Frontiers in toxicology · 2026
Clinical features of toxic encephalopathy induced by 1,2-dichloroethane.
СтатьяНазвание и аннотация: Перевод в очереди
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Chen Yuquan, Lin Yuqiang, Ye Yifan, Xie Meiwen, Chen Jiaqi, Yang Zhiqian, Wang Zhi
Аннотация
INTRODUCTION: 1,2-Dichloroethane (1,2-DCE) is a highly toxic industrial organic solvent that can cause acute toxic encephalopathy through occupational exposure, with underreported clinical data in English literature. To explore the clinical characteristics and patients' response to supportive treatments of toxic encephalopathy caused by 1,2-DCE.
METHODS: Fifty-nine patients with acute 1,2-DCE poisoning admitted to the hospital from January 2009 to December 2022 were selected. Patients were divided into three groups based on clinical manifestations: intracranial hypertension (Group A), limb tremors (Group B), and behavioral changes (Group C).
RESULTS: Toxicology testing found that 1,2-DCE was difficult to detect in serum after more than 24 h. Of the 59 patients, 45 (76.27%) achieved complete recovery, 10 (16.95%) achieved partial recovery, and 4 (6.78%) died. Statistical analysis showed a significant difference in recovery rates among the three groups (χ2 = 10.612, P < 0.05). There were no statistically significant differences in symptom and cranial imaging recovery times between the three groups.
CONCLUSION: Acute 1,2-DCE poisoning can cause severe toxic encephalopathy. Early and prolonged treatment with dehydrating agents and glucocorticoids is effective in improving prognosis, and patients with intracranial hypertension are at higher risk of death due to brain herniation.
METHODS: Fifty-nine patients with acute 1,2-DCE poisoning admitted to the hospital from January 2009 to December 2022 were selected. Patients were divided into three groups based on clinical manifestations: intracranial hypertension (Group A), limb tremors (Group B), and behavioral changes (Group C).
RESULTS: Toxicology testing found that 1,2-DCE was difficult to detect in serum after more than 24 h. Of the 59 patients, 45 (76.27%) achieved complete recovery, 10 (16.95%) achieved partial recovery, and 4 (6.78%) died. Statistical analysis showed a significant difference in recovery rates among the three groups (χ2 = 10.612, P < 0.05). There were no statistically significant differences in symptom and cranial imaging recovery times between the three groups.
CONCLUSION: Acute 1,2-DCE poisoning can cause severe toxic encephalopathy. Early and prolonged treatment with dehydrating agents and glucocorticoids is effective in improving prognosis, and patients with intracranial hypertension are at higher risk of death due to brain herniation.