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US
highly sensitive at differentiating a cyst from a solid liver lesion.
However, it is not as sensitive as computerized tomography (CT) or
magnetic resonance imaging (MRI) at detecting focal, solid liver lesions
presence of diffuse liver disease also lowers the sensitivity of US for the
detection of focal lesions
CT
best spatial resolution and the ability to study the entire liver in a single
breath-hold.
MRI
best imaging test for liver lesion detection and characterization, because
this modality provides high lesion-to-liver contrast and does not use
ionizing radiation.
The main drawbacks of MRI include its high cost, a long procedure time,
and the need for the patient to hold his breath for longer periods.
On a non enhanced CT-scan (NECT) liver tumors usually are not visible, because the
inherent contrast between tumor tissue and the surrounding liver parenchyma is too low.
hypervascular tumors will enhance via the hepatic artery, when normal liver parenchyma
does not yet enhances, because contrast is not yet in the portal venous system.
These
hypervascular tumors will be visible as hyperdense lesions in a relatively hypodense
liver.
However when the surrounding liver parenchyma starts to enhance in the portal
venous phase, these hypervascular lesion may become obscured.
Hypervascular tumors will enhance optimally at 35 sec after contrast injection (late
arterial phase).
This time is needed for the contrast to get from the peripheral vein to the hepatic artery
and to diffuse into the liver tumor.
hypovascular tumors are detected, when the normal liver parenchyma enhances
maximally.
These hypovascular tumors will be visible as hypodense lesions in a
relatively hyperdense liver.
tumors become visible, that either lose their contrast slower than normal liver, or wash
out their contrast faster than normal liver parenchyma.
These lesions will become
either relatively hyperdense or hypodense to the normal liver.
This phase can be valuable if you're looking for: fast tumor washout in
hypervascular tumors like HCC or retention of contrast in the blood pool as in
hemangiomas or the retention of contrast in fibrous tissue in capsules (HCC) or scar
tissue (FNH, Cholangioca)
EOVIST
What you give up: » Vascular phase optimization » Extracellular phase (becomes
“late dynamic”)
Benign
Cyst
Abscess
Hemangioma
FNH
Adenoma
Malignant
HCC
FLHCC
Metastases
CYST
US
Round, anechoic, well marginated
Thin-walled, no internal vascularity on Doppler
CT
Homogenous hypoattenuation
Imperceptible wall
No enhancement after IV contrast
MRI
T1: homogenous low signal intensity
T2: increased signal intensity, more so than other T2 hyperintense liver
lesions (e.g. hemangioma)
No enhancement after contrast administration
ABSCESS
US
Poorly demarcated, range from hypoechoic to hyperechoic
Enhancement during arterial phase, progressive washout during portal or
late phases
No enhancement of necrotic area
May or may not be septated
CT
Varied presentation, generally peripherally enhancing hypoattenuating
lesions
May be solid or contain gas (bubbles or air-fluid levels)
“Double target sign” – contrast CT shows central low attenuation
surrounded by high attenuating inner ring and low attenuating outer ring
Inner ring (abscess membrane) has early contrast enhancement that
persists on delayed imaging
Outer ring (liver parenchyma edema) enhances on delayed phase
MRI
T1: Usually heterogenously hypointense in center
T2: Hyperintense
T1 + gadolinium contrast: enhances the capsule and may allow
visualization of septations
HEMANGIOMA
US
Well defined hyperechoic lesions, small proportion (10%) are hypoechoic
which may be due to background of hepatic steatosis
Color doppler may show peripheral feeding vessels
Arterial: peripheral nodular discontinuous enhancement
Portal venous/delayed: continued “filling in” of lesion, hemangioma will
be hyperechoic relative to background liver
CT
Well defined
Non-contrast: hypoattenuating
Arterial: discontinuous, nodular, peripheral enhancement
Portal venous: progressive peripheral enhancement, more centripetal fill-in
Delayed: further irregular fill-in; iso/hyperattenuating
MRI
T1: hypointense
T2: hyperintense (not as intense as cyst though)
T1 + gadolinium contrast: peripheral discontinuous enhancement,
progressing centripetally
Retain contrast on delayed (>5 mins)
T1 + hepatobiliary contrast: delayed imaging may not be useful, variable
appearance from hypointense to diffuse and central enhancement
FNH
US
Echogenicity is variable – well marginated to isoechoic
Central scar, displacement of peripheral vasculature on color Doppler
Arterial: hyperechoic, prominent feeding vessel
Portal venous: centrifugal filling (vs. hemangioma/adenoma), sustained
enhancement in portal venous phase (vs. adenoma)
CT
Non-contrast: hypo or isoattenuating, hypoattenuating central scar
Arterial: hyperattenuating, central scar remains hypoattenuated
Portal venous: hypo/isoattenuating to liver, fibrotic scar may demonstrate
enhancement
MRI
T1: iso to hypointense, hypointense central scar
T2: iso to hyperintense, hyperintense central scar
T1 + Gadolinium: intense arterial phase enhancement, central fibrotic scar
retains contrast on delayed scans, isointense to liver on portal venous
phase
T1 + Eovist: early arterial enhancement, persists into delayed phases to a
greater degree than background liver due to presence of normal
hepatocytes and abnormal bile ductules (??????), fades to background
liver intensity on delayed hepatobiliary phase with small amount of
enhancement remaining (vs. adenomas which are hypointense on
hepatobiliary phase) (??????)
ADENOMA
US
Solitary well-demarcated heterogenous mass, variable echogenicity
Hypoechoic halo of focal fat sparing often seen
Arterial: hypervascular, early enhancement (similar to FNH, but more
enhancing)
Portal venous/delayed:
CT
Well marginated, generally isoattenuating
Hemorrhage can cause hyperattenuation, fat content can cas
hypoattenuation
Arterial: homogenous enhancement
Portal venous/delayed: isodensity
Calcifications may indicate areas of old hemorrhage
MRI
T1: variable, most are hyperintense
T2: hyperintense
T1 + Gadolinium: early arterial enhancement, nearly isointense on delayed
images
T1 + Eovist: hypointense on hepatobiliary phase due to reduced uptake
(vs. FNH which is iso/hyperintese)
HCC
US
Variable appearance depending on individual lesion size and echogenicity
of background liver
Small focal HCC appears hypoechoic
Larger lesions are heterogenous due to fibrosis, fatty change,
necrosis, calcification
Peripheral halo of hypoechogenicity may be seen with focal fatty
sparing
Arterial: enhancement from neovascularity
Portal venous: decreased echogenicity relative to background liver
(wash out)
CT
Various patterns can be seen depending on subtype of HCC (????????), so
ENHANCEMENT pattern is key to correct assessment of HCC. Classic
appearance is encapsulated mass that shows…
Vivid enhancement during late arterial phase, rapid wash
outiso/hypoattenuating in portal venous phase
MRI
T1: iso/hypointense compared with surrounding liver, if hyperintense may
be due to intratumoral fat or decreased intensity in surrounding liver
T2: typically moderately hyperintense
T1 + Gadolinium: rapid arterial enhancement, due to tumor supply from
hepatic artery rather than portal vein… rim enhancement may persist
(referred to as capsule)
LI-RADS to stratify lesions
T1 + Eovist: similar to Gadolinium based studies, LI-RADS is a bit
different
FLHCC
US
Variable appearance
Arterial: heterogenous enhancement
Portal venous: decreased echogenicity relative to liver (wash out)
CT
Single large tumors, dense fibrotic bands forming a central scar (can
resemble FNH), calcifications may be seen,
Arterial: enhancement
Portal venous/delayed: persistent enhancement of central scar
MRI
Hypointense scar on all phases (may occasionally be T2 hyperintense
mimicking FNH)
T1: iso/hypointense
T2: hypo/hyperintense
T1 + Gadolinium: arterial phase: heterogenous enhancement, portal
venous/delayed: iso/hypointense
METS
US
Rounded and well defined
Positive mass effect with distortion of adjacent vessels
Hypoechoic, with hypoechoic halo due to compressed/fat spared liver
Cystic, calcified, infiltrative and echogenic appearances are all possible
CT
Typically hypoattenuating on non-contrast
Enhance less than surrounding liver on contrast
Arterial: peripheral enhancement
Portal venous: central filling
Delayed: washout (helpful in differentiating from hemangioma)
MRI
More sensitive than CT for detection of liver metasteses
T1: moderately hypointense
T2: mild to moderately hyperintense
T1 + Gadolinium: enhancement can be lesional or perilesional
Small <1.5cm uniformly enhance
Large >1.5cm transient rim enhancement (with washout)
T1 + Eovist: useful for detection and confirmation of metastatic disease
Delayed phase: metastatic lesions don’t retain Eovist, appear as
“holes” in the liver
LI-RADS