Transcript Focal lesions in cirrhotic 2010

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
• 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
Cysts + Regenerative Nodules (RN)
Cysts
NECT
Hypodense
Enhancement
No
RN
Hyperdense
Minimal
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
Hemangioma in Cirrhotic
Liver
• Shrinks to Fibrotic Scar
2 years later
Only found a “scar” in explant
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: 31-35
Krinsky et al. Radiology 2001; 219: 445-454
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
Focal Confluent
Fibrosis
Note delayed enhancement
Confluent
Hepatic
Fibrosis
MRI Confluent
Hepatic Fibrosis
NC T1WI
HAP
delayed
Confluent
Hepatic
Fibrosis
T1 WI
T1 PVP
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
Low Grade Dysplastic Nodule
High 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
Cirrhotic Nodules
HAP
• visible only on NCCT & GRE
PVP
GRE
Regenerating
Nodules
T1 WI
Best seen on T2 WI
(hypointense,
multiple)
T2 WI
Regenerating Nodules
• hyperdense only on NECT
NCCT
HAP
PVP
Regenerating Nodules
• Importance of NCCT imaging
• Don’t call “hypervasc. HCC”
Regenerating Nodules
48 y/o man with cirrhosis
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
T1WI
Hyper on T1
Hypo on T2
(opposite of HCC)
T2WI
Dysplastic Nodules
Focal Nodule
Large
Hyper on NECT
Minimal vascularity
NECT
HAP
PVP
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
Focal Nodule
(same patient)
Hypoechoic mass
US-guided Bx
Confirmed dysplastic nodule
Courtesy: Mitch Tublin MD
UPMC
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)
Typical HCC
• screening CT
• chronic Hep C
• isodense on
NC + PVP
NC
HAP
PVP
HAP
Simplified Approach to Liver
Hemodynamics
increased dysplasia = more arterial, less portal
100
% arterial supply
80
% 60
40
20
0
% venous supply
Normal
RN
Dysplastic
Nodule
Well-diff
HCC
Mod-diff
HCC
NC
HCC moderately differentiated
• best on HAP
• “washes out” on PVP
HAP
PVP
HCC
- only or best seen on HAP
NC
HCC with capsule
HAP
PVP
HAP
HCC well-differentiated
• best on PVP
PVP
HCC Mod Differentiated
• Best on HAP
Small HCC
• only seen on HAP & MR
HAP
PVP
T1 NC
T1 PVP
T1 HAP
T2 WI
Small
HCC
HCC
• small tumor
• PV invasion
Tumor Thrombus:
•Contiguity w tumor
•Expansion of lumen
•Enhancing thrombus
HCC: Other Features
Focal fat
Calcifications
NECT
NECT
HAP
Lesion with
Focal fat in cirrhotic liver
= HCC
PVP
Nodular Lesions in Cirrhosis
CT
NC
Regenerative
Nodule
 or 
Dysplastic
Nodule
 or 
HAP
MR
PVP
Delay
 or 
Well-diff
HCC
 or   or 
Mod-diff
HCC
 or   or   or 

T1
HAP
PVP
T2
 or 
 or 
 or   or 
 or 

 or   or   or 


 or 

= not seen (isodense, isointense)
 = hyperdense (-intense) to liver
 = hypointense (-intense) to liver

 or 
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
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
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
HAP
Lobar “THAD”
• HCC obstructing RPV
PVP
PVP
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 Cirrhosis
Early draining vein
Small AP shunts are common, often resolve
Don’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)
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: 743-749
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