Figure 1
Post contrast sequential axial images showing psedolesion in segment II caused by aberrant vein.
Pseudolesion caused by aberrant venous drainage
SectionAbdominal imaging
Case TypeClinical Cases
AuthorsJain A, Ablett M.
Connected authors
47 years, male
Clinical History
Our patient was diagnosed with a pseudolesion in liver on a routine scan. It is crucial to recognise pseudolesions as they may be interpreted as true tumors. Understanding the underlying mechanisms of pseudolesions may help to recognize the wide variety of their CT appearances thus preventing unnecessary examinations and biopsy.
Imaging Findings
A 47 year old male patient underwent a venous phase helical CT scan of chest and abdomen for a suspicion of a lesion in the right apex on routine chest radiography. There was no abnormality in the chest. There was a large well defined geographic low attenuation area in the posterior aspects of hepatic segment II, which represented pseudolesion, caused by aberrant left gastric venous drainage (Fig. 1, 2).
Discussion
The prevalence of pseudolesions varies from 1-19.8% [1,2]. Several kinds of pseudolesions have been reported [3]. In non-cirrhotic livers they are subdivided into:
1) Due to extrinsic focal compression of the liver
2) Due to a “third inflow” of blood.
1) Pseudolesions caused by focal compression of the liver: These pseudolesions are caused by transient compression of the liver by a certain structure such as ribs or diaphram, which causes decreased transient portal perfusion at the subcapsular region.
They are seen as ill-defined areas of diminished portal perfusion usually at the portovenous phase.
2) Pseudolesions caused by ‘third inflow’: Small areas of liver tissue can be supplied by another venous system other than the hepatic artery and portal vein. This system may be composed of aberrant veins or parts of normal veins that directly enter the liver.
The 3 broad groups of third inflow pseudolesions are:
a) cholecystic veins through the liver bed – they either enter the liver through the liver bed or run through the Calot triangle and join the parabiliary veins at porta hepatis.
These pseudolesions are seen as enhanced areas around the gall bladder at the arterial phase.
b) parabiliary venous system: it lies with in the hepatoduodenal ligament and collects venous blood from the pancreatic head, distal stomach, and the bile duct system.
The left and right gastric veins normally drain directly into the portal vein proximal to the porta hepatis. In this case, the left gastric vein can clearly be seen to drain directly into hepatic segment-II.
Due to differences in the concentration of contrast medium in the portal vein supplying the rest of the liver and that in the left gastric vein supplying segment-II, a geographic area of relatively low attenuation results in segment-II. These pseudolesions can be typically seen in segment II [4]. Those caused by aberrant right gastric vein are seen in segment III or IV [3,4,5].
The timing of image acquisition influences the extent to which there is a difference in the attenuation of segment-II and the rest of the liver. A nonenhanced acquisition was not performed in this case; in a proportion of cases differences in attenuation of the liver into which there is aberrant venous drainage and liver into which there is normal portal venous drainage can occur on nonenhanced images due to differences in fat deposition within hepatocytes. Interestingly, this may result in either focal fatty sparing, as the blood entering the area of aberrant venous drainage contains less fat than blood in the portal vein; or focal fatty change, possibly due to differences in concentrations of intestinal hormones. The exact mechanism for both focal fatty sparing and focal fatty change is, however, poorly understood.
c) epigastric-paraumbilical venous system: this system consists of small veins around the falciform ligament that drain the anterior abdominal wall. These are the superior and inferior veins of Sappey and the vein of Burow. They are observed as low-attenuation areas.
1) Due to extrinsic focal compression of the liver
2) Due to a “third inflow” of blood.
1) Pseudolesions caused by focal compression of the liver: These pseudolesions are caused by transient compression of the liver by a certain structure such as ribs or diaphram, which causes decreased transient portal perfusion at the subcapsular region.
They are seen as ill-defined areas of diminished portal perfusion usually at the portovenous phase.
2) Pseudolesions caused by ‘third inflow’: Small areas of liver tissue can be supplied by another venous system other than the hepatic artery and portal vein. This system may be composed of aberrant veins or parts of normal veins that directly enter the liver.
The 3 broad groups of third inflow pseudolesions are:
a) cholecystic veins through the liver bed – they either enter the liver through the liver bed or run through the Calot triangle and join the parabiliary veins at porta hepatis.
These pseudolesions are seen as enhanced areas around the gall bladder at the arterial phase.
b) parabiliary venous system: it lies with in the hepatoduodenal ligament and collects venous blood from the pancreatic head, distal stomach, and the bile duct system.
The left and right gastric veins normally drain directly into the portal vein proximal to the porta hepatis. In this case, the left gastric vein can clearly be seen to drain directly into hepatic segment-II.
Due to differences in the concentration of contrast medium in the portal vein supplying the rest of the liver and that in the left gastric vein supplying segment-II, a geographic area of relatively low attenuation results in segment-II. These pseudolesions can be typically seen in segment II [4]. Those caused by aberrant right gastric vein are seen in segment III or IV [3,4,5].
The timing of image acquisition influences the extent to which there is a difference in the attenuation of segment-II and the rest of the liver. A nonenhanced acquisition was not performed in this case; in a proportion of cases differences in attenuation of the liver into which there is aberrant venous drainage and liver into which there is normal portal venous drainage can occur on nonenhanced images due to differences in fat deposition within hepatocytes. Interestingly, this may result in either focal fatty sparing, as the blood entering the area of aberrant venous drainage contains less fat than blood in the portal vein; or focal fatty change, possibly due to differences in concentrations of intestinal hormones. The exact mechanism for both focal fatty sparing and focal fatty change is, however, poorly understood.
c) epigastric-paraumbilical venous system: this system consists of small veins around the falciform ligament that drain the anterior abdominal wall. These are the superior and inferior veins of Sappey and the vein of Burow. They are observed as low-attenuation areas.
Differential Diagnosis List
Pseudolesion of liver caused by aberrant left gastric venous drainage.
Final Diagnosis
Pseudolesion of liver caused by aberrant left gastric venous drainage.
References
[1] Soyer P, Devine N, Somveille E, Rebibo G, Rambert C, Scherrer A (1996) Hepatic pseudolesion around the falciform ligament: prevalence on CT examination. Abdom Imaging 21(4):324-8. (PMID: 8661569)
[2] Koseoglu K, Ozsunar Y, Taskin F, Karaman C (2005) Pseudolesion of left liver lobe during helical CT examination: prevalence and comparison between unenhanced and biphasic CT findings. Eur J Radiol 54(3):388-92. (PMID: 15899341)
[3] Kengo Y, Hiroshi H, Toshiro K, Hiroyuki I, Hitoshi A, Kenji S et al. (2001) Unusual Hemodynamics and Pseudolesions of the Noncirrhotic Liver at CT. RadioGraphics 21: S81-S96. (PMID: 11598250)
[4] Terayama N, Matsui O, Tatsu T, Gabata T, et al. (2004) Focal sparing of fatty liver in segment II associated with aberrant left gastric vein. Br J Radiol. 2004 Feb;77(914):150-2. (PMID: 15010390)
[5] Takayasu K, Aoki K, Ichikawa T, et al. (1990) Aberrant right gastric vein directly communicating with left portal vein system: incidence and implications. Acta Radiol 31:575-577. (PMID: 2278780)
Case information
| URL: | https://www.eurorad.org/case/7101 |
| DOI: | 10.1594/EURORAD/CASE.7101 |
| ISSN: | 1563-4086 |
