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NUTRITION IN ICU BY : DR SITI AZILA MODERATOR : DR NIK AZMAN DATE : 12 TH JANUARY 2012

Nutrition in icu

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Page 1: Nutrition in icu

NUTRITION IN ICU

BY : DR SITI AZILAMODERATOR : DR NIK AZMAN DATE : 12TH JANUARY 2012

Page 2: Nutrition in icu

OUTLINES

History The Basis of Nutritional Support Physiologic Effect of malnourish Nutritional Requirement Supplimented nutrition Routes of administration ( Enteral,

parenteral)

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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?

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ICU Nutrition in the 1970s

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ICU NUTRITION THROUGH THE AGES

Overfeeding1980s

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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

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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

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THE BASIS OF NUTRITIONAL SUPPORT

Stress, acute illness, surgery or trauma produce major changes in the metabolic milieu of the body

changes in substrate utilizationaltered substance synthesis rateshypermetabolismcatabolism

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malnutritionin

the critically ill

Hypermetabolism

Stress

Changes in

substrate utilisation

Exogeneous steroids Prolonged bed rest

Immobility

Poor intake Surgery

FACTORS FAVOURING THE DEVELOPMENT OF MALNUTRITION IN THE CRITICALLY ILL

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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

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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.

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NUTRITIONAL SUPPORT IS NOT CRUCIAL IN “GUT

FAILURE”

Is that the right statement?

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TRY TELLING THE RESPIRATORY PHYSICIAN

THAT VENTILATORY SUPPORT IS NOT IMPORTANT IN

RESPIRATORY FAILURE

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NUTRITIONAL CARE PLAN

S ta nd ard nu trie n ts S p e c ia lity fo rm u las

E n te ra l n u trit ion

Y e s

P e rip he ra l P N C e n tra l P N

P a ren te ra l n u trit ion

N o

F u n ctio n a lG I tra ct

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PHYSIOLOGIC EFFECTS OF MALNUTRITION

PulmonaryDecreased diaphragmatic contractilityDepressed hypoxic drive & ventilatory drive to

CO2

CardiacDecreased contractility/response to inotropeVentricular dilatationRenalDecreased GFR Impaired Na+ excretion

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Hepatic• Altered CHO, protein & fat metabolism• Decreased protein synthesis• Decreased drug metabolism• Impaired bilirubin excretionHematology• Anaemia & coagulopathyImmune• Depressed T-cell functions• Impaired chemotaxis and phagocytosisGIT• Decreased gut motility• Gut atrophy• Increase gut permeability to intestinal bacteria

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NUTRITION REQUIREMENT

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1.Fluid 30-40 ml/kg BW

2. Energy 1. Total Energy expenditure2. Calorie/weight : 25-35

kcal/kg/day3. Indirect calorimetry

3. Protein Normal prot : 0.8 g/kg/dHD. CVVHD : 1.1 – 1.4 g/kg/dSepsis/trauma : 1.2 – 2.0 g/kg/dSevere burns : 2.5 – 4.0 g/kg/d

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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

NUTRITIONAL REQUIREMENTS

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NUTRITIONAL REQUIREMENTS

B a s a l E n e r g y E x p e n d i t u r e :H a r r i s - B e n e d i c t E q u a t i o n

E s t i m a t e b a s a l e n e r g y e x p e n d i t u r e u s i n g t h e H a r r i s - B e n e d i c te q u a t i o n s .

mM a

l ef

F e m a l e

I n p u t H e i g h t 1 7 2 c m c m i n i n

I n p u t W e i g h t 6 0 k g k g l b l b

I n p u t A g e 4 0 y r y r s m o m o s

S t r e s s F a c t o r I n f e c t i o n , s e v e r e

A c t i v i t y F a c t o r b r B e d r e s t a m A m b u l a t i n g

C a l c u l a t e C l e a r

B . E . E . = 1 4 8 1 k c a l / d

C a l o r i c R e q u i r e m e n t = 2 4 4 4 k c a l / d

http://www-users.med.cornell.edu/~spon/picu/calc/beecalc.htm

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Injury FactorMild illness 1 – 1.25 eg. minor op

1.2Moderate illness 1.25 – 1.5 eg skeletal trauma 1.35Severe illness 1.5 – 1.75 eg major

sepsis 1.60

Estimated Total Energy Requirement = BEE x Activity Factor x Injury Factor

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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

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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

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ESSENTIAL NUTRIENTSNUTRIENTS 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 AcidLinoleic & Linolenic acid.

VitaminsA, B, C, D, E, K.

MineralsElectrolyte : Na+, K+, Ca2+, Mg2+, Cl-Trace Element : Copper, Zinc, Selenium, Iron,

Manganase

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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

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ENTERAL FEEDING

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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

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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

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Delivery method Common indications Precautions

Nasogastric/orogastric

-Unable to consume oral nutrition ( eg. Intubated, sedated, neurologically impaired)- Hypermetabolism in the presence of functional GIT ( e.g. burns)

-Tube must be secured- Verify placement of tube by blue litmus method or by x-ray

Nasoduodenal/Nasojejunal

-inadequate gastric motility (e.g.gastroparesis)-Partial gastric outlet obstruction- Severe aspiration risk- Oesophageal reflex- After upper GI surgery

-Tube must be secured -Verify placement of tube by X-ray or endoscopically-Potential dumping syndrome

Gastrotomy-Percutaneous endoscopic (PEG)-Radiological-Surgical

-Anyone who requires medium to long term NG tube feeding ( > 1 mnth)-Head and neck injury/surgery

-Caution in patients with severe GE reflux or gastroparesis- Contraindicated in patients with ascites and coagulopathies.

Jejunostomy-PEJ-Surgical

- Injury, obstruction or fistula proximal to jejunum

- Potential dumping syndrome

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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 residuals ( > 150 to 200 ml)

Regurgitation of stomach contents/feeding while supine/delayed gastric emptying/tube dislodgement/ gastro-oesophageal reflux

Hyperglycaemia Diabetes/stress/trauma/corticosteroid/sepsis/refeeding syndrome

Hypoglycaemia Sudden cessation of tube feeding in patients on oral hypoglycaemic agents/insulin

Hypophosphataemia/hypokalaemia Refeeding syndrome / excessive losses

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Bowel obstruction

Ileus

Intestinal ischaemia

Clinical shock

CONTRA-INDICATIONS TO ENTERAL FEEDING

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PROTOCOL FOR ENTERAL FEEDING

Guidelines in Enteral_feeding.pdf

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PARENTRAL NUTRITION

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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

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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

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INDICATIONS

Indications ( usually) Indications ( sometimes)

Inability to absorb adequate nutrients via GITSevere acute pancreatitisSevere malnutrition/catabolism with non functioning GITComplete small bowel obstructionInability to feed enterally

Major surgery/stress when EN not expected to resume within 7-10 days.Enterocutaneous fistulaPartial small bowel obstructionIntractable vomitingSevere inflammatory bowel disease not responding to medical therapy

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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.

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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)

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Fat- Lipid emulsion available in concentrations of

10% and 20%. - Consequences of excess fat administration :

fat overload syndrome, impaired immune response.

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MACRONUTRIENTS

Nutrients Substrate Usual Amount

Maximum units of substrate

CHO Dextrose monohydrate = 3.4 kcal/g

40-60% of total kcal

7 g/kg/day

Protein Amino acid = 4 kcal/g

0.9 to 2.0 g/kg/d

2.5 g/kg/d

Fat Lipids = 9 kcal/g ( 20% emulsion provides 2 kcal/ml)

20-40% of total kcal

< 1 g/kg/d in high stress

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HOW TO CALCULATE TPN ?

Steps Example: A 56 y.o, 1.75 m tall, 70 kg man

1. Determine the protein requirement

70 kg x 1.5g/kg/d = 105 g/d ( = 16.8g N)

2. Determine the total caloric requirement

Using Harris Benedict equation: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 requirement between two energy substrate, CHO : fat ( 60:40 or 70:30)

If ratio 60:401950 x 0.6 : 1950 x 0.4 = 1170 : 780

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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 needed

If using 20% intralipid ( provides 2 kcal/ml) 780 kcal divide into 2 kcal/ml = 390 ml

7. Estimate fluid requirement 40 ml/kg/day x 70 kg = 2800 ml/dTherefore : 2800 – ( 500 + 390) = 1910 ml ( of water to be added to meet fluid requirement)

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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 / 24H

2800 ml / 24H = 117 ml/h

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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

COMPLICATIONS OF TPN

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ENTERAL VS. PARENTERAL NUTRITIONEnteral Parenteral

Advantages-Physiological-Simpler-Cheaper-No CVL required-Less monitoring-Less complication

Advantages-Independent of GIT functions

Disadvantages-Dependent on GIT functions-Diarrhea-Feed intolerance-NG tube – malposition, sinusitis-Pulmonary aspiration

Disadvantages-Non physiological-Requires venous access-Higher risk of systemic infection-Expensive-More complication

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Enteral Parenteral

Complications1. Mechanical-GEReflux-NG complication –

oesophageal perforation, throat injuries, tracheal placement, blockage, rupture oesophageal varices

2. Infection-Sinusitis, otitis-Pulmonary aspiration-Feed contamination3. GIT – nausea, vomit,

diarrhea4. Metabolic-dehydration,

hyperglycaemia-electrolyte abnormality-acid base imbalance

Complications1. CVL related

complication2. Fluid overload3. Hyperosmolar

dehydration syndrome – hyperglycaemia, osmotic diuresis

4. Electrolytes imbalance 5. Metabolic acidosis6. Hyperammonaemia7. Deficiency Syndromes8. Rebound hypoglycaemia

– if TPN stopped suddenly due to high level endogenous insulin

9. Overfeeding syndrome.

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SUPPLIMENTED NUTRITION

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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

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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

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Potential Beneficial Effects of Glutamine

Fuel forEnterocytes

Fuel forLymphocytes

Nuclotide Synthesis

Maintenance ofIntestinalMucosal Barrier

Maintenance ofLymphocyteFunction

Preservation of TCA Function

Decreased FreeRadical availability (Anti-inflammatory action)

GlutathioneSynthesis

GLNpool

GlutamineTherapy

Enhanced Heat Shock Protein

Anti-cataboliceffect

Preservation of Muscle mass

Reduced TranslocationEnteric Bacteriaor Endotoxins

Reduction ofInfectious complications

Inflammatory Cytokine Attenuation

NF-kB?

Preserved CellularEnergetics- ATP content

GLNPool

Critical Illness

Enhanced insulin sensitivity

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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

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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.

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ElectiveSurgery

Critically Ill

General Septic Trauma Burns Acute Lung Injury

Arginine Benefit No benefit (?) (Possible benefit)

No benefit

No benefit

Glutamine Possible Benefit

PN BeneficialRecom-mend

… EN Possibly

Beneficial:Consider

EN Possibly

Beneficial:Consider

Omega 3 FFA

… … … … … Recom-mend

Anti-oxidants

… Consider … … … …

Which Nutrient for Which Population?

Canadian Clinical Practice Guidelines JPEN 2003;27:355

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CONCLUSION

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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

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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_OF_PARENTERAL_NUTRITION.pdf

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Thank You for your attention