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Varices in the esophagus and stomach are present in about half of all cirrhosis patients. Each year, 5 percent to 20 percent of patients with cirrhosis experience the formation of varices. Once varices have been formed, 5 percent to 15 percent become large varices. Large varices are highly likely to rupture. Patients with more severe liver disease tend to have more varices, and their varices tend to be larger. Spontaneous rupture of these varices and severe bleeding occur when the pressure on the portal vein, expressed as the difference between the pressure in the portal vein and the pressure in the vein that drains out of the liver (the portal pressure gradient), is greater than 12 mm of mercury. Large varices have a 2-year risk of bleeding spontaneously in approximately 3 of every 10 cases. Small varices have a risk of only 1 in 10. Because it is difficult to determine that varices are developing, endoscopic evaluation of the esophagus and stomach is recommended at 1- to 2-year intervals in patients with cirrhosis to determine whether varices have formed and if they are large enough to require treatment to prevent bleeding.

Varices in the esophagus that are large or show evidence of high risk for bleeding should be considered for treatment to prevent bleeding (primary prophylaxis), such as the use of a class of drugs that block the action of the involuntary nervous system on the heart, and therefore relieve stress on the heart (nonselective beta blockers). An analysis of 11 prospective studies evaluating the effectiveness of nonselective beta blockers at preventing initial variceal bleeding showed that beta blockers decreased the risk of first bleed by at least 40 percent (25 percent in control subjects vs. 15 percent in the treatment group) after a median of 2 years. Isosorbide mononitrate and isosorbide dinitrate, which dilate both the veins and the arteries, have been evaluated for this purpose but have proven to be ineffective as single agents. Adding low doses of these medications, however, to a regimen of nonselective beta blockers may be of some help.

Treatment in the form of ligation of varices, in which elastic bands are placed around varices using a device attached to the end of the endoscope, also has proven to be effective but usually is reserved for patients who have large varices and cannot tolerate beta blockers. As mentioned, patients with esophageal varices may bleed spontaneously. Approximately half of these patients will stop bleeding spontaneously. The frequency of death for each of these episodes is 3 in 10. It is estimated that bleeding will recur within 6 weeks in 4 of 10 patients who have esophageal variceal bleeding. Thus, treatment of bleeding from esophageal varices has two components: immediate treatment to control the present bleed and additional treatment to prevent consequent bleeding (secondary prophylaxis).

In the United States the initial medical intervention for suspected variceal bleeding is to administer intravenous octreotide, which has been shown to safely and effectively control variceal bleeding by regulating vascular contraction and decreasing the pressure in the portal venous system. The method that has proven to be the best in controlling acute variceal hemorrhage is endoscopic banding of the esophageal varices. When banding is not possible, injecting the varices with scarring substances also can be used. Because cirrhotic patients with gastrointestinal bleeding are at high risk of developing serious infections, a prophylactic 7-day course of the antibiotic norfloxacin is recommended. A patient who has had the first episode of variceal bleeding faces an 8-in-10 chance of bleeding again in the next 3 years. In addition, treatment with nonselective beta blockers, in a manner similar to primary prophylaxis, should be given to patients who are not already receiving these drugs. Patients who cannot tolerate the medication, or for whom beta blockers are contraindicated, can be treated with repeated banding of the varices at 10- to 14-day intervals.

Patients who rebleed despite therapy with beta blockers and endoscopy should be considered for the TIPS procedure or surgery performing a distal spleno-renal shunt, thereby decreasing the high pressure of the veins by connecting the high-pressure vessels to the inferior vena cava system, which is a low-pressure system (it carries oxygen- poor blood to the heart from the lower half of the body). Despite the fact that TIPS is more effective than endoscopic therapy in decreasing rebleeding from esophageal varices, 1 in 3 of these patients will develop hepatic encephalopathy after TIPS, and this intervention does not affect survival rates. Because of the problems with encephalopathy and the cost of TIPS, this approach usually is reserved as rescue therapy. Liver transplantation is, of course, definitive therapy and should be considered for all of these patients.

Conclusions

In summary, it now is generally possible to accurately diagnose ALD, and new biomarkers or identifier proteins for detecting ongoing alcohol abuse and ALD are being investigated, as is the role of genetics in ALD. Although there are no FDA-approved therapies for alcoholic liver disease, lifestyle changes, nutritional support, and "off-label" therapies such as PTX can improve outcome. Similarly, new therapies for complications are improving quality of life and, in some cases, even reducing mortality rates.

Tags: Alcoholism

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