Sanyal assessment of a liver mass - American College of...
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Assessment of a Liver Mass: What do you need to knowy
Arun J Sanyal, M.B.B.S., M.D.
Charles Caravati Professor of Medicine
Vi i i C lth U i itVirginia Commonwealth University
CONFLICTS: US PI for Gideon Trial sponsored by Bayer
What to do with a liver mass?
• What could it be?– differential diagnosis varies based on whether d e e t a d ag os s a es based o et e
cirrhosis is present• Which diagnoses are particularly lethal if
missed?– hepatocellular and other cancers– non-malignant lesions that can bleed
• What are you going to do when you find it?– curative therapies for liver cancer– resection for high risk lesions for bleed– stop birth control pills for specific lesions
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Differential diagnosis of liver mass
• Cirrhosis presentHepatocellular CA– Hepatocellular CA
– Dysplastic nodules
– Regenerative nodules
– Cholangiocarcinoma
– Scar tissue
– HemangiomaHemangioma
– Other lesions commonly seen in non-cirrhotic liver
Clinical considerations in the diagnosis of a liver mass in cirrhosis
• Is cirrhosis present?H/O chronic liver
• Risk factors for HCC:Age– H/O chronic liver
disease
– Evidence of underlying chronic liver disease e.g. elevated liver enzymes
F t f i h i
– Age
– Male gender
– Alcohol + other liver disease
– Insulin resistance
– Obesity– Features of cirrhosis:
• Low platelets
• Synthetic dysfunction
• Features of portal HTN
y
– Diabetes
– Elevated AFP
– HVPG > 10 mm Hg
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Evaluation of a liver mass
CIRRHOSIS
PRESENT ABSENT
> 2 CM 1-2 CM < 1 CM
Imaging features used to diagnose HCC
• Presence of a visible mass with or without involvement of blood vessels etc
• Changes seen over time after injection of an intravenous contrast agent
• Tissue characteristics based on its content
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Size matters
Type of lesion Mean sizeType of lesion Mean size (cm)
Regenerative nodule
Low grade dysplastic nodule
High grade dysplastic nodule
Well differentiated HCC
< 1
1
1.3
1 6Well differentiated HCC
Classic HCC
1.6
2.2
Matsui O. Clin Gastroenterol Hepatol 2005;3:S136–S140
Natural history of HCC development
Matsui et al, Clin Gastroenterol Hepatol 2005;3:S136-S140
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Phases of blood flow in the liver
Arterialpeak Venousliver
peak
washout
Pre-contrast
Portalvein
0 5-20 60-90 200-300
seconds
Hepaticartery
Hepatocellular cancer
Hepatic artery and portal vein supply lost
Arterial neovascularization
Early enhancement
Washout in venous/delayed phase
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Regenerative nodule
Main blood supply from portal vein
Mild arterial enhancement
Strong venous enhancement
HCC: CT scan imaging
Pre-contrast arterial venous
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Additional MRI features of HCC
Variable intensity on T1-image Hyperintensity on T2-image
Diffuse hepatocellular cancer
Bright lesion in T2 weighted image Arterial enhancement with malignantPortal vein thrombosis
Willat, et al. Radiology 2008;247:311-330
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Confluent scar vs tumor:progressive enhancement in scar
Imaging criteria for diagnosis of HCC
Finding Sensitivity Specificity
Arterial enhancement
Delayed washout
Delayed enhancing capsule
> 90%
80%
89%
80%
95%
96%
Bright lesion on T2 images
80% 95%
Multiple sources
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Utility of imaging modalities for diagnosis of HCC
Modality Sensitivity SpecificityModality Sensitivity Specificity
Conventional US
Contrast-enhanced US
CT scan
MRI
45-92%
60-90%
68%
81%
40-90%
> 90%
> 95%
> 95%
Multiple sources
ALWAYS ORDER CONTRAST IMAGING WITH TUMOR PROTOCOL
What you need to know about AFP
• Normally produced in the fetus-fetal equivalent of albuminequivalent of albumin
• Elevated levels occurs due to:– Neonatal period– Pregnancy– Pregnancy-related disorders (omphalocele)– Germ cell tumors (testes and ovary)– Hepatocellular carcinoma– Hepatic regenerative activity
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Alternate biomarkers
• AFP-L3 (lectin-bound AFP), descarboxylprothrombin(DCP), glypican-3
• Relevant only when AFP > 10 or < 200
• If AFP-L3 > 10%, then:
– sensitivity: 70%
– specificity: 63%
• If AFP-L3 > 35%, then:
i i i 33%– sensitivity: 33%
– specificity: 100%
Evaluation of a liver mass
CIRRHOSIS
PRESENT ABSENT
> 2 CM 1-2 CM < 1 CM
4 phase CT or MRI
Tumordiagnosed
p
2nd modalityimaging
Biopsy
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Similar findings on two modalities allow HCC diagnosis to be made with high specificity
N= 89Nodules 1 2 cm in size in cirrhotic subjects
Modality sensitivity specificity PPV NPV
CEUS
MRI
CEUS + MRI
62
52
33
96
93
100
97
94
100
55
50
42
Nodules 1-2 cm in size in cirrhotic subjects
Forner, et al, Hepatology 2008;47:97-104
Evaluation of a liver massCIRRHOSIS
PRESENT ABSENT
> 2 CM 1-2 CM < 1 CM
4 phase CT or MRI4 phase CT or MRI
Tumordiagnosed
2nd modalityimaging
Biopsy
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Very early HCC• < 1 cm
• Neo-arterialization absent or incomplete
none or poor arterial enhancement– none or poor arterial enhancement
– non-specific washout
Duct cellsat interface of tumorat interface of tumorare less and replaced by tumor cells
Park et al, Cancer 2007;109:915–923.
Small HCC: diagnosis with MRI
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Super-paramegnetic iron oxide (SPIO)-MRI
Fe is taken up by Kupffer cells and make the liver look darker and making the tumor which lacks Kupffer cells stand out as a bright signal
Macarini, et al. Radiol Med 2009;114:1267–1282
Malignant tumors grow faster than benign tumors
Doubling time
• Malignant tumors: Median doubling time 120-180 days
• Benign tumors: > 1 yr
Taouli, et al. J Comput Assist Tomogr 2005;29:425–429
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Dysplastic nodules
• Isointense on T1 and T2 like regenerative nodules
• Low grade dysplasia: retain portal vein supply
• High grade dysplasia: increasing arterial enhancement and decreased
h tvenous enhancement
• T2 image bright if infarcted
• Nodule within nodule
Benign nodule masquerading as cancer: arterial enhancement without washout
Pre contrast Arterial phase Venous phase Delayed phase
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CT-arteriography for diagnosis of very small or indeterminate nodules
Pattern Findings correlateg
I
II
III
Nodule not seen, arterial and venous supply intact
Nodule hypodense-indicating decrease in arterial supply
Partial Hyperdense area in a nodule (neoarterialization) + loss of portal supply
Low gradeDysplasia
High gradeDysplasia
Early HCC in a nodule
IV
( ) p pp y
Diffusely hyperdense lesion with loss of portal supply
Classic HCC
AASLD guideline for evaluation of HCC
Refer to a transplant center early
Hepatology 2011 Mar;53(3):1020-2
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Differential diagnosis of liver masses when cirrhosis is not present
• In non-cirrhotic liverHemangioma– Hemangioma
– Focal nodular hyperplasia
– Hepatic adenoma
– Nodular regenerative hyperplasia
– Focal fat deposition
– Cystic lesions
– Hepatocellular cancer
Differential diagnosis of incidentalomas
Hemangioma FNH adenoma
Age 30-50 20-40 All ages
Gender
symptoms
US
CT enhancement
MRI
RBC scintiscan uptake
Calcification
F>M
Very rare
Hyperechoic
+++
CSF intensity
yes
Yes
F>>M
Rare
Varied
Central scar
Liver intensity
no
No
F>M*
FNH
Varied
Capsule
Liver intensity
No
NoCalcification
Risk of HCC
Risk of rupture
Yes
No
low
No
No
low
No
Yes
Yes
* Male predominant in glycogen storage diseases (types I and III)Bahirwani and Reddy, Aliment Pharmacol Ther. 2008 Oct 15;28(8):953-65
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Hepatic adenoma
Risk factors for HCC• > 5 cm 5 cm• rising AFP
Bahirwani and Reddy, Aliment Pharmacol Ther 2008 Oct 15;28(8):953-65
Focal nodular hyperplasia
• central scar• takes up biliary contrast
• Tc-colloid uptakepresent due toKupffer cells
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Take home messages
• Clinical assessment:– background likelihood of chronic liver disease– use of birth control pills– symptom status
• Asymptomatic solid solitary masses:– evaluate with CT scan with correct protocol– assess diagnosis, risk of bleeding and cancer
M i i h ti bj t• Masses in cirrhotic subject:– US used mainly for screening– 4 phase CT or MRI for lesion seen on other imaging– worry about HCC and follow AASLD guidelines
THANK YOU FOR YOUR ATTENTION