著者

広瀬 保夫 畑 耕治郎 本多 拓 山崎 芳彦 堀 寧 大関 暢

出版者

一般社団法人 日本救急医学会

雑誌

日本救急医学会雑誌 (ISSN:0915924X)

巻号頁・発行日

vol.12, no.3, pp.125-129, 2001

被引用文献数

3

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This report describes 7 victims of sodium azide poisoning caused by drinking poisoned water. Ten employees at the poisoning site developed symptoms immediately after ingesting coffee or tea made from hot water contained in a thermos bottle. Symptoms included altered consciousness, faintness, blackout, palpitation, nausea, and paresthesia of both hands and feet. Seven patients were transferred to our institution by ambulance. We assumed symptoms were caused by acute poisoning but the causative agent was unknown. We could not rule out cyanide poisoning because of the rapid emergence of symptoms suggesting circulatory failure, so we administered amyl nitrate, sodium nitrate, and sodium thiosulfate. Symptoms rapidly subsided. The causative agent was identified the next day as sodium azide. While the victims were being treated at the emergency room, 2 doctors, 3 nurses, and 1 pharmacist complained of faintness, headache, nausea, sensations of dyspnea and eye pain. These medical staff members had all either conducted gastric lavage or treated gastric contents. This strongly suggests that symptoms were caused by hydrazoic acid formed in a chemical reaction between sodium azide and gastric acid. Our experience underscores the potential hazard from hydrazoic acid faced by medical staff treating patients with oral sodium azide intoxication.

著者

広瀬 保夫 畑 耕治郎 本多 拓 山崎 芳彦 堀 寧 大関 暢

出版者

Japanese Association for Acute Medicine

雑誌

日本救急医学会雑誌 (ISSN:0915924X)

巻号頁・発行日

vol.12, no.3, pp.125-129, 2001-03-15 (Released:2009-03-27)

参考文献数

9

被引用文献数

1 3

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This report describes 7 victims of sodium azide poisoning caused by drinking poisoned water. Ten employees at the poisoning site developed symptoms immediately after ingesting coffee or tea made from hot water contained in a thermos bottle. Symptoms included altered consciousness, faintness, blackout, palpitation, nausea, and paresthesia of both hands and feet. Seven patients were transferred to our institution by ambulance. We assumed symptoms were caused by acute poisoning but the causative agent was unknown. We could not rule out cyanide poisoning because of the rapid emergence of symptoms suggesting circulatory failure, so we administered amyl nitrate, sodium nitrate, and sodium thiosulfate. Symptoms rapidly subsided. The causative agent was identified the next day as sodium azide. While the victims were being treated at the emergency room, 2 doctors, 3 nurses, and 1 pharmacist complained of faintness, headache, nausea, sensations of dyspnea and eye pain. These medical staff members had all either conducted gastric lavage or treated gastric contents. This strongly suggests that symptoms were caused by hydrazoic acid formed in a chemical reaction between sodium azide and gastric acid. Our experience underscores the potential hazard from hydrazoic acid faced by medical staff treating patients with oral sodium azide intoxication.