Detection of liver masses * arterial phase imaging * portal venous phase * equilibrium phase.

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Transcript of Detection of liver masses * arterial phase imaging * portal venous phase * equilibrium phase.

Detection of liver massesDetection of liver masses

* arterial phase imaging

* portal venous phase

* equilibrium phase

Characterization of liver massesCharacterization of liver masses

• Hypervascular lesions• Hypovascular lesions• Scar• Capsule • Calcification• Fat • Hemorrhage• Cystic components• Retraction of liver capsule• Peripheral enhancement & progressive fill in

• Minority of tumors contain calcifications , cystic components, fat or hemorrhage and will be detected on NECT.

• When we give IV contrast, it is important to understand that there is a dual blood supply to the liver.

• Normal parenchyma is supplied for 80% by PV & only for 20% by hepatic artery, so it will enhance in the portal venous phase.

• All liver tumors however get 100% of their blood supply from hepatic artery , so when they enhance it will be in arterial phase

• Small HCC in cirrhotic liver , not visible on NECT , clearly visible in arterial phase, and not visible in portal venous phase.

• In the arterial phase hypervascular tumors will enhance via the hepatic artery , when normal liver parenchyma does not yet enhances , because contrast is not yet in the portal venous system.

• These hypervascular tumors will be visible as hyperdense lesions in a relatively hypodense liver

• However when the surrounding liver parenchyma starts to enhance in the portal venous phase , these hypervascular lesions may become obscured.

• In the portal venous phase hypovascular tumors are detected when the normal liver parenchyma enhances maximally.

• These hypovascular tumors will be visible as hypodense lesions in a relatively hyperdense liver.

• In the equilibrium phase at about 10 minutes after contrast injection , tumors become visible, that either loose their contrast slower than the normal liver , or wash out their contrast faster than normal liver parenchyma. These lesions will become either relatively hyperdense or hypodense to the normal liver

• Above: arterial phase showing hypervascular FNH

• Middle: portal venous phase showing hypovascular metastases

• Down: equilibrium phase showing relatively dense cholangiocarcinoma

Arterial phase imagingArterial phase imaging

• Optimal timing and speed of contrast injection and type of CT scanner are very important for good arterial phase imaging.

Optimal timingOptimal timing

• Hypervascular tumors will enhance optimally at 35 seconds after contrast injection (late arterial phase)

• A patient who underwent two phases of arterial imaging at 18 and 35 seconds .

• In the early arterial phase we nicely see the arteries , but we only see some irregular enhancement within the liver .

• In the late arterial phase, we can clearly identify multiple tumor masses.

• Notice that in the late arterial phase, there has to be some enhancement of the portal vein .

• The only time that an arterial phase is needed is when you need an arteriogram , for instance as a roadmap for chemoembolization of a liver tumor.

Speed of contrast injectionSpeed of contrast injection

For arterial phase the best results are with an injection of 5 ml/sec

• Patient with liver cirrhosis and multifocal HCC injected at 2.5 ml/sec and at 5 ml/sec.

• At 5 ml/sec. there is far better contrast enhancement and better tumor detection.

Type of CT scannerType of CT scanner

• If you have a single slice scanner , it will take about 20 seconds to scan the liver.

• For late arterial phase imaging 35 sec. is the optimal time , so you start at about 25 seconds and end at about 45 seconds.

• However if you have 64 multislice scanner , you will be able to examine the whole liver in 4 seconds , so you start scanning at about 33 seconds.

Hepatic VenousPortal Venous

Tripple Phase Helical CTTripple Phase Helical CT

Foley, WD. Multiphase Hepatic CT with a Multirow Detector CT Scanner. 2000 (175): 679-685.

Axial C+ CT Arterial Phase

Axial C+ CT Portal Venous

Phase

Axial C+ CT Hepatic Venous

Phase

Contrast Injection

Arterial

0 15 30 45 60 75Time (sec)

Portal venous phasePortal venous phase

• Portal venous phase imaging work on the opposite idea . We image the liver when it is loaded with contrast through the portal vein to detect hypovascular tumors.

• The best moment to start scanning is at about 75 sec.,so this is a late portal phase , because enhancement of portal vein already starts at 35 sec in the late arterial phase.

• Late portal venous phase is also known as hepatic phase because there already must be enhancement of hepatic veins . If you don’t see enhancement of hepatic veins , you are too early.

• Hypovascular metastases seen as hypodense lesions in late portal venous phase

Liver metastases Liver metastases cancer coloncancer colon

Equilibrium phaseEquilibrium phase

• Starts when contrast is moving away from the liver and the liver starts to decrease in density .

• This phase begins at about 3-4 minutes after contrast injection and imaging is best done at 10 minutes after contrast injection.

• This phase can be valuable if you are looking for:

1- fast tumor washout in hypervascular tumors

2- retention of contrast in blood pool like in hemangioma

3- retention of contrast in fibrous tissue in capsule ( HCC )or scar tissue ( cholangiocarcinoma or FNH )

• 1- fast tumor washout in hypervascular tumors like HCC

• 2- retention of contrast in the blood pool as in hemangioma

• 3- retention of contrast in fibrous tissue in capsule ( HCC ) or scar tissue (cholangiocarcinoma , FNH)

Relative hyperdense lesions in Relative hyperdense lesions in the delayed phasethe delayed phase

• Fibrous tissue that’s well organized and dense is very slow to let iodine or gadolinium in.

• Once contrast gets in however, it is equally slow to get back out in the equilibrium phase.

• So when the normal liver parenchyma washes out, the fibrous component of the tumor will look brighter than the background liver tissue.

• Small cholangiocarcinoma not visible in portal venous phase , but seen as relative hyperdense lesion in the equilibrium phase.

Relative hypodense lesions in Relative hypodense lesions in delayed phasedelayed phase

• In the delayed phase, malignant tumors ( like HCC ) , the tumor is washed out more than the surrounding liver parenchyma .

• But benign tumors typically will not show this kind of wash out , but will stay isodense with liver parenchyma or some times more dense, in the equilibrium phase.

• These benign lesions don’t have enough neoplastic neovascularity to have a fast wash out.

• HCC in a cirrhotic liver. Notice fast wash out in equilibrium phase compared to surrounding liver parenchyma.

Blood pool and hemangiomaBlood pool and hemangioma

• Normally when we look at lesions filling with contrast, the density of these lesions is always compared to the density of the liver parenchyma.

• In hemangiomas, however you should not compare the density of the lesion to the liver but to the bloodpool

• This means that the areas of enhancement in a hemangioma should match the attenuation of the appropriate vessels { bloodpool } at all times.

• So, in the arterial phase the enhancing parts of the lesion must have almost the same attenuation value as the enhancing aorta.

• While in the portal phase, it must match the attenuation value of the portal vein . And so in venous or delayed phase.

• So, if it does not match the bloodpool in every single phase of contrast enhancement FOREGET the diagnosis of a hemangioma.

• Hemangioma in non-enhanced CT, late arterial, late portal venous, and equilibrium phase. Notice that the attenuation of the hemangioma matches the bloodpool in every single phase.

• Flash filling hemangioma in unenhanced, arterial & portal venous phase . Notice it matches the bloodpool.

Incidental hyper vascular lesionsIncidental hyper vascular lesions

• Hemangioma

• Focal nodular hyperplasia ( FNH )

• Adenoma

• Hepatocellular carcinoma ( HCC )

• Fibrolamellar hepatocellular carcinoma

• Hypervascular mtastases

• It is important to differentiate between “touch” and “don’t touch” lesions.

• Benign “don’t touch” hypervascular tumors include hemangioma, FNH, small adenoma.

• “touch lesions” iclude large adenoma ( more than 5 cm ) and malignant tumors like HCC , fibrolamellar HCC and metastases.

Benign hypervascularBenign hypervascular lesionslesions

Hemangioma Hemangioma

Hemangioma Hemangioma

• Bloodpool and hemangioma

• Normally when we look at lesions filling with contrast, the density of these lesions is always compared to the density of the liver parenchyma.

• In hemangiomas, however you should not compare the density of the lesion to the liver but to the bloodpool

• This means that the areas of enhancement in a hemangioma should match the attenuation of the appropriate vessels { bloodpool } at all times.

• So, in the arterial phase the enhancing parts of the lesion must have almost the same attenuation value as the enhancing aorta.

• While in the portal phase, it must match the attenuation value of the portal vein . And so in venous or delayed phase.

• So, if it does not match the bloodpool in every single phase of contrast enhancement , foreget the diagnosis of a hemangioma.

• Hemangioma in non-enhanced CT, late arterial, late portal venous, and equilibrium phase. Notice that the attenuation of the hemangioma matches the bloodpool in every single phase.

• Hemangiomas less than 1 cm frequently demonstrate immediate homogenous enhancement , isodense to aorta.

• Hemangiomas larger than 1 cm generally show slow centripetal spread of nodular enhancement

• Flash filling hemangioma in unenhanced, arterial & portal venous phase . Notice it matches the bloodpool.

• Giant hemangioma with scar tissue. Notice that the enhancement matches the bloodpool in all phases, central scar is hypodense on NECT & stays hypodense.

Progressive fill inProgressive fill in• The lesion definitely has some

features of hemangioma like nodular enhancement in the arterial phase & progressive fill in portal venous & equilibrium phase.

• In portal venous phase however the enhancement is not as bright as the enhancement of portal vein . The conclusion must be that this lesion doesn’t match blood pool in all phases , so it can’t be hemangioma.

• So progressive fill in is a non-specific feature of that can be seen in many other tumors like metastases or cholangiocarcinoma.

• The delayed enhancement in this lesion is due to fibrotic tissue in a cholangiocarcinoma & is a specific feature of this tumor

Rim enhancementRim enhancement

• The enhancement of a hemangioma starts peripheral. It is nodular or globular & discontinuous.

• Rim enhancement is continuous peripheral enhancement is never hemangioma.

• Rim enhancement is a feature of malignant lesions , especially metastases.

• Left: rim enhancement in breast carcinoma

• Right: nodular discontinuous enhancement in hemangioma

Atypical hemangiomaAtypical hemangioma

Hemangioma on USHemangioma on US

• Hemangioma on dynamic MRI will show the same enhancement characteristics as on contrast enhanced CT

Focal nodular hyperplasiaFocal nodular hyperplasiaFNHFNH

• Non-neoplastic, hyperplastic response to a congenital vascular malformation.

• At late arterial phase, FNH typically presents with bright homogenous enhancement , but less intense than the aorta with a hypodense central scar.

• Smaller (<3cm) FNH , often lack a central scar.

• At portal phase, FNH is often isoattenuating to the normal liver and may be difficult to delineate.

• Delayed phase often shows hyperattenuation of central scar due to late opacification of fibrous components ( or due to the AVM scar )

• No calcification, inhomogenity or capsule should be seen in FNH

• Best diagnostic clue: brightly and homogeneously enhancing mass in arterial phase on CT or MRI with delayed enhancement of the central scar.

• Central scar containing AVM

• Central scar seen in 2/3 of large and 1/3 of smal FNH.

• No malignant transformation

• No association with oral contraceptives.

• Nuclear study: normal or increase uptake {only FNH contains kuffer cells that cause increase uptake in 9% of cases }…….pathognomonic

• Classic FNH looks like a cross section of an orange ( central scar, radiating septa )

Hemangioma & FNHHemangioma & FNH

• FNH seen as hypervascular lesion in the late arterial phase & isodense in the portal venous phase . No scar was seen.

• T2W, T1W without gadolinium and a delayed phase after gadolinium.

AdenomaAdenoma

• Best diagnostic clue: spherical well defined hypervascular and heterogenous mass due to fat & hemorrhage .

• Symptomatic in 80%-abdominal pain- ( FNH asymptomatic in 80%)

• 98% in yoyung females taking oral contraceptives

• Not seen in males unless on anabolic steroids or with glycogen storage disease.

• Adenoma showing capsule in delayed phase

• Female with acute abdominal pain

• On portal phase, hypodense hepatic lesion with hemorrhage adjacent to it, extending subcapsularly.

• Fat in adenoma

• Hemorrhage in adenoma

Malignant hypervascular Malignant hypervascular lesionslesions

Hepatocellular carcinomaHepatocellular carcinomaHCCHCC

• Any hypervascular lesion in a cirrhotic liver is hepatocellular carcinoma untill proven otherwise.

• HCC may be solitary, multifocal or diffusely infiltrating.

• Large HCC typically have a mosaic appearance due to hemorrhage & fibrosis.

• HCC is a silent tumor, so if patients don’t have cirrhosis or hepatitis C , you will discover them in a late stage.

• They tend to be large with mozaic pattern , a capsule , hemorrhage and necrosis.

• HCC become isodense or hypodense to liver in the portal venous phase due to fast wash-out

• On delayed images, the capsule and sometimes septa demonstrate prolonged enhancement.

• Large HCC with mozaic pattern in a non cirrhotic liver

• Cirrhotic liver with hypervascular , inhomogenous lesion.

• The inhomogenous enhancement and partial capsule are helpful for the diagnosis of HCC

• Small HCC in cirrhotic liver not visible on NECT , clearly visible on arterial phase, and not visible in portal venous phase

• HCC in cirrhotic liver , notice fast wash out in equilibrium phase compared to surrounding liver parenchyma

PS: Triple Phase CTPS: Triple Phase CTAxial C- CT Axial C+ CT: Arterial Phase

Nodular liver

No discrete lesions

Film Findings: EarlyEarly hyperenhancinghyperenhancing lesionlesion

PS: Triple Phase CTPS: Triple Phase CT

Axial C+ CT: Portal Venous Phase Axial C+ CT: Delayed Phase

Quick washout of enhancing lesion

Film Findings: Hypoenhancing lesion with Hypoenhancing lesion with peripheral rim of enhancementperipheral rim of enhancement

????

• In the arterial phase we see two hypervascular lesions. Now do not just concentrate on the images, where you see the lesions best. You have to look at all the other images, because they give you the clue to the diagnosis. The upper images show a lesion that is isodens to the liver on the NECT. In the arterial phase there is enhancement, but not as dense as the bloodpool. In the portal venous phase the lesion is again isodense to the surrounding liver parenchyma and you can't see it. If you only had the portal venous phase you surely would miss this lesion. The lower images show a lesion that is visible on all images. You see it on the NECT and you could say it is hypodens compared to the liver. Does this help you? No, not in the least. However if you look at the bloodpool, you will notice that on all phases it is as dense as the bloodpool. So we have a HCC in the right lobe on the upper images and a hemangioma in the left lobe on the lower images. The key is to look at all the phases.

HCC & PV thrombosisHCC & PV thrombosis

Many patients with cirrhosis have portal venous thrombosis and many patients with HCC have thrombosis. These are two common findings and they can be coincidental. It is very important to make the distinction between just thrombus and tumor thrombus. First, if you have a malignant thrombus in the portal vein, it will always enhance and you'll see it best in arterial phase. Secondly, if you have a malignant thrombus in the portal vein, it will increase the diameter of the vessel. Sometimes a tumor thrombus may present with neovascularity within the thrombus .

• Above : diffusely enhancing tumor thrombus in HCC with portal venous thrombosis.

• Down: tumor thrombus with vessels within the thrombus

Fibrolamellar HCCFibrolamellar HCC

• Large hpervascular , heterogenously enhancing,lobulated mass in a normal, non-cirrhotic liver in young adult

• Central fibrotic scar in 60%

• Calcification in 70% of cases

• Normal alpha fetoprotein (increased in HCC)

• Non enhanced image , a fibrolamaellar HCC usually presents as a big mass with central calcification.

• FLC in late arterial phase , central calcification & heterogenous enhancement .

• Delayed phase with hypodense central scar

Hypervascular Hypervascular metastasesmetastases

Characteritics of hypervascular Characteritics of hypervascular metastasesmetastases

-a hyper vascular 1ry tumor like renal cell carcinoma, endocrine tumors( thyroid-islet cell – carcinoid) & some breast carcinoma

-often co-existing hypo and hypervascular metastases.

-larger lesions are often inhomogenous due to central necrosis.

Hypervascular metastasis Hypervascular metastasis

• Renal cell carcinoma• Islet cell tumors of pancreas• Thyroid carcinoma• Carcinoid • Malignant melanoma• Choriocarcinoma• Pheochromocytoma • 15 % of cancer breast

• Hypervascular metastases with typical peripheral enhancement

• Peripheral enhancement in metastases from breast carcinoma

Hypervascular metastasesHypervascular metastases

Hypervascular metastases Hypervascular metastases cancercancer breastbreast

Characterization of liver Characterization of liver massesmasses

• Scar

• Calcification

• Capsule

• Fat

• Blood

• Retraction of liver capsule

ScarScar

• Focal nodular hyperplasia …… AVM

• Fibrolamellar HCC ……………Fibrous tissue

• Cavernous hemangioma …….. Fluid• HCC• cholangiocarcinoma

Focal nodular hyperplasiaFocal nodular hyperplasia

Fibrolamellar HCCFibrolamellar HCC

HemangiomaHemangioma

Calcification Calcification

• Metastases

• Fibrolamellar HCC• Cholangiocarcinoma• hemangioma

Calcified mestastases Calcified mestastases ca ovaryca ovary

Calcified metastasesCalcified metastases

Fibrolamellar HCCFibrolamellar HCC

Capsule Capsule

• Hepatocellular carcinoma “ HCC “

• Adenoma • Biliary cystadenoma

HCCHCC

Adenoma Adenoma

Fat Fat

• Adenoma• HCC• Metastatic liposarcoma

• Angiomyolipoma

Adenoma Adenoma

Blood Blood

• HCC

• Adenoma

HCCHCC

Adenoma Adenoma

Retraction of liver capsuleRetraction of liver capsule

• Cholangiocarcinoma

• Breast cancer metastases

CholangiocarcinomaCholangiocarcinoma

Cancer breast metastasesCancer breast metastases

Hepatic CystHepatic Cyst

http://bb.westernu.edu/web/Pathology/webpath60/webpath/radiol/heparad/

Axial C+ CT

Film Findings:

Sharply demarcated, non enhancing, water-dense cyst.

Focal Nodular HyperplasiaFocal Nodular Hyperplasia

Axial C+ CT

Film Findings:

Enhancing lesion with central filling defect (central scar)

http://uuhsc.utah.edu/rad/medstud/BodyCaseStudies/BodyCase6a.htm

Hepatocellular AdenomaHepatocellular Adenoma

Axial C+ CT

Film Findings:

Multiple hypoenhancing heterogenous lesions

Enhancing hepatic veinsEnhancing hepatic veins

UpToDate: Hepatic Adenoma

HCC: MR ImagingHCC: MR Imaging

Axial T1 Weighted MR Precontrast

Axial T1 Weighted MR Arterial Phase

Axial T1 Weighted MR Portal-phase

• Variable intensity on T1 and T2 weighted imaging• Early arterial phase enhancement• Quick washout• Rim enhancement of fibrous capsule in portal/delayed

phases

Liver Metastasis (Colonic Liver Metastasis (Colonic Adenocarcinoma)Adenocarcinoma)

Axial C+ CT

Film Findings:

Multiple hypoenhancing heterogenous lesions

http://www.mypacs.net/repos/mpv3_repo/viz/full/11724/586248.jpg

Liver AbscessLiver Abscess

Axial C+ CT

Film Findings:

Well demaracated hypoenhancing lesion

Rim of increased Rim of increased enhancement relative to enhancement relative to central regioncentral region

http://www.e-radiography.net/ibase5/Hepatic/index.htm

• A Walk Through The Differential A Walk Through The Differential Diagnoses:Diagnoses:

Early arterial enhancement, fast washout, delayed fibrous capsule enhancement

Hepatocellular Carcinoma (HCC)

Mostly multiple low attenuation lesions, rim enhancement without “filling in”

Metastasis

Variable, central changes due to hemorrhage often seen

Hepatocellular

Adenoma

Early filling in arterial phase with central filling defect (scar)

Focal Nodular Hyperplasia (FNH)

Peripheral filling in of contrast over time

“Light Bulb Sign” on T2 MRI

Hemangioma

Sharply demarcated wall, water density, non-enhancing

Hepatic Cyst

PSClassical CT FindingsLesions

AbscessWell demarcated hypodense areas with peripheral enhancement, may see gas

ReferencesReferences

• The frequency and significance of small (less than or equal to 15 mm) hepatic lesions detected by CT EC Jones, JL Chezmar, RC Nelson and ME Bernardino Department of Radiology, Emory University School of Medicine, Atlanta, GA 30322. American Journal of Roentgenology, Vol 158, 535-539,

• Prevalence and Importance of Small Hepatic Lesions Found at CT in Patients with Cancer Lawrence H. Schwartz, MD, Eric J. Gandras, MD, Sandra M. Colangelo, MD, Matthew C. Ercolani, BS and David M. Panicek, MDRadiology. 1999;210:71-74.

• Small 'indeterminate' lesions on CT of the liver: a follow-up study of stability P J Robinson, MB, FRCP, FRCR, P Arnold, BSc and D Wilson, MScClinical Radiology Research Unit and Medical Physics Department, St James's University Hospital, Beckett Street, Leeds LS9 7TF, UKBritish Journal of Radiology (2003) 76, 866-874

• Small hypoattenuating hepatic lesions at Contrast-enhanced CT: Prognostic importance in patients with breast cancer. George A. Krakora, MD et alRadiology 2004; 233:667-673

• Benign hepatic tumours and tumour like conditions in men. by Karhunen PJ.J Clin Pathol. 1986 Feb;39(2):183-8.

• Introduction. In: Tumors of the liver and intrahepatic bile ducts. Page1-7. Atlas of tumor pathology, AFIP, Washington DC, 1988.

by Robert L. Craig • Fibrolamellar Hepatocellular Carcinoma: Imaging and Pathologic Findings in

31 Recent Cases Tomoaki Ichikawa, MD, Michael P. Federle, MD, Luigi Grazioli, MD, Juan Madariaga, MD, Michael Nalesnik, MD and Wallis Marsh, MDRadiology. 1999;213:352-361.