<unk>  were initially described as “dilated veins that bulge into the lumen, producing uneven worm like surface of the inside of esophagus. Varices in the<unk>  tract are thought to arise due to increased pressure in the portal venous system, leading to establishment of porto-systemic shunts. In the 20th century, sclerotherapy became an important treatment option in the management of variceal haemorrhage, especially with the advent of fibre-optic endoscopy. In 1950, The Sengstaken-Blakemore tube’s use was first described by Sengstaken and Blakemore and later used as a treatment option.<unk>  may be further classified into esophageal and gastric varices. Esophageal varices may be further divided according to various classification systems such as the Dagradi classification, Conn's classification, Pachquet classification, Westaby classification, Soehendra classification and Cales classification. Gastric varices may be classified according to Hoskins and Johnson’s classification, Mathur’s classification, Hashizume classification and Sarin's classification system. Varices arise from hemodynamic disturbance between the systemic and portal venous system. The majority of venous drainage of the<unk>  system occurs via the portal venous system. Whenever there is an interruption of drainage through the portal system (for example due to cirrhosis), the vessels contributing to the porto-caval shunts become more prominent due to increased pressure gradient. The interruption in blood flow leads to the creation collateral vessels that involve veins of the esophagus, stomach, pelvis (hemorrhoids), retroperitoneum, liver, abdominal wall, and other areas. Causes of<unk>  include all the causes of increased portal venous pressure, which may be divided into cirrhotic and non-cirrhotic causes. Non-bleeding varices are asymptomatic. Ruptured esophageal and gastric varices may lead to upper<unk>  bleeding and present with hematemesis. They must be differentiated from other causes of upper<unk>  bleeding such as peptic ulcer disease, esophagitis, gastritis, angiodysplasia, Dieulafoy's lesion, vascular ectasia, Mallory-Weiss tears, aorto-enteric fistulas and upper<unk>  tumors. Gastroesophageal varices are present in approximately 50,000 per 100,000 patients with cirrhosis, depending upon the clinical stage of the disease. The annual incidence of<unk>  ranges from a low of 7,000 per 100,000 individuals to a high of 8,000 per 100,000 individuals. Variceal hemorrhage occurs at a rate of around 10%-15% per year. If left untreated, recurrent variceal hemorrhage occurs in 60% of patients, usually within 1-2 years of the initial hemorrhage. Complications include, transient dysphagia, chest pain, esophageal ulceration, ulcerogenic bleeding, post-therapeutic hemorrhage, esophageal strictures, pleural effusions, pericarditis and portal vein thrombosis. Factors associated with a poor prognosis of presence of bacterial infections, HVPG >20 mm Hg, alcohol intake and obesity. The AIMS65 score is the best predictor of mortality in patients with variceal bleeding. Esophagogastroduodenoscopy (EGD) is the gold standard test for the diagnosis of<unk> . EGD should be performed once the diagnosis of cirrhosis is established. Physical examination of patients with<unk>  is usually remarkable for ascites, pallor, jaundice, tachycardia, low blood pressure in case of shock, hepatomegaly or shrunken liver (in case of cirrhosis), splenomegaly, altered mental status, palmar erythema, cyanosis and clubbing. X-ray taken after a barium swallow in cases of<unk>  may show multiple radiolucent filling defects. On CT scan<unk>  may appear as well-defined, tubular structures that have a smooth appearance with homogeneous attenuation. Upper endoscopy may be helpful in the diagnosis of gasteroesophageal varices. Findings on an upper endoscopy diagnostic of esophageal varices include visible submucosal tortuous veins, congested veins without compression during air insufflation, and grape-like varicose veins that may occlude the lumen. Medical therapy in cases of<unk>  includes goal-directed management of the cause of portal hypertension along with specific management of varices after their development. The treatment is aimed at optimizing portal venous inflow, portal pressure and portal resistance. The pharmacological therapy includes vasoconstrictors (beta blockers) and venodilators (nitrates). These therapies may be employed alone or in combination with endoscopic variceal ligation/sclerotherapy and transjugular intrahepatic shunt (TIPS) therapy depending upon the condition of the patient.
Gastrointestinal varices
Oral ulcer
Lower gastrointestinal bleeding
Esophageal varices
Upper gastrointestinal bleeding
Nosebleed
Stomach cancer
Bleeding esophageal varices