Hepatic Encephalopathy in Liver Cirrhosis

Abstract

The pathogenesis of hepatic encephalopathy (HE) is unknown. Many theories have been proposed. Most established therapies are based on such theories but since no theory has have ever been proved, therapies have to be considered empiric. The spectrum of HE ranges from minimal cerebral functional deficits, which can only be found by sensitive psychometric tests, to coma with signs of decerebration. HE has arbitrarily been divided into stages. A number of precipitating factors are known and the first line of therapy should always be the elimination of these factors. The differential diagnosis includes all states of impaired consciousness and deficits in cerebral function in patients with chronic liver disease, and clinical and biochemical tests to differentiate are indicated. The therapeutic options for HE include: protein restriction only for a limited time in comatous patients; nonabsorbable antibiotics (aminoglycosides), which because of adverse effects are also limited to higher grades of HE: intestinal cleansing which is applicable in all degrees of HE; lactulose, branched chain aminoacids and ornithin aspartate which have been proven to be effective and can be applied long term in patients with lower grades of HE.

Covert and Overt Hepatic Encephalopathy: Diagnosis and Management

“…Ammonia is generated from nitrogenous products in the diet, bacterial metabolism of urea and proteins in the gut, and from deamination of glutamine in the small intestine via glutaminase 20 . Normally, ammonia is converted to urea in the liver and then subsequently cleared by kidneys.…”

“…When administered, they are degraded by microbiota in the colon to short chain organic acids creating both an acidic environment and an osmotic gradient in the intestinal lumen 20 . The acidic environment created is hypothesized to reduce ammoniagenic bacteria and convert ammonia to non-absorbable ammonium.…”

“…The acidic environment created is hypothesized to reduce ammoniagenic bacteria and convert ammonia to non-absorbable ammonium. In addition, the increased osmolality also causes intestinal cleansing via removal of excess fecal nitrogen through a laxative effect 20 .…”

Emergencies of the Liver, Gallbladder, and Pancreas

“…Oxidative stress and inflammatory cytokines play a role as well. 7,33,35 The diagnosis of HE requires a thorough history as well as physical and laboratory/ radiological evaluation. The diagnosis should be suspected in any patient with known liver disease who presents with altered mental status and neuromuscular abnormalities.…”

Evaluation of Serum Ammonia in Hepatic Encephalopathy Patients and Its Correlation with Clinical Severity

“…The patho-physiology of HE is multifactorial with several circulating neurotoxins being proposed, but ammonia is strongly considered as a central factor in the pathogenesis of HE [8][9][10] . Ammonia is formed mainly from the nitrogenous products in the diet, bacterial metabolism of urea and proteins in the colon, and by de-amination of glutamine in the small intestine by glutaminase [11] . From the gut, ammonia is carried to the portal circulation and is converted to urea by the liver, which is subsequently excreted by the kidneys [9] .…”