Liver Flashcards
1
Q
How do you remember the Couinaud classification for the lobes of the liver?
What divides the superior from inferior segments?
What divides the segmental borders in the axial plane?
Each hepatic segment features its own:
Which lobe drains directly into the IVC?
A
- Portal veins divides superior from inferior segments.
- Hepatic veins
- Each hepatic segment features its own
- Central portal triad including branches of the portal vein, hepatic artery, and bile duct. Peripheral venous drainage to the hepatic veins and ultimately the IVC.
- The caudate lobe drains directly to the IVC, not into the hepatic veins. The caudate lobe is spared in early cirrhosis since the direct drainage to the IVC spares the caudate from increased venous pressures due to portal hypertension. This leads to compensatory hypertrophy of the caudate lobe, which is a typical morphologic change of early cirrhosis. Similarly, direct venous drainage to the IVC allows the caudate lobe to bypass the increased hepatic venous pressures seen in Budd-Chiari syndrome. Compensatory hypertrophy of the caudate lobe may preserve liver function in these patients.
2
Q
How many seconds following IV contrast administration for each below?
Portal Venous Phase
Arterial Phase
Late Arterial Phase
A
- Portal Venous Phase: 70 seconds
- Arterial Phase: 20-35 seconds
- Late Arterial Phase: 9-16 seconds after abdominal aortic enhancement, or approx 35 seconds after IV contrast injection.
3
Q
Fatty Liver (Hepatic Steatosis)
How do you diagnose on unenhanced CT?
How to diagnose on contrast-enhanced CT?
MRI?
A
- On unenhanced CT, the liver should be slightly hyperattenuating relative to the spleen. The traditional teaching is that steatosis is present if the liver attenuates at least 10 HU less than the spleen, although new work suggests that even a single HU of relative hypoattenuation compared to the spleen may represent hepatic steatosis.
- On contrast-enhanced CT, evaluation of hepatic steatosis is much less reliable compared to unenhanced CT due to different contrast uptake rates of the liver and the spleen. However, the liver is considered diffusely hypoattenuating if it attenuates at least 25 HU less than the spleen in the portal venous phase.
- In- and out-of-phase GRE MRI is a sensitive imaging technique to evaluate for the presence of (and to quantify the degree of) hepatic steatosis.
4
Q
Fatty Liver
What are the geographic regions that may exhibit focal fatty changes?
A
- Gallbladder fossa (drained by gallbladder vein).
- Subcapsular (along the falciform ligament).
- Periportal.
- Focal fat may also be nodular throughout the liver. An ultrasound would demonstrate multiple
- Hyperechoic lesions which would be hypoattenuating on CT. MRI shows pseudolesions drop in signal intensity on out-of-phase dual-phase GRE, consistent with nodular focal fat.
5
Q
What could amyloid deposition in the liver look like?
A
- Abnormal extracellular deposition of amyloid protein in the liver can cause focal or diffuse areas of decreased attenuation on CT imaging.
6
Q
Wilson disease
What is it and how does it look in the liver?
A
- Wilson disease causes high levels of copper to accumulate in the basal ganglia, cornea, and liver due to an autosomal recessive genetic defect. The liver may be hyperattenuating on CT with multiple nodules, eventually leading to hepatomegaly and cirrhosis.
7
Q
What are the two pathways to excess hepatic iron accumulation?
What does it look like on MRI (internal control in relation to what organ?)
A
- There are two pathways to excess hepatic iron accumulation. Accumulation within hepatocytes is seen in hemochromatosis. Uptake within the reticuloendothelial system RES causes hepatic Kupffer cell iron overload, as seen in hemosiderosis.
- Regardless of the etiology, the iron-overloaded liver is hypointense on all MRI sequences, relative to the paraspinal muscles as an internal control.
8
Q
Hemochromatosis
What is it?
Treatment?
Where does iron get deposited? What organs are normal?
A
- Hemochromatosis is the most common cause of iron overload, due to a genetic defect causing increased iron absorption. Excess iron is unable to be stored in the RES, so the spleen and bone marrow are not affected. Treatment of hemochromatosis is phlebotomy.
- Excess iron is deposited in hepatocytes (not the Kupffer cells that make up the intrahepatic RES), pancreas, myocardium, skin, and joints. Excess iron in hepatocytes can cause cirrhosis.
- The spleen and bone marrow are normal since the RES is not involved.
9
Q
Hemosiderosis
Where does iron get stored?
What causes it?
Treatment?
MRI imaging?
A
- Raffi MNEMONIC: HemoSiderosis - iron gets stored in the reS (in the Kupffer cells which also include spleen and bone marrow)
- Hemosiderosis is excess iron stored within the reticuloendothelial system, which may be due to frequent blood transfusions or defective erythrocytosis. Treatment of hemosiderosis is with iron chelators, not phlebotomy.
- The RES has a large capacity for iron. Iron stored in the RES is generally not harmful and the liver is normal in morphology, without cirrhosis.
- MRI imaging of hemosiderosis demonstrates hypointense liver on conventional MRI sequences, similar to hemochromatosis. Additionally, the spleen and bone marrow will also appear hypointense due to increased iron stores throughout the entire reticuloendothelial system.
10
Q
What is secondary hemochromatosis?
A
- Hemosiderosis is a precursor to secondary hemochromatosis. Secondary hemochromatosis is hepatic damage from iron overload after the RES system becomes saturated from prolonged hemosiderosis.
- When the RES becomes overwhelmed with iron, the hepatocytes begin to store the excess. Similar to hemochromatosis, hepatocyte iron uptake may lead to cirrhosis.
11
Q
DDx for hypoattenuating liver
A
- The liver is considered hypoattenuating if it attenuates less than the spleen on an unenhanced CT.
- Fatty liver (hepatic steatosis) is by far the most common cause of a diffusely hypoattenuating liver.
- Hepatic amyloid is rare and may cause either focal or diffuse hepatic hypoattenuation.
12
Q
DDx for hyperattenuating liver
A
- Hyperattenuating liver: The normal unenhanced attenuation of the liver is 30 to 60 HU. An absolute attenuation greater than 75 HU is considered hyperattenuating.
- Iron overload is by far the most common cause of a hyperattenuating liver.
- Medications (e.g., amiodarone, gold, and methotrexate).
- Copper overload (Wilson disease).
- Glycogen excess.
13
Q
Viral hepatitis - imaging appearance
A
- Patients with viral hepatitis often have a normal CT scan. Viral hepatitis may cause nonspecific CT findings, such as gallbladder wall thickening or periportal edema fluid on both sides of the portal veins).
14
Q
Hepatic Candidiasis
Seeding of liver from systemic fungal infection is coming from where?
CT appearance?
Candidiasis is almost always seen in which kind of patients?
DDx for multiple tiny hypoattenuating hepatic lesions
A
- Systemic fungal infection may seed the liver (and commonly the spleen as well) due to portal venous drainage of infected bowel.
- CT shows multiple tiny hypoattenuating microabscesses in the liver and the spleen, which may be rim-enhancing.
- Candidiasis is almost always seen in immunocompromised patients.
- The differential diagnosis for multiple tiny hypoattenuating hepatic lesions includes metastatic disease, lymphoma, biliary hamartomas, and Caroli disease.
15
Q
Hepatic Abscess
MCC?
Imaging features?
A
- Hepatic abscess is most commonly caused by a bowel process and resultant infectious nidus carried through the portal system to the liver. Common causes include diverticulitis, appendicitis, Crohn disease, and bowel surgery. E. coli is the most common organism. A primary hepatobiliary infection, such as ascending cholangitis, may be a less common cause.
- Imaging features of a hepatic abscess may mimic metastasis, appearing as a ring-enhancing mass on CT. On MRI, there is typically central hyperintensity on T2-weighted images with an irregular wall that enhances late. Perilesional enhancement may be present.
16
Q
Echinococcal Disease
Caused by what?
Endemic Where?
Associated with what specific job?
Imaging Characteristics?
A
- Hepatic echinococcosis is caused by ingestion of the eggs of Echinococcus granulosus, which is endemic in the Mediterranean basin and associated with sheep-raising.
- Echinococcal eggs can develop into hydatid cysts.
- On CT, a hydatid cyst is a well-defined hypoattenuating mass featuring a characteristic floating membrane or an associated daughter cyst. Peripheral calcification may be present.
24
Q
HCC
Major risk factor?
HCC is the diagnsosis until proven otherwise in what scenario?
What tumor marker is elevated and in what percent?
What is the characteristic imaging feature and how often does this occur?
Classic CT or MRI appearance?
What does a nodule in nodule appearance represent?
HCC tends to do what locally? Contrast this with mets?
Treatment options?
A
- Hepatocellular carcinoma (HCC) is the most common primary liver tumor. Cirrhosis is the major risk factor for the development of HCC.
- A hypervascular liver mass in a patient with cirrhosis or chronic hepatitis is an HCC until proven otherwise.
- Alpha-fetoprotein is elevated in approximately 75% of cases of HCC.
- Arterial phase enhancement is the characteristic imaging feature of HCC. However, between 10 and 20% of HCCs are hypovascular and thus slightly hypoenhancing relative to surrounding liver on arterial phase imaging.
- The classic CT or MRI appearance of HCC is an encapsulated mass that enhances on the arterial phase and washes out on portal venous phase. HCC may be difficult to detect on non-contrast or portal venous phase CT. On unenhanced MRI, HCC is characteristically slightly hyperintense on T2-weighted images relative to surrounding liver.
- The nodule in a nodule appearance describes an enhancing nodule within a dysplastic nodule and represents an early HCC.
- HCC is locally invasive and tends to invade into the portal and portal veins, IVC, and bile ducts. In contrast, metastases to the liver are much less likely to be locally invasive.
- Treatment options for HCC include partial hepatectomy, orthotopic liver transplantation, percutaneous ablation, and transcatheter embolization.
27
Q
Hepatic Metastases
Imaging appearance?
What are the classic hypervascular mets?
Calcifications can be seen in which mets? Prognostic implication?
MRI appearance?
What is pseudocirrhosis?
A
- Although metastases are supplied by branches of the hepatic artery induced by tumoral angiogenesis, most metastases are hypovascular and best appreciated on portal venous phase (in contrast to HCC, which is hypervascular and best visualized on late arterial phase).
- Hypervascular mets (best seen on arterial phase) classically include: Neuroendocrine tumors including pancreatic and carcinoid, RCC, Thyroid, Melanoma, Sarcoma. (similar to hemorrhagic mets in brain!)
- Colorectal and pancreatic adenocarcinoma metastases are typically hypovascular and can usually be diagnosed on portal venous imaging.
- Calcifications can be seen in mucinous colorectal tumors or ovarian serous tumors Calcification within a metastatic lesion may imply a better prognosis.
- On MRI, metastatic lesions tend to be hypointense on T1-weighted images and hyperintense on T2-weighted images. Blood products and melanin (as in melanoma) are T1 hyperintense.
- Pseudocirrhosis describes the macronodular liver contour resulting from multiple scirrhous hepatic metastases, which may mimic cirrhosis. Treated breast cancer is the most common cause of this appearance. Capsular retraction, although not always seen, is characteristic of pseudocirrhosis, and when present suggests pseudocirrhosis over cirrhosis.
29
Q
Epithelioid Hemangioendothelioma
What is it?
Imaging appearance?
A
- Epithelioid hemangioendothelioma is a rare vascular malignancy that characteristically causes multiple spherical subcapsular masses than can become confluent. The individual masses may have a halo or target appearance.
- Epithelioid hemangioendothelioma is one cause of capsular retraction.
33
Q
Focal Nodular Hyperplasia
What is it? Association?
Characteristic feature? Does it have a capsule?
Imaging appearance?
Ways to confirm?
A
- Focal nodular hyperplasia is disorganized liver tissue with no malignant potential. It is primarily seen in asymptomatic women and is not associated with oral contraceptives.
- FNH has a characteristic central “scar” which does not contain fibrotic tissue and is therefore not a true scar. Instead, the central area consists of T2-hyperintense ductules and venules, and demonstrates delayed enhancement. FNH does not have a capsule.
- FNH can be difficult to see without contrast on CT and T1- and T2-weighted MRI sequences. FNH avidly enhances during the arterial phase, then washes out very quickly. The portal venous phase will often show just the unenhanced scar, which enhances late.
- Kupffer cells and bile duct epithelium are both present. Kupfer cells may be confirmed by a sulfur colloid study (1/3 of the time) and bile duct cells can be seen on a HIDA scan. (or Gadoxetate disodium [premovist/eovist])
34
Q
Cavernous Hemangioma
What is it?
Epidemiology? What happens to a known hemangioma in a patient with early cirrhosis?
Range in size? What may happen to large ones on imaging?
What is the virtually pathognomonic imaging feature?
Unenhanced appearance?
A
- A hepatic hemangioma is a benign mass composed of disorganized endothelial-lined pockets of blood vessels, supplied by a branch of the hepatic artery at the periphery.
- Hemangioma is more common in females and uncommon in cirrhosis. When a known hemangioma is sequentially followed in a patient with early cirrhosis, the hemangioma involutes as the liver becomes more cirrhotic.
- Hemangiomas may range in size from <1 cm to >10 cm. Giant hemangiomas tend to have a non-enhancing central area representing cystic degeneration.
- A virtually pathognomonic imaging feature is peripheral, discontinuous, progressive, nodular enhancement. The attenuation (or signal intensity on MRI of the enhancement is identical to the aorta and features gradual centripetal fill-in on later phases.
- The unenhanced CT appearance of a hemangioma is a nonspecific hypoattenuating liver mass.
35
Q
Hepatic Adenoma
What is it?
Epidemiology? Risk factor?
Contrast to FNH
Risk of what? Treatment?
Multiple hepatic adenomas are seen in what dz?
What may be present, which tends to enhance late?
What two characteristics help differentiate from other hypervascular liver lesions?
A
- Hepatic adenoma is a benign hepatic neoplasm containing hepatocytes, scattered Kupfer cells, and no bile ducts.
- Adenoma s are much more common in females, especially with prolonged oral contraceptive use. When seen in males, adenoma may be associated with anabolic steroids.
- The absence of bile ducts makes a nuclear medicine HIDA scan a useful test to distinguish between focal nodular hyperplasia (which contains bile ducts and would be positive on HIDA) and a hepatic adenoma, which does not contain bile ducts.
- Adenomas have a relatively high risk of hemorrhage, which is often the presenting symptom. For this reason, incidentally discovered adenomas are usually resected.
- Multiple hepatic adenomas are seen in Von Gierke disease (type I glycogen storage disease).
- A pseudocapsule may be present, which tends to enhance late.
- Adenomas lack portal venous drainage and thus are hypervascular on arterial phase. The presence of microscopic fat, when present, is best seen on in- and out-of-phase MRI. Intralesional hemorrhage may cause T1 hyperintensity. Adenomas may be difficult to differentiate from other hypervascular liver lesions in the absence of fat or hemorrhage.
36
Q
Budd-Chiari
What is it?
Causes?
Acute presentation?
Vascular findings?
Acute intraparenchymal findings?
Chronic findings?
A
- Budd-Chiari is the hepatic venous outflow obstruction, which can be thrombotic or non-thrombotic.
- Budd-Chiari may be due to hypercoagulative states including hematological disorders, pregnancy, oral contraceptives, malignancy, infection, and trauma. It is very rare to have primary Budd-Chiari due to congenital hepatic vein anomaly.
- Acute Budd-Chiari presents with a clinical triad of hepatomegaly, ascites, and abdominal pain.
- Direct vascular findings include lack of flow within hepatic veins, thrombus in the hepatic veins/IVC, and the formation of collateral vessels.
- Acute intraparenchymal findings include an edematous peripheral liver with sparing of the caudate lobe. The caudate is spared as it drains directly into the IVC.
- Progressive liver failure may result in chronic disease, producing caudate lobe hypertrophy and atrophy of peripheral liver with prominent regenerative nodules.
42
Q
Overview of liver trauma
Grading
A
- The liver is the second most commonly injured solid organ due to blunt trauma, second to the spleen. The CT description and grading of liver injury are similar to splenic injury.
- The American Association for the Surgery of Trauma classification describes hepatic injury based on findings at laparotomy.
- The MDCT hepatic injury grading scale is based on CT findings and is more commonly used by radiologists. It is similar to the MDCT grading scale for splenic trauma.
