心肺蘇生中の呼気終末炭酸ガス濃度(以下ETCO2)は,動物実験において心臓マッサージの有効性ならびに,心拍再開の指標として有用とされている。さらに,心拍再開例の値は非再開例の値に比較し有意に高値であることから,心拍再開の可否を予測する手段としても期待されている。しかし,臨床において,最後の予測手段としての有用性については一定の見解が得られていない。そこで,今回,来院時心肺停止症例50例(外傷疾患は除外)についてETCO2が予測手段となるかどうか検討した。心拍再開の有無と記録開始1分前後のETCO2値との関係では,心拍再開例で非再開例に比較して有意に高値を示した(1.3±0.7% vs 0.7±0.4%)。しかし,個々の値では,低値であっても心拍再開する症例,また逆に高値であっても心拍再開をみない症例もあり,初期のETCO2の値から心拍再開の可否を推定することはむずかしいものと思われた。DOAの原因疾患別にみたとき,心停止の原因が非心疾患による症例では(呼吸器疾患もしくは脳疾患),蘇生例のETCO2値は非蘇生例に比較して有意に高く,さらに蘇生例では全例で0.8%以上であり,逆に0.8%以下では一例も蘇生されていない。すなわち非心疾患によるDOAではETCO2値が心拍再開の予後を予測する手段になる可能性が示唆された。臨床において,ETCO2が心拍再開の可否を予測できるかどうかについては依然議論の分かれるところである。しかし,その原因として背景にある心停止の原因の相違が影響していると推察され,すなわち心停止の原因が非心疾患の場合には有用である可能性が示唆された。
Soluble barium salts, commonly used in industrial fields, are highly toxic. Hypokalemia, arrhythmia and weakness are the common signs of barium salt poisoning and the lethal dose is thought to be about 1.0g. A 21-year-old man complained of vomiting, diarrhea and a tingling sensation after the accidental ingestion of barium chloride. Hypokalemia (3.2mEq/l) and electrocardiogram abnormality (giant U-wave) were also observed. The patient ingested only about 0.1g of barium chloride, but plasma barium concentration was 8.5μM (measured by ICP-AES; inductively coupled plasma emission spectroscopy). Other laboratory findings were normal. Magnesium sulphate was given orally (40g) for antagonistic action against that of barium and therapeutically 40mEq of potassium was infused intravenously over 6 hours. Potassium excretion into urine was 30.6mEq over 24 hours. At 45 hours after admission, plasma potassium had recovered to 4.3mEq/l. Electrocardiogram normalized within 3 hours, and gastrointestinal and neurological signs were absent by the next morning.The mechanism of cardiac toxicity in barium chloride poisoning has not yet been clearly defined. Although some of the ECG changes may be associated with hypokalemia, a Ca channel blocking mechanism could also be responsible.
The case of a 62-year-old male with acute development of a traumatic intracerebellar hematoma, which was identified on serial CT scans, is reported. The patient fell and struck his occiput when he was involved in a traffic accident on June 25, 1988. He complained of headache and vomited, and was transferred to this hospital within one hour after the accident. On admission, he was alert and well oriented. Plain skull roentgenogram showed a right occipital linear fracture. The initial CT scan showed a small high density area in the right cerebellar hemisphere suggesting a hematoma, associated with hemorrhage in the IVth ventricle and subarachnoid space. Gradually, the patient became drowsy and began vomiting frequently. CT scan performed 3 hours after injury revealed an increased volume of hematoma in the right cerebellar hemisphere with slight shift of the IVth ventricle to the opposite side. Emergency posterior fossa craniectomy was then performed 5 hours following injury and the hematoma was totally evacuated with debridement of the contused cerebellar hemisphere. The postoperative course was uneventful. At follow-up examination 4 months later the patient was found to be leading a normal life without any neurological deficit. Traumatic acute intracerebellar hematomas, unassociated with subdural or epidural hematoma of the posterior fossa, are relatively rare. Early diagnosis and management should be made so as not to result in fatal brain stem injury.
Three cases of bilateral epidural hematomas were found in a total of 153 cases of epidural hematoma over a period of 8 years among 2, 482 cases of head injury which required admission. In all cases, CT scan within 6 hours of head injury revealed simultaneous bilaterally-coexisting epidural hematomas. In two cases, skull x-ray films showed bilateral linear skull fractures. Under the skull fractures, acute bilateral epidural hematomas were demonstrated by CT scan. The origin of hematoma was thought to be related to the fractures. In one of the latter cases, skull x-ray films showed a linear skull fracture in the left fronto-parietal area and bilateral epidural hematomas were demonstrated by CT scan. A hematoma on the right side was thought to be the result of dural stripping caused by negative pressure at the site opposite the site of impact. In two of the three cases, hematomas were removed bilaterally. All patients were discharged without any major neurological deficit.