Esophageal varices are dilated submucosal veins that occur in patients with underlying portal hypertension, function as a shunt between the portal venous and systemic venous circulation, and can result in severe upper GI hemorrhage.

• Often asymptomatic until acute upper GI hemorrhage: Hematemesis, hypovolemia
• No physical findings specific for esophageal varices
• Stigmata of cirrhosis and portal hypertension may be evident: Palmar erythema, telangiectasias, gynecomastia, testicular atrophy, jaundice, caput medusae, lower extremity edema, ascites, splenomegaly, hemorrhoids, asterixis

• Portal hypertension results from obstruction to portal venous outflow, and varices subsequently develop in order to decompress the hypertensive portal vein and return blood to the systemic circulation.
• Varices may appear when portal vein pressures rise above 10 to 12 mm Hg.
• Cirrhosis is the most common cause of portal hypertension.

• Budd-Chiari syndrome, cirrhosis, portal vein thrombosis, schistosomiasis, Wilson disease
• Other causes of upper GI bleeding: Duodenal or gastric ulcers, gastric cancer, Mallory-Weiss tear

Upper endoscopy (Fig. E1), laboratory tests, and imaging

• CBC:
  1. Anemia (blood loss, nutritional deficiencies, alcohol myelosuppression)
  2. Thrombocytopenia (hypersplenism, alcohol myelosuppression)
• Renal function panel:
  1. Blood urea nitrogen: Often increased in setting of upper GI bleeding
  2. Creatinine: Often elevated by hypovolemia, monitor for hepatorenal syndrome
  3. Sodium: Dilutional hyponatremia
• Heme-positive stools
• Type and crossmatch: In preparation for blood transfusion
• INR/PT and PTT: Coagulation factors produced in liver and may be prolonged in liver disease or impairment
• Liver function tests: ALT/AST may be normal in cirrhotic patients due to longstanding fibrosis; elevated alkaline phosphatase and a direct hyperbilirubinemia may be present if cholestatic liver disease is present
• Serum albumin: Severe liver disease results in hypoalbuminemia

Invasive:

• Esophagogastroduodenoscopy (EGD) (upper endoscopy):
  1. In all patients with cirrhosis, screen for the presence or absence of varices and determine subsequent risk for variceal hemorrhage.
  2. In patients with small varices (<5 mm) repeat EGD in 2 yr (unless decompensation occurs).
  3. In patients with compensated cirrhosis who do not have varices, screening is repeated every 2 to 3 yr.
  4. In patients with decompensated cirrhosis (ascites, hepatic encephalopathy, variceal hemorrhage, or jaundice), it is repeated every yr or at the time of first decompensation.
  5. Emergently performed if there is evidence of acute upper GI bleeding to diagnose and treat variceal hemorrhage.

Noninvasive:

• Esophagography with barium can diagnose esophageal varices (Fig. E2).
• Capsule endoscopy can also diagnose esophageal varices, although sensitivity is not yet established.
• Computed tomography (CT) scan (Fig. E3).

• Endoscopic variceal ligation (Fig. E4) is an alternative to nonselective β-blockers for primary prophylaxis against variceal hemorrhage. It is also used in patients unable to tolerate β-blockers
  1. Typically for patients with medium or large varices at highest risk for hemorrhage (Child-Pugh B/C or red wale markings viewed on endoscopy)
  2. Usually two to four sessions
  3. May not be a permanent solution because varices can recur after initial eradication
  4. Associated with significant complications, including hemorrhage from banding-induced ulcerations
     1. Therefore should be performed by endoscopists with expertise in prophylactic banding
     2. First surveillance endoscopy 1 to 3 mo after obliteration, then every 6 to 12 mo indefinitely

• Variceal hemorrhage: Acute hemodynamic resuscitation with packed red blood cell transfusion, correct coagulopathy and thrombocytopenia, airway protection and intubation as necessary, antibiotics (ceftriaxone or norfloxacin) for SBP prophylaxis, octreotide maintained for 2 to 5 days in conjunction with endoscopic therapy. The use of balloon tamponade in the control of active variceal bleeding should be a last resort when other forms of therapy are not available or fail to achieve hemostasis. Balloon tamponade (Fig. E5) should be used only as a temporary means of stabilization and a bridge to a more definitive form of therapy.
• EGD to treat bleeding esophageal varices by esophageal band ligation or sclerotherapy (Fig. 6).

Figure 6 Algorithm for the Management of Bleeding Esophageal Varices

MELD, Model End State Liver Disease; RBC, Red Blood Cell; TIPS, Transjugular Intrahepatic Portosystemic Shunt.

From Feldman M et al: Sleisenger and Fordtran’s gastrointestinal and liver disease, ed 10, Philadelphia, 2016, Elsevier.

Primary prophylaxis (Fig. 7):

• Nonselective β-blockers such as propranolol (20 mg twice daily), nadolol (40 mg once daily), or carvedilol (6.25 mg twice daily)
  1. Increase as tolerated for goal heart rate of approximately 55 beats/min
  2. Blocks the adrenergic dilatory tone in mesenteric arterioles, resulting in unopposed alpha-adrenergic mediated vasoconstriction and therefore a decrease in portal inflow

Figure 7 Algorithm for the Primary Prophylaxis of Esophageal Variceal Hemorrhage in Patients with Cirrhosis

the Hepatic Vein Pressure Gradient (Hvpg) May Be Measured in Patients with Large Varices Before a Nonselective -Adrenergic Blocking Agent is Started and Remeasured 1 Mo after the Maximum Tolerated Dose of the -Blocker is Reached. The Goal of Treatment is to Reduce the Hvpg to <12 mm Hg or by 20%. Evl, Endoscopic Variceal Ligation.

From Feldman M et al: Sleisenger and Fordtran’s gastrointestinal and liver disease, ed 10, Philadelphia, 2016, Elsevier.

Secondary prophylaxis (Fig. E8):

• All patients with compensated cirrhosis who have bled from esophageal varices should receive esophageal band ligation and β-blockers, unless β-blockers are contraindicated.
  1. Transjugular intrahepatic portosystemic shunt or surgical shunt may be performed if bleeding from esophageal varices continues or recurs despite this dual therapy.
• For patients with decompensated cirrhosis there is evidence, although limited, against the use of prophylactic β-blockers due to the risk for increased mortality.

Figure E8 Algorithm for the Prevention of Recurrent Variceal Bleeding (Secondary Prophylaxis)

Evl, Endoscopic Variceal Ligation; TIPS, Transjugular Intrahepatic Portosystemic Shunt.

From Feldman M et al: Sleisenger and Fordtran’s gastrointestinal and liver disease, ed 10, Philadelphia, 2016, Elsevier.

Consultation with a gastroenterologist is recommended in all patients with cirrhosis or portal hypertension in order to screen for esophageal varices.

Cirrhosis (Related Key Topic)

Portal Hypertension (Related Key Topic)