IMAGING OF HEPATIC TUMOURS

Speaker: Dr Sharma (PG)Moderator: Dr Jatishwor Singh

(HOD)

INTRODUCTION Liver tumors can be divided into

nonneoplastic and neoplastic. They can be either hepatocellular,

cholangiocellular, Mesenchynal or other miscellenous catogory.

The aim of this seminar is to have a overview of hepatic tumours , imaging features and to highlight recent advances in this field.

Embryology of liver The liver primordium (third week)- appear

as outgrowth of the endodermal epithelium at the distal end of the foregut.

The hepatic diverticulum or liver bud, consists of rapidly proliferating cells that penetrate the septum transversum, which forms Hematopoietic cells, Kupffer cells, and connective tissue cells.

Epithelial liver cords intermingle with the vitelline and umbilical veins, which form hepatic sinusoids,parenchyma (liver cells) and lining of the biliary ducts.

FUNCTIONAL SEGMENTAL LIVER ANATOMY

GOLDSMITH &WIIDBURNE

COUINAUD & BISMUTH

CAUDATE CAUDATE 1

LEFT LOBE LEFT LATERALSEGMENT

SUP SUBSEGMENT 2

INF SUBSEGMENT 3

LEFT MEDIALSEGMENT

MED SUP SUBSEGMENT 4A

MED INF SUBSEGMENT 4B

RIGHT LOBE RIGHT ANTERIORSEGMENT

ANT INF SUBSEGMENT 5

ANT SUP SUBSEGMENT 8

RIGHT POSTERIORSEGMENT

POST INF SUBSEGMENT 6

POST SUP SUBSEGMENT 7

Vascular Distribution

Imaging Techniques X-RAYS ULTRASOUND Plain, Contrast , Doppler. COMPUTED TOMOGRAPHY SCAN (MDCT) PLAIN, CONTRAST MR IMAGING- PLAIN,CONTRAST,MRA, MRCP. RADIONUCLEIDE IMAGING. Miscellenous- Angiography , Contrast oil injection etc

Ultrasonography Ultrasound - Commonest, safest and

most widely used. Introduction of microbubbles contrast like

Livovist & perflurocarbon increased both sensitivity and specificity of detecting focal liver tumors.

Microbubble persist in liver within kupffer cells, producing bright enhancement.

Liver metastasis lacking kupffer cell will not enhance.

Overall lesion detection for USG equivalent to CT/MRI.

NCCT Not routinely done. May be used for identification of

calcification, hemorrhage, iron deposition, or determination of precontrast attenuation.

Also used for some neoplasm which become isoattenuated on postcontrast study.

Single phase contrast CT Bolus contrast enhanced CT, with

imaging in peak hepatic parenchymal enhancement (PV Phase).

Injection 125-150 ml 350mgI/ml contrast, followed by saline flush 20-50ml @ 3ml/sec is adequate.

Most useful for routine depection of liver abnormalities like focal lesions.

Multiphase CT Useful in detection of hypervascular

mass, characterization of liver mass, and preoperative planning.

Best performed on MDCT. Image acquisation- Early arterial phase

(25 sec) , Late hepatic arterial phase(35-40 s), and Portal venous phase (60-75 sec)

125-150ml contrast @5ml/sec.

In Arterial phase hypervascular tumors enhances via HA ,in a relatively hypodense liver.

In Portal venous phase , hypovascular tumors are detected, when the normal liver parenchyma enhances maximally and tumors will be hypodense lesions.

In Equilibrium phase, at about 10 minutes after contrast injection, tumors either lose their contrast slower than normal liver(hyperdense), or wash out their contrast faster than normal liver parenchyma(hypodense).

Cholangiocarcinoma – AP, PVP & EP. Delayed/prolonged Enhancement.

Tailored CT protocolsingle slice scanner-take about 20 seconds to scan the liver. 64-slice scanner-examine the whole liver in 4 seconds

Angiography assisted CT CT hepatic angiography-With catheter in

hepatic artery or celiac axis. CT arterial portography- catheter in SMA

or splenic artery. They are Replaced by newer advances

in MDCT and MRI. CT 1-4 wk after iodized oil inj. into HA is

used to detect small HCC. Oil is rapidly cleared by normal hepatic RE system within 1wk, but retained in vascular hepatic neoplasm, as hyperdense mass.

MRI- Plain T1,T2 and GRE sequences. Most tumours are SI in T1 w seq

(except for fat containing lesion and MM)

On T2 most masses are hyperintense. Other sequences used- Fat supressed,

STIR, HASTE etc.

Contrast MRI GD chelates- shorten t1 and t2 relxn. So

cause enhancement of t1. SPIO contrast-taken selectively by RES,

causes profound t2 shortening and normal hepatic signal loss. Tumour uptake depends on presence of kupffer cells.

Double contrast GD + SPIO has increased sensitivity for HCC in cirrhosis.

Mn-DPDP-T1 shortening agents taken up by hepatocytes. Better for metastasis.

Benign Liver tumorsNonneoplastic Neoplastic Potential

Hepatocellular origin

Necrotic noduleFocal nodular hyperplasiaNodular regenerative hyperplasiaRegenerative nodule.

Hepatocellular adenoma

Cholangiocellular origin

Simple cystPolycystic liver diseaseIntrahepatic choledochal cyst

AdenomaCystadenoma

Mesenchymal origin

Inflammatory tumor Hemangioendothelioma

Hemangioma Lymphangioma,LipomaAngiomyolipomaFibromaNeuroendocrine tumors

Other Hamartoma, TeratomaExtramedullary hematopoiesis

Malignant Neoplasms Hepatocellular Carcinoma Fibrolamellar Hepatocellular

Carcinoma Hepatocellular Carcinoma with

Sarcomatous Changes Cholangiocarcinomas Adenosquamous/Squamous Carcinoma Lymphoma Hepatoblastoma Sarcoma Metastases

Neoplasm in infants Benign Adenoma Hemangioendothelioma Malignant Hepatoblastoma Hepatocellular carcinoma Metastases Neuroblastoma Lymphoma Leukemia Sarcoma Rhabdomyosarcoma Teratocarcinoma

Simple Cysts Developmental cysts accounts for 5-14%. solitary or multiple with single epithelial lining.

Polycystic liver disease- assd with PCKD. D/T ductal plate malformation. Varying sizes. Imaging-

cystic lesions.

USG-anechoic, well-defined smooth capsule and exhibits posterior enhancement

CT- circumscribed near water attenuation. No enhancement. MRI- T1 T2 Non enhancing.

Complication-rare. Hemorrhage, Rupture

Simple cyst.

Complex cysts May have solid nodules,

thickened walls, hemorrhages,

Septations, Internal echo, Calcification etc

M Nodule

Biliary Hamartoma(von Meyenburg complex)

Dilated biliary duct with variable amount of fibrous stroma.

Arise from embryonic bile duct that fail to involute.

CT- small hypoattenuating cyst like structures with little or no enhancement.

MRI- multiple small lesions of cystic SI. Most do not enhance, but some show internal enhancement d/t compressed hepatic parenchyma.

Biliary Hamartoma

Peribiliary cyst. Cystic dilatation of obstructed periductal

gland adjacent to large I/H or E/H bile duct.

If extensive, a string-of-beads appearance is evident.

Usually asymptomatic. Imaging- discrete, clustered, cystic

structure with thin septa paralleling bile duct & central portal vein.

Peribiliary cyst- along bile ducts.

Adult Cavernous Hemangioma

Most common liver tumor in adults. Occurs at all ages. Typically <3cm.

Predominate in the posterior segment of the right lobe. Occasional patient develops multiple hemangiomas. Diffuse hemangiomatosis is rare.

Most hemangiomas are asymptomatic and discovered incidentally.

Giant hemangiomas (>4cm)can have unusual findings, like portal vein obstruction & tend to contain central scar.

Ultrasonography- Homogeneous, well marginated, and

hyperechoic tumor(70%). Less often- hyperechoic rim of varying thickness

with isoechoic or even hypoechoic center , post. acoustic enhancement , nonhomogenous centre, or scalloped margins may be seen.

Blood flow velocity is usually slow & Doppler US is noncontributory.

Microbubble-enhanced US- In AP, bright peripheral puddles and pools seen. With time centripetal progression with sustained enhancement in PVP. Delayed washout is common.

Hemangioma- hyperechoic tumor, AP( rim enhancement),delayed 142 sec (central fill-in).

CT- Hypodense to liver and isodense to blood. A

fibrotic component or thrombosis lowers CT density.

Postcontrast- irregular, nodular peripheral enhancement pattern during the arterial phase. Enhancement from the periphery toward the center, a prolonged tumor blush, vascular lakes, and delayed contrast washout.

Smaller ones are round diffusely enhancing while larger ones tend toward an oval or lobular shape.

Central scarring- Causes incomplete central opacification.

Hemangioma NECT, late arterial, late portal venous and equilibrium phase.

MRI

Most hemangiomas - Hypointense on precontrast T1, Hyperintense in T2.

Small hemangiomas-uniform enhancement, and larger ones usually show peripheral nodular enhancement progressing to uniform centripetal enhancement.

Large tumors tend to maintain a persistent central hypointensity.

Most hemangiomas increase lesion to- liver contrast on ferumoxides-enhanced T2-weighted MR images.

Hemangioma.T2-w ( hyperintense ) & T1-w FSE MRI(hypointense)

Scintigraphy

Both planar and SPECT Tc-99m–red blood cell imaging have high sensitivity and specificity in differentiating cavernous hemangiomas from other liver tumors.

Early perfusion phase Tc-99m–red blood cell scintigraphy shows a focal photopenic defect that gradually fills-in in a centripetal manner. A perfusion/ blood-pool mismatch is the hallmark.

Technetium-99m–sulfur colloid and hepatobiliary scintigraphy-- filling defect.

Infantile Hemangioma Especially assd with Kasabach-Merritt

syndrome. More common in girl and tends to be

multiple. With age, these tumors tend to involute with few sequelae.

Large hemangiomas in T2-weighted MRI appear hyperintense nodules containing fast flow flow voids and hyperintense tumors on GRE images.

Early rim enhancement after gadolinium, with progressive fill-in on delayed imaging

Regress after interferon-a-2a therapy.

FOCAL NODULAR HYPERPLASIA 2nd MC hepatic benign tumour. Mostly in young women. Majority < 5cm. Solitary in 75-80%. Typically

subcapsular. Usually nonencapsulated. Along with hepatocyte, BV, BD, and

kupffer cell, they contain central or eccentric fibrous scar with spoke-wheel radiating fibrous bands.

USG Subtle contour abnormality(stealth lesion)

and displacement of vascular structure. Echogenicity may vary from hypo to hyperechoic rarely.

Central scar- hypoechoic linear or stellate area.

Doppler- blood vessels can be seen coursing within central scar.

Microbubble contrast- AP-hypervascular with stellate lesional vessels

and tortuous feeding artery. PVP- Sustained enhancement with unenhanced

central scar.

FNH- Isoechoic, microbubble contrast ‘spoked-wheel’ pattern & central scar.

CT Homogenous iso/slight hypoattenuating. 1/3rd cases,well def. hypoattenuating scar. Prominent vasc supply marked

enhancement in AP (homogenous except for scar and septa).

Hepatic parenchymal phase– Iso attn. Delayed image- pseudocapsule

enhancement( compressed hepatic tissue). Fibrous scar- Hypo attn (AP), Enhance on

delayed images. 50% FNH takes up sulfur colloid in sulfur

scanning and 10% becomes “hot”.

FNH with central scar-NECT, PVP and Equilibrium phase

MRI

Unenhanced - similar to hepatic tissue. Iso/sl. hypo t1, Iso/sl. Hyper t2.

Central scar ½-¾ cases- hypo t1,hyper t2. Contrast-hyper (AP), Iso(PVP), scar

enhancement in delayed phases. Mn/t1 shortening Gd contrast- enhancement

in delayed image. SPIO- show signal loss.(lack specificity) Scintigraphy- rarely for confirmation of

diagnosis. FNH show sulfur colloic concentration.

Atypical features in 10-20%.

FNH- hypointense on T1and hyperintense on T2. Enhances with contrast.

99 mTc-HIDA --prolonged retention of tracer in the area of FNH.

Hepatocellular adenoma Uncommon benign primary neoplasm. Encapsulated. Usually solitary. 8-15 cm. F>M, increase in OCP users. Regress or

disappear after OCP withdrawl. Can have spontanous hemorrhage.

Adenomatosis- rare charecterised by numerous hepatic adenomas. F>M. Do not appear to be steroid dependent, and do not regress on steroid withdrawl. Show high risk of HCC.

USG Nonspecific. Echogenicity hypo/hyper/iso/mixed. Paucity of central vascular structure. Microbubble contrast has limited utility.

Majority are ‘cold’ on Tc-sulfur colloid imaging.

Adenomas are assd with glycogen storage disease in childrens.

Adenoma

CT-- variable

Unenhanced- Hypo attn (lipid, old hrge, necrosis) Hyper attn ( hrge, glycogen).

Contrast- Moderate enhancement (AP & early PVP). Homogenous enhancement if uncomplicated.

25% thin capsule seen- hypo attn (AP), hyper attn (PVP).

Adenoma

MRI Heterogeneous SI. Majority- hyper t1(lipid/hrge), iso/hyper

t2. Capsule – low SI.

Contrast GE seq- Usually hyperintense. May be iso/hypo.

SPIO- some show signal loss.

Hepatic adenoma - hypointense on T1, hyperintense on T2 &inhomogeneouscontrast enhancement

Angiomyolipoma Benign, unencapsulated mesenchymal

tumour. Contain SM,BV and adipose tissue. Vary in size. Solitary or multiple. USG-Well defined echogenic mass. CT- low attn lesion (<-20 HU) MRI– hyper T1, Hypo fat supression. Non fat component show early and

prolonged enhancement.

Hepatocellular carcinoma 90% primary hepatic malignancy. 5th MC cancer worldwide. AFP raised. M>F, solitary/multifocal/diffuse. 3 patterns- Nodular (mc) Massive pattern. Diffuse pattern. Expansive or invasive. Abnormal hepatocyte arranged in trabecular

sinusoidal pattern. Vascular tumour supplied by hepatic A.

Arterioportal shunting, spontanous hrge and rupture may occur rarely.

USG Variable. May be hypo/hyper or complex

echogenicity. Small<5cm-solid &hypoechoic. Thin

peripheral hypoechoic halo seen. Larger tumour becomes complex &

inhomogenous. Calcification rare. Doppler- High velocity flow &

neovascularity. Microbubble contrast- Hypervascular tmr

enhance in AP, ‘washout’ in PVP.

A) Exophytic HCC. (B) Multifocal HCC. ©nodular liver with suspicion of a lesion (D) contrast in the same patient as ©

CT Variable appearance. Mostly hypoattenuating. Some are

isoattenuating with hypo attng. capsule. Hyper attn- d/t hemorrhage. Hypo attn- d/t necrosis , fatty changes. Calcification- 5-10%. Contrast– Transiently hyper attn. in HAP.

But 20% appear hypo attn. in HAP. Fibrous capsule remain unenhanced.

Small HCC are homogenous and larger lesions are heterogenous.

PV(parenchymal)Phase- Isoattenuating. Rarely hypoattng. Tumour capsule/septa- enhances. Delayed images(3-6mt) Small percentage appear hypoattng. Fibrosis, capsule or septa show

prolonged enhancement. CECT can demonstrate vascular

invasion, A-P shunting, tumour thrombus etc.

NECT and Arterial phase image showing hypodense capsule of HCC

Multifocal hepatocellular carcinoma (postcontrast)

MRI Variable. T1- hypo/iso/hyper SI T2-hyperintense(70-90%). >3cm lesions

usually show hyperintensity. Capsule- appear hypointense rim in T1,

and in T2w. Either single hypointense rim or double

layer peripheral band( inner low signal fibrous tissue and outer high signal zone of vessels and ducts).

Internal Features: Intratumoural septa- thin. Hypointense in t1

and t2 w seq.Central scar – Low SI in T1. Low or high SI

in T2w. Contrast MRI Peak enhancement from 10s to 2 min., with

absent or minimal delayed enhancement. Most become isointense in PV Phase and

iso/hypo SI in equilibrium phase. Delayed Phase- washout of HCC(hypo SI)

and enhancement of capsule.

HCC-T1, T2 and Early contrast

CT 1-4wk after i/a injection of iodized oil, is capable of demonstrating small HCC missed by noninvasive technique.

CT arterial portography- sensitive for small HCC. But With 50% failure for setallite nodules.

Double contrast MRI study- SPIO followed

by Gd contrast study improve detection of HCC in cirrhosis Pt.

TNM staging of liver cancerPrimary tumor:Tx Cannot be assessed.T0 No evidence of primary tumor.T1 Solitary tumor without vascular invasion.T2 Solitary tumor with vascular invasion or multiple tumors, none >5cm.T3 Multiple tumors >5 cm or tumors involving major portal or hepatic branch.T4 Direct invasion of adjacent organs.

Lymph node involvement:

Nx Regional nodes cannot be assessed

N0 No regional nodes involved

N1 Regional nodes involved

Distant metastasis:

Mx Distant metastasis cannot be assessed

M0 No distant metastasis

M1 Distant metastasis

C/C Liver diseaseRegenerative nodule(Siderotic Nodule)

Dysplastic nodule Small HCC

Well defined enlarged parenchymal nodule

Hypo/iso/hyper T1Iso/Hypo T2(hypo SI d/t iron content- siderotic nodule)

X enhance HAP

GE Image- nodule within nodule app. Or Hyper I focus within hypo I nodule.

Nodule>1mm with dysplasia

Hypo/Hyper T1Iso/hypo T2

X enhance HAP

Enhance on CT & not on SPIO

HCC < 2cm.

Hypo/Hyper T1Iso/hyper T2Rarely hypo T2

Enhance in HAP.

Hypo attn on all CT phases & enhance on SPIO

Fibrolamellar HCC Histologic subtype of HCC. Occur in younger pt without underlying

liver disease. M>F. AFP Normal. Better prognosis. Malignant hepatocyte saperated into

cords by thin multilamellated fibrous strands.

Usually very large, aggressive local invasion, nodal or distant metastasis.

USG- variable echo. Punctate calcification and central echogenic scar.

CT: Large well defined lobulated mass showing heterogenous enhancement.

Central scar (50%).. Often show calcification. Delayed enhancement.

MRI: Hypo on T1, heterogenous hyper SI T2. Mass show heterogenous

enhancement, with no enhancement of central scar.

Central scar- Hypo SI in T1 and T2. Lack of delayed enhancement.

Fibrolamellar carcinoma with central calcifications-NECT, AP & PVP (radiating septa).

FS T2 and T1 GRE in AP and PVP (peripheral capsule and necrotic nodule)

Central scar

FNH Fibrolemellar HCC

USG

CT

T2 MRI

Enhancement

+++(hypoechoic)

Calcification rare.

Hyperintense on T2

delayed enhancement.

+++(echogenic)

Calcification Common

Hypointense on T2,

no delayed enhancement.

IH cholangiocarcinoma Adeno Ca from small intrahepatic bile

ducts. 2nd MC primary hepatic neoplasm(10%).

Firm hypovascular tumour with predominant fibrous stroma. Large amount of interstitial space in fibrous stroma causes slow diffusion of contrast.

Features- peripheral biliary ductal dilatation, PV encasement, segmental atrophy etc.

CT: Hypoattng mass with lobular margins,

showing mild early peripheral enhancement, gradual centripetal enhancement & delayed contrast pooling(10-20 min). Satellite nodules are frequent.

MRI: Hypo on T1, Hyper/Iso T2. Enhancement similar to CT.

Central Scar(50% Cases)- Hypo on T1 & hypo/iso/hyper T2.Delayed enhancement.

Hepatic and delayed phase in a patient with multifocal cholangiocarcinoma causing retraction of liver capsule

Metastases Liver is 2nd MC site of metastasis. Variable clinical and imaging

presentations. Precontrast images are important to

show calcification, and hemorrhage. Some Met like breast, colon, lung, and

carcinoid show retraction of adjacent liver capsule.

MDCT has advantage with thin section capability.

Hypovascular Metastasis

Hypervascular metastasis

Calcifying Metastasis

Colon adenocarcinomaPancreatic adenocarcinomaGastric adenocarcinomaTransitional cell carcinoma

Renal cell carcinomaNeuroendocrineIslet cell carcinomaCarcinoidMalignant pheochromocytomaThyroid carcinomaSome sarcomasMalignant melanoma

Mucin-producing adenocarcinomaOsteogenic or chondrosarcomaSome neuroendocrine tumors

USG Multiple solid lesion with hypoechoic halo(may

be d/t compressed nornal tissue, proliferating cells, fibrosis or vascularization).

Microbubble Contrast- AP-Hypervascular metastasis show

enhancement in HAP. Hypovasc. Met. Show enhancement less than liver.

PVP- Virtually all metastasis will be unenhanced relative to Liver in PVP(lack kipffer cells)..

USG- various features

ECHOGENIC MET. (hypervasc)

Hypoechoic met. (hypovasc)

Cystic met. Target lesion

Diffuse Disorganised(infiltrative)

GITRCCCarinoidChorio ca.Islet cell ca

BreastLungGastricPancreasLymphoma

Cystadeno caMucinous caSarcoma

Bronchogenic ca.

BreastLungMM

(a) Large necrotic metastasis. (b) Miliary metastases (c) Following microbubble contrast agent(d) Calcified metastases from breast carcinoma

CT-Hypovascular metastasis Most metastasis are hypovascular. CT- In Arterial Phase, most common

pattern is continuous ring like enhancement at periphery.

Hypoattenuating on PV Phase. Hypervascular metastasis: They are hyperattenuating in AP.

Becomes isoattenuating in PVP, so difficult to detect in PVP.

CT PVP-Multiple cystic liver metastases from a cystic pancreatic acinar carcinoma

Metastatic islet cell carcinoma. Precontrast and contrast- rim-enhancing nodules.

MRI Usually Hypo T1, Hyper T2. Hyper SI in T1- hemorrhagic, MM. 15-27% have central more hyperintense area in

T2(necrosis)– Target sign. 50% colorectal met. Show central area of low SI

relative to high SI tumour edge in T2- Halo sign. D/T Central desmoplasia and coagulative Necrosis.

Contrast: Hypovasc met.-Hypointense in HAP with

perilesional enhancement. Hypervasc met.- Hyperintense in HAP. Isointense in PVP.

Delayed images(5-10 min)- 1/4th of met. Show hypointense rim compared to centre of lesion(peripheral washout sign). Seen in hypervasc met > hypovasc met.

MRI and contrast CT are comparable- 80-90% sensitivity. MRI more sensitive for solitary metastasis.

CT remains the screening procedure of choice.

Pre op staging- CT,MRI &MDCT+Angio used. CTAP is being replaced by non-invasive Techniques.

Improvement of lesion detection with liver-specific agent-T1-weighted GRE image and Mangafodipir-enhanced MR

Hepatocyte-specific contrast agents- Early ring-like enhancement with delayed

washout.

Biliary Cystadenocarcimoma Uncommon biliary neoplasm. F>M, middle age patients. Unilocular or septated large cystic mass

containing mucinous or serous fluid. CT- Intrahepatic mass with non-enhancing

cystic spaces with high attenuating wall/septa. Mural or septal nodule when present enhances. Calcification may be seen.

MRI- Cystic locules with hypointense septa. T1-SI depend on fluid content. Serous- hypo, Mucinous-iso/hyper, Hrgic-hyper SI.

Epithelioid hemangioendothelioma

Rare neoplasm of vascular origin. Adults. F>M. Peripheral solid nodules composed of

myxoid stroma with relatively hypocellular center.

Usually multiple larger peripheral lesion coalescing to form confluent mass.

CT- Hypoattenuating mass showing peripheral enhancement.

MRI- Hypointense in T1, hyperintense in T2. Peripheral Enhancement Seen.

Epithelioid hemangioendothelioma – Contrast-CT -large heterogeneous, lobulated tumor involving both right and left lobes.

Primary hepatic Angiosarcoma

Rare,primary mesenchymal liver tumor. In Elderly men and have poor prognosis. Metastasis is common.

Association exists with prior exposure to certain chemical carcinogens.

Multifocal but well-marginated nodules throughout the liver.

USG- Large mass of mixed echogenicity. CT -Hypodense mass. Hetrog. enhancement. Hypointense on T1- and markedly

hyperintense on T2-w images, with hypointense septa in T2-weighted.

Angiosarcoma- T2W and AP CT and MRI showing non-enhancing lesionswith feeding artery

Primary Lymphoma Primary hepatic lymphomas are rare. Most of these tumors are Non-Hodgkin’s T-

cell lymphomas. Usually present as a discrete tumor. USG-Homogeneous lesions anechoic or

hypoechoic and mimic a cyst, although unlike a cyst they lack through transmission. Some are surrounded by a halo.

Most primary liver lymphomas are hypointense on T1- and hyperintense on T2-weighted images. They show heterogeneous postcontrast enhancement.

Secondary Lymphoma Non-Hodgkin’s lymphoma is more often

focal. Calcifications seen rarely. Portal and periportal intrahepatic

infiltrates causes jaundice. MRI-Hypointense on T1- and hypo- to

hyperintense on T2-weighted images. Postcontrast enhancement varies.

Use of phosphorus MR spectra from P-31 MR spectroscopy appears potentially useful.

NHL-contrast CT-Several focal hypodense tumors & intrahepatic tumor tracking along portal vessels.

Hepatoblastoma Most common primary liver neoplasm in

children under 3 years. Rarely seen in adults. M>F. Elevated AFP seen.

Prevalence is increased in Beckwith- Wiedemann syndrome and in hemihypertrophy.

Originates from embryonal hepatic tissue and usually consists of epithelial cells or mixture of epithelial and mesenchymal cells.

Readily metastasize. Vascular displacement or amputation may occur.

Imaging features similar to HCC. May have local invasion, cystic changes, necrosis or irregular shaped calcification.

US- Mixed echogenic large lesion with poorly defined margins.

CT- Hypodense mass. Variable enhancement.

MRI-Hypointense on T1- and hyperintense on T2. Heterogeneity is often evident.

Hepatoblastoma shows uptake of sulfur colloid; however, does not have uptake of both Tc-99m–sulfur colloid and HIDA.

Hepatoblastoma –Contrast CT- large slightly enhancing tumor containing central necrosis and calcifications

TSTC (too small to characterize)LesionsJones (1992), Schwartz (1999), Khalil (2005)

For lesions which, due to their small size and atypical imaging features, cannot be confidently categorized, the term TSTC lesions has been coined. Usually for lesion <15mm in CT/MRI.

Accounts abt.12% of liver lesions with a known Pt. with malignancy. (80% are benign).

Patient without a known malignancy –usually considered as benign.

Patient with a known malignancy-- a single TSTC lesion can be assumed as benign.

Even multiple TSTCs- mostly benign, esp. when they are small, sharply defined and hypodense.

Avoid 'we can't rule out metastases'

Chemoembolization Intraarterial embolization techniques used

to treat hepatocellular carcinomas consist of inert particle embolization, chemotoxic agents(chemoembolization), and injection of radioactive particles (radioembolization).

Transcatheter chemoembolization is commonly used using Ethiodol (Lipiodol).

Later, after injecting a chemotherapeutic agent, if needed, embolization of the vessel in question is performed using particulate matter.

CT shows residual Ethiodol retained in a multifocal hepatocellular carcinoma

Radioembolization Intrahepatic artery Tc-99m-MAA injection

estimates the relative tumor-to–normal parenchyma uptake of various size microspheres, including those containing therapeutic radiopharmaceutical agent

Hepatocellular carcinomas have also been embolized with iodine-131 iodized oil (Lipiodol) and gelatin sponges through a superselectively placed arterial catheter.

Provided long-term palliation without complications.

Percutaneous Techniques Hepatocellular carcinomas can be treated

using a direct percutaneous approach.injection of chemical agents such as

ethanol, acetic acid, and hot saline to induce tumor coagulation necrosis.

thermally mediated techniques such as radiofrequency (RF) ablation, laser photocoagulation, microwave therapy, and cryotherapy result in similar tumor cell death.

Imaging provides needle and catheter insertion guidance.

Most percutaneous ablation is performed using US guidance, although for tumors not visualized by US, MRI guidance in an open magnet is an option.

Either CT, contrast-enhanced US, or MR are used to detect residual tumors shortly after ablation.

Radiofrequency ablation of hepatocellular carcinoma. A: Pretherapy B: hyperdense center immediate post-therapy C: Residual changes are present 2 months.

Cryoablation Destroys tumor tissue by freezing. Liquid

nitrogen is the freezing Medium. Either a percutaneous or an open surgical

approach is used for cryoablation.US/MRI used.

Magnetic resonance guidance- identifies the tumor nodule in question and the size of the surrounding frozen liver tissue. An open MR unit reveals resultant ice balls as sharply defined expanding regions of signal loss encasing tumors S/O resultant necrosis.

REFERENCES: Lee/Sagel : CT With MRI Corr. 4th ed. Grainger/Allison : Diag.Radiology 5th ed. Skucas : Advanced Imaging Abd. 2006. Rumack : Diag. Ultrasonography 3rd ed. Margulis: GI Imaging AJR, Radiology.

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