Acutely decompensated cirrhosis and acute-on-chronic liver failure are conditions observed in patients with known chronic liver disease who have acute decompensation.
Acutely decompensated cirrhosis, refers to the development of ascites, encephalopathy, gastrointestinal hemorrhage, or any combination of these disorders in patients with cirrhosis.
Acute-on-chronic liver failure syndrome associated with a high risk of short-term death in patients with acutely decompensated cirrhosis.
Acute-on-chronic liver failure syndrome
occurs with systemic inflammation, proinflammatory precipitating events and is associated with single- or multiple-organ failure.
Acute-on-chronic liver failure is prevalent among patients with alcoholic cirrhosis.
Acute-on-chronic liver failure among patients nonelectively hospitalized for acutely decompensated cirrhosis, the prevalence of acute-on-chronic liver failure was 10%, and the 30-day mortality rate was 41% vs. 7% mortality in the absence of the syndrome).
A spike in hepatitis B virus infection is a common precipitating factor for acute-on-chronic liver failure in Asia.
In an study Asian Pacific study acute-on-chronic liver failure, 76% of patients had complications, including bacterial or fungal infection in 32% of patients, the hepatorenal syndrome in 15%, and gastrointestinal hemorrhage in 9%.
Patients with acute-on-chronic liver failure have intense systemic inflammation and oxidative stress.
In acute-on-chronic liver failure systemic inflammation correlates directly with the severity of the syndrome.
Bacterial infections and acute alcoholic hepatitis are two precipitants of systemic inflammation that are frequently associated with acute-on-chronic liver failure.
Ggastrointestinal hemorrhage may precipitate acute-on-chronic liver failure.
Severe hemorrhage may cause ischemic hepatitis, with cell necrosis and release of inflammatory stimuli.
Gastrointestinal hemorrhage confers a predisposition to the development of bacterial infections with chronic liver disease
In patients with cirrhosis who have a systemic inflammatory process and acute on-chronic liver disease, 40% are without any identified precipitating condition.
Translocation of bacterial by-products from the intestinal lumen to the systemic circulation may occur in chronic liver disease with acute liver failure.
The Model for End-Stage Liver Disease (MELD) with the addition of the serum sodium level score, and scores of failing organs, provides accurate prognostication for individual patients with acute-on-chronic liver failure.
Management is to diagnose and treat the precipitating event and then provide supportive therapy.
Infections, either precipitate or complicate the syndrome, in about 50% among patients with acute-on-chronic liver failure and 70% among patients with three or more organ failures.
Treatment for esophageal variceal bleeding includes the combination of a vasoconstrictor such as octreotide administered from the time of admission and maintained for 2 to 5 days.
Endoscopic therapy with endoscopic variceal ligation, performed at diagnostic endoscopy <12 hours after admission for esophageal bleeding.
Steroid therapy is indicated for patients with severe alcoholic hepatitis.
The ((Lille model)) score is used for early identification of patients who will not have a response to steroid treatment.
The score is calculated on the basis of age, bilirubin and albumin values, prothrombin time, baseline status with respect to renal failure, and the change in bilirubin levels between day 0 and day 7 of prednisolone therapy.
The score ranges from 0 to 1.
A score of 0.45 or higher at the seventh day of treatment indicates no improvement in the response to prednisolone and a low probability of short-term survival, as compared with patients who have a response; treatment should be discontinued.
A score below 0.45 indicates a positive response to treatment, which should be continued for up to 28 days.
Nucleoside or nucleotide analogues should be started in all patients with hepatitis B virus infection at presentation.
Acute kidney injury is the most common organ failure in patients with acute-on-chronic liver failure.
Hepatic encephalopathy is a complication of end stage liver failure.
Albumin dialysis, and extra corporeal liver assist device as compared with standard medical therapy, did not improve short-term survival among patients with acute-on-chronic liver failure.
After liver transplantation among patients with acute-on-chronic liver failure and one or two organ failures at 1 year does not differ significantly from the rate among patients without acute-on-chronic liver failure.
For patients with three or more organ failures, the 1-year post-transplantation survival rate may approach 80%, as compared with a survival rate of less than 20% among patients who do not undergo transplantation.