Michael P. Federle, MDAssociate Chair for Education

Department of Radiology

Stanford University

Focal Lesions in the Cirrhotic Liver

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

RN

NECT Enhancement

Cysts Hypodense No

RN Hyperdense Minimal

Cysts + Regenerative Nodules (RN)

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

2 years later

Only found a “scar” in explant

Hemangioma in Cirrhotic Liver

• Shrinks to Fibrotic Scar

HCC?

No! Cavernous Hemangioma

• Isodense to vessels

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: 31-35Krinsky et al. Radiology 2001; 219: 445-454

Confluent Hepatic Fibrosis(Focal Confluent Fibrosis)

Federle: DI: Abdomen

• 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

Focal Confluent Fibrosis

Note delayed enhancement

Confluent Hepatic Fibrosis

NC T1WI

HAPdelayed

MRI Confluent Hepatic Fibrosis

T1 WI

T1 PVP

Confluent Hepatic Fibrosis

T2 WI

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

Focal Lesions in the Cirrhotic Liver

• Regenerative nodules (RN)

• Dysplastic nodules

• Hepatocellular carcinoma (HCC)

Evolution of (some) Cirrhotic Nodules(Sakamoto hypothesis, 1991)

Regenerative Nodule

High Grade Dysplastic Nodule

Low Grade Dysplastic Nodule

Well-Differentiated HCC

Overt HCC (Moderately/Poorly Differentiated)

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

Regenerating Nodules

NCCT

HAP

PVP

GRE

Cirrhotic Nodules• visible only on NCCT & GRE

T1 WI

T2 WI

Best seen on T2 WI(hypointense, multiple)

Regenerating Nodules

NCCT

HAP

PVP

Regenerating Nodules • hyperdense only on NECT

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

48 y/o man with cirrhosisRegenerating Nodules

Cavernous Hemangiomas

48 y/o man with cirrhosis

Also has HCC

Must characterize lesions on all phases of CT or MR

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

Dysplastic Nodules

T1WI T2WI

Hyper on T1Hypo on T2(opposite of HCC)

Focal NoduleLargeHyper on NECTMinimal vascularity

NECT

HAP

PVP

Focal NoduleBright on T1WINo signal loss on OOP(= not focal fat)Dark on T2 WIMinimal Vascularity

T2WI

T1WI-IP T1WI-OOP

Dysplastic Nodule

HAP

PVP

Delayed

Focal Nodule (same patient)Hypoechoic massUS-guided BxConfirmed dysplastic nodule

Courtesy: Mitch Tublin MDUPMC

Hepatocellular Carcinoma (HCC)

• Heterogeneously hypervascular mass

• Washes out on delayed phase

• Invades veins (portal > hepatic)

Federle: DI: Abdomen

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)

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)

HCC within Dysplastic Nodule• “nodule-in-nodule” pattern

(each component has typical features)

NC PVP

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

HAP HAP

Simplified Approach to Liver Hemodynamics

increased dysplasia = more arterial, less portal

RN Mod-diffHCC

0

20

40

60

80

100

Normal DysplasticNodule

Well-diffHCC

%

% arterial supply

% venous supply

HCC moderately differentiated• best on HAP• “washes out” on PVP

NC

HAP

PVP

HCC - only or best seen on HAP

HCC with capsuleNC

HAP

PVP

HCC well-differentiated• best on PVP

HAP

PVP

HCC Mod Differentiated• Best on HAP

PVPHAP

Small HCC• only seen on HAP & MR

T1 NC

T1 PVP T2 WI

SmallHCCT1 HAP

HCC• small tumor• PV invasion

Tumor Thrombus:•Contiguity w tumor•Expansion of lumen•Enhancing thrombus

NECT

NECT

HAP

PVP

HCC: Other FeaturesFocal fatCalcifications

Lesion with Focal fat in cirrhotic liver= HCC

= not seen (isodense, isointense)

= hyperdense (-intense) to liver

= hypointense (-intense) to liver

Regenerative

Nodule

Dysplastic

Nodule

Well-diff

HCC

Mod-diff

HCC

PVPHAPT1 T2DelayPVPHAPNC

or

or

or

or

or

or

or or

or

or

or

or

or

or

or

or

or

or

CT MR

Nodular Lesions in Cirrhosis

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

• 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

HCC- Helical CT Accuracy

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

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

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

PVP

HAP

PVP

Lobar “THAD”• HCC obstructing RPV

AP Shunt• no tumor• resolved spontaneously

AP Shunt• ? Post-biopsy• visible vessels

AP Shunt• spontaneous

AP Shunts + Hemangioma • Shunts disappeared

• Hemangioma stable 3 yrs

AP Shunt in CirrhosisEarly draining vein

Small AP shunts are common, often resolveDon’t be too aggressive with Dx or Rx

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)

• 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: 743-749

Tumor Markers for HCC

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)

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

Summary

• Optimal CT + MR techniques are key

– Must include multiple phases, rapid bolus contrast administration

• Image-guided Bx and angiography often necessary