Ito H, Yamamoto S, Komai T, Mizukoshi H
J Neurosurg. 1976 Jul;45(1):26-31. doi: 10.3171/jns.1976.45.1.0026.
The authors describe studies performed on material aspirated from chronic subdural hematomas. Patients were given 51Cr-labeled red cells prior to aspiration, and it was possible to demonstrate that the mean daily hemorrhage into the hematoma space amounted to 10.2% of its volume. Immunoelectrophoresis of the aspirated hematoma fluid by monospecific anti-human fibrinogen revealed the presence of fibrin and fibrinogen degradation products that, measured by hemagglutination-inhibition immunoassay techniques, varied between 5.0 and 10,500 mug/ml with an average of 2604 mug/ml in 18 cases. The tissue activator was demonstrated by Todd's histological localization in the outer membrane of the chronic subdural hematoma in 11 cases, but not in the inner membrane. These results indicate that if a clot in the subdural space causes the formation of neomembrane, and excessive fibrinolysis occurs, the subdural clot would not only liquefy, but also enlarge by continuous hemorrhage from the neomembrane. Therefore, local hyperfibrinolysis and continuous bleeding are important in the etiology of the chronic subdural hematoma.
作者描述了对从慢性硬膜下血肿中吸出的物质所进行的研究。在抽吸之前给患者输注51Cr标记的红细胞,结果表明血肿腔内平均每日出血量相当于其体积的10.2%。用单特异性抗人纤维蛋白原对吸出的血肿液进行免疫电泳,发现存在纤维蛋白和纤维蛋白原降解产物,通过血凝抑制免疫测定技术测定,18例患者的含量在5.0至10500μg/ml之间,平均为2604μg/ml。在11例慢性硬膜下血肿的外膜中通过托德组织学定位法证实有组织激活剂,但内膜中未发现。这些结果表明,如果硬膜下间隙中的血凝块导致新膜形成,并且发生过度纤维蛋白溶解,硬膜下血凝块不仅会液化,还会因新膜持续出血而增大。因此,局部纤维蛋白溶解亢进和持续出血在慢性硬膜下血肿的病因学中很重要。