Lecture 11- Nutrition in Trauma
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NUTRITION IN TRAUMA
AND
GUT SPECIFIC RESUSCITATION
Warko Karnadihardja
2011
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RECENT ISSUES
The gut is one of the first organsexposed to shock and the last to beresuscitated in circulatory failure
Impairment of the gut plays a centralroles in the pathogenesis of infection,sepsis and even MODS
Heyland, Dhaliwal & Suchner. 2005
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TRAUMA CARE
Trauma is a multi system disease andas such, benefits from almost anyadvance in medical science
We can provide better managementfor trauma victims, as we learn moreabout physiology and biochemistry of
various organ systems
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MAJOR TRAUMA
Associated with Severe hemorrhage
Low-flow conditions
Tissue destruction and debris Gut bacterial translocation
Leading to:
Massive dyshomeostasis of
immunoinflammatory response
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THE RESPONSE
Starts within minutes following the
traumatic impact
Characterized by the immediateactivation of monocytes and
granulocytes
Leukocytic activation leads to anincreased synthesis and release of
inflammatory and anti-
inflammatory mediators
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Blood cytokine level during the first 24hours following trauma and hemorrhagic
shock
Faist E, Angele MK. In: Baue AE, et al. MOF. Springer 2000.
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MASSIVE DYSHOMEOTASIS
INDUCED BY MAYOR TRAUMA
Faist E, Angele M & Wichmann M, Trauma 5th edit. 2004
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Release of Mediators
Primed
WBCs
Primed
WBCs
Primed
WBCs
Primed
Inflammatory
Cells
Lung
Liver
Gut
Other
Organs
Systemic Release
of Cytokines
Local Activation of
Inflammatory Cells
LOCAL
TISSUE
RESPONSE
INITIAL INSULT
SYSTEMIC RELEASE OF
TOXIC MEDIATORS
GENERALIZED TISSUE INJURY
First Hit POST INJURYSystemic Activation of
Inflammatory CellsSecond Hit
Demling et al. Surg Clin North Am 74(3); 1994.
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Postinjury Hypermetabolism:
The Stage for MOF
O2 Deprivation/Injury
Endothelium
Macrophage
Neutrophil
Adrenal
Hypothalamus
Pituitary
Injury
Stress
Response
Tissue Necrosis
Inflammation
Gut Barrier Bacteria/EndotoxinTranslocation
IL1
TNFTXA2
PGE2
LTB4
PAF
O2OH
Proteases
Sensory
Perception
Catechols
Cortisol
Glucagon
Macroendocrine
Microendocrine
Evans & Park. Blackwell 1997.
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EARLY ENTERAL VS PARENTERALNUTRITION IN MAJOR TRAUMA (ATI 15-40)
( 11 PRCT, 2 META ANALYSIS, 1 MODEL)
Reduced septic morbidity
Increase lymphocytic count
Increase anastomotic strength in peritonitismodel
Support wound healing
Moore EE, Jones TN : J Trauma 1986Moore FA, Moore EE, Jones TN: J Trauma. 1989
Kudsk KA, Croce MA, Fabian TC et al : Ann Surg 1992
Moore FA, Feliciano DV, Andrassy RJ et al : Ann Surg. 1992
Khalili TM, Navarro RA, Meddleton J et al : An J Surg. 2001
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Schematic Representation of the Effect of Critical Illness on Gastrointestinal Function
Rolandelli RH & Koruda MJ : Surg. Crit. Care, 1994
Bowel rest/NPO
Malnutrition
Stress
Cardiac failure
Shock
Vasopressors
Achlorhydria
Antacids
H2 Antagonists
Intestinal obstruction,Ileus, Blind loop,Opiates, Ca channelblockers
Mucosal cellturnover
Mesentericblood flow
MotilityGastric pH
Mucosal atrophy
Mucosal sloughing
Intestinal bacterial
overgrowth
Breakdown
mucosal barrier
Translocation of
bacteria and toxins
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THE ROLE OF GUT IN DYSFUNCTIONINFLAMMATION TO MOF
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Gut: The Starter for MOF
Liver: The Motor for MOF
Delayed Enteral Feeding
Shock
Bacteria
Endotoxin
Kupffer Cell
Gut
Liver
ARDS
ATN
Stress
Immune
Injured Tissue
PGE2 =
IL1 =
TNFC3a,C5a
O2
Enteral NutritionEvans & Park. Blackwell 1997.
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HOW GUT DYSFUNCTION
HAPPENS IN MAJOR TRAUMA ? Might as complications of :
Abdominal compartment syndrome (ACS) whenintra-abdominal pressure (IAP) exceeds 25 cmH2O (Urinary bladder pressure)
Gastroparesis Impaired mucosal perfusion : shock results in
disproportionate splanchnic vasoconstriction Impaired intestinal transit: shock, bowel
manipulation and sepsis demonstrate impaired
small bowel transit Impaired gut absorptive capacity of small bowel:
absorption of glucose and amino acid isdepressed after trauma and sepsis.
Moore FA & Weisbroodt NW, 2003
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Stress Stratification by Metabolic
Criteria
Stress Urine Plasma Plasma Insulin Oxygen
Level Nitrogen Lactate Glucose Resistance Consumption
( g/day) (mM/L) (mg/dl) (mL/min/m2)
Low < 10 < 1.5 < 150 No < 140
Mid 1020 1.53.0 150-250 Some 140-180
High > 20 > 3 > 250 Yes > 180
Van der Berghe et al, 2001: Maintaining glucose levels below 110 mg/dL reduce
mortality and morbidity in ICU and in-hospital
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STRESS INDUCED HYPERGLYCEMIA
Acute or new hyperglycemia may occur
after :
Myocardial infarction Congestive heart failure
Cerebral vascular accident
Cardiopulmonary bypass
Burns
Major surgery or major trauma
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GLUCOSE CONTROL BY INSULIN FOR
CRITICALLY ILL SURGICAL PATIENTS
Hyperglycemia associated with
insulin resistance, is commonamong criticall ill pts, even those
who do not have diabetes.
It is a known factor for poorprognosis in hospitalized pts
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GUT-SPECIFIC RESUSCITATION
THE GOALS :
Early optimizing gut perfusion
Prevent reperfusion injury
THE PROTOCOL
Earlier use of PRBC, instead ofaggressive use of crystaloids to avoid
problematic bowel edema Or to use new blood substitutes and /
or hypertonic saline or colloids
Moore FA & Weisbroodt NW, 2003
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The Problems of Open
Abdomen
Have a high in-hospital mortality:
20%-30% in most series
Usually are heralded by a high ISS:25 9
And high serum lactate levels
indicative of severe ischemia
Stone PA et.al.; J.Trauma 2004; 57:1082-1086
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J Trauma, Dec 2008.65. 1520-152
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SUPPORTED
In part, by
Large scale collaborative project
award (U54-GM 62119) from theNational Institute of GeneralMedical Sciences. National
Institute of Health
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CONTRIBUTIONS
1. George E. OKoeje : Depart of Surgery,University of Washington Seattle,Washington
2. Joseph Cusheri : Depart of Surgery,
University of Washington Seattle,Washington
3. Ronald V.Maier : Depart of Surgery,University of Washington Seattle,
Washington4. Marilyn Shelton : Depart of Hospitality
and Nutrition, Harbor view MedicalCenter, Seattle, Washington
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5. Ernest E. Moore : Depart of Surgery,Univ of Colorado, Denver, Colorado
6. Stephen F.Lowry, VMDNJ-RWJMedical School, New Brunswich, NewJersey
7. Brain G Harbredit, Depart of Surgery,Univ of Kentucky, Louisville, Kentucky
CONTRIBUTIONS
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INTRODUCTION
Severely injured pts have markedmetabolic derangements, generallycharacterized by increased substrate
utilization and protein catabolism
Specialized nutritional support isbeneficial and improves important
clinical outcomes in the critically illHeyland DK et al : JPEN, 2003; 27, 74-83
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PROTOCOL GOALS
STANDARDS OPERATING PROCEDURE (SOP)
1. To optimize patient outcome through
enhancing tolerance of EN support andminimizing the complications
2. To generate guidelines that is basedupon the best available evidence
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SOPFor Nutritional Support of the Trauma Patients
1. Selection of the pts for nutritional support
2. Approach to initiation
3. Route of administration
4. Nutrient formulation5. Nutritional support monitoring
This set of guidelines is evidence-based
where possible and devised for pts with
severe multisystem injury, who have beenresuscitated from marked physiologic
derangements
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FORMULATION
Protein needs are initially : 1,5 to 2,0 gprotein/kg/d
Caloric needs : 25 to 30 kcal/kg/d Monitor :
Occult and potentially excessive calories Hyperglycemia Excess CO2 production Fluid/electrolytes
Blood stream infection PN lipids : limited to 1 g/kg/d ( EN lipids) =
less than 30% of total kcal
May AK et al : Ann Surg 1999; 65:560-574,
Dissonaike S et al. Crit Care 2007; 11; R114
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SUPPLEMENTATION
Recommendation: Standard high protein 1 kcal/ml formula When limiting volumes following large
volume resuscitation, open abdomens and
ongoing diuresis Higher caloric density 1,5-2.0 kcal/m
Specific Nutrients (additional) Glutamine
Arginine Ribonucleic acids Omega-3 /fatty acids
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IMMUNE ENHANCED
SUPPLEMENTATION
The beneficial effect in severely injuredhumans are uncertain Mendez C et al: J Trauma 1997, 42: 933-940
Kudsk KA et al : Ann Surg 1996; 224: 531-540 Combined supplementation of EN formula
with arginine, omega-3 fatty acids andglutamine does not reduce mortality,infections, or organ failure in critically ill pts
This constrasts with demonstrated reduction ininfections complications when are used inelective surgical pts
Heyland DK et al: JAMA, 2001; 286: 944-953
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IMMUNE ENHANCED SUPPLEMENTATION
Arginine increases nitric oxide (NO)production, while beneficially
influencing innate immune functionand infections outcomes in electivesurgery pts
Is detrimental in critically ill pts withsepsis
Sucher U, Heyland DK, Peter K: Br J Nutr 2002: 87 (S1), S121-S132
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GUT-SPECIFIC RESUSCITATION
THE GOALS :
Early optimizing gut perfusion
Prevent reperfusion injury
THE PROTOCOL
Earlier use of PRBC, instead ofaggressive use of crystalloids to avoid
problematic bowel edema Or to use new blood substitutes and /
or hypertonic saline or colloids
Moore FA & Weisbroodt NW, 2003
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MONITORING NUTRITIONAL
SUPPORTINCLUDES Bedside assessment of the patient
tolerance
Daily evaluation by the dietician toensure nutritional targets Biochemical monitoring The effect of massive resuscitation and
marked fluid shifts during initial post injuryweek generally preclude the use ofserum marker and body weight asindications
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MONITORING NUTRITIONAL
SUPPORT
Once the patient enters an
anabolic state, sufficient substrateis needed to rebuild proteins, healwound, and restore muscle mass
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MONITORING GI TOLERANCE
High gastric residual volumes have oftenbeen considered a marker for gastric intolerance of EN, reflux and bronchopulmonary aspiration of GI contents
Other manifestations: Poor gastric emptying Abdominal distention Abdominal tenderness Diarrhea Gastric ileus, infections colitis, intestinal
ischemia and necrosis ( < 1%)
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MONITORING GI TOLERANCE
Gastric aspirates are obtained every4 to 6 hours
Residual volume of > 300 ml,
mandates cessation of feeding withreassessment of residual volume 2hours later
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Gutt M, McFe J : Br J Surg 2010; 97:1629-1636
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Gutt M, McFe J : Br J Surg 2010; 97:1629-1636
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Gutt M, McFe J : Br J Surg 2010; 97:1629-1636
PLACEBO COCKTAIL
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PLACEBO COCKTAIL
VS
GSN COCKTAIL
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GSN COCKTAIL
Multivitamine capsules : 1 capsule daily (Forcevol)
Probiotic capsules : 3 x 1 capsule Trevis
Prebiotic powder : oligofructosa 16 g/day in twodivided doses
Glutamine
IV : dipeptiven 100 ml daily
Oral : glutamine Ox 5 g powder sachets 20 g/day
in four divided doseOrally or via NGT
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KEY THERAPEUTIC STRATEGY
METABOLIC RESUSCITATION OF G.I.T
By providing adequate nutrition ingeneral
Immunomodulatory substratesspecifically to maintain gut barrierintegrity
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The vicious cycle of oxygen free radical production in critically ill patient
Surgery, trauma
Ischemia/
reperfusion
OFR
Tissue injury
Hypoperfusion
Inflammation
Cytokines
Infection
Endotoxin, bacteria
Sepsis
SIRS
Macrophage
activation
(liver)
Monocytes/
leucocytes
activation
OFR
OFROFR
OFR
Cytokines
Heyland, Dhaliwal & Suchners, 2005
POTENTIAL ROLES AND SITES OF ACTION OF IMMUNO
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POTENTIAL ROLES AND SITES OF ACTION OF IMMUNO
NUTRIENTS IN SEPSIS
Sepsis
Glutamine
release
Free fatty acid
Immune response
Adipose tissue
Cytokines and stress hormones
MuscleGut Liver
Macrophages
OKG
GlutamineGlutamine
SCFAs
Arginine
n-3 PUFAs
n-3 PUFAs
n-3 PUFAs
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CONCLUSION
The gut of is one the first organs exposed toshock and the last to e resuscitated incirculatory failure
Impairment of the gut plays central role inthe pathogenesis of infection, sepsis andeven MODS
Metabolic resuscitation of the gut byadequate nutrition in general and specificimmunomodulating substrates to maintaingut barrier integrity and function will have tobe considered
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CONCLUSION
Enhancing the recovery of gut function or
curtailing the period of gut failure, might be
associated with improvements in patient
outcomes The return of adequate gut function can be
expedited with the use of GSN preparations
This was associated with an attenuation of
the acute phase response, decreasedseptic complications and a tendency
towards improved survival
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