• Most common primary
• 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.
• Usually solitary.
• Borders are clear.
• Not encapsulated.
• Various degenerative changes are seen in its
– Old and new thrombus formation.
– Necrosis, scarring, hemorrhage & calcification.
• Focal, homogenous, hypo vascular and
• Hypodense area with same density of aorta.
• Arterial phase-peripheral enhancement is seen
first, followed by gradual filling towards the
• Equilibrium phase-prolonged enhancement.
• In precontrast, arterial, equilibrium phases
tumor density is similar to that of aorta.
• Hypointense on T1.
• Hyperintense on T2.
• In T2 signal intensity is higher than that of
Focal nodular hyperplasia
• Second common benign lesion.
• Female >> male. 8:1
• Reactive change to abnormal circulation.
• Well defined lesion characterized by a central
• Usually asymptomatic.
• Epigastric pain and hepatomegaly are seen
• 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.
• Iso to hypoechoic.
• Colour doppler-central vascularity.
• Homogenous hypodense mass with a central
scar showing more marked hypodense.
• Arterial phase- brisk homogenous
• 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.
• Iso - hypointense on T1.
• Hyper - isointense on
• Central scar
– Hypointense on T1.
– Hyperintense on T2.
• Rare benign tumor in younger age group
compared to FNH.
• Solitary (80%).
• Females (90%).
• Predisposing factors-oral contraceptives,
anabolic steroids and glycogen storage disease.
• Clear border
• No capsule (fibrous capsule in some cases)
• Core - bleeding, necrosis, scar tissue
• Contains-fat & glycogen
• Neither portal vein nor bile ducts
• May be hypo, iso, hyperechoic.
• Typically heterogenous with areas of fluid
• Variable degrees of hemorrhage, necrosis &
• Calcification rare.
• Hypodense mass.
• Hyper attenuation areas in
case of ruptured.
• Area of necrotic foci and
scar tissue – hypodense
• Calcification is rare.
• Moderate tumor
enhancement in atrerial
• Hyper to isointense on T1
• Hypo to hyperintense on T2
• Hemorrhagic tumor hyperintense on T1 & T2
Hepatocellular nodules in cirrhosis
• Classified as regenerative nodule, dysplastic
• Regenerative nodules:
– USG and CT –too small to detect.
– When regenerative nodules contain iron, they are
termed siderotic nodules.
– Siderotic nodules- hyperdense on UECT and
hypointense on both T1 and T2.
• Dysplastic nodules :
– Rarely diagnosed by USG or CT
– MRI- Isointense with hyperintense foci on T1
– Hypo on T2.(opposite to HCC).
• Rare benign tumor.
• Composed of mature fat, blood vessels and
smooth muscle cells.
• It is not capsulated.
• Tuberous sclerosis is a known association of
• Solid mass containing markedly hypodense
• Arterial phase- partially enhancement often
with visualization of large central vessels.
• Hyperintense on both T1 & T2.
• Decreased intensity with fat suppression.
T1 Fat sup T1
• Lined by single layer of cuboidal epithelium.
• Older adults
• Clinical presentation
– Compressive symptoms (massive).
• Fine cystic lesion
with partial or
complete septa are
• In case of
septa and complex
• Smooth rimmed
• HU value near zero.
• No enhancement at all
• Hypointense on T1.
• Extremely hypointense on T2.
• Common infant benign lesion.
• Resembles capillary hemangioma seen in
infantile skin and mucosa.
• With in 6 months of birth.
• Solitary mass but may be multifocal.
• Typically large (1-20 cm).
• Hypodense area.
• 16%- calcification and hemorrhage.
• CECT – similar to that of cavernous
• MRI-Resemble those of hepatic hemangioma.
• Multi locular cystic liver mass.
• Originates from bile duct.
• Usually right hepatic lobe.
• Adults, Females >> males.
• Malignant transformation to cystadenocarcinoma
is not uncommon.
• Clincal presentation
– Chronic abdominal pain.
• Hypoechoic cystic lesion .
• Intracystic soft tissue components may be
• Focal calcification can occur.
• UECT – well defined hypodense lesion.
• Wall and internal septations are often
visualized (differentiate from simple cyst).
• CECT – cyst wall and soft tissue component
• 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).
• 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.