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17 Cards in this Set

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Focal Lesions in the Cirrhotic Liver
- Regenerative nodules (RN)
- Dysplastic nodules
- Hepatocellular carcinoma (HCC)
Regenerating Nodules
Usually too small to detect by imaging
- May be surrounded by fibrotic septa
- May contain iron, copper
Siderotic nodules
- Hyperdense on NCCT, disappear on HAP & PVP
- Hypointense on T2 MR, “bloom” on GRE
Larger or vascular/enhancing RN
- Can not be distinguished from dysplastic nodule or HCC
Dysplastic Nodules
- “Adenomatous hyperplasia” (old term)
- Are premalignant (larger, high-grade DNs)
- Rarely diagnosed by US or CT
Dysplastic Nodules
Small, low-grade DNs are often indistinguishable from regenerative nodules (by imaging + histology)
- Usually <1.5 cm diameter, minimal vascularity
- Usually hypointense on T2WI
Larger, high grade DNs are often indistinguishable from HCC
- Usually >2cm, moderate vascularity
- May be hyperintense on T2WI
Primary Criteria for Dx of HCC
- Mass-like arterial phase hyperenhancement with “washout” (becomes hypodense to liver)
- Tumor within the portal (or hepatic) vein
- Increase in size by > 10 mm within one year
HCC - Helical CT Pitfalls
THAD (transient hep. attenuation differences)
- Small peripheral wedge-shaped
- Ignore, usually due to AP shunt or aberrant veins
Larger segmental or lobar
- Often due to tumor occlusion of portal vein
Arterioportal shunt
- Common in cirrhosis
- Usually benign if small, peripheral, non-spherical, isodense on PVP, visible vessels into + out
Screening Recommendation for Known Cirrhosis
1. AFP and PIVKA II – every 3 months
2. Ultrasonography – every 3 or 4 months
- Most useful in less advanced cirrhosis
- Very nodular/coarse liver is difficult
3. CT or MR ~ every 12 months
- (For chronic hepatitis without cirrhosis, extend intervals)
4. For high clinical suspicion or indeterminate lesion, shorten intervals
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