Portal hypertension
From Wikipedia, the free encyclopedia
| Portal hypertension | |
| Classification and external resources | |
 |
|
|---|---|
| The portal vein and its tributaries. | |
| ICD-10 | K76.6 |
| ICD-9 | 572.3 |
| DiseasesDB | 10388 |
| eMedicine | radio/570 med/1889 |
| MeSH | D006975 |
In medicine, portal hypertension is hypertension (high blood pressure) in the portal vein and its tributaries.
It is often defined as a portal pressure gradient (the difference in pressure between the portal vein and the hepatic veins) of 5 mm Hg or greater.
Contents |
[edit] Causes
Many conditions can result in portal hypertension. In North America and Europe, it is usually the result of cirrhosis of the liver,[1] but can also result from alcoholic hepatitis, idiopathic non-cirrhotic portal hypertension, congenital hepatic fibrosis, partial nodular transformation, Budd-Chiari syndrome, portal vein thrombosis and, rarely, right heart failure. Schistosomiasis is a major cause worldwide,[2] especially in the less industrialized parts of the world.
[edit] Signs and symptoms
Consequences of portal hypertension are caused by blood being forced down alternate channels by the increased resistance to flow through the portal system. They include:
- Ascites (free fluid in the peritoneal cavity)[3]
- Hepatic encephalopathy
- Increased risk of spontaneous bacterial peritonitis
- Increased risk of hepatorenal syndrome
- Splenomegaly (enlargement of the spleen) with consequent sequestration therein of red blood cells, white blood cells, and platelets, together leading to mild pancytopenia
- Portacaval anastomoses (esophageal varices, gastric varices, hemorrhoids, caput medusae), with esophageal varices and gastric varices posing an ongoing risk of life-threatening hemorrhage, with haematemesis or melaena
[edit] Treatment
[edit] Medical management
Patients with portal hypertenson may undergo EGD to rule out esophageal varices, and perhaps correct them at the same time with banding or sclerotherapy.[4] Acute or severe complications may be treated with intravenous octreotide or terlipressin (an antidiuretic hormone analogue) to decrease the portal pressure. Octreotide inhibits the release of vasodilator hormones such as glucagon,[5] indirectly causing splanchnic vasoconstriction and decreased flow into the portal system.
Long-term treatment with a non-selective beta blocker is often commenced once portal hypertension has been diagnosed, and almost always if there has already been bleeding from esophageal varices. Typically, this is done with either propranolol or nadolol. The addition of a nitrate, such as isosorbide mononitrate, to the beta blocker is more effective than using beta blockers alone and may be the preferred regimen in those people with portal hypertension who have already experienced variceal bleeding.
[edit] Percutaneous interventions
Transjugular intrahepatic portosystemic shunting is the creation of a connection between the portal and the sytemic venous system. This is done by putting an artificial shunt tube through the liver under X-ray guidance. This allows creation of a low-resistance channel between the hepatic vein and the intrahepatic portion of the portal vein (usually the right branch). As the pressure in the systemic venous system is lower than that in a hypertensive portal system, this would decrease the pressure in the portal system and produce a decreased risk of bleeding complications. The commonest problem is blockage of the shunt which is as high as 50% in the first year. Another problem is an increased risk of hepatic encephalopathy, which may be unresponsive to conventional treatment in a proportion of cases.
[edit] Surgical interventions
- Sugiura operation
This operation is reported by Japanese surgeons in 1973. It is a technique to produce extensive gastroesophageal devascularization for the treatment of esophageal varices. The principle is to divide the esophageal and gastric venous plexus from the portal collateral vessels while preserving extra esophageal systemic venous collaterals (azygous system). Splenectomy is often required at the same time. The reported benefits of this procedure were low mortality, a low incidence of recurrent bleeding, and absence of hepatic encephalopathy when compared with series of nonselective shunts. Most authors outside of Japan failed to reproduce the exceptional results reported by Sugiura. The role of gastroesophageal devascularization (Sugiura-type procedures) for the treatment of variceal bleeding remains controversial in western countries. The modified Sugiura procedure may be an effective rescue therapy in patients who are not candidates for selective shunts, TIPS, or transplantation.[6]
This is the most definitive treatment of portal hypertension and cirrhosis.
[edit] References
- ^ Portal Hypertension at Merck Manual of Diagnosis and Therapy Home Edition
- ^ "Hepatic schistosomiasis.". Hepatology 1 (653). 1981.
- ^ "Portal Hypertension". http://www.clevelandclinic.org/health/health-info/docs/0200/0252.asp?index=4912. Retrieved on 2007-12-07.
- ^ Grace ND (1997 Jul). "Diagnosis and treatment of gastrointestinal bleeding secondary to portal hypertension". American College of Gastroenterology Practice Parameters Committee 92 (7): 1081-91.
- ^ Bloom SR; Polak JM. (1987 Aug 1). "Somatostatin". British Medical Journal (Clinical Research Edition) 295 (6593): 288-90.
- ^ Selzner M, Tuttle-Newhall JE, Dahm F, Suhocki P, Clavien PA (2001). "Current indication of a modified Sugiura procedure in the management of variceal bleeding". J Am Coll Surg 193 (2): 166–73. PMID 11491447.
[edit] External links
- VIDEO - Portal Hypertension: Shunt Surgery in the Era of Transplant and TIPS, Alysandra Lal, MD, speaks at the University of Wisconsin School of Medicine and Public Health (2007)
- Ascites at Merck Manual of Diagnosis and Therapy Home Edition
- 00863 at CHORUS
- Overview at Cleveland Clinic
- Children's Liver Disease Foundation
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