Imaging of the Liver and Intra-hepatic Biliary Tract: Volume 2: Tumoral Pathologies [1st ed.] 9783030390204, 9783030390211

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Medical Radiology · Diagnostic Imaging Series Editors: Hans-Ulrich Kauczor · Paul M. Parizel · Wilfred C.G. Peh

Emilio Quaia   Editor

Imaging of the Liver and Intra-hepatic Biliary Tract Volume 2: Tumoral Pathologies

Medical Radiology Diagnostic Imaging Series Editors Hans-Ulrich Kauczor Paul M. Parizel Wilfred C. G. Peh

For further volumes: http://www.springer.com/series/4354

Emilio Quaia Editor

Imaging of the Liver and Intra-hepatic Biliary Tract Volume 2: Tumoral Pathologies

Editor Emilio Quaia Radiology Unit Department of Medicine - DIMED University of Padova Padova Italy

ISSN 0942-5373     ISSN 2197-4187 (electronic) Medical Radiology ISBN 978-3-030-39020-4    ISBN 978-3-030-39021-1 (eBook) https://doi.org/10.1007/978-3-030-39021-1 © Springer Nature Switzerland AG 2021 This work is subject to copyright. All rights are reserved by the Publisher, whether the whole or part of the material is concerned, specifically the rights of translation, reprinting, reuse of illustrations, recitation, broadcasting, reproduction on microfilms or in any other physical way, and transmission or information storage and retrieval, electronic adaptation, computer software, or by similar or dissimilar methodology now known or hereafter developed. The use of general descriptive names, registered names, trademarks, service marks, etc. in this publication does not imply, even in the absence of a specific statement, that such names are exempt from the relevant protective laws and regulations and therefore free for general use. The publisher, the authors, and the editors are safe to assume that the advice and information in this book are believed to be true and accurate at the date of publication. Neither the publisher nor the authors or the editors give a warranty, expressed or implied, with respect to the material contained herein or for any errors or omissions that may have been made. The publisher remains neutral with regard to jurisdictional claims in published maps and institutional affiliations. This Springer imprint is published by the registered company Springer Nature Switzerland AG The registered company address is: Gewerbestrasse 11, 6330 Cham, Switzerland

Contents

Part I Hepatic Tumoral Pathology: Normal Liver  Hepatic Hemangioma, Focal Nodular Hyperplasia, and Hepatocellular Adenoma��������������������������������������������������������������������� 3 Luigi Grazioli, Barbara Frittoli, Roberta Ambrosini, Martina Bertuletti, and Francesca Castagnoli Inflammatory Liver Lesions �������������������������������������������������������������������� 49 Anna Sara Fraia, Silvia Brocco, and Emilio Quaia  Infectious Liver Diseases and Parasitic Lesions�������������������������������������� 67 Ali Devrim Karaosmanoglu, Aycan Uysal, and Musturay Karcaaltincaba  Imaging of Hepatic Cystic Tumors���������������������������������������������������������� 91 Vishal Kukkar and Venkata S. Katabathina Uncommon Liver Tumors ���������������������������������������������������������������������� 111 Ersan Altun and Katrina Anne Mcginty  Intrahepatic Cholangiocarcinoma and Mixed Tumors������������������������ 123 Jelena Kovač Liver Metastases�������������������������������������������������������������������������������������� 141 Martina Scharitzer, Helmut Kopf, and Wolfgang Schima Part II Hepatic Tumoral Pathology: Chronic Liver Disease and Liver Cirrhosis  Hepatocellular Carcinoma: Diagnostic Imaging Criteria�������������������� 177 Alessandro Furlan and Roberto Cannella Hepatocellular Carcinoma: Diagnostic Guidelines������������������������������ 191 Luis Martí-Bonmatí and Asunción Torregrosa  Benign Lesions in Cirrhosis�������������������������������������������������������������������� 215 Roberta Catania, Amir A. Borhani, and Alessandro Furlan  Pseudolesions in the Cirrhotic Liver������������������������������������������������������ 229 Rita Golfieri, Stefano Brocchi, Matteo Milandri, and Matteo Renzulli v

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Part III Therapy of Hepatic Tumours and Post-­treatment Changes in the Liver Percutaneous Ablation of Liver Tumors������������������������������������������������ 269 Arcangelo Merola, Silvia Brocco, and Emilio Quaia  Transarterial Chemoembolisation and Combined Therapy���������������� 283 Alberta Cappelli, Giuliano Peta, and Rita Golfieri Transarterial 90Yttrium Radioembolisation���������������������������������������� 319 Cristina Mosconi and Rita Golfieri  Imaging of Treated Liver Tumors and Assessment of Tumor Response to Cytostatic Therapy and Post-Treatment Changes in the Liver �������������������������������������������� 349 Silvia Brocco, Anna Sara Fraia, Anna Florio, and Emilio Quaia Part IV Special Topics  Hepatic Tumoral Pathology: The Pediatric Liver�������������������������������� 377 Gabriele Masselli, Marianna Guida, Silvia Ceccanti, and Denis Cozzi  Functional Imaging of the Liver ������������������������������������������������������������ 395 Simona Picchia, Martina Pezzullo, Maria Antonietta Bali, Septian Hartono, Choon Hua Thng, and Dow-Mu Koh

Contents

Part I Hepatic Tumoral Pathology: Normal Liver

Hepatic Hemangioma, Focal Nodular Hyperplasia, and Hepatocellular Adenoma Luigi Grazioli, Barbara Frittoli, Roberta Ambrosini, Martina Bertuletti, and Francesca Castagnoli

Contents 1    Hepatocellular Origin 1.1  Hepatocellular Adenoma

 4  4

2    Focal Nodular Hyperplasia (FNH)

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3    Nodular Regenerative Hyperplasia (NRH)

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4    Mesenchymal Origin 4.1  Hepatic Hemangioma

 36  36

References

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Abstract

Benign focal liver lesions can originate from all kind of liver cells: hepatocytes, mesenchymal and cholangiocellular line. Their features at imaging may sometimes pose difficulties in differential diagnosis with malignant primary and secondary lesions. In particular, the use of MDCT and MRI with extracellular and

L. Grazioli (*) Department of Radiology, ASST-Spedali Civili di Brescia, Brescia, Italy B. Frittoli · R. Ambrosini Radiology Service, Imaging Diagnostic Department, ASST-Spedali Civili di Brescia, Brescia, Italy M. Bertuletti · F. Castagnoli University of Brescia, ASST “Spedali Civili” University Hospital, Brescia, Italy

hepatobiliary Contrast Agents may help in correct interpretation and definition of hepatocellular or mesenchymal and inflammatory nature, allowing to choose the best treatment option. The peculiarities of main benign liver lesions at US, CT and MRI are described, with special attention to differential diagnosis and diagnostic clue.

The identification and imaging characterization of benign liver lesions is fundamental for differential diagnosis with malignant primary and secondary lesions. Likewise, differentiating between various benign lesions is of paramount importance because of their distinct management, which can range from no therapeutic treatment, to follow-up or biopsy for definitive confirmation, to surgical resection.

© Springer Nature Switzerland AG 2021 E. Quaia (ed.), Imaging of the Liver and Intra-hepatic Biliary Tract, Medical Radiology Diagnostic Imaging, https://doi.org/10.1007/978-3-030-39021-1_1

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Incidental focal liver lesions are for the most part benign, even in oncological patients. The most common benign focal liver lesions are hemangiomas which originate from the mesenchymal cellular line, followed by focal nodular hyperplasia (FNH) and hepatocellular adenoma (HCA), both originating from the hepatocellular line. We can identify and characterize these lesions by using various imaging techniques: US scan can identify liver lesions, but the use of contrast agents is in most cases necessary for correct characterization, whether during US (CEUS), CE-MDCT, or MRI with extracellular or hepatobiliary contrast agents. The peculiarities of the most common benign liver lesions at US, CT, and MRI are described with particular attention given to differential diagnosis and diagnostic clues. Recent guidelines about post-diagnostic management are also shown below.

1

Hepatocellular Origin

1.1

Hepatocellular Adenoma

Hepatocellular adenoma (HCA) is a rare benign liver lesion with an incidence of 1 case for 1,000,000 people: the incidence increases to 1–3 cases for 100,000  in females who use or have used oral contraceptives (OCPs) for long term (Cogley and Miller 2014). Although the precise pathogenic mechanism leading to hepatic adenomas is still unknown, the use of oral contraceptive and anabolic steroids and some congenital diseases such as glycogen storage diseases and metabolic syndrome are considered risk factors for development and progression of HCA. Men with metabolic syndrome are at a much higher risk (10 times more likely than females) for malignant degeneration of liver adenomas, although this is rare (5 cm), and histological subtype (β-catenin-­mutated) (Lee et al. 2014; Neri et  al. 2016). More than ten adenomas widespread into liver parenchyma configure “liver adenomatosis.”

HCA can be classified at least into four immunohistological subtypes (Lee et  al. 2014; Kaltenbach et al. 2016; Katabathina et al. 2011): 1. Inflammatory type (I-HCA) with serum amyloid A overexpression: they represent 45–55% of adenomas, initially described as telangiectatic FNH, characterized by inflammatory infiltrates and frequent sinusoidal dilatation, peliotic areas, dystrophic vessels, and ductular dilatations. 2. Hepatocyte nuclear factor 1α-mutated type (H-HCA): they represent 25–45% of adenomas and are characterized by predominant intralesional fat component due to activation of lipogenesis. 3. β-catenin-mutated type with upregulation of glutamine synthetase (β-HCA): they represent approximately 5–10% of adenomas, they are considered borderline lesions between HCA and HCC, and they occur more frequently in men and are associated with male hormone administration, glycogen storage disease, and familial adenomatous polyposis. 4. Unclassified type: this subtype encompasses HCAs without any genetic abnormalities ( 120 ms), with low signal intensity on T1w sequences (Klotz et  al. 2013; Chan et  al. 2002). In the case of “giant” HH, a central T2w hypointense portion may be observed, corresponding to hyalinized or thrombosed areas, sometimes with calcifications, with incomplete contrast filling (Fig. 16). Diffusion-weighted (DW) MRI is considered a useful technique for the detection and characterization of focal liver lesions. Using this

Hepatic Hemangioma, Focal Nodular Hyperplasia, and Hepatocellular Adenoma

a

b

c

d

e

f

Fig. 15  A 52-year-old male, chronic abdominal pain. US finding of nodular hyperechoic lesion in IIS. On T1w in/ opp imaging (a, b), the lesion appears hypointense (arrow in a); it’s brightly hyperintense on T2w acquisition with fat saturation (c). At DWI imaging (b0–b800), the signal intensity of the lesion is high due to shine-through effect (d, e), but the lesion doesn’t show restriction in the ADC

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map (f). During dynamic acquisition before and after i.v. administration of gadoxetic acid (g–j) with a slow flow injection rate (1 mL/s), the lesion shows globular enhancement (arrow in h) and almost complete fulfilling during PVP. The lesion appears slightly hypointense after 3 min during transitional phase (j), and it’s markedly hypointense after 10 min (HBP in k): cavernous hemangioma

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g

i

k

Fig. 1.15 (continued)

h

j

Hepatic Hemangioma, Focal Nodular Hyperplasia, and Hepatocellular Adenoma

a

b

c

d

e

g

Fig. 16  A 48-year-old, female, abdominal discomfort. US finding of heterogeneously hyperechoic mass in S5– S6. At MR examination the lesion is hypointense on T1 in/ opp-phase acquisitions (a, b) and brightly hyperintense T2-w image (c); the lesion does not show restriction on

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f

h

b50 (d), b800 (e) and ADC map (f); at T1w images with fat saturation (g) the lesion is hypointense. After Gd-BOPTA administration (h–j) the lesion shows typical globular enhancement, incomplete after 5′ (j): giant cavernous hemangioma

L. Grazioli et al.

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i

j

Fig. 16 (continued)

approach, benign lesions (mostly cyst and hemangioma) can be correctly categorized if they show high signal intensity on both T2w and b0 s/ mm2, with a progressive and significant signal intensity decrease at high b values 500/750  s/ mm2 and an apparent diffusion coefficient (ADC) signal that is subjectively higher than the adjacent liver (Parikh et  al. 2008). Some HHs may demonstrate residual high signal intensity on high b value images (500–750  s/mm2) and are more difficult to characterize at the qualitative assessment of DW MR images. This phenomenon, known as “T2w shine-through effect,” is explained by the influence of T2w properties to the DW images (being the other two factors involved in DW signal intensity the ADC and the spin density of the examined tissue). Moreover, the absence of restricted diffusion on a qualitative evaluation is supported by the quantitative assessment on the ADC map, with values that are always higher than hepatic parenchyma (2.17 ± 0.36 × 10 − 3 mm2/s) (Duran et al. 2014). The same peculiar aspect can be observed after bolus administration of EOB-DTPA due to its rapid hepatocyte intake. Indeed EOB vascular profile, in terms of globular and progressive fill­in, could not be typically evaluated, and, in late phases of dynamic evaluation, hemangiomas tend to appear iso- or hypointense, differently from what is seen when using vascular interstitial contrast agents (Fig. 17). Capillary hemangioma may be observed in almost 16% of all HH, 42% less than 1  cm in size. It consists of small vascular spaces, with

more abundant connective components, that may be the explanation for the different hemodynamic and contrast enhancement behavior (Klotz et al. 2013; Vilgrain et al. 2000). It may appear more frequently iso-hypoechogenic at US, due to tight vascular spaces and faster blood flow, with less reverberation of acoustic echoes and possible demonstration of intralesional flow at color Doppler evaluation. In steatotic liver, small capillary HH may demonstrate a perilesional hypoechogenicity at US, corresponding to the hyperattenuating rim at baseline CT and hyperintensity on T1w “chemical shift” images due to peritumoral sparing of fatty infiltration. At CT examination, the lesion may appear slightly hypodense or isodense before contrast medium injection, with early, homogeneous, and rapid and intense contrast enhancement, that follows the aortic enhancement in each phase, without any washing (Caseiro-Alves et  al. 2007; Youssef et  al. 2015). Furthermore, especially in small lesions (