Abstract

BACKGROUND: With the development of industry and agriculture, organotin compoundshave been widely used in China. Organotin compounds cause a common occupational poisoning.The toxicity of organotin was reported in animal studies; however the reports about human organotinintoxication are very rare. In this study we retrospectively analyzed the clinical manifestations of 15organotin-poisoned patients who had been treated at our hospital from 2002 through 2007. METHODS: Fifteen patients with organotin poisoning were admitted to Sir Run Run ShawHospital Affi liated to Zhejiang University School of Medicine from 2002 to 2007. They were 9 males and6 females, aged from 25 to 52 years. Clinical manifestations and Glasgow Coma Scales showed thatthe poisoning was mild in 4 patients, moderate in 6 and severe in 5. The severe patients were givenglucocorticoid after hospitalization by intravenous guttae of 500 mg methylprednisolone for the fi rst day, followed by 160 mg methylprednisolone per day for three days, and then 80 mg methylprednisoloneper day for another three days. Potassium glutamate and sodium glutamate were intravenously drippedto reduce blood ammonia; intravenous guttae plus oral administration of potassium 9 g/day was usedto correct intractable hypokalemia; sodium bicarbonate was used to correct metabolic acidosis, andsedatives were used to control spasm and twitch; mechanical ventilators were used in 4 patients withdyspnea. RESULTS: Most of the patients showed elevated level of blood ammonia, decreased level ofblood potassium and metabolic acidosis, but some had demyelination changes shown by CT and MRI.Treatments included correction of metabolic acids, blood potassium and ammonia, and mechanicalventilation when necessary. For patients with injuries of the nervous system, glucocorticoids weregiven immediately after hospitalization. These patients showed intractable hypokalemia and metabolicacidosis during the treatment. Forteen patients recovered completely without long-term side-effect. Onepatient in the aphasiac stage restored the linguistic capacity during a 6-month follow-up. CONCLUSIONS: Elevated level of blood ammonia, decresed level of blood potassium, andmetabolic acidosis are common in patients with organotin poisoning. Demyelination can be observed inpatients with severe poisoning. The abnormalities of the patients are reversible after suitable treatments

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