![]() As chronic injury promotes persistent fibrous formation, fibrosis can expand to bridge across lobules, between portal regions, and/or between portal regions and central veins. Initially, liver fibrosis remains limited to periportal or perivenular regions. 3 This results in islands of regenerative hepatocytes surrounded by fibrous tissue. 4, 5 The new thickened and congested space of Disse separates hepatocytes from sinusoidal blood flow. 3–5 This abnormal healing process is further driven by inflammatory cytokines and reactive oxygen species. 2 This leads to activation of peri-sinusoidal hepatic stellate cells, which transform into myofibroblasts that begin depositing an excess of fibrous extracellular matrix into the space of Disse and portal tracts. The process of liver fibrosis begins with hepatocytes undergoing cell death in response to liver injury. 1 In this review, we discuss the pathophysiology, clinical features and management of common complications of liver cirrhosis based on literature review and the current clinical practice guidelines of the AASLD. ![]() The transition from compensated to decompensated cirrhosis occurs at a rate of 5% per year and can be accompanied by a reduction in median survival time from 12 years to 2 years. Decompensated liver cirrhosis is characterized by complications of portal hypertension including ascites, spontaneous bacterial peritonitis, hepatic encephalopathy and variceal bleeding. ![]() Patients with compensated liver cirrhosis are often asymptomatic and possess indolent disease. Once the diagnosis of liver cirrhosis is established, it is important to distinguish between compensated and decompensated disease. While fibrosis was previously viewed as an irreversible disease process, further understanding of pathophysiology and risk factors shows that liver regeneration and regression of fibrosis is possible. The spectrum of chronic liver disease involves liver inflammation, fibrosis and cirrhosis. ![]()
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