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
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
20.
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
24.
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)
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
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
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
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
52.
53.
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)
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)
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
Editor's Notes
The metabolic response to fasting is an adaptation by the body to preserve protein by using alternative sources of energy.The carbohydrate deposits of the body last about 18 to 20 hours and new glucose is produced through gluconeogenesis of amino acids from the lean body mass. Ruderman NB. Muscle amino acid metabolism and gluconeogenesis. Annu Rev Med 1975;26:248
The initial response to fasting is mediated by a drop in serum insulin and an increase in glucagon. During this period energy is provided mainly by glucose from gluconeogenesis. However, lipolysis generates free fatty acids which are oxidized into ketones. After several days, most of the body organs are using ketones (acetoacetic, propionate, and butyric acids) for energy and gluconeogenesis decreases to half of the early phase. Brain, red blood cells, and nerve tissue still rely partially on glucose for energy.
This slide illustrates nitrogen losses in relation to trauma. With respect to protein, the greater the trauma, the greater the effect on the nitrogen balance. Similar to metabolic rate, patients experience nitrogen losses according to the severity and duration of the trauma.The normal range is indicated by the shaded area. The amount of protein requirement relative to calories increases in patients with metabolic stress.Long CL, et al. JPEN 1979;3:452-456.
G (gender)Female= 2, male = 1T= traumaB burnsO = obesity present =1 absent = 0
Calorie-to-nitrogen ratios can be used to prevent lean body mass from being utilized as a source of energy. Therefore, in the non-stressed patient, less protein is necessary to maintain muscle as compared to the severely stressed patient.
Rules of nine for adult and rules of 7 for chlidrenPercentage of burns
Sequestration -- >The action of forming a chelate or other stable compound with an ion or atom or molecule so that it is no longer available for reactions
1– controlenviroment, temp, maintain fluid, electrolytes balance, control pain, anxiety and covering wound healing2- adequate cal to prevent LOW > 10% UBW, adequate protein, vit & mineral supp.3- acute peptic ulcer of the duodenum resulting as a complication from severe burns when reduced plasma volume leads to sloughing of the gastric mucosa.
To find out nitrogen gms= protein in gms/ 6.25 500 ml of 8.5 amino acid has 42.5gms protein that divided by 6.25= 6.8 gms The calories from dextrose and lipids have 1000 and 510 calories respectively Now divide 1510 non protein calories/ 6.8 =222