64层螺旋CT静脉成像在肝硬化门脉高压症早期诊断中的价值

目的 探讨64层螺旋CT在肝硬化门脉高压的早期诊断.方法 研究经病理和/或临床诊断的42例肝硬化早期、中晚期病人64层螺旋CT门静脉及肝静脉血管成像表现,测量42例患者及15例健康者门静脉和肝右静脉管径并分析64层螺旋CT门脉血管成像法在肝硬化门脉高压症的早期诊断价值.结果 所有病人的观察血管在显示较佳的基础上,测得门静脉宽度(PV)在正常对照组(＜12 mm)与其他2组比较有显著性差异,肝硬化代偿组与失代偿组之间差异无明显统计学意义;肝右静脉宽度(RHV)在代偿期内径明显增宽,＞10 mm,而失代偿期肝静脉明显变窄,血管强化密度减低;PV/RHV比值在失代偿期约1.77±0.06,正常对照组及肝硬化代偿组PV/RHV均＜1.5.利用后处理软件最大密度投影(MIP)观察门静脉及肝右静脉血管,代偿组可显示3级以上的门静脉及肝右静脉,失代偿组肝右静脉显示欠佳,最多显示1级,门静脉属支走行扭曲且最多显示3级.结论 64层螺旋CT肝、门静脉血管成像对临床肝硬化门脉高压的早期诊断有重要临床意义.     

MSCT静脉成像应用于肝硬化门脉高压症的诊断效果分析

目的研究多层螺旋CT静脉成像(MSCTP)在肝硬化后门静脉高压症中的临床诊断价值。方法随机抽取2013年1月~2015年10月期间,我院接受MSCTP检查的患者45例作为研究对象,其中,32例肝静脉门静脉高压为门静脉高压症组,13例正常者为对照组。观察并比较两组的肝脏右静脉以及门静脉分支情况。结果两组血管显示都比较清晰。门静脉高压症组的PV以及RHV宽度,均显著低于对照组(P0.05)。RHV宽度内径于代偿期中有显著增宽的趋势,但在失代偿期中则有显著变窄的趋势。肝硬化门脉高压症者失代偿期中的PV/RHV值为(1.78±0.12),明显高于代偿期组以及对照组。组间差异显著,具有统计学意义(P0.05)。结论 MSCTP能够清晰地显示PV及RHV分支,准确观察和测量其管径,对肝硬化门静脉高压症的临床诊断具有重要指导价值。     

慢性重型肝炎门静脉系统血流动力学变化的研究

目的探讨慢性重型病毒性肝炎门静脉系统血流动力学变化.材料和方法应用多普勒超声检测30例慢性重型肝炎患者门静脉系统血流动力学变化,并与正常组(51例)、慢性肝炎组(61例)、代偿期肝硬化组(46例)、失代偿期肝硬化组(36例)进行对照研究.结果慢性重型肝炎门静脉直径稍宽于正常组,而明显低于失代偿期肝硬化,与慢性肝炎组及代偿期肝硬化无差异;门静脉血流速度、血流量显著低于对照各组;脾脏长径、脾静脉直径较正常组和慢性肝炎组增大、增宽,但明显小于失代偿期肝硬化,与代偿期肝硬化无差异;脾静脉血流量与各组比较均没有明显增加;脐静脉重开率显著高于慢性肝炎组及代偿期肝硬化组,与失代偿期肝硬化组无差异.结论慢性重型肝炎容易形成门静脉高压,门静脉血流灌注量明显减少,造成肝脏微循环障碍.     

多层螺旋CT肝脏灌注测量在肝硬化中的初步应用

目的探讨多层螺旋CT肝脏灌注测量在肝硬化中的应用价值。资料与方法37例接受多层螺旋CT肝脏灌注测量。20例无明显肝脏疾患的志愿者(正常组),17例肝硬化患者(肝硬化组),再按其肝硬化程度分为两组:9例为轻中度肝硬化(轻中度肝硬化组),8例为重度失代偿肝硬化(重度失代偿组)。计算各例的各项灌流指标并进行组间比较。结果(1)肝硬化组与正常组相比,门静脉灌流量(HPP)、门静脉灌流指数(PPI)明显减低[HPP:(0.49±0.19)ml·min-1·ml-1与(0.60±0.16)ml·min-1·ml-1,P=0.045;PPI:0.58±0.14与0.67±0.06,P=0.015],门静脉与肝动脉灌流比率(HPP/HAP)亦明显减低(1.63±0.87与2.12±0.65,P=0.04),肝动脉灌注指数(HPI)升高(0.42±0.14与0.33±0.06,P=0.015),提示肝硬化时HPP减少,门静脉血流在肝脏血供中的比例减少,而动脉的灌流比重增加;(2)重度失代偿组肝硬化HAP较轻中度组明显升高[分别为(0.48±0.16)ml·min-1·ml-1与(0.25±0.07)ml·min-1·ml-1,P=0.002],HPI亦明显升高(分别为0.54±0.10与0.32±0.07,P=0.0001),PPI则明显降低(分别为0.46±0.10与0.68±0.07,P=0.0001),提示不同程度肝硬化其灌注指标存在差异,灌注改变与肝硬化程度有关。结论肝脏CT灌注测量可以反映肝硬化的血流灌注改变,灌注值的变化也能够提示肝硬化的程度。     

失代偿期肝硬化肝内阳性结石CT分析

目的:分析失代偿期肝硬化肝内阳性结石发病情况。方法:随机选择正常肝脏、代偿期和失代偿期肝硬化各100例。结果:失代偿期肝硬化肝内阳性结石发病情况有:1发病率明显高于代偿期肝硬化,更高于正常人;2肝内结石的出现和增多与肝硬化肝形改变及肝功能损害程度有一定联系,但不成比例;3病程越长,发病率越高,胆石数目越多;4胆系感染机会越多,发病率越高;5弥漫性肝内胆管微小结石是弥漫型结节性失代偿期肝硬化的一个特殊表现。结论:组织、感染、代谢及体液等成石因素在失代偿期肝硬化形成恶性循环,其阳性结石发病率与代偿期显著差异(P<0.01)     

门静脉高压CT征象与肝纤维化、肝硬化病理分期关系的探讨

目的 探讨肝纤维化、肝硬化门静脉高压的CT征象与病理分期的关系.方法 对经肝穿刺病理活检确诊的肝纤维化S1期12例、S2期14例、S3期9例、S4期13例、典型肝硬化16例以及20例对照组行16层螺旋CT上腹部3期增强容积扫描,于门静脉期最大密度投影(MIP)图像上分别测量门静脉左支、门静脉右支、门静脉主干(MPV)、脾静脉(SV)和肠系膜上静脉(SMV)的管径,并观察各组门静脉侧支循环开放情况及有无腹水和脾脏肿大,将上述指标与病理分期作对照研究.门静脉系统各血管管径的比较采用单因素方差分析,组间两两比较用SNK法;多组腹水及侧支循环发生率的比较采用R×C表x2检验,组间行x2分割计算;运用Logistic回归分析探讨门静脉系统中对肝纤维化病理分期影响最大的血管.结果 对照组门静脉左支、门静脉右支、MPV、SV和SMV的管径分别为(0.98 ±0.11)、(1.00±0.12)、(1.33±0.11)、(0.75±0.10)和(1.07±0.12)cm,脾脏体积为(128.55±30.56)cm<'3>,无侧支循环开放和腹水.S1、S2、S3期组、S4期组或早期肝硬化组、典型肝硬化组SV管径逐渐增大,分别为(0.86±0.12)、(0.96±0.11)、(1.07±0.08)、(1.09±0.10)和(1.18±0.19)cm,各组与对照组间比较,差异均有统计学意义(P<0.05),重度肝纤维化(S3期组和S4期组)、典型肝硬化以及轻度肝纤维化(S1期组和S2期组)间差异均有统计学意义(P<0.05).Logistic回归分析显示,在门静脉各血管测量指标中,SV的标准化回归系数最大(2.719),且差异有统计学意义(P<0.01).典型肝硬化的侧支循环开放及腹水发生率明显高于正常肝脏和肝纤维化各期,S4期的侧支循环出现率明显高于对照组、S1期组及S2期组.结论 当慢性肝病发展至重度肝纤维化或早期肝硬化时,CT检查有助于早期诊断.     

肝性脑病的早期观察护理及预防

目的总结肝硬化失代偿期并发肝性脑病的护理措施,以提高临床护理水平。方法对肝硬化失代偿期患者密切观察病情变化,并发肝性脑病患者早期观察,早期诊断,及时有效的护理干预。结果37例患者及时发现肝性脑病的先兆,去除诱因,及早控制肝昏迷的发展,预后较好。结论肝硬化失代偿期并发肝性脑病患者早期的观察及护理干预。对及时治疗与控制疾病的发展具有积极作用。     

代偿期肝硬化MRI常规序列形态学分析和信号测量研究

目的 :探讨MRI常规序列形态学分析和信号测量对代偿期肝硬化的诊断价值。方法 :回顾性分析184例代偿期肝硬化患者(实验组)的上腹部MRI常规T1WI、FS-T1WI、T2WI和FS-T2WI图像,测量其信号强度,并与125例正常人(对照组)进行比较。结果:代偿期肝硬化T1WI及FS-T1WI示肝实质有稍高或高信号小或细小结节139例(75.54%);T2WI、FS-T2WI示肝实质有低信号小或细小结节78例(42.39%);肝脏表面不光滑,呈大小不等结节状或波浪状改变105例(57.07%);肝裂增宽58例(31.52%);肝叶比例失调86例(46.74%);肝脏缩小43例(23.37%);脾大156例(84.78%);门静脉高压征象15例(8.15%),包括门静脉、脾静脉增粗以及食管下段、胃底等静脉曲张。肝脏信号强度T1WI及FS-T1WI实验组显著低于对照组(P<0.05),T2WI及FS-T2WI显著高于对照组(P<0.05)。结论 :MRI常规序列形态学分析对代偿期肝硬化的诊断敏感且操作简便;肝脏信号强度在某种程度上可反映代偿期肝硬化肝脏的病理变化。     

16层螺旋CT评价肝硬化患者血流灌注参数变化

目的:探讨MSCT灌注成像技术在评估肝硬化血流动力学变化中的应用价值。材料和方法:对68例患者行肝灌注扫描,其中对照组29例,代偿期肝硬化22例,失代偿期肝硬化17例。通过扫描软件得出肝血流量(BF)、血容量(BV)、对比剂平均通过时间(MTT)、渗透表面积乘积(PS)、肝动脉灌注指数(HAF)。分析这些参数在肝硬化患者中的变化规律及临床意义。结果:对照组、代偿期肝硬化组和失代偿期肝硬化组的PS、HAF的均值是逐渐增加的。对照组、代偿期肝硬化组和失代偿期肝硬化组的BV、MTT均值是逐渐减小的。对照组、代偿期肝硬化组和失代偿期肝硬化组间的BF均值有显著性差异。结论:MSCT灌注成像技术可用来评价肝硬化血流动力学变化及其程度。     

多b值弥散加权成像对乙肝肝硬化分级的诊断价值探讨

目的探讨乙肝肝硬化患者不同肝叶磁共振弥散加权成像不同b值对肝硬化Child-Pugh分级的诊断价值。方法收集72例乙肝肝硬化患者和23例健康志愿者,其中肝硬化患者按Child-Pugh评分系统分为A、B、C三组分别为22例、26例和24例,均行肝脏MR-DWI扫描,设定不同的弥散敏感系数(b值)分别为0s/mm2、400s/mm2、600s/mm2、800s/mm2,测定每个受试者不同b值下肝脏各叶的ADC值。分别统计各b值肝左外叶、肝左内叶、肝右叶和肝尾状叶的ADC值,分析不同肝叶ADC值与Child-Pugh分级的相关性,使用ROC曲线评估肝叶ADC值对肝硬化分级的诊断效能。结果在不同b值下,肝硬化组肝脏ADC值均低于正常对照组,且各肝叶ADC值与肝硬化Child-Pugh分级均呈负相关(P0.05)。结论 DWI可以对乙肝肝硬化进行定量检查,有助于临床早期无创伤性评估肝硬化分级。     

经皮门静脉栓塞治疗肝癌的临床应用

目的探讨经皮选择性门静脉右支栓塞(PVE)在肝癌治疗中的应用价值。方法12例无手术切除指征的中晚期肝癌患者,在电视透视引导下经导管行经皮穿肝或穿脾行PVE。栓塞前、后用CT测量左侧肝叶的体积,并测量栓塞前后的门静脉压力、肝功能。结果12例患者均成功行经皮PVE,栓塞术后左肝叶代偿增生明显,其中3例PVE后顺利实行右肝切除术。PVE后未出现门静脉高压,肝功能损害轻,均未发现并发症。结论经皮选择性PVE能诱导非栓塞侧肝叶代偿性增生及栓塞侧肝叶萎缩,增加肿瘤手术切除机会,提高手术切除的安全性,对于无法手术切除的肝癌患者重新获得手术切除的机会,具有潜在的临床应用价值。     

能谱CT成像对肝硬化不同肝叶血流动力学的对比研究

目的 探讨能谱CT成像基物质分离技术在肝硬化患者不同肝叶血流动力学改变中的临床应用.方法 收集本院30例临床确诊为肝硬化的患者,行上腹部能谱CT增强扫描,扫描后重建单能量图像及基物质分离图像,在碘-水配对基物质图像上分别测量动脉期(AP)、门静脉期(VP)肝脏5叶(尾状叶、左外叶、左内叶、右前叶、右后叶)碘浓度(IC)及同层面腹主动脉碘浓度(ICaorta),分别计算出肝脏各叶动脉期碘分数(AIF)、门静脉期碘含量(PVIC)、动脉期及门静脉期标准化碘浓度(NIC),比较不同肝叶动脉期及门静脉期碘浓度(ICAP,ICVP)、AIF、PVIC、动脉期及门静脉期标准化碘浓度(NICAP,NICVP)等参数的差异.采用单因素方差分析对数据进行统计处理.结果 肝硬化患者尾状叶ICAP、ICVP,NICAP、NICVP,AIF均高于肝脏其余4叶,差异有统计学意义(P<0.05),但在肝脏其余4叶之间无明显统计学意义(P>0.05);PVIC在尾状叶稍低于其余4叶,但结果无统计学意义(P=0.929).结论 能谱CT基物质分离技术(碘基图)定量测量肝脏各叶IC可以评价肝硬化患者不同肝叶血流动力学的改变和差异,为临床提供更多的肝硬化血流改变信息.     

64层螺旋CT门静脉三维重组对门静脉高压侧支循环的研究及临床应用

目的：评价64层螺旋CT门静脉三维重组对门静脉高压侧支循环的诊断价值及临床应用。方法：正常者20例,肝硬化患者39例,行64层螺旋CT门静脉造影,容积数据采用最大密度投影（MIP）、容积再现法（VR）、表面遮盖法（SSD）、多平面重组（MPR）三维重组,观察门静脉高压肝内门静脉、属支及侧支循环的影像学特征。结果：64层螺旋CT门静脉三维重组能准确显示侧支循环分布范围、初步评估病变程度,门静脉高压症组门静脉属支管径显著大于正常组（P=0.000）,64层螺旋CT诊断食管胃底静脉曲张与胃镜诊断有高度一致性。结论：64层螺旋CT门静脉三维重组能够多角度、立体观察侧支循环情况,对预测其并发症、手术方案的制定具有重要的指导意义。     

Hepatic lobar atrophy following obstruction of the ipsilateral portal vein from hilar cholangiocarcinoma

Gross deformity of the liver associated with hilar carcinoma is rare. In 17 patients with hilar cholangiocarcinoma and intrahepatic bile duct dilatation, the relationships between lobar or segmental atrophy, compensatory hypertrophy, and patency of portal vein branches were evaluated with computed tomography (CT) and angiography. All six patients with obstructed or narrowed portal veins (group A) had lobar or segmental atrophy on CT scans and angiograms. Compensatory hypertrophy was observed in the unaffected lobe with a patent portal vein in five. In contrast, neither hepatic atrophy nor hypertrophy was demonstrated in the other 11 patients with patent portal veins. All group A patients had differences in hepatic attenuation on CT scans or dense opacification during the hepatogram phase of angiography. Biliary decompression was optimized when the bile duct selected for percutaneous drainage paralleled a patent portal vein. Knowledge of radiologic findings will assist in determining the primary site along the bile duct from which carcinoma has arisen.     

肝硬化Child-Pugh分级与LGV内径关系的MSCTA分析研究

目的探讨胃左静脉(LGV)和门静脉(PV)内径与肝硬化Child-Pugh分级间的关系。资料与方法应用16层螺旋CT对100例肝硬化患者和200名正常对照者行上腹部增强扫描,采用多平面重组(MPR)、最大密度投影(MIP)和容积重组(VR)对PV和LGV进行血管重建,测量LGV和PV主干的直径并进行统计学分析。结果总体肝硬化组LGV和PV管径与正常对照组比较明显增粗(P<0.05)。Child-A级和B级组PV最大内径较正常对照组和Child-C级组显著增粗(P<0.05)。Child-C级组和正常对照组、Child-A级和B级组PV最大内径比较差异无统计学意义(P>0.05)。正常对照组、肝硬化无腹腔积液组、肝硬化有腹腔积液组LGV内径逐渐增粗且差异具有统计学意义(P<0.05)。结论多层螺旋CT血管成像(MSCTA)可以清晰显示LGV和PV整体解剖结构,并能准确测量其内径,LGV和PV内径与肝硬化程度存在一定关系,但影响LGV和PV内径因素较多,不能单纯依靠管径大小评价肝硬化程度。     

Atrophy with compensatory hypertrophy of the liver in hepatic neoplasms: radiographic findings

Focal hepatic atrophy has numerous causes and in many cases is associated with compensatory hypertrophy. We have observed this phenomenon on CT in patients with hepatic neoplasms. Of 12 patients studied, eight had hepatic metastases, two had hepatocellular carcinoma, and two had bile-duct carcinoma. Focal changes in liver morphology (i.e., atrophy with compensatory hypertrophy) were found in five patients at presentation and developed after treatment with systemic or intraarterial chemotherapy in the others. Atrophic changes affected the right lobe in eight patients, the left lobe in three, and part of both lobes in one. Compensatory hypertrophy of part or all of the unaffected liver was found. Ten patients had obstruction of the portal vein branch to the atrophic segment, four of these 10 also had hepatic vein obstruction, and two of these 10 also had bile duct obstruction. Portal vein obstruction appears to be the most important element in the production of focal hepatic atrophy in patients with hepatic neoplasms. After treatment with chemotherapy, tumor regression and atrophy may be associated with compensatory hypertrophy and enlargement of the uninvolved part of the liver. This must not be mistaken for progression of disease.     

肝硬化门脉高压不常见门腔分流的MSCT表现

目的:探讨肝硬化门静脉高压不常见门腔分流的MSCT表现及诊断价值。方法:搜集256例肝炎后肝硬化并门静脉高压侧支血管形成患者的MSCT资料。受检者均行上腹部CT平扫及3期增强扫描,83例采用多平面重组(MPR)、曲面重组(CPR)、最大密度投影(MIP)、表面遮蔽显示(SSD)和容积再现(VR)等后处理方法进行血管成像。结果:本组共发现不常见门腔分流243处:食管旁静脉曲张61处(其中伴假肿瘤征16处)、胃肾静脉分流42处、脾肾静脉分流20处、椎旁静脉丛曲张21处、脐静脉和/或副脐静脉再通95处(其中脐静脉再通59处、副脐静脉再通30处、脐静脉和副脐静脉同时再通6处)、门静脉右后支瘤样扩张并向下腔静脉分流4处。门腔分流的主要CT表现为门静脉期可见门静脉属支与腔静脉系血管之间有异常交通。结论:MSCT可较好地显示肝硬化门静脉高压不常见门腔分流,对肝硬化门脉高压的临床诊断和治疗方案的确定有重要意义。     

Atrophy-hypertrophy complex in patients with cavernous transformation of the portal vein: CT evaluation

PURPOSE: To retrospectively evaluate the morphologic changes in the liver associated with cavernous transformation of the portal vein. MATERIALS AND METHODS: This study was institutional review board approved. Informed patient consent was not required. The computed tomographic (CT) results for 22 patients (14 male, eight female; mean age, 54 years) with cavernous transformation of the portal vein and no evidence of chronic liver disease at liver biopsy were retrospectively reviewed and compared with the CT results for 36 control subjects. Various morphologic changes in the hepatic lobes were qualitatively and quantitatively assessed by using the Student t test for unpaired data. RESULTS: Qualitative analysis revealed the atrophy-hypertrophy complex in most (n = 20, 91%) of the patients with cavernous transformation and in no control subjects. Atrophy of the left lateral segment and right liver lobe was seen in 16 (73%) and seven (32%) patients, respectively. Hypertrophy of the caudate lobe and liver segment IV was identified in 19 (86%) and 11 (50%) patients, respectively. All mean caudate lobe volume index values and mean caudate lobe-to-right lobe ratio values were significantly greater (P < .05) in the cavernous transformation group than in the control group. The mean segment IV diameter was significantly greater (41.6 vs 28.1 mm, P < .001) in the patients with cavernous transformation. Hepatic nodules and hepatic contour nodularity were not seen in the patients with cavernous transformation. CONCLUSION: The atrophy-hypertrophy complex is frequently observed in patients with cavernous transformation of the portal vein. Some findings, such as hypertrophy of the caudate lobe, mimic chronic liver disease or signs of portal hypertension, but left lateral segment atrophy and a normal or enlarged segment IV are distinctive findings of cavernous transformation.     

肝脏疾病的门静脉介入治疗

经门静脉系统的介入治疗在一些肝脏疾病的治疗中发挥重要作用,如肝细胞癌伴门静脉瘤栓、肝硬化门静脉高压症、门静脉血栓的介入治疗以及选择性门静脉栓塞诱导肝叶代偿性增生。本文主要介绍了这些介入疗法的途径、方法及疗效等情况。     

Post mortem CT demonstration of hemoperitoneum caused by rupture of a paraumbilical vein into a paraumbilical hernia in a man with liver cirrhosis and portal hypertension

In patients with liver cirrhosis and portal hypertension collateral circulation can develop to direct blood from portal to systemic veins allowing decompression of the portal system. A potential complication of portal hypertension is rupture of collateral vessels with subsequent fatal hemorrhage, occurring most commonly in the esophagus. The paraumbilical vein is a recognized collateral pathway in patients with portal hypertension however cases of rupture have been rarely documented. The authors report a case of hemoperitoneum caused by rupture of a paraumbilical vein into a paraumbilical hernia in a man with liver cirrhosis and portal hypertension. Post mortem CT imaging was valuable in localizing the source of hemorrhage in this case.