Current concepts in the pathophysiology and management of hepatic encephalopathy

Dr. Frederick is Director of Quality and Clinical Protocols for the Hepatology and Liver Transplant Program at California Pacific Medical Center in San Francisco, California.
Gastroenterology and Hepatology 04/2011; 7(4):222-33.
Source: PubMed


Hepatic encephalopathy (HE) represents a broad continuum of neuropsychological dysfunction in patients with acute or chronic liver disease and/or portosystemic shunting of blood flow. The pathophysiology of this disease is quite complex, as it involves overproduction and reduced metabolism of various neurotoxins, particularly ammonia. Recent hypotheses implicate low-grade cerebral edema as a final common pathway for the pathophysiology of HE. Management of this condition is multifaceted and requires several steps: elimination of precipitating factors; removal of toxins, both by reducing them at their source and by augmenting scavenging pathways; modulation of resident fecal flora; proper nutritional support; and downregulation of systemic and gut-derived inflammation.

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    • "This indicates that apart from hyperammonemia, other factors are also involved in the genesis of behavioral manifestations of TAA-induced encephalopathy. Possible additional factors that may contribute to TAA-induced encephalopathy include hypoglycemia, renal failure (Geller et al. 1988), or accumulation of other toxic products evident in liver failure (Frederick 2011). Hypothermia, also involved in toxic effects of TAA (Geller et al. 1988), was not evident in our study. "

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    • "There is a very high rate of mortality in this type.[7][8][9] Supportive care until spontaneous recovery is the only treatment strategy but does not occur in many patients.[9][10] To prevent death, liver transplantation is the only effective approach. "
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    ABSTRACT: As a serious neuropsychiatric disease, hepatic encephalopathy (HE) is a clinical condition with several types regarding chronicity and clinical diversity that can develop as a complication of both acute and chronic liver failure. This study evaluates changes in thioacetamide (TAA)-induced acute hepatic encephalopathy (AHE) in rat as an animal model. Both genders of C57BL6, BALB/C mice and Sprague Dawley rats; (10 animals in each group) were compared for induction of AHE to clarify which animal and gender were appropriate. The animals (10 male rats in each group) were categorized in 4 groups according to the dose of the TAA administered (200, 300 and 400 mg/kg of TAA at 24 h intervals for 4 days). A control group was treated with solvent of TAA which was water (5 ml/kg/day). The behavioral, biochemical markers of hepatic failure and histological aspects of thioacetamide (TAA) induced AHE and the correlation between the clinical severity and liver failure biomarkers were evaluated. Rat was shown to be an animal model of choice for AHE while the optimum dosage of TAA to induce AHE was 300 mg/kg/day at 24 h intervals for 4 days. The behavioral score was partially correlated with the rising of some biomarkers and pathological findings. Rat can be introduced as the animal of choice for AHE to study the pathophysiology, pharmacology and the survival rate of disease in liver transplant patients.
    03/2012; 14(3):164-70.
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    New Advances in the Basic and Clinical Gastroenterology, 04/2012; , ISBN: 978-953-51-0521-3
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