Calculators and Tools for Liver Disease and Cirrhosis

MELD-Na (Model for End-Stage Liver Disease with sodium) uses bilirubin, INR, creatinine, and sodium to predict 90-day mortality in cirrhosis. UNOS uses MELD-Na for organ allocation — higher scores receive priority. Key thresholds: MELD <10 = low mortality risk; 10–19 = moderate; ≥20 = high risk; ≥25 = typically warrants urgent transplant evaluation. MELD 3.0 (2022) incorporates sex assigned at birth to reduce gender disparity in transplant access. Patients with MELD ≥15 have a survival benefit from transplantation over medical management.

Child-Pugh scores five variables (bilirubin, albumin, PT/INR, ascites, encephalopathy) on a 1–3 scale each: Class A (5–6) = well-compensated cirrhosis, 1-year survival ~100%; Class B (7–9) = significant dysfunction, 1-year survival ~80%; Class C (10–15) = decompensated, 1-year survival ~45%. Child-Pugh is still widely used for surgical risk stratification (Child-Pugh A can tolerate resection; C cannot) and TIPS candidacy. MELD is preferred for transplant listing because it is objective, continuously updated, and validated prospectively. Both tools complement each other in clinical decision-making.

FIB-4 = (Age × AST) ÷ (Platelets × √ALT). For patients aged 35–65: FIB-4 <1.30 = low probability of advanced fibrosis (F0–F1, NPV ~90%); 1.30–2.67 = indeterminate (requires vibration-controlled transient elastography or liver biopsy); >2.67 = high probability of advanced fibrosis (F3–F4, PPV ~80%). AASLD 2023 recommends FIB-4 as the first-line non-invasive fibrosis assessment in MASLD/NAFLD (replacing liver biopsy for initial evaluation). Repeat annually in those with indeterminate FIB-4.

AST/ALT >2:1 is characteristic of alcoholic liver disease — alcohol impairs pyridoxal phosphate (vitamin B6) metabolism, which ALT synthesis depends on more than AST. A ratio >3:1 strongly suggests alcohol as the etiology. In viral hepatitis, NASH/MAFLD, and most non-alcoholic liver diseases, ALT typically exceeds AST (ratio <1). In advanced cirrhosis of any cause, the ratio may rise as hepatocyte loss reduces both enzymes proportionally. Always interpret transaminase ratios with absolute values — mildly elevated transaminases with a high ratio may still represent non-alcoholic disease.

Decompensated cirrhosis is defined by the development of: ascites (most common), variceal hemorrhage, hepatic encephalopathy, or jaundice (bilirubin >2.5 mg/dL) in a patient with previously compensated cirrhosis. Each episode of decompensation increases 1-year mortality significantly. Acute-on-chronic liver failure (ACLF) — acute decompensation with organ failure — carries 28-day mortality of 30–90% depending on ACLF grade. Management priorities: diuresis for ascites (spironolactone + furosemide), beta-blockers and banding for variceal prophylaxis, lactulose/rifaximin for encephalopathy, and urgent transplant evaluation.

Refer to hepatology for: FIB-4 >2.67 (high fibrosis risk), persistent transaminase elevation >6 months without identified cause, ALT or AST >3× ULN, suspected autoimmune hepatitis (positive ANA/ASMA), suspected hereditary hemochromatosis or Wilson's disease, suspected alcohol-related liver disease with markers of significant disease, HBsAg-positive with detectable HBV DNA, HCV with treatment eligibility, cirrhosis of any cause, or portal hypertension complications. Early hepatology involvement improves fibrosis staging accuracy, treatment initiation, and transplant preparation timing.