The pathogenesis of the nutritional problems can be summed as follows:

• The chronic inflammation and ongoing injury is a major form of stress, not unlike the healing decubitus ulcer.
• Cirrhosis leads to increased use of alternative energy sources by the body, specifically fats.
• Decreased liver and pancreatic function leads to poor GI absorption, particularly of fats and fat soluble vitamins.
  • Remember the fat soluble vitamins?
• Since there is poor fat absorption, this fuel comes from endogenous sources, leading to a net catabolic state.
• Early satiety leads to poor oral intake, further exasperating Mr. Bullroar's poor nutritional situation.
• In time there may even be problems of carbohydrate intolerance leading to overt diabetes.
• There is often increased muscle proteolysis, in an effort to raise serum levels of specific amino acids.
  • Leading to skeletal muscle wasting.
  • Aromatic amino acids, phenylalanine, tyrosine and tryptophan, increase disproportionately with rapid muscle proteolysis.
  • The imbalance between the serum levels of aromatic and branched chain amino acids (leucine, valine and isoleucine) is postulated to contribute to hepatic encephalopathy of terminal cirrhotic patients.

Is there much hope for Mr. Bullroar? Unfortunately not a lot. What can be done?