IMAGING OF BENIGN FOCAL LESIONS IN CHILDREN AND ADULTS

1. PRESENTOR : Dr Navni Garg
MODERATOR : Dr Sonal Krishan
SEMINARSEMINAR
JUNE 26,2014JUNE 26,2014
IMAGING IN BENIGN
HEPATIC MASSES

2.  Focal liver lesion is by definition a discrete
abnormality arising within the liver
 Features of intra hepatic lesion
 Most of the lesion within the liver with
respiration
 Bulging of the liver capsule
 Displacement and distortion of the portal
and hepatic vessels
 Post displacement of IVC

3. BENIGN HEPATIC MASSES
Developmental
Infective/Inflammatory :
 Pyogenic abscess
 Amoebic abscess
 Fungal abscess
 Hydatid cyst
Granulomatous:
 Tuberculosis
 Sarcoidosis
Neoplastic

4. Benign neoplasms
Hepatocellular
(hepatocyte)
Cholangiocellular
(bile duct epithelium)
Mesenchymal
Adenoma
FNH (2nd
most common)
Hepatic cysts
Biliary cystadenoma
Hemangioma
(most common)
Mesenchymal
hamartoma
Infantile hemangio-
Endothelioma
Lymphangioma/
Lipoma/fibroma/
Angiomyolipoma/
Leiomyoma/

5. Malignant neoplasms
Hepatocellular Cholangiocellular Mesenchymal
Cholangiocarcinoma
Cystadenocarcinoma
Angiosarcoma
Epitheliod
hemangio-
Endothelioma
Leiomyosarcoma
Lymphoma
Hepatcellular Ca
Fibrolamellar carcinoma
Hepatoblastoma
HEPATIC METASTASIS

6. Imaging modalities
99Tc-sulphur
colloid
PET CT
Nuclear Medicine
US
CT
MRI
CTAP
CE-USG
Nuclear
scans
Conventional
Radiological
Newer
methods
DWI
Elasto
graphy
99Tc-RBC
scan

7. MDCT protocol for hepatic imaging
Radiographics 2001

8. CT arterioportogapgy
scan(CTAP)
 Principle: tremendous enhancement of
normal liver parenchyma following the SMA
or splenic artery injection
 Technique-conventional angiogarphy.
End hole catheter in splenic artery /SMA
150 ml iodinated contrast 150 to 300 I/ml at 3 to
5 ml/s. Start scan at 30s.
Limitations – nontumous perfusion defect- d/t to
laminar flow in the PV, aberrant vascular supply
defect
RCNA 1998

9. CT arterioportogapgy
scan(CTAP)
 most sensitive technique for detection of
focal hepatic neoplasm.
 Sensitivity 80-90% for metastasis and 70%
for primary malignant neoplasm.higher
sensitivity for smaller liver SOL.
 Disadvantage-low specificity, cost and
need for the invasive procedure.
 Replacement with GD and ferumoxide
enhanced MRI may be reasonable.
RCNA 1998

10. CT hepatic angiography scan
 Principle: all hepatic neoplasm are largely
supplied by the hepatic artery.
 Technique: angiographic catheter is placed in
common hepatic artery. Scan delay 3-5 s of
contrast injection.70 ml of diluted iodinated 15-30
% at 2ml/s.
 Applications. use full in combination with the
CTAP scan for characterizing the lesions and for
for characterization of portal perfusion defect.
RCNA 1998

16. Iodized oil CT scan
 Principle: lipiodol -iodized ethyl ester of acids of
poppy seed oil.Prolonged retention of lipiodol in
highly vascular and abnormal tissue.
 Technique: two step procedure
Step 1- complete angiographic study f/b injection
of 5- 20ml of lipiodol in proper hepatic artery
beyond GDA .
Step 2- CT scan of liver in 7 to 28 days.
 Applications – highly sensitive method for
diagnosing small foci of the HCC and
intrahepatic metastatic nodule of HCC. Sensitivity
97%, specificity 76%, accuracy 88%.
 Can differentiate between dysplastic nodule and
small HCC

17. MRI in liver tumors
T1weighted breath hold spoiled gradient- entire liver
scanned in single breath hold ,TR-150-200ms, TE-
minimum,8x2+- fat sat
T2 weighted sequence-
SE T2 , TR 4000, TE- 100, with respiratory trigger.
FSE breath hold.
Fat suppression
Half Fourier acquisition single shot turbospin echoe.
Contrast enhanced sequences

18. MRI protocol
Radiographics 2000

19. MRI CONTRAST
AGENTS
IN LIVER IMAGING

20. MRI CONTRAST AGENTS
 Mri contrast maximises the SI b/w two
tissues by either increasing or decreasing
the SI of tissue relative to another
 Should produce large effect at low conc.,
s/b biocompatible, low tolerable
toxicity,stable invivo as well as invitro(shelf
life), s/b excreted in reasonable time, s/b
organ specific as far as possible.

21. TYPES OF MRI CONTRAST
T1 agents
 Transitional &
lanthanide (Gd) metal
ions
 Paramagnetic
substances (unpaired
e-)resultent fluctuating
magnetic field affect
proton relaxation
 Increases T1
relaxation
 Increases SI
T2 agents
 Feromagnetic & super
paramagnetic
substances, have little
effect on tissue
relaxivity
 Induce dephasing d/t
their net positive
magnetization
 Protons undergo
transverse relaxation/
T2 relaxation
 Decreased SI on T2 (-
ve contrast)

22. T1 AGENTS
FDA approved
IONIC
 Gd-DTPA (gadopantate dimeglumine)=
Magnevist
NONIONIC
 Gd-DTPA-BMA(gadopentate
diamide)=Omniscan
 Gd-HP-DO3A(gadoteridol)=Prohance
Approved in european
countries

23. T1 Agents
 Dose .1mmol/kg in adults & children> 2 yrs
Mt sequence & higher doses up to .3
mmol/kg can further increase lesion
conspicuity
 Gd chelates c/b used as T2 agents if used in
sufficiently high conc. T1 effect predominant
at low doses
 Gd chelates rapidly leave the vascular
spaces& after about 3 min. reach the
equlibrium through out ECF compartment.

24. T1 Agents
 Cross the BBB similar to iodinated
contrast used in CT ,thus anything which
enhances with CT also enhances with
MR contrast, detection better with MR
contrast d/t better inherent contrast of
image.
 S/E seen in 3-5 % of pt. Nausea
,transient rise of s.bilirubin & iron
 Can be safely given in pt. With impaired
renal function, however dialysis
recommended in pt. With severe renal
impairment.

25. ORGAN & TISSUE DIRECTED
CONTRASTAGENTS
1. Liver specific
2. Hepatobilliary agents
3. GI contrast
4. Blood pool agents

26. LIVER SPECIFIC AGENTS
 T2 agents/-ve contrast/RES agents
 Coated iron oxide particles of various
sizes. Phagocytosed by RES of liver,
spleen, BM, LN.
 Normal liver looses SI on T2 agents, Focal
liver lesions like mets which do not contain
kupffer cell c/b better seen.
 More specific the accumulation of agent in
target tissue better the result & lesion
tissue contrast
 SPIO (Ferum oxide/AMI-25, Magnetite/
Resovist/ SHU-555) & USPIO(AMI-227).

27. SPIO (super Paramagnetic iron oxide)
(50+- 19 nm)
1.Ferum oxide (Feridex/ AMI-25)
 FDA approved
 RES clears it (T1/2=8min.)
 Liver t1/2=2-3 days
 Dose 10-15 micro gm/kg
 Slow infusion over 30 min. (pre & post
contrast imaging inconvenience)
 S/E back ache,hypo tension (skilled
personnel & resuscitation equipment s/b
available when ever ferum oxide is
administered)

28. SPIO
2.Magnetite/resovit/SHU-555
 Phase III cl. trial
 Dose =40 microgram(comparable to AMI-
25)
 Particle size 61 nm.
 Max.hepatic signal loss in 10 min.

29. USPIO(ultra small SPIO)
 Particle size 17-20 nm
 Rapid infusion c/b given
 Small volume required
 S/E- back ache,hypo tension,flushing
 Taken up by normal & cirrhotic liver,FNH &
adenoma,but excluded from HCC
 Clinical trials have not been reported.

30. USPIO
AMI-227
 Blood t1/2 long=200 hrs=blood pool agent
 T2 - liver looses SI, BV dark
 Has gr. T1 effect.
 T1 -bright blood effect-delineates IV
thrombus better.
 Good balance ofT1 & T2 effect, by bolus
administration dynamic imaging of liver c/b
done.

31. HEPATO BILLIARY AGENTS
(T1 agents)
 Soluble paramagnetic molecule
 Substantial hepatic uptake & Prolonged
hepatocyte retention, billiary ex.
 T1agent – preferential T1
enhancement,beginning with in min &
lasting for 2 hrs, imaging performed during
window after renal clearance from blood &
ECF

32. HEPATO BILLIARY AGENTS
(T1 agents)
FDA APPROVED
1. Mangafodipir/Teslascan =Mn-DPDP(Mn
dipyridoxal diphosphate)
UNDER CLINICAL TRIAL
1. Multihance = Gd-BOPTA (Benzyl oxy
propionic tetra acetate)Gadobenate
dimeglumine
2. eovist = Gd-EOB-DTPA (gadoxitate)

33. Mangafodipir/Teslascan
 Dose 5-10 micromol/kg
 Enhances max. in 10 min.Imaging window 10
min-4hr
 Not effected by obstructed billiary system
 Focal liver lesion seen as hypointense lesion
 Mets –have no hepatocytes ,seen as low SI
with in enhanced normal liver,whenever
enhanement present (8%) seen as rim
enhancement attributed to c ompressed
hepatic tissue.

34. Mangafodipir/Teslascan
 HCC-show detectable enhancement in
100% cases,complex pattern-Uniform,
heterogenous;thick/nodular/peripheral;sept
al, capsular sparing,well defferentiated
HCC may become nearly isointense to
liver.
 Regenerating nodules-often enhances &
become more concipicuous on post
contrast images b/c cirrhotic/fatty liver
show decrease enhancement.

35. Classification of
Hepatocellular Nodules
 Regenerative or hyperplastic
nodules
Monoacinar regenerative
nodules
Diffuse nodular hyperplasia (with
fibrosis)
Nodular regenerative
hyperplasia
Multiacinar regenerative
nodules
Large regenerative nodule (if
0.5 cm)
Lobar or segmental
hyperplasia
Focal nodular hyperplaisa
•Dysplastic or neoplastic lesions
Hepatocellular adenoma
Dysplastic nodule
Hepatocellular carcinoma

36. Nodular regenerative
hyperplasia
 Diffuse regenerative nodule not associated
with of fibrosis.hyperplasic hepatocytes.
 A/W connective tissue disease,various drugs
like steroids and anti proliferative drugs Portal
hypertension in 50 %.
 Imaging- multiple nodule similar imaging
feature to normal liver parenchyma, may
contain hemorrhage
 On Tc 99 sulphur colloid scan diffuse or
patchy uptake.

37.  USG : iso to liver with asso portal HTN
findings
 CT : non enhancing multiple hypo nodules.
Hmg may occur
 MRI : hyper on T1 and hypo on T2

38. Regenerative nodule
 Localized proliferation of
the hepatocytes and their
supporting stroma.
 Siderotic /nonsiderotic
 Low signal on the T2 and
variable signal T1, no
enhancement on arterial
phase.
 may not be differentiated
from dysplastic nodule

40. Adenomatous hyperplastic
nodule(dysplastic nodule).
 Benign but premalignat, in cirrhotic liver.
 10 –14% of cirrhosis, massive hepatic
fibrosis
 Contains iron and supplied by portal vein
 NECT- may be hyperdense but mostly are
isoattenuating.
 CECT isoattenuating or slightly low
attenuating on arterial, portal and delayed
phase images and thus are difficult to
depict on CT.
 May show enhancement in minority of
cases similar to HCC.

41. Adenomatous hyperplastic
nodule(dysplastic nodule
 MRI- hyperintense on T1 w and hypointense
on T2,
 Nodule with in nodule on T2 s/o HCC
 CT arterioportography- to differentiat AHN&
HCC
 HCC supplied by hepatic artery so enhances
on CTAP whereas dysplastic nodule is
supplied by portal vein

42. dysplastic nodule.

43. dysplastic nodule. enhancing

44. HCC within a dysplastic nodule with MR
imaging–histologic correlation.

45. FNH
• Second MC benign lesion
• F>M , 3rd
to 5th
decade
•2% primary tumors in children
• Congenital vascular malformation -> hyperplasia of
hepatocytes
• Kupffer’s cell activity seen
•Well circumscribed , non encapsulated mass with central
scar surrounded by nodules of hyperplastic hepatocytes
and kupffer cells
•No hmg or necrosis
RadioGraphics 2010

46.  May be present on liver surface, nodules
due to AVM
 May be pedunculated
 Rt lobe > lt lobe
 > 7 cm in children

47. USG
 Subtle liver masses
homogeneous,iso -
hypoechoic to normal
liver
 Contour deformity
 Doppler :prominent
vasc in the central
scar, hypervascular
tumors
 Numerous scattered
arterial and venous
signals : comet tail
appearance

48. CONTRAST ENHANCED USG
 Arterial filling of
mass (centrifugal)
 Portovenous
phase : iso to liver
with central non
enhancing scar
 Delayed :
accumulation of
contrast in scar

49. FNH
• Centrifugal filling
• Stellate/linear/plica
ted non enhancing
central area
• Sustained portal
phase
enhancement
HEPATIC ADENOMA
• Centripetal filling
• No scar

50. NCCT
 Iso – hypodense
 Central hypodense scar
 Calcification rules out FNH
 Bulge deformity on liver surface

51. • Arterial Phase- Homogenous enhancement
• PV phase- Iso to liv with hypo enhancing central scar
• Delayed Phase- Iso /hypo to liver with hyperenhancing
scar
CECT

53. MRI
 T1 : Hypo/iso
 T2 : hyper
 Central scar is
hyper on T2 due to
vascular and
myxoid tissue

54. CEMRI
 Homogeneous enhancement with rapid
washout to isointensity with surrounding
liver tissue
 Scar shows delayed and persistent
enhancement

56. MRI
FNH
• 60-70% decrease
in signal intensity
on T2W SPIO MRI
( kupffer cell
containing )
• Homogeneous
• T1WI : iso /hypo
• Central scar
HEPATIC ADENOMA
• 20% decrease in
signal intensity on
T2W SPIO MRI
• Heterogenous
• T1WI : hyper

57.  Sulphur colloid scan : hot spot
 Angiography : hypervascular mass
possessing centrifugal or spoke wheel
pattern with dense tumor blush in
capillary ,portal venous phase

58. B. Op de Beeck et al. : European Journal of Radiology(1999)
• Rare
• Usually solitary, > 10 cm
• 30-50 y F> M
• Association with oral contraceptives,anabolic steroid intake
and GSD type I
& III
• Lacks portal tracts and terminal hepatic veins
-> necrosis, hemorrhage, and rupture common in
large tumors
HEPATOCELLULAR ADENOMA

59. USG
 Heterogeneous
echogenic due to
intratumoral fat
and glycogen
 Anechoic areas
may be present
due to hemorrage
and scar tissue

60. CONTRAST ENHANCED USG
intense rapid enhancement during arterial phase
less rapid washout during portal / sinusoid
at last becomes isoechoic to liver parenhyma

61.  Discrete perilesional feeding arteries
manifest as enhancement around the
tumor capsule
 Never seen in HCC

62. NCCT
 Iso-hypodense
 Hypodensity due to
excessive steatosis
 Hyperdense areas
due to hemorrage

64. TRIPHASIC STUDY
 ARTERIAL : HYPERDENSE
 PV : ISODENSE
 HV : HYPODENSE

65. • Tc 99 sulphur colloid –cold spot in 80% as
they lack kupffer cells
• MRI-iso to hyper on T1and T2 due to fat
and glycogen; capsule may be hypo on
T1WI
• Enhancement similar to CT
• SPIO- variable signal loss

66. a
Alvin C. Silva, MD et al .RadioGraphics 2009
c
b

67. HEPATIC SCINTIGRAPHY
 Uptake seen which doesnot get excreted
therefore delayed enhancement

68. Hepatic cyst
• Developmental benign, not
communicating with billiary tree
• Solitary unilocular cyst lined
bile duct epithelium.
• 5-14 % of general population
F>M (5:2)
• USG- anechoic with
imperceptible wall and post
acoustic enhancement.
• CT scan- water density
attenuation, no enhancement
• MRI : T1-hypo,T2-hyper
no enhancement
Cystic focal liver lesions

69. D/D
 Abscess
 Hydatid cyst
 Necrotic mets
 Hepatic cystadenocarcinoma
 Hematoma
 Intrahep GB

70. COMPLICATED CYST
 Because of hemorrage or infection in
simple cyst
 USG :Presence of internal echoes,
debris,thick septations, mural calcification
or nodules
 CT : septations,internal debris and wall
enhancement
 MRI : Hyper on both T1,T2 due to mixed
blood products

71. PERIBILIARY CYST
 Seen in pts with severe liver disease
 Small in size 0.2 – 2.5 cm
 Usually located centrally within porta
hepatis or at the junction of the main right
and left hep ducts
 Generally asymptomatic
 May rarely cause biliary obstruction
 Due to obstructed small periductal glands

72.  USG : discrete clustered cysts or tubular
appearing parastructures having thin septa
which parallel the bile ducts and portal
veins

73. POLYCYSTIC LIVER DISEASE
• More than 10 simple hepatic cysts
• Surrounding parenchyma frequently
contains von meyenburg’s complexes
• Associated with periductal fibrosis and bile
duct proliferation – congenital
fibropolycystic disease of liver
• Associated with autosomal dominant
polycystic kidney disease in 70%

74.  No corelation exists between severity of
renal ds and extent of liver involvement
 LFTs normal

75. Polycystic liver disease

76. Biliary Cystadenoma
• Slow growing multilocular cystic tumors
• 85 % : intrahepatic ( 55% - right lobe, 29%- left
lobe , 16% - both lobes)
• F>M
• May communicate with intrahepatic bile ducts and
secrete mucinous material into the duct
• Premalignant
• Calcification rare
• Avascular

77. • USG: 1.5-35 cm,
solitary cystic
mass , well defined
thick capsule,
mural nodules
seen in the
anechoic mass
• CT : Thin septa
show
enhancement

78. MRI
 T1WI-hypo, T2WI-
hyper, septations
are seen as dark
bands separating
high signal
intensity locules

79. • ↑ CA19-9 and CEA in intracystic fluid of
cystadenoma/ cystadenocarcinoma
• Polypoid, pedunculated excrescences with
coarse calcification in septa seen in
cystadenocarcinoma

80. HEMANGIOMA
• MC benign lesion of liver
• 2 MC hepatic tumor after metastasis
• Prevalence -- 1–2% to 20% (F:M= 2:1–5:1)
• More common in right lobe of liver
• More common in subcapsular location/around intrahepatic
vessels
• Blood filled vascular channels separated by thin fibrous
septa lined by flat endothelium
• No kupffer cells

81. • XRAY ABDOMEN : multiple calcific
phlebolith, numerous calcified
trebaculations and spicules arising from
central point and radiating towards
periphery

82. USG
 Sharply defined
 High reflective due
to multiple
interfaces between
vascular spaces
 Homogeneous
 Lobulated margins
if > 2.5 cm
 Involuting :
heterogeneous

83. CONTRAST ENHANCED USG
 Peripheral puddles of
enhancement
 Centripetal filling
 Complete fill in on
delayed imaging
 Sustained
enhancement
But all the phases of
enhancement must
have the same density
as the blood pool.

84. DYNAMIC CT IMAGING

85. FLASH HEMANGIOMAS
 Small hemangiomas may show fast
homogeneous enhancement ( flash filling)
 D/D : Small HCC , Hypervascular
metastasis
 So look at all phases to see if the
enhancing areas match the blood pool.

86.  Hemangiomas have peripheral nodular,
globular enhancement
 D/D : rim enhancement is continous
peripheral enhancement seen in malignant
lesions ( metastases)

87. MORPHOLOGY ON MRI
 Sharp geographic margins
 Lack of peripheral halo on T2WI
 Lack of deformity of the liver surface
 Superficial location
 Lack of displacement of hepatic vessels

88. MRI : T1- HYPO , T2 -HYPER

89. DYNAMIC MRI IMAGING WITH GADOBENATE
DIMEGLUMINE (MULTIHANCE)

90.  Hemangioma with central fibrosis :
hypointense on T2WI
 HCC and metastasis : hyperintense
necrotic area on T2WI
 Giant hemangioma : heterogeneous on
T2WI due to thrombosis,myxoid
tissue,fibrosis . May show irregular flame
shaped peripheral and central
enhancement

91. RBC SCINTIGRAPHY
 Hot spot on delayed Tc99 –RBC scan
 Scans are taken 1-2 hours after injection of
patient’s isotope labelled blood
 Progressive increase in ratio of blood pool
activity within the hemangioma to that of
surrounding liver because of retarded
blood flow in vascular sinusoids
 Initial photopenia with hot nodule on
delayed blood pool images

92. Angiography : Gold std
 Normal main and feeding vessels
 Early contrast accumulation within the
lesion during the late arterial phase
 Persists throughout the venous phase :
diagnostic
 Feeding vessels show crowding around
the lesion

93. Atypical hemangioma
Tommaso Vincenzo B et al,EJR 2007
• Only 55% cases show typical enhancement
patterns
• Atypical features : lesions >6-8cm
• Due to hemorrhage, necrosis, cystic change and
hyalinization
• Centrifugal (inside-out) enhancement
• Only peripheral enhancement
• Only central
• Diffuse

94. e
Baseline
LVP
Baseline
AP
PVP
Tommaso Vincenzo B et al,EJR 2007

95. Baseline PVPAP
10mins

96. CT finding useful in differentiating
liver tumor with central scar

97. Bile duct hamartoma
(Von Meyenburg complex)
• Incidental finding
• Due to failed involution of
embryonic bile duct
• Grayish white nodular 0.1-
1.5cm. Not communicating with
the billiary system
• USG :Multiple,anechoic
• CT : <1.5 cm,multiple
hypodense,no enhancement
Mortele KJ et al. RadioGraphics 2001;

98.  On USG, bright echogenic foci with ring
down artifacts occuring due to presence of
cholesterol crystals withih dilated tubules

99.  MRI : hypo on T1 and hyper on T2
Irregularly outlined. No enhancement/rim
enhancement ( due to compressed liver
parenchyma)
 MR CHOLANGIOGRAPHY :
multiple,tiny,cystic lesions that donot
communicate with biliary tree

100. Bile Duct Hamartoma
Mortele KJ et al. RadioGraphics 2001;

101. Liver cyst
 Varible sized
 Regular outline
 May be associated
with ADPKD
Biliary hamartoma
 <1.5 cm
 Irregular outline
 No such
association

102. • Include lipoma, myelolipoma
and angiomyolipoma
• A/W renal AML & tuberous
sclerosis(10%)
• USG- hyperechoic SOL.
• CT scan- radiolucent fat,
enhancement
• MRI- hyper on T1 & T2
Lipomatous tumours

103. Angiomyolipoma

104. Focal inflammatory lesions
• Abscesses
• Hydatid cysts

105. PYOGENIC LIVER ABSCESS
MC – STAPH, others : aerobic, non aerobic
Sources
 Ascending cholangitis from biliary tree
 Phlebitis secondary to diverticulitis,
appendicitis, pancreatitis , GI infections
 Arterial septicemia as result of
endocarditis,pneumonitis or osteomyelitis
 Direct extension from contigous organs
such as perforated ulcer, pneumonia,
pyelonephritis
 Iatrogenic causes

106. Pyogenic vs Amoebic
Biliary origin : multiple, both lobes
Portal vein source : solitary, right
lobe (65%), left lobe (12%), both
(23%)
CT: Round (60%)or irregularly
hypoattenuating area with
peripheral rim enhancement
Cluster sign : small abscesses
coalescing together
Double target sign : perilesional
edema
USG : Well defined or irregular &
thick walled lesion , hypoechoic
(36%)
Gas – echogenic foci ,
Fluid-fluid interface, internal
septations , debris
• Solitary unilocular
• Right lobe of liver (posterosuperior
segments)
•CT : hypoattenuating with peripheral
rim enhancement
•USG : Round or oval(82%)
• Absence of prominent abscess wall
• Hypoechoic compared to normal
liver with fine internal echoes (58 %)

107. 25sPyogenic abscesses

108. Pyogenic abscesses

109. Amoebic liver abscess

110. Cystic Hydatid Disease
Gharbi’s Classification of Cystic Hydatid Disease
Type Ultrasonographic features and patterns
I
Pure fluid collection - univesicular cyst
II
Fluid collection with a split wall- detached
laminated membrane (water-lily sign)-
III
Fluid collection with septa representing walls of daughter
cysts (honeycomb sign)
IV
Heterogeneous appearance - presence of matrix
- mimics a solid mass
V
Reflecting thick walls - calcifications

111. TYPE I TYPE III
TYPE IV TYPE V

112. CT
 Well defined, round or oval cystic mass
 Hyperdense to normal liver normally

113.  Detached
laminated
membranes : linear
areas of increased
attenuation

114.  Multiloculated,
daughter cysts
 Calcification : +/-

115. MRI
 T1WI : hypo
 T2WI : hyper
 Peri cyst has low signal on T1 and T2 due
to high collagen

116. Alveolar Echinococcosis
• E multilocularis is responsible parasite.
• Liver is MC (90%) site of E multilocularis , 70% rt. Lobe.
• Foxes - main host , rarely cats & dogs.
• Endemic in upper Midwest of USA, Alaska, Canada,
Japan, Central Europe, and parts of Russia
• Hilar infiltration in 50% of pts – dilatation of intrahepatic
bile ducts and invasion of the portal and hepatic veins,
with subsequent atrophy of the affected liver segments
due to hypoperfusion
Mortele KJ et al. RadioGraphics 2004;

117. • US - “hailstorm” pattern – multiple echogenic nodules with
irregular and indistinct margins
- Lesions with central liquefactive necrosis appear
hypoechoic, with some internal echoes and an irregular
hyperechoic border
• CT and MR - multiple irregular, ill-defined lesions scattered
throughout the involved liver that are generally hypo at
CT and hyperintense at T2WI.
- This mimic either metastases or pyogenic abscesses.
- little or no enhancement.
• D/D – Cystadenoma / Ca, peripheral cholangio Ca or
metastasis with peripheral bile duct dilatation.
Mortele KJ et al. RadioGraphics 2004;

121. FUNGAL ABSCESS
– Candidiasis
• Wheel within
wheel appearance
• Bulls eye /Target
lesion : hyper centre
with hypo rim
• Echogenic foci :
scar
• Uniformly
hypoechoic – M.C.

122. RadioGraphics 2001;

123. RadioGraphics 2001;

124. Focal hepatic
lesions
Solid hepatic
lesions
Cystic hepatic
lesions
Small
hemangioma
FNH Adenoma Metastasis
‘Washout’’
Capsule
+/- Fat
Post/delay
T2
Post/delay – ‘fades’
T2 iso
Central scarring
Gd
Ring
Enhancement
T2
Diffusion
Benign Malignant
Lymphoma
Prim/Sec
attenuation
T1
T2

125. Cystic hepatic
lesions
Developmental Miscellaneous
Hepatic
cysts
Bile duct
hamartoma
Rim
Enhancement
< 1.5cm
Biliary Cyst
adenoma/Ca
Hematoma
Multilocular
Mural nodules
Fib capsule, Calc
Variable SI
Bilioma
Neoplastic
Inflammatory
Abscess
Subcapsular
pseudocyst
Hydatid
cyst
Air, Enh wall
Double target sign
‘Cluster sign’
Low Att/
No wall/
enhancement
T1
T2
Calcification
Daughter cysts
Pericyst (T1,T2 )
Matrix (T1 T2 )
Lt. liver lobe
Signs of panc
Thin capsule
Signs of trauma
Low att at CT
Meth Hb at MRI
No capsule
No septa
No calcification
Solitary, hete
enh solid comp
T1
T2

126. D/D : Malignant cystic lesions
Cystic metastasis
 Ovarian tumors
 Teratomas
 Squamous cell Ca

127. Pediatric liver masses
• MC liver neoplasm in children, as in adults, is metastasis
• Most primary tumors are malignant,1/3rd
benign
• MC benign tumors are IHE, FNH, mesenchymal
hamartoma, NRH & hepatocellular adenoma
• Malignant – Metasasis, hepatoblastoma, HCC,
Lymphoma
• Others - Abcesses, hematoma
Ellen MC, et al. RadioGraphics 2010; 30:801–826

128. D/D of Pediatric liver tumors
• Age < 5years-hepatoblastoma ,IHE,mesenchymal
hamartoma, metastasis.
• Age> 5 years : HCC, adenoma and metastasis.
• AFP- HCC , hepatoblastoma
• Solitary vs multiple SOL- IHE, metastasis,
abscess,lymphoproliferative disease, adenoma,

129. Infantile hemangioendothelioma
• 90% before 6 months,F>M
• Mesenchymal tumor , vascular channels formed by
endothelial proliferation
• Usually presents as hepatomegaly/abdominal
mass/congestive heart failure due to AV Shunting in the
lesion/ thrombocytopenia due to platelet sequestration
(kasabach meritt syndrome )
• May be associated with cutaneous hemangiomas
Ellen MC, et al. RadioGraphics 2010; 30:801–826

130. TYPE 1
 Vasc channels lined by
endothelial cells
supported by reticular
fibres
TYPE 2
 Large irregular branching
spaces lined by immature
pleomorphic cells

131. USG
 Variable, highly echogenic
to hypoechoic /anechoic
mass.
 Celiac axis & CHA are
dilated
 Abdominal aorta caliber
below coeliac axis origin
reduces
 Hepatic veins become
prominent

132. CT
 Hypodense ,well
defined ,
homogeneous
nodule
 Calcification in
40%
 Centripetal filling
as in hemangioma.

133. MRI
• Hypointense on T1WI and hyperintense on
T2W
• Heterogeneous if necrosis, hemorrage and
fibrosis
• Feeder vessel-flow void
• Centripetal fill in of contrast post gadolinium

134. Mesenchymal hamartoma
• Benign cystic mesenchymal tumor
• < 2 years, M>F Abdominal distension
• Large mass(5-22cm),right lobe,
encapsulated and pedunculated,
gelatinous mesenchymal tissue with
cyst
Ellen MC, et al. RadioGraphics 2010; 30:801–826

135. USG
 Solid / cystic mass,
multilocular with anechoic
areas with echogenic
septae and stroma .

136. CT
 Complex mass,
low attenuation
areas separated
with enhancing
septa and stroma.

137. MRI
 Cystic component
is hyper on T2 and
mesenchymal
(stromal) tissue is
hypo on both T1
&T2

138. DW MRI in focal liver lesions
• With advances in hardware and coil systems, DW MRI –
now be applied to liver imaging with improved image quality.
• Enables qualitative & quantitative assessment of tissue
diffusivity (ADC) without Gd chelates, which makes it a
highly attractive technique, particularly in patients with
severe RF at risk for NSF.
• Detection and characterization with better results
compared with T2-WI.
• Should be interpreted in conjunction with conventional
sequences.
Taouli and Koh , Radiology 2010.

139. Taouli and Koh , Radiology 2010.

140. DWI in liver cysts

141. b=100
b=600
b =1000Hemangioma

142. b0
b100
b500 b1000
HCC
ADC

143. Lesion detection
Taouli and Koh , Radiology 2010.

145. Treatment assessment Taouli and Koh , Radiology 2010.

146. CONCLUSION
• Accurate clinical information needed to select the most
appropriate imaging modality
• Ultrasound is the initial modality for hepatic imaging
• Helical CT/ MRI are able to characterize the hepatic lesions
• DW-MRI has the potential to help detect and characterize
focal lesions in the liver.
• Knowledge of imaging features of liver lesions is essential to
avoid unnecessary work-up and to minimize patient anxiety