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Pronunciations ascites cholestasis cirrhosis computed tomography encephalopathy esophageal esophagus hepatic encephalopathy manometry pancreas ultrasonography vasopressin

Portal hypertension is abnormally high blood pressure in branches of the portal vein, the large vein that brings blood from the intestine to the liver.

• Cirrhosis is the most common cause in Western countries.
• The effects of portal hypertension can lead to an enlarged abdomen, abdominal discomfort, confusion, and internal bleeding.
• Doctors base the diagnosis on symptoms and results of a physical examination, sometimes with ultrasonography.
• Drugs can reduce blood pressure in the portal vein, but if internal bleeding occurs, emergency treatment is required.

The portal vein receives blood from the entire intestine and from the spleen, pancreas, and gallbladder. After entering the liver, the vein divides into right and left branches and then into tiny channels that run through the liver. When blood leaves the liver, it flows back into the general (systemic, or body-wide) circulation through the hepatic vein (see Blood Vessel Disorders of the Liver:Introduction).

Two factors can increase blood pressure in the portal blood vessels:

• Increased volume of blood flowing through the vessels
• Increased resistance to the blood flow through the liver

In Western countries, the most common cause of portal hypertension is increased resistance to blood flow caused by extensive scarring of the liver in cirrhosis, which is most often due to chronic excessive alcohol intake.

Portal hypertension leads to the development of new veins (called collateral vessels) that directly connect the portal blood vessels to the general circulation, bypassing the liver. Because of this bypass, substances (such as toxins) that are normally removed from the blood by the liver can pass into the general circulation. Collateral vessels develop at specific places. The most important are located at the lower end of the esophagus and at the upper part of the stomach. Here, the vessels become engorged and full of twists and turns—that is, they become varicose veins of the esophagus (esophageal varices) or stomach (gastric varices). These engorged vessels are fragile and prone to bleeding, sometimes seriously and occasionally with fatal results. Other collateral vessels may develop on the abdominal wall and at the rectum.

Portal hypertension often causes the spleen to enlarge because the pressure interferes with blood flow from the spleen into the portal blood vessels. Pressure in the portal blood vessels may cause protein-containing (ascitic) fluid from the surface of the liver and intestine to leak into the abdominal cavity. This condition is called ascites.

Esophageal Varices

Symptoms and Diagnosis

Portal hypertension itself does not cause symptoms, but some of its consequences do. If a large amount of ascitic fluid accumulates, the person's abdomen swells (distends), sometimes noticeably and sometimes enough to make the abdomen greatly enlarged and taut. This distention is painless. An enlarged spleen may cause a vague sense of discomfort in the upper left part of the abdomen. Esophageal and gastric varices bleed easily and sometimes massively. Much less commonly, varicose veins in the rectum bleed.

When substances that are normally removed from the liver pass into the general circulation and reach the brain, they may cause confusion or drowsiness (hepatic encephalopathy). Collateral vessels may be visible on the skin over the abdominal wall or around the rectum. Because most people with portal hypertension also have severe liver dysfunction, they may have symptoms of liver failure, such as a tendency to bleed.

Doctors can usually recognize hepatic encephalopathy based on symptoms and findings during the physical examination. Doctors can usually feel an enlarged spleen through the abdominal wall. They can detect fluid in the abdomen by noting abdominal swelling and by listening for a dull sound when tapping (percussing) the abdomen. An ultrasound scan may be used to examine blood flow in the portal vein and nearby blood vessels and to detect fluid in the abdomen. An ultrasound or computed tomography (CT) scan can be used to look for and examine collateral vessels. Rarely, a catheter is inserted through an incision in the neck and threaded through blood vessels into the liver or spleen to directly measure pressure in the portal blood vessels (manometry).

Treatment

To reduce the risk of bleeding from esophageal varices, a doctor may try to reduce pressure in the portal vein. One way is to drugs such as propranololSome Trade Names
INDERAL
or nadololSome Trade Names
CORGARD
.

Bleeding from esophageal varices is a medical emergency (see Gastrointestinal Emergencies: Abdominal Abscesses). Drugs such as vasopressinSome Trade Names
PITRESSIN
or octreotideSome Trade Names
SANDOSTATIN
may be given intravenously to constrict the bleeding veins, and blood transfusions are given to replace lost blood. An endoscopic examination is usually done to confirm that the bleeding is from varices. The veins can then be blocked off with rubber bands or with injections of a chemical given through the endoscope.

If the bleeding continues or recurs repeatedly, a surgical procedure may be done to create a bypass (called a shunt) between the portal venous system and the general (systemic, or body-wide) venous system. This bypass lowers pressure in the portal vein because pressure is much lower in the general venous system.

There are various types of portal-systemic shunt procedures. In one type, called transjugular intrahepatic portal-systemic shunting (TIPS), an x-ray-guided needle is passed through the liver to create a shunt connecting the portal vein directly with one of the hepatic veins. Shunt procedures are usually successful in stopping the bleeding but pose certain risks, such as hepatic encephalopathy (see Manifestations of Liver Disease: Hepatic Encephalopathy). The TIPS procedure, although less dangerous than other portal-systemic shunt procedures, may need to be repeated periodically because the shunt narrows in some people.

Last full review/revision August 2006 by Sidney Cohen, MD