OVERVIEW
Many raw materials, intermediates and end products of industrial production are toxic to humans and are called industrial poisons. Some of them can selectively damage peripheral nerves and cause toxic peripheral neuropathy. During the production, transportation, storage and use of industrial poisons, due to improper protection, the poisons can be absorbed through the respiratory tract and skin, resulting in the so-called toxic peripheral neuropathy of industrial poisons.
Causes
Can cause peripheral neuropathy of industrial poisons of many kinds, including the following categories: ① metal and metal-like, such as lead, bismuth, antimony, thallium, mercury, arsenic and its compounds; ② organic solvents or organic compounds, such as benzene, gasoline, methanol, n-hexane, methyl n-butyl ketone, carbon disulfide, trinitrophenol, carbon tetrachloride, trichloroethylene, chloropropylene, bromoform; ③ polymers such as vinyl chloride, styrene, acrylamide, butyraldehyde, etc.; (2) the use of industrial poisons in the production of peripheral neuropathy. Styrene, acrylamide, butadiene; ④ asphyxiating gases, such as carbon monoxide; ⑤ pesticides, such as organophosphorus, carbamates.
Except for a very few industrial poisons, such as hexachlorophenol, which mainly damages Schwann (Schwann) cells and causes demyelinating peripheral neuropathy, the vast majority of peripheral nerve damage caused by industrial poisoning is axonal degeneration.
Symptoms
1. Peripheral neuropathy
The onset of peripheral neuropathy caused by industrial poisons is slow and insidious, a few acute onset of disease (such as thallium poisoning), there are some poisons in acute poisoning does not appear peripheral nerve damage in the clinical manifestations, but in the 1 ~ 8 weeks after the recovery period of poisoning, the emergence of multiple peripheral neuropathy signs and symptoms, known as delayed-onset peripheral neuropathy, mainly in a variety of organophosphorus pesticides and arsenic trioxide poisoning.
Peripheral neuropathy caused by chronic poisoning by industrial poisons, mostly after a certain time of exposure to poisons, symmetrical motor sensory neuropathy of the distal extremities appeared. The manifestations are numbness and coldness of the hands and feet, and glove-stocking-like hyperalgesia of the extremities. Acute thallium or arsenic poisoning and delayed peripheral neuropathy after organophosphorus poisoning, there can be significant limb pain and nociceptive hypersensitivity, motor can be involved at the same time, manifested as distal limb muscle weakness, muscle atrophy and foot drop, Achilles tendon reflex is reduced or disappeared.
There are some industrial poisons caused by peripheral neuropathy, because of its damage to the nerve has a certain selectivity, the clinical performance has some characteristics. For example, in acrylamide poisoning, the distal extremity of the pars compacta and the spiral nerve endings in the muscle spindle are involved earlier, so the vibratory sensation and the Achilles tendon reflex disappear at an early stage; in the case of chloropropene poisoning neuropathy, there are obvious distal limb nociception and tactile dysesthesia, and the positional sensation is preserved intact; in the case of dimethyl aminopropyl cyanide poisoning, the nerves innervating the bladder are selectively damaged and lead to urinary retention; in the case of thallium poisoning, not only is there a polyneuropathy of the limbs, but there are also visual, motor, and triple-vision neuropathy. In thallium poisoning, there are not only multiple neuropathies in the limbs, but also multiple cerebral nerve damages such as optic, motor, trigeminal and facial nerves, and the clinical appearance of eyelid ptosis, diplopia and facial muscle paralysis.
2. Toxic peripheral neuropathy of common industrial poisons
(1) Arsenic poisoning Arsenic toxic peripheral neuropathy is rare, seen in industrial poisoning. Acute poisoning 1 ~ 3 weeks later often appear polyneuropathy, there are limb pain or radicular pain, nociceptive sensitization or hyperalgesia, deep sensory hyperalgesia, hand and foot paralysis and myasthenia, etc., there are similar to the performance of the GBS, preceded by severe gastrointestinal reactions, renal and hepatic failure. Severe cases may have arsenic encephalopathy, coma and convulsions. Workers with long-term exposure to arsenic operations or oral arsenic-containing drugs or endemic arsenic poisoning is often chronic, with slowly progressing clinical symptoms and sensory and motor involvement. Performance for the double lower extremity pain and distal extremity sensory impairment, such as glove, sock-like sensory loss, gradually developed to the double lower extremity weakness, tendon reflex disappearance. In the case of those who consume arsenic complex poisoning, gastrointestinal symptoms appear before peripheral neuropathy. The patient’s nails become brittle, white horizontal lines that arsenic line (Mees line), urine and hair arsenic discharge are significantly increased.
(2) Lead poisoning Lead can enter the body through the skin, respiratory tract and digestive tract, often occupational. Recently the disease has become very rare. Lead poisoning peripheral neuropathy clinical manifestations to movement disorder, upper extremity radial nerve damage symptoms are especially obvious, manifested as hanging wrist and finger can not be, after the other nerves can also be involved, the lower limbs can appear drop foot. Sensory impairment is rare, can be manifested as symmetrical polyneuritis or single such as peroneal neuritis.
(3) Mercury poisoning is common in the electronic chemical industry and pharmaceutical industry, mercury is divided into inorganic mercury (elemental mercury or mercury salts) and organic mercury in two forms, the clinical manifestations caused by poisoning are obviously different, organic mercury (such as methylmercury) poisoning is mainly damage to the central nervous system, the cerebral cortex and cerebellum, the damage to peripheral nerves is mainly in the back of the root ganglia, the front root is not involved, the clinical manifestations of speech disorders, ataxia, tubular vision, hearing disorders and severe mental symptoms. Clinical manifestations include speech disorders, ataxia, tubular vision, hearing disorders and severe psychiatric symptoms. Sensory disorders are manifested as perioral, tongue and distal extremity numbness. Elemental mercury poisoning is mainly dominated by peripheral nerve damage, which is characterized by muscle weakness and myasthenia with symptoms significantly heavier than sensory symptoms, symmetrical and active reflexes of the limbs, hand tremor, tongue tremor and lid tremor, which is sometimes easily confused with ALS.
(4) Thallium poisoning Metal thallium and its compounds are strong neurotoxins, and its soluble compounds can be absorbed through the digestive tract, respiratory tract, and skin to cause disease or death. The main symptoms of thallium poisoning are neurological and digestive symptoms and alopecia. Acute thallium poisoning is mostly caused by accidental intake or consumption of thallium-contaminated water or food, and in addition to acute gastrointestinal symptoms such as abdominal pain, diarrhea, vomiting, etc., the clinical symptoms of thallium poisoning can be seen after 4 days, and there will be multiple cerebral neurological damages such as optic, motility, trigeminal and facial nerves as well as limb polyneuropathy, which is mainly characterized as peripheral neuropathy of GBS-like or painful peripheral neuropathy, and pinprick-like peripheral neuropathy of limbs. The main manifestation is GBS-like peripheral neuropathy or painful peripheral neuropathy, with pinprick-like and burning pain in the limbs, sometimes with an ant-like sensation, starting from the toes or soles of the feet and progressing to the proximal end, with muscle weakness, hypotonia, and weakened tendon reflexes. In severe cases, there is pain and paralysis of the diaphragm and respiratory muscles, which can lead to respiratory distress or cessation. Chronic thallium poisoning at the initial onset of symptoms is not typical, there are similar to neurosis and atypical peripheral neuropathy manifestations, later the main symptoms of limb sensation and movement disorders, characterized by pain sensitivity, the later stage of muscle atrophy, and white horizontal lines on the nails, hair loss.
(5) Organophosphorus poisoning Late-onset neuropathy after organophosphorus poisoning is a serious toxic neuropathy, which can lead to permanent paralysis of limbs, this disease usually occurs in acute organophosphorus poisoning in 8-14 days, manifested as spasmodic pain in the gastrocnemius muscle, glove sock-like sensory deficits in the distal limbs, and gradually to the proximal end of the development of the distal limbs can be accompanied by distal limb weakness, gait unsteadiness and paralysis of the lower limbs, and the condition can be serious when it involves the upper limbs, appearing drop foot, drop wrist, drop wrist, and paralyzed upper limbs. In severe cases, the upper limbs may be involved, with drooping feet, drooping wrists, loss of Achilles tendon reflexes, and individual patients may have cone bundle involvement.
Examination
1. Laboratory examination
(1) Toxicology tests: Blood, urine, vomitus, and hair of suspected patients should be tested for heavy metals (lead, bismuth, antimony, thallium, mercury, arsenic and their compounds) and other types of toxic substances.
(2) Other blood tests including liver function, kidney function, blood sedimentation and other routine tests; rheumatic series immunoglobulin electrophoresis and other autoimmune-related serological tests.
2. Other auxiliary tests
(1) Electromyography
(2) Neurophysiologic examination.
(3) Tissue biopsy (including skin, peroneal nerve, muscle and kidney), if necessary, to differentiate from other sensory peripheral neuropathies.
Diagnosis
A definitive diagnosis of industrial poisoning should be made. The diagnosis of peripheral neuropathy is generally not difficult based on clinical signs, especially signs of impaired sensation, movement and reflexes in the extremities, combined with neuromyography. Its diagnostic significance lies in the etiological identification, that is, it is necessary to understand the occupational history in detail, including the type of exposure to poisons, time, concentration, the relationship between the emergence of peripheral neurological symptoms and the time of exposure to poisons, and whether there are patients in the same workshop or the same type of work with similar manifestations; the poisons in the production environment, and poisons or metabolites in the patient’s blood, urine, and vomitus are detected, and at the same time exclude the other peripheral neuropathies caused by non-industrial toxins, before a clear etiological diagnosis is made. The etiologic diagnosis can only be clarified by testing for toxins or metabolites in the production environment and in the patient’s blood, urine and vomiting, and by excluding other non-industrial toxicant-induced peripheral neuropathies.
The diagnosis of lead poisoning relies on a history of exposure, with clinical manifestations such as abdominal pain, anemia and peripheral neuropathy, blood lead levels above 70 mg/dL, and black lead lines in the gums. The diagnosis of thallium poisoning relies on a history of exposure, the presence of multiple peripheral neuropathies, abdominal pain, alopecia, white horizontal lines on the nails, and the measurement of blood and urine thallium levels.
Treatment
Acute poisoning, can be dealt with according to the general principles of first aid, oral poison available emetic, gastric lavage and diarrhea, pay attention to water, electrolyte balance. Chronic poisoning, mainly expelled poison treatment. ① lead poisoning treatment is first to stop the continued contact with lead and available sodium dimercaptosuccinic acid, sodium calcium edetate, sodium dimercaptopropanesulfonate and other lead expulsion, and a large number of applications of B vitamins; ② arsenic poisoning available dimercaptopropanol (BAL) arsenic, but also available for treatment with penicillamine; ③ thallium poisoning treatment principle is to immediately stop contact with the poison, and accelerate the excretion of toxic substances. Specific methods include the application of antidotes, such as Prussian blue, potassium chloride; continuous hemofiltration and hemodialysis; and the administration of sulfhydryl drugs, such as sodium dimercaptosuccinic acid, reduced glutathione and other complexing agents.
In addition to this, the vast majority of industrial toxins lack effective pro-discharge agents or antidotes. The application of high doses of B vitamins, adenosine triphosphate (ATP), coenzyme A and inosine has a promoting effect on the repair and functional reconstruction of nerve tissue.