Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2012;67(6):609-14.
doi: 10.6061/clinics/2012(06)11.

The diameter of the originating vein determines esophageal and gastric fundic varices in portal hypertension secondary to posthepatitic cirrhosis

Affiliations

The diameter of the originating vein determines esophageal and gastric fundic varices in portal hypertension secondary to posthepatitic cirrhosis

Hai-ying Zhou et al. Clinics (Sao Paulo). 2012.

Abstract

Objective: The aim of this study was to determine whether and how the diameter of the vein that gives rise to the inflowing vein of the esophageal and gastric fundic varices secondary to posthepatitic cirrhosis, as measured with multidetector-row computed tomography, could predict the varices and their patterns.

Methods: A total of 106 patients with posthepatitic cirrhosis underwent multidetector-row computed tomography. Patients with and without esophageal and gastric fundic varices were enrolled in Group 1 and Group 2, respectively. Group 1 was composed of Subgroup A, consisting of patients with varices, and Subgroup B consisted of patients with varices in combination with portal vein-inferior vena cava shunts. The diameters of the originating veins of veins entering the varices were reviewed and statistically analyzed.

Results: The originating veins were the portal vein in 8% (6/75) of patients, the splenic vein in 65.3% (49/75) of patients, and both the portal and splenic veins in 26.7% (20/75) of patients. The splenic vein diameter in Group 1 was larger than that in Group 2, whereas no differences in portal vein diameters were found between groups. In Group 1, the splenic vein diameter in Subgroup A was larger than that in Subgroup B. A cut-off splenic vein diameter of 8.5 mm achieved a sensitivity of 83.3% and specificity of 58.1% for predicting the varices. For discrimination of the varices in combination with and without portal vein-inferior vena cava shunts, a cut-off diameter of 9.5 mm achieved a sensitivity of 66.7% and specificity of 60.0%.

Conclusion: The diameter of the splenic vein can be used to predict esophageal and gastric fundic varices and their patterns.

PubMed Disclaimer

Conflict of interest statement

No potential conflict of interest was reported.

Figures

Figure 1
Figure 1
In a 56-year-old female with esophageal and gastric fundic varices secondary to posthepatitic cirrhosis, the computed tomography multiplanar reformation reconstruction images demonstrated esophageal varices (A and B, black arrow), and the inflowing vessel is the left gastric vein (A and B, white arrow) originating from the splenic vein (B, white arrowhead).
Figure 2
Figure 2
In a 48-year-old male with gastric fundic varices secondary to posthepatitic cirrhosis, the computed tomography multiplanar reformation reconstruction images show gastric fundic varices (A and B, black arrow) originating from the splenic vein (B, white arrow), which are associated with nephrogastric shunts (C, white arrowhead).
Figure 3
Figure 3
In a 43-year-old posthepatitic cirrhotic male with no collaterals, the computed tomography multiplanar reformation reconstruction images show ectasia of the portal vein (A and B, white arrow) and splenic vein (A and B, black arrow).
Figure 4
Figure 4
Receiver-operating characteristic (ROC) curves demonstrate the use of a cut-off splenic vein diameter of 8.5 mm in predicting the presence of esophageal and gastric fundic varices (A). A threshold diameter of 9.5 mm was used to discriminate isolated esophageal and gastric fundic varices from the varices associated with portal vein-inferior vena cava shunts (B).

Similar articles

Cited by

References

    1. Pinzani M, Rosselli M, Zuckermann M. Liver cirrhosis. Best Pract Res Clin Gastroenterol. 2011;25(2):281–90. - PubMed
    1. Iwakiri Y, Groszmann RJ. The hyperdynamic circulation of chronic liver diseases: from the patient to the molecule. Hepatology. 2006;43(2 Suppl 1) :S121–31. - PubMed
    1. Iwakiri Y. Endothelial dysfunction in the regulation of cirrhosis and portal hypertension. Liver Int. 2012;32(2):199–213. - PMC - PubMed
    1. Garini G, Delsante M, Iannuzzella F. Pathophysiology of portal hypertension and mechanisms of sodium and water retention in cirrhosis. Recenti Prog Med. 2011;102(3):134–40. - PubMed
    1. Nazyrov FG, Deviatov AV, Babadzhanov AKh, Sultanov SA. Specific development and course of portal hypertension complication in patients with hepatic cirrhosis of HBV and HCV etiology. Vestn Khir Im I I Grek. 2011;170(1):22–9. - PubMed

Publication types