lecture 11- nutrition in trauma

7/29/2019 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



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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



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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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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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lecture 11- nutrition in trauma

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