Imaging of aberrant left gastric vein and associated pseudolesions of segments II and III of the liver and mimickers

Abstract

We present imaging findings of aberrant left gastric vein (ALGV) and associated pseudolesions and mimickers including metastases and focal nodular hyperplasia. ALGV is formed due to interrupted involution of anastomotic omental veins, and it can drain into left portal vein or segments II and III of the liver as third inflow. Focal fat, focal fat sparing, and perfusion changes can be seen due to the presence of ALGV, which can mimic metastasis in cancer patients. ALGV may also serve as a pathway for direct tumor spread into the liver in patients with gastric cancer. Magnetic resonance imaging can be used as a problem solving tool in the presence of equivocal findings on ultrasonography and computed tomography. Pseudolesions of the liver are a well-known issue and have been reported in the literature. These pseudolesions are caused by aberrant hepatopedal venous flow other than portal venous system, also known as third inflow. Third inflow is most commonly due to aberrant right gastric, paraumbilical, and cholecystic veins (1-3). Pseudolesions caused by aberrant left gastric vein (ALGV) are considered to be a more rare entity (4).The purpose of this study is to illustrate ALGV drainage into the liver and associated pseudolesions of segments II and III of the liver. In addition, we illustrate imaging findings of the mimickers of these pseudolesions. Embryology and anatomyThe left gastric vein receives branches of the inferior paraesophageal region and minor curvature of the stomach. Thereafter, it runs along the hepatogastric ligament and merges with the left aspect of the portal vein or confluence of the portal and splenic veins. The right gastric vein also receives blood from minor curvature of the stomach and merges with the right aspect of the portal vein.Aberrant left and right gastric veins develop due to morphogenetic changes during the developmental process in the early embryonic life (5). The main cause is interrupted involution of the anastomotic omental veins, so that typical left gastric vein does not form. Anastomotic omental veins are the anastomoses between primitive foregut venous plexus and ductus venosus, which normally exist during early embryonic life (5, 6).

Volume change of segments II and III of the liver after gastrectomy in patients with gastric cancer

“…These small accessory veins are remnants of embryologic mesenteries, connecting hepatic circulation with the venous circulation of pancreatico-duodenal venous arcade, right gastric vein and left gastric vein which contribute venous circulation of gastric antrum (18). These veins are less often apparent in the portal phase of a CT in normal conditions and generally are well visualized on the setting of portal hypertension or acute cholecystitis (19). It was suggested that this anomalous venous drainage could be the cause of focal steatosis in certain segments of the liver due to insulin rich blood supply via pancreatico-duodenal venous arcade (19)(20)(21).…”

“…These veins are less often apparent in the portal phase of a CT in normal conditions and generally are well visualized on the setting of portal hypertension or acute cholecystitis (19). It was suggested that this anomalous venous drainage could be the cause of focal steatosis in certain segments of the liver due to insulin rich blood supply via pancreatico-duodenal venous arcade (19)(20)(21). In either total or distal subtotal open gastrectomy, this venous plexus is generally ligated during the operation and this situation might cause a venous ischemia causing volume decrease of the liver segments as mentioned in our study.…”

A Comprehensive Approach to Hepatic Vascular Disease

“…The left gastric vein receives branches from the inferior paraesophageal region and lesser gastric curvature and courses along the gastrohepatic ligament to drain into the left aspect of the portal vein. An aberrant left gastric vein drains directly into the liver and results in an area of relative hyperenhancement at the posterior edge of segments II and III (Fig 15) (33). The prevalence of aberrant left gastric vein has been reported to be 4% (32).…”

Can ultrasound elastography identify mass-like focal fatty change (FFC) from liver mass?

“…[ 25 – 27 ] However, mass-like FFC is induced by the inhomogeneous accumulation of intracellular fat within hepatic parenchyma due to altered blood supply and insulin level. [ 28 – 30 ] The SV of FFS has been mentioned by Guibal et al, [ 14 ] Heide et al, [ 15 ] and Ronot et al, [ 16 ] in their study. In the study by Guibal et al [ 14 ] by SWE, the mean SV on 3 FFS was 6.6 ± 0.3 kPa.…”