594012

research-article2015
NCPXXX10.1177/0884533615594012Nutrition in Clinical PracticeKozeniecki and Fritzshall

Invited Review
Nutrition in Clinical Practice
Volume XX Number X
Enteral Nutrition for Adults in the Hospital Setting Month 201X 1­–18
© 2015 American Society
for Parenteral and Enteral Nutrition
DOI: 10.1177/0884533615594012
ncp.sagepub.com
hosted at
Michelle Kozeniecki, MS, RD, CNSC1; and Rebecca Fritzshall, MS, RD, CNSC1 online.sagepub.com

Abstract
In patients unable to tolerate oral intake, multiple options of nutrient delivery are available to the clinician. Administration of enteral
nutrition (EN) has long been considered the standard of care for nutrition support among patients unable to meet energy and protein
requirements orally. Healthcare practitioners must make careful decisions related to ordering, administering, and monitoring EN therapy.
In the hospital setting, the registered dietitian is a key resource in enteral formula selection and method of administration, monitoring
for and troubleshooting EN-related complications, and transitioning to oral feeding. The hospital setting also presents many unique
challenges in providing optimal nutrition to the enterally fed patient. (Nutr Clin Pract. XXXX;xx:xx-xx)

Keywords
enteral nutrition; adults; nutrition therapy; nutritional support; hospitalization; nutrition assessment; malnutrition

Introduction result from inadequate nutrient intake in the hospital setting,

Enteral nutrition (EN) is defined as nutrition provided through
the gastrointestinal (GI) tract via a tube, catheter, or stoma that
delivers nutrients distal to the oral cavity.1 Enteral access
allows the short- and long-term delivery of nutrients to the
digestive tract of patients who cannot maintain their require-
ments with oral intake. Administration of EN has long been
considered the standard of care among patients unable to meet
energy and protein requirements orally. As such, many hospi-
talized patients in the United States receive EN. According to
the latest available statistics from the National Center for
Health Statistics, patients received EN during approximately
251,000 hospital stays in 2012, 78% of which were adults.2
The provision of EN not only provides micronutrients and
macronutrients but also supports the functional and structural
integrity of the largest immune organ in the body—the gut.
Some of the physiologic changes induced by the delivery of EN
include stimulating blood flow to maintain adequate perfusion,
stimulating intestinal motility/contractility, maintaining villous
height, promoting insulin sensitivity, supporting commensal bac-
teria, and attenuating oxidative stress and the systemic inflamma-
tory response to illness, among other things3-7 (Figure 1). These
physiologic changes help maintain intestinal barrier function
and therefore prevent increases in gut permeability and decrease
the virulence of pathogenic organisms (eg, bacterial transloca-
tion) often seen in patients with host immune deficiencies,
immunosuppression, stress, hypoperfusion, and disturbances in
normal gut flora due to lack of enteral stimulation.8
The prevalence of malnutrition in hospitalized patients has
been estimated at 30%–60%, with up to 69% of patients experi-
encing a decline in their nutrition status during hospitalization,9
and published reports consistently describe incomplete delivery
of EN.10-12 To prevent the downstream complications that can
including increased morbidity and mortality related to iatrogenic
malnutrition, longer lengths of hospital stay, and increased hos-
pital costs, healthcare providers must pay close attention to the
adequacy of EN intake and adjust therapies on a frequent basis.
The purpose of this article is to provide a basic review of EN in
the adult hospitalized patient to guide clinicians in the manage-
ment of EN. An interdisciplinary team approach is required for
the successful navigation of nutrition assessment, patient and
enteral access device selection, enteral formula selection and
method of administration, monitoring for and troubleshooting
EN-related complications, and transitioning to oral feeding.
Nutrition Assessment
A complete nutrition assessment includes a review of the
patient’s medical, surgical, social, and diet history, anthropo-
metric measurements, and laboratory data, as well as a verbal
discussion with the patient and/or caregiver and completion of
a nutrition-focused physical assessment. The intent of the
nutrition assessment is to document baseline nutrition param-
eters, identify risk factors for malnutrition and specific nutrient
deficits, establish individual nutrition needs, and identify any
factors that may influence the provision of nutrition support
therapy.13
From 1Department of Nutrition Services, Froedtert Hospital, Milwaukee,
Wisconsin.
Financial disclosure: None declared.
Corresponding Author:
Michelle Kozeniecki, MS, RD, CNSC, Froedtert Hospital, 9200 W.
Wisconsin Ave, Milwaukee, WI, 53226, USA.
Email: michelle.kozeniecki@froedtert.com

Downloaded from ncp.sagepub.com at CAMBRIDGE UNIV LIBRARY on August 1, 2015

2 Nutrition in Clinical Practice XX(X)

Figure 1.  Nutrition and nonnutrition benefits of early enteral nutrition. AGEs, advanced glycolytic endproducts; GI, gastrointestinal;
IgA, immunoglobulin A; MALT, mucosal-associated lymphoid tissue. Reprinted with permission from McClave SA, Martindale RG,
Rice TW, Heyland DK. Feeding the critically ill patient. Crit Care Med. 2014;42:2600-2610.

Identifying and Diagnosing Malnutrition
Currently, there is no single laboratory test or panel that can
accurately or consistently diagnose malnutrition. Despite
their widespread use as nutrition markers, serum proteins
such as albumin, prealbumin, and transferrin are now well
established as negative acute phase reactants that are sensi-
tive to acute and chronic inflammation.14,15 Severe, sustained,
or repeated bouts of inflammation correlate with adverse out-
comes. Since serum proteins correlate with the patient’s over-
all severity of illness and level of inflammation, they can be
useful predictors of morbidity and mortality in hospitalized
patients.15,16
In 2012, a standardized, etiology-based approach to diag-
nosing malnutrition in the adult hospitalized patient was devel-
oped.17 This approach recognizes the effects of acute and
chronic disease-related inflammation and includes the assess-
ment of 6 characteristics, and their respective thresholds, for both
moderate and severe malnutrition. Identification of 2 of 6 malnu-
trition characteristics (weight loss, insufficient energy intake,
depletion of subcutaneous fat, depletion of muscle mass, decline
in handgrip strength, and fluid accumulation) is needed to
diagnosis protein-energy malnutrition. It is important to note that
malnutrition can occur at any body mass index (BMI) and that
hepatic proteins can be within normal ranges in patients with
pure starvation-associated (noninflammatory) malnutrition.
Energy Needs
Energy needs in the hospitalized adult patient are generally
based on age, sex, BMI, body composition, and clinical status.
A.S.P.E.N. consensus guidelines suggest that most adults
require a range of 20–35 kilocalories per kilogram (kcal/kg).18
Indirect calorimetry (IC), which measures whole body oxygen
consumption and carbon dioxide gas exchange to yield resting
metabolic rate, is considered the gold standard for determining
energy needs in the acute care setting.19 However, IC is often
unavailable due to its high cost and the specialized training
required. Therefore, a number of predictive equations have
been developed to estimate energy needs in various patient pop-
ulations, although results do not always correlate with IC across
all patient populations and can vary with obesity, age, and
severity of illness. If used, equations must be applied in patients
similar to the reference population from which the equation was

Downloaded from ncp.sagepub.com at CAMBRIDGE UNIV LIBRARY on August 1, 2015

Kozeniecki and Fritzshall 3
derived, with the understanding that clinical judgment is still
required. Regardless of the method used to determine energy
needs, it is essential to adjust energy provision based on the
patient’s clinical status and response to nutrition therapy.
Protein Needs
Protein is essential for the structure, maintenance, and growth
of cells, tissues, enzymes, hormones, antibodies, and transport
carries. Daily protein requirements are based on a patient’s
age, weight, nutrition status, and the degree of stress imposed
by disease or injury. The Dietary Reference Intake (DRI) for
protein for healthy adults is 0.8 g/kg.20 Hospitalized patients
often experience accelerated muscle catabolism and net nega-
tive nitrogen balance due to acute or chronic illness(es).
Metabolically stressed adult patients generally require 1.2–2.0
g/kg of protein.21,22 The goal of protein provision in metaboli-
cally stressed patients is to achieve positive nitrogen balance,
or a state in which protein synthesis exceeds protein break-
down. Nitrogen balance studies can be useful in assessing the
adequacy of protein intake, although these studies may be dif-
ficult to conduct in the hospital setting due to the need for com-
plete and accurate measurements of intake (via oral, enteral,
and/or parenteral routes) as well as output (including urine,
stool, fistula, wound, and ostomy losses).
Fluid Needs
Water is the most abundant substance in the body, accounting
for 50%–60% of body weight. Total body water does vary with
age, weight, sex, and adiposity. The goal of fluid management
is to maintain adequate hydration, tissue perfusion, and elec-
trolyte balance. Healthy adults usually require 30–40 mL/kg
daily to achieve fluid balance.21 Assessing fluid status in hospi-
talized patients requires physical examination and the assess-
ment of intakes and outputs, weights, laboratory values, and
vital signs. Most fluid is lost from the GI tract and kidneys,
although a significant amount of fluid can also be lost through
the lungs and skin. Metabolic changes, such as fever and
hyperthyroidism, and medical therapy, such as diuretics or
dialysis, can contribute to fluid losses as well.
Micronutrient Needs
Micronutrients are required for effective metabolism and bio-
chemical processes. A patient’s specific vitamin and mineral
requirements vary depending on the patient’s nutrition and
clinical status. A multivitamin/mineral supplement is war-
ranted when the nutrition support regimen does not provide
sufficient amounts and no other form of nutrition is provided.
Patient Selection
Hospitalized patients with a functional GI tract, who are unable
to meet energy and protein requirements orally, are generally
Downloaded from ncp.sagepub.com at CAMBRIDGE UNIV LIBRARY on August 1, 2015
candidates for EN therapy. When oral intake is deemed unsafe,
insufficient, or impossible, the clinician must consider the risks
and benefits of EN therapy in the context of the patient’s diag-
nosis, clinical status, and prognosis and determine whether EN
is consistent with the patient and/or family’s wishes.13 Some
examples of conditions that merit consideration for EN therapy
include endotracheal intubation, swallowing difficulty due to
dysphagia, altered mental status or delirium, luminal obstruc-
tion in the head and neck area, the esophagus, or the stomach
from malignancy, or poor oral intake resulting in weight loss
and/or malnutrition. Patients with hypermetabolic and hyper-
catabolic states such as trauma, burns, and malignancy may
also benefit from EN therapy, as it may be difficult for them to
meet the needs with oral intake alone.
Contraindications to enteral feeding may include patients
with intractable vomiting or diarrhea, severe GI malabsorp-
tion, paralytic ileus, GI ischemia, severe short bowel syn-
drome, or high-output enterocutaneous fistula. Relative
contraindications include intestinal obstruction, diffuse perito-
nitis, or when nutrition intervention is not warranted or desired
by the patient or proxy.
Timing of Enteral Nutrition
Initiation of EN should always follow a complete evaluation
of the patient’s disease state, medical condition, and the rela-
tive risks and benefits. The timing, however, may depend on
the indication for EN as well as the patient’s nutrition state.
For most hospitalized patients, initiation of EN is recom-
mended when oral intake is absent or likely to be absent for a
period of 5–7 days.23 However, earlier initiation may be war-
ranted in the moderately or severely malnourished patient to
support metabolic demands and prevent functional decline.
This concept is also reflected in recommendations for the
postsurgical patient population, which state that EN should
be considered within 7 days of surgery in the normally or
overnourished, within 3–5 days of surgery in the moderately
malnourished, and within 1–2 days of surgery in the severely
malnourished.23 In the critically ill population, it is recom-
mended that EN should be started early within the first 24–48
hours following admission to the intensive care unit (ICU)22
due to the beneficial effects on intestinal physiology and
immunity discussed previously.
Enteral Access
The selection of an enteral access device should depend on the
patient’s disease state, GI anatomy, function and accessibility,
and expected duration of therapy.13 Short-term access options
include placement through the nose or mouth with the tip of the
feeding tube terminating within the stomach, past the pylorus,
or distal to the ligament of Trietz. For EN therapy lasting > 4
weeks, more permanent access options include gastrostomy,
jejunostomy, and gastrojejunostomy tubes. For all patients who
require an enteral access device, close monitoring is required
4 Nutrition in Clinical Practice XX(X)
Figure 2.  Common French sizes of adult enteral access devices.
to maintain patient safety and prevent events such as inadver-
tent tube displacement.
Enteral access devices vary with respect to tubing material
and size, which is measured using the French (Fr) scale. The
French size is a measure of the external diameter of a catheter.
One French unit is equal to 0.33 millimeters, so the larger the
French size, the larger the catheter. The most common tube
sizes used in the adult population range from 8–24 Fr24,25
(Figure 2). Large-bore (≥ 14 Fr) short-term access tubes are
made of a stiff polyvinyl material, are less likely to clog, and
are easier and more reliable when aspirating gastric contents.
Small-bore (8–12 Fr) tubes are made of silicone, polyurethane,
or a mixture and are softer and more comfortable for the patient
but are more prone to clogging and more difficult to use for
aspiration of gastric contents.26
Oro/Nasoenteric
Oroenteric and nasoenteric feeding tubes may be used as short-
term access (< 4 weeks’ duration) until more definitive mea-
sures are implemented. They can also provide opportunities to
assess patient tolerance of EN prior to placement of permanent
feeding tubes. Oroenteric (ie, orogastric) tubes are limited by
patient discomfort and are better tolerated in intubated and
sedated or chemically paralyzed patients. Large-bore nasoen-
teric tubes, when used, should be replaced with a more pliable
tube of smaller diameter within 5–7 days to potentially reduce
morbidity and improve patient discomfort.25
Oroenteric and nasoenteric feeding tubes can be placed at
the bedside or using endoscopic or fluoroscopic techniques.
Complications that may arise from oroenteric or nasoenteric
tube placement include epistaxis, sinusitis, esophageal perfora-
tion, and unintentional placement into the bronchopulmonary
tree. Bedside placement of nasoenteric (gastric or small bowel)
feeding tubes can be achieved without the use of technology,
however, use of an electromagnetic tube placement device has
demonstrated success rates as high as 90%.27-29 Achieving
placement within the jejunum is most reliably achieved with
endoscopic or fluoroscopic techniques. As a rule, confirmation
of the feeding tube tip position should be obtained prior to the
initiation of enteral support.18,25
Contraindications to short-term enteral access include cer-
tain patterns of facial fracture, obstruction of the GI tract distal
Downloaded from ncp.sagepub.com at CAMBRIDGE UNIV LIBRARY on August 1, 2015
to the site of access, esophageal varices or diverticula for risk
of bleeding, head and neck cancers, and upper GI tract stric-
tures so narrow that a tube cannot be passed through it. Disease-
related or medication-induced coagulopathies should trigger
heightened awareness for complication but generally do not
preclude placement.25,26
Enterostomy
For long-term enteral access (> 4 weeks’ duration), percutane-
ous feeding tubes can be placed using surgical, endoscopic,
fluoroscopic, and radiologic techniques. These tubes are typi-
cally made of silicone or polyurethane with a diameter of 14–28
Fr, with the exception of percutaneous endoscopic jejunosto-
mies, which are 8–12 Fr.24 Anatomic alterations, presence of
ostomy sites or drain tubes, or surgical scars may alter the loca-
tion for tube insertion. Once placed, percutaneous endoscopic
gastrostomy tubes may be used for feedings within 2 hours in
the adult population.30 Contraindications to placement include
presence of ascites, neutropenia, peritonitis, and neoplastic,
inflammatory, or infiltrative disease of the gastric/abdominal
wall.31
Complications from surgically placed tubes may include
bleeding, peristomal leakage, skin and soft tissue infection,
incisional hernia, injury to intra-abdominal viscera, and com-
plications associated with general anesthesia. Delayed compli-
cations may include buried bumper syndrome, gastric ulcers,
fistulas, and tumor tract seeding.32 Most bumper-type tubes
will need to be replaced every 1–2 years, or earlier if breakage,
occlusion, or dislodgement occurs. Balloon-type tubes, which
are filled with 5–10 mL of sterile water, are often used after the
removal of a bumper-type tube. To prevent balloon deflation
due to water leakage, the balloon water volume should be
checked every week. Due to degradation of the balloons, this
type of tube requires replacement every 3–4 months.32
Gastric vs Small Bowel Access
Gastric access is appropriate in most cases, as it allows for
more normal nutrient digestion and absorption and more versa-
tility in feeding regimen. Feeding into the stomach stimulates
the gastric phase of digestion and does not bypass any potential
sites for nutrient absorption. Small bowel feeding access may
Kozeniecki and Fritzshall 5
be achieved by passing a feeding tube past the pylorus (duode-
nal placement) or past the Ligament of Treitz (jejunal place-
ment) and is most appropriate for patients with gastric outlet
obstruction, gastroparesis, gastric fistula, pancreatitis, and
known reflux and aspiration of gastric contents.30 Although
several studies have demonstrated no difference in aspiration
risk between intragastric and small bowel feeding,33,34 small
bowel feeding has been promoted as a means to avoid
aspiration.
Maintaining Patient Safety
Patient safety should always be considered when providing
medical therapies, including the provision of EN. Two unique
issues that clinicians encounter in the hospital setting are
patient-initiated device removal and the high potential for
enteral misconnections. It is important for all members of the
healthcare team to be aware of the risk factors for both and to
employ prevention strategies to avoid patient harm.
The frequency of nasogastric tube removal has been
reported to be 28.9%, the highest rate among all removed
devices.35 Patient characteristics found to be closely associated
with tube removal include disorientation, restlessness, agita-
tion, and anxiety.36 Premature discontinuation of therapeutic
devices, including nasoenteric and percutaneous enterostomy
devices, may result in patient harm or injury. Of particular con-
cern is if inadvertent removal occurs before stoma tract matu-
ration, which usually occurs within 7–10 days. If the stoma
tract is not mature, the replacement tube cannot be reintro-
duced through the same tract but, rather, near the original site
to maintain apposition of the stomach to the abdominal wall.31
In addition to the harm that can be caused by tube displacement
itself, lack of enteral access can contribute significantly to
feeding delays, preventing the patient from receiving adequate
nutrition delivery.37 Several strategies have been proposed to
prevent self-initiated device removal including taping nasoen-
teric tubes to the patient’s face, inserting nasal bridles to secure
nasoenteric tubes, and using hand mittens or restraints.38,39 For
combative patients with enterostomies, abdominal binders can
be useful adjuncts following placement to prevent them access
to their tube.25 Some institutions employ constant observers to
watch patients to maintain patient safety.
An enteral misconnection is “an inadvertent connection
between an enteral feeding system and a non-enteral system
such as an intravascular line, peritoneal dialysis catheter, tra-
cheostomy, medical gas tubing, etc.”40 More than 116 cases of
enteral misconnections were reported between 1972 and 2010,41
and they continue to occur. Inadvertently delivering EN through
an intravenous system is a very serious event that can result in
patient death from embolus or sepsis. Both human factors and
physical and design factors have been identified as contributors
to enteral misconnections. Human factors include time con-
straints, fatigue, inadequate training, less than optimal room
lighting, and patient transfers. Physical and design factors
Downloaded from ncp.sagepub.com at CAMBRIDGE UNIV LIBRARY on August 1, 2015
include the use of universal connectors (ie, Luer connectors),
which allow connection between many types of therapeutic
devices, as well as inadvertent disconnection.40,42,43 In 2006, the
Joint Commission issued a sentinel event alert regarding tubing
misconnections44 and urged product manufacturers to imple-
ment “incompatibility by design” features for small-bore con-
nectors. Since then, a new standard for small-bore connectors
has been developed,45 and changes to the EN delivery system
have already been set in motion. On the nutrition end, a cross-
spike unique to EN (“nutrition source connector”) has been
developed and in use since 2012. On the patient end, a new
ENFit connector (“patient access connector”) has been devel-
oped for enteral administration sets, enteral syringes, and
enteral feeding tubes. To improve patient safety, the ENFit con-
nector will not allow connectivity with any other therapeutic
devices, will provide a locking feature to prevent disconnec-
tions, and will have a female connector that will fit only into a
new male patient-access feeding tube port.46
Enteral Formula Selection
Commercially prepared enteral formula emerged in the late
1960s and has undergone many changes in formulation since its
inception. Today, more than 100 enteral formulas are available
for use in the United States and vary greatly with respect to
concentration, macronutrient and micronutrient composition,
fiber content, and the addition of pharmacologically active sub-
stances intended to modulate the immune response. A detailed
review of enteral formula components and considerations for
use was recently published47; a summary is provided in Table 1.
Efficacy studies are not required before enteral products can be
manufactured and used in patient care because they cannot be
promoted as medications to treat specific diseases. To maintain
patient safety and prevent complications of bacterial contami-
nation, proper use of administration sets and formula storage
should also be taken into consideration when selecting an
enteral formula.
Nutrient Composition of Enteral Formulas
The concentrations of enteral formulas range from 1–2 kcal/
mL. Formulas with the lowest concentration are approximately
85% water and have an osmolality closer to that of the body’s
intracellular and extracellular fluids (285–290 mOsm/kg).
These formulas may be useful in patients with diarrhea to pre-
vent osmotic-induced dumping. Formulas with the highest
concentrations are approximately 70% water and may be used
in patients requiring a fluid restriction secondary to conditions
such as congestive heart failure, renal failure, liver failure, syn-
drome of inappropriate antidiuretic hormone, or hypervolemic
hyponatremia.
Carbohydrates represent the primary macronutrient in most
enteral formulas and are usually provided in the form of corn
syrup solids, hydrolyzed corn starch, and maltodextrin. Some
6 Nutrition in Clinical Practice XX(X)
Table 1.  Categories of Commercially Prepared Enteral Formulas and Modular Products.
Formula Type Characteristics and Variations
Polymeric Contains whole protein as the nitrogen source.
Content can vary greatly in terms of caloric density,
macronutrient distribution, amount and type of
fiber added, and vitamin, mineral, and electrolyte
composition.
Hydrolyzed or Proteins are hydrolyzed to peptides (peptide based),
“predigested” amino acids (elemental), or a combination of both
(semi-elemental).
Disease specific Content can vary greatly in terms of caloric density,
macronutrient distribution, amount and type of
fiber added, and vitamin, mineral, and electrolyte
composition.
•• Renal
•• Diabetic
•• Hepatic
•• Pulmonary
Immune modulating Contain any combination of pharmacologically
active substances such as arginine, glutamine,
ω-3 fatty acids, γ-linolenic acid, nucleotides, or
antioxidants. Can be polymeric or hydrolyzed.
Content can vary greatly in terms of caloric
density, macronutrient distribution, amount and
type of fiber added, and vitamin, mineral, and
electrolyte composition.
Modular products Contain predominantly 1 nutrient.
•• Protein
•• Carbohydrate
•• Lipid
•• Fiber
formulas may contain sucrose or fructose as well. Most enteral
formulas do not contain lactose and are gluten free.
Protein can be provided in various forms including intact or
hydrolyzed proteins from soy, casein, and whey, or as crystal-
line amino acids. Formulas containing hydrolyzed proteins and
amino acids are often termed semi-elemental and elemental,
respectively. Although they are marketed as being more easily
digested and better tolerated, the superiority of elemental vs
polymeric formulas has not been clearly demonstrated as there
is limited research in this area. However, hydrolyzed protein
formulas may be considered in patients with persistent diarrhea,
pancreatic disease, or other malabsorptive conditions.22
Fat is provided in enteral formulations as long-chain fatty
acids (LCFAs) obtained from corn, soybean, sunflower, and
safflower oils, as medium-chain triglycerides (MCTs) from
palm kernel and coconut oil, or as structured lipids that
combine LCFAs and MCTs on the same molecule. Some
formulas also contain eicosapentaenoic acid and docosa-
hexaenoic acid from fish oil. It is important to note that
although MCTs do not require bile salts or pancreatic enzymes
Downloaded from ncp.sagepub.com at CAMBRIDGE UNIV LIBRARY on August 1, 2015
Considerations
Suitable for patients with normal or near normal
functioning bowel (ie, no significant malabsorptive
disorders).
Suitable for patients with extensive impairment
of gastrointestinal function (ie, significant
malabsorptive disorders such as persistent diarrhea,
pancreatic disease, or significant gastrointestinal
resection). Not intended for routine use.
Use of some disease-specific formulas (pulmonary,
diabetic, and hepatic) is not currently supported by
strong research. Efforts should be made to avoid
overfeeding.
Intended to modulate immune function. Designed
with appropriate physiologic rationale for specific
patient populations, but due to conflicting
outcomes data, use should be determined on a
case-by-case basis.
Consider the size of the enteral access device as
some modular products may increase risk of tube
occlusion. Ensure adequate flushing before and
after administration of modular products.
for digestion and are metabolized at the cellular level without
the assistance of carnitine, they do not provide a source of
essential fatty acids and must be used in combination with
LCFAs.
Most enteral formulas have been designed to meet the DRI
for vitamins and minerals in a volume of 1–1.5 liters per day. If
the minimum volume required to meet the DRI is not consis-
tently being provided, supplemental vitamins and minerals
may be required. On the other hand, some formulas contain
increased amounts of certain vitamins or minerals. It is impor-
tant that the clinician pays particular attention to the amount of
vitamins and minerals being provided by all sources to avoid
the consequences of inadequate or excess intake.
Whereas some enteral formulas are fiber free, many contain
fiber in differing types and amounts to promote the health of
the GI tract and maintain regular bowel function. Insoluble
fiber acts as a bulking agent, increasing the speed at which
stool moves through the intestines, whereas soluble fiber keeps
the stool soft by absorbing water.48 Common sources of fiber
include soy fiber and guar gum. Many also contain prebiotics
Kozeniecki and Fritzshall 7
in the form of fructooligosaccharides, oligofructose, or inulin.
Manufacturers have also developed unique blends of fiber with
the theoretical intention of improving gut flora. The overall
fiber content of most enteral formulas is well below the recom-
mended 14 g/1000 kcal to achieve daily intakes of 25–38 g/
day. It has been recommended to avoid the use of fiber-con-
taining products in hypotensive patients at high risk for devel-
oping ischemic bowel and patients with severe dysmotility.22
Enteral Additives and Modular Products
Enteral formula can only be provided “as is.” Although there
are many different products on the market, it is not possible for
institutions to maintain a supply of them all. Therefore, a clini-
cian’s ability to meet the needs of all patients using the institu-
tion’s formulary may be limited. For some patients, their
“ideal” formula may not even exist. In these situations, the use
of modular products, which are administered separately from
the enteral formula, can be helpful. More than 20 modular
products are available in the United States. The largest compo-
nent of each modular product is usually a single nutrient.
Protein modulars are used most frequently, compared with fat
or carbohydrate modulars, to help meet the protein needs of
hypermetabolic or hypercatabolic patients or those with exces-
sive losses through wound exudate, fistula effluent, or thera-
pies such as continuous renal replacement therapy. Fiber
additives are also commonly used to help manage stool fre-
quency and consistency in the hospital setting.
Regulatory Standards
It is important to note that enteral formulas are considered
medical foods by the U.S. Food and Drug Administration
(FDA), defined as “a food which is formulated to be consumed
or administered enterally under the supervision of a physician
and which is intended for the specific dietary management of a
disease or condition for which distinctive nutritional require-
ments, based on recognized scientific principles, are estab-
lished by medical evaluation.”49 Although medical foods must
comply with all applicable FDA requirements for foods, they
are exempt from the labeling requirements for health claims
and nutrient content claims. Because the research of disease-
specific formulas with regard to improved clinical outcomes is
limited, it is important for the clinician to avoid using the
patient’s medical condition alone to guide enteral formula
selection.
Food Allergies, Sensitivities, and Strict
Dietary Practices
It is important for the clinician to keep in mind each patient’s
food allergies, sensitivities, and dietary practices when choos-
ing an enteral formula. As mentioned previously, most enteral
formulas do not contain gluten or lactose due to the
Downloaded from ncp.sagepub.com at CAMBRIDGE UNIV LIBRARY on August 1, 2015
commonality of gluten and lactose intolerance in the adult
population. For patients with food allergies such as egg, corn,
casein, whey, and soy, the clinician should refer to the most
recent product label, as ingredient lists may change due to
product reformulation and/or different suppliers providing
ingredients for the products. Most manufacturers will include
on the product label whether it is suitable for halal or kosher
practices. For vegan patients, attention should be paid to the
list of ingredients to ensure that the source of protein is derived
from soy rather than whey or casein.
Administration Sets and Hang Time
According to manufacturer guidelines, the hang time for sterile
formula in a closed system (eg, ready-to-hang bottles or bags
of formula) is 24–48 hours, whereas the hang time for a sterile
formula in an open system (eg, formula poured into an admin-
istration set) is 8 hours for hospitalized patients and 12 hours
for patients in the home setting.30 Any nonsterile formula (eg,
powder formula) that needs to be reconstituted by mixing with
sterile water should hang for no more than 4 hours; if not used
immediately, reconstituted formula can be refrigerated for up
to 24 hours after preparation.30 Open-system enteral adminis-
tration sets should be changed every 24 hours in the hospital
setting to prevent unacceptably high levels of bacteria from
accumulating in the tubing.50,51 Due to the increased nursing
time required to change enteral formula systems more fre-
quently and the reduced risk of contamination, many institu-
tions prefer to use closed-system enteral formulas as much as
possible. Additions to closed-system containers are to be
avoided.22
Initiation and Advancement
EN may be administered in a variety of ways, and the method
of administration can strongly affect the success of EN therapy.
To determine the most appropriate method of administration,
the clinician should consider the patient’s age, preexisting and
current medical condition(s), nutrition status and requirements,
the location of the feeding tube tip, and the patient’s expected
tolerance.
A study by Desachy et al52 compared the initial efficacy and
tolerability of early EN with immediate vs gradual introduction
of optimal flow rate among 100 shock-free intubated and
mechanically ventilated patients. In the immediate optimal
flow group, EN was initiated at the rate corresponding to 25
kcal/kg/day (average 75 mL/hour). In the gradual introduction
group, EN was initiated at a flow rate of 25 mL/hour and
increased in increments of 25 mL/hour every 24 hours until the
rate corresponding to 25 kcal/kg/day was reached (average of
76.5 mL/hour). Patients in the immediate group received a sig-
nificantly higher amount of calories compared with those in
the gradual group, with no differences in the rates of diarrhea
or suspected aspiration pneumonia. The authors concluded that
8 Nutrition in Clinical Practice XX(X)
Continuous (Set Rate- or Volume-Based)
1) Determine target volume: 1440 mL/day
2) Determine duration of therapy: 24 hours/day
3) Determine pump rate (Set Rate): 1440 mL ÷ 24 hours = 60 mL/hr
4) For volume-based feeding: Start with set rate and adjust based on the volume remaining and number of hours left in the day.
Maximum infusion rate may be institution-specific.
Intermittent and Bolus
1) Determine target volume: 1440 mL/day
2) Determine number of feedings per day: 3 feedings/day
3) Determine volume per feeding: 1440 mL ÷ 3 feedings = 480 mL per feeding
4) Determine duration of each feeding: 15-45 minutes per feeding, individualized based on patient tolerance
Figure 3.  Sample enteral nutrition calculations based on method of administration.
EN can be introduced at the optimal dose regimen in select
patients. Patients who may benefit from more conservative ini-
tiation and advancement of EN include patients who have not
been fed for an extended period of time; have not received
enteral nutrients in a long time; are hemodynamically unstable,
requiring vasopressors or inotropic agents; are chemically par-
alyzed; have recently undergone a significant bowel resection,
temporary abdominal closure, or multiple abdominal re-explo-
rations; or who have bowel wall edema.26
Delivery Methods
Continuous feeding is commonly used for the adult hospital-
ized patient requiring EN therapy and is achieved via pump
assist. The goal infusion rate is determined by dividing the
desired formula volume by the number of hours of administra-
tion. Because of the frequency with which enteral feeds are
interrupted in the hospital setting, resulting in delivery of only
50%-60% of prescribed EN volume on a daily basis, some
institutions have implemented a volume-based feeding proto-
col to ensure that the volume of EN prescribed to their patients
is actually provided.53,54 To allow for time away from feeding,
intermittent or bolus feedings may be used. Bolus feedings are
defined as formula delivered by gravity-assist or syringe over
approximately 15 minutes, whereas intermittent feedings are
usually delivered over 30–45 minutes via gravity assist or
pump assist.55 These feeding methods are usually reserved for
medically stable patients with feeding tubes terminating in the
stomach. Volumes typically range from 240–720 mL per feed-
ing, depending on individual tolerance, with a frequency from
2–6 times daily. Hospitalized patients may transition from 1
delivery method to another as their clinical status changes.
Sample calculations are provided in Figure 3.
Monitoring, Troubleshooting, and
Managing Complications
As patient condition can change quickly and frequently in the
hospital setting, continuous reassessment and reevaluation are
Downloaded from ncp.sagepub.com at CAMBRIDGE UNIV LIBRARY on August 1, 2015
required in order for the clinician to adapt the nutrition support
plan to the patient’s needs. Recommended monitoring for
patients receiving EN includes adequacy of intake; weight;
hydration status; electrolyte and acid-base balance; glycemic
control; presence of nausea, vomiting, abdominal distention,
pain, or discomfort; stool frequency and consistency; patency
of the enteral access device; and the potential for vitamin/min-
eral deficiencies and drug-nutrient interactions. The frequency
of monitoring should depend on the patient’s severity of ill-
ness, level of metabolic stress, and degree of malnutrition. This
section reviews some of the common and more serious compli-
cations seen in the adult hospitalized patient population,
including potential causes and strategies to mitigate them
(Table 2).
Refeeding Syndrome
The term refeeding syndrome is generally reserved to describe
the metabolic alterations that occur during nutrition repletion
of severely malnourished or starved individuals in amounts
greater than a weakened cardiopulmonary system can accom-
modate.87,88 Hypophosphatemia is considered the hallmark of
refeeding syndrome, although other clinical manifestations
include hypokalemia, hypomagnesemia, thiamin deficiency,
and sodium retention/fluid overload. Clinicians should always
consider the patient’s nutrition status when initiating EN, as
this can help determine the patient’s risk of developing meta-
bolic alterations that could potentially lead to multiorgan sys-
tem dysfunction and even death.89 Patients most at risk for
refeeding syndrome include those with minimal intake for > 7
days with evidence of metabolic stress; significant weight loss;
undernutrition as a result of chronic disease(s); anorexia ner-
vosa; persistent nausea, vomiting, or diarrhea; malabsorptive
conditions; or history of excessive alcohol intake.56,87,90
Although clinicians could be inclined to believe that refeeding
is unlikely among an increasing percentage of overweight and
obese patients, coupled with modern practices of conservative
energy provision, the prevalence of acute and chronic disease-
related malnutrition renders refeeding syndrome a very real
Kozeniecki and Fritzshall 9

Table 2.  Complications in Enterally Fed Patients and Prevention/Treatment Strategies.

Complication Cause Prevention/Treatment

Refeeding •• Rapid reintroduction of carbohydrates •• Correct electrolyte abnormalities prior to initiation and during
syndrome55-57 during nutrition repletion in severely delivery of nutrition
malnourished or starved individuals •• Start and increase calorie provision conservatively over the
course of 5–7 days
•• Minimal initial fluid and sodium provided
•• Supplement with 50–100 mg intravenous/oral thiamin for 5–7
days
Nausea/ •• Motion sickness •• Provide an anti-emetic regimen
vomiting58-63 •• Emotional stress •• Use prokinetic agents to increase gastric motility
•• Headaches or migraines •• Reduce, replace, or discontinue medications that delay gastric
•• Indigestion emptying
•• Delayed gastric emptying  •• Consider a lowfat, isotonic, or more calorically dense formula
  •• Ensure enteral formula and water flushes are delivered at room
temperature
•• Temporarily reduce the enteral infusion rate by 20–25 mL/
hour or extend the infusion time of cycled or intermittent feeds
•• Obtain postpyloric enteral access
Aspiration •• Contaminated oropharyngeal secretions •• Adequate handwashing and hand disinfection
pneumonia64 •• Elevate head of bed 30–45 degrees, especially while providing
enteral nutrition
•• Provide subglottic suctioning, drain condensate from ventilator
circuits, and provide chlorohexidine oral rinse as appropriate
•• Achieve adequate glucose control
•• Avoid unnecessary antibiotics
Diarrhea30,65-69 •• Medications •• Discontinue or reduce dose of offending medication, or replace
•• Infections, illness severity, and disease with alternative non–diarrhea-causing medication
states •• Change from liquid solution to tablet form or dilute hypertonic
•• Bacterial contamination medications
•• Enteral formula •• Identify and treat underlying medical/surgical issues and
infections
•• Consider adjusting the type of formula depending on disease
state to prevent malabsorption
•• Use a clean, aseptic technique when handling the feeding
system
•• Use sterile, liquid formula formulations over powder,
reconstituted formulas when possible
•• Limit formula hang time, especially when using an open
system
•• Provide education and training on policies, procedures, and
practices associated with preparing, storing, and administering
enteral formula
•• Adjust fiber type and/or amount provided; consider decreasing
insoluble fiber or increasing soluble fiber
•• Consider an isotonic formula or slower infusion rate
•• Try a peptide-based formula or one with a higher percentage
of fat from medium chain triglycerides or structured lipids
•• Ensure that the formula, modulators, and water flushes are
room temperature
Constipation70-75 •• Medications •• Adjust medications that decrease gastrointestinal motility
•• Laxative abuse •• Add or adjust bowel regimen
•• Inadequate fluid or fiber intake •• Use fiber-containing enteral formulas if no contraindication
•• Neuromuscular, hypothyroid, and exists
gastrointestinal disorders •• Increase amount of free water provided
•• Lack of physical activity •• Promote ambulation as able
(continued)

Downloaded from ncp.sagepub.com at CAMBRIDGE UNIV LIBRARY on August 1, 2015

10 Nutrition in Clinical Practice XX(X)
Table 2. (continued)
Complication Cause
Ileus22,76-81 •• Electrolyte imbalances
•• Major lower gastrointestinal surgeries
•• Delayed enteral nutrition
•• Inflammation
•• Medications
Clogged feeding •• Suboptimal flushing techniques
tube18,82-86 •• Improper medication administration
•• Precipitation of enteral formulas by
gastric acid
•• Small-bore feeding tubes
•• Formula composition
 
 
possibility. Based on case reports, refeeding syndrome can
manifest itself up to 5 days after the initiation of feedings.88
A variety of strategies have been suggested to prevent the
deleterious effects of refeeding syndrome. Any serum electro-
lyte abnormalities should be corrected prior to initiation of
nutrition. Calorie provision should be started and increased
conservatively, although recommendations vary. Common rec-
ommendations include starting energy intake at 15–20 kcal/kg/
day, 1000 kcal/day, or 50% of estimated needs57 and gradually
increasing to goal amounts over 5–7 days, keeping in mind that
the minimum carbohydrate requirement to suppress gluconeo-
genesis, spare proteins, and supply fuel to the central nervous
system is approximately 100–150 g/day.58 The amount of fluid
and sodium initially supplied should be minimized because of
the expansion of the extracellular water compartments and the
propensity to retain these during initial refeeding. Serum val-
ues of sodium, potassium, magnesium, and calcium should be
monitored daily during the first week and replaced as indi-
cated. Last, because thiamin is an essential cofactor in the
metabolism of carbohydrate, supplementation in the range of
50–100 mg/day intravenously or 100 mg orally for 5–7 days is
recommended for patients at risk for refeeding.87
Nausea/Vomiting
There are many causes of nausea and vomiting, which are often
quite similar. Common causes include motion sickness, emo-
tional stress (fear), headaches or migraines, indigestion, food
poisoning, various viruses, and certain smells or odors. The
most common cause of nausea and vomiting, especially in criti-
cally ill patients, appears to be delayed gastric emptying.59,60
Downloaded from ncp.sagepub.com at CAMBRIDGE UNIV LIBRARY on August 1, 2015
Prevention/Treatment
•• Correct electrolyte abnormalities
•• Consider initiating early enteral nutrition in setting of a mild to
moderate ileus
•• Limit sedatives and paralytic agents as much as possible  
•• Flush enteral devices with 20–30 mL of warm water every 4
hours during continuous feeds and before and after intermittent
feedings and medications
•• Avoid flushing enteral access devices with carbonated
beverages and juices
•• Minimize contact of liquid medications with enteral formula or
crush tablets into a fine powder before mixing with water
•• Avoid frequent checking of gastric residual volumes
•• Reference manufacturer recommendations to ensure the
enteral formula being used is compatible with the patient’s
enteral access device
•• Treat clogged tubes with a warm water flush with moderate
pressure, activated enzyme solutions, or an approved
declogging device
•• Replace enteral access device
Risk factors for delayed gastric emptying include hyperglyce-
mia, illness severity, low Glasgow Coma Score, elevated intra-
cranial pressure, traumatic brain injury, recent anesthesia or
surgery, surgical vagotomy, use of certain medications (eg, opi-
ates, analgesics, anticholinergics), rapid infusion of formula,
and the use of a high fat formula.59-62,91
Nausea and vomiting have been reported in up to 26% of
patients receiving EN therapy.63 Usually, these symptoms can be
successfully managed without needing to initiate parenteral nutri-
tion. Anti-emetic medications can help manage nausea quite
effectively if scheduled on a regular basis. Prokinetic agents such
as metoclopramide and erythromycin can increase gastric motil-
ity and are especially effective when used in combination.92 If
delayed gastric emptying is suspected, other interventions may
include reducing, replacing, or discontinuing opiates, analgesics,
and anticholinergics. Adjustments to the EN formula or regimen
should also be considered, if possible. Strategies may include
changing the enteral formula to one that is low in fat, isotonic, or
more calorically dense, ensuring that enteral formula and water
flushes are being administered at room temperature, temporarily
reducing the rate of enteral infusion by 20–25 mL/hour, extend-
ing the infusion time of cycled or intermittent feeds, and obtain-
ing postpyloric enteral access.60,61,63,91
Gastric Residual Volume and Aspiration
Pneumonia
Historically, gastric residual volumes (GRV) have been used to
assess tolerance to EN and determine one’s risk for aspiration/
aspiration pneumonia. This practice remains controversial as
neither the practice nor the method of checking GRV itself is
Kozeniecki and Fritzshall 11
Measure gastric residual volumes every 4 hours
or
Before intermittent feedings
GRV > 500 mL?
Yes
1.) Refeed residuals up to 500 mL
2.) Hold tube feeds for 1 hour and
recheck GRV
GRV > 500 mL?
No
Yes
1.) Discard residual (total amount)
2.) Restart tube feeds at half of the
previous rate (minimum 20 mL/hr).
Give half goal volume if intermittent.
3.) Notify physician
4.) Utilize strategies to reduce
aspiration risk and improve tolerance
Figure 4.  Sample algorithm for managing gastric residual volumes. EN, enteral nutrition; GRV, gastric residual volume; HOB, head of bed.
validated. Limitations to accurate measurement include the
position of the patient, type and size of the syringe used, and
the size, material, and position of the tip of the feeding tube.93
In addition, the quality (color, consistency) and composition of
gastric volumes are rarely differentiated and may include
recently administered medications and water flushes rather
than undigested formula alone.
Pneumonia and bacterial contamination of the respira-
tory tract are often caused by aspiration of contaminated
oropharyngeal secretions originating from the upper airway,
teeth, artificial airway, ventilator-circuit condensate, or
nasal sinuses.64 Additional data suggest the relative impor-
tance of oropharyngeal colonization over gastric colonization
in the development of ventilator-associated pneumonia.94-96
Nonnutrition prevention strategies, therefore, include (but are
not limited to) adequate handwashing and hand disinfection;
head of bed elevation of 30–45 degrees especially while
receiving EN; scheduled drainage of condensate from venti-
lator circuits (if applicable); subglottic suctioning; chloro-
hexidine oral rinse in selected patients; avoidance of
unnecessary antibiotics; and insulin therapy to maintain
serum glucose levels within the desired range.
Regarding GRV, the results of several studies have demon-
strated that a lower GRV cutoff value of 50–150 mL compared
with a higher cutoff of 250–500 mL does not decrease the risk of
Downloaded from ncp.sagepub.com at CAMBRIDGE UNIV LIBRARY on August 1, 2015
Strategies to reduce aspiration risk
and improve EN tolerance:
1.) Elevate HOB > 30°
2.) Good oral care
3.) Regular assessment of tube position
4.) Achieve glycemic control to prevent
gastroparesis
5.) Minimize use of narcotics and
sedatives
No
6.) Promote regular bowel movements
7.) Use prokinetic agents as indicated
8.) Place post-pyloric feeding tube
Are there other signs of intolerance?
Examples: abdominal distention,
firmness, or pain; retching/vomiting
Yes
1.) Hold tube feeds OR decrease
No rate by half
2.) Notify physician
3.) Utilize strategies to reduce
1.) Continue feeding aspiration risk and improve
tolerance
2.) Utilize strategies to reduce
aspiration risk and improve 4.) Restart/advance tube feeds
tolerance when issue resolved
regurgitation, aspiration, or pneumonia97-99 but instead increases
the unnecessary withholding of EN.100 It has been recommended
that interruption of EN should be avoided for GRV < 500 mL in
the absence of other signs and symptoms of intolerance (nausea,
vomiting, bloating, abdominal discomfort or distention) but that
close monitoring is warranted in patients with gastric residuals
between 200 and 500 mL, ensuring that all measures to reduce
aspiration risk are initiated.22 Recently, results from a large ran-
domized controlled trial suggest no beneficial effect of monitor-
ing GRV at all; however, these results represent primarily a
medical population with a low incidence of GI disorders.101
Although GRV may not be useful in determining aspiration risk,
it remains a simple and insightful tool to help clinicians detect
early signs of GI dysfunction, thereby allowing for timely inter-
vention. Figure 4 provides an example of an algorithm designed
to manage GRV and optimize patient tolerance to EN.
Diarrhea
Diarrhea is a serious condition and can cause electrolyte abnor-
malities, dehydration, loss of nutrients, fecal incontinence leading
to skin breakdown, malabsorption from increased transit time, and
inadequate nutrient intake from pausing or stopping EN. The inci-
dence of diarrhea in the hospital setting is difficult to determine
given the lack of a standardized definition and wide range of
12 Nutrition in Clinical Practice XX(X)

Table 3.  Categories of Diarrhea.66,106

Type Description Characteristics Common Causes

Dysmotility Altered gastric, small
bowel, or colonic motility
causing rapid transit time
or increased intestinal
motility
Inflammatory or Impaired water and
exudative electrolyte absorption due
to intestinal inflammation
Malabsorptive Damage to or loss of
absorptive ability causing
maldigestion of nutrients
Osmotic The bowel is unable to
reabsorb fluid as it passes
through the intestinal
lumen due to the presence
of nonabsorbable,
osmotically active solutes
Secretory An increase in the amount
of fluid drawn into the
intestinal lumen at a rate
exceeding the absorptive
capacity of the bowel
•• Alternating between •• Diabetic neuropathy
constipation and diarrhea •• Hyperthyroidism
•• Improvement overnight or •• Irritable bowel syndrome
when fasting •• Postsurgical (gastrectomy, vagotomy)
•• Intermittent, nonlocalizing
abdominal pain
•• Sensation of incomplete
evacuation after bowel
movement
•• Elevated white blood count •• Intestinal lumen damaged (graft-vs-host
•• Presence of mucus, blood, disease, radiation enteritis)
and/or plasma proteins in stool •• Small bowel disorders (Crohn’s disease,
ulcerative colitis)
•• Bloating •• Gastric bypass surgery
•• Excess gas •• Pancreatic insufficiency or disease
•• Steatorrhea •• Short bowel syndrome
•• Weight loss •• Small bowel bacterial overgrowth
  •• Small bowel mucosal diseases (celiac sprue)
•• Decreased stool with fasting •• Bowel resection or villi and brush border
or withholding the poorly atrophy
absorbed substrate •• Incomplete breakdown or malabsorption
•• Fecal osmotic gap > 50 of nutrients in small intestine (lactose,
mOsm/kg hyperosmolar substances, sugar alcohols, fat)
•• Stool volume of < 1 liter daily •• Medication induced (osmotic laxatives and
(usually proportionate to the antacids [magnesium, phosphate, sulfate],
offending substrate) sugar alcohol containing [mannitol, sorbitol,
xylitol])
•• Low or absent fecal osmotic •• Alcohol abuse
gap (< 50 mOsm/kg) •• Bile acid malabsorption
•• Stool volume of > 1 liter daily •• Endocrine disorders (hypothyroidism)
•• Unrelated with food intake or •• Hormones secreted by neuroendocrine
no change in stool with fasting tumors
  •• Infectious agents (Escherichia coli,
  Salmonella, Clostridium difficile)
•• Medication induced (antiarrhythmics,
antibiotics, antineoplastics, biguanides,
calcitonin, cardiac glycosides, colchicine,
nonsteroidal anti-inflammatory drugs,
prostaglandins, ticlopidine)
  •• Postsurgical (cholecystectomy, intestinal
resection)

patient populations studied.22,65,102 It has been reported that diar-
rhea occurs in 30% of patients on medical and surgical floors and
> 80% of patients in intensive care units.13,23 In tube-fed patients
alone, the incidence of diarrhea ranges from 11.3%–66.1%,
depending on the definition used.103 Definitions of diarrhea often
include frequency of bowel movements of 3 or more watery or
loose bowel movements in a 24-hour period, or stool weight of >
200 g/day. Descriptive terms such as passage of loose, unformed
stool or the presence of both abnormal stool frequency and liquid
consistency are also used.65,104,105 Although diarrhea is a com-
monly reported side effect of EN, it can also be caused by many
other factors in the hospitalized patient. Traditionally, diarrhea is
categorized as motility-related, malabsorptive, inflammatory/
exudative, secretory, or osmotic (Table 3). Therefore, managing
diarrhea in the enterally fed patient requires a systematic
approach prior to making changes to the enteral feeding regimen.
Understanding the type of diarrhea can help establish a differential
diagnosis and guide treatment strategies.
Infectious etiologies and medical conditions should always
be considered, evaluated, and treated appropriately if identi-
fied. Clostridium difficile infection is the most frequently iden-
tified cause of nosocomial diarrhea.107 The incidence and

Downloaded from ncp.sagepub.com at CAMBRIDGE UNIV LIBRARY on August 1, 2015

Kozeniecki and Fritzshall 13
duration of diarrhea has also been associated with severity of
illness, hypermetabolic stress, serum albumin level, decreased
immunity, glucose control, white blood cell count, and periph-
eral oxygen saturation.108-110
Medication administration also has the potential to contrib-
ute to diarrhea. Liquid medication solutions, for example, can
contain a number of poorly absorbed sweeteners (eg, sorbitol)
and stabilizers, which increase the osmolality of the medica-
tion and, therefore, the potential to cause diarrhea. As little as
10–20 g/day of sorbitol has been shown to produce GI side
effects (gas, cramping, bloating, and diarrhea) and doses ≥ 20
g/day can produce osmotic-induced dumping syndrome.70,111,112
A dose of 1.3–3.9 g of acetaminophen provides about 8–24 g
sorbitol.67 Other medications known to cause diarrhea include
antibiotics, antihypertensives, cholinergics, GI agents, glu-
cose-lowering agents, anti-inflammatory drugs, laxatives, pro-
kinetic agents, selective serotonin reuptake inhibitors, and
chemotherapy agents.68,104,113 Discontinuing or reducing the
dose of an offending medication or changing the form of the
medication can help reduce medication-induced diarrhea.
Addition of probiotics may attenuate diarrhea, especially if
associated with antibiotic use; however, more research is
needed to determine the strains and doses needed to provide
benefit.22,71 Antidiarrheal medications can also be considered.
After all other causes of diarrhea have been ruled out, an
assessment of the EN regimen may be warranted. EN-associated
diarrhea has been attributed to microbial contamination, low
fiber content, and hyperosmolarity of the EN formula.108 As
mentioned previously, many hospitals now use closed systems
of EN administration to reduce the risk of contamination. Use
of soluble fiber-containing enteral formula can help reduce the
incidence of diarrhea, as shown in a 2008 meta-analysis.114
Soluble fiber modular products can be used if such enteral for-
mulas are unavailable. Slowing the formula infusion rate or
changing to an iso-osmolar formula may also be beneficial,26
although the osmolarity of the EN formula is not thought to be
a major contributor to diarrhea in enterally fed patients with a
functioning GI tract.69 For patients with maldigestion or mal-
absorption, the addition of a semi-elemental or elemental for-
mula with greater percentage of fat from MCTs or structured
lipids may improve tolerance.115
Constipation
Constipation is also common among enterally fed patients,
especially the elderly and bedridden. In critically ill patients,
the incidence of constipation has been reported in the range of
15%-83%.72 Many definitions of constipation exist, although
most consistently identify infrequent and difficult defecation
as defining characteristics.114 The main causes of constipation
among patients receiving EN are medications (benzodiaze-
pines and opioids being the most common), inadequate fluid
intake or dehydration, inadequate fiber intake, and lack of
Downloaded from ncp.sagepub.com at CAMBRIDGE UNIV LIBRARY on August 1, 2015
physical activity.67,73,112 Other causes of constipation include
neuromuscular disorders, hypothyroid disorders, GI motility
disorders, and history of laxative abuse.112 Constipation can
cause abdominal distension or bloating, vomiting, fecal impac-
tion, and bowel perforation, therefore increasing the need for
nursing, medical, and/or pharmaceutical interventions.74 For
these reasons, constipation has been associated not only with
feeding intolerance and delays in EN therapy but also with dif-
ficulty weaning from mechanical ventilation in critically ill
patients, longer length of ICU stay, and decreased quality of
life.73-75
Management of constipation in the enterally fed patient
may include adjustments in fiber, fluid, and/or medications
with the goal of restoring normal bowel function and decreas-
ing symptoms related to constipation. Use of fiber-containing
enteral formulas can help to normalize bowel function and
reduce the need for laxatives.114,116 To minimize constipation
associated with increased fiber intake, at least 1 mL/kcal of
fluid is required.48 It is worth noting that the use of concen-
trated enteral formulas will likely require large water flush
volumes to meet this fluid requirement. If constipation does
not improve with increased fiber intake, or if fluid restriction
is warranted due to other medical conditions such as conges-
tive heart failure or renal disease, stool softeners, laxatives,
and/or enemas may be required to manage and prevent con-
stipation. Other patients who may require a scheduled bowel
regimen include those receiving medications that decrease GI
motility (eg, sedatives or opioids)75 or who are unable to
ambulate.
Ileus
The presence or absence of bowel sounds is often used to deter-
mine whether the GI tract is functional and may therefore deter-
mine EN initiation or delay.117 However, bowel sounds do not
always correlate with normal bowel function. In the setting of
ileus, for example, bowel sounds can range from hypoactive to
nonexistent, but in the setting of an obstruction, bowel sounds
may become louder, high-pitched, or even hyperactive.118 The
lack of peristalsis, which characterizes ileus, leads to the accu-
mulation of both gas and fluids within the bowel, causing
abdominal distension, nausea, and/or vomiting if gastric decom-
pression is not provided.76,77,119 Ileus occurs in 24%–75% of
postoperative patients and 50%–80% of critical care patients.77
Major lower GI surgeries are the most common cause of an
ileus, and other risk factors include infection and inflammation,
electrolyte imbalances, delayed EN, and the certain use of drugs
(sedatives, opioid analgesics, alpha-2 adrenergic receptor ago-
nists, and catecholamine vasopressors).22,78,119,120
After surgery, small bowel, gastric, and colonic motility are
regained within 24 hours, 1–2 days, and 3–5 days, respectively.79,119
Nutrition is commonly withheld in this population, or provided
parenterally, until return of bowel function due to concern that
14 Nutrition in Clinical Practice XX(X)
the digestive tract will not tolerate feedings following the manip-
ulation experienced during surgery and anesthesia. However, the
presence of enteral nutrients initiates intestinal propulsive activ-
ity and stimulates the secretion of various intestinal hormones,
which have a positive effect on GI motility.119 An early study
showed that EN can be safely initiated immediately postopera-
tively with ileus resolving within 48 hours.80 Other studies have
shown quicker return of bowel function with early enteral feed-
ing.81,82,121 For these reasons, guidelines support feeding through
mild to moderate ileus.22
Clogged Feeding Tubes
All feeding tubes are subject to mechanical complications such
as occlusion/clogging, for a variety of reasons. Usual causes
include suboptimal flushing techniques, improper medication
administration, precipitation of enteral formulas by gastric acid
(protein denaturation), and use of small-bore feeding
tubes.83,84,122 High-fiber and calorically dense formulas have
also been identified as risk factors for tube occlusion.
To prevent clogging, several strategies may be employed.
Enteral access devices should be flushed with 20–30 mL of
warm water every 4 hours during continuous feeding, before and
after intermittent feeding, and before and after medication
administration.18,85 Although liquids have long been considered
the preferred medication formulation selected for administration
via enteral feeding tubes,86 many are acidic. It is therefore impor-
tant to minimize contact with EN formulas as these acidic fluids
have a high potential to contribute to tube occlusion.123 If no
other alternatives are available, tablets should be crushed to a
fine powder before mixing with water to avoid accumulation of
pill fragments within the tube.83 Frequent checking of GRVs
should be avoided when possible to reduce the likelihood of tube
occlusion from precipitation of the enteral formula.84,122 In gen-
eral, most adult enteral formulas are manufactured to allow
smooth flow through enteral tube diameters as small as 8–12 Fr,
although it is best to reference the manufacturer’s recommenda-
tions when choosing an enteral formula to ensure that it is com-
patible with your patient’s enteral access device.
Once an enteral access device has become occluded, the cli-
nician must either remove and replace the device or remove the
clog. Several methods for restoring tube patency have been
described.84 In general, a warm water flush with moderate
pressure is recommended as the first-line treatment for clogged
feeding tubes. If this is not successful, activated enzyme solu-
tions can be used. Carbonated beverages and juices such as
cola and cranberry juice, respectively, are not recommended
due to their acidity and the potential to cause subsequent occlu-
sions. Several declogging devices are also available, including
the Intro-Reducer (Health Improvement Associates, Freeland,
MI, USA), the Clog Zapper (CorPak MedSystems, Buffalo
Grove, IL, USA), and the DeClogger (Bionix, Toledo, OH,
USA). If all attempts to restore patency to an existing enteral
access device fail, the clinician must replace the device.
Downloaded from ncp.sagepub.com at CAMBRIDGE UNIV LIBRARY on August 1, 2015
Drug-Nutrient Interactions
A drug-nutrient interaction involves alteration of the kinetics
(absorption, metabolism, disposition, or elimination) or
dynamics (clinical/physiological) of a drug or nutrition ele-
ment or a compromise in nutrition status as a result of the
action or side effect of a drug.18 There is no universal approach
to the management of drug-nutrient interactions in clinical
practice, however, several drugs are commonly thought to
require cessation of EN for up to 1–2 hours before and after
administration of the drug. Among these are levothyroxine,
carbidopa/levodopa, fluoroquinolones such as ciprofloxacin,
warfarin, and phenytoin. The proposed mechanisms are myr-
iad, including but not limited to protein binding, chelation
interaction with divalent cations, specific nutrient content of
the enteral formula, positioning of the enteral feeding tube, and
adsorption to the enteral tubing.13 Although it is important for
the clinician to be cognizant of potential drug-nutrient interac-
tions, it is also important to consider the quality of evidence on
this topic. The literature suffers many limitations including
lack of prospective, randomized, controlled trials and therefore
lacks strong evidence to support cessation of EN for medica-
tion administration. Furthermore, at this time there is no estab-
lished consensus in determining whether a drug-nutrient
interaction is even clinically significant. Holding EN for
administration of medications significantly challenges the abil-
ity of the clinician to provide adequate nutrition support.
Therefore, based on a risk-benefit analysis, the clinician’s
approach may include changing the management approach
immediately or continuing the current regimen and monitoring
for therapeutic effect or signs and symptoms of complications
associated with interaction.124 Future research should focus on
determining the effect of different feeding methods and enteral
formulations and validating the proposed mechanisms of spe-
cific nutrients on drug availability and metabolism.
Transitioning to Oral Intake
Although EN is often needed during critical and acute illness,
it should be discontinued when the patient can consume and
tolerate adequate amounts of an oral diet. The length of time
needed for this transition may vary considerably, depending on
the patient’s underlying illnesses and current medical condi-
tion. If the patient was mechanically ventilated for a prolonged
period of time, had a tracheostomy placed, or displays cogni-
tive deficits, altered mental status, or signs of difficulty with
swallowing, a swallow evaluation should be done prior to ini-
tiating an oral diet. Once a diet has been started, adjustments in
the enteral feeding schedule can help promote appetite and oral
intake while still providing adequate nutrition intake through
supplemental EN. Several strategies include nocturnal feeding,
intermittent feedings between meals, or stopping EN 1 hour
before meals. Prior to discontinuing EN, it is important to
assess the adequacy of oral energy and nutrient intake through
Kozeniecki and Fritzshall 15
food recall or a formal calorie count. When the patient is con-
suming 60%-75% of estimated energy and protein needs, the
clinician should consider stopping EN and removing the tem-
porary enteral access device. If the patient is unable to demon-
strate adequate oral intake for > 4 weeks, a permanent feeding
tube should be considered.
Transitioning to Home or an Alternate
Healthcare Setting With EN
For patients who are medically stable to discharge from the
hospital but are unable to achieve or maintain adequate nutri-
tion by the oral route, EN should be continued in the home or
alternate healthcare setting. Early discharge planning and
active communication with all members of the patient care
team (eg, physician, dietitian, nurse, social worker, and case
manager) are required for a successful transition.
The case manager can determine if the patient has appropri-
ate insurance coverage for home EN formula and supplies. As
many insurance companies follow Medicare guidelines, the
patient will likely need to meet criteria under the prosthetic
device benefit provision, which requires that the patient have
“a permanently inoperative internal body organ or function
thereof.”125 Specific criteria include anticipated length of ther-
apy for > 3 months, documentation of pathology to or nonfunc-
tion of the structures that normally permit food to reach the
digestive tract, or disease of the small bowel impairing diges-
tion and absorption of an oral diet.
Prior to discharge from the hospital, the clinician should be
sure that the patient has an appropriate route of administration,
is receiving the appropriate enteral formula and nutrient provi-
sion, and is using an appropriate delivery method. The formula
of choice and its administration should be well tolerated. The
clinician should reassess all nutrition needs and verify the indi-
cation for a specialized formula, if applicable. Intermittent
feedings using gravity bags or bolus feedings with syringes are
the preferred method of administration for gastric feedings. If
continuous gastric feedings are needed, Medicare and other
third party payers require documentation of medical necessity
or the failure of intermittent or bolus feedings before covering
the cost of a feeding pump.
Patient and caregiver education is important to ensure safe
and adequate administration of EN at home and should begin
early in the discharge planning process as well. Areas of educa-
tion from home EN include a comprehensive review of the
nutrition prescription (eg, name of the formula and volume
required, route of administration, method of administration,
feeding schedule, and volume/frequency water flushes), enteral
feeding equipment and techniques, and complications associ-
ated with EN therapy. The homecare agency can provide addi-
tional education once the patient is in the home setting.
Last, and of utmost importance, a primary clinician who
will be responsible for ordering and managing home EN should
Downloaded from ncp.sagepub.com at CAMBRIDGE UNIV LIBRARY on August 1, 2015
be identified prior to patient discharge from the hospital, and
the patient should follow up with this clinician soon after dis-
charge. The patient should be monitored periodically for
changes in his or her nutrition status and needs, fluid and elec-
trolyte balance, and tube placement and maintenance.
Summary
EN support has become a routine part of the care of hospital-
ized patients who have a functional GI tract but are unable to
meet their nutrition needs orally. All healthcare practitioners
should be familiar with patient selection, timing of EN initia-
tion, enteral access, and EN-related complications. Whereas
multidisciplinary management of EN is of utmost importance,
the registered dietitian is a key resource in determining indi-
vidual nutrition needs, selecting the appropriate enteral for-
mula, monitoring the adequacy of nutrient provision, and
assisting with EN-related complication management and the
transition to oral intake or to the home setting with EN. Due to
the prevalence of hospital malnutrition and its myriad conse-
quences including increased morbidity and mortality, longer
lengths of hospital stay, and increased hospital costs, it is
important to routinely monitor patients at risk for malnutrition
and to initiate safe, timely, and adequate EN therapy when
indicated.
Statement of Authorship
M. Kozeniecki and R. Fritzshall equally contributed to the con-
cepts and content presented in the manuscript; drafted and/or criti-
cally revised the manuscript; and agree to be fully accountable for
ensuring the integrity and accuracy of the work. All authors read
and approved the final manuscript.
References
1. Teitelbaum D, Guenter P, Howell WH, Kochevar ME, Roth J, Seidner
DL. Definition of terms, style, and conventions used in A.S.P.E.N. guide-
lines and standards. Nutr Clin Pract. 2005;20:281–285.
2. AHRQ Healthcare Costs and Utilization Project (HCUP) Nationwide
Inpatient Sample (NIS) 2012 data. http://hcup.ahrq.gov/. Accessed
February 1, 2015.
3. Kudsk KA. Current aspects of mucosal immunology and its influence by
nutrition. Am J Surg. 2002;183:390–398.
4. Jabbar A, Chang WK, Dryden GW, McClave SA. Gut immunology
and the differential response to feeding and starvation. Nutr Clin Pract.
2003;18:461–482.
5. Kang W, Kudsk KA. Is there evidence that the gut contributes to mucosal
immunity in humans? JPEN J Parenter Enteral Nutr. 2007;31:246–258.
6. McClave SA, Heyland DK. The physiologic response and associated
clinical benefits from provision of early enteral nutrition. Nutr Clin Pract.
2009;24(3):305–315.
7. McClave SA, Martindale RG, Rice TW, Heyland DK. Feeding the criti-
cally ill patient. Crit Care Med. 2014;42(12):2600–2610.
8. Vaishnavi C. Translocation of gut flora and its role in sepsis. Indian J Med
Microbiol. 2013;31:334–342.
9. Somanchi M, Tao X, Mullin GE. The facilitated early enteral and dietary
management effectiveness trial in hospitalized patients with malnutrition.
JPEN J Parenter Enteral Nutr. 2011;35(2):209–216.
16 Nutrition in Clinical Practice XX(X)
10. O’Meara D, Mireles-Cabodevila E, Frame F, et al. Evaluation of delivery
of enteral nutrition in critically ill patients receiving mechanical ventila-
tion. Am J Crit Care. 2008;17(1):53–61.
11. Quenot JP, Plantefeve G, Baudel JL, et al. Bedside adherence to clinical
practice guidelines for enteral nutrition in critically ill patients receiving
mechanical ventilation: a prospective, multi-centre, observational study.
Crit Care. 2010;14:R37.
12. Kemper M, Weissman C, Hyman AI. Caloric requirements and supply in
critically ill surgical patients. Crit Care Med. 1992;20(3):344–348.
13. Ukleja A, Freeman KL, Gilbert K, et al. Standards for nutrition support:
adult hospitalized patients. Nutr Clin Pract. 2010;25:403–414.
14. Jensen GL, Bistrian B, Roubenoff R, Heimburger DC. Malnutrition
syndromes: a conundrum vs continuum. JPEN J Parenter Enteral Nutr.
2009;33(6):710–716.
15. Fuhrman MP, Charney P, Mueller CM. Hepatic proteins and nutrition
assessment. J Am Diet Assoc. 2004;104(8):1258–1264.
16. Gibbs J, Cull W, Henderson W, Daley J, Hur K, Khuri SF. Perioperative
serum albumin level as a predictor of operative mortality and mor-
bidity: results from the National VA Surgical Risk Study. Arch Surg.
1999;134(1):36–42.
17. White JV, Guenter P, Jensen G, Malone A, Schofield M; Academy of
Nutrition and Dietetics Malnutrition Work Group; A.S.P.E.N. Malnutrition
Task Force; A.S.P.E.N. Board of Directors. Consensus statement of the
Academy of Nutrition and Dietetics/American Society for Parenteral and
Enteral Nutrition: characteristics recommended for the identification and
documentation of adult malnutrition (undernutrition). J Acad Nutr Diet.
2012;112(5):730–738.
18. A.S.P.E.N. Board of Directors and the Clinical Guidelines Task Force.
Guidelines for the use of parenteral and enteral nutrition in adult and
pediatric patients. JPEN J Parenter Enteral Nutr. 2002;26(1 suppl):1SA–
138SA.
19. Wooley JA, Sax HC. Indirect calorimetry: applications to practice. Nutr
Clin Pract. 2003;18(5):434–439.
20. Institute of Medicine, Food and Nutrition Board. Dietary Reference
Intakes for Macronutrients: Energy, Carbohydrate, Fiber, Fat, Fatty
Acids, Cholesterol, Protein and Amino Acids. Washington, DC: National
Academies Press; 2005:265–645.
21. Mirtallo J, Canada T, Johnson D, et al; Task Force for the Revision of Safe
Practices for Parenteral Nutrition. Safe practices for parenteral nutrition.
JPEN J Parenter Enteral Nutr. 2004;28(6):S39–S70.
22. McClave SA, Martindale RG, Vanek VW, et al; A.S.P.E.N. Board of
Directors; American College of Critical Care Medicine; Society of Critical
Care Medicine. Guidelines for the provision and assessment of nutrition
support therapy in the adult critically ill patient: Society of Critical Care
Medicine (SCCM) and American Society for Parenteral and Enteral
Nutrition (A.S.P.E.N.). JPEN J Parenter Enteral Nutr. 2009;33(3):
277–316.
23. Stroud M, Duncan H, Nightingale J. Guidelines for enteral feeding in adult
hospital patients. Gut. 2003;52(suppl 7):vii1–vii12.
24. Minard G. Enteral access. Nutr Clin Pract. 1994;9:172–182.
25. Miller KR, McClave SA, Kiraly LN, Martindale RG, Benns MV. A tuto-
rial on enteral access in adult patients in the hospitalized setting. JPEN J
Parenter Enteral Nutr. 2014;38(3):282–295.
26. Charney P, Malone A. ADA Pocket Guide to Enteral Nutrition. Chicago,
IL: D. Faulhaber; 2006.
27. Koopman M, Kudsk K, Szotkowski M, Rees SM. A team-based protocol
and electromagnetic technology eliminate feeding tube placement compli-
cations. Ann Surg. 2011;253(2):287–302.
28. Gray R, Tynan C, Reed L, et al. Bedside electromagnetic-guided feeding
tube placement: an improvement over traditional placement technique?
Nutr Clin Pract. 2007;22(4):436–444.
29. Rivera R, Campana J, Hamilton C, Lopez R, Seidner S. Small bowel feed-
ing tube placement using an electromagnetic tube placement device: accu-
racy of tip location. JPEN J Parenter Enteral Nutr. 2011;35(5):636–642.
Downloaded from ncp.sagepub.com at CAMBRIDGE UNIV LIBRARY on August 1, 2015
30. Bankhead R, Boullata J, Brantley S, et al. Enteral nutrition practice recom-
mendations. JPEN J Parenter Enteral Nutr. 2009;33(2):122–167.
31. Stayner JL, Bhatnagar A, McGinn AN, Fang JC. Feeding tube placement:
errors and complications. Nutr Clin Pract. 2012;27(6):738–748.
32. Toussaint E, Van Gossum A, Ballarin A, Arvanitakis M. Enteral access in
adults. Clin Nutr. 2015;34(3):350–358.
33. Kearns PJ, Chin D, Mueller L, Wallace K, Jensen WA, Kirsch CM. The
incidence of ventilator- associated pneumonia and success in nutrient
delivery with gastric versus small intestinal feeding: a randomized clinical
trial. Crit Care Med. 2000;28:1742–1746.
34. Strong RM, Condon SC, Solinger MR, Namihas BN, Ito-Wong LA, Leuty
JE. Equal aspiration rates from postpylorus and intragastric-placed small-
bore nasoenteric feeding tubes: a randomized, prospective study. JPEN J
Parenter Enteral Nutr. 1992;16:59–63.
35. Mion LC, Minnick AF, Leipzig RM, Catrambone CD, Johnson ME.
Patient-initiated device removal in intensive care units: a national preva-
lence study. Crit Care Med. 2007;35(12):2714–2720.
36. McGinnis C. The feeding tube bridle: one inexpensive, safe, and effective
method to prevent inadvertent feeding tube dislodgement. Nutr Clin Pract.
2011;26(1):70–77.
37. McClave SA, Sexton LK, Spain DA, et al. Enteral tube feeding in the
intensive care unit: factors impeding adequate delivery. Crit Care Med.
1999;27(7):1252–1256.
38. Kee YYK, Brooks W, Dhami R, Bhalla A. Evaluating the use of hand
control mittens in post stroke patients who do not tolerate naso-gastric
feeding. Cerebrovas Dis. 2007;23(suppl 2):93.
39. Popovich MJ, Lockrem JD, Zivot JB. Nasal bridle revisited: an improve-
ment in the technique to prevent unintentional removal of small-bore
nasoenteric feeding tubes. Crit Care Med. 1996;24(3):429–431.
40. Guenter P, Hicks RW, Simmons D, et al. Enteral feeding misconnec-
tions: a consortium position statement. Jt Comm J Qual Patient Saf.
2008;34(5):285–292.
41. Simmons D, Symes L, Guenter P, Graves K. Tubing misconnections: nor-
malization of deviance. Nutr Clin Pract. 2011;26(3):286–293.
42. Guenter P, Hicks RW, Simmons D. Enteral feeding misconnections: an
update. Nutr Clin Pract. 2009;24(3):325–334.
43. Guenter P. New enteral connectors: raising awareness. Nutr Clin Pract.
2014;29(5):612–614.
44. The Joint Commission Sentinel Event Alert. Tubing Misconnections—A
Persistent and Potentially Deadly Occurrence. http://www.jointcom-
mission.org/sentinel_event_alert_issue_36_tubing_misconnections—a_
persistent_and_potentially_deadly_occurrence/default.aspx. Published
2006. Accessed May 10, 2015.
45. ISO Small Bore Connectors Working Group. ANSI/AAMI/ISO 80369-
1:2010. Small Bore Connectors for Liquids and Gasses in Healthcare
Applications—Part 1: General Requirements. Arlington, VA: Association
for the Advancement of Medical Instrumentation; 2011.
46. Global Enteral Device Supply Association. Stay connected 2015. http://
www.stayconnected.org/index.html. Published December 2014. Accessed
May 10, 2015.
47. Brown B, Roehl K, Betz M. Enteral nutrition formula selection: current evi-
dence and implications for practice. Nutr Clin Pract. 2015;30(1):72–85.
48. Wong K. The role of fiber in diarrhea management. Support Line.
1998;20(6):16–20.
49. U.S. Food and Drug Administration. Draft guidance for industry: fre-
quently asked questions about medical foods. 2nd ed. http://www.fda.gov/
Food/GuidanceRegulation/GuidanceDocumentsRegulatoryInformation/
MedicalFoods/ucm054048.htm. Published 2013. Accessed February 3, 2015.
50. Kohn CL. The relationship between enteral formula contamination and
length of enteral delivery set usage. JPEN J Parenter Enteral Nutr.
1991;15:567–571.
51. Perez SK, Brandt K. Enteral feeding contamination: comparison of dilu-
ents and feeding bag usage. JPEN J Parenter Enteral Nutr. 1989;13:
306–308.
Kozeniecki and Fritzshall 17
52. Desachy A, Clavel M, Vuagnat A, Normand S, Gissot V, Francois B.
Initial efficacy and tolerability of early enteral nutrition with immedi-
ate or gradual introduction in intubated patients. Intensive Care Med.
2008;34:1054–1059.
53. Heyland DK, Murch L, Cahill N, et al. Enhanced protein-energy provision
via the enteral route feeding protocol in critically ill patients: results of a
cluster randomized trial. Crit Care Med. 2013;41:2743–2753.
54. Taylor B, Brody R, Denmark R, Southard R, Byham-Gray L. Improving
delivery through the adoption of the “Feed Early Enteral Diet Adequately
for Maximum Effect (FEED ME)” protocol in a surgical trauma ICU: a
quality improvement review. Nutr Clin Pract. 2014;29:639–648.
55. Lord L, Harrington M. Enteral nutrition implementation and management.
In: Merritt R, ed. The A.S.P.E.N. Nutrition Support Practice Manual.
2nd ed. Silver Spring, MD: American Society for Parenteral and Enteral
Nutrition; 2005:76–89.
56. Byrnes MC, Stangenes J. Refeeding in the ICU: an adult and pediatric
problem. Curr Opin Clin Nutr Metab Care. 2011;14:186–192.
57. National Institute for Health and Clinical Excellence. Nutrition support in
adults. Clinical guideline CG32.
58. Cahill GF. Starvation in man. N Engl J Med. 1970;282:668–675.
59. Chapman MJ, Nguyen NQ, Deane AM. Gastrointestinal dysmotility:
evidence and clinical management. Curr Opin Clin Nutr Metab Care.
2013;16(2):209–216.
60. Taylor SJ, Manara AR, Brown J. Treating delayed gastric emptying
in critical illness: metoclopramide, erythromycin, and bedside (cor-
trak) nasointestinal tube placement. JPEN J Parenter Enteral Nutr.
2010;34(3):289–294.
61. Ali T, Hasan M, Hamadani M, Harty RF. Gastroparesis. South Med J.
2007;100(3):281–286.
62. Sidery MB, Macdonald IA, Blackshaw PE. Superior mesenteric artery
blood flow and gastric emptying in humans and the differential effects of
high fat and high carbohydrate meals. Gut. 1994;35(2):186–190.
63. Malone A, Seres D, Lord L. Complications of enteral nutrition. In: Mueller
CM, ed. The A.S.P.E.N. Adult Nutrition Support Core Curriculum. Silver
Spring, MD: A.S.P.E.N.; 2012.
64. Kollef MH. The prevention of ventilator-associated pneumonia. N Engl J
Med. 1999;340:627–634.
65. Majid HA, Emery PW, Whelan K. Definitions, attitudes, and manage-
ment practices in relation to diarrhea during enteral nutrition: a survey of
patients, nurses, and dietitians. Nutr Clin Pract. 2012;27(2):252–260.
66. Juckett G, Trivedi R. Evaluation of chronic diarrhea. Am Fam Physician.
2011;84(10):1119–1126.
67. Beckwith MC, Feddema SS, Barton RG, Graves C. A guide to drug
therapy in patients with enteral feeding tubes: dosage form selection and
administration methods. Hosp Pharm. 2004;39(3):225–237.
68. Chang SJ, Huang HH. Diarrhea in enterally fed patients: blame the diet?
Curr Opin Clin Nutr Metab Care. 2013;16(5):588–594.
69. Thorson MA, Bliss DZ, Savik K. Re-examination of risk factors for non-
Clostridium difficil-associated diarrhoea in hospitalized patients. J Adv
Nurs. 2008;62(3):354–364.
70. Lefton J. Management of common gastrointestinal complications in tube-
fed patients. Support Line. 2002;24(1):19–25.
71. Hempel S, Newberry SJ, Maher AR, et al. Probiotics for the prevention
and treatment of antibiotic-associated diarrhea: a systematic review and
meta-analysis. JAMA. 2012;307(18):1959–1969.
72. Guerra TL, Mendonca SS, Marshall NG. Incidence of constipation in an
intensive care unit. Rev Bras Ter Intensiva. 2013;25(2):87–92.
73. Bittencourt AF, Martins JR, Logullo L, et al. Constipation is more fre-
quent than diarrhea in patients fed exclusively by enteral nutrition: results
of an observational study. Nutr Clin Pract. 2012;27(4):533–539.
74. Johanson JF. Review of the treatment options for chronic constipation.
Med Gen Med. 2007;9(2):25.
75. Mostafa SM, Bhandari S, Ritchie G, Gratton N, Wenstone R.
Constipation and its implications in the critically ill patient. Br J Anaesth.
2003;91(6):815–819.
Downloaded from ncp.sagepub.com at CAMBRIDGE UNIV LIBRARY on August 1, 2015
76. Phipps M, Bush JA, Buhrow D, et al. Ileus development in the trauma/
surgical intensive care unit: a process improvement evaluation. Dimens
Crit Care Nurs. 2011;30(3):164–168.
77. Caddell KA, Martindale R, McClave SA, Miller K. Can the intestinal dys-
motility of critical illness be differentiated from postoperative ileus? Curr
Gastroenterol Rep. 2011;13(4):358–367.
78. Aderinto-Adike AO, Quigley EM. Gastrointestinal motility problems in
critical care: a clinical perspective. J Dig Dis. 2014;15(7):335–344.
79. Wilson JP. Postoperative motility of the large intestine in man. Gut.
1975;16(9):689–692.
80. Moss G. Maintenance of gastrointestinal function after bowel surgery
and immediate enteral full nutrition. II. Clinical experience, with objec-
tive demonstration of intestinal absorption and motility. JPEN J Parenter
Enteral Nutr. 1981;5(3):215–220.
81. Hur H, Si Y, Kang WK, Kim W, Jeon HM. Effects of early oral feeding on
surgical outcomes and recovery after curative surgery for gastric cancer:
pilot study results. World J Surg. 2009;33(7):1454–1458.
82. Kasparek MS, Mueller MH, Glatzle J, et al. Postoperative colonic motility
increases after early food intake in patients undergoing colorectal surgery.
Surgery. 2004;136(5):1019–1027.
83. Marcuard SP, Perkins AM. Clogging of feeding tubes. JPEN J Parenter
Enteral Nutr. 1988;12:403–405.
84. Frankel EH, Enow NB, Jackson KC, Kloiber LL. Methods of restoring
patency to occluded feeding tubes. Nutr Clin Pract. 1998;13:129–131.
85. Scanlan M, Frisch S. Nasoduodenal feeding tubes: prevention of occlu-
sion. J Neurosci Nurs. 1992;24:250–259.
86. Gora ML, Tschampel MM, Visconti JA. Considerations of drug therapy in
patients receiving enteral nutrition. Nutr Clin Pract. 1989;4(3):105–110.
87. Kraft MD, Btaiche IF, Sacks GS. Review of the refeeding syndrome. Nutr
Clin Pract. 2005;20:625–633.
88. Skipper A. Refeeding syndrome or refeeding hypophosphatemia: a sys-
tematic review of cases. Nutr Clin Pract. 2012;27(1):34–40.
89. Weinsier RL, Krumdieck CL. Death resulting from overzealous total
parenteral nutrition: the refeeding syndrome revisited. Am J Clin Nutr.
1981;34:393–399.
90. Miller SJ. Death resulting from overzealous total parenteral nutrition: the
refeeding syndrome revisited. Nutr Clin Pract. 2008;23(2):166–171.
91. Rhoney DH, Parker D Jr, Formea CM, Yap C, Coplin WM. Tolerability of
bolus versus continuous gastric feeding in brain-injured patients. Neurol
Res. 2002;24(6):613–620.
92. Nguyen NQ, Chapman M, Fraser RJ, Bryant LK, Burgstad C, Holloway
RH. Prokinetic therapy for feed intolerance in critical illness: one drug or
two? Crit Care Med. 2007;35(11):2561–2567.
93. Edwards SJ, Metheny NA. Measurement of gastric residual volume: state
of the science. Medsurg Nurs. 2000;9:125–128.
94. Bonten MJM, Kullberg BJ, van Dalen R, et al. Selective digestive con-
tamination in patients in intensive care. The Dutch Working Group on
Antibiotic Policy. J Antimicrob Chemother. 2000;46:351–362.
95. Bergmans DC, Bonten MJ, Gaillard CA, et al. Prevention of ventilator-
associated pneumonia by oral decontamination: a prospective, random-
ized, double-blind, placebo-controlled study. Am J Respir Crit Care Med.
2001;164:382–388.
96. Bonten MJ, Gaillard CA, van Tiel FH, Smeets HG, van der Geest S,
Stobberingh EE. The stomach is not a source for colonization of the upper
respiratory tract and pneumonia in ICU patients. Chest. 1994;105:878–884.
97. Pinilla JC, Samphire J, Arnold C, Liu L, Thiessen B. Comparison of
gastrointestinal tolerance to two enteral feeding protocols in critically ill
patients: a prospective, randomized controlled trial. J Parenter Enter Nutr.
2001;25:81–86.
98. McClave SA, Lukan JK, Stefater JA, et al. Poor validity of residual vol-
umes as a marker for risk of aspiration in critically ill patients. Crit Care
Med. 2005;33:324–330.
99. Montejo JC, Miñambres E, Bordejé L, et al. Gastric residual volume dur-
ing enteral nutrition in ICU patients: the REGANE study. Intensive Care
Med. 2010;36(8):1386–1393.
18 Nutrition in Clinical Practice XX(X)
100. Mentec H, Dupont H, Bocchetti M, Cani P, Ponche F, Bleichner G.
Upper digestive intolerance during enteral nutrition in critically ill
patients: frequency, risk factors, and complications. Crit Care Med.
2001;29(10):1955–1961.
101. Reignier J, Mercier E, Le Gouge A, et al. Effect of not monitoring residual
gastric volume on risk of ventilator-associated pneumonia in adults receiv-
ing mechanical ventilation and early enteral feeding: a randomized con-
trolled trial. JAMA. 2013;309:249–256.
102. Whelan K, Schneider SM. Mechanisms, prevention, and management of
diarrhea in enteral nutrition. Curr Opin Gastroenterol. 2011;27(2):152–159.
103. Lebak KJ, Bliss DZ, Savik K. What’s new on defining diarrhea in tube-
feeding studies? Clin Nurs Res. 2003;12(2):174–204.
104. Eisenberg P. An overview of diarrhea in the patient receiving enteral nutri-
tion. Gastroenterol Nurs. 2002;25(3):95–104.
105. World Health Organization. Diarrhoeal disease. http://www.who.int/
mediacentre/factsheets/fs330/en/. Published April 2013. Accessed March
15, 2015.
106. Schiller LR. Secretory diarrhea. Curr Gastroenterol Rep. 1999;1(5):
389–397.
107. Gerding DN, Johnson S, Peterson LR, Mulligan ME, Silva J. Clostridium
difficile-associated diarrhea and colitis. Infect Control Hosp Epidemiol.
1995;16(8):495–477.
108. Jack L, Coyer F, Courtney M, Venkatesh B. Diarrhoea risk factors in
enterally tube fed critically ill patients: a retrospective audit. Intensive Crit
Care Nurs. 2010;26(6):327–334.
109. Huang HH, Hsu CW, Kang SP, et al. Association between illness severity
and timing of initial enteral feeding in critically ill patients: a retrospective
observational study. Nutr J. 2012;11:30.
110. Wierdsma NJ, Peters JHC, Weijs PJM, et al. Malabsorption and nutri-
tional balance in the ICU: fecal weight as a biomarker: a prospective
observational pilot study. Crit Care. 2011;15(6):R264.
111. Jain NK, Patel VP, Pitchumoni CS. Sorbitol intolerance in adults.
Prevalence and pathogenesis on two continents. J Clin Gastroenterol.
1987;9(3):317–319.
112. Lutomski DM, Gora ML, Wright SM, Martin JE. Sorbitol content of
selected oral liquids. Ann Pharmacother. 1993;27(3):269–274.
Downloaded from ncp.sagepub.com at CAMBRIDGE UNIV LIBRARY on August 1, 2015
113. Ratnaike RN, Jones TE. Mechanisms of drug-induced diarrhea in the
elderly. Drugs Aging. 1998;13(3):245–253.
114. Elia M, Engfer MB, Green CJ, Silk DB. Systematic review and meta-
analysis: the clinical and physiological effects of fibre-containing enteral
formulae. Aliment Pharmacol Ther. 2008;27(2):120–145.
115. Hegazi RA, Wischmeyer PE. Clinical review: optimizing enteral nutri-
tion for critically ill patients—a simple data-driven formula. Crit Care.
2011;15(6):234.
116. Shankardass K, Chuchmach S, Chelswick K, et al. Bowel function of
long-term tube-fed patients consuming formulae with and without dietary
fiber. JPEN J Parenter Enteral Nutr. 1990;14(5):508–512.
117. Rothnie NG, Harper RA, Catchpole BN. Early postoperative gastrointes-
tinal activity. Lancet. 1963;2:64–67.
118. Parrish CR. Enteral feeding: the art and the science. Nutr Clin Pract.
2003;18:76–85.
119. Holte K, Kehlet H. Postoperative ileus: a preventable event. Br J Surg.
2000;87(11):1480–1493.
120. Delaney CP, Senagore AJ, Gerkin TM, et al. Association of surgical care
practices with length of stay and use of clinical protocols after elective
bowel resection: results of a national survey. Am J Surg. 2010;199(3):
299–304.
121. Lassen K, Kjaeve J, Fetveit T, et al. Allowing normal food at will after
major upper gastrointestinal surgery does not increase morbidity: a ran-
domized multicenter trial. Ann Surg. 2008;247(5):721–729.
122. Powell KS, Marcuard SP, Farrior ES, Gallagher ML. Aspirating gastric
residuals causes occlusion of small-bore feeding tubes. JPEN J Parenter
Enteral Nutr. 1993;17(3):243–246.
123. Klang M, McLymont V, Ng N. Osmolality, pH, and compatibility of
selected oral liquid medications with an enteral nutrition product. JPEN J
Parenter Enteral Nutr. 2013;37(5):689–694.
124. Chan LN. Drug-nutrient interactions. JPEN J Parenter Enteral Nutr.
2013;37(4):450–459.
125. Centers for Medicare and Medicaid Services. National coverage deter-
mination (NCD) for enteral and parenteral nutritional therapy (180.2).
http://www.cms.gov/medicare-coverage-database/details/ncd-details.
aspx?NCDId=242&ver=1. Accessed March 7, 2015.