Cirrhosis, Portal Hypertension and Ascites

Cirrhosis creates two linked clinical problems: increased resistance to portal flow and reduced hepatocyte function. The first produces ascites, varices, and splenic sequestration; the second produces hypoalbuminemia, coagulopathy, jaundice, impaired detoxification, and encephalopathy. At the bedside, the most urgent problem is not always the most visible one. New gastrointestinal bleeding, altered mentation, hypotension, infection, or declining urine output can outrank routine management of abdominal distention. Chronic cirrhosis must be distinguished from acute liver failure (ALF). In an adult, ALF means acute liver injury with INR ≥1.5 and any degree of hepatic encephalopathy developing within roughly 26 weeks in a person without pre-existing cirrhosis or chronic liver disease. In a child, encephalopathy is not required: acute liver injury plus vitamin K–unresponsive coagulopathy meets pediatric criteria at INR ≥2.0 when encephalopathy is absent or at INR ≥1.5 when it is present. Suspected ALF requires ICU admission and early transplant-center contact rather than watchful waiting for neurologic deterioration. This lesson focuses on chronic cirrhosis, portal hypertension, and ascites; recognizing the distinction prevents chronic-disease routines from delaying an emergency transplant evaluation.