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

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

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or

or

or

or

or

or or

or

or

or

or

or

or

or

or

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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