Primary prophylaxis of gastric variceal bleeding: the choices need to be tested!!

Hepatology International (2021) 15:863–867 https://doi.org/10.1007/s12072-021-10227-1 EDITORIAL Primary prophylaxis of gastric variceal bleeding: the choices need to be tested!! Chitranshu Vashishtha1 · Shiv Kumar Sarin1 Received: 16 April 2021 / Accepted: 23 June 2021 / Published online: 10 August 2021 © Asian Pacific Association for the Study of the Liver 2021 Gastric varices (GV) pose a challenging problem in hepatology; due to the risk of severe variceal bleeding as well recurrent hepatic encephalopathy related to co-existent large spleno-renal shunts. Primary GV (varices seen in initial endoscopic examination, before any therapy) are seen in 17% of patients of liver cirrhosis, the prevalence being higher in bleeders than non-bleeders; 24% vs 7%. Secondary GV appear for the first time after therapy for esophageal varices (EV), and are seen in 9% of patients with portal hypertension [1]. The ‘Sarin Classification’ is universally applied to determine the natural history, choice of therapeutic intervention and likely outcomes in patient with GV [2]. According to it, GV are divided into two subgroups, the gastroesophageal varices (GOV) and isolated gastric varices (IGV). GOV are further subclassified as GOV1 when esophageal varices extend below the gastroesophageal junction along lesser curvature of stomach and as GOV2 when the esophageal varices extend into the fundus of stomach. IGV includes IGV1, when located in fundus, and IGV2, when located elsewhere in the stomach [2]. GOV1 constitute nearly 75%, GOV2—21%, IGV1 less than 2%, and IGV2 about 4% of all GV. The location of GV is important in predicting the frequency of bleed (IGV1 > GOV2 > GOV1). The GOV1 are in fact continuation of esophageal varices and the dominant afferent portal venous feeder is the left gastric vein originating from distal splenic vein, proximal part of main portal vein or splenoportal confluence. The hemodynamics and the management of GOV1 are similar to that of EV, i.e., endoscopic band ligation. For the same reason, bleeding from these veins has a favorable response to transjugular intrahepatic porto-systemic shunt (TIPS). For IGV1 and GOV2 collaterals, the dominant afferents are the * Shiv Kumar Sarin ; 1 Department of Hepatology and Liver Transplant, Institute of Liver and Biliary Sciences, New Delhi 110070, India posterior (64–70%) and short (25–64%) gastric veins arising from the proximal portion of splenic vein [3]. In about 10% patients with portal hypertension, spontaneous portosystemic shunts develop to accommodate the hyperdynamic and large blood volume in the portal circulation. The frequency of such shunts increases to about 85% in patients with GV. Predominantly these are left sided shunts, i.e., to the left of midline and include gastrorenal shunts (GRS), direct gastro-caval shunts and gastrocaval shunts via inferior phrenic vein. More than 90% of these shunts are GRS. Acute variceal bleed is a dreaded complication of portal hypertension with ~ 20% mortality risk at 6 weeks in cirrhosis [4]. GV attribute about 20% of all variceal bleeds, but they are associated with more risk of uncontrolled bleeding, higher transfusion requirements, rebleeding and death compared to EV. At present, the available treatment options for large (> 10 mm) and high risk GV (> 20 mm, with red color signs), without history of prior bleed, are obliteration by cyanoacrylate glue, occlusion through the spontaneous porto-systemic shunts or transjugular intrahepatic portosystemic shunt (TIPS) (Fig. 1). Use of cyanoacrylate glue is the treatment of choice for the control of acute GV bleed and for the prevention of rebleed from GV. Glue therapy offers a success rate close to 95% in the control of acute bleed and nearly 92% in preventing rebleed [5]. Only a very small proportion of patients with GV bleed fail to endotherapy, especially those with portal vein thrombosis, severe coagulopathy or with incomplete obturation [6]. Hepatic venous pressure gradient (HVPG) is the most important method to predict the risk of esophageal variceal bleeding, success of endotherapy and rebleeding. HVPG, however, does not correlate well with the risk of bleeding from GV and is not much different between bleeders and non-bleeders [7]. In fact, GV can bleed at HVPG less than 12 mm Hg, while the threshold of continued bleeding as well as early recurrence of bleeding from esophageal varices is considered to be 16 mmHg [8]. In GV, the risk of bleed 13 Vol.:(0123456789) 864 Hepatology International (2021) 15:863–867 Fig. 1  Anatomy of the portosystemic shunts, afferents, efferents and various treatment options. The white arrowheads denote the usual afferents of the gastric varices and black arrowheads denote the efferent pathway through gastrorenal shunt. BRTO balloon-occluded retrograde transvenous obliteration; GV gastric varices; IVC inferior venacava; LGV left gastric vein; LRV left renal vein; PGV posterior gastric vein; SGV short gastric vein; SMV superior mesenteric vein; SV splenic vein; TIPS transjugular intrahepatic portosystemic shunt (may be combined with variceal embolotherapy) depends on the size of varices (> 2 cm), wall tension, presence of red color signs on the varices, MELD ≥ 17 and presence of portal hypertensive gastropathy [7, 9]. Due to lack of correlation with HVPG, TIPS is not considered a very effective intervention in the control of acute GV bleed. In fact, in the absence of a large gastro-renal shunt, TIPS with afferent embolization should be preferred over TIPS alone [10]. The role of prophylactic TIPS in the prevention of first GV bleeding is another contentious area. Neither prophylactic surgical shunts, nor TIPS, have gained popularity in patients with large GV. Non-selective betablockers (NSBBs) are the mainstay for primary prophylaxis of esophageal varices. Whether substantial reduction of HVPG occurs by beta-blockers, and they can be of help in prevention of GV bleed, has not been well studied. In one study, propranolol was found to be superior to no-therapy, but inferior to glue therapy, in the prevention of first variceal bleed [7]. A recently published double-blind placebo-controlled RCT (PREDESCI) concluded that in compensated cirrhotics, NSBBs prevent not only variceal bleeding, but also other types of decompensation, including ascites [11]. However, patients of GV were not adequately represented in this study. Reduction in portal pressure is likely to reduce the frequency of decompensation episodes. Carvedilol, which is more potent than propranolol should be evaluated to achieve greater reduction in portal flow and decrease in the incidence of first bleed from GV. 13 Balloon-occluded retrograde transvenous obliteration (BRTO) procedure utilizes the GRS to access the GV. The GRS is occluded with a balloon and sclerosant is injected in the GV. This causes damage to the endothelial lining and complete occlusion or reduction of the vascular bed. Hence, BRTO is especially useful in (...truncated)