Esophageal Varices

Key Features

Essentials of Diagnosis

• Develop secondary to portal hypertension

• Found in 50% of patients with cirrhosis

• Upper gastrointestinal (GI) bleeding develops in one-third

• Diagnosis established by upper endoscopy

General Considerations

• Esophageal varices are dilated submucosal veins that develop in patients with underlying portal hypertension and may result in serious upper GI bleeding

• Bleeding most commonly originates in the distal 5 cm of the esophagus

• Bleeding from varices occurs in 30% of patients with esophageal varices

• In the absence of any treatment, variceal bleeding spontaneously stops in about 50% of patients

• Patients surviving this bleeding episode have a 60% chance of recurrent variceal bleeding, usually within the first 6 weeks

• Factors that may portend an increased risk of bleeding include

  • Size of the varices

  • Presence at endoscopy of red wale markings on the varix

  • Severity of liver disease (as assessed by Child-Pugh score)

  • Active alcohol abuse—patients with cirrhosis who continue to drink have an extremely high risk of bleeding

Clinical Findings

Symptoms and Signs

• Acute GI hemorrhage, usually severe, resulting in hypovolemia, postural vital signs, or shock

Differential Diagnosis

• Alcoholic gastritis

• Mallory-Weiss syndrome

• Portal hypertensive gastropathy

• Peptic ulcer disease

• Gastric or duodenal varices (rare)

• Vascular ectasias (angiodysplasias), eg, idiopathic arteriovenous malformation, CREST syndrome, hereditary hemorrhagic telangiectasia

Diagnosis

Laboratory Tests

• Complete blood count, platelet count, prothrombin time, INR

• Serum liver enzymes

• Creatinine, blood urea nitrogen

• If bleeding, blood type and cross-match

Diagnostic Procedures

• After the patient's hemodynamic status has been stabilized, emergent upper endoscopy is diagnostic

Treatment

Medications

• Antibiotic prophylaxis reduces the risk of serious infection in hospitalized patients with cirrhosis and upper GI bleeding

• Prophylactic administration of oral or intravenous antibiotics reduces the risk of serious infection to 10–20% as well as in-hospital mortality, especially in patients with Child-Pugh class C cirrhosis

  • Ceftriaxone 1 g/d intravenously for 5–7 days

• Vasoactive agents

  • Octreotide, (50 mcg intravenous bolus followed by 50 mcg/h intravenously) infusion reduces splanchnic and hepatic blood flow and portal pressures

  • Terlipressin (1–2 mg intravenous every 4 hours; not available in the United States) causes significant reduction in portal and variceal pressures and, where available, may be preferred over octreotide

• Combined vasoactive agents and endoscopic therapy (band ligation or sclerotherapy)

  • Superior to either modality alone in controlling acute bleeding and early rebleeding

  • May improve survival

• Vitamin K, 10 mg subcutaneously

• Lactulose 30 mL orally every 2–3 hours until evacuation occurs, then reduced to 15–45 mL/h every 8–12 hours as needed to promote 2–3 bowel movements daily for hepatic encephalopathy

• After bleeding ...