迟发性外伤性颅内血肿113例分析

目的总结和分析外伤性迟发性颅内血肿的临床特点及其影像学特征。方法对1995年1月至2003年3月住院治疗的外伤性迟发性颅内血肿患者病历资料进行回顾性分析。结果在同期住院治疗的1574例颅脑损伤患者中,有113例(7.2%)出现迟发性颅内血肿或因迟发性颅内血肿入院手术治疗,术后恢复良好18例(15.9%),中残29例(25.7%),重残25例(22.1%),植物生存17例(15.1%),死亡24例(21.2%)。结论外伤性迟发性颅内血肿有其明确的临床特点和典型的影像学特征,及早发现、及时手术抢救治疗,能显著改善外伤性迟发性颅内血肿的预后。     

急性颅脑伤术后再次开颅手术临床分析

目的:探讨急性颅脑伤术后再次出血行二次手术的原因与对策。方法:回顾性分析急性颅脑伤术后再次出现颅内血肿者28例。结果:根据格拉斯哥预后量表(GOS)评分:恢复良好者12例,中残3例,重残3例,植物生存1例,死亡9例。结论:能否预防颅脑外伤术后再次出血及早期诊断、及时手术治疗是提高患者生存率及生存质量的关键。     

Chronic subdural hematoma associated with dural metastasis leads to early recurrence and death: A single-institute,retrospective cohort study

The prevalence of chronic subdural hematoma (CSDH) associated with dural metastasis is uncertain, and appropriate treatment strategies have not been established. This study aimed to investigate the characteristics of and appropriate treatment strategies for CSDH associated with dural metastasis. We retrospectively reviewed the charts of 214 patients who underwent surgery for CSDH. The patients were divided into the dural metastasis group (DMG; n = 5, 2.3%) and no dural metastasis group (No-DMG; n = 209, 97.3%). Patient characteristics, treatment, and outcomes were compared between the two groups. Active cancer was detected in 31 out of 214 patients, 5 of whom (16.1%) had dural metastasis. In-hospital death (80.0% vs. 0%; p < 0.001) and recurrence within 14 days (80.0% vs. 2.9%; p < 0.001) and 60 days (80.0% vs. 13.9%; p = 0.002) were significantly prevalent in the DMG. All patients in the DMG developed subdural hematoma re-accumulation requiring emergent surgery because of brain herniation, and patients in the DMG had significantly worse recurrence-free survival (p < 0.001). This relationship remained significant (p < 0.001) even when the analysis was limited to the active cancer cohort (n = 31). CSDH associated with dural metastasis leads to early recurrence and death because of the difficulty in controlling subdural hematoma re-accumulation by common drainage procedures. Depending on the primary cancer status, withdrawal of active treatment and change to palliative care should be discussed after diagnosing CSDH associated with dural metastasis.     

Acute aortic syndromes: aortic dissections,penetrating aortic ulcers and intramural aortic hematomas

Acute aortic syndromes, including dissections, intramural hematomas and penetrating aortic ulcers, are a catastrophic clinical entity that are relatively uncommon. A high index of clinical suspicion along with proper imaging modalities are critical in making a prompt and accurate diagnosis for immediate management and to improve survival of the patient.     

Expression of the TGF-β–ALK-1 Pathway in Dura and the Outer Membrane of Chronic Subdural Hematomas

Neovascularization of the outer membrane plays a critical role in the development and enlargement of chronic subdural hematomas (CSHs) and vascular endothelial growth factor (VEGF) may promote their progression. However, the precise mechanisms remain to be determined. We focused on the signaling pathway upstream of VEGF, transforming growth factor β (TGF-β), and activin receptor-like kinase 1 (ALK-1) to identify the mechanisms underlying the neovascularization of the outer membrane of CSH. Retrospective comparative study was conducted on 15 consecutive patients diagnosed as CSH with burr-hole drainage. Dura and the outer membrane were collected. We immunohistochemically examined the expression of VEGF, integrin-α, TGF-β, and ALK-1 on the outer membrane and dura of CSH and compared our findings with control samples and the signal intensity of hematomas on computed tomography (CT) scans. VEGF and integrin-α expression was markedly up-regulated in both the dura and outer membrane of CSH, the expression of TGF-β and ALK-1 in the dura was slightly increased in the dura and markedly up-regulated in the outer membrane. There was no significant correlation between their expression and CT density. Here we first report the expression of TGF-β and ALK-1 in the outer membrane and dura mater of CSH. We suggest that the TGF-β–ALK-1 pathway and VEGF affect neovascularization and the progression of CSH.