Bleeding esophagogastric varices and ascites are the most serious complications of portal hypertension. Rupture of varices develops because of progressively rising portal pressure as rapid splanchnic blood flow combines with increasing portal vascular resistance (active congestion). The greater the restriction to transhepatic portal venous flow, the less the increment in splanchnic blood flow required to generate a venous pressure ultimately exceeding the bursting tension of thin-walled varices. Ascites, on the other hand, represents an imbalance of hydrodynamic forces in the microcirculation of the liver and digestive tract. Large amounts of fluid are driven out of the vascular space into visceral tissues. When the rate of lymph return to the systemic venous circulation fails to keep pace with increased capillary filtration, peritoneal transudation ensues. A complex sequence of events is then set into motion leading to renal salt and water retention. Plasma volume is restored, but at the same time hepatosplanchnic lymph formation is aggravated and a vicious cycle is thereby created. Treatment depends on reduction of lymph formation by indirect (dietary restriction of salt and water and diuretic drugs) or direct (portasystemic shunt) portal decompression or, alternatively, on acceleration of an already rapid lymph return (peritoneovenous shunt) to match the high rate of lymph production.
|Original language||English (US)|
|Number of pages||5|
|State||Published - Jan 1 1983|
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