MNT for Metabolic Stress:Sepsis, Trauma, Burns, Surgery
Metabolic Stress Sepsis (infection) Trauma (including burns) Surgery Once the systemic response is activated, the
physiologic and metabolic changes that follow are similar and may lead to septic shock.
Immediate Physiologic and Metabolic Changes after Injury or Burn
ADH, Antiduretic hormone; NH3, ammonia.
Metabolic Response to StressMetabolic Response to Stress
Involves most metabolic pathways Accelerated metabolism of LBM Negative nitrogen balance Muscle wasting
Involves most metabolic pathways Accelerated metabolism of LBM Negative nitrogen balance Muscle wasting
Ebb PhaseEbb Phase
Immediate—hypovolemia, shock, tissue hypoxia
Decreased cardiac output Decreased oxygen consumption Lowered body temperature Insulin levels drop because glucagon is
elevated.
Immediate—hypovolemia, shock, tissue hypoxia
Decreased cardiac output Decreased oxygen consumption Lowered body temperature Insulin levels drop because glucagon is
elevated.
Flow Phase
Follows fluid resuscitation and O2 transport
Increased cardiac output begins Increased body temperature Increased energy expenditure Total body protein catabolism begins Marked increase in glucose production, FFAs,
circulating insulin/glucagon/cortisol
Hormonal and Cell-Mediated Response
There is a marked increase in glucose production and uptake secondary to gluconeogenesis, and
—Elevated hormonal levels
—Marked increase in hepatic amino acid uptake
—Protein synthesis
—Accelerated muscle breakdown
Skeletal Muscle Proteolysis
From Simmons RL, Steed DL: Basic science review for surgeons, Philadelphia, 1992, WB Saunders.
Metabolic Changes in StarvationMetabolic Changes in Starvation
From Simmons RL, Steed DL: Basic science review for surgeons, Philadelphia, 1992, WB Saunders.
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
Starvation vs. Stress—cont’d 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 accelerated also
Hormonal Stress ResponseHormonal 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
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
Hormonal Stress Response—cont’dHormonal Stress Response—cont’d 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
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
CytokinesCytokines Interleukin-1, interleukin-6, and tumor
necrosis factor (TNF) Released by phagocytes in response to
tissue damage, infection, inflammation, and some drugs and chemicals
Interleukin-1, interleukin-6, and tumor necrosis factor (TNF)
Released by phagocytes in response to tissue damage, infection, inflammation, and some drugs and chemicals
Systemic Inflammatory Response Syndrome
SIRS describes the inflammatory response that occurs in infection, pancreatitis, ischemia, burns, multiple trauma, shock, and organ injury.
Patients with SIRS are hypermetabolic.
Multiple Organ Dysfunction Syndrome Organ dysfunction that results from direct
injury, trauma, or disease or as a response to inflammation; the response usually is in an organ distant from the original site of infection or injury
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
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
Bacterial Translocation across Microvilli and How It Spreads into the Bloodstream
Hypermetabolic Response to Stress—CauseHypermetabolic Response to Stress—Cause
Algorithm content developed by John Anderson, PhD, and Sanford C. Garner, PhD, 2000.
Hypermetabolic Response to Stress—PathophysiologyHypermetabolic Response to Stress—Pathophysiology
Algorithm content developed by John Anderson, PhD, and Sanford C. Garner, PhD, 2000.
Hypermetabolic Response to Stress—Medical and Nutritional Management
Algorithm content developed by John Anderson, PhD, and Sanford C. Garner, PhD, 2000. Updated by Maion F. Winkler and Ainsley Malone, 2002.
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
ASPEN
American Society of Parenteral and Enteral Nutrition
ASPEN
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
ASPEN’s Strength of Evidence Evaluation (adapted from AHRQ) A: there is good research-based evidence to
support the guideline (prospective, randomized trials).
B: There is fair research-based evidence to support the guideline (well-designed studies without randomization).
C: The guideline is based on expert opinion and editorial consensus
ASPEN Practice Guidelines for Critical Care Patients with critical illnesses are at nutrition risk and
should undergo nutrition screening to identify those who require formal nutrition assessment with development of a nutrition care plan. (B)
Specialized nutrition support (SNS) should be initiated when it is anticipated that critically ill patients will be unable to meet their nutrient needs orally for a period of 5-10 days. (B)
EN is the preferred route of feeding in critically ill patients requiring SNS. (B)
PN should be reserved for those patients requiring SNS in whom EN is not possible. ( C )
ASPEN BOD. JPEN 26;S92SA, 1992
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)
NUTRITIONAL ASSESSMENT
Clinical judgment must play a major role in deciding when to begin/offer nutrition support
Determination of Nutrient Requirements Energy Protein Vitamins, Minerals, Trace Elements Nonprotein Substrate
– Carbohydrate– Fat
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
Indirect Calorimetry
Better estimate in critically ill hypermetabolic patient
The “gold standard” in estimating energy needs in critical care
Can be used in both mechanically ventilated and spontaneously breathing patients (ventilated patients most accurate)
Equipment is expensive and not readily available in many facilities
GUIDELINES: Indirect Calorimetry in Critical Care R.16.1. Indirect calorimetry is the standard for
determination of RMR in critically ill patients since RMR based on measurement is more accurate than estimation using predictive equations. Strong, Imperative
When indirect calorimetry cannot be performed, predictive formulas may be necessary (Grade I)– ADA Evidence Analysis Library, accessed 10-06
Indirect Calorimetry
Requires appropriate calibration of equipment, attainment of a steady state for measurement, and appropriate timing of measurement
Requires interpretation by trained clinician Inaccurate in patients requiring inspired
oxygen (FiO2>60%), and with air leaks via the entrotracheal tube cuff, chest tubes or bronchopleural fistula
Respiratory Quotient Respiratory quotient (RQ) is the ratio of vCO2 and
vO2 and is a function of the mix of substrates being utilized for metabolism.
An RQ of <0.7 or > 1.0 may identify unusual metabolic or respiratory conditions, failure to adhere to the fasting requirement of the measurement protocol, and/or operator or equipment error.
A repeated measurement should be considered if an RQ value is outside the range of 0.70 to 1.0. – ADA Evidence Analysis Library, 10-06
Indications for Indirect Calorimetry
Patients with altered body composition (underweight, obese, limb amputation, peripheral edema, ascites)
Difficulty weaning from mechanical ventilation Patients s/p organ transplant Patients with sepsis or hypercatabolic states
(pancreatitis, trauma, burns, ARDS) Failure to respond to standard nutrition support
Malone AM. Methods of assessing energy expenditure in the intensive care unit. Nutr Clin Pract 17:21-28, 2002.
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.
Harris-Benedict Equation Monograph in 1919 described results of indirect
calorimetry on 239 healthy men and women of varying body sizes up to a BMI of 56 in men and 40 in women
Predicts BMR (RMR) with systematic overestimation of 5-15%
Random error greater in women than in men Stress and activity factors must be applied to
estimate total energy expenditure HB RMR X 1.3-1.5 used in critically ill patients
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)
Ireton-Jones Equations
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
Ireton-Jones 1997 Equations Three studies comparing RMR and the updated
Ireton-Jones 1997 equations report similar mean values
However, only 36% of subjects were predicted within 10% of RMR.
Further research in the critically ill population is needed regarding the Ireton-Jones 1997 equations (Grade III)– ADA Evidence Analysis Library,
accessed 10-06
Ireton-Jones 1992 Equations
Spontaneously-breathing patients: IJEE (s) = 629 – 11(A) + 25(W) – 609 (O)
Ventilator-dependent patients: IJEE (v) = 1925 – 10(A) + 5(W) + 281 (S)
+ 292 (T) + 851 (B)
Ireton-Jones Equations 1992
Where: A = age in years W = weight (kg) O = presence of obesity >30% above IBW from
1959 Metropolitan ht/wt tables or BMI >27 (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
Ireton-Jones Equations 1992
Seven studies comparing RMR and the Ireton-Jones 1992 equations report similar mean values
However, for an individual, energy predictions may be different by as much as 500 kcals (60% of subjects predicted within 10% of RMR). (Grade III)
• ADA Evidence Analysis Library, accessed 10-06
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.
Penn State Equations
Two studies comparing RMR and the Penn State equation report adequate precision (80% of non-obese subjects predicted within 10% of RMR).
Further research in the critically ill population is needed regarding the Penn State equation (Grade III)– ADA Evidence Analysis Library accessed 10-
06
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).
Swinamer Equation
In one positive quality cross-sectional study by MacDonald and Hildebrandt, 2003, 24-hour indirect calorimetry was performed on 76 critically ill patients with a mean APACHE II score of 12.6 +/- 7.5.
The Swinamer formula correlated with 24-hour measured RMR, with an r = 0.791 and r2 = 0.62 (P < 0.0001). The Swinamer equation predicted RMR within 20% of IC values 88% of the time for the entire population studied
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.
Further research is needed in critically ill patients with obesity.
Recommendations for Predicting RMR in Critically Ill Pts HBE should not be used to predict RMR in
critically ill patients (Grade I) Ireton-Jones 1997 should not be used to
predict RMR in critically ill patients (Grade II)
Ireton-Jones 1992 may be used to predict RMR in critically ill pts but errors will occur. (Grade III)– ADA Evidence Analysis Library, 10-06
Recommendations for Predicting RMR in Critically Ill Pts Penn State 2003 may be used in critically ill
patients, but errors will occur. (Grade III) Penn State 2003 or Ireton-Jones 1992 may
be used to predict RMR in critically ill OBESE patients, but errors will occur. (Grade III)– ADA Evidence Analysis Library, 10-06
GUIDELINES: Determining RMR in Critical Illness R.16.1. Indirect calorimetry is the standard
for determination of RMR in critically ill patients since RMR based on measurement is more accurate than estimation using predictive equations. Strong, Imperative
Critical Illness ADA Evidence Based Guidelines, 10-06
GUIDELINES: Determining RMR in Critical Illness R.16.2. If predictive equations are needed in
critically ill patients, consider using one of the following, as they have the best prediction accuracy of equations studied: Ireton-Jones, 1992, Penn State, 2003a or Swinamer. In some individuals, errors between predicted and actual energy needs will result in under- or over-feeding. Fair, Conditional
Critical Illness ADA Evidence Based Guidelines, 10-06
GUIDELINES: Determining RMR in Critical Illness R.16.3. The Harris-Benedict (with or without
activity and stress factors), the Ireton-Jones, 1997, and the Fick equation should not be considered for use in RMR determination in critically ill patients, as these equations do not have adequate prediction accuracy. In addition, the Mifflin-St. Jeor equation should not be considered for use in critically ill patients, as it was developed for healthy people and has not been well researched in the critically ill population. Strong, Imperative
Critical Illness ADA Evidence Based Guidelines, 10-06
GUIDELINES: Determining RMR in Critical Illness R.16.4. If predictive equations are needed
for critically ill mechanically ventilated individuals who are obese, consider using Ireton-Jones, 1992, or Penn State, 1998, as they have the best prediction accuracy of equations studied. In some individuals, errors between predicted and actual energy needs will result in under- or over-feeding. Fair, Conditional
Critical Illness ADA Evidence Based Guidelines, 10-06
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
What Weight Do You Use?
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
Objectives
First, fluid resuscitation and treatment of cause of hypermetabolism
When hemodynamically stable, begin nutrition support
Nutrition support may not result in +N balance – may slow loss of protein
Undernutrition can lead to protein synthesis, weakness, MODS, death
Nutrient Guidelines: Carbohydrate
Should provide 60 – 70% calories Maximum rate of glucose oxidation =
~5 – 7 mg/kg/min or 7 g/kg/day* Blood glucose levels should be monitored
and nutrition regimen and insulin adjusted to maintain glucose below 150 mg/dl
*ASPEN BOD. JPEN 26;22SA, 1992
Nutrient Guidelines: Fat Can be used to provide needed energy and
essential fatty acids Should provide 15 – 40% of calories Limit to 2.5g/kg/day or possibly 1 g/kg/day
IV* Caution with use of fats in stressed &
trauma pts – There is evidence that high fat feedings
(especially LCT) cause immunosuppression – New formulas focus on omega-3s
*ASPEN BOD. JPEN 26;22SA, 1992
Nutrient Guidelines: Protein
1.5 – 2.0 g/kg/day to start; monitor response Nonprotein calorie/gram of nitrogen ratio
for critically ill = 100:1 Giving exogenous aa’s decreases negative
N balance by supplying liver aa’s for protein synthesis
ASPEN BOD. JPEN 26;22SA, 1992
Nutrient Guidelines: Protein
No studies were found in generalized critical care populations that demonstrated a significant difference in mortality based on level of protein intake or delivery. In critically ill patients undergoing continuous renal replacement therapy, a single study indicates that protein intake > 2.0 g per kg per day is more likely to promote positive N balance (P=0.0001). And, while a more positive N balance is associated with decreased mortality, a higher protein intake was not associated with mortality.—ADA EAL 11-27-07
Nutrient Guidelines: Protein
To date, adequately powered studies have not been conducted to demonstrate a significant difference in rate of infectious complications when comparing critically ill patients with positive or negative N balance.
To date, no studies were found that demonstrated a significant difference in LOS or ICU length of stay based on level of protein intake or protein delivery. – ADA EAL, 11-27-07
Fluid and Electrolytes
Fluid 30-40 mL/kg or 1 to 1.5mL/kcal expended
Electrolytes/Vitamins/Trace Elements Enteral feedings: begin with RDA/AI
values PN: use PN dosing guidelines
ASPEN BOD. JPEN 26;23SA, 1992
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)
ASPEN BOD. JPEN 26;91SA, 1992
Immune-Enhancing EN in Critical Care The addition of immune-enhancing EN to enteral
feeding of severely ill ICU patients may be associated with increased mortality, though adequately powered trials have not been conducted (Grade III)
The addition of immune-enhancing EN to enteral feeding of moderate or less severely ill ICU patients demonstrates no effect on mortality (Grade II)– ADA Evidence Analysis Library Accessed 10-06
Immune-Enhancing EN in Critical Care The addition of immune-enhancing EN to enteral
feeding of critically ill ICU patients is not associated with fewer infectious complications (Grade III)
The addition of immune-enhancing EN to enteral feeding of critically ill ICU patients has limited impact on LOS (Grade II)
ADA Evidence Analysis Library Accessed 10-06
Immune-Enhancing EN in Critical Care The addition of immune-enhancing EN to enteral
feeding of critically ill ICU patients is not associated with reduced number of days on mechanical ventilation (Grade II).
The addition of immune-enhancing EN to enteral feeding of critically ill ICU patients is not associated with reduced cost of medical care (Grade III)– ADA Evidence Analysis Library Accessed 10-06
GUIDELINES: Immune-Enhancing EN in Critical Care R.3 Immune-enhancing EN is not recommended for routine use in critically ill patients in the ICU. Immune-enhancing EN is not associated with reduced infectious complications, LOS, reduced cost of medical care, days on mechanical ventilation or mortality in moderately to less severely ill ICU patients. Their use may be associated with increased mortality in severely ill ICU patients, although adequately-powered trials evaluating this have not been conducted. For the trauma patient, it is not recommended to routinely use immune-enhancing EN, as its use is not associated with reduced mortality, reduced LOS, reduced infectious complications or fewer days on mechanical ventilation. Fair, Imperative
Critical Illness ADA Evidence Based Guidelines, 10-06
Supplemental Glutamine (GLN) in Critical Care Alterations in glutamine metabolism can occur in
critical care, possibly affecting gut function PN solutions traditionally have not contained
glutamine because of instability in solution Animal and human studies suggest that
supplemental GLN in PN may have beneficial effects
Those benefits have not been demonstrated in EN
Glutamine Metabolism
NH2, Amine; NH3, ammonia.
From Simmons RL, Steed DL: Basic science review for surgeons, Philadelphia, 1992, WB Saunders.
EN vs PN in Critical Care
Adequately powered trials have not been found to enable evaluation of the impact of EN versus PN on mortality in critically ill patients (Grade V)
Enteral nutrition is associated with reductions in infectious complications in critically ill patients, when compared to PN (Grade I)
– ADA Evidence Analysis Library, accessed 10-06
EN vs PN in Critical Care
Adequately powered trials have not been found to enable evaluation of the impact of EN versus PN on LOS in critically ill patients (Grade V)
Enteral nutrition is associated with reduced cost of medical care in critically ill patients, when compared to PN (Grade II)
– ADA Evidence Analysis Library, accessed 10-06
GUIDELINES: EN vs PN in Critical Care R.1. If the critically ill ICU patient is
hemodynamically stable with a functional GI tract, then EN is recommended over PN. Patients who received EN experienced less septic morbidity and fewer infectious complications than patients who received PN. In the critically ill patient, EN is associated with significant cost savings when compared to PN. There is insufficient evidence to draw conclusions about the impact of EN or PN on LOS and mortality. Strong, Conditional
Critical Illness ADA Evidence Based Guidelines, 10-06
[Potential] Beneficial Effects of Postburn Early Enteral Nutrition Nutrient needs satisfied Improved tube feeding
tolerance Decreased incidence of
bacterial translocation Decreased number of
infectious episodes Decreased antibiotic
therapy
Improved nitrogen balance
Reduced urinary catecholamines
Diminished serum glucagon
Suppressed hypermetabolic response
Enhanced visceral protein status
*Mayes and Gottslich, Burns and Wound Healing. In The science and practice of nutrition support: A core curriculum. ASPEN 2001, p. 401
Early Enteral Nutrition (ADA EAL)
To date, adequately powered studies have not been conducted to demonstrate a significant difference in mortality when comparing early versus late EN in critically ill patients (Grade V)
In fluid-resuscitated, critically ill patients, EN started within 24-48 hours following injury or admission to the ICU reduces the incidence of infectious complications (Grade I)
• ADA Evidence Analysis Library, accessed 10-06
Early Enteral Nutrition (ADA EAL)
In fluid-resuscitated, critically ill patients, EN started within 24-48 hours following injury or admission to the ICU may reduce LOS (Grade II)
• ADA Evidence Analysis Library, accessed 10-06
GUIDELINES: Timing of Enteral Nutrition and Critical Illness R.2. 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. Strong, Conditional
Critical Illness ADA Evidence Based Guidelines, 10-06
Cautions Re/ Early Enteral Feeding in Critically Ill Patients Benefits cited are theoretical; many based on
animal studies During sepsis, the GI tract and liver are
susceptible to ischemia due to increased oxygen consumption and decreased blood flow
Enteral nutrition delivered to septic patients given vasoactive drugs may exacerbate this
EN should be initiated cautiously after hemodynamic stability is established
Brantley. Support Line; 24:10, 2003
Feeding Tube Placement in Critically Ill Patients R.4. Enteral Nutrition (EN) administered into the
stomach is acceptable for most critically ill patients.
Consider placing feeding tube in the small bowel when patient is in supine position or under heavy sedation.
If your institution's policy is to measure GRV, then consider small bowel tube feeding placement in patients who have more than 250ml GRV or formula reflux in two consecutive measures. Fair, Conditional A DA EAL accessed 11-27-07
Feeding Tube Placement in Critically Ill Patients Small bowel tube placement is associated with
reduced GRV. Adequately-powered studies have not been
conducted to evaluate the impact of GRV on aspiration pneumonia.
There may be specific disease states or conditions that may warrant small bowel tube placement (e.g., fistulas, pancreatitis, gastroporesis), however they were not evaluated at this phase of the analysis.
ADA EAL Guidelines accessed 11-27-07
Relationship Between Wt and Outcomes in Critically Ill Pts There is fair evidence that mortality is increased in
critically ill trauma patients with BMI > 30. Grade II
There is limited evidence that BMI > 30 is not associated with increased rate of infection in critically ill trauma patients. Grade III
There is fair evidence that LOS is increased in critically ill trauma patients with BMI > 30. Grade II
– ADA EAL 11-27-07
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
Charney P. Glycemic control in the ICU. In Sharpening Your Skills as a Nutrition Support Dietitian. DNS, 2003, p. 210
Glucose Control in Critical Illness
Survival is decreased in critically ill patients with hyperglycemia (Grade I)
Controlling BG is associated with fewer infectious complications in critically ill patients (Grade I)
There is fair evidence that controlling BG values in critically ill patients leads to a decrease in ICU LOS (Grade II)
– ADA Evidence Analysis Library Accessed 10-06
Glucose Control in Critical Illness
There is fair evidence that controlling BG values in critically ill patients is associated with reduced number of days on mechanical ventilation (Grade II)
There is limited evidence that controlling BG values in critically ill patients leads to a decrease in the cost of medical care (Grade III)– ADA Evidence Analysis Library Accessed 10-06
GUIDELINES: Blood Glucose Control in Critical Illness R.8.1 Evidence indicates that blood glucose under
140mg/dL is associated with decreased mortality, LOS and infectious complications in critically ill patients. Dietitians should promote attainment of these levels for BG control. Strong, Imperative
R.8.2 Dietitians should promote attainment of strict glycemic control (80-110mg/dL) to reduce time on mechanical ventilation in critically ill medical ICU patients. Strong, Imperative
Critical Illness ADA Evidence Based Guidelines, 10-06
MNT in Selected Populations in Critical Care
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.
ASPEN Practice Guidelines: Neurological Impairment Patients with neurologic impairment are at
nutrition risk and should undergo nutrition screening to identify those who require formal nutrition assessment with development of a nutrition care plan. (B)
SNS should be initiated early in patients with moderate or severe TBI. (B)
When SNS is required, EN is preferred if it is tolerated. ( C )
ASPEN BOD. JPEN 26;91SA, 1992
ASPEN Practice Guidelines: Neurological Impairment PN should be administered to patients with TBI
if SNS is indicated and EN does not meet the nutritional requirements. ( C )
Indirect calorimetry should be utilized, if available, to accurately determine nutrition requirements in patients with TBI and CVAs. (B)
Swallowing function should be evaluated to determine the safety of oral feedings and risk of aspiration before the initiation of an oral diet. (B)
ASPEN BOD. JPEN 26;91SA, 1992
Traumatic Brain Injury (TBI)
Use indirect calorimetry when available Use H/B x 1.4 stress factor Protein requirements estimated at 1.5 – 2.2
g/kg of body weight
Acute Spinal Cord Injury
Source: www.spinal-cord-injury-resources.com/ spinal-i...
Acute Spinal Cord Injury (SCI)
Energy requirement for SCI = 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
Nutrition Support in Surgery/Trauma
Graphic source www.nlm.nih.gov/.../ gallery/image/surgery.gif
ASPEN Practice Guidelines Perioperative Nutrition Support Preoperative SNS should be administered to
moderately-severely malnourished pts undergoing major gastrointestinal surgery for 7 to 14 days if the operation can be safely postponed. (A)
PN should not be routinely given in the immediate postoperative period to patients undergoing major gastrointestinal procedures. (A)
Postoperative SNS should be administered to patients who will be unable to meet their nutrient needs orally for a period of 7 to 10 days. (B)
ASPEN BOD. JPEN 26;96SA, 1992
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
Energy Requirements in Surgery or Trauma 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** Indirect calorimetry yields most accurate
estimates, particularly in pts difficult to assess
*ADA Evidence Analysis Library, accessed 10-06**ASPEN Nutrition Support Practice Manual, 2nd Edition, p. 278
Hypocaloric Feedings
Hypocaloric feedings have been recommended in specific patient populations
Aggressive protein provision (1.5-2.0 gm/kg/day
ASPEN Nutrition Support Practice Manual, 2nd Edition, p. 279
Zaloga GD. Permissive underfeeding. New Horizons 1994
Hypocaloric Feedings Have Been Recommended in: 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
Protein or Nitrogen Requirements in SurgeryProtein or Nitrogen Requirements in Surgery 1.2 to 1.5 g protein/kg BW
for anabolism mild or moderate stress Nitrogen requirement estimated from
energy requirements
1.2 to 1.5 g protein/kg BW
for anabolism mild or moderate stress Nitrogen requirement estimated from
energy requirements
Monitoring Response to MNT in Critical Care Pts Weight: may be difficult to obtain and
inaccurate d/t fluid shifts, dressings Indirect calorimetry: if available. Adjust
support as needed; use RQ to evaluate adequacy of support
Nitrogen balance: labor intensive. Can be used to assess metabolic state
Prealbumin: can reflect repletion once acute phase response has diminished
Monitoring Response to MNT in Critical Care R.6.1 Evaluating patient position should be
part of an EN monitoring plan. To decrease the incidence of aspiration pneumonia and reflux of gastric contents into the esophagus and pharnyx, critically ill patients should be placed in a 45-degree head of bed elevation, if not contraindicated. Strong, Imperative
Critical Illness ADA Evidence Based Guidelines, 10-06
GUIDELINES: Monitoring Response to MNT in Critical Care R.6.2 Evaluating GRV in critically ill patients is an
optional part of a monitoring plan to assess tolerance of EN. Enteral nutrition should be held when a GRV greater than or equal to 250ml is documented on two or more consecutive occasions. Holding EN when GRV is less than 250ml is associated with delivery of less EN. Gastric residual volume may not be a useful tool to assess the risk of aspiration pneumonia. Adequately-powered studies have not been conducted to evaluate the impact of GRV on aspiration pneumonia. Consensus, Imperative
Critical Illness ADA Evidence Based Guidelines, 10-06
GUIDELINES: Monitoring Response to MNT in Critical Care R.6.3 If the patient exhibits a history of
gastroparesis or repeated high GRVs, then consider the use of a promotility agent in critically ill ICU patients, if there are no contraindications. The use of a promotility agent (e.g., Metoclopramide) has been associated with increased GI transit, improved feeding tolerance, improved EN delivery and possibly reduced risk of aspiration. Strong, Conditional
Critical Illness ADA Evidence Based Guidelines, 10-06
GUIDELINES: Blue Dye Use and Critical Illness R.5. Blue dye should not be added to EN
for detection of aspiration. The risk of using blue dye outweighs any perceived benefit. The presence of blue dye in tracheal secretions is not a sensitive indicator for aspiration. Strong, Imperative
Critical Illness ADA Evidence Based Guidelines, 10-06
Monitoring Response to MNT in Critical Care Pts Intake and output: stooling, fluid balance Tolerance of feeding regimen (abdominal
exam, gastric residuals) Amount of nutrition prescription delivered;
support is often interrupted due to surgeries, dressing changes, intolerance, and therapy.
GUIDELINES: Monitoring Response to MNT in Critical Care R.7. Monitoring plan of critically ill patients must
include a determination of daily actual EN intake. Enteral nutrition should be initiated within 48 hours of injury or admission and average intake actually delivered within the first week should be at least 60-70% of total estimated energy requirements as determined in the assessment. Provision of EN within this time frame and at this level may be associated with a decreased LOS, days on the mechanical ventilation and infectious complications. Fair, Imperative
Critical Illness ADA Evidence Based Guidelines, 10-06