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Portal hypertension

The blood pressure within the portal vein in a normal person at rest is between 6 and 12 cm of water. In no cases it must exceed 25cm in healthy individuals. A rise in the portal venous pressure above this level indicates portal hypertension which, depends upon geographic, standing individual’s position, constitution etc.

Causes:
In many cases the obstruction occurs within the liver i.e. Intrahepatic. Sometimes the obstruction is below the liver i.e. prehepatic and rarely above the liver i.e. posthepatic.

Intrahepatic Lesions:
About 80% of cases the obstruction is due to the fibrotic changes in the liver that strangle the branches of portal vein within that organ. The fibrosis is almost due to the cirrhosis of the liver but rarely may be due to other causes e.g. Hepato-Splenic fibrosis (Banti’s) or sequalae to the acute viral hepatitis. During the cirrhosis (biliary, alimentary, post necrotic), portal venous pressure rises due to either mechanical obstruction or arterio-venous fistulas.
  • Mechanical Obstruction: may be due to:
    • Fibrosis
    • Regenerated mass of liver tissue in compensated cases
  • Arterio-Venous fistulas:
    Multiple minute intrahepatic arterio-venous fistulae develop (Hepatic arterial portal fistula, splenic arterial venous fistula, the factor of intersplenic origin) between the smaller branches of the hepatic artery and those of the portal vein. This may result by the deformity in the liver architecture in portal cirrhosis. The result is that the pressure of hepatic arterial system is transmitted to the portal venous system.
Prehepatic lesions:
It accounts for 20%, is usually congenital and common in children and adolescents. Occlusion either in the main portal vein or splenic vein i.e. before the vein has entered the liver. Such obstruction is due to:
  • Congenital malformation of vein: the vein being represented by cavernous spaces in the mesenchyme, rarely the vein may be congenitally absent
  • Thrombosis of the portal vein is usually a result of extension in the upward direction in the normal process of obliteration of umbilical vein in the neonates. Such extension of thrombosis is usually the result of umbilical sepsis. Rarely the thrombus in the portal vein may be post-traumatic as in adults
  • Posthepatic lesions:
    Posthepatic lesions are rare where the obstruction of the hepatic vein occurs or the site of obstruction is still above the liver e.g.
    • Occlusion of hepatic vein by malignant metastasis or by thrombosis (Budd-Chiari Syndrome)
    • Constrictive pericarditis
    • Right heart failure
    Pathological changes:
    As the blood in the portal circulation finds an obstruction, it tries to reach the heart via systemic circulation. The naturally existing collaterals between the portal and systemic circulation open up. The sites of porto-systemic anastomosis are:
    • At the lower end of the oesopahgus: Oesophageal branches of left gastric veins (portal) and lower oesophageal vein (systemic). The occurrence of oesophageal varices which, extend down into the stomach, there may be haemorrhage from rupture of these varices
    • Around the umbilicus: Paraumbilical vein accompanying with the round ligament of liver (portal) and superficial veins of the anterior abdominal wall. Overall the effect of pressure on these vessels results in Caput Medusae
    • At the Hilton line in the anal canal: Superior hemorrhoid veins (portal) and middle &inferior hemorrhoid veins (systemic). This obviously results in hemorrhoids but this is rare
    • In the retroperitoneal tissue and the extraperitoneal surface of the abdominal organs: This includes the group of superior & inferior mesenteric veins and retroperitoneal &subdiaphragmatic veins. The effect of these veins is unclear
    Enlargement of the spleen:
    Is believed to be the result of venous stasis.

    Blood changes:
    • Anaemia
    • Leucopenia
    • Thrombocytopenia
    • The blood changes are thought to be due to hypersplenism
    Clinical Features:
    • Bleeding from the varices is manifested as haemastemesis. Sometimes this bleeding can co-exist with peptic ulcers where it is difficult to differentiate
    • Ascites sometimes associated with oedema of the legs is obvious due to the abdominal fluid on the inferior vena cava
    • Splenomegaly
    • Caput Medusae around umbilicus
    • Anaemia
    Investigations:
    Blood examination:
    • Anaemia (microcytic, hypochromic)
    • Leukemia and
    • Thrombocytopenia
    Liver function test: poor
    Barium swallow examination: to detect oesophageal varices.
    Oesophagoscopy: to demonstrate varicose veins. It should be done with care as minor trauma can cause bleeding
    • Submucosal veins running I mucosa in three parallel lines and longitudinal lines (like piles)
    • Subepithelial dilated veins (running in zigzag course)

    Measurement of intrasplenic pressure
    Splenoportomanometry

     Treatment:
    Drug therapy:
    • Bed rest and sedatives
    • Vitamin K and blood transfusion
    • Sandostatin
    • Vasopressin
    • Propranolol
    Temponades:
    Occlusion of varicose veins by Sangstaken tube relieves hypertension by direct pressure. There is cylindrical balloon for lower oesophagus and spherical balloon for stomach to press upon veins. The varicose veins extend into the upper gastric wall.

    Surgical Methods:
    Ligation of varices (Crile’s):
    Oesophagus is isolated and clamped at cardia, then it is opened up longitudinally and varices are ligated with catgut sutures.
    Oesophageal transaction (Milnes Walket’s):
    Complete interruption of submucosal and subepithelial varices.
    Subcardiac gastric transaction (Tanner’s): Here the stomach is completely transacted two inches below the level of cardia. Then all vessels are ligated.

    Surgical treatment:
    Include the Decompression operations and Splenectomy.
    Portal Caval Shunts:
    These shunts are non-selective because there is evidence of thorough blood flow from portal to caval system without entering the liver. As a result we have decompression in portal system but severe encephalopathy does occur. This was the reason to selective shunts which itself decompresses the portal system and partially blood flows into the liver to avoid encephalopathy.
    After division, upper end of the portal vein is cut and anastomosed side-to-side with inferior vena cava.

    Spleno-renal anastomosis:
    After hypersplenism and when the portal vein is occluded by thrombosis, spleno-renal anastomosis is applied. When splenic vein is about 1cm in diameter then spleen is removed and cut end of the splenic vein is implanted into left renal vein. This is called side-by-side anastomosis.

    Superior mesenterico-caval anastomosis:
    This is done between superior mesenteric vein and inferior vena cava. When portal vein is thrombosed and splenic vein is less than 1cm in diameter. Lower cut end of the inferior vena cava is closed while the upper part is implanted end-to-end in the superior mesenteric vein.

    Complications:
    • Bleeding from enlarged varices especially from gastroesophageal junction
    • Ascites
    • Hypersplenism
    • Encephalopathy and coma
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    This article has been written by Dr. M. Javed Abbas.
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    01:17 09/02/2003