(Radiographics. 2001;21:S81-S96.)
© RSNA, 2001
Helping the Hepatic Surgeon |
Unusual Hemodynamics and Pseudolesions of the Noncirrhotic Liver at CT1
Kengo Yoshimitsu, MD,
Hiroshi Honda, MD,
Toshiro Kuroiwa, MD,
Hiroyuki Irie, MD,
Hitoshi Aibe, MD,
Kenji Shinozaki, MD and
Kouji Masuda, MD
1 From the Department of Clinical Radiology, Graduate School of Medical Sciences, Kyushu University, 3-1-1 Maisdashi, Higashi-ku, Fukuoka 812-8582, Japan. Presented as an education exhibit at the 2000 RSNA scientific assembly. Received February 2, 2001; revision requested March 9 and received April 16; accepted April 25. Address correspondence to K.Y. (e-mail: yoshimitsu@dr.hosp.kyushu-u.ac.jp).
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Abstract
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Recognition of pseudolesions of the liver at computed tomography (CT) is important because of their close resemblance to primary liver cancers or metastases. Two types of pseudolesion in the noncirrhotic liver include that due to transient extrinsic compression, typically caused by ribs or the diaphragm, and that due to a "third inflow" of blood from other than the usual hepatic arterial and portal venous sources: the cholecystic, parabiliary, or epigastric-paraumbilical venous system. Although the location of both types of pseudolesion are characteristic, their appearances at CT during arterial portography and CT during selective angiography vary from nonenhanced low-attenuation areas to well-enhanced high-attenuation areas, depending on the amount and timing of the inflow and presence or absence of focal metabolic alteration of the hepatocytes. Radiologists need to understand the underlying mechanism of these pseudolesions to better recognize the wide range of their appearances at CT.
Index Terms: Computed tomography (CT), perfusion study, 761.12114 • Liver, abnormalities, 761.91 • Liver, blood supply, 958.12914 • Liver, CT, 761.12114
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LEARNING OBJECTIVES
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After reading this article and taking the test, the reader will be able to:
- Define the two kinds of pseudolesions, namely those due to transient extrinsic compression and those due to the "third inflow."
- Describe the hemodynamics and CT findings of pseudolesions due to transient extrinsic compression.
- Describe the hemodynamics and CT findings of pseudolesions due to the third inflow.
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Introduction
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Understanding and diagnosing pseudolesions in the liver are important for radiologists, particularly in the treatment of known malignancies, because misinterpretation of pseudolesions as metastases may completely alter the choice of treatment. Several kinds of pseudolesions observed at computed tomography (CT) have been reported (1–5). In this article, we focus on those seen in the noncirrhotic liver and caused by unusual hemodynamics, and we exclude those related to cirrhosis and to apparent intrahepatic vascular compromise, including arterioportal shunting. For a better understanding and analysis of the underlying hemodynamics of pseudolesions, findings at CT during arterial portography and CT during selective angiography are shown.
Two basic assumptions may be made about the pseudolesions addressed in this article. First, because they are caused by unusual hemodynamics, they are observed only at contrast material–enhanced CT and not at unenhanced or equilibrium-phase CT. However, because persistence of this unusual hemodynamic state may result in focal metabolic alteration in the hepatocytes (focal sparing in the diffusely fatty liver or focal fatty infiltration), some pseudolesions are also visible at unenhanced or equilibrium-phase CT.
Focal sparing in a diffusely fatty liver may be explained as follows: Portal blood conveyed via the superior mesenteric vein contains abundant nutrition, including fat, and a lack or diminishment of the portal perfusion may result in less fatty change in hepatocytes, namely focal sparing, at the site of a pseudolesion (2). Focal fatty change may be more difficult to explain. Battaglia et al (6) speculated that venous blood from the pancreas may contain more insulin than that in the main portal vein, which would enhance the development of steatosis at the region with aberrant parabiliary venous drainage. This theory, however, cannot be applied to focal fatty change in other pseudolesions. For these, an imbalance of various amino acids and other substances, including intestinal hormones, due to lack of blood supply from the small intestine may play a role in the development of focal steatosis, as suggested in cases of fatty liver in patients with malnutrition or prolonged total parenteral nutrition (7–9). The true mechanism, however, of a portal perfusion defect that results in focal sparing in some patients and focal steatosis in others still remains unclear at present.
The pseudolesions described in this article can be roughly divided into two categories (Fig 1): those due to transient, extrinsic focal compression of the liver and those due to a "third inflow" of blood from other than the usual hepatic arterial and portal venous sources. In both conditions, portal perfusion is decreased while hepatic arterial perfusion remains unchanged in the area of the pseudolesions, but their CT appearances are different and varied. In this article, the nomenclature used to describe the segments of the liver is based on Couinaud’s system (10).
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Figure 1. Diagram shows the two types of pseudolesions: those due to transient extrinsic compression of the liver and those due to third inflow of blood from cholecystic veins, the parabiliary venous system, the epigastric-paraumbilical venous system, or aberrant veins.
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Pseudolesions Due to Compression of the Liver
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Underlying Hemodynamics
These pseudolesions are caused by transient compression of the liver by a certain structure, which typically occurs during a patient’s deep inspiration at the time of CT examination. This focal compression causes focal increase in the tissue pressure at the subcapsular region, resulting in decreased portal perfusion and little change in hepatic arterial perfusion (11,12). If this compression persists, the unusual hemodynamics result in focal fibrosis with deformity, a state classically known as "corset liver" (13). Corset liver, however, represents a true lesion and is beyond the scope of this article.
Because the compression that causes a pseudolesion of this category is transient, so is the hemodynamic alteration. Metabolic changes (focal sparing in the fatty liver or focal fat accumulation), therefore, are less likely to occur.
Appearances at CT
At CT during arterial portography, compression-type pseudolesions are shown as ill-defined areas of diminished portal perfusion just beneath the compressing structure. At CT during hepatic arteriography, there is little perfusion abnormality (12). At CT performed with intravenous contrast material, findings are similar to those seen at CT during arterial portography when images are obtained during the portal-dominant phase: an ill-defined low-attenuation area at the subcapsular region (12). For this type of pseudolesion to be diagnosed, there should be a compressing structure outside the liver that creates a concave deformity on the hepatic surface just adjacent to the low-attenuation area; in addition, the image should be obtained during the portal-dominant phase. No abnormal attenuation should appear on the unenhanced, arterial-phase, or equilibrium-phase images. Additional findings that may help radiologists differentiate pseudolesions from true lesions are the presence of portal branches within the pseudolesions (12) or their disappearance at repeated CT examination with different inspiration levels (Fig 2) (12).
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Figure 2a. Pseudolesion due to rib compression in a 45-year-old woman. (a) Early-phase incremental dynamic CT scan obtained during deep inspiration shows a low-attenuation area below the seventh rib (arrow). (b) CT scan obtained during arterial portography shows an area of portal perfusion diminishment (arrow) that corresponds to the pseudolesion in a. (c) CT scan obtained during hepatic arteriography shows little abnormality of hepatic arterial perfusion. (d) Early-phase incremental dynamic CT scan obtained during shallow inspiration shows no pseudolesion below the seventh rib. Instead, another pseudolesion appeared below the ninth rib (arrow). The anatomic relationship between the ribs and the liver is different from that seen in a.
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Figure 2b. Pseudolesion due to rib compression in a 45-year-old woman. (a) Early-phase incremental dynamic CT scan obtained during deep inspiration shows a low-attenuation area below the seventh rib (arrow). (b) CT scan obtained during arterial portography shows an area of portal perfusion diminishment (arrow) that corresponds to the pseudolesion in a. (c) CT scan obtained during hepatic arteriography shows little abnormality of hepatic arterial perfusion. (d) Early-phase incremental dynamic CT scan obtained during shallow inspiration shows no pseudolesion below the seventh rib. Instead, another pseudolesion appeared below the ninth rib (arrow). The anatomic relationship between the ribs and the liver is different from that seen in a.
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Figure 2c. Pseudolesion due to rib compression in a 45-year-old woman. (a) Early-phase incremental dynamic CT scan obtained during deep inspiration shows a low-attenuation area below the seventh rib (arrow). (b) CT scan obtained during arterial portography shows an area of portal perfusion diminishment (arrow) that corresponds to the pseudolesion in a. (c) CT scan obtained during hepatic arteriography shows little abnormality of hepatic arterial perfusion. (d) Early-phase incremental dynamic CT scan obtained during shallow inspiration shows no pseudolesion below the seventh rib. Instead, another pseudolesion appeared below the ninth rib (arrow). The anatomic relationship between the ribs and the liver is different from that seen in a.
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Figure 2d. Pseudolesion due to rib compression in a 45-year-old woman. (a) Early-phase incremental dynamic CT scan obtained during deep inspiration shows a low-attenuation area below the seventh rib (arrow). (b) CT scan obtained during arterial portography shows an area of portal perfusion diminishment (arrow) that corresponds to the pseudolesion in a. (c) CT scan obtained during hepatic arteriography shows little abnormality of hepatic arterial perfusion. (d) Early-phase incremental dynamic CT scan obtained during shallow inspiration shows no pseudolesion below the seventh rib. Instead, another pseudolesion appeared below the ninth rib (arrow). The anatomic relationship between the ribs and the liver is different from that seen in a.
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Among various CT techniques for scanning the liver, including incremental dynamic CT (12), helical CT, and multi–detector row CT, multi–detector row CT can provide the best portal-dominant-phase images and therefore delineate pseudolesions of this type most clearly (Fig 3). This fact deserves attention because multi–detector row CT is being used more frequently than before and may become the routine protocol for liver study in the near future. Figure 4 shows the time-attenuation curves for the abdominal aorta and the liver in correlation with the timing of scanning performed with three different CT protocols in our institution.
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Figure 3a. Different appearances of a pseudolesion due to rib compression in a 57-year-old man as imaged with three different CT techniques. (a) Early-phase incremental dynamic CT scan obtained with a 45-second delay, scanning speed of 1 second per section, table incremental speed of 10 mm per second, and 10-mm section thickness demonstrates a faint low-attenuation area (arrow). (b) Portal-phase helical CT scan obtained with 90-second delay, scanning speed of 1 second per section, pitch of 1:1, and 7-mm section thickness reveals a pseudolesion that is barely seen, probably because the scanning time was slightly later than a true portal-dominant phase. (c) Portal-phase multi-detector row CT scan obtained with 70-second delay, pitch of 3, and 3 x 4-mm detector configuration clearly shows a pseudolesion (arrow).
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Figure 3b. Different appearances of a pseudolesion due to rib compression in a 57-year-old man as imaged with three different CT techniques. (a) Early-phase incremental dynamic CT scan obtained with a 45-second delay, scanning speed of 1 second per section, table incremental speed of 10 mm per second, and 10-mm section thickness demonstrates a faint low-attenuation area (arrow). (b) Portal-phase helical CT scan obtained with 90-second delay, scanning speed of 1 second per section, pitch of 1:1, and 7-mm section thickness reveals a pseudolesion that is barely seen, probably because the scanning time was slightly later than a true portal-dominant phase. (c) Portal-phase multi-detector row CT scan obtained with 70-second delay, pitch of 3, and 3 x 4-mm detector configuration clearly shows a pseudolesion (arrow).
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Figure 3c. Different appearances of a pseudolesion due to rib compression in a 57-year-old man as imaged with three different CT techniques. (a) Early-phase incremental dynamic CT scan obtained with a 45-second delay, scanning speed of 1 second per section, table incremental speed of 10 mm per second, and 10-mm section thickness demonstrates a faint low-attenuation area (arrow). (b) Portal-phase helical CT scan obtained with 90-second delay, scanning speed of 1 second per section, pitch of 1:1, and 7-mm section thickness reveals a pseudolesion that is barely seen, probably because the scanning time was slightly later than a true portal-dominant phase. (c) Portal-phase multi-detector row CT scan obtained with 70-second delay, pitch of 3, and 3 x 4-mm detector configuration clearly shows a pseudolesion (arrow).
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Ribs.—
Pseudolesions due to rib compression are observed in approximately 14% of patients (12). The right seventh to eleventh ribs, which are curved medially and may compress the liver, have been reported to cause pseudolesions, most typically in segments V and VI (Fig 2) (12).
Diaphragm.—
Uneven contraction of the muscle bundles of the diaphragm can create pseudolesions around the dome of the liver, typically in segments VII and VIII (Fig 5). In our experience, elderly patients tend to have pseudolesions of this kind.
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Figure 5a. Pseudolesion due to diaphragmatic compression in a 62-year-old man. (a) Scan obtained during the early phase of incremental dynamic CT shows peripheral low-attenuation areas with a concave surface (arrow). (b) Delayed-phase incremental dynamic CT scan obtained 4 minutes after injection of contrast medium shows no abnormal attenuation.
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Figure 5b. Pseudolesion due to diaphragmatic compression in a 62-year-old man. (a) Scan obtained during the early phase of incremental dynamic CT shows peripheral low-attenuation areas with a concave surface (arrow). (b) Delayed-phase incremental dynamic CT scan obtained 4 minutes after injection of contrast medium shows no abnormal attenuation.
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Miscellaneous.—
In theory, any other structure, whether in its normal state or as a result of a pathologic condition, that is hard enough to compress the liver can cause a pseudolesion (Fig 6).
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Figure 6. Early-phase incremental dynamic CT scan shows a pseudolesion possibly due to compression by the prominent abdominal muscle (arrow) in a 42-year-old woman. No unusual vessels were evident to suggest Sappey veins (venae paraumbilicales) or epigastric veins around the round ligament of Cloquet.
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Pseudolesions Due to the "Third Inflow"
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Basic Anatomy and Underlying Hemodynamics
The liver is a unique organ in terms of its dual blood supply: namely, the hepatic arterial and portal venous systems. Small areas of liver tissue, however, are known to be supplied by another venous system (1,5,6,14–18). This system may be composed of aberrant veins or parts of normal veins that directly enter the liver independently of the portal venous system. Such veins communicate with intrahepatic portal branches to various degrees, focally decrease portal perfusion, and cause little change in the hepatic arterial perfusion. Because this hemodynamic state is persistent, focal metabolic changes (sparing in the fatty liver or fat accumulation) are occasionally observed in the pseudolesions of this category.
Cholecystic Vein through the Liver Bed.—
Cholecystic veins can be divided into two subgroups (14,19): small branches that directly enter the liver through the liver bed (segments IV and V) and those that run through the Calot triangle and join the parabiliary veins at the porta hepatis (Fig 7). The former drain the liver parenchyma around the body and fundus of the gallbladder and communicate with peripheral intrahepatic portal branches (14,19). They dilute the portal perfusion at these sites, causing pseudolesions.
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Figure 7. Drawing shows the anatomy of the parabiliary venous system. The portal vein is not shown. Abundant communication among the right gastric, pancreaticoduodenal, and cholecystic venous branches around the bile duct forms the parabiliary venous system. (Modified, with permission, from reference 20.)
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Parabiliary Venous System.—
This venous network or plexus is within the hepatoduodenal ligament, just anterior to the main trunk of the portal vein, and collects venous blood from the head of the pancreas, distal part of the stomach, and the bile duct system (Fig 7) (15,19). These veins usually join the main trunk or major branches of the portal venous system but occasionally enter the liver directly around the porta hepatis, which sometimes results in isolated perfusion (1,14,15,19). The cholecystic vein through the Calot triangle joins the parabiliary vein at the porta hepatis to form the superior or cephalic portion of the venous network; the pancreaticoduodenal vein conveys the blood from the region of the head of the pancreas to form the inferior and lateral portion of the network; and the right gastric or pyloric vein drains the distal part of the stomach on the side of the lesser curvature and forms the medial portion of the network. The aberrant drainage of these vessels into the liver causes a pseudolesion, typically at the dorsal aspect of segment IV. There are abundant communications among the branches of this venous network, and which vein predominates as the cause of a pseudolesion is dependent on the direction and amount of blood flow through these anastomoses. Multiple veins may be involved in the formation of a pseudolesion of this kind (15). In addition, the presence of hypervascular inflammation, a tumor, or surgical intervention in this region may change the flow through these anastomoses and, as a result, the appearance of the pseudolesion.
Embryologically, bile ducts, the parabiliary venous system, the hepatic artery, and segments I and IV of the liver develop late, around the 32nd–34th day of gestation; in contrast, the major portion of the liver and the portal venous system develop earlier, around the 26th–28th day (19). This difference may account for why aberrant drainage of the parabiliary venous system occasionally occurs in segments I and IV.
Epigastric-Paraumbilical Venous System.—
This system consists of small veins around the falciform ligament that drain the venous blood from the anterior part of the abdominal wall directly into the liver. This flow dilutes the portal perfusion at these sites, causing pseudolesions. These veins are roughly divided into three subgroups: the superior and inferior vein of Sappey and the vein of Burow (Fig 8) (21). The superior vein of Sappey drains the upper portion of the falciform ligament and medial part of the diaphragm and enters peripheral portal branches of the left hepatic lobe; it also communicates with branches of the superior epigastric or internal thoracic veins. The inferior vein of Sappey drains the lower portion of the falciform ligament and enters peripheral portal branches of the left hepatic lobe; it descends along the round ligament and communicates with branches of inferior epigastric veins around the navel. The vein of Burow also communicates with branches of inferior epigastric veins around the navel. However, it does not enter the liver directly but terminates in the middle portion of the collapsed umbilical vein, although some small communicating branches are present between it and the inferior vein of Sappey, namely, the intercalary veins (21). All of these veins can serve as collateral channels when vena caval obstruction occurs and flow through these vessels into the liver increases (17,22,23). The flow through these vessels may be reversed in cirrhotic livers or at portal hypertension, causing the vessels to serve as an efferent flow tract from the liver (5,24).
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Figure 8. Diagram shows the anatomy of the paraumbilical vein. The dotted line from the navel (N) toward the porta hepatis represents the obliterated umbilical vein or the round ligament.
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Appearances at CT
At CT during arterial portography, pseudolesions appear as ill- or well-defined areas of diminished portal perfusion (1,5,15,16,18,25,26). When communications between the third inflow vessel and intrahepatic portal venous branches are abundant, the flow between the two systems may be reciprocal and margins of the pseudolesion may be unclear. When no or little communication exists, namely, in a case of isolated perfusion of the third inflow, the pseudolesion may have clear margins. At CT during selective hepatic arteriography, there is little perfusion abnormality. If CT images are obtained during injection of contrast medium into the artery feeding the third inflow vessel, namely at CT during selective angiography, the pseudolesion is strongly enhanced. The findings at CT with intravenous contrast enhancement are the results of a combination of the three factors mentioned above and the attenuation change due to metabolic alteration.
Timing of imaging of the third inflow to the liver at intravenously enhanced CT is variable, and roughly depends on the anatomic distance between the pseudolesion and the organ from which the blood is conveyed. Blood enters the liver quickly via cholecystic veins through the liver bed, and the pseudolesion is therefore enhanced at the arterial phase of hepatic enhancement. Blood through the parabiliary venous system enters slightly later, and the pseudolesion is enhanced at the arterioportal phase. Blood via the epigastric-paraumbilical venous system reaches the liver rather late, around the late portal phase, and the pseudolesion is therefore rarely enhanced (Fig 3). However, the presence of inflammation or a tumor may change the vascularity and, as a result, the timing of the inflow as well.
The recognition of unusual vessels per se sometimes helps in the diagnosis of this type of pseudolesion at intravenously enhanced CT. If one can follow the unusual vessel entering the area of the pseudolesion, the diagnosis may be established.
Cholecystic Vein through the Liver Bed.—
Because of anatomic adjacency, pseudolesions due to this vein appear as enhanced areas around the gallbladder during the arterial phase of hepatic enhancement at intravenously enhanced CT (Fig 9) (14,27,28). This finding may be exaggerated in patients with acute cholecystitis or gallbladder carcinoma. Because these branches are short and directly enter the liver, it is unlikely they will appear at intravenously enhanced CT. For unknown reasons, focal fatty change is less likely to occur, although focal sparing in diffusely fatty liver tissue is common with these pseudolesions.
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Figure 9a. Pseudolesion due to cholecystic venous drainage through the liver bed in a 68-year-old man with a gallbladder carcinoma limited to the mucosa of the organ (not shown). (a) Unenhanced CT scan shows focal sparing around the gallbladder fossa in the diffusely fatty liver (arrow). (b) Arterial-phase helical CT scan shows enhancement of the spared area (arrow). (c) CT scan obtained during arterial portography shows an area of portal perfusion diminishment around the gallbladder (arrow). (d) CT scan obtained during selective cholecystic arteriography shows strong enhancement in the area around the gallbladder (arrow). (e) Venous-phase selective cholecystic arteriogram shows staining around the gallbladder due to cholecystic venous drainage (arrows).
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Figure 9b. Pseudolesion due to cholecystic venous drainage through the liver bed in a 68-year-old man with a gallbladder carcinoma limited to the mucosa of the organ (not shown). (a) Unenhanced CT scan shows focal sparing around the gallbladder fossa in the diffusely fatty liver (arrow). (b) Arterial-phase helical CT scan shows enhancement of the spared area (arrow). (c) CT scan obtained during arterial portography shows an area of portal perfusion diminishment around the gallbladder (arrow). (d) CT scan obtained during selective cholecystic arteriography shows strong enhancement in the area around the gallbladder (arrow). (e) Venous-phase selective cholecystic arteriogram shows staining around the gallbladder due to cholecystic venous drainage (arrows).
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Figure 9c. Pseudolesion due to cholecystic venous drainage through the liver bed in a 68-year-old man with a gallbladder carcinoma limited to the mucosa of the organ (not shown). (a) Unenhanced CT scan shows focal sparing around the gallbladder fossa in the diffusely fatty liver (arrow). (b) Arterial-phase helical CT scan shows enhancement of the spared area (arrow). (c) CT scan obtained during arterial portography shows an area of portal perfusion diminishment around the gallbladder (arrow). (d) CT scan obtained during selective cholecystic arteriography shows strong enhancement in the area around the gallbladder (arrow). (e) Venous-phase selective cholecystic arteriogram shows staining around the gallbladder due to cholecystic venous drainage (arrows).
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Figure 9d. Pseudolesion due to cholecystic venous drainage through the liver bed in a 68-year-old man with a gallbladder carcinoma limited to the mucosa of the organ (not shown). (a) Unenhanced CT scan shows focal sparing around the gallbladder fossa in the diffusely fatty liver (arrow). (b) Arterial-phase helical CT scan shows enhancement of the spared area (arrow). (c) CT scan obtained during arterial portography shows an area of portal perfusion diminishment around the gallbladder (arrow). (d) CT scan obtained during selective cholecystic arteriography shows strong enhancement in the area around the gallbladder (arrow). (e) Venous-phase selective cholecystic arteriogram shows staining around the gallbladder due to cholecystic venous drainage (arrows).
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Figure 9e. Pseudolesion due to cholecystic venous drainage through the liver bed in a 68-year-old man with a gallbladder carcinoma limited to the mucosa of the organ (not shown). (a) Unenhanced CT scan shows focal sparing around the gallbladder fossa in the diffusely fatty liver (arrow). (b) Arterial-phase helical CT scan shows enhancement of the spared area (arrow). (c) CT scan obtained during arterial portography shows an area of portal perfusion diminishment around the gallbladder (arrow). (d) CT scan obtained during selective cholecystic arteriography shows strong enhancement in the area around the gallbladder (arrow). (e) Venous-phase selective cholecystic arteriogram shows staining around the gallbladder due to cholecystic venous drainage (arrows).
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The typical location and nonnodular, ill-defined, amorphous shape of the pseudolesions make diagnosis relatively easy. In patients with gallbladder carcinomas, this pseudolesion should not be taken as a sign of hepatic invasion by the tumor (Fig 9) (14).
Parabiliary Venous System.—
Contrast medium flows into the pseudolesion approximately during the arterioportal phase, and both sparing in diffusely fatty liver tissue and focal steatosis are common. The attenuation of the pseudolesion, therefore, varies at intravenously enhanced CT. The typical location of this pseudolesion at the dorsal aspect of segment IV may be a key to correct diagnosis, but sometimes it is difficult to rule out a true lesion. The pseudolesion in this site is often, at least in part, well marginated, probably because of the isolated perfusion of this venous plexus.
Because the cholecystic venous branch through the Calot triangle is short and in a small anatomic space, it may rarely be recognized at intravenously enhanced CT. Pseudolesion due to this vein may manifest as focal steatosis (Fig 10) (14) or an early enhancing area in the left hepatic lobe in patients with acute cholecystitis (27,28).
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Figure 10a. Pseudolesion with focal steatosis in segment IV of a 66-year-old man due to cholecystic venous drainage through the Calot triangle. (a) Early-phase incremental dynamic CT scan shows a 1-cm-diameter low-attenuation area in segment IV (arrow). (b) CT scan obtained during arterial portography shows a portal perfusion defect (arrow). (c) CT scan obtained during cholecystic arteriography shows strong enhancement of a pseudolesion (arrow). (d) Venous-phase selective cholecystic arteriogram shows that a branch at the porta hepatis drains the area of the pseudolesion (arrow). (e) Spin-echo T1-weighted MR image (500/15 [repetition time msec/echo time msec]) obtained with a 1.5-T unit shows high signal intensity of the pseudolesion (arrow). (f) Spin-echo T1-weighted MR image (500/15) with fat saturation shows that the signal intensity of the pseudolesion is suppressed (arrow).
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Figure 10b. Pseudolesion with focal steatosis in segment IV of a 66-year-old man due to cholecystic venous drainage through the Calot triangle. (a) Early-phase incremental dynamic CT scan shows a 1-cm-diameter low-attenuation area in segment IV (arrow). (b) CT scan obtained during arterial portography shows a portal perfusion defect (arrow). (c) CT scan obtained during cholecystic arteriography shows strong enhancement of a pseudolesion (arrow). (d) Venous-phase selective cholecystic arteriogram shows that a branch at the porta hepatis drains the area of the pseudolesion (arrow). (e) Spin-echo T1-weighted MR image (500/15 [repetition time msec/echo time msec]) obtained with a 1.5-T unit shows high signal intensity of the pseudolesion (arrow). (f) Spin-echo T1-weighted MR image (500/15) with fat saturation shows that the signal intensity of the pseudolesion is suppressed (arrow).
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Figure 10c. Pseudolesion with focal steatosis in segment IV of a 66-year-old man due to cholecystic venous drainage through the Calot triangle. (a) Early-phase incremental dynamic CT scan shows a 1-cm-diameter low-attenuation area in segment IV (arrow). (b) CT scan obtained during arterial portography shows a portal perfusion defect (arrow). (c) CT scan obtained during cholecystic arteriography shows strong enhancement of a pseudolesion (arrow). (d) Venous-phase selective cholecystic arteriogram shows that a branch at the porta hepatis drains the area of the pseudolesion (arrow). (e) Spin-echo T1-weighted MR image (500/15 [repetition time msec/echo time msec]) obtained with a 1.5-T unit shows high signal intensity of the pseudolesion (arrow). (f) Spin-echo T1-weighted MR image (500/15) with fat saturation shows that the signal intensity of the pseudolesion is suppressed (arrow).
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Figure 10d. Pseudolesion with focal steatosis in segment IV of a 66-year-old man due to cholecystic venous drainage through the Calot triangle. (a) Early-phase incremental dynamic CT scan shows a 1-cm-diameter low-attenuation area in segment IV (arrow). (b) CT scan obtained during arterial portography shows a portal perfusion defect (arrow). (c) CT scan obtained during cholecystic arteriography shows strong enhancement of a pseudolesion (arrow). (d) Venous-phase selective cholecystic arteriogram shows that a branch at the porta hepatis drains the area of the pseudolesion (arrow). (e) Spin-echo T1-weighted MR image (500/15 [repetition time msec/echo time msec]) obtained with a 1.5-T unit shows high signal intensity of the pseudolesion (arrow). (f) Spin-echo T1-weighted MR image (500/15) with fat saturation shows that the signal intensity of the pseudolesion is suppressed (arrow).
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Figure 10e. Pseudolesion with focal steatosis in segment IV of a 66-year-old man due to cholecystic venous drainage through the Calot triangle. (a) Early-phase incremental dynamic CT scan shows a 1-cm-diameter low-attenuation area in segment IV (arrow). (b) CT scan obtained during arterial portography shows a portal perfusion defect (arrow). (c) CT scan obtained during cholecystic arteriography shows strong enhancement of a pseudolesion (arrow). (d) Venous-phase selective cholecystic arteriogram shows that a branch at the porta hepatis drains the area of the pseudolesion (arrow). (e) Spin-echo T1-weighted MR image (500/15 [repetition time msec/echo time msec]) obtained with a 1.5-T unit shows high signal intensity of the pseudolesion (arrow). (f) Spin-echo T1-weighted MR image (500/15) with fat saturation shows that the signal intensity of the pseudolesion is suppressed (arrow).
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Figure 10f. Pseudolesion with focal steatosis in segment IV of a 66-year-old man due to cholecystic venous drainage through the Calot triangle. (a) Early-phase incremental dynamic CT scan shows a 1-cm-diameter low-attenuation area in segment IV (arrow). (b) CT scan obtained during arterial portography shows a portal perfusion defect (arrow). (c) CT scan obtained during cholecystic arteriography shows strong enhancement of a pseudolesion (arrow). (d) Venous-phase selective cholecystic arteriogram shows that a branch at the porta hepatis drains the area of the pseudolesion (arrow). (e) Spin-echo T1-weighted MR image (500/15 [repetition time msec/echo time msec]) obtained with a 1.5-T unit shows high signal intensity of the pseudolesion (arrow). (f) Spin-echo T1-weighted MR image (500/15) with fat saturation shows that the signal intensity of the pseudolesion is suppressed (arrow).
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Aberrant pancreaticoduodenal veins arise from the region of the head of the pancreas and ascend within the anterior and lateral aspect of the hepatoduodenal ligament toward the porta hepatis. These veins may be recognized at intravenously enhanced CT (particularly at thin-section multi–detector row CT), but they are usually too small to be distinguished from branches of the common hepatic artery. The incidence of this aberrant vein is unknown. Only several cases have been reported in the literature, and most of them exhibit focal steatosis (Fig 11) (15,18).
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Figure 11a. Pseudolesion in segment IV due to an aberrant pancreaticoduodenal vein in a 54-year-old woman. Focal steatosis was proved with chemical shift MR images (not shown). (a) Early-phase incremental dynamic CT scan shows a faint low-attenuation area in segment IV (arrow). (b) CT scan obtained during arterial portography shows a portal perfusion defect (arrow). (c) CT scan obtained during pancreaticoduodenal arteriography shows strong enhancement of the pseudolesion (arrow). (d) Venous-phase selective pancreaticoduodenal arteriogram shows unusual vessels running along the hepatoduodenal ligament (arrow) toward segment IV.
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Figure 11b. Pseudolesion in segment IV due to an aberrant pancreaticoduodenal vein in a 54-year-old woman. Focal steatosis was proved with chemical shift MR images (not shown). (a) Early-phase incremental dynamic CT scan shows a faint low-attenuation area in segment IV (arrow). (b) CT scan obtained during arterial portography shows a portal perfusion defect (arrow). (c) CT scan obtained during pancreaticoduodenal arteriography shows strong enhancement of the pseudolesion (arrow). (d) Venous-phase selective pancreaticoduodenal arteriogram shows unusual vessels running along the hepatoduodenal ligament (arrow) toward segment IV.
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Figure 11c. Pseudolesion in segment IV due to an aberrant pancreaticoduodenal vein in a 54-year-old woman. Focal steatosis was proved with chemical shift MR images (not shown). (a) Early-phase incremental dynamic CT scan shows a faint low-attenuation area in segment IV (arrow). (b) CT scan obtained during arterial portography shows a portal perfusion defect (arrow). (c) CT scan obtained during pancreaticoduodenal arteriography shows strong enhancement of the pseudolesion (arrow). (d) Venous-phase selective pancreaticoduodenal arteriogram shows unusual vessels running along the hepatoduodenal ligament (arrow) toward segment IV.
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Figure 11d. Pseudolesion in segment IV due to an aberrant pancreaticoduodenal vein in a 54-year-old woman. Focal steatosis was proved with chemical shift MR images (not shown). (a) Early-phase incremental dynamic CT scan shows a faint low-attenuation area in segment IV (arrow). (b) CT scan obtained during arterial portography shows a portal perfusion defect (arrow). (c) CT scan obtained during pancreaticoduodenal arteriography shows strong enhancement of the pseudolesion (arrow). (d) Venous-phase selective pancreaticoduodenal arteriogram shows unusual vessels running along the hepatoduodenal ligament (arrow) toward segment IV.
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In 6%–24% of patients, common hepatic or right gastric arteriography shows drainage by an aberrant right gastric vein (1,15). According to our experience, this abnormal vessel is frequently observed to enter the area of a pseudolesion (dorsal aspect of segment IV) at intravenously enhanced CT. It can be a cause of focal steatosis (Fig 12) (1), focal sparing in a fatty liver (1), or an early enhancing pseudolesion (Fig 13).
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Figure 12a. Pseudolesion in segment IV of a 48-year-old woman due to an aberrant right gastric vein and possibly to an aberrant pancreaticoduodenal vein as well. Focal fatty accumulation was proved with chemical shift MR imaging (not shown). (a) Early-phase incremental dynamic CT scan shows a low-attenuation area in segment IV (straight arrow) and an aberrant right gastric vein (curved arrow). (b) CT scan obtained during arterial portography (same level as a) shows a well-marginated portal perfusion defect (arrow), which is suggestive of isolated perfusion. (c) CT scan obtained during arterial portography (2 cm cephalad to b) shows ill-defined portal perfusion defects in segments III (arrowhead) and IV (straight arrow), suggesting nonisolated perfusion. (d) CT scan obtained during right gastric arteriography (same level as b) shows strong enhancement of the dorsal half of the pseudolesion (straight arrow). An aberrant right gastric vein is also visible (curved arrow). (e) CT scan obtained during right gastric arteriography (same level as c) shows areas of strong enhancement in segments III (arrow) and IV (arrowhead) that are larger than the portal perfusion defects shown in c. No fatty change was proved in these areas. (f) Venous-phase selective right gastric arteriogram shows three aberrant vessels that ascend toward the porta hepatis and enter segment IV (curved solid arrow), the cephalic portion of segment IV (open arrow), and segment III (straight arrow) and that correspond to the three areas of portal perfusion diminishment at CT during arterial portography. (g) Venous-phase common hepatic arteriogram shows another vessel (arrows) ascending cephalad toward the region of segment IV, probably representing an aberrant pancreaticoduodenal vein and contributing to the development of the ventral half of the pseudolesion in segment IV. CT during selective angiography, however, was not performed.
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Figure 12b. Pseudolesion in segment IV of a 48-year-old woman due to an aberrant right gastric vein and possibly to an aberrant pancreaticoduodenal vein as well. Focal fatty accumulation was proved with chemical shift MR imaging (not shown). (a) Early-phase incremental dynamic CT scan shows a low-attenuation area in segment IV (straight arrow) and an aberrant right gastric vein (curved arrow). (b) CT scan obtained during arterial portography (same level as a) shows a well-marginated portal perfusion defect (arrow), which is suggestive of isolated perfusion. (c) CT scan obtained during arterial portography (2 cm cephalad to b) shows ill-defined portal perfusion defects in segments III (arrowhead) and IV (straight arrow), suggesting nonisolated perfusion. (d) CT scan obtained during right gastric arteriography (same level as b) shows strong enhancement of the dorsal half of the pseudolesion (straight arrow). An aberrant right gastric vein is also visible (curved arrow). (e) CT scan obtained during right gastric arteriography (same level as c) shows areas of strong enhancement in segments III (arrow) and IV (arrowhead) that are larger than the portal perfusion defects shown in c. No fatty change was proved in these areas. (f) Venous-phase selective right gastric arteriogram shows three aberrant vessels that ascend toward the porta hepatis and enter segment IV (curved solid arrow), the cephalic portion of segment IV (open arrow), and segment III (straight arrow) and that correspond to the three areas of portal perfusion diminishment at CT during arterial portography. (g) Venous-phase common hepatic arteriogram shows another vessel (arrows) ascending cephalad toward the region of segment IV, probably representing an aberrant pancreaticoduodenal vein and contributing to the development of the ventral half of the pseudolesion in segment IV. CT during selective angiography, however, was not performed.
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Figure 12c. Pseudolesion in segment IV of a 48-year-old woman due to an aberrant right gastric vein and possibly to an aberrant pancreaticoduodenal vein as well. Focal fatty accumulation was proved with chemical shift MR imaging (not shown). (a) Early-phase incremental dynamic CT scan shows a low-attenuation area in segment IV (straight arrow) and an aberrant right gastric vein (curved arrow). (b) CT scan obtained during arterial portography (same level as a) shows a well-marginated portal perfusion defect (arrow), which is suggestive of isolated perfusion. (c) CT scan obtained during arterial portography (2 cm cephalad to b) shows ill-defined portal perfusion defects in segments III (arrowhead) and IV (straight arrow), suggesting nonisolated perfusion. (d) CT scan obtained during right gastric arteriography (same level as b) shows strong enhancement of the dorsal half of the pseudolesion (straight arrow). An aberrant right gastric vein is also visible (curved arrow). (e) CT scan obtained during right gastric arteriography (same level as c) shows areas of strong enhancement in segments III (arrow) and IV (arrowhead) that are larger than the portal perfusion defects shown in c. No fatty change was proved in these areas. (f) Venous-phase selective right gastric arteriogram shows three aberrant vessels that ascend toward the porta hepatis and enter segment IV (curved solid arrow), the cephalic portion of segment IV (open arrow), and segment III (straight arrow) and that correspond to the three areas of portal perfusion diminishment at CT during arterial portography. (g) Venous-phase common hepatic arteriogram shows another vessel (arrows) ascending cephalad toward the region of segment IV, probably representing an aberrant pancreaticoduodenal vein and contributing to the development of the ventral half of the pseudolesion in segment IV. CT during selective angiography, however, was not performed.
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Figure 12d. Pseudolesion in segment IV of a 48-year-old woman due to an aberrant right gastric vein and possibly to an aberrant pancreaticoduodenal vein as well. Focal fatty accumulation was proved with chemical shift MR imaging (not shown). (a) Early-phase incremental dynamic CT scan shows a low-attenuation area in segment IV (straight arrow) and an aberrant right gastric vein (curved arrow). (b) CT scan obtained during arterial portography (same level as a) shows a well-marginated portal perfusion defect (arrow), which is suggestive of isolated perfusion. (c) CT scan obtained during arterial portography (2 cm cephalad to b) shows ill-defined portal perfusion defects in segments III (arrowhead) and IV (straight arrow), suggesting nonisolated perfusion. (d) CT scan obtained during right gastric arteriography (same level as b) shows strong enhancement of the dorsal half of the pseudolesion (straight arrow). An aberrant right gastric vein is also visible (curved arrow). (e) CT scan obtained during right gastric arteriography (same level as c) shows areas of strong enhancement in segments III (arrow) and IV (arrowhead) that are larger than the portal perfusion defects shown in c. No fatty change was proved in these areas. (f) Venous-phase selective right gastric arteriogram shows three aberrant vessels that ascend toward the porta hepatis and enter segment IV (curved solid arrow), the cephalic portion of segment IV (open arrow), and segment III (straight arrow) and that correspond to the three areas of portal perfusion diminishment at CT during arterial portography. (g) Venous-phase common hepatic arteriogram shows another vessel (arrows) ascending cephalad toward the region of segment IV, probably representing an aberrant pancreaticoduodenal vein and contributing to the development of the ventral half of the pseudolesion in segment IV. CT during selective angiography, however, was not performed.
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Figure 12e. Pseudolesion in segment IV of a 48-year-old woman due to an aberrant right gastric vein and possibly to an aberrant pancreaticoduodenal vein as well. Focal fatty accumulation was proved with chemical shift MR imaging (not shown). (a) Early-phase incremental dynamic CT scan shows a low-attenuation area in segment IV (straight arrow) and an aberrant right gastric vein (curved arrow). (b) CT scan obtained during arterial portography (same level as a) shows a well-marginated portal perfusion defect (arrow), which is suggestive of isolated perfusion. (c) CT scan obtained during arterial portography (2 cm cephalad to b) shows ill-defined portal perfusion defects in segments III (arrowhead) and IV (straight arrow), suggesting nonisolated perfusion. (d) CT scan obtained during right gastric arteriography (same level as b) shows strong enhancement of the dorsal half of the pseudolesion (straight arrow). An aberrant right gastric vein is also visible (curved arrow). (e) CT scan obtained during right gastric arteriography (same level as c) shows areas of strong enhancement in segments III (arrow) and IV (arrowhead) that are larger than the portal perfusion defects shown in c. No fatty change was proved in these areas. (f) Venous-phase selective right gastric arteriogram shows three aberrant vessels that ascend toward the porta hepatis and enter segment IV (curved solid arrow), the cephalic portion of segment IV (open arrow), and segment III (straight arrow) and that correspond to the three areas of portal perfusion diminishment at CT during arterial portography. (g) Venous-phase common hepatic arteriogram shows another vessel (arrows) ascending cephalad toward the region of segment IV, probably representing an aberrant pancreaticoduodenal vein and contributing to the development of the ventral half of the pseudolesion in segment IV. CT during selective angiography, however, was not performed.
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Figure 12f. Pseudolesion in segment IV of a 48-year-old woman due to an aberrant right gastric vein and possibly to an aberrant pancreaticoduodenal vein as well. Focal fatty accumulation was proved with chemical shift MR imaging (not shown). (a) Early-phase incremental dynamic CT scan shows a low-attenuation area in segment IV (straight arrow) and an aberrant right gastric vein (curved arrow). (b) CT scan obtained during arterial portography (same level as a) shows a well-marginated portal perfusion defect (arrow), which is suggestive of isolated perfusion. (c) CT scan obtained during arterial portography (2 cm cephalad to b) shows ill-defined portal perfusion defects in segments III (arrowhead) and IV (straight arrow), suggesting nonisolated perfusion. (d) CT scan obtained during right gastric arteriography (same level as b) shows strong enhancement of the dorsal half of the pseudolesion (straight arrow). An aberrant right gastric vein is also visible (curved arrow). (e) CT scan obtained during right gastric arteriography (same level as c) shows areas of strong enhancement in segments III (arrow) and IV (arrowhead) that are larger than the portal perfusion defects shown in c. No fatty change was proved in these areas. (f) Venous-phase selective right gastric arteriogram shows three aberrant vessels that ascend toward the porta hepatis and enter segment IV (curved solid arrow), the cephalic portion of segment IV (open arrow), and segment III (straight arrow) and that correspond to the three areas of portal perfusion diminishment at CT during arterial portography. (g) Venous-phase common hepatic arteriogram shows another vessel (arrows) ascending cephalad toward the region of segment IV, probably representing an aberrant pancreaticoduodenal vein and contributing to the development of the ventral half of the pseudolesion in segment IV. CT during selective angiography, however, was not performed.
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Figure 12g. Pseudolesion in segment IV of a 48-year-old woman due to an aberrant right gastric vein and possibly to an aberrant pancreaticoduodenal vein as well. Focal fatty accumulation was proved with chemical shift MR imaging (not shown). (a) Early-phase incremental dynamic CT scan shows a low-attenuation area in segment IV (straight arrow) and an aberrant right gastric vein (curved arrow). (b) CT scan obtained during arterial portography (same level as a) shows a well-marginated portal perfusion defect (arrow), which is suggestive of isolated perfusion. (c) CT scan obtained during arterial portography (2 cm cephalad to b) shows ill-defined portal perfusion defects in segments III (arrowhead) and IV (straight arrow), suggesting nonisolated perfusion. (d) CT scan obtained during right gastric arteriography (same level as b) shows strong enhancement of the dorsal half of the pseudolesion (straight arrow). An aberrant right gastric vein is also visible (curved arrow). (e) CT scan obtained during right gastric arteriography (same level as c) shows areas of strong enhancement in segments III (arrow) and IV (arrowhead) that are larger than the portal perfusion defects shown in c. No fatty change was proved in these areas. (f) Venous-phase selective right gastric arteriogram shows three aberrant vessels that ascend toward the porta hepatis and enter segment IV (curved solid arrow), the cephalic portion of segment IV (open arrow), and segment III (straight arrow) and that correspond to the three areas of portal perfusion diminishment at CT during arterial portography. (g) Venous-phase common hepatic arteriogram shows another vessel (arrows) ascending cephalad toward the region of segment IV, probably representing an aberrant pancreaticoduodenal vein and contributing to the development of the ventral half of the pseudolesion in segment IV. CT during selective angiography, however, was not performed.
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Figure 13a. Pseudolesion in segment IV due to aberrant right gastric venous drainage in a 72-year-old man with diffuse gastric carcinoma. Surgical ligation of the aberrant right gastric vein might have changed the status of flow within the parabiliary venous system and probably resulted in direct inflow of insulin-rich venous blood conveyed via the pancreaticoduodenal vein into segment IV. (a) Early-phase incremental dynamic CT scan obtained before surgery shows an aberrant right gastric vein (open arrow) and an enhanced area in segment IV (solid arrow), probably due to hypervascularity caused by the gastric cancer. (b) Early-phase incremental dynamic CT scan obtained after total gastrectomy shows severe fatty change of the area of the pseudolesion (arrow). Ascites due to peritoneal recurrence is also evident. (c) Postoperative ultrasonogram in a subcostal plane shows a hyperechoic area (arrow) that corresponds to the area of severe fatty change.
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Figure 13b. Pseudolesion in segment IV due to aberrant right gastric venous drainage in a 72-year-old man with diffuse gastric carcinoma. Surgical ligation of the aberrant right gastric vein might have changed the status of flow within the parabiliary venous system and probably resulted in direct inflow of insulin-rich venous blood conveyed via the pancreaticoduodenal vein into segment IV. (a) Early-phase incremental dynamic CT scan obtained before surgery shows an aberrant right gastric vein (open arrow) and an enhanced area in segment IV (solid arrow), probably due to hypervascularity caused by the gastric cancer. (b) Early-phase incremental dynamic CT scan obtained after total gastrectomy shows severe fatty change of the area of the pseudolesion (arrow). Ascites due to peritoneal recurrence is also evident. (c) Postoperative ultrasonogram in a subcostal plane shows | |
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Abstract
LEARNING OBJECTIVES
represents that of the cholecystic vein through the liver bed; ß, the parabiliary venous system; and 
, the epigastric-paraumbilical venous system.