GB 16379-1996 Diagnostic criteria and treatment principles for occupational toxic liver disease
Some standard content:
National Standard of the People's Republic of China
Diagnostic criteria and principles of management of occupational toxic hepatopathyGB16379—1996
Occupational toxic hepatopathy is a toxic liver disease caused by the absorption of chemical toxins in occupational contact. 1 Subject content and scope of application
This standard specifies the diagnostic criteria and management principles of occupational toxic hepatopathy. This standard is applicable to the diagnosis of occupational acute and chronic toxic hepatopathy caused by various chemical toxins. 2 Diagnostic principles
Based on the history of occupational contact, the exact clinical manifestations of liver disease, laboratory tests, combined with on-site hygiene and epidemiological surveys, and dynamic observation data, comprehensive analysis, and differential diagnosis are carried out to determine that the liver disease is indeed caused by the chemical toxins to be contacted before diagnosis can be made. If the manifestations of other system damage caused by virulence agents appear at the same time, it has important reference significance for etiological diagnosis. 3 Diagnosis and classification standards
3.1 Acute toxic liver disease
3. 1.1 Acute mild toxic liver disease
After absorbing a high concentration of liver poison in a relatively short period of time, if two of the following symptoms appear, it can be diagnosed as acute mild toxic liver disease: fatigue, loss of appetite, nausea, pain in the liver area, etc. a.
The liver is enlarged, soft, and tender, and may be accompanied by mild jaundice; b.
Routine liver function tests in acute toxic liver disease are abnormal. c.
3. 1.2 Acute moderate toxic liver disease
Patients with obvious fatigue, mental depression, anorexia, aversion to oil, nausea, abdominal distension, pain in the liver area, etc., liver enlargement, obvious tenderness, abnormal routine liver function test of acute toxic liver disease, and one of the following manifestations can be diagnosed as acute moderate toxic liver disease; a.
Moderate jaundice;
Splenomegaly;
Course of disease for more than four weeks.
3.1.3 Acute severe toxic liver disease
Patients with the following conditions based on the above clinical manifestations can be diagnosed as acute severe toxic liver disease: a.
Hepatic encephalopathy;
Obvious jaundice;
Appearance of ascites;
Hepatorenal syndrome,
Prolongation of prothrombin time to more than one times the normal value, accompanied by bleeding tendency. Approved by the State Bureau of Technical Supervision on May 23, 1996, and implemented from December 1, 1996
3. 2 Chronic toxic liver disease
3.2.1 Observation subjects
GB16379-1996
Workers who work with liver poisons have symptoms such as dizziness, fatigue, loss of appetite, or pain in the liver area; those whose liver is enlarged, soft, and tender, and whose liver function test is normal in the initial screening of chronic toxic liver disease. 3.2.2 Chronic mild toxic liver disease
Those who have symptoms such as fatigue, loss of appetite, nausea, upper abdominal fullness, or pain in the liver area; those whose liver is enlarged, soft or flexible, and tender, and whose liver function test is abnormal in the initial screening or re-screening of chronic toxic liver disease. 3.2.3 Chronic moderate toxic liver disease
Patients with any of the following manifestations may be diagnosed with chronic moderate toxic liver disease: the above symptoms are more severe, the liver tends to gradually enlarge or harden, accompanied by obvious tenderness; a.
fatigue and gastrointestinal symptoms are more obvious, serum transaminase activity, -glutamyl transpeptidase or -globulin are repeatedly abnormal or continuously elevated,
have clinical manifestations of chronic mild toxic liver disease, accompanied by splenomegaly. c
3. 2. 4 Chronic severe toxic liver disease
Based on chronic moderate poisoning, patients with any of the following manifestations may be diagnosed with chronic severe toxic liver disease: a.
liver cirrhosis,
accompanied by obvious kidney damage,
serum albumin continues to decrease.
4 Treatment principles
4. 1 Acute toxic liver disease
4. 1. 1 Etiological treatmentbZxz.net
Early etiological treatment, such as the use of complexing agents, special antidotes or blood purification therapy. 4.1.2 Symptomatic and supportive treatment
Bed rest, give a light diet rich in vitamins and easy to digest, intravenous injection or intravenous drip of glucose, vitamin C, etc., and appropriately select Chinese and Western medicines for the treatment of acute liver diseases; b.
c. Other reasonable treatments are given for systemic and other systemic damage. 4.1.3 Acute severe toxic liver disease
a. The focus is on treating liver damage, preventing and treating its complications, taking corresponding positive measures to block liver cell necrosis, promote liver cell regeneration, and strive for early recovery;
b. Glucocorticoids can be used, and the dosage and course of treatment can be adjusted in time according to the condition. Close observation should be carried out to prevent various side effects, and special attention should be paid to upper gastrointestinal bleeding. Other treatments can refer to the rescue treatment plan for fulminant hepatic failure. 4.2 Chronic toxic liver disease
4.2.1 Once the diagnosis is clear, the patient should rest and be hospitalized as much as possible. 4.2.2 A treatment plan should be formulated according to the condition. Rest should be the main treatment in the early stage. After the condition improves, appropriate activities can be carried out and normal life patterns can be gradually restored. It is advisable to choose a diet that is easy to digest and ensure necessary nutrition. Alcohol is prohibited and drugs that can cause liver damage are prohibited. 4.2.3 Symptomatic and supportive treatment are very important. Appropriate Chinese and Western medicine treatment should be used to avoid abuse. 4.2.4 For those with specific drug treatment indications for virulence agents, they can be used in a planned manner according to the condition. 5 Assessment of work capacity
5. 1 Acute toxic liver disease
5. 1. 1 After the recovery of acute mild toxic liver disease, the patient should be temporarily transferred from the original job; after the recovery of acute moderate toxic liver disease, the patient should generally not engage in liver poisoning work; after the recovery of acute severe toxic liver disease, the patient should not engage in poisoning work. 5.1.2 Those who still have obvious symptoms after the acute phase or whose liver function test has not recovered can be given rest and treatment according to their condition, and follow-up work should be done.
5.2 Chronic toxic liver disease
5.2.1 Observation subjects
Reexamine once every 2 to 3 months, and rescreen liver function tests or other examinations if necessary. The diagnosis should be made as soon as possible. Necessary treatment can be given during the observation period.
5. 2. 2 After the recovery of chronic mild toxic liver disease, the worker should be transferred away from liver poisoning work. 5.2.3 After the recovery of chronic moderate toxic liver disease, the worker should be transferred away from toxic and harmful work. 5.2.4 For chronic severe toxic liver disease, a long-term rest should be given. After treatment and rest, if the condition is significantly improved and the health condition allows, the worker can appropriately participate in light work without contact with harmful factors. 6 Requirements for health examination
6.1 Pre-employment physical examination
All workers who work with liver poisons should undergo a pre-employment physical examination. The items shall be in accordance with the requirements of internal medicine physical examination, including routine liver function tests and examination indicators for different poisons and serum HBsAg determination. 6.2 Regular physical examination
Workers who work with liver poisons should undergo a physical examination once a year. The examination items can refer to the pre-employment physical examination items. 7 Occupational contraindications
People with a history of liver disease of various causes who still often have obvious digestive tract symptoms or intermittent abnormal liver function tests, a.
People with hepatosplenomegaly,
Hepatitis B virus "carriers".
A1 Definition of liver poisons
GB 16379--1996
Definition and scope of liver poisons
(Supplement)
Various chemical poisons with the liver as the main target organ or one of the main target organs are called liver poisons. A2 Common varieties
According to domestic data, common liver poisons include: A2.1 Metals, metalloids and their compounds yellow phosphorus, phosphine, arsenic trioxide, arsenic, thallium, lead, antimony, decaborane, etc. A2.2 Halogenated hydrocarbons: carbon tetrachloride, chloroform, difluoroethane, trichloroethane, tetrafluoroethane, vinyl chloride, trichloroethylene, tetrachlorofluoroethylene, chloroprene, polychlorinated biphenyls, etc.
A2.3 Aromatic amino and nitro compounds: aniline, toluidine, chloroaniline, methoxyaniline (aminoanisole), ethoxyaniline (aminophenylethyl ether), xylidine, nitrobenzene, dinitrobenzene, trinitrobenzene, trinitrotoluene, nitrochlorobenzene, dinitrofluorobenzene, nitroaniline, 2,4,6-trinitromethylnitramine (tetryl), etc.
A2.4 Other ethanol, chloroethanol, pentachlorophenol, hydrazine, 1,1-dimethylhydrazine, dimethylformamide, organophosphorus pesticides, organofluorine pesticides, etc. A2.5 With the development of industrial and agricultural production, the above varieties will be continuously supplemented. A3 Toxicity of liver poisons
The toxicity of various liver poisons and the severity of toxic liver disease are affected by the exposure dose, mode, the presence or absence of joint effects and various individual factors. In diagnosis, it should be considered comprehensively from a holistic perspective. Appendix B
Key points for diagnosis and differential diagnosis
(Supplement)
B1 Key points for diagnosis
B1.1 Key points for diagnosis of acute toxic liver disease
According to occupational exposure history, on-site investigation, epidemiological history and biological monitoring, etc., obtain etiological information; a.
Comprehensively analyze symptoms, signs, liver function tests, and other necessary examinations to obtain the basis for acute liver disease; b.
Explore whether the liver disease is caused by poisons: whether the time of exposure to poisons and the onset of the disease, the nature of the poison's action and clinical manifestations, and whether the three aspects of possible c
absorbed dose and severity are consistent. If the basic conditions are consistent and the differential diagnosis is done well, the diagnosis can be initially confirmed; if there are any discrepancies, further examination and close observation can be carried out according to the specific situation in order to confirm the diagnosis. B1.2 Key points for diagnosis of chronic toxic liver disease
The disease has an insidious onset and progresses slowly. There is still a lack of sensitive and specific diagnostic indicators. Therefore, it is often difficult to draw a diagnostic conclusion based on a single clinical examination. Therefore, health monitoring must be carried out for liver poison workers to obtain the annual changes in various clinical manifestations after exposure to poisons. Providing more complete and comprehensive information is the main basis for a clear diagnosis. The main thinking of diagnosis is:
Based on the dynamic observation results of symptoms, signs, liver function tests and other examinations, to determine liver lesions; a.
b. Combine all the information on occupational exposure, conduct a comprehensive analysis, judge the relationship between liver lesions and exposure to poisons, and make a differential diagnosis to obtain an etiological diagnosis.
B2 Key points for differential diagnosis
B2.1 Key points for differential diagnosis from viral hepatitis GB16379-1996
Viral hepatitis is divided into hepatitis A, hepatitis B, hepatitis C (formerly known as post-transfusion non-A, non-B hepatitis), hepatitis D and hepatitis E (formerly known as epidemic or enteric non-A, non-B hepatitis). Viral hepatitis should be diagnosed based on a comprehensive analysis of epidemiological history, symptoms, signs and laboratory tests, and with reference to the diagnostic criteria revised by the National Conference on Viral Hepatitis (see Chinese Journal of Infectious Diseases, Issue 1, 1991). Serological markers are one of the main diagnostic indicators, but the diagnosis should not be made based on this marker alone. Table B1 Clinical and epidemiological significance of commonly used serological markers of viral hepatitis Hepatitis type
Serological markers
(five types)
Anti-HAV-IgM
Anti-HAV-IgG
Anti-HBs
Anti-HBc-IgM
Anti-HBc-IgG
Anti-HBe
Time of decline
Clinical and epidemiological significance
Type A Appears in the early stage of hepatitis, can be detected in the acute or recovery period within 3 to 4 months. Appears later than anti-HAV-IgM, lasts for several years or even decades. Can be detected at the end of the incubation period and one week before the onset of the disease, reaching a peak at the onset of the disease. 80% of acute hepatitis patients are in the recovery period of acute hepatitis, or have had hepatitis A in the past, indicating immunity. Acute incubation period, acute phase, chronic phase and "carrier" are important signs. Indicates the existence of HBV infection. Disappears within 1 to 3 months after the disease. If it has not turned negative within 6 months, it indicates the possibility of chronicity. Appears in the late stage of recovery from acute hepatitis, subclinical protection against HBV. Antibodies are also produced after infection and vaccination with hepatitis B virus vaccine. Indicates immunity
Appears when HBsAg carrier status disappears
Circulating serum can only be detected by adding detergent
Usually indicates viral replication, patient blood and
body fluids are infectious. This sign is generally not tested
Appears in the acute phase and recovery phase, 3 to 6 signs of recent infection and viral replication. Continuous positivity indicates prolonged disease activity and may decrease or disappear after a month. In the chronic stage, positivity often indicates activity. It appears 1 to 2 months after acute infection and persists, indicating that there has been hepatitis B virus infection for several years or more than ten years. It also appears after subclinical infection. It is a soluble component of the HBV core. Most of the cases are positive in the acute stage and disappear earlier than HBsAg. If it persists for more than 3 months, it may be produced during virus replication. Acute patients develop into chronic patients with transient positivity. In chronic patients, it is an important sign of HBV replication and the infectiousness of the patient. In the recovery stage of acute hepatitis, some chronic hepatitis cases appear about 3 to 6 months during the recovery stage of acute hepatitis and can last for more than several years. Chronic hepatitis virus is positive when replicating. Positive means that the virus replication is not active and the infectivity is low; HBsAg negative indicates that there has been HBV infection in the past. Hepatitis type Serological markers (five types) Anti-HCV Anti-HD-IgM Anti-HD-IgG Anti-HE-IgM Anti-HE-IgG GB 16379--1996 Continued Table B1 Time of decline Clinical and epidemiological significance Appears 2 to 6 months after onset, and remains positive in the late stage of acute hepatitis and chronic hepatitis in the chronic stage. Appears in acute and chronic infections Transiently positive in the acute stage and persists in chronic infections, both accompanied by HBsAg and anti-HBc positive
Both accompanied by HBs Ag and anti-HBc positive
Occurs in acute and chronic infections and when the infection has recovered. If anti-HBs and anti-HBc appear at the same time
Occurs in the acute phase and decreases in the recovery phase
The titer is low and difficult to detect
Currently, the most common viral hepatitis in my country is hepatitis B. IgG positive, indicating that hepatitis has been controlled
Diagnosis of acute cutaneous hepatitis
Table B2 Common patterns of clinical serum hepatitis B virus positive markers and their clinical and epidemiological significanceHBsAg
Anti-HBs
Anti-HBc-IgM
Anti-HBc-IgG
Anti-HBe
Clinical and epidemiological significance
Acute phase, active phase, highly contagious
After acute recovery phase, subclinical infection, continued positive after vaccination
Acute recovery phase, past infection, after subclinical infection, non-contagious
Chronic viral infection, no or little active viral replication, generally weakly contagious
May be in the recovery phase, or still have a low-grade infection, HBsAg Very low titer, undetectable
Acute latent period, acute phase and carriers, need to be followed up
Combined with clinical diagnosis, it can be diagnosed as acute hepatitis B, waiting
Special clinically, there is often severe or severe hepatitis
Explanation: Single anti-HBc positive, clinically possible, (1) past infection, has recovered, anti-HBc titer is low (or the method is not sensitive), so it is not detected; (2) there is still HBV infection, HBsAg titer is low, and it cannot be detected; (3) false positive. For those who have latent hepatitis B infection or hepatitis B virus "carriers", who develop liver disease symptoms and abnormal liver function tests after exposure to liver toxins, or those who have newly developed or combined viral hepatitis after the original occupational toxic liver disease is basically stable, the diagnosis and differential diagnosis are mainly based on the history of exposure to viral hepatitis and clinical manifestations, combined with occupational exposure history, poison type, dose, effect relationship, etc., and refer to serological markers for comprehensive analysis to reach a diagnosis.
B2.2 Key points for differential diagnosis from drug-induced liver disease The clinical manifestations of hepatocellular and mixed types in acute drug-induced liver disease and chronic active hepatitis type in chronic drug-induced liver disease are similar to those of acute and chronic toxic liver disease. Detailed inquiries about medical history and medication history are particularly important for diagnosis. The key points for differential diagnosis are: Detailed inquiries about past and current medication history, and understanding which drugs can cause which type of drug-induced liver disease,And analyze the relationship between the type of drug used, dosage, time and the time of liver damage, etc., 312
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b. It may be accompanied by manifestations of allergic reactions, such as rash, eosinophilia, etc., or other side effects of the pathogenic drug, c. For allergic drug-induced liver disease, the lymphoblast transformation test or macrophage (or leukocyte) migration inhibition test is positive, but the positive rate of skin test is very low, which can be used for reference: d. If the patient can get better quickly after stopping the drug and observing, it is conducive to the diagnosis of this disease. If the liver disease recurs after the drug is re-administered, the diagnosis can be established. However, the re-administration test may lead to serious consequences, even fatal, and should not be used lightly, e. Liver biopsy.
B2.3 Others
It should be differentiated from alcoholic liver disease, fatty liver caused by other causes, cirrhosis, idiopathic autoimmune chronic active hepatitis, metabolic liver disease and biliary tract disease. The key points of differentiation can be referred to relevant materials and will not be listed separately. B3 Clinical grading of hepatic encephalopathy
Four-degree classification method:
Grade I patients may have abnormal emotions, such as euphoria, multi-talk, depression, indifference, etc. Grade I patients may have abnormal personality and behavior, drowsiness, disorientation, confusion, and sometimes a state of trance, positive flapping tremor, hyperreflexia of tendons, and positive ankle clonus.
Sub-degree mania, drowsiness, and then coma, and still respond to stimulation. Grade V enters deep coma, has no response to stimulation, and tendon reflexes disappear. B4 Health monitoring should be carried out for workers who work with liver poisons. It is the main data for diagnosing occupational chronic toxic liver disease and should be implemented seriously. Appendix C
Clinical application of liver function tests
(supplement)
C1 The liver is the largest substantial organ in the body and has relatively complex physiological functions. It has functions such as digestion, metabolism, detoxification, excretion, storage, and participates in blood coagulation and immune reactions. Various liver function tests are designed for a certain function. There is no test that can reflect the full range of liver functions, so a reasonable choice is required. C2 The liver has strong reserve and regeneration capabilities. When liver damage is mild or chronic liver disease is relatively stable, liver function tests can be normal. Therefore, when liver function tests are normal, liver disease cannot be ruled out. On the contrary, when liver function tests are abnormal, it is not necessarily liver disease. C3 The purpose of liver function tests is:
Screening test for liver disease, that is, whether liver disease exists; differential diagnosis of liver disease,
Determination of the severity of liver disease,
d. Evaluation of treatment effects;
Follow-up of liver disease and estimation of prognosis.
C4 Clinicians must be familiar with the principles, clinical significance and evaluation of liver function tests in order to correctly select items and apply them reasonably. At present, there is still a lack of ideal liver function tests with high specificity and sensitivity for the diagnosis of toxic liver disease, so diagnosis must emphasize comprehensive analysis. Liver function tests are important, but not the only diagnostic indicator. C5 Based on the diagnosis needs of this disease and the current actual situation in my country, the liver function tests listed in this standard are described as follows: C5.1 Routine liver function tests for acute toxic liver disease: refers to serum alanine aminotransferase (ALT, i.e. GPT), serum bilirubin quantitative test or jaundice index; if necessary, serum bile acid determination, serum aspartate aminotransferase (AST, i.e. GOT), serum prealbumin (PA) or serum glutamyl transpeptidase (-GT) can be selected. C5.2 Initial screening liver function test for chronic toxic liver disease: During the regular examination of liver poison workers, ALT and serum bile acid determination are used as initial screening indicators. Appropriate liver function tests can also be selected as initial screening indicators based on the characteristics of specific poisons. 313
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C5.3 Liver function test for rescreening of chronic toxic liver disease: refers to serum protein electrophoresis, total protein and albumin, AST, Y-GT, transferrin, triglyceride or monoamine oxidase (MAO) determination, etc., which can be selected according to the specific clinical situation. Intravenous tryptophan tolerance test (ITTT) and indocyanine green retention test (ICG) are liver function tests with good sensitivity and specificity. If conditions permit, they can be used as rescreening indicators to improve the quality of diagnosis. C6 Other liver function tests such as serum lactate deaminase (LDH) and its isoenzymes (LDHs), arginine succinate lyase (ASAL), ornithine aminotransferase (OCT), glutathione-S-transferase (GST), alkaline phosphatase (AKP), adenosine deaminase (ADA), high-density lipoprotein (HDL), low-density lipoprotein (LDL) determination, etc., have been reported for the diagnosis or screening of toxic liver disease. However, since some items are not yet popular or have poor specificity, they are not included in this standard. The above items can be selected as diagnostic references according to specific clinical conditions.
C7 About breath test 14C and 13C marker breath test is a relatively new liver function test. These tests have the advantages of strong sensitivity and repeated measurement. They have been used in clinical screening tests for liver disease diagnosis. This test provides a new diagnostic indicator for occupational toxic liver disease. More data can be accumulated in practice. It is recommended that units with conditions can conduct further research. C8 About test methods The same liver function test has different test methods and normal values. Except for the items listed in Appendix D and E, this standard does not make unified regulations for other liver function test methods. Each unit can select appropriate methods and their normal values as standard recommendations according to specific conditions.
C9 Sensitive liver function tests that can reflect early liver damage are one of the key research topics at home and abroad in recent years. In clinical work, it is necessary to grasp the progress information, create conditions, and apply and accumulate experience in practice to continuously improve the quality of diagnosis of this disease. Appendix D
Method for determining the retention rate of indocyanine green (ICG) in blood (reference)
D1 Principle
Blood is collected 15 minutes after intravenous injection of indocyanine green, serum or plasma is separated, the concentration of indocyanine green is determined, and the average retention rate (R) is calculated. In various liver diseases, the retention rate of indocyanine green is higher than the normal value due to abnormal liver uptake and excretion functions. D2 Instrument
UV-visible spectrophotometer.
D3 Reagents
Indocyanine green injection.
D4 Operating steps
D4. 1 Dilute indocyanine green to 5 mg/mL with hot distilled water for injection. D4.2 The injection dose of indocyanine green is 0.5 mg/kg body weight. D4.3 After routine disinfection of the patient's elbow, first draw 5 mL of venous blood (or use heparin for anticoagulation) as a blank control tube, then inject indocyanine green within 30 seconds and start timing.
D4.4 At 15 minutes, draw 5 mL of venous blood (or use heparin for anticoagulation) from the patient's other elbow as the serum (or plasma) to be tested. D4.5 Separate serum or plasma from the drawn venous blood. D4.6 Take 1 mL of serum (or plasma) to be tested, add 2 mL of 0.9% sodium chloride and mix well. At a wavelength of 805 nm, use a blank tube (1 mL of serum or plasma before injection of ICG, add 2 mL of 0.9% sodium chloride and mix well) to calibrate the optical density to "0" point, read the optical density reading of the measuring tube, consult the standard curve, and obtain the ICG content in serum (or plasma) at 15 min. Calculate the average retention rate (R) according to formula (D1): 314
GB16379-1996
Serum ICG content at 15 min (mg/dL) × 100Ris(%) =
1(mg/dL)
Note: Assume that the ICG concentration in serum (or plasma) at injection time 0 is 1 mg/dL. D5 Drawing of standard curve
Indocyanine green 25mg, dilute to 250mL with distilled water to become indocyanine green standard stock solution. Prepare standard solution concentration according to Table D1: Table D1
Test tube number
Indocyanine green standard stock solution, mL
Normal human serum (plasma), mL
Distilled water, mL
Final indocyanine green concentration, mg/dL
Take 1mL of standard solution, add 1mL0.9% sodium chloride, then add 1mL normal human serum (or plasma) and mix well. Measure at 805nm wavelength with a spectrophotometer. The cuvette is 1cm. Use a blank tube (1mL normal human serum or plasma add 1mL0.9% sodium chloride, then add 1mL distilled water and mix well) to calibrate the density to "0" point. Read the optical density readings of each standard solution. Draw a standard curve with the optical density readings as the ordinate and the standard concentration as the abscissa.
D6Normal reference value
After 15 minutes, the average retention rate is less than 10%.
Appendix E
Intravenous tryptophan tolerance test
(reference)
E1Principle
Blood is drawn on an empty stomach and 45 minutes after intravenous injection of tryptophan, the free tryptophan and total tryptophan contents are determined. E2Instrument
E2.1Fluorescence spectrophotometer.
E2.2Portable high pressure sterilizer.
E2.3Ultrafilter (25 mm diameter needle type). E2.4Ultrafiltration membrane (model C×A-50, molecular weight cutoff value 50,000). E3Reagents
E3.11% tryptophan for intravenous injection.
E3.20.6 mol/L trichloroacetic acid (TCA). E3.32% formaldehyde.
E3.4 6 mmol/L ferric chloride (FeCl3)-0.6 mol/L TCA solution. Weigh 162 mg of FeCl: (MW=277.032) and dissolve it in 100 mL of 0. 6 mol/L TCA solution. E3.5Tryptophan standard solution
1mmol/L storage solution;
GB 16379-1996
boolmmol/L tryptophan standard application solution. E4 Operation method
E4.1 Fast for 12 hours, draw 3mL of venous blood, inject tryptophan at 4mg/kg body weight, and draw 3mL of blood from the other arm 45 minutes later. Measure the tryptophan content of serum twice.
E4.2 Prepare ultrafiltrate (for free tryptophan): install the treated ultrafiltration membrane in the ultrafilter, make sure the front side is facing up, tighten the filter, add 0.5mL of serum, install the filter on a plastic tube of appropriate diameter, put it in a centrifuge and centrifuge at 3500-4000r/min for 20 minutes to obtain ultrafiltrate.
E4.3 Preparation of serum supernatant (for total tryptophan): take serum and add an equal amount of 0.6mol/LTCA to mix and precipitate protein, centrifuge and take the supernatant for use.
E4.4 Fluorescent substance generation: Take 4 10mL graduated test tubes and add liquid as indicated: 1
UA (total color)
Serum supernatant
Ultrafiltrate
Standard solution
Distilled water
0. 6 mol/L TCA
2% formaldehyde
6 m mol/L FeCl
-0.6 mol/L TCA
Ue (free color)
S (standard)
B (blank)
The above tubes are covered with plastic test tube plugs for bacterial culture medium, and heated at high pressure in an autoclave for 20 min to generate fluorescent substances. After heating, cool down, add distilled water to the scale of 4mL, and measure the tryptophan content in a fluorescence spectrophotometer with an emission light wave of 448nm and an excitation light wave of 302nm.
E5 Calculation
Free tryptophan (μmol/L)
Total tryptophan (μ mol/L):
E6 Normal reference value
Free tryptophan
Total tryptophan
3~.7 μmol/L
30~~85 μ mol/L
gB × 10(μmol)
Uε—B
二B× 10(μ mol) × 2
F1 Treatment principles
GB163791996
Appendix F
Rescue and monitoring of occupational allergic severe toxic liver disease (supplement)
Occupational acute severe toxic liver disease is relatively rare, but once it occurs, the prognosis is poor, so early diagnosis and early treatment are very important. The principle of treatment is to remove the virus-causing substances and their metabolites in the body, antagonize their toxic effects, and prevent further damage to liver cells; adopt comprehensive treatment to improve the overall condition, restore the body's internal environment balance, promote liver cell regeneration, and prevent complications. F2 Monitoring purpose
The purpose of monitoring is to grasp the situation in a timely manner and make a comprehensive judgment of the condition, which can be used as the main basis for studying treatment plans. F3 Monitoring items
F3.1 Body temperature, pulse, respiration, consciousness, pupil size, check every 2 to 4 hours. F3.2 Closely observe changes in the condition, such as the degree of jaundice, bleeding tendency, presence or absence of liver odor and asterixis, abdominal distension, ascites, liver, spleen changes, etc.
F3.3 If the consciousness disorder tends to progress, pay special attention to whether there is disorientation, visual illusion, hallucination, persecution delusion, responsiveness to speech and pain stimulation, and changes in vestibular eye reflex, pupil light reaction, corneal reflex, etc. F3.4 Daily selective examination of the following items: blood routine, platelet count, serum bilirubin, ALT, prothrombin time, urine routine, stool occult blood test, etc. If the platelet count is reduced, add fibrinogen and plasma protamine paracoagulation test (3P), etc. F3.5 Other blood biochemical tests, fundus examination and B-type ultrasound examination, etc., can be selected and observed regularly in a planned and purposeful manner according to the condition.
F3.6 Regularly measure the concentration of blood and urine toxicants or their metabolites, as well as other laboratory diagnostic indicators. F4 Emergency measures
F4. 1 Etiological treatment, such as the use of special antidotes, chelating agents, etc., can be used for blood purification therapy when necessary. F4.2 Diet should be easy to digest, low-protein, low-fat diet, rich in vitamins, and maintain calorie supply, intravenous drip of 10% glucose, vitamin C, etc., regular insulin 12 U and potassium chloride 1 g can be added to every 1,000 mL of glucose solution, and attention should be paid to maintaining water and acid-base balance. F4.3 Adrenal cortex hormone - generally advocates early application. Commonly used dexamethasone 20 ~ 40mg / d, once or twice between 7-8 am every day, observe the efficacy and reaction after medication, and adjust in time. During the course of this drug treatment, special attention should be paid to preventing upper gastrointestinal bleeding. F4.4 Reduce blood ammonia, keep the stool unobstructed, and clean the enema when necessary; choose oral lactulose, neomycin, metronidazole (Flagyl) or ampicillin, etc., to inhibit the growth of bacteria in the intestine, reduce bacterial protein decomposition, and thus reduce the production of ammonia. F4.5 Give fresh plasma or human albumin, supplement coagulation factors, etc. to enhance the body's resistance. To promote liver cell regeneration, suckling pig liver growth hormone can be tried.
F4.6 Adjust amino acid metabolism disorders, intravenous drip of branched-chain amino acids such as liver and brain clear, BCAA-3H, six-combination amino acids, etc., to reverse the plasma branched-chain/aromatic amino acid ratio.
F4.7 Intravenous drip of sodium glutamate, potassium glutamate or -aminobutyric acid can help patients wake up. Intravenous drip of levodopa can remove and replace false neurotransmitters.
F4.8 This disease is often accompanied by kidney disease. Antibiotics that can easily cause kidney damage should not be used; analgesics and hypnotics that damage liver cells should also be banned.
GB16379-1996
F4.9 Do a good job of disinfection, isolation and nursing, and pay attention to preventing secondary infections, especially ascites infection and fungal infection of organs. Once it occurs, effective antibiotics should be used to quickly control the infection. F4.10 Other symptomatic and supportive treatments, such as the use of vitamin K and prothrombin complex, maintenance of microcirculation, and dialectical treatment of traditional Chinese medicine, are all comprehensive treatment measures and can be used as appropriate. According to current research, toxic liver disease is mainly caused by lipid peroxidation of liver cells and disorder of intracellular Ca++ balance, which leads to liver steatosis and necrosis. Therefore, antioxidants, free radical scavengers and calcium inhibitors have achieved certain therapeutic effects in experimental treatment, but their clinical application needs further discussion.
The above therapies can be determined according to the condition, medical conditions, etc., and clinical observation and summary should be done to improve the rescue effect. Appendix G
Health Monitoring Specifications for Workers of Liver Toxins (Trial) (Reference)
G1 Purpose of Health Monitoring
The main purpose of health monitoring for workers of liver poisons is to: prevent those with employment taboos from engaging in this operation, a.
b. Early detection of liver damage,
Formulate the diagnosis procedure of occupational chronic toxic liver disease, improve the quality of diagnosis, implement primary and secondary prevention measures, and achieve the goal of protecting the health of workers, and provide data for evaluating the labor and sanitation conditions in the workshop. G2 Health monitoring file content
G2.1 Pre-employment physical examination Those who engage in liver poison work must undergo a pre-employment physical examination to have a more comprehensive understanding of the employee's health status. The items include detailed medical history, physical examination, blood routine, liver function test, viral hepatic char serological markers and B-type ultrasound liver and spleen examination.
Liver function test can select one or two tests according to the type of exposure to poisons and local conditions, and there is no unified regulation for specific items. Viral hepatitis serological markers are generally tested with HBsAg as the initial screening, and other relevant indicators are tested when necessary. Appropriate examination items can be selected according to different types of poisons, exposure conditions and other situations. The purpose of pre-employment physical examination is to: a. Find those who are not suitable for liver poison work; b. As basic data for future health monitoring. G2.2After each examination, the results of each examinee will be comprehensively analyzed to fully understand their health status, including whether they have liver damage, and then treated accordingly. See the schematic diagram for details:
Healthy people
Continue to work
Employed
Employed as a doctor
Regular physical examination
Disease patients
Preliminary screening of liver
Function test
Observation subjects
Treat as appropriate
Rescreening of liver
Function test
Patients with liver disease
Diagnosis still unconfirmed
Patients with liver disease
Etiology
Chronic toxicity
Patients with liver disease
Other causes
Continue to observe, treat as appropriate
Healthy people
Other diseases
Healthy workers with liver poisons Diagram of health monitoring for workers—Treatment
—Treat as appropriate
—Continue to work
—Treat as appropriate
G3 Workshop labor hygiene survey provides environmental data for analyzing the health status of workers, and the results of health monitoring examinations are one of the main indicators for evaluating the labor hygiene conditions of workshops, so they are an indispensable item in health monitoring. 318
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