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GBZ79-2013 English PDF

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GBZ79-2013: Diagnosis of occupational acute toxic nephropathy
Status: Valid

GBZ79: Evolution and historical versions

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GBZ 79-2013English169 Add to Cart 3 days [Need to translate] Diagnosis of occupational acute toxic nephropathy Valid GBZ 79-2013
GBZ 79-2002English319 Add to Cart 3 days [Need to translate] Diagnostic Criteria of Occupational Acute Toxic Nephropathy Obsolete GBZ 79-2002

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Basic data

Standard ID GBZ 79-2013 (GBZ79-2013)
Description (Translated English) Diagnosis of occupational acute toxic nephropathy
Sector / Industry National Standard
Classification of Chinese Standard C60
Classification of International Standard 13.100
Word Count Estimation 7,730
Older Standard (superseded by this standard) GBZ 79-2002
Quoted Standard GB/T 16180
Regulation (derived from) Health-Communication (2013) 1
Issuing agency(ies) Ministry of Health of the People's Republic of China
Summary This standard specifies the principles of diagnosis of occupational acute toxic nephropathy, diagnostic classification and principles. This standard applies to occupational acute toxic nephropathy diagnosis and treatment.

GBZ79-2002: Diagnostic Criteria of Occupational Acute Toxic Nephropathy

---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.
(Occupational acute toxic nephropathy diagnostic criteria) ICS 13.100 C60 GBZ People's Republic of China National Occupational Health Standards Diagnostic criteria for occupational acute toxic nephropathy Diagnostic Criteria of Occupational Acute Toxic Nephropathy Released in.2002-04-08 2002-06-01 Implementation Issued by the Ministry of Health of the People's Republic of China

Foreword

Article 6.1 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. In a variety of professional activities, in a short period of time contact with some high concentrations and toxic chemicals can occur acute toxic kidney disease. At present there is no clear at home and abroad for the correct diagnosis and treatment of medical units for reference. To protect the health of the contact person, Effective prevention and treatment of occupational acute toxic kidney disease, according to recent clinical and laboratory research progress, the development of this standard. 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 Peking University Third Hospital Occupational Disease Research Center is responsible for the drafting, Shandong Provincial Hospital Occupational Diseases, Jilin Industrial workers in the hospital workers Institute of Occupational Disease Prevention and Control to participate in the drafting. This standard is interpreted by the Ministry of Health of the People's Republic of China. Diagnostic criteria for occupational acute toxic nephropathy Occupational acute toxic nephropathy refers to occupational activity, due to short-term exposure to large doses of chemical substances caused by To the kidney damage as the main performance of acute poisoning.

1 Scope

This standard specifies the diagnostic criteria and principles of occupational acute toxic nephropathy. This standard applies to occupational activity due to occupational chemicals caused by acute toxic kidney disease. In non - professional Activities due to other toxic substances caused by acute toxic kidney disease, 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. 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 occupational history of exposure to a large number of chemical substances in the short term, the typical clinical manifestations of acute kidney injury, the relevant experiments Room inspection results and on-site labor hygiene investigation, excluding other causes of similar diseases, can be diagnosed.

4 observation object

A large number of exposure to a large number of kidney poison in a short time, there is a transient acute renal damage manifestations of acute toxic nephropathy Object.

5 Diagnostic and grading standards

5.1 mildly toxic nephropathy Any person who has any of the following two manifestations. a) Urine continues to be positive; b) soy sauce color urine, laboratory tests showed occult blood test positive; c) hematuria, laboratory tests show a lot of red blood cells; d) see a large number of urine tube, or white blood cells, or a large number of renal tubular epithelial cells; e) Glomerular filtration rate (GFR) continued < 80 ml/min. 5.2 Moderate toxic nephropathy Any person who has any of the following two manifestations. a) urine output continued < 400ml/24h; b) Urine specificity continued < 1.012, or urine osmolality (Uosm) continued < 350mOsm/kgH2O; c) urinary sodium (UNa) sustained > 40 mmol/L, or filtered sodium excretion rate (FENa) sustained > 2%; d) GFR continued < 50ml/min; e) blood urea nitrogen (BUN) sustained > 7.0mmol/L ( > 20mg/dl), or daily increase > 3.5mmol/L ( > 10 mg/dl); f > serum creatinine (Pcr) > 177μmol/L ( > 2mg/dl), or daily increase > 89μmol/L ( > 1 mg/dl). 5.3 severe toxic nephropathy Any person who has any of the following two manifestations. a) Urine continued < 200 ml/24h; b) GFR continued < 30 ml/min; c) BUN sustained > 21mmol/L ( > 60mg/dl), or daily increase > 7.0mmol/L ( > 20mg/dl); d > Pcr sustained > 430μmol/L ( > 5 mg/dl), or daily increase > 177μmol/L ( > 2mg/dl); e) serum potassium (SK) sustained > 6.0 mmol/L ( > 6.0 mEq/L); f) symptoms of uremia such as nausea, vomiting, headache, drowsiness, trance, convulsions, coma, etc. Congestive heart failure, acute pulmonary edema, metabolic acidosis, hyponatremia, sepsis and other complications.

6 Principles of handling

6.1 Principles of treatment 6.1.1 Observe objects a) immediately from the toxic contact, the skin can be absorbed by the poison should be off the contaminated clothing, and washed with soap and water Skin; patients with gastrointestinal invasion, should be immediately gastric lavage; and then need to rest warm rest. b) patients with systemic poisoning, according to the treatment of poisonous poisoning conventional treatment; treatment should pay attention to careful Drugs with greater toxicity of the kidneys. c) carefully record the amount of liquid intake and close observation of urine routine examination results 2 to 3 days; abnormal need to be kidney Dirty function for further examination. 6.1.2 mild and moderate toxic nephropathy In addition to the above treatment, the following measures can be taken. a) have a special detoxification drugs can be used early, but each dose should be small; can be cleared by blood purification measures, Moderate poisoning patients can be used early this treatment. b) should pay attention to early prevention of insufficient blood volume, the lifting of renal vasospasm, improve renal microcirculation. c) early start diuretic therapy. d) early use of adequate glucocorticoid. e) the emergence of pigment proteinuria, should be early use of alkaline drugs. f) Oxygen free radical scavengers, calcium channel blockers, angiotensin converting enzyme inhibitors and other cellular interventions help Delay the progression of the disease, but need to be used early. 6.1.3 Severe Toxic Kidney Disease In addition to the above treatment, should pay attention to the following points. a) active use of blood purification therapy to prevent uremia, hyperkalemia, water poisoning, etc., and with the detoxification treatment Accelerated toxic discharge. b) active prevention of toxic organs caused by systemic damage to other organs, the protection of vital organs function. c) active prevention and treatment of infection and other complications; attention to a reasonable nutritional supplement. d) oliguria should limit the amount of liquid, proper diuretic; polyuria should pay attention to maintain the body of water and electrolyte balance. 6.2 Other treatments 6.2.l Observe the object After observing no obvious kidney damage and systemic poisoning performance, can return to the original job. 6.2.2 mildly toxic nephropathy After the cure can be engaged in the original job. 6.2.3 Moderate toxic nephropathy After curing can be engaged in normal work, but should avoid kidney poison contact. 6.2.4 Severe Toxic Kidney Disease After curing can be engaged in light work, and to avoid contact with kidney poison; if necessary, refer to GB/T 16180 treatment.

7 Correctly use the instructions in this standard

See Appendix A (informative).

Appendix A

(Informative) Correctly use the instructions in this standard A.1 This standard is mainly applicable to the use of working or productive contact, so that chemical substances in a relatively short period of time a greater amount of invasion of the body Caused by the acute toxicity of kidney damage diagnosis and treatment; due to chemical substances caused by renal tubular mechanical blockage (such as pigment Protein tube type, crystal, etc.), or by its immune mechanism caused by acute kidney damage (such as acute interstitial nephritis, pulmonary hemorrhage - Nephritis syndrome, etc.) are also applicable. Acute toxic nephropathy caused by environmental factors or drugs can refer to the use of this standard. This standard can also be used as other diseases caused by a variety of non-specific systemic pathology, such as hypoxia, shock, cardiopulmonary dysfunction And other causes of secondary acute renal damage diagnosis of the reference. A.2 Common occupational toxicities with direct kidney toxicity are. a. Heavy metals or metal-like compounds such as cadmium, mercury, chromium, Lead, bismuth, uranium, platinum, arsenic, phosphorus, etc .; b. Hydrocarbon compounds such as chloroform, carbon tetrachloride, trichlorethylene, ethylbenzene, naphthalene, Gasoline, etc .; c. Phenols such as phenol, cresol, resorcinol and the like; d. Pesticides, such as organic mercury, organic arsenic, organic chlorine, there are Machine phosphorus, organic fluorine, paraquat, etc .; e. Other compounds, such as synthetic dyes, glycols, acrolein, oxalic acid, pyridine, Morpholine and so on. Common occupational toxicity caused by indirect renal toxicity is mainly caused by acute intravascular hemolysis or the formation of denatured globin Body chemicals such as arsine, antimonide, tellurium, copper, nitro and amino compounds of benzene, insecticidal, Chrysanthemum, phenylhydrazine, coal tar derivatives, resulting in hemoglobin tube block renal tubules; and some compounds in the renal tubules The formation of crystalline or myoglobin tube type, can also cause renal tubular obstruction and even cause acute tubular necrosis. Many environmental factors and drugs also have direct or indirect renal toxicity, should pay attention to differential diagnosis. A.3 The incubation period of this disease is common for several hours to several tens of hours, so the observation period is at least two days. A.4 observation items in addition to the general clinical manifestations, the main urine, urine routine examination (including color, specific gravity, pH, eggs White and urine sediment examination, conditions can be used for urine osmotic pressure determination); the above check abnormalities, but after the review has been self-recovery , Is a transient kidney damage; if the previous indicators continue to be abnormal, should be occult blood test or urinary sodium, sodium filtration rate, Serum creatinine, urinary creatinine, glomerular filtration rate and other indicators of renal function for further examination. A.5 mildly toxic nephropathy should be noted with the identification of urinary tract infection, in addition to symptoms and signs, the urine see bacteria often infected with Important hints. A.6 is currently the most commonly used and more sensitive kidney function indicators are. (L) urine osmotic pressure (Uosm) urine osmotic pressure or osmotic concentration is the degree of urine concentration of the observed indicators, it can be anti- Reflective capacity of renal tubular. Although the urine specific gravity measurement also has this function, but susceptible to solute properties and molecular weight of the shadow Such as protein, sugar can exist in the proportion of urine increased; urinary osmotic pressure is only related to the number of solute particles, and its large Small irrelevant, so the more specific to more accurately reflect the renal tubular function. At present, the use of freezing point osmometer, vapor pressure penetration Pressure meter and other equipment for the determination, convenient and efficient, the results are more objective and reliable. Under normal circumstances Uosm more > 500mOsm/kgH2O, if Uosm < 350 mOsm/kgH2O, more suggestive of renal tubular dysfunction. (2) urinary sodium (UNa) renal tubular function is normal, the discharge of hypertonic hyponatremia, so under normal circumstances UNa will not More than 20mmol/L; when the renal tubular damage, the water absorption of sodium function was significantly reduced, so the discharge of low hypotonic high sodium, at this time UNa more > 40 mmol/L. Therefore, urine sodium can reflect the renal tubular function and help to identify prenatal nitrogen Hyperthyroidism and acute tubular necrosis. (3) filtered sodium excretion rate (FENa) It is defined as the total amount of urinary excretion of sodium per unit of time within the period of time by the kidney The percentage of total sodium filtered by the ball. This indicator not only contains urinary sodium factors, but also contains serum sodium, serum creatinine, muscle Anhydride, glomerular filtration rate and other functions, so the results are more objective and reliable, is currently recognized to reflect the best indicators of renal tubular function. The formula is. Urinary sodium concentration (mmol/L) Urinary creatinine concentration (ml/dl or μmol/L) FENa (%) = ---------- ÷ ------------- Serum sodium concentration (mmol/L) serum creatinine concentration (ml/dl or μmol/L) Under normal circumstances, FENa < 1%, if this value> 2%, then prompted renal tubular dysfunction. (4) Endogenous creatinine production rate (Ccr) This indicator is based on the body to produce a metabolite clearance to carry out Glomerular filtration ability to determine the need for injection of exogenous reference material, it is more simple and easy. Creatinine is high energy phosphate creatinine Dehydration dephosphoric acid products, the amount of production is very constant, normally completely through the urine, which in addition to a very small amount (< 5%) by the kidney Tube excreted, the vast majority of the Department of glomerular filtration, and not for the renal tubular reabsorption, so the clearance rate can be better reflected Glomerular filtration capacity. The formula is as follows. Urine creatinine concentration (mg/dl or μmol/L) 24 hours urine output (ml) 1.73 (m2) Ccr (ml/min) = -------------- × one by one ------ × --- one by one Serum creatinine concentration (mg/dl or μmol/L) 24 × 60 (min) S (m2) Where 1.73 is the body weight of adult body weight of 70kg S for the subject surface area, according to height, weight lookup table obtained; can also be calculated according to the following formula. S = [height (cm) x 0.0061 weight (kg) x 0.0128] -0.1529 1.73/S is roughly 1, the weight is too large This value is slightly less than 1, the weight is too light this value is slightly greater than 1. Ccr normal value of 80ml/min ~ 120ml/min, this value if the value is lower than the normal value of more than 50%, consider the acute Renal insufficiency of the possible; this value if not yet normal value of 25%, then prompted the emergence of acute renal failure. A.7 The focus of this disease treatment is the prevention and treatment of acute renal failure, the key is the emergence of acute renal insufficiency, That should be blocked early disease progression of the relevant ways. Clinical routine use of the measures are. a reasonable infusion and timely fill the blood volume, Use of microvascular dilators to relieve renal vasospasm to improve renal microcirculation, full diuretic to poison and metabolic waste Out, early enough to use glucocorticoids, active use of blood purification therapy, including blood purification therapy especially harmful to the blood Substance clearance has a significant effect. In general, hemoperfusion (HP) is more effective in removing exogenous toxicants For effective, plasma exchange (plasma exchange, PE) can also effectively remove the blood of harmful substances, but with too much blood, Difficult to be widely used; and various dialysis techniques such as hemodialysis (hemodialysis, HD), peritoneal dialysis (peritoneodialysis, PD) and so on the metabolic waste and molecular weight < 50kd exogenous harmful substances have a better clearance effect, for a variety of toxic Kidney disease, in particular, has occurred in acute renal dysfunction, it is a specimen of the treatment of both. This standard relaxes the conditions of blood purification therapy to promote early, that is, to determine the acute moderate toxic nephropathy Can be used in time, so that in addition to the purpose for treatment, but also become a prophylactic means of delaying the occurrence of toxic renal damage, is expected To improve the prognosis will play a good role.

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