肝硬化门静脉性胆病的影像表现

目的：探讨肝硬化门静脉高压性胆病（PB）的MSCT及MRI表现。方法：回顾性分析16例肝硬化PB患者的MSCT及MRI表现,分析门静脉血栓导致PB的解剖位置和临床表现。结果：16例患者中门静脉海绵样变13例,其中8例合并门静脉血栓;门静脉和／或门静脉分支血栓3例。16例患者中3例表现为肝内胆管扩张,9例表现为肝外胆管及一侧肝内胆管扩张,4例表现为肝外胆管和两侧肝内胆管扩张。本组病例门静脉系统侧支循环的类型包括食道一胃底静脉曲张13例（13／16,81％）、胰腺周围静脉曲张10例（10／16,63％）和胆囊静脉曲张10例（10／16,63%）。结论：肝硬化门静脉高压患者出现肝外或肝内胆管扩张时应考虑门静脉高压性胆病的可能。     

肝门部胆管癌影像学诊断

本文对５６例经手术和病理证实的肝门部胆管癌进行了影像学回顾性分析，直接法胆道造影（ＤＣ）表现征象可分为胆道梗阻、狭窄、息肉样变和右肝管狭窄伴左肝管梗阻。ＵＳ显示肝内胆管的扩张，肝门区低回声占位，胆管内低回声肿块，门静脉癌栓。ＣＴ可表现，肝内胆管扩张，肝门区软组织密度肿块，肝门区肿块有增强，胆囊变小或萎缩，左肝萎缩和右肝增大，作者认为：ＤＣ加上ＵＳ或ＣＴ是诊断肝门区胆管癌的首选方法。     

肝右叶缺如伴右侧胆管及右肾发育畸形一例

病例资料患者,女,43岁,右上腹疼痛数年,加重5 d。右上腹压痛,无反跳痛及移动性浊音,皮肤巩膜无黄染。多层螺旋CT平扫示肝脏体积明显缩小,胆囊位于肝脏右后方,在肝脏后方并可见迂曲的扩张的胆管,肝左叶胆管稍扩张,肝总管也明显扩张,右肾形态失常,体积明显缩小(图1)。增强扫描门静脉期见肝脏均匀强化,肝右叶未见明确显示,肝右叶胆管结构显示失常,门静脉主干及左支显示较清晰,右支未显示;右肾强化欠佳,体积明显缩小,形态不规整,皮质变薄,肾盂、肾盏变小,右肾动脉显示较细,左肾显示正常(图2、3)。剖腹探查显示肝右叶缺如,肝右胆管发育畸形扩张…     

常染色体隐性遗传多囊肾1例

患者男,10岁。脾肿大1年。实验室检查:AST20.6u/L,ALT24.9u/L,TB10.5umol/L,DB3.8umolL。影像学表现:肝脏体积增大,肝内实质密度尚均匀,肝内胆管囊状扩张,脾脏体积增大,约8个肋单位(图1)。双肾脏体积增大,实质内可见多发囊状低密度灶,增强扫描未见强化(图2,3)。诊断:常染色体隐性遗传多囊肾。讨论:常染色体隐性遗传多囊肾是一种少见的常染色体隐性遗传的致死性肾脏囊性病。染色体检查发现致病基因定位于第6对染色体。本病的发生率约为1/40000。根据其不同的病理及临床表现,又分为围生期型和儿童型。本病例为儿童型,儿童型以肝脏病变为…     

遗传性出血性毛细血管扩张症肝脏病变的 MDCT 影像学特征

目的：探讨遗传性出血性毛细血管扩张累及肝脏病变的M DC T影像学特征及临床意义。方法回顾分析9例经临床明确诊断的遗传性出血性毛细血管扩张累及肝脏的影像学资料并总结其影像特征。结果①肝动脉‐肝静脉分流4例：动脉期见增粗迂曲的肝动脉及提前显影的肝静脉;肝实质弥漫性分布小斑片状边缘模糊强化灶,门脉期等密度。其中3例肝门区胆管轻度扩张;②肝动脉‐门静脉分流1例：动脉期见扩张迂曲的肝动脉及提前显影的扩张门静脉;肝实质少量小斑片状强化灶,门脉期等密度;③肝动脉‐肝静脉分流合并肝动脉‐门静脉分流3例,动脉期肝动脉迂曲扩张,肝静脉和门静脉提前显影;肝实质弥漫性分布小斑片状强化灶,门脉期等密度;④门静脉‐肝静脉分流1例：动脉期未见扩张肝动脉,门脉期见扩张门静脉及其远端分支旁小斑片状强化灶,延迟期呈稍高密度。结论遗传性出血性毛细血管扩张症累及肝脏的CT影像表现具有特征性,充分认识其影像表现并结合临床对其诊断及鉴别诊断具有重要意义。     

肝脏囊虫感染的影像学表现

目的 探讨肝脏囊虫感染的影像学特征.方法 搜集8例患者临床及影像学资料,分析病灶分布、数量、大小、形态、密度/信号、强化方式及胆管扩张、脾大、淋巴结肿大、腹腔积液等影像学特点.结果 8例均为多发病灶,4例累及肝脏多叶,呈“簇样”不规则圆形/类圆形、结节状或蜂窝样表现,沿门静脉走行为主分布于肝脏深部或包膜下近肝表面,最大...     

自身免疫性肝炎致肝硬化的MRI表现及其临床价值

目的 探讨自身免疫性肝炎(autoimmune hepatitis,AIH)致肝硬化的MRI诊断特点,以提高其诊断准确性.资料与方法回顾分析经临床确诊为AIH所致肝硬化患者7例,所有患者均按肝功能Child-Pugh分级(A级2例,B级2例,C级3例)并行MR T,WI、T2WI、扩散加权成像(DWI)及动态增强扫描.2例行肝穿刺活检,2例经1～2年随访,分析其MRI表现并与病理、肝功能分级对照.结果 (1)肝脏形态学改变:5例(Child B、C级)全肝萎缩.3例(Child C级)肝脏内可见多个大小不等结节形成,可见结节融合,横径最大约为53 mm,结节信号表现多样,但在DWI上均呈低信号,部分结节增强后可见强化,随访后强化信号消失.(2)继发门静脉高压改变:除1例(Child A级)无明显继发门静脉高压表现,余6例门静脉主干增粗、胃底及脾静脉延长迂曲.7例脾均增大,2例(Child C级)脾内可见含铁血黄素沉积,其中1例伴有脾梗死.3例(Child C级)腹腔积液形成.(3)其他:1例(Child A级)肝内胆管轻度扩张.所有患者均无淋巴结改变.肝穿刺病理结果符合AIH致肝硬化表现.结论 AIH致肝硬化的MRI表现特点为:随着肝功能Child-Pugh分级的加重,肝脏形态学及继发门静脉高压改变随之加重;全肝萎缩,肝左外叶及尾状叶的代偿性增大少见;肝硬化结节形态、信号改变多样,癌变罕见;可伴有肝内胆管扩张;较少伴有淋巴结肿大.MRI可作为AIH致肝硬化的有效检查手段.     

不典型肝内胆管细胞癌合并脓肿的影像诊断要点

目的探讨不典型肝内胆管细胞癌合并肝脓肿的影像表现特征和诊断要点。方法回顾性分析1例经手术病理证实为肝内胆管细胞癌合并肝脓肿病人的临床资料、影像表现特征并复习相关文献。结果 MDCT平扫显示巨大不规则肿物,累及肝左叶及部分右前叶,肿物呈分叶状,内部密度不均,邻近血管无受侵、肝包膜无凹陷征;增强CT检查动脉期显示肿物呈多结节融合状,病灶边缘及内部各结节呈明显环形强化,门静脉期及平衡期肿物强化仍较明显。肝脏MRI平扫肿物呈不规则形稍长T1、稍长T2信号影,于DWI序列上显示不均匀较明显高信号,增强扫描表现类似于增强CT表现,另于MRI增强扫描门静脉期及平衡期可见肿物内局部区域呈分房状表现,增强程度更明显。结论不典型肝内胆管细胞癌合并肝脓肿兼具两种病变的影像表现。正确诊断需结合临床、实验室检查、超声表现并注重影像表现的细节信息。     

不典型肝内胆管细胞癌合并脓肿的影像学诊断要点

目的 探讨不典型肝内胆管细胞癌合并肝脓肿的影像表现特征和诊断要点。方法? 回顾性分析1例经手术病理证实为肝内胆管细胞癌合并肝脓肿病人的临床资料、影像表现特征并复习相关文献。结果? MDCT平扫显示巨大不规则肿物,累及肝左叶及部分右前叶,肿物呈分叶状,内部密度不均,邻近血管无受侵、肝包膜无凹陷征;增强CT检查动脉期显示肿物呈多结节融合状,病灶边缘及内部各结节呈明显环形强化,门静脉期及平衡期肿物强化仍较明显。肝脏MRI平扫肿物呈不规则形稍长T1、稍长T2信号影,于DWI序列上显示不均匀较明显高信号,增强扫描表现类似于增强CT表现,另于MRI增强扫描门静脉期及平衡期可见肿物内局部区域呈分房状表现,增强程度更明显。结论? 不典型肝内胆管细胞癌合并肝脓肿兼具两种病变的影像表现。正确诊断需结合临床、实验室检查、超声表现并注重影像表现的细节信息。     

丙硫咪唑治疗肝泡状棘球蚴病B超初步观察

本文报告口服ABZ1年治疗76例LAE,近期疗效满意。B超观察:病灶缩小,病灶的液化区增大,实质性病灶出现液化,病灶内均有钙化灶伴声影显示。治疗前6例黄疸患者肝内胆管扩张,治疗后5例扩张之胆管消失,黄疸消退,1例胆管仍有扩张,黄疸指数为20U。所有治疗者无新的病灶显示。门脉高压征象改善,脾脏缩小,腹壁静脉曲张消失,门静脉、脾静脉由增宽恢复至正常。正常肝实质代偿性增大。对未接受ABZ治疗的10例LAE随访观察症状均有加重,病灶均增大。     

Autosomal recessive polycystic kidney disease: radiologic-pathologic correlation.

Autosomal recessive polycystic kidney disease is a heritable but phenotypically variable disorder characterized by varying degrees of nonobstructive renal collecting duct ectasia, hepatic biliary duct ectasia and malformation, and fibrosis of both liver and kidneys. In the kidney, the dilated collecting ducts and interstitial fibrosis, when severe, may significantly impair renal function and result in hypertension and renal failure. Imaging typically shows large but reniform kidneys, diffusely increased renal parenchymal echogenicity at ultrasonography, and a striated nephrogram after contrast material administration. In the liver, periportal fibrosis accompanies the malformed and dilated bile ducts; this may result in portal hypertension. The liver may appear normal or may show intrahepatic biliary dilatation; once portal hypertension develops, splenomegaly and varices are usually evident. The relative degrees of kidney and liver involvement tend to be inverse: Children with severe renal disease usually have milder hepatic disease, and those with severe hepatic disease tend to evidence mild renal impairment. Presently, treatment consists of supportive management and control of hypertension. Replacement therapy for renal failure (dialysis or kidney transplantation) and control of portal hypertension (portal circulatory diversion or liver transplantation) may be necessary.     

Imaging findings in congenital hepatic fibrosis

Congenital hepatic fibrosis (CHF) is a rare congenital multisystemic disorder, mostly inherited in autosomal recessive fashion, primarily affecting renal and hepatobiliary systems. Main underlying process of the disease is the malformation of the ductal plate, the embryological precursor of the biliary system, and secondary biliary strictures and periportal fibrosis ultimately leading to portal hypertension. The natural course of the disease is highly variable ranging from minimally symptomatic disease to true cirrhosis of the liver. However, in most patients the most common manifestations of the diseases that are related to portal hypertension, particularly splenomegaly and bleeding varices. Many other disease processes may co-exist with the disease including Caroli's disease, choledochal cysts and autosomal recessive polycystic kidney disease (ARPKD) reflecting the mulstisystemic nature of the disease. The associating biliary ductal disease led the authors to think that all these entities are a continuum and different reflections of the same underlying pathophysiological process. Although, conventional method of diagnosis of CHF is the liver biopsy the advent of imaging technologies and modalities, today, may permit the correct diagnosis in a non-invasive manner. Characteristic imaging features are generally present and recognition of these findings may obviate liver biopsy while preserving the diagnostic accuracy. In this article, it is aimed to increase the awareness of the practising radiologists to the imaging findings of this uncommon clinical disorder and trail the blaze for future articles relating to this issue.     

Sonography of infantile polycystic kidney disease

Sonography was performed on five children, ages 1 day-9 years, who had classic infantile polycystic kidney disease and on one child who had glomerulocystic renal disease. Microcystic involvement of the kidneys in infantile polycystic kidney disease results in renal enlargement, increased echogenicity of renal parenchyma but good transmission of sound through the kidney, and poor definition of renal borders on sonograms. The periportal involvement of the liver in the classic infantile polycystic kidney disease may lead to hepatic fibrosis and portal hypertension. Less typical features include asymmetric renal enlargement and macrocysts in the renal parenchyma.     

Liver cysts in autosomal-dominant polycystic kidney disease: clinical and computed tomographic study

Hepatic CT findings were analyzed in 44 patients with autosomal-dominant polycystic kidney disease and were correlated with liver and renal function tests and liver, splenic, and renal CT volume measurements. CT showed many large liver cysts in 31.8% of patients, small liver cysts in 25%, and no liver cysts in 43.2%. Patients with many large cysts often showed increased liver volumes. Splenic volumes did not differ significantly in patients with and without liver cysts, suggesting that portal hypertension is rarely associated with cystic liver disease. There was no correlation between severity of liver involvement and extent of renal cystic disease as determined from urea nitrogen and creatinine levels and renal volumes. Liver function tests were normal except in two patients, one with a cholangiocarcinoma, which may have arisen from a cyst, and the other with an infected liver cyst and chronic active hepatitis. Accordingly, if liver function tests are abnormal, an attempt should be made to identify complications of polycystic liver disease such as tumor, cyst infection, and biliary obstruction. Such complications are rare but may be seen in patients whose lives are prolonged by dialysis and renal transplantation. CT is a useful method for detecting liver cysts and identifying patients at risk for these complications.     

Portal hypertension and obstructive jaundice after hepatic interventions: report of two unusual complications

We report two unusual complications after a transjugular intrahepatic portosystemic shunt and a biliary stent placement, respectively. One patient with cirrhosis and portal hypertension developed obstructive jaundice secondary to compression of the right hepatic duct by a stent graft placed in the transjugular intrahepatic portosystemic shunt. In another patient, biliary stents caused obstruction of the portal vein, resulting in symptomatic portal hypertension. An awareness of these possible complications is important for early diagnosis and appropriate treatment of such complications.     

Caroli disease: central dot sign in CT

Two adults with communicating cavernous ectasia of the biliary tract (Caroli disease) are described. Both patients had the pure form of the disease, characterized by saccular dilatation of intrahepatic bile ducts, multiple intrahepatic calculi, absence of portal hypertension, and associated cystic renal disease. Computed tomographic (CT) scans of the liver showed tiny dots with strong contrast enhancement within dilated intrahepatic bile ducts (the central dot sign). These intraluminal dots on CT scans corresponded to intraluminal portal veins on sonograms, findings indicating portal radicles surrounded by dilated intrahepatic bile ducts.     

Imaging and radiological interventions in extra-hepatic portal vein obstruction

Extrahepatic portal vein obstruction (EHPVO) is a primary vascular condition characterized by chronic long standing blockage and cavernous transformation of portal vein with or without additional involvement of intrahepatic branches, splenic or superior mesenteric vein. Patients generally present in childhood with multiple episodes of variceal bleed and EHPVO is the predominant cause of paediatric portal hypertension (PHT) in developing countries. It is a pre-hepatic type of PHT in which liver functions and morphology are preserved till late. Characteristic imaging findings include multiple parabiliary venous collaterals which form to bypass the obstructed portal vein with resultant changes in biliary tree termed portal biliopathy or portal cavernoma cholangiopathy. Ultrasound with Doppler, computed tomography, magnetic resonance cholangiography and magnetic resonance portovenography are non-invasive techniques which can provide a comprehensive analysis of degree and extent of EHPVO, collaterals and bile duct abnormalities. These can also be used to assess in surgical planning as well screening for shunt patency in post-operative patients. The multitude of changes and complications seen in EHPVO can be addressed by various radiological interventional procedures. The myriad of symptoms arising secondary to vascular, biliary, visceral and neurocognitive changes in EHPVO can be managed by various radiological interventions like transjugular intra-hepatic portosystemic shunt, percutaneous transhepatic biliary drainage, partial splenic embolization, balloon occluded retrograde obliteration of portosystemic shunt (PSS) and revision of PSS.     

Portal biliopathy: imaging manifestations on multidetector computed tomography and magnetic resonance imaging

Portal biliopathy refers to biliary abnormalities secondary to extrahepatic portal vein obstruction and cavernous transformation and is caused by vascular compression from peribiliary collateral vessels, producing segmental stenoses of the common bile duct and abnormal liver function test (LFT) results. A review of imaging studies yielded 18 patients with abnormal LFT results, biliary tract dilatation, and extrahepatic portal vein obstruction with cavernous transformation. Multidetector computed tomography and magnetic resonance imaging showed biliary stenotic segments in 11 patients secondary to extrinsic compression from enlarged peribiliary collaterals. Clinical and imaging follow-up demonstrated improvement in LFT results with minimal decrease in bile duct dilatation, eliminating percutaneous or endoscopic biliary intervention.     

Gd-EOB-DTPA enhanced MR imaging: Evaluation of biliary and renal excretion in normal and cirrhotic livers

Objective

The purpose of this study was to assess the difference in the activity of biliary and renal excretion between normal and cirrhotic livers on contrast-enhanced MR imaging obtained with gadolinium ethoxybenzyl diethylenetriaminepentaacetic acid (Gd-EOB-DTPA).

Methods

A total of 78 patients with cirrhotic liver (n = 44) and with normal liver (n = 34) underwent multi-phase Gd-EOB-DTPA enhanced MR imaging (arterial, portal, equilibrium, and three hepatobiliary phases (10, 15 and 20 min HP), respectively), and these contrast-enhanced images were qualitatively and quantitatively evaluated for the differences of the biliary and renal excretion between normal and cirrhotic livers.

Results

The timing of biliary excretion of contrast agents in the cirrhotic liver was significantly slower than that in the normal liver (P < 0.001). The degree of contrast enhancement in the common bile duct in the normal liver was significantly better than that in the cirrhotic liver (P = 0.003). Contrast agents were demonstrated in the duodenum at 20 min HP in 8/44 (18%) cirrhotic liver while they were seen in 15/34 (44%) normal liver (P = 0.013). The enhancement effects of renal medulla and portal vein at 20 min HP in the cirrhotic liver were significantly higher than those of normal liver (P = 0.043 and P < 0.001, respectively).

Conclusion

Biliary excretion of Gd-EOB-DPTA was impaired in cirrhotic livers in comparison with normal livers while renal excretion of Gd-EOB-DPTA was increased.     

黑血SPACE序列与MRCP、T2-HASTE在婴幼儿胆道成像中的对比应用

目的探讨磁共振黑血SPACE序列与MRCP、T2-HASTE在婴幼儿胆道成像中的对比应用价值。方法运用Siemens 3.0 T超导磁共振扫描仪对30例对照组患儿和12例罹患胆道疾病的婴幼儿进行全腹部常规MRI序列(包括T2-HASTE)以及黑血SPACE序列、MRCP检查,比较黑血SPACE序列与MRCP、T2-HASTE图像对正常胆道结构及病灶的显示能力。结果(1)对照组图像分析:黑血SPACE和MRCP对胆囊管、左右肝管及肝内二级胆管的显示能力较T2-HASTE好,且黑血SPACE序列显示门静脉的能力优于MRCP和T2-HASTE,但黑血SPACE与MRCP在显示胆道结构的能力方面差异无统计学意义。(2)病例组图像分析:黑血SPACE序列在清晰显示胆总管扩张的同时较MRCP拥有更好的组织对比度;黑血SPACE序列较MRCP、T2-HASTE更清晰的显示胆道闭锁患儿肝门区及门静脉周围的异常信号影(纤维斑块),并了解毗邻门静脉的走行及轮廓;黑血SPACE序列在显示微小胆管结石时优于T2-HASTE。结论黑血SPACE序列基本具备MRCP和T2-HASTE序列两者的优势,在观察婴幼儿胆道结构形态、轮廓及边缘的同时了解毗邻肝组织、血管(门静脉)的情况,且成像时间相对较短,但其运用于部分婴幼儿胆道成像时存在较多的运动伪影及肠气干扰,目前将其作为婴幼儿胆道成像的一种补充检查手段,针对不同疾病利用其不同优势,为胆道疾病的影像诊断提供更多助益。