PRESENTOR : Dr Navni Garg MODERATOR : Dr Sonal Krishan

SEMINARSEMINAR JUNE 26,2014 JUNE 26,2014

IMAGING IN BENIGN HEPATIC MASSES

Focal liver lesion is by definition a discrete abnormality arising within the liver

Features of intra hepatic lesion Most of the lesion within the liver with

respiration Bulging of the liver capsule Displacement and distortion of the portal and

hepatic vessels Post displacement of IVC

BENIGN HEPATIC MASSES

Developmental Infective/Inflammatory : Pyogenic abscess Amoebic abscess Fungal abscess Hydatid cystGranulomatous: Tuberculosis SarcoidosisNeoplastic

Benign neoplasms

Hepatocellular(hepatocyte) Cholangiocellular

(bile duct epithelium)Mesenchymal

Adenoma

FNH (2nd most common)

Hepatic cysts

Biliary cystadenoma

Hemangioma (most common)

Mesenchymal hamartoma

Infantile hemangio-Endothelioma

Lymphangioma/Lipoma/fibroma/Angiomyolipoma/Leiomyoma/

Malignant neoplasms

Hepatocellular Cholangiocellular Mesenchymal

Cholangiocarcinoma

Cystadenocarcinoma

Angiosarcoma

Epitheliod hemangio-Endothelioma

Leiomyosarcoma

Lymphoma

Hepatcellular Ca

Fibrolamellar carcinoma

Hepatoblastoma

HEPATIC METASTASIS

Imaging modalities

99Tc-sulphur colloid

PET CT

Nuclear Medicine

USCTMRI

CTAP

CE-USG

Nuclear scans

Conventional

Radiological

Newer methods

DWIElastography 99Tc-RBC

scan

MDCT protocol for hepatic imaging

Radiographics 2001

CT arterioportogapgy scan(CTAP) Principle: tremendous enhancement of

normal liver parenchyma following the SMA or splenic artery injection

Technique-conventional angiogarphy. End hole catheter in splenic artery /SMA 150 ml iodinated contrast 150 to 300 I/ml at 3 to

5 ml/s. Start scan at 30s.Limitations – nontumous perfusion defect- d/t to

laminar flow in the PV, aberrant vascular supply defect

RCNA 1998

CT arterioportogapgy scan(CTAP) most sensitive technique for detection of

focal hepatic neoplasm. Sensitivity 80-90% for metastasis and 70%

for primary malignant neoplasm.higher sensitivity for smaller liver SOL.

Disadvantage-low specificity, cost and need for the invasive procedure.

Replacement with GD and ferumoxide enhanced MRI may be reasonable.

RCNA 1998

CT hepatic angiography scan

Principle: all hepatic neoplasm are largely supplied by the hepatic artery.

Technique: angiographic catheter is placed in common hepatic artery. Scan delay 3-5 s of contrast injection.70 ml of diluted iodinated 15-30 % at 2ml/s.

Applications. use full in combination with the CTAP scan for characterizing the lesions and for for characterization of portal perfusion defect.

RCNA 1998

Iodized oil CT scan Principle: lipiodol -iodized ethyl ester of acids of

poppy seed oil.Prolonged retention of lipiodol in highly vascular and abnormal tissue.

Technique: two step procedureStep 1- complete angiographic study f/b injection of 5- 20ml of lipiodol in proper hepatic artery beyond GDA .Step 2- CT scan of liver in 7 to 28 days.

Applications – highly sensitive method for diagnosing small foci of the HCC and intrahepatic metastatic nodule of HCC. Sensitivity 97%, specificity 76%, accuracy 88%.

Can differentiate between dysplastic nodule and small HCC

MRI in liver tumors

T1weighted breath hold spoiled gradient- entire liver scanned in single breath hold ,TR-150-200ms, TE- minimum,8x2+- fat sat

T2 weighted sequence- SE T2 , TR 4000, TE- 100, with respiratory trigger. FSE breath hold.Fat suppressionHalf Fourier acquisition single shot turbospin echoe.

Contrast enhanced sequences

MRI protocol

Radiographics 2000

MRI CONTRAST AGENTSIN LIVER IMAGING

MRI CONTRAST AGENTS

Mri contrast maximises the SI b/w two tissues by either increasing or decreasing the SI of tissue relative to another

Should produce large effect at low conc., s/b biocompatible, low tolerable toxicity,stable invivo as well as invitro(shelf life), s/b excreted in reasonable time, s/b organ specific as far as possible.

TYPES OF MRI CONTRAST

T1 agents Transitional & lanthanide

(Gd) metal ions Paramagnetic

substances (unpaired e-)resultent fluctuating magnetic field affect proton relaxation

Increases T1 relaxation Increases SI (+contrast)

T2 agents Feromagnetic & super

paramagnetic substances, have little effect on tissue relaxivity

Induce dephasing d/t their net positive magnetization

Protons undergo transverse relaxation/ T2 relaxation

Decreased SI on T2 (-ve contrast)

T1 AGENTS

FDA approvedIONIC Gd-DTPA (gadopantate dimeglumine)=

Magnevist NONIONIC Gd-DTPA-BMA(gadopentate diamide)=Omniscan Gd-HP-DO3A(gadoteridol)=Prohance

Approved in european countries Gd-DOTA(gadoterate meglumine)= Dotarem

T1 Agents Dose .1mmol/kg in adults & children> 2 yrs

Mt sequence & higher doses up to .3 mmol/kg can further increase lesion conspicuity

Gd chelates c/b used as T2 agents if used in sufficiently high conc. T1 effect predominant at low doses

Gd chelates rapidly leave the vascular spaces& after about 3 min. reach the equlibrium through out ECF compartment.

T1 Agents Cross the BBB similar to iodinated contrast

used in CT ,thus anything which enhances with CT also enhances with MR contrast, detection better with MR contrast d/t better inherent contrast of image.

S/E seen in 3-5 % of pt. Nausea ,transient rise of s.bilirubin & iron

Can be safely given in pt. With impaired renal function, however dialysis recommended in pt. With severe renal impairment.

ORGAN & TISSUE DIRECTED CONTRASTAGENTS

1. Liver specific2. Hepatobilliary agents3. GI contrast4. Blood pool agents

LIVER SPECIFIC AGENTS T2 agents/-ve contrast/RES agents Coated iron oxide particles of various sizes.

Phagocytosed by RES of liver, spleen, BM, LN. Normal liver looses SI on T2 agents, Focal liver

lesions like mets which do not contain kupffer cell c/b better seen.

More specific the accumulation of agent in target tissue better the result & lesion tissue contrast

SPIO (Ferum oxide/AMI-25, Magnetite/ Resovist/ SHU-555) & USPIO(AMI-227).

SPIO (super Paramagnetic iron oxide) (50+\- 19 nm)

1.Ferum oxide (Feridex/ AMI-25) FDA approved RES clears it (T1/2=8min.) Liver t1/2=2-3 days Dose 10-15 micro gm/kg Slow infusion over 30 min. (pre & post contrast

imaging inconvenience) S/E back ache,hypo tension (skilled personnel

& resuscitation equipment s/b available when ever ferum oxide is administered)

SPIO

2.Magnetite/resovit/SHU-555 Phase III cl. trial Dose =40 microgram(comparable to AMI-

25) Particle size 61 nm. Max.hepatic signal loss in 10 min.

USPIO(ultra small SPIO) Particle size 17-20 nm Rapid infusion c/b given Small volume required S/E- back ache,hypo tension,flushing Taken up by normal & cirrhotic liver,FNH &

adenoma,but excluded from HCC Clinical trials have not been reported.

USPIO

AMI-227 Blood t1/2 long=200 hrs=blood pool agent T2 - liver looses SI, BV dark Has gr. T1 effect. T1 -bright blood effect-delineates IV

thrombus better. Good balance ofT1 & T2 effect, by bolus

administration dynamic imaging of liver c/b done.

HEPATO BILLIARY AGENTS(T1 agents) Soluble paramagnetic molecule Substantial hepatic uptake & Prolonged

hepatocyte retention, billiary ex. T1agent – preferential T1

enhancement,beginning with in min & lasting for 2 hrs, imaging performed during window after renal clearance from blood & ECF

HEPATO BILLIARY AGENTS(T1 agents)FDA APPROVED

1. Mangafodipir/Teslascan =Mn-DPDP(Mn dipyridoxal diphosphate)

UNDER CLINICAL TRIAL

1. Multihance = Gd-BOPTA (Benzyl oxy propionic tetra acetate)Gadobenate dimeglumine

2. eovist = Gd-EOB-DTPA (gadoxitate)

Mangafodipir/Teslascan Dose 5-10 micromol/kg Enhances max. in 10 min.Imaging window 10

min-4hr Not effected by obstructed billiary system Focal liver lesion seen as hypointense lesion Mets –have no hepatocytes ,seen as low SI with

in enhanced normal liver,whenever enhanement present (8%) seen as rim enhancement attributed to c ompressed hepatic tissue.

Mangafodipir/Teslascan

HCC-show detectable enhancement in 100% cases,complex pattern-Uniform, heterogenous;thick/nodular/peripheral;septal, capsular sparing,well defferentiated HCC may become nearly isointense to liver.

Regenerating nodules-often enhances & become more concipicuous on post contrast images b/c cirrhotic/fatty liver show decrease enhancement.

Classification of Hepatocellular Nodules Regenerative or hyperplastic

nodules Monoacinar regenerative

nodulesDiffuse nodular hyperplasia

(with fibrosis)Nodular regenerative

hyperplasia Multiacinar regenerative

nodules Large regenerative nodule (if

0.5 cm) Lobar or segmental

hyperplasiaFocal nodular hyperplaisa

•Dysplastic or neoplastic lesions Hepatocellular adenoma

Dysplastic noduleHepatocellular carcinoma

Nodular regenerative hyperplasia Diffuse regenerative nodule not associated with of

fibrosis.hyperplasic hepatocytes. A/W connective tissue disease,various drugs like

steroids and anti proliferative drugs Portal hypertension in 50 %.

Imaging- multiple nodule similar imaging feature to normal liver parenchyma, may contain hemorrhage

On Tc 99 sulphur colloid scan diffuse or patchy uptake.

USG : iso to liver with asso portal HTN findings

CT : non enhancing multiple hypo nodules. Hmg may occur

MRI : hyper on T1 and hypo on T2

Regenerative nodule Localized proliferation of

the hepatocytes and their supporting stroma.

Siderotic /nonsiderotic Low signal on the T2 and

variable signal T1, no enhancement on arterial phase.

may not be differentiated from dysplastic nodule

Adenomatous hyperplastic nodule(dysplastic nodule).

Benign but premalignat, in cirrhotic liver. 10 –14% of cirrhosis, massive hepatic

fibrosis Contains iron and supplied by portal vein NECT- may be hyperdense but mostly are

isoattenuating. CECT isoattenuating or slightly low

attenuating on arterial, portal and delayed phase images and thus are difficult to depict on CT.

May show enhancement in minority of cases similar to HCC.

Adenomatous hyperplastic nodule(dysplastic nodule MRI- hyperintense on T1 w and hypointense on T2, Nodule with in nodule on T2 s/o HCC CT arterioportography- to differentiat AHN& HCC HCC supplied by hepatic artery so enhances on

CTAP whereas dysplastic nodule is supplied by portal vein

dysplastic nodule. nonenhancing

dysplastic nodule. enhancing

HCC within a dysplastic nodule with MR imaging–histologic correlation.

FNH• Second MC benign lesion • F>M , 3rd to 5th decade•2% primary tumors in children

• Congenital vascular malformation -> hyperplasia of hepatocytes

• Kupffer’s cell activity seen

•Well circumscribed , non encapsulated mass with central scar surrounded by nodules of hyperplastic hepatocytes and kupffer cells•No hmg or necrosis

RadioGraphics 2010

May be present on liver surface, nodules due to AVM

May be pedunculated Rt lobe > lt lobe > 7 cm in children

USG Subtle liver masses

homogeneous,iso - hypoechoic to normal liver

Contour deformity Doppler :prominent vasc in

the central scar, hypervascular tumors

Numerous scattered arterial and venous signals : comet tail appearance

CONTRAST ENHANCED USG

Arterial filling of mass (centrifugal)

Portovenous phase : iso to liver with central non enhancing scar

Delayed : accumulation of contrast in scar

FNH • Centrifugal filling• Stellate/linear/

plicated non enhancing central area

• Sustained portal phase enhancement

HEPATIC ADENOMA• Centripetal filling• No scar

NCCT

Iso – hypodense Central hypodense scar Calcification rules out FNH Bulge deformity on liver surface

• Arterial Phase- Homogenous enhancement• PV phase- Iso to liv with hypo enhancing central scar• Delayed Phase- Iso /hypo to liver with hyperenhancing

scar

CECT

MRI

T1 : Hypo/iso T2 : hyper Central scar is

hyper on T2 due to vascular and myxoid tissue

CEMRI

Homogeneous enhancement with rapid washout to isointensity with surrounding liver tissue

Scar shows delayed and persistent enhancement

MRI

FNH• 60-70% decrease in

signal intensity on T2W SPIO MRI ( kupffer cell containing )

• Homogeneous• T1WI : iso /hypo• Central scar

HEPATIC ADENOMA • 20% decrease in

signal intensity on T2W SPIO MRI

• Heterogenous• T1WI : hyper

Sulphur colloid scan : hot spot Angiography : hypervascular mass

possessing centrifugal or spoke wheel pattern with dense tumor blush in capillary ,portal venous phase

B. Op de Beeck et al. : European Journal of Radiology(1999)

• Rare• Usually solitary, > 10 cm• 30-50 y F> M • Association with oral contraceptives,anabolic steroid intake and GSD type I & III• Lacks portal tracts and terminal hepatic veins -> necrosis, hemorrhage, and rupture common in large tumors

HEPATOCELLULAR ADENOMA

USG

Heterogeneous echogenic due to intratumoral fat and glycogen

Anechoic areas may be present due to hemorrage and scar tissue

CONTRAST ENHANCED USG intense rapid enhancement during arterial phase less rapid washout during portal / sinusoid at last becomes isoechoic to liver parenhyma

Discrete perilesional feeding arteries manifest as enhancement around the tumor capsule

Never seen in HCC

NCCT

Iso-hypodense Hypodensity due to

excessive steatosis

Hyperdense areas due to hemorrage

TRIPHASIC STUDY

ARTERIAL : HYPERDENSE PV : ISODENSE HV : HYPODENSE

• Tc 99 sulphur colloid –cold spot in 80% as they lack kupffer cells

• MRI-iso to hyper on T1and T2 due to fat and glycogen; capsule may be hypo on T1WI

• Enhancement similar to CT• SPIO- variable signal loss

a

Alvin C. Silva, MD et al .RadioGraphics 2009;c

b

HEPATIC SCINTIGRAPHY

Uptake seen which doesnot get excreted therefore delayed enhancement

Hepatic cyst

• Developmental benign, not communicating with billiary tree

• Solitary unilocular cyst lined bile duct epithelium.

• 5-14 % of general population F>M (5:2)

• USG- anechoic with imperceptible wall and post acoustic enhancement.

• CT scan- water density attenuation, no enhancement

• MRI : T1-hypo,T2-hyper no enhancement

Cystic focal liver lesions

D/D

Abscess Hydatid cyst Necrotic mets Hepatic cystadenocarcinoma Hematoma Intrahep GB

COMPLICATED CYST

Because of hemorrage or infection in simple cyst

USG :Presence of internal echoes, debris,thick septations, mural calcification or nodules

CT : septations,internal debris and wall enhancement

MRI : Hyper on both T1,T2 due to mixed blood products

PERIBILIARY CYST

Seen in pts with severe liver disease Small in size 0.2 – 2.5 cm Usually located centrally within porta

hepatis or at the junction of the main right and left hep ducts

Generally asymptomatic May rarely cause biliary obstruction Due to obstructed small periductal glands

USG : discrete clustered cysts or tubular appearing parastructures having thin septa which parallel the bile ducts and portal veins

POLYCYSTIC LIVER DISEASE

• More than 10 simple hepatic cysts • Surrounding parenchyma frequently

contains von meyenburg’s complexes• Associated with periductal fibrosis and bile

duct proliferation – congenital fibropolycystic disease of liver

• Associated with autosomal dominant polycystic kidney disease in 70%

No corelation exists between severity of renal ds and extent of liver involvement

LFTs normal

Polycystic liver disease

Biliary Cystadenoma

• Slow growing multilocular cystic tumors • 85 % : intrahepatic ( 55% - right lobe, 29%- left lobe

, 16% - both lobes)• F>M• May communicate with intrahepatic bile ducts and

secrete mucinous material into the duct• Premalignant • Calcification rare• Avascular

• USG: 1.5-35 cm, solitary cystic mass , well defined thick capsule, mural nodules seen in the anechoic mass

• CT : Thin septa show enhancement

MRI

T1WI-hypo, T2WI-hyper, septations are seen as dark bands separating high signal intensity locules

• ↑ CA19-9 and CEA in intracystic fluid of cystadenoma/ cystadenocarcinoma

• Polypoid, pedunculated excrescences with coarse calcification in septa seen in cystadenocarcinoma

HEMANGIOMA

• MC benign lesion of liver• 2 MC hepatic tumor after metastasis• Prevalence -- 1–2% to 20% (F:M= 2:1–5:1) • More common in right lobe of liver• More common in subcapsular location/around intrahepatic

vessels• Blood filled vascular channels separated by thin fibrous septa

lined by flat endothelium• No kupffer cells

• XRAY ABDOMEN : multiple calcific phlebolith, numerous calcified trebaculations and spicules arising from central point and radiating towards periphery

USG Sharply defined High reflective due to

multiple interfaces between vascular spaces

Homogeneous Lobulated margins if >

2.5 cm Involuting :

heterogeneous

CONTRAST ENHANCED USG Peripheral puddles of

enhancement Centripetal filling Complete fill in on

delayed imaging Sustained enhancement But all the phases of

enhancement must have the same density as the blood pool.

DYNAMIC CT IMAGING

FLASH HEMANGIOMAS

Small hemangiomas may show fast homogeneous enhancement ( flash filling)

D/D : Small HCC , Hypervascular metastasis

So look at all phases to see if the enhancing areas match the blood pool.

Hemangiomas have peripheral nodular, globular enhancement

D/D : rim enhancement is continous peripheral enhancement seen in malignant lesions ( metastases)

MORPHOLOGY ON MRI

Sharp geographic margins Lack of peripheral halo on T2WI Lack of deformity of the liver surface Superficial location Lack of displacement of hepatic vessels

MRI : T1- HYPO , T2 -HYPER

DYNAMIC MRI IMAGING WITH GADOBENATE DIMEGLUMINE (MULTIHANCE)

Hemangioma with central fibrosis : hypointense on T2WI

HCC and metastasis : hyperintense necrotic area on T2WI

Giant hemangioma : heterogeneous on T2WI due to thrombosis,myxoid tissue,fibrosis . May show irregular flame shaped peripheral and central enhancement

RBC SCINTIGRAPHY

Hot spot on delayed Tc99 –RBC scan Scans are taken 1-2 hours after injection of

patient’s isotope labelled blood Progressive increase in ratio of blood pool

activity within the hemangioma to that of surrounding liver because of retarded blood flow in vascular sinusoids

Initial photopenia with hot nodule on delayed blood pool images

Angiography : Gold std

Normal main and feeding vessels Early contrast accumulation within the

lesion during the late arterial phase Persists throughout the venous phase :

diagnostic Feeding vessels show crowding around

the lesion

Atypical hemangioma

Tommaso Vincenzo B et al,EJR 2007

• Only 55% cases show typical enhancement patterns• Atypical features : lesions >6-8cm • Due to hemorrhage, necrosis, cystic change and hyalinization• Centrifugal (inside-out) enhancement• Only peripheral enhancement • Only central • Diffuse

e

Baseline

LVP

Baseline AP

PVPTommaso Vincenzo B et al,EJR 2007

Baseline PVPAP

10mins

CT finding useful in differentiating liver tumor with central scar

Bile duct hamartoma(Von Meyenburg complex)

• Incidental finding• Due to failed involution of

embryonic bile duct

• Grayish white nodular 0.1-1.5cm. Not communicating with the billiary system

• USG :Multiple,anechoic• CT : <1.5 cm,multiple

hypodense,no enhancement

Mortele KJ et al. RadioGraphics 2001;

On USG, bright echogenic foci with ring down artifacts occuring due to presence of cholesterol crystals withih dilated tubules

MRI : hypo on T1 and hyper on T2 Irregularly outlined. No enhancement/rim enhancement ( due to compressed liver parenchyma)

MR CHOLANGIOGRAPHY : multiple,tiny,cystic lesions that donot communicate with biliary tree

Bile Duct Hamartoma

Mortele KJ et al. RadioGraphics 2001;

Liver cyst Varible sized Regular outline May be associated

with ADPKD

Biliary hamartoma <1.5 cm Irregular outline No such

association

• Include lipoma, myelolipoma and angiomyolipoma

• A/W renal AML & tuberous sclerosis(10%)

• USG- hyperechoic SOL.• CT scan- radiolucent fat,

enhancement• MRI- hyper on T1 & T2

Lipomatous tumours

Angiomyolipoma

Focal inflammatory lesions

• Abscesses• Hydatid cysts

PYOGENIC LIVER ABSCESSMC – STAPH, others : aerobic, non aerobicSources Ascending cholangitis from biliary tree Phlebitis secondary to diverticulitis, appendicitis,

pancreatitis , GI infections Arterial septicemia as result of

endocarditis,pneumonitis or osteomyelitis Direct extension from contigous organs such as

perforated ulcer, pneumonia, pyelonephritis Iatrogenic causes

Pyogenic vs Amoebic

Biliary origin : multiple, both lobesPortal vein source : solitary, right lobe (65%), left lobe (12%), both (23%)

CT: Round (60%)or irregularly hypoattenuating area with peripheral rim enhancement

Cluster sign : small abscesses coalescing together

Double target sign : perilesional edema

USG : Well defined or irregular & thick walled lesion , hypoechoic (36%)

Gas – echogenic foci ,Fluid-fluid interface, internal septations , debris

• Solitary unilocular

• Right lobe of liver (posterosuperior segments)

•CT : hypoattenuating with peripheral rim enhancement

•USG : Round or oval(82%)

• Absence of prominent abscess wall

• Hypoechoic compared to normal liver with fine internal echoes (58 %)

25sPyogenic abscesses

Pyogenic abscesses

Amoebic liver abscess

Cystic Hydatid Disease Gharbi’s Classification of Cystic Hydatid Disease

Type Ultrasonographic features and patterns

I Pure fluid collection - univesicular cyst

II Fluid collection with a split wall- detachedlaminated membrane (water-lily sign)-

III Fluid collection with septa representing walls of daughter cysts (honeycomb sign)

IVHeterogeneous appearance - presence of matrix- mimics a solid mass

V Reflecting thick walls - calcifications

TYPE I TYPE III

TYPE IV TYPE V

CT

Well defined, round or oval cystic mass Hyperdense to normal liver normally

Detached laminated membranes : linear areas of increased attenuation

Multiloculated, daughter cysts

Calcification : +/-

MRI

T1WI : hypo T2WI : hyper Peri cyst has low signal on T1 and T2 due

to high collagen

Alveolar Echinococcosis

• E multilocularis is responsible parasite.

• Liver is MC (90%) site of E multilocularis , 70% rt. Lobe.

• Foxes - main host , rarely cats & dogs.

• Endemic in upper Midwest of USA, Alaska, Canada, Japan, Central Europe, and parts of Russia

• Hilar infiltration in 50% of pts – dilatation of intrahepatic bile ducts and invasion of the portal and hepatic veins, with subsequent atrophy of the affected liver segments due to hypoperfusion

Mortele KJ et al. RadioGraphics 2004;

• US - “hailstorm” pattern – multiple echogenic nodules with irregular and indistinct margins

- Lesions with central liquefactive necrosis appear hypoechoic, with some internal echoes and an irregular hyperechoic border

• CT and MR - multiple irregular, ill-defined lesions scattered throughout the involved liver that are generally hypo at CT and hyperintense at T2WI. - This mimic either metastases or pyogenic abscesses. - little or no enhancement.

• D/D – Cystadenoma / Ca, peripheral cholangio Ca or metastasis with peripheral bile duct dilatation.

Mortele KJ et al. RadioGraphics 2004;

FUNGAL ABSCESS – Candidiasis

• Wheel within wheel appearance

• Bulls eye /Target lesion : hyper centre with hypo rim

• Echogenic foci : scar

• Uniformly hypoechoic – M.C.

RadioGraphics 2001;

RadioGraphics 2001;

Focal hepatic lesions

Solid hepaticlesions

Cystic hepatic lesions

Small hemangioma FNH Adenoma Metastasis

‘Washout’’Capsule +/- Fat

Post/delay T2

Post/delay – ‘fades’T2 iso

Central scarringGd

Ring Enhancement

T2Diffusion

Benign Malignant

Lymphoma

Prim/Sec attenuation

T1T2

Cystic hepaticlesions

Developmental Miscellaneous

Hepatic cysts

Bile ducthamartoma

Rim Enhancement

< 1.5cm

Biliary Cystadenoma/Ca

Hematoma

MultilocularMural nodules

Fib capsule, CalcVariable SI

Bilioma

Neoplastic Inflammatory

Abscess

Subcapsularpseudocyst

Hydatid cyst

Air, Enh wallDouble target sign

‘Cluster sign’Low Att/

No wall/ enhancement

T1 T2

CalcificationDaughter cysts

Pericyst (T1,T2 )Matrix (T1 T2 )

Lt. liver lobeSigns of pancThin capsule

Signs of traumaLow att at CT

Meth Hb at MRI

No capsuleNo septa

No calcification

Solitary, heteenh solid comp

T1 T2

D/D : Malignant cystic lesions

Cystic metastasis Ovarian tumors Teratomas Squamous cell Ca

Pediatric liver masses• MC liver neoplasm in children, as in adults, is metastasis

• Most primary tumors are malignant,1/3rd benign

• MC benign tumors are IHE, FNH, mesenchymal hamartoma, NRH & hepatocellular adenoma

• Malignant – Metasasis, hepatoblastoma, HCC, Lymphoma

• Others - Abcesses, hematoma

Ellen MC, et al. RadioGraphics 2010; 30:801–826

D/D of Pediatric liver tumors

• Age < 5years-hepatoblastoma ,IHE,mesenchymal hamartoma, metastasis.

• Age> 5 years : HCC, adenoma and metastasis.

• AFP- HCC , hepatoblastoma

• Solitary vs multiple SOL- IHE, metastasis, abscess,lymphoproliferative disease, adenoma,

Infantile hemangioendothelioma

• 90% before 6 months,F>M• Mesenchymal tumor , vascular channels formed by

endothelial proliferation • Usually presents as hepatomegaly/abdominal

mass/congestive heart failure due to AV Shunting in the lesion/ thrombocytopenia due to platelet sequestration (kasabach meritt syndrome )

• May be associated with cutaneous hemangiomas

Ellen MC, et al. RadioGraphics 2010; 30:801–826

TYPE 1 Vasc channels lined by

endothelial cells supported by reticular fibres

TYPE 2 Large irregular branching

spaces lined by immature pleomorphic cells

USG Variable, highly echogenic

to hypoechoic /anechoic mass.

Celiac axis & CHA are dilated

Abdominal aorta caliber below coeliac axis origin reduces

Hepatic veins become prominent

CT

Hypodense ,well defined , homogeneous nodule

Calcification in 40%

Centripetal filling as in hemangioma.

MRI• Hypointense on T1WI and hyperintense on T2W• Heterogeneous if necrosis, hemorrage and

fibrosis• Feeder vessel-flow void• Centripetal fill in of contrast post gadolinium

Mesenchymal hamartoma• Benign cystic mesenchymal tumor• < 2 years, M>F Abdominal distension• Large mass(5-22cm),right lobe,

encapsulated and pedunculated, gelatinous mesenchymal tissue with cyst

Ellen MC, et al. RadioGraphics 2010; 30:801–826

USG

Solid / cystic mass, multilocular with anechoic areas with echogenic septae and stroma .

CT

Complex mass, low attenuation areas separated with enhancing septa and stroma.

MRI

Cystic component is hyper on T2 and mesenchymal (stromal) tissue is hypo on both T1 &T2

DW MRI in focal liver lesions• With advances in hardware and coil systems, DW MRI – now be applied to liver imaging with improved image quality.

• Enables qualitative & quantitative assessment of tissue diffusivity (ADC) without Gd chelates, which makes it a highly attractive technique, particularly in patients with severe RF at risk for NSF.

• Detection and characterization with better results compared with T2-WI.

• Should be interpreted in conjunction with conventional sequences.

Taouli and Koh , Radiology 2010.

Taouli and Koh , Radiology 2010.

DWI in liver cysts

b=100

b=600

b =1000Hemangioma

b0 b100

b500 b1000

HCC

ADC

Lesion detection

Taouli and Koh , Radiology 2010.

Lesion characterisation

Treatment assessmentTaouli and Koh , Radiology 2010.

CONCLUSION• Accurate clinical information needed to select the most

appropriate imaging modality

• Ultrasound is the initial modality for hepatic imaging

• Helical CT/ MRI are able to characterize the hepatic lesions

• DW-MRI has the potential to help detect and characterize

focal lesions in the liver.

• Knowledge of imaging features of liver lesions is essential to

avoid unnecessary work-up and to minimize patient anxiety