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
15.
16.
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.
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.
21.
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.
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
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
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.