Improving Survival in Patients with Decompensated Cirrhosis

Abstract

Liver cirrhosis is defined as development of regenerative nodules surrounded by fibrous septa in response to chronic liver injury. This leads to vascular remodeling and giving rise to portal hypertension and end stage liver disease. Liver transplantation is the only treatment which improves both longevity and quality of life in patients with decompensated liver cirrhosis. However every patient with decompensated liver cirrhosis is not eligible for transplantation and it is not available for majority of the patients. Our current understanding of natural history, pathophysiology and treatment of complication has resulted in improved management quality of life and life expectancy in patients with decompensated liver cirrhosis. Median survival of patients with compensated cirrhosis is 12 years while that of decompensated patients is reduced to 2 years. Approximately 5 to 7% of the patients change from compensated stage to decompensated stage. Portal hypertension (PH) is a universal consequence of cirrhosis responsible for most of the complications like esophagogastric varices, variceal bleeding, ascites, spontaneous bacterial peritonitis, hepatorenal syndrome and hepatic encephalopathy. PH in cirrhosis is defined by hepatic venous pressure gradient (HVPG) more than 5mm of mercury. HVPG is indirect measure of portal pressure. Now it is clear that HVPG more than 10 is significant PH above which the complications like variceal bleed and ascites develop. Currently proposed classification of cirrhosis is based on the degree of PH and associated clinical features. Development of ascites, variceal bleed and hepatic encephalopathy is considered to be decompensated cirrhosis. PH results from increase in the intrahepatic resistance which has dynamic and fixed components and it is coupled with increase in the portal blood flow. Therapeutic interventions which can reduce the HVPG like non selective beta blockers and Transjugular intrahepatic porta systemic shunt (TIPS) can be helpful in combating complications of cirrhosis. And they have been shown to improve survival. Bacterial infection is common in cirrhosis with one month mortality of 30%. Oral prophylactic antibiotics or bowel decontamination have shown to improve long term outcome in patients with decompensated cirrhosis. Malnutrition is common in all patients with cirrhosis. Now it is clear there is no need of restricting the proteins in these patients. In fact nutritional therapy can improve survival, reduce the rate of infections, stay in ICU and hospital, and reduce post operative complications. Screening for hepatocellular carcinoma (HCC) can pick up very early disease and survival can be improved in these patients by offering curative treatment. Therapeutic modalities can reverse the cirrhosis. These modalities according to the etiology are (1) abstinence for alcoholic cirrhosis, (2) antiviral therapy for hepatitis B, (3) immunosuppression for autoimmune hepatitis, (4) relieving biliary obstruction in patients with secondary biliary cirrhosis, (5) antiviral therapy for hepatitis C and (6) relieving obstruction in patients with budd Chiari syndrome. Future therapies like antifibortic, antiangiogenic and anti coagulants may have potentials reducing fibrosis, reversing cirrhosis. Stem cell therapy may be helpful in patients with liver cirrhosis.