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Organotin poisoning refers to poisoning caused by exposure to excessive amounts of organotins. Trialkyl tin is mainly used in agriculture. Acute trialkyltin poisoning primarily damages the central nervous system, causing interstitial edema in the brain and spinal cord white matter, which leads to toxic encephalopathy. Chronic effects often present as a neurasthenic syndrome. Skin contact can cause burns, contact dermatitis, or allergic dermatitis. Dialkyltin primarily damages the liver and bile ducts. Treatment, apart from removing the source of exposure, mainly consists of symptomatic treatment and supportive therapy. Types of organotin compounds There are 4 types of organotin compounds: tetraalkyltin compounds, trialkyltin compounds, dialkyltin compounds, and monovalent alkyltin compounds. According to domestic and international case reports, the main organotin compounds that cause acute toxic encephalopathy include trimethyltin, trimethyltin chloride, triethyltin, triethyltin chloride, triethyltin bromide, triethyltin iodide, triethyltin hydroxide, triethyltin sulfate, bis(triethyl)tin sulfate, tributyltin chloride, triphenyltin chloride, stannic triphenylacetate, tetraethyltin, tetrabutyltin, tetraphenyltin, and triethyltin bromide (Umi San), among others. Physical and chemical properties: Organotin compounds are mostly solids or oily liquids, with a rotting-herb odor. It is volatile at room temperature, insoluble or poorly soluble in water, but soluble in organic solvents. Some of these compounds can be decomposed by bleaching powder or potassium permanganate to form inorganic tin. Opportunities for contact: Organotin compounds are primarily used as stabilizers for polyvinyl chloride plastics; they can also be employed as fungicides in agriculture, as anti-mold agents in paints, as anti-fouling agents underwater, and as rodenticides. Tetraalkyltin is an intermediate for the preparation of other organotin compounds. Water areas near ships and other vessels that use organotin anti-fouling coatings can become polluted. During operations, inadequate protection, equipment failure, or improper procedures can lead to workers being exposed to large amounts of organotin. Route of entry: Organotin compounds can generally be absorbed through the respiratory tract, while the degree of absorption through the skin and digestive tract varies depending on the specific compound. For example, light-chain alkyltin is absorbed rapidly through the gastrointestinal tract, whereas tricyclohexyltin hydroxide is hardly absorbed through the gastrointestinal tract. Trialkyltin is generally absorbed through the skin, but triphenyltin chloride and triphenyltin acetate do not easily penetrate intact skin. Symptoms of poisoning: Acute poisoning may have a certain incubation period, usually 1 to 5 days. During this period, the patient may show no symptoms or only mild symptoms such as dizziness and headache. These symptoms are intermittent in the early stage but become persistent later on; there is also listlessness and significant fatigue. In severe cases, the person may suddenly fall into a coma, and convulsions or respiratory arrest may also occur. Certain types, such as dibutyltin compounds, tributyltin compounds, triethyltin bromide, tetraethyltin, and triphenyltin acetate, can cause irritation in the eyes, nose, and throat, as well as burns. The symptoms of chronic poisoning are those of a neurasthenic syndrome, primarily including dizziness, headache, and fatigue, which are usually more severe in the afternoon; weight loss may also occur. First aid measures: 1. Immediately move away from the accident site to an area with fresh air. If the skin is contaminated, rinse it thoroughly immediately with clean water or soapy water. Rinse the eyes with clean water if they are contaminated. If swallowed accidentally, rinse the stomach immediately with water. 2. Since neurological symptoms may not be apparent during the incubation period of poisoning, the early symptoms are often non-specific, making it difficult to make a diagnosis at that stage. However, the condition progresses rapidly after onset; therefore, those with a significant history of exposure should stay in bed and be under observation for 5–7 days to allow for timely intervention. 3. Symptomatic and supportive treatment is provided based on the manifestations of poisoning caused by different organotin compounds. Hyperbaric oxygen therapy can be used if necessary; it is important to prevent those with severe mental symptoms from harming themselves or others. Patients with severe poisoning should also have their rest period appropriately extended even after clinical recovery. Accident cases: Major acute and subacute poisoning incidents include: In 1954 in France, the use of Stalinon either topically or orally led to 217 cases of poisoning, with 100 deaths. The main pathological change was leukoencephalomalacia, and the poisoning was primarily caused by the impurity triethylstannyl iodide. In 1998 in China, lard was stored in barrels that had previously contained tin methylmercaptide, resulting in poisoning cases; 94 cases were mild and 60 were severe, with mental symptoms being the main manifestation. The poisoning was primarily caused by the impurity tin trichloride. Another case of acute poisoning among maintenance workers was reported; the worker carried out pipeline maintenance without personal protective equipment and was exposed to vapors of a leaking tin methyl chloride mixture (containing approximately <0.1% tin trimethyl chloride, 80% tin dimethyldichloride, and 20% tin methylchloride) for about 4 hours. There were no symptoms on that day; the next day, she experienced dizziness, headache, nausea, and memory loss. She was hospitalized 3 days later, showing alternating episodes of depression and mania, and she tied up and beat her son for no reason, failing to remember what had happened afterward. Immediate and recent memory is significantly impaired. On the 14th day of hospitalization, paroxysmal epileptic seizures occurred, with 4 episodes within 3 days. Each episode lasts about 2 minutes. Physical examination: conscious, with a masked face, slow responses, decreased memory and calculation abilities, resting tremor in the fingers of both hands, and bilateral Babinski signs (-). No papilledema was observed during the fundus examination. The cerebrospinal fluid test was normal. The EEG showed mild abnormalities. The cranial CT is normal. The poisoning is mainly caused by trimethyltin chloride.