The Three Major Clinical Manifestations of Liver Cirrhosis and Portal Hypertension

Liver cirrhosis with portal hypertension presents several key clinical features, the most significant of which are ascites, the formation of collateral circulation, and splenomegaly accompanied by hypersplenism. These manifestations are described in detail below.

Ascites is one of the most prominent signs of decompensated liver cirrhosis. It results from a combination of reduced liver function and elevated portal venous pressure. Patients often experience abdominal distension, and in severe cases, massive fluid accumulation can lead to a visibly swollen abdomen. This condition may also contribute to the development of abdominal hernias, such as umbilical hernias. Furthermore, large volumes of ascites can push upward on the diaphragm, limiting its movement and potentially causing shortness of breath and palpitations.

Development of portosystemic collateral circulation is another hallmark of portal hypertension. Commonly observed collateral pathways include esophageal and gastric varices, abdominal wall vein dilation, hemorrhoidal vein expansion, retroperitoneal shunts, and splenorenal shunts. These alternative blood flow routes form as the body attempts to bypass the increased pressure in the portal system.

Splenomegaly and hypersplenism frequently occur early in the progression of liver cirrhosis. Increased resistance to blood flow in the splenic vein and backward transmission of portal pressure leads to passive congestion and enlargement of the spleen. Additionally, inflammatory substances from the gut enter the systemic circulation through portosystemic collaterals and are then taken up by the spleen. This triggers antigenic stimulation, leading to proliferation of mononuclear phagocytes within the spleen, contributing to both splenomegaly and overactive spleen function, known as hypersplenism.