|
KMID : 0882420080750010027
|
|
Korean Journal of Medicine
2008 Volume.75 No. 1 p.27 ~ p.36
|
|
|
Hepatic encephalopathy
|
|
Kim Chang-Wook
|
|
|
Abstract
|
|
|
|
Hepatic encephalopathy, one of the major complications of cirrhosis, is a neuropsychiatric syndrome caused by accumulation of toxins in the central nervous system following dysfunction in liver detoxification. Various manifestations makes it difficulty to diagnose and categorize hepatic encephalopathy. For the consistency in diagnosis and staging of hepatic encephalopathy, standardized nomenclature regarding forms of hepatic encephalopathy was proposed recently. Due to the poor understanding of pathophysiology, effective prevention or treatment options are limited. Based on the theory that intestinal-derived ammonia plays major role in the development of hepatic encephalopathy, therapeutic approaches are directed at reducing intestinal bacterial production of ammonia and facilitating its elimination. Non-absorbable disaccharides, antibiotics such as rifaximin and L-ornithine-L-aspartate are main therapies for hepatic encephalopathy. Alternative therapies such as benzodiazepine receptor antagonists, branched-chain amino acids, sodium benzoate and acarbose have limited data supporting their use. Precipitating factors must be looked into carefully and corrected immediately because most patients are usually present with precipitating factors. Hepatic encephalopathy without precipitating factors shows poor prognosis and could be candidate of liver transplantation.
|
|
|
KEYWORD
|
|
|
Hepatic encephalopathy, Terminology, Physiopathology, Therapy
|
|
|
FullTexts / Linksout information
|
|
|
|
|
Listed journal information
|
|
  
|
|