Cirrhosis is the end-stage of chronic liver disease characterized by irreversible replacement of normal hepatic parenchyma with fibrous scar tissue and regenerative nodules. Persistent hepatocyte injury (from alcohol, viral hepatitis, NAFLD, or autoimmune disease) triggers hepatic stellate cell activation, which produces excessive collagen deposition in the space of Disse. This fibrosis disrupts sinusoidal blood flow, increasing portal venous pressure above the normal 5-10 mmHg threshold. Portal hypertension (>12 mmHg) drives the formation of portosystemic collaterals (esophageal varices, caput medusae, hemorrhoids), splenomegaly with hypersplenism, and ascites through increased hydrostatic pressure combined with decreased oncotic pressure from impaired albumin synthesis. Hepatocyte loss also reduces synthesis of clotting factors (II, VII, IX, X), bile salts, and bilirubin conjugation, leading to coagulopathy and jaundice. Impaired ammonia metabolism by damaged hepatocytes leads to hyperammonemia and hepatic encephalopathy through glutamine accumulation in astrocytes causing cerebral edema. Ascites Assessment and Management is a clinical topic requiring comprehensive nursing knowledge and assessment skills. Understanding the pathophysiology, clinical presentation, diagnostic workup, and management principles enables practical nurses to provide safe, competent care within their scope of practice. Patients affected...