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Diagnostic criteria of occupational acute toxic hematologic disease caused by chemicals
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GBZ 75-2010
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| GBZ 75-2002 | English | 319 |
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Diagnostic Criteria of Occupational Acute Toxic Hematologic Diseases Caused by Chemicals
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PDF similar to GBZ75-2010
Standard similar to GBZ75-2010 GBZ 20 GBZ 57 GBZ 49 GBZ 82 GBZ 68 GBZ 77
Basic data | Standard ID | GBZ 75-2010 (GBZ75-2010) | | Description (Translated English) | Diagnostic criteria of occupational acute toxic hematologic disease caused by chemicals | | Sector / Industry | National Standard | | Classification of Chinese Standard | C60 | | Classification of International Standard | 13.100 | | Word Count Estimation | 7,796 | | Date of Issue | 2010-03-10 | | Date of Implementation | 2010-10-01 | | Older Standard (superseded by this standard) | GBZ 75-2002 | | Quoted Standard | GBZ 30; GBZ 59; GB/T 16180 | | Regulation (derived from) | ?Health-Communication (2010) 6 | | Issuing agency(ies) | Ministry of Health of the People's Republic of China | | Summary | This standard specifies the occupational acute toxic chemicals diagnosis and treatment of blood disorders principle. This standard applies to the diagnosis and treatment of various hematological diseases of occupational acute chemical poisoning caused. Diagnosis and treatment of non- occupational acute toxic blood diseases may also refer to this standard. |
GBZ75-2002: Diagnostic Criteria of Occupational Acute Toxic Hematologic Diseases Caused by Chemicals ---This is a DRAFT version for illustration, not a final translation. Full copy of true-PDF in English version (including equations, symbols, images, flow-chart, tables, and figures etc.) will be manually/carefully translated upon your order.
Diagnostic Criteria of Occupational Acute Toxic Hematologic Diseases Caused by Chemicals
ICS 13.100
C60
GBZ
People's Republic of China National Occupational Health Standards
Occupational acute chemical toxicity - Diagnostic criteria for blood system diseases
Diagnostic Criteria of Occupational Acute Toxic Hematologic Diseases
Caused by Chemicals
Released in.2002-04-08
2002-06-01 Implementation
Issued by the Ministry of Health of the People's Republic of China
Foreword
Article 5.1 of this standard is recommended and the remainder is mandatory.
According to the "People's Republic of China Occupational Disease Prevention Law" to develop this standard. Since the implementation of the standard date, the original standard
GB 17508-1997 inconsistent with this standard, subject to this standard.
In a variety of professional activities, may be in a short period of time exposure to some high concentrations and high toxicity of chemicals and then acute
poison. These chemicals can be known varieties, and some have been poisoned after a fashion is unknown its exact pathogenic varieties; some
Species caused by poisoning in the "list of occupational diseases" in the famous, and some are not yet included; some have independent diagnostic criteria, and some
It has not yet developed a separate diagnostic criteria. But all of the acute poisoning diseases have a common incidence of the law, it is necessary
Develop rules that should be observed when diagnosing acute poisoning.
The rules stipulated in this standard refer to the diagnosis of occupational acute chemical poisoning, which are used to ensure occupational
The unity of the diagnostic system of acute chemical poisoning, whether known or concealed by the cause, and whether it is caused by poisoning
Which target organ damage, can be in accordance with the provisions of this standard rules for diagnosis.
In the diagnosis of occupational acute chemical poisoning under the general heading, including the following 10 parts.
Part 1. Diagnostic criteria for occupational acute chemical poisoning (general);
Part 2. Occupational acute occult chemical poisoning diagnostic rules;
Part 3. Occupational acute chemical toxicity - Multiple diagnostic criteria for multiple organ dysfunction syndrome;
Part 4. Diagnostic criteria for occupational acute exogenous death;
Part 5. Occupational acute chemical toxicity - Criteria for the diagnosis of neurological diseases;
Part 6 Occupational acute chemicals - Criteria for the diagnosis of toxic respiratory diseases;
Part 7. Diagnostic criteria for occupational acute toxic liver disease;
Part 8. Diagnostic criteria for occupational acute toxic nephropathy;
Part 9 Occupational Acute Chemicals - Toxic Cardiac Disease Diagnostic Criteria;
Part 10 Occupational Acute Chemicals Toxicity Diagnostic criteria for blood system diseases;
Appendix A to this standard is an informative appendix.
This standard is proposed and centralized by the Ministry of Health of the People's Republic of China.
This standard by the Heilongjiang Provincial Institute of Occupational Health and Occupational Diseases, Shenyang City Institute of Labor and Health Occupational Diseases, Guangdong Province occupation
Disease prevention and control hospital is responsible for drafting; Liaoning Province Occupational Disease Prevention and Control Hospital, Jiangxi Province Institute of Labor and Health Occupational Diseases, Tongji Medical University
Belong to the Union Hospital, Panzhihua Labor Hygiene Research Institute to participate in the drafting.
This standard is interpreted by the Ministry of Health of the People's Republic of China.
Occupational acute chemical toxicity - Diagnostic criteria for blood system diseases
Occupational acute chemical poisoning Blood system disease refers to the workers in the short-term occupation of professional activities to absorb large doses
Caused by the blood system damage as the main clinical manifestations of acute systemic disease.
1 Scope
This standard specifies the diagnostic criteria and principles of occupational acute chemical toxicity of the blood system.
This standard applies to occupational activities in contact with this standard Appendix A of the blood poison caused by acute toxic blood system
disease. In the absence of occupational activities in the acute toxic blood system diseases, can also refer to the use of this standard.
2 normative reference documents
The terms of the following documents are hereby incorporated by reference into this standard. Any date that references the date of the document
All subsequent amendments (excluding corrigenda) or revisions do not apply to this standard, however,
The parties to the agreement are able to use the latest version of these documents. Those who do not mind the date of the reference file, its latest
The version applies to this standard.
Standard for the diagnosis of occupational acute insecticide
GBZ 71 Occupational Acute Chemical Poisoning Diagnostic Criteria (General)
Rules for the diagnosis of occupational acute occult chemical poisoning
Identification of Occupational Injury and Occupational Disease Disability in Staff and Workers GB/T 16180
3 diagnostic principles
According to the history of exposure to higher concentrations of chemical toxicants in the short term, the clinical manifestations of blood system damage
The results of the hematology laboratory tests, combined with the necessary field investigation data, exclude other causes, especially drug-induced
Blood disease, can be diagnosed as occupational acute chemicals poisonous blood system diseases.
4 clinical type and diagnostic grade
Occupational Acute Chemicals Toxicity The common clinical types of blood system diseases are as follows.
4.1 toxic hemolytic anemia
4.1.1 mild. poisoning after fatigue, chills, fever, low back pain, burnout, headache, nausea, vomiting, abdominal pain. skin
Sclera yellow dye, anemia appearance; blood test red blood cells and hemoglobin reduction, reticulocyte increase, Herne body
Urine; urinary occult blood positive, protein positive, red, white blood cells and tube, blood urea nitrogen base
This is normal.
4.1.2 severe. rapid onset, sudden chills, fever, delirium, convulsions, coma, cyanosis, scleral deep yellow dye, oliguria
Or no anuria, severe anemia; red blood cells and hemoglobin decreased significantly, reticulocytes increased significantly, Herne body mass out
Now, the urine was deep sauce, urine strong positive blood, blood urea nitrogen increased sharply, showing acute renal failure performance.
4.2 toxic hyperchromatic hemoglobinemia (MHb)
4.2.1 mild. general MHb concentration of 10% or more, lips around the cyanosis, can be asymptomatic.
4.2.2 moderate. MHb concentration of 40% to 60%, in addition to significant cyanosis, the emergence of hypoxia symptoms, such as headache, dizziness,
Fatigue, weakness, body aches, difficulty breathing, tachycardia, unresponsive, lethargy and so on.
4.2.3 severe. MHb concentration of 60% or more, the above symptoms were significantly increased, the face was cyanotic, urine was grape or
Dark brown, can occur in acute circulatory failure, coma, death.
4.3 toxic hematopoietic hemoglobinemia
4.3.1 mainly for hypoxia, may have cyanosis, headache, etc., some patients may coexist methemoglobin, hemolytic performance.
4.3.2 blood sulfide hemoglobin accounted for 2% of total hemoglobin, or even more than 10%.
4.4 toxic acute aplastic anemia
4.4.1 acute onset, was anemia, bleeding tendency, infection fever.
4.4.2 peripheral blood. red blood cells and hemoglobin decreased rapidly, the extreme reduction of white blood cells (neutrophils absolute < 0.5
× 109/L), platelet was significantly reduced (< 20 × 109/L), reticulocyte < l%, absolute value < l5 × 109/L.
4.4.3 bone marrow. nuclear cell proliferation is low, granulocyte, red and megakaryocyte cells were significantly reduced, the relative increase in the proportion of lymphocytes,
Plasma cells, reticular cells, tissue basophils are easy to see. Bone marrow biopsy hematopoietic tissue reduction, mostly replaced by adipose tissue.
4.5 toxic myeloid deficiency
4.5.1 acute onset, sudden chills, fever, sweating, headache, body and joint pain, followed by angina associated with submandibular,
Cervical lymph nodes, a few days after necrotic ulcers, common in the tonsils, soft palate, lips, tongue, skin, nasal cavity, rectum,
Anus and vagina, etc., and secondary sepsis.
4.5.2 peripheral blood. white blood cell count is extremely reduced, neutrophils can only account for 1% to 2%, red blood cells and platelets
The number of basic normal.
4.5.3 bone marrow. bone marrow in the sub-leaf nucleus, rod-shaped nucleus, young and middle and young cells often absent, only a small amount of the original grain and early
Granulocytes, but the proportion of plasma cells, lymphocytes and mononuclear cells increased, red and megakaryocyte lines were normal.
4.6 toxic vasculopathy purpura
4.6.1 skin bleeding, more common in the limbs, buttocks showed edema of the petechiaceae into a piece or into a bubble; also have blood in the stool, abdominal pain and
Joint pain and so on.
4.6.2 platelet count, bleeding or clotting time is normal, capillary brittleness positive.
4.7 Toxic thrombocytopenia
4.7.1 bleeding to limbs skin and nose, gums, tongue, oral mucosa is more common, rare hemoptysis, hematemesis, hematuria, black manure
And fundus and intracranial hemorrhage.
4.7.2 Platelet count reduction (< 50X109/L =.
4.7.3 bone marrow. megakaryocyte reduction, erythroid and granulosa cells roughly normal, may have nuclear left shift phenomenon.
4.7.4 bleeding time can be extended, blood clotting bad, abnormal prothrombin time, blood clotting time can be normal.
4.7.5 immune mechanism caused by thrombocytopenia, can detect platelet membrane-related antibodies.
4.8 toxic platelet dysfunction
4.8.1 symptoms of varying severity, more common nose bleeding, bleeding gums, severe cases can also have subcutaneous hematoma, hematuria, black manure and so on.
4.8.2 platelet count and out, clotting time is normal, platelet adhesion and platelet aggregation function decreased, platelet Ⅲ
Lack or release disorder.
4.9 toxic thrombinogen synthesis disorder
4.9.1 visible epistaxis, gingival bleeding, skin petechia or ecchymosis, excessive menstrual flow and hematuria, black manure, hemoptysis and intracranial
Bleeding and so on.
4.9.2 prothrombin time (PT) prolonged, white clay partial thromboplastin time (KPTT) prolonged, clotting time (CT)
And calcium recovery time.
4.10 Toxicity disseminated intravascular coagulation
4.10.1 seen in a variety of severe chemical poisoning poisoning.
4.10.2 Multiple bleeding tendency.
4.10.3 multiple microvascular thrombosis, the corresponding parts of the symptoms and signs of embolism.
4.10.4 is not easy to use the original disease explained microcirculation failure and shock.
4.10.5 laboratory tests. platelet showed a sustained reduction in dynamic; plasma fibrinogen content of less than 1.5 g/L or carried out
(PDP) greater than 20 mg/L; PT and KPTT prolonged; 3 P test positive or plasma fibrinogen degradation products (FDP) greater than 20 mg /
Long and so on.
5 Principles of handling
5.1 Principles of treatment
5.1.1 out of contact, eliminate pollution, quiet rest. If the indications can be applied special effects detoxification drugs.
5.1.2 toxic hemolytic anemia to take alkaline urine, as soon as possible the use of high-dose glucocorticoid control hemolysis, protection of kidney function
Can, severe use of blood purification therapy.
5.1.3 toxic hypergammic hemoglobinemia treatment can be used in the United States and blue and vitamin C and correct hypoxia and other symptomatic, support
Treatment. US blue dosage of 1mg/kg, slow intravenous injection, suffering from 6-phosphate dehydrogenase deficiency should not be applied to avoid hair
Health hemolytic reaction.
5.1.4 treatment of toxic thiogulinemia, mainly for symptomatic treatment, the use of US blue and vitamin C is invalid.
5.1.5 toxic acute aplastic anemia. blood transfusion, androgen and glucocorticoid application, control of infection, etc.
Type can choose to try anti-lymphoid (thymus) cell globulin, cyclosporin A or allogeneic bone marrow transplantation.
5.1.6 toxic granulocyte deficiency can be used granulocyte colony stimulating factor (GCSF).
5.1.7 toxic vasculopathy, toxic thrombocytopenia, toxic platelet dysfunction, toxic prothrombin
Synthetic disorders and toxic disseminated intravascular coagulation and other coagulation disorders, according to the principle of medical treatment.
5.2 Other processing
Toxic hemolytic anemia and toxic methemoglobinemia were cured, the mild were removed from the original species of visual disease
Situation and labor conditions, etc., medium and severe should be transferred from the original type of work. Hemolytic anemia according to the presence or absence of kidney damage
And the degree of arrangement of light work or rest.
Toxic hematopoietic hemoglobinemia, toxic myeloid deficiency, toxic acute aplastic anemia and toxic
Vascular purpura, toxic thrombocytopenia, toxic platelet dysfunction, toxic thrombinogen synthesis disorder and
Toxic disseminated intravascular coagulation and other coagulation disorders of the patient cured after the removal of the original species, rest or arrange light work.
6 Correct use of the description of this standard
See Appendix A (informative).
Appendix A
(Informative)
Correctly use the instructions in this standard
A.1 may cause common toxicities in occupational acute toxic blood system diseases
A.1.1 The meaning of occupational toxicants referred to in this standard
Occupational blood poison refers to the blood and/or hematopoietic tissue as the target organ or one of the main target organ or cause blood
The system changes to the main performance of the various chemical poisoning.
A.1.2 Common toxic substances that may cause blood changes
A.1.2.1 Toxicity caused by occupational acute toxic hemolytic anemia. arsine, copper sulfate, lead, chromic acid, naphthalene, antimony,
Ammonium halide, chlorate, methyl mercaptan, phenylhydrazine, benzene Amino nitro compounds (aniline, xylidine, nitrobenzene, dinitro
Benzene, trinitrotoluene, nitroaniline, nitro naphthylamine, nitrochlorobenzene, nitrochlorotoluene), azobenzene oxide, dichlorvos,
Dimethoate, parathion, paclitaxel, organochlorine pesticides, insecticidal squares, pyrethroids, propanil, pentachlorophenol, anti-kui, methamidophos,
Kill, double effect spirit, o-toluidine.
A.1.2.2 Toxicity of occupational acute toxic hypergammaglobulinemia
A.1.2.2.1 Aromatic amino nitro compounds
Aniline. aniline, phenylenediamine, methylaniline, dimethylaniline, ethylaniline, methoxyaniline, ethoxyaniline,
Methyl ethyl aniline, propionanilide, diaminoaniline, p-chloroaniline, o-chlorotoluene, p-bromoaniline, nitroaniline, p-
Nitroaniline, nitrotolaniline, methyltetetramolanilide, p-nitro-o-toluidine.
Phenyl hydroxylamine. phenyl hydroxylamine, chlorophenyl hydroxylamine.
Naphthylamine. nitronaphthylamine.
Nitrobenzenes. nitrobenzene, nitrotoluene, dinitrotoluene, dinitrobenzene, trinitrotoluene, nitrosobenzene,
Nitrochlorobenzene, nitrochlorobenzene, nitrochlorobenzene, m-chloronitrobenzene, dinitrochlorobenzene, p-aminopropenyl
ketone.
Phenols. p-aminophenols, methylaminophenols, dimethylaminophenols, pyrithione.
Phenylhydrazine. phenylhydrazine.
A.1.2.2.2 Pesticides. Insecticides (chlorpheniramidine), Chrysanthemum (p-chlorotoluene dimethyl thiourea), propanil (N-3,4
Chlorophenylpropionamide), herbicidal ether (2,4-dichlorophenyl-4-nitrophenyl ether), metoclopramide.
A.1.2.2.3 Other. nitrogen oxides, nitrites, nitrates, ethyl nitrite, chlorates, chlorites.
A.1.2.3 Toxicity caused by toxic thiogulinemia. generation of zinc (ethylene bis bis-thiocarbamate), acetophenone
Amine and so on.
A.1.2.4 Toxicants that cause toxic acute aplastic anemia. benzene, carbon tetrachloride, arsenic trioxide.
A.1.2.5 Poisoning caused by toxic myeloid deficiency. nitrogen mustard, thiotepine and so on.
A.1.2.6 Toxicants that cause toxic vasculopathy. gold, mercury, bismuth, twenty-two, organophosphates, military
Yi's gas, etc.).
A.1.2.7 Poisoning caused by toxic thrombocytopenia. benzene, lead, arsenic, iodide, trinitrotoluene, benzene arsine compounds,
Carbon tetrachloride, twenty-two, six six six, gold preparations, ethanol and so on.
A.1.2.8 Toxicities that cause toxic platelet dysfunction. Polyvinylpyrrolidine, potassium cyanide, iodoacetic acid, methyl nitrite,
Mercuric chloride, benzoic acid and so on.
A.1.2.9 Toxicants that cause toxic thrombinogen synthesis disorders. rodents, rodenticides, rodents and so on.
A.1.2.10 Toxicity caused by toxic disseminated intravascular coagulation
Various chemical toxicities Acute acute poisoning complicated with acute respiratory distress syndrome (ARDS), acute hemolysis, liver or kidney
Heavy damage, etc., can occur disseminated intravascular coagulation (DIC).
A.1.2.11 Other poisons in accordance with A1.1.
A.2 The scope of application of this standard
This standard applies to any occupational exposure to exposure to the blood poisoning listed in Appendix AI of this standard.
(Including subacute) toxic blood system diseases.
A.3 Diagnosis of occupational acute toxic blood system diseases, in addition to occupational exposure history, site investigation and monitoring data, Pro
Bed performance, should pay special attention to hematology laboratory tests. Check items in addition to routine examination, according to the blood disease Pro
Bed type and differential diagnosis.
A.4 Blood methemoglobin spectrophotometric method see GBZ 46.
Other hematological examinations, especially toxic and disseminated intravascular coagulation in laboratory tests and normal values can refer to
The latest version of the domestic practical medical and clinical hematology monograph.
A.5 plasma exchange and dialysis therapy is the rescue of acute severe acute hemolysis of the key measures should be used as soon as possible.
Toxicity of methemoglobinemia should be done early with american and vitamin C.
Toxic hematopoietic hemoglobinemia symptomatic treatment, Mei Lan and vitamin C is invalid.
Toxic acute aplastic anemia, toxic myeloid deficiency and toxic vasculopathy, toxic blood
Plate reduction, toxic platelet dysfunction, toxic thrombinogen synthesis disorder and toxic disseminated intravascular coagulation, etc.
Treatment of coagulation disorders is treated according to the principle of medical treatment.
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