Enteral Nutrition in the Critically Ill: Myths and

Misconceptions
Paul E. Marik, MD, FCCM, FCCP, ABPNS

Background: Nutritional support is an essential component of the

management of critically ill and injured ICU patients. Optimal provision of calories and protein has been demonstrated to reduce
morbidity, mortally, and length of ICU and hospital stay. Yet, a
large proportion of ICU patients receive inadequate nutrition.
Objective: To provide an evidence-base assessment of factors leading to inadequate enteral nutrition support in critically ill patients.
Data Source: Search of PubMed database and manual review of
bibliographies from selected articles.
Data Synthesis and Conclusions: A number of common myths and
misconceptions appear to play a major role in limiting the provision
of enteral nutrition in the critically ill. This article provides scientific data to debunk the most common myths and misconceptions
related to enteral nutrition. (Crit Care Med 2014; 42:962969)
Key Words: bowel sounds; enteral nutrition; ileus; myths; parenteral
nutrition; surgery

ver the past three decades, the understanding of the

molecular and biological effects of nutrients in maintaining homeostasis in the critically ill population has
made exponential advances. Nutrition support is now considered an essential component of the management strategy of
critically ill patients in the ICU (13). It has been well established that delivering early enteral nutritional (EN) support
reduces disease severity, diminishes complications, decreases
length of stay in the ICU, and favorably impacts patient outcome (110). Yet, a large proportion of ICU patients receive
inadequate nutritional support (1115). This appears to be
driven by a number of widespread myths and misconceptions
(1114, 16). This article reviews the most common misconceptions with the goal of optimizing nutritional support in critically ill patients.
Division of Pulmonary and Critical Care Medicine, Eastern Virginia Medical
School, Norfolk, VA.
The author has disclosed that he does not have any potential conflicts of
interest.
For information regarding this article, E-mail: marikpe@evms.edu
Copyright 2013 by the Society of Critical Care Medicine and Lippincott
Williams & Wilkins
DOI: 10.1097/CCM.0000000000000051

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MYTH NO. 1: STARVATION OR

UNDERNUTRITION IS OKAY
Nutrition is essential for survival. Adequate nutrition is essential for the critically ill patient to support anabolism, ameliorate uncontrolled catabolism, maintain a competent immune
system, and ultimately improve patient outcome. Nutrition
support attenuates the metabolic response to stress, limits oxidative cellular injury, and favorably modulates the immune
response (1721). In a large observational study conducted
in 167 ICUs, Alberda et al (15) demonstrated a strong association between the reduced provision of energy and protein
and worse outcomes. Weijs et al (22) demonstrated that optimal nutritional therapy (calories and protein) in mechanically ventilated critically ill patients was associated with a 50%
decrease in 28-day mortality. Similarly, Allingstrup et al (23)
demonstrated that in severely ill ICU patients, a higher provision of protein was associated with a lower mortality. The
energy deficit accumulated by underfeeding patients during
their ICU stay has been shown to be an important factor in
increasing the risk of adverse outcomes (2426). It, however,
needs to be recognized that these are observational studies
that may be confounded by severity of illness; less sick patients
who tolerate EN better are more adequately fed and have better outcomes. Despite this limitation, the Society of Critical
Care Medicine (SCCM) and American Society of Parenteral
and Enteral Nutrition (ASPEN) guidelines (1), as well as the
Canadian (3, 27) and European guidelines (2), all recommend
that EN be initiated within 48 hours in the critically ill patient
who is unable to maintain volitional intake. It is important to
emphasize that there is no known illness or disease that has
been demonstrated to benefit from starvation. However, it is
not uncommon for critically ill patients to be starved. In the
SepNet point prevalence study conducted in Germany, 10%
of ICU patients with sepsis received no nutritional support,
whereas only 20% received EN exclusively (11).
The role of an initial strategy of trophic feeding (or permissive underfeeding) in the critically ill patient is controversial. The EDEN study randomized patients (n = 1,000) with
acute lung injury to receive either trophic (20 kcal/hr) or full
feeding (2530 kcal/kg/d) for the first 6 days (28). After day
6, all patients who were still receiving mechanical ventilation
received the full feeding protocol. There was no difference in
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the number of ventilator-free days (primary outcome), 60-day

mortality, and other secondary endpoints between groups.
Follow-up of these patients showed no difference in physical
function (as assessed by the SF-36 questionnaire), psychological and cognitive function, and quality of life at 12 months (29).
The patients enrolled in the EDEN trial were well-nourished
overweight patients (mean body mass index, 30kg/m2) (28).
Moderate obesity has been shown to be protective during critical illness, the so-called obesity paradox (30). The findings of
the EDEN study may therefore not be generalizable to critically
ill patients who are malnourished. The results of the EDEN
trial are similar to a smaller study (n = 200) conducted by Rice
et al with a similar study design and patient population to the
EDEN trial (31). In the absence of a proven benefit of permissive underfeeding, critically ill patients should receive 20-25
kcal/kg/d and 1g/kg/d protein. The benefits of higher quantities of protein are controversial, with the SCCM/ASPEN guidelines recommending 1.22.0 g/kg/d (1), with some authorities
recommending up to 2.5 g/kg/d (32). However, increased provision of protein has not been demonstrated to limit muscle
wasting, loss of lean body mass, or improve clinical outcomes.
Bowel rest was popularized in the 1970s for the treatment
of active Crohn disease, colitis, acute and chronic pancreatitis, diverticulitis, and a number of other gastrointestinal (GI)
disorders (3339). It was postulated that EN would enhance
inflammation in these disorders while bowel rest would prevent further damage by removing the stimulus of luminal antigens and stimulation of bowel function. However, the concept
of bowel rest is seriously flawed. Starvation does not inhibit
bowel function, and this approach is akin to inducing asystole
to rest the heart. Starvation decreases splanchnic blood flow
and results in profound structural and functional changes to
the GI tract (see Myth No. 2: Parenteral Nutrition Is Safe section). Furthermore, recent data suggest that EN particularly
with a lipid- and protein-rich formula has a profound antiinflammatory effect on the GI mucosa (the gut-brain immune
axis) (40). The luminal presence of a lipid- and protein-rich
nutrition triggers a vagal reflex via peripheral cholecystokinin-1 receptors, which reduces local and systemic activation of
peripheral nicotinic acetylcholine receptors on inflammatory
cells (40). These data suggest that bowel rest is unlikely to be
beneficial. Indeed, EN has been demonstrated to improve the
outcome of the GI disorders for which bowel rest was considered the standard of care (4143).

MYTH NO. 2: PARENTERAL NUTRITION

IS SAFE
It is now widely accepted that the GI tract is the preferred route
of delivering nutritional support (44). Furthermore, consensus
guidelines strongly recommend enteral over parenteral nutrition (PN) in critically ill patients (13). The institution of
early EN in critically ill medical and postoperative patients has
been demonstrated to improve outcome (4, 6). Yet, PN continues to be widely used in patients who can be fed enterally. The
adverse sequela associated with PN results from the double
hit of not directly feeding the bowel, as well as the metabolic,
Critical Care Medicine

immunologic, endocrine, and infective complications associated with infusing a solution with a high glucose concentration and fat globules into a patients systemic venous system
(45). PN bypasses the gut and liver. EN stimulates the release
of a wide variety of enterohormones that play a crucial role in
regulating gut function and metabolic pathways. Furthermore,
the portal system supplies the liver with a rich source of nutrients and hormones, which are essential for hepatic function.
Lack of enteral feeding results in GI mucosal atrophy, bacterial
overgrowth, increased intestinal permeability, and translocation of bacteria and/or bacterial products. In a large cohort of
critically ill patients, Grau et al (46) demonstrated that PN was
strongly associated with the development of liver dysfunction,
whereas early EN was protective. EN has a major effect on the
gut-associated lymphoid tissue (GALT), which is the source of
most mucosal immunity in humans. PN results in rapid and
severe atrophy of this tissue (4750). In addition, to its effects
on the GALT, PN impairs humoral and cellular immunologic
defenses. PN is associated with impaired leukocyte chemotaxis, impaired phagocytosis, impaired bacterial and fungal
killing, and an attenuated inflammatory response (5153). PN
is associated with increased free radical formation (54); this
complication may be of considerable importance in critically
ill patients.
Heyland et al (55) performed a meta-analysis of PN (compared with no nutritional support) in critically ill patients.
These authors demonstrated that PN almost doubled the risk
of dying (relative risk [RR], 1.78; 95% CI, 1.112.85). The
SCCM/ASPEN guidelines state that Enteral nutrition is the
preferred route of feeding over parenteral nutrition (PN) for
the critically ill patient who requires nutrition support therapy
(Grade: B) and that if early EN is not feasible or available
the first 7 days following admission to the ICU, no nutrition
support therapy should be provided (1). However, if there is
evidence of protein-calorie malnutrition at admission and all
attempts at providing EN fail, the guidelines suggest that it is
appropriate to initiate PN as soon as possible following admission and adequate resuscitation (1, 5659).
Recently, the concept of supplemental PN has been popularized in patients who have a short-term contraindication to
EN or until full caloric goals are achieved (60). In a landmark
study, Casaer et al (61) randomized 4,640 ICU patients to either
early (within 48hr) or delayed (day 8) supplemental PN. In
this study, for every outcome measure investigated, the patients
who received early PN did worse. This included a group of
patients who received no concomitant EN (62). Furthermore,
they demonstrated a dose-response relationship; the more
PN the patients received, the greater the likelihood of harm.
Heidegger et al (63) randomized ICU patients to supplemental PN (between day 4 and day 8) or EN alone. Although the
published data suggested a lower rate of nosocomial infections
in the patients receiving supplemental PN, an intention-totreat analysis failed to show this benefit (64, 65). Furthermore,
there was no difference between groups for any of the secondary outcomes. Doig et al (66) randomized 1,372 patients
with relative contraindications to early EN to early PN or
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pragmatic standard of care. There was no difference in 60-day

mortality, ICU, or hospital length of stay although the early PN
group required 0.47 fewer days of ventilation. The study was
conducted over 5 years in 31 hospitals in Australia and New
Zealand; the number of screened patients nor the reasons why
EN was contraindicated were not provided. However, 62% of
those enrolled in this study were surgical patients; it is likely
that EN was not contraindicated in many of these patients (see
Myth No. 7: EN Is Contraindicated in Patients Without Bowel
Sound and/or a Postoperative Ileus section). The results of these
three studies fail to demonstrate a benefit from supplemental
PN (61, 63, 66). Furthermore, although limited short-term
PN may not be harmful (or beneficial), larger amounts of PN
appear to be associated with harm (62). The 2013 Canadian
Clinical Practice Guidelines strongly recommend that early
supplemental PN and high intravenous glucose not be used in
unselected critically ill patients (27).

MYTH NO. 3: EN CONTRAINDICATED WITH

VASOPRESSORS
Many critically ill patients are hemodynamically unstable and/or
require vasopressors/inotropes to maintain adequate blood pressure and cardiac output. Vasopressors improve hemodynamics by shunting blood from the gut and other peripheral organs
(i.e., bone marrow, skin, and kidneys) to the central circulation.
These nonessential organs are more sensitive to vasoconstriction than are central essential organs (i.e., heart and brain).
Thus, the effect of vasoconstrictor medications and hypotension
is a decrease in gut blood flow. It has, therefore, been postulated
that because these patients have limited oxygen delivery and that
by increasing GI oxygen demand with enteral feeding, intestinal
ischemia will develop. However, these propositions are based on
evidence from animal models where the mesenteric artery was
occluded and in patients with atherosclerotic occlusion of the
mesenteric arteries (67). Based on this information, many clinicians believe that EN will cause bowel ischemia and is contraindicated in patients receiving pressors. Anecdotal cases reports
of mesenteric ischemia in trauma patients receiving vasopressor agents (see below) are often cited to support this belief (68).
However, this theory is incorrect. Indeed, both experimental and
clinical studies demonstrate that EN increases gut blood flow and
protects against bowel ischemia. In the experimental and clinical
setting, enteral infusion of nutrients prevents adverse structural
and functional alterations of the gut barrier, increases epithelial
proliferation, maintains mucosal integrity, decreases gut permeability, improves gut blood flow, and improves local and systemic
immune responsiveness. These effects are mediated via both
direct and indirect (i.e., hormonal and neuronal) effects (6971).
In endotoxic and septic shock models, enteral feeding
improved hepatic artery and portal vein blood flow, superior
mesenteric artery blood flow, intestinal mucosal microcirculatory flow, hepatic microcirculatory flow, hepatic and intestinal tissue oxygenation, and hepatic energy stores (70, 72,
73). These experimental data have been confirmed by clinical studies. Revelly et al (74) evaluated EN in nine patients
requiring hemodynamic support by catecholamines 1 day
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after cardiac surgery. Patients were fed with postpyloric feeding tubes. During enteral feeding, cardiac index, indocyanine
green clearance, and glucose absorption increased while gastric tonometry remained unchanged. Similarly, Berger et al
(75) demonstrated close-to-normal paracetamol area under
the curve (a test of intestinal absorption) in hemodynamically unstable cardiac surgery patients receiving EN. Overall,
these studies indicate that enteral nutrients improve gut blood
flow with preservation of the bowel absorptive capacity during
vasopressor administration. The benefits of early EN in critically ill patients treated with vasopressors are supported by a
multicenter study, which demonstrated a lower hospital mortality in patients fed within 48 hours (34% vs 44%, p < 0.001)
(76). In this study, the benefits of early EN were greatest in the
sickest patients and those receiving multiple vasopressors.

MYTH NO. 4: EARLY EN IS NOT IMPORTANT

IN PATIENTS RECEIVING MECHANICAL
VENTILATION
The initiation of EN is often delayed in patients receiving
mechanical ventilation. It is likely that nutrition is not considered a priority and thus pushed to the back burner while
more acute issues take precedence. Furthermore, many may cite
older guidelines that stated that it was acceptable for mechanically ventilated patients to go a week without nutrition. In the
German Competence Network Sepsis (SepNet) study, mechanical ventilation was a strong predictor for the failure to provide
EN (11). Artinian et al (6) performed a retrospective analysis
of a prospectively collected large multicenter ICU database to
determine the impact of early enteral feeding on the outcome
of mechanically ventilated critically ill medical patients. In this
study, early EN (within 2 d of admission) was associated with
a significant reduction of ICU and hospital mortality. Barr et
al (77) demonstrated that the implementation of an evidencebased nutritional management protocol significantly shortened the duration of mechanical ventilation. In this study, EN
was associated with a reduced risk of death.

MYTH NO. 5: EN IS CONTRAINDICATED WITH

HIGH GASTRIC RESIDUAL VOLUME
Many clinicians monitor gastric residual volumes (GRV). The
presumption is that GRV measurements are accurate and useful markers for the risk of aspiration and pneumonia. Enteral
feeding is then interrupted when the GRV exceeds 150mL.
There is, however, no data to support this practice. High GRVs
(i.e., > 400mL) do not necessarily predict aspiration, and low
GRVs (i.e., < 100mL) are no guarantee that aspiration will not
occur. Interrupting EN when the GRV exceeds 100200mL
has not been shown to decrease the prevalence of aspiration.
McClave et al (78) randomized critically ill ventilated patients
to two management strategies using a GRV more than 200mL
or GRV more than 400mL for interrupting gastric feeding. In
this study, the prevalence of aspiration was similar between
groups. Similarly in a prospective multicenter study, Montejo et al (79) randomized patients to a control group (GVR
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> 200mL) or an intervention group in which tube feeds were

held when the GRV exceeds 500mL. In this study, there was no
difference in the risk of pneumonia, ventilator-free days, organ
failure, or mortality between groups. More recently, Reignier et
al (80) randomized mechanically ventilated patients to a group
in which the GVR was not monitored and a group in whom
tube feeds were held when the GRV exceeded 250mL. These
investigators demonstrated no difference in the risk of pneumonia between groups; however, the proportion of patients
receiving their caloric goal was higher in the no-GRV group.
It should, however, be noted that in this study, patients with
abdominal surgery within the past month; a history of esophageal, duodenal, pancreatic, or gastric surgery; a history of GI
bleeding; and contraindications to prokinetic agents were
excluded. These data suggest that there is poor relationship
between GVR and the risk of aspiration. Monitoring GVR may
not be necessary in patients at low risk for aspiration and may
only serve to reduce the amount of nutrition provided.

MYTH NO. 6: POSTPYLORIC FEEDING

REDUCES THE RISK OF ASPIRATION
As an extension of the myth that the GRV is associated with the
risk of aspiration pneumonia, many clinicians believe that all
critically ill patients should receive postpyloric feeding. Cleary,
there are some critically ill patients who have impaired gastric
motility (especially patients with diabetes) who cannot tolerate
early gastric feeds in whom EN is tolerated if delivered beyond
the pylorus (81). However, there is little consensus regarding
the issue as to whether the routine use of postpyloric feeding
decreases the risk of aspiration pneumonia. We performed a
meta-analysis comparing the risk of pneumonia in patients fed
gastrically versus postpylorically (82). In this meta-analysis,
the risk of pneumonia was unrelated to the route of feeding.
Ho et al (83) reported similar findings. However, a meta-analysis by Alhazzani et al (84) demonstrated a small reduction in
the risk of pneumonia with small bowel feeding without affecting mortality, ICU length of stay, or duration of mechanical
ventilation. We suggest placement of an orogastric tube and
early (within 12hr of ICU admission) initiation of EN in all
mechanically ventilated patients. In those patients who demonstrate intolerance to gastric feeding (abdominal distension,
regurgitation), we suggest the use of prokinetic agents (81, 85,
86). Should this approach fail, we would then place a postpyloric feeding tube. In patients with known gastric dysmotility
and those who are nursed supine (e.g., extracorporeal membrane oxygenation patients), we would suggest early placement
of a postpyloric feeding tube.

MYTH NO. 7: EN IS CONTRAINDICATED IN

PATIENTS WITHOUT BOWEL SOUND AND/OR
A POSTOPERATIVE ILEUS
In 1905, Cannon (87) was the first clinician to formally suggest a relationship between abdominal auscultation and bowel
function. Remarkably, abdominal auscultation has become part
of the standard physical examination of patients, and yet, no
Critical Care Medicine

studies have validated the value of this maneuver. Historically,

ICU nurses have been trained to auscultate each of the four
abdominal quadrants for the presence of bowel sounds, with
the presence of bowel sounds indicating that it is safe to feed
patients. Similarly, the return of bowel sounds after abdominal
surgery has been regarded as an indicator of the resolution of
postoperative ileus and an indicator that it is safe to commence
EN. However, the absence of bowel sounds does not mean that
the bowel is not working. Bowel sounds result from air moving through the small intestine. The presence of bowel sounds
requires swallowing of air and gastric emptying. Many seriously
ill patients have little movement of air from the stomach to the
small intestine and therefore have decreased bowel sounds. The
absence of bowel sounds after operation seems to result from
the emptiness of the gut. When fluid and air is injected into
the duodenum, sounds can be heard immediately (88).
Waldhausen et al (89) measured GI myoelectric and clinical
patterns of recovery after laparotomy. Small bowel myoelectric
activity returned immediately after surgery, whereas it took on
average 2.4 days for the return of bowel sounds and 5 days for
the passage of flatus. These authors were unable to find any correlation between bowel myoelectric activity and bowel sounds.
These data suggest that ausculting for bowel sound has limited
clinical utility and should not be used to guide the initiation of
EN. Indeed, multiple clinical trial have shown improved outcome with the early initiation of tube feeds following abdominal surgery in spite of the absence of bowel sounds or the
passage of flatus. Current guidelines recommend that in the
ICU patient population, neither the presence nor the absence
of bowel sounds nor evidence of the passage of flatus or stool
is required for the initiation of enteral feeding (1).

MYTH NO. 8: EN IS CONTRAINDICATED

FOLLOWING GI SURGERY
Classic surgical teaching suggests that due to reflex inhibition,
the alimentary tract becomes inactive after abdominal surgery
(88). The period of inactivity or postoperative ileus is thought to
last for 35 days during which time the patient is tided over by
gastric aspiration and parenteral fluids (88). It has been assumed
that the postoperative ileus precludes enteral feeding. Furthermore, it has been suggested that bowel distention following
enteral feeding would disrupt the anastomoses. Consequently,
EN is frequently withheld from postoperative abdominal surgery patients, particularly those with fresh GI tract anastomoses.
This approach is detrimental to patients and without scientific
evidence. Motility studies demonstrate return of small bowel
peristalsis within hours after laparotomy providing support
for early postoperative EN (89, 90). Over 30 years ago, Moss
(91) demonstrated the benefits of immediate EN following
laparotomy and colorectal excision. In this study, a full-strength
elemental diet was delivered into the duodenum immediately
postoperatively. Using radiolabelled albumin, he demonstrated
that 94% 4% of the albumin was absorbed with achievement
of a positive protein balance by 5 hours postoperatively. Furthermore, barium motility studies performed on the first postoperative day demonstrated clinically adequate peristalsis.
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In a canine model, Kawasaki et al (92) compared the effects

of EN versus PN on GI motility after open abdominal surgery.
They demonstrated that EN hastened recovery of GI motility.
Therefore, early postoperative enteral feeding may be an effective way to decrease the duration of postoperative ileus. This is
based on the fact that enteral feeding stimulates reflexes that
produce coordinated propulsive bowel activity and increase
the secretion of GI hormones that increase bowel motility (93).
Hence, early EN appears to be an effective means of treating an
ileus with starvation only serving to prolong the ileus.
The GI tract produces approximately 6L of fluid per day,
and it is illogical to propose that an additional liter or so of
tube feeds will cause excessive distention of the bowel with
anastomotic dehiscence. Furthermore, wound healing is critically dependent on an adequate supply of protein; starvation
with protein catabolism is likely to increase the risk of wound
dehisce. In an animal model, Moss et al (94) demonstrated
that early enteral feeding doubled the bursting pressure of
the colorectal anastomosis, with the anastomoses containing
significantly higher concentration of collagen and collagen
precursors than those of the unfed controls. Multiple experimental studies have demonstrated that early EN following
bowel surgery is associated with improved wound healing,
greater wound strength, and higher wound hydroxyproline
and collagen accumulation (95100). This may explain the
lower risk of anatomic leaks and fistulas in bowel surgery
patients who receive early enteral as opposed to delayed feeding or PN (5, 9, 101).
The experimental data demonstrating the benefit of early
EN are supported by a large number of studies which have
demonstrated the safety and improved outcomes associated
with early EN in patients who have undergone both small and
large bowel surgery. In 2001, we published a meta-analysis
of 15 randomized controlled trials that compared early with
delayed EN in postoperative patients (4). We demonstrated
that early EN was associated with a significantly lower risk of
infection (RR, 0.45; 95% CI, 0.30.66) and reduced length of
hospital stay (mean 2.2 d; 95% CI, 0.813.63 d). More recent
meta-analyses have reproduced these findings (5, 10). These
data clearly demonstrate that early EN following GI surgery is
feasible and that this intervention improves patient outcomes.
Concern has been raised that early enteral feeding may
cause bowel ischemia following abdominal surgery (68). This
is a very rare complication that was reported predominantly
between 1986 and 2000 with isolated cases reported subsequently (102108). Most of these patients had sustained traumatic injuries, and almost all had undergone a laparotomy with
surgical placement of a jejunostomy tube (68, 102104). Small
bowel necrosis is very rare in postoperative patients who are
initiated on early enteral feeding. Nevertheless, enteral feeding
should be advanced slowly in patients at risk (severe abdominal trauma, large burns), and they should be discontinued in
patients who developed abdominal complaints, such as pain,
distention, and vomiting, until the status of bowel integrity can
be evaluated. A semielemental formula may be advantageous
in these patients.
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MYTH NO. 9: EN IS CONTRAINDICATED IN

PATIENTS WITH AN OPEN ABDOMEN
Decompressive celiotomy has reduced the mortality of patients
with abdominal compartment syndrome (109). The management of these patients is challenging with the approach to the
route and timing of nutritional support being controversial.
Many patients are kept nil per os or receive PN on the assumption that these patients cannot be fed enterally due to bowel wall
edema and bowel dysfunction. However, clinical studies have
demonstrated that early EN is feasible in patients with an open
abdomen and that this approach is associated with improved
outcomes (110112). Collier et al (101) demonstrated that early
enteral feeding (within 4 d of celiotomy) was associated with
earlier closure of the abdominal cavity and less fistula formation when compared with the delayed initiation of EN.

MYTH NO. 10: EN IS CONTRAINDICATED IN

PATIENTS WITH PANCREATITIS
In patients with acute severe pancreatitis, classic teaching
suggested that total parenteral nutrition should be initiated
promptly and should judiciously replace nutrient deficits and
provide the extra energy imposed on the patient by the inflammatory process (113). It was claimed that this approach was
essential to rest the pancreas and that PN reduced mortality
(113). EN was considered an absolute contraindication as it
would stimulate the pancreas and worsen pancreatic inflammation. Randomized clinical trials comparing EN versus PN in
patients with moderate and severe pancreatitis have, however,
proven these recommendations to be wrong. Meta-analyses
have demonstrated that EN as compared with PN reduces
infectious complications (particularly pancreatic abscesses),
organ failure, length of hospital stay, and mortality (43, 114,
115). Nutritional support should be viewed as an active therapeutic intervention that improves the outcome of patients
with acute pancreatitis. EN should begin within 24 hours after
admission and following the initial period of volume resuscitation and control of nausea and pain. Patients with mild acute
pancreatitis should be started on a low-fat oral diet. In patients
with severe acute pancreatitis, EN may be provided by the gastric or jejunal route (114).

MYTH NO. 11: PATIENTS MUST BE FED

SEMIRECUMBENT AT 45
In an article published in 1999, Drakulovic et al (116) demonstrated a lower frequency of clinically suspected ventilator-associated pneumonia (VAP) in 39 intubated patients randomized
to the semirecumbent (45) as opposed to the supine body
position (47 patients). In this study, the risk of pneumonia was
highest for patients receiving EN in the supine body position.
Based on this small single-center study, it became standard of
care to nurse all ICU patients in a semirecumbent 45 position
particularly when receiving tube feeds. Indeed, the Centers for
Disease Control and Prevention (117), the Agency for Healthcare Research and Quality (118), and the Institute for Healthcare Improvement (119) suggest elevating the head of the bed to
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45 above horizontal to reduce gastroesophageal reflux and the

prevalence of nosocomial pneumonia. The results of the study
by Drakulovic et al (116) have, however, not been reproduced.
Van Nieuwenhoven et al (120) randomized 112 intubated
patients to the semirecumbent position with a target backrest
elevation of 45 and 109 patients to a supine position with a
backrest elevation of 10. Average elevations were 9.8 and 16.1
at day 1 and day 7, respectively, for the supine group and 28.1
and 22.6 at day 1 and day 7, respectively, for the semirecumbent group. The target semirecumbent position of 45 was not
achieved for 85% of the study time, and these patients more
frequently changed position than supine-positioned patients.
There was no difference in the risk VAP or any other outcome
variable between groups. In an observational study of 66 ventilated patients, Grap et al (121) reported a mean backrest elevation of 21.7 with no association between backrest elevation and
the Clinical Pulmonary Infection Score. Rose et al (122) performed 2,112 backrest elevation measurements in 371 patients
in 32 ICUs. Backrest elevation more than or equal to 45 was
recorded in 5.3% of instances and elevation of between 30 and
45 in 22.3% of instances (122). In this study, the mean backrest elevation was 23.8. These studies suggest that nursing a
patient semirecumbent at 45 is not feasible and attempts to do
so may not reduce the risk of VAP. When the head of the bed is
inclined at 45, the patient often slides down; most of the weight
of the upper body is applied on the sacral area, and this position
becomes uncomfortable for the patient. Furthermore, experimental models suggest that the semirecumbent position may
enhance the flow of mucous into the lungs with an increased
risk of bacterial colonization and pneumonia (123). Although
maintaining a patient supine (0) probably increases the risk
of pneumonia, there is no strong evidence that elevation of the
head of the bed between 10 and 30 is associated with a greater
risk of pneumonia than a semirecumbent 45 position.

CONCLUSION
We demonstrate that numerous myths and misconceptions
abound which act in concert to delay and limit the provision
of optimal nutritional support in critically ill patients. With
few exceptions, early EN is feasible and improves the outcome
of critically ill ICU patients. Such treatment should be considered the standard of care, and the early initiation of EN should
be used as an indicator of the quality of care delivered in ICUs.

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