REVIEW

C URRENT
OPINION Enteral nutrition in septic shock: a call for a
paradigm shift
Jayshil J. Patel a, Juan Carlos Lopez-Delgado b, Christian Stoppe c,d
and Stephen A. McClave e

Purpose of review
The purpose of this review is to identify contemporary evidence evaluating enteral nutrition in patients with
septic shock, outline risk factors for enteral feeding intolerance (EFI), describe the conundrum of initiating
enteral nutrition in patients with septic shock, appraise current EFI definitions, and identify bedside monitors
for guiding enteral nutrition therapy.
Recent findings
The NUTRIREA-2 and NUTRIREA-3 trial results have better informed the dose of enteral nutrition in critically
ill patients with circulatory shock. In both trials, patients with predominant septic shock randomized to
receive early standard-dose nutrition had more gastrointestinal complications. Compared to other
contemporary RCTs that included patients with circulatory shock, patients in the NUTRIREA-2 and
NUTRIREA-3 trials had higher bowel ischemia rates, were sicker, and received full-dose enteral nutrition
while receiving high baseline dose of vasopressor. These findings suggest severity of illness, vasopressor
dose, and enteral nutrition dose impact outcomes.
Summary
The provision of early enteral nutrition preserves gut barrier functions; however, these benefits are
counterbalanced by potential complications of introducing luminal nutrients into a hypo-perfused gut,
including bowel ischemia. Findings from the NUTRIREA2 and NUTRIREA-3 trials substantiate a ‘less is
more’ enteral nutrition dose strategy during the early acute phase of critical illness. In the absence of
bedside tools to guide the initiation and advancement of enteral nutrition in patients with septic shock, the
benefit of introducing enteral nutrition on preserving gut barrier function must be weighed against the risk
of harm by considering dose of vasopressor, dose of enteral nutrition, and severity of illness.
Keywords
circulatory shock, critical care, early acute phase of critical care, enteral nutrition, ICU, sepsis, septic shock

INTRODUCTION recent large multicenter randomized controlled tri-

Septic shock is characterized by circulatory, cellular,
and metabolic abnormalities related to dysregulated
immune and inflammatory responses from patho-
gen-associated molecular proteins and is clinically
recognized by hypotension necessitating vasoactive
support in a patient with an infection [1]. Many
patients with septic shock undergo mechanical ven-
tilation, which necessitates artificial nutrition. The
hypotensive period represents the early acute phase
of critical illness, which is hallmarked by height-
ened inflammation, catabolism, and proteolysis,
but also represents a window of opportunity to
bathe the intestinal mucosa.
For patients in septic shock, efforts to find the
optimal timing, route, and dose of enteral nutrition
are frustrating and often misdirected. Even though
als (RCTs) have shed light on the role, timing, and
dose of early enteral nutrition in mechanically ven-
tilated patients with septic shock, an encompassing
a
Division of Pulmonary and Critical Care Medicine, Medical College of
Wisconsin, Milwaukee, Wisconsin, USA, bMedical Intensive Care Unit,
Hospital Clínic de Barcelona, Barcelona, Spain, cUniversity Hospital,
W€ urzburg, Department of Anaesthesiology, Intensive Care, Emergency
and Pain Medicine, W€ urzburg, dDepartment of Cardiac Anesthesiology
and Intensive Care Medicine, Charit e Berlin, Berlin, Germany and
e
Department of Medicine, Division of Gastroenterology, Hepatology,
and Nutrition, University of Louisville, Louisville, Kentucky, USA
Correspondence to Jayshil J. Patel, MD, Medical College of Wisconsin,
Milwaukee, WI 53226, USA. E-mail: jpatel2@mcw.edu
Curr Opin Crit Care 2024, 30:165–171
DOI:10.1097/MCC.0000000000001134

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Copyright © 2024 Wolters Kluwer Health, Inc. All rights reserved.

Gastrointestinal system
KEY POINTS
 Septic shock impairs gut barrier functions and
represents the early acute phase of critical illness and
presents an opportunity to introduce enteral nutrition,
which has been shown to preserve gut
barrier functions.
 The NUTRIREA-2 and NUTRIREA-3 trials showed
introducing standard dose enteral nutrition in
mechanically ventilated patients with predominant
septic shock receiving high-dose vasopressor is harmful,
and trial results suggest a ‘less is more’ enteral
nutrition strategy.
 Accurate clinical and biochemical markers identifying
and predicting gastrointestinal dysfunction are not
available, and instead, two distinct levels of
gastrointestinal dysfunction, low and high-risk signs,
may better correlate to outcomes
 Assessment of enteral nutrition initiation and titration in
mechanically ventilated patients with septic shock
should consider dose of vasopressor, dose of enteral
nutrition to initiate, and severity of illness bearing in
mind low-risk signs and symptoms carry more
importance and may become a high-risk sign in
patients receiving high-dose vasopressor and/or has a
greater severity of illness.
regimen may never be established because ICU
patients are heterogeneous and have different nutri-
tion requirements, tolerance, and varying levels of
disease severity. Rather than seek a single enteral
nutrition strategy for all ICU populations, each
individual patient should be assessed for the chance
of benefit, risk for complications, and the degree to
which feeding will be tolerated.
The purpose of this review will be to identify
contemporary evidence evaluating the dose of early
enteral nutrition in patients with septic shock, out-
line recent evidence evaluating risk factors for
enteral feeding intolerance (EFI), describe the
conundrum of initiating enteral nutrition in
patients with septic shock, and appraise current
definitions of EFI and bedside monitors for guiding
nutrition therapy.
CONTEMPORARY EVIDENCE EVALUATING
NUTRITION IN CIRCULATORY SHOCK
The 2019 European Society of Parenteral and Enteral
Nutrition Critical Care Nutrition guideline indicates
that ‘in patients with septic shock receiving vaso-
pressors or inotropes, no evidence-based answer can
be proposed as no interventional studies have been
reported to date’ [2]. Since, the NUTRIREA-2 and
NUTRIREA-3 trials have better informed the role and
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dose of enteral nutrition in critically ill patients with
circulatory shock during the first week of critical
illness.
The multicenter NUTRIREA-2 trial randomized
more than 4000 mechanically ventilated patients in
circulatory shock, with two-third in septic shock, to
receive early full-dose enteral nutrition or early
parenteral nutrition during the first week of critical
illness to evaluate the primary outcome of 28-day
mortality [3]. The study found no between-group
differences in 28-day mortality. Of concern, patients
who received early full-dose enteral nutrition, com-
pared to early parenteral nutrition, had significantly
more vomiting (34 vs. 24%, P
0.0001), diarrhea (36
vs. 33%, P ¼ 0.007), and clinically relevant bowel
ischemia (2 vs. <1%, P ¼ 0.007) [3].
More recently, the multicenter NUTRIREA-3
trial randomized more than 3000 mechanically ven-
tilated patients with majority septic shock to
restricted calorie feeding (6 kcal/kg/day) or standard
calorie feeding (25 kcal/kg/day) to evaluate the pri-
&&
mary outcome of 90-day mortality [4 ]. More than
75% of patients received enteral nutrition. The trial
found no between-group differences on 90-day mor-
tality but the restricted calorie group, compared to
standard-dose, had a trend towards improved time
to weaning from vasopressor [hazard ratio 1.07; 95%
confidence interval (CI) 0.99–1.15, P ¼ 0.054] and
improved ICU mortality (32.7 vs. 29.5%, P ¼ 0.051)
&&
[4 ]. However, and as found in NUTRIREA-2,
patients who received early standard feeding, com-
pared to restricted feeding, had cumulatively higher
rates of vomiting (25.5 vs. 20.2%, P < 0.001), diar-
rhea (33.3 vs. 28.9%, P ¼ 0.004), and bowel ischemia
(1.8 vs. 0.9%, P ¼ 0.030) [4 ].
&&
The NUTRIREA-3 trial also found patients who
received early standard-dose feeding, compared to
restricted feeding, had more nongut-related compli-
cations, including hypophosphatemia (61.3 vs.
53.5%, P < 0.001), hyperglycemia (daily glucose
value of 13.6 vs. 11.6 mmol/l, P < 0.001), and fluid
overload with increased time to wean mechanical
ventilation (6 vs. 5 days, P ¼ 0.007) [4 ,9 ].
&& &
NUTRIREA-2 and NUTRIREA-3 trials are the larg-
est RCTs evaluating the route and dose of nutrition,
respectively, in critically ill patients with predom-
inant septic shock during the early acute phase of
critical illness. The findings of these studies do not
suggest that restricted feeding is superior to standard
full-dose feeding, but rather, early full-dose feeding
in patients with circulatory shock is harmful. The
bowel ischemia rate in patients receiving early full-
dose enteral nutrition in the NUTRIREA-2 and
NUTRIREA-3 trials was significantly higher than
reported in previous studies. The bowel ischemia
rate is 0.3% among contemporary retrospective and
Volume 30  Number 2  April 2024

prospective observational and RCTs that included
critically ill patients in circulatory shock receiving
enteral nutrition [5]. Of the comparable contempo-
rary RCTs, TARGET randomized more than 3900
critically ill patients, nearly two-third who were in
circulatory shock, to receive energy-dense or routine
nutrition during the first week of critical illness [6].
Patients in both groups commenced enteral nutri-
tion within 15 h of ICU admission and within 1 h of
randomization and received more calories than
patients in NUTRIREA-3; however, bowel ischemia
was observed in 27 of 1515 (1.8%) who received
standard-dose nutrition in NUTRIREA-3, compared
to two of 3957 patients (0.05%) in both groups in
TARGET [6,7]. Similarly, the CALORIES trial
randomized critically ill patients, more than 80%
in circulatory shock, to receive early enteral nutri-
tion or early parenteral nutrition during the first
week of critical illness. There was one patient
(0.08%) suspected of having bowel ischemia in
the 1197 patients randomized to early enteral nutri-
tion [mean 15.5 kcal/kg/day (7.3)] (Table 1) [8].
THE RELATIONSHIP BETWEEN SEVERITY
OF ILLNESS, VASOPRESSOR, AND DOSE
OF DELIVERED ENTERAL NUTRITION WITH
OUTCOMES
The severity of illness, vasopressor dose, and the
early full delivery of protein and calories to meet
requirements by enteral nutrition may explain the
rate of gastrointestinal complications, and particu-
larly, the high bowel ischemia rate in NUTRIREA-2
and NUTRIREA-3 [16]. First, patients in NUTRIREA-2
and NUTRIREA-3 represented a sick cohort of
patients. The mean baseline Sequential Organ
Failure Assessment (SOFA) score for patients in
both groups of NUTRIREA-2 was 11 (3), while
the median baseline SOFA score was 10 (IQR 8–13)
in both groups of NUTRIREA-3. In a prospective multi-
center observational study, Flordelis-Lasierra
found the SOFA score was associated with enteral
nutrition related complications [17]. The 90-day mor-
tality exceeded 40% in all patients in NUTRIREA-2 and
NUTRIREA-3. As a comparison, the mortality rate in
CALORIES and TARGET was under 40% [6,8].
Second, patients in NUTRIREA-2 and NUTRIREA-
3 received a baseline norepinephrine dose of at least
0.5 mg/kg/min, which was higher than any of the
other contemporary studies addressing use of enteral
nutrition in shock. Evidence suggests enteral nutri-
tion in patients receiving lower norepinephrine doses
is associated with improved clinical outcomes while
enteral nutrition with higher doses may promote EFI
and gastrointestinal dysfunction. In the largest obser-
vational study that stratified patients with circulatory
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Enteral nutrition in septic shock Patel et al.
shock based on NE dose, Ohbe et al. [10] found an
associated mortality benefit of early enteral nutrition
in critically ill patients who received low [odds ratio
(OR) 0.84, 95% CI 0.77–0.93) with <0.1 mg/kg/min]
and medium dose (OR 0.77, 95% CI 0.68–0.86 with
0.1–0.3 mg/kg/min) norepinephrine, but not in those
who received high dose (OR 0.96, 95% CI 0.81–1.14
with >0.3 mg/kg/min) norepinephrine [10]. The early
enteral nutrition dose was not reported. In a retro-
spective study of 319 patients receiving enteral nutri-
tion with (highest norepinephrine dose of 0.16 mg/
kg/min) and without vasopressor, Sabino et al. [11]
found no differences between rates of bowel ischemia
or emesis between groups, and in the four reported
cases of mesenteric ischemia, two occurred in
patients not receiving vasopressor. In an observatio-
nal study, Wang et al. [12] separated 66 patients with
circulatory shock receiving enteral nutrition, more
than 80% with septic shock, to those who developed
EFI and no EFI, and identified a mean NE equivalent
dose of 0.2 mg/kg/min predicted EFI with a sensitivity
of 88%. Qi et al. [13] recently found patients with
septic shock who tolerated enteral nutrition had a
lower norepinephrine dose [0.23 (0.07) vs. 0.28
(0.10) mg/kg/min, P ¼ 0.049].
Third, full feeding by enteral nutrition, at an
amount close to meeting protein/calorie require-
ments, may explain the higher rates of EFI and
nonocclusive bowel ischemia (NOBI). In a nested
cohort observational analysis of the EFFORT trial,
mechanically ventilated patients with mostly septic
shock (receiving norepinephrine equivalent dose of
0.3 mg/kg/min) who had received early enteral nutri-
tion at a dose of 13.5 kcal/kg/day had associated
improvement in ICU-free days, vasopressor-free
days, and duration of mechanical ventilation [14].
In a pilot RCT comparing early trophic rate enteral
nutrition to ‘no EN’ in mechanically ventilated
patients with septic shock, patients in the early
enteral nutrition arm were receiving a median nor-
epinephrine dose of 0.08 mg/kg/min (IQR 0.05–
0.25). There were more gastrointestinal complica-
tions reported in the ‘no EN’ group, compared to
early enteral nutrition, and no report of bowel
ischemia [15–17].
THE CONUNDRUM OF INTRODUCING
LUMINAL NUTRIENTS IN SEPTIC SHOCK
Within an intact gut, biochemical, physical, and
immunological barriers defend against intraluminal
pathogens and preserve gut-derived anti-inflamma-
tory responses. Septic shock related activation of
immune and inflammatory pathways incites a cyto-
kine storm [1]. Cytokines such as tumor-necrosis
factor alpha (TNF-a), interleukin-1 (IL-1), and
www.co-criticalcare.com 167
Gastrointestinal system

Table 1. Characteristics from contemporary randomized controlled trials that have enrolled patient in circulatory shock
(requiring vasopressor) and at least one arm of the trial evaluate early enteral nutrition
NUTRIREA-2 [3] NUTRIREA-3 [4 ] TARGET [6] CALORIES [8]
&&

Trial n ¼ 2410 n ¼ 3O36 N ¼ 3957 n ¼ 2388

Mortality
90-day EN: 45% low: 41.3% low: 25.7% EN: 39.1%
PN: 43% full: 42.8% high: 26.8% PN: 37.3%
28-day EN: 37% low: 33.2% low: 23% EN: 34.2%
PN: 35% full: 35.2% high: 22.9% PN: 33.1%
Patients in shock EN: 100% low 100% low: 62.7% EN: 84.6%
PN: 100% full 100% high: 63.1% PN: 80.9%
Patients in septic shock EN: 61% low: 58.7% low: 9.4% NR
PN: 64% full: 57.7% high: 9.1%
Vasopressor dose (median mg/kg/min) EN: 0.56 low: 0.5 NR NR
PN: 0.5 high: 0.5
Baseline severity of illness (mean or median) EN: SOFA of 11 EN: SOFA of 10 low: APACHE II of 22 EN: SOFA of 9.6
PN: SOFA of 11 PN: SOFA of 11 high: APACHE II of 22.1 PN: SOFA of 9.5
Calories delivered kcal/kg/day EN: 17.8 low: 7.2 low: 15.6 EN: 19.0
PN: 19.6 full: 22.0 high: 23.1 PN: 22.0
Protein delivered g/kg/day EN: 0.7 low: 0.4 low: 1.08 EN: 0.7
PN: 0.8 full: 1.0--1.3 high: 1.09 PN: 0.7
NOBN (bowel ischemia) EN: 1.6% low: 0.9% low 0.05% EN: 0.9%
PN: 0.4% full: 1.8% high 0.05% PN: 0.7%
Vomiting EN: 34% low: 20% low: 15.7% EN: 16.2%
PN: 24% full: 25% high: 18.9% PN: 8.4%
Diarrhea EN: 36% low: 29% low: 6% EN: 21%
PN: 33% full: 33% high: 7% PN: 16.2%
GI bleeding NR NR low: 0.05% EN: 0.7%
high: 0.15% PN: 0.3%

EN, enteral nutrition; IQR, interquartile range; NR, not reported; PN, parenteral nutrition.

interleukin-6 (IL-6) promote breakdown of barrier
defenses [18,19].
Gut microbiota establish symbiotic axes with
other organs, including the brain (gut-brain axis),
the heart (gut-heart axis), and the liver (gut-liver
axis) [20]. Septic shock pathophysiology and inter-
ventions (e.g., antibiotics) promote gut dysbiosis
[20]. Gut dysbiosis disrupts crosstalk with other
organs, suggesting the gut has a central role in
downstream complications. Impaired gut barrier
functions and dysbiosis have been shown to gener-
ate a gut-derived proinflammatory response [18,20].
Breakdown of gut barrier defenses allows increased
permeability, thinning of the mucus layer, and
accelerated apoptosis of the intestinal epithelium.
Immune dysregulation presents as the Systemic
Inflammatory Response Syndrome (SIRS), the emer-
gence of a virulent pathobiome is seen as ‘gut sepsis’,
and the ensuing pathophysiology contributes to
multiple organ failure [21,22].
The benefits from bathing the mucosa (with
enteral nutrition) include supporting the popula-
tion of the commensal microbiome, maintaining
gut barrier defenses, and promoting a robust but
appropriate immune response. Failing to take
advantage of introducing enteral nutrition results
in adverse consequences from not using the gut
[18,19].
On the contrary, introducing luminal nutrients
into critically ill patients with septic shock (receiv-
ing vasopressor) increases the risk of EFI and gastro-
intestinal dysfunction. Klanovicz et al. [23] applied
the European Society of Intensive Care Medicine’s
acute gastrointestinal injury (AGI) criteria to 163
mechanically ventilated patients with septic shock
and found AGI was frequent during the first week of

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ICU admission. AGI risk/dysfunction was found in
87% and AGI failure in 12% and higher heart rate
and lower mean arterial pressure were identified in
patients with AGI failure [23]. In an analysis of more
than 15 000 patients from an International Nutri-
&
tion Survey, Heyland et al. [24 ] found that sepsis is
associated with EFI (OR 1.34; 95% CI 1.17–1.54) and
the daily mortality hazard ratio increased by a factor
of 1.5 (95% CI 1.4–1.6; P < 0.0001) once EFI
occurred. As observed in the NUTRIREA trials, NOBI
is the gravest form of EFI [18]. NOBI is associated
with substantial morbidity and mortality and pre-
dicting it remains challenging [25].
STRATIFYING ENTERAL FEEDING
INTOLERANCE
The gut has a range of functions, but the symptoms
of gastrointestinal dysfunction have been limited to
detecting dysmotility in the traditional form of
hypoactive bowel sounds, abdominal distention,
nausea/vomiting, and cessation of passing gas and
stool [25,26]. However, clinical issues related to EFI
are counterintuitive. While traditional signs of dys-
motility occur in up to 85% of critically ill patients,
enteral nutrition is usually successful in over 90%
[27]. Over the past decade, there has been tremen-
dous effort to define EFI, but the counterintuitive
nature makes such a strategy difficult.
It may be more important to designate two
distinct levels of gastrointestinal dysfunction that
correlate to outcomes. Low-risk gastrointestinal dys-
function would be identified by bedside clinical
monitors of reduced bowel sounds, constipation
and obstipation, abdominal distention, and nau-
sea/vomiting. High-risk gastrointestinal dysfunc-
tion would be represented by increased intra-
abdominal hypertension, abdominal compartment
syndrome, and NOBI. Notably, the signs and symp-
toms of low-risk gastrointestinal dysfunction may
become an indication of high-risk gastrointestinal
dysfunction in patients with greater severity
of illness.
BEDSIDE AND BIOCHEMICAL MONITORS
OF GASTROINTESTINAL FUNCTIONS FOR
GUIDING NUTRITION THERAPY
Accurate clinical and biochemical markers predict-
ing EFI and gastrointestinal dysfunction are not
available. A recent scoping review found a lack of
a gold standard for monitoring gastrointestinal
functions in critically ill patients [26]. In a recent
systematic review assessing the accuracy of bio-
markers for NOBI, Reintam-Blaser et al. [31] found
18 biomarkers lacked sensitivity and specificity to
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Enteral nutrition in septic shock Patel et al.
predict NOBI. Recently, Franzosi et al. [32] collected
clinical parameters in 141 mechanically ventilated
patients with septic shock who tolerated and did not
tolerate nutrition therapy. At 12 h, mottling score
was a predictor of nutrition therapy failure [relative
risk (RR) 1.28, 95% CI 1.09–1.50] and over 48 h,
higher mottling score, higher serum lactate, and
higher norepinephrine dose were observed in
patients with nutrition intolerance, compared to
those who tolerated nutrition therapy [32]. Mottled
skin for predicting EFI in mechanically ventilated
patients with septic shock is compelling but war-
rants further evaluation.
Low-risk signs and symptoms do not serve the
clinician as a straightforward ‘start/stop sign’ for
initiating enteral nutrition and clinicians should
utilize these signs as bedside monitors with caution
and in context with severity of illness. Diarrhea as a
general bedside monitor is problematic because it is
related to EFI or bowel dysfunction in 20% of cases
[25,28]. The cause of diarrhea in the ICU is often
related to low volume incontinence, which may not
represent true diarrhea. The true cause of diarrhea in
the ICU is often linked to medications, reported in
over 60% of cases, and related to sorbitol, laxatives,
enemas, or suppositories used in a bowel regimen, or
antifungal or antibiotic agents [29]. Clostridioides
difficile is a cause for diarrhea in 17% [29].
Gastric residual volumes (GRVs) are a poor
marker of any adverse event related to enteral nutri-
tion, including nausea/vomiting, delayed gastric
emptying, regurgitation, aspiration, or pneumonia
[28]. Monitoring GRV does not protect against aspi-
ration or regurgitation, and monitoring has consis-
tently been an impediment to delivering enteral
nutrition [7]. Definitions of gastrointestinal dys-
function and EFI are overly dependent on GRVs,
and efforts to resurrect the use of GRV to the list of
intolerance monitors should be avoided [7]. Gastro-
intestinal bleeding in the ICU is usually not related
to and often decreases with enteral nutrition, as it
stimulates mucosal blood flow and reduces the risk
of stress gastritis [30]. Postrandomization occur-
rence of gastrointestinal bleeding was not reported
in the NUTRIREA-2 and NUTRIREA-3 trials and
reported in 4 of 3957 (0.1%) of patients in the
TARGET trial and eight of 1197 (0.7%) patients in
the enteral nutrition arm of the CALORIES trial
&&
(Table 1) [3,4 ,6,8].
Without context of severity of illness, presence or
absence of low-risk signs correlate poorly to true
gastrointestinal motility and function. Their pres-
ence may reflect clinical factors other than true gas-
trointestinal disease, such as co-interventions,
prolonged bed rest, or use of certain medications
including narcotics and sedatives [7,8]. Furthermore,
www.co-criticalcare.com 169
Gastrointestinal system
low-risk signs and symptoms may improve with
enteral nutrition initiation. Early provision of enteral
nutrition may prevent the emergence of these signs
and symptoms, minimizing the development of
abdominal distension, ileus, and the likelihood for
cessation of passing stool and gas. Delays in initiating
enteral nutrition may worsen these signs and symp-
toms [15]. Observing the patient response to the
‘challenge’ of initiating enteral nutrition may be
more useful to the clinician than the pretreatment
presence of these signs and symptoms.
CONCLUSION
Septic shock disrupts gut barrier functions and lumi-
nal nutrients have been shown to preserve them. In
the NUTRIREA-2 and NUTRIREA-3 trials, patients
with predominant septic shock receiving high-dose
vasopressor who were randomized to early full-dose
nutrition during the first week of critical illness had
more gut and nongut-related complications. There-
fore, introducing early full-dose enteral nutrition in
critically ill patients with greater severity of illness
receiving higher vasopressor dose is harmful and
poses a question: what is the goal for enteral nutrition
in the early acute phase of critical illness? Initiation of
enteral nutrition in patients with septic shock is an
exercise in assessing benefit (preserving gut barrier
functions) and harm (gastrointestinal dysfunction,
including NOBI). Early assessment should be done
with three crucial parameters in mind: norepinephr-
ine dose less than 0.3 mg/kg/min, enteral nutrition
dose less than 25% of protein/calorie requirements
and predicted mortality less than 40% using validated
severity of illness scores (e.g., SOFA score <9). If these
parameters are met, the window of opportunity may
be open to achieve the goal of preserving gut integrity
and barrier functions by using restricted dose enteral
nutrition to minimize complications. Recognizing
when these parameters are exceeded, however,
should alert the clinician of a significant increase in
risk for developing complications. Low-2risk signs
and symptoms carry more importance and may
become an indication of high risk in the critically
ill patient in septic shock when any one of these risk
parameters are not met. Overall, the findings from the
NUTRIREA-2 and NUTRIREA-3 trials lend credibility
towards a ‘less is more’ enteral nutrition strategy
during the early acute phase of critical illness.
Acknowledgements
None.
Financial support and sponsorship
None.
170 www.co-criticalcare.com
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Conflicts of interest
Jayshil Patel has consulted or Baxter and has served on
an advisory board for Fresenius Kabi. Juan Carlos Lopez
Delgado and Christian Stoppe have no conflicts of inter-
est. Stephen McClave has served as an education con-
sultant for Nestle, Abbott, and Fresenius Kabi.
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