![]() 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 authors declare that no patient data appear in this article.The spectrum of chronic liver disease involves liver inflammation, fibrosis and cirrhosis. The authors declare that they have followed the protocols of their work center on the publication of patient data. The authors declare that no experiments were performed on humans or animals for this study. Ethical disclosures Protection of human and animal subjects ![]() 4 ERCP treatment can be effective as a temporizing measure before surgery and can be definitive treatment for unsuitable surgical candidates. Surgery is the mainstay of therapy for Mirizzi syndrome. The Mirizzi syndrome is part of the differential diagnosis of obstructive jaundice and therefore the diagnostic approach usually begins with ultrasonography complemented by ERCP or magnetic resonance cholangiography.Ī useful classification system takes into account the presence and extent of a cholecystobiliary fistula, due to erosion of the anterior or lateral wall of the common bile duct by impacted stones. 1 The majority of the patients present the clinical triad of jaundice, fever, and right upper quadrant pain, showing in the laboratory evaluation elevations in the serum concentrations of alkaline phosphatase and bilirubin. The Mirizzi syndrome refers to common hepatic duct obstruction caused by an extrinsic compression from an impacted stone in the cystic duct or Hartmann's pouch of the gallbladder. 2) with subsequent patient referral to surgery (cholecystectomy plus closure of the fistula). Successful biliary decompression was performed by internal stenting ( Fig. 1), compatible with the diagnosis of Mirizzi syndrome. We performed an endoscopic retrograde cholangiopancreatography (ERCP) that clearly showed common hepatic duct compression by a large gallstone (20 mm) impacted in the cystic duct ( Fig. Abdominal ultrasound demonstrated a scleroatrophic gallbladder with cholelithiasis and an impacted large gallstone in the common bile duct with dilated common and intrahepatic bile ducts. Laboratory workup revealed leukocytosis (12.4 × 10 3 μL), elevated C-reactive protein (8.3 mg/dL) and cholestasis (bilirubin 5.4 mg/dL, alkaline phosphatase 893 U/L, gamma-glutamyl transferase 1143 U/L) with elevated liver enzymes (aspartate aminotransferase 231 U/L, alanine aminotransferase 178 U/L). Physical examination showed scleral icterus and right upper quadrant tenderness without inspiratory arrest at palpation (absent Murphy's sign). An 84-year-old woman presented with a 2-day history of jaundice, fever and abdominal pain.
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