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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).
Liver failure is the inability of the liver to perform its normal synthetic and metabolic functions as part of normal physiology. Two forms are recognised, acute and chronic (cirrhosis). [1] Recently, a third form of liver failure known as acute-on-chronic liver failure (ACLF) is increasingly being recognized. [2]
The third phase follows at 3 to 5 days, and is marked by complications of massive liver necrosis leading to fulminant liver failure with complications of coagulation defects, low blood sugar, kidney failure, hepatic encephalopathy, brain swelling, sepsis, multiple organ failure, and death. [10]
It is generally reserved for patients with fulminant liver failure, failure of shunts, or progression of cirrhosis that reduces the life expectancy to one year. [23] Survival rates in Budd–Chiari syndrome after liver transplantation are 76%, 71% and 68% after 1, 5 and 10 years respectively. [2]
Most hospitals stock the antidote (acetylcysteine), which replenishes the liver's supply of glutathione, allowing the NAPQI to be metabolized safely. [1] Without early administration of the antidote, fulminant liver failure follows, often in combination with kidney failure, and death generally occurs within several days.
Ischemic hepatitis, also known as shock liver, is a condition defined as an acute liver injury caused by insufficient blood flow (and consequently insufficient oxygen delivery) to the liver. [5] The decreased blood flow ( perfusion ) to the liver is usually due to shock or low blood pressure.
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Hepatotoxicity (from hepatic toxicity) implies chemical-driven liver damage. Drug-induced liver injury (DILI) is a cause of acute and chronic liver disease caused specifically by medications and the most common reason for a drug to be withdrawn from the market after approval.
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