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RADIOLOGICAL FEATURES OF COMMON FOCAL LIVER LESIONS WITH DIAGNOSTIC CHARACTERISTICS
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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
THANK U
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