RADIOLOGICAL FEATURES OF COMMON FOCAL LIVER LESIONS WITH DIAGNOSTIC CHARACTERISTICS

1. LIVER LESIONS
Maj Satyendra
Ref : Manorama berry
Gore Levine
Radiology assistant
Radiopedia

2. OBJECTIVE
1. Identify the most important features of common liver
tumors

3. 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

4. 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

5. HYPERVASCULAR LESIONS
Benign
 Hemangioma
 Adenoma
 FNH
Malignant
 HCC
 FLC
Metastasis
 RCC
 Melanoma
 NET

6. IMAGING TECHNIQUES
 plain radiography : gross hepatomegaly
 calcification
USG / CE-USG
CT
MRI
 Angiography
 Scintigraphy:
 Sulfur colloid , Tc99m labelled RBC’s
PET

7. 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

8. UNDERSTANDING THE PHASES
 Liver -dual blood
supply
 Normal parenchyma -
80% portal vein
 20% -hepatic artery
 All liver tumors blood
supply from hepatic
artery

9. 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

10. PORTAL VENOUS PHASE
 60- 80 sec
 To detect hypovascular
tumors

11. DELAYED PHASE
Begins at about >
180 sec
Best done at 10
minutes

12. 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

13. T1W T2W Gadolinium
MRI of Liver
Hepatocellular Ca
,iso or (fat degeneration)
Metastasis
Haemanigioma ++ (like CT)
Adenoma
often
FNH + delayed
FLC + delayed

14. 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

17. 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

18. 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.

19. PLAIN CT:
 HYPODENSE MASS

20. 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.

22. MR
 Marked hyperintensity
on T2 WI
 Light bulb sign
 Low intensity areas-fibrosis/
myxoid tissue/
thrombus

23.  <2 cm - uniform
early enhancement
 peripheral nodular
 Centripetally
enhancement.
 large (>5cms)
 peripheral nodular
enhancement
 Centre remains
hypointense.

24. GIANT CAVERNOUS HEMANGIOMA
 5 – 20 CMS.
 CAN BE CONFUSED
WITH METS /HCC

26. 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 %

27.  USG:
Large hyperechoic
lesion- glycogen / fat
Central anechoic
areas: zones of internal
haemorhage

28.  PLAIN CT: Low
density lesion (fat)
 High density lesion
( hge )
 CECT:
Hypervascular
lesion , rapid
washout
 Calcification +/- 5
%

29. MRI
 Heterogenous
 Increased T1
signal
Fat/ glycogen
Low signal –
hemorrhage/
necrosis/ scar
Hypointense
capsule T1 and T2 -
1/3rd
CSI –loss of
signal

30. 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

31.  USG:
Well defined isoechoic
mass
Homogenous
echotexture
Central hypo scar
Calcification seen in
1.4 % .
 DOPPLER:
stellate flow pattern
CEUS : central A with
centrifugal filling

32.  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.

33. 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.

34.  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.

35. 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

36.  CSI
 in-and out-of phase
 Signals of fat and
water cancel each
other in “out of phase”
image

37. HEPATOCELLULAR CARCINOMA
 Most common primary malignancy of the liver
 Rising incidence, attributed to a rise in hepatitis B
and C infection

38. 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

39. USG
 Small HCC’s
(<3cms)
 hypoechoic with
posterior acoustic
enhancement
 >3cms- mosaic or
mixed pattern

40. CT SCAN
 3 patterns:
 Solitary
 Multicentric
 Diffuse
 Large hypodense
mass
 Central low
attenuation due to
necrosis

41.  Focal calcification -
7.5%
 Majority -
hypervascular
 arterial phase
 Heterogenous
enhancement due to
central necrosis
 Isodense on delayed
images
 Angioinvasive: portal
vein /IVC

42. ARTERIAL PHASE
 Demonstration of
arterial branches
tumour
 Arterio portal shunts

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

45. 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.

46. 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

47. 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

48. Moderate
enhancement.
 Delayed enhancement
of scar
 Prognosis - good.

49. 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

50. 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

51. Hypervascular mets:
RCC, Thyroid,
carcinoid, melanoma,
islet cell tumor,
choriocarcinom.
 Calcified mets:
Mucinous CA of GI
tract (colon, stomach,
rectum), melanoma
ovarian ca.

52. Cystic mets:
 mucinous ovarian
ca, colonic ca

53. THANK U