Kompan Lidija
University Medical Center
Ljubljana
Slovenija
Constant supply
of substrates to generate ATP.
Evolution developed metabolic response to stress,
in which previous supply was supposed to cover all the needs.
This was essential for short term survival.
When extreme and long lasting,
it carries a danger of self destruction!
Metabolic response to critical illness
anearobic
Ketogenesis in stress
glycolisis
is supressed
Synthesis of acute proteins
VLDL FFA oxidation ~ glycogen
260g proteins/day
Alanine
gluconeogenesis
It is aimed at support of wound healing
Increased proteolysis
and hyperdynamic circulation. • Lypolisis
↑FFA, glycerol
Immune cells
Hyperglycemia in critical illness
• ↑ hepatic glucose production
• ↓ peripheral glucose uptake.
Peripheral Insulin Resistance
• ↑ insulin levels
We must be aware, that hyperglycemia can not be fully supressed by
exogenous insulin!
Toxic effects of severe hyperglycemia
• Glucose is pro-inflammatory. (glycans)
• Glycemia is independant risk factor for:
o infection
o myocardial dysfunction,
o poor outcome after brain trauma,
o neuromuscular weakness.
• Survivors experienced less variability
in glucose levels than the nonsurvivors.*
*Egi M et al: Variability of blood glucose concentration and short-term mortality in critically ill patients. Anesthesiology
2006; 105:244-252
Intensive insulin therapy (IIT) aiming
at achieving TGC
• Leuven I study *:
◦ 1,548 elective cardiac surgery.
◦ IIT group: blood glucose of 4.4 to 6.1 mmol/l,
control: 'conventional' target of 10 to 11.1 mmol/l.
◦ → ICU mortality was reduced from 8% to 4.6%.
• Leuven II study**, Krinsley***
*Van den Berghe G et al.: Intensive insulin therapy in the critically ill patients.
N Engl J Med 2001, 345:1359-1367
**Van den Berghe G, et al: Intensive insulin therapy in medical intensive care patients.
N Engl J Med 2006; 354:449-461
***Krinsley JS: Effect of an intensive glucose management protocol on the mortality of
critically ill adult patients. Mayo Clin Proc 2004; 79:992-1000
Criticism of IIT
CREATE-ECLA, DIGAMI-2, GIST, VISEP,
GLUCONTROL – ESICM study: 21 units, 1099 randomized patients.
Group A Group B
(n = 538) (n = 553) P
ICU death rate, % 12.27 9.76 0.186
(primary end-point)
Glycemia, mg/dl 118 (109-131) 144 (127-163) 10 mmol/l (180 mg/dl) is no longer an
acceptable target for insulin therapy.
Therefore:
•Because blood glucose levels of <8 mmol/l (140 mg/dl) were also
associated with improved outcome* → proposed levels 6 -8 mmol/l ?
•Insulin therapy without glucose control does not work.
*Krinsley JS . Mayo Clin Proc 2004; 79:992-1000
Finney SJ et al:. JAMA 2003; 290:2041-2047
Gabbanelli V, et al. Minerva Anestesiol 2005; 71:717-725
The aim of modern ICU nutriton:
• to limit endogenous loss by avoiding starvation,
• to maintain tissue function,
• to modify metabolic changes using special substates.
Nutritional support is accepted as an essential component
of care in the intensive care unit.
However,
•nutrition is not a magic tool, which will stop catabolism,
•and here are still unsettled questions.
Does every ICU patient need nutrition
support?
• It is generally accepted that nutritional support is needed at
patients at extreme risk and at those with pre-existing
malnutrition (NRS 2002).
• Therefore, nutritonal support is needed at most ICU patients.
ESPEN Guidelines on EN: Intensive care. Clinical Nutrition (2006) 25, 210-233.
When do we start nutrition
support?
Haemodynamically stable ICU patients who have funtioning gut
should be fed early (within 24 hours) using an appropriate amount of feed.
ESPEN Guidelines on EN: Intensive care. Clinical Nutrition (2006) 25, 210-233.
However, it is evident that not only early enteral, also early parenteral
nutrition reduces mortality!
Which is the optimal method for
providing nutrition :
enteral or parenteral?
Beneficial effects of enteral route have become well-established.
o on the gut,
o the immune system,
o the liver,
o and the host's endocrine and metabolic milieu
Therefore:
Heyland DK et al. Canadian clinical practice guidelines for nutrition support in mechanically ventilated,
critically ill adult patients. JPEN J Parenter Enteral Nutr. 2003;27:355-73.
ESPEN Guidelines on EN: Intensive care. Clinical Nutrition (2006) 25, 210-233.
Should we combine EN with PN?
Some degree of EN intolerance is common in ICU.
Therefore it is a practice to start combined nutrition.
(ESPEN Guidelines on EN: Intensive care. Clinical Nutrition (2006) 25, 210-233.
Try enteral route first and if it works,
there is no need to combine enteral with parenteral!
Which is the optimal access :
pre or post pyloric?
Enteral nutrition using a nasojejunal route seems not to be an efficacious
measure to decrease nosocomial pneumonia in critically ill patients.
Cook D. Crit Care 1997; 1: 3-9
Montejo JC, et al. Crit Care Med. 2002;30:796-800.
(ESPEN Guidelines on EN: Intensive care. Clinical Nutrition (2006) 25, 210-233.
Start gastric feeding and proceed to jejunal if it fails!
What are the measurements for
intolerance to EN?
1. Vomiting √
2. Diarrhoea ?
3. Abdominal distension ?
intraabdominal pressure <10 mmHg → successful EN*
4. Measaurement of gastric aspirate volume (GAV)?
• There is no “consensus” on a safe GAV in critically ill patient:
o minimal EN if GAV 600 -1200ml/24h **
o Continue EN if GAV 400- 500 ml/24h ***
o The trend may be more useful than use of a cutoff value ?
• GAV in a patient receiving continuous gastric feeding is unclear.
• GAV is also unreliable for predicting regurgitation and aspiration****, it´s
measurement does not prevent pneumonia, but body position does.*****
5. Biochemical parameters: triglicerides, urea, glucose.
*Burch JM, 1996 Surg Clin North Am
**AKE recomendations 2002
***ASPEN 2002
****Zaloga G. The myth of the gastric residual volume. Crit Care Med. 2005; 33:449-450
***** Drakulovic Lancet 1999
Feeding protocols
? metoclopropamide
Mentec H et al. Upper digestive intolerance during enteral nutrition in critically ill patients: Frequency, risk factors, and
complications. Crit. Care Med. 2001; 29:1955-1961.
What is the optimal amount od energy?
• TRADITIONAL: Harris-Benedict Equations
o Basal Energy Expenditure [BEE]
– BEE Male = 66.47 + 13.75(W) + 5.0(H) - 6.76(A)
– BEE Female = 655.1 + 9.56(W) + 1.85(H) - 4.68(A)
o Total Energy Expenditure [TEE]
– TEE = BEE (AF) (IF)
• AF = Activity Factor (confined to bed =1.2, Out of bed =1.3)
• IF = Injury Factor
– Mild: Surgery =1.2 ;
– Moderate: Pancreatitis =1.3, Infection =1.4, Trauma=1.5
– Severe: Burns=2.0, AIDS=2.0
• SCIENTIFIC: Indirect Calorimetry
– Most accurate way to determine energy expenditure
– REE = [3.9 (VO2) + 1.1 (VCO2) x 1.44]
ICU patients are very variable in their energy and food requirements.
The amount of energy is not important, as long as
excessive hypo or hyper- caloric feeding is avoided!
Krishnan J A. Chest. 2003;124:297-305:
33 to 65% of a target was associated with better outcome.
• However, early agressive EN in brain-injured → ↑ outcome
Taylor, CCM 1999
PRAGMATIC DAILY CALCULATION:
(ESPEN Guidelines on EN: Intensive care. Clinical Nutrition (2006) 25, 210-233.
What is the optimal amount od proteins?
TRADITIONAL: Nitrogen balance =[Nitrogen In] – [Nitrogen Out ]=
[gms diet protein/d x 0.16] – [gms of urinary urea nitrogen/day +
3gms(ubiquitous loss)]
Nowadays the non-protein cal. : N = 100:1 or even less.
Nutrition is not a magic tool, which will stop catabolism!
PRAGMATIC DAILY CALCULATION: up to 1.5g of protein/kg b.wt.
1gN = 6.25 g proteins = 25 g muscle
→for every 1.5g of protein give about 24 kcal or less,
in a 70kg man= 100g of protein and 1600 kcal per day
Which substrates and in what dose
does the ICU patient need?
Micronutritients
Micronutritient Enteral need Parenteral ICU recommendation
Current recommendations for vitamin supplementation
Copper 2-3 mg
Selenium* 50 μg
0.5-1.5 mg
are inadequate for ICU patients.1.5mg
30-60 μg 120 μg
Zinck* 15 mg 3.2 –6,5 mg 40 mg
Iron 10- 18 mg 1.2 mg 1.2mg
Chromium 50 -200 μg 10-20μg 20-30 μg
Vitamin C* 60 100mg 1000mg
Vitamin B1 1.5 mg 3mg 10- 100 mg
Vitamin B2 1.2 -1.7 mg 3 mg 10 mg
ESPEN Guidelines on EN: Intensive care. Clinical Nutrition (2006) 25, 210-233.
Vitamin B3 1.3 -1.9 40 mg 100 mg
Vitamin B6 2.0 -2.2 mg 4 mg 40 mg
3 μg
Vitamin B12 5 μg
Nutritionally complete EN meets RDA 4 μg
Vitamin A 1500- 3000 IU 3000 5000 IU
Vitamin E in 10 mg 200 to
8 - 10 mg IU volume from 1 IU 2 L.
Vitamin K 20-40 μg 15 mg 20 μg
Vitamin D 200 IU 0.4 mg 400 IU
Panthotenic ac. 4-7 mg 20 mg
Folic ac. 0.4 mg 2.5 mg
Biotin 100 -200 μg
Carbohydrates
• Non-protien calories from carbohydrate amounts 30% to 80%.
• Glucose requirements in acute stress decreases to 2.5- 4 mg/kg/ min.,
not less than 160 -220 g /day.
• Preferred parenteral carbohydrate is glucose.
• Enteral carbohydrates are mostly in the form of glucose polymers,
various types of fiber, fructose, and fluctooligosaccarides.
• The majority of enteral nutrtion products do not contain lactose.
• Fiber is also added to enteral formulas to improve stool consistency
and “feed” the colonic enterocyte.
Colonic enterocyte fiber-containing from short chain fatty acids ,
The effectiveness ofobtains its energyformulas has not been proven.
which are derived from bacterial digestion of fibre
Lipids
Optimum is debatable
•3% calories as fat is sufficient for essential FA requirements,
•10 -15% will minimize de novo lipogenesis,
•over 50% will affect CO2 production.
Due to ↓ ketogenesis in stress: ~ 1.4g/kg/day
Lipids in PN ?
Fat emulsions increase susceptibility to infection and prolong
respiratory failure.
Battistella FD, et al. A prospective, randomized trial of intravenous fat emulsion administration in trauma victims
requiring total parenteral nutrition. J Trauma. 1997;43:52-8.
In well nourished, tolerating EN, or on short-term PN
witholding parenteral lipids should be considered.
Heyland DK et al. Canadian clinical practice guidelines for nutrition support in mechanically ventilated, critically ill
adult patients. JPEN J Parenter Enteral Nutr. 2003;27:355-73.
Is ω- 3 alternative?
ESPEN Guidelines on EN: Intensive care. Clinical Nutrition (2006) 25, 210-233.
Medium-chain triglycerides (MCT) ?
• Do not require bile salts or pancreatic lipase for absorption and may
be used in patients with lipid malabsorption disorders.
• Not carnitine for intracellular difussion.
• Not precursors for prostglandins
• Induce ketogenesis
• However, MCT oil does not contain essential fatty acids and
may cause delayed gastric emptying.
• Maximum dose 0.5 mg/kg/min
Proteins and amino acids
• Dietary protein intake can replace protein losses,
but further protein sparing cannot be achieved once 1.5 g of
protein/kg b.wt. is provided.
• Parenteral solutions contain balanced essential and nonessential
mixtures of amino acids.
• Enteral formulas contain preferably intact proteins.
ESPEN Guidelines on EN: Intensive care. Clinical Nutrition (2006) 25, 210-233.
Predigested diets have little place in ICU
unless there is very little mass of bowel left, or bowel is grossly diseased.
What should we be giving?
Summary:
• Avoid overfeeding
• Avoid "predigested" foods if possible
• Give fibre if possible
• Give lots of vitamins
• 1 to 1.5 g/kg of quality protein with glutamine
supplementation.
It may be better to marginally underfeed the patient with
quality high-protein, fibre-containing food than
overfeed him/her.
Thank you!
Is ω- 3 alternative?
ESPEN Guidelines on EN: Intensive care. Clinical Nutrition (2006) 25, 210-233.
Medium-chain triglycerides (MCT) ?
• Do not require bile salts or pancreatic lipase for absorption and may
be used in patients with lipid malabsorption disorders.
• Not carnitine for intracellular difussion.
• Not precursors for prostglandins
• Induce ketogenesis
• However, MCT oil does not contain essential fatty acids and
may cause delayed gastric emptying.
• Maximum dose 0.5 mg/kg/min