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Liver

Parenchymal Disease

Nonalcoholic Fatty Liver Disease (NAFLD): Facts
Common cause of chronic liver disease
- Usually asymptomatic, mild elevation of aminotransferase levels
- Common in diabetics, obese (metabolic syndrome)
- Affects 15-25% of American adults (10% of kids)
Nonalcoholic steatohepatitis  (NASH)
- Subtype of NAFLD (25% of those w steatosis)
- Carries risk of progressive liver disease, cirrhosis
- Can only be diagnosed by Bx, not imaging
– (can’t distinguish NAFLD from NASH)
“CASH”: ChemoRx-associated steatohepatitis
- Common cause of liver dysfunction in cancer patients
- Associated with various agents
- May mask liver metastases on CT
- Liver injury may limit other therapeutic options (e.g., partial resection, ablation)
- Federle
Iron Deposition in the Liver: Facts
Hemochromatosis:
- Common autosomal recessive disorder, ? absorption of iron
- Deposited in hepatocytes, pancreas, heart, etc
- Leads to cirrhosis, HCC, “bronze” diabetes
- “Primary” = pancreatic involvement
Hemosiderosis:
- Due to hemolysis, transfusions
- Iron deposition in liver (RES), spleen
- “Secondary” = spleen
Steatosis (Fatty Infiltration of the Liver)
CT Findings
- Decreased density (less than spleen on NC, 25 HU less on CECT)
- Vessels course through undisturbed
- Geographic areas
--Can be rounded (esp ~ ligaments + vessels), resemble metastases
Nonalcoholic Fatty Liver Disease
Common cause of chronic liver disease
- Usually asymptomatic, mild elevation of aminotransferase levels
- Common in diabetics, obese (metabolic syndrome)
- Affects 15-25% of American adults (10% of kids)
Nonalcoholic steatohepatitis  (NASH)
- Subtype of NAFLD (25% of those w steatosis)
- Carries risk of progressive liver disease, cirrhosis
- May soon be #1 cause of cirrhosis + HCC in USA
- Can only be diagnosed by Bx, not imaging
- (can’t distinguish NAFLD from NASH)
“CASH”: ChemoRx-associated steatohepatitis
- Common cause of liver dysfunction in cancer patients
- Associated with various agents
- May mask liver mets on CT
- Liver injury may limit other Rx options (e.g., partial resection, ablation)
Diffuse Disease that May Simulate Fatty Liver
Diffuse tumor
- Lymphoma > mets > diffuse HCC
Diffuse infection
- Especially in AIDS (viral, mycobacterial, fungal, etc)
Diffuse acute liver injury
- Severe hepatitis
- Tylenol OD, mushroom poisoning
- Radiation hepatitis
Iron Deposition in the Liver
Hemochromatosis:
- Common autosom recess disorder, ­ absorption of iron
- Deposited in hepatocytes, pancreas, heart, etc
- Leads to cirrhosis, HCC, “bronze” diabetes
- “Primary” = pancreatic involvement
Hemosiderosis:
- Due to hemolysis, transfusions
- Iron deposition in liver (RES), spleen
- “Secondary” = spleen
Iron Deposition
CT:
- Liver much denser than spleen, muscle
- DDx: amiodarone Rx, glycogen storage disease, (Wilson’s disease – not!)
MR:
- Marked downward signal on T2 + T1WI
- T1WI: liver + spleen much darker than muscle
- Signal “drop-out” on in-phase GRE (opposite of steatosis)
Sarcoidosis of the Liver
- Periportal involvement
- Can simulate or lead to cirrhosis
- Hepatomegaly, splenomegaly, ­ periportal SI on T2WI
- Multifocal liver/splenic nodules
- Lung disease +/ or nodes (chest + abdomen)
Focal Lesions in the Cirrhotic Liver
Cysts, hemangiomas, focal fat, confluent fibrosis
- Can usually be diagnosed accurately
Hemangiomas shrink and become sclerosed in cirrhotic liver
- Often not identified in advanced cirrhosis
Focal fat
- Key is out-of-phase MR (focal sign dropout)
Brancatelli et al. Radiology 2001; 219: 69-74
Confluent Hepatic Fibrosis
(Focal Confluent Fibrosis)
Present in ~ 30% of advanced cirrhosis
- > 50% of PSC
Most common in anterior + medial segments
- Usually wedge-shaped lesion
80% have focal volume loss
- Capsular retraction, crowded vessels
Low density on NCCT
- Delayed persistent enhancement
- Can simulate tumor
Cirrhosis
- Chronic liver damage leading to fibrosis and nodular regeneration
- Most common causes:
- Alcoholism
- Hepatitis C
- Hepatitis B
- Biliary cirrhosis
- Metabolic Cirrhosis
- Primary Sclerosing Cholangitis
Cirrhosis
- CT Findings:
- Heterogeneous liver texture
- Surface nodularity
- High density nodules in the liver on non-contrast images
- Caudate Hypertrophy
- Transverse caudate width : right lobe width
- > 0.65
- Segmental hypertrophy of segments II and III
- Segmental atrophy of segments VI, VII, and IV
- Enlarged gallbladder fossa
- Enlarged periportal space
- Peribiliary Cysts
Iron Deposition
- Hemochromatosis (“primary”)
- Autosomal recessive
- Liver, Pancreas, Heart
- Cirrhosis, “bronze” diabetes
- Hemosiderosis (“secondary”)
- Transfusions or hemolysis
- Liver, Spleen
Iron Deposition
- CT:
- Liver denser than spleen and muscle
- Similar appearance with some drugs (amiodarone) and glycogen storage disease
Iron Deposition
- MR:
- Low signal on T2 and T1
- Liver and spleen lower in T1 signal compared to muscle
- Signal drop-out on in-phase GRE
Sarcoid
- Commonly involves liver, but rarely causes symptoms
- Multiple nodules in the liver and spleen
- Periportal involvement
- Hepatomegaly and splenomegaly
- Look for lymphadenopathy and lung disease
- Can lead to cirrhosis chronically
Passive Hepatic Congestion
- Reflux of contrast into dilated IVC and hepatic veins
- Can be seen with forceful injections in normal patients
- Heterogeneously enhancing liver
- “Mottled” or “Nutmeg” liver
- Poor enhancement of peripheral liver due to stasis of blood flow
- Hepatomegaly and ascites
Hepatic Infarction   
- Uncommon due to dual blood supply of the liver
- Usually hepatic arterial occlusion + portal vein abnormality
- Causes:
- Liver Transplant, Iatrogenic, Hypercoagulability, infection, vasculitis
Hepatic Infarction
- CT Findings:
- Usually wedge shaped, peripheral, and low attenuation
- Can be rounded or irregularly shaped
- Can evolve into bile lakes
- Gas can be seen in both sterile and infected infarcts
Portal Vein Thrombosis
- Causes:
- Cirrhosis and Portal Hypertension   
- Slow flow and stasis in portal vein combined with hypercoagulability
- 1% of patients with cirrhosis develop portal vein thrombosis
- Malignancy
- Hypercoagulable States
- Iatrogenic
- Unknown in 1/3 of cases
Portal Vein Thrombosis
- CT Findings:
- Filling defect in the vein
- Thrombus should show no enhancement
- Thread-and-streak sign: Tumor thrombus
- Arterial hyperenhancement in the thrombus
- Chronically, mural thickening along the periphery of the vein with calcification
- Cavernous transformation
Malignant Versus Benign Portal Vein Thrombosis
- Malignant portal vein thrombus
- 35% of patients with HCC
- Poor prognosis and high rates of recurrence
- Liver transplant is contraindicated
- Systemic chemotherapy only real option
- Liver transplant still potentially an option with bland thrombus
Cirrhosis
Chronic liver damage leading to fibrosis and nodular regeneration
Most common causes:
- Alcoholism
- Hepatitis C
- Hepatitis B
- Biliary cirrhosis
- Metabolic Cirrhosis
- Primary Sclerosing Cholangitis
Cirrhosis
CT Findings:
1. Heterogeneous liver texture
2. Surface nodularity
3. High density nodules in the liver on non-contrast images
4. Caudate Hypertrophy
- Transverse caudate width : right lobe width
- > 0.65
5. Segmental hypertrophy of segments II and III
6. Segmental atrophy of segments VI, VII, and IV
7. Enlarged gallbladder fossa
8. Enlarged periportal space
9. Peribiliary Cysts
Special Cases
1. Primary Sclerosing Cholangitis:
- Pseudotumoral enlargement of caudate
- DDX: Budd-Chiari Syndrome, PSC, and portal vein thrombosis
- Extensive periportal lymphadenopathy
2. Primary Biliary Cirrhosis
- “Lace-like fibrosis” with prominent regenerative nodules
Iron Deposition
1. Hemochromatosis (“primary”)
- Autosomal recessive
- Liver, Pancreas, Heart
- Cirrhosis, “bronze” diabetes
2. Hemisiderosis (“secondary”)
- Transfusions or hemolysis
- Liver, Spleen
Iron Deposition
1. CT:
- Liver denser than spleen and muscle
- Similar appearance with some drugs (amiodarone) and glycogen storage disease
2. MR
- Low signal on T2 and T1
- Liver and spleen lower in T1 signal compared to muscle
- Signal drop-out on in-phase GRE
Sarcoid
1. Commonly involves liver, but rarely causes symptoms
2. Multiple nodules in the liver and spleen
- Periportal involvement
- Hepatomegaly and splenomegaly
3. Look for lymphadenopathy and lung disease
4. Can lead to cirrhosis chronically