Gastric Varices

Gastric varices (GV) are distended veins caused by increased hydrostatic pressure in the portal system, with multiple etiologies. Bleeding may be acute or chronic. GV are often associated with liver disease and may occur together with esophageal bleeds. The former do not bleed as often as esophageal varices, and spontaneous cessation of bleeding is possible, with a risk of re-bleeding [1].

There are a number of classification systems used for GV. One such classification divides them into those caused by isolated splenic vein thrombosis (SVT), and those due to portal hypertension, the latter being the more frequently reported cause [2]. GV can occur through the short gastric veins in the case of SVT, and in this particular etiology, management is challenging as there tends to be multiple varices occurring simultaneously. Other classification systems include the Sarin and the Japanese vascular classification systems, which consider numerous factors such as the vasculature, location, and appearance of varices [3] [4].

The majority of individuals that have isolated GV are asymptomatic, and the diagnosis is made incidentally. Rupture of GV causes painless bleeding from the upper gastrointestinal (GI) tract. GV tend to bleed copiously, thus some patients may present in hypovolemic shock, and fatalities are more common compared to esophageal bleeds [2]. In cases with left-sided portal hypertension, additional signs such as ascites and abdominal pain may be noticed [5]. Splenomegaly may be found on clinical examination.

Other possible presentations are hematemesis which may consist of bright red blood or coffee grounds vomitus, melena, or hematochezia which can signify a massive upper GI bleed. Occult bleeds may only be detected through biochemical testing of stool.

In patients with gastric varices, it is important to investigate for the common underlying conditions. If varices are actively bleeding, the workup includes both diagnostic as well as therapeutic interventions, usually in the form of endoscopy. This is done after hypovolemia has been addressed with careful intravenous fluid therapy.

Laboratory investigations for liver disease, such as liver function tests and clotting studies, are usually conducted. Biopsy followed by histological analysis of liver tissue may also be carried out. Blood typing and crossmatching are also useful, as some people may require transfusion.

During the endoscopic evaluation, GV may be more adequately visualized by the insertion of a nasogastric tube for gastric lavage, endoscopic suction, or the use of prokinetic drugs to accelerate gastric emptying.

Radiological techniques are employed in the evaluation of the veins of the portal system. The modalities often used are:

• Endoscopy: This has a good detection rate, reported to be as high as 90% [6]. It is accurate in localizing the GV, and identifying non-variceal upper GI bleeding.
• Angiography.
• Ultrasonography: This can either be done via the trans-abdominal or endoscopic route and is instrumental in detecting splenic vein and pancreas pathologies. Endoscopic ultrasound is preferred, as it is more accurate [7].
• Computed tomography (CT) portography: This is carried out as a contrasted study, used in the evaluation of the portal system.
• Magnetic resonance imaging (MRI) [8].

1. Graham DY, Smith JL. The course of patients after variceal hemorrhage. Gastroenterology. 1981;80(4):800-809.
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3. Caldwell SH, Hespenheide EE, Greenwald BD, Northup PG, Patrie JT. Enbucrilate for gastric varices: extended experience in 92 patients. Aliment Pharmacol Ther. 2007;26(1):49–59.
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