GB 17058-1997 Diagnosis of occupational acute chemical poisoning Part 10: Diagnosis of occupational acute chemical poisoning blood system diseases
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GB17058—1997
In various occupational activities, people may be exposed to some high-concentration and highly toxic chemicals in a short period of time, and then suffer from acute poisoning. These chemicals may be known species, or their exact pathogenic species may not be known after poisoning has occurred. Some species of poisoning are listed in the "List of Occupational Diseases", while others are not yet included; some have independent diagnostic standards, while others have not yet developed independent diagnostic standards. However, all acute poisoning diseases have common pathogenic laws, and if necessary, rules that should be followed in diagnosing acute poisoning can also be formulated. The various rules specified in this standard 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 by poisoning, the diagnosis can be made according to the rules specified in this standard. Under the general title of "Diagnosis of Occupational Acute Chemical Poisoning", the following 10 parts are included. Part 1: General Principles for the Diagnosis of Occupational Acute Chemical Poisoning; Part 2: Diagnosis of Occupational Acute Hidden Chemical Poisoning; Part 3: Diagnosis of Multiple Organ Failure in Occupational Acute Poisoning; Part 4: Diagnosis of Sudden Death from Occupational Acute Chemical Sources; Part 5: Diagnosis of Nervous System Diseases in Occupational Acute Poisoning; Part 6: Diagnosis of Respiratory Diseases in Occupational Acute Chemical Poisoning; Part 7: Diagnosis of Occupational Acute Poisoning Liver Disease; Part 8: Diagnosis of Occupational Acute Poisoning Kidney Disease; Part 9: Diagnosis of Occupational Acute Chemical Poisoning Heart Disease; Part 10: Diagnosis of Occupational Acute Chemical Poisoning Blood System Diseases; This standard specifies the rules for the diagnosis of occupational acute toxic blood system diseases. Appendix A of this standard is a suggestive appendix. This standard was proposed by the Ministry of Health of the People's Republic of China. This standard was drafted by the Heilongjiang Provincial Institute of Labor Health and Occupational Diseases, Shenyang Municipal Institute of Labor Health and Occupational Diseases, and Guangdong Provincial Institute of Occupational Disease Prevention and Control. The participating units include: Liaoning Provincial Institute of Labor Health, Jiangxi Provincial Institute of Labor Health and Occupational Diseases, Union Hospital Affiliated to Tongji Medical University, and Panzhihua Institute of Labor Health and Protection. This standard is interpreted by the Chinese Academy of Preventive Medicine, the technical unit entrusted by the Ministry of Health. 407
National Standard of the People's Republic of China
Diagnosis of occupational acute chemical poisoning
Part 10: Diagnostic criteria of occupational acute toxichematologic diseases
GB17058—1997
Occupational acute chemical poisoning hematologic diseases refer to acute systemic diseases with hematologic damage as the main clinical manifestation caused by workers absorbing large doses of chemicals in a short period of time during their occupational activities. 1 Scope
This standard specifies the diagnostic criteria and treatment principles for occupational acute chemical toxicity blood system diseases. This standard applies to acute toxic blood system diseases caused by exposure to blood poisons listed in Appendix A of this standard during occupational activities. This standard can also be used as a reference for acute toxic blood system diseases occurring in non-occupational activities. 2 Referenced standards
The provisions contained in the following standards constitute the provisions of this standard through reference in this standard. When this standard is published, the versions shown are valid. All standards are subject to revision, and parties using this standard should explore the possibility of using the latest versions of the following standards. GB16852.1-1997 Diagnosis of occupational acute chemical poisoning Part 1: General principles for diagnosis of occupational acute chemical poisoning GB16852.2--1997 Diagnosis of occupational acute chemical poisoning Part 2: Diagnostic rules for occupational acute latent chemical poisoning
GB/T16180-1996 Identification of the degree of disability caused by work-related injuries and occupational diseases 3 Diagnostic principles
Based on the history of occupational exposure to high concentrations of chemical poisons in a short period of time, the appearance of clinical manifestations mainly characterized by blood system damage and related hematological laboratory test results, combined with necessary on-site investigation data, and after excluding other causes, especially blood diseases caused by drugs, it can be diagnosed as occupational acute chemical poisoning blood system disease. 4 Clinical types and diagnostic classification
Common clinical types of blood system diseases caused by occupational acute chemical poisoning are as follows: 4.1 Toxic hemolytic anemia
4.1.1 Mild poisoning: Fatigue, chills, fever, back pain, fatigue, headache, nausea, vomiting, and abdominal pain occur after poisoning. Yellowing of the skin and sclera, anemia appearance. Blood tests show a decrease in red blood cells and hemoglobin, an increase in reticulocytes, and the appearance of Hernzi bodies; urine routine tests show that the urine is red tea-colored, urine occult blood is positive, protein is positive, red and white blood cells and casts are present, and blood urea nitrogen is basically normal. 4.1.2 Severe poisoning: acute onset, sudden chills, high fever, delirium, convulsions, coma, purple, deep yellow sclera, oliguria or anuria, severe anemia, significant decrease in red blood cells and hemoglobin, significant increase in reticulocytes, large number of Hernzi bodies, dark soy sauce-colored urine, strong positive urine occult blood, sharp increase in blood urea nitrogen, and acute renal failure. 4.2 Toxic methemoglobinemia (MHb) 4.2.1 Mild poisoning: Generally, the MHb concentration is above 10%, the area around the lips is purple, and there may be no symptoms. 4.2.2 Moderate poisoning: MHb concentration is 40%~60%, in addition to significant ultraviolet, hypoxia symptoms appear, such as headache, dizziness, fatigue, weakness, body aches, dyspnea, tachycardia, slow reaction, drowsiness, etc. 4.2.3 Severe poisoning: MHb concentration is above 60%, the above symptoms are significantly aggravated, the face is purple, the urine is wine-colored or dark brown, acute circulatory failure, coma, and death may occur. 4. 3 Toxic sulfhemoglobinemia
4.3.1 The main manifestation is hypoxia, which may be purple, headache, etc. Some patients may also have hemolysis of methemoglobin. 4.3.2 Blood sulfhemoglobin accounts for 2% of the total hemoglobin, and even more than 10%. 4.4 Toxic acute aplastic anemia (severe-type I) 4.4.1 Acute onset, progressive anemia, bleeding tendency, infection and fever. 4.4.2 Peripheral blood picture: Red blood cells and hemoglobin decrease rapidly, white blood cells are extremely reduced (neutrophil absolute value <0.5×10°/L), platelets are significantly reduced (<20×10°/L), reticulocytes <1%, absolute value <15×10°/L. 4.4.3 Bone marrow picture: Nucleated cell proliferation is low, granulocytes, erythrocytes and megakaryocytes are significantly reduced, the proportion of lymphocytes is relatively increased, and plasma cells, reticular cells and tissue basophils are easy to see. Bone marrow biopsy shows a decrease in hematopoietic tissue, which is mostly replaced by adipose tissue. 4.5 Toxic agranulocytosis
4.5.1 Acute onset, sudden chills, high fever, sweating, headache, body and joint pain, followed by pharyngitis with submandibular and cervical lymphadenopathy. After a few days, there will be necrotic ulcers, which are common in tonsils, soft tissues, lips, tongue, skin, nasal cavity, rectum, anus and vagina, and sepsis will follow. 4.5.2 Peripheral blood picture: The white blood cell count is extremely reduced, and neutrophils can only account for 1%~~2%. The red blood cell and platelet counts are basically normal. 4.5.3 Bone marrow: In the bone marrow picture, lobed nuclei, rod-shaped nuclei, late and middle myelocytes are often absent, and only a small number of promyelocytes and promyelocytes are seen, but the proportion of plasma cells, lymphocytes and monocytes increases. The erythroid and megakaryocyte lines are roughly normal. 4.6 Toxic vascular purpura
4.6.1 Skin bleeding, mostly seen in the limbs and buttocks, showing edematous petechiae fused into pieces or blood bubbles; there are also blood in the stool, abdominal pain and joint pain. 4.6.2 Platelet count, bleeding or coagulation time is normal. Capillary fragility test is positive. 4.7 Toxic thrombocytopenia
4.7.1 Bleeding is common in the skin of the limbs and the nose, gums, tongue, and oral mucosa. Rare cases include hemoptysis, hematemesis, hematuria, black stools, and fundus and intracranial hemorrhage.
4.7.2 Decreased platelet count (<50×10°/L.) 4.7.3 Bone marrow: decreased megakaryocytes, and normal erythroid and granulocyte cells. There may be a nuclear left shift. 4.7.4 Bleeding time may be prolonged, blood clot retraction is poor, prothrombin consumption time is abnormal, and coagulation time may be normal. 4.7.5 Thrombocytopenia caused by immune mechanism can be detected with platelet membrane-related antibodies. 4.8 Toxic platelet dysfunction
4.8.1 Symptoms vary in severity, and common symptoms include nosebleeds and gingival bleeding.Severe cases may also have subcutaneous hematoma, hematuria, black stool, etc. 4.8.2 Platelet count and blood clotting time are normal. Platelet adhesion and platelet aggregation function are reduced. Platelet factor deficiency or release disorder. Www.bzxZ.net
4.9 Toxic prothrombin synthesis disorder
4.9.1 Epistaxis, gingival bleeding, skin petechiae or ecchymosis, excessive menstrual flow, hematuria, black stool, slight blood and intracranial hemorrhage can be seen. 4.9.2 Prothrombin time (PT) is prolonged, white clay partial thromboplastin time (KPTT) is prolonged, and coagulation time (CT) and recalcification time are prolonged.
Toxic disseminated intravascular coagulation
4.10.1 Seen in various severe chemical poisonings. 409
4.10.2 Multiple bleeding tendencies.
GB 17058—1997
4.10.3 Multiple microvascular thrombosis, symptoms and signs of embolism in the corresponding parts. 4.10.4 Microcirculatory failure and shock that are not easily explained by the primary disease. 4.10.5 Laboratory examination: platelets show a dynamic and persistent decrease, plasma fibrinogen content is less than 1.5g/L or progressively decreases; 3P test is positive or plasma fibrinogen degradation product (FDP) is greater than 20mg/L; PT and KPTT are prolonged, etc. 5 Treatment principles
5.1 Disconnect from contact, eliminate pollution, and rest quietly. If indicated, special antidote drugs can be used. 5.2 For toxic hemolytic anemia, alkalinize urine, use large doses of glucocorticoids as soon as possible to control hemolysis, protect kidney function, and use blood purification therapy for severe cases.
5.3 Treatment of toxic methemoglobinemia can be symptomatic and supportive treatment such as methylene blue and vitamin C and correction of hypoxia. The dosage of methylene blue is 1 mg/kg, slowly injected intravenously. It should not be used by patients with 6-phosphate glucose dehydrogenase deficiency to avoid hemolytic reaction. 5.4 Treatment of toxic sulfhemoglobinemia is mainly symptomatic treatment. The use of methylene blue and vitamin C is ineffective. 5.5 Toxic acute aplastic anemia: blood transfusion, application of androgens and glucocorticoids, infection control, etc. For severe cases, anti-lymphocyte (thymus) cell globulin, cyclosporin A or allogeneic bone marrow transplantation can be tried. 5.6 Toxic agranulocytosis can use granulocyte colony stimulating factor (GCSF). 5.7 Treatment of coagulation mechanism disorders such as toxic vascular purpura, toxic thrombocytopenia, toxic platelet dysfunction, toxic prothrombin synthesis disorder and toxic disseminated intravascular coagulation should be handled according to the principles of internal medicine treatment. 6 Assessment of work capacity
After patients with toxic hemolytic anemia and toxic methemoglobinemia are cured, whether patients with mild poisoning should be transferred from their original jobs depends on their condition and working conditions. Patients with moderate and severe poisoning should be transferred from their original jobs. Patients with hemolytic anemia should be assigned to light work or rest according to whether there is residual kidney damage and its degree.
Patients with coagulation mechanism disorders such as toxic sulfhemoglobinemia, toxic agranulocytosis, toxic acute aplastic anemia, toxic vascular purpura, neutrophilopenia, toxic platelet dysfunction, toxic prothrombin synthesis disorder and toxic disseminated intravascular coagulation should be transferred from their original jobs after recovery, and rest or be assigned to light work. 7 Health Examination Requirements
7.1 Workers who work with blood poisons should undergo a pre-employment physical examination, which includes an internal examination, and blood white blood cell count and cell classification, red blood cell count and (or) hemoglobin quantification, and platelet count. 7.2 After work, a regular physical examination should be conducted once a year. In addition to the pre-employment physical examination items, the examination items should include reticulocyte count, methemoglobin determination, Hernzi body examination, etc. according to the blood toxicity of the poison. 8. General Occupational Prohibition Certificate
a) Various blood diseases and hereditary red blood cell enzyme deficiency and platelet function deficiency. b) Kidney and liver diseases.
c) Obvious cardiopulmonary diseases.
GB 17058 - 1997
Appendix A
(Suggestive Appendix)
Instructions for the correct use of the standard
A1 Common poisons that may cause occupational acute toxic blood system diseases A1.1 Definition of occupational poisons in this standard Occupational blood poisons refer to various industrial chemical poisons that target blood and/or hematopoietic tissues or one of the main target organs or cause changes in the blood system as the main manifestation. A1.2 Common related poisons that may cause blood changes A1.2.1 Poisons that cause occupational acute toxic hemolytic anemia; arsenic, copper sulfate, lead, chromic acid, antimony, antimony, chlorate, methyl mercaptan, phenylhydrazine, aminonitro compounds of benzene (aniline, xylidine, nitrobenzene, dinitrobenzene, trinitrotoluene, nitroaniline, nitronaphthylamine, nitrobenzene, nitrochlorotoluene), azoxybenzene, dichlorvos, malathion, parathion, organochlorine pesticides, insecticides, pyrethroids, diquat, pentachlorophenol, antiqualin, methyl parathion, chlorpyrifos, dimethoate, and o-toluidine. A1.2.2 Toxic substances causing occupational acute toxic methemoglobinemia A1.2.2.1 Aromatic aminonitro compounds Anilines: aniline, phenylenediamine, methylaniline, dimethylaniline, ethylaniline, methoxyaniline, ethoxyaniline, methylethylaniline, propionaniline, diaminoaniline, p-chloroaniline, o-chlorotoluidine, p-bromoaniline, nitroaniline, p-nitroaniline, nitrotoluidine, methyltetranitroaniline, p-nitro-o-toluidine.
Phenylhydroxylamines: phenylhydroxylamine, chlorophenylhydroxylamine. Naphthylamines: nitronaphthylamine.
Nitrobenzenes: nitrobenzene, nitrotoluene, dinitrotoluene, dinitrobenzene, trinitrotoluene, nitrosobenzene, m-aminonitrotoluene, o-nitrochlorobenzene, p-nitrochlorobenzene, nitrofluorobenzene, m-chloronitrobenzene, dinitrochlorobenzene, p-aminopropiophenone. Phenols: p-aminophenol, methylaminophenol, dimethylaminophenol, pyroximate. Phenylhydrazines: phenylhydrazine.
A1.2.2.2 Pesticides: insecticide (chlorobenzene), chloranil (p-chloro-o-toluene dimethylsulfonamide), propanil (N-3,4-dichlorophenylpropionamide), herbicide (2,4-dichlorophenyl-4-nitrophenyl ether), chloranil. A1.2.2.3 Others: nitrogen oxides, nitrites, nitrates, ethyl nitrite, chlorates, fluorites. A1.2.3 Toxins causing toxic sulfhemoglobinemia: mancozeb (ethylene bisdithiocarbamate), acetanilide, etc. A1.2.4 Toxins causing neutrophilic acute aplastic anemia: benzene, carbon tetrachloride, and dichloromethane trioxide. A1.2.5 Toxins causing toxic agranulocytosis: nitrogen mustard, thiotepa, etc. A1.2.6 Toxins that cause toxic vascular purpura: gold, mercury, bismuth, 2,2,3, organophosphates, military poison gas (Lewis gas, etc.). A1.2.7 Toxins that cause toxic thrombocytopenia: benzene, lead, arsenic, iodide, trinitrotoluene, benzene compounds, carbon tetrachloride, 2,2,3, 666, gold preparations, ethanol, etc. A1.2.8 Toxins that cause toxic platelet dysfunction: polyvinylpyrrolidine, potassium cyanide, iodoacetic acid, methylmercuric nitrate, para-chloromercuric, benzoic acid, etc.
A1.2.9 Toxins that cause toxic prothrombin synthesis disorder: difacoum, warfarin, cypermethrin, etc. A1.2.10 Toxins that cause toxic disseminated intravascular coagulation Severe acute poisoning of various chemical poisons complicated by adult respiratory distress syndrome (ARDS), acute hemolysis, severe liver or kidney damage, etc., can cause disseminated intravascular coagulation (DIC). A1.2.11 Other poisons that meet the meaning of A1.1. A2 Scope of application of this standard
This standard applies to acute (including subacute) 411
toxic blood system diseases caused by exposure to blood poisons listed in Appendix A1 of this standard in any occupation.
GB17058-1997
A3 Diagnosis of occupational acute toxic blood system diseases,In addition to occupational exposure history, on-site investigation and monitoring data, and clinical manifestations, special attention should be paid to hematological laboratory tests. In addition to routine examinations, the examination items can be determined according to the clinical type of blood diseases and the need for differential diagnosis.
A4 The spectrophotometric determination of methemoglobin in blood can be found in Appendix B of GB11513-1989 Diagnostic Criteria and Treatment Principles for Occupational Acute Pesticide Poisoning.
Other hematological examinations, especially the laboratory examination methods and normal values of toxic disseminated intravascular coagulation, can refer to the latest version of practical internal medicine and clinical hematology monographs in China. A5 Plasma exchange and dialysis therapy are currently the key measures for rescuing acute severe toxic hemolysis and should be used as early as possible. Methylene blue and vitamin C should be used as early as possible for toxic methemoglobinemia. Toxic sulfhemoglobinemia should be treated symptomatically, and methylene blue and vitamin C are ineffective. The treatment of coagulation mechanism disorders such as toxic acute aplastic anemia, toxic granulocytosis and toxic vascular purpura, toxic thrombocytopenia, toxic platelet dysfunction, toxic prothrombin synthesis disorder and toxic disseminated intravascular coagulation shall be handled according to the principles of internal medicine treatment.
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