Gastrointestinal: Liver/Biliary Flashcards
1
Q
What is the hepatic bare area?
A
An area of the liver surface abutting the diaphragm that is not covered by visceral peritoneum
Note: An injury to the bare area can result in a retroperitoneal bleed.
2
Q
What parts of the liver are not covered by visceral peritoneum?
A
- Bare area
- Porta hepatis
- Gallbladder fossa
3
Q
What separates hepatic segments 7 and 8?
A
The right hepatic vein
4
Q
What separates hepatic segments 5 and 6?
A
The right hepatic vein
5
Q
What separates hepatic segments 4a and 8?
A
The middle hepatic vein
6
Q
What separates hepatic segments 4b and 5?
A
The middle hepatic vein
7
Q
What separates hepatic segments 2 and 4a?
A
The left hepatic vein/fissure for the ligamentum teres (falciform)
8
Q
What separates hepatic segments 3 and 4b?
A
The left hepatic vein/fissure for the ligamentum teres (falciform)
9
Q
What separates hepatic segments 2, 4a, 7, and 8 from segments 3, 4b, 5, and 6?
A
The portal vein separates the upper segments from the lower segments
10
Q
Why is hepatic segment 1 unique?
A
It is the caudate lobe and drains directly into the IVC (rather than into a hepatic vein)
Note: It also received blood supply from both the left and right portal veins.
11
Q
Cantlie’s line
A
Runs from the IVC to the middle of the gallbladder fossa (divides the liver into functional left and functional right hepatic lobes)
12
Q
What separates the liver into functional left and right hepatic lobes?
A
Cantlie’s line (running from the IVC to the middle of the gallbladder fossa)
13
Q
Why is the caudate lobe usually spared in Budd Chiari?
A
It receives blood from both the right and left portal veins
14
Q
Name the hepatic segments
A
15
Q
Why does the right hepatic lobe shrink and left hepatic lobe grow in cirrhosis?
A
The intrahepatic course of the right portal vein is longer and more susceptible to fibrosis, leading to right lobe atrophy
16
Q
What is the most common variant of the hepatic blood vessels?
A
Replaced right hepatic artery (originating from the SMA)
17
Q
What is the most common biliary variant?
A
Right posterior segmental duct draining to the left hepatic duct
18
Q
What are the normal MRI characteristics of the liver, spleen, and pancreas?
A
- Liver (T1 bright and T2 dark)
- Spleen (think water: T1 dark and T2 bright)
- Pancreas (T1 brightest and T2 dark)
Note: The pancreas is the brightest organ on T1 (think about all the pancreatic enzymes; the liver has enzymes also but not as many and isn’t as T1 bright).
19
Q
What fetal structure allows blood to bypass the liver in utero?
A
Ductus venosus
Note: This becomes the ligamentum venosum.
20
Q
How does blood get from the placenta to the heart in utero?
A
Placenta -> umbilical vein -> ductus venosus -> IVC -> right atrium
21
Q
A
Splenic vein
22
Q
A
SMA
23
Q
A
Pancreatic head
24
Q
A
Left renal vein
25
Aorta
26
IVC
27
How can you tell whether the pancreas is more hypoechoic that it should be?
If it is hypoechoic relative to the liver parenchyma it may be edematous
Note: The pancreas should be more echogenic than the liver.
28
Common bile duct
Note: "Mickey Mouse" sign.
29
Hepatic artery
Note: "Mickey Mouse" sign.
30
Portal vein
Note: "Mickey Mouse" sign.
31
A?
Left renal vein
32
C?
Pancreas
33
E?
Splenic vein
34
F?
SMA
35
Falciform ligament (ligamentum teres)
36
Common bile duct
37
Right hepatic artery
38
Portal vein
39
Why do hepatic abscesses almost always involve the right hepatic lobe?
The right portal vein has a longer intrahepatic course than the left (most pathogens spread through the portal vein to cause hepatic abscesses)
40
What common measurement is most specific for hepatic cirrhosis?
Caudate to right hepatic lobe ratio
Note: C/RL ratio > 0.75 is 99% specific for cirrhosis).
41
Which parts of the liver atrophy/hypertrophy in cirrhosis?
- Right lobe atrophies
- Left lobe and caudate hypertrophy
42
What is the most common cause of hepatic cirrhosis?
- Schistosomiasis (globally)
- EtOH cirrhosis (in US)
43
What are the common causes of portal hypertension?
- Pre-hepatic (portal vein thrombosis, tumor compression)
- Hepatic (cirrhosis, schistosomiasis)
- Post-hepatic (Budd-Chiari)
44
As fibrosis causes portal hypertension, what happens to velocities in the hepatic artery?
Velocities increase in the hepatic artery (to compensate for the reduced blood supply from the portal vein)
45
Transient hepatic attenuation differences
Areas of hepatic parenchymal hyperenhancement that are only visible during the arterial phase and then go away by the equilibrium/delayed phases
Note: This is due to the dual blood supply to the liver. Those areas of hyperenhancement are receiving a greater percentage of their blood supply from the hepatic artery rather than the portal vein.
46
What causes the regions of hyperenhancement in transient hepatic attenuation differences?
The hyperenhancing regions aren't getting enough portal venous flow so respond by increasing hepatic arterial flow (leading to hyperenhancement on arterial phases)
47
What are the most common causes of transient hepatic attenuation differences?
- Cirrhosis (usually subcapsular hyperenhancement)
- Portal vein branch thrombosis (usually larger wedge-shaped hyperenhancement)
- Mass (mass effect compressing the veins and/or tumor upregulating arterial flow)
- Abscess/infection (hyperemia of the arteries and/or edema compressing veins)
48
Why does there tend to be peripheral hyperenhancement and relative central hypoenhancement in cirrhotic livers?
The fibrosis that occurs in cirrhosis progresses from the periphery inward, reduced portal veinous flow to the periphery causes upregulation of hepatic arterial flow in the periphery (leading to relative hyperenhancement)
Note: This is the "central-peripheral" phenomenon.
49
What is the normal direction of flow in the portal veinous system?
Hepatopetal (towards the liver)
Note: Hepatofugal (Fugal means Flee away from the liver) flow is abnormal.
50
Why does flow sometimes reverse in the portal veins in cirrhosis rather than just clot off?
When pressures get too high in the liver, the portal veinous system can decompress through the creation of collaterals. The hepatic artery can't do this and instead decompresses by creating shunts to the portal veinous system. The shunting of blood from the hepatic artery to the portal vein is what causes portal veinous flow reversal.
51
Portal hypertensive colopathy
Edematous colon due to backup of pressure from the portal veinous system. This is usually worse on the right-sided colon because the left is more easily decompressed through the creation of collaterals (e.g. splenorenal shunt, short gastrics, esophageal varices, etc.)
Note: Portal hypertensive colopathy can resolve after a liver transplant.
52
Portal hypertensive gastropathy
Thickened gastric wall due to backup of pressure from the portal veinous system that can also cause GI bleeding
Note: This can happen even in the absence of gastric varices.
53
How do regenerative liver nodules appear on MRI as they progress to dysplastic nodules and HCC?
Regenerative nodules (T2 dark)
Dysplastic nodules (T2 isointense to dark)
HCC (T2 bright, enhancing)
Note: The "nodule within a nodule" (where there is a T2 bright spot within a T2 dark nodule) is concerning for transformation to HCC.
54
Why does hepatocellular carcinoma usually appear dark on delayed phase imaging with biliary contrast agents (e.g. Eovist)?
As hepatocytes become cancerous they usually lose the OATP bile uptake transporter which prevents those cells from taking up biliary contrast agents.
Note: A notable exception is well differentiated HCC, which maintains its OATP transporters, which is why this subtype actually appears bright on delayed imaging with biliary contrast agents.
55
Why are all lesions considered more suspicious in hepatic cirrhosis?
- Cirrhosis is a significant risk factor for HCC
- The squeezing process in cirrhosis that leads to portal hypertension also squeezes out most benign liver lesions (e.g. cysts and hemangiomas)
56
At what timepoinnt does the hepatic arterial phase occur?
25-30 seconds after injection
57
At what timepoints does the portal venous phase occur?
70 seconds after injection
58
What is the liver window?
Center: 100
Width: 200
59
How does gadolinium work as a contrast agent?
Gadolinium is paramagnetic, which causes T1 shortening (appearing bright on T1 images)
Note: Gadolinium is highly toxic and so is bound to a chelation agent to prevent it from killing the pt.
60
What are the major types of MRI contrast agents used in liver imaging?
- Extracellular (blood flow dependent: work just like iodine contrast agents in CT)
- Hepatocyte specific (taken up by hepatocytes and excreted into the bile)
61
What is the classic example of an extracellular MRI contrast agent?
Gd-DTPA (Magnavist)
62
What is the classic example of a hepatocyte specific MRI contrast agent?
Gd-EOB-DTPA (Eovist)
63
What are the main indications for using Gd-EOB-DTPA (Eovist)?
- Proving an FNH is an FNH
- Looking for bile leaks
- Looking for new metastases (once a baseline MRI has characterized any benign cysts/lesions present)
64
Is eovist a pure hepatocyte specific agent?
No, it also acts like a non-specific extracellular agent early on (55% ends up excreted into the bile)
65
What is the most common benign liver neoplasm?
Hemangioma (followed by FNH)
66
Are hemangiomas more common in men or women?
Women (5:1)
Note: They may also enlarge in pregnancy.
67
Classic ultrasound appearance of a hepatic hemangioma
- Hyperechoic (unless in a fatty liver)
- No internal flow on color Doppler (may have peripheral vascularity)
- Posterior acoustic enhancement is common
68
Classic CT/MRI appearance of a hepatic hemangioma
- Discontinuous peripheral nodular enhancement
- Isodense/isointense to aorta on all phases/sequences
69
If you were to biopsy a hepatic hemangioma, what type of biopsy would you need?
Core biopsy
Note: FNA will only show blood, not enough tissue.
70
Hepatic lesion that changes appearance during the course of a single ultrasound exam...
Think hemangioma (no other hepatic lesion does this)
71
What imaging study can be used to diagnose hepatic hemangiomas larger than 2 cm?
Tc-99m labeled RBCs
72
What is a giant hepatic hemangioma?
A hepatic hemangioma over 5 cm
73
Kasabach-Merritt syndrome
Consumptive coagulopathy due to a growing vascular tumor (e.g. giant hepatic hemangioma)
Note: This increases bleeding risk.
74
Flash filling hemangioma
Smaller (<2 cm) hemangiomas that homogeneously enhance "flash-filling" on arterial phase, but still remain isodense to blood pool on all phases
Note: They do not washout on delayed images the way HCC would.
75
If you were to biopsy focal nodular hyperplasia, where should you biopsy?
Through the central scar (if present)
Note: If you don't get the scar, the biopsy will just say normal hepatocytes.
76
Which hepatic lesion is classically seen in females on oral contraceptives?
Hepatic adenoma
Note: These are also often seen in men on anabolic steroids.
77
Focal nodular hyperplasia can develop after treatment with what chemotherapy agent?
Oxaliplatin
78
Classic appearance of focal nodular hyperplasia on MRI
Stealth lesion (isointense to liver on both T1 and T2)
Note: If there is a central scar, you may see that (which should show delayed enhancement).
79
How does FNH enhance on CT?
Homogenous enhancement on arterial phase (delayed enhancement of a central scar, if present)
Note: FNH should be isodense to the IVC, hemangiomas are isodense to the aorta.
80
What nuclear imaging study can be used to differentiate FNH from malignancy?
Sulfur colloid (FNH should have normal or increased uptake, since it contains normal liver cellularity)
Note: FNH also shows up on HIDA scintigraphy due to the normal liver cellularity.
81
Multiple hepatic adenomas...
- Glycogen storage disease (von Gierke)
- Liver adenomatosis
Note: Usually hepatic adenomas are solitary.
82
Why are hepatic adenomas sometimes surgically excised?
- Propensity to bleed
- Risk of degeneration into HCC
83
What is the most common location for a hepatic adenoma?
Right liver lobe (75%)
84
First line treatment for hepatic adenoma
Stop oral contraceptives (if taking) and repeat imaging
Note: Many hepatic adenomas regress after OCPs are stopped.
85
Which adenomas are often surgically resected?
Persistent adenomas that are >5 cm
86
What are the major subtypes of hepatic adenoma?
- Inflammatory (most common)
- HNF-1 alpha mutated
- Beta-catenin mutated
87
Which hepatic adenoma subtype has the highest rate of bleeding?
Inflammatory (also the most common subtype)
88
Which hepatic adenoma subtype is associated with having multiple hepatic adenomas?
HNF-1 alpha mutated
89
Which hepatic adenoma subtype is associated with anabolic steroids, glycogen storage disease, and familial adenomatous polyposis?
Beta catenin mutated
90
Is AFP elevated in HCC?
Almost always (80-95%)
91
Hepatic mass infiltrating the hepatic vein...
Think HCC
Note: HCC also invades the portal vein, but invasion of the hepatic vein is more specific.
92
Major risk factors for HCC
- Cirrhosis
- Hep B/C
- Hemochromatosis
- Glycogen storage disease
- Alpha 1 antitrypsin
93
What is a standard doubling time for HCC?
150-300 days
Note: There are 3 described growth patterns for HCC: slow (>300 days), medium (150-300 days), and fast (<150 days).
94
What is an appropriate follow up time for repeat imaging if you are not sure whether a lesion is HCC (despite exhausting all available imaging)?
3-4.5 months
95
What HCC subtype is more common in younger pts without cirrhosis and usually has a normal AFP?
Fibrolamellar HCC
Note: These often have a central scar and can be mistaken for FNH.
96
Does HCC tend to calcify?
Rarely
Note: The fibrolamellar HCC subtype does sometimes calcify (more often than classic HCC).
97
Which HCC subtype classically has a central scar?
Fibrolamellar subtype
Note: Don't confuse with FNH.
98
How can you differentiate FNH from fibrolamellar HCC?
Both usually have central scars, but the central scar in fibrolamellar HCC does NOT enhance and is usually T2 dark
Note: The central scar in FNH does enhance and is T2 bright.
99
Hepatic mass with a non enhancing, T2 dark central scar...
Think fibrolamellar HCC
100
Hepatic mass with an enhancing, T2 bright central scar...
Think FNH
101
Which HCC subtype is gallium avid on nuclear imaging?
Fibrolamellar HCC
102
Which HCC subtype is usually associated with a normal AFP level?
Fibrolamellar HCC
103
How can nuclear imaging studies help differentiate FNH from fibrolamellar HCC?
If the mass is sulfur colloid avid, it is likely FNH
If the mass is gallium avid, it is likely Fibrolamellar HCC
104
Risk factors for cholangiocarcinoma
- Primary sclerosis cholangitis (main risk factor in the western world)
- Recurrent pyogenic cholangitis (main risk factor in the eastern world)
- Caroli disease
- Hepatitis
- HIV
- History of cholangitis
- Liver worms (Clonorchis)
105
Why might a history of ulcerative colitis make you worry more about cholangiocarcinoma?
Ulcerative colitis is highly associated with primary sclerosis cholangitis (the major risk factor for cholangiocarcinoma in the western world)
106
Classic imaging appearance of cholangiocarcinoma
- Mass with delayed enhancement (due to fibrosis)
- Hepatic capsular retraction (due to fibrosis)
- Peripheral bile duct dilatation (due to fibrosis)
Note: Think of cholangiocarcinoma as a fibrotic scar tissue mass.
107
Classic clinical presentation of cholangiocarcinoma
Painless jaundice
108
Large hepatic mass that encases (not invades) the portal vein...
Think cholangiocarcinoma
Note: HCC is more likely to invade the portal vein.
109
Does cholangiocarcinoma have a tumor capsule?
No
110
Klatskin tumor
Cholangiocarcinoma that occurs at the bifurcation of the left and right hepatic ducts
Note: These can cause biliary obstruction even when very small.
111
What staging system is used to classify Klatskin tumors?
Bismuth-Corlette system
112
What does atrophy of a hepatic lobe suggest in the setting of cholangiocarcioma?
Biliary and/or vascular involvement of that lobe
Note: Imaging often underestimates disease burden. Look for these secondary signs of involvement.
113
What factors make a klatskin tumor less likely to be resectable?
- Proximal extent (extending deeper into the peripheral liver)
- Bilateral involvement (involving both the left and right hepatic ducts)
114
Elevated CEA and CA 19-9...
Think cholagniocarcinoma
115
Elevated CA 19-9 with normal CEA...
Think pancreatic cancer
116
Elevated CEA with normal CA 19-9...
Think colon cancer
117
Risk factor for hepatic angiosarcoma
- Arsenic exposure
- Polyvinyl chloride exposure
- Radiation
- Thorotrast exposure (history of time spent in Nazi Germany)
- Hemochromatosis
- NF1
118
What is the most common hepatic sarcoma?
Hepatic angiosarcoma (still extremely rare)
119
Imaging appearance of hepatic angiosarcoma
- Usually multifocal
- Propensity to bleed
120
Differential for a hepatic mass with hemorrhage
- Hepatic adenoma
- Hepatocellular carcinoma
- Hepatic angiosarcoma (rare)
121
Multilocular cystic lesion in the liver, possible biliary cystadenoma
Note: No reliable method to distinguish from biliary cystadenocarcinoma.
122
Multilocular cyst in the liver with a nodular enhancing solid component...
Think biliary cystadenocarcinoma
Note: An enhancing nodular solid component is the best way to distinguish this from a regular biliary cystadenoma.
123
Most common primary cancer to result in liver metastases
Colon cancer
124
Most common malignant mass in the liver
Metastasis (20-40x more common than a primary liver cancer)
125
What primaries are most common if you see calcified liver metastases?
Mucinous neoplasms:
- Colon
- Ovary
- Pancreas
126
What primaries are likely if you see hyperechoic liver metastases?
Think hypervacsular metastases:
- Renal
- Melanoma
- Carcinoid
- Choriocarcinoma
- Thyroid
- Islet cell
127
What primaries are likely if you see hypoechoic liver metastases?
Think hypovascular metastases:
- Colon
- Lung
- Pancreas
Note: Liver mets are more commonly hypoechoic than hyperechoic.
128
Multiple hyperechoic hepatic masses with hypoechoic halos...
Think hepatic metastases (with halos of fat-spared liver)
129
Hypotenuse liver masses with a continuous rim of enhancement...
Think liver metastases
Note: Hematic hemangiomas usually have a discontinuous rim on enhancement.
130
Why might hepatic metastases appear hyperdense on CT?
Hepatic metastases are usually hypodense, but can appear hyperdense if there is a background of fatty liver (hypodense liver parenchyma)
131
Pt has breast cancer and multiple hepatic hypodensities that are too small to further characterize...
Hepatic lesions that are too small to further characterize are still likely to be benign (90-95%) even in the setting of known malignancy (without definite hepatic mets)
132
Can lymphoma involve the liver?
Yes, Hodgkins lymphoma involves the liver 60% of the time and non-Hodgkins involves the liver 50% of the time
133
Imaging appearance of hepatic Kaposi sarcoma
AIDS pt with diffuse periportal hypoechoic infiltration (appears similar to biliary duct dilatation)
134
What ultrasound features suggest that a hepatic cyst might be something else (e.g. hydatid cyst)?
- Cyst larger than 2 cm
- Presence of membranes
- Abundant sediment in the cyst
135
What ultrasound features suggest that what looks like a hepatic hemangioma might be something else?
Internal flow on color Doppler
Note: Hemangiomas can have peripheral flow, but should now have internal flow.
136
Liver ultrasound
Think FNH
Note: This is the "spoke wheel" appearance of vascularity on Doppler.
137
Ultrasound features of FNH
- Difficult to see (isoechoic to liver)
- Look for bulging of the liver
- Central scar
- Spoke wheel appearance on doppler (vessels radiating out from a central point)
138
Classic ultrasound appearance of hepatic adenomas
- Round mass with well-defined borders and a hypoechoic halo of fatty sparing
- Peripheral flow on color Doppler (sometimes)
Note: Ultrasound appearance is highly variable due to the possibility of hemorrhage, fat, calcification, necrosis, etc.
139
Classic ultrasound appearance of HCC
- Cirrhotic liver contour (huge hint)
- Lots of internal and/or peripheral vascularity (not in the spoke wheel configuration seen in FNH)
- Thin peripheral hypoechoic halo (due to a fibrous capsule)
140
How does FNH appear on delayed eovist MRI sequence?
Bright
Note: HCC (other than well-differentiated HCC) will appear dark on this sequence due to loss of functional contrast uptake.
141
Which benign hepatic lesion classically contains microscopic fat (signal drop on in/out of phase imaging)
Hepatic adenoma
Note: Hepatic angiomyolipomas also usually contain microscopic fat, but usually have macroscopic fat also.
142
Hepatic mass with macroscopic fat on CT...
Think hepatic angiomyolipoma
Note: 50% of hepatic angiomyolipomas do not have macroscopic fat.
143
Hepatic angiomyolipomas are associated with...
Tuberous sclerosis
Note: This association isn't as strong as it is for renal angiomyolipomas.
144
Follow up for an incidental liver mass that homogeneously enhances on arterial or portal phase imaging
MRI (if >1.5 cm OR high risk pt: alcohol use, sex work, IV drug user, known cancer)
No follow up (if <1.5 cm AND low risk pt)
145
Which cystic kidney disease is also associated with hepatic cysts?
Autosomal dominant polycystic kidney disease
Note: Autosomal recessive polycystic kidney disease is more often associated with hepatic fibrosis.
146
Multiple AVMs in the liver and lungs with cirrhosis and a massively dilated hepatic artery...
Think hereditary hemorrhagic telangiectasia (Osler-Weber-Rendu)
147
Think hereditary hemorrhagic telangiectasia (Osler-Weber-Rendu)
Note: Multiple liver and lung AVMs.
148
Multiple hepatic AVMs in a pt with a brain abscess...
Think hereditary hemorrhagic telangiectasia (Osler-Weber-Rendu)
Note: The pulmonary AVMs also seen in this condition predispose to brain abscesses.
149
Think liver edema (e.g. hepatitis)
Note: This is the "starry sky" appearance due to prominence of the periportal fat against a background of hypoechoic liver.
150
Hepatic cyst containing gas...
Hepatic abscess
151
Classic cause of a single hepatic pyogenic abscess
Klebsiella
152
Classic cause of multiple hepatic pyogenic abscesses
E. coli
153
Classic ultrasound appearance of viral hepatitis
Starry sky (hypoechoic liver edema with bright spots of periportal fat)
154
Hepatic abscess
Note: This is the "double target" sign with central pus, peripheral hyperdense capsule, and surrounding hypodense edema.
155
What is the most common location for a hydatid cyst?
Liver (76%)
Note: Lung is the second most common (15%) followed by spleen (5%).
156
Hydatid cyst (Echinococcus infection)
Note: This is the "water Lilly" sign.
157
Hydatid cyst (Echinococcus infection)
Note: Daughter cysts within the cyst.
158
Treatment of hydatid cyst
Surgical resection (usually)
159
Treatment for amebic abscess in the left hepatic lobe
Emergent drainage (these can rupture into the pericardium)
160
Hepatic Schistosomiasis infection
Note: This is the "tortoise shell" appearance of the liver.
161
RUQ pain with history of pelvic inflammatory disease...
Fitz-Hugh-Curtis syndrome
Note: PID and right upper quadrant pain with enhancement of the liver capsule.
162
Focal fatty liver is most common in what locations?
- Next to the gallbladder
- Next to ligamentum theres (falciform ligament)
163
CT criteria for hepatic steatosis
- 40 HU or less
- More than 10 HU less than the spleen (on contrast enhanced CT)
164
US criteria for hepatic steatosis
Liver is hyperechoic to kidney
165
MRI criteria for hepatic steatosis
Signal dropout on out of phase imaging (by 2 standard deviations)
Note: Signal dropout will be maximal if there is 50% fat infiltration, if there is more infiltration than 50% the signal dropout will actually be less.
166
Hemochromatosis
Note: Liver is T2 hypointense relative to muscle. Normally liver should always be T2 hyperintense relative to muscle.
167
Which MRI sequence has the India ink artifact?
Out of phase imaging
168
Hemochromatosis
Note: Liver appears more hypointense on in phase imaging than out of phase imaging (this is the opposite of the signal dropout seen with microscopic fat).
169
Liver is T2 hypointense relative to muscle and the spleen is absent...
Think secondary hemochromatosis secondary to chronic hemolytic anemia
Note: The spleen is often surgically removed in the setting of chronic hemolytic anemia.
170
How can you differentiate primary vs secondary hemochromatosis on imaging?
Primary hemochromatosis tends to involve the pancreas and spare the spleen
Secondary hemochromatosis tends to involve the spleen and spare the pancreas
Note: Pancreas = primary and spleen = secondary.
171
What are the major causes of hemochromatosis?
- Primary (genetically inherited)
- Secondary (acquired due to chronic illness and/or multiple transfusions)
172
Budd-Chiari syndrome
Abdominal pain, ascites, and hepatomegaly secondary to hepatic vein thrombosis (more acute) or hepatic vein fibrosis (more chronic)
173
Risk factors for Budd-Chiari syndrome
Any hyper coagulable state (classically pregnancy)
174
Classic imaging findings of Budd-Chiari syndrome
- Thrombosed hepatic veins
- "flip-flop" pattern of enhancement in acute phase (delayed peripheral enhancement and central hepatic hypodensity)
- Nutmeg liver (inhomogenous mottled appearance)
- Hypertrophy of the caudate lobe (which has its own veinous drainage to the IVC)
175
What part of the liver hypertrophies in the setting of Budd-Chiari syndrome
The caudate lobe
Note: This is because it has its own veinous drainage to the IVC that wouldn't be affected by hepatic vein thrombosis.
176
"flip-flop" appearance of liver enhancement
Delayed enhancement of the peripheral liver resulting in peripheral enhancement with central hypodensity due to washout on portal veinous images. On arterial images this will be flip-flopped (central enhancement with peripheral hypodensity).
Note: This is classically seen in Budd-Chiari syndrome (hepatic vein thrombosis).
177
Nutmeg liver
Note: This is a perfusion abnormality, usually due to hepatic venous congestion (e.g. Budd-Chiari).
178
Differential for nutmeg liver
- Budd-Chiari (hepatic vein thrombosis)
- Hepatic veno-occlusive disease
- Hepatic congestion secondary to right heart failure
- Hepatic congestion secondary to constrictive pericarditis
179
How can you differentiate regenerative hyper plastic liver nodules from multifocal HCC?
T2 imaging (regenerative nodules are usually T2 dark/iso and HCC is usually T2 bright)
180
Classic clinical presentation of acute Budd-Chiari due to hepatic vein or IVC thrombus
Rapid-onset ascites
181
Differential for massive caudate lobe hypertrophy
- Budd-chiari Syndrome (hepatic vein thrombosis)
- Primar sclerosing cholangitis
- Primary biliary cirrhosis
182
Hepatic veno-occlusive disease
A form of Budd-Chiari that occurs due to occlusion of small hepatic venules
Note: The main hepatic veins and IVC will be patent, but portal waveforms will be abnormal (slow, reversed, to to-and-fro).
183
Common causes of hepatic veno-occlusive disease
- Alkaloid bush tea (common in Jamaica)
- Radiation/chemotherapy
184
Nutmeg liver, contrast reflux into hepatic veins, and increased portal veinous pulsatility...
Think passive hepatic congestions secondary to right heart failure or constrictive pericarditis
185
Portal vein thrombosis with cavernous transformation...
Cavernous transformation (many serpiginous vessels in the porta hepatis) indicates that the portal vein thrombosis is chronic (at least 12 months old)
186
History of metastatic breast cancer s/p treatment
Hepatic pseudocirrhosis
Note: Treated breast cancer metastases to the liver can give a cirrhotic appearance (multifocal liver retraction, caudate lobe hypertrophy).
187
Cryptogenic cirrhosis
Cirrhosis without a known cause (most are thought to be due to nonalcoholic fatty liver disease)
188
What is the most common disease requiring liver transplant?
Hepatitis C (followed by EtOH liver disease and cryptogenic cirrhosis)
189
Which vessels are anastomosed during liver transplant?
- IVC
- Hepatic artery
- Portal vein
- CBD
190
Which segments of the liver are most commonly transplanted?
Right lobe (segments 5-8) in adults
Note: In pediatric pts, segments 2-3 are usually transplanted.
191
Common contraindications to liver transplant
- Extrahepatic malignancy
- Advanced cardiac disease
- Advanced pulmonary disease
- Active substance abuse
Note: Portal hypertension is not a true contraindication, but does increase surgery difficulty and postoperative mortality.
192
What are the normal ultrasound findings for a liver transplant?
- Rapid systolic upstroke (diastolic to systolic in less than 80 msec)
- Resistive index 0.5-0.7
- Hepatic artery peak velocity < 200 cm/sec
193
What should the hepatic artery peak velocity be in healthy liver transplants?
<200 cm/sec
194
What should the resistive index be in healthy liver transplants?
0.5-0.7
195
How fast should the systolic upstroke be in healthy liver transplants?
Rapid (diastolic to systolic in less than 80 msec/0.08 sec)
196
What is the ultrasound sequence in the syndrome of impending thrombosis for liver transplants?
Over the 3-10 days post transplant:
1. Initial normal waveform
2. No diastolic flow
3. Dampening of systolic flow (trades parvus, resistive index < 0.5)
4. Loss of hepatic waveform
197
What percentage of hepatic blood flow comes from the portal vein?
70%
198
What is the most important vessel in liver transplants?
The hepatic artery (primary source of blood flow to the bile ducts)
Note: This is counterintuitive because normally the liver gets 70% of its blood flow from the portal vein.
199
When does ehpatic artery thrombosis tend to occur s/o liver transplant?
- Early (<15 days post op)
- Late (years later, usually due to chronic rejection or sepsis)
200
Is trades parvus of a transplanted hepatic artery more likely to be secondary to stenosis or thrombosis?
Tardus parvus is more likely secondary to stenosis
201
Think pneumobilia when gas is more central in the liver
Note: Bile ducts drain towards the porta hepatis.
202
Think portal venous gas when gas is more peripheral in the liver (within 2 cm of the liver capsule)
Note: Portal veins drain towards the periphery.
203
When should you consider branching air in the liver to be portal venous gas?
When it is peripheral (within 2cm of the liver capsule)
204
Common causes of pneumobilia
- Recent biliary instrumentation
- Anything that messes up the sphincter of Oddi (e.g. sphincterotomy)
205
Common causes of portal venous gas
- Bowel necrosis (look for pneumatosis)
- COPD
206
Jaundice, fever, and right upper quadrant pain...
Think bacterial cholangitis
207
Does primary sclerosis cholagnitis recur in pts s/o liver transplant?
Sometimes (20% of cases)
208
Cirrhotic liver with dilated intrahepatic bile ducts...
Think primary sclerosing cholangitis
Note: Intrahepatic bile duct dilatation is rare in other forms of cirrhosis due to the squeezing pathophysiology.
209
MRCP
Think primary sclerosing cholangitis
Note: This is the "withered tree" appearance due to multifocal intrahepatic strictures.
210
MRCP
Think primary sclerosis cholangitis
Note: This is the "beaded" appearance of intrahepatic bile ducts due to multifocal strictures and dilated segments.
211
Primary sclerosing cholangitis
Idiopathic disease characterized by progressive inflammation leading to multifocal strictures of the intrahepatic and/or extra hepatic bile ducts
Note: These pts are at high risk for cholangiocarcinoma.
212
AIDS pt
AIDS cholangiopathy
Note: This is an infection of the biliary epithelium (classically Cryptosporidium) that leads to multifocal bile duct strictures similar to primary sclerosis cholagnitis.
213
Differential for multifocal bile duct strictures
- Primary sclerosing cholangitis
- AIDS cholangiopathy
- Chemotherapy-induced cholangitis
- Recurrent pyogenic cholangitis (look for multiple pigmented stones)
214
Multifocal bile duct strictures and papillary stenosis...
Think AIDS cholangiopathy
Note: Papillary stenosis = sphincter of Odd dysfunction.
215
How do bile duct strictures differ in primary sclerosing cholangitis and AIDS cholangiopathy?
Extra hepatic bile duct strictures are rarely >5 mm in PSC, but often >2 cm in AIDS
Saccular deformities of the ducts are common in PSB but rare in AIDS
216
Where is recurrent pyogenic cholangitis common?
Southeast Asia
217
Multifocal intrahepatic bile duct dilatation containing multiple pigmented stones...
Think recurrent pyogenic cholangitis
218
Which hepatic lobe is more often involved in recurrent pyogenic cholangitis?
Left hepatic lobe
Note: This is because the biliary system is longer and flatter on the left (opposite of hematogenous processes, which prefer the right lobe).
219
Primary biliary cirrhosis
An autoimmune disease that results in destruction of the small and medium bile ducts resulting in progressive irregular dilatation of the intrahepatic bile ducts with normal extrahepatic bile ducts
Note: Early on, the bile ducts are normal.
220
Pt is positive for antimitochondrial antibodies...
Primary biliary cirrhosis
221
Pts with primary biliary cirrhosis are at an increased risk for...
HCC
222
Treatment for primary biliary cirrhosis
Ursodeoxycholic acid
223
Primary biliary sclerosis is most common in what pt population?
Middle-aged women
224
Long common channel
An anatomic variant in which the CBD and pancreatic duct fuse prematurely (at the level of the pancreatic head rather that at the normal location, just proximal to the sphincter of Oddi)
225
Pts with a long common channel are at increased risk for...
Pancreatitis
Note: A long common channel is premature fusion of the CBD and pancreatic duct.
226
Long common channel is associated with...
Type 1 choledochal cysts (focal dilatation of the CBD)
227
Todani classification of choledochal cysts
- 1 (focal CBD dilatation)
- 2 (CBD diverticulum)
- 3 (choledochocele)
- 4 (both intra and extra hepatic dilatation)
- 5 (intrahepatic only, AKA Caroli's)
228
Caroli's disease
Note: Large, saccular intrahepatic bile duct dilatation WITH "central dot sign" (portal vein surrounded by dilated bile ducts).
229
What does the "central dot sign" represent in Caroli's disease?
Portal veins (surrounded by dilated bile ducts)
230
Inheritence pattern of Caroli's disease
Autosomal recessive
231
Caroli's disease is associated with...
- Polycystic kidney disease
- Medullary sponge kidney
232
Complications of Caroli's disease
Cholestasis:
- Cholangiocarcinoma
- Cirrhosis
- Cholangitis
- Intraductal stones
233
Primary sclerosing cholangitis is associated with...
- Ulcerative colitis (80%)
- Crohns (20%)
234
How can you tell the difference between bile duct strictures due to cholagniocarcinoma vs benign causes (e.g. sclerosing cholangitis)?
Cholangiocarcinoma tends to produce long strictures with shouldering
Benign strictures tend to be abrupt and short
