Cirrhosis with the Most Pronounced Portal Hypertension

Among various types of cirrhosis, schistosomiasis-induced liver disease presents the most significant portal hypertension. Schistosomes primarily reside in the inferior mesenteric veins and rectal hemorrhoidal veins. The eggs are deposited in the submucosal layer of the intestine and travel through the portal venous system to the liver, where they cause major pathological changes in both the liver and colon.

In the early stages, the liver becomes visibly congested, swollen, and has a smooth surface interspersed with yellowish-brown granular nodules composed of parasite eggs. As the disease progresses, these egg-laden nodules in the intrahepatic branches of the portal vein lead to fibrous connective tissue proliferation, resulting in characteristic "pipestem" fibrosis. Due to circulatory disturbances, hepatocytes undergo atrophy, and the liver surface develops irregular, uneven nodules, ultimately forming a cirrhotic structure.

The thickening of the portal vein wall and the pre-sinusoidal blockage in its smaller branches contribute significantly to elevated portal pressure. This increased pressure manifests clinically as splenomegaly with hypersplenism, ascites, and upper gastrointestinal bleeding. Additional symptoms include fatigue, loss of appetite, and abdominal distension.

All patients exhibit some degree of spleen enlargement, with the organ sometimes reaching as far as the umbilicus. In early stages, the spleen remains soft, but it hardens over time due to intraparenchymal fibrosis and becomes less mobile because of surrounding adhesions. Approximately one-third of affected individuals develop ascites, which can be persistent and difficult to resolve. When esophageal and gastric varices rupture, patients may experience hematemesis and melena, which are serious complications requiring urgent medical attention.