Elevated pressure in the vein carrying blood to the liver, leading to distended veins, particularly in the oesophagus
- More common in adults, especially those over the age of 40
- More common in males
- Excessive alcohol consumption is a risk factor
- Genetics is not a significant factor
In a liver damaged by disease, normal blood flow may become blocked. This obstruction leads to portal hypertension, in which the pressure is increased inside the portal vein, a large vein that carries blood from the digestive tract to the liver. The high pressure forces blood through other smaller veins in the digestive tract. These veins become distended and fragile (like varicose veins in the legs), and are known as varices.
In most cases, varices develop at the lower end of the oesophagus. They are prone to rupture, and heavy bleeding from them can be life-threatening. In some cases, varices develop in other areas of the body, such as in the skin over the abdomen and in the rectum.
Portal hypertension occurs mainly in adults and is more common in men. The condition is often associated with excessive consumption of alcohol (see Alcohol and health).
What are the causes?
In Western countries, about 8 in 10 cases of portal hypertension are associated with cirrhosis, which is often due to chronic hepatitis or long-term alcohol abuse (see Alcohol-related liver disease). A blood clot blocking the portal vein, schistosomiasis, and in rare cases, congenital liver disorders may also cause portal hypertension.
What are the symptoms?
Portal hypertension is usually undetected until complications develop. If symptoms develop, they may include:
Swollen abdomen due to accumulation of fluid (ascites).
Visible swelling of the veins in the skin over the abdomen, sometimes around the navel.
In about 1 in 3 people with varices in the oesophagus, the veins eventually rupture. The bleeding is usually sudden and massive and leads to vomiting of blood and later passage of black, tarry faeces that contain partly digested blood (see Bleeding from the digestive tract). Loss of large volumes of blood can result in shock. If it is not treated immediately, shock may cause damage to internal organs and lead to disorders such as acute kidney failure and liver failure.
What might be done?
Your doctor will check for signs of portal hypertension if you have chronic hepatitis. Ultrasound scanning or CT scanning may be done to detect enlarged veins, or endoscopy may be used to visualize them (see Upper digestive tract endoscopy).
Usually, once the disorder has developed, liver damage is irreversible, but beta-blockers may be prescribed to lower pressure in the portal vein and decrease the risk of bleeding from varices.
Ruptured varices require urgent treatment in hospital with intravenous fluids and a blood transfusion, to replace lost blood. The source of internal bleeding will be investigated using endoscopy. If possible, the varices will be injected through the endoscope with a chemical that causes the vein to close and thus stops bleeding. Alternatively, bands may be placed around the varices during endoscopy. The drugs vasopressin, terlipressin, or octreotide may also be given to help reduce bleeding.
If these steps do not stop the bleeding, a tube encircled by a deflated balloon may be passed through the mouth into the oesophagus. The balloon is inflated to compress the varices and left in place until bleeding stops. In some cases, a procedure is carried out to allow blood from the digestive tract to bypass the liver: X-rays may be used to direct the insertion of a tube to connect the portal vein directly to the hepatic vein, through which blood normally leaves the liver.
What is the prognosis?
The outlook depends on whether or not varices develop and bleed and also on the severity of bleeding. About 7 in 10 people survive ruptured varices, but in over half of them bleeding will recur.
From the 2010 revision of the Complete Home Medical Guide © Dorling Kindersley Limited.
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