慢性硬脑膜下血肿发病机理的研究

pathogenesis of chronic subdural hematoma

报道慢性硬脑膜下血肿(CSDH)210例,180例行钻颅冲洗引流,30例行单纯冲洗而不作术后引流,均取得良好效果。17例血肿外包膜有大量新生毛细血管,均由一层内皮细胞组成,基底膜不完整,内皮细胞的间隙增宽,可见红细胞由内皮细胞间隙渗出。30例作血肿液及静脉血凝血及纤维溶解机制分析,发现血肿液中纤维蛋白原浓度较低,纤维溶解蛋白原产生物(FDP)浓度较高,血肿液中白陶土部分促凝血酶原激酶时间(KPTT)、凝血酶原时间(PT)、凝血酶时间(CT)均有明显延长,认为血液凝固系统与纤维蛋白溶解系统的过度活化是CSDH发生发展的基本病理因素,从而导致血肿膜微血管不断少量出血,使血肿逐步扩大的理论。

The paper offers a report of 210 cases of chronicsubdural hematoma (CSDH). of which 180 caseswere treated with burr and irrgation and drainagewhile 30 with irrigation without drainage. Bothtreatments proved to be satisfactory. In 17 casesthe external membrane of hematoma was rich inneocapillaries which were made of thin-layerendothelial cells. with incomplete basementmembrane. The gaps between endothelial cellswere rather wider. and it caused the erythrocytescoming in and out of there. Analysis of coagulationand fibrinolysis of the hematoma fluid and systematicvenous blood were performed in 30 cases. It wasdiscovered that fibrinogen concentration of thehematoma fluid was rather low and fibrinogen-degradtions prodllct (FDP) concentration compare-tivel high. While the systematic venous bloodsupplied normal coagulation parameter but thekaolin partial thromboplastin time(KPTT). prothrombintime (PT). thrombin time (TT) in hematomafluid were prolonged markedly, It was suggestedthat the overactivation in both clotting andfibrinolytic systems is the fundamental cause forgradually increase the size of CSDH. and alsosupports the theroy of continual minimal bleedingfrom hematoma membrane.