GBZ 26-2002 Diagnostic criteria for occupational acute trialkyltin poisoning
Some standard content:
ICS 13.100
National Occupational Health Standard of the People's Republic of China GBZ26—2002
Diagnostic Criteria of Occupational Acute Trialkyltin PoisoningPublished on April 8, 2002
Implemented on June 1, 2002
Ministry of Health of the People's Republic of China
Article 6.1 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 GB8784-1988 and this standard, this standard shall prevail. Acute trialkyltin poisoning may be caused by occupational activities involving exposure to trialkyltin. In order to protect the health of the exposed persons and effectively prevent and control trialkyltin poisoning, GB8784-1988 was issued. The main changes in this revision are: In combination with the research progress in recent years, the effects of trialkyltin on the nervous system of the middle plate are highlighted in the diagnostic criteria. Due to the different sites of toxicity of different types of trialkyltin compounds, the clinical manifestations are also different. Based on clinical case reports, this standard has been supplemented in the diagnosis and classification standards. 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 is drafted by the Shanghai Center for Disease Control and Prevention. The participating drafting units include Huashan Hospital Affiliated to Fudan University, Shanghai Sixth People's Hospital, and Shanghai Yangpu District Central Hospital. This standard is interpreted by the Ministry of Health of the People's Republic of China. Occupational acute trialkyltin poisoning diagnostic standard GBZ26-2002
Occupational acute trialkyltin poisoning is a systemic disease with central nervous system damage caused by short-term exposure to a large amount of trialkyltin in occupational activities. 1 Scope
This standard specifies the diagnostic criteria and treatment principles for occupational acute trialkyltin poisoning. This standard is applicable to the diagnosis and treatment of occupational acute trialkyltin poisoning, and can also be used as a reference for non-occupational acute trialkyltin poisoning.
2 Normative references
The clauses in the following documents become the clauses of this standard through reference in this standard. For all dated references, 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 all undated references, the latest versions are applicable to this standard.
GB/T16180
3 Diagnostic principles
Diagnostic criteria for occupational contact dermatitis
Diagnostic criteria for occupational chemical skin burnsDiagnostic criteria for occupational acute chemical toxicity of nervous system diseasesIdentification of the degree of disability caused by work-related injuries and occupational diseases of workers can be diagnosed only after the accurate history of occupational exposure to trialkyltin, combined with clinical symptoms, signs and relevant laboratory test results, reference to on-site labor hygiene surveys, comprehensive analysis, and exclusion of similar diseases caused by other reasons. 4 Contact reaction
After exposure to trialkyltin, there will be headache, dizziness, fatigue, and some contacts may have irritation symptoms of eyes, nose, and throat. After the contact is broken, the symptoms generally disappear within 24 hours. 5 Diagnosis and classification standards
5.1 Mild poisoning
After a latent period of several hours to several days after exposure to trialkyltin, one of the following conditions will occur: a) aggravated headache, dizziness, fatigue, mental fatigue, loss of appetite, nausea, sleep disorders, which may be accompanied by sweating or slow heart rate;
b) irritability, obvious memory impairment, and tinnitus and hearing loss. 5.2 Moderate poisoning
Symptoms such as extreme fatigue and mental depression, and one of the following conditions: a) Vomiting, weakened or absent abdominal wall reflexes and cremasteric reflexes; b) Confusion of consciousness and drowsiness
c) Obvious emotional disorders, such as depression, anxiety, indifference, irritability, etc.; d) Complex partial epileptic seizures.
5.3 Severe poisoning
One of the following conditions:
a) Coma, which may be accompanied by convulsions;
b) Obvious mental symptoms, such as rage, aggressive behavior, fabrication, hallucinations, etc., accompanied by disorientation; c) Grand mal epileptic seizures;
d) Obvious cerebellar damage.
Handling principles
Treatment principles
6.1.1 Immediately leave the scene and change contaminated clothing. If the skin or eyes are contaminated, they should be rinsed thoroughly with clean water immediately. 6.1.2 Those who have been exposed should be closely observed for 5 to 7 days, rest in bed, be given necessary examinations, and be given symptomatic treatment in a timely manner. 6.1.3 There is no specific antidote, and symptomatic and supportive treatment is the main treatment. Early, adequate, and short-term use of adrenal glucocorticoids. In case of cerebral edema, fluid intake should be controlled, and hypertonic dehydrating agents and diuretics should be given. Patients with moderate and severe poisoning can be treated with hyperbaric oxygen. When intracranial hypertension cannot be controlled by conventional treatment, surgical decompression can be considered. 6.2 Other treatments
Mildly poisoned patients can engage in normal work after recovery, but should not be exposed to organotin. Moderately and severely poisoned patients should be arranged to work without contact with poisons, depending on the recovery of the disease. Those who need to be assessed for their ability to work should be treated in accordance with GB/T16180. 7 Instructions for the correct use of this standard
See Appendix A (Informative Appendix).
Appendix AbZxz.net
(Informative Appendix)
Instructions for the correct use of this standard
A.1 This standard applies to acute poisoning by trialkyltin compounds and also to acute poisoning by tetraalkyltin compounds. A.2 Some varieties of this type of poison (such as triethyltin bromide, tributyltin compounds, etc.) can cause skin and mucous membrane irritation symptoms. However, the diagnosis of acute trialkyltin poisoning must be made based on systemic manifestations, combined with occupational history, on-site investigation and other necessary examinations, and comprehensive analysis can be made.
A.3 The incubation period is generally 1 to 5 days. In the early stage, there may be only mild neurotic symptoms or overexcitement. The symptoms are non-specific! It is often easy to misdiagnose. Therefore, for those who are exposed to a large amount of trialkyltin in a short period of time, even if there are no local irritation symptoms or systemic poisoning symptoms, they should be closely observed for 5 to 7 days. During the course of the disease, if the abdominal wall reflex or cremaster reflex changes from normal to weakened or disappeared, it indicates that the condition has worsened and should be treated in time.
A.4 This type of poison takes the central nervous system as the main target organ, but because the toxic sites of different types of trialkyltin are not exactly the same, the clinical manifestations of poisoning are not exactly the same. Trimethyltin mainly affects the limbic system and cerebellum. When the limbic system is damaged, obvious memory impairment, irritability, anxiety, depression, irritability, rage, aggressive behavior, confabulation, disorientation, hyperphagia, sexual dysfunction, and epilepsy (complex partial seizures and generalized tonic-clonic seizures) may occur. When the cerebellum is damaged, nystagmus, ataxia dysarthria (explosive speech or poetic speech), and ataxia mainly occur. Triethyltin is myelin toxic and causes leukoedema. Clinically, it is mainly manifested by intracranial hypertension, and severe cases have impaired consciousness.
A.5 Patients with acute trimethyltin poisoning may have cochlear hearing impairment, hearing loss or tinnitus. Therefore, for patients with hearing loss, electrical audiometry can be performed.
A.6 Acute trimethyltin poisoning epileptic seizures are mostly complex partial seizures, but can also be generalized tonic-clonic seizures, the latter of which is what was previously called a grand mal seizure. Complex partial seizures were previously called psychomotor seizures or lobar seizures, with prominent manifestations of impaired consciousness and mental symptoms. After each seizure lasts for several minutes or longer, consciousness gradually becomes clear, and the seizure process cannot be recalled. Although electroencephalogram examination is not specific, it can be used as an auxiliary diagnostic indicator. A.7 Urine tin determination can be used as an exposure indicator. Urine tin determination can be performed when diagnosis or differential diagnosis is required. A.8 When intracranial pressure is increased and cerebral edema is suspected, head CT or MRI examination can be performed. Lumbar puncture is generally not used as a routine examination item except for differential diagnosis.
A.9 Foreign reports have shown mild liver damage in cases of acute trimethyltin poisoning. Animal experiments have found that tributyltin chloride can cause fatty degeneration of the liver with focal necrosis, which should be paid attention to during observation and treatment. A.10 For toxic encephalopathy caused by poisoning with this type of poison, its diagnosis and treatment can refer to GBZ76; for skin burns or contact dermatitis caused by this type of poison, its diagnosis and treatment can refer to GBZ51 or GBZ20
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