LIVER

Presented by

Dr. Tahmina Islam

MD Third Part

Anatomy of Liver

• The liver is a large solid gland situated in the right upper quadrant of the abdominal cavity

• Weight: 1-2.5 kg varies with sex; age body mass .weight is maximal in 5th &6th decade then declines rapidly.

• Most of the liver is cover by ribs and costal cartilage except in the upper part of epigastrium where it is in contact with the anterior abdominal wall.

• It has 5 surfaces: -anterior -posterior -superior -inferior -right lateral

ANATOMICAL DIVISION

• Subdivided into 8 segments Landmark by hepatic and portal vein.

FUCTOINAL SEGMENT

On the basis of intrahepatic distribution of HV, PV and billiary ducts.

BLOOD SUPPLY

20% by hepatic artery80% by portal vein.

LYMPHATIC SUPPLY

Superficial :caval, hepatic, coeliac lymph node.Deep: nodes around IVC and hepatic nodes.

EMBRIOLOGY

Parenchyma: hepatic budSupporting stroma: septum transversum.

IMAGING OF LIVER

LIVER IMAGING FULFILS 4 PURPOSES • 1. It assess the cause of hepatomegaly or a

localized liver mass

• 2. it diagnoses a suspected neoplasm either primary or secondary

• 3. It excludes hepatic inflammatory or parasitic

disease.

• 4. It aid planning of therapy medical, interventional, radiological or surgical.

IMAGING METHOD

1) Simple x-ray

2) USG

3) CT

4) MRI

5) FLUROSCOPY

6) Angiography

PLAIN FILM DX • Hepatomegaly• Calcification• GassHEPATOMEGALY:only an appropriate estimation of liver size can be based on

the plain film appearanceRT LOBE -elevated rt hemidiaphram

-Depressed hepatic flexure and duodenum -bulging of the rt. Lateral properitoneal fat -occasional splaying of lower rib

LEFT LOBE- gastric fundus displaced downwards and laterally. -intra abdominal oesophagus elongated.

-extrinsic pressure on the lesser curvature of stomach. -sometimes posterior displacement of stomach. • PSEUDOHEPATOMEGALY=is noted in sever kyphoscoliosis

PLAIN FILM DX

• LOCALIZED MASS

Only visible if they lie adjacent to or deform one of the visible borders or cause a change in an adjacent

structure such as diaphragm.

• Before diagnosis of hepatomegaly it is essential to check the position of diaphragm.

PLAIN FILM DXCALCIFICATION

• Normal liver does not calcify even in old age.• Calcification frequently occurs in structure closely related to liver

such as costal cartilage ,kidney, pleura, GB.• To confirm intrahepatic calcification, lateral view is necessary.

PARENCYMAL CALCIFICATION

• Granuloma eg-TB …………………….multiple, scattered, nodular• Old abscess (pyogenic/amoebic)………..irregular, amorphous• Neoplasm: HCC……………………………..faint stippled or very rarely

“sunburst” type.• Mucous secreting adeno CA………………faint fluffy calcification • Medullary CA of thyroid ……………………faint fluffy calcification• Vascular :Haemangioma……………………rounded, speculated• Cyst: Hydratid cyst………………………….typical crumpled “eggshell”

or fine curvilinear

• Billiary: gall stone……………………………usually in GB and CBD

PLAIN FILM DX• GAS: not normally present in liver .

PATHOLOGY RADIOLOGICAL APPEARENCE

Parenchyma Abscess (by gass forming organism)

In tumour following therapeutic embolization or occurs spontaneously

Rounded space ,fluid level on horizontal beam

Scattered gas collection arranged in tumour distribution

Billiary ducts Rounded space ,fluid level on horizontal beam

Scattered gas collection arranged in tumour distribution

Seen centrally outlines major intrahepatic ducts and CBD

PV Necrotizing enterocolitis

Gut infraction

Hemorrhagic pancreatits

Gas reaches into peripheral

Branches

GENERALIZED INCRESED DENSITY OF LIVER IN PLAIN FILM

• 1) Hamochromatosis

• 2) Previous thorotrast injection.

• 3) Hepatic arterial embolization of neoplasm by lipoid or cytotoxic drugs

USG IN LIVER DISEASES

Most widely used modalities to detect liver disease due to availability, economical consideration and no radiation hazards

Some disease can be detected with almost same specificity by USG compared to CT.

APPEARANCE OF NORMAL LIVER IN USG:

Normal echo texture of liver parenchyma is homogenous and slightly more echo reflective than the adjacent renal cortex.

ECHOGENICITY

LIVER SPLEENHIGH RENTAL SINUS

RENTAL CORTEX RENTAL MEDULLA LOW

• The uniformity of liver tissue is interupted by portal vein.

• The portal vein branches may be identefied by their radiating pattern from the hilum & increased reflectivity of their walls .

• The hepatic veins radiate from IVC & right atrium & their walls are not usually distinguishable from the adjacent parenchyma.

• Diaphragm is routinely seen in transverse & sagittal plane highly echogenic membrane. it serve as a land mark for defining the pleural space & subdiaphramatic space & liver .

• Duplex sonography with pulsed droppler & colour dropler provide afor demonstrating vascular anatomy pathology.

GENERELIZED HYPERECHOIC

• Fatty changes in liver• Cirrhosis • Chronic hepatitis• Glycogen storage disease• Sarcoid infiltration

FOCAL HYPERECHOIC

• Metastasis (GIT,ovary,pacrease)• Capillary Haemangioma• Adenoma• FNH• Focal fatty infiltration• Abcess in early stage• Haematoma(early)• hepatoma

GENERALIZED HYPOECHOIC

• Acute hepatitis• Diffuse malignant infiltration (lymphoma)• Metastasis

FOCAL HYPOECHIC

• Cysts• Metastasis• Lymphoma• Abcess• Haematoma(late)• Sometimescavernous haemangioma

CT OF LIVER

• CT provides a global view of upper abdomen in axial section enabling clear demonstration of the liver anatomy of adjacent structures.

CT OF LIVER

• NORMAL LIVER IN CT• Normal liver parenchyma is homogenous with an

attenuation value of 54-60 HU, usually 8-10HU greater than the spleen. (due to high glycogen content)

• Vascular structures can be identified by their location on the unenhanced

• Images and confirmed by enhancement with I/V contrast.

• Intrahepatic Billiary tree is not normally visualized although the main rt and it hepatic ducts are increasingly demonstrated on modern system.

TECHNIQUES

• HELICAL/SPIRAL CT: Allows computed data acquisition of the upper abdomen in 20 sec or less using 5-8 mm thick section, providing truly contiguous image section.

• UNENHANCED IMAGING: It is necessary for assessing both diffuse Hepatic change such as fat infiltration and iron deposition and focalchanges such as calcification & hge.

• CALCIFICATION:

Haemangioendothelioma

Calcified metastasis of mucinous adenocarcinoma

Post inflammatory calcification i.e-alveolar echinocnccosis

• HAEMORRAGE:

Subcapsular

intraparenchymal

TECHNIQUES

• CONTRAST ENHANCED IMAGING: After intravenous administration of water soluble contrast medium. Biphasic nature of blood supply of liver contrast media uptake time are complex.

Hepatic perfusion cycle can be differentiated in to three idealized phase

1. Arterial phase

2. Redistribution or portal venous phase 3. Equilibrium or hepatic venous phase.

Majority of solid liver lesion have predominantly arterial blood supply.Portal phase imaging is used for detection of relatively hypo vascular lesion including the majority of diseases.

TECHNIQUES

• EARLY ARTERIAL PHASE=10sec after initiation of scanning .contrast enhanced abdominal aorta & hepatic artery without admixture of portal venous blood.

• LATE ARTERIAL PHASE=20sec after scanning initiation, clear depiction of hepatic artery & it branches & minimal enhanced portal venous blood.

• PORTAL VENOUS PHASE=30sec after scan initiation, visualization PV & its branches when HV still non enhanced .minimal contrast enhancement reach after 40sec.

• HEPATIC VENOUS PHASE=Acquared60sec after scan initiation &simultaneous enhancement of HV&PV.

• DELAYEDHEPATIC IMAGING

• EARLY DELAYED CT: used in selective cases over the first few minute after contrast administration to observe the pattern of enhancement in focal lesion eg; hge

• LATE DELAYED CT: Image taken after 4-5hrs.of contrast administration when the excreation of contrast by hepatocyte is in peak.

TECHNIQUES

• DUAL PHASE=known or suspected hyper vascular neoplasm outside the liver parenchyma & suspected hepatic metastasis .Here not include NECT. Breast ca RCC Melanoma Neuroendocrine tumor-islet cell tumor -carcinoid -thyroid ca

• TRIPPLE PHASE=NECT Hepatic arterial phase PVP

eg;cirrhosis HCC FNH Hepatic adenoma

• Cholangiocarcinomas =triple phase +delayed phase

TECHNIQUES• CT ATERIOGRAPHY: Not widely used due to hepatic artery

anatomy.

• CT ARTERIOPORTOGRAPHY (CTAP):

A selective arterial injection (usually up to sup.mesentric artery), thatdelivers a contrast medium bolus indirectly into the liver via portal vein

This technique maximize the differences b/w tumour (supplied hepatic artery) and normal hepatic parenchyma (supplied by portal vein)

For optimal enhancement 20-50 sec. required. Sensitive for subcentimetre lesion when compared to other

approaches. In presence of portal HTN or cirrhosis there may be delayed

enhancement and diversion of contrast medium away from the liver into Porto systemic shunt.

TECHNIQUES

• LIPIODOL CT

Selective arterial catheterization followed by injection of approximately 10ml of lipiodol.

Usually cleared by liver parenchyma 1 week.

Vascular tumour eg.HCC or Haemangioma may retain lipiodol possibly due to defect in wall of tumour vessels or kuffer cells to provide clearance.

MRI OF LIVER

MRI is more sensitive than CT & USG in detecting small lesion.

• INDICATION OF MRI

1.Cherecterization of diffuse or focal lesion of uncertain cause.

2.Determination of the extent & segment localization of hepatic malignancy before planned partial liver section.

3.Follow up cases primary &secondary malignancy.

MRI OF LIVERMRI helps in determing the following feature of a lesion

1. MORPHOLOGY: Size, shape, position, internal, structure of the lesion, margin & any sing of spread into the adjacent structure.

2. PHYSIOCHEMIAL COMPOSION: Water, fat, presence of blood, proteinaseous fluid

3. PERFUSION &LOCAL EXTRACELLULAR FLUID VOLUME:The rate, pattern & persistent of enhancement after contrast administration, a useful indication of local blood flow.

CELLUAR FUCTION: By tissue specific contrast media.Hepatocyte: gd.BOPTA(gadobenate dimeglumine)

gd.EOB-DTPA(gadoxetic acid disodium) mn.DPDP (mangofodipirtrisodium)

Kuffer cells-SPIO (super paramagnetic iron oxide)

TECHNIQUES • T1 weighted images: gives us the greatest magnitude of signal &therefore

the best information density

• T2 weighted images: provide high contrast b/w normal parenchyma &tissue with high water content.

Fat suppression: is achieved by applying a preparatory pulse at the resonant frequency of fat which effectively nulls out the contribution from fat protons, to the signal the signal produced by subsequent spin echo sequence .CHEMICAL SHIFT: The Technique exploits the slightly different resonant frequency fat and water protons

Voxel containing fat and water components appear brighter in “in phase” because fat and water signal are additive and darked in “out phase” images where the fat & water signals tends to cancel each other.

Evaluate effectively the fat containing tumour.

TECHNIQUES

GADOLINIUM ENHANCEMENT IMAGES A dynamic T1 wt series following intravenous inj.of gd is almost always helpful for lesion characterization and probably better than unenhanced T2 imaging for the early detection of small liver lesion.

• Hyper vascular lesions are best demonstrated at the arterial phase of enhancement (10-15sec.after the end of inj.)

• Hypo vascular lesions are best 20-25sec. of contrast inj.

• Delayed images (2-10 mins after inj. ) may be useful in lesion with a fibroid tissue component eg. Haemangomas, FNH, cholangiocarcinomas and to show peripheral wash out of malignant lesion.

TECHNIQUES

LIVER SPECIFIC CONTRAST MEDIUM:

• Kuffer cell agent :SPIO(size 30-200nm) Selectively taken by MNP cells of liver, spleen and bone marrow.

SPIO causes marked reduction in signal intensities in all sequences. This gives contrast b/w normal liver parenchyma with intrahepatic tumour. The neoplasm which consistently contain functioning

• RE cells: FNH Some liver adenomas

Well deffentiated HCC.

TECHNIQUES

• HEPATOCYTE AGENTS

Protein bound chelate of gd or Mn. In T1 wt images: normal parenchyma –hyperintence & tumour containing non-functioning hepatocyte eg.cyst, Haemangioma, metastasis appear hypointence.

RADIO-ISOTOPE SCANE OF LIVER

HEPATOCYTE (85%)-)IDA (Imidodiacacetic acid) agent used

KUFFER CELL (15%)-99mTc labeled colloid. 99mTc-colloid scan-diminished activity- localized and diffuse

RADIO-ISOTOPE SCANE OF LIVER

• LOCALIZED LESION/DEFECT: created by any lesion that does not contain R/E cells.

1. Metastasis 2. Hepatoma 3. Lymphoma 4. Angioma 5. Abcess 6. Cyst • DIFFUSE LOW ACTIVITY: 1. Cirrhosis 2. Portal vein thrombosis (decreased

hepatic perfusion) 3. Budd chiri 4. Extensive metastasis

RADIO-ISOTOPE SCANE OF LIVER

IDA SCAN: • Delayed uptake by liver with increased renal

excreation-impaired liver function

• Normal uptake delayed clearance-Billiary tract obstruction.

• Non-filling of GB by 60 min-acute or chronic cholecystitis

• Non-filling of GB by 4hrs-cystic duct obstruction.

HEPATIC DISORDERS

A) DIFFUSE LIVER DISEASE:

1) Acute viral hepatitis

2) Cirrhosis

3) Fatty infiltration

4) Hamochromatosis

5) Wilson’s disease

HEPATIC DISORDERS

B) FOCAL LIVER DISEASE:

1. NEOPLASM

a. benign- Haemangioma -Adenoma -FNH

b. malignant -1.Primary: HCC -Hepatoblatoma -fibro lamellar ca -cholengio ca -angiosarcoma

2. Secondaries or metastasis

HEPATIC DISORDERS 2. Cystic disease

a. polycystic disease b. simple cysts c. cystic metastasis

3. INFECTIVE a. pyogenic abcess b. Amoebic abcess c. Hydatid cyst d. TB e. Pneumocystitis

4. HEPATIC TRAUMA -Contusion

-Laceration

5. VASCULAR DISORDER-Budd chiari syndrome

-Hepatic venous congestion -Portal HTN

FATTY INFILTRATION • Due to excessive deposition of triglyceride in hepatocyte

• Cause

1. acute and chronic alcohol abuse 2. Obesity 3. DM 4. Malnourihment

5. Corticosteroid therapy 6. Ileal bypass 7. Chemotherapy 8. Cushing syndrome 9. Co-poisoning:

USG Marked increased echogenisity which obscures the portal vein margin. -liver may be mild to moderately enlarge. -poor delineation of right hemidiaphram -Divided in to3grades:

• GRADE-1: Only slight increase in fine echoes. -Normal visualization of intrahepatic vessels and diaphragm

• GRADE-2;Moderately increased echoes. Impaired visualization of intrahepatic vessels and diaphragm

• GRADE-3: sever increase in fine echoes poor delineation

D/D=Fibrosis

CT • Most commonly used technique for confirming and quantifying

• Attenuation decreased by approximately 1.6HU mg of triglyceride increased per gram of liver substance.

• Architecture of liver is preserved especially blood vessels.

• In sever cases, liver attenuation become lower than blood and and hepatic vasculature appear enhancement.

• Liver enhance normally after I/ V contrast.

• Normally liver is 8HUdenser than spleen , each mg of liver of TG per gm of liver decreased density by 1.6HU;

Visual liver less dense than spleen.

MRI

• Most sensitive method

• Chemical shift or in and out phase imaging .

• Uses fat saturation techniques to verify presence of fat .

FOCAL FAT DEPOSION

GB bed Segment IV. Subcapsular region.

• Diffuse fat accumulation in the liver at MR imaging. Axial T1-weighted GRE images show a marked decrease in the signal intensity of the liver.

•  Multifocal fat accumulation in the liver at MR imaging in a 48-year-old woman with breast cancer.T1-weighted GRE MR images show nodules (arrows) with a signal intensity loss on the opposed-phase image .

CIRRHOSIS OF LIVER Is the endpoint of wide variety of chronic disease process

• Cause - Chronic hepatitis - Alcohol abuse

- Hemocromatosis - Drug toxicity

- Chronic Billiary obstruction • This disease process causes: • Hepatic fibrosis Nodular regeneration

• Commonest finding in advanced cirrhosis is -Atrophy posterior segment VI, VII of right lobe

hypertrophy of caudate lobe (I) & left lateral segment (II, III)

• USG findings -Liver may be normal/enlarged in early stage but

small and contracted in chronic Cases.• Echogenisity may be increased courses• Liver contour may be irregular – knobby

protrusion and indentation.• In end stage cirrhosis, the vessels particularly

hepatic views may become attenuated and difficult to visualize.

IN DOPPLER USG

• Reduced main portal blood (less than 10 cms-1 mean peak)

• Occasionally, increased flow in a large recanalized paraumbillical vein will “steal” blood from right portal vein .

• Hepatic arterial flow is usually increased in advance cirrhosis, as the portal contribution to hepatocyte perfusion decreased—arterial dilatation—may produce confusion with bile ducts(enlarged)

CT • On unenhanced, regeneration areas have relatively

normal attenuation but advance fibrosis lowers overall attenuation.

• 4 different pattern of fibrosis: 1.patchy & poorly defined region of low attenuation on NEMDCT 2.Perilobular band of low attenuation in NEMDCT.3.Low-attenuation fibro tic bridging surrounding regenerative nodule.4.diffuse fibrosis causing high attenuation privascular cuffing .and accumulation of iron in hepatocyte increased it .

• These feature frequently co-exist, resulting parenchymal heterogeicity in both pre and post contrast film.

MRI

Relatively insensitive similar at CT finding.

LIVER SCANE

Normal liver accumulate 80-90 %of sulphur colloid in cirrhosis, increase colloid will be taken up by the spleen bone marrow &associated decreased uptake by liver (colloid shift)

ANGIOGRAPHY

Rarely done.Hepatic arteriography shows increased tortuosity of intrahepatic branches ,so called “corkscrew vessels”

HAEMOCHROMATOSIS/IRON OVER LOAD

• Causes iron deposition in both hepatocyte (leading to cirrhotic change) and other organ tissues such as myocardium, skin, endocrine glands.

• Manifestation during 4th -5th decade.

• Increased chance of malignant change.

TYPE

• Primary haemachromatosis (defect in intestinal mucosa, increased iron (Absorption). CLINICALY: Bronze diabetes: cirrhosis, DM, hyper pigmentation.

• Secondary haemachromatosis: multiple transfusion results from iron

uptake predominantly by the RE cells as kuffer cells in liver, bone marrow, spleen.

• R/E: USG: Hyper echoic liver

CT: Dense liver (>75 HU), much denser than spleen .

MRI: Most specific technique Liver and spleen are markedly hypointence on T2w image. When sever, then decreased intensity inT1w image Abnormally reduced signal on T2 is also noted in other

affected organs as LN, pancreas, adrenal, pituitary, bowel, and heart.

• T2-weighted gradient echo axial image in a patient with hemochromatosis demonstrates diffuse abnormal low signal intensity of the liver. The pancreas and spleen appear normal.

• Noncontrast CT scan in a 47-year-old man with sickle cell disease who had undergone multiple transfusions demonstrates diffuse increased attenuation of the liver, representing abnormal iron deposition. The spleen is small and calcified from autosplenectomy.

WILSON DISEASE

• Hepatolenticular degeneration.• Copper deposited in liver, cornea, lenticular,

nucleus of brain, kidney, joints.• May cause cirrhotic changes(macro nodular

type). No malignant transformation.• R/E: USG: Normal specific (normal/fatty change)

CT: increased attenuation

MRI: Increased signal in T1 &decreased signal in T2.

VIRAL HEPATITIS Causes: Hepatitis A, B, non A, nonB, delta virus. Other viruses—Cytomegalovirus virus Epstein-Bar virus Herpes simplex virus Rubella virus Yellow fever virus

R/F:USG

• Hepatomegaly is the most common manifestation.• Decreased parenchymal echogenisity• Prominent portal vein echo(starry sky appearance)• In GB-wall thickening may occur sludge.• Spleen-may be enlarged.

CT, MRI, ANGIOGRAPHY

limited value until cirrhotic change developed.

FOCAL LESION

HAEMANGIOMA

• Commonest benign hepatic tumour.

• Multiple Haemangioma-10% cases.

• Composed vascular channels of various sizes (cavernous to capillary) lined with endothelium often with intervening fibrous tissue of variable amount.

• 80% in female

TYPES

• TYPICAL HAEMANGIOMA-Small, asymptomatic• GIANT HAEMANGIOMA->5cm

R/F: USG :Homogeneous hyper echoic lesion 80 %( capillary)

Hypo echoic lesion 10% especially in fatty liver. Some adult and most neonatal and infantile H.

are cavernous type, which are hypoechoic. (As larger vascular channels).

Giant H. areheterogenous. Post .acoustic enhancement –common. No detectable signal in Doppler USG.

CT Well defined, lobulated lesion (hypo

dense) in pre-contrast scan . After contrast large heterogeneous lesion filling in centripetally & eventually merging with back ground parenchyma.

MRI

• Most specific and sensitive method for DX.• T1W-hypointense• T2W-hyperintense• After I/V Gd –DTPA-rapidly enhanced their

periphery. Then centripetally to become isointense with the adjacent parenchyma.

Hypo attenuating Haemangioma with "bright-dot" sign in 62-year-old woman with rectal carcinoma. Contrast-enhanced CT scan obtained during portal venous phase shows small hypo attenuating mass with tiny enhancing dots (arrows).

Hypo attenuating Haemangioma with "bright-dot" sign in 62-year-old woman with rectal carcinoma. Dynamic gadolinium-enhanced T1-weighted MR images obtained 1 min (C) and 5 min (D) after initiation of contrast agent administration show very slow enhancement (arrows), a finding that is known to be rare in small Haemangioma.

FOCAL NODULAR HYPERPLASIA (FNH)

• Most commonly occur in women aged 20-50 years.• Multiple lesions found in 20% cases.• Asymptomatic, may present with pain & hepatomegaly.• Relative with OCP consumption.

CHARECTERISTIC • Lack of true capsule.• Normal liver elements with lack of normal architecture.• Absent of portal tracts.• small bile ductule in cirrhotic liver. • Calcification and necrosis extremely rare .• No malignant transformation.• 50% FNH have a central stellate fibro vascular scar.

R/E • USG: Non specific finding .well defined mass iso,

hypo,hyper-refletivity related to adjacent normal liver parenchyma &detected mainly by their mass effect.

• CT : NECT : Isodense Mass effect (Compress adjacent vessels)

Central scar (Hypo dense) CECT : Arterial phase -> Markedly enhanced

except central scar. Feeding artery& central vein connected to HV.

• MRI : T1-> I so or Hypo intense ; Central scar – hypo. T2 -> Hyper intense • Rad scan : Norm. colloid uptake [as RE]

28-year-old woman with focal nodular hyperplasia with a retraction of the liver capsule. On hepatic helical CT scan , the mass shows an iso-attenuation with the liver parenchyma& The mass has a central fibro tic scar (small black). After contrast enhancement of the lesion.

ADENOMA • Rare benign tumour • Associated with glycogen storage disease Type I

(multiple)• OCP and androgenic steroid (solitary). • Vascular neoplasm with no portal tracts or bile ducts.• Kuffer cells are virtually absent (present in 20%)• Hemorrhage, thrombosis and nesrosis common.• Fat present.

R/F : USG : Iso to echogenic (if fat present) Heterogeneous if Hge and necrosis present.

• CT : NECT : Equal of lower attenuation of parenchyma.

If Hge -> Hyper dense CECT : Homogenous enhancement.• MRI : T1} Iso to hyper intense T2} Iso to hyper intense• Nuclear Scan : Activity to colloid (Different point from FNH)• Complication: Hge, Infarction, Malignant

degeneration.

HCC or HEPATOMA • Is the commonest primary malignant lesion of liver

• More common in 6th to 7th Decade. It may occur more earlier (3rd to 4th decade) in endemis areas like Asia and Africa.

• M:F = 5:1

• Predisposing factors : .Cirrhosis -> 5% develop HCC . (particularly post nesrotis cirrhosy) . Chronic hepatitis B -> 10% develop HCC . Hepatotoxins (Aflatoxin, OCP, Thorotrast) . Metabolic diseases -> (galactosemia,

glycogen storage disease, haemachromatosis) in pediatric patients.

• AFP level is increased.• • Type -> Focal or solitary

-> Multifocal (40%) -> Rarely diffuse

• (< 3cm) Larger lesions may show vascular invasive features, hemorrhage and contain areas of thrombosis and nearosis.

• May contain fat.

• R/F : USG : . Used for screening. . Small lesions may be hyper or hypoechoic. . Larger lesions show internal heterogeicity. portal vein involvement & thrombosis is a common

finding, causes loss of venous land mark ,echogenic material with in portal vein .dilatation of splenic &

portal vein

CT:NECT: Ill-defined low attenuation lesion (hypo dense), calcification 7.5%

CECT:Mosaic pattern of enhancement biphasic CT is most sensitive as10%

tumors are visible in arterial phase.CTfeature of portal venous invasion by HCC:1. Arterio-portal fistula2. Per portal streaks of high attenuation3. Dilatation of portal vein or its major branchesStraight line sign:

During CTAP,portal vein invasion may be demonstrated by complete nonenhancement of effected lobe.

• MRI:T1: Mostly hypo to iso intese

If fat containing tumor then hyperintence

T2: Always hyperintence

• CET1: hyperintence arterial phase.

• RADIO NUCLIDE SCANE: Non-Specific

• ANGIOGRAPHY: Hyper vascular, Dilated Arterial supply.

Transverse T1-weighted MR images in 50-year-old woman with cirrhosis secondary to autoimmune

hepatitis. There is marked signal intensity loss throughout the hepatic parenchyma (arrows) on the (a) in-phase image (repetition time msec/echo time msec, 170/4.4; 70° flip angle) in comparison with the (b) opposed-phase image (170/2.2, 70° flip angle), secondary to the presence of siderotic regenerative or dysplastic nodules.

FIBROLAMELLAR CARCINOMA

• Young adult• No sex predilection • USG :large solitary, well demarcated hyper reflective mass.• NECT: hyopodense frequently central calcification• CECT:inhomogenous enhacement arterial phase. necrosis –hypodense area delayed enhancement of the central scar• MRI: T1:hypointense T2:hyperintense &central scarhypointense• SPIO: not accumulate

HEPATOBLATOMA

• Occur with in 5years of age. • Malignant Childhood tumour• Incidence more in previously affected siblings ,familial

polyposis,trisomy18.• Associated with CVS anomaly, diaphramatic defect,UT anomaly.• R/F similar to hepatoma except that, 50%cases amorphous

calcificationUSG: mixed echogenic having calcificationNECT: hypodense with calcification

CECT: heterogenous hyperdense in arterial phaseMRI:T1-hypo

T2-hyper

Mixed echogenic structures having calcification in the lt. lobe of liver

INFANTILE HAEMANGIO ENDOTHELIOMA

• Benign lesion in new born• May be multi focal or solitary• Present 1st month of life• C/F: hepatomegaly High output CCF Hge consumptive coagulopathy cuteneous Haemangioma• Sinusoidal vascular channels lined by endothelial cells are Supported by connective tissue stoma.• Proliferation followed by involution ,which fibrous & fatty tissue accumulation

with areas of infarction &dystrophic calcification. • R/F:

CT: single, multiple intraparenchymal hepatic lesion with large high-flow feeding vessels.

INFANTILE HAEMANGIO ENDOTHELIOMA

• MRI:T 1:low signal

T2:high signal

• USG:ill defined isochoric mass with multiple vascular channel .

Ultrasound reveals a large, globular, well circumscribed hypoechoic mass within the left lobe of the liver. The blood vessels supplying the mass are tortuous and dilated, and demonstrate nonphasic low resistance brisk blood flow. Parasaggittal view of abdominal aorta demonstrates enlarged aortic caliber proximal to the celiac axis, with marked tapering of the aorta distal to the celiac axis.

Coronal T1 weighted views of the abdomen demonstrate a large, slightly nodular, well circumscribed mass within the left lobe of the liver. The mass demonstrates slightly heterogenous, but primarily decreased signal intensity with several punctate regions of increased signal intensity, suggestive of focal areas of hemorrhage. The T2 weighted axial views through the liver demonstrate well circumscribed mass within the left lobe of the liver with slightly heterogenous, but primarily increased signal intensity. There are numerous, prominent flow voids within the mass.

METASTASIS

• Liver is the most common metastatic site after regional LN.• Metastatic CA is most 20 times more common than then

primary.• Organ origin :GIT specially pancreases, colon, stomach &

breast ,lungs.• C/F: Hepatomegaly Abnormal liver enzyme . usually involved both lobe, in isolated cases

right lobe more common then left. commonly multiple50-98%.

R/F:USG

• Mostly multiple liver mass with variable sizes & shapes. Variable echogenicity with poorly defined margin.

ECHOGENIC MATASTASIS: Colonic CA Treated breast CAGIT primaryVascular metastasis (carcinoid,islets cell tumour

ECHOPENIC METASTASIS:LymphomapancreasesSarcomalung (adeno - CA)

• MIXED METASTASIS: Breast CA Rectal CA Cervical CA Lung CA

• CYST: Mucinous ovarian CA Colonic CA Chorio CA Cyst adenocarcinoma of pancrease

Bull eye or target lesion mainly seen from GIT.

CT: Enhancement character of metastatic lesion:(1) Although hepatic metastasis generally derive their blood supply from HA, they are less vascular than adjacent liver parenchyma.Metastatic tumour with increased vascularity than adjacent liver parenchyma are:

1) Liver 2) Kidney 3) thyroid 4) Neuroendocrine 5) Melanoma

(2) Less enhancement during portal venous phase.(3) Extra cellular space agent accumulate more in tumour tissue as metastases has a larger interstitial space.

NECT: Hypo denseCECT: Hypo dense and remain so on portal phase

images. Hyper vascular tumour are often visible as transiently in arterial phase and some become invisible in portal phase.

• CT is the most sensitive method for detecting subtle calcification.

Calcified liver metastases:1) Mucinous adeno carcinoma of –

• Colon • Brest • Ovary • Stomach2) Endocrine pancreatic carcinoma3) Neuroblastoma4) Medullary Ca of thyroid5) Renal cell Ca etc.

• Central Necrosis and rim enhancement clearly demonstrated on CT.

• MRI: T1W - Hypo intenseT2W - Hyper intense

• Nu. scan: Reduced areas of radio activity

Colon carcinoma metastasis on MRI. T2-weighted MRI of the liver shows two hyperintense masses. The high signal and heterogeneous nature of these tumors are typical for metastatic deposits. MRI is particularly helpful in the patient with suspected diffuse metastatic disease in whom CT or US might underestimate tumor burden.

Multiple metastases from breast cancer seen to better advantage using MRI than CT. A. Contrast-enhanced CT is normal. Metastases are not identified. B. T2-weighted MRI shows multiple liver metastases. In this case, MRI was considerably more sensitive for lesion detection than CT.

ABSCESS Pyogenic eg. E. Coil in adult, staphylococcus in children Amoebic by E. histolytica Fungal

C/F: • Hepatomegaly (tender), • Fever, • JaundiceCause: √Ascending cholangitis √ Trauma √ Surgery

R/F: • USG: Typically appears as solid spherical lesion with an ill defined

margin and low echoreflectivity. As abscess liquefy, a thickend and irregular wall becomes visible and necrotic centre often contains sparse echo’s from debris.

CT: Hypo dense, ill defined

CECT: Enhancement predominantly around the edge of the lesion. (If antibiotic treatment starts then this enhancement pattern is not apparent.

MRI: • T1- Hypo• T2- Hyper intense (mostly with a higher signal in outer margin)• After contrast Rim enhancement.

Am. Abscess: Usually solitary…Usually rt lobe ….. Irregular …….. Pt. moderately unwell ….. Yes

Pyo. Abscess: Usually multiple….Usually deeply situated....Irregular… Pr. very ill …………… Yes

Cyst: Multiple or solitary… …. Anywhere……..Sharp outline…..Usually asymptomatic…. No

Number Internal Location Clinical Wall Response to Presentation Metro

HYDATID DISEASE

• Organism: Echinococcues granulosus. Common in Rt lobe of liver.• Life cycle: E. granulosus is composed of scolex and only three

proglottids, making it one of the smallest tapeworms.• Dogs are definitive host, while sheep and human are intermediate

host.• In a typical life cycle, worm in dogs intestine liberates thousands of

eggs ingested by sheep (or human)The oncosphere embryos emerge in small intestine.Migrate to liver but also to lungs, bones and brain.The embryos developed in to large fluid filled “hydotid cyst”,

the inner germinal layer of which generates many protoscoleces within “brood capsule.”Life cycle is completed when the entrails (eg. liver

containing hydatid cyst) of slaughtered sheep are eaten by dogs.

• R/F : • USG: Variable maybe - As simple cyst Cyst with dependant debris Daughter cyst (cyst within cyst) Membrane separation (water lily sign) Wall calcification

• CT: Calcification + All above features.

• MRI: Nor sensitive to detect calcification.

CT scan shows renal hydatid with multiple daughter cysts.

CYSTIC DISEASEA SIMPLE LIVER CYST:

Frequent finding in USG. Incidence in 2.5% population. More common with aged, 7% in pt over 80yrs. Considered as cong. lesions, though exact pathogenesis in unknown. More common in women, especially in rt. Lobe

R/F: • USG: Anechoic, well defined imperceptible wall, most are 1-2cm in diameter. Distal acoustic enhancement is present. Thin septum may be soon.

CT: • Well defined• Mass of water density• No wall enhancement

MRI: • T1 Hypo intense• T2 Hyper intense

POLYCYSTIC LIVER DISEASE • Cong. hepatic fibroses and polycystic liver disease are a part

of spectrum of fibropolycystic disease of liver. • It is characterised by periductal fibrosis and aberrant bile duct

proliferation.• In A. dominant PC disease there may be kidney or liver involvement

of both 57 -74%.• >10 cysts are required to diagnose PC liver diseases.

• R/F: • USG: Extensive involvement with cysts that have irregular flattened shape.

• CT: • Multiple cysts in the liver• No enhancement• Calcification may be soon in the cyst walls.

• MRI: • T1 Hypo intense• T2 Hyper intense

HEPATIC TRAUMA May lead to –

I. Intraparenchymal laceration & haematomaII. Sub capsular haematomaIII. Capsular rupture with intraperitoneal Hge.

Secondary complications are: Ischemia and necrosis of part of liver Abscess Haemobilia Calcification Focal fibrosis Lobar/ segmental atrophy.

R/F: USG:• Intraperitoneal fluid (suggest cap. rupture and hge.) appears

as echo reflective (very recent) similar to adjacent parenchyma.

• Parenchymal laceration with adjacent hematoma appears mixed echogenic areas.

• Can be used as a modality for follow-up in known injury case.

CT: Method of choice for trauma evaluation in U/A. In NCCT laceration appears as low density area. Recent Hge appears higher attenuation than normal blood. Laceration that involves the hilum of demonstration of a major perfusion

deficit may indicate a major vascular injury.

Angiography: Only necessary when –

There is continuing Hge (life threatening) then it may demonstrate site of cause of Hge.

Therapeutic embolisation may aboid surgical intervention in this case.

VASCULAR LESIONS

BUDD-CHIARI SYNDROME Obstruction of hepatic veins 2ndary to obstruction of the

IVC by a membrane of thrombus of occlusion of the major hepatic vein branches is termed as BCS.

It may occur in associated with OCP use, Coagulopattries (eg. polycyethemia, TTP), secondary to compression of hepatic vein by tumours or following HV trauma of surgery.

In most pts. there is relative preservation of “Caudate lobe”.

Acute presentation with Hepatomegaly (congestion), Splenomegaly, Abd. Pain

& Ascites.

Some cases present insidiously with features of secondary portal HTN. In that case, periphery of liver atrophied with compensatory hypertrophy of

caudate lobe.

Type:-I. Occlusion of IVC with or without 2ndary occlusion of Hepatic

vein.

II. Occlusion of major Hepatic vein.

III. Veno occlusive disease of liver progressive thrombotic occlusion of small centri lobular vein.

R/F: USG: Hepatomegaly, Ascites (with caudate lobe preservation)

Doppler USG:

• Abnormal co-lateral veins passing through major hepatic veins or a cont. reversal of flow in a main hepatic vein.

• Walls of hepatic veins may be thickened and more echogenic.• Thrombus may be seen in hepatic veins.

CT:

• NTCT: Enlarge, Congested peripheral liver appears low attenuated than normal.

• CECT: Heterogeneous and reduced enhancement than normal. (D/D malignancy)* but “Caudate lobe” shows normal attenuation in both NECT and CECT.

MRI: Congested peripheral liver appears heterogeneous in both T1 & T2W2.

RAD. SCAN: Normal or increased caudate lobe activity and reduced activity in the remainder of liver.

ANGIOGRAPHY: Characteristic “spider web” appearance. “Web” or stenosis can be demonstrated by cerography.

PORTAL HYPERTENSION • Characterized by elevation of portal venous pressure above normal

(4-8 mm Hg). • Portal HTN is due to increased resistance in PV systems increased total portal venous bl. Folw.• Increased resistance may be due toI. Pre hepatic cause: Portal vein thrombosis –

» infection – portal pyaemia A. cholecystitis

» inflammation – pancreatitis, Nes. colitis» tumour – HCC, Pancreatic Ca, GastricCa. » trauma» coagulopathy» surgery (post. Liver transplant)

II. Hepatic cause: Damage of hepatocytes and fibrosisIII. Post hepatic: CCF, constrictive perisarditis, Hepatic vein occlusion,

supra hepatic IVC.

• R/F: USG:• Portal vein diameter is increased (normal 10-12 mm)• Periportal echogenecity is increased.• Spleen is enlarged with dialatation of splenic• Recanalization of the umbilical or Paraumbilical venis producing bull’s eye appearance in ligamentum teres and can be traced from left portal vein towards umbilicus an anechoic structure (Hepato fugal flow).• Ascites may be present.

• DOPPLER: is usually used to confirm the presence and direction of portal blood flow.

• CT/MRI:• Changes described by USG are better delineated.• MRA has now become the non-invasive method of choice

for assessing portal and hepatic venous vasculature.

• ANGIOGRAPHY: Now largely replaced by non-invasive method. But still be useful to confirm patency and flow reversal of portal vein.

MRI LIVER T1W T2W

Gadolinium

Hepatocellular Ca………... , iso or ……..… ………………………..

(due to fat degeneration) Metastases ……………….. …………… ………...............… ±* MRI with shows improved detection than CT. Haemangioma …………… ……………. ++ ………….. (like CT)* After admin. Of SPIO haemangiomas become hypo = to CSF at long TE

but metastasis remain hyper intense. Adenoma ……………… ………………….. * SPIO uptake is common.

Focal nodular hyperplasia • Central scar …… ……………… + .……………………• Margins …… isointense ………… ………………….. ±

* SPIO: T2 signal loss.Regenerating nodular... , isointense ……Haemochrmatosis/ … …………………….. ++Iron deposition

CT LIVER • HCC: NCCT

Hypo dense mass with central area of more hypo density due to necrosis. Mass may be isodense and in these cases contour change is only sign. Signs of cirrhosis.

• CONTRAST

Non-necrotic areas may appear hyper dense with enhancement, at times attenuation may be similar to less than liver. Rim enhancement may be present.

• Metastasis:

Most are hyper dense are usually hyper vascular, does not enhance after contrast.Hyper dense metastasis are hyper vascular like RCC, melanoma, chorio carcinoma.

• Hemangioma:

Enhancement is iso intense or hyper intense to aorta. Contrast will persist in delayed imaging and show peripheral globular pattern.

CT LIVER

• Focal nodular hyperplasia:NCCT:

Low density mass with central lower density representing fibrosis.

CONTRAST:• Iso intense to hyper intense,• Central low density area for scar.• In delayed image contrast may accumulate in

the scar.

Hepato cellular adenoma

NCCT:

• Well defined low attenuated mass, central scar of lower attenuation.

• Calcification is common, may occur in scar.

CONTRAST: Enhancement of tumour due to perivasculatity.

Hypato blastoma

NCCT:

Low density solid mass that may contain calcification.

CONTRAST:

Hyper vascular tumour, so intense contrast enhancement.

Lymphoma: Focal large mass of low attenuation. Diffuse masses may

of may not cause liver enlargement and difficult to

distinguish from normal liver

Thank you