Focal Lesions in the Cirrhotic Liver

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. RN Cysts + Regenerative Nodules (RN)

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

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: 445-454

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 delayed HAP MRI Confluent Hepatic Fibrosis

12. T1 WI T2 WI T1 PVP Confluent Hepatic Fibrosis

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) Low Grade Dysplastic Nodule Well-Differentiated HCC Overt HCC (Moderately/Poorly Differentiated) Regenerative Nodule High Grade Dysplastic Nodule

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 HAP PVP GRE • Cirrhotic Nodules • visible only on NCCT & GRE

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

20. NCCT HAP PVP • Regenerating Nodules • hyperdense only on NECT

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

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

23. 48 y/o man with cirrhosis Also has HCC 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: 445-454 Dodd et al. AJR 1999; 173: 1185 - 1192

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

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

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

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

34. Simplified Approach to Liver Hemodynamicsincreased dysplasia = more arterial, less portal 100 % arterial supply 80 % 60 40 20 % venous supply 0 RN Normal Dysplastic Nodule Mod-diff HCC Well-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 HAP PVP HCC with capsule

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

39. HCC Mod Differentiated • Best on HAP

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

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

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

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

44.                   or or or or or or or or or or or or or or or or or or Nodular Lesions in Cirrhosis CT MR NC HAP PVP Delay T1 HAP PVP T2 Regenerative Nodule    Dysplastic Nodule      Well-diff HCC         Mod-diff HCC         = 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: 763-767

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: 445-454

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 PVP PVP • Lobar “THAD” • HCC obstructing RPV