Diagnostic Ultrasound - Abdomen and Pelvis

Hepatic Cirrhosis
TERMINOLOGY
Definitions
• Chronic liver disease characterized by diffuse parenchymal
necrosis with extensive fibrosis and regenerative nodule
formation
○ Common end response of liver to variety of insults and
injuries
• Portal hypertension: Varices, ascites, splenomegaly
• Siderotic regenerative nodules
○ NECT: Increased attenuation due to iron content
○ CECT: Nodules disappear after contrast
– Nodules & parenchyma enhance to same level
• Dysplastic regenerative nodules
○ NECT: Large nodules are hyperdense (↑ iron + ↑
glycogen)
– Small nodules are isodense with liver (undetected)
○ CECT: Iso-/hyperdense to normal liver
IMAGING
General Features
MR Findings
• Best diagnostic clue
• Siderotic regenerative nodules: Paramagnetic effect of iron
○ Nodular contour, coarse echotexture ±hypoechoic
within nodules
nodules
○ T1WI: Hypointense
• Location
○ T2WI: Increased conspicuity of low signal intensity
○ Diffusely involving both lobes
○ T2 gradient-echo or FLASH: Markedly hypointense
• Size
○ Gamna-Gandy bodies (siderotic nodules in spleen)
○ General atrophy with relative enlargement of
– Caused by hemorrhage (portal hypertension) into
caudate/left lobes
splenic follicles
Ultrasonographic Findings
– T1 and T2WI: Hypointense
• Grayscale ultrasound
– T2 GRE and FLASH images: Markedly hypointense
○ Nodular liver surface contour
• Dysplastic regenerative nodules
○ Hepatomegaly (early stage)/normal size/shrunken
○ T1WI: Hyperintense compared to liver parenchyma
○ Enlarged caudate lobe & lateral segment of left lobe
○ T2WI: Hypointense relative to liver parenchyma
○ Atrophy of right lobe & medial segment of left lobe
• Fibrotic and fatty changes
○ Increased echogenicity of fissures & portal structures
○ T1WI: Fibrosis: Hypointense; fat: Hyperintense
○ Coarsened echotexture, increase parenchymal
○ T2WI: Fibrosis: Hyperintense; fat: Hypointense
echogenicity
Elastographic Findings
○ Steatosis
• Transient elastography (FibroScan, Echosens; Paris, France)
○ Regenerating nodules (siderotic)
○ Significant fibrosis ≥ 7.71 kPa (Metavir score F2)
– Iso-/hypoechoic nodules
○ Cirrhosis≥ 15.08 kPa (Metavir score F4)
○ Dysplastic nodules (> 1 cm)
○ Morbid obesity and ascites preclude use of elastography
– Considered to be premalignant
• Shear wave elastography
– Difficult to differentiate from small hepatocellular
○ Cutoff values for fibrosis are device-specific, measured in
carcinoma (HCC)
m/s
○ Compression of hepatic veins
– F2 > 1.34 m/s
○ Signs of portal hypertension
– F3 > 1.55 m/s
– Splenomegaly
– F4 > 1.8 m/s
– Portosystemic shunts, varices
– Ascites
DIFFERENTIAL DIAGNOSIS
○ Signs of hypoalbuminemia
– Ascites
Budd-Chiari Syndrome
– Edematous gallbladder wall and bowel wall
• Occluded or narrowed hepatic veins ± IVC, ascites
• Color Doppler
• Liver damaged, but no bridging fibrosis
○ Hepatic vein: Portalization of hepatic vein
• Ascites
– Loss of normal triphasic/flattened hepatic vein
• Acute phase: Hepatomegaly, hemorrhagic infarct
– Turbulence if hepatic vein compressed
• Chronic phase: Fibrosis (post infarct), large regenerative
○ Portal vein: Increased pulsatility, decreased velocity
nodules, collaterals
– Hepatofugal flow (away from liver)
• Caudate lobe sparing (enlargement)
○ Hepatic artery: Dilatation of hepatic arteries with
Hepatocellular Carcinoma
increased arterial flow
• Hypoechoic lesion within cirrhotic liver
– Hepatic artery hypertrophy often seen in setting of
• May see portal vein thrombosis/invasion
hepatofugal portal venous flow
Treated Metastatic Disease
CT Findings
• Example: Breast cancer metastases to liver
• Nodular contour & widened fissures
○ May shrink and fibrose with treatment simulating
• Atrophy of right lobe & medial segment of left lobe
nodular contour of cirrhotic liver
• Enlarged caudate lobe & lateral segment of left lobe
• Regenerative nodules; fibrotic & fatty changes
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Diagnoses: Liver
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