THE LIVER Methods of examination 1. US 2. CT 3. MRI 4. Nuclear medicine

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THE LIVER Methods of examination 1. US 2. CT 3. MRI 4. Nuclear medicine

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THE LIVER Methods of examination 1. US 2. CT 3. MRI 4. Nuclear medicine. CIRRHOSIS Pathologically cirrhosis consists of varying amounts of hepatic necrosis, fibrosis, fatty infiltration and nodular regeneration Types : - PowerPoint PPT Presentation

Transcript of THE LIVER Methods of examination 1. US 2. CT 3. MRI 4. Nuclear medicine

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THE LIVER

Methods of examination

1. US2. CT3. MRI4. Nuclear medicine

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CIRRHOSIS

Pathologically cirrhosis consists of varying amounts of hepatic necrosis, fibrosis, fatty infiltration and nodular regenerationTypes:1.Chronic sclerosing cirrhosis – minimal regenerative activity of hepatocytes, little nodule formation, liver is hard and small.

2. Nodular cirrhosis – regenerative activity with presence of many small nodules; initially the liver may be enlarged.

Causes – alcohol, hepatitis B, hemochromatosis

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Radiographic featuresLiver- Small liver, increased echogenicity, heterogeneous- Nodular surface- Regenerating nodules – hypoechoic- Unequal distribution of cirrhosis in different segments – left lobe appears larger than right lobe; lateral segment of left lobe enlarges, medial segment shrinks; ratio of the width of the caudate lobe to the right hepatic lobe is 0,6Portal hypertension- Collaterals – left gastric, paraesophageal, mesenteric, splenorenal- Splenomegaly- AscitesComplications – hepatocellular carcinoma, esophageal varices with bleeding

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FATTY LIVERCauses – obesity, alcohol, hyperalimentation, debilitation, chemotherapy, steroidsRadiographic findingsUS – fat increases liver echogenicity, renal cortex appears more hypointense relative to liver than normal, intrahepatic vessel borders become indistinct or cannot be visualized, nonvisualization of diaphragmCT – fatty areas are hypodense, hepatic and portal veins appear dense because of decreased parenchymal density

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PYOGENIC ABSCESSPathogens – Escherichia Coli, aerobic streptococci, anaerobesCauses – ascending cholangitis, trauma, surgery, portal phlebitis.Radiographic features- CT – hypodense with peripheral enhancement, no fill-in.- Double target sign – wall enhancement with surrounding

hypodense zone.- 30% contain gas.- any abscess can be drained percutaneously, particularly: deep

abscesses, no response to treatment, nonsurgical candidates.

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HYDATID DISEASEHumans are intermediate hosts of the dog tapeworm (taenia echinococcus). Two forms: E.granulosus – more common, few large cystsE.multilocularis – less common, more invasiveRadiographic featuresE.granulosus- well-delineated cysts- size of cysts usually very large- daughter cysts within larger cysts ( multiseptated cysts) are

pathognomonic- rimlike cyst calcification- double rim sign: pericyst, endocyst- enhancement of cyst wall

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E.multilocularis

- poorly marginated, multiple, hypodense liver lesions.- lesions are infiltrative (chronic granulomatous reaction with

necrosis, cavitation).-calcifications are punctate and dystrophic, not rimlike.

Complications- rupture into peritoneal, pleural, pericardial cavity- obstructive jaundice due to external compression or intrinsic

obstruction of biliary tree

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HEMANGIOMA- Frequency – 4-7% of population, 80% in females.Hemangiomas

may enlarge particularly during pregnancy or estrogen administration.

US- hyperechoic lesions 80%.- hypoechoic lesions especially in fatty liver.- giant hemangiomas are heterogeneous.- anechoic peripheral vessels may be demonstrated by color

Doppler .CT- hypodense, well-circumscribed lesion on precontrast scan

globular or nodular intense enhancement. MRI- hyperintense on heavily T2W sequences.- imaging modality of choice.Nuclear imaging (SPECT)- decreased activity on early dynamic images.- increased activity on delayed blood pool images.

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HEPATOCELLULAR CARCINOMA (HCC)Risk factors – cirrhosis, chronic hepatitis B, hepatotoxins, metabolic disease in paediatric patients Radiographic featuresGeneral- three forms – solitary, multiple, diffuse- portal and hepatic vein invasion is common- metastases – lung, adrenal, lymph nodes, bone

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CT- hypodense mass lesion- early arterial enhancement-Pseudocapsule

US- most small HCC are hypoechoic- larger HCC are heterogeneous-high-velocity Doppler pattern

Angiography - hypervascular- AV shunting is typical- Dilated arterial supply

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METASTASES30% of patients who die of malignancy have liver metastases.Colorectal carcinoma, stomach, pancreas, breast, lungSensitivity for lesion detection: CTAP – high-dose delayed CT – CECT,MRI – US- Echogenic MTS – GI malignancy, HCC, vascular- Hypoechoic MTS – lymphoma, bull’s eye pattern (hypoechoic halo around lesion)- Calcified metastases – all mucinous metastases – colon, thyroid, ovary, kidney, stomach- Cystic metastases – necrotic leyomiosarcoma

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PORTAL HYPERTENSIONCriteria – hepatic wedge pressure 10 mm Hg. Causes:PresinusoidalExtrahepatic (obstruction of portal vein) – thrombosis, compressionIntrahepatic (obstruction of portal venules) – hepatic fibrosis, infection SinusoidalCirrhosis ,sclerosing cholangitisPostsinusoidalBudd-Chiari syndrome, congestive heart failure Radiographic features- Portal vein diameter 13 mm- Collateral vessels – gastroesophageal varices via coronary vein, azygos; SMV collateral – mesenteric varices; splenorenal varices; IMV collateral – hemorrhoids- Splenomegaly- Ascites

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THE BILIARY SYSTEMMethods of examination

1. Abdominal plain film – gas or calcium in the biliary tract2. US3. CT4. MRI + MRCP5. ERCP6. PTC7. Scintigraphy

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ACUTE CHOLECYSTITISCauses - gallstone 95%US - Luminal distension 4cm- Wall thickening 5 mm (edema, congestion)- Gallstones- Pericholecystic fluidComplications - Gangrenous cholecystitis: rupture of GB- Emphysematous cholecystitis- Empyema

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CHRONIC CHOLECYSTITIS

- GB wall thickening (fibrosis, chronic inflammation)- Gallstones- Failure of GB to contract

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CHOLELITIASISTypes:Cholesterol stones are caused by precipitation of

supersaturated bile- Pigment stones – precipitate of calcium bilirubinate- Mixed stonesPredisposing factors:- Obesity- Hemolytic anemia- Abnormal enterohepatic circulation of bile salts- Diabetes- Cirrhosis- HyperparathyroidismUS – method of choice – hyperreflective image with

prominent posterior shadow; mobility of stones (exception – stones impacted in neck or stones adherent to wall)

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CHOLANGIOCARCINOMAAdenocarcinoma of the biliary tree.Clinical – jaundice, pruritus, weight loss.Treatment – pancreaticoduodenectomy or palliative procedures (

stent placement, biliary bypass)Location – hilar (originates from epithelium of main hepatic ducts or

junction –Klatskin tumor) + peripheral – originates from epithelium of intralobular ducts

Radiographic features- Dilated intrahepatic ducts- Hilar lesions – central obstruction + lesions are usually infiltrative

so that a mass is not usually apparent + encasement of portal veins causes irregular enhancement by CT

- Peripheral lesions – may present as a focal mass or be diffusely infiltrative + retain contrast materials on delayed scans + occasionally invade veins

- ERCP very useful

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THE PANCREASMethods of examination

1. CT2. US3. MRI + MRCP4. Arteriography

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PANCREATITISClassification - Mild acute pancreatitis (interstitial edema)- Severe acute pancreatitis (necrosis, fluid collections)- Chronic pancreatitis

Causes- Alcohol- Cholelitiasis- Abdominal trauma- Hyperlipidemia, hypercalcemia- Drugs – azathioprine, sulfonamides- Peptic ulcer- Pregnancy

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Imaging – CT stagingGrade A – normal pancreatic appearanceGrade B – focal or diffuse enlargement of pancreasGrade C – pancreatic abnormalities and peripancreatic

inflammationGrade D – 1 peripancreatic fluid collectionGrade E – 2 peripancreatic fluid collections and/or gasComplications- Necrosis - Acute fluid collections – enzyme-rich pancreatic fluid, no

fibrous capsule- Pseudocyst – encapsulated collection of pancreatic fluid- Abscess- Hemorrhage

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CHRONIC PANCREATITISProgressive, irreversible destruction of pancreatic parenchyma by repeated episodes of mild or subclinical pancreatitis.

Radiographic featuresCommonly small, atrophic pancreasFatty replacement, fibrosis, calcificationsIrregular dilatation of pancreatic duct

ComplicationsPseudocystsObstructed CBDVenous thrombosis – splenic, portal, mesentericCarcinomaMalabsorbtion

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NEOPLASMTypesExocrine pancreatic tumor – adenocarcinoma, cystic

neoplasmEndocrine pancreatic tumor – insulinoma, gastrinomaOther tumors – lymphoma, metastases

ADENOCARCINOMAClinical – jaundice, weight loss, Courvoisier sign

(enlarged, nontender gallblader)

Radiographic featuresMass effectAlterations of densityExtrapancreatic extensionVascular involvementMetastases

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