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BENIGN FOCAL
LESIONS
IN LIVER
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
Phases
 Liver -dual blood
supply
 Normal parenchyma -
80% portal vein
 20% -hepatic artery
 All liver tumors blood
supply from hepatic
artery
 Tumors enhance in
arterial phase.
 Liver will enhance in
the portal venous
phase
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
 Will be visible as hyperdense
lesions in a relatively
hypodense liver
Portal venous phase
 60- 80 sec
 To detect hypovascular
tumors
 also called the hepatic phase
because there is
enhancement of the hepatic
veins
Delayed Phase
 Begins at
about > 180
sec
 Best done at
10 minutes
CT LIVER – FOCAL HYPERENHANCING LESIONS
 During the arterial phase
 1. Hepatocellular carcinoma.
 2. Haemangioma.
 3. Focal nodular hyperplasia.
 4. Adenoma.
 5. Metastases – particularly carcinoid and pancreatic islet cell.
 Most metastases are hypovascular.
During the portal vein phase
 1. Haemangioma.
 2. Hepatocellular carcinoma – unusually. Most are isodense- or low-
attenuation during this phase.
 3. Venous collaterals – from an obstructed SVC to the IVC via
hepatic veins.
During the equilibrium phase
 1. Haemangioma – because of progressive fill-in.
 2. Cholangiocarcinoma.
 3. Solitary fibrous tumour.
 4. Treated metastases.
Hepatic cyst
• Single/multiple.
• Lined by single layer of cuboidal epithelium.
• Older adults
• Clinical presentation
– Asymptomatic
– Compressive symptoms (massive).
Autosomal dominant polycystic liver disease
• Multiple cysts (more than 10)
• Vary in size: 1-10 cm
• Water or hemorrhagic density
• Calcification of some cyst walls is seen
• No septations or mural nodularity
• Occasionally fluid levels seen
• Liver often distorted by innumerable cysts
usg
• Fine cystic lesion with
partial or complete
septa are often
visualized.
• In case of
complications –
debris, thickened septa
and complex internal
fluid.
ct
• Smooth rimmed
hypodense mass.
• HU value near zero.
• No enhancement at all
on CECT.
MR Findings
• Simple hepatic cyst & ADPLD
o T1WI: Hypointense
o T2WI: Hyperintense
o Heavily T2W images
• Markedly increased signal intensity
due to pure fluid content
• Sometimes indistinguishable from a
typical hemangioma
o MRCP: No communication with bile
duct
Differential diagnosis
1. Cystic or necrotic metastases
Demonstrate (e.g., ovarian
cystadenocarcinoma &
metastatic sarcoma)
o Debris
o Mural nodularity
o Thick septa
o Wall enhancement
Dd-2.Biliary cystadenocarcinoma
• Usually large in size
• Homogeneous, hypodense, water density
mass
o Rarely non septated
o Indistinguishable from large simple cyst
• Almost always has septations
• May show fine mural or septal
calcifications
• On contrast study
o Unilocular or multilocular
o Enhancement of capsule, septa & mural
nodules
Dd-3
Typical hepatic hemangioma
• Well-defined margins
• NECT: Isodense to blood
• CECT: Early peripheral nodular &
delayed centripetal
enhancement isodense to
enhanced vessels
• T1W: Hypointense
• T2WI: Markedly hyperintense
Sometimes indistinguishable from
simple hepatic cyst
DD-4 Pyogenic abscess
• Complex cystic mass
• Heterogeneous density
• Thick or thin multiple septations
• May show mural nodularity
• With or without hemorrhage
• May show fluid-debris levels
• Wall enhancement may be seen
• Absent or heterogeneous enhancement
of lesion
Dd-5 Hepatic hydatid cyst
• Large well-defined cystic liver
mass with numerous
peripheral daughter cysts
• With or without calcification &
dilated bile ducts
Cavernous hemangioma
• Most common
primary liver
tumor.
• All age groups.
• females >> males.
• Size less than 1
cm to 30 cm
(giant
hemangioma).
• No signs and
symptoms.
• When tumor
exceeds 4 cm
,abdominal
pain/discomfort or
a palpable mass.
• Rupture occurs
rarely.
characteristics
• Usually solitary.
• Borders are clear.
• Not encapsulated.
• Various degenerative changes are seen in its
centre.
– Old and new thrombus formation.
– Necrosis, scarring, hemorrhage & calcification.
Usg
Typical hemangioma
• Homogeneous hyperechoic mass with
acoustic enhancement
• Size: 2-10 cm
Giant hemangioma
• Lobulated heterogeneous mass with echoic border
• Size: More than 10 cm
Atypical hemangioma
• Well-defined
• Iso-/hypoechoic mass with echoic rim
Color Doppler
o Show filling vessels in periphery of
tumor
o No significant color Doppler flow in
center of lesion
• Power Doppler
o May detect flow within hemangiomas
o Flow pattern is nonspecific
o Similar flow pattern may be seen in
hepatocellular carcinoma & metastases
CT Findings
• NECT
o Small (1-2 cm) &
typical hemangioma (2-10 cm)
• Well-circumscribed, spherical to
ovoid mass isodense to blood
o Giant hemangioma (more than 10
cm)
• Heterogeneous hypodense mass
• Central decreased attenuation
(scar)
• CECT
o Small hemangiomas
("capillary"): Less than 2 cm
• Arterial & venous phases:
Show homogeneous
enhancement ("flash filling")
o Typical hemangiomas: 2-10 cm in
diameter
• Arterial phase:
Early peripheral, nodular or
globular, discontinuous enhancement
• Venous phase:
Progressive centripetal
enhancement to uniform filling, still
isodense to blood vessels
• Delayed phase:
Persistent complete filling
Giant hemangioma:
More than 10 cm in diameter
• Arterial phase:
Typical peripheral nodular or
globular enhancement
• Venous & delayed phases:
Incomplete centripetal
filling of lesion (scar does not
enhance)
o Atypical hemangioma: Inside to outside pattern
• Arterial phase:
No significant enhancement
• Venous & delayed phases:
Gradual enhancement
from center to periphery (centrifugal filling)
Baseline PVP
AP
10mins
o Hyalinized (sclerosed) hemangioma
• Shows minimal enhancement
• Cannot be diagnosed with confidence by imaging
o Hemangioma in cirrhotic liver
• Flash-filling of small lesions
• May lose characteristic enhancement pattern
• Capsular retraction
• Decrease in size over time
MR Findings
TlWI
o Small & typical hemangiomas
• Well marginated
• Isointense to blood or hypointense
o Giant hemangioma
• Hypointense mass
• Central cleft like area of marked decreased intensity (scar or fibrous tissue)
T2WI
o Small & typical hemangiomas
• Hyperintense, similar to CSF
o Giant hemangioma
• Hyperintense mass
• Marked hyperintense center (scar or fibrosis)
• Hypointense internal septa
T1 C+
o Small hemangiomas (less than 2 cm)
• Homogeneous enhancement in arterial & portal phases
o Typical & giant hemangiomas
• Arterial phase: Peripheral, nodular discontinuous enhancement
• Venous phase: Progressive centripetal filling.
• Central scar: No enhancement & remains hypointense
MRI : T1- HYPO , T2 –
HYPER - typical
Angiographic Findings
• Conventional
o Dense opacification of lesion
o "Cotton wool" appearance
• Pooling of contrast medium within
hemangioma
o Normal-sized feeders
o No neovascularity
o No arteriovenous shunting
o Typically retain contrast beyond venous
phase
DIFFERENTIAL DIAGNOSIS
Peripheral (intrahepatic)
cholangiocarcinoma
• Delayed persistent
enhancement, "fill in" may
mimic hemangioma
• Often heterogeneous, not
isodense with vessels on CT
• Not bright on T2WI
• Often invades/obstructs
vessels & bile ducts
Hypervascular metastases
• Hyperdense in late arterial phase images
• Hypo-or isodense on NECT & portal venous phase
• Treated metastases may mimic hemangioma on imaging (e.g., breast)
Focal nodular hyperplasia
• Second common
benign lesion.
• Female >> male. 8:1
• Reactive change to
abnormal circulation.
• Well defined lesion
characterized by a
central fibrous scar.
• Usually
asymptomatic.
• Epigastric pain
and
hepatomegaly
are seen
frequently.
characteristics
• Well-demarcated.
• Solitary mass without a capsule.
• Often located beneath the surface of liver.
• In central scar - feeding arteries, draining veins
connecting to hepatic vein.
• Necrosis and hemorrhage usually not seen.
Ultrasonographic Findings
• Real Time
o Well-demarcated liver lesion
o Mass: Mostly homogeneous &
isoechoic to liver
• Occasionally hypoechoic or
hyperechoic
o Central scar: Hypoechoic
o Prominent draining veins or
displacement of vessels
• Color Doppler
o "Spoke-wheel" pattern
• Large central feeding
artery with multiple small
vessels radiating
peripherally
o Large draining veins at
tumor margins
o High-velocity Doppler
signals
• Due to increased blood
flow or arteriovenous
shunts
Nuclear Medicine Findings
• Technetium Sulfur Colloid
o Normal or increased uptake
o Only FNH has both Kupffer cells & bile ductules
o Almost PATHOGNOMONIC in 60% of cases
• Tc-HIDA scan (hepatic iminodiacetic acid)
o Normal or increased uptake
o Prolonged enhancement (80%)
CT:
• Homogenous hypodense mass with a central
scar showing more marked hypodense.
• Arterial phase- brisk homogenous
enhancement.
• Portal phase-early wash out.
• Delayed phase-barely visible.
• If vessels radiating from central scar to the
periphery of the tumor is visualized , a near
definite diagnosis of FNH.
MRI
• Iso - hypointense on T1.
• Hyper - isointense on
T2.
• Central scar
– Hypointense on T1.
– Hyperintense on T2.
DIFFERENTIAL DIAGNOSIS
Hepatic adenoma
• Large tumor
• Symptomatic due to hemorrhage in 50%, scar atypical
• Usually heterogeneous due to hemorrhage, necrosis or fat
Cavernous hemangioma
• Only small ones with rapid enhancement simulate
FNH
• NECT: Isodense with blood vessels
• CECT: Peripheral enhanced areas stay isodense with
blood vessels
Fibrolamellar carcinoma
• Large (more than 12 cm)
heterogeneous mass
• Biliary, vascular & nodal
invasion
• Metastases (70% of cases)
• Fibrous scar
o Large & central or
eccentric with fibrous bands
&
calcification (68%)
o Hypointense scar on T2WI
Hepatocellular carcinoma
• Heterogeneous mass within cirrhotic liver
• Necrosis & hemorrhage
• Vascular & nodal invasion
Hypervascular metastasis
• Multiple lesions; older patient
Adenoma
• Rare benign
tumor in younger
age group
compared to
FNH.
• Solitary (80%).
• Females (90%).
• Predisposing factors-oral
contraceptives, anabolic
steroids and glycogen
storage disease.
• Abdominal
mass.
• Recurrent
abdominal pain.
• Acute abdomen
(tumor rupture).
Characteristics
• Clear border
• No capsule (fibrous capsule in some cases)
• Core - bleeding, necrosis, scar tissue
• Contains-fat & glycogen
• Neither portal vein nor bile ducts
Ultrasonographic Findings
• Real Time
o Well-defined, solid, echo genic mass
o Complex hyper & hypoechoic
heterogeneous mass with anechoic areas
• Due to fat, hemorrhage, necrosis &
calcification
• Color Doppler- Hypervascular tumor
o Large peripheral arteries & veins
o Intratumoral veins present
• Absent in FNH
• Useful discriminating feature for HCA
Nuclear Medicine Findings
• Technetium Sulfur Colloid
o Usually "cold" (photopenic): In 80%
o Uncommonly "warm": In 20%
• Due to uptake in sparse Kupffer cells
• HIDA scan
o Increased activity
• Gallium Scan
o No uptake
CT Findings
• NECT
o Well-defined, spherical mass
o Isodense to hypodense (due to
lipid)
o Hemorrhage: Intratumoral,
parenchymal or
subcapsular
o Fat or calcification seen (less
often than on MR)
•
CECT
o Arterial phase
• Heterogeneous, hyperdense enhancement
o Portal venous phase
• Less heterogeneous
• Hyper-, iso-, hypodense to liver
o Delayed phase (10 min)
• Homogeneous, hypodense
• Enhancement does not persist (due to arteriovenous shunting)
• Pseudocapsule: Hyperattenuated to liver & adenoma
o Large adenomas
• More heterogeneous than smaller lesions
MR Findings
• TlWI
o Mass: Heterogeneous signal intensity
• Increased signal intensity (due to fat & recent hemorrhage), more evident on MR
than CT
• Decreased signal intensity (necrosis, calcification, old hemorrhage)
o Rim (fibrous pseudocapsule): Hypointense
• T2WI
o Mass: Heterogeneous signal intensity
• Increased signal intensity (old hemorrhage/necrosis)
• Decreased signal intensity (fat, recent hemorrhage)
o Rim (fibrous pseudocapsule): Hypointense
•
T1 C+
o Gadolinium arterial phase
• Mass: Heterogeneous enhancement
o Delayed phase
• Pseudocapsule: Hyperintense to liver & adenoma
• Superparamagnetic iron oxide (SPIO)
o No uptake in adenoma
o Few cases take up SPIO (due to active Kupffer cells)
• Resulting in a decreased signal on T2WI
• Indistinguishable from FNH for these cases
• Uptake varies based on number of Kupffer cells
• Gd-BOPTA
(gadobenate
dimeglumine)
o Hepatocellular-
specific contrast
agent
o Adenoma
• No substantial
uptake
• Hypointense even
on delayed images
DIFFERENTIAL DIAGNOSIS
Hepatocellular carcinoma (HCC)
• May have identical imaging features as hepatic adenoma
• Histologically: May be difficult to distinguish well-differentiated
HCC from adenoma
• Biliary, vascular, nodal invasion & metastases establish that lesion is
malignant
Hepatic abscess
• Commonly – pyogenic,amebic and fungal.
• Via – portal vein, hepatic artery or bile duct.
• Solitary or multiple.
• Pyogenic – double structured hypodense area.
– CECT : double target sign.( arterial phase)
• Thick ring like stain (portal and venous phase)
• Amoebic – CECT- enhanced mural structure with hypodense
area at its lateral side owing to the presence of oedema.
• Fungal – CECT – faint ring like enhancement (arterial
phase)
– Hypodense (venous phase).
Hydatid cyst
• All age group.
• Caused by larva stage of adult tape worm.
Ct and mri
• Thick walled cystic lesions with internal round
periphery daughter cysts.
• Attenuation and signal intensity in mother
cyst is more than daughter cyst.
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

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benign focal lesions in liver.pptx

  • 2. 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
  • 3. Phases  Liver -dual blood supply  Normal parenchyma - 80% portal vein  20% -hepatic artery  All liver tumors blood supply from hepatic artery  Tumors enhance in arterial phase.  Liver will enhance in the portal venous phase
  • 4. 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  Will be visible as hyperdense lesions in a relatively hypodense liver
  • 5. Portal venous phase  60- 80 sec  To detect hypovascular tumors  also called the hepatic phase because there is enhancement of the hepatic veins
  • 6. Delayed Phase  Begins at about > 180 sec  Best done at 10 minutes
  • 7.
  • 8. CT LIVER – FOCAL HYPERENHANCING LESIONS  During the arterial phase  1. Hepatocellular carcinoma.  2. Haemangioma.  3. Focal nodular hyperplasia.  4. Adenoma.  5. Metastases – particularly carcinoid and pancreatic islet cell.  Most metastases are hypovascular.
  • 9. During the portal vein phase  1. Haemangioma.  2. Hepatocellular carcinoma – unusually. Most are isodense- or low- attenuation during this phase.  3. Venous collaterals – from an obstructed SVC to the IVC via hepatic veins.
  • 10. During the equilibrium phase  1. Haemangioma – because of progressive fill-in.  2. Cholangiocarcinoma.  3. Solitary fibrous tumour.  4. Treated metastases.
  • 11.
  • 12. Hepatic cyst • Single/multiple. • Lined by single layer of cuboidal epithelium. • Older adults • Clinical presentation – Asymptomatic – Compressive symptoms (massive).
  • 13. Autosomal dominant polycystic liver disease • Multiple cysts (more than 10) • Vary in size: 1-10 cm • Water or hemorrhagic density • Calcification of some cyst walls is seen • No septations or mural nodularity • Occasionally fluid levels seen • Liver often distorted by innumerable cysts
  • 14. usg • Fine cystic lesion with partial or complete septa are often visualized. • In case of complications – debris, thickened septa and complex internal fluid.
  • 15. ct • Smooth rimmed hypodense mass. • HU value near zero. • No enhancement at all on CECT.
  • 16.
  • 17. MR Findings • Simple hepatic cyst & ADPLD o T1WI: Hypointense o T2WI: Hyperintense o Heavily T2W images • Markedly increased signal intensity due to pure fluid content • Sometimes indistinguishable from a typical hemangioma o MRCP: No communication with bile duct
  • 18. Differential diagnosis 1. Cystic or necrotic metastases Demonstrate (e.g., ovarian cystadenocarcinoma & metastatic sarcoma) o Debris o Mural nodularity o Thick septa o Wall enhancement
  • 19. Dd-2.Biliary cystadenocarcinoma • Usually large in size • Homogeneous, hypodense, water density mass o Rarely non septated o Indistinguishable from large simple cyst • Almost always has septations • May show fine mural or septal calcifications • On contrast study o Unilocular or multilocular o Enhancement of capsule, septa & mural nodules
  • 20. Dd-3 Typical hepatic hemangioma • Well-defined margins • NECT: Isodense to blood • CECT: Early peripheral nodular & delayed centripetal enhancement isodense to enhanced vessels • T1W: Hypointense • T2WI: Markedly hyperintense Sometimes indistinguishable from simple hepatic cyst
  • 21. DD-4 Pyogenic abscess • Complex cystic mass • Heterogeneous density • Thick or thin multiple septations • May show mural nodularity • With or without hemorrhage • May show fluid-debris levels • Wall enhancement may be seen • Absent or heterogeneous enhancement of lesion
  • 22. Dd-5 Hepatic hydatid cyst • Large well-defined cystic liver mass with numerous peripheral daughter cysts • With or without calcification & dilated bile ducts
  • 23. Cavernous hemangioma • Most common primary liver tumor. • All age groups. • females >> males. • Size less than 1 cm to 30 cm (giant hemangioma). • No signs and symptoms. • When tumor exceeds 4 cm ,abdominal pain/discomfort or a palpable mass. • Rupture occurs rarely.
  • 24. characteristics • Usually solitary. • Borders are clear. • Not encapsulated. • Various degenerative changes are seen in its centre. – Old and new thrombus formation. – Necrosis, scarring, hemorrhage & calcification.
  • 25. Usg Typical hemangioma • Homogeneous hyperechoic mass with acoustic enhancement • Size: 2-10 cm
  • 26. Giant hemangioma • Lobulated heterogeneous mass with echoic border • Size: More than 10 cm
  • 27. Atypical hemangioma • Well-defined • Iso-/hypoechoic mass with echoic rim
  • 28. Color Doppler o Show filling vessels in periphery of tumor o No significant color Doppler flow in center of lesion • Power Doppler o May detect flow within hemangiomas o Flow pattern is nonspecific o Similar flow pattern may be seen in hepatocellular carcinoma & metastases
  • 29. CT Findings • NECT o Small (1-2 cm) & typical hemangioma (2-10 cm) • Well-circumscribed, spherical to ovoid mass isodense to blood o Giant hemangioma (more than 10 cm) • Heterogeneous hypodense mass • Central decreased attenuation (scar)
  • 30. • CECT o Small hemangiomas ("capillary"): Less than 2 cm • Arterial & venous phases: Show homogeneous enhancement ("flash filling")
  • 31. o Typical hemangiomas: 2-10 cm in diameter • Arterial phase: Early peripheral, nodular or globular, discontinuous enhancement • Venous phase: Progressive centripetal enhancement to uniform filling, still isodense to blood vessels • Delayed phase: Persistent complete filling
  • 32. Giant hemangioma: More than 10 cm in diameter • Arterial phase: Typical peripheral nodular or globular enhancement • Venous & delayed phases: Incomplete centripetal filling of lesion (scar does not enhance)
  • 33. o Atypical hemangioma: Inside to outside pattern • Arterial phase: No significant enhancement • Venous & delayed phases: Gradual enhancement from center to periphery (centrifugal filling)
  • 35. o Hyalinized (sclerosed) hemangioma • Shows minimal enhancement • Cannot be diagnosed with confidence by imaging o Hemangioma in cirrhotic liver • Flash-filling of small lesions • May lose characteristic enhancement pattern • Capsular retraction • Decrease in size over time
  • 36. MR Findings TlWI o Small & typical hemangiomas • Well marginated • Isointense to blood or hypointense o Giant hemangioma • Hypointense mass • Central cleft like area of marked decreased intensity (scar or fibrous tissue) T2WI o Small & typical hemangiomas • Hyperintense, similar to CSF
  • 37. o Giant hemangioma • Hyperintense mass • Marked hyperintense center (scar or fibrosis) • Hypointense internal septa T1 C+ o Small hemangiomas (less than 2 cm) • Homogeneous enhancement in arterial & portal phases o Typical & giant hemangiomas • Arterial phase: Peripheral, nodular discontinuous enhancement • Venous phase: Progressive centripetal filling. • Central scar: No enhancement & remains hypointense
  • 38. MRI : T1- HYPO , T2 – HYPER - typical
  • 39.
  • 40. Angiographic Findings • Conventional o Dense opacification of lesion o "Cotton wool" appearance • Pooling of contrast medium within hemangioma o Normal-sized feeders o No neovascularity o No arteriovenous shunting o Typically retain contrast beyond venous phase
  • 41. DIFFERENTIAL DIAGNOSIS Peripheral (intrahepatic) cholangiocarcinoma • Delayed persistent enhancement, "fill in" may mimic hemangioma • Often heterogeneous, not isodense with vessels on CT • Not bright on T2WI • Often invades/obstructs vessels & bile ducts
  • 42. Hypervascular metastases • Hyperdense in late arterial phase images • Hypo-or isodense on NECT & portal venous phase • Treated metastases may mimic hemangioma on imaging (e.g., breast)
  • 43.
  • 44. Focal nodular hyperplasia • Second common benign lesion. • Female >> male. 8:1 • Reactive change to abnormal circulation. • Well defined lesion characterized by a central fibrous scar. • Usually asymptomatic. • Epigastric pain and hepatomegaly are seen frequently.
  • 45. characteristics • Well-demarcated. • Solitary mass without a capsule. • Often located beneath the surface of liver. • In central scar - feeding arteries, draining veins connecting to hepatic vein. • Necrosis and hemorrhage usually not seen.
  • 46. Ultrasonographic Findings • Real Time o Well-demarcated liver lesion o Mass: Mostly homogeneous & isoechoic to liver • Occasionally hypoechoic or hyperechoic o Central scar: Hypoechoic o Prominent draining veins or displacement of vessels
  • 47. • Color Doppler o "Spoke-wheel" pattern • Large central feeding artery with multiple small vessels radiating peripherally o Large draining veins at tumor margins o High-velocity Doppler signals • Due to increased blood flow or arteriovenous shunts
  • 48. Nuclear Medicine Findings • Technetium Sulfur Colloid o Normal or increased uptake o Only FNH has both Kupffer cells & bile ductules o Almost PATHOGNOMONIC in 60% of cases • Tc-HIDA scan (hepatic iminodiacetic acid) o Normal or increased uptake o Prolonged enhancement (80%)
  • 49.
  • 50. CT: • Homogenous hypodense mass with a central scar showing more marked hypodense. • Arterial phase- brisk homogenous enhancement. • Portal phase-early wash out. • Delayed phase-barely visible. • If vessels radiating from central scar to the periphery of the tumor is visualized , a near definite diagnosis of FNH.
  • 51.
  • 52.
  • 53. MRI • Iso - hypointense on T1. • Hyper - isointense on T2. • Central scar – Hypointense on T1. – Hyperintense on T2.
  • 54.
  • 55. DIFFERENTIAL DIAGNOSIS Hepatic adenoma • Large tumor • Symptomatic due to hemorrhage in 50%, scar atypical • Usually heterogeneous due to hemorrhage, necrosis or fat Cavernous hemangioma • Only small ones with rapid enhancement simulate FNH • NECT: Isodense with blood vessels • CECT: Peripheral enhanced areas stay isodense with blood vessels
  • 56. Fibrolamellar carcinoma • Large (more than 12 cm) heterogeneous mass • Biliary, vascular & nodal invasion • Metastases (70% of cases) • Fibrous scar o Large & central or eccentric with fibrous bands & calcification (68%) o Hypointense scar on T2WI
  • 57.
  • 58. Hepatocellular carcinoma • Heterogeneous mass within cirrhotic liver • Necrosis & hemorrhage • Vascular & nodal invasion Hypervascular metastasis • Multiple lesions; older patient
  • 59.
  • 60. Adenoma • Rare benign tumor in younger age group compared to FNH. • Solitary (80%). • Females (90%). • Predisposing factors-oral contraceptives, anabolic steroids and glycogen storage disease. • Abdominal mass. • Recurrent abdominal pain. • Acute abdomen (tumor rupture).
  • 61. Characteristics • Clear border • No capsule (fibrous capsule in some cases) • Core - bleeding, necrosis, scar tissue • Contains-fat & glycogen • Neither portal vein nor bile ducts
  • 62. Ultrasonographic Findings • Real Time o Well-defined, solid, echo genic mass o Complex hyper & hypoechoic heterogeneous mass with anechoic areas • Due to fat, hemorrhage, necrosis & calcification • Color Doppler- Hypervascular tumor o Large peripheral arteries & veins o Intratumoral veins present • Absent in FNH • Useful discriminating feature for HCA
  • 63. Nuclear Medicine Findings • Technetium Sulfur Colloid o Usually "cold" (photopenic): In 80% o Uncommonly "warm": In 20% • Due to uptake in sparse Kupffer cells • HIDA scan o Increased activity • Gallium Scan o No uptake
  • 64. CT Findings • NECT o Well-defined, spherical mass o Isodense to hypodense (due to lipid) o Hemorrhage: Intratumoral, parenchymal or subcapsular o Fat or calcification seen (less often than on MR) •
  • 65. CECT o Arterial phase • Heterogeneous, hyperdense enhancement o Portal venous phase • Less heterogeneous • Hyper-, iso-, hypodense to liver o Delayed phase (10 min) • Homogeneous, hypodense • Enhancement does not persist (due to arteriovenous shunting) • Pseudocapsule: Hyperattenuated to liver & adenoma o Large adenomas • More heterogeneous than smaller lesions
  • 66.
  • 67.
  • 68.
  • 69. MR Findings • TlWI o Mass: Heterogeneous signal intensity • Increased signal intensity (due to fat & recent hemorrhage), more evident on MR than CT • Decreased signal intensity (necrosis, calcification, old hemorrhage) o Rim (fibrous pseudocapsule): Hypointense • T2WI o Mass: Heterogeneous signal intensity • Increased signal intensity (old hemorrhage/necrosis) • Decreased signal intensity (fat, recent hemorrhage) o Rim (fibrous pseudocapsule): Hypointense •
  • 70. T1 C+ o Gadolinium arterial phase • Mass: Heterogeneous enhancement o Delayed phase • Pseudocapsule: Hyperintense to liver & adenoma • Superparamagnetic iron oxide (SPIO) o No uptake in adenoma o Few cases take up SPIO (due to active Kupffer cells) • Resulting in a decreased signal on T2WI • Indistinguishable from FNH for these cases • Uptake varies based on number of Kupffer cells
  • 71. • Gd-BOPTA (gadobenate dimeglumine) o Hepatocellular- specific contrast agent o Adenoma • No substantial uptake • Hypointense even on delayed images
  • 72.
  • 73.
  • 74. DIFFERENTIAL DIAGNOSIS Hepatocellular carcinoma (HCC) • May have identical imaging features as hepatic adenoma • Histologically: May be difficult to distinguish well-differentiated HCC from adenoma • Biliary, vascular, nodal invasion & metastases establish that lesion is malignant
  • 75. Hepatic abscess • Commonly – pyogenic,amebic and fungal. • Via – portal vein, hepatic artery or bile duct. • Solitary or multiple.
  • 76. • Pyogenic – double structured hypodense area. – CECT : double target sign.( arterial phase) • Thick ring like stain (portal and venous phase) • Amoebic – CECT- enhanced mural structure with hypodense area at its lateral side owing to the presence of oedema. • Fungal – CECT – faint ring like enhancement (arterial phase) – Hypodense (venous phase).
  • 77.
  • 78. Hydatid cyst • All age group. • Caused by larva stage of adult tape worm.
  • 79. Ct and mri • Thick walled cystic lesions with internal round periphery daughter cysts. • Attenuation and signal intensity in mother cyst is more than daughter cyst.
  • 80.
  • 81. 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