GI Section III: Diffuse Liver Processes Flashcards
How to Call Fatty Liver on CT?
- < 40 HU on NECT
- < 100 HU on PVP
- < 25 HU less than the spleen
How to Call Fatty Liver on US?
Brighter than the kidney
How to Call Fatty Liver on MRI?
Two standard deviation difference between in and out of phase imagin
Out-of-phase SIGNAL DROP
What does signal drop out assume on MRI?
there is more water than fat in the liver
the degree of signal loss is maximum when the fat infiltration is 50% (exactly 1:1 signal loss)
When the percentage of fat grows larger than 50% you will actually see a less significant signal loss on out of phase imaging, relative to that maximum 50%.
What causes signal drop?
McDonalds, Burger King, and Taco Bell.
Additional causes include:
chemotherapv (breast cancer)
steroids
cystic fibrosis.
Iron overload
Hemochromatosis
You can show hemochromatosis is three main ways:
- The liver and spleen being T1 and T2 dark.
- T2 only: absent spleen (chronic hemolytic anemia = multiple blood transfusions = hemochromatosis = splenectomy), liver is darker (low signal) than muscle)
* On T2 a normal liver should always have a signal higher than muscle - Low signal on in phase, and high signal on out of phase. (“Iron on In-phase”)
FAT vs IRON in IP - OOP MRI
FAT - Signal Drop on OOP
IRON - Signal drop in IP
A. Hereditary hemochromatosis - Low signal Liver / Normal spleen
B. Prolonged treatment with phlebotomies: Normal Signal liver
C. Secondary hemochromatosis: Low signal on Liver and spleen
Hemocrhomatosis
Liver + Pancreas
Primary hemochromatosis
Hemochromatosis
Liver + spleen
Secondary hemochromatosis
Hemochromatosis
Genetic - increased absorption
Primary hemochromatosis
Hemochromatosis
Acquired - chronic illness, and multiple transfusions
Secondary hemochromatosis
How does the body react in secondary hemochromatosis?
result of either chronic inflammation or multiple transfusions.
body reacts by trying the “Eat the Iron,” with the reticuloendothelial system
Hypercoaguable patient (pregnant or idiopathic - mc example) = Hepatic vein thrombosis
Budd Chiary Syndrome
Budd-Chiary syndrome
- Obstruction - hepatic venous outflow
- Intrahepatic and systemic collateral veins
- Large regenerative (hyperplastic) nodules in a dysmorphic liver
- LArge caudate lobe (massive) - spared from separate drainage into IVC)
Early and delayed phases of liver enhancement
Budd-Chiari Syndrome
“flip-flop pattern
AP: Central enhancement Peripheral minumal
PVP: Central washout (Low attenuation) and high peripherally
Who gets a “Nutmeg Liver”
- Budd Chiari
- Hepatic Veno-occlusive disease
- Right Heart Failure (Hepatic Congestion)
- Constrictive Pericarditis
“nutmeg” with an inhomogeneous mottled appearance, and delayed enhancement of the periphery of the liver.
Budd-Chiari Syndrome
Regenerative (hyperplasic) nodules in Budd Chiari
High T1 low/iso T2
Budd-Chiarri vs HCC nodules
Big (>10cm) and small (<4cm) nodules in Budd chiarri = benign
Budd Chiari = T2 Dark
HCC = T2 bright
Acute vs Chronic Budd-Chiari syndrome
Acute = rapid onset ascites
Chronic = fibrosis of the intrahepati veins due to infplammateion
Who gets massive caudate lobe hypertrophy?
Budd-Chiari
Primary Sclerosing Cholangitis
Primary Biliary Cirrhosis
Budd Chiari that occurs from occlusion of the small hepatic venules (Instead of hepatic venous outflow)
Hepatic Veno-occlusive Disease
