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Esophageal Varices

Esophageal varices are dilated blood vessels within the wall of the esophagus. Patients with cirrhosis develop Portal Hypertension. When Portal Hypertension occurs, blood flow through the liver is diminished. Thus, blood flow increases through the microscopic blood vessels within the esophageal wall. As this blood flow increases, the blood vessels begin to dilate. This dilation can be profound. The original diameter the of blood vessels is measured in millimeters while the final, fully established, esophageal varix may be 0.5 to 1.0 cm or larger in diameter.

These blood vessels then continue to dilate until they become large enough to rupture. When esophageal varices rupture, patients become acutely ill. In fact, 50 percent of patients with esophageal varices will eventually bleed from the varices. The mortality rate for esophageal variceal bleeding, on the first event, is between 40 and 70 percent. Mortality is due to multiple factors:

  1. Liver failure
  2. Sepsis
  3. Exsanguination
  4. Cerebral edema.
  5. Complications associated with anemia.

The treatment for esophageal varices is directed immediately to control the bleeding, and then long-term medical therapy. Immediate control of bleeding is usually performed by endoscopic means. In fact, bleeding can be initially controlled in approximately 90 percent of cases. However, the failure rate for endoscopic therapy is between 10 and 30 percent. Thus, longer term therapy is required in order to prevent a patient from bleeding.

Variceal hemorrhage stops spontaneously in approximately 62 to 70 percent cases. However, recurrent bleeding occurs in 40 percent of patients within the next 72 hours. In fact, 60 percent of patients will rebleed within seven days of their initial bleeding. Although this type of bleeding will stop, it is the high rebleeding rate and the complications from acute hemorrhage which make control of bleeding mandatory in both the initial period of the variceal bleed and the chronic state after the patient has been stabilized.

Variants of esophageal varices are gastric varices. Gastric varices are dilated blood vessels that are found predominantly in the stomach. The true incidence of gastric varices is unknown. However, investigators have reported a wide incidence ranging between 20 and 70 percent in patients with esophageal varices. When gastric varices are identified without coexisting esophageal varices, a splenic vein thrombosis may be present.

Another variant of portal hypertension is portal hypertensive gastropathy. It is present in 50 percent of patients with portal hypertension. These patients have dilated arterioles and venules (small veins). This abnormality is seen usually in the fundus and cardia of the stomach (approximately 2/3 of the stomach). It is rarely seen in the antrum (last 1/3) of the stomach. It appears to have a "snake skin " or "reticulated" appearance.

Long-term treatment of portal gastropathy and gastric varices is with beta-blockers. They usually take the form of propranolol, a nonselective beta-blocker. These medications allow the pressure within the veins to be decreased, thus reducing the chance that bleeding will occur. Increased incidence of portal hypertensive gastropathy is noted in patients who undergo sclerotherapy for esophageal varices in the past.

Other treatments for upper GI bleeding associated with esophageal varices include vasopressin, vasopressin with nitroglycerin, somatostatin, balloon tamponade, TPSS (transhepatic portosystemic shunt), transhepatic catheter embolization, shunt surgery, gastric stapling and sclerotherapy with or without any.