Journal of Parenteral and Enteral

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''CAN WE FEED?'' A Mnemonic to Merge Nutrition and Intensive Care Assessment of the Critically Ill
Patient
Keith R. Miller, Laszlo N. Kiraly, Cynthia C. Lowen, Robert G. Martindale and Stephen A. McClave
JPEN J Parenter Enteral Nutr 2011 35: 643
DOI: 10.1177/0148607111414136

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Original Communication
“CAN WE FEED?”
A Mnemonic to Merge Nutrition and Intensive Care
Assessment of the Critically Ill Patient
Keith R. Miller, MD1; Laszlo N. Kiraly, MD2; Cynthia C. Lowen, RD1;
Robert G. Martindale, MD2; and Stephen A. McClave, MD1
Financial disclosure: none declared.
As care of the critically ill patient grows more complex, so does
the breadth of knowledge required of the intensivist to deliver
quality service. Nutrition is one area of many where the com-
plexity of care has grown and the opportunity for improving
patient outcomes has become evident. The use of mnemonics
has proven successful in compartmentalizing information that
must be considered in complex decision-making processes. The
authors propose one such mnemonic, “CAN WE FEED?” to
assist in the development and initiation of early enteral nutrition
therapy in the intensive care unit (ICU). Critical illness severity
(C), age (A), and nutrition risk screening (N) are considered
when performing a baseline evaluation of the critically ill
patient upon presentation to the ICU. Wait for resuscitation
(W) is a key component in the care of most critically ill patients
and is an important consideration prior to the initiation of feeding.
Clinical Relevancy Statement
With the luxury of the increasing availability of data to
guide decision making with regards to nutrition support
in the intensive care unit also comes a concurrent
increase in complexity. The multidisciplinary approach to
patient care has proven superior to traditional unilateral
care models but implies with it the assumption that all
involved caregivers are familiar with the various perspec-
tives of the others. The goal of this article is to provide the
intensivist, nutrition support team, and involved caregiv-
ers with a rational and easily applicable nutrition support
tool to apply to the critically ill patient.
From the 1University of Louisville, Louisville, Kentucky; and
2
Oregon Health Sciences University, Portland
Received for publication December 12, 2010; accepted for pub-
lication February 24, 2011.
Address correspondence to: Keith Miller, MD, Department of
Surgery, University of Louisville, ACB 2nd Floor, 550 South
Jackson St, Louisville, KY 40202; e-mail: Krmill10@gwise.louis-
ville.edu.
643
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Journal of Parenteral and
Enteral Nutrition
Volume 35 Number 5
September 2011 643-659
© 2011 American Society for
Parenteral and Enteral Nutrition
10.1177/0148607111414136
http://jpen.sagepub.com
hosted at
http://online.sagepub.com
Energy requirements (E) are determined using conventional
weight-based equations, indirect calorimetry, or combinations of
both techniques. The more practical aspects of support that fol-
low include formula selection (F), enteral access (E), efficacy
(E), and the determination of tolerance (D). With careful con-
sideration of these components through the use of the mne-
monic “CAN WE FEED?” the intensivist can successfully
implement a nutrition plan, and the clinical nutritionist can
appreciate where nutrition therapy appropriately intervenes in
the initial resuscitation and management of the critically ill
patient. (JPEN J Parenter Enteral Nutr. 2011;35:643-659)
Keywords:  nutrition assessment; enteral nutrition; parenteral
nutrition; tolerance
Introduction
Management of the critically ill patient has become
increasingly more complex in recent years as technologi-
cal and pharmaceutical advances provide the practicing
clinician with a growing armamentarium with which to
tackle specific disease processes. As the care of the
patient becomes more complex, attention to basic prin-
ciples and needs are often lost in the milieu of the hun-
dreds of decisions made each day by the clinician. As with
other aspects of care, nutrition support therapy in the
intensive care unit (ICU) has recently been scrutinized as
an area where improvements can be made.
In the past, delivery of nutrients to the ICU patient
was considered a supportive measure. But more recently,
with data showing an impact on patient outcome from
early enteral feeding and the use of pharmaconutrition,
that same nutrition intervention is being viewed as an
additional opportunity for therapeutic intervention. The
quality or content of intervention is at least as important
as the quantity.1
Goals of nutrition support therapy now focus on the
attenuation of oxidative stress by downregulating the
644   Journal of Parenteral and Enteral Nutrition / Vol. 35, No. 5, September 2011
severity of the systemic inflammatory responses, accentu-
ating the compensatory anti-inflammatory adaptive
immune response, and promoting an earlier return to a
physiologic baseline. It has become increasingly apparent
that the underused gut can contribute significantly to the
proinflammatory state of critically ill patients, further
emphasizing the role for early enteral nutrition (EN)
therapy in appropriate patients.2 As the dogma shifts,
several new decisions must be made with regard to the
appropriate timing, route, and initiation of feeding; con-
tent of the formula infused; dosing; and determination of
the patient’s metabolic state. The myriad decisions that
must be made in a multidisciplinary environment require
a close coordination of effort between the intensivist, the
nutritionist, and the nurse at the bedside.
Overview
As with many other complex decision-making processes,
an algorithm or mnemonic constructed to address each of
the important issues may be of benefit to the practicing
clinician. Several mnemonics have been introduced to
address the management of various aspects of critical
care. Among these, some are designed to address acute
issues such as the “A, B, Cs” of trauma, which emphasize
the immediate priority of care in the resuscitation and
stabilization of an acutely injured patient, including
Airway, Breathing, Circulation, Disability, and Exposure.3
Another mnemonic intended to address the daily issues of
patient care in the ICU (and remind the clinicians of
important ongoing aspects of care for the critically ill
patient) is “FAST HUG”—Feeding, Analgesia, Sedation,
Thromboembolic prophylaxis, Head-of-bed elevation,
stress Ulcer prevention, and Glucose control.4 We pro-
pose a simple mnemonic, “CAN WE FEED?” that inte-
grates the relevant issues with regards to both the critical
care assessment and the nutrition assessment of the
patient newly admitted to the ICU.
Important factors in the initial evaluation of the
critically ill patient include attention to the overall condi-
tion of the patient, pertinent comorbidities, and the criti-
cal illness severity (C). Age (A) alone provides prognostic
information and is a key predictor in patient outcome. A
quick nutrition risk screen (N) helps identify the baseline
nutrition status and determines the likelihood or risk that
deterioration of that status will occur quickly following
admission to the ICU.
After this baseline evaluation has been established,
the status of the resuscitative efforts must be addressed.
This is an important and somewhat controversial branch
point in the decision tree, when the appropriate timing to
institute nutrition support is determined. Although initi-
ating early EN as soon as possible is important, it is nec-
essary to wait for full resuscitation (W) to begin feeds.
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Once it has been determined that the patient is fully
resuscitated and thus a candidate for nutrition support
therapy, the patient’s energy requirements (E) must be
calculated. More practical details such as formula selec-
tion (F), type of enteral access (E), efficacy of support
(E), and determination of tolerance (D) follow. The
phrase “CAN WE FEED?” is a simple mnemonic that
addresses each of these issues and highlights the impor-
tance and order of priority for each component.
C: Critical Illness Severity
Disease severity by itself drives the need and timing of
nutrition therapy. Assessing and understanding the par-
ticular disease process that has resulted in admission or
transfer to the ICU, determining the severity of that ill-
ness, and identifying pertinent comorbidities are all
important steps in the nutrition evaluation of the indi-
vidual patient. The nature of the primary illness directly
affects the goals of nutrition therapy. Disease processes
such as sepsis, major gastrointestinal surgery, trauma,
large surface area burns, and pancreatitis result in
increased circulating levels of adrenocorticotropic hor-
mone (ACTH)5, epinephrine, glucagon, and cortisol and
are usually hypermetabolic in nature. As a general rule,
the sicker the patient, the more likely he or she is to ben-
efit from early enteral feeding. In rare instances where
patients in the ICU are not significantly stressed (such as
postoperative observation), nutrition support therapy may
not be indicated. Multiple scoring systems have been
proposed with regards to stratifying the physiologic stress
that each patient incurs from his or her specific disease
entity. The Abdominal Trauma Index (ATI) and Injury
Severity Score (ISS) are commonly used tools in the set-
ting of trauma.6,7 The Acute Physiology and Chronic
Health Evaluation (APACHE) scoring system is an
accepted measure across many medical and surgical dis-
ciplines to classify disease severity in the ICU based on
physiologic and laboratory variables. This system attempts
to factor in both acute and chronic conditions when
determining overall disease severity.8 A second scoring
system used in the critical care setting for prognostic pre-
diction as well as standardizing literature is the Sequential
Organ Failure Assessment (SOFA). Although it is a strong
predictor of mortality, the SOFA score also takes into
consideration 6 organ systems with a severity score
assigned from 1 to 4 and was designed initially to assess
morbidity in septic patients.9 Scoring systems such as
these help to determine “how sick” the patient is, define
those patients most likely to benefit from nutrition sup-
port therapy, and design the regimen best suited for their
condition.
For any patient, a comprehensive history, including
surgical and medical comorbidities, is required to

determine an appropriate nutrition support regimen.
Prior surgical alteration of normal gastrointestinal conti-
nuity (such as roux-en-Y gastric bypass, banding,
esophagectomy, partial/total gastrectomy, or colectomy)
should be considered when determining the conduit for
feeding, the composition of the diet, and the need for
parenteral supplementation. Patients with inflammatory
bowel disease and malassimilation have often undergone
multiple bowel resections, and their resultant functional
intestinal length and history of prior dietary adjustments
must be considered. In the patient with a preexisting
enteral access device, management decisions and the
ease of initiation of feeds are facilitated for the clinician.
Certain comorbidities should be taken under careful
consideration when developing a nutrition support plan.
Attention to glycemic control related to stress-induced
hyperglycemia has been shown to reduce polyneuropathy,
units of blood transfused, and requirements for mechani-
cal ventilation and even mortality regardless of prior his-
tory of diabetes or hyperglycemia.10,11 Awareness should
be heightened in those patients with documented preex-
isting disease. Regardless of the specific range that is
targeted for glucose control, profound hyperglycemia and
hypoglycemia can dramatically contribute to morbidity
and mortality. Preexisting liver or renal dysfunction is an
important consideration when contemplating nutrition
support therapy and can alter the substrates selected for
delivery.
Finally, a careful social history can be helpful, par-
ticularly with regards to alcohol intake and prior drug
abuse. In 1 study, 48% of daily caloric intake was derived
from alcohol in patients with documented alcoholic liver
disease.12 As a result, severe protein energy malnutrition
and concomitant micronutrient deficiencies are common.
Approximately 18% of male and female hospitalized drug
addicts are found to have severe malnourishment as
determined by subjective nutrition assessment.13
Malnutrition in the setting of substance abuse has been
shown to correlate to female sex, intensity of drug addic-
tion, anorexia, poor food and drink consumption, and
disturbance of social and familial support.13 The social
history remains an integral factor in determining the tim-
ing and character of nutrition support therapy.
A: Age
Age is an important independent variable in determining
the morbidity and mortality of the individual in most dis-
ease processes and should be considered when initiating
nutrition therapy. Age is included in many of the afore-
mentioned scoring systems, including the APACHE and
Ranson’s criteria. A slightly decreased metabolic rate and
a reduction in lean body mass may be expected in the
elderly patient. In conjunction with an increased protein
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“CAN WE FEED?” / Miller et al   645
requirement, early and adequate nutrition support ther-
apy of injured elderly patients becomes “the cornerstone
of successful trauma care.”13 A wide range of preexisting
factors contribute to malnutrition in the elderly patient,
many of which are influenced by the activity level of the
patient. Thomas et al reported an incidence of malnutri-
tion ranging from 5%–12% in the mobile patient to as
high as 40%–85% in the nursing home patient.14 The
causes of malnutrition are complex and multifactorial and
relate to inadequate intake, use of polypharmacy, and a
variety of psychological, social, and physiologic issues.15
Age is an independent variable in predicting mortality
regardless of nutrition status. Based on APACHE II scor-
ing calculations, a patient older than 75 years has a mor-
tality of 6.7% before entering any other variables into the
score using standard Web-available calculators.16 Any
patient older than 65 is assessed an additional 5 points to
his or her total APACHE II score.17 Using Ranson’s crite-
ria for pancreatitis, age older than 55 adds an additional
point to the patient’s total score. Although age is not a
specific factor in trauma scoring systems, the correlation
between mortality and ISS dramatically changes with
increasing age of the patient. In the study that introduced
the ISS in 1974, a patient younger than age 50 with an
ISS of 25 had a mortality of less than 10%. In contrast,
patients with the same ISS of 25 in the age range of 50–
69 and those with older than age 70 had mortalities of
25% and ≥40%, respectively.4 In the Nutritional Risk
Score 2002, age >70 adds 1 full point to the scores calcu-
lated for nutrition status and disease severity. Any score
≥3 warrants nutrition support therapy (Appendix 2).18 Age
should be part of the nutrition screening process
and remains an important determinant in overall patient
outcome.
N: Nutrition Risk Screening
Although visceral proteins have been used controversially
as markers for nutrition status in chronic disease and out-
patient settings, they clearly have little utility in the acute
critical care setting. Multiple factors explain the fallacy of
such use of these laboratory values. During acute illness,
increased vascular permeability with dramatic fluid shifts
are common and hepatic protein synthesis is reprioritized.
Both of these factors lead to reduced levels of albumin,
prealbumin, and transferrin. Increased production of
acute-phase reactants such as C-reactive protein (CRP),
fibrinogen, haptoglobin, and ferritin occurs at the expense
of reduced circulation of visceral proteins. Albumin remains
a powerful independent predictor for outcome upon admis-
sion to the ICU regardless of nutrition status.19 Visceral
protein levels, however, should never be used to determine
nutrition status or adequacy of nutrition support therapy in
the acute setting.20
646   Journal of Parenteral and Enteral Nutrition / Vol. 35, No. 5, September 2011
Other measures to evaluate nutrition status (bioelec-
tric impedance, muscle function studies, creatinine-
height index, anthropometric measures, and body
composition studies) are often cumbersome and impracti-
cal and have limited use in the critically ill patient.
Scoring systems are helpful in determining overall
disease severity and stratifying patient risk. A process by
which to define baseline nutrition status in the ICU, how-
ever, has proven quite difficult. Several similar scoring
systems have been developed in the past, including the
Nutritional Risk Index,21 Subjective Global Assessment,22
Nutritional Risk Screening,18 Mini Nutritional
Assessment,23 and the Malnutrition Universal Screening
Tool.24 Many of these tools are time-intensive, involve
parameters that are difficult to obtain, and require exten-
sive nutrition histories to complete.
The Nutritional Risk Screening (NRS-2002) was
developed by the European Society of Parenteral and
Enteral Nutrition (ESPEN). The NRS incorporates a
quick initial screening set comprising 4 questions regard-
ing body mass index (BMI), recent weight loss, dietary
intake, and illness severity.18 This screening set is easily
applied in the ICU setting. If the initial screening is posi-
tive, then a final more complete screening is performed to
document specific evidence of impaired nutrition status
and degree of disease severity. As can be seen by the
screening set, the majority of the patients in the ICU will
meet final screening criteria, as many are in fact critically
ill. For those patients admitted to the ICU who are not
severely ill (as determined in conjunction with severity of
illness scoring systems) and have no other risk factors, no
final screening is necessary (Appendix 2). The Subjective
Global Assessment (SGA) is an alternative screening tool
that incorporates aspects of the physical exam, comor-
bidities, weight, dietary history, and functional capacity to
determine an overall nutrition assessment. Although more
time-intensive, the SGA has proven useful and reproduc-
ible in the ICU setting in mechanically ventilated
patients.25
If a patient is identified to have severe nutrition
impairment and to require specialized nutrition therapy,
then consideration must be given to risk for the poten-
tially fatal complication of refeeding syndrome. Patients
who remain NPO (nil per os) for a prolonged period or
are chronically malnourished can experience acute
decompensation secondary to electrolyte and fluid shifts
once nutrition therapy is initiated. The hallmarks of this
syndrome include severely depressed serum levels of
phosphorus, magnesium, potassium, and calcium, as the
shift from chronic catabolism to anabolic metabolism
occurs. Cardiac abnormalities that may lead to death
include congestive heart failure and arrhythmias second-
ary to severe electrolyte abnormalities.26 Respiratory fail-
ure can occur as a result of decreased diaphragm
contractility (a phenomenon that can contribute to
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failure to wean from mechanical ventilation). If a patient
is identified to be at risk for refeeding syndrome, electro-
lyte replacement along with vitamin and mineral supple-
mentation should precede full caloric provision.27,28
Feeding should be started slowly (10 kcal/kg) and ramped
up slowly over 2–3 days while continued serial electrolyte
surveillance and replacement are performed.
The presence or absence of malnutrition upon admis-
sion to the ICU affects the need and timing of parenteral
nutrition (PN) therapy. In the rare patient who is deter-
mined to have severe protein energy malnutrition at the
time of presentation and in whom enteral support is not
feasible, use of early PN has been shown to decrease
morbidity.29,30 PN therapy should be withheld on admis-
sion to the ICU in patients not meeting criteria for mal-
nutrition or when the duration of parenteral therapy is
anticipated to be <7 days. Providing PN to such patients
accrues the added risk of infectious complications, with-
out the favorable outcome benefits of caloric replace-
ment.1 In the event that PN is deemed appropriate, the
soy-based parenteral lipids used in the United States
should be withheld for the first 7 days following the acute
insult because of their proinflammatory and immunosup-
pressive characteristics. These lipids may be added to the
regimen 7 days following the acute insult if long-term PN
therapy is warranted.1
W: Wait for Resuscitation
Resuscitation is an important component in the treatment
of the critically ill patient and should be assessed prior to
initiation of enteral or parenteral therapy. The importance of
this factor in the setting of trauma is evidenced by its posi-
tion in the primary survey, immediately following airway and
breathing stabilization. In the most severe form, hemody-
namic instability is characterized as shock. Shock is defined
by impaired tissue perfusion and a shift from aerobic to
anaerobic metabolism. This terminology has often been
applied to those patients presenting with systolic arterial
blood pressures of <90 mm Hg and signs of impaired end-
organ perfusion. Although cardiogenic, neurogenic, hemor-
rhagic, anaphylactic, and septic shock are specific entities
with regards to the nature of the insult, a combination of
these mechanistic factors is commonly in place, and the end
result often remains the same.31 The impaired perfusion or
inadequate oxygen utilization of specific tissues or organs
results in the accumulation of acid metabolites. A shift
toward anaerobic metabolism results in an increase in serum
lactate concentration, which is a powerful outcome predic-
tor when found in conjunction with metabolic acidosis.32
Splanchnic hypoperfusion results in the systemic release of
proinflammatory mediators, which serves to worsen the sys-
temic inflammatory response and contributes to the ongoing
cascade of inflammation.33

Splanchnic blood flow is increased by as much as
40%–60%34,35 in response to enteral feeding. In a study of
cardiac patients in the immediate postoperative period,
an increase in stroke volume and cardiac index was seen
and a decrease in systemic vascular resistance and mean
arterial pressure was noted following initiation of enteral
feeding.36 There is added risk associated with the initia-
tion of enteral feeding in the hypotensive patient, as a
marginally perfused gut is challenged with the metaboli-
cally demanding chore of absorption. Nonocclusive mes-
enteric ischemia, primarily of the superior mesenteric
artery,37 is a dreaded complication of early EN and is
associated with a mortality as high as 80%.38 The compo-
sition of the feeding affects the degree of splanchnic
vasodilation and metabolic demand, with hyperosmolar
formulas resulting in significantly more stress on the gut’s
absorptive capacities than iso-osmolar fluids. For this
reason, iso-osmolar formulas should be used if feeding is
being considered in the hypotensive patient requiring
vasopressive therapy.37 Appropriate volume resuscitation
should precede the initiation of EN therapy in hemody-
namically compromised patients.1
Appropriate volume expansion can be a daunting task
to achieve, and the evaluation of adequate resuscitation
may be difficult in many ICU patients. McCunn and
Dunton39 separate the resuscitative phase of shock into
measures conducted before and after appropriate inter-
ventions to address the etiology of the shock have been
undertaken. The goals of the first phase of resuscitation
include the determination of the underlying etiology of
the insult and expansion or restoration of intravascular
fluid volume. Techniques for assessing the overall success
of resuscitative measures continue to evolve and are a
cornerstone in the management of the critically ill patient.
Blood pressure, heart rate, capillary refill, respiratory
rate, and pulse oximetry are key parameters in assessing
the patient prior to the initiation of invasive monitoring.
Pressure data from central venous and pulmonary artery
catheters have been used to guide resuscitation. Their
usefulness has been questioned given the lack of correla-
tion between pressure readings and actual filling dynam-
ics and non-invasive monitoring techniques are becoming
more readily available and utilized.40,41 Strategies for
addressing shock and restoring tissue perfusion are
beyond the scope of this review. Intervascular volume
expansion with crystalloid (lactated Ringer’s solution) is
generally agreed upon as a first step, regardless of the
cause of shock.39 Transfusion of packed red blood cells to
increase oxygen-carrying capacity, initiation of inotropes
and vasopressors, and procedural/surgical intervention
are all therapies used during the resuscitative effort.
These parameters and interventions are mentioned only
in the context of determining a patient’s risk for complica-
tions from the initiation of EN therapy. The ideal or opti-
mal end points of resuscitation remain elusive.42,43
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“CAN WE FEED?” / Miller et al   647
Continued efforts at monitoring metabolic activity in
individual microvascular beds as indicators of global tis-
sue perfusion are in evolution. Continuous gastric
mucosal pH monitoring,44 sublingual capnometry,45 and
subcutaneous oxygen levels46 have all shown some prog-
nostic utility but provide little in the way of guidance
during resuscitative efforts. Muscle tissue oxygen tension
monitoring has shown some promise but remains experi-
mental.47 Currently, serial measurements of serum lac-
tate, base excess, and venous oxygen saturation remain
the targets most used for guiding resuscitative efforts.
Just as underresuscitation is thwart with conse-
quences, so too is overresuscitation. Noncardiogenic
pulmonary edema is often the most clinically obvious
result of overresuscitation, but excess crystalloid accu-
mulates in the bowel wall just as it does in the interstit-
ium of the lung.48 This is perpetuated by the capillary
leak that is often associated with acute illness and in its
worst form can contribute to the abdominal compart-
ment syndrome necessitating laparotomy. Although
abdominal compartment syndrome is a relatively rare
event and represents the extreme, reduced intestinal
motility attributed to overresuscitation and bowel wall
edema is common and can hamper future attempts at
nutrition support in the enteral form. Again, invasive
hemodynamic monitoring with frequent reassessment,
clinical exam, and timely intervention to address the pri-
mary insult are important components in preventing or
minimizing this complication.
The concept of resuscitation in the hemodynamically
unstable patient has recently been extended beyond fluid
volume management to preparation of the gut prior to
initiation of enteral feeding. Resuscitation of the gut with
delivery of enteral glutamine in the hemodynamically
compromised patient may provide beneficial effects
through proposed anti-inflammatory, tissue-protective
(via peroxisome proliferator-activated receptor [PPAR] γ
activation), and antioxidant properties.49-52 In 1 recent
trial, McQuiggan et al47 demonstrated that enteral glu-
tamine (0.5 g/kg/d) could be administered safely during
active shock resuscitation. The early infusion of glu-
tamine into the gut in the first 24 hours after admission
to the emergency room led subsequently to improved
tolerance once enteral feeds were later initiated.53
Aggressive volume resuscitation should be completed
before the critically ill patient becomes an appropriate
candidate for initiation of enteral feeding. However, the
timing of the initiation of feeds that follows becomes an
important factor in whether patient outcome is affected.
As a general rule, enteral therapy provided earlier rather
than later improves patient outcomes. Studies have shown
that initiation of early feeding during the first 24 to 48
hours of admission improves hospital length of stay, inci-
dence of infectious complications, and even mortality
compared to feeds started after that time point.54-59
648   Journal of Parenteral and Enteral Nutrition / Vol. 35, No. 5, September 2011
Although this premise is generally well accepted by clini-
cians, there exists a large gap between what physicians
intend to provide and what is actually delivered to the
patient. In 1 study performed in a level I trauma center,
22% of patients remained NPO for a mean of 5.2 days
after admission. Some of this delay may have been related
to concern for missed injury or the uncertainty surround-
ing the need for operative intervention for undeclared
concomitant injury in the setting of major trauma.60 As an
institution, having the expertise to accomplish rapid vol-
ume resuscitation, achieve early enteral access, have
protocols in place to reduce the risk of aspiration, and set
parameters for managing gastric residual volumes (GRVs)
all help facilitate delivery of early EN therapy. The key
issue is that once resuscitation is complete, rapid suffi-
cient delivery of EN should be initiated.
E: Energy Requirements
Most patients in the ICU are in a hypermetabolic cata-
bolic state. Plank and Hill61 demonstrated that increases
in caloric requirements over basal resting energy expendi-
ture peaked at 4 to 5 days postinsult but persisted as long
as 21 days after the initial injury to the trauma or burn
patient. Estimating or measuring energy expenditure
determines the goal of nutrition therapy. Providing calo-
ries as close to goal as possible is important, as a negative
caloric balance portends a poor prognosis and increased
morbidity.62 Exceptions should be considered. For exam-
ple, permissive underfeeding in the obese critically ill
patient, where hypocaloric (14–20 kcal/kg ideal body
weight [IBW]/d) protein-rich (2.0–2.5 g/kg IBW/d) diets
are used, has resulted in decreases in both infection and
hospital length of stay compared to eucaloric feeds.63,64
Hypocaloric PN, where 80% of requirements are deliv-
ered, may improve insulin sensitivity and outcome when
indicated. Permissive underfeeding in the nonobese
patient on EN remains controversial and cannot univer-
sally be recommended based on the available literature.
The overall caloric requirements for the individual
patient are often determined using simplistic weight-
based calculations (20–40 kcal/kg/d) or traditional predic-
tive equations such as the Harris-Benedict or the Penn
State equations. These equations are easy and practical to
use, as the patient’s age, weight, and height are the only
data points required to arrive at an estimate. Indirect
calorimetry remains the most accurate determination of
resting energy expenditure and caloric requirements.65
Multiple clinical variables affect the accuracy of the
results obtained from indirect calorimetry, including med-
ications such as paralytics and sedatives, the presence of
an air leak around chest tubes, failure to achieve true
steady state, and excess variability in measurements during
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the study interval. Other limiting factors with regard to
the use of calorimetry are availability of the technology,
local expertise, and cost.
Once caloric requirements are determined, protein
requirements should be calculated. A simplistic weight-
based calculation may be used, where protein provision is
determined by the equation 1.2–1.75 g/kg/d. Multiple
factors contribute to protein loss in the critically ill
patient, such as the metabolic insult itself (trauma, infec-
tion, pancreatitis, burns, and surgery), wounds, bed rest,
and certain medications (paralytic drugs, sedatives, ino-
tropic agents). These contributors result in mobilization
of labile protein from skeletal muscle, connective tissue,
and the unstimulated gastrointestinal tract.66 Sufficient
protein should be provided in critical illness. The goal of
protein provision is to maximize protein synthesis, in the
hope to meet or match catabolism. Efforts to reach nitro-
gen balance are important, but it is unrealistic to expect
a positive balance and net increases in lean body mass.
Particularly close attention to protein needs is warranted
in patients with large total body surface area burns, large
soft tissue defects, severe diarrhea, or other sources of
additional protein loss. Patients determined to have exten-
sive protein losses through any of these mechanisms may
require up to 2 g/kg actual body weight/d or higher.1
Protein requirements in the obese patient should be
based on IBW, with a goal of 2 g/kg IBW/d for BMI 30–40
and to 2.5 g/kg IBW/d for BMI >40.1
F: Formula Selection
Formulas vary according to factors such as caloric density,
source of macronutrients, micronutrients, fiber, and the
addition of pharmaconutrient agents. Standard enteral
formulas are likely appropriate for most noncritically ill
patients.
From the standpoint of formula selection, patients in
the ICU fall into 1 of 3 categories. The first category is
the subset of critically ill ICU patients who might benefit
from a pharmaconutrient formula, meaning that use of
such formula could change the course of their disease
process and improve their clinical outcome. Immune-
modulating pharmaconutrient formulas are specifically
recommended in patients undergoing major elective sur-
gery (esophageal, pancreatic, gastric), those sustaining
trauma with an ISS >18 or an ATI score >20, patients
with large surface area burns (>30% total body surface
area), those with head and neck cancer, and patients
requiring mechanical ventilation.27 Within this popula-
tion of patients are those diagnosed with acute respiratory
distress syndrome (ARDS)/acute lung injury (ALI).
Sufficient evidence suggests that these latter patients may
benefit from a nonarginine pharmaconutrient formula
with an anti-inflammatory lipid profile.67

The second category of patients includes those with
evidence of malassimilation. Patients with either impaired
digestion (ie, pancreatic insufficiency) or reduced
absorptive capacity (ie, malabsorption) may benefit from
small-peptide/medium-chain triglyceride (MCT) oil semi-
elemental formulas. Small peptides of 4–5 amino acids in
chain length have been shown to be more efficiently
absorbed than either intact protein or individual amino
acids. MCTs are efficient sources of fuel, as they do not
require the acyl-carnitine carrier for transport through
the mitochondrial membrane for oxidation and, unlike
long-chain fats, can be absorbed directly across the small
bowel mucosa into the portal vein. However, MCT oil
does not provide essential fatty acids (linoleic or linolenic
acid), which must be derived from long-chain fatty acids.
An alternative strategy in patients with malassimilation is
to provide a fiber-containing formula. Although most for-
mulas with fiber additives contain both insoluble and
soluble fibers, clinical benefits on outcome may be more
related to soluble fiber as a source of short-chain fatty
acids and an anti-inflammatory trophic effect on gut epi-
thelium via butyrate receptors. Of note, both soluble and
insoluble fiber should be used with caution in patients at
risk for bowel ischemia.
The third category that most likely makes up the
great majority of ICU patients comprises simply those
patients who do not fall into either of the above 2 groups.
These patients should be fed with a standard high-protein
enteral formula.
Pharmaconutrient Formulas
The use of immune-modulating pharmaconutrient for-
mulas is becoming increasingly more prevalent because of
growing data suggesting their potential beneficial effect
on patient outcome. Provision of fish oil in such formulas
increases the ratio of ω-3 to ω-6 fatty acids. ω-3 fatty
acids have been shown to enhance the anti-inflammatory
PPAR, stabilize the NFKB-IKK complex, and reportedly
shift lymphocytes to a more favorable anti-inflammatory
TH2 response.68,69
One component of pharmaconutrient formulas, argi-
nine, has been the subject of much debate and has led to
a general hesitancy in their use by some clinicians.
Arginine is a prominent intermediate in polyamine syn-
thesis (cell growth and proliferation) and proline synthe-
sis (wound healing and collagen synthesis). Arginine is
the only biosynthetic substrate for nitric oxide (NO) pro-
duction (via endothelial nitric oxide synthase [eNOS],
inducible NOS [iNOS], and neuronal NOS [nNOS]).
Arginine also serves as a potent modulator of immune
function via its effects on lymphocyte proliferation and
differentiation.70-73
The theoretical concept that arginine may pose a threat
to the critically ill patient is based on the perception that
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“CAN WE FEED?” / Miller et al   649
critically ill patients are often hemodynamically unstable,
with upregulated iNOS enzyme activity. Consequently, by
delivering supplemental arginine in metabolic states of
upregulated iNOS, an increase in NO production will
result. This increase in NO could then induce vasodila-
tion and hypotension, leading to even greater hemody-
namic instability.74
An alternate, equally valid hypothesis would be that
controlled vasodilation, promoted by arginine supplemen-
tation and increased NO production, would be beneficial
in critical illness and sepsis. This second hypothesis is
now being supported by human data. Three studies have
now been published in which supplemental arginine
given to patients in shock resulted in a clinical outcome
benefit without apparent harm.75-77
Additional metabolically active components com-
monly found in pharmaconutrient formulas include glu-
tamine, nucleic acids, and antioxidants. Because of the
availability of combination formulas, the benefits (and
detriments) of each individual component have been dif-
ficult to discern. Although a clear mortality benefit has
not yet been demonstrated with immune-modulating
pharmaconutrient formulas, meta-analyses have consist-
ently shown decreases in duration of mechanical ventila-
tion, length of stay, and infectious complications in
patients receiving these formulas compared to those
patients receiving standard enteral formulas.78-80
Provision of trace minerals is important in critical ill-
ness, as selenium, zinc, manganese, and copper play key
roles in tissue repair and the resolution of oxidative stress.
Micronutrient deficiencies result from a range of multiple
factors in the ICU setting, from the systemic inflamma-
tory response itself to losses through urine, exudative
wounds, surgical drains, and nasogastric decompression.
The oxidative stress of acute illness is amplified by certain
micronutrient deficiencies.81 Growing data support the
use of antioxidant cocktails in the acute resuscitation
phase to combat oxidative stress. A large study involving
more than 4000 trauma patients where half of the
patients were given vitamins C and E and selenium for 7
days demonstrated decreased lengths of stay and improved
mortality when compared to a retrospective cohort.82 A
randomized, prospective trial of 595 trauma patients per-
formed by Nathens et al demonstrated a decreased inci-
dence of organ failure and reduced ICU stay in trauma
patients given vitamin C and E supplementation.83
Although further study is needed to determine appropri-
ate dosing and timing, these interventions represent cost-
effective and low-risk therapies for potentially improving
patient outcomes.
Probiotics are an additional additive where conflicting
results in the literature have prevented widespread accept-
ance in the ICU. Potential benefits include the reduced
incidence of Clostridium difficile infection and colonic
vancomycin-resistant Enterococcus (VRE) colonization.
650   Journal of Parenteral and Enteral Nutrition / Vol. 35, No. 5, September 2011
Although small prospective, randomized controlled trials
in trauma, transplantation, and major abdominal surgery
patients suggest some improvement in outcome with the
use of probiotics, an additional trial performed in severe
acute pancreatitis demonstrated an increased mortality
associated with patients receiving probiotics.84-87 Due to
these conflicting findings, they cannot be routinely rec-
ommended in the critically ill patient.
Specialty Formulas
Specialty formulas are available for a variety of clinical
subset populations of patients, including those patients
with pulmonary disease, diabetes, renal insufficiency, and
hepatic dysfunction. Data are sparse to support the rou-
tine use of these diets.
No compelling data suggest the routine use of pulmo-
nary formulas in patients requiring prolonged mechanical
ventilation.88 These patients are important candidates for
indirect calorimetry, as overfeeding can subvert attempts
at weaning from mechanical ventilation. Pulmonary for-
mulations have a higher percentage of calories provided
from lipids in an attempt to decrease carbon dioxide pro-
duction. However, macronutrient composition and the
ratio of fat to carbohydrate in the formula do not alter
carbon dioxide production unless the patient is being
significantly overfed. In addition, the increased fat con-
tent in older pulmonary failure formulations comprised
relatively immunosuppressive ω-6 fatty acids.88 Greater
attention should be paid to overall volume status to avoid
fluid overload and resultant pulmonary complications. As
mentioned earlier, patients with ARDS or ALI may be
appropriate candidates for a pharmaconutrient formula
with an anti-inflammatory lipid profile, as use of such
formulas has been demonstrated to improve patient out-
come by reducing organ failure, hospital length of stay,
duration of mechanical ventilation, and mortality.1
Hepatic failure formulations are supplemented with
branched-chain amino acids (BCAAs). Aromatic amino
acids, which can compete with BCAAs for the same
receptors in the central nervous system, cross the blood-
brain barrier and contribute to encephalopathy. There is
some controversy over the utility of these formulas89
because of their low protein content and their failure to
demonstrate a reproducible benefit on patient outcome.90
Hepatic formulas should be reserved for patients with
hepatic failure whose encephalopathy is refractory to
standard therapy with lactulose and luminal acting anti-
biotics.89,90
Renal failure formulations, which comprise a high
concentration of essential amino acids, are actually low in
total protein and have reduced levels of phosphorus and
potassium. The rationale for such design relates to the
concept of nitrogen recycling (where nitrogen is used
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with essential amino acids to synthesize nonessential
amino acids), a process that does not occur to any appre-
ciable extent in the critically ill patient. Renal formulas
are rarely appropriate. Standard formulas should usually
be initiated, with close monitoring of fluid and electrolyte
status. In patients requiring hemodialysis or renal replace-
ment therapy, increased protein provision should be the
goal, with targets of up to 2.5 g/kg/d.1
E: Enteral Access
Obtaining appropriate enteral access often requires an
interdisciplinary approach, involving the expertise of
nursing staff, dietitians, intensivists, endoscopists, sur-
geons, and interventional radiologists. Few critically ill
patients tolerate an oral diet in the ICU. Three general
categories of options for enteral access exist: oro/nasal
access (nasogastric, orogastric, and nasojejunal tube),
percutaneous access (percutaneous endoscopic gastros-
tomy or PEG, PEG in combination with a jejunal tube or
PEG/J, and direct percutaneous endoscopic jejunostomy
or DPEJ), and surgical access (surgical gastrostomy or
jejunostomy). A nasoenteric tube can be used in patients
who are likely to require <4 weeks of EN therapy. In
patients anticipated to require >4 weeks of enteral feed-
ing, a more semipermanent percutaneously placed access
device should be considered.
Determining the level of infusion for EN within the
gastrointestinal tract is an important step in the appropri-
ate assessment for enteral access. Gastric feeding is usu-
ally preferred and represents the default route of delivery
as this level of infusion is easier, requires less expertise,
and is more physiologic, preventing the iatrogenic compli-
cations associated with hyperosmolar formula are deliv-
ered infusions into the small bowel. Gastric feeding
provides more options and even some additional benefits,
such as the ability to provide bolus feeds in rare circum-
stances where indicated and potentially to provide
increased protection from stress-induced gastropathy
(through a direct buffering effect of the formula in the
stomach, in addition to the stimulation of mucosal blood
flow seen from both gastric and postpyloric feeding).
Continuous gastric feeds are generally well tolerated.
Although patients on gastric feeds are at somewhat higher
risk for aspiration, they may not necessarily be at increased
risk for pneumonia (as pneumonia may be linked more
closely to aspiration of oropharyngeal secretions than
aspiration of gastric contents).91
Gastric dysmotility with delayed emptying is common
in the critically ill patient, and the causes are multifacto-
rial. Factors that contribute to this problem include
hyperglycemia, certain medications, electrolyte abnor-
malities, elevated intracranial pressures, sepsis, and

hyperosmolar formulas.92 In the setting of significant
gastric dysmotility, postpyloric tube placement is war-
ranted. Advantages of small bowel feeding include poten-
tially lower risks of aspiration and reduced stimulation of
pancreatic exocrine stimulation (which may be useful in
some patients with severe acute pancreatitis).93,94 The
placement of postpyloric tubes is somewhat more difficult
and more resource dependent. Bedside placement of
postpyloric small bowel tubes has been shown to be effec-
tive, with success rates up to 80% reported with trained
nursing and dietary personnel.95
In patients considered candidates for PEG place-
ment, nasogastric feeding trials are helpful beforehand to
ensure tolerance. If such trials prove unsuccessful, then
a combination PEG/J tube DPEJ tube or surgical jejunos-
tomy is an appropriate option.
E: Efficacy
Documenting efficacy or adequacy of EN therapy is
important because of tendencies toward a delay in the
initiation of feeds as well as the various difficulties
encountered during attempts to maintain target feeds.
Goals are rarely met secondary to underfeeding by physi-
cians and inappropriate cessation of anticipated infusion,
resulting in delivery of approximately 50% of goal calories
in the ICU setting.96 Some evidence suggests that an end
point of delivery closer to 60%–65% of goal calories is
needed to accrue the positive effects of enteral feeding
(maintenance of gut integrity, attenuation of oxidative
stress, and modulation of systemic immune responses).
One study performed by Ziegler et al97 showed that 60%–
70% of goal calories were required to maintain gut integ-
rity and prevent infection in burn patients. The cessation
of tube feeds in the ICU occurs readily as a consequence
of a variety of reasons, including placement of patients
NPO for procedures and tests, increased GRVs, tube dis-
placement/occlusion, plans for intubation or extubation,
nursing care, and feeding intolerance. In these instances,
two-thirds of the reasons for cessation have been shown
to be inappropriate.96 Clearly defining appropriate param-
eters that should trigger the cessation of feeding help
attains the proposed goals of support.
Securing nasoenteric tubes with a nasal bridle sub-
stantially decreases the incidence of dislodgement in
combative and agitated patients.92 Tube occlusion can
usually be ameliorated by infusing a declogging solution
comprising a pancrelipase tablet and bicarbonate tablet
crushed in 10 mL of warm water.98 The measurement of
GRVs has been shown to increase the incidence of tube
occlusion as much as 10-fold because the practice pulls
gastric acid into the tube in contact with the formula,
leading to clot formation.99 In the event that declogging
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“CAN WE FEED?” / Miller et al   651
maneuvers are unsuccessful, the tube usually must be
replaced.
An additional strategy for improving delivery of EN is
the implementation of feeding protocols in the ICU.
These protocols should include indications for the initia-
tion and cessation of enteral feedings and are similar to
those routinely used for glucose control. Protocols include
algorithms for early placement and confirmation of bed-
side feeding tubes, initial rate and ramp-up of formula
infusion, aspiration precautions, and strategies to manage
elevated GRVs. In 1 study, the aggressive implementation
of protocols to guide EN therapy for study patients in the
ICU increased the number of days enteral feeds were
infused over the first 10 days following admission to the
ICU (from 5.4 to 6.7 days, P = .04), which resulted in
significant decreases in hospital length of stay (35 to 25
days, P = .003) and mortality (37% to 27%, P = .058)
compared to control patients who did not receive such
implementation, respectively.100
D: Determine Tolerance
Poor tolerance of EN can result from multiple factors,
such as functional dysmotility, medications (narcotics,
proton pump inhibitors, H2 blockers, antibiotics, etc),
inadequate gastric decompression, overly aggressive feed-
ing, and hemodynamic instability.92 Classic clinical mark-
ers for intolerance include high GRVs, increased output
from a nasogastric aspiration tube, absence of flatus and
stool output, abdominal distention, diarrhea, and abdom-
inal pain.
An important step in the assessment of tolerance is
the evaluation of segmental contractility. Nasogastric out-
put >1200 mL per day and serial GRVs >400 mL suggest
poor gastric contractility. The absence of bowel sounds,
abdominal distension, and the presence of air/fluid levels
on abdominal radiographs are more specific to impaired
small bowel contractility.1 The absence of flatus and fecal
output give clues as to impaired colonic function. The
evaluation of segmental contractility allows for the appro-
priate selection of the conduit for enteral access and
whether appropriate decompression measures are
required. Electrolyte replacement should be undertaken
as needed and sedation/analgesia should be reevaluated
daily in the event of feeding intolerance.
Too much emphasis is placed on GRVs in the deter-
mination of feeding tolerance in the ICU. The practice
itself increases the incidence of tube occlusion and con-
sumes valuable nursing time. Automatic cessation of tube
feedings based on poorly standardized GRVs leads to fre-
quent inappropriate interruptions of the delivery of EN.
The perceived risk for continuing feeds despite elevated
GRVs is aspiration pneumonia. Studies in the past using
652   Journal of Parenteral and Enteral Nutrition / Vol. 35, No. 5, September 2011
very specific sensitive markers for aspiration (pepsin or
colorimetric microspheres) have shown no “consistent
relationship” between GRVs and aspiration events.101,102
The volume of gastric residual contents obtained is
dependent on certain tube characteristics. Nasogastric
tubes generate higher GRVs than PEG tubes, and aspira-
tion from larger bore tubes results in higher GRVs than
that from small-caliber tubes.103 Although GRVs provide
some information on tolerance, they must not be inter-
preted in a vacuum without consideration of other clini-
cal parameters. A more prudent approach is to avoid
automatic cessation of feeds for GRVs <500 mL in the
absence of other signs of intolerance. Instead, measures
to reduce risk from aspiration pneumonia should be
undertaken while the feeding continues, such as reassess-
ment of the need for sedation and analgesia, elevation of
the head of bed, optimization of oral health,90 utilization
of continuous feeds, addition of prokinetic agents, and
conversion to postpyloric feeding.
Although diarrhea is often interpreted as intolerance,
this complication should not lead inappropriately to the
cessation of tube feeds. Diarrhea is defined as >500 mL
of stool output per day through the rectum or >1,000 mL
of output from an ileostomy.92 “Diarrhea” in the ICU set-
ting often represents low-volume (<250 mL) inconti-
nence, which may be managed simply by a fecal
incontinence system. The most common cause of true
diarrhea in the ICU is the use of osmotic agents, such as
sorbitol preparations used as elixirs for the delivery of
medication. Infectious diarrhea, the most common of
which is C difficile, may be excluded through stool anti-
gen studies, stool cultures, or a toxin screen. The exten-
sive use of antibiotics in the critically ill patient population
and the resultant change in the microflora of the gut
render these patients particularly susceptible to virulent
strains of C difficile and should be ruled out or appropri-
ately treated before the initiation of antimotility agents.
The osmolarity of the tube feeding formulas may also be
the causative agent in <20% of cases.104,105 Other contrib-
uting factors to the development of diarrhea may include
reduced absorptive surfaces, decreased transit times,
gastric or colonic hypersecretion, and bacterial over-
growth. A prudent approach in the event of documented
diarrhea is to continue feedings while putative causes are
evaluated and eliminated. Regular dosing of opiates,
including loperamide, diphenoxylate, and paregoric, can
be helpful. The addition of fiber supplementation in
hemodynamically stable patients has been shown to
improve motility, absorb excess fluid, and may assist with
glucose control.106 The selection of a small-peptide,
medium-chain triglyceride formula may improve effi-
ciency of small bowel absorption and improve the symp-
toms of diarrhea as well.
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Conclusion
Nutrition support therapy in the ICU is growing increas-
ingly more complex. Important considerations include
the early initiation of enteral feeds, appropriate use of PN
for specific cases, careful choice of the enteral access
device and level of infusion, and selective utilization of
specialty formulas. Goals of nutrition support therapy
have been expanded from simply providing protein and
calories to the pursuit of broader avenues for therapeutic
intervention such as pharmaconutrition and immune
modulation. A multidisciplinary approach to nutrition
support is essential and cannot be emphasized enough.
This article attempts to integrate the clinical assessment
of the ICU patient by the critical care specialist, on one
hand, and the dietitian nutritionist, on the other. However,
the individuals who most often find “their hand on the
spigot” of delivering EN are the ICU nurses. It is hoped
that providing the integrated perspectives outlined in this
article will empower the nurse to assume a bigger role in
the nutrition management and optimal delivery of EN.
The “CAN WE FEED?” mnemonic allows integration of
the initial evaluation and resuscitation of the critically ill
patient with the nutrition assessment and derivation of
the plan for nutrition support therapy. Through the
implementation of this carefully designed process, the
chances for EN therapy to improve patient outcome may
be optimized.
Appendix A: Summary of “CAN WE FEED?”
Mnemonic
C  Critical Illness Severity
1. Comorbidities and severity of disease are impor-
tant considerations in the implementation of
enteral support therapy.
2. Glucose control is an important contributor to
morbidity and mortality in the critically ill patient
and is intimately associated with nutrition support
therapy.
3. Critical illness is a hypermetabolic state.
4. Multiple scoring systems exist for estimating
severity of illness, such as the Injury Severity
Score (ISS), Penetrating Abdominal Trauma
Index (PATI), Acute Physiology and Chronic
Health Evaluation (APACHE) II, Sequential
Organ Failure Assessment (SOFA), and Ranson’s
criteria. Severities of illness are important fac-
tors in considering the timing and route of nutri-
tion therapy.

A Age
1. Age is an important independent variable in evalu-
ating the critically ill patient.
2. Malnutrition is common in the elderly patient
population.
N  Nutrition Risk Screening
1. Determining baseline nutrition status is the first
step in the development of a nutrition plan.
2. Visceral proteins are of little value in the nutrition
assessment of the critically ill patient.
3. The Nutritional Risk Screening (NRS-2002) tool
is a quick and efficient way of estimating nutrition
status.
4. The most important step in preventing refeeding
syndrome is the identification of patients at risk
for this disorder.
W  Wait for Resuscitation
1. Resuscitation is paramount in the care of the
critically ill patient. Caution should be taken
when considering the initiation of enteral nutri-
tion (EN) therapy in hemodynamically unstable
patients requiring vasopressive medications.
2. Identifying hemodynamic instability through
measures such as lactate, base excess, and mean
arterial pressure help identify those patients at
risk of ischemia from early enteral feeding.
3. Early initiation of tube feeds portends good patient
outcomes.
E  Energy Requirements
1. Requirements are best determined using
traditional weight-based equations or indirect
calorimetry.
2. Protein requirements, of equal if not greater
importance than caloric needs, are more difficult
to determine in the obese patient.
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“CAN WE FEED?” / Miller et al   653
F  Formula Selection
1. Most patients are candidates for standard enteral
formulas.
2. Specialty formulas have little impact in the major-
ity of patients.
3. Pharmaconutrition formulas are appropriate in
select patients and may improve outcome when
compared to the use of standard enteral formulas.
E  Enteral Access
1. Most patients will tolerate gastric feeds.
2. In patients with true gastric dysmotility, nasojeju-
nal feeding is appropriate and bedside placement
is usually successful.
3. Percutaneous enteral access, such as percutane-
ous endoscopic gastrostomy or PEG, PEG in com-
bination with a jejunal tube or PEG/J, and direct
percutaneous endoscopic jejunostomy or DPEJ, is
appropriate for patients requiring >4 weeks of
nutrition support.
E Efficacy
1. Provision of approximately 55%–60% of caloric
requirements may be required to accrue the ben-
efits of EN therapy.
2. Feeding protocols in the intensive care unit can
improve delivery and prevent inappropriate cessa-
tion of feeds.
D  Determine Tolerance
1. Feeding intolerance is usually multifactorial.
2. The physical exam is an important component in
determining tolerance.
3. Gastric residual volumes should be interpreted in
the context of the clinical picture.
4. Diarrhea is rarely caused by tube feedings, and
alternative causes should be investigated prior to
stopping feeds.
654   Journal of Parenteral and Enteral Nutrition / Vol. 35, No. 5, September 2011

Appendix B:   ICU “CAN WE FEED?” Nutrition Screening Tool

C Comorbidities
Severity of Illness: Calculate score, as indicated by patient ICU admitting diagnosis
APACHE II _____
Ranson criteria  _____
SOFA _____
ISS _____

Preexisting conditions:
Diabetes mellitus?  □ Yes   □ No If yes, carefully target glucose control
Liver dysfunction?  □ Yes   □ No If yes, carefully monitor protein tolerance
Renal dysfunction?  □ Yes   □ No If yes, carefully monitor protein tolerance
Alcohol abuse and related malnutrition? □ Yes □ No If yes, carefully monitor for malnutrition and refeeding syndrome
Drug abuse and related malnutrition?   □ Yes □ No If yes, carefully monitor for malnutrition and refeeding syndrome

A AGE ________

N  Nutrition Risk Screening (NRS 2002 System)18

Initial Screening
BMI <20.5? □ Yes □ No
Weight loss in last three months? □ Yes □ No
Reduced dietary intake in past week? □ Yes □ No
Severe illness? □ Yes □ No

Final Screening (Complete if “yes” to any of above questions)

Part I Impaired Nutrition Status

Absent    Score 0:  Normal nutrition status
Mild     Score 1:   Wt loss >5% in three months or food Intake <50–75% normal in last week
Moderate   Score 2:   Wt loss >5% in last two months or BMI 18.5–20.5 Or food intake <25–50% normal in last week
Severe     Score 3:   Wt loss >5% in last month (>15% in last 3 mos) Or BMI < 18.5 + impaired general condition Or
food intake 0–25% normal in last week
Part II Severity of Disease
Absent    Score 0:  Normal nutrition requirements
Mild     Score 1:   Hip fracture, chronic patients (hemodialysis, diabetes, cancer, cirrhosis, COPD) with acute
complication
Moderate   Score 2:   Major abdominal surgery, stroke, severe pneumonia, hematologic malignancy
Severe     Score 3:   Head injury, bone marrow transplantation, APACHE II score >10
Total Nutrition Risk Score
Part 1 Impaired NS score ____ + Part II Severity of Disease Score ____ + 1 (if age > 70) ____ = ______Total
[If total of 3 or more, nutrition support is indicated. ]
W  Wait for Resuscitation
Proceed with caution if answer is Yes. Hold feeding if answer is No.
Fluid resuscitation complete? □ Yes □ No   CVP 8–12 mm Hg □ Yes □ No
Mean arterial pressure ≥65 mm Hg?  □ Yes   □ No   Serum lactate <2 mg/dL □ Yes □ No
Stable pressor agents for 24 hours? □ Yes □ No   Base excess < 5 mEq   □ Yes □ No
CVO2 ≥70% or MVO2 ≥65% □ Yes □ No
E  Estimated Energy Requirements
Calories:
BMI <30: Use 25–30 kcal/ kg ABW/day _____________ kcal ABW = Actual Body Weight
BMI ≥30: Use 11–14 kcal/ kg ABW/day _____________ kcal IBW = Ideal Body Weight
Protein:
BMI <30 Use 1.2–2.0 gm protein/kg ABW/day _____________ gms protein
BMI 30–40: Use ≥2.0 gm protein/kg IBW/day _____________ gms protein
BMI >40: Use 2.5 gm protein/ kg IBW/day _____________ gms protein
F  Formula Selection
Candidate for arginine-containing pharmaconutrition formula: □ Yes □ No
Criteria: Major surgery, trauma (ATI score >20), burns (TBSA >30%), head/neck cancer, critically ill on MV
Candidate for Anti-inflammatory Pharmaconutrition:  □ Yes □ No
Criteria: ARDS or ALI
Candidate for Malassimilation formula: Small peptide/ MCT oil □ Yes □ No
Fiber-containing □ Yes □ No
If no to all above, then candidate for standard enteral formula.
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 “CAN WE FEED?” / Miller et al   655

E  Enteral Access
Access site      Nasoenteric □ Yes □ No
           Oroenteric (concern for sinusitis) □ Yes □ No
           Percutaneous (anticipate feeds >4 wks) □ Yes □ No
Level of infusion   Stomach □ Yes □ No
           Postpyloric □ Yes □ No
           Below ligament of Treitz □ Yes □ No
Need for simultaneous gastric decompression (aspirate/feed tube) □ Yes □ No
E Efficacy
Days NPO _________ Cumulative Caloric Balance  __________
Initial Rate _________ Rapid ramp-up rate __________
Goal Rate _________ Goal volume/day __________
Initiate volume-based feeds □ Yes □ No [□ gastric (max 280 mL/ hour) □ postpyloric (max 150 mL/hour)]
D  Determine Tolerance
First Gastric Residual Volume >500 mL:
□ Continue current infusion, recheck in four hours □ Initiate narcan 8 mg in saline per tube q 6 hours
□ Normalize serum electrolytes  □ Elevate HOB
□ Initiate metaclopramide 10 mg IV q 6 hours □ Turn patient to right lateral decubitus position
Second Gastric Residual Volume >500 mL:
□ Hold enteral infusion □ Recheck GRV in 2 hours
□ Restart infusion once GRV <500 mL
Serum Glucose 80–150 mg/dL □ Yes □ No Passage of stool/gas □ Yes □ No
Diarrhea (>250 mL/day stool output per rectum Or >1000 mL/day output per ileostomy)
□ Remove sorbitol from oral/enteric medications
□ Obtain stool cultures/oxin assays to rule out infectious diarrhea
□ Initiate opiates once infectious etiology ruled out (lomotil, immodium, paregoric)
□ Consider fiber-containing formula and/or small peptide/MCT formula
□ Provide fiber additive

Adapted from Kondrup J, Allison SP, Elia M, Vellas B, Plauth M. ESPEN guidelines for nutrition support screening 2001. Clin Nutr.
2003;22(4):415-421.

Appendix C: Reference Information for
Scoring Systems
APACHE II
The Acute Physiologic and Chronic Health Evaluation
(APACHE) was developed by Knaus et al5 in 1985 to bet-
ter characterize severity of illness and is calculated from
independent variables, including age, temperature, hemo-
dynamics, arterial blood gas values, electrolytes, and renal
function. The score, calculated once upon initial presen-
tation to the intensive care unit (ICU), can be used to
predict mortality. The maximum APACHE II score is 71.
Online resources are readily available to aid in the calcu-
lation of APACHE II scores.16
Injury Severity Score
The Injury Severity Score (ISS) was developed in 1974
by Baker et al7 as a modification of the existing
Abbreviated Injury Score (AIS), in order to stratify risk
associated with multiple injuries sustained by trauma
patients. This somewhat complicated system is based on
the evaluation of 6 body regions (head/neck, face, chest,
abdomen, extremities, and external), with each injury
assigned an AIS ranging from 1 (minor) to 6 (unsurviv-
able). Only the most severe injury (highest score) is
considered from the 3 most severely injured regions.
Each of the 3 AIS values is squared and added
together for a maximum score of 75, which is deemed an
unsurvivable injury. The ISS correlates relatively well
with mortality with the caveat being that devastating
injuries to certain regions (for example, traumatic brain
injury) can result in low overall scores that still carry a
very high mortality.
Below is an example of what an APACHE II score
means relative to an ISS with regards to mortality. These
systems were obviously designed for different patient popu-
lations, but having some knowledge of what a particular
score means is useful.

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656   Journal of Parenteral and Enteral Nutrition / Vol. 35, No. 5, September 2011

APACHE II ISS Mortality, ISS Mortality,

Score Mortality, % Age <49, % Age >70, % SOFA
5 5 0 13 8–10
10 11 2 15 40–50
15 21 3 16 80
20 35 6 31 >80
30 70 21 65
40 91 47 92
50 98 75 100
55 98 89 100
75 — 100 100

Abdominal Trauma Index Ranson’s Score Mortality, %

The Penetrating Abdominal Trauma Index (PATI) was
developed in 1981 as a tool to assist with determining the
risk of postinjury complications following penetrating
abdominal trauma.6 The score is calculated by assigning
a risk factor (1–5) for each organ that is injured and mul-
tiplying this value by a severity of injury estimate. In the
group’s original article, the incidence of complications in
patients with a score of <25 was 5% for patients with stab
wounds and 7% for those with gunshot wounds. When
patients presented with a score >25, complications were
seen in 50% of patients with stab wounds and 46% of
patients with gunshot wounds.6
Sequential Sepsis-Related Organ Failure Assessment
The Sequential Organ Failure Assessment (SOFA) score,
developed by Vincent et al9 in 1996, considers 6 organ
systems, including respiratory, coagulation, liver, cardio-
vascular, central nervous system, and renal, and assigns a
severity of dysfunction score in a range between 1 and 4.
As discussed, scoring the system was originally developed
to assess morbidity rather than mortality but has been
proven to remain a powerful predictor of mortality in sep-
sis and has translated to other conditions. An additional
advantage of the SOFA scoring system is the ability to
repeatedly recalculate the score throughout the course of
the patient’s admission to reassess morbidity and mortality.
Ranson’s Criteria
Ranson’s criteria were developed in 1974 to estimate
prognosis and predict mortality in acute pancreatitis
based on 5 values collected at presentation (age, white
blood cell count, glucose, aspartate aminotransferase,
and lactate dehydrogenase) and 6 additional values
obtained at 48 hours (fluid sequestration, fall in hemato-
crit, PaO2, blood urea nitrogen, and base excess). The
maximum score is 11, and the mortality associated with
increasing scores is detailed below.17
1–2 1
3–4 15
5–6 40
>7 100
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