Pathophysiology
Clinical meaning
Cirrhosis represents the end-stage of chronic hepatic injury where iterative cycles of hepatocyte necrosis, inflammation, and regeneration produce progressive fibrosis that distorts the normal hepatic lobular architecture into regenerative nodules surrounded by fibrous septa. This architectural distortion has two fundamental pathophysiological consequences: loss of functional hepatocyte mass (causing synthetic failure) and increased intrahepatic vascular resistance (causing portal hypertension). The Child-Pugh score quantifies hepatic reserve using five clinical variables: serum albumin (reflecting synthetic capacity), total bilirubin (reflecting conjugation and excretion), INR (reflecting coagulation factor synthesis โ factor VII with its 6-hour half-life declines earliest), ascites (reflecting portal hypertension and sodium/water retention), and hepatic encephalopathy (reflecting impaired ammonia detoxification). Each variable is scored 1-3 points, yielding classes A (5-6, well-compensated), B (7-9, significant functional compromise), and C (10-15, decompensated). The MELD score uses a mathematical formula incorporating serum creatinine, total bilirubin, and INR to predict 90-day mortality and is the primary system for liver transplant organ allocation. MELD-Na adds serum sodium because hyponatremia (dilutional, from non-osmotic ADH release in cirrhosis) independently predicts mortality. Portal hypertension (hepatic venous pressure gradient >5 mmHg) becomes...