Industrial Toxic Toxic Peripheral Neuropathy

Introduction to Industrial Toxic Peripheral Neuropathy The raw materials, intermediates and final products in many industrial processes are toxic to humans and are called industrial poisons. Some of them can selectively damage peripheral nerves and cause toxic peripheral neuropathy. In the production, transportation, storage and use of industrial poisons, due to improper protection, toxic substances can be absorbed through the respiratory tract and skin, resulting in so-called occupational toxic peripheral neuropathy. There are many types of industrial poisons that can cause peripheral neuropathy, including the following categories: 1. Metal and metalloid lead, strontium, barium, strontium, mercury, arsenic and their compounds. 2. Organic solvent or organic compound benzene, gasoline, methanol, n-hexane, methyl n-butyl ketone, carbon disulfide, trinitrophenol, carbon tetrachloride, trichloroethylene, chloropropene, methyl bromide. 3. High molecular polymer vinyl chloride, styrene, acrylamide, butadiene. 4. Asphyxiating gas carbon monoxide. 5. Pesticide organic phosphorus, carbamates. basic knowledge The proportion of sickness: 0.01% Susceptible people: no specific population Mode of infection: non-infectious Complications: chronic pneumonia

Causes of industrial poisonous peripheral neuropathy

Causes:

Except for a few industrial poisons such as hexachlorophene, which mainly damage Schwann (Swanwang) cells and cause demyelinating peripheral neuropathy, the peripheral nerve damage caused by most industrial poisoning is axonal.

Pathogenesis:

Different chemical poisons differ in the target sites of peripheral nerves, and most of them invade distal axons, sputum, lead, maleic acid, hexachlorophenol and 6-aminonicotinamide, which mainly invade Schwann cells and myelin; ethanol, Glycerol thioethylamine mainly invades the perineurium membrane.

In the process of industrial poisons causing axonal damage, the functional state and degree of damage of the axo-transport system play an important role. The effects of industrial poisons on the axo-transport system are mainly as follows:

1. Destruction of the energy metabolism process, the energy metabolism of the axoplasmic transport is impeded, and the activity of the dynein is inhibited.

2. Damage to the skeleton structure of the axons.

3. Change the ion permeability of the plasma membrane in axons or cells, destroy the axoplasmic ion balance, and axoplasmic transport can also reverse the neurotoxicity of the neurotransmitters to the cell body, reducing the synthesis of neurotransmitters and neurofilaments. The diameter of the protrusion becomes smaller, and the distal end is denatured due to a nutritional disorder.

Some poisons (such as n-hexane) can also destroy the normal structure of the nerve fibers and microtubules in the axons, so that the nerve fibers are detached from the microtubules, and are rapidly transported to the distal end of the axons, and the nerve filaments accumulate at the distal end, resulting in far End axon swelling, degeneration, lead can inhibit the slow transport of nerve filaments and microtubules, destroy the axon skeleton system, arsenic can bind to thiol enzymes in mitochondria, form stable dimercapto esters, interfere with energy metabolism, affect axis In the power system of pulp transport, methylmercury can depolymerize microtubules in axons and block the forward and reverse transport of axoplasmics.

Industrial Toxic Peripheral Neuropathy Prevention

1. Strengthen labor protection education and implement protective measures. The Law of the People's Republic of China on Prevention and Control of Occupational Diseases requires that the health administrative departments of the local people's governments at or above the county level and other relevant departments should strengthen publicity and education on occupational disease prevention and control, popularize the knowledge of occupational disease prevention and control, and strengthen The employer's concept of occupational disease prevention and control raises the awareness of workers' self-health protection. This requires that leaders and workers at all levels of the enterprise must learn about occupational disease prevention and control in order to better prevent occupational diseases.

2. For suspected poisoning, stop contact with poison as soon as possible and try to remove the poison in the body.

Industrial poisonous peripheral neuropathy complications Complications chronic pneumonia

Systemic damage, especially liver, kidney damage and blood system lesions are more common.

Symptoms of Industrial Toxic Peripheral Neuropathy Common Symptoms Unstable gait, sensory disturbance, abdominal pain, drooping, vaginal hair loss, vaginal wrist, double eye, numbness, muscle atrophy, weakness

1. The general manifestations of peripheral neuropathy caused by industrial poisons. The incidence of peripheral neuropathy caused by industrial poisons is slow and insidious. A few are acute onsets (such as sputum poisoning), and some toxic substances do not show peripheral nerve damage during acute poisoning. Performance, and in the recovery period of poisoning after 1-8 weeks, the symptoms and signs of multiple peripheral neuropathy, called delayed peripheral neuropathy, are mainly found in various organophosphorus pesticides and arsenic trioxide poisoning.

The peripheral neuropathy caused by chronic poisoning of industrial poisons often occurs after exposure to poison for a certain period of time. Sympathetic motor neuropathy of the distal extremities appears in the limbs. It is characterized by numbness of the hands and feet, chills, feelings of gloves and socks in the limbs, acute sputum or arsenic poisoning and organic Delayed peripheral neuropathy after phosphorus poisoning can have significant limb pain and hyperalgesia. Exercise can be affected at the same time, manifested as distal muscle weakness, muscle atrophy and foot drop, and Achilles tendon reflexes are reduced or disappeared.

There are some industrial poisons caused by peripheral neuropathy, because of its selective selectivity to nerve damage, so the clinical manifestations have certain characteristics, such as acrylamide poisoning in the distal part of the limbs of the Pax body and the intramuscular spiral nerve endings involved Earlier, the vibrational sense and the Achilles tendon reflex disappeared early. When the chloropropene poisoning neuropathy, there are obvious pain and tactile dysfunctions in the distal part of the limb, and the positional sensation is well preserved. When dimethylaminopropane cyanide is poisoned, the selective damage dominates. The nerves of the bladder cause urinary retention. When poisoning, the brain damages the peripheral nerves of the limbs, and the motor fibers of the brain are also affected. Clinically, there are drooping eyelids, diplopia and facial paralysis.

2. Several common industrial poisonous peripheral neuropathy

(1) Arsenic-toxic peripheral neuropathy: It is the most common peripheral neuropathy of heavy metal poisoning. It can be caused by chronic contact or one-time inhalation of toxic doses in the digestive tract. Patients with acute poisoning begin to appear 4 to 6 weeks after exposure. Symptoms, and peaked within a few days, the onset of chronic arsenic-toxic peripheral neuropathy is concealed, development is very slow, and the sensory involvement is an early symptom of arsenic-toxic peripheral neuropathy, manifested as pain and paresthesia of both lower extremities, distal limb gloves and sock The feeling of sensation diminished, kinesthetic and positional sensation are obviously affected. After several days of feeling symptoms, muscle weakness begins to appear, which is characterized by complete flaccid paralysis of the lower extremities, sometimes involving the upper limbs, tendon reflexes often disappear, and common skin lesions Skin pigmentation, hyperkeratosis and nail changes (Mees line).

Neurophysiological examination showed that the nerve conduction velocity was normal or mildly slowed down, the amplitude of sensory evoked potential was significantly reduced, and the urinary arsenic was positive in the acute phase. The urinary arsenic concentration was greater than 0.1 mg/L, which was abnormal. The acute poisoning was usually greater than 1 mg/L. Arsenic can be detected in the hair within 2 weeks after arsenic poisoning, and it can last for several years, and the arsenic content of more than 0.1 mg per 100 mg of hair can be regarded as arsenic poisoning.

(2) Lead poisoning peripheral neuropathy: only seen in adults, infant lead poisoning can cause brain damage, lead can be absorbed through the lungs, skin and intestines, occupational lead poisoning is seen in ceramic glazing, battery manufacturing and paint workers, and other heavy metal poisoning Different, lead poisoning peripheral neuropathy mainly involves exercise fibers, and there are many sensory symptoms and signs. The wrist extensors and extensors of the sacral nerves are involved in the early stage, which is characterized by the weakness of the scapula and the extension of the fingers. Later, the other muscles of the upper limbs and the diaphragm are gradually involved. Usually not tired, occasionally involving the lower extremities, in rare cases can appear signs of upper motor neurons and lower motor neuron damage, which is easy to be confused with ALS, in addition lead poisoning can also cause abdominal pain, urate retention and gout.

Laboratory tests can find anemia, mild increase in cerebrospinal fluid protein, increased serum uric acid, elevated blood lead levels, blood lead levels greater than 70g can be considered abnormal, urine lead and urinary biliary excretion also increased, Patients with low blood lead levels should be treated with sodium calcium edetate 25 mg/kg once every 8 hours, orally, 24 hours urine lead up to 500 mg, which is important for diagnosis. Lead poisoning peripheral neuropathy The nerve conduction velocity detection is normal.

(3) Mercury poisoning: common in the electronic chemical industry and the pharmaceutical industry. Mercury is classified into inorganic mercury (elemental mercury or mercury salt) and organic mercury. The clinical manifestations caused by poisoning are significantly different. Organic mercury (such as methylmercury) Poisoning mainly damages the central nervous system, involving the cerebral cortex and cerebellum. The damage of peripheral nerves is mainly in the posterior root ganglion. The anterior root is not affected. The clinical manifestations are language disorders, ataxia, tubular vision, hearing impairment and severe mental symptoms. Sensory dysfunction is characterized by perioral, numbness of the tongue and distal extremities.

Elemental mercury poisoning is mainly caused by peripheral nerve damage, which is characterized by muscle weakness and muscle atrophy symptoms are significantly more sensitive than sensory symptoms, sometimes confused with ALS.

(4) scorpion poisoning: cockroach is the main component of rodenticide. poisoning is similar to lead poisoning. It mainly affects the central nervous system in children. It can cause peripheral nerve damage in adults. Symptoms of sensory and autonomic nerves are particularly prominent in sputum poisoning. Patients may have severe paresthesia and diffuse alopecia, sometimes with delayed cardiovascular autonomic dysfunction, and recovery is slow.

(5) Delayed neuropathy after organophosphorus poisoning: It is a serious toxic neuropathy, which can cause permanent limb paralysis. The incidence rate is high at home and abroad. This disease usually occurs 8 to 14 days after acute organophosphorus poisoning. For gastrocnemius tendon pain, the distal extremity gloves and sock-like sensory disturbances, and gradually develop to the proximal end, can be accompanied by distal extremities weakness, gait instability and lower extremity spasm, when the condition is serious, can affect the upper limbs, there are vertical feet , the wrist, the Achilles tendon reflex disappeared, individual patients may have pyramidal beam involvement, moderate and mild organophosphate poisoning, delayed neuropathy, neurological function can be restored to some extent within 1 to 3 years, but severely recovered Very difficult.

The diagnosis of industrial toxic peripheral neuropathy mainly depends on clinical symptoms and signs. Sural nerve biopsy and neurophysiological examination can identify the type of peripheral nerve damage, understand the patient's occupation history or the history of toxic contact, including the variety, quantity and time of exposure to poison. The relationship between the appearance of peripheral neurological symptoms and the contact with poisons and the presence of similar symptoms in other people who are exposed to the poison at the same time is extremely important for a definitive diagnosis. The final diagnosis depends on the environment in which the patient is exposed or the blood, urine, vomit and hair of the patient. Detection of endotoxin content.

The toxic effects of some chemicals on peripheral nerves have not yet been recognized. In this case, epidemiological studies should be conducted to find out the consistency of toxic contact in the affected population, and then these toxicants are used to replicate the animal model of peripheral nerve damage, thereby confirming its neurotoxicity. effect.

Inspection of industrial poisonous peripheral neuropathy

1. Detection of blood, urine, vomit and heavy metal (lead, strontium, barium, strontium, mercury, arsenic and its compounds) and other types of toxic substances in suspicious patients.

2. Other blood tests include liver function, kidney function, routine examination of erythrocyte sedimentation rate; rheumatism series, immunoglobulin electrophoresis and other serological tests related to autoimmunity.

3. Electromyography and neurophysiological examination.

4. Organize biopsy (including skin, sural nerve, muscle and kidney) as necessary to identify other sensory peripheral neuropathies.

Diagnosis and identification of industrial poisonous peripheral neuropathy

The first is the diagnosis and identification of toxic substances in industrial poisoning; the second is that industrial toxic peripheral neuropathy should be differentiated from peripheral neuropathy caused by other diseases and acute infectious polyneuritis.

The main points of identification are: 1 detection of the type and content of the poison; 2 electromyography and neurophysiological examination; 3 tissue biopsy (including skin, sural nerve, muscle) if necessary, and identification of other sensory peripheral neuropathy.

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