Morinaga K, Matsumoto Y, Hayashi S, Omiya N, Mikami J, Sato H, Inoue Y, Okawara S
Okawara Neurosurgical Hospital, Muroran, Japan.
No Shinkei Geka. 1995 Mar;23(3):213-6.
Subacute subdural hematoma was investigated in terms of findings in CT, MRI and operations and of onset mechanism. The subjects were 7 cases of subacute subdural hematoma in which CT and MRI were performed during the past 5 year period. Subacute subdural hematoma here was defined as a nonoperated case with acute subdural hematoma, accompanied by subacute exacerbation 1-3 weeks after head trauma. The time from the injury to the onset averaged 13.7 days. CT revealed mixed density in 4 cases, low density in 3 cases and cerebral atrophy in all cases, with increasing mass sign due to the enlarged low density area. MRI revealed mixed intensity in 5 cases and high intensity in 2 cases, with increasing mass sign due to the enlarged high intensity area. Operation disclosed the outer membrane of the hematoma only in 1 case, but the inner membrane could not be identified in any case. Analysis of the hematoma contents showed a low hemoglobin concentrations and a high level of methemoglobin. Lack of outer membrane in cases with subacute subdural hematoma suggests that this is a different disease entity from chronic subdural hematoma. It is surmised that subacute subdural hematoma is the result of subdural effusion in the subacute stage, because, judging from the findings of CT and MRI each performed over time, cerebrospinal fluid is considered accountable for the increase in the mass sign.
从CT、MRI检查结果、手术情况及发病机制方面对亚急性硬膜下血肿进行了研究。研究对象为过去5年期间行CT及MRI检查的7例亚急性硬膜下血肿患者。此处的亚急性硬膜下血肿定义为急性硬膜下血肿未经手术治疗的病例,头部外伤后1 - 3周出现亚急性加重。从受伤到发病的时间平均为13.7天。CT显示4例为混合密度,3例为低密度,所有病例均有脑萎缩,低密度区扩大导致占位征象加重。MRI显示5例为混合信号强度,2例为高信号强度,高信号区扩大导致占位征象加重。手术仅在1例中发现血肿的外膜,但在任何病例中均未发现内膜。血肿内容物分析显示血红蛋白浓度低,高铁血红蛋白水平高。亚急性硬膜下血肿病例缺乏外膜提示其与慢性硬膜下血肿是不同的疾病实体。据推测,亚急性硬膜下血肿是亚急性期硬膜下积液的结果,因为从不同时间进行的CT和MRI检查结果判断,脑脊液被认为是占位征象增加的原因。