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Acute liver failure.
Critical Care and Resuscitation : Journal of the Australasian Academy of Critical Care Medicine 1999 March
OBJECTIVE: To consider the classification and to present an approach to the diagnosis and management of complications associated with acute liver failure.
DATA SOURCES: A review of studies reported from 1966 to 1998 and identified through a MEDLINE search on treatment of acute liver failure.
SUMMARY OF REVIEW: Acute liver failure can be subdivided into hyperacute, (encephalopathy within 7 days of onset of jaundice) acute (8-28 days from jaundice to encephalopathy) and subacute (29 to 72 days from jaundice to encephalopathy) forms. Management of all forms involves largely supportive care until hepatocyte regeneration and recovery occurs (predominantly in the hyperacute group), or bridging supportive therapy until orthotopic liver transplantation can be performed. New therapies such as bioartificial liver support devices and ex-vivo liver perfusion offer exciting possibilities for this bridging therapy. While orthotopic liver transplantation remains the definitive treatment for many patients with acute liver failure, N-acetyl-cystine (150 mg/kg over 15 minutes followed by 12.5 mg/kg/hour) and PGE(1) (10 - 40 microg/hour) are reported to have an additional role and are being used increasingly in the management of all forms of acute liver failure.
CONCLUSIONS: Acute liver failure is the end stage of many acute viral and drug induced hepatic diseases. Management is largely supportive until hepatic repair or transplantation can be performed. Recently, additional hepatic protective, regenerative and supportive therapies have been successfully used.
DATA SOURCES: A review of studies reported from 1966 to 1998 and identified through a MEDLINE search on treatment of acute liver failure.
SUMMARY OF REVIEW: Acute liver failure can be subdivided into hyperacute, (encephalopathy within 7 days of onset of jaundice) acute (8-28 days from jaundice to encephalopathy) and subacute (29 to 72 days from jaundice to encephalopathy) forms. Management of all forms involves largely supportive care until hepatocyte regeneration and recovery occurs (predominantly in the hyperacute group), or bridging supportive therapy until orthotopic liver transplantation can be performed. New therapies such as bioartificial liver support devices and ex-vivo liver perfusion offer exciting possibilities for this bridging therapy. While orthotopic liver transplantation remains the definitive treatment for many patients with acute liver failure, N-acetyl-cystine (150 mg/kg over 15 minutes followed by 12.5 mg/kg/hour) and PGE(1) (10 - 40 microg/hour) are reported to have an additional role and are being used increasingly in the management of all forms of acute liver failure.
CONCLUSIONS: Acute liver failure is the end stage of many acute viral and drug induced hepatic diseases. Management is largely supportive until hepatic repair or transplantation can be performed. Recently, additional hepatic protective, regenerative and supportive therapies have been successfully used.
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