1. Focal Lesions in the Cirrhotic Liver
Michael P. Federle, MD
Associate Chair for Education
Department of Radiology
Stanford University

2. 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

3. Cysts + Regenerative Nodules (RN)
NECT
Enhancement
Cysts
Hypodense No RN
Hyperdense
Minimal

4. Cavernous Hemangioma Large ones have typical appearance
Very intense on T2WI
Nodular peripheral enhancement
Smaller (“capillary”) hemangiomas
May enhance homogeneously
Can be confused with HCC
Key is remaining isodense with vessels

5. Hemangioma in Cirrhotic Liver Shrinks to Fibrotic Scar
2 years later
Only found a “scar” in explant

6. HCC?
No!
Cavernous Hemangioma
Isodense to vessels

7. 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
High intensity on T2 – MR
Can simulate tumor
Ohtomo et al. Radiology 1993; 188: 31-35
Krinsky et al. Radiology 2001; 219:

8. 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
High intensity on T2 – MR
Can simulate tumor
Federle: DI: Abdomen

9. Focal Confluent Fibrosis
Note delayed enhancement

10. Confluent
Hepatic Fibrosis

11. NC T1WI
MRI Confluent
Hepatic Fibrosis
HAP
delayed

12. T1 WI
Confluent
Hepatic Fibrosis
T2 WI
T1 PVP

13. Peripheral Wedge-shaped Lesion
May appear central + round on axial section
Examples:
Focal confluent fibrosis
THADs
AP shunts

14. Focal Lesions in the Cirrhotic Liver
Regenerative nodules (RN)
Dysplastic nodules
Hepatocellular carcinoma (HCC)

15. Evolution of (some) Cirrhotic Nodules (Sakamoto hypothesis, 1991)
Regenerative Nodule
Low Grade Dysplastic Nodule
High Grade Dysplastic Nodule
Well-Differentiated HCC
Overt HCC
(Moderately/Poorly Differentiated)

16. 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

17. Regenerating Nodules

18. NCCT
Cirrhotic Nodules
visible only on NCCT & GRE
HAP
PVP
GRE

19. Regenerating Nodules T1 WI Best seen on T2 WI (hypointense, multiple)

20. NCCT
Regenerating Nodules
hyperdense only on NECT
HAP
PVP

21. Regenerating Nodules Importance of NCCT imaging
Don’t call “hypervasc. HCC”

22. Regenerating Nodules
48 y/o man with cirrhosis
Cavernous Hemangiomas

23. Also has HCC 48 y/o man with cirrhosis Must characterize lesions on
all phases of CT or MR

24. Dysplastic Nodules “Adenomatous hyperplasia” (old term)
Are premalignant
Rarely diagnosed by US or CT
MR – iso to hyperintense on T1
Hypo on T2 (opposite of HCC)
Should not enhance much on HAP
Diagnosed correctly 5 – 15% of cases
Krinsky et al. Radiology 2001; 219:
Dodd et al. AJR 1999; 173:

25. T1WI
T2WI
Hyper on T1
Hypo on T2
(opposite of HCC)
Dysplastic Nodules

26. Focal Nodule
Large
Hyper on NECT
Minimal vascularity
NECT
HAP
PVP

27. Focal Nodule Dysplastic Nodule T1WI-IP T1WI-OOP Bright on T1WI
No signal loss on OOP
(= not focal fat)
Dark on T2 WI
Minimal Vascularity
HAP
PVP
Delayed
T2WI
Dysplastic
Nodule

28. Focal Nodule (same patient) Hypoechoic mass US-guided Bx
Confirmed dysplastic nodule
Courtesy: Mitch Tublin MD
UPMC

29. Hepatocellular Carcinoma (HCC)
Heterogeneously hypervascular mass
Washes out on delayed phase
Invades veins (portal > hepatic)
Federle: DI: Abdomen

30. HCC - Helical CT Main imaging tool in most institutions
Must be multiphasic
Arterial phase ~ 25 – 35 seconds
Dual arterial, or test bolus is ideal
Portal venous ~ 60 – 70 seconds
Noncontrast
Very helpful for RNs, cysts
Delayed or equilibrium
Useful (but hard to justify 4 phase imaging)
Rapid injection (4 or 5 ml/sec); large volume
(2 ml/kg; > 150 ml)

31. HCC - Helical CT
Allows detection and characterization of most masses > 2 cm diameter
Accurately reflects morphology and hemodynamics of tumor
Small, well differentiated HCC
Still have portal venous supply
Often hypo – to isodense on NC + HAP
Hypodense on PVP
Capsule, fat common in well-differentiated
Most HCC (Best seen as hyperdense on HAP)

32. HCC within Dysplastic Nodule
“nodule-in-nodule” pattern
(each component has typical features)

33. NC
PVP
Typical HCC
screening CT
chronic Hep C
isodense on NC + PVP
HAP

34. Simplified Approach to Liver Hemodynamics increased dysplasia = more arterial, less portal
100
% arterial supply 80 % 60 40 20
% venous supply
Normal RN
Dysplastic
Nodule
Well-diff
HCC
Mod-diff
HCC

35. HCC moderately differentiated
best on HAP
“washes out” on PVP NC
HAP
PVP

36. HCC - only or best seen on HAP

37. NC
HCC with capsule
HAP
PVP

38. HCC well-differentiated
HAP
HCC well-differentiated
best on PVP
PVP

39. HCC Mod Differentiated
Best on HAP

40. Small HCC
only seen on HAP & MR
HAP
PVP

41. T1 NC
T1 HAP
Small
HCC
T2 WI
T1 PVP

42. HCC small tumor PV invasion Tumor Thrombus: Contiguity w tumor
Expansion of lumen
Enhancing thrombus

43. HCC: Other Features Lesion with Focal fat in cirrhotic liver = HCC
NECT
HCC: Other Features
Focal fat
Calcifications
NECT
HAP
PVP
Lesion with
Focal fat in cirrhotic liver
= HCC

44. Nodular Lesions in CirrhosisCT MR NC
HAP
PVP
Delay T1
HAP
PVP T2
Regenerative
Nodule  or   or   or 
Dysplastic
Nodule  or   or   or   or   or 
Well-diff
HCC  or   or     or   or   or  
Mod-diff
HCC  or   or   or    or    or  
= not seen (isodense, isointense)
 = hyperdense (-intense) to liver
 = hypointense (-intense) to liver

45. HCC - Helical CT Accuracy
Good for large tumors
Challenging in screening population (asymptomatic, normal tumor markers)
We miss (false + and neg) small HCCs (<2cm) frequently
However, we usually (> 95%, UPMC data) accurately guide Rx
Decision for follow-up, ablation, TACE, transplantation

46. HCC - Helical CT Accuracy
Multidetector CT and dual arterial phase imaging
Sensitivity (86%), positive pred value (92%)
Mean size of HCC (22 mm)
Much better results than other reports
Murakami et al. Radiology 2001; 218:

47. HCC - MR Accuracy Variable intensity of HCC on T1 MR
35% hyper -, 25% iso-, 40 % hypo
Hyperintense often well-differentiated, contain fat
Almost always hyperintense on T2 MR
Must have multiphasic study after bolus of Gd-DTPA
Most HCC are hypervascular/intense on HAP

48. HCC - MR Accuracy
Best studies with good reference standard (OLT, explantation) in screening population
Detect HCC in 50 – 65% of patients
Detect 35 – 50% of HCC tumors
Miss many tumors  20 mm
Hard to distinguish some RNs and dysplastic nodules
Krinsky et al. Radiology 2001; 219:

49. 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

50. HAP
Lobar “THAD”
HCC obstructing RPV
PVP
PVP

51. AP Shunt
no tumor
resolved spontaneously

52. AP Shunt
? Post-biopsy
visible vessels

53. AP Shunt
spontaneous

54. AP Shunts + Hemangioma
Shunts disappeared
Hemangioma stable 3 yrs

55. AP Shunt in Cirrhosis Early draining vein
Small AP shunts are common, often resolve
Don’t be too aggressive with Dx or Rx

56. HCC - Helical CT vs MR Comparable performance MR preference
Contrast allergy
Known steatosis
CT preference
Ascites, unstable, tachypneic patient
Both are evolving and improving (but often performed/interpreted poorly)

57. Tumor Markers for HCC Pitt Experience with 430 transplant recipients
Excluding 2 patients with HCC + markedly AFP
No significant difference in serum AFP in HCC, non-HCC groups
AFP often normal in small HCC
AFP often elevated in flare of hepatitis
Peterson et al. Radiology 2000; 217:

58. Screening Recommendation for Known Cirrhosis
AFP and PIVKA II – every 3 months
Ultrasonography – every 3 or 4 months
CT or MR – every 12 months
(for chronic hepatitis without cirrhosis, extend intervals)
(for high clinical suspicion or indeterminate lesion, shorten interval)

59. Summary US, CT, MR all useful in evaluation of cirrhosis
Large and symptomatic HCCs are easily detected and staged
Small HCCs in a screening population are more challenging
Some overlap in appearance of regenerative + dysplastic nodules + HCC

60. Summary Optimal CT + MR techniques are key
Must include multiple phases, rapid bolus contrast administration
Image-guided Bx and angiography often necessary