1 0 0 0 OA MRIにて下垂体後葉のT1高信号の消失を認めたSIADHの1例
- 著者
- 広瀬 保夫 岩松 宏 本多 拓 高橋 直也 田村 紀子 百都 健
- 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.8, no.12, pp.659-664, 1997-12-15 (Released:2009-03-27)
- 参考文献数
- 9
- 被引用文献数
- 1 1
We describe magnetic resonance imaging (MRI) findings of the syndrome of inappropriate secretion of antidiuretic hormone (SIADH). A 48 year-old man had been involved in a traffic accident and was admitted to our hospital. He was diagnosed as having a slight cerebral contusion and bone fractures in his bilateral lower extremities. His head injury was treated conservatively and his course was uneventful. Eight days after admission his consciousness deteriorated although the computed tomography was markedly improved. His laboratory data showed hyponatremia associated with continued urinary sodium loss and persistent secretion of vasopressin with markedly low plasma osmolality. The patient was diagnosed with SIADH and was treated with fluid restriction, sodium infusion and demeclocycline. T1-weighted MRI of his pituitary gland showed the absence of the high intensity signal of the posterior lobe. The high intensity signal appeared narrowly when his symptoms and hyponatermia improved, and disappeared when his symptoms and hyponatremia deteriorated. The high intensity signal observed with T1-weighted MRI of the normal posterior pituitary reflects an intact and functional neurohypophyseal system. This case suggested that neurosecretory vesicles were decreased despite high plasma vasopressin levels in SIADH patients.
1 0 0 0 アジ化ナトリウム集団中毒症例の検討
- 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
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.
1 0 0 0 OA アジ化ナトリウム集団中毒症例の検討
- 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
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.
