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. Acute toxic blood system diseases occurring in non-occupational activities can also be referred to this standard. GBZ 75-2002 Occupational Acute Chemical Toxic Blood System Disease Diagnosis Standard GBZ75-2002 Standard Download Decompression Password: www.bzxz.net

ICS 13.100
National Occupational Health Standard of the People's Republic of China GBZ75-2002
Diagnostic Criteria of Occupational Acute Toxic Hematologic Diseases Caused by Chemicals
Published on April 8, 2002
Implemented on June 1, 2002
Published by the Ministry of Health of the People's Republic of China
Article 5.1 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 GB17508-1997 and this standard, this standard shall prevail. 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 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 patterns of onset, 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 the poisoning, the diagnosis can be made according to the rules specified in this standard. Under the general heading of diagnosis of occupational acute chemical poisoning, the following 10 parts are included. Part 1 Diagnostic criteria for occupational acute chemical poisoning (general principles); Part 2
Diagnostic rules for occupational acute hidden chemical poisoning: Part 3
Part 4
Part 5
Part 6
Part 7
Diagnostic criteria for multiple organ dysfunction syndrome caused by occupational acute chemical poisoning; 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; Part 8
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.
This standard is proposed and managed 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, the Shenyang Municipal Institute of Labor Health and Occupational Diseases, and the Guangdong Provincial Institute of Occupational Disease Prevention and Control; the Liaoning Provincial Institute of Occupational Disease Prevention and Control, the Jiangxi Provincial Institute of Labor Health and Occupational Diseases, the Union Hospital Affiliated to Tongji Medical University, and the Panzhihua Institute of Labor Health and Protection participated in the drafting. The Ministry of Health of the People's Republic of China is responsible for interpreting this standard. Diagnostic Standard for Occupational Acute Chemical Toxicity Blood System Diseases GBZ75-2002
Occupational Acute Chemical Toxicity Blood System Diseases refer to acute systemic diseases with blood system 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 standards 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. Acute toxic blood system diseases occurring in non-occupational activities can also be used as a reference for this standard. 2 Normative References
The clauses in the following documents become the clauses of this standard through reference in this standard. For any dated referenced document, all subsequent amendments (excluding errata) or revisions are not applicable to this standard. However, parties reaching an agreement based on this standard are encouraged to study whether the latest versions of these documents can be used. For any undated referenced document, the latest version shall apply to this standard.
GB/T16180
3 Diagnostic principles
Diagnostic criteria for occupational acute insecticide poisoning Diagnostic criteria for occupational acute chemical poisoning (general principles) Diagnostic rules for occupational acute latent chemical poisoning Identification of the degree of disability caused by work-related injuries and occupational diseases of employees Based on the occupational exposure history of high concentrations of chemical poisons in a short period of time, the clinical manifestations mainly characterized by blood system damage and the relevant hematological laboratory test results, combined with the necessary on-site investigation data, and after excluding other causes, especially blood diseases caused by drugs, occupational acute chemical poisoning blood system diseases can be diagnosed. 4 Clinical types and diagnostic classification
Common clinical types of occupational acute chemical poisoning blood system diseases are as follows: 4.1 Toxic hemolytic anemia
4.1.1 Mild: Fatigue, chills, fever, back pain, fatigue, headache, nausea, vomiting, abdominal pain occur after poisoning. Skin and sclera are yellowed, and the appearance of anemia; blood tests show a decrease in red blood cells and hemoglobin, an increase in reticulocytes, and the appearance of Hernzi bodies: Urinalysis shows red tea-colored urine, positive urine occult blood, positive protein, red and white blood cells and casts, and blood urea nitrogen is basically normal.
4.1.2 Severe: 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 urine, strong positive urine occult blood, rapid increase in blood urea nitrogen, acute renal failure, 4.2 Toxic methemoglobinemia (MHb) 4.2.1 Mild: Generally, the MHb concentration is above 10%, the area around the lips is purple, and there may be no symptoms. 4.2.2 Moderate: MHb concentration is 40% to 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: 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 cause purple and headache. Some patients may also have methemoglobin and hemolysis. 4.3.2 Blood sulfhemoglobin accounts for 2% of the total hemoglobin, or even more than 10%. 4.4 Toxic acute aplastic anemia
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 (<20x10°/L), reticulocytes <1%, absolute value <15x10°/L. 4.4.3 Bone marrow: low proliferation of nucleated cells, significant decrease in granulocytes, erythrocytes and megakaryocytes, relatively increased proportion of lymphocytes, plasma cells, reticular cells and tissue basophils are easily seen. Bone marrow biopsy shows a decrease in hematopoietic tissue, 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, and necrotic ulcers after a few days, which are common in tonsils, soft tissues, lips, tongue, skin, nasal cavity, rectum, anus and vagina, and secondary sepsis. 4.5.2 Peripheral blood picture: White blood cell count is extremely reduced, neutrophils can only account for 1% to 2%, and red blood cell and platelet counts are basically normal.
4.5.3 Bone marrow: In the bone marrow, lobed nuclei, rod-shaped nuclei, late and middle myelocytes are often absent, and only a small number of promyelocytes and promyelocytes are seen. However, the proportion of plasma cells, lymphocytes and monocytes increases, and the erythroid and megakaryocyte systems are generally normal. 4.6 Toxic vascular purpura
4.6.1 Skin bleeding, mostly seen in the limbs, buttocks present edematous petechiae fused into pieces or blood blisters; there are also blood in the stool, abdominal pain and joint pain.
4.6.2 Platelet count, normal bleeding or coagulation time, positive capillary fragility test. 4.7 Toxic thrombocytopenia
4.7.1 Bleeding is more common in the skin of the limbs and the nose, gums, tongue, and oral mucosa. Rarely, there are hemoptysis, hematemesis, hematuria, black stools, and fundus and intracranial bleeding.
4.7.2 Decreased platelet count (<50X10°/L=4.7.3 Bone marrow: decreased megakaryocytes, normal erythroid and granulocyte cells, with 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, with epistaxis and gingival bleeding being common. Severe cases may also have subcutaneous hematoma, hematuria, and black stools. 4.8.2 Platelet count and blood clotting time are normal, platelet adhesion and platelet aggregation function are reduced, and platelet factor IIII is deficient or release disordered.
4.9 Toxic prothrombin synthesis disorder
4.9.1 Epistaxis, gingival bleeding, skin petechiae or ecchymosis, excessive menstrual flow, hematuria, black stools, hemoptysis, and intracranial hemorrhage may be seen.
4.9.2 Prothrombin time (PT) is prolonged, kaolin partial thromboplastin time (KPTT) is prolonged, and coagulation time (CT) and recalcification time are prolonged.
4.10 Toxic disseminated intravascular coagulation
4.10.1 Seen in various severe chemical poisonings. 4.10.2 Multiple bleeding tendencies.
4.10.3 Multiple microvascular thrombosis, with 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: platelet count is dynamically and continuously reduced; plasma fibrinogen content is less than 1.5g/L or progressively decreased; 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 Treatment principles
5.1.1 Disconnect from contact, eliminate pollution, and rest quietly. If indicated, specific antidotes can be used. 5.1.2 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. 5.1.3 For toxic methemoglobinemia, symptomatic and supportive treatments such as methylene blue and vitamin C and correction of hypoxia can be used. 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 reactions.
5.1.4 For the treatment of toxic sulfhemoglobinemia, symptomatic treatment is mainly used. The use of methylene blue and vitamin C is ineffective. 5.1.5 Toxic acute aplastic anemia: blood transfusion, application of male hormones and glucocorticoids, infection control, etc. For severe cases, anti-lymphocyte (thymus) cell globulin, cyclosporin A or allogeneic bone marrow transplantation can be tried. 5.1.6 Granulocyte colony stimulating factor (GCSF) can be used for toxic agranulocytosis. 5.1.7 Treatment of coagulation disorders such as 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. 5.2 Other treatments
After the patients with toxic hemolytic anemia and toxic methemoglobinemia are cured, whether the mild patients should be transferred from their original jobs depends on the condition and working conditions, while the moderate and severe patients should be transferred from their original jobs. Patients with hemolytic anemia should be arranged to do light work or rest according to whether there is residual kidney damage and its degree.
After the patients with coagulation disorders such as toxic sulfhemoglobinemia, toxic agranulocytosis, toxic acute aplastic anemia and toxic vascular purpura, toxic thrombocytopenia, toxic platelet dysfunction, toxic prothrombin synthesis disorder and toxic disseminated intravascular coagulation are cured, they should be transferred from their original jobs and rest or arranged to do light work. Instructions for the correct use of this standard
See Appendix A (Informative Appendix).
Appendix A
(Informative Appendix)
Instructions for the correct use of this standard
A.1 Common poisons that may cause occupational acute toxic blood system diseases A.1.1 Meaning of occupational poisons referred to in this standard Occupational blood poisons refer to various production chemical poisons that use blood and/or hematopoietic tissue as a target organ or one of the main target organs or cause changes in the blood system as the main manifestation. A.1.2 Common poisons that may cause blood changes A.1.2.1 Poisons that cause occupational acute toxic hemolytic anemia: arsenic, copper sulfate, lead, chromic acid, naphthalene, antimony, antimonide, chlorate, methyl mercaptan, phenylhydrazine, aminonitro compounds of benzene (aniline, xylidine, nitrobenzene, dinitrobenzene, trinitrotoluene, nitroaniline, nitronapthylamine, nitrochlorobenzene, nitrochlorotoluene), azoxybenzene, dichlorvos, malathion, parathion, organochlorine pesticides, insecticides, pyrethroids, diquat, pentachlorophenol, antiqualin, methyl parathion, chlorpyrifos, dimethoate, and o-toluidine.
A.1.2.2 Toxic substances causing occupational acute toxic methemoglobinemia A.1.2.2.1 Aromatic aminonitro compounds Anilines: aniline, phenylenediamine, methylaniline, dimethylaniline, ethylaniline, methoxyaniline, ethoxyaniline, methylethylaniline, lactanilide, 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, nitrochlorobenzene, m-chloronitrobenzene, dinitrochlorobenzene, p-aminopropiophenone.
Phenols: p-aminophenol, methylaminophenol, dimethylaminophenol, pyroximate. Phenylhydrazines: phenylhydrazine.
A.1.2.2.2 Pesticides: chlorpyrifos (chlorobenzene), chlorfenapyr (p-chloro-o-toluene dimethylthiourea), propanil (N-3,4-dichlorobenzyl lactam), herbicide (2,4-dichlorobenzyl-4-nitrophenyl ether), pyrocalyx. A.1.2.2.3 Others: nitrogen oxides, nitrites, nitrates, ethyl nitrite, chlorates, chlorites. A.1.2.3 Toxins causing toxic sulfhemoglobinemia: mancozeb (ethylenebisdithiocarbamate), acetanilide, etc.
A.1.2.4 Toxins causing toxic acute aplastic anemia: benzene, carbon tetrachloride, arsenic trioxide. A.1.2.5 Toxins that cause toxic agranulocytosis: nitrogen mustard, thiothiophene, etc. A.1.2.6 Toxins that cause toxic vascular purpura: gold, mercury, bismuth, 2,2,3, organophosphates, military poison gas (Lewis gas, etc.).
A.1.2.7 Toxins that cause toxic thrombocytopenia: benzene, lead, arsenic, iodide, trinitrotoluene, benzene compounds, carbon tetrachloride, 2,2,3, 666, gold preparations, ethanol, etc. A.1.2.8 Toxins that cause toxic platelet dysfunction: polyvinylpyrrolidine, potassium cyanide, iodoacetic acid, methylmercuric nitrate, para-chloromercuric, benzoic acid, etc.
A.1.2.9 Toxins that cause toxic prothrombin synthesis disorder: difacoum, warfarin, cypermethrin, etc. A.1.2.10 Toxins that cause toxic disseminated intravascular coagulation Severe acute poisoning by various chemical poisons complicated by acute respiratory distress syndrome (ARDS), acute hemolysis, severe liver or kidney damage, etc., may cause disseminated intravascular coagulation (DIC). A.1.2.11 Other poisons that meet the meaning of A1.1. A.2 Scope of application of this standard
This standard applies to acute (including occupational acute) toxic blood system diseases caused by exposure to blood poisons listed in Appendix AI of this standard under any occupational conditions. A.3 In the 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. A.4 For the spectrophotometric determination of methemoglobin in the blood, see GBZ46. For other hematological examinations, especially the laboratory examination methods and normal values ​​of toxic disseminated intravascular coagulation, please refer to the latest domestic edition of practical internal medicine and clinical hematology monographs. A.5 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 agranulocytosis and 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.1 Epistaxis, gingival bleeding, petechiae or ecchymoses on the skin, excessive menstrual flow, hematuria, black stools, hemoptysis, and intracranial hemorrhage may be seen.
4.9.2 Prolonged prothrombin time (PT), kaolin partial thromboplastin time (KPTT), coagulation time (CT) and recalcification time.
4.10 Toxic disseminated intravascular coagulation
4.10.1 Seen in various severe chemical poisonings. 4.10.2 Multiple bleeding tendencies.
4.10.3 Multiple microvascular thrombosis, with 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 Treatment principles
5.1.1 Disconnect from contact, eliminate pollution, and rest quietly. If indicated, special antidote drugs can be used 5.1.2 Toxic hemolytic anemia can be treated by alkalinizing urine, using large doses of glucocorticoids as soon as possible to control hemolysis, protect kidney function, and blood purification therapy for severe cases. 5.1.3 Toxic methemoglobinemia can be treated with symptomatic and supportive treatments 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.
5.1.4 The treatment of toxic sulfhemoglobinemia is mainly symptomatic treatment. The use of methylene blue and vitamin C is ineffective. 5.1.5 Toxic acute aplastic anemia: blood transfusion, application of male hormones and glucocorticoids, infection control, etc. For severe cases, anti-lymphocyte (thymus) cell globulin, cyclosporin A or allogeneic bone marrow transplantation can be tried. 5.1.6 Granulocyte colony stimulating factor (GCSF) can be used for toxic agranulocytosis. 5.1.7 The 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. 5.2 Other treatments
After the patients with toxic hemolytic anemia and toxic methemoglobinemia are cured, whether the mild cases should be transferred from their original jobs depends on the condition and working conditions, while the moderate and severe cases should be transferred from their original jobs. The patients with hemolytic anemia should be arranged to do light work or rest according to whether there is residual kidney damage and its degree.
After the patients with toxic sulfhemoglobinemia, toxic agranulocytosis, toxic acute aplastic anemia, toxic vascular purpura, toxic thrombocytopenia, toxic platelet dysfunction, toxic prothrombin synthesis disorder and toxic disseminated intravascular coagulation are cured, they should be transferred from their original jobs and rest or arranged to do light work. Instructions for the correct use of this standard
See Appendix A (Informative Appendix).
Appendix A
(Informative Appendix)
Instructions for the correct use of this standard
A.1 Common poisons that may cause occupational acute toxic blood system diseases A.1.1 Meaning of occupational poisons referred to in this standard Occupational blood poisons refer to various industrial chemical poisons that use blood and/or hematopoietic tissue as target organs or one of the main target organs or cause changes in the blood system as the main manifestation. A.1.2 Common poisons that may cause blood changes A.1.2.1 Poisons that cause occupational acute toxic hemolytic anemia: arsenic, copper sulfate, lead, chromic acid, naphthalene, antimony, antimonide, chlorate, methyl mercaptan, phenylhydrazine, aminonitro compounds of benzene (aniline, xylidine, nitrobenzene, dinitrobenzene, trinitrotoluene, nitroaniline, nitronapthylamine, nitrochlorobenzene, nitrochlorotoluene), azoxybenzene, dichlorvos, malathion, parathion, organochlorine pesticides, insecticides, pyrethroids, diquat, pentachlorophenol, antiqualin, methyl parathion, chlorpyrifos, dimethoate, and o-toluidine.
A.1.2.2 Toxic substances causing occupational acute toxic methemoglobinemia A.1.2.2.1 Aromatic aminonitro compounds Anilines: aniline, phenylenediamine, methylaniline, dimethylaniline, ethylaniline, methoxyaniline, ethoxyaniline, methylethylaniline, lactanilide, 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, nitrochlorobenzene, m-chloronitrobenzene, dinitrochlorobenzene, p-aminopropiophenone.
Phenols: p-aminophenol, methylaminophenol, dimethylaminophenol, pyroximate. Phenylhydrazines: phenylhydrazine.
A.1.2.2.2 Pesticides: chlorpyrifos (chlorobenzene), chlorfenapyr (p-chloro-o-toluene dimethylthiourea), propanil (N-3,4-dichlorobenzyl lactam), herbicide (2,4-dichlorobenzyl-4-nitrophenyl ether), pyrocalyx. A.1.2.2.3 Others: nitrogen oxides, nitrites, nitrates, ethyl nitrite, chlorates, chlorites. A.1.2.3 Toxins causing toxic sulfhemoglobinemia: mancozeb (ethylenebisdithiocarbamate), acetanilide, etc.
A.1.2.4 Toxins causing toxic acute aplastic anemia: benzene, carbon tetrachloride, arsenic trioxide. A.1.2.5 Toxins that cause toxic agranulocytosis: nitrogen mustard, thiothiophene, etc. A.1.2.6 Toxins that cause toxic vascular purpura: gold, mercury, bismuth, 2,2,3, organophosphates, military poison gas (Lewis gas, etc.).
A.1.2.7 Toxins that cause toxic thrombocytopenia: benzene, lead, arsenic, iodide, trinitrotoluene, benzene compounds, carbon tetrachloride, 2,2,3, 666, gold preparations, ethanol, etc. A.1.2.8 Toxins that cause toxic platelet dysfunction: polyvinylpyrrolidine, potassium cyanide, iodoacetic acid, methylmercuric nitrate, para-chloromercuric, benzoic acid, etc.
A.1.2.9 Toxins that cause toxic prothrombin synthesis disorder: difacoum, warfarin, cypermethrin, etc. A.1.2.10 Toxins that cause toxic disseminated intravascular coagulation Severe acute poisoning by various chemical poisons complicated by acute respiratory distress syndrome (ARDS), acute hemolysis, severe liver or kidney damage, etc., may cause disseminated intravascular coagulation (DIC). A.1.2.11 Other poisons that meet the meaning of A1.1. A.2 Scope of application of this standard
This standard applies to acute (including occupational acute) toxic blood system diseases caused by exposure to blood poisons listed in Appendix AI of this standard under any occupational conditions. A.3 In the 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. A.4 For the spectrophotometric determination of methemoglobin in the blood, see GBZ46. For other hematological examinations, especially the laboratory examination methods and normal values ​​of toxic disseminated intravascular coagulation, please refer to the latest domestic edition of practical internal medicine and clinical hematology monographs. A.5 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 agranulocytosis and 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.1 Epistaxis, gingival bleeding, petechiae or ecchymoses on the skin, excessive menstrual flow, hematuria, black stools, hemoptysis, and intracranial hemorrhage may be seen.
4.9.2 Prolonged prothrombin time (PT), kaolin partial thromboplastin time (KPTT), coagulation time (CT) and recalcification time.
4.10 Toxic disseminated intravascular coagulation
4.10.1 Seen in various severe chemical poisonings. 4.10.2 Multiple bleeding tendencies.
4.10.3 Multiple microvascular thrombosis, with 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 Treatment principles
5.1.1 Disconnect from contact, eliminate pollution, and rest quietly. If indicated, special antidote drugs can be used 5.1.2 Toxic hemolytic anemia can be treated by alkalinizing urine, using large doses of glucocorticoids as soon as possible to control hemolysis, protect kidney function, and blood purification therapy for severe cases. 5.1.3 Toxic methemoglobinemia can be treated with symptomatic and supportive treatments 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.
5.1.4 The treatment of toxic sulfhemoglobinemia is mainly symptomatic treatment. The use of methylene blue and vitamin C is ineffective. 5.1.5 Toxic acute aplastic anemia: blood transfusion, application of male hormones and glucocorticoids, infection control, etc. For severe cases, anti-lymphocyte (thymus) cell globulin, cyclosporin A or allogeneic bone marrow transplantation can be tried. 5.1.6 Granulocyte colony stimulating factor (GCSF) can be used for toxic agranulocytosis. 5.1.7 The 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. 5.2 Other treatments
After the patients with toxic hemolytic anemia and toxic methemoglobinemia are cured, whether the mild cases should be transferred from their original jobs depends on the condition and working conditions, while the moderate and severe cases should be transferred from their original jobs. The patients with hemolytic anemia should be arranged to do light work or rest according to whether there is residual kidney damage and its degree.
After the patients with toxic sulfhemoglobinemia, toxic agranulocytosis, toxic acute aplastic anemia, toxic vascular purpura, toxic thrombocytopenia, toxic platelet dysfunction, toxic prothrombin synthesis disorder and toxic disseminated intravascular coagulation are cured, they should be transferred from their original jobs and rest or arranged to do light work. Instructions for the correct use of this standard
See Appendix A (Informative Appendix).
Appendix A
(Informative Appendix)
Instructions for the correct use of this standard
A.1 Common poisons that may cause occupational acute toxic blood system diseases A.1.1 Meaning of occupational poisons referred to in this standard Occupational blood poisons refer to various industrial chemical poisons that use blood and/or hematopoietic tissue as target organs or one of the main target organs or cause changes in the blood system as the main manifestation. A.1.2 Common poisons that may cause blood changes A.1.2.1 Poisons that cause occupational acute toxic hemolytic anemia: arsenic, copper sulfate, lead, chromic acid, naphthalene, antimony, antimonide, chlorate, methyl mercaptan, phenylhydrazine, aminonitro compounds of benzene (aniline, xylidine, nitrobenzene, dinitrobenzene, trinitrotoluene, nitroaniline, nitronapthylamine, nitrochlorobenzene, nitrochlorotoluene), azoxybenzene, dichlorvos, malathion, parathion, organochlorine pesticides, insecticides, pyrethroids, diquat, pentachlorophenol, antiqualin, methyl parathion, chlorpyrifos, dimethoate, and o-toluidine.
A.1.2.2 Toxic substances causing occupational acute toxic methemoglobinemia A.1.2.2.1 Aromatic aminonitro compounds Anilines: aniline, phenylenediamine, methylaniline, dimethylaniline, ethylaniline, methoxyaniline, ethoxyaniline, methylethylaniline, lactanilide, 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, nitrochlorobenzene, m-chloronitrobenzene, dinitrochlorobenzene, p-aminopropiophenone.
Phenols: p-aminophenol, methylaminophenol, dimethylaminophenol, pyroximate. Phenylhydrazines: phenylhydrazine.
A.1.2.2.2 Pesticides: chlorpyrifos (chlorobenzene), chlorfenapyr (p-chloro-o-toluene dimethylthiourea), propanil (N-3,4-dichlorobenzyl lactam), herbicide (2,4-dichlorobenzyl-4-nitrophenyl ether), pyrocalyx. A.1.2.2.3 Others: nitrogen oxides, nitrites, nitrates, ethyl nitrite, chlorates, chlorites. A.1.2.3 Toxins causing toxic sulfhemoglobinemia: mancozeb (ethylenebisdithiocarbamate), acetanilide, etc.
A.1.2.4 Toxins causing toxic acute aplastic anemia: benzene, carbon tetrachloride, arsenic trioxide. A.1.2.5 Toxins that cause toxic agranulocytosis: nitrogen mustard, thiothiophene, etc. A.1.2.6 Toxins that cause toxic vascular purpura: gold, mercury, bismuth, 2,2,3, organophosphates, military poison gas (Lewis gas, etc.).
A.1.2.7 Toxins that cause toxic thrombocytopenia: benzene, lead, arsenic, iodide, trinitrotoluene, benzene compounds, carbon tetrachloride, 2,2,3, 666, gold preparations, ethanol, etc. A.1.2.8 Toxins that cause toxic platelet dysfunction: polyvinylpyrrolidine, potassium cyanide, iodoacetic acid, methylmercuric nitrate, para-chloromercuric, benzoic acid, etc.
A.1.2.9 Toxins that cause toxic prothrombin synthesis disorder: difacoum, warfarin, cypermethrin, etc. A.1.2.10 Toxins that cause toxic disseminated intravascular coagulation Severe acute poisoning by various chemical poisons complicated by acute respiratory distress syndrome (ARDS), acute hemolysis, severe liver or kidney damage, etc., may cause disseminated intravascular coagulation (DIC). A.1.2.11 Other poisons that meet the meaning of A1.1. A.2 Scope of application of this standard
This standard applies to acute (including occupational acute) toxic blood system diseases caused by exposure to blood poisons listed in Appendix AI of this standard under any occupational conditions. A.3 In the 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. A.4 For the spectrophotometric determination of methemoglobin in the blood, see GBZ46. For other hematological examinations, especially the laboratory examination methods and normal values ​​of toxic disseminated intravascular coagulation, please refer to the latest domestic edition of practical internal medicine and clinical hematology monographs. A.5 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 agranulocytosis and 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.1. Disconnect from contact, eliminate pollution, and rest quietly. If indicated, special antidotes can be used. 5.1.2. Alkalinize urine for toxic hemolytic anemia, use large doses of glucocorticoids as soon as possible to control hemolysis, protect kidney function, and use blood purification therapy for severe cases. 5.1.3. Treatment of toxic methemoglobinemia can be symptomatic and supportive with methylene blue and vitamin C, as well as correction of hypoxia. Methylene blue is used in a dose of 1 mg/kg, slowly injected intravenously. It should not be used by patients with 6-phosphate glucose dehydrogenase deficiency to avoid hemolytic reactions.
5.1.4. Treatment of toxic sulfhemoglobinemia is mainly symptomatic treatment. The use of methylene blue and vitamin C is ineffective. 5.1.5. Toxic acute aplastic anemia: blood transfusion, application of male hormones and glucocorticoids, infection control, etc. For severe cases, anti-lymphocyte (thymus) cell globulin, cyclosporin A or allogeneic bone marrow transplantation can be tried. 5.1.6 Granulocyte colony stimulating factor (GCSF) can be used for toxic agranulocytosis. 5.1.7 Treatment of coagulation disorders such as 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. 5.2 Other treatments
After the recovery of patients with toxic hemolytic anemia and toxic methemoglobinemia, whether to transfer from the original type of work for mild patients can be determined according to the condition and working conditions, while those with moderate and severe cases should be transferred from the original type of work. Patients with hemolytic anemia should be arranged to do light work or rest according to whether there is residual kidney damage and its degree.
Patients with toxic sulfhemoglobinemia, toxic agranulocytosis, toxic acute aplastic anemia, toxic vascular purpura, toxic thrombocytopenia, toxic platelet dysfunction, toxic prothrombin synthesis disorder and toxic disseminated intravascular coagulation and other coagulation mechanism disorders should be transferred from their original jobs after recovery, and rest or arrange light work. Instructions for the correct use of this standard
See Appendix A (Informative Appendix).
Appendix A
(Informative Appendix)
Instructions for the correct use of this standard
A.1 Common poisons that may cause occupational acute toxic blood system diseases A.1.1 Meaning of occupational poisons referred to in this standard Occupational blood poisons refer to various production chemical poisons that use blood and/or hematopoietic tissue as a target organ or one of the main target organs or cause changes in the blood system as the main manifestation. A.1.2 Common poisons that may cause blood changes A.1.2.1 Poisons that cause occupational acute toxic hemolytic anemia: arsenic, copper sulfate, lead, chromic acid, naphthalene, antimony, antimonide, chlorate, methyl mercaptan, phenylhydrazine, aminonitro compounds of benzene (aniline, xylidine, nitrobenzene, dinitrobenzene, trinitrotoluene, nitroaniline, nitronapthylamine, nitrochlorobenzene, nitrochlorotoluene), azoxybenzene, dichlorvos, malathion, parathion, organochlorine pesticides, insecticides, pyrethroids, diquat, pentachlorophenol, antiqualin, methyl parathion, chlorpyrifos, dimethoate, and o-toluidine.
A.1.2.2 Toxic substances causing occupational acute toxic methemoglobinemia A.1.2.2.1 Aromatic aminonitro compounds Anilines: aniline, phenylenediamine, methylaniline, dimethylaniline, ethylaniline, methoxyaniline, ethoxyaniline, methylethylaniline, lactanilide, 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, nitrochlorobenzene, m-chloronitrobenzene, dinitrochlorobenzene, p-aminopropiophenone.
Phenols: p-aminophenol, methylaminophenol, dimethylaminophenol, pyroximate. Phenylhydrazines: phenylhydrazine.
A.1.2.2.2 Pesticides: chlorpyrifos (chlorobenzene), chlorfenapyr (p-chloro-o-toluene dimethylthiourea), propanil (N-3,4-dichlorobenzyl lactam), herbicide (2,4-dichlorobenzyl-4-nitrophenyl ether), pyrocalyx. A.1.2.2.3 Others: nitrogen oxides, nitrites, nitrates, ethyl nitrite, chlorates, chlorites. A.1.2.3 Toxins causing toxic sulfhemoglobinemia: mancozeb (ethylenebisdithiocarbamate), acetanilide, etc.
A.1.2.4 Toxins causing toxic acute aplastic anemia: benzene, carbon tetrachloride, arsenic trioxide. A.1.2.5 Toxins that cause toxic agranulocytosis: nitrogen mustard, thiothiophene, etc. A.1.2.6 Toxins that cause toxic vascular purpura: gold, mercury, bismuth, 2,2,3, organophosphates, military poison gas (Lewis gas, etc.).
A.1.2.7 Toxins that cause toxic thrombocytopenia: benzene, lead, arsenic, iodide, trinitrotoluene, benzene compounds, carbon tetrachloride, 2,2,3, 666, gold preparations, ethanol, etc. A.1.2.8 Toxins that cause toxic platelet dysfunction: polyvinylpyrrolidine, potassium cyanide, iodoacetic acid, methylmercuric nitrate, para-chloromercuric, benzoic acid, etc.
A.1.2.9 Toxins that cause toxic prothrombin synthesis disorder: difacoum, warfarin, cypermethrin, etc. A.1.2.10 Toxins that cause toxic disseminated intravascular coagulation Severe acute poisoning by various chemical poisons complicated by acute respiratory distress syndrome (ARDS), acute hemolysis, severe liver or kidney damage, etc., may cause disseminated intravascular coagulation (DIC). A.1.2.11 Other poisons that meet the meaning of A1.1. A.2 Scope of application of this standard
This standard applies to acute (including occupational acute) toxic blood system diseases caused by exposure to blood poisons listed in Appendix AI of this standard under any occupational conditions. A.3 In the 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. A.4 For the spectrophotometric determination of methemoglobin in the blood, see GBZ46. For other hematological examinations, especially the laboratory examination methods and normal values ​​of toxic disseminated intravascular coagulation, please refer to the latest domestic edition of practical internal medicine and clinical hematology monographs. A.5 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 agranulocytosis and 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.1. Disconnect from contact, eliminate pollution, and rest quietly. If indicated, special antidotes can be used. 5.1.2. Alkalinize urine for toxic hemolytic anemia, use large doses of glucocorticoids as soon as possible to control hemolysis, protect kidney function, and use blood purification therapy for severe cases. 5.1.3. Treatment of toxic methemoglobinemia can be symptomatic and supportive with methylene blue and vitamin C, as well as correction of hypoxia. Methylene blue is used in a dose of 1 mg/kg, slowly injected intravenously. It should not be used by patients with 6-phosphate glucose dehydrogenase deficiency to avoid hemolytic reactions.
5.1.4. Treatment of toxic sulfhemoglobinemia is mainly symptomatic treatment. The use of methylene blue and vitamin C is ineffective. 5.1.5. Toxic acute aplastic anemia: blood transfusion, application of male hormones and glucocorticoids, infection control, etc. For severe cases, anti-lymphocyte (thymus) cell globulin, cyclosporin A or allogeneic bone marrow transplantation can be tried. 5.1.6 Granulocyte colony stimulating factor (GCSF) can be used for toxic agranulocytosis. 5.1.7 Treatment of coagulation disorders such as 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. 5.2 Other treatments Www.bzxZ.net
After the recovery of patients with toxic hemolytic anemia and toxic methemoglobinemia, whether to transfer from the original type of work for mild patients can be determined according to the condition and working conditions, while those with moderate and severe cases should be transferred from the original type of work. Patients with hemolytic anemia should be arranged to do light work or rest according to whether there is residual kidney damage and its degree.
Patients with toxic sulfhemoglobinemia, toxic agranulocytosis, toxic acute aplastic anemia, toxic vascular purpura, toxic thrombocytopenia, toxic platelet dysfunction, toxic prothrombin synthesis disorder and toxic disseminated intravascular coagulation and other coagulation mechanism disorders should be transferred from their original jobs after recovery, and rest or arrange light work. Instructions for the correct use of this standard
See Appendix A (Informative Appendix).
Appendix A
(Informative Appendix)
Instructions for the correct use of this standard
A.1 Common poisons that may cause occupational acute toxic blood system diseases A.1.1 Meaning of occupational poisons referred to in this standard Occupational blood poisons refer to various production chemical poisons that use blood and/or hematopoietic tissue as a target organ or one of the main target organs or cause changes in the blood system as the main manifestation. A.1.2 Common poisons that may cause blood changes A.1.2.1 Poisons that cause occupational acute toxic hemolytic anemia: arsenic, copper sulfate, lead, chromic acid, naphthalene, antimony, antimonide, chlorate, methyl mercaptan, phenylhydrazine, aminonitro compounds of benzene (aniline, xylidine, nitrobenzene, dinitrobenzene, trinitrotoluene, nitroaniline, nitronapthylamine, nitrochlorobenzene, nitrochlorotoluene), azoxybenzene, dichlorvos, malathion, parathion, organochlorine pesticides, insecticides, pyrethroids, diquat, pentachlorophenol, antiqualin, methyl parathion, chlorpyrifos, dimethoate, and o-toluidine.
A.1.2.2 Toxic substances causing occupational acute toxic methemoglobinemia A.1.2.2.1 Aromatic aminonitro compounds Anilines: aniline, phenylenediamine, methylaniline, dimethylaniline, ethylaniline, methoxyaniline, ethoxyaniline, methylethylaniline, lactanilide, 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, nitrochlorobenzene, m-chloronitrobenzene, dinitrochlorobenzene, p-aminopropiophenone.
Phenols: p-aminophenol, methylaminophenol, dimethylaminophenol, pyroximate. Phenylhydrazines: phenylhydrazine.
A.1.2.2.2 Pesticides: chlorpyrifos (chlorobenzene), chlorfenapyr (p-chloro-o-toluene dimethylthiourea), propanil (N-3,4-dichlorobenzyl lactam), herbicide (2,4-dichlorobenzyl-4-nitrophenyl ether), pyrocalyx. A.1.2.2.3 Others: nitrogen oxides, nitrites, nitrates, ethyl nitrite, chlorates, chlorites. A.1.2.3 Toxins causing toxic sulfhemoglobinemia: mancozeb (ethylenebisdithiocarbamate), acetanilide, etc.
A.1.2.4 Toxins causing toxic acute aplastic anemia: benzene, carbon tetrachloride, arsenic trioxide. A.1.2.5 Toxins that cause toxic agranulocytosis: nitrogen mustard, thiothiophene, etc. A.1.2.6 Toxins that cause toxic vascular purpura: gold, mercury, bismuth, 2,2,3, organophosphates, military poison gas (Lewis gas, etc.).
A.1.2.7 Toxins that cause toxic thrombocytopenia: benzene, lead, arsenic, iodide, trinitrotoluene, benzene compounds, carbon tetrachloride, 2,2,3, 666, gold preparations, ethanol, etc. A.1.2.8 Toxins that cause toxic platelet dysfunction: polyvinylpyrrolidine, potassium cyanide, iodoacetic acid, methylmercuric nitrate, para-chloromercuric, benzoic acid, etc.
A.1.2.9 Toxins that cause toxic prothrombin synthesis disorder: difacoum, warfarin, cypermethrin, etc. A.1.2.10 Toxins that cause toxic disseminated intravascular coagulation Severe acute poisoning by various chemical poisons complicated by acute respiratory distress syndrome (ARDS), acute hemolysis, severe liver or kidney damage, etc., may cause disseminated intravascular coagulation (DIC). A.1.2.11 Other poisons that meet the meaning of A1.1. A.2 Scope of application of this standard
This standard applies to acute (including occupational acute) toxic blood system diseases caused by exposure to blood poisons listed in Appendix AI of this standard under any occupational conditions. A.3 In the 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. A.4 For the spectrophotometric determination of methemoglobin in the blood, see GBZ46. For other hematological examinations, especially the laboratory examination methods and normal values ​​of toxic disseminated intravascular coagulation, please refer to the latest domestic edition of practical internal medicine and clinical hematology monographs. A.5 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 agranulocytosis and 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.2 Other treatments
After the patients with toxic hemolytic anemia and toxic methemoglobinemia are cured, whether the mild cases should be transferred from their original jobs depends on the condition and working conditions, while the moderate and severe cases should be transferred from their original jobs. The patients with hemolytic anemia should be arranged to do light work or rest according to whether there is residual kidney damage and its degree.
After the patients with toxic sulfhemoglobinemia, toxic agranulocytosis, toxic acute aplastic anemia, toxic vascular purpura, toxic thrombocytopenia, toxic platelet dysfunction, toxic prothrombin synthesis disorder and toxic disseminated intravascular coagulation are cured, they should be transferred from their original jobs and rest or arranged to do light work. Instructions for the correct use of this standard
See Appendix A (Informative Appendix).
Appendix A
(Informative Appendix)
Instructions for the correct use of this standard
A.1 Common poisons that may cause occupational acute toxic blood system diseases A.1.1 Meaning of occupational poisons referred to in this standard Occupational blood poisons refer to various industrial chemical poisons that use blood and/or hematopoietic tissue as target organs or one of the main target organs or cause changes in the blood system as the main manifestation. A.1.2 Common poisons that may cause blood changes A.1.2.1 Poisons that cause occupational acute toxic hemolytic anemia: arsenic, copper sulfate, lead, chromic acid, naphthalene, antimony, antimonide, chlorate, methyl mercaptan, phenylhydrazine, aminonitro compounds of benzene (aniline, xylidine, nitrobenzene, dinitrobenzene, trinitrotoluene, nitroaniline, nitronapthylamine, nitrochlorobenzene, nitrochlorotoluene), azoxybenzene, dichlorvos, malathion, parathion, organochlorine pesticides, insecticides, pyrethroids, diquat, pentachlorophenol, antiqualin, methyl parathion, chlorpyrifos, dimethoate, and o-toluidine.
A.1.2.2 Toxic substances causing occupational acute toxic methemoglobinemia A.1.2.2.1 Aromatic aminonitro compounds Anilines: aniline, phenylenediamine, methylaniline, dimethylaniline, ethylaniline, methoxyaniline, ethoxyaniline, methylethylaniline, lactanilide, 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, nitrochlorobenzene, m-chloronitrobenzene, dinitrochlorobenzene, p-aminopropiophenone.
Phenols: p-aminophenol, methylaminophenol, dimethylaminophenol, pyroximate. Phenylhydrazines: phenylhydrazine.
A.1.2.2.2 Pesticides: chlorpyrifos (chlorobenzene), chlorfenapyr (p-chloro-o-toluene dimethylthiourea), propanil (N-3,4-dichlorobenzyl lactam), herbicide (2,4-dichlorobenzyl-4-nitrophenyl ether), pyrocalyx. A.1.2.2.3 Others: nitrogen oxides, nitrites, nitrates, ethyl nitrite, chlorates, chlorites. A.1.2.3 Toxins causing toxic sulfhemoglobinemia: mancozeb (ethylenebisdithiocarbamate), acetanilide, etc.
A.1.2.4 Toxins causing toxic acute aplastic anemia: benzene, carbon tetrachloride, arsenic trioxide. A.1.2.5 Toxins that cause toxic agranulocytosis: nitrogen mustard, thiothiophene, etc. A.1.2.6 Toxins that cause toxic vascular purpura: gold, mercury, bismuth, 2,2,3, organophosphates, military poison gas (Lewis gas, etc.).
A.1.2.7 Toxins that cause toxic thrombocytopenia: benzene, lead, arsenic, iodide, trinitrotoluene, benzene compounds, carbon tetrachloride, 2,2,3, 666, gold preparations, ethanol, etc. A.1.2.8 Toxins that cause toxic platelet dysfunction: polyvinylpyrrolidine, potassium cyanide, iodoacetic acid, methylmercuric nitrate, para-chloromercuric, benzoic acid, etc.
A.1.2.9 Toxins that cause toxic prothrombin synthesis disorder: difacoum, warfarin, cypermethrin, etc. A.1.2.10 Toxins that cause toxic disseminated intravascular coagulation Severe acute poisoning by various chemical poisons complicated by acute respiratory distress syndrome (ARDS), acute hemolysis, severe liver or kidney damage, etc., may cause disseminated intravascular coagulation (DIC). A.1.2.11 Other poisons that meet the meaning of A1.1. A.2 Scope of application of this standard
This standard applies to acute (including occupational acute) toxic blood system diseases caused by exposure to blood poisons listed in Appendix AI of this standard under any occupational conditions. A.3 In the 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. A.4 For the spectrophotometric determination of methemoglobin in the blood, see GBZ46. For other hematological examinations, especially the laboratory examination methods and normal values ​​of toxic disseminated intravascular coagulation, please refer to the latest domestic edition of practical internal medicine and clinical hematology monographs. A.5 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 agranulocytosis and 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.2 Other treatments
After the patients with toxic hemolytic anemia and toxic methemoglobinemia are cured, whether the mild cases should be transferred from their original jobs depends on the condition and working conditions, while the moderate and severe cases should be transferred from their original jobs. The patients with hemolytic anemia should be arranged to do light work or rest according to whether there is residual kidney damage and its degree.
After the patients with toxic sulfhemoglobinemia, toxic agranulocytosis, toxic acute aplastic anemia, toxic vascular purpura, toxic thrombocytopenia, toxic platelet dysfunction, toxic prothrombin synthesis disorder and toxic disseminated intravascular coagulation are cured, they should be transferred from their original jobs and rest or arranged to do light work. Instructions for the correct use of this standard
See Appendix A (Informative Appendix).
Appendix A
(Informative Appendix)
Instructions for the correct use of this standard
A.1 Common poisons that may cause occupational acute toxic blood system diseases A.1.1 Meaning of occupational poisons referred to in this standard Occupational blood poisons refer to various industrial chemical poisons that use blood and/or hematopoietic tissue as target organs or one of the main target organs or cause changes in the blood system as the main manifestation. A.1.2 Common poisons that may cause blood changes A.1.2.1 Poisons that cause occupational acute toxic hemolytic anemia: arsenic, copper sulfate, lead, chromic acid, naphthalene, antimony, antimonide, chlorate, methyl mercaptan, phenylhydrazine, aminonitro compounds of benzene (aniline, xylidine, nitrobenzene, dinitrobenzene, trinitrotoluene, nitroaniline, nitronapthylamine, nitrochlorobenzene, nitrochlorotoluene), azoxybenzene, dichlorvos, malathion, parathion, organochlorine pesticides, insecticides, pyrethroids, diquat, pentachlorophenol, antiqualin, methyl parathion, chlorpyrifos, dimethoate, and o-toluidine.
A.1.2.2 Toxic substances causing occupational acute toxic methemoglobinemia A.1.2.2.1 Aromatic aminonitro compounds Anilines: aniline, phenylenediamine, methylaniline, dimethylaniline, ethylaniline, methoxyaniline, ethoxyaniline, methylethylaniline, lactanilide, 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, nitrochlorobenzene, m-chloronitrobenzene, dinitrochlorobenzene, p-aminopropiophenone.
Phenols: p-aminophenol, methylaminophenol, dimethylaminophenol, pyroximate. Phenylhydrazines: phenylhydrazine.
A.1.2.2.2 Pesticides: chlorpyrifos (chlorobenzene), chlorfenapyr (p-chloro-o-toluene dimethylthiourea), propanil (N-3,4-dichlorobenzyl lactam), herbicide (2,4-dichlorobenzyl-4-nitrophenyl ether), pyrocalyx. A.1.2.2.3 Others: nitrogen oxides, nitrites, nitrates, ethyl nitrite, chlorates, chlorites. A.1.2.3 Toxins causing toxic sulfhemoglobinemia: mancozeb (ethylenebisdithiocarbamate), acetanilide, etc.
A.1.2.4 Toxins causing toxic acute aplastic anemia: benzene, carbon tetrachloride, arsenic trioxide. A.1.2.5 Toxins that cause toxic agranulocytosis: nitrogen mustard, thiothiophene, etc. A.1.2.6 Toxins that cause toxic vascular purpura: gold, mercury, bismuth, 2,2,3, organophosphates, military poison gas (Lewis gas, etc.).
A.1.2.7 Toxins that cause toxic thrombocytopenia: benzene, lead, arsenic, iodide, trinitrotoluene, benzene compounds, carbon tetrachloride, 2,2,3, 666, gold preparations, ethanol, etc. A.1.2.8 Toxins that cause toxic platelet dysfunction: polyvinylpyrrolidine, potassium cyanide, iodoacetic acid, methylmercuric nitrate, para-chloromercuric, benzoic acid, etc.
A.1.2.9 Toxins that cause toxic prothrombin synthesis disorder: difacoum, warfarin, cypermethrin, etc. A.1.2.10 Toxins that cause toxic disseminated intravascular coagulation Severe acute poisoning by various chemical poisons complicated by acute respiratory distress syndrome (ARDS), acute hemolysis, severe liver or kidney damage, etc., may cause disseminated intravascular coagulation (DIC). A.1.2.11 Other poisons that meet the meaning of A1.1. A.2 Scope of application of this standard
This standard applies to acute (including occupational acute) toxic blood system diseases caused by exposure to blood poisons listed in Appendix AI of this standard under any occupational conditions. A.3 In the 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. A.4 For the spectrophotometric determination of methemoglobin in the blood, see GBZ46. For other hematological examinations, especially the laboratory examination methods and normal values ​​of toxic disseminated intravascular coagulation, please refer to the latest domestic edition of practical internal medicine and clinical hematology monographs. A.5 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 agranulocytosis and 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.10 Toxic substances that cause toxic disseminated intravascular coagulation Severe acute poisoning by various chemical poisons complicated by acute respiratory distress syndrome (ARDS), acute hemolysis, severe liver or kidney damage, etc., may cause disseminated intravascular coagulation (DIC). A.1.2.11 Other poisons that meet the meaning of A1.1. A.2 Scope of application of this standard
This standard applies to acute (including industrial acute) toxic blood system diseases caused by exposure to blood poisons listed in Appendix AI of this standard in any occupation. A.3 In the diagnosis of
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