The portal triad in hepatic cirrhosis

Although ascites, bleeding esophagogastric varices and fibrocongestive splenomegaly with hypersplenism compose a familiar triad in hepatic cirrhosis, the origin and progression of these complications involve much more than mere portal pressure elevation. Because critical events unfold in the relatively inaccessible hepatosplanchnic bed, methodology has been a major stumbling block to obtaining detailed hemodynamic and lymphodynamic data. Direct measurement of organ blood flow usually is made under artificial or less than ideal conditions, for example, at laparotomy, quantitation of portasystemic collateral venous flow is indirect and at best a rough approximation and examination of lymph flow and composition in the thoracic duct and its major tributaries in the liver and extrahepatic portal bed is limited. Nonetheless, based on fragmentary clinical data viewed in the context of numerous observations in experimental conditions mimicking the disordered portal circulation in hepatic cirrhosis, a more comprehensive understanding of these phenomena is slowly emerging. Viewed in the light of information available now, ascites begins with an imbalance of physiochemical forces at the capillary level in the liver and digestive tract. Large amounts of fluid are driven out of the vascular space into splanchnic tissues. When the rate of lymph return to the systemic venous circulation fails to keep pace with excessive capillary filtration, ascites appears. A complex sequence of events is then set into motion leading to salt and water retention and involving the renin-aldosterone system. Plasma volume is restored, but at the same time hepatosplanchnic lymph formation is further enhanced, and a vicious circle is created. Treatment depends upon reduction of lymph formation by indirect, dietary restriction of salt and water and diuretic drugs, or direct, portasystemic shunt, portal decompression or alternatively, upon acceleration of already rapid lymph return, lymph- venous or peritoneovenous shunt, to match the high rate of lymph production. Spontaneous rupture of esophagogastric varices develops because of the precipitous rise in portal pressure when increased splanchnic blood flow combines with progressively rising portal vascular resistance. The greater the restriction to transhepatic portal venous flow, the less of an increment in splanchnic blood flow is required to generate pressures that ultimately exceed the bursting tension of thin-walled varices. Treatment is based on attempts to lower resistance to esophagogastric venous flow, such as generalized or segmental portasystemic shunt or, in selected patients, to restrict hyperdynamic arterial inflow, such as splenectomy or splenic artery ligation. Splenomegaly in patients with disease of the liver primarily derives from hepatocellular dysfunction with compensatory reticuloendothelial hyperactivity in the congested spleen. Splenic arterial flow increases as the demand for blood flow rises from splenic work hypertrophy, and peripheral cytopenias may develop. Treatment of symptomatic hypersplenism requires reduction of splenic mass either by restricting splenic arterial inflow or ablating the spleen.