IMAGING OF

HEPATIC TUMOURS

Speaker: Dr Sharma (PG)

Moderator: Dr Jatishwor Singh (HOD)
 INTRODUCTION
 Liver tumors can be divided into
nonneoplastic and neoplastic.
 They can be either hepatocellular,
cholangiocellular, Mesenchynal or other
miscellenous catogory.
 The aim of this seminar is to have a
overview of hepatic tumours , imaging
features and to highlight recent
advances in this field.
 Embryology of liver
 The liver primordium (third week)- appear
as outgrowth of the endodermal epithelium
at the distal end of the foregut.
 The hepatic diverticulum or liver bud,
consists of rapidly proliferating cells that
penetrate the septum transversum, which
forms Hematopoietic cells, Kupffer cells,
and connective tissue cells.
 Epithelial liver cords intermingle with the
vitelline and umbilical veins, which form
hepatic sinusoids,parenchyma (liver cells)
and lining of the biliary ducts.
 FUNCTIONAL SEGMENTAL LIVER ANATOMY

GOLDSMITH & COUINAUD & BISMUTH

WIIDBURNE
CAUDATE CAUDATE 1
LEFT LOBE LEFT LATERAL SUP SUBSEGMENT 2
SEGMENT
INF SUBSEGMENT 3
LEFT MEDIAL MED SUP SUBSEGMENT 4
SEGMENT A
MED INF SUBSEGMENT 4
B
RIGHT LOBE RIGHT ANTERIOR ANT INF SUBSEGMENT 5
SEGMENT
ANT SUP SUBSEGMENT 8
RIGHT POSTERIOR POST INF SUBSEGMENT 6
SEGMENT
Vascular Distribution
 Imaging Techniques
 X-RAYS
 ULTRASOUND
Plain, Contrast , Doppler.
 COMPUTED TOMOGRAPHY SCAN (MDCT)
PLAIN, CONTRAST
 MR IMAGING- PLAIN,CONTRAST,MRA,
MRCP.
 RADIONUCLEIDE IMAGING.
 Miscellenous- Angiography , Contrast oil
injection etc
 Ultrasonography
 Ultrasound - Commonest, safest and most
widely used.
 Introduction of microbubbles contrast like
Livovist & perflurocarbon increased both
sensitivity and specificity of detecting focal
liver tumors.
 Microbubble persist in liver within kupffer
cells, producing bright enhancement.
Liver metastasis lacking kupffer cell will
not enhance.
 Overall lesion detection for USG equivalent
to CT/MRI.
 NCCT
 Not routinely done.
 May be used for identification of
calcification, hemorrhage, iron deposition,
or determination of precontrast
attenuation.
 Also used for some neoplasm which
become isoattenuated on postcontrast
study.
 Single phase contrast CT
 Bolus contrast enhanced CT, with
imaging in peak hepatic parenchymal
enhancement (PV Phase).
 Injection 125-150 ml 350mgI/ml
contrast, followed by saline flush 20-
50ml @ 3ml/sec is adequate.
 Most useful for routine depection of liver
abnormalities like focal lesions.
 Multiphase CT
 Useful in detection of hypervascular mass,
characterization of liver mass, and
preoperative planning.
 Best performed on MDCT.
 Image acquisation- Early arterial phase
(25 sec) , Late hepatic arterial phase(35-
40 s), and Portal venous phase (60-75
sec)
 125-150ml contrast @5ml/sec.
 In Arterial phase hypervascular tumors
enhances via HA ,in a relatively hypodense
liver.
 In Portal venous phase , hypovascular
tumors are detected, when the normal liver
parenchyma enhances maximally and
tumors will be hypodense lesions.
 In Equilibrium phase, at about 10 minutes
after contrast injection, tumors either lose
their contrast slower than normal
liver(hyperdense), or wash out their
contrast faster than normal liver
parenchyma(hypodense).
Cholangiocarcinoma – AP, PVP & EP.
Delayed/prolonged Enhancement.
 Tailored CT protocol
single slice scanner-take about 20 seconds to scan the liver.
64-slice scanner-examine the whole liver in 4 seconds
 Angiography assisted CT
 CT hepatic angiography-With catheter in
hepatic artery or celiac axis.
 CT arterial portography- catheter in SMA
or splenic artery.
They are Replaced by newer advances in
MDCT and MRI.
 CT 1-4 wk after iodized oil inj. into HA is
used to detect small HCC. Oil is rapidly
cleared by normal hepatic RE system
within 1wk, but retained in vascular
hepatic neoplasm, as hyperdense mass.
 MRI- Plain
 T1,T2 and GRE sequences.
 Most tumours are SI in T1 w seq (except
for fat containing lesion and MM)
 On T2 most masses are hyperintense.
 Other sequences used- Fat supressed,
STIR, HASTE etc.
 Contrast MRI
 GD chelates- shorten t1 and t2 relxn. So
cause enhancement of t1.
 SPIO contrast-taken selectively by RES,
causes profound t2 shortening and normal
hepatic signal loss. Tumour uptake
depends on presence of kupffer cells.
 Double contrast GD + SPIO has increased
sensitivity for HCC in cirrhosis.
 Mn-DPDP-T1 shortening agents taken up
by hepatocytes. Better for metastasis.
 Benign Liver tumors
Nonneoplastic Neoplastic Potential
Hepatocellular Necrotic nodule Hepatocellular adenoma
origin Focal nodular hyperplasia
Nodular regenerative
hyperplasia
Regenerative nodule.
Cholangiocellul Simple cyst Adenoma
ar origin Polycystic liver disease Cystadenoma
Intrahepatic choledochal cyst
Mesenchymal Inflammatory tumor Hemangioma
origin Hemangioendothelioma Lymphangioma,Lipoma
Angiomyolipoma
Fibroma
Neuroendocrine tumors
Other Hamartoma, Teratoma
Extramedullary hematopoiesis
 Malignant Neoplasms
 Hepatocellular Carcinoma
 Fibrolamellar Hepatocellular Carcinoma
 Hepatocellular Carcinoma with Sarcomatous
Changes
 Cholangiocarcinomas
 Adenosquamous/Squamous Carcinoma
 Lymphoma
 Hepatoblastoma
 Sarcoma
 Metastases
 Neoplasm in infants
 Benign
Adenoma
Hemangioendothelioma
 Malignant
Hepatoblastoma
Hepatocellular carcinoma
Metastases
Neuroblastoma
Lymphoma
Leukemia
Sarcoma
Rhabdomyosarcoma
Teratocarcinoma
 Simple Cysts
 Developmental cysts accounts for 5-14%.
solitary or multiple with single epithelial lining.

 Polycystic liver disease- assd with PCKD.

D/T ductal plate malformation. Varying sizes. Imaging- cystic lesions.

 USG-anechoic, well-defined smooth capsule and exhibits posterior

enhancement

 CT- circumscribed near water attenuation. No enhancement. MRI- T1 T2

Non enhancing.

 Complication-rare. Hemorrhage, Rupture

Simple cyst.
 Complex cysts
 May have
solid nodules,
thickened walls,
hemorrhages,
Septations,
Internal echo,
Calcification etc
M Nodule
Biliary Hamartoma(von Meyenburg complex)
 Dilated biliary duct with variable amount
of fibrous stroma.
 Arise from embryonic bile duct that fail
to involute.
 CT- small hypoattenuating cyst like
structures with little or no enhancement.
 MRI- multiple small lesions of cystic SI.
Most do not enhance, but some show
internal enhancement d/t compressed
hepatic parenchyma.
Biliary Hamartoma
 Peribiliary cyst.
 Cystic dilatation of obstructed periductal
gland adjacent to large I/H or E/H bile
duct.
 If extensive, a string-of-beads
appearance is evident.
 Usually asymptomatic.
 Imaging- discrete, clustered, cystic
structure with thin septa paralleling bile
duct & central portal vein.
Peribiliary cyst- along bile
ducts.
 Adult Cavernous Hemangioma
 Most common liver tumor in adults. Occurs
at all ages. Typically <3cm.
 Predominate in the posterior segment of
the right lobe. Occasional patient develops
multiple hemangiomas. Diffuse
hemangiomatosis is rare.
 Most hemangiomas are asymptomatic and
discovered incidentally.
 Giant hemangiomas (>4cm)can have
unusual findings, like portal vein
obstruction & tend to contain central scar.
Ultrasonography-
 Homogeneous, well marginated, and hyperechoic
tumor(70%).
 Less often- hyperechoic rim of varying thickness
with isoechoic or even hypoechoic center , post.
acoustic enhancement , nonhomogenous centre,
or scalloped margins may be seen.
 Blood flow velocity is usually slow & Doppler US
is noncontributory.
 Microbubble-enhanced US- In AP, bright
peripheral puddles and pools seen. With time
centripetal progression with sustained
enhancement in PVP. Delayed washout is
common.
Hemangioma- hyperechoic tumor, AP( rim
enhancement),delayed 142 sec (central fill-in).
 CT-
 Hypodense to liver and isodense to blood. A
fibrotic component or thrombosis lowers CT
density.
 Postcontrast- irregular, nodular peripheral
enhancement pattern during the arterial
phase. Enhancement from the periphery
toward the center, a prolonged tumor blush,
vascular lakes, and delayed contrast washout.
 Smaller ones are round diffusely enhancing
while larger ones tend toward an oval or
lobular shape.
 Central scarring- Causes incomplete central
opacification.
Hemangioma
NECT, late arterial, late portal venous
and equilibrium phase.
 MRI
 Most hemangiomas - Hypointense on
precontrast T1, Hyperintense in T2.
 Small hemangiomas-uniform enhancement,
and larger ones usually show peripheral
nodular enhancement progressing to
uniform centripetal enhancement.
 Large tumors tend to maintain a persistent
central hypointensity.
 Most hemangiomas increase lesion to- liver
contrast on ferumoxides-enhanced T2-
weighted MR images.
Hemangioma.
T2-w ( hyperintense ) &
T1-w FSE MRI(hypointense)
 Scintigraphy
 Both planar and SPECT Tc-99m–red blood
cell imaging have high sensitivity and
specificity in differentiating cavernous
hemangiomas from other liver tumors.
 Early perfusion phase Tc-99m–red blood
cell scintigraphy shows a focal photopenic
defect that gradually fills-in in a
centripetal manner. A perfusion/ blood-
pool mismatch is the hallmark.
 Technetium-99m–sulfur colloid and
hepatobiliary scintigraphy-- filling defect.
 Infantile Hemangioma
 Especially assd with Kasabach-Merritt
syndrome.
 More common in girl and tends to be
multiple. With age, these tumors tend to
involute with few sequelae.
 Large hemangiomas in T2-weighted MRI
appear hyperintense nodules containing fast
flow flow voids and hyperintense tumors on
GRE images.
 Early rim enhancement after gadolinium,
with progressive fill-in on delayed imaging
 Regress after interferon-a-2a therapy.
 FOCAL NODULAR HYPERPLASIA
 2nd MC hepatic benign tumour.
 Mostly in young women. Majority < 5cm.
 Solitary in 75-80%. Typically subcapsular.
 Usually nonencapsulated.
 Along with hepatocyte, BV, BD, and
kupffer cell, they contain central or
eccentric fibrous scar with spoke-wheel
radiating fibrous bands.
 USG
 Subtle contour abnormality(stealth lesion) and
displacement of vascular structure.
Echogenicity may vary from hypo to
hyperechoic rarely.
 Central scar- hypoechoic linear or stellate area.
 Doppler- blood vessels can be seen coursing
within central scar.
 Microbubble contrast-

AP-hypervascular with stellate lesional vessels

and tortuous feeding artery.
PVP- Sustained enhancement with unenhanced
central scar.
FNH-
Isoechoic, microbubble contrast ‘spoked-wheel’ pattern &
central scar.
 CT
 Homogenous iso/slight hypoattenuating.
 1/3rd cases,well def. hypoattenuating scar.
 Prominent vasc supply marked enhancement
in AP (homogenous except for scar and septa).
 Hepatic parenchymal phase– Iso attn.
 Delayed image- pseudocapsule
enhancement( compressed hepatic tissue).
 Fibrous scar- Hypo attn (AP), Enhance on
delayed images.
 50% FNH takes up sulfur colloid in sulfur
scanning and 10% becomes “hot”.
FNH with central scar-NECT, PVP and
Equilibrium phase
 MRI
 Unenhanced - similar to hepatic tissue. Iso/sl.
hypo t1, Iso/sl. Hyper t2.
 Central scar ½-¾ cases- hypo t1,hyper t2.
 Contrast-hyper (AP), Iso(PVP), scar
enhancement in delayed phases.
 Mn/t1 shortening Gd contrast- enhancement
in delayed image.
 SPIO- show signal loss.(lack specificity)
 Scintigraphy- rarely for confirmation of
diagnosis. FNH show sulfur colloic
concentration.
 Atypical features in 10-20%.
FNH- hypointense on T1and hyperintense on
T2. Enhances with contrast.
99 mTc-HIDA --prolonged retention of
tracer in the area of FNH.
 Hepatocellular adenoma
 Uncommon benign primary neoplasm.
 Encapsulated. Usually solitary. 8-15 cm.
 F>M, increase in OCP users. Regress or
disappear after OCP withdrawl.
 Can have spontanous hemorrhage.

 Adenomatosis- rare charecterised by

numerous hepatic adenomas. F>M. Do
not appear to be steroid dependent, and
do not regress on steroid withdrawl. Show
high risk of HCC.
 USG
 Nonspecific.
 Echogenicity hypo/hyper/iso/mixed.
 Paucity of central vascular structure.
 Microbubble contrast has limited utility.

 Majority are ‘cold’ on Tc-sulfur colloid

imaging.
 Adenomas are assd with glycogen
storage disease in childrens.
Adenoma
 CT-- variable

 Unenhanced- Hypo attn (lipid, old hrge,

necrosis) Hyper attn ( hrge, glycogen).

 Contrast- Moderate enhancement (AP &

early PVP). Homogenous enhancement if
uncomplicated.

 25% thin capsule seen- hypo attn (AP),

hyper attn (PVP).
Adenoma
 MRI
 Heterogeneous SI.
Majority- hyper t1(lipid/hrge), iso/hyper
t2.
 Capsule – low SI.

 Contrast GE seq- Usually hyperintense.

May be iso/hypo.

 SPIO- some show signal loss.

Hepatic adenoma - hypointense on T1,
hyperintense on T2 &inhomogeneous
contrast enhancement
 Angiomyolipoma
 Benign, unencapsulated mesenchymal
tumour.
 Contain SM,BV and adipose tissue.
 Vary in size. Solitary or multiple.
 USG-Well defined echogenic mass.
 CT- low attn lesion (<-20 HU)
 MRI– hyper T1, Hypo fat supression.
 Non fat component show early and
prolonged enhancement.
 Hepatocellular carcinoma
 90% primary hepatic malignancy.
 5th MC cancer worldwide. AFP raised.
 M>F, solitary/multifocal/diffuse.
 3 patterns- Nodular (mc)
Massive pattern.
Diffuse pattern.
 Expansive or invasive.
 Abnormal hepatocyte arranged in trabecular
sinusoidal pattern. Vascular tumour supplied by
hepatic A.
 Arterioportal shunting, spontanous hrge and
rupture may occur rarely.
 USG
 Variable. May be hypo/hyper or complex
echogenicity.
 Small<5cm-solid &hypoechoic. Thin
peripheral hypoechoic halo seen.
 Larger tumour becomes complex &
inhomogenous. Calcification rare.
 Doppler- High velocity flow &
neovascularity.
 Microbubble contrast- Hypervascular tmr
enhance in AP, ‘washout’ in PVP.
A) Exophytic HCC. (B) Multifocal HCC.
©nodular liver with suspicion of a lesion
(D) contrast in the same patient as ©
 CT
 Variable appearance.
 Mostly hypoattenuating. Some are
isoattenuating with hypo attng. capsule.
 Hyper attn- d/t hemorrhage.

Hypo attn- d/t necrosis , fatty changes.

 Calcification- 5-10%.
 Contrast– Transiently hyper attn. in HAP. But
20% appear hypo attn. in HAP. Fibrous
capsule remain unenhanced.
Small HCC are homogenous and larger lesions
are heterogenous.
 PV(parenchymal)Phase-
Isoattenuating. Rarely hypoattng.
Tumour capsule/septa- enhances.

 Delayed images(3-6mt)
Small percentage appear hypoattng.
Fibrosis, capsule or septa show
prolonged enhancement.
 CECT can demonstrate vascular invasion,
A-P shunting, tumour thrombus etc.
NECT and Arterial phase image showing
hypodense capsule of HCC
Multifocal hepatocellular carcinoma
(postcontrast)
 MRI
 Variable.
 T1- hypo/iso/hyper SI
 T2-hyperintense(70-90%). >3cm lesions
usually show hyperintensity.
 Capsule- appear hypointense rim in T1,
and in T2w.
Either single hypointense rim or double
layer peripheral band( inner low signal
fibrous tissue and outer high signal zone
of vessels and ducts).
 Internal Features:
Intratumoural septa- thin. Hypointense in t1
and t2 w seq.
Central scar – Low SI in T1. Low or high SI in
T2w.
 Contrast MRI

Peak enhancement from 10s to 2 min., with

absent or minimal delayed enhancement.
Most become isointense in PV Phase and
iso/hypo SI in equilibrium phase.
 Delayed Phase- washout of HCC(hypo SI) and
enhancement of capsule.
HCC-T1, T2 and Early contrast
 CT 1-4wk after i/a injection of iodized oil,
is capable of demonstrating small HCC
missed by noninvasive technique.

 CT arterial portography- sensitive for

small HCC. But With 50% failure for
setallite nodules.

 Double contrast MRI study- SPIO followed

by Gd contrast study improve detection of
HCC in cirrhosis Pt.
 TNM staging of liver cancer
Primary tumor: Lymph node Distant
Tx Cannot be assessed. involvement: metastasis:
T0 No evidence of primary tumor.
T1 Solitary tumor without vascular Nx Regional nodes Mx Distant
invasion. cannot be assessed metastasis
T2 Solitary tumor with vascular cannot be
invasion or multiple tumors, N0 No regional assessed
none >5cm. nodes involved
T3 Multiple tumors >5 cm or M0 No distant
tumors involving major portal or N1 Regional nodes metastasis
hepatic branch. involved
T4 Direct invasion of adjacent M1 Distant
organs. metastasis
 C/C Liver disease

Regenerative nodule Dysplastic nodule Small HCC

(Siderotic Nodule)
Well defined enlarged Nodule>1mm with HCC < 2cm.
parenchymal nodule dysplasia

Hypo/iso/hyper T1 Hypo/Hyper T1 Hypo/Hyper T1

Iso/Hypo T2 Iso/hypo T2 Iso/hyper T2
(hypo SI d/t iron Rarely hypo T2
content- siderotic
nodule)

X enhance HAP X enhance HAP Enhance in HAP.

GE Image- nodule Enhance on CT & not Hypo attn on all CT

within nodule app. Or on SPIO phases & enhance on
 Fibrolamellar HCC
 Histologic subtype of HCC.
 Occur in younger pt without underlying liver
disease.
 M>F. AFP Normal. Better prognosis.
 Malignant hepatocyte saperated into cords by thin
multilamellated fibrous strands.
 Usually very large, aggressive local invasion,
nodal or distant metastasis.
 USG- variable echo. Punctate calcification and
central echogenic scar.
CT: Large well defined lobulated mass
showing heterogenous enhancement.
Central scar (50%).. Often show
calcification. Delayed enhancement.

MRI:
Hypo on T1, heterogenous hyper SI T2.
Mass show heterogenous enhancement,
with no enhancement of central scar.
Central scar- Hypo SI in T1 and T2. Lack of
delayed enhancement.
Fibrolamellar carcinoma with central calcifications-
NECT, AP & PVP (radiating septa).
FS T2 and T1 GRE in AP and PVP
(peripheral capsule and necrotic nodule)
Central FNH Fibrolemellar HCC
scar

USG +++(hypoechoic) +++(echogenic)

Calcification rare. Calcification Common

CT

Hyperintense on T2 Hypointense on T2,

T2 MRI

delayed enhancement. no delayed enhancement.

Enhancement
 IH cholangiocarcinoma
 Adeno Ca from small intrahepatic bile
ducts. 2nd MC primary hepatic
neoplasm(10%).
 Firm hypovascular tumour with
predominant fibrous stroma. Large amount
of interstitial space in fibrous stroma
causes slow diffusion of contrast.
 Features- peripheral biliary ductal
dilatation, PV encasement, segmental
atrophy etc.
 CT:
Hypoattng mass with lobular margins,
showing mild early peripheral
enhancement, gradual centripetal
enhancement & delayed contrast
pooling(10-20 min). Satellite nodules are
frequent.
 MRI: Hypo on T1, Hyper/Iso T2.
Enhancement similar to CT.
Central Scar(50% Cases)- Hypo on T1 &
hypo/iso/hyper T2.Delayed
enhancement.
Hepatic and delayed phase in a patient with
multifocal cholangiocarcinoma causing
retraction of liver capsule
 Metastases
 Liver is 2nd MC site of metastasis.
 Variable clinical and imaging
presentations.
 Precontrast images are important to show
calcification, and hemorrhage.
 Some Met like breast, colon, lung, and
carcinoid show retraction of adjacent liver
capsule.
 MDCT has advantage with thin section
capability.
Hypovascular Hypervascular Calcifying Metastasis
Metastasis metastasis
Colon adenocarcinoma Renal cell carcinoma Mucin-producing
Pancreatic Neuroendocrine adenocarcinoma
adenocarcinoma Islet cell carcinoma Osteogenic or
Gastric adenocarcinoma Carcinoid chondrosarcoma
Transitional cell Malignant Some neuroendocrine
carcinoma pheochromocytoma tumors
Thyroid carcinoma
Some sarcomas
Malignant melanoma
 USG
 Multiple solid lesion with hypoechoic halo(may
be d/t compressed nornal tissue, proliferating
cells, fibrosis or vascularization).

 Microbubble Contrast-
AP-Hypervascular metastasis show
enhancement in HAP. Hypovasc. Met. Show
enhancement less than liver.
PVP- Virtually all metastasis will be unenhanced
relative to Liver in PVP(lack kipffer cells)..
 USG- various features

ECHOGENIC Hypoechoic Cystic met. Target lesion Diffuse

MET. met. Disorganised(
(hypervasc) (hypovasc) infiltrative)

GIT Breast Cystadeno ca Bronchogenic Breast

RCC Lung Mucinous ca ca. Lung
Carinoid Gastric Sarcoma MM
Chorio ca. Pancreas
Islet cell ca Lymphoma
(a) Large necrotic metastasis.
(b) Miliary metastases
(c) Following microbubble contrast agent
(d) Calcified metastases from breast carcinoma
 CT-Hypovascular metastasis
Most metastasis are hypovascular.
CT- In Arterial Phase, most common
pattern is continuous ring like
enhancement at periphery.
Hypoattenuating on PV Phase.
 Hypervascular metastasis:
They are hyperattenuating in AP.
Becomes isoattenuating in PVP, so
difficult to detect in PVP.
CT PVP-Multiple cystic liver metastases
from a cystic pancreatic acinar carcinoma
Metastatic islet cell carcinoma. Precontrast
and contrast- rim-enhancing nodules.
 MRI
 Usually Hypo T1, Hyper T2.
 Hyper SI in T1- hemorrhagic, MM.
 15-27% have central more hyperintense area in
T2(necrosis)– Target sign.
 50% colorectal met. Show central area of low SI
relative to high SI tumour edge in T2- Halo sign.
D/T Central desmoplasia and coagulative Necrosis.
 Contrast:
Hypovasc met.-Hypointense in HAP with
perilesional enhancement.
Hypervasc met.- Hyperintense in HAP.
Isointense in PVP.
 Delayed images(5-10 min)- 1/4th of met.
Show hypointense rim compared to centre
of lesion(peripheral washout sign). Seen in
hypervasc met > hypovasc met.
 MRI and contrast CT are comparable- 80-
90% sensitivity. MRI more sensitive for
solitary metastasis.
 CT remains the screening procedure of
choice.
 Pre op staging- CT,MRI &MDCT+Angio
used. CTAP is being replaced by non-
invasive Techniques.
Improvement of lesion detection with liver-
specific agent-T1-weighted GRE image and
Mangafodipir-enhanced MR
Hepatocyte-specific contrast agents- Early
ring-like enhancement with delayed
washout.
 Biliary Cystadenocarcimoma
 Uncommon biliary neoplasm.
 F>M, middle age patients.
 Unilocular or septated large cystic mass
containing mucinous or serous fluid.
 CT- Intrahepatic mass with non-enhancing
cystic spaces with high attenuating
wall/septa. Mural or septal nodule when
present enhances. Calcification may be seen.
 MRI- Cystic locules with hypointense septa.
T1-SI depend on fluid content. Serous-
hypo, Mucinous-iso/hyper, Hrgic-hyper SI.
 Epithelioid hemangioendothelioma
 Rare neoplasm of vascular origin.
 Adults. F>M.
 Peripheral solid nodules composed of
myxoid stroma with relatively hypocellular
center.
 Usually multiple larger peripheral lesion
coalescing to form confluent mass.
 CT- Hypoattenuating mass showing
peripheral enhancement.
 MRI- Hypointense in T1, hyperintense in
T2. Peripheral Enhancement Seen.
Epithelioid hemangioendothelioma –
Contrast-CT -large heterogeneous, lobulated
tumor involving both right and left lobes.
 Primary hepatic Angiosarcoma
 Rare,primary mesenchymal liver tumor. In
Elderly men and have poor prognosis.
Metastasis is common.
 Association exists with prior exposure to
certain chemical carcinogens.
 Multifocal but well-marginated nodules
throughout the liver.
 USG- Large mass of mixed echogenicity.
 CT -Hypodense mass. Hetrog. enhancement.
 Hypointense on T1- and markedly
hyperintense on T2-w images, with
hypointense septa in T2-weighted.
Angiosarcoma-
T2W and AP CT
and MRI showing
non-enhancing
lesionswith
feeding artery
 Primary Lymphoma
 Primary hepatic lymphomas are rare.
 Most of these tumors are Non-Hodgkin’s T-
cell lymphomas.
 Usually present as a discrete tumor.
 USG-Homogeneous lesions anechoic or
hypoechoic and mimic a cyst, although unlike
a cyst they lack through transmission. Some
are surrounded by a halo.
 Most primary liver lymphomas are hypointense
on T1- and hyperintense on T2-weighted
images. They show heterogeneous
postcontrast enhancement.
 Secondary Lymphoma
 Non-Hodgkin’s lymphoma is more often
focal.
 Calcifications seen rarely.
 Portal and periportal intrahepatic
infiltrates causes jaundice.
 MRI-Hypointense on T1- and hypo- to
hyperintense on T2-weighted images.
Postcontrast enhancement varies.
 Use of phosphorus MR spectra from P-31
MR spectroscopy appears potentially
useful.
NHL-contrast CT-Several focal hypodense
tumors & intrahepatic tumor tracking along
portal vessels.
 Hepatoblastoma
 Most common primary liver neoplasm in
children under 3 years. Rarely seen in
adults. M>F. Elevated AFP seen.
 Prevalence is increased in Beckwith-
Wiedemann syndrome and in
hemihypertrophy.
 Originates from embryonal hepatic tissue
and usually consists of epithelial cells or
mixture of epithelial and mesenchymal cells.
 Readily metastasize. Vascular displacement
or amputation may occur.
 Imaging features similar to HCC. May have
local invasion, cystic changes, necrosis or
irregular shaped calcification.
 US- Mixed echogenic large lesion with
poorly defined margins.
 CT- Hypodense mass. Variable
enhancement.
 MRI-Hypointense on T1- and hyperintense
on T2. Heterogeneity is often evident.
 Hepatoblastoma shows uptake of sulfur
colloid; however, does not have uptake of
both Tc-99m–sulfur colloid and HIDA.
Hepatoblastoma –Contrast CT- large
slightly enhancing tumor containing
central necrosis and calcifications
 TSTC (too small to characterize)Lesions
Jones (1992), Schwartz (1999), Khalil (2005)
 For lesions which, due to their small size and atypical
imaging features, cannot be confidently categorized, the
term TSTC lesions has been coined. Usually for lesion
<15mm in CT/MRI.
 Accounts abt.12% of liver lesions with a known Pt. with
malignancy. (80% are benign).
 Patient without a known malignancy –usually considered
as benign.
 Patient with a known malignancy-- a single TSTC lesion
can be assumed as benign.

 Even multiple TSTCs- mostly benign, esp. when they are

small, sharply defined and hypodense.

Avoid 'we can't rule out metastases'

 Chemoembolization
 Intraarterial embolization techniques used
to treat hepatocellular carcinomas consist
of inert particle embolization, chemotoxic
agents(chemoembolization), and injection
of radioactive particles (radioembolization).
 Transcatheter chemoembolization is
commonly used using Ethiodol (Lipiodol).
 Later, after injecting a chemotherapeutic
agent, if needed, embolization of the
vessel in question is performed using
particulate matter.
CT shows residual Ethiodol retained
in a multifocal hepatocellular
carcinoma
 Radioembolization
 Intrahepatic artery Tc-99m-MAA injection
estimates the relative tumor-to–normal
parenchyma uptake of various size
microspheres, including those containing
therapeutic radiopharmaceutical agent
 Hepatocellular carcinomas have also been
embolized with iodine-131 iodized oil
(Lipiodol) and gelatin sponges through a
superselectively placed arterial catheter.
 Provided long-term palliation without
complications.
 Percutaneous Techniques
 Hepatocellular carcinomas can be treated
using a direct percutaneous approach.
injection of chemical agents such as ethanol,
acetic acid, and hot saline to induce tumor
coagulation necrosis.
thermally mediated techniques such as
radiofrequency (RF) ablation, laser
photocoagulation, microwave therapy, and
cryotherapy result in similar tumor cell
death.
 Imaging provides needle and catheter
insertion guidance.
 Most percutaneous ablation is performed
using US guidance, although for tumors
not visualized by US, MRI guidance in an
open magnet is an option.

 Either CT, contrast-enhanced US, or MR

are used to detect residual tumors
shortly after ablation.
Radiofrequency ablation
of hepatocellular
carcinoma. A: Pretherapy
B: hyperdense center
immediate post-therapy
C: Residual changes are
present 2 months.
 Cryoablation
 Destroys tumor tissue by freezing. Liquid
nitrogen is the freezing Medium.
 Either a percutaneous or an open surgical
approach is used for cryoablation.US/MRI
used.
 Magnetic resonance guidance- identifies the
tumor nodule in question and the size of the
surrounding frozen liver tissue. An open MR
unit reveals resultant ice balls as sharply
defined expanding regions of signal loss
encasing tumors S/O resultant necrosis.
 REFERENCES:
Lee/Sagel : CT With MRI Corr. 4th ed.
Grainger/Allison : Diag.Radiology 5th ed.
Skucas : Advanced Imaging Abd. 2006.
Rumack : Diag. Ultrasonography 3rd ed.
Margulis: GI Imaging
AJR, Radiology.

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