老年者(65歳以上)の入浴中の突然死の発生機序を明らかにするため,秋田県内および秋田市と同等の都市規模を有する11の消防本部が,入浴中に発生したイベントにより医療機関に救急搬送した患者の実態調査を行った。また,これらのうち4都市については入浴環境および入浴習慣等についても調査した。さらに秋田市在住の健康高齢者(60歳以上)を対象に,入浴中の循環動態の変動(血圧,心拍数)を検査し室温や湯温との関連性を検討した。入浴中に救急要請のあった救急患者477人中,260人が心肺停止であり,そのうち老年者は210人であった。老年者の入浴中の心肺停止は冬季,自宅での発生が多く,大半は家族との同居形態であった。老年者の地域別発生率(管内の老年者人口10万人当たりの発生数)では青森が最多の41.6,最低は宮崎の11.0であった。対象とした都市のうち旭川市以外は,冬季の脱衣所の温度が居間や浴室よりも低かった。また,脱衣場での血圧は居間や浴室内よりも高い傾向にあった。入浴習慣と血圧変動では42℃以上の熱い湯に浸かる場合や湯に浸かる前に体を洗う場合の方が浴槽内での血圧低下の度合いが大きかった。以上から,冬季に多く発生する老年者の入浴中の心肺停止を防止するには,脱衣所の保温に注意し,適正な湯温での入浴など老年者の急激な血圧変動を来さないような配慮が必要である。また,複数での入浴や,家族による頻繁な声かけは早期発見につながる。したがって,老年者の入浴に際しては急激な血圧の変動を来さないような入浴環境の整備および入浴方法の啓発が重要である。

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In a case of iliopsoas abscess treated by computed tomography (CT) guided percutaneous drainage, a 72-year-old woman admitted to our hospital presented with a high-grade fever and pain in the left hip. Laboratory examination showed leukocytosis (white blood cell count 12, 600/mm³) and elevated C-reactive protein (11.6mg/dl). Plain X-ray film revealed no apparent abnormalities, but CT scan clearly showed an abscess formed in the left iliopsoas muscle. For treatment, we chose CT-guided percutaneous drainage because the lesion was localized in the iliac fossa. A drain catheter (sump tube) was inserted in the abscess cavity and about 300cc of purulent effusion was drained. After drainage, laboratory findings and clinical sympton improved gradually and CT after 3 weeks of follow-up showed the abscess to have disappeared. We found that CT-guided percutaneous drainage is effective in treating iliopsoas abscess, especially in the early stage. This drainage is less invasive than conventional surgical treatment, and we suggest that CT-guided percutaneous drainage may be the treatment of first choice when iliopsoas abscess is diagnosed early enough.

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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.

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A 63-year-old man began acting abnormally 2 days after development of a fever. He was admitted to a nearby hospital where a brain CT scan showed no abnormality. After experiencing a clonic convulsion the day following admission, he fell into a coma. Five days after admission, CT scans revealed low-density areas in the left temporal lobe, and acyclovir was administered based on a tentative diagnosis of herpes simplex encephalitis. Twelve days after admission, the patient was transferred to the Emergency Department of Kawasaki Medical School Hospital. MR imaging revealed bilateral expansion of the lesions, and his EEG showed periodic lateralized epileptform discharges (PLEDs) on both sides. HSV-DNA in his spinal fluid was positive as determined by PCR examination. Acyclovir 1, 500mg/day was continued for 3 weeks, and the patient's consciousness improved slightly. Although lesions improved, as indicated by MRI, SPECT showed high uptake on the left side at least up to 71 days after fever onset. The patient survived with apallic syndrome. Although pharmacological intervention improved the prognosis of this disease, treatment must be initiated promptly.

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We treated 3 patients who developed respiratory disorders due to aluminum silicate, a principal component of “Kitty litter” (cat dirt). Case 1 was a 37-year-old woman with dyspnea treated for bronchial asthma for 3 months from about September 1995. Dyspnea was exacerbated after inhalation of powder from Kitty litter. On admission, disturbance of consciousness and marked hypoxemia were noted, but the patient recovered through respiratory management. Bronchoscopy showed white sputum in each segment of the bronchi. Case 2 was a 48-year-old woman with a cough exacerbated from about November 1998. Moist rales were present in expiration on chest auscultation. Symptoms were resolved by the administration of bronchodilators and expectorants. Case 3 was a 45-year-old woman with dyspnea treated for bronchial asthma since about March 1998 without improvement. Moist rales were present in bilateral lung fields during inspiration and expiration. A diagnosis of pneumonitis was made based on chest computed tomography (CT) findings recovered by bronchodilators and expectorants. From the information obtained by inquiry about the disorder, all 3 patients were considered have problems related to Kitty litter. Silica was present in the sputum of all 3 in analysis using an X-ray microanalyzer. Kitty litter causes severe symptoms on massive inhalation and respiratory disorders by inhalation of even a small amount over a long period. Precaution are thus required for indoor use.

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