radiographic evidence of liver cirrhosis & sequelae ashley evans, ms3
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Radiographic Evidence of Liver Cirrhosis & Sequelae
Ashley Evans, MS3
Liver Cirrhosis
• Cirrhosis is the result of:Alcoholic liver disease Viral hepatitisPrimary biliary cirrhosis Primary sclerosing cholangitis Congestive hepatopathy, Wilson’s disease, Hemochromatosis,
In North America, ~75% of cirrhosis cases are attributed to chronic alcoholism1
Cirrhosis
• Among the leading causes of death in the western world
• Pathologically defined by 3 main characteristics: – Fibrosis– Nodular transformation– Distortion of hepatic architecture
Pathophysiology of CirrhosisInsult to Liver Cells
Cell Necrosis and Regeneration
Diffuse Fibrosis Regenerating Nodules
Destruction of Histological Structure
Hallmark Findings
• Nodular Liver• Portal Hypertension
• Hepatofugal Portal Venous Flow
– Portosystemic Vascular Shunts• Esophageal varices• Gastric varices• Superficial abdominal wall collaterals
– Ascites– Splenomegaly
• Hepatocellular Carcinoma• Hepatopulmonary Syndrome
Why Do We Image?
• Characterize the morphologic manifestations of the disease
• Evaluate the hepatic and extrahepatic vasculature
• Assess the effects of portal hypertension
• Detect hepatic tumors Numminen, et al. Scandinavian Journal of Gastroenterology; 2005
Imaging OptionsCT Scan
Ultrasound
MRI
Angiography
Murakami, Seminars, 2001.
Cirrhosis: Characteristic Findings
• Nodularity – Best seen affecting the liver
margin (especially left lateral)
• Cobblestone appearance
• Diffuse heterogeneity of liver parenchyma
• Atrophy of the right lobe and hypertrophy of the left and caudate lobes
Murakami, Seminars, 2001.
Van Beers, et al. AJR; 2001
CT Normal
MRI Chronic Cirrhosis
Cirrhosis: Early Imaging Changes
• Enlargement of the hilar periportal space
• Enlargement of the major interlobar fissure
• Expansion of pericholecystic space or gallbladder fossa
Numminen, et al. Scandinavian Journal of Gastroenterology; 2005
Portal Hypertension
• Responsible for the most devastating complications of end-stage liver disease:– Upper GI bleeding– Ascites– Hepatic encephalopathy
Portal Hypertension
• Extensive fibrosis of the spaces of Disse
• Nodular regeneration– Resistance to sinusoidal blood flow– Intrahepatic mesenteric vasodilators– Extra- and intrahepatic portosystemic
anastomoses develop to divert some portal venous blood directly into the systemic venous circulation
Kang, et al. Radiographics: 2002
Hepatofugal Blood Flow
Bryce, et al. AJR; 2003
79 yoF with alcoholic cirrhosis
The finding of a small main portal vein strongly correlates with hepatofugal flow6
Hepatofugal Blood Flow
Bryce, et al. AJR; 2003
49yoM Hep C cirrhosis
Enhancement of the portal vein during arterial phase indicates hepatofugal portal venous flow6
Portosystemic Vascular Shunts
• Variceal hemorrhage is a devastating complication that occurs in 25 to 40 percent of patients with cirrhosis – Gastroesophageal collaterals– Superficial collaterals– Splenorenal shunts– Retroperitoneal and mesenteric collaterals– Transhepatic Portosystemic collaterals
• Recanalized paraumbilical vein• Hepatic surface collaterals
Esophageal Varix
CT scan shows a tortuous, enlarged paraesophageal varix (arrows).
Kang, et al. Radiographics: 2002
Gastric Varix
Kang, et al. Radiographics: 2002
Axial CT scan shows dilated left gastric vein between the anterior wall of the stomach and the posterior surface of the left hepatic lobe
Anterior Abdominal Wall Collaterals
• CT appearance of the anterior abdominal wall in a normal patient at the level of the umbilicus
• CT showing multiple collateral superficial veins
Groves, et al. BJR; 2002
What is the significance of collateral vessels?
The maximal number of superficial collaterals on a CT image was significantly greater (p<0.02) in a cirrhotic cohort than a control cohort
Groves, et al. BJR; 2002
Ascites
• Def: accumulation of fluid within the peritoneal cavity
• Most common complication of cirrhosis– Due to elevated portal pressures, low albumin levels
• Nearly 60% of patients with compensated cirrhosis will develop ascites in 10 years– 2 year survival of patients with ascites is ~50%8
• Can develop into spontaneous bacterial peritonitis (SBP)
Ascites
• In most cases, the attenuation of the ascites is that of clear fluid, measuring around 0 HU
• If the attenuation of ascitic fluid is significantly greater than 0 HU, this should raise concern for hemorrhage or SBP
T2 weighted MRI with fluid around right lobe
Chopra, et al. Radiology; 1999
CT scan demonstrating ascites
Bryce, et al. AJR; 2003
Splenomegaly
• Common in patients with severe portal hypertension
• Although the spleen may become massive, it is usually asymptomatic
• May contribute to the thrombocytopenia or pancytopenia of cirrhosis
Splenomegaly
T1-weighted MRI demonstrates nodular liver, fibrosis,
splenomegaly.
Murakami, Seminars, 2001.
Hepatocellular Carcinoma
• Risk of HCC in patients with cirrhosis due to hepatitis C is approximately 100x the risk of non-infected cirrhotics (alcoholic cirrhosis is 2-3x increased risk)1.
• Incidence is rising in the United States– Has almost doubled over the past 20 years,
most likely due to rising incidence of Hep C
Detection of HCC
• Commonly diagnosed by ultrasound on routine screens of cirrhotic livers
• CT and MRI are useful to characterize any hepatic tumors detected by US
Ultrasound of well-differentiated HCC
Murakami, Seminars, 2001.
Hepatocellular Carcinoma
Large HCC shown by T1 spin echo (left) and T2 spin echo (right).
HCC show in precontrast CT (left), arterial phase (middle) and equilibrium phase (right).
Detection of HCC
• Detection of liver lesions is dependent on contrast difference between normal parenchyma and the nodules.– This is affected by cellularity, fibrosis, fatty
change and vascularity of nodules
• Arterial phase CT scan is thought to be the most useful technique for detecting hypervascular tumors such as HCC.
Hepatopulmonary Syndrome
• Defined by the triad of:– Liver disease– Increased A-a gradient on room air– Evidence for intrapulmonary vascular
abnormalities
• Signs and symptoms:– Dyspnea, platypnea, orthopnea
Hepatopulmonary Syndrome
• On CT scans, pulmonary vessels are enlarged, do not taper normally, extend to the pleural surface, and are most numerous in the bases
• The ratio of the diameter of the segmental arteries to the diameter of the accompanying bronchi is increased in hepatopulmonary syn.
Lee, et al. Radiology; 1998.
The End
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Liver Disease. 2001; 21(2):213-24.2. Gupta AA. Kim DC. Krinsky GA. Lee VS. “CT and MRI of cirrhosis and its mimics.” American
Journal of Roentgenology. 2004; 183(6):1595-601.3. Sheth S. Horton KM. Fishman EK. “Vascular sequelae of cirrhosis: evaluation with dual-phase
helical CT.” Abdominal Imaging. 2002; 27(6):720-7.4. Kang HK. Jeong YY. Choi JH. Choi S. Chung TW. Seo JJ. Kim JK. Yoon W. Park JG. “Three-
dimensional multi-detector row CT portal venography in the evaluation of portosystemic collateral vessels in liver cirrhosis.” Radiographics.2002; 22(5):1053-61.
5. Numminen K. Tervahartiala P. Halavaara J. Isoniemi H. Hockerstedt K. “Non-invasive diagnosis of liver cirrhosis: magnetic resonance imaging presents special features.” Scandinavian Journal of Gastroenterology. 2005; 40(1):76-82.
6. Bryce TJ. Yeh BM. Qayyum A. Pacharn P. Bass NM. Lu Y. Coakley FV. “CT signs of hepatofugal portal venous flow in patients with cirrhosis.” American Journal of Roentgenology. 2003;181(6):1629-33.
7. Van Beers BE. Leconte I. Materne R. Smith AM. Jamart J. Horsmans Y. “Hepatic perfusion parameters in chronic liver disease: dynamic CT measurements correlated with disease severity.” American Journal of Roentgenology. 2001; 176(3):667-73.
8. Goldberg, E., Chopra, S. “Overview of the complications, prognosis, and management of cirrhosis.” UTDOL. Aug 18, 2005.
9. Lee KN. Lee HJ. Shin WW. Webb WR. “Hypoxemia and liver cirrhosis (hepatopulmonary syndrome) in eight patients: comparison of the central and peripheral pulmonary vasculature.” Radiology. 1999; 211(2):549-53.
10. Chopra, S. Dodd, GD. Chintapalli, KN. Esola, CC. Chiatas, AA. “Mesenteric, omental and retroperitoneal edema in cirrhosis: frequency and spectrum of CT findings.” Radiology. 1999; 211: 737-742.