of blood is retained in the vascular bed of the abdominal organs and the sagging parts of the body; when lying down, the amount of blood returning to the heart increases, which significantly increases the heart shadow.
d. When lying down, the target-film distance changes from about 180cm to about 100cm, which significantly increases the heart-to-chest ratio. e. In the standing posteroanterior chest film, the heart is close to the film, and the magnification is small; while in the supine anteroposterior chest film, the distance between the heart and the film increases, the magnification is large, and the heart shadow is also significantly enlarged. B.6 Widening of the large blood vessels in the mediastinum: the shadow of the superior vena cava is more obvious. B.7 The position of the aortic bulb moves up, close to the level of the clavicle. B.8 The overlap of the bilateral scapula and the lung field may also affect the observation of the lesion. A small amount of pleural effusion cannot be displayed when lying down. Therefore, careful observation is required to avoid drawing wrong conclusions. ..com
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