Current status and future goals of the pharmacologic reduction of portal hypertension

Article Abstract:

Portal hypertension (increased pressure in the portal vein of the liver) can cause esophageal varices, which are enlarged, swollen and tortuous veins at the lower end of the esophagus. Pharmacologic treatment (medication) can reduce the pressure in the portal vein by one or both of two mechanisms: by decreasing the amount of blood coming into the vein from its tributaries, or by decreasing the resistance to blood flow in the vein as it passes through the liver. Some vasoactive medications are effective for a short time and are used to treat acute bleeding from varices; other medications can be taken over a long period and can be used to prevent gastrointestinal bleeding caused by portal hypertension. There are three classes of long-term medications: beta-adrenergic antagonists, alpha-2 adrenergic agonists, and 5-hydroxytryptamine (5-HT2) receptor antagonists. It appears that propranolol (a nonselective beta-adrenergic antagonist) reduces portal pressure (10 to 31 percent during short-term administration) in most patients, but there are patients who do not respond to this medication. These nonselective beta blockers lower pressure by reducing tributary blood flow. Clonidine, an alpha-2 adrenergic agonist, decreases the total outflow of the sympathetic nervous system and decreases vascular resistance. In one study clonidine reduced portal pressure by 19 percent. 5-HT2 receptor antagonists such as ketanserin may reduce portal pressure in patient who have cirrhosis of the liver by decreasing the pressure gradient of the hepatic veins, which return blood from the liver. If one drug is not being effective, either another type of drug or a combination of drugs may be tried. Several problems remain to be addressed: patient compliance, identification of non-responding patients; hemodynamic evaluation of treatment; and duration of treatment. (Consumer Summary produced by Reliance Medical Information, Inc.)

Causes of, Drug therapy, Adrenergic beta blockers, Adrenergic beta-antagonists, Propranolol hydrochloride, Propranolol, Clonidine, Adrenergic alpha blockers, Adrenergic alpha-antagonists, Ketanserin

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Evaluation of patients with portal hypertension

Article Abstract:

Portal hypertension (increased pressure in the portal vein of the liver), can cause esophageal varices, which are enlarged, swollen and tortuous veins at the lower end of the esophagus. Treatment of esophageal varices can be invasive (surgery or sclerotherapy) or noninvasive (drug therapy aimed at the underlying liver disease). In order to make the best treatment choice, full evaluation of the patient should be undertaken. The causes of the portal hypertension should be determined. The most common cause is cirrhosis (a degenerative disease in which liver tissue is replaced by fibrous tissue and fatty deposits), which obstructs the flow of blood through the liver causing portal hypertension. If varices can be identified by imaging (computed tomography; CT, or gastrointestinal series), endoscopy should be performed to determine their characteristics. Angiographic studies (X-ray examinations of the blood vessels following injection of radio-opaque contrast dye) are indicated if the patient is to undergo surgery. The liver disease should be evaluated, including any history of blood transfusions. The activity of the disease can be evaluated by routine blood chemistry tests and liver biopsy; patients with chronic disease and portal hypertension should also have serologic and immunologic evaluation. The functional ability of the liver needs to be evaluated; the presence of active disease does not necessarily indicate severe loss of function. Serial testing can quantify the progression of the disease and identify potential candidates for liver transplant. This evaluation is based on liver cell function, total liver blood flow, portal blood flow and systemic changes and liver size. (Consumer Summary produced by Reliance Medical Information, Inc.)

Care and treatment

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Selective shunts: the Johannesburg experience

Article Abstract:

The author's experience performing 141 selective shunts for treating portal hypertension (increased pressure in the portal vein of the liver) is reported. Portal hypertension frequently results from liver cirrhosis (degenerative disease in which liver tissue is replaced by fibrous tissue and fatty deposits), which obstructs the flow of blood through the liver. Esophageal varices and bleeding may result from portal hypertension. One hundred twenty-seven operations were performed electively; 56 percent of these were for alcoholic liver cirrhosis, 22 percent for other cirrhotic liver disease, and 24 percent were noncirrhotic. Adequate preoperative hospitalization (an average of 6 weeks) permitted improvement in Child's classification of liver cell failure prior to surgery. On admission there were 35 patients with Class A (least severe of the three classes) and 40 patients with Class C (the most severe); by the time of surgery, there were 72 patients with Class A and only one patient at Class C level. Recurrence of variceal bleeding was rare (4 percent of patients undergoing the standard splenorenal shunt procedure) and when it occurred it was due to shunt failure. Shunt failure occurred more often when selective shunt procedures other than splenorenal were performed. Postoperative encephalopathy occurred in 13 percent of patients, and not at all in the noncirrhotic patients. The main factor determining hospital mortality and long-term survival was the nature of the underlying liver disease. Nonalcoholics fared better than alcoholics. (Consumer Summary produced by Reliance Medical Information, Inc.)

Usage, Injuries, Surgery, Esophageal varices, Splenorenal shunt, Surgical, Surgical splenorenal shunt, Johannesburg

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