Esophageal Varices

Overview

Esophageal varices are dilated submucosal veins in the distal esophagus that develop as a consequence of portal hypertension, with the most common risk factor being cirrhosis. They are clinically significant because of their high risk of life-threatening upper gastrointestinal bleeding and account for 5-11% of upper GI bleeds. Early recognition and appropriate management are essential in both inpatient and outpatient settings.

Pathophysiology

Esophageal varices result from increased pressure within the portal venous system. Blood drains from portions of the GI tract into the portal vein which flows through the liver before returning to systemic circulation. The liver normally offers low resistance to portal blood flow, however, conditions impacting liver function such as cirrhosis increase the intrahepatic vascular resistance causing portal hypertension. Blood is then redirected thought portosystemic collateral pathways to bypass the liver due to the high pressure gradient. One of these collateral pathways involves veins in the distal esophagus which become thin and tortuous from the increased blood volume traveling through these vessels which lack structural support making them prone to rupture.

Clinical Manifestation

Many patients with esophageal varices are asymptomatic until bleeding occurs which can cause hematemesis, melena, or hematochezia. Additional symptoms of acute bleeding include lightheadedness, syncope, fatigue, weakness, hypotension, and tachycardia. Signs of chronic liver disease such as jaundice, ascites, spider angiomas, and splenomegaly may also be present. If left untreated bleeding varices can lead to hypovolemic shock.

Diagnosis

Upper endoscopy (EGD) remains the gold standard for screening. Patients with newly diagnosed cirrhosis should undergo screening endoscopy.

Treatment

In cases of acute bleeding endoscopic ligation is the treatment of choice as well as securing an airway, fluid replenishment, and correcting any coagulopathies present. Octreotide, a somatostatin analog, or vasopressin may also be used in cases of acute bleeds to reduce portal venous pressure.

Approximately 70% of varices rebleed within 1 year of the initial bleed (1/3 of these rebleeds are fatal) making prevention of rebleeding very important in treatment of patients with known esophageal varices. Non-selective beta blockers such as propranolol or nadolol are both used to reduce portal venous pressure outside of acute bleeds by 1) decreasing cardiac output due to β1 blockade and 2) causing splanchnic vasoconstriction due to β2 blockade. Beta blockers are contraindicated in acute bleeds to avoid lowering the tachycardic response to hypovolemia and reducing cardiac output. The long-acting nitrate Isosorbide may also be used to reduce esophageal variceal pressure. Additionally, a transjugular intrahepatic portosystem shunt (TIPPS) may be an option for patients with varices refractory to the above mentioned treatments.

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Quiz Question

• A patient with PMH significant for known liver cirrhosis comes to the emergency department endorsing hematochezia and fatigue over the past 48 hours. You suspect this patient may be suffering from an upper GI bleed due to bleeding esophageal varices. What initial labs would you order for this patient?

  CBC – anemia, thrombocytopenia

  CMP – liver function

  INR – coagulopathy due to cirrhosis

  Type and Screen – possible transfusion