Portal Hypertension

Question 1

Portal Hypertension

Answer 1

Increase in pressure in the portal system usually follows obstruction to the portal blood flow anywhere along its course. Portal veins have no valves and thus obstruction anywhere in the portal system raises pressure in all the veins proximal to the obstruction.

However, unless proved otherwise, portal hypertension means obstruction to the portal blood flow by cirrhosis of the liver.

Question 2

Based on the site of obstruction to portal venous blood flow, portal hypertension is categorised into 3 main types?

Answer 2

Intra-hepatic, posthepatic and prehepatic.

Question 3

Intrahepatic portal hypertension.

Answer 3

Cirrhosis is by far the commonest cause of portal hypertension.

Other less frequent intrahepatic causes are metastatic tumours, non-cirrhotic nodular regenerative conditions, hepatic venous obstruction (Budd-Chiari syndrome), veno-occlusive disease, schistosomiasis, diffuse granulomatous diseases and extensive fatty change.

Question 4

Post hepatic portal hypertension.

Answer 4

This is uncommon and results from obstruction to the blood flow through hepatic vein into inferior vena cava.

The causes are neoplastic occlusion and thrombosis of the hepatic vein or of the inferior vena cava (including Budd-Chiari syndrome).

Question 5

Prehepatic portal hypertension

Answer 5

Blockage of portal flow before portal blood reaches the hepatic sinusoids results in prehepatic portal hypertension.

Such conditions are thrombosis and neoplastic obstruction of the portal vein before it ramifies in the liver, myelofibrosis, and congenital absence of portal vein.

Question 6

Major Sequelae of portal hypertension:

Answer 6

1. Ascites
2. Varices
3. Splenomegaly
4. Hepatic encephalopathy

Question 7

Ascites

Answer 7

Ascites is the accumulation of excessive volume of fluid within the peritoneal cavity. It frequently accompanies cirrhosis and other diffuse liver diseases. Ascitic fluid is generally transudate with specific gravity of 1.010, protein content below 3 gm/dl and electrolyte concentrations like those of other extracellular fluids.

Pathogenesis. The ascites becomes clinically detectable when more than 500 ml of fluid has accumulated in the peritoneal cavity.

A. Systemic Factors: i) Decreased plasma colloid oncotic pressure ii) Hyperaldosteronism iii) Impaired renal excretion

B. Local Factors: i) Increased portal pressure ii) Increased hepatic lymph formation

Question 8

Varices (Collateral channels or Porto-systemic shunts)

Answer 8

As a result of rise in portal venous pressure and obstruction in the portal circulation within or outside the liver, the blood tends to bypass the liver and return to the heart by development of porto-systemic collateral channels (or shunts or varices). These varices develop at sites where the systemic and portal circulations have common capillary beds.

The principal sites are: i) Oesophageal varices ii) Haemorrhoids iii) Caput medusae iv) Retroperitoneal anastomoses

Question 9

Splenomegaly

Answer 9

The enlargement of the spleen in prolonged portal hypertension is called congestive splenomegaly.

The spleen may weigh 500-1000 gm and is easily palpable.

The spleen is larger in young people and in macronodular cirrhosis than in micronodular cirrhosis.

Question 10

Hepatic encephalopathy

Answer 10

Porto-systemic venous shunting may result in a complex metabolic and organic syndrome of the brain characterised by disturbed consciousness, neurologic signs and flapping tremors.

Hepatic encephalopathy is particularly associated with advanced hepatocellular disease such as in cirrhosis.