Cirrhosis 1. Background Definition: End-stage fibrosis and…
Cirrhosis 1. Background Definition: End-stage fibrosis and nodular regeneration of the liver resulting from chronic liver injury, leading to distortion of hepatic architecture, portal hypertension, and hepatic insufficiency. Pathophysiology: Chronic hepatocellular injury (inflammation, necrosis) → fibrosis → nodular regeneration → disruption of hepatic blood flow and function. Portal hypertension develops from increased intrahepatic resistance. Etiologies: Chronic viral hepatitis: HBV, HCV (most common worldwide). Alcohol-associated liver disease. Nonalcoholic steatohepatitis (NASH). Autoimmune hepatitis, hemochromatosis, Wilson disease, α1-antitrypsin deficiency, biliary disease. Epidemiology: A leading cause of death worldwide. Increasing prevalence due to metabolic syndrome and NAFLD/NASH. 2. History Early (compensated): Often asymptomatic or mild nonspecific fatigue, weakness, or anorexia. Decompensated (advanced): Jaundice Ascites Peripheral edema Hepatic encephalopathy (confusion, asterixis) Gastrointestinal bleeding from esophageal or gastric varices Easy bruising or prolonged bleeding (coagulopathy) Other features: Pruritus (especially in cholestatic causes) Dark urine / pale stools Sexual dysfunction, gynecomastia, menstrual irregularities (endocrine effects). 3. Exam Findings General: Jaundice, muscle wasting, fatigue. Skin: Spider angiomas, palmar erythema, bruising, jaundice. Abdomen: Hepatomegaly (early) → small, shrunken liver (late). Ascites, shifting dullness. Splenomegaly (portal hypertension). Caput medusae (distended abdominal veins). Neurologic: Asterixis, confusion (hepatic encephalopathy). Endocrine: Gynecomastia, testicular atrophy. 4. Making the Diagnosis A. Laboratory Findings LFT pattern: AST > ALT (esp. alcoholic), elevated bilirubin, low albumin, prolonged PT/INR. Other labs: Thrombocytopenia (splenic sequestration), hyponatremia. Confirmatory: Elevated serum fibrosis markers or biopsy (definitive but not always required). B. Imaging Ultrasound: First-line; shows nodular liver, splenomegaly, ascites. Elastography: Noninvasive measurement of liver stiffness. CT/MRI: Evaluate for nodularity, portal hypertension, HCC. C. Assessing Severity Child-Pugh score: Grades liver function (bilirubin, albumin, INR, ascites, encephalopathy). MELD score: Predicts mortality and determines liver transplant priority. D. Complications to Screen For Hepatocellular carcinoma (HCC): Ultrasound ± AFP every 6 months. Varices: Screening endoscopy. Hepatorenal syndrome spontaneous bacterial peritonitis (SBP) (ascites with >250 PMNs/µL, fever, abdominal pain) 5. Management A. General Management Treat underlying cause: Abstain from alcohol. Antivirals for HBV/HCV. Weight loss for NASH. Chelation (Wilson disease) or phlebotomy (hemochromatosis). Avoid hepatotoxins (NSAIDs, acetaminophen >2g/day). Vaccinations: HAV, HBV, influenza, pneumococcal. B. Management of Complications Complication Management Ascites Sodium restriction, diuretics (spironolactone ± furosemide), paracentesis, avoid NSAIDs Spontaneous Bacterial Peritonitis (SBP) Empiric cefotaxime; prophylaxis with norfloxacin or TMP-SMX Variceal Bleeding Octreotide, endoscopic band ligation, nonselective beta-blockers (propranolol/nadolol) for prevention Hepatic Encephalopathy Lactulose ± rifaximin, avoid sedatives Hepatorenal Syndrome Albumin, vasoconstrictors (midodrine/octreotide), treat precipitating factors C. Definitive Therapy Liver transplantation: Only curative option for end-stage disease. Indicated by MELD score ≥15 or recurrent decompensation. Question A 58-year-old man with a history of alcohol-associated cirrhosis presents with increasing abdominal distension and confusion over the past week. His temperature is 100.6°F (38.1°C), blood pressure 102/64 mm Hg, and pulse 96/min. On examination, he has jaundice, ascites with shifting dullness, and mild asterixis. Paracentesis reveals: WBC count: 420 cells/µL (80% neutrophils) Protein: 0.8 g/dL Culture: Escherichia coli Which of the following is the most likely complication responsible for this presentation?