Abstract

Chronic liver disease and decompensated cirrhosis are the major causes of morbidity and mortality in the world. According to current data, deaths due to liver cirrhosis constitute 2.4% of the total deaths worldwide. Cirrhosis is characterized by hepatocellular damage that leads to fibrosis and regenerative nodules in the liver. The most common causes of cirrhosis include alcohol consumption, hepatitis C, hepatitis B, and non-alcoholic fatty liver disease. Dysbiosis and intestinal bacterial overgrowth play a role in the development of complications of cirrhosis through translocation. In liver cirrhosis, ascites, gastrointestinal variceal bleeding, spontaneous bacterial peritonitis infection, hepatic encephalopathy, hepatorenal syndrome, hepatocelluler carcinoma are the most common complications. In addition, there are refractory ascites, hyponatremia, acute on-chronic liver failure, relative adrenal insufficiency, cirrhotic cardiomyopathy, hepatopulmonary syndrome and portopulmonary hypertension. In the primary prophylaxis of variceal bleeding, non-selective beta blockers or endoscopic variceal ligation are recommended for medium and large variceal veins. In current medical treatment, vasoactive agents, antibiotics, blood transfusion, endoscopic band ligation are the standard approach in the treatment of acute variceal bleeding. Sodium-restricted diet, diuretics and large-volume paracentesis are recommended in the management of ascites. In the treatment of hepatic encephalopathy, lactulose, branched chain amino acids, rifaximin and L-ornithine L-aspartate can be used. New therapeutic approaches such as ornithine phenyl acetate spherical carbon and fecal microbiota transplantation have shown beneficial effects on hepatic encephalopathy symptoms. In addition to their antioxidative, anti-proliferative and anti-inflammatory properties, statins have been shown to reduce the risk of decompensation and death by reducing portal pressure in compensated cirrhosis. In the treatment of liver failure, some artificial liver devices such as molecular adsorbent recirculating system, the single albumin dialysis system, fractionated plasma separation and adsorption are used until transplantation or regeneration. The purpose of this chapter is to review the most up-to-date information on liver cirrhosis and to explain the complications assessment, current management and potential treatment strategies in decompensated cirrhosis.

Highlights

  • Decompensated cirrhosis is characterized by the development of complications related to portal hypertension (PHT) such as variceal bleeding, ascites, spontaneous bacterial peritonitis (SBP), hepatic encephalopathy (HE), hepatorenal syndrome (HRS), or hepatopulmunary syndrome (HPS) in the presence of cirrhosis [1]

  • The second recommended method is the combination of diuretic agents and it is recommended to increase the dose of spironolactone and furosemide gradually to 400 mg and 160 mg/d [17]

  • It is recommended that the dose of diuretic be reduced to the lowest effective dose after the treatment goal is reached [19]

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Summary

Introduction

Decompensated cirrhosis is characterized by the development of complications related to portal hypertension (PHT) such as variceal bleeding, ascites, spontaneous bacterial peritonitis (SBP), hepatic encephalopathy (HE), hepatorenal syndrome (HRS), or hepatopulmunary syndrome (HPS) in the presence of cirrhosis [1]. The incidence of cirrhosis is 26 per 100,000 in Europe, and the incidence in Asia ranges from 16.5 per 100,000 in East Asia to 23.6 per 100,000 in Southeast Asia [3] It causes 1.2 million deaths due to complications of cirrhosis and 790.000 deaths due to liver cancer, accounting for 3.5% of all deaths worldwide [4]. Hepatitis B (HBV) incidence and complications decrease with HBV vaccination and antiviral treatment programs. Treatment strategy in decompensated cirrhosis patients should be aimed at preventing the progression of cirrhosis before complications occur. The ultimate treatment for decompensated cirrhosis should be aimed at regressing fibrosis by suppressing inflammation, normalizing liver cell number and function by regulating portal and arterial circulation, and restoring liver integrity [9]

Ascites
Classification of ascites
Uncomplicated ascites treatment
Findings
Refractory ascites
Gastrointestinal bleeding
Non-bleeding variceal treatment
Treatment in acute variceal bleeding
Hepatic encephalopathy
Hepatopulmonary syndrome
Acute on chronic liver failure
Artificial liver support systems
Conclusions
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