End-stage liver disease usually involves extensive hepatic parenchymal cells, with decreased regenerative capacity of liver tissue and extensive fibrosis of liver tissue leading to cirrhosis, resulting in liver metabolic function that cannot meet the needs of the body and eventually liver failure. Typical pathological changes of cirrhosis include diffuse fibrosis of liver tissue, formation of pseudobullets and regenerative nodules. Pre-sinusoidal fibrosis directly compresses blood flow in the confluent area, leading to increased resistance and blood flow in the portal system, resulting in portal hypertension and producing the triad of splenomegaly (hypersplenism), ascites and open portal collateral circulation (e.g., upper gastrointestinal varices). Cirrhosis results in decreased liver function, decreased albumin synthesis and decreased metabolism of the renin-angiotensin-aldosterone system causing sodium and water retention and accelerating ascites formation. It may also involve several organs such as brain, lung, heart, kidney and circulatory, blood, endocrine and digestive systems, resulting in a wide range of pathophysiological disorders in the organism.