Characteristics and natural history of gastric varices in portal hypertension.

INTRODUCTION : Portal hypertension can occur due to many reasons. One of the commonest causes for portal hypertension is cirrhosis. Other important causes are non cirrhotic portal fibrosis (NCPF) and extra hepatic portal vein obstruction (EHPVO). Portal pressure increases in cirrhosis initially as a result of an increased resistance to portal flow. This mostly results from fibrous tissue and regenerative nodules formation within the hepatic parenchyma which leads to distortion of the architecture of the liver. Along with this structural resistance to blood flow, there is an intra-hepatic constriction of the vessels that accounts for twenty to thirty percent of the increase in resistance within the liver. This happens because there is decreased synthesis of nitric oxide endogenously. The obstruction to the portal flow is at perisinusoidal level in NCPF but in EHPVO the obstruction is extra hepatic, which is commonly due to the formation of thrombosis in the portal vein. Porto-systemic collaterals are formed due to the development of portal hypertension. Although the collaterals are formed to relieve the portal pressure portal hypertension persists due to two causes: (1) an increase in portal venous inflow due to splanchnic arteriolar vasodilatation along with the formation of collaterals and (2) inadequate decompression of the portal venous system through the collaterals since they have a higher resistance than the normal liver. Therefore, an increased portal pressure gradient results from both an increase in portal blood inflow and increase in resistance to portal flow. Gastroesophageal varices are commonly seen in up to 50% of patients with cirrhosis.6 Gastric varices are seen in 20-25% of patients with portal hypertension. If the patient is not having varices it will develop at the rate of 8% per annum and one who have small varices will develop larger varices at 8% per year.. In few subsets of patients such as in primary biliary cirrhosis and hepatitis C with bridging fibrosis, even in the absence of overt cirrhosis they have propensity to develop varices in up to 16 % of the patients. Irrespective of the aetiology, the important and dreadful complication of varices is upper gastrointestinal bleeding. Prevalence of gastric varices is low when compared to esophageal varices. They are present in 6%-35% of patients with portal hypertension. The incidence of bleeding is about twenty-five percent in 2 years and highest bleeding rate is for fundal varices. Risk factors for gastric variceal haemorrhage include fundal varices size (large varices defined as >10 mm, medium -5-10 mm and small >5 mm), Child-Turcotte-Pugh score, particularly Child C status and endoscopic presence of variceal red spots (defined as localized reddish mucosal area or spots on the mucosal surface of a varix). The risk of bleeding with gastric varices is half that of esophageal varices. The transfusion requirement and mortality are high once the bleeding has occurred particularly for isolated gastric varices (IGV). Large gastric varices patients have a lower portal pressure compared to esophageal varices, which is due to the development of gastrorenal portosysytemic shunts, or large size of the varices resulting in increased wall tension. The type and prevalence of gastric varices varies greatly. AIM : The aim of this study is to assess 1. The prevalence of gastroesophageal varices in patients with portal hypertension in a tertiary referral centre 2. Characteristics of the gastric varices and 3. Natural history of gastric varices in portal hypertension. CONCLUSION : In conclusion, the results of our study confirm that the prevalence of gastroesophageal varices was low but within the range when compared with various studies. The type of the varices in Our study tallies with the international classification and the common type is GOV1 as denoted by many studies. GOV1 is relatively have a benign course and requires treatment only in the form of gastric variceal sclerotherapy if they bleed. For most GOV2 varices, endoscopic variceal obliteration therapy with N-Butyl 2- Cyanoacrylate is quite useful in arresting the bleeding and achieving the variceal obliteration. Although endoscopic therapy was effective in treating some patients with IGV1 varices, surgery was required in significant no. of patients to prevent re bleeding. In our study, the surgery was contemplated for such patients and also for other type of gastric varices because those patients were from far remote places where the immediate endoscopic intervention may not be feasible always. IGV2 cases were less in Our study and it might require long term follow up to identify such patients. Because the gastric varices have the potential to cause severe upper GI bleeding, its recognition is very important to manage the cases appropriately.