nutrition therapy in critical illness - ucsf cme baltz- ucsftraumaconfe… · nutrition therapy in...
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Nutrition Therapy in Critical Illness
Jami Baltz, RD, CNSDSan Francisco General Hospital and
Trauma [email protected]
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Objectives
• Discuss the hypermetabolism of the systemic inflammatory response and how it relates to nutrition and metabolic response.
• Identify the uses of enteral nutrition to address nutritional and inflammatory issues.
• Demonstrate the inadequacies of traditional approaches to nutrition assessment, intervention, and monitoring.
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Nutrition SupportSupportSupport Therapy: Modulating the Stress Response
and Systematic Immunity
Adjunctive Supportive
Care
Proactive Primary Therapy
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Rationale for Nutrition in the ICU
• Current Goals: "therapy not support"Evidence-based risk reduction– attenuate metabolic response– limit and reverse loss of lean body tissue– prevent oxidant stress– favorably modulate immune response
Martindale R, Maerz L. Current Opin Crit Care 12:290-294,2006
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Metabolic Comparisons: Stress vs. Starvation
↑↑↑↑Urine Nitrogen Loss↑↑↑↑Proteolysis↑↑↑Protein Synthesis↑↑↑Plasma Lipids↓↑↑Ketogenesis↑↑↓Blood Glucose↑↑↑↓Gluconeogenesis↑↓Insulin↑↑Glucagon
MixedFatPrimary Fuels↑↓RQ↑↑↓REE
StressStarvation
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Metabolic Changes to Stress:Resting Energy Expenditure
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3 phases of metabolic response
• Ebb Phase = Stress (0-48 hours)– ↓ Cardiac Output– ↓ Tissue perfusion– ↓ Oxygen Consumption– ↓ REE
Nutritional Goal: Metabolic Support
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3 Phases of metabolic response
• Flow Phase = catabolic (24+hours)– ↑ cytokines– ↑Counterregulatory hormones and ↑ catecholamines
– ↑ Insulin– ↑ O2 consumption,↑ REE– ↑ Catabolism
• Hyperglycemia, + fluid balance, - N balance– Shift toward production of positive acute phase
reactantsNutritional Goal: Metabolic Support
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3 Phases of Metabolic Response
• Repletion Phase = anabolic– Can last for months– May need up to 130% REE to support tissue
repair, repletion, and recovery
Nutritional Goal: shift from metabolic support to promotion of repletion
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Comparison of Measured Metabolic Rate
2015 (RQ 0.71)10
1492 (RQ 1.0)3
1820 (RQ 0.85)17
Measured Metabolic Rate
Hospital Day
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How can Nutrition affect Metabolic Response?
• Enteral preferred to Parenteral• Early Initiation of Enteral Nutrition• Appropriate macro and micronutrients
– Avoid Under/overfeeding– Pharmoconutients
• Meticulous glycemic control
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Enteral is Superior to Parenteral
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Human Studies: Enteral vs TPNWhat Does the Data Show?
Author
Moore
Kudsk
Hasse
Reynolds
Shirabe
Kalfarentzos
Windsor
Gramlich
Population
Trauma
Trauma
Hepatic transplant
GI surgery
Hepatic resection
Pancreatitis
Pancreatitis
Meta-analysis
Year
89
92
95
96
97
97
98
04
Benefit
↓ Infections
↓ Infections
↓ Infections
↓ Infections
↓ Infections
↓ Sepsis/Comp
↓ MOF/SIRS
↓ infections
48 studies in adult populations (46 in english literature)20 surgical, 9 critical care, 7 pancreatitis, 5 IBD, 3 Hepatic disease,3 mixed populations
General conclusions: fewer infections, shorter hospital stay
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TPN risks:Systemic Immune Suppression
• Mucosal atrophy/GALT atrophy• Overfeeding and hyperglycemia• IV Lipids• Catheter Infections
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Use of TPN in Critical Care• EN always first choice for Nutrition Therapy• Second choice depends on:
– Timing:– First week - STD (NPO)– After first week - PN
– Malnutrition (weight loss) - Prioritiesreversed
• No other options for IV fat source (Intralipid)– Omit if PN used over first week
• Minimal use of supplemental PN (no use first week)
Heyland (JAMA 1998; 280:2013), Braunschweig (AJCN; 74:534), McClave (JPEN 2009; 33:277)
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IV Lipids and Immune Function:Clinical Trials
↓Immune function
omega 3 ↓inflammation
IV LCT
Omega 3 vs Omega 6
Esophag
Sepsis
23
21
99
03
Furukawa
Mayer
↓ WBC functionVariousHome TPNx97Waitzberg
↑ infection+/- IV LCTTrauma5597Battisella
2x ↑ infectionHigh/LowBurn4395Garrel
OutcomeDesignPopulation
NYRAuthor
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Dietary Ω-6 FADietary Ω-6 FAMembrane phospholipids
lipoxygenasecyclooxygenaselipoxygenase
Dietary Ω-3 FADietary Ω-3 FA
Arachidonic acid Eicosapentaenoic acid (EPA)Docosahexaenoic acid (DHA)
Leukotrienes(4 series)
Proinflammatory Cell adhesiveChemotactic
Prostanoids & Thromboxanes
(2 series)Aggregates plateletsImmunosuppressive
Prostanoids & Thromboxanes
(3 series)Antiaggregatory
Non-immunosuppressive
Leukotrienes(5 series)
Anti-inflammatoryNonadhesive
You Are What You EatYou Are What You Eat
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The Anti-Inflammatory Effects of Enteral Nutrition
• Enteral nutrition can directly affect inflamed intestine
• Enteral nutrition can blunt acute inflammatory reactants
• Enteral formulas can have direct effect on cytokine/adhesion molecule expression by intestinal epithelium
Sanderson JPEN, 2005; 25:S134
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Early is Better than Later
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Early Enteral Feeding Meta-analysis
Trend to ↓infections and mortality
8 studies<24 to 48 hrHeyland. JPEN. 2003.
↓ Infections↓ LOS↑ Vomiting risk
11 studies837 patients
NPO vs <24 hr
Lewis. BMJ. 2001.
↓ Infections↓ LOS
15 studies753 patients
Feeding < or >36 hr
Marik. CCM. 2001.
OutcomeStudy Design
Study Parameters
Author/Journal
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“Effects of Early Enteral Feeding on the Outcomeof Critically Ill Ventilated Medical Patients”
• ICU patients• Retrospective review of prospectively collected data• N=4049
• 2537 patients fed < 48 hours• 1512 patients fed > 48 hours
• Propensity scoring system to control for confounding variables
• Conclusions:• 20% decrease in ICU mortality (18.1 vs 21.4%)• 25% decrease in hospital mortality (28.7 vs 33.5%)• Influence greatest in sickest patients
– Beneficial effect noted despite increase in VAP
• ICU patients• Retrospective review of prospectively collected data• N=4049
• 2537 patients fed < 48 hours• 1512 patients fed > 48 hours
• Propensity scoring system to control for confounding variables
• Conclusions:• 20% decrease in ICU mortality (18.1 vs 21.4%)• 25% decrease in hospital mortality (28.7 vs 33.5%)• Influence greatest in sickest patients
– Beneficial effect noted despite increase in VAP
Artinian V et al Chest 2006;129:960-967
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Effect of Early EN
• Local– Innate Immunity– Commensal Organisms
• Systemic– Acquired Immunity– Gut-Lung Conduit for Inflammation
Kudsk (Amer J Surg 2002; 183:390)
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Gut Associated Lymphoid TissueG.A.L.T.
• BM, spleen, LN2.5 x 1010 Ig producing cells
• Gut8.5 x 1010 Ig producing cells
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Quantity
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Quantity• Cumulative energy deficit correlated to:1
– Longer ICU stay– More days on mechanical ventilation– More complications
• Underfeeding2
– Lowest quartile (<6kcals/kg/day)• Increase risk bloodstream infections
• Overfeeding3
– Highest tertile (>66% recommended)• Highest mortality• Least likely to breath spontaneously at d/c
– Middle tertile had best outcomes
1Villet (Clin Nut 2005) 2Robinson (Crit Care Med 2004) 3Krishnan (Chest 2003)
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Consequences of Underfeeding
• Respiratory dysfunctionRespiratory muscle strengthVentilatory responseFailure to wean
• Low transport proteins in the absence of inflammation
• Poor wound healing
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Consequences of Overfeeding
• Hyperglycemia • Electrolyte imbalances • Fluid overload • Hyperlipidemia• Organ dysfunction• Hypermetabolism• Failure to wean (CO2 retention)
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Nutrient Delivery in Surgery and Critically Ill Populations
• Calories 20-35 kcal/kg/day• Carbohydrates 3-6 mg/kg/min
– 250-350 gm/day• Protein 1.25 - 2.0 gm/kg/day
– 80-150 gm/day• Lipids 10-30% of total calories
– Dependent on lipid composition• Vitamins/minerals/trace elements
– Adequate to meet needs
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Pharmoconutrients
• Glutamine• Omega 3 fish oils• Arginine• Anti-Oxidants
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“Glutamine: role in gut protection in critical illness”
• Critical illness• Alteration of gut epithelial cell function• +/- data for bacterial translocation• Gut as a source of pro-inflammatory cytokines
• Therapy should be targeted at • Protect epithelial from cell injury• Attenuate the elaboration of proinflammatory
mediators via gut based immune cells
Wischmeyer , PE Curr Opin Clin Nutr Metab Care 9:607-612,2006
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Proposed mechanisms for glutamines ability to attenuate the
SIRS response• Tissue protection
– Heat shock protein– Anti-apoptotic effect– Fuel source for
epithelial cells• Anti-inflammatory
– Attenuate NFkB– Enhanced PPAR
activation– Attenuation of cytokine
expression
• Preservation of tissue function in stress states– Preserves ATP in
sepsis and I/R– Preserves
mitochondrial function• Antioxidant
– Enhanced GSH– Attenuates iNOS in
sepsis and I/R– Reduction in oxidant
stress
Wischmeyer , PE Curr Opin Clin Nutr Metab Care 9:607-612,2006
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Enteral Feeding with EPA+GLAClinical Outcomes Summary
X 1
X 6
Reduced mortality
▲ 7
▲ 4
▲ 1
▲ 6
▲ 2,3,5
Safety
X 4Pediatric Burn
X 1
X 2,3
Fewer new
organ failures
Pediatric ICU
X 1X 1X 1Sepsis
X 6X 6X 6ALIX 3X 2,3X 2,3,5ARDS
Less time on
vent
Reduced ICU LOS
Improved oxygenstatus
Study Population
1. Pontes-Arruda A, et al: Crit Care Med 2006;34(9):2325-2333.2. Elamin E, et al: CHEST 2005;128:225S.3. Gadek J, et al: Crit Care Med 1999;27:1409-1420.4. Mayes, T, et al: J Burn Care Res 2008;29:82-88.5. Pacht E, et al: Crit Care Med 2003:31(2)491-500.
6. Singer P, et al: Crit Care Med 2006;34:1033-1038.7. Nadkarni V, et al: Crit Care Med 2005;33(Supp12)172M.
X = statistically significant▲ = EPA+GLA diet was found to be safe in these patient populations.
Safety variables measured were no different from the control group.
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Typical ALI/ARDS Inflammatory Response
Typical ALI/ARDS Inflammatory Response
Precipitatingevent
Increase inneutrophil
recruitment
Proinflammatoryeicosanoids and
free radicalsproduced
Pulmonaryinflammation
with loss of surfactant, edema andvasoconstriction
Impaired gasexchange and
poor oxygenation
Leading to deterioration of patient’s condition
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Immune Cell on Normal Lipids
PhospholipidMembraneAA
AA
AA
AA
AAAAAA
AAAA Arachinodic Acid -
Proinflammatory compounds
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Immune Cell on Special Fatty Acids
GOAL:DGLA
AAAAAA Less in cell
membrane
DGLA
DGLAEPA
EPA
EPA
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Arginine• Necessary for normal T lymphocyte function• Myeloid suppressor cells regulate availability of
arginine• Myeloid suppressor cells are capable of causing
states of severe arginine deficiency which impact production of nitric oxide
• Process is paralyzed during trauma and surgery -appears to be an arginine deficiency
– But NOT during sepsis!!! (when arginine metabolized, NO is produced)
(Popovic J. Nutr. 2007; 137:1681S)
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Monitoring Nutrition Therapy in Critical Care
• Indirect Calorimetry• Albumin• PreAlbumin• Nitrogen Balance
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Indications for Conducting RMR Measurements
• Inability to estimate energy expenditure with accuracy
• Inadequate clinical response using predictive equations
• Possible signs of malnutrition• Possible signs of overfeeding
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Indirect Calorimetry
• Measure change in concentration of inspired oxygen (vO2 in ml/min) and carbon dioxide excretion (vCO2 in ml/min) to determine resting metabolic rate (RMR)
• RMR (kcal/d) = {VO2 (3.94) + VCO2 (1.11)} * 1.440– Abbreviated Weir equation
• Respiratory Quotient RQ = vCO2/vO2
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Traditional View of RQ
1-1.2Lipogenesis1Carbohydrate oxidation
0.85Mixed substrate oxidation0.82Protein oxidation0.71Fat oxidation0.67EthanolRQSubstrate Utilization
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“Nutritionally Associated Increased Carbon Dioxide Production: Excess Total
Calories vs. High Proportion of Carbohydrate Calories”
• 20 mechanically ventilated patients in Pulmonary Intensive Care Unit
• Compare VCO2 from isocaloric nutritional regimens with varying concentrations of carbohydrates with VCO2 from low and high caloric nutritional regimens with constant concentrations of carbohydrates.
• Results:– VCO2 did not change with increasing CHO proportion.– VCO2 increased with increasing total calories (p < 0.05).
• Conclusions:– High caloric feeding increases VCO2 in contrast to high
percentage carbohydrate formulation. Thus moderate caloric intake appears to be more important in avoiding nutritionally related increases in VCO2 .
Talpers SS 1992; Chest 102:551-55
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“Clinical Use of the Respiratory Quotient Obtained from Indirect
Calorimetry”• Prospective, multicenter study• Determine the clinical use of RQ for monitoring adequacy
and tolerance of nutrition support • Results:
– Total of 263 long-term acute care adult patients receiving nutrition therapy
– Ratio of calories provided/required correlated with overall measure RQ (p < .0001; R2 = .16)
– Measured RQ compared to predicted reference RQ failed to differentiate appropriate from inappropriate feeding
– Increasing RQ correlated with increasing respiratory rate (p = .002 R2 = .04) and decreasing tidal volume (p = .002, R2 =.04)
McClave SA et al. JPEN, 2003;27:21-26
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Conclusion: Interpreting the RQ in Indirect Calorimetry
• RQ is a good marker of test validity (human biological range = 0.67-1.3)
• RQ doesn’t always reflect substrate use:– Inter-patient variability– The stress response– Underlying lung disease– Acid/base disturbances– Pharmacologic agents: propofol
McClave SA et al. JPEN 2003;27:21-26
• If < 0.7– Prolonged fast > 16
hrs– Ethanol metabolism
• If > 1.0– Recent excess caloric
intake
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Protein Markers
• Albumin, Prealbumin, Transferrin, Retinol Binding Protein
• Reflection of the acute phase response– Increases permeability and
reprioritization of hepatic protein synthesis
• DO NOT accurately represent nutrition status in critical care setting
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C-Reactive Protein
• Positive acute phase reactant - IL-6 stimulates release of CRP from liver– “hepatic reprioritization”
• Can be used to help interpret albumin/prealbumin values
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Biomarkers of Inflammation
0
5
10
15
20
PABCRP
PAB 4 4 13 19CRP 18.3 17.9 6.7 2
Week 1 Week 2 Week 3 Week 4
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Nitrogen Balance
• 1 gm nitrogen = 6.25 gm protein• N2 Balance = N2 intake – N2 output• Determine anabolic (+ N2 balance) vs. catabolic state
(- N2 balance) vs. equilibrium• Factors:
– Renal function: creatinine clearance of >40mL/min, or s.Creat <2.5 required to be accurate
– Wound, fecal, high output fistula losses
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Nitrogen Balance• Necessary data:
– 24 hour urine collection, volume in mL– Urine urea nitrogen (UUN) in grams– Accurate I/O’s essential and calorie count
• Nitrogen intake = 24 hour protein intake6.25
• Nitrogen output = 24 hour urine volume x UUN100,000
plus obligatory losses (generally 3-4 gm/day)
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Nitrogen Balance
• Limited Validity– Adequacy of urine collection– Unrecorded nitrogen losses from large
open wounds, severe burns, diarrhea, or renal or liver failure
– Ideally should be measured in “steady state” (impossible in critically ill)
– Interpret values based on patient’s clinical status (i.e. inflammatory state)
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A Vicious Cycle
• Inflammation and malnutrition both reduce transport protein concentrations by decreasing its rate of synthesis
• Inflammation is associated with greater fractional catabolic rate of transport proteins
• Inflammation promotes transfer of albumin out of the vascular compartment
• Vicious cycle of inflammation results in anorexia with decreased effective use of dietary protein and augmentation of catabolism
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If sources of inflammatory mediators are not controlled, nutrition support will not preserve catabolic lean tissue!!!
Kudsk, Trauma 5 ed., 2004
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In Conclusion:
• Feed enterally - do everything possible to use the gut!
• Start enteral nutrition within 24-48 hrs• Give the right amount - can cause more
metabolic stress - use IC• Pharmoconutrients
– Glutamine: gut protection– Omega- 3: ARDS/ALI/Sepsis– Arginine: trauma/surgery (avoid sepsis)
• There is no accurate measure of nutrition in critically ill
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References• McClave SA et al. Guidelines for the Provision and
Assessment of Nutrition Support Therapy in the Adult Critically Ill Patient: Society of Critical Care Medicine and American Society for Parenteral and Enteral Nutrition. JPEN J Parenter Enteral Nutr.2009; 33:277-316
• Heyland DK et al. Canadian Critical Care Clinical Practice Guidelines Committee. Canadian clinical practice guidelines for nutrition support in mechanically ventilated, critically ill adult patients.JPEN J Parenter Enteral Nutrition 2003;27:355-373
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THANK YOU!