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GBZ 73-2002 Diagnostic criteria for occupational acute chemical poisoning respiratory diseases

Basic Information

Standard ID: GBZ 73-2002

Standard Name: Diagnostic criteria for occupational acute chemical poisoning respiratory diseases

Chinese Name: 职业性急性化学物中毒性呼吸系统疾病诊断标准

Standard category:National Standard (GB)

state:in force

Date of Release2002-04-08

Date of Implementation:2002-06-01

standard classification number

Standard ICS number:Environmental protection, health and safety >> 13.100 Occupational safety, industrial hygiene

Standard Classification Number:Medicine, Health, Labor Protection>>Health>>C60 Occupational Disease Diagnosis Standard

associated standards

Publication information

publishing house:Legal Publishing House

ISBN:65036.74

Publication date:2004-06-05

other information

Drafting unit:Shanghai Yangpu District Central Hospital, Shenyang Institute of Labor Hygiene and Occupational Diseases

Focal point unit:Ministry of Health of the People's Republic of China

Proposing unit:Ministry of Health of the People's Republic of China

Publishing department:Ministry of Health of the People's Republic of China

Introduction to standards:

This standard specifies the diagnostic criteria and treatment principles for occupational acute chemical toxicity respiratory diseases. This standard applies to the diagnosis and treatment of occupational acute chemical toxicity respiratory diseases. GBZ 73-2002 Occupational Acute Chemical Toxic Respiratory Disease Diagnosis Standard GBZ73-2002 Standard download decompression password: www.bzxz.net

Some standard content:

ICS 13.100
National Occupational Health Standard of the People's Republic of China GBZ 73-2002
Diagnostic Criteria of Occupational Acute Toxic Pulmonopathy Caused by Chemicals
Published on 2002-04-08
Implemented on 2002-06-01
Published by the Ministry of Health of the People's Republic of China
3
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 GB16852.6-2000 and this standard, this standard shall prevail. The various rules specified in this series of standards involve the diagnosis of occupational acute chemical poisoning. These rules are used to ensure the unification of the diagnostic system of occupational acute chemical poisoning. Regardless of whether the cause is known or hidden, and regardless of which target organ is damaged after poisoning, the diagnosis can be made according to the rules specified in this standard. Under the general title of "Diagnostic Standards for Occupational Acute Chemical Poisoning", the following 10 parts are included: The scope defined in each part will be explained in the foreword and introduction of each part. Part 1
Diagnostic criteria for occupational acute chemical poisoning (general principles); diagnostic rules for occupational acute hidden chemical poisoning: Part 2
Part 3
Part 4
Part 5
Part 6
Part 7
Part 8
Diagnostic criteria for occupational acute chemical poisoning multiple organ dysfunction syndrome; diagnostic criteria for occupational acute chemical sudden death: diagnostic criteria for occupational acute chemical poisoning nervous system diseases: diagnostic criteria for occupational acute chemical poisoning respiratory system diseases; diagnostic criteria for occupational acute toxic liver diseases; diagnostic criteria for occupational acute toxic kidney diseases: Part 9
Diagnostic criteria for occupational acute chemical poisoning heart diseases: Part 10 Diagnostic criteria for occupational acute chemical poisoning blood system diseases: Appendix A of this standard is an informative appendix. Appendix B and C are normative appendices. This standard is proposed and managed by the Ministry of Health of the People's Republic of China. This standard was drafted by Shanghai Yangpu District Central Hospital and Shenyang Labor Health and Occupational Diseases Research Institute; Shanghai Sixth People's Hospital, Occupational Health and Poison Control Institute of China Center for Disease Control and Prevention, Heilongjiang Labor Health and Occupational Diseases Research Institute, Peking University Third Hospital, Shanghai Chemical Industry Occupational Disease Prevention and Treatment Institute, Huashan Hospital Affiliated to Fudan University, Shanghai Occupational Disease Hospital, School of Public Health of Fudan University, etc. participated in the drafting. This standard is interpreted by the Ministry of Health of the People's Republic of China. GBZ73—2002
Diagnostic Standard for Occupational Acute Chemical Toxic Respiratory Diseases Occupational acute chemical toxicity respiratory diseases refer to systemic diseases with respiratory system structural damage and acute functional disorders caused by short-term exposure to large amounts of chemicals in occupational activities. The most serious cases may develop acute respiratory distress syndrome (ARDS).
1 Scope
This standard specifies the diagnostic standards and treatment principles for occupational acute chemical toxicity respiratory diseases. This standard applies to the diagnosis and treatment of occupational acute chemical toxicity respiratory diseases. 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 to the agreement based on this standard are encouraged to study whether the latest versions of these documents can be used. For all references without dates, the latest versions are applicable to this standard.
GB/T16180
3 Diagnostic principles
Diagnostic criteria for occupational acute chemical toxicity nervous system diseases Diagnostic criteria for occupational acute toxic nephropathy Evaluation of the degree of disability caused by work-related injuries and occupational diseases of workers Based on the occupational history of short-term exposure to a large amount of chemicals, the clinical manifestations of acute respiratory system damage, combined with blood gas analysis and other examination findings, and reference to the on-site labor hygiene survey data, comprehensive analysis, and excluding similar diseases caused by other causes, the diagnosis can be made.
4 Irritation reaction
Patients with transient eye and upper respiratory tract irritation symptoms and no abnormal chest X-ray. 5 Diagnosis and classification standards
5.1.1 Mild toxic respiratory disease
Anyone with any of the following conditions can be diagnosed with mild toxic respiratory disease: a) Symptoms of eye and upper respiratory tract irritation, such as photophobia, tearing, sore throat, choking cough, chest tightness, etc., may also have aggravated cough, slightly mucous sputum, and occasionally blood in the sputum; physical signs include congestion and edema of the conjunctiva and pharynx; coarse breath sounds in both lungs, or scattered dry and wet rales: chest X-ray shows increased, thickened, extended, or blurred lung texture; consistent with acute tracheobronchitis or peribronchitis.
b) Symptoms are mainly asthma, especially difficult to exhale, accompanied by cough, chest tightness, etc. Physical signs include diffuse wheezing in both lungs, and chest X-ray may show no abnormalities. Asthma-like manifestations. 5.1.2 Moderate toxic respiratory disease
Anyone with any of the following conditions may be diagnosed with moderate toxic respiratory disease: a) Choking cough, sputum, shortness of breath, chest tightness, etc.; there may be blood in the sputum, dry and wet rales in both lungs, often accompanied by mild: chest X-ray shows punctate or small patchy shadows in both middle and lower lung fields: consistent with acute bronchopneumonia b) Cough, sputum, chest tightness and shortness of breath are more severe, breath sounds on both sides of the lungs are reduced, and there may be no obvious rales. Chest X-ray shows increased lung texture, widened hilar shadows, unclear boundaries, scattered small punctate shadows and reticular shadows in both lungs, reduced transparency of the lung fields, thickening of horizontal fissures, sometimes bronchial cuff sign and (or) Kline B lines: consistent with acute interstitial pulmonary edema.
c) Cough, expectoration, small to moderate amount of sputum, shortness of breath, mild purple, scattered moist rales in the lungs, chest X-ray shows a single or a few localized round shadows with clear outlines and increased density; consistent with acute localized alveolar pulmonary edemad) History of inhalation of hydrocarbons or other liquid chemicals, severe choking cough, expectoration, blood in sputum, rusty sputum, chest pain, dyspnea, rash, etc., often accompanied by fever, general malaise, etc.; chest X-ray shows thickened lung texture and small patchy shadows, more common on the lower right side, and a few may be accompanied by exudative pleurisy: consistent with acute inhalation 5.1.3 Severe toxic respiratory disease
Any person with any of the following conditions can be diagnosed with severe toxic respiratory disease: a) Severe cough, large amount of white or pink foamy sputum, dyspnea, obvious ulceration, dense moist rales in both lungs, chest X-ray shows that both lung fields have millet-like or cloud-like shadows of varying sizes and blurred edges, which can sometimes merge into large shadows, or are distributed in a butterfly shape: blood gas analysis Pa0z/Fi02≤40kPa (300mmHg); consistent with diffuse alveolar pulmonary edema or central alveolar pulmonary edema.
b) The above conditions are more serious, with a respiratory rate greater than 28 times/min or/and respiratory distress; chest X-ray shows extensive and mostly fused large shadows in both lungs: blood gas analysis oxygen partial pressure/oxygen concentration (Pa0z/Fi02)≤26.7kPa (20CmmHg): consistent with acute respiratory distress syndrome. c) Asphyxia.
d) Complications of severe pneumothorax, mediastinal emphysema or severe myocardial damage. e) Sudden death.
6 Treatment principles
6.1 On-site treatment
Immediately break away from contact, keep quiet and keep warm. Those who have irritation reactions should be closely observed. For patients who have been exposed to poisons that may cause delayed respiratory tract lesions (those with a long incubation period), the observation period should be extended. During the observation period, activities should be avoided and symptomatic treatment should be given. If necessary, preventive treatment drugs such as inhalation sprays, oxygen inhalation, injection of adrenal glucocorticoids, etc., and psychological treatment should be given to help control the progression of the disease. If the eyes are contaminated by chemicals, they must be rinsed thoroughly immediately. Never send to the hospital without rinsing to avoid irreversible serious eye lesions. Skin contamination and chemical burns should also be rinsed thoroughly on site before being sent to the hospital. 6.2
Treatment principles
Keep the airway open
Give nebulizer inhalation therapy, bronchial detoxifiers, defoaming agents such as dimethyl silicone oil, and perform tracheotomy when necessary. 6.2.2 Etiological treatment
If there are indications for the use of chelating agents, special antidotes, or blood purification therapy, use them in time. If a large amount of dust or liquid is inhaled, consider fiberoptic bronchoscopy to suck out the dust or liquid as soon as possible. 6.2.3 Reasonable oxygen therapy
Pay attention to reasonable oxygen therapy, maintain water and electrolyte balance, support treatment and prevent complications. 6.3 Other treatments
After mild and moderate toxic respiratory diseases are cured, the original work can be resumed. After severe toxic respiratory diseases are cured, in principle, they should be transferred away from irritating gas operations. If there are sequelae after acute toxic respiratory diseases, refer to GB/T16180 and treat them properly in combination with actual conditions. Instructions for the correct use of this standard
See Appendix A (Informative Appendix), Appendix B, and Appendix C (Normative Appendix). Appendix A
(Informative Appendix)
Instructions for the correct use of this standardwww.bzxz.net
A.1 There are many types of pathogenic chemicals that cause acute toxic respiratory damage. In Appendix B of this standard, common pathogenic varieties are listed and divided into two categories according to their mode of action, which is convenient for a more comprehensive understanding of the common types of virulence agents. A.2 The diagnostic principles and grading standards of this standard are general and applicable to the diagnosis of acute toxic respiratory diseases caused by various chemical species. When formulating diagnostic standards for various related species, the characteristics of acute poisoning of each species are added under the general diagnostic principles to make it consistent with the actual situation. A.3 Irritant reaction is a transient reaction to contact with irritant gas. It has not yet reached the level of poisoning. There are no obvious signs in the lungs, but there may be scattered rales occasionally. However, in order to prevent and timely discover delayed lesions and avoid aggravation of the condition due to improper treatment, it is included in the grading standard to arouse vigilance. When counting diseases, irritant reactions are not considered as poisoning cases. A.4 The principle of the grading standard is: comprehensive evaluation based on the location, range, nature and degree of hypoxemia of the lesion. In clinical practice, examination items can be selected according to the patient's condition, such as electrocardiogram, myocardial enzyme spectrum, liver and kidney function tests, etc., and judgment can be made from an overall perspective to make diagnosis and grading more practical. A.5 The severity of hypoxia is often closely related to respiratory system lesions, which is particularly obvious in acute poisoning. Therefore, the measured value of oxygen partial pressure (PaO2) is used as a reference indicator for graded diagnosis. Dynamic observation data must be available for evaluation, and technical errors should also be noted. During analysis, it should be understood that hypoxemia and tissue hypoxia are both related and not equivalent concepts, so as to correctly judge the condition. Mild poisoning generally does not cause hypoxemia, and the oxygen partial pressure (PaO2) of blood gas analysis is in the normal range of 10.7kPa~13.3kPa (80mmHg~100mmHg) or occasionally there is short-term mild hypoxemia, and the oxygen partial pressure (PaOz) of blood gas analysis is 8kPa~10.7kPa (60mmHg~80mmHg). Moderate poisoning is often accompanied by mild or moderate hypoxemia, and the oxygen partial pressure (PaO2) of blood gas analysis is 8kPa~10.7kPa (60mmHg80mmHg) or 8kPa~5.5kPa (60mmHg~41mmHg). Severe poisoning is accompanied by severe hypoxemia, and the oxygen partial pressure (PaO2) of blood gas analysis is <5.3kPa (40mmHg). A.6 The diagnostic indicators of acute respiratory syndrome in this standard are formulated with reference to domestic and international data in recent years, and can be applied to ARDS caused by direct and indirect causes. The value of PaO2/FIO2 is used as the main index for toxic diffuse alveolar pulmonary edema, and PaO2/FIO2<26.7kPa is used as the diagnostic index for ARDS, which minimizes the misdiagnosis of non-ARDS as ARDS. In this standard, the difference in diagnostic indicators for diffuse pulmonary edema and ARDS also reflects the difference in severity between the two, which is consistent with the view that there is a quantitative change to a qualitative change from diffuse pulmonary edema to ARDS. The index Q:/Q: reflecting pulmonary shunt is of certain significance for the diagnosis of ARDS, but since Qs/Qt needs to be carried out under oxygen absorption conditions, the mixed venous blood oxygen content needs to be measured during actual measurement, and there is a certain error between the results obtained by the current calculation formula and the actual measurement, A-aDO2, which is often difficult to perform in clinical practice, is also obtained by calculation and is rarely used, so it is not included in this standard. A.7 Aspiration pneumonia often has typical clinical manifestations, and the diagnosis is easy to make. The lesions are generally localized. However, if the amount of liquid or dust inhaled is too large, it can also cause diffuse pulmonary edema, which should be paid attention to. A.8 If the patient has a chronic respiratory disease in the past, after inhaling irritating gases, the condition may be more complicated after poisoning, or it may induce the original respiratory disease. In this case, diagnosis and treatment must take these factors into consideration to determine the graded diagnosis and formulate a treatment plan.
A.9 After severe toxic respiratory damage is cured, various diseases such as chronic bronchitis, emphysema, obstructive bronchiolitis, reactive airways dysfunction syndrome (RADS, reactive airways dysfunction syndrome), etc. may occur. The factors causing the above situation are complicated, and are related to the type of virulence agent, absorption mode, dosage, nature and severity of the lesion, treatment and the patient's health condition before the onset of the disease. It may be that the original disease is induced, or it may have nothing to do with the current poisoning. Therefore, the diagnosis should be comprehensively analyzed to draw an objective and realistic conclusion. It is not possible to diagnose all the above lesions as "sequelae" to avoid deviation. In the future, we should do a better job of tracking and follow-up to accumulate more information to provide accurate indicators for the diagnosis of sequelae. A.10 Etiological treatment refers to various treatment measures that promote the discharge of virulence agents or target their pathogenesis. Different treatment methods are used according to different types of poisons.
A.11 Hypoxia can cause many serious consequences, such as damage to mitochondria, insufficient and depleted adenosine triphosphate (ATP), and accelerated degradation of membrane phospholipids, leading to damage to biological membranes, overload of intracellular calcium ions, and increased generation of oxygen free radicals. These conditions further aggravate hypoxia and form a vicious circle. Therefore, early correction of hypoxia and control of disease progression are important links to prevent treatment contradictions. The oxygen supply method can be selected according to the patient's condition and objective conditions, and oxygen poisoning can be prevented under the condition of inhaling high-concentration oxygen. Blood gas analysis can be used as a monitoring indicator. The principle is to select the appropriate oxygen supply method according to the condition, use the lowest effective concentration of oxygen, and correct hypoxemia in the shortest time. Maintain the arterial oxygen partial pressure at 10.7kPa~13.3kPa (80mmHg~100mmHg). Severe patients are given positive ventilation from the mask (intermittent positive pressure oxygen supply) or positive end-expiratory pressure ventilation (PEEP) therapy. The end-expiratory pressure should be around 0.5kPa (5cmH,O column). High-frequency ventilation (HFV) or high-frequency jet ventilation has little effect on cardiac function and can achieve certain therapeutic effects. It can also be used. Inverse ventilation (IRV, inverseratio-ventilation) can also be used to treat ARDS. Extrapulmonary oxygen supply, such as photon blood therapy, can also be considered as an auxiliary treatment. Hyperbaric oxygen was rarely used to treat respiratory diseases in the past, and some people believed that it was a general contraindication for the treatment of ARDS. However, in recent years, there have been reports in China that hyperbaric oxygen has been used to treat acute toxic pulmonary edema and acute respiratory distress syndrome and has achieved certain efficacy. However, no consistent conclusion has been reached through clinical observation and animal experiments. Therefore, more data are needed to explore treatment indications and evaluate efficacy. Therefore, it cannot be included in the appendix as a routine treatment measure for reference. For example, when using hyperbaric oxygen, the air pressure used is relatively low [130~170kPa (1.3~1.7atm)], and the time is preferably 30~40min. A.12 Nonspecific antagonists are based on the pathogenesis of acute chemical toxic pulmonary edema and ARDS, and drugs are given to the main links of the disease to antagonize its effects and block the pathophysiological evolution of ARDS, so as to achieve the purpose of reducing lung and systemic damage. Therefore, it is one of the main treatment measures in rescue. Commonly used ones include adrenocortical hormones, oxygen free radical scavengers, calcium channel blockers, etc. The indications for the use of these drugs, the selection of drug types, dosages and courses of treatment, etc., can be reasonably used in the rescue according to the condition and the experience of the rescue team. A.13 Maintain good circulatory function, such as maintaining appropriate blood volume, improving cardiac pump function and correcting microcirculatory disorders, preventing microthrombosis, etc. Commonly used drugs include 6-542, Danshen, Chuanxiong, etc. A.14 Correct acid-base and electrolyte disorders In the course of pulmonary edema and ARDS, there are many types of acid-base poisoning, such as respiratory alkalosis caused by hyperventilation in the early stage, severe hypoxia with CO2 retention in the late stage, mixed acidosis, etc. There are also various electrolyte disorders. Targeted treatment measures should be taken according to clinical and laboratory results. A.15 Once a serious toxic respiratory disease develops a serious secondary infection, it will not only make the condition more serious and complicated, but also be one of the main reasons for the contradiction in treatment. A prolonged course of the disease can lead to the hyperplasia of granulation tissue in the lungs. Although the patient's survival period is prolonged, his life cannot be saved. Therefore, from the onset of the disease, various measures should be taken to prevent secondary infection, and close monitoring, timely detection and control are important links in treatment. A.16 Nutritional support. For acute and critically ill patients, in the high metabolic state, excessive energy consumption and insufficient nutrition intake during the course of the disease will lead to reduced immunity, easy secondary infection, respiratory muscle fatigue, and affect tissue repair. Therefore, nutritional support should be given as soon as possible, and calories should be supplemented in time. The total daily calories are about 150kJ/kg, and protein and fat account for about 20% and 30% of the total calories respectively.
A,17 Strengthen nursing work. During the whole process, improving nursing quality is the main link in rescue. A.18 The formulation of treatment plans should be guided by holistic thinking. Comprehensive treatment measures should be used for serious diseases, but medication should not be too abused. The efficacy and side effects should be closely observed. The treatment method should be adjusted in time according to the changes in the condition and preventive measures should be emphasized. Support and psychological treatment are very important to promote recovery. Patients with moderate and severe poisoning should be given necessary rehabilitation treatment during the recovery period.
A.19 Bedside chest X-rays are used for monitoring critically ill patients. Therefore, Appendix C of the standard proposes bedside radiography requirements for reference when using.
A.20 With the progress of scientific research, new methods and drugs are provided for clinical diagnosis and treatment, such as new diagnostic indicators, advanced imaging diagnostic methods and treatment measures. For example, exogenous nitric oxide is used to improve pulmonary perfusion: surfactant extracted from nature or artificially made is used; acinar is used for treatment, and intravenous oxygenator has been successfully developed to improve the shortcomings of PEEP. These drugs and measures have been reported for clinical application, but further research is needed before they can be widely used, so they are not included in this standard. Therefore, timely grasp the relevant information and apply it in combination with clinical practice. , and accumulate data to continuously improve the level of diagnosis and treatment, and contribute to the development of this discipline. A.21 Notes on reading films:
A.21.1 When performing bedside photography, the patient's position, photography position, respiratory state and focal length are different from those of conventional chest photography, and the imaging of various structures of the human body on the chest film also changes accordingly. Because the scapular swelling cannot be avoided outside the lung field, the sternoclavicular joint is not required to be symmetrical.
A.21.2 Before reading the film, you must understand the patient's condition and the photography conditions during the filming. A.21.3
When reading the film, you must fully consider the impact of different patients and photography conditions on the image. B.1 Toxic substances that directly damage respiratory tissues B.1.1 Irritant gases
Appendix B
(Normative Appendix)
Common types of virus-causing substances
B.1.1.1 Acids: nitric acid, hydrochloric acid, sulfuric acid, chromic acid, chlorosulfonic acid, etc. B.1.1.2 Nitrogen oxides: nitric oxide, nitrogen dioxide, nitrogen pentoxide, etc. B.1.1.3
Chlorine and other compounds: chlorine, hydrogen chloride, chlorine dioxide, phosgene, diphosgene, chloropicrin, maple dichloride, silicon tetrachloride, trichlorosilane, titanium tetrachloride, antimony trichloride, arsenic trichloride, phosphorus trichloride, phosphorus oxychloride, phosphorus pentachloride, boron trichloride, etc.
Sulfur compounds: sulfur dioxide, sulfur trioxide, hydrogen sulfide, etc. B.1.1.5
B.1.1.6 Ozone.
Ester: dimethyl sulfate, methyl formate, toluene diisocyanate, methyl chloroformate, etc. B.1.1.8
Metal compounds: silver oxide, hydrogen selenide, nickel pyrophosphate, vanadium pentoxide, etc. B.1.1.9
Aldehydes: formaldehyde, aldehyde, acrolein, trichloroacetaldehyde, etc. B.1.1.10
Fluorinated hydrocarbons: octafluoroisobutylene, fluorophosgene, hexafluoropropylene, cracking residual gas and pyrolysis gas of fluoropolymers, etc. Others: diborane, chloromethyl methyl ether, carbon tetrachloride, monomethylamine, dimethylamine, epichlorohydrin, etc. B.1.1.11
Military poisonous gases: nitrogen mustard, Adam's gas, Lewis gas, etc. B.1.1.12
Irritating metals: beryllium, cadmium, mercury, manganese, carbonyl nickel, vanadium pentoxide. B.1.3
Organic solvents: gasoline, kerosene, lubricating oil, diesel, etc. B.1.4Organic pesticides: organic phosphates, methyl bromide, phosphine, paraquat, etc. B.1.5Others: such as smoke from the combustion of certain substances, etc. B.2
Compounds that cause acute respiratory distress syndrome (ARDS) due to indirect damage. Severe toxic encephalopathy, liver disease, kidney disease, etc. caused by acute chemical poisoning can induce ARDS during the course of the disease. It is a common manifestation of multiple organ failure caused by acute poisoning and is an indirect damage-induced ARDS, which is more common in acute carbon monoxide poisoning, acute sodium pentachlorophenol poisoning, etc.
Appendix C
(Normative Appendix)
Special requirements for bedside chest radiography
C.1 Bedside chest radiography uses high-voltage photography technology. Technical specifications are the same as GB5906. 2 Before the existing bedside machine in this unit is updated, it is allowed to take chest radiographs with ordinary technology. C.2
Position: If the condition permits, take an anteroposterior chest radiograph in a sitting or semi-recumbent position as much as possible. Target-film distance: more than 90cm.2
Compounds that cause acute respiratory distress syndrome (ARDS) by indirect damage. Severe toxic encephalopathy, liver disease, kidney disease, etc. caused by acute chemical poisoning can induce ARDS during the course of the disease. It is a common manifestation of multiple organ failure caused by acute poisoning and belongs to ARDS caused by indirect damage. It is more common in acute carbon monoxide poisoning, acute sodium pentachlorophenol poisoning, etc.
Appendix C
(Normative Appendix)
Special requirements for bedside chest radiography
C.1 Bedside chest radiography uses high-voltage photography technology. Technical specifications are the same as GB5906. 2 Before the existing bedside machine in this unit is updated, it is allowed to take chest radiographs with ordinary technology. C.2
Position: If the condition permits, take an anteroposterior chest radiograph in a sitting or semi-recumbent position as much as possible. Target-film distance: more than 90cm.2
Compounds that cause acute respiratory distress syndrome (ARDS) by indirect damage. Severe toxic encephalopathy, liver disease, kidney disease, etc. caused by acute chemical poisoning can induce ARDS during the course of the disease. It is a common manifestation of multiple organ failure caused by acute poisoning and belongs to ARDS caused by indirect damage. It is more common in acute carbon monoxide poisoning, acute sodium pentachlorophenol poisoning, etc.
Appendix C
(Normative Appendix)
Special requirements for bedside chest radiography
C.1 Bedside chest radiography uses high-voltage photography technology. Technical specifications are the same as GB5906. 2 Before the existing bedside machine in this unit is updated, it is allowed to take chest radiographs with ordinary technology. C.2
Position: If the condition permits, take an anteroposterior chest radiograph in a sitting or semi-recumbent position as much as possible. Target-film distance: more than 90cm.
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