Hepatic Encephalopathy

last updated: May 9, 2016

Ammonia is generated in the intestines from different sources:

  • diet

  • deamination of glutamine (skeletal muscle has glutaminase)

  • breakdown of urea in the colon

 

Majority of the NH3 goes to the liver and metabolized to urea (urea cycle); small amount goes to the kidney and excreted as urea and some of the NH3 is taken up by skeletal muscle and converted to glutamine (acting as a buffer). When there is liver failure and/or portal-systemic shunts cause a rise in NH3 over coming the kidney and skeletal muscle role causing an accumulation of NH3 in the brain. NH3 affects astrocytes, specifically, by impairing the mitochondria and the glutamate-glutamine patheays between astrocytes and neurons.

 

Because skeletal muscle plays an important role in NH3 removal (buffer system), thus, malnutrition may further compound neuropsychiatric status.  

 

Gastrointestinal

  • diet: protein restriction does NOT appear to have any beneficial effect for cirrhotic patients during an episode of encephalopathy (Cordoba, 2003)

    • moderate intake 0.5 g/kg/day at first and shortly after return to normal protein intake (1-1.5 g/kg/day)

References

  • Cordoba, Journal of Hepatology October 2003

  • Amodio, Hepatology, July 2013

... but I would more especially commend the clinician who, in acute diseases, by which the bulk of mankind are cutoff, conducts the treatment better than others.
 
Hippocrates, 400 BC