hepatic cirrhosis is the clinical and pathologic result of a multifactorial chronic liver injury characterized by extensive fibrosis and nodular regeneration replacing the normal liver parenchyma . it is well known that cirrhosis is associated with a markedly increased risk of hepatocellular carcinoma ( hcc ) , the sixth most common malignancy worldwide and third most common cause of cancer related death . the detection of hepatic malignancy in cirrhotic patients is a diagnostic challenge due to distortion of the hepatic architecture . in this article we discuss and illustrate the wide spectrum of intra- and extrahepatic findings on computed tomography ( ct ) in patients with cirrhosis . common pathologic features of cirrhosis include hepatic fibrosis , nodular distortion of hepatic architecture , and perfusion abnormalities . bridging bands usually have variable thickness and may mimic a tumor capsule due to delayed contrast enhancement . focal confluent fibrosis is defined as a peripheral wedge - shaped hypoattenuated area on unenhanced and venous phase ct . on delayed phase , enhancement of overlying capsular retraction with volume loss in areas of focal confluent fibrosis is an important feature to differentiate this entity from malignant conditions   ( figure 1 ) . additional early detectable morphologic changes of the liver include widening of the porta hepatis , enlargement of the interlobar fissure , and expansion of pericholecystic space . during advanced stages shrinkage of the liver is seen , especially in alcohol - induced cirrhosis . the medial segment ( iv ) of the left lobe shrinks with concomitant hypertrophy of the lateral segments ( ii , iii ) , giving a  tongue - like  appearance . these changes lead to a nodular contour and heterogeneity of the liver , which is classically associated with cirrhosis . hepatic steatosis is a nonspecific reversible response of hepatocytes to chronic injury , commonly seen in alcohol - induced cirrhosis . when hepatosteatosis occurs , the average liver attenuation is at least 10 hounsfield units ( hu ) less than the splenic parenchyma on unenhanced ct . the identification of normal course vascular structures in areas of fatty infiltration is crucial to differentiate this abnormality from hepatic tumors . evolving hepatic nodular lesions are another important feature of cirrhosis . in attempt to standardize the terminology , an international working party has suggested terms and definitions of nodular lesions in cirrhotic patients . these are categorized as regenerative nodules , dysplastic nodules , and hcc . a regenerative nodule ( rn ) is a well - defined area of liver parenchyma that has enlarged in response to necrosis and altered circulation . based on gross morphologic features , the nodular regeneration can be classified as micronodular ( <3  mm in diameter ) or macronodular ( > 3  mm in diameter ) . unless a regenerative nodule contains iron , it is rarely seen on a noncontrast ct . if iron deposition is present ( siderotic nodule ) , the nodule appears hyperdense to the surrounding liver on a non - contrast ct ( figure 2 ) . micronodular changes are rarely identified on ct , despite being present in all cirrhotic livers . regenerative nodules do not enhance in the arterial phase ( figure 3 ) and are isodense to the remaining parenchyma on the venous phase , making them indistinguishable from the hepatic background . a combination of micro- and macronodular regeneration is the most common morphologic presentation seen in cirrhotic patients . a dysplastic nodule ( dn ) is defined as a nodular region of dysplastic hepatocytes without histologic features of malignancy . dns commonly measure 510  mm and most of them are undetectable by ct since , even after the administration of contrast , the majority is isoattenuating . dysplastic nodules can be further characterized as low grade or high grade , according to the degree of dysplasia . tumor angiogenesis appears to be a mandatory step in the evolution of dysplastic nodules to hcc . during this process , there is a progressive increase in the arterial supply and a concomitant decrease in the portal venous supply to these lesions . the major shift in angiogenesis typically occurs during the transition from low - grade dns to high - grade dns . new vessels composed of nontriadal arteries become dominant and the absence of portal tracts is noted . the increasingly dedifferentiated nodule appears more markedly enhanced on post - contrast early arterial phase image , occasionally mimicking an hcc ( figure 4 ) . several reports have described the detectability of dysplastic nodules on dynamic ct scans . in a large series of liver transplantation specimens , small dns ( < 5  mm ) the detection rate for dysplastic nodules smaller than 2  cm has been reported , in pretransplant three - phase helical ct study , to be 39% . hcc is a malignant neoplasm composed of cells with hepatocellular differentiation and is almost exclusively seen in patients with cirrhosis . the development of hcc in the cirrhotic liver is described either as de novo hepatocarcinogenesis or as a multistep progression , from low - grade dysplastic nodules to high - grade dysplastic nodule , then to dysplastic nodule with microscopic foci of hcc , then to small hcc , and finally to overt carcinoma . hcc is classified histologically as trabecular , pseudoglandular , compact , and scirrhous , with the trabecular pattern being the most common . the fibrolamellar type of hcc has distinct clinical , histologic , and prognostic features and is commonly seen in young patients with no history of cirrhosis or chronic liver disease . small lesions enhance homogeneously , while large lesions are heterogeneous with a characteristic mosaic pattern , due to intralesional necrosis . approximately 80%90% of hccs are highly vascular lesions demonstrating intense contrast enhancement during the arterial phase . in the venous phase , hcc demonstrates washout and becomes isodense with the liver parenchyma , thereby making its detection difficult . about 10%20% of hccs are hypovascular and show contrast enhancement slightly less than that in the surrounding liver on arterial phase images , making the imaging differentiation with dns difficult . the intranodular vascular changes of these lesions revealed by findings of ctap ( ct during arterial portography ) and ctha ( ct during hepatic angiography ) and correlated with histological analysis explain why high - grade dns and early - stage - well - differentiated hcc are hypodense relative to the surrounding liver . both lesions have decreased portal tracts ( including normal hepatic arteries ) , without increased abnormal arteries . and , when the increased abnormal arterial supply compensated for the decreased normal hepatic arterial supply , they are isodense . understanding this blood supply pattern is important for early detection , characterization , and treatment for early - stage hcc . most hccs have a fibrous capsule that is usually hypodense on hepatic arterial phase and enhance on delayed phase . hcc may present as a solitary mass ( figure 5 ) , a dominant mass with daughter lesions ( multicentric type ) ( figure 6 ) , or as a diffusely infiltrating neoplasm ( figure 7 ) . less frequently , it is multifocal with small foci usually less than 2  cm in both hepatic lobes , which may mimic liver metastasis . hcc is very locally invasive and may extend to the bile ducts , portal vein ( figure 8) , inferior vena cava ( ivc ) ( figure 9 ) , and hepatic veins . distant metastasis from hcc may be seen in the lungs , adrenals , adjacent lymph nodes , and bones . ct is accurate in staging hcc by detecting the number of lesions and involved segments , regional adenopathy , vascular tumor invasion , and metastases . the use of mdct with dynamic contrast - enhanced triple - phase technique and reformatted images is essential to detect small hcc lesions ; however , it remains the most challenging area in imaging cirrhotic liver . this technique demonstrates up to 30% more tumor nodules and in approximately 10% of cases of hcc will be the only phase to demonstrate the lesion   ( figure 10 ) . despite optimal arterial phase imaging , a large number of small ( < 1.5  cm ) hccs remain isodense relative to the background and go undetected on ct . reported sensitivity for dynamic triple - phase contrast enhanced ct ranges from 50% to 96% and the specificity from 75% to 96% . it is well known that to obtain the best conspicuity of lesions , thinner slices ( collimation , 1.5  mm ; image reconstruction interval , 3  mm ) and late arterial phase images ( 3035 seconds after injection of contrast medium ) should be acquired . on the basis of explanted livers , it has been reported that the detection of hepatocellular carcinomas smaller than 2  cm , using three - phase helical dynamic ct , was 60% and the detection of those larger than 2  cm was 82% . the reported sensitivity using previous state - of - the - art mr imaging technique and correlation with explanted liver pathologic results is also disappointing in detecting small hccs and dysplastic nodules smaller than 2.0  cm .   considering that in this country 60%90% of hccs occur in cirrhotic livers   and early - stage detection is difficult , the american association for the study of liver diseases ( aasld ) includes a recommendation for periodic imaging surveillance in patients with liver cirrhosis and stated that the diagnosis of hcc can be made safe if a mass larger than 1.0  cm shows typical features of hcc ( arterial hypervascularity and venous or delayed phase washout ) at contrast material enhanced ct or mri , obviating the need for biopsy if these features are present . in our institution , four - phase mdct is usually the preferred technique in our practice and contrast - enhanced mri is used for problem solving cases or in those patients with any contraindication for contrast - enhanced ct . arterioportal shunting is a well - known phenomenon that occurs in patients with cirrhosis and hcc . the typical imaging presentation is a wedge - shaped area of high attenuation seen on the arterial phase that becomes isodense to the liver parenchyma during the portal venous phase . the classic imaging finding is the presence of contrast material in distal portal branches , with minimal or no contrast in the proximal portal vein or superior mesenteric vein during the arterial phase . spontaneous rupture of hcc is an unusual complication identified in approximately 8% of the cases ( figure 11 ) . extrahepatic abnormalities associated with cirrhosis include portal hypertension , ascites , splenomegaly , diffuse intra and retroperitoneal edema , small bowel , and gallbladder wall thickening . portosystemic collaterals develop spontaneously , as blood flow is shunted away from the liver to low pressure systemic vessels ( hepatofugal flow )   ( figure 12 ) . gastrointestinal variceal bleeding is the most common clinical presentation in patients with altered flow dynamics . on unenhanced ct , varices may mimic adenopathy , masses , or nonopacified bowel loops . the left gastric venous collaterals ( coronary varices ) are seen in approximately 80% of cirrhotic patients . these vessels are located in the lesser omentum , between the medial wall of the upper gastric body and the posterior margin of the left lobe . a 5 - 6  mm left gastric vein on ct is an indicator of portal hypertension . esophageal varices are located in the wall of the lower esophagus and appear as intraluminal protrusions with scalloped borders ( figure 13 ) . paraesophageal varices are found around the esophageal wall and arise from the posterior branch of the left gastric vein , whereas the esophageal varices arise from the anterior branch . they appear as circular or tubular enhancing structures in the falciform ligament and are supplied by the left portal vein . caput medusae  refers to collateral vessels that radiate from the umbilicus and are situated in the subcutaneous fat . these varices are easily identified by their axial orientation and position in the perisplenic fat . the retrogastric varices are seen in the posteromedial aspect of the gastric fundus near the cardia and may be difficult to diagnose . retrogastric varices drain into the left renal vein through the gastrorenal shunt , whereas perisplenic varices drain directly into the left renal vein via the splenorenal shunt ( figure 15 ) . after administration of contrast , the portal vein shows a central hypodensity corresponding to the intraluminal thrombus . in this situation , the hepatic arterial flow to the liver is increased , developing scattered peripheral transient high attenuation areas known as transient hepatic attenuation differences . in subacute and chronic portal thrombosis , a cavernous transformation of the portal vein may manifest as multiple tubular collaterals in the porta hepatis ( figure 16 ) . when the portal vein is occupied by tumor thrombus , intraluminal enhancement may be seen . portal hypertension is considered the most common cause of splenomegaly in the united states ( figure 17 ) . foci of hemosiderin deposition in the spleen are seen in about 9%12% of patients with portal hypertension . these foci are called gamna - gandy bodies , and their ct imaging pattern varies from hypo- to hyperdense spots , depending on the presence of secondary calcium deposition ( figure 18 ) . mesenteric edema is defined as increased attenuation of the adipose tissue that surrounds the mesenteric vessels or their branches . inflammation , hemorrhage , neoplastic infiltration , and hypoproteinemia due to hepatic insufficiency are the most frequent conditions identified . the frequency of mesenteric edema in patients with cirrhosis is 86% , and it is usually associated with omental and retroperitoneal edema . most of the patients with mesenteric , omental , or retroperitoneal edema demonstrate a patchy , infiltrative pattern of fat stranding . focal edema may simulate a soft tissue mass . the severity of mesenteric edema parallels other manifestations of fluid overload in patients with cirrhosis such as subcutaneous edema , pleural effusion , and ascites . gastrointestinal wall thickening occurs in 64% of cirrhotic patients , usually as a result of submucosal edema . the jejunum and the ascending colon are the most common sites of involvement ( figure 19 ) . in almost all cases , the pattern of wall thickening is concentric with homogeneous enhancement after administration of intravenous contrast . the exact pathophysiologic mechanism leading to edema of the gallbladder wall is uncertain , but it is likely due to elevated portal venous pressure , decreased intravascular osmotic pressure , hypoproteinemia , or a combination of these factors . it is the most common complication of cirrhosis . within 10 years of the diagnosis of compensated cirrhosis , the development of ascites is the final consequence of anatomic and pathophysiologic abnormalities occurring in patients with cirrhosis . the formation of ascites is governed by the same principles as edema formation at other sites : net capillary permeability and the hydraulic / oncotic pressure gradients . patients with cirrhosis but without portal hypertension do not develop ascites . typical ascitic fluid in cirrhotic patients is a yellow - amber transudate with a total protein concentration of less than 2.5  g / dl and with relatively few cells ( figure 20 ) . hcc , its most lethal complication , is seen in 11% of cases after 5 years of hepatitis related cirrhosis . a triple phase evaluation of the liver with ct is essential to detect small hccs . the recognition of the extrahepatic abdominal complications is vital for adequate clinical assessment and treatment .
hepatic cirrhosis is the clinical and pathologic result of a multifactorial chronic liver injury . 
 it is well known that cirrhosis is the origin of multiple extrahepatic abdominal complications and a markedly increased risk of hepatocellular carcinoma ( hcc ) . 
 this tumor is the sixth most common malignancy worldwide and the third most common cause of cancer related death . with the rising incidence of hcc worldwide , awareness of the evolution of cirrhotic nodules into malignancy 
 is critical for an early detection and treatment . 
 adequate imaging protocol selection with dynamic multiphase multidetector computed tomography ( mdct ) and reformatted images is crucial to differentiate and categorize the hepatic nodular dysplasia . 
 knowledge of the typical and less common extrahepatic abdominal manifestations is essential for accurately assessing patients with known or suspected hepatic disease . 
 the objective of this paper is to illustrate the imaging spectrum of intra- and extrahepatic abdominal manifestations of hepatic cirrhosis seen on mdct .