Gastroesophageal varices
Gastroesophageal varices are dilated portosystemic collateral veins that form as portal pressure rises in cirrhosis, and their rupture causes acute variceal hemorrhage, a GI emergency treated with vasoactive therapy, prophylactic antibiotics, and urgent endoscopic band ligation. Screening endoscopy in cirrhotics guides primary prophylaxis with a nonselective beta-blocker or ligation, and survivors of a bleed require combined beta-blocker and serial ligation for secondary prophylaxis.
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What this article covers
- Overview
Definition: gastroesophageal varices are enlarged, tortuous submucosal veins in the distal esophagus and proximal stomach that form as extrahepatic portosystemic collateral pathways when portal…
- Epidemiology
Common in cirrhosis: roughly half of patients with cirrhosis have varices at diagnosis, and prevalence rises with worsening liver disease severity.
- Risk factors
Advanced cirrhosis: the dominant driver, through intrahepatic fibrosis, regenerating nodules, and increased intrahepatic vascular resistance; risk and size of varices increase with Child-Turcotte-Pugh class.
- Pathophysiology
Portal hypertension is the initiating lesion: cirrhosis distorts hepatic sinusoids and raises intrahepatic vascular resistance, while splanchnic vasodilation increases portal venous inflow, together raising pressure in the portal system.
- Clinical features
Asymptomatic until rupture: varices themselves cause no symptoms and are typically found on screening endoscopy performed for known or suspected cirrhosis.
- Differential diagnosis
Peptic ulcer disease: the most common overall cause of upper GI bleeding, with epigastric pain and hematemesis but no requirement for cirrhosis; endoscopy differentiates a visible vessel or clot in an ulcer base from a bleeding varix.
- Diagnosis
Confirmed by direct visualization at upper endoscopy, which also grades bleeding risk: varices are staged by size, small (<5 mm) versus large (≥5 mm), and by red wale marks (erythematous raised…
- Management
If varices are found on screening endoscopy in a patient who has never bled, start primary prophylaxis based on size: No varices: repeat screening endoscopy in 3 years (sooner if decompensation occurs).
- Complications
Hemorrhagic shock and death: the most feared outcome, with mortality driven by bleed volume, delay to endoscopic control, and severity of underlying liver disease.
- Prognosis
Bleeding risk scales with size and stigmata: large varices and those with red wale marks carry the highest risk of first hemorrhage, which is why they trigger prophylaxis.
- Prevention
Screen every cirrhotic patient with upper endoscopy before variceal bleeding occurs; repeat every 3 years if no varices, every 2 years for small varices without red wale marks, and more frequently in decompensated cirrhosis.
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Related articles
- Portal hypertension
Portal hypertension is elevated pressure in the portal venous system, most often from cirrhosis, that drives the major decompensating complications of chronic liver disease: varices, ascites, splenomegaly, and encephalopathy. Diagnosis rests on imaging and endoscopy for its downstream signs, and management combines treating the underlying cause with nonselective beta-blockade and, for refractory complications, TIPS.
- Cirrhosis
Cirrhosis is end-stage hepatic fibrosis with regenerative nodules, staged as compensated or decompensated by the onset of ascites, variceal hemorrhage, encephalopathy, or jaundice. Severity is graded by Child-Pugh class and MELD, and management centers on treating the underlying cause, surveillance for varices and hepatocellular carcinoma, and timely transplant referral once decompensation appears.
- Acute upper gastrointestinal bleeding
Acute upper gastrointestinal bleeding arises proximal to the ligament of Treitz and presents with hematemesis or melena, most often from peptic ulcer disease or bleeding gastroesophageal varices. Management sequences resuscitation, restrictive transfusion, IV proton pump inhibitor therapy, and, when varices are suspected, octreotide plus antibiotic prophylaxis, all before upper endoscopy within 24 hours, which is both diagnostic and therapeutic.