This document discusses nutritional support for ICU patients. It begins with a brief history of ICU nutrition and outlines the basis for nutritional support. Providing nutrition is important to prevent the physiologic effects of malnutrition, which can lead to organ dysfunction and poor outcomes. The nutritional requirements of ICU patients, including calories, protein, fluids and micronutrients are described. Enteral and parenteral routes of feeding administration are covered, along with their indications. Guidelines for initiating feeding, monitoring for complications, and calculating nutritional needs are provided. The goal of nutritional support is to improve patient outcomes by preventing and treating critical illness-related malnutrition.

1. BY : DR SITI AZILA
MODERATOR : DR NIK AZMAN
DATE : 12TH JANUARY 2012

2. OUTLINES
 History
 The Basis of Nutritional Support
 Physiologic Effect of malnourish
 Nutritional Requirement
 Supplimented nutrition
 Routes of administration ( Enteral, parenteral)

3. SIX SIMPLE QUESTIONS
 Why do we feed ICU patients?
 Which patients should we feed?
 When should we start to feed them?
 Which route should we feed by?
 How much feed should we give?
 What should the feed contain?

4. ICU Nutrition in the 1970s

5. ICU NUTRITION THROUGH THE AGES
Overfeeding
1980s

6. THE BASIS OF NUTRITIONAL SUPPORT
 Most patients in ICU are unable to tolerate normal
diet
 many of them are malnourished on admission
 nutrients can be delivered directly to the GIT by
feeding tubes( enteral feeding) or by intravenous (
parentral feeding)
 nutrition is provided against a bakground of a
continously changing physical status

7. THE BASIS OF NUTRITIONAL SUPPORT
 few data directly compare feeding with no
feeding in critical patients and it suggest
worse outcomes in underfed patients
 catabolism of critical illness causes
malnutrition
 malnutrition closely associated with poor
outcomes

8. THE BASIS OF NUTRITIONAL SUPPORT
 Stress, acute illness, surgery or trauma produce
major changes in the metabolic milieu of the body
 changes in substrate utilization
 altered substance synthesis rates
 hypermetabolism
 catabolism

9. Hypermetabolism Poor intake Surgery
malnutrition
Immobility
FACTORS FAVOURING THE DEVELOPMENT OF
Stress in
MALNUTRITION IN THE CRITICALLY ILL
the critically ill
Changes
in
Exogeneous steroids Prolonged bed rest
substrate
utilisation

10. CONSEQUENCES OF MALNUTRITION
 Increased morbidity and mortality
 Prolonged length of stay in ICU
 Impaired tissue function and wound healing
 Defective muscle function, reduced respiratory and
cardiac function
 Immuno-suppression, increased risk of infection

11.  Malnutrition causes widespread organ
dysfunction, ass. with poor healing, reduce
immune competence & poor weaning from
ventilator.
 Stress & sepsis further increase metabolic rate
& if the energy required is not met with
adequate dietary intake, it will results in
catabolism.
 Goal of nutritional support : to improve patients
outcome and reduce the morbidity and
mortality.

12. NUTRITIONAL SUPPORT IS NOT
CRUCIAL IN “GUT FAILURE”
Is that the right statement?

13. TRY TELLING THE RESPIRATORY
PHYSICIAN THAT VENTILATORY
SUPPORT IS NOT IMPORTANT IN
RESPIRATORY FAILURE

14. NUTRITIONAL CARE PLAN
Functional
GI tract
Yes No
Enteral nutrition Parenteral nutrition
Standard nutrients Speciality formulas Peripheral PN Central PN

15. PHYSIOLOGIC EFFECTS OF
MALNUTRITION
Pulmonary
 Decreased diaphragmatic contractility
 Depressed hypoxic drive & ventilatory drive to CO2
Cardiac
 Decreased contractility/response to inotrope
 Ventricular dilatation
Renal
 Decreased GFR
 Impaired Na+ excretion

16. Hepatic
• Altered CHO, protein & fat metabolism
• Decreased protein synthesis
• Decreased drug metabolism
• Impaired bilirubin excretion
Hematology
• Anaemia & coagulopathy
Immune
• Depressed T-cell functions
• Impaired chemotaxis and phagocytosis
GIT
• Decreased gut motility
• Gut atrophy
• Increase gut permeability to intestinal bacteria
•

17. NUTRITION REQUIREMENT

18. 1.Fluid 30-40 ml/kg BW
2. Energy 1. Total Energy expenditure
2. Calorie/weight : 25-35 kcal/kg/day
3. Indirect calorimetry
3. Protein Normal prot : 0.8 g/kg/d
HD. CVVHD : 1.1 – 1.4 g/kg/d
Sepsis/trauma : 1.2 – 2.0 g/kg/d
Severe burns : 2.5 – 4.0 g/kg/d

19. NUTRITIONAL REQUIREMENTS
 Total Energy Expenditure ( TEE) = BEE x Injury
Factor
 The BEE is the amount of energy required to
perform metabolic functions at rest, and is
influenced by both body size and illness
 BEE classically is estimated by the Harris-
Benedict equation:
 For men, BEE = 66.5 + (13.75 x kg) + (5.003 x cm) - (6.775 x age)
 For women, B.E.E. = 655.1 + (9.563 x kg) + (1.850 x cm) - (4.676 x age)
** BEE - Basal Energy Expenditure

20. NUTRITIONAL REQUIREMENTS
Basal Energy Expenditure:
Harris-Benedict Equation
Estimate basal energy expenditure using the Harris-Benedict
equations.
m
f
Ma
Female
le
172 cm in
Input Height cm in
60 kg lb
Input Weight kg lb
40 yr mo
Input Age yrs mos
Infection, severe
Stress Factor
br am
Activity Factor Bedrest Ambulating
Calculate Clear
1481
B.E.E. = 2444 kcal/d
Caloric Requirement = kcal/d
http://www-users.med.cornell.edu/~spon/picu/calc/beecalc.htm

21.  Injury Factor
 Mild illness 1 – 1.25 eg. minor op 1.2
 Moderate illness 1.25 – 1.5 eg skeletal trauma
1.35
 Severe illness 1.5 – 1.75 eg major sepsis
1.60
Estimated Total Energy Requirement =
BEE x Activity Factor x Injury Factor

22. INDIRECT CALORIMETRY
 Most accurate.
 Portable bedside system measuring of EE and resp
quotient by measuring and analysing the O2 consumed (
VO2) and the CO2 expired ( VCO2)
 Respiratory Quotient = CO2 production/O2consumption
RQ Interpretation
> 1.00 overfeeding
0.9 – 1.00 CHO oxidation
0.8 – 0.9 Mixed nutrients oxidation
0.7 – 0.8 Fat and protein oxidation

23. SOURCES OF ENERGY
 Carbohydrate, CHO
 Main source of energy, 60% of total energy requirement.
 2-3 g/Kg/day
 1 g CHO = 4 KCal
 Fat
 30-40% of caloric intake.
 1.5-2 g/Kg/day
 1 g Fat = 9 KCal
 Protein
 Not a major energy source. Provide essential & non essential
amino acids for protein synthesis. Use as energy substrate
(CHO @ Fat precursor) in excess.
 1-1.5 g/Kg/day
 1 g Protein = 4 Kcal. 1 g N2 = 6.25 g Protein.
 Non Protein Calories (CHO & Fat) : Nitrogen ratio = 80-200 :
1

24. ESSENTIAL NUTRIENTS
NUTRIENTS THAT CANNOT BE SYNTHESIZED FROM OTHERS.
 Essential Amino Acid
 Isoleucine, leucine, lysine, methionine, phenylalanine,
threonine, tryptophan, valine.
 Cysteine, tyrosine, histidine (in children).
 Arginine, glutamine (in critical ill state).
 Fatty Acid
Linoleic & Linolenic acid.
 Vitamins
 A, B, C, D, E, K.
 Minerals
 Electrolyte : Na+, K+, Ca2+, Mg2+, Cl-
 Trace Element : Copper, Zinc, Selenium, Iron,
Manganase

25. DAILY ALLOWANCES OF MINERALS, /KG/DAY
 Na+ 1-2 mmol
 K+ 0.7 - 1 mmol
 Ca2+ 0.1 mmol
 Mg2+ 0.1 mmol
 Phosphorus 0.4 mmol

26. ENTERAL FEEDING

27.  early feeding usually defined as starting within
the first 24-48 hours of admission
 meta-analysis suggests reduced infections if
patients are fed within 48 hours

28. BENEFIT OF ENTERAL FEEDING
 prevents gut mucosal atrophy by preserves
intestinal mucosal structure and function
 More physiological
 Relatively non-invasive, cheap, easier
 it reduces bacterial translocation and multi-organ
failure
 Reduced risk of infectious complications of PN

29. Delivery method Common indications Precautions
Nasogastric/ -Unable to consume oral nutrition -Tube must be secured
orogastric ( eg. Intubated, sedated, - Verify placement of tube by blue
neurologically impaired) litmus method or by x-ray
- Hypermetabolism in the
presence of functional GIT ( e.g.
burns)
Nasoduodenal/ -inadequate gastric motility -Tube must be secured
Nasojejunal (e.g.gastroparesis) -Verify placement of tube by X-ray
-Partial gastric outlet obstruction or endoscopically
- Severe aspiration risk -Potential dumping syndrome
- Oesophageal reflex
- After upper GI surgery
Gastrotomy -Anyone who requires medium to -Caution in patients with severe
-Percutaneous endoscopic (PEG) long term NG tube feeding ( > 1 GE reflux or gastroparesis
-Radiological mnth) - Contraindicated in patients with
-Surgical -Head and neck injury/surgery ascites and coagulopathies.
Jejunostomy - Injury, obstruction or fistula - Potential dumping syndrome
-PEJ proximal to jejunum
-Surgical

30. Reactions Possible causes
Diarrhoea +/- nausea and vomiting Medications/C. difficile/lack of dietary
fibre/hyperosmolar formula/bacterial
contamination/improper
administration/fat malabsorption
Constipation Inadequate fluid intake/insufficient
fibre/GI obstruction
Aspiration of tube feeding/high gastric Regurgitation of stomach
residuals ( > 150 to 200 ml) contents/feeding while supine/delayed
gastric emptying/tube dislodgement/
gastro-oesophageal reflux
Hyperglycaemia Diabetes/stress/trauma/corticosteroid/se
psis/refeeding syndrome
Hypoglycaemia Sudden cessation of tube feeding in
patients on oral hypoglycaemic
agents/insulin
Hypophosphataemia/hypokalaemia Refeeding syndrome / excessive losses

31. CONTRA-INDICATIONS TO ENTERAL FEEDING
 Bowel obstruction
 Ileus
 Intestinal ischaemia
 Clinical shock

32. PROTOCOL FOR ENTERAL FEEDING
 Guidelines in Enteral_feeding.pdf

33. PARENTRAL NUTRITION

34. TYPES OF TPN
1) Peripheral parenteral nutrition
- Temporary access ( up to 2 weeks)
- Limited caloric density
- High incidence of thrombophlebitis
- High-volume infusion may lead to fluid overload
- Osmolarity should not exceed 900 mOsm/l
- Access : peripheral veins

35.  Central parenteral nutrition
- Able to provide large nutrient, fluid and electrolyte
needs
- Recommended for prolonged IV nutritional support
- Access :
- central line : via subclavian, internal or
external jugular and femoral veins

36. INDICATIONS
Indications ( usually) Indications ( sometimes)
Inability to absorb Major surgery/stress when EN
adequate nutrients via GIT not expected to resume
Severe acute pancreatitis within 7-10 days.
Severe Enterocutaneous fistula
malnutrition/catabolism with Partial small bowel
non functioning GIT obstruction
Complete small bowel Intractable vomiting
obstruction Severe inflammatory
Inability to feed enterally bowel disease not
responding to medical
therapy

37.  Whenever possible, TPN should be instituted
simultaneously with enteral feeding. Partial feeding
via enteral route preserves intestinal mucosa
viability and may prevent bacterial translocation
through the gut wall.

38. SUBSTRATES IN TPN
 CHO
- Dextrose solution are available in concentration ranging
from 5-70%. Solutions greater than 10% must be
administered into the central vein.
- Consequences of excess CHO administration :
hyperglycaemia, glucosuria, synthesis and storage of
fat, hepatic steatosis, increase CO2 production.
 Protein
- Amino acids solutions are available in concentration of
3-15%.
- In critical illness, ensure that enough non protein
calories are administered for the optimal utilisation of
protein: approximately 100 kcal are needed for 1 g of
nitrogen ( 6.25 g of protein)

39.  Fat
- Lipid emulsion available in concentrations of 10%
and 20%.
- Consequences of excess fat administration : fat
overload syndrome, impaired immune response.

40. MACRONUTRIENTS
Nutrients Substrate Usual Amount Maximum
units of
substrate
CHO Dextrose 40-60% of total 7 g/kg/day
monohydrate = kcal
3.4 kcal/g
Protein Amino acid = 4 0.9 to 2.0 2.5 g/kg/d
kcal/g g/kg/d
Fat Lipids = 9 20-40% of total < 1 g/kg/d in
kcal/g ( 20% kcal high stress
emulsion
provides 2
kcal/ml)

41. HOW TO CALCULATE TPN ?
Steps Example: A 56 y.o, 1.75 m tall,
70 kg man
1. Determine the protein 70 kg x 1.5g/kg/d = 105 g/d ( =
requirement 16.8g N)
2. Determine the total caloric Using Harris Benedict equation:
requirement BEE = 66 + ( 13.7 x 70kg) + ( 15 x
175cm) – (6.8 x 56 yr) = 1519
kcal/day ( round off to 1500
kcal/day)
TEE = BEE x IF = 1500 x 1.3 =
1950 kcal/day
3. Divide the total caloric If ratio 60:40
requirement between two energy 1950 x 0.6 : 1950 x 0.4 = 1170 :
substrate, CHO : fat ( 60:40 or 780
70:30)

42. HOW TO CALCULATE TPN..
4. Determine calorie : nitrogen ratio 1950 : 16.8 = 116 : 1
5. Calculate amount of CHO needed If using 70% dextrose solution ( 100 ml
provide 70 g CHO x 3.4 kcal/g = 238
kcal)
1170 kcal / 238 kcal x 100 mls = 492
mls ~ 500 mls
6. Calculate amount of fat emulsion If using 20% intralipid ( provides 2
needed kcal/ml)
780 kcal divide into 2 kcal/ml = 390 ml
7. Estimate fluid requirement 40 ml/kg/day x 70 kg = 2800 ml/d
Therefore : 2800 – ( 500 + 390) = 1910
ml ( of water to be added to meet fluid
requirement)

43. 8. Order electrolytes: Na+, K+,
Mg2+, Ca, phosphorus, acetate
and chloride
9. Order multivitamin, trace
minerals and vitamin K if needed
10. Determine flow rates : volume / 2800 ml / 24H = 117 ml/h
24H

44. COMPLICATIONS OF TPN
 Catheter related sepsis - 3.5% increase in CRBSI
in a meta-analysis compared to EN
 Catheter Malposition
 pneumothorax
 hydrothorax
 Arterial puncture
 Metabolic
 Hyperglycaemia
 Hypoglycemia if TPN is abruptly stopped
 Increased CO2 production & increased O2 consumption if
infusion rates beyond 4 ml/kg/mt.
 Hypomagnesemia, hypophosphatemia if not supplemented
 Fatty liver

45. ENTERAL VS. PARENTERAL NUTRITION
Enteral Parenteral
Advantages Advantages
-Physiological -Independent of GIT functions
-Simpler
-Cheaper
-No CVL required
-Less monitoring
-Less complication
Disadvantages Disadvantages
-Dependent on GIT functions -Non physiological
-Diarrhea -Requires venous access
-Feed intolerance -Higher risk of systemic infection
-NG tube – malposition, sinusitis -Expensive
-Pulmonary aspiration -More complication

46. Enteral Parenteral
Complications Complications
1. Mechanical 1. CVL related complication
-GEReflux 2. Fluid overload
-NG complication – oesophageal 3. Hyperosmolar dehydration
perforation, throat injuries, syndrome –
tracheal placement, hyperglycaemia, osmotic
blockage, rupture diuresis
oesophageal varices 4. Electrolytes imbalance
2. Infection 5. Metabolic acidosis
-Sinusitis, otitis 6. Hyperammonaemia
-Pulmonary aspiration 7. Deficiency Syndromes
-Feed contamination 8. Rebound hypoglycaemia – if
3. GIT – nausea, vomit, diarrhea TPN stopped suddenly due
4. Metabolic to high level endogenous
-dehydration, hyperglycaemia insulin
-electrolyte abnormality 9. Overfeeding syndrome.
-acid base imbalance

47. SUPPLIMENTED NUTRITION

48. GLUTAMINE
 Non-essential amino acid – ‘conditionally essential’
in sepsis/major trauma
 Vital to gut, immune cells, and kidney
 Serves as metabolic fuel; precursor to DNA
synthesis
 BUT Levels drop after injury, exercise and stress.
Very low in critical illness first 72 hours
 Glutamine deficiency at onset of critical
illness/sepsis correlated with increased mortality

49. Immune enhanced diets
 Glutamine
 can prevent or ameliorate the gastrointestinal mucosal
atrophy seen during prolonged parenteral nutrition and
may help the gastrointestinal mucosa heal more promptly
after damage by either radiotherapy or chemotherapy
 Insufficient data to support the use of glutamine in the
critically ill, enteral glutamine supplementation may be of
benefit in trauma and burns patients

50. Potential Beneficial Effects of Glutamine
Enhanced Heat
Enhanced
insulin Decreased Free Shock Protein
sensitivity Radical availability NF-kB
(Anti-inflammatory action)
Inflammatory Cytokine ?
Attenuation
Glutathione
Glutamine Synthesis Reduced
Fuel for Maintenance of
Therapy Translocation
Intestinal Enteric Bacteria
Enterocytes
Mucosal Barrier or Endotoxins
Critical Illness GLN
GLN
Pool
pool Nuclotide
Synthesis
Preservation Reduction of
of TCA Function Fuel for Maintenance of Infectious
Anti-catabolic Lymphocyte complications
effect Lymphocytes
Function
Preserved
Cellular
Preservation of
Energetics-
Muscle mass
ATP content

51. Immune enhanced diets
 Arginine
 Arginine-supplemented parenteral nutrition show an
increased ability to synthesize acute phase proteins
when challenged with sepsis.
 No effect on mortality or infectious complications

52.  Omega – 3 Fatty Acids
 The polyunsaturated fatty acids in artificial feeding solutions
are mostly omega -6 fatty acids. Replacing these with omega-
3 fatty acids has anti-inflammatory effects:
1. production of less inflammatory eicosanoid derivatives
2. reduced cytokine production
Early clinical work in patients with ARDS using enteral feed
enriched in omega-3 fatty acids found a reduction in length of
ventilation and ICU stay.

53. Which Nutrient for Which Population?
Elective Critically Ill
Surgery
General Septic Trauma Burns Acute Lung
Injury
Arginine Benefit No benefit (?) (Possible No No
benefit) benefit benefit
Glutamine Possible PN … EN EN …
Benefit Beneficial Possibly Possibly
Beneficial: Beneficial:
Recom-
Consider Consider
mend
Omega 3 … … … … … Recom-
FFA mend
Anti- … Consider … … … …
oxidants
Canadian Clinical Practice Guidelines JPEN 2003;27:355

54. CONCLUSION

55.  Nutritional support is important in critically ill patients
because :
 Improves wound healing
 Decreases catabolic response to injury
 Improves GI function and structure,
 Reduces complications and length of stay.
 Reduces morbidity and mortality
 Feeding must be commenced as early as possible (
within 24H)
 Enteral feeding is always superior than parenteral
feeding

56. REFERENCES
 Oh’s Intensive Care Manual
 Bedside ICU handbook, 2nd edition, Dessmon YH
Tai , Thomas WK Lew & Loo Shi, Intensive Care
Units of Tan Tock Seng Hospital
 Basic Assessment & Support in Intensive Care
 http://www.pensma.org/index.cfm?&menuid=18
 http://eprints.usm.my/10377/1/THE_PRACTICE_O
F_PARENTERAL_NUTRITION.pdf