64层螺旋CT对门静脉海绵样变性的诊断价值

目的探讨64层螺旋CT在门静脉海绵样变性（CTPV）诊断中的价值。方法对CT检查发现的CTPV患者22例,采用MPR、MIP、VR等图像后处理技术显示异常的门静脉及侧支血管情况。结果 22例CTPV在CT平扫上显示门静脉结构不清,肝门区可见多发的结节状、条状软组织影。增强扫描显示6例动脉期肝实质灌注异常;门静脉期11例患者门静脉主干和（或）左右分支增粗,内可见充盈缺损,4例门静脉显示不清;2例门静脉主干和（或）左右分支在正常范围内;4例门静脉主干变细;1例门静脉主干受侵致管腔狭窄。胆管周围静脉丛（86.36%）、胆囊静脉（77.27%）及食管胃底静脉（77.27%）呈点状、细网状、簇状扩张。结论 64层螺旋CT能准确显示CTPV的部位、范围,立体地显示各曲张血管的走行及曲张程度,是检查CTPV的有效手段。     

门静脉海绵样变的MRI表现

<正>门静脉海绵样变性(cavernous transformation of portal vein,CTPV)是指由于不同病因导致门静脉主干和(或)分支完全或部分闭塞后,其周围形成海绵样扭曲的代偿静脉。CTPV构成的侧支静脉或旁路是机体保证肝脏血流量及肝脏营养的一种代偿改变,它是门静脉阻塞后病理改变的最终结果,在缓解门静脉高压过程中起重要作用。CTPV的诊断以往主要依靠彩色多普勒超声、数字减影血管造影     

肝包虫病合并门静脉海绵样变性的研究进展

肝包虫病灶压迫侵犯门静脉可引起门静脉海绵样变性(CTPV),其手术难度大,风险高,常规肝切除不能有效根治。简述了肝包虫病合并CTPV的病因、分型、临床表现、辅助检查,总结了其治疗策略。认为肝包虫病合并CTPV的治疗应在包虫病灶切除的基础上有效缓解门静脉高压,血管重建、离体肝切除和自体肝移植的应用在根治性切除方面发挥了重要作用。     

门静脉海绵样变性的临床诊疗进展

门静脉海绵样变性(cavernous transformation of portal vein,CTPV)是指门静脉主干或其分支受阻后,机体为维持肝脏血流灌注,在肝门区代偿性形成的大量海绵样侧支血管丛.该病较罕见,临床实践中缺乏对其病因及诊疗原则的认识.对于出现门静脉高压相关症状的患者需要采取积极治疗措施.治疗的主要目的是防治门静脉高压引起的上消化道出血和脾功能亢进,以及恢复肝脏门静脉血流灌注.需要在充分了解患者病情及每种治疗方式最佳适应症的基础上,采用个体化综合治疗策略.本文就CTPV的病因、诊断、分型、治疗方面的最新进展作一综述.     

原发性肝癌门脉癌栓螺旋CT双期扫描诊断价值

目的探讨原发性肝癌门静脉癌栓螺旋CT双期增强扫描诊断价值。方法对36例门静脉癌栓（TTPV）患者行螺旋CT双期增强扫描,观察门静脉癌栓在CT上的表现。结果36例TTPV患者在螺旋CT动态增强扫描时均显示出门静脉内癌栓及相关的阳性征象,表现为门静脉扩张、门静脉腔内充盈缺损及＂门静脉铸型＂,门静脉周围可见网状供血动脉。36例中,门静脉主干合并右支癌栓12例,门静脉主干合并左支癌栓8例,主干和左右支均有癌栓者9例,单纯右支癌栓4例,单纯左支癌栓3例。结论螺旋CT双期增强扫描是诊断门静脉癌栓的有效方法,可以完整地提供门静脉癌栓的全部资料。     

门静脉海绵样变的诊治进展

门静脉海绵样变(CTPV)是由于各种原因造成门静脉主干或分支、完全或部分阻塞,导致血管内血流受阻,门静脉压力增高,机体为缓解门静脉高压而形成大量的门静脉周围侧支血管而引起的疾病。因此,CTPV是一种代偿性病变,其代偿能力不够,无法阻止门静脉压力的上升,是导致肝前型门静脉高压的原因之一,约占门静脉高压症各病因的3.5%。因其在大体标本上表现为海绵样外观而被命名为CTPV。     

门静脉性胆道病的临床特征分析

目的 通过分析门静脉性胆道病（PB）患者的临床特征,旨在提高对PB的认识。方法 收集吉林大学第一医院近年来诊断为PB的22例患者的临床资料,并对患者的临床表现、肝功能、腹部彩色多普勒超声、腹部CT和肝胆核磁共振成像进行分析,描述胆道异常的影像学表现,侧支循环类型和血栓形成部位等特点。结果 本研究22例患者中,就诊的首发症状分别为：11例消化道出血,5例腹胀,3例腹痛,1例发热,1例腹部不适,1例牙龈出血。AST升高3例,ALT升高4例,GGT升高4例,ALP升高7例,CHE降低8例,Alb降低9例,Glo升高2例,TBil升高5例。20例患者有门静脉海绵样变性;2例存在门静脉系统血栓而无门静脉海绵样变性。22例患者均有胆管异常,其中2例仅为肝外胆管异常,12例仅为肝内胆管扩张,8例肝内外胆管均扩张。20例患者出现了不同部位的静脉曲张,其中19例主要表现为食管胃底静脉曲张,1例为胆囊周围静脉曲张,未见单纯肠系膜上静脉或脾静脉曲张。结论 PB无典型的临床症状及肝功能指标变化,但影像学均可见不同部位胆管扩张、狭窄或畸形,需扩大样本量对其诊断及治疗方式进行进一步探索。     

成人门静脉海绵样变性1例

门静脉海绵样变性（cavemous transformation of poemvein，cTPv）为肝前性门静脉高压症，主要表现为脾功能亢进症、食管、胃底静脉曲张及反复上消化道出血，临床上极为少见，易误诊为肝硬化。我院收治1例CTPV患者，现将临床资料分析报告如下。     

小儿门静脉海绵样变性临床特点

门静脉海绵样变性(cavernous transformation of the portal vein,CTPV)是指由各种原因引起的门静脉主干和(或)其分支阻塞,在其周围形成侧支静脉,是造成小儿肝前型门静脉高压的主要原因,约有10%的患儿死于反复上消化道大出血导致的休克.     

超声检查门静脉海绵样变特征表现

目的 探讨门静脉海绵样变(CTPV)及其相关并发症的超声表现特征,并分析了超声漏诊的原因。方法 2017年6月～2020年6月首都医科大学附属北京地坛医院诊治的101例CTPV患者,经CT和MRI增强扫描诊断,接受腹部超声检查。总结CTPV及其相关并发症超声图像表现特征,并分析超声漏诊的原因,提出解决策略。结果 在本组101例CTPV患者中,超声诊断82例(82.2%),漏诊19例(17.8%);在超声诊断病例中,82例(100.0%)患者门静脉主干及其分支周围出现广泛或局部蜂窝状粗细不等的血管结构,70例(85.4%)出现门静脉管壁增厚,76例(92.7%)在迂曲扩张的蜂窝状血管结构内部呈红蓝相间的丰富的血流信号,脉冲多普勒测得门静脉样低速血流频谱,10例(12.2%)门脉周围迂曲扩张蜂窝状血管压迫胆管,导致胆管扩张,8例(9.6%)出现胆囊增大,6例(7.4%)出现胆囊结石,5例(6.1%)出现胆管结石,5例(6.1%)出现门体分流。结论 超声是诊断CTPV的首选影像学方法,超声漏诊的原因主要为海绵样变血管腔细、病变范围小,腹部胀气,假性胆管肿瘤征,肋间隙或胸骨下角窄。利用腹腔积液和胆囊等声窗扫查肝脏,采用超声造影技术或结合其他影像学技术检查可减少漏诊。     

螺旋CT门静脉造影对门脉高压侧支循环的研究

目的探讨多排螺旋CT门静脉造影(CT portal venography,CTPV)显示肝硬化门脉高压侧支循环血管的临床应用价值。方法对92例肝硬化门脉高压的患者分别进行CT门脉造影,获得门脉侧支循环血管的清晰图像,测量门静脉主干和胃左静脉直径,将胃镜与CT门静脉造影两种技术进行比较。结果应用CT门静脉造影能清晰显示和测量门脉侧支循环的血管。CT门静脉造影与胃镜两种方法对食管和胃底曲张静脉的显示能力具有一致性,Kappa值分别为0.502和0.478。结论应用多排螺旋CT门静脉造影能很好显示和测量门体间侧支循环血管。联合应用多排螺旋CT门静脉造影与胃镜两种方法,对于肝硬化门静脉高压患者的诊断、病情判断和估计预后有帮助。     

门静脉海绵样变22例临床分析

目的 探讨门静脉海绵样变的临床特点、诊断方法及治疗.方法 对22例门静脉海绵样变患者的临床资料进行回顾性分析.结果 22例患者多以反复呕血便血、脾肿大、脾功能亢进为主要症状;肝功能检查多正常或仅表现为白蛋白的轻度降低.21例经超声检查确诊,1例经门静脉造影确诊.4例患者进行手术治疗,大多行脾切除,分流术加断流术.结论 门静脉海绵样变的临床表现以继发性门静脉高压为主,超声检查多能确诊.内科保守治疗效果不佳,手术以分流加断流术为主.     

门静脉海绵样变性病因及治疗

目的 探讨门静脉海绵样变性的病因和治疗。方法 对28例门静脉海绵样变性住院患者的临床资料进行回顾性分析。结果 2B例患者中15例（占53．6％）病因比较明确，13例（占46．4％）未发现明确病因；28例患者中20例有出血史，其中15例行内镜下套扎、硬化剂或组织胶注射治疗，随访4～96月，食管胃底静脉曲张基本消失，1例因食管溃疡再发出血，1例出现食管狭窄。结论 门静脉海绵样变性的病因为多因素；对有消化道出血的患者内镜下治疗可以起到急诊止血和预防再出血的作用。     

Plasma thrombopoietin in patients with cavernous transformation of the portal vein

Thrombopoietin (TPO), the primary regulator of thrombopoiesis, is produced mainly in the liver. Previous studies investigating blood TPO in chronic liver diseases revealed conflicting results. It has been suggested that hepatic TPO production is regulated by the portal blood supply to the liver. However, the role of TPO in the pathobiological basis of idiopathic portal vein thrombosis (PVT) and cavernous transformation of the portal vein (CTPV) has not been elucidated. The objective of this study is to assess plasma TPO concentrations in patients with CTPV. Eleven patients (4 men and 7 women, aged 38+/-12 years) with CTPV were studied. Sixteen healthy adults served as the control group (8 men and 8 women, aged 34+/-12 years). Median plasma TPO concentration was 326 pg/mL (range, 15-1402 pg/mL) in the patients with CTPV and 62.65 pg/mL (range, 38.5-102 pg/mL) in the control group (P = .003). In this study, we found significantly higher TPO concentrations in the plasma of patients with CTPV. The higher concentrations could be a result of the altered portal hemodynamics due to thrombosis. Moreover, TPO release by activated platelets might lead to the subsequent propagation of thrombosis in PVT.     

Transient perihilar attenuation difference in the liver on dynamic CT secondary to portal vein thrombosis: report of two cases

In two patients with portal vein thrombosis (PVT) accompanied by cavernous transformation, transient perihilar attenuation difference (TPAD) was demonstrated in the liver in the arterial phase of dynamic CT. It changed to an isodense shadow in the late phase. In one case, the area demonstrated as TPAD was well enhanced by postarterial portal CT, and in the other case, perihilar region was also densely opacified as contrasted by the peripheral area which was enhanced slightly with postarterial portography. It suggested that the TPAD area well supplied by portal blood flow via cavernous transformation and that the peripheral area surrounding TPAD was mainly supplied by increased hepatic arterial blood compensating for reduced portal flow. When the TPAD is found in the early phase of dynamic CT scan, attention should be paid to the existence of portal vein thrombosis (PVT). Chronic pancreatitis was the likely cause in one patient, and in the other it was idiopathic.     

Transient perihilar attenuation difference in the liver on dynamic CT secondary to portal vein thrombosis: Report of two cases

In two patients with portal vein thrombosis (PVT) accompanied by cavernous transformation, transient perihilar attenuation difference (TPAD) was demonstrated in the liver in the arterial phase of dynamic CT. It changed to an isodense shadow in the late phase. In one case, the area demonstrated as TPAD was well enhanced by postarterial portal CT, and in the other case, perihilar region was also densely opacified as contrasted by the peripheral area which was enhanced slightly with postarterial portography. It suggested that the TPAD area well supplied by portal blood flow via cavernous transformation and that the peripheral area surrounding TPAD was mainly supplied by increased hepatic arterial blood compensating for reduced portal flow. When the TPAD is found in the early phase of dynamic CT scan, attention should be paid to the existence of portal vein thrombosis (PVT). Chronic pancreatitis was the likely cause in one patient, and in the other it was idiopathic. The authors thank Professor Kunio Okuda, Chiba University School of Medicine, for his review. This study was supported by the Foundation for Promotion of Cancer Research.     

特发性门静脉高压症的彩色多普勒超声诊断与临床价值

目的探讨特发性门静脉高压症（IPH）的声像图特征,评价彩色多普勒对IPH的临床诊断价值。方法对25例IPH患者进行彩色多普勒超声检查,观察肝脏表面、内部回声、脾脏大小及肝内外门静脉系统等。结果25例患者中,25例均见门静脉肝内分支管壁增厚、回声增强、管腔狭窄甚至闭塞,15例实质回声增粗,门静脉海绵样变性22例,门静脉系统血栓5例,均为门静脉主干、脾静脉及肠系膜上静脉血栓,15例伴有胆道系统的异常。结论临床上不明原因的门脉高压及脾功能亢进患者均应进行彩色多普勒超声检查,肝内门静脉分支管壁增厚、管腔狭窄甚至闭塞的特征性改变及门静脉海绵样变性可提示IPH。