Causes
1. Prehepatic obstruction
- Splenic vein thrombosis
- Portal vein thrombosis
2. Intrahepatic obstruction
- Presinusoidal (fibrosis or infiltration outside the sinusoids) as in bilharziasis and metastasis.
- Sinusoidal as in cirrhosis
- Postsinusoidal as in veno-occlusive disease
3. Post hepatic obstruction of the portal vein flow
- Budd-Chiari syndrome
- Right sided heart failure
- Constrictive pericarditis
Pathophysiology
Portal hypertension leads to the opening of venous collateral circulation in many areas of the body (e.g. esophagus). These veins become dilated and are prone to bleeding.
Clinical picture
The major clinical manifestations of portal hypertension include hemorrhage from gastroesophageal varices, splenomegaly with hypersplenism, ascites, and acute and chronic hepatic encephalopathy. These are related, at least in part, to the development of portal-systemic collateral channels.
Consequences of portal hypertension
- Ascites (free fluid in the peritoneal cavity)
- Esophageal varices (dilated veins in the wall of the esophagus that are prone to bleed)
- Hemorrhoids
- Increased risk of spontaneous bacterial peritonitis
- Increased risk of hepatorenal syndrome
Diagnosis
- Ultrasound and CT scan reveals distention of portal vein and its collaterals.
- Endoscopy enables easy diagnosis and grading of varices.
- Celiac and superior mesenteric arteriography are used to determine the site of block and the extent of collaterals which is essential before procedures such as surgery, TIPS or hepatic transplantation.
Treatment
Surgical decompression procedures have been used for many years to lower portal pressure in patients with bleeding esophageal varices (see below). However, portal-systemic shunt surgery does not result in improved survival rates in patients with cirrhosis. Decompression can now be accomplished without surgery through the percutaneous placement of a portal-systemic shunt, termed a transjugular intrahepatic portosystemic shunt (TIPS).
B-Adrenergic blockade with propranolol or nadolol reduces portal pressure through vasodilatory effects on both the splanchnic arterial bed and the portal venous system in combination with reduced cardiac output.
