Portal Hypertension

Portal Hypertension

Increased resistance to portal blood flow may develop in a variety of circumstances which can be divided into prehapatic intrahepatic and posthepatic causes. The major prehepatic conditions are obstructive thrombosis and norrowing of the portal vein b

efore it ramifies within the liver. jMassive splenomegaly may also shunt excessive blood into the splenic vein. The major posthepatic causes are severe right sided heart failure constrictive pericarditis and hepatic vein outflow obstruction. The dominant intrahepatic cause is cirrhosis, accounting for most cases of portal hypertension. Far less frequent are schistosomasis massive fatty change diffuse fibrosing granulomatous disease such as sarcoidosis and military tuberculosis, and disease affecting the portal microcirculation exemplified by nodular regenerative hyperplasia.

Portal hypertension in cirrhosis results from increased resistance to portal flow at the level of the sinusoids and compression of central veins by perivenular fibrosis and expansile parenchymal nodules. Anastomoses between the arterial and portal systems in the fibrous bands also contribute to portal hypertension by imposing arterial pressure on the low pressure portal venous system. The four major cli

nical consequences are (1) ascites (2) the formation of portosystemic venous shunts (3) congestive splenomegaly and (4) hepatic encephalopathy.

Ascites

Ascites refers to the collection of excess fluid in the peritoneal cavity. It usually becomes clinically detectable when at least 500ml has accumulated but many liters may collect and cause massive abdominal distention. It is generally a serous fluid having less than 3 gm/dl of protein (largely albumin) as well as the same concentrations as in the blood of solutes such glucose sodium, and potassium. Influx of neutrophils suggests secondary infection whereas red cells point to possible disseminated intra abdominal cancer. With long standing ascites, seepage of peritoneal fluid through transdiaphragmatic lymphatics may produce hydrothorax, more often on the right side.

The pathogenesis of ascites is complex, involving the following mechanisms.

Sinusoidal hypertension , altering Starling forces and driving fluid into the space of disse, which is then removed by hepatic lymphatics; this movement of fluid is also promoted by hypoalbuminemia.

Percolation of hepatic lymp into the peritoneal cavity. Normal thoracic duct lymp flow approximates 800 to 1000 ml/dl. With cirrhosis, hepatic lymphatic flow may approach 20 L/day exceeding thoracic duct capacity. Hepatic lymp is rich in proteins and low in triglycerides, which is reflected in the protein rich ascitic fluid.

Intestinal fluid leakage. Portal hypertension also engenders increased perfusion pressure in intestinal capillaries.
The osmotic action of the protein rich ascitic fluid promotes movement of additional fluid out of intestinal cpillaries into the abdomen.

Renal retention of sodium and water due to secondary hyperaldosteronism.

Portosystemic shunts

With the rise in portal system pressure, bypasses develop whereever the systemic and portal circulation share common capillary beds. Principal sites are veins around and within the rectum (manifest as hemorrhoids); the cardioesophageal junction (producing esophagogastric varices); the retro peritoneum and the falciform ligament of the liver (involving periumbilical and abdominal wall collaterals). Although hemorrhoidal bleeding may occur, it is rarely massive or life threatening. Much more important are the esophagogastric varices that appear in about 65% of patientsw with advanced cirrhosis of the liver and cause massive hematemesis and death in about half of them. Abdominal wall collaterals appear as dilated subcutaneous veins extending from the umbilicus toward the rib margins (caput medusae) and constitute an important clinical hallmark of portal hypertension.

Splenomegaly

Long standing congestion may cause congestive splenomegaly. The degree of enlargement varies widely up to 1000 gm and is not necessarily correlated with other features of portal hypertension. Massive splenomegaly may secondarily induce a variety of hematologic abnormalities attributable to hypersplenism.
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