外伤性硬脑膜下积液转化成慢性硬脑膜下血肿的可能机制

目的 探讨外伤性硬脑膜下积液（TSE）转化为慢性硬脑膜下血肿（CSH）的机制。方法 CT或MRI随访TSE患者，并对部分积液和血肿的包膜作组织学检查以明确各期膜中细胞的类型。结果 TSE总数96个，转化为CSH44个，其中无症状31个。外膜显微解剖：TSE为幼稚成纤维细胞，少或无炎症细胞浸润。血肿初期：淋巴细胞浸润，毛细血管形成及局灶出血；中期：仍以淋巴细胞浸润为主，可见浆细胞，血管增多，红细胞呈弥漫性逸出；后期：多种炎症细胞并存尤是嗜酸性粒细胞出现。结论 CSH是部分TSE转归中的一个阶段，有症状只是少数病例。蛛网膜破口和TSE是局部炎性修复反应的始因，新生膜出血是修复蛛网膜的一种病理反应。

A possible mechanism of traumatic subdural effusion developing into chronic subdural hematoma

Objective To explore the possible mechanism for that traumatic subdural effusion(TSE) developed to chronic subdural hematoma(CSH).Methods Fifty-four patients of TSE were followed-up by computed tomography(CT) scans or magnetic resonance images(MRI).Some outer membranes in CSHs or hydromas were examined histologically for detecting their cellular types at(variant) stages.Results Of 96 TSEs,44 cases developed into CSHs(31 of those were asymptomatic).The microanatomy of hydroma membranes(6 cases) showed that immature fibroblasts were observed in the outer membranes,and there were no or little inflammatory cells infiltrated.Outer membranes of initial haematomas(4 cases) showed that fibrocollagenous tissue was still immature,lymphocytes were the main inflammatory cells infiltrated and there were some capillaries formed and bleedings locally.The membranes of mid-term haematomas(5 cases)showed increasingly the thickness of fibrocollagenous tissue and the amount of blood vessels.Lymphocytes were still the main inflammatory cells,but could find plasma cells,RBC leak out diffusly.In the later-term of haematoma(4 cases),fibroblasts were more maturer.Fibrocollagenous tissue became thicker.Various inflammatory cells were present,especially eosinophils appeared in a large amount in outer membranes.CSHs were then absorbed gradually.Conclusion CSH is one stage of some TSEs transmutation,and symptomatic CSH happens in a few cases only.We postulate that the laceration of arachnoid and the subdural liquid are the starting factors of local inflammation,and the haemorrhage in the neomembrane is a pathological response for reconstructing arachnoid in inflammation procedure.