Enteral Nutrition Guideline

Additional information

Contraindications to enteral nutrition (only 3):

  • Bowel obstruction
  • Bowel perforation
  • Proximal high output fistula
Relative contra-indications are:
Significant chance of gut hypoperfusion:
  • High dose vasopressors
  • Inadequate resuscitation
Note: Abdominal surgery and absence of bowel sounds are not contraindications to EN. Bowel sounds result from the combination of swallowed air and peristalsis. Sedated, mechanically ventilated, patients do not swallow air making the absence of bowel sounds meaningless.

Patients should be adequately resuscitated before feed is commenced.

Amount of feed

Target rate is 25 Kcal/kg/24h (ideal body weight)
This works out at about 1ml/kg/hour of 1 Kcal/ml feed.
Water requirements are 30 ml/kg/24h.
Additional water should be added to EN (enteral nutrition) to meet requirements (remember that water will allow additional sodium excretion and improve oedema if the kidneys are working).
TPN should be given at 50% of calculated requirements for 48h.
PN should be given through a dedicated central line lumen which is not used for anything else.
Glutamine should be included in PN for all patients.

Beware of re-feeding syndrome if malnourished (see later).

Timing and route

EN should be started early (24-48h).
PN should only be started if efforts to establish EN have failed by day 5-7.
PN should be started earlier if the patient is already malnourished.
No changes to the guideline are necessary for pancreatitis.

Rationale for guideline


In the UK, 40% of patients admitted to hospital are malnourished at the time of their admission.
The stress response in critical illness increases blood sugar (via increased cortisol, catecholamines and glucagon) but reduces the ability to utilise glucose with tissue resistance to insulin.
Starvation mobilises proportionally more fat for energy provision whereas critical illness mobilises mostly protein with breakdown of muscle.
The benefits of nutritional support include improved wound healing, decreased catabolic response to illness and improved gastrointestinal tract structure and function.
This results in a lower incidence of infectious complications and reduced hospital stay.


Impaired immune function

  • Delayed wound healing
  • infections
Muscle weakness
  • Prolonged weaning
  • Prolonged immobility
Decreased O2 delivery
  • Reduced cardiac output
  • Anaemia
  • Impaired ventilatory drive

Fatty liver
metabolic rate
  • Pyrexia
  • O2 consumption
  • CO2 production


Traditional assessment tools for nutrition are not validated in critically ill patients.
Confounding factors include oedema and altered pharmacodynamics.
Despite reduced glucose utilisation it is vital to provide adequate quantities of carbohydrate as some systems are unable to use other substrates.
Lipids are necessary to prevent free fatty acid deficiency.
Protein is essential to preserve muscle from breakdown and normal requirements are increased.

24h requirements


Water 30 ml/kg
Energy women 25; men 30 kcal/kg IBW
Protein 1-2 g/kg (1 g protein = approx 0.15 g N)
Nitrogen 0.2 g/kg (1 g N = approx 6.25g protein)
Glucose 3 g/kg
Lipid 2 g/kg
Na 1mmol/kg
K 1 mmol/kg
Ca/Mg 0.1 - 0.2 mmol/kg
PO4 0.5 mmol/kg


Fat soluble
- A,D E and K
Water soluble
- Thiamine, Riboflavin, Niacin, Pyridoxime, Biotin, B12, Folate, Ascorbic acid
Trace elements
- Iron, Copper, Selenium, Zinc, Chromium

Calorific requirements should be based on ideal body weight (IBW) as this is the major factor determining daily energy requirements.
The amount of vitamins, minerals and trace elements needed in critical illness is unknown.
Patients used to be given over their calorific requirements to compensate for the increased metabolic rate of critical illness but this has since been shown to have adverse outcomes.
>1/3 but <2/3 calculated requirements improved mortality and reduced ventilation (Krishnan et al Chest 2003; 124: 297 – 305)
The high energy requirements of critically ill decline swiftly.
Trials showing benefit of feeding do so despite ‘too little’ nutrition.
High levels of protein do not show better clinical outcomes.
High protein and energy feeding increases mortality in animal sepsis.
Mortality of very malnourished in refeeding camps increased with high protein (although we can monitor patients much more closely in ICU).
NICE recommend PN at rate of 50% for 1
st 48h.
EN can be given at full rate as often takes time to establish anyway.

Re-feeding syndrome

Malnourishment causes:
  • Depletion of K, Mg, PO4 and thiamin
  • Increased ICF and total body Na and water.
  • Reduced insulin
  • Impaired cardiac, renal and liver function
Feeding causes:
  • Shifts K, Mg and PO4 intracellularly and Na and water extracellularly.
  • Increases thiamin demand as cells switch back to carbohydrate metabolism from ketone production.
Can therefore cause:
  • Arrhythmias, heart failure, oedema, weakness, hyperglycaemia, Wernike-Korsakoff syndrome

Risks (need 1)
  • BMI <16
  • Unintentional weight loss >15% in last 3-6/12
  • Not fed for >10days
  • Low levels of K, PO4, Mg prior to feeding
Minor (need 2)
  • BMI <18.5
  • weight loss >10%
  • Not fed for >5days
  • alcohol abuse, drugs (insulin, chemo, antacids, diuretics)

Start feed at 50% or less and build up over 24-48h.
Close monitoring - ECG, fluid balance, electrolytes
Thiamin and other B vitamins (either thiamin + vit B co-strong NG
or IV pabrinex)
Enteral or IV supplementation of K (2-4mmol/kg), Mg (0.2-0.4mmol/kg) and PO4 (0.5mmol/kg) daily. Pre-feeding correction unnecessary as the deficit is intracellular which won’t be corrected without feeding but they should be started together.


Glutamine becomes an ‘essential’ amino acid during periods of critical illness. Important fuel for enterocytes and lymphoid cells, and facilitates nitrogen transport. Glutathione precursor.
Arginine modulates nitrogen balance, promotes T cell proliferation and stimulates macrophage and natural killer cell function.
Omega-3 fatty acids are anti-inflammatory agents and immune modulators.
These immune-enhancing nutrients may be added separately or in combination to provide targeted immunonutrition.

  • Glutamine in PN for all ICU patients and in EN for burns, trauma and elective surgical
  • Arginine in elective surgical (harmful in sepsis; no benefit in general ICU patients)
  • Omega 3 possibly beneficial in ALI
  • Antioxidants possibly beneficial in general ICU
Use is not supported in the wider critically ill population where there is no reduction in nosocomial infection rates or mortality.

Other additives

Fibre often used for both constipation and diarrhoea. Little evidence to support it.
Probiotics may have an as yet undefined role. BUT they increase mortality in SAP via bowel ischaemia so should not be used until supported by evidence.

Timing and route

There is general consensus among the critical care community that enteral nutrition should be started early (24-48h) with evidence (though weak) to support this - see below.


NICE - Early vs late postoperative enteral nutrition
Nutritional status improved. No significant differences in mortality, LOS or morbidity.
The table from NICE shows trends towards reduced morbidity (other than vomiting) for early feeding in post operative patients. Note the trend towards
reduced anastomotic breakdown with enteral nutrition.

Critically Ill

Early feeding
ACCEPT 2004.
Shorter length of hospital stay and trend to reduced mortality.
JAMA 2009.
No difference in LOS. Less renal dysfunction. Trend to reduced mortality.
ICM 2009;35(12):2018-2027 - systematic review
Early EN defined as within 24h.
Significant reduction in mortality and pneumonia.
BUT - Number of patients small and trials heterogenous.
Data therefore not robust enough to drive practice.
Did not include the above trial in JAMA 2009 which showed only trend to reduced mortality.

EN vs PN
Conflicting evidence
2 major meta-analyses using many of the same studies drew different conclusions
Heyland et al. JPEN 2003; 27(5):355-73. No mortality difference, reduced infectious complications for EN.
Simpson et al.
ICM 2005; 31(1):12-23. Mortality advantage for PN (but only in studies where EN delayed).

Early TPN vs late enteral or parenteral nutrition. Prospective observational.
JPEN 2011;35:160-168
The meta-analysis in ICM 2005;31:12-23 concluded early TPN better than late enteral (mortality reduction) but this is controversial due to the weakness of the evidence and the disagreement with Heyland’s 2003 meta-analysis.
The above 2011 JPEN study concluded early TPN results in greater intake of calories and protein but no outcome improvements.
EN is superior to PN in pancreatitis (see below).
Supports current recommendations to maximise enteral nutrition before starting TPN.
Benefit or harm from early TPN remains unclear - need decent trial.

Nutrition in pancreatitis

The surgeon 8 2010 105 – 110 - systematic review
NJ compared to PN reduces infectious complications, inflammation, organ failure and radiological changes of pancreatitis. No mortality difference.
NJ feeding safe if started within 6h.
NG equivalent to NJ.
Probiotics not beneficial and may increase mortality.

IV glutamine should be used in PN for pancreatitis.
No evidence for prokinetics in pancreatitis but there is in critically ill in general so should be used in SAP.
Antioxidants may be of benefit.

EN vs PN in pancreatitis
Cochrane review 2010
EN reduces mortality, infections, MOF and need for surgery compared to PN.
No of patients small.
EN should be started early and PN only used after several days of efforts to establish PN.

  • More physiological
  • Cheaper than PN
  • Decreases stress ulceration and GI haemorrhage
  • Prevention intestinal injury (gut villous atrophy and increased permeability)
  • Possible prevention bacterial translocation (but v. little evidence - only in rats) - prevent SIRS and MODS
  • Meet nutritional requirements of the bowel (50% small bowel, 80% large bowel met from gut lumen)
  • Preserve gut-associated lymphoid tissue
  • Tube insertion - perforation nasopharynx, oesophagus
  • Presence of tube - ulceration, discomfort
  • Admin of feed - abdo pain, distension, D, V, aspiration, VAP
  • Failure to tolerate feed by enteral route
  • High output fistulae
  • Less than 18 inches of small bowel
  • Catheter-related problems (infection, thrombosis, catheter misplacement)
  • Metabolic derangement (hyperglycaemia, electrolyte disturbances)
  • Acute fatty liver; hepatic dysfunction (cholestasis)
  • Fluid excess
  • Acid–base disturbance
  • Gut mucosal atrophy
  • Overfeeding

Glucose control

Tight glycaemic control
and hyperglycaemia increase morbidity and mortality in critically ill patients.
Optimal levels not established but 5-10 seems sensible.