- 1. Noraishah Mohamed NorDept Nutrition Sc. IIUM
2. Metabolic Stress Trauma MVA, gunshot, stab wound, falls,
burns Major cause of death and disability Active systemic response,
depend on: Pts age, previous health status, preexisting diseases,
type of infection, presence of multiple organ dysfunction syndrome
(MODS) There are many metabolic changes that occur inpatients who
are critically ill (eg sepsis, trauma) 3. Important to understand
these changes when implementing nutritional therapy Once the
systemic response is activated, the physiologic and metabolic
changes that follow are similar and may lead to septic shock Ebb
phase initial response to bodily insult, occur immediately
following injury (short term) Flow phase neuroendocrine response to
physiologic stress following the ebb phase (long term) 4. Metabolic
response during stress: Metabolic response to stress (tissue
injury, infection) is divided into the ebb and flow phaseEnergy
expenditure Flow Phase Ebb Phase Time 5. In the ebb phase, the body
shuts down and the metabolic rate decreases Leads to hypovolemic
shock: Blood pressure Cardiac output Body temperature tissue
perfusion O2 consumption metabolic rate Bodys protective response
(eg to blood loss) 6. However, once the blood pressure is
stabilized, the flow (recovery)phase begins Divided into 2
response: Acute Response: catabolism predominates glucocorticoids
glucagon catecholamines Release cytokines, lipid mediators Acute
phase protein (CRP) N2 excretion metabolic rate O2 consumptions
Impaired fuel utillization Adaptive Response: Anabolism
predominates Hormonal response gradually diminished hypermetabolic
rate Assoc with recovery Restore body protein Wound healing 7.
Metabolic changes in the stressed (critically illpatient): Energy
metabolism Protein metabolism Carbohydrate metabolism Fat
metabolism Others 8. In the acute response metabolism is increased
which requires energy However, the method of producing energy is
different to that of a normal state or in periods of fasting
(simple starvation) 9. Energy production in a normal(non fasting
state) Usually E is from carbohydrates from normal intake Complex
carbohydrate is broken down into glucose (preferred substrate for
the brain) Excess carbohydatre mainly converted to fat and stored
in adipose tissue 10. Metabolic Response to Fasting
IIIIIIIVVGLUCOSE UTILIZED
(g/hora)40ExogenousGlycogenGluconeogenesis302010LEGEND I IIIII IV
VFUEL FORGLUCOSE, GLUCOSE,BRAIN GLUCOSE GLUCOSE
GLUCOSEKETONESKETONESRuderman NB. Annu Rev Med 1975;26:248 11.
Metabolic Changes in Starvation 12. Metabolic Response to Trauma
Nitrogen Excretion (g/day) 13. Starvation vs. Stress Metabolic
response to stress differs from the responses to starvation.
Starvation = decreased energy expenditure, use of alternative
fuels, decreased protein wasting, stored glycogen used in 24 hours
Late starvation = fatty acids, ketones, and glycerol provide energy
for all tissues except brain, nervous system, and RBCs 14.
Hypermetabolic statestress causes accelerated energy expenditure,
glucose production, glucose cycling in liver and muscle
Hyperglycemia can occur either from insulin resistance or excess
glucose production via gluconeogenesis and Cori cycle. Muscle
breakdown also accelerated 15. Hormonal Stress Response
Aldosteronecorticosteroid that causes renalsodium retention
Antidiuretic hormone (ADH)stimulates renaltubular water absorption
These conserve water and salt to support circulatingblood volume
16. ACTHacts on adrenal cortex to release cortisol(mobilizes amino
acids from skeletal muscles) Catecholaminesepinephrine and
norepinephrinefrom renal medulla to stimulate
hepaticglycogenolysis, fat mobilization, gluconeogenesis 17.
Cytokines Interleukin-1, interleukin-6, and tumor necrosis factor
(TNF) Released by phagocytes in response to tissue damage,
infection, inflammation, and some drugs and chemicals 18. Nutrition
Care Prevent PEM and possible complication of nutritionsupport
Nutritional status prior to current illness is animportant
predictor of morbidity and mortality The level of injury will
determine the level ofmetabolic stress The Glasgow Coma scale (GCS)
score are usuallyused in critical ill pt. 19. Nutrition
Intervention Oral route is the preferred route to meet
therequirements However, for critically ill pt, usually the
requirementonly can be met via EN or PN There is evidence to
support early initiation of nutritionsupport with specific
metabolically stressed : acutepancreatitis, head injury and burns.
EN should be consider first before PN 20. Definition Sepsis: an
uncontrolled inflammatory response to infection or trauma
(immunosuppressive response to infection) Septic shock: hypotension
not reversed with fluid resuscitation and assoc with organ dysfx
SIRS: not necessarily caused by infection, may occur after major
surgery or trauma or with other condition such as myocardial
infraction MODS: result from the complications of sepsis or SIRS;
define as the present of the altered fx of 2 or > organs in
acutely ill pt 21. Diagnosis of Systemic Inflammatory Response
Syndrome (SIRS): Site of infection established and at least two of
thefollowing are present: Body temperature >38 C or 90
beats/minute Respiratory rate >20 breaths/min (tachypnea) PaCO2
12,000/mm3 or 10% bands (immature neutrophils)in the absence of
chemotherapy-induced neutropenia andleukopenia May be caused by
bacterial translocation Diagnostic criteria for MODS and
pathopysiology refer handout 22. Bacterial Translocation Changes
from acute insult to the gastrointestinal tract that may allow
entry of bacteria from the gut lumen into the body; associated with
a systemic inflammatory response that may contribute to multiple
organ dysfunction syndrome Well documented in animals, may not
occur to the same extent in humans Early enteral feeding is thought
to prevent this 23. Factors to Consider in Screening anICU Patient:
ICU medical admission Diagnosis, nutritional status, organ
function,pharmacologic agents Postoperative ICU admission Type of
Surgery, intraoperative complications, nutritional status,
diagnosis, sepsis/SIRS Burn or trauma admission Type of trauma,
extent of injury, GI function 24. ASPEN Guidelines ASPEN (American
Society of Parenteral and Enteral Nutrition) Objectives of optimal
metabolic and nutritional support in injury, trauma, burns, sepsis:
1. Detect and correct preexisting malnutrition 2. Prevent
progressive protein-calorie malnutrition 3. Optimize patients
metabolic state by managing fluidand electrolytes 25.
NUTRITIONALASSESSMENT Traditional methods not adequate/reliable
Urine urea nitrogen (UUN) excretion in gms per day may be used to
evaluate degree of hypermetabolism: 0 5 = normometabolism 5 10 =
mild hypermetabolism (level 1 stress) 10 15 = moderate (level 2
stress) >15 = severe (level 3 stress) 26. Determination of
NutrientRequirements Energy Protein Vitamins, Minerals, Trace
Elements Non-protein Calorie Carbohydrate Fat 27. Energy Enough but
not too much Excess calories: Hyperglycemia Diuresis complicates
fluid/electrolyte balance Hepatic steatosis (fatty liver) Excess
CO2 production Exacerbate respiratory insufficiency Prolong weaning
from mechanical ventilation 28. Predictive Equations for Estimation
ofEnergy Needs in Critical Care Harris-Benedict x 1.3-1.5 for
stress ASPEN Guidelines: 25 30 calories per kg per day*
Ireton-Jones Equations** Penn State equations Swinamer equation
*ASPEN Board of Directors. JPEN 26;1S, 2002 ** Ireton-Jones CS,
Jones JD. Why use predictive equations for energy expenditure
assessment? JADA 97(suppl):A44, 1997. **Wall J, Ireton-Jones CS, et
al. JADA 95(suppl):A24, 1995. 29. Harris-Benedict Equation(HBE)
InjuryStress Factor Minor surgery1.00 1.10Energy requirements for
Long bone fracture 1.15 1.30patient with cancer in bed Cancer 1.10
1.30 HBE = BEE x 1.10 x 1.2 Peritonitis/sepsis 1.10 1.30 Severe
infection/multiple trauma 1.20 1.40 Multi-organ failure syndrome
1.20 1.40 Burns1.20 2.00 Activity Activity Factor Confined to
bed1.2 Out of bed 1.3ADA: Manual Of Clinical Dietetics. 5th ed.
Chicago: American Dietetic Association; 1996Long CL, et al. JPEN
1979;3:452-456 30. Ireton-Jones 1997 EquationsVentilator-Dependent
Patients: EEE = 1784 11(A) + 5(W) + 244(G) + 239(T)
+804(B)Spontaneously-Breathing Patients: EEE = 629 11(A) + 25(W)
609(O) 31. Where: A = age in years W = weight (kg) O = presence of
obesity >30% above IBW (0 =absent, 1 = present) G = gender
(female = 0, male = 1) T = diagnosis of trauma (absent = 0, present
= 1) B = diagnosis of burn (absent = 0, present = 1) EEE =
estimated energy expenditure 32. Penn State Equation 1998 version:
RMR = BMR (1.1) + VE (32) + Tmax(140) - 5340 2003a version: RMR =
BMR (0.85) + VE (33) +Tmax (175) 6433 Equations use BMR calculated
using the Harris- Benedict equation, minute ventilation (VE) in
liters per min (L/min), and maximum temperature (Tmax) in degrees
Celsius. 33. Swinamer Equation EE = 945 (BSA) - 6.4 (age) + 108 (T)
+ 24.2 (breaths/min) + 81.7 (VT) 4349 Equation uses body surface
area (BSA) in squared meters (m2), temperature (T) in degrees
Celsius, and tidal volume (VT) in liters per minute (L/min). 34.
Estimation of RMR inObesity Harris-Benedict using actual weight x
1.2 (60% of subjects predicted within 10% of RMR) or an adjusted
weight x 1.3 (67% of subjects predicted within 10% of RMR) resulted
in the most accurate predictions. Penn State 2003a equation
predicts within 10% of RMR in 61% of subjects, the Penn State 1998
equation predicts within 10% of RMR in 67% of subjects
Ireton-Jones, 1992 equations predict within 10% of RMR in 72% of
subjects. 35. Recommendations forPredicting RMR in Critically
IllPts HBE should not be used to predict RMR in critically ill
patients Ireton-Jones 1997 should not be used to predict RMR in
critically ill patients Ireton-Jones 1992 may be used to predict
RMR in critically ill pts but errors will occur. ADA Evidence
Analysis Library, 10-06 36. ProteinStress Level No Stress Moderate
StressSevere StressCalorie:Nitrogen Ratio> 150:1 150-100:1<
100:1Percent Potein / Total< 15%15-20% > 20%
proteinCaloriesproteinproteinProtein / kg Body Weight0.81.0-1.2
g/kg/day 1.5-2.0 g/kg/dayg/kg/day 37. What Weight Do You Use?
Actual weight may be inaccurate in trauma and burnpatients who have
been fluid resuscitated Usual weights may not be available There is
no validation for the common practice of usingan adjusted body
weight for obese patients when usingHarris-Benedict since
Harris-Benedict equations werederived from studies done on healthy
people of all sizes Ireton-Jones uses actual weight in her
equations andthen adjusts for obesity 38. Lean body mass is highly
correlated with actual weight inpersons of all sizes Studies have
shown that determination of energy needsusing adjusted body weight
becomes increasinglyinaccurate as BMI increases However, some
studies suggest that high proteinhypocaloric feedings in obese
patients may betherapeutically useful Because overfeeding is more
problematic thanunderfeeding, could possibly use adjusted weight or
20-21kcal/kg actual BW in obese pts 39. Specialized Nutrients in
CriticalCare Include supplemental branched chain amino acids,
glutamine, arginine, omega-3 fatty acids, RNA, others Most studies
used more than one nutrient, making assessment of efficacy of
specific supplements impossible Immune-enhancing formulas may
reduce infectious complications in critically ill pts but not alter
mortality Mortality may actually be increased in some subgroups
(septic patients) 40. Timing of Enteral Nutrition andCritical
Illness If the critically ill patient is adequately
fluidresuscitated, then EN should be started within 24 to48 hours
following injury or admission to the ICU. Early EN is associated
with a reduction in infectiouscomplications and may reduce LOS. The
impact of timing of EN on mortality has not beenadequately
evaluated. 41. Monitoring Response to MNT inCritical Care Pts:
Blood Glucose Hyperglycemia (up to 200-220 mg/dl) in critically
illpatients was once considered acceptable Recent studies suggest
hyperglycemia is associated withinfection, morbidity, mortality New
goal is to keep BG as close to normal as possible.Target: 10 to
20%over baseline values)] 57. Hart et al (2001) found that a
high-carbohydrate diet, with 3% fat, 82% carbohydrates and 15%
protein, stimulated protein synthesis, increased endogenous insulin
production and improved lean body mass accretion compared to
high-fat diet. 58. Vitamins & Minerals Supplementation
Evidence-based guidelines for micronutrientsupplementation are
limited Vit C- collagen formation and antioxidant defense in
theimmune system and is involved in ATP production (66mg/kg/h
during the first 24 hours) Vit A immune fx & epithelialization
(1000 IU/1000kcal) Na & K restore via fluid therapy Ca
depression reduced with earlier ambulation &excersize Supp PO4
& Mg parenterally (to avoid GI irritation) Zn supp 220mg Zn
sulphate ( co fac in Vit E metab) 59. Methods of Nutritional
Support Pt with 40) Refeeding syndrome Severe malnutrition Trauma
patients following shock resuscitation Hemodynamic instability
Acute respiratory distress syndrome or COPD MODS, SIRS or sepsis
Aggressive protein provision (1.5-2.0 gm/kg/day 68. Although
overfeeding surgical patients should beavoided, prolonged
underfeeding may be equallyconcerning. This can compromise immune
function, delay woundhealing, exacerbate muscle wasting, and
prolong therecovery of nitrogen balance and visceral protein
levels. However, short-term hypocaloric feeding with 1-2 g
ofprotein per kilogram per day, particularly in the acutephase of
postoperative stress, may reduce metaboliccomplications while
supporting a reduction in negative
