Manganese poisoning

Introduction to manganese poisoning Acute manganese poisoning (manganese poisoning) can cause acute corrosive gastroenteritis or irritative bronchitis, pneumonia due to oral potassium permanganate or inhalation of high concentrations of manganese oxide fumes. Chronic manganese poisoning is mainly seen in workers who smoke long-term inhalation of manganese. The clinical manifestations are mainly extrapyramidal nervous system symptoms and neurobehavioral dysfunction and mental disorders. Manganese mining and smelting are more common in manganese exposure, and manganese electrode manufacturing. Welding and wind cutting manganese alloys as well as industrial workers manufacturing and applying manganese dioxide, permanganate and other manganese compounds. Manganese selectively acts on the thalamus, striatum, globus pallidus, substantia nigra, cerebral cortex and other brain regions. After manganese is consumed in animals, manganese in the hypothalamus and striatum can be increased by about 5 times, increasing in other brain regions. About 1 to 2 times, in the striatum, thalamus, midbrain, dopamine is reduced, high vanillic acid is increased, Na-k-ATPase and cholinesterase activity are increased, Mg-ATPase activity is changed, and monoamine oxidase activity is decreased. Pathological changes can be seen in neuronal degeneration and demyelination of nerve fibers, local blood vessels are congested, wall thickening, thrombosis and surrounding tissue edema and lymphocytic infiltration, etc., due to vascular lesions further aggravate the damage of nerve cells and nerve fibers, serious Manganese poisoning can cause degeneration of renal tubular epithelial cells, hepatic steatosis, myocardial and muscle fibers may have edema and degeneration, adrenal ischemia and partial necrosis. basic knowledge The proportion of illness: 0.0035% Susceptible people: no special people Mode of infection: non-infectious Complications: narcolepsy, dementia, depression

Causes of manganese poisoning

Manganese is mainly absorbed through the respiratory tract and the gastrointestinal tract. The skin absorbs very little. Manganese is in the blood and binds to 1 globulin in the blood in a bivalent form into a weak conjugate, which is distributed throughout the body, especially in the mitochondria-rich liver. There are many cells in the kidney, pancreas, heart, lung and brain. With the prolongation of time, the accumulated manganese in the body can be redistributed, and the manganese in the brain, hair and bones gradually increases accordingly; the manganese content in the brain can even exceed The accumulation of liver is mostly in the lenticular nucleus and cerebellum. Most of the manganese is secreted by the gallbladder, and is slowly discharged with the feces. A small amount of urine is discharged, and saliva, milk, and sweat glands are excreted in a small amount.

Manganese selectively acts on the thalamus, striatum, globus pallidus, substantia nigra, cerebral cortex and other brain regions. After manganese is consumed in animals, manganese in the hypothalamus and striatum can be increased by about 5 times, increasing in other brain regions. About 1 to 2 times, in the striatum, thalamus, midbrain, dopamine is reduced, high vanillic acid is increased, Na-k-ATPase and cholinesterase activity are increased, Mg-ATPase activity is changed, and monoamine oxidase activity is decreased. Pathological changes can be seen in neuronal degeneration and demyelination of nerve fibers, local blood vessels are congested, wall thickening, thrombosis and surrounding tissue edema and lymphocytic infiltration, etc., due to vascular lesions further aggravate the damage of nerve cells and nerve fibers, serious Manganese poisoning can cause degeneration of renal tubular epithelial cells, hepatic steatosis, myocardial and muscle fibers may have edema and degeneration, adrenal ischemia and partial necrosis.

The pathogenesis of chronic manganese poisoning has not yet been fully elucidated, but with neuronal degeneration, denervation of nerve fibers and decreased dopamine synthesis, and relatively enhanced excitatory effects of the acetylcholine transmitter system, leading to psycho-neuropathic symptoms and paralysis syndrome.

Manganese poisoning prevention

Chronic manganese poisoning is a disease caused by long-term exposure to manganese dust, which is mainly caused by nervous system changes. The prevention of manganese poisoning is mainly to strengthen ventilation and detoxification and personal protective measures.

Manganese poisoning complications Complications, narcolepsy, dementia, depression

Can be complicated by mental symptoms, such as significant mental changes, lethargy, dementia, apathy, indifference to things around, depression, involuntary crying, obsessive attitudes, impulsive behaviors, etc.

Symptoms of manganese poisoning Common symptoms Inability to abdominal pain, palpitations, nausea, chills, oral phantom contact, dizziness, hyperthermia, hemorrhagic shock

The diagnosis of acute manganese poisoning is not difficult. The diagnosis of chronic manganese poisoning should be based on the close history of manganese exposure and the neurological and psychiatric clinical manifestations of extrapyramidal lesions. Reference to the determination of manganese concentration in the air and urinary manganese, manure manganese The results should be differentiated from diseases such as tremor palsy and hepatolenticular degeneration caused by other causes.

Acute manganese poisoning is common in oral administration of 1% potassium permanganate solution, causing oral mucosal erosion, nausea, vomiting, and stomach pain; 3% to 5% solution occurs in gastrointestinal mucosal necrosis, causing abdominal pain, blood in the stool, and even shock; 5 to 19 g of manganese can be fatal, electric welding under poor ventilation conditions, inhalation of a large number of new manganese oxide fumes, sore throat, cough, shortness of breath, and sudden chills and high fever (metal smoke).

Chronic manganese poisoning is usually caused by exposure to manganese smoke and dust after 3 to 5 years or more. Early symptoms include dizziness, headache, limb pain, lower limb weakness and heavy, sweating, palpitations and mood changes, disease development, and muscle development. Increased tension, finger tremors, hyperreflexia, lack of interest in the surrounding things and emotional instability, typical tremor paralysis syndrome in the later stages, increased limb muscle tension and resting tremor, speech disorders, gait difficulties, etc. Crying, obsessive mentality, and impulsive behavior.

Manganese smoke can cause pneumonia, pneumoconiosis, and conjunctivitis, rhinitis and dermatitis can still occur.

Inspection of manganese poisoning

The upper limit of urinary manganese normal value does not exceed 0.54mol/L (0.03mg/L), and the manure manganese generally takes 40mg/kg as the upper limit of normal. The determination of urine and manure manganese can reflect the degree of manganese absorption in the near future. The upper limit of normal blood manganese is 9 .1mol/L (0.05mg/dl), because there is no regularity in blood manganese measurement, it is of little significance for diagnosis. Manganese is 7.2mg/kg for normal men and 13mg/kg for women, due to manganese on earth. Widely distributed, in different regions and eating habits can affect the body's manganese content, so the normal value of manganese in the biological specimens in vivo should be based on local normal values.

Patients with manganese poisoning may have urinary 17-ketosteroids, urinary dopamine and its metabolites increase, while vanillic acid content decreases, and EEG and EMG have abnormal changes.

Diagnosis and identification of manganese poisoning

Manganese poisoning should be distinguished from neurasthenia, peripheral neuritis, psychosis, tremor palsy, encephalitis sequelae, hepatolenticular degeneration, acute carbon monoxide poisoning, cerebral arteriosclerosis, and senile tremor.

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