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Nutritional requirements of the critically ill

Created: 21/5/2007

Nutritional requirements of the critically ill

Gina Tomlin
Chief dietician, John Radcliffe Hospital, Oxford

Focus on the role of nutrition provision in the critically ill

All patients should be guaranteed the amount of nutrition that prevents accelerated depletion. This gives the patient as long a time as possible to receive ICU therapy for their critical illness without the prospect of malnutrition intervening.

Why feed the critically ill patient?

For obvious ethical reasons there is an absence of well-designed prospective randomised controlled trials comparing the effects of feeding to witholding feeding on outcome from ICU treatment. Clinical depletion of lean body mass may occur after 14 days of starvation, although the consequences of withholding nutrition come into play before this. After 21 days of critical illness there is an average loss of 17% total body muscle stores. The majority of this loss (70%) comes from skeletal muscle, and this results in a decrease in muscle strength, muscle fatigue, delayed muscle relaxation and a delay in mobilisation during the post ICU recovery period. Unless contraindicated nutritional support should therefore be commenced as early as possible.

Contraindications to commencing feed (enteral or parenteral) on ICU:

  • Able to resume full oral diet within 3 days
  • Inappropriate for ethical reasons

Aims of nutritional support on the ICU:

  • Provide exogenous substrates to meet macro and micronutrient requirements in unconscious patients
  • Help protect vital visceral organs and attenuate breakdown of skeletal muscle
  • Reduce net protein catabolism

Effects of malnutrition on ICU outcome:

  • Impaired immunological function
  • Impaired ventilatory drive
  • Weakened respiratory muscles
  • Prolonged ventilator dependence
  • Increased infectious morbidity and mortality
  • Increased risk of complications
  • Poor wound healing
  • Increased length of ICU stay

Focus on the metabolic and nutritional response to critical illness

The Cuthbertson (1932) model of the metabolic response to injury includes 3 phases; ebb, flow catabolic and flow anabolic. The ebb phase is a period of severe shock characterised by depression of enzymic activity and oxygen consumption. Cardiac output is reduced and lactic acidosis is present. The flow catabolic phase is associated with fat and protein mobilisation, increased urinary nitrogen excretion and weight loss. The flow anabolic phase is associated with restoration of fat and protein stores and weight gain. In the flow phase the body is hypermetabolic, cardiac output, oxygen consumption and glucose production is increased and lactic acid is often normal. In the face of prolonged critical illness, the ebb and the flow catabolic phases are normally encountered whilst the patient is being treated on the ICU whereas the anabolic phase during the recovery period post ICU discharge.

In straightforward starvation the metabolic rate falls due to:

  • A reduction in the metabolically active tissue (e.g. skeletal muscle)
  • A reduction in physical activity
  • A decrease in metabolic activity of the remaining body tissues

However, in critical illness the hormonal balance is altered by the stress and inflammatory responses and a hypermetabolic response is seen. Nutritional consequences of this include:

  • An alteration in energy needs and production
  • Preferential catabolism for body glucose and protein stores
  • Limitation of intake by anorexia/inability to eat due to sedation/unconscious state
  • Possible decreased intestinal absorption if the gut is oedematous or poorly perfused
  • Fever
  • Increased production of immune cells and acute phase hepatic proteins
  • Sodium and fluid retention

Albumin levels are low as a result of the acute phase response and contribute significantly to the pathophysiological characteristics of the hypermetabolic response to critical illness. Therefore, a low albumin level is an unreliable marker of malnutrition in the critically ill.

The degree of hypermetabolism is proportional to the severity of the injury. Common causes for a larger hypermetabolic response include:

  • Burns
  • Septic shock
  • Perfusion deficit
  • Inflammation
  • Necrotic tissues
  • Head injury and multi trauma

When calculating nutritional requirements the degree for hypermetabolism is often referred to as a ‘stress factor’.

Focus on the nutritional requirements of a patient on the ICU

The nutritional requirements of the critically ill are made up of the following important components:

  • Total energy
  • Protein
  • Lipids (fat)
  • Carbohydrates
  • Micronutrients

Focus on the calculation of the nutritional requirements

Total energy

The total energy requirements of critically patients are given in recent guidelines issued by the European society of parenteral and enteral nutrition (‘ESPEN 2006’).

Acute initial phase of critical illness 20-25kcal/kg/day

Recovery/anabolic phase 25-30kcal/kg/day

The U.K. Parenteral and Enteral Nutrition group guidelines (‘PEN 2004’) recommend the use of the Schofield equation which works out an estimation for basal metabolic rate (dependent on age, sex and weight).

Focus on the Schofield equation

Females (kcal/day)

Males (kcal/day)

10-17yrs 13.4W + 692

10-17yrs 17.7W + 657

18-29yrs 14.8W + 487

18-29yrs 15.1W + 692

30-59yrs 8.3W + 846

30-59yrs 11.5W + 873

60-74yrs 9.2W + 687

60-74yrs 11.9W + 700

75yrs+ 9.8W +624

75yrs+ 8.3W + 820

  • W = weight in kg
  • A % adjustment is then made for activity and thermogenesis (temperature regulation and response to food intake):

        Bed bound immobile +10%
        Bed bound mobile/sitting +15-20%
        Mobile on the ward +25%

  • ICU patients often have <10% activity due to paralysis and degree of ventilatory support.
  • A further % adjustment is made for the ‘stress factor’/degree of hypermetabolism. Some examples seen in ICU patients:

        Infection 25-45%
        Uncomplicated surgery 5-10%
        Complicated surgery 25-40%
        Multi trauma and head injury 30-50%

Focus on Protein

Protein is also dependent on the degree of hypermetabolism.

Nitrogen g/kg/day


0.17 (0.14-0.20)

Hypermetabolic 5-25%

0.20 (0.17-0.25)

Hypermetabolic 25-50%

0.25 (0.20-0.30)

Hypermetabolic >50%

0.30 (0.25-0.35)


0.30 (0.20-0.40)

There is lack of consensus and evidence as to the ideal nitrogen requirements of a critically ill patient on the ICU and it is generally recommended that the patient will not gain from providing in excess of 0.20g nitrogen/kg/day. Nitrogen losses are large in critically ill patients and a positive nitrogen balance is virtually impossible to achieve.

In practice, nitrogen balance studies can be completed by collecting a 24 hour urinary urea and calculating nitrogen balance using the following approach:

Nitrogen balance = nitrogen intake – nitrogen output (g/day)

        Nitrogen intake = feed received in 24 hours (enteral/parenteral/oral)

        Nitrogen output = urinary urea/mmol/24 hours x 0.033 + obligatory losses + any extra renal losses

Obligatory losses are estimated as 2-4g nitrogen/day (skin, hair, faeces etc)

Extra renal losses include:

  • Pyrexia: 0.6g nitrogen/1° temperature rise
  • Inflammatory bowel disease
  • GI fistulae
  • Extensive bed sores
  • Burn exudates: 0.2g nitrogen/ degree surface area burn

Any attempt to increase protein intake above 0.20g/kg/day requires close monitoring of renal function (particularly urea levels) and further nitrogen balance studies to see if this is safely tolerated.

Focus on nitrogen balance in specific conditions

Renal failure – Haemofiltration is associated with increased protein losses of about 10%. Protein requirements alter depending on the type of renal replacement therapy applied and will be lower if the renal failure patient remains conservatively managed.

Liver failure – the requirements are dependent on the underlying functional capacity of the liver:

Compensated cirrhosis 0.19-0.20gN/kg/day

Decompensated cirrhosis 0.25-0.30gN/kg/day

Post-transplant 0.25-0.30gN/kg/day

Acute (fulminant) liver failure 0.20-0.25gN/kg/day

Focus on Lipid (fat) requirements

Critically ill patients require approximately 0.8-1.0g/kg/day of lipid.

It is important to note that propofol is a lipid source. Each ml contains of 1% propofol contains 0.9kcal and can increase the risk of both fat and total calorie overfeeding and micronutrient deficiency if feeding regimes are altered to compensate for its use.

Focus on Carbohydrate requirements

The PEN 2004 guidelines for the critically ill patient suggest using the glucose oxidation rate to determine the upper level of carbohydrate requirement:

Glucose oxidation rate = 4-7mg/kg/body weight/minute/day

Excess intake above this can result in hyperglycaemia, lipid synthesis and of particular relevance to the critically ill ventilator dependent patient, increased carbon dioxide production:

Carbohydrate + O2 = water + CO2 + energy production

Focus on Micronutrient requirements

There are no set levels for micronutrient requirements for the critically ill. In general aiming for the normal recommended daily allowance is suggested, which will be achieved by providing 1500ml of the majority of enteral nutrition feeds. However, as critical illness often involves excessive free radical production and oxidative stress some researches have suggested a potential role for increased supplementation with antioxidant nutrients. In estimating micronutrient requirements, consideration needs to be given to previous and current nutritional intake, micronutrient status, clinical signs of deficiency, possible drug interactions and known altered requirement due to specific disease states.
For example:

  • Thiamine deficiency in alcoholics
  • Vitamin B12 deficiency in patients post gastrectomy or total ileal resection
  • Zinc losses from pancreatic fistulae
  • Phosphate, magnesium and potassium deficiencies upon refeeding a malnourished patient

Micronutrient supplementation in patients with renal failure needs to be undertaken cautiously due to risks of toxicity.

Focus on complications associated with overfeeding (hyperalimentation)

Carbohydrate overfeeding

Carbohydrate overfeeding can potentially lead to hyperinsulinaemia, prolonged mechanical ventilation due to increased carbon dioxide production, fatty deposition in the liver, hepatomegaly and cholestasis.

Fat/lipid over feeding

Overfeeding fats can lead to fatty deposition in the liver, hepatomegaly, cholestasis and increased serum triglycerides.

Protein overfeeding

Protein overfeeding can increase ureagenesis that can further impair renal function if pre-existing kidney disease is present.

Focus on feeding protocols/flow charts for initiation of enteral feeding

These are used to establish safe feeding as early as possible and to highlight any problems associated with feeding. The evidence for gastric aspirates being a reliable marker for poor nutrition absorption is unreliable.

Key References

Cuthbertson DP.
Observation on the disturbance of metabolism produced by injury to the limbs.
Quarterly Journal of Medicine 1932; 25:233-246.

Weissman C, Kemper M, and Damask MC.
Effect of routine intensive care interaction on metabolic rate.
Chest 1984; 86: 815-18.

Schofield WN.
Predicting basal metabolic rate, new standards and review of previous work.
Hum Nutr Clin Nutr 1985; 44:1-19.

Klein CJ, Stanek GS, Wiles CE.
Overfeeding macronutrients to critically ill adults: metabolic complications.
J. American Dietetic Association 1998; 98: 795-806.

Heyland DK, Dhaliwal R, Drover JW et al.
Canadian clinical practice guidelines for nutrition support in mechanically ventilated, critically ill adult patients.
Journal of Parenteral and Enteral Nutrition 2003; 27: 355-73

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