Liver (for PBR 2) Flashcards
Term used for transient enhancement differences seen during either arterial phase imaging or portal venous imaging on MDCT or dynamic MRI
Transient hepatic attenuation differences (THAD) or
Transient hepatic intensity differences (THID) or
Transient hepatic enhancement differences (THED)
Findings in hepatic perfusion abnormalities
- Hyperenhancement in the arterial phase
- Isoenhancement in portal venous and delayed phase
- Isoattenuation on unenhanced CT
- Isointensity on MR unenhanced T1, T2, and DWI
Evidence of hepatomegaly
Round of the inferior border of the liver
Extension of the right lobe of the liver inferior to the lower pole of the right kidney
Liver length of how many centimeters is considered enlarged?
Greater than 15.5 cm
Measures in the midclavicular line
It is an elongated inferior tip of the right lobe of the liver
Reidel lobe
Normal variant - when present the left lobe of the liver is correspondingly smaller in size
Most common abnormality by hepatic imaging
Hepatic steatosis
Two most common cause of hepatic steatosis
Alcoholic liver disease
Nonalcoholic fatty liver related to metabolic syndrome
Reliable ultrasound finding of nonalcoholic steatohepatitis (NASH)
- Liver echogenicity is greater than the renal cortex
- Loss of visualization of normal echogenic portal triads
- Poor sound penetration with loss of definition of diaphragm
All three findings must be present to make an unquivocal US diagnosis
Unenhanced CT finding of NASH
- Liver attenuation is 10 HU less than spleen attenuation
OR
Liver attenuation is less than 40 HU - Blood vessels appear brighter than the dark liver on unenhanced CT
Sign seen with fatty liver being dark on unenhanced CT and bright on US
“Flip-flop” sign
Characteristic feature of fatty deposition on all modalities
- Lack of mass effect (no bulging of the liver contour or displacement of intrahepatic vessels)
- Angulated geometric boundaries between involved and uninvolved parenchyma
Most common pattern of fatty liver
a. Diffuse fatty liver
b. Focal fatty liver
c. Focal sparing
d. Multifocal fatty liver
e. Perivascular fatty liver
f. Subcapsular fatty liver
A. Diffuse fatty liver
MC locations of focal fat
Adjacent to the:
Falciform ligament
Gallbladder fossa
Porta hepatis
MC location of fat-spared area in fatty liver
Segment 4
Pattern of fatty liver which is only seen in patients with renal failure on peritoneal dialysis and only when insulin is added to the dialysate
Subcapsular fatty liver
High concentrations of insulin in the subcapsular lier lead to fat deposition
Liver disease that is characterized pathologically by:
- Diffuse parenchymal destruction
- Fibrosis with alteration of hepatic architecture
- Innumerable regenerative nodules (RN) that replace normal liver parenchyma
Cirrhosis
Imaging findings of cirrhosis (7)
- Hepatomegaly (early)
- Atrophy or hypertrophy of hepatic segments
- Coarsening of hepatic parenchymal texture
- Nodularity of the parenchyma, often most noticeable on the liver surface
- Hypertrophy of the caudate lobe and left lobe with shrinkage of the right lobe
- Regenerating nodules
- Enlargement of the hilar periportal space (>10mm)
Creator's notes: Early enlargement Atrophy Coarsening Nodularity Caudate lobe hypertrophy Enlargement of the hilar periportal space (1 cm)
Imaging finding of cirrhosis that reflects parenchymal atrophy
Enlargement of the hilar periportal space
Extrahepatic signs of cirrhosis
- Portosystemic collaterals (as evidence of portal hypertension)
- Splenomegaly
- Ascites
Different causes of nodules in a cirrhotic liver
- Regenerative nodules
- Dysplastic nodules
- Hepatocellular carcinoma
- Confluent fibrosis
- Focal fat infiltration
- Focal fat sparing
- Metastases (rare in cirrhosis)
Most common nodules of cirrhosis
Regenerative nodules
Regular pathologic feature of cirrhosis due to attempted repair of hepatocyte injury
Difference of low-grade dysplastic nodules and high-grade dysplastic nodules
Low-grade DN
- Minimal atypia, no mitosis, not premalignant
- Supplied by portain vein
- No arterial phase enhancement
- Progresses to high-grade
High-grade DN
- Moderate atypia, occasional mitosis, secrete AFP
- Not frankly malignant
- Blood supply by hepatic artery
- Show arterial phase enhancement
Siderotic nodules may be regenerative or dysplastic but are seldom benign.
What imaging finding would consider a benign siderotic nodule on MRI?
< 20 mm
Homogeneous on all sequences (low signal)
Isoenhance compared to background cirrhotic nodules in all phases
Major criteria for diagnosis of hepatocellular carcinoma (LIRADS)
- Hyperenhancement in arterial phase definitely greater than background liver
- “Washout”
- Threshold growth
Definition of “washout” of HCC
During contrast-enhanced study:
Visual hypointensity/ hypodensity of the lesion compared with background liver on portal venous and delayed phases
Definition of Threshold Growth in HCC
Diameter increase of the mass by 5 mm or more
50% increase in diameter compared to prior examination ≤6 months
100% increase in diameter compared to prior examination at >6 months
New 10-mm lesion regardless of time interval
Ancillary sings of HCC by LI-RADS criteria
*Low yield
- Mild to moderate hyperintensity on T2WI
- Restricted diffusion on MR
- Rim of perilesional enhancement (corona enhancement)
- Mosaic architecture
- “nodule within a nodule” (HCC developing within a DN)
- Intralesional fat
- Intralesional iron sparing
- Intralesional fat sparing
- Diameter increase less than that defined as threshold growth
LI-RADS criteria favoring benign nodule
*Low yield
5 and 6 - indicates no growth
- Homogeneous marked hyperintensity on T2
- Homogeneous marked hypointensity on T2 or T2*
- Intralesional vessels without distortion
- Nodule enhancement parallels blood pool
- Decrease diameter
- Stable diameter for > 2 years
*Creator's note simplify: #1 is a cyst #2 is probably a siderotic nodule #3 is a focal fat # 4 is probably a hemangioma
This refers to a bulging hypertrophied expanse of the liver surrounded by atrophic fibrotic liver parenchyma
Hypertrophic pseudomass
Imaging features that favor pseudomass over tumor include preservation of hepatic architectures and presence of undistorted vessels traversing the lesion
This refers to mass-like areas of fibrosis found in livers with advance cirrhosis
Confluent fibrosis
This is a pathologic increase in portal venous pressure that results in the formation of portosystemic collateral vessels that divert blood flow away from the liver and into the systemic circulation
Portal hypertension
Signs of portal hypertension
- Visualization of portosystemic collaterals
- Increased portal vein diameter (>13 mm)
- Increased superior mesenteric and splenic vein diameters (>10 mm)
- Portal vein thrombosis
- Calcifications in the portal and mesenteric veins
- Splenomegaly due to vascular congestion
- Ascites
- Reversal of flow in any portion of the portal venous system (hepatofugal flow)
What are the portosystemic collaterals affected in portal hypertension?
Coronary Gastroesophageal Splenorenal Paraumbilical Hemorrhoidal Retroperitoneal
Causes of portal vein thrombosis
Complication of cirrhosis
Portal vein invasion or compression by tumor
Hypercoagulable states
Inflammation (pancreatitis)
*Creator;s notes:
Cirrhosis, neoplasm, inflammation, blood problem
Characteristic of a malignant thrombus in the portal vein
It is contiguous with and extends from the primary tumor
Portal vein is expanded, filled with tumor in vein of the same imaging characteristics, including enhancement, as the primary tumor
Characteristic of a bland thrombus in the portal vein
It fills a portal vein of near-normal size
On MR bland thrombus is of low signal because of its hemosiderin content
Bland thrombus does not enhance
The thrombus is hyperintense on T1WI when acute and isointense when chronic
This develops when small collateral veins adjacent to the portal vein expand and replace the obliterated portal vein
Cavernous transformation of the portal vein
These collateral veins appear as a tangle of small vessels surrounding the thrombosed portal vein
This refers 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
Coagulation disorder
Membranous webs obstructing hepatic veins or IVC
Malignant tumor invasion
CE CT scan finding of Budd-Chiari syndrome
Early images - central liver enhancement prominently while the peripheral liver enhances weakly
Delayed images - the periphery of the liver is enhanced, while the contrast has washed out of the central liver
What is the “comma” sign?
It is a comma-shaped intrahepatic collateral vessels that may be seen on CT or MR in Budd-Chiari syndrome
Diffuse liver disease that is a common complication of congestive heart failure and constrictive pericarditis
Passive hepatic congestion
Imaging finding of passive hepatic congestion
Distention of hepatic veins and IVC
Reflux of intravenous contrast into hepatic veins and IVC
Increased pulsatility of the portal vein
Inhomogeneous contrast enhancement of the liver
Note: More of vessel findings
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
Imaging modality of choice for hemochromatosis
MRI
Susceptibility effect of iron, best appreciated on T2* images, causes loss of signal in tissues with excessive iron accumulation
What are the different patterns of hemochromatosis
Parenchymal pattern
Reticuloendothelial pattern
Renal pattern
Pattern of iron deposition seen with increased iron absorption of primary hemochromatosis and with secondary hemochromatosis caused by chronic anemias (thalessemia, congenital dyserythropoietic anemias, sideroblastic anemia)
Parenchymal pattern
This pattern shows decreased MR signal in the liver, pancreas, and heart
The spleen and bone marrow are spared
Pattern of iron deposition is seen in secondary hemochromatosis with iron overload caused by blood transfusions
Reticuloendothelial pattern
The excess iron accumulation occurs in reticuloendothelial cells in the liver, spleen, and bone marrow
MR shows diffuse decreased signal in all three areas
Pattern of iron deposition is rare but dramatic, occurring only in patients with intravascular hemolysis caused by mechanical heart valves
Renal pattern
Excess iron deposition occurs in the proximal convoluted tubules of the renal cortex causing loss of cortical signal on T1WI and T2WI, reversing the normal corticomedullary differentiation pattern
Attenuation value plain CT can detect when there is excess iron in the liver
72 HU
Other causes that can increased hepatic parenchymal attenuation (such as hemochromatosis)
Wilson diseases (copper deposition) Amiodarone treatment (iodine deposition) Colloidal gold
This may be an ominous imaging sign associated with bowel ischemia in adults and necrotizing entrocolilis in infants
Gas in the portal venous system
Less ominous, causes include recent colonoscopy, enema administration, gastrostomy tube placement, abdominal trauma, inflammatory bowel disease, perforated gastric ulcer, necrotizing pancreatitis, diverticulitis, and abdominal abscess
What are the most common hypervascular lesions in the normal liver parenchyma?
Hemangioma
Hepatic adenoma
Hypervascular metastases
What are the most common hypervascular lesions in the fibrotic liver and cirrhosis?
Hepatocellular carcinoma
Dysplastic nodules
Most common malignant mass in the liver
Metastases
Metastases in the liver most commonly originates where?
GI tract
Breast
Lung
Characteristic imaging finding of liver metastases on postcontrast CT and MR images
Band-like peripheral enhancement creating a “target lesion”
This mass is second only to metastases as a common cause of a liver mass
It is the most common benign liver neoplasm
Cavernous hemangioma
Consist of large, thin-walled, blood-filled vascular spaces separated by fibrous septa
Characteristic pattern of enhancement of hepatic cavernous hemangioma
Discontinuous nodular enhancement from the periphery of the lesion that gradually becomes isodense or hyperdense compared to the liver parenchyma
20 to 30 minutes following injection
Most common primary malignancy of the liver
Hepatocellular carcinoma
Three major patterns of large HCC (>2 cm)
Solitary massive
Multinodular
Diffuse infiltrative
Pattern of large HCC that has a single large mass with or without satellite nodules
Solitary massive HCC
Pattern of large HCC that appears as multiple discrete nodules involving larger area of the liver
Multinodular HCC
Pattern of large HCC that has innumerable tiny distinct nodules throughout the liver distorting the parenchyma but not causing a discrete mass
Diffuse HCC
Imaging characteristic of large HCC:
Hallmark finding on CE MDCT
Heterogeneous enhancement during arterial phase with RAPID WASHOUT of contrast during portal venous and delayed phase
Imaging characteristic of large HCC:
Related to portal vein compression or occlusion by the tumor with compensatory increase in hepatic arterial supply appearing wedge shaped and confined to the segment of the liver with compromised portal venous supply
Peritumoral arterial phase enhancment
Imaging characteristic of large HCC:
A pattern of confluent small nodules separated by thin septations and necrotic areas
Mosaic pattern
Best seen in T2
*Creators notes: Seems like a typical heterogeneous mass
Imaging characteristic of large HCC:
This is seen on CT, T1WI, and T2WI as a hypointense rind up to 4 mm thick consisting of an inner fibrous layer and an outer tissue layer of compressed bile ducts and blood vessels
Distinct tumor capsule
Imaging characteristic of large HCC:
Tumor projection through the capsule
Extracapsular extension of tumor with satellite lesions
Imaging characteristic of large HCC:
Portal vein or hepatic vein involvement seen as enhancing tumor and lack of flow within the blood vessels
Vascular invasion
Imaging characteristic of large HCC:
Occluded veins have expanded lumens, ill-defined walls
What DWI finding is seen?
Restricted diffusion
Imaging characteristic of large HCC:
What is the pattern of calcifications seen?
Punctate, stippled or rim-like
10% of caes
Imaging characteristic of large HCC:
Fatty metamorphosis within the tumor - This is best seen in what MR sequence?
Chemical shift MR
Imaging characteristic of large HCC:
This is seen as an early or prolonged enhancement of the portal vein or as as wedge-shaped area of parenchymal enhancement adjacent to the tumor
Arterioportal shunting
Imaging characteristic of large HCC:
Finding that causes the tumor to appear hyperdense on CT and T1 on MR
Excessive copper accumulation
*Creator’s notes: Bleed/ hemorrhage could also be the same
This refers to a benign solid mass consisting of abnormally arranged hepatocytes, bile ducts and Kupffer cells.
It is the second most common benign liver tumor
Solitary, less than 5 cm, hypervascular with central fibrous scar containing thick-walled vessels
Focal nodular hyperplasia
US finding of focal nodular hyperplasia
Very subtle mass, blending with surrounding parenchyma because the lesion consists of the same elements
A slight bulge in the liver contour or subtle alteration of parenchymal echogenicity may be the only clues
Color Doppler may shows central vascularity
CT scan finding of FNH
Unenhanced images: Slightly hypoattenuating lesions
Postcontrast - Intense homogeneous enhancement in arterial phase sometimes with visualization of large feeding vessels
Contrast washed early on portal venous phase
Lesion is isointense and commonly near-invisible on delayed-phase images
Key finding of FNH on MR
A key to diagnosis is to recognize that the lesion is near isointense to liver parenchyma on all precontrast MR sequences
The central scar, if present, is hypointense on T1 and hyperintense on T2
Hepatocyte-specific MR contrast agents show uptake within FNH appearing iso to hyperintense to parenchyma
Images are obtained how many hours after contrast administration?
1 to 3 hours
Benign tumor that carry a risk of life-threatening hemorrhage and potential for malignant degeneration
Found most commonly in women on long-term oral contraceptives
Additional risk factors: androgenic steroid intake and glycogen storage disease
Hepatic adenomas
US finding of hepatic adenoma
Well-circumscribed tumor that is usually heterogeneous depending on presence of fat, necrosis, hemorrhage, or rarely calcification
High fat content or acute intratumoral hemorrhage makes the lesion appear hyperechoic
Contrast -enhanced US shows prominent arterial phase enhancement
This disease is characterized by the presence of multple adenomas (>10) in an other wise normal liver in patients
Usually young women without risk factors for hepatic adenomas
Liver adenomatosis
Considered as a sperate clinical entity
A hepatocellular malignancy that typically present as large liver mass in an adolescent or young adult (ave age 23)
No risk factors for HCC
No AFP elevation
No cirrhosis or chronic liver disease
Surrounding liver is normal
Fibrolamellar carcinoma
Characteristic appearance of fibrolamellar carcinoma
Large, lobulated hepatic mass with central scar and calcifications
Creator’s notes: Similar to FNH
Finding of hepatic lymphoma
Diffusely infiltrative and undetectable by imaging methods
Poorly defined hypodense mass
Hypodense T1, variabal intensity T2
Lesion enhances poorly or not at all
MR finding of hepatic hematomas
Subacute - bright on T1WI (effect of methemoglobin)
Chronic hematomas - dark on T2WI (effect of hemosiderin)
Rim enhancement
Also known as Osler-Weber-Rendu syndrome
Autosomal dominant disorder of fibrovascular dysplasia resulting in multiple telangiectasias and arteriovenous malformations
Hereditary hemorrhagic telangiectasia
Clinical findings of hereditary hemorrhagic telangiectasia
Epistaxis
Intestinal bleeding
If AV fistulas in the liver: Pain, jaundice, portal hypertension, and high-output cardiac failure
In hereditary hemorrhagic telangiectasis
Term used for nodular transformation of the liver parenchyma without fibrosis
Pseudocirrhosis
In hereditary hemorrhagic telangiectasia:
What is the appearance of a telangiectasia
Hypervascular rounded masses resembling an asterisk
Usually a few millimeters in size
They may become confluent to form large vascular masses
This is a rare disorder associated with chronic wasting from cancer or tuberculosis, or associated with use of oral contraceptives or anabolic steroids
Peliosis hepatis
Imaging finding of peliosis hepatis
Cystic dilatation of the hepatic sinusoids and multiple small (1 to 3 mm) blood-filled spaces characterize the lesions
MR shows variable signal due to hemorrhage on T1
Hyperintense on T2
Imaging findings of benign hepatic cyst
US - anechoic with thin walls and may have fine thin septa
Posterior acoustic enhancement confirms their fluid nature
Internal debris - if they have internal hemorrhage or previous infection
CT - low internal attenuation near water, thin walls, and thin septa w/o enhancing solid components
MR - homogeneous low signal on T1W and homogeneous low signal on T2W
Cyst do not enhance
*Creator’s notes:
AS ALL CYST SHOULD BE
It is in the spectrum of autosomal dominant polycystic disease and occasionally occurs in the absence of polycystic kidneys
Polycystic liver disease
Number and size of cysts increase over time and may eventually result in massive hepatomegaly and affect hepatic function
Cysts are prone to hemorrhage and infection
Also known as von Meyenburg complexes
These are small benign neoplasms consisting of dilated cystic branching bile ducts embedded within fibrous tissue
Bile duct hamartomas
Bile duct hamartomas are best recognized on what modality?
MR
They appear as multiple tiny (<1 cm) cystic lesions throughout the liver
They are low signal on T1WI, high signal on T2WI, and show peripheral enhancement postcontrast
CT shows widespread tiny cystic lesions
The cysts are usually too small to be seen with US
Rare cystic neoplasm of the biliary epithelium
Tumors typically contain mucin and appear as large (up to 35 cm) multiloculated cystic mass
Biliary cystadenoma/ cystadenocarcinoma
Findings seen on biliary cystadenoma/ cystadenocarcinomas
Cyst adenomas - fine septations
Cystadenocarcinomas - may have mural nodules and papillary projections
Presence of thick, coarse calcifications favors:
a. Biliary cystadenoma
b. Biliary cystadenocarcinoma
b. Biliary cystadenocarcinoma
Usual pathogens that cause pyogenic abscess
E. coli
S. aureus
Streptococcus
Anaerobic bacteria
Imaging finding of pyogenic abscess
Echongenic/ appear solid on US
Peripheral rim enhances with contrast
Gas is present within the lesion
Amebic abscess is usually caused by what pathogen?
Entamoeba histolytica
Patient often resides or has travelled to endemic areas (India, Africa, the Far East, Central and South America)
“anchovy paste” material is seen on:
a. Pyogenic abscess
b. Amebic abscess
c. Hydatid cyst
b. Amebic abscess
Pathogen of hydatid cyst
Echinococcus granulosis or E. multilocularis tapeworn
Finding of hydatid cyst
Single or multiple cystic masses usually have well-defined walls that commonly calcify (50%)
The cyst wall and septations usually enhance
Daughter cysts may be visualized within the parent cyst
