What are the pillars of cirrhosis management in the inpatient setting?

Pillars of Cirrhosis Management in the Inpatient Setting

The core pillars of inpatient cirrhosis management are: (1) immediate diagnostic paracentesis to rule out spontaneous bacterial peritonitis, (2) aggressive management of acute decompensation events (variceal bleeding, ascites, hepatic encephalopathy), (3) infection prevention and treatment, (4) avoidance of nephrotoxic agents, and (5) early identification of acute-on-chronic liver failure (ACLF) to guide ICU-level care decisions. 1

Immediate Diagnostic Evaluation

Mandatory Paracentesis

• Perform diagnostic paracentesis without delay in ALL cirrhotic patients with ascites on hospital admission, regardless of symptoms. 1
• Repeat paracentesis immediately if the patient develops fever, shock, gastrointestinal bleeding, worsening hepatic encephalopathy, abdominal pain, or deteriorating liver/renal function. 1
• Ascitic neutrophil count >250/mm³ confirms spontaneous bacterial peritonitis (SBP) and mandates immediate empirical antibiotics. 1, 2
• Inoculate blood culture bottles at bedside to guide antibiotic selection. 1

ACLF Assessment

• Use the CLIF-SOFA score to identify ACLF, defined as acute decompensation with organ failure(s) and 28-day mortality ≥15%. 1
• ACLF grading predicts outcomes better than MELD or Child-Pugh scores and should guide ICU admission decisions. 1
• Do not deny ICU admission based solely on the presence of cirrhosis—ACLF patients benefit from critical care. 1

Management of Acute Decompensation Events

Variceal Hemorrhage

• Initiate vasoactive drugs (terlipressin, octreotide, or somatostatin) immediately upon suspicion of variceal bleeding, even before endoscopic confirmation. 2
• Start prophylactic antibiotics immediately—use ceftriaxone 1g/24h for up to 7 days in decompensated cirrhosis or quinolone-resistant settings; use norfloxacin 400mg twice daily in other patients. 2
• Use restrictive transfusion strategy with hemoglobin threshold of 7 g/dL, targeting 7-9 g/dL. 2
• Perform endoscopic band ligation within 12 hours once hemodynamically stable. 2
• Consider erythromycin 250mg IV 30-120 minutes before endoscopy to improve visualization (unless QT prolongation present). 2
• Use TIPS as rescue therapy for persistent bleeding or early rebleeding. 2

Ascites Management

• For tense ascites (Grade 3), perform therapeutic paracentesis followed by sodium restriction (<5g/day) and diuretic therapy. 2
• Start spironolactone 50-100mg/day (maximum 400mg/day) as first-line diuretic. 2
• Add furosemide 20-40mg/day (maximum 160mg/day) if needed for rapid diuresis. 2
• Fluid restriction is NOT necessary unless serum sodium <120-125 mmol/L. 2
• Avoid bed rest—excessive immobility causes muscle atrophy; mobilize patients unless complicated by bleeding, encephalopathy, infection, or hypotension. 2

Spontaneous Bacterial Peritonitis

• Start immediate empirical antibiotics based on context (community-acquired vs healthcare-associated), severity, and local resistance patterns—cefotaxime is widely studied but tailor to local ecology. 1
• Consider repeat paracentesis at 48 hours if inadequate response or if secondary bacterial peritonitis suspected. 1
• All patients with gastrointestinal bleeding and ascites require prophylactic antibiotics to prevent SBP development. 1

Critical Medication Management

Nephrotoxic Agent Avoidance

• Immediately discontinue NSAIDs—they reduce urinary sodium excretion and convert diuretic-sensitive ascites to refractory ascites. 2
• Stop ACE inhibitors and angiotensin receptor blockers. 2
• Avoid aminoglycosides and other nephrotoxic antibiotics when alternatives exist. 1
• Avoid large-volume paracentesis without albumin replacement and hypotensive drugs during acute variceal hemorrhage. 2

Diabetes Management in Decompensated Cirrhosis

• Screen all decompensated cirrhotic patients for diabetes (30% prevalence). 3
• Use insulin as the ONLY evidence-based treatment—initiate in hospital at 10 units or 0.1-0.2 units/kg body weight. 3
• Target fasting glucose ≤180 mg/dL to avoid hyperglycemic complications while minimizing hypoglycemia risk. 3
• Metformin is absolutely contraindicated due to lactic acidosis risk; sulfonylureas are contraindicated due to severe hypoglycemia risk. 3
• Do NOT use HbA1c for monitoring—altered red blood cell turnover makes it inaccurate. 3
• Recognize that hypoglycemic symptoms may mimic hepatic encephalopathy, creating diagnostic confusion. 3

Infection Prevention and Broad-Spectrum Coverage

Antibiotic Strategy

• Maintain low threshold for broad-spectrum antibiotics in patients with signs of sepsis or worsening encephalopathy. 1
• Cover enterobacteria, staphylococcal, and streptococcal species based on unit ecology. 1
• Consider prophylactic antibiotics for patients requiring frequent paracenteses or with history of SBP. 2

Nutritional Support

• Provide at least 35 kcal/kg body weight/day to maintain adequate nutrition. 2, 3
• High-protein diet of 1.2-1.5 g/kg/day prevents sarcopenia. 2, 3
• Recommend late-evening snack to reduce overnight catabolism. 3
• Perform rapid nutritional screening assuming high malnutrition risk if BMI <18.5 kg/m² or Child-Pugh C. 2
• Assess sarcopenia using CT scan, anthropometry, DEXA, or bioelectrical impedance analysis. 2

Treatment of Underlying Etiology

• Address the causative factor as a cornerstone of management—this can potentially reverse early cirrhosis and prevent progression. 2, 4
• For alcoholic cirrhosis, complete alcohol cessation may lead to "re-compensation" and improved outcomes. 2, 4
• For viral hepatitis-related cirrhosis, initiate antiviral therapy if HBV DNA ≥2,000 IU/mL using entecavir or tenofovir as first-line agents. 2
• All patients with decompensated cirrhosis should receive HBV treatment regardless of HBV DNA level. 2
• Interferon-α is absolutely contraindicated in decompensated cirrhosis due to risk of infection and hepatic failure. 2

Common Pitfalls to Avoid

• Failing to perform diagnostic paracentesis on admission is the most dangerous omission—SBP can be asymptomatic and rapidly fatal. 1
• Continuing NSAIDs, ACE inhibitors, or ARBs precipitates renal failure and refractory ascites. 2
• Using metformin or sulfonylureas in decompensated cirrhosis causes life-threatening complications. 3
• Overaggressive glycemic control increases hypoglycemia risk, which mimics hepatic encephalopathy. 3
• Denying ICU admission based solely on cirrhosis diagnosis deprives ACLF patients of potentially life-saving interventions. 1
• Delaying vasoactive drugs until endoscopic confirmation of varices worsens bleeding outcomes. 2
• Excessive bed rest causes muscle atrophy and sarcopenia—mobilize patients when safe. 2

Monitoring and Early Intervention

• Monitor for hepatorenal syndrome development, which represents extreme hemodynamic alterations. 5, 6
• Vigilantly monitor glucose during insulin initiation, as hypoglycemia symptoms overlap with hepatic encephalopathy. 3
• Consider measured GFR using exogenous marker clearance when possible, as creatinine-based equations are inaccurate in cirrhosis. 3
• If measured GFR <30 mL/min, consider combined liver-kidney transplantation rather than liver transplantation alone. 3