Nutritional Support in the ICU Sandra L Schoepfel MS RD RN CNSD Karl D Pilson MD Suresh Agarwal MD...

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Nutritional Support in the ICU

Sandra L Schoepfel MS RD RN CNSD

Karl D Pilson MD

Suresh Agarwal MD FACS

Boston Medical Center

Boston, MA

Rationale for Nutrition Support

• Limit catabolism – hypercatabolic state is driven by the underlying disease process and is not reversed by nutrition alone

• Offset muscle wasting and starvation induced immune depletion – loss of 1% per day lean body mass = 2% per day skeletal muscle

• Substrate for healing and preserve immune function• Increase survival• Nutritional therapy in the ICU is at best “supportive” –

cannot reverse hypermetabolism

Goals of Nutritional Support In The ICU

• Early intervention (after resuscitation)• Ensure adequate enteral access • Support the metabolic response to injury and

infection (bone marrow, acute phase proteins, wound healing)

• Correct fluid, metabolic and acid/base abnormalities

• Avoid overfeeding and hyperglycemia• ? reduce ventilator dependency

Achieving Nutritional Goals in the ICU is Difficult

• 1 year survey of ICU Nutritional Practice:• 3526 record feeding days were evaluated

– Desired intake was only achieved 52% of days– Ideal protein intake achieved in 54%– Ideal energy intake achieved in 66%– Ideal volume intake achieved in 75% of patients

» Binnekade JM. Crit Care 2005. Jun;9(3):R216-25

Baseline Patient Assessment

• No “single” test can be used as a completely reliable indicator of nutritional status

• Evaluation of weight loss and previous nutrient intake before admission

• Level of disease severity• Presence of comorbid conditions• Function of the gastrointestinal tract• Evaluation of biochemical indices• Measurement of body mass index

Nutritional Assessment – A Difficult Task in the ICU

• Medical, surgical and dietary history may be hard to obtain• Physical assessment may be confounded by volume

resuscitation (surgery, burn, trauma, infection)• Problems with Nutritional Assessment in ICU Patients

Parameter InvalidationWeight (BMI) Edema, fluids, diuretics

Anthropometrics Edema, observer variability

Albumin, Pre-Albumin Infection, inflammation, injury, renal failure

Nitrogen Balance Drainage tubes, wounds, renal failure

Factors That Increase Nutritional Risk

• Involuntary loss or gain of > 10% of usual BW within 6 months or > 5% of usual BW in 1 month, or a weight of 20% over or under ideal BW

• Presence of chronic disease• Increased metabolic requirements• Altered nutrient schedules (TF’s, PN) because of

recent surgery, illness• Impaired ability to ingest or absorb food

adequately for > 7 days

Malnutrition

• Recent surveys suggest that 33-53% of hospitalized patients suffer from moderate to severe malnutrition

• Souba W. N. Eng J Med 1997;336-41• Atalay BG. JPEN 2008 Jul-Aug;32(4):454• Delgado AF. Clinics 2008;63(3):357

• Assume some degree of malnutrition exists or will develop in all patients

• In the ICU: Malnutrition contributes to respiratory weakness, failure to wean from the ventilator, increased morbidity, mortality and hospital costs

Protein Markers in the ICU

• Traditional protein markers (albumin, prealbumin, transferrin, retinol binding protein) and may also be a reflection of the acute phase response and do not accurately represent nutritional status

• Improvement in hepatic protein levels indicate recovery, although not necessarily nutritional recovery

Stimuli for Stress Response

• Loss of blood volume• Emotion/pain/fear• Temperature• Infection• Tissue injury

Goals of Stress Response

• Maintain energy substrates (GLUCOSE)• Maintain oxygen delivery• Minimize further injury...

Greenfield 1997

Response to Stress/Injury

• Neurohormonal - "Counterregulatory hormones"– Glucagon– Epinephrine– Glucocorticoids

• Inflammatory mediators– IL-1, IL-2, IL-6– TNF-a– IFN-g

Metabolic Response During Sepsis – Carbohydrate Metabolism

• Pro-inflammatory cytokines potentiate the release of catabolic hormones (glucagon, catecholamines, and cortisol) stimulating glycogenolysis and gluconeogenesis to mobilize glucose

• Following the onset of sepsis, glycogen stores are depleted within hours, and endogenous lipid and protein become the major source of oxidative energy substrate

• As sepsis progresses, reduced splanchic blood flow and severe hepatic dysfunction eventually lead to hypoglycemia and decreased glucose production

Metabolic Response During Sepsis Protein Metabolism

• Amino acids released from skeletal muscle breakdown, connective tissue, and unstimulated gut are shunted to the liver, where they are used in gluconeogenesis and for the synthesis of acute-phase reactants

• The ureagenesis rate is increased, as well as the synthesis rates of creatinine, uric acid, and ammonia – all get excreted in the urine

• In an unfed, stressed patient, up to 250 g of lean body mass will be broken down each day

• The nitrogen loss of severe sepsis complicating recovery from trauma may exceed 30g/d

• Adequate nutrition support will not completely ablate the catabolic effects and response

Greenfield 1997

Metabolic Response During Sepsis Lipid Metabolism

• Lipolysis under catecholamine regulation• In early sepsis, catabolic hormones outweigh the effects

of anabolic hormones such as insulin and result in the breakdown of stored triglycerides to glycerol and free fatty acids affecting intracellular transport metabolism

• Sepsis impairs ketogenesis and the activity of lipoprotein lipase is suppressed

• Hyperlipidemia, hyperglycemia, hyperlactatemia, and high levels of circulating β-hydroxybutyrate often are present in severe sepsis

Metabolic Needs - How Much?

• Assessment of metabolic rate is an integral part of the nutrition care of the ICU patient

• Validity of multiple equations in this population has not been systematically evaluated

• Metabolic rate can be gauged by 3 methods:– Indirect calorimetry (“gold standard”)– Pulmonary artery catheter measurements using the Fick equation

VO²=cardiac output X 10 (CaO²-CvO²) where VO² is oxygen consumption in mL/min, cardiac output is in L/min, CaO² is concentration of oxygen in arterial blood (mL/dL), and CvO² is concentration of oxygen in mixed venous blood (mL/dL)

– Can be estimated using several predictive equations based on body size, degree of injury/illness, or degree of inflammatory response

• Given the limitations on the availability of indirect calorimetery, predictive equations are the mainstay of energy expenditure assessment in the ICU

Ideal Body Weight (IBW) The Hamwi Method

• Adult females– 100 lb (45kg) for the first 60 inches (152 cm) + 5 lbs

(2.3 kg) for every inch > 60– Ex: Ht. 5’4” (165.1 cm) = IBW of 120 lb or 54.5 kg)

• Adult males– 106 lb (48 kg) for the first 60 inches (152 cm) = 6 lbs

(2.7 kg for every inch > 60– Ex: Ht. 5’10” (180.3 cm) = IBW of 166 lb or 75.4 kg)

Evaluation of Body Weight Data

• Body Mass Index (BMI) - a weight-stature index, is use both as a measure of obesity and malnutrition.

• BMI = Weight (kg) ÷ Height² (m²)• Interpretation of BMI:

– 18.5 – 25 Normal weight– 25-29.9 Overweight– 30-34.9 Obesity grade I– 35-39.9 Obesity II– ≥40 Obesity grade III– 17-18.4 Protein-energy malnutrition grade I– 16-16.9 Protein-energy malnutrition grade II– <16 Protein-energy malnutrition grade III

• Individual variation is large so patients should not be misclassified as undernourished or obese using BMI alone

Goal Calculations - Harris-Benedict Equation

• Estimates Basal Energy Expenditure (BEE):

– Male BEE = 66 + (13.7 x Wt) + (5 x Ht) - (6.8 x age)

– Female BEE = 665 + (9.6 x Wt) + (1.8 x Ht) - (4.7 x age)

– Weight (Wt) in kilograms; Height (Ht) in centimeters

• BEE X Stress Factor (see below); this prediction method can overestimate or underestimate true resting metabolic rate and may be too unreliable for clinical use in the ICU

Conditions Energy Requirement ~ Kcal/kg/day ~Protein gm/kg/day

Elective Surgery 1.00-1.25 x BEE 25-30 1.0-1.2

Multiple Trauma 1.25-1.5 x BEE 25-35 1.4-1.5

Sepsis/Peritonitis 1.5 x BEE 25-35 1.4-2.0

Massive Burns >50% TBSA 1.75-2.0 x BEE 35-40 1.8-2.5

Goal Calculations – Ireton-Jones Equation 1992 vs 1997 Version

• Developed for intubated patients• RMR=(W x 5) – (A x 10) + (S x 281) + (T x 292) + (B x 851) +1925

for total calorie prescription where:• A=age

• W=wt in kg

• S=sex (1=male, 0=female)

• T=trauma (1=yes, 0=no)

• B=burns (1= yes, 0 = no)

• (This is the 1992 version)

• The corrected 1997 version of this equation does not perform as well as the 1992 version and is not recommended for use

Goal Calculations – Critically Obese

• Permissive underfeeding or hypocaloric feeding is recommended

• CALORIES: When BMI is >30 provide 11-14 kcal/kg ACTUAL body weight/day or 22-25 kcal/kg ideal body weight per day

• PROTEIN: When BMI is ≥ 30-40, provide ≥2.0 g/kg/ideal body weight per day and if BMI is ≥40, provide ≥2.5 g/kg ideal body weight per day

» Choban PS. Nutr Clin Pract. 2005;20:480-487.

Nitrogen Balance

• Used to reflect the balance between exogenous nitrogen intake and renal removal of nitrogen-containing compounds through stool, urine, skin, fistulas, wounds, etc.

• Measurement of nitrogen balance is most accurate in patient who receive a defined nutrient intake such as is in the case in those receiving enteral or parenteral nutrition

• Urea nitrogen urine concentration increases dramatically in the sickest of patients reflecting catabolism of protein associated with systemic inflammation

Greenfield 1997

Calculating Nitrogen Balance

• UUN excretion may differ from 3 to 5 grams

Problems With UUN

• UUN will be invalid if creatinine clearance is <50 mL/min• One cannot assume that moving nitrogen in a positive

direction always means that protein catabolism has decreased, particularly in inflammatory (disease and trauma) conditions

• Valid 24-hour urine collections are difficult to obtain• Alterations in renal function frequently occur in patient

with inflammatory metabolism, making standard nitrogen balance calculations inaccurate

Metabolic Cart / Indirect Calorimetry

• Measurement of O2 consumption (VO2) and CO2 production (VCO2) by a metabolic cart to allow for a Measured Resting Energy Expenditure (MREE) and Respiratory Quotient (RQ) (VCO2/VO2)

• RQ or respiratory quotient interpretation– 0.6-0.7 starvation/underfeeding– 0.84-0.86 desired range/mixed fuel utilization– 0.9-1.0 carbohydrate metabolism– 1.0+ overfeeding / lipogenesis

Clinical Indications for Indirect Calorimetry

• Factors causing predictive equations to be inaccurate (ARDS, large open wounds or burns, MSOF, sepsis, SIRS, ascites, multiple trauma, use of paralytic or barbiturate agents, and malnutrition with altered body composition like obesity or limb amputations)

• When patients fail to respond to nutrition support based on predictive equations during their clinical course (poor wound healing, failure to wean from vent and protein malnutrition) despite “adequate” support

• To evaluate whether under- or overfeeding is contributing to metabolic and respiratory derangements in ICU patients

Technical Factors Decreasing Indirect Calorimetry Accuracy

• Mechanical ventilation with FIO² ≥ 60• Mechanical ventilation with Positive End Expiratory

Pressure (PEEP) >12 cm H2O• Leak in the sampling system• Moisture in the system can affect the oxygen analyzer• Inability to collect all expired gases (leaking CT’s or

broncho-pleural fistula)• Supplemental O2 in spontaneously breathing patient• Dialysis or continuous renal replacement therapy in

progress• Errors in calibration of indirect calorimeter

» Wooley JA. Nutr Clin Pract. 2003;18:434-439.

Enteral vs. Parenteral?

• Several studies have compared each mode of therapy• Traditionally it’s been said: “Enteral is BETTER” and “If

the gut works, use it”– Earlier studies did not adjust for “overfeeding” and various rates

of hyperglycemia increasing infectious complications– Earlier meta-analyses failed to show benefit of TPN over EN

• PN use safer today with NST availability and tighter glucose control decreasing overall infectious complications

• Bistrian BR. Crit Care Med 2006;34:1525-1531

Enteral vs. Parenteral?

• Use the GI tract whenever possible• Contraindications to GI feeds

– Bowel obstruction / prolonged ileus > 7 day– High output fistula > 500 mL/d– Bowel ischemia– Intractable vomiting or diarrhea– Severe GI bleeding – Conditions precluding feeding tube placement (i.e. esophageal

tumor or tear)– Acute exacerbation of IBD with PO intolerance (malnutrition +

bowel rest > 7 days)– Failure of high risk, hypermetabolic patient to tolerate TF trials

ICU Enternal Feeding Algorithm

Nutrition Support Protocol For Mechanically Vented Patients

• Developed by multidisciplinary team approach– Timing of enteral nutrition– Identify high risk patients– Identify malnourished patients– Progression to minimal enteral nutrition goals (80%)– Monitor gastric residuals– Use of prokinetic agents or surgically placed jejeunal

tubes with gastric intolerance» Mackensiz SL. JPEN 2005;29(2):74-80

Results of Nutrition Support Protocol in Mechanically Vented Patients

• Percentage of patients receiving 80% of nutritional goals rose from 20% to 60% (p<0.001)

• Goal achieved in just 5 days• TPN use declined from 13% to 1.6% (p<0.02)• Significant increase in delivered calories• No data on the effect on outcome

» Mackensiz SL. JPEN 2005;29(2):74-80

Early Nutritional Support in the Mechanically Vented Patient

• 4,049 ventilated (>2 days) patients were studied• 2,537 (63%) labeled “Early Feeding” (<48 hours)• 1,512 (37%) labeled “Late Feeding Group”• Patients with contraindication to enteral diet

were excluded• Control for disease severity using separate

models with:• APACHE II, SAPS II, MPM-0

• Retrospective multi-institutional studyArtinian V, et al; Chest 2006;129(4):960-967

Effect of Early Feeding in Ventilated Patients

Outcomes EarlyLate Feeding p Value

ICU Mortality 18.10% 21.40% 0.01

Hospital Mortality 28.70% 33.90% 0.001

ICU Length of Stay 10.9 ± 8.1 10.2± 7.7 NS

Survival (vented over 30 days) ~58% ~52% 0.001

Artinian V, et al; Chest 2006;129(4):960-967

Timing of Enteral Feeds

• Many studies claim benefits to early EN• Meta-analysis that looked at 27 randomized,

prospective studies– Early EN had lower infections (RR 0.45)– Early EN had shorter LOS (2.2 days)

Marik PE, Zaloga GP. Crit Care Med. 2001;29:2264-2270

How Nutrition Support Goals Have Shifted in the ICU

Goals have become more focused on “nutrition therapy”

1. Attempt to attenuate the metabolic response to stress

2. Prevent oxidative cellular injury

3. Modulate the immune responseAim for early enteral nutrition, appropriate macronutrient and micronutrient delivery and meticulous glycemic control

Where to start?!

• Determine number of calories needed– Use predetermined “feeding weight” whether actual, ideal,

adjusted or usual body weight first– Utilize predictive equations, indirect calorimetry

• Determine normal or increased protein needs– Severity of injury, presence of wounds, fistulas, burns

• Determine if contraindication to fats– Sepsis, hemodynamic instability, hypertriglyceridemia

• Determine fluid needs• Determine mode of nutrition => use the GI tract

whenever feasible

ICU Nutrition Guidelines

Guidelines for the Provision and Assessment of Nutrition Support Therapy in the Adult Critically Ill Patient: Society of Critical Care Medicine and American Society for Parenteral and Enteral Nutrition: Executive Summary

Robert G. Martindale, MD, PhD; Stephen A. McClave, MD; Vincent W. Vanek, MD; Mary McCarthy, RN, PhD;Pamela Roberts, MD; Beth Taylor, RD; Juan B. Ochoa, MD; Lena Napolitano, MD; GailCresci, RD; American College of Critical Care Medicine; and the A.S.P.E.N. Board of Directors

Crit Care Med 2009;37(5):1757-1761

JPEN 2009;33(3):277-316

Guidelines developed that provided recommendations supported by review and analysis of the pertinent available current literature up to May 2008, by other national and international guidelines, and by the blend of expert opinion and clinical practicality. A grading system was used to help determine the level of evidence to support these recommendations.

Grading System Used for the Guidelines

• Grade of recommendation– A. Supported by at least two level I investigations– B. Supported by one level I investigation– C. Supported by level II investigations only– D. Supported by at least two level III investigations– E. Supported by level IV or level V evidence

• Level of evidence– Large, randomized trials with clear-cut results; low risk of false-

positive (alpha) error or false-negative (beta) error– Small, randomized trials with uncertain results; moderate to high

risk of false-positive (alpha) and/or false-negative (beta) error

Grading System Used for the Guidelines

– Nonrandomized, contemporaneous controls– Nonrandomized, historical controls– Case series, uncontrolled studies, and expert opinion

• Large studies warranting level I evidence were defined as those with 100 patients or those which fulfilled end

• point criteria predetermined by power analysis. Meta-analyses were used to organize information and to draw

• conclusions about overall treatment effect from multiple studies on a particular subject. The grade of

• recommendation, however, was based on the level of evidence of the individual studies.

Dellinger RP. Crit Care Med. 2004;32(11)(suppl):S446

“Guidelines”: Enteral Feeding

• Enteral Nutrition (EN) is the preferred route of feeding over parenteral nutrition (PN) (Grade B)

• EN should be started early within the first 24-48 hours following admission (Grade C) and feedings should be advanced toward goal over the next 48-72 hours (Grade E)

• EN should be withheld until the patient is fully resuscitated and/or hemodynamically stable (Grade E)

• Neither presence nor absence of bowel sounds, flatus, and stool is required for the initiation of EN (Grade B)

• Either gastric or small bowel feeding is acceptable (Grade C)

“Guidelines”: When to Use Parenteral Nutrition

• If early EN is not feasible or available over the first 7 days following admission to the ICU, no nutrition support (standard therapy) should be provided (Grade C)

• If there is evidence of protein-calorie malnutrition at admission and EN is not feasible, it is appropriate to initiate PN as soon as possible following admission and adequate resuscitation (Grade C)

• If a patient is expected to undergo major upper GI surgery and EN is not feasible, provide PN when: – Patient is malnourished. Initiate PN 5-7 days preoperatively and

continue into the postoperative period (Grade B)– The duration of therapy is anticipated to be ≥ 7 days (Grade B)

“Guidelines”: Dosing of Enteral Feeding

• The target goal of EN (defined by energy requirements) should be determined and clearly identified at the time of initiation of nutrition support therapy (Grade C)

• Efforts to provide > 50%-65% of goal calories should be made to achieve the clinical benefit of EN over the first week of hospitalization (Grade C)

• Initiating supplemental PN before 7-10 days when unable to meet energy requirements with EN alone does not improve outcome and may be detrimental to the patient (Grade C)

• In patients with BMI <30, protein requirements should be in the range of 1.2-2.0 g/kg/d actual body weight (Grade E)

• Critically ill obese patients with BMI >30, give 11-14 kcal/kg actual body weight/day or 22-25 kcal/kg IBW/d. Protein should be provided in a range of ≥2.0 g/kg IBW/d for BMI 30-40 and ≥2.5 g/kg IBW/d for BMI ≥40 (Grade D)

“Guidelines”: Selection of Appropriate Enteral Formula

• Immune-modulating formulations containing arginine, glutamine, nucleic acid, omega-3 fatty acids and antioxidants should be used for major elective surgery, trauma, burns, head and neck cancer, and critically ill patients on vents. Be cautious with severe sepsis for SICU patients (Grade A) and MICU patients (Grade B).

• Patients with ARDS and severe acute lung injury should receive a formula containing an anti-inflammatory lipid profile containing omega-3 fish oils, borage oil and antioxidants (Grade A)

What is Immunonutrition (IMN)?

• The term given to describe special enteral feeds containing:– Arginine– Omega-3 fatty acids– Nucleotides– + / - Glutamine – Antioxidants

Organs of the Immune System

Immunonutrition

• Glutamine – Most abundant AA in plasma and skeletal muscle; non-essential, but may be conditionally essential during catabolic stress. Has shown to be of benefit in burn, and trauma patients, but evidence is lacking in other critically ill patients.

• Arginine – conditionally essential amino acid thought to enhance the depressed immune responses associated with trauma, sepsis, or malnutrition.

• Nucleotides – precursor of DNA and RNA that are necessary for most cell functions, including protein synthesis. Demands during catabolic stress may exceed production.

• Omega-3 FA’s – “fish oil” with beneficial effects in septic patients, including modulating of leukocyte function and regulation of cytokine release through nuclear signaling and gene expression. The enhance the production of prostaglandin derivatives which play a role in accelerating the resolution of the pro-inflammatory state. IV omega-3 fatty acids are currently unavailable in parenteral emulsions in the United States.

• Antioxidants – thought to be of some benefit in severely stressed and septic patients, but exact amounts and combinations have yet to be determined for this population

What Is An Appropriate Gastric Residual Volume (GRV)?

• Threshold level of GRV tolerated by clinicians is of great debate!– No clinical significance of GRV < 200 ml– Stomach is a “distensible container” in which GRV

measurements don’t account for– Aspiration of TF’s is associated with a low morbidity

and an even lower mortality risk– Patients with high GRV >400 ml or who demonstrate

GI intolerance => consider NJT

EN Associated Bowel Necrosis

• Considered a very RARE complication < 1%• Most often reported with SB feeds• Exact cause is unclear - ? related to mucosal

perfusion, underlying bowel injury, excessive vasoconstriction or bacterial toxins

• No prospective randomized studies for TF’s w/ hypotension

Hemodynamic Instability

• High risk guidelines for a hypoperfused GI tract:– FiO2 >60– PEEP >5– Mean Arterial Pressure ≤ 75 mmHg– ? high dose pressors

• Levophed >8 mcg/min• Neosynephrine >40 mcg/min• Dopamine >15 mcg/kg/min

Recommendations For Feeding The Hypotensive Patient

• Hold feeds in hypotension:– Initiating pressor therapy– Increasing dose of pressors– Adding a second or third agent– Lactic acidosis

• OK to feed in hypotension on pressors:– Stable (24-48 hrs) or ing doses– MAP ≥75 mm/hg– Avoid fiber; stomach may be better than SB

• Hold feeds (on pressors) for any sign of intolerance:– NG output increases– New abdominal pain– Abdominal distention– Cessation of flatus, stool

Refeeding Syndrome

• Metabolic response caused by either enteral or parenteral nutrition

• Shift from stored body fat to CHO as primary fuel after prolonged NPO status

• Feeding causes insulin levels to rise creating intracellular movement of electrolytes

• Mg, K, PO4 levels may fall; can lead to arrhythmias, respiratory and cardiac failure, and death

• Prevention and therapy:– Correct electrolyte abnormalities BEFORE initiating nutrition

support, avoid overfeeding, and provide appropriate vitamin supplementation

Basic Parenteral Nutrition Calculations

• Amino Acids 4 kcal / g• Dextrose 3.4 kcal / g• Fat 10 kcals / g• 10% Lipids 1.1 kcal / mL• 20% Lipids 2 kcal / mL• 30% Lipids 3 kcal / mL

Basic Parenteral Nutrition Calculations

» Amino Acids 4%» Dextrose 15%» Lipids 2%» Total Volume 2000 mL

Grams AA = 4 grams X 2000 mL = 80 g X 4 kcal/g = 320 kcal

100 mL

Grams CHO = 15 grams X 2000 mL = 300 g X 3.4 kcal/g = 1020 kcal

100 mL

Grams Lipid = 2 grams X 2000 mL = 40 g X 10 kcal/g = 400 kcal

100 mL

TOTAL CALORIES = 1740

Parenteral Nutrition Formulation Additives

• Vitamins– Folate, Thiamine, Vitamin C, Zinc, Vitamin B12

• Trace Elements– Chromium, Copper, Zinc, Manganese, Selenium, Iron

• Electrolytes– Usually in the form of NaCl, NaAc, NaPO4, KCL, KAc,

KPO4, MgSO4, CaGluc

• Miscellaneous– H2 blockers, Heparin, Insulin, Glutamine

When Initiating PN Therapy

• CHO* - Start conservatively with 100-150 grams of dextrose per day advancing only when electrolytes and blood sugars are stable and repleted.

• Protein* - Amino acids should be limited initially to 1-1.2 gm/kg feeding weight due to their potential “refeeding effects“.

• Lipids** – Limit to ~1 gm/kg/d. Soy-based lipids have been shown to be immunosuppressive with proinflammatory characteristics so may have some benefit to withhold lipids or use with caution for the first 7 days in the ICU. Keep in mind that Propofol, is lipid based, and provides 1.1 kcal/mL.

*Patients should be monitored closely for refeeding syndrome for the first week of PN therapy.

**Essential Fatty Acid Deficiency (EFAD) may develop when no source of fatty acid is supplied for > 14 days. Minimum lipid requirements to prevent EFAD is 500 mL of a 20% fat emulsion (100 grams) over 24 hours given once a week

Overfeeding Consequences - 1

• Azotemia – Patients >65 years and patients given >2 gm/kg protein are at risk.

• Fat-overload syndrome – Recommended maximum is 1 gm lipid/kg/d. Infuse IV lipid slowly over 24 hours.

• Hepatic steatosis – Patients receiving chronic high-carbohydrate, very low fat TPN are at risk.

• Hypercapnia – Makes weaning difficult.

• Hyperglycemia – Increases risk of infection. Intake should not exceed 5 mg CHO/kg/min (4 mg/kg/min for diabetics).

Overfeeding Consequences - 2

• Hypertonic dehydration – Can be caused by high-protein formula with inadequate fluid provision.

• Hypertriglyceridemia – Propofol, high TPN lipid loads, and sepsis increase the risk. If the patient is hypertriglyceridemic, decrease lipid to an amount to prevent EFAD and monitor.

Consequences of Overfeeding-3

• Metabolic acidosis – Patients receiving low ratios of energy to nitrogen are at risk. Acidosis can cause muscle catabolism and negative nitrogen balance.

• Refeeding syndrome – Common in malnourished patients or those held NPO prior to initiation of feeding. Start feedings conservatively, advance gradually, and monitor Mg, Ph, and K closely.

Intensive Insulin Therapy in the Critically Ill

• PRCT, SICU ventilated pts (n=1548)• Intensive insulin therapy (BG 80-110mg/dl)

versus SSI (BG>215 mg/dl)• Results 5 day ICU stay (10 vs 20%) Hospital mortality x 34% Blood infections x 46% ARF requiring therapy x 41%

Van den Berghe G, et al. N. Engl J Med 001;345:1359-1367

Intensive Glycemic Control and Survival in SICU Patients

Van den Berghe G et al. N Engl J Med. 2001;345:1359-1367.

100

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0 20 40 60 80 100 120 140160

Intensive treatment

Conventional treatment

Intensive treatment

Conventional treatment

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0 50 100 150 200250

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A Days After Admission

B Days After Admission

42.5% reduction in mortality with intensive treatment; P<.04

34% reduction in mortality with intensive treatment; P<.01

ONLY REACHED SIGNIFICANCE for patients

in the SICU for 5 days or longer

Not so NICE (study) to follow

• Hypothesis: There is no difference in the relative risk of death between patient assigned a glucose range of 4.5 – 6.0 mmol/L (81-108 mg/dl) and those assigned a glucose range of 10.0 mmol/L, or less (180 mg/dl, or less). The primary end point would be defined as death from any cause within 90 days after randomization.

• International multi-center• 6104 ICU patients were randomized

• Conventional insulin group (n = 3054 assigned => 3010 after 90 days)

– Maintain 80-110 mg/dL

• Intensive insulin group (n = 3050 assigned => 3012 after 90 days)

– Maintain < 180 mg/dL

» The NICE-SUGAR Study Investigators. N Engl J Med 2009;360:1283-97

NICE-SUGAR RESULTS

• No difference– ICU LOS– Hospital LOS– Ventilator days– Renal replacement

therapy

• Severe hypoglycemia– Conventional insulin group 0.5%– Intensive insulin group 6.8%

• 90-day mortality in conventional insulin group

The NICE study showed no difference in ICU length of stay, hospital length of stay, days on the ventilator or need for renal replacement therapy. There was a significant incidence of severe hypoglycemia in the intensive therapy group combined with an increase in mortality of 27.5% vs 24.9% in the conventionally treated group.

Insulin Study Discrepancies

Van den Berghe• Majority PN

– Did not account exact amount of EN

• Majority CV surgery

NICE-SUGAR• > 70% nutrition received

from EN• Larger sample size• Mixed medical / surgical

Self Assessment

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References

• Pasquel FJ, Spiegelman R, McCauley M, et al. Hyperglycemia during total parenteral nutrition: An important marker of poor outcome and mortality in hospitalized patients. Diabetes Care. 2010;33:739-741.

• McClave SA, Martindale RG, Vanek VW, et al. Guidelines for the provision and assessment of nutrition support therapy in the adult critically ill patient:: Society of Critical Care Medicine (SCCM) and American society for Parenteral and Enteral Nutrition (ASPEN). JPEN. 2009;33:277-316.

• The NICE-SUGAR Study Investigators. N. Engl J Med. 2009;360:1283-1297.

• Sungurtekin H, Sungurtekin U, Oner O, Okke D. Nutrition assessment in critically ill patients. Nutr Clin Pract. 2008;23:635-641.

References

• Atalay BG, Yagmur C, Nursal TZ, et al. Use of subjective global assessment and clinical outcomes in critically ill geriatric patients receiving nutrition support. JPEN. 2008;32:454-459.

• Delgado AF, Okay TS, Leone C, et al. Hospital malnutrition and inflammatory response in critically ill children and adolescents admitted to a tertiary intensive care unit. Clinics. 2008;63(3)357-362.

• Bistrian BR, McCowen KC. Nutritional and metabolic support in the adult intensive care unit: Key controversies. Crit Care Med. 2006;34:1525-1531.

• Artinian V, Krayem H, DiGiovine B. Effects of early enteral feeding on the outcome of critically ill mechanically ventilated medical patients. Chest. 2006;129:960-967.

References

• Pontes-Arruda A, Aragao AM, Albuquerque JD. Effects of enteral feeding with eicosapentaenoic acid, gamma-linolenic acid, and antioxidants in mechanically ventilated patients with severe sepsis and septic shock. Crit Care Med. 2006;34:2325-2333.

• Van den Berghe G, Wilmer A, Hermans G, et al. Intensive insulin therapy in the medical ICU. N Engl J Med. 2006;354:449-461.

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Nutritional Support in the ICU Sandra L Schoepfel MS RD RN CNSD Karl D Pilson MD Suresh Agarwal MD...

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