focal lesions in the cirrhotic liver
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Focal Lesions in the Cirrhotic Liver. Michael P. Federle, MD Associate Chair for Education Department of Radiology Stanford University. Focal Lesions in the Cirrhotic Liver. Cysts, hemangiomas, focal fat, confluent fibrosis Can usually be diagnosed accurately - PowerPoint PPT PresentationTRANSCRIPT
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