Abdomen Breast Cardiovascular Chest Head/Neck Musculoskeletal

Neuroradiology Pediatrics More

Common Liver Tumors
Richard Baron
Radiology department of the University of Chicago

Hemangioma
Hepatocellular Carcinoma (HCC) Publicationdate 2006-07-15
Early appearance of HCC
Late appearance of HCC This article is based on a presentation given by
Differential diagnosis
Richard Baron and adapted for the Radiology Assistant
Hepatic Adenoma
Focal Nodular Hyperplasia (FNH) by Robin Smithuis.
Fibrolamellar carcinoma (FLC) Richard Baron is Chair of Radiology at the University
Cholangiocarcinoma of Chicago and well known for his work on hepatobili‐
Hepatic Metastases ary diseases.
Differential diagnosis He has been president of the Society of Computed
Liver abces Body Tomography and Magnetic Resonance.
In Part I a basic concept is given on how to detect and
characterize livermasses with CT.
In Part II the imaging features of the most common
hepatic tumors are presented.

Hemangioma

Hemangioma is the most common benign liver tumor.

It is composed of multiple vascular channels lined by
endothelial cells.
In 60% of cases more than one hemangioma is
present.
The size varies from a few millimeters to more than
10 cm (giant hemangiomas).
Calcification is rare and seen in less than 10%, usually
in the central scar of giant hemangioma.

CT will show hemangiomas as sharply defined

masses with the same density as the vessels on
NECT and CECT.
The enhancement pattern is characterized by sequen‐
tial contrast opacification beginning at the periphery
as one or more nodular areas of enhancement.
All these areas of enhancement must have the same
density as the bloodpool.
This means that in the arterial phase the areas of en‐
hancement must have almost the density of the aorta,
while in the portal venous phase the enhancement
must be of the same density as the portal vein.
Even on delayed images the density of a hemangioma
Typical hemangioma matches the bloodpool in every phase.
must be of the same density as the vessels.
 Finally most hemangiomas show complete fill in with
Abdomen Breast contrast.
Cardiovascular Chest Head/Neck Musculoskeletal

Neuroradiology Pediatrics More

Small hemangiomas may show fast homogeneous
enhancement ('flash filling').
Small HCC and hypervascular metastases may mimic
small hemangiomas because they all show homogen‐
eous enhancement in the arterial phase.
By looking at the other phases to see if the enhancing
Flash filling hemangioma in unenhanced, arterial and portal areas match the bloodpool, it is usually possible to
venous phase. Notice it matches the bloodpool. differentiate these lesions.

Large hemangiomas can have an atypical appear‐

ance.
Complete fill in is sometimes prevented by central
fibrous scarring.
These lesions need to be differentiated from other le‐
sions with a scar like FLC, FNH and Cholangiocar‐
cinoma.
Again looking at the bloodpool will help you.
On the left two large hemangiomas.
Notice that the enhancing parts of the lesion follow
the bloodpool in every phase, but centrally there is
scar tissue that does not enhance.

Giant hemangiomas with scar-tissue. Notice that the

enhancement matches the bloodpool in all phases. Central scar is
hypodens on NECT and stays hypodens.

Peripheral enhancement
The enhancement of a hemangioma starts peripheral
.
It is nodular or globular and discontinuous.
Rim enhancement is continuous peripheral enhance‐
ment and is never hemangioma.
Rim enhancement is a feature of malignant lesions,
especially metastases.

LEFT: rimenhancement in breast metastasis. RIGHT: nodular

discontinuous enhancement in hemangioma.

Progressive fill in
First look at the images on the left and describe what
you see. Then continue.

The lesion definitely has some features of a heman‐

gioma like nodular enhancement in the arterial phase
and progressive fill in in the portal venous and equilib‐
rium phase.
In the portal venous phase however, the enhancement
 is not as bright as the enhancement of the portal vein.
Abdomen Breast The conclusion must
Cardiovascular Chestbe,Head/Neck
that this lesion does not
Musculoskeletal
match bloodpool in all phases, so it cannot be a hem‐
angioma.
So progressive
Neuroradiology Pediatrics More fill in is a non-specific feature, that can
be seen in many other lesions like metastases or
primary liver tumors like cholangiocarcinoma.
The delayed enhancement in this lesion is due to
fibrotic tissue in a cholangiocarcinoma and is a spe‐
cific feature of these tumors.

Liver lesion showing nodular enhancement, progressive fill in and

delayed enhancement.

Ultrasound
Most hemangiomas are detected with US.
If you had to pick one word to characterize a heman‐
gioma on US, you would probably say 'hyperechoic'.
You have to realize however, that this simply means
that the lesion is hyperechoic to normal liver.
If the liver is hyperechoic due to steatosis, the heman‐
gioma can appear hypoechoic (figure).
Another important feature of hemangiomas is the in‐
LEFT: Classic US appearance of a [Link]: Also a creased sound transmission.
hemangioma but now in a hyperechoic liver, so the lesion is
relatively hypoechoic. Notice increased sound transmission.
This is because the lesion is made of these channels
containing blood.

Differential diagnosis
Hemangiomas must be differentiated from other le‐
sions that are hypervascular or lesions that show peri‐
pheral enhancement and progressive fill in.

Hepatocellular Carcinoma (HCC)

HCC is the most frequent abdominal malignancy

worldwide and is especially common in Asia and
mediterrean countries.
HCC may be solitary, multifocal or diffusely infiltrat‐
ing.
HCC consists of abnormal hepatocytes arranged in a
typical trabecular pattern.
Larger HCC lesions typically have a mosaic appear‐
ance due to hemorrhage and fibrosis.

In patients with cirrhosis or with hepatitis B/C our ma‐

jor concern is HCC, since 85% of HCC occur in these
patients.
If you take a cohort of patients with hepatitis C and
 you follow them for 10 years, 50% of them will have
Abdomen Breast end stage liver disease
Cardiovascular Chest and 25% will Musculoskeletal
Head/Neck have HCC.

Neuroradiology Pediatrics More

Early appearance of HCC
It is important to separate the early appearance from
the late appearance of HCC.
Nowadays we encounter very small HCC's in patients,
that we screen for HCC (figure).
These are small lesions that transiently enhance ho‐
mogeneously.
Small HCC seen only in arterial phase in a patient with cirrhosis. You will only see them in the arterial phase.
Sometimes there is rim enhancement and you might
mistake them for a hemangioma.
Always look how they present in the other phases and
compare with the bloodpool and remember that rim
enhancement is never hemangioma.
These early HCC's are very different from the large
ones that we see in the non-cirrhotic patients.

Late appearance of HCC

HCC is a silent tumor, so if patients do not have cir‐
rhosis or hepatitis C, you will discover them in a late
stage.
They tend to be very large with a mozaic pattern, a
capsule, hemorrhage, necrosis and fat evolution.
HCC becomes isodense or hypodense to liver in the
portal venous phase due to fast wash-out. On delayed
Large HCC with mozaik pattern in a non cirrhotic patient.
images the capsule and sometimes septa demon‐
strate prolonged enhancement.

HCC and Portal Vein thrombosis

Many patients with cirrhosis have portal venous
thrombosis and many patients with HCC have throm‐
bosis.
These are two common findings and they can be co‐
incidental.
It is very important to make the distinction between
just thrombus and tumor thrombus.
First, if you have a malignant thrombus in the portal
vein, it will always enhance and you'll see it best in ar‐
LEFT: Diffusely enhancing tumor thrombus in HCC with portal vein terial phase.
[Link]: Tumor thrombus with vessels within the Secondly, if you have a malignant thrombus in the
thrombus. portal vein, it will increase the diameter of the vessel.
Sometimes a tumor thrombus may present with
neovascularity within the thrombus (figure).

Differential diagnosis
Early HCC needs to be differentiated from other hy‐
pervascular lesions, that will be hyperdense in the ar‐
 terial phase.
Abdomen Breast First look at the images
Cardiovascular on the left and
Chest Head/Neck look at the en‐
Musculoskeletal
hancement patterns. Then continue.

Neuroradiology Pediatrics More

In the arterial phase we see two hypervascular le‐

sions.
Now do not just concentrate on the images, where
you see the lesions best.
You have to look at all the other images, because they
give you the clue to the diagnosis.
The upper images show a lesion that is isodens to the
liver on the NECT.
In the arterial phase there is enhancement, but not as
dense as the bloodpool.
In the portal venous phase the lesion is again
isodense to the surrounding liver parenchyma and
you can't see it.
NECT, arterial and portal venous phase in a patient with Hepatitis
If you only had the portal venous phase you surely
C with two lesions in the liver (arrows). would miss this lesion.
The lower images show a lesion that is visible on all
images.
You see it on the NECT and you could say it is hypo‐
dens compared to the liver.
Does this help you?
No, not in the least.
However if you look at the bloodpool, you will notice
that on all phases it is as dense as the bloodpool.
So we have a HCC in the right lobe on the upper im‐
ages and a hemangioma in the left lobe on the lower
images.
The key is to look at all the phases.

The importance of a non enhanced scan is demon‐

strated in the case on the left.
In the arterial phase we see a hyperdense structure in
the lateral segment of the left lobe of the liver.
This looks like an enhancing nodule very suspective
of early HCC.
However if we look at the NECT on the right, we'll no‐
tice, that it is not enhancement that we're looking at.
It is just a siderotic iron containing hyperdense nod‐
Arterial phase (left) and NECT (right) ule.
They are very common and are seen in up to 50% of
patients with cirrhosis.

10% of HCC are hypodense compared to liver.

The imaging findings will be non-specific.
The case on the left proved to be HCC.
 Abdomen Breast Cardiovascular Chest Head/Neck Musculoskeletal

Neuroradiology Pediatrics More

Hypovascular HCC seen in late portal venous phase

Hepatic Adenoma

Hepatocellular adenomas are large, well circum‐

scribed encapsulated tumors. They consist of sheets
of hepatocytes without bile ducts or portal areas.
80% of adenomas are solitary and 20% are multiple.
Adenomas typically measure 8-15 cm and consist of
sheets of well-differentiated hepatocytes.
Adenomas are prone to central necrosis and hemor‐
rhage because the vascular supply is limited to the
surface of the tumor.
The pathogenesis is believed to be related to a gener‐
alized vascular ectasia that develops due to exposure
of the liver to oral contraceptives and related syn‐
thetic steroids.
In young woman using contraceptives an adenoma is
the most frequent hepatic tumor.

CT will show most adenomas as a lesion with homo‐

geneous enhancement in the late arterial phase, that
will stay isodense to the liver in later phases.
Unfortunately, this homogeneous enhancement in the
late arterial phase is not specific to adenomas, since
small HCC's and hemangiomas as well as hypervas‐
cular metastases and FNH can demonstrate similar
enhancement in the arterial phase.
Malignant lesions however have a tendency to loose
their contrast faster than the surrounding liver, so they
may become relatively hypodense in later phases.
The finding of hemorrhage as an area of high attenu‐
ation can be seen in as many as 40% of adenomas.
This is however also a feature of HCC and large
hemangiomas.

Fat deposition within adenomas is identified on CT in

only approximately 7% of patients and is better depic‐
ted on MRI.
Typically adenomas have well-defined borders and do
not have lobulated contours.
A low-attenuation pseudocapsule can be seen in as
many as 30% of patients.
 This capsule will only show enhancement on delayed
Abdomen Breast scans.
Cardiovascular Chest Head/Neck Musculoskeletal
Coarse calcifications are seen in only 5% of patients.
On the left an adenoma with fat deposition and a
capsule. More
Neuroradiology Pediatrics

MRI usually is more sensitive in detecting fat and

hemorrhage.
Chemical-shift imaging showing loss of signal on out-
of-phase images can confirm the presence of fat.
HCC is known to contain fat in as many as 40% of le‐
sions, therefore the presence of fat does not help dif‐
ferentiate the lesions.

Adenomas may rupture and bleed, causing right up‐

per quadrant pain.
The two most common liver lesions causing hepatic
hemorrhage are HA and HCC.
Although adenomas are benign lesions, they can un‐
dergo malignant transformation to hepatocellular car‐
cinoma (HCC).
Although malignant transformation is rare, for this
reason, surgical resection is advocated in most pa‐
Adenoma with hemorrhage.
tients with presumed adenomas.

Significant overlap is noted between the CT appear‐

ances of adenoma, HCC, FNH, and hypervascular
metastases, making a definitive diagnosis based on
CT imaging criteria alone difficult and often not pos‐
sible.
Clinical correlation in such cases is most helpful.
In otherwise healthy young women using oral contra‐
ceptives, adenoma is favored.
Patients with glycogen storage disease, hemochro‐
matosis, acromegaly, or males on anabolic steroids
also are more prone to developing hepatic adenomas.
Enhancing adenoma with fat in the center
A history of cirrhosis and high AFP levels favor HCC.
A history of a primary hypervascular tumor favors
metastases.

As a result of the risk of intraperitoneal hemorrhage

and the rare occurrence of malignant transformation
to HCC, surgical resection has been advocated in
 most patients with presumed HA.
Abdomen Breast The risk of significant
Cardiovascular Chestbleeding fromMusculoskeletal
Head/Neck the tumor is as
high as 30%.
The exact risk of malignant transformation is un‐
known. More
Neuroradiology Pediatrics
Some advocate surgical resection only when tumors
are larger than 5 cm or when AFP levels are elevated,
since these two findings are associated with higher
risk of malignancy.
Adenoma showing capsule in delayed phase The value of percutaneous fine needle biopsy for the
diagnosis of HA is controversial for two reasons.
First, histologic studies may lead to misdiagnosis
when differentiating HA from FNH.
In addition, a considerable risk of hemorrhage exists
when biopsy is performed on these hypervascular tu‐
mors.
Adenomas may diminish after oral contraceptives are
discontinued, but this does not lower the risk of ma‐
lignant transformation.
When a definitive diagnosis of FNH can be made us‐
ing imaging studies, surgery can be avoided and le‐
sions can be observed safely using radiologic studies.
However, if HA or HCC remains in the differential dia‐
gnosis, surgery usually is indicated.

Focal Nodular Hyperplasia (FNH)

FNH is the second most common tumor of the liver.

FNH is not a true neoplasm. It is believed to represent
a hyperplastic response to increased blood flow in an
intrahepatic arteriovenous malformation.
All the normal constituents of the liver are present but
in an abnormally organized pattern.

US will show a FNH as a non specific ill-defined le‐

sion.
The central scar may be detected as a hyperechoic
area, but often cannot be differentiated.
With color doppler sometimes the vessels can be
seen within the scar.

CT will show FNH as a vascular tumor, that will be hy‐

perdens in the arterial phase, except for the central
scar.
On the left a typical FNH with a central scar that is hy‐
podens in the portal venous phase and hyperdens in
the equilibrium phase.

MRI will show a hypointense central scar on T1-

weighted images.
On T2-weighted images the scar appears as hyperin‐
tense in 80% of patients, which is very typical. How‐
ever in 20% of patients the scar is hypointense.
 Gadolineum enhanced MRI will reveal similar en‐
Abdomen Breast hancement patterns
Cardiovascular as on
Chest CECT.
Head/Neck Musculoskeletal

Neuroradiology Pediatrics More

The diagnosis of FNH is based on the demonstration

of a central scar and a homogeneous enhancement.
However, a typical central scar may not be visible in
as many as 20% of patients (figure).
Moreover a central scar may be found in some pa‐
tients with fibrolamellar hepatocellular carcinoma,
hepatic adenoma and intrahepatic cholangiocar‐
cinoma.
The key to the diagnosis in the lesion on the left is the
fact that it is isoattenuating to normal liver in the
portal venous phase and stays that way without a
wash out on the delayed phase (not shown).
This could also be an adenoma, but HCC would be un‐
FNH seen as hypervascular lesion in the late arterial phase and likely because they show a fast wash out.
isodense to normal liver in the portal venous phase. No scar was
seen.

If you look at the images on the left and just would

consider the T2W-images, what could be the cause of
the central area of high signal?

The most common cause would be central necrosis

in a tumor.
However if you look at the delayed phase, you will no‐
tice that this area enhances.
So this is fibrotic tissue and the diagnosis is FNH.
T2WI, T1WI without Gadolineum and a delayed phase after
Gadolineum.
Fibrolamellar carcinoma (FLC) has a dark scar on
T2WI and FNH has a brigth scar on T2WI in 80% of
the cases.
This means that at times the differential between
FNH and FLC will not be possible.

Fibrolamellar carcinoma (FLC)

FLC is an uncommon malignant hepatocellular tumor,

but less aggressive than HCC.
FLC characteristically manifests as a 10-20 cm large
hepatic mass in adolescents or young adults.
The typical risk factors for HCC such as cirrhosis, el‐
 evated alphafetoprotein, viral hepatitis, alcohol abuse
Abdomen Breast are absent.
Cardiovascular Chest Head/Neck Musculoskeletal
FLC characteristically appears as a lobulated hetero‐
geneous mass with a central scar in an otherwise nor‐
mal liver. Calcifications
Neuroradiology Pediatrics More occur in 30-60% of fibrolamel‐
lar tumors.

Imaging features of FLC overlap with those of other

scar-producing lesions including FNH, HCC, Heman‐
gioma and Cholangiocarcinoma.
FNH, in particular, may simulate FLC, since both have
similar demographic and clinical characteristics.
In contrast to FNH the central scar in FLC will usually
be hypointense on T2WI and will less often show
delayed enhancement.
LEFT: FLC in late arterial phase: central calcification and While FNH is always very homogeneous, FLC is usu‐
heterogenous enhancement in a lamellar pattern. RIGHT: venous
phase with hypodense central scar. ally heterogeneous following contrast administration.

On the left pathologic specimens of FLC and FNH.

At first glance they look very similar.
However when you look carefully you will notice the
lamellar and heterogenous structure of FLC com‐
pared to the homogeneous appearance of FNH.

On non enhanced images a FLC usually presents as a

big mass with central calcifications.

Cholangiocarcinoma

Cholangiocarcinoma usually presents as a mass of 5-

20cm. In 65% there are satellite nodules and in some
cases punctate calcifications are seen.
The diagnosis of a cholangiocarcinoma is often diffi‐
cult to make for a radiologist and even a pathologist.
That is because cholangiocarcinoma has a varied
morphology and histology.
It can be a constricting or an expanding lesion, be‐
cause it can have a fibrous or a glandular stroma.
It can be located anywhere in the intrahepatic bile
ducts or common bile duct.
 First look at the images on the left and try to find
Abdomen Breast Cardiovascular Chest Head/Neck Musculoskeletal
good descriptive terms for what you see. Then
continue.
Neuroradiology Pediatrics More
The lesion on the left has the folowing
characteristics:
The lesion is hypodens in the arterial and portal
venous phase with some peripheral
enhancement.
The lesion is hyperdense in the equilibrium
phase indicating dens fibrous tissue.
The lesion causes retraction of the liver capsule
The finding of an infiltrating mass with capsular re‐
traction and delayed persistent enhancement is very
Cholangiocarcinoma: Non enhanced, arterial, portal venous and typical for a cholangiocarcinoma.
equilibrium phase.

Infiltrative cholangiocarcinoma does not cause mass

effect, because when the stroma matures, the fibrous
tissue will contract and cause retraction of the liver
capsule.
There are not many tumors that cause retraction of
the liver capsule, since most tumors will bulge.
The most common tumor that causes retraction be‐
sides cholangiocarcinoma is metastatic breast can‐
cer.
This will give a pseudo-cirrhosis appearance.
Another cause of local retraction is atrophy due to bil‐
iary obstruction or chronic portal venous obstruction.

The case on the left demonstrates how difficult the

detection of ta cholangiocarcinoma can be.
Only on the delayed images at 8-10 minutes after con‐
trast injection a relative hyperdense lesion is seen.
This is the fibrous component of the tumor.

Some cholangiocarcinomas have a glandular stroma.

Hepatic Metastases
 The liver is the most common site of metastases.
Abdomen Breast The
Cardiovascular
most common Chest Head/Neck
organs Musculoskeletal
of origin are: colon, stom‐
ach, pancreas, breast and lung.
Most liver metastases are multiple, involving both
Neuroradiology Pediatrics More
lobes in 77% of patients and only in 10% of cases
there is a solitary metastasis.

Hypovascular metastases are the most common and

occur in GI tract, lung, breast and head/neck tumors.
They are detected as hypodense lesions in the late
portal venous phase.
In this phase the attenuation of the normal liver par‐
enchyma increases, revealing the relatively hypoatten‐
uating metastases, sometimes with peripheral en‐
hancement.
The rim enhancement that occurs represents viable
tumor peripherally, which appears against a less vi‐
able or necrotic center (figure).

Hypervascular metastases are less common and are

seen in renal cell carcinoma, insulinomas, carcinoid,
sarcomas, melanoma and breast cancer.
They are best seen in the late arterial phase at 35 sec
after contrast injection.
Although breast cancer metastases can be hypervas‐
cular, it was shown that routine use of adding arterial
phase imaging, did not show any advantage.

Calcified liver metastases are uncommon. Calcifica‐

tion can be seen in metastases of colon, stomach,
breast, endocrine pancreatic ca, leiomyosarcoma, os‐
teosarcoma and melanoma.
When calcified liver metastases are revealed by CT in
a patient with unknown primary tumor, colon cancer
will be the most likely cause.

Cystic liver metastases are seen in mucinous ovarian

ca, colon ca, sarcoma, melanoma, lung ca and carcin‐
oid tumor.

On MRI metastases are usually hypointense on T1WI

and hyperintense on T2WI.
Peritumoral edema makes lesions appear larger on
T2WI and is very suggestive of a malignant mass.
On dynamic contrast-enhanced MRi the characterist‐
ics of metastases are the same as for CECT.

Ultrasound findings
At US, metastases may appear cystic,hypoechoic,
isoechoic or hyperechoic.
 Bull's eye or target lesions is a common presentation
Abdomen Breast of metastases. InChest
Cardiovascular these Head/Neck
metastases Musculoskeletal
the halo is most
probably related to a combination of compressed nor‐
mal hepatic parenchyma around the mass and a zone
of cancer More
Neuroradiology Pediatrics cell proliferation.
This pattern suggests aggressive behavior and is
seen in bronchogenic, breast and colon carcinoma, .
However, this pattern is not specific for metastases
as it can also be seen in primary malignant liver neo‐
plasms (eg, HCC) and benign liver neoplasms (eg, ad‐
enoma in glycogen storage disease).
Calcified metastasis in a patient with colon cancer.
A similar appearance has been described with liver
abscesses.
Calcified metastases may shadow when they are
densely echogenic (figure). This pattern is commonly
seen in colorectal cancer.

Differential diagnosis
Metastases can look like almost any lesion that oc‐
curs in the liver.
Hypervascular metastases have to be differentiated
from other hypervascular tumors that can be multi‐
focal like hemangiomas, FNH, adenoma and HCC.
Hypovascular metastases have to be differentiated
from focal fatty infiltration, abscesses, atypical hypo‐
vascular HCC and cholangiocarcinoma.

Metastases in fatty liver

Focal fatty sparing in a diffusely fatty liver or foci of
focal fatty infiltration can simulate metastases.
However on nonenhanced scans these regions of fat
variation tend to be nonspherical and geographic,
with no mass effect or distortion of the local vessels.

On the other hand a fatty liver can also obscure meta‐

stases.
Metastasis difficult to detect on CECT in portal venous phase On a contrast enhanced CT hypovascular lesions can
(left). Better seen on NECT. be obscured if the liver itself is lower in density due to
fat deposition. On a NECT these lesions usually are
better depicted (figure).

If a patient is known to have a fatty liver, it is better to

do an MRI or ultrasound for the detection of liver‐
metastases.
On the left a patient with fatty infiltration of large
parts of the liver. No metastases were seen, but on an
ultrasound of the same region multiple metastases
were detected.
Steatosis of right liver lobe. No lesions detectable. On US multiple
lesions in the same region.
Abdomen Breast Cardiovascular Chest Head/Neck Musculoskeletal

Liver abces
Neuroradiology Pediatrics More

The presentation of liver abcesses is very much de‐

pendend on the way the bacteria have entered the
liver.
There are four routes for bacteria to get into the liver.
The common route is through the portal vein as a res‐
ult of abdominal infection.
The bacteria enter through the slow flow portal sys‐
tem and they are layered within the vessel.
The bacteria will fall down into the dependent portion
of the right lobe.
In sepsis the spread will be via the arterial system as
in patients with endocarditis and there will be multiple
abscesses spread out through the periphery of the
liver.
The biliary route is often the result of biliary manipula‐
tion as in ERCP. It is usually central in location and
then spreads out.
Finally there is a direct route as in penetrating injury
or direct spread of cholecystitis into the liver.

First look at the images on the left and try to find

good descriptive terms for what you see. Then
continue.

If you would describe the image on the left, you would

use terms as:
Hypovascular lesions
Low density, so it may be cystic i.e fluid
containing.
Liver abcess in a patient with diverticulitis. Clustered or satelite lesions. These lesions are
multiple, but not spread out through the liver.
Although it is difficult to see, there is also portal
venous thrombosis on the left.

So these findings suggest liverabscesses especially

because it's clustered.
Only when you have a population with livertrans‐
plants, bilomas in an infarcted area would look the
same.
If it wasn't clustered than any cystic tumor could look
like this.
It is very important to make the diagnosis of liver
absces because it is a benign disease that kills and
the radiologist may be the first to raise the suspicion.

Whenever you see a small cyst-like lesion in a patient

who recently underwent an ERCP, be very carefull to
 assume it is just a simple cyst.
Abdomen Breast Biliary abscessesChest
Cardiovascular start small but canMusculoskeletal
Head/Neck progress rapidly.
The figure on the left shows such a case.
Within 3 weeks the small lesion in the left liver lobe
progressed
Neuroradiology Pediatrics to this huge abces.
More
So any cystic structure near the biliary tract in a pa‐
tient, who recently has undergone a biliary procedure,
is suspicious of a liver abces.

LEFT: Small cyst-like lesion after recent ERCPRIGHT: 3 weeks

later a large absces had developed.

1. Oliver JH, Baron RL: State of the art, helical biphasic contrast enhanced CT of the liver: Technique, indications, interpret‐
ation, and pitfalls. Radiology 1996; 201:1-14.
2. Brancatelli G., Baron RL, Peterson MS, Marsh W. Helical CT screening for HCC in patients with Cirrhosis: Frequency and
causes of False-Positive interpretation. AJR 2003; ISO: 1007-1014.

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