MNT for Metabolic Stress

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


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


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


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


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


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


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


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)


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


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


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


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.


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


[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)


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)


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


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


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 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)


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)


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


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


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


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


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


MNT for Metabolic Stress

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