- •Foreword I
- •Foreword II
- •Preface
- •Contents
- •1 Abscesses – Pyogenic Type
- •3 Cyst I – Typical Small
- •4 Cyst II – Typical Large with MR-CT Correlation
- •5 Cyst III – Multiple Small Lesions with MR-CT-US Comparison
- •6 Cyst IV – Adult Polycystic Liver Disease
- •7 Cystadenoma / Cystadenocarcinoma
- •8 Hemangioma I – Typical Small
- •10 Hemangioma III – Typical Giant
- •11 Hemangioma IV – Giant Type with a Large Central Scar
- •13 Hemangioma VI – Multiple with Perilesional Enhancement
- •14 Hemorrhage
- •16 Mucinous Metastasis – Mimicking an Hemangioma
- •17 Colorectal Metastases I – Typical Lesion
- •18 Colorectal Metastases II – Typical Multiple Lesions
- •19 Colorectal Metastases III – Metastasis Versus Cyst
- •20 Colorectal Metastases IV – Metastasis Versus Hemangiomas
- •21 Liver Metastases V – Large, Mucinous, Mimicking a Primary Liver Lesion
- •24 Breast Carcinoma Liver Metastases
- •25 Kahler’s Disease (Multiple Myeloma) Liver Metastases
- •26 Melanoma Liver Metastases I – Focal Type
- •27 Melanoma Liver Metastases II – Diffuse Type
- •28 Neuroendocrine Tumor I – Typical Liver Metastases
- •29 Neuroendocrine Tumor II – Pancreas Tumor Metastases
- •30 Neuroendocrine Tumor III – Gastrinoma Liver Metastases
- •31 Neuroendocrine Tumor IV – Carcinoid Tumor Liver Metastases
- •32 Neuroendocrine Tumor V – Peritoneal Spread
- •34 Renal Cell Carcinoma Liver Metastasis
- •35 Cirrhosis I – Liver Morphology
- •36 Cirrhosis II – Regenerative Nodules and Confluent Fibrosis
- •37 Cirrhosis III – Dysplastic Nodules
- •38 Cirrhosis IV – Dysplastic Nodules – HCC Transition
- •39 Cirrhosis V – Cyst in a Cirrhotic Liver
- •40 Cirrhosis VI – Multiple Cysts in a Cirrhotic Liver
- •41 Cirrhosis VII – Hemangioma in a Cirrhotic Liver
- •42 HCC in Cirrhosis I – Typical Small with Pathologic Correlation
- •43 HCC in Cirrhosis II – Small With and Without a Tumor Capsule
- •44 HCC in Cirrhosis III – Nodule-in-Nodule Appearance
- •45 HCC in Cirrhosis IV – Mosaic Pattern with Pathologic Correlation
- •47 HCC in Cirrhosis VI – Mosaic Pattern with Fatty Infiltration
- •48 HCC in Cirrhosis VII – Large Growing Lesion with Portal Invasion
- •49 HCC in Cirrhosis VIII – Segmental Diffuse with Portal Vein Thrombosis
- •50 HCC in Cirrhosis IX – Multiple Lesions Growing on Follow-up
- •51 HCC in Cirrhosis X – Capsular Retraction and Suspected Diaphragm Invasion
- •52 HCC in Cirrhosis XI – Diffuse Within the Entire Liver with Portal Vein Thrombosis
- •53 HCC in Cirrhosis XII – With Intrahepatic Bile Duct Dilatation
- •54 Focal Nodular Hyperplasia I – Typical with Large Central Scar and Septa
- •55 Focal Nodular Hyperplasia II – Typical with Pathologic Correlation
- •57 Focal Nodular Hyperplasia IV – Multiple FNH Syndrome
- •58 Focal Nodular Hyperplasia V – Fatty FNH with Concurrent Fatty Adenoma
- •59 Focal Nodular Hyperplasia VI – Atypical with T2 Dark Central Scar
- •60 Hepatic Angiomyolipoma – MR-CT Comparison
- •61 Hepatic Lipoma – MR-CT-US Comparison
- •62 Hepatocellular Adenoma I – Typical with Pathologic Correlation
- •63 Hepatocellular Adenoma II – Large Exophytic with Pathologic Correlation
- •64 Hepatocellular Adenoma III – Typical Fat-Containing
- •65 Hepatocellular Adenoma IV – With Large Hemorrhage
- •77 Intrahepatic Cholangiocarcinoma – With Pathologic Correlation
- •78 Telangiectatic Hepatocellular Lesion
- •79 Focal Fatty Infiltration Mimicking Metastases
- •80 Focal Fatty Sparing Mimicking Liver Lesions
- •81 Hemosiderosis – Iron Deposition, Acquired Type
- •82 Hemochromatosis – Severe Type
- •83 Hemochromatosis with Solitary HCC
- •84 Hemochromatosis with Multiple HCC
- •85 Thalassemia with Iron Deposition
- •86 Arterioportal Shunt I – Early Enhancing Lesion in a Cirrhotic Liver
- •89 Budd-Chiari Syndrome II – Gradual Deformation of the Liver
- •90 Budd-Chiari Syndrome III – Nodules Mimicking Malignancy
- •92 Caroli’s Disease I – Intrahepatic with Segmental Changes
- •93 Caroli’s Disease II – Involvement of the Liver and Kidneys
- •95 Choledocholithiasis (Bile Duct Stones)
- •96 Gallbladder Carcinoma I – Versus Gallbladder Wall Edema
- •97 Gallbladder Carcinoma II – Hepatoid Type of Adenocarcinoma
- •98 Hilar Cholangiocarcinoma I – Typical
- •99 Hilar Cholangiocarcinoma II – Intrahepatic Mass
- •100 Hilar Cholangiocarcinoma III – Partially Extrahepatic Tumor
- •101 Hilar Cholangiocarcinoma IV – Metal Stent with Interval Growth
- •102 Hilar Cholangiocarcinoma V – Biliary Dilatation Mimicking Klatskin Tumor at CT
- •103 Primary Sclerosing Cholangitis I – Cholangitis and Segmental Atrophy
- •104 Primary Sclerosing Cholangitis II – With Intrahepatic Cholestasis
- •105 Primary Sclerosing Cholangitis III – With Intrahepatic Stones
- •106 Primary Sclerosing Cholangitis IV – With Biliary Cirrhosis
- •107 Primary Sclerosing Cholangitis V – With Intrahepatic Cholangiocarcinoma
- •108 Primary Sclerosing Cholangitis VI – With Hilar Cholangiocarcinoma
- •109 T2 Bright Liver Lesions
- •110 T1 Bright Liver Lesions
- •111 T2 Bright Central Scar
- •112 Lesions in Fatty Liver
- •113 Appendix I: MR Imaging Technique and Protocol
- •114 Appendix II: Liver Segmental and Vascular Anatomy
- •Subject Index
108 Part IIC – Primary Solid Liver Lesions in Cirrhotic Liver
51HCC in Cirrhosis X – Capsular Retraction and Suspected Diaphragm Invasion
Hepatic capsular retraction adjacent to hepatic tumor is rare, although this finding has been described in a variety of malignant tumors [intrahepatic cholangiocarcinoma, hepatocellular carcinoma (HCC), and colorectal metastases] and benign entities (confluent fibrosis and hemangioma). Although retraction of the liver capsule adjacent to a hepatic tumor was first described in epithelioid hemangioendothelioma, many radiologists consider this sign to be associated with cholangiocarcinoma. Rarely, HCC may present with this sign and in combination with other imaging findings such as high signal intensity on T2-weighted images, and subtle cirrhotic morphology may hamper the diagnosis. In addition, if subcapsular location coincides with the subphrenic location of HCC, the possibility of diaphragm invasion may be raised.
Literature
1.Miller WJ, Dodd GD III, Federle MP, Baron RL (1992) Epithelioid hemangioendothelioma of the liver: imaging findings with pathologic correlation. AJR 159:53 – 57
2.Outwater E (1993) Capsular retraction in hepatic tumors [letter]. AJR 160:422
3.Yang DM, Kim HS, Cho SW, et al. (2002) Various causes of hepatic capsular retraction: CT and MR findings. Br J Radiol 75:994 – 1002
4.Verhoef C, Holman FA, Hussain SM, et al. (2005) Resection of extrahepatic hepatocellular carcinoma metastasis can result in long-term survival. Acta Chir Belg 105:533 – 536
MR Imaging Findings
At MR imaging, subcapsular HCC may show retraction of the liver capsule. The signal intensity of such HCC may be exceptionally high on T2-weighted images and mimic cholangiocarcinoma. The high signal intensity strongly suggests high fluid content and may be related to the cholangiocellular differentiation or a mixed type of HCC at histology. On T1-weighted images the findings may be unremarkable. The lesions may show only subtle enhancement in the arterial phase. The enhancement of a tumor capsule in the delayed phase and subtle cirrhotic morphology of the liver may facilitate the correct diagnosis. Small recurrences of such HCCs may also display high signal on T2-weighted images and may be successfully removed at surgery (Figs. 51.1 – 51.3).
Differential Diagnosis
Large, single, intrahepatic lesions with high signal intensity on T2-weighted images and capsular retraction may mimic intrahepatic cholangiocarcinoma. In such cases, it is crucial to assess any capsular enhancement in the delayed phase, search for any subtle signs of cirrhosis at imaging, and look for the clinical indicators of parenchymal liver disease.
51 HCC in Cirrhosis X – Capsular Retraction and Suspected Diaphragm Invasion 109
Fig. 51.1. HCC, cirrhosis, large, drawings. T2 fatsat: HCC is hyperintense to the liver and surrounded by a (ruptured) tumor capsule; T1 in-phase: HCC is hyperintense to the liver; ART: HCC shows faint enhancement predomi-
Fig. 51.2. HCC, cirrhosis, large, MRI findings. A Axial TSE image (T2 fatsat): HCC is hyperintense to the liver, which is surrounded by a discontinuous dark tumor capsule; note also a subtle umbilication (arrow). B Axial inphase image (T1 in-phase): HCC is hypointense to the cirrhotic liver. C Axial arterial phase image (ART): HCC shows faint enhancement mainly in the periphery of the tumor. D Axial delayed phase image (DEL): HCC shows washout with enhanced capsule that particularly appears to be ruptured in
nantly in the periphery of the lesion; DEL: HCC shows washout with enhancement of the tumor capsule, which appears to be discontinuous at the subcapsular region (arrow)
the subcapsular region (arrow). E Sagittal delayed phase image (DEL): Fatty liver has become darker with persistent perilesional high signal (arrow). F Axial opposed-phase image (T1 opposed-phase): Note the peri-lesional compressed bright liver parenchyma (arrow). G Axial portal phase image (POR): a part of the HCC appears to be attached to the diaphragm, suspicious of extrahepatic tumor extension (arrow). H Axial SSTSE image (SSTSE): HCC is slightly brighter in the central part (arrow)
Fig. 51.3. HCC, cirrhosis, large, direct MR-pathology correlation. A Photograph of the resected specimen shows the HCC with a fibrous tumor capsule that is discontinuous at least at two places (arrow). The resection surfaces were considered to be free of tumor at pathology. B Photomicrograph shows large
glands within plates of abnormal hepatocytes that indicate a cholangiolar type of HCC. H&E, × 100. C, D Axial TSE and arterial phase images at 9 months follow-up show a recurrence at the diaphragm that was resected successfully (arrow)
110 Part IIC – Primary Solid Liver Lesions in Cirrhotic Liver
52HCC in Cirrhosis XI – Diffuse Within the Entire Liver with Portal Vein Thrombosis
Diffuse hepatocellular carcinoma (HCC) is present in up to 13 % of patients with HCC. The tumor can spread throughout the liver, and in some cases may replace almost the entire liver parenchyma by a permeative or extensive micronodular growth pattern. Extensive portal venous tumor thrombosis is a hallmark of such extensive diffuse HCC and the serum alpha-fetoprotein value is elevated in up to 78 % of patients. In addition, lymph node, bone, and lung metastases may be present. Diffuse HCC that infiltrates and replaces the entire liver may remain undetected on CT and US, mainly because of insufficient intrinsic soft tissue contrast in these modalities. The presence of portal venous tumor thrombosis is an important clue to the diagnosis.
Literature
1.Kanematsu M, Semelka RC, Leonardou P, et al. (2003) Hepatocellular carcinoma of diffuse type: MR imaging findings and clinical manifestations. JMRI 18:189 – 195
2.Okuda K, Noguchi T, Kubo Y, et al. (1981) A clinical and pathological study of diffuse type hepatocellular carcinoma. Liver 1:280 – 289
3.Tublin ME, Dodd 3rd GD, Baron RL (1997) Benign and malignant portal vein thrombosis: differentiation by CT characteristics. AJR 168:719 – 723
4.Hussain SM, Semelka RC (2005) Hepatic imaging: Comparison of modalities. Radiol Clin N Am 43:929 – 947
MR Imaging Findings
At MR imaging, the entire liver shows heterogeneous increased signal intensity on T2-weighted images with irregular contours and ascites (spleen, if normal, may be used as a reference). On T1weighted images, the liver may also appear heterogeneous with the presence of abnormally high signal at the level of the portal vein. Due to the presence of tumor thrombus, the portal vein is often expanded. On gadolinium-enhanced images, the entire liver shows marked heterogeneous or patchy enhancement in the arterial phase. The enhancement becomes more permeative or miliary in the delayed phase (Figs. 52.1, 52.2). US and CT may remain inconclusive in such cases (Fig. 52.3).
Differential Diagnosis
Hepatic vascular abnormalities such as bland portal vein thrombosis and Budd-Chiari syndrome may show some overlap on imaging with diffuse HCC, but the clinical settings and the relationship with the tumor markers differ considerably. Increased arterial enhancement of the liver due to altered vascularity is often a transient phenomenon, does not persist into the delayed phase and is often unaccompanied by tissue changes.
52 HCC in Cirrhosis XI – Diffuse Within the Entire Liver with Portal Vein Thrombosis 111
Fig. 52.1. HCC, cirrhosis, diffuse HCC with portal invasion, drawings. T2 fatsat: HCC is diffuse and hyperintense to the liver; note also the cirrhotic liver, a bright cyst (arrow) and ascites; T1 in-phase: HCC is hypointense to the liver;
Fig. 52.2. HCC, cirrhosis, diffuse HCC with portal invasion, MRI findings. A Axial TSE image (T2 fatsat): HCC is diffuse and hyperintense to the liver; note also the cirrhotic liver, a bright cyst (arrow) and ascites. B Axial in-phase image (T1 in-phase): HCC is hypointense to the liver. C Axial arterial phase image (ART): HCC shows heterogeneous permeative enhancement with the portal vein tumor thrombosis (solid arrows) and esophageal varices (open arrows). D Axial portal phase image (POR): The liver remains heterogeneous with portal vein thrombosis (solid arrows) and varices (open arrows). E Coronal
ART: HCC shows heterogeneous permeative enhancement with enhancement of the portal vein tumor thrombosis; DEL: the entire liver remains strongly heterogeneous
SSTSE image (SSTSE): Note the cirrhotic liver with diffuse HCC, a cyst, ascites, and enlarged spleen. F Coronal delayed phase image (POR): The liver shows strong heterogeneous enhancement due to the diffuse HCC. G Axial delayed phase image (POR) at another level shows the cyst (arrow) and the liver with septal enhancement. H MIP of the delayed phase image shows the recanalization of the ligament falciform (open arrows) and thrombosed right portal vein (solid arrow)
Fig. 52.3. HCC, cirrhosis, diffuse HCC with portal invasion, drawing and inconclusive US and CT prior to MRI. A Drawing shows the diffuse HCC within the cirrhotic liver. B Ultrasound was performed because of acute esophageal hemorrhage. No cause was found and the cirrhosis was not recognized. C and D
CT (following US) at two different anatomic levels showed a cyst (arrow) and “circulation changes”. No cause of bleeding was found and MRI was requested which is shown above