2. Outlines
Introduction remarks
Nutritional requirement at baseline
Metabolic response to stress and
alteration of nutritional requirement
Pitfalls in critical illness nutrition support
Special consideration (1) enteral vs. PN
Special consideration (2) Glutamine
3. Problems in critical care nutrition
Baseline malnutrition is common
Poor tolerance to feeding is the rule
Catabolic state resulting into protein loss
Poor wound healing, suppress immune
• Feeding-related complication easily seen
aspiration, VAP, line sepsis, re-feeding
syndrome, under/ overfeeding, LFT
derangement, electrolytes disturbance
4. What a normal person needs
Energy (measured in kCal)
CHO: 30-70% of total calories
Fats: 15-30% of total calories
Proteins: 1g/kg of body weight
Minerals: specific need for different metals
Vitamins
Water
5. 25-30 kCal per kg weight per day
Men: 66 + (13.7 × W) + (5 × H) − (6.8 ×
A)
women: 655 + (9.6 × W) + (1.8 × H) −
(4.7 × A)
W = body weight in kg
H = body height in cm
A = age in years
Harris-Benedict equations (basal
metabolic rate in kcal/day):
6. Amount of energy produced for
different substrates
Substrate Calorie content
kCal Kilo-joules
Protein 4 17
Carbohydrate 4* 17
Fat 9 38
*3.4 kcal if in solution form
7. Minerals
State of catabolism
Normal Mildly
catabolic
Severe
catabolic
Sodium 1-4 mEq 2-3 mEq 3-4 mEq
Potassium 0.7-0.9 mEq 2.0 mEq 3-4 mEq
Calcium 0.22 mEq 0.3 mEq 0.4 mEq
Phosphorous 0.3 mEq 0.8 mEq 1.2-2.0 mEq
Magnesium 0.3 mEq 0.3-0.4 mEq 0.6-0.8 mEq
Minerals requirement: per kg BW per day
8. Starvation vs. stress (injury)
Starvation: peripheral tissue adapted to
uptake free fatty acids and ketone derivatives
mobilized from adipose tissue. Prognosis
depends on availability of fat.
Stress: early protein breakdown to amino
acids which are used (1) gluconeogenesis;
(2)TCA cycle substrates. Prognosis depends
on cessation of catabolism.
12. Metabolic response to stress—
three phases
a) Ebb phase (early phase)
Immediately after injury
Decreased oxygen consumption, hypothermia,
lethargy
b) Flow phase (36-48 hours after injury)
Increased oxygen consumption, hyperthermia,
increased nitrogen excretion and catabolism
Lasts for days, weeks, or months until healing
c) Recovery phase
Anabolism to replace loss
13. Metabolic
response
Sequence of events
Sepsis/trauma
Tissue trauma
Septicemia
Cell deaths
local
inflammatory
response
wound healing
recovery
hypermetabolism
muscle wasting
immunosuppression
organ failure
mortality
Death
Malnutrition
New sepsis
Immobility
Ebb
phase
Flow
phase
Anabolic
phase
19. 70 kg patient in stress
Postoperative 25-30 kcal/kg BW/d 1750-2100 kcal/d
Poly-trauma 30-35 kcal/kg BW/d 2100-2450 kcal/d
Sepsis 25-40 kcal/kg BW/d 1750-2800 kcal/d
Burns 30-45 kcal/kg BW/d 2100-3150 kcal/d
Adjust energy supplement in sick person
20. Adjust protein requirement
1. Normal: 0.8 g/kg body weight
2. Moderate stress: 1.0 to 1.5 g/kg
body weight
3. Severe stress: 1.5 to 2.0 g/kg body
weight
28. To improve stability
Maintain final concentration of nutrients:
1. Amino acids 2.5%
2. Dextrose 3.3%
pH > 5.0
Mixing of TPN components (D, AA, Lip)
1. Avoid direct mixing of D and Lip }
2. Add Lip the last step }
Multi-chamber
29. Maximum dextrose infusion
For a 60 kg patient
Dextrose infusion should not be
greater than 0.36g/kg/hr
0.36 x 60 kg x 24 hr
= 518 grams per day
Excessive dextrose be converted to fat
causing fatty liver and LFT derangment
30. Estimate daily requirement by
calculating non-protein kcal : N
ratio
1. 150:1 unstressed patient
2. 100:1 severely stressed patients
3. 80:1 most severely stressed
Non-protein kcal = 3.4 kcal x
Dextrose in g + 1.1 kcal x 10% lipid in
volume
Proteins/ amino acids
31. IV Lipids
Isotonic and calorically dense, i.e. a good
source of calories for catabolic patients, or
patients with volume/ CHO restrictions
Can provide 60% of non-protein calories
Should not exceed 2.5g/kg lipids per day
4% of total caloric intake should be essential
fatty acids (EFA)
10% lipid contain 1.1 kcal/ml
32. IV lipids may be risky if
Contraindicated if
1. Abnormal lipid metabolism
2. Lipid nephrosis
3. Severe egg allergies
4. Acute pancreatitis with high TG
Cautious if
1. Chronic liver disease
2. Abnormal coagulation
3. Impaired pulmonary function
33. Medium chain triglycerides
Theoretically better for sick patients
1. Enter mitochondria independent of
carnitine, i.e. more ready for TCA
cycle
2. More ketones produced utilized by
peripheral tissue as energy source
Less proinflammatory
34. IV vitamins supplement
Supplements added into TPN just prior to
administration to prevent loss from light
Water-soluble vitamins (Soluvit) are given
with amounts greater than the RDA since
urinary losses increase with IV bolus
Fat-soluble vitamins (Vitalipid) can
accumulate, and are provided in amounts
equal to the RDA
35. Lactic Acidosis Traced to Thiamine Deficiency Related to
Nationwide Shortage of Multivitamins for Total
Parenteral Nutrition -- United States, 1997
Weekly
June 13, 1997 / 46(23);523-528
36.
37. In comparing TPN with EN
Myth: TPN is beneficial
Previous studies have flaws in design
1. Parenteral nutrition was compared with late
enteral nutrition
2. Nasogastric feeding was not based on
logical standardized protocol
3. Glycemic control not mentioned
4. Subgroup benefit: severe malnourished?
38. Meta-analysis comparing EN and PN
ICM 2005; 31:12-23
Nine studies from 465 publication. Included
studies are RCT for critically ill cases with
meaningful clinical outcomes
Primary analysis
1. Mortality: OR 0.51 (0.27-0.97) for PN
2. Infections: OR 1.66 (1.09-2.51) for PN
Subgroup: different timing of EN vs. PN
1. Mortality: OR 1.07, NS for PN vs. early EN
OR 0.29 (p=0.006) vs. late EN
2. Infection: OR 1.47, NS for PN vs. early EN
OR for PN vs. late EN not available
40. Potential risk of late enteral
feed
GI tract mucosa morphological change
1. Thinning of mucus covering layer
2. Simplification of microvilli
3. Reduced turnover of surface epithelia
4. Prolonged gut transit time
Possible net result
1. Relative malabsorption
2. Enhance bacterial +/- toxin translocation
44. What we are sure about TPN
More expensive
More infection
More demanding in nursing care
No concrete mortality benefit over the enteral
nutrition
Last resort in conditions with gut failure
Infection control strategy
Faster to reach feeding target
45. Glutamine story
Muscles: will be released to liver (as Alanine)
and kidney during catabolic state
Liver: raw material for gluconeogenesis;
important for urea cycle
Kidney: carrier for ammonia which is vital in
urinary acid excretion
Intestine: principal ‘food’ for epithelial cells
White cell: essential for differentiation
46.
47. At molecular level!
Enhanced heat shock protein expression
Reduced cellular apoptosis, in particular the
GI epithelial cells
Attenuation of cytokines release
Elevated Glutathione level at stress state
Attenuation of inducible nitric oxide synthase
(iNOs) activation during inflammation
48. What literature said about
glutamine clinical benefit
May reduce mortality
May reduce infectious complication
Route: intravenous route had more abundant
evidence
Dose: >0.5g/kg weight/ day
Particular benefit groups: Burns
Trauma
Critical sepsis
In conjunction with PN?
49. Meta-analysis of glutamine
supplementation in critical illness
Fourteen randomized studies, excluding
immune-modulating diet studies
Included trauma, burns, elective post-op,
medical/ surgical ICU cases
In 751 patients, glutamine associated with RR
0.78 (0.58-1.04) for mortality
In 326 patients, RR for hospital infections
0.80 (0.64-1.00)
In 541patients, shorter LOS seen (-2.6 days)
50. Meta-analysis of glutamine
supplementation in critical illness
Subgroups analysis
Elective OT: no effect on mortality
less infection (RR 0.36)
shorten LOS (-3.54 days)
ICU: trend to reduce mortality (RR 0.77)
trend to reduce infections (RR 0.86)
no effect on LOS
51. Meta-analysis of glutamine
supplementation in critical illness
Route: fewer death (RR 0.71) in
parenteral route but not enteral route.
LOS was shortened significantly (-2.8
days) for IV
Dose: high dose (0.2g /kg/ day) was
associated with fewer deaths (RR 0.71);
fewer infections (RR 0.58) and LOS (-
2.67 days); lower doses had no effect
CCM 2002; 30 (9): 2022-2029
52. Glutamine effect on intestinal
permeability
Measure by calculation of urinary lactulose:
mannitol ratio after oral ingestion. Increased
ratio for higher GI permeability
“Protective”: supplementation before or
immediately after OT, trauma or burns can
prevent GI permeability increase
“Therapeutic”: in established case of raised
permeability, glutamine cannot abolish the
disease
CCM 2005; 33: 1125-1135
53.
54. Effects on burn patient
CCM 2003; 31: 2444-2449
A prospective randomized double-blind
Randomized within 24 hours burn, with
surface area at least 20% involved
Exclude age >65, BSA >80%, CRF, CHF
Enteral supplement with Glutamine 26g/day
or isonitrogenous mixture
Positive blood cultures were 3x more common
in control (4.3 Vs. 1.2 days/pat)
Two death in treatment vs. 12 in control
55.
56.
57. Summary
In stress, modification of nutritional support
is important
Be careful about TPN
Supportive measures required to prevent
complication
Early feeding if possible
More evidence to be waited: immune
nutrition, glutamine supplement protocol