Multimedia
 | Media file 1: Patient with cirrhosis showing tortuous hepatic arteries in addition to enlarged left lobe and caudate (C) |
 | Media file 2: Coronal localizer magnetic resonance imaging (MRI) scan shows marked enlargement of the left lobe of the liver in another patient with cirrhosis. |
 | Media file 3: Female patient with cirrhosis showing "coarsened" echo texture and enlarged left lobe of liver |
 | Media file 4: More advanced cirrhosis. Computed tomography (CT) scan with a portal venous–phase image shows a markedly enlarged left lobe (L) and caudate (C), with an area of focal fibrosis and atrophy of the posterior right lobe, deforming contour (open arrow). Incidental note of prominent collaterals in lesser curvature region (white arrow) |
 | Media file 5: The expanded gallbladder fossa sign that was discussed by Ito and colleagues has a limited sensitivity (68%) in cirrhosis but is highly specific. 13 The authors described an enlarged, pericholecystic, fat-filled space that often contains collaterals (note the patent paraumbilical vein [arrow]), with no visualization of the medial segment of the left lobe of the liver at the level of the gallbladder fossa. |
 | Media file 6: Transverse view, real-time ultrasonogram (same patient as in Image 3) shows an irregular external contour of the left lobe (arrow). |
 | Media file 7: Computed tomography (CT) scan (same patient as in Images 3, 6) demonstrates irregularity of the external contour of the left lobe. |
 | Media file 8: Advanced cirrhosis. A nodular liver, echogenic in comparison to renal parenchyma (R), is seen. Ascites also is present. |
 | Media file 9: In cirrhosis, flow increases in the hepatic artery. In this patient, maximum flow was measured at 255 cm/sec. The resistive index increases in end-stage liver disease. |
 | Media file 10: Typical appearance of cirrhosis (in a 22-year-old female) on angiography. Injection of the celiac trunk demonstrates an enlarged hepatic artery. Intrahepatic branches are tortuous, with a "corkscrew" configuration. |
 | Media file 11: Spontaneous arteriovenous shunt in cirrhotic patient. Color flow Doppler ultrasonogram (a) of the right lobe of the liver demonstrates no focal mass and trace ascites (A), with region of interest shown for pulse Doppler trace (b) showing presence of shunt up to velocities of 170 cm/sec. |
 | Media file 12: Nontumorous arterioportal shunts occur spontaneously in cirrhosis. Occasionally, the configuration is more rounded, mimicking hepatocellular carcinoma. In this case, a spontaneous shunt is demonstrated as a wedge-shaped region of enhancement (arrow) in the periphery of the right lobe, noted only on early arterial-phase imaging. |
 | Media file 13: Secondary manifestations of cirrhosis include thickening and edema of the small and large bowel, as well as of the gallbladder wall, which is more common in the setting of ascites and hypoproteinemia. A thickened small bowel is demonstrated here in a 51-year-old patient who has cirrhosis with marked ascites. |
 | Media file 14: Computed tomography (CT) scan demonstrating edema of the colon in a patient with cirrhosis. Note the presence of marked ascites. |
 | Media file 15: Portal venous–phase computed tomography (CT) scan demonstrating a thickened gallbladder wall, splenomegaly, numerous collaterals within the omentum (arrow), and marked ascites (A). The liver is atrophic and irregular in its external contour. |
 | Media file 16: Extrahepatic manifestation of cirrhosis. Mesenteric edema and stranding is identified (open arrow). (Note marked splenomegaly.) Same patient: A computed tomography (CT) scan at more inferior level, the root of the mesentery, shows infiltration around the superior mesenteric vein and artery (arrow). |
 | Media file 17: A 56-year-old male with cirrhosis secondary to alcohol abuse. Technetium-99m (99mTc) sulfur colloid (6 millicuries) was administered intravenously. Planar images demonstrated splenomegaly with no focal defects. A single-photon emission computed tomography (SPECT) study showed a mild radiocolloid shift to the spleen and bone marrow, indicating the presence of "mild" portal hypertension. |
 | Media file 18: Splenomegaly with longitudinal dimensions of 12.95 cm in a patient with portal hypertension and splenorenal shunt |
 | Media file 19: Development of extensive collateral vessels at the lower esophagus, short gastric vessels places this 42-year-old patient with cirrhosis and portal hypertension at risk for a GI hemorrhage. Note ascites and marked splenomegaly. |
 | Media file 20: Same patient as in Image above, section more cranial. Varices are adjacent to and within the esophageal wall. |
 | Media file 21: A patent, collateral paraumbilical vein (arrow) arising in the ligamentum teres is an indication of the early development of portal hypertension in a 56-year-old female patient with cirrhosis. This can be traced to the umbilicus and its anastomosis with systemic, superficial abdominal wall vessels in Image below. |
 | Media file 22: Portal venous–phase computed tomography (CT) scan. Note the superficial vessel (arrow) anastomosing with the paraumbilical vessel (same patient as in Image above). |
 | Media file 23: A more advanced example of a patent paraumbilical vein, noted on a color flow Doppler ultrasonographic examination. Note the constant flow pattern on the Doppler flow trace, with a velocity of over 40 cm/sec. |
 | Media file 24: Magnetic resonance imaging (MRI) study. Ascites is present. Patent paraumbilical vessels appear as a bright signal intensity in the periumbilical region (arrow). |
 | Media file 25: In this computed tomography (CT) scan of a patient with long-standing cirrhosis, the arterial-phase image is indicated by enhancement of the aorta and hepatic arteries (enlarged, tortuous right hepatic artery [RHA], arrow). The intrahepatic left portal vein also is opacified (arrow), as are numerous enlarged paraumbilical collaterals. Simultaneous enhancement of arterial and portal structures on the early arterial-phase images indicates the presence of a large arterioportal venous shunt. Marked splenomegaly is present. Note also the prominent superficial veins in the abdominal wall. |
 | Media file 26: Same patient as in Image 25, section more caudal. The image shows a very large varix in the umbilical region (clinically evident as a caput medusa). |
 | Media file 27: Splenorenal shunt. This color flow Doppler ultrasonogram demonstrates collateral in the perisplenic region (open arrow), with simultaneous flow in the left renal vein (closed arrow). Contiguity was demonstrated on computed tomography (CT) scans (see Images 28, 29). |
 | Media file 28: Splenorenal shunt. Collateral vessels are identified medial to splenic hilum and anterior to upper pole left kidney (arrow). Note gallstones, which are frequently present in patients with cirrhosis. (Same patient as in Image 27.) |
 | Media file 29: Splenorenal shunt. A collateral vessel passes caudally (arrow) and enters the left renal vein (open arrow). (Same patient as in Images 27 and 28.) |
 | Media file 30: A more advanced example of a spontaneous splenorenal shunt, in a patient with alcohol-related cirrhosis. Upper figure: A large, dilated collateral vessel is present anterior to spleen (arrow). Lower figure: Collateral vessels contiguous with the perisplenic collateral vessel (arrow) feed into the left renal vein (open arrow). |
 | Media file 31: Recent development of a bland portal vein thrombus in advanced cirrhosis, with deficit of a Doppler ultrasonographic signal (arrow). Note the contracted liver and ascites. |
 | Media file 32: Vascularized thrombus (arrow) enhancing within the main portal vein on an arterial-phase computed tomography (CT) scan. A multifocal tumor is in the right lobe of the liver (M). |
 | Media file 33: Multifocal hepatocellular carcinoma in an elderly patient with cirrhosis who is presenting with fever. The arterial-phase image demonstrates regions of hypervascularity in both lobes of the liver, that do not persist into the portal venous–phase images. The portal vein is not occluded. Ascites is present. |
 | Media file 34: Screening for hepatocellular carcinoma. A real-time limited ultrasonogram (same patient as in Image 33) shows an inhomogeneous liver. No masses were appreciated. |
 | Media file 35: Screening real-time ultrasonographic study. A triple-phase computed tomography (CT) scan was negative. A guided, ultrasonographic biopsy showed hepatocellular carcinoma in the right lobe of the liver. Note the pseudo-capsule around the lesion (best seen on magnified view). |
 | Media file 36: Screening ultrasonogram in a patient with cirrhosis. A gray-scale real-time ultrasonogram shows a relatively hypoechoic region (<1 cm) near the gallbladder fossa (arrow). |
 | Media file 37: Arterial-phase computed tomography (CT) scan (same patient as in Image 36) shows focal fatty sparing adjacent to the gallbladder fossa (arrow), which mimics a small hepatocellular carcinoma. This abnormality became less visible on a subsequent CT-scan evaluation as the overall level of fatty infiltration decreased. |
 | Media file 38: A 51-year-old male who has cirrhosis with massive ascites. On kidney, ureters, bladder (KUB), and digital scout view, small bowel loops are seen primarily in the midabdomen. The abdomen appears hazy. A computed tomography (CT)–scan axial view confirms the presence of small bowel loops floating centrally in ascitic fluid and of the existence of fluid in paracolic gutters. |
 | Media file 39: Shunts may occur by way of the retroperitoneum and azygos pathways. A chest radiograph on a patient with such a configuration demonstrates an enlarged azygos vein at the level of the azygos arch (arrow). This can also be appreciated on a localizer magnetic resonance imaging (MRI) scan in the sagittal plane. |
 | Media file 40: A 48-year-old male with cirrhosis from hepatitis C with intractable ascites and pleural effusion. Chest radiograph obtained 1 day prior to a scintigraphic study shows right-sided pleural effusion. |
 | Media file 41: Hepatic hydrothorax. A 48-year-old male with cirrhosis from hepatitis C who has intractable ascites and pleural effusion. Technetium-99m (99mTc)–labeled, macroaggregated albumin (5.5 millicuries) was administered intraperitoneally. This planar image, obtained after 30 minutes, shows tracer activity within the peritoneal cavity, with radioactivity also distributed in the right pleural cavity (arrow), consistent with pleuroperitoneal fistula. Following the nuclear medicine study, a transjugular, intrahepatic, portosystemic shunt was placed, with reduction of the portosystemic pressure gradient from 16 mm Hg to 8 mm Hg (see Image 82). |
 | Media file 42: An abnormal soft-tissue density is seen (arrow) in the lower mediastinum, superimposed over the shadow of the descending aorta. This density represents massively dilated esophageal varices on the corresponding computed tomography (CT) scan (arrow), just above the level of the left hemidiaphragm, immediately adjacent to the aorta. |
 | Media file 43: Varices at the gastroesophageal junction (arrow), demonstrated on an upper GI series. The varices become more prominently seen on Valsalva maneuver. A computed tomography (CT) scan in the same patient shows enhancing collateral vessels. |
 | Media file 44: Characteristic unifocal hepatocellular carcinoma in male alcoholic with cirrhosis. Precontrast scan shows 4.7-cm hypo-attenuating lesion in the left lobe of the liver. |
 | Media file 45: Arterial-phase computed tomography (CT) scan (same patient as in Image 44). Increased attenuation in the lesion is demonstrated. |
 | Media file 46: Portal venous–phase computed tomography (CT) scan. The hepatic parenchymal enhancement is increased and the lesion has mixed hyperattenuated and hypo-attenuated regions, with a central area of hypo-attenuation. |
 | Media file 47: Regenerative nodules in patient with cirrhosis. Evanescent multiple subcentimeter hyper-attenuating lesions on arterial-phase imaging. It is difficult to distinguish these nodules from malignant lesions. The nodules represent a continuous spectrum of response to hepatic injury, with increasing levels of dysplasia culminating in hepatocellular carcinoma. |
 | Media file 48: Advanced multifocal hepatocellular carcinoma. A tumor nodule is in the right lobe, and there is an enlarged inferior vena cava with enhancement in the arterial phase (arrow), indicating malignant invasion |
 | Media file 49: Same patient as in Image 48. Arterial-phase computed tomography (CT) scan shows tumor hyperattenuation and mass with hyperattenuation within the inferior vena cava. |
 | Media file 50: Multifocal hepatocellular carcinoma (same patient as in Images 48-49). Note the prominent venous collaterals secondary to the inferior vena cava obstruction in the subcutaneous tissues. |
 | Media file 51: Arterial-phase and portal venous–phase computed tomography (CT) scans show multifocal lesions of hepatocellular carcinoma in the liver and demonstrate no opacification of the left portal vein from the thrombus (arrow). Minimal right portal opacification in the portal venous–phase image is seen. The patient presented with hematuria. |
 | Media file 52: Portal venous–phase computed tomography (CT) scan (same patient as in Image 51) shows collateral vessels. Enlarged portions of the right renal vein also are demonstrated (open arrow) and drain into the distended inferior vena cava (*). |
 | Media file 53: Color flow Doppler ultrasonogram (same patient as in Images 51-52) demonstrating a large mesorenal shunt with collateral flow and anastomosis to the right renal vein. |
 | Media file 54: Breast carcinoma can mimic cirrhosis, with enlargement of the left lobe, irregularity of the surface contour, and development of portal hypertension (see patent paraumbilical vein on insert). |
 | Media file 55: A 48-year-old male with cirrhosis from hepatitis C infection. Splenomegaly. A magnetic resonance imaging (MRI) pregadolinium scan demonstrates an isointense 5-cm x 6-cm tumor with a well-delineated capsule. The arterial-phase image (b) shows capsular enhancement. A computed tomography (CT) scan (d-f) of the same patient shows a lesion of slightly higher attenuation than the liver parenchyma on precontrast images, followed by minimal enhancement on the arterial phase (e) and becoming more iso-attenuating with the liver on portal venous–phase image (f). The second, smaller lesion (right lobe, posteriorly) is not evident on the pre- or arterial-phase images but becomes more hypo-attenuating on the portal venous phase. |
 | Media file 56: Arterial-phase, gadolinium-enhanced magnetic resonance imaging (MRI) scan in a patient with multifocal hepatocellular carcinoma (M) demonstrates a thrombus within the main portal vein that is vascularized. Note the thrombus (arrow, T) within the main portal vein, with an enhancing vessel (open arrow) leading to the thrombus. |
 | Media file 57: Real-time ultrasonography alone is a nonspecific screening modality. In this young female patient with cirrhosis caused by hepatitis C, numerous, well-defined, hyperechoic nodules are demonstrated on screening evaluation by real-time ultrasonography. |
 | Media file 58: Computed tomography (CT) scan in the arterial phase shows several transiently hyperattenuating regions (arrow) associated with areas of relative hypo-attenuation, which also were present on the precontrast evaluation. The CT scan was not felt to be diagnostic; thus, a magnetic resonance imaging (MRI) scan was obtained. |
 | Media file 59: Focal fatty infiltration. Magnetic resonance imaging (MRI) with axial inversion recovery, as well as axial and coronal T1-weighted, gradient echo scans with in-phase (right) and out-of-phase imaging (left), was performed. The in-phase coronal imaging demonstrated multiple lesions throughout the liver, which decreased in signal on the out-of-phase scan. This was diagnostic of a fatty content. None of these areas demonstrated increased signal on additional T2-weighted images (not shown) obtained throughout the liver. No appreciable mass effect, contour abnormality, or vessel displacement was seen. |
 | Media file 60: As portal hypertension develops, the flow within portal vessels can reverse as shunts develop. The flow in this patient was reversed in the main portal vein (the flow pattern is below the axis as the blood flow is directed away from the Doppler ultrasonographic probe). The flow was also reversed in the left portal vein (not shown) and in the intrapancreatic portion of the splenic vein (see 3 Images below). |
 | Media file 61: Flow is in the appropriate direction, away from the splenic hilum; however, this is because of the presence of a splenorenal shunt. |
 | Media file 62: Splenorenal shunt with continuous flow, as demonstrated on a pulse Doppler ultrasonogram (same patient as in 2 Images above). |
 | Media file 63: Splenorenal shunt visualized by color flow Doppler ultrasonography (same patient as in 3 Images above). |
 | Media file 64: Doppler ultrasonogram. A patient with cirrhosis who has a hypoechoic mass, as detected on a screening ultrasonogram. The cursor placed at the edge of the lesion shows a vascular shunt with a maximum velocity of over 50 cm/sec. |
 | Media file 65: Arterial-phase computed tomography (CT) scan reveals a 3-cm, hyper-attenuating mass in the left lobe of the liver in this patient with hemochromatosis (same patient as in Image 64). A biopsy demonstrated hepatocellular carcinoma. Several calcifications within the right lobe of the liver and spleen are granulomata. |
 | Media file 66: Color flow Doppler ultrasonogram shows a prominent feeding vessel (arrow) and a hypoechoic mass (M), in a patient who has cirrhosis with elevated alpha fetoprotein. Ascites (A) is noted. Computed tomography (CT) scanning confirmed a hyperattenuating hepatocellular carcinoma with satellite nodules in the right lobe of the liver. |
 | Media file 67: Color flow Doppler ultrasonogram of the liver (same patient as in Image 66) shows a right portal vein thrombosis as a filling defect in the portal vein (arrow). |
 | Media file 68: Multifocal hepatocellular carcinoma in a patient with underlying alcoholic cirrhosis and ascites (A). This color flow Doppler ultrasonogram shows multiple masses (M) displacing vessels within the right lobe of the liver. |
 | Media file 69: Multifocal hepatocellular carcinoma (same patient as in Image 68). The Doppler trace at the margin of the mass shows a shunt vascularity of 120 cm/sec. |
 | Media file 70: Gadolinium-enhanced magnetic resonance imaging (MRI) scan showing parenchymal enhancement, lower–signal-intensity tumor masses (M), and ascites (A). (Same patient as in Images 68-69.) |
 | Media file 71: Color flow Doppler evaluation (same patient as in Images 68-70) shows that the main portal vein (arrow) is occluded, with the collateral flow adjacent. |
 | Media file 72: Magnetic resonance imaging (MRI) scan (same patient as in Images 68-71) demonstrates vascularization within the thrombus, on the same arterial-phase image (arrow region of increased signal intensity) within the main portal vein. Compare the scan with a later-phase image, in which the relative signal intensity in the thrombus is reduced. |
 | Media file 73: Contrast-enhanced, harmonic ultrasonographic scans. A series of scans (same patient as in Images 68-72) were taken following a second intravenous injection of perfluorocarbon contrast. The baseline (a) shows a lesion in left lobe (arrow). The next image (b) was obtained after insonation at a high mechanical index (MI) (1.3), with diffuse echogenicity throughout the liver and lesion. A subsequent scan (c), which was taken at 2 minutes following microbubble destruction, was imaged using a low MI, and shows reperfusion of the tumor, with an echogenic signal appearing centrally. The next image (d), taken following a further delay (6 minutes after activation) shows that the signals persisted and that they brightened within lesion. |
 | Media file 74: Baseline, harmonic power Doppler image shows a minimal signal within a 5-cm hepatocellular carcinoma. Following the injection of ultrasonographic contrast, a feeding vessel was identified (arrow) and an immediate heterogeneous, bright signal occurred within the lesion. A relatively hypovascular region that was initially seen within the tumor filled in progressively (open arrow). Note that posteriorly, the kidney (K) shows progressive enhancement until image 4; a gradual reduction in enhancement is then seen. Doppler signals at 70 seconds are still above baseline. Contrast images obtained over 70-second interval. |
 | Media file 75: Indirect visualization of the portal venous system can be obtained by injection of the superior mesenteric artery with delayed imaging. This venous-phase angiogram shows prominent collaterals and faint opacification (arrow) of the portal vein. |
 | Media file 76: The hepatic venous wedge pressure can be measured after direct catheterization of a hepatic vein, temporarily occluding the vein with a balloon. In this study, the hepatic vein wedge pressure was 20 mm Hg, the free hepatic vein pressure was 8 mm Hg, the right atrial pressure was 4-8 mm Hg, the inferior vena cava at the level of the liver was 8 mm Hg, and the inferior vena cava below the liver was 9 mm Hg. The pressure gradient is the difference between the right atrial pressure and hepatic vein wedge pressure. |
 | Media file 77: Superior mesenteric artery, venous-phase injection (same patient as in Image 76 in Multimedia) opacifies the portal vein. A second catheter is in the hepatic vein. |
 | Media file 78: Splenoportography can be performed by direct splenic puncture (parenchymal blush, open arrow). This technique is no longer used, as alternative methods enable the portal system to be imaged, and pressure gradients are obtained via direct catheterization of the inferior vena cava and hepatic veins. However, this study from a past decade shows the delineation of collateral vessels and portal anatomy. Varices (arrow) are present at the gastroesophageal junction. |
 | Media file 79: Hepatic vein injection shows opacification of the hepatic vein, parenchymal staining, and opacification of the portal vein, indicating hepatofugal flow. |
 | Media file 80:
Transjugular intrahepatic portosystemic shunt
(TIPS). A patient with cirrhosis secondary to hepatitis B and C
developed refractory ascites, which on tap was bloody and
required multiple transfusions. A TIPS procedure was performed
emergently. Initial pressure measurements were obtained at the
level of the renal inferior vena cava (IVC) (13-14 mm Hg), the
IVC (13 mm Hg), and the right atrium (RA) (7 mm Hg), with a
13-mm hepatic vein–to–portal vein gradient and an
18 mm Hg pressure difference compared with the IVC
at the level of the liver, and a 24 mm Hg difference compared
with the RA. A 12 x 60 mm Wallstent was inserted from the distal main portal vein (MPV) to the hepatic vein, with an initial 13-14 mm Hg pressure gradient. The stent was dilated to 10 mm, with the gradient now 12 mm Hg, and was redilated to 12 mm. An additional Wallstent was inserted (14 x 40 mm), to increase the length of the TIPS and extend further into the hepatic vein, to the IVC. Final portal measurements: MPV and left portal vein (LPV), 18 mm Hg; mid-TIPS, 13 mm Hg; hepatic vein, 12 mm Hg; IVC 11, mm Hg; and RA, 10 mm Hg. The hepatic venous pressure gradient of 8 mm Hg was satisfactory. The contrast study showed the patent portal vein, the TIPS, and the IVC to the RA. |
 | Media file 81: Doppler ultrasonogram (same patient as in Image 80) shows the patency of the transjugular intrahepatic portosystemic shunt (TIPS), with a peak velocity of 247 cm/sec. |
 | Media file 82: Transjugular intrahepatic portosystemic shunt (TIPS) therapy for the treatment of refractory ascites; a 48-year-old male with intractable ascites and recurrent pleural effusion from a pleuroperitoneal fistula (see Images 40-41). A TIPS procedure was performed. A follow-up computed tomography (CT) scan 9 months later showed the TIPS catheter placed between the inferior vena cava and the middle hepatic vein, as well as resolution of the ascites and effusions (a). The patency of the shunt was confirmed by contrast enhancement on CT-scan and Doppler ultrasonographic evaluation (c), which showed the flow within shunt. |
 | Media file 83: Transjugular intrahepatic portosystemic shunt (TIPS) catheter patency; precontrast, harmonic ultrasonographic image (a). Following a high mechanical index pulse (1.3), microbubble destruction occurs and the microbubbles can be seen within the TIPS on a real-time image, appearing as a highly echogenic signal within the shunt (b). |
 | Media file 84: Maximum intensity projection (MIP); reformatted computed tomography (CT) scan showing extensive superficial paraumbilical collaterals in a cirrhotic patient with portal hypertension. The collaterals are extensively anastomosing with the systemic venous system through the internal epigastric veins. |
 | Media file 85: Three-dimensional reformat of a computed tomography (CT) scan shows the morphologic appearance of cirrhosis: a prominent left lobe and portal venous collateral vessels. |
 | Media file 86: Three-dimensional reformat of a computed tomography (CT) scan of a cirrhotic patient shows prominent collateral vessels arising from the portal system and extending to the GE junction (arrowed). |
 | Media file 87: Three-dimensional reformat of a computed tomography (CT) scan of a cirrhotic patient who has portal hypertension with prominent, paraumbilical collateral vessels. |
 | Media file 88: Three-dimensional reformat of a computed tomography (CT) scan showing prominent splenorenal collaterals adjacent to the superior pole of the left kidney |
 | Media file 89: Three-dimensional reformat of a computed tomography (CT) scan showing cavernous transformation in a cirrhotic patient who developed bland portal venous thrombosis. Note the serpiginous collateral vessels (arrow) in porta hepatitis. |
 | Media file 90: Computed tomography (CT) scan through the porta hepatis shows portal vein thrombosis and collateral vessels in cavernous transformation (arrow). |
More on Cirrhosis |
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Further Reading
Keywords
hepatic fibrosis, chronic end-stage liver disease, transjugular intrahepatic portosystemic shunt, TIP, hepatocellular carcinoma, HCCA, HCC, hepatic arterial circulation, portal venous circulation, hepatic vein pressure gradient, HVPG
