July 14, 2020
Metabolic Aspects of TPN Minimize

Metabolic aspects of TPN

There are numerous techniques for nutritional support, including specific (eg protein) or general (all nutrients) supplementation of diet and enteral feeding by nasogastric or nasojejunal tubes, percutaneous gastrostomy etc. Patients whose nutrient requirement cannot be met fully by enteral feeding, will require parenteral feeding either supplementary or as the sole source of nutrients (total parenteral feeding).

All patients requiring nutritional support require monitoring, involving clinical assessment eg weight, skinfold thickness, and laboratory investigations. the latter are particularly important in parenteral nutrition, as nutrients and a large volume of fluid are infused directly into the blood. Monitoring is required:

  1. to assess the adequacy of nutritional provision
  2. to detect metabolic complications 

Clinical monitoring:

Daily weight, vital signs, fluid input & output measurements, regular assessment for sepsis and oral hygiene.

Laboratory monitoring:

  1. Haemoglobin, white cell count,
  2. LFTs, potassium, calcium, magnesium, phosphate, glucose and triglycerides.
  3. Trace elements: Zinc, Copper, Selenium
  4. Vitamin analysis will depend on clinical situation but analysis may be invalidated by sepsis and inflammation (see below)
  5. CRP: since there are physiological changes in all the above biochemical markers with degrees of inflammation, CRP should be measured to evaluate the degree of pathophysiological interference.

In practice, the frequency of tests is determined by the patients overall clinical state or underlying illness, rather than the need to monitor nutritional support. Stable patients on long term eg home TPN require monitoring at intervals of approx 4-6 weeks. 

Effect of illness on plasma micronutrient concentrations


Minor inflammation
ie CRP ~ 20 mg/L

Major inflammation
ie CRP 100-200 mg/L


decreased by 40%

decreased by 60-90%


decreased by 10%

decreased by 40-60%


decreased by 10%

decreased by 40-60%


increased by 10-15%

increased by 30%

Vitamin A

decreased by 30-40%

decreased by 30%

Vitamin E


decreased by 20-30%

Vitamin D


decreased by <15%

Vitamin C

no data


Vitamin B6

no data

decreased by 40-50%

Vitamin B12


decreased by <10%



decreased by <15%

NB: vitamin B12 rises significantly in patients with liver disease


  1. Hyper & hypoglycaemia;
  2. Electrolyte disturbances esp potassium, magnesium and phosphate, due either to the quantity administered or redistribution consequent on insulin mediated glucose uptake.
  3. Trace element and vitamin deficiencies may be avoided by regular administration but cannot be reliably assessed by plasma concentrations in the presence of inflammation or infection.
  4. Hyperlipidaemia may be due to excess iv lipids, endogenous production, reduced catabolism or due to conversion from excessive carbohydrate infusion.
  5. Mild cholestatic abnormalities in LFTs are frequently seen but usually settle spontaneously; but excessive infusion of carbohydrates may produce a fatty liver with persistent elevation of transaminases.
  6. The administration of amino-acids gives rise to a mild metabolic acidosis (due to their breakdown). This may, if necessary, be treated by the concurrent use of the acetate rather than chloride salt of potassium.


  • Galloway P, McMillan DC, Sattar N. Effect of the inflammatory response on trace elements and vitamin status.  Ann Clin Biochem 2000;37:289-297.
  • Louw JA, Werbeck A, Louw MEJ, Kotze TJvW, Cooper R, Labadarios D. Blood vitamin concentrations during the acute-phase response. Crit Care Med 1992;20:934-941.
  • Duncan A, Talwar D, McMillan DC, Stefanowicz F, O’Reilly DStJ. Quantitative data on the magnitude of the systemic inflammatory response and its effect on micronutrient status based on plasma measurements. Am J Clin Nutr 2012;95:64–71.

JHB 22 Jan 2014


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