Decompensated chronic liver disease in the elderly, and the OPD approach to chronic liver disease

Definition. Cirrhosis is diffuse hepatic fibrosis with regenerative nodules. Decompensation is defined by the appearance of ascites, variceal bleeding, hepatic encephalopathy or jaundice (Baveno VII). Median survival is more than 12 years in compensated cirrhosis but about 2 years once decompensated.

Aetiology in the elderly. MASLD/MASH (now the commonest), alcohol-related liver disease, chronic hepatitis B and C, drug-induced injury, autoimmune hepatitis, primary biliary cholangitis, haemochromatosis, and cardiac (congestive) hepatopathy from right heart failure — a frequently missed cause in older patients.

Pathogenesis. Chronic injury activates hepatic stellate cells → fibrosis and nodules → increased intrahepatic resistance plus splanchnic vasodilatation → portal hypertension (HVPG >10 mmHg = clinically significant portal hypertension) → hyperdynamic circulation with effective arterial underfilling → activation of the renin-angiotensin-aldosterone and sympathetic systems → sodium and water retention producing ascites, dilutional hyponatraemia and hepatorenal syndrome. Systemic inflammation and bacterial translocation drive acute-on-chronic liver failure.

Precipitants of decompensation. Infection, especially spontaneous bacterial peritonitis; gastrointestinal bleeding; alcohol binge; dehydration or excessive diuresis; constipation; sedatives, opioids and NSAIDs; hepatotoxic drugs; portal vein thrombosis; hepatocellular carcinoma; and surgery.

Clinical features. Jaundice, ascites, oedema, spider naevi, palmar erythema, gynaecomastia, testicular atrophy, Dupuytren's contracture, caput medusae, splenomegaly, asterixis, and muscle wasting with sarcopenia. In the elderly, decompensation commonly presents as delirium, falls or functional decline rather than classical signs.

Approach to the OPD patient with chronic liver disease. History — quantified alcohol intake, all drugs including ayurvedic and over-the-counter preparations, transfusion, risk factors and family history. Examination for stigmata plus nutritional and frailty assessment. Baseline tests: LFT, PT/INR, albumin, complete blood count (thrombocytopenia suggests portal hypertension), renal function and electrolytes. Aetiological screen: HBsAg, anti-HCV, autoantibodies with IgG, ferritin and transferrin saturation, ceruloplasmin if under 55, alpha-1 antitrypsin, and lipid and glucose profile.

Staging and prognostic scoring. Child-Turcotte-Pugh score using bilirubin, albumin, INR, ascites and encephalopathy (A 5–6, B 7–9, C 10–15) and MELD, MELD-Na and MELD 3.0 for transplant prioritisation. Non-invasive fibrosis assessment with FIB-4, APRI and transient elastography — liver stiffness >15 kPa with platelets <150 × 109/L suggests clinically significant portal hypertension.

Management of the stable cirrhotic outpatient. Treat the cause — abstinence, antivirals, weight loss and metabolic control. Six-monthly ultrasound ± AFP for hepatocellular carcinoma surveillance. Screening endoscopy for varices (may be deferred if liver stiffness <20 kPa and platelets >150,000 — the Baveno "rule of five"); carvedilol as the preferred non-selective beta-blocker. Vaccinate against hepatitis A and B, influenza, pneumococcus and COVID-19; avoid NSAIDs, aminoglycosides and sedatives; salt restriction 5–6 g/day; and treat sarcopenia with 1.2–1.5 g/kg protein and a late evening snack.

Management of decompensation. Ascites — salt restriction, spironolactone with furosemide, large-volume paracentesis with albumin. Variceal bleeding — terlipressin, prophylactic antibiotics, band ligation, and early TIPS in high-risk patients. Encephalopathy — treat precipitants, lactulose plus rifaximin. Spontaneous bacterial peritonitis — cefotaxime plus albumin 1.5 g/kg on day 1 and 1 g/kg on day 3, followed by lifelong norfloxacin prophylaxis. Hepatorenal syndrome — terlipressin with albumin.

Complications and transplantation. Ascites, SBP, variceal bleeding, hepatic encephalopathy, hepatorenal and hepatopulmonary syndromes, portopulmonary hypertension, hepatocellular carcinoma, coagulopathy, malnutrition and sarcopenia, osteoporosis and cirrhotic cardiomyopathy. Refer for transplantation when MELD exceeds 15 or after the first decompensating event; carefully selected patients over 65–70 with good performance status and social support achieve about 80% five-year survival, so age alone is not a contraindication.

Baveno VII consensus (J Hepatol 2022;76:959) — introduced the concept of "recompensation" (resolution of ascites, encephalopathy and bleeding off diuretics and lactulose with sustained improvement in liver function after the cause is controlled), the "rule of five" for liver stiffness, and the principle that non-selective beta-blockers, preferably carvedilol, should be given to all patients with clinically significant portal hypertension to prevent the first decompensation (PREDESCI trial) — not merely to prevent variceal bleeding.

MASLD nomenclature and the first approved drug therapy. The 2023 multi-society Delphi consensus replaced NAFLD with MASLD, NASH with MASH, and introduced MetALD for combined metabolic and alcohol-related disease. Resmetirom (a thyroid hormone receptor-β agonist) received approval in 2024 as the first drug for MASH with F2–F3 fibrosis, and GLP-1 receptor agonists have shown histological benefit in MASH — a major shift from purely lifestyle-based management.