British Journal of Radiology (2004) 77, 150-152
© 2004 British Institute of Radiology
doi: 10.1259/bjr/86102770
Focal sparing of fatty liver in segment II associated with aberrant left gastric vein
N Terayama, MD
1
O Matsui, MD
1
H Tatsu, MD
1
T Gabata, MD
1
A Kinoshita, MD
2 and
K Hasatani, MD
2
1 Department of Radiology, Kanazawa University, Graduate School of Medical Science, Kanazawa 920-8641 and 2 Department of Internal Medicine, Suzu General Hospital, Suzu, Ishikawa, Japan
 |
Abstract
|
|---|
We present a patient with aberrant left gastric vein (LGV) that directly enters the posterior edge of segment II in the liver. The corresponding area was focally spared of fatty liver. We consider that this aberrant LGV contributed to the cause of focal sparing. This is the first report of the use of helical CT and Doppler ultrasound to depict the aberrant LGV that directly enters the liver.
|
Introduction
|
|---|
Non-portal venous flow draining into the liver such as the parabiliary venous system [1], and epigastric and cholecystic veins, cause pseudolesions in various locations of the liver on CT during arterial portography (CTAP) [2]. The aberrant right gastric vein, which is included in the parabiliary venous system, causes focal sparing of fatty liver as well as a pseudolesion at the posterior edge of segment IV in the liver [3]. The aberrant left gastric vein (LGV), which runs along the hepatogastric ligament and enters the liver [4], also causes pseudolesions in segments II and IV of the liver on CTAP [5]. We present a patient with focal sparing of fatty liver in segment II caused by the aberrant LGV that directly enters the liver. The aberrant LGV was visualized on helical CT, and hepatopetal flow was confirmed by colour Doppler ultrasound (US).
|
Case report
|
|---|
A 36-year-old asymptomatic man underwent a routine medical examination. Laboratory analysis revealed an increase in the serum levels of glutamic oxaloacetic transaminase (38 IU l-1; normal range, 13–34 IU l-1), glutamic pyruvic transaminase (83 IU l-1; normal range, 6–30 IU l-1), gamma glutamyl transferase (231 IU l-1; normal range, 7–47 IU l-1), total cholesterol (237 mg dl-1; normal range, 128–220 mg dl-1) and triglyceride (323 mg dl-1; normal range, 30–150 mg dl-1). Abdominal US (EUB-6000; Hitachi Medical Corporation, Tokyo, Japan) using a 5 MHz convex probe showed a fatty liver with a hypoechoic area at the posterior edge of segment II in the liver, suggestive of a focally spared area. Non-contrast CT (Somatome Plus 4; Siemens AG, Munich, Germany) showed that the corresponding area was slightly hyperdense compared with the surrounding liver. Post contrast helical CT was performed using the following parameters; 5 mm collimation, a scanning pitch of 1.0, and reconstruction of 5 mm intervals. Scanning was started 30 s after the beginning of the injection of 100 ml of contrast medium (iopamidol 300; Schering AG, Berlin, Germany) at a rate of 3.0 ml s-1. Post contrast helical CT revealed a blood vessel directly connected to the posterior edge of segment II in the liver (Figure 1
). This vessel ran along the distal section of the left gastric artery and it collected branches from the cardiac region of the lesser curvature of the stomach, suggesting that this vessel was the aberrant LGV. No tumourous lesions were detected. After CT examination, colour and pulse Doppler US performed on the vessel that was thought to be the aberrant LGV showed that the vessel entered the spared area of the fatty liver at the posterior edge of segment II (Figure 2), and that it exhibited a continuous venous flow waveform (Figure 3).
View larger version (125K):
[in this window]
[in a new window]
|
Figure 1. Post contrast helical CT at 5 mm intervals. The aberrant left gastric vein (arrows) runs along the distal portion of the left gastric artery (arrowheads) in the hepatogastric ligament and directly connects to the posterior edge of segment II in the liver.
|
|
View larger version (192K):
[in this window]
[in a new window]
|
Figure 2. Colour Doppler ultrasound revealed fatty liver with a hypoechoic area suggesting a focally spared area in the posterior edge of segment II. Hepatopetal flow towards the posterior edge of segment II is seen.
|
|
|
Discussion
|
|---|
The LGV collects branches from the cardiac region of the lesser curvature of the stomach and joins either the portal vein or the splenic vein. When present, the aberrant LGV runs along the hepatogastric ligament toward the left side of the hepatic hilus, enters the liver and joins the intrahepatic portal venous branch [4]. Miyaki et al reported the incidence of the aberrant LGV as 0.8% in an autopsy study [4]. The aberrant LGV is depicted by angiography and contrast enhanced CT. Radiological studies have reported that most aberrant LGVs join the portal venous branch at the hepatic hilus [6, 7], and that the aberrant LGV may be involved in the collateral pathway of the portal vein [7] and may cause pseudolesions on CTAP [5]. The aberrant LGV can also enter the liver directly and can give off small branches to the liver parenchyma [8]. If an area of the liver parenchyma is supplied by the aberrant LGV alone, or if the aberrant LGV connects with the small portal venous branch, CTAP may reveal a perfusion defect in the corresponding area.
In our patient, the aberrant LGV was revealed by non-invasive diagnostic modalities, including helical CT. Colour Doppler US was used to show that this aberrant LGV directly drained into the posterior edge of segment II of the liver. The corresponding area was found to be a focally spared area of fatty liver. To our knowledge, this is the first report of the aberrant LGV which directly enters the liver to have its hepatopetal flow clarified by colour Doppler US.
Pseudolesions in the gallbladder fossa and in the posterior edge of the segment IV of the liver which may be caused by decreased portal flow [3], are associated with the cholecystic vein and the aberrant right gastric vein (RGV), respectively. When the RGV, which usually enters the main portal vein, enters the liver directly at the posterior edge of segment IV, it is referred to as the aberrant RGV [2]. It is considered as the part of the parabiliary venous system [1, 9]. Such a vessel can cause a pseudolesion in that area, as well as inducing some parenchymal changes such as focal sparing of fatty liver or hyperplasia of cirrhotic liver [3, 9]. The aberrant RGV, however, rarely causes focal fatty infiltration at the posterior edge of segment IV [10]. It is uncertain why altered portal flow causes focal sparing and focal fatty infiltration. Several factors contribute to the pathogenesis of hepatic fatty infiltration. It has been suggested that free fatty acids and insulin play important roles. Insulin inhibits the oxidation of fatty acids and promotes the esterification of fatty acids into triglycerides that accumulate in hepatocytes [11]. It is speculated that because the parabiliary venous system mainly drains from the stomach, the level of dietary fat and insulin in this area is low, and thus focal sparing is noted [3]. Conversely, when this system mainly drains from the pancreaticoduodenal vein, the high level of insulin causes focal fatty infiltration in the supplied area of the liver [12]. In our patient, a focally spared area, in which the aberrant LGV entered, could have been caused by a decrease in fatty acids and insulin levels.
Several non-portal hepatopetal venous flows, such as the aberrant RGV draining into the posterior edge of segment IV and paraumbilical vein draining into the anterior edge of segment IV adjacent to the falciform ligament, can be depicted by colour Doppler US [13], whereas it may be difficult to detect these aberrant blood vessels by routine US. When using this technique, the contribution of aberrant blood vessels in pseudolesions, focally spared areas and focal fatty infiltration should be considered.
Received for publication November 28, 2002.
Revision received April 14, 2003.
Accepted for publication May 2, 2003.
|
References
|
|---|
- Couinaud C. The parabiliary venous system. Surg Radiol Anat 1988;10:311–6.[CrossRef][Medline]
- Matsui O, Takahashi S, Kadoya M, Yoshikawa J, Gabata T, Takashima T, et al. Pseudolesion in segment IV of the liver at CT during arterial portography: correlation with aberrant gastric venous drainage. Radiology 1994;193:31–5.[Abstract/Free Full Text]
- Matsui O, Kadoya M, Takahashi S, Yoshikawa J, Gabata T, Takashima T, et al. Focal sparing of segment IV in fatty livers shown by sonography and CT: correlation with aberrant gastric venous drainage. AJR Am J Roentgenol 1995;164:1137–40.[Abstract/Free Full Text]
- Miyaki T, Yamada M, Kumaki K. Aberrant course of the left gastric vein in the human. Possibility of a persistent left portal vein. Acta Anat 1987;130:275–9.[Medline]
- Hiwatashi A, Yoshimitsu K, Honda H, Kuroiwa T, Irie H, Tajima T, et al. Pseudolesion in segment II of the liver observed on CT during arterial portography caused by the aberrant left gastric venous drainage. Abdom Imaging 1999;24:357–9.[CrossRef][Medline]
- Tajima H, Murakami R, Kumazaki T. Aberrant left gastric vein directly draining into left portal venous system. A case report. Acta Radiol 1992;33:462–3.[Medline]
- Ohashi I, Ina H, Hanafusa K, Yoshida T, Himeno Y, Gomi N, et al. Aberrant left gastric vein demonstrated by helical CT. J Comput Assist Tomogr 1997;21:996–1000.[CrossRef][Medline]
- Ohkubo M. Aberrant left gastric vein directly draining into the liver. Clin Anat 2000;13:134–7.[CrossRef][Medline]
- Matsui O, Kadoya M, Yoshikawa J, Gabata T, Takahashi S, Ueda K, et al. Aberrant gastric venous drainage in cirrhotic livers: imaging findings in focal areas of liver parenchyma. Radiology 1995;197:345–9.[Abstract/Free Full Text]
- Kawamori Y, Matsui O, Takahashi S, Kadoya M, Takashima T, Miyayama S. Focal hepatic fatty infiltration in the posterior edge of the medial segment associated with aberrant gastric venous drainage: CT, US, and MR findings. J Comput Assist Tomogr 1996;20:356–9.[CrossRef][Medline]
- Wanless IR, Bargman JM, Oreopoulos DG, Vas SI. Subcapsular steatonecrosis in response to peritoneal insulin delivery: a clue to the pathogenesis of steatonecrosis in obesity. Mod Pathol 1989;2:69–74.[Medline]
- Fukukura Y, Fujiyoshi F, Inoue H, Sasaki M, Hokotate H, Baba Y, et al. Focal fatty infiltration in the posterior aspect of hepatic segment IV: relationship to pancreaticoduodenal venous drainage. Am J Gastroenterol 2000;95:3590–5.[CrossRef][Medline]
- Gabata T, Matsui O, Kadoya M, Ueda K, Kawamori Y, Yoshikawa J, et al. Aberrant gastric venous drainage into the medial segment: demonstration by color Doppler sonography. Abdom Imaging 1997;22:502–5.[CrossRef][Medline]
This article has been cited by other articles:
|
|
|
|
 
L.-P. Liu, B.-W. Dong, X.-L. Yu, D.-K. Zhang, X. Li, and H. Li
Analysis of Focal Spared Areas in Fatty Liver Using Color Doppler Imaging and Contrast-Enhanced Microvessel Display Sonography
J. Ultrasound Med.,
March 1, 2008;
27(3):
387 - 394.
[Abstract]
[Full Text]
[PDF]
|
|
|
Top
Abstract
Introduction
