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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_5762_Библиотеки_им_академика_М_И_Перельмана.pdf
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- •Preface
- •Contents
- •1.1 Historical Remarks
- •1.1.1 Contrast Enhanced Ultrasound
- •2.2 Machine Settings
- •1.4 CEUS Phases
- •1.8 Three-Dimensional (3D) CEUS
- •1.9 CEUS Guidelines
- •References
- •2.1 Introduction
- •2.2.2 Image Depth Penetration
- •2.2.3 Focus
- •2.2.5 Background Signal (Noise)
- •2.2.6 Dynamic Range
- •2.2.7 Frame Rate
- •2.6 Artifacts
- •2.6.1 Long Liver Enhancement
- •2.7 Safety
- •References
- •3.1 Introduction
- •3.7 Detection by Intraoperative Contrast Enhanced Ultrasound (IO-CEUS)
- •References
- •4: Malignant Liver Tumors
- •4.1 Hepatocellular Carcinoma
- •4.1.1 Introduction
- •4.1.6 Surveillance
- •4.1.7 CEUS LI-RADS
- •4.1.8 Small HCC
- •4.1.9 Treatment Response Follow Up
- •4.1.9.1 Ablation Therapy
- •4.1.9.2 Transarterial Chemoembolization
- •4.1.9.3 Targeted Therapy
- •4.2 Intrahepatic Cholangiocarcinoma
- •4.2.2 Imaging
- •4.2.2.1 Conventional Ultrasound Findings
- •4.2.2.2 Contrast Enhanced Ultrasound Findings
- •4.2.2.3 CT Findings
- •4.2.2.4 MRI Findings
- •4.2.2.5 Other Imaging Findings
- •4.2.2.6 Best Imaging Protocol Advices
- •4.2.3.1 Hepatocellular Carcinoma
- •4.2.4 Pathology
- •4.2.4.1 General Features
- •4.2.5 Clinical Issues
- •4.2.5.1 Presentation
- •4.2.5.2 Prognosis
- •4.2.5.3 Treatment
- •4.3 Liver Metastases
- •4.3.1 Terminology
- •4.3.2 Imaging Features
- •4.3.2.1 Conventional Ultrasound Findings
- •4.3.2.2 Contrast Enhanced Ultrasound Findings
- •4.3.2.3 CT Findings
- •4.3.2.4 MRI Findings
- •4.3.3.1 Hepatocellular Carcinoma
- •4.3.3.2 Intrahepatic Cholangiocarcinoma
- •4.3.3.3 Focal Fatty Liver Change
- •4.4 Dysplasia Nodules
- •4.4.1 Terminology
- •4.4.2 Imaging
- •4.4.2.1 Conventional Ultrasound Findings
- •4.4.2.2 Contrast Enhanced Ultrasound Findings
- •4.4.2.3 CT Findings
- •4.4.2.4 MRI Findings
- •4.4.2.5 Best Imaging Protocol Advices
- •4.4.4 Pathology
- •4.4.4.1 General Features
- •4.4.5 Clinical Issues
- •4.4.5.1 Presentation
- •4.4.5.2 Prognosis
- •4.4.5.3 Treatment
- •References
- •5: Benign Liver Tumors
- •5.1 Hepatic Hemangioma
- •5.1.1 Terminology
- •5.1.2 Imaging
- •5.1.2.1 Conventional Ultrasound Findings
- •5.1.2.2 Contrast Enhanced Ultrasound Findings
- •5.1.2.3 CT Findings
- •5.1.2.4 MRI Findings
- •5.1.2.5 Other Imaging Findings
- •5.1.2.6 Best Imaging Protocol Advices
- •5.1.3.1 Hepatocellular Carcinoma
- •5.1.3.2 Metastatic Hepatic Carcinoma
- •5.1.3.3 Focal Angiosarcoma
- •5.1.3.4 Abscess
- •5.1.3.5 Hepatic Adenoma
- •5.1.4 Pathology
- •5.1.4.1 General Features
- •5.1.5 Clinical Issues
- •5.1.5.1 Presentation
- •5.1.5.2 Prognosis
- •5.1.5.3 Treatment
- •5.2 Focal Nodular Hyperplasia
- •5.2.1 Terminology
- •5.2.2 Imaging
- •5.2.2.1 Conventional Ultrasound Findings
- •5.2.2.2 Contrast Enhanced Ultrasound Findings
- •5.2.2.3 CT Findings
- •5.2.2.4 MRI Findings
- •5.2.2.5 Other Imaging Findings
- •5.2.2.6 Best Imaging Protocol Advices
- •5.2.3.1 Hepatic Adenoma
- •5.2.3.2 Hepatocellular Carcinoma
- •5.2.3.3 Fibrolamellar Hepatocellular Carcinoma
- •5.2.4 Pathology
- •5.2.4.1 General Features
- •5.2.5 Clinical Issues
- •5.2.5.1 Prognosis
- •5.2.5.2 Treatment
- •5.3 Hepatocellular Adenoma
- •5.3.1 Terminology
- •5.3.2 Imaging
- •5.3.2.1 Ultrasonographic Findings
- •5.3.2.2 Contrast Enhanced Ultrasound Findings
- •5.3.2.3 CT Findings
- •5.3.2.4 MRI Findings
- •5.3.2.5 Imaging Recommendations
- •5.3.3.1 Focal Nodular Hyperplasia
- •5.3.3.2 Hepatocellular Carcinoma
- •5.3.3.3 Fibrolamellar Hepatocellular Carcinoma
- •5.3.3.4 Hepatic Hemangioma
- •5.3.4 Pathology
- •5.3.4.1 General Features
- •5.3.5 Clinical Issues
- •5.3.5.1 Presentation
- •5.3.5.2 Complications
- •5.4.1 Terminology
- •5.4.2 Imaging
- •5.4.2.1 Conventional Ultrasound Findings
- •5.4.2.2 Contrast Enhanced Ultrasound Findings
- •5.4.2.3 CT Findings
- •5.4.2.4 MRI Findings
- •5.4.2.5 Other Imaging Findings
- •5.4.2.6 Best Imaging Protocol Advices
- •5.4.3.1 Hepatocellular Carcinomas
- •5.4.3.2 Metastases
- •5.4.3.3 Hemangioma
- •5.4.4 Pathology
- •5.4.4.1 General Features
- •5.4.5 Clinical Issues
- •5.4.5.1 Presentation
- •5.4.5.2 Prognosis
- •5.4.5.3 Treatment
- •References
- •6: Rare Malignant Liver Tumors
- •6.1 Hepatic Lymphoma
- •6.1.1 Terminology
- •6.1.2 Imaging
- •6.1.2.1 Conventional Ultrasound Findings
- •6.1.2.2 Contrast Enhanced Ultrasound Findings
- •6.1.2.3 CT Findings
- •6.1.2.4 MRI Findings
- •6.1.2.5 Other Imaging Findings
- •6.1.2.6 Best Imaging Protocol Advices
- •6.1.4 Pathology
- •6.1.4.1 General Features
- •6.1.5 Clinical Issue
- •6.1.5.1 Presentation
- •6.1.5.2 Prognosis
- •6.1.5.3 Treatment
- •6.2.1 Terminology
- •6.2.2 Imaging
- •6.2.2.1 General Features
- •6.2.2.2 Conventional Ultrasound Findings
- •6.2.2.3 Contrast Enhanced Ultrasound Findings
- •6.2.2.4 CT Findings
- •6.2.2.5 MRI Findings
- •6.2.2.6 Other Imaging Findings
- •6.2.2.7 Imaging Recommendations
- •6.2.4 Pathology
- •6.2.4.1 General Features
- •6.2.5 Clinical Issues
- •6.2.5.1 Presentation
- •6.2.5.2 Prognosis
- •6.2.5.3 Treatment
- •6.3.1 Terminology
- •6.3.2 Imaging
- •6.3.2.1 Conventional Ultrasound Findings
- •6.3.2.3 Computed Tomography Findings
- •6.3.2.4 Magnetic Resonance Imaging Findings
- •6.3.2.5 Nuclear Medicine Findings
- •6.3.2.6 Imaging Recommendations
- •6.3.3.1 Focal Nodular Hyperplasia
- •6.3.3.2 Hepatocarcinoma
- •6.3.3.4 Hepatoadenoma
- •6.3.3.5 Intrahepatic Cholangiocarcinoma
- •6.3.4 Pathology
- •6.3.4.1 General Features
- •6.3.5 Clinical Issues
- •6.3.5.1 Presentation
- •6.3.5.2 Prognosis
- •6.3.5.3 Treatment
- •6.4 Hepatic Biliary Cystadenocarcinoma
- •6.4.1 Terminology
- •6.4.2 Imaging
- •6.4.2.1 Conventional Ultrasound Findings
- •6.4.2.2 Contrast Enhanced Ultrasound Findings
- •6.4.2.3 CT Findings
- •6.4.2.4 MRI Findings
- •6.4.2.5 Other Imaging Findings
- •6.4.2.6 Best Imaging Protocol Advices
- •6.4.3.1 Hepatic Biliary Cystadenoma
- •6.4.3.2 Simple Hepatic Cysts
- •6.4.3.3 Hemorrhagic Hepatic Cysts
- •6.4.3.4 Metastatic Tumor
- •6.4.3.5 Hepatic Abscesses
- •6.4.3.6 Hydatid Disease
- •6.4.3.9 Mesenchymal Hamartoma
- •6.4.4 Pathology
- •6.4.4.1 General Features
- •6.4.5 Clinical Issues
- •6.4.5.1 Presentation
- •6.4.5.2 Prognosis
- •6.4.5.3 Treatment
- •6.5 Neuroendocrine Neoplasm
- •6.5.1 Terminology
- •6.5.2 Image
- •6.5.2.1 Ultrasonographic Findings
- •6.5.2.2 Contrast Enhanced Ultrasound Findings
- •6.5.2.3 CT Findings
- •6.5.2.4 MR Findings
- •6.5.2.5 Other Imaging Finding
- •6.5.2.6 Best Imaging Protocol Advices
- •6.5.3.1 Hepatocellular Carcinoma
- •6.5.3.2 Metastatic Hepatic Carcinoma
- •6.5.4 Pathology
- •6.5.4.1 General Features
- •6.5.5 Clinical Issues
- •6.5.5.1 Presentation
- •6.5.5.2 Prognosis
- •6.5.5.3 Treatment
- •6.6.1 Terminology
- •6.6.2 Imaging
- •6.6.2.1 Conventional Ultrasound Findings
- •6.6.2.2 Contrast Enhanced Ultrasound Findings
- •6.6.2.3 CT Findings
- •6.6.2.4 MRI Findings
- •6.6.2.5 PET/CT Findings
- •6.6.2.6 Best Imaging Protocol Advices
- •6.6.3.1 Hepatocellular Carcinoma
- •6.6.3.2 Cholangiocarcinoma
- •6.6.3.3 Metastatic Liver Cancer
- •6.6.4 Pathology
- •6.6.5 Clinical Issues
- •References
- •7: Rare Benign Liver Tumors
- •7.1 Hepatic Angiomyolipoma
- •7.1.1 Terminology
- •7.1.2 Imaging
- •7.1.2.1 Conventional Ultrasound Findings
- •7.1.2.2 Contrast Enhanced Ultrasound Findings
- •7.1.2.3 CT Findings
- •7.1.2.4 MRI Findings
- •7.1.2.5 Other Imaging Findings
- •7.1.2.6 Best Imaging Protocol Advices
- •7.1.4 Pathology
- •7.1.4.1 General Features
- •7.1.5 Clinical Issues
- •7.1.5.1 Presentation
- •7.1.5.2 Prognosis
- •7.1.5.3 Treatment
- •7.2 Hepatic Biliary Cystadenoma
- •7.2.1 Terminology
- •7.2.2 Imaging
- •7.2.2.1 Conventional Ultrasound Findings
- •7.2.2.2 Contrast Enhanced Ultrasound Features
- •7.2.2.3 CT Findings
- •7.2.2.4 MRI Findings
- •7.2.2.5 Other Imaging Findings
- •7.2.2.6 Best Imaging Protocol Advices
- •7.2.3.1 Hepatic Biliary Cystadenocarcinoma
- •7.2.3.2 Simple Hepatic Cyst
- •7.2.3.3 Hemorrhagic Hepatic Cysts
- •7.2.3.4 Metastatic Tumor
- •7.2.3.5 Hepatic Abscesses
- •7.2.3.6 Hydatid Disease
- •7.2.3.9 Mesenchymal Hamartoma
- •7.2.4 Pathology
- •7.2.4.1 General Features
- •7.2.5 Clinical Issues
- •7.2.5.1 Presentation
- •7.2.5.2 Prognosis
- •7.2.5.3 Treatment
- •References
- •8: Hepatic Parasitosis
- •8.1 Terminology
- •8.1.1 Echinococcosis
- •8.1.2 Amebiasis
- •8.1.3 Schistosomiasis
- •8.2 Imaging
- •8.2.1 Conventional Ultrasound Findings
- •8.2.1.1 Echinococcosis
- •8.2.1.2 Amebiasis
- •8.2.1.3 Schistosomiasis
- •8.2.2 Contrast Enhanced Ultrasound Findings
- •8.2.2.1 Echinococcosis
- •8.2.3 CT Findings
- •8.2.3.1 Echinococcosis
- •8.2.3.2 Amebiasis
- •8.2.3.3 Schistosomiasis
- •8.2.4 MRI Findings
- •8.2.4.1 Echinococcosis
- •8.2.4.2 Amebiasis
- •8.2.4.3 Schistosomiasis
- •8.2.5 Other Imaging Findings
- •8.2.5.1 Echinococcosis
- •8.2.6 Best Imaging Protocol Advices
- •8.2.6.1 Echinococcosis
- •8.2.6.2 Amebiasis
- •8.2.6.3 Schistosomiasis
- •8.3 Pathology
- •8.3.1 General features
- •8.3.1.1 Echinococcosis
- •8.3.1.2 Amebiasis
- •8.3.2.1 Echinococcosis
- •8.4 Clinical Issues
- •8.4.1 Presentation
- •8.4.1.1 Echinococcosis
- •8.4.1.2 Amebic Liver Abscess
- •8.4.1.3 Schistosomiasis
- •8.4.2 Prognosis
- •8.4.2.1 Echinococcosis
- •8.4.2.2 Amebiasis
- •8.4.2.3 Schistosomiasis
- •8.4.3 Treatment
- •8.4.3.1 Echinococcosis
- •8.4.3.2 Amebiasis
- •8.4.3.3 Schistosomiasis
- •References
- •9: Hepatic Inflammatory Pseudotumor
- •9.1 Terminology
- •9.2 Imaging
- •9.2.1 Conventional Ultrasound Findings
- •9.2.2 Contrast Enhanced Ultrasound Findings
- •9.2.3 CT Findings
- •9.2.4 MRI Findings
- •9.2.5 Other Imaging Findings
- •9.2.6 Best Imaging Protocol Advices
- •9.3.1 Hepatocellular Carcinoma
- •9.3.2 Liver Metastasis Tumor
- •9.3.3 Intrahepatic Cholangiocarcinoma
- •9.3.4 Liver Abscess
- •9.4 Pathology
- •9.4.1 General Features
- •9.5 Clinical Issues
- •9.5.1 Presentation
- •9.5.2 Prognosis
- •9.5.3 Treatment
- •References
- •10: Hepatic Artery Aneurysm
- •10.1 Terminology
- •10.2 Hepatic Artery Aneurysm
- •10.3 Imaging
- •10.3.1 General Features
- •10.3.2 Radiographic Findings
- •10.3.3 DSA Findings
- •10.3.4 CT Findings
- •10.3.5 Conventional Ultrasound Findings
- •10.3.7 MRI Findings
- •10.3.8 Best Imaging Protocol Advices
- •10.3.9 Protocol Advice
- •10.5 Pathology
- •10.5.1 General Features
- •10.6 Clinical Issues
- •10.6.1 Presentation
- •10.6.2 Prognosis
- •10.6.3 Treatment
- •References
- •11: Peliosis Hepatis
- •11.1 Terminology
- •11.2 Imaging
- •11.2.1 Conventional Ultrasound Findings
- •11.2.2 Contrast Enhanced Ultrasound Findings
- •11.2.3 CT Findings
- •11.2.4 MRI Findings
- •11.2.5 Other Imaging Findings
- •11.2.6 Best Imaging Protocol Advices
- •11.3.1 Hepatic Adenoma
- •11.3.2 Hemangioma
- •11.3.3 Focal Nodular Hyperplasia
- •11.3.4 Hepatic Abscess
- •11.3.5 Hypervascular Metastases
- •11.3.6 Hepatocellular Carcinoma
- •11.3.7 Arteriovenous Malformations
- •11.4 Pathology
- •11.4.1 General Features
- •11.5 Clinical Issues
- •11.5.1 Presentation
- •11.5.2 Prognosis
- •11.5.3 Treatment
- •References
- •12.1 Introduction
- •12.8 Summary
- •References
- •References
- •14.1 Introduction
- •14.2 Indications
- •14.3 Equipment
- •14.4 3D-CEUS Procedures
- •14.5 Clinical Application
- •References
- •15: Future Prospects
- •15.2 Improved Liver Metastasis Detection (Sonazoid)
- •References

210
F. Mao et al.
8.2.6.2 Amebiasis
– The conclusive diagnosis is made by the detection of
serum antibodies to the amoeba with a combination of
image ndings.
8.2.6.3 Schistosomiasis
– Diagnosis is based on the nding of living eggs in stool
examination or positivity on serologic test.
8.3 Pathology
8.3.1 General features
8.3.1.1 Echinococcosis
• E. granulosus (causes CE) [13]
– Most common species
– Solitary in single organ involvement, 70% in liver,
25% in lungs
– Cyst enlarges 1–5cm per year, lled with clear uid
– Often with daughter cysts, inside which may merge
internal septation
– Three layers consist the wall of cyst under
microscopy
External layer is a peri-parasitic host tissue layer
that encompasses the larval endocyst, inltrated
with chronic inammatory cells, where variable
calcication may occur.
Laminated layer, the outer layer of the endocyst, is
1mm thick, avascular, eosinophilic, refractile, and
chitinous; strongly PAS+, GMS+.
Germinative layer, the innermost layer, gives rise to
brood capsules that enlarge to form protoscolices,
the separated capsules from the wall thus form a
sediment called “hydatid sand.”
• E. multilocularis (causes AE) [13]
– Less common and slower growing than that of E.
granulosus.
– Restricted to the cool region of Northern Hemisphere.
– Liver is the most affected initial organ (99% of cases),
maybe followed by metastasis or invasion to other
organs.
– Tissue invasion may simulate malignancy in each
focus.
– Foci with alveolar structure consisted of numerous
irregular small cysts in 1–20mm inltrative into adja-
cent tissue, with calcication and necrosis.
– cyst with a thinner peri-cystic rim and laminated layer
compared to E. granulosus, usually with no germinal
layer under microscopy.
8.3.1.2 Amebiasis
• Macroscopically, the hepatic amebic abscess is identied
as a well-delineated area lled with necrotic tissue of yellowish or creamy consistency [11].
• A rind of congested hepatic tissue surrounds the abscess.
• The necrotic materials can be solid, semi-liquid, sometimes containing mucus [11].
• The size of a hepatic abscess is variable, ranging from 5
to 15cm in diameter [11].
8.3.2 Staging, Grading, andClassication
8.3.2.1 Echinococcosis
• The World Health Organization Informal Working Group
on Echinococcosis (WHO-IWGE) classication of Cystic
Echinococcosis. In this classication, six cyst stages have
been assigned to three clinical groups:
– The “active” group includes developing cysts, which
may be unilocular (CE1) or multivesicular with daughter
vesicles (CE2) and which are usually found to be
viable.
– The “transitional” group (CE3) includes both cysts
with detachment of endocyst (CE3a) and predominantly solid cysts with daughter vesicles (CE3b).
– The “inactive” group (CE4 and CE5) exhibits involu-
tion and solidication of cyst content with increasing
degrees of calcication and is nearly always found to
be non-viable [9].
8.4 Clinical Issues
8.4.1 Presentation
8.4.1.1 Echinococcosis
• Clinical manifestation
– Asymptomatic for more than 10 years in slow-growing
cases [12].
– Depending on the size and location of lesion, epigas-
tric discomfort, chronic cough caused by mass effect
are often observed. Late phase of AE often presents
like malignant liver tumor causing liver dysfunction
and metastasis [12].

8 Hepatic Parasitosis
211
– Complications caused by rupture of cysts include bili-
ary obstruction and bronchi stulae, bacterial infection, and anaphylaxis [12].
• Laboratory
– Hydatid uid is the major antigenic source for echino-
coccosis immunodiagnosis, lipoproteins antigen B
(AgB), and antigen 5 widely used in serological assays
for CE, AE serology is more reliable on E. multilocu-
laris antigens (Em2 and Em492) [12].
8.4.1.2 Amebic Liver Abscess
• Clinical manifestation
– Right upper abdomen pain, fever, and hepatomegaly
are the predominant symptoms of hepatic amebiasis
[2].
– Jaundice is reported in cases with multiple lesions or a
very large abscess.
– Some important complications may occur as a result of
perforation.
– Pulmonary abscesses.
– Purulent pericarditis.
– Subphrenic abscesses and peritonitis.
• Laboratory
– A mild degree of anemia or leukocytosis is present.
– Serological methods include enzyme-linked immuno-
sorbent assay (ELISA), indirect hemagglutination
assay (IHA), and latex agglutination.
– The ELISA test for detection of the galactose-
inhibitable adherence protein of E. histolytica in serum
and feces appears to be the most reliable and sensitive
serology test.
8.4.1.3 Schistosomiasis
• Clinical manifestation
– Acute schistosomiasis is seldom recognized [14].
– Right after exposure, patients frequently complain of
itching that is caused by skin penetration by larvae
[14].
– Several weeks later, patients may complain of a variety
of symptoms including fever, chills, headache, hives,
or diarrhea [14].
– With diminishing of acute symptoms, the condition
moves into chronic process, with liver cirrhosis and
granulomatous inammation in the urinary tract and
lungs [14].
– The most important complication is periportal or
Symmers pipestem brosis of the liver, resulting in
splenomegaly and gastroesophageal varices [14].
• Laboratory
– The denitive diagnosis for a schistosome infection is
made by microscopic detection of eggs in stool (for S.
mansoni and S. japonicum) or urine (for S. haematobium) samples [14].
– Antigen tests use two proteoglycans, circulating anodic
antigens (CAAs) and circulating cathodic antigens
(CCAs) that can be detected in serum and in urine.
– Genomic tests targeting schistosome DNA sequences
enable a species-specic diagnosis [14].
8.4.2 Prognosis
8.4.2.1 Echinococcosis
• Curative treatment is achieved by the complete removal
of the cyst, CE has a better prognosis than AE [12].
• Because of the complications, prognosis ranges widely [12].
• While in general, the earlier the treatment, the lower the
grade of the mass, the less the number, and the smaller the
volume, the better the prognosis [12].
8.4.2.2 Amebiasis
• Amebicidal drugs are effective therapy.
• The time for termination of therapy varies from 1.5 to 23
months (median, 7 months).
• A residual hepatic cysts or focal regions may exist in
curative cases.
8.4.2.3 Schistosomiasis
• Curative rates of Praziquantel (PZQ) reach to 60–90% [14].
• While, re-infection is also a problem in endemic regions [14].
• The complication resulted from liver cirrhosis and urinary
bladder granulomatous inammation may affect the longterm prognosis of patients [14].
8.4.3 Treatment
8.4.3.1 Echinococcosis
• For CE, an image-based, stage-specic approach is help-
ful for choosing one of the following options: (1) percutaneous treatment, (2) surgery, (3) anti-infective drug
treatment, or (4) watch and wait [12].

212
F. Mao et al.
• For AE, early diagnosis and radical surgery remain one of
the key elements. However, most patients with AE are
diagnosed at a later stage, thus the backbone of AE treatment remains the continuous medical treatment [12].
8.4.3.2 Amebiasis
• The treatment of hepatic amebiasis is made by medical
therapy, with metronidazole as the initial drug, followed
by a luminal amebicide.
• In patients with large abscesses, and especially those with
no response to medical treatment, percutaneous drainage
must be performed under ultrasound or computerized
tomography guidance.
• Surgical drainage by laparotomy is reserved for patients
with secondary infections.
8.4.3.3 Schistosomiasis
• WHO recommends that PZQ be used at a single dose of
40mg/kg [14].
• Multiple features have made PZQ the drug of choice for
treating schistosomiasis, including [14]:
– It is effective against all the three major species, S.
mansoni, S. haematobium, and S. japonicum.
– It can be given as a single oral dose and is usually well
tolerated.
– Its relatively low cost.
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Hepatic Inflammatory Pseudotumor
YiDong, Pei-LiFan, andWen-PingWang
9
9.1 Terminology
• Inammatory pseudotumor of the liver (IPT) is a rare
benign lesion composed of brous tissue, lymphocytes,
histiocytes, and plasma cells.
• It was once described as an inammatory myobroblastic
tumor, histiocytoma, plasma cell granuloma, and
broxanthoma.
• Without specic clinical and imaging features, IPT is
often misdiagnosed as hepatic malignant tumors [1].
9.2 Imaging
9.2.1 Conventional Ultrasound Findings
• Conventional B mode ultrasound manifestation of IPT
varies in different lesions.
• Generally, most lesions show a heterogeneous hypoechoic
mass with an irregular shape, without acoustic enhancement behind (Fig.9.1).
• The common and specic imaging of IPT shows a well-
circumscribed hypoechoic mass with a dumbbell shape
(Fig.9.2).
• Color ow imaging can only detect blood signals at the
inammatory zone, because necrosis occurs inside the
lesions frequently (Fig.9.3).
• There are several types of IPT on contrast enhanced ultrasound (CEUS), including diffuse homogeneous hyperenhancement (Figs. 9.1 and 9.4), diffuse heterogeneous
hyperenhancement (Fig. 9.3), peripheral rim-like
enhancement, and diffuse isoenhancement (Fig. 9.5) in
arterial phase.
• Most IPT nodules show hypoenhancement during portal
venous and late phases (Figs.9.3, 9.4, 9.5, 9.6, and 9.7).
• Nonenhancement of the entire lesion at all phases is specic, which makes it easy to diagnose coagulative necrosis inside the lesions (Fig.9.8). Sometimes, a slim rim-like
hyperenhancement surrounding the lesion can be observed
in the arterial phase (Fig.9.2). Nowadays, such lesion is
called solitary necrotic nodule of the liver, pathologically
characterized by central necrotic core enclosed by a hyalinized brotic tissue containing elastic bers with inammatory cells.
• When it comes to the wash-in and wash-out patterns,
some IPT lesions with arterial hyperenhancement show
rapid wash-in and wash-out, while some IPT lesions show
quickly wash-in and slowly wash-out (Fig.9.9) [2].
• Centrifugal wash-out is of high diagnostic ability in differentiating IPTs from hepatocellular carcinomas
(Figs.9.1 and 9.6).
9.2.3 CT Findings
• IPT can manifest various patterns on images according to
9.2.2 Contrast Enhanced Ultrasound Findings
• Different lesions have different presentation enhancement
patterns due to different ratios of histological components
at different processes of inammatory.
Y. Dong (*) · P.-L. Fan · W.-P. Wang
Department of Ultrasound, Zhongshan Hospital, Fudan University,
Shanghai, China
e-mail: dong.yi@zs-hospital.sh.cn; fan.peili@zs-hospital.sh.cn
© The Author(s), under exclusive license to Springer Nature Singapore Pte Ltd. 2021
W.-P. Wang et al. (eds.), Contrast-Enhanced Ultrasound Imaging of Hepatic Neoplasms,
https://doi.org/10.1007/978-981-16-1761-4_9
different degrees of brosis and cellular inltration.
• Most tumors show low density on unenhanced CT, and
heterogeneously enhancement or peripheral delayed
enhancement in the arterial phase [3].
213

214
a
Y. Dong et al.
b
c
e
d
f
Fig. 9.1 A case of inammatory pseudotumor of the liver (IPT).
Multiple irregular heterogeneous hypoechoic lesions were detected
both in right lobe (a) and in left lobe (b) of liver on B mode ultrasound.
Dotted color ow signals could be detected inside the lesions (c).
Arterial Doppler spectrum with moderate resistance index (RI) as 0.64
was measured (d). The lesion showed homogeneous hyperenhancement
with a vague margin in arterial phase (e, f) followed by centrifugal
wash-out in portal and late phases (g, h, i) (arrow). This case was conrmed by surgery and histopathological results (j)

9 Hepatic Inammatory Pseudotumor
215
g
h
ji
Fig. 9.1 (continued)
9.2.4 MRI Findings
• On MRI, the lesions are hypointense on T1-weighted
images and isointense or heterogeneous hyperintense on
T2-weighted images.
• Peripheral enhancement without central enhancement is a
specic enhancement pattern of IPTs.
• During dynamic contrast enhanced MRI, most lesions
progressively or persistently enhance.
• The lesions show diffuse homogeneous or heterogeneous
hyperenhancement with delayed capsule-like enhancement without central enhancement.
• On DWI, all lesions are hyperintense in various degrees.
9.2.5 Other Imaging Findings
• FDG-PET sometimes confuses IPT with liver malignant
tumors.
• Some studies have reported that IPT shows high dose
uptake of FDG mimicking HCC lesions [4]. FDG uptake
can be observed in various diseases, not specic to liver
malignancies.
• IPT could show various manifestations on FDG-PET.
9.2.6 Best Imaging Protocol Advices
• The history and imaging manifestation of IPT is
nonspecic.
• In clinical practice, IPT cannot be discriminated from
malignant tumors.
• The following features are useful to make a diagnosis for
IPT.
– No enhancement of the entire tumor is observed.
– The IPT lesion has an irregular shape or a dumbbell
shape.

216
a
e
Y. Dong et al.
b
c
d
f
Fig. 9.2 A case of inammatory pseudotumor of the liver (IPT). A
hypoechoic lesion with dumbbell shape was detected in the right lobe
of liver (a). No ow signal could be detected in the lesion (b). The
lesion showed slim rim-like hyperenhancement surrounding the lesion
in the arterial phase (c), suggesting a hyalinized brotic tissue containing elastic bers with inammatory cells. The lesion showed nonenhancement at all phases (d, e, f), and the dumbbell shape of the lesion
was extremely clear in the late phase (f)

a
f
e
9 Hepatic Inammatory Pseudotumor
217
b
c
d
Fig. 9.3 A case of heterogeneous hypoechoic inammatory pseudotumor (IPT) lesion was detected on B mode ultrasound (a). Dotted color
ow signals could be detected in the periphery of the lesion (b). The
lesion showed heterogeneous hyperenhancement in arterial phase (c),
with multiple non-enhanced areas inside (d). During portal venous
phase, the lesion showed rapid wash-out and manifested hypoenhancement (e, f)

218
e
Y. Dong et al.
a
c
b
d
f
g
h
Fig. 9.4 A case of inammatory pseudotumor of the liver (IPT). A
hypoechoic heterogeneous focal liver lesion with a vague margin was
detected in the right lobe of liver (a). Dotted color ow signals could be
detected in the peripheral area of the lesion (b). The lesion showed heterogeneous hyperenhancement in arterial phase (c). When reaching the
peak enhancement, the enhanced area of lesion was larger than that on
B mode ultrasound (d, e). The lesion showed early wash-out at 27s
injection of contrast agents (f). During portal venous phase (g) and late
phase (h), the lesion showed hypoenhancement

a
e
9 Hepatic Inammatory Pseudotumor
219
b
c
d
f
Fig. 9.5 A case of heterogeneous hypoechoic inammatory pseudotumor of the liver (IPT) lesion with a vague margin and an irregular shape
was detected in the left lobe of liver (arrow) (a). The lesion showed
isoenhancement in the arterial phase (b, c) followed by wash-out in the
portal venous and late phase (arrow) (e, f). The shape and margin of the
lesion was much clearer in the late phase (arrow) (f)
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