Liver MRI + Masses

Hemangioma

• Disorganized mass of blood vessels ultimately supplied by the hepatic artery

• Commonly peripheral in liver

• CT = non-specific hypoattenuating liver mass

• T1: hypointense (relative to liver parenchyma)

  • Can be mildly hyper

• T2: hyperintense (relative to liver parenchyma)

• T1 C +: peripheral nodular discontinuous enhancement with centripetally filling

  • Retain contrast on delayed sequences

• Involute in cirrhosis

• Hemangiomatosis - tons of hemangiomas

  • Causes highoutput HF in kids

  • No real issues in adults

• Giant hemangioma = > 5 cm

Bile Duct Hamartoma

• aka von myenbeurg complex

• Cluster of disorganized bule duct

• Presentation

  • Simple cyst or

  • Solid enhancing nodule secondary to fibrous tissue

    • Concurrent intermediate signal on T2

• Seen in Caroli Disease

Cirrhosis

• Segments undergoing hypertrophy 1, 2, 3

  • The others undergo atrophy

• Caused by differences in portal venous flow with some areas having supply compressed and cut off by the fibrosis seen in cirrhosis

Liver Masses

Cystic Masses

General

• Broadly speaking there are 4 types of liver masses

  • Cystic

    • Typically all benign except for cystadenocarcinoma

  • Infectious

    • Pyogenic abscess

    • Amoebic abscess (entamoeba)

    • Fungal Abscess

  • Post-traumatic

    • Hematoma

    • Biloma

  • Solid

    • Benign

      • Adenoma

      • FNH

      • Hemangioma

    • Malignant

      • HCC

• Benign masses are typically cystic without enhancement

• Arterially enhancing masses that remain hyperintense or become isointense tend to be benign

Echinococcal Cyst

• Cystic, multiloculated lesion

• Classic T2 hypointense rim

• Stage 1 - simple appearing cyst

• Stage 2 - multiloculated cyst with internal smaller cysts

• Stage 3 - Wall calcification & eventually complete calcification

• Stage 4 - cyst rupture or complication

• Don’t biopsy these, causes rupture and anaphylaxis

  • Serology to diagnose

• Water lily sign

Fat & Water Related Artifacts

• Type 1 chemical shift

  • Only occurs in frequency encoding direction

  • Worse with

    • high field strength

    • More noticeable at a narrower receiver (readout) bandwidth

  • Seen with

    • Spin echo

    • Gradient echo

• Type 2 chemical shift - india ink

  • Dropout occurs on opposed phase

  • Only seen with gradient echo

    • Gradient echo has a 180 degree rephasing pulse

      • This is like re-starting the race between the fat and skinny guy so that the skinny guy cannot really get ahead of the fat guy

  • Fat and water are opposed and cancel signal - out of phase - occurs at 2.2 msec, 6.6, etc

  • Fat and water are aligned - in phase - occurs at 4.4 msec

  • Signal gets darker on out of phase = dropout on out of phase = fat (steatosis)

  • Signal gets brighter on out of phase = dropout on in phase = hemochromatosis

  • Key Note

    • The cycle of oppose and aligned phases will constantly continue to cycle indefinitely, so the water and fat will be opposed at 2.2, then aligned at 4.4, then opposed at 6.6 and so on

    • Now typically this doesn’t matter much but the following should be noted:

      • For a fatty liver the liver will be:

        • Dark on out of phase at 2.2 msec

        • Bright on in phase at 4.4 msec

        • Dark on out of phase at 6.6 msec

      • For an iron containing liver (hemochromatosis), the liver will be

        • Bright on out of phase at 2.2 msec

        • Dark on in phase at 4.4 msec

        • DARKER on out of phase at 6.6 msec

      • SO - you cannot really tell the difference between a fatty liver on a 6.6 msec out of phase an dan iron containing liver on the 6.6 msec out of phase

        • This is the reason why the OPPOSED (out of phase) 2.2 msec must be done first !

      • Note that for testing purposes the same phenomenon (gets progressively darker rather than dark-bright-dark-bright) will be seen with air (anywhere, i.e. in the bowel), metal clips (chole clips)

        • And remember that the brightest structue (brightest clips) = worst artifact = image obtained first (because they get progressively darker)

• Water

  • Spins fast

  • Long T1 relaxation time

• Fat

  • Spins slowly

  • Short T1 relaxation time

• Key formula

  • Frequency = field strength x Y

  • Increased field strength (3T scanner rather than 1.5T magnet) will worsen artifacts

  • Differences in frequency are less noticeable at a high bandwidth

    • Some charts and shit no body cares about, just memorize this

• Phase encoding direction —> AP —> pulsation artifact

  • Shorter

• Frequency encoding direction —> side to side —> white-black-white-black

• Note phase and frequency encoding directions will be opposite in breast, the above is only for body imaging

Fibrolamellar HCC

• Seen in younger patients (20-30 yos) who are otherwise healthy (i.e. - no cirrhosis)

  • Therefore LI-RADS typically does not apply

• Tend to be large 5-20 cm

• Central scar with arterially enhancing periphery

• AFP is normal

• Prognosis slightly better than regular HCC

Biliary Cystadenoma/Adenocarcinoma

• Middle aged women

• 2 flavors

  • With ovarian stroma

  • Without ovarian stroma

• Can be any size but usually large when found

• Basically a uniloculated or multiloculated fluid collection that has variable characteristics based on content

  • Looks like a giant simple cyst or some fucked up cyst

• No overt communication with the ducts

• Cannot differentiate between adenoma & adenocarcinoma based on imaging alone

Solid Lesions

Hepatic Adenoma

• Discontinuous pseudocapsule

• Many but not all will drop out on out of phase

  • Contain glycogen and fat

• Like to bleed

• No Kupffer cells

• Seen in

  • Estrogen use

  • Glycogen storage disease

• On US classically has large peripheral vessels and internal flow varies

Liver Nodules

• A fucked up liver will try and heal itself by making regenerative nodules

  • If you keep insulting the liver the regenerative nodules become dysplastic nodules

    • If you keep insulting the liver the dysplastic nodules become HCC

Dysplastic Nodules

• Liver trying to heal itself basically and forms a regenerative nodule which contains normal liver cells

• A regenerative nodule which has atypical cells is a dysplastic nodule

• T2 hypo

  • Will become iso to hyper over time as it becomes more malignant

• T1 hyper

  • Will be hypo over time as it becomes more malignant

• Enhancement similar to or less than liver signal, not hyperenhancement (not brighter than liver)

• Focal hyper-enhancing nodule in the larger overall nodule = nodule in nodule appearance

• On CT looks like what you think congestive hepatopathy looks like with lace-like fibrosis type shit

• Regenerative nodules seen in primary biliary cirrhosis too

Nodular regenerative hyperplasia

• Typically seen in response to budd-chiari

• Large regenerative nodules

• Hypodense rim and central scar, strongly resemble FNH

• Typically multiple

• Benign

Pyogenic Abscess

• Presents as multiple small heterogenous lesions that coalesce into one big heterogenous fuck

Infectious Liver Lesions

LI-RADS

• When can it be used

  • Must be an adult

  • Cirrhotic patient

  • Chronic Hep B infection

  • Hx of Hcc or prior Hcc

• 3 groups of patients

  • Group 1

    • Normal exam - surveillance in 6 months

    • LI-NC - exam is not satisfactory basically - repeat exam within 3 months

Hepatocellular Carcinoma

• Most common primary hepatic malignancy

• Believed to occur by chronic degeneration of a cirrhotic nodule that keeps getting more irregular

• Key finings

  • Arterial hyper-enhancement

  • Washout

  • Enhancing capsule

  • Interval growth (>50% growth within 6 months of prior exam)

References: