心肺停止蘇生後患者における,脳波とburst-suppression pattem(以下BSと略す)の意義を見いだすべく,出現率,出現時期や期間,および他の臨床検査との関わりなどについて検討した。対象は,当高度救命救急センターICUに入室した心肺停止蘇生後患者80例(男性46例,女性34例)で,ICU入室直後から経日的に脳波検査を施行した。その結果,(1) BS出現率は15.0% (12例)であり,いずれもその転帰は不良(死亡あるいは植物状態)であった。(2) BS出現12例のうち,1例のみがBS出現後,低振幅徐波を呈したが,その他のものはすべてisoelectric pattern(以下IPと略す)に移行し,BSは蘇生後3日目以降認められなかった。また,BSのうちburst出現時において50% (6例)に顔面を中心とした痙攣を認めた。(3) burstの持続時間とsuppressionの持続時間の比率と転帰との関係は明らかではなかった。(4) BS出現例においては91.7% (11例)が聴性脳幹反応にてI～IV波を認めたものの,66.7% (8例)は潜時が遅延していた。(5) 対光反射はBS出現例において58.3% (7例)に認めた。心肺停止蘇生後患者におけるBSの臨床的意義について種々の面から検討したが,BS出現例の転帰は不良であることは他家の報告と矛盾しない。一方,BSは蘇生直後から出現し,3日目以降は認められないこと,また,そのほとんどがBS出現後,IPに移行することが判明した。

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背景:敗血症時には心拍出量は増加するにもかかわらず酸素摂取率の低下から組織酸素代謝失調になるとされている。また敗血症では重要臓器,特にsplanchnic blood flowの相対的低下がおこることも酸素代謝失調の要因とされる。有効肝血流量はsplanchnicの血流と肝の代謝を反映する指標であるが,敗血症で起こる酸素摂取率の低下と有効肝血流量の関係は明らかではない。目的:敗血症患者で酸素摂取率と有効肝血流量との関係を検討すること。対象,方法:集中治療患者22名を対象とした。そのうち敗血症患者は12名であった。各患者において20mgのインドシアニングリーンを投与し,パルス式色素希釈法により心拍出量(CO),有効肝血流量(EHBF)を測定した。また肺動脈カテーテルを用い,全身酸素摂取率(O₂ER)を求めた。結果:敗血症患者では非敗血症患者に比べ,EHBF/CO比は有意に低下した(敗血症vs.非敗血症,0.08±0.03 vs. 0.21±0.06, p<0.001)。また,非敗血症ではEHBF/CO比とO₂ERには相関を認めなかったが,敗血症患者では有意な相関を認めた(r=0.73, p<0.01)。結語:敗血症患者でみられる全身酸素摂取率の障害は肝血流や肝細胞代謝の低下が要因となっている可能性が示唆された。

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A 47-year-old man admitted for a confused state and severe metabolic acidosis shortly after exposure to methylmercaptan. To treat methylmercaptan-induced cytotoxic hypoxia and resultant confusion status, mechanical ventilation was performed to maintain an adequate oxygen supply to organs, especially to the brain. Sodium nitrite (3%, total 40ml), which caused methemoglobinemia (maximally 22%), was given intravenously to remove methylmercaptan from the cytochrome oxidase complex. Oxygen content in arterial blood was maintained at over 15ml/dl throughout the time course in our intensive care unit. Jugular venous oxyhemoglobin (Hbo₂) decreased to 60%; Sjvo₂ (oxygen saturation in the jugular venous blood) was maintained at over 75%. His level of consciousness improved on the next day. The treatment for methylmercaptan poisoning is similar to that for hydrogen sulfide poisoning. Excessive sodium nitrite treatment might cause hypoxic hypoxia due to induced methemoglobinemia. Jugular venous Hbo₂ may indicate the adequate degree of induced methemoglobinemia at a point of the balance between oxygen delivery and consumption in the brain.

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Myocardial ultrasonic tissue characterization has been used recently for evaluating myocardial disease. However, it has been unknown whether myocardial ultrasonic tissue characterization is useful for detection of myocardial cotusion. We treated a patient with myocardial contusion in whom we observed changes in cyclic variation of myocardial ultrasonic integrated backscatter. A 61-year-old male was transported to Osaka Prefectural Nakakawachi Medical Center of Acute Medicine after suffering blunt anterior chest trauma due to motor vehicle accident. Second hospital day after the trauma, myocardial contusion showing diffuse left ventricular hypokinesia was diagnosed by electrocardiogram and echocardiogram. After diagnosing myocardial contusion, we evaluated the myocardial ultrasonic tissue characterization with an integrated backscatter imaging system. We analyzed cyclic variation of the integrated backscatter. Cyclic variation was measured in both the anterior and posterior myocardium at the left ventricle. The values of cyclic variation were consistent with recovery of left ventricular function. Thus, we conclude that integrated backscatter examination is a new technique that may be useful in the evaluating myocardial contusion.

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The case of 82-year-old female who presented with acute subdural hematoma (ASDH) secondary to ruptured intracranial aneurysm is reported. According to the history of the present illness, the patient had suddenly lost consciousness and was immediately brought to our hospital. There was no definite evidence of head trauma, and other etiologies, such as a cerebrovascular accident in her recent past history that might have caused ASDH, were also ruled out. Computed tomography (CT) on admission showed a right-sided ASDH with extension of the hematoma along the tentorium, but none of the characterstic features of subarachnoid hemorrhage (SAH) were observed. However, angiography with magnetic resonance imaging performed after the initial CT revealed a saccular aneurysm of the right internal carotid artery projecting posterolaterally. Emergency surgery was performed to remove the ASDH and clip the aneurysm neck in the acute stage. At surgery, marked adhesion of the arachnoid membrane and absence of cerebrospinal fluid flow were noted in the right sylvian and basal cisterns. Importantly, no clear evidence of SAH was observed during surgery. After removing the ASDH, the right internal carotid-posterior communicating (IC-PC) saccular aneurysm was successfully treated with a Yasagyl titanium clip. There are almost over 20 reports in the literature on ASDH caused by a ruptured aneurysm without evidence of SAH on a CT scan. Based on those reports and our own, ruptured aneurysm should be considered one of the causes of non-traumatic ASDH. In conclusion, the main cause of the occurrence of the phenomenon mentioned in our patient was probably related to the combined presence of the arachnoid adhesion in the sylvian cistern, the special shape of the aneurysm, and the direction in which the aneurysm projected.

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We report a case of a ruptured aneurysm arising from the distal anterior cerebral artery with acute subdural hematoma (SDH) but without subarachnoid hemorrhage. A 51-year-old man admitted in a coma following sudden headache but no history of trauma was found in CT to have a massive SDH on the left convexity. Angiography preceding evacuation of the hematoma showing an aneurysm at A2-A3, but we could not confirm whether it had ruptured because of a slight SDH at the interhemispheric fissure in CT. During the first operation, we conducted evacuation only; no brain or vessel damage was noted. Clipping was then applied to the aneurysm to confirm that it had ruptured and caused the SDH. Cases of ruptured aneurysm without subarachnoid hemorrhage are rare. Analysis by angiography is useful in locating the origin of the acute SDH in the presence of a nontraumatic SDH. In a patient with a ruptured aneurysm at the distal anterior cerebral artery with acute SDH, the discrepancy could be shown between the position of the ruptured aneurysm and the center of the SDH.

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