GB 8781-1988 Occupational acute carbon monoxide poisoning diagnostic criteria and treatment principles
Some standard content:
National Standard of the People's Republic of China
Occupational Acute Carbon Monoxide Poisoning
Diagnostic criteria and principles of management of occupational acute carbon monoxlde polsoningUDC616-057-616
-07/-08:667
GB 8781-88
Acute carbon monoxide poisoning is an acute cerebral hypoxia disease caused by inhalation of high concentrations of carbon monoxide (CO); a few patients may have delayed neuropsychiatric symptoms. Some patients may also have hypoxic changes in other organs. 7 Diagnostic Principles
According to the history of inhalation of high concentrations of carbon monoxide and the symptoms and signs of acute central nervous system damage, combined with the results of timely determination of carboxyhemoglobin (HbCO) in the blood, on-site hygiene investigation and data on determination of carbon monoxide concentration in the air, and after excluding other causes. Acute carbon monoxide poisoning can be diagnosed.
2 Diagnosis and classification standards
2.1 Contact reaction
Symptoms such as headache, dizziness, palpitations, nausea, etc., which disappear after inhaling fresh air. 2.2 Mild poisoning
Severe headache, dizziness, limb weakness, nausea, vomiting, b. Mild to moderate consciousness disorder, but no coma. Blood carboxyhemoglobin concentration may be higher than 10%. 2.3 Moderate poisoning
In addition to the above symptoms, consciousness disorder manifests as shallow to moderate coma, and recovers after rescue without obvious complications. Blood carboxyhemoglobin concentration may be up to 30%. 2. 4 Severe poisoning
Severe any of the following:
2. 4. 1 Consciousness disorder reaches deep coma or upper cerebral cortex, 2. 4. 2 Patients with impaired consciousness and any of the following symptoms: cerebral edema
shock or severe myocardial damage;
pulmonary edema:
respiratory failure;
upper gastrointestinal bleeding;
brain flat focal damage such as chain system or extrachain system damage signs, carboxyhemoglobin concentration can be higher than 50%,
2. 5 Delayed encephalopathy (neuropsychiatric complications) of intentional carbon monoxide poisoning Approved by the Ministry of Health of the People's Republic of China on February 22, 1988 and implemented on September 1, 1988
CB 878188
After the recovery of consciousness disorder in acute carbon monoxide poisoning, after a pseudo-recovery period of about 260 days, the following clinical manifestations appear: a. Mental and consciousness disorders are in the form of dementia, delirium or decerebrate state; b. Extracorporeal nerve disorders show the manifestation of Parkinson's syndrome; c. Pyramidal nerve damage (such as hemiplegia, positive pathological reflexes or urinary incontinence, etc.); l. Focal functional disorders of the cerebral cortex such as aphasia, blindness, etc., or secondary epilepsy. Head CT examination can reveal pathological areas of decreased density in the brain, and EEG examination can reveal moderate and severe abnormalities. 3 Treatment principles
3.1 Quickly move the patient away from the poisoning site to a ventilated place, loosen the collar, keep warm, and closely observe the state of consciousness. 3.2 Timely first aid and treatment
a. For mild cases, oxygen inhalation and symptomatic treatment can be given: b. For moderate and severe poisoning, oxygen inhalation treatment with normal pressure masks should be actively given, and hyperbaric oxygen treatment should be given if conditions permit. For severe poisoning, symptomatic and supportive treatments such as eliminating cerebral edema, promoting cerebral blood circulation, maintaining respiratory and circulatory functions, and calming the nerves should be given. Strengthen nursing care, prevent and treat complications, and prevent delayed encephalopathy. 3.3 For delayed encephalopathy, hyperbaric hypotension, cortical stimulants, hemodynamic agents or anti-Parkinson's disease drugs and other symptomatic and supportive treatments can be given.
4 Labor capacity assessment
4.1 Mild poisoning can still be performed in the original work after treatment. 4.2 After recovery from treatment, moderate poisoning should be temporarily separated from carbon monoxide work and reviewed regularly for 2 months. If there is no delayed encephalopathy, it can still be performed in the original work.
4.3 If there is severe poisoning or delayed encephalopathy, even if it is recovered after treatment, the worker should be transferred away from carbon monoxide work. 4.4 If there is incomplete organic nerve damage after half a year of treatment due to severe poisoning or delayed encephalopathy, the worker should be permanently transferred away from work involving exposure to carbon monoxide or other neurotoxic substances, and treatment and rest should be arranged according to the condition. 5 Requirements for health examination
5.1 Carbon monoxide workers should undergo a pre-employment physical examination, including detailed internal medicine, neurology and electrocardiogram examinations. 5.2 Personnel engaged in carbon monoxide work should undergo a physical examination every 1-3 years, and the examination items are the same as those for pre-employment physical examinations. 6 Occupational contraindications
6.1 Various organic diseases of the central and peripheral nervous systems. 6.2 Organic heart tube diseases.
A.1 Mild cognitive impairment
A.1.1 Confusion
GB8781--88
Appendix A
Classification and grading criteria for consciousness impairment
(Supplement)
Short-term transient decrease in consciousness clarity, lack of concentration, complete or partial loss of orientation, or accompanied by emotional reactions. A.1.2 Lethargy
The patient is in a state of pathological drowsiness. After receiving strong stimulation, he can wake up and basically respond, but his concentration is poor. After the stimulation stops, he will fall into a sleeping state.
A.1.3 Fragile state
Cannot perceive fine external stimulation, can only perceive large external stimulation and make corresponding responses, often have gaps in concentration, may have illegal behavior, sleepwalking or wandering.
A.2 Moderate consciousness disorder
A. 2. 1 Delirium
Consciousness is seriously unclear, with slight disturbances in attention and orientation. Self-recognition is good, but the ability to understand the disease is poor. There are obvious visual illusions and hallucinations, and fragmentary paranoia and psychomotor excitement may occur. A.3 Severe consciousness disorder
A.3.1 Light coma
Loss of consciousness. There may be defensive response to strong pain stimulation, various reflexes are present, and pathological reflexes may occur. Incontinence or retention of urine and feces. There are generally no obvious changes in respiration, blood pressure, and pulse. A. 3. 2 Moderate coma
Loss of consciousness. There is a painful expression on the face to strong stimulation, the medullary foramen reacts to light and the corneal reflex is slow, the sneezing and pharyngeal reflexes may disappear, the tendon reflexes are slow, and pathological reflexes appear. Incontinence or retention of urine and feces. There may be changes in respiration, blood pressure, and pulse. A.3.3 Deep coma
Nocturnal insomnia. No response to external stimuli. All reflexes including the reaction of the eye to light, corneal reflex, and swallowing reflex disappear. Pathological reflexes also disappear. Incontinence of urine and feces. May be accompanied by respiratory and circulatory failure. A.3.4 Decortical state
The patient can keep his eyes still but is unconscious. He is silent, motionless, does not take the initiative to eat or defecate, does not respond to calls, does not move when pushed, and has increased muscle tone.
GB 8781—88
Appendix B
Blood fluorocarbon hemoglobin determination method
(Supplement)
B.1 Spectrophotometric determination of blood carboxyhemoglobin D.1.1 Principle
Blood contains reduced hemoglobin (Hh), oxyhemoglobin (HbO2), carboxyhemoglobin (HbCO) and trace amounts of methemoglobin (MetHb). HbO2 and MetHb are reduced to Hb using the reducing agent sodium dithionite, and the blood only contains HaCO and Hb. HbCO has a maximum absorption peak at 420 nm, and Hb has a maximum absorption peak at 432 nm. The absorbance values of the blood sample under test at these two wavelengths are measured and substituted into the formula containing the pre-measured HbCO and Hb absorption coefficient to obtain the saturation of HbCO. B.1.2 Instruments and reagents
Domestic 721 or 751 spectrophotometer, carbon nitride gas (steel cylinder or using carbon monoxide generator as described in B.2) #steel cylinder general oxygen:
steel cylinder general nitrogen;
Blood diluent (Tris solution), weigh 1.21 g of hydroxymethylaminomethane (analytical grade), dissolve in 1 000 mt of hot distilled water sodium dithionite (analytical grade).
B.1.3 Operation steps
B.1.3.1 2 10 ml stoppered test tubes (one is a reagent blank tube, the other is a measurement tube). Put 2 glass balls in each and fill it with Tris solution (about 13~15 ml, the volume difference does not affect the measurement accuracy), add 40 mg of sodium dithionite to the blank tube [in the example mixing spoon]. B. 1. 3. 2 Use a hemoglobin tube to absorb 5 μl of earlobe blood and put it into a measuring tube, such as 10 mg of sodium dithionite; fill it up with Tris diluent and cover it tightly (do not let in bubbles), invert and mix. After 10-15 minutes, compare the color. B. 1. 3.3. Pour the reagent blank tube and the test solution in the assay tube into a 1 cm colorimetric ML. 1r, cover (do not allow air bubbles to enter), adjust the zero point with the reagent blank solution, and record the absorbance values of the assay solution at 420 and 432 nm (Aatb, Aa±). B.1.4 Saturation calculation
Hbco saturation is calculated according to the following formula:
An + t - Aut - nb
Hbco(%) - Am(4=A(- y 00
Wherein: a, aahcco are the absorption coefficients of Hb and HbCo at 420 and 432nm wavelengths. B.1.5 Determination of absorption coefficient
B.1.5.1 Take 2 ml of blood from a healthy person who does not smoke and is not exposed to carbon monoxide gas, add 1% heparin as an anticoagulant, and store for later use. B.1.5.2 Take a 5 ml test tube, absorb 0.5 ml of the original blood, and dilute it with 2 ml of Tris solution. B.1.5.3 Take 0.15~0.2 ml of the diluted blood above, put it into a 100 ml conical flask, add 60 ml of Tris solution and mix well. B.1.5. Preparation of B.1.5.4HbO2 solution: oxygenate the blood dilution solution B.1.5.3 for 20 minutes (30 ml/min). Preparation of B.1.5.5HbO2 solution: take half of B.1.5.4HbO2 solution, put it into a dry 50 ml conical flask, and pass carbon monoxide for 20 minutes (30 ml/min).
B.1.5.6 Take a 10 ml test tube, fill it with B.1.5.5HbCO2 solution, and then add 40 mg of sodium dithionite. Cover the stopper (do not let in air bubbles), mix, and test.
B.1.5.7Hb solution: pass the remaining half of B.1.5.4HbO2 solution through a container filled with distilled water at room temperature to saturate it with water vapor), and after 15 minutes, fill another 10 ml test tube. Add 40 mg sodium dithionite, cover with a stopper (do not allow air bubbles to enter), mix and wait for the test.
GB 878188
R.1.5.8 According to the conditions of B.1.3.3, the absorbance values of B.1.5.6IIbCO solution and 15.1.5.7Hb solution at 12 valence and 132Ttm wavelength are obtained as follows;
aHa.ahn.aho.ao
B.1.6 Precautions
Sodium dithionite is easily ineffective in the air and should be packaged in small bottles for use. Avoid contact with air and moisture. Fresh blood must be used for the determination of absorbance coefficient. Absorbance The coefficient value should be calibrated regularly. The test solution containing HhCO should be kept away from dust as much as possible. The color comparison should be done in time, otherwise the result will be too low. B.2 Carbon monoxide gas generation method Add 85% formic acid (analytical grade) to a flask equipped with a dropping funnel and a gas outlet tube. Add concentrated sulfuric acid to the dropping funnel. The generated carbon monoxide is introduced into a 2% NaOH gas washing bottle and then into the HbO solution. The operation should be carried out in a good fume hood. C.1 Preparation before inspection GB 878188 Electroencephalogram inspection method and judgment criteria (supplement) C.1.1 Explain the inspection requirements and precautions to the inspected person clearly, eliminate tension, keep him quiet, cooperate, reduce the source of artifacts, and conduct the inspection smoothly. C.1.2 The laboratory temperature is kept at around 20-26℃. Too cold will easily produce electromyographic artifacts. Overheating can easily cause sweating and unstable baselines. The light should be slightly dimmed to avoid direct sunlight on visual stimuli and the EEG inhibition reaction. C. 1. 3 Wash your hair the day before the examination.
C. 1. 4 The examination should be performed within 1~2 hours after a meal. It is not advisable to be on an empty stomach to prevent the influence of hypoglycemia. C.1.5 If a sedative is given to a very uncooperative patient, the name and dosage of the drug should be noted in the record. The influence of the drug should be considered during analysis. C.2 Operating procedures during the examination
C.2.1 Adjust the recording volume. Keep the baseline in the normal adjustment position: After checking the power supply voltage (220), turn on the main switch, preheat the tube type for 10~15 minutes (the full crystal type can be stable in 5~7 seconds), and check the supply of ink and recording paper. Then make a standard measurement (5mm is equivalent to 50 μV).
C.2.2 Part the hair at the location where the electrodes are placed, degrease it with 6~7% edible oil solution (or 70% ethanol), and secure the electrodes to the scalp with a suitable electrode cap.
C.2.3 After the electrodes are placed, check the resistance of each electrode immediately. It is generally between 10~20 k, and the values on both sides should be close. C.2.4 Adjust the pen: Check whether the shape or amplitude of the brain waves produced by each pen stroke is consistent. C.2.5 If necessary, adjust the following control buttons. Set the gain control to 10 μV/mm.
Set the time constant to 0.35.
The high frequency filter is at 15.
d. The paper feed speed is generally at 30mm/s; when encountering extremely fast activities, it can be turned to 60mm/s; and when studying slow activities, it can be turned to 15 mm/s.
C.2.6 Place scalp electrodes at conventional locations. When the electrodes are placed, ask the patient to lightly close their eyes and then begin recording. C.2:7 Routine examination, each area includes unipolar recording and bipolar recording, each group lasts 3-5 minutes. During unipolar recording, record 3 times of eye closure and hyperventilation for 3 minutes. The total recording time should not be less than 20 minutes. C.3 Electrode position
The location of the electrodes before the day is mainly measured by the daily measurement method. The locations of all electrodes should be strictly symmetrical, and the commonly used locations are: C. 3. 1 Anterior lairum: located 1 em inside the left and right hairlines, F is in a straight line with the pupil, and is the left and right forehead area. C.3.2 Central area: 3 cm away from the intersection (hui point) of the midline of the skull and the line connecting the two sides of the external ear holes, which is the left and right central area. C.3.3 Posterior frontal area: located at the point where the frontal area and the central area are equidistant. C.3.4 Occipital area: 3 cm above the tuberosity, 3 cm to the left and right sides are the left and right occipital areas. C.3.5 Frontal area: located at the point where the frontal area and the right central area are equidistant. It is the left and right prefrontal area. C.3.6 Proximal epilepsy area: located at the midpoint of the line connecting the left and right eye margins and the highest part of the auricle, which is the corresponding side proximal area. C.3.7 Middle area: the midpoint of the line connecting the external auditory canal opening and the central area is the left and right middle area. C.3.8 Posterior frontal area: located above the mastoid process. Together with the proximal area and the middle area, it forms a "品" shape. C.4 Lead method
GB8781-88
Generally, two methods are used: bipolar lead and unipolar lead. C.4.1 Bipolar lead: Every two effective electrodes are connected into a lead, and the potential difference between the two electrodes is recorded. Each two electrodes can be connected and recorded in sequence at equal distances on the head longitudinally (front-to-back) or laterally (left-to-right). C.4.2 Monopolar lead: Connect the "active electrode" on the scalp to the "reference electrode" (usually placed on the left and right earlobes). C. 5 Induced test
In order to increase the positive rate, physiological stimulation is used as a method to stimulate abnormal EEG. C.5.1 Hyperventilation: Take deep breaths at a rate of 20 to 24 times per minute for 3 minutes, and continue recording during hyperventilation and within 1 minute after termination.
C.5.2 Close your eyes quietly. Let the subject keep his eyes still for 4 to 5 minutes, then close his eyes again. After the background activity is restored, repeat 1 to 2 times. C.5.3 Flash stimulation: Place a flashlight 20 cm in front of the subject's eyes. The subject closes his eyes and sits quietly. First, give 3 flashes/s for 10 seconds, then give 18 flashes/s for 10 seconds, and then give 24 flashes/s after a full 10 seconds interval. There are 3 groups in total. C.6 Criteria for judging abnormal EEGbzxz.net
Adverse edge state
aa The wave rate is not well adjusted on both sides, and the frequency difference is 1.5 to 2 Within the cycle. The α wave amplitude is asymmetric on both sides, with a difference of more than 30%. b.
There are more low-amplitude 0 waves in the forehead.
d. The amplitude of the sum wave is higher than that of the α wave.
C.6.2 Mild abnormality
a. The α wave rate and amplitude are poorly regulated, the rate fluctuation exceeds 2.5 cycles/s, and the amplitude on both sides differs by more than 30%. b.
The rate is 7-8 cycles/s, and the amplitude is around 150uV. The occipital u wave has no inhibition of light.
The P wave amplitude is diffusely increased (50~-100uV) in the forehead, and the forehead has a medium amplitude (50~70μV). Every 4-cycle e wave or 1.5-3.5 cycles per second reaches 25%. Moderate abnormality
Occipital α The spikes disappear. There are limited or paroxysmal high-amplitude (51-70 μV) a activities in the forehead and chin. Paroxysmal or limited non-high-amplitude sharp waves, waves, activities or rhythms. A small or moderate amount of spikes or spike-slow wave combination. c.6.4 Highly abnormal
Continuous high-amplitude activities in the forehead and chin mixed with low-amplitude fast activities or a large amount of 0 and 6 waves. b.The rhythm disappears, replaced by paroxysmal or localized high-amplitude activity and 8 activity. ℃. A large number of high-amplitude spikes and spike-slow wave complexes. d
Hyperventilation and flash stimulation can induce high-amplitude spikes, spike-slow wave complexes and high-amplitude fast activity or limited slow activity. D.1 Scope of application of this standard
GB8781-88
Appendix D
Instructions for correct use of the standard
(Note:
This standard is applicable to acute poisoning caused by inhalation of high concentrations of carbon monoxide in production activities such as the steel industry, chemical industry, gas, coal, and transportation. The diagnosis of acute carbon monoxide poisoning in daily life is also referred to this standard. Whether long-term exposure to low concentrations of carbon monoxide can cause "chronic carbon monoxide poisoning" is still controversial and does not belong to the scope of application of this standard. D.2 The labor hygiene survey data at the poisoning site and the results of timely determination of the concentration of micro-carbon monoxide in the air are of reference significance for diagnosis. D.3 The disease is characterized by central nervous system damage caused by acute cerebral hypoxia as the main clinical manifestation, so it is not The same degree of consciousness disturbance is an important basis for clinical diagnosis and classification (see Appendix A). D.4 In acute carbon monoxide poisoning, abnormalities of other organs outside the brain may also occur, such as skin erythema and blisters, muscle swelling and pain, electrocardiogram or liver and kidney function abnormalities, mononeuropathy or auditory vestibular organ damage, etc. Since these abnormalities do not appear as early as central nervous system symptoms, are only seen in some patients, or are transient, they are not listed as the basis for diagnosis and classification in this standard. D.5 In acute carbon monoxide poisoning, if secondary cerebral edema (worsening of consciousness disturbance, seizures or decerebrate rigidity, positive pathological reflexes, increased slow waves on the electroencephalogram or papilledema), pulmonary edema, respiratory failure, shock, severe myocardial damage or upper gastrointestinal bleeding occur, all of which indicate a serious condition.
D.6 Blood carbon monoxide poisoning. If the hemoglobin (HbCo) is higher than 10%, it may indicate a history of exposure to high concentrations of carbon monoxide, which is of reference significance for the diagnosis and differential diagnosis of the disease. However, after leaving the poisoning scene, the HbC0 level in the blood will decrease, and sometimes it may not be parallel to the degree of clinical manifestations. Therefore, if the HbCO measurement is not timely, it should not be used as the basis for diagnostic grading. For patients who have been exposed to carbon monoxide for more than 8 hours, since the HbCo is mostly below 10%, it is generally not necessary to conduct HbCO monitoring. D.7 Delayed encephalopathy in acute carbon monoxide poisoning is different from sequelae. The latter's symptoms are directly continued from the acute phase, while delayed encephalopathy refers to the sudden appearance of consciousness and mental disorders, extrapyramidal system or pyramidal system after a period of time (2 to 6 days) after waking up from the coma due to acute carbon monoxide poisoning. Damage-based encephalopathy manifestations, moderate and severe acute carbon monoxide poisoning patients should be observed for 2 months after the process of clearing up. During the observation period, it is advisable to stay away from carbon monoxide work. DB Mild acute carbon monoxide poisoning needs to be differentiated from colds, hypertension, food poisoning, Meniere's syndrome, etc. Moderate and severe poisoning should pay attention to the differentiation from coma caused by other causes (such as diabetes, cerebrovascular accident, sleeping pill poisoning, etc.). For patients with delayed encephalopathy, it is necessary to differentiate and diagnose with other mental illnesses, Parkinson's disease, cerebrovascular disease, etc. Additional explanation,
This standard was proposed by the Occupational Disease Diagnosis Standard Subcommittee of the National Health Standard Technical Committee. This standard was drafted by the Institute of Labor Health and Occupational Diseases, Chinese Academy of Preventive Medicine, and the Institute of Labor Health of Anshan Iron and Steel Company. This standard was entrusted by the Ministry of Health to the Institute of Labor Health and Occupational Diseases, Chinese Academy of Preventive Medicine for interpretation. From the month of implementation of this standard, the draft of "Diagnosis, Treatment and Treatment Methods of Acute Carbon Monoxide Poisoning" promulgated by the former Ministry of Health in 1965 shall be invalidated.
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