LIVER LESIONSMaj Satyendra

Ref : Manorama berry

Gore Levine

Radiology assistant

Radiopedia

OBJECTIVE1. Identify the most important features of common

liver tumors

LIVER LESIONS MALIGNANT Metastasis Hepatocellular carcinoma

(hepatoma) Fibrolamellar carcinoma Intrahepatic

cholangiocarcinoma Hepatoblastoma Infantile

hemangioendothelioma Biliary cystadenoma

/cystadenocarcinoma Angiosarcoma Epithelioid

hemangioendothelioma Lymphoma

BENIGN Liver cysts Cyst adenoma Biliary hamartomas Hemangioma Focal nodular

hyperplasia Hepatic adenoma Regenerative nodules Atypical regenerative

nodules

LIVER LESIONS MALIGNANT Metastasis Hepatocellular carcinoma

(hepatoma) Fibrolamellar carcinoma Intrahepatic

cholangiocarcinoma Hepatoblastoma Infantile

hemangioendothelioma Biliary cystadenoma

/cystadenocarcinoma Angiosarcoma Epithelioid

hemangioendothelioma Lymphoma

BENIGN Liver cysts Cyst adenoma Biliary hamartomas Hemangioma Focal nodular

hyperplasia Hepatic adenoma Regenerative nodules Atypical regenerative

nodules

HYPERVASCULAR LESIONSBenign

Hemangioma Adenoma FNH

Malignant HCC FLC

Metastasis RCC Melanoma NET

IMAGING TECHNIQUES plain radiography : gross hepatomegaly

calcification USG / CE-USG CT MRI Angiography Scintigraphy:

Sulfur colloid , Tc99m labelled RBC’s PET

CT SCAN

Non contrast study:

Contrast study: arterial phase: 20-40secs Portal phase : 60-80secs Early delayed: > 180 sec

, best at 4 mins Late delayed : 4-6hrs

UNDERSTANDING THE PHASES Liver -dual blood

supply Normal parenchyma

- 80% portal vein 20% -hepatic artery All liver tumors

blood supply from hepatic artery

ARTERIAL PHASE

20- 40 sec Hypervascular

tumors enhance via the hepatic artery

Normal liver parenchyma not yet enhanced

Hypervascular tumors enhance optimally at 35 sec

PORTAL VENOUS PHASE

60- 80 sec To detect

hypovascular tumors

DELAYED PHASE

Begins at about > 180 sec

Best done at 10 minutes

  Pre contrast Arterial Phase Portal venous phase

Delayed

Hepatocelluar Ca Low attenuation Homogenous enhancement

Washout of lesion

Isodense

Adenoma Low attenuation Homogenous enhancement 85%

Iso or hypodense

Iso or hypodense

Haemangioma Low attenuation Peripheral puddles Partial Fill in Complete fill in

FNH Iso/Low attenuation

Homogenous enhancement

Hypodense Isodense

Hypervascular Mets Low attenuation Homogenous enhancement

Hypodense  

Metastasis Low attenuation Hypodense Hypodense  

Cyst Low attenuation No enhancement    

Abscess Low attenuation may have irregular margins

Transient regional enhancement

Ring enhancement

 

Multiphasic CT of Liver

T1W T2W Gadolinium Hepatocellular Ca

,iso or (fat degeneration)     Metastasis      Haemanigioma   ++   (like CT) Adenoma

 often     FNH   +   delayed 

 FLC   +   delayed  

MRI of Liver

LIVER CYSTS

Developmental - ? Origin from hamatomatous tissue

Do no communicate with biliary tree

Thin walled 1mm Unilocular Anechoic Water density 0-15 HU Non enhancing >10 consider ADPKD

HEMANGIOMA

Commonest benign tumor

Asymptomatic Large vascular

channels filled with slowly flowing blood

F> M (5:1) Multiple in 10%

cases 2-4cms-typical

characteristic

USG

Sharply defined Hyperechoic Homogenous Faint acoustic

enhancement >2.5cm Cystic and fibrotic

regions

Doppler : Filling vessel in the

periphery of the tumor but no significant colour flow.

PLAIN CT: HYPODENSE MASS

CECT: Early peripheral lesion

enhancement Progressive centripetal

opacification Isodense fill in on

delayed scans (<15 mins)

Central scar may be present

Upto 90% of hemangiomas meet these criteria.

MR

Marked hyperintensity on T2 WI

Light bulb sign

Low intensity areas- fibrosis/ myxoid tissue/ thrombus

<2 cm - uniform

early enhancement

peripheral nodular Centripetally

enhancement. large (>5cms)

peripheral nodular enhancement

Centre remains hypointense.

GIANT CAVERNOUS HEMANGIOMA 5 – 20 CMS.

CAN BE CONFUSED WITH METS /HCC

HEPATIC ADENOMA

Solitary >10 cm Pathology: absence of

kupffer cells, bile ducts ? malignant potential Female : age 20 – 40

yrs. H/o OCP/ anabolic

steroids

Central hge/ necrosis Thin capsule -30 %

USG: Large

hyperechoic lesion- glycogen / fat Central anechoic areas: zones of internal haemorhage

PLAIN CT: Low density lesion (fat)High density

lesion ( hge ) CECT:

Hypervascular lesion , rapid washout

Calcification +/- 5 %

MRI

Heterogenous Increased T1

signal Fat/ glycogenLow signal –

hemorrhage/ necrosis/ scar

Hypointense capsule T1 and T2

- 1/3rd CSI –loss of signal

FOCAL NODULAR HYPERPLASIA

Asymptomatic/incidental Etiology- unkn/ ? Cong

vascular malformation Female -20-50 yrs. Typical central stellate

fibrovascular scar - 50%

Hyper vascular Normal liver elements

Hepatocytes Non communicating bile

ducts, Kupffer cells Fibrous septa

USG: Well defined

isoechoic massHomogenous

echotextureCentral hypo scarCalcification seen

in 1.4 % .

DOPPLER: stellate flow pattern CEUS : central A with

centrifugal filling

NECT: Well defined with mass effect Attenuation same as that of

liver parenchyma/ less - fat Central scar common.

Arterial phase : Lesion enhance markedly and uniformly with the exception of central scar.

Portal phase : Isodense with liver

parenchyma Scar- low.

Delayed imaging : iso dense Scar may show enhancement.

MRI T1: Isointense T2: Slightly

hyperintense to isointense.

central scar is hypointense on T1 and hyperintense on T2.

Early homogenous enhancement of FNH , late enhancement of the central scar.

T2 WITH SPIO: FNH shows loss of signal due to

uptake of iron oxide particles by kupffer cells within the lesion. The degree of signal loss is greater than normal liver

T1 WITH Mn DPDP/ BOPTA FNH contains hepatocytes that take

up these agents resulting in hyperintensity of the lesion relative to the liver.

FOCAL FAT Diagnostic confusion

with tumors Common sites

Periportal region of the medial segment of left lobe (segment IV)

Either side of falciform ligament

Cranial aspect of GB fossa

Characteristic features: Geographic appearance Lack of mass effect Vessels through the

lesion

CSI in-and out-of phase

Signals of fat and water cancel each other in “out of phase” image

HEPATOCELLULAR CARCINOMA

Most common primary malignancy of the liver

Rising incidence, attributed to a rise in hepatitis B and C infection

RISK FACTORS: hepatitis B (HBV) infection hepatitis C (HCV) infection alcoholism biliary cirrhosis food toxins e.g. aflatoxins congenital biliary atresia inborn errors of metabolism

haemochromatosis

alpha-1 antitrypsin deficiency

type 1 glycogen storage disease

Wilson disease

USG Small HCC’s

(<3cms)hypoechoic

with posterior acoustic enhancement

>3cms- mosaic or mixed pattern

CT SCAN

3 patterns: SolitaryMulticentricDiffuse

Large hypodense mass

Central low attenuation due to necrosis

Focal calcification -7.5%

Majority - hypervascular arterial phase

Heterogenous enhancement due to central necrosis

Isodense on delayed images

Angioinvasive: portal vein /IVC

ARTERIAL PHASE

Demonstration of arterial branches tumour

Arterio portal shunts

Portal venous invasion by hepatocellular carcinoma. portal phase-expanded low attenuation focus in right portal vein.

MRI

Small HCC’s v/s regenerative Cirrhotic nodule: hyper on T1 , iso / hypo on T2

HCC : hyperintense on T2

HCC arising in a siderotic nodule: “nodule within a nodule” appearance

HCC - a small focus of high signal intensity within the low signal intensity nodule.

Hepatocellular carcinoma and regenerative nodule. T1w MRI (A) and T2w MRI (B) demonstrating a hepatocellular carcinoma (white arrowhead) and an adjacent atypical regenerative nodule (black arrowhead).

Majority of hepatomas have decreased signal intensity on T1WI -increased signal -fat or glycogen content

FIBROLAMELLAR CARCINOMA

Age group: 5 - 35yrs Spontaneous

No predisposing factor

Solitary lobulated well defined tumor containing a central fibrous scar.

Punctate calcification- in scar >50% cases

Moderate enhancement.

Delayed enhancement of scar

Prognosis - good.

FNH V/S FLC

Central scar of FNH -hyperintense on T2.

FNH rarely has calcification within the scar.

FNH - usually asymptomatic.

Biopsy normal hepatocytes with bile ductules in FNH Malignant, eosinophilic hepatocytes in FLC

METASTASIS

Most common Most common metastatic

site , after nodes Multiple lesions – common

Hypervascular mets DD -hemangiomas, FNH,

adenoma and HCC. 

Hypovascular mets DD-focal fatty infiltration,

abscesses, atypical hypovascular HCC

Hypervascular mets: RCC, Thyroid, carcinoid, melanoma, islet cell tumor, choriocarcinom.

Calcified mets: Mucinous CA of GI tract (colon, stomach, rectum), melanoma ovarian ca.

Cystic mets: mucinous ovarian

ca, colonic ca

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