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Cirrhosis, also known as liver cirrhosis or hepatic cirrhosis, chronic liver failure or chronic hepatic failure and end-stage liver disease, is an acute condition of the liver in which the normal functioning tissue, or parenchyma, is replaced with scar tissue and regenerative nodules as a result of chronic liver disease.
Chronic liver failure usually occurs in the context of cirrhosis, itself potentially the result of many possible causes, such as excessive alcohol intake, hepatitis B or C, autoimmune, hereditary and metabolic causes (such as iron or copper overload, steatohepatitis or non-alcoholic fatty liver disease).
It is also recommended that people with high risk signs are kept in hospital for at least 72 hours. [4] Those at low risk of re-bleeding may begin eating typically 24 hours following endoscopy. [4] If other measures fail or are not available, esophageal balloon tamponade may be attempted. [2]
In special cases where there is a higher risk with surgery, such as in the elderly, nonoperative management would include the infusion of packed red blood cells in an intensive care unit. [2] Typically hepatic injuries resulting from stab wounds cause little damage unless a vital part of the liver is injured, such as the hepatic portal vein ...
Acute liver failure is the appearance of severe complications rapidly after the first signs (such as jaundice) of liver disease, and indicates that the liver has sustained severe damage (loss of function of 80–90% of liver cells).
Viral hepatitis, primarily hepatitis B and hepatitis C, remains a leading cause of liver cirrhosis and liver cancer worldwide, despite advances in antiviral therapies and vaccination efforts. [50] Additionally, recent studies have highlighted lean steatotic liver disease (SLD), a subset of NAFLD, affecting over 12% of U.S. adults even in the ...
Cirrhosis alters bleeding pathways thus patients are simultaneously at risk of uncontrolled bleeding and forming clots. [3] A long-standing hindrance in flow as in chronic PVT, also known as portal cavernoma, can cause an increase in the hepatic venous pressure gradient (portal hypertension) and increased blood flow through subsidiary veins. [1]
An important non-genetic risk factor is the use of estrogen-containing forms of hormonal contraception, which is implicated in 22% of cases of Budd–Chiari syndrome. [2] Other less common risk factors include systemic diseases such as aspergillosis, Behçet's disease, connective tissue disease, mastocytosis, inflammatory bowel disease, HIV ...