Shimoji T, Sato K, Ishii S
Department of Neurosurgery, Juntendo Izunagaoka Hospital.
No Shinkei Geka. 1992 Feb;20(2):131-7.
Our report concerns 112 cases of chronic subdural hematoma (CSH). M:F ratio is 3.5:1. (Fig. 1). The etiology of CSH is as follows; mild head injury (71 pts.), post-craniotomy (3 pts.), post-V-P shunt (1 pt.) and unknown (37 pts.). All patients are diagnosed by CT scan. Twenty patients were followed up after the subdural space was expressed as low density on CT (Fig.2). 14 of these were found to have extremely thin subdural fluid collection without compression of the brain. Cisternography by using radioisotope and/or metrizamide was carried out in seven patients in whom the subdural fluid collection was found on CT, and in five of whom the dye flowing into the subdural space was retained for 24-48 hours (Fig. 3 a). For treatment, burr holes and irrigation of the hematoma was carried out and then a drain was inserted into the subdural space. The inner membrane of the chronic subdural hematoma was looked at in 19 patients during surgery. All but one showed the inner membrane totally covering the brain surface. However, in one patient the inner membrane didn't entirely cover the brain surface, suggesting that this was the condition just before the entire encapsulation of the hematoma (Fig. 4 b). It used to be considered that a blood clot in the subdural space is needed to develop a chronic subdural hematoma. However, since the introduction of CT scan, there have been many reports suggesting that chronic subdural hematoma has developed from subdural fluid collection without apparent evidence of blood clot after head injury. Therefore, it has been controversial whether the blood clot is absolutely essential to develop into the chronic subdural hematoma or not.(ABSTRACT TRUNCATED AT 250 WORDS)
我们的报告涉及112例慢性硬膜下血肿(CSH)。男女比例为3.5:1(图1)。CSH的病因如下:轻度头部损伤(71例)、开颅术后(3例)、脑室-腹腔分流术后(1例)及病因不明(37例)。所有患者均经CT扫描确诊。20例患者在CT显示硬膜下间隙为低密度后进行了随访(图2)。其中14例发现有极薄的硬膜下积液,无脑组织受压。对7例CT发现有硬膜下积液的患者进行了放射性核素和/或甲泛葡胺脑池造影,其中5例造影剂流入硬膜下间隙并滞留24 - 48小时(图3a)。治疗方法为钻孔引流血肿,然后在硬膜下间隙置入引流管。手术中观察了19例慢性硬膜下血肿的内膜。除1例患者外,其余患者的内膜均完全覆盖脑表面。然而,有1例患者的内膜未完全覆盖脑表面,提示这可能是血肿完全包裹前的状态(图4b)。过去认为硬膜下间隙有血凝块是形成慢性硬膜下血肿的必要条件。然而,自CT扫描应用以来,有许多报道表明慢性硬膜下血肿可由头部损伤后无明显血凝块证据的硬膜下积液发展而来。因此,血凝块对于发展为慢性硬膜下血肿是否绝对必要一直存在争议。(摘要截选至250字)