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- Increased portal venous pressure >5 mm Hg that occurs in association with splanchnic vasodilatation, portosystemic collateral formation, and hyperdynamic circulation
- Most commonly secondary to elevated hepatic venous pressure gradient (HVPG; the gradient between portal and central venous pressures)
- Course is generally progressive, with risk of complications including acute variceal bleeding, ascites, hepatic encephalopathy, and hepatorenal syndrome.
- Prevalence: <200,000 persons in the United States
- Predominant age: adult
- Predominant sex: male > female
Etiology and Pathophysiology
- Causes generally classified as follows:
- Prehepatic (portal vein thrombosis or obstruction)
- Intrahepatic (most commonly cirrhosis)
- Posthepatic (hepatic vein thrombosis, Budd-Chiari syndrome, right-sided heart failure)
- 90% of intrahepatic cases are due to cirrhosis secondary to the following:
- Virus (hepatitis B, hepatitis C, hepatitis D)
- Wilson disease
- Primary biliary cirrhosis (PBC)
- Increased HVPG results in venous collateral formation in the distal esophagus, proximal stomach, rectum, and umbilicus.
- Gastroesophageal variceal formation is found in 40% of patients with portal hypertension.
- Progression of portal hypertension results in splanchnic vasodilation and angiogenesis.
No known genetic patterns except those associated with specific hepatic diseases that cause portal hypertension
See “Etiology and Pathophysiology.”
In children, portal vein thrombosis is the most common extrahepatic cause; intrahepatic causes are more likely to be biliary atresia, viral hepatitis, and metabolic liver disease.