Gentleman Doli
08-14-2013, 01:34 PM
Acute liver failure (ALF) is an uncommon condition in which the rapid deterioration of liver function results in coagulopathy and alteration in the mental status of a previously healthy individual. Acute liver failure often affects young people and carries a very high mortality.
The term acute liver failure is used to describe the development of coagulopathy, usually with an international normalized ratio (INR) of greater than 1.5, and any degree of mental alteration (encephalopathy) in a patient without preexisting cirrhosis and with an illness of less than 26 weeks' duration.
Acute liver failure is a broad term that encompasses both fulminant hepatic failure (FHF) and subfulminant hepatic failure (or late-onset hepatic failure). Fulminant hepatic failure is generally used to describe the development of encephalopathy within 8 weeks of the onset of symptoms in a patient with a previously healthy liver. Subfulminant hepatic failure is reserved for patients with liver disease for up to 26 weeks before the development of hepatic encephalopathy.
There are important differences between FHF in children and FHF in adults. For example, in children with FHF, encephalopathy may be absent, late, or unrecognized. For a full discussion of the diagnosis and management of pediatric FHF, see Fulminant Hepatic Failure. The American Association for the Study of Liver Diseases has produced guidelines on the management of acute liver failure in adults.
Some patients with previously unrecognized chronic liver disease decompensate and present with liver failure; although this is not technically FHF, discriminating such at the time of presentation may not be possible. Patients with Wilson disease, vertically acquired hepatitis B, or autoimmune hepatitis may be included in spite of the possibility of cirrhosis if their disease has been manifest for less than 26 weeks.
The most important step in the assessment of patients with acute liver failure is to identify the cause, as certain causes demand immediate and specific treatment. Drug-related hepatotoxicity, especially from acetaminophen, is the leading cause of acute liver failure in the United States.
The most important aspect of treatment is to provide good intensive care support. Careful attention should be paid to fluid management and hemodynamics. Monitoring of metabolic parameters, surveillance for infection, maintenance of nutrition, and prompt recognition of gastrointestinal bleeding are crucial.
Various medications may be necessary because of the variety of complications that occur from fulminant hepatic failure. In specific cases, antidotes that effectively bind or eliminate toxins are essential.
The development of liver support systems provides some promise for patients with FHF, although it remains a temporary measure and, to date, has no impact on survival. Other investigational therapeutic modalities, including hypothermia, have been proposed but remain unproven.
The outcome of acute liver failure is related to the etiology, the degree of encephalopathy, and related complications . Although mortality from FHF remains significantly high, improved intensive care and use of orthotopic liver transplantation have improved survival from less than 20% to approximately 60%.
The term acute liver failure is used to describe the development of coagulopathy, usually with an international normalized ratio (INR) of greater than 1.5, and any degree of mental alteration (encephalopathy) in a patient without preexisting cirrhosis and with an illness of less than 26 weeks' duration.
Acute liver failure is a broad term that encompasses both fulminant hepatic failure (FHF) and subfulminant hepatic failure (or late-onset hepatic failure). Fulminant hepatic failure is generally used to describe the development of encephalopathy within 8 weeks of the onset of symptoms in a patient with a previously healthy liver. Subfulminant hepatic failure is reserved for patients with liver disease for up to 26 weeks before the development of hepatic encephalopathy.
There are important differences between FHF in children and FHF in adults. For example, in children with FHF, encephalopathy may be absent, late, or unrecognized. For a full discussion of the diagnosis and management of pediatric FHF, see Fulminant Hepatic Failure. The American Association for the Study of Liver Diseases has produced guidelines on the management of acute liver failure in adults.
Some patients with previously unrecognized chronic liver disease decompensate and present with liver failure; although this is not technically FHF, discriminating such at the time of presentation may not be possible. Patients with Wilson disease, vertically acquired hepatitis B, or autoimmune hepatitis may be included in spite of the possibility of cirrhosis if their disease has been manifest for less than 26 weeks.
The most important step in the assessment of patients with acute liver failure is to identify the cause, as certain causes demand immediate and specific treatment. Drug-related hepatotoxicity, especially from acetaminophen, is the leading cause of acute liver failure in the United States.
The most important aspect of treatment is to provide good intensive care support. Careful attention should be paid to fluid management and hemodynamics. Monitoring of metabolic parameters, surveillance for infection, maintenance of nutrition, and prompt recognition of gastrointestinal bleeding are crucial.
Various medications may be necessary because of the variety of complications that occur from fulminant hepatic failure. In specific cases, antidotes that effectively bind or eliminate toxins are essential.
The development of liver support systems provides some promise for patients with FHF, although it remains a temporary measure and, to date, has no impact on survival. Other investigational therapeutic modalities, including hypothermia, have been proposed but remain unproven.
The outcome of acute liver failure is related to the etiology, the degree of encephalopathy, and related complications . Although mortality from FHF remains significantly high, improved intensive care and use of orthotopic liver transplantation have improved survival from less than 20% to approximately 60%.