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
Slide 3
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
Slide 4
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
Slide 5
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
Slide 6
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
Invalidation
Weight (BMI)
Anthropometrics
Albumin, Pre-Albumin
Edema, fluids, diuretics
Edema, observer variability
Infection, inflammation, injury, renal failure
Nitrogen Balance
Drainage tubes, wounds, renal failure
Slide 7
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 (TFs, PN) because of
recent surgery, illness
Impaired ability to ingest or absorb food
adequately for > 7 days
Slide 8
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
Slide 9
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
Slide 10
Stimuli for Stress Response
Loss of blood volume
Emotion/pain/fear
Temperature
Infection
Tissue injury
Slide 11
Goals of Stress Response
Maintain energy substrates (GLUCOSE)
Maintain oxygen delivery
Minimize further injury...
Slide 12
Slide 13
Greenfield
1997
Response to Stress/Injury
Neurohormonal - "Counterregulatory hormones"
Glucagon
Epinephrine
Glucocorticoids
Inflammatory mediators
IL-1, IL-2, IL-6
TNF-a
IFN-g
Slide 14
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
Slide 15
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
Slide 16
Greenfield
1997
Slide 17
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 -hydroxybutyrate often are
present in severe sepsis
Slide 18
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
VO=cardiac output X 10 (CaO-CvO) where VO is oxygen
consumption in mL/min, cardiac output is in L/min, CaO is
concentration of oxygen in arterial blood (mL/dL), and CvO 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
Slide 19
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. 54 (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. 510 (180.3 cm) = IBW of 166 lb or 75.4 kg)
Slide 20
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) Height (m)
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
Slide 21
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
1.75-2.0 x BEE
35-40
1.8-2.5
Massive Burns >50% TBSA
Slide 22
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
Slide 23
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.
Slide 24
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
Slide 25
Slide 26
Greenfield 1997
Calculating Nitrogen Balance
UUN excretion may differ from 3 to 5 grams
Slide 27
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
Slide 28
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
Slide 29
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
Slide 30
Technical Factors Decreasing
Indirect Calorimetry Accuracy
Mechanical ventilation with FIO 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 CTs 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.
Slide 31
Enteral vs. Parenteral?
Several studies have compared each mode of therapy
Traditionally its 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
Slide 32
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
Slide 33
ICU Enternal Feeding Algorithm
Slide 34
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
Slide 35
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
Slide 36
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 study
Artinian V, et al; Chest 2006;129(4):960-967
Slide 37
Effect of Early Feeding in Ventilated
Patients
Early
Late
Feeding
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
~58%
~52%
0.001
Outcomes
Survival (vented over 30 days)
p Value
Artinian V, et al; Chest 2006;129(4):960-967
Slide 38
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
Slide 39
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 response
Aim for early enteral nutrition, appropriate
macronutrient and micronutrient delivery and
meticulous glycemic control
Slide 40
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
Slide 41
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.
Slide 42
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 falsepositive (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
Slide 43
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. Metaanalyses 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
Slide 44
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)
Slide 45
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)
Slide 46
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)
Slide 47
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 antiinflammatory lipid profile containing omega-3
fish oils, borage oil and antioxidants (Grade A)
Slide 48
What is Immunonutrition (IMN)?
The term given to describe special enteral feeds
containing:
Arginine
Omega-3 fatty acids
Nucleotides
+ / - Glutamine
Antioxidants
Slide 49
Organs of the Immune System
Slide 50
Immunonutrition
Glutamine Most abundant AA in plasma and skeletal muscle; nonessential, 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 FAs 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
Slide 51
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 dont account for
Aspiration of TFs 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
Slide 52
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 TFs w/
hypotension
Slide 53
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
Slide 54
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
Slide 55
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
Slide 56
Basic Parenteral Nutrition Calculations
Amino Acids
Dextrose
Fat
10% Lipids
20% Lipids
30% Lipids
4 kcal / g
3.4 kcal / g
10 kcals / g
1.1 kcal / mL
2 kcal / mL
3 kcal / mL
Slide 57
Basic Parenteral Nutrition Calculations
Amino Acids
Dextrose
Lipids
Total Volume
4%
15%
2%
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
Slide 58
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
Slide 59
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
Slide 60
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 highcarbohydrate, 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).
Slide 61
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.
Slide 62
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.
Slide 63
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
Slide 64
Intensive Glycemic Control and
Survival in SICU Patients
100
Intensive treatment
96
92
Conventional treatment
ONLY REACHED
SIGNIFICANCE for patients
in the SICU for
5 days or longer
88
42.5% reduction in
mortality with
intensive treatment;
P<.04
84
80
0
20 40 60 80 100 120 140
160
Days After
A
Admission
In-Hospital Survival (%)
Survival in ICU (%)
100
96
Intensive treatment
92
Conventional treatment
88
34% reduction in
mortality with
intensive treatment;
P<.01
84
80
0
50
100
B
Days
250 After
Admission
Slide 65
Van den Berghe G et al. N Engl J Med. 2001;345:1359-1367.
150
200
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
Slide 66
NICE-SUGAR RESULTS
No difference
ICU LOS
Hospital LOS
Ventilator days
Renal replacement
therapy
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.
Severe hypoglycemia
Conventional insulin group 0.5%
Intensive insulin group 6.8%
90-day mortality
in conventional insulin group
Slide 67
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
Slide 68
Self Assessment
Ready to test your knowledge?
Take the Review
Skip the Review
Slide 69
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;23:635641.
Slide 71
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)357362.
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.
Slide 72
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.
Binnekade JM, Tepaske R, Bruynzeel P, et al. Daily enteral feeding
practice on the ICU: attainment of goal and interfering factors. Crit
Care. 2005;9:R218-R225.
Mackenzie SL, Zygun DA, Whitmore BL, et al. Implementation of a
nutrition support protocol increases the proportion of mechanically
ventilated patients reaching enteral nutrition targets in the adult
intensive care unit. JPEN. 2005;29:74-80.
Slide 73
References
Kieft H, Roos A, Bindels A, et al. Clinical outcome of an
immune enhancing diet in a heterogeneous intensive
care population. Intensive Care Med. 2005;31:524-532.
McClave SA, et al. Poor validity of residual volumes as a
marker for risk of aspiration in critically ill patients. Crit
Care Med. 2005;33;449-450.
Choban PS, Dickerson RN. Morbid obesity and nutrition
support: is bigger different? Nutr Clin Pract.
2005;20:480-487.
Dellinger RP, Carlet JM, Masur H, et al; Surviving Sepsis
Campaign Management Guideline Committee. Surviving
Sepsis Campaign guidelines for management of severe
sepsis and septic shock. Crit Care Med. 2004;32:858873.
Slide 74
References
McClave SA, Chank WK. Feeding the
hypotensive patient: does enteral feeding
precipitate or protect against ischemic bowel?
Nutr Clin Pract. 2003;18:279-284.
Montejo JC, Zarazaga A , Lopez-Martinez J, et
al. Immunonutrition in the intensive care unit: a
systematic review and consensus statement.
Clin Nutr. 2003;22:221-233.
Wooley, JA, Sax HC. Indirect Calorimetry;
Applications to Practice. Nutr Clin Pract.
2003;18:434-439.
Slide 75
References
Van den Berghe G, Wouters P, Weekers F, et al.
Intensive insulin therapy in the critically ill patient. New
Engl J Med. 2001;345:1359-1367.
Marik PE, Zaloga GP. Early enteral nutrition in acutely ill
patients: a systematic review. Crit Care Med.
2001;29:2264-2270.
Souba WW, Austen WG. Nutrition and metabolism. In:
Greenfield LJ, Mulholland MW, Oldham KT, et al.
Surgery: Scientific Principles and Practice. 2nd ed. New
York, NY: Lippincott-Raven; 1997.
Souba WW. Nutritional Support. N. Engl J Med.
1997;336:41-48.
Slide 76