Gastroenterology training and education

How do you diagnose malnutrition in patients with liver disease?

This is very difficult. BMI may be difficult to use because cachexia may be masked by edema. However in general the following BMI indicates malnutrition in liver disease patients:

• BMI <22 in patients without ascites
• BMI <23 in patients with mild ascites
• BMI <25 in patients with tense ascites

Mid arm muscle circumference (MAMC) and triceps skin fold thickness may also be used to diagnose malnutrition.

SGA (subjective global analysis) is very reliable and specific in detecting malnutrition. ESPEN recommends use of SGA and/or anthropometrics (BMI/MAMC/ triceps skin fold thickness) to diagnose malnutrition.

Discuss enteral nutrition in alcoholic hepatitis (AH)/ cirrhosis of liver?

• Undernourished patients have a poor prognosis
• ESPEN (2006) recommends a calorie intake of 35-40Kcal/kg/day (dry body weight) and a protein intake of 1.2-1.5 g/kg/day (dry body weight)
• Use ONS or TF, if oral intake is not sufficient. Whole protein formulae should be used. Use of BCAA enriched formulae should be reserved, if hepatic encephalopathy develops despite appropriate medical treatment.
• ESPEN supports the insertion of fine bore NG tubes in patients with oesophageal varices.
• PEG is associated with a higher risk of complications (due to ascites and varices) and should be avoided.
• In the study by Cabre E et al (Hepatology 2000) EN was found to be as effective as steroids in alcoholic hepatitis.

When do you consider PN in AH or cirrhosis?
PN should be considered when oral/enteral intake is insufficient.

What are the energy requirements?

• Energy intake- 1.3 X BMR
  • CHO- 50-60 % of non protein requirements
  • Protein 1.2 gm/kg/day (1.5 gm/kg/day if severely malnourished)
  • Lipids- 40-50% of non protein requirements
  • In patients with ascites ideal weight according to the height should be used.
• Vitamins and minerals should be administered daily from the beginning. Due to the high risk of Wernicke’s encephalopathy, vitamin B1 must be administered prior to starting i.v. glucose in alcoholic patients.
• Lipid should be provided using emulsions with a content of n-6 unsaturated fatty acids lower than in traditional pure soy bean oil emulsions (n-6:n-3 = 8:1). New fat emulsions have a lower content in n-6 unsaturated fatty acids due to the admixture of MCT and/or olive oil and/or fish oil rendering them less suppressive on leucocyte and immune function and less pro-inflammatory modulators.
• A standard solution should be given in encephalopathy stage I-II and a liver-adapted complete amino acid solution should be given in encephalopathy stage III-IV. Such solutions contain an increased amount of branched-chain amino acids and lower content of aromatic amino acids, methionine and tryptophan. BCAA solutions lead to an improvement in mental state, but no definite benefit on survival.
• Like in other conditions, the administration of micronutrients has no proven therapeutic effect apart from the prevention or correction of deficiency states. Supplementing zinc and vitamin A may indirectly improve food intake and nutritional state by improving dysgeusia. Zinc and selenium deficiency have been observed in alcoholic and non-alcoholic liver disease. An impressive association between HE and zinc deficiency has been described in case reports. However oral zinc supplementation does not have a therapeutic effect on HE.  In a pragmatic approach, liberal supplementation is recommended in the first two weeks of nutritional support, because the laboratory diagnosis of a specific trace element or vitamin deficiency may be more costly, and would delay provision.

Discuss nutrition in AH/Cirrhosis?

• The prevalence of protein energy malnutrition increases from 20 % in Child-Pugh class A to over 60 % in class C
• In patients with cirrhosis, overnight fasting can cause depletion of glycogen stores and lead to a metabolic condition similar to prolonged starvation. Thus it is recommended that patients who need fasting should be given glucose IV at a rate equal to the endogenous hepatic production (2-3gm/kg/day).
• Due to psychomotor dysfunction oral nutrition often is not sufficient even in encephalopathy stage I-II.  Tube feeding should be considered to ensure adequate nutrient provision. PN should be considered in patients with unprotected airways and advanced HE.
• In the early postoperative phase often there is a disturbance of glucose metabolism associated with insulin resistance. Hyperglycaemia In this situation should be managed by reducing glucose intake because higher insulin doses are unable to increase glucose oxidation.

Discuss nutrition in acute Liver failure?

• As in other critically ill patients artificial nutrition in acute LF is indicated when the patient is considered unlikely to resume normal oral nutrition within the next 5 to 7 days.
• In acute liver failure resting energy expenditure is increased 1.2- to 1.3-fold compared to healthy individuals. Whenever possible, the individual energy requirement should be measured by use of indirect calorimetry.
• Sufficient glucose provision (2 – 3 g/kg/day) is mandatory for the prophylaxis or treatment of hypoglycaemia
• Lipid (0.8 – 1.2 g/kg/day). Most centers use LCT/MCT emulsion
• Amino acid administration is not mandatory in hyperacute LF. In acute or subacute LF, however, amino acids (0.8–1.2 g/kg/day in PN) or protein (0.8 – 1.2 g/kg/day) in enteral nutrition) should be used in order to support protein synthesis.
• The use of amino acid infusion often was omitted for fear of aggravating existing hyperammonaemia and hyperaminoacidaemia causing brain oedema and encephalopathy especially in hyperacute liver failure.
• Adequate metabolic monitoring is necessary in order to adapt nutrient provision to substrate utilisation. Strict control of the plasma levels of glucose (target: 5 – 8 mmol/L), lactate (target: < 5.0 mmol/L), triglycerides (target: < 3.0 mmol/L) and ammonia (target: < 100 micromole/L) are necessary for this purpose.

NB- BCAA are essential amino acids leucine, isoleucine and valine. In cirrhosis there are reduced body stores of BCAA. This directly or indirectly influence brain ammonia levels.

Ref

1. ESPEN guidelines