US VS CT VS MRI

MRI demonstrated to be more informative than US and CT in some studies

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

main limitations of US are high operator dependency, inability to detect

lesions <1 cm in size, and low specificity

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.

When performed properly, CT suffices for most clinical indications. Its

limitations include the need for a high radiation dose and a low sensitivity
for the detection and characterization of lesions smaller than 1 cm

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.

main advantages of contrast-enhanced MRI include a high spatial

resolution, better contrast sensitivity, better lesion detection and
characterization than with CT, and lack of 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.

CONTRAST VS. NON CONTRAST

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.

Only a minority of tumors contain calcifications, cystic components, fat or hemorrage

and will be detected on a NECT
Normal parenchyma is supplied for 80% by the portal vein and only for 20% by the
hepatic artery, so it will enhance in the portal venous phase.
All liver tumors however get 100% of their blood supply from the hepatic artery, so when
they enhance it will be in the arterial phase.
This difference in blood supply results in different enhancement patterns between liver
tumors and normal liver parenchyma in the various phases of contrast enhancement

TRIPLE PHASE CT (or any study for that matter)

arterial phase (30-35 seconds post contrast)

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.

portal venous phase (~75 seconds post contrast)

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.

equilibrium phase (~3 minutes post contrast)

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)

Hepatobiliary phase (~20minutes post contrast when using Eovist)

GADOLINIUM CONTRAST

Seven different contrast agents in use

All distribute in extracellular space
Eovist is designed for liver imaging and has 50% hepatic uptake after initial
extracellular phase

EOVIST

What you gain: » Liver lesion sensitivity, specificity, margins

» Hepatobiliary phase
Parenchymal enhancement
Biliary and bowel opacification

What you give up: » Vascular phase optimization » Extracellular phase (becomes
“late dynamic”)

When not to use: » Vascular indications » Inflammatory disease » Short-term

post-ablation, post-TACE » Probable hemangioma

TYPES OF LIVER LESIONS

 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
outiso/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