Liver Flashcards
Couinaud classification
8 segments
portal veins divide the superior from inferior segments
hepatic veins segments in axial planes; middle hepatic vein divides right and left lobes
caudate lobe drains into
IVC
compensatory hypertrophy of caudate lobe
morphological change of early cirrhosis; direct drainage into IVC spares caudate from increased venous pressures due to portal hypertension
portal venous phase, timing
routine CT abd/pelvis; 70 sec
arterial phase, timing
20-25 s after IV injection
however, optimal conspicuity in the late arterial phase ~35 sec
hepatic steatosis imaging
noncontrast CT: hyperattenuating to spleen; 10 HU greater than spleen
contrast enhanced CT: liver attenuates <25 HU than spleen
in and out of phase MRI: signal loss in liver on out of phase imaging
liver biopsy
liver decreased signal on in-phase images
hepatic iron overload due to longer TE; allows a longer dephasing time, exaggeration of T2*, and loss of signal
geographic regions of focal hepatic fat
gallbladder fossa, subcapsular (along falciform ligament), periportal, nodular throughout the liver
amyloid deposition in the liver
focal/diffuse areas of decreased attenuation on CT
wilson disease in the liver
high levels of copper (basal ganglia, cornea, liver)
hyperattenuating multiple nodules –> hepatomegaly/cirrhosis
pathways for hepatic iron accumulation
hemochromatosis and hemosiderosis
hemochromatosis, treatment
most common; genetic defect causing increased iron absorption; excess iron cannot be stored in the RES so deposited in hepatocytes, pancreas, myocardium, skin/joints
spleen/bone marrow normal
treatment phlebotomy
MR imaging of iron overload
hypointense liver
spleen/bone marrow hypointense in hemosiderosis
hemosiderosis, treatment
excess iron in the RES due to frequent blood transfusions or defective erythrocytosis
treatment: iron chelators
Ddx hypoattenuating liver (less than spleen)
fatty liver, hepatic amyloid
Ddx hyperattenuating
iron overload, medication (amiodarone, gold, methotrexate), copper overload, glycogen excess
<75 HU
viral hepatitis findings
nonspecific, gallbladder wall thickening or periportal edema
candidiasis
multiple tny hypoattenuating microabscesses in liver/spleen; may be rim enhancing
typically immunocompromised
Ddx for multiple tiny hypoattenuating hepatic lesions
metastases, lymphoma, biliary hamartomas, caroli disease, candidiasis
hepatic abscess cause, organism
typically bowel process (diverticulitis, appendicitis, Crohn disease, bowel surgery, ascending cholangitis) > nidus > portal system
E. coli
hepatic abscess imaging feature
rim enhancing mass
MRI: central hyperintensity on T2 with irregular wall that may enhance late
may mimic mets
echinococcal disease
ingestion of Echinococcus granulosus (Mediterranean basin) and associated with sheep-raising
echinococcal eggs –> hydatid cysts
imaging of echinococcis
well defined hypoattenuating mass featuring a floating membrane or an associated daughter cyst; peripheral calcifications may be present
Cirrhosis causes, types
repeated cycles of injury/repair –> fibrosis and attempted, disorganized regeneration
micronodular: metabolic causes (alcohol, steatohepatitis, hemochromatosis, Wilsons disease)
macronodular: postviral (hep B/C)
also inflammatory (PBC/PSC) and infectious
Signs of early cirrhosis on imaging
expansion of preportal space; atrophy of medial segment of L hepatic lobe, enlargement of the caudate lobe, empthy gallbladder fossa sign
secondary manifestations of cirrhosis
portal hypertension (splenomegaly, portosystemic collaterals/varices)
gallbladder wall thickening (hypoalbuminemia/edema)
Gamma Gandy bodies (splenic microhemorrhages), which appear hypointense on GRE
how is HCC formed
regenerative nodule > dysplastic nodule > HCC
regenerative nodule: supplied by portal vein, not premalignant, does not enhance
dysplastic nodule: premalignant, do not demonstrate arterial phase enhancement
MRI findings of regenerative and dysplastic nodules
regenerative: low T2, variable T1; enhance to the level of parenchyma or slight less
dysplastic: variable T1, hypointense T2 (high grade nodules will be T2 hyperintense); isoenhancing relative to liver
HCC tumor markers
AFP elevated in 75% of cases
imaging findings of HCC
hypervascular mass with cirrhosis
arterial phase enhancement, encapsulated, washes out on portal venous phase
T2 hyperintense on liver
locally invasive, can invade into portal veins, IVC, bile ducts
HCC treatments
partial hepatectomy, orthotopic liver translantation, percutaneous ablation, transcatheter embolization
fibrolamellar HCC
subtype that occurs in young patients without cirrhosis
AFP is not elevated
fibrolamellar HCC imaging findings
large heterogenous mass with a fibrotic central scar; capsular retraction possible, no capsule (unlike HCC)
T1/T2 hypointense scar
hepatic metastases enhancement
most mets (colorectal, pancreatic adenocarcinoma) are hypovascular best seen on portal venous phase
HCC is hypervascular, visualized on late arterial phase
hypervascular hepatic mets
neuroendocrine (pancreatic, carcinoid), RCC, thyroid, melanoma, sarcoma
calcifications with mets
seen with mucinous colorectal or ovarian serous tumors
imply better prognosis
T1 hyperintense lesions
blood products and melanin
metastatic lesions on MRI
hypointense T1, hyperintense T2
peudocirrhosis
macronodular liver contour from multiple scirrhous hepatic mets, mimics cirrhosis; will have capsular retraction
commonly breast cancer will do this
hepatic lymphoma
usually presents with splenomegaly and LAD
epithelioid hemangioendothelioma
multiple confluent spherical subcapsular masses; vascular malinancy
halo or target appearance
cause of capsular retraction
ddx capsular retraction
mets (mostly post treatment), fibrolamellar HCC, HCC (uncommon), epithelioid hemangioendothelioma, intrahepatic cholangiocarcinoma, confluent hepatic fibrosis
FNH associations, imaging
disorganized lvier tissue with no malignant potential
asymptomatic women , not associated with OCP
central scar (does not contain fibrotic tissue); no capsule T2 hyperintese area; avidly enhances during arterial phase and washes out quickly
sulfur colloid and HIDA visualizes?
sulfur colloid»_space; Kupffer cells
HIDA»_space; bile duct cells
hemangioma
benign mass of disorganized endothelial-lined pockets of blood vessels; more common in females
peripheral, discontinuous, progressive nodular enhancement; nonspecific hypoattenuating lesion on noncontrast CT
hepatic adenoma pathology
benign neoplasm: hepatocystes, scattered kupffer cells, no bile ducts (can differentiate on HIDA for FNH which has bile ducts)
hepatic adenoma
more common in females, prolonged OCPs or associated with anabolic steroids in men; high risk of hemorrhage
multiple hematic adenoma
von Gierke disease (type I glycogen storage disease)
adenoma on imaging
hypervascular on arterial phase; microscopic fat may be seen on in/out of phase MRI
intralesional hemorrhage will look like T1 hyperintensity
budd chiari pathology, causes
hepatic venous outflow obstruction
hypercoagulative states, hematolgic disorders, pregnancy, OCP, malignancy, infection, trauma
clinical triad of acute Budd Chiari
hepatomegaly, ascites, abdominal pain
budd chiari findings
edematous peripheral liver
progressive liver –> atrophy with caudate hypertrophy ;caudate spared as it drains directly into the IVC
veno-occlusive disease
destruction of post-sinusoidal venules with patent hepatic veins; seen in bone marrow transplate patients
cardiac hepatopathy
passive hepatic congestion from HF, constrictive pericarditis, right sided valvular disease –> cirrhosis
enlarged hepatic veins/IVC; reflux of contrast from right atrium
liver is enlarged with mottled enhancement; ascites present
congenital cystic liver disease
biliary hamartoma (von Meyenburg complex) and ADPLD
biliary hamartoma
incidental small cystic hepatic lesion; irregularly shaped simple cysts
autosomal dominant polycystic liver disease
40% of ADPKD have similar disease in the liver, called ADPLD
hepatic failure remains rare
most common organ injured in trauma? second most common?
spleen > liver
MDCT grading of hepatic injury
Grade I: Superficial laceration or subcapsular hematoma <1 cm in size.
• Grade II: Laceration or subcapsular/intraparenchymal hematoma >1 and <3 cm in size.
• Grade III: Laceration or subcapsular/intraparenchymal hematoma >3 cm in diameter.
• Grade IV: Massive hematoma >10 cm, or destruction/devascularization of one hepatic lobe.
• Grade V: Destruction or devascularization of both hepatic lobes.
