1. Noraishah Mohamed Nor
Dept Nutrition Sc.
IIUM

2. Metabolic Stress
 Trauma  MVA, gunshot, stab wound, falls, burns
 Major cause of death and disability
 Active systemic response, depend on:
 Pt‘s age, previous health status, preexisting diseases,
type of infection, presence of multiple organ
dysfunction syndrome (MODS)
 There are many metabolic changes that occur in
patients 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 phase
Energy 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
 Body‘s 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 ill
patient):
 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
I II III IV V
GLUCOSE UTILIZED (g/hora)
40 Exogenous
Glycogen
Gluconeogenesis
30
20
10
LEGEND I II III IV V
FUEL FOR GLUCOSE, GLUCOSE,
BRAIN
GLUCOSE GLUCOSE GLUCOSE
KETONES KETONES
Ruderman 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 state—stress 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
 Aldosterone—corticosteroid that causes renal
sodium retention
 Antidiuretic hormone (ADH)—stimulates renal
tubular water absorption
 These conserve water and salt to support circulating
blood volume

16.  ACTH—acts on adrenal cortex to release cortisol
(mobilizes amino acids from skeletal muscles)
 Catecholamines—epinephrine and norepinephrine
from renal medulla to stimulate hepatic
glycogenolysis, 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 nutrition
support
 Nutritional status prior to current illness is an
important predictor of morbidity and mortality
 The level of injury will determine the level of
metabolic stress
 The Glasgow Coma scale (GCS) score are usually
used in critical ill pt.

19. Nutrition Intervention
 Oral route is the preferred route to meet the
requirements
 However, for critically ill pt, usually the requirement
only can be met via EN or PN
 There is evidence to support early initiation of nutrition
support with specific metabolically stressed : acute
pancreatitis, head injury and burns.
 EN should be consider first before PN

21. 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

22.  Diagnosis of Systemic Inflammatory Response
Syndrome (SIRS):
 Site of infection established and at least two of the
following are present:
 Body temperature >38° C or <36° C
 Heart rate >90 beats/minute
 Respiratory rate >20 breaths/min (tachypnea)
 PaCO2 <32 mm Hg (hyperventilation)
 WBC count >12,000/mm3 or <4000/mm3
 Bandemia: presence of >10% bands (immature neutrophils)
in the absence of chemotherapy-induced neutropenia and
leukopenia
 May be caused by bacterial translocation
 Diagnostic criteria for MODS and pathopysiology refer handout

23. 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

25. Factors to Consider in Screening an
ICU 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

26. 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 patient‘s metabolic state by managing fluid
and electrolytes

27. NUTRITIONAL
ASSESSMENT
 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)

28. Determination of Nutrient
Requirements
 Energy
 Protein
 Vitamins, Minerals, Trace Elements
 Non-protein Calorie
 Carbohydrate
 Fat

29. 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

30. Predictive Equations for Estimation of
Energy 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.

31. Harris-Benedict Equation
(HBE)
Injury Stress Factor
Minor surgery 1.00 – 1.10 Energy requirements for
Long bone fracture 1.15 – 1.30 patient 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
Burns 1.20 – 2.00
Activity Activity Factor
Confined to bed 1.2
Out of bed 1.3
ADA: Manual Of Clinical Dietetics. 5th ed. Chicago: American Dietetic Association; 1996
Long CL, et al. JPEN 1979;3:452-456

32. Ireton-Jones 1997 Equations
Ventilator-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)

33. 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

34. 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.

35. 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).

36. Estimation of RMR in
Obesity
 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.

37. Recommendations for
Predicting RMR in Critically Ill
Pts
 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

38. Protein
Stress Level No Stress Moderate Stress Severe Stress
Calorie:Nitrogen Ratio > 150:1 150-100:1 < 100:1
Percent Potein / Total < 15% 15-20% > 20% protein
Calories protein protein
Protein / kg Body Weight 0.8 1.0-1.2 g/kg/day 1.5-2.0
g/kg/day g/kg/day

39. What Weight Do You Use?
 Actual weight may be inaccurate in trauma and burn
patients who have been fluid resuscitated
 Usual weights may not be available
 There is no validation for the common practice of using
an ―adjusted‖ body weight for obese patients when using
Harris-Benedict since Harris-Benedict equations were
derived from studies done on healthy people of all sizes
 Ireton-Jones uses actual weight in her equations and
then adjusts for obesity

40.  Lean body mass is highly correlated with actual weight in
persons of all sizes
 Studies have shown that determination of energy needs
using adjusted body weight becomes increasingly
inaccurate as BMI increases
 However, some studies suggest that high protein
hypocaloric feedings in obese patients may be
therapeutically useful
 Because overfeeding is more problematic than
underfeeding, could possibly use adjusted weight or 20-21
kcal/kg actual BW in obese pts

41. Specialized Nutrients in Critical
Care
 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)

42. Timing of Enteral Nutrition and
Critical Illness
 If the critically ill patient is adequately fluid
resuscitated, then EN should be started within 24 to
48 hours following injury or admission to the ICU.
 Early EN is associated with a reduction in infectious
complications and may reduce LOS.
 The impact of timing of EN on mortality has not been
adequately evaluated.

43. Monitoring Response to MNT in
Critical Care Pts: Blood Glucose
 Hyperglycemia (up to 200-220 mg/dl) in critically ill
patients was once considered acceptable
 Recent studies suggest hyperglycemia is associated with
infection, morbidity, mortality
 New goal is to keep BG as close to normal as possible.
Target: <150 mg/dl
 Use insulin drip and sliding scale; convert to
subcutaneous insulin as possible
 Can use intermediate insulins morning and evening once
feedings are tolerated and stable

44.  Survival is decreased in critically ill patients with
hyperglycemia
 Controlling BG is associated with fewer infectious
complications in critically ill patients
 There is fair evidence that controlling BG values in
critically ill patients leads to a decrease in ICU LOS
 Dietitians should promote attainment of strict
glycemic control (80-110mg/dL) to reduce time on
mechanical ventilation in critically ill medical ICU
patients

46. Head Injury

47.  Traumatic Brain Injury (TBI) Severely hypermetabolic
and catabolic
 The more severe the head injury, the greater the release
of catecholamines (norepinephrine and epinephrine) and
cortisol and the greater the hypermetabolic response.
 release of catecholamines, cortisol, & hypermetabolic
response
 Without rapid nutrition support  rapid LBM loss and
immunosuppression
 Glasgow Coma Scale (GCS) to evaluate pt‘s
consciousness:
 Sore 14–15 minor head injury
 Score 9 – 13  moderate head injury

48. MNT
 Energy:
 Use indirect calorimetry when available
 Use H/B x 1.4 stress factor
 GCS often EE
 Take into consideration the IV glucose (provide E) total
cal – the IV glucose E
 Protein:
 estimated at 1.5 – 2.2 g/kg of body weight
 BCAA help to restore plasma AA profile and nitrogen
bal

49.  Vitamins & Minerals
 Low plasma Vit B & C,
 Increase Zn excretion
 Fluid or/and sodium restriction

50. BURNS

51.  Definition: a result of tissue injury caused by exposure
to heat, chemical, radiation, or electricity
 May result from injury to the skin but damage may
extend into muscle and bone.
 When the burn injury exceeds 15 to 20% of the total
body surface area (TBSA), it results in systemic
disturbances, including a major stress response,
impaired immunity and extensive fluid redistribution

54.  The consequences of these metabolic alterations
include increased gluconeogenesis, increased
proteolysis, increased ureagenesis, sequestration of
micronutrients and altered lipid metabolism
 The metabolic response increased physiological
demands placed on the cardiac, pulmonary, renal
and other organ systems, complicates nutritional
support.
 Patients with major burn injuries also develop
immune system impairment, which predisposes them
to infection and multi-organ failure (MOF)

55. MNT
 Objectives:
 Maintain body mass, particularly lean body mass
 Prevent starvation and specific nutrient deficiencies
 Improve wound healing
 Manage infections
 Restore visceral and somatic protein losses
 Avoid or minimize complications associated with enteral
or parenteral nutrition

56.  Energy
 Based on size of burn (% TBSA)
 Use the Curreri Formula:
ER = 24kcal x kgUBW + 40 kcal x %TBSA (usually
200% REE)
OR
 Formula (Xie et al, 1993):
Energy expenditure (kcal/d) = (1000 kcal x BSA [m ]) +
2
(25 x %TBSA)
OR

57. Basal energy expenditure (BEE) per Harris-Benedict equation
Male: BEE = 66 + (13.7 x W) + (5 x H) – (6.8 x age)
Female: BEE = 655 + (9.6 x W) + (1.9 x H) – (4.7 x age)
Adjustments for burn severity
Extent of burn BEE Protein NPE:N ratio
Healthy individual 1.0 g/kg/d 150:1
Moderate burn (15–30% X 1.5 1.5 g/kg/d 100–120:1
TBSA)
Major burn (15–30% TBSA) X1.5–1.8 1.5–2 g/kg/d 100:1
Massive burn (≥ 50%) X1.8–2.1 2–2.3 g/kg/d 100:1
Activity factors: In bed = 1.2 Ambulatory = 1.3 Ventilated = 1.05

58.  ER for burned pediatric pts:
 Galveston Formula = 1800 kcal/m2 + 2200 kcal/m2
burn
 Polk Formula = (<3 y.o) = (60 kcal x wt) + (35kcal x %
TBSA)
 Important to remember that a progressive exercise
programme should always be combined with adequate
nutrition to enhance the restoration of muscle mass and
strength

59.  CHO
 50 to 60% or can be up to 70% of energy
 not to exceed 5 to 7 mg/kg/min in parenteral nutrition
 CHO need for protein sparing; but excess result in
hyperglacemia, osmotic diuresis, dehydration,
respiratory difficullity

60.  Protein:
 requirement due to losses via urine, wound,
gluconeogenesis and wound healing
 20 -25% of total calories (HBV protein)
 Pediatrics  2.5 – 3.0 g/kg (monitor renal fx & fluid
balance)
 BCAA‘s & arginine  improve wound healing & immunity
 Monitor BUN, serum creatinine, & hydration
 To estimate wound nitrogen loss:
 < 10% open wound = 0.02 g nitrogen/kg/d
 11 – 30% open wound = 0.05 g nitrogen/kg/d
 > 31 % open wound = 0.12 g nitrogen/kg/d

61.  Fats:
 Fat supplied at 15% of total energy reduced infectious
morbidity and shortened hospitalization time compared
to 35% of energy requirements being derived from fat.
 Increase omega- 3  may improve immune response
(inhibits production of prostaglandins & leukotrienes)
 Begin with 15 – 20% [monitor immune response,
feeding tolerance and serum TG (not rise > 10 to 20%
over baseline values)]

62.  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.

63.  Vitamins & Minerals Supplementation
 Evidence-based guidelines for micronutrient
supplementation are limited
 Vit C- collagen formation and antioxidant defense in the
immune system and is involved in ATP production (66
mg/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)

64. Methods of Nutritional Support
 Pt with <20% TBSA burn able to meet the regular
needs with regular hi-cal, hi-protein diet
 Use ‗concealed nutrients‘ – add protein to pudding,
milk etc
 Pt with major burn & EE require ETF or TPN (if
ileus not fx or do not tolerate TF)

65. Acute Spinal Cord Injury

66. MNT
 Energy :
 H/B x 1.1 x 1.2 (Barco et al, NCP 17;309-313, 2002)
 Pt with multi-traumas in addition to SCI may have
higher needs
 Protein needs:
 2 g/kg (Rodriguez DJ et al, JPEN 15:319-322, 1991)

67. Surgery/Trauma

68.  Def: an operative procedure used to diagnose, repair,
or treat an organ tissue. Can be further classify to
major/minor surgery
 The sign & symptoms experienced with surgery
depend to the type of procedure.
 Pt need to be fasted for 12 hr before surgery
 The progress of feeding from NBM/NPO to solid diet
should be done as quickly as possible
 The energy and protein should be individualize.

69. MNT
 Energy:
 HB x 1.0 – 1.3 depend on type of surgery
 Will vary with type of surgery, degree of trauma
 Use Ireton-Jones 1992 or Penn State if data is
available*
 Can use estimate of 25-30 kcals/kg to begin and monitor
response to therapy**
*ADA Evidence Analysis Library, accessed 10-06
**ASPEN Nutrition Support Practice Manual, 2nd Edition, p. 278
 Protein:
 Minor surgery : 1 -1.1 g/kg
 Major Surgery : 1.2 – 1.5 g/kg

70. ASPEN Practice Guidelines Perioperative Nutrition
Support
 Preoperative NS should be administered to moderately-
severely malnourished pts undergoing major
gastrointestinal surgery for 7 to 14 days if the operation
can be safely postponed.
 PN should not be routinely given in the immediate
postoperative period to patients undergoing major
gastrointestinal procedures.
 Postoperative NS should be administered to patients who
will be unable to meet their nutrient needs orally for a
period of 7 to 10 days.

71. Postoperative Nutrition Support
 Introduction of solid foods depends on condition of
GI
 Oral feeding may be delayed for first 24 – 48 hours
post surgery until return of bowel sounds, passage of
flatus or soft abdomen
 Traditional practice has been to progress from clear
liquids, to full liquids, to solid foods
 However, there is no physiological reason not to
initiate solid foods once small amounts of liquids are
tolerated

72. Hypocaloric Feedings
 Hypocaloric feedings have been recommended in
specific patient populations:
 Class III obesity (BMI>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

73.  Although overfeeding surgical patients should be
avoided, prolonged underfeeding may be equally
concerning.
 This can compromise immune function, delay wound
healing, exacerbate muscle wasting, and prolong the
recovery of nitrogen balance and visceral protein levels.
 However, short-term hypocaloric feeding with 1-2 g of
protein per kilogram per day, particularly in the acute
phase of postoperative stress, may reduce metabolic
complications while supporting a reduction in negative