FOCAL LIVER LESIONS.pptx MMMMMMMMMMMMMMM

FOCAL LIVER LESIONS
MODERATOR – DR. PRASANTHI MDRD
PRESENTOR – DR. SWETHA

Focal liver lesions
BENIGN
Hemangioma
Focal nodular
hyperplasia(FNH)
 Adenoma
Cyst
Abscess
MALIGNANT
Hepatocellular
carcinoma(HCC)
Fibrolamellar carcinoma(FLC)
Intrahepatic
cholangiocarcinoma(ICCA)
Metastases
Hepatoblastoma
Angiosarcoma

For detection, characterization & differentiation of
benign and malignant liver lesions.
Non contrast CT- Calcification, fat,
hemorrhage.
 Contrast CT- Arterial phase
Portal venous phase
Delayed phase

Arterial phase
20-40sec
Hypervascular tumors enhance via the hepatic artery,
when normal liver parenchyma does not yet enhance,
because contrast is not yet in the portal venous system.
Hypervascular tumors enhance optimally at 35 sec
after contrast injection.

Hypervascular lesions
Benign:

Hemangioma

Adenoma

FNH
Malignant:

HCC

Metastases(RCC,carcinoi
d,thyroid
ca,NET,sarcoma)

Portal venous phase
Normal liver parenchyma enhances in this phase.
To detect hypovascular tumors(more common,
majorities are metastases).
Scanning is done at about 75 seconds.

Delayed phase
Begins at about 3-4minutes after contrast
injection.
Valuable for washout of contrast (HCC), retention
of contrast in blood pool (hemangioma) &
retention of contrast in fibrous tissue (capsule of
HCC, central scar of FNH).

HEMANGIOMA
Commonest benign hyper vascular liver tumor.
Is composed of multiple vascular channels lined by endothelial
cells.
Usually asymptomatic & frequently diagnosed as an incidental
finding on imaging.
More common In female.
Size varies from a few mm to more than 10 cm (giant
hemangioma).
Calcification is rare & seen in <10%, usually in the central scar of
giant hemangioma.

USG
Typically well defined, homogeneous & hyperechoic
lesions(67%-79%).
May be hypoechoic, within background of fatty liver.
Post acoustic enhancement.
Giant hemangioma -heterogeneous with central hypo -
echoic foci.

On CT scan
CECT - Discontinuous, nodular, peripheral
enhancement starting at arterial phase & gradual
central filling in.
Retention of contrast in delayed phase.
Enhancement must match blood pool in each
phase(similar to aorta in arterial phase , portal vein in
portal venous phase).

MRI
T1WI: Hypo-intense relative to liver parenchyma.
T2WI: Significantly hyperintense –producing light bulb
appearance.
T1C+(GD):Nodular enhancement

FOCAL NODULAR HYPERPLASIA
2nd
most common benign tumor of liver.
Characterized by a central fibrous scar surrounded by
nodules of hyperplasic hepatocytes & small bile ductules.
More prevalent in women of reproductive age &
associated with OCP use.
Usually solitary(95%).
No capsule.
Asymptomatic.

USG
Subtle iso-echoic mass with contour abnormality.
Displacement of vascular structure.
Central scar- hypo-echoic linear or stellate
area, may be hyper-echoic.
Doppler study: well developed peripheral & central blood
vessels are seen.

CT SCAN
NECT: Homogeneous low density mass, often with a
central low density (central scar).
CECT: lesion enhance markedly & uniformly in arterial
phase with exception of central scar.
Isodense to normal liver parenchyma in PVP.
Contrast accumulates within the central scar in delayed
phase.

MRI
T1WI: Iso-intense to normal liver parenchyma.
T2WI: Iso to slightly hyper-intense.
Central scar is hypointense inT1WI & hyperintense
in T2WI

HEPATIC ADENOMA
Lacks of portal tracts, hepatic vein, kupffer cell & biliary
canaliculi. Fat & glycogen rich hepatocytes are often present.
Most common in women, with H/O OCP or anabolic steroid.
Usually solitary.
Central hemorrhage/necrosis.
Thin capsule.
 Complication: potential for rupture & may result
hemoperitonium , risk of malignant transformation.

USG
Nonspecific
The echogenecity may be
iso, hypo , hyperechoic or
mixed.

CT SCAN:
NECT: low attenuation mass (fat, glycogen), high
density if hemorrhage present.
CECT: early peripheral with centripetal
enhancement, no retention of contrast in
later phases because of AV shunting .

MRI
T1WI: mildly increased signal intensity( fat &
hemorrhage).
T2WI: heterogeneous with iso, hypo &
hyperintense areas.
Capsule-hypointense rim.
T1C+(GD) : similar to CECT.

HEPATOCELLULAR
CARCINOMA(HCC)
Commonest primary malignant neoplasm of liver.
Consists of abnormal hepatocytes arranged in a typical
trabecular pattern.
May be solitary, multiple nodules or diffusely
infiltrating.
80% of HCC occur in cirrhotic liver.
There is propensity toward venous invasion(PV>HV).

USG
 Variable in appearance.
usually hypoechoic.
A thin ,peripheral hypoechoic halo( fibrous capsule).
Larger tumors often are heterogeneous (necrosis,hge &
fibrosis).
May invade the portal & hepatic veins.
Most tumor will show central vascularity on Doppler
study.

CT SCAN
NECT: large hypodense mass, often with central area of
low attenuation(necrosis).
May be isodense to liver.
CECT: non necrotic area enhances strongly in arterial
phase & early washout in subsequent phases.
Detection of venous invasion (portal,hepatic veins,IVC).

MRI
T1WI : variable (fatty change, internal
fibrosis,hge)
T2WI : hyperintense
Capsule : hypo in T1 &T2WI
CEMR : similar to CECT

HCC RNs DPNs
NECT Hypo/ isodense Iso to liver except
siderotic nodule
Hypo to liver but
may be iso or hyper
CECT Early enhancement
in arteial phase &
early washout in
later phases.
Same as liver
parenchyma
Low grade- same as
liver parenchyma
High grade- early
enhancement in
arterial phase but
not early wash out
in delayed phase..
T1WI LOW SI variable High SI
T2WI High(mild to
moderate) SI
Iso/low SI iso/low SI
DWI Restricted diffusion no no

FIBROLAMELLAR CARCINOMA
 Histologic subtype of HCC.
Found in young adults & adolescents.
No coexisting liver disease.
Hemorrhage & necrosis –rare.
A fibrous central scar may present.
Calcification is common(within the scar in stellate
pattern).

USG
Echogenecity of FLC is variable.
Puncate calcification & central echogenic scar.
CT SCAN:
NECT: well defined ,low density mass with a more
low attenuating central scar.
CECT: moderate enhancement of the lesion with
delayed enhancement of scar.

MRI
T1WI: Isointense to normal liver.
T2WI: iso to slightly hyperintense.
Lac of hemorrhage & necrosis.(HCC- common).
Central scar is hypointense in both T1WI & T2WI

HCC FLC
Risk factor Occur in cirrhotic liver Normal liver
Age Old Age Young adult
S.AFP Elevated Normal
Central scar Less common More common
Hemorrhage, necrosis more less
Calcification
Portal vein thrombus
Less common
More common
More common
Less common

INTRAHEPATIC CHOLANGIOCARCINOMA
An adenocarcinoma, originates in small intrahepatic
ducts.
10% of all cholangiocarcinoma.
Usually large, firm masses with abundant fibrous tissue.
Desmoplastic reaction is prominent.
Age: 7th
decade. M>F.
Increased incidence- carolis disease, sclerosing
cholangitis, IH calculi & IBD.

ON USG
Mass-forming: tumors will be a homogeneous
mass of intermediate echogenicity with a
peripheral hypoechoic halo of compressed liver
parenchyma.
They tend to be well delineated but irregular in
outline and are often associated with capsular
retraction which, if present, helps distinguish
cholangiocarcinomas from other hepatic tumours

Periductal infiltrating: tumors typically are
associated with altered caliber bile duct (narrowed
or dilated) without a well-defined mass.
Intraductal: tumors are characterized by alterations
in duct caliber, usually duct ectasia with or without
a visible mass. If a polypoid mass is seen, it is
usually hyperechoic compared to surrounding
liver .

CT SCAN
NECT: well defined round to oval hypo dense mass.
CECT: typically shows early peripheral
 enhancement. Centre of the tumor remains no
enhanced (abundant fibrous stroma).
In delayed phase centre of the tumor is enhanced.
Capsule retraction and biliary dilatation adjacent to
mass is highly suggestive of ICCA.

MRI
The tumour is hypointense on T1WI & hyperintense on
T2WI with an irregular contour.
Strongly hyperintense areas on T2WI- necrosis.
DWI: peripherally hyperintense target appearance.
CEMRI is similar to CECT.

HCC IHCC
Pathology Soft tumor(lack of stroma) Hard mass(abundant
fibrous tissue)
Risk factor Cirrhosis, alcoholism Sclerosing cholangitis
carolies disease,IBD
Hge & necrosis Common rare
Capsular retraction Less common Common(fibrosis)
Vascular invasion common Less common
NECT Hypodense Homogenous hypodense
CECT Early enhancement(Arterial
phase),
early washout( later
phases).
Heterogeneous minor
peripheral enhancement
with gradual enhancement
centrally.

Metastases
Liver is the most common site of metastasis.
Usually multiple.
Majorities are hypovascular (GI tract,lung breast& head,neck
tumour, lymphoma).
Hypervascular metastasis are less .(NET, RCC, carcinoid, sarcoma,
melanoma).
Calcified metastases are uncommon( colon, stomach,
breast,melanoma).
Cystic meatstases occur from mucinous ca of ovary, colon, sarcoma,
melanoma).

USG
•rounded and well-defined
•positive mass effect with distortion of adjacent vessels
•hypoechoic: most common ~65% and is a concerning
feature
•hypoechoic halo due to compressed and fat-spared liver
•cystic, calcified, infiltrative, and echogenic appearances
are all possible

CT SCAN
NECT: Typically hypodense, may be iso or
hyperdense, cystic, mixed,calcified.
CECT: Enhancement is typically peripheral in
arterial phase & washout in delayed phase.

MRI
Variable but usually most metastatic nodules are
hypointense on T1W & hyperintense on T2WI.
High signal intensity in T1WI- mets from melanoma,
ca colon.
Higher signal on T2WI- mets with liquifective
necrosis.
CEMRI: variable.

hemangioma ICCA metastasis
age Any age Older age(7th
decade)
Older(but can
occur any age)
sex F M M=F
MRI(T2WI) Iight bulb
appearance
Hyperintense Variable
Cystic—light bulb
Post contrast Nodular
peripheral
enhancement
Mild
heterogenious
peripheral
enhancement,exc
ept central scar
Peripheral rim
like enhancement
Bile duct invasion no common Less common
Capsular
retraction
No common No

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