Clinical toxicology (Philadelphia, Pa.) · 2025
An outbreak of poisoning in Vietnam caused by the adulteration of alcoholic drinks with acetonitrile.
СтатьяНазвание и аннотация: Перевод в очереди
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Nguyen Tien H, Tran Son C, Le Thuan Q, Nguyen Dung T, Nguyen Chien M, Nguyen Tuan A, Nguyen Ngoc H, Tien Cao B, Vu Anh-Phuong, Nguyen Trung-Nguyen, Nguyen HoanVu N
Аннотация
INTRODUCTION: Acetonitrile causes potentially fatal inhibition of cytochrome c oxidase. We report a mass poisoning event linked to consumption of alcohol adulterated with acetonitrile.
METHODS: We performed a retrospective review of public health investigations, poison centre records, and hospital records of patients who presented to a tertiary hospital.
RESULTS: The mass poisoning potentially involved 80 individuals. Two died and 20 others were hospitalized. The hospital records of 14 patients were reviewed. The median time to first symptom was 6.5 h. The most common first symptoms were nausea and vomiting, followed by headache, abdominal pain, diarrhoea, confusion, and dizziness. Peak blood acetonitrile and cyanide concentrations were 170 mg/L and 0.398 mg/L, respectively. Eleven patients had increased lactate concentrations. Abnormalities of the corpus callosum were noted on neuroimaging in three patients. Eight patients were treated with extracorporeal elimination techniques. The median elimination half-life of acetonitrile was 40 h in patients who did not receive extracorporeal treatments and 28 h in patients who did.
DISCUSSION: The early symptoms and their observed delay are consistent with the findings described previously in acetonitrile poisoning. The abnormalities of the corpus callosum noted on neuroimaging in three patients may have been due to acetonitrile. The elimination half-lives of acetonitrile without extracorporeal treatments were similar to those previously reported.
CONCLUSIONS: Contamination of alcoholic drinks with acetonitrile resulted in 20 hospitalizations and two fatalities. In the 14 patients with hospital records, acetonitrile exposure was associated with delayed-onset gastrointestinal and neurological symptoms as well as increased lactate concentrations. Two patients required mechanical ventilation and vasopressor support for haemodynamic disturbances. Abnormalities of the corpus callosum were noted on neuroimaging in three patients, which might have been caused by acetonitrile. A shorter acetonitrile elimination half-life was noted in patients who received extracorporeal treatment. All patients who arrived at a medical facility survived to hospital discharge without severe residual symptoms.
METHODS: We performed a retrospective review of public health investigations, poison centre records, and hospital records of patients who presented to a tertiary hospital.
RESULTS: The mass poisoning potentially involved 80 individuals. Two died and 20 others were hospitalized. The hospital records of 14 patients were reviewed. The median time to first symptom was 6.5 h. The most common first symptoms were nausea and vomiting, followed by headache, abdominal pain, diarrhoea, confusion, and dizziness. Peak blood acetonitrile and cyanide concentrations were 170 mg/L and 0.398 mg/L, respectively. Eleven patients had increased lactate concentrations. Abnormalities of the corpus callosum were noted on neuroimaging in three patients. Eight patients were treated with extracorporeal elimination techniques. The median elimination half-life of acetonitrile was 40 h in patients who did not receive extracorporeal treatments and 28 h in patients who did.
DISCUSSION: The early symptoms and their observed delay are consistent with the findings described previously in acetonitrile poisoning. The abnormalities of the corpus callosum noted on neuroimaging in three patients may have been due to acetonitrile. The elimination half-lives of acetonitrile without extracorporeal treatments were similar to those previously reported.
CONCLUSIONS: Contamination of alcoholic drinks with acetonitrile resulted in 20 hospitalizations and two fatalities. In the 14 patients with hospital records, acetonitrile exposure was associated with delayed-onset gastrointestinal and neurological symptoms as well as increased lactate concentrations. Two patients required mechanical ventilation and vasopressor support for haemodynamic disturbances. Abnormalities of the corpus callosum were noted on neuroimaging in three patients, which might have been caused by acetonitrile. A shorter acetonitrile elimination half-life was noted in patients who received extracorporeal treatment. All patients who arrived at a medical facility survived to hospital discharge without severe residual symptoms.