We return to our 48-year-old patient: jaundiced, hypotensive, drowsy, and bleeding. In decompensated cirrhosis, every treatment targets a disrupted system — splanchnic vasodilation, portal hypertension, toxin accumulation, and renal hypoperfusion.

Although these patients look fluid overloaded, they are effectively hypovolaemic. Start with small aliquots of balanced crystalloid, avoiding 0.9% saline. In hepatorenal syndrome or tense ascites, 20% albumin is key — not just for volume expansion, but for circulatory and anti-inflammatory support.

Once volume is optimised, flow must be redirected. Terlipressin reverses splanchnic vasodilation, reduces portal pressure, and improves renal perfusion. If contraindicated, noradrenaline targeting a MAP ≥65 mmHg is an effective alternative.

Variceal bleeding reflects portal hypertension, not missing clotting factors. Use restrictive transfusion, correct platelets and fibrinogen selectively, start antibiotics early, and proceed to endoscopic banding once haemodynamically stable. Avoid blanket correction of INR — treat bleeding, not numbers.

Hepatic encephalopathy management focuses on reversing precipitants and reducing ammonia with lactulose and rifaximin, while protecting the airway in advanced grades. Infection screening is essential — SBP and sepsis worsen vasodilation and renal failure, with albumin improving outcomes.

Renal dysfunction is functional, not structural. Albumin plus vasoconstrictors can restore perfusion. Nutrition is critical: early enteral feeding with adequate protein supports recovery and ammonia clearance.

Bottom line: cirrhosis care works when physiology drives every decision.