Cirrhosis, Portal Hypertension and Ascites

A patient with cirrhosis may arrive with a distended abdomen, mild confusion or ankle oedema, but the most dangerous change may be less visible: falling renal perfusion, infection in ascitic fluid or bleeding from a portal-systemic collateral. These findings are connected rather than separate complications. This lesson uses that connection to guide assessment and priority decisions. Portal hypertension produces varices and splenic enlargement; splanchnic vasodilation makes the arterial circulation feel underfilled, so the kidneys retain sodium and water and ascites develops. As cirrhosis decompensates, ascites, variceal bleeding, hepatic encephalopathy and kidney injury can accelerate one another. The adult thresholds and treatment regimens below are the usual examination framework. Children require additional attention to the cause of portal hypertension, weight-based emergency treatment and developmental communication. A jaundiced infant is not simply a small adult with cirrhosis: persistent jaundice may signal biliary atresia, for which delay changes the chance of avoiding transplantation.