Chapter 27: Liver Diseases – Hepatitis & Cirrhosis Therapy

Cirrhosis, defined by the replacement of functional liver cells with nonfunctional scar tissue (fibrosis), is increasingly attributed to metabolic syndrome and alcohol abuse, though Hepatitis C remains a significant cause in older demographics. The progression of cirrhosis leads to critical complications stemming from elevated vascular resistance within the portal vein, known as portal hypertension (PH), which triggers systemic vasodilation and the activation of the RAAS system. Key complications include gastroesophageal varices, which are prophylacticly treated with nonselective beta blockers (NSBBs) such as propranolol, nadolol, or carvedilol to reduce portal pressure, or acutely managed with vasoactive therapy like octreotide during hemorrhage. Ascites, the pathological accumulation of fluid in the peritoneal space, is typically diagnosed using the Serum-Ascites Albumin Gradient (SAAG). First-line management for ascites involves diuretic therapy, with spironolactone preferred due to its targeting of underlying hyperaldosteronism, often in combination with furosemide, requiring careful monitoring to prevent kidney injury or electrolyte imbalance. A major risk for patients with ascites is spontaneous bacterial peritonitis (SBP), diagnosed by an ascitic fluid polymorphonuclear cell count of 250 cells/mm³ or more, which requires prompt empiric intravenous treatment with third-generation cephalosporins (e.g., ceftriaxone or cefotaxime). Hepatorenal syndrome (HRS) is a late-stage diagnosis of exclusion, characterized by profound kidney injury due to reduced blood flow, managed with combination therapy of albumin, octreotide, and midodrine to increase mean arterial pressure. Lastly, hepatic encephalopathy (HE), a neuropsychiatric complication caused by ammonia accumulation, is treated with lactulose to facilitate ammonia clearance, titrated to achieve two to three soft bowel movements daily, with the antibiotic rifaximin used as an adjunctive agent for refractory cases. The chapter also addresses viral hepatitis treatment, emphasizing that all HCV infections require treatment using Direct Acting Antivirals (DAAs) (e.g., combinations of NS3/4A, NS5A, and NS5B inhibitors), while chronic HBV is treated with nucleos(t)ide inhibitors (ETV, TAF, or TDF), often requiring indefinite therapy in cirrhotic patients.