Liver, Biliary tree and gallbladder Flashcards
current method of choice for most hepatic imaging
dynamic bolus contrast-enhanced MDCT
imaging used to characterize cavernous hemangiomas and focal nodular hyperplasia
radionuclide imaging
2/3 of hepatic blood supply comes from
portal vein
maximum enhancement of the liver parenchyma occurs at
60 to 120 seconds following hepatic arterial enhancement
2 major classes of gadolinium used in hepatic imaging
extracellular agents such as gadopentetate dimeglumine (magnevist) and liver specific contrast agent such as gadoxetate disodium (eovist)
imaging that is very useful for definitive diagnosis of cavernous hemangioma
radionuclide blood pool imaging
3 longitudinal plane landmarks of surgical liver segments
middle hepatic vein, IVC, gallbladder fossa
divides the right liver lobe in anterior and posterior segments
right hepatic vein
anterior segments of right liver lobe
segment 5 and 8
posterior segments of right liver lobe
segment 6 and 7
divides the left liver lobe into medial and lateral segments
left hepatic vein
divides the left liver lobe into superior and inferior segments
left portal vein
divides the right liver lobe into superior and inferior segments
right portal vein
segment 1 of liver is the _____ which extends between the fissuer of the ligamentum venosum and IVC
caudate lobe
hepatic venous drainage from caudate lobe is directly into the
IVC via small veins
difference of THADs or THIDs (transient hepatic attenuation differences) from true parenchymal abnormality
no associated mass effect, vessels traverse them without distortion, underlying liver parenchyma is preserved
“third inflow” of portal venous flow are from systemic veins in the
pericholecystic, parabiliary, epigastric-paraumbilical venous systems
hepatic arterial flow may be increased by
hypervascular tumors, arterioportal shunting, inflammation of adjacent orgas, aberrants hepatic arterial supply
normal liver length
15.5 cm
liver length is measured in
midclavicular line
normal variant of hepatic shape found most in women. refers to an elongated inferior tip of right liver lobe
Reidel lobe
most common abnormality demonstrated by hepatic imaging
fatty liver
includes a continuum of liver disease that extends from simple fatty liver through nonalcoholic steatohepatitis to cirrhosis
nonalcoholic fatty liver disease
at risk for NASH include
those with type 2 DM, metabolic syndrome
reliable US findings of fatty liver include
liver echogenicity greater than that of the renal cortex, loss of visualization of normal echogenic portal triads in the periphery of the liver, poor sound penetration with loss of definition of the diaphragm
on unenhanced CT, fatty liver is diagnosed when the liver is ___ HU less than the spleen attenuation or when the liver is less than ____ HU
10 HU less than the spleen or less than 40 HU
MR sequence most sensitive to diganosis of fatty liver
GRE
potential pitfall in MR diagnosis of fatty liver in patients with cirrhosis
Iron deposition, which also cause a loss of signal in our-of-phase MR imaging
characteristic feature of fatty liver deposition on all modalities include
lack of mass effect, angulated geometric boundaries between involved and uninvolved parenchyma
fatty changes can develop within ___ weeks of hepatocyte insult and may resolve within ____ days of removing the insult
3 weeks, 6 days
focal fatty infiltration is most common in what parts of the liver
adjacent to falciform ligament, GB fossa, porta hepatis
fat-spared area is most commonly in what segment
segment 4
used to quantify liver fat
MR spectroscopy
type of fatty liver distribution that is only associated with renal failure on peritoneal dialysis and only when insulin is added to the dialysate
subcapsular fatty liver
characterized pathologically by portal and perilobular inflammation and fibrosis
chronic hepatitis
causes of chronic hepatitis
chronic viral infection and hepatitis B and C
characterized pathologically by diffuse parenchymal destruction, fibrosis with alteration of hepatic architecture and innumerable regenerative nodules that replace normal liver parenchyma
cirrhosis
causes of cirrhosis
hepatic toxins (alcohol, drugs, aflatoxin from a grain fungus), infections, biliary obstruction and heredity (Wilson disease)
In asia and africa, most cases of cirrhosis are due to
chronic active hepatitis
morphologic alterations seen in cirrhosis
hepatomegaly, atrophy or hypertrophy of hepatic segments, coarsening of hepatic parenchymal texture, nodularity of the parenchyma, hypertrophy of caudate lobe and left lobe with shrinkage of right lobe, regenerating nodules, enlargement of hilar periportal space (>10 mm) reflecting parenchymal atrophy
extrahepatic signs of cirrhosis
presence of portosystemic collaterals as evidence of portal hypertension, splenomegaly and ascites
effective treatment for portal hypertension and long-term control of esophageal variceal bleeding
transjugular intrahepatic portosystemic shunts (TIPS)
well established effective treatment for end-stage liver disease
liver transplantation
mimics of cirrhosis include
diffuse hepatic nodularity or portal hypertension including pseuocirrhosis of treated breast cancer metastases, miliary metastases, sarcoidosis, schistosomiasis, Budd-Chiari syndrome, nodular regenerative hyperplasia, idiopathic portal hypertension, portal vein obstruction, biliary obstruction
constant feature of cirrhosis
nodules
causes of nodules in a cirrhotic liver
regenerative nodules, dysplastic nodules, HCC, confluent fibrosis, focal fat infiltration, focal fat sparing, metastases
micronodular pattern of cirrhosis include small RN with sizes of
< 3mm
macronodular pattern of cirrhosis include RN size of
> 3mm
regenerative nodules are supplied by
portal vein
describe cirrhotic nodules that are high in iron content and appear as low signal nodules on both T1 and T2
siderotic nodules
siderotic nodules may be considered benign when they are
< 20 mm in diameter, homogeneous on all image sequences, isoenhance compared to background cirrhotic nodules in all phases
most often involved part of the liver in confluent fibrosis
central portion of right hepatic lobe
appearance of acute liver fibrosis on MRI
bright on T2 due to high fluid content
chronic cirrhosis appears what on MRI
low in fluid content and appears dark on T2
pathologic increase in portal venous pressure that results in the formation of portosystemic collateral vessels that divert blood flow away from the liver into the systemic circulation
portal hypertension
causes of portal hypertension
progressive vascular fibrosis associated with chronic liver disease, portal vein thrombosis or compression and parasitic infections
complications of portal hypertension
hemorrhage from varices and hepatic encephalopathy
Signs of portal hypertension include
visualization of portosystemic collaterals, increased portal vein diameter, increased SMV and splenic vein diameters, portal vein thrombosis, calcifications in the portal and mesenteric veins, edem in the mesentery, omentum and retroperitoneum, splenomegaly, ascites, reversal of flow in any portion of the portal venous system
normal diameter of portal vein
<13mm
normal diameter of SMV and splenic vein
< 10mm
portosystemic collaterals
coronary, gastroesophageal, splenorenal, paraumbilical, hemorrhoidal and retroperitoneal
causes of portal vein thrombosis
as complication of cirrhosis, portal vein invasion or compression by tumor, hypercoagulable states or inflammation (pancreatitis)
refer to a group of disorders characterized by obstruction to hepatic venous outflow involving one or more hepatic veins
Budd-Chiari syndrome
causes of Budd-Chiari syndrome include
coagulation disorder, membranous webs, obstructing hepatic veins or IVC and malignant tumor invasion of the hepatic veins
in Budd-Chiari syndrome, caudate lobe is spared because
it has a separate venous drainage which the IVC
characteristic appearance of Budd-Chiari syndrome
early phase CT images show the markeldy heterogeneous liver with prominent central and weak peripheral enhancement
common complication of congestive heart failure and constrictive pericarditis wherein the hepatic venous drainage is impaired and the liver becomes engorged and swollen
passive hepatic congestion
radiographic findings of passive hepatic congestion
distention of hepatic veins and IVC, reflux of IV contrast into the hepatic veins and IVC, increased pulsatility of portal vein, and inhomogeneous contrast enhancement of the liver
this condition may primary resulting from a hereditary disorder that increases dietary iron absorption, or secondary due to excessive iron intake usually from multiple blood transfusions or chronic diseases including cirrhosis, myelodysplastic syndrome and certain anemias
hemochromatosis
reticuloendothelial pattern of iron deposition is seen in
secondary hemochromatosis with iron overload cause by blood transfusions
renal pattern of iron deposition appears
loss of renal cortical signal on T1 and T2, reversing the normal corticomedullary differentiation pattern
excess iron increases hepatic parenhcymal attenuation of ___ on noncontrast images
above 72 HU
an omnious imaging sign associated with bowel ischemia in adults and necrotizing enterocolitis in infants
gas in portal venous system
portal venous gas presents as
air-density tubular structures extending to the periphery of liver
pneumobilia presents as
central and does not extend into the peripheral 2 cm of the liver
LI-RADS category: definitely benign ; hemangioma, cyst, cystic biliary hamartoma, focal fat deposition or sparing, perfusion alteration, vascular anomalies, definite confluent fibrosis, hypertrophic pseudomass
LR-1
LI-RADS category: findings are less certain than for LR-1, persistent perfusion alteration, probable confluent fibrosis, pseudomass, cirrhosis-associated nodule, focal scars
LR-2
LI-RADS category: intermediate probability for HCC
LR-3
LI-RADS category: probably HCC
LR-4
LI-RADS category: Definitely HCC
LR-5
LI-RADS category: definitely tumor invading vein
LR-TIV
LI-RADS category: Treated posttreatment observation
LR-5 treated posttreatment observation
LI-RADS category: other malignancy which include cholangiocarcinoma, lymphoma, metastases
OM
Management of LR 1 and 2
Continued routine surveillance, as appropriate
management of LR-3
variable follow-up (depends on clinical consideration)
management of LR-4
Additional imaging, biopsy, treatment or close follow-up
management of LR-5 and LR-TIV
Treat without biopsy. Radiologic TNM staging
management of LR-5 treated posttreatment observation
close follow-up to asses treatment response. Retreat if needed
management of other malignancies
biopsy, additional imaging, treatment or close follow-up
In normal liver parenchyma, most common hypervascular lesions are
hemangiomas, FNH, hepatic adenoma and hypervascular metastases
In fibrotic liver and cirrhosis, the most hypervascular lesions are
HCC and dysplastic nodules
hepatic metastases most commonly originate from
GI, breast or lung