5-Year Survival Rate in Acute Decompensation in Cirrhosis Patient with Hepatitis

In decompensated cirrhosis due to hepatitis, the 5-year survival rate is 30% with continued drinking and 60% with abstinence from alcohol. 1

Survival Rates Based on Hepatitis Etiology and Decompensation Status

For patients with decompensated alcoholic liver cirrhosis, the 5-year survival rate is approximately 30% if drinking continues and 60% if abstinence is maintained 1
The 1-year mortality rate is 17% for patients with cirrhosis without complications, increasing to 20-64% once complications develop 1
When complications are present, the 5-year mortality rate approaches 58-85% 1
The median survival time for decompensated alcoholic liver cirrhosis is 61 months 1

For patients with decompensated cirrhosis due to chronic HBV infection, the 5-year survival rate is only 14-35% under conventional standard of care 2
In compensated cirrhosis, the survival is much better at 84% at 5 years and 68% at 10 years 1
Patients with compensated cirrhosis who are HBeAg-negative have significantly better 5-year survival (97%) than those who are HBeAg-positive (72%) 1

Decompensation may manifest with jaundice, ascites, variceal bleeding, or hepatic encephalopathy 2
The first decompensation event is a significant turning point, with median survival dropping from 10-12 years to only 1-2 years 3
At the time of diagnosis of alcoholic liver cirrhosis, it is accompanied by no complications in 24% of patients, ascites alone in 55%, variceal bleeding alone in 6%, combined ascites and variceal bleeding in 4%, and hepatic encephalopathy in 11% 1

The median survival time following onset of hepatic encephalopathy is 0.92 years and for ascites is 1.1 years 4
Among people with ascites, the annual incidence of spontaneous bacterial peritonitis is 11% and of hepatorenal syndrome is 8% 4
Hepatorenal syndrome is associated with a median survival of less than 2 weeks 4
80% of patients who continue drinking even in the presence of ascites will die within 7 months 1

According to multivariate analysis, a MELD score of >20 is the most robust predictor of mortality, with 58 times higher risk 5
Other predictors of poor survival include HBV DNA >7.4 log copies/ml, serum creatinine >1.2mg/dl, total bilirubin >3.7mg/dl, platelets count ≤0.75, and Child-Turcotte-Pugh score >10 5

Oral antiviral agents are effective in restoring liver function and improving survival in patients with decompensated cirrhosis, especially if therapy is initiated early enough 2
Post-treatment response with tenofovir for 24 months significantly improved hepatic functions and reversed decompensation in a majority of subjects 5
Clearance of HBeAg, whether spontaneous or after antiviral therapy, reduces the risk of hepatic decompensation and improves survival 1

Carvedilol or propranolol to prevent variceal bleeding 4
In a 3-year randomized clinical trial, nonselective β-blockers reduced the risk of decompensation or death compared with placebo (16% vs 27%) 4
Lactulose for hepatic encephalopathy, which was associated with reduced mortality relative to placebo (8.5% vs 14%) in randomized trials 4
Combination aldosterone antagonists and loop diuretics for ascites, which were more likely to resolve ascites (76% vs 56%) with lower rates of hyperkalemia (4% vs 18%) 4
Terlipressin for hepatorenal syndrome, which improved the rate of reversal from 39% to 18% 4

Treating the underlying cause can lead to cirrhosis regression 3
Addressing cofactors such as obesity, diabetes, dyslipidemia, and alcoholism may benefit patients 3
Management of precipitating factors such as infection, viral hepatitis, and hepatotoxic drugs is crucial 3

Approximately 1% to 4% of patients with cirrhosis develop hepatocellular carcinoma each year 4
HCC is associated with a 5-year survival of approximately 20% 4
The incidence of HCC is 7.2-16.0% in alcoholic liver cirrhosis, with a 1% annual risk in patients with decompensated alcoholic liver cirrhosis 1
Risk factors for HCC in patients with chronic HBV infection include male gender, family history of HCC, older age, presence of cirrhosis, and coinfection with hepatitis C virus 1