Masuda J, Yutani C, Waki R, Ogata J, Kuriyama Y, Yamaguchi T
Research Institute, National Cardiovascular Center, Osaka, Japan.
Stroke. 1992 Jun;23(6):843-50. doi: 10.1161/01.str.23.6.843.
We conducted the present study to elucidate the pathological mechanisms leading to intracranial hemorrhage complicating infective endocarditis.
Neurological, neuroradiological, and histopathological analyses were performed in 16 patients (one surgical and 15 autopsy cases), 12 men and four women 26-68 years of age, who had demonstrated central nervous system complications during the course of infective endocarditis.
Intracranial hemorrhage was found in all cases; parenchymal hematomas were found in 12 cases, hemorrhagic infarcts in four cases, and primary subarachnoid hemorrhages in two cases. Chronological analysis of neurological examination and computed tomographic scan of the brain confirmed that antecedent cerebral ischemic events had occurred in five of 12 patients showing parenchymal hematomas at autopsy. Hemorrhagic infarct, indicated by petechial or diffuse hemorrhages within the infarct, was seen in another four patients, so that hemorrhagic transformation of the ischemic infarct was confirmed in nine patients. Although mycotic aneurysms were found in five patients, only three of these were ruptured; the other two were occluded with septic emboli. Pyogenic arteritis without aneurysm was found to be distributed in the small cortical arterial branches located in the spaces of cortical sulci, with rupture occurring in five patients.
These results suggest that hemorrhagic transformation of the ischemic infarct due to septic emboli is the most frequent mechanism leading to intracerebral hemorrhage encountered in patients dying of infective endocarditis and that rupture of pyogenic arteritis may be responsible for such hemorrhage in many cases, with ruptures of mycotic aneurysms as an alternative mechanism.
我们开展本研究以阐明导致感染性心内膜炎并发颅内出血的病理机制。
对16例患者(1例手术病例和15例尸检病例)进行了神经学、神经放射学和组织病理学分析,这些患者年龄在26至68岁之间,包括12名男性和4名女性,在感染性心内膜炎病程中出现了中枢神经系统并发症。
所有病例均发现颅内出血;12例为实质血肿,4例为出血性梗死,2例为原发性蛛网膜下腔出血。对神经学检查和脑部计算机断层扫描进行时间顺序分析证实,在尸检时显示实质血肿的12例患者中,有5例先前发生过脑缺血事件。另外4例患者可见梗死区内有瘀点或弥漫性出血所提示的出血性梗死,因此9例患者证实有缺血性梗死的出血性转化。虽然5例患者发现有真菌性动脉瘤,但其中只有3例破裂;另外2例被感染性栓子阻塞。发现无动脉瘤的化脓性动脉炎分布于位于皮质沟间隙的小皮质动脉分支,5例患者发生破裂。
这些结果表明,感染性栓子导致的缺血性梗死的出血性转化是感染性心内膜炎死亡患者颅内出血最常见的机制,在许多情况下,化脓性动脉炎破裂可能是此类出血的原因,真菌性动脉瘤破裂是另一种机制。