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PHTN varices OLT

Matt Robinson Andrew Schumacher

Liver imaging
US, CT, MR US useful in spectral and colour doppler modes to demonstrate portal and hepatic venous flow, investigate biliary tree CT useful for anatomic distortions and mass lesions MR indications similar to CT (pipe dream)

hepatic vein

portal vein

triple phase CT liver


Noncontrast (unenhanced) hepatic arterial phase portal venous phase

radiological contrast media


all about iodine remainder of molecule is carrier, confers solubility, reduces toxicity all RCM are substituted benzoic acid derivatives (C2, C4, C6) monomers and dimers ionic (salts) and nonionic

RCM contd
rapidly partition into intravascular space and interstitium (except CNS) hydrophilic, minimal cellular uptake renal excretion (>90 % clearance w/i 12 hrs with normal kidney function)

ionic monomer (Hypaque, Gastrografin)

nonionic monomer (Optiray)

ionic dimer

nonionic dimer

Noncontrast
Noncontrast (unenhanced) necessary for assessing diffuse hepatic changes
fat infiltration Fe deposition

Focal changes
subtle calcification haemorrhage

portal phase: 150 ml of 60% radiocontrast medium, IV at 3 ml s1, data acquisition between 70 and 90 sec after injection
typically used for detection of relatively hypovascular lesions, including mets

biphasic: 45 ml s1 , arterial phase acquisition between 20 - 40 sec, portal phase between 60 80 sec after injection
primary liver lesions best seen in arterial phase

diffuse disease: fatty liver

diffuse disease: hemochromatosis

cirrhosis
endpoint of variety of chronic disease processes hepatocellular necrosis leading to
hepatic fibrosis nodular regeneration

early changes seen only histologically imaging cannot reliably distinguish micro- vs macronodular cirrhosis commonest finding: atrophy of posterior segments (VI, VII) of the right lobe hypertrophy of caudate lobe (I), lateral segments of left lobe (II, III) frequently seen

cirrhosis: vascular changes


hepatic, portal system dynamics radically altered increased overall hepatic blood flow (intrahepatic arteriovenous shunts) decreased hepatocellular perfusion (increased intrahepatic vascular resistance)

cirrhotic arteriogram

1) hepatocyte degeneration and intracellular accumulation


balloon degeneration foamy degeneration microvesicular steatosis

2) necrosis and apoptosis


usually centrilobular rarely midzonal or periportal Councilman bodies (fragmented nuclei) w/ apoptosis bridging necrosis (portal-portal, portalcentral, central-central fibrosis)

3) inflammation
periportal T cell infiltration macrophage scavenging of apoptotic debris granulomatous reaction

4) regeneration
micronodular macronodular

5) fibrosis
irreversible collagen deposition periportal, perivenular, Space of Disse fibrosis regenerative nodules surrounded by fibrotic scar tissue

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