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.
17
Q
Cirrhosis
Etiology and pathology
A
- Cirrhosis is caused by repeated cycles of injury and repair, which can be due to metabolic (alcohol, steatohepatitis, hemochromatosis, or Wilson disease), infectious (chronic hepatitis B or C), or inflammatory (primary biliary cirrhosis or primary sclerosing cholangitis) etiologies. The hallmarks of cirrhosis are fibrosis and attempted, disorganized regeneration.
- The micronodular form of cirrhosis is most often due to metabolic causes.
- The macronodular form of cirrhosis is most often post-viral (hepatitis B or C).
18
Q
What are the early signs of cirrhosis?
A
- One of the earliest signs of cirrhosis is expansion of the preportal space. Atrophy of the medial segment of the left hepatic lobe in early cirrhosis causes increased fat anterior to the right main portal vein.
- Enlargement of the caudate lobe is a specific sign of cirrhosis. Specifically, a caudate to right lobe size ratio of >0.65 highly suggests cirrhosis. As previously discussed, the caudate drains directly to the IVC, not via the hepatic veins, which results in compensatory caudate hypertrophy.
- The empty gallbladder fossa sign results when hepatic parenchyma surrounding the gallbladder is replaced with periportal fat.
19
Q
What are the secondary manifestations of cirrhosis?
What are Gamna-Gandy bodies?
A
- Portal hypertension causes splenomegaly, portosystemic collaterals, and varices.
- Gallbladder wall thickening is due to hypoalbuminemia and resultant edema.
- Gamna-Gandy bodies are splenic microhemorrhages, which appear hypointense on GRE.
20
Q
What is the pathway to hepatocellular CA?
A
- In the setting of cirrhosis, hepatocellular carcinoma (HCC) is thought to develop in a sequence from regenerative nodule to dysplastic nodule to HCC. Regenerative and dysplastic nodules cannot be reliably differentiated on imaging, and high-grade dysplastic nodules cannot be reliably differentiated from low-grade HCC.
21
Q
What is a regenerative hepatic nodule?
Imaging Characteristics on MR and contrast-enhanced MR?
A
- Regenerative nodule: A regenerative nodule is completely supplied by the portal vein and is not premalignant. A regenerative nodule should not enhance in the arterial phase.
- Most regenerative nodules show low signal intensity on T2-weighted images, with variable signal intensity on T1-weighted images. Rarely, a regenerative nodule may be hyperintense on T1-weighted images due to glycogen deposition.
- On contrast-enhanced MRI, most regenerative nodules enhance to the same (or slightly less) degree as the adjacent hepatic parenchyma.
22
Q
What is a dysplastic hepatic nodule?
Contrast to a regenerative nodule.
Imaging appearance?
A
- Unlike a regenerative nodule, a dysplastic nodule is premalignant. However, most dysplastic nodules do not demonstrate arterial phase enhancement (unless high grade), since blood supply is still from the portal vein.
- Dysplastic nodules are variable in signal intensity on T1-weighted images. Most dysplastic nodules are hypointense on T2-weighted images, although high-grade dysplastic nodules may be T2 hyperintense.
- Contrast-enhanced MRI shows low-grade dysplastic nodules to be iso-enhancing relative to the liver and thus indistinguishable from regenerative nodules. High-grade dysplastic nodules may demonstrate arterial enhancement and be indistinguishable from well-differentiated hepatocellular carcinoma.
23
Q
What is a siderotic hepatic nodule?
Imaging appearance?
Malignant potential?
A
- A siderotic nodule is an iron-rich regenerative or dysplastic nodule. A siderotic nodule is hypointense on T1 and T2*-weighted images and hyperattenuating on CT.
- A siderotic nodule is rarely, if ever, malignant.
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.
25
Fibrolamellar HCC
Who does it occur in?
Prognosis compared to regular 'ol HCC?
MR imaging appearance?
* Fibrolamellar carcinoma is a subtype of HCC that occurs in young patients without cirrhosis.
* The tumor tends to be large when diagnosed but has a better prognosis than typical HCC. Unlike in HCC, AFP is not elevated.
* On MRI, fibrolamellar HCC is a large, heterogeneous mass. A fibrotic central scar is classic, which is hypointense on T1- and T2-weighted images (in contrast, focal nodular hyperplasia features a T2 hyperintense scar that enhances late). Capsular retraction may be seen in 10%.
* Unlike HCC, the fibrolamellar subtype does not have a capsule, although there may be a pseudocapsule of peripherally compressed normal hepatic tissue.
26
What is hepatic capsular retraction?
DDx of capsular retraction?
Raffi Mnemonic: CHEFPF (5 cancers and a confluent hepatic fibrosis)
Capsular retraction is a focal concavity of the normally convex external liver contour.
* Intrahepatic **C**holangiocarcinoma.
* **H**epatocellular carcinoma (capsular retraction has been reported but is uncommon).
* **E**pithelioid hemangioendothelioma.
* **F**ibrolamellar hepatocellular carcinoma (10% of cases of fibrolamellar HCC).
* *Metastatic* (most commonly breast) tumor (more commonly **P**ost-treatment)
* Confluent hepatic **F**ibrosis (wedge-shaped fibrosis seen in cirrhosis, most commonly the medial segment of the left hepatic lobe or the anterior segment of the right hepatic lobe).
27
Hepatic Metastases
Imaging appearance?
What are the classic hypervascular mets?
Calcifications can be seen in which mets? Prognostic implication?
MRI appearance?
What is pseudocirrhosis?
* 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.
28
Hepatic Lymphoma
Prevalence? More commonly seen is what and what is that associated with?
* Primary hepatic lymphoma is very rare. Lymphomatous involvement of the liver tends to be secondary to systemic disease, with associated splenomegaly and lymphadenopathy.
29
Epithelioid Hemangioendothelioma
What is it?
Imaging appearance?
* 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.
30
What are the benign liver masses?
MNEMONIC: "Benign CHALC in the liver"
Cavernous hemangioma
Focal Nodular Hyperplasia
Hepatic Adenoma
Hepatic Lipoma
Biliary Cystadenoma
31
What are the malignant hepatic masses?
* HCC
* Fibrolamellar HCC
* Hepatic lymphoma (Primary = rare)
* Epithelioid hemangioendothelioma
* Hepatic mets
32
Name the benign liver masses in order of frequency
MNEMONIC: "Benign CHALC in the liver"
* Cavernous hemangioma
* Focal Nodular Hyperplasia
* Hepatic Adenoma
* Hepatic Lipoma
* Biliary Cystadenoma
33
Focal Nodular Hyperplasia
What is it? Association?
Characteristic feature? Does it have a capsule?
Imaging appearance?
Ways to confirm?
* 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
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 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
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?
* 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
Budd-Chiari
What is it?
Causes?
Acute presentation?
Vascular findings?
Acute intraparenchymal findings?
Chronic findings?
* 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.**
37
Hepatic Veno-occulusive disease
What is it?
Who is it seen in?
Imaging appearance
Contrast this to Budd-Chiari
* Veno-occlusive disease VOD is **the destruction of post-sinusoidal venules, with patent hepatic veins.** VOD is _seen in bone marrow transplant patients_, possibly due to chemotherapy.
* Imaging findings are **nonspecific. Periportal edema, narrowing of the hepatic veins, hepatomegaly, and heterogeneous hepatic enhancement** have been reported.
* In contrast to Budd-Chiari, **the caudate lobe is not spared.**
38
Cardiac Hepatopathy
What is it? Causes?
Imaging clues?
* Cardiac hepatopathy is **passive hepatic congestion from heart failure, constrictive pericarditis, or right-sided valvular disease, which ultimately may lead to cirrhosis.**
* Imaging clues **are enlarged hepatic veins and IVC, with reflux of intravenous contrast from the right atrium into the IVC and hepatic vein**s. The liver is typically enlarged and demonstrates _mottled enhancement. Ascites is usually present._
39
Biliary Hamartomas (von Meyenburg Complexes)
What are they?
Appearance?
* Biliary hamartomas are **incidental small cystic hepatic lesions that _do not communicate with the biliary tree_**, _caused by_ _embryologic_ _failure of normal bile duct formation._
* Biliary hamartomas **tend to be smaller and more irregularly shaped than simple cysts.**
40
What are the congenital cystic liver disease?
* Biliary hamartomas (von Meyenburg complex)
* Autosomal Dominant Polycystic Liver Disease
41
Autosomal Dominant Polycystic Liver Disease
What percent of patients with ADPKD have this?
Appearance?
* **40% of patients with autosomal dominant polycystic kidney disease ADPKD have a similar disease process in the liver.** Even in severe disease, hepatic failure is rare.
* On imaging, there are **innumerable non-enhancing simple cysts throughout the liver.**
42
Overview of liver trauma
Grading
* 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.
