Abstract
Cirrhosis is the end-stage manifestation of every chronic progressive liver disease. It is a diffuse process characterized by loss of hepatic parenchymna, formation of fibrous septa and regeneration nodules resulting in the distortion of the normal architecture and vascular anatomy. Approximately 40–60% of cases of liver cirrhosis in Europe and North America are due to alcohol abuse and nonalcoholic fatty liver disease, while 25–30% result from chronic viral hepatitis. The modern paradigm considers cirrhosis as a dynamic and potentially reversible disease. It consists of two different entities, compensated and decompensated cirrhosis, each with a distinct prognosis and different predictors of survival. Ascitis is the most common complication of cirrhosis, and approximately 60% of patients with compensated cirrhosis develop ascitis within 10 years during the course of their disease. Within the compensated stage, patients can be subclassified into those without varices (stage 1) and those with (stage 2). The threshold pressure of hepatic venous pressure gradient (HVPG) that predicts development of varices and decompensation is 10mm Hg (clinically significant portal hypertension). In decompensated stage, HVPG retains prognostic value but other parameters of liver insufficiency such as the MELD score are more predictive of death.
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