Management of Early (Compensated) Cirrhosis
The cornerstone of managing early compensated cirrhosis is aggressive treatment of the underlying etiology—which can potentially reverse early cirrhosis—combined with surveillance endoscopy for varices, strict avoidance of NSAIDs, and monitoring for decompensation. 1
Primary Treatment Strategy: Address the Underlying Cause
Treating the underlying liver disease is the single most important intervention in compensated cirrhosis because early cirrhosis with thin fibrous septa is potentially reversible. 2, 1
For viral hepatitis B: Initiate antiviral therapy with entecavir or tenofovir as first-line agents if HBV DNA ≥2,000 IU/mL, regardless of ALT levels, due to their potent antiviral efficacy and high genetic barrier to resistance. 2, 1 Long-term treatment is required. 2
For alcoholic cirrhosis: Complete and permanent cessation of alcohol is mandatory; this may lead to "re-compensation" and excellent long-term outcomes in some patients. 1
For viral hepatitis C: Direct-acting antivirals improve liver function and reduce portal hypertension. 1
For autoimmune hepatitis: Immunosuppressive therapy shows beneficial effects even in decompensated disease. 1
Correct aggravating conditions: Eliminate obesity, ongoing alcohol use, and drug-induced liver injury, as these measures can independently decrease portal pressure and reduce the risk of decompensation. 2
Varices Surveillance and Prophylaxis
All patients with compensated cirrhosis require screening endoscopy to assess for varices. 1
If no varices are present: Repeat endoscopy every 2 years if ongoing liver injury (e.g., obesity, alcohol use) or every 3 years if liver injury is quiescent (e.g., after viral elimination, alcohol abstinence). 2
If small varices are present: Repeat endoscopy every year with ongoing liver injury or every 2 years if liver injury is quiescent. 2
If decompensation develops: Perform repeat endoscopy immediately when this occurs. 2
Consider non-selective beta-blockers for prevention of variceal bleeding, though use with caution if severe or refractory ascites develops. 3
Hepatocellular Carcinoma Screening
Screen all patients with compensated cirrhosis for hepatocellular carcinoma with ultrasound every 6 months. 4, 3, 5
Medications to Strictly Avoid
NSAIDs are absolutely contraindicated in cirrhosis because they reduce urinary sodium excretion, precipitate renal dysfunction, and can convert diuretic-sensitive ascites to refractory ascites. 1
Discontinue ACE inhibitors and angiotensin receptor blockers as they can worsen renal function. 1
Avoid hepatotoxic medications and review all current medications for potential liver injury. 4
Monitoring and Laboratory Surveillance
Perform clinical assessment with laboratory tests and calculate Child-Pugh and MELD scores every 6 months. 5
Monitor complete blood count, comprehensive metabolic panel including liver function tests, electrolytes, and renal function. 4
Watch for signs of decompensation: ascites, hepatic encephalopathy, variceal bleeding, or jaundice. 4, 6
Nutritional and Lifestyle Management
Restrict dietary sodium to less than 5 g/day to help prevent ascites development. 1
Perform rapid nutritional screening in all patients, assuming high risk for malnutrition if BMI <18.5 kg/m² or Child-Pugh C. 1
Assess for sarcopenia using CT scan, anthropometry, DEXA, or bioelectrical impedance analysis. 1
Evaluate muscle function with handgrip strength and/or short physical performance battery. 1
Avoid excessive bed rest as it may cause muscle atrophy; patients can be managed outpatient unless complicated by bleeding, encephalopathy, infection, hypotension, or liver cancer. 1
Patient Education
Educate patients about disease management, including salt restriction, medication adherence, and recognition of warning signs such as increasing abdominal girth, confusion, or gastrointestinal bleeding. 1
When to Refer to Gastroenterology
Refer immediately to gastroenterology when any decompensation event occurs (ascites, variceal bleeding, hepatic encephalopathy, or jaundice). 1
Refer for evaluation of liver transplantation if MELD score reaches 15 or greater. 5
Refer if refractory ascites develops (requiring paracentesis more often than every 2 weeks). 1
Special Considerations for Mild Portal Hypertension (HVPG 5-10 mm Hg)
In patients with HVPG >5 but <10 mm Hg (mild portal hypertension), the mainstay of therapy is elimination of the etiologic agent rather than drugs acting on portal flow. 2
Non-selective beta-blockers are mostly ineffective at this stage because the hyperdynamic circulatory state is not fully developed. 2
These patients have a very low risk of clinical decompensation in the following 5 years. 2
Common Pitfalls to Avoid
Do not routinely measure HVPG outside clinical trials, as monitoring changes in HVPG should not be performed routinely. 2
Do not use noninvasive tests to monitor changes in portal pressure, as they do not correlate well with changes in HVPG. 2
Do not delay treatment of the underlying etiology, as the management paradigm has shifted from merely treating complications to preventing disease progression while patients remain compensated. 1
Recognize that median survival drops from >12 years in compensated cirrhosis to approximately 2 years after first decompensation, making prevention of that first decompensation event critical. 6