ASPEN

Enteral Nutrition Handbook Second Edition

Editors

Ainsley Malone,
MS, RD, LD, CNSC, FAND, FASPEN

Liesje Nieman Carney,

RD, CSP, LDN

Amy Long Carrera,

MS, RD, CNSC, CWCMS

Andrew Mays,
PharmD, BCNSP, CNSC
The American Society for Parenteral and Enteral Nutrition (ASPEN) is a scientific society whose members are
healthcare professionals—physicians, dietitians, nurses, pharmacists, other allied health professionals, and
researchers—dedicated to ensuring that every patient receives safe, efficacious, and high-quality patient care.
ASPEN’s mission is to improve patient care by advancing the science and practice of clinical nutrition and
metabolism.

NOTE: This publication is designed to provide accurate authoritative information with regard to the subject matter covered. It is sold with the
understanding that the publisher is not engaged in rendering medical or other professional advice. Trademarked commercial product names are used only
for education purposes and do not constitute endorsement by ASPEN.

This publication does not constitute medical or professional advice, and should not be taken as such. To the extent the information published herein may be
used to assist in the care of patients, this is the result of the sole professional judgment of the attending health professional whose judgment is the primary
component of quality medical care. The information presented herein is not a substitute for the exercise of such judgment by the health professional.

All rights reserved. No part of this may be used or reproduced in any manner whatsoever without written permission from ASPEN. For information, write:
ASPEN, 8401 Colesville Road, Suite 510, Silver Spring, MD 20910; call: (301) 587-6315; visit: www.nutritioncare.org; or email: aspen@nutr.org.

1 2 3 4 5 6 7 8 9 10

Copyright © 2019. American Society for Parenteral and Enteral Nutrition.

Print ISBN: 978-1-889622-39-2

eBook ISBN: 978-1-889622-40-8

Suggested citation: Malone A, Carney LN, Carrera AL, Mays A, eds. ASPEN Enteral Nutrition Handbook. 2nd ed. Silver Spring, MD: American
Society for Parenteral and Enteral Nutrition; 2019.

Printed in the United States.

 Contents

Preface

Editors, Contributors, and Reviewers

1 Nutrition Screening, Assessment, and Care Plan Development

2 Overview of Enteral Nutrition and Patient Selection

3 Enteral Access Devices

4 Enteral Formulas for Adult Patients

5 Enteral Formulas for Pediatric Patients

6 Enteral Nutrition Orders

7 Preparation, Labeling, and Dispensing of Enteral Nutrition

8 Administration and Monitoring of Enteral Nutrition

9 Complications of Enteral Nutrition

10 Medication Administration with Enteral Nutrition

11 Home Enteral Nutrition

Index
 Preface

We are pleased to present the second edition of the ASPEN Enteral Nutrition Handbook, a comprehensive guide
with up-to-date, specific information on how to safely, effectively, and confidently care for patients receiving enteral
nutrition (EN). Like its predecessor, this new edition features best-practice recommendations based on the most
current research and provides a wide variety of practical tools and tips to save time and elevate the quality of care.
This edition has been completely revised to reflect the many recent advancements in the science and practice of
EN therapy. For example, you will find guidance on using ENFit® devices for tube feeding and medication
administration, coverage of the indicators of malnutrition in adult and pediatric patients, and the latest
recommendations regarding the use of specialty formulas and blenderized tube feedings. There is a new chapter
focused on the preparation, labeling, and dispensing of EN, and this edition has divided the discussion of adult and
pediatric/infant formulas into separate chapters.
The content in this handbook is aligned with ASPEN’s evidence-based guidelines, core curriculum, practice
recommendations, and standards. The book is an invaluable resource for students and trainees in dietetics, medicine,
nursing, and pharmacy. Its “pocket guide” format and easy-to-follow clinical information will appeal to everyone
from the novice to the advanced practitioner.
We thank the many contributors and reviewers who shared their knowledge, analysis of the literature, and
clinical expertise in the area of EN support. It is our hope that this handbook improves the ordering, administration
and safety of EN support to patients.

Ainsley Malone, MS, RD, LD, CNSC, FAND, FASPEN

Liesje Nieman Carney, RD, CSP, LDN
Amy Long Carrera, MS, RD, CNSC, CWCMS
Andrew Mays, PharmD, BCNSP, CNSC
 Editors, Contributors, and Reviewers

Editors
Ainsley Malone, MS, RD, LD, CNSC, FAND, FASPEN
Clinical Practice Specialist
The American Society for Parenteral and Enteral Nutrition
Nutrition Support Dietitian
Mt. Carmel West Hospital
Columbus, OH

Liesje Nieman Carney, RD, CSP, LDN

Clinical Dietitian IV, Publication Specialist
Children’s Hospital of Philadelphia
Philadelphia, PA

Amy Long Carrera, MS, RD, CNSC, CWCMS

Lead Clinical Dietitian
Pacifica Hospital of the Valley
Los Angeles, CA

Andrew Mays, PharmD, BCNSP, CNSC

Clinical Pharmacy Specialist–Nutrition Support
University of Mississippi Medical Center
Jackson, MS

Contributors
Phil Ayers, PharmD, BCNSP, FASHP
Chief, Clinical Pharmacy Services, Mississippi Baptist Medical Center
Clinical Associate Professor, University of Mississippi School of Pharmacy
Jackson, MS

Lillian Harvey Banchik, MD, FACS, CNSC, FASPEN

North Shore University Hospital, Manhasset, NY
Assistant Clinical Professor, Donald and Barbara Zucker School of Medicine at Hofstra/Northwell
Long Island, NY

Sarah Ann Borowicz, MS, RDN, LDN

Clinical Pediatric Dietitian
Children’s Hospital of Philadelphia
Philadelphia, PA

Kelly Green Corkins, MS, RD-AP, CSP, LDN, FAND

Pediatric/CVICU Clinical Dietitian III
Department of Nutrition Therapy, Le Bonheur Children’s Hospital
Memphis, TN

Wendy Cruse, MMSc, RDN, CSPCC, CLS, CD

Pediatric/NICU Clinical Dietitian Senior
Riley Hospital for Children at Indiana University Health
Indianapolis, IN

Kathryn Drogan, MS, NP, ANP-BC

Nurse Practitioner
University of Rochester
Rochester, NY

Arlene A. Escuro, MS, RD, LD, CNSC, FAND

Advanced Practice II Dietitian
Cleveland Clinic
Cleveland, OH

John C. Fang, MD
Freston Takeda Professor of Medicine
Chief, Division of Gastroenterology, Hepatology, and Nutrition
Department of Internal Medicine, University of Utah Health
Salt Lake City, UT

Audrey Foster, MS, RDN, CNSC

Clinical Dietitian
Children’s Hospital of Philadelphia
Philadelphia, PA

Kimberly Gorsuch, BSN, RN

Gastroenterology/Nutrition Metabolic Support Care Manager
Cancer Treatment Centers of America
Comprehensive Care Network Chicago
Zion, IL

June Greaves, RD, CNSC, CDN, LD, LDN

A. Christine Hummell, MS, RD, LD, CNSC

Clinical Dietitian, Advanced Practitioner
Cleveland Clinic
Cleveland, OH

Deb Hutsler, MS, RD, LD

Manager of Nutrition Services
Akron Children’s Hospital
Akron, OH

Andrea K. Jevenn, MEd, RD, LD, CNSC

Advanced Practice II Dietitian
Cleveland Clinic Digestive Disease and Surgical Institute
Cleveland, OH

Merin Kinikini, DNP, FNP, RD, CNSC

Nurse Practitioner for Metabolic Nutrition Support Clinic, Intermountain Medical Center
Adjunct Faculty, University of Utah, College of Nursing
Salt Lake City, UT
Mary Kuehl, MS, RD, CNSC
Registered Dietitian
Shield HealthCare

Carolyn Kusenda, MS, RD, LD, CNSC, CSP

Clinical Nutrition Lead
Children’s Healthcare of Atlanta
Atlanta, GA

Rachel Larry, PharmD candidate

Student Pharmacist
University of Mississippi
Jackson, MS

Linda M. Lord, NP, ACNP-BC, CNSC

Nutrition Support Nurse Practitioner
University of Rochester Medical Center
Rochester, NY

Beth Lyman, MSN, RN, CNSC

Senior Clinical Program Coordinator, Nutrition Support, Co-Director of Nutrition Support
Children’s Mercy Kansas City
Kansas City, MO

Mary Marian, DCN, RDN, CSO, FAND

Assistant Professor of Practice and Director, Didactic Program in Dietetics
College of Agriculture and Life Sciences
Department of Nutritional Sciences
University of Arizona
Nutrition Consultant, AZ Oncology
Tucson, AZ

Karen Martin, MA, RDN, LD, FAND

Nutrition Support Specialist, Amerita Specialty Infusion
Neuromuscular Dietitian, UT Health San Antonio
San Antonio, TX

Mary S. McCarthy, PhD, RN, CNSC, FAAN

Nurse Scientist
Center for Nursing Science & Clinical Inquiry
Madigan Army Medical Center
Tacoma, WA

Jessica Monczka, RD, CNSC

Nutrition Support Specialist
Option Care Home Infusion
Denver, CO

Katina Rahe, BSN, RN, CPN

Enteral Access Team Nursing Program Coordinator
Children’s Mercy Kansas City
Kansas City, MO

Christina Ritchey, MS, RD, LD, CNSC

Consultant
Camarillo, CA
Caroline Steele, MS, RD, CSP, IBCLC, FAND
Director, Clinical Nutrition and Lactation Services
Children’s Hospital of Orange County
Orange, CA

Jacqueline Sullivan, MS, RD

Clinical Dietitian
SSM St Mary’s Hospital, Nutrition Services
Madison, WI

Reviewers
Anastasia E. Arena, BS, RD, LDN
Clinical Nutrition Specialist
Critical Care Medicine/Home Parenteral Nutrition Program
Boston Children’s Hospital
Boston, MA

Meg Begany, RD, CSP, CNSC, LDN

Neonatal Dietitian/Nutrition Support Service Specialist
Children’s Hospital of Philadelphia
Philadelphia, PA

Stephanie Dobak, MS, RD, LDN, CNSC

Clinical Dietitian
Thomas Jefferson University Hospital
Philadelphia, PA

June Garrett, MS, RDN-AP, CNSC, CLC

Clinical Dietitian
Children’s Hospital of Los Angeles
Los Angeles, CA

Peggi Guenter, PhD, RN, FAAN, FASPEN

Senior Director of Clinical Practice, Quality, and Advocacy
American Society for Parenteral and Enteral Nutrition
Silver Spring, MD

Lauren M. Hudson, MS, RD, LDN

Director, Clinical Nutrition Support Services
Hospital of the University of Pennsylvania
Philadelphia, PA

Carol Ireton-Jones, PhD, RDN, LD, CNSC, FASPEN

Nutrition Therapy Specialist
Good Nutrition for Good Living
Dallas, TX

Rachelle Kirsch, RD, LD, CNSC

Clinical Dietitian–Trauma
Baylor University Medical Center
Dallas, TX

Mark Klang, MS, PhD, RPh, BCNSP

Core Manager, Research Pharmacy
Memorial Sloan Kettering Cancer Center
New York, NY
Carolyn Kusenda, MS, RD, CNSC, CSP, LD
Clinical Nutrition Lead
Children’s Healthcare of Atlanta
Atlanta, GA

Carol McGinnis, DNP, APRN-CNS, CNSC

Clinical Nurse Specialist, Nutrition Support
Sanford USD Medical Center
Sioux Falls, SD

Kris M. Mogensen, MS, RD-AP, LDN, CNSC

Team Leader Dietitian Specialist
Department of Nutrition
Brigham and Women’s Hospital
Boston, MA

Susan Roberts, DCN, RDN, LD, CNSC, FAND

Area Director of Clinical Nutrition/Dietetic Internship Director
Baylor Scott & White Health/Aramark Healthcare
Dallas, TX

Carol J. Rollins, MS, RD, PharmD, CNSC, BCNSP, FASPEN

Clinical Professor
University of Arizona, College of Pharmacy, Department of Pharmacy Practice and Science
Tucson, AZ

David S. Seres, MD, ScM, FASPEN

Director of Medical Nutrition, Associate Clinical Ethicist, and Associate Professor of Medicine
Institute of Human Nutrition
Columbia University Irving Medical Center
NewYork-Presbyterian Hospital
New York, NY

Wednesday Marie A. Sevilla, MD, MPH, CNSC

Assistant Professor of Pediatrics
UPMC Children’s Hospital of Pittsburgh
Division of Pediatric Gastroenterology, Hepatology and Nutrition
Pittsburgh, PA

Allison Shaffer, RD, LDN

Registered Dietitian/Clinical Nutrition Specialist
Boston Children’s Hospital
Boston, MA

Erin Sullivan, RD, LDN

Pediatric Critical Care Dietitian
The Children’s Hospital of Philadelphia
Philaelphia, PA

Laura J. Szekely, MS, RD, LD

Supervisor, Nutrition Services
Akron Children’s Hospital
Akron, OH

Abby Wood, MS, RDN, CSO, LD, CNSC

Clinical Dietitian Specialist
Baylor University Medical Center
Dallas, TX
 CHAPTER 1

Nutrition Screening, Assessment, and Care Plan

Development

The Nutrition Care Pathway

In clinical practice, the nutrition screening and assessment processes focus on parameters that are easy to obtain,
cost effective, age appropriate, and clinically relevant. A complete nutrition assessment involves integrating
objective measures including growth history (for pediatric patients) and physical exam findings with subjective
clinical judgment to best identify patients who have or are at risk for malnutrition. Although the criteria for
identifying and diagnosing both adult and pediatric malnutrition have evolved over the last several decades, the
literature consistently demonstrates the need to assess information from the following 5 domains: (a)
anthropometrics, (b) etiology and chronicity (with or without inflammation), (c) mechanism, (d) nutrient imbalance,
and (e) functional/developmental outcomes. The ability to collect and appropriately assess these data is an important
proficiency in any clinician’s skill set and has remained an integral component within the scope of practice of
clinical nutrition professionals.
While pediatric and adult nutrition assessment share many of the same foundational requirements, pediatric
assessment also encompasses two additional pivotal concepts: oral motor skills and optimal growth. The latter is the
most important marker for assessing the nutrition status of a pediatric patient.
Nutrition screening and assessment are part of the nutrition care pathway and comprise a series of steps with
builtin feedback (see Figures 1-1 and 1-2).1–4 The information from the screening and assessment steps are used to
make a nutrition diagnosis and plan the intervention. Nutrition monitoring involves periodic measurement and
review of the individual’s assessment data for the purpose of modifying interventions to achieve desired clinical
outcomes.1,5
Nutrition Screening
Nutrition screening is the first step in the process to evaluate whether an individual is at risk of becoming
malnourished or is already malnourished. Screening thereby serves the purpose of identifying who would benefit
from a full nutrition assessment to determine appropriate interventions to minimize comorbidities and promote
improved patient outcomes.2,6,7 An effective nutrition screening tool should be valid and reliable, concise, and easy
to use by any clinician trained to screen the particular patient population.7
Information collected in a nutrition screening varies depending on the population and setting.2 Nutrition
screenings may solicit a wide range of information about the patient, including height (or length), recent weight
history, past and current nutrition interventions, clinical and diagnostic information, medical history, functional
status, and psychological and social status.6 Such information helps clinicians determine an individual’s nutrition
status and the likelihood that he/she will develop nutrient deficits during a course of treatment or hospitalization.
While informative, the interpretation of screening parameters often employs clinical judgment and therefore is
primarily subjective.1
A number of nutrition screening tools have been reviewed in the literature (see Tables 1-1 and 1-2 for
examples).6,8–18 Despite the variety of available tools, most have limitations. For example, they may not have been
evaluated for use in long-term care facilities or outpatient clinics; they may not address the screening needs of obese
patients; or they could have the potential for error if the necessary components are not readily available.19
Constraints in using existing screening tools for critically ill adults have led to the recommendation to use the
Nutrition Risk in Critically Ill (NUTRIC) tool or the Nutrition Risk Score (NRS-2002).20 Although there is a need
for valid and reliable tools, limited data demonstrating their effectiveness are currently available.6,8

TABLE 1-1. Selected Adult Nutrition Screening Instruments

Instrument
Description
(Evidence Grade)a
Intended population: Hospitalized medical-surgical and acute patients
Parameters used:
• Recent unintentional weight loss
• BMI
• Disea
se severity
• Impaired general condition
NRS-2002 (Grade • Age >70 y
I) Purpose: Originally designed as a tool to identify patients who would benefit
from nutrition support; also used to assess nutrition status and predict clinical
outcomes
Comments:
• Good validity against nutrition assessment/body composition
• Good to fair validity against SGA
• Poor validity against MNA
• Good to fair predictive validity for mortality, LOS, and complications
Intended populations: Oncology patients; acute and elderly hospitalized patients
Parameters used: Appetite, unintentional weight loss
Purpose: Quick to administer tool for screening/assessing nutrition status
and predicting clinical outcomes
MST (Grade II) Comments:
• Only tool available that is both valid and reliable for acute care/hospital-
based ambulatory care patients
• Good validity against SGA
• Performs poorly in predicting clinical outcomes
Intended populations: Hospitalized medical-surgical patients; elderly
hospitalized patients
Parameters used:
 • BMI
• Recent unintentional weight loss
• Problems with food intake
MUST (Grade II) • Disease severity
Purpose: Developed for screening in community settings; widely used in
Europe; for screening and assessing nutrition status and predicting clinical
outcomes
Comments:
• Good validity (by kappa) against SGA, NRS, assessment by dietitian
• Good to fair validity in multiple studies
• Good to fair predictor of LOS and mortality in malnourished patients
Intended population: Ambulatory, subacute, hospitalized elderly patients
Parameters used:
• Unintentional weight loss
• Appetite
• Food intake problem
• Disease severity
• Homebound
MNA-SF (Grade II) • Dementia/depression
Purpose: Easy and simple substitution for full MNA to screen and assess nutrition
status of older adults
Comments:
• Excellent validity against MNA (likely because of incorporation bias)
• Excellent sensitivity but poor specificity against nutrition assessment
or assessment by professional (too many false positives for malnutrition)
• Does not predict outcomes well in elderly patients
Intended population: Critically ill adult and elderly patients
Parameters used:
• APACHE II
• SOFA (with or without IL-6)
• Number of comorbidities
NUTRIC Score • Days from hospital to ICU admission
(not graded) Purpose: Quantification of risk of adverse outcomes that may be positively
affected by nutrition therapies
Comments:
• Higher scores correlated with increased mortality and longer duration
of mechanical ventilation
• Predictive of 28-day mortality
Abbreviations: APACHE, Acute Physiology and Chronic Health Evaluation; BMI, body mass index; ICU, intensive care unit; IL-6, interleukin-
6; LOS, length of stay; MNA, Mini Nutritional Assessment; MNA-SF, Mini Nutritional Assessment-Short Form; MST, Malnutrition Screening
Tool; MUST, Malnutrition Universal Screening Tool; NRS-2002, Nutritional Risk Screening 2002; NUTRIC, Nutrition Risk in Critically Ill; SGA,
subjective global assessment; SOFA, sequential organ failure assessment.
a
Evidence grades are from reference 6. Refer to the original article for additional information on the grades.
Source: Information is from references 6, 8, 10, and 11.

TABLE 1-2. Validated Nutrition Screening Tools for Hospitalized Pediatric Patients
Instrument Description
Intended population: Hospitalized, full-term children (all ages)
Parameters used:
• Simple questionnaire; caregiver can answer with a yes or no:
• Weight loss?
• Poor weight gain in last few months?
PNST • Decreased intake/appetite in last few weeks?
• Is the child overtly underweight?
Comments:
• Avoids anthropometric measures and growth references
• Reliability and reproducibility are limited
• Easy and simple
Intended population: Hospitalized children
Parameters used: 5-step scoring system:
1. BMI below the cutoff?
2. Weight loss?
3. Decreased intake?
4. Nutrition affected by recent admission/ condition?
PYMS 5. Calculate score
Comments:
• Identifies patients as at high, medium, or low risk of malnutrition
• Studies find to be the most accurate and most reliable in clinical settings
• Does not include impact of underlying disease
• Recommends a nutrition intervention for each risk
Intended population: Hospitalized children, ages 2-17 y
Parameters used: 5-step scoring system:
1. Diagnosis (with nutritional implication)
2. Nutrition intake
3. Weight and height
STAMP 4. Overall risk of malnutrition
5. Care plan
Comments:
• Identifies patients as at high, medium, or low risk of malnutrition
• Available for download from www.stampscreeningtool.org
• Recommends a nutrition intervention for each risk
Intended population: Children with cancer
Parameters used:
• Height
SCAN • Weight
• BMI
• Body composition
Comment: Identifies children with cancer who are at risk for malnutrition
Intended population: Hospitalized children, ages 3-18 y
Parameters used:
• Subjective clinical assessment
• High-risk diseases
 STRONGkids • Nutritional intake and losses (excessive diarrhea or vomiting)
• Weight loss or poor weight gain
Comments:
• Identifies risk of malnutrition in hospitalized patients
• Quick, reliable, and practical tool
Intended population: General pediatric population
Parameters used:
• Detailed questionnaire including gender, age, underlying disease,
anthropometrics (including weight, height, BMI), nutrition-related medical
history, and a complete physical examination
SGNA
Comments:
• Identifies malnourished children at higher risk of nutrition-associated
complications and prolonged hospitalization classifying patient as normal,
moderate, or severely malnourished
• Consists of both subjective and objective components

Nutrition Assessment and Indicators of Malnutrition

The nutrition assessment process identifies patients with malnutrition or other nutrition-related problems that may
require intervention. Alterations in nutrition status can be caused by altered nutrient intake, malabsorption, or altered
metabolism.21 Uncomplicated malnutrition is caused by an imbalance between nutrient intake and nutrient
requirements in the absence of disease or trauma.22
In the nutrition assessment, the clinician obtains and interprets information that can shed light on the patient’s
nutrition status. This information includes the patient’s medical and social history, food and nutrition-related history,
anthropometric data, laboratory test findings, results of medical tests and procedures, and the nutrition-focused
physical exam. To obtain information for the nutrition assessment, the clinician will review medical records, nutrient
intake records, diet histories, and available laboratory test data; interview the patient; and complete a physical
assessment.

Adult Malnutrition
Two important nutrition assessment tools used to identify malnutrition in adult patients are the subjective global
assessment (SGA) and the clinical characteristics of mal-nutrition described by the American Society for Parenteral
and Enteral Nutrition (ASPEN) and the Academy of Nutrition and Dietetics (AND). SGA is a well-tested and widely
accepted nutrition assessment tool that relies on weight history and dietary change, persistent gastrointestinal (GI)
symptoms, functional capacity, effects of disease on nutrition requirements, and changes in appearance as
determined by a physical exam (see Figure 1-3).23,24 On the basis of these parameters, clinicians categorize a
patient’s nutrition status as well nourished, moderate or suspected malnutrition, or severe malnutrition.
 In an effort to encourage consistency and promote objectivity for the diagnosis of malnutrition in hospitalized
patients, ASPEN and AND have published a list of specific malnutrition criteria within an etiology-based system
that account for a modern understanding of the effects of the inflammatory process.25,26 In many ways, the
ASPEN/AND criteria are similar to those used in the SGA (see Table 1-3).27 However, the ASPEN/AND method
identifies markers that may be used to analyze proinflammatory states during an acute illness or injury or during
chronic illness.25,27 Examples of diseases and conditions categorized as acute illness or injury include sepsis, closed
head injury, major abdominal surgery, or multiple trauma; these are associated with marked inflammatory response.
Inflammation of lesser intensities tends to be affiliated with chronic illnesses, such as chronic obstructive pulmonary
disease, organ failure, diabetes mellitus, obesity, or cancer.28,29 Although they are not all-inclusive listings, Tables 1-
4, 1-5, and 1-6 highlight practical indicators to assist the clinician in evaluating the presence and intensity of
inflammation in complex patient scenarios.23,25,27–38 The ASPEN/AND method also highlights risk factors for
malnutrition independent of inflammation—including social, environmental, and behavioral circumstances—that
may be found in patients with conditions such as anorexia nervosa.25

TABLE 1-3. Comparison of the SGA and ASPEN/AND Nutrition Assessment Methods

SGA ASPEN/AND Malnutrition Clinical Characteristics

Medical/nutrition history
• Weight changes • Unintentional weight loss
• Nutrition intake • Nutrition intake
• GI symptoms • No specific GI symptom review
• Functional status • Functional status
• Metabolic stress • Chronic illness, acute illness, or
from current disease state social/behavioral/environmentalcircumstances
Physical exam
• Muscle wastinga
• Temporalis
• Pectoralis
• Muscle wastinga
• Deltoids
• Quadriceps
• Scapular
• Deltoids
• Interosseous
• Quadriceps
• Gastrocnemius
• Loss of subcutaneous fata
• Loss of subcutaneous fata
• Orbital
• Triceps
• Triceps
• Chest
• Midaxillary line/iliac crest

• Edema • Fluid accumulation

• Effect on weight • Nutrition-related edema
• Ankles • Effect on weight
• Sacral area • Upper/lower extremities
• Ascites • Vulvar/scrotal edema
• Ascites
Laboratory data
 Laboratory data
• Not used • Used to determine presence and severity of inflammatory process
Abbreviations: AND, Academy of Nutrition and Dietetics; ASPEN, American Society for Parenteral and Enteral Nutrition; GI, gastrointestinal;
SGA, subjective global assessment.
a
Evaluation of muscle wasting and fat loss areas as described by the original methodologies.
Source: Information is from references 23, 25, and 27.

TABLE 1-4. Potential Inflammatory Markers

Indicators of Infectious
Examples Alternate Interpretations
Process
Biochemical markers
Serum proteins • Albumin: overhydration, nephrotic
syndrome, liver disease, heart
failure
• Transferrin: anemia, excess
• Low albumin excretion from kidneys
• Low prealbumin • Ferritin: frequent blood transfusions,
• Low transferrin porphyria, hemochromatosis,
• Elevated ferritin alcohol abuse
Blood glucose
• Elevated CRP • IV fluids with dextrose, medications
White blood cells
• Hyperglycemia (eg, steroids)
• Leukocytosis • Leukocytosis: medications, normal
• Leukopenia life-cycle variations (eg, pregnancy,
newborn infant)
• Leukopenia: medications, congenital
problems, autoimmune disorders,
vitamin deficiencies
Microbiological markers
Urine, fecal, blood, or other • Results positive for fungal,
body fluid cultures • n/a
bacterial, viral microbes
Vital signs
• Hypotension • Hypotension: dehydration,
Blood pressure
• Hypertension medications, heart disease,
pregnancy, blood loss
• Tachycardia
Heart rate • Hypertension: pain, medications,
• Bradycardia underlying disease/condition,
physical inactivity
• Tachycardia: uncontrolled pain,
heart conditions, dehydration,
tumors, hypertension,
medications, drug/alcohol abuse
• Bradycardia: hypothyroidism, heart
• Fevers damage/ disorder, COPD,
Temperature
• Hypothermia medications
 • Fevers: heat exhaustion,
medications
• Hypothermia: cold exposure, CNS or
endocrine dysfunction, metabolic
derangements

Abbreviations: CNS, central nervous system; COPD, chronic obstructive pulmonary disease; CRP, C-reactive protein; IV, intravenous; n/a,
not applicable. Source: Information is from references 25 and 28-38.

TABLE 1-5. Imaging Study and Procedure Results That May Indicate Inflammation

Study/Procedure Findings Indicative of Inflammatory Process

• Inflammation
• Pneumonia
Chest X-ray
• Pulmonary fistula
• Mass, nodule
• Abscess
• Pancreatitis
• Inflammation
CT scans
• Cancer
• Mass
• Obstruction
• Endocarditis
Echocardiogram
• Vegetations
• Radiation enteritis
• Esophagitis
• Gastritis
• Graft-versus-host disease
Endoscopy
(eg, colonoscopy, upper GI)
• Ulcers
• Fistula
• Enteritis
• Colitis
• Cancer
Abbreviations: CT, computed tomography; GI, gastrointestinal.
Source: Information is from references 27 and 28.

TABLE 1-6. Potential Signs of Inflammation from Clinical Inspection

Parameter for Inspection Potential Indicators of Inflammation

• Burns
• Rashes
• Wounds
Skin
• Erythema
 • Swelling
• Pain
• Red, swollen
Eyes • Tenderness, pain
• Drainage
Nose • Drainage
• Swelling
• Erythema
Mouth/gums
• Sores
• Pain
• Chills
• Night sweats
Miscellaneous
• Productive cough
• Painful urination
Source: Information is from reference 27.

Once the contextual influence of the inflammatory state is understood within an individual case, the
ASPEN/AND criteria can be evaluated (see Tables 1-7 and 1-8).25,39 Presentation of at least 2 of the 6 criteria
establishes the existence of malnutrition.25 The severity of those characteristics then determines whether the
condition is severe or nonsevere.25,40
The ASPEN/AND criteria for severe malnutrition in adults may be used when assigning the International Classi
fication of Diseases, 10th edition, Clinical Modification (ICD-10-CM) diagnosis code E43, Severe protein-energy
malnutrition, to patient documentation, and the ASPEN/AND criteria for nonsevere/moderate malnutrition may map
to the ICD-10-CM code E44.0, Malnutrition of moderate degree. Clinicians should consult with the health
information management or coding department about the use of ICD-10 codes.
Figure 1-4 provides a step-by-step schematic that can be used to apply the ASPEN/AND criteria.25,41 Two studies
published in 2018 concluded that adult patients identified with malnutrition by the ASPEN/AND criteria have higher
hospital mortality rates, longer lengths of stay, and increased likelihood of 30-day hospital readmission.42,43

Pediatric Malnutrition
Pediatric malnutrition is defined as “an imbalance between nutrient requirements and intake that results in
cumulative deficits of energy, protein, or micronutrients that may negatively affect growth, development and other
relevant outcomes.”44 After releasing the adult malnutrition criteria, ASPEN and AND developed a standardized set
of indicators to identify and document pediatric malnutrition (Table 1-9).45 Indicators of malnutrition in pediatric
patients include insufficient weight gain velocity and weight-for-length z scores in children under the age of 2 years;
weight loss and BMI-for-age z scores are more appropriate indicators in children older than 2 years. Mid–upper arm
circumference (MUAC) z scores may be used as an indicator of malnutrition in children ages 6–59 months.
Deceleration in either weight-for-length or BMI-for-age z scores and inadequate nutrient intake may be malnutrition
indicators from birth to adulthood. Accounting for the general aim for continued growth and development,
identification of 1 indicator is sufficient to establish the presence of malnutrition in pediatric patients (vs the adult
requirement for 2 indicators).45 Additionally, a deceleration or deviation from an initially established trend using
serial data points (>2) generally captures malnutrition status in pediatric patients better than a single data point.45
 In pediatrics, malnutrition status is typically identified by the degree of severity and degree of chronicity. As in
the adult criteria, the degree of malnutrition severity in pediatrics can range from mild to moderate to severe. Once a
degree of malnutrition is identified, the chronicity is then classified based on duration as either acute or chronic.
Acute malnutrition is defined as occurring in less than a 3-month span and typically results in a decline in weight
and often a correlating deceleration in weight for length (ages 0–2 years) or BMI (ages 2–20 years). In contrast,
chronic malnutrition is defined by duration longer than 3 months and often involves a correlating deceleration in
linear growth velocity (commonly referred to as “stunting”).45
The etiology of malnutrition should also be identified as part of the assessment. Malnutrition can be classified as
illness related or non–illness related. Mechanisms that may lead to malnutrition include decreased intake, increased
requirements, excessive losses, and impaired nutrient utilization.44,45

Components of the Nutrition Assessment

Medical and Nutrition History

Obtaining and evaluating detailed medical and nutrition histories is paramount to the nutrition assessment.
Clinicians can use information from these histories to determine how suboptimal nutrition status relates to intake
deficits, absorption/digestion issues, or both.22 The clinician conducting the nutrition assessment should therefore
review a patient’s medical history for relevant information about past and present acute and chronic diseases,
medications, diagnostic procedures, surgeries, and other therapies (eg, radio-therapy).2,5,46 The review of medications
should include prescription and nonprescription/over-the-counter drugs, vitamin and mineral supplements, and
herbal supplements. Whenever possible, information about complementary and alternative medical treatments and
the patient’s socioeconomic and psychosocial status should also be assessed.
Medical history information specific to pediatrics includes the mother’s health history during the pregnancy; the
patient’s prenatal and perinatal history; gestational age; history of prematurity; birth weight; classification as either
small or large for gestational age; and growth patterns for weight, length, and head circumference. If growth history
data are not included in the patient’s records, they can typically be obtained with permission of the
guardian/caregiver from the primary care physician. Other components of the history address the patient’s
developmental history, including problems with hypotonia or hypertonia as well as any delays in achieving
developmental milestones.
To best capture a patient’s nutrition history, the clinician must evaluate a variety of information, including recent
changes in appetite, ability to eat (or coordinate the suck/swallow/breathe pattern), bowel patterns, activity level,
nutrient intake, use of fad diets, feeding skills, types of feeding equipment used, food allergies and intolerances, and
use of oral supplements (Table 1-10). Additional components in the nutrition history for pediatric patients may
include maternal and infant issues related to breastfeeding; the adequacy of the human milk supply; the patient’s
overall tolerance of human milk or formula; the patient’s interest in feeding or refusal to eat or drink; duration,
frequency, and times of feedings; infant sleeping patterns; food-texture aversions; suck and swallow quality; and
symptoms of gastro esophageal reflux.

TABLE 1-10. Components of the Medical and Nutrition History

Component Examples
History (food records, diet recall, or feeding
Diet practices), dietary restrictions, alternative
and/or complementary practices
Drug allergies, food allergies, food intolerances,
Intolerances
food avoidances
Vitamin, mineral, or herbal supplements; oral
Supplementation
nutrition drinks; other products
Recent intentional or unintentional changes;
Weight
growth trends for infants and childrena
Chewing and swallowing abilities, salivation,
Dental/oral health dentition, pain, aphthous ulcers, other oral lesions,
taste changes
Mental status Altered mental status, delirium, dementia
Gastrointestinal Nausea, vomiting, heartburn, bloating, dyspepsia,
problems gas, diarrhea, constipation, steatorrhea
Chronic disease Long-term diseases affecting utilization of nutrients
Surgical resection or disease of gastrointestinal
Surgery tract, procedures involving other major organs
(eg, organ transplant)
Prescription and over-the-counter drugs, natural
health products, other dietary supplements; side
Medications
effects of medications and supplements; drug-
nutrient interactions
Illicit drugs and alcohol Use, amount, frequency
Food procurement, food preparation techniques,
physical limitations affecting food preparation; use
Socioeconomic factors
of/need for public aid assistance; level
of education; income level
Religion, customs, and their influence on eating
Cultural factors
patterns
Occupation, exercise regimen, sleep/rest pattern,
Physical activity dependence on a wheelchair, hypotonic
vs hypertonic conditions
a
See "Interpretation of Weight Data" later in this chapter.

Nutrition-Focused Physical Exam

The nutrition-focused physical exam (NFPE) is an excellent way to help evaluate nutrition status and has been
included in assessment criteria for SGA and the ASPEN/AND characteristics.23,25 The NFPE uses a body-systems
approach and includes a logical assessment from head to toe of muscle mass, subcutaneous fat stores, fluid status,
and vitamin and mineral abnormalities. NFPE techniques include visual inspection, palpation of specific body areas,
auscultation, and interviewing the patient and caregiver for further information and confirmation of findings.47 See
Tables 1-11, 1-12, and 1-13 for NFPE guidelines and suggested areas of the body that are conducive to evaluating
muscle mass, fat stores, and fluid accumulation.25,28,48,49

TABLE 1-11. Assessment of Body Areas for Fat Loss

Adult patients
Body Areas Nutrition Status
• Well nourished/normal: Soft, slightly bulging
fat tissue
• Mild to moderate loss: Faint to marginally
Orbital region:
dark circles, fairly hollow look
Orbital fat pads
• Severe loss: Deep depressions and sharp
features appearing hollow; dark circles; loose
skin
• Well nourished/normal: Plentiful fat tissue can
be grasped using the forefinger and thumb
Upper arm region: • Mild to moderate loss: Some tissue can be
Under triceps muscle grasped, but it is not abundant
• Severe loss: Very little tissue can be grasped;
examiner's forefinger and thumb touch
• Well nourished/normal: Iliac crest, spine, and
ribs are well covered; clinician cannot see/ feel
individual bones well; chest is full
• Mild to moderate loss: Iliac crest, spine, and
Thoracic and lumbar region:
rib bones are more apparent; some
Midaxillary line, ribs, lower back, iliac crest
depressions are visible between bones
• Severe loss: Iliac crest, spine, and rib bones
are very apparent/ prominent, easily visible;
deep depressions between bones
• Well nourished/normal: Rounded, full
Facial cheeks
(buccal pads)
• Mild to moderate loss: Pads are flat
• Severe loss: Face is hollowlooking, narrow
• Well nourished/normal: Plentiful fat tissue can
be grasped using the forefinger and thumb
Upper arm region: • Mild to moderate loss: Some tissue can be
Biceps/triceps grasped, but it is not abundant
 • Severe loss: Very little tissue can be grasped;
inspector's forefinger and thumb touch
• Well nourished/normal: Ribs do not show;
chest is full
• Mild to moderate loss: Spine and rib bones
Thoracic and lumbar region: are more apparent; some depressions are
Midaxillary line, ribs, lower back visible between bones
• Severe loss: Spine and rib bones are very
apparent/prominent, easily visible; deep
depressions between bones
• Well nourished/normal: Rounded, full
• Mild to moderate loss: Slight curvature, not
Buttocks (in infants) rounded
• Severe loss: Flat, wastedappearing; skin may
look wrinkled
Source: Information is from references 28, 48, and 49.

TABLE 1-12. Assessment of Body Area for Muscle Loss

Body Areas Nutrition Status

• Well nourished/normal:
• Adults: Bones are not evident in males; may
be visible/ somewhat noticeable in females
• Pediatrics: Bones are possibly visible but
not prominent
Clavicle bone region: • Mild to moderate loss:a
Pectoralis major, deltoid, trapezius muscles • Adults: Observable definition of bones in
males; bones are more prominent than
normal in females
• Pediatrics: Some protrusion of bones
• Severe loss: Obviously protruding bones,
sharp edges
• Well nourished/normal: Soft, rounded
features; curves at neck, shoulders, and upper
arms
Acromion bone region: • Mild to moderate loss:a Acromion process
Deltoid muscle and shoulders starting to look square, slightly protruding
• Severe loss: Shoulder-to-arm joint is square;
bone edges and acromion process are
easily observed, rigid/solid to touch
• Well nourished/normal: No significant or
obvious depressions; bones are not noticeable
• Mild to moderate loss:a
• Adults: Mild depressions, bones may be
 Scapular bone region: more prominent
Trapezius, supraspinatus, infraspinatus muscles • Pediatrics: Degree of wasting is variable,
may not be readily seen in all areas
• Severe loss: Protruding, visible bones; readily
observed depressions between shoulder and
spine or ribs and scapula

• Well nourished/normal:
• Adults: Soft, bulging muscle, easy to grasp;
potentially flat in some individuals
• Pediatrics: n/a
• Mild to moderate loss:a
• Adults: Slight depressions; dorsal bones may
Hand:
be more prominent
Interosseous muscle
• Pediatrics: n/a
• Severe loss:
• Adults: Hollowed areas at base of thumb-
forefinger intersection and along dorsal side
of hand
• Pediatrics: n/a
• Well nourished/normal: Muscles add soft,
rounded features; bones are not prominent
• Mild to moderate loss:a Kneecap and bones
Patellar region: are more noticeable, developing sharper edges
Knee, quadriceps muscles due to diminished muscle coverage
• Severe loss: Bones are
sharply prominent/square; minimal muscle is
appreciable around knee
• Well nourished/normal: Well-rounded
muscles; bone structure is not visible
Anterior thigh: • Mild to moderate loss:a Mild depression
Quadriceps muscles visible in inner thighs
• Severe loss: Inner thighs do not touch when
knees are pressed together and are visibly thin
• Well nourished/normal: Firm, well-developed,
easy-to-grasp muscle; potentially flat in
some adults
Posterior calf:
• Mild to moderate loss:a Poorly developed
Gastrocnemius muscle
muscle; thinner than usual
• Severe loss: Very little to no muscle definition;
thin, flat

Abbreviation: n/a, not applicable.

a
In pediatric patients, the described characteristics are for moderate loss only; in adults, the characteristics are found in both mild and
moderate losses.
Source: Information is from references 28, 48, and 49.
 TABLE 1-13. Assessment of Edema and Fluid Accumulationa

Examination method:
• Adults: Inspect upper thighs/flanks (or possibly scrotum/ vulva) in the activity-restricted patient;
inspect ankles/ calves in the mobile patient; in all patients, note ascites or anasarca.
• Pediatric patients: Use thumb to press on distal anterior foot (dorsal side) for 5 sec.
Status:
• Normal: No visual or palpable evidence of fluid accumulation
• Mild (1+) edema: Slight pitting (<2 mm); no distortion when thumb is pressed into skin on lower
extremity; pitting rapidly rebounds
• Moderate (2+) edema: Deeper pitting (2-4 mm) with pressure applied by thumb; slight swelling of
the extremity; indentation resolves after several seconds
• Severe (3-4+) edema: Deep (4-6 mm) to very deep (>6 mm) pitting when skin is pressed by thumb;
depression lasts for at least 1 min; extremity is obviously engorged
a
Causes of edema unrelated to nutrition must be ruled out to use this parameter as a criteria for malnutrition. Fluid accumulation masks
weight loss, and dehydration may artificially enhance loss of weight; therefore, nutrition assessment should be modified accordingly.
Source: Information is from references 25, 28, 48, and 49.

The assessment of sexual maturation, using Tanner staging (see Table 1-14), is a physical exam component of
the nutrition assessment unique to pediatrics. Tanner staging is based on the development of secondary sex
characteristics. In nutrition assessment of children and adolescents, the clinician should interpret findings related to
weight changes and growth patterns in the context of the patient’s stage of sexual maturity. In boys, the peak of the
rapid height growth occurs in Tanner stage 4. In girls, most linear growth is usually completed by the onset of
menarche. However, girls who enter puberty early may have more linear growth after menarche than girls who enter
puberty later. In pediatric patients, the rate of weight gain generally approximates the velocity of linear growth;
however, in females, the peak weight gain velocity occurs 6 to 9 months before the peak height change.50,51

TABLE 1-14. Tanner Stages of Development

Stage Girls Boys

1 Prepubescent Prepubescent
Pubic hair and breast buds Pubic hair appears, growth of
2 appear, increased activity of sweat genitalia, increased activity of sweat
glands glands
Continued enlargement of genitalia,
Breast enlargement, axillary hair changes in voice, faint
3
present moustache/ facial hair begins,
axillary hair present
Pubic hair thickens, voice deepens,
Nipple and areola become
4 facial hair increases, hair on
more pronounced, menarche begins
legs becomes darker
5 Breasts fully mature Genitalia fully mature
Source: Information is from references 50 and 51.

Anthropometric Assessment
Using Growth Charts
In pediatric practice, growth is the most important parameter for assessing the nutrition status of a pediatric patient.
It is assessed and monitored by plotting serial measurements of the patient’s anthropometric data, including weight,
length/height, BMI, and head circumference, as well as (when appropriate) MUAC and triceps skinfold (TSF)
thickness, on sex- and age-specific growth charts.52
In the United States, the World Health Organization (WHO) growth charts are used for term infants up to 2 years
of age.53 WHO growth standards are based on optimal growth of exclusively breastfed children.54 Centers for
Disease Control and Prevention (CDC) growth charts, which use data from 5 cross-sectional, nationally
representative health examination surveys, are used to plot weight, height, and BMI in patients ages 2 through 20
years.53
Specialized growth curves are available for premature infants55,56 and children with diagnoses such as Down
syndrome (trisomy 21),57 Turner syndrome,58 Williams syndrome,59 Prader-Willi syndrome,60 and cerebral palsy.61–63
Clinical judgment is particularly important when considering the use of such charts, which may be dated or based on
small, nongeneralizable sample populations.64 Specialized growth charts should be used in conjunction with WHO
and CDC growth charts to monitor a patient’s growth trends.64 See Table 1-15 for more information on selected
growth charts.53–56,62,63

TABLE 1-15. Examples of Growth Charts

Author Description
Target population: Infants and children from birth
to age 24 months (should reflect corrected age up
to age 3 years)
Parameters assessed:
• Weight for age
WHO54
• Length for age
• Weight/length for age
• Head circumference for age
Comments: Based exclusively on data
from breastfed infants; growth as the standard
Target population: Children ages 2-20 years
Parameters assessed:
• Weight for age
CDC53 • Length for age
• BMI for age
• Head circumference for age (to age 36 months)
Comments: Growth as reference, not a standard
Target population: Premature infants born at >23
weeks' gestational age
Parameters assessed:
• Weight for age
Olsen55
• Length for age
• Head circumference for age
Comments: Based on large US
population; separate charts for males and females
Target population: Premature infants born at 22
to <37 weeks' gestational age
Parameters assessed:
• Weight for age
Fenton56
 • Length for age
• Head circumference for age
Comments: 2003 Fenton growth chart postnatal
data matches WHO data
Target population: Children ages 2-20 years with
cerebral palsy
Parameters assessed:
• Weight for age
Brooks et al62
• Length for age
• BMI for age
Comments: 5 different charts based on gross
motor function
Abbreviations: BMI, body mass index; CDC, Centers for Disease Control and Prevention; WHO, World Health Organization.
Source: Information is from references 53-56, 62, and 63.

Measuring Body Weight

Body weight measurement can be accomplished in a variety of ways depending on the condition and age of the
patient.65,66 Methods include the following:

• Standing weight: Assess the patient’s ability to stand. Balance or recalibrate the scale and position the patient
on the center of the scale base. Obtain the measurement from the balance scale or digital readout. The
clothing worn by the patient, measuring equipment, and the time of day should all be uniform across
measurements, and these data should be documented along with the weight.
• Built-in bed scale weight: If patients have difficulty with balance while standing or have limited mobility, a
bed with a built-in scale can be used to measure weight. Before placing the patient in the bed, remove all
unnecessary pillows, blankets, and medical devices. Zero the bed scale, making sure to follow bed-specific
guidelines for accuracy. Transfer the patient to the center of the bed, without excessive clothing and shoes,
and follow the manufacturer’s instructions for measuring weight.67
• Sling weight: Roll the patient to one side and place the sling under the patient. Position the sling under the
patient evenly. Attach the sling to the scale and record the weight measurement.
• Wheelchair weight: Position the ramp for wheelchair access. Weigh the empty wheelchair and record the
weight of the chair. Repeat the procedure with the patient in the chair and deduct the chair weight from the
total weight.
• Infant gram scale or platform beam balance scale (for pediatric patients): It is preferable to weigh infants and
toddlers in the nude without clothing. Older children may be weighed while wearing underwear.

Body Mass Index and Weight for Length

BMI is a calculated measure using a person’s weight and height to estimate body mass.
BMI = Weight (kg)/(Height [m])2

BMI measures are classified as underweight, normal, overweight, or obese. In adults, BMI ≤18.4 is considered
underweight and BMI ≤17 indicates moderate or severe underweight.68 Of note, morbidity increases significantly
with BMI ≤16.69 Normal BMI ranges between 18.5 and 24.9, BMI between 25 and 29.9 is classified as overweight,
and BMI ≥30 is classified as obesity.68 In healthy older adults, the optimal BMI range is between 22 and 27.70
In pediatrics, a patient’s weight for length or BMI is assessed using sex-and age-specific growth charts or z
scores. For children ages 0 to 2 years, the CDC recommends plotting weight-for-length measurements on sex-
specific WHO weight-for-length growth curves.53 These curves reflect standards for how young children should
grow in ideal conditions.54 To assess weight in relation to height in children 2 to 29 years of age, BMI should be
plotted on the CDC’s sex-specific BMI-for-age growth charts.53 In children, BMI for age <5th percentile is classified
as underweight, BMI for age between the 85th and 94th percentile is classified as overweight, and obesity is defined
as BMI for age ≥95th percentile or BMI ≥30. BMI for age >99th percentile is considered severe obesity.71
There are limitations to the use of BMI in nutrition assessment. BMI does not differentiate fat mass, muscle
mass, and skeletal mass, and the calculation may be skewed by weight data that reflect fluid shifts in the setting of
critical or chronic illness.72 For example, older, athletic children with increased muscle mass may be misclassified as
overweight based on their BMI for age; therefore, other nutrition parameters may need to be used to assess body
composition.68

Waist Circumference
In adults, waist circumference is used to predict abdominal obesity and correlates with comorbid medical conditions
associated with increased visceral fat deposits or adipose tissue, including cardiovascular disease.68 To measure
weight circumference, use a flexible tape measure to measure the distance around the waist at the smallest area
immediately below the rib cage and directly above the umbilicus.

Ideal Body Weight

Ideal body weight (IBW) is an estimate of healthy weight for a patient. A commonly used, empiric method for
estimating IBW for adults in clinical settings is the Hamwi equation:73
IBW in Males = 106 lb (48 kg) for first 60 inches of height + 6 lb (2.7 kg) per each additional inch
IBW in Females = 100 lb (45 kg) for first 60 inches of height + 5 lb (2.3 kg) per each additional inch

Methods to estimate IBW in children include calculating the weight that would place the child at the 50th
percentile curve for BMI for age; the McLaren-Read method, in which a child’s stature is plotted on a weight-for-
stature chart and then IBW is estimated to be the weight along the 50th percentile curve for that height; and the
Moore method, which uses the weight along the same curve as height on a weight-for-stature chart.74 However, there
is no consensus on a standardized method, and the various methods provide a range of estimates.74 Furthermore,
anthropometric data for pediatric patients are frequently inaccurate, either because the information is out of date or
because height and/or weight were measured imprecisely, which throws an IBW estimate based on such data into
doubt.

Height/Length
Height (stature) can be measured directly or estimated using indirect methods such as knee height. Direct methods
using a stadiometer or measuring rod require the patient to stand erect or lie flat. For those who cannot be moved
and do not have musculoskeletal deformities, a recumbent bed length measurement can assist in determining height.
In pediatrics, recumbent lengths are measured with a length board for infants and toddlers. A stadiometer is used
for children ages 2 years and older (if they can stand). With a stadiometer, heights are measured in stocking feet and
with feet together, back straight, and arms hanging freely.

Head Circumference
Birth to age 36 months is a time of rapid brain growth. Head circumference should be routinely monitored during
this time.75 A flexible, narrow tape measure is used to measure the head circumference. Ideally, three measurements
are done, and the results averaged. The CDC and WHO have published growth curves and z score data to use in
assessing the measurements from 0–36 months and 0–24 months, respectively.53,54 Arrested head growth
(microcephaly) may indicate cranial defects or abnormal brain growth; accelerated growth may indicate catch-up
growth or developmental defects (eg, hydrocephalus).

Interpretation of Weight Data

In adults, comparison of a patient’s current and usual body weights can indicate the severity of malnutrition (see
Tables 1-7 and 1-8, earlier in this chapter).25 Recent involuntary weight changes can accurately predict nutrition
risk.25 When obtainable, the weight history of the individual is therefore more helpful than comparison of current
weight to IBW. Caution is recommended when interpreting current weight as a percentage of IBW.76 Body shape
and weight tend to vary across age and population groups, which can skew interpretation of IBW vs current
weight.76
Recent weight changes in children can indicate acute nutrition issues. A weight-for-age z score or percentile is
not independently indicative of nutrition issues. Weight gain velocity based on the WHO growth velocity standards
can be an indicator of undernutrition in children ages 0–24 months. Weight loss in patients older than 2 years can be
used to assess malnutrition (see Table 1-9, earlier in this chapter).
Factors that influence interpretation of weight measurements include the following:

• Edema, ascites, hydrocephalus, diuretic therapy, and other fluid alterations can significantly alter body
weight within short time periods.
• Fluid shifts from the intravascular space to the extra-vascular space and the intracellular space to the
extracellular space with a concurrent decline in lean body mass occur in malnutrition. Therefore, loss of lean
body mass may be masked, with little obvious change in weight, by fluid shifts.

Mid–Upper Arm Circumference and Triceps Skinfold Thickness

MUAC measures muscle, fat, and bone in the mid–upper arm, and TSF thickness measures subcutaneous fat stores
in the upper arm. Both MUAC and TSF thickness can be used to estimate the fat-free and fat mass in a body.
Clinicians require training to obtain reliable and reproducible measurements. Instructions for obtaining these
measurements are described in the National Health and Examination Survey Anthropometry Manual.77 These
measurements are appropriate for assessing change over time in individual patients. Single measurements are less
useful than serial measurements over time. A 2005 reference provides standards tables in the US population.78
MUAC should be used in nutrition assessment of pediatric patients as it can be an independent indicator of mal-
nutrition in children ages 6–59 months.45 TSF thickness is not used as an independent indicator of malnutrition, but
this measurement can be used to monitor progress of a nutrition intervention as fat lost or fat gained.

Bioelectrical Impedance Analysis

Bioelectrical impedance analysis (BIA) is a body composition assessment technique based on the principle that lean
tissue has higher electrical conduction and lower impedance than fat. Three types of BIA devices are available
(single-frequency, multiple-frequency, and spectroscopy). Using a standardized protocol, imperceptible, low
currents of electricity pass through electrodes attached to the extremities of an individual to measure resistance and
reactance to estimate fat-free mass and fat mass.79 BIA estimates of body composition are then calculated from the
data with established modeling or predictive equations that are device-specific.79,80
BIA has been favored over other methods to analyze body composition because it is portable, safe, easy to use,
and noninvasive, and because it obtains measures quickly and with relatively low associated costs. Various studies
have validated the use of BIA in healthy, normal weight individuals under highly controlled situations, and research
investigating the use of BIA to obtain raw bioimpedance values (eg, phase angle, impedance ratio, and fat-free mass
index) to evaluate nutrition status and clinical outcomes has had some promising results.79 However, other studies
attempting to use BIA to estimate whole body lean tissue of clinical populations have produced mixed results
regarding accuracy. Obese patients, and those with conditions that cause fluid overload, are particularly affected by
errors in whole body estimations based on BIA.79 Other factors affecting the precision or accuracy of BIA include
the electrolyte status and skin temperature of the patient, room temperature, proximity to other electronic devices or
metal, and variability in measurement protocols.80 For these reasons, the use of BIA in clinical settings may not be
appropriate. Further research on the use of BIA methods, especially in hospitalized patients, is needed.

Computed Tomography and Ultrasound

Within the last several years, computed tomography (CT) imaging and bedside ultrasound have emerged as valuable
tools for assessment of body composition. CT scans at the level of the third lumbar vertebra (L3) are precise,
accurate, and valid means to distinguish and quantify skeletal muscle and adipose tissue. These measures, obtained
by a trained clinician with the assistance of computer software, can then be used to estimate muscle volume
throughout the entire body. Repeated measures in certain patient populations also show that changes in lean tissue
can be observed and monitored through CT scans. However, this monitoring method is not a realistic option for all
patients because of its cost and the emission of high doses of radiation.81 Therefore, CT scans should not be obtained
for the sole purpose of nutrition assessment.
Bedside ultrasound has the ability to quantify muscle layer thickness and is generally regarded as safe,
noninvasive, portable, cost effective, and relatively easy to perform.82,83 It has been studied in a variety of
hospitalized and critically ill patient populations to measure muscle thickness, a proxy for lean soft tissue.81,82
Measurements taken at the quadriceps muscle have been shown to signify overall lean body mass.82,83 Bedside
ultrasound is less accurate than CT images, and the measurement can be subject to errors related to optimal
positioning of the transducer, muscle compressibility, presence of edema, variances between clinicians’ techniques,
and reliable site selection.81 However, given the benefits previously described, and the fact that an array of
disciplines can use bedside ultrasound in practice, this tool shows promise as a quantifiable method to assess lean
body mass.81–83

Functional Status
Malnutrition, especially when caused by disease, diminishes muscle strength, decreases muscle mass, and impairs
functional capacity over time.40,84 Both SGA and ASPEN/AND criteria recognize that strength and functional status
are important components of nutrition assessment in adults.23,25,45 However, it is also important to understand that
various factors unrelated to nutrition status can alter muscle function and strength, including acute and chronic
diseases, inflammatory states, sensory loss caused by neuromuscular damage, and atrophy from inactivity.84
Furthermore, impairment of muscle function has consequences regarding recovery from disease, morbidity, and
mortality.40 At this time, assessment of functional status is not routinely performed in the nutrition assessment of
pediatric patients.45
Handgrip strength can be measured with a handgrip dynamometer, and such measurements can be used as a
validated surrogate for upper body muscle strength in adults.84 Handgrip strength is feasible for bedside care in non-
critical-care situations and correlates well with other tests of muscle function, although it should be noted that age
and gender influence results and studies with younger adult patients demonstrate better correlations with nutrition
status than those with elderly patients.40 Variations in measurement technique, imprecise cutoff values, and a lack of
consensus on protocols are limitations of this method.40,84 Furthermore, clinicians must be trained in the proper use
of dynamometers, which may not be available in all facilities, and patients with certain diseases and conditions (eg,
dementia, arthritis, heavy sedation) may not be able to grip the tool.28,40,84 In addition to handgrip strength, other
measures of functional status have been proposed and may become of value for assessing different patient
populations as they become validated.40,84

Vitamin and Trace Mineral Abnormalities

The medical history, nutrition history, and NFPE are all used to assess patients for potential vitamin and trace
mineral deficits. Patients with malnutrition generally exhibit signs and symptoms associated with multiple nutrient
deficiencies rather than a single nutrient deficiency. Laboratory assessment is usually required to confirm clinically
abnormal signs and symptoms. Clinicians should consult with their facility’s laboratory regarding available tests,
reference ranges, and results indicative of micronutrient deficiency or toxicity. See Tables 1-16 through 1-19 for
guidance on assessment of vitamin and trace mineral status in adult and pediatric patients.85–87

TABLE 1-16. Possible Indicators of Vitamin Deficiency or Toxicity from the Physical Exam
or Medical History

Vitamin Indicators of Nutrient Imbalance

• Deficiency: Dermatitis, keratomalacia, infection (measles), night
A blindness, and xerophthalmia
• Toxicity: Liver damage, vascular dilation, flushing, and irritation
• Deficiency: Dermatitis, depression, alopecia, fatigue, muscle
Biotin pain, somnolence, anorexia, and paresthesia
• Toxicity: None known
• Deficiency: Pernicious (megaloblastic) anemia, glossitis, spinal
cord degeneration, and peripheral neuropathy
 Cyanocobalamin (B12) • Toxicity: (Rare) irritability, headache, insomnia, and interference
with B2 and B6

• Deficiency: Macrocytic anemia, stomatitis, paresthesia,

Folate (B9) diarrhea, glossitis, lethargy, and neural tube defects of fetus
• Toxicity: Diarrhea
• Deficiency: Pellagra: dementia (loss of memory), diarrhea,
dermatitis, headaches, and glossitis
Niacin (B5) • Toxicity: Osmotic diarrhea, oxalate kidney stones, interference
with anticoagulation therapy, and rebound deficiency after high
intake
• Deficiency: Fatigue, malaise, headache, insomnia, vomiting, and
Pantothenic acid (B3) abdominal cramps
• Toxicity: Acute: nausea, vomiting, headache, and dizziness
• Deficiency: Dermatitis, neuritis, irritability, glossitis,
cheilosis, depression, confusion, seizures, and microcytic anemia
Pyridoxine (B6)
• Toxicity: Chronic: peeling/scaly skin, bone pain, pseudotumor
cerebri, hepatomegaly, gingivitis, and alopecia
• Deficiency: Mucositis, glossitis, angular cheilitis or angular
stomatitis (cold sores), dermatitis, vascularization of cornea,
photophobia, lacrimation, decreased vision, impaired
Riboflavin (B2)
wound healing, and normocytic anemia
• Toxicity: Excess bone and soft tissue calcification, kidney
stones, constipation, myositis ossificans, and hypercalcemia
• Deficiency: Beriberi: cardiomyopathy, peripheral neuropathy,
Thiamin (B1) encephalopathy (Wernicke-Korsakoff syndrome), and lactic acidosis
• Toxicity: Prolonged clotting time
• Deficiency: Scurvy: capillary hemorrhage of gingiva, skin, and bone;
poor wound healing, enlargement and keratosis of hair follicles,
C
anemia, lethargy, and depression
• Toxicity: None known
• Deficiency: Rickets, osteomalacia, tetany, hypophosphatemia, and
D muscle weakness
• Toxicity: None known
• Deficiency: Hemolysis (in preterm infant), anemia, peripheral
E neuropathy, and myopathy
• Toxicity: Neuropathy

K • Deficiency: Bleeding, purpura, and bruising

• Toxicity: None known
Source: Information is from references 85 and 86.
 TABLE 1-17. Possible Indicators of Trace Mineral Deficiency or Toxicity from the Physical Exam
or Medical History

Mineral Indicators of Nutrient Imbalance

• Deficiency: Copper deficiency (90%-95% of
Ceruloplasmin plasma copper in ceruloplasmin)
• Toxicity: None known
• Deficiency: Neutropenia, microcytic anemia,
osteoporosis, decreased hair and skin
pigmentation, dermatitis, hypotonia, zinc
toxicity, growth failure, Wilson's disease, and
Copper
neuropathy
• Toxicity: Nausea, vomiting, epigastric pain,
cirrhosis, Fanconi nephropathy, corneal
pigmentation, and diarrhea
• Deficiency: Anemia and pica
Iron (ferritin)
• Toxicity: Hemosiderosis
• Deficiency: Muscle weakness and
pain; anemia; cardiomyopathy; growth failure
Selenium
• Toxicity: Hair loss, dermatitis, garlic odor,
brittle nails
• Deficiency: Growth failure,
dermatitis, hypogonadism, hypogeusia,
diarrhea, apathy, depression, impaired
Zinc
wound healing, and immunosuppression
• Toxicity: Nausea, vomiting, metallic taste,
chills, and headache
Source: Information is from references 85 and 86.

TABLE 1-18. Selected Laboratory Tests to Assess Vitamin Status

Vitamin Laboratory Assay

A Serum retinol or serum retinolbinding protein
Biotin Serum or urine
Cyanocobalamin (B12) Serum
Folate (B9) Serum
Niacin (B5) Urinary metabolites
Pantothenic acid (B3) Urine
Pyridoxine (B6) Serum or plasma
Riboflavin (B2) Urine
Thiamin (B1) Urine
 C Serum or plasma; whole blood, leukocyte-platelet
D Plasma 25-hydroxyvitamin D
E Plasma alpha-tocopherol (whole blood)
K PIVKA-II, INR, PT
Abbreviations: INR, international normalized ratio; PIVKA, protein induced by vitamin K absence; PT, prothrombin time.
Source: Information is from reference 87.

TABLE 1-19. Selected Laboratory Tests to Assess Trace Element Status

Trace Element Laboratory Assay

Ceruloplasmin Serum
Copper Serum value
Iron (ferritin) Serum
Selenium Serum
Zinc Serum value
Source: Information is from reference 87.

Nutrition Support Care Plan

Increased morbidity and mortality are associated with malnutrition.88,89 Malnutrition results in loss of lean body mass
and subsequent loss of structure or function of body systems. Impaired respiratory function, reduced cardiac
contractility, impaired renal function, altered immune function, and poor wound healing are known consequences of
malnutrition.90 Based on data gathered from the comprehensive nutrition assessment, clinicians make a nutrition
diagnosis and set a plan of care. Decisions involved in a nutrition intervention include timing of the intervention, the
route of therapy, and whether specialized nutrition formulations are needed.

Nutrition Diagnosis
A malnutrition diagnosis is associated with a longer hospital length of stay, increased comorbidities, higher medical
costs, and more ongoing medical care needs for a patient after discharge.90,91 The malnutrition criteria for adults and
pediatrics described earlier in this chapter should be used to accurately and uniformly diagnose malnutrition.
Documentation of the malnutrition diagnosis is important for timely interventions, reimbursement, and resource
allocation.

Nutrition Support Therapy

Integral to the process of nutrition care and the administration of nutrition support therapy is the decision regarding
the route of administration. In most cases, enteral nutrition (EN) is recommended when a patient’s nutrient
requirements are not met by oral intake and there is a functional GI tract of sufficient length and condition to allow
adequate nutrient absorption.92,93 Parenteral nutrition should be used when the GI tract is not functional or cannot be
accessed and in patients who cannot be adequately nourished by oral diets or EN.94 Indications for EN are discussed
in further detail in Chapter 2.

Timing of the Nutrition Intervention

Initiation of EN can be considered in well-nourished, stable adult patients unable to achieve 50% of their estimated
nutrient requirements orally after 7 days.92 For high-risk, hemodynamically stable, critically ill adults, it is
recommended that EN be initiated within 24–48 hours of initial trauma or medical insult if it is not possible to
maintain adequate volitional intakes and/or when patients are expected to require mechanical ventilation for at least
72 hours.20 For adult patients deemed severely malnourished, those with moderate to severe pancreatitis, or
individuals who just received a liver transplant, starting early EN within 24–48 hours is also recommended.
 Advancement of nutrition support to goal protein and energy ranges depends on risk of refeeding, clinical status,
and expected tolerance of therapy, but clinicians are encouraged to advance EN as quickly as the patient tolerates it.
For non–critically ill adult patients, as well as some hemodynamically stable critically ill adult patients, aiming to
achieve goal energy provisions within 24–48 hours of initiating EN will maximize nutrient delivery. Providing at
least 80% of estimated energy and protein goals within 48–72 hours of initiation can impart clinical benefit.20
Pediatric patients with insufficient oral intake require nutrition support therapy. According to expert consensus,
EN is the preferred route for delivery of nutrition for such patients, including those in an intensive care setting.
Initiation of EN within the first 24–48 hours of admission to a pediatric intensive care unit and reaching at least two-
thirds goal volume within the first week of critical illness have been associated with improved outcomes.93

Nutrition Monitoring and Evaluation

Once the nutrition assessment is complete and nutrition intervention begins, continuous reassessment (otherwise
known as monitoring) is needed.1 Many of the assessment parameters used initially are repeated serially to assess the
efficacy of the intervention and any potential complications associated with the therapy. The data collected also
determine the need to continue or cease nutrition care. See Chapter 8 for additional information.

Practice Resources

Malnutrition

• Jensen GL, Hsiao PY, D Wheeler. Adult nutrition assessment tutorial. JPEN J Parenter Enteral Nutr.
2012;36(3):267–274. doi:10.1177/014860711 2440284.
• American Society for Parenteral and Enteral Nutrition Malnutrition Committee. Malnutrition Matters: A
Call to Action for Providers Caring for Adult Patients (video). https://www.youtube.com/watch?
v=JORLgsyri5U&list=PL-rWCuTTwTKyItZtLZow_NLUJUeeM3JYU&index=5&t=0s. Published
September 2018. Accessed November 21, 2018.
• American Society for Parenteral and Enteral Nutrition Malnutrition Committee. Malnutrition Matters: A
Call to Action for Providers Caring for Pediatric Patients (video). https://www.youtube.com/watch?
v=tjyCepbtDT0&list=PL-rWCuTTwTKyItZtLZow_NLUJUeeM3JYU&index=5. Published September
2018. Accessed November 21, 2018.
• American Society for Parenteral and Enteral Nutrition. Malnutrition Toolkit website.
http://www.nutritioncare.org/MalToolkit. Accessed November 21, 2018.

Interpretation of Albumin and Prealbumin

• Chen Y, Henson S, Jackson AB, Richards JS. Obesity intervention in persons with spinal cord injury. Spinal
Cord. 2006;44(2):82–91. doi: 10.1038/sj.sc.3101818.
• Nova E, Lopez-Vidriero I, Varela P, et al. Indicators of nutritional status in restricting-type anorexia nervosa
patients: a 1-year follow-up study. Clin Nutr. 2004;23(6):1353–1359. doi:10.1016/j.clnu.2004.05.004.
• Jensen GL. Inflammation as the key interface of the medical and nutrition universes: a provocative
examination of the future of clinical nutrition and medicine. JPEN J Parenter Enteral Nutr. 2006;30(5):453–
463.
• Davis CJ, Sowa D, Keim KS, Kinnare K, Peterson S. The use of prealbumin and C-reactive protein for
monitoring nutrition support in adult patients receiving enteral nutrition in an urban medical center. JPEN J
Parenter Enteral Nutr. 2012;36(2):197–204. doi:10.1177/0148607111413896.

Nutrition-Focused Physical Exam

• Hamilton C, ed. Nutrition Focused Physical Exam: An Illustrated Handbook. Silver Spring, MD: American
Society for Parenteral and Enteral Nutrition; 2016.
 • DeTallo C, ed. The Practitioner’s Guide to Nutrition Focused Physical Exam of Infants, Children, and
Adolescents: An Illustrated Handbook. Silver Spring, MD: American Society for Parenteral and Enteral
Nutrition; 2019.

Anthropometrics

• National Center for Health Statistics. Growth charts. Centers for Disease Control and Prevention website.
http://www.cdc.gov/growthcharts. Accessed November 21, 2018.
• World Health Organization child growth standards. World Health Organization website.
http://who.int/childgrowth/standards/en. Accessed November 21, 2018.
• PediTools website (includes calculators for growth percentiles and z scores for WHO, CDC, Olsen, Down
syndrome, and MUAC growth curves). http://www.peditools.org. Accessed November 21, 2018.
• National Health and Nutrition Examination Survey (NHANES). Anthropometry procedures manual. Centers
for Disease Control and Prevention website.
https://www.cdc.gov/nchs/data/nhanes/nhanes_07_08/manual_an.pdf. Accessed November 21, 2018.
• University of Vermont Department of Food and Nutrition Sciences. Bioelectric impedance analysis tutorial.
University of Vermont website. http://nutrition.uvm.edu/bodycomp/bia/lesson1.html. Accessed November
21, 2018.
• Earthman CP. Body composition tools for assessment of adult malnutrition at the bedside: a tutorial on
research considerations and clinical applications. JPEN J Parenter Enteral Nutr. 2015;39(7):787–822.
doi:10.1177/0148607115595227.
• Gomez-Perez SL, Haus JM, Sheean P, et al. Measuring abdominal circumference and skeletal muscle from a
single cross-sectional CT image: a step-by-step guide for clinicians using National Institutes of Health
ImageJ. JPEN J Parenter Enteral Nutr. 2016;40(3):308–318. doi:10.1177/0148607115604149.
• Galindo Martín CA, Zepeda EM, Lescas Méndez OA. Bedside ultrasound measurement of rectus femoris: a
tutorial for the nutrition support clinician. J Nutr Metabol. 2017;2017: 2767232. doi:10.1155/2017/2767232.

Functional Status

• Dietitians in Nutrition Support. Handgrip Strength Assessment: A Skill to Enhance the Diagnosis of Disease
Related Malnutrition (toolkit). 2017. Available for purchase at https://www.dnsdpg.org/store.cfm.

References
1. Lacey K, Pritchett E. Nutrition care process and model: ADA adopts road map to quality care and outcomes
management. J Am Diet Assoc. 2003;103:1061–1072.
2. Field LB, Hand RK. Differentiating malnutrition screening and assessment: a nutrition care process
perspective. J Acad Nutr Diet. 2015;115(5):824–828.
3. American Society for Parenteral and Enteral Nutrition. Improve Patient Outcomes: A.S.P.E.N.’s Step by Step
Guide to Addressing Malnutrition. Silver Spring, MD: American Society for Parenteral and Enteral
Nutrition; 2015.
4. A.S.P.E.N. pediatric nutrition care pathway (age 1 month–18 years) (infographic). Malnutrition solution
center. American Society for Parenteral and Enteral Nutrition website.
https://www.nutritioncare.org/Continuing_Education/Programs/Malnutrition_Awareness/Malnutrition.
Accessed November 17, 2018.
5. Ukleja A, Freeman KL, Gilbert K, et al. Standards for nutrition support: adult hospitalized patients. Nutr Clin
Pract. 2010;25(4):403–414.
6. Skipper A, Ferguson M, Thompson K, Castellanos VH, Porcari J. Nutrition screening tools: an analysis of
the evidence. JPEN J Parenter Enteral Nutr. 2012;36(3):292–298.
7. Kruizenga HM, Van Tuldar MW, Seidell JC, et al. Effectiveness and cost-effectiveness of early screening
and treatment of malnourished patients. Am J Clin Nutr. 2005;82: 1082–1089.
8. van Bokhorst-de van der Schueren MA, Guaitoli PR, Jansma EP, de Vet HC. Nutrition screening tools: does
 one size fit all? A systematic review of screening tools for the hospital setting. Clin Nutr. 2014;33(1):39–58.
9. Academy of Nutrition and Dietetics. Nutrition screening adults: summary of all tools evaluated (2010).
Evidence Analysis Library website. https://www.andeal.org/topic.cfm?
cat=5437&conclusion_statement_id=251197&highlight=nutrition%20screen%20tool&home=1. Accessed
November 21, 2018.
10. Heyland DK, Dhaliwal R, Jiang X, Day AG. Identifying critically ill patients who benefit the most from
nutrition therapy: the development and initial validation of a novel risk assessment tool. Crit Care.
2011;15(6):R268.
11. Rahman A, Hasan RM, Agarwala R, Martin C, Day AG, Heyland DK. Identifying critically-ill patients who
will benefit most from nutritional therapy: further validation of the “modified NUTRIC” nutritional risk
assessment tool. Clin Nutr. 2016;35(1):158–162.
12. Lee YJ. Nutritional screening tools among hospitalized children: from past and to present. Pediatr
Gastroenterol Hepatol Nutr. 2018;21(2):79–85.
13. Joosten KFM, Hulst JM. Nutritional screening tools for hospitalized children: methodological
considerations. Clin Nutr. 2014;33:1–5.
14. Sermet-Gaudelus I, Poisson-Salomon AS, Colomb V, et al. Simple pediatric nutritional risk score to identify
children at risk of malnutrition. Am J Clin Nutr. 2000;72:64–70.
15. McCarthy H, Dixon M, Crabtree I, et al. The development and evaluation of the Screening Tool for the
Assessment of Malnutrition in Paediatrics (STAMP©) for use by healthcare staff. J Hum Nutr Diet. 2012;
25:311–318.
16. Huysentruyt K, Devreker T, Dejonckheere J, De Schepper J, Vandenplas Y, Cools F. Accuracy of nutritional
screening tools in assessing the risk of undernutrition in hospitalized children. J Pediatr Gastroenterol Nutr.
2015;61(2):159–166.
17. Murphy AJ, White M, Viani K, Mosby TT. Evaluation of the nutrition screening tool for childhood cancer
(SCAN). Clin Nutr. 2016;35(1):219–224.
18. Wonoputri N, Djais JT, Rosalina I. Validity of nutritional screening tools for hospitalized children. J Nutr
Metabol. 2014;2014:143649.
19. Jensen GL, Compher C, Sullivan DH, Mullin GE. Recognizing malnutrition in adults: definitions and
characteristics, screening, assessment, and team approach. JPEN J Parenter Enteral Nutr. 2013;37(6):802–
807.
20. McClave SA, Taylor BE, Martindale RG, et al. Guidelines for the provision and assessment of nutrition
support therapy in the adult critically ill patient: Society of Critical Care Medicine (SCCM) and American
Society for Parenteral and Enteral Nutrition (A.S.P.E.N.). JPEN J Parenter Enteral Nutr. 2016;40(2):159–
211.
21. Shronts EP, Cerra FB. The rational use of applied nutrition in the surgical setting. In: Paparella M, ed.
Otolaryngology. Philadelphia, PA: WB Saunders; 1990.
22. Jeejeebhoy KN. Nutritional assessment. Gastroenterol Clin North Am. 1998;27(2):347–369.
23. Detsky AS, McLaughlin JR, Baker JP, et al. What is subjective global assessment of nutritional status?
JPEN J Parenter Enteral Nutr. 1987;11:8–13.
24. Baker JP, Detsky AS, Wesson DL, et al. Nutritional assessment: a comparison of clinical judgment and
objective measurements. N Engl J Med. 1988;306:969–973.
25. White JV, Guenter P, Jensen G, et al. Consensus statement: Academy of Nutrition and Dietetics and
American Society for Parenteral and Enteral Nutrition: characteristics recommended for the identification
and documentation of adult malnutrition (undernutrition). JPEN J Parenter Enteral Nutr. 2012;36(3):275–
283. doi:10.1177/0148607112440285.
26. Guenter P, Jensen G, Patel V, et al. Addressing disease-related malnutrition in hospitalized patients: a call
for a national goal. Jt Comm J Qual Patient Saf. 2015;41(10):469–473.
27. JeVenn AK, Galang M, Hipskind P, Bury C. Malnutrition screening and assessment. In: Mueller CM, ed.
The ASPEN Adult Nutrition Support Core Curriculum. 3rd ed. Silver Spring, MD: American Society for
Parenteral and Enteral Nutrition; 2017:185–211.
28. Malone A, Hamilton C. The Academy of Nutrition and Dietetics/the American Society for Parenteral and
Enteral Nutrition consensus malnutrition characteristics: application in practice. Nutr Clin Pract.
2013;28(6):639–650.
29. Jensen GL, Hsiao PY, Wheeler D. Adult nutrition assessment tutorial. JPEN J Parenter Enteral Nutr.
2012;36(3):267–274.
30. Riley LK, Rupert J. Evaluation of patients with leukocytosis. Am Fam Physician. 2015;92(11):1004–1011.
31. McDowell S. What is leukopenia? Healthline. June 1, 2017. https://www.healthline.com/health/leukopenia.
Accessed June 15, 2018.
32. Marcin J. C-reactive protein test. Healthline. May 22, 2017. https://www.healthline.com/health/c-reactive-
protein. Accessed June 15, 2018.
33. Ferritin, serum. Mayo Medical Laboratories website. https://www.mayomedicallaboratories.com/test-
catalog/Clinical+and+Interpretive/88153. Accessed June 15, 2018.
34. Hypotension—what causes hypotension? National Heart, Lung, and Blood Institute website.
https://www.nhlbi.nih.gov/node/3740. Accessed June 15, 2018.
35. Tachycardia. Mayo Clinic website. https://www.mayoclinic.org/diseases-conditions/tachycardia/symptoms-
causes/syc-20355127. Accessed June 15, 2018.
36. Bradycardia. Mayo Clinic website. https://www.mayoclinic.org/diseases-conditions/bradycardia/symptoms-
causes/syc-20355474. Accessed June 15, 2018.
37. McCullough L, Arora S. Diagnosis and treatment of hypothermia. Am Fam Physician. 2004;70(12):2325–
2332.
38. Fever. Mayo Clinic website. https://www.mayoclinic.org/diseases-conditions/fever/symptoms-causes/syc-
20352759. Accessed June 15, 2018.
39. Norman K, Stobaus N, Gonzalez MC, Schulzke JD, Pirlich M. Hand grip strength: outcome predictor and
marker of nutritional status. Clin Nutr. 2011;30:135–142.
40. Jensen GL, Bistrian B, Roubenoff R, Heimburger DC. Malnutrition syndromes: a conundrum vs continuum.
JPEN J Parenter Enteral Nutr. 2009;33(6):710–716.
41. Jensen GL, Mirtallo J, Compher C, et al. Adult starvation and disease-related malnutrition: a proposal for
etiology-based diagnosis in the clinical practice setting from the International Consensus Guideline
Committee. JPEN J Parenter Enteral Nutr. 2010;34(2):156–159. doi:10.1177/0148607110361910.
42. Hudson L, Chittams J, Griffith C, Compher C. Malnutrition identified by Academy of Nutrition and
Dietetics/American Society for Parenteral and Enteral Nutrition is associated with more 30-day
readmissions, greater hospital mortality, and longer hospital stays: a retrospective analysis of nutrition
assessment data in a major medical center. JPEN J Parenter Enteral Nutr. 2018;42(5):892–897.
doi:10.1002/jpen.1021.
43. Ceniccola GD, Holanda TP, Pequeno RSF, et al. Relevance of AND-ASPEN criteria of malnutrition to
predict hospital mortality in critically ill patients: a prospective study. J Crit Care. 2018;44:398–403.
44. Mehta NM, Corkins MR, Lyman B, et al. Defining pediatric malnutrition: a paradigm shift toward etiology-
related definitions. JPEN J Parenter Enteral Nutr. 2013;37(4):460–481. doi:10.1177/0148607113479972.
45. Becker P, Carney LN, Corkins M, et al. Consensus statement of the Academy of Nutrition and
Dietetics/American Society of Parenteral and Enteral Nutrition: indicators recommended for the
identification and documentation of pediatric malnutrition (undernutrition). Nutr Clin Pract. 2015;
30(1):147–161. doi:10.1177/0884533614557642.
46. Ireton-Jones CS, Hasse JM. Comprehensive nutritional assessment: the dietitians’ contribution to the team
effort. Nutrition. 1992;8(2):75–81.
47. Fischer M, JeVenn A, Hipskind P. Evaluation of muscle and fat loss as diagnostic criteria for malnutrition.
Nutr Clin Pract. 2015;30(2):239–248.
48. Secker DJ, Jeejeebhoy KN. How to perform subjective global nutritional assessment in children. J Acad Nutr
Diet. 2012;112(3):424–431.
49. DeTallo C, ed. The Practitioner’s Guide to Nutrition Focused Physi cal Exam of Infants, Children, and
Adolescents: An Illustrated Hand book. Silver Spring, MD: American Society for Parenteral and Enteral
Nutrition; 2019.
50. Tanner JM. Growth in Adolescents. 2nd ed. Boston, MA: Blackwell Scientific Publications; 1962.
51. Chumlea WC. Physical growth and maturation. In: Samour PM, Lang CE, eds. Handbook of Pediatric
Nutrition. 3rd ed. Boston, MA: Jones & Bartlett; 2005:1–10.
52. Assessment of nutritional status. In: Kleinman RE, Greer FR, eds. Pediatric Nutrition. 7th ed. Elk Grove
Village, IL: American Academy of Pediatrics. 2014:609–642.
53. Centers for Disease Control and Prevention. Growth charts. https://www.cdc.gov/growthcharts/index.htm.
Accessed November 21, 2018.
54. World Health Organization child growth standards. World Health Organization website.
http://who.int/childgrowth/standards/en. Accessed November 21, 2018.
55. Olsen IE, Groveman SA, Lawson L, Clark RH, Zemel BS. New intrauterine growth curves based on United
States data. Pediatrics. 2010;125(2):e214–e224. doi:10.1542/peds.2009-0913.
56. Fenton TR, Kim JH. A systematic review and meta-analysis to revise the Fenton growth chart for preterm
infants. BMC Pediatr. 2013;13:59. doi:10.1186/1471-2431-13-59.
57. Cronk C, Crocker AC, Pueschel SM, et al. Growth charts for children with Down syndrome. Pediatrics.
1988;81: 102–110.
58. Lyon AJ, Preece MA, Grant DB. Growth curve for girls with Turner syndrome. Arch Dis Child.
1985;60:932–935.
59. Morris CA, Demsey MS, Leonard CL, et al. Height and weight of males and females with Williams
syndrome. Wil liams Syndr Assoc Newslett. Summer 1991:29–30.
60. Butler MG, Meany FJ. Standards for selected anthropometric measurements in Prader-Willi syndrome.
Pediatrics. 1991; 88:853–858.
61. Krick J, Murphy-Miller P, Zeger S, et al. Pattern of growth in children with cerebral palsy. J Am Diet Assoc.
1996; 96:680–685.
62. Brooks J, Day SM, Shavelle RM, Strauss DJ. Low weight, morbidity, and mortality in children with cerebral
palsy: new clinical growth charts. Pediatrics. 2011;128:e299. doi:10.1542/peds.2010-2801.
63. Cerebral palsy: new growth charts. Life Expectancy Project website.
http://www.lifeexpectancy.org/articles/newgrowthcharts.shtml. Accessed November 21, 2018.
64. Maternal Child and Health Bureau. The CDC growth charts for children with special health care needs
[training module]. http://depts.washington.edu/growth/cshcn/text/intro.htm. Accessed November 21, 2018.
65. Guenter PA, Smithgall JM, Williamson JM, Rombeau JL. Body weight. In: Rombeau JL, Caldwell MD,
Forlaw L, Guenter PA, eds. Atlas of Nutrition Support Techniques. Boston, MA: Little, Brown; 1989:1–12.
66. Heymsfield SB, Baumgartner RN, Pan SF. Nutritional assessment of malnutrition by anthropometric
methods. In: Shils M, Olson JA, Shike M, Ross AC. Modern Nutrition in Health and Disease. 9th ed.
Baltimore, MD: Williams and Wilkins; 1999.
67. Lippincott’s Nursing Procedures. 7th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2015.
68. National Heart, Lung, and Blood Institute. Clinical Guidelines on the Identification, Evaluation, and
Treatment of Overweight and Obesity in Adults: Executive Summary. Washington, DC: National Institutes of
Health; 2002.
69. World Health Organization. Obesity: preventing and managing the global epidemic. Report of a WHO
Consultation presented at: the World Health Organization; June 3–5, 1997; Geneva, Switzerland. Publication
WHO/NUT/NCD/98.1.
70. American Academy of Family Physicians, American Dietetic Association, and National Council on Aging.
Nutrition Inter ventions Manual for Professionals Caring for Older Americans. Washington, DC: Nutrition
Screening Initiative; 1992.
71. Barlow SE; Expert Committee. Expert Committee recommendations regarding the prevention, assessment,
and treatment of child and adolescent overweight and obesity: summary report. Pediatrics. 2007;120(Suppl
4):S164–S192.
72. Freeman DS, Sherry B. The validity of BMI as an indicator of body fatness and risk among children.
Pediatrics. 2009;124(Suppl 1):S23–S34. doi:10.1542/peds.2008 -3586E.
73. Hamwi GJ. Changing dietary concepts. In: Danowski TS, ed. Diabetes Mellitus: Diagnosis & Treatment.
Vol. 1. New York, NY: American Diabetes Association; 1964:73–78.
74. Phillips S, Edlbeck A, Kirby M, Goday P. Ideal body weight in children. Nutr Clin Pract. 2007;22(2):240–
245. doi:10.1177/0115426507022002240.
75. Sentongo T. Growth assessment and monitoring. In: Corkins MR, Balint J, Bobo E, Plogsted E, Yaworski
JA, eds. The A.S.P.E.N. Pediatric Nutrition Support Core Curriculum. 2nd ed. Silver Spring, MD: American
Society for Parenteral and Enteral Nutrition; 2010:142.
76. Knapp TR. A methodological critique of the “ideal weight” concept. JAMA. 1983;250:506–510.
77. Centers for Disease Control and Prevention. National Health and Nutrition Examination Survey (NHANES).
Anthropometry manual. https://wwwn.cdc.gov/nchs/data/nhanes/2013-
2014/manuals/2013_Anthropometry.pdf. Published January 2013. Accessed June 18, 2018.
78. McDowell MA, Fryar CD, Hirsch R, Ogden CL. Anthropo-metric reference data for children and adults:
U.S. population, 1999–2002. Adv Data. 2005;(361):1–5.
79. Mulasi U, Kuchnia AJ, Cole AJ, Earthman CP. Bioimpedance at the bedside: current applications,
limitations, and opportunities. Nutr Clin Pract. 2015;30(2):180–193.
80. Earthman CP. Body composition tools for assessment of adult malnutrition at the bedside: a tutorial on
research considerations and clinical applications. JPEN J Parenter Enteral Nutr. 2015;39(7):787–822.
81. Prado CM, Heymsfield SB. Lean tissue imaging: a new era for nutritional assessment and intervention.
 JPEN J Parenter Enteral Nutr. 2014;38(8):940–953.
82. Tillquist M, Kutsogiannis DJ, Wischmeyer PE, et al. Bedside ultrasound is a practical and reliable
measurement tool for assessing quadriceps muscle layer thickness. JPEN J Parenter Enteral Nutr.
2014;38(7):886–890.
83. Gruther W, Benesch T, Zorn C, et al. Muscle wasting in intensive care patients: ultrasound observation of
the M. quadriceps femoris muscle layer. J Rehabil Med. 2008; 40(3):185–189.
84. Russell MK. Functional assessment of nutrition status. Nutr Clin Pract. 2015;30(2):211–218.
85. Esper DH. Utilization of nutrition-focused physical assessment in identifying micronutrient deficiencies.
Nutr Clin Pract. 2015;30(2):194–202. doi:10.1177/0884533615573054.
86. McKeever L. Vitamins and trace minerals. In: Mueller CM, ed. The ASPEN Adult Nutrition Support Core
Curriculum. 3rd ed. Silver Spring, MD: American Society for Parenteral and Enteral Nutrition; 2017:139–
182.
87. Russell MK. Laboratory monitoring. In: Matarese LE, Gottschlich MM, eds. Contemporary Nutrition
Support Practice. Philadelphia, PA: WB Saunders; 2003:45–62.
88. Black DR, Sciacca JP, Coster DC. Extremes in body mass index: probability of health care expenditures.
Prev Med. 1994;23:385–393.
89. Seres DS. Nutritional assessment: current concepts and guidelines for the busy physician. Pract
Gastroenterol. 2003; 8:30–39.
90. Tignanelli CJ, Bukowiec JC. Hospital-based nutrition support: a review of the latest evidence. J Clin Nutr
Diet. 2017; 3:22. doi:10.4172/2472-1921.100057.
91. Abdelhadi RA, Bouma S, Bairdain S. Characteristics of hospitalized children with a diagnosis of
malnutrition: United States, 2010. JPEN J Parenter Enteral Nutr. 2016;40(5):623–635.
92. McClave SA, DiBaise JK, Mullin GE, Martindale RG. ACG clinical guideline: nutrition therapy in the adult
hospitalized patient. Am J Gastroenterol. 2016;111(3):315–334.
93. Mehta NM, Skillman HE, Irving SY, et al. Guidelines for the provision and assessment of nutrition support
therapy in the pediatric critically ill patient: Society of Critical Care Medicine and American Society for
Parenteral and Enteral Nutrition. JPEN J Parenter Enteral Nutr. 2017;41(5):706–742.
94. Worthington P, Balint J, Bechtold M, et al. When is parenteral nutrition appropriate? JPEN J Parenter
Enteral Nutr. 2017;41:324–377.
 CHAPTER 2

Overview of Enteral Nutrition and Patient Selection

Introduction
When adequate oral intake is compromised or contraindicated, nutrition support may be warranted for survival.
Enteral nutrition (EN), the provision of nutrients via the gastrointestinal (GI) tract through a feeding tube, is the
preferred route for delivering nutrition in patients who cannot meet their nutrition needs through voluntary oral
intake.1 When access is available and the GI tract can be safely used, EN is associated with numerous physiological,
metabolic, safety, and cost benefits over parenteral nutrition (PN).1
The physiological benefits of EN include using normal digestive and absorptive pathways. In contrast to PN,
nutrients that are administered enterally undergo first-pass metabolism, which promotes the efficient utilization of
nutrients. EN is also an important therapeutic tool that can diminish the adverse structural and functional
consequences associated with gut disuse.2 The presence of nutrients in the gut lumen, even in small amounts, helps
maintain normal digestive and absorptive functions of the GI tract. EN also assists with maintenance of the gut-
associated lymphoid tissue and mucosa-associated lymphoid tissue, both of which play an integral role in
immunity.2 In prospective, randomized clinical trials (RCTs), EN has been associated with reduced infectious
complications, likely through the maintenance of GI integrity.2–4 Alterations in gut integrity due to loss of villous
height, reduction in secretory immunoglobulin A production, and increased gut permeability can lead to systemic
infectious complications and multiorgan dysfunction syndrome.3,4 By maintaining gut integrity through the use of
EN, the stress and immune responses are modulated and disease severity may therefore be decreased.5,6 Lastly, EN is
also associated with fewer complications and is less expensive than PN. The time-tested adage “If the gut works, use
it” has become the guiding principle when identifying patients for EN.
Technological advancements in enteral formulations and equipment have greatly expanded the number of
patients who can receive EN. The EN use process (Figure 2-1) is the system within which EN is used.7 It involves a
number of major steps: initial patient assessment, recommendations for an EN regimen, selection of the enteral
access device (EAD), the EN prescription, review of the EN order, product selection or preparation, product labeling
and dispensing, administration of the EN to the patient, and patient monitoring and reassessment, with
documentation at each step. This process requires a multidisciplinary team of competent clinicians working in
concert to provide safe nutrition care.7 This chapter briefly surveys the various aspects of the process; refer to the
other chapters in this handbook for more detailed information.
History of Enteral Nutrition
In ancient times, equipment such as wooden or glass tubes was used to administer various combinations of liquids to
individuals who were unable or unwilling to consume adequate quantities of food.8 Given the difficulty and danger
involved in such attempts, enteral feeding was often viewed as an option of last resort. During the 18th and 19th
centuries, equipment remained fairly primitive, and nutrition choices were limited to liquids such as broth, milk,
eggs, and wine.9 In the late 19th century—a time when efficient nutrient absorption was thought to take place in the
colon—rectal feedings were commonly used to circumvent the challenges of achieving reliable access to the upper
GI tract.9
With the advent of modern medicine, technological advances have led to the availability of a plethora of EADs
and formulas that have improved the safety and efficacy of EN. Additionally, a multitude of studies have
demonstrated that improved outcomes are associated with EN.2–6,10–12

Indications for Enteral Nutrition and Patient Selection

A thorough nutrition assessment facilitates the identification of patients who may benefit from the initiation of
nutrition support (see Chapter 1). Data collected in the assessment process guide decisions related to nutrition
interventions by determining the most appropriate route for providing nutrition (see Figure 2-2), identifying the
optimal timing for initiation of therapy, establishing nutrient requirements, detecting potential complications, and
identifying any need for specialty formulations.13

The process of determining which patients actually should receive a feeding tube and EN can be quite
challenging. Table 2-1 lists important factors to consider before placement of any type of EAD. Addressing these
issues may take some time. Therefore, waiting a few days before placing a feeding tube may be appropriate for
patients who are not critically ill or malnourished. For critically ill patients, the patient should be hemodynamically
stable and fully resuscitated before EN support is initiated.14

TABLE 2-1. Factors to Consider Before Initiating Enteral Nutrition

• The patient's clinical and nutrition status, medical diagnosis, and prognosis
• Risks and benefits of therapy
• Discharge plans
• Quality of life
• Ethical issues
 • The patient's or family's wishes
• Cost and reimbursement issues

Individuals who have a functional GI tract but have clinical conditions in which oral intake is impossible,
inadequate, or unsafe are candidates for EN. EN should be considered for malnourished patients and those who are
at high risk for becoming malnourished because they cannot maintain adequate nutrition status through oral intake
alone. Other possible indications for EN include the following:

• Poor appetite, which may be associated with a chronic medical condition or treatment
• Dysphagia, which may be related to neurological disease, oropharyngeal dysfunction, or another issue
• Major trauma, burns, wounds, and/or critical illness

Additionally, severely malnourished preoperative patients who have a functional GI tract may benefit from a
course of EN prior to surgery.15
Infants and children have a higher rate of energy expenditure than adults; on a weight basis, energy requirements
are 3 to 4 times higher for infants than for adults. Therefore, infants and children are at greater risk for nutrition
compromise than adults.16,17 The nutrition goals for the pediatric patient are to provide adequate nutrition for growth,
development, and the preservation and proliferation of lean body mass.5,18 Extended periods of malnutrition during
childhood can manifest in growth failure and have adverse effects on cognitive and behavioral development. In
hospitalized children, malnutrition is associated with longer length of stay, higher infection rates, and worse clinical
outcomes (eg, longer times to wean off ventilator support).19,20 For these reasons, identifying malnutrition and
optimizing nutrition provision in children is vital.
Initiation of EN may be considered in infants and children who have a functioning GI tract in the following
circumstances:

• Prolonged nil per os (NPO) status during hospitalization:

• If the patient is age 1 year or older, consider EN if patient is NPO or is anticipated to remain NPO ≥5
days.21
• If the patient is younger than age 1 year, consider EN if the patient is NPO or is anticipated to remain NPO
≥3 days.21
• Disorders of oral feeding (eg, abnormal sucking and swallowing, discoordination, aspiration, dysphagia,
congenital abnormalities of upper GI tract, severe gastroesophageal reflux, esophagitis, feeding/oral
aversion, anorexia nervosa)21
• Disorders of digestion and/or absorption (eg, congenital abnormalities of the GI tract, GI dysmotility,
intractable diarrhea of infancy, autoimmune enter-opathy, immunodeficiency, short bowel syndrome, organ
transplantation, graft-versus-host disease, pancreatitis, cystic fibrosis)21
• Conditions with increased nutrient and/or metabolic requirements (eg, cystic fibrosis, burn, injury, recurrent
infection, congenital heart defects, chronic renal or pulmonary disease)
• Poor growth velocity (weight decrease of more than 2 standard deviations based on z score)
• Inadequate growth, weight loss, or no weight change21
• Weight for height less than the fifth percentile or z score of less than –2
• Mid–upper arm circumference less than the fifth percentile for age
• Inability to consume at least 80% of estimated energy needs by mouth22
• Disorders where EN is a key component of disease treatment, such as the use of exclusive EN for Crohn’s
disease, the ketogenic diet for epilepsy, or specialty formulas for inborn errors of metabolism21
Contraindications to Enteral Nutrition
In certain situations, patients should not receive EN. Table 2-2 summarizes selected contraindications to EN.14,21,23–25

TABLE 2-2. Selected Contraindications to Enteral Nutrition Support

Potential contraindications for patients of all ages:

• Nonoperative mechanical GI obstruction
• Hemodynamic instability (eg, mean arterial pressure <50 mmHg)
• 1 ntractable vomiting/diarrhea refractory to medical management
• Severe short bowel syndrome (<100 cm small bowel remaining)
• Distal high-output fistulas
• Severe GI bleed
• Severe GI malabsorptiona
• Inaccessible GI tract
• Aggressive intervention is not warranted or not desired by the patient
Relative contraindications in pediatric patients:
• Intestinal dysmotility
• Necrotizing enterocolitis
• Toxic megacolon
• Diffuse peritonitis
• GI bleeding
Abbreviations: EN, enteral nutrition; GI, gastrointestinal.
a
For example, EN failed as evidenced by progressive deterioration in the patient’s nutrition status.
Source: Information is from references 14, 21, and 23-25.

To determine whether contraindications are relative or absolute, the patient’s clinical status should be thoroughly
assessed. In particular, a thorough and objective evaluation of GI function is needed to identify any obstacle to
successful enteral feeding. Additionally, patients receiving EN should be monitored closely to detect any
complications or signs of intolerance that may require a change in the EN regimen.
Often, potential barriers to EN can be circumvented with careful selection of the appropriate EAD, formula, and
route of administration. For example, patients with minimally functional digestive and absorptive capabilities can
often be fed using elemental or small-peptide formulations (see Chapters 4 and 5 for further discussion on EN
formulas).
It was previously thought that paralytic ileus, defined as absence of bowel sounds or flatus, presented a
contraindication to enteral feedings. However, it is now known that the absence of bowel sounds does not preclude
safe EN.14 Ileus has varied effects on different areas of the intestine. For example, postoperative ileus appears to
affect colonic and gastric function to a greater extent than small intestinal function.26 While similar conditions, such
as partial small bowel obstruction and motility disorders, also present challenges to successful EN, these problems
are not considered absolute barriers.
Vomiting and diarrhea are frequently identified as contraindications to EN. Vomiting presents challenges in
maintaining nasal tube placement. However, successful enteral administration may be promoted by (a) the initiation
of small bowel feedings with simultaneous gastric decompression and (b) the use of prokinetic agents. Patients with
diarrhea should be evaluated to identify the cause (eg, Clostridium difficile infection or medications) and type of
diarrhea (osmotic vs secretory).14 The patient’s nutrition status as well as the risk for a general overall deterioration
in clinical status should also be considered (see Chapter 9 for further discussion of nausea and diarrhea).
In some situations, GI fistulas may preclude the initiation of EN. Enteral feedings are generally better tolerated
by patients with more proximal or distal fistulas (rather than midgut), and low to moderate fistula output. High-
output fistulas in the mid-jejunal area tend to be the most problematic. Patients should be monitored closely to
ensure efficacy and tolerance of EN support. An increase in fistula output with enteral feeding suggests that other
means of nutrition support, such as PN, may be indicated.
A mechanical obstruction of the GI tract, or pseudo-obstruction that does not resolve, is generally an absolute
contraindication to enteral feedings. Patients with a partial obstruction may receive EN; however, careful monitoring
is essential in order to ensure efficacy and tolerance of EN therapy.
The use of EN for patients with GI bleeding presents another clinical dilemma. GI bleeding was previously
considered an absolute contraindication for enteral feedings since the literature in the past suggested that any GI
bleeding was associated with adverse outcomes.27 Etiology, location, and severity of the bleeding are all factors that
should be evaluated before initiating enteral support. For most patients, lower GI bleeding does not affect the
administration of EN.28 Conversely, enteral feedings for patients who present with upper GI bleeding due to
esophageal varices, portal hypertension, or cirrhosis should be delayed until risk of bleeding has diminished.15
While the Society of Critical Care Medicine (SCCM) and American Society for Parenteral and Enteral Nutrition
(ASPEN) clinical practice guidelines for the provision of nutrition support for critically ill adults generally
recommend early initiation of EN in critically ill patients (see Optimal Timing for Enteral Nutrition section later in
this chapter), the guidelines also state that EN should be withheld for patients with hypotension (mean arterial
pressure <50 mmHg), during initiation of catecholamine agents (ie, dopamine, epinephrine, norepinephrine, etc),
and when doses of catecholamine agents are increased.14 In the NUTRIREA-2 study, critically ill patients who were
mechanically ventilated receiving vasopressor support and early EN experienced bowel ischemia to a greater degree
than patients receiving PN (19 patients in EN group vs 5 patients in PN group; P = 0.007), supporting the
importance of providing EN to stable patients.29 Conversely, stable patients receiving low-dose vasopressor support
had lower mortality rates for both intensive care unit (ICU) mortality and hospital mortality when EN was initiated
early.30
During periods of hemodynamic instability in pediatric patients, clinicians may be reluctant to provide EN
because of the risk of bowel ischemia. However, studies have shown that critically ill pediatric patients can tolerate
full-strength, continuous EN while receiving extracorporeal membrane oxygenation and tolerate EN administered at
the goal rate while receiving cardiovascular medication support (ie, vasopressors) that affect gut perfusion.31,32

Optimal Timing for Enteral Nutrition

The optimal times to initiate EN depend on the patient’s clinical and nutrition status (eg, medically stable, critically
ill, acutely ill, nourished, malnourished). Medical and nutrition assessment is required to determine the best timing
for the individual patient.

Medically Stable Patients

The precise length of time that a patient can tolerate suboptimal nutrition intake is unknown. In a 2017 consensus
document on the use of PN, PN support is recommended after 7 days in well-nourished, medically stable adult
patients who are unable to achieve 50% of estimated nutrient requirements.33 In this document, it is recommended
that in patients “at risk” for malnutrition, PN intervention should begin within 3–5 days with inadequate oral or
enteral intake. The principles underlying these recommendations can be applied to support the initiation of enteral
feedings in the patient unable to achieve adequate oral intake.
Worse outcomes, including increased morbidity and longer hospital length of stay, have been reported for
hospitalized adult patients who do not eat for 10 to 14 days following admission or surgery.14 The optimal timing to
promote positive clinical outcomes in general nonsurgical and non–critically ill patients requires further evaluation
in large clinical trials.

Critically Ill Patients

In contrast to patients who are medically stable, critically ill patients seem to benefit from early initiation of EN.
When EN initiation is delayed, patients are exposed to energy deficits, which are correlated with increased incidence
of complications in critical illness.34 Although the optimal timing for EN support in critically ill patients has not
been clearly elucidated, the SCCM/ASPEN guidelines for critically ill adults recommend initiating EN within 24 to
48 hours postoperatively or following injury requiring admission to the ICU because evidence suggests that early
initiation improves clinical outcomes.14 In agreement with adult critical care guidelines, recommendations for
patients in the pediatric intensive care unit (PICU) also support early EN initiation (ie, within 24–48 hours of PICU
admission).35
Starting EN as trophic feeds in the first week of critical illness may be an option for patients who cannot initially
tolerate full feedings. Several RCTs comparing EN therapy initiated with trophic feeding vs full feeding have found
no differences in outcomes.36–39
Most of the more recent studies of trophic vs full feeds have focused on the delivery of EN within the first week
of critical illness. No prospective RCTs have investigated whether delaying full feeds until the second week of
critical illness would be more beneficial than advancing more quickly to full feeds. Some researchers have theorized
that minimal feeding during the first week or “initial phase” of critical illness may be beneficial for critically ill
adults to promote autophagy during the height of critical illness; others advocate for the goal of providing full
nutrition support, if possible, at this critical time period.14,40,41 In published studies comparing underfeeding to full
feeding, 8 out of 9 studies report more favorable outcomes with underfeeding.42–50 After removing the studies with
methodological flaws, 4 observational studies and 1 RCT found worse outcomes were associated with full
feeds.42–45,47 In RCTs, investigators have found no difference in outcomes between the feeding strategies.36,38,39,46
The initial feeding goal for critically ill pediatric patients is to provide up to two-thirds of the estimated nutrient
needs in the first week of critical illness. Optimizing protein intake is also crucial to the recovery of PICU
patients.35,51,52 Efficient advancement of EN to achieve goal feeds is best supported by protocols or algorithms in the
PICU.53,54 Each medical center has different protocols or algorithms for feeding advancement in pediatric patients,
but the rates for initiation and advancement of tube feeds typically depend on the child’s body weight and overall
clinical status. See the Administration Methods section of this chapter for additional information.
Critically ill patients are a heterogeneous group. Clinicians must always monitor patients closely to avoid the
potential deleterious effects (eg, bowel ischemia, aspiration) of early EN.

Acutely Ill Patients

Several reviews comparing early EN versus early PN in acutely ill patients have been published. A criticism
commonly voiced regarding the results of these reviews is that the studies include heterogeneous populations,
making it difficult to determine what advantages are conveyed to specific populations. The results of several early
meta-analyses of RCTs of hospitalized patients clearly support recommendations to use early EN over early PN to
achieve positive clinical outcomes; however, more recent trials have found no difference in outcomes when
comparing early EN with early PN.29,55–58
Lack of consistency in the definition of “early” intervention is a limitation when comparing studies of early
nutrition support interventions. Protocols for early EN typically begin EN within 24 to 36 hours of admission, but
the initiation of feedings ranges from within 3 hours of injury to as late as 96 hours following hospitalization.14
Some evidence suggests that the time of initiation of feeding can make a difference in outcomes. When EN was
initiated less than 72 hours postadmission, it was associated with a 2-day reduction in length of stay, compared with
EN initiated more than 72 hours following admission.14 Given the inconsistent results and methodological flaws in
studies of early nutrition support interventions, further research is clearly needed to delineate more precisely the
optimal timing and amount delivered for nutrition intervention in acutely ill patients.

Enteral Access Device Selection

The selection of the correct EAD is critical to the successful delivery of EN. Factors influencing the selection
include the following:

• Clinical status and patient history

• Functional status of the GI tract (eg, gastric emptying, absorptive capacity)
• Anatomy of the GI tract
• Expected duration of EN: short term (eg, <4 weeks) vs long term (eg, >4 weeks)
• Aspiration risk
• Patient wishes
• Quality of life
 Refer to Chapter 3 for additional information on the various feeding routes and EAD types available for
administering EN formulations, including their benefits, limitations, and potential complications.

Formula Selection and Preparation

Many types of EN formulas are available in the marketplace. Most medical institutions have an established EN
formulary that reflects the needs of their patient populations, and outpatients can either receive formula from an
infusion or durable medical equipment company or purchase standard EN formulas over the counter. Before
selecting an EN formula, the clinician should complete a comprehensive assessment of the patient’s nutrition needs,
clinical status, and possible benefits that may be derived from the formula.
Standard adult formulas, ranging from 1 kcal/mL to 2 kcal/mL with varying amounts of protein, are readily
available and are recommended for most adult patient populations (see Chapter 4). Standard pediatric formulas are
indicated for patients ages 1 to 13 years. These products typically provide 1 kcal/mL (30 kcal/oz). Most pediatric
formulations are available as ready-to-feed products and some are available in the retail setting (see Chapter 5).
Homemade or commercially prepared blenderized tube feedings (BTFs) derived from whole food may also be used
in EN therapy for adults and children. However, these types of formulas may increase the risk for microbial
contamination and clogging of the feeding tube.38 Refer to Chapters 4, 5, 7, 8, and 11 for additional information on
BTFs.
Human milk (HM) is typically the first choice for neonates; however, the optimal choice for a specific infant
depends on the family’s feeding goals. HM is assumed to be between 19 and 20 kcal/oz, although the energy density
can vary. Standard infant formulas are available over the counter. To match the energy provided by HM, standard
dilution of infant formula ranges from 19 to 20 kcal/oz. See Chapter 5 for additional information on the selection of
HM and infant formulas.
The concentration of energy provided by powdered formulas may be adjusted by altering the amount of fluid
mixed with the powder. See Chapter 7 for guidance on the preparation of powdered formulas.
Nutrient levels in both liquid and powdered products can be adjusted with the addition of a variety of modular
components that augment energy, protein, fiber, and micronutrients. For example, modulars may be used to increase
the energy density of feeds for pediatric patients while avoiding the high renal solute load of excessively
concentrated formula. The osmolarity of the final formula must be considered to avoid hyperosmolar formula, which
may not be well tolerated in some infants and children.59 See Chapters 4 and 5 for additional information on modular
products.
Pediatric and adult enteral formulas do not generally meet the patient’s fluid requirements. Additional fluid is
therefore needed to maintain normal fluid status. Infants should rarely be offered free water because of the possible
risk for oral water intoxication, which can cause hyponatremia, convulsions, and even death.60 See Chapter 1 for
information on assessing fluid status, Chapter 6 for information on the fluid requirements in the nutrition
prescription, and Chapter 9 for guidance on dehydration prevention.
Regardless of the type of tube feeding used, clinicians must follow best-practice recommendations for the safe
storage, preparation, labeling, and dispensing of EN products. These recommendations are reviewed in Chapter 7.

Administration Methods
Bolus, intermittent, continuous, and cyclic methods are options for administering EN. The following should be
considered when choosing an administration method:

• The patient’s clinical status and GI function

• Location of feeding tube tip location
• The patient’s functional status, quality of life, and treatment preferences

When initiating feedings, clinicians should select the infusion method that promotes the best initial tolerance of
EN and is most likely to meet the patient’s nutrition needs. The infusion method may be changed, if necessary or
desirable, once feedings are established with good tolerance.
The following reviews the various infusion methods. Refer to Chapter 8 for additional information on
administration methods. Note: Before initiating any type of enteral feeding, tube placement should be confirmed
with imaging or by checking the medical record for documentation of what type of tube was placed and precisely
where the tip of the feeding tube is located.

Bolus Infusion
Bolus feedings use a syringe or gravity drip via a feeding container to infuse a specific volume of enteral formula
over a short period of time (eg, ≤30 minutes), several times throughout the day. For example, a bolus feeding
regimen might be to infuse 1 can (237 mL) of formula over 10–15 minutes every 3 to 4 hours, 4 or more times per
day during the daytime. The volume infused per feeding can range widely depending on the patient’s tolerance. The
rate at which the volume is infused can also be adjusted depending on the patient’s tolerance.
The advantages of bolus feedings are that they reflect typical eating patterns, allow for greater ambulation than
other administration methods, and are inexpensive.61 For some patients, providing feedings only during the day may
improve their quality of life and support their autonomy. In infants, bolus feedings can be helpful when the goal is to
increase the amount of oral intake because patients can drink part of the feeding and then the remaining amount can
be provided as a bolus through a feeding tube. Bolus feedings are generally only used when feeding into the
stomach.

Intermittent Infusion
Like the bolus method, the intermittent method infuses a specific volume of enteral formula over a specific amount
of time, several times per day. However, the intermittent method infuses the volume of feeding over a longer period
of time (eg, 20–60 minutes in adults; 120–180 minutes in pediatrics); typically intermittent feedings are
administered 4 or more times per day every 3 to 4 hours. The volumes infused can be similar to those used with
bolus feedings. An infusion pump or the gravity-drip method can be used to infuse the intermittent feeding.
Intermittent feedings are typically used for patients receiving gastric feedings. They may be used prior to trying
bolus feedings or tried when bolus feedings are poorly tolerated.

Continuous Infusion
Continuous infusions run 24 hours a day at a steady rate (mL/h) that provides adequate total volume to meet the
patient’s nutrition prescription. The volume infused can range widely (eg, from less than 50 mL/h to more than 150
mL/hour in adults), depending on the patient’s nutrition prescription and feeding tolerance. Continuous infusion is
most often administered using an enteral infusion pump or can be delivered via the gravity-drip method.62
Continuous infusions can be used when the feeding tube tip is in any location (gastric or postpyloric) because the
formula is administered in a slow and steady fashion. This administration method is most often used for critically ill
patients or when administering feedings into the small bowel.62 A variety of EN infusion pumps are available on the
market, including small, lightweight pumps for home use. See Chapter 11 for additional information on EN in the
home setting.

Cyclic Feedings
Cyclic feedings are similar to continuous feedings, except the daily volume of EN formula is infused in less than 24
hours. Like continuous feedings, cyclic feedings can be administered via an EN infusion pump or gravity drip.
With cyclic feedings, the rate (mL/h) of administration may be increased while the feeding times are condensed.
For example, if a patient has been receiving EN at a rate of 100 mL/h over 24 hours, the EN volume may be
increased to 135 mL/h and infused over 18 hours to provide a similar volume per day. As long as the patient is
tolerating the EN, the rate of EN administration could be continually increased while the time span for infusing the
formula is decreased to as little as 8 hours per day.
Compared with continuous feedings, the primary advantage of cyclic feedings is that time off the pump may
give the patient more autonomy and improved quality of life. Cyclic feedings are also an option when nocturnal
feedings are desired. For example, a patient may consume a normal diet during the day with nightly EN feedings
supplementing oral intake. Sometimes, infants will be allowed to work on oral feeding with oral/nasogastric boluses
during the day while catching up on energy and/or volume with overnight continuous feeds. This technique is
especially helpful in children who are already sleeping through the night and may enhance quality of life for both the
patient and family if the patient is receiving EN at home.
Volume-Based Administration
Volume-based feedings can be used to achieve established nutrient goals in some patients. Rather than using a fixed
rate of infusion, clinicians using this method can adjust the rate of feeding throughout the day based on the volume
needed per day to achieve the patient’s nutrient goals. This approach to EN administration is discussed in greater
detail in Chapter 8.

Advancing Enteral Nutrition

The SCCM/ASPEN clinical practice guidelines for critically ill adults recommend that EN should be advanced to
goal within 48–72 hours or provide at least 80% of nutrient needs in the first week of ICU admission in patients who
are stable and have been adequately resuscitated.14 Patients should be monitored closely for refeeding syndrome and
be reevaluated for feeding tolerance until stable.
The SCCM/ASPEN recommendation reflects evidence showing that the administration of trophic feeds—which
are usually begun in the critically ill adult at a rate from 10 to 20 mL/h—for up to 6 days is associated with positive
clinical outcomes such as less GI intolerance (ie, diarrhea), more ventilator-and ICU-free days, fewer infectious
complications, and reduced 60-day mortality when compared to full feeds.30,36 Trophic feeds may be sufficient to
maintain GI physiology and immune-enhancing benefits in patients who are at low to moderate nutrition risk and
adequately nourished upon admission.14 However, in many relevant studies, patients in the full-feeding groups never
achieved their prescribed nutrient needs, which complicates the comparison of trophic and full-feeding strategies.46,63
In 2 observational studies, when greater amounts of energy and protein were provided to critically ill patients at high
nutrition risk, feedings administered for at least 12 days were associated with better outcomes such as reduced
mortality.64,65 More specifically, these investigators suggest that providing sufficient protein is important to improve
ICU outcomes; meeting the energy goal seems less crucial. These findings are supported by others.66–68
Non–critically ill adult patients may begin EN at their goal rate when continuous infusions are used. Feedings
are started at full strength. When patients cannot start at their goal rate, feedings can begin at a rate of 25–30 mL/h
and be advanced as tolerated in increments of 20–30 mL/h every 4–8 hours until the goal rate is achieved.
In adults, bolus feedings are typically begun at 120–237 mL for the first feeding, with subsequent feedings
increased by similar volumes every 3–4 hours as tolerated. Patients should also be monitored for refeeding
syndrome.
In pediatrics, the volumes for initiating and advancing EN are tailored to reflect the size and age of the infant or
child. It is rare to start EN at the goal rate for non–critically ill pediatric patients. Full-strength feedings are
preferred. Laboratory values should be monitored for refeeding syndrome during the initiation and advancement of
nutrition support in children who are malnourished or taking in minimal energy.

Challenges Associated with Enteral Nutrition

Many of the common challenges associated with EN may be prevented if patients are assessed thoroughly and
monitored closely.7,14,69 See Chapter 1 for information on nutrition assessment, Chapter 8 for further discussion of
monitoring patients receiving EN, and Chapter 9 for a review of complications associated with EN.
The establishment of institutional policies and procedures can promote the safe delivery of optimal EN and
reduce costs such as those associated with hospital admissions. Protocols addressing the following are
recommended:7

• EAD assessment and care (Chapter 3)

• Formula and modular handling, preparation, labeling, and storage (Chapter 7)
• EN hang-time requirements (Chapter 8)
• Administration of medications (Chapter 10)
• Standardization of EN delivery and advancement (Chapter 8)
• Clarification of EN orders
• Review of EN errors
• Establishment of competency measurements for EN providers
Ethical Considerations
Artificial nutrition, including EN, is not associated with improved outcomes during advanced dementia and other
terminal illnesses, and it may result in increased burdens.14,70 When patients have advanced dementia or another
terminal illness, decisions to initiate, continue, or withdraw nutrition support can be ethically challenging and may
generate considerable distress among patients, family members, clinicians, and other caregivers. Careful
consideration and respect must be given to the patient and family’s wishes regarding the placement of a feeding tube
or the cessation of aggressive therapies, including EN. In such circumstances, the healthcare team should review the
risks and benefits with all involved in the patient’s care. Factors such as the patient’s religious and cultural beliefs as
well as the patient’s wishes should also be considered.
Guidelines are available from a variety of professional organizations to help guide decision-making related to
ethical decisions involved in whether to initiate, withhold, or withdraw support.14,70–73 Table 2-3 summarizes selected
legal and ethical recommendations from ASPEN.14,70–73

TABLE 2-3. Selected Legal and Ethical Recommendations Regarding Nutrition Support Therapy

• Legally and ethically, nutrition support therapy should be considered a medical therapy.
The decision to receive or refuse nutrition support therapy should reflect the autonomy and wishes of
• the patient. Clinicians should consider the benefits and burdens of nutrition support therapy, and the
interventions required to deliver it, before offering this therapy.
The healthcare team should strive for clear communication with the patient and his or her caregivers,
• family, and/or surrogate decision-makers.

Clinicians should be familiar with current evidence of the benefits and burdens of nutrition support
• therapy.

Adult patients should be encouraged to have living wills and/or advance directives and to discuss
• with their loved ones their wishes in the event of a serious or terminal accident or disease. These
directives should address the use of nutrition support therapy.
Competent patients or the legal surrogate of incompetent patients shall be involved in decisions
regarding the withholding or withdrawal of treatment. Incompetent patients' wishes (as documented
• in advance directives) shall be considered in making decisions to withhold or withdraw nutrition
support therapy.
Nutrition support therapy should be modified or discontinued when there are disproportionate
• burdens for the patient or when benefit to the patient can no longer be demonstrated.

Institutions should develop clear policies regarding the withdrawal or withholding of nutrition support
• therapy and communicate these policies to patients in accordance with the Patient Self-
Determination Act.
Source: Information is from references 14 and 70-73.

References
1. 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(suppl):1SA–
138SA. (Errata JPEN J Par enter Enteral Nutr. 2002;26:144.)
2. Jabbar A, Chang WK, Dryden GW, McClave SA. Gut immunology and the differential response to feeding
and starvation. Nutr Clin Pract. 2003;18(6):461–482.
3. Kudsk KA. Current aspects of mucosal immunology and its influence by nutrition. Am J Surg.
2002;183(4):390–398.
4. Kang W, Kudsk KA. Is there evidence that the gut contributes to mucosal immunity in humans? JPEN J
Parenter Enteral Nutr. 2007;31(3):246–258.
5. Windsor AC, Kanwar S, Li AG, et al. Compared with parenteral nutrition, enteral feeding attenuates the
 acute phase response and improves disease severity in acute pancreatitis. Gut. 1998;42(3):431–435.
6. Ammori BJ. Importance of the early increase in intestinal permeability in critically ill patients. Eur J Surg.
2002; 168(11):660–661.
7. Boullata J, Carrera AL, Harvey L, et al. ASPEN safe practices for enteral nutrition therapy. JPEN J Parenter
Enteral Nutr. 2016;41(1):15–103. doi:10.1177/0148607116673053.
8. Randall JT. The history of enteral nutrition. In: Rombeau JL, Caldwell MD, eds. Clinical Nutrition: Enteral
and Tube Feed ing. 2nd ed. Philadelphia, PA: WB Saunders; 1990.
9. Harkness L. The history of enteral nutrition therapy: from raw eggs and nasal tubes to purified amino acids
and early postoperative jejunal delivery. J Am Diet Assoc. 2002;102(3): 399–404.
10. Heyland DK, Dhaliwal R, Drover JW, Gramlich L, Dodek P; Canadian Critical Care Clinical Practice
Guidelines Committee. Canadian clinical practice guidelines for nutrition support in mechanically ventilated,
critically ill adult patients. JPEN J Parenter Enteral Nutr. 2003;27(5):355–373.
11. Doig GS, Heighes PT, Simpson F, Sweetman EA, Davies AR. Early enteral nutrition, provided within 24 h
of injury or intensive care unit admission, significantly reduces mortality in critically ill patients: a meta-
analysis of randomised controlled trials. Intensive Care Med. 2009;35(12):2018–2027.
12. Tian F, Heighes P, Allingstrup MJ, Doig GS. Early enteral nutrition provided within 24 hours of ICU
admission: a meta-analysis of randomized controlled trials. Crit Care Med. 2018;46(7):1049–1056.
doi:10.1097/CCM.00000000 00003152.
13. Ukleja A, Gilbert K, Mogensen KM, et al. Standards for nutrition support: adult hospitalized patients. Nutr
Clin Pract. 2018;33(6):906–920. doi:10.1002/ncp.10204.
14. McClave SA, Taylor BE, Martindale RG, et al. Guidelines for the provision and assessment of nutrition
support therapy in the adult critically ill patient: Society of Critical Care Medicine (SCCM) and American
Society for Parenteral and Enteral Nutrition (A.S.P.E.N.). JPEN J Parenter Enteral Nutr. 2016;40(2):159–
211.
15. Weimann A, Braga M, Carli F, et al. ESPEN guideline: clinical nutrition in surgery. Clin Nutr. 2017;36:623–
650.
16. Chwals WJ. Energy metabolism and appropriate energy repletion in children. In: Baker S, Baker R, Davis A,
eds. Pediatric Nutrition Support. Boston, MA: Jones and Bartlett Publishers; 2007:66.
17. Institute of Medicine. Recommended Dietary Allowances. 10th ed. Washington DC: National Academies
Press; 1989.
18. Sentongo T. Assessment of nutrition status by age and determining nutrient needs. In: Corkins M, ed. The
A.S.P.E.N. Pedi atric Nutrition Support Core Curriculum. 2nd ed. Silver Spring, MD: American Society for
Parenteral and Enteral Nutrition; 2015:531–565.
19. Carvalho-Salemi J, Salemi J, Wong-Vera M, et al. Malnutrition among hospitalized children in the United
States: changing prevalence, clinical correlates, and practice patterns between 2002 and 2011. J Acad Nutr
Diet. 2018;118(1):40–51.
20. Becker P, Carney L, Corkins M, et al. Consensus statement of the Academy of Nutrition and
Dietetics/American Society for Parenteral and Enteral Nutrition: indicators recommended for the
identification and documentation of pediatric malnutrition (undernutrition). Nutr Clin Pract.
2015;30(1):147–161.
21. Yi DY. Enteral nutrition in pediatric patients. Pediatr Gastroen terol Hepatol Nutr. 2018;21(1):12–19.
22. Axelrod D, Kazmerski K, Iyer K. Pediatric enteral nutrition. JPEN J Parenter Enteral Nutr. 2006;30(1
Suppl):S21–S26.
23. Bankhead R, Boullata J, Brantley S, Corkins M, et al. Enteral nutrition practice recommendations. JPEN J
Parenter Enteral Nutr. 2009;33(2):122–167.
24. DiBaise J, Parrish CR. Short bowel syndrome in adults— part 5: trophic agents in the treatment of short
bowel syndrome. Pract Gastroenterol. 2015;39(5):10–18.
25. Corkins M, ed. The A.S.P.E.N. Pediatric Nutrition Support Core Curriculum. 2nd ed. Silver Spring, MD:
American Society for Parenteral and Enteral Nutrition; 2015.
26. 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.
27. MacLaren R, Jarvis CL, Fish DN. Use of enteral nutrition for stress ulcer prophylaxis. Ann Pharmacother.
2001;35: 1614–1623.
28. McClave SA, Change WK. When to feed the patient with gastrointestinal bleeding. Nutr Clin Pract.
2005;20:544–550.
29. Reignier J, Boisramé-Helms J, Brisard L, et al. Enteral versus parenteral early nutrition in ventilated adults
with shock: a randomized, controlled, multicenter, open-label, parallel-group study (NUTRIREA-2). Lancet.
2018;391:133–143.
30. Khalid I, Doshi P, DiGiovine B. Early enteral nutrition and outcomes of critically ill patients treated with
vasopressors and mechanical ventilation. Am J Crit Care. 2010;19(3): 261–268.
31. Greathouse K, Sakellaris K, Tumin D, et al. Impact of early initiation of enteral nutrition on survival during
pediatric extracorporeal membrane oxygenation. JPEN J Parenter Enteral Nutr. 2018;42(1):205–211.
32. King W, Petrillo T, Pettignano R. Enteral nutrition and cardiovascular medications in the pediatric intensive
care unit. JPEN J Parenter Enteral Nutr. 2004;28:334–338.
33. Worthington P, Balint J, Bechtold M, et al. When is parenteral nutrition appropriate? JPEN J Parenter
Enteral Nutr. 2017;41(3):324–377. doi:10.1177/0148607117695251.
34. Villlet S, Chiolero RL, Bollmann MD, et al. Negative impact of hypocaloric feeding and energy balance on
clinical outcome in ICU patients. Clin Nutr. 2005;24(4):502–509.
35. Mehta N, Skillman H, Irving S, et al. Guidelines for the provision and assessment of nutrition support
therapy in the pediatric critically ill patient: Society of Critical Care Medicine and American Society for
Parenteral and Enteral Nutrition. JPEN J Parenter Enteral Nutr. 2017;18(7):675–715.
36. National Heart, Lung, and Blood Institute Acute Respiratory Distress Syndrome (ARDS) Clinical Trials
Network, Rice TW, Wheeler AP, et al. Initial trophic vs full enteral feeding in patients with acute lung
injury: the EDEN randomized trial. JAMA. 2012;307(8):795–803.
37. Arabi YM, Aldawood AS, Haddad SH, et al. Permissive underfeeding or standard enteral feeding in
critically ill adults. N Engl J Med. 2015;372(25):2398–2408.
38. Rice TW, Mogan S, Hays MA, Bernard GR, Jensen GL, Wheeler AP. Randomized trial of initial trophic
versus full-energy enteral nutrition in mechanically ventilated patients with acute respiratory failure. Crit
Care Med. 2011;39(5):967–974.
39. Charles EJ, Petroze RT, Metzger R, et al. Hypocaloric compared with eucaloric nutritional support and its
effect on infection rates in a surgical intensive care unit: a randomized controlled trial. Am J Clin Nutr.
2014;100(5):1337–1343.
40. Marik PE. Is early starvation beneficial for the critically ill patient? Curr Opin Clin Nutr Metab Care.
2016;19(2):155–160.
41. Patel JJ, Martindale RG, McClave SA. Controversies surrounding critical care nutrition: an appraisal of
permissive underfeeding, protein, and outcomes. JPEN J Parenter Enteral Nutr. 2018;42:508–515.
42. Krishnan JA, Parce PB, Martinez A, Diette GB, Brower RG. Caloric intake in medical ICU patients:
consistency of care with guidelines and relationship to clinical outcomes. Chest. 2003;124(1):297–305.
43. Ash J, Gervasio JM, Zaloga GP. Does the quantity of enteral nutrition affect outcomes in critically ill trauma
patients? JPEN J Parenter Enteral Nutr. 2005;29(suppl):S10.
44. Arabi YM, Haddad SH, Tamim HM, et al. Near-target caloric intake in critically ill medical-surgical patients
is associated with adverse outcomes. JPEN J Parenter Enteral Nutr. 2010;34(3):280–288.
45. Crosara IC, Melot C, Preiser JC. A J-shaped relationship between caloric intake and survival in critically ill
patients. Ann Intensive Care. 2015;5(1):37.
46. Arabi YM, Aldawood AS, Haddad SH, et al. Permissive underfeeding or standard enteral feeding in
critically ill adults. N Engl J Med. 2015;372(25):2398–2408.
47. Braunschweig CA, Sheean PM, Peterson SJ, et al. Intensive nutrition in acute lung injury: a clinical trial
(INTACT). JPEN J Parenter Enteral Nutr. 2015;39(1):13–20.
48. Heyland DK, Cahill N, Day AG. Optimal amount of calories for critically ill patients: depends on how you
slice the cake! Crit Care Med. 2011;39(12):2619–2626.
49. Ibrahim EH, Mehringer L, Prentice D, et al. Early versus late enteral feeding of mechanically ventilated
patients: results of a clinical trial. JPEN J Parenter Enteral Nutr. 2002;26(3):174–181.
50. Casaer MP, Wilmer A, Hermans G, Wouters PJ, Mesotten D, Van den Berghe G. Role of disease and
macronutrient dose in the randomized controlled EPaNIC trial: a post hoc analysis. Am J Respir Crit Care
Med. 2013;187(3):247–255.
51. Mehta N, Bechard L, Cahill N, et al. Nutritional practices and their relationship to clinical outcomes in
critically ill children—an international multicenter cohort study. Crit Care Med. 2012;40(7):2204–2211.
52. Joffe A, Anton N, Lequier L, et al. Nutritional support for critically ill children. Cochrane Database Syst
Rev. 2016;(5): CD005144.
53. Wong J, Ong, C, Han W, et al. Protocol-driven enteral nutrition in critically ill children: a systematic review.
JPEN J Par enter Enteral Nutr. 2014;38(1):29–39.
54. Martinez E, Bechard L, Mehta N. Nutrition algorithms and bedside nutrient delivery practices in pediatric
intensive care units: an international multicenter cohort study. Nutr Clin Pract. 2014; 29(3):360–367.
55. Braunschweig CL, Levy P, Sheean PM, et al. Enteral compared with parenteral nutrition: a meta-analysis.
Am J Clin Nutr. 2001; 74:534–542.
56. Peter JV, Moran JL, Phillips-Hughes J. A meta-analysis of treatment outcomes of early enteral versus early
parenteral nutrition in hospitalized patients. Crit Care Med. 2005;33:213–220.
57. Windsor AC, Kanwar S, Li AG, et al. Compared with parenteral nutrition, enteral feeding attenuates the
acute phase response and improves disease severity in acute pancreatitis. Gut. 1998;42:431–435.
58. Harvey SE, Parrott F, Harrison DA, et al. Trial of the route of early nutritional support in critically ill adults.
N Engl J Med. 2014;371(18):1673–1684.
59. Alpers DH, Stenson WF, Bier DM, eds. Manual of Nutritional Therapeutics. 3rd ed. Boston, MA: Little
Brown and Company; 1995:281–320.
60. Keating JP, Schears GJ, Dodge PR. Oral water intoxication in infants: an American epidemic. Am J Dis
Child. 1991;145(9):985–990. doi:10.1001/archpedi.1991.0216009 0037018.
61. Seron-Arbeloa C, Zamora-Elson M, Labarta-Monzon L, Mallor-Bonet T. Enteral nutrition in critical care. J
Clin Med Res. 2013;5(1):1–11.
62. Read J, Guenter P. ASPEN Enteral Nutrition by the Numbers: EN Data Across the Healthcare Continuum.
Silver Spring, MD: American Society for Parenteral and Enteral Nutrition; 2017.
63. Rice TW, Wheeler AP, Thompson BT, et al. Initial trophic vs full enteral feeding in patients with acute lung
injury: the EDEN randomized trial. JAMA. 2012;307(8):795–803.
64. Compher C, Chittams J, Sammarco T, Nicolo M, Hey-land D. Greater protein and energy intake may be
associated with improved mortality in higher risk critically ill patients: a multicenter, multinational
observational study. Crit Care Med. 2017;45(2):156–163.
65. Yeh DD, Cropano C, Quraishi SA, et al. Implementation of an aggressive enteral nutrition protocol and the
effect on clinical outcomes. Nutr Clin Pract. 2017;32(2):175–181.
66. Wijs PJ, Stapel SN, de Groot SD, et al. Optimal protein and energy nutrition decreases mortality in
mechanically ventilated, critically ill patients: a prospective observational cohort study. JPEN J Parenter
Enteral Nutr. 2012;36(1):60–68.
67. Nicolo M, Heyland DK, Chittams J, Sammarco T, Compher C. Clinical outcomes related to protein delivery
in a critically ill population: a multicenter, multinational observation study. JPEN J Parenter Enteral Nutr.
2016;40(1):45–51.
68. Zusman O, Theilla M, Cohen J, Kagan I, Bendavid I, Singer P. Resting energy expenditure, calorie and
protein consumption in critically ill patients: a retrospective cohort study. Crit Care. 2016;20(1):367.
69. Drake R, Ozols A, Nadeau WJ, Braid-Forbes MJ. Hospital inpatient admissions with dehydration and/or
malnutrition in Medicare beneficiaries receiving enteral nutrition: a cohort study. JPEN J Parenter Enteral
Nutr. 2018;42(4):730–738. doi:10.1177/0148607117713479.
70. A.S.P.E.N. Ethics Position Paper Task Force, Barrocas A, Geppert C, Durfee SM, et al. A.S.P.E.N. ethics
position paper. Nutr Clin Pract. 2010;25(6):672–679.
71. O’Sullivan Maillet J, Baird Schwartz D, Posthauer ME; Academy of Nutrition and Dietetics. Position of the
Academy of Nutrition and Dietetics: ethical and legal issues in feeding and hydration. J Acad Nutr Diet.
2013;113:828–833.
72. American Medical Association Code of Medical Ethics’ opinions on care at the end of life. Virtual Mentor.
2013;15(12): 1038–1040.
73. American Nurses Association. Position statement. Nutrition and hydration at the end of life. 2017.
https://www.nursingworld.org/~4af0ed/globalassets/docs/ana/ethics/ps_nutrition-and-hydration-at-the-end-
of-life_2017june7.pdf. Accessed December 14, 2018.
 CHAPTER 3

Enteral Access Devices

Introduction
The selection of an enteral access device (EAD) requires an evaluation of the patient’s disease state, upper
gastrointestinal (GI) anatomy (including past surgeries), GI motility and function, and the estimated length of
therapy. Determination of the appropriate type and location of the feeding tube is critical to the success of enteral
feeding. The clinician must weigh the overall risks vs benefits to the patient whenever a feeding tube is considered.
Advance directives and religious, cultural, and ethical issues must also be considerations, especially in end-stage or
terminal disease states. See Chapter 2 for additional information on ethical issues related to enteral nutrition (EN)
therapy.

Selection of Enteral Access Devices

Once the decision has been made to administer EN, the next decision is to select the type of EAD. Primary factors to
consider in this decision include how long EN therapy will likely be required, where the EN should be delivered (ie,
at what level—gastric or small bowel), patient preferences, risk factors associated with the type of EAD, and tube
characteristics. The specific type of feeding tube a patient receives may also depend on the expertise and availability
of nutrition support clinicians at the particular institution. See Figure 3-1 for a decision algorithm for tube selection
based on anticipated duration of need and patient preferences, goals, and aspiration risk.

Anticipated Duration of Enteral Nutrition Therapy

Clinicians should consider the estimated duration of enteral therapy when determining whether to place (a) an
orogastric (OG), nasogastric (NG), or nasoenteric (NE) tube or (b) an enterostomy (gastrostomy, gastrojejunostomy,
or jejunostomy) tube. EADs inserted via the nasal and oral routes (Figure 3-2) are usually placed for short-term use
(<4–6 weeks) in the hospitalized patient. They can also provide an opportunity to assess tolerance of enteral
feedings prior to placement of enterostomy tubes when longer-term access is required. Additionally, there are many
situations when NG and NE feeding tubes are appropriate for use in the outpatient setting, especially in the pediatric
population.1 (NE tubes include nasoduodenal and nasojejunal tubes.)
 OG and NG feeding tubes can be placed at the bedside (either blindly or using electromagnetic guidance),
endoscopically, or under fluoroscopic guidance.2 Some patients or caregivers are able to self-place OG or NG tubes.
However, the placement of an NE feeding tube should only be performed by clinicians who have been properly
trained to insert the device. Insertion techniques are described in greater detail later in this chapter.
Decisions regarding the selection of an EAD for long-term EN (>4–6 weeks) involve the anticipated length of
EN therapy, the patient’s disposition, and the special needs of the patient and caregivers. For long-term EN,
enterostomy tubes are placed into the stomach or small bowel using a variety of techniques (ie, endoscopic,
fluoroscopic, laparoscopic, and open surgical laparotomy routes). Placing a long-term EAD with local anesthesia of
the abdominal wall with or without intravenous (IV) sedation by fluoroscopic and endoscopic routes is often a better
option than placement under general anesthesia, especially in patients with extensive comorbidities. See the section
on insertion of long-term EADs later in this chapter for additional information.
To clarify the terminology, enterostomy tubes placed via endoscopy are called percutaneous endoscopic
gastrostomy (PEG) or percutaneous endoscopic jejunostomy (PEJ) tubes; when enterostomy tubes are placed
radiologically or surgically, they are simply called gastrostomy tubes (which may be further classified as balloon or
nonballoon gastrostomy tubes), gastrojejunostomy tubes, or jejunostomy tubes. When a gastrostomy tube is placed at
the bedside, it should not be referred to as a PEG tube.
Gastrostomy tubes are generally the preferred EAD for medium-term and long-term EN therapy, unless the use
of gastrostomy tubes is medically contraindicated.3 Two studies of adult patients with persistent dysphagia due to
neurologic diseases randomly assigned patients to be fed via an NG tube or a PEG tube.4,5 These studies found that
the patients fed with a PEG tube had greater weight gain and fewer missed feedings, whereas the patients fed by NG
received significantly less formula because of tube difficulties. In 1 of the studies, patients with NG tubes were
switched to a PEG tube if they experienced difficulties (usually displacement) with the NG tube; at the end of 4
weeks, only 1 of 19 patients had an NG tube in place.5
When long-term enteral access is needed, the condition of the external abdominal wall, the ability to correct
coagulopathies, and the patient’s tolerance to sedation and general anesthesia must be assessed. Other factors to
evaluate are the presence of open wounds or fistulas on the exterior abdominal wall, the presence of ostomies or
future requirements for ostomies, the patient’s need for other percutaneous or intra-abdominal infusion devices and
peritoneal dialysis catheters, the patient’s history of previous abdominal surgeries, and the condition of the upper GI
anatomy.

Level of Delivery
EN can be delivered either into the stomach or into the small bowel. Gastric access relies on a functional stomach
free of delayed gastric emptying, aspiration from gastric contents, obstruction, or fistulas. In patients who have had
previous gastric bypass surgery, the EAD can be placed into the gastric remnant, which is typically accessed through
laparoscopic surgery.6,7 Small bowel placement and feedings are more appropriate than gastric for patients with
gastric outlet obstruction, gastroparesis, reflux with aspiration of gastric contents, or superior mesenteric artery
syndrome, and when patients have failed gastric feeds (including patients with pancreatitis).2,8 Gastrojejunal access
with a single combined gastrojejunostomy tube or with separate gastrostomy and jejunostomy tubes allows for
simultaneous gastric decompression and small bowel feedings.9,10
In most cases, including in some patients with previous gastric surgery, gastric access is chosen first. The largest
multicenter randomized controlled trial (RCT) comparing gastric vs small bowel feeding in critically ill patients
found no difference in the most important outcomes, including length of stay, mortality, nutrient delivery, and
incidence of pneumonia. Two meta-analyses have found that gastric feedings were initiated sooner than small bowel
feedings because gastric feedings avoided the delay from difficulties in obtaining postpyloric placement.11,12 The
most recent guidelines from the Society of Critical Care Medicine (SCCM) and American Society for Parenteral and
Enteral Nutrition (ASPEN) on nutrition support in critically ill adults aggregated data from relevant RCTs and found
that small bowel feeding decreases the risk of pneumonia; however, there are no differences in length of stay or
mortality between small bowel and gastric feeding.13 The ASPEN/SCCM guidelines recommended that if timely
obtainment of small bowel enteral access is not feasible, early EN via the gastric route may provide more benefit
than delaying feeding initiation while awaiting small bowel access.13
Existing data are insufficient to make universal recommendations regarding the optimal site to deliver EN to
critically ill children. On the basis of observational studies, SCCM and ASPEN suggest that the gastric route is the
preferred site for EN in critically ill pediatric patients.14 The postpyloric or small intestinal site for EN may be used
for pediatric patients unable to tolerate gastric feeding or for those at high risk for aspiration.14

Device-Related Risk Assessment

When selecting an EAD, the risk factors associated with the type of device must be considered. For example, a
concern with NG feedings in critically ill patients has been the risk of reflux associated with bronchopulmonary
aspiration and pneumonia. Multiple studies and meta-analyses have attempted to address this issue.11,12,15
Complications that may occur with gastrojejunostomy tubes include a gastric lumen that is too small to decompress
adequately; a tendency to clog, leading to frequent replacements; and the jejunal extension tube migrating back into
the stomach. In a 2016 case report of jejunal perforation in 3 low–birth weight infants due to gastrojejunostomy tube
placement, the authors recommended caution when infants with a clinical indication for gastrojejunostomy tube
weigh <10 kg.16 Reported complications related to jejunostomies in pediatric patients have included dislodgement,
bowel obstruction, tube leakage, and wound dehiscence in one-third of the patients studied, with most complications
occurring within 4 weeks of surgery.17 Complications related to EADs are discussed in greater detail later in this
chapter.

Tube Characteristics
Physical Characteristics
Patient comfort, tube performance, and available commercial options are important considerations when choosing a
feeding tube. Most commercially manufactured feeding tubes are made of polyurethane or silicone, each with its
specific advantages and disadvantages (Table 3-1).18

TABLE 3-1. Comparison of Polyurethane and Silicone Tube Characteristics

Polyurethane Silicone
Comfort Lower Higher
Stiffness Higher Lower
Wall width Thinner Thicker
 Fungal degradation More resistant Less resistant
Percutaneous abdominal feeding
Common use Nasoenteric feeding tubes
tubes
Source: Reprinted with permission from reference 18: Fang JC, Kinikini M. Enteral access devices. In: Mueller CM, ed. The ASPEN Adult
Nutrition Support Core Curriculum. 3rd ed. Silver Spring, MD: American Society for Parenteral and Enteral Nutrition; 2017:251-264.

Most short-term feeding tubes are constructed of polyurethane, which can provide a relatively larger inner tube
diameter for a given outer diameter size, thereby decreasing the risk of clogging. Most percutaneous tubes are
constructed from silicone because of its inherent material compliance and comfort.
Rubber-and latex-based tubes (eg, Foley-type catheters and red rubber tubes) are not indicated for feeding. These
are inferior tubes because (a) they degrade rapidly; (b) they lack internal (red rubber tubes) or external (red rubber
tubes and Foley-type catheters) retention devices; and (c) their use puts the patient at risk for enteral misconnections
with non-enteral devices. Tube connections and misconnections are discussed in greater detail later in this chapter.

Tube Configurations
As shown in Table 3-2, NE and enterostomy tubes are measured by their external diameter in French size (1 Fr =
0.33 mm).18,19 However, flow through the tube and a tube’s susceptibility to clogging depend on the inner diameter,
which may vary depending on the specific material used to construct the tube. In general, a polyurethane tube will
have a larger internal diameter than a silicone tube of the same outer diameter.

TABLE 3-2. Nasoenteric and Enterostomy Tube Types, Sizes, and Lengths

Tube Type Size, Fr Length, cm

Nasogastric (for adults) 8-16 38-91
Nasogastric (for pediatrics) 3.5-16 15-170
Nasoenteric (for adults) 8-12 91-240
Nasoenteric (for pediatrics) 3.5-16 15-170
Gastrostomy 12-30 n/a
Gastrojejunostomy 6-14 n/a
Jejunal extension through existing gastrostomy 8-12 15-95
Dual-lumen (gastric and jejunal) 16-30 n/a
Single lumen (jejunal only) 12-24 15-58
Low-profile gastrostomy (replacement) 12-24 0.8-6.0
Low-profile gastrojejunostomy 14-22 15-45
1 Fr = 0.33 mm; n/a, not applicable.
Source: Adapted with permission from reference 18: Fang JC, Kinikini M. Enteral access devices. In: Mueller CM, ed. The ASPEN Adult
Nutrition Support Core Curriculum. 3rd ed. Silver Spring, MD: American Society for Parenteral and Enteral Nutrition; 2017:251-264. Pediatric
data are from reference 19.

NE feeding tubes come in a wide array of diameters and lengths, with a variety of options such as stylets,
feeding and medication ports, and distal weighted and unweighted tips. A stylet or guidewire is included with most
NE feeding tubes to provide tube structure and/or guidance while inserting these relatively floppy tubes. Stylets and
guide-wires are designed to be shorter than the length of the tube and have a flexible distal tip to avoid perforation of
the GI mucosa/wall when placing the tube. A water-activated lubricant coats the tube’s internal lumen to allow for
easier removal of the stylet or guidewire after the tube is in place. Commercially available NE feeding tubes have a
single lumen with either 1 port for feeding or 2 ports in a Y configuration, 1 for feeding and 1 for medication
administration and/or irrigation. These ports can accommodate either a feeding set or a syringe or both. Dual ports
can allow for concomitant feeding and medication administration and/or irrigation. However, to minimize the risk of
tube clogging, medications should be administered separately through the tube only after enteral feedings are held
and the feeding tube is flushed with water. (See Chapter 10 for further information on administration of medication
via the feeding tube.)
Weighted tube tips were once thought to facilitate transpyloric passage. However, critical analysis of the
literature has not demonstrated a clear advantage of either weighted or unweighted tips.20 In fact, a study showed
that weighted tips were less likely to migrate into the small bowel, and there have been reports that the weighted tip
can separate from the tube and become a foreign body.20,21
Feeding tube tips come in a wide variety of shapes and sizes, and the number, size, and location of distal end
openings can also vary. There are no data to demonstrate that any particular design is preferable. Therefore, the
choice of feeding tube tip is determined by the personal preference of the individual clinician, the patient’s
preference, and available stock from the institution.
The internal retention bolster of the percutaneous enter-ostomy tube is constructed of either solid material
(silicone or polyurethane) or silicone balloons (Figure 3-3).18 Solid internal bolsters are commonly used in initial
percutaneous enterostomy tube placement. Balloon-type internal bolsters (or encapsulated internal bolsters) are
commonly inserted when a tube is fluoroscopically or surgically placed or when a tube is replaced. The balloons
generally have a lifespan of only 3–6 months, whereas solid internal bolsters typically last 1 year or longer.22
Enterostomy feeding tubes typically have 2 ports: 1 for feeding and 1 for medication and/or irrigation. If the internal
bolster is of the balloon type, an additional third port is present for balloon inflation or deflation.

Traditionally, 2-piece gastrojejunostomy feeding tubes are placed by passing a smaller-bore jejunal extension
tube through an existing gastrostomy tube through the pylorus, beyond the duodenum, and into the jejunum. There
are also single-piece gastrojejunostomy tubes manufactured with designated gastric and jejunal lumens to allow for
both jejunal feeding and gastric decompression.
Direct jejunostomy tubes are placed directly into the jejunum without passage through the stomach. There are no
enterostomy tubes commercially available for this specific use; clinicians usually use smaller-bore percutaneous
gastrostomy tubes but place them directly into the jejunum.
Low-profile tubes are skin-level devices. They can be placed as the initial feeding tube, but they are typically
used as replacement devices for gastrostomies and gastrojejunostomies. The length of the existing stoma tract is
measured before the most appropriately sized low-profile device is chosen and placed. Commercially available low-
profile devices have either balloon or solid internal bolsters (Figure 3-4).18 Balloon-type internal bolsters are used
more commonly because they can be easily replaced by simply deflating the balloon and sliding the tube, without
trauma, in or out of the existing stoma tract.
 In pediatric patients, it is common practice to use a low-profile balloon gastrostomy tube as the initial
gastrostomy tube. Caregivers are taught to replace the low-profile balloon gastrostomy tube at home.
Solid internal bolster replacement tubes require an obturator to deform the internal bolster to allow it to be
inserted through the stoma tract. There is also a unique solid internal bolster tube that is constrained in a capsule
such that it can be placed like a balloon-type tube, with minimal trauma; once placed, the capsule is split and the
bolster deployed.

Insertion of Short-Term Enteral Access Devices

As noted previously, OG, NG, and NE feeding tubes are inserted when short-term access (<4–6 weeks) is indicated.
Short-term EADs can be passed transorally or transnasally, although the nasal approach is better tolerated in the
conscious patient. During the first 4 to 6 months of life, the infant is an obligate nose breather; therefore, an OG
feeding tube may be the best option in these patients. However, in a study with a crossover design, 32 infants
showed no significant difference in apnea or bradycardia using either the OG or NG tube.23
NG or NE feeding tube placement is contraindicated if the patient has an obstructing head, neck, and esophageal
pathology or injury that would make insertion unsafe. Once placed, NG or NE feeding tubes should not be used until
proper position of the EAD is confirmed.24,25 It is imperative that clinicians use only evidence-based methods to
verify OG, NG, or NE tube placement, such as measuring the pH of aspirate, evaluating a radiograph, or using
specific technology that is proven to accurately determine placement.
NG tubes are the easiest feeding tubes to insert. Placement may be performed by a clinician with the appropriate
training, competencies, and privileges to do so. When possible, larger, stiffer tubes used for gastric decompression
should be converted to a smaller-bore feeding tube (6–12 Fr) for patient comfort and to decrease the risk of
associated complications.
The most reliable method for measuring the length of NG tube necessary for gastric placement is known as
NEMU (which is shorthand for “direct distance from nose to earlobe to midumbilicus”), although many clinicians
use a NEX (nose-to-earlobe-to-xiphoid process) measurement in adult patients.26 For either an NEMU or NEX
measurement, the patient is positioned as upright as possible and an NG tube is passed through a patent naris. If the
patient is alert, he or she can help guide the tube appropriately through the esophagus by dry-swallowing or taking
sips of water through a straw while the tube is being inserted and advanced.
Once the tube is in position at the predetermined length, attempted aspiration of gastric contents and auscultation
of insufflated air over the stomach using a 30-to 60-mL syringe may be attempted. The volume, color, and pH level
of the aspirate can be assessed. (To measure pH, place a drop of aspirate on a colorimetric pH strip.) Fasting gastric
fluid typically is clear and colorless (pH <3) or grassy green (pH <5) and is of larger volume. In contrast, gastric
fluid from a tube that has perforated into the pleural space is small in volume and has a pale-yellow serous
appearance with pH of >7. Clinicians should not assess the position of a placed tube by the visual appearance of
aspirated gastric contents; auscultation of insufflated air; or the absence of coughing, choking, or respiratory
distress.27–29
Correct initial position of an NG tube should be confirmed by first checking the pH of gastric aspirate, with the
desired result being ≤5.5 for all patients from neonates to older adults.30–33 Although many institutions use
abdominal radiograph as their gold standard for assessing the initial placement of a feeding tube, the National Health
Service (NHS) in the United Kingdom has reported multiple problems with inaccurate interpretation of
radiographs.32,34 Furthermore, a study conducted in a neonatal intensive care unit in Korea compared the
interpretation of radio-graphs for OG tube placement by pediatric residents with interpretation by staff with
expertise in interpreting radio-graphs and found that the residents correctly marked the position of the OG tube tip
only 85.7% of the time.35
Both the American Association of Critical-Care Nurses and NHS recommend that the pH of aspirate be
evaluated to assess placement of NG feeding tubes inserted at the bedside.31,34 The NHS does not recommend
radiographic confirmation of an NG tube as the first-line placement verification method.31 Continuous feedings can
skew the pH measurement, and it is recommended the feeds be held for 10–20 minutes (longer for patients receiving
high administration rates).30 The use of an acid-suppressing medication does not necessarily mean the pH will be
≥5.5 and is not a contraindication for checking pH.36
An abdominal radiograph should be obtained to confirm tube position in certain situations, such as cases with a
pH measurement of ≥6 or when aspirate cannot be collected from the NG tube even after the patient is repositioned.
Radiographic confirmation may also be warranted if the patient has a high-risk condition, such as critical illness
with intubation; decreased or absent gag or cough reflex; neurologic impairment with decreased level of
consciousness; sedation and/or chemical paralysis; or clinical status that warrants use of an X-ray even though pH is
less than 5 or 5.5. ASPEN’s New Opportunities for Verification of Enteral Tube Location (NOVEL) Project has
published additional information and an algorithm to help clinicians place NG tubes in pediatric patients.30 To learn
more about the NOVEL Project or download the algorithm, visit the NOVEL web page
(www.nutritioncare.org/NOVEL).
When a radiograph is necessary, it should be done in such a way that the tube can be traced from the pharynx to
the stomach with the tip within the frame of the radio-graph.36 The report needs to specifically state that the tube
placement is appropriate to use for feeding or medication administration.36 Use of abdominal radiograph to assess
NG tube placement is not common in pediatric care settings, but many adult centers continue to consider radio-
graphic assessment to be the “gold standard” method.3,19
Nursing documentation of the NG tube insertion procedure must include the centimeter mark that is visible at the
naris. Once the NG tube is in place, nurses should recheck the centimeter mark to determine whether it has changed,
which would indicate tube migration. Currently, there is no evidence to guide practice regarding how often to
routinely reconfirm placement. If there are indicators that the tube has migrated while in place, such as vomiting or
deep coughing, the pH of an aspirate sample should be checked and the patient’s respiratory status should be
thoroughly assessed.
Carbon dioxide (CO2) monitoring can help clinicians determine when an NG or NE tube has taken an inadvertent
course into the trachea during the insertion process.37–40 Use of capnography or a colorimetric CO2 detector
(Medtronic, Minneapolis, MN) assumes that a tube misplaced into the respiratory tract will reveal (a) a characteristic
exhaled CO2 waveform when attached to CO2 monitoring equipment or (b) a color change when using the
calorimetric CO2 detector. However, CO2 detection cannot determine whether the depth of insertion into the GI tract
is proper; therefore, radiography and/or pH testing should be used to verify that the tip position is appropriate before
enteral feeding is initiated or whenever dislodgement is suspected. Tube migration is further discussed in the Tube
Maintenance Considerations section later in this chapter.
NE feeding tubes are placed anywhere distal to the pylorus, with NJ tubes positioned distal to the ligament of
Treitz. NE tubes, which are more difficult to place than NG tubes, can be placed blindly at the bedside,
endoscopically, or fluoroscopically.
Bedside placement usually requires specialized training and should be done by an experienced clinician. A
number of methods have been described for bedside blind placements,41 including a method described by Zaloga.42
In this technique, the patient lies on his or her right side, and a feeding tube with bent tip is passed through a naris
into the stomach. The tip of the tube is bent by removing the stylet and bending it 30° about 2 cm from the distal end
and reinserting it into the feeding tube. A 60-mL syringe is used to pump air into the stomach. The bend allows for
the tip of the tube to cover a greater surface area during rotation and helps the tip to “hook” the pyloric outlet during
tube advancement. After air insufflation, the feeding tube is slowly rotated and advanced in short (4-to 5-cm) bursts
until it is inserted the appropriate length (ie, compatible with a small bowel location). The tube is allowed to slowly
advance and is not forced forward. Prokinetic agents (erythromycin or metoclopramide) may be used as adjuvants to
bedside placement techniques and may increase success rates.43 A meta-analysis recently showed the most effective
maneuvers to assist with postpyloric tube placement are air insufflation and the use of prokinetic agents in adult
patients.44 The authors of that review did not recommend use of prokinetic agents in children when placing a
postpyloric feeding tube.44 Finally, compared with feeding tubes with weighted tips, feeding tubes with unweighted
tips have been shown to increase the likelihood of transpyloric passage.20
 NE feeding tube placement is reliably achieved with endoscopic or fluoroscopic techniques. However, these
methods are costlier and require advanced training, and endoscopy is more invasive than the bedside method.
Radiographic confirmation of placement is not required for these methods.
When inserting NE tubes in pediatric patients, it is most important to swaddle the child and slowly advance the
tube 5–10 cm past the measured number obtained using the NEMU method at the umbilicus. Older children will
require advancement of the tube up to 20 cm past that number.
Infants with increased work of breathing can pose a challenge for NG or NE tube placement. Blowing in the
patient’s face to elicit a startle reflex will cause the infant to swallow, which facilitates proper tube passage. It is
typical to slowly instill a small volume of sterile water (3–10 mL) to help “float” the tube postpylorically and to
check for a “snap back” of an empty syringe when attempting to aspirate. When water is slowly instilled during tube
advancement, kinking of the tube is readily identified and remedied; a kinked tube will result in a false-positive
“snap back.” NG or NE tubes are secured to the cheek with a skin-protectant base and transparent tape. An
abdominal radiograph is required to confirm placement for any patient who has a blindly placed NE tube. It is
uncommon in pediatrics to change the position of the child during tube placement unless placement is difficult.
Prokinetic agents are not often used when placing feeding tubes in pediatric patients.
Efforts are being made to improve technological aids for tube insertion. An electromagnetic placement device
system has been developed to assist with NG and NE tube placement. An electromagnetic signal is sent by a
transmitter at the distal end of the feeding tube stylet to a receiver unit, which is positioned on the patient’s chest at
the xiphoid process (corresponding to the base of the diaphragm). The triangulated signal from the tip of the feeding
tube stylet is tracked on a portable monitor as the tube is advanced through the esophagus and into the stomach and
small intestine.45 The most recent version of this system provides both anterior and lateral positioning screens,
allowing 2-dimensional tracking of the tube tip. This technology has reported success rates of 70%–90% when
physicians or nurses pass the feeding tube into the small intestine.46–48 Before using this technology, clinicians
should be trained with a combination of didactic and clinical observation, and periodic competency assessment after
initial training is recommended. The electromagnetic placement device system has been approved by the US Food
and Drug Administration (FDA) for confirmation of the final tip position by qualified operators, without the need
for radiographic confirmation. However, tracheobronchial misplacements have been reported with the device, and
radio-graphic confirmation is suggested if there is any concern for incorrect tube position.49
Another technological innovation is a single-use, small-bore NG feeding tube with a miniature camera
embedded in the distal end to aid in tube placement. This system allows clinicians to visually identify anatomical
markers during the placement procedure. Preliminary studies have demonstrated correct identification of gastric
mucosa in ≥90% of patients.50,51
When placing NG or NE tubes, clinicians must be aware that malpositioning may occur without any apparent
symptoms, particularly in patients with decreased level of consciousness.24,52,53 Also, the auscultatory method or
bubbling of air from the proximal end of the tube placed in water cannot reliably differentiate placement in the
esophagus, stomach, or small bowel from tracheobronchial placement and therefore should not be used to assess
tube tip location.30,31,36,52 Pulmonary aspiration, pneumonia, and pneumothorax have been reported with all tube
insertion methods, including use of the electromagnetic signal device technology.54
The overall success rate for NG or NE tube placement is high (90%–100%), but the success rate for placement in
the distal duodenum is lower (84%–90%), and the success rate is just 25%–50% for placement past the ligament of
Treitz, no matter which insertion method is employed.55 Table 3-3 summarizes the ASPEN practice
recommendations for short-term feeding tube placement.3

TABLE 3-3. Practice Recommendations for Short-Term Feeding Tube Placement

For all blindly placed tubes, obtain evidence-based confirmation of proper tube positioning in the GI
1.
tract prior to initial use.
Do not rely on the auscultation method to differentiate between gastric and respiratory placement or
2.
to differentiate between gastric and small bowel placement.
Mark the exit site of a feeding tube at the time of the initial radiograph; observe for a change in the
external tube length during feedings. If a significant increase in the external length is observed, use
3.
 other bedside tests to help determine whether the tube has become dislocated. If in doubt, obtain a
radiograph to determine tube location.
In pediatric and neonatal patients, the first-line method to verify NG tube placement is pH
measurement of aspirate, with a cutoff level of ≤5.5. When pH is greater than this number, pH is
unattainable, or a radiograph is clinically indicated, radiographic assessment is the best
4.
practice. The use of radiography in children should be judicious given the cumulative effect of
radiation exposure. It is also noted that several cases have been identified where the X-ray has
been misinterpreted by a physician who is not trained in radiology.
Consider pH measurement of aspirate as the first-line method for NG tube placement in adult
patients. A radiograph would be the first- or second-line method to confirm that any blindly placed
5.
tube (small-bore or large-bore) is properly positioned in the GI tract prior to the tube's initial use for
administering feedings and medications in adult patients.
When attempting to insert a feeding tube into the stomach of an adult patient, it may be helpful to
6. use capnography to detect inadvertent entry of the tube into the trachea. Be aware that radiographic
confirmation is needed before the tube is used for feedings.
When attempting to insert a feeding tube into the small bowel, observe for a change in the pH and
7. appearance of aspirates as the tube progresses from the stomach into the small bowel; use the
findings to determine when a radiograph should be done to confirm small bowel placement.
Abbreviations: GI, gastrointestinal; NG, nasogastric.
Source: Adapted with permission from reference 3: Boullata JI, Carrera AL, Harvey L, et al. ASPEN safe practices for enteral nutrition
therapy. JPEN J Parenter Enteral Nutr. 2016;41(1):15-103. doi:10.1177/0148607116673053.

Insertion of Long-Term Enteral Access Devices

As discussed earlier in this chapter, enterostomy tubes are placed when long-term enteral access (>4–6 weeks) is
anticipated. These tubes may be placed by endoscopic, radiologic, or surgical (laparoscopic or open) methods. All of
these methods have similar success rates; however, endoscopic or fluoroscopic techniques have less morbidity and
cost less than surgical methods; therefore, endoscopic and fluoroscopic methods are more commonly employed.56–60
The choice of procedure depends on local resources and expertise, anatomical considerations (eg, contraindications
to endoscopic or radiologic placement), and whether the patient is undergoing surgery for another reason where
operative gastrostomy can be performed in combination with the primary surgical procedure. See Table 3-4 for
practice recommendations for long-term EAD placement.61

TABLE 3-4. Practice Recommendations for Long-Term Enteral Access Device Placement

Long-term feeding devices should be considered in adults, children, and infants, including neonates
1.
after term age, when the need for enteral feeding exceeds at least 4-6 weeks.
In premature infants with the ability to eat by mouth at the normal time for development of oral
2. feeding skills, a longterm feeding device should not be considered before the usual age of
development of independent oral feeding.
Evaluation by a multidisciplinary team is indicated prior to insertion of a long-term feeding device to
establish whether (a) benefit outweighs the risk of access placement; (b) insertion of a feeding tube
3.
near the end of life is warranted; or (c) insertion of a feeding tube is indicated in the situation where
patients are close to achieving oral feeding.
Abdominal imaging should be performed prior to longterm feeding device placement if a possible
4.
anatomical difficulty exists.
Gastrostomy tube placement does not mandate fundoplication. The possible exception is children
5.
with neurologic impairment who also have abnormal pH probe findings.

Direct placement of a jejunostomy tube is indicated in patients requiring long-term small bowel
 6. feeding. For patients who require gastric venting or decompression, consideration of a
gastrojejunostomy tube is appropriate. In the pediatric population, gastrojejunostomy tubes are not
typically the first enterostomy tube placed.
Low-profile devices require periodic resizing to increase the length of the stem of the device.
7. Resizing should occur with any significant growth or weight change and, in the pediatric population,
twice a year for patients under the age of 5 years and annually for patients after the age of 5 years.
Document tube type, tip location, and external markings in the medical record and in follow-up
8.
examinations.
Avoid placement of catheters or tubes not intended for use as enteral feeding devices, such as
urinary or GI drainage tubes, which usually do not have an external anchoring device. Use of such
9. tubes leads to enteral misconnection as well as tube migration, which can potentially cause
obstruction of the gastric pylorus or small bowel and aspiration. In the rare instances that a non-
enteral feeding tube is placed, use an anchoring device to keep the tube from migrating.
Abbreviation: GI, gastrointestinal.
Source: Adapted with permission from reference 61: Bankhead R, Boullata J, Brantley S, et al. Enteral nutrition practice recommendations.
JPEN J Parenter Enteral Nutr. 2009;33(2):122-167.

Gastrostomy Tubes
Commercially available percutaneous gastrostomy tubes with balloon-type or solid distensible internal bolsters can
be placed initially or for replacement by endoscopic or radiologic methods. Solid internal bolsters are not susceptible
to balloon deflation and may be less susceptible to inadvertent dislodgement than balloon internal bolster
gastrostomy tubes.

Percutaneous Endoscopic Placement

PEG is the most commonly used technique for obtaining long-term gastric access. It is generally performed under
moderate IV sedation.62 Absolute contraindications for endoscopic placement of a gastrostomy tube include
obstruction of the GI tract proximal to the stomach and the inability to transilluminate the abdominal wall for
identification of a safe abdominal access site.63 Additional relative contraindications include ascites, coagulopathy,
gastric varices, morbid obesity, and neoplastic, infiltrative, or inflammatory disease of the gastric or abdominal
wall.64 If a patient is not already receiving a broad-spectrum antibiotic, a single dose of an appropriate antibiotic
administered prophylactically before tube placement has been shown to decrease peristomal infection rates.65–67 PEG
placement offers several advantages over other methods. For example, clinicians can perform it at the bedside; it
does not expose the patient to radiation; and clinicians can perform diagnostic and therapeutic endoscopic
procedures simultaneously.
Routine preprocedural testing of coagulation parameters and platelets is no longer recommended for patients
undergoing endoscopic tube placement; however, these tests should be considered if the patient is at risk for
abnormal coagulation due to anticoagulant medication, medical history of excessive bleeding, or recent antibiotic
use. American Society for Gastrointestinal Endoscopy guidelines consider placement of a percutaneous feeding tube
to be a high-bleeding-risk procedure.68 Thienopyridines (eg, clopidogrel) should be held, whenever possible, for 5 to
7 days before PEG placement. If holding the thienopyridine is not possible, some institutions will add epinephrine to
the lidocaine for local anesthesia (vasoconstriction), avoid vessels on the skin and mucosa, and make sure the
bolsters are relatively firm (not tight) for 3 to 4 days before loosening them.68,69 Aspirin regimens should be
continued in patients with high thromboembolic risk.68 Warfarin should be held 5 days before PEG placement, and
patients at high risk for clots may be bridged with short-acting heparin. The new, direct-acting oral anticoagulants
should be held for at least 48 hours before high-risk procedures and restarted up to 48 hours after the procedure,
depending on renal function.69
The most common method of PEG insertion is the “pull” technique first described by Ponsky.70 Air is insufflated
into the stomach, and the optimal site for placement is determined through simultaneous endoscopic
transillumination noted on the abdominal wall and finger indentation at the site visualized endoscopically. A
sounding needle is inserted initially to confirm a safe track. A small incision is then made at this site, and a larger-
bore (14- to 18-Fr) needle/trocar is inserted through the abdominal wall and into the stomach. A guidewire is passed
through the needle/trocar, snared endoscopically, and withdrawn through the mouth. A gastrostomy tube is affixed
to the guidewire and pulled through the esophagus into the stomach and out the abdominal wall. The gastrostomy
tube is held in place by a solid distensible internal bolster as well as an external bumper (see Figure 3-5).71

Percutaneous Radiologic Placement

Two common methods for placing percutaneous gastrostomy tubes fluoroscopically are the antegrade (transoral) and
the retrograde (transabdominal) techniques. With either method, identification of a safe window can be aided by
using oral barium administered the day before the procedure to opacify the colon; more commonly, an abdominal
computed tomography (CT) scan or ultra-sound examination can be performed and/or reviewed prior to the
procedure. If patients are not already receiving a broad-spectrum antibiotic, a single dose of an appropriate antibiotic
is administered prophylactically for fluoroscopic placement using the antegrade method; prophylactic antibiotic
administration is optional for the retrograde method.
Advantages of fluoroscopic gastrostomy placement include the following: Some patients will not need sedation;
placement can be done in patients with severe stenosis/trauma of the upper GI tract; and the risk of tumor seeding
from active upper aerodigestive tract cancers may potentially be decreased when the retrograde approach is used.72
Society of Interventional Radiology guidelines designate these procedures as category 2, implying a moderate risk
of bleeding. Those guidelines recommend the following:72

1. Correct international normalized ratio to ≤1.5.

2. Verify that platelet count is >50,000.
3. Withhold clopidogrel for 5 days before the procedure.
4. Do not withhold aspirin.
5. Withhold 1 dose of low-molecular-weight heparin before the procedure.
6. Measurement of partial thromboplastin time is recommended only for patients receiving unfractionated
heparin.

However, some institutions do not routinely check coagulation status when there is no reason to suspect
coagulopathy before tube placement.
In the retrograde method, an NG tube is placed to insufflate the stomach, a safe window is identified under
fluoroscopy, and 1–4 T-fasteners are used to perform a gastropexy to secure the stomach wall to the abdominal wall.
The stomach is then punctured, usually with an 18-gauge needle directed toward the pylorus, to facilitate future
conversion of the gastrostomy tube to a gastrojejunostomy tube if the latter type of tube is needed later. A guidewire
is advanced through the needle, and the tract is dilated sequentially until it is a large enough for the gastrostomy
tube. The gastrostomy tube is placed through the tract using a peel-away sheath, and contrast material is injected to
confirm correct tube placement.63
In the antegrade technique, 2 tubes are usually advanced into the stomach—an NG tube is used to inflate the
stomach with air, and an OG tube is used to insert and advance a snare. However, it is possible to use only 1 OG
catheter, which can be used to inflate the stomach and then introduce the snare. The stomach is punctured
percutaneously with a needle under fluoroscopic guidance, and a wire is introduced. The OG snare is then used to
grasp the wire and pull it out of the mouth, giving wire access from the mouth, down the esophagus, and out of the
gastric puncture. The percutaneous gastrostomy tube is introduced over this wire, and the tube is pulled out of the
anterior abdominal wall (similar to the endoscopic pull method), which allows for placement of a standard PEG-type
gastrostomy tube with a solid distensible internal bolster.73

Surgical Placement
Gastrostomy tube insertion using the laparoscopic or open method is performed in the operating room using general
anesthesia. Placement of these tubes may take place during other operative procedures, including tracheostomy, or
when endoscopic or fluoroscopic methods fail.
Laparoscopic techniques access the peritoneal cavity by way of small ports that enter through the abdominal
wall. A pneumoperitoneum is created by way of a port inserted through the umbilicus, and a camera is passed
through this site. A second port enters the left upper quadrant of the abdomen and is used to access the stomach. T-
fasteners are placed to approximate the stomach to the abdominal wall. A gastrostomy tube is then placed over a
guidewire into the stomach. A third port may be placed in the right upper quadrant so atraumatic graspers can be
inserted to hold the stomach in place.74
The Stamm technique is the most commonly used open surgery technique for placement of a gastrostomy
tube.75,76 It requires a small laparotomy in the upper midline of the abdomen. The gastrostomy tube is brought into
the stomach through a small incision in the upper abdominal wall. Another small incision is then made into the
stomach through which the feeding tube enters and around which a purse-string suture is placed to secure the
stomach around the gastrostomy tube. The stomach is then sutured to the anterior abdominal wall. This tube is held
in place with an inflated balloon.

Percutaneous Gastrojejunostomy Tubes

With a gastrojejunostomy tube, 1 lumen opens to the stomach and the distal opening is in the jejunum, so the patient
can benefit from gastric decompression while receiving enteral feeds into the small bowel (see Figure 3-6).77 A
gastrojejunostomy tube should be placed any time that enteral feeding into the small bowel with simultaneous
stomach decompression is required. It may be indicated in patients with gastric feeding intolerance, impaired gastric
motility, a previous gastric surgery, or pancreatitis, and in those undergoing pancreatic surgery.78,79

Percutaneous endoscopic gastrojejunostomy (PEGJ) may be performed initially or at any time after gastrostomy
tube placement. In this procedure, a guidewire is placed through the existing gastrostomy and then grasped
endoscopically and carried into the jejunum. The endoscope is then withdrawn, leaving the guidewire in place. The
jejunal extension tube is threaded over the guidewire and placed within the small bowel.64,80
 A more recently described PEGJ technique uses reclosable clips. The jejunostomy feeding tube with a suture on
its tip is inserted through the PEG or existing gastrostomy stoma into the stomach lumen. A clip is passed through
the working channel of an endoscope and used to grasp the suture and drag the tube into the jejunum as the endo-
scope is advanced. The suture is then clipped to the jejunal mucosa, securing the feeding tube to the small bowel.81
Another PEGJ technique uses an ultrathin endoscope (5–6 mm in diameter) or pediatric bronchoscope (3–4 mm)
passed through a large-diameter gastrostomy tube or mature gastrostomy tract into the small intestine. A guide-wire
is fed through the endoscope deep into the small bowel, and the endoscope is removed. The gastrojejunostomy tube
is then passed over the wire into position, and the wire is removed.82
Fluoroscopy may be used as an adjunct with any method of endoscopic placement. However, it is not absolutely
required.
Fluoroscopic techniques to provide gastrojejunal access are becoming much more common for both initial and
replacement gastrojejunostomy feeding tubes. Initial steps are similar to the previously described fluoroscopic
gastrostomy placement. For initial placement, the stomach is punctured in the direction of the pylorus to facilitate
placement of the gastrojejunostomy. A guiding catheter and/or wire is advanced through the gastrostomy to or
beyond the ligament of Treitz, and the jejunal extension tube is advanced over the wire into the jejunum.83,84
Fluoroscopic techniques can be used when the patient cannot undergo endoscopy. However, fluoroscopic
placement cannot be done at the bedside; it requires transport of the patient to the radiology suite.
Gastrojejunostomy tubes can be placed during laparotomy or by laparoscopic technique using any of the
previously described laparoscopic gastrostomy methods. Using manual and/or endoscopic methods, the jejunostomy
tube is positioned into the small bowel through the gastrostomy.

Percutaneous Direct Jejunostomy Tubes

Direct percutaneous jejunostomy using either endoscopic or fluoroscopic guidance is technically much more
difficult than percutaneous gastrostomy and therefore is not available in all institutions. Success rates range from
68% to 100% for endoscopic jejunostomy and from 87% to 100% for fluoroscopic jejunostomy.72 Endoscopic
jejunostomy tubes may be more stable than fluoroscopically placed tubes because the endoscopic tubes have solid,
mushroom-type internal bolsters and larger tube diameters (14- to 20-Fr tubes are used in endoscopic placement; 10-
to 14-Fr tubes are placed fluoroscopically). Because endoscopic and radiologic methods for jejunostomies are more
complex, surgical jejunostomies are usually more commonly performed, although this depends on local expertise
and availability.
Direct PEJ is a modification of the PEG technique. A colonoscope or enteroscope is advanced through the
stomach into the small bowel. Transillumination and finger palpation are performed over the jejunum instead of the
stomach. A sounding needle and/or trocar is passed through the anterior abdominal wall into the jejunum. An
insertion wire is advanced through the trocar and grasped. The procedure is then completed in the same manner as
the “pull-type” PEG.85 Higher rates of successful endoscopic placement have been reported when balloon enter-
oscopy and general anesthesia are used.86,87
Interventional radiologists have a variety of methods to place direct jejunostomy tubes. The initial step in all
methods is to identify a target bowel loop. Historically, this has been done by advancing an angiographic catheter
into the proximal jejunum and insufflating it with air and contrast or by placing an angioplasty balloon or snare loop
in the desired location to serve as a target.88,89 More recently introduced methods to identify the proximal jejunal
loop include (a) ultrasound guidance following injection of the saline solution and contrast agent, and (b) use of
cone fluoroscopy CT.90 Once the jejunal loop is identified by any method, it is accessed with a needle, and a T-
fastener device is used to secure the jejunal loop against the abdominal wall. A guidewire is then advanced through
the needle, the tract is dilated, and the jejunostomy tube is placed and injected with contrast to confirm the position.
The technique of laparoscopic jejunostomy is similar to laparoscopic gastrostomy. Ports are placed in the left
upper quadrant and lower abdominal midline. The jejunum is manipulated to affix it to the abdominal wall with T-
fasteners. A guidewire is then placed into the lumen of the jejunum, and a jejunostomy tube is advanced into the
small bowel through a peel-away sheath. An advantage with this approach is that a larger-diameter tube (18–20 Fr)
with a solid bolster can be placed.
An open jejunostomy is placed using the Witzel technique (Figure 3-7).77 In this procedure, a submucosal tunnel
is created in the small bowel through which the jejunostomy tube is threaded. This method helps prevents leakage of
small bowel contents onto the abdominal wall.77,91
 Placing a needle-catheter jejunostomy by laparotomy or laparoscopy is a less common procedure.77 In this
procedure, a needle is threaded into the small bowel and a guidewire is passed into the jejunum. A small
jejunostomy catheter (5–8 Fr) is passed over the guidewire into the jejunum. The small-bore size of needle-catheter
jejunostomies makes them prone to occlusion.

Low-Profile Devices
Low-profile (skin-level) devices are excellent options for the patient who is concerned about cosmetic appearance
and does not wish to have a feeding tube concealed or exposed through clothing. These devices may also be more
comfortable for the patient who is active, sleeps in the prone position, only needs intermittent therapy, or is at risk
for pulling out a standard-profile tube. Low-profile EADs are the preferred option for pediatric patients because
these devices are easier to secure and less likely to be inadvertently dislodged. Balloon low-profile devices allow
caregivers to manage and replace in the home setting. To attach a feeding connector to the skin-level device,
reasonable manual dexterity or caregiver assistance is needed.
In adult patients, skin-level devices are usually placed as an exchange or replacement tube for a preexisting
gastrostomy tube; however, they can also be placed at the time of initial tube placement.92 In pediatric patients, they
are typically placed as the initial EAD.93 The devices are held in place with an inflated internal balloon or a
distensible internal retention bolster that requires an obturator for placement. Low-profile, 1-piece
gastrojejunostomy tubes are also available for jejunal feeding with or without gastric decompression.

Tube Maintenance Considerations

Maintaining Proper Placement

Once the feeding tube tip is properly positioned, it is necessary to verify that the tube has remained in the desired
location (either the stomach or small bowel). Unfortunately, a nasally placed or transgastric small bowel tube may
migrate upward into the stomach, or a nasally placed gastric tube may migrate downward into the small bowel; the
worst-case scenario is when a tube tip displaces upward into the esophagus.94 Obviously, X-rays cannot be obtained
multiple times a day to confirm tube location; thus, clinicians may employ bedside methods for this purpose. These
methods include the following:95
 • Determining whether the external length of the tubing has changed since the time of the confirmatory
radiograph
• Detecting any change in the measurement marking on the tube at the naris
• Observing for negative pressure when attempting to withdraw fluid from the feeding tube
• Observing for unexpected changes in gastric residual volumes (GRVs)
• Measuring the pH of the feeding tube aspirates

In a prospective study, observing for changes in external tube length was helpful in identifying outward
migration of feeding tubes into the esophagus, as well as proximal migration from the small bowel into the
stomach.95 To allow for assessment of tube length, the measurement marking where a confirmed properly placed OG
or NG tube exits the mouth or nares should be recorded in documentation accessible to all clinicians. Negative
pressure is more likely to be felt during attempts to aspirate fluid from a small bowel tube than from a gastric tube.96
A sharp increase in GRV may indicate displacement of a small bowel tube into the stomach.97 Testing the pH of
feeding tube aspirates is most likely to be helpful prior to an intermittent or bolus feeding, when less of the tube
feeding formula is present (formula can alter the pH). For tubes placed using electromagnetic guidance, the stylet
with transmitter can be re inserted to check the distal location of the tip.
As noted previously, the auscultatory method cannot distinguish between gastric and small bowel placement,
and it cannot detect when the tube tip is in the esophagus. This method should not be used to evaluate tube
placement.53,98

Tube Securement and Connections

There is nothing inherent to the design of available nasally placed tubes to prevent migration inward or outward.
Therefore, an additional mechanism is needed to secure the tube to the nose or face. Nasal tubes are typically
secured near the nares with tape, adhesive strips, a transparent physiologic dressing, or a nasal bridle. Securement is
frequently done with adhesive tape that is split part way and wrapped around the tube and then attached to the nose,
or it may be done with semipermeable transparent dressing, adhesive skin-closure strips, or manufactured fixation
devices. After providing some slack so as not to exert pressure on the nares, the remaining tube length can then be
brought to the side of the face and secured to the cheek with tape, adhesive strips, or a transparent physiologic
dressing. For infants, it is important to watch the pacifier and make sure it does not catch in securement products.
Nasal bridles are typically reserved for patients who are at risk for pulling at their tubes or those with facial
burns, but they can be used in any patient. Use of a nasal bridle involves a technique that results in small-bore tubing
or twill tape entering 1 naris, looping around the nasal septum, and exiting the other naris. The 2 ends are then
secured together, forming the bridle, and the feeding tube is clipped or tied to it. When the feeding tube is pulled or
tugged, the bridle is also tugged and the patient feels nasal septal discomfort. There is a commercially manufactured
nasal bridle that uses a magnetic retrieval technique to facilitate the movement of the blue polymer hypoallergenic,
latex-free tubing (bridle) around the nasal septum (Applied Medical Technology, Brecksville, OH).
A meta-analysis found that nasal bridles were more effective for tube securement and preventing tube
dislodgement when compared to adhesive tape.99 This technique should be avoided in those patients with nasal
airway obstructions and abnormalities and with facial or anterior cranial fractures. Excessive traction on a nasal
bridle may cause serious nasal injury, and it is recommended to further secure the tube by other means.
As noted previously, percutaneous feeding tubes have an internal securement device or bolster to prevent
external displacement, and most have an external securement device preventing internal displacement. Those that do
not have the external retention device should be secured with tape, adhesive strips, sutures, or commercial tube-
attachment devices. For patients who tend to pull at their percutaneous feeding tube, the tube should either be tucked
away under clothing, covered with an abdominal binder, cut down to an external length of 6 to 8 cm, and/or
transitioned to a low-profile feeding tube. Placing the patient’s hands in mittens is another option to deter pulling.
The use of medications or physical restraints is discouraged because those methods can increase the risk of agitation
and delirium.
To administer formula, medication, or water to the patient, the EAD must be connected to a syringe or feeding
bag. Misconnections between EADs and unrelated delivery systems such as IV lines, respiratory tubing, or urinary
devices can lead to deleterious outcomes, including serious injury or death. The FDA has received reports of 2
deaths and 24 serious injuries related to enteral misconnections just since 2011. Furthermore, it is thought that many
enteral misconnections do not get reported to the FDA. In response to such safety issues, the FDA published safety
considerations regarding the risk of enteral feed misconnections with non-enteral small-bore connectors in 2015.100
Healthcare facilities are encouraged to implement procedures and policies to reduce enteral misconnection risk.3,101
See Table 3-5 for recommendations to prevent enteral misconnections.

TABLE 3-5. Practice Recommendations for Enteral Misconnection Prevention

Review currently used systems to assess practices that include the potential for misconnection,
1.
including nonstandard, rigged work-arounds (Luer adapters, etc).
Train nonclinical staff and visitors not to reconnect lines but to seek clinical assistance instead.
2. Only clinicians or users knowledgeable about the use of the device should make a reconnection,
and they should do so under proper lighting.
Do not modify or adapt IV or feeding devices because doing so may compromise the safety
3.
features incorporated into their design.
When making a reconnection, practitioners should routinely trace lines back to their origins and
4.
then verify that they are secure.
Route tubes and catheters that have different purposes in unique and standardized directions (eg,
5. IV lines should be routed toward the patient's head, and enteric lines should be routed toward the
feet).
When arriving at a new setting or as part of a hand-off process, staff should recheck connections
6.
and trace all tubes.
Label or color-code feeding tubes and connectors, and educate staff about the labeling or color-
7.
coding process in the institution's enteral feeding system.
Identify and confirm the EN label, because a 3-in-1 PN admixture can appear similar to an EN
8. formulation bag. Label the EN bags with large, bold statements such as “WARNING! For Enteral
Use Only—NOT for IV Use.”
9. Transition to enteral-specific connectors such as ENFit®.
Purchase an adequate number of enteral pumps so that IV pumps are not used for enteral delivery
for adult patients. When syringe pumps are used in neonatal ICUs for human milk or other
feedings, they should be clearly distinct from syringe pumps used for IV or other medical
10.
purposes. Ideally, enteral feeding pumps should be a different model, a different color, or as
different in appearance from IV pumps as possible. Enteral feeding pumps should be clearly
labeled as enteral feeding pumps.
Avoid buying prefilled enteral feeding containers, except for those with design technology
labeled non-IV-compatible. In all cases, verify that the enteral administration set is packaged with
the enteral feeding bag or container before it is sent to the patient care unit. (The set should be
11.
secured to the bag, perhaps with a rubber band, or preattached sets should be requested from the
manufacturer.) In either case, the objective is to prevent bags or containers from being spiked with
IV administration sets.
Purchase and use enteral syringes with ENFit connectors instead of Luer-lock syringes to draw up
and deliver medications into the enteral feeding system. Include pharmacy department
12.
recommendations to verify the correct syringe type, along with dispensing and proper labeling
protocols.
Abbreviations: EN, enteral nutrition; GI, gastrointestinal; ICU, intensive care unit; IV, intravenous; PN, parenteral nutrition.
Source: Adapted with permission from reference 3: Boullata JI, Carrera AL, Harvey L, et al. ASPEN safe practices for enteral nutrition
therapy. JPEN J Parenter Enteral Nutr. 2017;41(1):15-103. doi:10.1177/0148607116673053.
 To address the risk of enteral misconnections, the International Organization for Standardization (ISO) has
published design standard ISO 80369-3 (commonly known as ENFit®). Enteral device manufacturers produce EADs
with this connection to comply with the standard and improve patient safety (see Figure 3-8). Use of the ENFit
connection is considered an effective method to reduce enteral misconnection risk because the ENFit connection is
not physically compatible with non-enteral devices. The FDA released a letter on September 7, 2018, encouraging
healthcare facilities to adopt the ISO 80369-3 connection.102 The Global Enteral Device Supplier Association
(GEDSA) is a nonprofit group created to promote the global adoption of ENFit connectors.103,104 At the time of
publication of this handbook, US healthcare facilities, manufacturers, and distributors are undergoing the transition
from legacy to ENFit devices.104 More information on ENFit may be found on GEDSA’s website
(www.stayconnected.org).

Nasal, Oral, and Skin Care

Regardless of the feeding tube type or insertion technique, all patients receiving EN require appropriate oral
hygiene. Oral care is especially important for preventing aspiration pneumonia in ventilator-dependent patients or in
those with a depressed level of consciousness.105
Patients with nasal feeding tubes benefit from skin care to the nasal area to prevent or address harm caused by
prolonged exposure to tape and adhesive products. Periodic repositioning of the nasal tube and efforts to avoid
pressure on the nares are necessary to prevent pressure necrosis.
In patients with enterostomy feeding tubes, the area around the tube’s exit site should be cleaned with mild soap
and water daily. The area should then be rinsed and dried thoroughly, including underneath the external retention
device. Routine use of antibiotic ointments or hydrogen peroxide at the tube site is not recommended. Hydrogen
peroxide can impede wound healing and cause skin irritation. Antibiotic ointments are not routinely necessary and
can promote yeast overgrowth with chronic use. Dressings are not needed at the tube site unless there is concern
about drainage (some drainage is common).
Patients with enterostomies are at risk for skin breakdown with redness or excoriation at the exit site. Zinc-based
products, such as diaper rash creams or absorptive powders, can be applied and the site covered with a semi-
permeable/breathable drainage sponge. If there is excessive site leakage, a dressing that is manufactured to wick
away moisture is preferable to gauze. Alcohol-free, skin-barrier films or skin-barrier wafers can be used. Scattered,
reddened and raised papules spreading from the stoma outward may indicate a candidal infection. This type of
fungal infection can be treated by directly applying a topical antifungal, such as nystatin powder or cream, and a
zinc oxide cream coating twice daily and then covering the area with a split-gauze dressing. Clinicians should
consult with a wound or stoma nurse if these first-line treatments are ineffective.
Hypertrophic granulation tissue growth may develop at the stoma site, manifesting as reddened, lumpy, moist,
shiny tissue growth protruding from the site. The presence of this excess tissue may, but does not always, lead to
increased site drainage as the seal around the tube is compromised. The treatment involves dissolution of the
granulated tissue, most commonly with silver nitrate applicators. If that fails, topical corticosteroid can be applied
with a cotton tip applicator as needed. Other treatment options include mometasone furoate 0.1% once daily or
triamcinolone acetonide 0.1% 3 times daily. Care must be taken not to apply the corticosteroid on healthy skin
because it will cause tissue thinning of the skin over time. As a last resort, surgical excision of granulation tissue can
be undertaken. A skilled clinician must perform the surgical intervention because the tissue can bleed easily, and a
thorough assessment is needed to rule out malignancy.
 To minimize the risk for granulation tissue, the site must be kept as dry as possible, the tube should be secured to
prevent movement, and the movable external attachment device or low-profile tube should be positioned about a
dime’s width from the skin.

Exchange and Removal of Enterostomy Feeding Tubes

Depending on the tube type and provider’s discretion, enterostomy tubes may be safely removed after the tract has
matured, which usually happens 4–8 weeks after insertion in adults. In patients who are slow to heal or receiving
steroids or immunosuppressive agents, longer wait times (up to 3 months) are advised. In pediatric patients, waiting
4–12 weeks may be advised.106 Early dislodgement or removal of newly placed enterostomy tubes may result in the
stomach falling away from the abdominal wall, allowing gastric contents to leak into the peritoneum. Inadvertent
tube dislodgement before tract maturation requires tube replacement with the assistance of endoscopy, interventional
radiology, or surgical intervention.
Removal of enterostomy tubes should be performed only by those trained and/or credentialed to do so. Removal
of a percutaneous gastrostomy tube with an internal solid bolster is accomplished at the bedside using the traction
pull method. The patient is placed in the supine position with knees bent to relax the abdominal muscles. The
exposed gastric tube is firmly grasped and pulled using constant traction while the abdomen is held down around the
stoma site for countertraction. The internal bolster deconforms through the stomal tract. Some clinicians cut the
percutaneous gastrostomy tube close to the site, which allows the internal bolster to fall inside the stomach;
however, the severed bolster could potentially cause a subsequent bowel obstruction. For devices held in place with
an inflated balloon, the balloon is deflated and the tube is gently removed.
To insert replacement percutaneous feeding tubes with balloon internal bolsters, the deflated replacement tube is
lubricated with water-soluble gel and inserted into the stoma tract and then the balloon is inflated with distilled or
sterile water. Generally, 5–20 mL of sterile or distilled water should be used for gastric tubes and 2–3 mL should be
used for small bowel tubes; follow the manufacturer’s recommendations to determine the water volume to use.
Clinicians can use stoma-measuring devices to select the appropriate replacement tube length when replacing a
standard-profile tube with a low-profile tube or when there is uncertainty about the length of the low-profile
replacement tube needed.

Complications of Enteral Access Devices

Nasal Tube Complications

Complications of nasally placed feeding tubes can be divided into those that occur during the insertion procedure
and those that occur postprocedure. Procedure-related complications include epistaxis, aspiration, tube
misplacement, esophageal perforation, and circulatory or respiratory compromise. The most-dreaded procedure-
related complication is initial misplacement of the nasal tube into the bronchopulmonary tree. This complication has
been reported to occur in 1.2%–2.3% of blind tube placements and may lead to pneumothorax, hemopneumothorax,
empyema, or pneumonia.107 Death has been reported to occur in 0.1%–0.5% of all blind tube placements, and the
estimated mortality rate is 15% when a tube is misplaced into the bronchopulmonary tree.108,109 Patients at the
highest risk for feeding tube malposition include those who are critically ill, sedated, or intubated; patients with
altered mental status; and those who have poor cough reflex.107 Patients who require repeated tube placements or
experience difficult tube placements are also at increased risk. Best practices for confirming tube position are
reviewed earlier in this chapter.
Postprocedural complications include tube malfunction, tube displacement or dislodgement, tube clogging,
pressure-related skin breakdown, sinusitis, aspiration, and intestinal ischemia. Malfunction of the tube, which
includes breaking, cracking, or kinking, occurs 11% to 20% of the time.110,111
Tube dislodgement seems to be a fairly frequent occur-rence. In a study of 49 intensive care units (ICUs), 28.9%
of NG tubes were reported to have dislodged.112 As noted earlier in the chapter, once a feeding tube is placed and the
tube tip is determined to be in the proper position, the tube must be secured to prevent inward or outward migration.
A tube can displace inward or outward by slipping through the external securement device. Tube dislodgement has
been associated with patients who are agitated, confused, or restless, as well as those who have infections, untoward
medication side effects, or a Glasgow coma scale score <9.112,113 For these high-risk patients and patients with facial
wounds or burns, a nasal bridle may be a good securement option. See the Tube Securement and Connections
section earlier in this chapter for cautions regarding the use of nasal bridles.
In patients with nasally placed tubes, the incidence of sinusitis is approximately 12%.114 Sinusitis is believed to
be secondary to obstruction of physiological sinus drainage by the nasal tube; therefore, it may be prudent to avoid
larger-diameter or stiffer tubes. Although the overall incidence of sinusitis is relatively low, incidence increases in
patients who have both a nasoenteric tube and an endotracheal tube.115

Enterostomy Tube Complications

Complications of enterostomy tubes can be divided into major complications and those that tend to have less clinical
significance. Major complications include aspiration, hemorrhage, peritonitis/necrotizing fasciitis, and death.
Complications that are usually less serious include peristomal infection, peristomal leakage, buried bumper
syndrome, inadvertent removal, and fistulous tracts.18
Another way to classify enterostomy-related complications is as procedural vs postprocedural events. Incidence
of procedure-related complications (eg, intraprocedural aspiration, hemorrhage, perforation of the GI lumen, and
prolonged ileus) has been estimated to be 1.5%–4%; procedure-related mortality occurs in less than 2% of cases.116
Risk factors for aspiration include the supine position, advanced age, need for sedation, and neurologic
impairment.117 Pneumoperitoneum as a result of the percutaneous procedure is common, and, in the absence of
peritoneal signs, it is of no clinical consequence.118 Infusion of water-soluble contrast with fluoroscopic or CT
imaging is the test of choice if perforation and peritonitis are suspected.
Peristomal infection is the most common complication of gastrostomy tube placement.65,119 Most of these
infections are mild, presenting with a painful area surrounding the tube with marked redness and induration. Early
evaluation and management of peristomal wound infection and treatment with oral antibiotics are usually sufficient
interventions. However, signs of systemic toxicity (ie, fever, tachycardia, hypotension) require hospital admission
and IV antibiotics. Local wound care and incision and drainage of any significant fluid collections are the keys to
successful management.66,120 In rare cases, necrotizing fasciitis with high risks for morbidity and mortality can
develop from peristomal infection. Necrotizing fasciitis is an emergent condition requiring surgical debridement,
broad-spectrum antibiotics, and ICU admission.
Significant leakage around the gastrostomy site should be addressed promptly (see Table 3-6).121 Of note, the
color of the drainage around a gastrostomy tube does not necessarily signify infection—even green or cloudy yellow
drainage, which may otherwise appear purulent, may be normal for gastric fluid. Prolonged exposure of the skin to
gastrostomy secretions can lead to pain, skin breakdown, cellulitis, or a yeast infection. Risk factors include
infection, excessive cleansing with irritant solutions (eg, hydrogen peroxide, povidone-iodine), an external bumper
that is either too loose or too tight, internal balloon deflation or rupture, and excessive tension and side torsion on
the external portion of the feeding tube. Prompt treatment of infection, good ostomy skin care, adjustment of the
outer bumper, checking for appropriate balloon volume, and stabilizing the gastrostomy tube to prevent torsion on
the tube will address these issues.122 Converting a gastrostomy to a gastrojejunostomy tube may be indicated to
decrease leakage of formula. With a gastrojejunostomy, the gastric port can be used for drainage while feeding is
infused through the jejunal port.

TABLE 3-6. Management of Drainage at an Enterostomy Tube Site

Type of Drainage Management Recommendations

• Monitor for skin irritation and breakdown.
• Clean site with mild soap and water.
• Check water in the balloon/external bolster position if
Thin clear (serous) appropriate.
• Confirm size of the tube is appropriate.
• Use a skin-barrier product to protect the skin (cream,
powder) or a moisture-wicking dressing.
• Assess gastrostomy site for skin breakdown.
 • Assess whether a traumatic event occurred.
• Identify where drainage is originating.
Pink/bleeding • Clean site with mild soap and water.
serosanguineous • Check water in the balloon if appropriate.
• Confirm size is appropriate.
• If skin breakdown is present, use a moisture-wicking
dressing.
• Consider using a silver-impregnated dressing.
• Monitor site for skin breakdown.
• Clean site with mild soap and water.
Mucous—thick/clear white/cloudy
• Use a skin-barrier product to protect the skin (cream,
powder) or a moisture-wicking dressing.
• Monitor site for signs and symptoms of infection and for
skin breakdown.
• Clean site with mild soap and water.
• Check water in the balloon/external bolster position if
Purulent yellow/ green thick appropriate.
• Confirm size is appropriate.
• Use a moisture-wicking dressing.
• If skin breakdown is present, consider using a silver-
impregnated dressing.
• Protect skin from drainage, and monitor the site for skin
breakdown.
• Clean site with mild soap and water.
• Check water in the balloon/external bolster position, if
Thin, bright-yellow
appropriate.
• Confirm size of the tube is appropriate.
• Use a skin-barrier product to protect the skin (cream,
powder) or a moisture-wicking dressing.
• Protect skin from drainage, and monitor site for skin
breakdown.
• Monitor bowel movements and feeding tolerance.
• Clean site with mild soap and water.
• Check water in the balloon/external bolster position, if
Formula/food intake
appropriate.
• Confirm size of the tube, if appropriate.
• Vent gastric port to release any air in the stomach.
• Use a skin-barrier product to protect the skin (cream,
powder) or a moisture-wicking dressing.
• This is an indication that an injury has occurred to the
gastric mucosa. Patient should be seen by a medical
provider, and close follow-up is needed.
• Monitor site for skin breakdown.
• Monitor site for signs and symptoms of infections.
 • Monitor site for signs and symptoms of buried bumper
Dark-brown/black syndrome or other injury to stomach mucosa.
• Confirm size is appropriate.
• Protect skin from drainage with moisture-wicking dressing
or skin-barrier products.
• Consider whether patient needs a proton pump inhibitor to
decrease the acidic environment and promote healing of
the gastric mucosa.

Source: Adapted with permission from reference 121: Abdelhadi RA, Rahe K, Lyman B. Pediatric enteral access device management. Nutr
Clin Pract. 2016:31: 748-761.

Buried bumper syndrome (Figure 3-9) is the embedding of the internal retention device into the gastric mucosa.71
It can cause pain, tube obstruction, and stoma site drainage and may lead to GI bleeding, perforation, peritonitis,
abdominal abscesses, or phlegmon.123 Risk factors include excessive tension between the internal and external
bumpers, poor wound healing, and significant weight gain or abdominal distention that causes progressive tightness
of the external bumper.124–126 Buried bumper syndrome is highly suspected when a gastrostomy tube cannot be easily
rotated or moved inward. Treatment is based on maintaining the existing stoma tract while restoring the internal
bumper entirely within the stomach lumen; if that approach fails, tube removal and replacement may be
warranted.127,128 To prevent this complication, it is important to not place the external bumper too tightly and to
loosen it if the patient gains a substantial amount of weight or has a distended abdomen.

A rare but serious complication is tumor implantation and metastasis at the gastrostomy tube site in patients with
upper aerodigestive cancers. This complication may result from direct shearing of cancer cells during gastrostomy
tube placement and subsequent tumor seeding at the tube site or from hematogenous spread of circulating tumor
cells to a wound site. In a report of 218 patients with head and neck cancer with viable tumor at the time of PEG
placement, 2 patients (0.92%) experienced PEG-site meta stasis.129 This may have been caused by cancer cells
adhering to the endoscope and then seeding at the gastrostomy site. Gastrostomy-site tumors can be treated with
palliative radiation or resection, but overall prognosis is poor. Because this complication has for the most part been
reported with endoscopically placed gastrostomy tubes using the transoral approach, alternate tube placement
methods, such as radiologic techniques using the transabdominal approach, can be considered in patients with active
aerodigestive cancers.
Peritonitis can result from the premature removal of the percutaneous enterostomy tube before the stoma tract
has matured (ie, within the first few days to weeks after insertion). If the stomach or small bowel falls away from the
abdominal wall when the EAD is prematurely removed, gastric or small bowel contents can leak into the
peritoneum. Gastrostomy tract maturation begins to take place in the first 7 to 10 days following initial gastrostomy
tube placement, but it is recommended to wait at least 30 days for fusion between the stomach and peritoneum to
occur.3,116 Peritonitis can also occur during either initial placement or replacement if the tip of the tube is
malpositioned into the peritoneum and enteral formula infuses into the peritoneal cavity.
Given the risk for peritonitis, unintended gastrostomy tube removal should be addressed urgently. If a
gastrostomy tube is removed or dislodged prior to stoma tract maturation, the tube should be immediately replaced
with endoscopic or fluoroscopic guidance. After stoma tract maturation has occurred, a replacement tube can be
placed at the bedside or in an outpatient setting without endoscopy or fluoroscopy. If a standard replacement tube is
not promptly available, a suitably sized Foley-type or uro-logical red rubber catheter might be used to keep the tract
open until a standard replacement tube can be placed. However, this intervention should be temporary and done only
as a last resort. As noted earlier, these types of tubes are not indicated for enteral use and are not compatible with
ENFit connections on feeding sets and syringes. Alternatively, tape may be used to hold the damaged tube in place
until replacement can be achieved. Some patients are provided with a backup gastrostomy tube to be used for
replacement in an emergency. If there is any concern about improper replacement, the tube position should be
checked either radiographically with injection of contrast or by direct endoscopic visualization.
A cohort study published in 2015 sheds light on gastrostomy-related complications in pediatric patients.130 The
authors reviewed charts of 591 infants and children with PEG tubes, and the data collected indicated that mortality
in the pediatric population was relatively low compared to the adult population cohort. Mortality in the pediatric
patients was linked to comorbidities. In this review, infection at the stoma site was the most common complication
with PEG placement. The presence of a ventriculoperitoneal shunt was a greater risk factor than other neurologic
abnormalities. From the data reviewed, the authors predicted that 1 in 4 pediatric patients would have a
complication, an extended hospital stay, or an additional procedure requiring anesthesia after the placement of a
PEG. Laparoscopic techniques to place PEG tubes may have lower complication rates.130
Other studies involving pediatric patients have investigated the risk for gastroesophageal reflux disease (GERD)
following PEG tube placement.131,132 That risk seems to be minimal even when predicted based on preplacement
studies. However, pediatric patients with a neurologic impairment are at increased risk for GERD after PEG tube
placement.131,132
Patients with gastrojejunostomy tubes and jejunostomy tubes are at risk for many of the complications associated
with gastrostomy tubes. Compared with gastrostomy feeding tubes, gastrojejunostomy feeding tubes are associated
with higher risks of tube occlusion and kinking because the jejunostomy tube has a smaller diameter and longer
length. To help prevent tube clogging, medications should be administered through the much-larger-diameter
gastrostomy port of the gastrojejunostomy tube when possible (tube clogging is discussed in greater detail in the
next section of this chapter).
A unique complication of transgastric GI and trans-gastric jejunal tubes is the retrograde migration of the
jejunostomy tube tip back into the stomach.72 Further complications may occur when the type of ostomy tube is
incorrectly identified (eg, a balloon gastrostomy tube is confused with a gastrojejunostomy tube). This risk can be
prevented when clinicians clearly understand and carefully inspect the labeling of the various ports (gastric, jejunal,
or balloon). In addition, there should be clear documentation regarding which port is used for enteral formula
delivery, which is used for water administration, and which is for medication administration (see Chapter 10).
A pediatric study described outcomes for patients requiring primary gastrojejunostomy tube placement.133 The
primary indications for gastrojejunostomy tube placement in this study were GERD, aspiration, and growth failure;
secondary comorbidities included complex cardiac disease, prematurity, respiratory disease, and neurologic
conditions. Of the 90 patients in the study, 16 had a complication of tube occlusion, tube migration, or jejunal
perforation. The 30-day complication rate was 6.7%, and the mortality rate at 30 days was 4.4%.133
Complications specific to direct jejunostomy tubes include jejunal volvulus, small bowel perforation, and
persistent enterocutaneous fistulas after the tube is removed.72 However, jejunostomy tubes have the advantage of a
more stable jejunal tip placement because they are inserted directly into the jejunum. Jejunal volvulus is a rare but
potentially devastating complication of direct jejunostomy placement.134 A retrospective study that compared
outcomes of primary placement of jejunostomy tube and gastrojejunostomy tubes found comparable complication
rates except that more pericatheter leakage was seen with the jejunostomy tubes.135
Gastrojejunostomy or direct jejunostomy intermittent feeding into the small bowel can result in dumping
syndrome. The rapid infusion of tube feeding directly into the small bowel causes a release of gut hormones that
shifts the fluid from the bloodstream into the bowel. The bowel becomes distended, and patients can experience
diarrhea, abdominal discomfort and bloating, lightheadedness, and potential fainting.
Tube Clogging
Tube clogging is a frequent problem across all types of tubes, with incidence reported to be as high as 23%–35%;
when tubes become clogged, they often must be replaced.136 Risk factors for tube clogging include longer tube
lengths, smaller internal tube calibers, inadequate water flushing, contaminated formula, improper medication
delivery, and use of the tube to measure GRVs.137
The first strategy to unclog a feeding tube usually involves attaching a 60-mL syringe of warm water to the tube,
using the syringe plunger to push the water into the tubing, massaging the tubing to loosen the clog, and then pulling
back on the plunger to dislodge the clog. If this technique is ineffective, water penetration may be tried. Remove all
fluid from the tube, instill the tube with warm water, and clamp the tube for 20–60 minutes, periodically moving the
plunger back and forth to help loosen the clog.138–140
If water penetration fails, a declogging solution can be tried. A prospective study demonstrated that pancreatic
enzyme activated with bicarbonate was more effective than traditional measures for resolving feeding tube clogs.141
This declogging solution is made by first dissolving ¼ teaspoon of baking soda or a crushed 650-mg non-enteric-
coated sodium bicarbonate tablet in 10 mL of warm water and then adding the contents of an opened 12,000-U
pancrelipase capsule (Creon) or a crushed 10,440 U pancrelipase tablet (Viokace) to the solution; the solution is
ready for use when all ingredients are fully dissolved.29 To use the solution, all the fluid from the feeding tube
should be withdrawn, the declogging solution instilled, and the tube clamped for up to 60 minutes. Afterward, the
solution should be withdrawn to see whether the clog releases. The declogging technique with activated pancreatic
enzyme can be repeated once. Once a clog is successfully withdrawn, a water flush should be administered to clear
the tube.
An intermittent activated pancreatic enzyme lock has been suggested once weekly to prevent clogging in tubes
prone to clogging.29 A commercially available pancreatic enzyme cocktail (Clog Zapper, Avanos, Alpharetta, GA) is
available in a preloaded syringe that is activated with water and gains close proximity to the clog through a smaller-
bore tube placed inside the feeding tube. A 100% declogging success rate was reported with up to 2 attempts in
feeding tubes with formula clogs.142
Another option is mechanical dislodgement of tube occlusion. This may be achieved using a cytology brush, an
endoscopic retrograde cholangiopancreatography catheter, corrugated plastic rods (Bionix, Toledo, OH), or a
machine-operated wire encased in a sheath that mechanically breaks up clogs with a back and forth motion (Tube-
Clear, Actuated Medical, Bellefonte, PA).
Regular flushing of the tube is critical to maintain tube patency, with water as the fluid of choice. If medication
is administered via the feeding tube, a water flush should be administered before and after each medication.143 A
pharmacist should be consulted if any medications are to be administered via the feeding tube. For example, some
medications require activation in the stomach and should not be administered via a postpyloric route. See Chapter 10
for additional information on medication administration. Table 3-7 summarizes practice recommendations related to
tube patency.3,29

TABLE 3-7. Practice Recommendations to Maintain Tube Patency

1. Use the largest-bore enteral tube possible that will be comfortable for the patient.
2. Follow best practices for enteral medication administration.a
3. Flush the tube with water every 4-8 hours during continuous feedings.
4. Flush the tube with water before and after all bolus enteral feeds.
5. Consult treating provider for the appropriate amount of water flushes.
a
See Chapter 10.

References
1. Northington L, Lyman B, Guenter P, Irving SY, Duesing L. Current practices in home management of
nasogastric tube placement in pediatric patients: a survey of parents and homecare providers. J Pediatr Nurs.
2017;33:46–53.
2. Vanek VW. Ins and outs of enteral access. Part 1: short-term enteral access. Nutr Clin Pract.
2002;17(5):275–283.
3. Boullata JI, Carrera AL, Harvey L, et al. ASPEN safe practices for enteral nutrition therapy. JPEN J
Parenter Enteral Nutr. 2016;41(1):15–103. doi:10.1177/0148607116673053.
4. Norton B, Homer-Ward M, Donnelly MT, Long RG, Holmes GK. A randomised prospective comparison of
percutaneous endoscopic gastrostomy and nasogastric tube feeding after acute dysphagic stroke. BMJ.
1996;312(7022):13–16.
5. Park RH, Allison MC, Lang J, et al. Randomised comparison of percutaneous endoscopic gastrostomy and
nasogastric tube feeding in patients with persisting neurological dysphagia. BMJ. 1992;304(6839):1406–
1409.
6. Attam R, Leslie D, Freeman M, Ikramuddin F, Andrade R. EUS-assisted, fluoroscopically guided
gastrostomy tube placement in patients with Roux-en-Y gastric bypass: a novel technique for access to the
gastric remnant. Gastrointest Endosc. 2011;74(3):677–682. doi:10.1016/j.gie.2011.05.01.
7. Moon R, Teixeira A, Potenza K, Jawad M. Routine gastrostomy tube placement in gastric bypass patients:
impact on length of stay and 30-day readmission rate. Obes Surg. 2013;23(2):216–221. doi:10.1007/s11695-
012-0835-5.
8. Levy H. Nasogastric and nasoenteric feeding tubes. Gastroin test Endosc Clin N Am. 1998;8(3):529–549.
9. Albrecht H, Hagel AF, Schlechtweg P, Foertsch T, Neurath MF, Mudter J. Computed tomography-guided
percutaneous gastrostomy/jejunostomy for feeding and decompression. Nutr Clin Pract. 2017;32(2):212–
218.
10. Haskins IN, Strong AT, Baginsky M, et al. Comparison of laparoscopic jejunostomy tube to percutaneous
endoscopic gastrostomy tube with jejunal extension: long-term durability and nutritional outcomes. Surg
Endosc. 2018;32(5):2496–2504.
11. Ho KM, Dobb GJ, Webb SA. A comparison of early gastric and post-pyloric feeding in critically ill patients:
a meta-analysis. Intensive Care Med. 2006;32(5):639–649.
12. Marik PE, Zaloga GP. Gastric versus post-pyloric feeding: a systematic review. Crit Care. 2003;7(3):R46–
R51.
13. McClave SA, Taylor BE, Martindale RG, et al. Guidelines for the provision and assessment of nutrition
support therapy in the adult critically ill patient: Society of Critical Care Medicine (SCCM) and American
Society for Parenteral and Enteral Nutrition (A.S.P.E.N.). JPEN J Parenter Enteral Nutr. 2016;40(2):159–
211.
14. Mehta NM, Skillman HE, Irving SY, et al. Guidelines for the provision and assessment of nutrition support
therapy in the pediatric critically ill patient: Society of Critical Care Medicine and American Society for
Parenteral and Enteral Nutrition. JPEN J Parenter Enteral Nutr. 2017;41(5): 706–741.
15. Heyland DK, Drover JW, Dhaliwal R, Greenwood J. Optimizing the benefits and minimizing the risks of
enteral nutrition in the critically ill: role of small bowel feeding. JPEN J Parenter Enteral Nutr. 2002;26(6
Suppl):S51–S55.
16. Massoumi R, Akdelhafeez HA, Christensen MA, Vo NJ. JPEN J Parenter Enteral Nutr. 2016;40(8):1177–
1182.
17. Egnell C, Eclborg S. Grahnquist L. Jejunostomy enteral feeding in children: outcome and safety. JPEN J
Parenter Enteral Nutr. 2014;38(5):631–636.
18. Fang JC, Kinikini M. Enteral access devices. In: Mueller CM, ed. The ASPEN Adult Nutrition Support Core
Curriculum. 3rd ed. Silver Spring, MD: American Society for Parenteral and Enteral Nutrition; 2017:251–
264.
19. Lyman B, Kemper CA, Northington L, et al. Use of temporary enteral access devices in hospitalized
neonatal and pediatric patients in the United States. JPEN J Parenter Enteral Nutr. 2016;40(4):574–580.
20. Lord LM, Weiser-Maimone A, Pulhamus M, Sax HC. Comparison of weighted vs unweighted enteral
feeding tubes for efficacy of transpyloric intubation. JPEN J Parenter Enteral Nutr. 1993;17(3):271–273.
21. Meyer TE, Verbrugge JK, Neutze JA. Ruptured, weighted, enteral feeding tube tip presenting as enteric
foreign objects. Radiol Case Rep. 2010;5:429.
22. Heiser M, Malaty H. Balloon-type versus non-balloon-type replacement percutaneous endoscopic
gastrostomy: which is better? Gastroenterol Nurs. 2001;24(2):58–63.
23. Bonhorst B, Cech K, Peter C, Doerdelmann M. Oral versus nasal route for placing feeding tubes: no effect
on hypoxemia and bradycardia in infants with apnea of prematurity. Neo natology. 2010;98(2):143–149.
24. Rassias AJ, Ball PA, Corwin HL. A prospective study of tracheopulmonary complications associated with
the placement of narrow-bore enteral feeding tubes. Crit Care. 1998;2(1): 25–28.
25. Marderstein EL, Simmons RL, Ochoa JB. Patient safety: effect of institutional protocols on adverse events
related to feeding tube placement in the critically ill. J Am Coll Surg. 2004;199(1):39–50.
26. Ellett ML, Beckstrand J, Flueckiger J, Perkins SM, Johnson CS. Predicting the insertion distance for placing
gastric tubes. Clin Nurs Res. 2005;14(1):11–31.
27. Metheny N, Reed L, Berglund B, Wehrle MA. Visual characteristics of aspirates from feeding tubes as a
method for predicting tube location. Nurs Res. 1994;43(5):282–287.
28. Metheny NA. Preventing respiratory complications of tube feedings: evidence-based practice. Am J Crit
Care. 2006;15(4): 360–369.
29. Lord LM. Enteral access devices: types, function, care, and challenges. Nutr Clin Pract. 2018;33(1):16–38.
30. Irving SY, Lyman B, Northington L, Bartlett JA, Kemper C. Nasogastric tube placement and verification in
children: review of the current literature. Crit Care Nurs. 2014;34(3):67–78.
31. American Association of Critical-Care Nurses. AACN Practice Alert: Verification of Feeding Tube
Placement (Blindly Inserted). Aliso Viejo, CA: American Association of Critical-Care Nurses; 2010.
32. National Health Service. Nasogastric tube misplacement: continuing risk of death and severe harm. Patient
safety alert. https://improvement.nhs.uk/resources/patient-safety-alerts. Published July 2016. Accessed
August 9, 2018.
33. Meert KL, Calverly M, Kelm LM, Metheny NA. The pH of feeding tube aspirates from critically ill infants.
Am J Crit Care. 2015;24(5):72–77.
34. National Health Service. Resource set: initial placement checks for nasogastric and orogastric tubes.
https://improvement.nhs.uk/documents/193/Resource_set__Initial_placement_checks_for_NG_tubes_1.pdf.
Published July 2016. Accessed August 9, 2018.
35. Lee KH, Cho HJ, Kim EY, Son DW, et al. Variation between residents and attending staff interpreting
radiographs to verify placement of nutrition access devices in the neonatal intensive care unit. Nutr Clin
Pract. 2015;30(3):389–401.
36. Patient Safety Movement Foundation. APSS—actionable patient safety solutions: challenge 15. Nasogastric
feeding and drainage tube placement and verification. https://patientsafetymovement.org/actionable-
solutions/challenge-solutions/nasogastric-feeding-and-drainage-tube-placement-and-verification. Accessed
December 23, 2018.
37. Asai T. Use of a capnograph during feeding tube insertion. Crit Care Med. 2002;30(7):1674.
38. Araujo-Preza CE, Melhado ME, Gutierrez FJ, Maniatis T, Castellano MA. Use of capnometry to verify
feeding tube placement. Crit Care Med. 2002;30(10):2255–2259.
39. Kindopp AS, Drover JW, Heyland DK. Capnography confirms correct feeding tube placement in intensive
care unit patients. Can J Anaesth. 2001;48(7):705–710.
40. Burns SM, Carpenter R, Truwit JD. Report on the development of a procedure to prevent placement of
feeding tubes into the lungs using end-tidal CO2 measurements. Crit Care Med. 2001;29(5):936–939.
41. DeLegge MH. Enteral access and associated complications. Gastroenterol Clin North Am. 2018;47(1):23–
37.
42. Zaloga GP. Bedside method for placing small bowel feeding tubes in critically ill patients. A prospective
study. Chest. 1991;100(6):1643–1646.
43. Booth CM, Heyland DK, Paterson WG. Gastrointestinal promotility drugs in the critical care setting: a
systematic review of the evidence. Crit Care Med. 2002;30(7):1429–1435.
44. Tiancha H, Jiyong J, Min Y. How to promote bedside placement of postpyloric feeding tubes: a network
meta-analysis of randomized controlled trials. JPEN Parenteral Enteral Nutr. 2015;39(5):521–530.
45. Powers J, Luebbehusen M, Spitzer T, et al. Verification of an electromagnetic placement device compared
with abdominal radiograph to predict accuracy of feeding tube placement. JPEN J Parenter Enteral Nutr.
2011;35(4):535–539.
46. Akers AS, Pinsky M. Placement of a magnetic small bowel feeding tube at the bedside. JPEN J Parenter
Enteral Nutr. 2017; 41(3):496–499.
47. Smithard D, Barrett NA, Hargroves D, Elliot S. Electromagnetic sensor-guided enteral access systems: a
literature review. Dysphagia. 2015;30(3):275–285.
48. Gerritsen A, van der Poel MJ, de Rooij T, et al. Systematic review on bedside electromagnetic-guided,
endoscopic, and fluoroscopic placement of nasoenteral feeding tubes. Gastro intest Endosc. 2015;81(4):836–
847e2.
49. Bourgault AM, Aguirre L, Ibrahim J. Cortrak-assisted feeding tube insertion: a comprehensive review of
adverse events in the MAUDE database. Am J Crit Care. 2017;26(2):149–156.
50. Wischmeyer PE, McMoon MM, Waldron NH, Dye EJ. Successful identification of anatomical markers and
 placement of feeding tubes in critically ill patients via camera-assisted technology with real-time video
guidance. JPEN J Parenter Enteral Nutr. 2019;43(1):118–125. doi:10.1002/jpen.1313.
51. Mizzi A, Cozzi S, Beretta L, Greco M, Braga M. Real-time image-guided nasogastric feeding tube
placement: a case series using Kangaroo with IRIS technology in an ICU. Nutrition. 2017;37:48–52.
52. Metheny N, Dettenmeier P, Hampton K, Wiersema L, Williams P. Detection of inadvertent respiratory
placement of small-bore feeding tubes: a report of 10 cases. Heart Lung. 1990;19(6):631–638.
53. Metheny N, McSweeney M, Wehrle MA, Wiersema L. Effectiveness of the auscultatory method in
predicting feeding tube location. Nurs Res. 1990;39(5):262–267.
54. US Food and Drug Administration. Feeding tube placement systems—letter to health care providers.
https://www.fda.gov/MedicalDevices/Safety/LetterstoHealthCareProviders/ucm591838.htm. Published
January 16, 2018. Accessed December 29, 2018.
55. McClave SA, Chang WK. Complications of enteral access. Gastrointest Endosc. 2003;58(5):739–751.
56. Cosentini EP, Sautner T, Gnant M, Winkelbauer F, Teleky B, Jakesz R. Outcomes of surgical, percutaneous
endoscopic, and percutaneous radiologic gastrostomies. Arch Surg. 1998; 133(10):1076–1083.
57. Moller P, Lindberg CG, Zilling T. Gastrostomy by various techniques: evaluation of indications, outcome,
and complications. Scand J Gastroenterol. 1999;34(10):1050–1054.
58. Laasch HU, Wilbraham L, Bullen K, et al. Gastrostomy insertion: comparing the options—PEG, RIG or
PIG? Clin Radiol. 2003;58(5):398–405.
59. Stiegmann GV, Goff JS, Silas D, Pearlman N, Sun J, Norton L. Endoscopic versus operative gastrostomy:
final results of a prospective randomized trial. Gastrointest Endosc. 1990;36(1):1–5.
60. Scott JS, de la Torre RA, Unger SW. Comparison of operative versus percutaneous endoscopic gastrostomy
tube placement in the elderly. Am Surg. 1991;57(5):338–340.
61. Bankhead R, Boullata J, Brantley S, et al. Enteral nutrition practice recommendations. JPEN J Parenter
Enteral Nutr. 2009;33(2):122–167.
62. Duszak R Jr, Mabry MR. National trends in gastrointestinal access procedures: an analysis of Medicare
services provided by radiologists and other specialists. J Vasc Interv Radiol. 2003;14(8):1031–1036.
63. Lorentzen T, Skjoldbye B, Nolsoe C, Torp-Pedersen S, Mygind T. Percutaneous gastrostomy guided by
ultrasound and fluoroscopy. Acta Radiol. 1995;36(2):159–162.
64. DiSario JA, Baskin WN, Brown RD, et al. Endoscopic approaches to enteral nutritional support. Gastrointest
Endosc. 2002;55(7):901–908.
65. Gossner L, Keymling J, Hahn EG, Ell C. Antibiotic prophylaxis in percutaneous endoscopic gastrostomy
(PEG): a prospective randomized clinical trial. Endoscopy. 1999;31(2): 119–124.
66. Jain NK, Larson DE, Schroeder KW, et al. Antibiotic prophylaxis for percutaneous endoscopic gastrostomy.
A prospective, randomized, double-blind clinical trial. Ann Intern Med. 1987;107(6):824–828.
67. Allison MC, Sandoe JA, Tighe R, et al. Antibiotic prophylaxis in gastrointestinal endoscopy. Gut.
2009;58(6):869–880.
68. Acosta RD, Abraham NS, Chandrasekhara V, et al. The management of antithrombotic agents for patients
undergoing GI endoscopy. Gastrointest Endosc. 2016;83(1):3–16.
69. Veitch AM, Vanbiervliet G, Gershlick AH, et al. Endoscopy in patients on antiplatelet or anticoagulant
therapy, including direct oral anticoagulants: British Society of Gastroenterology (BSG) and European
Society of Gastrointestinal Endos-copy (ESGE) guidelines. Endoscopy. 2016;48(4):385–402.
70. Ponsky JL, Gauderer MW. Percutaneous endoscopic gastrostomy: a nonoperative technique for feeding
gastrostomy. Gastrointest Endosc. 1981;27(1):9–11.
71. Heximer B. Pressure necrosis: implications and interventions for PEG tubes. Nutr Clin Pract. 1997;12:256–
258.
72. Itkin M, DeLegge MH, Fang JC, et al. Multidisciplinary practical guidelines for gastrointestinal access for
enteral nutrition and decompression from the Society of Interventional Radiology and American
Gastroenterological Association (AGA) Institute, with endorsement by Canadian Interventional Radiological
Association (CIRA) and Cardiovascular and Interventional Radiological Society of Europe (CIRSE).
Gastroenterology. 2011;141(2):742–765.
73. Crowley JJ, Hogan MJ, Towbin RB, et al. Quality improvement guidelines for pediatric gastrostomy and
gastrojejunostomy tube placement. J Vasc Interv Radiol. 2014;25(12): 1983–1991.
74. Peitgen K, von Ostau C, Walz MK. Laparoscopic gastrostomy: results of 121 patients over 7 years. Surg
Laparosc Endosc Percutan Tech. 2001;11(2):76–82.
75. Grant JP. Comparison of percutaneous endoscopic gastrostomy with Stamm gastrostomy. Ann Surg.
1988;207(5):598–603.
 76. Vanek VW. Ins and outs of enteral access: part 2—long-term access—esophagostomy and gastrostomy. Nutr
Clin Pract. 2003;18(1):50–74.
77. Vanek VW. Ins and outs of enteral access. Part 3: long-term access—jejunostomy. Nutr Clin Pract.
2003;18(3):201–220.
78. Rombeau JL, Twomey PL, McLean GK, Forlaw L, Del Rio D, Caldwell MD. Experience with a new
gastrostomy-jejunal feeding tube. Surgery. 1983;93(4):574–578.
79. Mack LA, Kaklamanos IG, Livingstone AS, et al. Gastric decompression and enteral feeding through a
double-lumen gastrojejunostomy tube improves outcomes after pancreaticoduodenectomy. Ann Surg.
2004;240(5):845–851.
80. DeLegge MH, Duckworth PF, McHenry L, Foxx-Orenstein A, Craig RM, Kirby DF. Percutaneous
endoscopic gastrojejunostomy: a dual center safety and efficacy trial. JPEN J Parenter Enteral Nutr.
1995;19(3):239–243.
81. Udorah MO, Fleischman MW, Bala V, Cai Q. Endoscopic clips prevent displacement of intestinal feeding
tubes: a long-term follow-up study. Dig Dis Sci. 2010;55(2):371–374.
82. Adler DG, Gostout CJ, Baron TH. Percutaneous transgastric placement of jejunal feeding tubes with an
ultrathin endo-scope. Gastrointest Endosc. 2002;55(1):106–110.
83. Ho CS. Radiologic placement of gastrostomy/jejunostomy tubes in high-risk patients. Nutr Clin Pract.
1997;12(1 Suppl): S17–S19.
84. Ho CS, Yeung EY. Percutaneous gastrostomy and transgastric jejunostomy. AJR Am J Roentgenol.
1992;158(2):251–257.
85. Shike M, Latkany L, Gerdes H, Bloch AS. Direct percutaneous endoscopic jejunostomies for enteral feeding.
Gastrointest Endosc. 1996;44(5):536–540.
86. Al-Bawardy B, Gorospe EC, Alexander JA, et al. Outcomes of double-balloon enteroscopy-assisted direct
percutaneous endoscopic jejunostomy tube placement. Endoscopy. 2016; 48(6):552–556.
87. Velazquez-Avina J, Beyer R, Diaz-Tobar CP, et al. New method of direct percutaneous endoscopic
jejunostomy tube placement using balloon-assisted enteroscopy with fluoros-copy. Dig Endosc.
2015;27(3):317–322.
88. Richard HM, Widlus DM, Malloy PC. Percutaneous fluoroscopically guided jejunostomy placement. J
Trauma. 2008; 65(5):1072–1077.
89. Yang ZQ , Shin JH, Song HY, et al. Fluoroscopically guided percutaneous jejunostomy: outcomes in 25
consecutive patients. Clin Radiol. 2007;62(11):1061–1068.
90. Sparrow P, David E, Pugash R. Direct percutaneous jejunostomy—an underutilized interventional
technique? Cardiovasc Intervent Radiol. 2008;31:336–341.
91. Skandalakis LJ, Skandalakis JE. Small intestine. In: Skandalakis LJ, Skandalakis JE, eds. Surgical Anatomy
and Technique: A Pocket Manual. 4th ed. New York, NY: Springer; 2014: 405–414.
92. Yarze JC, Herlihy KJ, Fritz HP, et al. Prospective trial evaluating early initiation of feeding in patients with
newly placed one-step button gastrostomy devices. Dig Dis Sci. 2001;46(4):854–858.
93. Gothberg, G, Bjornsson, S. One-step insertion of low-profile gastrostomy in pediatric patients vs pull
percutaneous endoscopic gastrostomy. JPEN J Parenter Enteral Nutr. 2016; 40(3):423–430.
94. Metheny NA, Spies M, Eisenberg P. Frequency of nasoenteral tube displacement and associated risk factors.
Res Nurs Health. 1986;9(3):241–247.
95. Metheny NA, Titler MG. Assessing placement of feeding tubes. Am J Nurs. 2001;101(5):36–45.
96. Harrison AM, Clay B, Grant MJ, et al. Nonradiographic assessment of enteral feeding tube position. Crit
Care Med. 1997;25(12):2055–2059.
97. Welch SK, Hanlon MD, Waits M, Foulks CJ. Comparison of four bedside indicators used to predict
duodenal feeding tube placement with radiography. JPEN J Parenter Enteral Nutr. 1994;18(6):525–530.
98. Metheny N. Preventing respiratory complications of tube feedings: evidence-based practice. Am J Crit Care.
2006;15(4): 360–369.
99. Bechtold ML, Nguyen DL, Palmer LB, Kiraly LN, Martin-dale RG, McClave SA. Nasal bridles for securing
nasoenteric tubes: a meta-analysis. Nutr Clin Pract. 2014;29(5):667–671.
100. US Food and Drug Administration. Safety considerations to mitigate the risks of misconnections with small-
bore connectors intended for enteral applications: guidance for industry and Food and Drug Administration
staff.
https://www.fda.gov/downloads/medicaldevices/deviceregulationandguidance/guidancedocuments/ucm313385.pdf
Published February 2015. Accessed December 29, 2018.
101. US Food and Drug Administration. Medical device connectors.
 https://www.fda.gov/MedicalDevices/ProductsandMedicalProcedures/GeneralHospitalDevicesandSupplies/TubingandLuerMisc
Updated September 2018. Accessed December 29, 2018.
102. US Food and Drug Administration. The FDA encourages use of enteral device connectors that reduce risk of
misconnection and patient injury [letter].
https://www.fda.gov/downloads/MedicalDevices/ResourcesforYou/Industry/UCM619782.pdf. Published
September 7, 2018. Accessed December 29, 2018.
103. Global Enteral Device Supplier Association website. http://gedsa.org. Accessed December 29, 2018.
104. Stay Connected website. http://stayconnected.org. Accessed December 23, 2018.
105. Speck K, Rawat N, Weiner NC, Tujuba HG, Farley D, Berenholtz S. A systematic approach for developing a
ventilator-associated pneumonia prevention bundle. Am J Infect Control. 2016;44(6):652–656.
106. Lyman B, Shah SR. Nutrition access. In: Corkins MR, ed. The A.S.P.E.N. Pediatric Nutrition Support Core
Curriculum. 2nd ed. Silver Spring, MD: American Society for Parenteral and Enteral Nutrition; 2015:567–
582.
107. Krenitsky J. Blind bedside placement of feeding tubes: treatment or threat? Pract Gastroenterol.
2011;35:32–42.
108. McWey RE, Curry NS, Schabel SI, Reines HD. Complications of nasoenteric feeding tubes. Am J Surg.
1988;155(2): 253–257.
109. de Aguilar-Nascimento JE, Kudsk KA. Clinical costs of feeding tube placement. JPEN J Parenter Enteral
Nutr. 2007; 31(4):269–273.
110. Patrick PG, Marulendra S, Kirby DF, DeLegge MH. Endoscopic nasogastric-jejunal feeding tube placement
in critically ill patients. Gastrointest Endosc. 1997;45(1):72–76.
111. Bosco JJ, Gordon F, Zelig MP, Heiss F, Horst DA, Howell DA. A reliable method for the endoscopic
placement of a nasoenteric feeding tube. Gastrointest Endosc. 1994;40(6):740–743.
112. Mion L, Minnick AF, Leipzig RM, Catrambone C, Johnson M. Patient-initiated device removal in intensive
care units: a national prevalence study. Crit Care Med. 2007;35(12): 2714–2720.
113. Chang LY, Wang KWK, Chao YF. Influence of physical restraint on unplanned extubation of adult intensive
care patients. Am J Crit Care. 2008;17(5):408–415.
114. George DL, Falk PS, Umberto Meduri G, et al. Nosocomial sinusitis in patients in the medical intensive care
unit: a prospective epidemiological study. Clin Infect Dis. 1998;27(3):463–470.
115. Metheny NA, Hinyard LJ, Mohammed KA. Incidence of sinusitis associated with endotracheal and
nasogastric tubes: NIS database. Am J Crit Care. 2018;27(1):24–31. doi:10.4037/ajcc2018978.
116. Lynch CR, Fang JC. Prevention and management of complications of percutaneous endoscopic gastrostomy
(PEG) tubes. Pract Gastroenterol. 2004;28:66–77.
117. Safadi BY, Marks JM, Ponsky JL. Percutaneous endoscopic gastrostomy. Gastrointest Endosc Clin N Am.
1998;8(3):551–568.
118. Wojtowycz MM, Arata JA, Micklos TJ, Miller FJ. CT findings after uncomplicated percutaneous
gastrostomy. AJR Am J Roentgenol. 1988;151(2):307–309.
119. James A, Kapur K, Hawthorne AB. Long-term outcome of percutaneous endoscopic gastrostomy feeding in
patients with dysphagic stroke. Age Ageing. 1998;27(6):671–676.
120. Akkersdijk WL, van Bergeijk JD, van Egmond T, et al. Percutaneous endoscopic gastrostomy (PEG):
comparison of push and pull methods and evaluation of antibiotic prophylaxis. Endoscopy. 1995;27(4):313–
316.
121. Abdelhadi RA, Rahe K, Lyman B. Pediatric enteral access device management. Nutr Clin Pract. 2016;
31:748–761.
122. McClave SA. Managing complications of percutaneous and nasoenteric feeding tubes. Techniques
Gastrointest Endosc. 2001;3(1):62–68.
123. Cyrany J, Rejchrt S, Kopacova M, Bures J. Buried bumper syndrome: a complication of percutaneous
endoscopic gastrostomy. World J Gastroenterol. 2016;22(2):618.
124. Segal D, Michaud L, Guimber D, Ganga-Zandzou PS, Turck D, Gottrand F. Late-onset complications of
percutaneous endoscopic gastrostomy in children. J Pediatr Gastroen terol Nutr. 2001;33(4):495–500.
125. Venu RP, Brown RD, Pastika BJ, Erikson LW. The buried bumper syndrome: a simple management
approach in two patients. Gastrointest Endosc. 2002;56(4):582–584.
126. Walton GM. Complications of percutaneous gastrostomy in patients with head and neck cancer—an analysis
of 42 consecutive patients. Ann R Coll Surg Engl. 1999;81(4):272–276.
127. Ma MM, Semlacher EA, Fedorak RN, et al. The buried gastrostomy bumper syndrome: prevention and
endoscopic approaches to removal. Gastrointest Endosc. 1995;41(5): 505–508.
128. Boyd JW, DeLegge MH, Shamburek RD, Kirby DF. The buried bumper syndrome: a new technique for safe,
endoscopic PEG removal. Gastrointest Endosc. 1995;41(5):508–511.
129. Cruz I, Mamel JJ, Brady PG, Cass-Garcia M. Incidence of abdominal wall metastasis complicating PEG tube
placement in untreated head and neck cancer. Gastrointest Endosc. 2005;62(5):708–711.
130. McSweeney ME, Kerr J, Jiang H, Lightdale JR. Risk factors for complications in infants and children with
percutaneous endoscopic gastrostomy tubes. J Pediatr. 2015;166:1514–1519.
131. Suksamanapun N, Mauritz FA, Franken J, van der Zee DC, Herwaarden-Lindeboom MY. Laparoscopic
versus percutaneous endoscopic gastrostomy placement in children: results of a systematic review and meta-
analysis. J Minim Access Surg. 2017;13(2):81–88. doi:10.4103/0972-9941.181776.
132. Aumar M, Lalanne A, Guimber D, et al. Influence of percutaneous endoscopic gastrostomy on
gastroesophageal reflux disease in children. J Pediatr. 2018;197:116–120.
133. Onwubiko C, Weil BR, Bairdain S, et al. Primary laparoscopic gastrojejunostomy tubes as a feeding
modality in the pediatric population. J Pediatr Surg. 2017;52:1421–1425.
134. Maple J, Baron T, Petersen B. The frequency, severity, and spectrum of adverse events associated with direct
percutaneous endoscopic jejunostomy (DPEJ). Gastrointest Endosc. 2005;61(5):AB80.
135. Kim CY, Engstrom BI, Horvath JJ, et al. Comparison of primary jejunostomy tubes versus
gastrojejunostomy tubes for percutaneous enteral nutrition. J Vasc Int Radiol. 2013; 24(12):1845–1852.
136. Dandeles LM, Lodolce AE. Efficacy of agents to prevent and treat enteral feeding tube clogs. Ann
Pharmacother. 2011;45(5):676–680.
137. Lord L. Maintaining hydration and tube patency in enteral tube feedings. Safe Pract Patient Care.
2012;592:1, 5–11.
138. Arriola TA, Hatashima A, Klang MG. Evaluation of extended-release pancreatic enzyme to dissolve a clog.
Nutr Clin Pract. 2010;25(5):563–564.
139. Fisher CB, Blalock B. Clogged feeding tubes: a clinician’s thorn. Pract Gastroenterol. 2014;38:16–22.
140. Marcuard SP, Stegall KS. Unclogging feeding tubes with pancreatic enzyme. JPEN J Parenter Enteral Nutr.
1990;14(2): 198–200.
141. Marcuard SP, Stegall KL, Trogdon S. Clearing obstructed feeding tubes. JPEN J Parenter Enteral Nutr.
1989;13(1):81–83.
142. Lazar J. Treatment of feeding tube occlusions [abstract]. Nutr Clin Pract. 2011;26(1):94–102.
143. Boullata JI. Drug administration through an enteral feeding tube. Am J Nurs. 2009;109(10):34–43.
 CHAPTER 4

Enteral Formulas for Adult Patients

Introduction
This chapter reviews the composition of enteral formulas, applications of enteral nutrition (EN) formulas in clinical
practice, the rationale for the use of specialized formulas in adult patient care, and the development of an enteral
product formulary. The focus of this chapter is EN for adult patients, although the general information on formula
composition, food allergies and intolerances, and developing an enteral product formulary is also applicable in the
pediatric setting. Pediatric and infant formulas are discussed in greater depth in Chapter 5.
Today, more than 100 enteral formulas are available in the United States. These products vary greatly with
respect to concentration, macronutrient and micronutrient composition, fiber content, and elements proposed to
support immune function. Table 4-1 reviews terms commonly used to classify EN formulas.

TABLE 4-1. Terms Commonly Used in the Classification of Enteral Formulas

Term Definition
Standard or polymeric formula Formula containing intact macronutrients.
Type of tube feeding used for patients who cannot tolerate
semisynthetic formulas or who wish to consume whole foods.
BTFs are formulated with a mixture of blenderized
Blenderized tube feeding (BTF) food sources, with or without the addition of commercial
enteral formula. They are recommended for patients with a
healed feeding site and for those who adhere to recipe
instructions, food safety practices, and tube maintenance.
Formula containing partially or completely hydrolyzed
Elemental and semi-elemental formula
nutrients to maximize nutrient absorption.
A formula used for patients with an organ dysfunction or a
Disease-specific formula
specific metabolic condition.
Product used for supplementation, to create a formula, or to
Modular
add to nutrient content of a formula.

Federal Regulations
Under federal law, enteral formulas are not considered drugs or conventional foods. Instead, they are categorized as
medical foods. A medical food is defined in the 1988 Orphan Drug Act as follows:1
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 requirements, based on recognized scientific principles, are established by
medical evaluation.

Manufacturers can include “structure and function” claims about enteral formulas on product labels without the
approval of the US Food and Drug Administration. Enteral formulas are also not required to meet Nutrition Facts
labeling requirements mandated for conventional foods.2 As discussed in Chapter 5, federal regulation of infant
formulas is more stringent.

Formula Selection Algorithm

Limited direct data are available regarding the efficacy and outcomes associated with the use of specific enteral
formulas. This lack of efficacy data makes it challenging for nutrition support clinicians to select the best enteral
formula for an individual patient. Figure 4-1 is an algorithm that clinicians may use to select formulas for adult
patients.3 It may be used when EN is first initiated or as the EN prescription is reevaluated throughout the patient’s
medical care.

Formula Composition
Most enteral formulas are complete nutrition, containing macro-and micronutrients in proportions to meet the
nutrient requirements of most patients. See Table 4-2 for common macronutrient sources in EN formulas.

TABLE 4-2. Macronutrient Sources in Enteral Formulas

Macronutrient Polymeric Formula Hydrolyzed Formula

• Corn syrup solids
• Hydrolyzed cornstarch • Cornstarch
• Maltodextrin • Hydrolyzed cornstarch
Carbohydrate
• Sucrose • Maltodextrin
• Fructose • Fructose
• Sugar alcohols
• Casein
• Sodium, calcium, magnesium, • Hydrolyzed casein
 and potassium caseinates • Hydrolyzed whey protein
Protein • Soy protein isolate • Crystalline L-amino acids
• Whey protein concentrate • Hydrolyzed lactalbumin
• Lactalbumin • Soy protein isolate
• Milk protein concentrate

• Borage oil
• Canola oil
• Corn oil • Fatty acid esters
• Fish oil • Fish oil
• High-oleic sunflower oil • Medium-chain triglycerides
• Medium-chain triglycerides • Safflower oil
Fat
• Menhaden oil • Sardine oil
• Mono- and diglycerides • Soybean oil
• Palm kernel oil • Soy lecithin
• Safflower oil • Structured lipids
• Soybean oil
• Soy lecithin

Carbohydrate
Carbohydrate is the primary macronutrient and principal energy source in most enteral formulas. Carbohydrate
typically supplies 28% to 90% of the energy in enteral formulas, and it contributes to the osmolality, digestibility,
and sweetness of the formula.4 Most formulas contain oligosaccha-rides or polysaccharides. Polymeric formulas use
primarily corn syrup solids as their source of carbohydrate, whereas hydrolyzed formulas use maltodextrin or
hydrolyzed cornstarch.4,5 Oral products contain simpler or less-complex carbohydrates such as sucrose to increase
the palatability of the product. Because of the prevalence of lactose intolerance, most adult formulas do not contain
lactose.5

Fiber
Fiber is added to some enteral formulas. When selecting an enteral formulation for a patient, it is important to note
whether the product is supplemented with soluble or insoluble fiber. Most formulations contain a combination of
both soluble and insoluble fiber. Soluble fiber is fermented by the gut microbiota in the distal intestine to produce
short-chain fatty acids (SCFAs). SCFAs are a source of energy for colonocytes, help increase intestinal mucosal
growth, and may help control diarrhea by increasing sodium and water absorption.5 Insoluble fiber is not effectively
fermented by the gut microbiota, but it may help to decrease transit time by increasing fecal weight.5
Some enteral formulas contain prebiotic fibers, fructooligosaccharides (FOS), and inulin. These products may
provide benefits to some patients by promoting growth of beneficial bacteria in the distal bowel to produce SCFAs.6
The patient’s tolerance of fiber-supplemented enteral formulas should be monitored closely, particularly in
critically ill patients. Cases of bowel obstruction from the use of these formulas have been reported.7,8 For patients
who are critically ill and at risk for bowel ischemia (eg, in cases of hemodynamic instability or vasopressor therapy),
administering a fiber-free formula may be a safer option.9,10
A number of clinical studies have examined the effects of fiber-containing formulas on gut function; their
findings have been inconsistent. A meta-analysis confirmed that the incidence of enteral feeding–related diarrhea is
reduced by the inclusion of fiber into enteral diets.11 However, when intensive care unit (ICU) and non-ICU patients
were analyzed separately, no differences in the incidence of diar-rhea were shown in ICU patients. Mixed-fiber
formulas were found to be better tolerated than single-fiber types of formulas. The same review found that fiber may
also speed up transit time, increase fecal bulk, reduce constipation, and improve gut barrier function through the
stimulation of colonic bacteria in both healthy volunteers and hospitalized patients.11 See Table 4-3 for practice
recommendations on managing diarrhea with fiber.10,12
 TABLE 4-3. Practice Recommendations: Managing Diarrhea with Fibera

AND Evidence Analysis Library recommendations:

• Diarrhea may be reduced in the adult critically ill patient when guar gum is included in the EN
regimen (Grade II, fair).
• The impact of other types of fiber on reducing diarrhea is unclear due to variations in the fiber
combinations and amounts used in studies (Grade II, fair).
SCCM/ASPEN recommendations:
• We suggest that EN not be automatically interrupted for diarrhea but rather that feeds be continued
while evaluating the etiology of diarrhea in an ICU patient to determine appropriate treatment (expert
consensus).
• Consider use of a commercial mixed-fiber-containing formulation if there is persistent diarrhea
(expert consensus).
• Avoid both soluble and insoluble fiber in critically ill patients at high risk for bowel ischemia or
severe dysmotility (expert consensus).
• Consider 10-20 g of a fermentable soluble fiber supplement given in divided doses over 24 hours
as adjunctive therapy if there is evidence of diarrhea (expert consensus).
Abbreviations: AND, Academy of Nutrition and Dietetics; ASPEN, American Society for Parenteral and Enteral Nutrition; EN, enteral nutrition;
ICU, intensive care unit; SCCM, Society of Critical Care Medicine.
a
Refer to the original sources for guidance on evidence grading.
Source: Adapted from references 10 and 12.

Fat
The fat component of enteral formulas is a concentrated source of energy and a source of essential fatty acids (ie,
linoleic acid and linolenic acid). Long-chain triglycerides (LCTs) and medium-chain triglycerides (MCTs) may be
found in enteral formulas. Corn and soybean oil are the most common sources of LCTs; safflower, canola, and fish
oils are also used in enteral formulas.4,5
Palm kernel and coconut oil may be included in enteral formulas as a source of MCTs. MCTs are absorbed in the
portal circulation and do not require chylomicron formation. MCTs are cleared from the bloodstream rapidly, and,
once in the cell, they can cross the mitochondrial membrane for oxidation without the need for carnitine.5 How-ever,
MCT oil provides no essential fatty acids; therefore, most enteral formulas contain a mixture of LCT and MCT.
Some enteral formulas contain structured lipids as their fat source. Because structured lipids feature a mixture of
long-chain fatty acids (LCFAs) and medium-chain fatty acids (MCFAs) on the same glycerol molecule, they offer
the advantages of MCFAs and include enough LCFAs to meet essential fatty acid needs.
Some enteral formulas have been designed with an altered ratio of ω-6 to ω-3 fatty acids to include more ω-3
fatty acids. The rationale is that ω-3 fatty acids are metabolized to prostaglandins of the 3 series and leukotrienes of
the 5 series, which have anti-inflammatory properties, whereas ω-6 fatty acids are metabolized to prostaglandins of
the 2 series and leukotrienes of the 4 series, which tend to be proinflammatory and immunosuppressive.4

Protein
Protein is a source of nitrogen and energy in enteral formulas. Enteral formulas may contain intact protein, hydro-
lyzed protein, or free amino acids.5
Intact protein refers to whole protein or protein isolates. Casein and soy protein isolates are the most commonly
used types of intact protein. Lactalbumin, whey, and egg albumin are also sources of intact protein. Formulas with
intact protein require normal levels of pancreatic enzymes for digestion and absorption.
Formulas with hydrolyzed protein, small peptides, dipep-tides and tripeptides, and free amino acids are referred
to as semi elemental or elemental formulas.4 These types of formulas are intended for patients with malabsorption,
pancreatic dysfunction, or prolonged bowel rest following major abdominal surgery or other evidence of
gastrointestinal (GI) dysfunction.

Vitamins and Minerals

Most adult enteral formulas provide adequate amounts of vitamins and minerals to meet the Dietary Reference
Intakes (DRIs) when provided in volumes of 1000 to 1500 mL/d. However, some disease-specific enteral formulas
may have amounts of specific vitamins and minerals that are higher or lower than the DRI.5 When considering the
adequacy of micronutrients in the individualized EN prescription, it is important to assess the amount of vitamins
and minerals being provided by all sources of nutrition relative to the needs of the specific patient.3 It is the
clinician’s responsibility to carefully evaluate the products available in the formulary to select the most appropriate
EN formula to avoid adverse clinical outcomes associated with inadequate or excessive micronutrient intakes.

Water
Adult enteral formulas contain roughly 70% to 85% water by volume.13,14 In general, the more energy dense the
formula is, the less water it contains.
Enteral formulas are not intended to meet the patient’s fluid needs. When calculating the patient’s total fluid
intake, only the volume of water in the formula is considered. For example, if a formula is 75% water by volume,
1000 mL of formula would count as 750 mL of fluid. Most patients receiving EN require an additional source of
water to meet their hydration needs. Supplemental free water is often provided through the feeding tube as flushes
for hydration and to maintain feeding tube patency. Intravenous (IV) fluids must be accounted for and adjusted as
required while a patient is receiving EN. Chapter 6 presents sample calculations for determining the contributions of
enteral formula and flushes to daily fluid goals.

Osmolality
Osmolality is the concentration of free particles, molecules, or ions in a given solution, and it is expressed as
milliosmoles per kilogram of water (mOsm/kg).15 The osmolality of adult enteral formulas typically ranges from 280
to 875 mOsm/kg.4
Hypertonic enteral formulas (osmolality >320 mOsm/kg) have frequently been blamed for problems related to
formula intolerance (eg, diarrhea). However, the osmolality of an enteral formula has little to do with formula
tolerance. GI tolerance or diarrhea is often related to the severity of illness, comorbid conditions, or the concomitant
use of hypertonic medications administered through the enteral access device.16 Some items included in clear and
full liquid diets routinely used by hospitalized patients, as well as many medications, are more hyperosmolar than
enteral formulas. Refer to Chapter 9 for further information on enteral feeding complications and tolerance.

Food Allergies and Intolerances

To minimize the risk for adverse reactions to ingredients in enteral formulas, it is important that the patient undergo
a comprehensive nutrition assessment, including evaluation of any reports of food allergies or intolerances in the
medical records or diet history (see Chapter 1). True food allergies involve an adverse immune system response to a
food protein.17 In the United States, about 4% of adults and 5% of children have food allergies.18 Food intolerances,
such as lactose intolerance, are adverse reactions to foods that do not involve the immune system.17
Most enteral formulas do not contain gluten or lactose. However, they may contain common allergens such as
egg, corn, casein, whey, or soy. The Food Allergen Labeling and Consumer Protection Act (FALCPA) of 2004,
which applies to medical foods (including enteral formulas), requires that the label of a food that contains an
ingredient that is or contains protein from a “major food allergen” declare the presence of the allergen in the manner
described by the law.2 FALCPA identifies 8 foods or food groups as the major allergens: milk, eggs, fish, crustacean
shellfish, tree nuts, peanuts, wheat, and soybeans.
Manufacturers periodically change ingredients in formulas. When selecting EN for patients with food allergy or
food intolerance, the clinician should always refer to the most recent product label.

Formulas for Specific Diseases or Conditions

Specialized formulas cover a wide range of formulas designed for a variety of clinical scenarios. Some are intended
for patients with specific disease states such as acute kidney injury (AKI), diabetes, hepatic disease, or pulmonary
disease. Others are marketed for use in hypermetabolic disease and inflammatory states such as those occurring in
critical illness.

The brand names mentioned in this chapter do not constitute a comprehensive list of all relevant products on the
market in the United States or other countries. Mention of a product does not imply an endorsement.
Manufacturers periodically introduce, withdraw, and alter products. Before using any product, nutrition
support clinicians should review the label and product website for current information on ingredients, nutrient
composition, and instructions for use. If those resources are insufficient, contact the manufacturer or the
formulary manager for additional information. Selected manufacturer websites are listed at the end of the
chapter.

Gastrointestinal Disorders and Malabsorption

Elemental and semi-elemental formulas have partially or completely hydrolyzed macronutrient content and are
designed for patients with known GI disorders or for those who exhibit signs and symptoms of intolerance to
standard polymeric formulas.4–6 Before assuming that a patient cannot tolerate a formula, nutrition support clinicians
should thoroughly investigate the etiology of a patient’s diarrhea or malabsorption (ie, assess types and formulations
of medications, mode of EN delivery, and possible infectious causes).10 See Chapter 9 for additional information on
diarrhea and other complications of EN.
Elemental and semi-elemental formulas may be useful in patients with malabsorption, pancreatic dysfunction, or
prolonged bowel rest following major abdominal surgery (see Table 4-4 for examples of these products). In these
products, carbohydrate is included as hydrolyzed cornstarch, maltodextrin, or fructose; protein is provided as
hydrolyzed casein, hydrolyzed whey, soy protein isolate, or crystalline amino acids; and lipids are from fatty acid
esters or MCTs.

TABLE 4-4. Selected Enteral Formulas Marketed for Use in Gastrointestinal Disorders and
Malabsorption

Product Manufacturer
Peptamen Nestlé
Peptamen 1.5 Nestlé
Peptamen 1.5 with Prebiol Nestlé
Peptamen AF Nestlé
Peptamen Intense VHP Nestlé
Peptamen with Prebiol Nestlé
Tolerex Abbott
Vital 1.0 Cal Abbott
Vital 1.5 Cal Abbott
Vital AF 1.2 Cal Abbott
Vital High Protein Abbott
Vital Peptide 1.5 Cal Abbott
Vivonex Plus Nestlé
Vivonex RTF Nestlé
Vivonex T.E.N. Nestlé
The brand names mentioned in this table may not constitute a comprehensive list of all relevant products on the market in the United States
or other countries. Mention of a product does not imply an endorsement.

The use of peptide-based formulas has not been extensively evaluated, and available findings are inconsistent.
Two studies found that the incidence of diarrhea was reduced by using a peptide-based formula,19,20 but other studies
found that the frequency of diarrhea increased or stayed the same following the change to a peptide-based
formula.21,22 A few of these elemental and semi-elemental formulations also contain components such as ɷ-3 fatty
acids, glutamine, and prebiotics such as FOS and inulin.4 A small, prospective randomized pilot study found
significantly fewer days with adverse events and undesired GI complications using a specialized peptide-based
formula containing ɷ-3 fatty acids compared to a standard polymeric formula.23 Further research is warranted on the
efficacy of specialized formulas for GI disorders containing added components such as prebiotics and ɷ-3 fatty
acids. See Table 4-5 for practice recommendations on formula selection for critically ill patients with GI disorders
and malabsorption.10

TABLE 4-5. Practice Recommendations: Enteral Formula Selection for Critically Ill Patients
with Gastrointestinal Disorders and Malabsorptiona

SCCM/ASPEN recommendations:
• Avoid the routine use semi-elemental or elemental formulas in critically ill patients because no clear
benefit to patient outcome has been shown in the literature (expert consensus).
• Consider use of small-peptide formulas in the patient with persistent diarrhea, with suspected
malabsorption or lack of response to fiber (expert consensus).
Abbreviations: ASPEN, American Society for Parenteral and Enteral Nutrition; SCCM, Society of Critical Care Medicine.
a
Refer to the original article for guidance on evidence grading.
Source: Adapted from reference 10.

Wound Healing
Wound healing is a complex process that involves a cascade of events to repair and heal damaged tissue. Enteral
formulas marketed for oral intake or tube feeding in patients with wounds or pressure injuries contain a combination
of nutrients that are thought to aid the healing process (see Table 4-6). Energy; protein; vitamins A, C, and E; zinc;
copper; iron; and arginine have all been linked to the wound-healing process.24 Several studies demonstrate that
malnutrition adversely affects wound healing and adequate nutrition is required for healing to occur.25,26

TABLE 4-6. Selected Enteral Formulas Marketed for Use in Wound Healing

Product Manufacturer
Impact® Nestlé
Impact® Peptide 1.5 Nestlé
®
Replete Nestlé
Replete with Fiber® Nestlé
®
Perative Abbott
®
Pivot 1.5 Cal Abbott
Promote® Abbott
®
Promote with Fiber Abbott
The brand names mentioned in this table may not constitute a comprehensive list of all relevant products on the market in the United States
or other countries. Mention of a product does not imply an endorsement.
 A meta-analysis by Cereda and colleagues found that individuals with pressure injuries expended more energy
compared with controls and were usually characterized as having negative nitrogen balance.27 For adults with a
pressure injury who are identified as being at risk for malnutrition, the National Pressure Ulcer Advisory Panel
(NPUAP) recommends an energy goal of 30–35 kcal per kg body weight per day.24 The NPUAP practice guidelines
also recommend that energy intake be adjusted based on a patient’s weight change or level of obesity, and that
individuals who have had significant unintended weight loss may need additional energy intake.24
Protein is vital for growth and maintenance of cells, promotion of positive nitrogen balance, and provision of
structure. All stages of wound healing require adequate protein for wound closure, and increased protein levels have
been linked to improved healing rates.26,28 For adults with existing pressure injury, as well as those at risk for
pressure injury and malnutrition, NPUAP recommends providing 1.25 to 1.5 g protein per kg body weight per day.24
Reassessment of a patient’s protein requirement is recommended as the patient’s condition changes.24
A 2014 systematic review concluded that research on nutrition supplements enriched with various nutrients to
promote wound healing should be interpreted with caution because the studies were small, included heterogeneous
populations with high dropout rates, and examined various types of oral nutrition supplements.29 The authors noted
that this conclusion should not be interpreted to mean that nutrition interventions have no effect on pressure injury
healing; to the contrary, they emphasized that individuals at risk for malnutrition and those identified as
malnourished should receive nutrition interventions based on a nutrition assessment.
Another systematic review, published in 2017, evaluated 3 studies on the use of formulas enriched with arginine,
zinc, and antioxidants as oral supplements and tube feedings. The authors of this review found that, compared with
control interventions, the use of these formulas was associated with significantly higher reduction in pressure injury
area; also, a higher proportion of patients using the formulas had a 40% or greater reduction of pressure injury size
at 8 weeks when compared with controls.30

Diabetes/Glucose Intolerance
Enteral formulas designed for glucose intolerant patients typically contain less carbohydrate (33% to 40% of total
energy) and more fat (44% to 49% of total energy) than a standard polymeric formula; diabetes-specific formulas
also include 14 to 15 g fiber per liter.31,32 These formulas are based on the premise that the reduced carbohydrate
content, greater amount of fat (particularly monounsatu-rated fats), and inclusion of fiber will result in better
glycemic control. However, the American Diabetes Association (ADA) no longer recommends specific percentages
of macronutrients for the hospitalized patient.33
Table 4-7 lists selected formulas marketed for use in patients with diabetes or glucose intolerance. These
formulas may contain pureed foods, arginine, ω-3 fatty acids, or fructose; they may also be high in monounsaturated
fats with reduced amounts of saturated fat. Diabetes-specific products tend to be more costly than standard formulas.

TABLE 4-7. Selected Enteral Formulas Marketed for Use in Patients with Diabetes or Glucose
Intolerance

Product Manufacturer
®
Diabetisource Nestlé
Glucerna® Abbott
Glytrol® Nestlé
The brand names mentioned in this table may not constitute a comprehensive list of all relevant products on the market in the United States
or other countries. Mention of a product does not imply an endorsement.

Recommendations about the use of specialized formulas for patients with diabetes or glucose intolerance are
varied (see Table 4-8). The Society of Critical Care Medicine/American Society of Parenteral and Enteral Nutrition
(SCCM/ASPEN),10 American College of Gastroenterology (ACG),34 and the Canadian Clinical Practice Guidelines
(CPG) for Nutrition Support in the Mechanically Ventilated, Critically Ill Adult35 from the Clinical Evaluation
Research Unit in Kingston, Ontario, oppose their use, whereas ADA33 is supportive.
 TABLE 4-8. Practice Recommendations: Enteral Formula Selection for Patients with Diabetesa

SCCM/ASPEN recommendations (critically ill patients):

• Use a standard polymeric formula when initiating EN in ICU (expert consensus).
• Avoid routine use of all specialty formulas (expert consensus).
ACG recommendations (hospitalized patients):
• A standard polymeric or high-protein standard formula should be routinely used in the hospitalized
patient requiring EN (conditional recommendation, very low level of evidence).
• Routine use of disease-specific formulas (diabetes) is discouraged (conditional recommendation,
very low level of evidence).
ADA recommendations (hospitalized patients with diabetes):
• Diabetes-specific formulas appear to be superior to standard formulas in controlling postprandial
glucose, A1C, and insulin response.
CPG recommendations (critically ill patients):
• Data are insufficient to recommend high fat/low CHO enteral nutrition for critically ill patients.
Abbreviations: A1C, hemoglobin A1C; ACG, American College of Gastroenterology; ADA, American Diabetes Association; ASPEN, American
Society for Parenteral and Enteral Nutrition; CHO, carbohydrate; CPG, Canadian Clinical Practice Guidelines; EN, enteral nutrition; ICU,
intensive care unit; SCCM, Society of Critical Care Medicine.
a
Refer to the original sources for guidance on evidence grading.
Source: Adapted from references 10 and 33-35.

The differences in recommendations are at least partly explained by the distinctive missions of the organizations
that published them; also, the recommendations do not all focus on the same target populations. Guidelines from
SCCM/ASPEN and CPG are for critically ill patients.10,35 Hospitalized patients are the target for the ACG
guidelines,34 which were derived from those developed for critically ill patients. ADA guidelines are for hospitalized
patients with diabetes.33
Based on expert consensus, SCCM/ASPEN guidelines recommend avoiding the routine use of most specialty
formulas, including diabetes-specific products, in critically ill patients, citing the lack of benefit in patient
outcomes.10 The ACG guideline for hospitalized patients is identical to that from SCCM/ASPEN, stating that routine
use of disease-specific (ie, diabetes-specific) enteral formulas should be avoided.34
Having identified only 3 studies for evaluation, the CPG guideline states that data are insufficient to recommend
high-fat, low-carbohydrate enteral formulas.35 Notably, the objective of the CPG was not to evaluate the
effectiveness of diabetes-specific formulas but to determine the impact of high-fat, low-carbohydrate pulmonary
enteral formulas in reducing ventilator days in critically ill patients. However, a study involving a diabetes-specific
formula was part of the analysis for this guideline, and that study showed better glycemic control with the diabetes-
specific product. On the other hand, the diabetes-specific formula did not alter clinical outcomes (mortality,
infections, intensive care length of stay, and number of ventilator days). Consequently, CPG notes that glycemic
control may be better in critically ill patients who receive a diabetes-specific formula.35
For hospitalized patients with diabetes requiring EN, ADA recommends the use of diabetes-specific enteral
formulas, rather than standard enteral formulas, for better control of postprandial glucose, hemoglobin A1C
(HbA1C), and insulin response. In support of this recommendation, ADA references the results of several meta-
analyses evaluating the effects of diabetes formulas compared with standard products in individuals with diabetes.33
For example, ADA considered an early (2005) meta-analysis, in which diabetes formulas were identified as
those containing >60% fat, monounsaturated fatty acids, fructose, and fiber; this review demonstrated improved
glycemic control with these specialty formulas.36 However, it is difficult to apply the findings of this meta-analysis
to present-day EN therapy because the current diabetes-specific formulas have a lower fat content (44%–49%).
ADA also cited a 2014 systematic review by Ojo and Brooke of 5 studies comparing diabetes-specific vs
standard formulas in patients with diabetes.37 The authors found that use of diabetes-specific formulas resulted in
improved post-prandial glucose, HbA1c, and insulin response. However, it is difficult to cite these findings to
support the use of diabetes-specific enteral formulas for patients with diabetes because the studies evaluated in this
meta-analysis had only a few tube-fed patients (n = 46) and these patients had varying degrees of severity of illness
while using all feeding administration methods (bolus, intermittent, and continuous feeding).37
The ADA recommendation for diabetes-specific enteral formulas does not note any clinical benefit for the
patient with diabetes other than improved glycemic control.33 How-ever, in studies cited by ADA, hyperglycemia
persisted, albeit at lower levels, when diabetes-specific formulas were used.33,38–40 In patients with diabetes who
received standard formulas, blood glucose levels were 172.8–223.2 mg/dL vs 156.6–176.4 mg/dL in patients
receiving the diabetes-specific products.38–40 Although these findings were statistically significant, the decline in
blood glucose levels associated with diabetes-specific formulas may not be sufficient enough to substantially alter
clinical treatment of hyperglycemia in the hospitalized patient. Insulin therapy remains the best way to control
hyperglycemia in the hospitalized patient.33,41
Research continues to examine the effectiveness of diabetes-specific enteral formulas. Although recent studies
have associated diabetes-specific enteral formulas with improvement in glycemic control, the conclusions in each
case are not generalizable due to the limitations of the study designs.42–44 Well-designed research is needed to
evaluate the role of EN and diabetes-specific formulas on the management, clinical outcomes, and quality of life of
malnourished patients with diabetes or with stress-induced hyperglycemia.
Because there is insufficient evidence to support the routine use of diabetes-specific formulas, it is appropriate to
start with a standard enteral formula while closely monitoring the patient’s blood glucose levels and using insulin as
needed for glycemic control. If glycemic control is difficult to achieve with a standard formula, then a diabetes-
specific formula may be tried; however, hyperglycemia may arise from multiple etiologies, and as noted above,
insulin is the preferred treatment.

Hepatic Failure
Enteral formulas marketed for use in patients with liver disease (Table 4-9) have increased amounts of branched-
chain amino acids (BCAAs). They also have reduced amounts of aromatic amino acids (AAAs), total protein,
sodium, and fluid.

TABLE 4-9. Selected Enteral Formula Marketed for Use in Patients with Hepatic Failure

Product Manufacturer
®
NutriHep Nestlé
The brand name mentioned in this table may not be the only relevant product on the market in the United States or other countries.
Mention of a product does not imply an endorsement.

In persons with cirrhosis, concentrations of AAAs (phenylalanine, tyrosine, and tryptophan) are increased due to
impaired metabolism, and concentrations of BCAAs (valine, leucine, and isoleucine) are decreased because BCAAs
are used for glutamine synthesis, which is needed as a source of energy.45 AAAs compete with BCAAs at the blood-
brain barrier, and that leads to a greater number of false neurotransmitters that stimulate additional ammonia
production. Development of hepatic enteral formulas is based on the concept that restoration of the plasma BCAA-
to-AAA ratio would reduce hepatic encephalopathy (HE) and restore muscle mass.46
Guidelines for the use of hepatic formulas vary, depending on the target patient population of the guidelines and
the desired outcomes to be achieved by the guidelines (see Table 4-10).10,34,47 Lactulose and antibiotics can be
effective treatments for persons with HE. For this reason, SCCM/ASPEN and ACG do not recommend using
BCAA-containing enteral formulas for HE patients.10,34 The American Association for the Study of Liver Diseases
does not support protein restriction in patients with cirrhosis because a chronic inflammatory state is associated with
that condition.47

TABLE 4-10. Practice Recommendations: Enteral Formula Selection for Patients with Hepatic
Failurea

SCCM/ASPEN recommendations (critically ill patients):

 • Use standard polymeric formula in ICU patients with acute and chronic liver disease (expert
consensus).
• There is no evidence of further benefit of BCAA formulas on coma grade in the ICU patient with HE
who is already getting luminal antibiotics and lactulose (expert consensus).
AASLD recommendations (patients with HE in chronic liver failure):
• Daily protein intake should be 1.2-1.5 g/kg/d (Grade I, A, strong recommendation).
• Oral BCAA supplementation may allow recommended nitrogen intake to be achieved and
maintained in patients with HE who are intolerant of dietary protein (Grade II-2, B, weak
recommendation).
• Oral BCAA supplementation can be used as an alternative or additional agent to treat patients
nonresponsive to conventional therapy (Grade I, B, weak recommendation).
ACG recommendations (hospitalized patients):
• A standard polymeric or high-protein standard formula should be routinely used in the hospitalized
patient requiring EN (conditional recommendation, very low level of evidence).
• Routine use of organ-specific formulas (hepatic) is discouraged (conditional recommendation, very
low level of evidence).
Abbreviations: AASLD, American Association for the Study of Liver Diseases; ASPEN, American Society for Parenteral and Enteral Nutrition;
BCAA, branch-chained amino acid; EN, enteral nutrition; HE, hepatic encephalopathy; ICU, intensive care unit; SCCM, Society of Critical
Care Medicine.
a
Refer to the original sources for guidance on evidence grading.
Source: Adapted from references 10, 34, and 47.

Persons with hepatic dysfunction will likely tolerate a standard, polymeric enteral formula. A fluid-restricted
formula may be needed if the patient has ascites or edema. If HE is refractory to medical treatment (eg, lactulose,
rifaximin), a trial of a hepatic formula may be warranted, but prolonged use of hepatic formulas could worsen
malnutrition because these products are low in protein. Nutrition support clinicians must weigh benefits, costs, and
efficacy to determine whether a hepatic formula would be a good option.3

Immune-Enhancing Nutrition
Enteral formulas marketed as immune-enhancing or immune-modulating nutrition contain supplemental amounts of
L-arginine, nucleotides, ω-3 fatty acids, and/or antioxidants in addition to nutrient substrates essential for general
nutrition and metabolism (see Table 4-11 for selected products). The goal of immune-enhancing formulas is not only
to provide sufficient nutrition but also to modulate immunity during stress in specific patient populations. These
formulas vary considerably in composition. Immune-enhancing formulas are the most studied of the specialty
enteral formulas; however, the studies lack uniformity in patient populations, formulas studied, and outcomes
measured, thus making it difficult to develop recommendations for use.

TABLE 4-11. Selected Enteral Formulas Marketed as Immune-Enhancing Products

Product Manufacturer
®
Impact Nestlé
Impact® Peptide 1.5 Nestlé
®
Perative Abbott
®
Pivot 1.5 Cal Abbott
The brand names mentioned in this table may not constitute a comprehensive list of all relevant products on the market in the United States
or other countries. Mention of a product does not imply an endorsement.
Specific immune-modulating nutrients have unique roles during stress and trauma (see Table 4-12).48 Argi-nine
and glutamine are nonessential amino acids under normal circumstances, but they become essential during stress
because the demand for them increases and exceeds endogenous supplies.48 Compared with ω-6 fatty acids, ω-3 fatty
acids produce fewer inflammatory prostaglandins and leukotrienes. When consumed, ω-3 fatty acids replace ω-6
fatty acids in cellular membranes, which reduces inflammation during stress.48

TABLE 4-12. Functions of Immunonutrients

Immunonutrient Functions
• T-cell lymphocyte proliferation and function
• Proline synthesis for wound healing
Arginine
• Substrate for nitric oxide production for blood circulation
and vascular tone
• Primary fuel for small bowel, lymphocytes, and
macrophages
Glutamine • Gluconeogenesis
• Heat shock protein induction to modulate inflammation
and oxidation at cellular level
• Bases of RNA, DNA, ATP, and other dinucleotides
Nucleic acids
• Cellular proliferation and immunity
(ω-3 fatty acids (EPA, DHA) • Reduction in inflammation
Abbreviations: ATP, adenosine triphosphate; DHA, docosahexaenoic acid; DNA, deoxyribonucleic acid; EPA, eicosapentaenoic acid; RNA,
ribonucleic acid.
Source: Adapted from reference 48.

Table 4-13 reviews guidelines regarding the use of immune-enhancing nutrition.10,34,35 The rationales for the
guidelines are based on evidence of reduced infection, shortened length of stay, and potential harm associated with
immune-enhancing nutrition.
SCCM/ASPEN suggest using immune-enhancing nutrition containing at least arginine and fish oil in patients
with severe trauma, those with traumatic brain injury, and postoperative surgical ICU patients who had major
surgery.10 Routine use of immune-enhancing nutrition in the medical ICU or patients with severe sepsis is not
suggested by SCCM/ASPEN because studies do not show clinical benefits.10
The guidelines from ACG are similar to those of SCCM/ASPEN. Immune-enhancing formulations containing
arginine and fish oil should be used for patients who have had major surgery and are in a surgical ICU setting but
not routinely used for patients in the medical ICU.34
Formulations containing arginine could worsen hemo-dynamic instability in a septic patient because arginine is a
precursor of nitric oxide. This is the rationale for the guideline from CPG against the routine use of EN with arginine
in critically ill patients.35 However, CPG does not extend this recommendation to the elective surgery patient
population.
As noted in Table 4-13, guidelines also exist for EN with glutamine and antioxidants. Because these
immunonutrients are in products in various amounts and in different combinations, it is difficult to develop
recommendations for their use. CPG does not recommend supplemental enteral glutamine because a large study
noted a trend toward a higher mortality rate in critically ill medical patients and a lack of benefit in reducing
infections.35 There is ongoing research to evaluate the effects of immune-enhancing nutrition in the pre-and
postoperative periods for various surgical procedures and also during certain disease states. Immune-modulating
formulas are probably most beneficial for the following patient populations: patients in the pre-and postoperative
periods who are having major elective surgery, critically ill postoperative patients, and those with severe trauma or
traumatic brain injury.
 TABLE 4-13. Practice Recommendations: Use of Immune-Enhancing Enteral Formulas in
Critically Ill Patientsa

SCCM/ASPEN recommendations:
• Immune-modulating enteral formulations (arginine with other agents, including EPA, DHA,
glutamine, and nucleic acid) should not be used routinely in MICU patients (very low quality of
evidence).
• Data are insufficient to recommend placing a patient with severe acute pancreatitis on immune-
enhancing formulation (very low quality of evidence).
• We suggest that immune-modulating formulations containing arginine and fish oil be considered in
patients with severe trauma (very low quality of evidence).
• We suggest the use of either arginine-containing immune-modulating formulations or EPA/DHA
supplement with standard enteral formula in patients with traumatic brain injury (expert consensus).
• We suggest the routine use of an immune-modulating formula (containing both arginine and fish oils)
in the SICU for the postoperative patient who requires EN therapy (moderate to low quality of
evidence).
• We suggest providing combinations of antioxidant vitamins and trace minerals in doses reported to
be safe for critically ill patients who require specialized nutrition support (low quality of evidence).
• We suggest supplemental enteral glutamine not be added to EN routinely in critically ill patients
(moderate quality of evidence).
• We suggest immune-modulating formulas not be routinely used in patients with severe sepsis
(moderate quality of evidence).
• No recommendation can be made regarding selenium, zinc, and antioxidant supplementation during
sepsis due to conflicting studies (moderate quality of evidence).
ACG recommendations:
• Immune-enhancing formulas containing arginine and fish oil should be used for patients who have
had major surgery and are in SICU (conditional recommendation, very low level of evidence).
• Immune-enhancing formulas containing arginine and fish oil should not be routinely used for patients
in MICU (conditional recommendation, very low level of evidence).
CPG recommendations:
• EN supplemented with arginine and other select nutrients is not recommended for critically ill
patients.
• EN supplemented with glutamine is not recommended for critically ill patients.
Abbreviations: ACG, American College of Gastroenterology; ASPEN, American Society for Parenteral and Enteral Nutrition; CPG, Canadian
Practice Guidelines; DHA, docosahexaenoic acid; EN, enteral nutrition; EPA, eicosapentaenoic acid; MICU, medical intensive care unit;
SCCM, Society of Critical Care Medicine; SICU, surgical intensive care unit.
a
Refer to the original sources for guidance on evidence grading.
Source: Adapted from references 10, 34, and 35.

Pulmonary Failure and Acute Respiratory Distress Syndrome

Table 4-14 lists selected enteral formulas marketed for use in patients with pulmonary failure or acute respiratory
distress syndrome (ARDS). The enteral formulas in this category are intended to help critically ill patients wean off
mechanical ventilation.

TABLE 4-14. Selected Enteral Formulas Marketed for Use in Patients with Pulmonary
Dysfunction
 Product Manufacturer
Nutren® Pulmonary Nestlé
Oxepa®a Abbott
Pulmocare® Abbott
The brand names mentioned in this table may not constitute a comprehensive list of all relevant products on the market in the United States
or other countries. Mention of a product does not imply an endorsement.
a
Marketed specifically for patients with acute respiratory distress syndrome.

Pulmonary failure–specific products are high in fat and low in carbohydrate content (55%–56% fat, 26%–28%
carbohydrate), which is supposed to reduce carbon dioxide production and respiratory quotient. However, as bedside
indirect calorimetry became available, it was theorized that excessive energy intake, not carbohydrate intake, may
have been contributing to excess carbon dioxide production. (Notably, excess carbon dioxide production can occur
in patients due to fever, thyrotoxicosis, increased catabolism that occurs with sepsis or use of steroids, exercise, or
metabolic acidosis without any correlation to nutrition intake.49) Also, the high ω-6 fatty acid contents of several
pulmonary formulas could worsen inflammation; the ratio of ω-6 fatty acids to ω-3 fatty acids is 4:1.31,32 Based on
these findings, as well as the high cost of specialty EN products, pulmonary failure–specific EN formulas are not
recommended (see Table 4-15).10,34,35

TABLE 4-15. Practice Guidelines: Formula Selection for Patients With Pulmonary Dysfunctiona

SCCM/ASPEN recommendations:
• Use a standard polymeric formula when initiating EN in the ICU setting (expert consensus).
• Avoid routine use of organ-specialty (pulmonary) formulas in critically ill patients in a MICU and
disease-specific formulas in the SICU (expert consensus).
• Specialty high-fat/low-carbohydrate formulas designed to manipulate respiratory quotient and reduce
CO2 should not be used in ICU patients with acute respiratory failure (very low quality of evidence).
• Fluid-restricted, energy-dense EN formula should be considered for patients with acute respiratory
failure (especially if in a state of volume overload) (expert consensus).
• We are unable to make a recommendation for routine use of an enteral formula characterized by an
antiinflammatory lipid profile (ω-3 fish oils, borage oil) and antioxidants in patients with ARDS and
severe ALI due to conflicting data (low to very low quality of evidence).
ACG recommendations:
• A standard polymeric or high-protein standard formula should be routinely used in the hospitalized
patient requiring EN (conditional recommendation, very low level of evidence).
• Routine use of organ-specific formulas (pulmonary) is discouraged (conditional recommendation,
very low level of evidence).
• We are unable to make a recommendation for nonarginine anti-inflammatory EN formulas in
ARDS/ALI due to conflicting results.
CPG recommendations:
• Unable to make a recommendation for high-fat/low-carbohydrate EN for critically ill patients due
to insufficient data.
• Use of EN with fish oils, borage oils, and antioxidants should be considered in patients with ALI and
ARDS.
ACG, American College of Gastroenterology; ALI, acute lung injury; ARDS, acute respiratory distress syndrome; ASPEN, American Society
for Parenteral and Enteral Nutrition; CO2, carbon dioxide; CPG, Canadian Clinical Practice Guidelines; EN, enteral nutrition; ICU, intensive
care unit; MICU, medical intensive care unit; SCCM, Society of Critical Care Medicine; SICU, surgical intensive care unit.
a
Refer to the original sources for guidance on evidence grading.
Source: Adapted from references 10, 34, and 35.

With increasing understanding of ARDS and acute lung injury, an enteral formula was designed to reduce
inflammation, using a high-fat, low-carbohydrate formula as its base with the additions of ω-3 fatty acids
(eicosapentaenoic and docosahexaenoic acids); borage oil, which contains γ-linolenic acid (GLA); and antioxidants.
When ω-3 fatty acids are provided enterally, they will replace the ω-6 fatty acid arachidonic acid in cellular
membranes, resulting in production of anti-inflammatory or less-inflammatory eicosanoids.50 GLA also inhibits
production of proinflammatory metabolites deriving from arachidonic acid. Recommendations for using ω-3 fatty
acids and GLA-supplemented pulmonary formulas vary, in part because of variations in the methodologies used to
analyze product research (see Table 4-15).10,34,35
Fluid-restricted formulas may be beneficial for patients with respiratory failure who are experiencing volume
overload, pulmonary edema, and renal failure with decreasing urinary output. These complications can worsen
outcomes.10 A standard or possibly fluid-restricted enteral formula is likely the most cost-effective product for
patients with respiratory failure who require mechanical ventilation. Additional information on fluid-restricted
formulas is presented later in this chapter.

Renal Failure
Enteral formulas developed for use in patients with renal dysfunction are energy dense and have restricted amounts
of electrolytes (sodium, potassium, phosphorus, magnesium). The types and amounts of protein in such formulas
vary, depending on the intended use of the product. Some formulas are protein restricted for nondialyzed patients.
Other formulas have greater amounts of complete proteins to meet the needs of patients receiving intermittent hemo-
dialysis. See Table 4-16 for examples of these products.

TABLE 4-16. Selected Enteral Frmulas Marketed for Use in Patients with Renal Dysfunction

Product Manufacturer
Nepro® Abbott
Novasource Renal® Nestlé
®
Renalcal Nestlé
®
Suplena Abbott
The brand names mentioned in this table may not constitute a comprehensive list of all relevant products on the market in the United States
or other countries. Mention of a product does not imply an endorsement.

The contents of the renal formulas mostly adhere to the electrolyte and fluid recommendations for chronic
kidney disease (CKD) developed by the Kidney Disease: Improving Global Outcomes (KDIGO) CKD Workgroup
for the nondialysis patient.51 For the patient with CKD who is not receiving dialysis, protein intake should be limited
to 0.8 g/kg/d, and sodium, phosphate, and potassium should be restricted, if needed.51 For persons with CKD who
are receiving hemodialysis or peritoneal dialysis, protein intake increases to at least 1.2–1.3 g/kg/d.52
AKI is a different disorder than CKD, and there is no formula marketed specifically for it. The National Kidney
Foundation Disease Outcomes Quality Initiative and SCCM/ASPEN recommend not restricting protein intake
during AKI as an attempt to postpone dialysis.10,53 According to the KDIGO Work Group for Acute Kidney Injury,
suggested protein intakes for patients with AKI are 0.8–1 g/kg/d for noncatabolic, nondialyzed patients; 1–1.5
g/kg/d for patients on renal replacement therapy; and ≤1.7 g/kg/d for patients receiving continuous renal replacement
therapy (CRRT) and those who are hypercatabolic.53 In contrast, SCCM/ASPEN guidelines on AKI use standard
ICU recommendations for protein intake: 1.2–2 g/kg/d (using actual body weight) or, if receiving CRRT, ≤2.5
g/kg/d.10
Table 4-17 presents practice recommendations for the use of renal disease–specific formulas.10,34,51–53 Above all,
the patient’s fluid balance, electrolyte status, use of dialysis, and type of dialysis should be assessed to select the
appropriate EN formula. After determining the patient’s nutrition prescription, the nutrition support clinician should
compare the nutrient contents of the renal disease–specific formulas to those of standard formulas to select the
product that will be the best fit for the patient.
 TABLE 4-17. Practice Recommendtions: Selection of Enteral Formulas for Patients with Renal
Dysfunctiona

SCCM/ASPEN recommendations:
• We suggest that ICU patients with AKI should be placed on a standard enteral formula and that
standard ICU recommendations for protein (1.2-2 g/kg actual body weight) and energy (25-30
kcal/kg/d) provision should be followed. If significant electrolyte abnormalities develop, a specialty
formula designed for renal failure (with appropriate electrolyte profile) may be considered (expert
consensus).
• Patients receiving frequent hemodialysis or CRRT should increase protein intake, up to a maximum
of 2.5 g/kg/d (very low quality of evidence).
• Protein should not be restricted in patients with renal insufficiency as a means to avoid or delay
initiating dialysis therapy (very low quality of evidence).
ACG recommendations:
• A standard polymeric formula or a high-protein standard formula should be used routinely in the
hospitalized patient requiring EN (conditional recommendation, very low level of evidence).
KDIGO recommendations:
• We suggest avoiding protein restriction with the aim of preventing or delaying initiation of renal
replacement therapy (2D: very low level of evidence).
• CKD (no dialysis): We suggest limiting protein intake to 0.8 g/kg/d and restricting phosphorus,
potassium, and sodium (2B for persons without diabetes: moderate quality of evidence; 2C for
persons with diabetes: low quality of evidence).
• AKI: Suggested protein intakes are 0.8-1 g/kg/d for noncatabolic, nondialyzed patients, 1-1.5 g/kg/d
for dialyzed patients, and up to 1.7 g/kg/d for patients on CRRT and the hypercatabolic patient (2D:
very low quality of evidence).
Ikizler recommendation:
• For patients with CKD who are on hemodialysis or peritoneal dialysis, the suggested minimum
protein intake is 1.2-1.3 g/kg/d.
Abbreviations: ACG, American College of Gastroenterology; AKI, acute kidney injury; ASPEN, American Society for Parenteral and Enteral
Nutrition; CKD, chronic kidney disease; CRRT, continuous renal replacement therapy; EN, enteral nutrition; ICU, intensive care unit; KDIGO,
Kidney Disease: Improving Global Outcomes; SCCM, Society of Critical Care Medicine.
a
Refer to the original sources for guidance on evidence grading.
Source: Adapted from references 10, 34, and 51-53.

Conditions Requiring Fluid Restrictions

Certain patients may need a fluid-restricted enteral formula (see Table 4-18 for examples of these products). Fluid-
restricted EN formulas are energy dense (1.5–2 kcal/mL). As noted earlier in this chapter, fluid-restricted EN
formulas may be considered for patients with pulmonary failure. They may also be appropriate for persons with
other organ dysfunctions such as congestive heart failure or renal failure and for patients with ascites or selected
other medical conditions (eg, syndrome of inappropriate anti-diuretic hormone secretion, hypervolemic
hyponatremia). A fluid-restricted formula may also be used to provide sufficient nutrition without a large volume
during specific types of EN administration, such as cyclic or bolus feedings, or when transitioning from enteral to
oral feedings. However, adequate free water must be provided to prevent dehydration while using concentrated EN
for these situations.

TABLE 4-18. Selected Fluid-Restricted Enteral Formulas

 Product Manufacturer
Isosource® 1.5 Cal Nestlé
®
Nutren 1.5 Nestlé
Nutren® 2.0 Nestlé
Osmolite® 1.5 Cal Abbott
®
TwoCal HN Abbott
The brand names mentioned in this table may not constitute a comprehensive list of all relevant products on the market in the United States
or other countries. Mention of a product does not imply an endorsement.

The SCCM/ASPEN guidelines include several recommendations for use of fluid-restricted EN for critically ill
patients.10 These guidelines recommend a standard polymeric EN formula rather than disease-specific formulas,
unless the use of an immune-modulating formula would be optimal based on the patient’s disease state.
SCCM/ASPEN’s definition of a standard polymeric EN formula is one that is 1.0–1.5 kcal/mL. According to
SCCM/ASPEN, 2 kcal/mL formulas are rarely needed unless volume needs to be restricted (ie, in renal failure).10
Refer to Table 4-19 for practice recommendations.10

TABLE 4-19. Practice Recommendations: Using Fluid-Restricted Enteral Formulas in Critically Ill
Patientsa

SCCM/ASPEN recommendations:
• Use a standard polymeric formula (ie, 1-1.5 kcal/mL) when initiating EN in critically ill patients
(expert consensus).
• Use fluid-restricted, energy-dense EN formulations for patients with acute respiratory failure
(especially if in a state of volume overload) (expert consensus).
Abbreviations: ASPEN, American Society for Parenteral and Enteral Nutrition; EN, enteral nutrition; SCCM, Society of Critical Care Medicine.
a
Refer to the original source for guidance on evidence grading.
Source: Adapted from reference 10.

Obesity and Bariatric Surgery

Specialty enteral formulas have been developed to promote weight loss and provide sufficient protein to promote
healing and preserve muscle mass in patients after bariatric surgery (see Table 4-20). These formulations often
contain hydrolyzed proteins, fish oil, fiber, and antioxidants. They are therefore also used in the ICU for obese
patients who require high-protein, hypocaloric EN and to prevent over-feeding in critically ill patients who are
receiving significant amounts of energy from propofol (an IV sedation agent that provides 1.1 kcal/mL infused).

TABLE 4-20. Selected Enteral Formulas Marketed for Use in Patients Requiring Hypocaloric,
High-Protein Feedings

Product Manufacturer
Peptamen Intense® VHP Nestlé
Vital® High Protein Abbott
The brand names mentioned in this table may not constitute a comprehensive list of all relevant products on the market in the United States
or other countries. Mention of a product does not imply an endorsement.
Table 4-21 reviews recommendations related to the use of hypocaloric, high-protein EN.10,34,35,54 In guidelines on
care for patients recovering from bariatric surgery, the American Association of Clinical Endocrinologists (AACE),
the Obesity Society (TOS), and the American Society for Metabolic and Bariatric Surgery (ASMBS) recommend at
least 60 g protein intake per day during the early postoperative stage and up to 1.5 g protein per kg ideal body
weight. This recommendation is based on studies showing that higher protein intakes (80–90 g/d) are associated
with reduced loss of lean body mass.54 In this guideline, AACE/TOS/ASMBS acknowledge that patients may need
EN but make no recommendation for the ideal enteral formula or energy intake level.54 SCCM/ASPEN, CPG, and
ACG recommend high-protein, hypocaloric feedings for critically ill patients with obesity (body mass index >30)
because high-protein, hypocaloric nutrition may aid in increasing insulin sensitivity, promote weight loss, reduce
ICU and hospital mortality, and improve respiratory function.10,34,35

TABLE 4-21. Practice Recommendations: Enteral Formula Selection for Patients with Obesitya

SCCM/ASPEN recommendations (critically ill obese patients):

• Use high-protein hypocaloric feeding for obese ICU patients (expert consensus).
• If available, use an enteral formula with low caloric density and a reduced NPC:N in the adult obese
ICU patient (expert consensus).
• Energy intake: We suggest that, for all classes of obesity, energy intake from EN should not exceed
65%-70% of target energy requirement as determined by IC. If IC is unavailable, we suggest using
the weight-based equation 11-14 kcal/kg actual body weight per day for patients with BMI in the
range of 30-50 and 22-25 kcal/kg ideal body weight per day for patients with BMI >50
(expert consensus).
• Protein intake: We suggest that protein should be provided in a range from 2.0 g/kg ideal body
weight per day for patients with BMI of 30-40 up to 2.5 g/kg ideal body weight per day for patients
with BMI ≥40 (expert consensus).
ACG recommendations (critically ill obese patients):
• Permissive (hypocaloric) underfeeding is an acceptable alternative to full feeding in critically ill obese
(BMI >30) patients (conditional recommendation, very low level of evidence).
• Protein intake: 2.0-2.5 g/kg ideal body weight.
• Energy intake: 60%-65% estimated or measured energy expenditure.
CPG recommendations (critically ill obese patients):
• Intentional underfeeding of calories (not protein) should be considered in obese patients at low
nutrition risk. However, this recommendation does not apply to patients at high nutrition risk.
AACE/TOS/ASMBS recommendations (patients receiving early postoperative care following
bariatric surgery):
• Protein intake should be individualized, assessed, and guided by an RD (Grade D).
• Minimal protein intake of 60 g/d and up to 1.5 g/kg ideal body weight should be adequate; intake of
up to 2.1 g/kg ideal body weight should be assessed on an individualized basis (Grade D).
Abbreviations: AACE, American Association of Clinical Endocrinologists; ACG, American College of Gastroenterology; ASMBE, American
Society for Metabolic and Bariatric Surgery; ASPEN, American Society for Parenteral and Enteral Nutrition; BMI, body mass index; CPG,
Canadian Clinical Practice Guidelines; EN, enteral nutrition; IC, indirect calorimetry; ICU, intensive care unit; NPC:N, nonprotein calorie-to-
nitrogen ratio; RD, registered dietitian; SCCM, Society of Critical Care Medicine; TOS, the Obesity Society.
a
Refer to the original sources for guidance on evidence grading.
Source: Adapted from references 10, 34, 35, and 54.

Blenderized Tube Feedings

Blenderized tube feedings (BTFs) are commercially available products and homemade preparations that blend whole
food ingredients to a consistency that can be administered through a feeding tube. BTFs can be used for partial,
supplemental, or complete EN support.
A variety of commercially prepared BTFs are available (see Table 4-22). Some of these products are made for
bolus feeding only. Others may need to be strained or thinned with water for gravity feedings or are intended to
supplement commercial formula or food to meet nutrient needs.

TABLE 4-22. Selected Commercial Food-Based Enteral Formulas/Meals

Product Manufacturer
Compleat® Nestlé
Compleat® Organic Blends Chicken Garden Blend Nestlé
®
Compleat Organic Blends Plant-Based Blend Nestlé
Kate Farms® Standard Formula 1.0 Kate Farms
®
Kate Farms Peptide 1.5 Kate Farms
®
Liquid Hope Functional Formularies
Real Food Blends™ Beef, Potatoes & Spinach Real Food Blends
Real Food Blends™ Chicken, Carrots & Brown Rice Real Food Blends
Real Food Blends™ Quinoa, Kale & Hemp Real Food Blends
Real Food Blends™ Salmon, Oats & Squash Real Food Blends
The brand names mentioned in this table may not constitute a comprehensive list of all relevant products on the market in the United States
or other countries. Mention of a product does not imply an endorsement.

Homemade BTFs are made from whole foods and usually prepared using a meal plan or recipe. Depending on
the patient’s nutrient needs, medical condition, and family support, the amount of blended food in homemade tube
feeding can range between 1% and 100%.55 A patient might choose to use a commercial food-based enteral formula
or add a small amount of blended food to his or her current feeding plan, while another patient may desire to have
100% of nutrition provided by blended food.
To promote the safe initiation of a BTF regimen and choose the appropriate BTF recipe or product, the nutrition
support clinician must assess the patient, with emphasis on the following factors:3,55–57

• Medical history
• Tolerance or intolerance of current or past enteral feeding regimen
• Food intolerances and food allergies
• Lifestyle
• Ethnic and religious preferences
• Ability to obtain and store ingredients and tools for preparing a homemade BTF

After a patient begins a BTF regimen, a trained registered dietitian should perform periodic nutrition
reassessments and offer continuing patient education on safe preparation, administration, and storage of the
formula.56 Chapter 11 provides additional information on the use of BTFs in the home setting.

Modular Products
Many modular products are available to fortify EN, including protein powders and liquids, liquid fat, MCT oil,
soluble fiber, and specific amino acids (eg, glutamine, arginine) (see Table 4-23). Liquid modular products are often
hyperosmolar.
 TABLE 4-23. Selected Examples of Modular Products

Nutrient(s) Product Manufacturer

Protein Beneprotein® Nestlé
®
ProMod Liquid Protein Abbott
®
ProSource No Carb Medtrition
ProSource® Plus Liquid Protein Medtrition
®
ProSource Protein Powder Medtrition
ProSource® TF Medtrition
Pro-Stat® Max Nutricia
®
Pro-Stat Sugar Free Nutricia
Pro-Stat® Sugar Free AWC Nutricia
®
Fiber Fiber-Stat Nutricia
®
NutriSource Fiber Nestlé
Protein and fiber Pro-Stat® Renal Care Nutricia
®
Fat MCT Oil Nestlé
Microlipid™ Nestlé
The brand names mentioned in this table may not constitute a comprehensive list of all relevant products on the market in the United States
or other countries. Mention of a product does not imply an endorsement.

Instructions for mixing and administering modulars must be carefully followed because many of these products
can occlude feeding tubes. Modular products can be diluted or dissolved in an appropriate volume of water and
administered via the feeding tube. Additional water flushes before and after the modular is administered help
maintain patency of the enteral access device. See Chapter 3 for additional information on preventing tube
occlusion.
In the home setting, administering modular products for the person receiving EN will be an additional task for
the caregiver; the ease of providing modulars at home will depend on the caregiver’s capabilities and the time
dedicated for feeding administration. See Chapter 11 for further information on EN in the home setting.
Protein modulars, which provide 6 to 15 g of protein per serving, rank as the most widely used of the modular
components. This is because many enteral products may not provide adequate protein for certain patient populations
(eg, critically ill patients, patients receiving CRRT).10 Patient-specific factors must be taken into account when
choosing between protein modulars.
There are multiple types of protein modulars, including those with complete protein (whey, casein), collagen-
based products, and specific amino acids (arginine, glutamine).58 Only complete protein modulars contain all 9
essential amino acids. Protein modulars that contain only collagen lack tryptophan. Therefore, it may be necessary to
supplement tryptophan via other protein modulars in patients receiving collagen-based protein modulars. If
indicated, single-entity arginine and glutamine modulars are available.
The other types of modulars are used less frequently. Fermentable soluble fiber may promote bowel health and
reduce diarrhea and may be added if the EN formula is fiber-free and supplementation is indicated based on patient
status.10,34 MCT oil can be used to boost energy intake in persons with chylous leaks because it bypasses the
lymphatic system for absorption. If enterally fed, these patients receive very-low-fat EN. However, MCT does not
contain essential fatty acids. A liquid fat modular can also be used to provide energy, but a high fat intake could
promote delayed gastric emptying. Above all, the nutrition support clinician should thoroughly assess the patient to
determine which modulars, if any, are appropriate for the EN regimen.

Developing an Enteral Product Formulary

Many healthcare organizations choose to develop an enteral formulary to save money, improve patient care, and
help with inventory control. A multidisciplinary formula selection committee will represent the perspectives of
dietitians, pharmacists, physicians, administrators, and individuals working in the supply chain. The committee can
evaluate formulas in each category. Evidence-based research should guide the committee in the selection of
products; such research is especially helpful when considering specialty and disease-specific formulas. The
following factors should be considered when evaluating an enteral product formulary:

• Patient acuity
• EN formula categories
• Current product utilization
• Contractual requirements
• Substitution list in case of product shortages
• Frequency of enteral product formulary review (eg, every year or every 2 years)
Competitive bidding practices and policies that scrutinize nonformulary requests and encourage automatic
substitution for nonformulary products promote formulary adherence and cost containment.59 It may be most
economical to select all products from the same manufacturer if that company can provide an appropriate product
for each category.

Product Resources

US Contact Information for Enteral Formula and Modular

Manufacturers Website
Abbott Nutrition http://abbottnutrition.com
Functional Formularies http://functionalformularies.com
Kate Farms http://katefarms.com
Medtrition https://www.medtrition.com
Nestlé Nutrition http://nestlehealthscience.us
Nutricia https://www.nutricia.com
Real Food Blends http://realfoodblends.com

References
1. US Food and Drug Administration. Medical foods guidance documents & regulatory information.
https://www.fda.gov/Food/GuidanceRegulation/GuidanceDocumentsRegulatoryInformation/MedicalFoods/default.htm
Updated December 2017. Accessed November 26, 2018.
2. US Food and Drug Administration. Food guidance regu lation.
https://www.fda.gov/downloads/Food/GuidanceRegulation/GuidanceDocumentsRegulatoryInformation/UCM500094.pdf
Accessed September 24, 2018.
3. Escuro AA, Hummell AC. Enteral formulas in nutrition support practice: is there a better choice for your
patient? Nutr Clin Pract. 2016;31(6):709–722.
4. Roberts S, Kirsch R. Enteral nutrition formulations. In: Mueller CM, ed. The ASPEN Adult Nutrition Support
Core Cur riculum. 3rd ed. Silver Spring, MD: American Society for Parenteral and Enteral Nutrition;
2017:227–249.
5. Malone AM. Enteral formulations. In: Cresci GA, ed. Nutrition Support for the Critically Ill Patient. 2nd ed.
Boca Raton, FL: CRC Press; 2015:259–277.
6. Brown B, Roehl K, Betz M. Enteral formula selection: current evidence and implications for practice. Nutr
Clin Pract. 2015;30(1):72–85.
7. Scaife CL, Saffle JR, Morris SE. Intestinal obstruction secondary to enteral feedings in burn trauma patients.
J Trauma. 1999;47:859–863.
8. McIvor AC, Meguid MM, Curtas S, Kaplan DS. Intestinal obstruction from cecal bezoar: a complication of
fiber-containing tube feedings. Nutrition. 1990;6:115–117.
9. McClave SA, Chang WK. Feeding the hypotensive patient: does enteral feeding precipitate or protect against
ischemic bowel? Nutr Clin Pract. 2003;18:279–284.
10. McClave SA, Taylor BE, Martindale RG, et al. Guidelines for the provision and assessment of nutrition
support therapy in the adult critically ill patient: Society of Critical Care Medicine (SCCM) and American
Society for Parenteral and Enteral Nutrition (ASPEN). JPEN J Parenter Enteral Nutr. 2016;40(2):159–211.
11. Elia M, Engfer MB, Green CJ, Slik DB. Systematic review and meta-analysis: the clinical and physiological
effects of fibre-containing formulae. Aliment Pharmacol Ther. 2008;27(2): 120–145.
12. Academy of Nutrition and Dietetics Evidence Analysis Library. Enteral nutrition and fiber.
http://www.andeal.org. Accessed May 21, 2018.
13. Malone AM. Enteral formula selection. In: Charney P, Malone A, eds. Academy of Nutrition and Dietetics
Pocket Guide to Enteral Nutrition. 2nd ed. Chicago, IL: Academy of Nutrition and Dietetics; 2013:120–152.
14. Lipp J, Lord LM, Scholer LH. Fluid management in enteral nutrition. Nutr Clin Pract. 1999;14:232–237.
15. Trujillo E. Enteral nutrition: a comprehensive overview. In: Matarese LE, Gottschlich MM, eds.
Contemporary Nutrition Support Practice: A Clinical Guide. Philadelphia, PA: WB Saunders;1998:192–201.
16. Parrish CR, Krenitsky J, Perkey KG. Enteral feeding challenges. In: Cresci GA, ed. Nutrition Support for the
Critically Ill Patient. 2nd ed. Boca Raton, FL: CRC Press; 2015:291–311.
17. American Academy of Allergy, Asthma, and Immunology. Food allergies, symptoms, diagnosis and
treatment. https://www.aaaai.org/conditions-and-treatments/allergies/food-allergies. Accessed September 24,
2018.
18. National Institute of Allergy and Infectious Diseases. Food allergy. https://www.niaid.nih.gov/diseases-
conditions/food-allergy. Accessed September 24, 2018.
19. Mowatt-Larssen CA, Brown RO, Wojtysiak SL, Kudsk KA. Comparison of tolerance and nutritional
outcome between a peptide and a standard enteral formula in critically ill, hypoalbuminemic patients. JPEN
J Parenter Enteral Nutr. 1992;16(1):20–24.
20. Brinson RR, Kolts BE. Diarrhea associated with severe hypoalbuminemia: a comparison of a peptide-based
chemically defined diet and standard enteral alimentation. Crit Care Med. 1988;16(2):130–136.
21. Dietscher JE, Foulks CJ, Smith RW. Nutritional response of patients in an intensive care unit to an elemental
formula vs a standard enteral formula. J Am Diet Assoc. 1998;98:335–336.
22. Heimburger DC, Geels VJ, Bilbrey J, Redden DT, Keeney C. Effects of small-peptide and whole-protein
enteral feedings on serum proteins and diarrhea in critically ill patients: a randomized trial. JPEN J Parenter
Enteral Nutr. 1997;21:162–167.
23. Seres DS, Ippolito PR. Pilot study evaluating the efficacy, tolerance, and safety of a peptide-based enteral
formula versus a high protein enteral formula in multiple ICU settings (medical, surgical, cardiothoracic).
Clin Nutr. 2017;36:706–709.
24. National Pressure Ulcer Advisory Panel, Europe Pressure Ulcer Advisory Panel, Pan Pacific Pressure Injury
Alliance. Prevention and Treatment of Pressure Ulcers: Clinical Practice Guide line. Perth, Australia:
Cambridge Media; 2014.
25. Litchford MD, Dorner B, Posthauer ME. Malnutrition as a precursor of pressure ulcers. Adv Wound Care.
2014;3(1):54–63.
26. Posthauer ME, Dorner B, Schols JMGA. The role of nutrition for pressure ulcer management: National
Pressure Ulcer Advisory Panel, European Pressure Ulcer Advisory Panel, and Pan Pacific Pressure Injury
Alliance white paper. Adv Skin Wound Care. 2015;28(4):175–188.
27. Cereda E, Klersy C, Rondanelli M, Caccialanza R. Energy balance in patients with pressure ulcers: a
systematic review and meta-analysis of observational studies. J Am Diet Assoc. 2011;111(12):1868–1876.
28. Posthauer ME, Marian M. Wound healing. In: Mueller CM, ed. The ASPEN Adult Nutrition Support Core
Curriculum. 3rd ed. Silver Spring, MD: American Society for Parenteral and Enteral Nutrition; 2017:419–
434.
29. Langer G, Fink A. Nutritional interventions for preventing and treating pressure ulcers. Cochrane Database
Syst Rev. 2014;(6):CD003216.
30. Cereda E, Neyens JCL, Caccialanza R, Rondanelli M, Schols JMGA. Efficacy of a disease-specific
nutritional support for pressure healing: a systematic review and meta-analysis. J Nutr Health Aging.
2017;21(6):655–661.
31. Abbott Nutrition website. http://Abbottnutrition.com. Accessed October 2, 2018.
32. Nestlé Health Science website. http://www.NestleHealthScience.us. Accessed October 2, 2018.
33. American Diabetes Association. Standards of medical care in diabetes 2018. Diabetes Care. 2018;14(Suppl
1):S1–S172.
34. McClave SA, DiBaise JK, Mullin GE, Martindale RG. ACG clinical guideline: nutrition therapy in the adult
hospitalized patient. Am J Gastroenterol. 2016;111:315–334.
35. Critical Care Nutrition at the Clinical Evaluation Research Unit. Canadian clinical practice guidelines for
nutrition support in the mechanically ventilated, critically ill adult 2015. http://www.criticalcarenutrition.org.
Accessed April 30, 2018.
36. Elia M, Ceriello A, Laube H, Sinclair AJ, Engfer M, Stratton RJ. Enteral nutritional support and use of
diabetes-specific formulas for patients with diabetes. Diabetes Care. 2005;28(9):2267–2279.
37. Ojo O, Brooke J. Evaluation of the role of enteral nutrition in managing patients with diabetes: a systematic
review. Nutrients. 2014;6(11):5142–5152.
38. Mesejo A, Acosta JA, Ortega C, et al. Comparison of a high protein disease-specific enteral formula with a
high-protein enteral formula in hyperglycemic critically ill patients. Clin Nutr. 2003;22(3):295–305.
39. Ceriello A, Lansink M, Rouws CHFC, van Laere KMJ, Frost GS. Administration of a new diabetes-specific
enteral formula results in an improved 24 h glucose profile in type 2 diabetic patients. Diabetes Res Clin
Pract. 2009;84(3):259–266.
40. Alish CJ, Garvey WT, Maki KC, et al. A diabetes-specific enteral formula improves glycaemic variability in
patients with type 2 diabetes. Diabetes Technol Ther. 2010;12(6):419–425.
41. Corsino L, Dhatariay K, Umpierrez G. Management of diabetes and hyperglycemia in hospitalized patients.
In: Endotext [internet]. National Library of Medicine website.
http://www.ncbi.nlm.nih.gov/books/NBK279093. Accessed October 15, 2018.
42. Hamdy O, Ernst FR, Baumer D, Mustad V, Partridge J, Hegazi R. Differences in resource utilization
between patients with diabetes receiving glycemia-targeted specialized nutrition vs standard nutrition
formulas in U.S. hospitals. JPEN J Parenter Enteral Nutr. 2014;38(2 suppl):86S–91S.
43. Lansink M, Hofman Z, Genovese S, Rouws CH, Ceriello A. Improved glucose profile in patients with type 2
diabetes with a new, high-protein, diabetes-specific tube feed during 4 hours of continuous feeding. JPEN J
Parenter Enteral Nutr. 2017;41(6)968–975.
44. Mesejo A, Monteio-Gonzalez JC, Vaquerizo-Alonso C, et al. Diabetes-specific enteral formula in
hyperglycemic, mechanically ventilated, critically ill patients: a prospective, open-label, blind-randomized,
multi-center study. Crit Care. 2015;9:390. doi:10.1186/s13054-015-1108-1.
45. Abdelsayed GG. Diets in encephalopathy. Clin Liver Dis. 2015;19:497–505.
46. Bémeur C, Desjardins P, Butterworth RF. Role of nutrition in the management of hepatic encephalopathy in
end-stage liver failure. J Nutr Metab. 2010;2010:489823. doi:10.1155/2010/489823.
47. Vilstrup H, Amodio P, Bajaj J, et al. Hepatic encephalopathy in chronic liver disease: 2014 practice
guideline by the American Association for the Study of Liver Diseases and the European Association for the
Study of the Liver. Hepa tology. 2014;60:715–735.
48. Rosenthal MD, Vanzant EL, Martindale RG, Moore FA. Evolving paradigms in the nutritional support of
critically ill surgical patients. Curr Probl Surg. 2015;52(4):147–182. doi: 10.1067/j.cpsurg.2015.02.003.
49. Feller-Kopman DJ, Schwartzstein RD. Mechanisms, causes, and effects of hypercapnia. UpToDate website.
https://www.uptodate.com/contents/mechanisms-causes-and-effects-of-hypercapnia. Published Sept 8, 2017.
Accessed October 25, 2018.
50. Shirai K, Yoshida S, Matsumaru N, Toyoda I, Ogura S. Effect of enteral diet enriched with eicosapentaenoic
acid, gamma-linolenic acid, and antioxidants in patients with sepsis-induced acute respiratory distress
syndrome. J Intensive Care. 2015;3(1):24.
51. Kidney Disease: Improving Global Outcomes (KDIGO) CKD Work Group. KDIGO 2012 clinical practice
guideline for the evaluation and management of chronic kidney disease. Kidney Int Suppl. 2013;3(1):1–150.
52. Ikizler TA. A patient with CKD and poor nutritional status. Clin J Am Soc Nephrol. 2013;8(12):2174–2182.
53. Kidney Disease: Improving Global Outcomes (KDIGO) Acute Kidney Injury Work Group. KDIGO clinical
practice guideline for acute kidney injury. Kidney Int Suppl. 2012;2(1):1–138.
54. Mechanick JI, Youdim A, Jones DB, et al. Clinical practice guidelines for the perioperative nutritional,
metabolic, and nonsurgical support of the bariatric surgery patient—2013 update: cosponsored by American
Association of Clinical Endocrinologists, the Obesity Society, and American Society for Metabolic &
Bariatric Surgery. Surg Obes Relat Dis. 2013;9(2):159–191.
55. Walia C, Van Hoorn M, Edlbeck A, Feuling MB. The registered dietitian nutritionist’s guide to homemade
tube feeding. J Acad Nutr Diet. 2017;117(1):11–16.
56. Escuro AA. Blenderized tube feeding: suggested guidelines to clinicians. Pract Gastroenterol.
 2014;38(12):58–66.
57. Carter H, Johnson K, Johnson TW, Spurlock A. Blended tube feeding prevalence, efficacy, and safety: what
does the literature say? J Am Assoc Nurs Pract. 2018;30(3):150–157.
58. Castellanos VH, Litchford MD, Campbell WW. Modular protein supplements and their application to long-
term care. Nutr Clin Pract. 2006;21:485–504.
59. Wildish DE. Enteral formulary management: a cost-effective approach. Can J Diet Pract Res.
2006;67(4):193–198.
 CHAPTER 5

Enteral Formulas for Pediatric Patients

Introduction
Choosing the appropriate formula is particularly important when caring for a growing and developing pediatric
patient. To select the best enteral nutrition option for a patient, the nutrition support clinician must first perform a
complete nutrition assessment and identify any nutrition-related diagnoses or symptoms and medical conditions that
may affect the individual’s energy and nutrient needs (see Chapter 1). This chapter focuses on formula selection for
pediatric and infant patients. Chapter 4 provides general information on formula composition, food allergies and
intolerances, and developing an enteral product formulary.

The brand names mentioned in this chapter do not constitute a comprehensive list of all relevant products on the
market in the United States or other countries. Mention of a product does not imply an endorsement.
Manufacturers periodically introduce, withdraw, and alter products. Before using any product, nutrition
support clinicians should review the label and product website for current information on ingredients, nutrient
composition, and instructions for use. If those resources are insufficient, contact the manufacturer or the
formulary manager for additional information. Selected manufacturer websites are listed at the end of the
chapter.

Federal Regulations

Medical Foods
Under US law, enteral formulas (adult and pediatric) are classified as medical foods. A medical food is defined in
the 1988 Orphan Drug Amendments as follows:1
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 requirements, based on recognized scientific principles, are established by
medical evaluation.

The US Food and Drug Administration (FDA) regulates the manufacturing of medical foods. However, it does
not require the inclusion of Nutrition Facts on the product label of a medical food. Also, manufacturers do not need
FDA approval to make structural or functional claims about medical foods. Even without prior FDA approval, these
claims cannot be misleading or disease related. An example of an allowed claim is “This product contains short-
chain fructooligosaccharides to stimulate the growth of beneficial bacteria in the colon.” There is scientific evidence
that this claim is true. However, although we understand that beneficial bacteria in the gut play a role in immune
health, a manufacturer cannot claim that the product “strengthens your immune system.” The American Society for
Parenteral and Enteral Nutrition (ASPEN) recommends that nutrition support clinicians interpret the content and
health claims of enteral formulas with caution until more specific regulations are in place.2

Infant Formulas
An infant formula is defined by the Federal Food, Drug, and Cosmetic Act as “a food which purports to be or is
represented for special dietary use solely as a food for infants by reason of its simulation of human milk or its
suitability as a complete or partial substitute for human milk.”1 Compared with enteral products, infant formulas are
more highly regulated with regard to quality control, labeling, nutrient requirements, formula recall, notification of
new products, and exempt products.
An infant formula is considered exempt if it is designed to meet the nutrition needs of a specific population, such
as premature infants. This designation does not exempt the formulas from regulation. Instead, they need to meet
criteria established for the specific need of the population for which they are intended.
In 2014, the FDA finalized a rule that established standards to ensure all manufactured infant formula is safe and
supports healthy growth. Under these regulations, whenever a new formula is released to the market or an already
available formula undergoes any major formulation changes, the manufacturer needs to file notification with the
FDA and have studies that show infants have normal growth on the petitioned formulas. Additionally, the new
standards require testing for the harmful pathogens Salmo nella and Cronobacter, and infant formulas must be tested
for the content of every nutrient in every lot of finished infant formula, both before entering the market and at the
end of the products’ shelf life.3
In response to the incidence of Enterobacter sakazakii (now called Cronobacter sakazakii) infection resulting in
meningitis, necrotizing enterocolitis, and bacteremia in neonates fed cow’s milk–based powdered infant formulas,
the Centers for Disease Control and Prevention (CDC) and FDA recommend that powdered infant formulas not be
used in neonatal intensive care settings unless there is no alternative available.4,5 The American Academy of
Pediatrics (AAP) also warns against the use of powdered infant formulas in term infants less than 2 months of age
and infants with underlying medical conditions.6 The infection risks and associated recommendations have resulted
in hospitals implementing policies to primarily feed neonates and high-risk infants the commercially sterile liquid
forms of formulas (ie, ready-to-feed [RTF] and concentrated products) when available.

Formula Composition
For an overview of enteral formula composition (ie, carbohydrate, fiber, fat, protein, vitamins, minerals, water, and
osmolality), refer to Chapter 4. Specific information about the composition of pediatric and infant formulas is
presented later in this chapter.

Pediatric Enteral Formulas

Pediatric enteral formulas are designed for children from 1 to 13 years of age who require tube feedings to meet
nutrient needs. These formulas are designed to meet the needs of children 1–8 years old in 1000 mL/d and children
9–13 years old in 1500 mL/d. Most types of pediatric formulas are reviewed in this chapter. One exception is
products for children with inborn errors of metabolism; the treatment of those patients is beyond the scope of this
handbook.
Adult specialty formulas can be considered when an appropriate pediatric formula is not available. However,
when considering the use of these products, nutrition support clinicians must pay special attention to the nutrition
needs for growth and development in the pediatric patient.

General Purpose (Polymeric) Pediatric Formulas

General purpose or polymeric pediatric formulas are designed to meet the nutrition needs for growth and
development of children when used as the sole source of nutrition (see Table 5-1). These products are available in
various energy concentrations from 0.63 kcal/mL to 1.5 kcal/mL and typically meet the Dietary Reference Intakes
(DRIs) for children ages 1–8 years in 1000 mL/d and ages 9–13 years in 1500 mL/d. Most polymeric products are
available with or without fiber, are considered appropriate for lactose intolerance, are gluten free, and are kosher.7
Manufactured pediatric blenderized enteral products are considered a subcategory of polymeric formulas (see next
section of this chapter).

TABLE 5-1. Examples of General Purpose/Polymeric Enteral Formulas Marketed for Pediatric
Patients

Indications for Use Characteristics Product Examples (Manufacturers)

• Boost Kid Essentials (Nestlé)a
• Boost Kid Essentials 1.5 (Nestlé)a
 • Boost Kid Essentials 1.5 (Nestlé)a
• Compleat Pediatric (Nestlé)
• Compleat Pediatric Reduced Calorie
(Nestlé)
• Supplemental or sole source of • Intact macronutrients • Compleat Pediatric Organic Blends
nutrition for children without • May or may not (Nestlé)
food allergies or contain fiber • Nutren Junior (Nestlé)a
significant malabsorption • May be made with • Pediasure Enteral Formula 1.0 Cal
issues whole foods (Abbott)a
• Pediasure 1.5 (Abbott)a
• Pediasure Grow and Gain
Therapeutic Shake (Abbott)a
• Pediasure SideKicks 0.63 Cal Shake
(Abbott)
The brand names mentioned in this table may not constitute a comprehensive list of all relevant products on the market in the United States
or other countries. Mention of a product does not imply an endorsement.
a
Available with or without fiber.

Polymeric formulas primarily contain intact proteins and typically require normal digestion.8 These products can
be orally consumed or administered into the stomach or the small intestine, and they are typically well tolerated in
patients with normal digestive capacity. They usually contain cow’s milk as the protein source in the form of milk
protein concentrate, whey protein concentrate, and/or sodium and calcium caseinates. The blenderized products may
contain other nonmilk sources of protein; therefore, careful attention to the label and current formulation of these
enteral products is important (as it is with all formula products).
Common carbohydrate sources for polymeric products are maltodextrin and sugar. Compared with formulas for
enteral use only, oral products or products for both oral and tube feeding usually contain more sugar or added
sweeteners for taste. It is important to note that sugar and sweeteners can increase the osmolality of the enteral
formula. Fiber sources are usually a combination of soluble and insoluble fibers, including oat fiber, soy fiber,
fructooligosaccharides, pea fiber, and inulin.
Sources of fat in polymeric products include soybean oil, canola oil, soy lecithin, and medium-chain
triglycerides (MCTs). Some products may contain the long-chain polyunsaturated fatty acids (LCPUFAs)
docosahexaenoic acid (DHA) and arachidonic acid (ARA), which are found in human milk (HM) and are associated
with neurodevelopment in infants. LCPUFAs are discussed in further detail in the Infant Formulas section of this
chapter.

Blenderized Tube Feedings

Blenderized tube feedings (BTFs) have recently regained their popularity in the pediatric population. The BTF may
be made by blending whole foods with added liquid, or a commercially available BTF product containing whole
foods may be used. The foods in a BTF may include a variety of table foods and/or baby foods from animal or plant
protein sources, grains, fruits, and vegetables. Fat and carbohydrates may be added to meet a patient’s essential fatty
acid and energy needs. The liquid source may be a commercially available formula, but water, cow’s milk, nondairy
“milks,” and electrolyte-containing fluids are also used. The final blenderized feeding plan must be analyzed to
determine whether it is nutritionally complete. There are guidelines on recipe development as well as when it is
appropriate for a patient to receive a BTF.9–12
There are reports of BTFs being especially beneficial in children with intestinal failure, as well as those
following the ketogenic diet, those with food sensitivities, and those whose tolerance of commercial formulas is
poor.13,14 Multiple reports indicate that BTFs help improve retching, gagging, dumping syndrome, and
constipation.9,15,16 Some families prefer this type of feeding because it uses whole foods and offers customizability
for children who follow a vegetarian or gluten-free diet or have other food preferences or restrictions.
Vieira and associates conducted a cross-sectional study in Brazil comparing contamination of 33 samples of
commercial BTFs (some RTF formulas and some powdered products reconstituted with water) and 33 samples of
home-blenderized formulas in the home care setting. Escherichia coli and mesophilic and coliform bacteria were
detected in samples from all 3 groups. The bacteria counts in the home-blenderized formula and reconstituted
powdered formula samples were higher than in the RTF samples. The authors attributed contamination in the
reconstituted formula samples to the water used in mixing.17 Refer to Chapters 4, 8, and 11 for additional
information on BTFs.

Semi-Elemental (Peptide-Based) Pediatric Formulas

Semi-elemental or peptide-based pediatric formulas are designed for children with impaired gastrointestinal (GI)
function or those who had trouble tolerating the polymeric formula.18 Most are marketed for use in children between
the ages of 1 and 13 years; there is also a peptide-based product marketed for adolescents ages 14 years and older
(see Table 5-2). These products are not intended for the treatment or prevention of allergies or allergic reactions.
Like the polymeric products, the peptide-based pediatric products typically meet the DRIs for children 1–8 years old
in 1000 mL/d and children 9–13 years old in 1500 mL/d. The product marketed for use in adolescents meets the
DRIs for 14-to 18-year-old adolescents in 1000 mL/d.

TABLE 5-2. Examples of Semi-Elemental/Peptide-Based Formulas Marketed for Pediatric

Patients

Indications for Use Characteristics Product Examples (Manufacturers)

• Pediasure Peptide 1.0 Cal (Abbott)
• Cow's milk protein • Pediasure Peptide 1.5 Cal (Abbott)
• Intolerance of polymeric hydrolyzed to peptides
• Peptamen Junior (Nestlé)a
formulas • Some fat may be from
• Peptamen Junior 1.5 (Nestlé)a
• May be indicated for medium-chain
patients with triglycerides • Peptamen Junior with Prebio
(Nestlé)
malabsorption disorders • May or may not contain
fiber • Peptamen Junior HP (Nestlé)
• Vital Peptide 1.5 Cal (Abbott)b
The brand names mentioned in this table may not constitute a comprehensive list of all relevant products on the market in the United States
or other countries. Mention of a product does not imply an endorsement.
a
Available with or without fiber.
b
Marketed for use in adolescents ages ≥ 14 years.

Peptide-based formulas are acceptable for patients with lactose intolerance and are gluten free. Some, but not all,
products meet kosher guidelines; compliance will be clearly indicated on the label. Some products used for oral or
tube feeding are flavored.
Peptide-based formulas contain partially hydrolyzed protein, resulting in di-or tri-peptides and other short-chain
peptides.7,18 Research comparing outcomes of peptide-based formulas compared to polymeric formulas is limited,
and many studies show no difference in outcomes.8 The protein source is hydrolyzed cow’s milk protein
(hydrolyzed whey protein or hydrolyzed sodium caseinate). Carbohydrate sources are maltodextrin, hydrolyzed
cornstarch, and sugar. Sources of fat include soybean oil, canola oil, soy lecithin, structured lipids, and MCTs. Some
products contain soluble fibers or prebiotics in the form of fructooligosaccharides, guar gum, and inulin.

Elemental Pediatric Formulas

Pediatric elemental formulas may be appropriate for patients with malabsorption disorders and GI impairment,
including short bowel syndrome or intestinal failure; severe food allergies, such as food protein–induced
enterocolitis syndrome; and eosinophilic GI disorders (see Table 5-3). Pediatric elemental products are designed for
children 1 year of age or older. Note: Most pediatric (“Junior”) elemental formulas have an infant formula
counterpart. The ingredients in these paired products and their manufacturing processes are similar, with the
intention of making the transition from the infant formula to the pediatric product relatively straightforward.
 TABLE 5-3. Examples of Elemental Enteral Formulas Marketed for Pediatric Patients

Indications for Use Characteristics Product Examples (Manufacturers)

• Malabsorption disorders • Alfamino Junior (Nestlé)
and GI impairment • Elecare Junior (Abbott)
• Short bowel syndrome or • Amino acid based • Neocate Junior (Nutricia)
intestinal failure • Some fat is from MCTs • Neocate Junior with Prebiotics
• Severe food allergies (Nutricia)
• Eosinophilic GI disorders • Vivonex Pediatric (Nestlé)
Abbreviations: GI, gastrointestinal; MCT, medium-chain triglyceride.
The brand names mentioned in this table may not constitute a comprehensive list of all relevant products on the market in the United States
or other countries. Mention of a product does not imply an endorsement.

Because elemental products are amino acid based, they are considered hypoallergenic. The most common
carbohydrate source is corn syrup solids; less-common carbohydrate sources include potato starch and tapioca
starch. Fat sources include high-oleic safflower oil, refined or modified palm kernel and/or coconut oil for MCT
content, MCT oil, soy oil, DHA, and ARA. The percentage of MCT varies from product to product; if fat
malabsorption is a concern, read the product information to make the best choice for the patient. As of 2019, 1
product containing prebiotics was available in the US market (see Table 5-3). Similar to polymeric and semi-
elemental products, elemental products may be flavored or unflavored.

Modified-Fat Pediatric Formulas

Modified-fat formulas are designed for use in patients with long-chain oxidative disorders and chylous leaks (see
Table 5-4). The protein sources are intact cow’s milk whey and caseinates. Carbohydrate sources include
maltodextrin and corn syrup solids. These products usually contain a lower percentage of calories from fat, and
approximately 80% of the fat is from MCT. MCT is transported via the portal system while long-chain triglycerides
(LCTs) are transported through the lymphatic system. Fat sources are modified palm kernel oil and/or coconut oil,
which are high in MCTs, and walnut oil, which is a fat rich in LCTs. To prevent essential fatty acid deficiency, it is
important to provide at least 10% of total energy intake as fat and 2%–4% of total energy intake as the essential fatty
acid linoleic acid.19 In addition, DHA and ARA may be added. Manufacturers recommend monitoring the essential
fatty acid status of patients using these products.

TABLE 5-4. Examples of Modified-Fat Formulas Marketed for Use in Pediatric Patients

Indications for Use Characteristics Product Examples (Manufacturers)

• Intact protein
• Long-chain oxidative
• Low fat with a high • Lipistart (Vitaflo)
disorders and chylous
leaks
percentage of medium- • Monogen (Nestlé)
chain triglycerides
The brand names mentioned in this table may not constitute a comprehensive list of all relevant products on the market in the United States
or other countries. Mention of a product does not imply an endorsement.

Renal Pediatric Formulas

In the United States, 1 pediatric formula product is marketed to meet the specific nutrition needs of children with
acute kidney injury or chronic kidney disease (see Table 5-5). This product is available in powdered form and is a
high-calorie product with limited amounts of protein, calcium, chloride, phosphorus, potassium, and vitamin A. The
protein source is whey protein concentrate with some free amino acids, and the carbohydrate source is glucose syrup
solids. Fat is from palm kernel, palm, canola, and sunflower oils, and the product contains DHA and ARA.

TABLE 5-5. Example of an Enteral Formula Marketed for Use in Pediatric Patients with Renal
Disease

Indications for Product Example

Characteristics
Use (Manufacturer)
• Acute kidney
• High calorie with limited amounts of protein,
injury
calcium, phosphorus, chloride, potassium, and • Renastart (Vitaflo)
• Chronic kidney vitamin A
disease
The brand name mentioned in this table may not be the only relevant product on the market in the United States or other countries. Mention
of a product does not imply an endorsement.

Infant Formulas
The AAP states that HM is the preferred source of nutrition for all term and preterm infants for the first year of
life.20 According to the CDC, as of 2015, the percentage of US infants ever receiving HM was 83.2%, which exceeds
the Healthy People 2020 breastfeeding rate objective of 81.9%.21,22
Still, many infants in the United States rely on infant formula for some portion of their nutrition. Infant formula
is designed to be similar in composition to HM, the optimal nutrition for a growing infant.23 Although infant
formulas differ in exact composition, those regulated under the Infant Formula Act have all been shown to promote
normal physical growth.24 Compared with HM, infant formula typically contains higher concentrations of macro-
and micronutrients to compensate for the potentially lower bio-availability of nutrients from formula.
Infant formulas are available in RTF, concentrated liquid, and powdered forms. The first 2 forms are
commercially sterile, whereas powdered forms are not. RTF products do not require mixing and are the easiest to
use. Concentrated formulas and powdered formulas require the addition of water. When a product is available in
multiple forms, the RTF is usually most expensive, concentrated formula is typically less costly, and powdered
formula is the least-expensive option.

Additives in Infant Formulas

According to the Infant Formula Act, manufacturers are required to submit new ingredients to the FDA to be
approved as a food additive or GRAS (Generally Recognized as Safe) for use in infant formulas. Current infant
formulations contain a mixture of some of the following functional ingredients: DHA and ARA; probiotics,
prebiotics, and synbiotics; nucleotides; and milk fat globule membranes (MFGMs). However, manufacturers are
unable to make formulas that provide the hormones, immunoglobulins, enzymes, and live cells found in HM.25

DHA and ARA

As mentioned earlier in this chapter, DHA and ARA are LCPUFAs found in HM. They can also be converted in the
body from the essential fatty acids alpha-linolenic acid and linoleic acid. The amounts of DHA and ARA in HM
vary depending on maternal intake. DHA and ARA are important components of cell membrane structure and neural
tissue structure and function.26 They are the most abundant LCPUFAs in the brain and are considered important in
cognitive development.27 Most infant formulas in the United States have added DHA and ARA.

Prebiotics, Probiotics, and Synbiotics

Prebiotics are carbohydrates that are fermentable and not fully digested in the small intestine. The most common
prebiotics in HM and infant formulas are fructooligosaccharides and galactoligosaccharides. These ferment and
produce short-chain fatty acids, which are energy for the colonocytes. The prebiotic fibers stimulate the growth of
the normal bacteria in the colon while preventing the growth of the pathogenic bacteria.28,29
Probiotics are live bacteria that adhere to the colon and increase the barrier function of the intestine. Prebiotics
combined with probiotics are called synbiotics, and they may enhance the immunological function of the gut.29
Infant formulas with prebiotics and/or probiotics have been shown to decrease duration of diarrhea related to an
illness and may be protective against necrotizing enterocolitis.28,30

Nucleotides
Nucleotides are considered “conditionally essential” during infancy because of the increased need for them during
periods of accelerated growth. These nonprotein nitrogenous compounds are precursors of nucleic acids and a
component of coenzymes.31 Research suggests that nucleotide supplementation in infant formulas supports immune
function in the GI tract and may enhance mucosal recovery after intestinal injury.32

Milk Fat Globule Membranes

MFGMs are the newest additive to infant formulas. MFGMs are found in both HM and cow’s milk. Because
MFGMs are naturally present in cow’s milk, they are found to some extent in any cow’s milk–based infant formula.
However, processing denatures MFGMs, which lessens their concentration in infant formula. Therefore,
manufacturers may choose to supplement products with additional MFGMs.33,34
Components of the MFGMs are biologically active and important in immune function, development of the
central nervous system, and digestion.34,35 Infant formula supplemented with MFGMs appears to narrow the
cognitive development gap seen between breastfed and formula-fed infants.35

Standard Cow’s Milk–Based Formulas for Term Infants

Standard infant formulas (Table 5-6) are designed to resemble the nutrient composition of HM. In HM,
approximately 6% of energy is from protein, 40%–45% is from carbohydrate, and 50% is from fat. Term infant
formulas have 19 to 20 kcal/oz. Although the energy content of HM varies, it is within a similar range.

TABLE 5-6. Examples of Standard Term Infant Formulas

Indications for Use Characteristics Product Examples (Manufacturers)

• When human milk is • Enfamil NeuroPro (Mead Johnson)

• Derived from cow's milk
unavailable or • Enspire (Mead Johnson)
• Designed to resemble the
contraindicated • Gerber Good Start Gentle (Gerber)a
nutrient composition of
• Human milk • Similac Advance (Abbott)
human milk
supplementation • Similac Pro-Advance (Abbott)
The brand names mentioned in this table may not be the only relevant products on the market in the United States or other countries.
Mention of a product does not imply an endorsement.
a
100% partially hydrolyzed protein.

Most standard formulas intended for term infants contain intact protein derived from cow’s milk. One standard
formula contains 100% partially hydrolyzed protein. (Other partially hydrolyzed formulas are further discussed later
in this chapter.) The protein content in term infant formulas ranges from 2 to 2.2 g per 100 kcal and provides 8%–
12% of energy. The amount of protein in term infant formula is higher than in HM to compensate for lower
bioavailability.
The ratio of whey-to-casein content in HM is variable (from 80:20 early in lactation to approximately 60:40 in
mature milk) but always higher than the ratio in cow’s milk (18:82). The whey-to-casein ratio of standard cow’s
milk–based formulas varies from being the same as its original source, cow’s milk protein (18:82) to being more
similar to HM (80:20).
The fat source in these formulas is a blend of vegetable oils and typically provides 40%–50% of energy. Lactose
is the main carbohydrate source, as it is in HM. Other sources of carbohydrate found in standard infant formula
include oligosaccharides, maltodextrin, and sucrose.
Lactose-free and reduced-lactose standard infant formulas are available (Table 5-7); they contain corn syrup
solids, maltodextrin, cornstarch, and sucrose as the carbohydrate sources. Because these products contain trace
amounts of lactose, they are not indicated in infants with galactosemia.

TABLE 5-7. Examples of Lactose-Free Standard Term Infant Formulas

Indications for Use Characteristics Product Examples (Manufacturers)

• Lactose intolerance
• Contain trace amounts of • Similac Sensitive (Abbott)
• Not indicated for lactose • Similac Pro-Sensitive (Abbott)
galactosemia
The brand names mentioned in this table may not be the only relevant products on the market in the United States or other countries.
Mention of a product does not imply an endorsement.

The AAP recommends that infants who are formula fed receive an iron-fortified infant formula. The AAP also
recommends vitamin D supplementation to meet the DRI for all infants whose formula intake is less than 32 oz/d.25

Lower-Calorie (19 kcal/oz) Standard Infant Formulas

Most standard formulas available for term infants in the United States provide 20 kcal/oz; however, lower-calorie
standard formulas (19 kcal/oz) have recently been made available. The rationale for lower-calorie products is based
on published data measuring the calorie content in HM36 and donor HM37 as well as concerns about the incidence of
childhood obesity.
In 2015 Abrams and Hawthorne conducted a systematic review of 4 European controlled trials in full-term
infants to assess growth outcomes when infants were fed formulas lower in protein and energy than traditional cow’s
milk protein–based infant formulas.38 Although the formulas in this investigation differed from formulas historically
available in the United States, their concentrations of energy and protein were similar to calorie and protein levels in
recently introduced lower-calorie products in the United States. The authors concluded that the range of protein and
energy delivery from the lower-energy, lower-protein formulas is associated with adequate growth despite small
variances in growth and body composition differences. The studies in the systematic review showed that full-term
infants receiving formula lower in protein and energy content grew similar to breastfed infants. However, Abrams
and Hawthorne suggest cautious use of these products, especially in former preterm infants and infants born small
for gestational age, until further long-term studies are conducted.38
Notably, the Special Supplemental Nutrition Program for Women, Infants, and Children has not approved the
use of 19 kcal/oz formulas. Therefore, some powdered, concentrated liquid, and RTF products may be available for
both retail purchase and hospital use in both 19 kcal/oz and 20 kcal/oz concentrations. These products may have
similar labels, which could lead to confusion among consumers.

Soy-Based, Lactose-Free Infant Formulas

Soy-based infant formulas (Table 5-8) contain soy protein isolate. One product contains partially hydrolyzed soy
protein as the protein source. L-methionine, taurine, and L-carnitine are added to compensate for the naturally low
content of these amino acids in soy protein. Soy-based infant formulas are available as 19 and 20 kcal/oz products.
The protein content is 2.45–2.66 g per 100 kcal, which is slightly higher than the protein content of cow’s milk–
based infant formulas to compensate for the lower quality of soy protein. The fat source of soy-based infant
formulas is a blend of vegetable oils. These formulas are lactose free and contain corn syrup solids, corn
maltodextrin, and sucrose as the carbohydrate sources. Soy-based formulas are lower in osmolality than cow’s milk–
based formulas.

TABLE 5-8. Examples of Soy Protein-Based Infant Formulas

Indications for Use Characteristics Product Examples (Manufacturers)

• Galactosemia
 • Galactosemia
• Transient lactase
deficiency • Enfamil Prosobee (Mead Johnson)
• Cow's milk allergy if not • Gerber Good Start Soy (Gerber)a
• Lactose free
associated with soy • Similac for Diarrhea (Abbott)b
protein allergy • Similac Soy Isomil (Abbott)
• Caregiver's preference for
vegetarian option
The brand names mentioned in this table may not constitute a comprehensive list of all relevant products on the market in the United States
or other countries. Mention of a product does not imply an endorsement.
a
Partially hydrolyzed soy protein.
b
Contains fiber.

Soy protein isolate contains phytates, which may inhibit mineral absorption (primarily calcium, phosphorus,
iron, and zinc). To compensate, the calcium and phosphorus concentrations of soy-based formulas are approximately
30% higher compared to standard cow’s milk–based formula. Soy-based formulas are fortified with iron and zinc,
similar to standard cow’s milk–based formulas for term infants. Their vitamin D content is similar to that of standard
formula.
There has been much debate on the safety of soy-based infant formulas. A systematic review with meta-analysis
was published in the British Journal of Nutrition in 2014.39 The authors found that children fed soy-based infant
formulas had similar anthropometric growth outcomes as children fed standard cow’s milk–based formula or HM.
Despite the high levels of phytates and aluminum in soy-based infant formula, the infants’ serum zinc and calcium
levels and bone mineral content were also found to be similar. The authors concluded that soy-based infant formulas
are safe options for term infants requiring this type of formula.39
The AAP has provided guidelines on the indications for use of soy-based infant formulas.40 Because soy
formulas are lactose free, they are recommended for infants with galactosemia (hereditary lactase deficiency) and
infants with documented transient lactase deficiency. It is also indicated when an infant who is not allergic to soy
protein has an immunoglobulin E–associated allergy to cow’s milk protein. Soy-based formulas are an acceptable
option for a term infant whose parents seek a vegetarian alternative to cow’s milk–based formula.
Due in part to the higher phytate and aluminum content of these formulas, the AAP recommends that soy
protein–based formulas not be given to preterm infants with birth weights less than 1800 g.40 These formulas do not
promote optimal weight gain, linear growth, or bone mineralization in this population. Preterm infants receiving
these formulas have been reported to have lower serum levels of phosphorus, higher serum levels of alkaline
phosphatase, and higher frequency of osteopenia. High amounts of aluminum present in soy protein–based formulas
compete with calcium absorption and may contribute to osteopenia in preterm infants.
Fruzza and colleagues have reported that soy protein interferes with the absorption of exogenous thyroid
hormone used to treat congenital hypothyroidism.41 There-fore, it is prudent to avoid soy protein–based formulas in
the presence of hypothyroidism. The authors state that increased monitoring and increasing the dose of thyroid
replacement therapy is warranted when infants with hypothyroidism are receiving soy protein–based formulas.
There are several additional instances when soy protein–based infant formulas are contraindicated. Soy protein–
based infant formulas are not recommended in the prevention of colic or atopic disease. Infants with food protein–
induced enterocolitis or enteropathy should not be fed soy-based formula because proteins from both cow’s milk and
soy are the most common causes of these conditions, and 25%–64% of affected infants have allergies to both types
of proteins.40,42 Soy-based formula containing sucrose is contraindicated in infants with either sucrose-isomaltase
deficiency or hereditary fructose intolerance.40

Antiregurgitation Infant Formulas

Two standard cow’s milk protein–based infant formulas contain added rice starch to reduce reflux symptoms (Table
5-9). These products are slightly thicker in viscosity than standard infant formulas. Because they thicken in the low
pH of the stomach, they may not be as effective when given with an antacid. Both products are predominately
casein-based and contain 2.14–2.5 g of protein per 100 kcal. One is lactose free and contains corn syrup solids, rice
starch, and sucrose as the carbohydrate sources. The other has a carbohydrate source of approximately 60% lactose,
with the rest of the carbohydrate from rice starch and maltodextrin. Fat sources are vegetable oils, including
safflower, sunflower, soy, coconut, and palm olein oils. Unlike standard infant formula mixed with infant cereal or
thickeners, these formulas do not provide more energy from carbohydrate than standard formula would, and they
flow freely through a standard nipple. Clinicians should be aware that these formulas have a slightly higher viscosity
than standard formulas, so they may not flow through a feeding tube as easily, especially if the formula is
concentrated.

TABLE 5-9. Examples of Infant Formulas Marketed to Reduce Regurgitation

Indications for Use Characteristics Product Examples (Manufacturers)

• Contain added& rice
• To reduce reflux& starch • Enfamil AR (Mead& Johnson)
symptoms • Slightly higher& viscosity • Similac for Spit Up& (Abbott)a
than& standard formulas
The brand names mentioned in this table may not constitute a comprehensive list of all relevant products on the market in the United States
or other countries. Mention of a product does not imply an endorsement.
a
Lactose free.

The North American and European Societies for Pediatric Gastroenterology, Hepatology, and Nutrition updated
their clinical guidelines on the management of gastroesophageal reflux disease in 2018.43 They state that the use of
antiregurgitation formula may reduce visible regurgitation; however, it is unclear if this type of formula improves
other reflux symptoms or has adverse effects. The guidelines suggest considering the provision of lower volumes of
formula to reduce the incidence of reflux symptoms; also, if severe symptoms persist, a trial of an extensively
hydro-lyzed or amino acid–based formula may be warranted.

Low-Electrolyte/Low-Mineral Infant Formula for Renal Disease

As of 2019, 1 term infant formula is marketed for use in infants with renal disease (Table 5-10). This formula is
lower in phosphorus to assist in the management of hypocalcemia and hyperphosphatemia, especially in infants with
impaired renal function. Protein sources include whey protein concentrate and sodium caseinate. The protein content
is 2.2 g per 100 kcal. The whey-to-casein ratio is 60:40. This product has a slightly lower potential renal solute load
(18.3 mOsm per 100 kcal) than standard term infant formulas (18.6–19.6 mOsm per 100 kcal) and is isotonic. The
carbohydrate source is lactose. Fat sources include safflower, soy, and coconut oils. This product is lower in
calcium, phosphorus, and potassium than standard cow’s milk–based formulas. It is also low in iron (0.7 mg per 100
kcal). An iron supplement is indicated for infants receiving this formula. DHA and ARA are not added to this
formula. This product is available in powdered form only.

TABLE 5-10. Example of a Low-Mineral Infant Formula

Indications for Use Characteristics Product Example (Manufacturer)

• Contains less calcium,
phosphorus, and
• Renal disease potassium than standard • Similac PM 60/40 (Abbott)
term infant formulas
• Contains lactose
The brand name mentioned in this table may not constitute a comprehensive list of all relevant products on the market in the United States or
other countries. Mention of a product does not imply an endorsement.

Modified-Fat Infant Formula

As of 2019, 1 infant formula that is low in LCTs and high in MCTs is marketed in the United States to meet the
needs of infants with chylothorax (Table 5-11). The whey-to-casein ratio is 60:40, and the formula contains 3.5 g of
protein per 100 kcal. The product is only available as a RTF commercially sterile liquid and provides 30 kcal/oz;
however, the formula can be diluted with water to provide a lower energy density. This formula is lactose free and
has corn syrup solids as its carbohydrate source. Fat constitutes 46% of total energy, with MCTs providing 83% of
the fat. Soy oil provides the other source of fat as well as essential fatty acids.

TABLE 5-11. Example of a Modified-Fat Infant Formula

Indications for Use Characteristics Product Example (Manufacturer)

• Chylothorax
• Low in LCTs and high in
• Chylous ascites • Enfaport (Mead Johnson)
MCTs
• Intestinal lymphangiectasia
Abbreviations: LCT, long-chain triglyceride; MCT, medium-chain triglyceride.
The brand name mentioned in this table may not constitute a comprehensive list of all relevant products on the market in the United States or
other countries. Mention of a product does not imply an endorsement.

Partially Hydrolyzed Infant Formulas

Partially hydrolyzed infant formulas (Table 5-12) contain protein in the form of peptides from partially broken-down
whey protein or a combination of partially hydrolyzed whey and either casein protein or whey protein concentrate
solids. Partially hydrolyzed formulas have a lower concentration of intact cow’s milk protein than standard term
infant formulas. Compared with formulas containing extensively hydrolyzed protein, the partially hydrolyzed
formulas contain cow’s milk peptides and thus may elicit an allergic reaction in patients with cow’s milk protein
allergy.25 The protein content in these formulas is between 2.2 and 2.3 g per 100 kcal.

TABLE 5-12. Examples of Partially Hydrolyzed Infant Formulas

Indications for Use Characteristics Product Examples (Manufacturers)

• Intended • Enfamil NeuroPro Gentlease
• Lower concentration of
to improve symptoms
intact cow's milk (Mead Johnson)a
of fussiness, gas, and
protein than • Enfamil Reguline (Mead Johnson)a
colic
in standard term • Gerber Good Start Soothe (Gerber)a
• Not intended for cow's infant formulas
milk protein allergy • Similac Total Comfort (Abbott)b
The brand names mentioned in this table may not constitute a comprehensive list of all relevant products on the market in the United States
or other countries. Mention of a product does not imply an endorsement.
a
Reduced lactose.
b
Trace lactose.

These formulas are lactose free or reduced in lactose content compared with HM. In addition to or in place of
lactose, other carbohydrate sources may include corn maltodextrin, corn syrup solids, and sucrose. Fat sources for
these products include a blend of vegetable oils such as safflower, sunflower, soy, coconut, palm olein, and DHA
and ARA.
These low-lactose products are marketed to improve symptoms such as fussiness, crying, and gas associated
with lactose intolerance. Partially hydrolyzed formulas are not considered hypoallergenic, and they are not effective
nor indicated for use in infants with cow’s milk protein allergy.42

Extensively Hydrolyzed Protein Infant Formulas

Infant formulas that are considered hypoallergenic contain extensively hydrolyzed protein. Extensively hydro-lyzed
protein formulas (Table 5-13) contain whey and casein protein from cow’s milk that has been heat-treated for
hydrolysis and/or enzymatically hydrolyzed. The extensively hydrolyzed proteins are broken down into short-chain
peptides and amino acids. These products are supplemented with amino acids. The protein content is 2.6–2.8 g per
100 kcal.

TABLE 5-13. Examples of Extensively Hydrolyzed Infant Formulas

Indications for Use Characteristics Product Examples (Manufacturers)

• Cow's milk allergy • Gerber Extensive HA (Gerber)a
• Soy protein allergy • Considered hypoallergenic • Nutramigen (Mead Johnson)
• Fat malabsorption if • Lactose free • Pregestimil (Mead Johnson)a
formula contains medium-
• Similac Alimentum (Abbott)a
chain triglycerides
The brand names mentioned in this table may not constitute a comprehensive list of all relevant products on the market in the United States
or other countries. Mention of a product does not imply an endorsement.
a
Contains medium-chain triglycerides.

Extensively hydrolyzed formulas are lactose free. The carbohydrate sources are corn syrup solids, corn
maltodextrin, tapioca starch, potato starch, modified cornstarch, and sucrose. According to the AAP, formulas
labeled as hypoallergenic should demonstrate in clinical trials to not provoke reactions in 90% of infants with
confirmed cow’s milk allergy with 95% confidence.42 The AAP recommends use of extensively hydrolyzed infant
formulas in infants with cow’s milk and soy protein allergies.42
One of the formulas in this category is indicated for infants with cow’s milk protein allergy and has long-chain
fatty acids (LCFAs) as its fat source. The fat source in the other 3 products in this category is a combination of
LCFAs and MCTs. Infants with liver disease, cystic fibrosis, chylothorax, and intestinal failure who have fat
malabsorption and lack adequate bile salt may benefit from a hydrolyzed formula containing MCTs because MCTs
do not require bile salt to form a micelle for absorption.25 The amount of fat from MCTs in these formulas is 33%–
55%.

Amino Acid–Based Infant Formulas

Amino acid–based infant formulas (Table 5-14) contain 100% free amino acids. These formulas contain 2.8–3.1 g of
protein per 100 kcal. Amino acid–based infant formulas are also lactose free and contain corn syrup solids and
modified tapioca starch as the carbohydrate sources. The fat source is a combination of LCFAs and MCTs, with
MCTs providing 33%–43% of the energy from fat. The AAP recommends that a free amino acid–based product is
indicated when a formula-fed infant has severe allergies and an extensively hydrolyzed infant formula has not
resolved symptoms.25

TABLE 5-14. Examples of Amino Acid–Based Infant Formulas

Indications for Use Characteristics Product Examples (Manufacturers)

• Alfamino Infant (Nestlé)a
• Severe cow's milk allergy • Elecare for Infants (Abbott)a
• Contain 100% free amino
• Severe soy protein allergy • Neocate Infant (Nutricia)a
acids
• Fat malabsorption • Neocate Syneo Infant (Nutricia)a
• PurAmino (Mead Johnson)
The brand names mentioned in this table may not constitute a comprehensive list of all relevant products on the market in the United States
or other countries. Mention of a product does not imply an endorsement.
a
Contains medium-chain triglycerides.

Preterm Infant Enteral Formulas

Human Milk Fortifiers

The AAP recommends HM for preterm infants and advises that it should be fortified for infants born weighing less
than 1500 g.44 Commercially available pasteurized liquid HM-based fortifiers as well as liquid and powdered cow’s
milk protein–based fortifiers are used to increase the nutrient content of HM by providing additional energy, protein,
iron, vitamin D, calcium, phosphorus, and sodium (Table 5-15).45 The AAP, FDA, and CDC advise against the use
of powdered formulas in neonatal intensive care units (NICUs).4,6

TABLE 5-15. Examples of Human Milk Fortifiers

Indications for Use Characteristics Product Examples (Manufacturers)

• Enfamil HMFAL (Mead Johnson)a
• Enfamil Human Milk Fortifier Powder
(Mead Johnson)a
• Prolacta +4 H2MF (Prolacta
Bioscience)b
• To fortify HM • Concentrated products
• Similac Human Milk Fortifier
Concentrated Liquid (Abbott)a
• Similac HMF HPCL (Abbott)a
• Similac Human Milk Fortifier Powder
(Abbott)a
The brand names mentioned in this table may not constitute a comprehensive list of all relevant products on the market in the United States
or other countries. Mention of a product does not imply an endorsement.
Abbreviations: HM, human milk; HMFAL, human milk fortifier acidified liquid; HMF HPLC, human milk fortifier hydrolyzed protein
concentrated liquid.
a
Derived from cow’s milk.
b
Derived from HM.

Preterm Infant Formulas

Preterm infant formulas (Table 5-16) are higher in protein, calcium, phosphorus, vitamins A and D, sodium, and
other nutrients to meet the high nutrition needs of the preterm infant. They are only available as sterile liquid. They
are available in 20, 24, and 30 kcal/oz RTF forms in 2-oz bottles.

TABLE 5-16. Examples of Infant Formulas Marketed for Preterm Infants

Indications for Use Characteristics Product Examples (Manufacturers)

• Higher in protein
• Oral and enteral feeding and select micronutrients
• Enfamil Premature High Protein
of very-low-birth- than standard term
(Mead Johnson)
weight infants formulas
• Similac Special Care High Protein
when human milk is not • Available as 20, 24,
(Abbott)
sufficiently available and 30 kcal/oz ready-to-
feed products
 feed products
The brand names mentioned in this table may not constitute a comprehensive list of all relevant products on the market in the United States
or other countries. Mention of a product does not imply an endorsement.
Preterm infant formulas are high in protein and provide a range of 3–3.6 g of protein per 100 kcal. One brand has
a whey-to-casein ratio of 80:20, and the other available product has a ratio of 60:40. Lactose is the source of 15%–
50% of the carbohydrate; corn syrup solids and maltodextrin provide the rest. Preterm formulas are reduced in
lactose because the intestinal lactase content is lower in preterm infants than in term infants. Both available preterm
formulas are high in MCTs, with 40%–50% of energy from fat calories provided by MCTs. The other fat sources are
coconut, soy, and sunflower oils. These products are designed to be lower in LCFAs because the intestinal content
of lipase and bile salts in preterm infants is lower than in term infants.
Preterm infant formulas are indicated for oral and enteral feeding of very-low-birth-weight infants when
maternal HM and donor HM are not sufficiently available.46 These products are not intended for infants who weigh
more than 3600 g because the formulas could provide excessive fat-soluble vitamins and protein to such patients.

Preterm Infant Discharge Formulas

Transitional formulas (Table 5-17) contain higher amounts of protein and minerals to support growth in preterm
infants at the time of discharge from the NICU and after discharge from the hospital. They are higher in these
nutrients compared with standard term infant formula and lower compared with preterm infant formula. Typically,
preterm infants are transitioned from preterm infant formula to these formulas as early as 34 weeks’ postmenstrual
age or when preparing for discharge to home. The standard energy concentration is 22 kcal/oz, and the formulas are
available in RTF and powdered forms. There is no consensus on the benefits on growth and development in infants
receiving these formulas compared with standard term infant formulas.47 Preterm infants without significant medical
complications and growing well on the preterm discharge formula can be transitioned to term infant formulas at 6–9
months of age; however, there is no consensus on the appropriate time to transition.48 It is important to monitor
growth in former preterm infants to allow for individualized nutrition plans.

TABLE 5-17. Examples of Transitional Infant Formulas Marketed for Preterm Infants

Product Examples
Indications for Use Characteristics
(Manufacturers)
• Protein and select
micronutrient levels
• May promote growth in infants born • Enfamil Enfacare
are higher than
prematurely who are (Mead Johnson)
in standard term formulas
being discharged • Similac Neosure (Abbott)
but lower than
in preterm formulas
The brand name mentioned in this table may not constitute a comprehensive list of all relevant products on the market in the United States or
other countries. Mention of a product does not imply an endorsement.

Increasing the Nutrient Density of Infant Formulas

Infants with increased energy and protein requirements and/or those needing a fluid restriction based on their
medical condition may need a formula with an increased energy density. This can be accomplished by mixing
powdered infant formula or a liquid concentrate with less water than is required for standard dilution. Another
option is to add a modular product. The clinician needs to consider the age and medical condition of the infant along
with the components of the infant formula being concentrated when formulating a recipe with increased energy
density.49
Modular carbohydrate and fat products have the advantage of increasing the energy concentration without
significantly increasing the osmolality or renal solute load.50 This can be important for infants with renal issues. The
disadvantage of using modulars is that it alters the proportions of macronutrients in the formula and provides lower
micronutrient concentrations.
Increasing the energy density using only the powdered formula or liquid concentrate maintains the macro-
nutrient distribution and increases the micronutrient density as well. This method also increases the osmolality and
renal solute load.
When a formula with more than 27 kcal/oz is to be used, consider using modular products. Monitor hydration
status of infants receiving infant formulas concentrated to higher energy densities.

Modular Products
Modular products can be used to increase the energy density of infant, pediatric, and adult enteral formulas. They
can be added to the formula prior to the administration of the tube feeding or mixed with water and administered as
a bolus separate from the tube feeding. Available modular products include fiber, intact or extensively hydrolyzed
protein, carbohydrate, MCT, emulsified LCT, and combinations of macronutrients. Specific macronutrient modular
products may be used to modify the macronutrient distribution of products to meet the disease-specific needs of a
patient.

Practice Resources

Manufacturer Information

Selected Manufacturers of Infant Formulas Selected Manufacturers of Pediatric Enteral Formulas

Manufacturer URL
Abbott Nutrition www.abbottnutrition.com
Earth’s Best https://earthsbest.com
Gerber https://medical.gerber.com/products/formulas
The Honest Company www.honest.com
Mead Johnson www.meadjohnson.com/pediatrics/us-en
Nestlé Health Science www.nestlehealthscience.us
Nutricia www.nutriciahealthcare.com
Perrigo Nutritionals (manufacturer of store brands) www.perrigonutritionals.com
Prolacta Bioscience www.prolacta.com

Selected Manufacturers of Pediatric Enteral Formulas

Manufacturer URL
Abbott Nutrition www.abbottnutrition.com
Functional Formularies www.functionalformularies.com/nourish.html
Kate Farms www.katefarms.com/for-clinicians
Nestlé Health Science www.nestlehealthscience.us
Nutricia www.nutriciahealthcare.com
RealFood Blends www.realfoodblends.com
Vitaflo www.nestlehealthscience.us/vitaflo-usa

ASPEN Guidelines and Resources

Boullata JI, Carrera AL, Harvey L, et al. A.S.P.E.N. safe practices for enteral nutrition therapy. JPEN J Parenter
Enteral Nutr. 2017;41(1):15–103. doi:10.1177/0148607116673053.
Fallon EM, Nehra D, Potemkin AK, et al. A.S.P.E.N. clinical guidelines: nutrition support of neonatal patients at
risk for necrotizing enterocolitis. JPEN J Parenter Enteral Nutr. 2012;36(5):506–523.
Jaksic T, Hull MA, Modi B, Ching A, George D, Compher C; A.S.P.E.N. Board of Directors. A.S.P.E.N. clinical
guidelines: nutrition support of neonates supported with extra-corporeal membrane oxygenation. JPEN J
Parenter Enteral Nutr. 2010;34(3):247–253.
Jesuit C, Dillon C, Compher C, A.S.P.E.N. Board of Directors, Lenders CM. A.S.P.E.N. clinical guidelines:
nutrition support of hospitalized pediatric patients with obesity. JPEN J Parenter Enteral Nutr. 2010:34(1):13–
20.
Mehta NM, Skillman HE, Irving SY, et al. Guidelines for the provision and assessment of nutrition support therapy
in the pediatric critically ill patient: Society of Critical Care Medicine and American Society for Parenteral and
Enteral Nutrition. JPEN J Parenter Enteral Nutr. 2017;41(5):706–742.
Nehra D, Carlson SJ, Fallon EM, et al. A.S.P.E.N. clinical guidelines: nutrition support of neonatal patients at risk
for metabolic bone disease. JPEN J Parenter Enteral Nutr. 2013;37(5): 570–598.
Sabery N. A.S.P.E.N. clinical guidelines: nutrition support of children with human immunodeficiency virus
infection. JPEN J Parenter Enteral Nutr. 2009;33(6):588–606.
Wales PW, Allen N, Worthington P, et al. A.S.P.E.N. clinical guidelines: support of pediatric patients with intestinal
failure at risk of parenteral nutrition–associated liver disease. JPEN J Parenter Enteral Nutr. 2014;38(5):538–
557.

References
1. Federal Food, Drug, and Cosmetic Act, §412, Title 21. Code of Federal Regulations 106,107.
2. Bankhead R, Boullata J, Brantley S, et al. Enteral nutrition practice recommendations. JPEN J Parenter
Enteral Nutr. 2009;33:122–167.
3. 21 CFR 107: Infant formula. US Food and Drug Administration website.
https://www.accessdata.fda.gov/scripts/cdrh/cfdocs/cfCFR/CFRSearch.cfm?CFRPart=107&showFR=1.
Updated April 1, 2018. Accessed October 9, 2018.
4. American Academy of Pediatrics. CDC, FDA advise against powdered formula in NICUs. AAP News.
http://www.aappublications.org/content/20/5/219.1. Published May 1, 2002. Accessed October 9, 2018.
5. American Academy of Pediatrics Committee on Nutrition. Nutritional needs of the preterm infant. In:
Kleinman RE, Greer FR, eds. Pediatric Nutrition. 7th ed. Elk Grove Village, IL: American Academy of
Pediatrics; 2014:83–122.
6. Jason J. Prevention of invasive Cronobacter infections in young infants fed powdered infant formulas.
Pediatrics. 2012;130:1–9.
7. Vermilyea S, Goh VL. Enteral feedings in children: sorting out tubes, buttons, and formulas. Nutr Clin Pract.
2016;31: 59–67.
8. Brown B, Roehl K, Betz M. Enteral nutrition formula selection: current evidence and implications for
practice. Nutr Clin Pract. 2015;30:72–85.
9. Bobo E. Reemergence of blenderized tube feedings: ex ploring the evidence. Nutr Clin Pract.
2016;31(6):730–735. doi:10.1177/0884533616669703.
10. Epp L. Blenderized feeding options—the sky’s the limit. Pract Gastroenterol. 2018;42(6):30–39.
11. Escuro AA. Blenderized tube feeding: suggested guidelines to clinicians. Pract Gastroenterol.
2014;38(12):58–66.
12. Walia C, VanHoorn M, Edlbeck A, Feuling MB. The registered dietitian nutritionist’s guide to homemade
tube feeding. J Acad Nutr Diet. 2017;117(1):11–16. doi:10.1016/j. jand.2016.02.007.
13. Samela K, Mokha J, Emerick K, Davidovics ZH. Transition to a tube feeding formula with real food
ingredients in pediatric patients with intestinal failure. Nutr Clin Pract. 2017;32(2):277–281.
doi:10.1177/0884533616661011.
14. Gallagher K, Flint A, Mouzaki M, et al. Blenderized Enteral Nutrition Diet Study: feasibility, clinical and
microbiome outcomes of providing blenderized feeds through a gastric tube in a medically complex pediatric
population. JPEN J Parenter Enteral Nutr. 2018; 42(6):1046–1060. doi:10.1002/jpen.1049.
15. Pentiuk S, O’Flaherty T, Santoro K, Willging P, Kaul A. Pureed by gastrostomy tube diet improves gagging
and retching in children with fundoplication. JPEN J Parenter Enteral Nutr. 2001;35(3):375–379.
 doi:10.1177/0148607110377797.
16. O’Flaherty T, Santoro K, Pentiuk S. Calculating and preparing a pureed-by-gastrostomy-tube (PBGT) diet
for pediatric patients with retching and gagging postfundoplication. ICAN Infant Child Adolesc Nutr.
2011;3(6):361–364. doi:10.1177/1941406411423702.
17. Vieira MMC, Santos VFN, Bottoni A, Morais TB. Nutritional and microbiological quality of commercial
and homemade blenderized whole food enteral diets for home-based enteral nutritional therapy in adults.
Clin Nutr. 2018; 37(1):177–181. doi:10.1016/j.clnu.2016.11.020.
18. Escuro AA, Hummel AC. Enteral formulas in nutrition support practice: is there a better choice for your
patient? Nutr Clin Pract. 2016;31:709–722.
19. Mogensen KM. Essential fatty acid deficiency. Pract Gastroen terol. 2017;41(6):37–44.
20. American Academy of Pediatrics Section on Breastfeeding. Breastfeeding and the use of human milk.
Pediatrics. 2012; 129(3):e827–e841. doi:10.1542/peds.2011-3552.
21. Centers for Disease Control and Prevention. Breastfeeding report card. United States 2014.
https://www.cdc.gov/breastfeeding/pdf/2014breastfeedingreportcard.pdf. Published July 2014. Accessed
October 9, 2018.
22. Healthy People 2020. https://www.healthypeople.gov. Accessed October 9, 2018.
23. Schulman AJ. A concise history of infant formula (twists and turns included). Contemp Pediatr.
2003;20(2):91–103. http://www.contemporarypediatrics.com/pediatrics/concise-history-infant-formula-
twists-and-turns-included. Accessed October 9, 2018.
24. Rossen LM, Simon AE, Herrick KA. Types of infant formulas consumed in the United States. Clin Pediatr.
2016;55(3): 278–285.
25. American Academy of Pediatrics Committee on Nutrition. Formula feeding of term infants. In: Kleinman
RE, Greer FR, eds. Pediatric Nutrition. 7th ed. Elk Grove Village, IL: American Academy of Pediatrics;
2014:61–82.
26. Qawasmi A, Landeros-Weisenberger A, Leckman JF, et al. Meta-analysis of long-chain polyunsaturated
fatty acid supplementation of formula and infant cognition. Pediatrics. 2012;129:1141–1149.
27. Hadders-Algra M. Effect of long-chain polyunsaturated fatty acid supplementation on neurodevelopmental
outcome in full-term infants. Nutrients. 2010;2:790–804.
28. Patel RM, Denning PW. Therapeutic use of prebiotics, probiotics and postbiotics to prevent necrotizing
enterocolitis: what is the current evidence? Clin Perinatol. 2013;40(1):11–25.
29. Murguia-Peniche T, Mihatsch WA, Zegarra J, et al. Intestinal mucosal defense system, part 2: probiotics and
prebiotics. J Pediatr. 2013;162(3 suppl):S64–S71.
30. Wall R, Ross RP, Ryan CA, et al. Role of gut microbiota in early infant development. Clin Med Pediatr.
2009;3:45–54.
31. Hess JR, Greenberg NA. The role of nucleotides in the immune and gastrointestinal systems: potential
clinical applications. Nutr Clin Pract. 2012;27:281–294.
32. Singhal A, Kennedy K, Lanigan J, et al. Dietary nucleotides and early growth in formula-fed infants: a
randomized controlled trial. Pediatrics. 2010;126:e946–e953.
33. Hernell O, Timby N, Domellöf M, Lönnerdal B. Clinical benefits of milk fat globule membranes for infants
and children. J Pediatr. 2016;173(Suppl):S60–S65. doi:10.1016/j.jpeds.2016.02.077.
34. Billeaud C, Puccio G, Saliba E, et al. Safety and tolerance evaluation of milk fat globule membrane-enriched
infant formulas: a randomized controlled multicenter non-inferiority trial in healthy term infants. Clin Med
Insights Pediatr. 2014;8:51–60. doi:10.4137/CMPed.S16962.
35. Timby N, Domellöf E, Hernell O, Lönnerdal B, Domellöf M. Neurodevelopment, nutrition, and growth until
12 mo of age in infants fed a low-energy, low-protein formula supplemented with bovine milk fat globule
membranes: a randomized controlled trial. Am J Clin Nutr. 2014;99(4):860–868.
doi:10.3945/ajcn.113.064295.
36. de Halleux V, Rigo J. Variability in human milk composition: benefit of individualized fortification in very-
low-birth-weight infants. Am J Clin Nutr. 2013;98(suppl):529S–535S.
37. Wojcki KY, Rechtman DJ, Lee ML, Montoya A. Macro-nutrient analysis of a nationwide sample of donor
breast milk. J Am Diet Assoc. 2009;109:137–140.
38. Abrams SA, Hawthorne KM. A systematic review of controlled trials of lower-protein or energy-containing
infant formulas for use by healthy full-term infants. Adv Nutr. 2015; 6(2):178–188.
39. Vandenplas Y, Castrellon PG, Rivas R, et al. Systematic review with meta-analysis: safety of soya-based
infant formulas in children. Br J Nutr. 2014;111(8):1340–1360.
40. Bhatia J, Greer F, Committee on Nutrition. Use of soy protein-based formulas in infant feeding. Pediatrics.
 2008; 121(5):1062–1068.
41. Fruzza AG, Demeterco-Berggren C, Jones KL. Unawareness of the effects of soy intake on the management
of congenital hypothyroidism. Pediatrics. 2012;13(3): e699–e702. doi:10.1542/peds.2011-3350.
42. American Academy of Pediatrics. Committee on Nutrition. Hypoallergenic infant formulas. Pediatrics.
2000;106(2): 346–349.
43. Rosen R, Vandenplas Y, Singendonk M, et al. Pediatric gastroesophageal reflux clinical practice guidelines:
joint recommendations of the North American Society for Pediatric Gastroenterology, Hepatology, and
Nutrition and the European Society for Pediatric Gastroenterology, Hepatology, and Nutrition. J Pediatr
Gastroenterol Nutr. 2018;66(3):516–554. doi:10.1097/MPG.0000000000001889.
44. American Academy of Pediatrics Committee on Nutrition. Breastfeeding. In: Kleinman RE, Greer FR, eds.
Pediatric Nutrition. 7th ed. Elk Grove Village, IL: American Academy of Pediatrics; 2014:41–60.
45. Ziegler EE. Human milk and human milk fortifiers. In: Koletzko B, Poindexter B, Uauy R, ed. Nutritional
Care of Pre term Infants: Scientific Basis and Practical Guidelines. Basel, Switzerland: Karger; 2014:215–
227.
46. Hay WW, Hendrickson KC. Preterm formula use in the pre-term very low birth weight infant. Semin Fetal
Neonatal Med. 2017;22(1):15–22. doi:10.1016/j.siny.2016.08.005.
47. Nzegwu NI, Ehrenkranz RA. Post-discharge nutrition and the VLBW infant: to supplement or not
supplement? Clin Perinatol. 2014;41(2):463–474. doi:10.1016/j.clp.2014.02.008.
48. Andrew B, Pellerite M, Myers P, Hageman J. NICU follow-up: medical and developmental management age
0 to 3 years. NeoReviews. 2014;15(4):123–132.
49. Nevin-Folino NL, Loughead JL, Loughead ML. Enhanced-calorie formulas: considerations and options.
Neonatal Netw. 2001;20(1):7–15.
50. Pereira-da-Silva L, Diaz MP, Virella D, Moreira AL, Serelha M. Osmolality of preterm formulas
supplemented with nonprotein energy supplements. Eur J Clin Nutr. 2008; 62(2): 274–278.
 CHAPTER 6

Enteral Nutrition Orders

Introduction
The process of communicating the enteral nutrition (EN) order involves a number of steps and includes several
essential elements, which are also to be included on the patient-specific label for the dispensed EN (see Chapter 7
for additional information on labeling). The goal is to communicate the order to all healthcare providers for the
benefit of the patient. The nutrition support clinician ordering EN needs to have an understanding of adult and
pediatric nutrient requirements and the potential for ordering errors that can occur with an EN prescription. This
chapter reviews general considerations for EN ordering, adult and pediatric nutrient dosing requirements, methods
of administration, selected special considerations, and sample calculations.

General Considerations
Ordering decisions should factor in patient-specific variables, such as current disease state, nutrition status, available
enteral access, condition of the gastrointestinal (GI) tract, and estimated age-specific nutrition requirements. An
institution should construct an EN formulary that is broad enough to provide for the nutrition needs of its patients
without becoming overwhelming to manage. See Chapter 1 for discussion of nutrition assessment, Chapter 3 for
details about enteral access, and Chapter 4 for additional information on formularies.

Nutrient Requirements
Nutrient requirements for EN can reasonably be based on the Dietary Reference Intakes (DRIs).1 These nutrient
standards are based on data generated from epidemiological, depletion-repletion, and clinical intervention studies
using appropriate indicators of nutrient adequacy, including clinical and functional outcome markers. The DRIs—or,
more specifically, the Recommended Dietary Allowances (RDAs) and Adequate Intakes (AIs)—are estimates for
healthy individuals to prevent deficiencies and minimize the risk from nutrition-related chronic disease and
developmental dis orders. Therefore, nutrition support clinicians must recognize certain inherent limitations about
the application of RDAs and AIs for patients receiving EN. First, the DRIs are designed to be met from a usual diet.
Also, although the RDAs and AIs take individual variability into account, the DRIs are not intended for use in
people with acute or chronic disease.
Enteral formulas can provide daily vitamin and mineral intakes to achieve requirements for most individuals
(adults and pediatrics). However, some patients may require additional micronutrient supplementation. Clinicians
should assess patients for signs and symptoms of nutrient deficiencies and use clinical judgment regarding the
appropriateness of administering micronutrient supplements. See Table 6-1 for practice recommendations related to
nutrient requirements.

TABLE 6-1. Practice Recommendations for Determining Nutrient Requirements

1. Determination of nutrient requirements should be individualized, based on assessment of body

composition and function, and fall within acceptable ranges, while taking physiological and
pathophysiological conditions into account.
2. When determining requirements for pediatric patients, also consider the individual's needs with
 regard to growth and development.

Adult Patients
The usual maintenance goals for energy and protein for adult patients receiving EN are presented in Table 6-2.2,3

TABLE 6-2. Estimated Energy and Protein Requirements for Adult Patients

Parameter Critically III Patients Stable Patients

Energy, kcal/kg/d 25-30 20-30
Protein, g/kg/d 1.5-2 1-1.5
Source: Data are from references 2 and 3.
According to the third edition of The ASPEN Adult Nutrition Support Core Curriculum,4 initial fluid needs
(mL/d) can be estimated for adults by calculating the average of results from the following 2 formulas:

• Equation 1 (based on body weight and age):

◦ Ages 18–55 years: 35 mL × Body Weight (kg)
◦ Ages 56–75 years: 30 mL × Body Weight (kg)
◦ Ages > 75 years: 25 mL × Body Weight (kg)
• Equation 2 (Holliday-Segar formula adjusted for age):
◦ Ages ≤ 50 years: 1500 mL for First 20 kg Body Weight + [20 mL × Remaining Body Weight (kg)]
◦ Ages > 50 years: 1500 mL for First 20 kg Body Weight + [15 mL × Remaining Body Weight (kg)]

When using such estimates, clinicians must exercise careful clinical judgment regarding the individual’s fluid
status. Fluid prescriptions should take into account the patient’s weight, age, and clinical condition and address any
additional fluid losses that require replacement.4

Pediatric Patients and Neonates

The usual goals for energy, protein, and fluid intake for pediatric patients are presented in Tables 6-3, 6-4, and 6-5.5
For guidelines on usual vitamin, mineral, and electrolyte requirements, refer to the DRIs.1

TABLE 6-3. Daily Energy Requirements for Pediatric Patients

Age Group Energy Requirements,a kcal/kg/d

Preterm neonates 90–120
<6 mo 85–105
6–12 mo 80–100
1–7 y 75–90
7–12 y 60–75
12–18 y 30–50
aAssumes normal age-related organ function and normal losses.
Source: Adapted with permission from reference 5: Ayers P, Guenter P, Holcombe B, Plogsted S, eds. A.S.P.E.N. Parenteral Nutrition
Handbook. 2nd ed. Silver Spring, MD: American Society for Parenteral and Enteral Nutrition; 2014:124.
 TABLE 6-4. Daily Protein Requirements for Pediatric Patients

Age or Weight Group Protein Requirements,a g/kg/d

Preterm neonates 3-4
Birth to age 1 y 2-3
Weight >10 kg or ages 1-10 y 1-2
Ages 11-17 y 0.8-1.5
a
Assumes normal age-related organ function and normal losses.
Source: Adapted with permission from reference 5: Ayers P, Guenter P, Holcombe B, Plogsted S, eds. A.S.P.E.N. Parenteral Nutrition
Handbook. 2nd ed. Silver Spring, MD: American Society for Parenteral and Enteral Nutrition; 2014:124.

TABLE 6-5. Daily Fluid Requirements for Pediatric Patients

Body Weight Fluid Requirements,a mL/kg

<1-1.5 kg 150
1.5-2.5 kg 120
First 10 kg 100
Second 10 kg 50
Each additional kg 20
a
Assumes normal age-related organ function and normal losses.
Source: Adapted with permission from reference 5: Ayers P, Guenter P, Holcombe B, Plogsted S, eds. A.S.P.E.N. Parenteral Nutrition
Handbook. 2nd ed. Silver Spring, MD: American Society for Parenteral and Enteral Nutrition; 2014:125.

Methods of Administration
EN may be administered as bolus, intermittent, continuous, or volume-based feedings.

• Bolus feedings deliver a specific volume of formula, typically using either a syringe or gravity drip via a
feeding container, over a short period of time (eg, <30 minutes). Bolus feeding may be more physiological
than intermittent or continuous feedings because bolus feedings tend to mimic the normal intake of an oral
diet. Bolus feedings also may help prevent constipation by inducing the gastrocolic reflex.
• Intermittent feedings are delivered via a feeding container or bag for 30–60 minutes, with or without the use
of an enteral feeding pump.6
• Continuous feedings are feedings administered using a feeding pump at a constant hourly rate of EN
administration; they may be provided around the clock or as a cyclic feeding (eg, administered for 8 hours
nightly).
• With volume based feedings, a total volume of EN to be administered in 24 hours is prescribed and there is
an option to adjust the administration rate from time to time within the 24-hour period, as long as the
required total volume is administered.

Initiation and Advancement of Enteral Feedings

Adult Patients
There are limited prospective data to form strong recommendations regarding the best starting administration rate
for initiation of enteral feeding. Stable patients tolerate a fairly rapid progression of EN, generally reaching the
established goal within 24 to 48 hours of initiation.7 Initiating EN with “half-strength” or diluted enteral formulas is
unnecessary, and the lower osmolality and higher pH of diluted formulas may increase the risk of microbial
contamination.8

Bolus Feedings and Intermittent Feedings

Bolus and intermittent feedings are intended for gastric feeding; bolus feeding directly into the small bowel can lead
to abdominal pain, distention, and diarrhea. Gastric feedings may be initiated with full-strength formula 3 to 8 times
per day, with increases of 60 to 120 mL every 8 to 12 hours, as tolerated, up to the goal volume (ie, the amount of
formula that closely meets the patient’s predicted nutrient needs). When additional water is necessary to meet fluid
requirements, it is administered as intermittent flushes throughout the day. Monitoring of GI tolerance is essential in
formula titration toward the goal.

Pump-Assisted Feedings
A pump is generally required for small bowel feedings and is preferred for gastric feedings in critically ill patients
because the slower administration rate of continuous feedings often enhances tolerance while decreasing the risks of
complications. Pump-assisted feedings are also used when a volume-based feeding protocol is followed.
Conservative initiation and advancement rates are recommended for patients who are critically ill and those who
have not been fed enterally for an extended period of time. In practice, formulas are frequently initiated at 10–40
mL/h and advanced to the goal rate in increments of 10–20 mL/h every 8 to 12 hours, as tolerated. This approach
can usually be used with isotonic formulas as well as high-osmolality or elemental products.9 There is some
evidence that EN can begin at goal rates in stable, adult patients.6,10

Pediatric Patients
When determining the best way to deliver the EN prescription, the patient’s status and current clinical condition
should be considered. For example, in critically ill patients with labile hemodynamics or children with significant
mal-absorption, continuous feeds may be the safest course of action and promote optimal nutrient absorption. In
stable children, bolus or intermittent feedings will more closely mimic what the child’s normal diet would have been
if the patient were able to ingest food orally.11
Initiation and advancement of enteral feedings in pediatric patients is guided by clinical judgment and
institutional practices in the absence of prospective controlled clinical trials. Generally, children are started on an
isotonic formula and the rate is advanced based on feeding tolerance, with the goal of providing 25% of total energy
needs on Day 1.12 When giving gastric feedings, it is possible to concentrate formula once feeding tolerance is
demonstrated, which allows fluid-restricted children to receive more calories.
For patients fed via the gastric route, bolus feedings can be considered. Bolus feeds should not be given over a
shorter period of time than the child would be expected to consume an oral feeding and should not be spaced out at
intervals longer than normal age-based mealtimes.
Children may receive a combination of daytime bolus feeds and nighttime continuous feeds. Continuous feeds
may be better tolerated overnight due to decreased risk of gastroesophageal reflux. For children at home, continuous
feeds overnight may also be a more practical regimen for caregivers.13
However, continuous feeds given via short-term enteral access (eg, nasogastric or nasojejunal tubes) should be
used with caution, especially in the home setting where 24-hour continuous monitoring may not be available. The
feeding tube could be dislodged and pose an aspiration risk if feedings are inadvertently infused above the
esophageal-gastric sphincter.
In general, infant feeding intervals should be every 3–4 hours for a total of 6–8 feeds per day. Older children
may tolerate their full daily volume with 4–5 bolus feedings per day or a combination of daytime bolus and
nighttime continuous feedings. Maximum volumes for continuous and bolus feedings are determined by the child’s
response to the regimen, weight gains, and overall GI status.

Bolus Feedings
To initiate bolus feeds, first determine the daily goal volume of formula and then divide the volume into the desired
number of bolus feeds. Initiate full-strength bolus feeds at 25% of the goal and increase the daily volume by 25%, as
tolerated, up to the goal volume.8 Infants generally eat every 2–3 hours; therefore, bolus feeds should be given in a
similar manner, such as a feeding every 3 hours around the clock (~8 feeds per day). Older children may be able to
tolerate their full volume in 4–5 feeds per day given every 3–4 hours during the day and not require feedings
overnight.
Bolus feedings may be given by several methods. The syringe bolus method involves pouring formula into a
standard 60 mL syringe and allowing it to flow into the tube by gravity. The gravity bag method uses special bags
with a roller clamp on the tubing that allows the formula to flow faster or slower into the tube; this method usually
delivers the feed more slowly than the syringe bolus method. Infants and small children are often given their bolus
feeds on a feeding pump. The pump can be set to deliver bolus or intermittent feeds at a predetermined rate. An
example of a bolus feed via pump would be 90 mL every 3 hours, given over 1 hour via pump at 90 mL/h.

Pump-Assisted (Continuous) Feedings

Continuous EN administered via pump is required if the patient is being fed postpylorically and is recommended if
the patient is critically ill, is hemodynamically unstable, or has significant malabsorption. Full-strength, continuous
EN via pump can be initiated at 1 to 2 mL/kg/h and advanced by 1–2 mL/kg/h every 8 hours, as tolerated, until the
goal volume is achieved.14

Special Considerations

Critically Ill Children

EN is the preferred mode of nutrient delivery and can be safely provided to critically ill infants and children with a
wide variety of diagnoses when the GI tract is functional. However, pediatric intensive care unit (PICU) patients
may not tolerate the initiation and advancement recommendations for the non–critically ill child.
Achieving at least two-thirds of the prescribed energy intake within 5 to 7 days of PICU admission has been
associated with lower 60-day mortality and improved outcomes.15 Initiating EN within 24–48 hours of PICU
admission is recommended16 and has been associated with improved clinical outcomes. Institutional guidelines using
a stepwise, algorithmic approach should be in place to guide initiation and advancement, assess tolerance, and
monitor delivery of the prescribed amounts. A nutrition support team, including a dietitian, is an integral part of the
PICU team and can help to ensure timely and appropriate nutrition interventions throughout the course of therapy.16
The 2017 guidelines for the provision and assessment of nutrition support therapy in the pediatric critically ill
patient from the Society of Critical Care Medicine and American Society for Parenteral and Enteral Nutrition
(ASPEN) suggest that the gastric route may be preferred for patients in the PICU, based on available observational
studies and a weak GRADE (Grading of Recommendations, Assessment, Development, and Evaluations)
recommendation.16 There is not enough evidence to determine whether continuous or intermittent gastric feeding
would be optimal. In patients who are unable to tolerate gastric feeding and those at high risk for aspiration,
postpyloric feeds may be preferable.
Energy needs in critically ill pediatric patients vary widely, and patients in the PICU should be reevaluated
frequently to ensure the appropriateness of the energy prescription. If indirect calorimetry (IC) is available, it should
be used to determine the energy requirements and guide daily order adjustments. If IC is unavailable, the use of the
RDAs or Harris-Benedict equations is not recommended. The Schofield or Food Agriculture Organization/World
Health Organization/United Nations University equations may be used to predict energy expenditure in critically ill
pediatric patients.17–19 Stress factors may be added to these calculations based on the clinical condition of the
individual patient.
When predictive equations are used to estimate energy needs, patients should be routinely monitored for
potential signs of overfeeding, such as elevations in glucose, triglyceride, or carbon dioxide levels, and signs of
underfeeding, such as prolonged ventilator dependence and increased length of PICU stay. Anthropometric
measurements such as weight and mid–upper arm circumference can also be used to monitor adequacy of energy
prescription, although availability and accuracy of these values can be an issue in the critically ill patient.16
Protein requirements are elevated during critical illness; therefore, using the RDA values to determine protein
goals is not recommended for critically ill patients. Optimal protein dosages for critically ill pediatric patients are not
known. Observational studies have indicated a positive association between higher protein delivery and clinical
outcomes. A minimum protein intake of at least 1.5 g/kg/d is recommended to prevent cumulative negative protein
balance, with greater amounts recommended for infants and young children.20,21 Modular protein supplements may
be required in addition to the enteral formula to fully meet the elevated protein requirements of critical illness.
Preterm Infants
Infants with growth failure are at risk for poor developmental outcomes. In addition, poor growth can contribute to
hospital complications—such as necrotizing enterocolitis (NEC), infection and sepsis, and broncho-pulmonary
dysplasia—as well as longer-term problems, such as increased incidence of cerebral palsy and neuro-developmental
deficits.22 Early EN stimulates gut motility and maturation, and human milk (HM), which has important anti-
infectious effects, can be protective against feeding intolerance, NEC, and late-onset sepsis.23,24
Infants with NEC have been shown to have significantly more neurodevelopmental impairment than age-
matched peers.25 Whether that outcome is inevitable or can be changed by nutrition intervention is not known.
Parenteral nutrition is the initial mode of nutrition support for the premature infant and should be started as soon as
possible after birth.26 The timing of the initiation of EN depends on the gestational age of the infant and the patient’s
clinical condition. The concern about NEC governs the timing and advancement of enteral feedings. Research has
been conducted for over 40 years, but investigations to date have failed to identify the optimal feeding method to
prevent NEC.26 Current recommendations include exclusive use of HM, rather than cow’s milk–based products or
formula; initiating minimal EN within the first 2 days of life; and advancing EN by 30 mL/kg/d for infants weighing
1000 g or more.27 For infants weighing less than 1000 g, starting EN at a more conservative rate of 15–20 mL/kg/d
and advancing the volume by 15–20 mL/kg/d may be warranted.28 The safety of early EN initiation and the
relatively faster advancement rate have been confirmed in recent studies as well as a 2017 Cochrane review of 10
randomized controlled trials involving 3753 infants. That review found no increase in NEC when EN was advanced
at a faster rate (30–40 mL/kg/d) versus a slower rate (15–20 mL/kg/d).29 This meta-analysis also concluded that
slower advancement resulted in several days’ delay in establishing full EN and may have been associated with an
increased risk of invasive infection.29
Feeding infants HM exclusively also seems to be protective against NEC. Infants who exclusively receive HM,
including those who are provided supplementation with banked donor HM and HM-based fortifier, have
demonstrated reduced incidence of NEC compared with infants who receive preterm infant formula or a cow’s
milk–based fortifier.30–32 Use of standardized feeding protocols and earlier fortification of HM have been shown to
improve growth for infants receiving HM exclusively.33 However, infants fed HM and HM-based fortifiers
exclusively may have poorer rates of weight gain and growth when compared with those who are fed cow’s milk–
based fortifiers and formula. Consequently, the optimal regimen remains unclear.34
The optimal frequency and route of EN delivery is unclear. In theory, postpyloric feedings are advantageous
because of the decreased potential for gastroesophageal reflux and aspiration into the lungs. However, feeding by
this route may impair the secretion of intestinal hormones and growth factors.35 This method also bypasses the
stomach, whose acidic environment serves as a barrier against potentially pathogenic organisms. Placing a post-
pyloric feeding tube is a challenge, and there are reports of complications, including intestinal perforation and
pyloric stenosis.36,37 Based on the limited evidence available, post-pyloric feeds do not seem to offer increased
benefit over the gastric route.
The advantages and disadvantages of continuous vs intermittent EN in preterm infants are also frequently
debated. Historical trials have pointed toward a worsening of respiratory complications with bolus feeds.38,39 The
continuous feeding method may reach goal feeding volumes faster and promote a faster weight gain.40,41 A 2011
Cochrane review tried to answer the question of which feeding method was best for premature infants weighing less
than 1500 g.42 In a review of 7 trials with over 500 infants, the authors did not find adequate evidence to determine
the best feeding method for low-birth-weight premature infants. Subgroup analysis did reveal faster weight gain and
a trend toward earlier discharge for infants weighing less than 1000 g who were fed continuous nasogastric feeds.42
It is important to note that there are varying degrees of NEC, as well as medical vs surgical types. Patients with
moderate to severe medical NEC or surgical NEC require extremely conservative initiation and advancement of
enteral feedings. See Table 6-6 for additional guidance on feedings for premature infants.27–29

TABLE 6-6. Practice Recommendations for Premature Infant Feedings

For premature infants weighing ≥1000 g who are at risk for NEC, minimal EN should be initiated
1. within the first 2 days of life at 30 mL/kg/d and advanced by 30 mL/ kg/d to a goal of 150-180
mL/kg/d.
 2. For premature infants weighing <1000 g at risk for NEC, minimal EN should be initiated within the
first 2 days of life at 15-20 mL/kg/d and increased by 15-20 mL/kg/d to a goal of 150-180 mL/kg/d.
Strong consideration should be given to the exclusive use of human milk and human milk-based
3.
fortifiers for premature infants at risk for NEC.
Institution-specific standardized feeding protocols for initiation and advancement of feeds should be
4.
used for preterm infants whenever clinically appropriate.
Abbreviations: EN, enteral nutrition; NEC, necrotizing enterocolitis. Source: Information is from references 27-29.

Postoperative Initiation of Enteral Feedings

Traditionally, clinicians were taught that postoperative feedings should wait until there is evidence that (a) bowel
function has returned (as evidenced by flatus or a bowel movement) and (b) the effects of the anesthetic have
diminished enough that the patient can protect the airway when swallowing. This teaching was not based on any
studies but reflected the fear that early postoperative feedings were associated with complications. For example, it
was thought that narcotic pain control might result in an ileus and a patient who was fed too soon could vomit and
aspirate.
These traditional assumptions have been challenged by a variety of studies supporting earlier postoperative
initiation of feedings. For example, the change in approach is clearly demonstrated in an article by Collier and
colleagues about the enteral feeding of patients with an open abdomen following trauma.43 In this retrospective
review, patients with an open abdomen who were fed within 4 days of celiotomy had earlier wound closure, fewer
fistulas, and lower hospital charges when compared with patients whose enteral feedings were initiated more than 4
days after celiotomy.
The patients of greatest concern with regard to EN complications are those who undergo a form of GI surgery.
However, in a randomized controlled trial of patients undergoing elective segmental intestinal or rectal resection,
investigators used a protocol to introduce solids the evening of postoperative Day 1, without waiting for flatus or a
stool, and found that these patients were discharged earlier and had no increase in complications compared with
patients receiving traditional care.44 Another prospective study began a regular diet at 8 hours after GI surgery and
found good tolerance.45
In another investigation, patients undergoing gastrectomy for gastric cancers were randomly assigned to either a
solid diet on demand or the conventional regimen in which a solid diet was initiated on Day 10 after surgery.
Compared with the control group, the patients in the on-demand group had improved clinical outcomes, were able to
tolerate an oral diet sooner, and had shorter hospitalizations.46
Malhotra and associates studied patients presenting emergently with enteric perforations complicated by sepsis
and peritonitis.47 Half of the participants were randomly assigned to receive nasogastric feedings within 48 hours of
surgery. Compared with the controls, the patients who received early feedings had no increase in complications and
experienced less weight loss.47
In a multicenter prospective trial, newborns begun on small feedings by nasogastric tube within 24 hours of
surgery for GI anomalies, without waiting for flatus or stool passage, were compared with a control group who were
fasted until resolution of postoperative ileus. The early feeding group tolerated the feedings without complications
and were discharged sooner than the control group.48
Lewis and colleagues conducted a meta-analysis of 11 studies that began feedings within 24 hours of surgery
compared with a standard waiting period. The analysts concluded that there is no advantage to waiting and found
that patients receiving early feedings had a lower infection rate and were discharged 0.84 days sooner.49
Very few complications have been reported with early postoperative feedings. The most serious complication
has been bowel necrosis; a review of 9 studies in which enteral feedings were responsible for bowel ischemia found
necrosis rates ranging between 1% and 12%.50 The authors of this review indicated that abdominal distention, sepsis,
or worsening general condition should prompt evaluation and discontinuation of enteral feedings.50
The studies reviewed here and others like them are difficult to compare because of the wide variety of surgeries
done before the trials. There is also little literature regarding the optimal composition of the first feedings or the rate
at which they should be initiated and advanced. See Table 6-7 for practice recommendations for the initiation of EN
after surgery.44,45
 TABLE 6-7. Practice Recommendation for Initiating Feedings Postoperatively

Enteral feedings should be started postoperatively in surgical patients without waiting for flatus or a
bowel movement.
The current literature indicates that these feedings can be initiated within 24 to 48 hours.
Source: Information is from references 44 and 45.

Initiation of Feedings After Placement of a Long-Term Enteral Access Device

Several studies of EN after percutaneous endoscopic gastrostomy (PEG) placements in adults have been published.
Two studies with more than 20 patients in each group found no difference in complications with patients fed 3 hours
after placement, compared with those fed the following day.51,52 In another study, adults were administered 50 mL of
diatrizoate sodium into PEGs 3 hours after placement, and no evidence of leakage was found in X-ray of the
abdomen.53 In a more rigorous study, adult patients were randomly assigned to receive formula feedings at 4 hours
or 24 hours after PEG placement. This study, which had over 50 patients in each group and measured post-feeding
residuals, noted no differences in the incidence of complications or in the amount of gastric residuals.54 In a review
paper, Kirby and colleagues described their first 55 PEG placements and stated that they began a trial administration
of water at 2 hours postprocedure without increased complications.55 According to the abstract of an article
published in Spanish, a randomized trial compared a group of patients who began feeding within 30 minutes after
PEG placement with a control group who were not fed for 24 hours postprocedure, and no notable differences in the
complication rates were found between the 2 groups.56
EN can be initiated safely in pediatric patients within 6 hours of gastrostomy tube placement, whether the tube
was inserted using a percutaneous endoscopic, laparoscopic, or open placement method. Earlier initiation of EN
following gastrostomy placement may result in shorter hospital length of stay and is not associated with increased
complications.57 See Table 6-8 for practice recommendations regarding initiation of EN after placement of a
gastrostomy tube.51–57

TABLE 6-8. Practice Recommendation for Initiating Feedings After Placement of a Gastrostomy
Tube

A gastrostomy tube may be used for feedings within several hours of placement. Current literature
supports the initiation of feeding within 2 hours in adults and 6 hours in infants and children.
Source: Information is from references 51-57.

Best Practices in Enteral Nutrition Orders

The use of standardized EN orders offers many advantages. These include the prevention of errors of
omission/commission, the standardization of terminology, and— most importantly—the protection of patient safety.

Elements of the Order

According to ASPEN recommendations, patient-specific EN orders should always include the following 4 essential
elements: (a) patient information; (b) EN formula name; (c) delivery route and access device; and (d) administration
method and rate.8 Additionally, orders should include the water flush type, volume, and frequency and may include
other ancillary or supplemental elements. Crucial information about the EN prescription must be provided on the
labeled product as well as in the order. (See Chapter 7 for more information on labeling requirements.)

Patient Information
The order should clearly state the patient’s name, date of birth, weight, location, and medical record number. Other
relevant information such as allergies and dosing weight should be included.8

EN Formula Name
The formula should be clearly identified in the order by a descriptive generic name, and the use of product-specific
names should be avoided entirely or secondary to the use of the generic term. Examples of generic names (which
should be standardized by the organization) include “standard,” “isotonic,” “calorie-dense,” “semi-elemental,” and
“peptide-based.” The rationale for using generic names is to minimize prescriber confusion. For pediatric patients,
the final energy concentration (kcal/oz) should be noted with the formula name.8
Formula orders should also include options for the administration of modular products used to enhance the
protein, carbohydrate, fat, or fiber content of the enteral regimen. In the adult population, these products are usually
not added to enteral formula. Instead, they are administered separately to the patient via the enteral access device.
Orders for modulars should indicate the prescribed amounts, the frequency of administration, and other instructions.
In the neonatal and pediatric population, fluid tolerance limits are a concern; therefore, the base formula is often
augmented with a modular macro-nutrient. When this type of manipulation to infant or pediatric formula is
prescribed, the base formula, the modular product, and the base and final concentration of formula per 100 kcal are
all considered.58,59 If modu-lars are added to infant or pediatric formula in the home setting, it is important to teach
the parents or caregivers the proper method to prepare a formula with additives. See Chapters 4, 5, and 7 for
additional information on modular products.

Delivery Site (Route) and Enteral Access Device

The order must clearly identify the delivery site (route) for formula administration.6 This information, which is
based on the enteral tube’s distal tip position (gastric or small bowel), helps prevent wrong-site connections and
errors in administration. Multiple instances of enteral misconnections have been reported in the literature.60
Additionally, the order must document the specific enteral access device to be used (eg, nasogastric, orogastric,
gastrostomy, nasojejunal, orojejunal, jejunostomy, or gastrojejunostomy).8

Administration Method and Rate

The administration method (bolus, gravity, or continuous feeds), volume or rate of administration, and timing of
formula delivery within a specified period of time (24 hours, cyclic or volume-based rates) should all be clearly set
forth in an EN order.8

Additional Orders
An EN order can be entered as a single order representing a specific prescription, or multiple orders can be made as
part of a larger protocol that directs advancement of EN from initiation to a goal rate or volume that represents a
nutritionally adequate endpoint. The inclusion of transitional orders will direct weaning from EN, and supplemental
orders may address various patient-care issues related to EN.
Any additional orders that differ from the standard formula rate, route, and volume prescriptions should be
clearly documented.8 These types of orders can include the following:

• Advancement orders: These orders direct the progression of an EN regimen from initiation through to an
endpoint or goal formula volume over a specified time period. Increases in formula volume or rate of
administration to achieve a goal should be clearly stated. EN advancement orders also need to be coordinated
with decreases in parenteral nutrition or intravenous fluids.
• Transitional orders: These orders document incremental decreases in formula volume over a period of time
to accommodate increases in oral intake.
• Ancillary or supplemental orders: Routine or ancillary orders depend on both the population and the setting.
These orders are based on institutional policies for care of the enterally fed patient, such as orders for
flushing the enteral access device, head-of-bed elevation, weight checks, and the monitoring of laboratory
parameters. Supplemental orders could also include orders to confirm enteral access device position,
nutrition support service consultation, or pharmacy consult for enteral drug administration.

Enteral Nutrition Order Forms

Orders may be entered through a computerized prescriber order entry (CPOE) system or using a standardized
electronic template. When the standardized order is incorporated into an electronic health record, further protection
is added against inappropriate orders involving omissions or transcription errors. Paper forms should be used only if
CPOE or electronic forms are unavailable. Completely handwritten orders and telephone orders should be avoided
to minimize the possibility of tran scription errors. Only those abbreviations, acronyms, symbols, and numerical
expressions considered acceptable by the institution should be used in the EN ordering process.8
Whether built into a CPOE system or on a hard copy, the EN order form must contain the 4 essential elements of
an EN order and include transitional and supplemental orders.8 The example in Figure 6-1 should be adapted to meet
the needs of each individual institution.

Many institutional settings use CPOE systems, which should address each of the elements shown in Figure 6-1
(eg, a separate screen in sequence for each element). Ideally, CPOE should also provide clinical decision support.
For example, if a postpyloric enteral access device order is selected, the intermittent administration delivery
screen(s) would not be an option. These systems should be designed with detailed order sets that promote safety by
using drop-down menus within each element of an EN order, including required fields, with limited opportunity to
enter any information as free text. Such menus may facilitate standardized advancement of initial administrations to
goal volumes, uniform enteral access device flushing volumes and methods, and population-specific ancillary
orders. See Table 6-9 for a summary of practice recommendations for EN ordering.8

TABLE 6-9. Practice Recommendations for Enteral Nutrition Ordering

Develop and design standardized EN orders (CPOE or editable electronic templates, or paper as a
1. last resort) for adult and pediatric EN regimens to aid prescribers in meeting each patient's nutrition
needs and to improve order clarity.
Include all critical elements in the EN orders: (1) patient identifiers, (2) the formula name, (3) the
EAD site/device, (4) the administration method and rate, plus (5) water flush type, volume, and
2. frequency. Incorporate the feeding advancement order, transitional orders, and implementation of
complementary orders into protocols. All elements of the EN order must be completed when EN is
modified or reordered.
 3. Avoid the use of unapproved abbreviations or inappropriate numerical expressions.
Encourage the use of generic terms to describe EN formulas. All elements of the EN order must be
4.
completed when EN is modified or reordered.
Provide clear instructions related to modular products, including product dose, administration
5.
method, rate, and frequency.
Establish and enforce policies and procedures that clearly describe the preparation of powdered EN
products, including who will evaluate compatibility, measure the dose, reconstitute the product, what
6.
diluent and source will be used, the location of preparation, labeling including beyond use date and
time, and storage.
Abbreviations: CPOE, computerized prescriber order entry; EAD, enteral access device; EN, enteral nutrition.
Source: Reprinted with permission from reference 8: Boullata J, Carrera AL, Harvey L, et al. ASPEN safe practices for enteral nutrition
therapy. JPEN J Parenter Enteral Nutr. 2017;41(1):15-103. doi:10.1177/0148607116673053.

Sample Calculations
Figure 6-2 illustrates one method of calculating the appropriate EN prescription of formula and water for an adult
patient. Figure 6-3 shows the calculations for a fluid-restricted patient requiring EN with similar provision of energy
and protein. Figure 6-4 provides a sample of the calculations for a pediatric patient.
Practice Resources

Resource URL
Food and Nutrition Information Center DRI
https://fnic.nal.usda.gov/fnic/dri-calculator
Calculator for Professionals
Nutrition and Food Web Archive includes several
calculators relevant to calculating enteral nutrition http://www.nafwa.org
prescriptions)

References
1. Institute of Medicine. Dietary Reference Intakes: The Essen tial Guide to Nutrient Requirements.
Washington, DC: National Academies Press; 2006.
2. McClave SA, Taylor BE, Martindale RG, et al. Guidelines for the provision and assessment of nutrition
support therapy in the adult critically ill patient: Society of Critical Care Medicine (SCCM) and American
Society for Parenteral and Enteral Nutrition (ASPEN). JPEN J Parenter Enteral Nutr. 2016;40:159–211.
3. 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(suppl):1SA–
138SA. (Errata: JPEN J Parenter Enteral Nutr. 2002;26:144.)
4. Canada TW, Lord LM. Fluids, electrolytes, and acid-base disorders. In: Mueller CM, ed. The ASPEN Adult
Nutrition Support Core Curriculum. 3rd ed. Silver Spring, MD: American Society for Parenteral and Enteral
Nutrition; 2017:113–138.
5. Ayers P, Guenter P, Holcombe B, Plogsted S, eds. A.S.P.E.N. Parenteral Nutrition Handbook. 2nd ed. Silver
Spring, MD: American Society for Parenteral and Enteral Nutrition; 2014.
6. Rees RG, Keohane PP, Grimble GK, Frost PG, Attrill H, Silk DB. Tolerance of elemental diet administered
without starter regimen. BMJ. 1985;290:1869–1870.
7. Doley J, Phillips W. Overview of enteral nutrition. In: Mueller CM, ed. The ASPEN Adult Nutrition Support
Core Curriculum. 3rd ed. Silver Spring, MD: American Society for Parenteral and Enteral Nutrition;
2017:213–226.
8. Boullata J, Carrera AL, Harvey L, et al. ASPEN safe practices for enteral nutrition therapy. JPEN J Parenter
Enteral Nutr. 2017;41(1):15–103. doi:10.1177/0148607116673053.
9. 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.
10. Mentec H, Dupont H, Bocchetti M, et al. Upper digestive intolerance during enteral nutrition in critically ill
patients: frequency, risk factors, and complications. Crit Care Med. 2001; 29:1955–1961.
11. Monczka J. Enteral nutrition support: determining the best way to feed. In: Corkins M, Balint J, Bobo E, et
al, eds. The A.S.P.E.N. Pediatric Nutrition Support Core Curriculum. 2nd ed. Silver Spring, MD: American
Society for Parenteral and Enteral Nutrition; 2015:583–592.
12. Marchand V. Enteral nutrition tube feedings. In: Baker S, Baker R, Davis A, eds. Pediatric Nutrition
Support. Boston, MA: Jones and Bartlett; 2007;249–260.
13. Enteral nutrition. In: Kleinman RE, ed. Pediatric Nutrition Handbook. 6th ed. Elk Grove Village, IL:
American Academy of Pediatrics; 2009:541–556.
14. Bankhead R, Boullata J, Brantley S, et al. Enteral nutrition practice recommendations. JPEN J Parenter
Enteral Nutr. 2009;33(2):122–167.
15. Mehta NM, Bechard LJ, Cahill N, et al. Nutritional practices and their relationship to clinical outcomes in
critically ill children—an international multicenter cohort study. Crit Care Med. 2012;40:2204–2211.
16. Mehta NM, Skillman HE, Irving SY, et al. Guidelines for the provision and assessment of nutrition support
therapy in the pediatric critically ill patient: Society of Critical Care Medicine and American Society for
Parenteral and Enteral Nutrition. JPEN J Parenter Enteral Nutr. 2017;41(5):706–742.
17. van der Kuip M, Oosterveld MJ, van Bokhorst-de van Schueren MA, et al. Nutritional support in 111
 pediatric intensive care units: a European survey. Intensive Care Med. 2004;30:1807–1813.
18. Schofield WN. Predicting basal metabolic rate, new standards and review of previous work. Hum Nutr Clin
Nutr. 1985; 39(suppl 1):5–41.
19. World Health Organization. Energy and Protein Requirements: Report of a Joint FAO/WHO/UNU Expert
Consultation. Technical report series 724. Geneva, Switzerland: World Health Organization; 1985.
20. Jotterand Chaparro C, Laure Depeyre J, Longchamp D, et al. How much protein and energy are needed to
equilibrate nitrogen and energy balances in ventilated critically ill children? Clin Nutr. 2016;35:460–467.
21. Bechard LJ, Parrott JS, Mehta NM. Systematic review of the influence of energy and protein intake on
protein balance in critically ill children. J Pediatr. 2012;161:333–339.
22. Prince A, Groh-Wargo S. Nutrition management for the promotion of growth in very low birth weight
premature infants. Nutr Clin Pract. 2013;28(6):659–668.
23. Ziegler EE. Meeting the nutritional needs of the low-birth-weight infant. Ann Nutr Metab. 2011;58(suppl
1):8–18.
24. Tsang RC, Uauy R, Koletzko B, et al. Nutrition of the Preterm Infant: Scientific Basis and Practical
Guidelines. 2nd ed. Cincinnati, OH: Digital Educational; 2005.
25. Rees CM, Pierro A, Eaton S. Neurodevelopmental outcomes of neonates with medically and surgically
treated necrotizing enterocolitis. Arch Dis Child. 2007;92:F193–F198.
26. Greer FR. Nutrition support of the premature infant. In: Baker SR, Baker RD, Davis AM, eds. Pediatric
Nutrition Sup port. Sudbury, MA: Jones and Bartlett; 2007:383–392.
27. Fallon E, Nehra D, Potempkin A, et al. A.S.P.E.N. clinical guidelines: nutrition support of neonatal patients
at risk for necrotizing enterocolitis. JPEN J Parenter Enteral Nutr. 2012;36(5):506–523.
28. Dutta S, Singh B, Chessell L, et al. Guidelines for feeding very low birth weight infants. Nutrients.
2015;7:423–442.
29. Oddie SJ, Young L, McGuire W. Slow advancement of enteral feed volumes to prevent necrotising
enterocolitis in very low birth weight infants. Cochrane Database Syst Rev. 2017; (8):CD001241.
doi:10.1002/14651858.CD001241.pub7.
30. Sullivan S, Schanler RJ, Kim JH, et al. An exclusively human milk-based diet is associated with a lower rate
of necrotizing enterocolitis than a diet of human milk and bovine milk-based products. J Pediatr.
2010;156:562–567.
31. Cristofalo EA, Schanler RJ, Blanco CL, et al. Randomized trial of exclusive human milk versus preterm
formula diets in extremely premature infants. J Pediatr. 2013;163:1592–1595.
32. Herrman K, Carroll K. An exclusively human milk diet reduces necrotizing enterocolitis. Breastfeed Med.
2014;9: 184–190.
33. Huston RK, Markell AM, McCulley EA, et al. Improving growth for infants ≤1250 grams receiving an
exclusive human milk diet. Nutr Clin Pract. 2018;33(5):671–678. doi:10.1002/ncp.10054.
34. Quigley M, Embleton ND, McGuire W. Formula versus donor breast milk for feeding preterm or low birth
weight infants. Cochrane Database Syst Rev. 2018;(6):CD002971. doi:10.1002/14651858.CD002971.pub4.
35. Milner RD, Minoli I, Moro G, et al. Growth and metabolic and hormonal profiles during transpyloric and
nasogastric feeding in preterm infants. Acta Paedriatr Scand. 1981;70:9–13.
36. McAlister WH, Seigel MJ, Shackelford GD, et al. Intestinal perforation by tube feedings in small infants:
clinical and experimental studies. Am J Roentgenol. 1985;145:687–691.
37. Raine PA, Goel KM, Young DG, et al. Pyloric stenosis and transpyloric feeding. Lancet. 1982;2:821–822.
38. Blondheim O, Abbasi S, Fox WW, et al. Effect of enteral gavage feeding rate on pulmonary functions of
very low birth weight infants. J Pediatr. 1993;122:751–755.
39. Nelle M, Hoecker C, Linderkamp O. Effects of bolus tube feeding on cerebral blood flow velocity in
neonates. Arch Dis Child Fetal Neonatal Ed. 1997;76:F54–F56.
40. Dsilna A, Christensson K, Alfredsson L, et al. Continuous feeding promotes gastrointestinal tolerance and
growth in very low birth weight infants. J Pediatr. 2005;147:43–49.
41. Silvestre MA, Morbach CA, Brans YW, et al. A prospective randomized trial comparing continuous versus
intermittent feeding methods in very low birth weight infants. J Pediatr. 1999;134:293–297.
42. Premji SS, Chessel I. Continuous nasogastric milk feeding versus intermittent bolus milk feeding for
premature infants less than 1500 grams. Cochrane Database Syst Rev. 2011;(11): CD001819.
doi:10.1002/14651858.CD001819.pub2.
43. Collier B, Guillamondegui O, Cotton B, et al. Feeding the open abdomen. JPEN J Parenter Enteral Nutr.
2007;31:410–415.
44. Delaney CP, Zutshi M, Senagore AJ, Remzi FH, Hammel J, Fazio VW. Prospective, randomized, controlled
 trial between a pathway of controlled rehabilitation with early ambulation and diet and traditional
postoperative care after laparotomy and intestinal resection. Dis Colon Rectum. 2003;46:851–859.
45. Lucha PA, Butler R, Plichta J, Francis M. The economic impact of early enteral feeding in gastrointestinal
surgery: a prospective survey of 51 consecutive patients. Am Surg. 2005;71(3):187–190.
46. Hirao M, Tsujinaka T, Takeno A, Fujitani K, Kurata M. Patient-controlled dietary schedule improves clinical
outcome after gastrectomy for gastric cancer. World J Surg. 2005; 29:853–857.
47. Malhotra A, Mathur AK, Gupta S. Early enteral nutrition after surgical treatment of gut perforations: a
prospective randomized study. J Postgrad Med. 2004;50:102–106.
48. Ekingen G, Ceran C, Guvenc BH, Tuzlaci A, Kahraman H. Early enteral feeding in newborn surgical
patients. Nutrition. 2005;21:142–146.
49. Lewis SJ, Egger M, Sylvester PA, Thomas S. Early enteral feeding versus “nil by mouth” after
gastrointestinal surgery: systematic review and meta-analysis of controlled trials. BMJ. 2001;323:1–5.
50. Melis M, Fichera A, Ferguson MK. Bowel necrosis associated with early jejunal feeding: a complication of
postoperative enteral nutrition. Arch Surg. 2006;141:701–704.
51. Brown DN, Miedema BW, King PD, Marshall JB. Safety of early feeding after percutaneous endoscopic
gastrostomy. J Clin Gastroenterol. 1995;21:330–331.
52. Choudhry U, Barde CJ, Markert R, Gopalswamy N. Percutaneous endoscopic gastrostomy: a randomized
prospective comparison of early and delayed feeding. Gastrointest Endosc. 1996;44:164–167.
53. Nolan TF, Callon R, Choudry U, Reisinger P, Shaar CJ. Same day use of percutaneous endoscopic
gastrostomy tubes: radiographic evidence of safety. Am J Gastroenterol. 1994;89:1743.
54. McCarter TL, Condon SC, Aguilar RC, et al. Randomized prospective trial of early versus delayed feeding
after percutaneous endoscopic gastrostomy placement. Am J Gastroen terol. 1998;93:419–421.
55. Kirby DF, Craig RM, Tsang T K, Plotnick BH. Percutaneous endoscopic gastrostomies: a prospective
evaluation and review of the literature. JPEN J Parenter Enteral Nutr. 1986;10:155–159.
56. Carmona-Sanchez R, Navarro-Cano G. Percutaneous endoscopic gastrostomy: is it safe to start eating
immediately? Rev Gastroenterol Mex. 2002;67:6–10.
57. Jensen AR, Renaud E, Drucker NA. Why wait: early enteral feeding after pediatric gastrostomy tube
placement. J Pediatr Surg. 2017;53:656–660.
58. Klein CJ. Nutrient requirements for preterm infant formulas. J Nutr. 2002;132(6 suppl):1395S–1577S.
59. Raiten DJ. LRSO report: assessment of nutrient requirements for formulas. J Nutr. 1998;128(11
suppl):2059S–2293S.
60. Guenter P, Hicks RW, Simmons D, et al. Enteral feeding misconnections: a consortium position statement. Jt
Comm J Qual Patient Saf. 2008;34:285–292.
 CHAPTER 7

Preparation, Labeling, and Dispensing of Enteral

Nutrition

Introduction
The safe and accurate provision of enteral nutrition (EN), including human milk (HM) for infants as well as infant,
pediatric, and adult formulas, within the healthcare setting is critical for ensuring patient safety and promoting
positive outcomes.1,2 Some patients require individualized enteral feeding regimens. In the pediatric setting,
fortification of HM or the use of powdered or concentrated liquid formulas may be required to modify the nutrient
density of EN (see Chapter 5).3–5 In both the adult and pediatric settings, modulars may be mixed with water and
administered as a bolus separate from the tube feeding. In the pediatric setting, modular products may also be added
to formula prior to the administration of the tube feeding (see Chapters 4 and 5 for additional information on
modulars).5 The more extensively enteral feedings are manipulated, the greater the risks are for preparation errors
and contamination—and both types of risk may be life threatening.2,4,6 Consequently, it is imperative that healthcare
facilities critically evaluate their processes and implement well-defined procedures that employ best practices for the
preparation, labeling, and dispensing of HM and formulas for infant, pediatric, and adult patients.

Microbiology and Contamination of Enteral Nutrition

Microbial contamination of EN may occur at any step in the preparation, dispensing, and administration process:
during expression and collection of HM, in the manufacturer’s production of formulas, during preparation and
storage within the healthcare facility, or when EN is administered to the patient.1
Enteral feedings as a source of hospital-associated infections have been reported in the literature.7–15 HM and
enteral formulas provide ideal growth media for microbes (nutrients, moisture, oxygen, and the proper pH).1 Both
normal flora and pathogenic microorganisms are common in the hospital environment.16,17 Of particular concern are
those that are resistant to heat, antibiotics, and disinfectants as well as those that continue to grow at refrigerator
temperatures.8,9,13,17–20 While pathogenic microorganisms are of greatest concern, even the introduction of those not
considered pathogenic, such as gram-positive rods (including Bacillus), is concerning, especially for
immunocompromised patients, because infections and sepsis have been linked to such species in the neonate.7,21–24 In
addition to contamination of feedings during preparation and administration, retrograde contamination has also been
described in the literature, potentially affecting up to 85% of EN feedings in the neonatal intensive care setting.25
Potential points of contamination for EN in the healthcare setting are identified in Figure 7-1 (formula) and Figure 7-
2 (HM).
Reducing Risks for Contamination and Preparation Errors
Optimal processes are needed to reduce the risk of enhancing growth of microbes that may be present in nonsterile
feedings as well as risk of introducing new microorganisms to sterile and nonsterile feedings.2 Recommendations for
safe practices in the preparation and dispensing of EN have been widely published, with emphasis on the importance
of preparation location, aseptic technique, trained staff, and prevention of misadministration of HM and/or
formulas.1,2,26–28 Individual state regulations and Joint Commission standards require healthcare institutions to
prepare food and nutrition products (which includes HM and formulas) under proper conditions, taking sanitation,
storage, and security into account.1,29
See Table 7-1 for practice recommendations for safe preparation of enteral formulas.2 Additional
recommendations specific to the safe preparation of HM, infant and pediatric formulas, and blenderized tube
feedings (BTFs), as well as the labeling of EN, are addressed later in this chapter. For resources on hand hygiene,
refer to the Suggested Reading and Practice Resources section at the end of the chapter.
 TABLE 7-1. Practice Recommendations for Safe Preparation of Enteral Nutrition Formulas

1. Use competent personnel trained to follow strict aseptic technique for formula preparation.
Establish and follow protocols for preparation, handling, and storage of commercial and handmade
2.
EN.
3. Use a closed EN system when possible.
If using an open system, use formula decanted from container with a screw cap instead of a flip
4.
top, if possible.
Use effective hand hygiene and a clean work space when handling enteral formulas. When gloves
5.
are used, they must be clean gloves, not having been involved in other unrelated tasks.
Use equipment dedicated for EN use only. Keep all equipment as clean and dry as possible. Store
6.
clean equipment away from potential sources of contamination.
Follow practice recommendations, manufacturer guidelines, and/or facility policies for
7.
administration hang times.a
8. Use strict aseptic technique for powdered formula preparation.
9. Refrigerate unused formula and use within 24 hours of preparation or opening.
Expose reconstituted formulas to room temperature for no longer than 4 hours. Discard unused
10.
formula after this time.
11. Use a sterile water source for formula reconstitution.
12. Avoid mixing additives directly into formula when possible.
13. Periodically survey and regularly monitor adherence to safety protocols.
Abbreviation: EN, enteral nutrition.
a
See Chapter 8 for additional information on hang times.
Source: Information is from reference 2.

Formula Selection and Storage

While illness related to contaminated formulas is not common, it is suspected that incidents may be under-
reported.30,31 Furthermore, ingestion of contaminated formulas could result in serious injury or death.30,31 The US
Food and Drug Administration (FDA) is responsible for monitoring microbiological quality of commercial
formulas.32–34 (See Chapters 4 and 5 for additional information on FDA regulation of formula.)
Commercially sealed liquid formulas are sterile as long as the packaging remains intact. Commercial powdered
formulas are not sterile at the time of manufacture; therefore, extra care is required to prevent both the proliferation
of existing microbes and the introduction of new organisms. Contamination of powdered infant formulas with
Cronobacter (a gram-negative member of the Entero bacteriaceae family that is found in the environment and a
variety of foods) and Salmonella has been reported in the literature. Powdered formulas should only be used within
the healthcare setting if no commercially sterile alternative is available.1,30,35–37 Liquid formulas are heat sterilized,
making them preferable for immunocompromised and hospitalized patients.
Sterile ready-to-feed (RTF) formulas pose the lowest risk with regard to contamination because they require no
preparation prior to use; therefore, they should be used in healthcare facilities when nutritionally appropriate.1
However, care must still be taken to avoid contamination during feeding administration. Research has shown that
bedside handling of sterile RTF formulas may still result in microbial growth.7 As discussed in the next sections of
this chapter, use of closed EN systems, when available, and safe practices for hang times further reduce risk of
contamination.1,2,14
Unopened formulas should be stored in a dry area at room temperature (13°C/55°F to 24°C/75°F) to minimize
risks to the products’ nutrient and physical integrity. These products should be rotated using “first in, first out”
(FIFO) storage techniques.1,38–40 Storage of opened containers of formula and prepared feedings is discussed later in
the chapter.

Closed vs Open Enteral Nutrition Systems

A closed EN system uses a bag or rigid container of liquid formula that is prepackaged by the manufacturer and
ready to administer (hang). With an open EN system, formula is decanted into an enteral container before
administration. Use of closed EN systems involves less manipulation of enteral formulas and feeding administration
sets, which reduces the risk of contamination.41–45 Using a closed system has also been shown to reduce nursing
time.42 How-ever, closed systems tend to be more expensive and are not appropriate for all situations. When open
EN systems are used, hand hygiene, proper handling and storage procedures, and observation of recommended hang
times reduce risk of contamination.
According to findings from a survey of American Society for Parenteral and Enteral Nutrition members
published in 2017, the use of open systems in acute care was 25% for adults, 62% for pediatrics, and 76% for
neonates.46 These data may reflect the lack of availability of pediatric or infant formulas in closed systems (many
infant and pediatric formulas are powders that require reconstitution). In long-term acute care hospitals, closed
systems are used 87% of the time; notably, most patients in this setting are adults. In home care, 11% of the survey
respondents used closed systems. This finding may reflect the use of bolus feedings in this setting.46

Hang Times
Exceeding the recommended hang time for EN is a safety risk whether a closed or open system is used.
Manufacturer hang time recommendations for closed EN containers vary but may be up to 48 hours; hang times for
EN administered in an open system are considerably shorter (see Chapter 8). Refer to facility-specific policies when
determining all hang times.2

Effective Use of Technology

Utilization of technology, including use of bar code scanning systems, may reduce risk of preparation errors by
automating enteral recipe calculations, automating calculation of expiration dates and times, ensuring proper HM
identification, and confirming correct formula and additive product identities.1,3,6,7,28,47 Furthermore, technology may
promote improved staff efficiency while allowing for automated tracking of a variety of metrics, including
productivity, compliance, errors and near misses, and product lot numbers in the event of a recall.1,3,6,7,28,47

Water Safety
Commercially prepared sterile water as a source of purified water is preferred for formula preparation, hydration,
and feeding tube flushes within the acute care setting and with immunocompromised patients due to the potential for
contamination of tap water.2,48 Chilling sterile water prior to formula preparation is recommended to assist the final
product in reaching appropriate storage temperatures (≤4°C [≤40°F]) as quickly as possible.1,49
If commercial sterile water is not available, tap water may be sterilized by bringing the water to a full rolling boil
for 1–2 minutes and allowing to cool. However, sterilizing does not make the water purified; this requires
filtration.2,39,40,50 Knowledge of the lead content of the water supply (available from the Environmental Protection
Agency website) is important if tap water is used because lead is known to be harmful to health, particularly in
infants, children, and pregnant women.51

Additives
Addition of any component to EN increases the risk of introducing microbes into the final product, as well as other
risks such as clogged tubing. In the pediatric setting, macro-nutrient modular products may be added to feedings at
the time of preparation. Additives that are considered medications (such as vitamin/mineral preparations and
electrolytes) should be administered by appropriately licensed staff; addition of such items is generally considered
outside the scope of practice of the feeding preparation room.1 (See Chapter 10 for additional information on
medication administration.) Colorants have been linked to serious adverse outcomes and risk of contamination;
therefore, colorants should not be added to feedings for any reason (including detection of aspiration).52

Preparation Space, Equipment, and Staffing

The benefits of a dedicated centralized space with dedicated trained staff for the preparation of HM and pediatric
formulas have been well documented in the literature. 1,6,7,26,28,47,53,54 Published recommendations for the pediatric
setting suggest a preparation space solely designated for preparing enteral feedings that supports aseptic technique
and is physically separate from patient care areas.1,6,7,28,55 The space should allow for an efficient and logical
workflow from clean to dirty for optimal function and safety.1,55,56 Such a model reduces the risk of contami-nation,
preparation errors, and HM errors (use of the wrong patient’s HM).6,7,26,28,47,53,54 Furthermore, many states now
require a designated feeding preparation space for new neonatal intensive care unit construction.55,57–67

Equipment and Supplies

Refrigerators and Freezers
Refrigerators are necessary both for ingredient storage and for holding of the final prepared product.1 Facilities
preparing HM will also require freezer storage.1 The overall capacity and number of refrigerators and freezers
required will be based on the type of EN managed (HM, pasteurized donor HM, and/or formula), taking into account
the space necessary for ingredient storage and volume of feedings prepared daily.1
Guidelines for storage times and temperatures for HM provided to healthy infants at home are available from the
Centers for Disease Control and Prevention and the Academy of Breastfeeding Medicine.68,69 Within the healthcare
setting, however, the recommended temperature ranges and duration of storage are more conservative to prevent
illness in immunocompromised patients.1,2,27,68 Facility refrigerators must have the ability to maintain temperatures
between 2°C and 4°C (35°F and 39°F), while HM storage freezers must sustain temperatures of ≤4°C
(≤39°F).1,2,8,68–70 Often, laboratory-or pharmacy-grade units are preferred for their ability to better maintain desired
temperatures despite frequent opening.1
Refrigeration unit temperatures should be confirmed using a thermometer that meets the National Institute of
Standards and Technology requirements.1 A temperature monitoring system with an alarm to alert staff of
temperatures outside the desired ranges promotes patient safety and can prevent HM waste in the event of equipment
malfunction.1 It may also be prudent to have HM refrigerators and freezers plugged into outlets that provide
emergency power to prevent loss in the event of a power outage.5,27,70 Once HM has thawed, it must be used within
24 hours or discarded; however, HM that is partially thawed and still contains ice crystals may be refrozen.1,27
Refrigerators used to store EN should be regularly cleaned and well organized using FIFO storage methods.1 Use
of plastic bins or resealable plastic bags may help with organization and FIFO and lessens the risk for errors by
keeping each individual patient’s EN separated from others.1 This may be particularly important for HM feedings,
which, if fed to the incorrect patient, constitute a bodily fluid exposure.1 Access to EN refrigerators and HM freezers
should be limited to authorized staff to reduce risk of error, tampering, and waste.1,27

Sinks and Dishwashers

Recommendations for the pediatric setting include use of a separate, hands-free sink for hand hygiene.1 See
Suggested Reading and Practice Resources at the end of the chapter for additional information on hand hygiene.
If nondisposable items are used for EN preparation, proper equipment for sanitation is required. A commercial
dishwashing machine, separate from the facility’s foodservice dishwasher, is recommended.1 Wash temperatures of
66°C (150°F) and rinse temperatures of 82°C (180°F) are needed to meet National Sanitation Foundation standards
as well as most local codes.71,72 Alternatively, reusable items may be hand-washed in a single-compartment sink and
autoclaved or sanitized using a 3-compartment sink (wash, rinse, and chemically sanitize).73

Carts
Delivery carts may be needed to transport prepared feedings from the preparation area to the patient unit(s).
Temperature maintenance of 2°C–4°C (35°F–39°F) for facility-prepared EN is critical to prevent microbial growth
and possible foodborne illness.73 The time and distance required for EN delivery will determine the type of cart
needed. Feedings may be transported in ice baths; alternatively, insulated carts and temperature-controlled carts are
available for appropriate temperature maintenance.1

Laminar Flow Hood

While a laminar flow hood may provide an additional barrier to potential contaminants, a hood is not required for
EN preparation.1 Commonly used in the preparation of sterile pharmaceutical products, use of a laminar flow hood
is not required for the preparation of oral (ie, nonsterile) medications, and its use with nonsterile products (including
HM and powdered formulas) does not result in a sterile final product.74,75 If a laminar flow hood is used, staff must
be adequately trained and demonstrate competency on well-defined operating procedures.1

Measuring and Mixing Devices

All items used in the preparation and storage of pediatric EN should be made of bisphenol A (BPA)–free and di(2-
ethylhexyl) phthalate (DEHP)–free food-grade plastic or stainless steel; glass items (such as graduated cylinders or
beakers) are not recommended because of the risk of glass particles.72 Reusable items should be sanitized between
uses with different formulas to prevent cross contamination of allergens and between individual patient HM
preparations to prevent biological cross contamination. Single-use, disposable items may be preferred for ease and
sanitation.
Liquid ingredients should be measured using graduated cylinders, beakers, liquid measuring cups, or syringes.1
Powdered ingredients should be measured using a gram scale accurate to 0.1 g.1
Scoops and household measurements should not be used for EN preparation in healthcare facilities because of
the high variability of the measuring devices themselves as well as variability in packing the powder.1,76 Research
has shown that inconsistencies in packing and technique contribute to differences of 10%–25% when scoops or
household measurements are used.77 Calibration of scales should be conducted per manufacturer guidelines and per
facility biomedical engineering standards to verify the accuracy of weights.1
Whisks with solid handles and immersion blenders with removable blades are both acceptable types of mixing
devices because they may be properly cleaned and sanitized.1,72 Upright blenders are not recommended for the
preparation of EN because it is not possible to adequately sanitize parts and gaskets.1

Storage Containers
When HM and prepared EN are stored, food-grade and BPA-and DEHP-free storage containers with leak-proof,
solid surface lids must be used.27,78 Single-use containers and syringes must be clean, but they do not need to be
sterile as there is no evidence that use of nonsterile items results in higher microbial counts in collected HM or
prepared EN.1,27 Reusable containers must be appropriately cleaned and sanitized between uses.1

Thawing and Warming Equipment

Microwave ovens must not be used for thawing HM or warming EN because there is a potential for nutrient losses
and a risk of hot spots within the feeding, which could cause burns.38,49,79–81 Safe methods of thawing frozen HM and
warming prepared EN include use of water baths, bead baths, and commercial milk warmers.27,81,82 Tap water is a
potential source of microbial contamination; therefore, steps must be employed to prevent water from coming into
contact with the feeding itself if water baths or water-based commercial warmers are utilized.82,83

Staff Hygiene and Apparel

Use of disposable gowns over clean scrubs or other professional attire is recommended when preparing EN.1 Gowns
should be changed between type of formula preparation (such as between milk-based formulas and hypoallergenic
formulas) to prevent cross contamination of allergens from residue that may be present on the gown.
Personal protective items such as a bonnet or hairnet and beard cover (if needed) should be used when preparing
HM and formulas.1 As allowed by the facility, a face mask may be used for minor illnesses (if changed frequently);
however, staff preparing EN should be in good health and follow the facility’s employee health standards.84
To minimize risk for infection transmission, EN preparation staff should have short, unpolished, natural
nails.85–87 Gloves are recommended, but they are not required in the handling of HM and EN if effective hand-
washing techniques are employed.1,27 Furthermore, gloves should not be considered a substitute for appropriate hand
hygiene.16

Preparation, Dispensing, and Administration of Human Milk and Pediatric Enteral

Nutrition

Human Milk
Policies for the use of HM within the healthcare setting must address more than breastfeeding.3 HM for hospitalized
infants is typically expressed, stored, thawed, fortified, and fed (either by mouth or via tube).3 Therefore, systems
must be in place to preserve HM nutrients and immune factors during storage and processing and document
appropriate expiration dates/times, while reducing risk of contamination, fortification errors, and
misadministration.3,27,88 Expressed HM is not sterile and contains beneficial microorganisms (probiotic organisms
and commensal, nonpathogenic organisms that support establishment of optimal gut flora).1 However, if HM is not
collected under sanitary conditions, stored at proper temperatures, and safely transported to the hospital, it may
become contaminated by harmful viruses and/or bacteria.27,89,90 Proper cleaning of breast pumps and personal
collection kits is critical to decrease contamination rates at the time of HM expression and subsequent risk of
infection, sepsis, and/or feeding intolerance in the preterm or ill infant.77,88,89,91–95 Donor HM that has been
appropriately commercially pasteurized is sterile, but it may still become contaminated during storage, handling, and
administration if improper procedures are used.1
It is imperative that HM be labeled clearly to prevent administration errors. Preprinted labels and/or bar coding
systems may help avoid HM administration errors. See the Labeling Enteral Nutrition section later in this chapter for
additional information on labeling elements for HM.

Preparation Steps in the Healthcare Setting

HM and pediatric enteral formulas should be prepared in a dedicated space that supports aseptic technique by trained
staff using well-defined procedures that promote accuracy in fulfillment of the provider order. Table 7-2 provides an
overview of steps for HM and pediatric EN preparation within the hospital setting.1,2 EN in home care is discussed in
Chapter 11.

TABLE 7-2. Steps for Human Milk and Pediatric Enteral Nutrition Preparation

Perform hand hygiene:

• Upon entry into the preparation area;
1. • After sanitizing work spaces;
• Before and after preparing each type of formula and each individual patient's human milk;
• As needed for ongoing aseptic technique.
Don appropriate personal protective gear as outlined by facility policies (such items may include
2.
gowns, bonnets or hairnets, beard covers, masks).
3. Confirm the provider's order.
4. Confirm the recipe for fortified human milk or formula.
Sanitize preparation surfaces:
• Prior to initiating feeding preparation;
5.
• Before and after each type of formula and each individual patient's human milk;
• As needed for ongoing aseptic technique.
Assemble needed supplies and ingredients:
• Employ first-in-first-out techniques for formulas, fortifiers, modulars, and human milk bottles.
• Thaw human milk using appropriate techniques, taking care to avoid waste.
6.
• Perform a double-check procedure to confirm correct human milk before decanting, combining,
preparing, or relabeling any human milk. This double-check procedure may be (a) a manual 2-
person verification of a minimum of 2 patient identifiers; or (b) bar code scanning.

7. Don gloves (following hand hygiene) prior to preparing the human milk or formula feeding.

Measure ingredients using appropriate equipment and

 aseptic technique.
8.
• Measure human milk, sterile water, and liquid formulas using graduated cylinders, beakers,
liquid measuring cups, or syringes.
• Measure powdered ingredients using a gram scale.
• Verify that equipment is clean and sanitized to prevent cross contamination of microbes and
allergens.
9. Combine ingredients in a clean disposable container or a reusable clean and sanitized container.
Decant prepared enteral nutrition into a closed
container for delivery.
• No more than 24-hour volumes may be prepared.
10.
• Feedings may be dosed into units for individual feedings or in bulk volumes.
• New, clean disposable containers may be sterile or nonsterile.
• Reusable containers must be cleaned and sanitized between uses.
11. Label each container: See the labeling recommendations later in this chapter.
Refrigerate prepared human milk or formula immediately in the preparation area, patient
12.
unit refrigerator, or patient in-room refrigerator for up to 24 hours after preparation.
Source: Information is from references 1 and 2.

Dispensing and Administration

Closed, food-grade containers should be used to deliver prepared HM and EN; feedings dispensed in single doses
reduce risk of contamination by limiting handling at bedside.1 If bulk volumes (up to a 24-hour supply) are prepared,
care must be taken to avoid introduction of contaminants when each feeding is retrieved.1,16 Temperatures must be
maintained during delivery from the preparation area to the patient unit or room.1 Adherence to proper hang times,
tubing changes, and EN expiration times during administration is critical for infection prevention.2 HM and facility-
prepared formulas should not be held at room temperature for more than 4 hours.2,15,25,96 Sterile RTF formulas should
not exceed hang times of 4 hours for neonates (infants younger than 30 days) and immunocompromised
infants/children; 8-hour hang times are acceptable for sterile RTF formulas for nonimmunocom-promised pediatric
patients older than 30 days.2,15,25,96 Any pediatric EN remaining in the bottle 1 hour after an oral feeding has begun
should be discarded due to potential bacterial contamination from the oral flora.49 See Chapter 8 for additional
information on administration and monitoring of EN.

Blenderized Tube Feedings

The term blenderized tube feeding may refer to either homemade or commercially prepared blended whole foods.
Both types of BTF are gaining popularity with patients receiving EN.97–99 BTF can be provided exclusively or in
conjunction with a standard polymeric formula.
A disadvantage to the use of homemade BTF is the risk of cross contamination and potential for foodborne
illness. Once prepared, homemade BTF should be immediately used or refrigerated at appropriate temperatures.100
Home-made BTF should not be held at room temperature for more than 2 hours due to concerns about bacterial
contamination. For this reason, a bolus regimen is recommended instead of continuous infusion.100 Refrigerated
homemade BTF that is not used within 24 hours of preparation should be discarded. Commercially prepared BTFs
have longer hang times of 8–12 hours, depending on manufacturer recommendations.97
Another disadvantage to homemade BTF is the potential for clogged feeding tubes, which may be related to
varying consistencies in the blended formula. The FDA has published recommendations on the preparation of home-
made BTF to prevent clogged feeding tubes, including use of high-end blenders or increasing blend time with
existing blenders.101 Additional recommendations on administration of homemade BTF are found in Table 7-3, the
practice resources at the end of this chapter, and Chapters 8 and 11.2 See Chapters 4, 5, and 8 for additional
information on commercially prepared BTF products.
 TABLE 7-3. Practice Recommendations for Blenderized Tube Feedings

Prepare homemade BTF using safe food-handling techniques, and store at refrigerator
1.
temperature immediately after preparation. Discard any unused portion after 24 hours.
Sanitize mechanical devices (eg, blenders) used to prepare homemade BTF after each use, using
2.
an established protocol.
3. Limit the hang time of homemade BTF to ≤2 hours.
Limit the hang time of commercial BTF to 8-12 hours or per manufacturer recommendation (similar
4.
to other open system EN feeding systems).
Abbreviations: BTF, blenderized tube feeding; EN, enteral nutrition.
Source: Adapted with permission from reference 2: Boullata JI, Carrera AL, Harvey L, et al. ASPEN safe practices for enteral nutrition
therapy. JPEN J Parenter Enteral Nutr. 2017;41:15-103. doi:10.1177/0148607116673053.

Labeling Enteral Nutrition

Patient-specific, standardized labels for EN decrease potential confusion when a patient is transferred to a different
unit within a facility, or when a new staff member takes over a patient’s care.2 For example, “Not for IV Use” helps
decrease the risk for an enteral misconnection. Proper labeling also allows for a final check of that enteral formula
against the prescriber’s order.2,102 (See Chapter 6 for additional information on EN orders.)
To avoid misinterpretation, EN should be treated as a medication, and a standardized label should be affixed to
all EN formula administration containers (bags, bottles, syringes used in syringe pumps). Care should be taken in
developing a label that is clear and concise and of a size that fits neatly on the container (see Figures 7-3, 7-4, and 7-
5 for examples).2 In some institutions it may not be possible to print standardized labels. Some formula
manufacturers provide labels to document important elements on the formula container. In all cases, the critical label
elements (Table 7-4) should be listed on the enteral product container or label.2 See Table 7-5 for a summary of
practice recommendations for EN labeling.2
TABLE 7-4. Components of the Formula Label

Labeling of enteral formula:

• Patient's name
• Medical record ID number
• Formula name and strength of formula, if diluted
• Date and time formula prepareda
• Date and time formula hunga
• Administration route
Rate of administration expressed as mL/h over 24 hours if continuous administration or “Rate not to
•
exceed ______” or “Volume not to exceed _______”
• Administration duration and rates are to be expressed on the label if the EN is cycled or intermittent
• Initials of who prepared, hung, and checked the EN against the order
• Appropriate hang time (expiration date and time)
 • Dosing weight if appropriate
• “Not for IV Use”
Labeling of incoming human milk:
• Infant's name
• Medical record ID number
• Dosing weight
• Date and time that HM was expressed
• Medication or supplements being taken by the mother
• Specify whether HM is fresh or frozen
• Contents in syringe/container (expressed HM)
• If frozen, date and time HM was thawed
• Expiration date (based on whether the HM was fresh or frozen)
• “Not for IV Use”
Fortified HM also includes:
◦ Name of fortifier
•
◦ Final concentration
◦ Date and time formula prepared
• Initials of who prepared, hung, and checked the EN against the order
Abbreviations: EN, enteral nutrition; HM, human milk; ID, identification; IV intravenous.
a
The date-time of formula prepared and the date-time of formula hung may be different, so note both.
Adapted with permission from reference 2: Boullata JI, Carrera AL, Harvey L, et al. ASPEN safe practices for enteral nutrition therapy. JPEN
J Parenter Enteral Nutr. 2017;41:15–103. doi:10.1177/0148607116673053.

TABLE 7-5. Practice Recommendations for Labeling of Enteral Nutrition

Include all the critical elements of the EN order on the EN label: patient identifiers, formula type,
1. enteral delivery site (route and access), administration method and type, and volume and
frequency of water flushes.
Standardize the labels for all EN formula containers, bags, or syringes to include who prepared the
2.
formula, date/time it was prepared, and date and time it was started.
Express clearly and accurately on all EN labels in any healthcare environment what the patient
was ordered. Given changes to administration rates/volumes, consider patient-specific labels that
3. state:
a. “Rate not to exceed ______”
b. “Volume not to exceed ______”
Include on the label of HM stored in the hospital: contents in container, infant's name, infant's
4. medical record number, date and time of milk expressed, maternal medications, fortifiers added,
and energy density.
State on the HM label whether the milk is fresh or frozen, date and time the milk was thawed, and
5. the appropriate expiration date. Bar codes, special colors, or symbols may be used to further
identify the HM.
Label commercial enteral containers “Not for IV Use” to help decrease the risk for an enteral
6.
misconnection.
 Carefully check commercial enteral container labeling against the prescriber's order. Be aware of
7. sound-alike or look-alike product names that may be mixed up on the order or during selection of
the product.
Abbreviations: EN, enteral nutrition; HM, human milk.
Adapted with permission from reference 2: Boullata JI, Carrera AL, Harvey L, et al. ASPEN safe practices for enteral nutrition therapy. JPEN
J Parenter Enteral Nutr. 2017;41:15-103. doi:10.1177/0148607116673053.

Quality Assurance
EN handling processes should be routinely evaluated to determine their ongoing quality effectiveness and safety.
Examples of methods for quality assurance monitoring include the Hazard Analysis Critical Control Point (HACCP)
system and the plan-do-check-act (PDCA) process.7,70,103–105 The HACCP system uses a scientific approach to
identify critical control points in the provision of nutrition products and implement safeguards at those points to
prevent microbial contamination.7,70,103,104 Originally used for healthcare food service, many facilities have extended
the use of HACCP to EN (including HM).7,70,103,104 Table 7-6 provides an overview of the HACCP plan process.70
The steps in the PDCA model proceed in a cyclical manner, allowing for a systematic approach for implementing a
new process as well as a method for ongoing monitoring and adjustments.105

TABLE 7-6. Steps in a Hazard Analysis Critical Control Point Plan

1. Assessment of potential hazards

2. Identification of critical control points (CCPs)
3. Establishment of policies and procedures for CCPs
4. Monitoring of CCPs
5. Planning for procedure failures and corrective actions
6. Verification that systems and procedures are working
7. Record keeping
Source: Information is from references 1, 7, 70, 103, and 104.

Policies and procedures should reflect current practice and be easily accessible to provide guidance to staff.
Regular assessment of staff competency (both within the preparation room and at bedside) is crucial to verify
compliance and identify gaps in training or the process.

Suggested Reading and Practice Resources

Hand Hygiene

• Centers for Disease Control and Prevention. When and how to wash your hands.
https://www.cdc.gov/handwashing/when-how-handwashing.html. Updated March 2016. Accessed
November 8, 2018.
• Association for Professionals in Infection Control and Epidemiology. Guide to hand hygiene programs for
infection prevention. http://www.apic.org/Professional-Practice/Implementation-guides#HandHygiene.
Published 2016. Accessed November 8, 2018.
• World Health Organization. WHO guidelines on hand hygiene in health care: a summary.
http://apps.who.int/iris/bitstream/10665/70126/1/WHO_IER_PSP_2009.07_eng.pdf. Published 2009.
Accessed November 8, 2018.

Human Milk and Infant/Pediatric Formulas

 • Steele C, Collins EA, eds. Infant and Pediatric Feedings: Guidelines for Preparation of Human Milk and
Formula in Health Care Facilities. 3rd ed. Chicago, IL: Academy of Nutrition and Dietetics; 2018.
• Centers for Disease Control and Prevention. How to keep your breast pump kit clean: the essentials.
https://www.cdc.gov/healthywater/hygiene/healthychildcare/infantfeeding/breastpump.html. Updated August
2017. Accessed November 8, 2018.

Blenderized Tube Feedings

• Fessler TA. Home tube feeding with blenderized foods. Oley Foundation website.
https://oley.org/page/hometf_blenderfoods?&terms=%22blenderized%22. Updated September 2016.
Accessed November 8, 2018.
• Escuro A. Blenderized tube feeding: suggested guidelines to clinicians. Pract Gastroenterol.
2014;38(12):58–66. https://www.practicalgastro.com/article/144773/Blenderized-Tube-Feeding-Suggested-
Guidelines. Accessed November 8, 2018.
• Epp L. Blenderized feeding options—the sky’s the limit. Pract Gastroenterol. 2018;42(6):30–39.
https://www.practicalgastro.com/article/183989/Blenderized-Feeding-Options-Skys-the-Limit. Accessed
December 30, 2018.

References
1. Steele C, Collins EA, eds. Infant and Pediatric Feedings: Guidelines for Preparation of Human Milk and
Formula in Health Care Facilities. 3rd ed. Chicago, IL: Academy of Nutrition and Dietetics; 2019.
2. Boullata JI, Carrera AL, Harvey L, et al. ASPEN safe practices for enteral nutrition therapy. JPEN J
Parenter Enteral Nutr. 2017;41:15–103. doi:10.1177/0148607116673053.
3. Steele C, Czerwin A, Bixby C. Breast milk bar code scanning results in time savings and staff efficiency. J
Acad Nutr Diet. 2015;115(1):23–26.
4. Vermilyea S, Goh VL. Enteral feedings in children: sorting out tubes, buttons, and formulas. Nutr Clin Pract.
2016; 31(1):59–67.
5. Drenckpohl M, Bowers L, Cooper H. Use of the Six Sigma methodology to reduce incidence of breast milk
administration errors in the NICU. Neonatal Netw. 2007;26(3): 161–166.
6. Steele C, Bixby C. Centralized breastmilk handling and bar code scanning improve safety and reduce
breastmilk administration errors. Breastfeed Med. 2014;9(9):426–429. doi:10.1089/bfm.2014.0077.
7. Steele C, Short R. Centralized infant formula preparation room in the neonatal intensive care unit reduces
incidence of microbial contamination. J Am Diet Assoc. 2008;108: 1700–1703.
8. Iversen C, Forsythe SJ. Comparison of media for the isolation of Enterobacter sakazakii. Appl Environ
Microbiol. 2007;73: 48–52.
9. Kandhai MC, Reij MW, Grognou C, van Schothorst M, Gorris LGM, Zwietering MH. Effects of preculturing
conditions on lag time and specific growth rate of Enterobacter saka zakii in reconstituted powdered infant
formula. Appl Environ Microbiol. 2006;72:2721–2729.
10. Marino LV, Goddard E, Whitelaw A, Workman L. Prevalence of bacterial contamination of powdered infant
feeds in a hospital environment. S Afr Med J. 2007;97:534–537.
11. Buyukyavuz BI, Adiloglu AK, Onal S, Cubukcu SE, Cetin H. Finding the sources of septicemia at a neonatal
intensive care unit: newborns and infants can be contaminated while being fed. Jpn J Infect Dis.
2006;59:213–215.
12. Giovannini M, Verduci E, Ghisleni D, Salvatici E, Riva E, Agostoni C. Enterobacter sakazakii: an emerging
problem in paediatric nutrition. J Int Med Res. 2008;36:394–399.
13. Iversen C, Lane M, Forsythe SJ. The growth profile, thermo-tolerance and biofilm formation of Enterobacter
sakazakii grown in infant formula milk. Lett Appl Microbiol. 2004;38:378–382.
14. Mathus-Vliegen L, Binnekade J, de Hann R. Bacterial contamination of ready-to-use 1-L feeding bottles and
administration sets in severely compromised intensive care patients. Crit Care Med. 2000;28:67–73.
15. Perry J, Stankorb S, Salgueiro M. Microbial contamination of enteral feeding products in thermoneutral and
hyperthermal ICU environments. Nutr Clin Pract. 2015;30:128–133.
16. Boyce JM, Pittet D. Guideline for hand hygiene in health-care settings: recommendations of the Healthcare
Infection Control Practices Advisory Committee and the HICPAC/SHEA/APIC/IDSA Hand Hygiene Task
 Force. Infect Control Hosp Epidemiol. 2002;23(12 Suppl):S3–S40.
17. Goff HD. Microbial growth. Dairy science and technology education series. University of Guelph Food
Science website. https://www.uoguelph.ca/foodscience/book-page/microbial-growth. Accessed November 9,
2018.
18. Centers for Disease Control and Prevention. Diagnosis and management of foodborne illnesses: a primer for
physicians. MMWR Morb Mortal Wkly Rep. 2001;50(RR-02):1–69.
19. Nair MK, Joy J, Venkitanarayanan KS. Inactivation of Enterobacter sakazakii in reconstituted infant formula
by monocaprylin. J Food Prot. 2004;67(12):2815–2819.
20. Brett MM, McLauchlin J, Harris A, et al. A case of infant botulism with a possible link to infant formula
milk powder: evidence for the presence of more than one strain of Clos tridium botulinum in clinical
specimens and food. J Med Micro biol. 2005;54:769–776.
21. Hilliard NJ, Schelonka RL, Waites KB. Bacillus cereus bacteremia in a preterm neonate. J Clin Microbiol.
2003;41: 3441–3444.
22. Adler A, Gottesman G, Dolfin T, et al. Bacillus species sepsis in the neonatal intensive care unit. J Infect.
2005;51(5):390–395.
23. Ko KS, Oh WS, Le MY, et al. Bacillus infantis sp. nov. and Bacillus idriensis sp. nov., isolated from a
patient with neonatal sepsis. Int J Syst Evol Microbiol. 2006;56(Pt 11):2541–2544.
24. Boyle RJ, Robins-Browne RM, Tang MLK. Probiotic use in clinical practices: what are the risks? Am J Clin
Nutr. 2006; 83:1256–1264.
25. Hurrell E, Kucerova E, Loughlin M. Neonatal enteral feeding tubes as loci for colonization by members of
the Entero bacteriaceae. BMC Infect Dis. 2009;9:146.
26. National Association of Neonatal Nurses. The use of human milk and breastfeeding in the neonatal intensive
care unit. Position statement #3065. http://nann.org/about/position-statements. Published 2015. Accessed
November 8, 2018.
27. Jones F. Best Practice for Expressing, Storing and Handling Human Milk in Hospitals, Homes, and Child
Care Settings. 3rd ed. Fort Worth, TX: Human Milk Banking Association of North America; 2011.
28. Moro GE, Arslanoglu S, Bernito E, et al. Human milk in feeding premature infants: from tradition to
bioengineering. J Pediatr Gastroenterol Nutr. 2015;61(Suppl 1):S1–S19.
doi:10.1097/MPG.0000000000000897.
29. The Joint Commission. The Joint Commission Comprehensive Accreditation and Certification Manual 2017
(E-dition). https://e-dition.jcrinc.com. Accessed May 3, 2017.
30. Food and Agriculture Organization of the United Nations/World Health Organization. Enterobacter
sakazakii and other microorganisms in powdered infant formula. Food and Agriculture Organization website.
http://www.fao.org/docrep/007/y5502e/y5502e00.htm. Published 2004. Accessed November 9, 2018.
31. US Food and Drug Administration. FDA and CDC update: investigation of Cronobacter bacteria illness in
infants. https://www.cdc.gov/media/releases/2011/s1230_Cronobacter.html. Published December 30, 2011.
Accessed December 30, 2018.
32. US Food and Drug Administration. Code of Federal Regulations. Title 21: Food and Drugs. Part 106: infant
formula requirements pertaining to current good manufacturing practice, quality control procedures, quality
factors, records and reports, and notifications. Part 107: infant formula. April 1, 2016.
https://www.accessdata.fda.gov/scripts/cdrh/cfdocs/cfcfr/CFRSearch.cfm. Accessed November 13, 2017.
33. US Food and Drug Administration. Code of Federal Regulations. Title 21: Food and Drugs. Part 113:
thermally processed low-acid foods packaged in hermetically sealed containers.
https://www.accessdata.fda.gov/scripts/cdrh/cfdocs/cfcfr/CFRSearch.cfm?CFRPart=113. Accessed
November 14, 2017.
34. US Food and Drug Administration. Current Good Manufacturing Practices, quality control procedures,
quality factors, notification requirements, and records and reports, for infant formula; correction. a rule by
the Food and Drug Administration on 7/15/2014. Federal Register. 2014;79:41127.
https://www.federalregister.gov/documents/2014/07/15/201416476/current-good-manufacturing-practices-
quality-control-procedures-quality-factors-notification. Accessed November 9, 2018.
35. Food and Agriculture Organization of the United Nations/World Health Organization. Safe preparation,
storage and handling of powdered infant formula. World Health Organization website.
http://www.who.int/foodsafety/publications/powdered-infant-formula/en. Published 2007. Accessed
November 9, 2018.
36. Jason J. Prevention of invasive Cronobacter infection in young infants fed powdered infant formulas.
Pediatrics. 2012;130(5): e1076–e1084.
37. Forsythe S. Cronobacter species. Culture. 2010;31(1):1–8.
38. US Food and Drug Administration. FDA takes final step on infant formula protections.
https://www.fda.gov/ForConsumers/ConsumerUpdates/ucm048694.htm. Published June 4, 2014; updated
January 4, 2018. Accessed April 26, 2018.
39. Abbott Nutrition. How to make a bottle. Similac website. https://similac.com/baby-feeding/formula/how-to-
make-bottle. Accessed November 9, 2018.
40. Abbott Nutrition. Recommended storage guidelines for Abbott Nutrition pediatric products.
https://static.abbottnutrition.com/cms-prod/abbottnutrition-2016.com/img/13-
14_Recommended_Storage_Guidelines_for_Abbott_Nutrition_Pediatric_Products_tcm1310-72819.pdf.
Accessed November 9, 2018.
41. Beattie TK, Anderton A. Decanting versus sterile prefilled nutrient containers—the microbiological risks in
enteral feeding. Int J Environ Health Res. 2001;11:81–93.
42. Marlon ND, Rupp ME. Infection control issues of enteral feeding systems. Curr Opin Clin Nutr Metab Care.
2000;3(5):363–366.
43. Vanek V. Closed versus open enteral delivery systems: a quality improvement study. Nutr Clin Pract.
2000;15(5):234–243.
44. Phillips W. Economic impact of switching from an open to a closed enteral nutrition feeding system in an
acute care setting. Nutr Clin Pract. 2013;28(4):510–514.
45. Lyman B, Gebhards S, Hensley C, Roberts C, San Pablo W. Safety of decanted enteral formula hung for 12
hours in a pediatric setting. Nutr Clin Pract. 2011;26:451–456.
46. Read J, Guenter P. ASPEN Enteral Nutrition by the Numbers: EN Data Across the Healthcare Continuum.
Silver Spring, MD: American Society for Parenteral and Enteral Nutrition; 2017.
47. Oza-Frank R, Kachoria R, Dail J, Green J, Walls K, McClead RE. A quality improvement project to
decrease human milk errors in the NICU. Pediatrics. 2017;139(2 suppl):S1–S13.
48. US Environmental Protection Agency. The Safe Drinking Water Act. https://www.epa.gov/sdwa. Accessed
November 9, 2018.
49. American Academy of Pediatrics Committee on Nutrition. Formula feeding of term infants. In: Kleinman
RE, Greer FR, eds. Pediatric Nutrition. 7th ed. Elk Grove Village, IL: American Academy of Pediatrics;
2014:66–68.
50. American Academy of Pediatrics. How to safely prepare formula with water.
https://www.healthychildren.org/English/ages-stages/baby/feeding-nutrition/Pages/How-to-Safely-Prepare-
Formula-with-Water.aspx. Updated July 3, 2018. Accessed November 9, 2018.
51. US Environmental Protection Agency. Basic information about lead in drinking water.
https://www.epa.gov/ground-water-and-drinking-water/basic-information-about-lead-drinking-water.
Accessed November 9, 2018.
52. Corkins MR, Griggs KC, Groh-Wargo S, et al. Standards for nutrition support: pediatric hospitalized
patients. Nutr Clin Pract. 2013;28(2):263–276.
53. Paul E. Minimizing patient safety events through a multidisciplinary approach to human milk management.
ICAN Infant Child Adolesc Nutr. 2015;7(5):258–261.
54. Gabrielski L, Lessen R. Centralized model of human milk preparation and storage in a state-of-the-art human
milk lab. ICAN Infant Child Adolesc Nutr. 2011;3:225–232.
55. Facilities Guidelines Institute. Standard A2.1-7.2.3.2(3) and Standard 2.1-7.2.3.3(5). In: Guidelines for
Design and Construc tion of Hospital and Health Care Facilities. Washington, DC: American Institute of
Architects; 2014:91–92.
56. White RD, Smith JA, Shepley MM. Recommended standards for newborn ICU design. J Perinatol.
2013;33(suppl): S2–S16.
57. Massachusetts Department of Public Health. Compliance checklist IP6: neonatal intensive care unit.
http://www.mass.gov/eohhs/docs/dph/quality/hcq-plan-review/ip06.pdf. Published May 2015. Accessed
November 8, 2018.
58. Oklahoma State Department of Health. OAC 310:667-49-4 General medical surgical hospital construction
requirements—nurseries.
https://www.ok.gov/health2/documents/Medical%20Surgical%20Hospital_Nurseries.docx. Accessed
November 8, 2018.
59. Texas Administrative Code. Title 25 health services, part 1, Department of State Health Services, chapter
133 hospital licensing, subchapter 1 physical plant and construction requirements, rule 133.163 spatial
requirements for new construction. http://texreg.sos.state.tx.us/public/readtac$ext.TacPage?
 sl=T&app=9&p_dir=F&p_rloc=149501&p_tloc=237062&p_ploc=222130&pg=17&p_tac=&ti=25&pt=1&ch=133&rl=163
Accessed November 8, 2018.
60. US Department of Defense. DOD space planning criteria. Chapter 430: neonatal intensive care unit June 1,
2016. Whole Building Design Guide website.
https://www.wbdg.org/FFC/DOD/MHSSC/spaceplanning_healthfac_430_2016.pdf. Accessed November 8,
2018.
61. Georgia Department of Community Health. 2010 guidelines for design and construction of health care
facilities. https://weblink.dch.georgia.gov/WebLink8/1/doc/307664/Electronic.aspx. Accessed November 8,
2018.
62. Oregon Health Authority. FPS newborn nursery units rulesheet.
https://public.health.oregon.gov/ProviderPartnerResources/HealthcareProvidersFacilities/FacilitiesPlanningSafety/Documents/F
Accessed November 8, 2018.
63. Michigan Department of Consumer and Industry Services Bureau of Health Systems Division of Health
Facilities and Services. 2007 minimum design standards for health care facilities in Michigan.
https://www.michigan.gov/documents/mdch/bhs_2007_Minimum_Design_Standards_Final_PDF_Doc._198958_7.pdf
Accessed November 8, 2018.
64. Office of Statewide Health Planning and Development. Interior environment. In: 2016 California Building
Code. 2016:662. California Building Standards website. http://www.bsc.ca.gov/Codes.aspx. Accessed
November 8, 2018.
65. Illinois General Assembly. Title 77: public health, chapter I: Department of Public Health, subchapter b:
hospitals and ambulatory care facilities, part 250 hospital licensing requirements, section 250.1830 general
requirements for all obstetric departments.
http://ilga.gov/commission/jcar/admincode/077/077002500O18300R.html. Accessed November 20, 2016.
66. New York City Department of Health. Article 115 Prescription Formula Preparation Facilities.
https://www1.nyc.gov/assets/doh/downloads/pdf/about/healthcode/health-code-article115.pdf. Accessed
November 8, 2018.
67. Office of the Revisor of Statutes. Minnesota administrative rules. https://www.revisor.mn.gov/rules/?
id=4645.1200. Published 2000. Accessed November 9, 2018.
68. Eglash A, Simon L, Academy of Breastfeeding Medicine. ABM clinical protocol #8: human milk storage
information for home use for full-term infants, revised 2017. Breastfeed Med. 2017;12:390–395.
69. Centers for Disease Control and Prevention. Proper handling and storage of human milk.
https://www.cdc.gov/breastfeeding/recommendations/handling_breastmilk.htm. Updated September 2018.
Accessed November 9, 2018.
70. Cossey V, Jeurissen A, Thelissen MJ, Vanhole C, Schuer-mans A. Expressed breast milk on a neonatal unit:
a hazard analysis and critical control points approach. Am J Infect Con trol. 2011;39(10):832–838.
71. NSF International, American National Standards Institute. NSF/ANSI 3: Commercial warewashing
equipment. In: NSF International Standard/American National Standard for Food Equipment. Ann Arbor,
MI: NSF International; 2012.
72. NSF International, American National Standards Institute. NSF/ANSI 51: Food equipment materials. In:
NSF Interna tional Standard/American National Standard for Food Equipment. Ann Arbor, MI: NSF
International; 2015.
73. US Food and Drug Administration. FDA food code. 2013.
https://www.fda.gov/food/guidanceregulation/retailfoodprotection/foodcode/default.htm. Accessed May 4,
2017.
74. United States Pharmacopeial Convention. USP 795 pharmaceutical compounding—nonsterile preparations.
In: USP Compounding Compendium 2016. Rockville, MD: United States Pharmacopeial Convention;
2016:31–38.
75. United States Pharmacopeial Convention. USP 797 Pharmaceutical compounding—sterile preparations. In:
USP Compounding Compendium 2016. Rockville, MD: United States Pharmacopeial Convention: 2016:39–
84.
76. Renfrew MJ, Ansell P, Macleod KL. Formula feed preparation: helping reduce the risk; a systematic review.
Arch Dis Child. 2003;88:855–858.
77. Bower A, Wiesenfeld HC, Kloesz JL, et al. Cronobacter sakazakii infection associated with feeding
extrinsically contaminated expressed human milk to a premature infant—Pennsylvania, 2016. MMWR Morb
Mortal Wkly Rep. 2017;66(28):761–762.
78. Chang JC, Chen CH, Fang LJ, Tsai CR, Chang YC, Wang TM. Influence of prolonged storage process,
 pasteurization, and heat treatment on biologically-active human milk proteins. Pediatr Neonatal.
2013;54:360304366.
79. De la Fuente M, Olano A, Juraz M. Mineral balance in milk heated using microwave energy. J Agric Food
Chem. 2002;10:2274–2277.
80. Mohrenschlager M, Weigl LB, Haug S, et al. Iatrogenic burns by warming bottles in the neonatal period:
report of two cases and review of the literature. J Burn Care Rehabil. 2003;24(1):52–55.
81. Bransburg-Zabary S, Virozub A, Mimouni F. Human milk warming temperatures using a simulation of
currently available storage and warming methods. PLoS One. 2015;10(6):1–13.E0128806.
doi:10.1371/journal.pone.0128806.
82. Steele C, Gonzalez B, Gornick W. Thawing human milk for hospitalized infants: use of a laboratory bead
bath may be an effective method for large quantities. J Acad Nutr Diet. 2018;118(5):801–804.
83. Cervia JS, Ortolano GA, Canonica FP. Hospital tap water: a reservoir of risk for health care-associated
infection. Infect Dis Clin Pract. 2008;16(6):349–353.
84. Centers for Disease Control and Prevention. Prevention strategies for seasonal influenza in healthcare
settings. https://www.cdc.gov/flu/professionals/infectioncontrol/healthcaresettings.htm. Published February
13, 2018. Accessed April 26, 2018.
85. McNeil SA, Foster CL, Hedderwick SA, Kauffman CA. Effect of hand cleansing with antimicrobial soap or
alcohol-based gel on microbial colonization of artificial fingernails worn by health care workers. Clin Infect
Dis. 2001;32: 367–372.
86. Association of Perioperative Registered Nurses. Hand hygiene. http://www.aorn.org/guidelines/clinical-
resources/clinical-faqs/hand-antisepsis-hygiene. Accessed May 19, 2017.
87. Moolenaar RL, Crutcher M, San Joaquin VH, et al. A prolonged outbreak of Pseudomonas aeruginosa in a
neonatal intensive care unit: did staff fingernails play a role in disease transmission? Infect Control Hosp
Epidemiol. 2000;21:80–85.
88. Peters MD, McArthur A, Munn Z. Safe management of expressed breast milk: a systematic review. Women
Birth. 2016;29(6):473–481.
89. Centers for Disease Control and Prevention. How to keep your breast pump kit clean: the essentials.
https://www.cdc.gov/healthywater/hygiene/healthychildcare/infantfeeding/breastpump.html. Updated August
2017. Accessed November 8, 2018.
90. Lawrence RM. Transmission of infectious diseases through breast milk and breastfeeding. In: Lawrence RA,
Lawrence RM, eds. Breastfeeding: A Guide for the Medical Profession. 7th ed. Maryland Heights, MO:
Elsevier Mosby; 2011:406–473.
91. Becker GE, Smith HA, Cooney F. Methods of milk expression for lactating women. Cochrane Database
Syst Rev. 2015;(2): CD006170. doi:10.1002/14651858.CD006170.pub4.
92. Boo NY, Nordiah AJ, Alfizah H, Nor-Rohaini AH, Lim VK. Contamination of breast milk obtained by
manual expression and breast pumps in mothers of very low birthweight infants. J Hosp Infect. 2001;
49(4):274–281.
93. Smith SL, Serke L. Case report of sepsis in neonates fed expressed mother’s milk. J Obstet Gynecol Neonat
Nurs. 2016; 45:699–705.
94. Karimi M, Eslami Z, Shamsi F, Moradi J, Ahmadi AY, Baghianimoghadam B. The effect of educational
intervention on decreasing mothers’ expressed breast milk bacterial contamination whose infants are
admitted to neonatal intensive care unit. J Res Health Sci. 2013;l13(1):43–47.
95. Weems MF, Dereddy NR, Arnold SR. Mother’s milk as a source of Enterobacter cloacae sepsis in a preterm
infant. Breast feed Med. 2015;10(10):503–504.
96. Petersen S, Greisen G, Krogfelt K. Nasogastric feeding tubes from a neonatal department yield high
concentrations of potentially pathogenic bacteria—even 1 day after insertion. Pediatr Res. 2016;80:395–400.
97. Bobo E. Reemergence of blenderized tube feedings: exploring the evidence. Nutr Clin Pract.
2016;31(6):730–735.
98. Martin M, Gardner G. Home enteral nutrition: updates, trends, and challenges. Nutr Clin Pract.
2017;32(6):712–721.
99. Epp L, Lammert L, Vallumsetla N, et al. Use of blenderized tube feeding in adult and pediatric home enteral
nutrition patients. Nutr Clin Pract. 2017;32(2):201–205.
100. Epp L. Blenderized feeding options—the sky’s the limit. Pract Gastroenterol. 2018;42(6):30–39.
https://www.practicalgastro.com/article/183989/Blenderized-Feeding-Options-Skys-the-Limit. Accessed
December 30, 2018.
101. US Food and Drug Administration; Guha S, Myers MR, Silverstein J, Antonino MJ, Cooper J. Feeding tubes
 and transition to ENFitTM: creating science around infinite user variables. Stay Connected website.
http://stayconnected.org/wp-content/uploads/2017/08/FDA.Blenderized-Update-upload.pdf. Accessed
January 2, 2019.
102. Perry AG, Potter PA. Clinical Nursing Skills & Techniques. 6th ed. St. Louis, MO: Mosby; 2006:1032.
103. Oliveira M, Batista C, Aidoo K. Application of hazard analysis critical control points system to enteral tube
feeding in hospital. J Hum Nutr Diet. 2001;14:397–403.
104. Carvalho M, Morais T, Amaral D, Sigulem D. Hazard analysis of critical control point system approach in
the evaluation of environmental and procedural sources of contamination of enteral feedings in three
hospitals. JPEN J Parenter Enteral Nutr. 2000;24:296–300.
105. American Society for Quality. Plan-do-check-act (PDCA) cycle. http://asq.org/learn-about-quality/project-
planning-tools/overview/pdca-cycle.html. Accessed November 9, 2018.
 CHAPTER 8

Administration and Monitoring of Enteral Nutrition

Introduction
Clinicians must be cognizant of many factors when developing an individualized enteral nutrition (EN) regimen. For
example, EN can be supplemental nutrition for patients who are unable to meet nutrition needs with an oral diet
alone, or it can meet 100% of an individual’s nutrition needs. It can be administered through a temporary enteral
access device (EAD), such as a nasogastric feeding tube, or a long-term EAD, such as a gastrostomy or jejunostomy
feeding tube (see Chapter 3). Feeding modalities include the syringe method (also known as bolus feeding), gravity-
bag feeding, and pump-assisted feedings. Patients and care givers vary in terms of their ability and availability to
administer EN. An individual’s medical history, gastro intestinal (GI) status, and ability to participate in the feeding
process will all influence the selection of the optimal EN regimen for that patient. Insurance coverage is an
important consideration, particularly when selecting an EN feeding regimen for the hospitalized patient who will be
discharged to receive EN therapy in another setting. Above all, while considering these variables and others, the
clinician must remember that, if medically possible, the desired outcome of the EN regimen is to restore the patient’s
ability to meet nutrition needs via oral diet and end dependency on nutrition support.

Implementation of Enteral Nutrition Feedings

After the patient undergoes a comprehensive nutrition assessment, the nutrition support clinician can develop an
individualized EN regimen, establish nutrition goals, and either initiate EN or assist the ordering practitioner with
EN initiation. After initiation of the EN regimen, the clinician should closely monitor the safety of EN, the
advancement of feedings, and the patient’s metabolic and GI tolerance of the prescribed feeding regimen. (See
Chapter 6 for information on ordering, initiating, and advancing EN.) While EN is being administered, clinicians
must adjust the regimen as needed to prevent complications and achieve nutrition goals. At this time, clinicians may
also be required to provide education on feeding administration (eg, hang times, water flushes, and proper feeding
administration techniques), patient positioning, or the feeding equipment.

Reducing Microbial Contamination Risks

Microbial contamination of EN formula or administration sets can occur at any step of the feeding delivery process.
For example, bacterial contamination of EN has been attributed to touch contamination, formula
preparation/addition of modular to commercially manufactured formulas, extended hang times of the enteral formula
beyond manufacturer guidelines/facility policy, use of administration sets for more than 24 hours, and endogenous
retrograde growth.1–8 The consequences of EN contamination can be serious. It has been associated with nosocomial
infections, feeding intolerance (diarrhea), infectious enterocolitis, vomiting, fever, abdominal distention, aspiration
pneumonia, and sepsis.1,4,5,8,9 See Chapter 7 for discussion of the contamination points in the formula and human
milk (HM) preparation processes.
Based on results of testing and reports about microbial contamination, criteria have been established for how
long various types of formula preparations can safely hang in ambient environments, the recommended use of
administration sets, safe feeding administration procedures, and proper hand hygiene (see Table 8-1 for selected
recommendations).1 At the federal level, the US Food and Drug Administration (FDA) has established standards for
unacceptable levels of bacterial contamination in medical foods that FDA inspectors of medical food firms must
immediately report (Table 8-2).10 As discussed in Chapter 5, federal regulations for infant formulas are distinct from
those for medical foods such as adult and pediatric enteral formulas.
 TABLE 8-1. Practice Recommendations to Promote Safe Handling of Enteral Nutrition

1. Use a closed EN delivery system when possible.

Follow the manufacturer's recommendations for duration of infusion through an intact delivery
2.
device (container and administration set).
Do not reuse the enteral delivery device for open or closed systems (container and administration
3.
set in excess of what is recommended by the manufacturer).
If open systems are used, follow recommended hang times and avoid topping off remaining
formula, which may result in a continuous culture for exponential microbial growth.
a. Limit infusion time for open EN feeding systems to 4-8 hours maximum (12 hours in the home
4. setting).
b. Limit infusion time for a reconstituted powder product or modular to 4 hours maximum.
c. Change the delivery device (container and administration set) according to the manufacturer's
recommendations for open systems.
Be aware that the addition of modular units to an open feeding system may result in an
5.
unacceptable risk of contamination in hyperthermal environments.
To limit the risk of microbial growth and biofilm formation, avoid unnecessary additions to the EN
6. administration set. If additional equipment, such as 3-way stopcocks, is used, follow manufacturer
recommendations or facility protocol for change and cleaning practices.
Establish and follow protocols for preparation, handling, and storage of commercial and handmade
EN.
a. Educate those who prepare and administer EN about hand hygiene (a critical point) and safe
handling of EN preparation and administration; extend education to patients and family
members/care givers who will continue this practice into the home setting.
b. Use effective hand hygiene in all aspects of EN preparation and administration. When gloves
are used, they must be clean gloves, not having been involved in other nonrelated tasks. The
7. importance of hand washing in minimizing transference of microbial growth and preventing
hospital-acquired infections cannot be overstressed.
c. Give preference to selecting systems that require minimal handling.
d. Use a clean work surface for EN preparation.
e. Use equipment dedicated for EN use only.
f. Store EN formula according to the manufacturer's instructions. Store prepared or opened ready-
to-feed solutions in an appropriate refrigerator, discarding any used solutions within 24 hours of
preparation or opening.
Periodically survey and regularly monitor adherence to the above-listed protocols. Document
8.
findings and take appropriate actions if protocols are not followed.
Reduce potential for touch contamination of EN-related equipment as well as risk of exposure to
body fluids by reducing interruptions to the system, providing a clean work surface (eg, small clean
9.
towel under tube/ administration connection), and, when interruptions are necessary, using only
washed hands and gloves.
Keep all equipment, including syringes and containers for flush and medication administration, as
10.
clean and dry as possible. Store clean equipment away from potential sources of contamination.
Consider whether microbial growth related to EN might be implicated as part of the diagnosis
11.
when patients have adverse conditions such as diarrhea.
Abbreviation: EN, enteral nutrition.
Source: Reprinted with permission from reference 1: Boullata JI, Carrera AL, Harvey L, et al. ASPEN safe practices for enteral nutrition
therapy. JPEN J Parenter Enteral Nutr. 2017;41(1):15-103. doi:10.1177/0148607116673053.
 TABLE 8-2. FDA Guidance on Inspection of Medical Foods for Contamination

FDA inspectors of firms manufacturing, distributing, or repacking medical foods must immediately report
findings of any of the following:
• Any aerobic agar plate growing >104 cfu/mL
• Positive for coliform and Escherichia coli
• Presence of Salmonella spp., Listeria monocytogenes, or staphylococcal enterotoxin
• Bacillus cereus subsample >1000 organisms/g
• Aerobic plate count subsample >10,000 organisms/g, or ≥3 subsamples exceed 1000 organisms/g
Source: Adapted from reference 10.

Environmental Controls and Temperature

The environment in which enteral formula is prepared and ambient temperatures when the formula is administered
can affect microbial growth. The American Society for Parenteral and Enteral Nutrition (ASPEN) has recommended
that “the environment in which enteral nutrition preparation takes place should be controlled to reduce the risk of
contamination.”11 When this recommendation was published in 2009, it was endorsed by the Academy of Nutrition
and Dietetics, American Society of Health-System Pharmacists, and Institute for Safe Medication Practices. The
ASPEN recommendations for safe practices in EN were updated in 2017.1

Hang Times and Administration Set Use

To reduce the risk for contamination, hang time protocols for EN must be enforced. The recommended hang time
will vary depending on the type of product administered, the administration system, and the care setting. For
example, the FDA has recommended that reconstituted enteral formulas prepared from powdered products (which
are not sterile) hang no more than 4 hours; this recommendation was issued in response to deaths of infants who
consumed infant formula contaminated with Cronobacter sakazakii (formerly called Enterobacter sakazakii).12,13
Other recommendations regarding hang times have been published by ASPEN. See Figure 8-1 for a summary.1

The literature suggests that limiting formula hang time lowers the risk for bacterial contamination. Although
patient safety is the paramount concern, shortening hang times increases supply costs. Therefore, healthcare
providers have an incentive to create protocols that promote safety without incurring undue expense. Neely and
associates investigated whether the hang time protocol for feeding administration sets in a burn unit could be
extended from a very conservative approach of 1 administration set every 4 hours to a longer hang time of 8 hours.6
The investigation used both commercially prepared formulas and the specialized, hospital-specific standard tube
feeding formula (designed for burn patients) made of multiple separate components. The extended hang time was
not associated with an increase in microbial load, unacceptable levels of contamination, or a higher rate of
nosocomial infections, and changing the protocol to 8-hour hang times reduced supply costs. The investigators
suggest that the microbial load did not increase with the 8-hour hang time because the hospital-specific formula was
refrigerated after preparation until needed and only 4 hours’ worth of formula was administered at a time. In
addition, diligent aseptic technique was followed during preparation and during administration of the feedings.
Improper handling of the enteral feeding administration set and feeding port increases the risk for microbial
contamination. Touch contamination by the nursing staff is a particular risk because they are typically the personnel
most involved in manipulating the enteral feeding system. In a study of handling techniques in a pediatric hospital,
Lyman and colleagues estimated contamination rates of enteral formula and/or administration sets to be between
19% and 59% and determined that 17 of the 24 species found to contaminate EN originated from skin or oral flora.2
This study compared sterile water rinse of administration sets, refrigeration of administration sets that were not
rinsed, and ready-to-hang formula with the administration set capped off and left at room temperature. The sterile
water rinse and unrinsed refrigerated techniques showed similar bacterial growth of 11.4% and 10.3%, respectively.
The ready-to-hang samples had 4.4% bacterial growth. The authors then factored in nursing labor and supply costs
for each technique. The sterile water rinse technique significantly increased the overall expense, while ready-to-hang
systems were deemed the most effective, in relation to decreasing bacterial contamination, supply, and labor costs.2
In a 1992 study, Payne-James and colleagues investigated retrograde contamination with 3 types of
administration sets: feeding set without drip chamber, feeding set with drip chamber, and feeding set with antireflux
ball valve. The authors found that the drip chamber on the administration set showed less bacterial growth than the
no-drip chamber and drip chamber with antireflux ball valve.14
A potential source of bacterial contamination of EN is endogenous retrograde growth stemming from secretions
of the throat, lungs, and stomach that enter the feeding tube and migrate toward the connection site of the
administration set.8 Mathus-Vliegen and colleagues found that feeding containers and/or administration sets tested
positive for the same predominant bacteria found from the cultures of the throat, lung and stomach, including 4
pathogenic species that are mobile and can easily grow upstream.8
One high-risk group for microbial infections is neonates. Hurrell and associates reported that opportunistic
pathogens (including Enterobacteriaceae spp.) were found growing in 76% of neonatal enteral feeding tubes tested
after being in place for <6 hours to >48 hours.15 The feeding regimen (HM, fortified HM, ready-to-feed formula,
reconstituted powdered formula, or a mixture) did not seem to affect microbial growth. Mehall and colleagues also
studied neonatal feeding tubes and found them to be a reservoir for antibiotic-resistant pathogens that could be
transmitted to other infants.16 In that study of 50 tube-fed neonates, formula-fed infants had significant feeding
intolerance when fed with contaminated tubes, and 4 infants developed necrotizing enterocolitis that required
surgery. Contamination was more prevalent in those infants receiving H2 receptor antagonists.16 Juma and Forsythe
investigated the colonization of feeding tubes in neonates with a wide range of bacterial and fungal organisms.17 The
potential for these organisms to translocate and cause systemic infections in immunocompromised infants with
increased mucosal permeability and underdeveloped gut microflora was explored. See Chapter 7 for guidance on the
use of infant formulas and HM in EN.

Modulars
Modulars, especially those in powdered form, are not sterilized at the end of the manufacturing process and may
increase the risk of bacterial contamination.3 Prepared enteral formulas with the addition of modular products should
be refrigerated when not in use, and unused product should be discarded after 24 hours of mixing.1 See Chapter 7 for
additional information on preparing enteral formulas as well as infant formulas and HM.

Blenderized Tube Feedings

Microbial contamination of blenderized tube feedings (BTFs) may cause foodborne illness.9 BTFs can be
contaminated at multiple points in the preparation and administration process. Ingredients in BTFs may be
contaminated, or improper food handling techniques may be used during preparation of the BTF, while cleaning
equipment, in food storage, or during feeding administration.7,18
Research on the incidence of bacterial contamination of BTFs and associated infections is scant. In a study
conducted in Iran, where BTFs are widely used in hospitals, Jalali and associates studied samples of BTFs prepared
in a hospital kitchen under the supervision of a nutritionist and then delivered to patient wards in closed containers
and refrigerated until time of use. In 76 samples collected immediately after preparation, variable counts of coliform
and Staphylococcus aureus were found in all samples. In 76 samples taken at 18 hours after preparation, 68 samples
(90%) were positive for coliform and 72 samples (95%) were positive for S. aureus. Tests did not detect Salmonella
spp. or Listeria monoocytgenes.7
In a study by Gallagher et al, 20 pediatric patients who were fed via gastrostomy tubes were switched to a
blenderized food diet from commercial enteral formulas.19 These patients exhibited improved GI tolerance (patients
with >1 episode of vomiting per week decreased from 76% to 53%, and patients experiencing gagging or retching
decreased from 82% to 47% by the end of the study). Investigators also reported increased intestinal bacterial
diversity. Patients did require 50% more energy intake while fed with BTFs.
To reduce the risk for microbial contamination, hospital-or home-prepared BTFs should be treated in the same
manner as reconstituted powdered formulas with respect to preparation in a controlled environment, handling,
storage, and administration. The Academy of Nutrition and Dietetics has published guidelines to minimize
contamination of BTFs from preparation to administration and meet food safety standards.20 It is recommended that
BTFs should be prepared and handled according to safe food handling and preparation guidelines; hospital-prepared
or home-blended products must be refrigerated until administered and between feedings; and unused portions must
be discarded after 24 hours. The maximum hang time for home-or hospital-blended BTFs at room temperature is 2
hours.1,20 Hang times for commercial BTFs may be different.

Enteral Feeding Pumps

The first commercial enteral feeding pump, which used rotary and linear peristaltic mechanisms to compress and
decompress fluid against rollers, was introduced in 1956. Use of enteral pumps took off in the 1970s, coinciding
with the development of commercially manufactured enteral formulas. Pump design advanced to use volumetric
mechanisms that improved the accuracy of measuring a preset volume of formula into a cassette before delivering
the formula at a controlled rate into the infusion tubing. By the late 1990s, enteral feeding pumps were enhanced
with safety features, including microprocessor controls, display screens, programming options, alarm alerts, error
messages, automatic water flush features, anti-free-flow protection, administration-set security doors, and safeguards
against overinfusion.21 Today, enteral feeding pumps offer even more sophisticated features, such as ambulatory
functionality (ie, a battery-operated pump and bag can be carried in a shoulder bag or backpack), delivery of a
controlled amount of enteral feedings, automatic priming, dose-volume settings, memory/feeding history
information, easy-to-load cassettes, and one-handed pump setup.21
Current enteral feeding pumps can be programmed at rates of 0.1 mL/h (a specialized infant feeding pump
designed for low-volume/HM feedings) to 600 mL/h. Enteral feeding pumps can be programmed for continuous,
intermittent, or bolus feedings. According to manufacturer manuals, the accuracy of flow rates ranges from ±5% to
10%. Flow-rate accuracy depends on hang height, which ranges from about 6 to 18 inches above the pump,
depending on the pump model. When the specialized pediatric low-volume/HM feeding pump is used with a feeding
rate of <0.1 mL/h, the pump should be level with the patient.
If a feeding pump fails to deliver feedings within the manufacturer’s accuracy specification, the pump should be
recalibrated. Pump manufacturers recommend that enteral feeding pumps should routinely be recalibrated every 2
years.
Use of enteral feeding pumps is recommended for patients receiving tube feedings into the small bowel.1 The
jejunum secretes fluid in response to hyperosmolar solutions, and rapid infusion of such a formula into the small
bowel may result in abdominal distention, hyperperistalsis, and diarrhea.21 In addition, because the stomach reservoir
is bypassed, patients may experience bloating and diarrhea if bolus or gravity feedings are administered through a
jejunal tube. A slow, controlled rate of infusion can avoid or reduce these symptoms. The addition of anti-free-flow
devices on the administration set protects against the possibility of free-flow incidents, preventing large volumes of
feeding from entering the GI tract as a single bolus feeding.21
Critically ill patients may also benefit from pump-assisted enteral feedings because continuous infusion of
formula may improve tolerance.1,22 Patients who experience enteral feeding aspiration, gastroesophageal reflux,
vomiting, or unresolved diarrhea may benefit from controlled-rate, small-volume feedings administered by an
enteral feeding pump.21,23
To deliver EN as prescribed, enteral feeding pumps must be used correctly. Walker and colleagues investigated
discrepancies between 24-hour enteral feeding pump histories and the hourly EN provision documented by the
nursing staff at a facility that had changed which type of enteral feeding pump it used.24 The researchers determined
that the enteral formula was rarely hung according to the manufacturer’s specifications and improper hang height
accounted for the delivery discrepancies. Improper hang height can result in underfeeding. At the conclusion of this
study, nursing staff was trained on the proper hang height for accurate nutrition support delivery, and the facility’s
EN protocol was updated accordingly.24 See Table 8-3 for recommendations regarding the use of enteral feeding
pumps.1,25

TABLE 8-3. Practice Recommendations for the Use of Enteral Feeding Pumps

Enteral feeding pumps should deliver the prescribed volume within 10% accuracy for children and
•
adults.
• Enteral feeding pumps should have a flow accuracy within 5% accuracy for neonatal patients.
Zero the volume delivery amount on the feeding pump at the beginning of a time period, such as
•
usual intake and output assessment period.
For pediatric patients, pumps should have an alarm for no flow or occlusion (even at low infusion
• rates) and automatic anti-free-flow protection should the tubing become disconnected from the pump.
A lockout feature to prevent settings from being changed is also preferable.25
Ensure that institutional biomedical engineering departments periodically test, according to
• manufacturer recommendations, whether pumps continue to meet the accuracy rates and whether
alarms function.
Human milk infused at low rates should be administered via syringe pump with the syringe tip
•
elevated.
Feeding pumps used for patients requiring enteral nutrition at home should have features that
•
promote safety and minimize sleep disturbances.
Source: Information is from references 1 and 25.

Protocols on Preventing Pulmonary Aspiration

Healthcare facilities should have in place protocols to minimize pulmonary aspiration risk in patients receiving EN.
For example, clinicians should be trained regarding best practices for positioning the patient during feeding (see
Table 8-4).1,26,27 Protocols related to pulmonary aspiration risk should also address the use of gastric residual
volumes (GRVs). ASPEN recommends the following:1

TABLE 8-4. Practice Recommendations on Positioning Patients Receiving Enteral Nutrition

Elevate the head of the bed at least 30° while patients are receiving EN, unless an elevated position
• is medically contraindicated. If there is a contraindication, consider the reverse Trendelenburg
position.
If it is necessary to lower the head of the bed for a procedure or because of a medical
•
contraindication, return the patient to an elevated head-of-the-bed position as soon as possible.
Pediatric patients over 12 months of age are to be elevated at least 30° while tube feeding is infusing
•
and for an additional 30 minutes after the feeding, unless elevation is medically contraindicated.26,27
• Infants under 1 year of age should sleep on their backs without the head of the bed being elevated.
Source: Information is from references 1, 26, and 27.

GRV measurements may not need to be used as part of routine care to monitor ICU [intensive care unit] patients on EN. For those patient care areas
where GRVs are still utilized, holding EN for GRVs <500 mL in the absence of other signs of intolerance should be avoided. A gastric residual volume
of between 250 and 500 mL should lead to implementation of measures to reduce risk of aspiration.
 This recommendation is based on a lack of evidence that GRVs are sufficiently predictive of risk to warrant
routine use of the invasive procedure, which “leads to increased EAD clogging, inappropriate cessation of EN,
consumption of nursing time, and allocation of healthcare resources and may adversely affect outcome through
reduced volume of EN delivered.”1 Refer to Chapter 9 for further discussion of preventing aspiration risk.

Feeding Tube Patency

Feeding tubes are prone to clogging for a variety of rea-sons, including an accumulation of formula sediment in the
lower portion of the tube, especially during slow administration rates of energy-dense and fiber-containing
formulas.28 To minimize the risk for tube clogging, clinicians should follow protocols for flushing adequate volumes
of water through tubes; completely grind medications into a fine powder before dissolving them in purified water;
avoid mixing medications together; limit the frequency of GRV checks; and avoid administering acidic fluids
through the tube.1,29,30 See Chapter 10 for information on recommended medication administration techniques.
Nasogastric and jejunostomy tubes are more likely than other tubes to clog because of their long lengths and
narrow diameters.29 Clogging may be caused by the acidic contents of gastric residual aspiration in the feeding
tube.1,29,30 Historically, colas, meat tenderizers, and acidic juices have been used to clear clogs. However, acidic
juices may worsen clogs because the proteins in the enteral formula coagulate in an acid environment.30,31 It is
crucial to restore tube patency when a clog is suspected. See Table 8-51 and Chapter 3 for additional guidance on the
management of tube patency.

TABLE 8-5. Practice Recommendations on Maintaining and Monitoring Feeding Tube Patency

Flush feeding tubes with 30 mL of water every 4 hours during continuous feeding or before and
1.
after intermittent feedings in adult patients.
Limit gastric residual checks as acidic gastric contents may cause protein in enteral formulas to
2.
precipitate within the lumen of the tube.
Flush the feeding tube with 30 mL of water after gastric residual volume measurements in an adult
3.
patient.
Flush feeding tubes in neonatal and pediatric patients with the lowest volume of water necessary
4. to clear the tube, unless the patient needs additional fluids to meet fluid needs. In some neonate
patients with strict fluid limits, a small amount of air may be used to flush the tube.
Purified water is recommended for use in tube flushes in adult and neonatal/pediatric patients
5.
before and after medication administration.
Adhere to protocols that call for proper flushing of tubes before and after medication
6.
administration.
Use an enteral feeding pump when patients, such as neonates, require slow rates of enteral
7.
feeding, and respond promptly to pump alarms.
Source: Adapted with permission from reference 1: Boullata JI, Carrera AL, Harvey L, et al. ASPEN safe practices for enteral nutrition
therapy. JPEN J Parenter Enteral Nutr. 2017;41(1):15-103. doi:10.1177/0148607116673053.

Monitoring

Goals and Scope of Monitoring

Careful monitoring of patients receiving EN is imperative to optimize patient safety, assess the effectiveness of
nutrition support, and avoid potential deleterious complications. An important part of monitoring is investigating
and promptly resolving problems related to EN. To attain positive clinical outcomes related to the provision of EN,
the clinician needs a thorough understanding of pathophysiology; energy and macronutrient metabolism; and fluid,
electrolyte, and micronutrient disorders.
The preeminent goals of monitoring EN are to (a) evaluate the adequacy of energy, nutrient, and fluid provision;
(b) minimize risk factors for feeding intolerance and other complications; and (c) detect and resolve any
complications or other problems as soon as possible. In the acute care and subacute care settings, responsibility for
monitoring tolerance and identifying complications frequently rests with the nursing staff, who then bring concerns
to nutrition support specialists for recommendations. See Chapter 3 for information on mechanical complications
and Chapter 9 for a review of GI-related and metabolic complications.
While patients are receiving EN, their nutrition and clinical status must be periodically reassessed. The
frequency of reassessment is based on the patient’s stability and tolerance of EN. The scope of the nutrition
reassessment resembles that of the initial nutrition assessment (see Chapter 1) while being guided by patient-specific
goals of the nutrition care plan (eg, to maintain or improve nutrition/clinical status, transition the patient to another
care setting, or enhance the patient’s quality of life).
The periodic nutrition assessments in the monitoring period should include the following:1,32,33

• Medical, surgical, social, and diet histories

• Anthropometric measurements
• Laboratory and diagnostic studies
• Nutrition-focused physical exam
• Handgrip strength and functional status

Surrogate markers such as energy intake, body weight, serum protein levels, nitrogen balance, body
composition, and functional status have been used to assess the adequacy of the nutrition support regimen.34
However, many of these measures are influenced by the patient’s clinical status and, therefore, may not accurately
reflect the patient’s nutrition status. Serum proteins (albumin and prealbumin) and C-reactive protein are indicators
of an inflammatory process and may serve as predictors of morbidity and mortality, but they are not accurate
measures of nutrition status.1,35 Nutrition status is an intermediate marker that acts as a stepping-stone to the ultimate
goal of achieving positive clinical outcomes (eg, wound healing, weight gain, decreased infectious complications,
reduced length of stay).
Table 8-6 summarizes suggested monitoring parameters for patients receiving EN.1,27,34,36 In addition to
monitoring the factors outlined in this table, clinicians monitoring patients receiving EN must verify that the EN
regimen includes routine procedures designed to promote safety (Table 8-7).1 To advance the safety and cost-
effectiveness of patient care, the nutrition support clinician must also provide ongoing education related to optimal
EN delivery for other members of the healthcare team.1

TABLE 8-6. Monitoring Parameters for Patients Receiving Enteral Nutrition Support

Nutrition-focused physical exam, including clinical signs of energy, fluid, and nutrient excess or
•
deficiency
• Vital signs
• Actual energy, fluid, and nutrient intake (oral, enteral, and parenteral) vs nutrition goals
• Measurement of output (urine, GI fluids, wound losses, chest tube drainage, etc)
• Weight trends
Growth trends for infants and children (appropriate weight gain and linear growth, head
•
circumferences for children up to 3 years of age)36
Laboratory data,a including:
• CBC, glucose, BUN, creatinine, electrolytes, calcium, magnesium, phosphorus, LFTs,
triglycerides, serum proteins, PT/INR, urine glucose, urine sodium, urine-specific gravity
◦ Vitamin D (25,OH) levels in pediatric patients
• Review of medications and any vitamin, mineral, or herbal supplements
 • Diagnostic studies
Changes in GI function indicating tolerance of nutrition therapy (eg, ostomy output, stool frequency
• and consistency, presence of blood in the stool, presence of abdominal distention/firmness,
increasing abdominal girth, nausea, vomiting)
• Signs and symptoms of complications of EN therapyb
For infants and children, apnea and bradycardia with feeds, which may be exacerbated by gastric
• distention27

• Functional status (eg, handgrip strength)

• Skin integrity status
Abbreviations: BUN, blood urea nitrogen; CBC, complete blood count; GI, gastrointestinal; INR, international normalized ratio; LFT, liver
function test; PT, prothrombin time.
a
The burden of the test, including consideration of the blood volume required to do the test, should be balanced by the benefit or usefulness
of the results, particularly in those patients who have been on a stable enteral regimen.
b
Refer to Table 8-7 for additional information on monitoring and preventing EN-related complications.
Source: Information is from references 1, 27, 34, and 36.

TABLE 8-7. Practice Recommendations for Monitoring and Preventing Complications

1. Evaluate all enterally fed patients for risk of aspiration.

2. Use ENFit® feeding sets, tubes, and syringes to avoid misconnections with intravenous lines.
3. Verify that the feeding tube is in the proper position before initiating feedings.
Keep the head of the bed elevated at least 30° at all times during the administration of enteral
4.
feedings, unless contraindicated.
In those facilities where GRV is utilized as a monitoring parameter, a GRV >500 mL should result
in holding EN and reassessing patient tolerance by use of an established algorithm including
5.
physical assessment, GI assessment, evaluation of glycemic control, minimization of sedation, and
consideration of promotility agent use, if not already prescribed.
Consider a feeding tube placed well beyond the pylorus when GRVs are consistently measured at
6.
>500 mL.
Abbreviations: EN, enteral nutrition; GI, gastrointestinal; GRV, gastric residual volume.
Source: Adapted with permission from reference 1: Boullata JI, Carrera AL, Harvey L, et al. ASPEN safe practices for enteral nutrition
therapy. JPEN J Parenter Enteral Nutr. 2017;41(1):15-103. doi:10.1177/0148607116673053.

A plan for monitoring EN therapy, including short- and long-term goals, should be documented in the patient’s
initial nutrition care plan as well as in specific plans of care, such as clinical pathways. Once tolerance of enteral
feedings is established, the frequency of monitoring is influenced by the patient’s disease, severity of illness, degree
of malnutrition, and level of metabolic stress.37,38 To provide adequate nutrition, it is often necessary to make
adjustments based on the patient’s clinical status.
The administration of EN may be interrupted for procedures/tests, surgery, medical interventions and therapies,
activities of daily living, periods of GI distress, medication administration, and elevated GRVs. Any interruptions
that can affect adequate delivery of nutrition support and hydration should be addressed during the monitoring
process. Progress toward nutrition goals should be documented within the medical record. If goals of therapy are not
being achieved, the nutrition care plan should be revised.32

Meeting Targets for Nutrient Delivery

Once enteral feeding orders have been written, it is essential for the nutrition support clinician to verify that the tube
feedings are actually being administered as ordered (see Chapter 6 for information on EN orders). Multiple studies
show that delivery of EN to hospitalized patients often falls short of established goals.37–40 Scheduled and
unscheduled interruptions, inadequate nutrient prescriptions, or other barriers (eg, mechanical, GI, or infectious
complications) are all factors cited that contribute to the inadequate provision of EN.37 A study in burn patients
found that the amount of energy received by patients was significantly less than the prescribed amount on all study
days (first 2 weeks of admission).41 The most common reasons why the EN prescription was not met were EN not
being administered at the goal rate (35%); feedings being held for surgery (24%); physician-or nurse-directed
interruptions to feedings (16%); and feeding intolerance (11%). The average time per day that EN was not
administered was 8.9 hours.41
Volume-based feeding is one strategy to meet the EN goal in cases where EN is frequently interrupted. With this
technique, a set volume of formula is prescribed for the day and the nurses compensate for the time that the tube
feeding is stopped by adjusting the hourly rate of administration as needed to meet the daily goal.42
When achievement of the established EN goal is not feasible in critically ill patients, administering a smaller
volume of EN during the first week of ICU admission seems to be adequate to achieve positive outcomes.22,37,38,43,44
Kudsk and colleagues found that adult trauma patients receiving as little as 15 kcal/kg/d via EN demonstrated
improved outcomes as compared with patients receiving parenteral nutrition (PN).43 Others have found that the
delivery of approximately 14–18 kcal/kg/d or 60% to 70% of enteral feeding goal has also been favorable.37,38
However, before this is accepted as the standard of care, larger clinical trials must take place to delineate the optimal
timing and critical amount of enteral formulation needed to promote positive outcomes.

Transitional Feedings
Management of a patient’s transition from PN to tube feeding or oral intake, or from tube feeding to oral intake, is
one of the most challenging aspects of nutrition support. The process of weaning a patient off nutrition support
should be individualized, with tactics, goals, and timing that reflect the patient’s clinical status.1

Parenteral Nutrition to Tube Feedings

When transitioning from PN to tube feeding, a reasonable approach is to begin tapering PN when tube feedings are
providing 33% to 50% of the patient’s nutrient requirements. As EN progresses, the PN formulation can be
decreased such that total intake (ie, EN and PN) meets nutrient requirements. Once tube feedings are well tolerated
and provide 60%–75% of nutrient requirements, PN can be dis continued.33 In pediatric patients whose EN is being
advanced at a very conservative rate to the EN goal, it may be necessary to continue PN beyond the point when EN
meets 75% of nutrient requirements to provide total intake that adequately promotes optimal growth and
development.45

Tube Feeding to Oral Intake

Transition from tube feeding to voluntary oral intake also requires careful management. Close monitoring reduces
the risk that EN will be discontinued prematurely, which can lead to nutrient inadequacy and weight loss. After EN
is discontinued, it may be prudent to delay removing the EAD until it is confirmed that the transition to oral intake is
a success; this conservative approach to EAD removal can minimize the risks associated with device reinsertion in
the event that the patient must resume EN because appetite and oral intake do not continue to improve as expected.
On the other hand, continuing EN when a patient is consuming an adequate amount orally could potentially interfere
with the patient’s appetite and motivation to eat and may cause overfeeding.
The transition phase from EN to oral intake may begin as soon as a patient is alert and able to manage the
mechanics of chewing and swallowing. Consultation with and input from speech-language pathologists can help
clinicians identify the presence of dysphagia early in the transition process. Once a patient is cleared to safely
consume a specific diet consistency (eg, blended foods), he or she should be encouraged to choose appropriate foods
at meals and snacks. Enteral tube feedings can be held for approximately 1 hour before scheduled meals to stimulate
appetite. Nocturnal infusion of tube feedings can also provide supplemental nutrition for patients who do not yet
meet nutrition needs via oral intake during the day. When voluntary intake approaches 50% of nutrient requirements
for more than 2 to 3 consecutive days, either the infusion rate of tube feedings can be slowed or the number of
feedings each day can be progressively decreased.
Another method to help patients transition to oral intake is to use postmeal bolus feedings. To take advantage of
the hunger drive, oral intake is optimal when the stomach is not full. Administering a feeding immediately after a
meal therefore reduces the impact that EN has on the patient’s appetite. The feedings can be varied according to the
adequacy of each meal. For example, suppose a patient would need 480-mL boluses of enteral formula 3 times daily
when consuming no food orally. If he or she does not eat a meal or eats very little, a 480-mL bolus feeding should
be administered. If the patient eats about half of a “usual” meal (as based on the patient’s or caregiver’s opinion of
what is normal for the patient), 240 mL of formula should be administered. The entire bolus feeding could be
omitted if the patient eats all or most of a “usual” meal. Clinical trials are needed to confirm the efficacy of this type
of schedule; however, anecdotal reports suggest that this system helps the patient who is transitioning back to oral
intake by providing a way to promote adequate nutrition.1

Transitioning Hospitalized Patients to Other Settings

When a hospitalized patient is expected to need EN for a prolonged period, the nutrition support clinician may be in
a position to oversee the patient’s transition to receive EN at home or in a long-term care or rehabilitation setting.
An important aspect of transition planning is to establish a feeding schedule that is safe and meets nutrition goals
while being as convenient for the patient’s lifestyle as possible. At this juncture, reimbursement issues may
influence the choice of enteral formulation or the type of equipment available for use at home or in a long-term
care/rehabilitation facility.
Communication with the home care provider or facility nursing staff regarding the patient’s nutrition care plan is
essential for success in achieving therapeutic goals. To promote a seamless transition to home, the clinician may also
assist with supply acquisition and patient/family teaching in preparation for discharge. Smooth transition to home
for pediatric patients with complex medical needs and enteral feeds requires contributions from a multidisciplinary
team, including care coordinators, nurses, physicians, dietitians, and speech therapists.46
The EN regimen should be well tolerated before a patient is discharged from the hospital. The feeding schedule
and method of feeding should be adjusted and simplified to accommodate individual and/or caregiver schedules.
Gravity bag or syringe may be the preferred method to administer gastric feedings in the home setting.33 If an EN
feeding pump is needed to administer gastric feedings at home, insurance providers may require supportive
documentation of the need.33
Patients receiving EN at home and their caregivers will need ongoing education on the feeding regimen and
possible complications. Feeding tolerance and the adequacy of the nutrition goals should be routinely monitored by
home care providers. See Chapter 11 for a detailed review of EN in the home setting.

Termination of Nutrition Support

The ASPEN standards of practice for hospitalized patients recommend that hospitals develop protocols to address
the termination of nutrition support therapy.32 These protocols should be designed to allow clinicians to use clinical
judgment in accordance with accepted standards of medical ethics, institutional policies, and state and federal laws.
Nutrition support may be modified or discontinued when there are disproportionate burdens on the patient or when
feedings are no longer beneficial to the patient. Functionally competent patients of all ages, parents/guardians,
and/or the legal surrogates of minor or incompetent patients should be involved in any decisions regarding the
withholding or withdrawing of nutrition support. A patient’s wishes for care should be considered in making
decisions to withhold or withdraw EN. Refer to Chapter 2 for a more detailed discussion of this issue.

References
1. Boullata JI, Carrera AL, Harvey L, et al. ASPEN safe practices for enteral nutrition therapy. JPEN J
Parenter Enteral Nutr. 2017;41(1):15–103. doi:10.1177/0148607116673053.
2. Lyman B, Williams M, Sollazzo J, et al. Enteral feeding set handling techniques: a comparison of bacterial
growth, nursing time, labor and material costs. Nutr Clin Pract. 2017;32(2): 193–200.
3. Perry J, Stankorb SM, Salgueiro M. Microbial contamination of enteral feeding products in thermoneutral
and hyper thermal ICU environments. Nutr Clin Pract. 2015;30(1):128–133.
4. Hsu TC, Chen NR, Sullivan MM, et al. Effect of high ambient temperature on contamination and physical
stability of one-liter ready-to-hang enteral delivery systems. Nutrition. 2000;16:165–167.
5. Areval-Manso JJ, Martinez-Sanchez P, Juarez-Martin B, et al. Preventing diarrhoea in enteral nutrition; the
impact of the delivery hang set hang time. Int J Clin Pract. 2015; 69(8): 900–908.
6. Neely AN, Mayes T, Gardner J, Kagan RJ, Gottschlich MM. A microbiologic study of enteral feeding hang
 time in a burn hospital: can feeding costs be reduced without compromising patient safety? Nutr Clin Pract.
2006;21:610–616.
7. Jalali M, Sabzghabaee AM, Badri SS, Soltani HA, Maracy MR. Bacterial contamination of hospital-prepared
enteral tube feeding formulas in Isfahan, Iran. J Res Med Sci. 2009; 14(3):149–156.
8. Mathus-Vliegen EM, Bredium MWJ, Binnekade JM. Analysis of site of bacterial contamination in an enteral
feeding system. JPEN J Parenter Enteral Nutr. 2006;30(6):519–525.
9. Bobo E. Reemergence of blenderized tube feedings: exploring the evidence. Nutr Clin Pract.
2016;31(6):730–735.
10. US Food and Drug Administration. Compliance program guidance manual: medical foods program—import
and domestic. Chapter 21: food composition, standards, labeling and economics, program 7321.002.
Implementation date: August 24, 2006, completion date: September 30, 2008.
https://www.fda.gov/downloads/food/complianceenforcement/ucm073339.pdf. Accessed December 16,
2018.
11. Bankhead R, Boullata J, Brantley S, et al. Enteral nutrition practice recommendations. JPEN J Parenter
Enteral Nutr. 2009;33(2):122–167.
12. Centers for Disease Control and Prevention. Enterobacter saka zakii infections associated with the use of
infant formula— Tennessee 2001. MMWR Morb Mortal Wkly Rep. 2002; 51(14):298–300.
13. Centers for Disease Control and Prevention. Cronobacter species isolation in two infants—New Mexico,
2008. MMWR Morb Mortal Wkly Rep. 2009;58(42):1179–1183.
14. Payne-James JJ, Rana SK, Bray JM, McSwiggan DA, Silk D. Retrograde (ascending) bacterial
contamination of enteral diet administration sets. JPEN J Parenter Enteral Nutr.1992;16(4):369–373.
15. Hurrell E, Kucerova E, Loughlin M, et al. Neonatal enteral feeding tubes as loci for colonisation by members
of the Enterobacteriaceae. BMC Infect Dis. 2009;9:146.
16. Mehall J, Kite C, Gilliam C, Jackson R, Smith S. Enteral feeding tubes are a reservoir for nosocomial
pathogens. J Pediatr Surg. 2002;37(7):1011–1012.
17. Juma N, Forsythe S. Microbial biofilm development on neonatal enteral feeding tubes. Adv Exp Med Biol.
2015;830: 113–121.
18. Vieira MMC, Santos VFN, Bottoni A, Morais TB. Nutritional and microbiological quality of commercial
and homemade blenderized whole food enteral diets for home-based enteral nutritional therapy in adults.
Clin Nutr. 2018;37(1): 177–181. doi:10.1016/j.clnu.2016.11.020.
19. Gallagher K, Flint A, Mouzaki M, et al. Blenderized enteral nutrition diet study: feasibility, clinical and
microbiome outcomes of providing blenderized feeds through a gastric tube in a medically complex pediatric
population. JPEN J Parenter Enteral Nutr. 2018;42(6):1046–1060.
20. Tutor S, Bennett K. Blenderized tube feeding. In: Steele C, Collins E, eds. Infant and Pediatric Feedings:
Guidelines for Prepa ration of Human Milk and Formula in Health Care Facilities. 3rd ed. Chicago, IL:
Academy of Nutrition and Dietetics; 2019: 173–183.
21. White H, King L. Enteral feeding pumps: efficacy, safety, and patient acceptability. Med Devices.
2014;7:291–298.
22. McClave SA, Taylor BE, Martindale RG, et al. Guidelines for the provision and assessment of nutrition
support therapy in the adult critically ill patient: Society of Critical Care Medicine (SCCM) and American
Society for Parenteral and Enteral Nutrition (ASPEN). JPEN J Parenter and Enteral Nutr. 2016;40(2):159–
211.
23. Scott R, Bowling TE. Enteral tube feeding in adults. J R Coll Physicians Edinb. 2015;45:46–54.
24. Walker R, Probstfeld L, Tucker A. Hang height of enteral nutrition influences the delivery of enteral
nutrition. Nutr Clin Pract. 2018;33(1):151–157. doi:10.1177/0884533617700132.
25. Hutsler D, Szekely L. Delivery and bedside management of feedings. In: Steele C, Collins E, eds. Infant and
Pediatric Feedings: Guidelines for Preparation of Human Milk and Formula in Health Care Facilities. 3rd
ed. Chicago, IL: Academy of Nutrition and Dietetics; 2019:201–215.
26. Hockenberry MJ, Wilson D, eds. Wong’s Nursing Care of Infants and Children. 9th ed. St. Louis, MO:
Elsevier; 2011.
27. Bowden VR, Greenberg CS. Feeding, enteral. In: Bowden VR, Greenberg CS, eds. Pediatric Nursing
Procedures. 4th ed. Philadelphia, PA: Wolters Kluwer; 2016:301–309.
28. Lord LM. Restoring and maintaining patency of enteral feeding tubes. Nutr Clin Pract. 2003;18:422–426.
29. Lord LM. Enteral access devices: types, function, care, and challenges. Nutr Clin Pract. 2018;33(1):16–38.
30. Garrison CM. Enteral feeding tube clogging: what are the causes and what are the answers? A bench top
analysis. Nutr Clin Pract. 2018;33(1):147–150.
31. Dandeles LM, Lodolce AE. Efficacy of agents to prevent and treat enteral feeding tube clogs. Ann
Pharmacother. 2011; 45:676–80.
32. Ukleja A, Gilbert K, Mogensen K, et al. Standards for nutrition support: adult hospitalized patients. Nutr
Clin Pract. 2018;33(6):906–920.
33. Kozeniecki M, Fritzshall R. Enteral nutrition for adults in the hospital setting. Nutr Clin Pract.
2015;30(5):634–651.
34. Doley J, Phillips W. Overview of enteral nutrition. In: Mueller CM, ed. The ASPEN Adult Nutrition Support
Core Curriculum. 3rd ed. Silver Spring, MD: American Society for Parenteral and Enteral Nutrition;
2017:214–225.
35. Matarese L, Charney P. Capturing the elusive diagnosis of malnutrition. Nutr Clin Pract. 2017;32(1):11–14.
36. Weckwerth J. Monitoring enteral nutrition support tolerance in infants and children. Nutr Clin Pract.
2004;19(5):496–503.
37. Adam S, Batson S. A study of problems associated with the delivery of enteral feeding in critically ill
patients in five ICUs in the UK. Intensive Care Med. 1997;23:261–266.
38. Rice TW, Swope T, Bozeman S, Wheeler AP. Variation in enteral nutrition delivery in mechanically
ventilated patients. Nutrition. 2005;21:786–792.
39. Ibrahim EH, Mehringer L, Prentice D, et al. Early versus late enteral feeding of mechanically ventilated
patients: results of a clinical trial. JPEN J Parenter Enteral Nutr. 2002;26:174–181.
40. Krishnan JA, Parce PB, Martinez A, et al. Caloric intake in medical ICU patients: consistency of care with
guidelines and relationship to clinical outcomes. Chest. 2003;124:297–305.
41. Sudenis T, Hall K, Carlotto R. Enteral nutrition: what the dietitian prescribes is not what the burn patient
gets! J Burn Care Res. 2015;36(2):297–305.
42. Taylor B, Brody R, Denmark R, Southard R, Byham-Gray L. Improving enteral 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.
43. Kudsk KA, Minard G, Croce MA, et al. A randomized trial of isonitrogenous enteral diets after severe
trauma: An immune-enhancing diet reduces septic complications. Ann Surg. 1996;224:531–543.
44. Taylor S, Fettes S, Jewkes C, et al. Prospective, randomized, controlled trial to determine the effect of early
enhanced enteral nutrition on clinical outcome in mechanically ventilated patients suffering head injury. Crit
Care Med. 1999;27:2525–2531.
45. Worthington P, Balint J, Bechtold M. When is parenteral nutrition appropriate? JPEN J Parenter Enteral
Nutr. 2017; 41: 324–377.
46. Sevilla W, McElhanon B. Optimizing transition to home enteral nutrition for pediatric patients. Nutr Clin
Pract. 2016; 31(6):762–768.
 CHAPTER 9

Complications of Enteral Nutrition

Introduction
Enteral nutrition (EN) therapy is the preferred feeding modality when the gastrointestinal (GI) tract is functional but
the patient is unable to orally consume adequate nutrients. The enteral route is promoted as an efficacious and cost-
effective method of providing nutrients to patients, compared to the parenteral route. However, EN is not without its
challenges and risks for serious complications. This chapter reviews selected GI and metabolic complications of EN
that can contribute to a patient’s morbidity and mortality (Table 9-1). Chapter 3 examines complications specific to
feeding tubes, and formula-related issues (eg, microbial contamination) are addressed in Chapter 7. Most EN-related
complications can be prevented with planning and bedside care using best-practice protocols. Ongoing monitoring
and reassessment should be a standard component of follow-up care (see Chapter 8).

TABLE 9-1. Selected Medical Complications Related to Enteral Nutritiona

Gastrointestinal-related complications:
• Nausea and vomiting
• Abdominal distention
• Maldigestion and malabsorption
• Diarrhea
• Constipation
• Gastroesophageal reflux
• Pulmonary aspiration
Metabolic alterations:
• Refeeding syndrome
• Electrolyte and mineral imbalances
• Vitamin deficiencies
• Fluid imbalances
• Hypercapnia
• Glucose intolerance
• Essential fatty acid deficiency
a
Refer to Chapter 3 for information on complications related to enteral access devices, such as tube misplacement, occlusion, or migration;
buried bumper syndrome; and site irritation/ulceration.

Gastrointestinal-Related Complications

Nausea and Vomiting

Nausea and/or vomiting occur in approximately 12% to 26% of patients who receive EN,1–3 and in up to 46% of
critically ill patients.4 Vomiting, especially in minimally responsive patients, may increase the risk of pulmonary
aspiration, pneumonia, and sepsis, although evidence in support of this hypothesis is weak.
Multiple etiologies for nausea and vomiting are associated with EN. Delayed gastric emptying, or gastroparesis,
is most often blamed.5,6 Potential causes of and interventions for slowed emptying are listed in Table 9-2.3–11

TABLE 9-2. Possible Causes of and Interventions for Delayed Gastric Emptying

Causes:
• Hypotension
• Hypokalemia
• Sepsis
• Medications (eg, anesthesia, anticholinergics, opioids)
• Diabetes mellitus and other metabolic diseases (eg, hypothyroidism, electrolyte disorders, renal
failure)
• Surgery (including vagotomy)
• Formula-related issues:
◦ Excessively rapid infusion of formula
◦ Use of cold formula
◦ Use of formula with a high fat content
Interventions:
• Reducing or discontinuing opioid and anticholinergic medications and finding substitutes for other
problematic medications when clinically appropriate
• Improving glucose control
• Positioning the feeding tube in a postpyloric location, although this may not resolve vomiting and
may require concomitant gastric drainage
• Switching to a low-fat and/or isotonic formula (low fiber)
• Administering the feeding solution and all flushes at room temperature
• Reducing the rate of infusion
• Administering a prokinetic agent (eg, metoclopramide, erythromycin)
Source: Information is from references 3–11.

Nausea and vomiting in critically ill patients may be caused by something other than delayed gastric emptying,
such as adverse effects of medication, soy allergy, or lactose intolerance. (Note: Enteral formulas administered to
critically ill patients are lactose free.) The etiology of nausea should be identified, if possible, instead of assuming
that it is related to EN.
If nausea or vomiting occur as the rate of administration or bolus volume of the EN increases, one approach is to
decrease the rate or volume to the last tolerated amount, with an attempt to increase the rate again after symptoms
abate. Closed-system delivery methods and selection of a polymeric formula, rather than peptide-based or elemental
formula, may reduce nausea associated with formula smell and appearance.8,9 Evidence-based, nurse-driven
protocols can standardize approaches to GI complications and may result in timely delivery of nutrition and
achievement of feeding goals.12,13
The presence of abdominal distention in a patient with nausea indicates a need to perform more detailed
abdominal assessments. Obstipation or fecal impaction may also lead to abdominal distention and nausea,
particularly in the institutionalized or chronically critically ill patient. The development of abdominal distention
during EN in conjunction with other symptoms, such as early satiety, vomiting, lack of flatus, and no bowel
movements, may be suggestive of severe constipation or fecal impaction or the more serious postoperative ileus or
paralytic ileus, which can lead to delays in feeding and extended hospital stay.9,14,15
One of the adverse consequences of ileus is intestinal dilatation and increased abdominal pressure, which in turn
may increase gastric residual volume (GRV) and the risk for vomiting.14 Postoperative ileus usually resolves without
intervention within 24–72 hours of surgery, but it may last for days to weeks. It is important to rule out ileus or other
type of GI pathology (eg, acute megacolon, acute colonic pseudo-obstruction) that could lead to enteric ischemia,
intestinal perforation, and increased mortality.14
Current evidence-based guidelines suggest omitting use of routine GRV assessment because GRVs do not
correlate with EN intolerance and do not decrease the incidence of ventilator-associated pneumonia.8,16 If GRV is
evaluated and measurements are low (<300–500 mL) and yet nausea persists, antiemetic medications may resolve
the problem. While GRV is not useful in determining aspiration risk, this bedside assessment technique can be a
valuable tool for detecting early signs of GI dysfunction and feeding intolerance, thus allowing for prompt
intervention.8

Abdominal Distention
Abdominal distention is a common reason why EN is interrupted.8 Distention (with or without elevated GRV) and
its associated symptoms of bloating and cramping may be the result of ileus, obstruction, obstipation, ascites, lactose
intolerance, or diarrheal illness.14,15
As previously mentioned, excessively rapid formula administration, infusion of cold formula, or initial use of a
fiber-containing formula may occasionally contribute to abdominal distention.8,17 Abdominal distention is diagnosed
by visual inspection and palpation, as well as from patient report. Evidence is lacking regarding how to define a
significant increase in abdominal girth. Therefore, careful clinical and radiological evaluation remain the most
practical means of assessment.
Distention caused by ileus or mechanical bowel obstruction may be diagnosed from a flat and upright abdominal
X-ray or abdominal computed tomography scan. Obtaining upper GI radiology with small bowel follow-through,
along with observation of intestinal anatomy and motility, can provide additional insights into the clinical situation.
If intestinal integrity and function are normal, EN may be continued so long as the patient is closely monitored.
Guidelines support enteral feeding through mild to moderate ileus.16 However, the discontinuation of feedings
may be necessary if motility is poor or if the bowel is markedly dilated. Parenteral nutrition (PN) may be considered
if the GI tract will be inaccessible or the patient will be unable to tolerate EN while awaiting return of bowel
function.8

Maldigestion and Malabsorption

Maldigestion refers to impaired breakdown of intact macro-nutrients (eg, lactose) into absorbable forms.
Malabsorption is defective mucosal uptake and transport of nutrients (fat, carbohydrate, protein, vitamins,
electrolytes, minerals) or water from the small intestine.
Disorders that lead to carbohydrate maldigestion and malabsorption are commonly divided into primary and
secondary forms.18 Primary forms include rare congenital defects in specific brush-border enzymes or transport
mechanisms, and secondary are those that arise from any condition affecting structural integrity or function of the
pancreas and small intestine.
It is extremely important to not confuse disaccharidase deficiency, malabsorption, and intolerance as these are
distinctive conditions and are not treated in the same manner.18 Similarly, carbohydrate intolerance, which is a
common condition, must be differentiated from carbohydrate malabsorption, which involves deficiencies in various
enzymes and transporters.18
Absorption depends on many factors, including gastric emptying, small intestinal motility and transit, presence
of pancreatic enzymes, contact surface area, and depth of the diffusion barrier of the absorptive epithelium.5 General
clinical manifestations of malabsorption include abdominal pain, unexplained weight loss, flatulence, bloating,
steatorrhea, and diarrhea.18 Other documented problems associated with malabsorption are related to vitamin or
mineral deficiencies; these conditions include anemia, tetany, bone pain and pathologic fractures, bleeding,
dermatitis, neuropathy, glossitis, and edema.19
Screening and diagnosis of malabsorption may include the following:

• Gross and microscopic examination of the stool to determine fat and protein content of a random stool
collection (in a qualitative study) and measure serum carotene concentration.
• Imaging studies of intestinal transit time and motility.
 • Evaluation of intake-output balance: A quantitative fecal fat study is the most traditional test used in an
inpatient or ambulatory setting to diagnose pancreatic exocrine insufficiency. For this test, the patient
consumes a diet containing 100 g of fat and stool is collected for 72 hours. Modifications can be made to this
procedure for patients unable to tolerate such a high fat content. In general, if more than 7% of the total
amount of fat consumed is obtained from the stool collection, that indicates fat malabsorption. A result of 15
g/d or greater indicates severe steatorrhea.20
• Assessment of maldigestion/malabsorption of specific nutrients: Evaluation may include lactose tolerance
tests, the Schilling test to screen for abnormal absorption of vitamin B12, and various radioisotopic
methodologies for identification of iron, calcium, various amino acids, folic acid, pyridoxine, and vitamin D
malabsorption. Hydrogen and methane concentrations in breath samples can help diagnose lactose, fructose,
sucrose, and sorbitol malabsorption.18
• Endoscopic small bowel biopsy: This test is helpful in diagnosing various mucosal disorders such as celiac
disease, tropical sprue, inflammatory bowel disease, and Whipple’s disease.

Causes of maldigestion/malabsorption include gluten-sensitive enteropathy, Crohn’s disease, diverticular

disease, radiation enteritis, enteric fistulas, HIV infection, pancreatic insufficiency, short bowel syndrome, and
numerous other disorders. The rate and extent of glucose absorption are greatly reduced in the critically ill
population.
Knowledge of the patient’s medical history and selection of an appropriate enteral product should help minimize
the likelihood of malabsorption and maldigestion during enteral feeding. The use of a semi-elemental or elemental
formula with a greater percentage of medium-chain triglycerides or structured lipids may improve tolerance.8 It is
best practice in the intensive care unit (ICU) to initiate feedings early. Although early feeding has not been shown to
affect subsequent gastric emptying or GI hormones, it may improve subsequent nutrient absorption.21 PN may be
necessary in patients who do not respond to efforts to improve GI tolerance of EN.

Diarrhea
Diarrhea is a commonly reported problem in patients receiving EN.22 Estimates of its incidence in enterally fed
patients range from 2% to 95%.23,24 The variation in estimates is related to the lack of a common definition of diar-
rhea. It can be defined as stool weight of more than 200 g/d, but it is frequently defined clinically as 3 or more
watery or loose stools in a 24-hour period.15,25,26 Stool volume can be measured by placing a collection device in the
toilet or by using a bedpan. In incontinent patients, volume can be estimated by measuring rectal tube or rectal
pouch output or weighing the soiled pad beneath the patient after each stool (assuming 1 g = 1 mL of stool).
Diarrhea can be categorized as motility-related, malabsorptive, inflammatory/exudative, secretory, or osmotic. A
systematic approach is required to identify the underlying cause and implement appropriate treatment strategies.15,26
Clinicians should always thoroughly investigate the etiology of diarrhea while initiating appropriate medical and
nutrition-related interventions to address the problem (see Table 9-3).9,15,16,26 Diarrhea may be caused by intolerance
of specific components in enteral formula (eg, lactose, sucrose, fructose, soy), or it may be related to the
characteristics of the formula (eg, high osmolality, low fiber content, high amounts of fermentable oligosaccha-rides,
disaccharides, monosaccharides, and polyols)15,22,24 However, most standard 1 kcal/mL formulas are now lactose free
and isotonic and contain only a moderate amount of fat. Consequently, formula intolerance is a less common cause
of diarrhea than some might assume. More common causes include medications (eg, antibiotics, liquid medications
in a sorbitol base, glucose-lowering agents, stool softeners, prokinetics, proton pump inhibitors) and infection (eg,
Clostridium difficile). Other possible etiologies include steatorrhea, small intestine bacterial overgrowth (SIBO), and
various GI diseases such as short bowel syndrome (SBS).

TABLE 9-3. Selected Options for Addressing Clinically Significant Diarrhea in Patients Receiving
Enteral Nutrition

Option Comments
Before assuming diarrhea is related to enteral
 Medical assessment nutrition, rule out infectious or inflammatory
causes, fecal impaction, or known problematic
medications.
Consultation with a pharmacist may help the
Consider changes to the medication regimen if
clinician determine whether discontinuing,
drugs are the suspected cause of diarrhea
reducing, or reformulating medication is an option.
Carefully choose agents that are not hyperosmolar
Administer an antidiarrheal agent (eg, loperamide, or in a sorbitol base; these may worsen diarrhea.
diphenoxylate) once an infectious etiology has Consult with a pharmacist regarding sorbitol
been ruled out or is being treated content of liquid medications because the
sweetener is not always listed as an ingredient.9
In the hemodynamically stable ICU patient
specifically, the routine use of a soluble fiber
additive should be considered as a prophylactic
Use an enteral formula with a blend of soluble and
measure to help maintain commensal microbiota
insoluble fiber15,26
and promote bowel health. The recommended
dose is 10-20 g given as a supplement in divided
doses over 24 hours.16
Consider a small-peptide formulation if the patient
Switch the patient from a hyperosmolar enteral has persistent diarrhea or suspected
formula to a more isotonic formula malabsorption, or if he or she does not respond to
fiber supplementation.15,16,26
Consider administering probiotics to patients with
For example, in trials, Lactobacillus GG has been
specific clinical conditions if randomized controlled
associated with improved outcomes in patients
trials have demonstrated both safety and outcome
with antibiotic-associated diarrhea.16
benefits16

When diarrhea occurs, the patient’s medication regimen should be among the first areas of investigation.
Antibiotics can cause diarrhea without necessarily causing Clostridium difficile overgrowth. Any drug given via a
jejunal feeding tube should be appropriately diluted with water to avoid a dumping-like syndrome associated with
hyperosmolality. For example, some drugs, such as potassium chloride liquid, should be mixed with a minimum of
30 to 60 mL per 10 mEq dose to avoid direct irritation of the gut.9 Refer to Chapter 10 for additional information on
medication administration in patients receiving EN.
Microbial contamination of the enteral feeding solution can cause infectious diarrhea or other problems and is a
particular risk for vulnerable hosts such as neonates, critically ill patients, and immune-suppressed patients.
Additionally, proton pump inhibitors and histamine2 receptor antagonists diminish the gastric acid microbial barrier;
therefore, patients taking these drugs may be at increased risk of enteric infections, which may predispose them to
greater risk of morbidity related to formula contamination.27 The risk of EN contamination is less when closed
enteral formula systems are used and greater when open systems are used.8,28 Refer to Chapter 7 for additional
information on closed vs open systems and the prevention of microbial contamination.
Patients receiving EN who have malabsorptive conditions (eg, SBS, pancreatic insufficiency) may experience
steatorrhea (the malabsorption of fat), which is made clinically obvious by frothy, odoriferous stools. The condition
is confirmed by a fecal fat analysis (quantitative or qualitative). A lower-fat enteral formula may reduce the
symptoms of fat malabsorption. Enteral formulas with fat in the form of medium-chain triglycerides may provide an
alternative source of energy in the presence of fat malabsorption. Inclusion of pancreatic enzymes in the patient’s
drug regimen may help if pancreatic dysfunction is present.20
Bacterial overgrowth in the GI tract can cause severe enteritis with marked diarrhea, fever, and even sepsis.
Conditions that predispose patients to SIBO include intestinal stasis and low acid states due to gastric resection or
possibly the use of proton pump inhibitors, which are common in GI surgical patients and those with chronic
pancreatitis. Up to 40% of patients with pancreatic insufficiency will develop SIBO.20 Symptomatic patients should
receive oral antimicrobial therapy that targets both aerobic and anaerobic organisms, as well as interventions to
decrease bacterial colonization.20
Many primary diseases of the intestine, including inflammatory bowel disease, SBS, gluten-sensitive
enteropathy, and acquired immunodeficiency syndrome, may result in malabsorption or secretory diarrhea.
Recognition and treatment of these diseases can minimize diarrhea. In some patients with GI disease, the use of
elemental or semi-elemental products with a greater percentage of fat from medium-chain triglycerides may
facilitate absorption.16
In patients with SBS, malabsorption can lead to severe diarrhea or significant ostomy losses. Whether the overall
bowel functions as if it is shortened or it has actually been resected, patients may require relatively large doses of
antimotility medications to control stool output. If all strategies to promote EN tolerance have been exhausted,
patients with SBS may require PN to supplement enteral nutrient delivery.
Although lactase deficiency is common in illness, lactose intolerance is not a significant issue with EN therapy
because, as previously noted, most formulas are lactose free. However, a patient may have diarrhea associated with
lactose intolerance during the transition from EN to oral intake. It may be prudent to reduce or eliminate milk
products from the diet, provide lactose-reduced dairy products or oral lactase, or advance to a low-lactose solid diet.
A potential consequence of diarrhea occurring with EN is incontinence-associated dermatitis, which can lead to
excoriation and skin breakdown. In situations where stool may come into prolonged contact with the skin, measures
should be taken to prevent skin breakdown. One option is the topical application of skin protectants such as a
moisture barrier cream or liquid protectant film.29 Another option is the application of a stool collection apparatus
such as a rectal pouch. The perineal skin should be inspected frequently, treated with gentle cleaning, and kept as
dry as possible.

Constipation
Defining constipation is difficult because normal defecation varies from person to person.30 The best clinical
definition of constipation is the accumulation of excess waste in the colon, often to the transverse colon or even the
cecum, associated with infrequent and difficult defecation.8
Constipation is a common problem for enterally fed patients, particularly those who are elderly and/or
bedridden.8 Multiple observational studies in critically ill patients defined constipation as the inability to pass stool
within 72 hours of admission; applying this definition, the incidence of constipation in the ICU is as high as 50%–
83%. In the critically ill patient, constipation is associated with early satiety and feeding intolerance, and it may
increase intra-abdominal pressure, making weaning from a ventilator more difficult; for these reasons, constipation
can interfere with nutrition goals in critically ill patients.31 Other symptoms associated with constipation include
abdominal distention, bloating, and vomiting; consequences of severe constipation may include fecal impaction or
bowel perforation requiring urgent nursing, medical, or pharmaceutical interventions.8,32
In patients receiving EN, the residue and extent of absorption of an EN product are factors to consider when
investigating the occurrence of constipation. A predigested, low-residue product may be completely absorbed,
resulting in a stool frequency of less than once a week. A plain abdominal X-ray may be ordered for diagnosis to
clearly differentiate constipation from small bowel obstruction or ileus.
With uncomplicated constipation, there is rarely any small bowel dilatation. A variant of constipation is
impaction of stool in the rectal vault. Impaction can be diagnosed and treated by rectal exam. Enemas, cathartics,
and even endos-copy may be required to treat severe impaction. Impaction should also be considered in patients,
particularly those who are elderly or bed-bound, when stool volumes have been small and then become liquid.
Liquid stool will seep around an impaction (obstipation). In addition, impaction may be the cause of delirium and
agitation in older adults.
Common causes of constipation in patients receiving EN include specific medications (eg, benzodiazepines and
opioids), inadequate fluid intake or dehydration, inadequate fiber intake, and lack of physical activity.8,33 To avoid
dehydration, it is important to provide adequate fluid during EN. Hydration may be problematic when a
concentrated formula is needed for fluid restriction. If usual hydration guidelines are contraindicated, consider a
stool softener and/or a laxative or cleansing enema.28,32,33
Inadequate fiber intake results in infrequent bowel movements without significant buildup of waste in the colon.
Fiber propels waste through the colon; use of a fiber-containing formula may be particularly important for the
patient who requires long-term tube feeding.8,30 If fiber is added to the enteral regimen, patients must receive a
minimum of 1 mL of fluid per kcal to prevent solidification of waste in the colon and constipation. Given that
isotonic EN formulas contain only 80%–85% of water by volume, additional fluid is often needed to facilitate
regular stool output and minimize the chance of impaction.8,28,30,32,33
Inadequate physical activity contributes to constipation. Patients should be encouraged and/or assisted to
ambulate whenever possible.
Of note, a systematic review and meta-analysis of the use of bowel protocols in ICU patients found a lack of
significance for unit bowel protocols to reduce either the occurrence of constipation and feeding intolerance or days
on mechanical ventilation.30 Feeding protocols that provide evidence-based guidance for early identification of and
intervention for constipation are recommended.9,16,33

Gastroesophageal Reflux
In healthy individuals, physiological reflux is cleared by a peristaltic wave, assisted by gravity in the erect person,
and acid is neutralized by swallowed saliva, which is high in bicarbonate.14 Delayed gastric emptying raises
intragastric pressure and threatens the integrity of the gastroesophageal barrier. Medications commonly administered
in the hospital and ICU settings (eg, opioids, nitrates, calcium channel blockers, theophylline, diazepam, and
barbiturates) have the potential to relax the lower esophageal sphincter and contribute to reflux.14
Percutaneous endoscopic gastric tubes have been found to reduce, although not completely prevent, occurrence
of reflux in both ventilated and nonventilated patients.34 Postpyloric feeding reportedly minimizes microaspiration
and pneumonia; however, duodenogastric reflux has been documented in patients fed in this manner.14 A duodenal
feeding tube may be inserted at the bedside using blind insertion techniques or newer electromagnetic placement
devices, whereas jejunal tube placement is most reliably achieved with endoscopic or fluoroscopic techniques.8,28
Distal jejunal placement beyond the ligament of Treitz is recommended for patients with gastric outlet obstruction,
gastroparesis, gastric fistula, pancreatitis, and known reflux and aspiration of gastric contents.8,28
Controversy exists as to whether postpyloric feeding is associated with improved tolerance, fewer complications,
or favorable patient outcomes. The most recent nutrition therapy guidelines published concluded that small bowel
feeding may reduce regurgitation, aspiration, and pneumonia; however, no difference has been found between small
bowel and gastric feedings in mortality, hospital or ICU length of stay, duration of mechanical ventilation, or time to
achieve goal EN.16 Best practices to minimize gastro esophageal reflux in patients receiving EN include elevating
the head of the bed at least 30°, altering the EN delivery method from bolus or intermittent to continuous, using pro
kinetic agents as appropriate for gastric feeding, diverting the level of feeding to a postpyloric location, and
transitioning to oral nutrition as quickly and safely as possible.8,16

Pulmonary Aspiration
Aspiration can be defined as the inhalation of material into the airway. This material may include nasal and oral
pharyngeal secretions as well as reflux of liquids, food, and other gastric contents.35 Symptoms associated with
clinically significant aspiration include dyspnea, tachypnea, wheezing, frothy or purulent sputum, rhonchi and rales,
tachycardia, fever, cyanosis, anxiety, and agitation. Pulmonary aspiration of tube feeding formula can also be
asymptomatic (ie, silent aspiration). In fact, aspiration of saliva is a normal phenomenon during sleep. Pneumonia
can result from pulmonary aspiration of tube feeding formula; however, aspiration of very small amounts of fluid
alone is insufficient to cause pneumonia.17
Despite correlations between aspiration and tube feeding, causal relationships have not been established. The
progression of pulmonary aspiration of feeding formula to aspiration pneumonia is hard to predict and may depend
on the quantity and acidity of the formula in addition to the particulates and contaminants in the formula. Age,
immune status, and comorbidities also influence the tendency toward aspiration pneumonia development. When the
quantity and acidity of the formula overwhelm either the patient’s natural defense mechanisms or the patient’s
altered pulmonary defense mechanisms, pneumonia is more likely to occur.
Aspiration pneumonia is estimated to account for 5%–15% of pneumonia in hospitalized patients.36 How-ever,
unless a patient is discovered regurgitating and then develops a new pulmonary infiltrate on radiographic film,
proving that aspiration was the cause of the pneumonia is difficult.37.38 The incidence of pulmonary aspiration in
tube-fed patients varies depending on the patient population studied and the technique used to identify aspiration. In
the critically ill patient population, the risk for pulmonary aspiration is thought to be increased because patients are
in a prolonged supine position and are likely to have endotracheal intubation, delayed gastric emptying, and a
decreased level of consciousness. Risk factors for aspiration include sedation, the use of paralytic agents, supine
patient positioning, gastric tube feedings, malpositioned feeding tubes, mechanical ventilation, vomiting,
gastroesophageal reflux disease, transportation within the hospital, staffing level of nursing, and advanced patient
age.39,40

Methods to Determine Aspiration Risk

Patients at risk for aspiration should be identified based on their diagnosis, clinical factors, and physical findings.
Any clinical signs of sepsis, the level of sedation, and the influence of vasopressor agents should be closely
monitored.39 The patient should be assessed for level of consciousness, feelings of fullness, nausea, and abdominal
distention, and vital signs should be routinely evaluated.
Historically, measurement of GRV has been used to monitor patients for the risk of aspiration. However,
although much research has been conducted to define an acceptable range for GRVs, investigators have not been
able to identify the precise level of GRV that places the patient at greatest risk for obvious GI intolerance. Therefore,
it is unclear how GRV values might best be applied in decision-making about when to advance or discontinue
feedings. In clinical guidelines on nutrition support for critically ill patients, the Society of Critical Care Medicine
and American Society for Parenteral and Enteral Nutrition suggest that GRVs should not be used as part of routine
care to monitor mechanically ventilated patients in the ICU receiving EN. The rationale for this recommendation is
that the procedure may have adverse outcomes and GRVs do not correlate with incidence of pneumonia,
regurgitation, or aspiration.16 If ICUs do use GRVs to assess aspiration risk, the guidelines recommend that
clinicians should not hold EN if a patient’s GRV is less than 500 mL unless there are other signs of intolerance.16 It
is appropriate to abruptly cease enteral feeding upon overt regurgitation or aspiration.
If GRVs are assessed and a patient’s GRVs are in the range of 250 to 500 mL, clinicians may want to consider a
step wise approach to assess the potential for GI intolerance. Elevated and increasing GRVs may be a symptom of
another underlying problem manifesting itself as delayed gastric emptying. If serial measurements reveal a change in
GRV, other potential causes of the change must be investigated.41
Even if the GRV is less than 250 mL, assessment of aspiration risk should continue.42 Just as high GRVs should
not automatically result in holding of enteral feedings, low GRVs should not result in decreased vigilance in the
monitoring of signs and symptoms of GI intolerance.
When clinicians choose to assess GRVs, they must understand that procedures for measuring GRVs are poorly
defined and not standardized. Unreliable methods are often used to detect aspiration. For example, using a syringe to
withdraw gastric contents will not consistently result in aspiration of the total volume of fluid present in the
stomach.43
Furthermore, many variables can affect the accuracy of bedside GRV measurements. These include the type of
feeding tube used when performing the measurement, the position of the feeding tube ports in the GI tract, and the
patient’s position.
Large GRVs are detected more often when large-bore sump tubes are used for the measurement. Using small-
bore tubes can underestimate the GRV. A study of 645 dual measurements made by using small-bore feeding tubes
and large-bore sump tubes concurrently present in the stomach of 62 critically ill patients indicated that large GRVs
were detected 2 to 3 times more often with large-bore sump tubes.44 Regardless of the size of the feeding tube used,
ports positioned at the gastroesophageal junction will result in a negligible GRV in most cases.45
Patient positioning may reasonably be assumed to affect the amount of GRV obtained; this factor may be of
greater significance in infants than in adults.45,46 In a study of 10 critically ill patients, McClave and associates found
no difference in GRVs obtained when the patients were supine vs in a right lateral decubitus position;45 similarly,
van der Voort and Zandstra reported that GRVs were similar when 19 critically ill patients were prone as opposed to
supine.47 In contrast, Malhotra and coauthors reported significantly higher GRVs from 27 preterm babies when they
were supine as opposed to prone.48
Finally, there is no established consensus about how frequently to monitor GRVs, if they are monitored.
Numerous studies have documented evaluation of GRV from every 4 to every 12 hours, depending on when the
feedings were initiated and the previous GRV obtained.45

Methods to Detect Aspiration

There is no validated method currently in clinical use to detect aspiration of tube feeding formula. In the past, blue
food coloring was added to enteral formula to attempt to detect aspiration of gastric feedings. However, in 2003, the
US Food and Drug Administration issued a public health advisory describing the association between FD&C Blue
#1 dye and patient fatalities from hypotension and metabolic acidosis, as well as blue discoloration of the skin,
organs, and body fluids.49 Given these safety concerns, the blue dye method is no longer used. Notably, it was also
shown to be ineffective in detecting aspiration.50
The use of glucose oxidase strips to test tracheal secretions for glucose from enteral formula is also problematic
because investigators have found glucose in tracheal secretions of unfed patients.43 Because there are no reliable
methods to detect formula aspiration in tube-fed patients, clinicians should prioritize strategies to minimize risk
factors for delayed gastric emptying, aspiration, and aspiration pneumonia.

Strategies to Prevent Aspiration

Because pulmonary aspiration can have life-threatening complications, prevention of aspiration and the
identification of high-risk patients are crucial. During gastric feedings, it is extremely important to raise the head of
the bed to 30°–45° or position the patient upright in a chair, if possible.28 The patient should be monitored at least
every 4 hours for proper positioning.28 This simple measure has been associated with decreased esophageal and
pharyngeal reflux of gastric contents and a decreased incidence of aspiration pneumonia.51 If head-of-the-bed (HOB)
elevation is contraindicated, the reverse Trendelenburg position should be considered for patients receiving gastric
feeds.28
The National Pressure Ulcer Advisory Panel recommends limiting the HOB elevation to 30° for patients on
bedrest, unless contraindicated, to reduce the risk for pressure ulcers, which are more likely to occur with higher
HOB elevations.52 Schallom and colleagues reviewed research aimed at lowering aspiration risk as well as that
directed at preventing pressure ulcers and recommend that HOB elevation decisions should be made in the context
of each patient’s overall condition.53 Critically ill patients who require mechanical ventilation and heavy sedation are
at the highest risk for aspiration and may benefit more from the 45° HOB elevation with periodic lowering of the
head of the bed to 30°. HOB elevation of 30° is recommended for critically ill patients at less risk for aspiration and
patients who are not critically ill. Infants under 1 year of age should sleep on their back and not have the head of the
bed elevated.28 In all cases, pressure-relieving measures should be employed.
When tube-fed patients are unable to effectively clear their airway secretions, additional precautions must be
taken. Sedative use should be minimized; feeding tube placement and GI intolerance should be assessed at 4-hour
intervals; bolus feedings should be avoided; endotracheal cuff pressures should be maintained at appropriate levels;
and secretions above cuff should be cleared before deflation.54 Oral care at least twice daily helps decrease the
bacterial load of the oral cavity.55
If patients experience feeding intolerance involving high GRVs or emesis, interventions to consider include a
slower infusion rate, use of a prokinetic agent (metoclopramide or low-dose erythromycin), or switching to small
bowel tube feedings. The possibility that the feeding tube is malpositioned should also be considered when nausea
and emesis occur. In 1 investigation, 25 of 201 critically ill patients were found to have malpositioned feeding tubes
that increased the risk for aspiration.56 If the open ports within the tube tip lie in the esophagus, the risk of
regurgitation and aspiration likely increases. After a feeding tube is placed in the antrum of the stomach or the small
bowel, the feeding tube should be marked at the exit site or the tube length should be measured and documented so
that placement can be checked every 4 hours or per the institution’s protocol.28 Obtaining a residual from a nasally
or orally placed small bowel feeding tube or from the jejunal port of a transgastric jejunal feeding tube is a useful
technique to detect inadvertent upward dislocation of the tip of the feeding tube into the stomach. Residual volumes
from the small bowel are typically quite low (eg, <10 mL); a sudden sharp increase in residual volume (eg, ≥100
mL) is a good indication that the tube has migrated up into the stomach.57
The use of care protocols may minimize aspiration risk. Metheny and colleagues compared usual care of
critically ill, tube-fed patients to care guided by an aspiration risk-reduction protocol (ARRP), which called for HOB
elevation of at least 30° (unless contraindicated) and an algorithmic approach for elevated GRVs that directed small
bowel feeding tube placement.58 In the usual care group, 88% aspirated and 48% developed pneumonia. In the
ARRP group, 39% aspirated and 19% developed pneumonia. The authors concluded that strict HOB elevation when
appropriate and the use of an ARRP to manage elevated GRVs in critically ill, tube-fed patients can significantly
lower the incidence of aspiration and aspiration-related pneumonia.
In a randomized, controlled, double-blind trial comparing the efficacy of combination therapy with erythromycin
and metoclopramide to erythromycin alone, Nguyen and associates defined feeding intolerance as (a) 2 or more
GRVs ≥250 mL within the first 24 hours, or (b) any 6-hour GRV ≥250 mL thereafter while receiving EN at a rate of
≥40 mL/h. They used the 250-mL threshold for the GRV as an indication for therapy, not for holding enteral feeds.
They found that the combination therapy was more effective in improving the outcomes of enteral feedings in
critically ill patients.59

Metabolic Alterations
With the exception of refeeding syndrome, EN by itself is unlikely to be the cause of significant metabolic
derangements or specific nutrition deficiencies. However, many patients undergoing EN support have underlying
conditions that predispose them to metabolic derangements.
Malnourished children are at increased risk for metabolic problems. All moderately to severely malnourished
children should have serum potassium, phosphorus, magnesium, and glucose levels checked at least daily during the
first week of initiation of nutrition support, as well as periodically during the gradual advancement of feedings.60

Refeeding Syndrome
Re-initiation of carbohydrate-containing feeding of severely malnourished patients may result in refeeding
syndrome, in which there are acute intracellular shifts of electrolytes as cell anabolism is stimulated.61–65 Refeeding
syndrome can affect the cardiac, respiratory, hepatic, and neuromuscular systems, possibly leading to various
clinical complications, including hematologic, neuromuscular, cardiac, and respiratory dysfunction and even death.
Refeeding syndrome can result in acute decreases in circulating levels of potassium, magnesium, and
phosphorus. Serum levels should be monitored very closely, and deficiencies should be treated as needed to
maintain normal circulating levels. Many patients with refeeding syndrome also require thiamin and folate
supplementation.63–66
Patients at high risk for refeeding syndrome and other metabolic complications should be followed closely, and
depleted levels of minerals and electrolytes should be corrected before feedings are initiated.28 When monitoring
metabolic parameters prior to the initiation of enteral feedings and periodically during EN therapy, clinicians should
follow protocols and consider the patient’s underlying disease state and length of therapy.
Prevention of refeeding syndrome is of utmost importance.67 Stanga and colleagues highlighted 7 cases that
exhibited 1 or more features of refeeding syndrome, including deficiencies and low plasma levels of potassium,
phosphorous, magnesium, and thiamin. These metabolic issues were compounded further by salt and water
retention.68 The aforementioned hallmarks of refeeding syndrome responded to specific interventions. In most cases,
these abnormalities could have been anticipated and prevented.67,68
For at-risk patients, nutrition support should be initiated at approximately 25% of the estimated energy goal and
advanced over 3 to 5 days to the goal rate.28 Serum electrolytes and vital signs should be monitored carefully after
nutrition support is started.28,66

Electrolyte and Mineral Imbalances

Electrolytes are lost via stool, ostomies, fistulas, emesis, venting gastrostomy tubes, urine, and skin. Patients with
excessive losses may need increased intake of various electrolytes. Potassium, magnesium, and phosphorus are
required for optimal protein synthesis. The kidneys are primarily responsible for excretion of potassium,
magnesium, and phosphorus; intake of these may need to be restricted in patients with renal insufficiency or failure.
Serum concentrations should be monitored at intervals based on patient acuity, and electrolytes and minerals should
be replaced as needed to keep serum levels within the normal range.69

Sodium
Sodium is the primary extracellular cation in the body and the major controller of osmolality. Clinical features of
hyponatremia and hypernatremia relate to the nervous system and include the following: depressed mentation,
confusion, irritability, obtundation, coma, seizures, nausea, vomiting, anorexia, and headache. Serum sodium
represents a ratio of sodium to water.69
Abnormal circulating levels of sodium primarily reflect the status of body water. A relative excess of water
compared with sodium results in hyponatremia, while a relative excess of sodium compared with water results in
hyper-natremia. A common cause of hyponatremia in hospitalized patients is the excessive effect of arginine
vasopressin (“antidiuretic hormone”) as with the syndrome of inappropriate antidiuretic hormone secretion
(SIADH), which results in retention of water in excess of sodium. SIADH can result from a variety of causes,
including intracranial hemorrhage, trauma, tumor, or encephalitis; carcinoma of the lung, duodenum, pancreas,
thymus, or lymph nodes; pneumonia; tuberculosis; lung abscess; cystic fibrosis; or certain medications. The most
common cause of hypernatremia in tube-fed patients is dehydration due to water losses in excess of sodium (eg,
excess sweating, osmotic diuresis causing exorbitant urinary losses, limited water intake). Thus, hypernatremia is
treated primarily by administration of fluid, and hyponatremia is treated by fluid restriction.69
Hypernatremia and hyponatremia also can be caused by high and low sodium intake, respectively, in relation to
output. Most enteral formulas contain low amounts of sodium. Patients with increased sodium losses require sodium
replacement. Sodium chloride may be judiciously included in the flush solution. The amount of salt used is based on
the sodium deficit, the volume of fluid losses, and the organ from which the fluids originated. Conversely, the
sodium content of intravenous (IV) fluids needs to be calculated when hypernatremia is evaluated. See Tables 9-4
and 9-5 for additional information on hypo- and hypernatremia.17,69

TABLE 9-4. Hyponatremia

Possible EN-Associated Causes Preventive or Therapeutic Measures

• SIADH causing water retention and dilution of
• Restrict fluid.
sodium
• Monitor sodium level daily.
• Hepatic, cardiac, or renal insufficiency
• Assess fluid status.
• Provide diuretic therapy, if indicated.
• Reduced sodium intake relative to output
• Restrict fluid and/or sodium.
• Provide sodium-containing replacement fluids to
• High gastrointestinal output (vomiting, diarrhea)
offset losses.
Abbreviations: EN, enteral nutrition; SIADH, syndrome of inappropriate antidiuretic hormone secretion.
Source: Information is from references 17 and 69.

TABLE 9-5. Hypernatremia

Possible EN-Associated Causes Preventive or Therapeutic Measures

• Inadequate fluid intake with increased fluid loss
• Monitor daily fluid intake and outputs.
(sweating, osmotic diuresis)
• Increased sodium intake (IV fluid) • Monitor electrolytes, BUN, and Cr daily.
• Monitor body weight daily; weight change >0.2
kg/d reflects change in ECF volume.
• Estimate fluid loss. Mild loss is indicated by 3%
• Depletion of total body sodium, extracellular decrease in body weight; moderate loss is
mass, extracellular fluid indicated by a 6% decrease; and severe loss is
a 10% decrease.
• Replace fluid loss via enteral or parenteral route
to replete ECF.
Abbreviations: BUN, blood urea nitrogen; Cr, creatinine; ECF, extracellular fluid; EN, enteral nutrition; IV, intravenous.
Source: Information is from references 17 and 69.

Potassium
Potassium is the primary intracellular cation in the body and the major determinant of electrical membrane potential.
Decreased concentrations of potassium (ie, hypokalemia) result in cardiac arrhythmias, muscle weakness, impaired
protein synthesis, and impaired insulin secretion. Potassium deficiency results from losses in the stool, GI secretions,
and urine (especially with diuretics). Elevated serum potassium (hyperkalemia) is often caused by poor kidney
function. Traumatic injuries that release potassium from injured cells can also cause hyperkalemia.69 See Tables 9-6
and 9-7 for additional information on hypo-and hyperkalemia.17,69

TABLE 9-6. Hypokalemia

Possible EN-Associated Causes Preventive or Therapeutic Measures

• Effect of ADH and aldosterone
• Supplement potassium to normal serum values
• Diuretic therapy
before initiation of tube feeding.
• Excessive losses (with diarrhea or via
• Monitor serum potassium daily until levels are
nasogastric tube)
stable with patient at goal EN rate.
• Metabolic alkalosis
• Supplement potassium and chloride.
• Insulin therapy
• Consider supplementation protocol.
• Dilution
Abbreviations: ADH, antidiuretic hormone; EN, enteral nutrition.
Source: Information is from references 17 and 69.

TABLE 9-7. Hyperkalemia

Possible EN-Associated Causes Preventive or Therapeutic Measures

• Correct acidosis, if possible; recheck serum
potassium.
• Metabolic acidosis • Correct serum potassium before initiation of EN,
if possible.
• Monitor serum potassium daily.
• Poor perfusion (eg, congestive heart failure) • Treat cause of poor perfusion.
• Administer potassium-binding resin, glucose,
• Renal failure
and/or insulin therapy.
• Excessive potassium intake from EN, IV fluid, • Eliminate potassium from IV fluids; reduce
oral diet potassium in EN and oral diet.
Abbreviations: EN, enteral nutrition; IV, intravenous.
Source: Information is from references 17 and 69.

Calcium
Calcium is the primary divalent cation of the extracellular fluid and is essential for regulating processes that require
movement in the body (eg, excitation-contraction coupling in cardiac, smooth, and skeletal muscles;
neurotransmission; hormonal secretion; ciliary motion; cell division).70 Calcium circulates in the blood in 3
fractions: ionized, chelated, and protein bound. The ionized fraction is physiologically active and homeostatically
regulated, and the best measure of circulating calcium status is the ionized calcium level. Total calcium levels,
which are measured by most laboratories, do not accurately reflect ionized calcium status.69
Ionized calcium levels are usually obtained with a parathyroid hormone level when serum total calcium values
are persistently low despite attempts to normalize them. In the absence of an ionized calcium measurement,
clinicians often use the following equation to determine a corrected or adjusted value, although the reliability of this
calculation has been questioned:
Adjusted Serum Calcium Value (mg/dL) = [Normal Serum Albumin (g/dL) − Observed Serum Albumin (g/dL) × 0.8] + Observed Serum
Calcium (mg/dL)

If adequate dietary calcium is not received over the short term, it will be mobilized from bone and will not be
immediately reflected in serum levels. Long-term depletion of calcium from bones may lead to osteopenia or
osteoporosis. Conversely, excess calcium administration during ischemic and septic states can cause cellular
injury.69 Calcium should be administered to patients in the smallest amounts possible to maintain normal
concentrations.

Phosphorus
Phosphorus is a source of cellular energy (eg, adenosine triphosphate, creatine phosphate), a component of cyclic
adenosine monophosphate and cyclic guanosine mono-phosphate (important intracellular messengers), a component
of 2,3-diphosphoglycerate (important for oxygen offloading from hemoglobin), and synthesis of nucleotides. Most
circulating phosphorus is in the ionized form.69,70
Phosphorus depletion (hypophosphatemia) causes a sick-cell syndrome in which all cells of the body (eg, in the
immune system, muscle, and liver) demonstrate diminished function. Respiratory arrest can occur with severe
phosphorus depletion. Common causes of hypophosphatemia are administration of large amounts of carbohydrate
(ie, phosphorus shifts intracellularly when glucose enters the cell), administration of drugs (eg, insulin, epinephrine,
phosphate-binders, sucralfate), and phosphate losses from the GI tract and kidneys.69
Serum phosphorus concentrations should be monitored based on patient acuity and replacement provided as
necessary. If levels are severely low, phosphorus should be administered intravenously. See Tables 9-8 and 9-9 for
additional information on hypo-and hyperphosphatemia.17,69

TABLE 9-8. Hypophosphatemia

Possible EN-Associated Causes Preventive or Therapeutic Measures

• Refeeding syndrome • Supplement phosphorus to reach normal levels
• Excessive energy intake before initiation of tube feeding.
• Monitor serum phosphorus daily and replete as
• Binding by sucralfate, antacids
necessary with changing clinical course.
• Supplement phosphorus as sodium or
• Insulin therapy potassium form, as clinically indicated, via
enteral or parenteral route.
Abbreviation: EN, enteral nutrition.
Source: Information is from references 17 and 69.

TABLE 9-9. Hyperphosphatemia

Possible EN-Associated Cause Preventive or Therapeutic Measures

• Administer phosphate-binder therapy.
• Renal insufficiency • Choose EN product with lower phosphorus
content.
Abbreviation: EN, enteral nutrition.
Source: Information is from references 17 and 69.

Magnesium
Magnesium is an important cofactor for many essential enzymes. Magnesium depletion (hypomagnesemia) can
result from urinary and GI losses or decreased dietary intake. Hypomagnesemia predisposes a patient to cardiac
arrhythmias and cellular injury.69 See Tables 9-10 and 9-11 for additional information on hypo- and
hypermagnesemia.17,69

TABLE 9-10. Hypomagnesemia

Possible EN-Associated Causes Preventive or Therapeutic Measures

• Supplement magnesium to normal serum values
• Excessive GI losses (diarrhea, high ostomy before initiation of tube feeding.
output) • Monitor serum magnesium daily until levels are
• Malabsorption stable with patient at goal EN rate.
• Consider supplementation protocol.
Abbreviations: EN, enteral nutrition; GI, gastrointestinal.
Source: Information is from references 17 and 69.

TABLE 9-11. Hypermagnesemia

Possible EN-Associated Causes Preventive or Therapeutic Measures

• Renal failure
• Excessive magnesium intake from EN and/or • Reduce magnesium in EN and oral diet.
oral diet
Abbreviation: EN, enteral nutrition.
Source: Information is from references 17 and 69.

Zinc
Zinc plays important roles in immune function, wound healing, vitamin A metabolism, glucose control, cellular
proliferation, and more. Table 9-12 reviews causes of and interventions for zinc deficiency (hypozincemia).71

TABLE 9-12. Hypozincemia

Possible EN-Associated Cause Preventive or Therapeutic Measures

• Supplement zinc via enteral or parenteral route.
• Excessive losses (via nasogastric tube, protein-
• Monitor for signs and symptoms of zinc
losing enteropathy, ostomy, wound)
deficiency, such as hair loss.
Abbreviation: EN, enteral nutrition.
Source: Information is from reference 71.

Vitamin Deficiencies
Patients who receive nutrition support may develop vita-min deficiencies, which are often the result of inadequate
vitamin intake (ie, intake that fails to match requirements or compensate for losses) or poor absorption.
Malnourished patients are at increased risk of developing vitamin deficiencies while receiving EN therapy because
of their depleted state when nutrition support is initiated.
Fat-soluble vitamins (vitamins A, D, E, and K) require pancreatic enzymes and bile for absorption.
Concentrations of these vitamins may be low in patients with pancreatic insufficiency, cirrhosis, or malabsorption
syndromes. Vitamin K is required for activation of coagulation proteins, and vitamin D is necessary for the
maintenance of circulating calcium. Table 9-13 reviews causes and interventions for vitamin K deficiency.71

TABLE 9-13. Vitamin K Deficiency

Possible EN-Associated Causes Preventive or Therapeutic Measures

• Inadequate vitamin K intake in diet
• Supplement vitamin K.
• Prolonged use of low-fat or low-vitamin K
• Consider probiotic agents.
formula
• Measure prothrombin time and partial
• Cirrhosis, malabsorption, pancreatic
thromboplastin time or INR daily until stable.
insufficiency
Abbreviations: EN, enteral nutrition; INR, international normalized ratio.
Source: Information is from reference 71.

Common water-soluble vitamin deficiencies include folate, ascorbic acid, and thiamin. Humans are almost
entirely dependent on dietary sources for these vitamins and require constant intake to maintain normal stores.71
Thiamin is an essential vitamin for carbohydrate metabolism, including glucose. In the United States, chronic
alcoholism, advanced age, long-term malnutrition, malabsorption syndromes, prolonged antacid therapy (thiamin is
destroyed in alkaline pH), and dialysis are common causes of thiamin deficiency. Thus, many of these patients are
provided thiamin and folic acid upon hospital admission. See Table 9–14 for additional information on thiamin
deficiency.71

TABLE 9-14. Thiamin Deficiency

Possible EN-Associated Causes Preventive or Therapeutic Measures

• Chronic alcoholism
• Thiamin supplementation for 3-7 days (IV for 3
• Advanced age
days, PO for 7 days).
• Long-term malnutrition
• Consider addition of folate and
• Refeeding syndrome
multivitamin/mineral in cases of alcoholism,
• Malabsorption
refeeding syndrome, malabsorption, or chronic
• Antacid therapy disease.
• Dialysis, diuretic
Abbreviations: EN, enteral nutrition; IV, intravenous; PO, per os (by mouth).
Source: Information is from reference 71.

Fluid Issues
Dehydration and overhydration are risks for patients receiving EN (see Tables 9-15 and 9-16).17 All enteral
prescriptions should include the patient’s fluid requirements as calculated by a qualified clinician who has done a
thorough review of the patient’s current clinical status, including fluid losses that require replacement (see Chapter 1
for additional information on assessment). The risk for dehydration is higher in older adults because they have
decreased lean body mass and therefore have diminished water reserves. Equations used to estimate fluid
requirements should take into account the patient’s weight, age, and clinical condition (see Chapter 6).69

TABLE 9-15. Dehydration

 Possible EN-Associated Causes Preventive or Therapeutic Measures
• Monitor daily fluid intake and output (urine,
ostomy, fistula outputs).
• Monitor body weight daily and assess for
edema. Weight change >0.2 kg/d reflects a
• Excessive fluid loss (vomiting, diarrhea, gastric
change in ECF volume.
tube loss)
• Estimate fluid losses. Mild loss is indicated by
• Inadequate fluid intake
3% decrease in body weight; moderate loss is
• Administration of formula concentrated in energy
indicated by a 6% decrease; and severe loss is
and protein to a patient who cannot express
a 10% decrease.
thirst
• Monitor serum electrolytes, urine-specific
gravity, BUN, and Cr daily. BUN:Cr is usually
10:1 in state of normal hydration.
• Provide enteral or IV fluid as indicated.
Abbreviations: BUN, blood urea nitrogen; Cr, creatinine; ECF, extracellular fluid; EN, enteral nutrition; IV, intravenous.
Source: Information is from reference 17.

TABLE 9-16. Overhydration

Possible EN-Associated Causes Preventive or Therapeutic Measures

• Monitor fluid intake and output daily.
• Excessive fluid intake
• Monitor edema.
• Rapid refeeding • Assess fluid status daily.
• Catabolism of lean body mass with potassium
• Monitor body weight daily.
loss
• Monitor weight. Weight change >0.2 kg/d
reflects a change in ECF volume.
• Refeeding syndrome • Monitor aldosterone levels, which will be
elevated with sodium retention.
• Consider use of less-concentrated formula.
• Renal, hepatic, or cardiac insufficiency • Provide diuretic therapy.
Abbreviations: ECF, extracellular fluid; EN, enteral nutrition.
Source: Information is from reference 17.

Dehydration results when fluid needs are not being met. Treatment of dehydration is aimed at restoring
intravascular volume.
Even though tube feeding formulas are liquid, they typically will not meet total fluid needs. Tube feeding
formulas are approximately 67%–87% water. Most patients receiving EN will require the equivalent of about 15%–
30% of the formula volume in additional water to meet normal fluid requirements. Nutrition support clinicians must
be mindful of other sources of fluids (IV fluids, oral intake, flushes after medication administration, etc) when
managing EN regimens.
Dehydration also occurs when extra body fluid losses (eg, water loss from skin during fever, loose stools,
emesis, large draining wounds, chronic drooling, drains, ostomy/fistula/gastric outputs, paracentesis losses, losses
through lactation and overuse of diuretics) are not met by fluid intake. The volume of these losses should be
measured (if possible) or estimated and then repleted. Wound dressings could be weighed before and after
placement to measure fluid loss from wounds. Excessive diaphoresis that soaks bed linens has been associated with
the loss of 1 liter of fluid.69,72
The use of high-protein or concentrated formulas can increase dehydration risk. High-protein formulas may
cause an osmotic diuresis due to the high renal solute load and loss of body water. Concentrated feeding formulas
contain 67%–75% water and are used commonly for patients with advanced renal disease, those who are fluid
overloaded, and those receiving intermittent feedings who are unable to handle a larger volume of feeding
administered during a given time period. In the latter case, a lower volume of concentrated formula is given and the
extra water needed is administered in between the feedings. See Chapter 4 for additional information on high-protein
and concentrated formulas.
Early signs of dehydration include dry mouth and eyes, thirst, dark urine with a strong odor, lightheadedness
upon standing, headache, fatigue, loss of appetite, flushed skin, and heat intolerance. Orthostatic hypotension (a drop
in systolic blood pressure by ≥20 mmHg upon standing) is usually present in dehydrated patients. Dehydration can
progress to include dysphagia, muscle cramps, painful urination, sunken eyes with dim vision, poor skin turgor
(sternum: >2 seconds), clumsiness, and delirium.69 An increasing serum sodium concentration, blood urea nitrogen
(BUN) level, or BUN-creatinine ratio suggests dehydration. An elevated urine-specific gravity (>1.028) together
with low urine output also points to dehydration.
Chronic overhydration may precipitate edema and congestive heart failure. Treatment is aimed at excess fluid
removal through diuresis or dialysis.69
After the initial fluid prescription is documented, a patient’s fluid status must be monitored closely and fluid
intake adjusted based on intake and outputs, laboratory values, and clinical status. Patients and their caregivers
should be educated on the signs and symptoms of dehydration and overhydration so that adjustments to the nutrition
regimen can be made in a timely manner.

Hypercapnia and Acid-Base Disorders

Hypercapnia (elevated blood levels of carbon dioxide [CO2]) with resultant respiratory acidosis is a theoretical
nutrition concern in patients on ventilators or those retaining CO2 (such as patients with markedly diminished
pulmonary function). Because the metabolic by-products of carbohydrate metabolism are CO2 and water, it was
theorized that restricting dietary carbohydrate would decrease CO2 production. However, this treatment approach
has not resulted in a clinical benefit, and it is now recognized that CO2 production is more affected by excess total
energy. Perceived differences in CO2 production between formulas with high vs lower fat content may be due to fat-
induced slowing of gastric emptying.73 See Table 9-17 for additional information on hypercapnia.17

TABLE 9-17. Hypercapnia

Possible EN-Associated Causes Preventive or Therapeutic Measures

• Use IC to measure energy requirement, if
possible.
• Overfeeding of energy
• If IC is unavailable, provide only maintenance
energy needs until hypercapnia resolves.
• Provide appropriate balance of carbohydrate,
• Excessive carbohydrate provision in patient with
protein, and fat. Consider providing fat to supply
respiratory dysfunction
30% of total energy.
Abbreviations: EN, enteral nutrition; IC, indirect calorimetry.
Source: Information is from reference 17.

Glucose Intolerance
Hyperglycemia is more common with PN than with EN. The enteral products developed to reduce hyperglycemia
are higher in fat and contain fiber, both intended to slow gastric emptying. This may not be desirable in acutely ill
patients in whom antropyloric dysfunction (poor gastric emptying, gastroparesis) commonly complicates gastric
feeding. Slow advancement of the feeding formula and close collaboration with the medical team should allow
adequate glucose control with standard feeding products.
Glycemic control should be considered a primarily medical issue in the acutely ill patient. Enteral products
marketed for patients with diabetes may help improve the ease of glycemic control in chronic care, but they have not
yet been proven effective in acutely ill patients.74 See Tables 9-18 and 9-19 for further information on hyper-and
hypoglycemia.75 For further information on formulas marketed for glycemic control, refer to Chapter 4.

TABLE 9-18. Hyperglycemia

Possible EN-Associated Causes Preventive or Therapeutic Measures

• Correct serum glucose before initiation of EN, if
possible.
• Monitor serum glucose every 6 hours, or per
• Refeeding syndrome
protocol.
• Diabetes mellitus, sepsis, catabolism, trauma, or
• Treat underlying disease.
other disease states or conditions
• Maintain appropriate intervascular volume and
• Insulin resistance
hydration.
• Glucocorticoids
• Provide appropriate pharmacological
• Excessive carbohydrate
intervention.
• Consider providing 30% of total energy as fat.
• Consider use of an enteral product with fiber.
Abbreviation: EN, enteral nutrition.
Source: Information is from reference 75.

TABLE 9-19. Hypoglycemia

Possible EN-Associated Cause Preventive or Therapeutic Measures

• Monitor serum glucose every 6 hours, or per
protocol.
• Abrupt cessation of EN in a patient receiving
• Treat with IV or enteral glucose to increase
insulin or other hypoglycemic drug
serum level to >100 mg/dL.
• Taper EN gradually.
Abbreviations: EN, enteral nutrition; IV, intravenous.
Source: Information is from reference 75.

Essential Fatty Acid Deficiency

Patients receiving EN may be at risk for essential fatty acid deficiency. The EN prescription for the types and
amount of lipids should be based on careful, individualized assessment. Essential fatty acid deficiency is further
reviewed in Table 9-20.76

TABLE 9-20. Essential Fatty Acid Deficiency

Possible EN-Associated Causes Preventive or Therapeutic Measures

• Provide at least 4% of energy needs as linoleic
 • Inadequate linoleic acid intake acid.
• Poor absorption due to Crohn's disease, short • Add modular fat component to EN if needed.
bowel syndrome • Provide soybean oil via enteral route (1.1-1.6 g/d
based on age, gender).
Abbreviation: EN, enteral nutrition.
Source: Information is from reference 76.

References
1. Montejo JC. Enteral nutrition-related gastrointestinal complications in critically ill patients: a multicenter
study. The Nutritional and Metabolic Working Group of the Spanish Society of Intensive Care Medicine and
Coronary Units. Crit Care Med. 1999;27:1447–1453.
2. Montejo JC, Grau T, Acosta J, et al. Multicenter, prospective, randomized, single-blind study comparing the
efficacy and gastrointestinal complications of early jejunal feeding with early gastric feeding in critically ill
patients. Crit Care Med. 2002;30:796–800.
3. Wasseem S, Moshiree B, Dragonov PV. Gastroparesis: current diagnostic challenges and management
considerations. World J Gastroenterol. 2009;15(1):25–37.
4. Davies AR, Bellomo R. Establishment of enteral nutrition: prokinetic agents and small bowel feeding tubes.
Curr Opin Crit Care. 2004;10:156–161.
5. Chapman MJ, Nguyen NQ , Deane AM. Gastrointestinal dysmotility: evidence and clinical management.
Curr Opin Clin Nutr Metab Care. 2013;16(2):209–216.
6. Taylor SJ, Manara AR, Brown J. Treating delayed gastric emptying in critical illness: metoclopramide,
erythromycin, and bedside (Cortrak) nasointestinal tube placement. JPEN J Parenter Enteral Nutr.
2010;34(3):289–294.
7 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;35:186–190.
8. Kozeniecki M, Fritzshall R. Enteral nutrition for adults in the hospital setting. Nutr Clin Pract.
2015;30(5):634–651.
9. Btaiche IF, Chan L, Pleva M, Kraft MD. Critical illness, gastrointestinal complications, and medication
therapy during enteral feeding in critically ill adult patients. Nutr Clin Pract. 2010;25(1):32–49.
10. Ali T, Hasan M, Hamadani M, Harty RF. Gastroparesis. South Med J. 2007;100(3):281–286.
11. Parkman HP, Hasler WL, Fisher RS, et al. American Gastroenterological Association technical review on the
diagnosis and treatment of gastroparesis. Gastroenterology. 2004;127:1592–1622.
doi:10.1053/j.gastro.2004.09.055.
12. Marshall AP, Cahill NE, Gramlich L, MacDonald G, Alberda C, Heyland DK. Optimizing nutrition in
intensive care units: empowering critical care nurses to be effective agents of change. Am J Crit Care.
2012;21(3):186–194. doi:10.4037/ajcc2012697.
13. Williams TA, Leslie GD, Leen T, Mills L, Dobb GJ. Reducing interruptions to continuous enteral nutrition
in the intensive care unit: a comparative study. J Clin Nurs. 2013; 22(19–20):2838–2848.
doi:10.1111/jocn.12068.
14. Aderinto-Adike AO, Quigley EM. Gastrointestinal motility problems in critical care: a clinical perspective. J
Dig Dis. 2014;15(7):335–344. doi:10.1111/1751-2980.12147.
15. Frazer C, Hussey L, Bemker M. Gastrointestinal motility problems in critically ill patients. Crit Care Nurs
Clin N Am. 2018;30:109–121.
16. McClave SA, Taylor BE, Martindale RG, et al. Guidelines for the provision and assessment of nutrition
support therapy in the adult critically ill patient: Society of Critical Care Medicine (SCCM) and American
Society for Parenteral and Enteral Nutrition (A.S.P.E.N.). JPEN J Parenter Enteral Nutr. 2016;40(2):159–
211. doi:10.1177/0148607115621863.
17. Malone AN, Seres DS, Lord L. Complications of enteral nutrition. In: Mueller CM, ed. The ASPEN Adult
Nutrition Support Core Curriculum. 3rd ed. Silver Spring, MD: American Society for Parenteral and Enteral
Nutrition; 2017:265–284.
18. Omer A, Quigley EMM. Carbohydrate maldigestion and malabsorption. Clin Gastroenterol Hepatol.
2018;16(8):1197–1199. doi:10.1016/j.cgh.2018.01.048.
19. Rezaie A, Buresi M, Lembo A, et al. Hydrogen and methane-based breath testing in gastrointestinal
disorders: the North American consensus. Am J Gastroenterol. 2017;112:775–784.
20. Berry AJ. Pancreatic enzyme replacement therapy during pancreatic insufficiency. Nutr Clin Pract.
2014;29(3):312–321.
21. Nguyen NQ , Burgstad C, Bellon M, et al. Delayed enteral feeding impairs intestinal carbohydrate
absorption in critically ill patients. Crit Care Med. 2012;40(1):50–54.
22. Chang S, Huang H. Diarrhea in enterally fed patients: blame the diet? Curr Opin Clin Nutr Metab Care.
2013;16:588–594.
23. Whelan K. Enteral tube feeding diarrhea: Manipulating the colonic microbiota with probiotics and
prebiotics. Proc Nutr Soc. 2007;66:299–306.
24. Whelan K, Schneider SM. Mechanisms, prevention, and management of diarrhea in enteral nutrition. Curr
Opin Gas troenterol. 2011;27:152–159.
25. Wierdsma NJ, Peters JH, Weijs PJ, et al. Malabsorption and nutritional balance in the ICU: fecal weight as a
biomarker: a prospective observational pilot study. Crit Care. 2011; 15(6):R264.
26. de Brito-Ashurst I, Preiser JC. Diarrhea in critically ill patients: the role of enteral feeding. JPEN J Parenter
Enteral Nutr. 2016;40(7):913–923.
27. Imhann F, Vich Vila A, Bonder MJ, et al. The influence of proton pump inhibitors and other commonly used
medication on the gut microbiota. Gut Microbes. 2017;8:351–358.
28. Boullata JI, Carrera AL, Harvey L, et al. ASPEN safe practices for enteral nutrition therapy. JPEN J
Parenter Enteral Nutr. 2017;41(1):15–103.
29. Brennan MR, Milne CT, Agrell-Kann M, Ekholm BP. Clinical evaluation of a skin protectant for the
management of incontinence-associated dermatitis. J Wound Ostomy Continence Nurs. 2017;44(2):172–180.
30. Lord LM. Maintaining hydration and tube patency in enteral tube feedings. Safe Pract Patient Care.
2011;5(2):1–11.
31. Mostafa SM, Bhandari S, Ritchie G, Grotton N, Wen-stone R. Constipation and its implications in the
critically ill patient. Br J Anaesth. 2003;91(6):815–819.
32. Johanson JF. Review of the treatment options for chronic constipation. Med Gen Med. 2007;9(2):25–59.
33. Bittencourt AF, Martins JR, Logullo L, et al. Constipation is more frequent than diarrhea in patients fed
exclusively by enteral nutrition: results of an observational study. Nutr Clin Pract. 2012;27(4):533–539.
34. Schallom M, Orr J, Metheny N, Pierce J. Gastroesophageal reflux in critically ill patients. Dimens Crit Care
Nurs. 2013; 32:69–77.
35. Zaloga GP. Aspiration-related illnesses: definitions and diagnosis. JPEN J Parenter Enteral Nutr. 2002;26(6
Suppl):S2–S7.
36. Dibardino DM, Wunderink RG. Aspiration pneumonia: a review of modern trends. J Crit Care.
2015;30(1):40–48.
37. Hamaoui E. Gastroesophageal reflux during gastrostomy feeding. JPEN J Parenter Enteral Nutr.
1995;19:172–173.
38. Gustke RF, Varma RR, Soergel KH. Gastric reflux during perfusion of the proximal small bowel.
Gastroenterology. 1970; 59:890–895.
39. Metheny N, Clouse RE, Chang YH, et al. Tracheobronchial aspiration of gastric contents in critically ill
tube-fed patients: frequency, outcomes, and risk factors. Crit Care Med. 2006;34:1007–1015.
40. Kollef MH, von Harz B, Prentice D, et al. Patient transport from intensive care increases the risk of
developing ventilator associated pneumonia. Chest. 1997;112:765–773.
41. McClave SA, Lukan JE, Stefater JA, et al. Poor validity of residual volume as a marker for risk of aspiration
in critically ill patients. Crit Care Med. 2005;33:324–330.
42. McClave SA, Demeo MT, DeLegge MH, et al. North American Summit on Aspiration in the Critically Ill
Patient: consensus statement. JPEN J Parenter Enteral Nutr. 2002;26 (6 Suppl):S80–S85.
43. Metheny NA, Dahms TE, Stewart BJ, Stone KS, Frank PA, Clouse RE. Verification of inefficacy of the
glucose method in detecting aspiration associated with tube feedings. Medsurg Nurs. 2005;14:112–121.
44. Metheny NA, Stewart J, Nuetzel G, Oliver D, Clouse RE. Effect of feeding-tube properties on residual
volume measurements in tube-fed patients. JPEN J Parenter Enteral Nutr. 2005;29:192–197.
45. McClave SA, Snider HL, Lowen CC, et al. Use of residual volume as a marker for enteral feeding
intolerance: prospective blinded comparison with physical examination and radiographic findings. JPEN J
Parenter Enteral Nutr. 1992;16: 99–105.
46. Metheny NA. Preventing respiratory complications of tube feedings: evidence-based practice. Am J Crit
Care. 2006;15: 360–369.
47. van der Voort PH, Zandstra DF. Enteral feeding in the critically ill: comparison between the supine and
prone positions: a prospective crossover study in mechanically ventilated patients. Crit Care. 2001;5:216–
 220.
48. Malhotra AK, Deorari AK, Paul VK, Bagga A, Singh M. Gastric residuals in preterm babies. J Trop Pediatr.
1992;38: 262–264.
49. US Food and Drug Administration. FDA Public Health Advisory: Reports of Blue Discoloration and Death
in Patients Receiving Enteral Feedings Tinted With The Dye, FD&C Blue No. 1.
https://www.fda.gov/forindustry/coloradditives/coloradditivesinspecificproducts/inmedicaldevices/ucm142395.htm
Published September 29, 2003. Accessed December 12, 2018.
50. Metheny NA, Dahms TE, Stewart BJ, et al. Efficacy of dye-stained enteral formula in detecting pulmonary
aspiration. Chest. 2002;122:276–281.
51. Drakulovic MB, Torres A, Bauer TT, et al. Supine body position as a risk factor for nosocomial pneumonia
in mechanically ventilated patients: a randomized trial. Lancet. 1999;354(9193):1851–1858.
52. National Pressure Ulcer Advisory Panel, European Pressure Ulcer Advisory Panel, Pan Pacific Pressure
Ulcer Alliance. Prevention and Treatment of Pressure Ulcers. Perth, Australia: Cambridge Media; 2014.
53. Schallom M, Dykeman B, Metheny N, Kirby J, Pierce J. Head-of-bed elevation and early outcomes of
gastric reflux, aspiration and pressure ulcers: a feasibility study. Am J Crit Care. 2015;24(1):57–66.
54. American Association of Critical-Care Nurses. AACN practice alert: prevention of aspiration in adults.
https://www.aacn.org/clinical-resources/practice-alerts/prevention-of-aspiration Published February 1, 2016.
Accessed December 19, 2018.
55. American Association of Critical-Care Nurses. AACN practice alert: oral care for acutely and critically ill
patients. https://www.aacn.org/clinical-resources/practice-alerts/oral-care-for-acutely-and-critically-ill-
patients. Published June 2017. Accessed December 12, 2018.
56. Metheny NA. Preventing respiratory complications of tube feedings: evidence-based practice. Am J Crit
Care. 2006;15(4): 360–369.
57. Braunschweig CL, Levy P, Sheean PM, Wang X. Enteral compared with parenteral nutrition: a meta-
analysis. Am J Clin Nutr. 2001;74:534–542.
58. Metheny NA, Davis-Jackson J, Stewart BJ. Effectiveness of an aspiration risk-reduction protocol. Nurs Res.
2010;59(1): 18–25.
59. 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.
60. A.S.P.E.N. Board of Directors. 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.
61. Jolly AF, Blank R. Refeeding syndrome. In: Zaloga G, ed. Nutrition in Critical Care. St. Louis, MO: Mosby;
1994:765–782.
62. Bowling TE, Silk DB. Refeeding remembered. Nutrition. 1995;11:32–34.
63. Solomon SM, Kirby DF. The refeeding syndrome: a review. JPEN J Parenter Enteral Nutr. 1990;14:90–97.
64. Parli SE, Ruf KM, Magnuson B. Pathophysiology, treatment, and prevention of fluid and electrolyte
abnormalities during refeeding syndrome. J Infus Nurs. 2014;37(3):197–202.
doi:10.1097/NAN.0000000000000038.
65. Mehanna HM, Moledina J, Travis J. Refeeding syndrome: what it is, and how to prevent and treat it. BMJ.
2008; 336(7659):1495–1498. doi:10.1136/bmj.a301.
66. Kraft MD, Btaiche IF, Sacks GS. Review of the refeeding syndrome. Nutr Clin Pract. 2005;20:625–633.
67. Friedli N, Stanga Z, Sobotka L, et al. Revisiting the refeeding syndrome: results of a systematic review.
Nutrition. 2017;35: 151–160. doi:10.1016/j.nut.2016.05.016.
68. Stanga Z, Brunner A, Leuenberger M, et al. Nutrition in clinical practice—the refeeding syndrome:
illustrative cases and guidelines for prevention and treatment. Eur J Clin Nutr. 2008;62:687–694.
69. Canada TW, Lord LM. Fluids, electrolytes, and acid-base disorders. In: Mueller CM, ed. The ASPEN Adult
Nutrition Support Core Curriculum. 3rd ed. Silver Spring, MD: American Society for Parenteral and Enteral
Nutrition; 2017:113–138.
70. Zaloga GP, Chernow B. Divalent ions: calcium, magnesium, and phosphorus. In: Chernow B, ed. The
Pharmacologic Approach to the Critically Ill Patient. 3rd ed. Baltimore, MD: Williams & Wilkins;
1994:777–804.
71. McKeever L. Vitamins and trace elements. In: Mueller CM, ed. The ASPEN Adult Nutrition Support Core
Curriculum. 3rd ed. Silver Spring, MD: American Society for Parenteral and Enteral Nutrition; 2017:140–
182.
72. Russell MK. Monitoring and complications. In: Charney P, Malone A, eds. ADA Pocket Guide to Enteral
Nutrition. Chicago, IL: American Dietetic Association, 2005.
73. Akrabawi SS, Mobarhan S, Stoltz RR, Ferguson PW. Gastric emptying, pulmonary function, gas exchange,
and respiratory quotient after feeding a moderate versus high fat enteral formula meal in chronic obstructive
pulmonary disease patients. Nutrition. 1996;12:260–265.
74. Malone AM. Enteral formula selection: a review of selected product categories. Pract Gastroenterol.
2005;29:44–74. https://med.virginia.edu/ginutrition/wp-content/uploads/sites/199/2015/11/MaloneArticle-
June-05.pdf. Accessed December 12, 2018.
75. Walker R, Tucker AM, Birtcher KK. Diabetes mellitus. In: Mueller CM, ed. The ASPEN Adult Nutrition
Support Core Cur riculum. 3rd ed. Silver Spring, MD: American Society for Parenteral and Enteral
Nutrition; 2017:675–700.
76. Hise M, Brown JC. Lipids. In: Mueller CM, ed. The ASPEN Adult Nutrition Support Core Curriculum. 3rd
ed. Silver Spring, MD: American Society for Parenteral and Enteral Nutrition; 2017:71–96.
 CHAPTER 10

Medication Administration with Enteral Nutrition

Introduction
Patients receiving enteral nutrition (EN) often require administration of medications through that same enteral access
device (EAD). By appreciating the complexity of drug administration through a feeding tube and using appropriate
administration techniques, nutrition support clinicians can reduce the risk for obstructed tubes, reduced drug
efficacy, and increased drug toxicity. To maximize the best use of medication in patients receiving EN,
administration techniques should ensure bioavailability without further complicating the patient’s overall care. See
Table 10-1 for selected factors to review when considering administration of oral drug products through an enteral
feeding tube.

TABLE 10-1. Selected Factors to Review Before Administering Medications via an Enteral
Feeding Tube

• Length of a patient's functional bowel beyond the tube's distal tip

• Internal diameter and length of the tube
• Composition of the tube
• Routine flushing regimen
• Location of the distal end of the feeding tube relative to the site of drug absorption
• Size of the opening(s) at the distal end of the feeding tube
• Need to keep a drug separate from a tube feeding formula
• Size of the enteral syringe [pressures]

Recommendations for administering medication via enteral feeding tubes are available.1–9 However, since the
1980s, surveys of enteral drug administration practices and techniques have demonstrated a gap between best-
practice recommendations and actual practice. These surveys suggest that only 5%–43% of practitioners flush tubes
before or between the administration of medications, only 32%–51% administer drugs separately from one another,
only 44%–64% dilute liquid medication, and 75%–85% avoid crushing modified-release dosage forms.10–16 Some of
these practices may contribute to measurable adverse outcomes—in particular, tube obstruction, reduced drug
efficacy, and increased drug toxicity. Best-practice techniques for medication administration through a feeding tube
are reviewed in this chapter.

Dissolution and Absorption of Drugs

Commercially available drugs that are intended for systemic effect after oral administration are designed with the
physiology of the healthy, intact gastrointestinal (GI) tract in mind. Immediate-release dosage forms begin to
disintegrate and dissolve in the stomach before entering the small bowel environment, where dissolution and
absorption continue. Although some drug absorption may occur throughout the GI tract by mass effect, the sites of
absorption for specific drugs are distinct and sometimes unknown.
Administration of a drug via an enteral feeding tube may bypass the required environment for optimal
dissolution and absorption of the medication. For example, when administered as a medication, iron is
predominantly absorbed in the duodenum following gastric dissolution. Thus, administration through a tube with the
distal opening in the jejunum risks poor bioavailability of the iron.9 Prior to administration of medication through a
feeding tube, the location of the distal tube tip should be noted (see Chapter 3 for information on tube tip
verification).

Enteral Access Devices and Medication Administration

For both accurate drug dosing and safe intraluminal pressures, only syringes manufactured and intended for enteral
use should be used to measure and administer a medication through an enteral feeding tube. Only specially designed
enteral syringes with ENFit® connectors will fit into ENFit enteral feeding devices, and those syringes should be
used exclusively to deliver medications via a feeding tube. The Low-Dose Tip ENFit syringes have minimal dead
space and have been shown to accurately deliver low-volume liquid medications.17,18
The ENFit connector is the new International Organization for Standardization (ISO) 80369-3 standard for
enteral feeding device connectors. This connector is designed to prevent misconnection of enteral feeding lines to
intravenous lines or other commonly encountered connectors not intended for enteral feeding delivery. Its unique
design is only compatible with ENFit tubing, therefore promoting patient safety and reducing the risk for a severe or
fatal administration error. For any EAD that does not yet have an ENFit connector, a temporary transition adapter is
available to connect the traditional enteral port to the ENFit administration set until new ENFit tubing is available.
Ultimately, all ENFit feeding tubes will use the ENFit connection. The ENFit syringe is available in 2 configurations
—standard dose and low dose. ENFit-labeled enteral devices with medication or feeding ports are only compatible
with ENFit medication syringes. ENFit syringes and connectors are available in a wide variety of sizes to allow for
medication and formula delivery. Refer to Chapter 3 for illustrations of ENFit connectors.

Dosage Forms
Commercially available oral drug dosage forms are solids (eg, capsules, tablets) or liquids (eg, solutions,
suspensions). Most tablets and capsules are immediate-release products (eg, compressed tablets, hard gelatin
capsules), which contain the active drug molecule along with excipients (non-therapeutic ingredients required to
formulate the product). These products are designed to allow the drug contents to be released within minutes of
reaching the stomach following oral administration. Many drugs are also offered as modified-release products (eg,
delayed- or extended-release), or as complex formulations.19,20
Solutions are homogeneous liquid mixtures in which the active medication is uniformly dissolved in the diluent.
The diluent often contains water and a variety of other solvents (eg, ethanol); contents of the diluent are chosen
based on the solubility of the active drug. The viscosity and osmolality of a solution vary with the drug and solvent.
With regard to enteral administration, disadvantages of solutions include the increased potential for drug instability
due to hydrolysis or oxidation.
Suspensions are heterogeneous liquids containing a poorly soluble active medication “floating” in a liquid
medium that contains suspending or thickening agents. Disadvantages of suspensions for enteral administration
include their viscosity and the potential that dispersed particles will settle, making it more difficult to deliver the
medication to the site of drug absorption through an enteral feeding tube. Regardless of the container volume,
suspensions should be shaken well immediately before the drug is administered via an EAD.

Crushing and Diluting Medications

Except for tablets that disperse easily when placed in an enteral syringe with water, contents of an appropriate tablet
or capsule should be crushed to a fine powder before being dispersed, dissolved, or suspended in an appropriate
volume of sterile water.21 See Figure 10-1 for an example of a medication-crushing device. Advantages of the
smaller particle size are improved suspension and decreased likelihood that a tube or its distal exit site(s) will be
obstructed. A disadvantage is increased risk of interaction with other medication particles found in the water if
nonpurified water is used. Flushing the enteral feeding tube between medications decreases the incidence of enteral
tube occlusions.22
 Some tablets are very small, very hard, or film coated, making them difficult to crush. Enteric and film coatings
do not crush well and tend to aggregate in clumps when diluted in water, thereby increasing the risk of clogging.
Modified-release dosage forms should not be crushed for administration via feeding tubes because destroying the
protective coating on a drug may make the medication much less effective or may result in an excessive—even fatal
—dose of the drug being released at one time.5,23 Instead, a more appropriate dosage form or therapeutic equivalent
should be considered.
Interfering with the integrity of intact liquid-filled gel capsules poses another level of complexity as it is difficult
to ensure accurate doses, so these forms of medication are also best avoided in enterally fed patients. Injectable
dosage forms are generally not considered appropriate for administration through a feeding tube because they are
designed for a physiological site with different characteristics.
Commercially available liquid formulations of a drug are not necessarily the best delivery option for a patient.
The solvents, solubilizing agents, and excipients in such formulations may be factors that contraindicate enteral
administration.24 Also, in fluid-restricted patients, a balance between the patient’s fluid requirements and the
minimal volume required to dilute medications for enteral feeding tube administration must be realized.
Liquid dosage forms often must be further diluted with sterile water prior to administration through an enteral
feeding tube. The viscosity and osmolality of the liquid dosage form, the internal diameter and length of the tube,
and the location of the distal tip all must be considered when determining the final diluted volume of the liquid drug
formulation. High-osmolality medicines may cause emesis and diarrhea; however, diluting medications to achieve a
lower osmolality is not always possible.
Suspensions tend to have much higher viscosity than solutions. Some suspensions are granular and may contain
modified-release particles. The resistance to flow through an enteral feeding tube can be reduced through dilution
but still may not be adequate to overcome a narrow tube. Dilution of each liquid medication prior to administration
is associated with improved delivery of the drug dose to the distal end of the tube.25,26
Liquid medication formulations may contain a number of excipients in addition to the drug and liquid. Several
poorly absorbed sweeteners and stabilizers are used in liquid drug products; such additives invariably increase a
product’s osmolality and potential to cause diarrhea. Electrolyte-containing liquids also contribute to high
osmolality.

Drug Interactions
Pharmacists and other clinicians do not routinely mix different medications in the same intravenous bag or syringe
without first ensuring the stability and compatibility of the drugs. Similar precautions should be taken during
preparation of medication for administration through enteral feeding tubes. Suboptimal drug administration has been
identified as more common in patient care units that did not establish drug preparation and administration
protocols.27
Interactions involving medication administered to patients receiving EN include those that pose a compatibility
problem and those that influence the stability of the drug or nutrient. These interactions can result in feeding tube
occlusion, altered drug or nutrient delivery and bioavail-ability, or altered GI tract function.
Occlusion of feeding tubes and altered clinical responses to drug therapy as a result of inappropriate enteral
administration techniques are not routinely captured in medication error event rates. Regardless of etiology,
obstruction (“clogging”) of a feeding tube is both time- and resource-intensive to address; therefore, it is best to
prevent clogs (see Chapter 3 for techniques to prevent feeding tube obstruction). Results of a national survey suggest
that drug-related feeding tube obstruction exceeds 10% if modified-release dosage forms are routinely crushed.15
Whenever a drug formulation is altered—whether by crushing, adding to fluid, or combining with other substances,
drug stability may be compromised.

Drug Added to Enteral Nutrition

In patient care settings that do not use a closed EN feeding system, the opportunity to add medication to EN
formulas may still exist. However, this practice is not recommended. There is a risk that the formula could be
contaminated during the mixing process. Also, mixing medication with formula would require knowledge we
generally do not have about the drug’s compatibility with the formula, the stability of each component of the final
mixture, and the therapeutic efficacy of the mixture.
Several older papers described the compatibility of a relatively small number of medications when admixed with
a limited number of commercially available EN formulas.28–33 This research shows that the type and concentration of
protein, as well as the fiber and mineral content of the EN formula, are factors that influence compatibility, while
drug product variables include pH, viscosity, osmolality, alcohol, and mineral content.29,31 Few of these studies
evaluated nutrient stability. Notably, 2 of the papers concluded that concentration of the medication may be
significantly affected when mixed with formula,30,32 and another reported that 95% of incompatible admixtures result
in clogged feeding tubes, of which less than one-third could be resolved by flushing with water.31
The available data on compatibility and stability of formula-drug mixtures cannot be extrapolated to different
forms of the same medication, different medications in the same drug class, or different enteral feeding formulas.
For example, a liquid morphine product of lower concentration may result in phase separation and protein
precipitation of an EN formula while a more concentrated version of the same drug may not.28

Drug Added to Drug

Combining drugs into one mixture for enteral administration is not recommended. The design of immediate-release
oral products is based on the intended use through oral ingestion with 120–240 mL of water. Once in the gastric
lumen, the water and endogenous secretions initiate the process of breaking down the tablet or capsule and
dispersing the particles widely with continued dilution in the large volume of the stomach; subsequently, the broken-
down and diluted drug empties into the duodenum and further disperses and dilutes in the large surface area of the
small bowel. Combining 2 or more medications within the confined space of a mortar under a pestle or other tablet-
crushing device may cause a chemical reaction much greater than the reaction that would occur when combining
drugs orally. The applied force used in combining drugs before administration, and the resultant increase in particle
surface area exposed, could accelerate changes in molecular structure and formation of complexes with subsequent
changes in physical and chemical properties of each drug. When considering the various excipients also occupying
that confined, nonphysiological space, the potential for chemical reactions increases even further. Any new dosage
form created by crushing and mixing together 2 or more medications (and their excipients) must still be expected to
release each drug in a known and consistent manner following administration.21 This information is not available for
most medications.
Combining liquid drug products requires knowledge of each solvent’s physicochemical properties to minimize
disruption of drug solubility and stability. Therefore, combining multiple liquid drug products can be quite complex,
with the solubility of the products altered by each new additive in the mix. Again, the stability and compatibility of
mixtures is impractical to predict.

Specific Drug-Nutrient Interactions

There are many potential drug-nutrient interactions involving EN therapy; however, a few drugs are particularly
troublesome and generate more discussion than most. Four of these drugs are discussed here.

Phenytoin
Phenytoin is the most noteworthy drug for interaction with EN therapy. Many studies and case reports have been
published, but findings from prospective, randomized controlled trials (RCTs) are limited. There are multiple
theories regarding the interaction and many proposed solutions. Four RCTs of phenytoin and EN in healthy
volunteers have been reviewed.34,35 Only 1 RCT investigated whether EN formulation delivered through a feeding
tube affects phenytoin; the others investigated the effect of oral EN on the drug. None of these RCTs documented an
interaction between phenytoin and EN formulations. However, 25 reports and studies with less-rigorous designs (no
randomization or placebo control) supported an interaction in patients.34 Theories regarding the mechanism of
interaction focus on issues related to pH and phenytoin binding, either to tubing or to an EN component.36–40 Issues
related to dosage form (eg, suspension, chewable tablets, capsule, parenteral solution), chemical form (eg, phenytoin
acid vs phenytoin sodium), and solubility are encompassed in the discussion of pH.36–38 Of the various methods
proposed to manage the phenytoin-EN interaction, none are completely reliable, and monitoring of serum phenytoin
concentrations and patient-specific pharmacokinetic parameters is highly recommended. Holding administration of
the EN formulation for at least 1 hour, and possibly 2 hours, before and after phenytoin administration seems to
produce the most consistent results.41,42 However, some practitioners elect not to hold EN; they should monitor
serum concentrations accordingly. Dilution of phenytoin suspension (1:1) is recommended when the suspension is
administered through a feeding tube.39 Regardless of the method used, consistency of administration is important to
control 1 of the variables influencing the phenytoin concentration.

Carbamazepine
Carbamazepine is a relatively insoluble drug and is acid stable; thus, slow gastric emptying improves its bio-
availability. Limited data suggest EN therapy reduces bioavailability, possibly by altering solubility. Relative bio-
availability of 90% was reported in a randomized cross-over study comparing administration of carbamazepine
suspension via nasogastric tube with continuous EN and oral intake after an overnight fast in 7 healthy men.43 Serum
carbamazepine concentrations with tube feeding were significantly lower at 8 hours, and the lower maximum
concentration approached statistical significance, although the small size of the study limited the ability of
investigators to show significance. In an vitro study, recovery of carbamazepine was 58% when the drug was mixed
with an intact protein enteral formulation, compared with 79% recovery after the drug was mixed with a simulated
gastric juice.44 Recovery when carbamazepine was mixed with the EN formulation and simulated intestinal juice was
59%. These findings suggest that postpyloric administration of carbamazepine may result in poor bioavailability.
Binding of carbamazepine to a component of enteral formulations has not been demonstrated; thus, it is unclear if
holding administration of the enteral formulation for 2 hours before and after the drug dose, as has been
recommended, is the best method of mitigating this potential interaction.45,46 Carbamazepine suspension should be
diluted at least 1:1 with water if the medication is administered via a feeding tube because drug loss in the feeding
tube seems to be reduced with dilution.47

Fluoroquinolones
Bioavailability of fluoroquinolone antibiotics seems to be reduced by enteral formulations. Studies in healthy
volunteers reported a 25% to 28% decrease in ciprofloxacin bio-availability when the drug was administered with an
enteral formulation, and decreases of 27% to 67% have been reported in hospitalized patients.48–50 Reduced
bioavailability has also been reported with repeated doses of ciprofloxacin via nasogastric tube in critically ill
patients receiving continuous infusion of an enteral formulation.51,52 Jejunal feeding has the greatest impact on
reducing ciprofloxacin bioavailability and may increase the risk for treatment failure.50,53 However, it is unclear
whether reduced bioavail-ability with gastric feeding is clinically significant because serum drug concentrations
above the minimum inhibitory concentration (MIC) for many pathogenic microorganisms have been reported.54 This
response will depend on the microorganism and its MIC given that the therapeutic effect of fluoroquinolones is
driven by adequate peak-to-MIC or area under the drug-concentration curve (AUC)-to-MIC ratio.
Complexation of ciprofloxacin with divalent cations in the enteral formulation was initially thought to be
responsible for reduced bioavailability. Fluoroquinolones are known to bind with divalent cations, and
manufacturers of these medications advise separating drug administration from intake of foods, dietary supplements,
or other drugs containing calcium, magnesium (eg, antacids), or iron. However, one in vitro study failed to find a
correlation between cation content of the enteral formulation and the loss of different fluoroquinolones mixed into
the formulation.55 Ciprofloxacin loss was greatest (82.5%), followed by levofloxacin (61%) and ofloxacin (46%).
The amount of loss seemed to increase with the degree of hydrophilicity of the individual drug. Better
bioavailability of ofloxacin (90%) compared with ciprofloxacin (72%) has also been reported in healthy volunteers
receiving the antibiotics with an enteral formulation.48 The current recommendation is to hold administration of EN
for at least 1 hour before a fluoroquinolone dose and 2 hours after the dose.46 This approach seems to minimize
effects of the interaction on ciprofloxacin and norfloxacin, and it is the safest approach for all fluoroquinolones
unless drug-specific data clearly demonstrate an absence of a drug-nutrient interaction.

Warfarin
The interaction between warfarin and vitamin K in enteral formulations was a classic interaction of concern until the
vitamin K content of most products was modified to ≤100 mcg/1000 kcal. Resistance to the anticoagulant effect of
warfarin was still observed when the drug was coadministered with EN; the protein content of the formulation was
suspected to be causative. However, warfarin resistance due to protein binding has not been adequately studied to
confirm whether that is the mechanism of interaction.56
Clinicians may elect to manage the warfarin-EN interaction by separating the drug from the formula, increasing
the warfarin dose, choosing an alternative anticoagulant therapy, or even using an elemental formula. (Note:
Elemental formulas are costly and high in osmolality, and their use requires justification.) Holding administration of
the EN formulation for at least 1 hour before and after the warfarin dose is expected to mitigate the interaction.57
Nonetheless, response to warfarin therapy must be closely monitored when EN therapy is started, stopped, or
altered. Interactions involving warfarin can be life threatening.

Planning the Patient’s Medication Regimen

Each patient’s medication regimen should be individualized. Pharmacists can provide necessary information on the
physicochemical properties of a drug as well as interpretation of published stability and compatibility data. This
guidance from the pharmacist can be applied to an individual patient’s drug regimen and allow for more informed
decision-making by the entire healthcare team.
A multidisciplinary intervention program involving guidelines, nurse education, and pharmacist
recommendations has been shown to be effective in promoting the most appropriate drug administration practices
and techniques, thereby reducing tube obstructions and drug errors.27 Several strategies may help minimize the risk
for adverse outcomes for patients receiving EN who are also being administered medications. For example, the
entire medication regimen may be simplified, a medication that is not immediately needed may be temporarily
discontinued, or dosing schedules may be altered to avoid administration of medications at the same time as enteral
feedings.5 Additionally, dosage forms or routes of administration may be altered, or the patient may be switched to a
therapeutically similar drug product that is better suited for administration via the feeding tube.5 The creation of
extemporaneous medication formulas for individual patients may sometimes be the best option, particularly in
pediatric practice settings.58,59 Specific medication formulas may be found in the literature.58–60 Aside from ensuring
drug stability, the data should additionally reflect that the labeled drug dose can ultimately be delivered to the site at
the distal end of the enteral feeding tube without significant loss.

Medication Administration Technique

To optimize therapeutic response of the medication and prevent complications such as tube occlusion, clinicians and
caregivers should carefully follow documented procedures and guidelines for medication administration through an
enteral feeding tube.1 As discussed earlier, important concepts to consider include tube size and location of the tube
tip. Administration of enteral formula is temporarily held while each medication is administered enterally. The
period of time that the formula is held will depend on the interaction potential between the administered drug and
the enteral formula. See Table 10-2 for practice recommendations and medication administration techniques.1

TABLE 10-2. Practice Recommendations and Procedures for Medication Administration Through
an Enteral Access Device

Develop policies and procedures to ensure safe practices by staff across all departments involved
1.
with enteral medication preparation and administration.
Identify drug, dose, dosage form, route (ie, enteral), and access device (eg, nasoduodenal tube) in
2.
the prescriber's order.
 3. Have a pharmacist review each medication order to determine whether the enterally administered
medication will be safe, stable, and compatible as ordered.
Institute and follow nursing policies and procedures to prepare and administer each medication
4.
safely.
5. Provide nonsterile compounding pharmacy services to support medication preparation.
Use best practices as per USP <795> for any enteral drug preparations compounded in advance
(ie, not for immediate use); these should include:
a. Reference to published stability data clearly described with citations in the organization's master
6. formulation records
b. Documenting in a permanent compounding record
c. Providing a beyond use date
d. Storage in a container consistent with the stability/ compatibility literature and USP <795>
7. Do not add medication directly to an enteral feeding formula.
8. Administer each medication separately through an appropriate access.
Avoid mixing together different medications intended for administration through the feeding tube,
9. given the risks for physical and chemical incompatibilities, tube obstruction, and altered
therapeutic drug responses.
Use available liquid dosage forms only if they are appropriate for enteral administration. If liquid
10. dosage forms are inappropriate or unavailable, substitute only immediate-release solid dosage
forms.
Prepare approved immediate-release solid dosage forms of medication for enteral administration
according to pharmacist instructions. Techniques may include:
11. a. Crush simple compressed tablets to a fine powder and mix with purified water.
b. Open hard gelatin capsules and mix powder containing the immediate-release medication with
purified water.
12. Use only appropriate instruments to measure and prepare enteral medication.
Use only clean enteral syringes (>20 mL with ENFit device) to administer medication through an
13.
EAD.
Provide appropriate tube irrigation around the timing of drug administration:
a. Prior to administering medication, stop the feeding and flush the tube with at least 15 mL water.
b. Administer the medication using a clean enteral syringe.
14.
c. Flush the tube again with at least 15 mL water, taking into account the patient's volume status.
d. Repeat with the next medication.
e. Flush the tube 1 final time with at least 15 mL water.
Restart the feeding in a timely manner to avoid compromising nutrition status. Hold the feeding by
15.
30 minutes or more only if separation is indicated to avoid altered drug bioavailability.
Consult with an adult or pediatric pharmacist for patients who receive medications coadministered
16.
with EN.
Abbreviations: EAD, enteral access device; EN, enteral nutrition.
Source: Adapted with permission from reference 1: Boullata JI, Carrera AL, Harvey L, et al. ASPEN safe practices for enteral nutrition
therapy. JPEN J Parenter Enteral Nutr. 2017;41:15–103.

Conclusion
Best practice in drug administration through enteral feeding tubes requires dedicated time and resources.
Implementing standardized protocols for drug administration through an enteral feeding tube can reduce
inconsistencies in practice that may otherwise interfere with appropriate medication delivery.1,16,24 Such protocols, as
well as clear communication among members of the interdisciplinary team and careful documentation of patient care
(including medication and EN orders), are essential to the safe and effective delivery of drugs via EADs.

Practice Resources and Suggested Readings

Boullata JI. Guidebook on Enteral Medication Administration. Silver Spring, MD: American Society for Parenteral
and Enteral Nutrition; 2018.
Boullata JI, Carrera AL, Harvey L, et al. ASPEN safe practices for enteral nutrition therapy. JPEN J Parenter
Enteral Nutr. 2017;41:15–103.
Boullata JI. Drug administration through an enteral feeding tube. Am J Nurs. 2009;109(10):34–42.
Boullata JI, Armenti VT. Handbook of Drug Nutrient Interactions. 2nd ed. New York, NY: Humana Press; 2010.
GEDSA. ENFit® medical guidelines: research and position statements. GEDSA website.
http://stayconnected.org/enfit-medical-guidelines.Accessed October 22, 2018.
GEDSA. Procedure for inpatient settings: preparing and administering medications using ENFit®. GEDSA website.
http://stayconnected.org/wp-content/uploads/2017/02/medication-administration-poster.pdf. Accessed October
22, 2018.
Institute for Safe Medication Practices website. www.ismp.org.Accessed October 22, 2018.
McCabe BJ, Frankel EH, Wolfe JJ. Handbook of Food Drug Inter actions. Boca Raton, FL: CRC Press; 2003.
Mitchell J. Oral dosage forms that should not be crushed. Institute for Safe Medication Practices website.
www.ismp.org/tools/donotcrush.pdf. Published November 20, 2016. Accessed October 22, 2018.
Williams NT. Medication administration through enteral feeding tubes. Am J Health Syst Pharm. 2008;65:2347–
2357.
Wohlt PD, Zheng L, Gunderson S, Balzar SA, Johnson BD, Fish JT. Recommendations for the use of medications
with continuous enteral nutrition. Am J Health Syst Pharm. 2009;66: 1458–1467.

References
1. Boullata JI, Carrera AL, Harvey L, et al. ASPEN safe practices for enteral nutrition therapy. JPEN J
Parenter Enteral Nutr. 2017;41:15–103.
2. Lehmann S, Barber JR. Giving medications by feeding tube: how to avoid problems. Nursing.
1991;21(11):58–61.
3. McConnell EA. Giving medications through an enteral feeding tube. Nursing. 1998;28:66.
4. Gilbar PJ. A guide to enteral drug administration in palliative care. J Pain Symptom Manage. 1999;17:197–
207.
5. 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;39:225–237.
6. Dickerson RN. Medication administration considerations for patients receiving enteral tube feedings. Hosp
Pharm. 2004;39:84–89,96.
7. Magnuson BL, Clifford TM, Hoskins LA, Bernard AC. Enteral nutrition and drug administration,
interactions, and complications. Nutr Clin Pract. 2005;20:618–624.
8. Rollins C, Thomson C, Crane T. Pharmacotherapeutic issues. In: Rolandelli RH, Bankhead R, Boullata JI,
Compher CW, eds. Clinical Nutrition: Enteral and Tube Feeding. 4th ed. Philadelphia, PA:
Elsevier/Saunders; 2005:291–305.
9. White R, Bradnam V. Handbook of Drug Administration via Enteral Feeding Tubes. London, UK:
Pharmaceutical Press; 2007.
10. Leff RD, Roberts RJ. Enteral drug administration practices: report of a preliminary survey. Pediatrics.
1988;81:549–551.
11. Mateo MA. Nursing management of enteral tube feedings. Heart Lung. 1996;25:318–323.
12. Belknap DC, Seifert CF, Peterman M. Administration of medications through enteral feeding catheters. Am J
Crit Care. 1997;6:382–392.
13. Schmieding NJ, Waldman RC. Nasogastric tube feeding and medication administration: a survey of nursing
practices. Gastroenterol Nurs. 1997;20:118–124.
14. Seifert CF, Johnston BA. Drug administration through enteral feeding catheters [letter]. Am J Health Syst
Pharm. 2002;59:378–379.
15. Seifert CF, Johnston BA. A nationwide survey of long-term care facilities to determine the characteristics of
medication administration through enteral feeding catheters. Nutr Clin Pract. 2005;20:354–362.
16. Boullata JI, Hudson LM, Spencer CT, Preston AM, Oakes BA. Drug administration by feeding tube: results
 of a practice-based survey [abstract]. Nutr Clin Pract. 2007; 22:126.
17. Guenter P, Lyman B. ENFit enteral nutrition connectors. Nutr Clin Pract. 2016;31(6):769–772.
18. GEDSA. Reducing the risk of medical device tubing mis-connections: ENFit® Low Dose Tip Syringe
review. http://stayconnected.org/wp-content/uploads/2016/04/GEDSA-Low-Dose-Syringe-End-User-LDT-
Preso-FINAL.pdf. Published 2016. Accessed October 22, 2018.
19. Franceschinis E, Voinovich D, Grassi M, et al. Self-emulsifying pellets prepared by wet granulation in high-
shear mixer: influence of formulation variables and preliminary study on the in vitro absorption. Int J Pharm.
2005;291:87–97.
20. Matteucci ME, Brettmann BK, Rogers TL, Elder EJ, Williams RO, Johnston KP. Design of potent
amorphous drug nanoparticles for rapid generation of highly supersaturated media. Molec Pharm.
2007;4:782–793.
21. USP. USP NF 41–NF 36. Rockville, MD: United States Pharmacopeial Convention; 2018.
22. Scanlan M, Frisch S. Nasoduodenal feeding tubes: prevention of occlusion. J Neurosci Nurs. 1992;24:256–
259.
23. Schier JG, Howland MA, Hoffman RS, Nelson LS. Fatality from administration of labetalol and crushed
extended-release nifedipine. Ann Pharmacother. 2003;37:1420–1423.
24. Madigan SM, Courtney DE, Macauley D. The solution was the problem. Clin Nutr. 2002;21:531–532.
25. Clark-Schmidt AL, Garnett WR, Lowe DR, Karnes HT. Loss of carbamazepine suspension through
nasogastric feeding tubes. Am J Hosp Pharm. 1990;47:2034–2037.
26. Seifert CF, McGoodwin PL, Allen LV. Phenytoin recovery from percutaneous endoscopic gastrostomy
Pezzer catheters after long-term in vitro administration. JPEN J Parenter Enteral Nutr. 1993;17: 370–374.
27. van den Bemt PM, Cusell MB, Overbeeke PW, et al. Quality improvement of oral medication administration
in patients with enteral feeding tubes. Qual Saf Health Care. 2006;15: 44–47.
28. Udeani GO, Bass J, Johnston TP. Compatibility of oral morphine sulfate solution with enteral feeding
products. Ann Pharmacother. 1994;28:451–455.
29. Altman E, Cutie AJ. Compatibility of enteral products with commonly employed drug additives. Nutr
Support Serv. 1984; 4(12):8,10,11,14.
30. Holtz L, Milton J, Sturek JK. Compatibility of medications with enteral feedings. JPEN J Parenter Enteral
Nutr. 1987;11: 183–186.
31. Burns PE, McCall L, Worsching R. Physical compatibility of enteral formulas with various common
medications. J Am Diet Assoc. 1988;88:1094–1096.
32. Strom JG, Miller SW. Stability of drugs with enteral nutrient formulas. Ann Pharmacother. 1990;24:130–
134.
33. Crowther RS, Bellanger R, Szauter KE. In vitro stability of ranitidine hydrochloride in enteral nutrient
formulas. Ann Pharmacother. 1995;29:859–862.
34. Au Yeung SC, Ensom MH. Phenytoin and enteral feedings: does evidence support an interaction? Ann
Pharmacother. 2000;34:896–905.
35. Doak KK, Curtis EH, Dunnigan KJ, et al. Bioavailability of phenytoin acid and phenytoin sodium with
enteral feedings. Pharmacotherapy. 1998;18:637–645.
36. Splinter MY, Seifert CF, Bradberry JC, et al. Recovery of phenytoin suspension after in vitro administration
through percutaneous endoscopic gastrostomy Pezzer catheters. Am J Hosp Pharm. 1990;47:373–377.
37. Fleisher D, Sheth N, Kou JH. Phenytoin interaction with enteral feedings administered through nasogastric
tubes. JPEN J Parenter Enteral Nutr. 1990;14:513–516.
38. Hooks MA, Longe RL, Taylor AT, Francisco GE. Recovery of phenytoin from an enteral nutrient formula.
Am J Hosp Pharm. 1986;43:685–688.
39. Cacek AT, DeVito JM, Koonce JR. In vitro evaluation of nasogastric administration methods for phenytoin.
Am J Hosp Pharm. 1986;43:689–692.
40. Guidry JR, Eastwood TF, Curry SC. Phenytoin absorption on volunteers receiving selected enteral feedings.
West J Med. 1989;150:659–661.
41. Gilbert S, Hatton J, Magnuson B. How to minimize interaction between phenytoin and enteral feedings: two
approaches—therapeutic options. Nutr Clin Pract. 1996;11:28–31.
42. Bauer LA. Interference of oral phenytoin absorption by continuous nasogastric feedings. Neurology.
1982;32:570–572.
43. Bass J, Miles MV, Tennison MB, et al. Effects of enteral tube feeding on the absorption and
pharmacokinetic profile of carbamazepine. Epilepsia. 1989;30:364–369.
44. Kassam RM, Friesen E, Locock RA. In vitro recovery of carbamazepine from Ensure. JPEN J Parenter
 Enteral Nutr. 1989;13: 272–276.
45. Estoup M. Approaches and limitations of medication delivery in patients with enteral feeding tubes. Crit
Care Nurs. 1994;14:68–79.
46. Engle KK, Hannawa TE. Techniques for administering oral medications to critical care patients receiving
continuous enteral nutrition. Am J Health Syst Pharm. 1999;56: 1441–1444.
47. Clark-Schmidt AL, Garnett WR, Lowe DR, Karnes HT. Loss of carbamazepine suspension through
nasogastric feeding tubes. Am J Hosp Pharm. 1990;47:2034–2037.
48. Mueller BA, Brierton DG, Abel SR, Bowman L. Effect of enteral feeding with Ensure on oral
bioavailabilities of ofloxacin and ciprofloxacin. Antimicrob Agents Chemother. 1994;38: 2101–2105.
49. Piccolo ML, Toossi Z, Goldman M. Effect of coadministration of a nutritional supplement on ciprofloxacin
absorption. Am J Hosp Pharm. 1994;51:2697–2699.
50. Healy DP, Brodbeck MC, Clendening CE. Ciprofloxacin absorption is impaired in patients given enteral
feedings orally and via gastrostomy and jejunostomy tubes. Antimicrob Agents Chemother. 1996;40:6–10.
51. Mimoz O, Binter V, Jacolot A, et al. Pharmacokinetics and absolute bioavailability of ciprofloxacin
administered through a nasogastric tube with continuous enteral feeding to critically ill patients. Intensive
Care Med. 1998;24:1047–1051.
52. de Marie S, VandenBergh MFQ , Buijk SL, et al. Bioavail-ability of ciprofloxacin after multiple enteral and
intravenous doses in ICU patients with severe gram-negative intra-abdominal infections. Intensive Care
Med. 1998;24:343–346.
53. Sahai J, Memish Z, Conway B. Ciprofloxacin pharmaco-kinetics after administration via a jejunostomy tube.
J Anti microb Chemother. 1991;28:936–937.
54. Cohn SM, Sawyer MD, Burns GA, et al. Enteric absorption of ciprofloxacin during tube feeding in the
critically ill. J Antimicrob Chemother. 1996;38:871–876.
55. Wright DH, Pietz SL, Konstantinides FN, Rotschafer JC. Decreased in vitro fluoroquinolone concentrations
after admixture with an enteral feeding formulation. JPEN J Par enter Enteral Nutr. 2000;24:42–48.
56. Penrod LE, Allen JB, Cabacungan LR. Warfarin resistance and enteral feedings: 2 case reports and a
supporting in vitro study. Arch Phys Med Rehabil. 2001;82:1270–1271.
57. Dickerson RN, Garmon WM, Kuhl DA, Minard G, Brown RO. Vitamin K-dependent warfarin resistance
after concurrent administration of warfarin and continuous enteral nutrition. Pharmacotherapy.
2008;28:308–313.
58. Trissel LA. Trissel’s Stability of Compounded Formulations. 6th ed. Washington, DC: APhA Publications;
2018.
59. Jew RK, Soo-Hoo W, Erush SC, Amiri E. Extemporaneous For mulations for Pediatric, Geriatric and
Special Needs Patients. 3rd ed. Bethesda, MD: American Society of Health-System Pharmacists;2016.
60. Dansereau RJ, Crail DJ. Extemporaneous procedures for dissolving risendronate tablets for oral
administration and for feeding tubes. Ann Pharmacother. 2005;39:63–67.
 CHAPTER 11

Home Enteral Nutrition

Introduction
Home enteral nutrition (HEN) therapy delivers nutrients via a tube into the gastrointestinal (GI) tract to patients who
are medically stable, living in the community, and unable to meet their nutrition needs orally. HEN may be
appropriate for patients with neurological or neuromuscular dysfunction, head and neck or upper GI cancers,
malabsorptive conditions, anorexia, failure to thrive, or other conditions.1
This chapter focuses on special issues associated with HEN. Enteral nutrition (EN) providers can play an
important role in facilitating the transition from hospital to home by clarifying EN orders, educating patients and
their care-givers, and arranging for timely delivery of supplies. Some home infusion and durable medical equipment
(DME) companies have nutrition support clinicians who provide nutrition assessments and monitor patient progress.
However, many patients are discharged home without such support.
Enteral access devices, EN formulas, administration schedules, and the frequency and intensity of laboratory and
clinical monitoring can differ substantially from hospital to home. In the hospital, trained clinicians administer EN.
In contrast, HEN is administered by the patient, family member, or other caregiver. The goal of care at the time of
discharge and beyond is to provide appropriate, individualized, compassionate, cost-effective, and safe HEN
support.

Benefits and Goals of Home Enteral Nutrition

Discharging a patient home on EN may have many advantages over prolonged hospitalization. Benefits include
greater participation in activities of daily living, decreased cost of care, and reduced potential for hospital-acquired
infection. Given current incentives to discharge patients from acute care settings as well as the aging of the US
population, patients receiving EN are likely to have multiple chronic medical comorbidities that require home health
care.2,3 When indicated, HEN provides the most physiological mode of nutrient delivery for medically complex
patients in the least restrictive environment.
Patient and home assessment, as well as proper management and monitoring, are essential to the safe and cost-
effective delivery of HEN. Collaborative planning during the discharge process for a patient going home on EN
should include attention to the HEN prescription, consideration of the patient’s financial resources, the plan for
follow-up, and education of the patient and/or caregiver.

Statistics on Enteral Nutrition in the Home Setting

Capturing demographic data on patients receiving HEN is difficult for a variety of reasons. There is no formal
registry for patients receiving HEN; therefore, estimates regarding this population have largely been compiled based
on data analysis of HEN studies.4 In addition, patients receiving HEN may bypass traditional providers and obtain
EN supplies and formula on their own.
In 2017, the American Society for Parenteral and Enteral Nutrition (ASPEN) published a comprehensive data
analysis report regarding patients receiving EN.4 This report focused on the use of EN across the care spectrum,
including in the home setting, and it analyzed the number of patients receiving HEN, the types of formulas
delivered, the types of feeding tubes placed, and routes of EN administration. As part of that EN market report,
ASPEN conducted a survey of its members on a variety of EN practices and found that 44 of 492 survey
respondents (8.9%) cared for patients receiving HEN. Survey respondents reported that their agency was caring for
between 1 and 764 EN patients (average: 467 EN patients per agency). Of these patients, 75% were adults, 22%
were pediatric patients, and 3% were infants or neonates.4 In addition, about 23% of hospitalized EN patients were
reportedly discharged home while receiving EN. Extrapolating from this information, it is estimated that
approximately 50,000 US patients go home on EN per year.4
Regarding types of formulas used for HEN patients, the ASPEN survey found that most patients (59%) received
standard intact nutrient formulas. The remaining patients received hydrolyzed protein/amino acid formulas (23%),
disease-specific formulas (12%), formulas intended for patients with inherited diseases of metabolism (3%), and
blenderized tube feedings (BTFs) (2%).4 BTFs are discussed in greater detail later in this chapter. See Chapters 4
and 5 for additional information on types of formula.
ASPEN also collected survey data on the types of feeding tubes used. Respondents reported that most patients
receiving HEN (75.4%) had gastrostomy tubes, 8.6% had gastrojejunostomy tubes, 8.1% had jejunostomy tubes, and
7.9% had short-term nasogastric or nasoenteric tubes. The ASPEN survey also found that 23% of patients in the
home setting received continuous feedings via pump, 17% received intermittent feedings via pump, and 60%
received bolus or intermittent feedings via gravity or syringe.4

Transition to Home

Patient Evaluation
Careful consideration must be taken when evaluating a patient for HEN. To successfully transition a patient to HEN,
several criteria should be met. At the very minimum, the patient should be willing to enterally feed at home; the
patient or a caregiver should be capable of administering EN; and the patient’s tolerance to the prescribed enteral
regimen should be evident. Table 11-1 provides a checklist of criteria that optimize a successful transition to home.5
It is important to note that not all criteria may be met in every case.5

TABLE 11-1. Discharge Preparation Checklist for Patients to Receive Home Enteral Nutrition

Category Responsible Professionals

Patient assessment
• Patient is deemed medically stable for discharge
• Primary medical team
• Patient exhibits tolerance of current feeding
• Registered dietitian
regimen
• Bedside nursing staff
• Patient is deemed able to tolerate planned home
• Case manager
progression of feedings
• Social worker
• Patient or caregiver exhibits willingness to
• Home care company representative
continue administering enteral nutrition at home
Home environment
• Adequate structure
• Electrical access
• Adequate physical access (bathroom/ramp)
• Case manager
• Heat and air conditioning
• Social worker
• Clean water supply
• Home care company representative
• Clean area for formula preparation
• Road accessibility
• Communication access: telephone or cell phone
Caregiver education
• Identification of caregivers

• Development of training schedule with identified

 • Development of training schedule with identified
caregivers
• Primary medical team
• Education on feeding tube care and
• Bedside nursing staff
troubleshooting
• Registered dietitian
• Education on assessment of feeding tolerance
• Home care company representative
• Education on formula preparation and feeding
• Pharmacist
schedule
• Education on route of administration (bolus,
gravity, pump)
• Education on enteral medication administration
Discharge planning
• Identification of primary physician to manage
enteral feedings
• Communication with primary physician about • Primary medical team
clinical status • Inpatient care management team or professional
• Initial postdischarge appointment set who can coordinate insurance coverage and
• Appointments for other subspecialty clinics as contact home care companies
needed • Case manager or care coordinator
• Coordination with home care company for • Social worker
feeding tube supply and formula
• Coordination with home nursing
Source: Adapted with permission from reference 5: Sevilla WM, McElhanon B. Optimizing transition to home enteral nutrition for pediatric
patients. Nutr Clin Pract. 2016; 31(6):762-768. doi:10.1177/0884533616673348.

Selection of Providers of Supplies and Services

Providers of HEN supplies and services include DME companies, home infusion companies, and home health
agencies. A DME company typically provides formula and supplies, as well as medical equipment such as beds,
walkers, wheelchairs, and respiratory equipment. Home infusion companies may provide not only formula and
supplies but also medications administered intravenously and pharmacy and nursing services. Home health agencies
may provide nursing services for education, training, and clinical monitoring.
The case manager, care coordinator, or social worker who is assisting in the transition to home is responsible for
educating the patient regarding options for HEN providers. When selecting a provider, the following should be
considered: the patient’s insurance coverage, the availability of a registered dietitian and/or nutrition support team,
the provider’s hours of operation, its compliance with HEN standards of care, and whether it is accredited by an
organization such as the Joint Commission, Accreditation Commission for Health Care, or Community Health
Accreditation Program.6,7

Discharge Plan
The discharge process should begin as soon as the health-care team determines that a patient may need HEN. The
patient or caregiver is expected to become proficient in administering the formula, checking enteral access
placement if needed, and maintaining skin integrity at the access site.8 A collaborative approach from the multi-
disciplinary team and home care supplier is key to a safe and smooth transition. Table 11-2 lists ways that the
multidisciplinary team can help facilitate the discharge process.7

TABLE 11-2. Tips to Facilitate Discharge of Patients Who Will Receive Home Enteral Nutrition

Obtain required diagnostic tests and procedures to demonstrate medical necessity and verify

• insurance coverage.
 • Document the diagnosis requiring enteral nutrition for
treatment.
• Establish feeding access.
• Determine the patient's tolerance to the enteral formulation.
• Explain to the patient and caregiver the risks and benefits of home nutrition support.
Assess the patient's or caregiver's ability to perform activities of daily living and enteral nutrition-
•
related tasks.
Assess the learning needs of the patient and caregivers and provide appropriate patient education.
•
If necessary, develop patient-specific learning materials to address literacy or language barriers.
Engage the patient and family in a discussion about their expectations of involvement in daily care;
•
include social workers or interpreters as needed in this discussion.
• Conduct psychosocial assessment of the patient.
• Identify caregiver(s).
• Determine the home care provider(s).
Identify all necessary home infusion therapies and the follow-up communication required by each
•
provider (blood samples for laboratory tests, wound care, etc).
• Identify who will prescribe the home enteral nutrition orders after discharge.
Establish the type and amount of communication desired by the physician and nutrition support
•
team after discharge.
Educate the patient and family on how to contact the nutrition support team and reasons for urgent
•
after-hours contact.
Source: Adapted with permission from reference 7: Konrad D, Mitchell R, Hendrickson E. Home nutrition support. In: Mueller CM, ed. The
ASPEN Adult Nutrition Support Core Curriculum. 3rd ed. Silver Spring, MD: American Society for Parenteral and Enteral Nutrition; 2017:765-
784.

In addition to the multidisciplinary team, the home care supplier plays an integral role in the discharge process.
For example, the home care supplier may have a clinical representative meet with the patient prior to discharge to
assist in evaluating the patient and educating the patient and family on how to use the feeding pump. The enteral
supplier should also review the discharge order to verify that all equipment and supplies necessary to safely
administer the feeding are on the prescription.
Plans for the discharge home of pediatric patients receiving EN can vary significantly from plans used for the
adult population. The coordination involved with discharging a medically complex child home can be especially
challenging, and the risk for EN-related complications is considerable. Enteral devices used for children may vary
from those of adults. For example, low-profile feeding devices (which require extension sets to feed) are commonly
used. The pediatric patient may need to have their stomach vented or have gastric contents intermittently or
continuously drained. Selection of an enteral provider with expertise in pediatric EN is imperative when dealing
with this population.
Whether the patient is a child or an adult, patient and caregiver education is an important component of the
transition to home. Education should begin as early as possible and include written and verbal forms of
communication.8 See the Patient Education section of this chapter for further discussion of this topic.

Insurance Coverage
HEN may be covered by Medicare, Medicaid/Medicaid managed care, private insurance plans, and other entities.
Medicare covers HEN under Part B, the DME benefit. Patients who qualify for Medicare must meet specific criteria
for HEN, as outlined here:9
 • There is evidence of dysphagia.
• An emptying study for dysmotility and malabsorption is documented.
• Duration of EN is expected to last >90 days (continued need must be documented annually).
• EN is required to provide sufficient nutrients to maintain the patient’s weight and strength commensurate
with his or her overall health status.
• If oral intake continues, EN must constitute most of the patient’s nutrition intake.
• Additional documentation is needed if the patient’s EN requirement is <750 or >2000 kcal/d.

State Medicaid programs cover medical assistance for certain individuals and families with low incomes and
limited resources. The rules for Medicaid reimbursement eligibility, payment rates, and types of reimbursement vary
by state. The requirements should be reviewed on a case-by-case basis for each individual and state.
Some payers may require prior authorization for coverage of enteral formula and/or supplies—and coverage
varies widely. Prior to discharge, it should be determined if formula and supplies are covered by the patient’s
individual health plan, and if medical justification or prior authorization is required. Ideally, HEN coverage should
be evaluated before the enteral access device is placed. Insufficient insurance coverage for HEN may put undue
financial burden on the patient or caregiver.

Patient Education
Clinicians involved in care of the patient receiving EN should contribute to the development and provision of a
standardized patient nutrition education program (see Table 11-3).8 Adequate education increases knowledge and
may reduce therapy-related complications, improve clinical outcomes, bolster caregiver knowledge and confidence,
and increase compliance with the treatment regimen.10,11 It is beneficial to assess the patient’s or care-giver’s
learning style and provide education in the most appropriate format for the individual learner (eg, use print material,
audio recordings, videos, and/or teaching kits).5 Printed material should be developed at a reading level of fifth to
sixth grade and avoid unnecessary use of medical and technical terms.7

TABLE 11-3. Practice Recommendations for Patient/ Caregiver Education About Home Enteral
Nutrition

1. Begin the referral process once the decision for EN therapy is made.
2. Begin education for the patient receiving EN at home prior to placement of the EAD.
Provide patient and caregiver education that is comprehensive, includes education materials
3.
related to EN therapy, and uses a standard checklist.
Provide the patient and caregiver with verbal and written
education that covers the following topics:
• Reason for EN and short-term and long-term nutrition goals (eg, weight goal)
• Feeding device, route, and method; formula; and feeding regimen
• Supplies needed to administer enteral tube feedings at home
• Use and cleaning of equipment, including administration/feeding set, infusion pump, and syringe
• Care of the feeding tube and access site, such as securing, flushing, and unclogging the tube
4. and stoma care
• Nutrition and hydration guidelines: feeding plan/ regimen, water flushes, hydration monitoring
• Weight schedule, laboratory test recommendations
• Safe preparation and administration of formula
• Safe preparation and administration of medications
• Proper position during and after feedings
 • Recognition and management of complications (mechanical, gastrointestinal, and metabolic)
• Available resources, emergency care plan, and healthcare contacts
Use demonstration and teach-back method of patient education to assess comprehension.
5. • Use various methods of education to take into account various learning styles.
• Implement an EN education checklist to assist with the discharge coordination process.
Abbreviations: EAD, enteral access device; EN, enteral nutrition.
Source: Adapted with permission from reference 8: Boullata JI, Carrera AL, Harvey L, et al. ASPEN safe practices for enteral nutrition
therapy. JPEN J Parenter Enteral Nutr. 2017;41(1):15-103. doi:10.1177/0148607116673053.

Patient and caregiver instruction on the enteral access device is an important element of HEN education.5 When
discharged to home, some patients may require a combination of feeding methods, such as bolus feedings with a
syringe during the day and continuous pump feeds at night. Specific print material regarding all the different routes
of administration used (eg, bolus feeding, gravity feeding, or pump feeding) should be included in patient education.
Education materials should detail the route of administration and the care and handling of the formula and the
enteral access device (see Table 11-4).5,7 Safety issues should be reviewed repeatedly with patients and caregivers.
After discharge to the home, ongoing education on safe handling techniques and the importance of a controlled,
clean environment for HEN administration is imperative to avoid infectious complications.

TABLE 11-4. Components of Patient Education about Using an Enteral Access Device

• Name and composition of enteral formula

• Methods for formula inspection, storage, preparation, and administration
• Formula hang time limits
• Infusion method (bolus, gravity, pump) and schedule
• Instructions for water flushes
• Instructions for administering medications via the feeding tube (if applicable)
• Identification of the type of tube, tube size (French), and date of placement
• Manufacturer's name and how to access manufacturer's information
• Enteral access device care
• Instructions for tube reinsertion (nasal) or instructions for securing the tube
• Signs and symptoms of complications
• Information for reordering supplies (company name and phone number)
• Contact name and phone number of the physician who ordered enteral nutrition
Source: Information is from references 5 and 7.

Patient education materials should also include information regarding the patient’s or caregiver’s expectations
and potential complications of HEN, with emphasis on problems that may require emergency interventions or
rehospitalization. Tables 11-5 through 11-13 list selected complications that should be covered in patient/caregiver
education for patients receiving long-term HEN.12,13 The HEN provider as well as the home health nurse should
instruct patients regarding these complications at the start of care and continually throughout the duration of therapy.
Refer to Chapters 3 and 9 for additional information on EN complications.
 TABLE 11-5. Key Points for Patient Education on Nausea and Vomiting

Signs and symptoms:

• Abdominal distress, distention, feeling bloated
• Cramping
• Vomiting/dry heaves/retching
• Cold sweat
Possible causes:
• Feeding too quickly
• Formula is too concentrated
• Intolerance to formula ingredients
• Incorrect positioning of patient during feeds
• Contaminated formula
• Formula is too cold
• Constipation
Action steps:
• To lessen risk of nausea and vomiting, patient should sit up at ≥30° angle during feed and remain
upright for 30 minutes after feeding.
• Discuss medication use with healthcare provider.
• Discuss formula and infusion rate with healthcare provider.
• Allow formula to reach room temperature prior to use.
• Verify proper storage and preparation of formula.
• If vomiting continues, stop feeding and call doctor.
Source: Information is from references 12 and 13.

TABLE 11-6. Key Points for Patient Education on Dehydration

Signs and symptoms:

• Excessive thirst
• Dry mouth, cracked lips
• Weight loss
• Fever
• Decreased urine output
Possible causes:
• Persistent diarrhea and/or vomiting
• Prolonged fever
• Insufficient fluid intake
Action steps:
• Administer fluids via tube.
• Call healthcare provider.
Source: Information is from references 12 and 13.
 TABLE 11-7. Key Points for Patient Education on Constipation

Signs and symptoms:

• Infrequent and/or hard stool
• Bloating, gas
• Cramping or other pain
Possible causes:
• Inadequate fluid intake
• Medication side effect
• Inadequate fiber intake
• Decreased physical activity
• Dysmotility
Action steps:
• Ensure prescribed volume of formula and fluid is given.
• Discuss formula and medication use with healthcare provider.
• Increase physical activity if safe to do so.
Source: Information is from references 12 and 13.

TABLE 11-8. Key Points for Patient Education on Diarrhea

Signs and symptoms:

• Abdominal pain or cramping
• Frequent, loose, and/or watery stool
Possible causes:
• Side effect of medication
• Intolerance to formula
• Bowel disorder
• Infection
Action steps:
• Check with prescriber or pharmacist to evaluate whether medication is cause of diarrhea.
• Discuss formula and infusion rate with healthcare provider.
• Allow formula to reach room temperature prior to use.
• Follow recommendations for proper storage and preparation of formula.
Source: Information is from references 12 and 13.

TABLE 11-9. Key Points for Patient Education on Aspiration

Signs and symptoms:

• Vomiting
• Heartburn
• Coughing or choking with difficulty breathing
• Chest pain
• Fever
 • Shortness of breath
• Pneumonia
Possible causes:
• Diminished gag reflex
• Gastroesophageal reflux
• Swallowing disorder
• Silent aspiration
• Esophageal narrowing
• Decreased motility of esophagus and/or stomach
• Incorrect positioning of patient during feeds
• Tube migrated out of place
Action steps:
• Stop feeding, and open clamp to drain stomach contents if possible.
• Contact doctor.
• Patient should sit up ≥30° during feed and remain in an upright position for at least 30 minutes after
feed.
Source: Information is from references 12 and 13.

TABLE 11-10. Key Points for Patient Education on Site Irritation and/or Tube Leaking

Signs and symptoms:

• Irritated skin or rash around tube
• Burning pain
• Foul odor or local infection
• Sinus or ear infection (in patients using nasogastric or nasojejunal tubes)
• Granulation, or extra tissue built up around the insertion site
• Visible leakage from tube or around tube
• Multiple soaked dressings that require changing more than twice per day
Possible causes:
• Poorly fitting tube
• Tube tugging at exit site
• Improper skin care
• Broken tubing, cap, or antireflux valve
• Repeat clamping at same site
• Accidental cutting of the tube
Action steps:
• Stop feeding.
• If possible, clamp the tube between the patient's body and the problem area.
• Wash skin with warm water and mild soap, and pat dry. Apply a dry dressing as needed.
• Call doctor or home care nurse.
• Apply barrier cream to protect skin as needed.
Source: Information is from references 12 and 13.
 TABLE 11-11. Key Points for Patient Education on Tube Displacement

Signs and symptoms:

• Tube has come out of body or has moved out of place
• Choking
• Difficulty breathing
• Nausea/vomiting
• Abdominal pain
• Diarrhea
Possible causes:
• Tube inadequately secured
• Accidental or excessive pulling of the tube
• Frequent vomiting
• Deflated balloon (if applicable)
Action step: Discontinue feeding and contact healthcare provider.
Source: Information is from references 12 and 13.

TABLE 11-12. Key Points for Patient Education on Tube Obstruction/Blockage

Signs and symptoms:

• Inability to flush tube with water, infuse tube feeding, or administer medication via tube
• Bulging of tube when feeding or flushing
Possible causes:
• Medicine administered improperly
• Tube not flushed properly
• Putting soda through the tube
• Administering feedings or other substances that are too thick, sticky, or large to pass through tube
• Tube clamp is closed
• Infusion rate is too slow
Action steps:
• Make sure the tube clamp is open.
• Do not force formula or medication into a clogged tube.
• Try to flush the tube with a syringe filled with warm water. Pull the plunger back on syringe. Try
flushing again with warm water.
• If flushing does not work, contact healthcare provider.
Source: Information is from references 12 and 13.

TABLE 11-13. Key Points for Patient Education on Pump or Power Failure

Signs:
• Unable to start pump
 • Repeated alarms without obvious cause
• Excess formula left in the bag after recommended feeding time is complete
Possible causes:
• Power failure/low battery
• Pump charger parts are not properly connected
• Pump is unplugged
• Pump malfunction
Action steps:
• Check whether pump is plugged in.
• Check that the wall socket is functioning.
• Check that battery is charged.
• Stop pump, and check user's manual for instructions.
• If pump will not work, contact home care provider.
Source: Information is from references 12 and 13.

Education may also include lists of resources and support organizations dedicated to tube feeding. Two of the
largest patient support organizations are the Oley Foundation (www.oley.org) and Feeding Tube Awareness
Foundation (www.feedingtubeawareness.org). Such organizations may provide education, consumer events, online
communities, equipment/supply exchange programs, and a sense that others are undergoing the same issues related
to HEN.

Patient Monitoring
A major goal of monitoring patients who receive HEN is to prevent hospital readmission related to the enteral
feeding. The appropriate type and amount of monitoring can vary widely and will depend on many factors, including
the patient’s age, medical condition, and insurance coverage. Pediatric patients may be regularly monitored by
health-care providers in an outpatient setting, such as a specialty clinic. This type of monitoring may be less
common in the adult population.
The medical supply provider may also offer a degree of monitoring. This entity may have communication with
the patient at least monthly for reorder of supplies. Some companies employ registered dietitians to assist in
troubleshooting EN-related issues. Ultimately, however, patients/caregivers should refer to their healthcare providers
for medical issues.

Patient Outcomes
The reporting and evaluation of outcomes is an important aspect of home care to promote continued quality
improvement of HEN. ASPEN has established nutrition support standards for HEN that can be used as a guide for
tracking patient outcomes.6 If possible and practical, clinicians should utilize these standards as well as their
organization’s policies and procedures when developing tools to track outcomes. Ideally, data should be collected on
mortality, hospital readmissions, complications, customer satisfaction, and problem reporting and resolution.6

Blenderized Tube Feedings

An increasing number of families are preparing homemade BTFs or at least discussing them with their nutrition
support clinicians. There has also been a sharp increase in the number of commercially available whole food–based
formulas entering the market. These trends may reflect the desire of patients to reduce their intake of processed
enteral formulas and consume more formulas prepared from whole foods, which patients may perceive to have
emotional and nutritional benefits. Increased interest in BTFs may also stem from financial and nutrition-related
challenges associated with obtaining and using commercial formulas (eg, insurance limitations, gastrointestinal
symptoms, intolerance of commercially prepared enteral formulas, or food allergies/intolerances).
Clinicians should therefore be prepared to educate patients and caregivers about the following aspects of using
BTFs:14,15
 • Safe food practices for preparation and storage of homemade BTFs
• The time and effort required by families to make and use BTFs
• Cost considerations (insurance companies do not usually cover the cost of food used in homemade BTFs)
• Methods to evaluate the nutrient content of BTFs
• How to choose homemade BTF recipes and plan for nutritionally complete feedings
• Whether BTFs can be administered via the patient’s enteral access device:
• Feeding tubes less than 10 Fr may be too small for blenderized formulas.
• Diluting formulas to pass through tubes may diminish the amount of nutrients delivered.
• Patients with a jejunostomy may not tolerate BTFs because the tubes are small in diameter and feedings
are delivered into the small intestine; these patients should only use BTFs under medical supervision.
• Homemade BTFs should not be kept at room temperature for more than 2 hours (unlike commercially
prepared liquid formulas, homemade formula is not sterile); therefore, BTFs may not be safe for
continuous feedings.
• BTF infusion through an enteral feeding pump could block the pump’s air sensors, which might allow air
to enter the stomach.

Use of BTF does not have to be an all-or-none proposition, and combinations of commercial standard enteral
formulas, commercial BTFs, and homemade BTFs may be used to meet all nutrition needs or to complement an
existing feeding regimen. Several of the numerous resources on homemade blenderized diets to assist
patients/caregivers and clinicians in meeting the nutrition needs of those who want to pursue this method are listed
in the next section under Patient Education and Support.

Practice Resources

Professional Resources

• Agency for Clinical Innovation and the Gastroenterological Nurses College of Australia. A Clinician’s
Guide: Caring for People With Gastrostomy Tubes and Devices. Chatswood, Australia: Agency for Clinical
Innovation; 2014.
• Boullata JI, Carrera AL, Harvey L, et al. ASPEN safe practices for enteral nutrition therapy. JPEN J
Parenter Enteral Nutr. 2017;41(1):15–103. doi:10.1177/0148607116673053.
• Durfee SM, Adams SC, Arthur E, et al. A.S.P.E.N. standards for nutrition support: home and alternate site
care. Nutr Clin Pract. 2014;29(4):542–555.
• Lyman B, Rempel G, Windsor K, Guenter P. Use of nasogastric feeding tubes for children at home: a
template for caregiver education. Nutr Clin Pract. 2017;32(6):831–833.
• University of Virginia School of Medicine. GI Nutrition Support Team website.
www.ginutrition.virginia.edu. Accessed November 15, 2018. (Go to Clinician Resources tab for blenderized
recipes.)

Patient Education and Support

• Blenderized tube feeding (handout for parents). Seattle Children’s website.

www.seattlechildrens.org/globalassets/documents/for-patients-and-families/pfe/pe442.pdf. Accessed
November 15, 2018.
• Complex Child website. GI section. www .complex child .com /gi .html. Accessed November 15, 2018.
• Feeding Tube Awareness Foundation. www.feedingtubeawareness.org. Accessed November 15, 2018.
• Food for Tubies website. www.foodfortubies.org. Accessed November 15, 2018.
 • Klein MD, Morris SE. Homemade Blended Formula Hand book. Tucson, AZ: Mealtime Notions; 2007.
Available for purchase at www.mealtimenotions.com.
• Oley Foundation. www.oley.org. Accessed November 15, 2018.
• US Department of Agriculture. Choose My Plate website. www.choosemyplate.gov. Accessed November
15, 2018.

References
1. Delegge MH. Home enteral nutrition. JPEN J Parenter Enteral Nutr. 2002;26(5 Suppl):S4–S7.
2. McCall N, Petersons A, Moore S, Korb J. Utilization of home health services before and after the balanced
budget act of 1997: what were the initial effects? Health Serv Res. 2003;38(1):85–106.
3. Castellanos VH, Silver HJ, Gallagher-Allred C, Smith TR. Nutrition issues in the home, community, and
long-term care setting. Nutr Clin Pract. 2003;18(1):21–36.
4. Read J, Guenter P. ASPEN Enteral Nutrition by the Numbers: EN Data Across the Healthcare Continuum.
Silver Spring, MD: American Society for Parenteral and Enteral Nutrition; 2017.
5. Sevilla WM, McElhanon B. Optimizing transition to home enteral nutrition for pediatric patients. Nutr Clin
Pract. 2016; 31(6):762–768. doi:10.1177/0884533616673348.
6. Durfee SM, Adams SC, Arthur E, et al. A.S.P.E.N. standards for nutrition support: home and alternate site
care. Nutr Clin Pract. 2014;29(4):542–555.
7. Konrad D, Mitchell R, Hendrickson E. Home nutrition support. In: Mueller CM, ed. The ASPEN Adult
Nutrition Support Core Curriculum. 3rd ed. Silver Spring, MD: American Society for Parenteral and Enteral
Nutrition; 2017:765–784.
8. Boullata JI, Carrera AL, Harvey L, et al. ASPEN safe practices for enteral nutrition therapy. JPEN J
Parenter Enteral Nutr. 2017;41(1):15–103. doi:10.1177/0148607116673053.
9. Centers for Medicare & Medicaid Services. National coverage determination (NCD) for enteral and
parenteral nutritional therapy (NCD 180.2). Medicare Coverage Database website.
https://www.cms.gov/medicare-coverage-database/overview-and-quick-search.aspx. Published 1984.
Accessed November 16, 2018.
10. Weston-Eborn R, Sitzman K. Selecting effective instructional resources. Home Healthc Nurse. 2005;23:402–
403.
11. Schweitzer M, Aucoin J, Docherty SL, Rice HE, Thompson J, Sullivan DT. Evaluation of a discharge
education protocol for pediatric patients with gastrostomy tubes. J Pediatr Health Care. 2014;28:420–428.
doi:10.1016/j.pedhc.2014.01.002.
12. Agre P, Brown P, Stone K. Tube feeding troubleshooting guide. The Oley Foundation.
https://cdn.ymaws.com/oley.org/resource/resmgr/Docs/TF_Troubleshooting_Guide_201.pdf. Updated May
2018. Accessed November 16, 2018.
13. Agency for Clinical Innovation. Feeding tubes—troubleshooting.
https://www.aci.health.nsw.gov.au/__data/assets/pdf_file/0019/154801/feed_tube_troubleshooting.pdf.
Updated August 2007. Accessed November 16, 2018.
14. Martin K, Gardner G. Home enteral nutrition: updates, trends, and challenges. Nutr Clin Pract.
2017;32(6):712–721. doi:10.1177/0884533617701401.
15. Escuro A. Blenderized tube feeding: suggested guidelines to clinicians. Pract Gastroenterol.
2014;38(12):58–64. https://www.practicalgastro.com/pdf/December14/Blenderized-Tube-Feeding-
Suggested-Guidelines.pdf. Accessed November 16, 2018.
 Index

Page numbers followed by f indicate figures, those followed by t indicate tables.

AAA (aromatic amino acids), 184–185

AACE (American Association of Clinical Endocrinologists), 199, 201, 201t
AAP (American Academy of Pediatrics), 216, 225, 230, 233, 239–242
AASLD (American Association for the Study of Liver Diseases), 185, 186t
abdominal distention, 358–359
Academy of Nutrition and Dietetics (AND)
adult malnutrition assessment, 12, 14, 15t, 18–19, 20t–22t, 23f, 45
managing diarrhea with fiber, 171t
pediatric malnutrition assessment, 24, 25t
ACG (American College of Gastroenterology), 181t, 182, 185, 186t, 189, 191t, 193t, 200t, 201
acid-base disorders, 392
acute kidney injury, 195, 196t, 225t
acutely ill patients, timing for enteral nutrition in, 78
acute respiratory distress syndrome (ARDS), 191–194
ADA (American Diabetes Association), 180, 181t, 182–183
additives in infant formulas, 226–228
adequate intake (AI), 254
administration set use, 332–333 adults
advancing enteral nutrition, 85–86
body mass index (BMI), 39
edema assessment, 35t
EN administration methods, 258–259
EN delivery route selection, 69f
EN formula selection, 79–80
EN formulas for, 164–206
estimating energy and protein requirements, 256t
fat loss, assessment for, 30t
ideal body weight, 40, 42
malnutrition, 11–19, 15t, 20t–22t, 23f
nutrient requirements, 255–256, 255t
nutrition assessment, 2, 3f
nutrition screening tools for, 6t–10t
sample EN prescription calculations, 277f–279f
standard EN label template, 307f
timing of nutrition intervention, 52–53, 76
waist circumference, 40
weight changes, 42
AI (adequate intake), 254
allergy
cow’s milk protein, 232t, 233, 237–239, 238t–240t
 food, 174–175
hypoallergenic infant formulas, 238
American Academy of Pediatrics (AAP), 216, 225, 230, 233, 239–242
American Association for the Study of Liver Diseases (AASLD), 185, 186t
American Association of Clinical Endocrinologists (AACE), 199, 201, 201t
American Association of Critical-Care Nurses, 110
American College of Gastroenterology (ACG), 181t, 182, 185, 186t, 189, 191t, 193t, 200t, 201
American Diabetes Association (ADA), 180, 181t, 182–183
American Society for Metabolic and Bariatric Surgery (ASMBS), 201, 201t
American Society for Parenteral and Enteral Nutrition (ASPEN)
adult malnutrition assessment, 12, 14, 15t, 18–19, 20t–22t, 23f, 45
advancing enteral nutrition, 85
ethical and legal recommendations, 88t
guidelines for enteral nutrition, 74–75, 101
home enteral nutrition statistics, 427–428
home enteral nutrition support standards, 442
New Opportunities for Verification of Enteral Tube Location (NOVEL) Project, 110–111
pediatric malnutrition assessment, 24, 25t
practice recommendations
critically ill children, 262
diabetes, 181t
fluid-restricted formulas, 198, 199t
gastric residual volumes measurement, 338–339
gastrointestinal disorders and malabsorption, 178t
hepatic failure, 185, 186t
immune-enhancing formulations, 189, 191, 190t–191t
managing diarrhea with fiber, 171t
obesity, 200t, 201
placement of short-term feeding tube, 115t
pulmonary dysfunction, 193t
renal dysfunction, 195, 196t
safe handling of enteral nutrition, 327, 328t–329t
amino acid-based infant formulas, 240, 240t
AND. See Academy of Nutrition and Dietetics (AND)
anthropometric assessment, 34–45
bioelectrical impedance analysis, 43–44
body mass index (BMI), 39–40
body weight measurement, 36, 38–39
computed tomography and ultrasound, 44–45
growth charts, 34–36, 37t–38t
head circumference, 41–42
height/length, 41
ideal body weight (IBW), 40–41
interpretation of weight data, 42–43
mid–upper arm circumference (MUAC), 35, 43
triceps skinfold (TSF) thickness, 35, 43
waist circumference, 40
weight-for-length, 39–40
antibiotics, 136, 141
antiregurgitation infant formulas, 234–235, 234t
apparel, for staff, 301–302
arachidonic acid (ARA), 194, 219, 223–227, 237
ARDS (acute respiratory distress syndrome), 191–194
aromatic amino acids (AAAs), 184–185
ARRP (aspiration risk-reduction protocol), 376
ASMBS (American Society for Metabolic and Bariatric Surgery), 201, 201t
ASPEN. See American Society for Parenteral and Enteral Nutrition (ASPEN)
aspiration. See pulmonary aspiration
aspiration risk-reduction protocol (ARRP), 376
aspirin, 119

bacteria. See also contamination

in blenderized tube feedings (BTFs), 220
in infant formulas, 216
bacterial overgrowth, 362, 365
bariatric surgery, enteral formulas for, 198–201
BCAAs (branched-chain amino acids), 184–185
BIA (bioelectrical impedance analysis), 43–44
bicarbonate, for unclogging tubes, 150
bioelectrical impedance analysis (BIA), 43–44
bleeding, gastrointestinal, 74
blenderized tube feedings (BTFs), 80, 165t, 202–203, 202t, 292, 428
contamination, reducing risks for, 333–334
enteral formulas for pediatrics, 219–220
home enteral nutrition, 443–445
preparation of enteral nutrition formulas, 305–306, 306t
body mass index (BMI), 24, 25t, 39–40
body weight measurement, 36, 38–39
bolsters, 105–108, 106f–107f
bolus infusion/feeding, 82, 257–259, 261
branched-chain amino acids (BCAAs), 184–185
breast milk. See human milk
bridle, nasal, 131–132, 140
BTFs. See blenderized tube feedings
buried bumper syndrome, 144–145, 145f

calcium, 381, 383

Canadian Clinical Practice Guidelines (CPG), 181t, 182, 189, 191t, 193t, 200t, 201
carbamazepine, 412–413
carbohydrate in enteral nutrition formulas, 168t, 169, 219
carbon dioxide monitoring, 111
carts, delivery, 299
Centers for Disease Control and Prevention (CDC), 35, 41, 216, 297
children. See pediatrics
chronic kidney disease, 194–195, 196t–197t, 225t
clogging of enteral access devices, 80, 103–105, 139, 148–151, 151t, 409, 443t
Clostridium difficile, 73, 362
compatibility, drug, 408
complications of enteral access devices, 139–151
enterostomy tube, 140–141, 142t–144t, 144–149, 145f
nasal tube, 139–140
tube clogging, 149–151, 151t
complications of enteral nutrition, 354–395, 355t
gastrointestinal-related, 355–376, 355t
abdominal distention, 358–359
constipation, 366–368
diarrhea, 361–366, 363t–364t
gastroesophageal reflux, 368–369
maldigestion and malabsorption, 359–361
nausea and vomiting, 355–358
pulmonary aspiration, 370–376
metabolic alterations, 355t, 377–395
 acid-base disorders, 392
electrolyte and mineral imbalances, 378–386, 380t–382t, 384t–386t
essential fatty acid deficiency, 393, 395t
fluid imbalances, 388–392, 389t–390t
glucose intolerance, 392–393, 394t
hypercapnia, 392, 393t
refeeding syndrome, 377–378
vitamin deficiencies, 386–388, 387t–388t
computed tomography, 44–45
computerized prescriber order entry (CPOE), 274
connections, 103, 133, 135f, 147, 272
constipation, 366–368, 438t
contamination, 289–290, 364–365
inspection of medical foods for, 330t
potential points of, 290f
reducing risks for, 290–296, 326–335
ASPEN recommendations for, 327, 328t–329t
blenderized tube feedings, 333–334
environmental controls and temperature, 327
hang times and administration set use, 330–333, 331t
inspection of medical foods, 330t
modulars, 333–334
continuous infusion/feeding, 83, 258, 261
continuous renal replacement therapy (CRRT), 195
cow’s milk-based infant formulas, 228–229, 228t
CPG (Canadian Clinical Practice Guidelines), 181t, 182, 189, 191t, 193t, 200t, 201
CPOE (computerized prescriber order entry), 274
critically ill patients
advancing enteral nutrition in, 85
delivery site, 101–102
ordering enteral nutrition for children, 262–263
timing for enteral nutrition in, 76–78
Cronobacter sakazakii, 216
CRRT (continuous renal replacement therapy), 195
crushing medications, 406–408, 406f
cyclic feedings, 83–84

dehydration, 388–392, 389t, 438t

delayed gastric emptying, 356, 356t, 368–369, 371–372
delivery route selection in adults, 69f
dermatitis, incontinence-associated, 366
DHA (docosahexaenoic acid), 219, 223–227, 237
diabetes, enteral formulas for, 180–184, 180t–181t
diarrhea, 361–366, 363t–364t
causes of, 362, 364–366
as enteral nutrition contraindication, 73
fiber and, 169–170, 171t
incontinence-associated dermatitis, 366
options for addressing, 363t–364t
patient education on, 439t
Dietary Reference Intakes (DRIs), 172–173, 217, 254
diluting medications, 407–408
discharge
home enteral nutrition plan, 431–433, 432t
preparation checklist, 429t–430t
preterm infant discharge formulas, 243–244, 244t
dishwashers, 298–299
dislodgment, tube, 140
DME (durable medical equipment), 425, 428, 430, 433
docosahexaenoic acid (DHA), 219, 223–227, 237
dosage forms, 405–406
drainage, 136–137, 141, 142t–144t, 144
DRIs (Dietary Reference Intakes), 172–173, 217, 254
drug(s). See also medication administration
added to enteral nutrition, 409–410
combining drugs, 410–411
constipation induced by, 367–368
crushing and diluting medications, 406–408, 406f
diarrhea induced by, 362, 364
dissolution and absorption of, 403–404
dosage forms, 405–406
nutrient interactions, 411–415
carbamazepine, 412–413
fluoroquinolones, 413–414
phenytoin, 411–412
warfarin, 415
drug interactions, 408–409
durable medical equipment (DME), 425, 428, 430, 433
dynameter, handgrip, 46
EADs. See enteral access devices
edema, assessment of, 35t
education, for home enteral nutrition patients, 434–440, 435t–444t
aspiration, 440t
constipation, 438t
dehydration, 438t
diarrhea, 439t
enteral access device use, 436t
nausea and vomiting, 437t
practice recommendations for, 435t
pump or power failure, 444t
site irritation and/or tube leaking, 441t
tube displacement, 442t
tube obstruction/blockage, 443t
electrolyte and mineral imbalances, 378–386, 380t–382t, 384t–386t
calcium, 381, 383
magnesium, 385, 385t–386t
phosphorus, 383–384, 384t–385t
potassium, 380–381, 382t
sodium, 379–380, 380t–381t
zinc, 386, 386t
elemental formulas, 172, 176, 222–223, 223t
EN. See enteral nutrition
energy
requirements of adults, 256t
requirements of pediatrics, 256t
ENFit, 133, 134t–135t, 147, 404–405
enteral access devices (EADs), 96–151
bolsters, 105–108, 106f–107f
for children, 433
clogging of, 80, 103–105, 139, 148–151, 151t, 409, 443t
complications, 139–151
enterostomy tube, 140–141, 142t–144t, 144–149, 145f
 nasal tube, 139–140
in pediatrics, 147–149
tube clogging, 149–151, 151t
long-term
gastrostomy tubes, 118–123, 121f
insertion of, 116–129, 117t
low-profile devices, 129
percutaneous direct jejunostomy tubes, 126–129, 128f
percutaneous gastrojejunostomy tubes, 123–126, 124f
medication administration and, 404–405, 417t–418t
ordering enteral nutrition, 272
patient education, 436t
selection, 79, 97–108
algorithm, 97f
anticipated duration of therapy, 98–100
device-related risk assessment, 102
level of delivery, 100–102
tube characteristics, 102–108
short-term, insertion of, 108–115, 115t–116t
tube characteristics, 102–108, 103t
physical characteristics, 102–103
tube configurations, 103–108, 104t, 106f–107f
tube maintenance considerations, 130–139
exchange and removal of enterostomy feeding tubes, 137–139
nasal, oral, and skin care,136–137
proper placement, maintaining, 130–131
tube securement and connections, 131–133, 134t–135t, 135f
tube tips, 105
enteral feeding pumps. See pumps, enteral feeding
enteral nutrition (EN). See also home enteral nutrition (HEN)
administration methods, 81–84, 258–261
for adults, 258–259
bolus, 82, 257–259, 261
continuous, 83, 258, 261
cyclic feedings, 83–84
intermittent, 82–83, 258–259
for pediatrics, 259–261
pump-assisted, 259, 261
volume-based, 84, 258
advancing, 85–87
benefits of, 65–66
challenges with, 86–87
closed vs open systems, 294–295
complications. See complications of enteral nutrition
considerations before initiating, 70t
contamination risks, reducing, 326–335
contraindications, 72–75, 72t
drug added to, 409–410
ethical considerations, 87, 88t
history of, 67–68
implementation of feedings, 326
indications for, 68–72
medication administration. See medication administration
overview of, 65–66
parenteral nutrition versus, 65–66, 76, 78
patient selection, 68–72
 process, 66, 67f
timing for, 75–78
enteral nutrition formulas. See also infant formulas
for adults, 164–206
blenderized tube feedings (BTFs), 202–203, 202t
classification of, 165t
composition of, 168t, 216
carbohydrate, 166, 168t, 169
fat, 168t, 170–172
fiber, 169–170, 171t
osmolality, 173–174
protein, 168t, 172
vitamins and minerals, 172–173
water, 173
disease-specific, 175–201
acute respiratory distress syndrome, 191–194
diabetes/glucose intolerance, 180–184, 180t–181t
gastrointestinal disorders and malabsorption, 176–177, 177t–178t
hepatic failure, 184–187, 185t–186t
immune-enhancing nutrition, 187–191, 187t–188t, 190t–191t
obesity and bariatric surgery, 198–201, 200t–201t
pulmonary failure, 191–194, 192t–193t
renal disease, 194–197, 195t–197t
wound healing, 177–180, 178t
elemental, 172, 176, 222–223, 223t
federal regulations, 165–166, 214–216
fluid-restricted, 185, 194, 197–198, 198t
food allergies and intolerances, 174–175
formulary, developing enteral product, 205–206
labeling, 166, 214, 307–308, 307f–309f, 310t–311t
modular, 80, 165t, 203–205, 204t, 206t, 245, 263, 271–272, 288, 296, 326, 333–334
for pediatrics, 213–245
elemental, 222–223, 223t
general purpose (polymeric), 217, 218t, 219
modified-fat formulas, 223–224, 224t
renal disease formulas, 224–225, 225t
semi-elemental (peptide-based), 220–222, 221t
peptide-based, 176, 220–222, 221t
powdered, 80, 216, 220, 224, 226, 231, 236, 241–245, 288, 293, 299–300, 333
preparation. See preparation of enteral nutrition formulas
selection, 79–81, 166, 167f, 293–294
semi-elemental, 172, 176, 220–222, 221t
storage, 293–294
enteral nutrition orders. See ordering enteral nutrition
enterostomy tubes
complications, 140–141, 142t–144t, 144–149, 145f
exchange and removal of, 137–139
tube configurations, 103–108, 104t, 106f–107f
equipment and supplies, 297–301
essential fatty acids, 170, 393, 395t
ethical considerations in enteral nutrition, 87, 88t
extensively hydrolyzed infant formulas, 238–240, 239t
FALCPA (Food Allergen Labeling and Consumer Protection Act), 174–175
fat
in enteral nutrition formulas, 168t, 170–172, 219, 223–224
modified-fat formulas
 infant, 236, 237t
for pediatrics, 223–224, 224t
fat loss, assessment for, 30t–31t
FDA (Food and Drug Administration), 114, 166, 214–216, 293, 327, 330t
fecal fat study, 360, 365
federal regulations, 165–166, 214–216
Feeding Tube Awareness Foundation, 439
feeding tube patency, 339–340, 340t
feeding tubes. See enteral access devices
fiber, in enteral nutrition formulas, 169, 170, 171t, 219
fistulas, gastrointestinal, 74
fluid accumulation, assessment of, 35t
fluid imbalances, 388–392, 389t–390t
dehydration, 388–392, 389t, 438t
overhydration, 388, 390t, 391–392
fluid requirements
for adults, 255–256
for pediatrics, 257t
fluid-restricted formula, 185, 194, 197–198, 198t
fluoroquinolones, 413–414
fluoroscopy, 99, 106, 112–113, 116, 120–123, 125–127, 141, 147, 369
food allergies and intolerances, 174–175
Food Allergen Labeling and Consumer Protection Act (FALCPA), 174–175
Food and Drug Administration (FDA), 114, 166, 214–216, 293, 327, 330t
formulary, developing enteral product, 205–206
formulas. See enteral nutrition formulas
fortifiers, human milk 241–242, 241t
fructooligosaccharides (FOS), 169

gamma-linolenic acid (GLA), 192, 194

gastric residual volume (GRV), 357
aspiration risk, 371–373
assessment of, 130–131, 149, 337–339, 340t, 344, 344t, 358, 371–373
preventing aspiration and, 337–338, 375–376
gastroesophageal reflux, 148, 368–369
gastrointestinal contraindications for enteral nutrition, 73–74
gastrointestinal disorders, enteral nutrition formulas for, 176–177, 177t–178t
gastrointestinal-related complications of enteral nutrition, 355–376, 355t
abdominal distention, 358–359
constipation, 366–368
diarrhea, 361–366, 363t–364t
gastroesophageal reflux, 368–369
maldigestion and malabsorption, 359–361
nausea and vomiting, 355–358
pulmonary aspiration, 370–376
gastrojejunostomy, 99–100
percutaneous endoscopic gastrojejunostomy, 124–125
placement, 123–126, 124f
gastroparesis (delayed gastric emptying), 356, 356t, 368–369, 371–372
gastrostomy tubes
classification of, 99–100
initiation of feedings after placement, 269–270, 270t
insertion, 118–123
percutaneous endoscopic placement, 118–120, 121f
percutaneous radiologic placement, 120–123
surgical placement, 123
GLA (gamma-linolenic acid), 192, 194
Global Enteral Device Supplier Association (GEDSA), 133. See also ENFit
glucose intolerance, 180–184, 180t–181t, 392–393, 394t
GRADE (Grading of Recommendations, Assessment, Development, and Evaluations), 262
granulation tissue, 137
growth charts, 34–36, 37t–38t
GRV. See gastric residual volume (GRV)

handgrip strength, 46
hang times, 295, 330–333, 331t
Hazard Analysis Critical Control Point (HACCP) system, 308–309, 312t
head circumference, 41–42
head-of-bed (HOB) elevation, 374–376
height, assessment of, 41
HEN. See home enteral nutrition
hepatic encephalopathy, 185, 187
hepatic failure, enteral nutrition formulas for, 184–187, 185t–186t
history of enteral nutrition, 67–68
HM. See human milk
HMF (human milk fortifier), 241–242, 241t
HOB (head-of-bed) elevation, 374–376
home enteral nutrition (HEN), 425–447
benefits and goals of, 426
blenderized tube feedings, 443–445
discharge plan, 431–433, 432t
discharge preparation checklist, 429t–430t
insurance coverage, 433–434
patient education, 434–440, 435t–444t
patient evaluation, 428
patient monitoring, 440–442
patient outcomes, 442
selection of providers of sup-plies and services, 428, 430–431
statistics on, 427–428
human milk (HM), 80, 219, 225–230, 232
label template, 309f
potential contamination points, 291f
preparation, dispensing, and administration, 288–289, 296–298, 302–305, 304t–305t
for preterm infants, 264–265
human milk fortifier (HMF), 241–242, 241t
hydrogen peroxide, 136
hydrolyzed protein, 168t, 172, 176, 198, 221t, 222, 229, 231, 237–240, 238t–239t, 245
hygiene and apparel, staff, 301–302
hypercapnia, 392, 393t
hyperglycemia, 183–184, 392–393, 394t
hyperkalemia, 380–381, 382t
hypermagnesemia, 385, 386t
hypernatremia, 379–380, 381t
hyperphosphatemia, 384, 385t
hypertonic enteral formulas, 174
hypoglycemia, 392–393, 394t
hypokalemia, 380–381, 382t
hypomagnesemia, 385, 385t
hyponatremia, 379–380, 380t
hypophosphatemia, 384, 384t
hypotension, 75
hypozincemia, 386, 387t
ideal body weight (IBW), 40–41, 42
ileus, 73, 266, 268, 357–359, 367
immune-enhancing nutrition, 187–191, 187t–188t, 190t–191t
immunonutrients, 188t
impaction, fecal, 357, 367–368
incontinence-associated dermatitis, 366
indirect calorimetry, 263
infant formulas, 225–245
additives, 226–228
amino acid–based, 240, 240t
antiregurgitation, 234–235, 234t
extensively hydrolyzed, 238–240, 239t
federal regulations, 215–216
human milk fortifiers, 241–242, 241t
human milk label template, 309f
increasing nutrient density of, 244–245
lactose-free standard, 229, 230t
low-calorie standard, 230–231
low-electrolyte/low-mineral for renal disease, 235–236, 236t
modified-fat, 236, 237t
partially hydrolyzed, 237–238, 238t
preterm, 241–244, 242t, 244t
soy-based, 231–234, 232t
standard cow’s milk-based, 228–229, 228t
infection, peristomal, 136, 141, 144, 147
inflammation
markers of, 16t–17t
nutrition assessment and, 12, 14
signs from clinical inspection, 19t
study/procedure results indicative of, 18t
insoluble fiber, 169
insurance coverage, 433–434
intact protein, 172
intermittent infusion/feeding, 82–83, 258–259
intolerance, food, 174–175
inulin, 169

jejunal volvulus, 149

jejunostomy tubes, 98–101, 107, 340
complications, 148–149
insertion, 126–129, 128f
Joint Commission, 291, 431

kidney disease. See renal disease

Kidney Disease: Improving Global Outcomes (KDIGO), 195–196

labeling, 166, 214, 307–308

components of label, 310t
practice recommendations, 311t
templates, 308f, 309f
lactase deficiency, 366
lactose-free infant formulas
amino acid-based, 240
extensively hydrolyzed, 239
partially hydrolyzed, 237–238
soy-based, 231–234, 232t
 standard, 229, 230t
laminar flow hood, 299
LCFAs (long-chain fatty acids), 171–172
LCPUFAs (long-chain polyun-saturated fatty acids), 219, 226, 240
LCTs (long-chain triglycerides), 170–171
leakage, 102, 136, 140–141, 142t–144t, 144, 149, 441t
legal recommendations, 88t
length, assessment of, 41
liquid medication formulations, 407–408
long-chain fatty acids (LCFAs), 171–172, 239–240, 243, 245
long-chain polyunsaturated fatty acids (LCPUFAs), 219, 226, 240
long-chain triglycerides (LCTs), 170–171, 224, 236, 237t
low-calorie standard infant formulas, 230–231
low-electrolyte/low-mineral infant formulas, 235–236, 236t
low-profile devices, 129

magnesium, 385, 385t–386t

malabsorption, 176–177, 177t–178t
maldigestion, 359–361
malnutrition
in adults, 11–19, 15t, 20t–22t, 23f
diagnosis, 49–50
pediatric, 19, 24, 25t, 26, 70, 377
Malnutrition Screening Tool (MST), 6t
Malnutrition Universal Screening Tool (MUST), 7t
MCFAs (medium-chain fatty acids), 171–172
MCTs (medium-chain triglycerides), 170–171, 205, 219, 222–224, 236, 237t, 239–240, 243, 245
measuring and mixing devices, 299–300
Medicaid, 433–434
medical food, 166, 214, 330t
medical history, 26–27, 28t–29t
medically stable patients, timing for enteral nutrition in, 75–76
Medicare, 433
medication administration, 402–419
best practices, 403
crushing and diluting medications, 406–408, 406f
dissolution and absorption of drugs, 403–404
dosage forms, 405–406
drug added to drug, 410–411
drug added to enteral nutrition, 409–410
drug interactions, 408–409
drug-nutrient interactions, 411–415
enteral access devices and, 404–405
planning for, 403t, 415–416
technique, 416, 417t–418t
medium-chain fatty acids (MCFAs), 171–172
medium-chain triglycerides (MCTs), 170–171, 205, 219, 222–224, 236, 237t, 239–240, 243, 245
metabolic complications of enteral nutrition, 355t, 377–395
acid-base disorders, 392
electrolyte and mineral imbalances, 378–386, 380t–382t, 384t–386t
essential fatty acid deficiency, 393, 395t
fluid imbalances, 388–392, 389t–390t
glucose intolerance, 392–393, 394t
hypercapnia, 392, 393t
refeeding syndrome, 377–378
vitamin deficiencies, 386–388, 387t–388t
MIC (minimum inhibitory concentration), 414
microbial contamination. See contamination
micronutrient supplements, 254–255
mid–upper arm circumference (MUAC), 24, 25t, 35, 43, 71
milk fat globule membranes (MFGMs), 227–228
minerals
in enteral nutrition formulas, 172–173
imbalances, 50t, 378–386
trace, 46, 50t–51t
minimum inhibitory concentration (MIC), 414
Mini Nutritional Assessment–Short Form (MNA-SF), 7t–8t
misconnections, 103, 118t, 133, 134t–135t, 172, 307, 344t, 404
misplacement, tube, 139
MNA-SF (Mini Nutritional Assessment–Short Form), 7t–8t
modified-fat formulas
for infants, 236, 237t
for pediatrics, 223–224, 224t
modular products, 80, 165t, 203–205, 204t, 206t, 245, 263, 271–272, 288, 296, 326, 333–334
monitoring, 341–346
evaluation and, 53
goals and scope of, 341–344, 343t–344t
meeting targets for nutrient delivery, 345–346
MST (Malnutrition Screening Tool), 6t
MUAC, 24, 25t, 35, 43, 71
muscle loss, assessment for, 32t–34t
MUST (Malnutrition Universal Screening Tool), 7t

nasal bridle, 131–132, 140

nasal care, 136
nasal tubes
complications, 139–140
location of distal tip, 98f
nasoenteric (NE), 98–99, 103–105, 104t, 108, 111, 113–115
nasogastric (NG), 98–100, 108–115, 130
nasojejunal (NJ), 112, 122
National Health and Examination Survey Anthropometry Manual, 43
National Health Service (NHS), 109–110
National Pressure Ulcer Advisory Panel, 179
nausea, 355–358, 437t
necrotizing fasciitis, 141, 264–266
NEMU measurement, 109, 113
New Opportunities for Verification of Enteral Tube Location (NOVEL) Project, 110–111
NEX measurement, 109
NFPE (nutrition-focused physical exam), 27, 29, 30t–35t, 34
NRS (Nutrition Risk Score), 5, 6t
nucleotides, 227
NUTRIC (Nutrition Risk in Critically Ill) tool, 8t
nutrient-drug interactions, 411–415
nutrient requirements, 254–257, 255t–257t
adults, 255–256, 255t
pediatric, 256–257, 257t
nutrition assessment
in adults, 2, 3f
anthropometric assessment, 34–45
components of, 26–49
functional status, 45–46
 malnutrition indicators and, 5–26
adult malnutrition, 11–19
pediatric malnutrition, 19–26
medical and nutrition history, 26–27, 28t–29t
pediatric, 2, 4f
physical exam, nutrition-focused, 27, 29, 30t–35t, 34
subjective global assessment (SGA), 11–12, 13f–14f
vitamin and trace mineral abnormalities, 46, 47t–50t
nutrition care pathway, 1–2
adult, 2f
pediatric, 3f
nutrition diagnosis, 49–50
nutrition-focused physical exam (NFPE), 27, 29, 30t–35t, 34
nutrition intervention, 52–53
nutrition monitoring. See monitoring
Nutrition Risk in Critically Ill (NUTRIC) tool, 5, 8t
Nutrition Risk Score (NRS), 5, 6t
nutrition screening, 2–5
adult algorithm, 3f
pediatric algorithm, 4f
tools for adult patients, 6t–10t
tools for pediatric patients, 9t–11t
nutrition support care plan, 49–53

obesity, enteral formulas for, 198–201, 200t–201t

Obesity Society, the (TOS), 199, 201, 201t
obstipation, 357
obstruction, GI, 74
Oley Foundation, 439
omega-3 fatty acids, 172, 176–177, 187–188, 194
omega-6 fatty acids, 172, 188
oral care, 136
ordering enteral nutrition, 253–281
administration methods, 257–258
advancement orders, 273
ancillary or supplemental, 273–274
best practices, 270–276, 276t
calculating prescriptions, 277, 277f–281f
for critically ill children, 262–263
elements of order, 271–274
forms for, 274–276, 275f
general considerations, 254
initiation and advancement of feedings, 258–261, 266–269, 269t, 269–270
nutrient requirements, 254–257, 255t–257t
for preterm infants, 264–266, 267t
transitional orders, 273
orogastric (OG) tube feeding, 98–99, 110, 122, 130
Orphan Drug Act, 166, 214
osmolality of enteral formulas, 173–174
overhydration, 388, 390t, 391–392

pancreatic enzyme, for unclogging tubes, 150–151

parenteral nutrition (PN)
enteral nutrition vs, 65–66, 76, 78
timing of nutrition intervention, 76, 78
transition to tube feeding, 346
partially hydrolyzed infant formulas, 237–238, 238t
PDCA (plan-do-check-act) process, 310
Pediatric Nutrition Screening Tool (PNST), 9t
pediatrics
advancing enteral nutrition, 86
body mass index (BMI), 39–40
body weight measurement, 39
critically ill patients, 101–102
edema assessment, 35t
energy requirements, 70
enteral access devices for, 433
enteral formulas, 80, 213–245
enteral nutrition administration methods, 259–261
enteral nutrition contraindications, 72t
enteral nutrition indications and patient selection, 70–71
enteral nutrition orders, 262–263, 264–266, 267t
enteral nutrition preparation, dispensing, and administration, 302–305, 304t–305t
enteral nutrition prescription calculations, 280f–281f
exchange and removal of jejunostomy tubes, 138
fat loss, assessment for, 31t
fluid requirements for, 257t
gastroesophageal reflux, 148 gastrostomy-related complications in, 147–149
growth charts, 34–36, 37t–38t
head circumference, 41
ideal body weight, 40–41
infections in neonates, 333
length measurement, 41
malnutrition, 19, 24, 25t, 26, 70
mid–upper arm circumference (MUAC), 43, 71
nutrient requirements, 256–257, 257t
nutrition assessment, 2, 4f
nutrition screening tools for, 9t–11t
timing for enteral nutrition, 53, 76–77
weight changes, 42
Pediatric Yorkhill Malnutrition Score (PYMS), 9t
PEG. See percutaneous endoscopic gastrostomy (PEG)
PEGJ (percutaneous endoscopic gastrojejunostomy), 124–125
PEJ (percutaneous endoscopic jejunostomy), 99, 126
peptide-based formula, 176, 220–222, 221t
percutaneous endoscopic gastrojejunostomy (PEGJ), 124–125
percutaneous endoscopic gastrostomy (PEG), 99–100, 106f
complications in pediatrics, 147–148
initiation of feedings after placement, 269–270, 270t
placement, 118–120, 121f
percutaneous endoscopic jejunostomy (PEJ), 99, 126
percutaneous radiologic placement, 120–123
peritonitis, 146–147
phenytoin, 411–412
phosphorus, 383–384, 384t–385t
physical exam, nutrition-focused (NFPE), 27, 29, 30t–35t, 34
plan-do-check-act (PDCA) process, 310
PN. See parenteral nutrition
pneumonia, 101–102, 114, 136, 139, 369–370, 372, 374, 376
pneumoperitoneum, 141
PNST (Pediatric Nutrition Screening Tool), 9t
polymeric pediatric formulas, 217, 218t, 219
Ponsky technique, 120
positioning patients, 339t
postoperative initiation of enteral feedings, 266–269, 269t
postpyloric feeding, 112, 265, 369
potassium, 380–381, 382t
prebiotics, 176–177, 222–223, 226–227
preparation of enteral nutrition, 79–81
additives, 296
blenderized tube feedings (BTFs), 305–306, 306t
closed vs open systems, 294–295
effective use of technology, 295
equipment and supplies, 297–301
errors, reducing risks for, 290–296
formula selection and storage, 293–294
hang times, 295
human milk (HM), 302–305, 304t–305t
recommendations for safe, 292t
space for, 296–297
staff hygiene and apparel, 301–302
water safety, 295–296
pressure injuries, 177–180, 374–375
preterm infants
enteral formulas, 241–244, 242t, 244t
ordering enteral nutrition for, 264–266, 267t
probiotics, 227
protein in enteral nutrition formulas, 168t, 172
hydrolyzed, 168t, 172, 176, 198, 221t, 222, 229, 231, 237–240, 238t–239t, 245
intact, 172
modular products, 204t, 205
soy-based infant formulas, 231–234, 232t
wound healing and, 179
protein requirements
adults, 256t
pediatrics, 257t
pulmonary aspiration, 370–376
gastric residual volume (GRV) and, 337–338, 371–373, 375–376
methods to detect, 373–374
methods to determine risk, 371–373
patient education, 440t
prevention strategies, 337–339, 374–376
pulmonary disease enteral formulas, 182, 191–194, 192t–193t
pumps, enteral feeding, 335–337, 338t
pump-assisted feedings, 259, 261
pump or power failure, patient education on, 444t
PYMS (Pediatric Yorkhill Malnutrition Score), 9t

quality assurance, 308–309, 312, 312t

Recommended Dietary Allowance (RDA), 254, 263

refeeding syndrome, 85–86, 377–378
refrigerators and freezers, 297–298
regurgitation, infant formulas to reduce, 234–235, 234t
renal disease
adult enteral nutrition formulas, 194–197, 195t–197t
infant formulas for, 235–236, 236t
pediatric enteral nutrition formulas, 224–225, 225t
renal replacement therapy, 195

SBS (short bowel syndrome), 362, 365–366

SCAN (Screening Tool for Childhood Cancer), 10t
SCCM (Society of Critical Care Medicine), 74, 85, 101, 171t, 178t, 181t, 185, 189, 190t, 193t, 195, 196t, 198, 199t–
200t, 201, 262
SCFAs (short-chain fatty acids), 169
Screening Tool for Assessment of Malnutrition in Paediatrics (STAMP), 10t
semi-elemental formulas, 172, 176, 220–222, 221t
SGA (subjective global assessment), 11–12, 13f–14f, 45
SGNA (Subjective Global Nutritional Assessment), 11t
short bowel syndrome (SBS), 362, 365–366
short-chain fatty acids (SCFAs), 169
SIADH (syndrome of inappropriate antidiuretic hormone secretion), 379
SIBO (small intestine bacterial overgrowth), 362, 365
sinks and dishwashers, 298–299
sinusitis, 140
skin care, 136–137, 441t
small intestine bacterial over-growth (SIBO), 362, 365
Society of Critical Care Medicine (SCCM), 74, 85, 101, 171t, 178t, 181t, 185, 189, 190t, 193t, 195, 196t, 198, 199t–
200t, 201, 262
sodium, 379–380, 380t–381t
soluble fiber, 169
soy-based infant formulas, 231–234, 232t
stability, drug, 408
staff hygiene and apparel, 301–302
Stamm technique, 123
STAMP (Screening Tool for Assessment of Malnutrition in Paediatrics), 10t
steatorrhea, 360, 362, 365
stoma
care of, 136–137
measurement of, 138
peristomal infection, 141
tract maturation, 146–147
stool volume, measurement of, 361–362
storage containers, 300–301
strength assessment, 45–46
STRONGkids, 10t
Subjective Global Assessment (SGA), 11–12, 13f–14f, 45
Subjective Global Nutritional Assessment (SGNA), 11t
suspensions, 408
synbiotics, 227
syndrome of inappropriate anti-diuretic hormone secretion (SIADH), 379

Tanner staging, 27, 29, 36t

termination of nutrition support, 349
T-fasteners, 122–123, 127
thawing and warming equipment, 301
thiamin deficiency, 387–388, 388t
thienopyridines, 119
trace minerals, 46, 50t–51t
transitional feedings
parenteral nutrition to tube feeding, 346
tube feeding to oral intake, 346–348
transitioning hospitalized patients to other settings, 348–349
triceps skinfold (TSF) thickness, 35, 43
tube displacement, patient education on, 442t
tube leaking, patient education on, 441t
tumor implantation and meta-stasis, 146

ultrasound, 45

vitamin(s)
abnormalities, 46, 47t–49t
deficiencies, 46, 47t–49t, 386–388, 387t–388t
thiamin deficiency, 48t, 387–388, 388t
vitamin K deficiency, 49t, 387, 387t
in enteral nutrition formulas, 172–173
status assessment tests, 51t
toxicities, 46, 47t–49t
volume-based feedings, 84, 258
vomiting, 73, 355–358, 437t

waist circumference, 40
warfarin, 119, 415
water content in enteral formulas, 173
water safety, 295–296
weight data interpretation, 42–43
weight-for-length, 24, 25t, 39–40
weight gain velocity, 24, 25t, 29, 34, 42
Witzel jejunostomy technique, 127, 128f
World Health Organization (WHO), 35, 41–42
wound healing, enteral formulas for, 177–180, 178t

zinc, 386, 386t

zinc oxide, 136–137