重症脑出血微创术后下呼吸道感染病原学分析

目的:重症脑出血微创术后气管切开病人痰培养病原菌分布与耐药情况分析,其院内感染发生的原因、探讨防治对策。方法:应用痰培养检出的病原菌及耐药性分析。结果:重症脑出血微创术后气管切开病人下呼吸道感染41例,其中G-杆菌26例占63.4%,G 球菌15例占36.6%,其中金葡菌11例,药敏仍以敏感菌株为主,但耐药菌株有增多趋势。结论:重症脑出血微创术后气管切开病人下呼吸道感染以G-杆菌为主,G 球菌以金葡菌为主,仍以敏感菌珠为主,耐药有增多趋势。万古霉素对G 球菌,氨曲南对G-杆菌敏感性较敏感,故在培养结果未出来之前经验用药是非常重要的。     

利多卡因治疗外伤性蛛网膜下腔出血疗效分析

目的探讨早期静脉注射利多卡因对外伤性蛛网膜下腔出血（tsAH）继发性脑损伤的治疗作用。方法重度颅脑损伤后SAH患者60例（GCS评分≤8分）。随机分为治疗组（早期静脉注射利多卡因组）和对照组。在治疗前后对患者均进行GCS评分、颅内压（ICP）测定以及头部CT、发射计算机体层摄影（ECT）、经颅多普勒（TCD）检查。结果利多卡因治疗7d后即出现颅内压降低、挫伤脑组织血流供应改善、脑水肿减轻，与对照组比较，有明显差异（P〈0．01）；GCS评分在利多卡因治疗7d、14d后较对照组明显增加（P〈0．01）。结论早期静脉注射利多卡因能明显减轻颅脑损伤后SAH继发性脑组织损伤的程度，有利于神经功能的早期恢复。     

Treatment Outcomes in Spontaneous Intracranial Hypotension: Do Epidural Blood Patches Stop the Leaks?

Abstract:   Spontaneous intracranial hypotension (SIH) is a postural headache syndrome unrelated to dural puncture. Because of the increasing failure of epidural blood patch (EBP) to relieve headache in SIH, we retrospectively investigated the epidemiological features and treatment outcomes in 55 cases of SIH. The study population was stratified by age and sex; continuous variables were compared for differences by t -tests; categorical variables were compared by Chi-squared analysis or Fisher exact tests. Significant differences were identified by P values of 0.05 or less. The mean age of the study population was 44 ± 12 years with a female to male ratio of 1.3:1.0. Men presented with subdural hematomas ( P  = 0.001) more often than women. Meningeal enhancement on contrast magnetic resonance imaging (MRI) was the most consistent radiographic finding. Radionuclide cisternography (RC) demonstrated thoracolumbar dural leaks in 16 of 22 patients. EBP failures were more common in patients aged 40 and younger than in older patients ( P  = 0.003). Postural headache from SIH was not uniformly responsive to EBP, and had significant comorbidities, especially in men. The management of postural headache in SIH by other techniques to restore brain position and cerebrospinal fluid dynamics should be investigated.     

磁场治疗白兔脑出血的安全性及疗效的实验研究

目的　探讨磁场治疗对实验性脑出血的治疗作用和安全性。方法　实验一 :5 0只大耳白兔被钩破大脑中动脉以建立脑出血模型。用CT扫描和解剖的方法观察脑出血的情况。实验二 :45只大耳白兔随机分为 0 .4T组、0 .8T组和对照组 ,每组 15只。每只白兔均采用实验一的方法建成脑出血模型。磁疗前CT扫描观察出血情况 ,磁疗后CT扫描观察血肿吸收情况。结果　实验一 :5 0只大耳白兔大脑中动脉钩破术后均出现对侧后下肢无力 ,肌张力降低 ,回缩反射减弱或消失。CT和解剖证实有脑出血。实验二 :45只大耳白兔均成功建成脑出血模型。磁疗前CT扫描 3组之间脑出血差异无显著性意义 (P >0 .0 5 ) ;磁疗后CT扫描 2磁疗组之间血肿吸收差异无显著性意义 (P >0 .0 5 ) ,与对照组比较血肿吸收差异有显著性意义 (P <0 .0 1)。结论　用钩破兔大脑中动脉的方法可建立脑出血动物模型。磁场治疗可促进实验性白兔脑出血的血肿吸收 ,且不产生继发性脑出血     

青光眼术后早期眼内出血的原因分析

目的分析青光眼术后早期眼内出血的原因，以预防眼内出血的发生。方法对261例（共493只眼）手术治疗的青光眼病人进行回顾性分析。结果术后早期发生眼内出血者17例，共17眼（前房出血6例，眼底出血11例），年龄均在68岁以上。其中闭角型青光眼术前持续性高眼压14眼，新生血管性青光眼3眼；伴糖尿病者6例，伴高血压者5例。结论青光眼术后早期发生眼内出血的主要原因是术前顽固性高眼压。其次与高龄和是否伴有糖尿病、高血压有一定关系。     

TCD观察动脉瘤性SAH后脑血管痉挛的血流动力学改变

目的探讨动脉瘤性蛛网膜下腔出血(SAH)后脑血管痉挛的血流动力学改变。方法经CT、DSA证实为动脉瘤性SAH患者179例,床旁经颅超声多谱勒(TCD)在术前、术后1~3d、5~7d、9~11d、12~14d记录并分析大脑中动脉(M CA)的血流参数及频谱改变。结果M CA平均血流速度(Vm)于SAH后1~3d开始升高,5~7d、9~11d达到高峰;L I(血管痉挛指数)为3~6时预后良好;>6时可以出现神经系统功能损害,颅内压增高且有脑血管痉挛(CV S)者预后较差。结论TCD能无创、实时评价SAH后CV S的动态变化,可以推断SAH后CV S的严重程度及临床转归。     

Non-HIV-Related Progressive Multifocal Leukoencephalopathy (PML): A Tertiary Cancer Center Experience

In the course of 1 year at a tertiary cancer center, 3 patients (2 men; 1 woman; age 51-75 years) were seen in neurological consultation (1.5% of all consultations). Clinical course in all patients was of a progressive neurologic disorder not consistent with either a primary or secondary malignancy. Magnetic resonance (MR) imaging was most informative with respect to diagnosis and subsequent management. Brain biopsy was performed in all patients to assist in both diagnosis and prognostication. All patients were determined to have progressive multifocal leukoencephalopathy (PML) by brain biopsy.     

Foley尿管气囊压迫治疗骶前静脉丛大出血的评价(附6例报告)

目的:评价直肠癌根治术中用Foley尿管气囊压迫治疗骶前静脉丛大出血(MPVP)的临床价值。方法:分析1995~2005年用Foley尿管气囊压迫治疗骶前静脉丛大出血6例的临床资料。结果:6例骶前大出血中全部用Foley尿管气囊压迫控制出血,术中出血量为800~1700mL,Foley尿管于术后4d拔除3例,5d1例,6d2例,均无再出血,会阴切口均一期愈合。结论:Foley尿管气囊压迫治疗骶前静脉丛大出血是一种简单安全有效的治疗方法。     

血红素氧合酶-1与脑出血的继发性损害

自发性脑出血是指非外伤性脑实质出血,发病率高,死亡率高[1],且脑出血后患者多遗留不同程度的神经功能障碍。因此,探讨脑出血后脑组织损伤的病理生理机制对于改善脑出血病情及预后是十分必要的。大量研究表明自发性脑出血后造成的脑损伤存在多种机制[2]:早期血肿机械占位效应、