Liver Flashcards
Liver anatomy
- Segments not typically seen on frontal view.
- % of blood to the liver from where and % w/O2.
- Most common portal vein branching pattern.
- % variant PV patterns.
- 2nd most common PV pattern.
- Where do the hepatic veins run in ech segment?
- 6, 7.
- 75% from portal vein, but provides only 50% of O2.
- Bifurcation into RPV/LPV then RPV bifurcating into RA and RP.
- 25%
- Trifurcation: LPV, RAPV, RPPV.
- Periphery.
- What do the following divide:
- RHV
- MHV
- LHV/falciform ligament
- Portal vein
- What’s the significance of Cantlie’s line?
- RHV: 7/8, 6/5.
- MHV: 8/4A, 5/4B
- LHV/falciform: 4A/2, 4B/3
- PV: divides upper & lower segments
- Cantlie’s: same division as the MHV.
- Significant as it divides the liver into functional L/R hepatic lobes.
- It runs from the IVC to the middle of the GB fossa.
Liver anatomy: caudate
- Which veins drain this into the IVC?
- Why the caudate hypertrophies in early cirrhosis.
- What other disease causes hypertrophy.
- What is the portal supply to the caudate?
- Veins of Spieghel.
- The caudate may be supplied by R & LPVs. Early in cirrhosis, the caudate is spared of disease from the separate IVC drainage, so the higher pressures don’t affect it as much, then hypertrophies to compensate for crap liver parenchyma.
- Budd-Chiari; direct IVC drainage allows the caudate to bypass the higher HV pressures.
- Branches of BOTH, RPV & LPV supply the caudate.
Liver anatomy: caudate hypertrophy
- DDx (5) & most common.
- How to quantify hypertrophy.
- Cut-off for cirrhosis.
- DDx:
- Cirrhosis: most common
- cavernous transformation of the portal vein
- Budd-Chiari
- PSC (end stage)
- congenital hepatic fibrosis.
- Caudate-right lobe ratio:
- Take axial slice immediately below MPV bifurcation & draw 3 lines:
- Line 1: R lateral to the PV.
- Line 2: L lateral border of the caudate.
- Line 3: midway b/w the PV & IVC in the caudate.
- Take axial slice immediately below MPV bifurcation & draw 3 lines:
- Caudate-right lobe ratio: >0.65 = high likelihood of cirrhosis.
- Name the 3 bare areas of the liver.
- What’s the significance of these?
- Porta hepatis, bare area, GB fossa.
- An injury to the bare area can cause a retroperitoneal bleed.
CT of the liver
- Timing of arterial & PV phase.
- Vascularity of most hepatic mets. The exception.
- Vascularity of most 1º benign & malignant liver masses. Phase they’re most prominent.
- 25-30 & 70 secs.
- Mets: hypovascular (see pic). Exception: breast, which can be iso on PV phase & more conspicuous on unenhanced.
- Hypervascular. Most prominent in arterial, typically late arterial (35s).
MRI of the liver:
- Mets/primary enhancement patterns compared to CT.
- Sequences for intracytoplasmic lipid/steatosis.
- 2 types of hepatic MR contrast agents.
- What does Gad do to be bright?
- Same. Mets: hypo; primaries: hyper.
- In/out of phase.
- Extracellular & hepatocyte-specific.
- Shortens T1, just like blood, calcium, melanin, etc.
MR contrast agents: extracellular
- What do these act like?
- Where do they flow?
- Example?
- Purpose?
- CT iodinated contrast.
- Stay outside the cell (extracellular) & are blood flow dependent.
- Magnevist (Gd-DTPA).
- Hepatic lesion detection & characterization; liver vasculature evaluation.
MR contrast agents: hepatocyte-specific
- Where do they flow?
- Examples?
- Is Eovist a pure hep-specific agent?
- When phases are taken
- Purposes?
- 2 other problematic lesions that uptake this?
- Distributes into the vascular then extravascular spaces during arterial, PV & late dynamic phases, then taken up by hepatocytes by the OATP bile uptake transporter into the cell; then excreted into bile.
- Eovist, Primovist.
- No, 55% is excreted into bile.
- MRCP: 5 mins; HPB phase: 20 mins.
- Assess focal liver lesions found on other studies; contrast b/w normal hepatocytes and:
- Great for proving an FNH is an FNH (it uptakes at 20 mins) and not an adenoma.
- Great for finding new mets once all other benign lesions are found: mets don’t uptake.
- HCC surveillance.
- Cholangiogram: bile leaks, GB obstruction.
- FNH, well-differentiated HCC.
Diffuse liver disease: NAFLD
Px: 2 types; components of metabolic syndrome (4).
Ex: prevalence.
Ix: NCCT normal app of liver relative to spleen; HUs.
- NCCT abnormal HU.
- CECT abnormal HU.
- More sensitive test for steatosis.
Px: steatosis, steatosis w/inflammatory activity (steatohepatitis); NAFLD, obesity, insulin resistance, dyslipidemia.
Ex: 15%.
Ix: liver should be slightly hyperattenuating relative to spleen; normal liver 10HU < spleen.
- NCCT: liver >10HU less than spleen.
- CECT: liver >25HU less than spleen in PV phase.
- MR in/out of phase sequences.
DDx hypoattenuating liver (2)
- steatosis: by far the most common
- amyoidosis: rare & may be focal or diffuse
DDx hyperattenuating liver (4)
- Iron overload: by far the most common.
- Medications: amiodarone, gold, methotrexate.
- Copper overload (Wilson’s).
- Glycogen excess.
DDx diffuse/focal hepatic steatosis (5)?
- obesity
- DM
- EtOH
- exogenous steroids
- drugs: amiodarone, methotrexate, chemo
Normal liver attenuation
- Normal NCCT liver range.
- NCCT normal app of liver relative to spleen; HUs.
- Defn hyperattenuating liver.
- NCCT abnormal HU.
- CECT abnormal HU.
- More sensitive test for steatosis.
- Normal NCCT range: 30-60 HU.
- Liver should be slightly hyperattenuating relative to spleen; normal liver 10HU < spleen.
- Hyper: >75HU.
- NCCT: liver >10HU less than spleen.
- CECT: liver >25HU less than spleen in PV phase.
- MR in/out of phase sequences.
Diffuse liver disease: focal fat
Px: why does this form.
- What do the veins of Sappey drain & what can these cause?
Ix: 3 features compared to real masses.
Px: variations in PV supply delivers fat differently, and third inflow (aberrant R gastric venous drainage, veins of Sappey, vein of Burow).
- Sappey: paraumbilical veins draining the ant abdo wall & diaphragm; can cause hot quadrate sign when there is systemic venous obstruction.
Ix:
- No mass effect.
- Vessels run through it, no vessel distortion.
- Characteristic locations:
- GB fossa
- Subcapsular, along the falciform
- Periportal
- Nodular, throughout the liver: hyperechoic on US, hypoattenuating on CT; drop out on OOP GRE.
Diffuse liver disease: NAFLD
Ix: How MR in/out works.
- How this differs from iron overload on in/out.
Ix: when water & fat protons are in the same MR voxel the fat/water signals are summed in in-phase, subtracted in out-of-phase.
- Steatosis: high signal on in-phase, low on out-of-phase.
- Iron overload: low on in-phase, higher on out-of-phase.
Diffuse liver disease: amyloid
Ex: common in liver?
Ix: CT: typical app.
Ex: no, uncommon in liver.
Ix: CT: decreased attenuation, hepatomegaly, “lardaceous liver”.
Diffuse liver disease: Wilson disease
Px: cause; genetics; where else does the deposn occur; most common manifestation in childhood; hepatic sequelae.
Ix: general findings; unique hepatic findings in Wilson’s.
Px: copper accumulation; AR genetic defect; liver, basal ganglia, cornea.
- Most common manifestation: hepatic dysfunction.
- hep sequelae: hepatomegaly + cirrhosis.
Ix: general: hyperattenuation + cirrhosis
- Unique: multiple nodules, perihepatic fat layer + normal caudate.
Diffuse liver disease: hepatic iron overload
- 2 pathways
- Most common
- Pathology of each
- Ix: general appearance on MR
- Hemochromatosis & hemosiderosis
- Hemochromatosis most common
- Hemochrom: accumulation in hepatocytes.
-
Hemosid: accumulation in the RES causes hepatic Kupffer cell iron overload.
- Kupffer cells are hepatic macrophages which sit in the sinusoids b/w the portal and hepatic veins.
- Ix: Fe overload is always hypo on MR relative to the paraspinal muscles.
Diffuse liver disease: hepatic iron overload, hemosiderosis
Hepatic infection: viral hepatitis
Ix: most sens sign
- US
- CT: nonspecific findings.
- Most sens sign: hepatomegaly.
- US: hepatomeg, starry sky appearance, GB wall thickening, periportal edema.
- CT: hepatomeg, possible decreased attenuation, possible periportal/hepatoduodenal lymphadenopathy.
- MR: increased periportal T2 (edema).
DDx multiple tiny hepatic hypoattenuating lesions
- Mets
- Candidiasis
- biliary hamartomas (von Meyenberg complexes)
- Caroli disease
- lymphoma
Hepatic infection: candidiasis
Px: which organs often involved.
Ex: almost always seen in who & in particular?
Ix: CT app.
Tx: mortality?
Px: liver + spleen; invade the intestinal mucosa during periods of marked neutropenia & invade liver through the portal circulation.
Ex: immunocompromised pts., especially those w/hematologic malignancies + chemo.
Ix: CT: tiny hypoattenuating foci which may be rim-enhancing.
Tx: mortality high (30%) despite antifungals.
Hepatic infection: abscess
Px: most common general cause; common causes; less common cause; most common organism.
Ix: CT-1
MR-4
Px: bowel process; diverticulitis, appendicitis; ascending cholangitis; E. coli.
Ix: CT: ring-enhancing lesion
MR: T2 central hyperintensity, irregular wall that enhances late, perilesional enhancement.
Hepatic infection: echinococcal disease/hydatid cyst
Px: bug; where it’s from; associated w/?
US-2
CT-4
Px: Echinococcus granulosus; Mediterranean basin; sheep farming.
US: complex, primarily hypoechoic mass containing a hyperechoic undulating membrane.
CT: fluid-attenuation mass w/a characteristic floating membrane +/- a daughter cyst; peripheral calcs may be present.
Cirrhosis-pathology
- General path.
- Causes: 3 families.
- Micronodular vs. macronodular causes.
Etiology:
- Repeated cycles of injury + repair.
- Metabolic: NASH, EtOH, hemochromatosis, Wilson disease.
- Infectious: chronic Hep B or C.
- Inflammatory: PBC, PSC.
- Micronodular: often due to metabolic.
- Macronodular: often post-viral.
Cirrhosis-early signs
- Earliest sign & cause.
- Specific sign.
- Another 2 signs.
- Least reliable sign.
2dry manifestations: 3 from PHTN; cause of GB wall thickening; splenic finding & how to see them.
- Expansion of the preportal space; atrophy of medial segment of L lobe, so increased fat anterior to the RMPV.
- Caudate enlargement w/caudate to R lobe ratio >0.65.
- Empty GB fossa w/increased fat around the GB; stigmata of PHTN (varices, ascites, splenomeg).
- Least reliable sign: hepatic surface nodularity.
2dry manifestations: varices, portosystemic collaterals, splenomegaly; hypoalbuminemia & resultant edema; Gamna Gandy bodies, which are splenic microhemorrhages & are hypo on GRE.
Pathway to HCC
- Sequence of path development.
- Can the above nodules be differentiated on imaging?
-
Regenerative nodules:
- Blood supply?
- Malignant?
- App on arterial phase?
- MR app-4.
-
Dysplastic nodules:
- Malignant?
- Blood supply & app on arterial phase?
- MR app-4.
-
Siderotic nodules:
- What is this? Malignant?
- CT-1
- MR-2
*
- Regenerative nodule → dysplastic nodule → HCC.
- No. Regen not from dysplastic and high-grade dysplastic not from HCC.
-
Regenerative nodules:
- Portal vein
- Malignant–no.
- App on arterial phase: non-enhancing.
- MR-T2 low, T1 variable, rarely T1 hyper as may contain glycogen; enhance similarly, or less, than liver.
-
Dysplastic nodules:
- Malignant: yes, malignant potential.
- Blood supply & app on arterial phase: same as regens, i.e., PV & no enhancement, so can’t tell them apart.
- MR app-T2 low, but high grade may be T2 hyper, T1 variable, low grade lack enhancement; high grade can enhance, hence can’t tell them apart from HCC.
-
Siderotic nodules:
- Fe-rich regen or dysplatic nodule. Rarely malignant.
- CT-hyperattenuating, just like Fe in the liver.
- MR-T1, T2* hypo.
Malignant hepatic masses: HCC
- The most common 1° liver tumour?
- The biggest RF?
- What’s the tenet re: a pt w/cirrhosis or chronic hepatitis?
- % of cases where AFP is elevated.
- Classic CT/MR Ix appearance of HCC.
- Classic MR Ix app of HCC.
- Significance of the nodule in a nodule appearance?
- Diff b/w HCC & mets re: invasion.
- HCC.
- Cirrhosis.
- A hyperenhancing mass in this kind of pt is HCC until proven otherwise.
- AFP up in 75% only.
- Classic general Ix app: capsulated mass w/early enhancement & washout.
- MR:
- Dysplastic nodule w/early HCC inside.
- HCC tends to be locally invasive, mets aren’t.
HCC tumour vs. bland thrombus
- Criteria to distinguish PV tumour thrombus from bland thrombus (3)?
- Contiguity w/parenchymal tumour.
- Expansion of the vein lumen.
- Enhancing thrombus.
Hepatic tumour markers:
- Name the 2 tumour markers used in primary hepatic cancers.
- Draw the table of the 2 and their cut offs for high probability of these cancers.
- What are the key numbers in this table?
- AFP: HCC
- CA 19-9: intrahepatic cholangiocarcinoma.
- 100: for moderate elevation, moderate-high probability.
- >200: marked elevation, moderate-high probability.
LI-RADS
- What does a LI-RADS score signify?
- In who should LI-RADS be used?
- Not used?
- Major criteria.
- Factors favouring HCC.
- Factors favouring benignity.
- RR for HCC.
- Used: RFs for HCC (cirrhosis, chronic HBV, etc.).
- <18yo, cirrhosis 2dry to congenital hep fibrosis or vascular disorders, e.g., Budd-Chiari.
-
Major:
- Non-rim arterial enhancement: compared to background liver.
- Non-peripheral washout: relative hypointensity compared w/background liver at PV & delayed phases.
- Enhancing capsule/pseudocapsule: can be seen in PV or delayed.
- Threshold growth: increase >=50% in <=6 months.
-
Favouring HCC:
- Non-enhancing capsule.
- Nodule-in-nodule.
- Mosaic architecture.
- Fat in mass, more than liver.
- Blood products in mass.
-
Favouring benignity:
- Size stable >=2 yrs.
- Size reduction.
- Homogeneous T2 hyper or hypo T2 or T2*.
- Undistorted vessels.
- Parallels blood pool enhancement.
- Hepatobiliary phase iso.
- List the algorithm of how to use LI-RADS.
- How do you determine LR4 or 5 in the diagonal box?
- Draw the LI-RADS table.
- First determine if there is enhancement.
- Look at the type of enhancement: non-rim is more suspicious than hypo or iso.
- Gauge lesion size.
- Finally, look for typical HCC features to use in the table, e.g., enhancing capsule, non-peripheral washout, threshold growth.
- Diagonal box: LR4 = enhancing capsule only; LR5 = washout or growth.
Malignant hepatic masses: Fibrolamellar HCC
Ex: typical; prognosis; AFP?
Ix:
- MR-4
- How the MR app differs from FNH? From HCC?
- Capsular retraction?
- Capsule?
Ex: young pts w/o cirrhosis; better prognosis than HCC; AFP not elevated.
Ix:
- MR: large, heterogeneous w/fibrotic central scar that’s T1/T2 hypo.
- FNH: scar that enhances late.
- 10% may have capsular retraction.
- No capsule, unlike HCC, but may show a pseudocapsule of peripherally compressed normal hepatic tissue.
Malignant liver masses: hepatic angiosarcoma
- Commonality?
- RFs.
- Ex?
- Ix?
- Mets?
- DDx?
- Prognosis?
- Rare, but the 3rd most common primary liver tumour.
- RFs: thorotrast, radiation.
- 60-70yo, M>F, 4:1.
- Variable appearance given their pleomorphic histology: hetero hypervascular mass w/irregular margins.
- May be solitary or multiple.
- PET avid.
- Lung & spleen; may see a pleural effusion.
-
DDx:
- Hepatic angiosarcoma
- HCC: conventional or fibrolamellar
- Mets
- Poor; median survival = 6 mos; survival uncommon beyond 1 year.
Malignant hepatic masses: hepatic mets
- Typical CT Ix app of hepatic mets.
- DDx hypervascular mets.
- 2 mets w/calcs.
- Prognosis w/calcs.
- Typical MR app of mets.
- Most common cause of pseudocirrhosis.
- Hypovascular on PV phase, e.g., colorectal & pancreatic adeno.
- Renal, thyroid, chorioca, PNET, carcinoid, melanoma, sarcoma.
- Mucinous colorectal or ovarian serous.
- Calcs = better prognosis.
- MR: T1 hypo unless hemorrhagic, T2 hyper.
- Treated breast ca mets.
Malignant hepatic masses: lymphoma
- What is more common 1° or 2dry?
- With what cell type?
- 2 associated findings.
- Typical CT, MR Fx?
- 2dry BY FAR!
- NHL.
- Splenomegaly, lymphadenopathy.
- CT: hypo.
- MR: T1 hypo, T2 hyper.
Malignant hepatic masses: epithelioid hemangioendothelioma
Px: what is this; grade.
Ex: how common; sex, age.
Ix: general; US-2; CT-4, specific sign; MR-3.
Tx: clinical course; prognosis; preferred Tx; mets?
Px:
- Low to intermed grade malignant hepatic vascular tumour.
Ex:
- Rare!
- F>M 3:2, 30-40yos.
Ix:
- General: multiple peripheral solid nodules often w/capsular retraction.
- US: often hypoechoic but may be mixed.
- CT: multiple hypoattenuating lesions in both lobes; can coalesce; may have halo or target enhancement; capsular retraction; hepatic or PV branches may taper & terminate at the edge of these lesions = lollipop sign.
- MR: T1 hypo, T2 hyper, halo enhancement.
Tx:
- Variable clinical course.
- Prognosis more variable than other hepatic malignancies.
- Mets ~30%, typically lung.
- Tx: xplant as they are often diffuse or resection if not.
DDx: hepatic capsular retraction
- Mets: most commonly post-Tx breast.
- Intrahepatic cholangio
- Epitheliod hemangioendothelioma
- Confluent hepatic fibrosis: wedge-shaped, most commonly medial segment L lobe or anterior segment R lobe.
- Fibrolamellar HCC: 10% of cases
- HCC: has been reported but uncommon
Confluent hepatic fibrosis
Px: general cause; 2 specific; in what 2 conditions is it more common.
Ix: common chars; what segments; generally, what is less common than w/cholangio
CT-3, MR-4; LR calssification.
DDx: 3
Px:
- Generally, chronic liver injury.
- Most commonly by cirrhosis or hepatic vascular injury.
- 2 conditions: PSC & EtOH cirrhosis.
Ix: wedge-shaped, in medial L lobe or anterior R (segs 4, 5, 8); capsular retraction w/crowded vessels; dilated ducts less common than w/cholangio.
- CT: hypo on arterial & PV; fibrosis may gradually enhance.
- MR: T1 hyp, T2 hyper, progressive enhancement but no enhancement w/Eovist; no fat signal.
DDx:
- HCC: no capsular retraction.
- Cholangio: more masslike; dilated ducts more common.
- Epithelioid hemangioendothelioma: different enhancement; lollipop; rounded.
Benign liver masses: FNH
Px: tissue type; 2 cell types; malignant potential?; contents of scar; capsule?
Ex-2.
CT/MR-3.
Nucs-2
Px: disorganized hepatic tissue; contains Kupffer cells & bile duct cells; ZERO malignant potential; scar = ductules + venules; no capsule.
Ex: women, but no association w/OCPs.
CT/MR:
- T2: scar is hyper.
- Avid arterial phase enhancement.
- PV: stealth lesion, will often show only dark scar.
- Early washout.
Nucs:
- Kupffer cells can be confirmed w/sulfur colloid 1/3 of the time.
- Bile ducts can be seen on HIDA.
Benign liver masses: hemangioma
Px: cell type; blood supply; size range; char of giant hemangs.
Ex: 2; significance w/cirrhosis.
US-1
CT/MR-pathognomonic feature; enhancement relative to Ao.
Px: disorganized endothelial-lined pockets of blood vessels; supplied by a hepatic artery branch at the periphery; <1cm-10cm.
- Giant hemangiomas: tend to have non-enhancing central areas, which are cystic degeneration.
Ex: like FNH, adenomas, more common in females & uncommon in cirrhosis as they tend to involute as the liver becomes more cirrhotic.
US: homogenously echogenic.
CT/MR: hypoattenuating in non-contrast studies; peripheral, nodular discontinuous, progressive (centripetal) enhancement. Follows Ao on all sequences.
Benign liver masses: hepatic adenoma
Px: general path; cell types-2; cell type absent; vascular feature; malig degen?
Ex: 2; if in males, RF; other RFs.
Sx: common presenting symptom & why; assoc Syndrome & underlying cause.
Ix-3
US-1
CT-2
MR-2
Nucs: what nucs scan is useful & why.
DDx: 5
Tx: 1 & why.
Px: hormone-induced; hepatocytes (w/tons of glycogen) + Kupffer cells; no bile ducts; rarely can degenerate into HCC, particularly in men.
Ex: F>M, assoc w/OCP use; if in males, assoc w/exogenous steroid use.
- Other RFs: glycogen storage diseases, obesity, metabolic syndrome, DM.
Sx: hemorrhage as they are hypervascular; von Gierke disease (type 1 glycogen storage disease).
Ix: usually solitary, often subcapsular, R lobe.
US: echogenic due to fat.
CT: hypervascular; may have a late enhancing pseudocapsule.
MR: dark on OOP b/c of intralesional fat.
Nucs: HIDA to distinguish adenoma from FNH as FNH contains bile ducts, adenomas do not.
DDx:
- HCC: washout & rim enhancement, different demographics.
- Fibrolamellar HCC: has scar, calcs more common
- FNH: T2 bright scar, retains Eovist.
- Mets: fat less common.
Tx: resection as they have risk of hemorrhage.
HIDA scan:
- Aka
- General function
- Radiotracer used
- How it works.
- Dx uses (7)
- Cholescintigraphy
- Looks at anatomy & function of the biliary system.
- Tc-99m-IDA analog, or hepatic IDA, hence HIDA
- Like Eovist, IDA radiotracers are taken up by hepatocytes & excreted into the biliary system.
- Acute chole: this is the most common use after an equivocal US; if the tracer does not enter the GB after a sufficient length of time then the cystic duct is obstructed.
- Chronic chole: diagnosed if an adequate % of bile + radiotracer doesn’t exit the GB after CCK.
- Biliary atresia in neonates.
- Bile leak: if tracer spreads outside biliary system.
- Biliary obstruction: tracer does not progress into duodenum.
- Biliary dilatation: for choledochal cysts.
- Sphincter of Oddi dysfunction.
Vascular liver disease: Budd-Chiari
Px: defn-; 2 general causes; specific causes-5; rare cause.
Sx-clinical triad.
US-vascular Fx-3
CT-acute Fx-2; chronic Fx-3.
Px: defn-hepatic venous outflow obstruction; 2 general causes: thrombotic or non-thrombotic; specific causes-OCPs, pregnancy, cancer, infection, trauma; rare cause-congenital HV anomaly.
Sx-abdo pain, hepatomegaly, ascites.
US-vascular Fx:
- Lack of HV flow.
- HV/IVC thrombus.
- Collateral vessels.
CT:
- Acute Fx: edematous peripheral liver (see below); caudate sparing.
- Chronic Fx: caudate lobe hypertrophy; peripheral liver atrophy; regenerative nodules.
Vascular liver disease: veno-occlusive disease
Px: 2.
Ex: 2.
Ix: 5.
Px:
- Destruction of post-sinusoidal vessels w/patent hepatic veins.
Ex:
- Bone marrow pts, possible 2dry to chemo.
Ix: non-specific:
- Hepatomegaly.
- Periportal edema.
- Hepatic vein narrowing: no blood is going to them.
- Heterogeneous parenchymal enhancement.
- No sparing of the caudate.
Vascular liver disease: cardiac hepatopathy
Px: 4; sequela.
Ix: 6
Px:
- Passive hepatic congestion from:
- Heart failure; constrictive pericarditis; R-sided valve failure.
- Any of these may lead to cirrhosis.
Ix:
- Enlarged IVC & hepatic veins.
- Reflux of IV contrast from the R atrium into the HVs
- Hepatomegaly + mottled parenchyma.
- Ascites.
Congenital cystic liver disease: biliary hamartomas (von Meyenburg complexes)
Px: 3.
Ex-1, sex.
Ix: app relative to simple cysts
DDx: 4
Px: small, clusters of dilated bile ducts forming hepatic cystic lesions that DO NOT communicate w/the biliary tree.
- They are embryonic failure of normal bile duct formation.
Ex: rare, ~3%; F:M, 3:1.
Ix: smaller & more irregularly shaped
DDx:
- Multiple liver mets: more variable size & prominent enhancement.
- Multiple liver microabscesses: may restrict diffusion.
- Multiple small hepatic cysts.
- Caroli disease: will have central dot sign.
Congenital cystic liver disease: ADPCLD
Ex-1
Sx-1
Ix: 2
Prognosis: 1
Ex:
- 40-90% of pts w/ADPKD have this.
Sx: even if severe, liver failure is rare.
Ix: Innumerable nonenhancing simple cysts throughout both liver lobes. No lobe is spared!
Prognosis: the # & size of cysts increase w/age.
Liver trauma
- Most commonly injured solid organ in blunt trauma? Liver?
- Name 2 hepatic trauma classification systems and what each is based on?
- List the 5 grades of the MDCT hepatic injury scale.
- What grade is the following?
- Most common = spleen; liver is 2nd.
- American Assoc for the Surgery of Trauma (AAST); based on findings at laparotomy.
- MDCT hepatic injury scale: CT findings.
- Grade 1: superficial lac or subcapsular hematoma <1cm.
- Grade 2: lac or subcapsular/intraparenchymal hematoma 1-3cm.
- Grade 3: lac or subcapsular/intraparenchymal hematoma >3cm.
- Grade 4: massive hematoma >10cm, or destruction, devascularization of 1 hepatic lobe.
- Grade 5: destruction/devasc of both hepatic lobes.
- Dx: grade 4: active bleeding + deep lac.
- Spontaneous hemorrhage from a mass within a cirrhotic liver is almost always what?
- HCC rupture.
- They will also tend to show washout
- Spontaneous hemorrhage is classic, although unusual.
- Like this example, you may see a sentinel clot adjacent to the mass (curved arrow).
78yo female w/cirrhosis & abdo discomfort.
Dx & why?
HCC.
- Focal fat, calcs & hypervascular foci which washout, especially w/in a cirrhotic liver are diagnostic of HCC.
- While macroscopic fat & calcs are unusual features of HCC, in a cirrhotic liver, they are HCC until proven otherwise.
44yo male w/focal liver lesion. Dx?
- Flash-filling hemangioma.
- It follows blood pool on all phases.
- Smaller hemangiomas don’t always demonstrate peripheral nodular peripheral centripetal enhancement and may be homogeneously hypervascular in arterial phase, like this one.
- FNH: always on the DDx for a lesion like this, but most are iso to liver on NCCT and portal venous.
- Adenomas: rare in men & often have lipid, hemorrhage or capsules.
How does viral hepatitis differ from NASH and EtOH hepatitis in liver appearance?
Unlike the other two where steatosis is involved, viral hepatitis rarely results in significant alteration of the liver attenuation.
55yo male w/a pancreatic tumour. What accounts for the wedge-shaped hypervacular regions indicated by the arrows on arterial phase images?
THADs: transient hepatic attenuation differences.
- The mets have occluded PV branches which cause the THADs.
- In a pt w/a GI malignancy, the presence of a THAD should prompt a careful search for subtle mets causing the THAD.
36yo male w/large hepatic mass identified on sonography for RUQ pain. Dx?
Dx: Cavernous hemangioma.
- Most of the mass is isodense to blood pool on NCCT.
- On arterial & PV phase, enhancing portions of the mass are peripheral, nodular, discontinuous & isodense to blood pool, diagnostic of hemangioma.
- Large hemangiomas often have a central or eccentric scar that is hypodense to the rest of the lesion on all phases.
- Focal calcs within the scar are also common in giant hemangiomas.
- Not FNH as the scar would enhance brightly on delayed.
34yo male w/AIDS & wt loss. Dx?
Dx: NHL
- Immunosuppressed pts (AIDS, xsplant) are at markedly increased risk for developing NHL.
- Any focal abdominal visceral or nodal mass should be considered NHL until proven otherwise.
Px:
Ex:
Sx:
US-
CT-
MR-
DDx:
Tx:
Px:
Ex:
Sx:
US:
CT:
MR:
DDx:
Tx:
DDx GB wall thickening:
Biliary:
- cholecystitis
- GB cancer
- adenomyomatosis
- PSC
- AIDS cholangitis
Non-biliary:
- hepatitis
- ascites
- cirrhosis
- PHTN
- hypoproteinemia
- lymphatic obstruction
Adenomyomatosis is most commonly associated with?
- cholelithiasis
Type 1 choledochoceles are associated w/increased risk of what 2 entities?
- Cholangiocarcinoma & GB cancer.
What is the most appropriate management for this finding in a pt w/RUQ pain?
- Dx: type 1 choledochocele w/dilation & an intraluminal papillary mass.
- ERCP for further evaluation & tissue sampling for diagnosis.
What is the most common complication associated w/choledochoceles?
- Biliary & pancreatic calculi.
- Cholangioca is the 2nd most common complication.
Which types of biliary cysts/choledochoceles are typically treated w/a Roux-en-Y hepaticojejunostomy?
- 1 & 4.
- Choledochal cysts are a premalignant state w/cancer occurring more frequently and earlier than in the general population. Risk increases w/age. Most common cancer = adenoca.
- 90% of carcinomas occur in these types, both which involve the EHDs, so the recommendation is for removal.
- Type 4 always includes the EHDs, but type 4a includes intra as well, and 4b, is multiple strictures of the EHD.
- Treatments for the others:
- Type 2: cyst excision.
- Type 3: sphincterotomy or endoscopic resection.
What is present in 70-90% of pts w/GB cancer?
Gallstones.
- Malignancy risk is higher in pts w/larger gallstones & longer duration of cholelithiasis.
The most common appearance of GB cancer is?
- A mass filling the GB lumen (40-65% of pts show this).
What does a parvus tardus waveform mean, generally?
Upstream stenosis.
- How does biliary epithelium differ from hepatic parenchyma re: its blood supply?
- It only receives blood from the hepatic arteries, whereas the hepatic parenchyma receives a dual supply.
- So the biliary epithelium is vulnerable to ischemic injury.
- Ischemic type biliary lesions (see below, resulting in dilated ducts), can result if there is HA stenosis.
Identify the labeled structures:
A: caudate
B: left lateral segment
C: ligamentum venosum
D: umbilical portion of the LPV
Identify the following structures:
E: MPV
F: CBD
G: RHA
- What is one of the hallmarks of HCC?
- Why do they wash out?
- Preferential arterial blood supply, hence early arterial enhancement.
- Diminished portal venous supply of HCC compared to surrounding liver, so it doesn’t receive as much PV blood.
- What is the LI-RADS score for this lesion?
- What characteristics cause a LR5 lesion?
- LR5.
- >20mm, arterial hyperenhancement, delayed washout.
- >10mm w/1 or 2 of the 3 features:
- Interval growth
- Enhancing capsule
- Non-peripheral washout
Draw the LI-RADS chart
- Which marker is elevated in fibrolamellar HCC?
- Which is not?
- Elevated: bhCG.
- Not: AFP.
