Esophageal varices

Article Abstract:

Portal hypertension (increased pressure in the portal vein of the liver), can cause esophageal varices, enlarged, swollen and tortuous veins at the lower end of the esophagus. These varices are susceptible to ulceration and bleeding. Bleeding may be anticipated based upon the size and pressure of the varices, endoscopic appearance of red spots, and the severity of the related liver failure. Bleeding may be prevented by improving the underlying liver disease and avoidance of aspirin and nonsteroidal anti-inflammatory medications. Sixty-five percent of patients with cirrhosis of the liver (degenerative disease in which liver tissue is replaced by fibrous tissue and fatty deposits) will not bleed within two years of diagnosis; however, 50 percent will die as a result of the first hemorrhage. The use of sclerotherapy, injection of a hardening agent through the esophagus into esophageal varices, to prevent bleeding is controversial; however, sclerotherapy is effective in controlling active bleeding in 85 to 95 percent of patients treated. Prior to sclerotherapy, drug therapy is often begun with either vasopressin, vasopressin with nitroglycerine or somatostatin-type medications. These medications, although they may stop the bleeding themselves, are usually used to prepare the patient for more definite treatment. If sclerotherapy is not effective, emergency surgery is usually performed. Rebleeding may possibly be prevented by sclerotherapy, and if this is not successful, surgery must be performed. Use of propranolol is safe, but its effectiveness is not confirmed. These treatments may stop bleeding, but mortality is not affected; this ultimately depends on the function of the liver cells. Once the patient has been stabilized, the possibility of liver transplant should be evaluated. (Consumer Summary produced by Reliance Medical Information, Inc.)

Portal hypertension

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A hepatologist's view of variceal bleeding

Article Abstract:

Patients with cirrhosis of the liver have a 50 percent risk of dying from one single episode of bleeding esophageal varices (enlarged, swollen and tortuous veins at the lower end of the esophagus, the canal extending from throat to stomach). Cirrhosis, a degenerative disease of the liver, results in obstruction of the blood flow through the liver, causing portal hypertension (increased pressure in the portal vein of the liver), which in turn can cause esophageal varices. Once esophageal varices have been identified, 25 to 33 percent of patients will have bleeding, usually within the first year, with a risk of 70 percent for recurrent bleeding. The treatment of choice for severe acute bleeding is injection sclerotherapy, injection of a sclerosing (hardening) agent, through the esophagus, into esophageal varices; reported success rates range from 75 to 90 percent. Medications such as vasopressin plus nitroglycerine (vasoconstrictors and vasodilators) are currently being studied and used for minor bleeding episodes. Emergency surgery which shunts blood away from the portal system has a high mortality; however, a newer procedure of staple transection of the esophagus may be used. Another procedure is ligation (tying off) of the varices performed through an endoscope. Methods of preventing recurrent bleeding include chronic sclerotherapy for patients who have decompensated liver cirrhosis; medical treatment with beta-adrenergic blockers (propranolol or nadolol) may be used for patients who have good function of the liver. Prevention of initial variceal bleeding using beta-adrenergic blockers is being studied. Use of sclerotherapy or shunt surgery as prevention methods does not appear to be justified. (Consumer Summary produced by Reliance Medical Information, Inc.)

Surgery, Portacaval anastomosis, Portal vein bypass

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Status of sclerotherapy for variceal bleeding in 1990

Article Abstract:

Injection sclerotherapy, injection of a hardening agent through the esophagus into esophageal varices, has three different roles: it may be used to control active bleeding, to prevent rebleeding, or used prophylactically to prevent initial bleeding. The role best supported by available research is that of controlling active bleeding. In two controlled studies of patients actively bleeding, control was achieved in 74 and 92 percent of patients. For patients whose bleeding has stopped, sclerotherapy may be combined with diagnostic endoscopy (visualization of the interior of the esophagus using an illuminated optic instrument). This may also be performed immediately on actively bleeding patients to stop bleeding, if competent personnel are available. Sclerotherapy may also be used to prevent rebleeding in patients who have spontaneously stopped bleeding. A poorly functioning liver has been found to be predictive of early rebleeding. The use of repeated sessions of sclerotherapy has been shown to reduce the number of rebleeding episodes, but not necessarily the number of patients experiencing rebleeding. The influence of long-term sclerotherapy on survival is controversial, and the need for such an intense regimen has been questioned. Sclerotherapy, as a prophylactic measure, does not appear to be justified unless criteria are able to be defined so that high-risk patients can be identified. (Consumer Summary produced by Reliance Medical Information, Inc.)

Evaluation, Injuries

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