Portal hypertension

Anatomy/physiology:

The portal vein is formed by the union of the superior mesenteric vein and the splenic vein

The pressure within it is usually 5-8mmHg, with only a small gradient across the liver to the hepatic vein, in which blood is returned to the IVC

Portal hypertension can be classified according to the site of obstruction:

Prehepatic:

Due to blockage of the portal vein before the liver

Intrahepatic:

Due to distortion of the liver architecture, which can be either:

Pre-sinusoidal (e.g. in schistosomiasis), or

Post-sinusoidal (e.g. in cirrhosis)

Posthepatic:

Due to venous blockage outside the liver (rare)

As portal pressure rises > 10-12mmHg, the compliant venous system dilates and collaterals occur with the systemic venous system

The main sites of the collaterals are the:

Gastro-oesophageal junction

Rectum

Left renal vein

Diaphragm

Retroperitoneum

Anterior abdominal wall (via the umbilical vein)

The collaterals at the gastro-oesophageal junction (varices) are superficial in position and tend to rupture

Common causes:

Prehepatic:

Portal vein thrombosis

Intrahepatic:

Cirrhosis

Schistosomiasis

Congenital hepatic fibrosis

Posthepatic:

Budd-Chiari syndrome

Veno-occlusive disease

Right heart failure (rare)

Constrictive pericarditis

Clinical features:

Pts with portal hypertension are often asymptomatic and the only clinical evidence is splenomegaly

Clinical features of chronic liver disease are usually present

Presenting features may include:

Portal hypertension

Haematemesis/malaena from rupture of gastro-oesophageal varices

Ascites

Encephalopathy