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Critical Care Nutrition
Dr Alfred YF Chan
ICU, PYNEH
23/6/2006
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
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
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
 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):
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
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
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.
Food intake
Fasting
Proteolysis
Negative N balance
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
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
Oxygen
consumption
Time
Stress
Ebb
Flow Recovery
Ebb phase
Physiology change Clinical Effect
 blood glucose
 lactate
free fatty acids
 catecholamine
 glucagon
 cardiac output
Below normal
core temperature
 oxygen consumption
Flow phase
Physiology change Clinical effects
 catecholamine
 glucagon
 cortisol
 insulin
 cardiac output
 temperature
 aldosterone
 ADH
IL1, IL6, TNF
spillage from
wound
 consumption
of glucose, FFA,
amino acid
 O2 consumption
fluid retention
SIRS
N or  glucose
N or  FFA
normal lactate
 CO2 production
 heat production
multi-organ
failure
Physiological outcome in
stress
 Diabetogenic
 Ketogenic
 Proteolytic
 Fluid retention
 Sympathetic hypertonia
 Immunosuppression
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
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
TPN preparation—why bother?
All-in-one Multi-chamber
Instability of lipid-containing TPN
Creaming Aggregation Coalescence Cracking
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
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
 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
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
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
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
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
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
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?
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
Prolonged period of fasting
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
Mortality
LOS
Infection
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
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
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
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?
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)
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
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
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
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
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
Thank you for not eating
now

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critical care nutrition.ppt

  • 1. Critical Care Nutrition Dr Alfred YF Chan ICU, PYNEH 23/6/2006
  • 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.
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  • 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
  • 15. Ebb phase Physiology change Clinical Effect  blood glucose  lactate free fatty acids  catecholamine  glucagon  cardiac output Below normal core temperature  oxygen consumption
  • 16. Flow phase Physiology change Clinical effects  catecholamine  glucagon  cortisol  insulin  cardiac output  temperature  aldosterone  ADH IL1, IL6, TNF spillage from wound  consumption of glucose, FFA, amino acid  O2 consumption fluid retention SIRS N or  glucose N or  FFA normal lactate  CO2 production  heat production multi-organ failure
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  • 18. Physiological outcome in stress  Diabetogenic  Ketogenic  Proteolytic  Fluid retention  Sympathetic hypertonia  Immunosuppression
  • 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
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  • 27. Instability of lipid-containing TPN Creaming Aggregation Coalescence Cracking
  • 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
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  • 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
  • 42. LOS
  • 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
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  • 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
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  • 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
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  • 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
  • 58. Thank you for not eating now