Update on the Management of Gastric Varices

Xuefeng Luo; Virginia Hernández-Gea


Liver International. 2022;42(6):1250-1258. 

In This Article

Abstract and Introduction


Gastro-oesophageal varices are the major clinical manifestations of cirrhosis and portal hypertension. Although less frequent than oesophageal varices (EV), bleeding from gastric varices (GV) is generally more severe and associated with higher mortality and a greater risk to rebleed. According to Sarin's classification, GVs are categorized into four types based on their location within the stomach and relationship with EV. Currently, treatment options for the management of GV include beta-blockers, endoscopic band ligation, endoscopic cyanoacrylate injection, EUS-guided coil/cyanoacrylate injection, transjugular intrahepatic portosystemic shunts and balloon-occluded retrograde transvenous obliteration. The best treatment strategy of GV remains controversial because of the heterogeneity of GV, lack of high-quality data and suboptimal trial design of the studies available. The proper treatment algorithm may require adequate endoscopic and imaging evaluation by a multidisciplinary team with multiple treatment options available. This review describes the hemodynamic features of GV, pharmacological, endoscopic and interventional radiological treatment options for GV.


In the course of cirrhosis, portal hypertension causes a vast variety of spontaneous portosystemic collaterals of which gastro-oesophageal varices are the most significant.[1] With disease progression and exacerbation of portal pressure, the collaterals enlarge and eventually rupture causing variceal bleeding. Despite improved clinical management, variceal bleeding is still a major complication of portal hypertension and a leading cause of mortality in cirrhotic patients.

Gastric varices (GV) are found in about 20% of patients with cirrhosis.[1] According to the Sarin classification, GV can be categorized into four types based on their location within the stomach and relationship with oesophageal varices (EV).[2] Gastro-oesophageal varices type 1 (GOV1) are a continuation of EV into the lesser curvature of the stomach. Gastro-oesophageal varices type 2 (GOV2) represents a continuation of EV into the fundus of the stomach. Isolated gastric varices type 1 (IGV1) are those located in the fundus of the stomach and isolated gastric varices type 2 (IGV2) refers to GV located anywhere in the stomach (Figure 1). In 1992, Sarin et al reported that GOV1 represents 75%, GOV2 21%, IGV1 less than 2% and IGV2 4% of all GV.[2]

Figure 1.

Endoscopic classification system for GV

As a general consideration, GV tend to bleed less frequently than EV; however, rupture of GV is associated with more severe haemorrhage, higher mortality and a greater risk of rebleed after spontaneous haemostasis.[1,3,4] This review will focus mainly on GOV2/IGV1 called thereafter GV, as GOV1 shares a similar vascular anatomy with EV and should be managed equally to EV.