肝外胆管细胞癌所致肝实质一过性密度差异研究

目的 探讨肝外胆管细胞癌所致胆系扩张的肝实质--过性密度差异(transient hepatic parenchyma)attenuation differences,THAD)的影像学表现.资料与方法 56例肝外胆管细胞癌致胆系扩张患者行肝脏三期动态扫描均可见THAD.分析THAD的影像学特征及THAD与胆系扩张程度的相关性.结果 56例共测量肝内胆管222段,其中轻度扩张46段,中度扩张98段,重度扩张78段.柱状或分枝状THAD(Ⅰ型)在胆管轻度扩张肝段的发生率明显低于胆管中、重度扩张肝段(X2=186.68,P<0.005).肝内胆管重度扩张时,扩张程度呈扇形或不规则片状THAD(Ⅱ型)发生率明显增高(t'=5.16,P<0.05)0 II型THAD阳性组95%可信区间下限为9.3mm.Ⅲ型THAD阳性组与阴性组胆囊横径均数存在差异,其差异具有统计学意义(t'=6.46,P<0.05).Ⅲ型THAD阳性组胆囊横径均数95%可信区间下限为28.2mm.结论 肝外胆管细胞癌所致胆系扩张的THAD的影像学表现主要有3种:(1) Ⅰ型.沿胆管分布的柱状或分枝状THAD,边界不清,肝内胆系扩张＞5mm时常见;(2) Ⅱ型.扇形或不规则片状THAD,边界清楚或不清楚,肝内胆系扩张＞9.3mm时常见;(3) Ⅲ型.胆囊旁肝实质内弧形片状THAD,边界不清,胆囊横径＞28.2mm时常见.     

肝胆管细胞癌并发肝脓肿的MSCT诊断

目的:探讨肝胆管细胞癌并发肝脓肿患者的MSCT诊断价值。方法:收集15例肝胆管细胞癌合并肝脓肿患者的MSCT资料进行回顾性分析。结果:15例患者CT平扫图像上发现31处边界模糊的低密度病灶,包括15处肝内胆管细胞癌和16处肝脓肿。病灶位于肝右叶者12处,位于肝左叶者19处,其中10例患者肝胆管细胞癌和肝脓肿位于同一肝段或肝叶,5例患者肝胆管细胞癌和肝脓肿位于不同肝段或肝叶。15处肝胆管细胞癌中,肿块型5处,表现为肝实质内轻～中度环形强化结节,常不伴有周围胆管扩张;管周浸润型4例,表现为沿胆管纵轴生长的树枝状肿块,伴有周围胆管扩张;肿块并管周浸润型6例,表现为肝实质内轻～中度延迟强化结节,常伴周围胆管扩张。16处肝脓肿病灶动态强化CT图像上,表现为中央完全强化者3处;中央不完全强化者6处,其中表现为伴中央小范围不强化者2处,表现为花簇状、多间隔强化者4处;表现为中央不强化者7例,称为肝脓肿的典型表现,即周围环形强化而中央不强化。结论:肝内胆管细胞癌和肝脓肿有着不同的强化特征,因此动态增强CT对同时患有肝胆管细胞癌和肝脓肿的患者有重要价值。     

肝外胆管细胞癌的CT诊断

目的:分析肝外胆管细胞癌的CT表现,探讨其诊断价值。材料和方法:23例病理证实的肝外胆管癌均行螺旋CT动态增强检查和ERCP检查,分析其影像表现和诊断准确性。结果:CT诊断符合率78.3%(18/23),均表现为特征软组织肿块(直接征象)和肝内胆管及胆总管扩张(间接征象)。CT同时提供了较好的肿瘤分期诊断。ERCP诊断符合率91.3%(21/23),表现为肝内胆管均呈不同程度的扩张,肝外胆管狭窄、截断。CT结合ERCP后全部诊断正确,并提供详细信息。结论:肝外胆管细胞癌的螺旋CT检查有较好的诊断,结合ERCP可以获得更高的诊断准确率。     

囊性肝内胆管细胞癌与肝脓肿CT征象及鉴别诊断

目的:探讨囊性肝内胆管细胞癌与肝脓肿的CT征象及鉴别诊断。方法:搜集经临床穿刺及手术病理证实的21例囊性肝内胆管细胞癌(22个病灶)及26例肝脓肿的CT资料(29个病灶),并采用卡方检验对两组的常见形态征象进行分析。结果:靶征、分隔状强化征、边缘环形强化完整征及肿块缩小征在肝脓肿组的分布明显高于囊性肝内胆管细胞组(P<0.05)。边缘环形强化不完整征、向心性延迟强化征及肝被膜回缩征在囊性肝内胆管细胞组的分布明显高于肝脓肿组(P<0.05)。灌注异常在两组的出现率无明显差异。结论:囊性肝内胆管细胞癌与肝脓肿CT征象有相似之处,靶征、分隔状强化征、边缘环形强化完整征及肿块缩小征提示肝脓肿的可能性大,边缘环形强化不完整征、向心性延迟强化征及肝被膜回缩征提示囊性肝内胆管细胞癌的可能性大,对各个征象的详细分析和比较是鉴别诊断的重要依据。     

不典型末梢型肝内胆管细胞癌MSCT影像学特征

目的探讨末梢型肝内胆管细胞癌MSCT影像学征象,提高术前影像诊断水平。方法回顾性分析12例经病理证实的不典型末梢型肝内胆管细胞癌的影像学资料。结果CT平扫病灶均为稍低密度,增强扫描动脉期6例见不均匀轻度强化,3例呈富血供强化;门脉期及延迟期5例病灶渐进性、向心性持续轻度强化,5例轻度环状强化,2例病灶未进一步强化;肝包膜皱缩5例,肝叶萎缩4例,周围胆管轻度扩张3例,合并胆管结石3例。结论不典型末梢型肝内胆管细胞癌平扫呈边缘模糊稍低密度影,增强动脉期呈轻度不均匀性环状强化,延迟期渐进性强化为特点,周围胆管扩张、肝叶萎缩及肝包膜皱缩是其重要间接征象。     

肝内胆管细胞癌的多层螺旋CT诊断价值

目的:探讨肝内胆管细胞癌的CT表现,加深对肝内胆管细胞癌的认识。方法:回顾性分析14例经病理证实的肝内胆管细胞癌的CT影像学表现。结果:14例中8例边界模糊的类圆形低密度肿块,11例伴肝内胆管扩张,6例边界较清晰。增强扫描8例早期肿块周边呈不规则强化;4例周边呈环形或结节状明显强化;2例无明显强化;延时扫描所有病灶均延迟强化。结论:多层螺旋CT扫描显示肝内胆管细胞癌有一定的特征性,具有较高的诊断价值。     

周围型肝内胆管细胞癌的CT诊断及鉴别诊断

目的:探讨周围型肝内胆管细胞癌的诊断及鉴别诊断,提高对周围型胆管细胞癌的认识.方法:回顾性分析对23例经手术病理证实的周围型胆管细胞癌的常规CT平扫及增强扫描.结果:CT平扫所有病灶均为低密度,大小约2.5~8.0cm,平均为5.0cm.19例为单发病灶,4例为多发大小不一病灶,其中肝内胆管扩张18例,肝内胆管结石6例,肝叶变形萎缩9例,局部肝轮廓凹陷6例,增强扫描:动脉期和静脉期可见边缘不规则断续的轻度晕圈状强化,内部出现不同程度线样及条网状强化.延迟扫描:随时间延长病灶逐步进一步强化,密度等于或大于同层肝组织.结论:周围型肝内胆管细胞癌的表现有一定特征性,实质性病灶延迟强化及病灶内胆管扩张是胆管细胞癌的特征表现.     

肝内胆管细胞癌的CT诊断

目的探讨肝内胆管细胞癌的CT增强特征及其病理基础,提高该病CT诊断的准确性。方法15例经病理证实的肝内胆管细胞癌,均行CT平扫及增强扫描,其中,6例加做CT延时扫描。结果15例平扫表现为低密度病灶伴肝内胆管扩张8例,合并肝内胆管结石4例,合并钙化2例;增强扫描呈线样强化7例,呈网格样强化6例,结节样强化1例,无明显强化1例;病理显示肝内胆管细胞癌纤维组织丰富,血管稀少。结论CT平扫病灶呈低密度而增强扫描呈线样及网格样强化对肝内胆管细胞癌的诊断及鉴别诊断有重要意义。     

肝内胆管细胞癌的CT诊断

目的：探讨肝内胆管细胞癌的CT表现及其诊断价值。方法对28例经手术或穿刺活体组织检查经病理证实为肝内胆管细胞癌患者的CT表现进行分析。结果28例肝内胆管细胞癌患者的30个病灶CT平扫均为低密度,病变区或其周围见胆管扩张,其中15例见肝包膜回缩征,11例为肝内胆管结石术后。增强扫描动脉期病灶边缘环形增强9例。门静脉期11例中央网格样增强。延迟期8例呈向心性增强,密度略高于正常肝实质。结论肝内胆管细胞癌CT表现具有一定特异性,有利于肝内胆管细胞癌诊断。     

不同形态类型肝内胆管细胞癌的CT诊断

目的：探讨不同形态类型肝内胆管细胞癌的CT表现。方法：回顾性分析经病理证实的20例肝内胆管细胞癌的形态特点和动态增强CT表现。结果：20例肝内胆管细胞癌中肿块型14例，管周浸润型4例，管内生长型2例。肿块型平扫表现为不规则低密度肿块，动态扫描早期肿瘤周边呈环状强化，中心部分早期呈轻度强化或不强化，延迟期呈现持续性强化为特征性表现；管周浸润型表现为沿胆管树走行的分枝状软组织肿块，边缘不清，远侧胆管扩张，动态扫描肿瘤呈渐进性延迟强化；管内生长型表现为扩张胆管内的乳头状或结节状病变，动态扫描早期呈轻度均匀性强化，延迟期无强化。结论：不同形态类型肝内胆管细胞癌的CT表现不同，术前影像学检查明确ICC的形态学类型，有助于临床选择合理的治疗方案并判断患者预后。     

Meaning and etiopathogenesis of sectorial transient hepatic attenuation differences (THAD)

PURPOSE: To examine sectoral transient hepatic attenuation differences (THAD) in an attempt to correlate semeiotics with etiopathogenesis and to deduce a possible diagnostic value. MATERIALS AND METHODS: Over a period of three years (January 1998-January 2001) we observed 130 THAD in 988 patients, and we selected 30 sectoral THAD in 18 patients (10 males and 8 females), ranging in age from 24 to 82 years (average = 63.3). The 18 patients comprised 6 cancer patients undergoing CT staging/restaging, 5 cirrhotic patients being studied for possible hepatocellular carcinoma, 7 patients undergoing helical CT to further investigate clinical and/or US findings. For each patient a biphasic helical CT liver examination was performed, during the arterial and portal dominant phase. After the first diagnosis, all patients were followed up for 12 months with at least one US and helical CT examination; 8/18 were also studied by MRI. RESULTS: Thirty THAD were associated with 14 metastatic lesions, 4 hepatocellular carcinomas, 1 cholangiocarcinoma of the liver, 4 haemangiomas, 3 abscesses, 1 FNH, 2 cases of arterioportal shunting (APS) and 1 fine-needle percutaneous biopsy. Nine THAD turned out to be the sole sign of disease and occurred at least 3/6 months before the causal focal lesion had become detectable. At the first examination, all focal lesions had a maximum diameter of 2 cm; the size of THAD varied from 1 to 5 cm. All of the THAD were sectoral, with the base side represented by the glissonian capsule and the apex towards the parenchyma. 27/30 THAD were connected to focal lesions: 24/27 were fan-shaped and the lesion was situated at the apex of the triangle; 3/27 were roughly wedge-shaped and the lesion was entirely inscribed in the hyperattenuating area. 3/30 were not connected to focal lesions, being in 2 cases fan-shaped and in only one case irregularly shaped. CONCLUSIONS: Sectoral THAD may or may not be connected to focal lesions. Whenever a sectoral THAD not connected to a focal lesion is detected, all of the possible causes should be considered: portal or superhepatic vein thrombosis, traumatic (biopsy) or cirrhotic intraparenchymal APS, or a benign occult nodule. If none of these explanations are confirmed, we should consider the possibility of an occult malignant lesion.     

Transient hepatic attenuation differences (THAD) not connected to focal lesions

PURPOSE: To report our experience with helical CT evaluation of transient hepatic attenuation differences (THAD), and in particular of those not associated with focal lesions, in an attempt to provide an aetiopathogenetic picture that accounts for the morphology, evolution and density of THAD. MATERIALS AND METHODS: Between January 1998 and January 2001 we observed THAD in 130/988 biphasic helical CT liver examinations performed in the arterial and portal dominant phase. THAD were associated to focal hepatic lesions in 87 patients; in 43 patients there was no such association. This second group of patients, composed of 23 males and 20 females ranging in age from 17 to 80 years (average = 58.8), was enrolled in the study. THAD were associated to: Budd-Chiari syndrome (9), portal venous thrombosis (10), liver cirrhosis (7), acute inflammation of an adjacent organ (4), dilatation of the entire biliary tree (3), hepatic stasis caused by heart failure (2) and constrictive pericarditis (1), fine-needle percutaneous biopsy (2), arterioportal shunting (2), parenchymal compression by fractured ribs (2) and by a strengthened phrenic pillar (1). THAD were evaluated according to extension, morphology and density. For each case at least 10 density measurements were performed by sampling regions of interest on the parenchyma with THAD and on the contralateral parenchyma. The results (mean and standard deviation) were compared to those relative to 30 healthy patients. 22/43 patients were followed up for 6#150;24 months by at least one US and helical CT examination. During CT, the direct appreciation of vascular thrombus during the portal dominant phase was also considered. RESULTS: We detected 18 localised and 25 diffuse THAD. The localised sectoral THAD (11), wedge-shaped with clear border sign, were associated to thrombosis of a portal branch (6), fine-needle percutaneous biopsy (2), arterioportal shunting (2) and partial Budd-Chiari syndrome (1). The localised non-sectoral THAD (7), with variable morphology and without the clear border sign, were associated to acute inflammation of an adjacent organ (4) and to parenchymal compression by the ribs or diaphragm (3). Diffuse THAD associated to Budd-Chiari syndrome (8) and to heart failure (3) showed mosaic enhancement of hepatic parenchyma (patchy pattern); those linked to portal trunk thrombosis (4) and cirrhosis (7) revealed predominant enhancement of external hepatic parenchyma (central-peripheral phenomenon); finally, those concurrent with dilatation of the entire biliary tree showed parenchymal enhancement close to the dilated bile ducts (peribiliary pattern). Follow-up (22/43) demonstrated complete THAD regression after removal (5/22) and less conspicuity of THAD after partial overcome of the stoppage (1/22). In 2/22 cases of arterioportal shunting no substantial changes were seen. The remaining 14/22 cases showed a gradual, slow tendency towards THAD regression with hypotrophy of the involved parenchyma and compensatory contralateral hypertrophy even in the case of endurance of the causative agents. CONCLUSIONS: Based on our experience and the literature we suggest a classification for THAD unrelated to focal hepatic lesions. We recognise 4 causes: portal vein stoppage-obstruction, portal in-flow diversion, trauma and inflammation. When THAD is related to the first three causes pathogenesis is portal hypoperfusion. In the fourth group the mediators of the arterial phenomena are those of inflammation even though portal hypoperfusion might be involved as well. THAD identification makes the detection of vascular thrombi easier by comparison with their direct finding during the portal dominant phase. Finally, THAD are to be investigated for their potential utility in the detection and characterisation of several hepatic diseases. As a consequence, hepatic CT studies cannot ignore arterial dominant phase evaluation, even if no focal hepatic lesions are expected.     

Transient hepatic attenuation difference (THAD) in patients without neoplasm: frequency, shape, distribution, and causes.

Transient hepatic attenuation difference (THAD) is a valuable finding in detecting hypervascular lesions. However, similar findings are also observed in patients even without known hepatic diseases. We elucidate the characteristic findings and the causes of THAD in patients without hepatic neoplasm in this article. Dual-phased contrast-enhanced CT studies performed in 450 patients were reviewed, and THAD was observed in 42 (9.3%). THAD was linear or wedge-shaped and was seen contiguous to the liver surface with a relatively obscure margin in 40 of the 42 cases. The most common cause of THAD was chronic cholecystitis followed by previous biliary surgery. THAD was also seen in 30 patients with no hepatic diseases in whom it had a tendency to locate around the gallbladder fossa or in the periphery of the liver particularly in the left lobe. The knowledge of the prevalence, shape, distribution and causes of THAD is essential for the evaluation of contrast-enhanced CT images obtained during the arterial phase.     

胆管癌误诊和漏诊的影像学分析

目的：分析胆管癌误诊和漏诊的原因，评价不同检查方法对肝门区胆管癌诊断的价值，提高胆管癌的影像学诊断和鉴别诊断水平。方法：收集31例临床和病理诊断为胆管癌的病例(ERCP检查31例，B超检查31例，25例CT检查，11例行MRCP检查)，回顾性分析不同检查方法的影像学表现。结果：31例中发生在肝门区的胆管癌25例。2例初次ERCP显示胆管内出血，再次行鼻胆管造影后诊断为胆管癌，4例合并有总胆管结石。6例为总胆管中下段癌。初次诊断准确性为90．3％。11例MRCP中9例显示病变，2例显示不满意，7例显示胆管或胆囊结石。25例CT中23例显示肝内胆管扩张，9例显示肝门区肿块，2例见后腹膜转移淋巴结，1例见肝内多发性转移瘤。12例初次诊断正确(48％)。B超检查23例提示肝内胆管扩张，6例提示总胆管结石，18例诊断为胆囊炎、胆囊结石，8例提示胆管占位(25．8％)。结论：良好的直接胆管造影是诊断胆管癌的金标准，MRCP可以在一定程度上准确显示病变的范围，是ERCP的良好补充，很大程度上取代了诊断性ERCP；CT诊断的关键在于显示扩张的胆管和梗阻的定位，肝门区梗阻多为胆管癌所致。多种影像检查方法的结合明显提高了诊断的准确性，对胆管癌治疗方案的选择有重要价值。     

肝门胆管癌的CT诊断

目的:评价螺旋CT对肝门胆管癌的诊断价值。方法:回顾性分析14例经病理证实的肝门部胆管癌的CT表现,评价其对病灶的显示情况及定性诊断的准确率。结果:平扫表现为肝门区低密度软组织肿块;增强扫描14例均有延迟强化;增强检查能更清楚显示肝内胆管扩张和胆管壁增厚。结论:螺旋CT扫描对肝门胆管癌的诊断具有重要意义。     

肝内外胆管癌的螺旋CT诊断

目的:探讨肝内外胆管癌的螺旋CT表现及鉴别诊断。方法:收集23例经手术、病理证实的肝内外胆管癌,回顾性分析其螺旋CT平扫及动态增强表现。结果:肝内胆管癌5例,CT平扫为边缘欠清的低密度病灶中可有高密度钙化影,增强扫描随时间延长病灶由边缘向中央逐步强化,最后病灶强化高于正常肝实质,病灶周围可见扩张的肝内胆管。肝门胆管癌6例,CT表现为肝内胆管扩张,胆总管或左右肝管起始部狭窄、充盈缺损、轻中度强化的肝门软组织肿块。中下段胆管癌12例,CT表现为肝内胆管扩张、病变以上胆总管扩张、病变处胆总管狭窄、中断,梗阻近端胆管壁不均匀增厚、腔内见软组织结节影或周围软组织肿块。结论:肝内胆管癌及肝门部胆管癌根据CT动态增强表现不难作出诊断,胆总管癌须认真分析CT薄层放大增强表现鉴别其他低位梗阻性胆道疾病后作出诊断。     

肝外胆管细胞癌的多层螺旋CT诊断价值

目的 探讨多层螺旋CT(MSCT)对肝外胆管细胞癌的诊断价值.方法 回顾性分析27例经病理确诊的肝外胆管癌的临床资料及MSCT图像特征,20例行平扫及四期动态增强扫描(即早动脉期,晚动脉期,门脉期及延迟期),7例仅行增强扫描.结果 肝门区胆管癌15例,胆总管癌12例;不同部位,不同生长方式的胆管癌CT表现各具特点,除延迟强化等直接征象外,肝叶萎缩,胆管扩张等间接征象亦具有特征性.结论多层螺旋CT对于肝外胆管细胞癌具有较高的诊断价值.     

Transient hepatic attenuation differences on dynamic computed tomography

Transient hepatic attenuation differences (THAD) are occasionally noted on dynamic CT in patients with portal vein obstruction, arterioportal shunt, liver tumor, and liver abscess. We report four additional cases of THAD with unreported and/or unexplained etiology.     

磁共振VIBE增强扫描联合冠状位T2WI诊断肝外远端胆管癌

目的探讨MR三维容积内插体部检查(volume interpolated body examination,VIBE)增强联合冠状位T2WI诊断肝外远端胆管癌的价值。方法 17例经手术病理证实的肝外远端胆管癌行MR冠状位T2WI、VIBE增强扫描,观察病灶的MR表现,测量病灶长度。结果 17例肝外远端胆管癌在冠状位T2WI上表现为肝外远端胆管梗阻,10例于胆管梗阻处见软组织肿块、3例见胆管壁增厚,同周围组织相比呈低信号。VIBE动态增强扫描17例病灶均呈进行性强化,10例肿块者中2例均匀性强化,8例肿块边缘强化更明显;7例胆管壁增厚、强化,在轴位VIBE图像上呈"环"形强化,在冠状位VIBE图像上,5例呈平行的"线条"状强化,2例呈"V"形强化。病灶平均长度为18.7 mm。结论 VIBE增强联合冠状位T2WI能较好地显示肝外远端胆管癌。     

磁共振快速三维容积动态增强联合MRCP诊断肝外胆管癌

目的：评价磁共振肝脏快速三维容积动态增强（LAVA）联合MRCP诊断肝外胆管癌的价值。方法：回顾性分析15例经手术、病理证实的肝外胆管癌常规MR平扫、LAVA增强和MRCP表现。结果：15例肝外胆管癌发生于肝外胆管近段者7例,远段者6例,另2例发生于肝外胆管近段及远段上部。MR平扫主要表现为肝门部、胆管区软组织肿块或胆管壁不规则增厚。2例未见明确的软组织肿块及胆管壁增厚。LAVA增强扫描动脉期病灶轻至中度强化。门脉期及延迟期中至明显强化,另2例平扫未见明确的病灶影者于LAVA薄层扫描发现胆管壁不规则偏心性增厚且强化。MRCP显示扩张的肝内外胆管及梗阻部位的狭窄、中断、截断和管腔内的充盈缺损。3例伴肝内转移灶。4例伴有肝门部及腹膜后淋巴结转移。结论：IAVA和MRCP联合应用能较好地对肝外胆管癌进行诊断,提高早期管壁浸润型胆管癌的检出率．并能准确描述和评价胆管癌扩散及浸润范围。