Cirrhosis Decompensation: 9 Essential Management Rules

Calculate the Child-Pugh score and the MELD-Na score on admission and at every subsequent decompensation event. These two scores guide transplant referral, antibiotic prophylaxis decisions, and the safety of further interventions.

Perform diagnostic paracentesis in every patient admitted with ascites or with worsening hepatic function, even if the abdomen feels unchanged. Sub-clinical infection is the trigger in roughly a third of admissions.

Refer for liver transplantation evaluation at the first decompensation event regardless of MELD. Listing decisions are made later by the transplant team, but the conversation has to start early.

Stop nephrotoxins on admission: NSAIDs, aminoglycosides, IV contrast where avoidable, and proton pump inhibitors prescribed without indication. These accelerate hepatorenal physiology faster than any other intervention worsens it.

Start spironolactone 100 mg and furosemide 40 mg orally once daily together in patients with moderate ascites. Maintain the 100:40 mg ratio as you titrate — this preserves normokalaemia and matches the aldosterone-driven physiology.

Titrate every 3–5 days in steps of 100 mg spironolactone and 40 mg furosemide, up to maxima of 400 mg and 160 mg respectively. Aim for weight loss of 0.5 kg per day without peripheral oedema and 1 kg per day with peripheral oedema.

Counsel patients on sodium restriction of less than 88 mmol (2 g) per day. Diuretics will fail unintentionally if dietary sodium remains uncontrolled.

Stop diuretics if serum sodium falls below 120 mmol/L, creatinine rises above 2.0 mg/dL (180 µmol/L), encephalopathy develops, or potassium falls below 3.0 or rises above 6.0 mmol/L.

Switch to amiloride 10–40 mg daily for spironolactone-related painful gynaecomastia. Eplerenone is an alternative but is more expensive and offers no efficacy advantage.

Perform large-volume paracentesis as first-line therapy for tense or refractory ascites. Single-session removal of more than 5 litres requires intravenous albumin at 6–8 g per litre removed to prevent post-paracentesis circulatory dysfunction.

Send ascitic fluid for cell count and culture with every paracentesis. A polymorphonuclear count of 250 cells/mm³ or higher confirms spontaneous bacterial peritonitis and mandates empirical third-generation cephalosporin therapy.

Initiate albumin 1.5 g/kg at diagnosis and 1.0 g/kg at day 3 in patients with SBP and either creatinine above 1.0 mg/dL, BUN above 30 mg/dL, or bilirubin above 4 mg/dL.

Prescribe long-term oral antibiotic prophylaxis (norfloxacin 400 mg daily or ciprofloxacin 500 mg daily) for survivors of a first SBP episode and for selected patients with low-protein ascites and advanced liver disease.

Identify and treat the precipitant in every episode of overt encephalopathy. The differential includes infection (especially SBP and UTI), gastrointestinal bleeding, electrolyte disturbance, dehydration from over-diuresis, constipation, recent benzodiazepine or opioid use, and acute kidney injury.

Start lactulose 25 mL orally every 1–2 hours until the first bowel movement, then titrate to a target of two to three soft bowel movements per day. Stool frequency — not blood ammonia — is the dosing endpoint.

Deliver lactulose by nasogastric tube or as a retention enema (300 mL lactulose in 700 mL water, held for 30–60 minutes) in patients who cannot safely swallow.

Add rifaximin 550 mg twice daily to lactulose for secondary prophylaxis after a second overt encephalopathy episode, or earlier if lactulose alone fails to maintain remission. Continue indefinitely unless the trigger is permanently reversible.

Do not restrict protein intake. Target 1.2–1.5 g/kg/day to prevent sarcopenia, which itself predisposes to encephalopathy. Vegetable and dairy protein are better tolerated than animal protein in patients prone to recurrent episodes.

Avoid empirical ammonia level testing as a diagnostic or monitoring tool. Diagnosis and response are clinical — normal ammonia does not exclude encephalopathy and elevated ammonia does not confirm it.

Apply Baveno VII non-invasive criteria to defer screening endoscopy in compensated cirrhosis: liver stiffness below 20 kPa and platelets above 150 × 10&sup9;/L identifies patients at very low risk of high-risk varices and avoids unnecessary upper endoscopy.

Prescribe a non-selective beta-blocker (NSBB) for any patient with clinically significant portal hypertension, even before varices appear. Carvedilol 6.25–12.5 mg daily is now preferred over propranolol for most patients because it lowers portal pressure more reliably.

Perform prophylactic endoscopic variceal ligation (EVL) for medium or large varices in patients who cannot tolerate or are intolerant to NSBB. Band every 2–4 weeks until varices are eradicated, then surveillance EGD at 3–6 months and yearly thereafter.

Do not combine NSBB and prophylactic banding routinely for primary prophylaxis — the additive benefit is small and the complication rate of combined therapy is higher. Reserve combined therapy for secondary prophylaxis after a first bleed.

Initiate vasoactive therapy (terlipressin, octreotide, or somatostatin) at the moment variceal bleeding is suspected — before endoscopy. Continue for 2–5 days.

Prescribe ceftriaxone 1 g IV daily for up to 7 days at admission for any cirrhotic patient with upper GI bleeding, irrespective of ascites status. Antibiotic prophylaxis reduces mortality, rebleeding, and infection.

Perform endoscopic band ligation within 12 hours of presentation in haemodynamically stable patients. Sclerotherapy is reserved for cases where banding is technically impossible.

Consider pre-emptive TIPS within 72 hours of admission in Child-Pugh class C (10–13 points) or class B with active bleeding at endoscopy. Early TIPS reduces rebleeding and mortality compared with continued medical therapy.

Transfuse to a haemoglobin target of 7–8 g/dL using a restrictive strategy. Over-transfusion raises portal pressure and increases rebleeding risk.

After a first variceal bleed, prescribe combined NSBB plus serial banding to eradication as secondary prophylaxis. This combination outperforms either modality alone.