Cirrhosis

Cirrhosis is permanent scarring and regenerative nodule formation that distort the liver’s normal architecture. It creates two related clinical problems: blood cannot pass easily through the liver, and the remaining hepatocytes cannot perform synthesis, metabolism and detoxification normally. Portal hypertension develops through two additive mechanisms. Fibrosis, nodules and dysfunctional sinusoidal endothelium increase resistance inside the liver. At the same time, splanchnic arterioles dilate, sending more blood into the portal circulation and creating a hyperdynamic circulation. The result is increasing portal pressure, collateral veins and reduced effective arterial filling. [1] Once portal hypertension becomes clinically significant, usually at a hepatic venous pressure gradient (HVPG) of at least 10 mmHg, the patient is at risk for varices, ascites and other decompensating events. An HVPG above 12 mmHg is associated with the pressure range in which variceal bleeding becomes more likely. [1] Ascites is not simply “too much fluid.” Splanchnic vasodilation makes the arterial circulation appear underfilled even when the total body water is high. The renin-angiotensin-aldosterone system, sympathetic nervous system and antidiuretic hormone then retain sodium and water. This is why sodium...