RSNA_ESRLiverOncologyX2011

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Essentials in Oncologic Imaging What Radiologists Need to Know Liver: Primary, Metastases Richard Baron, M.D. University of Chicago

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oncology

Transcript of RSNA_ESRLiverOncologyX2011

Essentials in Oncologic ImagingWhat Radiologists Need to Know

Liver: Primary, Metastases

Richard Baron, M.D.University of Chicago

Liver Malignancies• Primary

– Hepatocellular Carcinoma (~85 – 90%)– Cholangiocarcinoma (~5 – 10%)– Rare tumors (Angiosarcoma, Lymphoma, Epithelioid

Hemangioendothelioma, others)

• Metastases

HCC without cirrhosis

Mosaic and capsuleMosaic and capsuleMosaic and capsule

HCC in Cirrhosis

• 10 – 14% of advanced cirrhosis harbors HCC• 25% of Hepatitis B/C patients develop HCC within

10 years• Compare to risk of colon cancer in 50 y.o.:

< 1% prevalence, 7% lifetime incidence

Patients %HCC

Alcohol 86 10%B Hepatitis 22 27%C Hepatitis 99 22%B/C Hepatitis 22 18%C Hep/Alcohol 22 18%PBC 47 2%PSC 31 0%Other 99 8%

430 14% 59 pts

Screening Cirrhosis: 1329 patientsPeterson et al, Radiology, 2000

Patients %HCC

Alcohol 86 10%B Hepatitis 22 27%C Hepatitis 99 22%B/C Hepatitis 22 18%C Hep/Alcohol 22 18%PBC 47 2%PSC 31 0%Other 99 8%

430 14% 59 pts

Screening Cirrhosis: 1329 patientsPeterson et al, Radiology, 2000

Pathogenesis of HCC:Key Role of Dysplastic Nodules

• Regenerative Nodule

• Large Regenerative Nodule

• Dysplastic Nodule

• HCC

• HCC (nodule-in-nodule)

Dysplastic Nodules: MR

CT: ~ 10% Lim et al, BJR 2004

MR: 10 – 15% Krinsky, Radiology 2001

CT: ~ 10% Lim et al, BJR 2004

MR: 10 – 15% Krinsky, Radiology 2001

Dysplastic Nodules:Low Grade

- Nuclear atypia is minimal- Portal tracts present

High Grade- High nuclear cytoplasmic ratio- Rare mitotic figures- Resistance to iron accumulation-New vessels (nontriadal arteries) increase -Portal flow to nodules decreases

HCCAP

PV

HCC: DetectionPatientDetection

LesionDetection Study

CT 67 – 73% 35% Peterson, 2000

MR 77% 37% Krinsky, 2001

MRDual Contrast

91% Bhartia, 2003

US ~ 50% ~ 35% multiple

48 y.o. male, chronic hepatitis C Solitary 2.5 cm lesion

APAPAP PVPVPV EQEQEQ

A. Biopsy LesionB. Confirm with MR examC. Make Rx plans as HCCD. F/U imaging in 3 - 6 mos.

What would be next best stepTo plan appropriate treatment?

HCC Dx: 2005 AASLD CRITERIA

> 20 mm Liver Lesion, chronic liver diseaseOne imaging technique with typical HCC

(AP hypervascularity & EQ washout)One imaging technique showing a mass with

AFP levels > 200 ng/ml

10-20 mm Two imaging techniques with typical HCC (AP hypervascularity & washout

< 10 mm Repeat US every 3-6 months for 2 yrs

American Association for the Study of Liver Diseases (AASLD) Practice Guideline. Hepatology 2005;42:1208

APAP

PVPV

EQ

> 10 mm Liver Lesion, chronic liver diseaseOne imaging technique with typical HCC

(AP hypervascularity & EQ washout)

< 10 mmRepeat US every 3-6 months for 2 years

American Association for the Study of Liver Diseases (AASLD) Practice Guideline. Bruix and Sherman. Hepatology 2010

APAP

PVPV

EQ

HCC Dx: 2010 AASLD CRITERIA

Why is non biopsy Dx important?2009

2011

01/22/2008 Value of Equilibrium Phase CT

10/30/2007

Pre Early arterial Late arterial Portal Equilibrium

Courtesy of M. Hori , Osaka

‘Peliotic HCC’

AP AP PV

PV EQ

T1

T2 2 hr

AP PV EQ

• O’Malley et al (Am J. Gastro 2005): 28% HCC

– Doubling time – 6 mos.

• Jeong et al (AJR, 2002): 13% HCC

• Most small enhancing nodules are not HCC

• Delay, washout characteristics helpful in characterizing

• Multimodality imaging & Follow-up imaging essential

Small (10-20 mm) Enhancing CT/MR Nodules

HCC: MRI signal intensities

AP EQ Delay T1 T2 DWI

Enhancing Nodule: Value of T2 characteristics

AP EQ

“Nodule in

Nodule”Evolution

OP T1 F/U OP T1

IP T1 OP T1

2007 f/u 2007

2008

Evolution Dysplastic Nodule to HCC2005

T2 T1

2006 2007

Hypovascular Nodules

10 – 15% of small HCC are hypovascular

60% of small hypoattenuating nodules transformed to enhancing vascular lesions(Takayasu et al, AJR, 2006)

APAPAP

AP

PVPV

EQEQ

PV

EQ

2008

2009

Diagnosis of Small NodulesForner et al, Hepatology, 2007

Serially followed cirrhotic patients for 3 yrs

89 patients developed NEW nodule60 HCC, 1 cholangiocarcinoma28 benign nodules (regenerative/dysplastic predominate)

24/89 nodules = hypovascular (only 2/24 = HCC)

STAGING HCC: TNM basedT1 Solitary TumorT2 Solitary Tumor with microvascular invasion,

OR multiple tumor (< 3 cm); T3 Multiple tumors > 3cm,

OR tumor involving a major venous branchT4 Tumor(s) with direct invasion of

adjacent organs other than gallbladder

N1 Regional lymph node metastasisM1 Distant Metastasis

STAGING HCC: TNM based

I T1 N0 M0II T2 N0 M0IIIA T3 N0 M0IIIB T4 N0 M0IIIC Any T N1 M0IV Any T Any N M1

Solitary Tumor

Multiple tumor (< 3 cm);

Extrahepatic HCC: 148 of 403 patients (37%)

Lungs 55%Lymph Nodes 53%

Regional 41%Distant 12%

Bone 28%Adrenal 11%Peritoneum 11%Brain 2%All other sites 7%

Ferris et al, Radiology, 2000

48 y.o. male, chronic hepatitis C 3 lesions; Largest = 3 cm

APAP PVPV EQEQAP PV EQ

A. Biopsy largest lesionB. F/U in 3 mos to show stabilityC. Proceed to transplantation list

without further stepsD. Patient is not candidate for

transplantation

To evaluate for possible liver transplantation, which is next best step ?

Liver Transplantation• UNOS HCC MELD score upgrade to

22 (15% mortality in 3 mos)

• Milan criteria:– Single tumor 2 – 5.0 cm

– Multifocal tumor (3 nodules, <3 cm each)

– No extrahepatic spread or macrovascular invasion

Mazzaferro et al. N Engl J Med 1996;334:693-699.

False Positive CT DiagnosisHYPERVASCULAR

Reg/Dysplastic NodulesFocal FibrosisPeliosisA-P Shunting/THAD

HYPOVASCULAR

Focal FibrosisReg Nodules (and

infarcted nodules)Fibrosed Hemangiomas

False Positive CT DiagnosisHYPERVASCULAR

Reg/Dysplastic NodulesFocal FibrosisPeliosisA-P Shunting/THAD

HYPOVASCULAR

Focal FibrosisReg Nodules (and

infarcted nodules)Fibrosed Hemangiomas

Summary of key issues in HCC

• Very common in chronic liver disease

• Detection difficult despite claims in literature

• US/CT/MRI can all be used as screening tools, but require optimizing techniques

• Liver transplantation often only real cure option

• Radiology assessment/reports are critical to determining patient treatment options

• Wording, number and exact size of lesions (to decimal point) in radiology reports have dramatic impact on care

A. Contrast washout key to diagnosisB. Most lesions show homogeneous

retention of contrast material C. Usually vascular lesions with

marked arterial enhancementD. Can range from near water density

to densely solid lesions

In imaging Hepatic Cholangiocarcinoma, which of the following is true?

Cholangiocarcinoma• Gross pathologic structure

– Annular, constricting– Infiltrative and expanding– Intraluminal, polypoid

• Underlying histologic stroma– Fibrous versus glandular stroma

• Locations– Intrahepatic, Proximal CBD, Distal

• Associations: PSC, Choledochal cysts; infections, chemical toxins

~ 10%Intrahepatic

Spectrum of Cholangiocarcinoma Pathology

Fibrous Stroma Glandular Stroma

Mixed Stroma

Cholangiocarcinoma: Fibrous Stroma

+C EQ

+C EQ

Cholangiocarcinoma: Glandular Stroma

Cholangiocarcinoma: Contrast Enhancement

STAGING Chol CA: TNM basedT1 Solitary TumorT2 Solitary Tumor with microvascular invasion,

OR multiple tumor (< 5 cm); T3 Multiple tumors > 5cm,

OR tumor involving a major venous branchT4 Tumor(s) with direct invasion of

adjacent organs other than gallbladder

N1 Regional lymph node metastasisM1 Distant Metastasis

Treatment and Staging Impact

Surgery is only cure possibility

Imaging role preparing for resection:

Exclude AdenoCa metastasis from unknown primary

Poor prognosis: Multiple nodules; bi-lobar disease; vascular invasion; positive lymph nodes

Difficult surgery: Central lesions; chronic liver disease

Surgery offered to potentially resectable patients regardless of stage

Value of Delay Equilibrium Phase

Liver Metastases

• Most common liver malignancy• Generally variable, noncharacteristic features

Does not meet classic benign dx (cyst, hemangioma, or FNH) with known primary tumor

• Site of origin can occasionally be suggested

Liver Metastases

• Hypovascular (colon, lung, pancreas, many others)• Hypervascular (renal, islet cell, breast, thyroid, sarcomas)• Ca++ in mucinous tumors (colon, ovary)• Change over time in appropriate setting

Significance of Small (<1.0 – 1.5 cm) Hepatic Lesions

2,978 Cancer Patients378 Small Lesions44 Considered Metastases on Follow-Up

Schwartz et al., Radiology, 1999

Recon thickness 10 mm 7.5 mm 5.0 mm 2.5 mm

No. Lesions 90 112 137 167

Weg, et. al., Radiology, 1998

58 year old breast cancer patient

T2CT Gd

Biliary Hamartomas

Colon CaColon CaColon Ca Islet Cell CaIslet Cell CaIslet Cell Ca

EQ

DWIAP

AP

Liver Specific Contrast Agents

DWI

T1

T2

+C EQPV Gd

Carcinoid Metastasis

T2 AP PV EQ

Prior CTPrior CTPrior CT F/U CTF/U CTF/U CT

Cystic Metastases

Key findings:− thick, irregular rind−mural nodule− fluid-debris level

Sarcomas (and GIST)Mucin Producing Tumors

Ovarian, colon, mucinous pancreasPost Treatment Necrosis

GIST Mets

GIST

6 month follow-up

Choi Criteria: GISTJ. Clin Oncol 2007; 25:1753-1759

Complete Response

Disappearance of all lesionsNo new lesions

PartialResponse

Size of 10% OR tumor density > 15% on CT

StableDisease

Size of < 30% or of < 20%

ProgressiveDisease

> 20% increase in sum of target lesions diameters

Liver Tumors: Practical Summary• Understanding the clinical setting is essential

– Chronic Liver Disease– Presence of other primary tumor and type

• Optimizing imaging and contrast techniques– Vary with underlying type of tumor suspected

• Regular communications and interactions with oncologists/hepatologists/surgeons is essential