出血性脑梗死的临床分析

目的：研究出血性脑梗死的原因、影像学及临床特征。方法：分析116例出血性脑梗死的原因、影像学及临床特征（出自1990-2001年治疗的2050例脑梗死病例）。结果：2050例脑梗死中出血性脑梗死占5.66％，最常见的原因是脑梗死（62.06%），特别是心源性。最早出现的出血性脑梗死为脑梗死后17小时。78例为血肿型，38例非血肿型。结论：出血性脑梗死应严格控制血压、血糖。临床症状及体征不变或加重，特别是脑梗死或大面积脑梗死，应检查或复查CT和（或）MRI。发现出血性脑梗死，应立即停用抗凝、溶栓治疗。     

出血性脑梗死危险因素分析

通过对３１例经头颅ＣＴ扫描证实的出血性脑梗死患者的回顾性分析，以期获得对该病较全面的认识，从而有利于预防和早期诊断与治疗。本组３１例出血性脑梗死中属皮质型９例，血肿型７例，梗死灶内渗血型１５例。     

缺血性和出血性脑梗死的螺旋CT鉴别诊断

目的分析螺旋CT对缺血性和出血性脑梗死的鉴别诊断作用。方法选取50例缺血性脑梗死患者(缺血性脑梗死组)和42例出血性脑梗死患者(出血性脑梗死组),2组均行螺旋CT扫描,并分析其CT图像的特征。结果缺血性脑梗死组病变部位额顶叶11例,颞顶叶18例,基底节8例,小脑7例,一侧大面积脑梗死6例;出血性脑梗死组患者中病变部位额顶叶8例,颞顶叶12例,基底节9例,小脑10例,一侧大面积脑梗死的有3例;缺血性脑梗死组CT征象为脑回征25例,浮云征20例,假肿瘤征5例;出血性脑梗死组CT表现为非血肿型24例,血肿型18例。结论螺旋CT能够清晰显示缺血性和出血性脑梗死特征,在其诊断和鉴别诊断中应用价值高。     

出血性脑梗死37例临床分析

目的提高对出血性脑梗死的发病规律、临床特点的认识和指导临床治疗。方法回顾分析37例出血性脑梗死病例,根据其临床表现、影像资料及预后进行分型。结果出血性脑梗死的临床表现取决于继发性出血的时间和出血量的多少,按发病时间及部位可分为早发型、迟发型及血肿型、不规则型。早发型及血肿型预后较差。结论出血性脑梗死分型不同,预后不同。治疗上应分型分治,个体化治疗。     

脑梗死后出血性转化患者血浆白细胞介素1β、6、10含量的变化

目的观察脑梗死后出血性转化患者血浆IL-1β、IL-6、IL-10的变化,探讨脑梗死出血性转化与脑梗死后炎性反应之间的关系。方法 60例脑梗死并发出血性转化患者按出血严重程度分为HI-1型15例,HI-2型15例,PT-1型15例,PT-2型15例。按年龄、性别、神经功能缺损评分(NIHSS)、出血部位、治疗措施相匹配的原则选取无出血性转化的脑梗死患者作为对照组。分别为:HI-1型对照组15例,HI-2型对照组15例,PT-1型对照组15例,PT-2型对照组15例。测定所有患者入院2 d清晨血浆IL-1β、IL-6、IL-10、S-100β蛋白浓度。结果和相对应的对照组相比出血性转化患者发病初期IL-1β、IL-6浓度显著高于对照组,而IL-10、S-100β蛋白的浓度无明显差别。结论在同样程度脑损伤的情况下,急性期的高水平的促炎性细胞因子IL-1β、IL-6可能是通过炎性反应促进了血脑屏障的破坏和脑梗死后出血性转化的发生。     

出血性脑梗死CT与临床分析

目的 探讨出血性脑梗死的病因、CT和临床表现。方法 回顾我院收治的35例HI的临床资料，分析其病因、CT及临床表现的改变。结果 出血性脑梗死最常见病因为心源性脑栓塞．以梗死后第2周发病率最高．血肿型症状重，有占位效应；非血肿型症状轻，但恢复慢。结论 对初诊为脑梗死的患者临床症状继续加重或出现新的症状体征以及按脑梗死治疗效果不明显时。应及时行头颅CT扫描，以相应调整治疗方案。     

出血性脑梗死58例临床分析

目的 探讨出血性脑梗死的病因、发病机制及影像学特点.方法 对58例经颅脑CT/MRI证实的出血性脑梗死患者的临床和影像资料进行分析.结果 出血性脑梗死发生率为7.05%,好发于心房纤颤、大面积梗死、溶栓、降纤、抗凝患者;影像学上表现为非血肿型占86.21%,血肿型占13.79%.结论 脑栓塞、大面积脑梗死、溶栓、降纤、...     

出血性脑梗死38例临床分析

出血性脑梗死是脑梗死病人因梗死区内血液再灌注引起的继发性出血。自CT和MBI问世以来，临床诊断也日渐增多。尤其是近年来溶栓和抗凝药的普遍使用，出血性梗死引起了广泛关注。我院1998～2002年共收治脑梗死857例，其中出血性梗死38例，现对其有关问题进行探讨。     

出血性脑梗死36例临床分析

目的：探讨出血性脑梗死患者的临床特点，发病机制及预防策略。方法：回顾性分析36例出血性脑梗死患者的临床资料，结果：大面积梗死患16例，原梗死灶出血20例，梗死后第2周发生出血8例，第一周内发生出血19例，出血性脑梗死中分水岭梗死不少见，并发高血糖者是发生出血性梗死后的一个重要危险因素。出血性脑梗死病例头痛发生率高。注意临床观察，及时复查CT，以利诊断。结论：需溶栓的病例，可先行SPEGT检查进行筛选。再定治疗方案。     

出血性脑梗死42例随访观察

目的探讨出血性脑梗死(HI)的病因、临床特点及其预后。方法回顾性分析42例出血性脑梗死及12例大面积脑梗死未出血患者的临床资料并进行2年随访。结果HI的主要病因为脑栓塞，占71．4％，并以心源性栓塞为主.HI常发生于脑梗死后2周内。发生出血性梗死后原有症状加重，危险性增加，但长期预后较非出血性大面积脑梗死的好转率高。结论HI是影响患者生存的严重并发症，及时诊治可改善预后。     

磁敏感加权成像在出血性脑梗死诊断中的初步应用

目的 探讨磁敏感加权成像(SWI)诊断出血性脑梗死的临床价值.方法 20例亚急性期出血性脑梗死患者分别行常规MRI、扩散加权成像(DWI)和SWI检查,根据图像分析结果比较不同扫描序列所显示的梗死灶内出血灶数目及其阳性检出率;测量SWI序列出血最大层面出血灶面积和T2WI序列梗死灶最大层面的梗死灶面积,并行相关分析;观...     

磁敏感加权成像在出血性脑梗死诊断中的初步应用

目的探讨磁敏感加权成像（SWI）诊断出血性脑梗死的临床价值。方法20例亚急性期出血性脑梗死患者分别行常规MRI、扩散加权成像（DWI）和SWI检查,根据图像分析结果比较不同扫描序列所显示的梗死灶内出血灶数目及其阳性检出率;测量SWI序列出血最大层面出血灶面积和T2WI序列梗死灶最大层面的梗死灶面积,并行相关分析;观察SWI序列对梗死灶内静脉血管的显示程度,以及梗死灶以外区域微出血灶的诊断敏感性。结果20例患者SWI序列均显示梗死灶内出血,两名医师共诊断43个出血灶,其中SWI序列显示42个、T1WI序列25个、DWI序列15个、T2WI序列12个;SWI序列阳性检出率与T1WI、T2WI、DWI序列相比,差异具有统计学意义（X^2=51．516,P=0．000）。T2WI序列梗死灶最大层面的梗死灶面积为（18．08±12．47）cm^2,SWI为（5．02±6．27）cm^2,梗死灶面积与出血灶范围之间呈明显正相关（r=0．562,P=0．010）。其中,13例患者SWI序列检出梗死灶以外区域的微出血灶;12例显示梗死灶内小静脉血管分支减少和（或）变细,6例血管增多、增粗和（或）扭曲。结论SWI序列对出血性脑梗死病灶内出血的显示优于常规MRI和DWI序列,并能显示梗死灶内静脉血管的变化及梗死灶以外区域的微出血灶,可作为诊断出血性脑梗死的MRI常规扫描序列。     

大脑中动脉高密度征与大面积脑梗死预后的相关性研究

目的探讨大脑中动脉高密度征(HMCAS)与大面积脑梗死预后的关系。方法回顾性分析我院139例大面积脑梗死患者的影像学及临床资料。结果根据OCSP分型:98例(98/139)完全前循环梗死(TACI),41例(41/139)部分前循环梗死(PACI)。据首次CT检查中是否出现HMCAS分两组,HMCAS组58例(58/139);非HMCAS组81例(81/139);所有患者因不符合溶栓指征未行溶栓治疗,其中34例(34/139)患者发生梗死后出血。HMCAS组伴出血者21例(21/58),死亡者11例(11/58),非HMCAS组伴出血者13例(13/81),死亡者5例(5/81)。HMCAS组的出血率、死亡率明显高于非HMCAS组。差异具有统计学意义(χ2出血率=7.43,χ2死亡率=5.43,P0.05)。大面积脑梗死患者出现HMCAS,其伴梗死后出血的发生率和死亡率均高于无HMCAS患者。结论 HMCAS出现可以作为脑梗死预测梗死后出血的指标之一,并可提示大面积脑梗死预后不佳。     

真性红细胞增多症并发脑卒中27例临床分析

目的 探讨真性红细胞增多症(PV)并发脑卒中的临床特点及治疗方法.方法 对27例PV并发脑卒中患者的临床资料进行回顾性分析.结果 (1)本组PV并发脑梗死22例(81.5%),其中多发性脑梗死18例(66.7%);短暂性脑缺血发作2例(7.4%);脑出血2例(7.4%);蛛网膜下腔出血(SAH)1例(3.7%).均符合PV的临床表现和体征及血象、骨髓象的改变.(2)影像学检查显示脑梗死以多发小梗死灶多见(66.7%),常见于脑叶、基底节、内囊;脑出血的出血灶内密度不均匀,周边水肿明显.(3)本组采用静脉放血加小剂量化疗治疗,脑卒中痊愈8例,显著进步18例,无效1例.结论 PV并发脑卒中以脑梗死多见,其中又以多发性梗死为主,并发脑出血和SAH较少,采用静脉放血加小剂量化疗治疗的效果较好.     

列线图风险预测模型评估未溶栓治疗的出血转化和脑梗死再发风险

目的 建立列线图风险预测模型评估未溶栓治疗的出血转化和脑梗死再发风险.方法 回顾性分析未给予溶栓治疗的脑梗死病人118例,单因素回归分析得到发生出血转化(HT)的危险因素,多因素回归Logistic分析出独立危险因素,同时利用R软件构建未溶栓治疗的出血转化和脑梗死再发风险的列线图预测模型.结果 年龄(OR=4.084,...     

Hemorrhagic transformation in cerebral embolism

We studied the mechanism of hemorrhagic infarction after acute cerebral embolism in 160 patients by brain computed tomography and angiography. Hemorrhagic infarction during the month after the embolic event was evident in 65 patients (40.6%). Initial angiography a median of 1.5 (range 1-60) days after the event revealed occlusion of the cerebral arteries in 117 of 142 patients (82.4%), and reopening of the vessels was observed in 56 (94.9%) of 59 patients who had follow-up angiography a median of 20 (range 3-47) days after the event. The incidence of hemorrhagic infarction was higher in patients greater than or equal to 70 years old (31 of 61, 50.8%) than in those aged 50-69 years (27 of 72, 37.5%) or less than 50 years (seven of 27, 25.9%) (greater than or equal to 70 vs. less than 50, p less than 0.05). In patients with moderate or large infarcts, hemorrhagic infarction developed in 50.0% or 51.5%, respectively, while in those with small infarcts it developed in only 2.9% (p less than 0.05). No correlation was found between hemorrhagic infarction and history of hypertension or blood pressure during the acute stage of stroke. Thrombolytic and/or anticoagulant therapy did not affect the incidence of hemorrhagic infarction (40.0% with vs. 40.7% without therapy) but tended to cause massive hematoma. Our results indicate that hemorrhagic transformation in cerebral embolism is caused not only by reopening of the occluded vessels but also by other factors such as age and size of the infarct. Hypertension per se seems to be less important for hemorrhagic infarction.(ABSTRACT TRUNCATED AT 250 WORDS)     

Late-onset hemorrhagic infarction in patients with patent foramen ovale: reports of two cases]

We presented here two patients with hemorrhagic infarction occurred during subacute phase of brain embolism. The patients were 71-year-old and 73-year-old men who suffered from brain infarction of the left posterior cerebral artery and right middle cerebral artery territory, respectively. Both of them were diagnosed as having cryptogenic stroke and patent foramen ovale. After transferred to rehabilitation hospitals taking aspirin for a secondary prevention of stroke, they developed hemorrhagic infarction at day 17 and day 19, respectively. Their blood pressure remained within normal range throughout acute and subacute phase. Although most of hemorrhagic infarction occurs within 24 hours of stroke onset, some patients develop symptomatic hemorrhagic infarction even after 10 days. We need to be careful about late-onset hemorrhagic infarction, because many patients are now transferred early to rehabilitation hospitals to facilitate dedicated systematic rehabilitation.     

磁敏感加权成像对大面积脑梗死后出血转化早期诊断临床价值的预探索研究

目的 探讨磁共振成像（magnetic resonance imaging,MRI）磁敏感加权成像（susceptibility-weightedimaging, SWI）技术在早期诊断大面积脑梗死后出血转化（hemorrhagic transformation,HT）中的价值。 方法 纳入39例经磁共振确诊的大面积脑梗死患者为研究对象,在发病72 h内行头颅计算机断层扫 描（computed tomography,CT）和SWI检查,比较两种检查方法对脑梗死后HT的检出率及敏感性。参考 欧洲协作性急性卒中研究（European Cooperative Acute Stroke Study,ECASS）分型标准对脑梗死后HT 患者的HT进行分级,比较HT分级在两种检查方法中的差异,分析脑梗死后HT分级与美国国立卫生研 究院卒中量表（National Institutes of Health Stroke Scale,NIHSS）评分的相关性。 结果 SWI、CT两种方法诊断脑梗死HT的阳性率分别为61.54％和12.82％（P <0.001）;SWI检出发生 脑梗死后HT者24例,其中1级占12.82%;2级占25.64%;3级占15.48%;4级占7.69%;经Spearman相关性 分析,SWI序列的HT分级与临床NIHSS评分的增长呈正相关（R =0.94,P <0.01）。 结论 SWI技术可以早期、敏感评价大面积脑梗死后HT。     

CT-detected hemorrhagic infarction; relation with the size of the infarct, and the presence of midline shift

The incidence of mass effect indicated by midline shift, and the incidence of hemorrhagic infarction were studied in 952 consecutive CT scans with supratentorial infarcts. Hemorrhagic infarction was found in 5.1% indicating that the incidence of hemorrhagic infarction during life is far less than was suggested from pathological studies. Midline shift was found in 3.6% and, accordingly, the chance of finding a hemorrhagic infarct with mass effect indicated by a shift of the midline would be 0.2% if these 2 phenomena were not related. However, this incidence appeared to be 12 times higher, indicating they are closely related. In addition, the incidence of hemorrhagic infarcts and midline shift were both related to large infarcts with bad outcome. Cardiac emboli were not more prevalent in patients with hemorrhagic infarcts than in a control series, indicating that cardiac emboli do not produce hemorrhagic infarction more often than other causes of cerebral infarction, and that cardiac embolic cause cannot be inferred from hemorrhagic infarction on CT. This probably also applies to carotid emboli. When anticoagulation is considered in patients with cerebral infarction, CT-confirmed hemorrhagic infarction and shift of midline structures as well as decreased consciousness are contraindications to such treatment. In their absence, and in the absence of general contraindications, anticoagulant treatment can safely be started.     

出血性脑梗死的相关危险因素分析

目的探讨出血性脑梗死的相关危险因素。方法回顾性分析本院2007-09~2010-08收住的685例脑梗死患者的临床资料。结果出血性脑梗死组患者在大面积梗死、房颤、高血压、高血糖等方面的发生率均高于同期非出血性脑梗死组。结论大面积梗死、房颤、高血压、高血糖等是出血性脑梗死的相关危险因素。