AMERICAN SOCIETY FOR PARENTERAL AND ENTERAL NUTRITION

The A.S.P.E.N. Nutrition Support Practice Manual

2nd Edition

EDITOR-IN-CHIEF

Russell Merritt, MD, PhD

Medical Director, Nutrition
Ross Products Division, Abbott Laboratories
Columbus, OH

SECTION EDITORS

Mark H. DeLegge, MD
Associate Professor of Medicine
Director, Section of Nutrition
Digestive Disease Center
Medical University of South Carolina
Charleston, SC

Beverly Holcombe, PharmD, BCNSP

Clinical Specialist
Department of Pharmacy
University of North Carolina Hospitals
Chapel Hill, NC

Charles Mueller, PhD, RD, CNSD

General Clinical Research Center
Department of Medicine
Weill/Cornell Medical College
New York, NY

Juan Ochoa, MD, FACS

Associate Professor of Surgery and Critical Care
University of Pittsburgh
Pittsburgh, PA

Karen Ringwald Smith, MS, RD, LDN

Clinical Coordinator/Research and Education Coordinator
Clinical Nutrition Services
St. Jude Children’s Research Hospital
Memphis, TN

W. Frederick Schwenk II, MD

Professor of Pediatrics
Mayo Clinic College of Medicine
Rochester, MN

MANAGING EDITOR

Peggi Guenter, PhD, RN, CNSN

A.S.P.E.N. Managing Editor for Special Projects
Silver Spring, MD
A.S.P.E.N. is a scientific society whose members are health care professionals-physicians, dietitians, nurses, pharmacists,
other allied health professionals, and researchers- dedicated to assuring that every patient receives optimal nutrition care.

A.S.P.E.N.’s mission is to serve as a preeminent, interdisciplinary, research-based, patient-centered clinical nutrition

society throughout the world.

NOTE: This publication is designed to provide accurate authoritative information in 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. Trade-
marked commercial product names are used only for education purposes and do not constitute endorsement by A.S.P.E.N.

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 A.S.P.E.N. Printed in the United States of America. For information write: American Society for Parenteral and
Enteral Nutrition (A.S.P.E.N.), 8630 Fenton Street, Suite 412, Silver Spring, MD 20910-3805; (301) 587-6315,
www.nutritioncare.org, email:[email protected].

Copyright © 2005. American Society for Parenteral and Enteral Nutrition.

ISBN #1-889622-06-0
 American Society for
Parenteral and Enteral Nutrition

Contents

INTRODUCTION
Russell Merritt, MD, PhD

I Fundamentals of Nutrition Support Practice and Management

S E C T I O N E D I T O R : Beverly Holcombe, PharmD, BCNSP
0

1 Nutrition Assessment and Decision Making

Kathy Pesce-Hammond, MS, RD, LD, CNSD, RN, CNSN; Jacqueline Wessel, MEd, RD, CSP,
CNSD,CLE

2 Nutritional Goals and Requirements

Maria Luisa Forchielli MD; Sarah J. Miller PharmD

3 Enteral Access and Infusion Equipment

Donald K. Kirby MD, CNSP; Marianne Opilla, RN, BSN, CNSN

4 Enteral Formulations
Mary Marian MS, RD; Susan J. Carlson, MMSc, RD, CSP, LD, CNSD

5 Enteral Nutrition Implementation and Management

Linda Lord NP, RN, MS, CNSN; Michelle Harrington, MS, RD, CSP, CNSD, LDN

6 Parenteral Nutrition Access and Infusion Equipment

Elizabeth A. Krzywda, RN, ANP, MSN; Charles Edmiston, Jr., PhD

7 Parenteral Nutrition Formulations: Preparation and Ordering

Vanessa J. Kumpf, PharmD, BCNSP; Jay M. Mirtallo, MS, RPh, BCNSP, Craig Peterson, RD,
CNSD

8 Parenteral Nutrition Implementation and Management

Gordon S. Sacks, PharmD, BCNSP, FCCP; Susan Mayhew, PharmD, BCNSP; Debbie John-
son, RN, MSN

9 Drug Nutrient Interactions

Michael S. Nyffeler, PharmD, BCNSP; Eric Frankel, PharmD, BCNSP; Edmund Hayes,
PharmD; Stephanie Mighdoll, PharmD

II Immune Driven Conditions

S E C T I O N E D I T O R : Karen Ringwald-Smith, MS, RD

10 HIV Infection/Acquired Immunodeficiency Syndrome

Cade Fields-Gardner, MS, RD, LD, CD

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11 Cancer 0
Elaine B. Trujillo, MS, RD; Sara L. Bergerson, MS, RD; Jennifer C. Graf, MS, RD;
Madeline Michael, MPH, RD

12 Solid Organ Transplantation 0

Mary Kramlich, MS, RD, LD, CNSD; Angie Iverson RD, LMNT; Vincent Armenti, MD, PhD;
Jeanette M. Hasse, PhD, RD, LD, FADA, CNSD

13 Hematopoietic Stem Cell Transplantation 0

Paula M. Charuhas, MS, RD, FADA,CNSD; Ann Lipkin, MS, RD,CNSD;
Polly Lenssen, MS, RD, FADA; Kerry McMillen, MS,RD

III Gastrointestinal Related Conditions

S E C T I O N E D I T O R : Mark DeLegge, MD

14 Diarrhea 0
Mark R. Corkins, MD, CNSP, FAAP; James Scolapio, MD, CNSP

15 Pancreatic Disease 0
Maria R. Mascarenhas, MBBS; Donna Divito,RD, CNSD; Stephen A. McClave, MD

16 Inflammatory Bowel Disease 0

William A. Faubion, Jr., MD; Darlene G. Kelly, MD, PhD

17 Liver Disease 0
Jeannette M. Hasse, PhD, RD, LD, FADA,CNSD; Stuart S. Kaufman, MD;
Erin Fennelly, RD, CNSD

18 Neurologic Diseases 0
Elizabeth Gleghorn, MD; Karen Amorde-Spalding, MS, RD, CSP;
Mark H. Delegge, MD, FACG

IV Surgical and Critically Ill Conditions 0

S E C T I O N E D I T O R : Juan Ochoa, MD, FACS

19 Perioperative 0
Stephen L. Barnes, MD; Marjorie Swintosky, MS, RD; Andrew C. Bernard, MD;
Paul Kearney, MD, FACS

20 Nutrition in Critical Illness, Including Immunonutrition 0

Imad F. Btaiche, PharmD, BCNSP; Paul Marik, MD, FCCM, FCCP; Juan Ochoa, MD, FACS;
Robert G. Martindale, MD, PhD, FACS; Jeffrey E. Salon, MD, FACP, FCCP, FCCM

21 Trauma 0
Rosemary A. Kozar, MD, PhD; Margaret M. McQuiggan, MS, RD, LD, CNSD;
Frederick A. Moore, MD

22 Indirect Calorimetry in Critically Ill Patients 0

Jennifer A. Wooley, MS, RD, CNSD

23 Nutrition Support for Adult Patients with Acute Renal Failure 0

Kathleen D. Liu, MD, PhD; Annette Stralovich-Romani, RD, CNSD;
Glenn M. Chertow, MD, MPH

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24 Nutrition Support for Pediatric Patients with Acute Renal Failure 0

Carolyn L. Abitbol, MD; Marie Rossique, PharmD; Mirta Rios, RD

25 Burns 0
Michele M. Gottschlich, PhD, RD; Theresa Mayes, RD

26 Neonatal Intensive Care 0

Winston W. K. Koo, MB, BS, FRACP; Kathleen McLaughlin, MS, RNC, NNP;
May Saba, PharmD, BCNSP

V Metabolic Conditions 0
S E C T I O N E D I T O R : W. Frederick Schwenk, MD

27 Diabetes Mellitus 0
M. Molly McMahon, MD

28 Obesity 0
Julie L. Roth, MD; Robert F. Kushner, MD; Eden Bateman, MS, RD, LD

29 Inborn Errors of Metabolism 0

Margretta R. Seashore, MD, FAAP, FACMG; Crystal A. Reil, RD, CD-N

30 Chronic Kidney Disease 0

Charles J. Foulks, MD, FACP, FACN

31 Pregnancy 0
David Frankenfield, MS, RD

32 Anorexia Nervosa 0
J. Scott Whittaker, BSc, MD; Laura Sware, RD; Lori Hards, BSc, RD

VI Site Related and Ethical Issues 0

S E C T I O N E D I T O R : Charlie Mueller, PhD, RD, CNSD

33 Acute Care Organizations 0

Denise Baird Schwartz, MS, RD, FADA, CNSD; Carolyn M. Apovian, MD, FACN

34 Long Term Care 0

Mary Ellen Posthauer, RD,CD,LD; Gretchen Robinson, MS, RD, LD, FADA

35 Considerations for Home Nutrition Care 0

Debra S. Kovacevich, RN, MPH; Marsha E. Orr, RN, MS

36 Ethics 0
Julie O’Sullivan Maillet, PhD, RD, FADA

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 American Society for
Parenteral and Enteral Nutrition

Contributors

Carolyn Abitbol, MD Susan J Carlson, MMSc, RD, CSP, LD, William Faubion, MD
Professor of Pediatrics CNSD Assistant Professor of Medicine
University of Miami Neonatal Dietitian Mayo Clinic College of Medicine
Division of Pediatric Nephrology Children’s Hospital of Iowa at the Division of Gastroenterology, Hepatology,
Miami, FL University of Iowa Hospitals Internal Medicine
Iowa City, IA Mayo Clinic
Caroline M. Apovian, MD, FACN Rochester, MN
Associate Professor of Medicine Paula M. Charuhas, MS, RD, FADA,
Boston University School of Medicine CNSD Erin Fennelly, RD, CNSD
Director, Nutrition & Weight Management Clinical Dietitian/Pediatric Nutrition Georgetown University Transplant Institute
Center Specialist Washington, DC
Boston Medical Center Seattle Cancer Care Alliance
Boston, MA Seattle, WA Cade Fields-Gardner, MS, RD, LD, CD
Director of Services
Vince Armenti, MD, PhD Glenn M. Chertow, MD, MPH The Cutting Edge
Professor of Surgery Temple University Division of Nephrology Cary, IL
Department of Surgery/Abdominal Organ Department of Medicine Research
Transplant Program University of California, San Francisco Maria Luisa Forchielli, MD
Philadelphia, PA San Francisco, CA Pediatric Department
University of Bologna
Stephen L. Barnes, MD Mark R. Corkins, MD, CNSP, FAAP Bologna, Italy
Major, United States Air Force Assistant Professor of Pediatrics
Center for Sustainment of Trauma and James Whitcomb Riley Hospital for Charles Foulks, MD, FACP, FACN
Readiness Skills Children/Indiana University School of Professor of Medicine, Texas A&M
University Hospital Medicine University System Health Science Center
Cincinnati, OH Indianapolis, IN Division Director of Nephrology-
Hypertension
Eden Bateman MS, RD, LD Mark H. Delegge, MD, FACG Vice Chairman of External Affairs
Wellness Institute, Northwestern Memorial Associate Professor of Medicine Department of Medicine
Hospital Director, Section of Nutrition Scott & White Clinic & Hospital
Chicago, IL Digestive Disease Center Temple, TX
Medical University of South Carolina
Sara L. Bergerson, MD, RD Charleston, SC Eric H. Frankel, PharmD,MSE, BCNSP
Clinical Research Dietitian Nutrition Support Coordinator
National Institutes of Health Donna DiVito, RD, CNSD Covenant Health System
Clinical Center Nutrition Dept. Department of Clinical Nutrition Lubbock, TX
Bethesda, MD Children’s Hospital of Philadelphia
Philadelphia, PA David Frankenfield, MS, RD
Andrew C. Bernard, MD Chief Clinical Dietitian
Assistant Professor of Surgery Charles E. Edmiston Jr., PhD Milton S. Hershey Medical Center
Division of General Surgery Associate Professor of Surgery Hershey, PA
University of Kentucky Department of Surgery
Lexington, KY Medical College of Wisconsin Elizabeth Gleghorn, MD
Milwaukee, WI Director, Division of Pediatric
Imad F. Btaiche, PharmD, BCNSP Gastroenterology, Hepatology, and
Pharmacy Department Nutrition
University of Michigan Hospitals Children’s Hospital and Research Center
Ann Arbor, MI Oakland, CA

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Michele M. Gottschlich, PhD, RD, CNSD Paul A Kearney, MD, FACS Robert F. Kushner, MD
Director, Nutrition Services Professor of Surgery Professor of Medicine, Northwestern
Shriners Hospitals for Children Section Head, Trauma and Surgical Critical University Feinberg School of Medicine
Cincinnati, OH Care Medical Director, Wellness Institute,
Division of General Surgery Northwestern Memorial Hospital
Jennifer C. Graf, MS, RD University of Kentucky Medical Center Chicago, IL
Clinical Dietitian Lexington, KY
National Institutes of Health Polly Lenssen, MS, RD, FADA
Clinical Center Nutrition Dept. Darlene G Kelly, MD PhD Clinical Nutrition Manager
Bethesda, MD Associate Professor of Medicine Childrens’ Hospital & Regional Medical
Mayo Clinic Center
Kathy Pesce-Hammond, MS, RD, LD, Division of Seattle, WA
CNSD, RN, CNSN Gastroenterology/Hepatology/Internal
Coordinator, Continuing Education Medicine Ann Connell Lipkin, MS, CNSD
Clinical Nutrition Specialist Rochester, MN Clinical Dietitian II
Chartwell Diversified Services, Inc. Childrens’ Hospital & Regional Medical
Lilburn, GA Donald F. Kirby, MD CNSP Center
Professor, Virginia Commonwealth Seattle, WA
Lori Hards, BSc, RD University School of Medicine
University of British Columbia Medical College of Virginia Hospitals Kathleen D. Liu, MD, PhD
Vancouver, BC Section of Nutrition University of California, San Francisco
Richmond, VA San Francisco, CA
Michelle Harrington, MS, RD, CSP,
CNSD, LDN Winston Koo, MB, BS, FRACP Linda M. Lord, NP, MS, CNSN
Nutrition Information Specialist Professor of Pediatrics Nutrition Support Service
McNeil Nutritionals Wayne State University Strong Memorial Hospital
Fort Washington, PA Department of Pediatrics Rochester, NY
Hutzel Hospital
Jeanette Hasse, PhD, RD, LD, FADA, Detroit, MI Julie O’Sullivan Maillet, PhD, RD, FADA
CNSD Professor and Associate Dean for Academic
Transplant Nutrition Specialist Debra S. Kovacevich, RN, MPH Affairs and Research
Transplant Services Home Care Services University of Medicine and Dentistry of New
Baylor University Medical Center University of Michigan Hospitals and Health Jersey-School of Health Related
Dallas, TX Centers Professions
Ann Arbor, MI Newark, NJ
Edmund M. Hayes, PharmD
Departments of Pharmacy and Medicine Rosemary Kozar, MD, PhD Mary Marian, MS, RD
University Medical Center Associate Professor Clinical Nutrition Research Specialist
State University of New York at Stony Brook University of Texas Medical School University of Arizona College of Medicine
Stony Brook, New York, Houston, TX and Northwest Medical Center
Tucson, AZ
Angela K Iverson, RD, LMNT Mary Kramlich, MS, RD, LD,CNSD
Pediatric Dietitian Transplant Nutrition Specialist Paul E. Marik, MD, FCCM, FCCP
University Hospital Transplant Services Chief of Pulmonary and Critical Care
The Nebraska Medical Center Baylor University Medical Center Medicine
Omaha, NE Dallas, TX Thomas Jefferson University School of
Medicine
Deborah Johnson, RN, MSN Elizabeth Krzywda, ANP, MSN Philadelphia, PA
Meriter Hospital Adult Nurse Practitioner
Madison, WI Department of Surgery Robert G. Martindale, MD, PhD, FACS
Medical College of Wisconsin Professor of Surgery
Stuart S. Kaufman, MD Milwaukee, WI Chief, Gastrointestinal Surgery
Children’s National Medical Center and Department of Surgery
Georgetown University Transplant Institute Vanessa J. Kumpf, PharmD, BCNSP Medical College of Georgia
Washington, DC Clinical Specialist Augusta, GA
Nutrishare, Inc.
Elk Grove, CA Maria Mascarenhas, MBBS
Director, Nutrition Support Service
Children’s Hospital of Philadelphia
Philadelphia, PA

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 C oRn et rviibeuwt oe r s

Theresa Mayes, RD Frederick Moore, MD Julie L. Roth, MD

Registered Dietitian James H. “Red” Duke Jr. Professor Assistant Professor of Medicine,
Shriners Hospitals for Children and Vice Chairman, Department of Surgery Northwestern University
Cincinnati, OH Medical Director, Trauma Services Feinberg School of Medicine
University of Texas Medical School Wellness Institute, Northwestern Memorial
Susan L Mayhew, PharmD, BCNSP Houston, TX Hospital
Nutrition Support Specialist Chicago, IL
Coordinator, Pharmacy Education and Michael S. Nyffeler, PharmD, BCNSP
Residency Programs Clinical Specialist Nutrition Support Mary Saba, PharmD, BCNSP
Columbus Regional Healthcare System Meriter Hospital Clinical Coordinator
Columbus, OH Madison, WI Wayne State University
Children’s Hospital of Michigan
Stephen A. McClave, MD Juan Ochoa, MD, FACS Department of Pharmacy Services
Professor of Medicine Associate Professor of Surgery and Critical Detroit, MI
Division of Gastroenterology/Hepatology. Care
University of Louisville University of Pittsburgh Gordon S Sacks, PharmD, BCNSP, FCCP
Louisville, KY Pittsburgh, PA Clinical Associate Professor
University of Wisconsin, Madison
Kathleen McLaughlin, MS, RNC, NNP Marianne Opilla, RN, BSN, CNSN School of Pharmacy
Neonatal Nurse Practitioner Nutrition Support Nursing Madison, WI
Hutzel Hospital / Women’s Hospital Medical College of Virginia Hospitals
Detroit, MI Richmond, VA Jeffrey E. Salon, MD, FACP, FCCP,
FCCM
M. Molly McMahon, MD Marsha E. Orr, RN, MS Medical Director, Medical Nutrition
Associate Professor of Medicine Faculty, Department of Nursing Ross Products Division, Abbott Laboratories
Division of Endocrinology, Diabetes, California State University Columbus, OH
Metabolism, Fullerton, CA
Nutrition, and Internal Medicine Margretta R. Seashore, MD, FAAP,
Mayo Clinic College of Medicine Craig Petersen, RD, CNSD FACMG
Rochester, MN Pediatric Nutrition Support Specialist Professor, Genetics and Pediatrics
University of California, Davis Med Center Director, Genetics Consultation Service
Kerry McMillen, MS, RD Sacramento, CA Department of Genetics
Clinical Dietitian Yale University School of Medicine
Seattle Cancer Care Alliance Mary Ellen Posthauer, RD, CD,LD Attending Physician
Seattle, WA Corporate Consultant Yale-New Haven Hospital
Supreme Care West New Haven, CT
Margaret M. McQuiggan, MS, RD, LD, Evansville, IN
CNSD Denise Baird Schwartz, MS, RD, FADA,
University of Texas Medical School Houston Crystal Reil, RD, CD-N CNSD
Department of GI Nutrition Genetic Nutritionist Nutrition Support Coordinator
Houston, TX Department of Genetics Providence Health System
Yale University School of Medicine San Fernando Valley Service Area
Madeline Michael, MPH, RD Yale-New Haven Hospital Burbank, CA
Chief, Clinical Nutrition Services New Haven , CT
National Institutes of Health James S. Scolapio, MD, CNSP
Clinical Center Nutrition Dept. Mirta Rios, RD Associate Professor of Medicine
Bethesda, MD Jackson Memorial Hospital Director of Nutrition
Miami, FL Mayo Clinic
Stephanie Mighdoll, PharmD Jacksonville, FL
Albany College of Pharmacy Gretchen Robinson, MS, RD, LD, FADA
Albany, NY Consultant Dietitian Karen Amorde-Spalding, MS, RD, CSP
Ada, OH Children’s Hospital Oakland
Sarah J Miller, PharmD Oakland, CA
Professor, Dept. Pharmacy Practice Annette Stralovich-Romani, RD, CNSD
University of Montana University of California, San Francisco Marjorie Swintosky, MS, RD
Missoula, MT San Francisco, CA University of Kentucky Medical Center
Lexington, KY
Jay Mirtallo, MS, RPh, BCNSP Marie Rossique, PharmD
The Ohio State University Medical Center Jackson Memorial Hospital
Dept. of Pharmacy Miami, FL
Columbus, OH

© 2005 A.S.P.E.N. www.nutritioncare.org. A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. xi
Reviewers

Laura Sware, RD Jacqueline Wessel, MEd, RD, CSP, CNSD, Jennifer A. Wooley, MS, RD, CNSD
University of British Columbia CLE Nutrition Support Service
Vancouver, BC Cincinnati Children’s Hospital Medical St. Joseph Mercy Health System
Center Ann Arbor, MI
Elaine B. Trujillo, MS, RD Cincinnati, OH
Nutritional Science Research Group
Division of Cancer Prevention J. Scott Whittaker, MD
National Cancer Institute Clinical Professor, Gastroenterology
National Institutes of Health University of British Columbia
Rockville, MD Vancouver, BC

xii A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. © 2005 A.S.P.E.N. www.nutritioncare.org.
 American Society for
Parenteral and Enteral Nutrition

Reviewers

Carolyn L. Abitbol, MD Randy Bechtel, PharmD, BS Ronni Chernoff, PhD, RD

Professor of Pediatrics Metabolic Support and Clinical Pharmacy Associate Director, GRECC; Professor of
Division of Pediatric Nephrology Manager Geriatrics
University of Miami School of Medicine Freeman Health System CAVHS & University of Arkansas for
Miami, FL Joplin, MO Medical Sciences
Little Rock, AR
Phyllis B. Acosta, MS,MPH, DrPH, RD Bruce Ryan Bistrian, MD, PhD
Director of Metabolic Diseases (retired) Professor of Medicine Kathy Clark, MS, RD, CNSD,LD
Ross Products Division, Abbott Laboratories Harvard Medical School Metabolic Support Dietitian
Columbus, OH Beth Israel Deconess Medical Center Freeman Health System
Boston, MA Joplin, MO
Maria R. Andrews, MS, RD, FADA,
CNSD, LDN
Donna Zimmaro Bliss, PhD, RN, FAAN Charlene Compher, PhD, RD, FADA,
Chief, Nutrition & Food Service
Associate Professor and Professor in Long- CNSD, LDN
New Mexico VA Health Care System
Term Care of Elders Assistant Professor of Nutrition Science
Albuquerque, NM
University of Minnesota School of Nursing University of Pennsylvania School of
Deborah A. Andris, MSN, ANP Minneapolis, MN Nursing
Nurse Practitioner; Bariatric Surgery Clinical Nutrition Support, Hospital of the
Program Carol Braunschweig, PhD University of Pennsylvania
Medical College of Wisconsin Associate Professor Philadelphia, PA
Milwaukee, WI University of Illinois at Chicago
Chicago, IL Mark R. Corkins, MD, CNSP, FAAP
Caroline Apovian, MD Assistant Professor of Pediatrics
Director, Center for Nutrition and Weight Pamela Brown, MD, PhD James Whitcomb Riley Hospital for
Management Clinical Assistant Professor of Pediatrics and Children/Indiana University School of
Associate Professor of Medicine Communicable Diseases Medicine
Boston University School of Medicine University of Michigan Medical Center Indianapolis, IN
Boston, MA Ann Arbor, MI
Catherine M. Crill, PharmD, BCPS,
David A. August, MD Susan J Carlson MMSc, RD, CSP, LD, BCNSP
Associate Professor of Surgery, Chief, CNSD Assistant Professor of Pharmacy and
Division of Surgical Oncology Neonatal Dietitian Pediatrics
UMDNJ/ Robert Wood Johnson Medical Children’s Hospital of Iowa at the University of Tennessee Health Science
School and The Cancer Institute of New University of Iowa Hospitals Center
Jersey Iowa City, IA Memphis, TN
New Brunswick, NJ

Robin Bankhead, MS, CRNP, CNSN David Charney, MD, FACP Susan Curtas, RN, MSN
Department of Surgery Riverside Nephrology Association Clinical Nurse Specialist and Research
Temple University Hospital Columbus, OH Manager
Philadelphia, PA Cleveland Clinic Foundation
Pamela Charney, MS,RD, LD, CNSD Cleveland, OH
Jacqueline R. Barber, PharmD, FASHP, PhD Candidate
BCNSP School of Health Related Professions Joan Daniels, RD
Clinical Associate Professor University of Medicine and Dentistry of New Division of Pediatric Nephrology
University of Minnesota, Minneapolis, MN Jersey Mott Children’s Hospital
Pharmacy Clinical Specialist Newark, NJ University of Michigan
Methodist Hospital, Department of Pharmacy Ann Arbor, MI
St. Louis, MN

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Reviewers

Roland Dickerson, PharmD Kalman E. Holdy, MD, ABPNS Carol McGinnis, RN, MS, CNSN
Professor of Pharmacy Medical Director of Clinical Nutrition Clinical Nurse Specialist
University of Tennessee Health Science Sharp Memorial Hospital Sioux Valley Hospital USD Medical Center
Center San Diego, CA Sioux Falls, SD
Memphis, TN
Wanda H. Howell, PhD, RD Louise R. Merriman, MS, RD, CN/D
Mark Fishbein, MD University Distinguished Professor Corporate Manager, Clinical Nutrition
Associate Professor Nutritional Science Dept. New York Presbyterian Hospital
Southern Illinois University School of University of Arizona New York, NY
Medicine Tucson, AZ
Department of Pediatrics Sarah J. Miller, PharmD, MS
Springfield, IL Deborah Johnson, RN, MSN Professor, University of Montana School of
Clinical Nurse Specialist Pharmacy
Amy Andolina Fisher RN, MS, CNSN Meriter Hospital Missoula, MT
Nutrition Support Nurse Madison, WI
Lucile Packard Childrens Hospital Gayle Minard, MD
Palo Alto, CA Kimberly Joseph, MD, FACS, CNSP Professor of Surgery
Director, Trauma Intensive Care Unit The University of Tennessee Health Science
M. Patricia Fuhrman, MS, RD, LD, J.H. Stroger Hospital of Cook County Center
FADA, CNSD Department of Trauma Memphis, TN
Area Clinical Nutrition Marketing Director Chicago, IL
Coram Healthcare Ethel L. Mitty, EdD, RN
St. Louis, MO Kenneth A. Kudsk, MD, FACS Adjunct Clinical Professor of Nursing
Professor of Surgery, Vice Chairman of Research Associate
Susan T. Fussell, PhD, RD, CNSD Surgical Research New York University
Pediatric Clinical Nutrition Specialist University of Wisconsin-Madison Division of Nursing
Duke University Medical Center Madison, WI New York, NY
Durham, NC
Jennifer Lefton, RD, LD/N, CNSD Barry Mizock, MD
Debra K. Gardner, PharmD Clinical Dietitian II Cook County Hospital
Specialty Practice Pharmacist, Women and Jackson Memorial Hospital Chicago, IL
Infants Miami, FL
Ohio State University Medical Center Joseph A. Molnar, MD, PhD
Columbus, OH Neal S. LeLeiko, MD, PhD Assistant Professor of Plastic and
Professor of Pediatrics Brown School of Reconstructive Surgery
Donald E. George, MD Medicine Wake Forest University School of Medicine
Chief, Division of GI/Nutrition Director of Pediatric Gastroenterology, Winston-Salem, NC
Nemours Children’s Clinic Nutrition and Liver Diseases
Jacksonville, FL Hasbro Children’s Hospital and The Steve Montoya, MD
Rhode Island Hospital Medical Director
Kathleen Gura, PharmD, BCNSP, FASHP Providence, RI Angelo Dialysis Centers
Clinical Pharmacist GI/Nutrition San Angelo, TX
Team Leader, Surgical Program Mary Marian, RD, MS
Children’s Hospital of Boston Clinical Nutrition Research Specialist Charles Mueller, PhD, RD, CNSD
Boston, MA University of Arizona College of Medicine General Clinical Research Center
and Northwest Medical Center Department of Medicine
Gregory A. Hale, MD Tucson, AZ Weill/Cornell Medical College
Clinical Director, Division of Stem Cell New York, NY
Transplantation Ainsley M. Malone, MS, RD, LD, CNSD
St. Jude Children’s Research Hospital Nutrition Support Team Diane Olson, RD, CNSD
Memphis, TN Pharmacy Department Registered Dietitian
Mt. Carmel West Hospital Mayo Clinic
Michelle Harrington, MS, RD, CSP, Columbus, OH Rochester, MN
CNSD, LDN
Nutrition Information Specialist Todd W. Mattox, PharmD, BCNSP Adele K. Pattinson, RD, LD, CNSD
McNeil Nutritionals Coordinator, Nutrition Support Team Nutrition Support Dietitian/ Home Enteral
Fort Washington, PA H. Lee Moffitt Cancer Center and Research Coordinator
Institute Mayo Clinic Medical Center
Linda Heller, MS, RD, CSP Tampa, FL Rochester, MN
Childrens Hospital of Los Angeles
Los Angeles, CA

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 Reviewers

Marcia Kalista-Richards, MPH, RD, David S. Seres, MD, CNSP Susan J. Whitmire, RD, CNSD, LDN
CNSD, LDN Assistant Professor Nutrition Support Dietitian
Nutrition Support-Renal Dietitian Albert Einstein College of Medicine Geisinger Medical Center
Easton Hospital/Sodexho Co. New York, NY Danville, PA
Easton, PA
Marcia Silkroski RD Marion Winkler, MS, RD, LDN, CNSD
Carol J. Rollins, MS, RD, CNSD, PharmD, Executive Director Surgical Nutrition Specialist
BCNSP Nutrition Advantage Rhode Island Hospital and Brown University
Coordinator, Nutrition Support Team and Chester Springs, PA School of Medicine
Clinical Associate Professor Providence, RI
University Medical Center and University of David L. Sigalet, MD, PhD, FRCSC, FACS
Arizona, College of Pharmacy Director of Pediatric General Surgery Patricia Worthington, RN, MSN, CNSN
Tucson, AZ Professor, University of Calgary, Alberta Nutrition Support Clinical Nurse Specialist
Children’s Hospital Thomas Jefferson University Hospital
Pamela Rothpletz-Puglia, EdD, RD Calgary, Alberta, CANADA Philadelphia, PA
Nutrition Practitioner and Research Associate
Francois-Xavier Bagnoud Center Edwin Simpser, MD Jane Anne Yaworski, MSN, RN
University of Medicine and Dentistry of Chief Medical Officer Clinical Nurse Specialist for Nutrition
New Jersey St. Mary’s Hospital for Children Support and Intestinal Care
Newark, NJ Bayside, NY Children’s Hospital of Pittsburgh
Pittsburgh, PA
Mary Krystofiak Russell MS, RD Joyce K Stechmiller, ARNP, PhD
Director, Nutrition Services Associate Professor Yi-Hao Yu, MD, PhD, CNSP
Duke University Hospital Department of Adult and Elderly Nursing Director, Adult PN/Nutrition Service
Durham, NC University of Florida Columbia-Presbyterian Hospital
College of Nursing Assistant Professor of Medicine
Nancy Sacks, MS, RD Gainesville, FL Columbia University College of Physicians
Research Coordinator and Surgeons
Division of Oncology John A. Tayek, M.D. Department of Medicine, Division of
Children’s Hospital of Philadelphia Associate Professor of Medicine-In Preventive Medicine and Nutrition
Philadelphia, PA Residence New York, NY
David Geffen School of Medicine at UCLA
Philip J. Schneider, RPh, MS, FASHP Harbor-UCLA Medical Center Gary P. Zaloga, MA, MD
Clinical Professor and Director Department of Internal Medicine Medical Director, Methodist Research
Latiolais Leadership Program Torrance, CA Institute
Division of Pharmacy Practice and Clinical Professor of Medicine
Administration Melody Thompson, MS, RD Indiana University School of Medicine
College of Pharmacy Clinical Nutrition Specialist Indianapolis, IN
The Ohio State University Ross Products Division, Abbott Laboratories
Columbus, OH Columbus, OH

W. Frederick Schwenk II, MD Charles W. Van Way, III, MD

Professor of Pediatrics Ralph R. Coffey Professor and Chair of
Mayo Clinic College of Medicine Surgery
Rochester, MN School of Medicine, University of Missouri-
Kansas City
Douglas L. Seidner, MD Kansas City, MO
Director, Nutrition Support and Vascular
Access Department
Program Director, Fellowship in Clinical
Nutrition
Digestive Disease Center
The Cleveland Clinic Foundation
Cleveland, OH

© 2005 A.S.P.E.N. www.nutritioncare.org. A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. xv
 Russell Merritt, MD, PhD

Introduction

Background Clinical Care

Health Care Management/Administration

T he purpose of this manual is to help practitioners and healthcare

organizations implement appropriate and up-to-date nutrition
support practices based on the American Society for Parenteral and
Age Groups(s) of interest
Condition/Disease Specific Information

Depending on the categories chosen, the next query, subcategories of

Enteral Nutrition (A.S.P.E.N.) Guidelines, Safe Practices, and Stan-
dards of Practice.1-6 The goal of A.S.P.E.N. is to assure that every per- the above, appear and can be chosen to further specify the search.
son receives optimal nutrition care.7 In pursuing this vision, the Society Using this approach, the information on the CD matching the selected
establishes guidelines for the use of parenteral and enteral nutrition criteria will be brought into a printable view on the screen in the order
(which assess the strength of evidence behind each set of recommen- the material is contained in the Manual. Keywords can then be typed
dations); actively promotes education related to nutritional support; in to even further narrow the search of the material appearing on the
and stresses the importance of interdisciplinary collaboration in clin- screen. The other search function is to access whole chapters via the
ical care, education and research. Among A.S.P.E.N.’s objectives is the table of contents screen.
development of clinical nutrition standards and programs for special-
ists and generalists working in integrated healthcare systems.8 Contents of Manual
The concept for the first edition of this manual emerged from dis-
cussions of the A.S.P.E.N. Publications Committee in 1994-1995 and This manual describes methods for achieving safe and effective nutri-
was approved by the Board of Directors in 1995. The Committee rec- tion support. No attempt has been made to limit information to that
ognized the need for A.S.P.E.N. to articulate methods of nutrition sup- derived exclusively from randomized clinical trials or meta-analyses
port useful for the implementation of clinical practice guidelines as there are many clinical nutrition practices that remain to be com-
(CPG) in an era when medical practice is becoming increasingly inter- prehensively studied. At some future date, it may be possible to sub-
disciplinary and protocol-driven. In 2002, the Board of Directors ject the practices described in this practice manual to more formal
approved a second edition to update the content and offer a new CD analysis15 to develop more detailed CPG’s which meet recommended
format. criteria.16 In its current form, we believe the Manual can be used to
The editors have designed this manual to be useful to all practice dis- implement CPG’s by virtue of its clinical applicability, clinical flex-
ciplines within A.S.P.E.N. and to other healthcare professionals looking ibility, clarity and multidisciplinary process.16
for guidance on the methods of providing nutrition support including The manual does not specifically address indications for nutrition
practitioners, clinical administrators, and representatives of third-party support as they have been addressed elsewhere.1-3,5,17-19 With the down-
payors seeking to identify appropriate nutrition support practices. This ward pressure currently being exerted on the U.S. healthcare budget,
manual is a practical “how to” volume which provides focused infor- there will inevitably be heavy scrutiny of nutrition support and evo-
mation on the implementation of multidisciplinary nutrition support. It lution of the indications for nutrition support. In order to be effec-
was developed using a “traditional” approach that is based on practices tively assessed, healthcare practices need to be well-delineated and, to
that have evolved from relevant clinical research and multidisciplinary some extent, standardized. This assures competence, safety and cost-
clinical practices.9 The volume draws from the relevant medical and predictability, even when cost-effectiveness is unknown or unad-
nutrition literature, available textbooks, A.S.P.E.N.’s Core Curricu- dressed. Well-delineated practices can be adapted to specific
lum,10 and clinical expertise applied in a manner consistent with the institutional needs and reassessed on an ongoing basis through ran-
A.S.P.E.N. Standards, Safe Practices, and Guidelines.1-6,11-14. domized clinical trials and continuous quality improvement (CQI) pro-
grams. While the methods presented in this manual are state-of-the-art
and consistent with the A.S.P.E.N. Guidelines and Safe Practices, they
How To Use This Manual do not imply exclusion of other clinical approaches to specific situa-
The Compact Disc (CD) version of this manual is designed to create tions. As with all clinical medicine, the professional judgment of the
electronic portability and accessibility of this manual and to facilitate attending health care professional is the primary component of quality
searches for specific information. There are two search functions. The medical care and the propriety of a specific procedure must be assessed
first is a query-based searching function to find information specific to by the attending healthcare professional in light of all the circumstances
an inquiry. All paragraphs in the manual have been tagged for search- presented by the individual patient and the resources particular to the
ing according to the categories listed below. A series of levels of cat- locality of practice.4
egories are used in the search function. In the query mode the next level General nutrition support practices relevant to most types of
forces a choice of broad categories including: patients are presented in Chapters 1-9 and these are followed by Chap-

© 2005 A.S.P.E.N. www.nutritioncare.org. A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. xvii
Introduction

ters 10-32 on specific conditions which are commonly managed at Such teams may have either centralized, complete control over
least in part by nutrition support. In these disease-specific chapters the nutrition support or function in a consultative mode. Typical com-
authors describe the unique aspects of the conditions, including the position includes physician, nurse, dietitian, and pharmacist.20 Other
pattern and mechanism of nutrition depletion, unique nutrition require- individuals may be included. A.S.P.E.N. has previously published stan-
ments and potential complications of nutrition support that require spe- dards of practice for the nutrition-support physician, pharmacist, nurse
cific monitoring. Age-specific issues are included in each chapter. The and dietitian.11-14,23,24 An anthology of nutrition support team literature
remaining four chapters focus on practices relevant to specific sites of is available from A.S.P.E.N. While the roles of individuals on the nutri-
delivering nutrition care and the ethical issues important to nutrition tion support team have been well-described, the practice of nutrition
support. support is becoming increasingly interdisciplinary at the bedside.25
Some functions may be suitable for trained technicians under profes-
sional supervision. Important non-clinical roles of the NST include
Integration of Nutrition Support into Patient Care data collection for CQI related to nutrition support, analysis of the
In the context of this volume, nutrition support refers to the use of resultant data base, and implementation of indicated improvements in
foods and medical foods for specific conditions, enteral nutrition practices.
provided by tube-access to the gastrointestinal tract and parenteral The structures and reporting relationships of agencies providing
nutrition. The delivery of nutrition support is a multidisciplinary, spe- home nutrition support are potentially even more variable than those
cialized practice which is utilized for almost all types of patients and providing inpatient nutrition support, as the focus of the particular
extends beyond the hospital into alternative care sites such as long- home agency may be predominately for infusion care, nutrition sup-
term care facilities and homes. Differences in hospital size, patient port, nursing care or oncology management. The management of such
population, healthcare delivery setting, local expertise, organizational teams may be hospital-directed, nurse-agency directed, home-infusion
structure and financial payment relationships dictate that there cannot company directed, or report directly to an insurer. While the organiza-
be a single safe and effective system for providing nutrition support. tional structures conducive to providing nutrition support vary with the
Certain clinical activities are generally expected to reside in specific type of organization, it is still possible to describe clinical procedures
departments. utilized for patient care independent of organizational framework.5
One well-established model for providing nutrition support is the This volume provides such information.
Nutrition Support Team (NST).20-21 In its Standards, A.S.P.E.N. defines
the NST as, “A multi-disciplinary group of health care professionals Certification
with expertise in nutrition who aid in the provision of nutrition sup-
port.” While all of the functions of a formal NST relative to patient care The National Board of Nutrition Support Certification offers creden-
need to be performed, an NST is but one organizational approach to tialing for three of the major disciplines involved in nutrition support
meet nutrition needs of patients. Wesley has previously summarized — physicians, dietitians, and nurses. Nutrition Support certification of
the role and the perceived cost-effective benefits of nutrition support pharmacists is offered by the Board of Pharmaceutical Specialties. The
teams20: American Board of Physician Nutrition Specialists offers broad nutri-
tion certification for Physician Nutrition Specialists.
1. Recognition and treatment of malnutrition Certification by professional organizations relevant to nutrition
2. Reduction of mechanical and metabolic complications of enteral support can be used by hospitals as part of their process for defining
and parenteral nutrition clinical privileges.26 Some hospitals also establish a local credential-
3. Reduction of morbidity and mortality ing procedure for nutrition support such as passing a basic nutrition
4. Reduction in the cost of providing nutrition support by facilitating support examination or completing an orientation program. Such pro-
the appropriate use of enteral and parenteral therapies cedures are a part of the process of assuring quality nutrition support.
5. Provision for more cost-effective selection of products
6. Reduction in costly wastage of formula Accreditation
7. Selection of appropriate nutrition support equipment and devices
8. Reduction in length of stay and costs to the hospital In 1986, the Joint Commission on Accreditation of Healthcare Orga-
9. Reduction in liability exposure nizations (JCAHO), initiated its Agenda for Change.27 This culminated
10. Selection and monitoring of appropriate laboratory tests. in the 1995 and later editions of its Accreditation Manual for Hospitals
(AMH) and a new approach to assessing the adequacy of medical care,
While other models may meet the needs of particular environments, including nutrition.21 The goal was to reformulate JCAHO standards,
the NST can be viewed as the de facto gold standard for delivering develop performance indicators and redesign the accreditation survey
nutrition support. Some have justified personnel by using the projected process to make the process patient-focused. Similar changes have
cost savings from nutrition support teams resulting from decreased been made in the JCAHO Accreditation Manuals for Home Care and
medical complications and decreased nutrition product wastage. For Long-Term Care.28
example, the Centers for Disease Control & Prevention have provi- JCAHO defines nutrition care as, “intervention and counseling of
sionally determined that “trained personnel designated with the individuals to promote appropriate nutrition intake based on the nutri-
responsibility to insert and maintain the intravascular devices provide tional assessment and information about food, other sources of nutri-
a service that effectively reduce catheter-related infections and overall ents, and meal preparation consistent with the patient’s cultural
costs”.22 They further state, “As with vascular devices used for other background and socioeconomic status. Nutrition therapy, a component
purposes, the use of specially trained personnel to inspect and main- of medical treatment, includes enteral and parenteral nutrition”.4 The
tain the catheter appears to reduce the rate of infection in patients A.S.P.E.N. standards for nutrition support of hospitalized adult and
receiving TPN [total parenteral nutrition].” pediatric patients are consistent with the JCAHO approach.1,2,29,30

xviii A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. © 2005 A.S.P.E.N. www.nutritioncare.org.
 Introduction

Clinical Pathways 4. A.S.P.E.N. Board of Directors and The Clinical GuidelinesTask

Force. Guidelines for the use of parenteral and enteral nutrition in
One mechanism by which clinical care standards, best management adult and pediatric patients. J Parenter Enteral Nutr 2002; 26
practices, cost-containment and CQI activities can be integrated and (1 Suppl):1SA-138SA.
focused is by the use of Clinical Pathways. Clinical Pathways are most 5. A.S.P.E.N. Board of Directors. Standards for home nutrition sup-
commonly and most effectively developed locally through the involve- port. Nutr Clin Pract 1999; 14:151-162.
ment of affected individuals and organizational entities to develop a 6. Task Force for the Revision of Safe Practices for Parenteral Nutri-
standardized way of managing specific medical problems.31,32 With the tion. Safe practices for parenteral nutrition. J Parenter Enteral
use of such algorithms, medical orders and nursing procedures are Nutr 2004;28:S39-S70.
largely incorporated into protocols and expected outcomes are defined. 7. A.S.P.E.N. Board of Directors. Itinerary for tomorrow. A.S.P.E.N.’s
Medical charting may be limited to describing variances from the path-
new strategic plan. Nutr Clin Pract 1995; 10:243-247.
way or from expected outcomes in contrast to traditional descriptive
8. Eddy DM. Practice policies: Where do they come from? JAMA
medical charting.33 Such pathways can be applied to specific diagnoses
1990; 263(9):1265-1275.
(e.g. pneumonia) or to medical practices such as the provision of
9. Gottschlich MM, Matarese LE, Shronts EP. Nutrition Support
enteral or parenteral nutrition. Ideally, local clinical pathways are
Dietetics Core Curriculum. 2 ed. Silver Springs, MD: A.S.P.E.N.,
based on a thorough assessment of the relevant medical literature and
1993.
consideration of guidelines and standards of care established by
10. Gottschlich MM.(ed). The Science and Practice of Nutrition
national professional societies or other experts who have developed
Spport: A Case-Based Core Curriculum. A.S.P.E.N./Kendall
guidelines for specific diagnoses or procedures.
Hunt Dubuque, IO. 2001.
Patient outcome data and variances from the CPG or clinical path-
ways can be analyzed to improve local practices or to benchmark local 11. A.S.P.E.N. Board of Directors. Standards of practice: Nutrition
practices and outcomes versus historical performance or other data support pharmacist. Nutr Clin Pract 1999; 14:275-281.
sets.31,34 Such analyses can be restricted to medical issues, financial 12. A.S.P.E.N. Board of Directors. Standards of practice for nutri-
issues, or most commonly, a combination of these.34 Since best prac- tion support dietitians. Nutr Clin Pract 2000; 53:53-59.
tices develop in evolutionary fashion, such a process needs to become 13. A.S.P.E.N. Board of Directors. Standards of practice: Nutrition
a major part of institutions’ CQI activities. It is anticipated that the pro- support nurse. Nutr Clin Pract 2001; 16:56-62.
cedures and paradigms included in this manual can be used by local 14. A.S.P.E.N. Board of Directors. Standards of practice: Nutrition
groups charged with the responsibility for developing clinical path- support physician. Nutr Clin Pract 2003;18:270-275.
ways, for assessing the efficacy or cost-effectiveness of local nutrition 15. Agency for Health Care Policy and Research. Clinical Practice
practices or for understanding the procedures involved in appropriate Guideline Development (AHCPR Publication No 93-0023). 1993.
and safe utilization of nutrition support. A.S.P.E.N. has also developed Rockville, MD, U.S. Department of Health and Human Service.
a generic set of clinical pathways for the use of parenteral and enteral 16. Clinical Practice Guidelines—Directions for a New Program.
nutrition which may be helpful in this process.4 Washington, DC: National Academy Press, 1990.
17. American College of Physicians. Parenteral nutrition in patients
receiving cancer chemotherapy. Ann Intern Med 1989; 110(9):
Acknowledgements 734-736.
The editorial board expresses its appreciation to the authors for updat- 18. American Gastroenterological Association. Medical position
ing this manual and expanding its content and to the reviewers who statement: guidelines for the use of enteral nutrition. Gastroen-
worked with the authors to assure that the practices described are con- terology 1995; 108:1280-1301.
sistent with the best current scientific evidence and clinical judgment. 19. Sitzmann JV, Pitt HA. Statement on guidelines for total parenteral
Just as this manual has been developed for a multidisciplinary audi- nutrition. Dig Dis Sci 1989;(4):34-496.
ence, the process of its development has involved the multiple profes- 20. Wesley JR. Nutrition support teams: past, present, and future.
sional disciplines of A.S.P.E.N. in an effective interdisciplinary Nutr Clin Pract 1995; 10(6):219-228.
collaboration. Acknowledgement of the first edition authors can be 21. JCAHO. 2004 Comprehensive Accreditation Manual for Hospi-
found following the text of each chapter and their chapter base for this tals: The Official Handbook (CAMH). Oakbrook Terrace, IL,
second edition is appreciated. Special accolades are in order for Dr. 2004.
Peggi Guenter whose tireless nurturing of the chapters and the edito- 22. Department of Health and Human Services, Centers for Disease
rial staff on behalf of the A.S.P.E.N. administration made final publi- Control and Prevention. Draft guideline for prevention of intravas-
cation of the second edition possible. cular device-related infections. Fed Reg 1995; 60:49978-50006.
23. Greer FR. Reimbursement for foods for special dietary use. Pedi-
REFERENCES atrics 2003; 111(5 Pt 1):1117-1119.
1. A.S.P.E.N. Board of Directors and Task Force on Standards for 24. Mattox TW. Drug use evaluation approach to monitoring use of
Specialized Nutrition Support for Hospitalized Adult Patients. total parenteral nutrition: a review of criteria for use in cancer
Standards for specialized nutrition support: Adult hospitalized patients. Nutr Clin Pract 1993; 8(5):233-237.
patients. Nutr Clin Pract 2002; 17:384-391. 25. Vogel DP. Patient-focused care. Am J Hosp Pharm 1993;
2. A.S.P.E.N. Board of Directors and Task Force on Standards for 50(11):2321-2329.
Specialized Nutrition Support for Hospitalized Pediatric Patients. 26. Davis AM, Baker SS, Leary RA. Advancing clinical privileges for
Standards for specialized nutrition support: Hospitalized pediatric nutrition support practitioners: The dietitian as a model. Nutr Clin
patients. Nutr Clin Pract 2005; 29:103-116. Pract 1995; 10:98-103.
3. A.S.P.E.N. Board of Directors. Standards for nutrition support for 27. Dougherty D, Bankhead R, Kushner R, Mirtallo J, Winkler M.
adult residents of long-term care facilities. Nutr Clin Pract 1997; Nutrition care given new importance in JCAHO standards. Nutr
12:284-293. Clin Pract 1995; 10:26-31.

© 2005 A.S.P.E.N. www.nutritioncare.org. A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. xix
Introduction

28. JCAHO. 2004 Comprehensive Accreditation Manual for Long 32. Lykins TC. Nutrition support clinical pathways. Nutr Clin Pract
Term Care (CAMLTC). Oakbrook Terrace, IL: Joint Commission 1996; 11(1):16-20.
Resources, 2004. 33. Hronek C. Redesigning documentation: clinical pathways, flow-
29. August DA, Kushner RF. A.S.P.E.N. Standards for Nutrition Sup- sheets, and variance notes. MedSurg Nurs 1995; 4(2):157-159.
port: Hospitalized Patients. Nutr Clin Pract 1995; 10(6):206-207. 34. Clare M, Sargent D, Moxley R, Forthman T. Reducing health care
30. JCAHO Standards: Environment of Care List of Standards TX.4. delivery costs using clinical paths: a case study on improving hos-
Retrieved 10/11/2004 from http://www.nyspi.org/jcho/jcahotx pital profitability. J Health Care Finance 1995; 21(3):48-58.
4.htm.
31. Flanel DF, Fairchild MM. Continuous quality improvement in inpa-
tient clinical nutrition services. J Am Diet Assoc 1995; 95:65-74.

xx A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. © 2005 A.S.P.E.N. www.nutritioncare.org.
 SECTION EDITOR
Beverly Holcombe, PharmD, BCNSP
I
Fundamentals of Nutrition
Support Practice and
Management
1 Nutrition Assessment and Decision Making

2 Nutritional Goals and Requirements

3 Enteral Access and Infusion Equipment

4 Enteral Formulations

5 Enteral Nutrition Implementation and Management

6 Parenteral Nutrition Access and Infusion Equipment

7 Parenteral Nutrition Formulations

8 Parenteral Nutrition Implementation and Management

9 Drug Nutrient Interactions

 Kathy Pesce-Hammond, MS, RD, LD, CNSD, RN, CNSN;
Jacqueline Wessel, MEd, RD, CSP, CNSD, CLE
1
Nutrition Assessment and
Decision Making

I n clinical practice, the nutrition assessment process focuses on

parameters that are easy to obtain, cost-effective, age-appropriate,
and clinically relevant. Nutrition assessment involves carefully selected
by general hospital staff. An example of a simple screening tool is
shown in Table 1-1.
B. Screening should be done within 24 hours of admission (for hospi-
objective parameters, in combination with a comprehensive physical talized patients) or at the outpatient visit.
exam and subjective parameters, to provide the best information for C. Nutrition screening of the elderly should not be overlooked, in view
identifying those with preexisting malnutrition or those at risk. of the prevalence of chronic illness and socioeconomic factors that
In this chapter, discussion of pediatric and adult assessment has are likely to place them at nutritional risk.9,10
been combined. Much of pediatric and adult nutrition assessment is D. Screening parameters unique to pediatric patients include gesta-
similar. Concepts unique to pediatrics are development of oral motor tional age (for neonates and infants), weight for age or length, and
skills and growth. This chapter will also describe the nutrition care head circumference for children less than 2 years of age. Growth
process. parameters are plotted on an appropriate growth chart such as the
National Center for Health Statistics growth charts.11,12
I. Background: The Nutrition Care Process
II. Nutrition Screening
III. Nutrition Assessment III. Nutrition Assessment
IV. Nutrition Support Decision Making
A. Introduction
References
1. The nutrition assessment process identifies patients who are at
nutritional risk.
I. Background: The Nutrition Care Process a) Adults who are nutritionally-at-risk are those who have actual
or potential for developing malnutrition. Factors indicative
A. Nutrition care process: Nutrition screening and assessment are part
of malnutrition include involuntary loss or gain of ≥10% of
of the nutritional care process and comprise a series of steps with
usual body weight within 6 months or ≥5% of usual body
built-in feedback.1,2
weight in 1 month; body weight of 20% over or under ideal
B. Nutrition assessment is a systematic process of obtaining, verifying,
and interpreting data to make decisions about the nature and cause body weight, especially in the presence of chronic disease or
of nutrition-related problems. The type of data collected depends on increased metabolic requirements; and inadequate nutrition
the practice setting.1 intake, including an impaired ability to ingest or absorb food
C. The nutrition assessment process includes screening and a more adequately.13
comprehensive assessment of nutritional status. Data from nutrition b) Neonates who are nutritionally-at-risk are those who are very
screening and the more comprehensive nutrition assessment are low birth weight (<1500 gm) or low birth weight (<2500 gm)
used to identify nutritional problems, including malnutrition, the even in the absence of gastrointestinal, pulmonary, or cardiac
risk for developing malnutrition, or specific nutrition-related prob- disorders; have birth weight less than 2 standard deviations
lems. The nutrition assessment and diagnostic process is not static below the mean; or have acute weight loss of 10% or more.3
but continuous. c) Children are nutritionally-at-risk if they have a weight for
D. Nutrition interventions are specific to nutrition diagnoses. All inter- length or weight for height less than the 10th percentile or
ventions must be based on scientific principles and, when available, greater than the 90th percentile, increased metabolic require-
evidence-based practice.2 ments, impaired ability to ingest or tolerate oral feedings,
E. Nutrition monitoring involves periodic measurement and review documented inadequate provision or tolerance of nutrients,
of the individual’s assessment data for the purpose of modifying or inadequate weight gain or a significant decrease in an
interventions as needed to achieve desired clinical outcomes.2 See individual’s usual growth percentile.3
Figure 1-1 for an illustration of the process.2,3 2. Alterations in nutritional status occur because of altered nutritional
intake, malabsorption, or altered metabolism.14
3. Uncomplicated malnutrition is caused by an imbalance between
II. Nutrition Screening
nutrient intake and requirements in the absence of disease or
A. Nutrition screening is the first step in the nutrition care process.1 trauma.15
Screening identifies individuals who require a more comprehensive 4. Historically, nutrition assessment has consisted of a combination
nutrition assessment and who are at nutritional risk.4–8 Screening of subjective and objective parameters. Subjective parameters
parameters should be simple, efficient, and able to be implemented include the medical and nutrition histories. Objective parameters

© 2005 A.S.P.E.N. www.nutritioncare.org. A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. 3
S E C T I O N I Fundamentals of Nutrition Support Practice and Management

FIGURE 1-1. Adult Nutrition Screening and Assessment Algorithm

Admission
Inpatient
Evaluation of care no Discharge
care setting longer planning
Acute required
Patient
screening Not at risk inpatient
care
Progressing
required
toward goals
At risk

Development Implementation
Patient Patient Goals Termination
of nutrition of nutrition
assessment monitoring achieved of therapy
care plan care plan
Change in
status

Patient
reassessment
and updating
of nutrition
care plan

Reprinted with permission from the American Society of Parenteral and Enteral Nutrition.2

include the physical examination, anthropometric measurements, 3. Subjective Global Assessment (SGA): The SGA is a nutritional
various body composition methodologies, laboratory tests, and assessment tool that relies on history of weight and dietary
clinically specific parameters.16 change, persistent gastrointestinal symptoms, functional capac-
B. Medical and nutritional history ity, effects of disease on nutritional requirements, and physical
1. Medical history includes acute and chronic diseases, medications, appearance. The SGA has been well tested and is widely accepted
diagnostic procedures, surgeries, and other therapies (ie, chemo- as a practical and reliable tool for nutrition assessment.18,19 On
therapeutics, immunosuppressives).2,8,17 The review of medica- the basis of these parameters, clinicians categorize patients’
tions should include prescription and nonprescription drugs, nutritional status as well nourished, moderate or suspected
vitamin and mineral supplements, and other over-the-counter malnutrition, or severe malnutrition. See Table 1-3 for SGA
drugs. History also includes alternative medical treatments and features.
socioeconomic status whenever possible. Medical history infor- C. Physical examination
mation specific to pediatrics includes maternal and prenatal 1. The physical examination is an excellent tool to help evaluate
health history; perinatal history; gestational age; history of pre- nutritional status.20–22 A physical examination uses a systems
maturity; birth weight; whether small or large for gestational approach and includes a logical assessment from head to toe. See
age; and growth patterns for weight, length, and head circum- Table 1-4 for full physical examination guidelines.
ference. Growth records can typically be obtained with per- 2. Specific to pediatrics is the assessment of sexual maturation using
mission from the primary care physician. Other components of Tanner staging (Table 1-5). Tanner staging is based on the devel-
the history are developmental history including problems with opment of secondary sex characteristics. In adolescents, nutrition
hypotonia or hypertonia; and any problem with developmental assessment findings may be altered depending on the stage of sex-
milestones. ual maturity. In males the peak of the rapid height growth occurs
2. Nutritional history includes recent changes in appetite or weight, in Tanner Stage 4. In females by the onset of menarche, the major-
ability to eat, bowel habits, activity level, nutrient intake, use of ity of linear growth has been completed. However, girls who enter
diets, feeding skills, types of feeding equipment used, food aller- puberty early may have more linear growth after menarche than
gies or intolerances, and use of oral supplements (Table 1-2). The girls who enter puberty later. The rate of weight gain approxi-
history is important to set a baseline to assist in establishing the mates the velocity of linear growth, although in females, the peak
etiology of nutritional impairment, such as impediments to eating, weight gain velocity occurs 6 to 9 months before the height rate
absorbing, or both.15 change.23,24
Nutritional history unique to pediatrics includes interest in D. Anthropometric parameters
feeding; feeding refusals; duration of feedings; frequency and 1. Body weight25
times of feedings; whether getting up at night to feed; feeding jags; a) Body weight measurement26
problems in acceptance of textures; suck and swallow quality; and (1) Standing weight: Use uniform clothing, equipment, and
symptoms of gastroesophageal reflux. time of day and document these data with the weight

4 A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. © 2005 A.S.P.E.N. www.nutritioncare.org.
 S E C T I O N I Fundamentals of Nutrition Support Practice and Management

TABLE 1-1. Admission Nutrition Screening Tool

A. Diagnosis D. Weight history

If the patient has at least ONE of the following diagnoses, circle and pro-
Any recent unplanned weight loss? No____ Yes ____
ceed to section E to consider the patient AT NUTRITIONAL RISK and stop
here. Amount (lbs or kg) _______________

Anorexia nervosa/bulimia nervosa If yes, within the past _________ wks or _________ mos
Malabsorption (celiac sprue, ulcerative colitis, Crohn’s disease, short-
Current weight (lbs or kg) _______________
bowel syndrome)
Multiple trauma (closed-head injury, penetrating trauma, multiple Usual weight (lbs or kg) _______________
fractures)
Decubitus ulcers Height (ft, in, or cm) _______________
Major gastrointestinal surgery within the last year Find percentage usual wt – current wt
Cachexia (temporal wasting, muscle wasting, cancer, cardiac) 2 100 = _____% wt loss
of weight loss: usual wt
Coma
Diabetes Compare the % wt loss with the chart values and circle the
End-stage liver disease appropriate value
End-stage renal disease
Nonhealing wounds Length of time Significant (%) Severe (%)

1 wk 1–2 >2
B. Nutrition intake history 2–3 wks 2–3 >3
If the patient has at least ONE of the following symptoms, circle and pro- 1 mo 4–5 >5
ceed to section E to consider the patient AT NUTRITIONAL RISK and stop 3 mos 7–8 >8
here. 5+ mos 10 >10

Diarrhea (>500 mL 2 2 days) If the patient has experienced a significant or severe weight loss,
Vomiting (>5 days) proceed to section E and consider the patient AT NUTRITIONAL RISK.
Reduced intake (< 1⁄2 normal intake for >5 days)
E. Nurse assessment
C. Ideal body weight standards
Using the above criteria, what is this patient’s nutritional risk?
Compare the patient’s current weight for height to the ideal body weight (check one)
chart on the back of this form.
____ LOW NUTRITIONAL RISK
If at <80% of ideal body weight, proceed to section E to consider the
patient AT NUTRITIONAL RISK and stop here. ____ AT NUTRITIONAL RISK

From Kovacevich DS, Boney AR, Braunschweig CL, et al. Nutrition risk classification: a reproducible and valid tool for nurses. Nutr Clin Pract. 1997;12:20–25 with permission.

measurement. Assess the patient’s ability to stand. Balance (1) A commonly used method for determining IBW in clinical
or recalibrate the scale and position the patient on the cen- settings is the Hamwi rule of thumb method.27 In this
ter of the scale base. Obtain the measurement from the bal- method, males are given 106 lbs (48 kg) for the first 5 ft
ance scale or digital readout. (1.5 m) and an additional 6 lbs (2.7 kg) for each inch
(2) Bed or sling weight: Roll the patient to one side and place (2.54 cm) over 5 ft. Females are given 100 lbs (45 kg) for
the sling under the patient. Position the sling under the the first 5 ft and an additional 5 lbs (2.3 kg) for each inch
patient evenly. Attach the sling to the scale and record over 5 ft. To account for a large frame, 10% of body
the weight measurement. weight is added; and for a small frame, 10% of body
(3) Wheelchair weight: Position the ramp for wheelchair weight is subtracted from the initial calculated weight.
access. Weigh the empty wheelchair and record the weight (2) Reference data on body weight are available from the
of the chair. Repeat the procedure with the patient in the National Health and Nutrition Examination Surveys
chair and deduct the chair weight from the total weight. (NHANES). These reference tables provide the most up-
(4) Pediatric weights are measured nude in infants and toddlers, to-date weight available for the US population and reflect
and in underpants only for older children, using infant national diversity.28,29 See Tables 1-6 and 1-7.
scales or a platform beam balance scale. (3) Adjustments in IBW estimates are made for patients
b) Ideal body weight (IBW) with amputations to account for the missing body part(s)

© 2005 A.S.P.E.N. www.nutritioncare.org. A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. 5
S E C T I O N I Fundamentals of Nutrition Support Practice and Management

TABLE 1-2. Components of the Medical and TABLE 1-3. Features of Subjective Global Assessment
Nutritional History (SGA)

Diet History (usual meal pattern), restrictions, alter- (Select appropriate category with a checkmark, or enter numerical
native, complementary value where indicated by “#”.)
Allergies Food, intolerances, avoidances
A. History
Supplementation Vitamin, mineral, oral nutritional drinks, other
products 1. Weight change
Weight Recent changes—intentional, nonintentional Overall loss in past 6 mos: amount = # __________ kg;
Dental/oral Chewing, swallowing ability, salivation, denti- % loss = # __________
tion, pain Change in past 2 wks: ____ increase, ____ no change,
Mental status Altered mental status, delirium, dementia ____ decrease
Gastrointestinal Nausea, vomiting, heartburn, bloating,
2. Dietary intake change (relative to normal)
dyspepsia, gas, diarrhea, constipation,
____ No change
steatorrhea
____ Change ____ duration = # __________ weeks
Chronic disease Long-term diseases affecting utilization of
____ Type: ____ suboptimal solid diet
nutrients
____full liquid diet
Surgery Surgical resection or disease of gastrointesti-
____ hypocaloric liquids ____ starvation
nal tract
Medications Prescription, over the counter, other 3. Gastrointestinal symptoms (that persisted for >2 wks)
Drug/alcohol Use, amount ____ none____ nausea ____ vomiting
Economic factors Food procurement, preparation, physical ____ diarrhea ____ anorexia
limitations of food preparation, public aid
4. Functional capacity
assistance
____ No dysfunction (eg, full capacity)
Cultural factors Religion, education, and customs and their
____ Dysfunction ____ duration = # __________ wks
influence on eating patterns
____ Type: ____ working suboptimally
Physical activity Occupation, exercise regimen, sleep/rest
____ ambulatory
pattern
____ bedridden

5. Disease and its relation to nutritional requirements

Primary diagnosis (specify)
(Figure 1-2).30 Estimated ideal weight = [(100 – percent of Metabolic demand (stress): ____ no stress ____ low stress
amputation)/100] × estimated ideal weight for original
____ moderate stress ____ high stress
height.
c) Height/length/head circumference B. Physical (for each trait specify 0 = normal, 1+ = mild,
(1) Pediatrics: Recumbent lengths are measured with a length 2+ = moderate, 3+ = severe)
board for infants and toddlers and a stadiometer for chil- # ____ loss of subcutaneous fat (triceps, chest)
dren who are more than 3 years old (if they can stand). # ____ muscle wasting (quadriceps, deltoids)
Heights are measured in stocking feet and with feet
# ____ ankle edema
together, back straight, and arms hanging freely. Head cir-
# ____ sacral edema
cumference is measured until approximately 36 months.
A flexible, narrow tape measure is used. Ideally, three # ____ ascites
measurements are done, and the results averaged. Arrested C. SGA rating (select one)
head growth (microcephaly) may indicate cranial defects ____ A = Well nourished
or abnormal brain growth; accelerated growth may indi-
____ B = Moderately malnourished (or suspected of being
cate catch-up growth or developmental defects (eg, hydro-
malnourished)
cephalus).
(2) Height is measured directly or indirectly. Direct methods ____ C = Severely malnourished
using a stadiometer or measuring rod require the patient
to stand erect or lie flat. For those who cannot be moved Reprinted with permission from Detsky AJ, McLaughlin JR, Baker JP, et al. What is
and do not have musculoskeletal deformities, a recum- subjective global assessment of nutritional status? J Parenter Enteral Nutr. 1987;11:9.
bent bed length measurement can assist in determining
height. Frame size can be determined by dividing the
height in centimeters by the circumference of the wrist in illustrates guidelines used to interpret weight data, including
centimeters. ideal, current, and usual weight and percentage of weight
2. Interpretation of weight data change. Of these, the change in recent weight most accurately
a) Comparison to ideal and usual weight: Weight comparisons predicts nutritional risk.29 When obtainable, the weight history
in adults can indicate severity of malnutrition. Table 1-8 of the individual is more helpful than comparison to IBW. Cau-

6 A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. © 2005 A.S.P.E.N. www.nutritioncare.org.
 TABLE 1-4. A Sample Outline for the Nutrition-Focused Physical Examination

This table is not intended to be a complete list of nutritional or non-nutritional causes for presenting physical signs and symptoms. This table serves only as an example and may need to be modified
using clinical judgment.

What Exam May Reveal in Regard to

System Nutrition Physical Exam Focus Nutritional/Metabolic Status Non-Nutritional Examples of Similar Findings

General Using inspection:

© 2005 A.S.P.E.N. www.nutritioncare.org.

survey Body weight for height, alertness, any general wasting of Lack of calories and protein, ability to independently Endocrine disorders, osteogenic disorders, menopausal
muscle or fat stores, coordination, speech, growth, body feed, or degree of vitamin, mineral, or trace element changes
movements deficiency

Vital signs Temperature Increased temperature—increase in energy and fluid Vital signs reflect major disease or illness factors and
requirements nutrition assists in preventing or decreasing severity
Respiration Increased rate, labor-intense—influences calorie and Increases with hyperthyroidism, increased temperature,
protein requirements along with quantity of food eaten anxiety, pain, exercise, medication
at one time and type of food (eg, calorically dense)
Pulse Heart rate increases with anemia Decreases with sleep/rest, organic heart disease,
hypothyroidism, and medications
Blood pressure Diet modification such as calculated sodium used for Blood loss, heart attack and heart failure, irregular heart
high blood pressure rate, and certain medications lower blood pressure

Dehydration lowers blood pressure

Skin Inspect and palpate:

Color Pallor—iron, folate, or B12 deficiency Skin pigmentation disorders, disease of the bone
marrow, hemorrhage, arsenic ingestion, steroids, low
volume, low perfusion states
Lesions, pigmentation Dermatitis—essential fatty acid, zinc, niacin, or Hypersensitivity reactions, connective tissue disease,
riboflavin deficiency burns, Addison’s disease

Pellagrous dermatitis—niacin, tryptophan Thermal, sun, or chemical burns; Addison’s disease,

psoriasis
Flaky paint dermatitis—hyperpigmented areas on thighs,
buttocks—protein
Petechiae, ecchymosis Vitamin C deficiency, vitamin K deficiency Hematologic disorder, trauma, liver disease, anticoagu-
lant disorder, Cushing’s disease
Wound healing degree, pressure ulcers Poor wound healing—zinc, vitamin C, protein deficiency Diabetes, use of steroids, AIDS, malignancy

A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed.

Moisture, turgor Poor skin turgor—poor fluid status Heart failure, kidney disease, liver disease

7
S E C T I O N I Fundamentals of Nutrition Support Practice and Management

(Continued)
8
TABLE 1-4. A Sample Outline for the Nutrition-Focused Physical Examination (Continued)

What Exam May Reveal in Regard to

System Nutrition Physical Exam Focus Nutritional/Metabolic Status Non-Nutritional Examples of Similar Findings

Skin Sweat may influence temperature and fluid status

(Continued)
Edema—generalized (anasarca) with accumulation of
serum in connective tissue
Texture Scaly, dry—vitamin A deficiency or essential fatty acid Hypothyroidism, dermatitis, hygiene, uremia, psoriasis,
deficiency environmental factors, aging
Little lumps (or nodules) on elbows or eyelids present in

A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed.

those with high cholesterol levels
Temperature Warmth will influence temperature status and hence
fluid and energy
Cold will influence temperature status and energy
S E C T I O N I Fundamentals of Nutrition Support Practice and Management

demand

Nails Inspect and palpate:

Shape, color, angle contour, lesions Spoon-shape (koilonychia)—iron deficiency COPD, heart disease, aortic stenosis
Lackluster, dull—protein Infection, congenital systemic lupus erythematosus
Mottled, pale, poor blanching—vitamin A, C

Scalp/hair Inspect and palpate:

Shape and symmetry of scalp, masses Softening or craniotabes—vitamin D deficiency; open Hydrocephalus
anterior fontanel (usually closes by ~18 mos of age)

Hair distribution, color, and texture Dull, lackluster, thin, sparse—protein, iron, zinc, or Chemical effects, hypothyroidism, chemotherapy,
essential fatty acid deficiency psoriasis, color treatment
Easily pluckable—protein deficiency

Alternating bands of light and dark hair in young children Chemically processed or bleached hair
(flag sign)—protein deficiency

Face (general) Inspect and palpate:

Shape and symmetry May influence ability to eat if masses are present See skin assessment
Moon face—protein-calorie deficiency
Bilateral temporal wasting—protein-calorie deficiency
Color, temperature, lesions, texture Review skin assessment Usually affected by a neuromotor dysfunction or disease
Pallor—iron, folate, or B12 deficiency

© 2005 A.S.P.E.N. www.nutritioncare.org.

 Cranial nerves (really part of the neurological exam, but Cranial nerves are not usually a direct cause of nutrition de-
more practical at this point) ficiency but once injured affect nutritional status indirectly

CN V (trigeminal)— assess muscles of mastication— Control main muscles of chewing Neuromuscular disorder, paralysis
test by clenching teeth and feeling masseter and
Note asymmetry in jaw movement or pain clenching
temporal muscles
teeth

CN VII (facial)—test by raising eyebrows, frowning, smil- Weakness, asymmetry affect chewing and holding food Bell’s palsy, paralysis
ing, showing upper and lower teeth

© 2005 A.S.P.E.N. www.nutritioncare.org.

CN IX (glossopharyngeal)—gag reflex Supplies nerve stimulation to muscle in throat, provides
intervention to parotid glands that secrete saliva to
assist with digestion, and stimulates the back one third
of tongue with taste and touch

CN X (vagus)—tickle back of throat—gag reflex, phonate Provides impulses to throat to allow movement and swal- Brain stem tumor, neck injury, lesion on cranial nerve,
“ahh” and watch movement of soft palate and pharynx, lowing, peristalsis motion of the gut in digesting food; vocal cord weakness
voice quality note any dysphagia, fluids regurgitating through nose
(important to note gag reflex if placing tube since post-
pyloric placement needed if absent to prevent aspiration)

CN XI (accessory)—test by shrugging shoulders and Moves trapezius and sternomastoid muscle Neck injury, torticollis
moving chin to left and right against resistance

CN XII (hypoglossal)—test by sticking tongue out and Movement of tongue Lower motor neuron lesions
wiggling side to side Improper alignment and movement may influence the Bilateral upper motor neuron lesion
ability to chew properly

Eyes Inspect and palpate:

Adjustment to night Night blindness—vitamin A deficiency Tapetoretinal degeneration, status post panretinal
photocoagulation, photic exhaustion (all day in bright
Any vision impairment Affects ability to shop, cook, eat, etc
sun; short-term effects), advanced glaucoma

Skin color and texture, cracks, brows, lids Cracked and reddened corners of eyes (angular Infection, foreign objects, allergic reaction, seborrheic
palpebritis)—riboflavin, niacin deficiency dermatitis
Dry, grayish, yellow or white rings of whitish-yellow
cholesterol deposits around edges of eye

Sclerae Foamy spots on eyes (Bitot’s spots)—vitamin A deficiency Pterygium, Gaucher’s disease
Dull, dry rough appearance—vitamin A deficiency Chemical, environmental
Pallor—iron, folate, or B12 deficiency

(Continued)

A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed.

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S E C T I O N I Fundamentals of Nutrition Support Practice and Management
10
TABLE 1-4. A Sample Outline for the Nutrition-Focused Physical Examination (Continued)

What Exam May Reveal in Regard to

System Nutrition Physical Exam Focus Nutritional/Metabolic Status Non-Nutritional Examples of Similar Findings

Eyes Conjunctiva Dull, dry, rough appearance to inner lids (conjunctival Chemical, environmental
(Continued) xerosis) —vitamin A deficiency
Cornea Dull, milky, or opaque (corneal xerosis)—vitamin A Rule out cataracts
deficiency

Softening (keratomalacia)—vitamin A deficiency

Nose Inspect and palpate external and internal structures:

A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed.

Shape, septum, nares, mucosa, discharge Influences decision of nasal tube placement if polyps,
obstruction, or prior surgery present. Redness of sinus
tract should also be noted. Size of nare to use when
inserting tube (may choose larger one).
S E C T I O N I Fundamentals of Nutrition Support Practice and Management

Skin Scaly, greasy, with gray or yellowish material around

nares (nasolabial seborrhea)—riboflavin, niacin, pyridox-
ine deficiency
CN I (olfactory) Identify smell that influences food eaten—favorable
smells assist with enhancing appetite

Oral cavity:
Lips Inspect and palpate:
Color, temperature, texture, cracking, lesions, symmetry Bilateral cracks, redness of lips (angular stomatitis)— Poor-fitting dentures, herpes, syphilis
riboflavin, niacin, pyridoxine deficiency

Vertical cracks of lips (cheilosis)—riboflavin, niacin AIDS (Kaposi’s sarcoma), environmental exposure
deficiency
Mucosa Inspect and palpate:
Color, texture, lesions, integrity, moisture Pallor—iron, B12, or folate deficiency Side effects of medications

Dryness—hydration status

Cracking—vitamin C deficiency

General inflammation—B complex, iron, C deficiency Infection, trauma, dryness with aging, autoimmune dis-
orders, cancer therapy, irritants, drug therapy

Tongue Inspect and palpate:

Color Magenta color—riboflavin deficiency Crohn’s disease, infection

Beefy red color and atrophied taste—niacin, folate, White overgrowth may be a sign of fungal infection

© 2005 A.S.P.E.N. www.nutritioncare.org.

riboflavin, iron, B12 deficiency
 Texture, moisture, lesions, symmetry Smooth, slick, loss of papillae—folacin, niacin, iron, Cancer therapy, aging, dryness of mouth, influenza, mul-
riboflavin, B12 deficiency tiple medications, diabetes mellitus

Distorted taste (dysgeusia), Diminished taste Zinc deficiency

(hypogeusia)

Teeth Inspect and palpate:

State of repair, missing, dentures, color Influence ability to chew and texture of food able to Trauma, syphilis, aging, poor dental hygiene, improper-
handle fitting dentures

© 2005 A.S.P.E.N. www.nutritioncare.org.

Teeth vary in shades of white

Excess caries—excess sugar Eating disorders, xerostomia, radiation, poor dental

hygiene

White or brownish patches (mottled)—fluoride excess Enamel hypoplasia, erosion

Gums Inspect and palpate:

Lesions, integrity Spongy, bleeding, receding—vitamin C deficiency Phenytoin and other medication, poor hygiene, lym-
phoma, polycythemia, thrombocytopenia
Moisture Dry—fluid status

Color Pale—iron deficiency

Neck Inspect and palpate:

Vasculature appearance Distended neck veins—fluid status (overload) Disease or illness processes

Range of motion Influences ability to coordinate mechanics of eating

Symmetry, midline structures (trachea, thyroid) Enlarged thyroid—iodine deficiency Cancer, allergy, cold, infection

Parotid gland Located anterior to earlobe—bilateral enlargement— Cysts, tumor, hyperparathyroidism

protein deficiency or bulimia

Thorax and
lungs:
Thorax Inspect and palpate:
(general) Muscle and fat, accessory muscle usage (use of abdomi- Prominent bony skeleton with muscle and fat wasting—
nal muscles, some of muscles between ribs, and some calorie and protein depletion
neck muscles besides the diaphragm) Respiratory muscle mass and strength decrease with
calorie protein depletion

Lungs While assessing this region also note any vascular Assessment should be noted to ensure that access
access devices present device is intact without redness or drainage or swelling
so that nutrition therapy can be continued without risk of
complications

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S E C T I O N I Fundamentals of Nutrition Support Practice and Management

(Continued)
12
TABLE 1-4. A Sample Outline for the Nutrition-Focused Physical Examination (Continued)

What Exam May Reveal in Regard to

System Nutrition Physical Exam Focus Nutritional/Metabolic Status Non-Nutritional Examples of Similar Findings

Thorax and Inspect and palpate: Most causes are non-nutritional but influence nutrition
lungs: Rate and depth of respiration Increased and labor–intense uses more energy therapy:
(Continued) Fluid status may influence fluid requirements and nutri-
Fremitus (usually assessed by having patient say “99”;
tion regimen such as parenteral nutrition fluid volume
the vibration in examiner’s hand is decreased when fluid
has filled the space between lung and chest wall)

Also influence acid-base status

A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed.

Percuss:
Chest wall Assess fluid collections

Auscultate:
Breath sounds Abnormal breath sounds such as rales (crackles) present
S E C T I O N I Fundamentals of Nutrition Support Practice and Management

with fluid overload

Rhonchi also increase the work of breathing and present
when fluid is in the airways

Cardiovascular Inspect and palpate:

Neck vein distention Neck vein distention, edema influences fluid status: Edema can be systemic or local in etiology:
edema
Pitting edema—condition resulting from accumulation of Systemic causes include heart failure, hypoalbumine-
interstitial fluid—may occur in protein malnutrition and mia, salt and water retention; local causes include
is thought to result from decreased venous colloid pres- venous stasis, lymphatic stasis, or prolonged
sure exerted from low serum albumin levels dependency
(<2.5 mg/dL)
Heart failure, pregnancy, immobilization, and varicose
veins

Rhythm/rate Irregular rhythm may be related to potassium excess or Cardiopulmonary conditions or influences
deficiency, calcium deficiency, magnesium deficiency or
excess, phosphorus deficiency

Increased rate (tachycardia)—thiamine, fluid Organic heart disease, severe chronic lung disease,
(dehydration) respiratory insufficiency, drug toxicity, excess alcohol
ingestion
Auscultate:
Rate, sounds S3 presence (with edema, dyspnea, loud crackles that do
not disappear with cough)—fluid excess

Abdomen Inspect:
Color, contour Scaphoid appearance—loss of subcutaneous fat—

© 2005 A.S.P.E.N. www.nutritioncare.org.

caloric deprivation
 Rounded to protuberant—gas distention, obesity Pregnancy
Rounded with tight, glistening skin, fine veins able to be
seen, everted umbilicus (ascites)—fluid, sodium concerns

Muscle development Poor muscle tone or wasting muscle—poor activity or Postpartum, neuromuscular decline, surgery
nutritional depletion

Texture See skin assessment

Wounds Poor wound healing—protein or calorie inadequacy, vita-

© 2005 A.S.P.E.N. www.nutritioncare.org.

min C or zinc depletion

Feeding devices, ostomies Feeding devices and ostomies should be assessed at this
time—intact without drainage, erythema, swelling, or
odor. Surrounding skin should also be pink without
drainage, redness, or tenderness.

Auscultate:
Bowel sounds No sounds/hypoactive—influences the decision of what Bowel obstruction after surgery, trauma injury, or
route of feeding should be used diseases of the bowel peritonitis, paralytic ileus

Percuss:
For tympany Hyperactive—influences what type of feeding route can Gastroenteritis
be used and even the enteral substrate used if diarrhea High-pitched tinkling—early obstruction
is present
Percuss:
For tympany, dullness, density of abdominal contents, Tympany should be present since the air in the intestines Neoplastic disease, cirrhosis, infections, hematologic
and liver span (takes practice to acquire this skill) rises when supine disorders, AIDS, megaloblastic anemia

Check liver, which is a solid organ and sounds dull

(combine with palpation to check for hepatomegaly)—
protein deficiency

Palpate:
Texture, temperature, specific organs such as liver Warm to touch as with rest of body—temperature that Note: From a nutritional standpoint, if the patient
increases calorie and fluid requirements complains of any discomfort or pain, then palpation or
percussion should be done only by a physician or
physician-appointed attendee

Kidneys Inspect:
Color and clarity Dark, concentrated urine—could be a sign of Infection, sepsis, hematuria
dehydration

Light, dilute urine—could be a sign of overhydration Diabetes insipidus

A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed.

(Continued)

13
S E C T I O N I Fundamentals of Nutrition Support Practice and Management
14
TABLE 1-4. A Sample Outline for the Nutrition-Focused Physical Examination (Continued)

What Exam May Reveal in Regard to

System Nutrition Physical Exam Focus Nutritional/Metabolic Status Non-Nutritional Examples of Similar Findings

Musculo- Inspect:
skeletal Size, shape, symmetry, deformity, involuntary movements Craniotabes (<1 yr of age), softening of occipital, parietal
area—vitamin D deficiency
Inspect and palpate:
Head and neck movement, arms, fingers, wrists, elbows, Frontal or parietal bossing (infants), swelling or thicken-
and shoulders for strength, range of motion, and fluid, ing of front and sides of head—vitamin D deficiency
swelling, and pulses Open anterior fontanelle (persistent at >18 mos of
age)—vitamin D deficiency

A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed.

Inability to flex, extend, and rotate neck influences nutri-
tion by interfering with ability to feed or make hand-to-
mouth contact

Fat and muscle wasting in temporal regions, thorax, del- Muscular dystrophy, deep vein thrombosis, arthritis,
S E C T I O N I Fundamentals of Nutrition Support Practice and Management

toid muscle, fine muscles of hand, decreased range of malignancy, paralysis, renal dysfunction, liver dysfunc-
motion, swelling, impaired joint mobility- protein and tion, trauma, osteomalacia, hyperparathyroidism
calorie deprivation
Swollen, painful joints—vitamin C deficiency Connective tissue disease

Epiphyses at wrist—vitamin C or D deficiency Trauma, deformity, or congenital causes

Assess range of motion of upper extremities so ability to

feed independently and hand-to-mouth coordination can
be evaluated

Assess finger manipulations for assistive devices for

feeding

Inspect and palpate:

Legs for hip strength and edema, hair distribution, Muscle wasting noted on buttocks, gastrocnemius mus- Trauma, congenital deformity, renal disease, deep vein
pulses cle of legs, prominent body skeleton—calorie protein thrombosis, arthritis, chronic renal failure, pituitary
deficiency; also may be thiamine deficiency, vitamin C tumor, idiopathic hypopituitarism, growth hormone
deficiency, phosphorus deficiency, calcium deficiency deficiency
Rickets, knock knees, bowleg—vitamin D, calcium, phos-
phorus epiphyseal enlargement—vitamin D (painless),
vitamin C (painful)
Swollen, painful joints—vitamin C
Dwarfism—zinc

© 2005 A.S.P.E.N. www.nutritioncare.org.

 Neurologic Inspect:
Alertness, orientation, gross and fine motor skills (in con- Cranial nerves (see Face row) Polyneuropathy of diabetes mellitus, weakness due to
junction with musculoskeletal system), paresthesias, myogenic disorders
Motor weakness (lower extremities)—thiamine
tremors, weakness, dementia, coordination, reflexes
deficiency

Tests:
Alertness: general conversation and asking basic ques- Mental confusion, hyperirritability, apathy—protein Lyme disease, polyneuropathy of diabetes mellitus, col-
tions such as time, date, year, name, family peripheral neuropathy, thiamine, B12, B6 deficiency lagen vascular disease
Muscle tone: feeling muscle’s resistance to passive

© 2005 A.S.P.E.N. www.nutritioncare.org.

stretch by, for example, taking patient’s hand with yours
and while supporting elbow flexing and extending
patient’s fingers, wrist, and elbow, and putting the shoul-
der through range of motion. For legs, support the
patient’s thigh with one hand, grasp foot with other, and
flex and extend knees and ankles.
Muscle strength: have patient place hands (right then
left) against yours and push as hard as he or she can and
for lower extremities have the patient place right and
then left foot in your hand and push against your hand
Coordination: observe patient touching finger to nose and
mouth and even raising eating utensils to mouth
Reflexes: detect central nervous system disturbances Vibratory sense decrease, loss of position sense, loss of Hypothyroidism, sarcoidosis, amyloidosis, uremia,
using a reflex hammer with the pointed end to strike ankle or knee jerks bilaterally—thiamine, B12 malignancy
small areas and the larger, flatter end used in larger
Hyperactive reflexes—hypocalcemia Tetanus, upper motor neuron disease
areas (patellar or brachioradialis)
Reflexes usually tested—biceps, triceps, brachioradialis, Hypoactive reflexes—hypokalemia Neurologic disorders
abdominal, patellar, ankle, and plantar (graded 0–4+) Hypoactive Achilles, patellar reflexes—thiamine, B12 Neurologic disorders

Tetany—lips, tongue, fingers, feet, generalized muscle Neurologic disorders, respiratory alkalosis
aching, spasm—calcium, vitamin D, or magnesium
deficiency

Calf tenderness bilaterally—thiamine deficiency Deep vein thrombosis, peripheral neuropathy of other
causes

Dementia—niacin, B12 Head trauma, cardiac arrest, cerebral hemorrhage, brain

tumor, degenerative brain diseases

AIDS, acquired immunodeficiency syndrome; COPD, chronic obstructive pulmonary disease.

Reprinted from Hammond K. The nutritional dimension of physical assessment. Nutrition.1999;15:412-417 with permission from Elsevier Science.

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S E C T I O N I Fundamentals of Nutrition Support Practice and Management
S E C T I O N I Fundamentals of Nutrition Support Practice and Management

actual weight × 100

TABLE 1-5. Tanner Stages of Development23,24 Acute nutritional status =
50th percentile weight/height
Stage Girls Boys actual weight × 100
Chronic nutritional status =
50th percentile height/age
1 Prepubescent Prepubescent
d) Weight comparisons in adults can indicate severity of mal-
2 Pubic hair appears, breast Pubic hair appears, growth nutrition (Table 1-8). In adults, developing malnutrition is
buds, increased activity of of genitalia, increased evidenced by an involuntary loss or gain of ≥10% of usual
sweat glands activity of sweat glands body weight within 6 months or ≥5% of usual body weight
in 1 month, or a weight 20% over or under IBW.58
3 Breast enlargement, axillary Continued enlargement of e) Factors that influence interpretation of weight measurements
hair present genitalia, changes in voice, (1) Edema, ascites, diuretic therapy, and other fluid alterations
can significantly alter body weight within short time periods.
faint moustache/facial hair
(2) Fluid shifts from the intravascular space to the extra-
begins, axillary hair present
vascular space and the intracellular space to the extracel-
lular space with a concurrent decline in lean body mass
4 Nipple and areola become Pubic hair thickens, voice occur in malnutrition. Therefore, loss of lean body mass
more pronounced, menarche deepens, facial hair may be masked, with little obvious change in weight.
begins increases, hair on legs 3. Body mass index (BMI): BMI is a measure of weight for height.
becomes darker
Weight ( kg )
a) BMI is calculated as follows: BMI =
5 Breasts fully mature Genitalia fully mature Height 2 ( m )

b) In adults, a BMI of less than 15 kg/m2 is associated with a

significant increase in morbidity,59 while a BMI of less than
tion is recommended when using percent IBW.31 Body shape 18.5 kg/m2 is considered underweight. A healthy weight is
and weight tend to vary across age and population groups.29 considered a BMI between 18.5 and 24.9 kg/m2.2,4,60 Accord-
b) Growth charts: Various growth charts have been used for pre- ing to the National Institutes of Health, a BMI between 25
term infants,32–42 term infants, children, and adolescents.43 The and 29.9 kg/m2 is considered overweight and a BMI ≥ 30 is
Babson and Benda chart for premature infants44 has been obese.60 For the elder healthy adult, the BMI range is between
recently updated.32 Postnatal growth parameters should be cor- 22 and 27 kg/m2.61
rected for gestational age at birth for premature infants.45–47 c) The CDC growth charts with BMI for age,11 male or female,
Weight, length, and head circumference are monitored for are recommended to assess weight in relation to height for
infants up to 36 months old.48 Weight-for-length graphs are children 2 to 20 years of age. A BMI in the 85th to 95th per-
available for infants, children, and adolescents.43 Specialized centile means that a child is considered to be at risk for being
growth curves are available for children with diagnoses such as overweight. Some athletic children who are not overweight
Trisomy 21; Turner, Williams, and Prader-Willi syndromes; may fall into these categories due to increased muscle mass.40,41
and quadriplegic cerebral palsy.49–53 Most commonly, a stan- See Appendix 1-1 for CDC growth charts.
dard reference chart such as that from the Centers for Disease 4. In adults, abdominal girth measurement is commonly used to
Control and Prevention (CDC) is used in conjunction with a indicate risk of coronary artery disease and other morbidity.62,63
specialized curve for evaluation.11,48,54 Average weight gains per The waist circumference is measured by obtaining the distance
day according to gestational age from birth to 24 months are around the smallest area right below the rib cage and above the
listed in Table 1-9. Table 1-10 lists growth rates for weight, umbilicus. The measurement is used to determine excess abdom-
length, and head circumference by birth weight group and sex. inal fat. Waist girth circumference is not very useful for those
Table 1-11 gives general guidelines for weight gain, height, and with a BMI ≥ 35 kg/m2 since at this level the incremental pre-
head circumference from the age of 1 year to adolescence. dictive power is lost.
Z scores can also be used as part of the evaluation process. Nor- 5. Mid-arm circumference (MAC), mid-arm muscle circumfer-
mal is accepted as lying between ±2 standard deviations from ence (MAMC), and skinfold thickness (ST) estimate lean and
the mean. This range includes 95% of the reference population. fat mass.64,65 The techniques and standards have been widely
Malnourished children have a weight or weight-for-height published elsewhere.28
Z score of −2 or below. Serial Z scores can be used to evaluate a) MAC, MAMC, and ST measurements are appropriate for
the effects of dietary intervention, especially for populations.55 assessing change over time in individual patients. Single mea-
c) Weight changes: Recent weight changes in children can indi- surements are less useful than serial measurements over time.
cate acute nutrition issues. Significant weight losses for chil- b) Major limitations to these measurements include fluid shifts,
dren are considered to be >2% in 1 week, >5% in 1 month, changes in hydration status, and interobserver variability.
>7.5% in 3 months, and >10% in 6 months.56 The National E. Creatinine height index (CHI)64–68: CHI has traditionally been men-
Center for Health Statistics data—or more recently, CDC tioned as part of the nutritional assessment but is seldom used clini-
growth charts—are used to determine the percentiles.11,12,57 cally. Creatinine is the metabolic end-product of muscle and dietary
See Appendix 1-1 for CDC growth charts. protein creatine. Endogenous muscle creatine is released at a constant

16 A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. © 2005 A.S.P.E.N. www.nutritioncare.org.
 S E C T I O N I Fundamentals of Nutrition Support Practice and Management

TABLE 1-6. Weight in Pounds for Males 20 years and Over-number of Examined Persons, Mean, Standard Error of the
Mean, and Selected Percentiles, by Race-ethnicity and Age: United States, 1988-199428

Number of Standard Selected percentile

Race-ethnicity examined error of
and age persons Mean the mean 5th 10th 15th 25th 50th 75th 85th 90th 95th

All race/ethnicity groups1

20 years and over 7,942 180.7 0.83 131.3 140.1 145.5 155.9 175.9 199.2 214.3 226.1 243.8
20–29 years 1,630 172.1 1.37 126.9 134.0 138.7 147.5 164.9 187.6 205.2 217.7 236.8
30–39 years 1,481 182.5 1.49 136.1 142.1 148.1 158.2 175.9 200.9 217.4 226.4 247.9
40–49 years 1,226 187.3 1.67 135.4 145.1 150.9 163.6 180.7 206.5 223.3 232.5 256.4
50–59 years 855 189.2 1.76 139.6 150.1 158.4 166.7 184.7 206.8 221.6 231.5 251.3
60–69 years 1,175 182.8 1.44 134.5 141.9 148.8 160.1 181.1 203.3 216.4 224.4 236.2
70–79 years 875 173.6 1.57 128.7 136.3 141.2 151.4 171.3 191.2 205.7 211.4 227.1
80 years and over 700 157.8 1.63 114.3 123.5 128.5 140.1 155.8 173.1 185.2 193.4 204.7

Non-Hispanic white
20 years and over 3,287 183.1 0.97 135.1 142.9 149.1 159.1 178.0 201.9 216.5 227.2 245.6
20–29 years 393 173.7 1.99 130.6 137.3 142.8 149.6 166.2 188.5 206.2 219.5 234.6
30–39 years 454 185.6 1.96 138.7 145.3 152.2 162.1 179.6 204.5 220.4 226.6 250.9
40–49 years 428 189.5 2.04 139.9 148.6 155.0 166.2 181.9 206.8 224.6 233.1 259.4
50–59 years 418 191.5 1.80 145.3 155.1 161.7 169.5 187.3 209.5 224.6 232.9 252.8
60–69 years 510 185.4 1.56 137.6 143.7 151.9 163.6 183.9 205.3 217.4 225.7 236.7
70–79 years 524 175.1 1.45 132.0 139.0 144.1 153.6 172.5 192.6 206.0 211.6 227.3
80 years and over 560 159.0 1.31 114.6 124.6 131.7 141.2 157.1 173.8 185.7 193.5 205.3
Non-Hispanic black
20 years and over 2,113 181.5 1.09 129.3 136.7 143.0 153.0 176.0 201.1 217.7 231.1 255.1
20–29 years 488 181.6 2.14 130.1 136.2 140.7 151.9 173.9 197.5 219.6 238.6 269.1
30–39 years 497 182.4 2.00 131.7 141.1 146.4 153.1 176.6 199.4 215.7 230.0 261.6
40–49 years 370 185.4 2.11 131.7 139.9 145.6 156.3 179.1 207.7 222.2 234.7 254.1
50–59 years 217 186.0 3.09 128.9 135.2 144.8 158.4 182.3 207.8 223.6 232.4 265.9
60–69 years 295 176.9 2.25 124.2 133.6 141.3 152.6 172.0 199.1 216.4 226.1 241.1
70–79 years 187 169.9 2.63 130.1 132.1 144.0 167.7 190.6 202.1 213.1 *
80 years and over 59 155.4 4.48 * * * 133.1 157.9 173 * * *
Mexican American
20 years and over 2,256 170.5 1.01 125.8 134.4 139.9 148.1 166.4 188.1 202.6 212.2 228.3
20–29 years 674 162.3 1.46 123.4 129.1 134.9 141.7 157.5 175.9 191.6 201.0 220.1
30–39 years 474 173.0 1.83 126.8 136.7 143.1 153.0 169.3 189.9 204.1 210.2 234.5
40–49 years 381 181.4 2.13 139.5 144.4 149.9 160.2 175.1 202.5 214.3 223.5 240.8
50–59 years 178 182.2 3.08 144.6 150.2 158.5 179.2 199.4 213.4 221.2 *
60–69 years 337 172.3 1.91 134.8 139.2 142.2 150.2 170.1 191.6 202.2 213.1 223.5
70–79 years 149 160.7 2.89 126.9 131.9 139.9 164.5 178.7 186.8 193.6 *
80 years and over 63 145.7 3.56 * * * 129.6 146.8 154.5 * * *

* Figure does not meet standard of reliability or precision.

1 Includes all other race-ethnicity groups not listed separately.

rate. Creatinine excretion correlates with lean body mass and body
CHI =
(actual 24-hour creatinine excretion )
weight. It has been estimated that 18 to 20 kg of muscle is needed to
yield 1 g of urinary creatinine per day.
( expp ected creatinine excretion )
1. CHI is calculated by comparing the actual measured creatinine 2. Expected creatinine excretion is calculated as follows: IBW (kg)
excretion value with an expected value from reference values for multiplied by 23 mg/kg for males and by 18 mg/kg for females.
the same height and gender as follows:

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S E C T I O N I Fundamentals of Nutrition Support Practice and Management

TABLE 1-7. Weight in Pounds for Females 20 Years and Over—Number of Examined Persons, Mean, Standard Error of the
Mean, and Selected Percentiles, by Race-Ethnicity and Age: United States, 1988-199428

Number of Standard Selected Percentile

Race-Ethnicity Examined Error of
and Age Persons Mean the Mean 5th 10th 15th 25th 50th 75th 85th 90th 95th

All race/ethnicity groups1

20 years and over 8,764 152.3 0.81 105.5 112.0 117.1 125.5 144.4 171.3 190.5 202.7 225.6

20–29 years 1,665 141.7 1.25 102.9 108.0 111.2 118.3 133.2 157.3 175.2 188.9 216.5
30–39 years 1,775 154.2 1.46 106.2 112.5 117.4 125.4 144.0 172.7 195.7 211.9 232.9
40–49 years 1,368 157.4 1.58 109.2 116.9 122.6 130.0 150.6 175.6 193.8 209.4 230.3
50–59 years 1,006 163.7 1.85 114.0 120.2 125.7 135.1 157.2 185.8 201.6 213.3 239.9
60–69 years 1,172 155.9 1.57 109.0 115.6 121.9 130.3 151.4 174.7 191.1 202.2 220.7
70–79 years 988 148.2 1.66 100.5 110.5 116.3 125.0 142.4 166.8 180.6 189.5 213.8
80 years and over 790 133.2 1.50 92.0 100.0 105.4 114.1 131.4 149.4 159.1 168.7 186.3

Non-Hispanic white
20 years and over 3,758 150.7 0.91 105.6 112.1 117.0 125.0 143.0 169.3 187.5 200.2 221.2

20–29 years 452 140.1 1.92 102.9 108.7 111.2 118.1 130.4 153.0 171.1 185.6 218.8
30–39 years 579 151.4 2.06 105.4 112.1 116.6 123.6 141.6 170.0 192.6 207.5 227.7
40–49 years 477 155.1 2.10 109.7 117.2 122.8 129.2 147.7 172.1 191.6 202.7 227.1
50–59 years 484 163.5 2.17 115.0 120.6 125.8 135.2 157.1 185.4 200.2 211.2 239.8
60–69 years 501 155.4 1.91 110.0 115.9 122.1 130.9 151.5 172.7 190.9 201.2 219.5
70–79 years 644 147.0 1.64 100.8 111.1 116.3 124.4 141.6 164.5 178.1 187.3 206.2
80 years and over 621 132.9 1.39 92.1 100.1 105.5 114.2 131.3 149.1 158.9 167.1 185.9

Non-Hispanic black
20 years and over 2,495 168.2 1.07 110.7 118.9 125.6 137.4 161.1 191.1 211.8 226.8 250.8

20–29 years 563 155.6 1.83 106.7 112.1 118.1 128.0 146.9 177.4 193.1 208.1 224.0
30–39 years 626 169.0 2.03 114.8 120.7 127.0 136.6 159.9 192.1 215.1 230.7 251.7
40–49 years 456 180.2 2.53 116.5 124.0 134.4 146.4 171.7 204.7 227.5 245.7 276.4
50–59 years 275 177.6 2.94 112.6 123.8 137.4 148.1 174.4 203.7 220.2 236.0 250.2
60–69 years 300 173.4 2.84 114.0 125.6 135.2 145.0 168.1 193.3 209.1 219.9 253.1
70–79 years 182 166.0 3.45 124.1 127.5 138.1 159.7 185.2 205.4 228.6
80 years and over 93 138.7 3.65 111.0 117.0 136.1 151.0 176.5

Mexican American
20 years and over 2,135 151.6 1.12 105.6 112.9 118.3 127.1 145.4 171.2 185.9 196.6 217.1

20–29 years 575 142.5 1.68 101.4 105.7 110.5 119.0 136.9 157.3 177.6 188.3 205.7
30–39 years 493 154.6 2.05 107.1 114.6 120.1 129.9 145.7 174.2 191.2 208.0 229.6
40–49 years 367 163.0 2.13 117.1 125.4 130.9 139.7 157.8 180.0 194.0 204.6 225.9
50–59 years 193 156.0 2.64 121.5 123.2 134.8 153.8 175.7 182.7 192.2
60–69 years 321 154.4 2.19 114.5 118.6 125.1 133.2 148.3 171.1 181.1 193.4 214.2
70–79 years 127 140.2 3.04 113.7 121.7 135.5 153.2 163.8
80 years and over 59 118.4 3.83 * * * 96.7 116.0 135.2 * * *

* Figure does not meet standard of reliability or precision.

1 Includes all other race-ethnicity groups not listed separately.

NOTE: Pregnant women are excluded.

18 A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. © 2005 A.S.P.E.N. www.nutritioncare.org.
 S E C T I O N I Fundamentals of Nutrition Support Practice and Management

FIGURE 1-2. Percent of Body Weight Contributed by TABLE 1-8. Evaluation of Body Weight Data
Individual Body Parts
weight
% of IBW = x 100
IBW
8% 80% to 90% = mild malnutrition
Body Part
70% to 79% = moderate malnutrition
0% to 69% = severe malnutrition
Head & neck
Trunk without limbs current weight
2.7% Hand % of UBW = x 100
usual weight
Forearm without hand
5% 50% Forearm with hand 85% to 95% = mild malnutrition
1.6% Upper arm 75% to 84% = moderate malnutrition
Entire arm 0% to 74% = severe malnutrition
0.7% Foot
Lower leg without foot usual weight—curent weight
% of recent weight = x 100
10.1% Lower leg with foot usual weight
16%
Thigh
Entire leg Significant weight loss Severe weight loss
4.4%
Time (%) (%)
1.5%
1 wk 1–2 >2
1 mo 5 >5
Reprinted from the Journal of the American Dietetic Association, 95, Osterkamp LK, 3 mos 7.5 >7.5
Current perspective on assessment of human body proportions of relevance to 6 mos 10 >10
amputees, 215–218, 1995, with permission from American Dietetic Association.
IBW, ideal body weight; UBW, usual body weight
Adapted with permission from Blackburn GL, Bistrian BR. Nutritional and metabolic
3. Dietary protein may contribute up to 20% of the excreted crea- assessment of the hospitalized patient. J Parenter Enteral Nutr. 1977;1(1):11–22.
tinine.
4. Interpretation of CHI: 90–80%, mild depletion; 60% to 80%,
moderate depletion; <60%, severe depletion.
5. Several factors affect the measurement of CHI: addition of meat acute inflammation. Proteins that increase in concentration at least
to a previously meat-free diet, strenuous exercise, second half of 25% (due to inflammation) by virtue of increased hepatic synthe-
menstrual cycle, lean tissue loss with aging, renal impairment, sis are referred to as positive acute-phase proteins (Table 1-12).73
rhabdomyolysis, bed rest, and catabolic states; an incomplete Of these proteins, C-reactive protein is the most frequently cited as
24-hour urine collection will invalidate creatinine excretion an indicator of inflammation. Altered hepatic synthesis of positive
results but may be recognized. and negative acute-phase proteins during inflammatory metabo-
6. Creatinine excretion can also assist in verifying the accuracy of lism presumably facilitates immune function and tissue repair.
24-hour urine collections for nitrogen balance determinations, as 3. In addition to inflammation, serum concentrations are affected by
daily creatinine excretion should vary little over the short term. liver and renal function, hydration, pregnancy, iron deficiency,
F. Bioelectrical impedance analysis (BIA)63,64,69,70 and blood loss. Substantial published reports correlating hepa-
1. BIA is a body composition measurement technique based on the tic protein concentrations with morbidity and mortality have
principle that lean tissue has higher electrical conduction and lower replaced previously published conclusions that low concentra-
impedance than fat. It uses resistance and reactance to estimate tions are associated primarily with malnutrition. The earlier
fat-free and fat mass. reports did not account for or consider the variable of inflam-
2. An imperceptible, low electric current (900 A; frequency, 50 kHz) mation.74 As such, serum hepatic protein levels assist in the iden-
is passed through electrodes attached to the extremities of a patient tification of patients who are the most morbid and, thus, at risk for
to measure resistance and reactance. developing nutritional deficits and in need of carefully monitored
3. Factors that affect reliable BIA measurements include hydra- nutrition support interventions.
tion, electrolyte abnormalities, and lack of standards for specific H. Nitrogen balance65,72,75,76
body sizes. 1. Nitrogen balance evaluates adequacy of protein intake relative
G. Hepatic transport proteins68,71,72 to need. Nitrogen metabolism is dependent on both energy and
1. Serum hepatic transport protein concentrations have historically protein intake. Increasing energy intake often improves nitrogen
been thought to be markers for malnutrition. Those used to assess balance.
malnutrition are albumin, transferrin, prealbumin, and retinol- 2. Nitrogen balance is calculated as follows:
binding protein, which are synthesized in the liver.
2. These proteins have been referred to as negative acute-phase Nitrogen balance (g/d) = (Protein intake/6.25) −
proteins because they decrease in serum concentration (due to (urinary nitrogen{mostly urea} + fecal losses +
decreased hepatic synthesis) at least 25% in response to chronic or obligatory losses)

© 2005 A.S.P.E.N. www.nutritioncare.org. A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. 19
S E C T I O N I Fundamentals of Nutrition Support Practice and Management

TABLE 1-9. Infant Weight Gain (g/d) According to Gestational Age

Age

Gestational Age (wks) Postterm Age (mos)

Term to
Age at Birth (wks) Sex 28–32 32–36 36–40 3 mos 3–6 6–9 9–12 12–18 18–24

28–32 M* 32 ± 7 32 ± 7 32 ± 7 26 ± 7 16 ± 6 12 ± 4 6±1 6±1 5±1

F* 27 ± 6 27 ± 6 27 ± 6 23 ± 4 16 ± 3 13 ± 4 7±1 7±1 6±2
M + F** 30 ± 5 32 ± 6 26 ± 5 29 ± 6 19 ± 3 13 ± 4 9±3

33–36 M* 32 ± 7 32 ± 7 28 ± 6 20 ± 5 14 ± 4 11 ± 4 8±3 6±2

F* 30 ± 6 30 ± 6 27 ± 6 20 ± 5 14 ± 4 10 ± 4 8±3 7±2
M + F** 32 ± 6 26 ± 5 29 ± 6 19 ± 3 13 ± 4 9±3

37–42 (term) M* 31 ± 7 21 ± 6 16 ± 4 12 ± 6
F* 27 ± 6 21 ± 6 16 ± 6 11 ± 4
M + F** 29 ± 6 19 ± 3 13 ± 4 9±4
M*** 30 21 15 11 7 (6–8) 6 (5–7)
(21–36) (20–22) (15–16) (12–12)
F*** 24 20 15 11 7 (6–8) 6 (5–7)
(20–33) (18–22) (13–16) (9–12)

F, female; M, male; SD, standard deviation

*From Fomon SJ, ed. Infant Nutrition. 2nd ed. Philadelphia, PA: WB Saunders; 1973. Values given are mean ± 1 SD.
**From Babson and Benda.44 Values were calculated from growth chart and are mean ± 2 SD.
***From Hamill PVV, Drizd RA, Johnson CL, et al. Physical growth: National Center for Health Statistics percentiles. Am J Clin Nutr. 1979;32:607–615. Values represent the mean.
Values in parentheses include the 5th to 95th percentiles.
Reprinted with permission from the Ohio Neonatal Nutritionists. Nutritional Care for High Risk Newborns. Philadelphia, PA: George F. Stickley; 1985:207.

3. Nitrogen intake, assuming usual protein and amino acid sources, 3. DHR is a measure of cell-mediated immunity. This involves
is calculated by dividing grams of protein intake by 6.25 to obtain intradermal injection of an antigen to which the individual has
grams of nitrogen intake. Specialized enteral or parenteral formu- probably been exposed. An appropriate induration response in a
lations may have a slightly different conversion factor. healthy person indicates immunocompetence. Anergy is associ-
4. Total nitrogen output is determined by measuring 24-hour urinary ated with malnutrition. DHR testing is not a useful parameter in
nitrogen and adding fecal and other obligatory losses (generally individuals with infection, cancer, immunosuppressive disease or
an additional 2–4 g/d). medications, renal failure, liver disease, or trauma.77
5. For clinical purposes, nitrogen balance calculations using urinary 4. TLC is an indicator of immune function that reflects the status of
urea nitrogen instead of total urinary nitrogen are more practical B cells or T cells. TLC is calculated by multiplying the white blood
and generally suffice. cell count by the percentage of lymphocytes.
6. The goal for nitrogen balance is zero (or equilibrium) for main- 5. TLC is not necessarily a specific indicator of nutritional status
tenance or 2 to 4 g for repletion. A positive nitrogen balance since it decreases with age, acquired immunodeficiency syn-
reflects that nitrogen intake exceeds nitrogen losses; however, it dromes, and radiotherapy. Other non-nutritional factors that affect
does not reveal which tissues are being repleted and may not cor- TLC include hypoalbuminemia, metabolic stress, infection, can-
relate with changes in hepatic transport proteins that are affected cer, and long-term diseases.
as much by stress and hepatic diseases as by protein status. J. Vitamin and trace mineral abnormalities16,25,65
7. The validity of nitrogen balance is affected by severe nitrogen 1. The clinical evaluation (medical history, nutritional history,
retention disorders (eg, creatinine clearance) < 50 units or severe physical exam) provides the basis for evaluating patients for
hepatic failure), completeness of the 24-hour urine collection, and potential vitamin and trace mineral deficits.
completeness of the record of protein or amino acid intake. 2. Laboratory assessment is usually required to confirm clinically
I. Immunocompetence77–79 suspicious signs and symptoms.
1. Malnutrition is associated with immunosuppression. 3. Patients with malnutrition generally exhibit symptoms associated
2. Delayed hypersensitivity reactivity (DHR) and total lympho- with multiple micronutrient deficiencies rather than a single nutri-
cyte count (TLC) have been used to detect malnutrition-related ent deficiency. See Tables 1-13 and 1-14 for assessment of vitamin
immunosuppression in uncomplicated malnutrition. and trace mineral status.

20 A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. © 2005 A.S.P.E.N. www.nutritioncare.org.
 S E C T I O N I Fundamentals of Nutrition Support Practice and Management

TABLE 1-10. Toddler Growth Rates of Weight, Length, and Head Circumference by Birth Weight Group and Sex

Group I* Group II** Group III***

Male Female Male Female Male Female

n = 65 n = 67 n = 200 n = 226 n = 168 n = 155

Growth rate (g/d)

12 mos 9.3 ± 1.6 8.9 ± 1.8 9.0 ± 1.6 9.0 ± 1.7 9.1 ± 1.6 8.9 ± 1.9
24 mos 5.7 ± 1.3 5.6 ± 1.4 5.6 ± 1.3 5.9 ± 1.6 5.9 ± 1.5 6.0 ± 2.0
36 mos 4.2 ± 1.2 4.3 ± 1.3 4.2 ± 1.2 4.6 ± 1.5 4.6 ± 1.5 4.7 ± 2.2
n = 64 n = 67 n = 200 n = 224 n = 168 n = 154

Growth rate (mm/mo)

12 mos 13.0 ± 1.1 13.0 ± 1.3 12.3 ± 1.1 12.4 ± 1.1 12.0 ± 1.0**** 12.0 ± 1.0****
24 mos 8.0 ± 1.0 8.4 ± 1.0 8.0 ± 0.9 8.4 ± 1.0 8.0 ± 0.9 8.2 ± 0.9
36 mos 6.0 ± 1.0 6.5 ± 0.9 6.1 ± 0.8 6.6 ± 1.0 6.3 ± 0.9 6.6 ± 0.9

Head circumference
n = 65 n = 66 n = 198 n = 226 n = 169 n = 155

Growth rate (mm/mo)

12 mos 3.1 ± 0.3 3.0 ± 0.4 3.0 ± 0.4 3.0 ± 0.4 3.0 ± 0.3 3.0 ± 0.3
24 mos 1.3 ± 0.2 1.3 ± 0.2 1.4 ± 0.3 1.4 ± 0.3 1.5 ± 0.2**** 1.5 ± 0.2****
36 mos 0.7 ± 0.1 0.8 ± 0.2 0.9 ± 0.2 0.9 ± 0.2 0.9 ± 0.2**** 0.9 ± 0.2****

Values (except n) are expressed as mean ± standard deviation.

*Birth weight # 1250 g.
**Birth weight $ 1251 g but # 2000 g.
***Birth weight $ 2001 g but # 2500 g.
****p < 0.001
Reprinted with permission from Casey PH, Kraemer HC, Bernbaum J, et al. Growth patterns of low birth weight preterm infants: longitudinal analysis of a large, varied sample.
J Pediatr. 1990;117:298–307; and Casey PH, Kraemer HC, Bernbaum J, et al. Growth status and growth rates of a varied sample of low birth weight preterm infants: longitudinal
cohort from birth to three years of age. J Pediatr. 1991;119:599–605.

IV. Nutrition Support Decision Making

TABLE 1-11. General Growth Guidelines for Children
and Adolescents55 Increased morbidity and mortality are associated with malnutrition.80–82
Malnutrition results in loss of lean body mass and subsequent loss of
Age Weight Height Circumference structure or function. Impaired respiratory function, reduced cardiac
(yrs) gain (cm/yr) (cm/yr) contractility, impaired renal function, altered immune function, and poor
wound healing are known consequences of malnutrition.58,80,81 Based on
Preschool 1–2 3.5 kg/yr 12 5 data gathered from the comprehensive nutritional assessment, a nutrition
4 2–4 kg/yr 6–8 <1 diagnosis is made and a plan of care set forth. Nutritional intervention
decisions include timing, nutrient needs, route of therapy, and whether
Middle 7 2 kg/yr 5–6 specialized nutritional formulations are needed. See Figure 1-3 for a
childhood 10 4 kg/yr 5–6 decision-making algorithm.
A. Nutrition diagnosis
Adolescent 14–18 13 kg over 4 yrs 9.5–10.3 1. Malnutrition is often diagnosed as mild, moderate, or severe, as
boys seen in Table 1-8. This model is based on weight loss, while other
Adolescent 13–16 11 kg over 3 yrs 8.4–9.0 models are a combination of nutritional assessment parameters.
An example of the latter is the Nutrition Risk Index, which strat-
girls
ifies nutritional status based on serum albumin and percentage of
usual body weight.83
2. Marasmus and kwashiorkor are other diagnostic terms used to
describe malnutrition. While these terms traditionally labeled

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S E C T I O N I Fundamentals of Nutrition Support Practice and Management

marasmus malnutrition as depleted fat and muscle stores and the

TABLE 1-12. Acute-Phase Protein Classification kwashiorkor type as pure protein malnutrition, these terms are con-
and Function troversial. Both refer to states of uncomplicated malnutrition,
which is a rare occurrence in acute care settings. Further, kwashi-
Positive Negative Function orkor, first described in malnourished children in the 1930s, may
actually be a condition of undernutrition and inflammation rather
Fibrinogen Clotting process than uncomplicated protein deficiency.84
3. Coding for malnutrition diagnoses can be found in Chapter 33.
Prothrombin Clotting process B. Timing of nutritional intervention
1. A well-nourished adult patient without excessive metabolic stress
Antihemophilic Clotting process can be expected to tolerate little or no nutrition for up to 7 days.2
Plasminogen Clotting process In adults, it is reasonable to initiate specialized nutrition support
(provision of nutrients orally, enterally, or parenterally with
Complement proteins Complement cascade, in- therapeutic intent) within 7 to 14 days of inadequate oral intake
(C1s, C1, C2, B, C3, cluding cell lysis, opsonic or if inadequate oral intake is expected over a period of at least
C4, C5, C56, 1NH) action, and target roles in 7 to 14 days.2,8
immune response 2. Pediatric patients have increased metabolic rate nutrient needs
for growth, and lower nutrient reserves. Surgery or a short-term
Pancreatic secretory Protease enzyme inhibitor illness can alter a child’s nutritional status rapidly.85 Early intro-
trypsin inhibitor that prevents damage to duction of nutrition support is thought to be indicated for chil-
dren at high risk of malnutrition or those who are malnourished.
a1-Antitrypsin healthy tissue
For example, initiation of parenteral nutrition on the first or sec-
a-Antichymotrypsin
ond day of life in premature infants has been shown to be bene-
Haptoglobulin Binding of free hemoglobin, ficial for improving early growth86,87 and establishing positive
nitrogen balance.88 For those under 2 years with malnutrition
inhibition of prostaglandin
prior to admission, initiation of trophic feedings within 8 hours has
synthesis
been suggested, along with advancing to the nutrition goal within
Ceruloplasmin Binding of copper, 48 hours if tolerated.89 For older children, it is suggested that nutri-
tion support start within the first 18 hours and be advanced as
antioxidant
tolerated within 24 to 36 hours to goal.
C-reactive protein Complement activation, C. Mode of nutrition intervention. Integral to the process of nutrition
opsonization of DNA and cell care and the administration of specialized nutrition support is the
decision on route of administration (Figure 1-3).2
membrane debris for sub-
1. Indications for enteral nutrition. Enteral nutrition should generally
sequent scavenging
be given in preference to parenteral nutrition when nutritional
requirements are not met by oral intake and there is a functional
Albumin Binding of multiple mole-
gastrointestinal tract of sufficient length and condition to allow
cules, antioxidant, plasma
adequate nutrient absorption.2 See Chapter 5 for further indications
oncotic pressure
and enteral nutrition management.
2. Indications for parenteral nutrition. Parenteral nutrition should
Prealbumin Thyroxine transport and for-
be used when the gastrointestinal tract is not functional or cannot
mation of a complex with
be accessed and in patients who cannot be adequately nourished
retinol binding protein
by oral diets or enteral nutrition.2 See Chapter 8 for parenteral
nutrition indications and management.
Retinol-binding Retinol transport
3. Specialized nutrition support may be needed for management of
protein
specific conditions such as renal failure, liver failure, or critical
Transferrin Iron absorption and transport illness.
D. Nutrition monitoring and evaluation
Fibronectin Opsonization of noxious 1. Once the nutrition assessment is complete and nutrition inter-
agents, enhancing immune vention begins, continuous reassessment (otherwise known as
monitoring) is needed. Many of the assessment parameters used
clearance
initially are repeated serially to assess the efficacy of therapy
Insulin-like Promotion of protein syn- related to desired outcomes and for potential complications asso-
growth factor thesis in liver and muscle ciated with the therapy.
2. The data collected also determine the need for continued nutrition
and inhibition of lipolysis
care or discharge from nutrition care.1,2
(Nutrition assessment chapters from the 1st edition were con-
Reprinted with permission from Mueller C. True or false: serum hepatic tributed by Eva Politzer Shronts, Judith Fish, Kathy Pesce-
protein concentrations measure nutritional status. Support Line. Hammond, Kimberly A. Klotz, Jacqueline Wessel, and Geraldine
2004;26(1):8–16. A. Hennies.)

22 A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. © 2005 A.S.P.E.N. www.nutritioncare.org.
 S E C T I O N I Fundamentals of Nutrition Support Practice and Management

TABLE 1-13. Assessment of Vitamin Status64,72

Vitamin Laboratory assay Normal vvalues Signs of deficiency Signs of toxicity

Niacin (B5) Urinary niacin >1.6 mg per g of Pellegra, dermatitis, dementia, death, Liver damage, vascular dilation,
Metabolites creatinine loss of memory, headaches, glossitis flushing, and irritation

Folate (B9) Serum folate >6.0 ng/mL Macrocytic anemia, diarrhea, glossitis, None known
lethargy, and stomatitis

Cyanoco- Serum B12 >150 pg/mL Pernicious anemia, glossitis, spinal None known
balamin (B12) cord degeneration, and peripheral
neuropathy

Thiamine (B1) Urinary thiamine >60 mcg per g of Beriberi, paresthesias, nystagmus, (Rare) irritability, headache, insomnia,
creatinine impaired memory, congestive heart and interference with B2 and B6
failure, lactic acidosis, and Wernicke-
Korsakoff syndrome

Riboflavin (B2) Urinary riboflavin >80 mcg per g of Mucositis, dermatitis, cheilosis, None known
creatinine vascularization of cornea, photophobia,
lacrimation, decreased vision, impaired
wound healing, and normocytic anemia

Pyridoxine (B6) Plasma B6 >50 ng/mL Dermatitis, neuritis, convulsions, and None known
microcytic anemia

Pantothenic Urinary >1 mg/d Fatigue, malaise, headache, insomnia, Diarrhea

acid (B3) pantothenic acid vomiting, and abdominal cramps

Biotin Serum biotin 0.5–2.7 ng/mL Dermatitis, depression, alopecia, None known
lassitude, somnolence, anorexia, and
paresthesias

Ascorbic acid Serum ascorbic acid >0.30 mg/dL Enlargement and keratosis of hair Osmotic diarrhea, oxalate kidney stones,
(C) follicles, impaired wound healing, and interference with anticoagulation
anemia, lethargy, depression, bleed- therapy
ing, and ecchymosis

A Plasma vitamin A >20 mcg/dL Dermatitis, night blindness, kera- Acute: nausea, vomiting, headache,
tomalacia, and xerophthalmia dizziness; chronic: peeling skin, gingivitis,
and alopecia

D Plasma 25- 29.4 ± 15.7 ng/mL Rickets, osteomalacia, and muscle Excess bone and soft tissue calcification,
hydroxyvitamin D weakness kidney stones, and hypercalcemia

E Plasma alpha- >0.5 mg/dL Hemolysis, anemia, neuronal axonopa, Prolonged clotting time
tocopherol thy, and myopathy

K Prothrombin time Clotting with 1 s of Bleeding, purpura, and bruising Jaundice

laboratory control

© 2005 A.S.P.E.N. www.nutritioncare.org. A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. 23
S E C T I O N I Fundamentals of Nutrition Support Practice and Management
TABLE 1-14. Assessment of Trace Mineral Status64,72

Trace Laboratory Normal

Mineral Assay Serum Values Signs of Deficiency Signs of Toxicity

Zinc Serum value 50–150 mcg/dL Dermatitis, hypogeusia, diarrhea, apathy, depression, Nausea, vomiting, metallic taste,
impaired wound healing, immunosuppression chills, headache

Copper Serum value 70–150 mcg/dL Neutropenia, microcytic anemia, osteoporosis, decreased Nausea, vomiting, epigastric
hair and skin pigmentation, dermatitis, hypotonia pain, diarrhea

Chromium Serum value 1–3 mg/mL Glucose intolerance, peripheral neuropathy, increased None known
serum cholesterol and triglyceride, insulin resistance

Manganese Serum value 2–3 mcg/dL Nausea, vomiting, dermatitis, color changes in hair, Extrapyramidal symptoms,
hypocholesterolemia, growth retardation encephalitis like symptoms

Selenium Serum value 0.01–0.34 mcg/dL Muscle weakness and pain, cardiomyopathy Hair loss, dermatitis, garlic odor,
brittle nails

Molybdenum Neutron 0.4–0.5 mg/mL Tachycardia, tachypnea, altered mental status, vision Increased copper excretion
changes, headache, nausea, vomiting

FIGURE 1-3. Routes to Deliver Nutrition Support to Adults: Clinical Decision Algorithm

Nutrition assessment

Diffuse peritonitis,
Functional GI Tract intestinal abstruction,
intractable vomiting, ileus,
Yes No
intractable diarrhea,
gastrointestinal schemia

Enteral nutrition Parenteral nutrition

Long-term Short-term
gastrostomy nasogastric
jejunostomy nasoduodenal
nasojejunal
GI function Short-term Long-term or fluid restrition

Normal Compromised Peripheral PN Central PN

Standard nutrients Speciality formulas GI function returns

Nutrient tolerance Yes No

Adequate Inadequate Adequate

progress to PN supplementation progress to more
oral feedings complex diet and oral
feedings as tolerated

Progress to total
enteral feedings
Reprinted with permission from American Society for Parenteral and Enteral Nutrition.2

24 A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. © 2005 A.S.P.E.N. www.nutritioncare.org.
 S E C T I O N I Fundamentals of Nutrition Support Practice and Management

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26 A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. © 2005 A.S.P.E.N. www.nutritioncare.org.
 APPENDIX

1-1
Pediatric Growth Charts

Centers for Disease Control and Prevention, National

Center for Health Statistics in collaboration with
the National Center for Chronic Disease Prevention
and Health Promotion. Growth charts. 2000.
Available at: http://www.cdc.gov/growth charts.
Accessed November 23, 2004.

© 2005 A.S.P.E.N. www.nutritioncare.org. A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. 27
 Birth to 36 months: Boys NAME
Length-for-age and Weight-for-age percentiles RECORD #

Birth 3 6 9 12 15 18 21 24 27 30 33 36
in cm AGE (MONTHS)
cm in
41 41 L
40 95 40 E
100 90 100 N
39 39
75 G
38 38
95 50 95 T
37 37 H
25
36 36
90 10 90
35 5 35
34
85
33
32 95 38
80 17
31
L 90 36
30
E 75 16
N
29
75
34
G 28
70 15
T 27 32
H 26 50
65 14
25 30 W
24 25 E
60 13
23 28 I
10 G
22 55 12 H
5 26
21 T
20 50 11 24
19
18 45 10 22
17
16 40 9 20
15
8 18

16 16
7 AGE (MONTHS)
kg lb
12 15 18 21 24 27 30 33 36
14
6 Mother’s Stature Gestational
W Father’s Stature Age: Weeks Comment
E 12
Date Age Weight Length Head Circ.
I 5 Birth
G 10
H
T
4
8
3
6
2
lb kg
Birth 3 6 9
Pubished May 30, 2000 (modified 4/20/01).
SOURCE: Developed by the National Center for Health Statistics in collaboration with
the National Center for Chronic Disease Prevention and Health Promotion (2000).
http://www.cdc.gov/growthcharts
 Birth to 36 months: Girls NAME
Length-for-age and Weight-for-age percentiles RECORD #

Birth 3 6 9 12 15 18 21 24 27 30 33 36
in cm AGE (MONTHS)
cm in
41 41 L
40 40 E
100 95 100
39 90 39 N
38 G
75 38
95 95 T
37 50 37 H
36 25 36
90 90
35 10 35
5
34
85
33
32 38
80 95 17
31
L 30 36
75 90 16
E
N
29
34
G 28
70 75
15
T 27 32
H 26 65 14
25 50 30 W
24 E
60 13
23 25 28 I
G
22 55 12 H
10 26
21 5 T
20 50 11 24
19
18 45 10 22
17
16 40 9 20
15
8 18

16 16
7 AGE (MONTHS)
kg lb
12 15 18 21 24 27 30 33 36
14
6 Mother’s Stature Gestational
W Father’s Stature Age: Weeks Comment
E 12
Date Age Weight Length Head Circ.
I 5 Birth
G 10
H
T
4
8
3
6
2
lb kg
Birth 3 6 9
Published May 30, 2000 (modified 4/20/01).
SOURCE: Developed by the National Center for Health Statistics in collaboration with
the National Center for Chronic Disease Prevention and Health Promotion (2000).
http://www.cdc.gov/growthcharts
 Birth to 36 months: Boys
Head circumference-for-age and NAME
Weight-for-length percentiles RECORD #

Birth 3 6 9 12 15 18 21 24 27 30 33 36
in cm AGE (MONTHS) cm in H
E
95 A
52 90 52
D
20 75 20
50 50 C
50
I
25 R
H 19 19
48 48 C
E 10 U
A 5 M
D 18 46 46 18 F
E
R
C 44 44 E
I 17 17 N
R C
C 42 42 E
U 16
M 40 50
F 22 48
E
15 38 21 46
R
E 20 44
N 36 19 42
14
C
E
95
18 40
34 90
17 38
13 75
36
32 50
16
34
12 25 15
30 10 32
5 14
30 W
13 28 E
12 I
26 G
24 11 11 24 H
22 10 10 22 T
20 9 9 20
18 8 8 18
16 7 7 16
W
E 14 14
6 6
I 12 12
G 5 5
10 kg lb
H 4 LENGTH
T 8 cm
64 66 68 70 72 74 76 78 80 82 84 86 88 90 92 94 96 98100
6 3
26 27 28 29 30 31 32 33 34 35 36 37 38 39 40 41 in
4 2
Date Age Weight Length Head Circ. Comment
2 1
lb kg
cm 46 48 50 52 54 56 58 60 62
in 18 19 20 21 22 23 24

Published May 30, 2000 (modified 10/16/00).

SOURCE: Developed by the National Center for Health Statistics in collaboration with
the National Center for Chronic Disease Prevention and Health Promotion (2000).
http://www.cdc.gov/growthcharts
 Birth to 36 months: Girls
Head circumference-for-age and NAME
Weight-for-length percentiles RECORD #

Birth 3 6 9 12 15 18 21 24 27 30 33 36
in cm AGE (MONTHS) cm in H
E
A
52 52
D
95
20 90 20
50 50 C
75 I
50 R
H 19 19
48 48 C
E 25 U
A 10 M
D 18 46 5 46 18 F
E
R
C 44 44 E
I 17 17 N
R C
C 42 42 E
U 16
M 40 50
F 22 48
E
15 38 21 46
R
E 20 44
N 36 19 42
14
C 95
E 18 40
34 90
17 38
13 75 36
32 16
50 34
12 25
15
30 32
10 14
5 30 W
13 28 E
12 I
26 G
24 11 11 24 H
22 10 10 22 T
20 9 9 20
18 8 8 18
16 7 7 16
W
E 14 14
6 6
I 12 12
G 5 5
10 kg lb
H 4 LENGTH
T 8 cm
64 66 68 70 72 74 76 78 80 82 84 86 88 90 92 94 96 98100
6 3
26 27 28 29 30 31 32 33 34 35 36 37 38 39 40 41 in
4 2
Date Age Weight Length Head Circ. Comment
2 1
lb kg
cm 46 48 50 52 54 56 58 60 62
in 18 19 20 21 22 23 24

Published May 30, 2000 (modified 10/16/00).

SOURCE: Developed by the National Center for Health Statistics in collaboration with
the National Center for Chronic Disease Prevention and Health Promotion (2000).
http://www.cdc.gov/growthcharts
 2 to 20 years: Boys NAME
Stature-for-age and Weight-for-age percentiles RECORD #

12 13 14 15 16 17 18 19 20
Mother’s Stature Father’s Stature cm in
Date Age Weight Stature BMI*
AGE (YEARS) 76
95
190
74
90
185 S
75
72
180 T
50 70 A
175 T
25 68 U
170 R
10 66
165 E
in cm 3 4 5 6 7 8 9 10 11 5
64
160 160
62 62
155 155
S 60 60
T 150 150
A 58
T 145
U 56
140 105 230
R
54
E 135 100 220
52
130 95 95 210
50
125 90 200
90
48 190
120 85
46 180
115 80
75
44 170
110 75
42 160
105 50 70
150 W
40
100 65 140 E
25
38 I
95 60 130 G
10
36 90 5 H
55 120
T
34 85 50 110
32 80 45 100
30
40 90
80 35 35 80
W 70 70
30 30
E 60 60
I 25 25
G 50 50
H 20 20
40 40
T
15 15
30 30
10 10
lb kg AGE (YEARS) kg lb
2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20
Published May 30, 2000 (modified 11/21/00).
SOURCE: Developed by the National Center for Health Statistics in collaboration with
the National Center for Chronic Disease Prevention and Health Promotion (2000).
http://www.cdc.gov/growthcharts
 2 to 20 years: Girls NAME
Stature-for-age and Weight-for-age percentiles RECORD #

12 13 14 15 16 17 18 19 20
Mother’s Stature Father’s Stature cm in
Date Age Weight Stature BMI*
AGE (YEARS) 76
190
74
185 S
72
180 T
70 A
95
175 T
90
68 U
170 R
75 66
165 E
in cm 3 4 5 6 7 8 9 10 11 50
64
160 25 160
62 62
155 10 155
60 5 60
150 150
58
145
56
140 105 230
54
S 135 100 220
T 52
A 130 95 210
50
T 125 90 200
U
48 190
R 120 85
E 95 180
46
115 80
44 170
110 90 75
42 160
105 70
150 W
40 75
100 65 140 E
38 I
95 60 130 G
50
36 90 H
55 120
25 T
34 85 50 110
10
32 80
5
45 100
30
40 90
80 35 35 80
W 70 70
30 30
E 60 60
I 25 25
G 50 50
H 20 20
40 40
T
15 15
30 30
10 10
lb kg AGE (YEARS) kg lb
2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20
Published May 30, 2000 (modified 11/21/00).
SOURCE: Developed by the National Center for Health Statistics in collaboration with
the National Center for Chronic Disease Prevention and Health Promotion (2000).
http://www.cdc.gov/growthcharts
2 to 20 years: Boys NAME
Body mass index-for-age percentiles RECORD #

Date Age Weight Stature BMI* Comments

BMI

35

34

33

32

31

30
95
29

BMI 28
90
27 27
26 85 26
25 25
75
24 24

23 23
50
22 22

21 21
25
20 20
10
19 19
5
18 18

17 17

16 16

15 15

14 14

13 13

12 12

2 2
kg/m AGE (YEARS) kg/m
2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20

Published May 30, 2000 (modified 10/16/00).

SOURCE: Developed by the National Center for Health Statistics in collaboration with
the National Center for Chronic Disease Prevention and Health Promotion (2000).
http://www.cdc.gov/growthcharts
34 A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. © 2005 A.S.P.E.N. www.nutritioncare.org.
2 to 20 years: Girls NAME
Body mass index-for-age percentiles RECORD #

Date Age Weight Stature BMI* Comments

BMI

35

34

33

32

95
31

30

29

BMI 28
90

27 27
26 85 26
25 25

24 75 24

23 23

22 22
50
21 21

20 20
25
19 19
10
18 5
18

17 17

16 16

15 15

14 14

13 13

12 12

2 2
kg/m AGE (YEARS) kg/m
2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20

Published May 30, 2000 (modified 10/16/00).

SOURCE: Developed by the National Center for Health Statistics in collaboration with
the National Center for Chronic Disease Prevention and Health Promotion (2000).
http://www.cdc.gov/growthcharts
© 2005 A.S.P.E.N. www.nutritioncare.org. A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. 35
 NAME
Weight-for-stature percentiles: Boys RECORD #

Date Age Weight Stature Comments kg lb

76
34
33
72
32
31 68
30
29 64
28
lb kg 27 60
95
26 26
56 56
25 25
90
24 85 24
52 52
23 75 23

48 22 22 48
50
21 21
25
44 20 20 44
10
5
19 19
40 18 18 40

17 17
36 36
16 16
15 15
32 32
14 14
13 13
28 28
12 12

24 11 11 24
10 10
20 9 9 20
8 8
lb kg STATURE kg lb
cm 80 85 90 95 100 105 110 115 120

in 31 32 33 34 35 36 37 38 39 40 41 42 43 44 45 46 47

Published May 30, 2000 (modified 10/16/00).

SOURCE: Developed by the National Center for Health Statistics in collaboration with
the National Center for Chronic Disease Prevention and Health Promotion (2000).
http://www.cdc.gov/growthcharts

36 A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. © 2005 A.S.P.E.N. www.nutritioncare.org.
 NAME
Weight-for-stature percentiles: Girls RECORD #

Date Age Weight Stature Comments kg lb

76
34
33
72
32
31 68
30
29 64
28
lb kg 27 60
95
26 26
56 56
25 90 25
24 85 24
52 52
23 75 23

48 22 22 48
50
21 21

44 20 25 20 44
19 10 19
5
40 18 18 40

17 17
36 36
16 16
15 15
32 32
14 14
13 13
28 28
12 12

24 11 11 24
10 10
20 9 9 20
8 8
lb kg STATURE kg lb
cm 80 85 90 95 100 105 110 115 120

in 31 32 33 34 35 36 37 38 39 40 41 42 43 44 45 46 47

Published May 30, 2000 (modified 10/16/00).

SOURCE: Developed by the National Center for Health Statistics in collaboration with
the National Center for Chronic Disease Prevention and Health Promotion (2000).
http://www.cdc.gov/growthcharts

© 2005 A.S.P.E.N. www.nutritioncare.org. A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. 37
 Maria Luisa Forchielli, MD;
Sarah J. Miller, PharmD
2
Nutritional Goals and
Requirements

Introduction 2. Morbidity and mortality are less likely and the need for hospital-
ization and further treatments may be reduced, which has implica-
Due to nutrition’s direct impact on health and disease, nutritional goals
tions for cost containment.
and requirements for patients under medical care should be set as clearly D. Benefits from nutritional therapy have been detected in both
as possible. These goals and requirements are constantly revised, fol- “healthy” children and children receiving treatments for various
lowing the progressive understanding of the quantitative and qualitative diseases either in the hospital or at home. Overall pediatric nutri-
role of nutrients in biological pathways and clinical outcomes. This tional goals can be summarized as follows:
chapter describes current nutritional goals and requirements in health 1. To avoid limitations in the rate of growth and reverse weight loss
and disease. or extreme conditions such as failure to thrive. In the presence of
a disease, ponderal and/or statural growth are usually affected—
I. Nutritional Goals the former in acute conditions, both in chronic ones. Proper nutri-
II. Overall Nutritional Requirements tional intervention allows catch-up growth.5–7
III. Nutritional Requirements for Health and Disease (Enteral and 2. To maintain positive nitrogen balance, necessary for growth, tis-
Parenteral Nutrition) sue repair, and subsequent multiorgan functioning. Children are
References at greater risk than adults of protein wasting because of a propor-
tionally higher basal metabolic rate and protein turnover.8,9 Chil-
dren can lose as much as one third of their lean body mass in 3 to
I. Nutritional Goals 5 days after caloric stores are depleted.10 Malnutrition can lead to
A. Nutritional goals are different for different interventional appli- progressive muscle weakness, altered respiratory function,
cations. For example, goals of nutrition support for therapeutic impaired immune response, and other hazards of debilitation,
aims are often different from goals for prevention of nutrient defi- including cellular and mitochondrial impairments.
3. To reduce short- and long-term morbidity (eg, infectious episodes
ciency, which, in turn, may be different from goals for prevention
of various origins such as respiratory and intravenous [IV]
of chronic disease.
catheter-related infections or postoperative complications) and
B. Nutrition plays an important role in disease evolution and signifi-
mortality. Evidence in this regard exists for both in- and out-
cantly affects patient response to disease, and consequently out-
patients suffering from different diseases (eg, human immuno-
comes. With regard to the role of nutrition in disease evolution, it is
deficiency virus, cancer requiring bone marrow transplant).11,12
well recognized that
4. To avoid or diminish the rate of long-term disabilities. Cognitive
1. Malnutrition and malabsorption of macro- and/or micronutrients
and behavioral development is influenced by adequate nutrition.
contribute to many disease outcomes (malnutrition: cancer, acute
For instance, extreme situations such as failure to thrive—as well
and chronic infections, etc; malabsorption: gastrointestinal dis- as singular deficiencies regarding iron, iodine, zinc, and so forth—
eases such as celiac disease or inflammatory bowel disease, have been associated with poor cognitive and behavioral perform-
hereditary diseases such as cystic fibrosis, etc). For example, sur- ances in children of different ages. Energy and nutrients such as
vival is typically shorter in cancer patients who have already lost polyunsaturated fatty acids (PUFA) are also implicated in cogni-
weight prior to beginning chemotherapy.1 Another example of tive and behavioral performance.13–15
how malnutrition affects disease outcome is provided by children 5. To reduce costs for the patient and for the health care system.
with Crohn’s disease.2 Malnutrition in these children can con- With the advent of home-based nutrition support and the reduc-
tribute to growth failure and delayed sexual maturation. tion in complication rates, patients tend to have briefer hospital-
2. Malnutrition increases both morbidity and mortality. Hospitalized izations. The choice of nutrition intervention has a profound
patients are at risk (up to 65%) of developing malnutrition. No impact on costs. A report on home nutrition support showed
major changes in this percentage have been detected over the enteral nutrition (EN) to cost, on average, one sixth of home par-
years.3,4 The vicious circle of malnutrition and infections has been enteral nutrition (PN) and to halve the hospital admissions/year/
well documented. patient rate.16
C. Reversal or alteration of disease outcomes is possible through 6. To improve quality of life. Although difficult to assess and quan-
appropriate nutrition support3,4: tify, quality of life appears to be enhanced, especially during
1. The clinical course of disease may be improved through avoiding home nutrition support. Happiness, activity, sense of freedom,
or correcting macro- and micronutrient deficiencies. Improve- and willingness to socialize were reported to be improved in chil-
ments involve anthropometric parameters and body metabolism. dren on both home EN and PN.17,18

38 A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. © 2005 A.S.P.E.N. www.nutritioncare.org.
 S E C T I O N I Fundamentals of Nutrition Support Practice and Management

E. Goals of nutrition support in adults lipids and fibers are now included. For each nutrient, specific indica-
1. The primary goal of nutrition support in adults should be to tors are used to set the requirements.
improve clinical outcome. To achieve this goal, provision of D. Energy is measured in calories (in the United States) with specific
nutrition support is based on two different rationales: respect to its individual components:
a) To prevent starvation-induced complications (eg, death, infec- 1. Basal metabolic rate (BMR): the energy necessary to allow nor-
tion). This rationale is indisputable and includes patients who, mal function at the cellular, organ, and systemic levels, and to
without nutrition support, would eventually die from starvation maintain homeostasis, body temperature, and heart and respira-
because they cannot eat. tory rate when the body is in a fasted state for 12 hours, awake, and
b) To alter favorably the natural history or treatment of a spe- in a thermoneutral environment. BMR decreases proportionally
cific disease process. with age.22 Approximately two thirds of BMR is used by the fat-
(1) This goal is based on correcting nutritional or metabolic free mass in both adults and children.23 More specifically, BMR is
deficiencies that arise from a disease or treatment so that directly proportional to metabolically active organ mass such as
outcome will improve. heart, central nervous system, liver, and kidneys in infants and
(2) The role of nutrition support in this scenario is controver- children, and to metabolically active muscle mass in adults.24
sial because improvements in prognostic markers such BMR at rest, but not fasted, is called resting energy expenditure
as serum protein concentrations, nitrogen balance, and (REE). REE and BMR are often used interchangeably, even
weight gain have not consistently been accompanied by though the former can be approximately 10% higher than the lat-
clinical benefits.19–21 ter. In young infants, growth may account for as much as 25% to
2. Nutrition therapy should be directed toward a specific objective, 33% of total energy expenditure.
with the intent of improving outcome. Depending on the patient’s 2. Thermic effect of food (TEF): the energy required to allow diges-
nutritional status and clinical condition, this objective may be as tion, absorption, and storage of nutrients. TEF is influenced by
follows: energy intake, time of delivery, and meal composition for both EN
a) To diminish the rate of weight loss and body protein turnover. and PN.25 The highest thermic effect is seen for proteins (protein
This is the goal in markedly catabolic patients (eg, severely synthesis from amino acids requires 25% to 57% of their energy
injured patients). content), followed by carbohydrates (glycogen from glucose
b) To maintain body weight and lean body mass. This is the requires 4%) and lipids (lipids from lipids or glucose require 2%
goal in patients who cannot eat for indefinite or long periods: and 28%, respectively).26 Metabolic response to food (TEF) may
patients with certain intestinal disorders (eg, short-bowel syn- account for 5% to 10% of energy expenditure.
drome, long-term obstruction), permanent neurologic impair- 3. Losses: the energy lost in stool and urine.
ment, or oropharyngeal dysfunction. 4. Activity: the energy required for physical activity. Activity
c) To achieve weight gain and anabolism. This is the goal in requirements are expressed as percentage increases over BMR
depleted patients. requirements. With regard to activity, percentage increases over
BMR requirements can range from 5% to 10% of the daily
energy expenditure in premature neonates and up to 50% in 8- to
II. Overall Nutritional Requirements 12-year-old children. These values decrease with illnesses and
A. The human body requires the daily provision of macronutrients hospitalization. Activity typically represents about a 5% increase
(carbohydrates, fats, and proteins) and micronutrients (vitamins and over BMR in hospitalized adults but can be much higher.27
trace elements) along with water and electrolytes. Macronutrients 5. Growth: the energy cost for new tissue to be generated. It is
have an energetic and structural-functional role, while micro- approximately 5 kcal/g of body weight, ranging from 3 to 6 kcal/g
nutrients are vital regulators of cellular, metabolic, or structural according to type of tissue. Except in young infants, growth repre-
components. Nutrient requirements have been established according sents a very small part of the total energy requirement.28
to age, gender, weight, and/or height. 6. Illness/stress: any amount of energy to overcome other non-
B. For patients under medical care, nutrients can be delivered enterally physiologic or “stress” conditions, usually expressed by a BMR
and/or parenterally. The enteral route includes the physiological correction factor.
route of ingestion of food by mouth as well as the introduction of 7. The sum of the first five energy components above is called total
nutrients directly into the stomach or duodenum/jejunum by enteric energy expenditure (TEE). Each component should not be seen
tubes or stoma. Nutritional requirements depend on the patient’s as a separate contributor to TEE, as they are all intertwined and
health status. Nutritional requirements for healthy people refer subject to wide variability.
specifically to food ingested orally. Those for people using PN 8. The minimum level of energy compatible with health is termed
are set for people with acute or chronic illness that renders their maintenance energy requirement.
gastrointestinal tract either nonfunctional or inaccessible. The E. Proteins (nitrogen) are critical for body homeostasis. Appropriate
requirements for healthy people or for people using PN can indi- nitrogen and energy intakes along with body metabolism help main-
rectly be applied to EN, but only partially and with adjustments. tain nitrogen balance. In disease states, due to higher turnover and
Recommendations for the enteral and the parenteral requirements catabolism of endogenous proteins, this balance may become nega-
can overlap. tive. Although proteins are not one of the two major macronutrients
C. Given extreme inter- and intrapersonal variability and difficulties in for supplying energy, they can be used for energy when energy
assessing nutrient requirements in studies on healthy subjects, sug- intake is insufficient.
gested intakes are reference standards and are continuously revised F. Lipids are energy dense, facilitate the absorption of fat-soluble vita-
to reflect advances in knowledge. Requirements have been exten- mins and their precursors, and are structural components of cell
sively investigated for energy, protein, and some micronutrients. membranes and some hormones. They consist of saturated and unsat-
The list is growing, however, and other nutrients such as specific urated (mono- and polyunsaturated) fatty acids, phospholipids, and

© 2005 A.S.P.E.N. www.nutritioncare.org. A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. 39
S E C T I O N I Fundamentals of Nutrition Support Practice and Management

cholesterol. Among these, only the PUFA (omega-3 and omega-6) 120 kcal/kg/day promotes weight gains approximating the
are essential components of the diet, as humans cannot synthesize intrauterine growth rate. Greater weight gains associated
them. For this reason, dietary reference intakes have been set only with greater energy intakes are thought to reflect fat depo-
for PUFA. For the others, only limitations of daily intakes are avail- sition.35 In conditions such as BPD, 150 kcal/kg/day may
able. The recent attention to PUFA is due to their immunomodula- be required. Both carbohydrate and fat are provided as
tory effects: anti-inflammatory effects in the omega-3 series and energy sources to provide a balanced PN formulation.
pro-inflammatory effects in the omega-6 series, through modulation Provision of fat in addition to carbohydrate for energy
of different prostaglandins, thromboxanes, leukotrienes, and lipox- decreases the volume needed for the PN formulation,
ins.29 Other PUFA functions include alteration in membrane fluid- decreases the respiratory quotient, may help avoid fatty
ity, additional immunomodulatory effects through intracellular infiltration of the liver, and prevents deficiency of essential
signal transduction and changes in gene expression, and modifica- fatty acids.
tions of the intestinal bacterial ecosystem due to a hypothesized b) Protein. The protein requirement varies according to body
disruption of the wall membrane.29 They are also important for weight and is highest in the most immature infants. Provision
development and maintenance of the eye and brain. of amino acids is necessary to reverse the 1% daily loss of
G. Fiber requirements have been set because of the recently recognized endogenous protein stores by premature infants. The protein
importance of functional fibers. All fibers are nondigestible carbo- loss begins the first day after birth. Clinical conditions includ-
hydrates, but functional fibers are defined as those that have bene- ing surgery, necrotizing enterocolitis, sepsis, and BPD may
ficial physiological effects in humans. These beneficial effects increase protein requirements.
include laxation, improvement in blood lipid concentrations, and (1) Net protein utilization depends on energy intake. Protein
reduction in glycemic response. Different functional fibers demon- utilization ensures growth and minimizes complications.
strate differing effects on these physiological responses. High rates of protein utilization (protein not used exclu-
H. Micronutrient requirements remain largely empirical due to assess- sively as an energy source) are achieved with 150 to 200
ment problems and lack of knowledge. Vitamin requirements are nonprotein kcal per g of nitrogen (24–32 nonnitrogen kcal
better characterized than those of trace elements. per g of protein). If energy intake is deficient (<150 non-
protein kcal per g of nitrogen), endogenous proteins are
oxidized to produce the needed energy and nitrogen bal-
III. Nutritional Requirements for Health and Disease ance becomes negative. If protein intake is suboptimal,
(Enteral and Parenteral Nutrition) increasing energy intake will spare protein for lean tissue
A. Premature infants gain, but only up to a certain level. Above this level, protein
1. The goal is to achieve a postnatal growth rate approximating nor- gain plateaus.
mal fetal intrauterine growth rates (weight, length, and head cir- (2) Conditionally essential amino acids for preterm infants
cumference). This is not usually possible in the first 1 to 2 weeks include tyrosine, cysteine, and taurine in addition to the
of life. Growth parameters are routinely plotted on Babson-Benda other amino acids essential for term infants.
or Lubchenco growth grids to determine trends. Weight gain (3) EN. The protein requirement for appropriate growth in
should approximate 10–20 g/kg/day for preterm infants After premature infants is estimated at 2.5 to 4 g/kg/day, which
reaching 2.5 kg, daily weight gain is around 20 to 30 g/day. is primarily devoted to preserving or depositing lean body
Length and head circumference gains are expected to be between mass. Excessive protein administration (>6 g/kg/day) has
0.7 and 1 cm/week.30 The goal is accretion of protein, fat, and been associated with adverse effects, including azotemia,
minerals approximating normal fetal intrauterine accretion rates. pyrexia, and lower IQ scores. Inadequate (<2.5 g/kg/day)
2. EN and PN requirements are shown in Table 2-1.31–39 protein intake is associated with slow growth and decreased
a) Energy. Actual energy needs are affected by weight, gestational nitrogen retention.31
age, postnatal age, gender, environment, feeding regimen and (a) Human milk varies with stage of lactation. Early milk is
composition, activity, rate of growth, and development. Energy 60% to 90% whey protein and 10% to 40% casein.
needs increase with fever, cardiac failure, major surgery, Within 1 to 2 weeks, the ratio becomes closer to 50:50.
severe sepsis, long-term growth failure, protein-calorie mal- (b) Formulas designed for premature infants or fortified
nutrition, and chronic lung disease (bronchopulmonary dys- human milk are required to provide adequate protein.
plasia [BPD]). Energy intake below or above requirements Standard infant formulas do not provide adequate
may lead to growth retardation or excessive fat accumulation, protein.
respectively. (4) PN. The protein requirement to approximate intrauterine
(1) EN. The energy requirement for premature infants is nitrogen accretion is estimated at 3 to 4 g/kg/day, with a
approximately 120 kcal/kg/day (50 kcal/kg for mainte- minimum concomitant delivery of 60 to 90 nonprotein
nance plus 70 kcal/kg for a daily weight gain of 15 g/kg), kcal/kg/day. Azotemia may result from administration of
with a range of 105 to 130 kcal/kg/day. Most energy com- >4 g/kg/day in low birth weight infants. Current practice is
ponents are extrapolated from the norm to provide ade- to initiate amino acids just after birth at variable doses of 1
quate energy for catch-up growth, high energy costs of to 3 g/kg/day. Doing so could decrease subsequent protein
thermoregulation and body functions, and inefficient uti- requirements for catch-up growth. The target for normal-
lization of ingested nutrients. ization of plasma amino acids during PN is generally set at
(2) PN. Because energy is not required for digestion, there are the postprandial amino acid concentrations for the term
no absorptive losses, activity is limited, and cold stress is breast-fed infant. For this reason, specific amino acid
reduced, energy requirements for PN are lower than for formulations have been designed with the addition of
EN. After the first 2 weeks of life, energy intake of 90 to taurine, glutamate, aspartate, and cysteine; the reduction

40 A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. © 2005 A.S.P.E.N. www.nutritioncare.org.
 S E C T I O N I Fundamentals of Nutrition Support Practice and Management

TABLE 2-1. Guidelines for Daily Nutrient Intakes of Enterally or Parenterally Fed Preterm Infants31–39

Nutrient Unit measurement Suggested enteral intake Suggested parenteral intake

Fluid mL/kg/day 120–200 100–150

Energy kcal/kg/day 105–130 90–120
Protein g/kg/day 2.5–4 3–4
Carbohydrate 40%–50% total energy 6–15 mg/kg/minute
Fat 40%–55% total energy
g/kg/day 5–7 1–3
Minerals
Calcium mg/kg/day 100–220 40-80
Phosphorus mg/kg/day 60–140 31-62
Magnesium mg/kg/day 8–15 3.6-6
Iron mg/kg/day 2–4 —
Sodium mEq/kg/day 2–7 2–5
Potassium mEq/kg/day 2–3 2–4
Chloride mEq/kg/day 2–7 As needed to maintain acid-base balance
Zinc mcg/kg/day 600–3000 400
Copper mcg/kg/day 110–160 20
Iodine mcg/kg/day 30–60 1
Selenium mcg/kg/day 1.3–4.5 1.5-2
Chromium mcg/kg/day 0.1–2.25 0.05-0.2
Molybdenum mcg/kg/day 0.3 0.25
Manganese mcg/kg/day 0.75–7.5 1
Vitamins
Vitamin A* IU/kg/day 700–1500 1643; max 2300 IU/day (500 mcg/kg/day,
max 700 mcg/day)
Vitamin D** IU/day 400 160; max 400 IU/day (4 mcg/day; max
10 mcg/day
Vitamin E*** IU/day 6–12 2.8; max 7 IU/day (2.8 mg; max 7 mg/day)
Vitamin K mcg/kg/day 8–10 80; max 200 mcg/day
Thiamine mcg/kg/day 180–240 350; max 1200 mcg/day
Riboflavin mcg/kg/day 250–360 150; max 1400 mcg/day
Niacin mg/kg/day 3.6–4.8 6.8; max 17 mg/day
B6 mcg/kg/day 150–210 180; max 1000/day
B12 mcg/kg/day 0.30 300; max 1000/day
Folic acid mcg/kg/day 25–50 56; max 140/day
Biotin mcg/kg/day 3.6–6 6; max 20/day
Pantothenic acid mg/kg/day 1.2–1.7 2; max 5/day
Vitamin C mg/kg/day 18–24 25; max 80/day
Carnitine mg/kg/day — 10–30

*Vitamin A (retinol) 0.3 mcg = 1 IU.

**Vitamin D 0.025 mcg = 1 IU.
***Vitamin E 1 mg = 1 IU.
The following conversion factors apply to: Ca 40 mg=1 mmol=2 mEq; P 31 mg=1 mmol; Mg 24 mg=1 mmol=2 mEq; Na 23 mg=1 mmol= 1 mEq; K 39 mg=1 mmol= 1 mEq; Cl 35 mg=1
mmol= 1 mEq.

© 2005 A.S.P.E.N. www.nutritioncare.org. A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. 41
S E C T I O N I Fundamentals of Nutrition Support Practice and Management

of methionine, glycine, and alanine; and an increase of erides (MCT) more effectively than long-chain ones,
arginine and leucine. The N-acetyl-L-tyrosine salt is a because their concentration of bile salts is low. For-
more soluble form of tyrosine. Cysteine, along with glu- mulas for premature infants include both MCT and
tamine and glycine, is a precursor of glutathione. These long-chain triglycerides in various concentrations.
formulations have been demonstrated to improve weight The European Society for Pediatric Gastroenterology,
gain, nitrogen balance, and mineral solubility. Hepatology and Nutrition (ESPGHAN) has recom-
c) Carbohydrate. Carbohydrate delivery is recommended to be mended limiting the amounts of MCT to <40% of total
40% to 50% of the total caloric intake. Infants with chronic calories in preterm formula.40 MCT do not provide
lung diseases benefit from as little as 35% of energy as carbo- essential fatty acids and do not promote the absorption
hydrates. of minerals. Therefore, essential fatty acids and fat-
(1) EN. The carbohydrate composition of preterm infant for- soluble vitamins have to be supplied when formulas
mulas is generally equally divided between lactose and with high MCT content (>80%) are used.
glucose polymers. (2) PN. Lipids are provided as IV fat emulsions (IVFE) (see
(a) Glucose polymers may be digested more effectively Chapter 7) at a dose of 1 to 3 g/kg/day (30%–60% of
than lactose by premature infants early in life. nonprotein calories when full calories are administered).
(b) Glucose polymers contribute fewer osmotic particles Lipids should be provided from the first day of life, because
to formula than do individual glucose molecules. premature infants do not have essential fatty acid stores.
(c) Lactose appears to lower intestinal pH, facilitating Serum triglycerides should be monitored, with values <200
absorption of some minerals (eg, calcium) and devel- mg/dL considered acceptable. A continuous infusion and
opment of normal flora. 20% IVFE promote optimal metabolic tolerance. No
(d) Functional fibers or prebiotics such as galactooligosac- adverse effects have been observed in terms of lung dys-
charide and oligofructose may improve the intestinal function.
ecosystem (development of beneficial flora such as e) Fluids. Fluid requirements are generally higher for EN than
Lactobacillus and Bifidobacterium, change in pH, PN and should take into account the following points:
enterocyte and immune system maturation). Oligo- (1) Diuresis during the first 1 to 2 weeks of life results in a 5%
saccharides are present in breast milk but not current to 15% weight loss in premature infants. Fluids must be
North American formulas. adjusted accordingly, based on urine parameters (mainte-
(2) PN. Carbohydrate is provided as dextrose (D-glucose) in nance of specific gravity between 1.010 and 1.016 g/mL,
the monohydrate form at 3.4 kcal/g. Dextrose is the major flow 2–3 mL/kg/hour by day 3 and up to 6 mL/kg/hour
contributor to the osmolarity of the PN formulation. later, osmolality 200–400 mOsm/kg of water) and normal
(a) Current practice is to initiate glucose approximating the serum sodium values.
rate of endogenous glucose production (6 mg/kg/ (2) Higher fluid intake may be required to meet energy needs
minute for infants weighing <1000 g; 8 mg/kg/minute after 2 weeks of life. Tolerance to increased fluids depends
for infants weighing >1000 g) with stepwise advance- on the clinical condition (eg, BPD and patent ductus arte-
ments of 1 to 2 mg/kg/minute to a maximum of 15 mg/ riosus are exacerbated by excessive fluid intake). Pre-
kg/minute to optimize glucose tolerance. Serum and mature infants are susceptible to both dehydration and
urine glucose monitoring provides an indication of fluid overload.
acute intolerance reflected as hyperosmolarity and (3) The infant’s environment and other factors directly affect
osmotic diuresis. Glucose delivery of >26 mg/kg/ fluid requirements. Examples that increase requirements
minute may result in fatty infiltration of the liver. are exposure to radiant warmers, phototherapy, fluid
(b) Nonprotein calories need to be balanced between glu- losses (diarrhea, glycosuria), or respiratory distress.
cose and fat. Glucose without fat increases water Examples that decrease requirements are oliguria and
retention and may thereby worsen existing respiratory conditions of neutral thermal range or high ambient
compromise. Glucose alone may exacerbate fatty humidity.
infiltration of the liver. (4) EN. Ranges are 120 to 200 mL/kg/day or 100 to 160 mL/
d) Lipids. Fat delivery is recommended to be at 40% to 55% of 100 kcal. Infants weighing <1000 g preferably require 150
total calories. The essential fatty acid requirement is estimated to 200 mL/kg/day. Infants weighing >1000 g require 120 to
at approximately 3–12% of total calories. 150 mL/kg/day.
(1) EN. The lipid requirement is 4.5 to 6 g/100 kcal, or 5 to (5) PN. Infants weighing <1000 g require 150 mL/kg/day;
7 g/kg/day. infants weighing >1000 g require 100 to 150 mL/kg/day.
(a) The recommended omega-6 (C18:2ω-6) to omega-3 Some infants require >150 mL/kg/day, depending on their
(C18:3ω-3) ratio ranges from 5:1 to 15:1, while the environmental situation.
ratio of their derivatives, docosahexaenoic acid (DHA) f) Vitamin, mineral, and trace element recommendations
(C22:6ω-3) to arachidonic acid (ARA)(C20:4ω-6), for EN and PN have been developed for premature infants
ranges from 1:1 to 1:2.7. Inclusion of one international (Table 2-1).31–39 PN requirements are generally lower than EN
unit of vitamin E per g of linoleic acid will prevent per- requirements.
oxidation of unsaturated lipids in food and tissues. (1) Vitamins. Preterm infants do not have fat-soluble vitamin
PUFA content has been revised in some formulas to reserves at birth. Requirements may change based on the
include DHA and ARA. quality and quantity of nutrient intake.
(b) Premature infants (especially if <34 weeks of gesta- (a) EN. In general, specific formulas and fortified breast
tional age) may absorb and use medium-chain triglyc- milk supply adequate amounts. Most water-soluble

42 A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. © 2005 A.S.P.E.N. www.nutritioncare.org.
 S E C T I O N I Fundamentals of Nutrition Support Practice and Management

vitamins are affected by macronutrient intake and osteopenia in infants requiring long-term PN. Long-
exposure to environmental factors. For instance, expo- term diuretic use or aluminum contamination of the
sure to light or phototherapy destroys riboflavin. components of PN formulations may further deplete
(b) PN. A preterm parenteral multivitamin preparation calcium reserves. At birth, the magnesium level is ele-
has not yet been developed. Current practice is to use vated and, upon its normalization, IV supplementa-
2 mL/kg/day of a pediatric multivitamin to a maxi- tion can start.
mum of 5 mL/day. The American Society for Clinical (3) Trace elements. Zinc and copper are required for growth.
Nutrition recommends intakes of 500 mcg/kg/day vita- Deficiencies of zinc (alteration of the intestine, skin,
min A and approximately 3 mg/kg/day of vitamin E, immunity, and growth) and copper (hypochromic anemia,
and these should be started just after birth.37 When osteoporosis, and neutropenia) can occur. Zinc require-
other intakes are compared with estimates, at the cur- ments may increase in infants with high stool output,
rent doses, water-soluble vitamins largely cover the gastrointestinal fluid losses, or renal failure.
recommended needs. Ascorbic acid and riboflavin are (a) EN. Zinc and copper have a limited absorption rate:
given in excess. 36% and 60% from fortified human milk and preterm
(2) Minerals. Premature infants require higher calcium, formula for zinc, and 10% to 30% for copper. They
phosphorus, and magnesium intakes than do term exhibit competition for absorption and may be involved
infants to promote intrauterine accretion rates and to in drug-nutrient interactions. Recommendations for
prevent osteopenia. An infant in utero accrues 75% of its zinc are 600 to 1500 (up to 3000) mcg/kg/day and for
total body calcium from gestation weeks 24 to 40. Drugs copper 110 to 160 mcg/kg/day.
such as corticosteroids, furosemide, theophylline, and (b) PN. Copper and manganese need to be omitted in the
caffeine cause calcium loss. Due to high urinary sodium presence of cholestasis as indicated by direct bilirubin
losses during the first 3 weeks of life, premature infants > 2 mg/dL. Selenium, chromium, and molybdenum
require more sodium. Therefore, 5 to 7 mEq/kg/day of need to be omitted in infants with renal dysfunction.
sodium are recommended in infants <32 weeks gesta- g) Other. Carnitine: Premature infants receiving exclusively PN
tional age, while 3 to 5 mEq/kg/day are more appropri- need carnitine to allow fat oxidation at the mitochondria.
ate for less premature infants. After that critical time and Estimates range from 10 and 20, with supplementation up to
upon stabilization and growth, premature infants require 30 mg/kg/day without risk of side effects.
2 to 4 mEq/kg/day of sodium along with equal amounts B. From infancy to adolescence
of chloride and potassium. Some of the anion is com- 1. The child’s age-specific regular growth and development are the
monly provided as acetate to decrease the likelihood of final tests of nutritional needs. Appetite and self-selection usually
metabolic acidosis. result in adequate nutrient intake for the normal, healthy child.
(a) EN. The following points are emphasized: When illness or physical disability prevent adequate nutrient
i) Mineral bioavailability averages 60% for cal- intake, requirements must be artificially determined considering
cium, 70% for phosphorus, and 50% for magne- the disease factor involved. In this case, ongoing reassessments of
sium. Mineral absorption is improved with the many nutrients are essential, especially for energy expenditure.
addition of MCT, lactose, enrichment with vita- For healthy children and adults, a joint committee of the govern-
min D and minerals, and appropriate quantity of ments of Canada and the United States, after reassessing the pre-
calcium and phosphorus. vious recommended dietary allowances (RDAs) plus the qualities
ii) Standard infant formulas and unfortified human of subsequent studies, has developed dietary reference intakes
milk do not provide enough calcium and phospho- (DRI) (full reports are available at www.nap.edu). DRI define the
rus to meet the mineral needs of preterm infants. levels of nutrient intake that are necessary to achieve good health
Fortified human milk or formulas specifically and avoid adverse effects. These levels, obtained after selecting
designed for premature infants provide higher cal- specific indicators, are age-specific and identify first and second
cium and phosphorus delivery and appropriate semesters (0–6 months and 7–12 months) of life, infants, toddlers,
amounts of sodium, potassium, and chloride (see children, and adolescents. No similar age-specific nutritional rec-
Chapter 4). ommendations are available for sick children nourished either
iii) Preterm infants require more iron. Iron require- enterally or parenterally. DRI include the RDA plus three other
ments are between 2 and 4 mg/kg/day, to be started reference values41,42:
within 2 months of age or at doubling of weight. a) Adequate intake (AI): the usual intake at or above which
Iron absorption is enhanced in premature infants. there is a low probability of inadequacy (replaces RDA when
Formulas specifically for premature infants are RDA cannot be determined)
iron fortified (see Chapter 4). b) Tolerable upper level (UL): the average daily nutrient intake
(b) PN. Specific IV recommendations are as follows: A level above which adverse effects may arise
calcium-phosphorus ratio of 1.3:1 (≥1:1 molar) repli- c) Estimated average requirement (EAR): the average daily
cates the fetal mineral accretion ratio and allows for nutrient intake level that meets the requirements of half the
the highest retention of both minerals, provided they healthy individuals of a specific age and gender
are supplied together and daily. Addition of calcium 2. Energy needs. Pediatric energy needs originate from mainte-
and phosphorus to PN is limited by solubility (see nance, activity, and growth. Each component is subject to age
Chapter 7). Cysteine HCl increases calcium/phosphorus variability because maintenance progressively declines from
solubility. It is frequently impossible to provide ade- birth to adolescence, activity increases during childhood, and
quate amounts of these minerals for prevention of growth has two major spikes during infancy and adolescence.

© 2005 A.S.P.E.N. www.nutritioncare.org. A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. 43
S E C T I O N I Fundamentals of Nutrition Support Practice and Management

TABLE 2-2. Criteria and Dietary Reference Intake Val- TABLE 2-3. Equations for Predicting REE from
ues for Energy by Active Individuals by Life Body Weight45
Stage Group*43
Sex and age range (yrs) Equation to derive REE (kcal/day)
Active PAL EER (kcal/day)
Life Male
stage group Criterion Male Female 0– < 3 (60.9 x wt) – 54
3– <10 (22.7 x wt) + 495
0–6 mos Energy expenditure plus 570 520 (3 mos) 10–18 (17.5 x wt) + 651
energy deposition Female
7–12 mos ≤ 743 676 (9 mos) 0– < 3 (61 x wt) – 51
1–2 yrs ≤ 1046 992 (24mos) 3– <10 (22.5 x wt) + 499
3–8 yrs ≤ 1742 1642 (6 yrs) 10–18 (12.2 x wt) + 746
9–13 yrs ≤ 2279 2071 (11 yrs)
14–18 yrs ≤ 3152 2368 (16 yrs) REE, resting energy expenditure; wt = weight in kilograms.
Printed with permission from World Health Organization. Energy and Protein Require-
ments Technical Report Series, No 724. Geneva, Switzerland: World Health Organiza-
EER = estimated energy requirement; PAL = physical activity level.
tion; 1985.
*For healthy, moderately active Americans and Canadians.
Printed with permission from the Institute of Medicine. Dietary Reference Intakes for
Energy, Carbohydrate, Fiber, Fat, Fatty Acids, Cholesterol, Protein, and Amino Acids double-labeled water. Table 2-2 summarizes the recom-
(Macronutrients). Washington, DC: National Academy Press; 2002. mended energy intake.43
(2) Energy needs for stressed infants/children/adolescents.
See PN section.
a) EN b) PN
(1) Energy needs for healthy infants/children/adolescents. The (1) In the presence of illness or disability, DRI may not apply
estimated requirement is defined as the average dietary secondary to decrease in activity or growth or change in
energy intake that is predicted to maintain energy balance thermic effect of food. Energy expenditure may shift from
in healthy individuals of a defined age, gender, weight, growth to the needs of acute illness.44
height, level of physical activity, and deposition of new tis- (2) The starting point for the estimation of an individual’s
sues. Physical activity is classified into four levels (seden- energy expenditure is the BMR or the REE. Approaches for
tary, low active, active, and very active) with different estimating BMR or REE differ according to the number of
coefficients. The activity-level coefficient is approximately variables included (eg, age, sex, weight, height.) The World
1.25 to 1.4. Estimates have been extrapolated from Health Organization equations are two examples of energy
reported energy intakes and body mass index data, factorial expenditure estimates based on weight, age, and/or sex (see
approaches, and measurements of energy expenditure by Tables 2-3 and 2-4).45–47

TABLE 2-4. Basal Metabolic Rate Requirement in kcal/Day Based on Body Weight46,47

Kg Male Female Kg Male Female Kg Male Female Kg Male Female

3 150 (120*) 136 (144*) 16 750 747 38 1305 1207 62 1660 1572
4 210 (191*) 205 (191*) 17 780 775 40 1340 1241 64 1690 1599
5 270 274 18 810 802 42 1370 1274 66 1725 1626
6 330 336 19 840 827 44 1400 1306 68 1765 1653
7 390 395 20 870 852 46 1430 1338 70 1785 1679
8 445 448 22 910 898 48 1460 1369 72 1815 1705
9 495 496 24 980 942 50 1485 1399 74 1845 1731
10 545 541 26 1070 984 52 1505 1429 76 1870 1756
11 590 582 28 1100 1025 54 1555 1458 78 1900 1781
12 625 620 30 1140 1063 56 1580 1487 80 1935 1805
13 665 655 32 1190 1101 58 1600 1516 82 1970 1830
14 700 687 34 1230 1137 60 1630 1544 84 2000 1855
15 725 718 36 1270 1173

*From reference 46. These values differ from those in reference 47. Printed with permission from World Health Organization. Energy and Protein Requirements Technical Report
Series, No 522. Geneva, Switzerland: World Health Organization; 1973.

44 A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. © 2005 A.S.P.E.N. www.nutritioncare.org.
 S E C T I O N I Fundamentals of Nutrition Support Practice and Management

ommendations used, calorie distribution among lipids,

Table 2-5. Daily Energy Requirements for Pediatric carbohydrates, and proteins should be carefully prescribed.
Patients on Parenteral Nutrition38 3. Protein needs
a) EN
Age kcal/kg (1) Healthy infants/children/adolescents. DRI values may be
used to determine protein needs. Acceptable protein intake
<6 mos 85–105 should range between 10% and 20% of total calories.
6–12 mos 80–100 These values are based on a combination of intake,
>1–7 yrs 75–90 growth, nitrogen accretion, and nitrogen balance data. AI
(or RDA) and EAR are also provided (Table 2-6).43
>7–12 yrs 50–75
(2) Stressed infants/children/adolescents. See PN section.
>12–18 yrs 30–50 b) PN
(1) In the stressed child, protein requirements are increased.
Reprinted from Task Force for the Revision of Safe Practices for Parenteral Nutrition. Rates of catabolism and synthesis of proteins are higher.
Safe practices for parenteral nutrition. J Parenter Enteral Nutr. 2004;28:S39–S70, with Protein recommendations are listed in Table 2-7.38
permission from A.S.P.E.N. (2) Provision of approximately 12% to 16% of calories as
protein minimizes negative nitrogen balance.
(3) To maximize protein utilization and avoid gluconeogene-
(3) Illness tends to decrease activity but may increase energy sis, appropriate calorie distribution and intake are essential.
expenditure. Therefore, estimates of BMR or REE (Tables A nonprotein calorie-to-nitrogen ratio of 150:1 to 300:1
2-3 and 2-4) must be corrected by a factor of 0.7 for starva- is most likely to achieve positive nitrogen balance. The
tion, 1 to 1.2 for minimal stress, 1.2 to 1.5 for moderate ratio should be determined based on age, metabolic stress,
stress, and 1.5 to 2 for severe stress. nutritional intake and status, and ongoing losses.
(4) Indirect calorimetry may be used to determine the actual (4) 1 g/kg/day daily advances in protein intake are suggested,
energy expenditure of a specific child with greater accu- after starting at an initial rate of 0.5 g/kg/day.
racy. Measurements of resting metabolic expenditure can (5) All formulations contain crystalline amino acids.
be adjusted for activity and other factors as needed. This (a) Children under 1 year of age have special amino acid
determination may help to reduce the likelihood of under- requirements, and therefore the IV formulations used
or overfeeding. See Chapter 22. are as discussed under the PN section for premature
(5) Energy estimates for pediatric patients on PN are provided infants. In patients older than 1 year, adult formula-
by A.S.P.E.N. (Table 2-5).38 Regardless of the energy rec- tions can be used. These formulations are designed to

Table 2-6. Criteria and Dietary Reference Intake Values for Protein by Life Stage Group43

AI or RDA for
Reference Individual EAR RDA
(g/day) (g/kg/day) (g/kg/day)
AI AMDR
Life stage Ggroup Criteria Male Female Male Female Male Female (g/kg/day) %

0–6 mos Average consumption of

protein from human milk 9.1 (AI) 9.1 (AI) 1.52 ND
7–12 mos Nitrogen equilibrium
+ protein deposition 13.5 (AI) 13.5 (AI) 1.10 1.10 1.50 1.50 ND
1–3 yrs " 13.0 13.0 0.88 0.88 1.10 1.10 5–20
4–8 yrs " 19.0 19.0 0.76 0.76 0.95 0.95 10–30
9–13 yrs " 34.0 34.0 0.76 0.76 0.95 0.95 10–30
14–18 yrs " 52.0 46.0 0.73 0.71 0.85 0.85 10–30
>18 yrs Nitrogen equilibrium 56.0 46.0 0.66 0.66 0.80 0.80 10–35

AI, adequate intake (the observed average or experimentally determined intake by a defined population or subgroup that appears to sustain a defined nutritional status, such as
growth rate, normal circulatory nutrient values, or other functional indicators of health; used if sufficient scientific evidence is not available to derive an EAR; for healthy infants
receiving human milk, the AI is the mean intake; not equivalent to an RDA); AMDR, acceptable macronutrient distribution range (the intake for a particular energy source associ-
ated with a reduced risk of chronic disease while providing intakes of essential nutrients); EAR, estimated average requirement (the intake that meets the estimated nutrient needs
of half of the individuals in a group); ND, not determinable; RDA, recommended dietary allowance (the intake that meets the nutrient need of almost all [97%–98%] individuals in a
group).
Printed with permission from Institute of Medicine. Dietary Reference Intakes for Energy, Carbohydrate, Fiber, Fat, Fatty Acids, Cholesterol, Protein, and Amino Acids (Macronutri-
ents). Washington, DC: National Academy Press; 2002.

© 2005 A.S.P.E.N. www.nutritioncare.org. A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. 45
S E C T I O N I Fundamentals of Nutrition Support Practice and Management

needs be given as carbohydrate to limit fat and possibly pro-

Table 2-7. Daily Protein Requirements for Children tein intake in the diet.41 The acceptable carbohydrate intake
on Parenteral Nutrition with Normal as a percentage of energy should be 45% to 65% of total calo-
Organ Function38 ries in all age groups. EAR for carbohydrates has been estab-
lished only for older adolescents and adults, based on the
Age g/kg average amount of glucose used by the brain. Pediatric data
have been extrapolated from adults (Table 2-8).43
Neonates 3–4 b) PN. Carbohydrates should comprise 40% to 60% of the total
Infants (1-12 months) 2–3 caloric intake. Dextrose monohydrate is used as the major
Children (above 10 kg or 1 through 10 years) 1–2 source of energy in PN and contributes to PN osmolality.
Adolescents (11 through 17 years) 0.8–1.5 Glucose infusion rates of 5 to 13 mg/kg/minute are generally
tolerated. Above 14 mg/kg/minute, complications such as liver
fatty infiltration, hypertriglyceridemia, hyperglycemia, and
Reprinted from Task Force for the Revision of Safe Practices for Parenteral Nutrition. excessive carbon dioxide production may occur. In general, the
Safe practices for parenteral nutrition. J Parenter Enteral Nutr. 2004;28:S39–S70 with infusion rate usually starts at 5 to 7 mg/kg/minute and
permission from A.S.P.E.N.
advances daily by 2 to 4 mg/kg/minute.
5. Fat. Fat requirements range from 25% to 55% of total calories,
meet the amino acid requirements of orally fed adults with a minimum requirement of 3% to 4% of calories as essential
and contain high levels of methionine, glycine, and fatty acids (1%–3% as linoleic and close to 1% as linolenic acid).
phenylalanine and low levels of branched-chain amino a) EN. Fat does not have DRI values, with few exceptions (AI
acids, cysteine, and tyrosine. for infants of 31 g/day in the age range 0–6 months and
(b) Glutamine, a primary fuel for intestinal mucosa and 30 g/day from 7–12 months, obtained from average consump-
immune cells and precursor for nucleotide synthesis tion data of total fat from human milk). More detailed recom-
and the antioxidant glutathione, seems to improve mendations are available for the essential PUFA (Table 2-9).43
nitrogen balance, gut barrier functions, and mortality The American Academy of Pediatrics Committee on Nutri-
and morbidity in selected patients. Limited stability in tion and the National Cholesterol Education Program have
PN still limits its use in the United States. agreed that fat and cholesterol should not be restricted in
4. Carbohydrate. Without carbohydrate in the diet, lipolysis, lim- children less than 2 years of age. In children over 2 years of
ited ketone accumulation, and transient protein breakdown may age, the American Academy of Pediatrics recommends 30%
occur. Fifty to 100 g per day of carbohydrate usually prevents or of calories from fat, with less than 10% from saturated fat,
minimizes these effects. and less than 300 mg of cholesterol daily. Acceptable enteral
a) EN. The subcommittee on the 10th edition of the RDA rec- fat intake as a percentage of energy is 25% to 30% (up to
ommended that beyond infancy, greater than 50% of energy 55% in infants).

Table 2-8. Criteria and Dietary Reference Intake Values for Carbohydrate by Life Stage Group43

EAR (g/day) RDA (g/day)

AMDR
Life stage group Criteria Male Female Male Female AI (g/day) %

0–6 mos Average content of human milk 60 ND

7–12 mos Average intake from human milk plus
complementary foods 95 ND
1–3 yrs Extrapolation from adult data 100 100 130 130 45–65
4–8 yrs Extrapolation from adult data 100 100 130 130 45–65
9–13 yrs Extrapolation from adult data 100 100 130 130 45–65
14–18 yrs Extrapolation from adult data 100 100 130 130 45–65
>18 yrs Brain glucose use 100 100 130 130 45–65

AI, adequate intake (the observed average or experimentally determined intake by a defined population or subgroup that appears to sustain a defined nutritional status, such as
growth rate, normal circulatory nutrient values, or other functional indicators of health; used if sufficient scientific evidence is not available to derive an EAR; for healthy infants
receiving human milk, the AI is the mean intake; not equivalent to an RDA); AMDR, acceptable macronutrient distribution range (the intake for a particular energy source associ-
ated with a reduced risk of chronic disease while providing intakes of essential nutrients; reflects the source of kcal to maintain body weight); EAR, estimated average requirement
(the intake that meets the estimated nutrient needs of half of the individuals in a group); ND, not determinable; RDA, recommended dietary allowance (the intake that meets the
nutrient need of almost all [97%–98%] individuals in a group).
Printed with permission from Institute of Medicine. Dietary Reference Intakes for Energy, Carbohydrate, Fiber, Fat, Fatty Acids, Cholesterol, Protein, and Amino Acids (Macronutri-
ents). Washington, DC: National Academy Press; 2002.

46 A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. © 2005 A.S.P.E.N. www.nutritioncare.org.
 S E C T I O N I Fundamentals of Nutrition Support Practice and Management

Table 2-9. Criteria and Dietary Reference Intake Values for PUFA by Life Stage Group43

Linoleic Acid Linolenic Acid

`
AI (g/day) AI (g/day)
AMDR AMDR
Life stage group Criteria Male Female % Male Female %

0–6 mos Average consumption of total fat from 4.4 4.4 ND 0.5 0.5 ND
human milk
7–12 mos Average consumption of total fat from 4.6 4.6 ND 0.5 0.5 ND
human milk and complementary foods
1–3 yrs Median intake of specific PUFA from CSFII 7.0 7.0 5–10 0.7 0.7 0.6–1.2
4–8 yrs Median intake of specific PUFA from CSFII 10.0 10.0 5–10 0.9 0.9 0.6–1.2
9–13 yrs Median intake of specific PUFA from CSFII 12.0 10.0 5–10 1.2 1.0 0.6–1.2
14–18 yrs Median intake of specific PUFA from CSFII 16.0 11.0 5–10 1.6 1.1 0.6–1.2

AI, adequate intake (the observed average or experimentally determined intake by a defined population or subgroup that appears to sustain a defined nutritional status, such as
growth rate, normal circulatory nutrient values, or other functional indicators of health; used if sufficient scientific evidence is not available to derive an EAR; for healthy infants
receiving human milk, the AI is the mean intake; not equivalent to an RDA); AMDR, acceptable macronutrient distribution range (the intake for a particular energy source associ-
ated with a reduced risk of chronic disease while providing intakes of essential nutrients; reflects the source of kcal to maintain body weight); CSFII, Continuing Survey of Food
Intake by Individuals; ND, not determinable; PUFA, polyunsaturated fatty acids.
Printed with permission from Institute of Medicine. Dietary Reference Intakes for Energy, Carbohydrate, Fiber, Fat, Fatty Acids, Cholesterol, Protein, and Amino Acids (Macronutri-
ents). Washington, DC: National Academy Press; 2002.

b) PN
(1) High glucose loads expose the patient to fatty liver infil-
Table 2-10. Criteria and Dietary Reference Intake Val-
tration and possibly metabolic and respiratory stresses. ues for Total Fiber by Life Stage Group43
The minimum fat requirement is determined by essential
fatty acid need, and the daily maximum is 50% to 60% of AI (g/day)
energy. Fats provide concentrated energy and decrease IV Life stage
osmolality. Fat emulsion infusion rate starts at 1 g/kg/ group Criteria Male Female
day with increments of 0.5 to 1 g/kg/day. A 20% fat emul-
sion supplies 2 kcal/mL. Continuous infusions are better 0–6 mos — ND ND
tolerated. 7–12 mos — ND ND
(2) Fat emulsion formulations come from soybean oil, saf- 1–3 yrs Intake level shown to provide the 19 19
flower oil, or both, with different long-chain fatty acid
greatest protection against
(LCFA) content. The combination of MCT with LCFA
coronary heart disease (14 g/1000
formulations are under investigation. MCT are better
hydrolyzed, with less storage in the body. kcal of required energy) ? median
6. Fiber. AI estimates are available exclusively for EN. Recom- energy intake level (kcal/1000
mendations are shown in Table 2-10.43 kcal/day)
7. Vitamins and minerals 4–8 yrs " 25 25
a) EN 9–13 yrs " 31 26
(1) The DRI provide recommendations based on dietary 14–18 yrs " 38 26
intakes, a factorial approach of nutrient retention, and 19–50 yrs " 38 25
estimates of physiological needs extrapolated from pre- >51 yrs " 30 21
vious studies in adults or children (see Tables 2-11 and
2-12).42,48–50 Upper Levels are also available for most
vitamins and minerals. Requirements are usually met by AI, adequate intake (the observed average or experimentally determined intake by a
eating a variety of foods. The nutrient content of enteral defined population or subgroup that appears to sustain a defined nutritional status,
such as growth rate, normal circulatory nutrient values, or other functional indicators
formulations mirrors these recommendations.
of health; used if sufficient scientific evidence is not available to derive an EAR; for
(2) Administration of vitamin K to newborn infants is recom- healthy infants receiving human milk, the AI is the mean intake; not equivalent to an
mended for the prevention of hemorrhagic disease. Breast- RDA); ND, not determinable.
fed or formula-fed infants receive one intramuscular dose Printed with permission from Institute of Medicine. Dietary Reference Intakes for
of 0.5 to 1.0 mg at birth or later, or multiple oral doses of Energy, Carbohydrate, Fiber, Fat, Fatty Acids, Cholesterol, Protein, and Amino Acids
1.0 to 2.0 mg. (Macronutrients). Washington, DC: National Academy Press; 2002.

© 2005 A.S.P.E.N. www.nutritioncare.org. A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. 47
S E C T I O N I Fundamentals of Nutrition Support Practice and Management

Table 2-11. Dietary Reference Intakes (DRIs): Recommended Intakes for Individuals, Vitamins
Food and Nutrition Board, Institute of Medicine, National Academies

Panto-
thenic
Life stage Vit A Vit C Vit D Vit E Vit K Thia- Ribo- Niacin Vit B6 Folate Vit B12 acid Biotin Choline
group (µg/d) a (mg/d) (µg/d) b,c (mg/d) d (µg/d) (mg/d) (mg/d) (mg/d) e (mg/d) (µg/d) f (µg/d) (mg/d) (µg/d) (mg/d) g

Infants
0–6 mo 400* 40* 5* 4* 2.0* 0.2* 0.3* 2* 0.1* 65* 0.4* 1.7* 5* 125*
7–12 mo 500* 50* 5* 5* 2.5* 0.3* 0.4* 4* 0.3* 80* 0.5* 1.8* 6* 150*
Children
1–3 y 300 15 5* 6 30.0* 0.5 0.5 6 0.5 150 0.9 2* 8* 200*
4–8 y 400 25 5* 7 55.0* 0.6 0.6 8 0.6 200 1.2 3* 12* 250*
Males
9–13 y 600 45 5* 11 60.0* 0.9 0.9 12 1.0 300 1.8 4* 20* 375*
14–18 y 900 75 5* 15 75.0* 1.2 1.3 16 1.3 400 2.4 5* 25* 550*
19–30 y 900 90 5* 15 120.0* 1.2 1.3 16 1.3 400 2.4 5* 30* 550*
31–50 y 900 90 5* 15 120.0* 1.2 1.3 16 1.3 400 2.4 5* 30* 550*
51–70 y 900 90 10* 15 120.0* 1.2 1.3 16 1.7 400 2.4 h 5* 30* 550*
> 70 y 900 90 15* 15 120.0* 1.2 1.3 16 1.7 400 2.4 h 5* 30* 550*
Females
9–13 y 600 45 5* 11 60.0* 0.9 0.9 12 1.0 300 1.8 4* 20* 375*
14–18 y 700 65 5* 15 75.0* 1.0 1.0 14 1.2 400 i 2.4 5* 25* 400*
19–30 y 700 75 5* 15 90.0* 1.1 1.1 14 1.3 400 i 2.4 5* 30* 425*
31–50 y 700 75 5* 15 90.0* 1.1 1.1 14 1.3 400 i 2.4 5* 30* 425*
51–70 y 700 75 10* 15 90.0* 1.1 1.1 14 1.5 400 2.4 h 5* 30* 425*
> 70 y 700 75 15* 15 90.0* 1.1 1.1 14 1.5 400 2.4 h 5* 30* 425*
Pregnancy
14–18 y 750 80 5* 15 75.0* 1.4 1.4 18 1.9 600 j 2.6 6* 30* 450*
19–30 y 770 85 5* 15 90.0* 1.4 1.4 18 1.9 600 j 2.6 6* 30* 450*
31–50 y 770 85 5* 15 90.0* 1.4 1.4 18 1.9 600 j 2.6 6* 30* 450*
Lactation
14–18 y 1,200 115 5* 19 75.0* 1.4 1.6 17 2.0 500 2.8 7* 35* 550*
19–30 y 1,300 120 5* 19 90.0* 1.4 1.6 17 2.0 500 2.8 7* 35* 550*
31–50 y 1,300 120 5* 19 90.0* 1.4 1.6 17 2.0 500 2.8 7* 35* 550*

Note: This table (taken from the DRI reports, see www.nap.edu) presents Recommended Dietary Allowances (RDAs) in bold type and Adequate Intakes (AIs) in ordinary type fol-
lowed by an asterisk (*). RDAs and AIs may both be used as goals for individual intake. RDAs are set to meet the needs of almost all (97 to 98 percent) individuals in a group. For
healthy breastfed infants, the AI is the mean intake. The AI for other life stage and gender groups is believed to cover needs of all individuals in the group, but lack of data or
uncertainty in the data prevent being able to specify with confidence the percentage of individuals covered by this intake.
a As retinol activity equivalents (RAEs). 1 RAE = 1 µg retinol, 12 µg b-carotene, 24 µg b-carotene, or 24 µg b-cryptoxanthin. The RAE for dietary provitamin A carotenoids is twofold

greater than retinol equivalents (RE), whereas the RAE for preformed vitamin A is the same as RE.
b As cholecalciferol. 1 µg cholecalciferol = 40 IU vitamin D.

c In the absence of adequate exposure to sunlight.

d As a-tocopherol. a-Tocopherol includes RRR-a-tocopherol, the only form of α-tocopherol that occurs naturally in foods, and the 2R-stereoisomeric forms of

a-tocopherol (RRR-, RSR-, RRS-, and RSS-α-tocopherol) that occur in fortified foods and supplements. It does not include the 2S-stereoisomeric forms of a-tocopherol
(SRR-, SSR-, SRS-, and SSS-a-tocopherol), also found in fortified foods and supplements.
e As niacin equivalents (NE). 1 mg of niacin = 60 mg of tryptophan; 0–6 months = preformed niacin (not NE).

f As dietary folate equivalents (DFE). 1 DFE = 1 µg food folate = 0.6 µg of folic acid from fortified food or as a supplement consumed with food = 0.5 µg of a supplement taken on an

empty stomach.
g Although AIs have been set for choline, there are few data to assess whether a dietary supply of choline is needed at all stages of the life cycle, and it may be that the choline

requirement can be met by endogenous synthesis at some of these stages.

h Because 10 to 30 percent of older people may malabsorb food-bound B12, it is advisable for those older than 50 years to meet their RDA mainly by consuming foods fortified with

B12 or a supplement containing B12.

i In view of evidence linking folate intake with neural tube defects in the fetus, it is recommended that all women capable of becoming pregnant consume 400 µg from supplements

or fortified foods in addition to intake of food folate from a varied diet.

j It is assumed that women will continue consuming 400 µg from supplements or fortified food until their pregnancy is confirmed and they enter prenatal care, which ordinarily

occurs after the end of the periconceptional period—the critical time for formation of the neural tube.
Copyright 2004 by the National Academy of Sciences. Reprinted with permission from National Academy Press.

48 A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. © 2005 A.S.P.E.N. www.nutritioncare.org.
 S E C T I O N I Fundamentals of Nutrition Support Practice and Management

Table 2-12. Dietary Reference Intakes (DRIs): Recommended Intakes for Individuals, Elements
Food and Nutrition Board, Institute of Medicine, National Academies

Life Chro- Mag- Man- Molyb- Phos- Selen- Potas-

stage Calcium mium Copper Fluoride Iodine Iron nesium ganese denum phorus ium Zinc sium Sodium Chloride
group (mg/d) (µg/d) (µg/d) (mg/d) (µg/d) (mg/d) (mg/d) (mg/d) (µg/d) (mg/d) (µg/d) (mg/d) (g/d) (g/d) (g/d)

Infants
0–6 mo 210* 0.2* 200* 0.01* 110* 0.27* 30* 0.003* 2* 100* 15* 2* 0.4* 0.12* 0.18*
7–12 mo 270* 5.5* 220* 0.5* 130* 11.0 75* 0.6* 3* 275* 20* 3 0.7* 0.37* 0.57*

Children
1–3 y 500* 11.0* 340 0.7* 90 7.0 80 1.2* 17 460 20 3 3.0* 1.0* 1.5*
4–8 y 800* 15.0* 440 1.0* 90 10.0 130 1.5* 22 500 30 5 3.8* 1.2* 1.9*

Males
9–13 y 1,300* 25.0* 700 2.0* 120 8.0 240 1.9* 34 1,250 40 8 4.5* 1.5* 2.3*
14–18 y 1,300* 35.0* 890 3.0* 150 11.0 410 2.2* 43 1,250 55 11 4.7* 1.5* 2.3*
19–30 y 1,000* 35.0* 900 4.0* 150 8.0 400 2.3* 45 700 55 11 4.7* 1.5* 2.3*
31–50 y 1,000* 35.0* 900 4.0* 150 8.0 420 2.3* 45 700 55 11 4.7* 1.5* 2.3*
51–70 y 1,200* 30.0* 900 4.0* 150 8.0 420 2.3* 45 700 55 11 4.7* 1.3* 2.0*
> 70 y 1,200* 30.0* 900 4.0* 150 8.0 420 2.3* 45 700 55 11 4.7* 1.2* 1.8*

Females
9–13 y 1,300* 21.0* 700 2.0* 120 8.0 240 1.6* 34 1,250 40 8 4.5* 1.5* 2.3*
14–18 y 1,300* 24.0* 890 3.0* 150 15.0 360 1.6* 43 1,250 55 9 4.7* 1.5* 2.3*
19–30 y 1,000* 25.0* 900 3.0* 150 18.0 310 1.8* 45 700 55 8 4.7* 1.5* 2.3*
31–50 y 1,000* 25.0* 900 3.0* 150 18.0 320 1.8* 45 700 55 8 4.7* 1.5* 2.3*
51–70 y 1,200* 20.0* 900 3.0* 150 8.0 320 1.8* 45 700 55 8 4.7* 1.3* 2.0*
> 70 y 1,200* 20.0* 900 3.0* 150 8.0 320 1.8* 45 700 55 8 4.7* 1.2* 1.8*

Pregnancy
14–18 y 1,300* 29.0* 1,000 3.0* 220 27.0 400 2.0* 50 1,250 60 13 4.7* 1.5* 2.3*
19–30 y 1,000* 30.0* 1,000 3.0* 220 27.0 350 2.0* 50 700 60 11 4.7* 1.5* 2.3*
31–50 y 1,000* 30.0* 1,000 3.0* 220 27.0 360 2.0* 50 700 60 11 4.7* 1.5* 2.3*

Lactation
14–18 y 1,300* 44.0* 1,300 3.0* 290 10.0 360 2.6* 50 1,250 70 14 5.1* 1.5* 2.3*
19–30 y 1,000* 45.0* 1,300 3.0* 290 9.0 310 2.6* 50 700 70 12 5.1* 1.5* 2.3*
31–50 y 1,000* 45.0* 1,300 3.0* 290 9.0 320 2.6* 50 700 70 12 5.1* 1.5* 2.3*

Note: This table presents Recommended Dietary Allowances (RDAs) in bold type and Adequate Intakes (AIs) in ordinary type followed by an asterisk (*). RDAs and AIs may both be
used as goals for individual intake. RDAs are set to meet the needs of almost all (97 to 98 percent) individuals in a group. For healthy breastfed infants, the AI is the mean intake.
The AI for other life stage and gender groups is believed to cover needs of all individuals in the group, but lack of data or uncertainty in the data prevent being able to specify with
confidence the percentage of individuals covered by this intake.
Sources: Dietary Reference Intakes for Calcium, Phosphorous, Magnesium, Vitamin D, and Fluoride (1997); Dietary Reference Intakes for Thiamin, Riboflavin, Niacin, Vitamin B6,
Folate, Vitamin B12, Pantothenic Acid, Biotin, and Choline (1998); Dietary Reference Intakes for Vitamin C, Vitamin E, Selenium, and Carotenoids (2000); Dietary Reference Intakes
for Vitamin A, Vitamin K, Arsenic, Boron, Chromium, Copper, Iodine, Iron, Manganese, Molybdenum, Nickel, Silicon, Vanadium, and Zinc (2001); and Dietary Reference Intakes for
Water, Potassium, Sodium, Chloride, and Sulfate (2004). These reports may be accessed via http://www.nap.edu.
Copyright 2004 by the National Academy of Sciences. All rights reserved. Reprinted with permission from National Academy Press.

(3) Vitamin D supplementation (200–400 international with an additional source of iron such as iron-fortified
units/d) is recommended for breast-fed infants and older cereal by 4 to 6 months of age. Other sources of iron in
infants (>6 months), especially those with limited expo- addition to cereal may be beneficial after 6 months of age.
sure to sunlight. b) PN
(4) Iron-fortified formula should be provided to infants who (1) Guidelines for the provision of IV vitamins and trace
are not breast-fed. The breast-fed infant should be provided elements in pediatrics follow the indications of the

© 2005 A.S.P.E.N. www.nutritioncare.org. A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. 49
S E C T I O N I Fundamentals of Nutrition Support Practice and Management

Subcommittee on Pediatric Parenteral Nutrient Require-

ments from the Committee on Clinical Practice Issues of the Table 2-13. EER for Healthy Adults43
American Society for Clinical Nutrition and A.S.P.E.N.36–38
(2) The multivitamin needs of term infants are commonly met Men age 19 years and older:
by a pediatric multivitamin at 2 mL/kg up to a maximum of EER = 662 – 9.53 (age in yrs) + PA (15.91 × weight in kg)
5 mL/day (dose used in children up to 11 years old). For + 539.6(height in m)
children over 11 years of age, the adult version of multi- PA = 1.00 for sedentary men
vitamins will meet estimated requirements plus the addi- PA = 1.11 for low-activity men
tion of vitamin K (2–4 mg/week or 1 mg/day).51 See
PA = 1.25 for moderate-activity men
Chapter 8, Table 8-6, for PN multivitamins.
PA = 1.49 for high-activity men
(3) The trace element needs are described in Chapter 8,
Table 8-7. Women age 19 years and older:
(4) If the patient is to be on PN for >1 month, supplemental
EER = 354 – 6.91 (age in yrs) + PA (9.36 × weight in kg) + 726 (height
selenium and possibly molybdenum should be added.
Selenium should be provided at 2 to 3 mcg/kg/day (maxi- in m)
mum: 40–60 mcg/day), while molybdenum requirements PA = 1.00 for sedentary women
may be met by providing 0.25 mcg/kg/day (maximum: PA = 1.12 for low-activity women
5 mcg/day). Also, carnitine can become deficient in long- PA = 1.27 for moderate-activity women
term PN patients receiving all their calories from PN. The PA = 1.45 for high-activity women
recommended IV intake is 10 to 30 mg/kg/day (maximum
100 mg/day). Harris-Benedict equations
(5) If liver or renal complications occur, some trace element Men 66.42 + 13.75 (weight in kg) + 5.00 (height in cm)
regimens have to be reformulated for PN patients (see – 6.78 (age in yrs)
Section III.A.2.f).(3).(b)). Women 655.1 + 9.65 (weight in kg) + 1.85 (height in cm) – 4.68
8. Fluids and electrolytes. Body homeostasis is maintained by fluids, (age in yrs)
which are the bulk of body weight in children (60%–70%) and
especially in neonates (up to 80%). To maintain water and elec-
trolyte homeostasis and to allow metabolic processes (including EER, estimated energy requirements; PA = physical activity coefficient.
the effects of insensible and sweat losses), a certain amount of Printed with permission from Institute of Medicine. Dietary Reference
fluid has to be introduced daily regardless of health conditions. Intakes for Energy, Carbohydrate, Fiber, Fat, Fatty Acids, Cholesterol, Protein,
Maintenance is mainly dependent on TEE and environmental tem- and Amino Acids (Macronutrients). Washington, DC: National Academy
Press; 2002.
perature, whereas deficit replacements seem to be directly related
to the size of the deficit and the body mass. Factors such as losses
and organ dysfunction may require volume individualization. b) Energy requirement may be measured by indirect calorimetry
New DRI for some electrolytes can be found in Table 2-12.52 if equipment is available; this measurement may be particu-
a) Fluid maintenance requirements can be computed following larly valuable in the critically ill patient. The value derived is
the A.S.P.E.N. recommendations based on the Holliday-Segar REE, which is the energy expended at rest (not necessarily
method. The Holliday-Segar formula estimates fluid needs by fasting). Then appropriate factors can be applied to account
calculating energy expenditure and relating this to water for physical activity.
losses and water of metabolism. The formula is based on c) In the absence of indirect calorimetry capability, various
energy expenditure for bed rest and therefore may not be ade- methods are used to estimate energy requirements of sick
quate for highly active children: patients.55,56
(1) 2 to 10 kg, 100 mL/kg (1) Harris-Benedict equations (Table 2-13) derived from
(2) 10 to 20 kg, 1000 mL + 50 mL/kg for each kg over 10 healthy adults, adjusted for activity and stress, have been
(3) 20 kg and up, 1500 mL + 20 mL/kg for each kg over 2038 widely applied to sick patients to predict REE.
b) Another method, based on body surface area, can be accurate (2) Alternatively, more recently, regression equations based
for children of abnormal height for weight: 1500 to 1700 mL/ on sick populations have been derived; two of the more
m2/day.53 commonly used are the Ireton-Jones equations (Table 2-
c) Based on caloric intake, infant and child fluid needs are, 14).57 These equations already factor in the stress level of
respectively, 1.5 and 1 mL/kcal of energy expenditure. the patient.
d) PN electrolyte recommendations are outlined in Chapter 8, (3) Also frequently used is the simple calculation of energy
Table 8-2.38,54 Addition of calcium and phosphorus to PN is requirement based on kcal per kg body weight. The typ-
limited by solubility. ical range is 20 to 35 total kcal per kg body weight per
C. Adults day.36
1. Energy requirements (4) With most of these methods, the question of what body
a) Estimated energy requirement (EER) as defined by the Insti- weight to use in a patient who is significantly above ideal
tute of Medicine (IOM) for healthy adults is the dietary energy body weight must be addressed. See Chapter 28 for a dis-
intake predicted to maintain energy balance in a healthy cussion of this topic.
adult of a defined age, gender, weight, height, and level of (5) Another source of confusion when applying these equa-
physical activity consistent with good health.43 EER equations tions is whether to express energy requirements in terms
for men and women are given in Table 2-13.43 of total kcal or nonprotein kcal. In the early days of PN,

50 A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. © 2005 A.S.P.E.N. www.nutritioncare.org.
 S E C T I O N I Fundamentals of Nutrition Support Practice and Management

in enteral feeding products. MCT are a source of some of the

Table 2-14. Ireton-Jones Equations for Estimation of fat in many enteral formulas and serve as a readily utilizable
Energy Requirements of Hospitalized energy source.
Patients57 g) Special considerations in the elderly. Both REE and physical
activity decrease with age; the decrease in REE is primarily
Spontaneously breathing patients: due to decrease in lean body mass and increase in fat mass
kcal/day = 629 – 11 (age in yrs) + 25 (weight in kg) – 609(O)* with age. Individual differences in the elderly make estima-
tion of energy requirements challenging.
Ventilator-dependent patients: 2. Protein requirements
kcal/day = 1784 – 11 (age in yrs) + 5 (weight in kg) + 244(S) ** a) The RDA for protein for healthy adults is 0.8 g/kg/day (Table
+ 239(T)*** + 804(B)**** 2-6).43
b) Protein requirements for catabolic patients are generally
higher, in the range of 1.2 to 2.0 g/kg/day.36,38 About 25% to
*
O stands for obesity (>30% above initial weight from 1959 Metropolitan Life Insur- 30% of protein intake should typically be provided by
ance tables or body mass index > 27 kg/m2): use 1 if present and 0 if absent. essential amino acids.36
**S stands for sex: use 1 for male and 0 for female.

***
c) Adequate kcal must be provided along with protein to ensure
T stands for diagnosis of trauma: use 1 if present and 0 if absent.
****B stands for diagnosis of burn: use 1 if present and 0 if absent.
the proper utilization of protein.
Reprinted from Ireton-Jones C, Jones JD. Improved equations for predicting energy
d) Patients with certain disease states such as renal failure and
expenditure in patients: the Ireton-Jones equations. Nutr Clin Pract. 2002;17:29–31 end-stage liver disease may require protein restriction (see
with permission from A.S.P.E.N. disease-specific chapters 17, 23, 24 and 29).
e) Provision of individual amino acids for specific situations
may be beneficial, although general recommendations cannot
kcal requirements were often referred to in terms of non- yet be made.36
protein kcal, since it was felt that the protein supplied by f) Although there has been some suggestion that protein require-
the nutrient solution was being given not to act as an ments may be increased in the elderly, the RDA for adults
energy source for the body but rather as a substrate for 50 years and older was set at the same level as for younger
synthesis of lean body mass. The recent trend is to express adults (0.8 g/kg/day).43
energy requirements in terms of total kcal, since the body 3. Fluid requirements
does not distinguish that infused protein is not to be used a) Typical fluid requirements for adults are 20 to 40 mL/kg/day or
as a fuel source. 1 to 1.5 mL/kcal of energy expended.36,38,41,52 Fluid supplied by
d) Energy requirements of patients requiring nutritional support nutritional support should be individualized on the basis of
should generally be met through provision of a mixed fuel patient inputs and outputs and estimates of insensible losses.
system, that is, one providing substantial kcal from both car- b) Fluid requirements of the elderly are similar to those quoted
bohydrate and fat. Carbohydrate should generally be provided above. However, many elderly persons are underhydrated, due
at a rate not to exceed 7 g/kg/day (about 5 mg/kg/minute).36 to impaired thirst mechanisms and inability to obtain or con-
Fat should generally be provided at a rate not to exceed 2.5 g/ sume liquids by themselves, thus making attention to intake
kg/day; at least 1% to 2% of kcal should be derived from and output data critical in this population.58 On the other hand,
linoleic and 0.5% from alpha-linolenic acid to prevent essen- fluid may sometimes need to be restricted in the ill elderly due
tial fatty acid deficiency.36 Many clinicians would limit fat to underlying conditions such as congestive heart failure.
infusion to closer to 1 g/kg/day, especially in critically ill and 4. Electrolyte requirements
immunocompromised adults. The typical distribution of car- a) Daily electrolyte requirements for generally healthy people
bohydrate and fat in PN solutions is about 70% to 85% non- receiving PN or EN as published by A.S.P.E.N. are shown in
protein kcal as carbohydrate and 15% to 30% nonprotein kcal Table 2-15.36,38 Note that some of these values for enteral elec-
as fat. Corresponding distributions for EN would be about trolytes are slightly different from the AI and RDA values
65% to 80% nonprotein kcal as carbohydrate and 20% to 35% recently published by the IOM and presented in Table 2-12.
nonprotein kcal as fat. b) The requirements of ill patients receiving these therapies can
e) Carbohydrate in PN is provided exclusively as dextrose in the be much different, especially in the presence of organ dysfunc-
United States. Carbohydrate sources for EN are more varied. tion, thus necessitating close clinical and laboratory monitor-
Starch or glucose polymers found in standard formulas require ing of these patients.
digestion to be absorbed. The formulas that require less diges- 5. Vitamin requirements
tive function typically contain oligosaccharides as the carbo- a) Vitamin requirements for patients receiving enteral feed-
hydrate source. ings are based on the RDA or, if no RDA has been set for a
f) Commercially available lipid for IV infusion in the United particular vitamin, the AI.42,48–50 See Table 2-11 for vitamin
States is derived from soybean oil or a combination of soy- recommendations for healthy persons on oral diets; these
bean and safflower oils. These emulsions contain LCFAs. recommendations can be extrapolated with caution to patients
Use of MCT as an IV fat source remains investigational in the on enteral feedings.36
United States, although commercial products containing a b) Parenteral vitamin requirements are poorly defined. Current
blend of MCT and long-chain triglycerides for IV use are parenteral recommendations are largely based on guidelines
available in several other countries. Fat sources in standard adopted by the American Medical Association Department of
adult EN formulas include vegetable oils such as soy or corn Foods and Nutrition, which were approved by the Food and
oil rich in PUFA. Canola oil is another common source of fat Drug Administration (FDA) in 1979.59 Amendments to these

© 2005 A.S.P.E.N. www.nutritioncare.org. A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. 51
S E C T I O N I Fundamentals of Nutrition Support Practice and Management

iodine and molybdenum are not well defined, and therefore

Table 2-15. Daily Adult Enteral and Parenteral Elec- these minerals are not routinely added to PN solutions.
trolyte Requirements Assuming Normal However, some commercially available multiple–trace ele-
Age-Related Organ Function36 ment solutions contain these minerals. Many patients on
long-term PN will require parenteral iron supplementation;
Enteral Parenteral many clinicians wait until laboratory abnormalities consis-
tent with iron insufficiency develop before supplementing
Sodium 500 mg (22 mEq) 1–2 mEq/kg with parenteral iron.
c) Trace element RDAs and AIs are generally identical for older
Potassium 2 g (51 mEq) 1–2 mEq/kg
adults and younger adults. The two exceptions are the AI val-
Chloride 750 mg (21 mEq) As needed to maintain acid-base ues for chromium, which are lower for adults 51 years old
balance and older than for younger adults, and the RDA for iron,
which is lower for postmenopausal women than for pre-
Acetate — As needed to maintain acid-base
menopausal women.
balance
Calcium 1200 mg (60 mEq) 10–15 mEq (Nutritional Requirements chapters from the 1st edition were con-
tributed by Harry C. Sax, Wiley W. Souba, Nancy Baugh, Marilyn A.
Magnesium 420 mg (35 mEq) 8–20 mEq
Recupero, and John A. Kerner Jr)
Phosphorus 700 mg (23 mmol) 20–40 mmol
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ments in patients receiving EN are generally set in accord and micronutrient supplement in undernourished children in Indonesia. Eur
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b) Recommendations for parenteral chromium, copper, man- 14. Heird WC. The role of polyunsaturated fatty acids in term and preterm infants
ganese, and zinc were set by the Nutrition Advisory Group and breastfeeding mothers. Pediatr Clin North Am. 2001;48:173–188.
of the Department of Foods and Nutrition, American Med- 15. Lucas A. Does early diet program future outcome? Acta Paediatr.
ical Association, in 1979 (Chapter 8, table 8-5).62 The Amer- 1990;365(suppl):S58–S67.
16. Reddy P, Malone M. Cost and outcome analysis of home parenteral and
ican Medical Association has not published updates to these
enteral nutrition. J Parenter Enteral Nutr. 1998;22:302–310.
recommendations; however, other definitive guidelines have
17. Holden CE, Puntis JWL, Charlton CPL, et al. Nasogastric feeding at
set copper and manganese recommendations at levels sig- home: acceptability and safety. Arch Dis Child. 1991;66:148–151.
nificantly lower than those originally recommended and 18. De Potter S, Goulet O, Lamor M, et al. Two hundred sixty-three patient-
have also set a recommendation for the parenteral require- years of home parenteral nutrition in children. Transplant Proc. 1992;
ment for selenium.36,38 Note that parenteral requirements for 24:1056–1057.

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19. DeCicco M, Panarello G, Fantin D, et al. Parenteral nutrition in cancer 41. Food and Nutrition Board, National Academy of Sciences, National
patients receiving chemotherapy: effects on toxicity and nutritional status. Research Council. Recommended Dietary Allowances. 10th ed. Washington,
J Parenter Enteral Nutr. 1993;17:513–518. DC: National Academy Press; 1989.
20. Sax HC, Warner BW, Talamini MA, et al. Early total parenteral nutrition 42. Institute of Medicine. Dietary Reference Intakes for Calcium, Phosphorus,
in acute pancreatitis: lack of beneficial effects. Am J Surg. 1987;153: Magnesium, Vitamin D, and Fluoride. Washington, DC: National Academy
117–124. Press; 1997.
21. Valdivieso M, Frankmann C, Murphy WK, et al. Long-term effects of 43. Institute of Medicine. Dietary Reference Intakes for Energy, Carbohydrate,
intravenous hyperalimentation administered during intensive chemother- Fiber, Fat, Fatty Acids, Cholesterol, Protein, and Amino Acids (Macro-
apy for small cell bronchogenic carcinoma. Cancer. 1987;59:362–369. nutrients). Washington, DC: National Academy Press; 2002.
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maturity and during late gestation and early infancy. Pediatrics. 1971; 45. World Health Organization. Energy and Protein Requirements. Technical
47(suppl 2):169–179. Report Series, No 724. Geneva, Switzerland: World Health Organization;
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nents of fat-free mass in humans. Am J Clin Nutr. 1992;55:790–794. previous work. Hum Nutr Clin Nutr. 1985;39C(S1):5–41.
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Advances in Obesity Research. Volume 2. London, UK: Newman Publ; 48. Institute of Medicine. Dietary Reference Intakes for Thiamin, Riboflavin,
1978:211–228. Niacin, Vitamin B6, Folate, Vitamin B12, Pantothenic Acid, Biotin, and
27. Payne PR, Waterlow JC. Relative energy requirement for maintenance, Choline. Washington, DC: National Academy Press; 1998.
growth, and physical activity. Lancet. 1971;2:210–211. 49. Institute of Medicine. Dietary Reference Intakes for Vitamin C, Vitamin E,
28. Frankenfield DC, Wiles CE 3rd, Bagley S, et al. Relationships between Selenium, and Carotenoids. Washington, DC: National Academy Press;
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29. Teitelbaum J, Walker WA. Review: the role of omega 3 fatty acids in intes-
Arsenic, Boron, Chromium, Copper, Iodine, Iron, Manganese, Molybdenum,
tinal inflammation. J Nutr Biochem. 2001;12:21–32.
Nickel, Silicon, Vanadium, and Zinc. Washington, DC: National Academy
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sea level: standards obtained from measurements in 7 dimensions of infants
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born between 25 and 44 weeks of gestation. Pediatrics. 1969;74:901–910.
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on Nutrition. Pediatric Nutrition Handbook. 4th ed. Elk Grove, IL: tion. In: Kleinman RE, ed. Pediatric Nutrition Handbook. 4th ed. Elk
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Duggan C., eds. Nutrition in Pediatrics. 3rd ed. Hamilton, Ontario: BC care unit. Nutr Clin Pract. 2002;17:21–28.
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36. A.S.P.E.N. Board of Directors and the Clinical Guidelines Task Force. weight adjustments currently used to estimate energy expenditure in hos-
Guidelines for the use of parenteral and enteral nutrition in adult and pedi- pitalized patients. J Parenter Enteral Nutr. 2002;26:231–238.
atric patients. J Parenter Enteral Nutr. 2002;26(1 suppl):1SA–138SA. 57. Ireton-Jones C, Jones JD. Improved equations for predicting energy expen-
37. Greene HL, Hambridge KM, Schanler R, et al. Guidelines for the use of vita- diture in patients: the Ireton-Jones equations. Nutr Clin Pract. 2002;17:
mins, trace elements, calcium, magnesium, and phosphorus in infants and 29–31.
children receiving total parenteral nutrition: report of the Subcommittee on 58. Castellanos VH, Silver HJ, Gallagher-Allred C, et al. Nutrition issues in the
Pediatric Parenteral Nutrient Requirements for the Committee on Clinical home, community, and long-term care setting. Nutr Clin Pract. 2003;18:
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Nutr. 1998;48:1324–1342. 59. American Medical Association, Department of Foods and Nutrition.
38. Task Force for the Revision of Safe Practices for Parenteral Nutrition. Safe Multivitamin preparations for parenteral use. A statement by the Nutrition
practices for parenteral nutrition. J Parenter Enteral Nutr. 2004;28: Advisory Group. J Parent Enteral Nutr. 1979;3:258–261.
S39–S70. 60. Food and Drug Administration. Parenteral multivitamin products: drugs
39. Denne SC, Clark SE, Poindexter BB. Nutrition and metabolism in the for human use: drug efficacy study implementation: amendment. Federal
high-risk neonate. In: Fanaroff AA, Martin RJ, eds. Neonatal-Perinatal Register. April 20, 2000;65(77):21200–21201.
Medicine. Diseases of the Fetus and Infant. St Louis, MO: Mosby; 61. Chernoff R. Normal aging, nutrition assessment, and clinical practice.
1997:562–621. Nutr Clin Pract. 2003;18:12–20.
40. Aggett PJ, Haschke F, Heine W, et al. Comment on the content and compo- 62. American Medical Association. Guidelines for essential trace element
sition of lipids in infant formulas. ESPGHAN Committee on Nutrition. preparations for parenteral use. A statement by the Nutrition Advisory
Acta Paediatr Scand. 1991;80:887–896. Group. J Parenter Enteral Nutr. 1979;3:263–267.

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 Donald F. Kirby, MD, CNSP;
Marianne Opilla, RN, BSN, CNSN
3
Enteral Access and
Infusion Equipment

Introduction 1. Short—term feeding tubes (<3 weeks)

a) Patients not undergoing laparotomy—nasogastric or orogas-
Patients who are unable to meet their nutritional requirements with oral
tric, nasoenteric or oroenteric: Orogastric tube feedings may
intake frequently need supplementation, either enterally or parenterally.
be better tolerated in premature and small infants, as they are
The enteral route is preferred whenever possible because it is associated
obligatory nasal breathers. Orogastric feedings are also indi-
with lower costs, fewer complications, and improved outcome. In this
cated for children with choanal atresia or basilar skull fracture
chapter, we discuss how to choose among the multiple enteral access
who cannot feed orally.
routes and tubes that are available. We also address how to care for the
b) Patients undergoing laparotomy for another indication: Gas-
tubes and administration devices.
trostomy, jejunostomy (standard), needle catheter jejunostomy
(NCJ), or a nasoenteric tube can be placed during surgery.
I. Background
2. Long-term feeding tubes adults >4–8 weeks; pediatrics >4–
II. Selection of Enteral Feeding Route
6 weeks)
III. Short-Term Nonsurgical Prepyloric Tubes
a) Patients not undergoing laparotomy: percutaneous endoscopic
IV. Short-Term Nonsurgical Postpyloric Tubes
gastrostomy (PEG), percutaneous endoscopic jejunostomy
V. Short-Term Surgical Pre- and Postpyloric Tubes
(PEJ), percutaneous radiologic gastrostomy, percutaneous
VI. Long-Term Prepyloric Tubes
radiologic jejunostomy, laparoscopic gastrostomy or jejunos-
VII. Long-Term Postpyloric Tubes
tomy, or cervical pharyngostomy/esophagostomy (not com-
VIII. Selection of Access Device Features
monly done)
IX. Care of Feeding Tubes
b) Patients undergoing laparotomy for feeding tube placement:
X. Selection of Infusion Equipment
gastrostomy, transgastric jejunostomy, jejunostomy
References
B. Does the patient need pre- or postpyloric access? Technically,
Suggested Readings
prepyloric tubes are the easiest to insert, and they have the advantage
of delivering feeds in a more “standard” physiologic manner into the
I. Background. To choose the proper access device after deter- stomach. However, some patients may have severe reflux or delayed
mining that enteral feeding can be used, the clinician needs to ask sev- gastric emptying, necessitating postpyloric access to prevent tube
eral questions: feeding–related aspiration (TFRA). The more distal to the stomach
the ___location of feeding delivery, the less likely TFRA is to occur.1–3
A. How long will feeding be required? Thus, the optimal postpyloric tube placement is in the fourth portion
B. Can the patient tolerate gastric feeding, or is postpyloric (or ideally, of the duodenum or past the ligament of Treitz.
post–ligament of Treitz) access required? C. Who has the interest and expertise to place tubes? Choices include
C. Who is available with the expertise to place the access (ie, nurse, gastroenterologists, surgeons, dietitians, nurses, and radiologists.
dietitian, surgeon, endoscopist, or radiologist)? After the access Most specialists favor specific tubes and access methods, so the
tube has been placed, further decisions about infusion equipment route of insertion varies among them. Methods of access insertion
are necessary. These decisions are somewhat dictated by the route include blind passage, operative, endoscopic, laparoscopic, and
and type of tube selected as well as by the availability of personnel radiologic placement.
and resources. D. In children, a gastrostomy tube is the most common method for long-
term enteral access. Gastrostomy avoids nasopharyngeal irritation
II. Selection of Enteral Feeding Route (Figure 3-1) and the psychosocial issue of the nasoenteric tube. Gastrostomy tubes
have larger diameters than jejunostomy tubes and are less likely
A. The estimated length of time that tube feeding will be required is an to clog.
important issue that should be addressed before access placement. If
feeds are needed for only a short time, tubes that are easily placed
with low-risk procedures are usually recommended; however,
III. Short-Term Nonsurgical Prepyloric Tubes
occlusion and displacement rates are higher with these tubes. More A. Nasogastric tubes (NGTs). Commonly used, traditional NGTs (eg,
complex, higher-risk procedures (ie, surgery) may be required to Salem sumps) may perform many functions in addition to feeding,
secure permanent tubes. Children’s growth will need to be moni- such as decompression of the stomach, administration of medica-
tored so that feeding tube shaft lengths can be changed as needed and tion, and measurement of gastric pH or residuals. NGTs are made
complications prevented. in various sizes (5F–18F), but, to avoid clogging, at least a 10F tube

54 A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. © 2005 A.S.P.E.N. www.nutritioncare.org.
 S E C T I O N I Fundamentals of Nutrition Support Practice and Management

anesthetized patients, the left lateral decubitus position may

FIGURE 3-1. Enteral access feeding options. Artwork by decrease this risk. The tube is carefully directed back through
Mary Beatty, McGuire Veteran’s Affairs the nares to the hypopharynx. When the tip is in the posterior
Medical Center Media Department, Rich- pharynx, the patient should be asked to take small sips of
mond, VA. water or initiate dry swallows to facilitate passage of the tube
past the upper esophageal sphincter (UES). If the patient begins
ORO-NASO- to cough or cannot speak, the tube should be retracted because
ENTERIC ROUTES it may be in the trachea. Once the tube has passed the UES, it
Oro-Nasogastric is important to be aware of any intrinsic esophageal disease
Oro-Nasoduodenal Cervical (esophageal stricture, tumor, or diverticulum) that may impede
Oro-Nasojejunal pharyngostomy safe passage to the lower esophageal sphincter (LES). Disor-
or esophgostomy
ders of the LES, such as achalasia, may also hinder tube pas-
Upper sage into the stomach. If significant resistance is met, the
esophageal
Sphincter procedure should be terminated and the reason for the resist-
Lesser curve Lower ance should be assessed. Another method of placement may
esophageal need to be used.
Sphincter
2. Insertion: complicated. A stethotube is a feeding tube that is
adapted to a stethoscope.5 If the feeding tube is passed incorrectly
Pylorus
into the trachea, there will be a very loud noise, indicating that the
Cardia tube should be removed and redirected. In comatose or anes-
thetized patients, a laryngoscope may be used to help guide the tube
Greater curve
past the UES into the esophagus and beyond. A physician who is
comfortable with the technique generally performs this procedure.
PEG; PEJ;
PEG/J; button 3. Documentation of placement. Auscultation of air insufflation over
portions (1-4) of 2 1 gastrostomy the midepigastrium has been used to document passage of the
the duodenum ligament of tube into the stomach. Caution is needed because inadvertent pul-
4
treitz monary placement can result in bronchial sounds being trans-
3 mitted through the diaphragm, simulating gastric placement.6
Jejunostomy
Auscultation alone should not be used to confirm tube placement.
However, a positive air insufflation test combined with aspiration
is required for commercially available enteral formulations. For of gastric contents is a fairly reliable predictor of successful
improved patient comfort, some institutions use small-caliber tubes placement. X-ray verification of tube placement remains the gold
(8F–12F) for short-term nasogastric feedings. standard; it also shows whether the tube is in the preferred antral
1. Insertion: uncomplicated position or is curled.
a) If the tube is to be inserted through the nose, it is important 4. Pros. Nasogastric tubes are available in a variety of sizes and tube
to obtain a history of sinus problems, deviated septum, fre- materials, making it possible to select the smallest size that will
quent nosebleeds, known platelet or bleeding disorders, recent allow the appropriate enteral formulation to be infused by the
head or facial trauma, or difficulty with a previous nasal tube administration method intended. Placement is generally easy,
passage. Before tube passage, the nasal passages should be especially in an alert, cooperative patient. Larger-caliber tubes
inspected. If the patient already has a tube (nasotracheal) and ease of replacement permit bolus feeding and administration
in one nostril, the NGT is best placed in the other nostril. of medication.
Hanson’s formula4 has been used to estimate the length of tube 5. Cons. Nasogastric tubes are contraindicated if severe coagulopa-
needed to pass 1 to 10 cm beyond the gastric cardia in adults: thy, severe thrombocytopenia, some nasal and facial fractures, or
[(NEX − 50)/2] + 50 cm, where N = tip of nose, E = earlobe, and esophageal obstruction is present. In addition, intrinsic problems
X = xiphoid process. of the esophagus (masses, diverticula, or strictures) or disorders
b) The tube is marked 50 cm from its tip and, with the patient’s of the LES (hypertensive LES or achalasia) can increase the
head in a neutral position, is placed along the shortest course risk of complications, such as bleeding, perforation, or coiling
with the end of the tube at the tip of the nose (N) passing to of the tube in the esophagus, and result in aspiration of feeding.
the earlobe (E) and then to the xiphoid process (X). A second 6. Complications (Table 3-1)
mark is made on the tube at the point where the tube meets B. Orogastric tubes. The oral route may be preferred when nasal or
the xiphoid process. The length of tube insertion should be facial trauma, head injury, sinusitis, or other factors prevent a tube
halfway between the xiphoid process mark and the 50-cm from being placed nasally. In addition, the oral route may be a good
mark. A simplified method is also used, whereby the tube is option in patients who are sedated, paralyzed, or mechanically ven-
measured from the tip of the patient’s nose to the earlobe and tilated. Orogastric tubes are used for premature infants, as they are
from the earlobe to the xiphoid process. Some commercially obligatory nasal breathers.
available feeding tubes have markings to denote length. 1. Pros. The incidence of sinusitis is lower than with nasoenteric
c) Lubrication of the tube with a water-soluble lubricant facili- tubes.
tates passage; use of local anesthetic jelly (eg, 2% lidocaine 2. Cons. Orogastric tubes are not tolerated for prolonged periods in
jelly) may promote comfort and improve success in an alert alert patients; tubes may be damaged by teeth.
patient. To decrease the risk of aspiration, the head of the bed 3. Complications. Except for nasal-related events, the complica-
should be raised or the patient should sit up. In comatose or tions are similar to those for nasogastric tubes (Table 3-1).

© 2005 A.S.P.E.N. www.nutritioncare.org. A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. 55
S E C T I O N I Fundamentals of Nutrition Support Practice and Management

2. Pros. Postpyloric feeding tubes are usually of smaller diameter

Table 3-1. Potential Complications of Nasogastric than standard NGTs and cause less patient discomfort. Delayed
and Nasoenteric Tubes gastric emptying does not preclude feeding.
3. Cons. It may be difficult to achieve postpyloric or post–ligament
Nasal mucosal ulceration Gastrointestinal bleeding of Treitz positioning. Small-caliber tubes may preclude adminis-
Clogging Epistaxis tration of some medications. Infusion pumps are usually required
Esophageal perforation Otitis media for infusion of enteral formulations.
Pneumothorax Pulmonary aspiration 4. Complications (Table 3-1)
Pulmonary intubation Pyriform sinus perforation B. Oroenteric. There are the same indications for oral placement as for
orogastric tubes, and there are similar complications as for naso-
enteric tubes except for nasal-related events.
Adapted with permission from Kirby DF, DeLegge MH. Enteral nutrition: the challenge
of access. In: Kirby DF, Dudrick SJ, eds. Practical Handbook of Nutrition in Clinical
Practice. Boca Raton, FL: CRC Press; 1994:87–117. V. Short-Term Surgical Pre- and Postpyloric Tubes
A. Gastrostomy. If a patient is already undergoing laparotomy, a gas-
trostomy or jejunostomy tube can easily be placed even for short-
term use. For example, someone undergoing a partial gastrectomy
IV. Short-Term Nonsurgical Postpyloric Tubes
may have a gastrostomy and jejunostomy tube placed. The gastros-
A. Nasoenteric. These tubes are ideal if short-term feeds are required tomy would initially be used for decompression; the jejunostomy
but the patient is at high risk of aspiration, esophageal reflux, or would be used for immediate postoperative feedings. See Section
delayed gastric emptying. It is assumed that if the tip of the tube is VI.A.3.
placed past the pyloric sphincter, the risk of TFRA is reduced. B. Jejunostomy (standard). See above and Section VII.A.3.
However, duodenogastric reflux is limited only if the tube is in the C. NCJ These are small-caliber jejunal tubes that can be easily placed
distal third of the duodenum and preferably past the ligament of Tre- at surgery. Older models were 5F, which predisposed them to clog-
itz.7 Newer tubes have a separate gastric port for gastric suction, ging. Newer versions are 7F or 8F, which allows administration of
decompression, or medication delivery, with a second lumen for enteral formulations with extra protein or fiber.
simultaneous small-bowel feeding. These tubes are generally more 1. Pros. These are easily placed, with a low risk of enteric leak if
difficult to place and may require pharmacologic, endoscopic, inadvertently dislodged.
intraoperative, or radiologic assistance.8,9 2. Cons. They require diligent nursing care because they are easily
1. Nasoenteric tube insertion methods occluded. Infusion pumps are required for administration of enteral
a) pH sensors. Small-bowel tubes with pH sensors are available. formulations. Medications can rarely be infused through NCJs.
It is assumed that an increase in pH over the presumed gastric 3. Complications (Table 3-2)
reading is consistent with the end of the tube entering the duo- D. Surgical nasoenteric. Some surgeons provide short-term enteral
denum. In one study, the pH profile and radiograph were in access postoperatively by manually guiding a nasoenteric tube
agreement in 87% of the cases, but small-bowel tube ___location through the stomach, then through the duodenum, and into the small
was not discussed.10 bowel during laparotomy. The frequency and success of this practice
b) Pharmacologic measures. Medications with promotility prop- are not known.
erties have been used to facilitate passage of feeding tubes into
the small intestine. Metoclopramide (10 mg intravenously)
VI. Long-Term Prepyloric Tubes. Gastrostomy. Although sur-
has been studied the most and appears to be most effective
gical gastrostomy has been performed for over 150 years, technical
when given about 15 minutes before tube insertion. Only dia-
advances and procedural improvements have made PEG a preferred
betic patients appear to benefit from a dose of metoclopramide
method of gastrostomy placement if the patient is not undergoing
given after tube placement.11 When used in low doses, the
laparotomy for another reason.16 Gastrostomies can also be placed
antibiotic erythromycin also has promotility properties and
radiologically or laparoscopically. There are no significant differences
can be useful for tube placement. In adults, an intravenous (IV)
dose of 500 mg administered prior to tube insertion has been
reported to facilitate tube placement.11,12 In children, a dose of
3 mg/kg given intravenously 1 hour prior to tube insertion has
been reported.13 (Note that this is an off-label use for erythro- Table 3-2. Potential Complications of Jejunostomy
mycin.)
(All Methods)
c) Fluoroscopy. Radiologic techniques can be very useful for
placing nasoenteric tubes. Passage into the third portion of the Pneumatosis intestinalis Bowel obstruction
duodenum or beyond was successful in 86% of attempts in one
Bleeding Tube occlusion
study.14 Procedures can be performed in the radiology depart-
Dislodgment Stomal leakage
ment or at the bedside if portable fluoroscopy is available.
d) Endoscopy. Endoscopy can facilitate feeding-tube placement Tube deterioration Wound infection
into the small bowel; however, in adults, tubes of sufficient Volvulus
length (>105 cm) need to be used.15 Friction from the endo-
scope may drag tubes back as the endoscope is removed, so Adapted with permission from Kirby DF, DeLegge MH. Enteral nutrition: the challenge
postprocedure radiographs are recommended. Success rates of of access. In: Kirby DF, Dudrick SJ, eds. Practical Handbook of Nutrition in Clinical
90% to 95% have been reported with this technique. Practice. Boca Raton, FL: CRC Press; 1994:87–117.

56 A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. © 2005 A.S.P.E.N. www.nutritioncare.org.
 S E C T I O N I Fundamentals of Nutrition Support Practice and Management

in complication rates among the different methods of gastrostomy inser- a temporary gastrostomy because the tract closes spontaneously
tion; however, nonoperative access is less costly.17 Local expertise is after the tube is removed. A gastropexy is performed in which
an important deciding factor for determining how a gastrostomy is the stomach is sutured to the abdominal wall. Once postproce-
placed. dure healing is complete, a reliable, established tract for replac-
ing tubes exists. Gastrostomy tube placement itself may alter the
A. Gastrostomy insertion methods.
contour of the stomach enough to cause some gastroesophageal
1. PEG. Prior to an attempt to place a PEG, a screening upper
reflux. Children with documented gastroesophageal reflux or gas-
endoscopy is performed to make sure that there are no con-
tric aspiration may need a fundoplication procedure performed
traindications to the procedure such as a large ulcer (higher risk
with the surgical gastrostomy, which may obviate the need for
of ulcer perforation) or a gastric or duodenal mass or obstruction.
postpyloric feedings. A pyloroplasty may be performed also if
Conscious sedation is usually sufficient to perform the procedure,
delayed gastric emptying has been documented.
but occasionally deep sedation with propofol or even general
B. Pros. These tubes allow long-term access and are easily cared for
anesthesia may be required.
and replaceable. Bolus feeding and administration of medication
After the initial endoscopy, the patient is placed supine and
are possible because of the large caliber of the tube.
an area of transillumination in the left upper quadrant is identi- C. Cons. Compared with the oral or nasal route, this technique is more
fied. When a proposed site is located, palpation with a finger is invasive.
used to indent the insufflated stomach. The site is then prepped D. Complications (Table 3-3)
with iodine swabs and infiltrated with 1% lidocaine solution. A
1-cm skin incision is made, and a catheter is placed through the
incision into the stomach. A suture or guidewire is placed VII. Long-Term Postpyloric Tubes. Jejunostomy. As with
through the catheter and grasped with a snare. The endoscope, gastrostomy, many methods of jejunostomy insertion are now possi-
snare, and suture are removed from the patient. The PEG tube is ble, including operative, percutaneous endoscopic, radiologic, and
tied onto the suture coming from the mouth and then pulled laparoscopic placement. Indications for jejunal access include reflux
through the mouth, esophagus, and stomach to reach the ante- esophagitis, gastric aspiration, gastroparesis, insufficient stomach rem-
rior abdominal wall. The endoscope is reinserted and the intra- nant because of previous resection, and establishment of access for post-
gastric position of the PEG bumper is visualized. The endo- operative feeding after major surgical procedures and of feeding access
scope is removed from the patient, and the external bumper and in patients who have unresectable gastric or pancreatic cancers. During
urgent abdominal surgery, jejunostomy placement to facilitate early
a feeding adapter are placed.
postoperative feeding should be considered.
Kits are commercially available with tube sizes from 14F to
28F. Adults commonly have 20F tubes placed. Larger tubes may A. Methods of insertion21–23
be required to insert a smaller feeding tube into the small intestine 1. Percutaneous gastrojejunostomy—also called a JET-PEG or jeju-
if small bowel feedings are desired. Infants and children often have nal extension through a PEG. This jejunal feeding tube is a small
14F tubes placed, but later 18F to 20F tubes are necessary to facil- 9F to 12F tube that is dragged or passed over a guidewire into the
itate flow rates commensurate with growth. small bowel through a previously placed PEG. Initial versions of
2. Radiologic. Gastrostomy tubes may be placed with radiologic this tube were unsatisfactory in their design, were difficult to
guidance, which avoids passage of the endoscope through a place past the proximal duodenum, and often migrated back into
bacteria-laden oral cavity. This reduces the risk of contamination the stomach. Devices now available are easier to place in the dis-
of the subcutaneous tissues and avoids general anesthesia that tal duodenum or jejunum and are more reliable because the like-
may be required for surgical placement. In patients with head and lihood of migration is greatly decreased. To decrease the inci-
neck cancer, there is a very small but real risk of causing PEG dence of TFRA, the feeding port must be located in the distal
stoma site metastases when pulling a tube through the oropharynx. duodenum or jejunum. Although placement of a primary Per-
This risk can be obviated by doing the procedure radiologically cutaneous Endoscopic Jejunostomy (PEJ) tube (tube placed with
or endoscopically by the introducer technique.18,19 Fluoroscopy the PEG technique directly into the small intestine) as the initial
is the most commonly used imaging modality; however, ultra- procedure is not as common as the PEG procedure, it is becom-
sonography or computed tomography can provide additional ing more widely practiced. It has been performed in patients with
information about intra-abdominal structures that may be over- normal anatomy and in those who have had gastric resection.24–27
lying the stomach or provide a safe tract when endoscopic tran- There are also commercially available dual-lumen tubes that
sillumination fails. The size of feeding tubes varies from 10F to have both a gastric and a jejunal port. These are usually placed
28F. The two most common complications associated with radi-
ologic placement are tube clogging and displacement; these
complications often lead to catheter replacement. If stabilizing Table 3-3. Potential Complications of Gastrostomy
sutures are used, larger tubes with a lower rate of dislodgment or
clogging can be inserted.
(All Methods)
3. Surgical. Most operative gastrostomies are performed under gen-
Aspiration Bleeding Tube occlusion
eral anesthesia in an operating room, but doing so can escalate
costs. Surgical gastrostomies have been performed under con- Dislodgment Pneumoperitoneum Stomal leakage
scious sedation. Operative gastrostomies are very cost-effective Tube deterioration Wound infection
when done during another intra-abdominal procedure. An opera-
tive alternative to laparotomy is laparoscopic insertion.20 Adapted with permission from Kirby DF, DeLegge MH. Enteral nutrition: the challenge
Surgical placement in pediatric patients is most commonly of access. In: Kirby DF, Dudrick SJ, eds. Practical Handbook of Nutrition in Clinical
achieved with a Stamm gastrostomy procedure. This is technically Practice. Boca Raton, FL: CRC Press; 1994:87–117.

© 2005 A.S.P.E.N. www.nutritioncare.org. A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. 57
S E C T I O N I Fundamentals of Nutrition Support Practice and Management

through mature gastrostomy tracts and can be placed radiologi- periods for gastric drainage, decompression, lavage, or diagnostic
cally or endoscopically. The fact that the internal retention device procedures.32
is a balloon often limits these devices’ use. When the balloon fails 2. Polyurethane or silicone tubes are better for long-term use
(usually within 3 months), the entire tube must be replaced. because they are more flexible and less irritating to tissue. Most
These tubes are too large to be used in infants and small pediatric small-bowel feeding tubes are made of polyurethane or silicone.
patients. Polyurethane tubes may have improved longevity, but this con-
2. Radiologic jejunostomy. Radiologists can insert a small feeding cept needs further investigation.33 Silicone tubes are flexible and
tube through the stomach and fluoroscopically guide it through may collapse when assessing gastric residuals. Fungal coloniza-
the pylorus to the duodenojejunal flexure. This provides small- tion has been associated with silicone rubber PEG tubes and may
bowel feeding with a reduced risk of TFRA, but because smaller contribute to tube failure over time.34
catheters (10F) are placed by this technique, a higher obstruction 3. Latex tubes are still available but should not be used in patients
rate is expected. One series retrospectively compared surgical gas- who are allergic to or at high risk of developing an allergy to latex.
trostomy with radiologic percutaneous jejunostomy transgastric, In addition, latex tubes need to be replaced more frequently
in which ultrasound and fluoroscopy were used to insert a feeding because of susceptibility to degradation by microbes and gas-
tube through the stomach wall and then a 10F catheter was passed tric acid.
to the duodenojejunal junction.28 Complications were fewer in 4. Red rubber catheters are soft and pliable, which makes them easy
the nonsurgical jejunostomy group, despite the fact that the stom- to place at the time of surgery. Although the tubes are generally
ach wall was not fixed to the anterior abdominal wall. However, large enough to infuse enteral formulations and medications, they
radiologic techniques do not allow for placement of feeding tubes are subject to gastric acid degradation and are used mostly for
of sufficient size to provide both gastric and small-bowel access. gastric gavage feeding or jejunostomies. If long-term feeding is
Some centers are now performing dual-lumen gastrojejunos- required, another feeding tube material should be considered after
tomies. The gastric port is 16F with a 10F jejunal port. While this the short-term problem has been addressed.
may allow for decompression of the stomach or medication B. Weighted versus nonweighted. It is commonly believed that
administration and feeding into the jejunum, the tube sizes may weighted tubes are easier to pass into the small bowel when they are
be associated with a higher rate of occlusion. More long-term being placed blindly; however, nonweighted tubes have actually
data are needed. Direct percutaneous access to the jejunum has been shown to pass at a higher rate.35 In theory, weight may help keep
been performed under radiologic control; however, this is techni- the tube in place, but this concept has not been proven.
cally more difficult. C. Use of a stylet. A stylet may facilitate passage of a small, very pliable
3. Open surgery. Surgical placement of jejunostomy tubes has been tube. Reinsertion of the stylet after removal is not recommended
performed for over 100 years. A variety of techniques are avail- because it may pass through the wall of the tube and perforate the gas-
able, including Witzel jejunostomy (probably the most common), trointestinal tract. Stylets may need to be lubricated before the tube
Roux—en-Y jejunostomy, serosal tunnel jejunostomy, button is used. Obtain information about any product before using it, espe-
jejunostomy, and laparoscopic jejunostomy.29,30 Numerous tubes cially for the first time; do not assume that all tubes are alike.
have been used, including red rubber catheters, biliary T tubes, and D. Tube length. The length of a nasoenteric tube may influence its
dialysis catheters. Surgical gastrojejunostomy tubes, which allow ability to pass the duodenojejunal junction. In adults, tubes longer
gastric decompression or medication administration in addition than 105 cm are preferred if passage past the ligament of Treitz is
to jejunal feeding, are also available. The common belief that only desired.11
elemental diets should be given through jejunostomy tubes has E. Low-profile device (LPD) versus standard gastrostomy
been shown to be untrue.31 Standard polymeric diets containing 1. LPDs are cosmetically appealing to patients and may decrease the
fiber can be used; however, the catheter must be flushed rou- possibility of pyloric obstruction from inward migration of the
tinely to maintain tube patency. feeding tube. LPDs are composed of an internal stabilizer, a shaft,
B. Pros. These tubes decrease the risk of TFRA. Early postoperative an external stabilizer, a connecting tube, and an antireflux valve to
feeding is possible in most patients except those who are hemo- keep gastric contents from leaking onto the skin. It is important to
dynamically unstable, have peritonitis, or have a bowel obstruction. choose the appropriate shaft length. If the shaft is too short, the
C. Cons. An infusion pump is required. Administration of medication patient may develop pressure necrosis of the skin or the internal
is precluded in some instances but is dependent on the size of the stabilizer may become embedded in the wall of the stomach. If the
T-tube. Invasive procedures are required for access. Outside con- adult patient gains or loses 10 pounds, the shaft length should be
nectors are prone to break and may require replacement of the entire reevaluated.36 In infants and children, the size must be reevaluated
T-tube. The tubes are difficult if not impossible to replace unless a routinely and the shaft replaced to accommodate growth. One
mature tract has developed. design allows the physician to customize the shaft length, as the
D. Complications: similar to PEG (Table 3-2) tube resembles a standard PEG tube. The shaft length is deter-
mined and then a valve-and-collar assembly is put into place. This
obviates the need for multiple LPDs with various shaft lengths
VIII. Selection of Access Device Features. When a par- in inventory.
ticular enteral access device is being selected, the tube’s composition,
2. Initial placement of an LPD should be performed by a physi-
intended use, estimated length of time required, cost-effectiveness, and
cian. Contraindications to switching to an LPD are gastros-
features (eg, stylet, weighted tip, length of tube) should be considered.
tomies placed by the Witzel and Janeway surgical techniques or
A. Tube composition patients who require gastric decompression. LPDs may not be a
1. In the presence of gastric secretions, polyvinyl chloride tubes good choice for patients with tracheostomies, neurology patients
harden and become brittle with time, which may cause tissue irri- with spastic posturing, or other patients with increased abdominal
tation or necrosis. Thus, these tubes should be used only for short pressure. In these patients, forceful coughing or movement can

58 A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. © 2005 A.S.P.E.N. www.nutritioncare.org.
 S E C T I O N I Fundamentals of Nutrition Support Practice and Management

damage or expel the device or cause leakage of gastric contents ment the external length in the medical record daily. If no
and lead to maceration of the abdominal wall.37,38 external markings are on the tube, an indelible mark can be
made on the tube and used to monitor position.34 Gastrostomy
tubes with internal bumpers should be pushed in several cen-
IX. Care of Feeding Tubes. Feeding tubes require regular
timeters and the tube rotated 360°. In pediatric patients, the
assessment and monitoring to ensure continued correct placement
tube is rotated 360° but not pushed in. If this is not possible,
and to avoid complications such as skin breakdown or infection.
a buried bumper may be developing, and the patient will
When problems arise, early intervention is key to maintaining enteral
need to be referred to an experienced health care provider for
access. This section reviews significant care issues for each type of
further care and ultimate replacement.1,43
feeding tube, with special emphasis on routine tube care, skin care,
b) LPDs should also be monitored daily. The tube should have
and replacement.
some movement (ie, you should be able to slide the tube in
A. Oro- or nasogastric and oro- or nasoenteric tubes. Care of orally or and out about 0.5 inch). An LPD should be gently pushed in
nasally inserted tubes requires vigilance in checking placement, approximately 0.5 inch and rotated 360° daily to prevent the
protecting the mucosal surfaces, and flushing routinely. balloon or internal bumper from adhering to the gastric wall.
1. Checking placement. Placement of the tube should be checked For infants and small children, the LPD should be pushed in
every 8 hours during continuous feedings and before each inter- approximately one-eighth inch and rotated.
mittent feeding. Verification methods include x-ray, marking the 2. Care of exit site and tube
tube where it exits the patient and measuring it, checking the pH a) Exit site assessment. Check for erythema (initially, a small
of the aspirate, observing the color of the aspirate, and ausculta- amount of serosanguineous drainage can be expected), edema,
tion.39 Any time tube misplacement or displacement is suspected, warmth, and exudate. Foul-smelling drainage is a sign of infec-
a roentgenogram should be taken. tion. Also monitor for skin breakdown, pressure necrosis,
2. Protecting the mucosal surfaces.40 Mucosal irritation of the hypergranulation (keep site dry), gastric leakage (identify the
nasopharynx may occur anywhere along the path of the feeding cause; do not just try to repair), displacement (tube movement
tube. >1 inch for adults and >0.25 inches for infants and small chil-
a) Inspect the nares, mouth, and pharynx daily for skin irritation, dren), and enlargement of the stoma tract (stabilize tube; avoid
ulceration, pressure necrosis, and lesions. excessive tube movement.
b) Clean the nares daily with warm water or saline and keep b) Skin care. When the tube tract is new and has drainage or crust-
mucous membranes moist with petroleum jelly. If the nares ing, clean the exit site with diluted hydrogen peroxide. After the
are crusty, clean them with dilute hydrogen peroxide and then tract is healed, clean the site daily with soap and water. Clean
moisturize. carefully under external bumpers or disks to keep dry and clean
c) Change the fixator device or tape on the nose or mouth as and to check for excessive pressure. External bumpers and disks
needed if loose or soiled and at least every 3 to 5 days. In- should be just above skin level and not taut against the skin.
correct taping can lead to pressure necrosis. c) Dressings. Dressings are commonly used for 48 hours after ini-
d) Maintain good oral hygiene. Even when patients are not eat- tial placement when the tract is considered an open wound,
ing, their teeth should be brushed at least twice a day. If gum when the tract is soiled, or when the patient is at high risk for
inflammation is present, the patient may benefit from an oral inadvertent tube removal.
antiseptic rinse (eg chlorhexidene gluconate). Tube-fed pa- 3. Tube stabilization. Stabilizing a tube can reduce the risk of tube
tients receiving antibiotics may benefit from an oral antifungal displacement, pain, and enlargement of the tract.
formulation (eg, nystatin 500, 000 units applied to the oral cav- a) Sutures or T- fasteners may be present to secure gastrostomy
ity 4 times a day) to help prevent overgrowth of fungus. or jejunostomy tubes. If a gastrostomy tube has anchoring
3. Flushing routinely. Tubes should be flushed with water every sutures or T- fasteners, check with the physician about possi-
6 hours during continuous feeds, between and after medica- ble removal when the tract is healed. Most jejunostomy tubes
tions, after intermittent feeds, after residuals are checked, and require a secure suture at all times.
if feeds need to be turned off for more than 4 to 6 hours. b) Anchoring devices can secure the tube and protect the skin from
In children, the flushing volume should be scaled down to the the effects of frequent dressing changes.44,45 Anchoring devices
size of the child. typically last twice as long as tape. Examples of anchoring
4. Replacement. Orally or nasally placed tubes should be replaced devices are Hollister Drain/ Tube Attachment Device (Hol-
only when necessary (eg, tube occlusion, problems at the inser- lister, Libertyville, IL), Cath-Secure (MC Johnson, Naples,
tion site). Any time a tube is replaced, placement should be ver- FL), and Flexi-Trak (ConvaTec, Skillman, NJ). If adhesive
ified (see Section III.A.3). Some parents/caregivers learn to tube holders are used, the exit site must be cleaned around
place and remove their infant’s or child’s orogastric or naso- the tube daily and as needed to prevent accumulation of tissue
gastric feeding tube and do so routinely at home. The American debris.
Academy of Pediatrics recommends that NGTs be changed from c) If the tube has a balloon, check the water in the balloon at least
one nostril to the other every 1 to 3 weeks to decrease sinus and once a week.
ear infections. d) Patients with enteral devices or tubes may shower or bathe
B. Gastrostomy and jejunostomy tubes. The care of these tubes in- according to the directions of their health care provider.
cludes maintaining patency, protecting the skin at the exit site, and If a bumper or disk is present, the skin underneath it should
preserving proper placement and integrity of the tube.37,40–42 be dried carefully to prevent maceration from trapped
1. Checking placement moisture.36,37
a) For traditional gastrostomy and jejunostomy tubes, measure 4. Irrigation (see Section IX.A.3)
the length of the tube protruding from the abdomen and docu- 5. Replacement of gastrostomy tubes

© 2005 A.S.P.E.N. www.nutritioncare.org. A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. 59
S E C T I O N I Fundamentals of Nutrition Support Practice and Management

a) Maturation of the tract generally occurs in 2 to 3 weeks in the c) Hydrocolloids and pectin wafers (eg, Stomadhesive, Duo-
adult patient and 6 weeks in the pediatric patient. This DERM [ConvaTec, Skillman, NJ]) can also be used to pre-
process takes longer if the patient is immunocompromised, vent skin breakdown at the exit site and at sites distant from
diabetic, or severely malnourished.41 If the tract is disturbed the exit site. These should be placed on clean, dry skin and
during this time, the stomach may separate from the abdom- changed when soiled to prevent trapped moisture.
inal wall. During the maturation process, only a physician
should change the gastrostomy tube; a radiologic procedure
(eg, fluoroscopy, contrast study) may be indicated to confirm
X. Selection of Infusion Equipment50,51
proper tube replacement. Once the tract is fully mature, A. Times to use an infusion pump
nurses may replace tubes—depending on their knowledge 1. Enteral infusion pumps are designed and used exclusively for
and experience, facility policies, and state regulations—if delivery of tube feedings. A pump should be considered when
a health care provider orders it. Some parents/caregivers a controlled volume or infusion rate is desired. Continuous drip
become comfortable enough to replace their child’s gastros- feedings via pump may improve gastrointestinal tolerance and
tomy tube through a mature tract. reduce the risk of aspiration associated with reflux.52 Generally,
b) If the tube is inadvertently removed, it should be replaced as postpyloric feedings require a pump.
soon as possible; the tract can close within hours of the inci- 2. Intravenous infusion pumps should not be used for enteral for-
dent. The patient can be instructed to take the tube (so care- mulation delivery because of the risk of inadvertent connection
givers know what type and size tube is being used) to an of tube feeding to an IV site. In addition, IV pumps have unnec-
acute-care facility for replacement, taught how to replace the essary alarms and are more costly than enteral pumps.
tube in an emergency situation, or instructed to call a home- B. Pump selection. Issues to consider when selecting a pump include
care nurse. how easy the product is to use and who will be operating the pump
c) Gastrostomy tubes should be replaced when they show signs (nurse, patient, or caregiver), the patient’s size and overall condi-
of degradation, balloon breakage, malfunction, or irreversible tion (which can affect the ability to lift or move a pump), and the
occlusion. Removal of any tube requires knowledge of the patient’s ambulation status.
tube type and initial placement procedure. For example, C. Pumps for the outpatient
some endoscopically placed tubes require endoscopy for 1. Pump requirements. Some special considerations with regard to
tube removal. pump selection are necessary for patients who receive feeds in the
d) Replacement gastrostomy tubes are usually inserted when home setting.
the tract is well formed and further endoscopy is not neces- a) Most pumps come with a built-in carrying handle and pole
sary.41 Many replacement tubes are made of silicone. If a clamp. In the home setting, pumps should be portable or
latex tube (eg, Foley catheter) is selected as a replacement attached to a mobile pole. Some pumps are designed with
tube, providers should be aware of possible latex sensitivi- shoulder straps or a carrying case for ease of transport, which
ties. There are a variety of replacement gastrostomy tubes is ideal for school or work.
and LPDs on the market with balloons or solid bolsters. b) All pumps have rechargeable batteries and run on AC power.
e) Jejunostomy tubes are almost always replaced or changed by Pumps should have a battery life of at least 8 to 12 hours; some
a health care provider with specialized education, training, pumps have 24-hour batteries.
and experience in the procedure. They are replaced surgically, 2. Reimbursement in the home-care setting varies greatly among
endoscopically, or via fluoroscopy in radiology.46 payers. Most payers have very rigid criteria, and the necessity of
C. Problem skin care. The most crucial step in preventing or mini- a pump must be documented before reimbursement is approved.
mizing skin problems is early identification and removal of the D. Infusion pump mechanics
problem. 1. Fluid delivery mechanisms53
1. Hypergranulation (everted mucosa) typically develops when the a) Rotary peristaltic devices. The pump insert is looped around the
exit site remains moist or the tube is not stabilized and moves in pump rotor. The pressure of the rotary mechanism against the
the stoma. Keeping the site dry and stabilizing the tube may help tubing pulls the fluid out of the bag and through the adminis-
prevent this problem. Excessive growth (>0.25 inch for adults; tration set. The infusion rate is determined by the speed of the
>2 mm for pediatric patients) of granulation tissue can be elimi- rotor. For the infusion rate to remain accurate, the rotor assem-
nated around the tube by carefully cauterizing with silver nitrate bly must be installed and operating correctly, and the pump
sticks.37,47 insert must be placed in accordance with the manufacturer’s
2. For other skin problems, the cause should be identified and instructions.
removed, if possible. Certain liquid or solid barriers can be used b) Cassette devices. These pump sets incorporate a measured-
to protect the skin as it heals.48,49 volume cassette that works with the pumping mechanism to
a) Minor skin breakdown. If there is slight irritation, a protective deliver enteral fluid to the patient. These sets tend to be less
skin barrier (eg, zinc oxide). susceptible to alarm conditions than rotary peristaltic devices.
b) Skin that is already denuded. Dry the skin well and dust with Cassette devices may not deliver reconstituted powdered for-
a powder (eg, Stomadhesive [ConvaTec, Skillman, NJ]). Then mulations accurately; manufacturers’ recommendations should
apply a waterproof ointment (eg, Critic Aid Skin Paste be followed.
[Coloplast, Marietta, GA]). If the patient is not receiving an 2. Infusion rates. All pump manufacturers claim an accuracy rate of
acid-suppressing medication (eg, histamine-2 receptor antago- ±10% of the selected flow rate. Formulation viscosity affects the
nist [eg, ranitidine, famotidine] or a proton pump inhibitor [eg, accuracy of the flow rate. Adding a powdered protein supplement
omeprazole]), then this may be necessary to decrease the risk to a ready-to-feed formulation may also reduce the expected infu-
of acid damage to the skin. sion rate.54 Institutions should evaluate the delivery accuracy of the

60 A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. © 2005 A.S.P.E.N. www.nutritioncare.org.
 S E C T I O N I Fundamentals of Nutrition Support Practice and Management

pump and follow manufacturers’ instructions for their selection of 7. Gutske RF, Varma RR, Soergel KH. Gastric reflux during perfusion of the
enteral formulations. Administration sets and tubing should have a proximal small bowel. Gastroenterology. 1970;59:890–895.
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3. Automatic flush systems. Some manufacturers provide pumps ing in critically ill patients [abstract]. Gastrointest Endosc. 1995;41:370.
9. Baskin WN, Johanson JF. An improved approach to the delivery of enteral
with automatic flush systems. These pumps combine infusion of
nutrition in the intensive care unit. Gastrointest Endosc. 1995;42:161–165.
the enteral formulation with programmable water flushes. The
10. Heiselman DR, Vidovich RR, Milkovich G, Black LD. Nasointestinal
flush feature can be turned off if manual flushing is desired.55
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trol. Troubleshooting guidelines are usually located on the side 11. Booth CM, Heyland DK, Paterson WG. Gastrointestinal promotility drugs
of the pump. in the critical care setting: a systematic review of the evidence. Crit Care
a) Low battery power. When this alarm sounds, battery operation Med. 2002;30:1429–1435.
should be stopped. Ideally, the pump should be plugged in to an 12. Griffith DP, McNally AT, Battey CH, et al. Intravenous erythromycin facil-
electrical outlet whenever feasible, not only to provide elec- itates bedside placement of postpyloric feeding tubes in critically ill adults:
tricity to run the pump but also to recharge the battery. The bat- a double-blind, randomized, placebo-controlled study. Crit Care Med.
tery is primarily a backup system in case of a power outage and 2003;31:315–316.
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b) Flow obstruction alarm. An alarm sounds when fluid is not pyloric intubation. J Pediatr Gastroenterol Nutr. 1990;11:45–47.
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E. Cleaning and maintenance. The pump should be of a simple design Endosc 1990;36:1–5.
and have as few crevices as possible, because residue and dirt may 18. Thakore JN, Mustafa M, Suryaprasad S, Agrawal S. Percutaneous endoscopic
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should be unplugged and cleaned weekly with a mild soap and warm 19. Hunter JG. Tumor implantation at PEG exit sites in head and neck cancer
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F. Pump servicing. With use, the rotor mechanism may wear and no
20. Edelman DS, Unger SW. Laparoscopic gastrostomy and jejunostomy:
longer exert correct pressure, resulting in inaccurate volume deliv- review of 22 cases. Surg Laparosc Endosc. 1994;4:297–300.
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tomy (EPJ): an alternative for operative catheter-jejunostomy [abstract].
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intubation by feeding tubes with stethoscopic guidance: the “stethotube” 30. Reed DN. Percutaneous peritoneoscopic jejunostomy. Surg Gynecol
[abstract]. Gastroenterology. 1993;104:A623. Obstet. 1992;174:527–529.
6. Metheny N, McSweeney M, Wehrle MA, Wiesema L. Effectiveness of 31. Collier P, Kudsk KA, Glezer J, Brown RO. Fiber-containing formula and
the auscultatory method in predicting feeding tube ___location. Nurs Res. needle catheter jejunostomy: a clinical evaluation. Nutr Clin Pract.
1990;39:262–267. 1994;9:101–103.

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S E C T I O N I Fundamentals of Nutrition Support Practice and Management

32. Petrosino BM, Christian BJ, Wolfe J, Becker H. Implications of selected 47. Kaufman MW, Faller NA, Lawrence KG. Low profile gastrostomy devices.
problems with naso-enteral tube feedings. Crit Care Nurs Q. 1989; Gastroenterol Nurs. 1995;18:171–176.
12:1–18. 48. Maklebust J. Using wound care products to promote a healing environment.
33. Grant JP. Percutaneous endoscopic gastrostomy: initial placement by sin- Crit Care Nurs Clin N Am. 1996;8:141–158.
gle endoscopic technique and long-term follow-up. Ann Surg. 1993; 49. Hagelgans NA, Janusz HB. Pediatric skin care issues for the home care
217:168–174. nurse: part 2. Pediatr Nurs. 1994;20:69–75.
34. Iber FL, Livak A, Patel M. Importance of fungus colonization in failure of 50. Lehmann S. Nutrient infusion devices. In: Teasley-Strausburg KM, Cerra
silicone rubber percutaneous gastrostomy tubes (PEGs). Dig Dis Sci. 1996; FB, Lehmann S, Shronts EP, eds. Nutrition Support Handbook: A Com-
41:226–231. pendium of Products with Guidelines for Usage. Cincinnati, OH: Harvey
35. Lord LM, Weiser-Maimone A, Pulhamus M, Sax HC. Comparison of Whitney Books; 1992:259–272.
weighted vs unweighted enteral feeding tubes for efficacy of transpyloric 51. Saladow J. Making sense of the options: enteral infusion pumps. Infusion.
intubation. J Parenter Enteral Nutr. 1993;17:271–273. 1995;2:22–27
36. Faller NA, Lawrence KG, Ferraro CB. Gastrostomy replacement feeding 52. Minard G, Lysen LK. Enteral access devices. In: Gottschlich MM, ed. The
tube: the long and short of it. Ostomy Wound Management. 1993;39:26–33. Science and Practice of Nutrition Support. Dubuque, IA: Kendall/Hunt;
37. Townsend LC. Practical considerations of the gastrostomy button. Gastro- 2001:178–181.
enterol Nurs. 1991;14:18–26. 53. Goff K. The nuts and bolts of enteral infusion pumps. MedSurg Nurs.
38. Lehmann S. Parenteral and enteral access devices. In: Teasley-Strausburg 1997;6:9–15.
KM, Cerra FB, Lehmann S, Shronts EP, eds. Nutrition Support Handbook: 54. Dietscher JE, Foulks CJ, Watts M. Accuracy of enteral pumps: in vitro per-
A Compendium of Products with Guidelines for Usage. Cincinnati, OH: formance. J Parenter Enteral Nutr. 1994;18:359–361.
Harvey Whitney Books; 1992:228–257. 55. Guenter P. Tube feeding administration. In: Guenter P, Silkroski M, eds.
39. Metheny N. Verification of feeding tube placement. In: Silver E, Gussler Tube Feeding Practical Guidelines and Nursing Protocols. Gaithersburg,
JD, eds. Current Issues in Enteral Nutrition Support: Report of the First MD: Aspen Publishers; 2001:81–94.
Ross Conference on Enteral Devices. Columbus, OH: Ross Products Divi-
sion, Abbott Laboratories; 1996:34–41.
40. Teasley-Strausburg KM, Lehmann S. Guidelines for administration of nutri- SUGGESTED READINGS
tion support and nutrition support service forms. In: Teasley-Strausburg Ireton-Jones C, Hennessy K. Care of patients receiving home enteral nutrition.
KM, Cerra FB, Lehmann S, Shronts EP, eds. Nutrition Support Handbook: Infusion. 1996;2:30–43.
A Compendium of Products with Guidelines for Usage. Cincinnati, OH: Marks JM, Ponsky JL. Access routes for enteral nutrition. Gastroenterologist.
Harvey Whitney Books; 1992:321–330. 1995:3:130–140.
41. Eisenberg PG. Gastrostomy and jejunostomy tubes. RN. 1994;57:54–59. Payne KM, King TM, Eisenach JB. The technique of percutaneous endoscopic
42. Broscious SK. Preventing complications of PEG tubes. Dimens Crit Care gastrostomy: a safe and cost-effective alternative to operative gastrostomy.
Nurs. 1995;14:37–41. J Crit Ill. 1991;6:611–619.
43. Boyd JW, DeLegge MH, Shamburek RD, Kirby DF. The buried bumper Vanek V. Ins and outs of enteral access, I: short-term enteral access. Nutr Clin
syndrome: a review of the literature and a new technique for safe, endo- Pract. 2002;17:275–283.
scopic PEG removal. Gastrointest Endosc. 1995;41:508–511. Vanek V. Ins and outs of enteral access, II: long-term enteral access—
44. Blaylock B, Clayton G, Milnes M, Foster C. A catheter anchoring device. esophagostomy and gastrostomy. Nutr Clin Pract. 2003;18:50–74.
Ostomy Wound Management. 1993;39:36–43. Vanek V. Ins and outs of enteral access, III: long-term access—jejunostomy.
45. Wilson RE. Case study: a system for stabilizing percutaneous tubes. Nutr Clin Pract. 2003;18:201–220.
Ostomy Wound Management. 1994;40:44–49. Young M, McClure E, Thimsen-Whitaker K. Management of percutaneous
46. Stogdill BJ, Page CP, Pestana C. Nonoperative replacement of a jejunos- tubes. In: Bryant RA, ed. Acute and Chronic Wounds and Nursing Man-
tomy feeding catheter. Am J Surg. 1984;147:280–282. agement. St Louis, MO: Mosby Year Book; 1992:213–247.

62 A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. © 2005 A.S.P.E.N. www.nutritioncare.org.
 Mary Marian, MS, RD;
Susan J. Carlson, MMSc, RD, CSP, LD, CNSD
4
Enteral Formulations

Introduction ance in many populations and because lactase production

may be decreased during illness.
Numerous commercially prepared enteral formulations are available (2) Sucrose is added to some infant formulations in conjunc-
and include standard formulations and specialty products designed to tion with maltodextrin to provide carbohydrate, requiring
provide nutrition support for specific disease states. It is important to different enzyme systems for digestion and absorption. It
choose formulations that deliver the most beneficial and cost-effective also increases the sweetness of the formula.
enteral nutrition support. The formulations can be grouped by compo- 2. The percentage of energy in products contributed by carbohy-
sition to facilitate formula selection. Once a formulation has been cho- drate varies from <30% to >90% depending on the condition for
sen, the compounding (if necessary) and delivery must be undertaken which the product was formulated (see pulmonary disease and
in a manner that will avoid potential infectious complications. glucose intolerance formulations). In pediatric products, the per-
centage of calories from carbohydrate ranges from 42% to 58%,
I. Composition and Characteristics of Enteral Formulations while in infant formulations it ranges from 40% to 54%.
II. Adult Enteral Formulations 3. Modular carbohydrate products are available in liquid or powder
III. Pediatric Enteral Formulations for use in modifying the carbohydrate content of an existing prod-
IV. Infant Enteral Formulations uct. The carbohydrate content ranges from 50 to 95 g of carbohy-
V. Preterm Infant Enteral Formulations drate per 100 g of product.
VI. Reducing Contamination of Enteral Formulations B. Fat
References 1. Commonly used fat sources include the following:
a) Vegetable oils such as corn, canola, soybean, sunflower, and
safflower. Vegetable oils, which contain long-chain triglyc-
I. Composition and Characteristics
erides (LCTs), contribute essential fatty acids, moderate osmo-
of Enteral Formulations
lality, and enhance palatability.
A. Carbohydrate b) Medium-chain triglyceride (MCT) oil. MCT oil (Mead John-
1. Commonly used carbohydrate sources include maltodextrin, mod- son, Evansville, IN) does not require bile salts or pancreatic
ified cornstarch, and corn syrup. Each of these carbohydrate lipase for absorption into portal circulation. It also stimulates
sources is derived from cornstarch. Other carbohydrate sources the pancreas less than LCTs. MCT oil is useful as an alternative
often used in infant formulas are lactose and sucrose. The size of calorie source for patients with malabsorption disorders.3
individual carbohydrate polymers is defined by dextrose equiva- c) Long-chain polyunsaturated fatty acids including arachidonic
lents (DEs). A low DE value indicates a complex carbohydrate acid (ARA), an omega-6 fatty acid, and docosahexaenoic acid
source (unaltered cornstarch, DE = 1), whereas a high DE value (DHA), an omega-3 fatty acid, are supplied from fungal and
indicates a simpler source (dextrose, DE = 100).1 algae sources.4 These fatty acids are considered by some to be
a) Maltodextrin, with a DE of <20, is the most complex carbohy- essential in infancy, particularly in the very lowbirthweight
drate source commonly added to enteral formulas. Important infant, because of their role in visual and neural development.5,6
characteristics of maltodextrin include ease of digestion and rel- 2. The percentage of energy from fat ranges from approximately
atively low osmotic contribution to an enteral formulation.1 1% to 55% in adult formulations according to the formulation’s
b) Modified cornstarch is variable and cannot be characterized intended use. For example, products designed for patients with
by a specific DE. Modified cornstarch is used to reduce osmo- pulmonary disease and glucose intolerance are high in fat, whereas
lalities in products with otherwise high osmolalities. products designed for patients with intestinal malabsorption are
c) Corn syrup, with a DE value ranging from 20 to 65, is a sim- lower in total fat and LCTs. Pediatric formulations contain 25% to
pler form of carbohydrate than maltodextrin. Like malto- 46% of the calories from fat, while infant formulations range from
dextrin, it is a product of cornstarch hydrolysis.1 35% to 50%. The higher fat content of infant formulations reduces
d) Monosaccharides and disaccharides, such as lactose and the osmolality of the feeding and provides the necessary fat intake
sucrose, have a high DE value and osmolality. for growth.
(1) Lactose is routinely used in standard infant formulations 3. Modular fat products can be used to increase the fat content of an
to mimic the carbohydrate found in human milk. Lactose enteral formulation. MCT oil may be added to a product to increase
may also enhance the absorption of calcium from these for- its caloric density and provide a readily absorbable source of calo-
mulations.2 Most adult medical nutritional products are ries. Vegetable oils available for purchase in the grocery store can
lactose-free because of the prevalence of lactose intoler- be used as a source of fat. Microlipid (Novartis Medical Nutrition,

© 2005 A.S.P.E.N. www.nutritioncare.org. A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. 63
S E C T I O N I Fundamentals of Nutrition Support Practice and Management

Minneapolis, MN) contains emulsified safflower oil (50% fat imately 12% of calories from protein. Infant formulations con-
emulsion) and may be used to increase the caloric and linoleic acid tain 8% to 13% of calories from protein.
content of an enteral feeding regimen. In general, emulsified lipid 3. Modular protein products are indicated when the protein content
products are better choices for tube feedings, because unemulsi- of an enteral nutrition regimen needs to be increased without
fied oils separate out of the feeding formulation over time and cling greatly increasing the caloric content or volume of the regimen.
to enteral feeding tubes and administration containers.7 Most protein modules contain polymeric protein such as calcium
C. Protein. Products traditionally are broadly characterized according caseinate, whey protein, or egg albumin (eg, ProMod, Ross Prod-
to their protein type. ucts, Columbus, OH).
1. Commonly used protein sources include the following: D. Water content
a) Cow milk protein, whey protein isolates, caseinates, soy pro- 1. The energy density of a formulation is dictated largely by the
tein isolates, milk protein concentrate, or beef. Intact protein amount of water in the formulation.
or polymeric formulations contain these types of protein. 2. Infant formulations providing energy densities of 20 to 24 kcal/
b) Enzymatically hydrolyzed casein, whey, lactalbumin, wheat, fluid ounce (0.67–0.8 kcal/mL) have the highest water content,
and soy or meat protein. Oligomeric or semielemental formu- ranging from 88% to 90%.
lations contain protein sources that have undergone enzymatic 3. Formulations that provide 1 kcal/mL are approximately 75% to
hydrolysis (these formulations are often termed peptide based). 85% water.
Peptide chain length may vary from product to product depend- 4. Formulations that provide 2 kcal/mL are approximately 70%
ing on the degree of hydrolysis. water. These concentrated formulations are often indicated in
c) Free amino acids. Monomeric or elemental formulations con- adult patients who require fluid restriction.
tain free amino acids. Use of free amino acids enables manip- E. Fiber
ulation of the amino acid composition of a product and 1. Common types of fiber added to enteral formulations include the
avoidance of allergens in certain populations. following:
d) Other amino acids that may be added to enteral formulations a) Soy polysaccharide. This predominantly insoluble fiber is the
include methionine (soy infant formulas). branched-chain most prevalent fiber source in fiber-containing enteral formu-
amino acids (BCAAs), glutamine, and arginine. These nutri- lations. Soy polysaccharide may prevent constipation, increase
ents are added to certain formulations because of their pro- stool volume, and decrease gastrointestinal (GI) transit time in
posed roles in nutrition support of critically ill patients. (See critically ill patients.1 In infants, soy polysaccharide can be
immunomodulating formulations and formulations for gastro- used to firm stools in the case of diarrhea.
intestinal impairment and liver disease.) b) Gum arabic, guar gum, and pectin. These fibers are categorized
(1) BCAAs (valine, leucine, and isoleucine) are metabolized as soluble fibers. Products that contain soluble fibers may
by skeletal muscle instead of liver. These amino acids act improve glucose tolerance, lower serum cholesterol (if used
as a key nitrogen source for synthesis of protein and the over the long term), and maintain the ileal and colonic mucosal
amino acids alanine and glutamine during periods of stress. production of short-chain fatty acids, which are trophic to those
In addition, BCAAs have been promoted for use in liver mucosal surfaces.1 Partially hydrolyzed guar gum reportedly
disease when disorders of aromatic amino acid (AAA) also decreases the incidence of enteral nutrition–related diar-
metabolism occur.8,9 rhea in non–critically ill and critically ill patients with sepsis.12
(2) L-glutamine appears to be a conditionally essential amino c) Fructooligosaccharides (FOSs) have recently been added to
acid during stress-induced conditions. Although glutamine some enteral formulations. FOSs are naturally occurring, non-
is the most abundant free amino acid in the body, during digestible sugars that are selectively used by bifidobacteria in the
times of stress and infection, glutamine levels throughout human intestinal tract. FOS has been demonstrated to improve
the body fall as production through transamination of intestinal flora, relieve constipation, improve blood lipids, and
α-ketoglutarate or glutamate is unable to meet the increased suppress production of putrefactive substances. Excess FOS
demands.10 Glutamine is the preferred energy source for (more than approximately 45 g for adults) causes diarrhea in
rapidly replicating cells in both the small intestinal mucosa humans.13 Lower doses (eg, 30 g/day) may cause flatulence.
and the immune system. Feeding enteral formulations 2. Fiber-containing formulations can create complications in patients
supplemented with glutamine has been associated with who are fluid restricted or have delayed GI transit. Patients receiv-
improved microbial colonization patterns, reduced bacte- ing fiber-containing formulations should be monitored for symp-
rial overgrowth, and improved clinical outcome.11 toms of GI intolerance (eg, abdominal distention, gas, cramping,
(3) Like L-glutamine, L-arginine is considered an essential impaction, or bezoar formation).14
amino acid under certain conditions, including metabolic 3. The fiber content of adult formulations ranges from 0–22 g/L.
stress and infection. It also serves as a substrate for the pro- Pediatric formulas contain 0–8 g/L. Infant formulations do not
duction of nitric oxide. Arginine has been shown to convey routinely contain fiber.
potential benefits, including improving cell-mediated F. Micronutrients
immunity following injury, enhancing proliferation of 1. Adult formulations
fibroblasts and collagen (thus promoting wound healing), a) When provided in adequate volume, nutritionally complete
and improving nitrogen balance in critically ill patients.11 products meet 100% of the US recommended Dietary Refer-
2. The protein content in adult formulations ranges from approxi- ence Intakes (DRI). The volume required to provide the RDI
mately 6% to 32% of calories. Products designed for renal dis- varies greatly among products (≤1–4 L).
ease can contain very low amounts of protein, whereas stress and b) Patients who do not receive volumes of formulations adequate
immune-enhancing formulations contain up to 94 g/L. Pediatric to provide the RDI should receive a multivitamin and mineral
formulations have little variation in protein content, with approx- supplement unless contraindicated.

64 A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. © 2005 A.S.P.E.N. www.nutritioncare.org.
 S E C T I O N I Fundamentals of Nutrition Support Practice and Management

c) Some disease-specific enteral formulations are not nutrition- B. Cancer

ally complete. Decisions to supplement patients must be made 1. Weight loss and loss of functional tissue (lean body mass) is a com-
on the basis of an individual patient’s condition and severity mon problem in patients with advanced cancer despite aggressive
of organ dysfunction. (See disease-specific chapters.) nutritional interventions. Continued deterioration of nutritional
2. Pediatric and infant formulations status is thought to result from changes mediated by proinflam-
a) Most pediatric formulations meet 100% of the US RDI in matory cytokines, hormones, and other tumor-derived metabolites.
1000 mL for children from 1 to 8 years of age and in 1500 mL Enteral formulations enriched with fish oils (omega-3 fatty acids)
for children from 9 to 13 years of age. and other immune-promoting substrates have been used in
b) Infant formulations patients with GI cancers. The results of their use as revealed in
(1) Most infant formulations are designed to meet vitamin and clinical studies have been promising.15–20
mineral requirements as outlined by the Infant Formula 2. Formulation characteristics
Act. Products for infants with certain diseases (eg, inborn a) Osmolality is 635 mOsm per kg of water.
errors of metabolism) are exempt from some of the nutri- b) Energy density is 1.27 kcal/mL.
ent requirements in the Infant Formula Act. c) The protein provided is approximately 64 g/L (21% of total
(2) Infants and children with very low energy needs may be energy).
unable to meet micronutrient needs with formula alone if d) Carbohydrate sources include corn syrup solids, maltodextrin,
fed to their energy need. Nutrients at highest risk for insuf- sugar, fructooligosaccharides, gum arabic, and soy fiber.
ficient intake include calcium and phosphorus. A multi- e) Omega-3 fatty acids are provided through a unique blend of
vitamin and mineral supplement should be provided to sardine oil and canola oil. Additionally, MCT oil, soybean oil,
meet nutrient goals for these nutrients. and lecithin are included as fat sources (18% of total calories).
3. Clinical studies comparing the use of immune-enhancing for-
mulations with standard formulations when enteral support is
II. Adult Enteral Formulations required for patients undergoing surgery for GI cancer have
A. General-purpose formulations yielded mixed results.14–18 The contrasts in study results are
1. These formulations are generally palatable, easily absorbed, eco- likely due to differences in study design and the insufficient
number of patients enrolled in each of the studies. Despite the
nomical, and useful for most patients except those with special
flaws in study design, subanalysis of many of these studies sug-
metabolic needs or intolerance. These formulations may be the
gests a role for immune-enhancing formulations for malnour-
sole source of nutrition, or they may be used to supplement in-
ished patients undergoing surgery for upper GI cancer (both
adequate oral intake.
pre- and postoperatively).18 To obtain the maximal benefits
2. Formulation characteristics
associated with using these formulations, patients should be fed
a) The osmolality for oral formulations generally ranges from iso-
for at least 5 to 7 days.19
tonic to hypertonic (ie, about 300–700 mOsm per kg of water).
4. Consumption of a nutritional supplement enriched with fish oil
b) Energy density ranges from 1 to 2 kcal/mL.
(providing 2 g/day of eicosapentaenoic acid [EPA]) for at least
c) Protein content is between 35 and 62 g/L. The protein is high
3 weeks was associated with gains in weight and lean body mass
quality and is commonly provided as milk protein concen-
and reduced levels of several inflammatory biomarkers in severely
trate, casein, or soy protein. These intact proteins are readily
cachectic patients with pancreatic cancer cachexia.20 However, fur-
broken down to peptides and amino acids in most clinical sce- ther research is needed to determine specifically which patients
narios, with the possible exception of conditions where the with cancer cachexia are likely to benefit from consumption of this
bowel absorptive surface is severely eroded. supplement.
d) To minimize osmolality, carbohydrates are provided in com- D. Critical care/immunomodulating
plex forms. 1. Patients with trauma, sepsis, burns, or postsurgical stress are in a
e) Fats are provided as MCTs and LCTs, usually providing 29% relative state of immunosuppression. When these patients must
to 38% of calories. undergo surgical procedures, they have high rates of infectious
B. Nutrient-dense formulations complications such as pneumonia, intra-abdominal abscess, and
1. These formulations are designed for use in patients who require wound infections. Commercially prepared enteral formulations
fluid restriction (eg, patients with cardiac, renal, pulmonary, or have been developed through fortifying standard enteral formula-
hepatic failure). tions with omega-3 fatty acids, nucleotides, arginine, and gluta-
2. Formulation characteristics mine. Unfortunately, it is still unclear which of these substrates is
a) These formulations are generally hypertonic, as the osmolal- responsible for the immune-enhancing benefits associated with
ity ranges from 640 to 950 mOsm per kg of water. these formulations. The results from clinical studies and meta-
b) Energy density ranges from 2 to 2.25 kcal/mL. analyses suggest that the use of immune-enhancing formulations
c) Protein sources include sodium and calcium caseinates, soy for patients posttrauma and perioperative patients may reduce the
and milk protein isolates, and milk protein concentrate at 57 to number of overall infectious complications. Furthermore, clinical
84 g/L. trials investigating immunomodulating formulations have demon-
d) Carbohydrate is supplied by corn syrup, maltodextrin, hydro- strated decreased antibiotic use, fewer days on mechanical venti-
lyzed cornstarch, and/or sucrose as 39% to 45% of total lation, decreased length of hospitalization, and, ultimately, reduced
calories. health care costs.21–25
e) Fat content includes various combinations of soy, corn, saf- 2. Critically ill patients have been found to have reduced levels of
flower, MCT, and canola oils in amounts ranging from 30% to antioxidants (vitamins C and E, retinol, beta-carotene, and sele-
55% of total calories. nium). Whether supplementation with therapeutic levels of these

© 2005 A.S.P.E.N. www.nutritioncare.org. A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. 65
S E C T I O N I Fundamentals of Nutrition Support Practice and Management

micronutrients results in positive clinical outcomes has yet to be increased mortality rate when fed an immune-enhancing
determined. Excess supplementation may be undesirable. diet. A third study reported a decreased incidence of mor-
3. Formulation characteristics tality. Therefore, the use of immune-enhancing diets in this
a) Osmolality is moderate, at a range of 375 to 630 mOsm per patient population requires further study.
kg of water. E. Diabetes/glucose intolerance
b) Energy density ranges from 1 to 1.5 kcal/mL. 1. Patients with diabetes mellitus or stress-induced glucose intoler-
c) The high protein content (55–84 g/L) is uniquely formulated ance have difficulty tolerating the carbohydrate content of general-
to include the following: purpose enteral formulations. Hyperglycemia is associated with
(1) Arginine and glutamine, which, as previously discussed, an increased risk for infectious complications, so promoting
may be conditionally essential during stress and are sup- glycemic control is important when providing nutrition support.
plemented in some of the stress formulations In addition to pharmacotherapeutic interventions, a number of
(2) BCAAs, which are essential amino acids mobilized from commercially prepared fiber-containing, reduced carbohydrate,
skeletal muscle during stress. Supplemental BCAAs may modified fat formulations are now available for enteral feeding for
preserve muscle in metabolically stressed patients; how- patients with poor glucose control.28
ever, studies have not consistently shown improved clinical 2. Formulation characteristics
outcomes.26,27 a) These formulations are essentially isotonic.
(3) Nucleotides, which are required by rapidly proliferating b) Energy density is 1 to 1.2 kcal/mL.
tissues such as the intestinal epithelium. Nucleotides also c) An intact protein source provides 42 to 63 g/L.
enhance lymphocyte proliferation and responsiveness. d) Carbohydrate is primarily polysaccharide, with fructose for
(4) Carbohydrate sources, which include maltodextrin or hydro- flavor, and provides 31% to 40% of total calories.
lyzed cornstarch. Fiber may also be provided as hydrolyzed e) Fiber content ranges from 8 to 21 g/L. Fiber sources vary but
guar gum or soy fiber. generally are derived from hydrolyzed guar gum, soy fiber,
(5) Fat sources, which contribute between 20% and 55% of acacia, cellulose, soy polysaccharides, pectin, gum arabic, or
total calories. Long-chain omega-3 fatty acid content is fruit and vegetable fiber.
one of the defining characteristics of this category of for- f) Fat provides 40% to 50% of calories; the ratio of omega-6 to
mulations. Inflammatory mediators normally produced omega-3 fats is variable. There is generally a greater proportion
during critical illness may be minimized with adminis- of fat calories than is recommended by the American Diabetes
tration of omega-3 fatty acids because their metabolism Association for healthy patients with diabetes.29,30
produces prostaglandins and thromboxanes of a less g) There is limited published evidence that the use of these spe-
inflammatory and less immunosuppressive nature than cialty formulations results in improved glucose control in hos-
the products of omega-6 fatty acid metabolism. Supple- pitalized patients, especially the critically ill. Patients with
mentation with omega-3 fatty acids has been shown to glucose intolerance should be carefully evaluated for con-
attenuate the inflammatory response, stabilize the nuclear comitant morbidities (eg, gastroparesis, renal impairment)
factor-Κ-B complex, possess antithrombotic properties, when selecting the appropriate formula. Improved glycemic
reduce platelet adhesion, enhance neutrophil function, control can reduce diabetic gastroparesis. Important goals of
and support membrane stability and microvasculature nutrition therapy should include avoiding overfeeding and
profusion.11 controlling glucose through administration of insulin, if
(6) Structured lipids, which are also added to some of the needed.
immunomodulating formulations. Structured lipids are F. Hepatic disease
chemical combinations of long-, medium-, and short-chain 1. Patients with decompensated liver disease are typically malnour-
fatty acids on a single glycerol backbone. The resultant ished and benefit from nutritional supplementation. Some patients
product has improved absorption (compared with LCT), who have worsening encephalopathy when they receive standard
minimizes immune dysfunction,11 and can provide essential enteral formulations may improve when given a formulation con-
fatty acids. taining a higher BCAA-to-AAA ratio. Hepatic disease formula-
d) A variety of commercially prepared formulations are avail- tions should not be used in patients with nonencephalopathic
able with various substrates added that may modulate the manifestations of liver disease.31
immune system. According to the recommendations of the 2. Formulation characteristics
US Summit on Immune-Enhancing Enteral Therapy25 held a) These formulas are hypertonic, with osmolalities of >450
in 2000, immune-enhancing formulations may be beneficial mOsm per kg of water.
for the following: b) Energy density ranges from 1.2 to 1.5 kcal/mL.
(1) Patients undergoing major elective GI surgery, especially c) To minimize ammonia production, protein content is low
malnourished patients (40–46 g/L). BCAAs are provided in greater amounts than
(2) Patients with blunt and penetrating torso trauma AAAs because of the increased quantities of AAAs in patients
(3) Malnourished patients undergoing surgery for head and with liver failure. This abnormal AAA-to-BCAA ratio, which
neck cancer results in AAAs acting as false neurotransmitters, is one of the
(4) Patients with severe head injury theoretical etiologies of hepatic encephalopathy.31
(5) Burn patients d) Carbohydrate is supplied as maltodextrin and sucrose.
(6) Ventilator-dependent non-septic patients at risk for infection e) Hepatic formulations are low in fat because absorption can be
(7) Patients needing formulations for a minimum of 5 days impaired as a result of cholestasis.
(8) Patients with preexisting severe sepsis. Two studies suggest 3. Clinical studies have not demonstrated improved outcomes in
that patients with preexisting severe sepsis may have an patients who received formulations high in BCAAs.31,32 Use of

66 A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. © 2005 A.S.P.E.N. www.nutritioncare.org.
 S E C T I O N I Fundamentals of Nutrition Support Practice and Management

these formulations should be restricted to patients who present e) Fat content ranges from approximately 1% to 39% of total
with grade II or greater encephalopathy or whose grade of ence- calories.
phalopathy worsens as nutrition support with a standard enteral f) These products are nutritionally complete and provide 100%
formulation is advanced. of the RDI in approximately 950 mL to 2 L.
G. Impaired GI digestion or absorption 3. Studies show that jejunal administration of specialized enteral
1. In certain disease states, there may be impaired absorption of nutrition support not only is well tolerated but also attenuates the
nutrients. Absorption may be enhanced with the use of a chemi- inflammatory response, reduces hyperglycemia and infectious
cally defined formulation. Also, because they are less viscous, complications, and hastens recovery from the pancreatic insult
chemically defined formulations are commonly used in patients compared with parenteral nutrition.38–40 While the “ideal” enteral
with needle catheter jejunostomies to minimize catheter clog- formulation for patients with pancreatitis has not been agreed
ging. Conditions that can benefit from the use of a chemically upon, clinical studies where enteral nutrition has been successfully
defined formulation include the following: employed have generally used peptide-based formulations with
a) Diffuse diseases of the intestinal mucosa, such as celiac dis- good tolerance.
ease, inflammatory bowel disease, and enterokinase deficiency I. Pulmonary disease
b) Critical illness, especially after shock, trauma, sepsis, or 1. Formulations for use in patients with long- or short-term pul-
surgery monary disease are designed based on the theory that, when
c) Pancreatic or bile salt deficiencies more energy is provided from fat and less from carbohydrate, a
d) Intestinal atrophy or loss of absorptive surface, as with pro- patient’s carbon dioxide production will be lowered and thereby
longed nothing-by-mouth status, profound malnutrition, and the amount of carbon dioxide retention will be reduced. Addi-
short-bowel syndrome tionally, some investigators have demonstrated significantly
2. Formulation characteristics reduced time on mechanical ventilation for patients who receive
a) Semi-elemental or peptide-based formulations have a lower these formulations.41,42
osmolality than elemental formulations but a higher osmolal- 2. Formulation characteristics
ity than polymeric formulations. a) These formulas are moderately hypertonic (330–650 mOsm
b) Energy density ranges from 1 to 1.5 kcal/mL. per kg of water).
c) Protein is supplied as crystalline amino acids (elemental for- b) Energy density is 1.5 kcal/mL.
mulations) or as hydrolyzed whey, casein, wheat protein, soy, c) Protein content ranges from 63 to 75 g/L.
or lactalbumin or a mixture of free amino acids and hydrolyzed d) Carbohydrate sources include sucrose, maltodextrin, and
protein. hydrolyzed cornstarch, which contribute between 28% and
d) The fat content ranges from very low fat (1% of total calories) 40% of total calories. Some pulmonary formulations also
to 30% of total calories. contain fiber (8 g/L) from sources including hydrolyzed guar
e) Peptides may be better absorbed than free amino acids by gum and soy fiber.
both healthy and diseased guts.33 Individual amino acids are e) Fat content ranges from approximately 38% to 55% of total
absorbed by a less efficient, passive diffusion mechanism. calories.
However, tolerance and clinical outcomes with peptide-based f) These products are nutritionally complete and provide 100%
formulations have not been demonstrated to be superior to the of the RDI in ≤1 L.
outcomes of polymeric formulation use.34,35 Additional con- g) Formulations designed for patients with Acute Respiratory Dis-
cerns of using these products include increased cost, evidence tress Syndrome (ARDS) also contain borage and sardine oils.
that less complex products are less trophic to the GI tract and 3. In general, studies demonstrating the benefits of pulmonary for-
may increase the risk of bacterial translocation, and deleterious mulations over general-purpose formulations have been criticized
effects on immunocompetence.36,37 To summarize, these prod- for having a small sample size.41,42 Recent studies suggest that
ucts should be reserved for use in patients with disease states avoiding overfeeding of energy is as effective in reducing PCO2,
that lead to malabsorption of conventional polymeric formula- as is a low-carbohydrate feeding regimen.43 Thus, pulmonary for-
tions and in patients who have demonstrated intolerance to mulations may not provide clinically significant benefits above
polymeric feedings. those of a nutrition support regimen that provides adequate
H. Pancreatitis (instead of excessive) energy regardless of the carbohydrate-to-
1. Traditionally, parenteral nutrition was the preferred method of fat ratio.
providing specialized nutrition support to patients with severe 4. Conversely, a recent clinical study reported positive clinical out-
pancreatitis because it was thought that not using the GI tract comes with the use of an enteral formulation specifically designed
would result in less stimulation of and more rest for the pancreas. for patients with ARDS. Although this product provides a high fat
However, evidence has accumulated that favors the use of enteral content, the fat composition has been altered to provide greater
nutrition support for patients with pancreatitis when specialized amounts of EPA and gamma-linolenic acid. This combination
nutrition support is warranted. (See Chapter 15.) has been shown to alter membrane phospholipid makeup, sub-
2. Formulation characteristics sequently resulting in the synthesis of the less inflammation-
a) Elemental and peptide-based formulations generally range in producing eicosanoids.44 Improved clinical outcomes included
osmolality from 270 to 650 mOsm per kg of water. decreased length of stay and fewer ventilator days.
b) Energy density ranges from 1 to 1.5 kcal/mL. 5. Ambulatory patients with long-term pulmonary disease often need
c) Protein content ranges from 21 to 94 g/L. an oral supplement because these patients have high energy needs,
d) Carbohydrate sources include maltodextrin, and hydrolyzed fatigue easily, and often have trouble eating and breathing simul-
cornstarch, sucrose, and soy fiber; carbohydrates generally taneously, which makes it difficult to consume adequate energy
contribute 36% to 91% of total calories. and protein from common foods. Energy-dense products allow

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S E C T I O N I Fundamentals of Nutrition Support Practice and Management

such patients to consume a large amount of energy and protein in ever, the optimal amount of arginine needed to promote wound
a small volume and with little effort. healing is unknown. As previously discussed, several formula-
J. Renal disease tions are available that contain not only arginine but other sub-
1. Enteral formulations for patients with renal disease must provide strates associated with wound healing.
adequate nutrients and minimize complications such as fluid over- e) Carbohydrate sources include hydrolyzed cornstarch, sucrose,
load, uremia, and elevated serum electrolyte and mineral concen- maltodextrin, and corn syrup solids. Many formulations also
trations. To achieve these goals, renal formulations typically are offer fiber supplementation with hydrolyzed guar gum, soy
energy dense, low in electrolyte and mineral contents, and mod- fiber, or soy polysaccharides.
erate in protein content. f) Fat generally comprises 25% to 40% of total calories. Sources
2. Formulation characteristics include palm kernel, sunflower, canola, safflower, and MCT
a) These formulations are very hypertonic, with osmolalities oil; soy lecithin; and menhaden fish oil.
ranging from 570 to 700 mOsm per kg of water. g) Nutrition is one of many factors that influence wound healing.
b) Energy density is 2 kcal/mL. A variety of commercially prepared enteral formulations are
c) Protein content ranges from 30 to 75 g/L. Protein sources now available that contain greater levels of vitamins A, C, and
include sodium, calcium and magnesium caseinates, milk pro- E as well as zinc. While clinical studies have found these
tein isolate, whey protein, and free amino acids. micronutrients to play an important role in wound healing, sup-
d) Carbohydrate sources include maltodextrin, sucrose, fructose, plementation beyond the RDI has not been shown to improve
corn syrup, and hydrolyzed cornstarch. wound healing when no clinical deficiency exists. In some
e) Fat sources include safflower, soy, canola, corn, and MCT oil cases, excess supplementation may be detrimental.
and contribute 35% to 46% of calories. 3. Poor nutritional status has been linked with the development of
f) Some formulations are not nutritionally complete; some are pressure ulcers. Provision of adequate nutrition is key in preven-
essentially vitamin- and mineral-free, and others contain some tion and treatment. To promote positive patient outcomes as well
water-soluble vitamins and no fat-soluble vitamins or minerals as wound healing, the choice of the “optimal” enteral formula-
3. Historically, enteral renal formulations with protein sources tion should be dictated by both the patient’s clinical status and
derived chiefly from essential amino acids were used for patients nutritional requirements.
with short-term renal failure who could not tolerate dialysis, or for 4. Arginine, glutamine, omega-3 fatty acids, vitamins A and C, and
whom dialysis was being postponed or avoided. However, today zinc are specific substrates frequently associated with stimulating
most patients with acute renal failure are dialyzed; therefore, the immunocompetence and enhanced wound healing postburn. The
use of these formulations is rarely warranted. A variety of formu- results of clinical trials using commercially prepared enteral for-
lations designed for patients with impaired renal function are avail- mulations to alter clinical outcomes are mixed.45,47 In one study,
able with modified electrolyte and micronutrient compositions. burn patients receiving a formulation high in protein and low in fat
These formulations may be appropriate for patients whose serum but fortified with omega-3 fatty acids, arginine, cysteine, histidine,
electrolyte and mineral levels are difficult to control. vitamins A and C, and zinc experienced fewer overall infections
K. Wound healing and had a shortened length of hospitalization.47 Another study
1. Obesity, poor oxygenation, infection, aging, impaired immune found that an immune-enhancing formulation fortified with
function, vascular insufficiency, and some medications can impair omega-3 fatty acids, nucleotides, and arginine provided no signif-
wound healing.45 Poor nutrition can also contribute to delayed and icant benefits.45 The A.S.P.E.N. Clinical Guidelines for the Use of
impaired wound healing. Reportedly, enteral nutrition is associ- Parenteral and Enteral Nutrition in Adult and Pediatric Patients
ated with improvements in wound healing when compared with state that “there is no current role for the routine use of specific
parenteral support.46 The optimal provision of both macro- and nutrients in burn patients.”48
micronutrients is required for cellular, collagen, and connective
tissue synthesis. Of the micronutrients, vitamins A, E, K, and C,
III. Pediatric Enteral Formulations
thiamine, riboflavin, and zinc have been identified with improved
wound healing.46 The conditionally essential amino acid arginine A. General-purpose formulations
may also enhance wound repair.46 1. General-purpose formulations are designed for children from 1
2. Formulation characteristics to 10 years of age who require tube feedings or oral formula sup-
a) Osmolality is moderate, at a range of 300 to 630 mOsm per plements to meet nutrient needs. These formulations are avail-
kg of water. able in two forms, one for tube feeding and the other for use as
b) Energy density ranges from 1 to 1.5 kcal/mL. an oral supplement.
c) The high protein content (55–84 g/L) generally is provided 2. Formulation characteristics
by protein sources similar to those discussed in the immune- a) The enteral tube-feeding products are isotonic, with osmo-
modulating formulation section; it typically includes sodium lalities of 335 to 380 mOsm per kg of water. The osmolali-
and calcium caseinates, L-arginine, whey and wheat protein ties of the oral formulations are higher, ranging from 430 to
hydrolysates, soy protein isolate, and free amino acids. 520 mOsm per kg of water.
Some formulations are supplemented with L-arginine and b) Energy density is 30 kcal/fluid ounce (1 kcal/mL).
L-glutamine. c) Protein sources are typically sodium and calcium caseinates,
d) L-arginine may be a conditionally essential amino acid to pro- milk protein, and/or whey protein concentrate. A blenderized
mote wound healing. Arginine supplementation has been found formulation also contains beef as a protein source. All prod-
not only to improve nitrogen balance but also to enhance ucts contain at least one source of cow milk protein. The pro-
immune function and increase hydroxyproline accumulation in tein content of these formulations ranges from 30 to 38 g/L,
healthy people supplemented with arginine for 2 weeks.46 How- with most formulas containing 30 g/L.

68 A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. © 2005 A.S.P.E.N. www.nutritioncare.org.
 S E C T I O N I Fundamentals of Nutrition Support Practice and Management

d) Carbohydrate sources are typically maltodextrin and sucrose. e) Fat sources include corn oil and MCTs. The MCT oil com-
Other carbohydrate sources include fructose, apple juice, poses 87% of the fat. The product contains 48 g/L.
fruits, and vegetables. The sucrose content is higher in oral f) Because the LCT content is low, the content of essential fatty
supplements (30%–70% of carbohydrate) than in tube-feeding acids is also low (3.4 g linoleic acid/L). Long-term use of this
products (13% of carbohydrate) to enhance flavor. The carbo- product, particularly in patients with fat malabsorption, may
hydrate content of these formulations ranges from 110 to induce essential fatty acid deficiency. When this product was
138 g/L. Products are available with and without fiber. Fiber labeled as an infant formulation, infants with hepatocellular
sources include soy fiber, pea fiber, gum arabic, oat fiber, car- disease fed the high-MCT formulation developed an increased
boxymethylcellulose, oligofructose, fruits, and vegetables. triene:tetraene ratio consistent with essential fatty acid defi-
The fiber content of the fiber-containing products ranges from ciency. When fed formulations containing only 50% of fat
4.4 to 8 g/L. calories as MCT, the same infants were able to maintain essen-
e) Fat sources include high oleic sunflower and safflower oils, tial fatty acid stores.49 This high-MCT formulation should be
canola oil, corn oil, soy oil, beef fat, and MCT. The fat content avoided in infants with fat malabsorption. Infants requiring a
ranges from 37 to 50 g/L. high-MCT formulation for management of chylous leak syn-
B. Chemically defined formulations dromes may require a secondary source of essential fatty acids
1. The chemically defined formulations are designed for 1- to such as intravenous fat emulsions if the formulation is used for
10-year-old children with severe protein allergies, malabsorp- extended periods.
tion, and/or GI tract impairment. The nutrient content varies
widely from product to product. Product selection should be deter-
IV. Infant Enteral Formulations
mined by matching the disease condition with the appropriate
nutrient composition. Peptide products with moderate MCT oil A. Standard cow milk–based formulations for term infants
content are designed for children with malabsorption syndromes. 1. Cow milk formulations are indicated as routine feedings for
Free amino acid products are indicated for children with severe infants.
protein allergies who demonstrate an allergic response to the 2. Formulation characteristics
extensively hydrolyzed protein found in the peptide products. a) These formulations are isotonic, with osmolalities ranging
2. Formulation characteristics from 280 to 300 mOsm per kg of water.
a) Osmolality of the chemically defined formulas is typically b) Standard energy density is 20 kcal/fluid ounce (0.67 kcal/mL).
higher than the that of general-purpose pediatric formulations The formulations are also available in 24 kcal/fluid ounce
due to the predigested nature of the protein source. The most ready-to-feed bottles (0.8 kcal/mL) for hospital use.
hypertonic formulas contain free amino acids as their protein c) Protein sources include whey protein concentrate, sodium
source. The osmolalities of these products range from 260 to caseinate, nonfat milk, and hydrolyzed reduced-minerals whey
820 mOsm per kg of water. protein concentrate. The protein content of these formulas, at
b) Caloric density ranges from 20 kcal/fluid ounce (0.8 kcal/mL) standard dilution, is 1.4 g/100 mL (2.1 g/100 kcal).
to 30 kcal/fluid ounce (1 kcal/mL). d) Lactose is the carbohydrate source. The carbohydrate con-
c) Protein sources include whey hydrolysates, soy hydrolysates, tent at standard dilution ranges from 7.1 to 7.5 g/100 mL
pork hydrolysates, and free amino acids. The protein content (10.6–11.2 g/100 kcal).
ranges from 24 to 32 g/L (30–32 g/1000 kcal). e) Fat sources include high oleic safflower and sunflower oils,
d) Carbohydrate sources include corn syrup solids, maltodextrin, soy oil, coconut oil, palm olein, and safflower oil. The fat con-
modified cornstarch, and sucrose. All products are lactose- tent at standard dilution ranges from 3.4 to 3.6 g/100 mL
free. The carbohydrate content ranges from 107 to 138 g/L (5.1–5.4 g/100 kcal).
(107–162 g/1000 kcal). f) The formulations are available with and without added ARA
e) Fat sources include high-oleic safflower oil, soy oil, canola oils, and DHA. Studies evaluating the effect of very long chain
and MCT. The fat content ranges from 24 to 49 g/L (30–49 g/ fatty acids on visual and neural development have had con-
1000 kcal). MCTs range from 25% to 60% of the fat content. flicting results, with some studies showing improved visual
C. High-MCT formulations and mental development and others demonstrate no effect.5,6
1. These formulations were initially designed for children with fat These differences in outcomes may reflect differing formula
digestion, absorption, and transport disorders, as MCTs are easier compositions, differing levels of very long chain fatty acid
to digest and absorb than LCTs. The use of a diet low in LCTs has supplementation, and differing levels of essential fatty acids.
also been recommended in the treatment of patients with chylous g) Some cow milk formulations contain added nucleotides.
leak syndromes (chylothorax and chylous ascites) and in disor- Studies have shown that the addition of a particular amount of
ders of fatty acid transport (lymphangiectasia). As MCTs are nucleotides to infant feedings (72 mg/L) enhances antibody
transported via the portal system instead of the lymphatic system, response to specific immunizations and lymphocyte matura-
they may minimize lymphatic flow. tion so that they are closer to those of breast-fed infants.50
2. Formulation characteristics h) Cow milk formulations are available with two levels of iron.
a) The high-MCT formulation is isotonic, with an osmolality of Only the formulations with the higher iron content are indi-
350 mOsm per kg of water. cated for routine use in infant feedings.51
b) The caloric density is 30 kcal/ounce (1.01 kcal/mL). i) Cow milk formulations are available in ready-to-feed, con-
c) The protein source is sodium caseinate. The protein content centrated liquid (40 kcal/fluid ounce), and powder forms.
of the formulation is 35 g/L. B. Cow milk–based lactose-free formulations
d) Carbohydrate sources include corn syrup solids and sucrose. 1. “Lactose-free formulations” are cow milk–based lactose-free
The product is lactose-free and contains 114 g/L. products marketed as an alternative to soy formulations for infants

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S E C T I O N I Fundamentals of Nutrition Support Practice and Management

with symptoms thought to be related to lactose intake. The for- protein allergies. The second category contains extensively hydro-
mulations are considered very low in lactose but are not indicated lyzed protein and a blend of LCTs and MCTs. This formulation
for use in infants with galactosemia. may be used for infants with cow milk or soy protein allergies but
2. Formulation characteristics is also indicated for infants with malabsorption syndromes such as
a) These formulations are hypotonic, with osmolalities of approx- short-bowel syndrome and cystic fibrosis. The third category con-
imately 200 mOsm per kg of water. tains free amino acids and low amounts of MCTs. This formula-
b) Standard energy density is 20 kcal/fluid ounce (0.67 kcal/mL). tion is indicated for infants who continue to demonstrate allergic
c) The protein source is milk protein isolate. The protein content symptoms on extensively hydrolyzed protein formulations. It is
is 1.4 g/100 mL (2.1 g/100 kcal). also often used for infants with serious malabsorption.
d) Carbohydrate sources include maltodextrin, corn syrup solid, 2. Formulation characteristics
and sucrose. The carbohydrate content is approximately 7.2 g/ a) These formulations have osmolalities ranging from 320 to
100 mL (10.8 g/100 kcal). 500 mOsm per kg of water.
e) Fat sources include high oleic safflower and sunflower oils, soy b) Standard energy density is 20 kcal/fluid ounce (0.67 kcal/mL).
oil, coconut oil, and palm olein. The fat content is approxi- c) Protein sources include extensively hydrolyzed casein and free
mately 3.6 g/100 mL (5.4 g/100 kcal). These formulations con- amino acids. Casein hydrolysate formulations also contain
tain added ARA and DHA. added L-cystine, L-tyrosine, and L-tryptophan. The protein
f) These formulations contain added nucleotides. content ranges from 1.8 to 2.1 g/100 mL (2.7–3.1 g/100 kcal).
g) Cow milk–based lactose-free formulations are available in d) Carbohydrate sources include corn syrup solids, modified
ready-to-feed, concentrated liquid (40 kcal/fluid ounce), and cornstarch, modified tapioca starch, dextrose, and sucrose. All
powder forms. formulations are lactose-free. The carbohydrate content ranges
C. Soy-based lactose-free formulations from 6.8 to 9.1 g/100 mL (10.2–13.6 g/100 kcal).
1. Soy-based formulations are cow milk protein–and lactose-free. e) Fat sources include canola, coconut, corn, high oleic safflower,
They have been marketed for use with fussy babies and infants safflower, sunflower, and soy oils, as well as palm olein.
with allergies, lactose intolerance, or galactosemia. The American Hydrolyzed casein formulations also contain ARA and DHA.
Academy of Pediatrics recommends the use of soy formulations Hydrolyzed casein formulations have an MCT content of 0%
for infants with galactosemia, infants with documented lactose to 60% of fat calories. Free amino acid formulations have an
intolerance, or infants with vegetarian parents who want a plant- MCT content of 5% to 33% of fat calories. The fat content
based formulation for their children. Eighty six percent of patients ranges from 2.6 to 3.8 g/100 mL (4.2–5.7 g/100 kcal).
with IgE-mediated cow milk protein allergy tolerated soy for- f) Chemically defined formulations are available in a variety of
mula.52 The academy states that soy formulations are not effec- forms. All products are available in a powder form, and the
tive for treatment of colic and should not be used for infants with hydrolyzed formulations are also available in a ready-to-feed
GI cow milk protein allergy or premature infants weighing less form. One hydrolyzed formulation is also available to hospitals
than 1800 g.53 as a concentrated liquid.
2. Formulation characteristics 3. Approximately 2% to 3% of formula-fed infants will develop
a) These formulations are hypotonic, with osmolalities of an allergy to cow milk protein. The incidence is increased in
approximately 200 mOsm per kg of water. infants with a family history of allergy. Two forms of cow milk
b) Standard energy density of these formulations is 20 kcal/fluid protein allergy/intolerance have been identified. The first form
ounce (0.67 kcal/mL). is immunoglobulin-E (IgE) mediated and presents as urticaria,
c) The protein source is soy protein isolate. L-methionine is added respiratory difficulties, vomiting, and anaphylaxis. The second
to improve the biological value of the soy protein. The protein form, non-IgE mediated, presents as GI symptoms such as vom-
content ranges from 1.6 to 1.9 g/100 mL (2.4–2.8 g/100 kcal). iting, diarrhea, bloody stools, and enterocolitis. Infants with IgE-
d) Carbohydrate sources include corn syrup, corn maltodextrin, mediated allergies will often tolerate soy formulations without
and sucrose. The carbohydrate content ranges from 6.8 to development of a secondary allergy to soy. Infants with non-
7.4 g/100 mL (10.1–11.1 g/100 kcal). IgE-mediated GI protein intolerance are at high risk of devel-
e) Fat sources include high oleic safflower and sunflower oils, oping a soy allergy. The American Academy of Pediatrics
coconut oil, soy oil, and palm olein. The fat content ranges Committee on Nutrition recommends that breast milk, extensively
from 3.4 to 3.6 g/100 mL (5.1–5.5 g/100 kcal). These formu- hydrolyzed formulations, or free amino acid formulations be used
lations are available with and without added ARA and DHA. for infants with “non-IgE-associated syndromes such as entero-
f) One ready-to-feed soy formulation contains added soy fiber colitis, proctocolitis, malabsorption syndrome, or esophagitis.”57
with a fiber content of 0.6 g/100 mL (0.9 g/100 kcal). Soy poly- 4. Approximately 10% of infants with colic have a cow milk pro-
saccharide added to infant formulations has been found to tein allergy that may respond to a chemically defined diet.58
improve stool consistency and reduce duration of diarrhea in E. Low electrolyte/mineral formulations for renal disease
infants and toddlers suffering from gastroenteritis or antibiotic- 1. Hypocalcemia and hyperphosphatemia are common complica-
induced diarrhea.54–56 tions in infants with renal disease. Diets low in phosphorus are
g) Soy formulations are available in ready-to-feed, concentrated indicated to minimize the development of bone disease.
liquid (40 kcal/ounce), and powder forms. 2. Formulation characteristics
D. Chemically defined formulations a) Osmolality is isotonic, at 280 mOsm per kg of water.
1. Three different chemically defined formulations are available. b) Standard energy density is 20 kcal/fluid ounce (0.67 kcal/mL).
Indications for each formulation vary. The first category contains c) Protein sources include whey protein concentrate and sodium
extensively hydrolyzed protein and LCTs as the fat source. This caseinate. The whey to casein ratio is 60:40. The protein con-
formulation is designed for use in infants with cow milk or soy tent is 1.5 g/100 mL (2.2 g/100 kcal).

70 A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. © 2005 A.S.P.E.N. www.nutritioncare.org.
 S E C T I O N I Fundamentals of Nutrition Support Practice and Management

d) The carbohydrate source is lactose. The carbohydrate content ounce (74 kcal/100 mL). The energy density of preterm
is 6.8 g/100 mL (10.2 g/100 kcal). human milk mixed with a powdered fortifier at standard dilu-
e) Fat sources include corn, coconut, and soy oils. The fat con- tion (4 packets HMF:100 mL breast milk) is 24 kcal/fluid
tent is 3.7 g/100 mL (5.6 g/100 kcal). ounce (80 kcal/100 mL).
f) This product has a lower content of calcium, phosphorus, potas- c) Protein sources include nonfat milk, milk protein isolate, whey
sium, and chloride than standard cow milk formulations. It is protein concentrate, and whey protein isolate hydrolysate. The
also low in iron, containing 0.47 mg/100 mL (0.7 mg/100 kcal). protein content of the liquid fortifier is 2.2 g/100 mL, and for-
An iron supplement is indicated for patients using this product. tified preterm milk made with the liquid fortifier at standard
g) This product is available in powder form only. dilution contains 1.8 g/100 mL (2.4 g/100 kcal). The protein
F. Thickened formulations content of powdered fortifiers ranges from 1 to 1.1 g/4 packets,
1. Gastroesophageal reflux and regurgitation are common symptoms and fortified preterm milk made with the powdered fortifier at
in newborns, peaking at approximately 4 months of age and resolv- standard dilution contains 2.3 to 2.5 g/100 mL (2.9–3.1 g/
ing by the end of the first year of life.59 Although controversial, 100 kcal).
thickening of infant formulations is a common practice in the man- d) Carbohydrate sources include corn syrup solids and lactose.
agement of gastroesophageal reflux and has been recommended by The carbohydrate content of the liquid fortifier is 8.5 g/100 mL,
the North American Society for Pediatric Gastroenterology and and fortified preterm milk made with the liquid fortifier at stan-
Nutrition as a treatment for this condition.60 Thickening of infant dard dilution contains 7.6 g/100 mL (9.5 g/100 kcal). The car-
formulas is often accomplished by adding rice cereal to a standard bohydrate content of powdered fortifiers ranges from <0.4 to
cow milk formula. This method of thickening formula increases 1.8 g/4 packets, and fortified preterm milk made with the pow-
the energy density and alters the nutrient composition of the dered fortifier at standard dilution contains 6.6 to 8.2 g/100 mL
product. An infant formulation product with added rice starch (8.2–10.2 g/100 kcal).
that thickens when exposed to gastric acid has been developed. e) Fat sources include soy oil, coconut oil, and MCTs. The fat
Its nutrient composition is comparable to that of standard infant content of the liquid fortifier is 4.4 g/100 mL, and fortified
formulations. preterm milk made with the liquid fortifier at standard dilu-
2. Formulation characteristics tion contains 4.1 g/100 mL (5.1 g/100 kcal). The fat content
a) The osmolality is isotonic, at 240 mOsm per kg of water. of powdered fortifiers ranges from 0.36 to 1 g/4 packets, and
b) Energy density of the formula is 20 kcal/fluid ounce fortified preterm milk made with the powdered fortifier at
(0.67 kcal/mL). standard dilution contains 4.1 to 4.9 g/100 mL (5.1–6.1 g/
c) Protein content is nonfat milk, with 1.7 g protein/100 mL 100 kcal).
(2.5 g/100 kcal). f) Calcium and phosphorus content is increased in HMFs, and,
d) Carbohydrate sources include lactose, rice starch, and malto- when mixed at standard dilution, makes the calcium content
dextrin. The carbohydrate content is 7.4 g/100 mL (11 g/ 3 to 5 times greater than that found in preterm milk. The phos-
100 kcal). phorus content is increased to a greater degree, ranging by
e) Fat sources include palm olein, soy oil, coconut oil, high oleic four- to six fold the content of preterm human milk. In gen-
sunflower oil, and single-cell oils rich in DHA and ARA. The eral, the HMF provides a lower increase in mineral intake.
fat content is 3.4 g/100 mL (5.1 g/100 kcal). g) HMFs are available with and without added iron. Iron-
f) The formulation is available in only a ready-to-feed form. containing HMFs have 1.4 mg iron/4 packets (1.8 mg iron/
3. Several studies have shown that thickened infant formulations 100 mL fortified human milk). Infants receiving HMFs without
reduce overt signs of gastroesophageal reflux.61,62 While thick- added iron require an oral iron supplement.
ening agents may reduce regurgitation, subclinical acid reflux 3. The addition of HMFs to human milk has been found to promote
may continue. Infant formulations thickened with carob bean short-term increases in weight, length, and head circumference.63
gum have been found to reduce the frequency and reflux height B. Preterm formulations
of nonacid (pH > 4) regurgitations but not the frequency and 1. Preterm infant formulations are designed to provide increased
duration of acid reflux (pH < 4).62 protein, mineral, electrolyte, and vitamin intakes in a form that is
easy to digest and absorb.
2. Formulation characteristics
V. Preterm Infant Enteral Formulations a) These formulations are isotonic, with osmolalities ranging
A. Human milk fortifiers from 280 to 310 mOsm per kg of water.
1. Preterm infants have increased needs for protein, minerals, and b) Standard energy density is 24 kcal/fluid ounce (0.8 kcal/mL).
electrolytes to support the rapid growth and bone mineralization These products are also available in a 20 kcal/fluid ounce
normally occurring during the final trimester of pregnancy. Human (0.67 kcal/mL) form.
milk, ideal for term infants, requires supplementation to meet the c) Protein sources include nonfat milk and whey protein con-
needs of the growing preemie. Human milk fortifiers (HMFs) are centrate. The whey protein fraction is 50% to 60% of the total
powders or liquids that are mixed with human milk to increase protein content. The protein content ranges from 2.2 to 2.4 g/
the protein, mineral, electrolyte, and vitamin content. 100 mL (2.7–3 g/100 kcal).
2. Formulation characteristics d) Carbohydrate sources include corn syrup solids and lactose.
a) Osmolality of human milk fortified with HMF ranges from The lactose content is approximately 50% of the total carbohy-
285 mOsm per kg of water (liquid fortifier) to 320 to 385 mOsm drate content. The carbohydrate content ranges from 8.5 to 9 g/
per kg of water (powdered fortifier). 100 mL (10.6–11.2 g/100 kcal).
b) Energy density of preterm human milk mixed with a liquid e) Fat sources include soy oil, coconut oil, and MCTs. MCTs
fortifier at the standard dilution (1:1 ratio) is 22 kcal/fluid comprise approximately 40% to 50% of the total fat content.

© 2005 A.S.P.E.N. www.nutritioncare.org. A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. 71
S E C T I O N I Fundamentals of Nutrition Support Practice and Management

The fat content ranges from 4.1 to 4.4 g/100 mL (5.1–5.5 g/100 fluid volumes. These infants will benefit from concentrating
kcal). Preterm infant formulations contain ARA and DHA. formulations. When increased nutrient density formulations are
f) Preterm infant formulations are available with or without iron. produced by decreasing the amount of water added to formula
To meet the iron needs of the growing premature infant, the powders or concentrates, the balance of nutrients is maintained.
iron-containing form is recommended. Infants with increased energy needs but little increase in other
3. Clinical studies have shown improved early growth in infants fed nutrient may tolerate the use of carbohydrate or fat modulars to
preterm formulations versus standard formulations. Growth dif- increase the energy density of the formulation. Infants with
ferences between the groups tend to disappear as the infants age increased protein needs, such as infants on peritoneal dialysis
into late childhood and early adolescence.64 One study suggested or small preterm infants, may benefit from concentrated for-
that at the age of 7 to 8 years, neurodevelopmental outcome was mulations and/or the use of a protein modular.
improved in former preterm infants who received preterm for- b) Increasing nutrient density usually increases formulation osmo-
mulations versus standard-term formulations in the first few lality. Concentrating formulations will cause a substantial
weeks of life.64 increase in osmolality, particularly in formulations that are
C. Preterm discharge formulations hypertonic at standard dilution. Carbohydrate modulars made
1. Preterm infants are frequently discharged to home before reaching from glucose polymers are also hypertonic and will generally
term gestation. In addition, many preterm infants have delayed increase osmolality to the same degree as an equicaloric
growth during hospitalization and will benefit from increased pro- increase in formulation concentration.67 Fat modulars are iso-
tein and mineral intakes after discharge to promote catch-up tonic and will therefore have no effect on formulation osmolal-
growth. The preterm discharge formulations are designed for ity. As the protein used in protein modulars is a whole protein
preterm infants nearing hospital discharge and at home throughout (whey protein concentrate or sodium, calcium caseinates),
the first year of life. these products also have minimal effects on osmolality. Often,
2. Formulation characteristics feeding osmolality is influenced more by the administration of
a) These formulations are hypotonic, with osmolalities ranging hypertonic oral medication than by the increase in nutrient den-
from 230 to 250 mOsm per kg of water. sity. Best practice is to avoid mixing medications with enteral
b) Standard energy density is 22 kcal/fluid ounce (0.74 kcal/mL). formulations. Medications should be given separately as
c) Protein sources include nonfat milk and whey protein con- boluses. In general, increases in formula osmolality are well tol-
centrate. The protein content is approximately 2 g/100 mL erated if the concentration is advanced slowly and attention is
(2.7 g/100 kcal). paid to tolerance with each concentration change.
d) Carbohydrate sources include corn syrup solids and lactose. c) Infants, particularly newborns and preterm infants, have imma-
The lactose content is 40% to 60% of the total carbohydrate ture kidneys unable to concentrate urine when fluid intake is
content. The carbohydrate content is approximately 7.7 g/ limited. Renal solute load refers to the amount of solute present
100 mL (10.4 g/100 kcal). in the diet (protein, sodium, potassium, chloride, and phospho-
e) Fat sources include high oleic sunflower oil, soy oil, coconut rus) that must be excreted by the kidneys.68 Formulations with
oil, and MCTs. MCTs comprise approximately 20% to 25% of a higher renal solute load will potentially require increased
the total fat content. The fat content is approximately 4 g/100 mL water content for excretion of the solutes. Increasing the con-
(5.4 g/100 kcal). centration of the formulation and adding protein modulars will
f) The calcium and phosphorus content of preterm discharge for- increase renal solute load, while adding carbohydrate or fat
mulations is approximately 2.5 to 3 times the mineral content modulars will have minimal effect or may slightly decrease the
of term infant formulations. renal solute load. Other factors must be considered when
g) All preterm discharge formulations have added iron (1.3 mg/ evaluating the risk of increasing renal solute load. As infants
100 mL). mature, their ability to concentrate urine increases and renal
3. Clinical studies suggest that the use of nutrient-enriched formu- solute load becomes less of a problem. Rapidly growing infants
lations in preterm infants after discharge improves growth in will incorporate solutes into newly formed tissue and renal
weight, length, and head circumference.65,66 The benefit in weight solute will decrease. Increased insensible fluid losses from
was most pronounced in the first few months after discharge.66 fever or diarrhea and limited volume intake will increase the
The difference in height has persisted as long as 18 months.65 risk of dehydration, as less fluid is available for excretion of
D. Infant formulations with increased nutrient density renal solutes. Generally, infants will tolerate moderate advances
1. Infants with increased nutrient requirements or those requiring in renal solute load (ie, increasing formulation concentration to
fluid restriction may require increased nutrient density formula- 24 or 27 kcal/fluid ounce). Infants will also tolerate increases in
tions. Nutrient-dense formulations can be produced by concen- formulation concentration to 30 kcal/fluid ounce if fluid intake
trating formulas or by including modular nutrient additives of exceeds 100 mL/kg per day. It is important to carefully moni-
carbohydrate, protein, or fat. Before the nutrient density of for- tor hydration status in all infants receiving concentrated enteral
mulations is altered, several consequences of the formulation formulations.
change should be considered. d) Products made from powders or concentrated liquids, particu-
a) Maintaining nutrient balance. When increasing the nutrient larly in a home environment with questionable sanitation, may
density of formulations, it is important to keep in mind the put the infant at risk of receiving contaminated formulations.
actual nutrient requirements of the infant and the effect of Sanitation issues are compounded as more and more additives
changing formulation density on nutrient intakes. Fluid- are incorporated into the enteral formulation. Whenever pos-
restricted infants require formulations with an increased sible, recipes for preparing formulations at home should be
nutrient density of all nutrients. Energy, protein, minerals, simple and have a limited number of additives, to minimize the
electrolytes, and vitamins all need to be provided in smaller risk of preparation errors and microbial contamination.

72 A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. © 2005 A.S.P.E.N. www.nutritioncare.org.
 S E C T I O N I Fundamentals of Nutrition Support Practice and Management

2. Methods 3. Reducing contamination during preparation.

a) Increasing nutrient density by concentrating formulation a) When possible, formulations should be mixed, reconstituted,
(1) Formulations are concentrated by using smaller volumes and diluted in a centralized ___location (eg, enteral formulary
of water in formulation recipes. This method is easy to room or pharmacy). Mixing equipment must be cleaned
incorporate when formulations are available in a powder meticulously.
or concentrated liquid form. b) In most instances, formulations can be reconstituted and diluted
(2) In some instances (eg, preterm formulations), the products with tap water. However, in areas where the water supply is
are available in only a ready-to-feed form. To increase the of questionable quality or in severely immunocompromised
nutrient density of preterm formulations, term formulation patients, it may be prudent to use distilled or sterile water.
concentrated liquids or powders or preterm infant dis- c) Infant feedings require additional formulation preparation
charge formulation powders must be added to the ready- safeguards. Whenever possible, sterile ready-to-feed formu-
to-feed preterm formulation. Concentrated liquids are lations or concentrated liquid formulations should be used.
preferred over powders in preterm infant formulations, as Formulation powders should be weighed (not measured) and
concentrated liquids are sterile. Addition of a term formu- should be used only when no liquid forms are available.70 For-
lation to a preterm infant formulation will alter nutrient mulations should always be prepared with sterile water.70
composition and reduce, in particular, the protein and min- 4. Formulations should be stored according to manufacturers’ rec-
eral density. ommendations.
(3) Infants receiving breast milk who require formulations a) Expired or damaged formula containers should be discarded.70
with increased nutrient density are a particular challenge. b) Unopened ready-to-feed formulations should be stored in a
The nutrient density of term breast milk feedings may be cool, dark place. They should not be stored in direct sunlight
increased by adding term infant formulation powders or or near direct heat such as a radiator. Once opened, formula-
concentrated liquids. In preterm infants, term infant con- tions may be stored in a refrigerator for up to 48 hours.71
centrated liquids or preterm infant discharge formulation c) Reconstituted or diluted formulations be stored in a refriger-
powders may be added to fortified human milk to increase ator for a maximum of 24 hours.71
nutrient density above 24 kcal/fluid ounce. Concentrated d) Additional guidelines for infant formulation storage include
liquid are preferred over powders in preterm infant feed- the following:
ings because concentrated liquids are sterile. The addition (1) Prepared infant formulations should be chilled to 40°F
of extra packets of HMF is generally discouraged because within 1 hour of preparation.70
nutrient intakes of calcium and phosphorus increase sub- (2) Opened ready-to-feed containers and prepared infant for-
stantially and may cause hypercalcemia and hyperphos- mulations should be stored in a refrigerator and used within
phatemia. 24 hours.70
b) Increasing nutrient density by adding modular ingredients. (3) Human milk may be stored frozen in a home-style freezer
Adding fat, carbohydrate, or protein modulars to infant for- for 3 months. It may be stored in a deep freeze (−20°C or
mulations will alter the nutrient balance of the feeding regi- −4°F) for 12 months.70
men. When nutrient density is increased in this manner, careful (4) Fresh human milk may be stored in a refrigerator for
attention must be paid to the effect of these additives on intakes 48 hours. Thawed or fortified human milk should be
of other nutrients. stored and used within 24 hours.70
5. Reducing contamination during administration
a) Formulation hang time
VI. Reducing Contamination of Enteral Formulations (1) Canned, ready-to-use formulations generally can be hung
A. Complications related to contamination for 8 to 12 hours at room temperature, but manufacturers’
1. Some degree of microbial contamination of formulations is almost guidelines should be followed. In general, it is best to fill
inevitable during feedings. Contamination of enteral feedings may the reservoir using clean technique as infrequently as hang
cause GI colonization, septicemia, nosocomial pneumonia, and time restrictions allow.
diarrhea.69–75 Sources of contamination include formulation (2) Reconstituted powdered formulations generally can be
ingredients, mixing equipment, delivery systems, handling during hung for 4 to 6 hours at room temperature.
assembly of the administration system, unsanitary formula prepa- (3) Prefilled administration sets (bag/container) can generally
ration areas and patient care units, health care providers, family be hung for 2 to 48 hours, or according to the manufac-
members, and patients. Dangerous concentrations of organisms turers’ recommendations.74
result from heavy initial contamination or inappropriately long b) Administration set hang time
hang times of the formulation or administration set.69 Because (1) Refillable sets (bag/container and tubing) can be used in a
infants are more susceptible to infection, guidelines for prepa- short-term care setting for about 24 hours.74
ration, storage, and administration of infant feedings are more (2) It has been suggested that refillable administration sets
conservative than those for children and adults.70 (bags/containers and tubing) may be used for up to 72 hours
2. Hazard Analysis Critical Control Point (HACCP) is a systematic in long-term care facilities; no differences in adverse effects
approach to minimizing the potential for contamination. It is (eg, fever, pneumonia, diarrhea, vomiting) were noted
important to identify critical points where contamination of enteral between delivery sets used for 24 versus 72 hours. How-
formulations may occur to reduce the possibilities for microbial ever, no bacterial counts were performed. Thus, use of refill-
contamination and/or food-borne disease. HACCP also aids in pro- able delivery sets for longer than 24 hours in settings other
viding safe and accurate nutrition products as mandated by the than long-term care facilities requires further investigation.75
Joint Commission on Accreditation of Healthcare Organizations. c) Infant feeding delivery guidelines

© 2005 A.S.P.E.N. www.nutritioncare.org. A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. 73
S E C T I O N I Fundamentals of Nutrition Support Practice and Management

(1) Hang times for human milk and infant formulas should intensive care unit patients: results of a multicenter, prospective, random-
not exceed 4 hours.70 ized, clinical trial. Crit Care Med. 1995;23:436–449.
(2) Syringe tubing should be changed every 4 hours in infants 23. Heys SD, Walker LG, Smith I, Eremin O. Enteral nutritional supple-
receiving continuous infusion feedings.70 mentation with key nutrients in patients with critical illness and cancer:
a meta-analysis of randomized controlled clinical trials. Ann Surg.
1999;229:467–477.
(Enteral Formulations chapter from the 1st edition was contributed by 24. Beale RJ, Bryg DJ, Bihari DJ. Immunonutrition in the critically ill: a sys-
Kelley Olree, Joseph Vitello, Jacqueline Sullivan, and Carol Kohn- tematic review of clinical outcome. Crit Care Med. 1999;27:2799–2805.
Keeth) 25. Kudsk KA, Moore F, Martindale RT, et al. Consensus recommendations
from the U.S. Summit on Immune-Enhancing Enteral Therapy. J Parenter
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19. Sax HC. Effect of immune enhancing formulas (IEF) in general surgery 43. Talpers SS, Romberger DJ, Bunce SB, et al. Nutritionally associated
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 Linda Lord, NP, RN, MS, CNSN;
Michelle Harrington, MS, RD, CSP, CNSD, LDN
5
Enteral Nutrition
Implementation and
Management
Introduction pH and flora and inhibits opportunistic bacterial overgrowth in
the small bowel.
When the gastrointestinal (GI) tract is functional, enteral feeding is the
c) The presence of nutrients in the gut, especially complex pro-
preferred route for nutrition support. This type of feeding provides
teins and fats, supports the mucosa’s critical immunologic bar-
many physiologic, metabolic, safety, and cost benefits over parenteral
rier function by triggering feeding-dependent neuroendocrine
feedings.1 Tube feedings can range from providing adjunctive support
activity. Subsequently, this activity appears to stimulate the
to providing complete nutrition therapy. Enteral feedings can be admin-
manufacture of immunoglobulins in the gut, particularly secre-
istered and scheduled in a variety of ways. Practitioners who are famil-
iar with these options can recommend regimens that accommodate each tory immunoglobulin A, which is important for preventing bac-
patient’s needs and lifestyle. Selection of the optimal enteral regimen terial adherence and translocation.3
depends on a number of factors, such as the patient’s nutritional and 2. Safety benefits. Enteral feeding is generally considered safer than
clinical status, GI function, age, and level of activity. Practitioners need parenteral feeding, when administered cautiously and with ongo-
to be aware of these factors so that enteral feedings can be administered ing monitoring, and with the appropriate modifications made to
successfully and safely. A well-tolerated enteral regimen that meets the the regimen as needed.
patient’s needs can reduce the length of time that support is necessary 3. Cost benefits. Enteral feeding generally costs less than parenteral
and improve the disease treatment outcome; it can also assist in the feeding, including the costs for formula, equipment, administra-
growth and development of the pediatric patient.2 tion, and monitoring in both the hospital and outpatient settings.
B. Indications for enteral feeding4
I. Benefits, Indications, and Contraindications for Enteral Feedings 1. Inability to consume or absorb adequate nutrients. Enteral support
II. Implementation of Enteral Feedings is considered in patients who have demonstrated inability to meet
III. Monitoring and Management of Enteral Feedings nutritional needs by mouth and are assessed as being at high risk
IV. Complications and Management of Enteral Feedings for or as being malnourished. Enteral support is indicated when
V. Transitioning from Enteral Nutrition Support patients’ volitional intake is inadequate to meet two thirds to three
References quarters of their daily energy needs. The duration of acceptable
inadequate intake is based on several factors, such as a patient’s
age, nutritional status, expected illness and catabolic severity,
I. Benefits, Indications, and Contraindications for length of illness, and expected duration of poor nutrient intake or
Enteral Feedings
absorption. Adult patients who do not eat or receive nutrition sup-
A. Benefits of enteral feeding port for more than 10 to 14 days after hospital admission or after
1. Physiologic/metabolic benefits surgery have been reported to have worse clinical outcomes,
a) The gut can be used for the administration of complex nutrients longer hospitalizations, and higher costs of care.5–7 However, it is
(eg, intact protein, peptides, fiber) that cannot be given intra- often difficult to prospectively identify patients who will meet
venously. Nutrients absorbed through the GI tract via the por- these criteria. Therefore, it may be prudent to initiate the appropri-
tal vein enter the liver and are processed before they enter the ate modality of nutrition support in patients with inadequate oral
systemic circulation or are disposed of as waste products. Many intake for 7 to 14 days, or in those in whom inadequate oral intake
nutrients enter the systemic circulation intact. This mechanism is anticipated for more than 7 to 14 days.5
(first-pass metabolism) allows for more effective utilization of a) Children. Children possess lower energy substrate stores rela-
nutrients. tive to their rate of energy expenditure and therefore are at ear-
b) In addition to the systemic benefits, enteral feedings have local, lier risk for nutritional compromise than adults.8 The nutrition
trophic beneficial effects on the GI mucosa, maintaining its goals for the pediatric patient are to provide adequate nutrition
absorptive structures by nourishing the enterocytes directly to for growth, development, and the preservation of lean body
support epithelial cell repair and replication. Enteral nutrients mass.9 Extended periods of malnutrition during childhood can
provide a complex systemic stimulus that leads to gut protec- manifest in growth failure, as well as have adverse effects on
tion related to stress and corticosteroid use and reduces the risk cognitive and behavioral development.2,10
of inflammation, ulceration, and bleeding. Luminal nutrients, b) Additional criteria for consideration of enteral tube feeding in
such as glutamine and short-chain fatty acids, are used as fuel children who have a functioning GI tract include
by the cells of the small bowel and colon, respectively. The (1) no weight gain or weight loss for 3 consecutive months
presence of nutrients in the gut also helps maintain normal gut (2) weight for height less than the fifth percentile

76 A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. © 2005 A.S.P.E.N. www.nutritioncare.org.
 S E C T I O N I Fundamentals of Nutrition Support Practice and Management

(3) triceps skin fold measurement less than the fifth percentile 7. GI ischemia. Certain disease states or medical treatments can
for age reduce blood flow to the gut and cause GI ischemia. Examples
(4) total oral feeding time greater than 4 to 6 hours per day11 include critically ill patients with low cardiac output, sepsis, and
2. Functional or partially functional gut. Patients with a functional gut multiorgan failure. Even a relatively brief reduction in mesenteric
who are unable or not allowed to eat should receive enteral instead blood flow can cause rapid changes in the GI mucosa, reducing the
of parenteral feedings. Even patients with only a partially func- absorptive and barrier functions of the gut. Therefore, the benefits
tional gut can often tolerate some enteral feeding, but may require of enteral feeding may be less clear-cut in patients with cardio-
a combined regimen (ie, both parenteral and enteral nutrition) to pulmonary instability. However, enteral nutrition has been shown
meet total nutritional needs. to improve blood flow in the gut and to maintain the barrier effect
C. Possible contraindications to enteral feeding. Contraindications to of the intestine.12,13 The challenge with such patients is to determine
enteral feeding are usually relative or temporary rather than absolute. when the physiologic balance has shifted and enteral feedings will
Potential contraindications include clearly be beneficial rather than problematic. With chronic occlu-
1. Terminal illness. Before enteral nutrition support is initiated in sive or compression syndromes that limit enteric blood supply, a
patients who are terminally ill, the potential benefits should be potential risk for worsening ischemia and necrosis exists.
weighed against the risk of potential problems. Potential problems 8. Ileus. Paralytic ileus occurs quite frequently in acutely ill patients.
include aspiration, diarrhea, overhydration, discomfort, and inter- Common surgical causes include perforation, anastomotic leaks,
ference with personal dignity. intraperitoneal hemorrhage, peritonitis, and other intra-abdominal
2. Short bowel. Patients with a short bowel often require parenteral infections. Nonsurgical causes include ischemia, hypokalemia,
nutrition (PN) for 1 to 3 months after surgery while the remaining head or spine injury, uremia, adverse drug effects, thyroid defi-
bowel adapts to allow adequate nutrient absorption. Depending ciency, and severe, uncontrolled diabetes. Ileus affects the small
on the length of the remaining absorptive small bowel, some bowel to a lesser degree than the stomach and large bowel. Persis-
patients may require long-term PN or parenteral fluid, electrolyte, tent gastric ileus usually can be circumvented with small-bowel
and mineral replacement. feeding tube placement and gastric decompression.
3. Obstruction. Complete mechanical obstruction of the GI tract 9. GI inflammation. Inflammation or enteritis may have several
below the duodenum, or pseudo-obstruction that cannot be etiologies, including inflammatory bowel disease, radiation, or
resolved, is a contraindication to enteral feeding. Partial obstruc- chemotherapy. Bowel rest (with PN) has been prescribed in an
tion of the GI tract often can be circumvented but requires ongo- effort to achieve remission during acute Crohn’s disease flare-ups,
ing monitoring of GI status as well as recurrent evaluation of the but studies have failed to demonstrate any improvement in long-
most appropriate feeding site, formula, and equipment. term outcomes.14
4. GI bleeding. The etiology, severity, and ___location of acute GI bleed- 10. Pancreatitis. Bowel rest also is frequently prescribed for pancre-
ing, as well as the need for immediate GI evaluation and treatment, atitis; however, several studies have reported successful use of
are determinants of the feasibility of enteral feedings. Chronic, enteral nutrition support without exacerbation of pancreatitis.15,16
slow upper GI bleeding is not necessarily a contraindication to The degree of pancreatic stimulation is dependent on the ___location
enteral feedings but may be accompanied by anorexia and frequent of the feeding tube in the GI tract, as well as the composition of the
nausea or vomiting. Small-bowel feedings may be better tolerated enteral formula. Less stimulation occurs when the feedings are
than gastric feedings in these patients. delivered distally in the intestinal tract, and lower-fat formulations
5. Vomiting and diarrhea. Protracted vomiting and diarrhea are are tolerated best.17,18
not absolute contraindications to enteral feedings; however, the
cause(s) of either should be carefully assessed. Vomiting can make
it difficult to keep a nasally placed tube in position. Patients with
II. Implementation of Enteral Feedings
frequent episodes of nausea or vomiting may better tolerate small- The patient’s type of access, tolerance of feedings, absorptive capacity,
bowel feedings with gastric decompression or may benefit from volume requirements, amount of oral intake, and lifestyle are determi-
the use of prokinetic agents. Patients with diarrhea should be nants of the delivery method and duration of the daily tube feedings.19
assessed for the type of diarrhea (osmotic or secretory) and for pos- A. Delivery methods
sible causes other than the enteral feedings, such as Clostridium 1. Gravity controlled. This manually controlled method of infusing
difficile or oral medications (eg, sorbitol-containing medications; formula is used almost exclusively for gastric feedings. A specific
antibiotics; H2-receptor antagonists; antineoplastics; laxatives; volume of formulation is hung in a plastic feeding bag or rigid
antacids; prokinetic agents; potassium, magnesium, phosphorus plastic container with tubing on an intravenous (IV) pole above the
supplements). In cases of mild to moderate vomiting or diarrhea, insertion site of the feeding tube. The tubing is fitted with a roller
judicious waiting for symptomatic improvement is sometimes clamp, to control the infusion rate of the formulation, and a con-
warranted. Depending on the patient’s nutritional status and poten- nector, to permit attachment to the patient’s feeding tube. Feedings
tial for depletion, PN may be indicated until symptoms abate. may be provided over several minutes to hours depending on
6. Fistulas. When patients have fistulas, it is prudent to choose a patient tolerance. A drawback to this method is that the formula
feeding site away from the fistula to optimize nutrient absorption infusion rate can fluctuate during the feeding as a result of positional
and minimize losses. Patients with fistulas in the more proximal changes or increases in gastric pressure.20 Gravity-controlled feed-
or more distal gut are easier to feed enterally, and those with low ings are indicated only for neurologically intact patients who can
to moderate fistula output are usually amenable to enteral feed- reliably protect their airways. Most often this method is used with
ing. High-output midgut (jejunal) fistulas are more problematic. ambulatory patients (ie, in-home care or long-term care facilities).
Patients with fistulas require careful monitoring to ensure that a) Continuous gravity feedings. These feedings are provided over
nutrient, electrolyte, and fluid needs are met and that the feedings 24 hours and can be accomplished with the use of high-quality
are not exacerbating the problem. gravity-feeding equipment and a roller clamp to control the

© 2005 A.S.P.E.N. www.nutritioncare.org. A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. 77
S E C T I O N I Fundamentals of Nutrition Support Practice and Management

infusion rate. This method may result in occasional incidents of B. Initiation of enteral feedings. Currently, it is recommended that feed-
unintentionally rapid infusion rates or interruptions. Poor- ings in adults and children be initiated with full-strength formula at
quality tubing or clamps make controlling the rate very diffi- a slow rate and steadily advanced. This approach allows goal rates
cult, and the patient may inadvertently receive a bolus feeding. to be achieved earlier and reduces the risk of microbial contamina-
b) Intermittent gravity feedings. Intermittent feedings are gener- tion by minimizing the number of times the formula is manipulated.
ally well tolerated if a maximum of 200 to 300 mL is adminis- Experience has shown these regimens to be well tolerated, partially
tered over 30 to 60 minutes every 4 to 6 hours.21 A prescription because of the widespread use of pumps for controlling infusion
for an intermittent gravity feeding might read as follows: rates. Protocols for introducing tube feedings vary and should be
provide 240 mL of formula every 4 hours; infuse over 1 hour; individualized to fit the needs of the patient as well as the realities of
precede and follow with a 30-mL flush of tap water. the care environment.
c) Bolus feedings. Bolus feedings are the infusion of a predeter- During feeding advancement, only one change should be made at
mined volume of formula at specified intervals by gravity or by a time to allow for tolerance assessment. If poor tolerance of the
syringe over a short period. The rate of infusion is controlled by enteral regimen is demonstrated, either the formula volume or the
either regulating the roller clamp or adjusting the syringe pres- concentration should be decreased. It is important to allow adequate
sure. Feedings are generally accomplished over several minutes time for the patient to tolerate the modified regimen before further
but may be best tolerated when provided at less than 60 mL/ advances are attempted. Occasionally it becomes necessary to
minute. In some settings, a large piston syringe (usually 50 mL change the formula to achieve improved feeding tolerance. After the
or larger) is used to draw up and administer formula directly patient is receiving and tolerating the goal regimen, modifications to
into the patient’s feeding tube. When a syringe is used, the infu- the feeding schedule may be attempted to accommodate the patient’s
sion rate can be gravity-controlled by either raising or lowering and family’s lifestyle.22
the syringe (plunger absent) or by slowly pushing the plunger 1. Bolus feedings and gravity-controlled feedings
inward. Rapid infusion of formula may cause discomfort, lead- a) Adults. Usually only gastric feedings are well tolerated when
ing to the misconception that the formula instead of the admin- provided as a bolus or gravity feeding. The feedings are usually
istration method is not being tolerated. A feeding prescription initiated with full-strength formula 3 to 8 times per day, with
might read as follows: provide 240 mL of formula every 3 hours increases of 60 to 120 mL every 8 to 12 hours as tolerated up to
over at least 4 minutes; precede and follow with a 30-mL flush the goal volume. Formula (ie, elemental, hypertonic, poly-
of tap water. Bolus feedings are the easiest, least expensive meric, or isotonic) does not require dilution unless additional
delivery method and are more physiologic because they mimic water is necessary to meet fluid requirements. Careful moni-
normal feedings. The patient reaps the additional benefit of toring of gastric residual volumes and GI tolerance may help to
freedom of movement and breaks from feeding. Disadvantages facilitate increases in formula intake to the goal volume. Some
include increased risk of aspiration, volume intolerance, vom- patients may require bolus feedings to be delivered by gravity
iting, or delayed gastric emptying.11 over 15 to 20 minutes or in smaller volumes more frequently.
2. Pump assisted. Continuous pump feedings are indicated when b) Children. Bolus feedings may be started with 25% of the goal
there is a high risk for aspiration, with volume sensitivity, with volume divided into the desired number of daily feedings. For-
small-bowel feedings, sometimes with delayed gastric motility, mula volume may be increased by 25% per day as tolerated,
and in sicker or hospitalized patients. Continuous feedings allow divided equally between feedings.22
for maximal nutrient absorption and improved tolerance.11 Pump- 2. Pump-assisted feedings. A pump is usually required for small-
assisted feedings help to prevent GI complications associated with bowel feedings and is preferred for gastric feedings in critically
rapid infusion, such as nausea, cramping, and diarrhea. Pumps are ill patients, as the slower infusion rate of continuous feedings
also more appropriate in patients who have tenuous fluid balance; often enhances tolerance. Conservative initiation and advance-
if programmed correctly, they can help to prevent fluid overload. ment rates are recommended for patients who are critically ill,
Usual equipment includes a disposable pump set (container and have not been fed enterally for some time, or require hydrolyzed
tubing with drip chamber and connector) and the pump itself. Con- or high-osmolality formula.
trolled infusion is accomplished by threading the tubing through a) Adults. Formulas are initiated at full strength at 10 to 40 mL/
the pump’s electronic sensors and cassette or pumping mechanism. hour and advanced to the goal rate in increments of 10 to
Portable “backpack”-style pumps are available for patients who 20 mL/hour every 8 to 12 hours as tolerated. This approach
require feedings while participating in their normal daily activities. can usually be used with isotonic as well as high-osmolality
a) Continuous pump feedings are delivered via a stationary or or elemental products.
ambulatory pump at a prescribed rate without interruption.19 b) Children. A full-strength, isotonic formula can be started at 1 to
b) Cyclic feedings are generally administered over 8 to 20 hours 2 mL/kg/hour and advanced by 0.5 to 1 mL/kg/hour every 6 to
per day, depending on the patient’s volume tolerance. This 24 hours until the goal volume is achieved. Preterm, critically
cycle allows for freedom from the feeding equipment for at ill, or malnourished children who have not been fed enterally
least a few hours each day. Transitioning from continuous to for an extended period may require a lower initial volume of
cyclic feedings typically is attempted as the patient recovers 0.5 to 1 mL/kg/hour.23
mobility and independence. Feedings may be provided at night
(nocturnal feedings) in an effort to allow patients to experience
III. Monitoring and Management of Enteral Feedings
hunger and gradually increase their oral intake during the day.22
c) Intermittent pump feedings are used to deliver predetermined A. Assessment of GI tolerance
volumes more accurately over a specified period. This accu- 1. Abdominal discomfort. Subjective signs of tube-feeding intoler-
racy is helpful in managing patients that are at risk for aspira- ance include feelings of abdominal fullness, cramping, and pain.
tion resulting from a rapid infusion rate. Possible etiologies of GI discomfort that result from the provi-

78 A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. © 2005 A.S.P.E.N. www.nutritioncare.org.
 S E C T I O N I Fundamentals of Nutrition Support Practice and Management

sion of tube feedings include rapid administration of feeding, tial complications, the volume of fluid remaining in the stomach
hyperosmolar solutions, medications, excess air in the stomach during feeding (the residual volume) is measured to monitor the
or intestines, tube migration from stomach to small intestine, safety of advancing or continuing enteral feeds.24,25 Gastric
infection, cold formula, bacterial contamination, and fat or lactose motility is affected by disease, mechanical obstruction, and cer-
intolerance.11 tain medications.26
a) If GI symptoms are attributable to hyperosmolar solutions, One episode of high residual volume should not automatically
decrease the concentration of the formula and consider adding prompt cessation of feedings in the absence of physical exami-
glucose polymers or fat to increase calories as needed. nation or radiographic abnormalities; rather, signs and symptoms
b) If GI symptoms are thought to be caused by medications that of intolerance should be monitored carefully.24–27 Patients with
are administered through the feeding tube, determine whether frequently elevated gastric residual volumes may benefit from
it is feasible to dilute the medication, change the form of the feeding tube placement beyond the ligament of Treitz.26
medication (ie, change to parenteral), or change to a different a) Frequency of checking residuals. Gastric emptying of enteral
medication. feedings can be assessed by checking residuals prior to each
c) If GI symptoms are due to fat intolerance, consider using a for- intermittent feed or every 4 hours with continuous feeds.11
mula that contains a higher proportion of fat from medium- b) Method for obtaining residuals. Residuals are obtained by
chain triglycerides. aspirating through the feeding tube with a syringe and mea-
d) Intolerance can also be attributed to delayed gastric emptying, suring the formula and fluid withdrawn. The aspirating syringe
motility disorders of the small and large intestine, intestinal needs to be fairly large, generally at least 50 mL for small-bore
spasms or ischemia, and fiber-containing formulas. (12F or less) feeding tubes and at least 30 mL for gastrostomy
2. Nausea and vomiting. Nausea and vomiting may be caused by gas- tubes. Smaller syringes exert a higher pressure per square inch
tric irritation or atony, rapid administration of the tube-feeding for- and may cause the tube to collapse. If unable to aspirate, inject
mula, medications, feeding tube migration from the intestine to the 3 to 5 mL of air or water into the feeding tube and reattempt.
stomach, distal obstruction, anxiety, and other disease states. Nau- Residuals contain formula, digestive juices, and electrolytes
sea and vomiting may also indicate feeding tube migration, such and therefore should be reinstilled through the feeding tube
as a balloon gastrostomy causing a gastric outlet obstruction. (unless there is a large amount).
3. Abdominal distension. Abdominal circumference can be meas- c) Parameters for holding feedings. Isolated episodes of high gas-
ured daily at the level of the iliac crest to monitor changes in tric residuals are not always associated with abdominal symp-
abdominal distension. Holding enteral feedings may be indicated toms. The amount of gastric residuals obtained depends on the
if the circumference exceeds the baseline measurement by 8 to amount and timing of the last feeding, medications, and the
10 centimeters. ___location of the feeding tube tip. The patient’s activity and posi-
4. Bowel sounds. The absence or presence of bowel sounds is not tioning may also affect the gastric emptying rate.11 The resid-
always a good indicator of bowel function. Fluid and air must be ual may be clear, indicating the presence of gastric juices, or
present in the GI tract for bowel sounds to be heard. For example, may contain partially digested formula.
in patients with nasogastric tubes for decompression and suction, (1) Adults. When a residual reaches ≥200 mL with a naso-
bowel sounds may not be heard despite good bowel function. gastric tube or ≥100 mL with a gastrostomy tube, associ-
Conversely, “bowel sounds” may be heard if the suction is not ated signs or symptoms of intolerance should be assessed.25
turned off prior to auscultation. (2) Infants and children. Slowing or stopping feedings in
5. Stool pattern. Stool volume, frequency, consistency, and color infants and children has been recommended if residual vol-
should be noted for any patient receiving enteral tube feedings. ume exceeds twice the hourly infusion volume during con-
The patient’s baseline or normal bowel pattern should be noted tinuous feedings or exceeds 50% of the infusion volume
and used as a basis for comparison. during bolus feedings.28
a) Diarrhea. Strategies to prevent and manage diarrhea include d) It is believed that aspiration from a gastrostomy tube is less
avoiding the provision of antibiotics or medications that cause likely to yield gastric residuals because of the tube’s posi-
diarrhea whenever medically feasible, decreasing the osmolal- tioning in the anterior portion of the stomach, compared with
ity of hypertonic formulas, decreasing the tube-feeding infusion a nasogastric tube. Therefore, high residuals from a gastros-
rate, altering the fat source and content when indicated, and tomy tube are more worrisome. If abdominal discomfort or
increasing fluid replacement. distension is present, feedings should be held. Further workup
b) Constipation. Possible dietary causes of constipation include with roentgenograms may be indicated. If the abdominal
inadequate fiber intake, inadequate fluid intake, or medications exam is benign, feedings should be delayed for at least 1 hour
that slow peristalsis. Strategies to prevent or manage constipa- and residuals rechecked. If high residuals persist without
tion include using fiber-containing formulas, monitoring that associated clinical signs and symptoms, a promotility agent
free water intake is adequate, supplementing with prune juice, (eg, erythromycin, metoclopramide) may be tried. Another
and identifying medications that may be causing constipation option is to insert a transpyloric feeding tube and perform gas-
(eg, narcotics) and finding appropriate substitutions when tric decompression as necessary. Residuals cannot always be
possible.11 aspirated from jejunal or duodenal tubes.11 Intolerance of
B. Aspiration precautions small-bowel feedings can be identified when a patient expe-
1. Tube-feeding residuals. Gastric residuals are frequently used to riences abdominal distention, discomfort, and/or diarrhea.
monitor the safety and gastric emptying of tube feedings. When If a patient develops feeding intolerance with small-bowel
gastric emptying is delayed or gastric secretion is excessive, fluid feedings, the previously tolerated formula strength or vol-
accumulates in the stomach and may result in vomiting, aspira- ume should be reinstituted and feeds gradually advanced as
tion, abdominal distention, or cramping. To prevent these poten- tolerated.9

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S E C T I O N I Fundamentals of Nutrition Support Practice and Management

2. Head-of-bed elevation. The effect of head elevation in patients fed a) Physical assessment. Possible clinical signs and symptoms of
through small-bore tubes or enterostomies has not been deter- overhydration include edema, high urine output, dilute urine
mined; however, the semirecumbent position (≥30° elevation) specific gravity, hypertension, respiratory insufficiency, con-
has been recommended for all tube-fed patients to minimize the gestive heart failure, and rapid weight gain. Possible signs
potentially life-threatening consequences of aspiration.29,30 Aspi- of dehydration include decreased urine output or number of
ration of pharyngeal and gastric secretions can still occur in some wet diapers in infants; concentrated, strong-smelling urine;
patients (even those not fed), and large-bore tubes may disrupt the elevated urine specific gravity; dry lips and mucous mem-
function of the lower esophageal sphincter (LES), increasing the branes; poor skin turgor; sunken eyes (and fontanelle in infants);
risk of aspiration. flat neck veins; lethargy; hypotension; tachycardia; elevated
C. Aspiration detection blood urea nitrogen (BUN) level; constipation; and rapid
1. Clinical signs and symptoms. When a significant amount of enteral weight loss.34
formula is aspirated, sudden onset of dyspnea, tachypnea, wheez- b) Intake and output. In the euvolemic patient, fluid intake should
ing, rales, tachycardia, cyanosis, decreased oxygenation, anxiety, approximately equal output. Fluid can be provided orally, with
and agitation can occur. Smaller amounts of formula may be aspi- enteral feedings, or intravenously. Fluid output occurs prima-
rated over time with no apparent clinical symptoms. A subsequent rily through the kidneys and, to a lesser extent, through the skin
fever can signal the development of aspiration pneumonia. and lungs and in the feces. Insensible fluid loss in afebrile
2. Roentgenogram findings are nonspecific and lack sensitivity adult patients with intact skin approximates 10 mL/kg/day.
for the detection of aspiration. There are many causes of pul- Approximately 40 mL/100 kcal per 24 hours replaces insen-
monary infiltrates, including pneumonia, contusion, atelectasis, sible losses in pediatric patients.35 Fluid needs increase with
and hemorrhage. The appearance of new infiltrates in dependent warmer weather, diarrhea, fever, vomiting, high nasogastric
lung fields in a patient lacking other causes of infiltrates suggests drainage, excessive diaphoresis, polyuria, open wounds, fistula/
aspiration. ostomy losses, and thermal injuries. These losses should be
3. Use of coloring agents. Blue dye has been used to tint tube-feeding appropriately replaced with fluid and electrolytes. For each
formulas as a method for determining the presence of formula degree of body temperature above 38°C, insensible fluid loss is
in tracheal aspirates. It was thought that this method would help increased by 5 mL/kg per 24 hours. Diarrhea output should be
detect pulmonary aspiration in tube-fed patients. The sensitiv- monitored and replaced milliliter for milliliter.35,36 In addition,
ity, specificity, and safety of this method have not been ade- liters of fluid can leak from the vascular compartment into the
quately evaluated. The percentage of patients who will develop interstitial spaces in patients with vasodilatation or low serum
clinically significant aspiration whether or not coloring is detected oncotic pressure. In these conditions, fluid intake needs to be
has not been determined. Most important, a Food and Drug increased to compensate for the losses or fluid shifts and to
Administration Public Health Advisory issued September 29, maintain adequate intravascular volume. The clinician should
2003, reported blue discoloration and death in patients receiv- also account for any factors or conditions that may result in
ing tube feedings containing FD&C Blue No. 1 dye.31 Blue dis- fluid retention and could necessitate fluid restriction. Fluid
coloration of the skin, urine, feces, and serum has been reported restriction may be indicated in certain disease states, such as
in patients receiving this dye in their tube feedings, and in some cardiac, liver, pulmonary, and renal dysfunction. Electrolyte
the dye has been associated with refractory hypotension, meta- disturbances and medications can also alter fluid needs.
bolic acidosis, and death. Case reports reveal that critically ill c) Weight changes. Fluid changes can be determined by daily
patients, especially those who have increased intestinal perme- changes in body weight. One kilogram of weight change is
ability, are at risk for these complications. Based on these equivalent to 1 L of fluid.
reports, patients with sepsis, severe burns, trauma, shock, surgi- 2. Determining fluid requirements. Calculate water needs.
cal interventions, renal failure, celiac sprue, and inflammatory a) Adults. There are several ways to calculate normal free water
bowel disease may be at risk for systemic toxicity of blue dye requirements for enterally fed, afebrile adults.37 Either of the
absorption from enteral tube feedings. Other disadvantages of following methods is intended to replace urine and insensible
this method include the false elevation of gastric pH, positive fluid losses: provide 1 mL of water per calorie fed, or provide
Hemoccult stool tests, formula manipulation, and the potential 30 to 35 mL of water per kilogram of body weight per day.
to induce an allergic response. Blue food colorings or methyl- b) Children. See Chapter 2 on nutrient requirements.
ene blue may still be used when checking for fistulas (ie, tracheal- 3. Providing extra fluids. Fluids can be given orally, intravenously,
esophageal fistula) in hemodynamically stable patients, if with medications, with the enteral tube feeding, and as tube-
provided in unit-of-use containers (ie, an ampule of methylene feeding flushes. Additional water requirements can be provided
blue) to minimize contamination risk. as tube flushes or intravenously. Calculate how much extra fluid
4. Tracheal glucose measurements. It has been reported that aspira- a patient needs as follows:
tion of tube-feeding formulas may be determined by a positive- a) Determine how much fluid is being taken in orally and assess
glucose result in the tracheal aspirate,32 but the sensitivity and the patient’s ability to consistently ingest that amount.
specificity of this method have not been adequately tested. High b) Determine the volume of fluids being given intravenously.
tracheal concentrations of glucose have been found in intubated c) Determine the water content of the tube-feeding product being
patients, both fed and not fed, and often are not associated with delivered. Most infant and pediatric enteral formulas contain
clinical evidence of aspiration. High tracheal concentrations of approximately 85% to 90% free water (850 to 900 mL per L of
glucose also may be found in diabetic patients with high serum formula), while most adult formulas contain 80% to 85% water
concentrations of glucose.33 (800 to 850 mL per L of formula). Calorically dense or con-
D. Hydration status centrated formulas may contain as little as 60% water (600 mL
1. Assessing hydration status per L of formula).38

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 S E C T I O N I Fundamentals of Nutrition Support Practice and Management

d) Determine the amount of water being provided with flushes and mittent feeding or medication.43 Medications should be admin-
medications that are being administered via the feeding tube. istered separately, and 5 to 10 mL of water should be provided
e) Subtract the patient’s fluid intake (total of steps a–d) from the between each one. Gastric acids coagulate most intact protein
daily amount required and provide the remainder throughout formulations, so it is recommended that a feeding tube be
the day as water flushes via the enteral feeding tube. Note that flushed with 30 mL of warm tap water before and after check-
if IV fluids are discontinued, water intake by the feeding tube ing for feeding residuals.44 It is important to subtract the amount
may need to be increased. of water flushed from the obtained residual volume.
f ) Assess the patient’s body weight, presence of edema, BUN, b) Children. Most pediatric tubes are not routinely flushed with
serum sodium, adequacy of intravascular volume, and urine water to prevent clogging unless recurrent problems occur. It
output. is important to consider the size of the child when providing
E. Assessment of nutrient intake flushes. Infants’ feeding tubes should be flushed with only 3 to
1. Assess actual nutrient intake. Calculate the macronutrients and 5 mL of water before and after medication administration,
energy being provided from the patient’s oral intake, tube feedings, because they may not tolerate large amounts of calorie-free
and dextrose-containing IV fluids. Often patients do not receive fluid. Older toddlers are also provided small volumes of
their full enteral nutrition prescriptions for various reasons, such flushes following medication administration in an effort to pre-
as the scheduled administration of medications, tests or proce- vent fluid excess.22
dures, or daily therapies. 2. Choice of irrigant. No irrigant has been shown to be more effec-
2. It is important for ongoing assessment of actual intake to deter- tive than water in preventing tube clogging. Water and carbon-
mine whether changes in the nutrition support regimen are indi- ated beverages were shown to be equally effective in preventing
cated to provide the daily prescribed volume of formulation more tube clogging, and both were superior to cranberry juice. The
accurately and consistently. lower pH of cranberry juice can cause clogging by precipitating
F. Oral stimulation for children certain proteins.45
1. Infants and young children who have received exclusive enteral J. The underlying medical condition(s) should be reassessed on an
tube feedings or PN for extended periods may experience diffi- ongoing basis to evaluate the feasibility of transitional feeding and
culties when oral foods are introduced.39 Early and frequent oral initiating or increasing oral intake.
stimulation is necessary in such patients to minimize the poten-
tial for developing oral feeding difficulties and aversions.
IV. Complications and Management of
2. Solid food feedings should be used particularly in infants in the
Enteral Feedings46–58
first year of life at developmentally appropriate ages. Even though
the nutrients may not be bioavailable, if these behaviors are not A. Mechanical complications and management
initiated and learned at this time, problems such as aversive behav- 1. Complications during placement of feeding tube (see Chapter
iors toward eating are likely to manifest when the child is physi- 3).57,59 Proper assessment of feeding-tube placement can prevent
ologically able to eat by mouth.40 feedings from being delivered to the wrong site. Techniques for
3. If oral intake of fluids or solids is not medically feasible, non- determining feeding-tube position include roentgenogram, tube-
nutritive sucking (sucking on a pacifier while being tube-fed) feeding aspiration (with assessment of pH, bile, volume of aspi-
should be encouraged in infants. rate), use of special feeding tubes that measure pH or motility,
G. Body weight auscultation, and laryngoscopy.
1. Ideal conditions. If possible, patients should be weighed in the a) Upper airway injury during placement of feeding tubes may
morning—before eating, drinking, or the infusion of the tube- result in lacerations or bleeding of the nasal or oral cavity (espe-
feeding formula but after voiding—using the same scale, and with cially in patients with coagulopathy or thrombocytopenia).
minimal clothing. b) Lower airway injury during placement of feeding tubes may
2. Frequency. Patients should be weighed once or twice per week. result in perforation of the trachea or pulmonary parenchyma
More frequent measurements are useful in critically ill patients, in (pneumothorax).57,59 Pulmonary placement of feeding tubes is
patients whose fluid status is unstable, or in infants and growing more likely in obtunded patients, in patients with impaired pha-
children. ryngeal sensation (impaired cough or gag reflex), and with the
H. Biochemical and hematological indices. The use of laboratory values use of small-bore feeding tubes.
as monitoring parameters during enteral nutrition support is individ- c) GI tract injuries during feeding tube insertion include perfo-
ualized, and the frequency depends on the severity of the underlying ration (peritonitis) or laceration with GI bleeding. Other GI
medical condition, degree of malnutrition, level of metabolic stress, complications include intraperitoneal placement of the feeding
and presence of nutrient and electrolyte deficiencies.41 Typically, lab- tube and pneumoperitoneum.
oratory monitoring is indicated less frequently in patients receiving d) Abdominal infection and abscess formation. Contamination
enteral nutrition than PN because of the ability of the GI tract to reg- of the peritoneum with resultant infection can occur from per-
ulate the absorption of electrolytes and minerals. However, baseline foration of the GI tract or leakage following percutaneous or
metabolic and nutrition assessment parameters should be obtained surgical tube placement.
(see Chapter 1).42 Follow-up laboratory work is then obtained based e) Respiratory compromise may occur during feeding tube place-
on the patient’s clinical status. ment as a result of interference with oxygenation or aspiration
I. Maintaining feeding tube patency of secretions.
1. Method to irrigate the tube f ) Increased intracranial pressure and aggravation of brain
a) Adults. To keep tubes patent, feeding ports should be flushed ischemia may occur during tube placement in patients with
with warm water (at least 20–30 mL for adults) every 4 hours intracranial lesions or bleeding.
for continuous feedings as well as before and after each inter- 2. Complications from the presence of a feeding tube56

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S E C T I O N I Fundamentals of Nutrition Support Practice and Management

a) Upper airway complications. Nasopharyngeal erosions and 4. Declogging methods. Feeding tubes are more successfully de-
necrosis, sinusitis, otitis media, loosening and evulsion of teeth, clogged when intervention is initiated immediately after the
bacteremia (especially in immunocompromised patients and obstruction is noted and if the obstruction is close to the proximal
patients with poor oral or dental hygiene), and interference with tube opening.71,72
dental hygiene (oral tubes). Many of these complications are a) Irrigants. Warm water initially should be used as an irrigant.
more common with the use of larger, stiffer tubes and can be If ineffective, enzyme treatments can be initiated.73 Papain
minimized by the use of small-bore feeding tubes and meticu- (meat tenderizer) and carbonated beverages showed no sig-
lous nursing care. nificant advantage over distilled water in dissolving coagu-
b) Lower airway complications.60 Feeding into the trachea or lated formula. However, a solution of digestive enzymes
lung with resultant pneumonia, respiratory distress, acute res- (pancrelipase) mixed with sodium bicarbonate (to activate the
piratory failure, empyema, and adult respiratory distress syn- enzyme) has been shown to be fairly effective in dissolving
drome. Proper assessment of tube ___location can prevent these formula occlusions.73–75
complications. (1) With a 30- to 50-mL syringe, aspirate as much liquid as
c) GI injuries. Esophagus: erosions, aggravation of variceal bleed- possible from the feeding tube so that the declogging solu-
ing (rarely occurs with soft, small-bore feeding tubes). Stom- tion can come in contact with the obstruction.
ach: erosions, ulcer bleeding, and gastric outlet obstruction. (2) Instill 5 mL of warm water with a 30- to 50-mL syringe
Small intestine: erosions, ulcer bleeding, obstruction, and under manual pressure for 1 minute and use a back-
volvulus. Other: buried bumper syndrome (ie, percutaneous and-forth motion with the plunger to help dislodge the
endoscopic gastrostomy placement), misplaced fasteners, occlusion.
necrotizing fascitis, wound infection, cellulitis, stomal leakage, (3) Clamp the tube for 5 to 15 minutes.
hematoma, tube dislodgment, extrusion or migration of feeding (4) Try to aspirate or flush with warm water.
tubes, subcutaneous emphysema, and enterocutaneous fistulas (5) If the tube remains clogged, prepare a pancrelipase solu-
(eg, from percutaneous or surgical tube placement). tion buffered with a sodium bicarbonate tablet (eg, 1
3. Tube clogging. Tube clogging is caused by viscous formulas, inap- crushed pancrelipase tablet or 1⁄4 teaspoon of pancrelipase
propriate medication administration, formula residue, and inade- powder + 1 non-enteric-coated sodium bicarbonate [324
quate flushing.26 mg] tablet) or 1⁄8 tsp of baking soda dissolved in 5 mL of
a) Tube clogging is more likely with intact protein products and warm water. Follow steps 1 to 4 with the pancrelipase solu-
viscous formulas (calorically dense and fiber-containing prod- tion instead of water, and repeat once if necessary. When
ucts).44,61,62 Clogging may also be caused by product microbial declogging feeding tubes, be certain the tube tip is not inad-
contamination that leads to formula coagulation63 or by the vertently positioned in the lung because enzymes or water
aspiration of residuals (gastric fluid coming in contact with for- can severely damage the pulmonary tissue.
mulation in the feeding tube).64 To prevent tube clogging, the b) Mechanical methods. Insertion of the following instruments
tubing should be flushed before and after each intermittent into the feeding tube is generally used as a final attempt to
feeding and every 4 to 6 hours with continuous feeds.65 Other declog the tube and should be performed by experienced
strategies to prevent clogging include flushing the tube after practitioners only. In each case, the instrument used needs to
aspirating for residuals, using an infusion pump to infuse vis- be premeasured so it does not exceed feeding-tube length.
cous formulations, responding to an occlusion alarm on a pump Feeding-tube stylets should not be used to clear an obstruc-
as soon as possible, and using clean technique when adminis- tion, because they may cause tube perforation and trauma to
tering enteral feedings to minimize contamination. the GI mucosa.74
b) Clogging caused by medications. Inadequately crushed tablets, (1) Small-diameter catheter. Introduce a small-diameter cathe-
medications administered together (causing precipitation), ter into the clogged feeding tube. Instill declogging solution
interaction with formulation, or inadequate tube flushing can in close proximity to the obstruction.71,73 After feeding-tube
cause clogging. Clogging can be prevented by flushing feeding length is verified, mark the catheter appropriately and insert
tubes with water (about 30 mL) before administering medica- it into the feeding tube up to the point of obstruction. Ini-
tion, as well as between each medication (at least 5 mL), and tially, warm water is infused through the catheter and a
after the administration of all medications is complete (about back-and-forth motion is used to dislodge and dissolve the
30 mL).66 Avoid mixing a drug with any enteral formulation occlusion. If this method fails, the pancrelipase solution
unless it has been shown to be compatible. Provide liquid forms technique (see above) can be used.
of medications whenever possible and use elixirs or suspen- (2) Endoscopy/cytology brushes.61—Insert an endoscopy/
sions rather than syrups (which have a lower pH and can easily cytology brush through the tube lumen to break up an
clump tube-feeding products).67 Solid dosage forms, such as obstruction. The feeding tube is then flushed with water.
simple compressed tablets, should be crushed into a fine pow- (3) Declogger devices. These devices are made of plastic and
der and diluted with enough water to dissolve the powder. come in various lengths and diameters, which conform to
Enteric-coated or sustained-release tablets should not be various feeding-tube lengths and diameters. The threaded
crushed. Bulk-forming agents should be avoided because they end of the device is inserted into the feeding tube with a
congeal rapidly when mixed with water and can clog the twisting motion. After the clog is penetrated, the device is
tube.43,68,69 (See Chapter 9 for further discussion of medication moved in a back-and-forth motion to dislodge the clog. This
administration via enteral feeding tubes.) is followed by a water flush.
c) Clogging attributable to feeding-tube characteristics. Less 5. Aspiration is a potentially lethal complication of enteral feed-
clogging occurs with polyurethane tubes than with silicone ing.50,76,77 Clinically significant aspiration pneumonia is esti-
tubes.65,69,70 mated to occur in 5% of gastric-fed patients. It can result in

82 A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. © 2005 A.S.P.E.N. www.nutritioncare.org.
 S E C T I O N I Fundamentals of Nutrition Support Practice and Management

cough, bronchospasm, pulmonary edema, pneumonia, empyema, rhea in tube-fed patients.81–87 Antibiotics, H2-receptor antagonists,
and respiratory failure. antineoplastics, laxatives, antacids, and potassium and phosphate
a) Risk factors include decreased level of consciousness, dimin- supplements are medications that commonly contribute to the
ished cough or gag reflex, neurologic injury, incompetent LES, development of diarrhea. The cause of diarrhea is often multi-
gastroesophageal reflux, supine position, use of large-bore factorial (Table 5-1). The best treatment for diarrhea remains
feeding tubes, large gastric residuals, and gastroparesis. Most unclear. It is rarely necessary to stop enteral feedings; diarrhea usu-
aspiration is of oral-pharyngeal secretions, not gastric contents. ally subsides as the cause is eliminated (eg, infection, drug, toxin,
b) Aspiration of gastric contents may be prevented by providing fecal impaction). However, in infants, increases in stool volumes
smaller, more frequent feedings in patients receiving inter- of greater than 20 mL/kg per day are often an indication for less
mittent tube feedings; using small-bowel feeding tubes (and aggressive enteral feeding advancement.40 Whenever possible, the
gastric decompression); using promotility agents; periodically offending medication(s) should be discontinued. It is important to
assessing gastric residuals; and keeping the head of the bed rule out infection or the presence of enteric pathogens such as
elevated (≥30°). C difficile before using antimotility agents, because increased
6. Miscellaneous. Other mechanical complications are tube knot- bowel motility is one mechanism for eliminating infecting organ-
ting; perforation of the feeding tube with the guidewire (which isms and toxins from the GI tract. Antimotility agents may enhance
also could perforate the bowel); inability to remove the guidewire bacterial growth and toxin absorption. Agents used include
because of knotting, kinking, or poor lubrication; tube deteriora- adsorbents (eg, kaolin, pectin) and antimotility agents (eg, lop-
tion; dislodgment; and migration. eramide, diphenoxylate/atropine, paregoric, tincture of opium).
B. GI complications Pancreatic enzymes may be useful in patients with pancreatic
1. Gastroparesis is not a complication of feeding but may be pres- insufficiency. If diarrhea persists despite treatment of enteric
ent in patients who require enteral feeding. It predisposes the pathogens or disease-related causes, antidiarrheal therapy, and
patient to gastroesophageal reflux and aspiration. Gastroparesis medication adjustments, the enteral formulation should be evalu-
results from altered gut neurologic or muscular function (eg, neu- ated. The addition of fiber to the enteral formulation may help bulk
ropathy in patients with diabetes mellitus) and release of media- up the stool and promote more normal bowel function. Peptide-
tors that inhibit gastric emptying (eg, during critical illness). based and elemental enteral formulas have been associated with
Consistently high gastric residuals may be an indicator of gastro- improved GI tolerance but should be used judiciously due to their
paresis. For patients with impaired gastric motility, the use of higher cost.87 Diluting the feeding formula or administering par-
promotility agents such as metoclopramide and erythromycin enteral albumin rarely improves feeding tolerance and is not rec-
should be considered. ommended. Hypoalbuminemia does not cause diarrhea but rather
2. Gastroesophageal reflux occurs in most patients at some time.78 serves as a marker for patients with underlying inflammatory dis-
Reflux can occur when gastric pressure exceeds LES pressure. ease, increased gut permeability, and hypercatabolism.
Gastric pressure is increased by large gastric volumes and
increased abdominal pressure due to fluid (eg, ascites). Reflux may
be greater when the patient is in the supine position, especially if a
large-bore feeding tube is in place.30 Complications of reflux
TABLE 5-1. Possible Causes of Diarrhea in
include esophagitis, vomiting, and aspiration. Gastroesophageal Tube-Fed Patients
reflux and secondary aspiration can be minimized by maintaining
low gastric volumes, keeping the head of the bed elevated, and Non-formula-related diarrhea
using agents that increase LES pressure (eg, metoclopramide). Medications (sorbitol-based elixirs, antibiotics, H2-receptor
3. Duodenal-gastric (DG) reflux is common but does not usually antagonists, laxatives, magnesium, and phosphorus)
present a clinical problem. The finding of bile or small-bowel feed- Mediators released during inflammatory syndromes and sepsis
ings in the stomach is not a contraindication to enteral feedings. It Pancreatic insufficiency
is important to evaluate the clinical significance of the DG reflux.
Delayed feedings causing bowel atrophy or long-term parenteral
Large-volume DG reflux may indicate impaired small-bowel
nutrition only
motility and can increase gastric residual volume. DG reflux is
reduced by promotility agents and more distal placement of small- Increased bowel motility
bowel feeding tubes. It is usually minimal when the feeding tube Pathogenic bacteria (Clostridium difficile, enterotoxins)
is beyond the ligament of Treitz.79 Bacterial overgrowth
4. Diarrhea occurs in 2% to 63% of enterally fed patients, depend- Cytomegalovirus
ing on how it is defined.80–87 Diarrhea is generally defined as the Inflammatory bowel disease
passage of more than 200 grams of stool per day, but it is fre- Impaction
quently defined clinically as three or more liquid stools per day.86
It is important to note that the stool is usually pasty in patients fed Short-bowel syndrome
non-fiber-containing liquid formulas. Many patients also develop Formula-related diarrhea
rectal incontinence as a result of their illness. Thus, a patient with
Rapid infusion rate
multiple small-volume bowel movements does not necessarily
Rapid initiation and progression of feedings in the small bowel
have diarrhea. Impaction should be ruled out in patients with ooz-
ing stools. Diarrhea rarely results from the enteral formula but High fat intake
rather indicates malfunction of the GI tract (eg, malabsorption, Lactose intolerance
excess secretion), bacterial overgrowth, or the presence of toxins. Microbial contamination of formula
Medications have been reported to cause 61% of the cases of diar-

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S E C T I O N I Fundamentals of Nutrition Support Practice and Management

5. Constipation can result from inactivity, decreased bowel motility, tion, coma, seizures, nausea, vomiting, anorexia, and headache.
decreased fluid intake, impaction, or lack of dietary fiber. Poor Altered circulating levels of sodium primarily reflect the status
bowel motility and dehydration may lead to impaction and abdom- of body water. An excess intake of water compared with sodium
inal distension (from obstruction). Other common causes include results in hyponatremia, while an excess intake of sodium com-
the use of antimotility agents such as anticholinergics, opioids, pared with water results in hypernatremia. The most common
calcium-channel antagonists, and certain chemotherapy agents cause of hyponatremia in hospitalized patients is the syndrome
such as vincristine. Neuromuscular blockers do not paralyze gut of inappropriate antidiuretic hormone (SIADH), which results
smooth muscle but may slow bowel motility via anticholinergic in retention of water in excess of sodium. SIADH can result
actions. Constipation is often improved by the provision of ade- from a variety of causes, including intracranial hemorrhage,
quate hydration and the use of fiber-containing formulas, stool sof- trauma, tumor, or encephalitis; carcinoma of the lung, duode-
teners, and bowel stimulants. Laxatives and enemas may improve num, pancreas, thymus, or lymph nodes; and pneumonia, tuber-
symptoms in these patients. An abdominal roentgenogram may be culosis, lung abscess, cystic fibrosis, or certain medications.
needed as a diagnostic tool. The most common cause of hypernatremia is dehydration due
6. Malabsorption without diarrhea. The most common causes are to water losses in excess of sodium (eg, excess sweating, excess
medications (eg, antibiotics, sorbitol-containing medications, H2 urinary loss of water because of osmotic diuresis, limited water
antagonists), impaired digestion (pancreatic insufficiency, dimin- intake). Thus, hypernatremia is treated primarily by adminis-
ished gut mucosal enzymes, insufficient bile secretion), and tration of fluid, and hyponatremia is treated by fluid restriction.
impaired absorption (due to underlying injury or disease of the gut). Hypernatremia and hyponatremia also can be caused by high
and low sodium intake, respectively, in relation to output. Most
C. Metabolic complications. Metabolic complications are less prevalent
enteral formulas contain low amounts of sodium. Patients with
with enteral than parenteral feedings due to the buffering effects of
increased sodium losses require replacement. Table salt may be
the gut and liver, which can help to prevent rapid metabolic
judiciously added to the formula or the flush solution. The
changes.34 However, it is still prudent to perform thorough ongoing
amount of salt used is based on the sodium deficit, the volume
assessments of patients receiving enteral nutrition support.
of fluid losses, and the organ from which the fluids came. Con-
1. Hyperglycemia. Most enterally fed patients do not develop hyper-
versely, the sodium content of IV fluids needs to be calculated
glycemia. Hyperglycemia may occur in some patients because of
when hypernatremia is evaluated.
underlying diabetes mellitus or insulin resistance (precipitated by c) Potassium is the primary intracellular cation in the body and
the illness or by medications such as glucocorticoids). Carbohy- is the major determinant of electrical membrane potential.
drate feeding can increase blood glucose concentrations in these Decreased concentrations of potassium result in cardiac
patients. Hyperglycemia should be treated because it impairs arrhythmias, muscle weakness, and impaired protein synthesis.
immune function, increases the risk of infection, increases post- Potassium deficiency results from losses in the stool, GI secre-
ischemic neuronal damage, and results in fluid and electrolyte tions, and urine (especially with diuretics).
losses. In critically ill patients, hyperglycemia increases in-hospital d) Calcium is the primary divalent cation of the extracellular fluid
mortality, bloodstream infections, incidence of acute renal failure and is essential for regulating processes that require movement
requiring dialysis or hemofiltration, need for red cell transfusions, in the body (eg, excitation-contraction coupling in cardiac,
and critical illness polyneuropathy.88 Blood glucose levels should smooth, and skeletal muscle; neurotransmission; hormonal
be monitored at periodic intervals in all patients receiving enteral secretion; ciliary motion; or cell division).89 Calcium circulates
nutrition support. It is important to treat the underlying disease in the blood in three fractions: ionized, chelated, and protein
(eg, infection, inflammation), maintain intravascular volume, and bound. The ionized fraction is physiologically active and home-
prevent electrolyte disturbances. If blood glucose concentra- ostatically regulated. Total calcium levels (measured by most
tions remain elevated (>110 mg/dL) in critically ill patients at the laboratories) may not accurately reflect the ionized calcium sta-
carbohydrate level needed by the patient, insulin should be admin- tus of sick patients. The best measure of circulating calcium
istered and titrated to achieve blood glucose concentrations that are status is the ionized calcium level. Ionized calcium levels are
below this range. In nonacute hyperglycemic patients who have usually obtained with a parathyroid hormone level when serum
not been previously diagnosed with diabetes mellitus or are not total calcium values are persistently low despite attempts to
being treated with corticosteroids, a workup for diabetes mellitus normalize them. In the absence of an ionized calcium mea-
should be initiated. surement, practitioners often use the following equation to
2. Electrolyte and mineral deficiencies89 (Table 5-2) determine a corrected value:
a) Electrolytes are lost via stool, ostomies, fistulae, urine, and skin.
Patients with excessive losses may need increased intake of var- [normal serum albumin ( mg dL )
ious electrolytes. Potassium, magnesium, and phosphorus are − observed serum albumin ( mg dL ) × 0.8]
required for optimal protein synthesis. The kidneys are prima- + observed serum calcium ( mg dL )
rily responsible for excretion of potassium, magnesium, and = corrected serum calcium value ( mg dL )
phosphorus; intake of these ions may need to be decreased in
patients with renal insufficiency or failure. Serum concentra- If adequate dietary calcium is not received over the short term,
tions should be monitored at intervals based on patient acuity, it will be mobilized from bone. However, long-term depletion
and electrolytes and minerals should be replaced as needed to of dietary calcium may lead to osteopenia or osteoporosis.
keep serum levels within the normal range. Conversely, excess calcium administration during ischemic
b) Sodium is the primary extracellular cation in the body and and septic states can cause cellular injury. Calcium should be
the major controller of osmolality. Clinical features of hypo- administered to patients in only the amounts required to main-
natremia and hypernatremia relate to the nervous system and tain normal concentrations. Some experts believe that calcium
include depressed mentation, confusion, irritability, obtunda- intake should be decreased or completely restricted for a short

84 A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. © 2005 A.S.P.E.N. www.nutritioncare.org.
 TABLE 5-2. Electrolyte/Mineral Imbalances

Mineral Physiologic Function Clinical Features Etiologies Treatment

Sodium 1. Primary extracellular cation Altered CNS function; disorientation, 1 Hyponatremia results from 1. Hyponatremia is treated
2 Extracellular osmolality depressed mentation, confusion, retention of water in excess of by limiting the intake
3 Exchange of K+, H+, Ca++, H2O irritability, coma, seizures, nausea, sodium (ie, from excess ADH of free water and in-

© 2005 A.S.P.E.N. www.nutritioncare.org.

vomiting, weakness or water intake); rarely does low creasing water excretion.
sodium intake contribute. 2. Hypernatremia is treated
2. Hypernatremia results from with water administration
water loss in excess of or salt removal plus water
sodium or excess intake of salt repletion..

Potassium 1 Primary intracellular cation 1. Hypokalemia: cardiac arrhythmias, 1. Hypokalemia results from loss 1 Hypokalemia is treated
2. Electrical membrane potential bradycardia, muscle weakness, of potassium from the body in by administering K+.
paralysis, hyporeflexia, paresthesias, urine, stool, wounds, or through 2. Hyperkalemia is treated
ileus, impaired protein synthesis the skin (not matched by intake) by antagonizing K+
2. Hyperkalemia: bradycardia, heart or shift of K+ into cells (refeeding). effect on the cell
block, dysrhythmias, diminished 2. Hyperkalemia results from excess membrane with calcium
cardiac conduction, weakness, excess entry of K+ into the (only emergencies),
paralysis, paresthesias, hyporeflexia extracellular space from dietary shifting K+ into cells
intake or release from tissues (ie, (insulin and glucose,
cell necrosis) and/or decreased bicarbonate), and removing
renal excretion. K+ from the body (diuretics,
kayexalate).

Calcium 1. Primary extracellular divalent 1. Hypocalcemia causes bone loss, 1. Hypocalcemia results from 1. Hypocalcemia is treated
cation weakening of bones, hypotension, from decreased PTH or vitamin D with calcium administra-
2. Excitation-contraction coupling, poor cardiac contraction. action on bone; chelation tion; mild hypocalcemia is
secretion neurotransmission, 2. Hypercalcemia causes hypertension, may also cause hypocalcemia. well tolerated over the
cellular messenger, activator of impaired cardiac function, and altered 2. Hypercalcemia results from short term (a few weeks)
enzymes mentation and can lead to renal stones excess Ca++ intake or excess and may be protective
3. Major regulator of all processes and tissue calcification. release of Ca++ from bone (ie, against ischemic and
that require movement 3 Calcium status is best determined using cancer, hyperparathyroidism, inflammatory-mediated
ionized calcium levels. immobilization). cellular injury.

(continued)

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S E C T I O N I Fundamentals of Nutrition Support Practice and Management
86
TABLE 5-2. Electrolyte/Mineral Imbalances

Mineral Physiologic function Clinical features Etiologies Treatment

2. Hypercalcemia is treated by
decreasing Ca++ intake, Ca++
excretion (with diuretics
and sodium), and decreas-
ing bone release of

A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed.

calcium.

Phosphorus Cellular energy, second 1. Depletion results in diminished 1. Low levels result from 1. Depletion is treated by ad-
messengers, 2,3-DPG, DNA, RNA immune, muscle, hepatic, and other decreased PO4 intake, excess ministering enteral or IV PO4.
organ functions. loss from the body, or shift of 2. Excess PO4 states are y
S E C T I O N I Fundamentals of Nutrition Support Practice and Management

2. Excess usually causes symptoms by PO4 into cells (ie, refeeding treated by decreasing PO4
lowering Ca++ levels. syndrome). intake, increasing PO4 loss
3. Ca-PO4 precipitation is likely when 2. High levels result from excess from the body (diuretics, PO4
Ca x PO4 product >60 mg/dL. intake, diminished renal excretion, binders such as aluminum-
or release of PO4 from tissues containing antacids), or
(cell lysis). shifting PO4 intracellularly
(glucose and insulin).

Magnesium Regulates PTH and vitamin D 1. Depletion results in cardiac arrhythmias, 1. Depletion results from 1. Depletion is treated with
secretion or action, Na+-K+ muscle weakness, hypokalemia, decreased intake and excess enteral or IV Mg++.
ATPase activity, cyclase activity, hypocalcemia. body losses (urine, stool, skin); 2. Excess states are treated by
Ca++ channels; also a cofactor for 2. Excess results in CNS depression, levels may also decrease when limiting intake and increas-
many enzymes muscle weakness; very high levels Mg++ shifts into cells (ie, ing losses from urine.
can cause paralysis and cardiac arrest. refeeding syndrome).
2. Excess states result from
increased intake and decreased
renal excretion.

ADH, antidiuretic hormone; ATPase, adenosine triphosphatase; CNS, central nervous system; DPG, diphosphoglycerate ; IV, intravenous; PTH, parathyroid hormone.

© 2005 A.S.P.E.N. www.nutritioncare.org.

 S E C T I O N I Fundamentals of Nutrition Support Practice and Management

period after the onset of critical illness, although this belief is b) Water-soluble vitamins. The most common deficiencies are of
controversial. folate, ascorbic acid, and thiamine. Humans are almost entirely
e) Phosphorus plays an important role in the body.89 It is a source dependent on dietary sources for these vitamins and require con-
of cellular energy (eg, adenosine triphosphate, creatine phos- stant intake to maintain normal stores. Thiamine is an essential
phate), a component of cyclic adenosine monophosphate and vitamin for carbohydrate metabolism (including glucose). In the
cyclic guanosine monophosphate (important intracellular mes- United States, chronic alcoholism, advanced age, long-term
sengers), a component of 2,3-diphosphoglycerate (important malnutrition, malabsorption syndromes, prolonged antacid
for oxygen offloading from hemoglobin), and synthesis of therapy (thiamine is destroyed in alkaline pH), and dialysis are
nucleotides. Most circulating phosphorus is in the ionized form. the most common causes of thiamine deficiency. Thus, many
Phosphorus depletion causes a sick-cell syndrome in which all of these patients are provided thiamine upon hospital admission.
cells of the body demonstrate diminished function (eg, immune 5. Dehydration is a risk for patients receiving enteral nutrition sup-
system, muscle, liver). Respiratory arrest can occur with severe port, and the etiology is multifactorial. Water needs average 1 mL
phosphorus depletion. Common causes of hypophosphatemia per calorie consumed in adults. Dehydration may result from the
are administration of large amounts of carbohydrate (phospho- use of concentrated formulations, which contain less water. In
rus shifts intracellularly when glucose enters the cell), admin- addition, high-protein feeds may cause an osmotic (urea) diure-
istration of drugs (insulin, epinephrine, phosphate-binding sis and loss of body water. Dehydration also may result when
antacids, sucralfate), and phosphate losses from the GI tract and body fluid losses are not met by fluid intake (eg, water loss from
kidneys. Serum phosphorus concentrations should be moni- skin during fever, from urine, from stool, or from fistula/ostomy
tored based on patient acuity and replacement provided as nec- output). An increasing serum sodium concentration, BUN, or
essary. If levels are severely low, IV phosphorus should be BUN/creatinine ratio suggests dehydration. Treatment is aimed
administered. at restoring intravascular volume and fluid balance.
f ) Magnesium is an important cofactor for many essential
enzymes.89 Magnesium depletion can result from losses in GI V. Transitioning from Enteral Nutrition Support
fluids or urine or from decreased intake in the diet. Magne-
sium depletion predisposes a patient to cardiac arrhythmias Before beginning the process of weaning from tube feedings, the
and cellular injury. patient should have an adequate nutrition status or the ability to return
3. Refeeding syndrome to normal status by eating. In addition, it is important to ensure that the
a) Refeeding of severely malnourished patients may result in patient’s fluid needs are being met either by tube or orally during the
“refeeding syndrome,” in which there are acute intracellular transitional phase.
shifts of electrolytes as cell anabolism is stimulated.90–92 A. Transitioning from continuous tube feedings. When a patient is tran-
sitioning from full enteral nutrition support, physiologic preparation
Refeeding syndrome is a potentially life-threatening com-
should be initiated by providing the patient bolus feedings through-
plication that may occur with the rapid reintroduction of
out the day to simulate meals and snacks. This strategy is imple-
carbohydrate-containing feedings in severely malnourished
mented in an effort to stimulate hunger and to achieve the
patients. Hematologic, neuromuscular, cardiac, and respira-
association of satiety with feedings.11 Initially, oral intake can be
tory dysfunction has been observed in severe cases.93 Refeed-
minimal and coupled with supplemental feedings via tube after each
ing syndrome can result in acute decreases in circulating
meal to provide the majority of nutrition needs. As oral intake
levels of potassium, magnesium, and phosphorus. Serum lev-
increases, tube-feeding formula volume is decreased, keeping the
els should be monitored and replacement should be provided combined regimen isocaloric.94 Another option is to provide a por-
as needed to maintain normal circulating levels. Many of tion of the tube feedings by continuous drip at night, ending at least
these patients also require thiamine supplementation.92 1 hour before the first meal. This allows freedom from tube feeding
b) Children. Malnourished children are at greater risk for meta- during the day and helps promote an appetite. This also is useful in
bolic problems. All moderately to severely malnourished chil- patients who have short-bowel syndrome and require small, frequent
dren should have serum potassium, phosphorus, magnesium, feedings to optimize intestinal absorption. If the patient is receiving
and glucose levels checked at least daily during the first week elemental tube feedings due to intestinal malabsorption or if weight
of initiation of nutrition support, as well as periodically dur- gain is deemed inadequate, additional calories may need to be pro-
ing the gradual advancement of feedings.41 vided via the feeding tube, but efforts to continue to increase the
4. Vitamin deficiencies may develop in patients who receive nutri- intake of oral foods should still be encouraged.
tion support. Deficiencies commonly result from inadequate vita- B. Discontinuing tube feedings. When the patient is able to consume
min intake (which fails to match requirements or losses) or poor 75% of nutrition needs by mouth, the tube feeding can be discon-
absorption. Malnourished patients are at higher risk of develop- tinued but the feeding tube left in place. Before the feeding tube is
ing vitamin deficiencies due to their depleted state when nutrition removed, factors that should be considered include the type of tube
support is initiated. (See Chapter 1 for clinical manifestations of placement (ie, nasogastric vs. a more permanent gastrostomy), the
vitamin deficiencies.) underlying medical condition(s) that necessitated the tube, whether
a) Fat-soluble vitamins (vitamins A, D, E, and K) require pancre- fluid needs can be met, and whether medications can be adminis-
atic enzymes and bile for absorption. Concentrations may be tered without the tube. It is especially helpful to observe patients
low in patients with pancreatic insufficiency, cirrhosis, or mal- who have received long-term enteral nutrition support during an
absorption syndromes. Vitamin K is synthesized by gut bac- acute illness to determine the future necessity of the tube.11
teria, and concentrations may be decreased in patients who
receive antibiotics. Vitamin K is required for synthesis of coag- (Enteral Nutrition Management chapters from the 1st edition were
ulation proteins, while vitamin D is necessary for the mainte- contributed by Linda Lord, Linda Trumbore, Gary Zaloga, Kristy
nance of circulating calcium. Gibbons, Nancy Cyr, Michael L. Christensen, and Richard A. Helms)

© 2005 A.S.P.E.N. www.nutritioncare.org. A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. 87
S E C T I O N I Fundamentals of Nutrition Support Practice and Management

REFERENCES 26. A.S.P.E.N. Board of Directors. Guidelines for the use of parenteral and
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23:31–34. 32. Winterbauer RH, Durning RB Jr, Barron E, et al. Aspirated nasogastric feed-
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Crit Care Nurs. 1994;5:450–458. 36. Ellis KJ, Shypailo RJ, Wong WW. Measurement of body water by multi-
13. Martindale RG. Enteral feeding during states of marginal visceral blood frequency bioelectrical impedance spectroscopy in a multiethnic pediatric
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Ross Conference on Enteral Devices. Columbus, OH: Ross Products; 37. Lipp J, Lord LM, Scholer LH. Fluid management in enteral nutrition. Nutr
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14. Greenberg GR, Fleming CR, Jeejeebhoy KN, et al. Controlled trial of 38. Mahan L, Arlin M, eds. Krause’s Food, Nutrition & Diet Therapy. 8th ed.
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Gut. 1988;29:1309–1315. 39. Huggins PS, Tuomi SK, Young C. Effects of nasogastric feeding tubes
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the puzzle [editorial]. J Parenter Enteral Nutr. 1995;19:93–94. 157–161.
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alcoholic pancreatitis. J Am Coll Nutr. 1995;14:662–665. patient receiving home parenteral and enteral nutrition. Nutr Clin Pract.
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enteral nutrition in adult and pediatric patients. J Parenter Enteral Nutr. 41. A.S.P.E.N. Board of Directors. Guidelines for the use of parenteral and
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18. Ragins H, Levenson SM, Singer R, et al. Intrajejunal administration of an 2002;26:16SA–17SA.
elemental diet at neutral pH avoids pancreatic stimulation. Am J Surg. 1973; 42. A.S.P.E.N. Board of Directors. The 1995 standards for nutrition support of
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19. Weckwerth J, Nelson J, O’Shea R. Home nutrition support. In: Gottschlich 43. Scanlan M, Frisch S. Nasoduodenal feeding tubes: prevention of occlusion.
M, Matarese L, Shronts E, eds. Nutrition Support Dietetics Core Curriculum. J Neurosci Nurs. 1992;24:256–259.
Silver Spring, MD: A.S.P.E.N; 1993:467–473. 44. Marcuard S, Perkins A. Clogging of feeding tubes. J Parenter Enteral Nutr.
20. Nevin-Folino N, Miller M. Enteral nutrition. In: Queen Samour P, King Helm 1988;12:403–405.
K, Lang CE, eds. Pediatric Nutrition. Gaithersburg, MD: Aspen Publishers; 45. Methany N, Eisenberg P, McSweeney M. Effect of feeding tube properties
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21. Heitkemper M, Martin D, Hansen B, et al. Rate and volume of intermittent 46. Kudsk KA, Minard G. Enteral nutrition. In: Zaloga GP, ed. Nutrition in
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22. Harrington M, Lyman B. Special considerations for the pediatric patient. 47. Silk DBA, Payne-James JJ. Complications of enteral nutrition. In:
In: Guenter P, Silkroski M, eds. Tube Feeding: Practical Guidelines and Romeau JL, Caldwell MD, eds. Clinical Nutrition: Enteral and Tube
Nursing Protocols. Gaithersburg, MD: Aspen Publishers; 2001:139–188. Feeding. 2nd ed. Philadelphia, PA: WB Saunders; 1990:510–531.
23. Akers SM, Groh-Wargo SL. Normal nutrition during infancy. In: Queen 48. Bastow MD. Complications of enteral nutrition. Gut. 1986;27(suppl 1):
Samour P, King Helm K, Lang CE, eds. Pediatric Nutrition. Gaithersburg, 51–55.
MD: Aspen Publishers; 1999:65–97. 49. Kirby DF, DeLegge MH. Enteral nutrition: the challenge of access. In: Kirby
24. Burd RS, Lentz C. The limitations of using gastric residual volumes to DF, Dudrick SJ, eds. Handbook of Nutrition in Clinical Practice. Boca
monitor enteral feedings: a mathematical model. Nutr Clin Pract. 2001;16: Raton, FL: CRC Press; 1994:87–104.
349–354. 50. Zaloga GP. Enteral nutrition in the critically ill. In: Chernow B, ed. The
25. McClave SA, Snider HI, Lowen CC, et al. Use of residual volume as a Pharmacologic Approach to the Critically Ill Patient. 3rd ed. Baltimore,
marker for enteral feeding intolerance: prospective blinded comparison MD: Williams & Wilkins; 1994:1034–1050.
with physical examination and radiographic findings. J Parenter Enteral 51. Cabre E, Gassull MA. Complications of enteral feeding. Nutrition. 1993;
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52. Eddy VA, Snell JE, Morris JA Jr. Analysis of complications and long-term 75. Marcuard SP, Stegall KS. Unclogging feeding tubes with pancreatic
outcome of trauma patients with needle catheter jejunostomy. Am Surg. enzyme. J Parenter Enteral Nutr. 1990;14:198–200.
1996;62:40–44. 76. Hamaoui E. Gastroesophageal reflux during gastrostomy feeding. J Parenter
53. Fleming CR. Hepatobiliary complications in adults receiving nutrition Enteral Nutr. 1995;19:172–173.
support. Dig Dis. 1994;12:191–198. 77. Gustke RF, Varma RR, Soergel KH. Gastric reflux during perfusion of the
54. O’Keefe KP. Complications of percutaneous feeding tubes. Emerg Med proximal small bowel. Gastroenterology. 1970;59:890–895.
Clin North Am. 1994;12:815–826. 78. Mullan H, Roubenoff RA, Roubenoff R. Risk of pulmonary aspiration
55. Bowling TE, Silk DB. Enteral feeding: problems and solutions. Eur J Clin among patients receiving enteral nutrition support. J Parenter Enteral Nutr.
Nutr. 1994;48:379–385. 1992;16:160–164.
56. Bohnker BK, Artman LE, Hoskins WJ. Narrow bore nasogastric feeding 79. Pratt JC, Tolbert CG. Tube feeding aspiration. Am J Nurs. 1996;96:37.
tube complications. A literature review. Nutr Clin Pract. 1987;2:203–209. 80. Koruda MJ. Diarrhea-diagnosis and treatment. In: Zaloga G, ed. Nutrition
57. Miller KS, Tomlinson JR, Sahn SA. Pleuropulmonary complications of in Critical Care. St. Louis, MO: Mosby; 1994:815–829.
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58. Metheny N. Minimizing respiratory complications of nasoenteric tube mula not necessarily the cause. Am J Med. 1990;88:91–93.
feeding: state of the science. Heart Lung. 1993;22:213–223. 82. Mobarhan S, DeMeo M. Diarrhea induced by enteral feeding. Nutr Rev.
59. Roubenoff R, Ravich WJ. Pneumothorax due to nasogastric feeding tubes. 1995;53:67–70.
83. Eisenberg PG. Causes of diarrhea in tube-fed patients: a comprehensive
Report of four cases. Arch Intern Med. 1989;149:184–188.
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60. Montecalvo MA, Steger KA, Farber HW, et al. Nutritional outcome and
84. Bowling TE. The Sir David Cuthbertson Medal Lecture. Enteral-feeding-
pneumonia in critical care patients randomized to gastric versus jejunal tube
related diarrhoea: proposed causes and possible solutions. Proc Nutr Soc.
feedings. The Critical Care Research Team. Crit Care Med. 1992;10:
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85. Heimburger DC, Sockwell DG, Geels WJ. Diarrhea with enteral feeding:
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prospective reappraisal of putative causes. Nutrition. 1994;10:392–396.
tubes [letter]. Gastrointest Endosc. 1986;32:55.
86. Bliss DZ, Guenter PA, Settle RG. Defining and reporting diarrhea in tube-
62. Hofstetter J, Allen LV Jr. Causes of nonmedication-induced nasogastric fed patients—what a mess! Am J Clin Nutr. 1992;55:753–759.
tube occlusion. Am J Hosp Pharm. 1992;49:603–607. 87. Fuhrman MP. Diarrhea and tube feeding. Nutr Clin Pract. 1999;4:83–84.
63. Kohn CL. The relationship between enteral formula contamination and 88. Van den Berghe G, Wouters P, Weekers, F, et al. Intensive insulin therapy
length of enteral delivery set usage. J Parenter Enteral Nutr. 1991;5:567–571. in critically ill patients. New Engl J Med. 2001;345:1359–1367.
64. Powell KS, Marcuard SP, Farrior ES, et al. Aspirating gastric residuals causes 89. Zaloga GP, Chernow B. Divalent ions: calcium, magnesium, and phospho-
occlusion of small-bore feeding tubes. J Parenter Enteral Nutr. 1993;17: rus. In: Chernow B, ed. The Pharmacologic Approach to the Critically Ill
243–246. Patient. 3rd ed. Baltimore, MD: Williams & Wilkins; 1994:777–804.
65. Sensibile J, Agrecy J, Griggs M, Lovoy K, Smart J. Breakout session. 90. Jolly AF, Blank R. Refeeding syndrome. In: Zaloga G, ed. Nutrition in
Group II: salvage of the clogged feeding tube: tricks of the trade. Nutr Clin Critical Care. St. Louis, MO: Mosby; 1994:765–782.
Pract. 2000;15:S74–S75. 91. Bowling TE, Silk DB. Refeeding remembered. Nutrition. 1995;11:32–34.
66. Williams PJ. How do you keep medicines from clogging feeding tubes? Am 92. Solomon SM, Kirby DF. The refeeding syndrome: a review. J Parenter
J Nurs. 1989;89:181–182. Enteral Nutr. 1990;14:90–97.
67. Altman E, Cutie AJ. Compatibility of enteral products with commonly 93. A.S.P.E.N. Board of Directors. Guidelines for the use of parenteral and
employed drug additives. Nutr Supp Serv. 1984;4:8, 10, 11, 14. enteral nutrition in adult and pediatric patients. J Parenter Enteral Nutr.
68. Holtz L, Milton J, Sturek JK. Compatibility of medications with enteral 2002;26:39SA–41SA.
feedings. J Parenter Enteral Nutr. 1987;11:183–186. 94. Reimers K, Carlson S, Lombard K. Nutritional management of infants with
69. Hearne BE, Besser PM, Groshen S, et al. In vitro flow rates of enteral solu- bronchopulmonary dysplasia. Nutr Clin Pract. 1992;7:127–132.
tions through nasoenteric tubes. J Parenter Enteral Nutr. 1984;8:456–459.
70. Petrosino BM, Meraviglia M, Becker H. Mechanical problems with small- SUGGESTED READINGS
diameter enteral feeding tubes. J Neurosci Nurs. 1987;19:276–280. Clevenger F, Rodriguez D. Decision-making for enteral feeding administration:
71. Bommarito AA, Heinzelmann MJ, Boysen DA. A new approach to the the why behind where and how. Nutr Clin Pract. 1995;10:104–113.
management of obstructed enteral feeding tubes. Nutr Clin Pract. 1989:4: Ideno K. Enteral nutrition. In: Gottschlich M, Matarese L, Shronts E, eds.
111–114. Nutrition Support Dietetics: Core Curriculum. 2nd ed. Silver Spring, MD:
72. Mateo MA. Maintaining the patency of enteral feeding tubes. Online A.S.P.E.N.; 1993:71–104.
J Knowledge Synth Nurs. 1994;1(Doc 9):1–13. Kudsk K. Clinical applications of enteral nutrition. Nutr Clin Pract. 1994;9:
73. Marcuard SP, Stegall K, Trogdon S. Clearing obstructed feeding tubes. 165–171.
J Parenter Enteral Nutr. 1989;3:81–83. Rolandelli R, DePaula J, Guenter P, et al. Critical illness and sepsis. In: Rombeau
74. Webber-Jones J, Sweeney K, Winterbottom A, et al. How to declog a feeding J, Caldwell M, eds. Clinical Nutrition: Enteral and Tube Feeding. 2nd ed.
tube. Nursing. 1992;22:62–64. Philadelphia, PA: WB Saunders; 1990:288–305.

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 Elizabeth A. Krzywda, RN, APN, MSN;
Charles E. Edmiston Jr, PhD
6
Parenteral Nutrition
Access and Infusion
Equipment
Introduction a) Modified Seldinger technique: Venipuncture and passage of a
guidewire through the needle are followed by removal of the
The development of central venous access devices is closely linked to needle and catheter placement over the guidewire.
the development of total parenteral nutrition. Today, the use of central b) Peel-away introducer sheath and tissue dilator: The catheter
venous access has become a standard for a multitude of intravenous passes through the introducer into the vein and the introducer
(IV) therapies. Vascular access is both an art and a science. Decisions tears longitudinally, leaving the catheter in place.
and practices related to device selection, placement, and maintenance as c) Introducers should be 0.2F to 0.5F sizes larger than the catheter
well as appropriate use of infusion systems affect the success of par- to prevent bleeding or air embolism.
enteral nutrition administration. This chapter addresses the following: 2. Cut down: Surgical dissection is followed by isolation of the
vessel and catheter placement. This technique is most often used
I. Central Venous Access: General Principles
to access the cephalic, external, or internal jugular vessels.
II. Central Venous Catheter Placement
3. Tunneled: A catheter segment of approximately 6 cm is tunneled
III. Central Venous Catheter Features
from the selected skin exit site through the subcutaneous tissues
IV. Central Venous Catheter Types
to the venipuncture site.
V. Central Venous Catheter Selection
B. Complications
VI. Central Venous Catheter Care and Maintenance
1. Pneumothorax is the most common immediate complication of
VII. Peripheral Access
percutaneously placed subclavian catheters. The incidence is
VIII. Infusion Delivery Devices
1% to 4%.3
IX. Infusion Delivery Device Selection Criteria
2. Arterial puncture is the most common complication associated
References
with the percutaneous internal jugular approach.3
3. A wide variety of technical and mechanical complications during
I. Central Venous Access: General Principles catheter placement have been reported, including pneumothorax,
A. Central venous access provides for infusion and blood withdrawal catheter malposition, arrhythmias, air and catheter embolization,
from the central circulation. vascular injury, cardiac injury, pleural injury, mediastinal injury,
B. Access is facilitated through the use of specialized catheters with neurologic injury, and thoracic duct injury.3
distal tip placement into the vena cava adjacent to the right atrium. 4. Pericardial tamponade is the most lethal complication, with a
C. The most common venipuncture sites are the subclavian, jugular, mortality rate between 65% and 90%. The relationship of this
femoral, cephalic, and basilic veins. complication to catheter placement is addressed by the Food and
D. Primary indications for central venous infusions include chemother- Drug Administration with the recommendation that the catheter
apy, antibiotic administration, and parenteral nutrition (PN). Central tip not be placed in or allowed to migrate into the heart. This rec-
access allows for use of therapy toxic to the endothelium of small ommendation is controversial and is not universally supported
veins due to medication pH, osmolarity, and volume; vesicant prop- by clinical practice or research.3
erties of some medications; and length of therapy. C. Setting
E. The risk of infectious complications decreases with standardization 1. Catheter placement can take place in the operating room or a
of aseptic care, staff experience with device placement, and adequate variety of other settings, such as bedsides, minor procedure
nursing staff. Specialized IV teams have been effective in decreasing rooms, physicians’ offices, and interventional radiology suites.
catheter-related infections.1 2. Currently, implanted and tunneled catheters are most commonly
placed in the operating room or interventional radiology suite. Flu-
oroscopy is often used to verify catheter placement, and the patient
II. Central Venous Catheter Placement receives local anesthesia and at times supplemental IV sedation.
A. Methods 3. Regardless of the setting in which central venous catheters
1. Percutaneous approach: Commonly used to access subclavian, (CVCs) are placed, it is imperative that catheter tip ___location be
internal and external jugular, or antecubital vessels. The subcla- confirmed by chest x-ray or fluoroscopy before the start of therapy.
vian vein is often easiest to cannulate in emergent situations such In the pediatric population, proper catheter tip placement should
as profound volume depletion or shock. Ultrasound guidance be confirmed and/or revalidated as the patient grows and matures.
during internal jugular venous catheterization reduces the num- D. Patient preparation
ber of catheterization failures, the mechanical complications, and 1. Placement of CVCs for PN should always be done on an elective
the time required for insertion.2 basis, allowing for adequate patient preparation (Section II.F).

90 A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. © 2005 A.S.P.E.N. www.nutritioncare.org.
 S E C T I O N I Fundamentals of Nutrition Support Practice and Management

2. Appropriate explanation to the patient is essential. a) Great range of flexibility, excellent physical strength, and
3. Patient or parent/guardian consent is required. resistance to hydrolytic enzymes
E. Strategies for preventing infection b) When used for short-term access, results in more infrequent
1. The best results are achieved when strict infection control pro- inflammatory changes and thrombophlebitis than with poly-
tocols are followed, regardless of the type of catheter and tetrafluoroethylene, polyvinyl chloride, or polyethylene
dressing.1 c) When used for long-term access, requires anticoagulation to
a) Hand washing prevent thrombus formation
b) Aseptic site and hub care 4. Polytetrafluoroethylene (Teflon, DuPont)8
c) Port sterilization before access a) Extremely stable; demonstrates nonadhesive, antifriction
d) Monitoring of the catheter site appearance properties; resistant to degradative enzymes
2. Maximal sterile barrier precautions consist of mask, cap, sterile b) catheter surface
gloves, sterile gown, and large sterile drape. The use of maximal c) Generally unsuitable for long-term use because of rigidity,
barrier precautions during CVC placement minimizes catheter which causes irritation of the intima, leading to thrombus
contamination and subsequent catheter infections.4 formation
3. Site choice may influence infection risk. Subclavian veins have a 5. Silicone elastomer (Silastic, Dow Corning)9
lower risk than jugular or femoral veins. Internal jugular a) High degree of elasticity and flexibility, causing minimal
catheters that are close to oropharyngeal secretions and difficult damage to the intima
to immobilize may have the highest risk of infection.1,2 b) Biomaterial most often used for long-term indwelling devices
4. Techniques used to decrease infections include placing catheters c) Resistant to hydrolytic enzymes; hydrophobic surface resists
with a minimal number of lumens, using silver-chelated cuffs, bacterial adherence
tunneling catheters, and using antibiotic-impregnated catheters. d) Considered to be chemically inert in blood because of the
5. Blood sampling through catheters, especially in acutely ill ability of the surface to adsorb host protein without triggering
patients, should be minimized. the complement cascade.
6. CVCs that are no longer needed should be removed. e) Guidewire or peel-away introducer required for insertion
7. Routine CVC exchange over a guidewire is no longer recom- because of soft texture
mended in view of increased mechanical and infectious com- 6. Coated/bonded catheters10
plications.1,2 a) Antimicrobial-impregnated catheters, either chlorhexidine and
F. Patient evaluation: before catheter placement silver sulfadiazine or minocycline and rifampin, are the most
1. Vascular access history: previous lines, infection, thrombosis, or frequently used.
difficult placement b) The use of these catheters may reduce the risk of catheter-
2. Physical findings at or near access site: lesions, tumors, previous related bloodstream infections and associated costs in high-
surgical procedures, venous abnormalities, or burns risk patient populations.
3. Specific disease states: lung and breast cancers, pneumonia, c) Long-term studies will be required to determine whether
coagulopathies, cervical masses, and adenopathy microbial resistance is an issue with these catheters.
4. Medication history: attention to anticoagulants, including aspirin, B. Lumens
nonsteroidal anti-inflammatory drugs, warfarin, and unfraction- 1. Many catheters are available in multilumen versions.
ated as well as low–molecular weight heparins. Warfarin should 2. Multilumen catheters provide for simultaneous infusion of multi-
be withheld the day before CVC placement, and prothrombin time ple or incompatible drugs.
should be checked the day of catheter placement. Unfractionated 3. The design varies across manufacturers in terms of both lumen
heparin infusions should be withheld 4 hours before the proce- size and intravascular or lumen openings. Lumens may exit at the
dure.3 Low–molecular weight heparin therapy should be discon- catheter tip or along the distal side of the catheter.
tinued 12 hours prior to the procedure. 4. While studies have not consistently demonstrated an increased
5. Laboratory evaluation: A complete blood cell count, including risk of infectious complications, selection of the catheter with
platelet count and the differential, is necessary. The need for addi- the minimal number of lumens required to administer therapy is
tional laboratory evaluations is based on the clinician’s assess- recommended.11
ment.3 Neutropenia has been identified as a significant risk factor C. Cuffs: a subcutaneous anchor and a mechanical barrier to infection12
in the placement of tunneled CVCs.5 1. Polyethylene eterphthalate (Dacron, DuPont) cuffs are attached
to tunneled catheters. These cuffs, positioned in the subcutaneous
tissue, anchor the catheter by facilitating fibrous ingrowth.1
III. Central Venous Catheter Features
2. Collagen cuffs impregnated with silver ions can be attached to
A. Materials the catheter at insertion or are available preattached. The gradual
1. Polyvinyl chloride6 release of the silver ion exerts a short-term antimicrobial activ-
a) Relatively stiff ity, but studies have not demonstrated efficacy. The use of silver-
b) Common complications: thrombosis and phlebitis impregnated cuffs with tunneled devices has not been shown to
c) Infrequently used offer an added benefit.1
2. Polyethylene7 D. Specialized valve: A pressure-sensitive three-way slit valve
a) High tensile strength (Groshong, Bard) prevents retrograde blood flow, possible catheter
b) Minimal intimal irritation when used for short-term access occlusion, and air embolism. This valve is positioned distally along
c) Associated with platelet adherence and fibrous capsule forma- the side of the catheter; the distal end is closed. The design to prevent
tion in long-term access retrograde blood flow eliminates the need for daily heparinized
3. Polyurethane8 saline flushes and catheter clamping.

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S E C T I O N I Fundamentals of Nutrition Support Practice and Management

E. Catheter diameter/circumference and therefore greater costs may be incurred for long-term home
1. Diameter: expressed in millimeters defining both the internal care, external catheter breakage is possible, and repairs may be dif-
and external diameters ficult because no standard repair kit is available. Infection preven-
2. French size: circumference of the outer diameter in millimeters tion protocols should be followed as for centrally placed catheters.
3. Gauge: inversely related to the catheter’s outer diameter D. Ports
4. Catheters with similar external diameters can have a 30% differ- 1. Description: a subcutaneous injection port with a self-sealing sili-
ence in internal lumen size depending on the catheter material. A cone septum and a catheter. Septum diameters are 6.4 to 19.1 mm;
ratio of the inner to the outer diameter represents this feature. For septum depth, 5.1 to 13 mm. A septum can withstand approxi-
example, polytetrafluoroethylene, polyurethane, and polyethylene mately 1000 to 2000 punctures using a special noncoring needle.
have a ratio of 0.75, compared with 0.38 for silicone catheters. The anterior chest wall is the most common placement site,
5. Catheter length although a smaller peripheral port can be placed in the abdomen,
a) Catheter length is dependent on the site of insertion. groin, or antecubital vessels. Ports are available in a dual-lumen
b) Silicone catheters can be trimmed at the time of insertion. version, with preattached or separate catheters for attachment to
c) Tapered-tipped catheters are inserted without alteration. the port chamber at the time of placement.
2. Alternative port designs include reservoirs without corners and
possible areas of residual or “sludge” collection; ports with
IV. Central Venous Catheter Types1,12,13
access parallel to the skin rather than perpendicular to the skin,
A. Nontunneled central venous access catheters which is the more common design; and a “needleless” port that
1. Description: single- and multilumen catheters, placed using a per- is accessed with a needlelike device.
cutaneous approach into the jugular, subclavian, or femoral ves- 3. Indications: used for long-term intermittent IV access; at times,
sels. The preferred site is the subclavian vein. Length, 6 to 30 cm; this has included daily PN.
gauge, 14 to 27. 4. Advantages: Site care is needed only when the port is accessed,
2. Indication: usually used in the acute-care setting for short- heparinization is needed only monthly if the port is not in use,
duration therapy, such as inpatient PN. An exception is the the patient’s body image remains intact, and there are no exter-
Hohn (Bard) catheter, which is made of silicone and may be nal components for breakage.
placed for home infusions. 5. Disadvantages: Needle access is required, needle displacement
3. Advantages: economical, easily removed, and easily exchanged from the reservoir is possible, placement must occur in an operat-
over a guidewire. ing room or a special room, and removal requires a minor surgical
4. Disadvantages: requires heparin flushing and sterile dressing procedure.
changes. Patient self-care is difficult, and catheter breakage is
possible. There are sutures at the exit site, which may become
V. Central Venous Catheter Selection
detached and result in catheter dislodgment.
B. Tunneled cuffed catheters (Hickman/Broviac/Groshong [Bard]) A. Clinicians experienced in the many facets of vascular access are
1. Description: single and multilumen catheters placed percuta- key to appropriate device selection. Interdisciplinary collaboration
neously, most often into the jugular or subclavian veins or via as well as input from the patient and caregivers will enhance device
cut down into the cephalic vein. These catheters use a Dacron selection.
cuff and are tunneled in the subcutaneous tissue. Length, 55 to B. CVC device selection is a process that appropriately matches the
90 cm; gauge, 2.7 to 19.7 (dual lumen). patient, the disease, the therapy, and the catheter.
2. Indication: extended IV therapy often administered on an out- C. Patient assessment
patient basis, including home PN, chemotherapy, and pain 1. Preoperative evaluation (Section II.F)
management. 2. Activity level
3. Advantages: can be used for extended periods of time, require 3. Body image concerns
minimal dressing care, can be repaired externally, can be cared 4. Physical ability to care for catheter
for by patients, and are secured with a subcutaneous cuff. 5. Cognitive abilities
4. Disadvantages: require an operating room or a special room for 6. Caregiver involvement
placement and routine heparin flushes (exception: Groshong); 7. Patient’s diagnosis and future activity level
may be difficult to remove. 8. Financial considerations
C. Peripherally inserted central catheter (PICC)11 a) Cost of the device
1. Description: single- or double-lumen catheters, placed percuta- b) Cost of the insertion
neously into the antecubital vessels. Length, 33.5 to 60 cm; c) Costs associated with care and maintenance
gauge, 14 to 60. d) Potential costs of complications
2. Indications: used for patients requiring access for several weeks D. Duration and type of therapy
to several months. PICCs have been used in the acute-care setting 1. Length (see Table 6-1): Estimated length of therapy is one of the
as well as for outpatient therapies including PN. most significant variables in catheter choice.
3. Advantages: eliminate the risks associated with thoracic catheter a) Patients requiring long-term outpatient therapy are best
placement. For adults, placement can occur at the patient’s bed- served by a tunneled cuffed catheter, an implanted port, or a
side or home. In most states, placement can be performed by PICC. If therapy is daily, implanted ports may not be the opti-
specially trained registered nurses, thereby decreasing the cost mal choice, as frequent needle access can lead to skin irrita-
associated with placement. tion and may make patient self-care difficult.
4. Disadvantages: require routine heparin flushing and site care. b) Either peripheral access or nontunneled central venous
There is a higher rate of catheter malposition, self-care is difficult access and PICCs can serve patients requiring acute short-

92 A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. © 2005 A.S.P.E.N. www.nutritioncare.org.
 S E C T I O N I Fundamentals of Nutrition Support Practice and Management

B. Flushing: maintains catheter patency and reduces fibrin or thrombus

TABLE 6-1. Length of Therapy for Various Types of formation. In addition, very low doses (1 mg/day) of warfarin can
Venous Access protect against thrombosis in patients with long-term central venous
access.16
Type of Access Length of Therapy 1. Frequency and dosage are dependent on catheter type, usage,
and institutional protocols.
Nontunneled CVC Weeks 2. Although saline and heparin have been shown to be equally effi-
Tunneled CVC Months to years cacious for flushing peripheral catheters, most protocols endorse a
PICC Months heparin solution for routine flushing of CVCs (except Groshong).
Port Months to years 3. There is a lack of consensus regarding the volume, frequency,
and concentration of heparinized solutions for flushing.
a) Flushing volumes range from 1 to 5 mL.
CVC, central venous catheter; PICC, peripherally inserted central catheter.
b) Heparin concentrations range from 1 to 1000 units/mL; the
concentration most frequently used is 10 units/mL.
term infusion therapy, depending on whether the prescribed c) Flushing is most often done daily, except for with ports, which
therapy mandates central access. are flushed every 4 weeks.
2. Type: Single infusion or multiple infusions differentiate the need 4. Groshong catheters are flushed weekly with sodium chloride
for single- versus multiple-lumen catheters. Most patients requir- 0.9% (normal saline).
ing home PN can be managed with a single-lumen catheter, infus- C. Hub care: reduces intraluminal contamination at the catheter hub.
ing PN nightly and other IV medications around the scheduled Disinfection, often with 70% alcohol, is done during manipulations
PN infusion. (eg, tubing changes) at the catheter hub.1
3. Need for frequent blood sampling D. In the hospital setting, IV tubing is changed no more frequently than
4. Drug volume and rate of administration every 72 hours, with the exception of tubing used for blood infusions
and intravenous fat emulsions, which should be changed within
VI. Central Venous Catheter Care and Maintenance 24 hours.1 In the home setting, PN tubing should be changed daily.
E. Port access mandates skin antisepsis before needle insertion. Pro-
A. Site care: considered one of the most important measures for tocols vary from aseptic technique to sterile technique with a mask
decreasing catheter-related infections; aimed at reducing micro- and sterile gloves when ports are accessed.
bial colonization through skin antisepsis and dressings at the F. Specific CVC care and maintenance (see Table 6-2)
insertion site G. Long-term complications17
1. Common antiseptics include chlorhexidine 2%, povidone-iodine 1. Infection (see Chapter 8)
10%, alcohol 70%, and tincture of iodine. The use of acetone to 2. Occlusion and thrombosis (see Chapter 8)
defat the skin has been shown to have no efficacy in reducing 3. Catheter breakage
catheter infections. A 2% chlorhexidine–based preparation is the a) External catheter segment. Tunneled, cuffed long-term
agent of choice for cleaning the skin prior to access.1,12 catheters can be repaired with proprietary repair kits. If
2. Antimicrobial ointments should not be used.1 Studies addressing these kits are not immediately available, a temporary repair
the application of antimicrobial ointments to the skin site have can be done with a 16-gauge blunt-end needle inserted into
contradictory findings. There is concern that fungal infections the catheter and secured. Catheters that cannot be repaired
may be associated with the use of antibacterial ointments. must be removed and replaced.
3. Protocols vary with the type of catheter dressing, the interval for b) Fracture of the internal catheter segment is related to catheter
dressing changes, and the frequency of site observation for signs “pinch-off syndrome.” Access devices are inserted via the
of local infection. The two types of dressings most often used are subclavian vein course between the clavicle and the first
transparent dressings and gauze dressings. Either sterile gauze or rib. In certain patients, this anatomical angle is narrow and
sterile transparent semipermeable dressing can be used to cover causes catheter compression that presents as occlusion.
the catheter site. Tunneled CVC sites that are well healed may not This syndrome is confirmed when the occlusion is relieved
require a dressing.1,14 with postural changes, such as raising the arm, and by radi-
a) Gauze dressings should be replaced every 2 days; transparent ologic findings of catheter luminal narrowing in this area.
dressings should be changed every 7 days.1 Although this complication is rare, it can result in catheter
b) The simplicity of gauze dressings makes patient self-care embolus. Catheter removal is appropriate with pinch-off
easier. syndrome. Replacement should be on the opposite side if
c) Transparent dressings allow for continuous inspection of the possible; use of a more lateral approach may prevent this
site and aid in securing the catheter. complication.18
4. A sustained-release chlorhexidine gluconate patch is available for 4. Catheter malposition can present as a catheter malfunction with
placement around the catheter insertion or exit site. A gauze or symptoms of thrombosis, occlusion, or perforation. Catheters
transparent dressing is then applied over the patch. Limited stud- with tip malposition can be replaced or repositioned under fluoro-
ies have shown a reduction in the rate of catheter-related blood- scopic guidance.
stream infections.
5. Collodion, a solution of pyroxylin in ether and alcohol that pro-
VII. Peripheral Access19
vides an occlusive transparent film after application, has been
used as a dressing. This dressing is both bacteriostatic and in- A. Parenteral nutrition may be administered by peripheral venous
expensive, but very limited studies are available to date.15 access when the therapy is expected to be short term (10 –14 days),

© 2005 A.S.P.E.N. www.nutritioncare.org. A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. 93
S E C T I O N I Fundamentals of Nutrition Support Practice and Management

TABLE 6-2. CVC Maintenance

Catheter Type Site Care Flushing

Nontunneled CVC Dressing: transparent or gauze Internal volume: 0.1±0.53 mL

Transparent enhances catheter stability 1±2 mL flush is adequate
Performed as a sterile dressing Frequency: usually daily
Skin antisepsis protocols include one or a combination of
the following: (1) 70% alcohol(3 swabs); (2) 10%
povidone-iodine (3 swabs).

Tunneled cuffed CVC Dressing: transparent or gauze until incision heals Internal volume: 0.15–1.8 mL
Dressings often discontinued once incision heals and suture is removed. Frequency: usually daily
Performed as sterile dressing antisepsis (see above) Groshong catheters: 5 mL 0.9%
Hydrogen peroxide may be used to remove crusting at the site saline weekly

PICC Dressing: transparent preferred to enhance catheter stability Internal volume: 0.04–1.2 mL
Performed as sterile dressing antisepsis (see above) 2–3 mL flush adequate
Dressings required as long as catheter is in place Frequency: daily

Ports Dressing until incision healed (several days postop) Internal volume: 0.5–1.5 mL
Transparent dressing when port is accessed to stabilize needle At least 3 mL adequate
Huber needle change at least every 7 days Frequency: every 4 weeks
Skin antisepsis as above prior to needle placement
Sterile approach is recommended during needle insertion and dressing change

CVC, central venous catheter; PICC, peripherally inserted central catheter.

Reprinted with permission from Krzywda EA, Andris DA, Edmiston CE, Wallace JR. Parenteral access devices. In: Gottschlich MM, ed. The Science and Practice of Nutrition Sup-
port: A Case-Based Core Curriculum. Dubuque, IO: Kendall Hunt/American Society for Parenteral and Enteral Nutrition; 2001:225–250.

fluid restriction is not necessary, and formulation osmolarity is distance from the site of thrombophlebitis, preferably on the
<600 to 900 mOsm/L. contralateral side.
B. Adequate peripheral veins are necessary for successful peripheral G. Prophylaxis against peripheral vein thrombophlebitis during periph-
venous access administration. eral venous access19
C. General principles of catheter care and maintenance, as noted above, 1. Combine heparin (1 unit/mL) and hydrocortisone (10 mg/L).
apply to peripheral catheters. This approach has not been evaluated in the pediatric popula-
D. Peripheral catheters include standard peripheral cannulas, midline tion, however.
catheters, and midclavicular catheters. Often referred to as extended- 2. Use topical nonsteroidal anti-inflammatory creams and gels.
dwell peripheral catheters, midline catheters are advanced approxi- 3. Minimize solution osmolarity to <600 mOsm/L. There are some
mately 5 to 7 inches into the vein, and midclavicular catheters reports of infusions of 800 to 1000 mOsm/L with the use of meas-
involve distal tip placement at the axillary and subclavian junction. ures such as the addition of heparin and hydrocortisone.
Neither of these placements provides central venous access. Midline 4. Buffer infusion formulations with sodium bicarbonate within the
catheters are not recommended for administration of PN due to the pH range 7.2 to 7.4.
risk of upper extremity thrombosis. 5. Include iso-osmolar lipid emulsions to provide additional calories
E. Peripheral catheters remain at risk for complications associated and lower osmolarity.
with infection and occlusion; however, the principal complication
is peripheral vein thrombophlebitis. VIII. Infusion Delivery Devices
F. Catheter recommendations for peripheral venous access A. Infusion delivery devices provide for accurate and safe administra-
1. Use fine-bore cannulas. tion of IV therapies, including PN.
2. Polyurethane is the preferred catheter material. B. Significant technological advancements in these devices are related
3. Use large veins and avoid placement across joints. to the expansion of home IV therapies over the past 2 decades.
4. Inspect cannula site daily. C. Device classification1
5. Standard peripheral cannulas require site rotation every 72 to 96 1. Gravity infusion devices: manual regulation of drop chamber,
hours in adult patients but are not routinely changed in the pedi- associated with a high degree of inaccuracy, not used for PN
atric population. Midline catheters may be used for up to 4 weeks, infusions
and midclavicular catheters may be used for 2 to 3 months.19 2. Controllers: maintain a regular drop rate with no mechanical
6. The cannula should be removed as soon as thrombophlebitis parts, incapable of high volumes, not used for PN
develops. The replacement cannula should be inserted at some 3. Syringe devices: control fluid delivery from a syringe and a

94 A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. © 2005 A.S.P.E.N. www.nutritioncare.org.
 S E C T I O N I Fundamentals of Nutrition Support Practice and Management

Table 6-3. Summary of Ambulatory and Stationary Infusion Devices20–22

Ambulatory infusion devices Stationary infusion devices

Availability >25 devices marketed Approximately 10 devices marketed

Size Small and lightweight (approximately 8 ounces) Heavier (approximately 12 pounds)
Patient mobility Designed for patient to remain ambulatory Mounted on pole—requires patient to remain homebound
Flow rate/volumes Wide range Wide range
Alarms/safety measures Wide range Wide range
Automatic programming Yes Yes
Administration set Many require proprietary set May use generic set
Cost acquisition Usually 20% to 25% more expensive Lower up-front cost
Patient indications Allows for mobility Use for nighttime infusions

CVC, central venous catheter; PICC, peripherally inserted central catheter.

Reprinted with permission from Krzywda EA, Andris DA, Edmiston CE, Wallace JR. Parenteral access devices. In: Gottschlich MM, ed. The Science and Practice of Nutrition Sup-
port: A Case-Based Core Curriculum. Dubuque, IO: Kendall Hunt/American Society for Parenteral and Enteral Nutrition; 2001:225–250.

motor-driven piston, appropriate for low-volume infusions, used E. Reimbursement: Increasingly, providers are choosing stationary
for neonatal PN infusion devices because of the lower acquisition prices and the
4. Infusion pumps ability to use less costly administration sets.
a) Electronic devices that provide accurate volume (rate) control
and free-flow protection; visual and auditory safety alarms (Parenteral Nutrition Access and Infusion Equipment chapters from
indicate increased pressure or air within the system and signal the first edition were contributed by Elizabeth A. Krzywda, Charles E.
infusion completion. Additional features may include pro- Edmiston, Jr, Kristy Gibbons, Nancy Cyr, Michael L. Christensen,
grammable automatic cycling and rate tapering. and Richard A. Helms)
b) The basic types commonly used for PN administration are
REFERENCES
ambulatory infusion devices and stationary infusion devices.
D. Comparative features of ambulatory infusion devices and stationary 1. O’Grady NP, Alexander M, Dellinger EP, et al. Guidelines for the preven-
infusion pumps (see Table 6-3) tion of intravascular catheter-related infections. Centers for Disease Con-
trol and Prevention; Aug 9, 2002. MMWR Recomm Rep. 51(RR-10):1–29.
2. McGee DC, Gould MK. Preventing complications of central venous
IX. Infusion Delivery Device Selection Criteria 20–22 catheterization. N Engl J Med. 2003;348:1123–1133.
3. Whitman ED. Complications associated with the use of central venous
A. Appropriate device selection, especially in the outpatient setting or access devices. Curr Probl Surg. 1996;33:311–378.
alternative site, is dependent on the patient, the therapy (length and 4. Raad II, Hohn DC, Gilbreath BJ, et al. Prevention of central venous
type), and cost-effectiveness/reimbursement. catheter-related infections by using maximal sterile barrier precautions
B. Key patient characteristics during insertion. Infect Control Hosp Epidemiol. 1994;15:231–238.
1. Age, diagnosis, and overall condition 5. Howell PB, Walters PE, Donowitz GR, Farr PM. Risk factors of infection
2. Ambulation status of adult patients with cancer who have central venous catheters. Cancer.
3. Lifestyle and mobility 1995;15:1367–1374.
6. Kim SW, Petersen RV, Lee ES. Effect of phthalate plasticizers on blood
4. Manual dexterity
compatibility of polyvinyl chloride. J Pharm Sci. 1976;65:670–673.
5. Cognitive ability
7. Williams D. Implantable prostheses. Phys Med Biol. 1980;25:611–636.
6. Caregiver involvement 8. Larsson N, Stemberg K, Linder L, Curelaru I. Cannula thrombophlebitis:
C. Therapy a study in volunteers comparing polytetrafluoroethylene, polyurethane,
1. Single infusion or multiple drugs and polyamide-ether-elastomer cannula. Acta Anaesthesiol Scand.
2. Continuous or intermittent infusion 1989;33:223–231.
3. Length of infusion cycle 9. Trooskin SZ, Mikulaschek AW. Biomaterials used for catheters. In: Greco
4. Volume of infusion RS, ed. Implantation Biology. Boca Raton, FL: CRC Press; 1994:270–271.
D. Cost-effectiveness of the infusion device21,22 10. Shorr AF, Humphreys CW, Helman DL. New choices for central venous
1. Ease of staff training catheters. Chest. 2003;124:275–284.
2. Ease of patient training 11. Orr M. Issues on the management of percutaneous central venous catheters:
single and multiple lumens. Nurs Clin North Am. 1993:28:911–919.
3. Complications associated with device
12. Crnich CJ, Maki DG. The promise of novel technology for the prevention
4. Pharmacy time
of intravascular device-related bloodstream infection, I: pathogenesis and
5. Amount of waste and ease of disposal short-term devices. Clin Infect Dis. 2002;34:1232–1242.
6. Storage space at both patient’s home and provider’s ___location 13. Crnich CJ, Maki DG. The promise of novel technology for the prevention
7. Product availability and manufacturer’s support of intravascular device-related bloodstream infection, II: long-term
8. Downtime and repair costs devices. Clin Infect Dis. 2002;34:1362–1368.
9. Inventory costs 14. Zitella L. Central venous catheter site care for blood and marrow transplant
10. Overall product reliability recipients. Clin J Oncol Nurs. 2003;3:289–298.

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S E C T I O N I Fundamentals of Nutrition Support Practice and Management

15. Babycos CR, Barracos A, Mancuso J, Turner-Marse T. Collodion as a 21. Saladow J. Ambulatory electronic infusion systems: making sense of the
safe, cost-effective dressing for central venous catheters. South Med J. options. Infusion. July 1995:9–21.
1990;83:1286–1288. 22. Saladow J. Stationary infusion pumps used in home care: making sense of
16. Bern MM, Lokich JJ, Wallach SR, et al. Very low doses of warfarin can the options. Infusion. September 1995:11–17.
prevent thrombosis in central venous catheters. Ann Intern Med.
1990;112:423–428.
17. Moureau N, Poole S, Murdock MA, Gray SM, Semba CP. Central venous SUGGESTED READINGS
catheters in home infusion care: outcomes analysis in 50,471 patients. Holcombe BJ. Adult parenteral nutrition. In: Young LY, Koda-Kimble MA, eds.
J Vasc Interv Radiol. 2002;13:1009–1016. Applied Therapeutics: The Clinical Use of Drugs. 8th ed. Philadelphia, PA:
18. Andris D, Krzywda EA, Schulte W, Ausman R, Quebbeman EJ. Pinch-off Lippincott Williams and Wilkins; 2004:35.
syndrome: a rare etiology for central venous catheter occlusion. J Parenter Task Force for the Revision of Safe Practices for Parenteral Nutrition. Safe prac-
Enteral Nutr. 1994;18:531–533. tices for parenteral nutrition. J Parenter Enteral Nutr. 2004;28:S29-S70.
19. Payne-James J, Khawala HT. First choice for total parenteral nutrition: the Vanek VW. The ins and outs of venous access: part I. Nutr Clin Pract.
peripheral route. J Parenter Enteral Nutr. 1993;17:468–478. 2002;17:85–98
20. Saladow J. Ambulatory systems for I.V. antibiotic therapy: making sense Vanek VW. The ins and outs of venous access: part II. Nutr Clin Pract.
of the options. Infusion. April 1995:17–29. 2002;17:142–155.

96 A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. © 2005 A.S.P.E.N. www.nutritioncare.org.
 Vanessa J. Kumpf, PharmD, BCNSP;
Jay M. Mirtallo, MS, RPh, BCNSP;
Craig Petersen, RD, CNSD 7
Parenteral Nutrition
Formulations: Preparation
and Ordering
Introduction 2. Carbohydrate source: Carbohydrate serves as the primary energy
substrate in a PN formulation. The patient’s energy requirements
Parenteral nutrition (PN) is defined as nutrients provided intravenously. and glucose oxidation rate, and the desired balance of carbohydrate
From a pharmaceutical perspective, a PN formulation is a complex and fat calories, determine the amount of carbohydrate in a given
admixture of individual chemicals, all having physicochemical proper- PN admixture.
ties that influence their behavior when combined in a single container. a) Dextrose monohydrate is used almost exclusively in PN solu-
A thorough understanding of the available nutrient products used in the tions as the source of carbohydrate calories. Dextrose mono-
PN admixture is necessary to formulate a safe and clinically appropri- hydrate provides 3.4 kcal/g, and base solutions are available
ate end product. The many factors that influence the end product include in a range of concentrations, from 5% to 70%.
concentration, composition, and pH of base solutions; stability of base b) Glycerol is a naturally occurring sugar alcohol that is used as
solutions; microbial growth potential; and compatibility of nutrient an alternative source of energy in some PN formulations. It
components. This chapter provides an overview of these issues in both yields 4.3 kcal/g and has been shown to be protein sparing when
the adult and pediatric populations. Guidelines regarding appropriate used concomitantly with amino acids.3
ordering and labeling of PN formulations are also provided with the 3. Fat source: Fat is delivered in the form of stabilized emulsions.
intent to promote safe practice. These emulsions provide essential fatty acids and are a concen-
trated source of calories.
I. Formula Design
a) Long-chain fatty acid (LCFA) emulsions currently are the only
II. Compatibility Issues
commercially available source of intravenous fat emulsions
III. Stability Issues
(IVFE) in the United States. These fat emulsions are made from
IV. Microbial Growth Potential
either soybean oil or a mixture of safflower and soybean oils.4,5
V. Automated Compounding
VI. Off-Site Compounding Centers They are available as concentrations of 10%, 20%, and 30% fat
VII. Ordering PN Formulations emulsions. IVFE also contain egg phosphatides as an emulsi-
VIII. Labeling PN Formulations fier and glycerol to adjust the osmolarity.
References b) Medium-chain fatty acid (MCFA)/LCFA physical mixtures
are available in Europe. Two separate triglyceride sources,
MCFA and LCFA, are combined to create these mixtures.
I. Formula Design MCFA/LCFA mixtures take advantage of the fact that MCFAs
A. Components of a PN admixture are more rapidly oxidized for energy than LCFAs. The LCFA
1. Protein source: Amino acids are included in the PN admixture as provides a source of essential fatty acids.6
the source for new protein synthesis. c) MCFA/LCFA structured lipids are similar to the MCFA/LCFA
a) Crystalline amino acid solutions are classified as either stan- physical mixture in that they combine the properties of the two
dard or specialized. The standard amino acid solutions contain types of fatty acids. However, the structured lipid is created
a balanced or physiologic mixture of essential and nonessen- through hydrolysis of triglycerides and transesterification of
tial amino acids.1 The base solutions are available in a range of fatty acids to form a composite triglyceride molecule that has
concentrations from 3% to 20%. The specialized amino acid various proportions of both MCFA and LCFA. The structured
solutions contain mixtures of amino acids designed to meet lipids are thought to have an advantage over the physical mix-
disease- or age-specific amino acid requirements. ture of MCFA and LCFA because of a slower rate of release
b) Amino acid compositions of commercially available formula- and utilization of the MCFA.6 These products are currently
tions intended for infant use have an amino acid profile that has investigational only.
been demonstrated to result in plasma amino acid levels in the 4. Water: Sterile water is added to most PN admixtures to adjust the
same range as those seen 2 hours postprandial in the breast-fed total volume of fluid needed to meet the prescribed 24-hour fluid
infant. These specialized amino acid formulations also contain intake via PN. This is a convenient and economical way to create
taurine, which is involved in the conjugation of bile acids. Cys- a PN admixture when concentrated dextrose, amino acids, and
teine can be added separately at the time of preparation. Infant IVFE are used as the base products.
amino acid formulations are more acidic than standard amino 5. Electrolytes: Electrolytes are included in the PN admixture to
acid products.2 This acidity enhances calcium and phosphorus maintain electrolyte homeostasis. Electrolyte balance is depend-
solubility and allows higher concentrations of these two nutri- ent on many factors, such as renal function, acid-base balance,
ents without causing precipitation. gastrointestinal losses, and medications. Therefore, electrolyte

© 2005 A.S.P.E.N. www.nutritioncare.org. A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. 97
S E C T I O N I Fundamentals of Nutrition Support Practice and Management

intake needs to be individualized in many patients. In stable, Single-entity parenteral vitamin products include vitamin B1
uncomplicated patients, a multiple-electrolyte formulation con- (thiamine), vitamin B2 (riboflavin), vitamin B6 (pyridoxine),
taining standard doses of several electrolytes or several single- vitamin B12 (cyanocobalamin), folic acid, vitamin C, vitamin A,
entity electrolyte solutions may be used in a PN admixture. The and vitamin K. Vitamin D can also be given by intramuscular
electrolyte composition of PN admixtures is also dependent on administration.
the compatibility of each electrolyte with the other components 7. Trace minerals are essential to normal metabolism and growth.
of the PN admixture (see Section II.B). Although relatively minute amounts of trace minerals are
a) Sodium is available as the chloride, acetate, bicarbonate, phos- required, deficiency states may develop fairly rapidly when
phorus, or lactate salt. The bicarbonate form should not be used increased metabolic requirements (eg, burn injury), increased
in PN admixtures, as it may cause precipitation of other addi- losses (eg, large-volume fistula output), or rapid growth are
tives, particularly calcium and magnesium. Lactate is consid- present. The recommended daily requirement (plus supplemen-
ered an inferior choice relative to acetate, as acetate is more tal replacement doses as needed for increased requirements or
readily metabolized to bicarbonate intravenous (IV) sodium losses) should be included in all PN admixtures. There are, how-
and is dosed in milliequivalent units. ever, clinical conditions necessitating trace mineral restriction
b) Potassium is available as the chloride, acetate, or phosphorus (eg, decreased copper and manganese excretion with biliary dis-
salt. IV potassium is dosed in milliequivalent units. ease), and therefore the recommended daily requirement may
c) Phosphorus is available as the sodium or potassium salt. IV need adjustment. Trace minerals available for parenteral admix-
phosphorus is dosed in millimoles. ture include chromium, copper, iodine, iron, manganese, molyb-
d) Magnesium is available as the sulfate or chloride salt. IV mag- denum, selenium, and zinc.
nesium is dosed in milliequivalent units. a) Standard multiple–trace element solutions are available in sev-
e) Calcium is available as the chloride or gluconate salt. Calcium eral combinations with as few as four (chromium, copper, man-
gluconate is the preferred form of calcium for PN admixtures ganese, zinc) and as many as seven (chromium, copper, iodine,
because it is more stable in solution and, therefore, is less likely manganese, molybdenum, selenium, zinc) trace elements. The
to dissociate and form a precipitate with phosphorus. IV cal- doses of each trace element in the recommended daily volume
cium is dosed in milliequivalent units. for admixture usually are based on the American Medical Asso-
f) The choice of the chloride versus acetate salt of sodium and ciation National Advisory Group recommendations for daily
potassium depends on the patient’s acid-base status. Generally, parenteral trace element intake.10 Separate products exist for
acid-base balance can be maintained by using approximately adult and pediatric patients.
equal amounts of chloride and acetate (ie, a 1:1 ratio). Acetate b) Single-entity trace element solutions are available to use when
and chloride are also present in the base amino acid solutions individual trace element requirements cannot be met with the
in various amounts. If a patient has altered acid-base status, the multiple–trace element products. Single-entity products exist
chloride-acetate ratio may need to be adjusted. For example, if for chromium, copper, iodine, iron, manganese, molybdenum,
metabolic acidosis is present, maximum acetate and minimum selenium, and zinc. Iron dextran may be added to non-IVFE-
chloride should be used in the PN admixture. Conversely, if containing PN formulations but requires caution due to com-
metabolic alkalosis is present, maximum chloride and mini- patibility limitations.11 It should not be added to a total nutrient
mum acetate should be used. admixture (TNA) because it can destabilize the IVFE (see Sec-
6. Vitamins are added to the PN admixture daily, usually as a fixed tion II.C.2). Iron sucrose and sodium ferric gluconate provide
dose using a multivitamin preparation. Parenteral vitamins have therapeutic options for the parenteral supplementation of iron,
limited stability once they are added to the PN admixture. In gen- but compatibility data with PN formulations are not available.11
eral, they are stable for 24 hours.7 B. Contaminants of PN formulation components: Many components of
a) Adult: Available parenteral multivitamin products for adults the PN formulation have been shown to be contaminated with trace
contain 12 or 13 known vitamins (with or without vitamin elements such as zinc, copper, manganese, chromium, selenium, and
K). In 2000, the US Food and Drug Administration (FDA) aluminum.12 Manganese and aluminum appear to be the most clini-
amended requirements for marketing an “effective” adult cally relevant trace element contaminants.
parenteral vitamin formulation and recommended changes to 1. Aluminum: Toxicity due to aluminum contamination in PN for-
the 12-vitamin formulation that had been available for over mulations can cause significant clinical problems.13 As a result,
20 years.8 The new requirements call for increased dosages of the FDA developed regulations that require manufacturers to
vitamins B1 (thiamine), B6 (pyridoxine), C (ascorbic acid), and disclose on the label the aluminum content of small- and large-
folic acid as well as addition of vitamin K. An adult parenteral volume parenteral products used in the preparation of PN (as of
vitamin formulation meeting the 2000 reformulation require- July 2004).14
ments but without vitamin K has also received FDA approval a) The safe limit of aluminum in PN has been set at 5 mcg/kg/
and is commercially available. day.14
b) Pediatric: Parenteral multivitamin products are available for b) The intent of the regulation is to educate health care practi-
pediatric patients who are up to age 11 years or who weigh up tioners about aluminum exposure and facilitate the preparation
to 40 kg. They are formulated to comply with the Subcommit- of low-aluminum parenteral solutions to patients in high-risk
tee on Pediatric Parenteral Nutrient Requirements of the Com- groups.
mittee on Clinical Practice Issues of the American Society for c) High-risk groups include infants and neonates receiving PN for
Clinical Nutrition.9 a period longer than 10 days and any patient receiving long-
c) Individual vitamin products are used to supplement multivita- term PN who has renal compromise.
min doses when a deficiency state exists or when there are d) Renal compromise is associated with central nervous system
increased needs because of a disease or clinical condition. manifestations of aluminum toxicity.

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e) Infants and neonates are extremely vulnerable to aluminum (5) Ease of administration for home PN patients: Using a sin-
toxicity, which is manifested by alterations in bone formation gle container per day rather than piggybacking a separate
and mineralization, encephalopathy, and impaired neurologic container of lipid into the PN admixture is simpler for most
development.13,14 These patients are at higher risk because of patients. It eliminates the need for two separate infusion
the excess aluminum burden per kg body weight infused with pumps and administration sets. As a result, it can signifi-
PN, the infant’s inability to regulate the body’s aluminum con- cantly improve quality of life.
tent due to immature renal function, and the impact of alu- (6) Better fat utilization: A slow, continuous infusion of IVFE
minum on growth and development. has been shown to be better tolerated than a shorter IVFE
f) Aluminum contamination of products used in PN preparation infusion period, as demonstrated by reticuloendothelial
comes primarily from raw materials during the manufacturing system impairment.18,19
process and can therefore vary by manufacturer and lot. The alu- b) Disadvantages
minum sources of most concern are calcium and phosphate salts. (1) Diminished stability and compatibility: Addition of IVFE
g) Adults receiving long-term home PN have had problems with to the PN admixture decreases the overall stability of the
osteopenia and bone mineralization, in part caused by alu- fat emulsion. If the fat emulsion separates from the other
minum.13 This problem has been partially improved by the components after it is prepared and then is infused, there
replacement of casein hydrolysates with crystalline amino could be potentially life-threatening consequences (see
acid products as the source of protein and reduction in the alu- Section III.B). There are limitations to the amounts of
minum in PN formulations. nutrients that can be combined when IVFE is present in
2. Manganese: Manganese toxicity associated with PN has been the PN admixture. This is due to the properties of the fat
reported, most notably in long-term home PN patients.15 Hyper- emulsion and the ease with which it can be disrupted by
manganesemia may lead to manganese deposition in the basal substances such as divalent and trivalent electrolytes (see
ganglia and neurological symptoms. Manganese contamination of Section II.B.).
PN additives has been identified as a factor contributing to hyper- (2) Impaired visual inspection of the TNA: Addition of IVFE
manganesemia. The level of contamination appears to vary by renders the PN admixture opaque. Therefore, visual inspec-
manufacturer and lot number. Manganese concentrations ranging tion, one of the most frequently used methods of checking
from 8 to 22 mcg per total daily volume have been reported in PN for solution impurities or precipitates, is obscured. This
formulations with no added manganese.16 It may, therefore, be increases the risk of infusing an admixture that may harm
necessary to eliminate the use of multiple–trace element products the patient.20–21
that contain added manganese in long-term home PN patients D. Order of admixing: The order in which the components of a PN
with hypermanganesemia and instead use single-entity trace admixture are combined can affect the overall stability of the final
element solutions. product. The additive sequence in compounding must be opti-
C. Types of PN formulations mized and validated as a safe and efficacious method.22 The order
1. Dextrose/amino acids (2-in-1): Dextrose and amino acids are of admixing is determined by the method used (eg, automated vs
mixed with electrolytes, vitamins, and trace elements. These for- gravity).
mulations are typically mixed in single-liter volumes. However, in 1. Automated compounding: The procedure depends on the spe-
some circumstances the components may be in a container that pro- cific automated compounding device being used. Assistance in
vides a 24-hour supply of nutrients. IVFE are infused separately. optimizing the compounding order for automated devices should
2. TNAs: Under specific circumstances, IVFE can be admixed be obtained through consultation with the manufacturer of
with the other components of PN to create a TNA.17 All the par- macronutrients being used as well as the manufacturer of the com-
enteral nutrient components are mixed in one container that sup- pounding device because brand-specific issues might influence the
plies the 24-hour nutrient intake. There are both advantages and compatibility of the final formulation.22
disadvantages associated with a TNA when compared to a 2-in-1 2. Gravity transfer: The steps below should be followed in the order
formulation with a separate IVFE infusion.18 presented (step a first and step j last) to optimize the stability of
a) Advantages the PN admixture.23
(1) Decreased nursing time: Since a TNA system uses only one a) Combine dextrose, amino acids, and water.
container per day, nursing time involved in IV setup and b) Add phosphorus.
administration is decreased. c) Add sodium, potassium, and magnesium (in any order).
(2) Decreased risk of touch contamination: Fewer manipula- d) Add trace minerals.
tions of the catheter and administration set are required, e) Agitate the solution well.
decreasing the risk of touch contamination. This may f) Add calcium (or a calcium-containing multielectrolyte solu-
decrease the risk of catheter-related infection. tion) and agitate the solution well again.
(3) Decreased pharmacy preparation time: Compared with g) Observe the solution for precipitates or contaminants (eg,
admixing multiple single-liter containers of the PN admix- rubber cores). If either is present, discard the solution. If a
ture for each patient each day, it takes less time to admix a precipitate is present, review the quantities of additives for
single 24-hour supply of the PN admixture, especially if an incompatibilities (especially calcium and phosphorus; see Sec-
automated compounder is available. tion II.B.1) and adjust nutrient doses as needed to achieve com-
(4) Cost savings: Less nursing and pharmacy time plus fewer patibility (see Section II.B.1.e). Review the order of mixing and
materials used in admixing and administering the PN for- remix the solution.
mulation result in lower cost. For example, the infusion h) If a TNA is being admixed, add the IVFE next, gently agi-
pump and administration set for a separate IVFE infusion tate, and observe for signs of the emulsion cracking (see
are not required. Section III.B.2).

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S E C T I O N I Fundamentals of Nutrition Support Practice and Management

i) Add vitamins last, as close to the time of administration of the this results in the formation of insoluble product. Calcium salts are
PN admixture as possible. For home PN patients, the patient one of the most reactive compounds and readily form insoluble
or caregiver should add vitamins just prior to infusion. products with a number of additives. Dibasic calcium phosphate
j) Note that when a TNA is admixed, dextrose and IVFE should is one of the most dangerous combinations and has resulted in
never be added directly to one another. The low pH of dextrose embolic deaths when infused.20 Although the potential for precip-
solutions will disrupt the IVFE. itation of calcium phosphate is well documented, this precipitation
E. Admixture osmolarity refers to the osmoles of solute per liter of solu- remains difficult to predict because of the many contributing fac-
tion. Osmolarity is measured in milliosmoles per liter (mOsm/L). PN tors.21 Some of the known factors include the following:
admixture osmolarity is important because the IV access site used for a) Increased temperature increases the likelihood of a precipitate
a given infusion is dictated by admixture osmolarity. The higher the forming because of increased dissociation of calcium from
osmolarity, the larger the vein needed to accommodate the formula- gluconate and of potassium and sodium from phosphate. This
tion. A formulation with high osmolarity infused into a small periph- increases the chance for collision between the calcium and
eral vein will cause irritation and pain, with damage to the vessel phosphate ions.
(phlebitis), which will necessitate frequent changes of the IV site. b) Calcium gluconate is the preferred salt form of calcium, as it
1. Central vein infusion guidelines: Due to the high osmolarity of is more stable than an equivalent amount of calcium chloride.22
most PN formulations, they are limited to administration through c) Increased solution pH increases the likelihood of precipitation
a central venous access catheter with tip placement in the superior because the amount of dibasic phosphate is increased. An acidic
vena cava adjacent to the right atrium.22,24 Because of the high rate pH is more favorable to calcium phosphate solubility. Acidity
of blood flow through the central vein, the formulation is rapidly is especially influenced by the type and amount of amino acid
diluted and is not harmful to the vessel. There are no known upper solution used, as pH varies with the many available amino acid
limits to solution osmolarity via the central vein; however, the products. The pH of the amino acid solution helps maintain the
maximum is usually limited by the concentration of available base pH of the PN admixture because of its buffering capacity.
solutions used in compounding the PN formulation. Neonatal/infant amino acid solutions are specifically designed
2. Peripheral vein infusion guidelines: Typically, a peripheral vein with a lower pH to enhance calcium and phosphorus solubility.
can tolerate a formulation of up to 600 mOsm/L without any irri- Addition of L-cysteine hydrochloride to the PN formulation
tation or damage. As the osmolarity of the formulation increases containing neonatal/infant amino acid solutions will further
above 600 mOsm/L, the likelihood of vein irritation and dam- reduce pH and improve solubility.27
age increases. Data indicate that an appropriate standard max- d) Order of mixing is extremely important to avoid the formation
imum osmolar concentration for a peripheral PN admixture is of an insoluble precipitate (see Section I.D). In general, phos-
900 mOsm/L.25 phate should be added first, and calcium should be added near
3. Estimating osmolarity: Formulation osmolarity can be estimated the end of the compounding sequence to take advantage of the
by adding the osmolar contribution from each component of the maximum volume of the PN formulation.22
PN formulation and dividing by the total volume (in liters) of the e) Increased quantities of calcium and phosphorus in the PN
formulation. The approximate osmolar contribution of commonly admixture favor precipitation. Clinicians should refer to doc-
used components of a PN admixture is as follows22: umented solubility curves provided by the manufacturers of
a) Amino acids: 1 g = 10 mOsm amino acid products and published sources to guide calcium
b) Dextrose: 1 g = 5 mOsm and phosphorus limitations.2 When a PN order is written for
c) 20% IVFE: 1 g = 0.71 mOsm (product dependent) potentially incompatible amounts of calcium and phosphorus,
d) Calcium gluconate: 1 mEq = 1.4 mOsm verification of the patient’s requirements should be obtained
e) Magnesium sulfate: 1 mEq = 1 mOsm and adjustments in the doses should be made as appropriate.28
f ) Potassium (chloride, acetate, or phosphate salt): 1 mEq = In some cases, if high calcium or phosphorus requirements
2 mOsm exist, the requirement for one of the electrolytes may need to
g) Sodium (chloride, acetate, or phosphate salt): 1 mEq = be met by some route and vehicle other than the PN admixture.
2 mOsm f) Increased time of exposure of calcium and phosphorus in the
PN admixture may result in formation of an insoluble precip-
itate. The likelihood increases as the PN admixture warms.
II. Compatibility Issues
Therefore, frequent agitation and observation for precipitates
A. General considerations: Ensuring compatibility among all the com- in the product are important.
ponents of a PN admixture is a prerequisite to using PN safely. Every g) It should be emphasized that precipitation of calcium phosphate
effort must be made to ensure compatibility to avoid complica- (or any other substance) is obscured by the presence of IVFE in
tions.20–22 Although data do not exist to predetermine the compatibil- a TNA. Therefore, additional caution is warranted when a TNA
ity of every possible nutrient combination in a PN admixture, general is prepared, and calcium and phosphorus limitations must be
guidelines do exist and are key to minimizing the risk of incompati- known and followed.
bility. An appropriate caution, however, is “When in doubt, don’t.” 2. Bicarbonate salts are incompatible with PN admixtures and should
The factors known to affect the compatibility of any given additive not be used. Bicarbonate reacts with calcium to form the insoluble
include concentration, temperature, pH, length of time of exposure of product calcium carbonate.22 The addition of bicarbonate to the
the additive and the PN admixture, and order of mixing.26 The most acidic PN admixture can also result in formation of carbon
common compatibility issues will be discussed here. dioxide and loss of the bicarbonate ion.
B. Nutrient additives C. TNA
1. Calcium and phosphorus: Solid precipitates can develop when an 1. General considerations: Adding IVFE to a PN admixture changes
incompatible combination of salts is added to a PN formulation; the overall physiochemical properties of the product. Most notable

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is the fact that when dextrose and IVFE alone are combined, they may be dramatically altered. The general factors affecting PN
are incompatible with each other because the low pH of IV dex- admixture stability are discussed below.
trose solutions disrupts the IVFE. The presence of the amino acids 1. Temperature: Whereas it typically is assumed that increasing tem-
serves as a buffer and facilitates a stable admixture. The presence perature helps substances dissolve or stay in solution better, the
of IVFE also further limits the compatibility of other additives. converse is true for PN admixtures. With increased temperature,
Strict adherence to published compatibility guidelines5 is critical there is increased dissociation of electrolytes, resulting in an
to avoid disrupting the TNA (see Section III.B) or developing a increased likelihood of the formation of salts that will precipitate,
potentially lethal precipitate.20,21 for example, calcium phosphate (see Section II.B.1.a). Further-
2. Iron dextran: Iron is a trivalent cation (Fe+3) that can destabilize more, the degradation of several amino acids (eg, tryptophan,
the TNA when iron dextran is added to the formulation. The arginine, methionine) is hastened by room temperature, compared
higher the cation valence, the greater the destabilizing power; to refrigerator temperature.22
thus, iron is more disruptive than calcium and magnesium (diva- 2. pH: pH has variable effects, depending on the nutrient in question.
lent cations), which are more disruptive than sodium and potas- For example, IVFE are more stable at higher pH values, whereas
sium (monovalent cations). There is no safe concentration of iron a lower pH value is favorable to calcium phosphate solubility.
dextran in any TNA.22,29 However, iron dextran can be added to Therefore, the specific composition of an individual PN admix-
non-IVFE-containing PN formulations, within limits.11 ture must be taken into consideration when stability is evaluated
D. Medication additives relative to pH.
1. In general, the PN admixture should not be used as a drug deliv- 3. Light and oxygen exposure: Light and oxygen exposure enhances
ery vehicle. Data on medication compatibility with PN formula- the degradation of some nutrients, including selected vitamins and
tions are limited, identifying physical compatibility, which is only amino acids. During storage, PN admixtures should be protected
one of several variables that influence complete bioavailability of from light. Light protection is generally not considered necessary
both the drug and the nutrient provided by PN.21 while a PN admixture is being infused into the patient because of
2. In some cases there is no reasonable alternative to medication the relatively short time of exposure (eg, ≤24 hours). However, it
administration with PN. When medications are being admixed with may be prudent to consider using light-protective coverings for PN
the PN formulation, the following issues need to be addressed30: formulations exposed to high levels of ultraviolet light (pho-
a) Medication stability and compatibility with 2-in-1 or TNA is totherapy lights) or fluorescent light, due to the susceptibility of
assured. vitamins, particularly vitamin A, to photodegradation.
b) Evidence supports the efficacy of the medication administered 4. Composition: The specific doses and combinations of nutrients
in this manner. can greatly affect the stability of a PN admixture. As discussed in
3. Studies of medication compatibility in PN found compatibility Section II, some nutrients have a destabilizing effect when in the
to differ for TNA or 2-in-1 formulas.31,32 Therefore, compati- presence of other nutrients. For example, dextrose and IVFE can-
bility with one PN admixture does not predict compatibility not be directly admixed because of the effect of the low pH of the
with another. dextrose solution on the integrity of the IVFE. Divalent and triva-
a) The physical compatibility of 102 drugs with 2-in-1 PN for- lent cations are known to be potentially disruptive of a TNA
mulations simulating y-site administration has been deter- admixture because of the effect of these ions on IVFE integrity.
mined.32 Twenty drugs, including amphotericin B, acyclovir, 5. Order of admixing (see Section I.D)
sodium bicarbonate, and ciprofloxacin, were found to be B. TNAs
incompatible. 1. General considerations: The issues of TNA stability are fre-
b) The physical compatibility of 106 drugs with TNA formula- quently related to compatibility. The presence of IVFE in the
tions simulating y-site administration has been determined.32 TNA alters the physicochemical character of the PN admixture.
Twenty-three drugs were found to be incompatible. The TNA is an oil-in-water emulsion that is inherently less sta-
c) Many of these interactions and incompatibilities could be ble than a 2-in-1 formulation, which is completely water-based.
identified by careful inspection of the PN formulas for pre- All the factors that affect stability in a PN formulation tend to do
cipitates, discoloration, haziness, or breaking of the emulsion. so to a greater extent with a TNA. Therefore, a more conserva-
d) Compatibility information should be derived for the PN for- tive approach to interpreting admixture guidelines for compati-
mulation that most closely matches the one prescribed for the bility is needed followed to avoid disruption of the TNA or
patient in question. formation of a visually undetectable precipitate.20,21
4. Coadministration or admixture of medications known to be 2. Stages of TNA deterioration: The integrity of a TNA is depend-
incompatible with PN should be prevented.33 In the absence of ent on the oil droplets remaining dispersed throughout the aque-
reliable information concerning compatibility of a specific drug ous phase. If the oil droplets are allowed to aggregate, they can
with PN, the medication should be administered separate from eventually cause complete separation into oil and water phases,
the PN.33 and the TNA that is no longer safe for infusion. The stages of
deterioration or cracking of the TNA are as follows17:
a) Aggregation (flocculation): Fat droplets aggregate to form
III. Stability Issues larger droplets but can be redispersed with gentle agitation.
A. General considerations: As with compatibility, many factors influ- b) Creaming: The larger fat droplets that have aggregated rise to
ence the stability of PN admixtures. Stability and compatibility are the surface and form a cream layer; this stage can be reversed
often overlapping issues, as the conditional incompatibility of indi- with gentle agitation.
vidual nutrients renders the admixture less stable. Each nutrient c) Coalescence: The fat droplets aggregate into significantly
additive in a PN admixture has its own inherent stability profile, larger droplets, creating an irreversible separation of the oil
which once combined with the other PN admixture components and water phases and an unusable TNA.

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S E C T I O N I Fundamentals of Nutrition Support Practice and Management

d) Oiling out: There is continued coalescence, with total, irre- should successfully complete a process validation of aseptic
versible separation of the oil and water phases and an un- technique before being allowed to admix PN. Process simu-
usable TNA. lation of the PN formulation may also be used but is more
C. Vitamins difficult since the PN formulation itself may limit or inhibit
1. General considerations: Light exposure and time are the primary microbial growth if inadvertently contaminated during the
factors affecting vitamin stability in PN admixtures. Vitamins compounding process.
should be added as the last component when a PN admixture is 2. Nutrient composition
prepared (see Section I.D). Once the vitamins have been added, a) PN admixtures can serve as an ideal growth environment for
the PN admixture should be infused within 24 hours to limit loss some microorganisms. These organisms may be introduced
of potency. into the admixture when it is compounded or when the it is
2. Specific vitamin considerations manipulated during administration.
a) Ascorbic acid (vitamin C) breakdown is hastened by the pres- b) The ability of the PN admixture to support the growth of con-
ence of copper. The addition of ascorbic acid in a batch fashion taminants depends on nutrient composition. When the individ-
has caused degradation, resulting over time in the formation of ual base components are compared, IVFE are better than amino
oxalic acid. Oxalic acid readily reacts with free calcium to form acids, which are better than dextrose, in supporting microbial
calcium oxalate precipitates.22 proliferation. When nutrient components are admixed, TNAs
b) Thiamine may be destroyed by sodium bisulfite but appears are more likely to support microbial proliferation than 2-in-1
to be stable in the presence of sodium hydrosulfite. Sodium formulations.
bisulfite or sodium hydrosulfite is used in some commercially 3. Temperature: Room temperature facilitates and refrigerator tem-
prepared crystalline amino acid solutions as an antioxidant. perature retards microbial growth.
c) Riboflavin degradation is increased by light exposure. 4. pH: An acidic environment inhibits bacterial growth, which is
d) Vitamin A may adsorb to plastic bags and tubing. Vitamin A in partly why a 2-in-1 formulation is less likely than a TNA to sup-
the form of retinol is less susceptible to adsorption than retinol port proliferation of bacteria. However, fungi can rapidly pro-
palmitate. Substantial amounts of vitamin A can also be lost liferate in a 2-in-1 formulation despite the lower pH.
over time due to degradation.34 5. Time frame
D. 2-in-1 base solutions are stable for various lengths of time depending a) Lipid emulsions support the growth of bacteria and fungi that
on the storage conditions; 2-in-1 solutions cannot be commercially can reach clinically significant numbers within 24 hours. The
premixed because the temperatures required for autoclave sterili- Centers for Disease Control and Prevention (CDC) recom-
zation caramelize the dextrose (a process known as the Maillard mends that IVFE infused separately from PN formulations be
reaction). Caramelization is detected by the presence of a brown completed within 12 hours of hanging the container.37
coloration in the 2-in-1 formulation. b) TNAs support the growth of bacteria and fungi but at a slower
rate than IVFE alone. The CDC recommends that a TNA be
completed with 24 hours of hanging the solution.37
IV. Microbial Growth Potential c) 2-in-1 formulations support fungi but do not support bacte-
A. General considerations: Safe administration of a PN admixture is ria. Like TNAs, they should be infused within 24 hours of
dependent on the product being free of microbial contamination. initiating the infusion to avoid clinically significant fungal
Strict adherence to infection control admixing guidelines and vali- proliferation.22
dation of an aseptic compounding technique are imperative. Profes- B. Microbes of greatest clinical significance: There have been reports of
sional organizations have published guidelines for compounding infectious complications associated with a contaminated PN admix-
and dispensing sterile products. The American Society of Health- ture. The following organisms related to PN contamination have been
System Pharmacists has published guidelines35 on quality assurance reported:
for pharmacy-prepared sterile products, while the United States 1. Candida albicans in 2-in-1 formulations7
Pharmacopeia publishes the official compendium The United States 2. Malassezia furfur in IVFE38
Pharmacopeia and The National Formulary, which includes a chap- 3. Coagulase-negative staphylococci in neonates receiving IVFE in
ter on pharmaceutical compounding of sterile preparations.36 The the intensive care unit39
following factors influence the sterility of the PN admixture: 4. Staphylococcus saprophyticus in TNAs40
1. Sterile compounding procedure: Sterile products are divided into
three levels of risk on the basis of the probability of exposing mul-
V. Automated Compounding
tiple patients to microbial and physical contaminants.35,36 Draw-
ing a sterile product into a sterile syringe or transferring a sterile A. General characteristics
product from a vial into a commercially produced intravenous bag 1. An automated compounding device (ACD) is a mechanical sys-
is an example of a low-risk process. Medium risk is the level tem usually made up of numerous stations, each designated for
assigned for automated compounding of PN formulations. a component of the PN admixture. Some ACDs are limited to
a) PN admixtures should be prepared in a class 100 environment preparation of the base components (dextrose, amino acids,
(ie, fewer than 100 particles of a size 0.5 µm/cu ft of air). This sterile water, and IVFE), whereas other systems include up to
is best achieved by using a laminar flow hood. 23 channels to accommodate micronutrients as well.
b) Personnel are required to wear clean gowns or coveralls, as 2. ACDs admix PN formulations under computer-assisted com-
scrub attire by itself is not acceptable. Gloves and masks are mands connected to special hardware housed with sterile, dispos-
recommended during the compounding process. able compounding sets. Based on prescribed dose, information
c) Process validation of aseptic procedures is recommended for regarding the specified volume of each ingredient is fed to the
PN formulations.35 Individuals involved in PN compounding appropriate channels for the compounding process.

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B. Guidelines on safe use: Due to the risk level of the compounding pro- 4. Trailing zeroes should never be used, and the use of decimals
cedure, it is recommended that automated PN compounding include should be avoided whenever possible. Leading zeroes should be
the following22,41: used for doses less than one measurement unit.46
1. Pharmacist validation of data entered into the compounding device 5. Units of measure on the PN order form should be consistent with
prior to PN preparation the recommended PN label format (see Section VIII).
2. Performance of end-product checks to verify compounding 6. Ingredients should be listed in the same order on the PN order form
accuracy and the PN label to facilitate verification of the PN contents against
3. Periodic observation by the operator of the device to ensure that it the PN order.
is working properly C. Mandatory components of the order form: The design of PN order
C. Advantages (compared with manual compounding) forms may differ from institution to institution to account for specific
1. Potential reduction in labor needs and concerns. However, the following recommendations are
2. More efficient use of materials: Bulk volumes of additives can be deemed to be necessary for all PN order forms22:
used for compounding multiple patients’ PN admixtures. Fewer 1. Type of access (central or peripheral vein)
needles and syringes are needed for manually adding components. 2. Height, weight, diagnosis, PN indication
3. Less likelihood of contamination during compounding because 3. Contact number for reference person and prescriber
of less manual manipulation 4. Hang time guidelines
4. Availability of safety and quality assurance checks 5. Safeguards to avoid incompatibilities
D. Disadvantages (compared with manual compounding) 6. Warning mechanism for excessive rate of nutrient administration
1. Potential user error D. Recommended components of the order form: Although not consid-
2. Potential equipment malfunction ered mandatory, these items are strongly recommended for inclusion
3. Susceptibility to power outages on the PN order form (or back of the form)22:
1. Nutrient dosing guidelines based on weight and age
2. Recommended nutrient ranges, including maximum and minimum
VI. Off-Site Compounding Centers
amounts, when applicable
A. Definition: an off-site IV admixture center providing IV com- 3. Guidelines to assist in nutrient and volume calculations
pounding services that are shared by multiple institutions, elimi- 4. Monitoring guidelines
nating the need for each institution to have its own dedicated IV 5. Guidelines for stopping or interrupting the PN infusion
admixture facility42 6. Specific content of multivitamin and trace element preparations
B. Potential advantages available
1. Greater efficiency in staffing, materials use, and inventory con- 7. Specific amino acid and IVFE brands available
trol, especially in institutions with a small volume of PN patients 8. Insulin guidelines
2. Standardization of procedures with improved quality control E. Sample order form (Figure 7-1): A sample adult PN order form is pro-
3. More efficient use of space vided as a guide to meeting criteria for mandatory and strongly rec-
C. Potential disadvantages ommended items for inclusion. Its content must be adapted to meet
1. Logistics of communicating orders and order changes the needs of the individual institution based on patient population,
2. Logistics of transporting products from the off-site admixture prescribing patterns, and judgment by the health care professional.
center to the institution
3. Less ability to assess quality control measures at the outside
facility
VIII. Labeling PN Formulations
A. General considerations: The way PN ingredients are labeled varies
considerably.22 PN base components (dextrose, amino acids, and
VII. Ordering PN Formulations
IVFE) have been labeled as the volume of the percent of original con-
A. General considerations: Many of the errors associated with the use centration added, the percent of final concentration after admixture,
of PN formulations are related to the complex nature of the order- and either the grams per liter or the grams per total volume of PN
ing process. Clinical errors have been associated with the manner admixed. Additives, especially electrolytes, have been labeled as
in which orders were created and communicated and lack of uni- mEq or mmol and as quantity per day, per kg, per liter, or per 100 mL.
formity in the ordering process from institution to institution.22 1. Misinterpretation of the dextrose content of a PN label led to an
Standardizing the order-writing process has been shown to reduce error in PN preparation that caused a patient’s death.47 Hepatic tox-
prescribing errors.43–45 A set of minimum standards for creating a PN icity resulted from an iron overdose caused by the misinterpreta-
order form have been recommended to reduce errors and improve tion of a PN label for iron dextran (1 mL) where the original
patient safety.22 solution containing 50 mg/mL was used rather than a pre diluted
B. Clarity of the order form: A PN order form should be designed so that product having a concentration of 1 mg/mL.48
all health care professionals who use it understand it. The following 2. Quantity per total volume: With use of a 24-hour nutrient infusion
principles have been recommended to promote order form clarity22: system, quantity per total volume is most consistent with that of a
1. Organization: The form should be organized simply and be easy nutrient label, requiring the least number of calculations to deter-
to scan for completeness. mine the nutrient dose per day.
2. All nutrients should be clearly identified. B. PN label template (see Figures 7-2 through 7-4): Due to the complex
3. Adequate space should be provided to allow clear handwriting. nature of the label, there are several points that should be clarified.
However, the use of a standardized PN order form should dramat- 1. Amount/day is the only column required on the adult label (Fig-
ically reduce the need for the prescriber to hand write items, thus ure 7-2). A second, optional column may be added reflecting
reducing the likelihood of misinterpretation. amount/L.

© 2005 A.S.P.E.N. www.nutritioncare.org. A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. 103
 FIGURE 7-1. Parenteral Nutrition Order Form Template

Physician Orders
PARENTERAL NUTRITION (PN) - ADULT
Primary Diagnosis: _________________________________________ Ht: __________cm Dosing Wt:_____kg
PN Indication:________________________________________ Allergies: ______________________________

Instructions: This form must be completed for a new order or continuation of PN and faxed to the Pharmacy by [Insert Time] to receive same day preparation. PN
administration begins at [Insert Time]. Contact the Nutrition Support Service at (XXX) XXX-XXXX for additional information.

Administration Route: CVC or PICC Note: Proper tip placement of the CVC or PICC must be confirmed prior to PN infusion
Peripheral IV (PIV) (Final PN Osmolarity ≤ _________ mOsm/L)

Monitoring: Daily weights, Strict input & output, Bedside glucose monitoring every _____ hours
Na, K, Cl, CO2, Glucose, BUN, SCr, Mg, PO 4 every __________________
T. Bili, Alk Phos, AST, ALT, Albumin, Trigl ycerides, Calcium every _____________

Base Solution: Parenteral nutrition MUST be administered through a dedicated infusion port and filtered with a 1.2-micron in-line
Select one filter at all times. Discard any unused volume after 24 hours.

PERIPHERAL 2-in-1 CENTRAL 2-in-1 CENTRAL 3-in-1

Dextrose _____ g Dextrose _____ g Dextrose _____ g
Amino Acids (Brand _________) _____ g Amino Acids (Brand _________) _____ g Amino Acids (Brand ___________) _____ g
For patients with PIV and established glucose For patients with CVC or PICC and established glucose Fat Emulsion (Brand ___________) _____ g
tolerance; Provides ______ kcal; Maximum Rate tolerance; Provides ______ kcal; Maximum Rate not to
not to exceed ______ mL/hour exceed ______ mL/hour
For patients with CVC or PICC and established glucose / fat
emulsion tolerance; Provides ______ kcal; Maximum Rate not to
exceed ______ mL/hour
RATE & VOLUME: ______ mL/hour for _____ hours = ______ mL/day
Use of additional fat emulsion not required with 3-in-1 base
Must specify solution

or CYCLIC INFUSION: ______ mL/hour for _____ hours, then ______ mL/hour for _____ hours = ______ mL/day

Fat Emulsion (Brand ____________) – via PIV or CVC with 2-in-1 base solutions (Select caloric density & volume)

10% 250 mL Infuse at ______ mL/hour over _____ hours Frequency _____________
20% 500 mL (Note: Infusions < 4 or > 12 hours not recommended) Discard any unused volume after 12 hours.

Additives: (per day) Normal Dosages Additives: (per day)

Sodium Chloride ______ mEq 1-2 mEq Sodium/kg/day Regular Insulin ________ units
as Acetate ______ mEq pH or CO2 dependent Recommend if hyperglycemic, start with
as Phosphate ______ mmol of PO4 Consider if hyperkalemic 1 unit for every 10 g of dextrose
Potassium Chloride ______ mEq 1-2 mEq Potassium/kg/day
as Acetate ______ mEq pH or CO2 dependent Pharmacy Use Only: Ca/PO4
as Phosphate ______ mmol of PO4 20-40 mmol/day (1 mmol Phos = 1.5 mEq K) Limit Checked ____
Calcium Gluconate ______ mEq 5-15 mEq/day (Note: Some brands of amino acids
Magnesium Sulfate ______ mEq 8-24 mEq/day contain phosphate)

Adult Multivitamins mL/day Contains Vitamin K 150 mcg

Adult Trace Elements mL/day Zn __ mg, Cu __ mg, Mn __ mg, Cr __ mcg, Se __ mcg (with normal hepatic function)
H2 Antagonist _________ ______ mg ____ mg/day with normal renal function
Other:

Physician's Signature: __________________________________PagerNumber:__________Date/time:_________

Orders transcribed by: __________ Date/time: ___________ Orders verified by: ___________Date/time:________
SEND COMPLETED ORDERS TO PHARMACY File under: Physician Orders
Reprinted from Task Force for the Revision of Safe Practices for Parenteral Nutrition. Safe practices for parenteral nutrition. J Parenter Enteral Nutr. 2004;28:S39–S70 with per-
mission.

104 A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. © 2005 A.S.P.E.N. www.nutritioncare.org.
 S E C T I O N I Fundamentals of Nutrition Support Practice and Management

FIGURE 7-2. Standard PN Label Template: Adult Patient FIGURE 7-3. Standard Parenteral Nutrition Label
Template: Neonate or Pediatric Patient
Institution/Pharmacy Name, Address, and Pharmacy Phone Number
Institution/Pharmacy Name, Address, and Pharmacy Phone Number
Name ____________________ Dosing Weight __________
Location _______________ Name ____________________ Dosing Weight __________
Administration Date/Time _________ Expiration Date/Time _________ Location _______________
Administration Date/Time _______ Do Not Use After: Date/Time ______
Base formula Amount/day (Amount/L)
Base formula Amount/day (Amount/L)
Dextrose g (g/L)
Amino acidsa g (g/L) Dextrose g/kg g
IVFEa g (g/L) Amino acidsa g/kg g

Electrolytes Electrolytes
Sodium chloride mEq (mEq/L) Sodium chlorideb mEq/kg mEq
Sodium acetate mEq (mEq/L) Sodium acetateb mEq/kg mEq
Sodium phosphate mmol of P (mmol/L) Potassium chloride mEq/kg mEq
(mEq of Na) (mEq/L) Potassium acetateb mEq/kg mEq
Potassium chloride mEq (mEq/L) Potassium phosphate mmol of P/kg mmol of P
Potassium acetatem Eq (mEq/L) (mEq of K)/kg (mEq of K)
Potassium phosphate mmol of P (mmol/L) Sodium phosphateb mmol of P/kg mmol of P
(mEq of K) (mEq/L) (mEq of Na)/kg (mEq of Na)
Calcium gluconate mEq (mEq/L) Calcium gluconate mEq/kg mEq
Magnesium sulfate mEq (mEq/L) Magnesium sulfate mEq/kg mEq

Vitamins, trace elements, and medications Vitamins, trace elements, and medications
Multiple vitaminsa mL Multiple vitaminsa mL/kg mL
Multiple trace elementsa mL Multiple trace elementsa mL/kg mL
Insulin units (units/L) L-cysteine mg/kg mg
H2 antagonistsa mg H2 antagonistsa mg/kg mg
L-carnitine mg/kg mg
Rate ___ mL/hour Volume ___ mL Infuse over ___
hours Rate ___ mL/hour Volume ___ mL Infuse over 24 hours

Formulation contains _____ mL plus _____ mL overfill Admixture contains _____ mL plus _____ mL overfill
Discard any unused volume after 24 hours ***Central Line Use Only***
Central Line Use Only a Specify product name.
b Since the admixture usually contains multiple sources of sodium, potassium, chlo-
aSpecify product name. ride, acetate, and phosphorus, the amount of each electrolyte/kg provided by the PN
Reprinted from Task Force for the Revision of Safe Practices for Parenteral Nutrition. admixture is determined by adding the amount of electrolyte provided by each salt.
Safe practices for parenteral nutrition. J Parenter Enteral Nutr. 2004;28:S39–S70 with Reprinted from Task Force for the Revision of Safe Practices for Parenteral Nutrition.
permission. Safe practices for parenteral nutrition. J Parenter Enteral Nutr. 2004;28:S39–S70 with
permission.

2. For neonatal or pediatric patients, nutrient doses should be labeled

as amount/kg/day. PN labels for these patients should include a
column for amount/day and amount/kg/day (Figure 7-3). Optional 9. Rate should be expressed in mL/hour over 24 hours. If the PN
columns may be added to reflect amount/L or amount/100 mL. is cycled, the infusion duration and rates are to be expressed on
3. If IVFE are not included in the PN formulation, this line may be the label.
omitted from the label. Figure 7-4 provides a label template for 10. For use in the home setting, ingredients to be added at home
IVFE administered separate from the PN formulation. should be labeled as patient additives.
4. The dosing weight (the weight used to calculate nutrient doses) is 11. An auxiliary label may be used to provide supplemental infor-
required on the label. mation thought to be useful but not required on the PN label.
5. The PN label should specify the route of administration. C. Practice guidelines22
6. If the PN contains overfill, it should be clearly stated on the label. 1. Labels for PN formulations shall be standardized.
7. The administration date and time and expiration date and time a) The amount per day of nutrients and medications is required
should be expressed clearly on the label. on the label.
8. The phosphorus content should be expressed as both the mmol b) Using the quantity per liter option supports programs that
quantity of phosphorus and the mEq quantity of the salt’s cation, continue to admix PN in 1-liter volumes.
potassium, or sodium. c) The dosing weight is required on the label.

© 2005 A.S.P.E.N. www.nutritioncare.org. A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. 105
S E C T I O N I Fundamentals of Nutrition Support Practice and Management

10. American Medical Association Department of Foods and Nutrition. Guide-

FIGURE 7-4. Standard IVFE Label Template: Adult, lines for essential trace element preparations for parenteral use. A statement
Neonate, or Pediatric Patient by an expert panel. JAMA. 1979;241:2051–2054.
11. Kumpf V. Update on parenteral iron therapy. Nutr Clin Pract. 2003;18:
Institution/Pharmacy Name, Address, and Pharmacy Phone Number 318–326.
12. Pluhator-Murton MM, Fedorak RN, Audette RJ, et al. Trace element con-
Name ____________________ Dosing Weight __________ tamination of total parenteral nutrition, I: contribution of component solu-
Location _______________ tions. J Parenter Enteral Nutr. 1999;23:222–227.
13. ASCN/ASPEN Working Group on Standards for Aluminum Content of Par-
Administration Date/Time _______ Expiration Date/Time ______
enteral Nutrition Solutions. Parenteral drug products containing aluminum as
Volume Amount/kg/day Amount/day an ingredient or a contaminant: response to food and drug administration
notice of intent and request for information. Am J Clin Nutr. 1991;53:399–402.
Intravenous fat emulsiona(%) ___ mL ________ g/kg _______ g 14. Aluminum in large and small volume parenterals used in total parenteral
nutrition. Food and Drug Administration, Docket No. 90N-0056. Federal
Infusion rate ___ mL/hour Infuse over ___ hours Register. January 26, 2000;65(17):4103–4111.
15. Dickerson RN. Manganese intoxication and parenteral nutrition. Nutrition.
May contain overfill––Discard any unused volume after 12 hours 2001;17:689–693.
For peripheral or central line administration 16. Kurkus J, Alcock NW, Shils ME. Manganese content of large-volume
parenteral nutrition solutions and of nutrient additives. J Parenter Enteral
a
Specify product name. Nutr. 1984;8:254–257.
Reprinted from Task Force for the Revision of Safe Practices for Parenteral Nutrition. 17. Brown R, Quercia RA, Sigman R. Total nutrient admixture: a review.
Safe practices for parenteral nutrition. J Parenter Enteral Nutr. 2004;28:S39–S70 with J Parenter Enteral Nutr. 1986;10:650–658.
permission. 18. Driscoll DF. Total nutrient admixtures: theory and practice. Nutr Clin Pract.
1995;10:114–119.
19. Jensen GL, Mascioli EA, Seidner DL, et al. Parenteral infusion of long- and
2. Auxiliary labels may be used to provide information not already medium-chain triglycerides and reticuloendothelial system function in
included on the label. man. J Parenter Enteral Nutr. 1990;14:467–471.
3. Pharmacist-to-pharmacist communication is required when a 20. Hill SE, Heldman LS, Goo EDH, et al. Fatal microvascular pulmonary
patient transfers between health care environments, to ensure emboli from precipitation of a total nutrient admixture solution. J Parenter
Enteral Nutr. 1996;20:81–87.
the accurate transfer of the PN prescription.
21. McKinnon BT. FDA safety alert: hazards of precipitation associated with
4. The PN label must be compared to the PN order for accuracy and
parenteral nutrition. Nutr Clin Pract. 1996;11:59–65.
to verify expiration date prior to administration. 22. Task Force for the Revision of Safe Practices for Parenteral Nutrition. Safe
practices for parenteral nutrition. J Parenter Enteral Nutr. 2004;28:S39–S70.
(Parenteral Nutrition Formulation chapters from the 1st edition were 23. Bertch KE, McKinnon BT. Pharmaceutical issues for parenteral nutrition
contributed by Kathleen M. Strausburg, Kristy Gibbons, Nancy Cyr, solutions. In: Christensen ML, McKinnon BT, eds. Nutrition Support Phar-
Michael L. Christensen, and Richard A. Helms) macy: Selected Cases for Self-Study. Silver Spring, MD: A.S.P.E.N.;
1995:7–1 to 7–17.
24. A.S.P.E.N. Board of Directors and the Clinical Task Force. Guidelines for
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the use of parenteral and enteral nutrition in adult and pediatric patients.
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parenteral amino acids. Nutr Clin Pract. 2001;16:219–225. 25. Isaacs JW, Millikan WJ, Stackhouse J, et al. Parenteral nutrition of adults
2. Amino acid injection. In: Trissel LA, ed. Handbook on Injectable Drugs. with 900-milliosmolar solution via peripheral vein. Am J Clin Nutr.
12th ed. Bethesda, MD: American Society of Health-System Pharmacists; 1977;30:552–559.
2003:45–90. 26. Johnson GC, Anderson JD. Compounding considerations. In: Teasley-
3. Singer P, Bursztein S, Kirvela O, et al. Hypercaloric glycerol in injured Strausbury KM, ed. Nutrition Support Handbook: A Compendium of Prod-
patients. Surgery. 1992;112:509–514. ucts with Guidelines for Usage. Cincinnati, OH: Harvey Whitney Books;
4. Driscoll DF. Intravenous lipid emulsion: 2001. Nutr Clin Pract. 2001;16: 1992:133–146.
215–218. 27. Eggert LD, Risho WJ, MacKay MW, et al. Calcium and phosphorus com-
5. Fat emulsion, intravenous. In: Trissel LA, ed. Handbook on Injectable Drugs. patibility in parenteral nutrition solutions for neonates. Am J Hosp Pharm.
12th ed. Bethesda, MD: American Society of Health-System Pharmacists; 1982;39:49–53.
2003:562–582. 28. Mirtallo JM. The complexity of mixing calcium and phosphate. Am J Hosp
6. Driscoll DF, Adolph M, Bistrian BR. Lipid emulsions in parenteral nutrition. Pharm. 1994;51:1535–1536.
In: Rombeau JL, Rolandelli RH, eds. Clinical Nutrition: Parenteral Nutri- 29. Driscoll DF, Bhargava HN, Li L, et al. Physicochemical stability of total
tion. 3rd ed. Philadelphia, PA: WB Saunders; 2001:35–39. nutrient admixtures. Am J Hosp Pharm. 1995;52:623–634.
7. Mirtallo JM. Parenteral formulas. In: Rombeau JL, Rolandelli RH, eds. Clin- 30. Driscoll DF, Baptista RJ, Mitrano FP, et al. Parenteral nutrient admixtures as
ical Nutrition: Parenteral Nutrition. 3rd ed. Philadelphia, PA: WB Saunders; drug vehicles. Theory and practice in the critical care setting. Ann Pharma-
2001:118–137. cother. 1991;25:276–283.
8. Food and Drug Administration. Parenteral multivitamin products: drugs 31. Trissel LA, Gilbert DL, Martinez JF, et al. Compatibility of parenteral
for human use: drug efficacy study implementation: amendment. Federal nutrient solutions with selected drugs during simulated Y-site administra-
Register. April 20, 2000;65(77):21200–21201 tion. Am J Health-Syst Pharm. 1997;54:1295–1300.
9. Greene HL, Hambidge KM, Schanler R, Tsang RC. Guidelines for the use 32. Trissel LA, Gilbert DL, Martinez JF, et al. Compatibility of medications with
of vitamins, trace elements, calcium, magnesium, and phosphorus in infants 3-in-1 parenteral nutrient admixtures. J Parenter Enteral Nutr. 1999;23:67–74.
and children receiving total parenteral nutrition: report of the Subcommit- 33. A.S.P.E.N. Board of Directors and the Clinical Guidelines Task Force.
tee on Pediatric Parenteral Nutrient Requirements from the Committee on Drug-nutrient interactions, IX: guidelines for the use of parenteral and
Clinical Practice Issues of the American Society for Clinical Nutrition. Am enteral nutrition in adult and pediatric patients. J Parenter Enteral Nutr.
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34. Howard L, Chu R, Feman S, et al. Vitamin A deficiency from long-term 41. American Society for Health-System Pharmacists. ASHP Guidelines on Safe
parenteral nutrition. Ann Intern Med. 1980;93:576–577. Use of Automated Compounding Devices for the Preparation of Parenteral
35. American Society for Health-System Pharmacists. ASHP guidelines on Nutrition Admixtures. Am J Health-Syst Pharm. 2000;57:1343–1348.
quality assurance for pharmacy-prepared sterile products. Am J Health-Syst 42. Fauber WS, Cosnotti SJ, Mady RL. Offsite intravenous admixture center
Pharm. 2000;57:1150–1169. shared by health-system facilities. Am J Hosp Pharm. 1995;52:2550–2555.
36. USP General Chapter <797> pharmaceutical compounding–sterile prepa- 43. Petros WP, Shank WA. A standardized parenteral nutrition solution: pre-
rations. United States Pharmacopeial Convention. Pharmacopeial Forum. scribing, use, processing, and material cost implications. Hosp Pharm.
2003;29(4):940–965. 1986;21:648–656.
37. Centers for Disease Control and Prevention. Guidelines for the prevention of 44. Mitchell KA, Jones EA, Mequid MM, et al. Standardized TPN order form
intravascular catheter-related infections. MMWR. 2002;51(No RR-10):1–29. reduces staff time and potential for error. Nutrition. 1990;6:457–460.
38. Shek YH, Tucker MC, Viciana AL, et al. Malassezia furfur-disseminated 45. Cerra FB. A standardized TPN order form reduces staff time and potential
infection in premature infants. Am J Clin Pathol. 1989;92:595–603. error [editorial]. Nutrition. 1990;6:498–499.
39. Freeman J, Goldmann DA, Smith NE, et al. Association of intravenous lipid 46. ISMP list of error-prone abbreviations, symbols, and dose designations.
emulsion and coagulase-negative staphylococcal bacteremia in neonatal ISMP Medication Safety Alert. 2003;8(24):3–4.
intensive care units. N Engl J Med. 1990;323:301–308. 47. Carey LC, Haffey M. Incident: home TPN formula order misinterpreted
40. Llop JM, Mangues I, Perez JL, et al. Staphylococcus saprophyticus sepsis after hospital admission. Home Care Highlights. spring 1995:7.
related to total parenteral nutrition admixture contamination. J Parenter 48. Iron overdose due to miscommunication of TPN order. Error alert. Pharm
Enteral Nutr. 1993;17:575–577. Today. September 1995:52.

© 2005 A.S.P.E.N. www.nutritioncare.org. A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. 107
 Gordon S. Sacks, PharmD, BCNSP, FCCP;
Susan Mayhew, PharmD, BCNSP;
Debbie Johnson, RN, MSN 8
Parenteral Nutrition
Implementation and
Management
Introduction D. A.S.P.E.N. has also developed specific guidelines for implemen-
tation of PN in pediatric patients1
Parenteral nutrition (PN) is the provision of intravenous nutrients to
patients whose gastrointestinal (GI) tract is not functioning or cannot be
accessed and to patients whose nutritional needs cannot be met with oral III. Initiation of PN
diets or enteral tube feeding. Recognized as a major medical advance in
A. PN may be initiated in adult patients who are hemodynamically
the past 50 years, PN has provided lifesaving therapy for patients who
stable, who are able to tolerate the fluid volume necessary to pro-
could not otherwise be nourished. Because of its complexity, PN ther-
apy requires careful monitoring by trained clinicians to avoid serious vide significant macronutrient intake, and who have central vascu-
complications. New knowledge and technological advances have lar access. If access to a central vein cannot be obtained, PPN
resulted in appropriate patient selection and therapies that have steadily should be considered. PPN is more commonly used in neonatal and
improved patient safety. pediatric populations than in adults.
B. For preterm neonates, PN is a cornerstone of postnatal care and ini-
I. Background tiation is advocated as soon as clinically possible after birth, often
II. Situations in Which PN Is Commonly Used on day 1 of life. Goals for initiation and advancement of protein,
III. Initiation of PN carbohydrate, fat, and fluid intake in term and preterm neonates are
IV. Administration of PN listed in Chapter 26. Goals for fluid intake, energy, and protein in
V. Monitoring and Management of PN infants, children, and adolescents are listed in Chapter 2.
VI. Complications of PN C. The usual goals for protein, carbohydrate, fat, and fluid intake for
VII. Transitional Feeding and Discontinuing PN adult patients on PN are presented in Table 8-1.
References D. Guidelines for mineral and electrolyte intake are presented in Table
Suggested Readings 8-2 for pediatric patients and in Table 8-3 for adult patients.2–4
E. Electrolytes may be manipulated to avoid electrolyte and acid-
I. Background base imbalance. Although it is inappropriate to use PN to manage
short-term fluid and electrolyte shifts, the fluid, mineral, and elec-
PN refers to a combination of nutrients—crystalline amino acids, dex- trolyte content of PN is frequently individualized. Consideration
trose, fat emulsions, electrolytes, vitamins, and minerals—administered is given to the patient’s existing deficits, dry weight, ongoing
intravenously. losses, and changes in organ function or drug therapy.
A. PN was developed in the late 1960s to provide nutrition for those F. Recommendations for vitamin and trace element intake are given
without a functioning GI tract. in Tables 8-4 and 8-5 for adult PN formulations and in Tables 8-6
B. PN was initially called intravenous (IV) hyperalimentation, but and 8-7 for pediatric PN formulations.5,6
now the terms PN and central PN are more often used. G. Generally, the patient should have satisfactory hydration, elec-
C. PN administered via a peripheral vein is called peripheral PN
trolyte, and acid-base status prior to the initiation of PN. Individual-
(PPN).
ized PN may help balance hydration, electrolytes, and acid-base
D. PN admixtures are of two types.
status. However, to best achieve nutritional goals with PN, the
1. Mixtures of dextrose, amino acids, vitamins, and minerals are
hydration, electrolyte, and acid-base status of the patient should be
referred to as 2-in-1. IV fat emulsions (IVFE) are infused
corrected as much as possible before PN is started.
separately.
H. The initial PN for adults is based on ability to tolerate volume and
2. Total nutrient admixtures (TNAs), 3-in-1, or all-in-one formu-
macronutrients.
lations are terms for PN that contains IVFE in the same con-
tainer with crystalline amino acids, dextrose, vitamins, and 1. As protein intake in an adult is associated with minimal meta-
minerals. bolic side effects, the maximum amount of protein (up to 60–
70 g/L) can be given on day 1. The initial maximum carbohy-
drate given in an adult is usually 150 to 200 g per day or a 15%
II. Situations in Which PN Is Commonly Used to 20% final dextrose concentration. For adult patients with dia-
A. The indication for PN is a nonfunctioning or inaccessible GI tract. betes mellitus or hyperglycemia of stress, 100 to 150 g per day
B. The anticipated duration of PN is at least 7 days. of dextrose or a 10% to 15% final dextrose concentration can be
C. The American Society for Parenteral and Enteral Nutrition administered initially.7
(A.S.P.E.N.) has developed specific guidelines for implementa- 2. For most adult patients, PN may be increased so that energy and
tion of PN in adult patients.1 protein goals are achieved by day 2 or 3. Many institutions, how-

108 A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. © 2005 A.S.P.E.N. www.nutritioncare.org.
 S E C T I O N I Fundamentals of Nutrition Support Practice and Management

TABLE 8-1. Suggested Nutrient Intake for Adult TABLE 8-3. Daily Electrolyte Guidelines for Adult Par-
Patients on Parenteral Nutrition* enteral Nutrition Formulations2–4

Critically ill patients Stable patients Standard daily Factors Tthat

Nutrient requirement increase needs Dosage form
Protein 1.2–1.5 g/kg/d 0.8–1.0 g/kg/d
Carbohydrate Not >4 mg/kg/min Not >7 mg/kg/min Calcium 10–15 mEq High protein intake Ca gluconate
Lipid 1 g/kg/d 1 g/kg/d Magnesium 8–20 mEq GI losses, drugs, Mg sulfate
Total calories 25–30 kcal/kg/d 30–35 kcal/kg/d** refeeding
Fluid Minimum needed to deliver 30–40 mL/kg/d*** Phosphorus 20–40 mmol High dextrose loads, Na phosphate
adequate macronutrients refeeding K phosphate
Sodium 1–2 mEq/kg Na phosphate
*Estimated dry weight is used as the basis of calculations. For obese patients, 120% Na chloride
of ideal weight is used as the basis for calculations. Na acetate
**Varies according to activity levels. Na lactate
***May vary if the patient has ongoing fluid losses.
Potassium 1–2 mEq/kg Diarrhea, vomiting, K phosphate
NG suction K acetate
ever, can provide patient-specific PN formulations with K chloride
increased nutrient density, so volume is not a limiting factor.
a) The dextrose content of the PN can be increased if the patient GI, gastrointestinal; NG, nasogasric.
has capillary blood glucose values consistently ≤180 mg/dL.
b) The IVFE in the PN can be increased if the patient has serum
triglycerides ≤400 mg/dL.
I. The initiation rate of PN for neonatal and pediatric patients will daily increments until energy goals are achieved or the maximum
often replace maintenance IV fluids, thereby meeting maintenance of 12 to 14 mg/kg/minute is reached (about 19 g/kg/day).1 The
fluid requirements. Generally, the time to reach energy and pro- upper limit of carbohydrate intake appears to peak between the
tein goals with PN is inversely related to age. For example, 3 to ages of 1 to 3 years and gradually decreases with age, approach-
5 days of PN therapy (advanced incrementally each day) are gen- ing adult values (5–6 mg/kg/minute or 9 g/kg/day) during ado-
erally required for neonatal patients before nutritional goals are lescence (8–10 mg/kg/minute or 12–14 g/kg/day).8 When IVFE
reached, whereas for children and adolescents, PN goals can often are administered to supplement nonprotein calories, dextrose
be met in 48 to 72 hours. intake at or below the upper limit is generally sufficient for ade-
1. Daily protein requirements are inversely related to developmen- quate weight gain.
tal age and weight. Initial protein doses for preterm neonates 3. IVFE provide a concentrated source of energy and prevent
range from 1 to 2 g/kg/day and are increased daily by 0.5 to essential fatty acid deficiency (EFAD). Preterm neonates are
1 g/kg/day to a goal of 3 g/kg/day for most neonates and infants. especially prone to developing EFAD because of low body fat
Protein requirements in healthy individuals decline to about 1.5 stores. For neonates receiving PN, IVFE should be initiated
to 2 g/kg/day around 1 year of age and by adolescence approach within 3 days of birth and are usually started at doses of 0.5 to
adult values, with requirements generally ranging from 0.8 to 1 g/kg/day and advanced daily (in increments of 0.5–1 g/kg/
1.5 g/kg/day. day) to a goal dose of 3 g/kg/day. For term neonates, infants,
2. Dextrose infusions are generally initiated at doses that approxi- and children, IVFE are commonly initiated at 1 g/kg/day and
mate endogenous glucose production rates (about 6–8 mg/kg/ advanced daily to a goal of 2 to 3 g/kg/day for children and
minute for neonates and infants) and are increased gradually in generally 2 g/kg/day for adolescents.

TABLE 8-2. Daily Electrolyte and Mineral Requirements for Pediatric Patients*2–4

Electrolyte Preterm neonates Infants/children Adolescents and children >50kg

Sodium 2–5 mEq/kg 2–5 mEq/kg 1–2 mEq/kg

Potassium 2–4 mEq/kg 2–4 mEq/kg 1–2 mEq/kg
Calcium 2–4 mEq/kg 0.5–4 mEq/kg 10–20 mEq/d
Phosphorus 1–2 mmol/kg 0.5–2 mmol/kg 10–40 mmol/d
Magnesium 0.3–0.5 mEq/kg 0.3–0.5 mEq/kg 10–30 mEq/d
Acetate As needed to maintain acid-base balance As needed to maintain acid-base balance As needed to maintain acid-base balance
Chloride As needed to maintain acid-base balance As needed to maintain acid-base balance As needed to maintain acid-base balance

*Assumes normal age-related organ function.

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TABLE 8-4. Recommendations for Vitamin Intake TABLE 8-6. Daily Dose Recommendations for Pediatric
in Adults5–6 Multivitamins* 5–6

Vitamin Daily dose Manufacture AMA-NAG

Vitamin A 3300 IU Weight (kg) Dose Weight (kg) Dose

Vitamin D 200 IU
Vitamin E 10 IU <1 1.5 mL <2.5 2 mL/kg
Vitamin K 150 mcg 1–3 3.25 mL >2.5 5 mL
Thiamine (B1) 6 mg >3 5 mL
Pyridoxine (B6) 6 mg
Cyanocobalamin (B12) 5 mcg *Assumes normal age-related organ function. Pediatric multivitamin formulation
Pantothenic acid 15 mg (5 mL): A 2300 IU, D 400 IU, E 7 IU, K 200 mcg, ascorbic acid 80 mg, thiamine 1.2 mg,
Biotin 60 mcg riboflavin 1.4 mg, niacin 17 mg, pantothenic acid 5 mg, pyridoxine 1 mg, cyanocobal-
Ascorbic acid 200 mg amin 1 mcg, biotin 20 mcg, and folic acid 140 mcg.
Folic acid 600 mcg
Niacin 40 mg
Riboflavin 3.6 mg
IV. Administration of PN
A. Proper central venous catheter (CVC) tip placement must be con-
firmed prior to initial PN administration as well as any time signs
and symptoms indicate a compromised catheter position.
J. After a review of organ function, medication profile, and serum B. Because it is hypertonic, central PN is administered via a CVC
concentrations, electrolytes are manipulated according to the fol- with the distal tip placed in the superior vena cava adjacent to the
lowing general guidelines: right atrium.1,9,10
1. Because magnesium, phosphorus, and potassium needs C. Infusion of PN via a peripheral vein requires careful consideration
increase with anabolism and are carbohydrate dependent, reple- of the formulation’s osmolarity along with judicious monitoring of
tion levels of these minerals may be needed for the first few the venous access site for signs of phlebitis and/or infiltration.
days of PN. D. The use of femoral catheters for adult PN administration should be
2. Potassium, magnesium, and phosphorus administration is ad- avoided unless no other access can be obtained. These catheters are
justed according to changes in the serum concentrations and associated with a higher risk of venous thrombosis and catheter-
renal function. related sepsis.11,12 However, in pediatric patients, femoral catheters
K. Elevated serum or capillary glucose concentrations or fluid volume have a lower incidence of mechanical complications and may have
intolerance may preclude an increase in glucose concentration or an infection rate similar to catheters not placed in the femoral vein.12
PN volume, respectively. If fluid restriction is necessary, the E. The use of in-line filters is recommended during the administration
required amounts of protein and energy substrate are concentrated of PN because the filters can eliminate or reduce the infusion of par-
within the volume tolerated. ticulates, microprecipitates, microorganisms, pyrogens, and air.13–15
L. Because of reduced dextrose concentration and osmolarity, PPN 1. A 0.22-micron filter should be used for 2-in-1 formulations.
can be initiated at greater volumes than central PN formulations.
1. If PPN is 5% dextrose, it may be initiated at the same rate as
peripheral IV fluids.
2. Osmolarity restrictions usually preclude adding large amounts TABLE 8-7. Trace Element Daily Requirements for Pedi-
of electrolytes to PPN. The maximum osmolarity for PPN is atric Patients* 5–6
900 mOsm/L. A formula to estimate the osmolarity of formu-
lations is in Chapter 7. Additional electrolyte supplements may Term
be delivered via the GI tract or a peripheral vein. Preterm neonates,
neonates infants Children Adolescents
Trace <3 kg 3–10 kg 10–40 kg >40 kg
TABLE 8-5. Recommended Trace Element Intake in
Adult Patients on Parenteral Nutrition5–6 Zinc 400 50–250 50–125 2–5 mg
Copper 20 20 5–20 200–500 mcg
Trace element Standard daily intake Manganese 1 1 1 40–100 mcg
Chromium 0.05–0.2 0.2 0.14–0.2 5–15 mcg
Chromium 10–15 mcg Selenium 1.5–2 2 1–2 40–60 mcg
Copper 0.3–0.5 mg
Manganese 60–100 mcg
*Assumes normal age-related organ function. Recommended intakes of trace
Selenium 20–60 mcg elements cannot be achieved through the use of a single pediatric multiple–trace ele-
Zinc 2.5–5 mg ment product. Only through the use of individualized trace element products can rec-
ommended intakes of trace elements be achieved.

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2. A 1.2-micron filter should be used for TNA formulations. M. Patients may tolerate the PN infusion better if the refrigerated PN
3. Alternatively, a 1.2-micron filter may be used for all PN for- is removed from the refrigerator 30 to 60 minutes prior to the infu-
mulations. sion time; patients occasionally complain of discomfort when the
4. Occlusion of a filter during PN infusion could be indicative of a chilled formulation is infused into the central circulation.9
problem; the filter may be replaced but should never be N. Patients receiving PN formulation for the first time should be mon-
removed altogether. itored closely for any adverse reactions.
F. PN final containers and administration sets free of the plasticizer
di(2-ethylhexyl)phthalate (DEHP) should be used to prevent DEHP V. Monitoring and Management of PN
contamination of TNAs or separate IVFE infusions.16 DEHP is
highly lipophilic, and IVFE are capable of extracting DEHP from A. Serious complications can be associated with PN administration.
the polyvinyl chloride (PVC) containers/administration sets. DEHP The potential for serious complications with PN is unacceptably high
is a known neurotoxic, hepatoxic, and carcinogenic agent in animal unless careful monitoring is conducted by experienced clinicians.
models. The use of DEHP-free bags and tubing is especially impor- B. Monitoring by experienced clinicians can control costs and mini-
tant in chronic long-term patients, pregnant patients, and pediatric mize complications. Suggested protocols for monitoring PN in
patients receiving PN. neonates/pediatric patients and adults are shown in Tables 8-8 and
G. Administration sets9,12 8-9, respectively.
1. PN administration sets are changed using aseptic technique and C. Once it is determined that an individual requires PN, the goals for
universal precautions. specialized nutrition support should be set with specific markers and
2. TNA administration sets are changed every 24 hours and imme- outcomes.1,22 These goals may include the following:
diately upon suspected contamination, or if the product 1. Stabilization of weight or moving toward goal weight
integrity has been compromised. 2. Improvement or replenishment of protein stores
3. 2-in-1 administration sets are changed every 72 hours. 3. Normalization of clinical laboratory values
4. Administration sets for a separate IVFE infusion are discarded 4. Reduction in morbidity/mortality
after use, or at least every 12 hours if the IVFE is infused con- 5. Improvement in quality of life
tinuously. 6. Optimization of clinical outcomes
H. PN is to administered via an infusion pump having adequate pro- D. Nutrition monitoring should be conducted and monitored parame-
tection from “free flow” and reliable audible alarms.9,17,18 ters compared to the goals of the nutrition care plan.
1. Infusion pumps ensure accurate volume (rate) control and con- 1. All individuals receiving PN should be monitored for fluid,
tain safety alarms (visual and auditory) for sensing air and electrolyte, and acid/base imbalances.
pressure changes in the IV tubing; some pumps also have a pro-
grammable rate-cycling feature to minimize infusion errors.
These infusion pump features are key to ensuring safe PN admin-
TABLE 8-8. Monitoring—Neonates/Pediatric Patients
istration because of the hypertonic nature, fluid volume, dextrose
content, and potassium content of the PN formulation. on PN
2. Regular infusion pump preventative maintenance and testing
Parameter Initial Daily Weekly
should be performed, as health care practitioners administering
the PN rely on the pump and its alarms to optimize safe infusion
of the PN formulation. Anthropometric
I. Medical devices for PN administration should minimize the risk Weight ● ●
of needle-stick injuries and patient/caregiver exposure to blood- Length ● ●*
borne pathogens.19–21 Head circumference ● ●*
1. Federal agencies have published standards to prevent needle- Physical examination ● ●
stick injuries in health care settings and enforcement procedures Fluid balance ● ●
regarding occupational exposure to blood-borne pathogens. Metabolic assessment
These standards are laws and are enforced in the same manner as Na, K, Cl, CO2 ● ● ●**
other Occupational Safety and Health Administration laws.
Ca, Phos, Mg ● ●
2. Health care providers administering PN should take an active
Glucose ● ● ●**
role in identifying, evaluating, and selecting available effective
medical devices to reduce exposure to blood-borne pathogens, BUN/Cr ● ●
for instance, needle-less systems to draw blood or the applica- Liver profile ● ●
tion of a needle-free catheter patency device to the CVC that Triglycerides ●*** ●
eliminates the backflow of blood into the catheter lumen. Urine glucose ● ●
J. The PN infusion should be completed within 24 hours of initiation.12 Complete blood count ● ●
K. IVFE infused separately from the PN formulation should be com- Prealbumin ●**** ●
pleted within 12 hours of entry into the original container.12
L. Each PN formulation should be inspected prior to administration,
BUN, blood urea nitrogen.
and the PN formulation should not be infused if visual changes or *Weekly until 3 months of age.
precipitates are apparent.14 The pharmacist evaluates the PN for- **Daily until stable, then once or twice weekly.
mulation before dispensing, and the nurse, patient, or caregiver is ***Initially and before each advancement of intravenous fat emulsions, then once
responsible for ongoing evaluation of the PN prior to and during weekly. If septic, more frequent monitoring is prudent.
the infusion. ****Prealbumin approaches adult values at approximately 3 months of age.

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S E C T I O N I Fundamentals of Nutrition Support Practice and Management

demonstrated. The health care provider needs to be alert to

TABLE 8-9. Monitoring for Adult Patients on potential changes in fluid status and should closely monitor
Parenteral Nutrition intake and output, presence of edema, vital signs, and weight
with attention to changes, patterns, or trends that could indicate
Critically ill Stable problems or progress toward achieving nutrition goals.
Parameter Baseline patients patients E. It is important that the health care provider periodically compare the
actual PN infused into the patient with the recommended, measured,
Chemistry screen Yes 2–3x/week Weekly or estimated nutrition needs to ensure optimal treatment.
(Ca, Mg, LFTs, P) F. The nutrient content of the administered PN should be regularly
Electrolytes, BUN, Yes Daily 1–2x/week compared with predicted energy and protein needs. Changes in clin-
creatinine ical condition and activity level may require periodic reassessment
of energy requirements.
Serum triglycerides Yes Weekly Weekly
G. GI function and readiness for oral/enteral feeding should be assessed
CBC with differential Yes Weekly Weekly
whenever the patient’s clinical condition changes.
PT, PTT Yes Weekly Weekly H. Adjustments of the PN formula may be necessary as oral intake
Capillary glucose 3x/day 3x/day (until 3x/day (until begins or improves.
consistently consistently I. Regular assessments and meticulous care of the parenteral access
<200 mg/dL) <200 mg/dL) device ensure a reliable delivery system for the PN and minimize
Weight If possible Daily 2–3x weekly infection.
Intake and output Daily Daily Daily unless fluid J. Extensive attention is directed toward monitoring the patient’s
status is as- physiological response to PN therapy, but it is equally important to
sessed by assess, monitor, and manage the patient’s developmental, emo-
physical exam tional, and psychological response to PN.
Nitrogen balance As needed As needed As needed
Indirect calorimetry As needed As needed As needed VI. Complications of PN
Although widely reported, complications of PN can be minimized
BUN, blood urea nitrogen; CBC, complete blood count; LFT = liver function test; PT, when a multidisciplinary team of trained professionals monitors PN
prothrombin time; PTT, partial thromboplastin time. therapy and venous access devices.
A. Peripheral venous access catheters for PN
1. The indication for PPN infusion is a short-term need for PN.
a) In general, it is inappropriate to manage short-term fluid, 2. The patient receiving PPN should have no fluid restrictions.
electrolyte, and acid-base imbalances by PN alone. However, 3. Infusion of PN via a peripheral vein requires careful considera-
adjustments in fluid, electrolyte, and acid-base content of PN tion of the formulation’s osmolarity (<900 mOsm/L) along with
may avoid the risk and expense inherent in providing supple- judicious monitoring of the venous access site for phlebitis
mental fluids and electrolytes. and/or infiltration.
b) PN volume may be concentrated for patients at risk for vol- 4. The peripheral venous access catheter should be removed as
ume overload or expanded to meet the needs of patients with soon as thrombophlebitis develops or an infiltration is noted.
increased fluid requirements. 5. The Centers for Disease Control and Prevention (CDC) recom-
c) The electrolyte composition of PN may be varied based on mends the following12:
the electrolyte profile, changes in clinical status, organ func- a) Replace peripheral venous catheters at least every 72 to
tion, and medications. 96 hours in adults to prevent phlebitis and bacterial catheter
d) Acid-base disorders of metabolic origin may respond to colonization. However, in pediatric patients, the risk for
adjustments in the amount of chloride or acetate in PN. phlebitis is not increased with the duration of catheter days, so
e) Acid-base disorders of respiratory origin will usually respond the peripheral venous catheter should be left in place until the
to correction of the underlying problem or adjustments of the IV therapy is completed unless complications (phlebitis,
ventilator.23 infiltration) occur.
2. All patients receiving PN should be monitored for proper glu- b) Use a transparent, semipermeable polyurethane dressing or a
cose control. gauze dressing to cover the peripheral access site.
3. One or more visceral protein concentrations (eg, albumin, preal- c) Replace the dressing when the catheter is removed or
bumin, transferrin) should be evaluated with consideration given replaced, or when the dressing becomes damp, loosened, or
to their half-life and changes in patient fluid status, organ func- soiled.
tion, and presence of infection. If an unsatisfactory response is 6. Hydrocortisone and heparin may be added to 2-in-1 PN for-
observed, a nitrogen-balance study may be used to guide nutrient mulations to decrease phlebitis.
intake. Serum albumin concentration is a poor marker of nutri- B. CVCs for PN
tional repletion or depletion because of its long half-life and large 1. General information
body pool. However, serum albumin has been shown to be an a) Central PN is administered via a CVC with the distal tip
excellent prognostic marker for patient outcome. placed in the superior vena cava adjacent to the right atrium.14
4. Typically, laboratory monitoring of serum chemistries and vis- b) Proper CVC tip placement must be confirmed before initi-
ceral proteins is more frequent when PN is initiated and ating PN, as well as any time signs or symptoms indicate an
decreases in frequency once a degree of metabolic stability is improper catheter position.

112 A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. © 2005 A.S.P.E.N. www.nutritioncare.org.
 S E C T I O N I Fundamentals of Nutrition Support Practice and Management

c) Venous access catheters should be promptly removed when 3. Infectious complications

no longer needed. a) It has been estimated that over 200,000 nosocomial blood-
2. Catheter occlusion: the inability to infuse a solution and/or stream infections occur yearly in the United States and that
aspirate a blood sample the majority of these infections are associated with venous
a) Thrombotic occlusion9,17 access devices.30
(1) Intraluminal clotting as a result of inadequate flushing or b) Catheter-related infection accounts for nearly 75% of all com-
blood reflux. Treat by instilling a thrombolytic agent plications seen in pediatric patients receiving PN therapy.31
directly into the catheter, not to exceed the volume capac- c) The multidisciplinary health care team providing and moni-
ity of the catheter. Protocols for the organizational use of toring the efficacy of the PN therapy has a responsibility to
thrombolytic agents to restore catheter patency must be minimize catheter infections.
developed. (1) Reductions in catheter-associated sepsis occur when
(2) Fibrin sheath/fibrin sleeve at the distal catheter tip: par- specially trained registered nurses care for the CVC.1
enteral admixtures can be infused without trouble, but (2) Proper hand hygiene procedures—involving hand wash-
blood samples cannot be aspirated. Thrombolytic agents ing with conventional antiseptic-containing soap and
directly instilled into the catheter exceeding the volume water or with waterless alcohol-based gels or foams—
capacity of the catheter may correct this problem, or an must be observed.
endovascular procedure to remove the fibrin sheath may (3) Care and maintenance of the CVC must be performed
be needed to salvage the catheter. according to published standards.9,12
(3) Subclavian vein thrombosis. Subclavian vein thrombosis (4) Aseptic technique must be observed for the insertion and
can occlude a catheter and manifest clinical symptoms of care of the intravascular catheter.
vascular obstruction. Symptoms include neck vein disten- (5) The CDC also makes the following recommendations12:
tion, edema, pain or tingling over the ipsilateral arm and (a) To prevent catheter-related infections, adult CVCs or
neck, throat tightness, and prominent anterior chest wall percutaneously inserted central catheters (PICCs)
vein distention. This situation is serious and requires should not be routinely replaced. The CDC makes no
immediate physician intervention. Catheter-related sub- recommendations in this area for pediatric patients.
clavian thrombosis is the most common cause of upper (b) CVCs or PICCs should not be removed on the basis of
arm extremity deep vein thrombosis, and there is a 12% fever alone. Use clinical judgment regarding removal
of the catheter if infection is detected elsewhere or if a
incidence of pulmonary embolus with a subclavian throm-
noninfectious cause of fever is suspected.
bosis.24,25 Treatment of the subclavian thrombosis may
(c) If no evidence of infection is present, guidewire
include catheter removal, elevation of the affected arm,
exchange to replace a nontunneled catheter should be
catheter-directed thrombolytic agent infusion, systemic
performed only to replace a malfunctioning catheter.
infusion of a thrombolytic agent, and/or endovascular
(d) If a multilumen catheter is used for fluids, one port
stenting.
should be designated exclusively for PN administra-
b) Nonthrombotic occlusion
tion. A CVC should have the minimum number of
(1) Intraluminal drug precipitates can result in catheter
ports/lumens necessary for clinical management of
occlusions.
the patient.
(2) Catheter irrigations with 0.1N hydrochloric acid may dis-
(e) Antibiotic lock solutions should not be routinely
solve occlusions caused by calcium phosphate or other
used in an attempt to prevent catheter-related blood-
mineral precipitates by decreasing the pH and improving stream infection.
solubility.26 (f) Clean skin should be disinfected with an appropriate
(3) Catheter irrigations with a 70% ethanol-in-water solution antiseptic before catheter insertion and during dress-
or 0.1N sodium hydroxide may be used to clear an occlu- ing changes. A 2% chlorhexidine-based prep is pre-
sion caused by fat emulsion.27,28 ferred (no recommendations for chlorhexidine in
(4) Protocols for the organizational use of precipitant clear- infants <2 months can be made), though tincture of
ance agents to restore catheter patency must be developed. iodine, an iodophor, or 70% alcohol can be used. No
c) Mechanical occlusion topical antibiotic ointment or creams should be placed
(1) Catheter malposition, external catheter or infusion on catheter insertion sites (except dialysis catheters)
clamps, kinking of the catheter, and/or constricting because of the potential for antimicrobial resistance
sutures should be assessed for and corrected. and fungal infections. Organic solvents (eg, acetone,
(2) “Pinch-off syndrome”: Intermittent mechanical obstruc- ether) should never be applied to the skin. The
tion/occlusion is related to postural changes caused by catheter insertion site should then be covered with
catheter compression between the clavicle and first rib.29 either a sterile gauze or a sterile, transparent, semiper-
In certain patients, an anatomic narrow triangle exists at meable dressing. Gauze dressings should be changed
the junction of the axillary and subclavian vein. This junc- every 2 days, and sterile, transparent dressings should
tion is in the lateral aspect of the clavicle, and “pinch-off” be changed at least weekly, depending on the patient’s
may occur with medial placement of the CVC. Changing clinical circumstances.
the patient’s position by raising the ipsilateral arm (open- (g) All catheter injection ports should be cleansed with
ing the angle) relieves the occlusion. Chest x-rays will 70% alcohol or an iodophor before the system is
demonstrate a luminal narrowing of the catheter at this accessed.
site. Catheter removal is recommended, as the pinch-off (h) The CDC has published specific guidelines for the
syndrome can lead to catheter transection and embolus. care of umbilical catheters.12

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S E C T I O N I Fundamentals of Nutrition Support Practice and Management

C. GI tract
1. Disuse of the GI tract can lead to some degree of villous atro- TABLE 8-10. Suggested Guidelines for Monitoring and
phy and possibly bacterial translocation. Managing PN-Associated MBD
2. Bacterial translocation may be avoided with enteral feeding, but
the amount and type of enteral feeding required to prevent bac- 1. Evaluate all patients receiving long-term PN >1 year for MBD.
terial translocation is unknown. 2. Monitor for physical signs of MBD: loss of height, bone or back
3. Hepatobiliary complications32 pain.
a) Mildly elevated transaminase and alkaline phosphatase con- 3. Provide adequate amounts of minerals in the PN solution for
centrations usually occur 2 weeks after PN is initiated. bone remodeling, including calcium 15 mEq, phosphorus
b) Elevated serum bilirubin is seen less often, and jaundice does
15 mM, magnesium (adjust amount for serum and urine levels).
not occur in most adults.
4. Reduce higher protein doses to 1 g/kg/day once nutritional
c) Elevated enzyme concentrations may return to normal while
the patient is still on PN but almost always normalize when status is stable.
PN is stopped. 5. Treat metabolic acidosis with adequate amounts of acetate in
d) Causes of hepatic abnormalities related to PN include steato- PN solutions.
sis, especially with infusion of carbohydrate at rates greater 6. Monitor serum (at least monthly) calcium, phosphorus, magne-
than 5 mg/kg/minute, and sepsis. sium, and acetate concentrations. Maintain normal concentra-
e) A metabolic complication seen more frequently in the pedi- tions by adjusting amounts in the PN solutions. Specific markers
atric population than in adults is the development of PN- of bone metabolism may be of further help.
associated cholestasis (PNAC), the most life-threatening
7. Obtain 24-hour urine collection for calcium and magnesium
long-term complication of PN therapy in children.
every 6 to 12 months. Adjust PN to maintain positive balances.
f) The incidence of PNAC in children receiving long-term PN
is estimated at 30% to 60%.33 8. Obtain DEXA measurement and refer patient to endocrinologist
g) The etiology of PNAC is believed to be multifactorial. It has for evaluation and pharmacologic therapy if low bone mineral
been associated with recurrent sepsis, delays in enteral feed- density (T-score below –1). Repeat DEXA every 1 to 2 years.
ing, bacterial overgrowth, excessive dextrose administra- 9. Minimize steroid use and all medications known to cause bone
tion, altered amino acid profiles, prematurity, low birth resorption.
weight, long duration of PN, short-bowel syndrome, and ele- 10. Promote exercise or refer to physical therapist.
vated levels of lithocholic acid. 11. Encourage cessation of smoking.
h) While no definitive preventive measure is known, efforts to
minimize the incidence of PNAC should be directed toward
early initiation of EN, prevention and aggressive treatment Reprinted with permission from Hamilton C. Parenteral nutrition-associated metabolic
of sepsis, avoidance of overfeeding, and use of cyclic PN for bone disease. Support Line. 2003;25(5):7–13.
prolonged therapy.1
i) A sustained upward trend of conjugated bilirubin and alkaline
3. Refeeding syndrome is defined as a constellation of fluid,
phosphatase serve as a warning that the patient may be at risk
micronutrient, electrolyte, and vitamin imbalances that occurs
of developing PNAC and should prompt reevaluation of the
PN regimen and transition to EN when medically possible. within the first few days after refeeding of starved adult
4. Management of PN-induced hepatobiliary abnormalities usu- patients.35 It is potentially life-threatening if not recognized
ally includes giving about one third of calories as IVFE, cycling and treated promptly.
the PN so that the patient is off PN 8 to 10 hours per day, and a) This syndrome may involve hemolytic anemia, respiratory
using enteral nutrition to stimulate bile flow. distress, paresthesias, tetany, and cardiac arrhythmias.
D. Metabolic b) Biochemical findings include hypophosphatemia, hypomag-
1. Osteopenia of prematurity, also commonly termed metabolic nesemia, and hypokalemia.
bone disease (MBD), is a complication of long-term PN ther- c) Proposed risk factors for refeeding syndrome include alco-
apy. While the incidence of MBD is unknown, the patient pop- holism, anorexia nervosa, marasmus, rapid refeeding, and
ulation at highest risk of developing MBD is premature excessive dextrose infusion.
infants (<34 weeks gestation at birth or <1.5 kg birth weight). d) Suggested prevention of refeeding syndrome in the adult
Major factors compromising bone mineralization are deficien- includes addressing repletion of serum potassium, magne-
cies in phosphorus, calcium, and vitamin D. Aluminum, found sium, and phosphorus concentrations before initiating PN;
as a contaminant in PN formulations, may also decrease the rate limiting initial carbohydrate to 150 g/day and fluid to
of bone formation and mineralization. Amounts of aluminum 800 mL/day in at-risk patients; providing adequate amounts
exceeding 5 mcg/kg/day may be associated with bone toxicity. of potassium, magnesium, phosphorus, and vitamins in initial
The severity of MBD can vary from mild subclinical bone under- PN; and increasing carbohydrate-dependent minerals in pro-
mineralization to nontraumatic fractures. Maximizing calcium portion to increases in carbohydrate when PN is advanced.
and phosphorus intake soon after birth to match intrauterine 4. Hyperglycemia
accretion rates can help prevent the development of MBD. Cal- a) The incidence of hyperglycemia appears to be inversely
cium and phosphorus intake at a ratio of 1.7:1 (Ca:P) by weight related to developmental age and weight in the pediatric pop-
has produced mineral retention of approximately 90% in very ulation. In neonates, hyperglycemia is defined as a plasma
low birth weight infants receiving PN.34 glucose concentration >150 mg/dL or a whole-blood glucose
2. MBD can also occur in adults on long-term PN therapy. See concentration >125 mg/dL. Prematurity, excessive dextrose
Table 8-10 for monitoring and management guidelines for MBD. infusions via PN, sepsis, surgery, or respiratory distress may

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contribute to hyperglycemia. To minimize the risk of hyper- and displacement of albumin-bound bilirubin by free fatty
glycemia in pediatric patients, as well as to avoid elevations in acids.1
CO2 in the systemic circulation, dextrose infusion rates in PN c) In adult patients, IVFE should be limited to the provision
should not exceed 10 to 14 mg/kg/min.1 To control PN-asso- of essential fatty acids (eg, 250 mL of 20% IVFE, once or
ciated hyperglycemia in infants, continuous insulin infusion twice weekly) when triglyceride concentrations rise above
can be administered in a safe and effective manner.36 400 mg/dL.42
b) Risk factors for hyperglycemia (nonfasting blood glucose d) Withholding IVFE must be considered when triglyceride con-
>180 mg/dL) in adults include metabolic stress, medica- centrations are greater than 500 mg/dL or in the presence of
tions, obesity, and diabetes mellitus. lipemic serum. Topical administration of soybean or safflower
c) Techniques to minimize hyperglycemia in an adult receiving oil may be a useful alternative under these conditions since
PN include glucose monitoring every 6 hours with initiation topical linoleic acid is transcutaneously absorbed directly into
of PN; administration of dextrose in amounts less than the plasma without exacerbating hypertriglyceridemia.42
maximum glucose oxidation rate (<4 mg/kg/minute); and E. Fluid and electrolytes43
administration of decreased amounts of dextrose initially in 1. Hyponatremia is frequently noted in patients receiving PN. The
at-risk patients (100–150 g/day or 2–3 mg/kg/minute). most common cause of hyponatremia is administration of
d) For patients previously treated with insulin or oral hypo- excessive hypotonic fluid. Other causes include nephritis, adre-
glycemic agents, a basal amount of human regular insulin nal insufficiency, congestive heart failure, the syndrome of
should be added to the PN formulation to keep blood glucose inappropriate antidiuretic hormone, and cirrhosis with ascites.
concentrations below 180 mg/dL. Symptoms of hyponatremia include confusion, hypotension,
e) Only regular human insulin is compatible with PN formula- irritability, lethargy, and seizures. Depending on the etiology,
tions. Other insulin products such as NPH, ultralente, lente, hyponatremia is usually treated with fluid restriction or diuret-
lispro, aspart, and glargine are not compatible with PN. ics. If sodium intake is inadequate and the clinical condition
f) A regimen of 0.1 units of insulin per gram of dextrose in the warrants additional sodium intake, sodium may be increased in
PN infusion can be used as a starting dose.37,38 If the blood glu- the PN formulation.
cose is >300 mg/dL, PN should not be initiated until glycemic 2. Hypernatremia occurs infrequently. Possible causes of hyperna-
control is improved (<180 mg/dL). tremia include inadequate free water administration, excessive
g) In general, the dextrose content of the PN should not be water loss (as with fever, burns, osmotic diuresis hyperventila-
increased until glucose concentrations during the previous tion), or excessive sodium intake. Symptoms of hypernatremia
24-hour period are consistently <180 mg/dL. include thirst, decreased skin turgor, and mild irritability. Increas-
h) If hyperglycemia persists when 0.3 units of insulin per gram ing fluid intake usually treats hypernatremia; less often, reducing
of PN dextrose is exceeded, initiation of a separate IV insulin sodium content in the PN formulation treats it.
infusion should be considered to achieve more appropriate 3. Hypokalemia may be caused by inadequate potassium intake,
glycemic control. refeeding syndrome, or excessive losses with diarrhea or intes-
i) The amount of insulin that adheres to the PN bag and tubing tinal fluids. Drugs such as loop and thiazide diuretics, cathartics,
made from ethyl vinyl acetate or PVC is approximately 5% to and some antibiotics or antifungals (eg, amphotericin B) may
15%39; therefore, insulin requirements may appear slightly increase urinary potassium losses. Hypomagnesemia may also
higher than they actually are. give rise to hypokalemia. Symptoms of hypokalemia include
5. Hypoglycemia can develop rapidly in neonates, young infants, nausea, vomiting, confusion, arrhythmias, respiratory depres-
and some adults upon interruption of PN. sion, and cardiac arrest. Increasing the potassium content of the
a) Preterm neonates are at increased risk for developing hypo- PN by providing it through a peripheral vein or by the GI route
glycemia because of immature homeostatic mechanisms, lim- may treat hypokalemia. If potassium is to be administered via a
ited glycogen stores, and increased glucose requirements.40 peripheral vein or via the GI tract, it is necessary to collaborate
b) Hypoglycemia can be seen within 15 to 30 minutes after stop- with the pharmacist, as potassium supplements are very hyper-
ping PN, suggesting that glucose concentrations should be tonic and can cause significant irritation to the peripheral vein or
checked within 15 to 60 minutes.41 PN can be tapered over 1 the GI mucosa. If hypomagnesemia is present, it should be cor-
to 2 hours prior to discontinuation to prevent hypoglycemia rected first to facilitate correction of hypokalemia.
episodes.1 This tapering process is usually accomplished dur- 4. Hyperkalemia may be caused by renal dysfunction, administra-
ing the transition period between PN and enteral feeding. tion of excessive potassium, metabolic acidosis, or potassium-
6. Hyperlipidemia sparing medications (eg, angiotensin-converting enzyme [ACE]
a) Triglyceride (TG) levels provide a reasonable estimate of lipid inhibitors). Symptoms of hyperkalemia include diarrhea, pares-
clearance and should be maintained below 200 mg/dL in pedi- thesia, tachycardia, oliguria, and cardiac arrest. Hyperkalemia
atric patients. Hypertriglyceridemia in pediatric populations is may be managed by reducing potassium intake or, if severe, by
usually due to excessive fat administration, uncontrolled using potassium exchange resins, insulin and dextrose, inhaled
hyperglycemia, excessive carbohydrate administration with- beta agonists, or dialysis.
out hyperglycemia, prematurity, low birth weight, or sepsis. 5. Hypocalcemia may caused by decreased vitamin D intake,
b) If baseline TG concentrations are <200 mg/dL, IVFE can be hypoparathyroidism, citrate binding of calcium with blood
administered and TG concentrations monitored. A rise of product administration, or hypoalbuminemia. Hypomagne-
≥50 mg/dL warrants a temporary discontinuation or reduction semia may also contribute to hypocalcemia. Symptoms of
in the infusion rate. Clinical consequences of hypertriglyc- hypocalcemia include tetany, irritability, seizures, and ventricu-
eridemia include reduced oxygenation, impaired leukocyte lar arrhythmias. Hypocalcemia that is independent of hypoalbu-
function, deposition of lipids in the reticuloendothelial cells, minemia may be treated with calcium supplementation.

© 2005 A.S.P.E.N. www.nutritioncare.org. A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. 115
S E C T I O N I Fundamentals of Nutrition Support Practice and Management

6. Hypercalcemia may be caused by renal failure, tumor lysis syn- who are elderly or debilitated, those with malignancy, and those
drome, bone cancer, administration of excess vitamin D, pro- who eat ethnic foods not available in the hospital setting.
longed immobilization and stress, or hyperparathyroidism. 4. Adult patients with known diabetes mellitus or clinically induced
Symptoms of hypercalcemia include confusion, dehydration, insulin resistance require special monitoring to set up a safe tran-
muscle weakness, nausea, vomiting, and coma. Hypercalcemia sitional feeding plan.
may be treated by administering isotonic saline, inorganic phos- B. To guide the transition from PN to full oral intake, a bedside calo-
phate, corticosteroids, bisphosphonates, or mithramycin. rie count may be performed when the patient is eating a substantial
7. Hypomagnesemia may be caused by refeeding syndrome, alco- amount of food with a consistent appetite or effort but unsure of
holism, diuretic use, prolonged nasogastric suction, increased how much may have been tolerated or consumed. This count may
stool output, diabetic ketoacidosis, or magnesium-wasting med- be used to guide the reduction or discontinuation of PN.
ications. Symptoms of hypomagnesemia include cardiac arrhyth- C. Although it has been documented that nondiabetic adult patients
mias, tetany, convulsions, and muscular weakness. Parenteral suffer minimal ill effects, abrupt discontinuance of PN may poten-
magnesium supplementation should be used to treat moderate tiate rebound hypoglycemia in patients who are not being fed orally
and severe hypomagnesemia since orally administered magne- or enterally.
sium products are poorly absorbed. 1. PN may be rapidly discontinued in an adult patient who is toler-
8. Hypermagnesemia may be seen with excessive magnesium ating tube feeding in amounts adequate to maintain serum glu-
intake in renal insufficiency. Symptoms of hypermagnesemia cose levels.
include respiratory paralysis, hypotension, premature ventricular 2. Decreasing the PN infusion rate by one-half for 1 to 2 hours
contractions, lethargy, coma, liver dysfunction, and cardiac before discontinuation may minimize the risk of rebound hypo-
arrest. Hypermagnesemia is usually treated by decreasing magne- glycemia.
sium intake. Severe hypermagnesemia may necessitate dialysis.
3. If PN is abruptly discontinued, a 10% dextrose solution may be
9. Hypophosphatemia may be seen with refeeding syndrome, long-
administered for a few hours. This practice is unnecessary
term alcoholism, and inadequate phosphorus intake. Symptoms
when discontinuing PPN.
of hypophosphatemia include congestive heart failure, arrhyth-
4. Capillary glucose concentrations may be measured 30 to 60 min-
mias, nausea and emesis, altered red blood cell morphology,
utes after cessation of a central PN formulation, and oral or IV
hemolytic anemia, leukocyte dysfunction, ataxia, short-term
carbohydrate can be given as appropriate if hypoglycemia is
paralysis, lethargy, confusion, coma, acute respiratory failure,
suspected.
acute tubular necrosis, and bicarbonate and glucose wasting.
D. Oral or enteral tube feeding may be initiated when the patient has
Moderate and severe hypophosphatemia should be treated with
IV phosphate supplementation since oral phosphate products are demonstrated return of GI function.
poorly absorbed. E. Initiation of oral intake requires GI function, minimal risk for
10. Hyperphosphatemia may be seen with administration of excess aspiration, and patient motivation.
phosphate or with renal insufficiency. Symptoms of hyperphos- F. In some circumstances, a swallowing evaluation may be useful in
phatemia include paresthesias, flaccid paralysis, mental confu- determining readiness for oral feeding and can dictate the type and
sion, hypertension, and cardiac arrhythmias. Tissue calcification texture of foods introduced.
may occur with prolonged elevated levels. Decreasing phospho- G. PN may have a negative effect on appetite. If more than 25% of
rus intake and/or using enteral phosphate binders may treat caloric needs are provided as PN, reduced oral intake can be
hyperphosphatemia. expected.46
1. When oral intake equals 500 kcal/day in an adult patient, the
carbohydrate and protein in the PN should be reduced by an
VII. Transitional Feeding and Discontinuing PN44,45 amount equal to the amount consumed orally.
A. The ultimate goal for patients receiving PN is to return to as nearly 2. Subsequent decreases in the PN should continue as oral intake
normal food intake as tolerated. The period during which oral or increases.
enteral feeding is initiated and PN is discontinued may be termed 3. Once an adult patient is taking 60% of goal energy and protein
the transitional period. The transition from PN to oral intake or via the oral route, PN may be stopped.
enteral tube feeding should be accomplished in an orderly fashion H. For adults who do not achieve acceptable oral intake within a few
to avoid the potential for deterioration in nutritional status when days, enteral tube feeding should be considered.
PN is discontinued. I. For adults who have been receiving substantial amounts of elec-
1. In pediatric patients, discontinuation of PN is generally a more trolytes in the PN, oral or IV electrolyte supplements may be
gradual process than in adult patients. needed.
a) PN is tapered as enteral feeds are advanced. Ideally, the com-
bination of PN and enteral feedings will meet all estimated (Parenteral Nutrition Management chapters from the 1st edition were
nutritional goals during the transitional period. contributed by Annalynn Skipper, Keith Millikan, Kristy Gibbons,
b) In practice, PN is generally continued until about 75% to Nancy Cyr, Michael L. Christensen, and Richard A. Helms)
80% of energy needs (90–100 kcal/kg) are met enterally.
2. For many adult patients, PN may be discontinued as soon as they REFERENCES
are able to tolerate solid foods. These patients are usually 1. A.S.P.E.N. Board of Directors and the Clinical Guidelines Task Force.
younger, well nourished before PN, not debilitated, free of malig- Guidelines for the use of parenteral and enteral nutrition in adult and pedi-
nancy, and without oral intake for less than 1 to 2 weeks. atric patients. J Parenter Enteral Nutr. 2002;26(suppl):1SA–138SA.
3. For other adult patients, a detailed transitional feeding plan may 2. Institute of Medicine. Minerals. Recommended Dietary Allowances. 10th ed.
be needed. Candidates for transitional feeding include those Washington, DC: National Academy Press; 1989:174–194.

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3. Baumgartner TG. Clinical Guide to Parenteral Micronutrition. 3rd ed. 25. Horattas MC, Wright DJ, Fenton AH, et al. Changing concepts of deep
Fujisawa USA; Deerfield, IL 1997. venous thrombosis of the upper extremity: report of a series and review of
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intravenous hyperalimentation of underweight adult subjects. J Clin Invest. 26. Shulman RJ, Reed T, Pitre D, et al. The use of hydrochloric acid to clear
1975:55:94–104. obstructed central venous catheters. J Parenter Enteral Nutr. 1988;12:
5. American Medical Association Department of Foods and Nutrition. Multi- 509–510.
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sory Group. J Parenter Enteral Nutr. 1979:3:258–262. occlusion. J Parenter Enteral Nutr. 1987;11:507–508.
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lines for essential trace element preparations for parenteral use: a statement solution to clear partially occluded vascular access ports. J Parenter Enteral
by an expert panel. J Am Med Assoc. 1979;241:2051–2054. Nutr. 1993;17:289–291.
7. McMahon M, Manji N, Driscoll DF, Bistrian BR. Parenteral nutrition in 29. Andris DA, Krzywda EA. Catheter pinch-off syndrome: recognition and
patients with diabetes mellitus: theoretical and practical considerations. management. J Intravenous Nurs. 1997;20:233–237.
J Parenter Enteral Nutr. 1989;13:545–553. 30. Maki DG, Stolz SM, Wheeler S, et al. Prevention of central venous
8. Kalhan SC, Kilic I. Carbohydrate as nutrient in the infant and child: range catheter–related bloodstream infection by use of an antiseptic-impregnated
of acceptable intake. Euro J Clin Nutr. 1999;53(suppl 1):S94–S100. catheter: a randomized, controlled trial. Ann Intern Med. 1997;127:
9. Intravenous Nurses Society. Infusion nursing: standards of practice. 257–266.
J Intravenous Nurs. 2000;23(suppl):S1–S88. 31. Adal KA, Farr BM. Central venous catheter-related infections: a review.
10. A.S.P.E.N. Board of Directors and the Task Force on Standards for Spe- Nutrition. 1996;12:208–213.
cialized Nutrition Support for Hospitalized Adult Patients. Standards for 32. Fleming CR. Hepatobiliary complications in adults receiving nutrition
specialized nutrition support: adult hospitalized patients. Nutr Clin Pract. support. Dig Dis. 1994;12:191–198.
2002;17:384–391. 33. Suita S, Ikeda K, Nagasaki A, et al. Follow-up studies of children treated
11. Harden JL, Kemp C, Mirtallo J. Femoral catheters increase risk of infec- with a long-term intravenous nutrition during the neonatal period. J Pediatr
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12. Centers for Disease Control and Prevention. Guidelines for the prevention 34. Pelegano JF, Rowe JC, Carey DE, et al. Simultaneous infusion of calcium
of intravascular catheter-related infections. MMWR. 2002;51(No. RR-10). and phosphorus in parenteral nutrition for premature infants: use of physi-
13. Bethune K, Allwood M, Grainger C, Wormleighton C. British Pharmaceu- ologic calcium/phosphorus ratio. J Pediatr. 1989;114:115–119.
tical Nutrition Group Working Party. Use of filters during the preparation 35. Brooks MJ, Melnik G. The refeeding syndrome: an approach to under-
and administration of parenteral nutrition: position paper and guidelines standing its complications and preventing its occurrence. Pharmacother-
prepared by a British pharmaceutical nutrition group working party. Nutri- apy. 1995;15:713–726.
tion. 2001;17:403–408. 36. Collins JW Jr, Hoppe M, Brown K, et al. A controlled trial of insulin infusion
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parenteral nutrition. J Parenter Enteral Nutr. 2004;28:S39–S70. intolerance. J Pediatr. 1991;118:921–927.
15. Food and Drug Administration. Safety alert: hazards of precipitation asso- 37. McCowen KC, Malhotra A, Bistrian BR. Stress-induced hyperglycemia.
ciated with parenteral nutrition. Am J Hosp Pharm. 1994;51:1427–1428. Crit Care Clin. 2001;17:107–124.
16. Dickerson RN. Di(2-ethylhexyl)phthalate as a plasticizer for intravenous 38. McCowen KC, Bistrian BR. Hyperglycemia and nutrition support: theory
bags and tubing: a toxicological quandary. Nutrition. 1997;13:1010–1012. and practice. Nutr Clin Pract. 204;19:235–244.
17. Krzywda EA, Andris DA, Edmiston CE, Wallace JR. Parenteral access 39. Marcuard SP, Dunham B, Hobbs A, Caro JF. Availability of insulin from total
devices. In: Gottschlich MM, ed. The Science and Practice of Nutrition parenteral nutrition solutions. J Parenter Enteral Nutr. 1990;14:262–264.
Support: A Case-Based Core Curriculum. Dubuque, IA: Kendall/Hunt; 40. Farrag HM, Cowett RM. Glucose homeostasis in the micropremie. Clin
2001:225–250. Perinatol. 2000;27:1–22.
18. JCAHO. 2005 National Patient Safety Goals FAQs. www.jcaho.org/ 41. Werlin SL, Wyatt D, Camitta B. Effect of abrupt discontinuation of high
accredited+organizations/patient+safety/05+npsg/05_npsg.html glucose infusion rates during parenteral nutrition. J Pediatr. 1994;124:
Accessed December 8, 2004 441–444.
19. US Department of Health and Human Services, Public Health Service, 42. Sacks GS, Mouser JF. Is IV lipid emulsion safe in adult patients with
Centers for Disease Control and Prevention, National Institute for Occupa- hypertriglyceridemia? Nutr Clin Pract. 1997;3:120–123.
tional Safety and Health Settings (NIOSH). Preventing Needlestick 43. Brown RO, Dickerson RN. Drug-nutrient interactions. Am J Managed
Injuries in Health Settings. NIOSH Publication No 2000-108. Cincinnati, Care. 1999;5:345–352.
OH:NIOSH;November; 1999. 44. Wagman LP, Miller KB, Thomas RB, Newsome HH, Weir GC. The effect
20. US Department of Labor, Occupational Safety and Health Administration. of acute discontinuation of total parenteral nutrition. Ann Surg. 1986;204:
Enforcement Procedures for the Occupational Exposure to Bloodborne 524–529.
Pathogens. Directives No CPL 2-2.44D. Effective date: November 5, 1999. 45. Winkler MF, Pomp A, Caldwell MD, Albina JE. Transitional feeding: the
US Department of Labor, Washington DC, 1999. relationship between nutritional intake and plasma protein concentrations.
21. US Department of Labor, Occupational Safety and Health Administration. J Am Diet Assoc. 1989;89:969–970.
Occupational Exposure to Bloodborne Pathogens; Needlesticks and Other 46. Gil KM, Skeie B, Kvetan V, Askanazi J, Freidman MI. Parenteral nutrition
Sharp Injuries; Final Rule Federal Legislation, Public Law 106-430. Effec- and oral intake: effect of glucose and fat infusions. J Parenter Enteral Nutr.
tive date: April 18, 2001. US Department of Labor, Washington DC, 2001. 1991;15:426–432.
22. A.S.P.E.N. Board of Directors. Clinical Pathways and Algorithms for
Delivery of Parenteral and Enteral Nutrition in Adults. Silver Spring, MD: SUGGESTED READINGS
American Society for Parenteral and Enteral Nutrition; 1998. Klein S, Kinney J, Jeejeebhoy K, et al. Nutrition support in clinical practice:
23. Nehme AE. Nutritional support of the hospitalized patient: the team con- review of published data and recommendations for future research direc-
cept. JAMA. 1980;243:1906–1908. tions. J Parenter Enteral Nutr. 1997;21:133–156.
24. Kerr TM, Lutter KS, Moeller DM, et al. Upper extremity venous thrombo- Rombeau JL, Rolandelli RR, eds. Clinical Nutrition: Parenteral Nutrition.
sis diagnosed by duplex scanning. Am J Surg. 1990;160:202–206. 3rd ed. Philadelphia, PA: WB Saunders; 2001.

© 2005 A.S.P.E.N. www.nutritioncare.org. A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. 117
 Michael S. Nyffeler, PharmD, BCNSP;
Eric Frankel, PharmD, BCNSP; Edmund Hayes, PharmD;
Stephanie Mighdoll, PharmD 9
Drug-Nutrient Interactions

Introduction (2) For liquid medications in solution, the rate-limiting step

to absorption is blood perfusion of the intestines, where
The goal of a multidisciplinary approach to monitoring enterally and
absorption takes place.2 Adequate perfusion of the small
parenterally fed patients for drug-nutrient interactions is to maximize
bowel is necessary for proper absorption. Disease states,
the therapeutic response to the medication administered without
edema, surgery, and sepsis may decrease perfusion.
adversely affecting enteral nutrition tolerance. This chapter addresses
(3) Absorption of medication may be altered by factors such
principles of drug absorption, distribution, and metabolism along with
as the presence of other drugs, the gastric emptying rate,
potential drug-nutrient interactions in these patients.
the route of administration, the ___location of the distal tip of
the enteral tube, or the presence of food.
I. Background
d) Factors that alter medication absorption
II. Enteral Incompatibilities
(1) Approaches to enhance absorption
III. Medication Administration via Enteral Feeding Tubes
(a) Use liquid medications to bypass the dissolution step; if
IV. Parenteral Considerations
tablets are used, they should be pulverized to enhance
V. Effects of Medications on Clinical Laboratory Values
dissolution and subsequent absorption.3
VI. Effects of Drugs on Nutrition and Metabolism
(b) Administer liquid medications or pulverized tablets
References
with adequate fluid. Fluid helps expand the stomach,
Suggested Readings
thereby enhancing the rate of gastric emptying.
(c) Many enterally fed patients do not meet their daily fluid
I. Background requirements with enteral feeding alone, and they
require additional free water throughout the day. When-
A. Absorption
ever possible, administer additional free water flushes
1. Enteral
in conjunction with scheduled medications. These
a) Absorption requires movement of medication from the gas-
flushes provide an excellent medium for delivery of
trointestinal (GI) tract into the general circulation. Not all of
medication, enhance its absorption, and maintain
a drug dose is necessarily absorbed, and not all absorbed drug
enteral tube patency.
reaches the systemic circulation as active drug. Some of the
(2) Factors that may inhibit optimal absorption
absorbed drug is eliminated or metabolized in the GI tract or
(a) Enteral tubes are placed with the distal tip in the stom-
liver before it reaches its site of action. Absorption of med-
ach, duodenum, or jejunum. Absorption may become
ication is generally what is affected when drug-nutrient inter-
actions occur in enterally fed patients. an issue for medications when the distal end of the
b) Bioavailability is the percentage of the original dose that enteral feeding tube is placed beyond the main site of
reaches the systemic circulation as active drug1; the process absorption.
of bioavailability is distinctly different from absorption. i) Itraconazole is a medication that requires an acidic
c) Disintegration and dissolution of a drug in the aqueous diges- environment to ensure proper dissolution when
tive fluid must occur prior to absorption, if the medication is administered as a solid dosage form. Absorption
not already in solution. Medications that are formulated as sus- will be poor if delivered in the jejunum because dis-
pensions must also undergo dissolution. Once a medication has solution is inadequate. The liquid form, on the other
dissolved, it can then diffuse across the intestinal mucosa.2 hand, is already dissolved and does not require the
(1) For most solid-dose forms (tablets, capsules), the rate- acidic environment of the stomach for dissolution
limiting step of absorption is dissolution.2 Disintegration is to occur; therefore, it is amenable to postpyloric
the process of a solid-dose form breaking down into administration. Extemporaneous preparations of
smaller particles, which improves the rate at which a drug itraconazole are not reliably absorbed.4–5 No studies
then dissolves so that absorption may occur. Stomach to date have evaluated itraconazole absorption with
churning in the presence of aqueous fluids aids in disinte- concurrent enteral feedings.
gration and dissolution. Once the components of the tablet ii) The main site of absorption of ciprofloxacin is the
have been adequately reduced in size, they leave the stom- upper part of the intestinal tract.6 Studies have indi-
ach and enter the small bowel, where the majority of cated mixed results with respect to ciprofloxacin
absorption occurs. The small bowel provides a large surface absorption via feeding tubes. When ciprofloxacin is
area and is well perfused to enhance the absorption process.2 administered via a jejunostomy tube, reduction in

118 A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. © 2005 A.S.P.E.N. www.nutritioncare.org.
 S E C T I O N I Fundamentals of Nutrition Support Practice and Management

absorption may result in treatment failure; there- enters the bloodstream can affect its bioavailability. Most par-
fore, this type of administration is not advised.7 enterally administered drugs enter the bloodstream via the
(b) Medications delivered directly into the jejunum rather capillary or venous circulation. In contrast, enterally adminis-
than the stomach can be expected to have a decreased tered drugs (with a few exceptions for gastric, sublingual, and
transit time, reducing the amount of time during which buccal administration) will enter the portal circulation and be
the medication can be absorbed. Tablets delivered transported to the liver before entering the general circulation.
directly into the jejunum lose the positive churning Since this occurs only after initial absorption, it is referred to
and dissolution activity of the stomach, yet the jejunum as the first-pass effect. The liver is the major site of biotrans-
is still a viable option for administration of most formation of organic substances and exerts a profound effect
medications.3 on many enterally absorbed substances. Dosage differences
(c) Some medications (eg, penicillin, tetracycline, for drugs given orally versus parenterally can be large; in the
rifampin), are better absorbed when taken “on an case of propranolol, for instance, the oral dose is approxi-
empty stomach.” Patients who receive continuous mately 10 times the IV dose. First-pass effect can also change
feeding by gastric tube never have an empty stomach. the action of a drug. The composition of early pediatric par-
To optimize absorption of such medications, tube enteral amino acids was based on the amino acids in human
feeding should be held approximately 30 to 60 min- breast milk. However, because human breast milk undergoes
utes before and 30 minutes after the medication is biotransformation by the liver before entering the general cir-
administered; the tube-feeding schedule should then culation and parenteral amino acids bypass the liver entirely,
be readjusted to meet the patient’s total 24-hour parenteral amino acids for neonates are now designed to
nutritional needs. match the serum aminograms of breast-fed infants, not the
(d) If patients develop GI intolerances during tube feedings amino acid composition of human breast milk.
(eg, nausea, vomiting, diarrhea, increased gastric resid- B. Distribution
uals, cramping), the medication profile should be 1. Volume of distribution defined. When a substance enters the
reviewed for potential causative agents. Whenever pos- body, it is distributed via the bloodstream to many tissues. It
sible, change to medications with therapeutic equiva- achieves varying concentrations in these tissues based on the sol-
lents or change the route of administration before ubility of the drug and its affinity for each tissue. If a drug has a
considering discontinuation of tube feeding. high affinity for muscle or fat, serum levels of the drug will be
(e) Use of prokinetic agents (eg, metoclopramide) may lowered. An artificial construct called apparent volume of distri-
decrease transit time, alter absorption of some medica- bution or simply volume of distribution (Vd) is used to predict the
tions, and contribute to diarrhea.8 kinetics of a substance. Volume of distribution is defined as the
(f) Medications that delay gastric emptying or decrease volume in which the substance entering the body would need to
GI motility be diluted to achieve the observed serum levels. The volume of
i) Anticholinergics (eg, antihistamines, tricyclic distribution is expressed in liters per kilogram of body weight to
antidepressants, phenothiazines, medications for correct for differing body weights. If the drug is highly water sol-
Parkinson’s disease) cause smooth muscle relax- uble and primarily found in body water, it will have a volume of
ation and inhibit gastric motility.9 distribution of 0.6 L/kg. The same dose of a drug that is lipid sol-
ii) Aluminum-containing antacids delay gastric uble will achieve lower serum levels, and its volume of distribu-
emptying. tion will be greater than 0.6 L/kg. For example, digoxin is widely
iii) Narcotics interfere with normal peristalsis and distributed in body tissue and has a Vd of 7 L/kg. A drug that is
delay gastric emptying.9 concentrated intravascularly will have a Vd less than 0.6 L/kg.
2. Parenteral Sulfisoxazole has a Vd of 0.16 L/kg.10
a) Parenteral routes of drug delivery. Technically, the term par- 2. Protein binding. Many substances bind to protein. Protein binding
enteral refers to all drug administration other than by the GI may increase the length of time a drug remains in the body while
tract. Commonly, the term is used to refer to the intravenous also attenuating its serum levels. The metabolism of the substance
(IV) route, where the drug is injected into the body. Par- by the liver may be decreased, as only the unbound substance is
enteral delivery of medication avoids the issue of absorption, available for biotransformation.
as the entire dose will enter the body. Once the drug is in the 3. Solubility and tissue distribution. The solubility of a substance
bloodstream, the action of the drug is the same without has a profound effect on its distribution within the body. Water-
regard for administration route. With few exceptions, oral soluble or hydrophilic substances are principally distributed
administration of drugs is favored, as is oral administration within the fluid compartments of the body.
of nutrients. C. Metabolism.
b) Effect of route on kinetics. A large variety of drug delivery 1. Liver enzyme systems. Many drugs are metabolized via the cyto-
routes fall under the umbrella of parenteral administration. chrome P-450 (CYP450) enzyme system. Although numerous
Rapid IV infusion (IV push), controlled IV infusion over a enzyme families within CYP450 have been identified, CYP3A4 is
short period of time (IV piggyback or secondary administra- involved with the metabolism of most drugs currently on the mar-
tion), and continuous IV infusion (IV drip) are all common ket.11 Other isoenzymes commonly associated with drug metabo-
parenteral drug administration methods. Intra-arterial delivery lism include CYP1A2, CYP2C19, and CYP2D6.12 Nutrients, like
is also done for certain drugs to deliver a concentrated dose to drugs, can inhibit or induce the effects of these metabolic
a specific organ. enzymes. When the enzyme that is responsible for the metabolism
c) Effect of entry point into bloodstream (first-pass effect or lack of a particular drug is induced, the serum level of the drug is
of same affecting systemic dose). The point at which a drug decreased. The opposite effect on the drug would occur if the

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S E C T I O N I Fundamentals of Nutrition Support Practice and Management

enzyme were being inhibited. Following are examples of some drug. Drugs that undergo enterohepatic cycling include ethinyl
nutrients that affect the various CYP450 enzymes: estradiol18 and antibiotics such as macrolides, ceftriaxone, naf-
a) Broccoli, brussels sprouts, and charcoal-broiled meats can cillin, and doxycycline.19
induce CYP1A2. Therefore, any drug that is metabolized by
CYP1A2 could become toxic when taken with either broccoli
II. Enteral Incompatibilities. Every available dosage form
or brussels sprouts. Some of the drugs that are metabolized
has the potential to cause undesirable effects or incompatibilities
by CYP1A2 are acetaminophen, amitriptyline, caffeine,
when combined with enteral feeding formulations or adminis-
clozapine, cyclobenzaprine, desipramine, diazepam, ethinyl
tered to the enterally fed patient.
estradiol, fluvoxamine, haloperidol, imipramine, methadone,
naproxen, nortriptyline, olanzapine, ondansetron, propranolol, A. Physical incompatibility is a chemical instability that occurs when
ritonavir, tamoxifen, theophylline, verapamil, and warfarin. two susceptible substances are mixed together. This incompatibility
b) Grapefruit (juice) inhibits CYP1A2 and CYP3A4, and there- results in an actual physical change between two substances. A typi-
fore any drug metabolized by either of these two CYP iso- cal example is the formation of a precipitate.
enzymes could become toxic when routinely taken with 1. A common reaction that may occur with enteral formulations is
grapefruit juice. Some drugs metabolized by CYP1A2 are listed formation of a precipitate (eg, curdling, flocculation, altered
above. Examples of drugs that are metabolized by CYP3A4 enteral formulation consistency, viscosity [coagulation, thick-
are acetaminophen, alprazolam, amiodarone, amitriptyline, ening, gelling, or thinning]).
atorvastatin, buspirone, caffeine, carbamazepine, cerivas- 2. Physical incompatibilities may cause feeding tubes to occlude.
tatin, chlorpheniramine, chlorpromazine, cimetidine, cis- 3. See Table 9-1 for physical compatibilities with selected enteral
apride, clarithromycin, clindamycin, clomipramine, feeding formulations.
clonazepam, cocaine, codeine, cyclophosphamide, B. Pharmaceutical incompatibility is an alteration in the drug form itself
cyclosporine, delavirdine, dexamethasone, dextromethor- that interferes with drug efficacy, potency, or tolerance. Medications
phan, diazepam, diltiazem, disopyramide, dolasetron, in specialized dosage forms (ie, enteric coated, sustained release, or
donepezil, doxorubicin, enalapril, erythromycin, estrogens sublingual) typically are not amenable to administration via a feed-
(oral), felodipine, fentanyl, flutamide, glyburide, haloperi- ing tube. A pharmacist should evaluate all dosage forms prior to
dol, hydrocodone, imipramine, indinavir, itraconazole, administration via a feeding tube to determine appropriateness.
ketoconazole, lansoprazole, lidocaine, losartan, lovastatin, C. Physiologic incompatibility is the result of a nonpharmacologic
methadone, miconazole, midazolam, mirtazapine, nelfinavir, action incurred by the medication itself or by the medium in which
nifedipine, nimodipine, ondansetron, oral contraceptives, it is suspended. This type of incompatibility occurs when liquid
paclitaxel, pravastatin, prednisone, quinidine, quinine, medications have a high osmolality or contain a significant amount
rifampin, ritonavir, saquinavir, sertraline, sildenafil, simvas- of sorbitol. Patients typically experience nausea, increased gastric
tatin, tacrolimus (oral), tamoxifen, temazepam, teniposide, ter- residuals, bloating, cramping, and diarrhea.
fenadine, testosterone, theophylline, trazodone, triazolam, D. Pharmacologic incompatibility results when a medication alters tol-
verapamil, vinblastine, and vincristine. erance of the enteral nutrition or PN regimen because of the med-
2. Cranberry juice has been recently reported in the literature ication’s mechanism of action. This incompatibility frequently
to inhibit CYP2C9 and thus warfarin metabolism, resulting leads to either a greater pharmacologic effect of the medication than
in an increased International Normalized Ratio (INR) and initially intended (eg, abdominal cramping or diarrhea related to use
bleeding.13 of prokinetic agents) or an unintended side effect of the medication
D. Excretion. Excretion is the process by which a drug or a metabolite (eg, increased gastric residuals caused by narcotic analgesics).
is eliminated from the body without further chemical change.14 E. Pharmacokinetic incompatibilities occur when the enteral or par-
1. Urinary. Renal excretion is the major pathway for the elimination enteral feeding regimen alters the bioavailability, absorption, dis-
of most water-soluble drugs and their metabolites. Alteration in tribution, metabolism, and/or elimination of the medication, or
renal function will have a profound effect on the clearance of when the medication alters nutrient function. Common medica-
drugs and may result in increased serum levels or prolonged tions that cause pharmacokinetic interactions involving enteral
half-life. Dosage adjustments may be necessary according to nutrition include phenytoin, warfarin, ciprofloxacin, and any
a patient’s renal function. Antibiotics such as penicillins, medication that should be taken on an empty stomach in order to
cephalosporins, aminoglycosides, vancomycin, and fluoro- maximize absorption.
quinolones are cleared renally.15 Ranitidine is primarily elimi-
nated via the urine; approximately 70% of an IV dose is excreted
III. Medication Administration via
unchanged.16 Analgesics that are excreted in the urine unchanged
Enteral Feeding Tubes
or as metabolites include nonsteroidal anti-inflammatory drugs,
COX-2 inhibitors (eg, celecoxib), opioids, and tramadol.17 A. Medication dosage forms that can be administered via enteral tubes.
2. GI. Drugs and their metabolites are also excreted into the bile. Medications that can be given via enteral tubes include immediate-
Protein transporters usually mediate this process. Drugs and their release oral tablets, hard gelatin capsules, soft gelatin capsules, and
metabolites enter the duodenum via the common bile duct, liquid formulations. All medications should be mixed with appropri-
move through the small intestine, and are excreted in the stool. ate diluents and administered separately; the feeding tube should be
The drugs may be reabsorbed from the intestine. Some drugs will flushed with water before and after each medication is administered
be reabsorbed back into the bloodstream and return to the liver by to minimize incompatibilities and prevent occlusion.
the enterohepatic circulation. The drug then undergoes further 1. Immediate-release oral medications. Most simple, compressed
metabolism or is secreted back into bile. This process, referred to tablets, including film- and sugar-coated and hard gelatin cap-
as enterohepatic cycling, may extend the duration of action of a

120 A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. © 2005 A.S.P.E.N. www.nutritioncare.org.
 S E C T I O N I Fundamentals of Nutrition Support Practice and Management

TABLE 9-1. Physical Compatibilities With Enteral Feeding Products

TwoCal Ensure Ensure Osmolite Osmolite

Drug HN Plus HN 1 cal HN Vivonex Comments

Acetaminophen/Codeine Elixir C C C
Acetaminophen Elixir C C C C C C
Actifed Syrup C C C C C
Amoxicillin Suspension C C C C
Amphogel I C C Thickens on contact
Bactrim Suspension C C C C C C
Benadryl Elixir C C C C C C
Bentyl Liquid I C Thickens on contact
Benylin DM C C C C C
Cephalexin Suspension C C C C C C
Cephulac C C C C C
Cibalith-S I I I I C Clumping
Compazine Elixir C C
Dexamethasone Elixir C C C C C C
Dimetane Elixir I I I I I C Gelatinous formation
Dimetapp Elixir I I I I I C Enteral product breaks down
Docusate Liquid C C C C C C
Donnatal Elixir C C C C C C
Doxepin Concentrate C C C C C C
EES Granules C C C C C
Feosol Elixir I I I I I C Complete gel formation
Fleet Phospho-Soda I I I C Instant clumping
Gantrisin Suspension C C C C C C
Gevrabon Liquid I C
Griseofulvin Suspension C C
Guaifenesin Liquid I I I I I C Flocculate precipitate
Haldol Drops C C C C C C
Imodium Liquid C C C
KCl Oral Liquid I I I I I Interphase incompatibility
Klorvess Granules C C C C
Lanoxin Elixir C C C C C C
Lasix Liquid C C C C C
Mandelamine Granules C C C C C
Mandelamine Suspension I I I I Gelatinous tacky formation
MCT Oil I I Adhesive gelatinous mass formation
Mellaril Concentrate C C
Mellaril Solution I I I I C Granular formation
Mestinon Suspension C C C C C
Milk of Magnesia C
Morphine Liquid C C C
Mylanta C C C
Mylanta II I I Thickening on contact
Navane Concentrate C C C C C C
Neo-Calglucon Syrup I I I I I C Adhesive gelatinous mass
Nitrofurantoin Suspension C C C C C C
Organidin Elixir C C C C C
Paregoric Elixir I I I C Instant clumping
Periactin C C C
Phenergan Syrup C C C C C

(Continued)

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S E C T I O N I Fundamentals of Nutrition Support Practice and Management

TABLE 9-1. Physical Compatibilities With Enteral Feeding Products (Continued)

TwoCal Ensure Ensure Osmolite Osmolite

Drug HN Plus HN 1 cal HN Vivonex Comments

Phenobarbital Elixir C C C C C C
Reglan Syrup C C
Riopan I C Thickening on contact
Simethicone Drops C C C C C C
Slo-Phyllin Syrup C C C C C
SSKI Liquid C C C C C
Sudafed Syrup C I I I I C Viscous gelatinous formation
Sumycin Syrup C C C C
Tagamet Elixir C I I C Thickening on contact
Terpin Hydrate Elixir C C C C C
Theolair Liquid C C C C
Theragran Liquid C C C C
Thorazine Concentrate I I I I C Granulation and particle formation
Triaminic Syrup I C C C C C
Zinc Sulfate I

C, compatible; I, incompatible
References
Lutomski DM, Gora ML, Wright SM, Martin JE. Sorbitol content of selected oral liquids. Ann Pharmacother. 1993;27:269–274.
Miller SJ, Oliver AD. Sorbitol content of selected sugar-free liquid medications. Hosp Pharm. 1993;28:741–744, 755.
Niemiec PW, Vanderveen TW, Morrison JI, Hohenwarter MW. Gastrointestinal disorders caused by medications and electrolyte solution osmolality during enteral nutrition. J Par-
enter Enteral Nutr. 1983;7:387–389.

sules filled with a fine powder, are amenable to administration via tions exceeding 300 mOsm/kg require GI dilution to approach
a feeding tube. the isotonic state to aid absorption; if the amount of fluid that
a) Tablets must be crushed to a fine powder (eg, with a mortar moves into the GI tract exceeds the absorptive capacity of the
and pestle) and mixed with water before administration. The intestinal tract, diarrhea will result.
finer the powder the better, both to enhance absorption and e) The stomach may be more tolerant of hyperosmolar medica-
reduce the risk of tube occlusion. tions than the small intestine because of the stomach’s inherent
b) Hard gelatin capsules filled with a fine powder should be ability to dilute hypertonic solutions with gastric juice before
opened and mixed thoroughly with water before administra- emptying the gastric contents into the duodenum.
tion. Soft gelatin capsules can be emptied by creating a pin- f) Administration of undiluted hyperosmolar liquid medications
hole in one end of the capsule and squeezing out the contents. directly into the duodenum or jejunum should be approached
The contents can then be mixed with water. Precise dosing cautiously, as it causes a significant influx of water and elec-
may not be possible, as it is difficult to remove all the cap- trolytes into the GI tract, which could contribute to bloating,
sule’s contents. nausea, cramping, diarrhea, and electrolyte imbalances.
2. Liquid medications20–22 are the preferred alternative for adminis- g) Complications can be avoided by diluting hypertonic liquid
tration via an enteral feeding tube because of better absorption and medications with an appropriate amount of water. The site of
decreased potential for enteral tube occlusions. However, liquid medication delivery and the tonicity of the medication influ-
medications are not without potential for producing adverse ence the amount of water required. More diluent may be
effects. needed to dilute medications administered into the small
a) Liquid medications may cause physiologic incompatibilities intestine than into the stomach.
(eg, diarrhea, elevated gastric residuals, distended abdomen, h) Coordinate the patient’s need for additional water with
cramping). amounts of water needed to dilute hypertonic medications.
b) These responses may not be attributed initially to the enteral i) Osmolalities of liquid medications can reach as high as
feeding formulation and may be misdiagnosed as a tube- 9000 mOsm/kg of water. Check with the manufacturer or
feeding intolerance. read the package insert for more information.23,24
c) The “intolerance” may in fact be attributable to the liquid med- j) Medications that contain sorbitol often cause a physiologic
ication preparation, as these medications often have a high incompatibility (eg, diarrhea, bloating, cramping). Doses as
osmolality or contain large amounts of sorbitol.23–26 low as 10 g have been known to cause mild GI distress, with
d) Hyperosmolar liquid medications may cause diarrhea, cramp- 20 g or more causing more severe symptoms.26 Children may
ing, and increased gastric residuals. The osmolality of GI tract be more susceptible to the effects of sorbitol than adults.
secretions is approximately 300 mOsm/kg. Liquid medica-

122 A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. © 2005 A.S.P.E.N. www.nutritioncare.org.
 S E C T I O N I Fundamentals of Nutrition Support Practice and Management

(1) Sorbitol is considered an inert ingredient that is added to crushed enteric-coated aspirin may produce some GI upset
enhance palatability and improve stability. Sorbitol may or irritation associated with aspirin, but the overall effi-
be present in all liquid medications except tinctures and cacy of the medication will most likely be unaltered.
emulsions. None of the reconstituted antibiotic prepara- (2) Enteric coating protects a number of medications (eg, eryth-
tions are known to contain sorbitol.27 romycin base, erythromycin stearate, pancrelipase) from
(2) The sorbitol content of a liquid medication may vary destruction in the acidic environment of the stomach prior
among manufacturers. Manufacturers do not list the sor- to absorption in the small intestine. Upon entering the
bitol content on the label. The best source for determin- alkaline environment of the duodenum, the enteric coating
ing whether sorbitol is present is the package insert, but will dissolve and release the medication for absorption.
the manufacturer must be contacted to obtain the actual These medications require an intact enteric coating to pre-
sorbitol content. serve the integrity of the active drug during its passage
(3) The total daily dose of sorbitol provided by all liquid med- through the stomach to ensure bioavailability.29
ication preparations administered must be considered. (3) If a medication has an enteric coating solely for the pur-
(4) Common offending agents are acetaminophen elixir, pose of preventing destruction from acidic acid, adminis-
theophylline solutions, valproate, and guaifenesin syrup. tration via a feeding tube beyond the pylorus is acceptable.
These medications contain large quantities of sorbitol, Check with a pharmacist to verify the purpose of the
and numerous doses may be given in a 24-hour period. enteric coating.
Any product may have a high concentration of sorbitol, 2. Sublingual or buccal medications20
but if the product dose in milliliters is small, the actual a) These medications are placed under the tongue or in the cheek
dose of sorbitol may also be quite small. pouch and absorbed into the systemic circulation.
(5) Options for avoiding problems with sorbitol include b) Administration via feeding tube is not recommended.
changing to another manufacturer’s product, using ther- 3. Sustained-release (SR) tablets or SR capsules.20,21 Crushing these
apeutically equivalent products that have less or no sor- medications is not recommended, as significant pharmaceutical
bitol, changing the route of administration, and using incompatibilities or toxicities could occur.
tablets or capsules that do not exhibit pharmaceutical a) Administering crushed SR tablets or capsules delivers a bolus
incompatibility. of drug that was intended to be delivered over 6 to 24 hours.
3. Suspensions The bolus causes high peaks with a potential for toxicity fol-
a) Suspensions present few incompatibility concerns. lowed by low troughs and inadequate coverage.
b) Suspensions do not contain sorbitol. b) Emptying capsules with extended-release beads into feeding
c) Suspensions may be hyperosmolar; adding water to the dose tubes is not recommended because it increases the potential
will reduce tonicity. for tube occlusions.
d) Antibiotics are often available as suspensions. The diarrhea c) Dissolving the beads in water or NaCl 0.9% solution is not
that may occur is a direct side effect of the antibiotic and is not recommended because it will adversely affect the integrity of
related to the suspension form. Recolonization of the GI tract the beads’ outer coating. This can affect the integrity of the
may be useful in these cases. medication and compromise the time-release properties.
4. Granular-type medications d) Alternative therapeutic equivalents must be considered.
a) Psyllium hydrophilic mucilloid and cholestyramine resin may (1) Use a liquid therapeutic equivalent or a crushable
be added to a patient’s regimen to control diarrhea. Cholestyra- immediate-release medication, or choose an alternative
mine resin may also be added as a hypercholesterolemia agent. delivery route (eg, parenteral, rectal).
b) These medications require dilution with water before admin- (2) If a therapeutically equivalent immediate-release medica-
istration. The granules rapidly absorb water and expand to tion is available as a tablet or liquid, it will require more
form a gelatinous mixture that may occlude the enteral tube; frequent administration, usually at the same total daily
small-bore feeding tubes are more problematic than larger dose as the SR form.
gastric tubes. (3) Monitor for appropriate clinical response and, whenever
c) Metamucil may be administered by mixing 4 g with 80 mL of warranted, adequate blood concentrations.
water and completing the dose administration within 5 minutes 4. A comprehensive list of oral solid dosage products that should
or less.28 The quick administration minimizes expansion of the not be crushed is available.20
granules and decreases the risk of tube occlusion. 5. Syrups29–31
d) A therapeutically equivalent medication should be considered a) A physical incompatibility may occur when syrups are mixed
if the patient has a small-bore feeding tube. with enteral formulations. Syrups with a pH of ≤4 can denature
B. Medication dosage forms not recommended for administration the protein in the enteral formulation, leading to an increase in
via tube viscosity that may contribute to feeding tube occlusions.
1. Enteric coated medications20,21 b) It is important to be aware of the protein source of the enteral
a) Crushing these medications may induce a pharmaceutical formula. Syrup preparations administered with whole-protein
incompatibility. A therapeutic equivalent or alternative admin- formulations have been shown to cause physical incompati-
istration route should be considered. bilities; those with free amino acids or hydrolyzed formula-
b) It is important to understand the purpose of the enteric coating tions are not as affected by concurrent administration of syrup.
and the ___location of the tip of the feeding tube. c) Physical incompatibilities (clumping, etc) cannot be avoided
(1) Enteric coating may protect the stomach lining. Certain by diluting the syrup or the enteral formulation. Not all syrup
formulations of aspirin are coated to decrease the gastric products have an acidic pH ≤4. If there is suspicion that the
irritation often associated with its use. Administering a product has a low pH, the pH may be tested with pH paper or

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S E C T I O N I Fundamentals of Nutrition Support Practice and Management

a small amount of the syrup may be mixed with a sample (f) An orally disintegrating form of lansoprazole is avail-
amount of the enteral formulation to observe any affect on the able. This dosage form circumvents the feeding tube
formulation stability. route, as the pellets dissolve in the patient’s mouth and
d) Alternatively, a compatible therapeutically equivalent med- do not require swallowing.
ication (ie, a tablet or capsule form that could be sufficiently (g) A powder formulation of omeprazole is commercially
pulverized and diluted in water) can be selected or an alterna- available and can be reconstituted for administration
tive route of administration can be used. If the incompatible via enteral feeding tubes.
syrup must be administered via the feeding tube, the steps b) Enteric-coated tablets
below should be followed: (1) Crushing enteric-coated tablets has the same effect as
(1) Stop the tube feeding. crushing the enteric-coated beads in capsules.
(2) Flush the feeding tube with 30 mL of water to clear the (2) A pantoprazole extemporaneous solution can be prepared
tube of all formulation. using sodium bicarbonate 4.2% solution.39,40
(3) Administer the syrup via the tube. c) Alternative options. Use an H2 antagonist when possible.
(4) Flush the tube with 30 to 60 mL of water to clear the tube (1) H2 antagonists are available in liquid form and in easily
of residual syrup and ensure tube patency. dissolved tablets and capsules.
(5) Resume the tube feeding. (2) Use parenteral proton pump inhibitor or H 2 antagonists
C. Drug-nutrient interactions. Drug-nutrient interactions are situations only when the GI tract cannot be used.
in which the ultimate effect of a drug is altered by a nutrient or the 2. Phenytoin. Impaired absorption of phenytoin is a pharmacoki-
ultimate effect of a nutrient is altered by a drug. Interactions could netic incompatibility41–44 that is well documented in the literature.
involve any of the previously mentioned types of incompatibilities. a) There appears to be impairment in absorption, but there is
1. Proton pump inhibitors available as capsules or tablets32 debate about where and how the interaction occurs. Possible
a) Capsules containing enteric-coated beads reasons for impaired absorption include the following:
(1) Enteric coating preserves the integrity of the medication (1) The protein source of the enteral formulation may con-
until it reaches the alkaline pH of the duodenum, where tribute to the interaction. Calcium caseinate protein sources
the coating dissolves and absorption begins. may impair absorption more than sodium caseinates.
(2) Dissolving the beads in water removes the protective (2) The phenytoin suspension may bind to the enteral feed-
enteric coating, exposing the medication inside to a basic ing tube.
environment. In this basic environment, the active med-
(3) The phenytoin suspension has poor solubility and may con-
ication begins to degrade, thereby decreasing its overall
tribute to poor absorption.
effectiveness. Mixing with water also causes the beads to
(4) There may be decreased gastric emptying, with subsequent
clump as the enteric coating dissolves. Clumping con-
destruction of phenytoin by gastric acid.
tributes to occlusion of enteral feeding tubes.
(5) Drug administration via a tube placed in the distal jejunum
(3) Two alternative methods of delivery have published
reduces transit time and time for drug absorption.
support.
(6) Patients have decreased GI transit time (ie, the drug
(a) The contents of the capsule (omeprazole, lansoprazole,
spends less time in the GI tract).
esomeprazole) may be mixed in an acidic fruit juice
b) Patients receiving enteral formulations may need much
such as orange juice or apple juice. The enteric coating
higher phenytoin doses than usual to maintain therapeutic
will remain intact until the beads reach the basic envi-
blood levels.
ronment of the duodenum. One concern with this
approach is that the intact beads may occlude small- c) Seizures are a potential consequence of inadequate phenytoin
bore feeding tubes. Not all of the dose is administered blood levels.
to the patient, as the beads can collect and remain d) Strategies to maintain therapeutic phenytoin levels and pro-
lodged in the syringe hub.32,33 vide adequate protection from seizures include the following:
(b) The beads can be dissolved in sodium bicarbonate (1) Hold the tube feeding 2 hours before and 2 hours after
8.4% solution, creating a simplified suspension. Sta- administering the phenytoin dose. Adjust the tube-feeding
bility is maintained at this high pH.34 schedule to accommodate the total 24-hour requirement.
(c) Extemporaneous simplified suspensions of omeprazole (2) Dilute the phenytoin with water (30–60 mL) before admin-
and lansoprazole can be prepared. These formulations istration. The water may enhance dissolution and improve
have proven to be effective in maintaining adequate absorption.
buffering of stomach contents in the critically ill popu- (3) Monitor blood levels more frequently when changing from
lation.35,36 One study involving healthy individuals an established therapeutic parenteral dose via vein to the
administered esomeprazole via a feeding tube immedi- suspension form administered via the feeding tube.
ately after the drug was mixed with water demonstrated (4) Consider administering the parenteral form of phenytoin
good results.37 via enteral tube if problems persist in maintaining thera-
(d) The commercially available lansoprazole packets peutic levels. Supporting evidence at this time is limited to
should not be administered via a feeding tube. The a single-dose trial in healthy subjects, which is not ade-
product contains particles or gums that will occlude a quate to establish this route as a reliable alternative. The
feeding tube.38 parenteral form is hyperosmolar and must be diluted before
(e) Simplified suspensions of proton pump inhibitor administration.45
should be administered via feeding tubes to avoid tube (5) Phenytoin toxicity can occur as the patient transitions from
occlusion. tube feeding to oral feedings, because of the removal of the

124 A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. © 2005 A.S.P.E.N. www.nutritioncare.org.
 S E C T I O N I Fundamentals of Nutrition Support Practice and Management

offending interaction. Monitor the phenytoin levels closely the enteral route.58
until stable. i) It may not be advisable to change ciprofloxacin to
(6) Consider the use of IV phenytoin or fosphenytoin in dif- the feeding tube route if pseudomonal respiratory
ficult situations. tract infection is being treated. The feeding tube
3. Warfarin. A decreased therapeutic response to warfarin has been route should be acceptable for patients with urinary
noted in patients receiving enteral tube feeding.46–48 tract infections.
a) The altered response was initially thought to be related to the ii) For a more detailed discussion on this topic, refer
high vitamin K content of enteral formulations. to a review article by Nyffeler.59
(1) The vitamin K content could antagonize warfarin activity. (3) Levofloxacin. No information is presently available.
(2) Subsequently, the vitamin K content was reduced in most (4) Gatifloxacin. A single-dose prospective two-way crossover
enteral products. trial in critically ill patients comparing AUC for the par-
(3) Warfarin resistance continues to be reported in the enteral product to a single dose administered via a feeding
literature. tube with concurrent enteral feeding did not demonstrate a
b) Warfarin is a highly protein-bound drug. difference in overall bioavailability.60
(1) It has a protein-binding level in serum of 97.4% to 99.9%. 5. Atovaquone. A single-dose trial of atovaquone suspension admin-
(2) It may bind to the protein in the enteral formulation. istered to healthy patients within 1 hour of an enteral supplement
c) One letter to the editor indicated success in one patient when produced levels of absorption similar to those taking it with a
the warfarin was administered during the 6-hour break in the normal breakfast.61
patient’s daily 18-hour cycle.49 6. Carbamazepine
d) Warfarin drug-nutrient interactions are less consistent than a) Administration with concurrent tube feedings should not be a
phenytoin drug-nutrient interactions. problem if an appropriate dilution-and-flush routine is used.
e) Monitor anticoagulant activity closely while the patient is on b) One trial demonstrated that administration of undiluted carba-
enteral tube feeding. mazepine suspension via a polyvinyl feeding tube resulted in
f) Evaluate warfarin dose, anticoagulant goals, and monitoring decreased absorption. Diluting the suspension prior to admin-
parameters closely as the patient transitions to an oral diet or istration produced more normal delivery.62
begins a bolus, intermittent gravity tube-feeding regimen. c) An insignificant reduction in overall absorption was demon-
4. Quinolones strated in a small trial of healthy patients. This was a crossover
a) Significant controversy surrounds the use of quinolones trial that demonstrated 90% bioavailability of carbamazepine
administered simultaneously with enteral feedings. Efficacy is suspension when taken after fasting or with continuous enteral
best measured by evaluating the area under the curve (AUC) feedings.63
data and comparing these data to the minimum inhibitory con- d) Serum concentrations should be monitored closely after
centration (MIC) of the bacterial strain being treated. patients are started on carbamazepine and enteral feedings. A
b) The AUC measures the total amount of quinolone that is consistent method of administration should be used.
absorbed over time. The AUC/MIC ratio is the most important e) A report describes the use of an extended-release version of
predictor of efficacy.50 carbamazepine (Carbatrol) via feeding tubes in pediatric
c) Concurrent administration of quinolones with medications patients.64 This trial administered the contents of the capsule
that are high in aluminum, magnesium, iron, and calcium can via feeding tubes. No mention was made of carbamazepine
impair absorption, resulting in a clinically significant decrease levels or side effects, but the patient’s family noted frequent
in absorption.51 occlusion of the feeding tube. Administering capsule contents
d) High concentrations of the following cations in enteral feed- via feeding tubes always presents the potential for occluding
ing formulations may also impair quinolone absorption. the feeding tube and is probably best avoided.
(1) Ofloxacin 7. Carbidopa/levodopa
(a) A single-dose trial with a crushed tablet administered a) No trials have evaluated absorption of carbidopa/levodopa
with a bolus of Ensure (Ross Products) produced a with concurrent enteral feedings.
10% reduction in the AUC.52 b) Extrapolations have been made from the data showing a
(b) This was not a significant reduction compared to taking decreased effect when the medication was taken with a
on an empty stomach with water. high-protein meal. The amino acids in the high-protein meal
(2) Ciprofloxacin inhibited transport across the blood-brain barrier via a com-
(a) There have been mixed results depending on what petitive uptake mechanism.
patient groups were studied and how the medication c) If patients are receiving intermittent feedings, doses should be
was administered. administered during off-time. Another option is to explore
i) Single-dose trials in which the tablet was crushed alternative medications for Parkinson’s that do not exhibit this
and administered simultaneously with a bolus of interaction.
enteral feedings demonstrated reduced absorp- 8. Clarithromycin. Administration of suspension, which contains
tion.53–55 granules, may result in occluded feeding tubes.
ii) Nonsurgical, critically ill patients receiving contin- 9. Hydralazine. Absorption in continuous enteral feedings is compa-
uous enteral tube feeding and receiving multiple rable to that of fasted patients.65
doses of ciprofloxacin have demonstrated adequate 10. Fluconazole
absorption.56,57 a) A number of trials in patients in intensive care unit support the
(b) Adequate GI tract function must be established prior administration of fluconazole via a feeding tube in conjunction
to changing ciprofloxacin from the parenteral route to with continuous enteral feedings.66,67

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S E C T I O N I Fundamentals of Nutrition Support Practice and Management

b) Postpyloric administration in trauma patients has also demon- 7. Differentiate medication-induced GI intolerance from enteral
strated adequate absorption.68 delivery system- or formula-induced GI intolerance.
11. Tacrolimus. One study demonstrated that absorption of tacrolimus 8. Continually and consistently monitor the patient’s therapeutic
was no different whether the enteral feedings (Osmolite, Ross drug response to all medications.
Products) were held 1 hour before and 8 hours after tacrolimus
administration or administered in conjunction with continuous
enteral feedings.69
IV. Parenteral Considerations. Patients receiving parenteral
nutrition (PN) are often treated concomitantly with medications,
12. Theophylline
both orally and parenterally. The clinician should be aware of the
a) Theophylline and/or aminophylline absorption is probably not
physical compatibility of parenteral medications as well as the
impaired when the medication is administered with enteral
effects of medications on laboratory measurements and the overall
feedings, but serum levels may be affected by the presence of
nutrition status of the patient. The compatibility of PN formula-
enteral feedings.
tions infused with other additives is often influenced by the expo-
b) The initiation of enteral feeding stimulates liver enzymes that sure time between the nutrients and additives present. A useful
contribute to the metabolism of theophylline, subsequently reference for the compatibility of medications and PN formulations
reducing theophylline levels.70 is by Trissel (see Suggested Readings).
c) Two single-dose trials in healthy patients did not demonstrate
a reduction in absorption when a long-acting theophylline A. Secondary medications (Y site). Usually, secondary or IV piggyback
preparation was taken and an hourly enteral supplement medications are coinfused simultaneously with a primary infusion.
drunk. Neither trial used feeding tubes.71,72 In most cases, the primary IV infusion contains relatively low con-
13. Sucralfate centrations of electrolytes and poses few compatibility problems.
a) Sucralfate is a medication that may be used for stress ulcer Also, the of time for contact with the secondary IV infusion is rela-
prophylaxis, esophageal ulcerations, or gastric reflux disease. tively short. Most significant interactions are time and concentration
Sucralfate must be administered into the acidic environment dependent. The situation becomes more complicated if a PN formu-
of the stomach in order to be converted to the active moiety. lation is used as the primary IV infusion. Numerous additives may
This is difficult to accomplish when patients are on continuous be, either individually or in combination, incompatible with concen-
enteral feedings. trated secondary medications. In the presence of limited venous
b) An additional problem with mixing enteral feedings and access, medications with borderline stabilities should be diluted or
sucralfate is the risk of developing a bezoar. This occurs administered at a Y site proximal to the patient. Otherwise, a separate
when a complex forms between the sucralfate and the pro- infusion port or injection site should be used for secondary medica-
tein component of the enteral feeding supplement.73,74 tions where stability after exposure to PN is questionable.
14. Levothyroxine B. Stability of added ingredients. Numerous additives are combined in
a) There is concern that interaction with the soy content in an a PN formulation. PN is frequently considered as a vehicle for med-
enteral feeding formulation could impair the absorption of ication administration. However, because of the complexity of the
levothyroxine. formulations and the potential for incompatibilities and interac-
b) Only data to support this direct interaction was done a at a tions, admixing PN with medications is not advised. See Chapters 7
time when it was more common for adult enteral formulations and 8 for discussions on PN formulations and physicochemical
to be soy based.75 Although some adult formulas may contain interactions.
some soy protein, this interaction has not been studied using C. Administration sets. Regular insulin is often either coadministered
currently available enteral formulations. Without supporting or added to the PN formulation for glucose management. Insulin
binds to the surface of the delivery container and the administration
evidence, it is not necessary to hold enteral feedings for
set. Binding is particularly problematic with polyvinyl chloride
administration of levothyroxine.
containers. The extent of binding to a particular container is also
D. Summary
influenced by the formulation within the container. The effect of the
1. Develop multidisciplinary standards and practice protocols to
formulation on the extent of insulin binding to container surface is
ensure the safe, consistent care and monitoring of the enterally fed
as follows (from greatest binding to least)76: NaCl 0.9% (normal
patient who needs to receive medication via an enteral tube. Doing
saline) > dextrose > amino acids > albumin. Therefore, the same
so will have the following results:
dose of insulin will have a different amount of activity depending on
a) Ensures optimal therapeutic response to medication and
the vehicle in which it is administered. The higher the concentration
enteral nutrition
of insulin, the lower the extent of binding, because there are a lim-
b) Minimizes side effects and complications of administration
ited number of binding sites per container. The route of administra-
of the medication
tion and the insulin product (insulin lispro, insulin aspart, insulin
c) Optimizes effectiveness of therapies and interventions
regular, insulin NPH, insulin glargine) will also have a major effect
d) Optimizes cost-effectiveness of therapies and interventions
on the action of this drug.77
2. Consult a pharmacist to review the patient’s medication profile
D. Predicting interactions
before administering a medication via an enteral feeding tube.
1. Reviewing the package insert for the pH of a medication may
3. Confirm proper placement of the enteral tube before adminis- provide information for predicting compatibility with a PN for-
tration of medication. mulation. Medications that are weak acids or bases are formu-
4. Do not mix any medications directly with enteral formulations. lated at a pH that optimizes their solubility. IV medications that
5. Administer each medication separately. produce extreme changes in the final pH of the reconstituted
6. Flush the enteral feeding tube with water before and after each product, such as phenytoin, tend to be most reactive and therefore
medication is administered. capable of significant incompatibilities.

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 S E C T I O N I Fundamentals of Nutrition Support Practice and Management

2. Injectable medications that contain cosolvents, such as propy- 2. Drugs that affect metabolic rate include thyroid hormones and
lene glycol or ethanol, have the greatest potential for interaction steroids (anabolic, corticosteroid).82,83
if coadministered with a PN formulation or other large-volume 3. Chemotherapeutic agents. Emetogenic agents stimulate the
parenteral infusion. Examples include furosemide, diazepam, chemotherapeutic trigger zone in the central nervous system.
digoxin, phenytoin, and etoposide. Examples include cisplatin, high-dose methotrexate, and doxo-
rubicin.84,85
4. Drugs that affect appetite or taste86,87
V. Effects of Medications on Clinical
a) Drugs that cause anorexia: diuretics, estrogens, sympath-
Laboratory Values
omimetics (including decongestants), and serotonin uptake
A. Interference of drugs with laboratory tests. Drugs may interfere with antagonists such as fluoxetine and sertraline
substrates within the body and alter clinical laboratory values. In b) Drugs that stimulate appetite: methylprogesterone, dronabi-
some cases, organ dysfunction can produce aberrant values, which nol, cyproheptadine, and tricyclic antidepressants such as
may be misinterpreted as related to nutrition therapy. It is important amitriptyline and imipramine
for the clinician to differentiate between the adverse effects of med- c) Drugs that cause dry mouth: anticholinergics, diuretics,
ications and other causes of changes in nutrition indices. Table 9-2 methyldopa, and antihistamines
lists some of the more prevalent and clinically significant alterations d) Drugs that cause a bad taste87: gold products, metronidazole,
in laboratory values. penicillins, and some other antibiotics
B. Analytical interference of medications. Medication interactions e) Drugs that decrease taste87: azathioprine and phenytoin
with laboratory tests can occur through several mechanisms of f) Drugs that affect taste acuity87: captopril and other angiotensin-
interference.78 Medications can both increase and decrease labora- converting enzyme inhibitors, chlorpromazine
tory values through different mechanisms. 5. Drugs with GI effects86
a) Drugs that cause nausea or vomiting: anticholinergics, auto-
nomic agents, beta blockers such as propranolol or labetalol,
VI. Effects of Drugs on Nutrition and Metabolism and emetogenic cancer chemotherapeutic agents
A. Drug-nutrient interactions. The following is not intended to be an b) Drugs that cause gastritis or ulcers: corticosteroids such as
all-inclusive list. Individual agents are mentioned only to provide a dexamethasone, methylprednisolone, hydrocortisone, non-
concrete illustration of the root cause of interactions. steroidal anti-inflammatory agents (indomethacin, ketorolac),
1. Antibiotics inhibit or kill susceptible bacteria. These may include and serotonin reuptake antagonists
gut bacteria responsible for vitamin K production. Since vitamin c) Drugs that alter intestinal motility86: decrease in motility—
K is essential for the production of clotting factors II (prothrom- opiates, anticholinergics, and phenothiazines such as chlorpro-
bin), VII, IX, and X, reduced vitamin K can result in decreased mazine; increase in motility—metoclopramide, erythromycin,
coagulation and bleeding. Antibiotics differ in the extent of this and cisapride
effect.79 d) Drugs that can damage GI tract mucosa: colchicine and cyto-
2. Some medications may affect hepatic protein synthesis. Chloram- toxic agents
phenicol is one of these. It also decreases the amount of iron incor- e) Drugs that can cause diarrhea: Many drugs can induce diar-
porated into heme, resulting in decreased hemoglobin synthesis.80 rhea as a result of an adverse reaction or toxicity. Additionally,
3. Certain diuretics may increase urinary excretion of potassium, drugs can significantly alter GI flora, which can precipitate
magnesium, and zinc.79 Other diuretics may spare potassium diarrhea. Antibiotics, quinidine, digoxin, and theophylline are
while increasing the urinary excretion of sodium. examples of medications that induce diarrhea.84
4. Medications used to treat or prevent ulcer disease, such as hista- f) Drugs that can cause abdominal pain and cramping: estro-
mine2 receptor antagonists and proton pump inhibitors, raise gens79,86
the gastric pH. This can result in decreased iron absorption. 6. Drugs that can affect the pancreas79,84,86
There may also be a decrease in the secretion of intrinsic fac- a) Drugs that can cause or exacerbate pancreatitis: diuretics,
tor.79 Histamine2 receptor antagonists can prevent metabolic estrogens, anticonvulsants, corticosteroids, azathioprine,
alkalosis, which occurs when patients have losses of gastric cyclosporine, carbamazepine, alcohol, antibiotics, and
secretions such as through nasogastric tubes connected to asparaginase
external suction. This is an example of a medication affecting b) Drugs that can alter pancreatic secretions: octreotide
nutrient absorption. c) Drugs that can alter pancreatic hormone release: insulin,
5. Drugs may also affect the pharmacodynamics of a nutrient at its asparaginase, beta blockers, glucocorticosteroid, octreotide,
site of action. There is a report of hydralazine interfering with growth hormone
the activity of pyridoxine, resulting in peripheral neuropathy.79 7. Drugs that can affect liver function
Phenytoin can increase inactivation of 25-hydroxy vitamin D, a) Thiazides: increase glycogen synthesis and increase glyco-
potentially leading to osteomalacia or rickets.79 genolysis
B. Medication-metabolic interactions. Drugs can alter metabolism. b) Drugs that can induce drug-metabolizing enzymes: barbitu-
Alterations are seen in appetite, digestion, and absorption; organ rates, alcohol, theophylline, diazepam, cimetidine, and
integrity and nutrient-processing capabilities; nutrient incorporation; erythromycin88
and nutrient metabolism and excretion. The following are examples c) Drugs that inhibit drug-metabolizing enzymes: cyclosporine,
of drugs that affect general nutritional status: isoniazid, chloramphenicol, amphotericin B, cytotoxic agents,
1. Growth hormone is a potent anabolic agent that affects protein, tricyclic antidepressants, steroids, long-acting antihistamines
carbohydrate, and fat metabolism. It increases protein synthesis such as terfenadine and astemizole, thiazides, allopurinol,
and nitrogen retention.81 anesthetics, antibiotics, and anti-inflammatory agents81,89

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S E C T I O N I Fundamentals of Nutrition Support Practice and Management

TABLE 9-2. Drug Interference With Clinical Laboratory Values (Continued)

Increase/
Drug Laboratory test decrease Mechanism of action

Acetaminophen Alkaline phosphatase Increase Hepatic necrosis associated with high drug concentration
Bilirubin Increase Hepatic damage with overdose
Glucose Decrease GOD-PERID method, measured by MediSense Precision QID
Acyclovir Alkaline phosphatase Increase Increased liver function tests
Decrease Leukopenia
Bilirubin Increase Increased liver function tests
Creatinine Increase Reversible renal failure
Aluminum antacids Phosphorus Decrease Binds to phosphorus in gastrointestinal tract
Amiodarone Alkaline phosphatase Increase Hepatitis, asymptomatic change in liver function enzyme
Bilirubin Increase Cholestasis, hepatitis
Prealbumin Decrease Probable direct effect on clearance or synthesis
Amitriptyline Alkaline phosphatase Increase May rarely cause hepatitis, hypersensitivity
Amphotericin B Bilirubin Increase May cause hepatocellular dysfunction
BUN Increase Nephrotoxic effect
Creatinine Increase Nephrotoxic effect
Magnesium Decrease Nephrotoxic effect
Potassium Decrease Altered distal tubule permeability
Ampicillin Sodium Increase Measured by ISE without predilution
Ascorbic acid Bilirubin Increase SMA 12/60 method
Urine sugar (False +) Clinitest
Atenolol Glucose Increase or Altered glucose regulation mediated by beta-2 receptors
decrease
Barium Potassium Decrease Impaired cellular discharge
Beta-2 agonists Potassium Decrease Facilitates intracellular uptake
Beta-adrenergic Potassium Increase Aldosterone effect
blockers
Bicarbonates Chloride Decrease Induced metabolic alkalosis
Potassium Decrease Induced metabolic alkalosis
Calcium Potassium Increase Emission spectrum interferes with that of potassium in direct flame
photometric method
Sodium Increase Emission spectrum interferes with that of sodium in direct flame
photometric method
Captopril Potassium Increase Hypoaldosterone, impaired excretion
Carbamazepine Alkaline phosphatase Increase Hepatotoxicity
Bilirubin Increase Hepatotoxicity
Cephalexin Alkaline phosphatase Increase Transient hepatitis and cholestatic jaundice reported
Creatinine Increase Jaffe methods, Technicon SMAC, Serno Centrifichem
Chlorambucil Bilirubin Increase Hepatotoxicity

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TABLE 9-2. Drug Interference With Clinical Laboratory Values (Continued)

Increase/
Drug Laboratory test decrease Mechanism of action

Chloramphenicol Bilirubin Increase Hepatotoxicity

BUN Decrease Berthelot method
Increase Nesslerization method
Chlordiazepoxide Bilirubin Increase Infrequent cholestatic effect
Chlorfibrate Sodium Decrease Increased ADH
Chloroquine Bilirubin Increase Hemolytic anemia due to G6PD deficiency
Chlorpromazine Alkaline phosphatase Increase Hepatic sensitivity to drug (up to 2% of patients)
Glucose Increase Abnormally high after repeated doses
Chlorpropamide Sodium Decrease Increased inappropriate ADH secretion
Cholestyramine Cholesterol Decrease Increases fecal excretion of bile acids
Cisplatin Magnesium Decrease Renal wasting
Potassium Decrease Renal wasting
Citrates Calcium Decrease EDTA titration method
Magnesium Decrease Complexes with calcium in fluorometric test
Clonidine Sodium Increase By effect on renal tubules
Corticosteroids Calcium Decrease Metabolic effect
Chloride Decrease Decreased reabsorption
Increase By salt/water retention
Glucose Increase Gluconeogenesis
Phosphorus Decrease Glucose utilization
Potassium Decrease Renal potassium wasting
Sodium Increase By salt/water retention
Cyclophosphamide Bilirubin Increase Hepatotoxicity
Sodium Decrease Increased ADH/water retention
Cyclosporine Potassium Increase Impaired excretion
Diethylstilbestrol Bilirubin Increase Hepatotoxicity
Calcium Increase Elevations over baseline level
Digoxin Potassium Decrease Impaired K/Na pump
Diltiazem Alkaline phosphatase Increase Mild increases in enzyme activity
Bilirubin Increase Mild transient increase
Uric acid Increase May cause gout as a side effect
Enalapril Potassium Increase Hypoaldosterone, impaired excretion
Erythromycin Alkaline phosphatase Increase May cause intrahepatic cholestasis (reversible)
Bilirubin Increase Cholestatic effect in 15% of patients
Estrogens Dexamethasone (False +) Due to increased corticosteroid binding globulin
suppression test

(Continued)

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TABLE 9-2. Drug Interference With Clinical Laboratory Values (Continued)

Increase/
Drug Laboratory test decrease Mechanism of action

Ethacrynic acid Bicarbonate Increase By alkalosis

Calcium Decrease Renal wasting
Chloride Decrease By diuretic effect
Magnesium Decrease Impaired reabsorption
Potassium Decrease By diuretic action
Sodium Decrease By diuretic effect
Fat emulsion Bilirubin Decrease May affect accuracy
Furosemide BUN Increase Nephrotoxic effect: usually dehydration
Calcium Decrease Diuretic action
Chloride Decrease Diuretic effect
Glucose Increase Diabetogenic action of drug
Magnesium Decrease Diuretic action
Potassium Decrease Diuretic action
Sodium Decrease Diuretic effect
Gentamicin Magnesium Decrease Associated with massive urinary loss of magnesium and potassium
and renal tubular toxicity
Potassium Decrease Associated with massive urinary loss of magnesium and potassium
and renal tubular toxicity
Glutamine Phenytoin Increase Significant increase in children
Growth hormone Phosphate Increase Metabolic effect
Total protein Increase Increased protein synthesis
Heparin Calcium Decrease EDTA titration method
Decrease Fluorometric titration method
Potassium Increase Impaired aldosterone synthesis
Sodium Decrease Increases sodium excretion
Hydrochlorothiazide Bicarbonate Increase By alkalosis
Bilirubin Increase Cholestatic jaundice
Calcium Increase Impaired excretion
Glucose Increase Glucose intolerance associated with potassium depletion
Potassium Decrease By diuretic action
Indomethacin Alkaline phosphatase Increase Hepatotoxicity
Bilirubin Increase Cholestatic jaundice
Glucose Increase No mechanism known
Potassium Increase ISE method
Urea nitrogen Increase Occasionally to upper normal
Insulin Potassium Decrease Intracellular shift
Total protein Increase Increased protein synthesis

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TABLE 9-2. Drug Interference With Clinical Laboratory Values (Continued)

Increase/
Drug Laboratory test decrease Mechanism of action

Isoniazid Alkaline phosphatase Increase Hepatotoxicity

Bilirubin Increase Cholestatic jaundice
Laxatives Magnesium Decrease From malabsorption and diarrhea
Potassium Decrease From malabsorption and diarrhea
Sodium Decrease From malabsorption and diarrhea
Lithium Magnesium Increase Affect membrane transport
Magnesium hydroxide Phosphorus Decrease Binding effect
Magnesium salts Calcium Increase EDTA titration method
Mannitol Sodium Decrease By diuretic effect
Meperidine Glucose Increase Mechanism unknown
Metformin Bicarbonate Decrease Acidosis
Iron Decrease Impaired B12 absorption
Methotrexate Alkaline phosphatase Increase Hepatotoxicity
Bilirubin Increase Hepatotoxicity
Methyldopa Bilirubin Increase Hepatotoxicity
Chloride Increase By salt/water retention
Sodium Increase By salt/water retention
Urine ketone Increase Affect alkaline nitroprusside procedure
Metoclopramide Potassium Decrease About 0.3 mmol/L
Metoprolol Alkaline phosphatase Increase Increased enzyme activity
Metronidazole Glucose Decrease Hexokinase/G6PD method
Du Pont academic method
Morphine Urine volume Decrease Increased ADH
Niacin Alkaline phosphatase Increase Hepatic impairment
Bilirubin Increase Hepatic impairment
Glucose Increase Glucose intolerance may occur
Uric acid Increase Hyperuricemia may occur
Nitrofurantoin Bicarbonate Decrease By nephrotoxicity
Creatinine Increase Jaffe-Fading-Fraction method
Nonsteroidal anti- Potassium Increase Impaired potassium secretion, hypoaldosteronism
inflammatory drugs
Oral contraceptives Glucose Increase Alters glucose tolerance test
Sodium Increase By salt/water retention
Total protein Decrease Decreased protein synthesis; increases 3 years after administration
Oxazepam Bilirubin Increase Possible hepatotoxicity
Glucose Increase Affects o-toluidine/neocuprion method
Oxytocin Sodium Decrease At induction of labor, also observed in infant

(Continued)

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S E C T I O N I Fundamentals of Nutrition Support Practice and Management

TABLE 9-2. Drug Interference With Clinical Laboratory Values (Continued)

Increase/
Drug Laboratory test decrease Mechanism of action

Penicillin Albumin Decrease BCG method

Potassium Decrease If intravenous sodium penicillin infused
Decrease Large doses given intravenously (especially carbenicillin and
ticarcillin) may cause hypokalemia due to the large amount of non-
reabsorbable anion in the distal renal tubules
Urine glucose Increase Ames Clinitest tablets
Phenobarbital Calcium Decrease Metabolic effect with long-term therapy
Folate Decrease Low levels in 27% to 91% of treated epileptics
Phenothiazines Bilirubin Increase Intrahepatic cholestatic syndrome
Phosphate Decrease Affects methods using phosphomolybdate
Phenytoin Alkaline phosphatase Increase Hepatotoxicity (in 42% of 60 patients treated for >10 yrs)
Folate Decrease Low level after extended therapy
Glucose Increase Inhibitory effect on insulin secretion
Phosphates Calcium Decrease Emission flame method
Probenecid Bilirubin Increase Hepatotoxicity
Urine protein Increase Nephrotoxic effects
Procainamide Potassium Increase ISE method
Propranolol Glucose Decrease May precipitate overt diabetes
Increase In long-term dialysis, due to beta blockade
Triglycerides Increase After therapy for >10 wks
Quinidine Bilirubin Increase Hemolysis effect
Rifampin Bilirubin Increase Yellow coloration interferes with several analytical methods
Glucose Increase Du Pont academic method
Risperidone Glucose Increase Infrequent diabetes mellitus observed
Potassium Decrease Hypokalemia observed
Sodium Decrease Hyponatremia observed
Saline infusions Chloride Increase Without addition of other anions, normal saline is hyperchloric with
respect to physiologic extracellular fluid
Sildenafil Alkaline phosphatase Increase Abnormal liver function tests
Glucose Increase Unstable diabetes or hyperglycemia observed
Decrease Hypoglycemic reactions observed
Spironolactone Potassium Increase Blunted normal response to aldosterone
Sodium Decrease By diuretic effect
Succinylcholine Potassium Increase Transient effect: general anesthesia
Sulcrafate Phosphate Decrease Comparable to aluminum hydroxide
Sulfonylureas Alkaline phosphatase Increase Elevation with cholangiolitis
BUN Increase Diacetyl method

132 A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. © 2005 A.S.P.E.N. www.nutritioncare.org.
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TABLE 9-2. Drug Interference With Clinical Laboratory Values (Continued)

Increase/
Drug Laboratory test decrease Mechanism of action

Sulfonylureas (Continued) Sodium Decrease Potentiates vasopressin, causes water retention

Tetracycline Glucose Decrease Ascorbic acid in preparation may affect glucose oxidase procedure,
by GOD/POD-PAP method.
Increase MBTH procedure of Neeley, slight effect on hexokinase, o-toluidine
methods
Phosphate Decrease May occur with Fanconi syndrome
Increase May occur with nephrotoxicity
Sodium Increase May cause hypernatremia with renal impairment
Theophylline Bilirubin Decrease Diazo reaction (general)
Glucose Decrease Hypoglycemia observed with acute and chronic overdoses
Potassium Decrease Renal/gastrointestinal cellular shift
Thiazide diuretics Bilirubin Increase Cholestatic hepatitis
Calcium Increase Renal retention: up to 0.25 mEq/L
Chloride Decrease Impaired tubular reabsorption
Glucose Increase Decreased glucose tolerance
Magnesium Decrease Diuretic effect
Sodium Decrease Diuretic effect
Thyroid preparations Glucose Increase Promotes mobilization of glycogen stores
Tolbutamide Alkaline phosphatase Increase Hepatotoxicity
Cholesterol Decrease Inhibits hepatic synthesis
Triamterene Bicarbonate Decrease By nephrotoxicity
Tube feedings Magnesium Increase Especially in high rate and renal failure
Valproic acid Alkaline phosphatase Increase Acute hepatic centrilobular necrosis
Bilirubin Increase Abnormal liver function tests
Sodium Decrease Hyponatremia and inappropriate ADH secretion
Sodium Increase Technicon SRA-2000
Valsartan Potassium Increase Serum potassium may increase 20%
Vancomycin BUN Increase Nephrotoxicity
Vasopressin Sodium Decrease Water retention
Verapamil Urine sodium Increase Marked increase in hypertensives
Vincristine Sodium Decrease Increased inappropriate secretion of ADH
Vitamin K Bilirubin Increase Increases bilirubin by hemolyzing G6PD-deficient red blood

ADH, antidiuretic hormone; BUN, blood urea nitrogen; EDTA = ethylenediaminetetraacetic acid; G6PD = glucose-6-phosphate dehydrogenase; ISE, ion-sensitive electrode
(laboratory method)
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S E C T I O N I Fundamentals of Nutrition Support Practice and Management

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36. Tsai WL, Poon SK, Yu HK, et al. Nasogastric lansoprazole is effective in 61. Freeman CD, Klutman NE, Lamp KC, Dall LH, Strayer AH. Relative
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col Ther. 2000;1:123–127. enteral nutrition supplement. Ann Pharmacother. 1998;32:1004–1007.
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Aliment Pharmacol Ther. 2003;18:581–586. Pharm. 1990;47:2034–2037.
38. Prevacid [package insert]. Lake Forest, IL: TAP Pharmaceuticals; 2003. 63. Bass J, Miles MV, Tennison MB, Holcombe BJ, Thorn MD. Effects of
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39. Ferron GM, Ku S, Abell M, et al. Oral bioavailability of pantoprazole bamazepine suspension. J Clin Pharmacol. 2001;41:183–186.
suspended in sodium bicarbonate solution. Am J Health Syst Pharm. 64. Riss JR, Kriel RL, Kammer NM, Judge MK, Montgomery MJ. Adminis-
2003;60(13):1324–1329. tration of Carbatrol to children with feeding tubes. Pediatr Neurol.
40. Dentinger PJ, Swenson CF, Anaizi NH. Stability of pantoprazole in an 2002;27:193–195.
extemporaneously compounded oral liquid. Am J Health Syst Pharm. 65. Semple HA, Koo W, Tam YK, Ngo LY, Coutts RT. Interactions between
2002;59:953–956. hydralazine and oral nutrients in humans. Ther Drug Monit. 1991;13:
41. Bauer LA. Interference of oral phenytoin absorption by continuous naso- 304–308.
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43. Fleischer D, Sheth N, Kou JH. Phenytoin interaction with enteral feed- 67. Buijk SL, Gyssens IC, Mouton JW, Verbrugh HA, Touw DJ, Bruining HA.
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1990;14:513–516. ically ill surgical patients with invasive mycoses and compromised gastro-
44. Rodman DP, Stevenson TL, Ray TR. Phenytoin malabsorption after intestinal function. Intensive Care Med. 2001;27:115–121.
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68. Davis GA, Rapp RP, Kearney PA, Ensom MH. Pharmacokinetics of flucona- 84. McEvoy G, ed. American Hospital Formulary Service, Drug Information
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69. Murray M, Grogan TA, Lever J, Warty VS, Fung J, Venkataramanan R. 85. Obama M, Cangir A, Van Eys J. Nutrition status and anthracycline cardio-
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70. Fagan TC, Walle T, Oexmann MJ, et al. Increased clearance of propranolol 87. Maslakowski CJ. Drug-nutrient interactions/interrelationships. Nutr Supp
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75. Pinchera A, MacGillivray MH, Crawford JD, et al. Thyroid refractoriness in
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76. Seres DS. Insulin adsorption to parenteral infusion systems: case report
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77. AHFS Drug Information 2003. Bethesda, MD: American Society of Health and clearance due to obesity. J Pharmacol Exp Ther. 1981;217:681–685.
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with protein calorie malnutrition. Am J Clin Nutr. 1975;26:977–981. Roe DA. Handbook on Drug and Nutrient Interactions. Chicago, IL: American
81. Anderson KE, Conney AH, Dappas A. Nutrition and oxidative drug metab- Dietetic Association; 1989.
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mal and kwashiorkor serum. South Afr Med J. 1977;52:522–525.

136 A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. © 2005 A.S.P.E.N. www.nutritioncare.org.
 SECTION EDITOR
Karen Ringwald-Smith, MS, RD
II
Immune Driven
Conditions

10 HIV Infection/Acquired Immunodeficiency Syndrome

11 Cancer

12 Solid Organ Transplantation

13 Hematopoietic Stem Cell Transplantation

 Cade Fields-Gardner,
MS, RD, LD, CD
10
HIV Infection/Acquired
Immunodeficiency
Syndrome
Introduction aphthous ulcers, gingival erythema, Herpes spp. lesions, oral
hairy leukoplakia, and Kaposi’s sarcoma.
Infection with the human immunodeficiency virus (HIV) has become c) Gastrointestinal manifestations include esophageal ulcers,
a global pandemic, with prevalence ranging from 0.5% in the United abdominal pain, biliary tract dysfunction, pancreatitis, and
States and many Western countries to nearly 40% in some transitional diarrhea (often associated with opportunistic infection).
and developing nations.1 While death rates have declined dramatically d) Weight loss episodes are commonly associated with oppor-
in the United States, there are an estimated 40,000 new infections tunistic infections.
yearly, with a trend toward increasing numbers of HIV diagnoses.2,3
e) Hematologic, neurologic, and neoplastic problems are asso-
A dramatic (>80%) decline in perinatal transmission has been seen
ciated with chronic or untreated HIV disease and immune
with the use of antiretroviral (ARV) therapies, which are nearly 100%
dysfunction.
effective in preventing transmission from mothers to children.4,5 The
B. Treatments include ARV drugs targeted to various segments of the
majority of new infections in the United States are seen in the popula-
HIV life cycle, prevention and treatment for opportunistic infec-
tion categories of women and ethnic minorities.6 The natural history of
tions, and prevention and treatment for a variety of symptoms that
HIV infection and its symptomatic manifestation of acquired immun-
complicate disease treatment.
odeficiency syndrome (AIDS) vary widely among individuals.7–9 HIV
1. The introduction and routine use of combination ARV therapies
infects many cells and proliferates in activated CD4+ T cells. A back-
ground on the life cycle of HIV is helpful, and several online sources has resulted in a 50% decline in death rates in the United States.
are available.10 It is speculated that use of ARV therapies may also reduce the
incidence of HIV infection for the future, assisting in efforts to
I. Overview of HIV Infection and AIDS eradicate the pandemic.14–17
II. Nutritional Aspects of HIV Infection 2. ARV treatment is not universally used or available. General rec-
III. Nutritional Assessment in HIV Infection ommendations suggest the initiation of ARV therapy if there is
IV. Goals of Nutritional Therapy and Nutrition Decision Making severe immune compromise as evidenced by CD4 cell counts of
V. Nutritional Management in HIV Infection <200/uL in adults, adolescents, and children older than 6 years;
References or <500/uL in children aged 1 to 5 years; or <750/uL in children
Suggested Reading under 1 year old.18,19 In addition, patient medical and nutritional
history should play a role in choosing the most appropriate reg-
imens. For instance, for a patient with a history of cardiovascu-
I. Overview of HIV Infection and AIDS lar disease, regimens less likely to elevate blood lipids may be
A. Several aspects of primary (initial) and chronic infection with HIV preferred.
can affect health and nutritional well-being. 3. Prophylaxis for opportunistic infections may include antibiotic
1. The acute viral syndrome that develops 2 to 4 weeks after expo- medications.12 Interactions with ARVs and additive risk for side
sure to HIV may include weight loss, fatigue, and fever. Gastro- effects should be considered in choices for prevention and treat-
intestinal manifestations during this time include abdominal pain, ment for opportunistic infections.20
vomiting, and diarrhea.11 4. Additional treatment may be required for diseases affecting
2. Immune deficiency resulting from the dysfunction and destruc- nutritional status, such as diabetes, cancer, and cardiovascular
tion of immune cells can lead, predictably, to opportunistic infec- disease. Please refer to chapters on individual disease states for
tion and neoplasm.12 treatment recommendations. Prior to treatment, special attention
3. HIV is found in many tissues and may continue to be harbored should be paid to potential interactions of diet and therapies with
regardless of viral load measures and ARV therapy.13 ARV medications
4. Various manifestations of chronic HIV infection and treatments 5. Variations in quality of care have been documented and may
can directly affect the maintenance and restoration of nutritional be related to several factors, including CD4 count and medical
status.11 insurance.21
a) Chronic HIV infection can result in various metabolic alter-
ations, including hypertriglyceridemia, hyperglycemia, lactic
acidosis, insulin resistance, and altered body shape.
II. Nutritional Aspects of HIV Infection
b) Oral manifestations are more common in immunosuppressed A. Nutritional alterations occur in primary infection and throughout
patients and may include candidiasis (oral and esophageal), the disease process.

© 2005 A.S.P.E.N. www.nutritioncare.org. A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. 139
SECTION II Immune Driven Conditions

1. Individuals experience primary infection differently. As with other 1. HIV can infect and affect organ function. Gastrointestinal, liver,
infections, primary infection with HIV can lead to catabolism of kidney, pancreas, adrenal, and sex organ functions may be
lean tissues and alterations in nutrient metabolism. Symptoms adversely affected.
associated with primary infection that specifically affect nutrition- a) If HIV infection is introduced through the gastrointestinal
al status may include anorexia, nausea, vomiting, diarrhea, and tract, gastrointestinal compromise may occur early.44,45
fever. (1) Symptoms and risk factors for compromise may include
2. Malnutrition, wasting, and altered metabolism are relatively com- malabsorption of macronutrients and micronutrients, diar-
mon and in some cases clinically significant, particularly in symp- rhea, and lactose intolerance.
tomatic phases of the disease. (2) Reduced food and nutrient intake may result in weight loss.
a) Malnutrition may start early in chronic HIV infection, with b) Liver manifestations are common in persons who are infected
altered body composition and mild to moderate gastro- with HIV and are being treated for it.46,47
intestinal dysfunction.22–24 (1) Alterations may be due to inflammatory response to
b) Weight loss and wasting, while common, are not necessarily infection.
a component of the natural history of HIV disease.25,26 Weight (2) Additional alterations may result from medication, nutri-
loss episodes continue to be common regardless of the use of ents, and other treatments.
ARV medications.27 (3) Coinfection with hepatitis A, B, or C or other hepatitis
c) Weight loss is related to the following: viruses may lead to additional nutritional risk. Patients
(1) Reduced intake or loss of nutrients that may be due to with hepatitis C coinfection on ARV therapies may be at
oral manifestations, diarrhea, vomiting, fever, and sweat- higher risk for developing disease- and nutrition-related
ing28,29 complications, such as diabetes.48 ARV therapies may inter-
(2) Malabsorption of nutrients related to HIV or other infec- act with treatments for hepatitis C coinfection and should
tion in the gastrointestinal tract, hepatobiliary dysfunc- be closely monitored to maintain the efficacy of both
tion, and pancreatic dysfunction30,31 therapies.49,50
(3) Increased catabolism of body tissues in response to HIV c) Pancreatic function affects both absorption and metabolism
or opportunistic infection and neoplasm32 of nutrients.
(1) Exocrine pancreatic function can be compromised by
(4) Viral load with each log increase in levels associated with
infection and by medication interactions. Altered exocrine
a 1.68 kg weight loss and a 1.58 increased likelihood of
pancreatic function can lead to fat malabsorption and
weight loss33
steatorrhea in some cases.51,52
d) Altered metabolism of nutrients may include changes in
(2) Endocrine pancreatic function can be compromised by
absorption, utilization, and losses.34,35
infection and altered hormonal milieu.53
(1) Altered organ function related to inflammatory response,
d) Adrenal gland function may be altered, leading to changes in
HIV or opportunistic infection, and cancers can lead to
inflammatory responses and other hormones.54–56
changes in nutrient needs and tolerances.
e) Sex hormone alterations may be related to other hormonal
(2) Nutrients associated with inflammatory response may
alterations and to weight and subcutaneous fat losses.57
indicate more about infection severity than nutritional sta-
f) Changes in growth hormone levels and circadian rhythms have
tus but are still important indicators of disease and nutri-
been reported and may lead to weight loss, alterations in body
tional status changes.36,37 composition, and anabolic blocks.58
(a) HIV is a chronic inflammatory disease, and long-term g) Alterations in thyroid hormone levels have been documented.
alterations in nutrient status may be related to disease Hypothyroidism may be more prevalent in HIV-infected men
process as well as nutritional status changes. than in women and more commonly associated with low CD4
(b) Albumin levels that quickly drop are more likely to be counts. The potential of ARVs to alter thyroid levels remains
indicative of infection than of a change in nutritional equivocal.59,60
status.38,39 C. Nutritional compromise can be related to chronic HIV infection
(c) Nutrients bound to albumin are also likely to be altered and opportunistic conditions.
during an inflammatory response, with or without a 1. Chronic HIV infection and intermittent opportunistic infections
significant change in nutritional status.40 For instance, or cancers related to immune compromise can also alter nutri-
changes in zinc status may be related to inflamma- tional status according to the site affected and the severity of the
tion, hydration, or hemolysis.41 Whether albumin can infection or cancer.
be used as an adequate indicator of nutritional status 2. Nutritional compromise can further impair immune function and
may depend on the severity of an inflammatory the ability to withstand opportunistic events.61
response. Additional information, such as C-reactive D. Nutritional alterations occur with ARV and other treatments.
protein levels, may help to establish the severity of 1. The introduction of combination therapy with ARVs has resulted
inflammation. in a 50% decline in the death rate due to HIV infection.6
(d) Nutrients such as iron may be shunted to storage forms 2. Medication interactions with food and nutrient metabolism can
during inflammatory responses. Care should be taken compromise nutritional status and lead to additional acute and/or
in both diagnosing iron deficiency and treating poten- chronic disease characterized by gastrointestinal, liver, kidney,
tial deficiency with supplements (which may be con- pancreatic, and other organ dysfunction. See Table 10-1 for poten-
traindicated in chronic inflammatory conditions, such tial interactions and other effects of ARVs.20
as HIV infection).42,43 a) Once initiated, it is likely that medication therapies will be
B. Alterations in organ and other tissue function can be related to HIV long-term and possibly lifelong. Adherence is an important
infection. part of an integrated health care plan. Adherence is supported

140 A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. © 2005 A.S.P.E.N. www.nutritioncare.org.
 S E C T I O N I I Immune Driven Conditions

TABLE 10-1. Potential Nutrition Interactions With Antiretroviral Therapies

Generic name (brand name)

Class of drug (manufacturer) Diet and nutrition interactions

Abacavir (Ziagen) Diet interactions: Take with or without food; caution with alcohol
Protease inhibitor
Potential side effects: nausea/vomiting, anorexia, abdominal pain, diarrhea, anemia, pancreatitis, lactic acido-
(GlaxoSmithKline)
sis (rare); may increase triglycerides, slight glucose intolerance

Amprenavir (Agenerase) Diet interactions: Take with or without food but not with high-fat meal (>50 g); avoid vitamin E supplements;
Protease inhibitor take 1 hour apart from antacids
(GlaxoSmithKline)
Potential side effects: diarrhea, nausea/vomiting, taste changes, stomach upset, diabetes, fatigue, increased
cholesterol, increased triglycerides, anemia

Atazanavir (Reyataz) Diet interactions: Take with food

Protease inhibitor
Potential side effects: abdominal pain, anorexia, aphthous stomatitis, colitis, constipation, gastroenteritis, taste
(Bristol-Myers Squibb)
changes, increased high-density lipoprotein cholesterol, increased bilirubin, lactic acidosis, potential for altered
fat deposition

Delavirdine (Rescriptor) Diet interactions: Take with or without food; do not take with antacids or magnesium-containing supplements;
NNRTI (Agouron) can take with acidic beverage (eg, cranberry juice); avoid alcohol

Potential side effects: increased thirst, anorexia, dry mouth, nausea/vomiting, gastritis, diarrhea, constipation,
flatulence

Didanosine (Videx) Diet interactions: Take without food on an empty stomach; do not take with acidic beverage or food, aluminum-
NRTI (Bristol-Myers Squibb) containing antacids, or magnesium-containing supplements; avoid alcohol

Potential side effects: anorexia, diarrhea, weight loss, anemia, nausea/vomiting, constipation, dry mouth, taste
changes, pancreatitis (increased risk with alcohol; decreased risk in pediatric patients), lactic acidosis (rare),
increased triglycerides

Efavirenz (Sustiva) Diet interactions: Do not take with high-fat meal (>40–60 g); avoid alcohol
NNRTI
Potential side effects: anorexia, nausea/vomiting, diarrhea, increased cholesterol, increased
(Bristol-Myers Squibb)
triglycerides

Emtricitabine (Emtriva) Diet interactions: Take with or without food

NRTI (Gilead)
Potential side effects: nausea/vomiting, diarrhea

Enfurvitide (Fuzeon) Diet interactions: Subcutaneous injection with no food interactions

Fusion inhibitor (Roche)
Potential side effects: diarrhea, nausea, fatigue, taste change, decreased appetite, potential for pancreatitis

Fosamprenavir (Lexiva) Diet interactions: Take with or without food

Protease inhibitor
Potential side effects: nausea/vomiting, diarrhea, increased triglycerides
(GlaxoSmithKline)

Indinavir (Crixivan) Diet interactions: Take without food on an empty stomach or with very low calorie/low protein snack (note: no
Protease inhibitor (Merck) food restriction when taken with ritonavir); take with plenty of fluids

Potential side effects: nausea/vomiting, abdominal pain, taste changes, diarrhea, kidney stones, diabetes
(rare), insulin resistance, increased triglycerides, increased cholesterol; increased indirect bilirubin in pediatric
patients should be closely monitored

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SECTION II Immune Driven Conditions

TABLE 10-1. Potential Nutrition Interactions With Antiretroviral Therapies (Continued)

Generic name (brand name)

Class of drug (manufacturer) Diet and nutrition interactions

Lamivudine (Epivir) Diet interactions: Take with or without food

NRTI (GlaxoSmithKline)
Potential side effects: nausea/vomiting, abdominal cramps, diarrhea, anorexia, pancreatitis, lactic acidosis (rare)

Lopinavir (Kaletra) Diet interactions: Take with or without food; meals with >15 g fat increase absorption
Protease inhibitor (Abbott)
Potential side effects: abdominal pain, diarrhea, nausea, increased triglycerides, increased cholesterol

Nelfinavir (Viracept) Diet interactions: Take with food; mixing powder with acidic food or beverage results in bitter taste
Protease inhibitor (Agouron)
Potential side effects: diarrhea, flatulence, nausea, abdominal pain, diabetes (rare), increased or decreased glu-
cose

Nevirapine (Viramune) Diet interactions: Take with or without food

NNRTI (Roxane)
Potential side effects: nausea/vomiting, abdominal pain, fatigue, hepatotoxicity

Ritonavir (Norvir) Diet interactions: Take with food; meals with >15 g fat increase absorption
Protease inhibitor (Abbott)
Potential side effects: nausea/vomiting, diarrhea, taste changes, anorexia, upset stomach, abdominal pain,
weight loss, diabetes, increased triglycerides, increased cholesterol

Saquinavir (Invirase, Diet interactions: Take with high-calorie, high-fat meal unless combined with ritonavir; grapefruit juice increas-
Fortovase) es retention
Protease inhibitor (Roche)
Potential side effects: nausea, diarrhea, constipation, abdominal pain, taste changes, impaired glucose toler-
ance

Stavudine (Zerit) Diet interactions: Take with or without food; avoid alcohol
NRTI (Bristol-Myers Squibb)
Potential side effects: nausea/vomiting, diarrhea, anorexia, weight loss, abdominal pain, peripheral neuropathy

Tenofovir (Viread) Diet interactions: Take with food

NRTI (Gilead)
Potential side effects: nausea/vomiting, diarrhea, abdominal pain, lactic acidosis (rare)

Zalcitabine (Hivid) Diet interactions: Take without food on an empty stomach; avoid alcohol
NRTI (Roche)
Potential side effects: anorexia, oral/esophageal ulcers, nausea/vomiting, diarrhea, constipation, weight loss,
abdominal pain, dry mouth, peripheral neuropathy, lactic acidosis (rare), pancreatitis (rare), increased triglyc-
erides, impaired glucose tolerance

Zidovudine (Retrovir) Diet interactions: Take with or without food, preferably not with high-fat meal; may require zinc, copper supple-
NRTI (GlaxoSmithKline) mentation

Potential side effects: anorexia, nausea/vomiting, upset stomach, constipation, anemias

NNRTI, Nonnucleoside Reverse Transcriptase Inhibitor; NRTI, Nucleoside Reverse Transcriptase Inhibitor.

in part by nutritional interventions.62 Research is continuing to (1) Protease inhibitors have been associated with glucose
explore the possible advantages and disadvantages of planned intolerance or insulin resistance.
treatment interruptions.63,64 (2) Nucleoside reverse transcriptase inhibitors have been
b) Specific ARVs are associated with glucose intolerance, insulin associated with anemias.
resistance, dyslipidemia, and a variety of anemias.65–68 See c) Treatment recommendations for these problems are outlined
Table 10-1 for potential nutrient interactions reported with by the Adult and Pediatric AIDS Clinical Trials Groups and
ARV medications. others.69,70

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d) Many ARVs are associated with anorexia, nausea and vomit- associated with insulin resistance and altered fat metab-
ing, diarrhea, constipation, abdominal pain, dry mouth, taste olism. Central fat deposition can be assessed through
changes, and other potential interactions that can reduce food anthropometric measures, magnetic resonance imag-
intake, absorption, and increase losses.20 ing, or computed tomography scans of an abdominal
E. Nutritional compromise in pediatric patients cross-section at the L4–L5 level.
1. Nutritional compromise in the forms of stunting, weight loss, b) Bioelectrical impedance analysis (BIA)
failure to thrive, gastrointestinal dysfunction, and developmen- (1) BIA evaluation should use equations validated for use in
tal delay are among the problems commonly seen in pediatric HIV infection.78
patients with HIV disease. (2) BIA can be compared to expected or functional levels of
2. Subclinical hypothyroidism has been documented and has the BCM (muscle and organ tissue estimate), extracellular tis-
potential to lead to developmental abnormalities.71 Thyroid func- sue (bone, collagen, and extracellular fluid estimate), and
tion monitoring has been suggested. fat (both stored and essential functional fat tissues).
3. Children with growth failure may have altered levels of thyroid (3) A 5% loss of BCM from function levels or baseline indi-
and insulin-like growth factor.72 cates wasting and risk for functional loss of tissues and
increased risk of mortality.
(4) An increase in extracellular tissue can indicate an active
III. Nutritional Assessment in HIV Infection inflammatory process in normally hydrated persons.
A. Specific nutrition-related assessment factors are strong predictors of (5) A decrease in fat stores indicates a calorie imbalance and
morbidity and mortality. Weight loss and wasting as indicated by can also reflect peripheral fat losses. This problem may
loss of weight, fat-free mass, body cell mass (BCM), and fat tissues feed a cycle of insulin resistance, leading to additional
are strong predictors of mortality in persons with HIV infection. peripheral fat losses and alterations in other hormonal
Despite the use of effective ARV therapies, the incidence of wasting balances.
may be on the rise.73 c) Other physical examination findings include
B. General assessment for adults will include the evaluation criteria (1) General appearance
for other patients as described in the general nutrition assessment (2) Signs and symptoms of nutrient deficiency and excess (see
chapter. Chapter 1 for more detail)
d) Food and other nutrient intake compared to estimated needs
1. Nutrition assessment includes basic evaluation of
and anticipated contraindications, upper limits, and other lim-
a) Physical findings
itations due to organ dysfunction, inflammatory processes, and
(1) Anthropometry to evaluate weight for height, weight
other conditions the patient experiences
changes, changes in or high-risk patterns of body dimen-
(1) Ability to eat, gastrointestinal function, and risk or indica-
sions, and body composition evaluation
tion of altered nutrient metabolism should be reviewed to
(a) While the numbers of AIDS cases reported has been
determine the appropriate mode of nutrition intervention
reduced, the relative numbers of cases that are defined by
and support.
wasting continues to hover around 20%. Current research
(2) Included in this evaluation are physical activity levels,
suggests that wasting episodes continue to occur regard-
psychosocial and economic limitations, and other factors
less of the use of ARVs in as many as 40% of HIV-infect- that can affect nutritional intake and nutrition security
ed patients.27 (the ability to maintain a steady and adequate supply of
(b) Indicators of wasting in chronic HIV infection include74 required nutrients).
i) Weight decrease of more than 10% over a 6-month (3) Specific evaluation of dietary intake along with physical
period and laboratory evaluation can be used to determine poten-
ii) Loss from baseline or expected values of 5% BCM tial deficiencies and toxicities (see Chapter 1).
iii) Body mass index of <20 (a) Several nutrient deficiencies or metabolism alterations
(c) Additional measures of body dimensions and fat folds may be seen. Most commonly, nutrients associated with
may help to characterize altered body shape and fat inflammation, including iron, zinc, and antioxidants,
deposition associated with chronic HIV infection, treat- may be altered.
ment, and nontreatment host factors.75–77 (b) Supplementation to overcome reduced levels of nutri-
(2) Commonly reported altered body shape changes have been ents or anticipated additional nutrient needs can
related to both chronic infection and medications used to increase the risk for nutrient toxicity. Nutrient supple-
treat HIV infection. mentation should be monitored closely. In most cases,
(a) Subcutaneous fat losses can occur all over the body it may be better to initiate a balanced multivitamin
but are most noticeable in peripheral limbs and facial and mineral supplement than to supplement individual
areas. Consequences of subcutaneous fat loss can nutrients.
include the initiation or exacerbation of insulin resist- e) Medical history, including disease status, presence of oppor-
ance and a reduced substrate for maintenance of sex tunistic infections and neoplasms, existence of cofactors that
hormones and normal bone metabolism. Subcutaneous can affect nutritional status, and medication history
fat losses can be assessed through anthropometric f) Laboratory evaluation, including disease status and markers
measures as well as dual energy x-ray absorptiome- of nutritional status
try of soft tissues in peripheral limbs. (1) Review current and past markers of disease status, includ-
(b) Fat deposition is generally centrally located in the ing CD4 and CD8 cell counts and viral loads. Past or cur-
abdomen, chest, back, and nape of neck areas. Central rent history of low T-cell counts and high viral load is asso-
fat deposition, sometimes known as central obesity, is ciated with greater risk for adverse effects of disease and

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SECTION II Immune Driven Conditions

treatments such as insulin resistance, altered body fat depo- severe immunosuppression, neurological disorders, and
sition, and osteoporosis. developmental delay.
(2) Note that chronic inflammatory process and dehydration (2) Several common problems are specifically related to nutri-
may affect nutritional status markers such as albumin, tion and can be treated by combinations of therapies that
prealbumin, zinc, and iron. include nutrition-related strategies.
(3) Additional evaluation may include biochemical indices (a) Oral lesions are associated with CD4 counts, and gin-
of concomitant disease such as C-reactive protein for car- gival lesions were found to be the most common man-
diovascular disease and active inflammatory response, ifestations in children.82 Dental treatment access and
glycosylated hemoglobin, oral glucose tolerance tests, and utilization may be underused by children with HIV
C-peptide for insulin resistance. infection.83
C. Additional clinical risk factors and indicators should be assessed. (b) Fever is related to opportunistic infections.
1. Other common chronic diseases that may complicate treatment (c) Nausea, vomiting, diarrhea, malabsorption, and anorex-
of HIV infection and associated malnutrition include diabetes, ia may be related to HIV infection, opportunistic dis-
cardiovascular disease, osteopenia and osteoporosis, renal dys- ease, other comorbidities, or medication therapies.
function, liver disease, respiratory disease, and cancer. (d) Folate and iron-associated anemias have been docu-
2. Smoking and alcohol intake can affect nutrient intake and metab- mented in children. Neurologic deficits are associated
olism. with folate deficiency, and iron-related anemia is asso-
a) Alterations in organ function and greater risk for adverse ciated with chronic disease. Additional nutrients can
effects of medications and chronic HIV infection have been be lost through vomiting and diarrhea.
suggested by cohort studies. Examples include the following: b) In addition to clinical problems, psychosocial and economic
(1) Coinfections, interactions with additional medications issues may compromise nutritional status. A child with a care-
used to treat coinfections or neoplasms, and the long-term taker who is also HIV-infected may not be receiving adequate
effects of cortisol and other hormonal changes associated care. Additional support for nutrition may include connection
with chronic inflammatory processes can contribute to with community resources and additional health care social
changes in liver, kidney, pancreas, intestinal, and other support resources.
organ systems. c) There may be nutrition-related interactions with medications.
(2) Liver toxicity and interactions with foods or coinfections d) Cardiovascular function may be worse in children born to
can lead to medication intolerance in cases of medica- women with HIV infection and especially in HIV-infected
tions that are heavily metabolized by the liver. children.84
(3) Nephrotoxicity and other kidney disease can increase the e) Anemia may be common in children, particularly those with
prenatal exposure to ARV medications.67
potential toxicity of medications and adverse effects on
f) Similar patterns of metabolic and body shape alterations are
nutritional status.
seen in children and adults.85
(4) Gastrointestinal infection by HIV and other infectious
g) Some medications may affect children differently than adults.
disease can reduce the absorption of both nutrients and
For instance, the protease inhibitor indinavir is associated
medications.
with increased indirect bilirubin, which may be clinically in-
b) Complicated interactions with medications, hormonal milieu,
consequential in adult patients but more threatening to health
food intake and absorption, organ function, and cellular dam-
and survival in children. On the other extreme, very little
age should be taken into consideration. Examples include the
pancreatitis has been reported in children taking the nucleo-
following:
side reverse transcriptase inhibitor didanosine, although pan-
(1) Medications can alter lipid and glucose metabolism, cause
creatitis is a common occurrence in adults. Finally, while
symptoms such as anorexia and diarrhea, and lead to liver nephrolithiasis is a potential problem with both adults and
and kidney cell damage. children taking indinavir, it may be more difficult to ensure
(2) Hormonal changes associated with chronic inflammation adequate fluid intake (estimated at 48 ounces) in small chil-
and weight changes may include insulin resistance, hypo- dren to prevent the problem.
gonadism, and growth hormone resistance. Alterations in h) Different forms of medications are used with newborns and
body composition may include changes in muscle tissues, infants than adults. In some cases, it is a challenge to adminis-
fat deposition patterns, bone tissue metabolism, and oxida- ter liquids and improve the tolerance of bad-tasting medica-
tive stress-related cellular damage. tions, such as ritonavir.
D. General assessment will include items outlined in Chapter 1. Please 2. Physical examination
refer to that chapter for details. Pediatric-specific nutritional assess- a) Anthropometry, specifically serial measures of body dimen-
ment in HIV infection background information includes79,80 sions, which can identify particular types of problems and
1. Disease process their severity
a) Presence of HIV infection, level of immune function mark- (1) A declining trajectory of weight for age measures may
ers, and clinical class of disease progression are strong indi- indicate calorie imbalance and is a strong indicator of risk
cators of nutritional risk.81 for malnutrition-related problems and mortality.
(1) Comorbidities can include a number of opportunistic or (2) A declining trajectory of height for age measures is asso-
other complications related or unrelated to HIV infection ciated with chronic malnutrition, protein imbalance, and
and its treatment. Examples include failure to thrive, micronutrient deficiencies (eg, zinc) and is a strong indi-
cardiovascular disease, glucose intolerance and diabetes, cator of risk of morbidity and mortality.
renal disease, hepatic disease, pulmonary disease, a myr- (3) A declining trajectory of weight for height or body mass
iad of opportunist infections and neoplasms related to index measures is an indicator of calorie imbalance but

144 A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. © 2005 A.S.P.E.N. www.nutritioncare.org.
 S E C T I O N I I Immune Driven Conditions

may not consider existing stunting processes and is a implemented with extreme caution as the body may respond
weaker indicator of risk for malnutrition-related compli- dramatically if there are hidden opportunistic infections.94
cations. Increased availability of nutrients, particularly amino acids, in
(4) Midarm and head circumferences can be compared to a severely malnourished person with hidden infections (infec-
norms. tions that are not accompanied by fever or other indicators
(5) Growth velocity has been correlated to survival in HIV- because of a lack of nutritional stores to mount an adequate
infected children. Best predictors of mortality were height inflammatory response) can lead to a sudden, severe inflam-
growth, viral load, and CD4 count. Weight gain and head matory response that increases the risk of severe reactions that
circumference growth may not be as well correlated with can lead to multiorgan failure and death.
survival rates in this population.86 Shorter survival times b) Different mechanisms for weight loss can yield differences in
are associated with poor nutritional status.87 body composition changes during wasting, which can alter the
b) BIA level of nutritional risk. In most cases, opportunistic infection
(1) Equations may be different for children. is associated with a cachectic form of weight loss.95
(2) Lean body mass as expressed by BIA is a strong indica- c) Treatment of HIV infection may alter energy expenditure and
tor for nutritional risk. risk for malnutrition, both by decreasing energy expenditure
3. Dietary intake through lowering of HIV viral burden and by increasing
4. Laboratory analysis for disease factors and nutritional indices. energy expenditure through a mechanism independent of
Nutritional indices may be affected by inflammatory processes ARV therapies.96,97
(eg, albumin, zinc, selenium). 2. Protein turnover rates may be higher in HIV infection regardless
5. In many cases, the diagnosis of HIV infection and related disease of energy expenditure. Both calorie and protein balance appear to
is not disclosed to the child. In some cases, the diagnosis is dis- be important to maintaining growth in children.98 Level of protein
closed to only selected caregivers. These limitations should be intake is related to the maintenance and preservation of BCM in
considered in evaluating and planning for nutrition-related inter- HIV.99 Alterations in BCM may differ in patients with coinfec-
ventions, especially those that support medication adherence.88,89 tions.100 Protein intake remains related to the preservation of
BCM tissues.
3. Micronutrient interventions may be important to maintain ade-
IV. Goals of Nutritional Therapy and Nutrition quate intake and appropriate body tissue levels.101,102
Decision Making a) Micronutrient supplementation efforts should be approached
A. Primary goals for nutrition-related therapies include survival and with care due to the potential for toxic levels and the lack of
maintenance of body and cognitive functions, growth, and devel- knowledge about nutrient tolerance in asymptomatic and
opment in pediatric patients.90 symptomatic HIV-infected individuals.
B. Medication efficacy is dependent on nutritional status and can be b) Antioxidant therapy using micronutrients has been explored
affected by nutrient intake. Nutrition-related interventions should with equivocal results. Beta-carotene supplementation has
support medication adherence and efficacy. Because the use of ARV shown transient increases in CD4 cell count. Whey protein,
therapies results in a decline in infectivity, supporting medication N-acetyl cysteine, and other strategies to improve glutathione
content have increased the antioxidant capacity of the body.
efficacy through nutrition education and intervention becomes of
Additional efforts to improve antioxidant status and keep
primary importance to transmission prevention efforts.14–17
oxidative stress in check with nutrient supplementation are
C. Nutrition-related interventions should also aim to prevent or reduce
topics of ongoing research.
the adverse effects of chronic HIV infection, other concomitant dis-
B. Interventions to improve and maintain nutritional status should
ease, and therapies.
include education and counseling on basic nutritional principles and
1. Maintenance of nutritional status supports maintenance of
individualized strategies for maintaining adequate food and nutri-
immune function and resistance to opportunistic disease.
ent intake despite the challenges of disease and medications. As
Well-nourished children may respond well to ARV therapies, but
with other diseases, all HIV-infected patients should have access
response has not been tested in undernourished children.91
to nutrition-related care. Care should be provided in a nonjudg-
2. Education and counseling should include support for adherence mental and safe environment with consideration of all the psychoso-
to medication regimens. cial and economic factors that can ultimately affect nutritional status
and health care.103
V. Nutritional Management in HIV Infection 1. Patient education should include basic nutrition principles, food
and water safety, physical activity maintenance, and nutrition-
A. Alterations in nutrient requirements that may occur include the related symptom management strategies.
following: 2. Patient counseling should be tailored to specific risk factors and
1. Energy needs may increase. Increases in resting energy expendi- nutritional needs.
ture have been documented across the disease spectrum.92 a) Weight loss and wasting should be prevented whenever pos-
However, total energy expenditure depends on current nutrition- sible and reversed as soon as feasible. Nutrition-related inter-
al status and the amount of BCM (calorie-using tissues) in the ventions can improve important nutrition-related markers of
body.93 The increase in energy needs is variable and dependent on weight, fat-free mass, and body mass index.73,104,105
two factors: inflammatory process and amount of metabolizing b) Symptoms of HIV infection, opportunistic disease, and med-
protein stores (BCM). ication interactions should be addressed, and nutrition should
a) Severely wasted patients may have lower total energy expen- be tailored to the patient’s food preferences and tolerances.106
ditures and may not have the protein stores required to mount Care should be taken to anticipate the potential adverse effects
an inflammatory response. In such cases, refeeding should be of disease and treatments. The patient’s diet plan may include

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SECTION II Immune Driven Conditions

contingent dietary alterations related to anticipated problems. 2. In both adults and children, enteral nutrition support presents
Past concepts of palliative care should be integrated into pri- challenges for the HIV-infected patient with immune compromise
mary care for HIV-infected patients at all points in chronic (CD4 cell counts of <200/uL in adults, adolescents, and children
HIV disease.107 older than 6 years, or <500/uL in children aged 1 to 5 years,
(1) A strong emphasis on palliative care has previously been or <750/uL in children under 1 year old), but standard practice
reserved for hospice patients. With longer-term survival guidelines should be sufficient to provide safe and effective enter-
in HIV, symptom management and coping skills to main- al nutrition therapy options.117
tain nutritional status become important in chronic HIV a) The standard of care for other tube-fed adult and pediatric
infection across the spectrum of disease. patients applies, with special attention to sterile/aseptic tech-
(2) A patient interview might include questions about symp- niques and methods. The use of ready-to-feed or prepared
toms that may require palliation, such as diarrhea, nausea/ powder products depends on the level of immune compro-
vomiting, anorexia, pain, and fatigue, and other symptoms mise as indicated by CD4 cell counts and the potential for
that may interfere with health maintenance, medication infection in the particular setting (eg, acute care, home care).
adherence, and quality of life. b) The fact that several organ systems may be affected with severe
c) Specific diets may be used to address chronic disease cofac- immune compromise should be considered in tailoring therapy.
tors such as insulin resistance and diabetes, cardiovascular Plans should include strategies to maintain gut mucosa and
disease, renal dysfunction, and liver disease 108 immunity.
3. Oral nutrient supplementation may be required if it is deter- c) Close monitoring for infection and other complications will
mined that foodstuffs will not meet extraordinary requirements be required.
related to disease, gastrointestinal dysfunction, or neurologic dys- D. HIV-specific considerations in parenteral nutrition support (adult
function. and pediatric) include the following:
a) Nutrients lost through fever, diarrhea, and vomiting should be
1. In both adults and children, parenteral nutrition support presents
replaced. Oral rehydration therapy in addition to macronutri-
challenges for the HIV-infected patient with severe immune
ent and micronutrient supplementation may be required.
compromise.
b) Weight loss and nutrient deficits may be selectively treated
a) The standard of care for other parenterally fed adult and pedi-
with supplemental nutrients.
atric patients applies, with special attention to sterile/aseptic
(1) Care should be taken to ensure that supplemental nutri-
techniques and methods. With appropriate care, line sepsis may
ents do not adversely interact with medications and other
or may not be more common in immune compromise.118,119
dietary nutrients.
While treatment for HIV infection has reduced the risk of
(2) Nutrient supplementation should be tailored according to
catheter-associated infection rates by improving immune
patient risk factors and needs. High-protein supplemen-
competence, close monitoring for infectious complications
tation may not be advisable in populations at high risk for
is required.120
renal insufficiency.
(3) Limitations of effectiveness may be related to metabolic b) The fact that several organ systems may be affected with
alterations that produce an anabolic block.109 severe immune compromise should be considered in tailoring
c) Multi-micronutrient supplements have been investigated and therapy. Alterations in liver, pancreas, or kidney functions, for
show some promise for slowing the progression of HIV instance, may require altered formulations, rates of infusion,
infection to AIDS.110,111 Caution is suggested for iron supple- and methods of delivery. See chapter 11 for cancer, chapter 15
mentation in patients with a low serum iron level, owing to for pancreatitis, chapter 17 for liver disease, and chapter 23, 24
the potential for toxicity and the increased risk for bacterial and 30 for kidney failure for more tailored feeding strategies.
infections. c) Opportunistic infection treatment is essential to achieving
d) Complementary and alternative medicine may include nutritional repletion using parenteral nutrition.121
nutrient-based therapy. E. Nonnutrient adjunctive therapies to achieve nutrition-related goals
(1) Both nutrient and nonnutrient therapies in doses higher may include treatment for nutrition-related symptoms, anemias and
than in common food intake may be categorized as phar- other altered laboratory values, wasting, altered body fat deposi-
maceutical therapies. tion, osteopenia and osteoporosis, altered organ functions, altered
(2) Care should be taken to consider the potential for nutrient- hormonal milieu, inflammatory processes, anabolic blocks, and
drug interactions.112 reduced levels of physical activity. Examples include the following:
C. HIV-specific considerations in enteral nutrition support (adult and 1. Chronic diarrhea may benefit from a full evaluation to identify
pediatric) include the following: the cause, to match appropriate treatment with antidiarrheal
1. Standard indications for enteral nutrition can be used in adults medications, enteric-coated pancrelipase, and hydration strate-
and children with HIV infection and immune compromise. gies (oral or intravenous rehydration therapy).
a) Children who fail oral supplementation, have severe growth 2. Appetite loss may benefit from medications that stimulate the
and development failure, or have neurologic dysfunction that appetite, such as dronabinol or megestrol acetate, or strategies to
prevents adequate oral nutrient intake should be considered overcome anabolic blocks, such as testosterone replacement or
for enteral nutrition.113 growth hormone therapy.
b) Severe malabsorption and/or gastrointestinal infections may 3. Chronic anemias may be treated with medications to improve
require special formulations or consideration for parenteral red blood cell production.
nutrition.114 4. Hypogonadism, anemia, muscle wasting, and bone losses may
c) Immune-enhancing formulas may or may not provide added benefit from testosterone replacement or supplemental anabolic
benefit.115,116 steroids.

146 A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. © 2005 A.S.P.E.N. www.nutritioncare.org.
 S E C T I O N I I Immune Driven Conditions

5. Muscle wasting, bone losses, altered fat deposition, and growth 16. Clements MS, Prestage G, Grulich A, VanDeVen P, Kippax S, Law MG.
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© 2005 A.S.P.E.N. www.nutritioncare.org. A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. 149
 Elaine B. Trujillo, MS, RD;
Sara L. Bergerson, MS, RD;
Jennifer C. Graf, MS, RD;
Madeline Michael, MPH, RD
11
Cancer

Introduction 2. Cancer trends6

a) The incidence of all childhood cancers has fluctuated but has
Cachexia is often observed in patients with cancer and is associated with generally increased over the period 1975–2000 for 0- to 19-
increased morbidity and decreased quality of life and survival. The eti- year-olds.
ology of weight loss and cachexia in cancer patients includes decreased b) The largest increase in incidence for all cancers occurred dur-
intake, altered metabolism, and increased catabolism. This chapter ing 1975–1986.
addresses pediatric and adult nutritional issues and adjuvant therapy for c) Hepatic tumors had the largest percent increase in incidence for
patients with cancer, along with education for patients and caregivers. 1975–2000, followed by soft-tissue sarcomas and renal tumors.
d) Mortality from cancer has steadily decreased over the period
I. Background 1975–2000.
II. Nutritional Alterations in Patients With Cancer e) The 5-year survival rates for all cancers steadily increased
III. Nutritional Assessment of Patients With Cancer from 1975 to 1995.
IV. Criteria for Intervention and Goals of Therapy f) The 5-year survival rates from 1985 to 1999 were highest for
V. Nutritional Management retinoblastoma, followed by renal tumors, germ-cell tropho-
VI. Patient and Caregiver Education Internet Resources blastic and other gonadal neoplasms, and carcinomas and other
References malignant epithelial neoplasms. Hepatic tumors had the low-
est 5-year survival rate during the period.
3. Cancer types more likely to result in nutritional alterations
I. Background. More than 1 million Americans are diagnosed with
a) At diagnosis
cancer each year. Cancer is the second leading cause of death after heart
(1) Children have lower energy reserves and higher metabolic
disease, claiming 23% of total deaths in the United States. Although
demands than adults and are therefore more likely to expe-
overall cancer death rates and incidence rates have remained stable over
rience nutritional depletion, particularly during growth
the past few years, mortality rates of the four most common cancers
spurts.7–10
(lung, colorectal, breast, and prostate) have continued to decline.1 The
(2) At presentation, patients with sarcomas frequently have
leading cancers affecting men and women of all races are prostate can-
compromised nutritional status.11 Patients with intra-
cer and breast cancer, respectively.
abdominal solid tumors were significantly more malnour-
A. Adults—Cancer types more likely to result in nutritional alterations ished than patients with leukemia or extra-abdominal solid
1. There is a relation between malnutrition/weight loss and tumor tumors at diagnosis.12
type.2 Generally, malnutrition is more prevalent in patients with (3) Nutritional status may be related to the length of time until
cancer of the proximal gastrointestinal (GI) tract.3 diagnosis. Patients with prolonged time to diagnosis may
2. Patients with pancreatic or gastric cancer had the highest preva- experience more nutritional compromise.
lence of weight loss (83%–87%).4 (4) Patients with acute lymphoblastic leukemia (ALL), high-
3. Patients with non-Hodgkin’s lymphoma with less favorable out- risk malignant disease, or various solid tumors had doc-
comes, colon cancer, prostate cancer, and lung cancer had a 48% umented increases in catabolism prior to therapy, with
to 61% prevalence of weight loss.4 protein breakdown significantly greater than protein syn-
4. Weight loss occurs in 43% to 61% of patients with lung cancer, thesis.13
depending on the stage of the disease.5 b) After therapy
5. Patients with subtypes of non-Hodgkin’s lymphomas with more (1) The frequency, intensity, and type of chemotherapy regi-
favorable outcomes, breast cancer, acute non-lymphocytic leu- mens may affect nutritional status. Patients with soft-tissue
kemia, and sarcomas had the lowest prevalence of weight loss sarcomas and osteosarcomas had greater decreases in
(31%–41%) in this study.4 weight-for-height compared to patients with other types of
B. Pediatrics cancer, which may be attributed to aggressive and frequent
1. Cancer among children ages 0 to 19 years chemotherapy.11 Steroid use in the treatment of other
a) The most common childhood cancers are leukemias, fol- cancers (eg, ALL) may have prevented this decrease
lowed by cancer of the central nervous system, lymphomas, in weight-for-height. However, height-for-age Z scores
and reticuloendothelial neoplasms for all races. decreased after therapy in patients with ALL, with a corre-
b) Leukemias are more common among 1- to 4-year-olds, whereas sponding decrease in lean body mass and increase in body
lymphomas are more common among 15- to 19-year-olds. fat.14 Survivors of ALL were shown to have decreased

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 S E C T I O N I I Immune Driven Conditions

height-for-age standard deviation scores during treatment (2) Mucositis, a result of the effect of cancer therapy on rapidly
and up to 20 years postdiagnosis, while their body mass dividing cells, can occur along the GI tract but occurs more
index (BMI) standard deviation significantly increased dur- often in the mouth. Mucositis often occurs 5 to 7 days after
ing the period from diagnosis to final height.15,16 This ten- chemotherapy and generally persists with bone marrow
dency toward overweight in ALL survivors may be related suppression from the treatment. Clinical manifestations
in part to decreases in physical activity.16–18 include erythema, dryness, ulcers, bleeding, and pain. It is
(2) There are inconsistent results regarding metabolic rate estimated to occur in 40% of cancer patients, and the inci-
before and after chemotherapy in patients with ALL.19–22 dence is the highest in bone marrow transplant patients.30
The difference in results may be related to the tumor burden (3) Radiotherapy has direct short- and long-term effects on
prior to chemotherapy.20 ALL patients with a greater tumor olfactory and secretory function, the digestive tract, and the
burden had higher resting energy expenditures than those mucous membranes. Long-term bone, dental, olfactory,
with lower tumor burden initially. This difference disap- secretory, and digestive sequelae can lead to reduced food
peared after 1 to 2 weeks of chemotherapy, because the rest- intake and/or malabsorption of nutrients.3
ing energy expenditure decreased in the group that had a c) Operative therapy may result in altered intake. Surgery of the
high tumor burden.20 head and neck may result in dysphagia. Pre- and postoperative
(3) Patients with cancers of the central nervous system tend nil per os and restrictive diets such as clear liquids further affect
to require enteral nutrition or parenteral nutrition (PN) for nutrient intake.
greater lengths of time than do lymphoma, leukemia, and d) Biotherapy is associated with decreased appetite and fatigue.30
bone marrow transplant patients (but not patients with solid Biotherapy, also known as biologic therapy or immunotherapy,
tumors), likely owing to the effect of the disease on neuro- is intended to strengthen the immune system’s ability to recog-
logical processes involved with eating.23 nize and attack cancer cells. Biotherapy is a diverse group
of therapeutic strategies for cancer and includes immuno-
therapy, agents that inhibit angiogenesis or invasion, growth
II. Nutritional Alterations in Patients With Cancer factor modulation, and small molecules (inhibitors of signal
Cachexia comes from the Greek words kakos hexos, which literally transduction).31 Although some of these treatments stimulate
means “bad condition of the body.” It is estimated to affect more than immune reactions against cancer cells, they sometimes inter-
80% of patients with advanced malignant disease. It is defined as a state fere with immunity against infections. People who receive bio-
of malnutrition characterized by anorexia, weight loss, muscle wasting, logical therapies may be at risk for immunosuppression and
asthenia, depression, chronic nausea, and anemia and results in psycho- neutropenia.32
logical distress, changes in body composition, and alterations in carbo- e) Physical obstruction of the GI tract (stomach, small intestine,
hydrate, lipid and protein metabolism.24,25 Alterations may occur in or colon) is generally associated with decreased intake or eme-
tissue water content, in acid-base balance, and in the concentrations of sis after intake. Intestinal obstruction is well recognized in
electrolytes, vitamin or mineral concentrations. These metabolic abnor- patients with progressive advanced gynecological and GI can-
malities may impair nutritional status and contribute to cachexia through cers, especially those with colon cancer or with metastasis from
the depletion of fat, protein, water, and mineral stores.26 The degree of ovarian cancer.33,34
cachexia is inversely correlated with the survival time of the patient, and f) Dysphagia, especially due to head and neck cancer, leads to
it implies a poor prognosis.27 significant weight loss even in the presence of reported nor-
A. Weight loss and cachexia mal appetite.35
1. Altered intake g) Depression, feelings of overwhelming sadness, and the fear and
a) Anorexia or the loss of appetite and early satiety is present in anxiety that accompany a diagnosis of cancer may lead to
up to one half of newly diagnosed cancer patients.4,28 Anorexia decreased intake. In the Psychosocial Collaborative Oncology
results in decreased food intake and weight loss and may lead Group Study, in which 215 adults with various types of cancers
to the development of malnutrition. Symptoms that interfere were studied, 47% of the subjects had a clinically apparent
with food intake and are likely to be related to anorexia include psychological disorder. Two thirds had either reactive anxiety
early satiety, taste alterations, smell alterations, meat aversion, or depressed mood, and 13% had major depression.36 Depres-
and nausea/vomiting.29 The pathogenesis of cancer anorexia is sion has been associated more commonly with pancreatic
multifactorial and is associated with disturbances of the central cancer than with most other cancers.37
physiological mechanisms controlling food intake. Several fac- 2. Energy expenditure
tors that appear to play key roles in the development of cancer a) Tremendous variability in resting energy expenditure measure-
anorexia include hormones (leptin), neuropeptides (neuro- ments has been reported in malnourished patients with cancer,
peptide Y), cytokines (interleukin-1 and -6, tumor necrosis fac- ranging from hypometabolism to hypermetabolism.38
tor [TNF]), and neurotransmitters (serotonin and dopamine).29 b) Elevated resting energy expenditure was reported in pancreatic
b) Cancer treatment modalities, such as chemotherapy and radio- and lung cancer patients and unchanged in patients with gastric
therapy, may cause nausea, vomiting, diarrhea, mucositis, and and colorectal cancer.28,39
taste alterations. These side effects ultimately may decrease c) Hypermetabolism and weight loss are significant predictors of
food intake and cause learned food aversions. decreased survival.38
(1) Nausea and vomiting are the most feared side effects of d) In a group of almost 300 patients with various types of cancer,
cancer treatment. Acute nausea and vomiting occurs dur- about one half had elevated resting energy expenditures. The
ing the first 24 hours after treatment. Highly emetogenic increase in energy expenditure was not associated with a dif-
chemotherapy, such as cisplatin and cyclophosphamide, ferent dietary intake compared to normometabolic patients.40
may cause nausea and vomiting after 24 hours.30 Feedback regulation of dietary intake in relation to energy

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S E C T I O N I I Immune Driven Conditions

expenditure is frequently lost in patients with cancer, so that ated with cancer cachexia. Cytokines are a diverse group of sol-
hypermetabolism is not compensated for by an increase in uble glycoproteins and low–molecular weight peptides that
spontaneous food intake as it is in normometabolism.38,40 mediate interactions between cells and regulate cell and tissue
3. Decreased absorption41 functions.46 In relation to cancer cachexia, they modulate gas-
a) Treatment modalities, such as surgery, chemotherapy, and tric motility and emptying, either in the GI tract or via the brain,
radiotherapy, may result in malabsorption. by altering efferent signals that regulate satiety.47 Although ele-
(1) Operative therapy may result in intestinal ileus and stasis of vated levels of numerous cytokines were found in the blood and
bowel contents, which adversely affects absorption. Pan- urine of cancer patients, the absence of clinically detectable
creatic resection may be associated with malabsorption of cytokine levels does not exclude the idea that cytokines play a
fat and protein. Gastric resection may lead to dumping syn- role in systemic effects.46,48
drome. Large segment resection of the small bowel or colon (1) TNF was one of the first cytokines thought to play a role
may affect absorption of nutrients, fluid, and electrolytes in cancer cachexia. Early studies found that mice with
and sometimes results in long-term PN dependency. tumors producing TNF also developed cachexia and that
(2) Chemotherapeutic agents often cause severe GI symp- weight loss was reversed with TNF-neutralizing anti-
toms, such as mucositis and diarrhea, which may result in bodies.46,49 TNF also suppresses lipoprotein lipase activ-
malabsorption. ity in adipocytes.50
(3) Radiotherapy causes both acute and delayed reactions that (2) Interleukin-1 (IL-1) is associated with the initiation of
affect intestinal absorption. Acute reactions usually occur anorexia by blocking neuropeptide Y (NPY)–induced
within days to weeks of therapy and include enteritis, feeding.47,51
diarrhea, and decreased production of saliva with con- (3) TNF and IL-1 may increase the levels of corticotropin-
sequently reduced enzymes. Late reactions to radiation releasing hormone, which is a central nervous system neu-
therapy include persistent mucosal inflammation, intes- rotransmitter that suppresses food intake and the release of
tinal fibrosis, and stricture.42 glucose-sensitive neurons and ultimately decreases food
b) Tumor involvement of the GI tract may result in mechanical intake.47,52,53
obstruction, with decreased absorption and diarrhea. Serosal (4) Interleukin-6 (IL-6) and leukemia inhibitor factor (LIF)
involvement of the bowel may cause functional malabsorp- are produced by some cancers and may contribute to
tion, pseudo-obstruction, or intestinal ileus, precluding opti- cachexia.46,50,54 Ciliary neurotropic factor, which is a mem-
mal absorption. ber of the family of cytokines that includes IL-6 and LIF, is
c) Stasis of bowel contents from partial or complete intestinal
expressed in skeletal muscle and induces potent cachectic
obstruction may lead to bacterial overgrowth and interfere
effects and acute-phase proteins in tumor-bearing mice.47,50,55
with absorption of nutrients.
(5) Interferon (IFN)-γ may be involved in cancer cachexia. In
4. Changes in the immune system
animals, the provision of antibodies against IFN-γ reversed
a) It is now established that nutritional deficiency is commonly
the wasting syndrome, which clarified that there was an
associated with impaired immune responses, particularly cell-
endogenous production of IFN-γ.47,56
mediated immunity, phagocyte function, cytokine production,
(6) Lipid-mobilizing factor induces lipolysis and correlates
secretory antibody response, antibody affinity, and the comple-
with weight loss.57
ment system.43 Nutritional deprivation, such as protein energy
(7) Proteolysis-inducing factor induces protein degradation in
malnutrition, often causes immunodeficiency, leading to
increased frequency and severity of infection and an increased skeletal muscle by upregulating the ubiquitin-proteasome
incidence of common infections affecting the upper and lower proteolytic pathway and by decreasing protein synthe-
respiratory, urinary, and genital tracts.44 In a study that exam- sis.28,58 This factor also may increase cytokines and acute-
ined the relationship between nutritional status as indicated by phase proteins.28,59,60
the presence or absence of the cutaneous delayed hypersensi- b) Leptin, neuropeptides, and uncoupling proteins
tivity response and treatment-related morbidity, disease recur- (1) Leptin acts to control food intake and energy expenditure
rence, and survival at 2 years in 67 head and neck patients, via neuropeptideric effector molecules within the hypothal-
survival was improved in patients whose cell-mediated immu- amus.61 TNF, IL-1, and LIF increase plasma levels of lep-
nity was preserved compared with those who were anergic at tin, despite a decrease in food intake that would normally
completion of treatment. Morbidity due to surgical therapy and suppress leptin expression.62–64 Increased leptin levels may
tumor recurrence rates were also higher in the anergic group.35 contribute to anorexia by preventing the normal compensa-
b) Immunodeficiency may result from treatment. Operative tory mechanisms in light of decreased food intake. Results
intervention, radiation therapy, and chemotherapeutic agents on leptin levels are not consistent. Leptin levels were not
all affect cell-mediated immunity, even in well-nourished elevated in tumor-bearing rats and in patients with cancer
subjects.41,45 cachexia.65–67 On the other hand, very low levels of leptin
c) T-cell function is also altered with certain hematologic malig- with high levels of inflammatory cytokines were found in
nancies, whereas humoral (B-cell) immunity is affected in patients with advanced-stage cancer.68
chronic lymphocytic leukemia and multiple myeloma.41 (2) NPY is the most potent feeding-stimulatory peptide acti-
d) Immunoglobulin A deficiency, noted in many malnourished vated by the fall of leptin. NPY is thought to restore normal
patients, may play a role in facilitating bacterial translocation energy balance and body fat stores under conditions of
and absorption of endotoxin into the circulation.41 energy deficit, the signals of which are falling leptin and/or
5. Hormones and cytokines insulin.62
a) Cytokines and other mediators play a major role in the complex (3) Uncoupling protein (UPC) 1, 2, and 3 may be involved in
cascade of biological responses leading to the wasting associ- the control of energy metabolism. They are mitochondr-

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 S E C T I O N I I Immune Driven Conditions

ial membrane proteins that mediate proton leakage and 3. Lipid metabolism
decrease the coupling of respiration to adenosine diphos- a) Patients with cancer cachexia have a profound loss of adipose
phate phosphorylation, resulting in the generation of heat tissue due to an increase in lipolysis and a reduction in lipo-
instead of adenosine triphosphate. UPC 1 is expressed only genesis.28,50,52
in brown adipose tissue, which in adult humans is very b) Cancer patients with weight loss have a higher turnover of
scarce and probably not functional.69 UPC 2 is distributed both glycerol and free fatty acids.28
and expressed in most tissues. UPC 3 is expressed in brown c) Patients with cancer have been shown to have significantly
adipose tissue and skeletal muscle and may be of significant reduced levels of lipoprotein lipase, the enzyme responsible
importance in energy expenditure. Changes in UPC expres- for triglyceride clearance from plasma.50,52
sion may be induced by tumor products of cytokines.28 d) The lipid profile in cancer patients is characterized by
B. Metabolic alterations. Although altered nutrient intake and anorexia decreased high-density lipoproteins, decreased low-density
contribute to cancer cachexia, decreased food intake alone does not lipoproteins, and relatively high serum triglycerides.77,78
entirely account for the weight loss seen in cancer patients.70 This is Hypertriglyceridemia is a consequence of the decreased
evident in studies in which the loss of muscle and adipose tissue pre- lipoprotein lipase activity, which results in a decrease in the
cedes the fall in food intake and the provision of extra calories does plasma clearance of both endogenous and exogenous triglyc-
not result in weight gain.70,71 It is clear that the cachectic cancer erides.52
patient uses nutrients ineffectively and seems unable to adapt to the C. Micronutrient deficiencies. Dietary compounds may affect cancer
malnourished state as normal humans do by conserving lean body development through several mechanisms, including the alteration of
mass.72 carcinogen metabolism, antioxidation, enhancement of differentia-
1. Glucose homeostasis tion and growth inhibition, and immunologic modulation.79
a) There is an elevation in Cori cycle activity in malnourished 1. Vitamins
cancer patients, and this increased activity accounts for a) Vitamin C and Vitamin E act as antioxidants, stimulate the
approximately 300 kcal per day loss of energy.28,73 The immune system, and reduce nitrite, which prevents the for-
demand for glucose carbons by the tumor tissue can increase mation of nitrosamine and nitrosamine compounds known to
demand for glucose production by the liver, especially if glu- induce tumor formation in experimental animals and humans.79
cose cannot be fully oxidized by the tumor tissue itself. The b) Studies on vitamins reveal reduced levels associated with dif-
inability to effectively oxidize glucose may explain why some ferent malignancies. Reduced levels of vitamins and minerals
cancer patients exhibit an increase in Cori cycle activity and were found in the following cancer sites:
elevated glucose production.73 (1) Vitamin A levels in colorectal cancer and esophageal can-
b) Increased lactate levels and production rates in cancer patients cer80,81 and in pretreatment pediatric leukemia and lym-
are due to increased glycolysis and lactate release by the tumor phoma82
tissue and skeletal muscle tissue. Glucose is the main energy (2) Beta-carotene in lung cancer, gastric cancer, pancreatic
source of most solid tumors, and it is highly used by the tumor cancer, oral cancer, and thyroid cancer83–87 and in pediatric
and host, with an associated release of substantial amounts of leukemia, lymphoma, and malignant bone tumors82
lactate. Lactate is then regenerated into glucose by the liver (3) Vitamin E in lung cancer, gastric cancer, pancreatic can-
through the Cori cycle.70 cer, prostate cancer, and gallbladder cancer79,83–85,88 and in
c) Gluconeogenesis is increased to maintain glucose homeostasis pediatric leukemia, lymphoma, malignant bone tumors,
in the cancer patient. Amino acids and glycerol from muscle and central nervous system tumors82
and fat breakdown, respectively, are used as the main substrates (4) Vitamin C in lung cancer, gastric cancer, pancreatic can-
in gluconeogenesis.70 The reduced plasma levels of alanine, cer, esophageal cancer, colon cancer, and prostate can-
glycine, and glutamine seen in cachectic cancer patients may be cer81,83–85,88,89
caused by an increase in their use by the liver for glucose pro- (5) Vitamin D (and calcium) in colon cancer89
duction.74 c) A multivitamin and mineral supplement may be recommended
d) Glucose production, glucose intolerance, and insulin resistance for patients with an inadequate nutrient intake. Further evalua-
often are increased in cancer patients. Glucose use by skeletal tion of vitamin and mineral status may be indicated if deficien-
muscle is reduced due to insulin resistance. The counter regula- cies are suspected, such as in patients with prolonged poor
tory hormones, such as glucocorticoids and glucagons, increase nutrient intake and/or with malabsorption, and repletion may be
and may contribute to insulin resistance.52 warranted.
2. Protein metabolism 2. Trace elements
a) Increased muscle catabolism. Muscle wasting is common in a) Selenium, zinc, manganese, and copper are cofactors for vari-
cancer patients and contributes to the asthenia, or lack of ous antioxidant enzymes such as glutathione peroxidase, RNA
strength, seen in these patients. It is caused by an increase in polymerase, superoxide dismutase, and diamine oxidase.79
protein breakdown and, to a lesser extent, a decrease in protein b) Metabolism of metals, especially zinc, is affected in patients
synthesis.70 with cancer. There is an increase in urinary zinc with a variety
b) Negative nitrogen balance may be present, whole body protein of tumors, such as melanoma, gynecologic malignancies, and
turnover is increased, and amino acid turnover is altered.58,75 lung cancer. Low zinc levels were reported in the serum and tis-
c) Decreased muscle protein synthesis and increased liver and sues of cervical cancer patients90 and in patients with prostate
tumor protein synthesis occur. There is a shift from normal cancer and breast cancer,88,91,92 as well as in pediatric patients
muscle protein and other tissue protein synthesis to increased with leukemia, lymphoma, malignant bone tumors, and tumors
hepatic protein synthesis, which is reprioritized with an of the central nervous system.82 Zinc is released during protein
increased production of acute-phase proteins.50,58,76 catabolism bound to amino acids and may pass the glomerular

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S E C T I O N I I Immune Driven Conditions

membrane.80 Zinc deficiency may occur if nutrient intake is ical score of the completed PG-SGA can guide the nutrition
poor or GI losses are great. intervention pathway and assist in determining effective
c) Copper functions as a cofactor in metabolic substrate path- strategies, such as patient education, symptom management,
ways and nucleic acid synthesis. Levels may be low second- aggressive oral nutrition, and enteral/parenteral support. An
ary to chronic decreased intake and absorption. observational study of cancer patients demonstrated that the
d) Selenium deficiency has been reported in cancer patients, par- scored PG-SGA is a simple, valid, and reliable assessment
ticularly those who are chronically malnourished or dependent tool.100 The scored PG-SGA was adopted by the Oncology
on home nutrition support. Low serum and tissue selenium lev- Nutrition Dietetic Practice Group of the American Dietetic
els were reported in patients with cervical cancer.90 Reduced Association as the standard for nutrition assessment of cancer
levels of serum selenium were found in patients with hepato- patients.
cellular carcinoma and breast cancer.91–93 2. History and medication use
e) Selenium deficiency is common among newly diagnosed pedi- a) A detailed nutritional focused history should supplement other
atric cancer patients, even in the absence of malnutrition.94 parts of the nutritional evaluation. In cancer patients, a focused
f) Low serum, biliary, and tissue concentrations of selenium and history should evaluate for any impediments to food intake and
zinc were reported in patients with carcinoma of the gallblad- tolerance, including previous medical conditions or surgeries,
der as compared to patients with cholelithiasis.79 taste alterations and food aversions, complementary and alter-
g) The copper-to-zinc ratio was demonstrated to be useful as a native therapies (including supplements, herbs, and botanicals),
diagnostic tool in GI, lung, and gallbladder cancer and may rigid or restrictive dietary habits, food allergies, and oral or den-
contribute to an early diagnosis of these cancers.79,95,96 tal disease. Family members and significant others may provide
D. Electrolyte disturbances useful information in the assessment.
1. Hypercalcemia, hyperphosphatemia, hypocalcemia, and hyper- b) A history should be used to assess the impact that a medical
kalemia are associated with tumor lysis syndrome (TLS).97 TLS condition, medication, and/or modified diet may have on nutri-
frequently occurs in patients with lymphoma and is defined as the tional care during treatment. If a patient has difficulty eating
metabolic derangements produced by rapid tumor breakdown, during cancer treatment, it may be appropriate to liberalize or
which can occur either spontaneously from rapid tumor growth discontinue a previously prescribed diet. A history of GI sur-
followed by spontaneous tumor cell death or as a consequence of gery might necessitate an adjustment in a patient’s dietary pat-
therapy. It is characterized by hyperuricemia due to DNA break- tern or consideration for nutrition support.
down, hyperkalemia related to cytosol breakdown, hyperphos- 3. Physical examination and functional assessment. A physical
phatemia due to protein breakdown, and hypocalcemia secondary examination and functional evaluation are incorporated in the
to the hyperphosphatemia. As phosphate levels rise, serum calcium PG-SGA.
decreases.97 a) Body weight is the most basic anthropometric measure. Body
2. Hypocalcemia, hypomagnesemia, and hypophosphatemia are weight evaluation provides a simple, dependable, and proven
often observed in association with the use of platinum-containing measure of nutritional risk. More than 45% of hospitalized
therapy, and hyponatremia often accompanies treatment with adult cancer patients have been identified as having significant
cyclophosphamide and vincristine.97 (>10%) weight loss (from usual weight).101 Unlike people expe-
riencing starvation who lose fat while lean body mass is pre-
served, cancer patients lose both fat and lean body mass.28
III. Nutritional Assessment of Patients With Cancer Percent body weight loss from usual weight correlates with
A. Adults complications and mortality.102 Multiple factors (eg, ___location
1. Screening and stage of tumor, cancer treatment) affect weight status.102
a) Early assessment of nutritional risk and serial reassessments Since weight loss may be masked by altered fluids (eg, edema,
throughout a cancer patient’s course are necessary to ensure that ascites), hydration status should be taken into consideration.
interventions are timely and effective.98 The focus of nutritional Timely intervention for weight loss is essential, since weight
assessments varies depending on a patient’s situation and loss may be stabilized or reversed in some cancer patients if
needs. quickly identified.98 When body weight is being evaluated, a
b) The Patient-Generated Subjective Global Assessment (PG- comparison should be made to usual or normal weight, not a
SGA), a modification of the Subjective Global Assessment, is reference standard. Accurate body weight may be needed to cal-
an outcome-based assessment tool developed specifically for culate a treatment dose.
cancer patients (see Figure 11-1). It is applicable in varied b) The physical examination should evaluate for muscle wasting
health care settings and can be used to identify and prioritize and edema or ascites. A decrease in protein and fat stores and
nutritional risk and capture short-term changes in nutritional an associated increase in extracellular fluid accounts for the
status.98,99 The PG-SGA is formatted so that components of the changes in body composition observed in cancer patients.41
medical history can be completed first by the patient using a Peripheral edema suggests increased extracellular fluid or
check-box format. This segment includes four sections: short- decreased visceral protein stores.41 Temporal wasting is a
term weight status, food intake change, nutrition impact symp- hallmark of cachexia that is seen in patients with depleted
toms, and functional capacity. A three-part physical assessment lean body mass. However, muscle mass in cachectic cancer
section evaluating metabolic demand of underlying disease and patients may be underestimated, limiting the usefulness of
degree of metabolic stress, and a subjective evaluation of fat this measurement.41 While muscle wasting is apparent in
stores, muscle status, and fluid status, are then completed by the cachectic patients, it may be more subtle in obese patients.
clinician. In addition to a global rating of nourishment status, c) A functional assessment should determine a patient’s ability
the scored PG-SGA incorporates a numerical score. The numer- to perform activities of daily living. This evaluation should

154 A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. © 2005 A.S.P.E.N. www.nutritioncare.org.
 S E C T I O N I I Immune Driven Conditions

FIGURE 11-1.

Scored Patient-Generated Subjective Patient ID Information

Global Assessment (PG-SGA)

History (Boxes 1-4 are designed to be completed by the patient.)
1. Weight (See Worksheet 1) 2. Food Intake: As compared to my normal intake, I would
rate my food intake during the past month as:
In summary of my current and recent weight: unchanged (0)
more than usual (0)
I currently weigh about _______ pounds less than usual (1)
I am about _________ feet _________ tall I am now taking:
normal food but less than normal amount (1)
One month ago I weighed about _________ pounds little solid food (2)
Six months ago I weighed about _________ pounds only liquids (3)
only nutritonal supplements (3)
During the past two weeks my weight has: very little of anything (4)
decreased (1) not changed (0) increased (0) only tube feedings or only nutrition by vein (0)
Box 1 Box 2
3. Symptoms: I have had the following problems that have kept 4. Activities and Function: Over the past month, I
me from eating enough during the past two weeks (check all would generally rate my activity as:
that apply): normal with no limitations (0)
no problems eating (0)
not my normal self, but able to be up and
no appetite, just did not feel like eating (3)
about with fairly normal activities (1)
nausea (1) vomiting (3)
constipation (1) diarrhea (3) not feeling up to most things, but in bed or chair
mouth sores (2) dry mouth (1) less than half the day (2)
things taste funny or have no taste (1) smells bother me (1) able to do little activity and spend most
problems swallowing (2) feel full quickly(1) of the day in bed or chair (3)
pain; where? (3)________________ pretty much bedridden, rarely out of bed(3)
other** (1) ______________________________________________ Box 4
** Examples: depression, money, or dental problems
Additive Score of the Boxes 1-4
Box 3 A
The remainder of this form will be completed by your doctor, nurse, or therapist. Thank you.
5. Disease and its relation to nutritional requirements ( See Worksheet 2)
All relevant diagnoses (specify) _______________________________________________________
Primary disease stage (circle if known or appropriate) I II III IV Other _________________
Age ________ Numerical score from Worksheet 2 B
6. Metabolic Demand (See Worksheet 3)
Numerical score from Worksheet 3 C

Numerical score from Worksheet 4 D

7. Physical (See Worksheet 4)

Global Assessment (See Worksheet 5) Total PG-SGA score

Well-nourished or anabolic (SGA-A)
(Total numerical score of A+B+C+D above)
Moderate or suspected malnutrition (SGA-B)
Severely malnourished (SGA-C) (See triage recommendations below)

Clinician Signature ___________________________ RD RN PA MD DO Other ___ Date _______

Nutritional Triage Recommendations: Additive score is used to define specific nutritional interventions including patient &
family education, symptom management including pharmacologic intervention, and appropriate nutrient intervention
(food, nutritional supplements, enteral, or parenteral triage). First line nutrition intervention includes optimal symptom management.
0-1 No intervention required at this time. Re-assessment on routine and regular basis during treatment.
2-3 Patient & family education by dietitian, nurse, or other clinician with pharmacologic intervention as indicated by symptom
survey (Box 3) and laboratory values as appropriate.
4-8 Requires intervention by dietitian, in conjunction with nurse or physician as indicated by symptoms survey (Box 3).
>9 Indicates a critical need for improved symptom management and/or nutrient intervention options.

© FD Ottery, 2001 email: [email protected] or [email protected] Reprinted wtih permission

© 2005 A.S.P.E.N. www.nutritioncare.org. A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. 155
S E C T I O N I I Immune Driven Conditions

FIGURE 11-2.

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determine and then compare preexisting abilities and deficits B. Pediatrics

to those after diagnosis and treatment. The Karnofsky Perfor- 1. Screening
mance Status Scale can classify a patient’s functional impair- a) A PG-SGA for pediatric oncology has yet to be validated.
ment. This scale may be used to compare the effects of varied However, many of the areas covered by the adult PG-SGA
treatments and to assess the prognosis in individual patients. may also be applied to pediatrics, with some additions.
Generally, the lower the Karnofsky score, the poorer the sur- b) These additions include current height-for-age and weight-for-
vival prognosis for cancer patients.103 height or BMI-for-age as well as recent growth trends; food
d) Functional limitations may affect a patient’s ability to pur- intake change; nutrition impact symptoms (nausea, vomiting,
chase, prepare, and eat food without assistance.104 A rehabili- diarrhea, constipation); and functional capacity.
tation therapy referral may be appropriate if the patient has 2. History and medication use
significant deficits. a) A diet history similar to that described for adults should be per-
e) Assessment of muscle function using tests such as grip formed with the child and family. It should also include assess-
strength, respiratory muscle function, and electrical stimula- ment of feeding behavior and skills. In addition, the family’s
tion of specific muscles has effectively detected malnutrition- viewpoints about nutrition and the child’s level of understand-
related changes before biochemical levels fall.105 ing of the importance of nutrition should be assessed. These
f) Pain in cancer patients may be related to physical factors, such factors may have an impact on the child’s motivation to eat
as the disease itself, cancer treatment, or psychological vari- when not feeling well, to try oral nutritional supplements, and
ables.106 Since uncontrolled pain may affect a patient’s appetite to tolerate specialized nutrition support.
and ability to eat, an assessment of pain should be an integral b) A medical history, including medication use, should be used
part of a nutrition assessment of cancer patients. when establishing the nutrition care plan and interpretating
4. Biochemical and laboratory tests nutrition laboratory tests. Numerous medications often needed
a) A measure of visceral proteins is used to judge protein status during disease and treatment, including antibiotics and diuret-
and effectiveness of nutritional repletion. Although serum ics, can alter vitamin, mineral, and electrolyte status. Certain
albumin is commonly used to evaluate nutritional status, its medications may have greater nutritional impact in children.
ability to reflect nutritional status is questionable, however For example, glucocorticoids, which are often used chroni-
it is considered predictive of morbidity and mortality. Pre- cally in leukemia and lymphoma treatment, interfere with bone
albumin, with its shorter half-life, provides a better indication metabolism, causing decreased bone mineral density.111 Sup-
of nutritional status and nutritional recovery during nutri- plementation with calcium and vitamin D has been shown to
tional support, and also serves as a prognostic indicator of significantly reduce the effects of corticosteroids on bone min-
outcome.107 eral density in adults,112 and supplementation with calcium and
b) A low albumin, and to a lesser extent a lowered prealbumin, vitamin D should be seriously considered in children receiving
may reflect poor nutrition but may also indicate infection, over chronic steroids to ensure appropriate bone mineral accretion
hydration, and decreased synthesis due to cytotoxic agents.107 during childhood. However, recommended doses of calcium
c) Laboratory tests to identify micronutrient deficiencies may and vitamin D in children receiving steroids are not clear, so
be appropriate in limited circumstances when other areas of children who are taking calcium and vitamin D supplements
assessment suggest deficits. should be closely monitored for the development of hyper-
d) Objective parameters, such as anthropometrics and biochemi- calcemia and hypercalciuria.
cal and immunological measures, support other aspects of the 3. Physical examination and functional assessment
nutritional assessment. However, their validity and predictive a) Anthropometrics
capability as sole measures have been questioned since non- (1) Weight and height are essential tools in assessing acute and
nutritional factors may skew results. chronic nutritional status and changes in nutritional status
5. Quality of life (QOL) in children. Height-for-age is a measure of chronic or long-
a) Disease- and treatment-related symptoms affect a cancer term nutrition in children. Weight-for-height or BMI-for-
patient’s ability to eat and, therefore, are important aspects of a age can be used to assess acute or recent nutritional status.
patient’s QOL. A patient’s willingness to eat also can be neg- The criteria for poor growth or malnutrition in children have
atively affected by financial constraints, depressed psycho- included any of the following: weight-for-height or height-
logical state, and poor attitude. Ultimately, disinterest in eating for-age that is 2 standard deviations below the mean for sex
can lead to social isolation and conflict with caregivers and and age113; the downward crossing of more than 2 major
friends. percentile markings on the National Center for Health Sta-
b) Weakness and fatigue, resulting from poor nutritional status and tistics (NCHS) growth charts from a child’s established
treatment side effects, may limit a patient’s ability to work and growth curve114; or the stages of acute and chronic mal-
carry out activities of daily living, thereby compromising nutrition described by the Waterlow criteria.115 The valid-
QOL.108 ity of specific cutoffs based on the 2000 NCHS pediatric
c) A patient’s well-being is composed of a physical component BMI-for-age data as a screen for underweight has yet to be
and a spiritual, psychological, and emotional component; both assessed. However, the World Health Organization defines
components are crucial to a patient’s QOL and should be BMI below the 5th percentile as an indication of under-
addressed in assessment.106,109 weight.113 Meeting any of these criteria indicates the need
d) In a study of patients with head and neck cancer receiving for nutrition assessment. Keep in mind that serial measure-
radiation treatment, individualized nutrition counseling for ments of growth over time provide much more information
symptom management not only improved nutrient intake but regarding the individual’s nutritional status than a single
positively influenced QOL.110 point on the growth chart. A patient who has a decrease in

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S E C T I O N I I Immune Driven Conditions

height-for-age or weight-for-age or BMI-for-age from the protein consumption. The liver may not be able to synthe-
patient’s established curve can cause greater concern (even size albumin at a rate that surpasses loss. Knowledge of
if the patient’s current point is above the 10th percentile) the patient’s hydration status is also important for accurate
than a child who is below the 5th percentile but following interpretation of body weight. Pain assessment is included
his or her established curve. Overweight and its comor- in the physical evaluation as a factor that may reduce a
bidities can also be problematic in children with cancer. child’s appetite or capacity to eat.
BMI-for-age is used to classify adolescents as at risk for (4) Functional assessment should determine the patient’s abil-
overweight if between the 85th and 95th percentile and as ity to perform activities of daily living as compared to pre-
overweight if at the 95th percentile or greater.116,117 treatment capacity as well as to developmental stage.
Recommendations for appropriate nutrition intervention Having enough strength and energy to play is important
as well as referral for additional medical workup have psychosocially in children and should be considered as part
been described for healthy children over 2 years of age of the functional assessment.
with elevated BMIs based on their age and their BMI- 4. Biochemical and laboratory tests
for-age percentile.116,117 These recommendations can be a) As in adults, serum albumin and prealbumin122 can be useful
applied to cancer survivors. However, weight mainte- tools to assess the visceral protein status of children. A Pre-
nance and weight loss recommendations for patients albumin in Nutritional Care Consensus Group123 developed the
currently battling cancer are not appropriate except in following levels of nutritional risk based on prealbumin levels:
extreme cases, as the patient is likely to experience unin- Less than 5 mg/dL indicates a poor prognosis; 5.0 to 10.9 mg/dL
tentional weight loss. indicates significant risk and calls for aggressive nutrition
(2) When interpreting weight and height, one should bear in support; and 11.0 to 15.0 mg/dL suggests increased risk with
mind that other factors such as tumor size and hydration sta- recommendation for close monitoring. When using this scale,
tus can affect weight. Medication and length and type of bear in mind that each medical institution has its own normal
treatment can affect growth. These factors should be con- standards for laboratory values based on analytical methods
sidered when evaluating growth and determining the cause used, so that the values listed above may not exactly reflect the
of growth delays in children. values in a given institution. In addition to indicating current
b) Body composition nutritional status, prealbumin, with its rapid 2-day turnover rate,
(1) Caliper skinfold and circumference measurements should is useful in early assessment of the effectiveness of nutri-
be used as part of a complete nutritional assessment and tion repletion regimens. A 1 mg/dL increase in prealbumin
can be especially useful in situations where loss of lean per day indicates adequate nutrition support in malnourished
body mass may not be apparent because of overall body patients.123,124 Increasing trends in prealbumin suggest that at
weight maintenance due to edema. Triceps skinfold thick- least 65% of energy and protein needs are being met.123 How-
ness, mid–upper arm circumference, mid–upper arm mus- ever, numerous non nutrition factors may affect interpretations
cle area, and subscapular skinfold thickness are common of both albumin and prealbumin levels. Infection, extremes in
anthropometric measurements. Caliper skinfold measure- hydration, liver synthetic function, protein-losing enteropathies,
ments and circumference measurements can be compared corticosteroid therapy, surgery, and impaired renal function may
to reference tables based on the age and sex of the child to alter albumin and/or prealbumin levels.125
determine relative fat and lean body mass composition.118 b) Absolute neutrophil count is important to monitor, as neutro-
Typically, values less than the 5th percentile for sex and penic patients must be especially careful to avoid food-borne
age are consistent with acute malnutrition.119 A triceps skin- pathogens.
fold thickness greater than the 95th percentile in a child c) Electrolyte and mineral wasting can be due to medications used
with a BMI-for-age above the 85th percentile can confirm in cancer treatment and management or to side effects of can-
that the child’s BMI is elevated due to excessive fat rather cer therapy, such as diarrhea and vomiting. Serum potassium,
than substantial lean body mass or frame size.116 Skinfold magnesium, calcium, and phosphorous levels should be moni-
and circumference measurements can be used to track tored regularly and replaced, if low. Note that total serum cal-
changes in an individual patient over time when collected cium and magnesium levels underestimate true status when
serially (every 3–6 months). The methodology for per- albumin is low. Serum ionized calcium and magnesium levels
forming anthropometrics is described elsewhere.120 more accurately reflect true calcium and magnesium status
(2) Bioelectrical impedance analysis can be used in older chil- when albumin is decreased.
dren to determine total body composition. This is a quick, d) Glucose and lipids may be elevated with some commonly
noninvasive tool and also can be used to track changes over used medications, such as corticosteroids, and should be mon-
time. However, factors such as fluid status may affect the itored regularly.
validity of results. This tool has been validated in well- 5. QOL
nourished and malnourished children.121 a) A poor QOL can affect a patient’s nutritional status. Children
(3) A physical exam should involve assessment of muscle or may be physically and socially isolated due to infection or risk
fat depletion, fluid status, gastrointestinal symptoms, and of infection. Long-term isolation may cause them to become
pain. Edema may manifest as a clinical symptom of hypo- bored, anxious, and depressed, leading to poor intake. Recre-
albuminemia, in which case aggressive protein repletion ation therapists, psychiatrists/psychologists, and spiritual advi-
measures are often indicated. In some cases, severe hypo- sors can be consulted to help in these situations.
albuminemia is due to protein losses via gut or capillary b) Conversely, poor nutrition may lead to a poor QOL. Under-
leakage, and increases in visceral protein levels may be nourished patients are likely to feel fatigued and weak, which
limited by the rate of synthesis by the liver rather than by can affect their ability to play and enjoy life.

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c) Poor intake by the child may also affect the parent’s QOL. Par- c) Changes in taste
ents often equate good eating with good health, so poor intake d) Dry mouth
can cause them much distress. e) Fatigue
d) QOL is an important issue to be assessed periodically as chil- f) Endocrinological effects (adverse endocrinological effects of
dren undergo therapy or to evaluate when assessing the effec- cranial radiation have been reviewed)141–143
tiveness of a palliative treatment in children who are at the end 3. Nutritional considerations for immunotherapy
of life, but QOL is difficult to measure in children.126 First, chil- a) Nausea, vomiting
dren pass through numerous developmental stages of physical, b) Mucositis
emotional, cognitive, and social functioning, meaning that no c) Diarrhea
single measure can appropriately assess children of all ages.127 d) Changes in taste
Assessment tools must consider the developmental stage of the e) Dry mouth
child being evaluated in terms of the child’s ability to use the 4. Nutritional considerations for surgery
tool (Likert scale vs yes/no options) as well as the tool’s ability a) One week before an operative procedure, patients should stop
to address the factors that may affect the child’s QOL (fear of all herbal products or supplements (eg, borage or fish oil, vita-
pain vs concern about appearance).126 Longitudinal assess- min E) that may affect blood thinning, unless otherwise advised
ment of children may require use of different tools as they by their physician.144
develop. Second, a proxy respondent is necessary for assess- b) Nutritional considerations vary depending on type and degree
ment of very young children who are unable to express their of surgical intervention. Potential issues depend on the patient’s
feelings in the structured manner of an assessment tool. mechanical and physical impairment and ability to ingest,
However, proxy respondents may not accurately represent digest, and absorb adequate nutrients.
the child’s perceptions or priorities. In a systematic review c) The patient’s perioperative and long-term nutritional needs
of studies examining proxy reports of QOL, children with should be taken into account and planned for from the onset.
chronic illness and their parents were found to have good B. Adults
agreement for domains reflecting physical activity, physical 1. Criteria for intervention145
symptoms, and somatic distress but poor agreement for a) Preoperative tube-feeding or PN support provided for at least 7
domains reflecting social and emotional issues.128 Parents to 14 days preoperatively may benefit moderately and severely
have been found to rate their children’s functioning in certain malnourished cancer patients, but the potential benefits of nutri-
categories and overall QOL as lower than the children’s rat- tion support should be appraised against the inherent risks of
ings, possibly due to differences in perception of the situa- nutrition support and the delay in surgery.
tion.128,129 For example, parents may be considering long-term b) Specialized nutrition support should not be used routinely in
outcomes such as future fertility or compromised education, well-nourished or mildly malnourished patients receiving sur-
while a young child may be concerned with immediate con- gery, chemotherapy, or radiation therapy when reasonable oral
sequences, such as missing friends.129 This is not to say, how- intake is anticipated.
ever, that parental concerns are not important. c) Specialized nutrition support is indicated in selected patients
e) Specific QOL assessment tools for use during cancer therapy who are receiving cancer treatment and who are either severely
in children include the Miami Pediatric Quality of Life Ques- malnourished or unable to consume and/or absorb an adequate
tionnaire,130 the Pediatric Oncology Quality of Life Scale,131 oral diet for an extended period of time.
and the Behavioral, Affective, and Somatic Experiences d) Palliative specialized nutrition support is seldom indicated in
Scale.132 A common modular instrument (which combines patients with terminal cancer that is unresponsive to conven-
generic as well as disease-specific scales) is the Pediatric Qual- tional therapy.
ity of Life Inventory.133 Tools used to assess QOL of childhood 2. Goals
cancer survivors include the Minneapolis-Manchester Quality a) Maintenance of nutritional status or reversal of protein-calorie
of Life Instruments for both youth and adolescents.134,135 Other malnutrition
tools have also been used to measure the QOL of pediatric (1) The caloric needs of cancer patients depend on the tumor
cancer patients after treatment.136–140 type and other medical factors such as fever or infection.
Caloric needs are not static and can vary with medical
changes throughout the treatment course.
IV. Criteria for Intervention and Goals of Therapy
(2) Nutrition support should provide calories sufficient to meet
A. Nutritional considerations for specific cancer treatments a cancer patient’s needs by minimizing body catabolism
1. Nutritional considerations for chemotherapy without overfeeding. A variety of empiric formulas are
a) Nausea and vomiting available to estimate energy needs. See Chapter 2. How-
b) Mucositis ever, ongoing monitoring is essential to ensure that the
c) Constipation caloric estimate is appropriate. Providing most cancer
d) Diarrhea patients with 25 to 35 kcal/kg per day is a reasonable esti-
e) Neutropenia mate.106 Although not routine and felt by some to be con-
f) Changes in taste troversial, the use of indirect calorimetry to measure resting
g) Loss of appetite energy expenditure in the clinical setting may be of value.
2. Nutritional considerations for radiation therapy (3) A cancer patient’s degree of catabolism will dictate protein
a) Mucositis requirements. Generally, an intake of 1.2 to 1.5 g/kg/d pro-
b) Diarrhea, nausea, vomiting if the GI tract is in the radiation tein is adequate,106 although hypermetabolic or extremely
field wasted patients may have higher requirements.

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S E C T I O N I I Immune Driven Conditions

(4) Although visceral proteins are influenced by non nutritional in pediatric ALL.161,162 Conversely, patients with pediatric
factors, monitoring them may provide an indication of a lymphoma and solid tumor with localized disease and
patient’s protein status, and a nitrogen balance evaluation with good nutritional status at time of referral had signif-
may be appropriate in selected cases. icantly improved likelihood of survival compared to
b) Decreased morbidity, improved survival, and improved QOL patients with poor nutritional status at referral. This sig-
(1) There is no definitive evidence that specialized nutrition nificance did not hold true for patients with regional and
support in cancer patients increases treatment tolerance, metastatic disease.158
decreases treatment complications, or extends survival; (2) Tolerance to treatment and treatment delays varies with
therefore, the effects of nutrition support in this regard type of cancer. Patients with ALL and Wilms’ tumor who
remain controversial.146,147 were malnourished at diagnosis required a reduction in
(2) Provision of nutrition support to selected patients with drug therapy compared to patients who were well nour-
cancer may improve QOL. As expectations of quality vary ished at diagnosis, owing to poor tolerance of drug ther-
with individual patients, decision making requires multi- apy.9,157 Treatments were delayed in significantly more
disciplinary assessment and should be addressed on a patients with Stage IV neuroblastoma who were malnour-
case-by-case basis. ished at diagnosis or who had early decrease in nutritional
(3) Use of home PN in a group of appropriately selected can- status than in patients who were well nourished at diag-
cer patients resulted in improved performance status and nosis or who had early improvement in their nutritional
reported improved QOL (judged as returning to work or status.159
previous activity level).98 (3) Nutritional status may serve as a marker, rather than a
(4) There is no conclusive evidence in humans that feeding cause, of a particular outcome in cancer patients. There is
cancer patients to replete the host will stimulate further insufficient evidence to support the assertion that improve-
tumor growth.148,149 ments in nutritional status will result in improved patient
(5) In head and neck cancer, preexisting poor intake com- outcomes.
monly results from alcohol and nicotine abuse and diffi- b) Indications for nutrition support
culty swallowing due to obstruction from tumor. Multiple (1) Specialized nutrition support and dietary interventions must
treatment modalities—such as surgery, radiation, and be implemented to support normal growth and development
chemotherapy—may be employed and may affect diet tol- and to provide the energy needed in patients who cannot
erance and adequacy of intake. Multiple studies show that meet requirements via oral intake.99
early enteral feeding with percutaneous endoscopic gastros- (2) Palliative specialized nutrition support in terminally ill
tomy (PEG) or surgical jejunostomy before or during children with cancer is rarely indicated.99
cancer treatment can minimize weight loss, dehydration, (3) Newly diagnosed pediatric cancer patients tend to consume
and interruptions in treatment and can limit hospital 90% or less of the recommended dietary allowance for
admissions.147,150–153 Prospective, randomized clinical trials calories but have adequate protein intake.12,163 However,
(PRCTs) have failed to show improved survival in patients disease progression plus side effects from therapy may
receiving parenteral or tube-feeding support with their can- result in decreased oral consumption and the need for nutri-
cer treatment.154 tion support.164
(6) Some nutrients, such as glutamine, arginine, essential fatty (4) A task force formed by the American Academy of Pediatrics
acids, and nucleic acids, were evaluated as having specific developed criteria for nutrition intervention in pediatric
biologic effects on the tumor and the host. The potential cancer patients.8 Andrassy and Chwals165 and Ollenschlager
benefits of these specific nutrients, individually or com- et al166 slightly modified and contributed to the criteria,
bined, in enhancing immune function, lessening the inflam- which include
matory response, and enabling recovery from surgery are (a) Weight loss of more than 5% of preillness body weight
inconclusive.145,151,155 (b) Weight less than 90% of ideal body weight (IBW) or
C. Pediatrics weight-for-height less than 10th percentile on NCHS
1. Criteria for intervention growth curves.167 The NCHS growth chart showing
a) Nutritional status is related to relapse rates and survival as BMI-for-age can be used for older children.
well as to tolerance of treatment in pediatric oncology. This (c) Serum albumin less than 3.2 mg/dL (barring acute
relationship varies based on the type and stage of cancer. metabolic stress within the last 14 days)
(1) The cancer relapse rate has been shown to be increased in (d) Triceps skinfold less than the 5th percentile for age
patients who are malnourished at diagnosis or referral in and sex
ALL156,157 and in solid tumors.158 Five-year disease-free sur- (e) Decrease of weight- and/or height-for-age across 2 per-
vival was significantly greater for patients with ALL who centile increments on the NCHS growth curves
were well nourished compared to patients with ALL who (f) Oral intake less than 70% of that needed for growth for
were malnourished at diagnosis.157 The time to relapse or more than 5 days in well-nourished patients
death was significantly longer in patients with Stage IV (g) Expected GI dysfunction for more than 5 days in well-
neuroblastoma who were well nourished at diagnosis nourished patients
compared to those who were malnourished at diagnosis (h) High risk for malnutrition based on type of tumor and
and received PN.159 However, nutritional status was not cancer therapy
related to survival in these patients, in a group of pediatric (i) Delayed cutaneous hypersensitivity anergy in children
patients in El Salvador and Brazil that included various over 2 years old prior to treatment
types of cancer,159,160 or in two large retrospective studies (5) Oral intake

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 S E C T I O N I I Immune Driven Conditions

(a) Numerous studies show that pediatric cancer patients (h) The beneficial nutritional effects of PN fail to persist
tend to experience significant weight loss and have once PN is discontinued if the patient’s clinical situa-
decreases in arm muscle area and triceps skinfold mea- tion has not improved.173
surements on an oral diet.10,168,169 (i) Comparing results from different studies is difficult
(b) Patients who experienced intervention by a registered because of variability in the type and stage of cancer, the
dietitian while on an oral diet had significantly more type of therapy, the stage of treatment, and nutritional
weeks at a stable weight than did patients who did not status. Furthermore, small sample sizes may prevent
receive intensive nutritional intervention.166 detection of differences between groups.
(c) Counseling must be individualized to the type and 2. Goals
stage of cancer, the degree of disease, symptoms, and a) Growth and/or maintenance of nutritional status or reversal of
the type and stage of treatment. protein-calorie malnutrition
(6) Enteral nutrition support (1) Body weight should be greater than IBW.8
(a) Indications for enteral support in children are similar to (2) Arm fat area should be greater than the 10th percentile for
those in adults. In addition, children who fail to gain age and sex.8
weight should be considered for nutrition support. (3) Serum albumin should be greater than 3.2 mg/dL.8
(b) Studies reveal that pediatric cancer patients significantly (4) Calorie and protein needs vary with age, disease state, type
increase their body weight after 1, 3, and 4 months of of treatment, presence of fever, infection, wound status,
tube feeding.168,170,171 activity level, and individual needs. See Chapter 2 for help
(c) In malnourished cancer patients, 60% of the patients with determining calorie and protein needs.
reached 95% of their IBW in a mean of 4.9 months of (5) Fluid balance is important. See Chapter 2 for help with
tube feeding, and the remaining patients gained at least determining fluid requirements.
7% of their IBW in that time.172 (6) Vitamin and mineral deficiency should be prevented. Mon-
(d) Lack of randomized studies has hampered the ability to itor mineral and electrolyte levels regularly and other vita-
determine the effectiveness of enteral nutrition support mins and minerals when deficiency or toxicity is suspected.
in pediatric cancer patients. For example, vitamin K levels may decrease with long-
(7) PN support term antibiotic therapy, and copper and manganese levels
(a) Indications for PN in children are similar to those in may exceed normal levels when provided in TPN during
adults. cholestasis.180,181
(b) Numerous PRCTs have examined the effectiveness of b) Decreased morbidity, improved survival, and improved QOL
PN at nutritionally repleting pediatric cancer patients (1) Improvement in nutritional status has not clearly been
and improving their clinical outcome. shown to increase the survival or treatment tolerance in
(c) PRCTs in primarily well-nourished cancer patients pediatric oncology patients.
demonstrate that PN given for 17 to 104 days is able to (2) Improvement in nutritional status can theoretically enhance
significantly increase weight and nitrogen balance and QOL by increasing energy level and wound healing and
results in increases in arm muscle area and triceps skin- reducing risk of infection. However, the inconvenience of
fold measurements. In addition, PN promotes mainte- some nutrition interventions (eg, time-consuming tube-
nance of total leukocyte and absolute granulocyte counts feeding regimen that interferes with play time) may out-
compared to those of control groups.169,173,174 weigh the potential benefits. The pros and cons should be
(d) Other PRCTs in primarily well-nourished patients who presented to the child and family, allowing them to make the
were given PN through the first cycle of chemotherapy final decision.
until recovery from myelosuppression showed no dif-
ference in survival rates, tumor response, or duration of
V. Nutritional Management
myelosuppression and actually showed shorter remis-
sion in patients with parenteral nutrition (PN) than in A. Management for specific cancer treatments
controls.174,175 1. Pharmacological
(e) Nonrandomized studies that administered PN for a) Commonly used antiemetics include 182
approximately 4 weeks showed a significant increase (1) Serotonin-receptor antagonists (eg, ondansetron,
from baseline in arm muscle area, triceps skinfold meas- granisetron)
urements, subscapular skinfold measurements, and per- (2) Phenothiazines (eg, promethazine, chlorpromethazine)
centage of diagnosis weight. Serum transferrin, albumin, (3) Antihistamines (eg, diphenhydramine, hydroxyzine)
prealbumin, and retinol-binding protein levels were (4) Benzodiazepines (eg, lorazepam)
increased. In addition, there was a significant decrease (5) Steroids (eg, dexamethasone)
in treatment delays compared to those in nourished (6) Cannabinoids
patients receiving enteral nutrition.10,176–179 b) Prevention/treatment of mucositis182
(f) Overall, PN seems to improve nutritional status but (1) Salt, soda rinse
not clinical outcome. (2) Chlorhexidine
(g) The duration of PN provision necessary to achieve nutri- (3) Mouthwash consisting of diphenhydramine, antacid, and
tional repletion is difficult to predict. Nine to 14 days of lidocaine
PN resulted in a slight weight gain and a significant c) Bowel medications
increase in serum transferrin levels, but only 9 of 15 sub- (1) Stool softeners (docusate)
jects repleted their weight, whereas all but 1 subject (2) Bulk laxatives (psyllium, calcium polycarbophil,
repleted their weight on 28 days of PN.10 methylcellulose)

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(3) Lubricants (mineral oil) (4) Do not force children to eat if they refuse.
(4) Osmotic agents (glycerin, lactulose) h) Dry mouth
(5) Saline laxatives (magnesium salts, sodium biphosphate/ (1) Select sweet or sour foods.
phosphate) (2) Moisten or puree dry foods.
(6) Stimulants (bisacodyl, cascara sagrada, senna) (3) Sip water frequently.
(7) Antidiarrheals (bismuth subsalicylate, difenoxin, kaolin/ i) Fatigue
pectin, loperamide, opium tincture) (1) Consume small, frequent meals.
2. Nutritional (2) Choose high-calorie and protein- and nutrient-dense foods.
a) Nausea and vomiting 3. Complementary and alternative approaches
(1) Consume small, frequent meals or snacks. a) Although gaps still exist, research is growing that indicates
(2) Eat slowly. that complementary and alternative medicine (CAM) thera-
(3) Choose cold, nonodorous foods. pies can be effectively integrated into conventional medicine.
(4) Select light, starchy, low-fat foods. Current evidence indicates that CAM usage is more effective
(5) Avoid very sweet or spicy foods. in relieving cancer-related symptoms than in slowing disease
(6) Save favorite foods for periods without nausea or vomiting. progression.183
(7) Rest and sit up after eating. b) CAM therapies commonly used by cancer patients that can be
(8) Refrain from eating prior to therapies that cause nausea or recommended for use183 include acupuncture for chemotherapy-
vomiting. related nausea and vomiting or for pain, massage (except deep
b) Mucositis tissue or forceful) for anxiety or pain, moderate exercise to min-
(1) Choose bland, cold, soft foods. imize fatigue, psychological and mind-body techniques (eg
(2) Moisten dry foods. support groups, relaxation training, imagery), reduction of ani-
(3) Cut food into small pieces or puree. mal and saturated fat, and addition of soy in the diet of well-
(4) Use a straw with fluids. nourished men with prostate cancer.
(5) Coordinate eating with analgesic use. c) Some CAM therapies should be discouraged in cancer
c) Constipation patients.183 These include very restrictive diets in patients with
(1) Obtain adequate fluid intake. poor nutritional status; antioxidants in patients undergoing radi-
(2) Increase insoluble fiber consumption.
ation or chemotherapy; supplements with anticoagulant effects
(3) Drink hot beverages prior to the usual time of bowel move-
in patients with thrombocytopenia, patients undergoing anti-
ments.
coagulation therapy, and postoperatively; acupuncture in
(4) Incorporate physical activity as permitted by the medical
patients with thrombocytopenia and anticoagulation therapy;
team.
and high-dose vitamin A and vitamin C in all cancer patients.
d) Diarrhea
d) Any CAM therapy should be discouraged if any of the fol-
(1) Consume extra fluid and potassium-rich food sources.
lowing apply:
(2) Increase intake of soluble fiber and reduce insoluble fiber
(1) It delays conventional treatment.
consumption.
(2) It has not been scientifically proven to be efficacious.
(3) Avoid lactose and sugar alcohols.
(3) It is provided by an unlicensed practitioner.
(4) Select low-fat foods.
(5) Consume foods and beverages at room temperature. (4) It requires injection of substances not approved by the US
e) Neutropenia Food and Drug Administration.183
(1) Choose foods less likely to contain a high bacterial load. B. Adults
(a) Wash raw fruits and vegetables well and reject any that 1. Special aspects of diet and nutritional supplements
have indications of damage or spoilage. a) Aggressive strategies to optimize oral intake and tolerance
(b) Avoid unpasteurized products and ripened, soft cheeses. should be instituted early, especially for patients with preexist-
(2) Follow safe handling, storage, thawing, and cooking pro- ing nutritional problems. A patient’s calorie and protein needs
cedures for meat, fish, poultry, and eggs. should be determined, diet strategies and oral supplements
(a) Keep raw meat, fish, and poultry separated from other should be instituted, unnecessary diet restrictions should be
foods to prevent cross-contamination. eliminated, and eating times should be planned to be separated
(b) Store frozen foods at 0°F and refrigerated foods at 35 from treatment sessions.98
to 40°F. b) Physiological and mechanical considerations of the disease
(c) Thaw foods in the refrigerator, in the microwave, or in and/or treatment may necessitate an alteration in the cancer
cold water that is changed every 30 minutes. patient’s diet.184 These considerations include the following:
(d) Cook meat (including deli meats), fish, poultry, and (1) Multiple feedings and postgastrectomy diet after gastric
eggs until well done (160°F). resection
(e) Do not leave perishable foods unrefrigerated for more (2) A soft diet for esophageal strictures
than 2 hours. Dispose of leftovers after 2 to 3 days. (3) A low-fat diet with or without enzyme supplementation
f) Taste changes. Choose flavorful foods as tolerated, such as for improved absorption in patients with pancreatic insuf-
sour, seasoned, and spicy foods. ficiency
g) Loss of appetite (4) Low fiber and lactose for radiation enteritis
(1) Consume small, frequent meals. c) Oral supplements are a valuable addition to the diets of cancer
(2) Save beverages for the end of meals. patients. The use of oral supplements resulted in significantly
(3) Give priority to high-calorie and protein- and nutrient- increased protein and calorie intake without reducing foods con-
dense foods. sumed in a group of cancer patients counseled to use nutrition

162 A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. © 2005 A.S.P.E.N. www.nutritioncare.org.
 S E C T I O N I I Immune Driven Conditions

supplements between meals and at bedtime.185 A limitation of (2) In cachectic cancer patients, given the metabolic alter-
oral supplementation use is taste fatigue; therefore, ongoing ations from advanced or untreated disease, the goal of
evaluation of acceptance is necessary, as are plans to provide nutrition support may be to minimize wasting rather than
varied alternatives for patients with anticipated long-term needs. to nutritionally replete the patient.
d) There is evidence from animal studies that polyunsaturated b) Monitoring (see Chapter 8 for PN monitoring)
fatty acids can promote cell growth by stimulating cell prolif- 4. CAM aspects. Cancer patients may use a variety of CAM thera-
eration and by inhibiting apoptosis. Fish oil, on the other pies in conjunction with or as a substitute for conventional
hand, can reduce the tumor growth rate and decrease host treatment.189 Many cancer patients are motivated to seek CAM
body weight loss in animals. In humans, a small, pilot trial of therapies as a means of self-healing and of maintaining optimism
20 patients with pancreatic cancer was conducted in which when faced with the uncertainty of their disease.190 Patients should
patients were given an eicosapentaenoic acid (EPA)–enriched be questioned about possible use of CAM therapies throughout
supplemented oral diet.186 Cachexia was reversed, and body treatment. Clinicians need to communicate openly and without
weight was increased at 3 and 7 weeks. However, these results judgment so patients feel comfortable disclosing CAM usage.
could not be replicated in a follow-up study of 200 patients with Reputable and up-to-date Web sites and resources are available,
pancreatic cancer, possibly because several patients in the con- so clinicians have access to reliable information describing the
trol group were taking EPA.187 growing number of CAM therapies and detailing some dangerous
e) Cancer patients can benefit from nutrition counseling not only interactions between these therapies and allopathic medicines.
before and during treatment but also later in their course. Can- 5. Ethical issues
cer survivors are interested in making lifestyle changes to a) The goals of nutritional care in the framework of cancer treat-
improve their diet and physical activity level. According to a ment should be discussed with patients and their caregivers
survey, approximately 66% of survivors reported making proactively in an open, straightforward, supportive manner.
lifestyle changes, 40% made one or more dietary changes, 21% Patients should recognize the short- and long-term nutritional
started a new physical activity, and 48% started taking dietary consequences of their treatments. For example, certain GI sur-
supplements.188 geries may necessitate long-term nutrition support or special
f) Information on food safety issues should be incorporated into diet modifications. Radiation treatment may cause lasting
the nutrition education provided to neutropenic patients. mucosal damage that affects diet tolerance. Patients requiring
2. Special aspects of enteral nutrition massive surgery and tube feeding, such as head and neck
a) Indications and goals patients, have unique ethical issues related to disfigurement and
(1) Aggressive nutritional support with enteral nutrition should dysfunction.33,98,191
be considered in selected instances in cancer patients who b) Transitioning a patient from active nutritional care to end-of-
are unable to attain adequate oral intake. Patients with small- life care can present numerous challenges. The provision or
bowel resections and patients with mucosal injury from withdrawal of nutrition support to patients with advanced dis-
chemotherapy or radiation who are unable to ingest and/or ease is an issue that evokes medical, emotional, ethical, and
digest nutrients may benefit from enteral feeding. Critically legal considerations. Ethical decision making should involve
ill cancer patients may also benefit from enteral nutrition.150 the multidisciplinary team, including the patient and caregivers,
(2) The aim of enteral feeding is to meet macronutrient, and should account for patient needs for autonomy, QOL, and
micronutrient, and fluid needs with acceptable GI tolerance. a holistic structure. While there may be facility guidelines to
(3) Cycled and intermittent feedings may be well tolerated, help decision making, ultimately decisions need to be made on
allow patients more mobility, and encourage some oral an individualized, case-by-case basis.191–196
intake. The ultimate goal is to transition to an oral diet as c) Given that cancer patients are interested in CAM therapies, it
soon as the patient is able to attain adequate intake by mouth. is crucial for clinicians to recognize their ethical obligation
b) Monitoring when recommending, allowing, and guiding patients to these
(1) Cancer patients should be monitored for aspiration risk and therapies and modalities. It is necessary to keep in mind the
GI tolerance. Preexisting treatment-related side effects, risk-to-benefit ratio when determining the appropriateness of
such as nausea or diarrhea, may be exacerbated during any therapy, especially when there is limited or no scientific
enteral feeds. In postoperative patients, ileus may preclude evidence to support it.197
tolerance; and in critically ill patients who are receiving 6. Patient and caregiver education
mechanical ventilation, poor perfusion may limit ability to a) Review all drug-nutrient interactions that apply to the patient.
maintain enteral feeds. b) Educate the patient and family about the nutrition side effects
(2) Nasoenteric feeding tubes may be contraindicated in commonly experienced with the cancer therapy being used and
patients with severe thrombocytopenia, significant mucosi- how to maximize calorie and protein intake when the patient
tis, or recent extensive neck resection. faces these side effects.
(3) Immune-suppressed patients should be educated regarding c) Teach the patient and caregivers the principles of the neutro-
careful tube-feeding technique to minimize the risk of feed- penic diet and when it is to be followed.
ing-related infection. d) When implementing specialized nutrition support, help the
3. Special aspects of PN patient and family to understand the reason it is being used,
a) Indications and goals how the nutrients are being delivered, and the risks and ben-
(1) PN is recommended in appropriately chosen cancer patients efits associated with the feeding method.
who need aggressive nutrition support when tube feeding e) Share the known effects of the CAMs being used with the
has been unsuccessful or when use of the GI tract is not patient and family, being sure to emphasize, when appropriate,
appropriate (eg, obstruction, high-output fistula). the possible unknown effects due to lack of controlled studies.

© 2005 A.S.P.E.N. www.nutritioncare.org. A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. 163
S E C T I O N I I Immune Driven Conditions

f) As long-term effects become known, patients with good out- 1.58 episodes/1000 days of GT use,172 or 4.5 episodes/
comes to therapy should be educated on nutrition-related prob- 1000 days of PEG use201 in pediatric cancer patients.
lems they may face later in life and the need for follow-up. 3. Special aspects of PN
C. Pediatrics a) Goals
1. Special aspects of diet and nutritional supplements (1) Growth. Adequate calories, protein, and micronutrients
a) When the appetite is at a preillness level, follow a well- should be provided to support growth along the NCHS
balanced diet with a variety of foods according to the Food growth curves.
Guide Pyramid and Dietary Guidelines. (2) Catch-up growth. If the patient has protein calorie malnu-
b) If appetite or intake is compromised, make high-calorie, trition, catch-up growth and repletion of lean body mass is
high-protein, and nutrient-dense foods a priority in the diet. the goal.
A multivitamin/multimineral supplement may be indicated. (3) Prealbumin levels and trends. These can be monitored as
However, extra iron should be avoided in patients who undergo one measure of the adequacy of energy and protein intake.
numerous blood transfusions, and folate supplements should Increases of 1 mg/dL per day indicate appropriate effec-
not be given with methotrexate therapy. tiveness of the nutrition regimen.123,124
c) Avoid favorite foods during periods of nausea and vomiting (4) Replacement of any minerals and electrolytes that are
or therapies that lead to GI upset in order to minimize learned being wasted, and provision of additional micronutrients
aversions to those foods. at levels indicated by secondary conditions. For example,
d) Oral supplements may be used to increase nutrient intake. voluminous diarrhea may require the provision of addi-
(1) Pediatric supplements are designed to meet the nutrient tional zinc.
needs of children aged 1 to 10 years. (5) Minimization of metabolic disturbances associated with
(2) Modular supplements (protein, carbohydrate, lipid) may PN. Glucose should be maintained at less than 180 mg/dL,
be given to increase intake of a particular macronutrient. and triglycerides should not exceed 300 mg/dL.
(3) In cases of diarrhea or malabsorption, low osmolar nutri- (6) Avoidance of refeeding syndrome by repleting mineral and
tional supplements that contain hydrolyzed carbohydrate electrolyte levels prior to starting PN and by initiating PN
and protein and a higher percentage of medium-chain slowly in cases of severe malnutrition.
triglycerides may be appropriate. These supplements should b) Monitoring
be flavored when taken orally. (1) Major complications with catheter insertion include hemo-
(4) The safety of fish oil supplementation in children has not thorax and infection at the insertion site, reported in one
been well studied. study to occur at a rate of 4.4%.203 A minor complication is
2. Special aspects of enteral nutrition hematoma, which reportedly occurred at a rate of 6.7%.203
a) Goals (2) The most commonly reported complication with PN is sep-
(1) Growth. Provide adequate calories, protein, and micronu- sis. PN patients had significantly more days with fever;
trients to support growth along the NCHS growth curves. however, the catheter tip never cultured positively.204
(2) Tolerance of feeds. The type of formula, concentration, Catheter-related sepsis has been reported to occur at a rate
and rate must be well tolerated by the patient to promote of 3%.205 This rate seems to vary depending on the nutri-
optimal absorption of the nutrients provided. tional status of the patient, with significantly more sepsis
(3) Minimization of the burden associated with tube feeding. occurring in malnourished patients on PN than in well-
Cycle the tube feeding, as tolerated, overnight, so that days nourished patients on PN.205
are free for eating and playing, and so feedings are less (3) Metabolic complications also can develop. They include
often interrupted by medical procedures performed during hyperglycemia, hypophosphatemia, altered electrolytes,
the day. If the patient is unable to take anything by mouth, and increases in liver function tests and bilirubin levels.
then provide boluses, as tolerated, to mimic meals during 4. CAM aspects. Reports from studies conducted in 1997–2000 in the
the day. United States suggest that anywhere from 47% to 84% of pediatric
(4) Prealbumin. Increase prealbumin by 1 mg/dL per day.123,124 cancer patients have used at least one CAM since diagnosis.206–208
b) Monitoring The most popular CAMs reported in these studies were faith heal-
(1) The most common complications associated with naso- ing, diet changes, and dietary or herbal supplements. Literature on
gastric tubes (NGTs) in pediatric cancer patients are tube the safety and efficacy of herbal supplements in children is lack-
dislodgment due to vomiting and feeding intolerances (diar- ing. In general, concerns include adverse interactions with stan-
rhea, nausea, vomiting).198,199 Diarrhea can often be con- dard medications and/or contamination of the herbal supplements
trolled by adjusting the rate, strength, or osmolarity of with agents that can cause illness. Other CAMs include hypnosis
feeds.172,198 Nausea and vomiting are well managed pharma- and art therapy, the benefits of which have been reported in chil-
cologically.199 No episodes of epistaxis, sinusitis, or GI dren.209–211 The International Society of Pediatric Oncology (SIOP)
bleeding were reported,198,199 even in patients who had working committee on psychosocial issues in pediatric oncology
NGTs placed during thrombocytopenia and neutropenia.198 developed guidelines for the use of nonconventional therapies in
(2) Minor complications associated with PEGs and gastros- childhood cancer.212 The committee recommended that the health
tomy tubes (GTs) are common and primarily include inser- care team not automatically discourage the use of CAM therapies
tion site inflammation.170,172,200–202 Other complications if they are deemed nonharmful, even if the patient or family bene-
include feeding discharge from the GT site and GT occlu- fits only psychologically.212 On the other hand, the health care team
sion.170,172,200–202 should attempt to maintain open communication with the patient
(3) Major complications included systemic infection and and family about use of nonconventional therapies and should be
peritonitis. The rate of these ranged from 3% to 7%,170,200 vigilant about discouraging therapies that may be harmful, either

164 A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. © 2005 A.S.P.E.N. www.nutritioncare.org.
 S E C T I O N I I Immune Driven Conditions

physically or psychologically.212 The committee also warned that 4. Cancer Research and Prevention Foundation, www.prevent-
parents should be wary of therapies that have the following char- cancer.org
acteristics: the therapy is a secret that is known only by the pro- a) The mission of the Cancer Research and Prevention Founda-
moter of the therapy; the therapy is touted as a cure for a wide tion is the prevention and early detection of cancer through
range of cancers; the promoter attacks the medical community or scientific research and education. It focuses on cancers that
claims to be persecuted by it; or treatment with the therapy requires can be prevented through lifestyle changes or early detection
a large sum of money to be paid up front.212 followed by prompt treatment. These include breast, cervical,
5. Ethical issues colorectal, lung, oral, prostate, skin, and testicular cancers.
a) The same ethical considerations that exist for adult cancer b) The Web site spotlights topics and discusses cancer prevention
patients exist for pediatric cancer patients. in the news. There is information for patients and researchers.
b) The use of specialized nutrition support in terminally ill patients 5. Diet Guidelines for Immunosuppressed Patients, www.fhcrc.
is controversial but should be considered if it may improve org/clinical/ltfu/
QOL. a) The Web site of the Fred Hutchinson Cancer Research Center
c) Discontinuance of nutritional support can be the factor that in Seattle, Washington.
transitions the parents/caregivers to acceptance of the end-of- b) The site provides guidelines for adult and pediatric patients,
life status of their child. Sensitivity to the significance of nutri- including a patient and caregiver resource manual with guide-
tion to the family and caregivers in this regard is very important. lines on food and water safety, diet, adult nutrition, pediatric
6. Patient and caregiver education nutrition, and GI diets.
a) The same topics should be covered with pediatric patients that 6. National Cancer Institute, www.cancer.gov
are covered with adults (see Section V.B.6). a) A comprehensive site that includes information on cancer top-
b) With increasing survival of pediatric cancer patients, the long- ics, clinical trials, cancer statistics, research and funding, and
term effects of cancer treatments must be considered. Long- news.
term gastrointestinal toxicity may be one adverse effect of b) Eating Hints for Cancer Patients, http://www.cancer.gov/
cancer therapy in patients who survive into adolescence and cancertopics/eatinghints, provides nutritional advice for
adulthood.213 Survivors of ALL tend to become overweight by before treatment begins, advice on managing eating problems
the time they reach their final height,15,16 and decreased physical during treatment, special notes for caregivers, discussion of
activity has been purported to be a likely cause.17,18 Survivors of the posttreatment period, recipes, and more.
brain tumors may also experience intractable weight gain if 7. OncoLink, http://www.oncolink.upenn.edu/
the hypothalamus is damaged during therapy.214 Numerous a) The Web site of the Abramson Cancer Center of the University
long-term health-related issues secondary to radiotherapy and of Pennsylvania.
chemotherapy have been reviewed.140–142 As long-term effects b) This site highlights daily and weekly cancer-related news and
continue to become known, patients with good outcomes to offers a newsletter. There are sections on types of cancer, treat-
therapy should be educated on possible nutrition-related prob- ment options, coping with cancer, clinical trials, cancer
lems they may face later in life and the need for follow-up. resources, and expert advice.
8. Oncology Nutrition Dietetic Practice Group, www.oncologynu-
trition.org
VI. Patient and Caregiver Education Internet a) The Oncology Nutrition Dietetic Practice Group is a dietetic
Resources practice group of the American Dietetic Association. Its mis-
sion is to provide direction and leadership for quality oncol-
A. Internet resources for the patient and caregiver
ogy nutrition practice through education and research. It is a
1. American Cancer Society, www.cancer.org
national organization with over 1200 members.
a) Contains information for patients, family and friends, sur-
b) The practice of oncology nutrition covers research, preven-
vivors, health information seekers, American Cancer Society
tion, treatment, recovery, palliative care, and hospice. Oncol-
supporters, and professionals.
ogy nutritionists provide dietetic professionals with resources
b) The health information section contains information about
and networking opportunities to deal with the complexities of
food and fitness, such as guidelines for eating well and being
oncology practice. Members work in clinical, public health,
active, cooking smart, and taking control of one’s weight; the
education, and research settings.
power of fruits and vegetables; recipes; and nutrition during
treatment.
2. American Institute for Cancer Research, www.aicr.org (Cancer chapters from the 1st edition were contributed by Virginia
Hermann, Patricia Fuhrman, Peggy Borum, Karyl Rickard, Barbara
a) AICR is the cancer charity that fosters research on diet and
Godshall, Angelita Lopez, and Robert Weetman)
cancer prevention and educates the public about the results.
b) The site contains information for survivors and health pro-
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47–52; quiz 54–55. MA. Use of unconventional therapies by children with cancer at an urban
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 Mary Kramlich, MS, RD, LD, CNSD;
Angie Iverson, RD, LMNT;
Vincent Armenti, MD, PhD;
Jeanette Hasse, PhD, RD, LD, FADA, CNSD
12
Solid Organ Transplantation

Introduction a) Maintenance regimens are designed to provide long-term

immunosuppression to prevent rejections.
Solid organ transplantation outcomes may be influenced by nutritional b) These regimens are typically initiated soon after transplan-
factors such as preoperative malnutrition or obesity. Postoperative tation and include one or two drugs often combined with a
immunosuppressive medication regimens often affect nutritional man- corticosteroid.
agement along with growth and development in pediatric patients. c) Recent attempts have been designed to withdraw corticosteroids
Nutrition-related medication side effects, oral nutrition therapy, and over some period or even avoid corticosteroids completely.
enteral and parenteral nutrition management will be addressed in this d) Maintenance therapy agents include combinations of cyclos-
chapter.
porine or tacrolimus with either mycophenolate mofetil or
sirolimus.
I. Indications for Transplantation
e) Two new immunosuppressive agents on the horizon are
II. Immunosuppression
myfortic (Novartis Pharmaceutical Corporation, East Hanover,
III. Nutritional Factors Influencing Postoperative Outcomes
NJ) and Certican (Novartis Pharmaceutical Corporation),
IV. Nutrition Assessment
which have mechanisms of action similar to mycophenolate
V. Nutrient Requirements
mofetil and sirolimus, respectively.
VI. Nutrition Goals for Posttransplant Maintenance Phase
C. There is potential for drug-nutrient interactions (Table 12-2).
VII. Enteral Nutrition
VIII. Parenteral Nutrition
IX. Oral Nutrition III. Nutritional Factors Influencing
X.Patient Education Postoperative Outcomes
References
A. Malnutrition
1. Malnutrition reduces posttransplant survival.
I. Indications for Transplantation. Organ transplantation is a) Malnutrition increased risk for morbidity and mortality post
indicated for individuals who have organ failure that is no longer “cur- liver transplant in several studies,18–23 although findings by
able” with current medical and surgical therapies. See Table 12-1 for Figueiredo et al and Stephenson et al did not support this
specific disease states that may lead to organ transplantation. correlation.24,25
b) Madill et al reported that lung transplant recipients with a body
mass index (BMI) <17 kg/m2 had a 4-fold greater risk of dying
II. Immunosuppression within 90 days posttransplant compared with a normal weight
A. Organ transplant recipients are maintained on immunosuppressive group, although the finding was not statistically significant.16
regimens to prevent rejection. c) Frazier et al reported that mortality was increased in heart
B. Immunosuppression is designed to disable or destroy various com- transplant recipients who were malnourished.26
ponents of the immune response; this is typically achieved with mul- d) Becker et al showed that hypoalbuminemia in kidney trans-
tiple drug therapy. Regimens fall into three categories: plant recipients increased rates of cytomegalovirus infection
1. Induction regimens and graft failure and was associated with a trend for reduced
a) The aim of these regimens is to avoid rejection and establish survival.27
good graft function within the early postoperative course. 2. Malnutrition increases blood loss and use of blood products dur-
b) Induction regimens usually involve biologic agents, including ing liver transplant surgery.24,25,28
antilymphocyte sera (polyclonal or monoclonal antibodies) or 3. Malnutrition increases length of intensive care unit (ICU)22,24 and
interleukin-2 receptor blockade. hospital stay after liver transplant.22,25,29
c) Examples include Thymoglobulin, ATGAM, basiliximab, dac- 4. Malnutrition impairs wound healing.
liximab, and muromonab CD3 (Table 12-2) 5. Physical deconditioning, associated with malnutrition, may also
2. Antirejection regimens increase length of hospital stay and rehabilitation.
a) Antirejection regimens are high-dose, short-term treatments B. Obesity
aimed at reversing acute rejection. 1. Lung. Madill et al reported that lung transplant patients with a BMI
b) Agents include corticosteroids, Thymoglobulin, or muromonab >27 kg/m2 had an increased mortality within 90 days posttrans-
CD3 (Table 12-2). plant as well as an increased length of ICU stay.16
3. Maintenance regimens 2. Kidney and kidney/pancreas

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S E C T I O N I I Immune Driven Conditions

TABLE 12-1. Common Diagnoses Leading to Organ Transplantation

Organ Adult Pediatric

Liver transplant1–4 • Alcoholic cirrhosis • Pediatric

• Viral hepatitis—hepatitis B and C (fulminant and • Acute and chronic hepatitis—fulminant hepatic
chronic) failure, chronic viral hepatitis with cirrhosis
• Cholestatic disease—primary biliary cirrhosis, • Intrahepatic cholestasis—idiopathic neonatal hep-
primary sclerosing cholangitis atitis, Alagille’s syndrome, familial intrahepatic
• Metabolic disease—hemochromatosis, Wilson’s cholestasis (Byler’s disease)
disease, alpha 1-antitrypsin deficiency, glycogen • Cholestatic disease—extrahepatic biliary atresia,
storage disease sclerosing cholangitis
• Nonalcoholic steatohepatitis • Metabolic disease—alpha-1-antitrypsin deficiency,
• Autoimmune disease tyrosinemia, Wilson’s disease, perinatal hemochro-
• Miscellaneous—cryptogenic liver failure, polycystic matosis, glycogen storage disease
liver disease, hepatocellular carcinoma, Budd-Chiari
syndrome, sarcoidosis

Kidney transplant3,5,6 • Diabetes mellitus • Obstructive uropathy

• Hypertension • Aplastic/hypoplastic/dysplastic kidneys
• Chronic glomerulonephritis • Focal segmental glomerulosclerosis
• Systemic lupus erythematosus • Reflux nephropathy
• Chronic pyelonephritis • Chronic glomerulonephritis
• Polycystic kidney disease • Syndrome of agenesis of abdominal musculature
• Hyperoxaluria • Medullary cystic disease/juvenile nephronophthisis
• Vasculitis • Hemolytic uremic syndrome
• Nephritis • Congenital nephritic syndrome
• Polycystic kidney disease

Pancreas transplant3,7,8 • Type 1 diabetes mellitus is the indication for 99% of • Pancreas transplantation is uncommon in pediatric
pancreas transplants patients
• Islet cell transplantation is another option for • A pancreas graft is sometimes included in a multi-
patients with type 1 diabetes mellitus visceral transplant

Small-bowel • Indicated for patients with irreversible intestinal failure who cannot tolerate parenteral nutrition due to life-
transplant3,9–13 threatening complications such as cholestatic liver disease, loss of venous access, repeated central line sepsis
• Causes of intestinal failure include mesenteric thrombosis, necrotizing enterocolitis, Crohn’s disease, desmoid
tumor, Gardner’s syndrome, ischemia, pseudo-obstruction, trauma, intestinal volvulus, radiation enteritis

Heart transplant3,14,15 • Primary cardiomyopathy • Complex congenital heart disease

• Coronary artery disease • Primary cardiomyopathy
• Inoperable ischemic coronary disease • Hypoplastic left heart syndrome
• Endocardial fibroelastosis
• Acquired heart disease

Lung transplant3,14,16,17 • Cystic fibrosis • Cystic fibrosis

• Chronic obstructive pulmonary disease • Primary pulmonary hypertension
• Pulmonary hypertension • Chronic obstructive pulmonary disease
• Bronchiectasis • Alpha-1-antitrypsin deficiency
• Pulmonary fibrosis • Idiopathic pulmonary fibrosis
• Emphysema • Interstitial lung disease
• Eisenmenger’s syndrome • Congenital heart disease
• Bronchiolitis obliterans • Bronchiolitis obliterans
• Alpha-1-antitrypsin deficiency • Desquamative interstitial pneumonitis
• Scleroderma

172 A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. © 2005 A.S.P.E.N. www.nutritioncare.org.
 S E C T I O N I I Immune Driven Conditions

TABLE 12-2. Immunosuppressant Drugs, Nutritional Side Effects, and Interventions

Drug Activity Nutritional side effects Suggested nutrition therapy

Antilymphocyte Binds with lymphocytes, resulting in Fever and chills Provide nutrient-dense foods patient will eat
serum (ATGAM, Thy- phagocytosis Increased risk of infection, Ensure that patient is receiving adequate
moglobulin) Inhibits and destroys lymphocytes profound leukopenia protein

Azathioprine Inhibits purine nucleotide synthesis, Nausea, vomiting Try antiemetic medications; if vomiting does not
(Imuran) blocking T- and B-lymphocyte Diarrhea subside, consider tube feeding or PN
proliferation Sore throat/mucositis Review drugs and substitute for those that may
Altered taste acuity be causing diarrhea; make sure that patient
Macrocytic anemia is receiving adequate fluid to replace losses
Pancreatitis Provide foods that will not irritate throat
Offer a variety of foods with different tastes
Make sure folate intake is adequate
Initiate EN or PN if pancreatitis is severe

Basiliximab Acts against the interleukin-2R-alpha None reported

(Simulect) chain (CD25) on activated
T-lymphocytes and inhibits
interleukin-2-mediated activation
of lymphocyte

Corticosteroids Anti-inflammatory properties Hyperglycemia Monitor blood sugar and need for long-term
(methyl- Inhibits cell-mediated—and, to a Sodium retention diabetes diet and hypoglycemic agents
prednisone, lesser degree, humoral— Ulcers Avoid high-sodium foods
prednisone, immunity Osteoporosis Avoid foods that irritate stomach
prednisolone, Inhibits lymphocyte proliferation Hyperphagia Ensure adequate calcium and vitamin D intake;
Solu-Medrol, Inhibits lymphokine production Impaired wound healing consider need for calcitriol, fluoride, or estro-
Solu-Cortef) and increased infec- gen
tion risk Behavior modification to prevent overeating
Hypertension Ensure adequate protein intake; consider need
Pancreatitis for vitamins A or C or zinc
Avoid high-sodium foods, maintain healthy
weight
Initiate EN or PN if pancreatitis is severe

Cyclosporine Inhibits cell-mediated immunity; Hyperkalemia Restrict high-potassium foods

(Neoral, inhibits T-cell proliferation Hypomagnesemia Supplement with high-magnesium foods or
Sandimmune) Suppresses interleukin-2 production Hypertension supplements
Prevents gamma-interferon release Hyperglycemia Avoid high-sodium foods, maintain healthy
Hyperlipidemia weight
Monitor blood sugar and need for long-term
diabetes diet and hypoglycemic agents
Limit fat intake to <30% calories during long-
term phase; maintain healthy weight

Daclizumab None reported

(Zenapax)

© 2005 A.S.P.E.N. www.nutritioncare.org. A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. 173
S E C T I O N I I Immune Driven Conditions

TABLE 12-2. Immunosuppressant Drugs, Nutritional Side Effects, and Interventions (Continued)

Drug Activity Nutritional Side Effects Suggested Nutrition Therapy

Muromonab- Blocks T3 antigen recognition and Nausea, vomiting Try antiemetic medications; if vomiting does not
CD3 (OKT3) T-cell effector function Diarrhea subside, consider tube feeding or PN
Causes T-cell lysis Anorexia Review drugs and substitute for those that may
be causing diarrhea; make sure that patient
is receiving adequate fluid to replace losses
Offer frequent meals of nutrient-dense foods

Sirolimus Blocks the response of T- and B-cell Hyperlipidemia Limit fat intake to <30% calories during long-
(Rapamycin, Rapa- activation by cytokines, which Gastrointestinal disorders term phase; maintain healthy weight
mune) prevents cell-cycle progression and (constipation, Monitor for adequate nutrient intake
proliferation diarrhea, nausea/
vomiting, dyspepsia)

Tacrolimus Suppresses T cell-mediated immunity Nausea, vomiting Try antiemetic medications; if vomiting does not
(Prograf, FK506) and interleukin-2 production Hyperkalemia subside, consider tube feeding or PN
Hyperglycemia Avoid high-potassium foods
Abdominal distress Monitor blood sugar and need for long-term
diabetes diet and hypoglycemic agents
Monitor oral intake; consider alternate methods
of nutrition support if intake is suboptimal

Mycophenolate Inhibits DNA synthesis and mixed Diarrhea Review drugs and substitute for those that may
mofetil (CellCept) lymphocyte production be causing diarrhea; make sure that patient
Inhibits antibody formation is receiving adequate fluid to replace losses

EN, enteral nutrition; PN, parenteral nutrition.

Reprinted from Hasse JM. Solid organ transplantation. In: Matarese LE, Gottschlich MM, eds. Contemporary Nutrition Support Practice: A Clinical Guide,. 2nd ed. Philadelphia, PA:
Elsevier; 2003:560–573 with permission from Elsevier.

a) Obesity may increase the risk of delayed renal graft function.30–33 b) Table 12-8 summarizes nutrition considerations associated
b) Obesity has been shown to adversely affect graft survival in with common posttransplant complications.
some31,32,34–37 but not all studies.33,38 2. Pediatric. See Table 12-7.
3. Liver. Obesity may delay wound healing, prolong ventilator
time, and increase postoperative infections.39–41
VI. Nutrition Goals for Posttransplant
Maintenance Phase
IV. Nutrition Assessment. A combination of objective and sub-
A. Adult
jective parameters form the basis of a comprehensive nutrition assess-
1. Attain/maintain appropriate weight.
ment (see Table 12-3 for assessment guidelines specific to transplant
a) Excess weight gain posttransplant has been well docu-
recipients).
mented.52,59–64
b) Posttransplant obesity is attributed to numerous factors, includ-
ing the side effects of corticosteroids (hyperphagia, increase in
V. Nutrient Requirements adipose stores), pretransplant obesity, improved gastrointesti-
A. Pretransplant nal (GI) absorption, limited exercise, and noncompliance with
1. Adult. See Table 12-4; review other chapters on nutritional care dietary recommendations.5,42,65,66
of adult patients with specific organ failure c) Regular exercise is encouraged for weight maintenance as well
2. Pediatric. See Tables 12-5 and 12-6; review other chapters on as promotion of lean muscle tissue; posttransplant patients
nutritional care of pediatric patients with specific organ failure are at risk for increased muscle loss due to the side effects of
B. Postoperative corticosteroids.
1. Adult d) Weight loss recommendations posttransplant are similar to gen-
a) Table 12-7 highlights postoperative nutrient requirements. eral population guidelines (ie, exercise, diet modifications).67

174 A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. © 2005 A.S.P.E.N. www.nutritioncare.org.
 S E C T I O N I I Immune Driven Conditions

TABLE 12-3. Nutrition Assessment Criteria for Organ Transplant Patients5,9,14,42–48

Components of
an assessment Assessment parameters

Medical • Patient age • Previous surgeries (other than transplant) such as GI

history • Etiology, duration, and severity of organ failure prior to trans- surgeries (eg, noting ___location and extent of intestinal re-
plantation sections in small-bowel transplant recipients)
• Time since transplant and current transplant function • Other supportive therapies (eg, hemodialysis, oxygen, heart
• Other organ damage (eg, renal insufficiency, diabetes, assist devices if pretransplant)
cardiovascular disease) • History of diabetes mellitus and level of glucose control
• GI conditions (eg, nausea, vomiting, diarrhea, GI bleeding) or • Functional ability, energy level, attendance at work or school
diseases (eg, Crohn’s disease, celiac sprue, gastro-
esophageal reflux) • Current diet prescription

Nutrition • Diet history to assess quality and quantity of intake • Use of nutrition supplements, including vitamin, mineral, and
history • Medication history to identify drug-nutrient interactions herbal preparations
• Previous enteral or parenteral nutrition support; type and • Psychosocial and economic conditions to determine patient’s
amount of formula or caregiver’s ability to obtain/prepare food and comply with
• For infants, consideration of route of feeding and type of for- diet
mula if bottle-fed • Changes in appetite, taste acuity, satiety
• Fluid and electrolyte supplementation • Dietary restrictions
• Food allergies and intolerances
• Religious or cultural food preferences

Physical • Mental status • Skin color, dryness, turgor, and integrity

examination • Muscle and fat stores • Oral/dental health
• Edema or ascites

Anthropo- • Height or length • Tricep skinfold and midarm muscle circumference measure-
metric • For children, weight and percentile for age, weight for length ments may be helpful if measured serially over time
measurements percentile, head circumference and percentile for age • Hand grip strength may be an indirect measure of muscle
• Weight history (to assess degree of fluid retention and stores
weight loss)

Laboratory • Tests to evaluate transplant graft function • Hepatic transport proteins: not especially helpful in the post-
tests • Serum electrolytes operative period because concentrations are affected by
• Serum glucose and, if indicated, hemoglobin A1c and fluid status, liver and kidney function, and vitamin status
C-peptide levels • Iron studies
• Tests to evaluate renal function, such as blood urea nitrogen • Serum lipid levels
and creatinine • Fat-soluble vitamin levels (for patients with malabsorption)

Other tests • Subjective global assessment may be helpful as an initial • The D-xylose test is recommended for small-bowel trans-
assessment tool plant recipients 30 days posttransplant and then weekly
• Bioelectrical impedance is probably not an accurate measure to evaluate intestinal graft function and carbohydrate
of protein calorie malnutrition in fluid-overloaded patients absorption
• Creatinine-height index is influenced by renal function
• Dual-energy x-ray absorptiometry can accurately measure
bone density and body fat
• Indirect calorimetry can accurately determine resting energy
expenditure

GI, gastrointestinal

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S E C T I O N I I Immune Driven Conditions

(1) Osteopenic effects of immunosuppressive drugs (specifi-

TABLE 12-4. Pretransplant Calorie and Protein Goals for cally, corticosteroids and cyclosporine)
Solid Organ Transplant Candidates (2) Pretransplant risk factors such as type of pretransplant dis-
ease, vitamin D deficiency, hypogonadism, impaired absorp-
Nutrition Goal tion or inadequate intake of calcium, reduced physical
activity, and preexisting bone disease
Calorie Needs b) Treatment includes
(1) Adequate calcium intake (1500 mg per day) with vitamin D
Weight 1.2 to 1.3 x basal energy expenditure (by Harris- (2) Regular resistance exercise to improve bone density82
maintenance Benedict equation), depending on activity level (3) Smoking avoidance
(4) Annual bone density testing to monitor bone health
30 kcal/kg (5) Treatment with estrogen and/or bisphosphonates (indicated
for certain patients)83–85
Weight gain 1.5 x basal energy expenditure 4. Achieve normal serum lipid levels.
a) Risk factors for posttransplant hyperlipidemia include immuno-
35 to 40 kcal/kg
suppressive medications (especially sirolimus, corticosteroids,
and cyclosporine)52,86–88 as well as obesity, genetic predisposi-
Weight loss Deficit of 500 to 1000 kcal/day, depending on tion, diabetes mellitus, sedentary lifestyle, renal dysfunction,
current intake, anticipated time until transplant, high-fat diet, antihypertensive drugs, and proteinuria.
and ability to exercise b) Treatment of hyperlipidemia includes
(1) Dietary changes
Protein Needs (2) Lipid-lowering agents
(3) Fish oil supplementation, whose benefits are being studied
Maintenance 0.8 to 1.2 g/kg/d 5. Achieve normal blood pressure.
a) Transplant patients are at risk for increased blood pressure
Repletion 1.3 to 2.0 g/kg/d caused by corticosteroids and cyclosporine.
b) Treatment includes weight management, antihypertensive
Dialysis Hemodialysis: 1.2 to 1.5 g/kg/d medications, and a dietary restriction of 2 to 4 g sodium per day.
6. Wean nutrition support.
Peritoneal: 1.5 g/kg/d
a) Patients should achieve adequate intake with oral diet.
b) Small-bowel transplant recipients may require a period of nutri-
Adapted from Hasse JM. Solid organ transplantation. In: Matarese LE, Gottschlich tion support and/or intravenous (IV) fluids.
MM, eds. Contemporary Nutrition Support Practice: A Clinical Guide. 2nd ed. Philadel- B. Pediatric
phia, PA: Elsevier; 2003:560–573 with permission from Elsevier.
1. Obtain adequate calories and protein; needs reflect recommended
daily allowance (RDA) for age if there is good graft function, min-
imal complications, and appropriate growth since transplant.
e) Although limited data are available, small-bowel transplant
2. Achieve appropriate catch-up and long-term growth (Table 12-9).
patients appear to be at low risk for posttransplant obesity due
to decreased intestinal absorption.9 a) Growth retardation often occurs in pediatric patients prior to
2. Optimize diabetes management. transplantation.
a) Transplant patients are at higher risk of developing diabetes 68–72 b) The use of corticosteroids after transplantation can com-
due to immunosuppressive medications (eg, corticosteroids, pound this problem; however, the use of alternate-day pred-
tacrolimus, cyclosporine); the incidence of diabetes may lower nisone can reduce the growth-depressing effects of steroids89;
as corticosteroid doses are reduced.73 withdrawal of corticosteroids can also result in improved
(1) Cyclosporine and tacrolimus inhibit insulin secretion, catch-up growth.
increase insulin resistance, and exert a direct toxic effect c) Liver and heart recipients normally experience catch-up
on beta cells74; tacrolimus may be more diabetogenic than growth during the first posttransplant year if chronic rejec-
cyclosporine.75 tion is absent90; however, patients with poor graft function,
(2) Corticosteroids cause insulin resistance, increase gluco- those requiring high-dose corticosteroids due to rejection, or
neogenesis and glucagon production, and antagonize those requiring multiple operations are more likely to con-
peripheral glucose uptake.74,76,77 tinue to experience poor linear growth.89
b) Other risk factors for the development of diabetes include d) Children with renal failure have short stature for multiple rea-
heredity, obesity, and renal insufficiency. sons. Optimizing nutrition support, supplementing with oral
c) Diabetes treatment should include an appropriate carbohy- bicarbonate, preventing renal osteodystrophy, and treating
drate-controlled diet, self-monitoring of blood glucose, and anemia prior to transplantation can help stabilize growth.91
medication as needed (insulin or oral agents).70–72 (1) The use of recombinant human growth hormone before
d) Weight management, lipid control, and exercise are stressed transplant in patients with chronic renal failure has been
for patients with diabetes. shown to result in improved growth.91
3. Prevent and treat bone mass loss. (2) Some studies indicate that catch-up growth occurs in only
a) Posttransplant patients are at increased risk for bone loss78–81 30% to 50% of children after renal transplantation; it
due to occurs most often in children less than 6 years old rather

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 S E C T I O N I I Immune Driven Conditions

TABLE 12-5. Nutrition Considerations for Pediatric Transplant Candidates10,45,48–50

Considerations

Diet factors • Oral intake can be maximized by concentrating infant needs may make it difficult to meet 100% of nutritional
formulas needs with breast milk unless the mother is willing to pump
• Modular protein, fat, and carbohydrate components can be and additives are added to the milk
added to food or formulas to increase nutrient density • Most intestinal transplant candidates will have oral aver-
• If early satiety or tiring while feeding occur, offer patients sions; patients should receive as much oral stimulation as
small, frequent meals possible: bottles should be offered to children <1 year of age
• If an infant is breast-feeding, continue as long as he or she and solid food should be introduced at normal developmen-
gains weight and grows well; increased calorie and protein tal milestones

Nutrition • Tube feeding is indicated if patients are severely malnour- • Patients awaiting heart transplantation or requiring extracor-
support ished or unable to achieve adequate nutrient intake by poreal membrane oxygenation may also require PN
considerations mouth; when possible, tube feedings should be administered • Patients with severe esophagitis or gastric varices secondary
nocturnally or with a nipple/bolus schedule during the day to to liver disease may require PN if oral intake is inadequate
preserve as much oral intake as possible and prevent devel- and placing a nasogastric tube is contraindicated due to
opment of oral aversions bleeding risk
• If a patient is not growing adequately despite tube feedings,
PN is indicated to maximize nutritional status prior to trans-
plant

Pre-liver • Biliary atresia is the most common cause of liver disease in ❍ Infant formulas high in medium-chain triglycerides are
transplant pediatric patients helpful in reducing steatorrhea and improving growth
❍ Calorie requirements may be as high as 180% of the RDA • Patients with noncholestatic liver disease require 100% to
for calories and up to 4 g protein per kg per day due to 120% of the RDA for calories, 2.2 to 2.5 g protein per kg per
malabsorption of nutrients day for infants, and the RDA for protein for children ages
❍ Malabsorption of fat and fat-soluble vitamins also occurs; 1 year to 18 years
fat-soluble vitamin supplementation is frequently required
(see TABLE 12-6)

Pre-intestinal • Patients awaiting intestinal transplant are dependent upon • Protein requirements are 1.8 to 2.5 g per kg per day
transplant PN • Hypertriglyceridemia occurs frequently in patients awaiting
• Calorie needs are normally less than the RDA combined liver and intestinal transplantation
• If the patient is stable, 70 to 80 calories per kg per day are • Adequate fat (0.5 g/kg/day) should be provided to prevent
adequate for growth essential fatty acid deficiency

Pre-kidney • Calorie and protein requirements vary depending on need for • Electrolyte requirements need to be individualized based on
transplant dialysis and type of dialysis serum levels

Pre-heart • Calorie needs vary greatly • Calorie needs for children with congenital heart disease vary
transplant • Infants and children requiring ventricular assist devices or widely but may be 150 calories per kg per day or higher
extracorporeal membrane oxygenation prior to transplanta- • Children with less advanced heart disease will have calorie
tion are often dependent upon PN and protein needs similar to the RDA for their age
• Calorie requirements are typical for other children requiring
PN, approximately 80% to 85% of the RDA

Pre-lung • Most children requiring lung transplantation have CF; this • Because the degree of lung disease is quite advanced in
transplant population has specific nutrient requirements many patients with CF awaiting lung transplantation, tube
feeding may be required to meet nutrient needs

CF, cystic fibrosis; PN, parenteral nutrition; RDA, recommended daily allowance.

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S E C T I O N I I Immune Driven Conditions

7. Treat posttransplant diabetes mellitus (PTDM).

TABLE 12-6. Fat-Soluble Vitamin Recommendations for a) The incidence of hyperglycemia and PTDM ranges from 4%
Pediatric Liver Transplant Candidates45 to 41%.
b) Significant risk factors for the development of PTDM include
Vitamin Daily Recommended Amount first-degree family history of type 2 DM, second-degree family
history of type 2 DM, tacrolimus use, and hyperglycemia
Vitamin A, emulsified A 5000 to 15 000 International Units occurring in the 2 weeks after transplantation.
Vitamin D, 25 (OH) D 5 to 7 mcg/kg c) Patients with family history of DM or hyperglycemia may
Vitamin E, D-alpha-tocopherol 15 to 25 International Units/kg benefit from the avoidance of tacrolimus in the immediate
Vitamin K 2.5 to 5 mg posttransplant period.100
d) If PTDM develops, patients and families will need in-depth
dietary counseling to learn management principles.
8. Avoid obesity.
than older children92; however, there are reports of signif- a) Corticosteroids, inactivity, and poor dietary habits can con-
icant catch-up growth in children of pubertal age. tribute to the development of obesity in children after trans-
e) Lung and intestinal transplant recipients require more im- plantation.
munosuppression than other organ transplant recipients. b) Patients and families should be counseled on healthy eating
(1) Antirejection medications, specifically corticosteroids, can habits and the importance of daily exercise.
result in additional growth delay.
(2) After 5 years post small-bowel transplant, it appears that
VII. Enteral Nutrition
children do begin to experience catch-up growth in the
absence of renal failure or chronic rejection.93 A. Indications
3. Overcome oral aversions. 1. Advantages of early posttransplant enteral nutrition have been
a) This is primarily a complication in intestinal transplant recipi- documented in adults.101–106
ents; these children have not developed normal oral motor skills a) Benefits include promotion of protein metabolism, improve-
due to long-term dependence on parenteral nutrition (PN). ment in wound healing, maintenance of gut immunity, and pre-
b) Most small-bowel transplant recipients will require intensive vention of infectious complications.
posttransplant feeding therapy to achieve adequate nutritional b) The use of probiotics in early enteral nutrition to reduce bac-
intake by mouth.10 terial translocation and decrease the risk of infections is being
c) Patients with a long dependence on tube feedings or PN prior studied in posttransplant populations.107
to transplantation will require feeding therapy to meet nutri- 2. If a feeding tube is not placed at the time of transplantation, indi-
tional needs orally. cations for enteral nutrition include
4. Achieve normal blood pressure. a) Prolonged ventilator requirements
a) A sodium-restricted diet is recommended for patients who b) Postsurgical complications
have posttransplant hypertension (HTN). c) Failure to eat adequately when an oral diet is initiated
b) HTN is common after pediatric kidney transplantation and d) Severe malnutrition
can be associated with graft failure; higher systolic blood e) Physical deconditioning or overall weakness and failure to
pressure in the first few posttransplant months is associated thrive
with decreased renal allograft function in children 1 year after f) Gastroparesis
transplantation.94 g) Oral aversion
c) By 1 year after liver or heart transplantation, most patients are h) Growth failure in children
normotensive and do not require antihypertensive therapy.95 3. A transplant recipient who develops a critical illness at any time
d) HTN is also common in lung transplant recipients; patients posttransplant should be assessed for nutritional risk, and nutrition
with cystic fibrosis should restrict dietary sodium with caution. support should be considered (Figure 12-1).
5. Prevent and treat bone loss. 4. Following small-bowel transplantation, enteral nutrition is not
a) Long-term corticosteroid use can lead to bone loss over time.96 initiated until approximately 1 to 2 weeks after transplantation,
b) Corticosteroids are often discontinued or changed to alternate- when the postoperative ileus is resolved and it is verified that
day dosing in the first 6 to 12 posttransplant months to maxi- there is no anastomotic leakage; the patient is gradually weaned
mize long-term growth and minimize bone loss.97 off PN as enteral nutrition tolerance is established (meeting 50%
c) Calcium intake should meet the RDA for age. of needs).9
d) Vitamin D levels should be monitored and supplemented with B. Route of feeding
400 to 1000 International Units per day if needed. 1. Small bowel
e) Daily exercise is recommended to minimize bone disease. a) Nasoenteral—indicated for postoperative feedings if gastric
6. Achieve and maintain normal serum lipid levels. emptying is delayed and possibly to reduce risk of aspiration.
a) Elevated serum cholesterol and triglyceride levels can occur b) Jejunostomy—indicated for longer-term feedings. These
in children posttransplantation, most commonly in renal and tubes have a higher complication rate and risk compared with
heart transplant recipients.98 nasoenteral tubes and may be placed during small-bowel
b) Family history of hyperlipidemia correlates with increased risk. transplantation.
c) Complete serum lipid profiles should be performed, counsel- 2. Gastric
ing regarding dietary changes provided, and lipid-lowering a) Nasogastric—indicated for patients in whom aspiration risk
agents prescribed as needed.99 is reduced and gastric emptying is normal.

178 A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. © 2005 A.S.P.E.N. www.nutritioncare.org.
 S E C T I O N I I Immune Driven Conditions

TABLE 12-7. Nutrient Recommendations for Organ Transplant Recipients During Postoperative Stage or
Subsequent Critical Illness

Nutrient Adult recommendations5,9,14,42,44 Pediatric recommendations10,43,46–48,51

Calories 130% to 150% of calculated basal energy expenditure or • Needs vary depending upon clinical status
measure with indirect calorimetry • Up to 130 kcal/kg for patients with open wounds, sepsis, pre-
existing malnutrition, history of growth failure, cardiac fail-
• Calorie needs are individualized considering pretransplant
ure, or respiratory distress
nutritional status, postoperative stress factors, and presence
• 80 to 90 kcal/kg for infants and preschoolers without
of steatorrhea
complications
• Adjustments may be made for obese patients
• 50 to 60 kcal/kg for adolescents
• Ventilator dependence decreases calorie needs due to
decreased respiratory effort and inactivity
• Research indicates that the increase in energy expenditure
associated with surgery lasts only 24 hours

Protein 1.5 to 2 g/kg 2 times the RDA for age during the recovery period
• Protein catabolism is increased owing to surgical stress and • Protein needs are elevated in the first 2 weeks posttransplant
high-dose corticosteroids to account for protein catabolism from corticosteroids and
• Adjust for nitrogen balance studies, decubitus, wounds, increased needs for wound healing
fistulas, dialysis, and additional posttransplant surgeries • If renal function is poor (without dialysis), decrease protein
intake to 0.75 to 1.25 x the RDA

Carbohydrate 50% to 70% of nonprotein calories 50% to 60% of calories

• Hyperglycemia may occur as a result of immunosuppressive • Hyperglycemia may occur as a result of immunosuppressive
medications (corticosteroids, tacrolimus, cyclosporine), meta- medications (corticosteroids, tacrolimus, cyclosporine), meta-
bolic stress, or infection bolic stress, or infection
• Hyperglycemia may be a risk factor for infection • Hyperglycemia may be a risk factor for infection
• Treat hyperglycemia with short-acting and long-acting insulin • Insulin may be required
as indicated; consider insulin drip during critical conditions • Glucose should not be overfed; doing so could create more
• For small-bowel transplant recipients, limit lactose for post- problems with hyperglycemia or hypercapnia
operative secondary lactase deficiency

Fat 30% of calories 30% of calories

• Monitor serum triglyceride and cholesterol levels • Medications, sepsis, and liver or kidney dysfunction can
• Sirolimus (an immunosuppressant) can cause significant increase the incidence of hypertriglyceridemia
hyperlipidemia • Despite much research studying the effects of intravenous fat
• Fish oil (n-3 fatty acids) may reduce the nephrotoxic effects of on immune function and pulmonary function, there are not
cyclosporine enough data suggesting that lipids should be held for these
• For small-bowel transplant recipients, initially provide reasons
medium-chain triglycerides • Discontinue intravenous lipids if serum triglyceride levels
exceed 400 mg/dL

Fluid 30 mL/kg; adjust based on output Daily maintenance needs for pediatric patients:
• Adjust intake based on output from urine, drains, wounds, • mL/kg
diarrhea, nasogastric tube suction, fistulas, and para- or ❍1 to 10 kg: 100 mL/kg
thoracentesis ❍11 to 20 kg: 1000 mL plus 50 mL for every kg >10
• In pancreas transplant recipients with urinary drainage of ❍ 21 to 40 kg: 1500 mL plus 20 mL for every kg >20

exocrine secretions, losses can be as high as 2 to 3 L/day • Body surface area: 1500 to 2000 mL/m2
• In small-bowel transplant recipients, ostomy output can be as • Fluid may be restricted to less than maintenance if there is
high as 4 L/day edema, congestive heart failure, or renal failure

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S E C T I O N I I Immune Driven Conditions

TABLE 12-7. Nutrient Recommendations for Organ Transplant Recipients During Postoperative Stage or
Subsequent Critical Illness (Continued)

Nutrient Adult recommendations5,9,14,42,44 Pediatric recommendations10,43,46–48,51

Fluid • Fluid needs may be increased with fever, diarrhea, or vomit-

(Continued) ing; high volumes of gastric output need to be replaced;
kidney recipients often require additional fluid to replace
urine output
• Intestinal transplant patients will require intravenous re-
placement fluids for ileostomy output >35 to 40 mL/kg/day

Electrolytes • Hypernatremia may require additional free water administration

• Hyponatremia may require fluid restriction
• Hyperkalemia may occur with tacrolimus, cyclosporine, potassium-sparing diuretics, renal insufficiency, or metabolic acidosis
• Hypokalemia may be caused by potassium-wasting diuretics, amphotericin, refeeding syndrome, diarrhea, and fistulas
• Hyperphosphatemia may occur with renal insufficiency
• Hypophosphatemia may occur with refeeding syndrome or administration of corticosteroids
• Hypermagnesemia may occur with renal insufficiency
• Hypomagnesemia may be caused by cyclosporine, tacrolimus, diuretics, refeeding syndrome, diabetic ketoacidosis, and diarrhea;
oral magnesium supplements may cause diarrhea
• Bicarbonate loss may occur with urinary diversion of transplanted pancreas exocrine secretions or ostomy output in small-bowel
transplantation

Vitamins and • A multivitamin/mineral supplement is recommended

minerals • Adequate calcium for age is needed for bone health and prevention of osteopenia
• Vitamin C and B6 may be low in post–kidney transplant patients31
• Hyperhomocysteinemia is correlated in renal transplant recipients with renal function and status of vitamin B6, B12, and
folate53–58
• Patients with cystic fibrosis need water-miscible forms of fat-soluble vitamins
• Zinc and vitamin C may help with wound healing
• Zinc levels may be decreased in small-bowel transplant recipients due to high stomal losses requiring supplementation of zinc

RDA, recommended daily allowance.

b) Gastrostomy—indicated for long-term feedings when aspira- (1) Immunosuppressive medications can affect potassium,
tion risk is reduced and gastric emptying is normal. Gastros- magnesium, phosphorous, and calcium levels.
tomy tubes may be contraindicated if posttransplant ascites is (2) Formulas with reduced potassium and/or phosphorus may
present. be helpful for patients with renal failure with hyperkalemia
C. Indications for formula selection and hyperphosphatemia
1. Adults d) Fluid content
a) Protein content (1) Calorie-dense formulas may be indicated for patients with
(1) A high-nitrogen formula may be indicated for postoperative fluid overload or reduced urine output.
recovery and in situations such as critical illness or sepsis in (2) Fluid should be increased for patients with hypernatremia,
which protein needs are increased; a modular protein may fever, increased losses via drains, wounds, nasogastric tube,
be used to meet needs. or diarrhea.
(2) Glutamine-enhanced, small-peptide formulas may be (3) IV fluids may be required for small-bowel transplant recip-
advantageous for small-bowel transplant recipients receiv- ients when PN is discontinued.
ing early feedings following transplantation. 2. Children
b) Calorie contribution a) Age of patient
(1) Enteral nutrition may be required to meet all or part (1) Children should be given age-appropriate formulas.
of the patient’s estimated needs, depending on oral (2) Infants can normally resume breast-feeding or feeding with
intake. formulas they were receiving prior to transplantation.
(2) Calorie-dense formulas are indicated when patients are (3) Liver recipients requiring a hydrolyzed-protein formula
unable to tolerate high infusion rates to meet needs. pretransplant for malabsorption will usually tolerate an
c) Electrolyte content intact-protein formula after transplantation.

180 A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. © 2005 A.S.P.E.N. www.nutritioncare.org.
 S E C T I O N I I Immune Driven Conditions

TABLE 12-8. Nutrition Support Considerations for Specific Posttransplant Complications

Transplant
complication Nutrition considerations

Rejection • Rejection rates are reduced in malnourished patients • If muromonab-CD3 is used to treat rejection, nausea, vomit-
• Antirejection medications have many nutritional side effects ing, diarrhea, and headache, it may prevent adequate dietary
• Corticosteroids increase protein catabolic rate and effects intake
are dose dependent; protein catabolism increases during
rejection treatment

Infection • Immunosuppressed patients are at increased risk of infection • Antimicrobial agents may cause gastrointestinal upset and
• Malnutrition also increases the rate of infection affect dietary intake or cause diarrhea

Wound • Severely malnourished or obese patients are at increased

healing risk of wound complications

Renal • If renal replacement therapy is required, 5–10 g amino acids • 43%–45% of glucose is absorbed from dialysate with con-
insufficiency may be lost in dialysate tinuous hemodialysis
• During hemofiltration, 300 g glucose can be absorbed over
24 hours from glucose-rich replacement fluids

Hyperglycemia • Hyperglycemia is common due to metabolic stress, insulin • Infection rates are higher in diabetic patients than in nondia-
resistance caused by corticosteroids, and inhibition of islet betic patients
cell function and insulin release by cyclosporine and
tacrolimus

Surgical • Vascular complications, postoperative bleeding, or complica- • Edema and ascites may respond to sodium restriction
complications tions requiring further surgery will delay oral intake • Intestinal complications (diarrhea, ulcers, etc) may require
• Severe pancreatitis or ileus may be indications for nutrition that the route of feeding or type of food be altered
support

Adapted from Hasse JM. Nutrition assessment and support of organ transplant recipients. J Parenter Enteral Nutr. 2001;25(3):120–131 with permission from A.S.P.E.N.

b) Calorie content transplantation; tube feedings should be initiated slowly

(1) Infant formulas provide 20 kcal/oz, and most children’s (eg, 5 mL/hour) and advanced gradually (eg, 5 mL/hour
formulas provide 30 kcal/oz; these are normally adequate per day).108
to meet posttransplant requirements. e) Fat content. A low-fat formula containing MCT oil may be pre-
(2) Occasionally, 1.5 and 2.0 kcal/mL formulas are used for scribed if a patient develops chylothorax. If the condition does
pediatric transplant recipients if a severe fluid restriction is not resolve, PN with bowel rest is prescribed.109
required due to a complication such as renal failure. D. Complications. Posttransplant enteral complications for organ trans-
c) Osmolality plant patients are similar to those of postsurgical patients. See Chap-
(1) Isotonic formulas can be initiated full strength at low rates ter 5. In addition, the following should be done:
and advanced as tolerated. 1. Monitor stomal output and absorption in small-bowel transplant
(2) Small-bowel transplant recipients often receive a diluted patients.
formula initially, but it is concentrated as needed to meet 2. Evaluate potential causes of diarrhea, commonly found in trans-
fluid and calorie goals. plant recipients:
d) Protein content a) Cytomegalovirus invasion of the intestine
(1) Protein content should be adequate to meet posttransplant b) Clostridium difficile
needs. c) High levels of tacrolimus
(2) For patients with reduced calorie needs due to intubation, d) Mycophenolate mofetil
pretransplant obesity, and so on, protein modulars can be 3. Gastroparesis may be present posttransplant110; patients may
added to formulas to meet protein needs. require a prokinetic agent to tolerate tube feeds.
(3) Small-bowel transplant recipients should receive a hydro- E. Home enteral nutrition
lyzed, low-osmolality formula containing medium-chain 1. Patients may be sent home with tube feedings when the only fac-
triglycerides (MCTs) for the first 4 to 6 weeks following tor keeping them hospitalized is inadequate oral intake; most

© 2005 A.S.P.E.N. www.nutritioncare.org. A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. 181
S E C T I O N I I Immune Driven Conditions

pediatric intestine recipients will require tube feeding after hospi-

TABLE 12-9. Estimation of Catch-up Requirements tal discharge.
2. Usually, nocturnal tube feedings are recommended for home
1. Plot the child’s height and weight on the National Center for enteral nutrition; limiting factors include the inability to control
Health Statistics growth chart blood sugars with nocturnal tube feeds or intolerance of the higher
2. Determine the child’s recommended calories for age (recom- tube feed rate required to meet calorie/protein needs.
mended daily allowance [RDA]) 3. Appetite enhancers (eg, megestrol acetate) may stimulate appetite
3. Determine the ideal weight (50th percentile) for the child’s height and oral intake in adults.
4. Multiply the RDA calories by ideal body weight for height (kg) 4. Patients should be encouraged to try oral nutrition supplements
5. Divide this value by the child’s actual weight and/or between-meal snacks to improve intake.
5. Outpatient calorie count records should be kept by the patient or
Catch-up growth requirement = Calories required for weight family members and reviewed 1 to 2 times per week by a dietitian
to determine when enteral nutrition can be discontinued.
RDA calories for age (kcal/kg/day) x Ideal weight for height (kg)
Actual weight (kg)
VIII. Parenteral Nutrition
Protein requirement = Protein required for weight
A. Indications
RDA protein for age x Ideal weight for height (kg) 1. Prolonged ileus
Actual weight (kg) 2. Fistula or intestinal perforations
3. Bowel obstruction
Adapted from Peterson K, Washington JS, Rathburn J. Team management of failure- 4. GI bleed
to-thrive. J Am Diet Assoc.1984;84:810–815 with permission from the American 5. Pancreatitis (when tube feeding is not tolerated)
Dietetic Association. 6. Severe malabsorption or diarrhea

FIGURE 12-1. Algorithm for Providing Nutrition Support to a Critically Ill Organ Transplant Recipient

Critically ill organ

transplant patient

Malnourished
Well
or extended
nourished
NPO

Expect NPO Expect NPO Functional Nonfunctional

status <3 days status >3 days GI tract GI tract

Hold TF PN
nutrition
support

Does not GI
Diet NPO >3 Tolerates No GI
tolerate function
initiated days TF function
TF returns

Continue
Monitor Not able
Able to eat TPN and
intake to eat
reassess

Continue
Adequate Inadequate
TF and
reassess

Reprinted with permission from Hasse JM, Chinnakotla S. Solid organ transplantation. In: Cresci G, ed. Nutrition Support for the Critically Ill Patient: A Guide to Practice.
Boca Raton, FL: CRC Press; in press.

182 A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. © 2005 A.S.P.E.N. www.nutritioncare.org.
 S E C T I O N I I Immune Driven Conditions

7. Severe esophagitis (when tube feeding or oral diet is not tolerated) 2. Monitor patients for vomiting, diarrhea, abdominal distension, or
8. Small-bowel transplantation9,43 other GI complications.
a) PN is usually initiated within 24 to 48 hours posttransplant when 3. Initiate calorie counts to monitor the transition from parenteral
the patient and his or her electrolyte and fluid status are stable. or enteral nutrition to oral intake.
b) PN is continued until the patient can meet about 50% of esti- 4. Appetite enhancers (eg, megestrol acetate) can be considered for
mated needs with enteral nutrition. adult patients with loss of appetite and without functional swal-
c) PN may need to be resumed if the patient experiences severe low problems.
rejection or infection. 5. Dysphagia
B. Formula selection a) Dysphagia frequently occurs in posttransplant patients who
1. Provide solution that most closely meets needs and is tolerated. require prolonged intubation, who have tracheostomies, and/or
2. For small-bowel transplant patients, providing glutamine sup- who have physical deconditioning.
plement may improve repair of small-bowel mucosa.111,112 b) Swallow evaluations and/or dysphagiagrams are indicated to
C. Complications evaluate patients’ capacity for oral intake and safe progression
1. See Chapter 8. In addition, consider hydration and weight; fluid of diet.
balance and weight should be closely monitored, noting edema
and ascites and losses (urine, stool, ostomy, drains).
2. Posttransplant patients may be at greater risk for hyperglycemia
X. Patient Education
and hypertriglyceridemia secondary to immunosuppressive A. Discuss nutrient intake goals with patients and caregivers to achieve
medications. improvement in nutritional status (and growth in children). Goals are
D. Home PN individualized and should be reassessed during follow-up visits.
1. Adult small-bowel transplant recipients may require home PN to B. Maintenance needs for adults:
provide all or part of their nutrition needs. 1. Calories: 1.2 to 1.3 × basal energy expenditure (BEE) to maintain
2. Most pediatric intestinal transplant recipients are weaned from weight; small-bowel transplant patients may need higher calorie
PN prior to discharge from the hospital. amounts at 1.3 to 1.5 × BEE.
2. Protein: 0.8 to 1.3 g/kg (depends partly on maintenance corticos-
teroid dose); small-bowel recipients require 1.0 to 1.5 g/kg.
IX. Oral Nutrition
3. Carbohydrate: 50% to 60% of calories adjusting for hyper-
A. Diet initiation glycemia control; 20 g to 30 g fiber per day; small-bowel trans-
1. Adult—varies among transplant type plants should include lactose as tolerated.
a) Heart, lung. Diet is usually initiated within 24 to 48 hours 4. Fat: 25% to 35% total calories, 10% to 15% of calories as mono-
posttransplant. unsaturated fat, <300 mg cholesterol; for small-bowel transplants,
b) Kidney. Diet is usually initiated within 24 hours posttrans- reintroduce long-chain triglycerides as tolerated.
plant; diet is restricted as needed (ie, fluid, potassium, sodium, C. Instruct the patient and caregivers about individualized diet modi-
phosphorus, and concentrated carbohydrates). fications for
c) Liver. Diet is usually initiated within 48 to 72 hours post- 1. Weight control—calorie-controlled diet, behavior control related
transplant; most frequent diet restriction is concentrated car- to eating habits and hyperphagia from corticosteroids, daily
bohydrates for hyperglycemia. activity, and exercise
d) Pancreas. Diet is usually initiated within 5 days posttransplant 2. Diabetes mellitus—carbohydrate-controlled diet, self-monitoring
when nasogastric decompression is discontinued; a prokinetic of blood glucose, medication administration, daily activity, and
agent may be needed for gastroparesis. exercise
e) Small-bowel transplant9 3. Dyslipidemia—low saturated fat, low simple carbohydrate, calo-
(1) Oral diet is not initiated until tube feeding tolerance has rie-controlled diet; weight maintenance; possibly drug therapy
been established, about 1 to 2 weeks posttransplant. and/or fish oil therapy; daily activity; and exercise
(2) Low-fat, lactose-free, no-caffeine diet is provided (lym- 4. HTN—2 to 4 g per day sodium diet, weight maintenance, possi-
phatics and lacteals are severed at time of transplant; a lac- bly drug therapy, daily activity, and exercise
tase deficiency may exist); the low-fat and lactose-free 5. Electrolyte balance—monitoring of potassium, phosphorus, and
restrictions should be continued for 4 to 6 weeks post- magnesium; restricting or supplementing as needed
transplant. 6. Vitamin/mineral supplementation—daily multivitamin and min-
(3) A prokinetic agent or antidiarrheal may be indicated eral supplement; consideration of need for additional calcium
depending on GI motility. and vitamin D for osteopenia
2. Pediatric D. Food safety113
a) Oral diets are initiated 3 to 4 days posttransplant if the patient 1. Adequately cook all animal foods.
is extubated and bowel function has returned. a) No raw seafood (eg, sushi, raw oysters, ceviche)
b) A clear liquid is usually initiated; the diet is advanced to a reg- b) No raw eggs
ular diet as tolerated. 2. Wash fresh fruits and vegetables with a scrub brush, even when
B. Oral supplements. Use of oral nutrition supplements is encouraged the outer covering will not be consumed.
to improve calorie and protein intake. Select a supplement on the 3. Certain foods are prohibited:
basis of patient age, diet restrictions, and preference. a) Grapefruit, grapefruit juice—contain flavonoids, naringin, and
C. Monitoring and intervention aglycone naringenin, which inhibit cytochrome P450 enzymes
1. Patients frequently complain of decreased appetite, dysgeusia, and increase serum concentrations of cyclosporine and
early satiety, abdominal fullness, bloating, or food aversions. tacrolimus

© 2005 A.S.P.E.N. www.nutritioncare.org. A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. 183
S E C T I O N I I Immune Driven Conditions

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17. Boucek M, Edwards L, Keck B, et al. The Registry of the International prehensive Guide to Transplant Nutrition. Chicago, IL: American Dietetic
Society for Heart and Lung Transplantation: Fifth Official Pediatric Association; 2002:58–89.
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18. Selberg O, Bottcher J, Tusch G, Pichlmayer R, Henkel E, Muller M. Iden- Hasse JM, Blue LS, eds. Comprehensive Guide to Transplant Nutrition.
tification of high- and low-risk patients before liver transplantation: a Chicago, IL: American Dietetic Association; 2002:216–225.
prospective cohort study of nutritional and metabolic parameters in 150 44. Obayashi PAC. Adult pancreas transplantation. In: Hasse JM, Blue LS,
patients. Hepatology. 1996;25(3):652–657. eds. Comprehensive Guide to Transplant Nutrition. Chicago, IL: Ameri-
19. Porayko MK, DiCecco S, O’Keefe SJ. Impact of malnutrition and its ther- can Dietetic Association; 2002:90–105.
apy on liver transplantation. Semin Liver Dis. 1991;11(4):305–314. 45. Becht MB, Pedersen S, Ryckman F, Balistreri W. Growth and nutritional
20. Lautz H, Selberg O, Körber M, Bürger M, Müller MJ. Protein-calorie mal- management of pediatric patients after orthotopic liver transplantation.
nutrition in liver cirrhosis. Clin Invest. 1992;70:478–486. Gastroenterol Clin North Am. 1993;22:367–380.
21. Harrison J, McKiernan J, Neuberger JM. A prospective study on the effect 46. Fulton JA, McKenna A. Pediatric lung transplantation. In: Hasse JM, Blue
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22. Pikul J, Sharpe MD, Lowndes R, Ghent CN. Degree of preoperative mal- 47. Connolly C. Pediatric kidney transplantation. In: Hasse JM, Blue LS, eds.
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48. Sutton MM. Pediatric liver transplantation. In: Hasse JM, Blue LS, eds. 75. Heisel O, Heisel R, Balshaw R, Keown P. New onset diabetes mellitus in
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49. Ford EG. Nutrition support of pediatric patients. Nutr Clin Pract. 1996;11: 76. Silva F, Queirós J, Vargas G, Henriques A, Sarmento A, Guimarãs S. Risk
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50. Smith P. Primary care in children with congenital heart disease. J Pediatr tion after renal transplantation. Transplant Proc. 2000;32:2609–2610.
Nurs. 2001;16(5):308–319. 77. Jawad F, Rizvi SAH. Posttransplant diabetes mellitus in live-related renal
51. Shulman R, Phillips S. Parenteral nutrition in infants and children. J Pedi- transplantation. Transplant Proc. 2000:32:1888.
atr Gastroenterol Nutr. 2003;36:587–607. 78. Ulivieri FM, Piodi LP, Aroldi A, Cesana BM. Effect of kidney transplan-
52. du Plessis AS, Randall H, Escreet E, et al. Nutritional status of renal trans- tation on bone mass and body composition in males. Transplantation.
plant patients. S Afr Med J. 2002;92(1):68–74. 2002;73(4):612–615.
53. Arnadottir M, Hultberg B, Vladov V, Nilsson-Ehle P, Thysell H. Hyper- 79. Aroldi A, Tarantino A, Montagnino G, Cesana B, Cocucci C, Ponticelli C.
homocysteinemia in cyclosporine-treated renal transplant recipients. Effects of three immunosuppressive regimens on vertebral bone density
Transplantation. 1996;61(3):509–512. in renal transplant recipients. Transplantation. 1997;63:380–386.
54. Arnadottir M, Hultberg B, Wahlberg J, Fellström B, Dimény E. Serum 80. Kwan JTC, Almond MK, Evans K, Cunningham J. Changes in total body
total homocysteine concentration before and after renal transplantation. bone mineral content and regional bone mineral density in renal patients fol-
Kidney Int. 1998;54:1380–1384. lowing renal transplantation. Miner Electrolyte Metab. 1992;18:166–168.
55. Huh W, Kim B, Kim SJ, et al. Changes of fasting plasma total homocys- 81. Epstein S, Shane E, Bilezikian JP. Organ transplantation and osteoporo-
teine in the early phase of renal transplantation. Transplant Proc. 2000;32: sis. Curr Opin Rheumatol. 1995;7:255–261.
2811–2813. 82. Braith RW, Mills RM, Welsch MA, Keller JW, Pollock ML. Resistance
56. Fonseca I, Queirós JM, Satos JM, et al. Hyperhomocysteinemia in renal exercise training restores bone mineral density in heart transplant recipi-
transplantation: preliminary results. Transplant Proc. 2000;32:2602–2604. ents. J Am Coll Cardiol. 1996;28(6):1471–1477.
57. Kim SI, Yoo TH, Song HY, et al. Hyperhomocysteinemia in renal trans- 83. Isoniemi H, Appelberg J, Nilsson C-G, Makela P, Risteli J, Hockerstedt K.
plant recipients with cyclosporine. Transplant Proc. 2000;32:1878–1879. Transdermal oestrogen therapy protects postmenopausal liver transplant
58. Stein G, Muller A, Busch M, Fleck C, Sperschneider H. Homocysteine, women from osteoporosis. A 2-year follow-up study. J Hepatol. 2001;34:
299–305.
its metabolites, and B-group vitamins in renal transplant patients. Kidney
84. Reeves HL, Francis RM, Mana DM, Hudson M, Day CP. Intravenous
Int. 2001;59(suppl 78):262–265.
bisphosphonate prevents symptomatic osteoporotic vertebral collapse in
59. Trust NHS. The effect of dietary intervention on weight gain after renal
patients after liver transplantation. Liver Transpl Surg. 1998;4(5):404–409.
transplantation. J Ren Nutr. 1998;8:137–141.
85. Ninkovic M, Love S, Tom BDM, Bearcroft PW, Alexander GJ, Compston
60. Mor E, Facklam D, Hasse J, et al. Weight gain and lipid profile changes in
JE. Lack of effect of intravenous pamidronate on fracture incidence and
liver transplant recipients: long term results of the American FK506 multi-
bone mineral density after orthotopic liver transplantation. J Hepatol.
center study. Transplant Proc. 1995;27:1126.
2002;37:93–100.
61. Everhart JE, Lombardero J, Lake JR, Wiesner RH, Zetterman RK, Hoof-
86. Kasiske BL, Uman AJ. Persistent hyperlipidemia in renal transplant
nagle JH. Weight change and obesity after liver transplantation: incidence
patients. Medicine. 1987;66:309–316.
and risk factors. Liver Transplant Surg. 1998;4:285–296.
87. Baumgardner GL, Wilson GA, Tso PL, et al. Impact of serum lipids on
62. Ragsdale D. Nutritional program for heart transplantation. J Heart Trans-
long term graft and patient survival after renal transplantation. Trans-
plant. 1987;6(4):228–233.
plantation. 1995;60:1418–1421.
63. Hussaini SH, Oldroyd B, Stewart SP, et al. Effects of orthotopic liver 88. Eich D, Thompson JA, Ko D, et al. Hypercholesterolemia in long-term
transplantation on body composition. Liver. 1998;18(3):173–179. survivors of heart transplantation: an early marker of accelerated coronary
64. Pischon T, Sharma AM. Obesity as a risk factor in renal transplant artery disease. J Heart Lung Transplant. 1991;10(1 pt 1):45–49.
patients. Nephrol Dial Transplant. 2001;16:14–17. 89. Balistreri W, Bucuvalas J, Ryckman F. The effect of immunosuppression on
65. Lopes IM, Martin N, Errasti P, Martinez JA. Benefits of a dietary inter- growth and development. Liver Transplant Surg. 1995;1(5, suppl 1):64–73.
vention on weight loss, body composition and lipid profile after renal 90. Fine RN. Growth following solid-organ transplantation. Pediatr Trans-
transplantation. Nutrition. 1999;15:7–10. plant. 2002;6:47–52.
66. Hines L. Can lowfat/cholesterol nutrition counseling improve food intake 91. Furth S, Hwang W, Yang C, Neu A, Fivush B, Powe N. Growth failure,
habits and hyperlipidemia of renal transplant patients? J Ren Nutr. risk of hospitalization and death for children with end-stage renal disease.
2000;10:30–35. Pediatr Nephrol. 2002;17:450–455.
67. Munoz SJ. Long term management of the liver transplant recipient. Med 92. Simon D, Rosilio M, Maisin A, et al. Post graft development of short chil-
Clin North Am. 1996;80:1103–1120. dren treated with growth hormone before kidney graft. Pediatr Nephrol.
68. Navasa M, Bustamante J, Morroni C, et al. Diabetes mellitus after liver 1999;13:723–729.
transplantation: prevalence and predictive factors. J Hepatol. 1996;65: 93. Iverson AK. Long term growth and nutritional status in pediatric small
64–71. bowel transplant [abstract]. Nutr Clin Pract. 2002;17:56.
69. Weir MR, Fink JC. Risk for posttransplant diabetes mellitus with current 94. Mitsnefes MM, Omoloja A, McEnery PT. Short-term pediatric renal trans-
immunosuppressive medications. Am J Kidney Dis. 1999;34:1–13. plant survival: blood pressure and allograft function. Pediatr Transplant.
70. Obayashi PAC. Posttransplant diabetes mellitus: cause, impact, and treat- 2001;5:160–165.
ment options. Nutr Clin Pract. 2004;19:165–171. 95. Atkison P, Ross C, Williams S, et al. Long-term results of pediatric liver
71. Davidson J, Wilkinson A, Dantal J, et al. New-onset diabetes after trans- transplantation in a combined pediatric and adult transplant program.
plantation: 2003 international consensus guidelines. Transplantation. CMAJ. 2002;166(13):1663–1671.
2003;75(10, suppl):SS3–SS24. 96. Sprague S. Mechanism of transplantation-associated bone loss. Pediatr
72. Marchetti P. New-onset diabetes after transplantation. J Heart Lung Trans- Nephrol. 2002;14:650–653.
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1998;41:203–205. 98. Silverstein D, Palmer J, Polinsky M, Braas C, Conley S, Baluarte HJ. Risk
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99. Chin C, Rosenthal D, Bernstein D. Lipoprotein abnormalities are highly 106. Pescovitz MD, Mehta PL, Leapman SB, Milgrom ML, Jindal RM, Filo RS.
prevalent in pediatric heart transplant recipients. Pediatr Transplant. Tube jejunostomy in liver transplant recipients. Surgery. 1995;117:642–647.
2000;4:193–199. 107. Rayes N, Seehofer D, Hansen S, et al. Early enteral supply of lactobacil-
100. Greenspan L, Gitelman S, Leung MA, Glidden D, Mathias R. Increased lus and fiber versus selective bowel decontamination: a controlled trial in
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analysis. Pediatr Nephrol. 2002;17:1–5. 108. Strohm S, Koehler A, Mazariegos G, Reyes J. Nutrition management in
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patients undergoing liver transplantation. J Parenter Enteral Nutr. 1995; 109. Buttiker V, Fanconi S, Burger R. Chylothorax in children: guidelines for
19:437–443. diagnosis and management. Chest. 1999;116:682–687.
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liver transplantation for acute hepatic failure: report of four cases. Trans- paresis after combined heart and lung transplantation. J Clin Gastroenterol.
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103. Anbar R, Lipa R, Zinger P, Mor E. The role of nutritional support in trans- 111. Nemoto A, Krajack A, Suzuki T, et al. Glutamine metabolism of intestine
plant recipients: two case reports. Transplant Proc. 2003;35:614–616. grafts: influence of mucosal injury by prolonged preservation and trans-
104. Wicks C, Somasundaram S, Bjarnason I, et al. Comparison of enteral feed- plantation. Transplant Proc. 1996;28:2545–2546.
ing and total parenteral nutrition after liver transplantation. Lancet. 1994; 112. Schroeder P, Schweizer E, Blomer A, Deltz E. Glutamine prevents
344:837–840. mucosal injury after small bowel transplantation. Transplant Proc. 1992;
105. Mehta PL, Alaka KJ, Filo RS, Leapman SB, Milgrom ML, Pescovitz MD. 24:1104.
Nutrition support following liver transplantation: a comparison of jejunal 113. Cabelof D. Preventing infection from foodborne pathogens in liver trans-
versus parenteral routes. Clin Transplant. 1995;344:837–840. plant patients. J Am Diet Assoc. 1994;94(10):1140–1144.

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 Paula M. Charuhas, MS, RD, FADA, CNSD;
Ann Lipkin, MS, RD, CNSD;
Polly Lenssen, MS, RD, FADA;
Kerry McMillen, MS, RD
13
Hematopoietic Stem
Cell Transplantation

Introduction B. The preparative conditioning regimen consists of cytotoxic chemo-

therapy directed at eradicating the malignancy or defective stem
Hematopoietic stem cell transplantation (HSCT) is an accepted thera- cells with or without total body irradiation (TBI) and possibly local
peutic modality for many diseases, including hematologic malignancies, irradiation.
some malignant solid tumors, immunodeficiency syndromes, nonma- 1. Myeloablative conditioning regimens deliver high-dose chemothe-
lignant hematologic disorders of the bone marrow, inherited storage dis- rapy and radiation to eliminate disease and ablate bone marrow.
eases, and some autoimmune disorders. The objective is to replace the 2. Some myeloablative regimens use reduced conditioning to reduce
malignant or defective marrow to restore hematopoietic and immuno- toxicity.
logic function. While the diversity of applications for and approaches to
3. Nonmyeloablative conditioning regimens deliver low-dose chemo-
HSCT has expanded significantly in the last decade, it remains a highly
therapy and radiation to develop a mixed immune system or
morbid treatment in terms of potentially fatal toxicities, nutrition impli-
chimera. Candidates for nonmyeloablative conditioning regimens
cations, and, among children, developmental sequelae. This chapter
include
reviews the nutritional consequences of HSCT and offers guidelines for
a) Older patients
nutrition management of transplant-related complications and nutrition
b) Patients with relapsed malignancy following myeloablative
support practices.
HSCT
c) Patients with pretransplant comorbidities (ie, hepatic compro-
I. Overview of Diseases and Conditions Treated by HSCT
II. Types of Transplants mise) that make them ineligible for conventional transplant
III. Nutritional Aspects of HSCT d) Patients with nonmalignant disorders in which it is not neces-
IV. Nutrition Assessment sary to ablate diseased tissues
V. Nutrition Therapy C. An infusion of hematopoietic stem cells follows the conditioning
VI. Nutrition Management regimen.
VII. Patient and Caregiver Education D. Sources for new stem cells are
References 1. Bone marrow
2. Peripheral blood
I. Overview of Diseases and Conditions 3. Umbilical cord blood
Treated by HSCT1 E. Three types of HSCT1
1. Autologous: patient receives stem cells from him- or herself
A. Hematologic malignancies: acute leukemias; chronic leukemias; 2. Syngeneic: patient receives stem cells from a genetically identi-
lymphomas; multiple myeloma; myelodysplastic syndromes cal twin
(ie, refractory anemias) 3. Allogeneic: patient receives stem cells from a related or unrelated
B. Malignant solid tumors: advanced-stage neuroblastoma; refractory donor
Ewing’s sarcoma; ovarian cancer; prostate cancer; testicular can-
cer; renal cell carcinoma
C. Immunologic disorders: severe combined immunodeficiency dis- III. Nutritional Aspects of HSCT
ease; Wiskott-Aldrich syndrome; other cellular immunodeficiencies A. Multiple oral and gastrointestinal (GI) toxicities
D. Nonneoplastic disorders of hematopoiesis: severe aplastic anemia; 1. Mucositis and esophagitis
β-thalassemia major; Fanconi’s anemia; paroxysmal nocturnal a) These involve an inflammation of the epithelial tissue that may
hemoglobinuria
vary in severity from cracked and painful lips and mouth sores
E. Nonmalignant congenital disorders: storage diseases (ie, Gaucher’s
(ulcers on tongue/cheek) to bleeding mucosa with epithelial
disease); lysosomal diseases (ie, Lesch-Nyhan syndrome); muco-
loss. The mucositis may be present throughout the entire GI
polysaccharidoses (ie, Hurler’s syndrome; Hunter’s disease); muco-
tract.
lipidoses (ie, metachromatic leukodystrophy; Niemann-Pick disease);
b) They are an expected complication of myeloablative condition-
infantile osteopetrosis
ing regimens; often, oral or intravenous (IV) opioids are needed
F. Autoimmune disorders: multiple sclerosis; systemic lupus erythe-
for pain management.
matosus; systemic sclerosis
c) Methotrexate, used to prevent graft-versus-host disease
(GVHD), aggravates ulceration and thinning of the oral
II. Types of Transplants
mucosa.
A. The objective of HSCT is to replace the malignant or defective bone d) Symptoms may develop as early as 4 days after chemother-
marrow to restore hematopoietic and immunologic function. apy and several days after TBI starts.

© 2005 A.S.P.E.N. www.nutritioncare.org. A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. 187
S E C T I O N I I Immune Driven Conditions

e) Healing begins with marrow engraftment (absolute neutrophil c) SOS is characterized by subendothelial edema, endothelial cell
count >500/cm3). damage with microthrombosis, fibrin deposition, and expres-
f) Oral glutamine supplementation has not been effective in sion of factor VIII and von Willebrand’s factors within venu-
decreasing the incidence or severity of mucositis.2 lar walls. Hepatic necrosis follows these events in severe SOS,
2. Altered salivation with a reported survival of 38%.8
a) Xerostomia (oral dryness) is associated primarily with TBI but d) Clinical symptoms associated with SOS:
also with antiemetics, antidepressants, and opiate-containing (1) Weight gain with concomitant ascites
pain medications. (2) Increased serum bilirubin and jaundice
b) Saliva production diminishes and saliva becomes thick and (3) Hepatomegaly
viscous. (4) In severe cases, hepatorenal failure and encephalopathy
3. Taste alterations 2. Nutrition management of SOS
a) Dysgeusia (impaired taste) and hypogeusia (diminished taste) a) Minimize fluid retention by concentrating PN fluids.
are primarily an effect of TBI. b) Eliminate sodium from PN and diet.
b) Medications such as morphine and antibiotics may induce c) Remove or reduce copper and manganese from PN for per-
taste changes. sistent hyperbilirubinemia (ie, serum bilirubin >10.0 mg/dL).
c) Altered salivation and dry mouth affect taste due to decreased Ensure that patient continues to receive adequate zinc.
saliva production. Saliva is essential for taste perception, as d) Monitor serum triglyceride levels. If fasting serum levels are
food particles must be in solution to stimulate taste bud recep- >500 mg/dL, provide a minimal amount of IV fat emulsion
tor cells.3 Taste loss is temporary, with recovery between 30 and (ie, 4%–8% of total energy support).
50 days posttransplant.4 e) Consider obtaining indirect calorimetry measurements to
d) Sweet is the first taste to return, followed by bitter, sour, and ensure that the patient is not being overfed, and adjust energy
salty.4 support as appropriate.
4. Nausea and vomiting C. GVHD
a) These are associated with the preparative conditioning regimen, 1. GVHD is a T-cell–mediated immunologic reaction of engrafted
such as myeloablative agents (alkylating agents, TBI); other
lymphoid cells against the tissues of the host.
supportive care medications (antibiotics, cyclosporine, inter-
2. The incidence increases in mismatched and unrelated donor
leukin-2, trimethoprim-sulfamethoxazole, and mycophenolate
transplants.9
mofetil); GI infections (eg, cytomegalovirus, Helicobacter
3. The major target organs affected are the skin, mouth, GI tract, and
pylori); intestinal GVHD; and fluid and electrolyte imbalances.
liver. Ocular and pulmonary symptoms have also been described.9
b) Antiemetics are routinely administered to prevent and con-
a) Skin GVHD is characterized by a pruritic, maculopapular, and
trol symptoms. Initially, postablation symptoms are severe
erythematous rash. In severe cases, it may evolve into ulcer-
and patients often require regularly scheduled IV antiemet-
ations, blisters, and desquamation that necessitates burn care.
ics. IV antiemetics are changed to oral forms with symptom
Chronic skin GVHD can result in pigment changes, contrac-
improvement.
ture, and scleroderma.
5. Anorexia
b) Oral GVHD is associated with pain, ranging from mild sensi-
a) Anorexia has a multifactorial etiology.
b) Loss of appetite during and immediately postconditioning ther- tivity to frank mucosal ulceration. Oral GVHD may also
apy may be related to mouth pain, nausea and vomiting, elec- cause xerostomia.
trolyte imbalances, psychological factors, and medications. c) Gastrointestinal GVHD
After engraftment, loss of appetite may stem from these factors (1) Esophageal complications associated with GVHD include
as well as ongoing delayed gastric emptying, taste alterations, dysphagia with esophageal webbing or strictures.
GI infections, esophageal ulcers, or upper intestinal GVHD. (2) Intestinal complications are characterized by anorexia, nau-
c) Prolonged use of parenteral nutrition (PN) post-HSCT has been sea, vomiting, severe abdominal pain/cramping, and high-
associated with anorexia and delayed resumption of oral intake.5 volume watery diarrhea. In severe cases, the disease may be
6. Diarrhea and steatorrhea life-threatening, with mucosal ulceration, extensive bleed-
a) Diarrhea is associated with high-dose cytoreductive therapy, ing, and mucosal sloughing. Mucosal degeneration asso-
oral antibiotics, intestinal infections, GI GVHD, lactose intol- ciated with GVHD also induces fat malabsorption and
erance, gastric motility agents, and magnesium salts. intestinal protein losses (ie, protein-losing enteropathy).
b) Liver and intestinal GVHD may produce steatorrhea and fat Upper-gut GVHD is characterized by anorexia, nausea, and
malabsorption. vomiting.
7. Dietary guidelines for managing oral and GI toxicities associated d) Liver GVHD presents as cholestasis, elevated alkaline phos-
with HSCT are shown in Table 13-1.6 phatase and serum bilirubin levels, jaundice, hepatomegaly,
B. Sinusoidal obstructive syndrome (SOS) (also known as hepatic and, in severe cases, encephalopathy and hepatorenal failure.
veno-occlusive disease) 4. Nutritional consequences associated with GVHD can be extensive.
1. SOS is the leading cause of morbidity and mortality in the first Hypermetabolism, tissue damage, fluid and electrolyte imbal-
2 months posttransplant. ances, and medication-induced effects all affect nutritional status.
a) The incidence varies from 1% to 2% in some conditions (ie, thal- 5. GVHD can be hyperacute, acute, and/or chronic.
assemia) but may be as high as 50% in patients with preexisting a) Hyperacute GVHD generally occurs before engraftment and
hepatic compromise.7 primarily affects the skin.9
b) Patients with a history of hepatitis and second transplants are b) Acute GVHD develops posttransplant and is graded by sev-
at increased risk of developing SOS. eral criteria (Table 13-2).10

188 A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. © 2005 A.S.P.E.N. www.nutritioncare.org.
 S E C T I O N I I Immune Driven Conditions

TABLE 13-1. Dietary Guidelines for Managing Common Nutrition Problems Associated With HSCT

Oral and esophageal mucositis • Involve the patient in grocery shopping, meal planning, and simple
• Try soft/puree-textured or blenderized liquid diet.
meal preparation.
• Try smooth, bland, moist foods (custard, cream soups, mashed potatoes). • Encourage relaxation techniques and light exercise before meals,
• Offer soft, nonirritating, cold foods (popsicles, ice cream, frozen which may help improve food intake.
yogurt, slushes). Nausea and vomiting
• Encourage frequent mouth rinsing to remove food and bacteria and
promote healing. • Try high-carbohydrate foods and fluids (crackers, toast, gelatin) as
well as nonacidic juices.
Xerostomia (oral dryness) • Try small, frequent feedings.
• Offer moist foods (stews, casseroles, canned fruit) and liquids. • Offer cold, clear liquids and solids.
• Add extra sauces, gravies, margarine, butter, and broth to foods. • Avoid overly sweet or high-fat foods.
• Encourage liquids with meals. • Avoid feeding in a stuffy, too-warm room or one filled with cooking
• Add vinegar or pickles to foods. odors or other potentially disagreeable odors.
• Offer lemon-flavored, sugarless candy to help stimulate saliva. • Encourage the patient to drink or sip liquids frequently throughout
• Encourage good oral hygiene. the day; having the patient use a straw may help.
• Try commercial saliva substitutes. • Encourage rest periods after meals (but discourage reclining).
• Avoid offering favorite foods when the patient is nauseated; it may
Thick, viscous saliva and mucous cause a permanent dislike of the food.
• Encourage adequate fluid intake. • Observe whether there is a pattern to when nausea occurs or what
• Offer clear liquids (tea, popsicles, slushes, warm broth). causes it (specific foods, events, surroundings); suggest appropriate
• Encourage good oral hygiene. changes in diet or schedule.

Dysgeusia (impaired taste) Diarrhea

• Flavor poultry, fish, eggs, and dairy products. • Try a low-fat, low-fiber diet.
• Enhance food taste with herbs, spices, flavor extracts, and marinades. • Avoid caffeine.
• Offer cold, nonodorous foods. • Offer cold or room-temperature foods and beverages, which may be
• Offer fruit-flavored beverages. better tolerated.
• Try highly aromatic foods. • Offer low lactose intake.
• Try tart foods like oranges or lemonade, which may have more taste. • Encourage adequate fluids to prevent dehydration.
• Offer fluids with meals to help take away bad tastes in the mouth. • Avoid excessive fruit juice ingestion.
• Encourage good oral hygiene. Constipation
Anorexia • Encourage fluids.
• Offer small, frequent meals of nutrient-dense foods. • Offer a hot beverage in the morning or evening to help stimulate a
• Use carbohydrate supplements and protein powders. bowel movement.
• Create a pleasant mealtime atmosphere by enhancing food aromas, • Offer high-fiber foods.
using colorful place settings, and offering foods with varied colors
and textures.

Adapted with permission from Charuhas PM. Introduction to marrow transplantation. Oncol Nutr Diet Pract Group Newsletter. 1994;2:2–9.

c) Chronic GHVD generally develops 4 to 7 months posttrans- d) Table 13-3 discusses the dietary management of intestinal
plant but has been found to occur as early as 2 months or as GVHD.13
late as 2 years after transplant from nonidentical related and e) Medications and therapy may have significant nutritional con-
unrelated donors. The greatest risk factor for development of sequences (Table 13-4).14
chronic GVHD is the prior development of acute GVHD.11 D. Renal complications
(1) Nutrition problems reported at 1 year post transplant in 1. Multifactorial etiology
patients with chronic GVHD include weight gain, weight a) Chemotherapeutic agents and TBI, which may cause kidney
loss, oral sensitivity, xerostomia, stomatitis, anorexia, reflux, damage
diarrhea, malabsorption, and osteoporosis.12 b) Medications such as cyclosporine, tacrolimus, ampho-
(2) Community-based nutrition monitoring is necessary for tericin, aminoglycosides, vancomycin, and trimethoprim-
patients with chronic GVHD after discharge from the trans- sulfamethoxazole, which are associated with renal damage
plant center. and renal insufficiency

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S E C T I O N I I Immune Driven Conditions

TABLE 13-2. Clinical Manifestations and Staging of Acute GVHD

Organ Clinical manifestations Differential Histology Staging

Skin Erythematous, maculo- Chemo/radiotherapy Basal vaculopathy Stage 1: <25% rash

papular rash often effect, drug allergy, dyskeratosis, Stage 2: 25% to 50% rash
involving palms and soles; viral exanthem, exocytosis of Stage 3: generalized
may become confluent; infection lymphocytes, erythroderma
severe disease: bullae edema, dermal- Stage 4: bullae
described as tender, epidermal
like a sunburn, pruritic separation

Liver Painless jaundice with Veno-occlusive Lymphocytic Stage 1: bili 2 to 3 mg/dL

conjugated disease, drug infiltration of bile Stage 2: bili 3.1 to 6 mg/dL
hyperbilirubinemia toxicity, viral ducts, bile duct Stage 3: bili 6.1 to 15 mg/dL
and increased alkaline infection, sepsis damage with Stage 4: bili >15 mg/dL
phosphatase epithelial cell
dropout

GI tract Upper: nausea, vomiting Infection (bacterial. Crypt cell necrosis Stage 1: diarrhea >500 mL/day
anorexia. Lower: diarrhea, viral, C. Difficile), and dropout; Stage 2: diarrhea >1000 mL/day
crampy abdominal pain, toxicity from mucosal separation Stage 3: diarrhea >1500 mL/day
distention, ileus, GI conditioning and sloughing Stage 4: ileus, bleeding
bleeding regimen

Bili, bilirubin; GI, gastrointestinal; GVHD, Graft Versus Host Disease.

Reprinted with permission from Vogelsang GB, Lee L, Bensen-Kennedy DM. Pathogenesis and treatment of graft-versus-host disease after bone marrow transplant. Ann Rev Med.
2003;54:29–52.

c) Radiocontrast agents compromised liver function, those taking high-dose vitamin

d) Intravascular volume depletion A supplements preadmission, or children),18,19 discontinue
e) Tumor lysis syndrome or decrease IV multivitamin if appropriate depending on
f) Sepsis vitamin A and retinol binding protein levels. Toxicity symp-
g) Hepatorenal syndrome toms are known to occur at vitamin A levels 11⁄2 to 2 times
h) Thrombotic microangiopathies: hemolytic uremic syndrome normal20 in some patients who develop renal failure during
and thrombotic thrombocytic purpura15,16 hospitalization and receive PN support.
(1) These are associated with TBI and exacerbated by (2) Provide a complete complex of water-soluble vitamins and
cyclosporine. folic acid to compensate for ultrafiltrate losses.21,22 Ensure
(2) The common pathology is partial or complete occlusion that vitamin K needs are met.
of the arterioles and capillaries by thrombi containing (3) Provide additional protein supplementation (baseline needs
multiple platelet remnants. The result is consumption of plus 0.2 mg/kg/day) to compensate for filtered amino acid
platelets, fragmentation of red cells, and diverse organ losses.23
dysfunction. (4) Control serum glucose levels to prevent excessive glucose
(3) HSCT nephropathy presents as nephrotic syndrome with losses.24 Adjusting total kilocalorie intake in nutrition sup-
membranous nephropathy.17 port may be necessary to compensate for extra dextrose pro-
(4) Diffuse proliferative glomerulonephritis has also been vided through continuous renal replacement therapy.
reported and may be an effect of GVHD.17 (5) Calcium and magnesium losses are high.25 Patients treated
2. Nutritional management with citrate anticoagulation therapy are likely to require IV
a) Maintain sufficient intravascular volume. calcium supplementation.
b) Correct electrolyte imbalances. E. Infection
c) Maximize nutrition within fluid allowance. 1. Infection can be a major source of morbidity and mortality.
d) If continuous venovenous hemofiltration/hemodialysis or Patients are at risk for viral (ie, cytomegalovirus; varicella zoster;
intermittent hemodialysis is instituted, herpes simplex), bacterial (ie, coagulase-negative Staphylococcus;
(1) Assay serum vitamin A levels if the patient is to continue Pseudomonas aeruginosa), and fungal (ie, Candida glabrata;
on therapy for an extended period (correcting for retinol- Aspergillus fumigatus) infections.
binding protein levels). For patients at high risk of toxicity 2. Oropharyngeal, esophageal, and GI infections may influence the
at low doses of parenteral vitamin A intake (ie, those with patient’s ability to ingest and tolerate oral feedings.

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 S E C T I O N I I Immune Driven Conditions

TABLE 13-3. GI GVHD Diet Progression13

Phase Clinical Symptoms Diet Nutrition Support

1. Bowel rest GI cramping Oral: NPO PN with supplemental zinc and

Large-volume watery diarrhea or active possibly copper
GI bleeding
Depressed serum albumin
Severely reduced transit time
Small-bowel obstruction or diminished
bowel sounds
Nausea and vomiting

2. Introduction of Minimal GI cramping Oral: isosmotic, low- residue, low- PN

oral feeding Diarrhea less than 500 mL/day lactose beverages, initially Trophic enteral feeds of semiele-
Guaiac-negative stools 60 mL every 2 to 3 hours, for mental formula if patient
Improved transit time (minimum several days unable to eat
1.5 hours)
Infrequent nausea and vomiting

3. Introduction Minimal or no GI cramping Oral: allow introduction of solid Begin to cycle and decrease PN
of solids Formed stool food, once every 3 to 4 hours: Advance feeds slowly (small
minimal lactose, low fiber, low boluses or continuous infusion)
fat (20–40 g/day), low total if patient unable to eat
acidity, no gastric irritants

4. Expansion Minimal or no GI cramping Oral: minimal lactose, low fiber, Nighttime supplemental PN if oral
of diet Formed stool low total acidity, no gastric irri- intake less than needs or
tants; if stools indicate fat mal- patient unable to maintain
absorption: low fat weight owing to malabsorption
Enteral feed schedule and formula
dependent on any residual GI
symptoms

5. Resumption No GI cramping Oral: progress to regular diet by Discontinue PN

of regular diet Normal stool introducing 1 restricted food Supplemental enteral feeds if
Normal transit time per day: acid foods with meals, patient unable to eat adequate
Normal albumin fiber-containing foods, lactose- nutrients
containing foods; order of addi-
tion will vary depending on
individual tolerances and pref-
erences
Patients no longer exhibiting
steatorrhea should have the fat
restriction liberalized slowly

GI, gastrointestinal; GVHD, graft-versus-host disease; NPO, nil per os.

3. Treatment includes antiviral, antibiotic, and/or antifungal medica- F. Osteoporosis27

tions, which may induce anorexia, nausea, vomiting, diarrhea, and 1. Osteoporosis is a significant cause of morbidity, with subsequent
possible nutrient malabsorption, necessitating increased fluids and fractures and joint avascular necrosis (AVN). Osteoporosis has
electrolytes. been reported in 8% of adult autologous HSCT patients28 and 18%
4. Lipids do not increase bacteremia or fungemia when provided of allogeneic HSCT patients with chronic myeloid leukemia.29
in typical doses (25%–30% of total calories) for critically ill 2. The pathogenesis is complex and incompletely understood. Post-
patients.26 transplant steroid use is associated with an odds ratio of 14.4 for

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S E C T I O N I I Immune Driven Conditions

TABLE 13-4. Therapies Used for Prophylaxis and Treatment of GVHD14

Medication Nutritional Implications

Antithymocyte globulin Nausea and vomiting; diarrhea; stomatitis

Azathioprine Nausea and vomiting; anorexia, diarrhea; mucosal ulceration; esophagitis; steatorrhea
Beclomethasone dipropionate Xerostomia; dysgeusia; nausea
Budesonide None known
Corticosteroids Sodium and fluid retention resulting in weight gain or hypertension; hyperphagia; weight gain; hypokalemia;
skeletal muscle catabolism and atrophy; gastric irritation and peptic ulceration; osteoporosis; growth retardation
in children; decreased insulin sensitivity and impaired glucose tolerance; hyperglycemia or steroid-induced dia-
betes; hypertriglyceridemia
Cyclosporine Nausea and vomiting; renal insufficiency; magnesium wasting; potassium wasting
Extracorporeal photopheresis IV fluid may be necessary to maintain adequate hydration status; monitor calcium status if citrate anticoagulant
is used, because it may bind calcium and induce hypocalcemia
Methotrexate Nausea and vomiting (mild to moderate); anorexia; mucositis and esophagitis; diarrhea; renal and hepatic
changes; decreased absorption of vitamin B12, fat, and D-xylose; hepatic fibrosis; change in taste acuity
Methoxsalen (in conjunction with Nausea; hepatotoxicity
psoralen + ultraviolet A light)
Monoclonal antibodies Nausea and vomiting
Mycophenolate mofetil Nausea and vomiting; diarrhea
Sirolimus Hypertriglyceridemia
Tacrolimus Nephrotoxicity; hyperglycemia; hyperkalemia; hypomagnesemia
Thalidomide Constipation; nausea; xerostomia
Ursodeoxycholic acid Nausea and vomiting; diarrhea; dyspepsia

GVHD, graft-versus-host disease; IV, intravenous

the occurrence of AVN. TBI is associated with an adjusted odds c) As glucocorticoid doses are tapered to below 5 mg per day,
ratio of 3.2 for the occurrence of AVN.30 It is also thought that osteoblast function recovers and the suppressive effects on
hypogonadism plays a role. bone formation are reversed. Adverse effects of cyclosporine
3. Medications and tacrolimus remain, both the direct effects on the skeleton
a) Furosemide and heparin have negative effects on bone min- and the indirect effects that occur as a result of the nephrotoxi-
eral density. city. Bone resorption remains elevated.
b) Glucocorticoids lower osteoblast levels, shorten osteoblast life 5. Prevention and management of osteoporosis32
span, and reduce osteoblast function. Early in the course of glu- a) Baseline and serial dual-energy x-ray absorption scans are
cocorticoid use, there may be increased bone resorption. How- important for monitoring status.
ever, with chronic long-term use, glucocorticoids are associated b) Calcium and vitamin D supplementation for patients treated
with decreased bone resorption. with corticosteroids, based on duration of supplementation14:
c) Glucocorticoids cause decreased intestinal calcium absorption (1) 1 to 5 years: 600 to 800 mg calcium; 400 international units
and increased renal calcium excretion.31 vitamin D
d) Cyclosporine and tacrolimus are associated with bone loss, (2) 6 to 8 years: 800 to 1200 mg calcium; 400 international
but the mechanisms are unclear. units vitamin D
4. Two main phases of bone loss exist and are distinguished from (3) >9 years: 1500 mg calcium; 400 to 800 international units
each other by the presence or absence of glucocorticoids. vitamin D
a) During the first 6 months posttransplant, serum markers of bone c) Hormone replacement therapy (HRT) is used in postmenopausal
formation are suppressed and urinary markers show increased women and in men with low levels of serum testosterone.32
bone resorption. d) Bisphosphonates are recommended for adults when glucocor-
b) Nephrotoxic effects of cyclosporine and tacrolimus cause ticoid therapy is initiated, for patients with documented osteo-
declines in renal function and decreased synthesis of 1,25-OH porosis, for patients who have had fractures while treated with
vitamin D, resulting in inhibited intestinal calcium transport. HRT, and for patients in whom HRT is poorly tolerated.32
Parathyroid hormone levels increase, resulting in osteoclast- e) Bisphosphonate use is not well studied in the pediatric popu-
mediated bone resorption. lation.

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f) Weight-bearing and resistive exercise is also recommended. 6. Pediatric patients

G. Endocrine dysfunction33 a) For infants, determine if breast-fed or formula-fed. If infant
1. Thyroid dysfunction is associated with TBI. is breast-fed, encourage weaning, as breast milk contains live
2. Treatment with glucocorticoids suppresses the pituitary adrenal T-lymphocytes; if formula-fed, determine infant formula and
axis. Recovery is related to the duration and intensity of gluco- concentration.
corticoid therapy. b) Evaluate stage of eating development (ie, cup vs bottle; pureed
3. Pancreatic function changes occur with GVHD. vs table food; self-feeding skills).
a) Insulin resistance and hyperglycemia are associated with c) Assess for oral aversions.
steroid therapy for GVHD. Long-term effects include insulin B. Physical examination
resistance, impaired glucose tolerance, diabetes, and the core 1. Assess for presence of obesity, emaciation, dehydration, ascites,
signs of the metabolic syndrome. or edema.
(1) Insulin therapy and instruction related to diabetes are 2. Assess musculature, physical abilities, and activity level.
necessary. 3. Evaluate for signs of vitamin or mineral deficiency (ie, eyes, mouth,
(2) Dietary management includes modification of carbohydrate hair, nails, skin).
intake. 4. Assess for presence of stomas.
(3) Weight control is essential. C. Anthropometry
b) Alterations in lipid metabolism may occur as a result of steroid 1. Obtain baseline height and weight to determine body surface area.
and cyclosporine therapy. a) Assess weight changes, body mass index (BMI), ideal body
c) Extensive chronic GVHD can result in pancreatic scarring weight, percent ideal body weight, and if appropriate, adjusted
and reduced function, with effects on endocrine and exocrine weight.
function. b) In pediatric patients, assess growth history, weight-for-age,
4. Reproductive failure is common following HSCT. height- or length-for-age, and weight-for-length or BMI-for-age.
5. Vitamin D deficiency may occur with chronic GVHD due to c) These measurements may be used to determine chemotherapy
diarrhea and malabsorption and decreased exposure to sunlight and other medication dosages.
(patients are encouraged to apply daily sunblock therapy). Serum d) Chronic disease and prior treatment may affect growth, devel-
levels of 25-OH vitamin D should be monitored. opment, and physical abilities (ie, activities of daily living,
H. Growth and development issues34,35 exercise tolerance).
1. Growth hormone deficiency is common in children who have 2. Obtain baseline arm circumference and skinfold measurements
received prior cranial radiation and/or been treated with TBI or to assess somatic muscle protein and adipose reserves. These
busulfan plus cyclophosphamide. measurements may be helpful in further assessing the patient’s
2. Effects include decreased growth velocity, decreased bone min- nutritional status.
eral density, and delayed onset of puberty. 3. Establish baseline anthropometry, which provides landmark data
3. Regular long-term follow-up evaluations are necessary to detect for serial measurements.
occurrence of endocrine gland dysfunction. 4. Obtain head circumference in children less than 36 months old.
4. If abnormal endocrine function is detected, appropriate hormonal D. Laboratory parameters
therapy may improve growth and development. 1. Obtain baseline serum values of:
a) Electrolytes
b) Glucose
IV. Nutrition Assessment
c) Creatinine
A. Nutrition history d) Blood urea nitrogen
1. The nutrition history should include a comprehensive evaluation e) Calcium
of current oral and GI symptoms associated with the disease or f) Magnesium
prior therapy. g) Phosphate
a) Chewing or swallowing difficulties h) Albumin or prealbumin
b) Mucositis and esophagitis i) Liver function enzymes
c) Dental health, including denture fit and presence of oral j) Cholesterol and triglyceride
abrasions 2. Assay serum ferritin levels in patients with a history of multiple
d) Taste alterations blood transfusions to assess for iron overload.
e) Xerostomia 3. Hematologic indices such as hemoglobin, hematocrit, and total
f) Heartburn or reflux lymphocyte count are readily affected by disease and treatment,
g) Nausea and vomiting so they are not valid parameters for nutrition assessment of
h) Early satiety HSCT patients.
i) Anorexia E. Medications
j) Changes in bowel habits 1. Medications often affect appetite or alter GI function.
2. Assess current dietary modifications or unproven diets. 2. Analgesics, narcotics, antiemetics, antacids, laxatives, antibi-
3. Assess food allergies or intolerances. otics, diuretics, and corticosteroids all have nutritional implica-
4. Evaluate current use and dosage of vitamin and mineral sup- tions. See Tables 13-4 and 13-5.
plements, herbal supplements, and other integrative medicine 3. Assess for drug-nutrient interactions.
therapies. F. Quality of life
5. Evaluate past or current use of nutritional supplements, enteral 1. Assess physical strength, usual activity level, and any changes in
nutrition, PN, or fluid support. activity level.

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S E C T I O N I I Immune Driven Conditions

2. To provide nutrition support during regimen-related toxicities,

TABLE 13-5. Nutritional Implications of Medications prolonged anorexia, and GVHD in order to minimize loss of lean
Used During Hematopoietic Stem Cell body mass and maintain fluid and electrolyte balance
Transplantation14 B. Nutrient requirements
1. Energy14
Nutritional a) Increased energy requirements due to the preparative regi-
Medication Classification implications men, fever, infections, acute GVHD, metabolic complica-
tions, and growth demands of children
Amphotericin Antifungal Nephrotoxicity including b) Estimating energy requirements early posttransplant
(1) Infants and very young children: basal metabolic rate
azotemia; hypokalemia;
(BMR) × 1.6 to 1.814,37
hypomagnesemia; (2) Children (up to 16 years of age and ≤ 75 kg): BMR × 1.614,37
increased creatinine; (3) Older adolescents (>16 years of age or >75 kg): basal
anorexia; nausea and energy expenditure (BEE) × 1.5 to 1.614,38
vomiting (4) Adults: BEE × 1.514,38 or 30 to 35 kcal/kg/day39,40
(5) Following engraftment and resolution of metabolic com-
Busulfan Alkylating agent Nausea and vomiting; plications, energy needs decrease to BEE × 1.3 for adults
anorexia; hepatic toxicity; and BMR × 1.4 to 1.6 for children and adolescents.
(6) When possible, use metabolic chart measurements in
absorption impaired by
complex patients (ie, patients on long-term nutrition sup-
food
port or with significant body composition changes).
2. Protein14
Cyclophosphamide Alkylating agent Nausea and vomiting a) Increased protein is provided for tissue repair after cyto-
reductive therapy and to spare breakdown of lean body mass.
Foscarnet Antiviral agent Nephrotoxicity; potassium, b) Guidelines for protein support
magnesium, calcium, and (1) Ages 1 to 6: 2.5 to 3.0 g/kg/day
(2) Ages 7 to 10: 2.4 g/kg/day
phosphorus wasting;
(3) Ages 11 to 14: 2.0 g/kg/day
pancreatitis
(4) Ages 15 to 18: 1.8 g/kg/day
(5) Adults: 1.5 g/kg/day
Melphalan Alkylating agent Nausea and vomiting; c) Needs may be further increased during high-dose cortico-
anorexia; diarrhea; hepatic steroid therapy and during active GVHD.
toxicity; metallic taste d) If hepatic, renal, or neurologic function is altered, protein
intake may need to be modified.
Pamidronate Bisphosphonate Hypophosphatemia; 3. Fat
a) Typical intake is 15% to 30% of total energy.
hypocalcemia;
b) Maximum dose of intravenous lipid must not exceed 60% of
hypokalemia;
total energy intake, or no more than 3 g/kg/day.
hypomagnesemia c) Monitor weekly serum triglyceride levels when supporting
patients with >40% total energy from fat.
Thiotepa Alkylating agent Nausea and vomiting; d) Fat should account for a minimum of 4% to 8% of total calo-
mucositis and esophagitis ries, to prevent essential fatty acid deficiency.
4. Carbohydrate
a) Carbohydrate typically comprises 50% to 60% of total energy
Trimethoprim- Antibiotic Anorexia; nausea and
support.
sulfamethoxazole vomiting; stomatitis; diar-
b) Recommended carbohydrate infusion rates during PN:
rhea; nephrotoxicity; (1) Infants and children: ≤15 mg/kg/min
increased liver function (2) Adolescents: 7 to 10 mg/kg/min
tests; possible folate defi- (3) Adults: <5 mg/kg/min
ciency; possible decreased c) Hyperglycemia (preexisting or induced by PN or steroids)
vitamin K absorption often mandates a lower carbohydrate delivery.
5. Fluids14
a) Fluid needs are dependent on clinical status.
(1) ≤10 kg: 100 mL/kg/day
2. Assess level of pain and pain control, which may interfere with (2) 11 to 20 kg: 1000 mL + 50 mL/kg for each kg >10 kg/day
oral intake. (3) 21 to 40 kg: 1500 mL + 20 mL/kg for each kg >20 kg/day
(4) >40 kg: 1500 mL/m2/day
V. Nutrition Therapy b) Fluid needs are increased with fever, excessive GI losses,
hypermetabolism, high-output renal failure, nephrotoxic med-
A. Goals of nutrition support ications, and during HSCT conditioning.
1. To identify patients at nutritional risk early to avert morbidity c) Fluid restrictions may be necessary during compromised
associated with malnutrition36 organ function and iatrogenic volume overload.

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 S E C T I O N I I Immune Driven Conditions

6. Vitamins and minerals (2) Hyperkalemia: Causes include excessive supplementation,

a) Specific vitamin and mineral recommendations for HSCT potassium-sparing diuretics, renal insufficiency, tacrolimus,
patients are not known. and tumor lysis syndrome.
b) Oral multivitamin and mineral supplementation with 100% of e) Sodium
the dietary reference intakes for age is recommended for all (1) Hyponatremia: Causes include excessive GI losses, fluid
patients for 1 year posttransplant and longer in patients who retention, excessive IV or oral fluid or free water intake,
remain on long-term immunosuppressive medications. hyperglycemia, medications (ie, cyclophosphamide; cyclo-
c) Because patients undergoing HSCT often require administra- sporine; furosemide), and syndrome of inappropriate
tion of blood products and experience iron overload, supple- antidiuretic hormone.
mental iron is not recommended. (2) Hypernatremia: Causes include inadequate fluid replace-
d) IV vitamin and mineral recommendations are based on the ment during GI losses, aggressive diuretic therapy, and
American Medical Association recommendations for daily fever.44
requirements.41,42 f) Phosphorus
e) Provide additional vitamin C in PN during HSCT to promote (1) Hypophosphatemia: Causes include diabetes mellitus,
tissue recovery via collagen biosynthesis after cytoreductive medications (ie, corticosteroids; cyclophosphamide; fos-
therapy.14 carnet; sirolimus), refeeding syndrome, renal acidosis, and
(1) <31 kg, additional 250 mg of vitamin C per day steatorrhea.
(2) ≥31 kg, additional 500 mg of vitamin C per day (2) Hyperphosphatemia: Causes include excessive phosphorus
(3) Additional vitamin C, which may act as a pro-oxidant, is intake, multiple myeloma, myelogenous leukemia, renal
contraindicated in patients with serum ferritin levels >1000 failure, and tumor lysis syndrome.
mcg/L, to decrease oxidative damage from release of free g) Calcium
iron.43 (1) Hypocalcemia: Causes include medications (ie, cortico-
(4) During hemodialysis, discontinue additional vitamin C to steroids; foscarnet; pamidronate) and vitamin D deficiency.
prevent secondary oxalosis. (2) Hypercalcemia: Causes include lymphoma, metastatic
f) Malabsorptive disorders, such as with liver or intestinal GVHD breast cancer, multiple myeloma, renal failure, and tumor
or long-term oral antibiotic therapy, may precipitate a vitamin lysis syndrome.
K deficiency.
8. Drug-nutrient interactions (Tables 13-4 and 13-5)14
(1) Pediatric IV multivitamin preparations (used for patients
<11 years old) contain vitamin K, while only some adult
IV preparations (used for patients ≥11 years old) do. VI. Nutrition Management
(2) For pediatric patients >11 years old, add 200 mcg/day of
A. Oral feedings
vitamin K.
1. Oral feedings are indicated for patients with a functional GI tract
(3) For adults, add 10 mg/week of vitamin K.
and good nutritional status.
g) Additional zinc supplementation is indicated in patients who
2. High-calorie, high-protein intake is emphasized, supplemented
develop diarrhea, with a suggested replacement guideline of
by nutrient-dense snacks as necessary.
1 mg/100 mL stool when volume exceeds
3. Liquid, blended, or soft diets may be necessary in patients with
(1) 250 mL for patients <20 kg
chewing or swallowing difficulties due to mucositis, esophagitis,
(2) 500 mL for patients 20 to 40 kg
(3) 1000 mL in patients >40 kg14 or oral GVHD.
h) In the presence of hepatic failure, eliminate the biliary excreted 4. Nutrient modifications may be necessary.
trace elements copper and manganese from PN solutions. a) A lactose-restricted diet is indicated for diarrhea.
i) Calcium and vitamin D supplementation is recommended for b) A sodium-restricted diet is indicated in patients with ascites
patients maintained on high-dose corticosteroids when dietary or significant edema as a result of cardiac dysfunction or
intake is inadequate. (See Section III.F.5.b).) medication-induced fluid retention.
7. Electrolytes c) Potassium or phosphorus restriction is occasionally necessary
a) Electrolyte requirements vary widely, because medications in patients with renal dysfunction.
and GI losses influence needs. d) If total calories and simple carbohydrate intake are greater than
b) Serum electrolyte levels should be closely monitored, espe- needs, restriction is indicated in steroid-induced hyperglycemia
cially for patients maintained on PN or IV hydration contain- (>180 mg/dL). (See III.G.3.a). However, diet modifications
ing electrolyte additives. generally do not avert the need for insulin administration (short-
c) Magnesium acting with meals and long-acting if morning blood glucose is
(1) Hypomagnesemia: Causes include diarrhea and steatorrhea, elevated).
malabsorption syndromes, medications (ie, amphotericin, 5. A five-phase diet regimen has been developed for patients with
cyclosporine; foscarnet; tacrolimus), refeeding syndrome, GI GVHD with moderate to excessive diarrhea (Table 13-3).13
and severe malnutrition. 6. Elimination of foods most commonly associated with food-borne
(2) Hypermagnesemia: Causes include discontinuation of a illness as well as food and herbal sources of fungal organisms is
magnesium-wasting medication, excessive supplementa- recommended until all immunosuppressive therapy has been dis-
tion, and renal insufficiency. continued (Table 13-6).
d) Potassium a) Safe food handling and preparation methods are probably
(1) Hypokalemia: Causes include GI losses, medications more beneficial than restriction of individual foods.45
(ie, amphotericin; corticosteroids; furosemide; foscar- b) There is no scientific evidence to support restricting fruits and
net), refeeding syndrome, and anabolism. vegetables or providing only well-cooked foods.

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S E C T I O N I I Immune Driven Conditions

(1) Receive nonmyeloablative or reduced-intensity condi-

TABLE 13-6. Diet Guidelines for Immunosuppressed tioning regimens
Patients (2) Fail to recover appetite and resume eating after engraft-
ment and resolution of conditioning-related mucositis and
These guidelines are intended to minimize the introduction of patho- esophagitis45
genic organisms into the gastrointestinal tract by food while maximiz- (3) Have chronic GVHD (ie, oral; esophageal; liver; pul-
ing healthy food options for immunosuppressed patients. The monary; weight loss; quiescent phases of GI)
guidelines should be coupled with food safety education to ensure (4) Have neurological complications that preclude safe swal-
proper food preparation and storage in the home and hospital kitchen. lowing
High-risk foods identified as potential sources of organisms known to (5) Are ventilated
cause infection in immunosuppressed patients are restricted. 2. Access
a) Nasoenteric
In general, autologous transplant patients follow the diet during
(1) Gastric feeding may be tried initially. Postpyloric place-
the first 3 months after hematopoietic stem cell transplantation. Allo-
ment is sometimes necessary in patients with delayed gas-
geneic transplant patients should follow the diet until they are off all tric emptying and frequent emesis.
immunosuppressive therapy (ie, cyclosporine, tacrolimus, pred- (2) Self-propelling tubes have been used with partial success
nisone). in the early posttransplant period.47
b) Percutaneous endoscopic or surgically placed gastrostomies
Food restrictions
(1) Platelets >50 000 units/L and absolute neutrophil count
• Raw and undercooked meat (including wild game), fish, shellfish, >1000 cm2 are recommended for safe placement.
poultry, eggs, sausage, bacon (2) Pretransplant placement needs to occur 3 to 4 weeks prior
• Raw tofu, unless pasteurized or aseptically packaged to conditioning and period of neutropenia to ensure ade-
• Luncheon meats (including salami, bologna, hot dogs, ham), unless quate healing.
heated until steaming (3) Posttransplant placement is dependent on the clinical status
• Refrigerated smoked seafood typically labeled as lox; kippered, of the patient; a trial of nasoenteral feeding is appropriate
nova-style, or smoked fish; fish jerky (unless contained in a cooked prior to placement.
3. Complications
dish)
a) Dislodgment of nasoenteral tubes, necessitating frequent
• Pickled fish
replacement47,48
• Unpasteurized milk and raw milk products, nonpasteurized cheese, b) Delayed gastric emptying, especially among allograft recipi-
and unpasteurized yogurt ents.49 Prokinetic agents or jejunal feeds may ameliorate the
• Soft and blue-veined cheeses, including brie, Camembert, feta, situation50; however, not all patients tolerate prokinetic agents.
farmer’s, blue, Gorgonzola, Roquefort, Stilton c) Poor tolerance of rapid advancement of feeds when transi-
• Mexican-style soft cheeses, including queso blanco and queso tioning from PN after myeloablative conditioning
fresco d) Infections and gastric leakage at gastrostomy sites. Gastric
• Cheese containing chili peppers or other uncooked vegetables leakage requires special protection of the skin during the neu-
• Fresh salad dressings (stored in the grocer’s refrigerated case) tropenic period to prevent breakdown.51,52
containing raw eggs or contraindicated cheeses e) Inadequate energy intake. With a predominantly enteral
approach early post-HSCT, inadequate energy intake results in
• Unwashed raw vegetables and fruits and those with visible mold
weight loss, decreased body cell mass, and increased frequency
• All raw vegetable sprouts (alfalfa, mung bean, all others)
of malnutrition, as it supplies on average less than 50% of
• Unpasteurized commercial fruit and vegetable juices needs.47,53,54 PN51,52 or a combination of enteral feedings and PN
• Raw honey; honey in the comb may be needed.55
• All miso products (including miso soup); tempeh; maté tea f) Inadequate protein intake. In children, modular protein addi-
• All moldy and outdated food products tives often are required to meet high protein needs.
• Raw, uncooked brewer’s yeast g) Inadequate electrolyte and mineral intake, specifically inade-
• Well water, unless boiled for 1 minute quate magnesium, calcium, phosphorus, and zinc with enteral
feeds.53,56 IV supplementation of magnesium and phosphorus
Source: Courtesy of the Nutrition Program, Seattle Cancer Care Alliance, 2004.
may be needed to avoid excessive diarrhea.
h) Malabsorption in patients with chronic GVHD or pancreatic
insufficiency. This necessitates semi-elemental or elemental
formulas with supplemental vitamins and minerals.
C. PN
c) The effect of these diet modifications is unknown and war- 1. Indications
rants further research.46 a) PN is associated with improved long-term disease-free sur-
B. Enteral nutrition vival compared to hydration support in allogeneic patients
1. Indications receiving myeloablative conditioning regimens.57
a) Patients with a functional GI tract who are either under- b) Candidates include patients who
nourished or who have poor oral intake that is expected to (1) Receive high-intensity conditioning regimens and experi-
continue for 1 week or longer ence severe GI toxicity that precludes adequate intake.55
b) Candidates include patients who The length of time before starting PN will depend on the

196 A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. © 2005 A.S.P.E.N. www.nutritioncare.org.
 S E C T I O N I I Immune Driven Conditions

nutritional status of the patient, the risk of GVHD, and the clinical trials are needed to ensure that they have no adverse
expected duration of GI toxicity. effect on GVHD or survival before specific recommenda-
(2) Develop severe intestinal GVHD or other GI toxicities, tions can be made. Alanyl-glutamine dipeptide was associ-
such as high-volume infectious diarrhea ated with significantly more relapses in patients undergoing
(3) Fail to receive adequate nutrition via the enteral route, espe- autologous HSCT in one randomized study.60
cially children who need adequate nutrition to maximize (2) Lipids are not associated with an increased incidence of
growth and development and malnourished patients with bacteremia or fungemia.23 (See Section III.E.4.)
minimal reserves D. Nutrition support monitoring
2. Access 1. Monitor alterations in medical condition and nutritional status,
a) Most patients have dual-lumen central venous access as a stan- treatment-related symptoms, and modifications in nutrient require-
dard of care for infusion of chemotherapy, blood products, and ments.
intravenous medications for several months and sometimes 2. Monitor weights and intake and output daily during early post-
even years (in patients with severe chronic GVHD) post-HSCT. grafting period. Monitor weights weekly in patients with chronic
Occasionally, single-lumen access requires cycling of PN GVHD.
because of competition with other IV therapies. 3. Monitor laboratory parameters for abnormalities at least 3 times
b) Line infections are common, and line removal may require per week and in some critical cases daily in the early posttransplant
use of peripheral PN until central access is reestablished. period.
3. Complications a) Serum glucose, creatinine, blood urea nitrogen, and electrolytes
a) Hyperglycemia management will depend on clinical status, are often needed daily, with adjustments to PN required.
etiology, and institutional practice, with the goal to achieve a b) Serum phosphate, magnesium, calcium, and albumin are needed
glucose level as close to normal as is safely possible. twice weekly.
(1) Patients with preexisting diabetes need insulin titrated c) Blood lipids are needed weekly in patients with preexisting
to each advancement of dextrose toward goal dextrose hyperlipidemia; liver, renal, or pancreatic dysfunction; or pro-
(approximately 40% of total energy needs). Achieving tight longed course of medication associated with hyperlipidemia
control may require an insulin drip with glucose monitor- (ie, corticosteroids, sirolimus, cyclosporine).
ing every 2 hours. If an insulin drip is not available, a base d) Liver function tests are needed twice weekly.
amount of insulin may be added to the PN and sliding-scale e) Prealbumin is not useful in the early postgrafting period,
coverage provided every 4 to 6 hours to maintain a serum because prealbumin parallels neutrophil count.
glucose level of <180 mg/dL. If a patient is clinically stable f) If the patient is on long-term PN, check serum zinc, copper,
and needs predictable amounts of insulin, then a lower level carnitine, selenium, manganese, and chromium.
of glucose may be safely achieved. g) If the patient is on long-term tube feeding and has chronic
(2) Patients who develop hyperglycemia on PN or with the GVHD, check serum vitamins A and D.
addition of corticosteroids may have partial replacement of 4. Assess the adequacy of nutrition support daily during the early
dextrose with lipid calories (in the absence of hyper- postgrafting period, while maintained on enteral feedings or PN
triglyceridemia) and/or insulin added. Target glucose will support, and when transitioning to an oral diet.
depend on the clinical stability of the patient and the abil-
ity to monitor glucose/adjust insulin frequently (ie, via
insulin drip or base amount in PN with sliding-scale cov- VII. Patient and Caregiver Education
erage as discussed above). Patients on a tapering cortico- A. Discuss increased nutrient requirements during HSCT.
steroid schedule need to be monitored closely for decreased B. Review nutrient and fluid goals.
insulin needs; those on a stable alternate-day schedule C. Review nutrition support feeding modalities (ie, oral, enteral,
may be managed with a base amount of insulin in PN with and/or parenteral).
sliding-scale coverage for steroid days. D. Review safe food handling and high-risk foods to avoid.
b) Hypertriglyceridemia (ie, serum triglyceride >500 mg/dL) E. Instruct on pertinent dietary modifications.
due to medications or organ dysfunction requires reduction of 1. GI diets (Table 13-3)13
IV lipids to 4% to 8% of total energy. 2. Corticosteroid-induced hyperglycemia (see Section III.G.3.a)
c) Essential fatty acid deficiency occurs rapidly in patients sup- 3. Osteoporosis prevention (see Section III.F.5)
ported without lipids. Only in patients with grossly lipemic F. Discuss dietary guidelines for managing common posttransplant
serum should lipids be withheld entirely. nutrition problems (Table 13-1).6
d) Cholestasis and gallbladder sludge occur several weeks after G. Establish a mechanism for nutrition follow-up as needed.
HSCT in patients on PN. Specialized pediatric amino acid solu-
tions should be used in infants and can be considered in chil-
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1. Horowitz MM. Uses and growth of hematopoietic cell transplantation. In:
ursodiol is recommended, along with initiation of oral or enteral
Blume KG, Forman SJ, Appelbaum FR, eds. Thomas’ Hematopoietic Cell
feeds as soon as possible.
Transplantation. 3rd ed. Malden, MA: Blackwell Publishing; 2004:9–15.
e) Infections are higher in patients on PN.57,58 While bacteremia 2. Clarkson JE, Worthington HV, Eden OB. Interventions for preventing oral
may be treatable, in allogeneic patients infections may activate mucositis for patients with cancer receiving treatment [Cochrane Review].
life-threatening flares of GVHD. Transition to enteral feeds The Cochrane Library. 2003;issue 3.
should be considered in patients with recurring infections. 3. Pedersen AM, Bardow A, Beier Jensen S, Nauntofte B. Saliva and gastro-
(1) Glutamine-enriched PN solutions have been recommended intestinal functions of taste, mastication, swallowing and digestion. Oral
to reduce infectious complications,59 but larger, controlled Dis. 2002;8:117–129.

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4. Barale KV, Aker SN, Martinsen CS. Primary taste thresholds in children 28. Schimmer AD, Mah K, Bordeleau L, et al. Decreased bone mineral density
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1982;6:287–290. row Transplant. 2001;28:387–391.
5. Charuhas PM, Fosberg KL, Bruemmer B, et al. A double-blind randomized 29. Kiss TL, Abdolell M, Jamal N, et al. Long term medical outcomes and qual-
trial comparing outpatient parenteral nutrition with intravenous hydration: ity of life assessment of patients with chronic myeloid leukemia followed
effect on resumption of oral intake after marrow transplantation. J Parenter at least 10 years after allogeneic bone marrow transplantation. J Clin Oncol.
Enteral Nutr. 1997;21:157–161. 2002;20:2334–2343.
6. Charuhas PM. Introduction to marrow transplantation. Oncol Nutr Diet 30. Fink JC, Leisenring WM, Sullivan KM, et al. Avascular necrosis following
Pract Group Newsletter. 1994:2:2–9. bone marrow transplantation: a case control study. Bone. 1998;22:67–71.
7. Shulman HM, Hinterberger W. Hepatic veno-occlusive disease—liver tox- 31. Zeitler PS, Travers S, Kappy MS. Advances in the recognition and treat-
icity syndrome after bone marrow transplantation. Bone Marrow Trans- ment of endocrine complications in children with chronic illness. Adv Pedi-
plant. 1992;10:197–214. atr. 1999;46:101–149.
8. Vogelsang GB, Dalal J. Hepatic venoocclusive disease in blood and bone mar- 32. American College of Rheumatology Ad Hoc Committee on Glucocorti-
row transplantation in children: incidence, risk factors, and outcome. J Pedi- coid-Induced Osteoporosis. Recommendations for the prevention and treat-
atr Hematol Oncol. 2002;24:706–709. ment of glucocorticoid-induced osteoporosis 2001 update. Arthritis Rheum.
9. Sullivan KM. Graft-vs-host disease. In: Blume KG, Forman SJ, Appelbaum 2001;44:1496–1503.
FR, eds. Thomas’ Hematopoietic Cell Transplantation. 3rd ed. Malden, 33. Brennan BM, Shalet SM. Endocrine late effects after bone marrow trans-
MA: Blackwell Publishing; 2004:635–664. plant. Br J Haematol. 2002;118:58–66.
10. Vogelsang GB, Lee L, Bensen-Kennedy DM. Pathogenesis and treatment 34. Shalet SM, Brennan BMD. Growth and growth hormone status after a bone
of graft-versus-host disease after bone marrow transplant. Ann Rev Med. marrow transplant. Hormone Res. 2002;58(suppl 1):86–90.
2003;54:29–52. 35. Darzy KH, Shalet SM. Radiation induced growth hormone deficiency. Hor-
11. Bhushan V, Collins, RH. Chronic graft-vs-host disease. JAMA. 2003;290: mone Res. 2003;59(suppl 1):1–11.
2599–2603. 36. Lenssen P, Aker SN. Adult hematopoietic stem cell transplantation. In:
12. Lenssen P, Sherry ME, Cheney CL, et al. Prevalence of nutrition-related Hasse JM, Blue LS, eds. Comprehensive Guide to Transplant Nutrition.
problems among long-term survivors of allogeneic marrow transplantation. Chicago, IL: American Dietetic Association; 2002:123–152.
J Am Diet Assoc. 1990;90:835–842. 37. Altman PL, Dittmer DS. Metabolism. Bethesda, MD: Federation of Amer-
13. Gauvreau JM, Lenssen P, Cheney CL, et al. Nutritional management of ican Societies for Experimental Biology; 1968.
patients with intestinal graft-versus-host disease. J Am Diet Assoc. 38. Harris JA, Benedict FG. Biometric Studies of Basal Metabolism in Man.
1981;79:673–677. Publication 279. Washington, DC: Carnegie Institution; 1919.
14. Seattle Cancer Care Alliance. Hematopoietic Stem Cell Transplantation 39. Geibig CB, Owens JP, Mirtallo JM, et al. Parenteral nutrition for marrow
Nutrition Care Criteria. 2nd ed. Seattle, WA: Seattle Cancer Care Alliance; transplant recipients: evaluation of an increased nitrogen dose. J Parenter
2002. Enteral Nutr. 1991;15:184–188.
15. Byrnes JJ, Hussein AM. Thrombotic microangiopathic syndromes after 40. Peters E, Beck J, Lemaistre C, et al. Changes in resting energy expenditure
bone marrow transplantation. Cancer Invest. 1996;14:151–157. (REE) during allogeneic bone marrow transplantation (ABMT) [abstract].
16. Elliott MA, Nichols WL. Thrombotic thrombocytopenic purpura and Am J Clin Nutr. 1990;51:521.
hemolytic uremic syndrome. Mayo Clinic Proc. 2001;76:1154–1162. 41. American Medical Association, Department of Foods and Nutrition. Mul-
17. Suehiro T, Masutani K, Yolotama M, et al. Diffuse proliferative glomeru- tivitamin preparations for parenteral use: a statement by the nutrition advi-
lonephritis after bone marrow transplantation. Clin Nephrol. 2002;58: sory group. J Parenter Enteral Nutr. 1979;3:258–262.
231–237. 42. American Medical Association. Guidelines for essential trace element
18. Hathcock JN, Hattan DG, Jenkins MY, et al. Evaluation of vitamin A toxi- preparations for parenteral use: a statement by the nutrition advisory group.
city. Am J Clin Nutr. 1990;52:183–202. J Parenter Enteral Nutr. 1979;3:263–267.
19. Vitamin A toxicity. Med Lett Drugs Ther. 1980;22:19–20. 43. Gordon LI, Brown SG, Tallman MS, et al. Sequential changes in serum iron
20. Gleghorn EE, Eisenberg LD, Hack S, et al. Observations of vitamin A tox- and ferritin in patients undergoing high-dose chemotherapy and radiation
icity in three patients with renal failure receiving parenteral alimentation. with autologous bone marrow transplantation: possible implications for
Am J Clin Nutr. 1986;44:107–112. treatment-related toxicity. Free Radic Biol Med. 1995;18:383–389.
21. Story DA, Ronco C, Bellomo R. Trace element and vitamin concentrations 44. Adrogué HJ, Madias NE. Hypernatremia. New Engl J Med. 2000;342:
and loss in critically ill patients treated with continuous venovenous 1493–1499.
hemofiltration. Crit Care Med. 1999;27:220–223. 45. American Society for Parenteral and Enteral Nutrition. Guidelines for the
22. Fortin MC, Amyot SL, Geadah D, Leblanc M. Serum concentrations and use of parenteral and enteral nutrition in adult and pediatric patients. J Par-
clearances of folic acid and pyridoxal—5′-phosphate during venovenous enter Enteral Nutr. 2002;1S:83SA–85SA; 124SA–126SA.
continuous renal replacement therapy. Intensive Care Med. 1999;25: 46. Moody K, Charlson ME, Finlay J. The neutropenic diet: what’s the evi-
594–598. dence. J Pediatr Hematol Oncol. 2002;24:717–721.
23. Maxvold NJ, Smoyer WE, Custer JR, Bunchman TE. Amino acid loss and 47. Sefcick A, Anderton D, Byrne JL, et al. Naso-jejunal feeding in allogeneic
nitrogen balance in critically ill children with acute renal failure: a prospec- bone marrow transplant recipients: results of a pilot study. Bone Marrow
tive comparison between classic hemofiltration and hemofiltration with Transplant. 2001;28:1135–1139.
dialysis. Crit Care Med. 2000;28:1161–1165. 48. Lenssen P, Bruemmer B, McDonald GB, Aker S. Nutrient support in
24. Frankenfield DC, Reynolds HN. Nutritional effect of continuous hemo- hematopoietic cell transplantation. J Parenter Enteral Nutr. 2001;25:219–228.
diafiltration. Nutrition. 1995;11:388–393. 49. Eagle DA, Gian V, Lauwers GY, et al. Gastroparesis following bone mar-
25. Klein CJ, Moser-Veillon PB, Schweitzer M, et al. Magnesium, calcium, row transplantation. Bone Marrow Transplant. 2001;28:59–62.
zinc, and nitrogen loss in trauma patients during continuous renal replace- 50. Roberts SR, Miller JE. Success using PEG tubes in marrow transplant
ment therapy. J Parenter Enteral Nutr. 2002;26:77–93. recipients. Nutr Clin Pract. 1998;13:74–78.
26. Lenssen P, Bruemmer B, Bowden RA, et al. Intravenous lipid dose and inci- 51. Pedersen AM, Kok K, Petersen G, et al. Percutaneous endoscopic gastros-
dence of bacteremia and fungemia in patients undergoing bone marrow tomy in children with cancer. Acta Paediatr. 1999;88:849–852.
transplantation. Am J Clin Nutr. 1998;67:927–933. 52. Barron MA, Duncan DS, Green GJ, et al. Efficacy and safety of radiologi-
27. Cohen A, Shane E. Osteoporosis after solid organ and bone marrow trans- cally placed gastrostomy tubes in paediatric haematology/oncology
plantation. Osteoporos Int. 2003;14:617–630. patients. Med Pediatr Oncol. 2000;34:177–182.

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53. Langdana A, Tully N, Molloy E, et al. Intensive enteral nutrition support in 57. Weisdorf SA, Lysne J, Wind D, et al. Positive effect of prophylactic total
paediatric bone marrow transplantation. Bone Marrow Transplant. 2001;27: parenteral nutrition on long-term outcome of bone marrow transplantation.
741–746. Transplantation. 1987;43:833–838.
54. Szeluga DJ, Stuart RK, Brookmeyer R, et al. Nutritional support of bone 58. Lough M, Watkins R, Garden OJ, et al. Parenteral nutrition in bone marrow
marrow transplant recipients: a prospective randomized clinical trial com- transplant recipients. Clin Nutr. 1986;9:97–102.
paring total parenteral nutrition to an enteral feeding program. Cancer Res. 59. Murray SM, Pindoria S. Nutrition support in bone marrow transplant
1987;47:3309–3316. patients [Cochrane Review]. The Cochrane Library, 2002;issue 3.
55. Hopman GD, Pena EG, Le Cessie S, et al. Tube feeding and bone marrow 60. Pytlik R, Penes P, Patorkova M, et al. Standardized parenteral alanyl-
transplantation. Med Pediatr Oncol. 2003;40:375–379. glutamine dipeptide supplementation is not beneficial in autologous trans-
56. Papadopoulou A, MacDonald A, Williams MD, et al. Enteral nutrition after plant patients: a randomized, double-blind, placebo controlled study. Bone
bone marrow transplantation. Arch Dis Child. 1997;77:131–136. Marrow Transplant. 2002;30:953–961.

© 2005 A.S.P.E.N. www.nutritioncare.org. A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. 199
SECTION EDITOR
Mark DeLegge, MD
III
Gastrointestinal Related
Conditions

14 Diarrhea

15 Pancreatic Disease

16 Inflammatory Bowel Disease

17 Liver Disease

18 Neurologic Diseases
 Mark R. Corkins, MD, CNSP, FAAP;
James Scolapio, MD, CNSP
14
Diarrhea

Introduction 7. Diarrhea can be classified as osmotic, hypersecretory, mal-

absorptive, inflammatory, and dysmotility related.
Diarrhea is a symptom of a variety of diseases. Many steps are required 8. Initial examination of the stool for blood, white blood cells, and
to break down the food we ingest into the basic building blocks that are fat globules is helpful.
metabolized or used by our bodies. A failure in one of the many com- 9. Red and white cells in the stool suggest an inflammatory process,
ponents of the digestive process can result in malabsorption. At the usually of the colon. Examples include Crohn’s colitis, idio-
most basic level, diarrhea is a reflection of malabsorption. One diffi- pathic ulcerative colitis, and malignancy.
culty is that this single symptom, diarrhea, can be the result of so many 10. Stool samples should be tested for pathological organisms,
different processes and that these etiologies may require dramatically including ova and parasites, and C diff toxin (made by the organ-
different treatments and nutritional approaches. ism Clostridium difficile).
11. Diarrhea that is purely hypersecretory (bile salt induced, hor-
I. General Principles monally mediated); osmotic (disaccharidase deficiency, laxative
II. Acute Diarrhea abuse); dysmotility related (irritable bowel, diabetic, post-
III. Chronic Diarrhea surgical); or malabsorptive (celiac disease, bacterial overgrowth,
References pancreatic disease, Whipple’s disease, tropical sprue) usually
does not present with blood or white cells in the stool.
I. General Principles 12. Other fecal testing that is commonly done in the pediatric popu-
lation includes the Clinitest for reducing substances (detects most
A. Epidemiology unabsorbed dietary carbohydrates except sucrose) and stool pH
1. The best estimate for children under age 5 years in the United to detect fermentation of unabsorbed carbohydrates.
States is 3.2 episodes of diarrhea a year.1,2
13. Clinitest-positive stools with low pH indicate that the small intes-
2. Because children become dehydrated more frequently than
tine is not digesting and absorbing dietary carbohydrates. This
adults, the economic impact of diarrhea is also higher in children.
can be due to a variety of causes, including viral enteritis and con-
In a survey of a large privately insured population, diarrhea
genital enzyme deficiencies.
accounted for 4% of all hospitalizations and 2% of all outpatient
14. If malabsorption is suspected, a 72-hour collection for stool vol-
visits in children under 5 years of age.3
ume and fecal fat should be performed while the adult patient is
3. Acute diarrhea of short duration is not life-threatening in the United
on a 100-g fat diet. In children, no specific diet is recommended,
States, where good nutrition predominates. In other areas of the
world, diarrhea is the leading killer of malnourished children. but a 3-day diet record is kept. The grams of fat consumed are
4. Worldwide, diarrhea accounts for 21% of all deaths in children then calculated for the 72 hours of the collection.
less than 5 years of age, which represents 2.5 million deaths a 15. Steatorrhea in adults is defined as fat excretion of greater than
year.1 7 grams/24 hours. If greater than 7 g of fecal fat is found, further
5. Persistent diarrhea is always a clinical concern because it can testing is required for a specific diagnosis. In children, the grams
lead to malnutrition. of fat in the stool and the grams of fat consumed are used to cal-
B. Diagnostic evaluation culate a percentage of fat lost. In children under 6 months of age,
1. Diarrhea is defined as 250 mL of stool per day, or ≥3 loose up to 15% of dietary fat can be excreted normally; after this age,
stools a day,4 or total fluid loss in the stool greater than 10 mL/ the excretion should be less than 7%.6
kg/day in children.5 16. Testing may also include an upper endoscopic small-bowel
2. Chronic diarrhea is diarrhea that lasts longer than 2 weeks. biopsy for histopathology as well as a small-bowel aspirates to
3. Fecal urgency and incontinence are different from diarrhea. rule out bacterial overgrowth.
4. Having patients chart stool frequency and volume is often a 17. If chronic pancreatic insufficiency is thought to be causing the
helpful start in the diagnostic process. malabsorption, a sweat chloride test (in pediatric patients)
5. Associated symptoms are also very important in making a diag- and/or a duodenal aspirate should be obtained after intravenous
nosis. Weight loss and oily stool would suggest a malabsorptive (IV) administration of either cholecystokinin or secretin.
process. 18. Stool osmolality can also give a general idea of the etiology of
6. Other important historical data include previous gastrointestinal the diarrhea. The stool cannot have an osmolality less than that
surgical history (eg, short-bowel syndrome, bacterial over- of serum, even if secretory. If it does, the sample may have been
growth); previous abdominal radiation treatment; and travel, tampered with in some manner. The values to use are as follows7:
sexual, medication, and family history. a) Normal: mean stool osmolality 275–290 mOsm/kg water

© 2005 A.S.P.E.N. www.nutritioncare.org. A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. 203
S E C T I O N I I I Gastrointestinal Related Conditions

b) Osmotic diarrhea: mean stool osmolality 400 mOsm/kg water and other helminths can also cause a long-standing diarrhea that
c) Secretory: mean stool osmolality 280 mOsm/kg water will require treatment.
19. A small-bowel x-ray can reveal a number of abnormalities asso- B. Antibiotics and drugs
ciated with malabsorption, such as Crohn’s disease, jejunal diver- 1. One drug-associated cause of diarrhea is abuse of stool softeners
ticulosis, radiation enteritis, and infiltrative disease of the small and laxatives. Many of over-the-counter antacids can also result
intestine. A complete blood cell count and chemistry panel should in diarrhea, as can promotility agents such as metoclopramide and
also be checked in patients with chronic diarrhea. Further labo- erythromycin.
ratory testing should be based on clinical suspicion of a specific 2. Osmolality is an important potential cause of diarrhea. A survey of
disease process. 58 commercially available solutions and suspensions found that 56
20. The role of capsule endoscopy in the workup of chronic diarrhea had an osmolality greater than 1000 mOsm/kg.12 Many pediatric
is not well defined. suspensions are made with syrups containing sorbitol, which can
lead to osmotic diarrhea. In a report of adults in an intensive care unit
receiving IV aminophylline or an oral solution containing sorbitol,
II. Acute Diarrhea
the IV patients had diarrhea only 4% of the hospital days compared
A. Infectious diarrhea to 43% of the patients on the oral solution.13
1. By far the most common cause of acute diarrhea is viral gastro- 3. The common occurrence of diarrhea during antibiotic therapy is
enteritis. well recognized. A recent study of children on antibiotics found
2. The damage to the enterocytes results in a temporary malabsorp- that 11% developed diarrhea; this increased to 18% in children
tion with diarrhea. less than 2 years of age.14 It is widely believed that the antibiotics
3. The most common viral pathogens are rotavirus, enteric ade- alter the natural anaerobic flora of the gastrointestinal tract.15
novirus, Norwalk virus, calicivirus, and astrovirus.8 There are 4. C difficile accounts for 10% to 20% of antibiotic-associated diar-
rapid stool antigen tests for rotavirus and adenovirus. rhea.15 C diff produces toxins that are responsible for pseudomem-
4. Bacterial causes are usually diagnosed by stool culture. Dis- branous colitis, which can occur with use of both oral and IV
covering the etiology of most viral and bacterial causes is not antibiotics. Most cases are mild and resolve in 2 to 3 weeks.
crucial, as the treatment is largely supportive. 5. The diagnosis is made by obtaining a stool cytotoxin test for the
5. Nutrition support of infectious diarrhea first focuses on restoring B toxin.
hydration. 6. The first response is discontinuation of the antibiotic if possible.
6. Recent guidelines for treatment of children with diarrhea have When symptoms are persistent or severe, metronidazole 250 to
been uniform in their recommendations.4,9,10 If a child presents 500 mg (30 mg/kg/day in children) 3 to 4 times per day for 10 days
clinically dehydrated, the first step, if clinically reasonable, is an is the drug of choice.
oral rehydration solution; hydration can usually be completed in 7. A recent meta-analysis has supported the use of probiotics to pre-
less than 4 hours. vent antibiotic-associated diarrhea.16
7. Severe dehydration should be initially treated with IV fluid 8. A randomized trial also has suggested that adults given regular
replenishment, but even then, once the patient has improved, intake of yogurt (227 g twice a day) containing active cultures
oral rehydration can be attempted. had a reduced incidence of antibiotic-associated diarrhea.17 An
8. Following rehydration, the recommendations in acute diarrhea infant formula with fiber has been used to firm up loose stools in
are to return to a normal diet as soon as possible.4,9,10 Breast-fed this situation.
infants should continue breast-feeding. Formula-fed infants C. Enteral feeding
should continue to receive full-strength formula. In most situa- 1. Diarrhea is one of the most common complications reported
tions, no benefit has been shown of using lactose-free formulas. with enteral feeding, occurring in up to 30% of patients.
Older children and adults should resume appropriate solids with- 2. The causes include the concurrent use of antibiotics, C difficile
out restriction.4 toxin, antacids, or the use of sorbitol-based liquid medications
9. Food-borne illnesses often present with diarrhea. These ill- and magnesium in the formula.
nesses arise from consumption of raw or poorly cooked food as 3. Prior to investigation of the cause of the diarrhea, the amount
well as unpasteurized milk or juices, home-canned goods, fresh of stool volume should be determined, since stool incontinence
produce, or soft cheeses made from unpasteurized milk.11 The is often reported as diarrhea even when the volume is less than
diarrhea is caused by toxins produced by the bacteria in the food 200 mL/day.
or by the contaminating agents themselves. The incubation time 4. Two reviews of this subject found that for the overwhelming
for these illnesses ranges from several hours to several days. majority of patients on enteral feedings, the cause of the diarrhea
The diagnosis is suggested by a careful history of the patient’s was not the formula, even if the formula was hypertonic.18,19
dietary intake. 5. Careful review of the patient’s current medical record, includ-
10. For the majority of these patients, the recommended treatment is ing medications, is very important.
supportive care to maintain hydration, usually with oral hydra- 6. Bacterial contamination of the enteral formula has been reported
tion.11 The nutritional therapy is the same as for other infectious to cause colonization of the intestinal tract and diarrhea. This
causes of diarrhea. problem can be minimized by proper formula handling, includ-
11. In persistent diarrhea, a parasite must be suspected and the ova ing limiting infusion time or hang time to 8 to 12 hours. A closed
and parasite screen should be performed. It is important to iden- delivery system has also been shown to significantly reduce the
tify these, as treatment can prevent malnutrition and shorten the risk of formula contamination.
course of illness. 7. If the formula is thought to be the culprit after other causes have
12. There are rapid antigen tests for Giardia and Cryptosporidia, the been excluded, then the formula can be changed to help man-
most common parasites. Various types of tapeworms, amoeba, age this problem.

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8. Confusion still exists regarding the dilution of a hypertonic for- 4. Deficiencies of fat-soluble vitamins A, D, E, and K; iron; folic
mula and the development of diarrhea. When the formula is fed acid; and calcium are also common.
into the stomach, the osmolarity of the formula should not mat- 5. This disorder is much more common in persons of Northern
ter. Occasionally, feeding a hypertonic formula into the small European extraction, who tend to carry certain human leukocyte
intestine may cause diarrhea. antigen (HLA) types, including DQw2.28 Population-based sero-
9. Starting the infusion slowly usually suffices, and dilution of logic surveys have noted a prevalence of celiac disease of 1 in 250
the formula is rarely needed. Changing to a different formula to 500 individuals in most countries studied, including the United
(ie, a fiber-based formula) may be helpful in some cases of States. Siblings who share the specific HLA type of DQw2 have
tube feeding–related diarrhea. a 40% likelihood of concordance for celiac disease; monozygotic
10. Using antidiarrheal agents while continuing tube feeds is help- twins have a 70% concordance.
ful in many cases. 6. Several other disease associations have been described, primarily
11. Patients should not be switched to parenteral nutrition for with juvenile-onset diabetes, short stature, cystic fibrosis, and
tube feeding–related diarrhea unless the above-mentioned Down’s syndrome.29
approaches fail. 7. The most important environmental factor in celiac disease is
D. Allergic disorders gluten. The harmful proteins are gliadins (wheat), hordeins (bar-
1. Diarrhea can be one of the manifestations of food allergy. ley), and secalins (rye).
2. The most common allergy is cow’s milk allergy in infants. 8. This disorder can show up at any age after the introduction of
3. The frequency of food allergies is highest the first several years of gluten-containing foods, although the peak is during the first and
life, with an estimated 6% to 8% of children affected in the first second years of life.30
year of life.20 The incidence falls with age to the adult level of 1% 9. Breast-feeding may reduce the likelihood of the infant develop-
to 2%. ing celiac disease at an early age.
4. In developed countries, the incidence of cow’s milk allergy in 10. Patients with celiac disease have a loss of their intestinal villi as
infants is 2% to 5% of all infants.21 These infants often present with a result of the inflammatory cross-reaction, with resultant mal-
other symptoms besides diarrhea, including gastroesophageal absorption. The inflammatory response consists of increased
reflux, blood in the stool (visible or detected during testing), and numbers of T lymphocytes, plasma cells, and macrophages in
irritability. the lamina propria and increased numbers of lymphocytes in the
5. Most infants develop symptoms shortly after the introduction of surface layer of the epithelium. The changes may be patchy and
cow’s milk–based formula.21 Some infants appear to be sensitized affect a variable length of small bowel.
before birth and will even develop a reaction to the small quanti- 11. The villi are shortened and flattened, and the crypts are increased
ties of milk protein present in human breast milk. Nearly 100% of in depth.
infants resolve this gastrointestinal allergy by 2 years of age, and 12. In addition to the malabsorptive symptoms, including diarrhea
the majority do so before their first birthday.22 and weight loss, atypical clinical presentations of celiac disease
6. Therapeutically, the logical first step is a trial of soy formula. include isolated iron deficiency anemia (with or without heme-
7. Only about half of infants with cow’s milk–induced enteritis or positive stool), osteoporosis, stunting of growth in children,
colitis will respond to soy formula.23 The American Academy of tetany, infertility, dementia, and dermatitis herpetiformis (bullous
Pediatrics (AAP) recommends that such infants be treated with a skin rash).
hydrolyzed cow’s milk formula. 13. Although very good antibody tests are now available, the gold
8. A small subset of infants mount an immune response even to standard for diagnosis continues to be the histological demon-
the hydrolyzed formulas and require feedings with an amino stration of the characteristic lesion in the small intestine and the
acid–based formula.24–26 subsequent clinical response to a gluten-free diet.
9. One important point is that these infants are not lactose intolerant 14. Serological testing offers methods to screen individuals suspected
(in the absence of severe enteropathy) and do not have an immune of having celiac disease without the need for invasive endoscopy.
response to lactose.27 A milk-based lactose-free formula contains Of the serological antibodies, the immunoglobulin A (IgA)
the proteins of the standard formulas, and using this type of for- endomysial antibody (an indirect immunofluorescent assay) is the
mula will not resolve the problem. most sensitive and specific for the diagnosis of celiac disease.
15. Endomysial IgA antibody titers diminish with the institution of
a gluten-free diet, often within weeks, and by 6 months may be
III. Chronic Diarrhea (Cystic fibrosis and inflamma-
undetectable.
tory bowel diseases are covered in Chapters 15
16. The therapy for celiac disease is both simple and difficult. The
and 16, respectively.)
institution of gluten-free diets should result in prompt and often
A. Celiac disease dramatic improvements in patient’s symptoms. Recovery appears
1. Celiac disease, also known as gluten-sensitive enteropathy, is to be more rapid in children.
characterized by inflammation of the small-intestine mucosa 17. Dietary advice from a dietitian experienced in gluten-free diets
that results from a genetically based immunologic intolerance is very important to the treatment of patients with celiac disease.
to ingested gluten. Patients should also take an active role in self-education.
2. This disorder is now known to arise due to a cross-reaction 18. There are celiac disease support groups and volumes of infor-
between the gluten protein of certain cereal grains and the mation regarding celiac disease via the Internet. Patients need
human enzyme transglutaminase.28 to understand that the disease is lifelong and requires a lifetime
3. The inflammation occurring in celiac disease typically produces of avoidance of gluten protein.
a malabsorptive syndrome, with diarrhea, steatorrhea, and loss 19. Gluten is normally found in products containing wheat, barley,
of weight or failure to thrive. or rye.28 Other grains are acceptable but may be contaminated

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S E C T I O N I I I Gastrointestinal Related Conditions

during production at facilities that also process wheat, barley, or mum of 25 g a day in adults.31 When starting to take fiber,
rye (Table 14-1). patients may complain of bloating or diarrhea. This usually
20. Secondary lactose intolerance is common but usually resolves improves with time.
once the damage to the small intestine is healed. Folate defi- 11. Foods high in undigestible carbohydrates, such as beans, cab-
ciency is also common. bage, and brussels sprouts, should be avoided.
21. Specific minerals such as iron, calcium, and magnesium may 12. Because lactase deficiency may produce symptoms similar to
need to be replaced if deficient. Rarely, a celiac patient will those of IBS, a trial of lactose restriction would also be indi-
develop refractory disease. Noncompliance with a gluten-free cated. (See Section III.D.)
diet should first be considered as the cause. 13. Other dietary factors may also exacerbate IBS symptoms, includ-
22. Other causes of refractory celiac symptoms include T-cell small- ing excess use of alcohol or coffee, or diets that contain sorbitol.
bowel lymphoma, collagenous sprue, and ulcerative jejunoileitis. C. Toddler’s diarrhea (chronic nonspecific diarrhea, irritable colon of
Endoscopic, radiographic, and surgical testing is often required childhood)
to make these diagnoses. 1. This is a common presentation to pediatric caregivers during the
23. Occasionally, a patient with refractory celiac disease will require toddler years.
parenteral nutrition (PN). 2. This is a functional disorder. The Rome criteria define it as daily
B. Irritable bowel syndrome passage of three or more large, unformed stools, for 4 or more
1. Irritable bowel syndrome (IBS) is a diagnosis of exclusion. The weeks, with onset in infancy or preschool years. There is no evi-
diagnosis can often be made on the basis of the history, physi- dence of poor weight gain if the diet is adequate.32
cal examination, and simple blood screening. 3. The common presentation is a toddler who has a normal to
2. Chronic, nonprogressive symptoms of abdominal pain; alter- slightly increased frequency of extremely liquid stools but is
nating diarrhea and constipation in the absence of nocturnal otherwise normal to examination and healthy by history.
symptoms; weight loss; fever; anemia; or blood in the stool 4. The child has normal growth and development despite having
should raise the possibility of this diagnosis. what the parents often describe as “explosive” stools that often
3. The etiology is unknown, but IBS is most likely related to some contain recognizable vegetable and other food particles.33
form of disordered gastrointestinal motility. In children, this is 5. It is believed that this diarrhea arises because meals fail to inter-
often associated with some dyspepsia. rupt the migrating motor complex.32
4. Symptoms reported more commonly in IBS patients include relief 6. Some authorities believe toddler’s diarrhea is more common in
of abdominal pain with bowel movements, increased mucus on patients with a family history of IBS.33
the stool, and the sensation of incomplete evacuation of stool. 7. A major contributor to this disorder is the intake of fluids with a
5. Psychosocial factors, including anxiety, depression, and stres- high carbohydrate level. Parents often believe that older infants
sors, often worsen symptoms. and toddlers need to drink juice, and juices, soft drinks, or pow-
6. In older patients, a colonic neoplasm must always be excluded. dered drinks (all liked for their sweet taste) can come to replace
7. Celiac disease should also be excluded. Many patients who are higher-quality liquids in the diet.
labeled as having IBS are later found to have celiac disease. 8. The diagnosis is supported by a thorough dietary history, includ-
8. Dietary therapy for IBS, especially in children with dyspepsia, ing assessment for overfeeding, fruit juice/sorbitol intake, and
may be helpful. Dietary triggers, including fried foods, spicy excessive dietary reliance on carbohydrates rather than fats.32,34
foods, high-fat foods, and carbonated and caffeinated beverages 9. The initial dietary therapy is to eliminate these fluids com-
should be avoided.31 pletely from the toddler’s diet (although it is crucial that the par-
9. Another dietary intervention that has been shown to be very ents not create a highly restrictive diet).34 Elimination normally
helpful is increased dietary intake of fiber in the form of bran, results in a dramatic improvement in the patient’s stools.
or use of commercial fiber preparations such as psyllium or 10. A high-fat, low-carbohydrate diet is recommended to reduce the
methylcellulose. intestinal motility.33 This includes restarting whole milk, the food
10. Fiber is usually prescribed based on a patient’s age. The ini- that has often been removed from the patient’s diet. The symp-
tial dosage is approximately 5 g a day, increasing to a maxi- toms resolve by the time the child reaches school age.32
D. Lactose intolerance
1. Lactase deficiency is the most common disaccharidase deficiency.
2. Because lactose cannot be hydrolyzed and absorbed, it passes
TABLE 14-1. Celiac Disease Diet into the colon, where osmotically active substances are formed
that induce diarrhea.
Do Not Eat Do Eat Caution Advised 3. Infants born at term have adequate lactase levels in the brush
border cells of the small intestine to digest the lactose found in
Wheat (all types) Plain rice Processed foods human breast milk.
Barley (including wild) Oats (contaminated 4. Congenital lactase deficiency is an extremely rare autosomal
recessive disease that results in severe diarrhea and weight loss
Soy sauce (made Tapioca mills)
in early infancy.
with wheat) Potato Pharmacy products
5. In most populations, the lactase level normally declines after
Licorice Legumes (binder) infancy.
Prepared soups Soy Cold cuts 6. In some ethnic groups, this developmental lactase deficiency is
Prepared sauces Corn Caramel coloring more common. People of African, Asian, and South American
and dressings Spice extracts heritage tend to exhibit lactase deficiency more often than do
people from other cultures.

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7. A temporary secondary lactase deficiency may occur following gastric tube). The volume of drip feedings is initially low and is
acute gastroenteritis in children. Secondary lactase deficiency can advanced according to patient tolerance. Tolerance can be
also occur in other disease processes of the intestinal mucosa, assessed by measuring the volume of stool and the amount of
such as celiac disease, short-bowel syndrome, and inflammatory carbohydrate in the stool via the Clinitest method for reducing
bowel disease. substances.
8. Clinical symptoms following the intake of milk or milk products 12. In extreme cases, PN may be needed until the mucosa is able to
include abdominal bloating, increased flatus, nausea, and some- reconstitute itself and the patient can be transitioned off PN to
times loose to watery stools. full-drip enteral feeds, then to intermittent bolus feedings, and
9. Weight loss and wasting is not part of this clinical entity, unless eventually to completely oral intake.
associated with an underlying disorder. 13. This disorder is normally transient, with complete resolution
10. The hydrogen breath test is the most accurate indirect method eventually; the goal is to prescribe the least invasive therapy
for detecting lactase deficiency. Breath hydrogen is measured at possible.
30- to 60-minute intervals for 2 to 4 hours following a 50-gram F. Short-bowel syndrome
oral lactose dose. A sustained rise in breath hydrogen of greater 1. Short-bowel syndrome is a collection of signs and symptoms
then 20 ppm above baseline indicates lactose malabsorption. occurring after intestinal resection and characterized by weight
11. Patients may also note symptoms during lactose administration, loss, malabsorption of fluids, and malabsorption of micro- and
which supports the diagnosis. macronutrients.
12. Lactase levels can be directly measured in small intestinal biopsy a) In adults, the most common etiologies include small-bowel
samples from patients who undergo endoscopic procedures. resection for Crohn’s disease and vascular events such as
13. Patients with mild symptoms can manage the condition by reduc- acute mesenteric ischemia.
ing the amount of milk products in their diets. Patients with more b) In adults, the normal small intestine is approximately 600 cm
severe symptoms may need to ingest only milk products with in length and the colon, approximately 150 cm.
enzymatic products added or to eliminate lactose from their diets. c) The incidence of short-bowel syndrome is split almost evenly
E. Intractable/protracted diarrhea of infancy between pediatric and adult populations.38 The etiologies are
1. There is a small subset of infants who, after a significant different in pediatric cases. The leading causes in pediatric
gastrointestinal illness, have persistent diarrhea (lasting more cases are intestinal volvulus, intestinal atresia, necrotizing
than 2 weeks). enterocolitis, and complications of gastroschisis.38
2. The diffuse mucosal injury that is present is believed to arise d) Patients with a preserved colon had lower fecal volumes and
either from formula protein intolerance or following an infectious fecal energy loss than patients without a colon.39
e) Patients with less than 150 to 200 cm of remaining small
enteritis.33,35
intestine without a colon may have significant energy and
3. This injury can result in secondary formula-protein intolerance
fluid losses and may require PN for survival.
and a mild inflammation with mild malabsorption.33,35 The mal-
f) Patients with a partial or complete remaining colon in conti-
absorption is frequently manifested by the presence of carbo-
nuity with the small intestine may not have significant fluid
hydrates in the stool, noted by a positive Clinitest.
and energy loss until less than 50 to 70 cm of the small bowel
4. Once there is malabsorption, malnutrition may quickly develop.
remains. With shorter lengths, patients may require PN for
Malnutrition may place the patient at risk for infections and
survival.
repeated mucosal injury, resulting in a vicious cycle.
g) In infants, the crucial factor determining small-bowel length
5. This disorder has been renamed “protracted diarrhea of infancy”
needed is the ileocecal valve. If the valve is present, survival
by some authorities to differentiate it from disorders in which is possible with 20 to 40 cm of intestine; if not, greater than
infants truly have unrelenting (and thus intractable) diarrhea.36 40 cm is usually required.38 Survival of infants with less than
6. Other disorders such as autoimmune enteropathy and congeni- 20 cm of small intestinal is rare.38
tal enterocyte disorders must be eliminated as the cause of the h) The remaining intestine can often compensate or adapt with
diarrhea.36,37 time. The results of this compensation can be observed clini-
7. Fortunately, this disorder will usually resolve with time and cally in the form of patient weight gain, reduced intestinal fluid
good nutrition. losses, and stabilization of micronutrients. These changes usu-
8. Previously, many of these infants required an extended course ally are clinically obvious approximately 3 months after intes-
of PN. The development of hydrolysate and amino acid–based tinal resection and may continue for years.
formulas has made this approach unnecessary for most patients. 2. Dietary management
9. PN may be required initially, but enteral feedings are crucial to a) Specific dietary recommendations should be based on the
speed the resolution of this disorder.33,35 PN is sometimes used to presence or absence of a colon. Those with a colon should
begin reversing the general malnutrition while allowing for time consume a high-carbohydrate/low-fat (HCLF) diet.
to restore the normal gastrointestinal mucosa. It is important to b) The colon can convert complex carbohydrates by bacterial
maintain normal hydration and electrolytes, including zinc. fermentation to short-chain fatty acids (acetate, propionate,
10. These infants are usually first tried on a lactose-free formula, and butyrate), which can provide a source of up to 500 calo-
most often a protein hydrolysate formula. If small amounts of ries per day.40 Also, short-chain fatty acids stimulate colonic
this formula are tolerated, the volume is advanced as tolerated. sodium and water absorption.
If the hydrolysate formula is met with evidence of intolerance, c) In patients with a colon, an HCLF diet can reduce fecal losses
then an amino acid–based formula is initiated.35 This type of of energy by 500 kcal/d compared to the low-carbohydrate/
formula is usually well tolerated. high-fat (LCHF) diet.40 In contrast, patients with end jejunos-
11. In some infants with more severe mucosal injury, a continuous tomies excrete equal amounts of calories on both types of
drip of the amino acid–based formula is necessary (via naso- diets.40–43

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S E C T I O N I I I Gastrointestinal Related Conditions

d) Use of lactose in diets of patients with short-bowel syndrome a) Octreotide, a synthetic octapeptide analogue of somatostatin,
should be individualized since most patients can tolerate dairy has many effects on the gastrointestinal tract. It reduces splanch-
products.44 nic blood flow and inhibits gastric, pancreatic, and small-bowel
e) Patients with short-bowel syndrome who have had more than secretions that inhibit intestinal adaptation and increase fecal fat
60 cm of terminal ileum resected or diseased should receive losses. All of these changes can negatively affect nutrient assim-
vitamin B12.45 For replacement, 1000 mcg should be given ilation and absorption.
intramuscularly once a month. b) In perfusion studies, it has been shown that somatostatin has no
f) Patients with colonic continuity are at increased risk of oxalate effect on jejunal absorption of sodium and water. Therefore, the
nephropathy and should be placed on low-oxalate diets if 24- improved balance is most likely the result of reduced water and
hour urinary oxalate levels are elevated. Increasing dietary cal- electrolyte secretion.
cium and using an HCLF diet may also be helpful.46 c) A double-blind, placebo-controlled study of six TPN-dependent
g) In infants, fats are better tolerated than carbohydrates and the patients with short-bowel syndrome without a colon reported
nutritional needs for fats are higher. improved sodium and fluid balance with octreotide, but TPN
h) Infants with short-bowel syndrome tend to develop formula nutrient requirements could not be reduced.59
protein allergies. The use of a hydrolysate protein formula is d) In another study, 10 patients who had been dependent on home
recommended; in rare cases, an amino acid–based formula PN (HPN) for 1 to 15 years and who had end jejunostomies and
will be required.47 The feedings should be administered con- no colons were treated in an open-labeled trial with 100 mcg of
tinuously to maximize absorption. octreotide, administered subcutaneously 3 times a day.60 Sig-
i) In infants, feeding formulas should be started as soon as possi- nificant improvement was noted in fluid (30%–40% reduction),
ble after surgery and advanced as tolerated. The measurement sodium, potassium, and chloride balance. Despite improvement
of stool volume and the amount of reducing substances (Clin- in net fluid secretion, all but one patient remained in negative
itest) are used to guide advancement.47 At the developmentally balance, and HPN could not be discontinued.
appropriate time, small amounts of oral solids should be initi- e) An open-labeled trial evaluated the effects of the long-acting
ated to prevent the child from having a feeding aversion when release analogue of octreotide during a 15-week period in eight
he or she is older.47 TPN-dependent patients with short-bowel syndrome.61 They
j) Children are susceptible to the same vitamin and mineral defi- reported no statistically significant decrease in stool weight
(despite a positive trend) or in stool sodium, potassium, or fat.
ciencies as adults, so vitamin and mineral levels should be
5. Growth hormone and glutamine
monitored and supplemented at the appropriate doses.
a) Negative studies
3. Oral rehydration solutions
(1) In a randomized, double-blind, placebo-controlled crossover
a) Most of the published success with oral rehydration solutions
study, 10 patients with short-bowel syndrome who were
(ORSs) has been in the context of treating patients with cholera,
treated for 8 weeks with subcutaneous human recombinant
in which such solutions have substantially reduced mortality.
growth hormone reported no significant changes in absorp-
b) Few data are available on ORS efficacy in short-bowel syn-
tive capacity.62
drome. The sodium concentration of the effluent is almost con-
(2) A randomized, double-blind, placebo-controlled cross-
stant, at approximately 90 mmol/L.
over study in eight patients with short-bowel syndrome
c) ORSs work by the solvent drag mechanism in the jejunum.
evaluated the effects of oral administration of glutamine
Nutrients such as glucose promote the passive absorption of
(0.45 g/kg per day) with a constant HCLF (60%:20%)
electrolytes and water. To avoid osmotically driven secretion of diet. No significant changes were seen in the measured
salt and water, solutions should be isotonic with plasma. They parameters.63
should also be balanced in sodium and glucose content to pro- (3) A randomized, double-blind, placebo-controlled crossover
mote sodium and glucose cotransport. Standard “sport drinks” study with subcutaneous human recombinant growth hor-
have a high sugar content and too little sodium. In studies in rats mone, oral glutamine, and a constant HCLF (60%:20%)
and in humans, the optimal ORS has a sodium concentration of diet for 21 days was completed in eight HPN-dependent
at least 90 mmol/L.48 patients who had short-bowel syndrome.64 There was no
d) Rice-based ORSs (such as Ceralyte [Cera Products, Colum- significant improvement in fecal volume, fecal fat, nitro-
bia, MD], 40 g of rice carbohydrate; osmolality, 225 [sodium, gen, or D-xylose absorption.
50 mmol/L], 235 [sodium 70], or 260 [sodium 90]) allow (4) A randomized, placebo-controlled, double-blind crossover
more glucose delivery to the small intestine without increas- study of eight patients with short-bowel syndrome treated
ing the osmotic load from free glucose. with their usual diets, human recombinant growth hor-
e) The addition of glutamine to a standard rehydration formula mone, and oral and parenteral glutamine for 28 days was
did not enhance sodium absorption in a study of six patients performed.65 No improvement was observed in the absorp-
with end jejunostomies.49 tion of carbohydrate, fat, or nitrogen. Stool weight and stool
f) Eight case reports50–58 showed successful results (defined as electrolytes were unchanged.
discontinuation of parenteral fluids and electrolytes) of ORSs b) Positive studies
with sodium concentrations between 77 and 116 mmol/L. The (1) An open-labeled study evaluated the effects of subcuta-
mean length of jejunum in these studies was 100 cm (range, 25– neous human recombinant growth hormone, parenteral
180 cm). Two of the patients had parts of their colon remaining: glutamine or oral glutamine, and an HCLF (60%:20%,
one still had 25 cm and one had 30 cm of small intestine. including soluble fiber) diet on eight HPN-dependent
g) Intake is often limited by palatability. Commercial products patients with short-bowel syndrome. There was a signifi-
with a better taste have been marketed. cant increase in the absorption of total calories, protein,
4. Octreotide carbohydrate, sodium, and water.66

208 A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. © 2005 A.S.P.E.N. www.nutritioncare.org.
 S E C T I O N I I I Gastrointestinal Related Conditions

(2) The open-label study of eight patients was expanded to an 9. Armon K, Stephenson T, MacFaul R, et al. An evidence and consensus based
additional 31 HPN-dependent patients. The growth hor- guideline for acute diarrhoea management. Arch Dis Child. 2001;85:132–142.
mone dose was reduced.67 At the end of the 21-day treat- 10. Sullivan PB. Nutritional management of acute diarrhea. Nutrition. 1998;14:
ment period, 57% of patients did not require TPN, 30% 758–762.
11. Tan LJ, Lyznicki J, Adcock PM, et al. Diagnosis and management of food-
had reduced TPN requirements, and 13% had no change.
borne illnesses: a primer for physicians. MMWR Recomm Rep. 2001;50:1–69.
The side effects of the treatment were minor and consisted 12. Dickerson RN, Melnik G. Osmolality of oral drug solutions and suspen-
of fluid retention and arthralgias, both of which varied sions. Am J Hosp Pharm. 1988;45(4):832–834
with the growth hormone dose. 13. Hill DB, Henderson LM, McClain CJ. Osmotic diarrhea induced by sugar-
(3) The latest prospective, randomized, double-blind, placebo- free theophylline solution in critically ill patients. J Parenter Enteral Nutr.
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alone for 3 weeks in 12 TPN-dependent patients with short- 14. Turck D, Bernet J-P, Marx J, et al. Incidence and risk factors of oral antibiotic-
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Health Organ. 2003;81:197–204. 30. Pietzak MM, Catassi C, Drago S, et al. Celiac disease: going against the
2. Kotloff KL, Wasserman SS, Steciak JY, et al. Acute diarrhea in Baltimore grains. Nutr Clin Pract. 2001;16:335–344.
children attending an outpatient clinic. Pediatr Infect Dis J. 1988;7:753–759. 31. Hyams JS. Chronic and recurrent abdominal pain. In: Hyman PE, ed. Pedi-
3. Zimmerman CM, Bresee JS, Parashar UD, et al. Cost of diarrhea-associated atric Functional Gastrointestinal Disorders. New York, NY: Academy Pro-
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dren in the United States. Pediatr Infect Dis J. 2001;20:14–19. 32. Rasquin-Weber A, Hyman PE, Cucchiara S, et al. Childhood functional
4. King CK, Glass RI, Bresee JS, et al. Managing acute gastroenteritis among gastrointestinal disorders. Gut. 1999;45(suppl 2):1160–1168.
children. MMWR Recomm Rep. 2003;52:1–16. 33. Vanderhoof JA. Chronic diarrhea. Pediatr Rev. 1998;19:418–422.
5. Guandalini S. Acute diarrhea. In: Walker WA, Durie PR, Hamilton JR, 34. Hyams JS. Diet and gastrointestinal disease. Curr Opin Pediatr. 2002;
Walker-Smith JA, Watkins JB, eds. Pediatric Gastrointestinal Disease. 3rd 14:567–569.
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6. Huynh H, Couper R. Pancreatic function tests. In: Walker WA, Durie PR, 14:775–779.
Hamilton JR, Walker-Smith JA, Watkins JB, eds. Pediatric Gastrointesti- 36. Goulet O. Intractable diarrhea of infancy. In: Walker WA, Durie PR, Hamil-
nal Disease. 3rd ed. Hamilton, Ontario: BC Decker; 2000:1515–1528. ton JR, Walker-Smith JA, Watkins JB, eds. Pediatric Gastrointestinal Dis-
7. Walker-Smith JA, Hamilton JR, Walker WA. Practical Paediatric Gas- ease. 3rd ed. Hamilton, Ontario: BC Decker; 2000:762–772.
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38. Sigalet DL. Short bowel syndrome in infants and children: an overview. 55. MacMahon RA. The use of the World Health Organization’s oral rehydra-
Semin Pediatr Surg. 2001;10:49–55. tion solution in patients on home parenteral nutrition. J Parenter Enteral
39. Nordgaard I, Hansen BS, Mortensen PB. Importance of colonic support for Nutr. 1984;8:720–721.
energy absorption as small-bowel failure proceeds. Am J Clin Nutr. 56. Ward K, Murray B, Neale G. Treatment of salt losing ileostomy diarrhoea with
1996;64:222–231. an oral glucose polymer electrolyte solution. Ir J Med Sci. 1984;153:77–78.
40. Nordgaard I, Hansen BS, Mortensen PB. Colon as a digestive organ in 57. Camilleri M, Prather CM, Evans MA, et al. Balance studies and polymeric
patients with short bowel. Lancet. 1994;33:373–376. glucose solution to optimize therapy after massive intestinal resection.
41. Woolf GM, Miller C, Kurian R, et al. Diet for patients with short bowel: Mayo Clin Proc. 1992;67:755–760.
high fat or high carbohydrate? Gastroenterology. 1983;84:823–828. 58. Beaugerie L, Cosnes J, Verwaerde F, et al. Isotonic high-sodium oral rehy-
42. McIntyre PB, Fitchew M, Lennard-Jones JE. Patients with a high jejunos- dration solution for increasing sodium absorption in patients with short-
tomy do not need a special diet. Gastroenterology. 1986;91:25–33. bowel syndrome. Am J Clin Nutr. 1991;53:769–772.
43. Jeppesen PB, Mortensen PB. The influence of a preserved colon on the 59. Ladefoged K, Christensen KC, Hegnhoj J, et al. Effect of a long acting
absorption of medium chain fat in patients with small bowel resection. Gut. somatostatin analogue SMS 201-995 on jejunostomy effluents in patients
1998;43:478–483. with severe short bowel syndrome. Gut. 1989;30:943–949.
44. Marteau P, Messing B, Arrigoni E, et al. Do patients with short-bowel syn- 60. O’Keefe SJ, Peterson ME, Fleming CR. Octreotide as an adjunct to home
drome need a lactose-free diet? Nutrition. 1997;13:13–16. parenteral nutrition in the management of permanent end-jejunostomy syn-
45. Behrend C, Jeppesen PB, Mortensen PB. Vitamin B12 absorption after ile- drome. J Parenter Enteral Nutr. 1994;18:26–34.
61. Nehra V, Camilleri M, Burton D, et al. An open trial of octreotide long-acting
orectal anastomosis for Crohn’s disease: effect of ileal resection and time
release in the management of short bowel syndrome. Am J Gastroenterol.
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46. Dobbins JW, Binder HJ. Effect of bile salts and fatty acids on the colonic
62. Ellegard L, Bosaeus I, Nordgren S, et al. Low-dose recombinant human
absorption of oxalate. Gastroenterology. 1976;70:1096–1100.
growth hormone increases body weight and lean body mass in patients with
47. Vanderhoof JA, Young RJ. Enteral nutrition in short bowel syndrome.
short bowel syndrome. Ann Surg. 1997;225:88–96.
Semin Pediatr Surg. 2001;10:65–71.
63. Scolapio JS, McGreevy K, Tennyson GS, et al. Effect of glutamine in short-
48. Lennard-Jones JE. Oral rehydration solutions in short bowel syndrome.
bowel syndrome. Clin Nutrition. 2001;20:319–323.
Clin Ther. 1990;12(suppl A):129–137.
64. Scolapio JS, Camilleri M, Fleming CR, et al. Effect of growth hormone,
49. Beaugerie L, Carbonnel F, Hecketsweiler B, et al. Effects of an isotonic glutamine, and diet on adaptation in short-bowel syndrome: a randomized,
oral rehydration solution, enriched with glutamine, on fluid and sodium controlled study. Gastroenterology. 1997;113:1074–1081.
absorption in patients with a short-bowel. Aliment Pharmacol Ther. 1997; 65. Szkudlarek J, Jeppesen PB, Mortensen PB. Effect of high dose growth hor-
11:741–746. mone with glutamine and no change in diet on intestinal absorption in short
50. Newton CR, Gonvers JJ, McIntyre PB, et al. Effect of different drinks on bowel patients: a randomized, double blind, crossover, placebo controlled
fluid and electrolyte losses from a jejunostomy. J Royal Soc Med. study. Gut. 2000;47:199–205.
1985;78:27–34. 66. Byrne TA, Morrissey TB, Nattakom TV, et al. Growth hormone, glutamine,
51. Rodriguez-Iturbe B, Herrera J, Garcia R. Relationship between glomerular and a modified diet enhance nutrient absorption in patients with severe
filtration rate and renal blood flow at different levels of protein-induced short bowel syndrome. J Parenter Enteral Nutr. 1995;19:296–302.
hyperfiltration in man. Clin Sci (Lond). 1988;74:11–15. 67. Byrne TA, Persinger RL, Young LS, et al. A new treatment for patients with
52. Crow M, Meyer GW. “Cholera solution” in short bowel syndrome. South short-bowel syndrome. Growth hormone, glutamine, and a modified diet.
Med J. 1978;71:1303. Ann Surg. 1995;222:243–255.
53. Griffin GE, Fagan EF, Hodgson HJ. Enteral therapy in the management of 68. Seguy D, Vahedi K, Kapel N, et al. Low-dose growth hormone in adult
massive gut resection complicated by chronic fluid and electrolyte deple- home parenteral nutrition-dependent short bowel syndrome patients: a posi-
tion. Dig Dis Sci. 1982;27:902–908. tive study. Gastroenterology. 2003;124:293–302.
54. Laustsen J, Fallingborg J. Enteral glucose-polymer-electrolyte solution in 69. Jeppesen PB, Hartmann B, Thulesen J, et al. Glucagon-like peptide 2
the treatment of chronic fluid and electrolyte depletion in short-bowel syn- improves nutrient absorption and nutritional status in short-bowel patients
drome. Acta Chir Scand. 1983;149:787–788. with no colon. Gastroenterology. 2001;120:806–815.

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 Maria R. Mascarenhas, MBBS;
Donna Divito, RD, CNSD;
Stephen A. McClave, MD 15
Pancreatic Disease

Introduction 2. Autodigestion of the gland by these enzymes is normally pre-

vented by storage of these lytic enzymes in a precursor form and
This chapter focuses on nutritional aspects of acute and chronic pancre- by synthesis of protease inhibitors, which rapidly inactivate the
atitis in adults and children and on cystic fibrosis (CF), the most com- enzymes.4
mon cause of pancreatic insufficiency. While CF is genetic in origin, 3. Pancreatitis is caused either by premature (intrapancreatic) activa-
pancreatitis may be related to predisposing genes and congenital struc- tion of these lytic enzymes or by disruption of the balance between
tural abnormalities as well as infectious and inflammatory etiologies. the activated protease enzymes and protease inhibitors.5
I. Background: Acute Pancreatitis C. Etiology
II. Nutritional Aspects of Acute Pancreatitis 1. In adults, acute pancreatitis involves long-term ethanol abuse in
III. Nutritional Alterations in Acute Pancreatitis >75% of patients.5 Fifteen percent of cases are idiopathic or due
IV. Focused Assessment to gallstones.5 The remaining 10% are related to pancreas divi-
V. Goals of Therapy sum, trauma, hyperparathyroidism and hypercalcemia, hyperlipi-
VI. Management demia, post–endoscopic retrograde cholangiopancreatography
VII. Background: Chronic Pancreatitis (post-ERCP), medications, and biliary dyskinesia.
VIII. Nutritional Aspects of Chronic Pancreatitis 2. In children, acute pancreatitis is caused by trauma, viral infections,
IX. Focused Assessment multisystem disease (systemic lupus erythematosus, Kawasaki
X. Goals of Therapy disease, hemolytic uremic syndrome, and inflammatory bowel
XI. Management disease), congenital anomalies of the ducts, or medications, or
XII. Background: Pancreatic Insufficiency, Including Cystic Fibrosis is idiopathic.
XIII. Nutritional Aspects of Pancreatic Insufficiency
XIV. Nutritional Alterations in Pancreatic Insufficiency
XV. Focused Assessment
II. Nutritional Aspects of Acute Pancreatitis
XVI. Goals of Therapy A. Factors promoting nutritional deterioration
XVII. Management 1. Protein and energy requirements increase because of the physio-
References logic stress of acute pancreatitis.
2. Reduced oral intake occurs because of abdominal pain with food
I. Background: Acute Pancreatitis ingestion, nausea and vomiting, gastric atony and paralytic ileus,
or partial duodenal obstruction from pancreatic enlargement, or
A. Definitions
in association with ethanol addiction.
1. Pancreatitis is a diffuse inflammatory process of the pancreas
3. Increased nutrient losses result from maldigestion and reduced
with variable involvement of other regional tissues and/or remote
absorption of luminal nutrients, excessive loss of protein because
organ systems.1,2
2. Eighty percent of hospital admissions for pancreatitis are mild in of inflammation of peritoneal and retroperitoneal surfaces, diar-
severity.3 Most patients experience a self-limited hospital course, rhea, or formation of pancreatic fistulas.
can be supported with intravenous (IV) fluid resuscitation and B. Concept of pancreatic rest
analgesia, and rapidly return to an oral diet. 1. An ongoing precept of management that has not changed over
3. Severe pancreatitis (20% of hospital admissions for pancreatitis)3 the years is the concept of pancreatic rest. Reducing pancreatic
is characterized by organ failure, peripancreatic fluid collection, exocrine secretion and diminishing stimulation of the gland has
or evidence of necrosis on dynamic computed tomography (CT) been found to allow resolution of the inflammatory process when
scans. These patients tend to have a longer hospital stay, with mild.
higher mortality, and are more likely to require nutrition support. 2. What has changed is the understanding of what pancreatic rest
Recurrent acute pancreatitis involves flare-ups of pancreatic means. In the past it was felt that enzyme output from the pancreas
inflammation with abdominal pain and elevated amylase and had to be reduced to basal unstimulated levels; it is now understood
lipase concentrations. The gland returns to normal function and that reducing secretion may be sufficient to allow resolution of
anatomy between bouts. inflammation.
B. Pathophysiology 3. Previous prospective randomized controlled trials of severe pan-
1. The exocrine pancreas secretes amylase, lipase, carboxypeptidase, creatitis in which the sole management strategy was putting the
phospholipase A, chymotrypsinogen, aminopeptidase, trypsino- pancreas to rest (using cimetidine, nasogastric aspiration, somato-
gen, and cholesterase. statin, etc) all failed to show an impact on patient outcome.6

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S E C T I O N I I I Gastrointestinal Related Conditions

4. Putting the pancreas to rest and using the gut are not incompati- be offset by the stimulation of inhibitory factors such as pan-
ble concepts; both can be accomplished simultaneously. creatic inhibitory polypeptide, pancreatic polypeptide YY and
5. Fortunately for the clinician, management may be guided by the bile salts.7
patient’s symptoms; placing a tube in the duodenum and monitor- c) There is evidence for a beneficial effect of stimulation of the
ing enzyme output from the pancreas is not required. GI tract at this level. In a study by McClave et al, three patients
C. Stimulation of pancreatic secretion randomized to EN had resolution of symptoms and normal-
1. Multiple factors are involved in stimulation of the pancreas, includ- ization of amylase on jejunal feeds.36 Upon advancement to
ing neural stimulants (the vagus nerve), chemical stimulants (lumi- clear liquids by mouth, there was an exacerbation of symptoms
nal protein, fat, and gastric acid), mechanical stimulants (distension and development of hyperamylasemia. Placing the patients
of the gastric wall), and hormonal stimulants (gastrin, secretin, back on jejunal feeds resolved symptoms and normalized amy-
vasoactive intestinal peptide, and cholecystokinin [CCK]).7 lase until efforts to advance diet could be tried again at a later
2. Stimulants may act directly or indirectly on pancreatic secre- date.36 In a fourth patient, after amylase/lipase levels normal-
tion.7 Pancreatic secretion involves gut luminal stimulants, and ized and abdominal pain resolved on jejunal feeds, a dramatic
the evidence that similar stimulation can occur from IV nutrients exacerbation of the systemic inflammatory response syndrome
is controversial.8 (SIRS) occurred a week later, when the tube was found to
3. Effect of IV nutrients on pancreatic secretion be displaced from the jejunum into the stomach. Replacing the
a) Animal studies on the effect of IV nutrients are inconclusive.9–18 tube in the jejunum allowed resolution of the SIRS response,
b) Among human studies, while one report in a single patient and eventually the patient was advanced successfully to oral
showed stimulation of pancreatic secretion from IV fat emulsion diet and discharged.36
(but not IV amino acid and glucose),19 seven other studies in 6. A second factor in the safety of EN in pancreatitis involves the con-
patients with pancreatitis,20–22 postoperative patients with surgi- tent of the formula infused into the GI tract. At any given level of
cally created pancreatic fistulas,23,24 or healthy volunteers25,26 the GI tract, infusion of protein or fat causes greater stimulation of
showed no effect of IV nutrients on pancreatic secretion. pancreatic exocrine output than infusion of carbohydrate.7,37
c) There is controversy over IV fat emulsion. The consensus opin- a) Intact protein and individual amino acids may cause greater
ion from available studies is that hypertriglyceridemia resulting stimulation than small-chain oligopeptides.37 Long-chain fat
from infusion of fat is the most likely cause of an exacerbation causes greater stimulation than medium-chain triglycerides
of pancreatitis; a flare of pancreatitis resulting from IV fat infu- (MCTs).7
sion in the absence of hypertriglyceridemia is unlikely.4,27–32 b) Evidence for the effect of diet content on pancreatic enzyme
output was shown by Grant et al in a postoperative patient
Multiple studies with more than 100 pancreatitis patients have
receiving jejunal feeds.38 Switching from a nearly fat-free, ele-
shown IV fat emulsion to be a safe component of parenteral
mental formula to a standard formula containing long-chain fat
nutrition (PN).33
led to a statistically significant increase in lipase output (but no
4. Effect of enteral nutrients on pancreatic inflammation
change in fluid volume, bicarbonate, or amylase output).38
a) It appears from a large prospective case series that the worst
c) In a prospective series of patients with acute pancreatitis,
effect of early advancement to oral diet or use of the gut is an
patients treated with oral fat-free, elemental formula (all of
uncomplicated exacerbation of symptoms, which was shown to
whom had resolution of symptoms and normalization of serum
occur in approximately 21% of patients.34
amylase) developed an exacerbation of symptoms and hyper-
b) A true exacerbation of the disease process of pancreatitis
amylasemia when advanced to a full oral diet.37 Placing the
occurred in only 4.3% of cases.34 Prolongation of hospitaliza-
patients back on the oral fat-free, elemental formula resolved
tion and length of stay in the intensive care unit (ICU) was seen symptoms and normalized amylase again.
in those patients who experienced a symptomatic relapse com- 7. Tolerance of EN is variable, not an “all or nothing” phenomenon,
pared to patients who did not.34 However, early use of the gut and may be envisioned as a balance on a graded scale. The biggest
did not prolong hospitalization. factor determining tolerance is disease severity, which in turn is
c) Exacerbation of symptoms appears to be simply a sign that related to the presence or absence (and degree) of pancreatic
inflammation within the gland has not resolved and the necrosis.
patient is not ready for dietary advancement. Ranson’s warn- a) With greater degree of necrosis, disease severity is increased,
ing 25 years ago35 that early oral intake would induce late the enteral formula may need to be infused lower in the GI tract,
complications (specifically, abdominal abscess) has not been and the standard enteral formula may need to be replaced by
corroborated. either a nearly fat-free, elemental formula or a semielemental,
5. Evidence for the safety of early enteral nutrition (EN) in acute pan- small-peptide formula with MCT oil.
creatitis was first established by a prospective randomized trial b) While a recent study by O’Keefe et al made clear that patients
comparing EN with PN therapy in 1997.36 No significant differ- randomized to EN have significantly greater increases in
ence in medical outcome parameters between the two groups was trypsin, amylase, and lipase output than similar patients ran-
shown, including days to normalization of amylase, days to oral domized to PN,39 the degree of stimulation is tolerated in
diet, length of hospitalization, length of time in the ICU, percent most patients, and resolution of inflammation within the gland
nosocomial infections, and mortality.36 still occurs.
a) There are three phases of stimulation of pancreatic secretory D. Role of gut integrity. For years, emphasis on pancreatic rest deterred
output: the cephalic, gastric, and intestinal phases.7 At each recognition of the role of gut integrity in critical illness. The gut is
level, multiple stimulatory factors are invoked. the largest immune organ in the body and has been described as the
b) Feeding lower in the gastrointestinal (GI) tract, especially at or motor of the multiorgan failure sepsis syndrome. The degree to
below the ligament of Treitz, tends to invoke fewer stimulatory which gut integrity is maintained in the critical care setting affects
factors. The few stimulatory factors invoked at this level may patient outcome.

212 A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. © 2005 A.S.P.E.N. www.nutritioncare.org.
 S E C T I O N I I I Gastrointestinal Related Conditions

1. Effects of enteral feeding insulin is required in as many as 81% of patients who were not dia-
a) EN maintains gut integrity by sustaining closure of the para- betic before the onset of pancreatitis.30 Carbohydrate intolerance
cellular channels between the intraepithelial cells of the intes- has been shown to increase mortality by up to 15%.51
tinal mucosa. It also stimulates immunoglobulin A and bile 2. Changes in fat metabolism occur in only 12% to 15% of
salts, which coat bacteria within the lumen of the gut. Peristal- patients30,52,53 (particularly hypertriglyceridemia) and have been
sis helps wash the bacteria downstream, and thus the overall shown to increase mortality by up to 33%.51 Chronic pancreati-
number of enteric bacteria is held in check. tis causes steatorrhea once about 90% of the gland is destroyed
b) EN stimulates blood flow to the gut, which helps prevent and may result in weight loss and associated fat-soluble vitamin
ischemia/reperfusion injury.40 deficiencies.
c) EN helps maintain the mass of gut-associated lymphoid tis- C. Micronutrient deficiencies
sue and mucosal-associated lymphoid tissue at distant sites 1. Hypocalcemia occurs in 25% of patients52 because of decreased
such as the lungs, liver, and kidneys.40,41 parathyroid hormone secretion, increased calcitonin, hypomag-
d) Whether or not EN is provided helps set the tone for the sys- nesemia, hypoalbuminemia, and saponification of calcium with
temic immune response at the level of the gut. EN stimulates free fatty acids.30
the proliferation of CD4 helper T-cell lymphocytes in the 2. Long-term ethanol abuse predisposes patients to hypomagne-
lamina propria of the gut to proliferate down a Th2 and Th3 semia, decreased zinc concentrations, and deficiencies of thi-
pathway generating interleukin-4, interleukin-10, and trans- amine and folate.
forming growth factor β, all of which serve to downregulate 3. Clinical vitamin B12 deficiency may result from a deficiency of
GI inflammation.40 the pancreatic protease required to degrade the binding of the R
2. Effects of starvation protein with vitamin B12.5
a) Failure to provide EN leads to increased gut permeability
(opening of the paracellular channels between the intraepi-
IV. Focused Assessment
thelial cells) and increased systemic bacterial challenge to the
patient (with increased circulating systemic endotoxemia). A. History and physical exam
b) Patients with severe pancreatitis and multiorgan failure have 1. Etiologic clues that should be elicited from the interview with the
a 16-fold increase in gut permeability beyond that found in patient include long-term excess ethanol use, symptoms referable
mild pancreatitis.42 Following major insult or injury, a starved to gallbladder disease or gallstones, prescription and over-the-
gut becomes a proinflammatory organ. counter medicines, and history of remote trauma (in which the
(1) Activation of macrophages at the level of the gut by either pancreas might have been injured by a steering wheel or bicycle
increased permeability/bacterial challenge or subclinical handlebars).
ischemia/reperfusion injury leads to priming of neutrophils, 2. Symptoms that should be elucidated in the history include the char-
which in turn circulate out to distant organ sites. acter and time course of the abdominal pain, the presence of nau-
(2) Subsequent activation of these neutrophils by hypotension sea and vomiting, weight loss, diarrhea, new onset of abdominal
or hypoxemia leads to release of superoxide radicals and distension (which may indicate pancreatic ascites), muscle cramps
exacerbation of systemic oxidative stress.40,43 (related to electrolyte disturbances), and easy bruising (reflecting
3. Stress responses in pancreatitis vitamin K insufficiency).
a) Prospective randomized controlled trials of patients with acute 3. The physical exam must carefully evaluate fluid status and abdom-
pancreatitis placed on EN have shown patients with EN to have inal tenderness or mass and should document any findings of xan-
less stress-induced hyperglycemia, reduced use of antioxidant thomas as a result of hyperlipidemia, jaundice as a result of
defenses, faster decline in C-reactive protein levels, faster res- extrinsic common bile duct compression from an enlarged pan-
olution of SIRS, and less disease severity compared to similar creas, bruising around the umbilicus or flanks from retroperitoneal
patients receiving PN.44–46 bleeding, Chvostek’s sign (hypocalcemia), or subcutaneous nod-
b) The greater the degree of severity of acute pancreatitis, the ules from fat necrosis.54
greater the importance of maintaining gut integrity and the more B. Determination of disease severity
likely the outcome parameters will be affected by the route of 1. An APACHE II score of ≥10 and Ranson criteria of ≥3 identify
nutritional support.36,44,46,47 patients with severe pancreatitis who are likely to have pancre-
atic necrosis on CT scan, a 38% rate of complications, and an
associated 19% mortality rate.54–56 These patients represent 20%
III. Nutritional Alterations in Acute Pancreatitis
of hospital admissions for pancreatitis, have almost no likelihood
A. Metabolic stress state-. The metabolism of acute pancreatitis involves of successfully advancing to oral diet within 7 days,54–56 and are
a classic stress state very similar to that in sepsis,48,49 with measured favorably affected by the use of EN rather than PN.
resting energy expenditure as high as 139% of the value predicted by 2. Patients with lower scores (APACHE II ≤9, Ranson criteria ≤2)
the Harris-Benedict equation.50 More patients with acute pancreatitis have mild to moderate pancreatitis, are unlikely to have necrosis
are hypermetabolic than patients with chronic pancreatitis (61% vs on CT scan, and have a very low complication rate (6%) and close
33%, respectively).50 When pancreatitis is complicated by sepsis, to no mortality. They have over an 81% chance of advancing to
energy expenditure may be increased by as much as 15%.50 oral diet successfully within 7 days and thus may be supported
B. Changes in substrate metabolism with IV fluid resuscitation and analgesia alone without nutritional
1. Changes in carbohydrate metabolism4,30 caused by increased cor- support.54–56
tisol and catecholamine secretion, increased glucagon/insulin 3. If there is a discrepancy between the two scoring systems, patients
ratio, impaired β-cell function, and insulin resistance lead to evi- with severe pancreatitis may be identified by a tendency for the
dence of glucose intolerance in 40% to 90% of patients,4,30 and APACHE II score to increase by 3 points over the first 48 hours,

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S E C T I O N I I I Gastrointestinal Related Conditions

whereas patients with mild to moderate disease severity demon- c) The nonsignificant trends seen in these small studies suggest
strate a decrease in the APACHE II score by 1 point over the same that the issue of gut integrity and EN versus starvation is a
period.54–56 much more important clinical factor than some negative effect
4. Admission bedside judgment and its associated clinical assessment from PN.
have been shown to have a 34% to 44% sensitivity for identifying B. Tolerance of EN
patients with severe pancreatitis, which is significantly less than 1. Clinical experience with EN and expertise in placing and main-
the sensitivity of 63% seen for the APACHE II score.56,57 After 48 taining feeding tubes low in the GI tract vary among institutions.
to 72 hours, the sensitivity of clinical assessment increases to 44% a) In one center in Great Britain, there were minimal problems
to 66%, but this is significantly less than the increased sensitivity involving tolerance of EN in acute pancreatitis. Out of
of 75% to 82% seen with either the APACHE II score or the Ran- 16 patients randomized to EN, 5 showed some degree of ileus
son criteria.56,57 requiring only a decrease in the infusion rate for 2 to 4 days
(before resuming the full rate of feeding).62
b) In contrast, a separate group from Great Britain attempted to
V. Goals of Therapy place all patients with acute pancreatitis on EN and was suc-
A. EN versus PN cessful in only 53%; 47% of patients ultimately received total
1. Six prospective randomized trials have now shown a number of parenteral nutrition (TPN) alone or no nutritional therapy.63
significant benefits and an overall favorable impact on patient 2. Duration of ileus is important. In a prospective, nonrandomized
outcome from use of EN, compared to use of PN, in patients with consecutive case series, duration of ileus was a factor in whether
severe acute pancreatitis.36,42,45,47,58,59 patients tolerated EN.63 No patients in whom the duration of ileus
2. McClave et al showed a fivefold reduction in the cost of nutri- was ≥6 days tolerated advancement to EN. If duration of ileus was
tional support with EN compared to PN.36 limited to ≤5 days, 50% of those patients tolerated EN. However,
3. Abou-Assi et al showed faster time to resolution of the disease if the nutrition support team was aggressive in placing tubes and
process (defined by resolution of abdominal pain, near normal- was able to minimize the duration to <2 days, 92% of the patients
ization of amylase, and successful advancement to clear liquid tolerated EN.63
3. While there is wide individual enteral feeding tolerance, most
diet) by nearly 1 full week in the EN group compared to the PN
patients tolerate enteral feeding below the ligament of Treitz.
group (6.2 vs 11.8 days, respectively, P < .05).46
a) Eatock et al randomized patients with acute, severe pancre-
4. Kalfarentzos et al showed a reduction in overall complications
atitis to nasogastric or nasojejunal feeds64; the groups behaved
from 75% in patients receiving PN to 45% in those receiving EN
indistinguishably.
(P < .05). Septic complications were cut nearly in half, from 50%
b) In contrast, two patients39 demonstrated intolerance to infusion
to 28%, comparing patients receiving PN to those receiving EN
of nasojejunal feeds, with exacerbation of pain and elevation of
(P < .03).47
serum amylase levels, in a situation where the tubes were doc-
5. Olah et al similarly showed a reduction in septic complications,
umented to be 10 cm or more below the ligament of Treitz.
again by half, from 27% to 12%, comparing those patients receiv-
C. Methods to enhance efficacy of EN
ing PN to those receiving EN, respectively (P = .08).58
1. Immunonutrition. In other disease processes, such as major elec-
6. Two meta-analyses aggregating the data from these six prospec- tive surgery, burns, and trauma, immune-enhanced diets have
tive randomized trials have now been performed. shown even greater benefits on patient outcome than use of stan-
a) S. A. McClave et al (unpublished data), showed that infectious dard enteral formulas.65
complications were reduced by half with use of EN (RR = 0.52, a) Concern has been raised that in an acute stress state such as
P < .05), compared to use of PN. pancreatitis, stimulation of interferon-gamma receptors would
b) P. Marik and G. Zaloga (oral communication, January 2004) cause macrophages to take up arginine and produce nitric
showed that the need for surgical intervention was also reduced oxide, a compound that can lead to hypotension, vasodilation,
by half in patients receiving EN (RR = 0.48, P < .05) compared and clinical shock.66
to those receiving PN. Marik also showed a significant reduc- b) Only one small study has compared a high arginine-
tion in hospital length of stay by a mean of nearly 3 days in supplemented immune formula to a standard enteral formula
those patients receiving EN, compared to those placed on PN. in acute pancreatitis. It showed a reduction in ICU length of
Marik and Zaloga found trends in reduced mortality and non- stay from 34.8 to 8.6 days and hospital length of stay from
infectious complications in the group receiving EN compared 38.4 to 27.2 days (comparing controls on standard formula
to patients receiving PN, but the differences did not reach sta- and those receiving immunonutrition, respectively, P =
tistical significance. nonsignificant [ns]).67
7. Two studies have compared EN with no nutritional therapy in 2. Probiotics. In a small study, Lactobacillus added to an enteral for-
patients with acute pancreatitis.60,61 mula infused into patients with acute pancreatitis resulted in a
a) Pupelis et al showed that markers of systemic inflammation and reduction in intra-abdominal abscess and infected pancreatic
oxidative stress (TNF, interleukin-6, and C-reactive protein lev- necrosis from 30.4% to 4.5% (P = 0.023) and a reduction in hos-
els) were all lower in a small group of patients randomized to pital length of stay from 21.4 to 13.7 days (P = ns), compared to
EN compared to those patients receiving conventional therapy similar patients receiving an enteral formula with heat-inactivated
with no nutritional support.60 Lactobacillus.68
b) Powell et al showed that overall complications were reduced by D. Role of PN
half, from 29% to 15%, and mortality was cut to one third, from 1. Early PN studies
28% to 9%, in a small group of patients receiving EN, com- a) Early, nonrandomized, poorly controlled retrospective and
pared to conventional therapy with no nutritional support.61 prospective studies suggested that early use of PN, even with

214 A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. © 2005 A.S.P.E.N. www.nutritioncare.org.
 S E C T I O N I I I Gastrointestinal Related Conditions

lipids, was safe in patients with pancreatitis,4,69–71 reduced the D. Using adjunctive therapy. Patients should receive aggressive fluid
overall complication rate by up to 60%,72 and reduced mortal- resuscitation, repletion of electrolytes and micronutrients, ade-
ity by 8% to 25%.51,72–74 quate analgesia to control pain, and a broad-spectrum antibiotic
b) In contrast, two early retrospective reviews showed no (eg, imipenem) to reduce septic complications.77
effect of PN on the clinical course or rate of complications E. Using PN
in pancreatitis.22,75 1. Progression to PN should be entertained only in patients who
2. Prospective randomized trials with PN. Only one prospective demonstrate clear-cut intolerance to enteral feeding or who show
randomized trial compared patients with mild to moderate pan- increasing pain with increases in amylase and lipase on EN.
creatitis placed on early PN with a control group of patients who 2. PN should not be initiated until after 5 to 7 days.
received only IV fluid resuscitation, nasogastric decompression, 3. Slightly underfeeding (providing 80% of requirements) and
and analgesia.55 advancing slowly (only as control of serum glucose between 80
a) Compared with the control group, the early PN patients had a and 110 mg/dL will allow) may enhance the efficacy of PN.
significantly longer length of hospitalization and a higher 4. A mixed-fuel regimen should be used and patients should be
catheter sepsis rate. watched closely for evidence of hypertriglyceridemia and hyper-
b) There was no difference in days to advancement to clear liquids, calcemia (either of which can exacerbate pancreatitis).
return of amylase to normal levels, or overall complications. F. Watching for development of complications
c) The study concluded that widespread use of PN might not be 1. Failure of patients with mild pancreatitis to improve within 48 to
warranted in pancreatitis.55 72 hours of admission should prompt further evaluation for evi-
3. Timing of PN dence of complications, pancreatic necrosis, or organ failure.1
a) Based on the limited experience of comparing PN with no 2. Patients with protracted complications, such as pancreatic fistu-
nutritional therapy, and the more extensive experience of com- las, ascites, or pseudocyst, still may be placed on jejunal feeding
paring PN with EN, the timing of PN becomes important in as long as there is no evidence for increasing inflammation, sig-
patients with severe acute pancreatitis in whom EN is not fea- nificant increases in serum amylase and lipase, or worsening of
sible. In these patients, initiating PN within 48 hours of admis- the complicating process.
sion to the ICU may exacerbate the stress response and worsen G. Treating pediatric patients. Treatment of pediatric patients is mainly
outcome. It may be prudent to withhold nutrition support for 5 supportive and consists of hydration maintenance, pain control, and
to 7 days, until the peak of systemic inflammation has passed, control of vomiting. Nutritional therapy is mainly via PN, since there
before initiating PN. are few studies showing the efficacy of enteral feeds in pediatric
b) In one study, an effort was made to enhance the efficacy of PN patients.
in pancreatitis by adding IV glutamine to the PN. Patients
receiving PN with glutamine compared to those receiving PN
VII. Background: Chronic Pancreatitis
alone saw a reduction in hospital length of stay by 4 days (from
25 to 21 days, P = .07), a reduction in sepsis from 36% to 21% A. Definition. Chronic pancreatitis (CP) is a persistent inflammatory
(P = ns), and a reduction in the duration of nutritional therapy condition of the pancreas characterized by progressive, irreversible
from 16 to 10 days (P = .03).76 damage to the pancreas, leading to extensive fibrosis and the destruc-
tion of both exocrine and endocrine tissue.
1. Several retrospective studies reported that the annual incidence
VI. Management
of CP ranges from 3.5 to 10 cases per 100 000.78
A. Determining the severity of pancreatitis 2. As CP is seen mainly in adults, most of the discussion in this
1. An APACHE II score of ≤9 with ≤2 Ranson criteria identifies section will focus on the care of adults with this disorder.
patients with mild pancreatitis, who are not likely to need nutri- 3. Management in pediatric patients is similar to that in adults,
tion support, should progress to an oral diet within 7 days, and with the exception of alcohol abstinence. Alcohol ingestion is
should show rapid resolution of their disease process. not an etiologic factor in pediatric patients.
2. An APACHE II score of ≥10 with ≥3 Ranson criteria identifies 4. CP is a common and debilitating disorder with high morbidity.
patients with severe pancreatitis, who are at higher risk for com- 5. Complications include malnutrition, pain, poor quality of life
plications and will require (aggressive) nutrition support. These (QOL), diabetes mellitus, and malabsorption.
patients should be evaluated for evidence of multiple organ fail- 6. The most common clinical presentation in these patients is
ure and pancreatic necrosis. abdominal pain, diarrhea, and weight loss.
B. Initiating EN 7. Most patients present with a variable course of intermittent
1. Enteral access should be achieved fluoroscopically or endoscop- acute flares of abdominal pain that become constant as the dis-
ically with a nasoenteric tube placed at or below the ligament of ease evolves.
Treitz. 8. With destruction of the gland, diarrhea due to fat malabsorption
2. Enteral infusion may be started with a standard enteral formula. If develops, leading to progressive weight loss.
there is added concern in a particular patient about potential intol- 9. The natural history of the disease and the prognosis in these
erance, a low-fat elemental formula or a small peptide semiele- patients is somewhat variable, being associated with a high
mental formula (which should cause less stimulation of pancreatic morbidity rate and a mortality rate of up to 50% over 20 years.79
exocrine secretion) may be used. 10. Patients who continue to consume alcohol are more likely to
C. Monitoring. Patients should be watched closely for the possibility of develop complications, such as acute episodes of pancreatitis,
tube migration and for evidence of intolerance (eg, nausea/vomiting, formation of pseudocysts, duodenal obstruction, splenic vein
increasing abdominal pain, worsening fever, sudden elevations in thrombosis, and biliary strictures. These complications lead to
serum amylase/lipase). surgical intervention in approximately 50% of patients.80

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S E C T I O N I I I Gastrointestinal Related Conditions

11. At the end stage of disease, diabetes mellitus and malnutrition 4. The main reason for poor oral intake is persistent epigastric
are common. abdominal pain (90% of patients), which is exacerbated by eat-
B. CP is differentiated from acute pancreatitis by evidence of permanent ing and often accompanied by nausea and vomiting.
damage to the anatomy or function of the gland, documented by cal- 5. The exact cause of the pain is unknown.
cifications on abdominal radiographic film, ductal changes on ERCP, a) It is theorized that oral intake stimulates exocrine secretion of
and evidence of endocrine insufficiency (diabetes) or exocrine insuf- pancreatic juices released through scarred abnormal ducts,
ficiency (steatorrhea). which in turn causes an increase in ductal pressure, a decrease
C. Causes in blood flow, and possible ischemic injury to the gland.
1. Multiple etiologies are involved in the pathogenesis of CP. They b) Poor outflow of digestive enzymes may trigger autodigestion
include alcohol ingestion, pancreatic duct obstruction, acute pan- of pancreatic tissue and subsequent inflammation.
creatitis, pancreas divisum, CF, hereditary pancreatitis, idiopathic 6. Poor nutritional intake may also be related to continued ethanol
pancreatitis, autoimmune disorders, metabolic disorders (hyper- consumption and associated poor diet.
triglyceridemia and hyperparathyroidism), trauma, and nutritional 7. Gastroparesis has been noted in 44% of patients with exocrine
causes in tropical Africa and Asia. insufficiency due to small-duct CP.89
2. In Western countries, alcohol consumption is the main cause in 8. A subset of patients, usually with more advanced disease, may
70% to 90% of cases.81–85 develop gastroduodenal obstruction.
a) For the disease process to develop, consumption of 150 to 9. A large pseudocyst or diffuse inflammation of the pancreatic
175 grams of alcohol per day is required for a duration rang- head may cause gastric outlet obstruction, resulting in nausea
ing from 5 years up to 18 years for men and up to 11 years for and vomiting.
women.86 10. Another component of malnutrition in these patients results
b) At this level of consumption, however, only 10% to 15% of from advanced destruction of the pancreas due to maldigestion
patients will develop CP. and steatorrhea; this occurs in 25% to 45% of patients.88,90–92
3. CP involves virtually the same etiologic possibilities as acute a) Patients usually have three to four loose, bulky, greasy, foul-
smelling stools per day and often mention having oil droplets
pancreatitis, with two exceptions: gallstone disease and biliary
in the stools that are difficult to flush.
dyskinesia (which cause only acute pancreatitis and not CP).
b) Symptoms differ from those of patients with a classic mal-
4. CP is rare in children and is due to hereditary causes, congenital
absorptive process, which is typically characterized by watery
anomalies, and CF.
diarrhea, abdominal bloating, and cramping.
D. Pathophysiology
c) This difference in symptomatology is due to better preserva-
1. CP is an inflammatory disorder of the pancreas resulting in
tion of carbohydrate absorption in the patients with maldiges-
anatomic changes that include the infiltration of chronic inflam-
tion from CP.
matory cells and fibrosis of the gland. Depending on the stage of
11.The exocrine pancreas also produces bicarbonate, which is
disease, patients may present with or without functional abnor-
secreted with digestive enzymes in response to a meal.
malities and abdominal pain.
a) The bicarbonate helps neutralize gastric acid in the duodenum,
2. CP starts with pancreatic injury and is characterized by loss of which would otherwise cause breakdown of pancreatic
endocrine and exocrine function due to destruction of the acinar enzymes and bile salts.
and islet cells and replacement of the gland by fibrous tissue. b) Without bicarbonate present, both bile salts and enzymes are
3. Clinical presentation correlates with the severity of the histologic inactivated by the gastric acid, which worsens maldigestion.93
abnormalities. 12. It has been shown that protein malabsorption is less than fat mal-
4. Loss of exocrine function leads to malabsorption, maldigestion, absorption because trypsin is less vulnerable to acid destruction
steatorrhea, weight loss, and malnutrition. Pancreatic function than is lipase.94
has to fall below 10% for this to occur.87 13. Patients with CP and maldigestion are at risk for deficiencies of
5. Initially, histologic changes are patchy. These changes often vitamins and trace elements.
progress to replacement of a large part of the gland by fibrous scar a) Vitamin B12 concentrations are low in an estimated 10% to
tissue. 15% of patients with CP, but hematologic and neurologic com-
6. CP differs from acute pancreatitis in that fibrosis and loss of exo- plications are rare.95 When present, the deficiency may be cor-
crine tissue are present before and after an acute exacerbation. rected either by supplementing B12 with monthly injections or
by administrating pancreatic enzymes.
VIII. Nutritional Aspects of Chronic Pancreatitis b) Patients with CP are at significant risk for malabsorption of
fat-soluble vitamins (A, D, E, and K), but only very rarely does
A. Factors causing nutritional abnormalities it lead to overt clinical deficiency in specific vitamins.
1. Malnutrition is a multifactorial process in CP and is commonly c) Compared to a healthy control population, these patients have
a later manifestation of the disease. A multitude of factors, rang- been shown to have lower plasma levels of antioxidants, such
ing from poor oral intake and hypermetabolism to maldigestion as selenium, vitamins A and E, xanthine, beta-carotene, beta-
and endocrine dysfunction, predispose the patient with CP to cryptoxanthine, and lycopene.96,97
protein-calorie malnutrition. d) Hemorrhagic complications from vitamin K deficiency are
2. There is stepwise deterioration as the disease progresses, lead- sporadic.
ing to protein-calorie malnutrition.88 e) Once thought to be insignificant, vitamin D malabsorption
3. The major events that lead to malnutrition include poor oral leading to secondary hyperparathyroidism and either osteo-
intake, maldigestion resulting in malabsorption, hypermetabo- malacia or osteoporosis has been documented in 20% of
lism, and endocrine dysfunction. patients with CP. A study by Haaber et al showed that approx-

216 A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. © 2005 A.S.P.E.N. www.nutritioncare.org.
 S E C T I O N I I I Gastrointestinal Related Conditions

imately half of patients with CP and up to 69% of those with lection period. The coefficient of fat absorption is calculated from
documented steatorrhea had bone-mineral density Z scores <1, the amount of fat ingested and excreted and normally is more
with mean 25 (OH)D and 1,25 (OH)-2D serum levels below than 93%.
normal.98
14. Up to one third of patients have chronic persistent pancreatic
inflammation that causes a continuous hypermetabolic state,
X. Goals of Therapy
which plays a role in the development of malnutrition in these A. The goals of therapy include correction of malnutrition, improvement
patients. of nutritional status, correction of vitamin and mineral deficiencies,
a) Hypermetabolism (with a resting energy expenditure >110%) maintenance of glucose homeostasis, correction of malabsorption,
was shown in 65% of patients with alcohol-induced CP who improvement of bone mineral density, abstinence from alcohol inges-
were underweight versus 20% in patients who were of normal tion, control of pain, and improved QOL.
weight.87 B. The success of nutritional therapy is dependent upon abstinence from
b) Hypermetabolism was associated with up to a 10% to 20% alcohol and control of abdominal pain. Nutritional support varies
loss of body weight. The mechanism of hypercatabolism may depending on disease severity.
include alcohol toxicity and inflammatory effects.99–102 C. Continued oral intake is preferred to the provision of artificial enteral
15. Insulin-dependent diabetes develops on average 7 to 15 years feeds or PN.
after the diagnosis is made. D. Supplementation with pancreatic enzymes helps to control pain and
a) 90% of the insulin-producing beta cells must be destroyed improve digestion.
before this complication manifests. E. Specific vitamin deficiencies should be anticipated and treated
b) Accompanying the destruction of beta cells is the loss of appropriately.
glucagon-producing alpha cells. F. Careful assessment, design of the proper nutritional regimen, and
c) Twenty to thirty percent of these patients are insulin-depend- documentation of response to therapy are all required to reduce the
ent diabetics who are difficult to manage, with labile blood morbidity seen in CP.
glucose levels and frequent hypoglycemic episodes.5,103
d) Ketoacidosis is uncommon because of preservation of some
beta cell function.104 XI. Management
e) Wide swings in blood glucose levels and continued abnormal-
A. Successful intervention depends on two strategies that must be used
ities in carbohydrate metabolism may contribute to delayed
in conjunction with nutritional therapy: absolute abstinence from
gastric emptying.
alcohol and control of pain.
B. Presence of comorbid conditions. Complications seen with CP include
B. Endoscopic therapy may be needed to remove pancreatic obstruc-
diabetes, pseudocysts of the pancreas, biliary strictures, gastroduo-
tions106 such as stones and strictures, for stent placement and drainage
denal obstruction, GI bleeding, splenic vein thrombosis, and pan-
of pseudocysts, to block or destroy pancreatic nerves for pain control,
creatic cancer.
and to place jejunal tubes for pancreatic rest.
C. Surgical therapy is indicated for patients with ongoing biliary and
IX. Focused Assessment duodenal obstruction, pancreatic duct stenosis, and pseudocysts and
A. The diagnosis of CP is based on tests that assess pancreatic func- consists mainly of pancreatic resection or drainage procedures for
tion and morphology. pain relief.
B. An accurate nutritional assessment must be obtained in patients D. If pancreatic resection is performed, as much pancreatic tissue as
with CP, and evaluation of the severity of malabsorption is needed possible should be conserved to decrease surgical morbidity.
before a course of treatment can be selected. E. Pain control. Controlling abdominal pain is also an important strat-
C. Subjective global assessment, described by Detsky et al, is one meas- egy for correcting malnutrition in patients with CP.
ure that can be used to screen for significant nutritional risk.105 Other 1. Controlling abdominal pain requires putting the pancreas to rest
data collected during the history and physical exam should include through reduction in stimulation of pancreatic exocrine secretion.
body mass index (BMI), amount of weight loss, and anthropometric 2. Control of pain may stimulate increased appetite and nutritional
measurements. intake.
D. Laboratory data that need to be included are vitamin D and vitamin F. Oral enteral therapy
B12 levels. 1. Nutritional therapy may use the traditional oral route with a restric-
E. The presence of steatorrhea, due to pancreatic exocrine insuffi- tive diet designed to reduce stimulation of the pancreas, with or
ciency, can be assessed by either a quantitative or qualitative stool without supplemental enzymes.
collection. Both methods require adherence to a strict diet of 100 g 2. Some patients with CP with signs of mild malnutrition may be
of fat per day, starting 3 days prior to the study. able to consume adequate calories through an oral diet without
1. The quantitative method is the gold standard to estimate stool fat. exacerbation of abdominal pain.
Stool is collected for 72 hours; an abnormal result is the presence a) High-fat diets are associated with more amylase and lipase
of >7 g of fat (or >7% of the ingested dose) per day. secretion than are high-carbohydrate diets.
2. The qualitative method involves collecting one stool specimen, b) While protein may be a stronger pancreatic stimulant than car-
then staining for fat with Sudan III stain. Greater than 6 fat glob- bohydrate, one study showed that varying the protein content
ules per high-power field is considered to be abnormal. from 10% to 40% of calories failed to produce a difference in
3. In pediatric patients, assessment includes a 72-hour fecal fat col- pancreatic enzyme secretion.107
lection while the patient is on a high-fat diet (3–4 grams of c) The recommended diet for patients with CP is high in calo-
fat/kg/day) and recording all foods ingested during the stool col- ries (35 kcal/kg/day), high in protein (1.0–1.5 g/kg/day),

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S E C T I O N I I I Gastrointestinal Related Conditions

high in carbohydrate percentage, and moderate in fat (0.7– 2. As in patients with CF, PERT is given with meals, with snacks,
1.0 g/kg/day).108 and sometimes at bedtime.
3. Vegetable fats are thought to be better tolerated than animal fats, 3. There are two types of enzyme preparations: enteric-coated
because they cause less stimulation of pancreatic secretion. (Creon, Pancrease, Ultrase) and non-enteric-coated (Viokase,
G. Pancreatic enzyme replacement therapy (PERT) pancrelipase). See Table 15-1.
1. The two goals of treatment with pancreatic enzyme supple- 4. The enteric-coated forms are designed to resist inactivation by
ments are control of malabsorption and relief of pain. gastric acid as the medication passes through the stomach.

TABLE 15-1. Commonly Available Pancreatic Enzyme Supplements

Manufacturer Lipase Protease Amylase

Brand-Name Enzymes (Headquarters) (USP Units) (USP Units) (USP Units)

Creon Microminispheres 5 Solvay Pharmaceutical, Inc 5000 18 750 16 600

(Marietta, GA)

Creon Microminispheres 10 10 000 37 500 33 200

Creon Microminispheres 20 20 000 75 000 66 400

Pancrecarb MS-4 Digestive Care, Inc 4000 25 000 25 000

(Bethlehem, PA)

Pancrecarb MS-8 8000 45 000 40 000

Pancrease Ortho-McNeil Pharmaceutical, Inc 4500 25 000 20 000

(Raritan, NJ)

Pancrease MT-4 4000 12 000 12 000

Pancrease MT-10 10 000 30 000 30 000

Pancrease MT-16 16 000 48 000 48 000

Pancrease MT-20 20 000 44 000 56 000

Ultrase Axcan Scandipharm, Inc 4500 25 000 20 000

(Birmingham, AL)

Ultrase MT-12 12 000 39 000 39 000

Ultrase MT-18 18 000 58 500 58 500

Ultrase MT-20 20 000 65 000 65 000

Viokase 8 tablet A.H. Robins Co 8000 30 000 30 000

Richmond, VA

Viokase 16 tablet 16 000 60 000 60 000

Viokase 16 800 70 000 70 000

each 0.7 g powder (1⁄4 teaspoon)

USP, US Pharmacopeia

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5. Once the preparation is in the proximal small bowel, the 2. There are no reported prospective randomized trials of PN in
increase in pH causes dissolution of the enteric coating and patients with CP. Anecdotally, PN has been used to provide pan-
the active enzymes are released. creatic rest in patients with painful symptomatic flares.
6. Because lipase can be destroyed by gastric acid with pH <4, the 3. Disadvantages and complications from use of PN include
non-enteric-coated forms should be given with simultaneous increased cost (compared to EN), greater risk of catheter-related
acid suppression (using either proton pump inhibitor or hista- sepsis and thrombosis, and higher incidence of hyperglycemia
mine-2-receptor antagonist agents).97,109,110 and other metabolic derangements. Such PN-related complications
7. These two general types of enzyme preparations (enteric- occurred in 35% of patients in one study.116
coated and non-enteric-coated) are equally effective in patients 4. In general, PN should be used only in patients with CP in whom
with CP.110 signs of small-bowel dysmotility develop or enteral access to the
8. To treat steatorrhea in adults with CP, approximately 10% of small bowel is not available.
the amount of lipase normally produced by the pancreas should I. Enteral tube feeding
be delivered to the duodenum, timed to be present when the food 1. Enteral therapy (tube feeds) is helpful and has been shown to
is passing through the proximal small bowel.111 This amount improve weight gain, improve QOL, and reduce narcotic use.
of enzyme has been shown to be equivalent to approximately The principle of reducing pancreatic stimulation by distal feed-
30 000 international units of lipase per meal,112 thus requiring 4 ing is the same as that for acute pancreatitis.117–121
to 8 tablets at each meal and at bedtime and 2 to 3 tablets with 2. Patients with continued weight loss and poor response to oral
snacks. pancreatic enzymes may gain sufficient calories from supple-
9. One study showed steatorrhea to be significantly reduced from mental formulas containing MCT oil.
24 to 10 g of fat/day with appropriate enzyme therapy.113 a) MCT oil minimizes pancreatic secretion because of its direct
a) A favorable response to treatment does not necessarily require absorption by the intestinal mucosa into the portal venous sys-
repeat stool collection but may be determined by a clinical tem in the absence of lipase, colipase, or bile salts.108,122
improvement in stool consistency, loss of visible fat in the b) In healthy volunteers, mean peak CCK levels were lower with
stool, relief of diarrhea, and weight gain.111 the administration of formula composed of hydrolyzed pep-
b) With correct dosing, there is usually improvement in symp- tides and MCT oil, compared to levels seen in response to an
toms, but steatorrhea may not be totally corrected. oral high-fat meal. In a 10-week pilot study of eight patients
c) Tolerance of the enzyme supplements may be a problem in with CP and postprandial pain, daily provision of three to four
some patients due to nausea, bloating, cramping, constipa- cans of a small-peptide formula with MCT oil improved pain
tion, or diarrhea. scores in 62%.123
d) Failure of therapy most commonly is due to inadequate 3. In the few, mostly uncontrolled and retrospective studies evaluat-
dosing, patient noncompliance, or improper use of acid- ing the use of enteral feedings in patients with CP, enteral feeding
suppressive medications, as in CF. has been shown to be superior to PN and in some instances to oral
(1) Changing to a different preparation, decreasing daily fat diet.
intake to <60 grams, or increasing dosage to >30 000 a) In a group of patients with necrotizing exacerbations of CP,
international units of lipase per meal may improve symp- those on nasojejunal feedings had fewer complications, required
tomatic response. fewer surgical interventions, and demonstrated improved heal-
(2) If these measures fail to resolve symptoms, then other ing compared to those on PN.124
causes of malabsorption, such as small-bowel bacterial b) In a separate study in patients with refractory acute pancre-
overgrowth, should be investigated. Intestinal bacterial atitis, patients sent home on jejunal feeds were less likely to
overgrowth was found in approximately one third of be rehospitalized than patients on an oral diet.125
patients with pancreatic exocrine insufficiency from CP.114 4. Enteral feedings maintain gut integrity,126 which in turn reduces
10. PERT can also be used to manage abdominal pain. The mecha- the levels of proinflammatory cytokines generated by the gut that
nism of pain relief from the enzyme preparations may involve contribute to hypermetabolism.
suppressing the feedback mechanism of CCK-induced pancreatic 5. The main indication for direct enteral access is the need for
secretion. prolonged (>30 days) jejunal access to manage CP and its
a) Preparations high in trypsin (>50 000 international units) complications.
should be used. 6. Complications such as pseudocysts, ascites, and fistula are not a
b) Surprisingly, two trials using non-enteric-coated preparations contraindication to jejunal feeding. For patients in whom perma-
reported relief of pain, while four other trials using enteric- nent enteral access is anticipated, preliminary placement of a
coated preparations did not report effective relief of pain. nasojejunal tube is recommended to see if the patient tolerates
c) A recent consensus review recommended a trial of pancreatic postpyloric feedings.
enzymes for pain, particularly in patients with less advanced 7. Placement of a percutaneous gastrojejunostomy, surgical jejunos-
disease in whom other treatments have failed.115 tomy tube, percutaneous endoscopic gastrojejunostomy, or direct
H. PN percutaneous endoscopic jejunostomy depends on the patient’s
1. For the 10% to 15% of patients who are found to be intolerant of clinical status, the institution’s expertise, and whether the patient
or unable to sustain adequate nutritional intake with a low-fat diet has had previous abdominal surgery.
and pancreatic enzyme supplementation, more invasive methods J. Antioxidants
for nutritional therapy may be required.5 Either PN or enteral tube 1. There is some evidence supporting the use of antioxidants in
feeding can provide adequate nutritional support while minimally patients with CP to help reduce the amount of oxidative stress
stimulating the pancreas, reducing abdominal pain, and decreasing created by elevated proinflammatory cytokines and the associ-
the likelihood of complications associated with CP. ated hypermetabolic rate.

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S E C T I O N I I I Gastrointestinal Related Conditions

2. Supplementation of vitamins E and C with selenium and other position delta F508 in the encoded CFTR.130,133,134 Many other
trace elements has shown favorable clinical outcomes, with a manifestations are described.
decrease in pain and reduced number of hospital admissions.127,128 2. Other causes of PI are rare and include Shwachman-Diamond
3. A larger retrospective study showed that patients on antioxidant syndrome, Alagille’s syndrome, Pearson’s pancreas/marrow syn-
therapy had a decreased need for surgical intervention, reduced drome, Jeune’s thoracic dystrophy, and Johanson-Blizzard syn-
number and intensity of painful attacks, and fewer absences from drome.
work.129 C. Pathophysiology
4. Studies indicate that in pancreatic exocrine insufficiency, malab- 1. Mutations in the CFTR gene result in alterations in fluid and elec-
sorption of vitamin D is most likely to result in deficiency, in turn trolyte content of all secretions in the body due to defective CFTR
leading to osteomalacia and osteoporosis. Patients with advanced anion channel transport.
disease should be placed on vitamin D supplementation. The 25- a) The damage is seen mainly in the lungs, pancreas, GI tract,
hydroxylated form of vitamin D, calcifediol, is more readily liver, sweat glands, and vas deferens.
absorbed than vitamin D2 (calciferol). Adult dosing starts at 20 mcg b) These abnormalities are mainly in sodium, chloride, bicar-
per day, with maintenance dosing ranging from 20 to 100 mcg bonate, and water content and result in changes in the viscos-
per day. Close monitoring of calcium levels is needed to avoid ity of all exocrine secretions.
hypercalcemia. c) In the pancreas, pancreatic fluid becomes viscid and obstructs
smaller pancreatic ducts. This results in duct dilatation, inflam-
XII. Background: Pancreatic Insufficiency, mation, interstitial fibrosis, and even more obstruction and
Including Cystic Fibrosis destruction of the pancreas with atrophy and fatty replacement.
This process starts in utero; at birth, the majority of patients
A. The two most common causes of pancreatic insufficiency (PI) with CF have PI.
emerging in childhood are CF and Shwachman syndrome (PI, neu- d) In patients with PS, recurrent pancreatitis leads to ongoing
tropenia, thrombocytopenia, anemia, short stature, and metaphyseal damage to the pancreas.
dysostosis). e) In time, PS leads to PI.130,135,136 In older patients, endocrine
B. CF is an autosomal recessive genetic disorder and is the most com-
function is affected, with loss of islet cells and the develop-
mon inherited exocrine disease of the pancreas.
ment of CF-related diabetes mellitus (CFRD).
1. It results in PI in the majority of patients with CF and is caused
2. PI in CF manifests clinically as malabsorption, fat-soluble vitamin
by mutations in the CF transmembrane conductance regulator
deficiencies, edema, hypoproteinemia, weight loss, and failure to
(CFTR) gene.
thrive.
2. So far, more than 1000 CFTR gene mutations have been described.
D. Factors causing nutritional abnormalities
3. CF was once primarily a pediatric disease, since the life expectancy
1. PI causes increased fecal losses
was low. Now, CF is fast becoming an adult disease, as patients are
a) PI leads to steatorrhea, hypoproteinemia, essential fatty acid
surviving longer.
(EFA) deficiency, and micronutrient deficiencies. Protein losses
C. EN is a mainstay of nutritional therapy for CF.
in stool are due to malabsorption.
D. PN is used in critically ill patients who cannot tolerate EN or whose
caloric needs cannot be met with EN. b) Chronic liver disease and cirrhosis associated with CF worsen
E. It is important to sustain nutrition growth and development for maldigestion due to reduced bile salts.
improved outcome (morbidity and mortality). The many improve- c) Patients with meconium ileus can have intestinal resections,
ments in clinical care have resulted in improved survival for patients leading to short-bowel syndrome, decreased absorptive surface
with CF. area, and nutrient and bile salt losses.
F. It is clear that improvement in nutritional status plays an important d) Older patients with CF can develop diabetes mellitus, which
role in maintaining pulmonary status. leads to glucosuria, further contributing to nutrient losses.
e) Hypoproteinemia and edema are seen in infants and in patients
with liver disease.
XIII. Nutritional Aspects of Pancreatic Insufficiency 2. Decreased intake
A. Definitions. PI refers to abnormal pancreatic exocrine function, a) Reduction in oral intake may occur for a variety of reasons, includ-
which affects protein, fat, and carbohydrate digestion and absorption. ing post-tussive emesis, gastroesophageal reflux, esophagitis, liver
Fat is the most significant dietary component that is malabsorbed. disease, meconium ileus equivalent, salt depletion, micronutrient
1. Pancreatic sufficiency (PS) is seen in 10% to 15% of patients deficiency (zinc deficiency), and psychosocial causes.
with CF. These patients have sufficient (but often severely dimin- b) Patients often have a loss of appetite during acute exacerbations
ished) pancreatic exocrine function to achieve normal fat absorp- of pulmonary infections.
tion.130 Patients with PS have less severe mutations and disease c) Medications (eg, antibiotics) can contribute to anorexia.
and longer survival. d) Some patients may have decreased intake if advised to be on a low-
2. Patients with CF and PS are at 900-fold increased risk for acute fat diet or prescribed unpalatable semielemental or elemental diets
or recurrent episodes of acute pancreatitis78 relative to the gen- or supplements containing MCT.
eral population, and some of these patients go on to develop e) Despite a high energy intake and control of malabsorption with
PI.131–134 Imaging of the pancreatic and biliary trees should be enteric-coated enzymes, some children remain malnourished.137
done in CF patients with recurrent pancreatitis. f) In contrast to energy deficiency, which often exists in the mal-
B. Causes nourished child or adult with CF, protein intake is usually good.
1. Mutations in the CFTR gene result in a secretory defect in all g) Protein deficiency is usually seen in the first year of life, when
epithelial cells. The most severe mutation is a 3-pair deletion at protein and energy requirements are high.

220 A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. © 2005 A.S.P.E.N. www.nutritioncare.org.
 S E C T I O N I I I Gastrointestinal Related Conditions

(1) Breast milk may not contain enough protein for the infant with a) Symptoms are rare except in patients with severe deficiencies,
CF, even though the protein in breast milk is more bioavail- who can have the skin changes as well as thrombocytopenia
able than the protein from cow’s milk–based formulas. and poor wound healing.
(2) Edema and hypoproteinemia have been described in infants b) Fat malabsorption and inadequate EFA intake relative to oxida-
with CF fed soy formulas. tive stress or possibly from a defect in EFA metabolism are
3. Increased needs likely contributors.
a) Children with CF have a 5% to 20% increase in resting energy 8. Sodium depletion may present as hyponatremic dehydration,
expenditure, after allowing for malnutrition and lung dis- lethargy, weakness, and metabolic alkalosis in newly diagnosed
ease.138–140 patients and in the summer in patients who have inadequate salt
b) Studies have noted greater increases in resting energy expen- intake.
ditures of females than males.138–140 9. Beta-carotene
c) Chronic pulmonary infections contribute to increased energy a) Studies have shown low levels of beta-carotene in patients
needs. with CF. These levels improved with supplementation.154–156
d) Increased energy expenditure contributes to the negative energy b) There are not enough data at this time to suggest routine sup-
balance.141 Total energy expenditure is increased, and appetite plementation. The suggested intake of five servings of fruits
may not increase to compensate for the increased requirements and vegetables per day will increase the intake of beta-carotene.
and fecal energy losses. C. Bone health
1. Osteoporosis and osteopenia are commonly reported complica-
tions of CF in adults. Studies have shown inconsistent results for
XIV. Nutritional Alterations in bone mineral density in children and adolescents with CF com-
Pancreatic Insufficiency pared to controls.157–163
A. Growth and puberty 2. Factors contributing to bone disease in CF include low body
1. Poor growth and weight gain have been demonstrated in children weight; gonadal dysfunction; reduced weight-bearing physical
activity; poor nutritional intake; PI; malabsorption and/or
and adolescents with CF.141,142
decreased intake of calcium, magnesium, vitamin K, and vitamin
a) Malnutrition can vary from mild to severe.
D; corticosteroid use; pubertal delay; chronic respiratory acido-
b) There are critical periods in the life of a patient with CF: the
sis; inflammatory cytokines; and liver disease.
first 12 months after diagnosis, birth to 12 months (for infants
diagnosed prenatally), and the peripubertal period. It is criti-
cal that normal growth occur during these periods.142 XV. Focused Assessment
2. Delayed puberty is seen in CF and is thought to be related to
A. Growth and physical findings
malnutrition.
1. According to the CF Foundation, all pediatric patients should
a) Swedish researchers found delayed puberty and hypogonadism
have their weight, height/length, and head circumference (from
in CF despite good nutritional status independent of age at
birth to 24 months) monitored every 3 months. If growth is sub-
menarche, growth, or nutritional or clinical parameters.143 optimal, then infants should be seen every 2 to 4 weeks and older
b) The CF Foundation consensus report on nutrition concluded children every 4 to 6 weeks until nutritional status reaches an
that delayed puberty should be considered a marker for nutri- acceptable level.
tional failure.142 a) Acceptable growth is defined as % ideal body weight (IBW)
3. Although growth hormone deficiency is uncommon, growth hor- 90% (all ages), weight-for-length >25th percentile (0–2 years),
mone therapy improves height velocity and muscle mass in and BMI >25th percentile (2–20 years).
patients with CF.144–146 b) Patients at risk for nutritional failure include those whose length
B. Micronutrients or height has not reached genetic potential (all ages), whose
1. Deficiencies of fat-soluble vitamins (vitamins A, D, E, and K), %IBW is ≤90% with a history of weight loss or plateauing of
minerals (iron, zinc), electrolytes (sodium), and EFAs can occur weight (all ages), whose weight-for-length is between the 10th
due to malabsorption, increased needs, and decreased intake. and 25th percentile (0–2 years), and whose BMI is between the
2. Vitamin A deficiency is common in CF and can be seen in 15% 10th and 25th percentile (2–20 years).
to 40% of patients.147–150 It may be manifested as night blindness, c) Patients with nutritional failure are those whose length/height
increased intracranial pressure, and conjunctival xerosis, or just is <5th percentile, whose %IBW is <90% (all ages), whose
as low levels without any clinical manifestations. weight-for-length is <10th percentile (0–2 years), and whose
3. Vitamin D deficiency is present in 10% to 40% of patients151 but BMI is <10th percentile (2–20 years).
rarely presents as rickets or osteomalacia. It is believed to con- 2. Adult patients with CF should have their IBW determined initially.
tribute to the bone disease seen in CF. Patients should also be questioned about their usual body weight
4. Vitamin E deficiency is frequently seen in patients with CF and can (UBW). Thereafter, at every office visit, their weight should be
present with hemolytic anemia, neuropathy (decreased vibration compared to their IBW and UBW.
sense and proprioception), ophthalmoplegia, and ataxia.152 a) Malnutrition can be defined based on the %IBW as severely
5. Vitamin K deficiency can present with coagulopathy and bone malnourished (<75%), moderately malnourished (75%–79%),
disease and is more common in infants and patients with chronic mildly malnourished (80%–84%), underweight (85%–89%),
liver disease.153 and adequately nourished (≥90%). Improved weight gain is
6. Deficiencies of vitamins B6 and B12 and zinc are seen in patients related to better pulmonary function.164
with CF.142 b) BMI can also be determined at every visit and every attempt
7. EFA deficiency is seen in patients with PI and PS. made to keep patients’ BMI within a range of 20 to 25. Any

© 2005 A.S.P.E.N. www.nutritioncare.org. A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. 221
S E C T I O N I I I Gastrointestinal Related Conditions

patient with a BMI of <19 is significantly malnourished and C. Evaluation for malabsorption
needs aggressive nutritional intervention. Arm anthropometry 1. All patients should be evaluated for symptoms and signs of fat
may also be helpful.165 malabsorption at every visit. Evaluation may consist of determin-
3. Height is an effective screening tool in patients with CF. ing whether the patient has abdominal pain, bloating, gas, floating
a) Height measurements at or below the 5th percentile for age in stools, and diarrhea.
young children are associated with decreased life expectancy.166 2. If patients have any of the above symptoms in conjunction with
b) Biological parental height should be determined at diagnosis weight loss, lack of adequate weight gain, and growth failure, a
and used as a guide to determine mid-parental height and hence, more detailed assessment should be performed. It should consist of
growth potential. a 72-hour fecal fat determination and 3-day diet record with notes
4. The CF Foundation recommends that %IBW be used and calcu- on the number of enzyme capsules used and stool description.
lated according to the Moore et al method.167 3. Patients with PS should have a fecal elastase level at regular
a) Studies have shown that patients with mild to moderate lung intervals to monitor pancreatic function.
disease, PI, and normal IBW had greater deficits in muscle mass D. Laboratory assessment
than in fat stores.137,168 1. It is recommended that all patients with CF have laboratory stud-
b) Arm anthropometry should be a component of care of the ies checked at diagnosis and at least once a year.142 Studies
patient with CF. It is recommended that arm anthropometrics include a complete blood count to screen for anemia, serum albu-
be done at diagnosis and annually. min, retinol, 25-hydroxy vitamin D, and alpha-tocopherol levels.
5. Pubertal status should be determined annually and may be assessed EFA status should be checked in all infants and those with poor
by physical examination or by the self-assessment method.169 It is weight gain.
important that patients progress though puberty in a normal fash- 2. Vitamin K status should be assessed in patients at diagnosis and
ion. (See Chapter 1.) in those with hemoptysis, hematemesis, and liver disease. The
6. Bone health is another important part of the nutritional assessment. CF Foundation recommends that a PIVKA-II level be checked.
3. The CF Foundation recognizes that there is no acceptable test
It should include information about any history of atraumatic bone
currently available to check zinc status in patients with poor
fractures, poor growth, and/or bone mineral deficits noted on pre-
growth. Therefore, it is recommended that a 6-month trial of zinc
vious radiographs and dual x-ray absorptiometry (DXA) studies.
supplementation be initiated, with growth status periodically
a) In the patient with growth failure and short stature, DXA
reassessed to evaluate efficacy.
results may be difficult to interpret and therefore may be more
4. Visceral protein status should be assessed in all patients at risk of
informative if obtained serially to detect a trend rather than by
and/or diagnosed with nutritional failure by obtaining a serum
comparing bone densitometry values to those of age- and sex-
albumin level.
matched controls.
5. Iron studies alone may not be helpful in the patient with CF,
b) All children 8 years and older who have risk factors for poor because infection will affect the reliability of the results. Soluble
bone health should have a whole-body and lumbar spine DXA transferrin receptor levels are not affected by infection and inflam-
done.142 mation and are a better reflection of iron status.
c) At-risk patients include those who are listed for a lung trans- E. Presence of comorbid conditions
plant and have end-stage lung disease, those who have bone 1. Malnourished patients should be assessed for the presence of co-
fractures associated with low-impact activity, those receiving existing conditions. The following conditions are known to affect
chronic corticosteroid therapy, and those with delayed puberty, nutritional status: behavioral disorders, active pulmonary disease,
nutritional failure, liver disease, or short-bowel syndrome. sinus disease, gastroesophageal reflux,171 CFRD,172,173 and liver
d) The CF Foundation recommends that laboratory testing (serum disease.174
calcium, phosphorus, magnesium, parathormone, and 25- 2. Consideration should be given to ruling out the presence of other
hydroxy vitamin D levels), as well as a detailed diet history GI disease processes, such as lactose intolerance, infections (bacte-
for calcium and vitamin D intake, be obtained as part of a rial, parasitic), bacterial overgrowth, celiac disease, inflammatory
comprehensive assessment. bowel disease, short-bowel syndrome, and fibrosing colonopathy.
e) Since physical activity is an important factor in bone health, The latter should be suspected in any patient with a chronic his-
an exercise history is also recommended.159 tory of ingestion of high-dose PERT, GI symptoms, and growth
B. Diet history abnormalities.175
1. A dietary history should be done by a registered dietitian at least F. Determinants of disease severity
once a year in all children with CF. It may include a 24-hour dietary 1. There is a direct association between degree of undernutrition
recall, a 3-day written dietary record, an assessment of nutrient and and severity of pulmonary disease.20 Morbidity and mortality are
supplement intake, and anticipatory dietary and feeding behavior related to progressive lung disease.176,177
guidance.142 2. Female patients with CF appear to have a worse prognosis than
2. Patients should be questioned about a history of enzyme use with males, especially during adolescence. The reasons are unknown.178
meals and snacks.
3. More patients are trying complementary and alternative thera-
XVI. Goals of Therapy
pies,170 so a history of the use of these therapies should be taken.
4. More frequent or detailed diet evaluations may need to be done A. Normal growth
in those patients with failure to thrive, poor weight gain, and 1. The goals of nutritional therapy include promoting/obtaining
signs/symptoms of fat malabsorption. normal growth in all patients with CF.
5. The diet history should also evaluate any abnormalities in eating 2. The CF team should monitor growth and nutritional status closely.
behavior in the infant, toddler, child, or adolescent. Eating disor- This includes assessment of growth and pubertal status and early
ders can occur in adolescents with CF. initiation of appropriate nutritional interventions.

222 A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. © 2005 A.S.P.E.N. www.nutritioncare.org.
 S E C T I O N I I I Gastrointestinal Related Conditions

B. Maintained or improved nutritional status

1. All nutritional and growth abnormalities should be aggres- TABLE 15-2. Calculations of Energy Requirements
sively addressed. in Patients With Cystic Fibrosis
2. All abnormal vitamin and mineral and EFA levels should be cor-
rected and periodically reassessed. Energy needs = [REE × (AF + DC)] × 0.93/CFA
C. Promotion of optimal outcomes
1. Optimal outcomes can be achieved by periodic assessments of REE = resting energy expenditure or basal metabolic rate, which can
adherence to PERT by the CF team, especially by the registered be calculated using the World Health Organization energy equation
dietitian. In addition to a detailed history of the enzyme dose pre- for weight (Energy and Protein Requirements. Technical Report Series
scribed, the timing of enzyme consumption, and the storage of
No 724. Geneva, Switzerland: World Health Organization; 1985)
enzymes, a stool history and an evaluation of growth status are
critical.
2. It may be necessary to perform a 72-hour stool fat collection in AF = activity factor:
addition to a 3-day diet history with documentation of PERT 1.3 = confined to bed
usage and stool pattern. 1.5 = sedentary
3. Guidelines for screening and treatment of bone disease,159 liver 1.7 = active
disease,174 and CFRD172 are available from the CF Foundation.
4. DXA scans should be done in at-risk patients and at regular inter- DC = disease coefficient:
vals in patients with an abnormal DXA scan. 0 = normal lung function or FEV1 = 80% predicted or greater
0.2 = moderate lung disease or FEV1 = 40% to 79% predicted
XVII. Management 0.3 = severe lung disease or FEV1 = less than 40% predicted
A. Energy and macronutrient needs FEV = forced expiratory volume
1. The CF Foundation recommends a high-energy balanced diet
with adequate protein and unrestricted fat appropriate for age CFA = coefficient of fat absorption; if the value is not known,
and clinical state. use 85%
2. The new nutrition guidelines from the CF Foundation suggest
a diet that contains 35% to 40% of calories as fat.168
Adapted with permission from Baker RD, Borowitz D, Stallings VA. Consensus report
3. There are many methods to calculate energy needs in patients with on nutrition for pediatric patients with cystic fibrosis, 2002. J Pediatr Gastroenterol
CF. In 1990, the CF consensus conference report recommended a Nutr. 2002;35(3):246–259.
standard method to calculate energy needs taking into account
malabsorption and pulmonary status.142 (See Table 15-2.)
4. When weight gain is needed, energy needs are generally increased 12. Breast milk is the diet of choice for infants with CF. Some infants
by 250 to 1000 calories. may need caloric supplementation using formula or molecular
5. Energy needs should be periodically reassessed in conjunction additives (fat and/or carbohydrate) to breast milk (eg, Polycose,
with other nutritional assessment indices to ensure that energy vegetable oil, Microlipid, MCT, and Duocal).
intake is optimal. a) There is no advantage to recommending that the newly diag-
6. If no weight gain occurs, energy intake should be increased by nosed infant with CF be given elemental or partially digested
10% to 20%, with weight reassessed to determine adequacy. formula.
7. For adequately nourished patients with CF without associated b) If the mother chooses not to or cannot breast-feed her infant,
complications (normal nutritional status, well-controlled mal- then a cow’s milk–based formula can be used.
absorption, and normal pulmonary function), energy require- c) If the infant is not gaining weight appropriately, then the
ments are generally about 105% to 115% of the recommended caloric density of formula should be increased.
daily allowance (RDA). 13. The timing of the introduction of solids into the infant’s diet
8. Energy needs for patients with mild to moderate lung disease, should follow the recommendation of the American Academy
malabsorption, and nutritional failure are often in the range of of Pediatrics.179 When infants are fed cereals, breast milk or for-
120% to 150% of the RDA. mula rather than water or juice should be used as the mixing
9. Patients with severe lung disease may require up to 200% of the agent to provide additional calories.
RDA. However, some patients may compensate for increased 14. Patients with short-bowel syndrome, liver disease, uncontrolled
energy needs by decreasing physical activity, especially when malabsorption, and/or feeding intolerances may require a par-
they have pulmonary exacerbations. tially digested or semielemental formula such as Pregestimil
10. Most patients with CF ingest a diet with adequate to high levels (Mead Johnson Nutritionals, Evansville, IN) or Alimentum (Ross
of protein. Products Division, Columbus, OH) to promote optimal absorp-
11. Patients with CF typically will require a diet with 35% to 40% tion. Butter, margarine, or vegetable oil may be added to baby
of total daily energy intake contributed by fat, higher than the food for extra calories.
recommendations for the general US population (<30% of total 15. Toddlers, children, and adolescents benefit from a high-calorie,
daily energy intake as fat). well-balanced diet consisting of three meals and three snacks
a) Fat intake should never be restricted for patients with PI, and daily, consisting of energy-dense foods and homemade or com-
all patients should be prescribed a high calorie intake. mercial shakes.
b) Patients with recurrent pancreatitis should ingest a low-fat a) Simultaneously, energy intakes typically decrease due to ano-
diet during the acute episode. These patients usually revert rexia, fatigue, nausea, and vomiting, subsequently resulting
to their regular-fat diet once the acute episode has resolved. in weight loss and deterioration in nutritional status.

© 2005 A.S.P.E.N. www.nutritioncare.org. A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. 223
S E C T I O N I I I Gastrointestinal Related Conditions

b) Initiation of appropriate medical interventions (ie, IV antibi- d) Serum glucose levels should be checked in patients at risk
otics, increased airway clearance, etc) generally results in the for developing CFRD: patients with poor weight gain, feed-
return of appetite, increased energy intake, and ultimately ing intolerance, or corticosteroid use; and adolescents and
weight gain and improved nutritional status. young adults.
16. The first step in nutritional therapy is to counsel the patient and e) If excessive bloating occurs, a prokinetic medication to
family to increase consumption of nutritionally dense foods. It improve gastric emptying and a semielemental formula can be
is important that any commercial supplements used do not tried.
replace the patient’s usual food intake. While most practition- 24. PN is used infrequently in patients with CF. It is indicated in
ers use commercially available supplements for CF patients, neonates with meconium ileus in the perioperative period,
other approaches to increasing dietary intake may be equally patients with poor nutritional status and poor oral intake who are
valid. There appears to be limited efficacy for augmenting intake not candidates for tube feeds or who refuse tube feeds, patients
orally.180,181 who have respiratory distress or failure while waiting for a post-
17. Patients who do not respond to the above interventions will likely pyloric tube to be placed, patients who are vomiting and have
need aggressive nutrition support such as tube feeds (nasogastric, significant weight loss and malabsorption, and patients with
gastric, and jejunal). short-bowel syndrome who do not tolerate tube feeds.182
18. Indications for specialized nutrition support include poor weight 25. Patients with EFA deficiency (EFAD) unresponsive to enteral
gain for 6 to 12 months, poor nutritional status, and nutritional linoleic acid supplementation benefit from the administration of
failure in the pre–lung transplant and pre–liver transplant patient. IV fat.183
19. Before the initiation of nutrition support (enteral or parenteral), 26. Anabolic agents have been used in the management of patients
patients need to be appropriately educated and the topic discussed with CF diagnosed with nutritional failure. Insulin has been
in a positive light and proposed as supportive therapy. shown to improve weight gain and fasting hyperglycemia.184
a) A trial of nasogastric tube feeds prior to gastrostomy tube a) Use of growth hormone therapy has resulted in increased
placement is optimal. growth and weight, improved pulmonary function, and
b) The patient who develops gastroesophageal reflux with naso- fewer hospitalizations.185
gastric feeds that is unresponsive to medical therapy is con- b) Growth hormone therapy has been shown to decrease inflam-
sidered a candidate for jejunal feeds after an appropriate matory cytokine levels and result in less protein catabo-
evaluation by a gastroenterologist. lism.144
c) Nocturnal continuous feeds are often initiated to allow for c) Growth hormone therapy is not widely used, and the deci-
consumption of usual daytime nutrition intake and ambula- sion to start therapy must be made in consultation with an
tion. However, this type of regimen often has a negative impact endocrinologist.
on oral intake at breakfast. d) Trials with megestrol acetate have resulted in increased
d) Standard polymeric nutrient-dense commercially prepared appetite and weight gain.186
enteral formulations (1–2 cal/mL) are generally well toler- 27. Behavioral interventions are part of the management of the
ated. Usually, 30% to 50% of the total daily energy intake is patient with abnormal behaviors related to feeding.187
provided at night. B. Micronutrients
e) Tube feeding rates need to be adjusted depending on weight 1. Standard age-appropriate doses of water-soluble vitamins should
gain. Infants may need 120 to 150 cal/kg/day for catch-up be prescribed for all patients with CF.
growth and nutritional rehabilitation. This is usually pro- a) There are age-specific recommendations for vitamins A, D,
vided as a continuous nocturnal infusion for 30% to 50% of E, and K for patients with CF.142 (See Table 15-3.)
the total daily energy intake and as bolus or intermittent b) A common practice is to give patients with PI age-appro-
feeds during the day after the infant has been given an oppor- priate multivitamin doses (1–2 per day) and to give extra
tunity to feed orally. vitamin E.142
f) Signs of feeding intolerance are generally exhibited as nau- c) It is recommended that all pediatric patients with CF receive
sea, bloating, diarrhea, and anorexia. 0.3 to 0.5 mg of vitamin K daily.
20. PERT is usually given at the beginning of the feed; if needed, it d) Patients with liver disease and adults who have hemoptysis
is also provided midway through and at the end of feeds. and are frequently on antibiotics will require significantly
21. Some patients benefit from the use of very low fat elemental higher doses of vitamin K.
formulas, which do not require PERT. e) Adult patients should ingest 2.5 to 5 mg/week of vitamin K.164
22. Feeding intolerance may be addressed through the use of a com- 2. Patients consuming PERT should ingest their vitamin supplements
bination of enteric-coated and powdered PERT, concentrated with meals.
formulas, predigested formulas containing MCT, and/or low-fat 3. It is important to monitor fat-soluble vitamin status on a yearly
formulas. basis per the CF Foundation’s recommendations.
23. Patients with CFRD may require specialized formulas as well 4. Adult patients consuming two tablets per day of specially for-
as the use of insulin during tube feeds to avoid hyperglycemia. mulated vitamins for CF should be ingesting sufficient vitamins.
a) Patients at risk for CFRD may also develop this complica- 5. Supplementation of sodium starting at diagnosis and especially
tion during nutritional therapy. during the summer months is necessary for patients with CF.
b) All patients with suspected CFRD should have their blood a) This can be done by carefully adding extra salt to formula or
sugars checked 2 to 3 hours after the start of the tube feeds diet in infants and by offering salty foods and sport drinks to
and at the end of feeds on 2 to 3 separate nights.114 older patients.142
c) If the serum glucose value is more than 180 mg/dL, insulin b) The sodium requirement for infants without CF is 2 to 4 mEq/
should be administered.142 kg/day; infants with CF have higher requirements.

224 A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. © 2005 A.S.P.E.N. www.nutritioncare.org.
 S E C T I O N I I I Gastrointestinal Related Conditions

TABLE 15-3. Vitamin Supplements in Patients With CF

Age 0–12 months 1–3 years 4–8 years >8 years Adults

Vitamin A (international units) 1500 5000 5000–10 000 10 000 10 000

Vitamin E (international units) 40–50 80–150 100–200 200–400 200–400

Vitamin D (international units) 400 400–800 400–800 400–800 400–800*

* With additional sunlight exposure.

Adapted with permission from Baker RD, Borowitz D, Stallings VA. Consensus report on nutrition for pediatric patients with cystic fibrosis, 2002. J Pediatr Gastroenterol Nutr.
2002;35(3):246–259.

6. All patients should consume daily reference intake (DRI) levels lection for fecal fat, measuring fecal elastase, or measuring
for calcium daily (0–6 months: 210 mg; 6–12 months: 270 mg; fecal trypsin/chymotrypsin.
1–3 years: 500 mg; 4–8 years: 800 mg; 9–18 years: 1300 mg; 2. PERT should be prescribed for all patients with CF and PI at
19–51 years: 1000 mg; 51–70 years: 1200 mg). Note that the diagnosis. (See Table 15-1.)
requirements are in milligrams of elemental calcium per day. 3. All PS patients should have their pancreatic status monitored as
a) Patients with low bone mineral content (osteopenia and osteo- clinically indicated to determine if they have developed PI,
porosis) may need to increase their calcium intake. especially if they have genetic mutations associated with PI.
b) The upper limit for calcium is 2500 mg of elemental calcium 4. PERT only partially corrects fat malabsorption.130
per day. 5. Excessive PERT dosing is associated with the development of
c) Recommended vitamin D intakes have been clearly defined by fibrosing colonopathy.175
the CF Foundation.142 6. In 1995, the CF Foundation published dose recommendations
7. The CF Foundation recommends that any patient suspected of hav- for PERT. Infants should be given doses of 1500 to 2500 lipase
ing zinc deficiency receive a trial of zinc supplements for 6 months. units/kg body weight/meal, and older children and adolescents
a) Growth should be monitored during this period, with improve- should be given doses of 500 to 2500 lipase units/kg body weight/
ments in growth indicative of successful treatment. meal. Ranges of 500 to 4000 lipase units/g of fat/day should not
b) Zinc supplementation is also beneficial in the patient with low be exceeded. PERT should be given with all foods and milk
vitamin A status who does not respond to vitamin A supple- products.188
mentation, since zinc and vitamin A deficiency are interrelated. 7. PERT is not required with simple carbohydrates but is required
c) Zinc deficiency is generally manifested as poor growth, when starchy foods are ingested.
altered taste, and skin rash (acrodermatitis enteropathica). a) PERT is required with the consumption of breast milk and
8. It is common practice to treat EFAD with vegetable oils that are predigested formula, since both MCTs and long-chain triglyc-
high in linoleic/linolenic acids (eg, flaxseed oil, canola oil, wal- erides require lipase for digestion, although MCTs require
nut oil). Cold-water marine fish is another source of EFA and less.189
long-chain polyunsaturated fatty acids. b) PERT should be taken before each meal and snack.
a) All patients should meet the DRI requirements for linolenic c) If meals last longer than 30 minutes, it is recommended that the
acid. enzyme dose be split, with a half-dose given at the start of the
b) Patients with PI will need higher intakes to compensate for meal and the rest of the dose given halfway through the meal.
malabsorption. 8. Infants and children who cannot swallow the PERT capsules
c) The administration of IV fat during hospitalizations using a should be given their enzymes in applesauce immediately before
dose of 1 g/kg/day for the duration of the hospital stay may be eating.
beneficial in patients with documented EFAD. a) Parents are instructed to open the capsules and mix the beads
d) Patients at risk for EFAD include those with nutritional failure, with applesauce, which has an acidic pH.
those with moderate to severe lung disease, and those with b) Parents and caregivers should be educated to frequently check
frequent hospital admissions for pulmonary exacerbations. the infant’s mouth for retention of beads to prevent oral ulcer-
e) There are not enough data at this time to recommend DHA ations.
supplements to all patients with CF.139 c) A skin barrier cream may be needed to prevent perianal skin
9. Pediatric recommendations for iron and fluoride supplementa- irritation from the enzymes.
tion follow the American Academy of Pediatrics guidelines.179 d) Older children are encouraged to swallow enzyme capsules
Older patients and adult women with CF who are menstruating when they are able to do so.
may need supplemental iron, depending on the results of blood 9. Since the commonly available PERT products are porcine in
tests of iron status. origin, patients with pork allergy should not use them.
C. Pancreatic Enzyme Replacement Therapy (PERT) 10. Significant drug interactions can occur with PERT and calcium
1. At diagnosis, all patients with CF should have their pancreatic carbonate and magnesium hydroxide. Therefore, coadministra-
function assessed. This can be done by obtaining a 72-hour col- tion of these products should be avoided.

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11. Patients with CF have been shown to have gastric hypersecretion Owens, Anne M. Davis, Susan S. Baker, Robert D. Baker, and Valerie
and pancreatic secretions that are deficient in bicarbonate. This Marchand)
results in an acidic duodenal pH, which does not allow for opti-
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133. Cohn JA, Friedman KJ, Noone PG, et al. Relation between mutations of the report. CF Foundation. 2002;10(4):1–35.
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339(10):653–658. sity in normal-growing patients with cystic fibrosis. Acta Paediatr. 2003;92:
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138. Allen JR, McCauley JC, Selby AM, et al. Differences in resting energy
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in cystic fibrosis. Am J Clin Nutr. 1999;70(3):378–383.
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164. Lloyd-Still JD, Bibus DM, Powers CA, et al. Essential fatty acid defi-
139. Shepherd RW, Greer RM, McNaughton SA, et al. Energy expenditure in
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166. Beker LT, Russek-Cohen E, Fink RJ. Stature as a prognostic factor in cys-
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tic fibrosis survival. J Am Diet Assoc. 2001;101:438–442.
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167. Moore BJ, Durie PR, Forstner GG, et al. The assessment of nutritional sta-
142. Baker RD, Borowitz D, Stallings VA. Consensus report on nutrition for tus in children. Nutr Res. 1985;57:97–99.
pediatric patients with cystic fibrosis, 2002. J Pediatr Gastroenterol Nutr. 168. Stettler N, Kawchak DA, Boyle LL, et al. Prospective evaluation of
2002;35(3):246–259. growth, nutritional status, and body composition in children with cystic
143. Johannesson M, Gottlieb C, Hjelte L. Delayed puberty in girls with cys- fibrosis. Am J Clin Nutr. 2000;72:407– 413.
tic fibrosis despite good clinical status. Pediatrics. 1997;99:29–34. 169. Stern RC, Canda ER, Doershuk CF. Use of nonmedical treatment by cys-
144. Hardin DS, Ellis KJ, Dyson M, Rice J, McConnell R, Seilheimer DK. tic fibrosis patients. J Adolesc Health. 1992;13:612–615.
Growth hormone decreases protein catabolism in children with cystic 170. Malfroot A, Dab I. New insights on gastro-esophageal reflux in cystic
fibrosis. J Clin Endocrinol Metab. 2001;86(9):4424–4428. fibrosis by longitudinal follow-up. Arch Dis Child. 1991;66:1339–1345.
145. Hardin DS. Growth problems and growth hormone treatment in children 171. Moran A, Doherty L, Wang X, et al. Abnormal glucose metabolism in cys-
with cystic fibrosis. J Pediatr Endocrinol Metab. 2002;15(2):731–735. tic fibrosis. J Pediatr. 1988;133:10–17.
146. Hardin DS, Stratton R, Kramer JC, et al. Growth hormone improves 172. Moran A, Hardin D, Rodman D, et al. Diagnosis, screening and manage-
weight velocity and height velocity in prepubertal children with cystic ment of cystic fibrosis–related diabetes. A consensus report. Diabetes Res
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147. Palin D, Underwood BA, Denning CF. Effect of oral zinc supplementa- 173. Morris NM, Udry JR. Validation of a self-administered instrument to
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149. Lindblad A, Diczfalusy U, Hulcrantz R, Thorell A, Strandvik B. Vitamin 175. Fitzsimmons SC, Bukhart GA, Borowitz D, et al. High-dose pancreatic-
A concentration in the liver decreases with age in patients with cystic enzyme supplements and fibrosing colonopathy in children with cystic
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150. Rayner RJ, Tyrell JC, Hiller EJ, et al. Night blindness and conjunctival xero- 176. Kerem E, Reisman J, Corey M, et al. Prediction of mortality of patients
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180. Hanning RM, Blimke C, Bar-or O, et al. Relationships among nutritional 188. Borowitz DS, Grand RJ, Durie PR, et al. Use of pancreatic enzyme supple-
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230 A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. © 2005 A.S.P.E.N. www.nutritioncare.org.
 William A. Faubion, Jr, MD;
Darlene G. Kelly, MD, PhD
16
Inflammatory Bowel
Disease

Introduction 2. Restricted to the left colon in 40–50% of cases (isolated rectal or

rectosigmoid involvement)
The inflammatory bowel diseases (IBD) primarily include Crohn’s dis- 3. Remainder of cases extend proximally to involve mucosa beyond
ease and ulcerative colitis. These diseases can significantly impact an the splenic flexure. Twenty percent have pancolitis or involvement
individual’s nutritional status, and conversely, nutritional status can alter of the entire colon often with a short segment of terminal ileum
the disease course and outcome of therapies. Nutrient deficiencies result involved due to “backwash ileitis.”
from decreased intake, altered digestions and absorption, increased 4. Usually presents with bloody diarrhea, urgency, and sometimes
losses or requirements, and drug-nutrient interactions. This chapter will incontinence
describe the disease background, therapy options, and nutritional sup-
port practices.
III. Pharmacologic Therapy
I. Background A. Corticosteroid therapy most efficacious, rapidly active therapy avail-
II. Pathophysiology of Inflammatory Bowel Disease able for moderate to severely active IBD, effective in approximately
III. Pharmacologic Therapy 80% of cases4
IV. Nutritional Status in Inflammatory Bowel Disease B. 5-ASA products (mesalamine and sulfasalazine) effective in mild
V. Nutrition Support in Crohn’s Disease to moderately active UC and CD5–8
VI. Nutrition Support in Ulcerative Colitis 1. In UC, 5-ASA products have been shown to prolong remission.9,10
VII. Summary 2. In UC, 5-ASA products are associated with lower colon cancer
References rates.11,12
3. The immunomodulatory agents 6-mercaptopurine (6-MP) and
I. Background azathioprine are effective in the maintenance of remission in CD
and are empirically believed to be effective in UC.13–20 Azathi-
A. Inflammatory bowel disease (IBD) is an incurable relapsing disorder aprine/6-MP is also successfully used to heal fistulizing disease.21
B. It is characterized by chronic inflammatory involvement of the C. Methotrexate useful in the induction of remission and maintenance
small and large intestine of remission of CD in adults22 and in children.23
C. It occurs both in children and adults D. Newer “biologic” therapies, such as the monoclonal antibody to
D. Prevalence in U.S. only studied in Olmsted County, Minnesota1,2 TNFα, infliximab, are extremely effective in adults with moderate
1. Crohn’s disease (CD) for 1991 was 133 per 100,000 to severely active CD.
2. Ulcerative colitis (UC) was 229 per 100,000 residents 1. Induction24,25 and maintenance of remission26,27
3. Similar to European data 2. Perianal fistula healing28,29
E. Lifetime costs of care for Crohn’s disease approximately $125,000 per 3. Prospective30 and retrospective31 studies of pediatric patients have
patient3 shown similar efficacy in moderate to severely active CD, includ-
ing fistulizing disease.
II. Pathophysiology of Inflammatory Bowel Disease E. Antibiotics, particularly metronidazole and ciprofloxacin, are use-
ful in CD
A. Crohn’s Disease 1. Treatment of perianal disease
1. Can involve any portion of the alimentary tract from the mouth 2. Maintenance of post-operative remission32,33
to the anus 3. The high incidence of peripheral neuropathy severely limits the
2. In 80–90% of cases the small intestine is involved, particularly utility of metronidazole in CD
the terminal ileum 4. Antibiotics have not shown a consistent effect in UC, except in
3. Interspersed areas of normal mucosa are typical the case of pouchitis post colectomy.33
4. Inflammation of the bowel is patchy and involves the full thick- 5. No pediatric-specific data for antibiotics
ness of the intestine
5. Fistulae to other segments of involved bowel, adjacent organs IV. Nutritional Status in Inflammatory Bowel Disease
(bladder, uterus), and skin occur in 20–40% of patients.
6. Often presents with abdominal pain, fever, diarrhea, and weight loss A. Malnutrition in CD and to a somewhat lesser extent in UC is
B. Ulcerative Colitis common34
1. Mucosal disease restricted to the colon. It begins in the rectum in 1. Nutritional deficiencies or inability to maintain body weight occurs
a continuous distribution without interspersed normal mucosa. in 65–78% of those with CD and in 18–62% of those with UC.35,36

© 2005 A.S.P.E.N. www.nutritioncare.org. A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. 231
S E C T I O N I I I Gastrointestinal Related Conditions

2. Growth impairment found in 5% of children with CD.37 c) Steroids alter mineral and protein metabolism
3. At some point in the course of their disease, 75% of children with 7. Specific nutrient deficiencies
CD and 10% of children with UC have growth failure.35,38 a) Vitamins: A, D, E, K, C, B12, folic acid; more common in CD
B. Cause of malnutrition is multi-factorial (Table 16-1). b) Minerals: Copper, Calcium, Magnesium, Iron, Selenium, Zinc;
1. Reduced oral intake caused by: more common in CD
a) Pain c) Hypoalbuminemia in 25–80% of patients with CD and 26–50%
b) Obstructive bowel symptoms of those with UC35
c) Diarrhea d) Anemia in about 50% of patients with CD, primarily the result
d) Anorexia (possibly cytokine-induced) of malabsorption, and in up to 80% of those with UC, largely
e) Dysgeusia (secondary to medications or zinc deficiency)39 caused by blood loss
f) Acutely ill children consume less than 40 to 80% of estimated e) Electrolytes are often depleted as a result of diarrhea in both
needs38 CD and UC.
2. Maldigestion secondary to fistulae or surgically diverted intestine
3. Malabsorption due to bacterial overgrowth, enterocyte injury,
V. Nutrition Support in Crohn’s Disease
small intestinal resection, or bile acid wasting
4. Increased nutrient losses through bleeding, diarrheal losses, A. Use as primary therapy
fistulous drainage 1. Parenteral nutrition (PN) induces remission during acute attacks,
5. Alterations in energy expenditure but upon resuming oral diet, recurrence rates are high and do not
a) Total energy expenditure in quiescent and active CD is not justify the cost or risk associated with PN.42–44
significantly different than in normal volunteers39,40 2. No confirmed benefit for bowel rest in CD compared to enteral
b) Resting energy expenditure is increased in active CD, but feedings.45
activity level was decreased, making total energy expenditure 3. Meta-analyses comparing clinical remission with steroids was 80%
identical to normals40 versus 60% with elemental or polymeric enteral feedings46–48
6. Drug-nutrient interactions 4. No advantage for enteral elemental diets compared with semi-
a) Sulfasalazine decreases absorption and alters metabolism of elemental and polymeric formula diets (61% versus 65% remis-
folic acid sion rates) in adults47,48 and in pediatric patients48
b) TNFα antibody may alter protein metabolism 5. In pediatric CD, no difference in remission rate between elemen-
tal diets and corticosteroids, each achieving remission 75–90% of
the time48–51
B. In very extensive CD, PN may be required when the oral or tube
TABLE 16-1. Causes of Malnutrition in IBD enteral route is not possible until remission can be achieved or sur-
gery is performed.
Possible causes C. Correction of malnutrition is an important component of treatment.
of malnutrition General etiology Specific etiology D. Peri-operatively, PN in malnourished patients has shown
1. Fewer post-operative complications52
Decreased oral Altered taste Zn deficiency or 2. Improved clinical course53
intake (Dysgeusia) Metronidazole 3. Decreased length of bowel requiring resection, but at the expense
of a longer hospitalization54
Anorexia Cytokines (TNFa) 4. PN should be restricted to seriously malnourished patients sched-
uled for elective or semi-elective procedures or patients with
Pain Stricture, mucosal inflammation who are not responding to pharmacologic therapy
and who are not candidates for enteral nutrition support.
inflammation, or diarrhea
E. In growth failure, nocturnal enteral feeding stimulates growth55 with
significant height and weight gains compared to controls on standard
Maldigestion Enteric fistulae Poor exposure to therapy.56
digestive enzymes F. To induce healing of enterocutaneous fistulae
1. Fistulae may result in altered nutritional status, particularly of
Malabsorption Carbohydrate Enterocyte damage fluid, electrolytes, and zinc.57
Bacterial overgrowth 2. About 38% of fistulae initially close spontaneously with bowel
rest and PN, but recurrence is common with refeeding.58
Fat Enterocyte damage 3. If closure of a fistula is not achieved during several weeks of PN
Bile acid deficiency use, infliximab can be used in an attempt to avoid surgery.
(terminal ileal involve- G. Dietary modification is only indicated in IBD in patients with CD
where one or more non-obstructive strictures necessitates dietary
ment or resection)
fiber restriction.
Bacterial overgrowth
Extensive surgical
resection VI. Nutrition Support in Ulcerative Colitis
A. No support for concept that improved nutritional status coupled
Protein Inflamed tissue with bowel rest would achieve clinical remission and avoid colec-
tomy in UC

232 A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. © 2005 A.S.P.E.N. www.nutritioncare.org.
 S E C T I O N I I I Gastrointestinal Related Conditions

B. Role for specific nutrients in UC: 9. Anonymous. An oral preparation of mesalamine as long-term maintenance
1. Decreased relative risk of development of cancer or dysplasia in therapy for ulcerative colitis. A randomized, placebo-controlled trial. The
patients taking 0.4 and 1 mg folate daily59 Mesalamine Study Group. Ann of Intern Med. 1996;124:204–211.
2. Omega-3 fatty acids as a nutritional supplement decreased dis- 10. Miner P, Hanauer S, Robinson M, et al. Safety and efficacy of controlled-
release mesalamine for maintenance of remission in ulcerative colitis. Pen-
ease activity and was steroid sparing60–63
tasa UC Maintenance Study Group. Dig Dis & Science. 1995;40:296–304.
11. Eaden J. Review article: the data supporting a role for aminosalicylates in
VII. Summary the chemoprevention of colorectal cancer in patients with inflammatory
bowel disease. Aliment Pharm & Therap. 2003;18:15–21.
A. IBD is associated with significant nutritional risk; thus patients with 12. Eaden J, Abrams K, Ekbom A, et al. Colorectal cancer prevention in ulcer-
these diseases require ongoing assessment and intervention to cor- ative colitis: a case-control study. Aliment Pharm Therap. 2000;14:145–153.
rect nutritional deficits. 13. Rhodes J, Bainton D, Beck P, et al. Controlled trial of azathioprine in
B. Mechanisms for malnutrition in patients with IBD include decreased Crohn’s disease. Lancet. 1971;2:1273–1276.
nutrient intake, maldigestion, malabsorption, increased losses, 14. Klein M, Binder HJ, Mitchell M, et al. Treatment of Crohn’s disease with
increased requirements, and drug-nutrient interactions. azathioprine: a controlled evaluation. Gastroenterology. 1974;66:916–922.
C. Patients with CD do not require more energy than other patients. 15. Present DH, Korelitz BI, Wisch N, et al. Treatment of Crohn’s disease with
D. Bowel rest with PN has no advantage over enteral nutrition in the 6-mercaptopurine. A long-term, randomized, double-blind study. New Engl
management of patients with active CD, unless complicated by the J Med. 1980;302:981–987.
16. Ewe K, Herfarth C, Malchow H, et al. Postoperative recurrence of Crohn’s
presence of high output fistulae or high-grade small bowel obstruc-
disease in relation to radicality of operation and sulfasalazine prophylaxis:
tion, or in cases where the active disease is not responding to aggres-
a multicenter trial. Digestion. 1989;42:224 –232.
sive pharmacological therapy. 17. Willoughby JM, Beckett J, Kumar PJ, et al. Controlled trial of azathioprine
E. Elemental formulae have no advantage over polymeric diets. in Crohn’s disease. Lancet. 1971;2:944 –947.
F. Oral nutrition is the preferred route of feeding in patients with uncom- 18. Summers RW, Switz DM, Sessions JT Jr, et al. National Cooperative Crohn’s
plicated CD. Disease Study: results of drug treatment. Gastroenterology. 1979;77:
G. Peri-operative nutrition support may be indicated in patients with 847–869.
IBD who are severely malnourished prior to elective or semi-elective 19. Candy S, Wright J, Gerber M, et al. A controlled double-blind study of aza-
operations. thioprine in the management of Crohn’s disease. Gut. 1995;37:674–678.
H. In children with growth failure resulting from CD, nocturnal enteral 20. Oren R, Moshkowitz M, Odes S, et al. Methotrexate in chronic active
nutrition may stimulate growth. Crohn’s disease: a double-blind, randomized, Israeli multicenter trial. Am J
I. In cases of fistulae associated with CD, a brief course of bowel rest Gastro. 1997;92:2203–2209.
21. Sandborn W, Sutherland L, Pearson D, et al. Azathioprine or 6-mercaptop-
and parenteral nutrition may achieve fistula healing, but relapse rates
urine for inducing remission in Crohn’s disease. Coch Data Sys Rev. 2000;
are high.
2:CD000545.
J. PN and tube enteral nutrition have no therapeutic role in uncompli- 22. Feagan BG, Rochon J, Fedorak RN, et al. Methotrexate for the treatment
cated UC. of Crohn’s disease. The North American Crohn’s Study Group Investiga-
tors. New Engl J Med. 1995;332:292–297.
(IBD chapter from the 1st edition was contributed by Darlene G. Kelly 23. Mack DR, Young R, Kaufman SS, et al. Methotrexate in patients with
and Jan U. Burnes) Crohn’s disease after 6-mercaptopurine. J Pediatr. 1998;132:830–835.
24. D’Haens G, Van Deventer S, Van Hogezand R, et al. Endoscopic and his-
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S E C T I O N I I I Gastrointestinal Related Conditions

33. Shen B, Achkar JP, Lashner BA, et al. A randomized clinical trial of 49. Sanderson IR, Udeen S, Davies PS, et al. Remission induced by an ele-
ciprofloxacin and metronidazole to treat acute pouchitis. Inflamm Bowel mental diet in small bowel Crohn’s disease. Arch Dis Child. 1987;62:
Dis. 2001;7:301–305. 123–127.
34. Kelly DG, Fleming CR. Nutritional considerations in inflammatory bowel 50. Heuschkel RB, Menache CC, Megerian JT, et al. Enteral nutrition and corti-
diseases. Gastro Clin No Am. 1995;24:597–611. costeroids in the treatment of acute Crohn’s disease in children. J Ped Gastro
35. O’Keefe SJ. Nutrition and gastrointestinal disease. Scand J Gastroenterol- Nutr. 2000;31:8–15.
ogy Suppl. 1996;220:52–59. 51. Ruemmele FM, Roy CC, Levy E, et al. Nutrition as primary therapy in
36. Burke A, Lichtenstein GR, Rombeau JL. Nutrition and ulcerative colitis. pediatric Crohn’s disease: fact or fantasy? J Pediatr. 2000;136:285–291.
Baillieres Pract Res Clin Gastroenterol. 1997;11:153–174. 52. Rombeau JL, Barot LR, Williamson CE, Mullen JL. Preoperative total par-
37. Booth IW. The nutritional consequences of gastrointestinal disease in ado- enteral nutrition and surgical outcome in patients with inflammatory bowel
lescence. Acta Paediat Scand Suppl. 1991;373:91–102. disease. Am J Surg. 1982;143:139–143.
38. Oliva MM, Lake AM. Nutritional considerations and management of the 53. Eisenberg HW, Turnbull RB Jr, Weakley FL. Hyperalimentation as prepara-
child with inflammatory bowel disease. Nutrition. 1996;12:151–158. tion for surgery in transmural colitis (Crohn’s disease). Dis Col Rect. 1974;
39. Chan AT, Fleming CR, O’Fallon WM, et al. Estimated versus measured 17:469–475.
basal energy requirements in patients with Crohn’s disease. Gastroenterol- 54. Lashner BA, Evans AA, Hanauer SB. Preoperative total parenteral nutri-
ogy. 1986;91:75–78. tion for bowel resection in Crohn’s disease. Dig Dis Science. 1989;34:
40. Stokes MA, Hill GL. Total energy expenditure in patients with Crohn’s dis- 741–746.
ease: measurement by the combined body scan technique. J Parenter 55. Wilschanski M, Sherman P, Pencharz P, et al. Supplementary enteral nutrition
Enteral Nutr. 1993;17:3–7. maintains remission in paediatric Crohn’s disease. Gut. 1996;38:543–548.
41.Geerling BJ, Badart-Smook A, Stockbrugger RW, Brummer RJ. Comprehen- 56. Belli DC, Seidman E, Bouthillier L, et al. Chronic intermittent elemental
sive nutritional status in patients with long-standing Crohn disease currently diet improves growth failure in children with Crohn’s disease. Gastro-
in remission. Am J Clin Nutr. 1998;67:919–926. enterology. 1988;94:603–610.
42. Shiloni E, Coronado E, Freund HR. Role of total parenteral nutrition in the 57. Yamazaki Y, Fukushima T, Sugita A, et al. The medical, nutritional and surgi-
treatment of Crohn’s disease. Am J Surg. 1989;157:180–185. cal treatment of fistulae in Crohn’s disease. Jap J Surgery. 1990;20:376–383.
43. Dickinson RJ, Ashton MG, Axon AT, Smith RC, Yeung CK, Hill GL. Con- 58. Afonso JJ, Rombeau JL. Nutritional care for patients with Crohn’s disease.
trolled trial of intravenous hyperalimentation and total bowel rest as an Hepato-Gastroenterology. 1990;37:32–41.
adjunct to the routine therapy of acute colitis. Gastroenterology. 1980;79: 59. Lashner BA, Provencher KS, Seidner DL, et al. The effect of folic acid sup-
1199–1204. plementation on the risk for cancer or dysplasia in ulcerative colitis. Gas-
44. McIntyre PB, Powell-Tuck J, Wood SR, et al. Controlled trial of bowel rest troenterology. 1997;112:29–32.
in the treatment of severe acute colitis. Gut. 1986;27:481–485. 60. Hawthorne AB, Daneshmend TK, Hawkey CJ, et al. Treatment of ulcerative
45. Greenberg GR, Fleming CR, Jeejeebhoy KN, et al. Controlled trial of colitis with fish oil supplementation: a prospective 12 month randomised
bowel rest and nutritional support in the management of Crohn’s disease. controlled trial. Gut. 1992;33:922–928.
Gut. 1988;29:1309–1315. 61. Lorenz R, Weber PC, Szimnau P, et al. Supplementation with n-3 fatty
46. Messori A, Trallori G, D’Albasio G, et al. Defined-formula diets versus acids from fish oil in chronic inflammatory bowel disease—a randomized,
steroids in the treatment of active Crohn’s disease: a meta-analysis. Scand placebo-controlled, double-blind cross-over trial. J Intern Med. 1989;225:
J Gastro. 1996;31:267–272. 225–232.
47. Fernandez-Banares F, Cabre E, Esteve-Comas M, et al. How effective is 62. Lorenz-Meyer H, Bauer P, Nicolay C, et al. Omega-3 fatty acids and low
enteral nutrition in inducing clinical remission in active Crohn’s disease? carbohydrate diet for maintenance of remission in Crohn’s disease. A ran-
A meta-analysis of the randomized clinical trials. J Parenter Enteral Nutr. domized controlled multicenter trial. Study Group Members (German
1995;19:356–364. Crohn’s Disease Study Group). Scand J Gastro. 1996;31:778–785.
48. Griffiths AM, Ohlsson A, Sherman PM, et al. Meta-analysis of enteral nutri- 63. Aslan A, Triadafilopoulos G. Fish oil fatty acid supplementation in active
tion as a primary treatment of active Crohn’s disease. Gastroenterology. ulcerative colitis: a double-blind, placebo-controlled, crossover study. Am
1995;108:1056–1067. J Gastro. 1992;87:432–437.

234 A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. © 2005 A.S.P.E.N. www.nutritioncare.org.
 Jeanette M. Hasse, PhD, RD, LD, FADA, CNSD;
Stuart S. Kaufman, MD;
Erin Fennelly, RD, CNSD 17
Liver Disease

Introduction (2) Chemical toxicity (eg, poisonous mushrooms or industrial

poisons)
As a primarily metabolic organ, the liver orchestrates a complex array e) Inherited disorders—includes metabolic diseases such as:
of physiologic and biochemical processes, one of which is the regula- (1) Hemochromatosis—iron overload
tion of protein and energy metabolism. Consequently, it is not surpris- (2) Wilson’s disease—copper overload
ing that protein calorie malnutrition (PCM) is a common complication (3) Alpha-1-antitrypsin deficiency
of advanced liver disease. The demonstration that PCM is an independ- f ) Other
ent risk factor for predicting clinical outcomes in cirrhosis and the fact (1) Systemic diseases—includes rheumatoid arthritis, systemic
that nutritional intervention may improve survival, surgical outcome, lupus erythematosus, polymyalgia, polyarteritis nodosa,
liver function, and hepatic encephalopathy have made the recognition of Sjögren’s syndrome, autoimmune disease
PCM an important factor in the management of liver disease patients. (2) Non-alcoholic steatohepatitis (NASH)
The aim of the present chapter is to provide a practical approach to the (3) Vascular conditions—Budd Chiari syndrome, hepatic
nutrition management of patients with liver disease, recognizing there is venoocclusive disease
insufficient information for proscriptional recommendations. (4) Infectious—parasitic, bacterial, fungal, and granulomatous
liver disease
I. Overview of Liver Disease 2. Duration
II. Metabolic Alterations in Chronic Liver Disease a) Acute—sudden and massive destruction of liver cells3
III. Protein-Calorie Malnutrition (PCM) in Liver Disease (1) Fulminant—severe liver dysfunction with hepatic encepha-
IV. Nutrition Assessment lopathy and coagulopathy that develop within 2 weeks of
V. Objectives of Nutritional Therapy illness onset; no previous history of liver dysfunction
VI. Feeding Goals (2) Subfulminant—hepatic encephalopathy and coagulopathy
VII. Methods of Nutrient Delivery develop in 2 to 8 weeks of onset of illness
VIII. Patient Education (3) Late-onset liver failure—hepatic encephalopathy and coag-
References ulopathy develop within 8 to 24 weeks of onset of illness
b) Chronic—at least a 6-month course
B. Pediatric—Nutrition support is relevant primarily to chronic fibro-
I. Overview of Liver Disease cirrhotic disorders and acute liver failure
A. Adult1,2 1. Fulminant and subfulminant liver failure
1. Types a) Viruses (A to G viruses)
a) Viral hepatitis—inflammation of the liver caused by b) Certain inborn errors (eg, neonatal hemochromatosis)
(1) Hepatitis A—transmitted by the oral-fecal route c) Toxins (eg, poisonous mushrooms)
(2) Hepatitis B and C—transmitted via body fluids 2. Chronic liver disease
(3) Hepatitis D—only occurs in patients infected with hepa- a) In infants, disorders include:
titis B (1) Intrahepatic and extrahepatic biliary obstructive disorders
(4) Hepatitis E—transmitted via the oral-fecal route; hepatitis (eg, biliary atresia, familial intrahepatic cholestasis, Alagille
E is rare in the U.S. but is seen more often in Asia, Africa, Syndrome)
and Mexico (2) Metabolic disorders involving the hepato-biliary system
b) Alcohol—most common liver disease in the United States; such as cystic fibrosis, Niemann-Pick disease type C
progresses in 3 stages b) In older children, disorders include:
(1) Hepatic steatosis (1) Late onset of symptomatic alpha-1-antitrypsin deficiency
(2) Alcoholic hepatitis (2) Secondary hemochromatosis
(3) Alcoholic (Laennec’s) cirrhosis (3) Autoimmune liver disease
c) Cholestatic disease—involves the bile ducts (4) Chronic hepatitis C and human immunodeficiency virus
(1) Primary biliary cirrhosis—destruction of small and inter- (HIV; rarely)
mediate-sized intrahepatic bile ducts
(2) Sclerosing cholangitis—inflammation of segments of extra- II. Metabolic Alterations in Chronic Liver Disease
hepatic bile ducts; may involve intrahepatic ducts
d) Toxic hepatitis—often includes: A. Accelerated starvation—The preferred fuel in cirrhotic patients is
(1) Drug toxicity (eg, acetaminophen) fat. This phenomenon is especially apparent after an overnight fast,

© 2005 A.S.P.E.N. www.nutritioncare.org. A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. 235
S E C T I O N I I I Gastrointestinal Related Conditions

as fat supplies approximately 75% of calories compared with 35% 2. Alcohol inhibits meal-stimulated hepatic protein synthesis.
in normal subjects.4 3. Alcohol increases intestinal permeability, which increases endo-
B. Protein imbalance toxin uptake and cytokine-induced muscle proteolysis.
1. The starvation response is accelerated with increased skeletal mus- 4. Alcohol provides “empty” calories.
cle breakdown to supply substrate for gluconeogenesis and energy a) Alcohol has a theoretic caloric density of 7 kcal/g but its calo-
expenditure.5 Protein catabolism is not as easily suppressed by ries are oxidized less efficiently than other carbohydrates and
feeding as in normal individuals. lipid.
2. Hepatic encephalopathy—Neuro-psychiatric abnormalities may b) Alcohol replaces other nutrient-dense energy sources.
occur with advanced acute or chronic liver failure. These mental c) Alcohol-induced cirrhosis generally results in decreased mus-
status alterations may range from mild behavioral changes to deep cle mass but a relative sparing of fat stores compared with
coma (Table 17-1). nonalcoholic cirrhosis.
a) Sub-clinical hepatic encephalopathy is present in 70% of pa-
tients with cirrhosis and does not require any specific nutri-
tional therapy. III. Protein-Calorie Malnutrition (PCM) in
b) Hepatic encephalopathy associated with liver failure is the Liver Disease
third most common cause of death in patients with cirrhosis A. Adult
and is responsible for approximately 20% of the deaths from 1. Prevalence
this disease. a) PCM is uncommon in chronic liver disease without cirrhosis.
c) Although the pathogenesis of hepatic encephalopathy remains Nutritional management is based on standard recommenda-
poorly defined, all the proposed toxins (ammonia, mercaptans, tions that are not disease-specific.
fatty acids, γ-aminobutyric acids, altered plasma amino acid b) In contrast with non-cirrhotic liver disease, PCM is highly
profile, and endogenous benzodiazepines) appear to be related prevalent in all forms of cirrhosis.5,11 In alcoholic cirrhosis,
in part to protein feeding. PCM severity correlates with liver dysfunction (as measured
d) Overt encephalopathy is almost always associated with some
by serum bilirubin and international normalized ratio [INR]).
precipitating event, such as gastrointestinal (GI) bleeding,
c) Characteristics of PCM are influenced by the etiology of the cir-
infection or sepsis, fluid and electrolyte imbalances, consti-
rhosis, ie, the type of underlying liver disease (see Table 17-2).
pation, acid-base abnormalities, or inappropriate use of sedat-
2. The cause of PCM is multifactorial (see Table 17-3).
ing drugs. In 5% or less of patients with cirrhosis, hepatic
a) Anorexia is prevalent. Central appetite suppression can be
encephalopathy may be precipitated by dietary protein intake
caused by increased pro-inflammatory cytokine production.
(especially animal protein) without any other precipitating
b) Diagnostic and therapeutic procedures interrupt eating and
factor. These patients are considered protein intolerant and
contribute to low intake. Typical intakes meet ∼ 50% of needs
may benefit from a diet enriched in branched-chain amino
during the first 10 days of hospitalization.12
acids (BCAA).6–10
e) More than 95% of patients with cirrhosis tolerate diets of mixed c) Early satiety can be caused by gastric compression from ascites
proteins (up to 1.5 g/kg/d for adults, up to 4 g/kg/d for children and hepatosplenomegaly.
receiving tube feeding, and up to 2.5 g/kg/d for children receiv- d) Dysgeusia is probably related to zinc deficiency and unpalat-
ing parenteral nutrition); some studies suggest a benefit of able diets.
BCAAs over standard amino acids in these patients.6–10
C. Metabolic alterations in alcoholic liver disease
1. Alcohol has deleterious effects on muscle protein status inde-
pendent of associated liver injury. TABLE 17-2. Pattern of Malnutrition
in Chronic Liver Disease

Reduced
TABLE 17-1. Four Stages of Hepatic Encephalopathy Muscle Loss of Synthetic
Wasting Fat Stores Function
Stage Symptoms
Alcohol ● ■ ▲
I mild confusion, agitation, irritability, sleep disturbance,
decreased attention Viral ▲ ▲ ■
II lethargy, disorientation, inappropriate behavior,
drowsiness Primary biliary
cirrhosis ● ● ■
III somnolent but arousable, incomprehensible speech,
confused, aggressive when awake Primary sclerosing
IV Coma cholangitis ▲ ■ ■

Reprinted with permission from Hasse JM, Matarese LE. Nutritional care in diseases ■, mild abnormalities; ▲, moderate abnormalities; ●, severe abnormalities
of the liver, biliary system, and exocrine pancreas. In: Mahan LK, Escott-Stump S, eds. Reprinted from McCullough AJ. Malnutrition in liver disease. Liver Transplant.
Krause’s Food, Nutrition, and Diet Therapy. 11th ed. Philadelphia: W.B. Saunders Com- 2000;6(4 suppl 1):S85–S96 with permission of Wiley-Liss, Inc., a subsidiary of John
pany; 2004:738–767. Wiley & Sons, Inc.

236 A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. © 2005 A.S.P.E.N. www.nutritioncare.org.
 S E C T I O N I I I Gastrointestinal Related Conditions

(2) Bleeding due to portal hypertension contributes to intestinal

TABLE 17-3. Etiologic Factors for Protein Calorie Mal- protein loss. Because hemoglobin lacks the essential amino
nutrition in Cirrhosis acid isoleucine, hemoglobin is a relatively low-quality pro-
tein source.
Adults Children (3) Large-volume paracentesis may also cause a loss of 10–
20 g of protein.
Reduced nutrient intake* Reduced nutrient intake* (4) Portal hypertension impairs GI motility and increases GI
• Anorexia • Anorexia protein loss.
• Increased satiety • Increased satiety (5) Small intestinal bacterial overgrowth associated with cir-
• Nausea and vomiting • Nausea and vomiting rhosis also increases fat and protein losses.
• Iatrogenic (protein, 3. Prognosis—PCM adversely affects clinical outcomes in cirrhotic
fluid/salt restriction) adult patients (Table 17-5). Successful nutritional intervention
may improve liver function, short-term survival, and outcome fol-
lowing liver transplantation.
Malabsorption* Malabsorption
B. Pediatric considerations with PCM of chronic liver disease
• Pancreatic and bile salt • Pancreatic and bile salt 1. Prevalence
deficiency deficiency a) PCM incidence in children with liver disease is approximately
• Enteropathy • Portal hypertension 60%.15
• Small intestinal bacterial b) Metabolic and nutritional abnormalities develop and become
overgrowth apparent more rapidly than in adults due to higher metabolic
rates associated with body growth.5
2. Etiology of PCM is similar to adults with chronic liver disease
Altered protein and energy Altered energy metabolism
(Table 17-3).
metabolism • Increased resting energy a) Reduced nutrient intake is the most important factor.
• Alcohol toxicity on energy and expenditure b) Malabsorption occurs with diseases that have coincident pan-
protein • Increased active energy creatic insufficiency (eg, Alagille syndrome and cystic fibrosis).
• Amino acid oxidation expenditure c) Increased energy consumption
• Increased protein breakdown (1) Resting energy expenditures (REE) are generally increased
• Accelerated fat oxidation and per kg of total body weight by about 140% to 160% or to
gluconeogenesis approximately 75 kcal/kg/d.16,17
(a) Increased REE results from relative increase in body
cell compartment as a fraction of total body weight due
Fasting status
to reduction in the (less metabolically active) body fat
(if hospitalized) for compartment.
• Diagnostic testing (b) Also, energy expenditure per unit of body cell compart-
• Gastrointestinal bleeding ment is increased, likely because of increased activity
• Altered neurologic status of futile metabolic pathways (eg, cyclical fatty acid syn-
thesis and degradation) and possibly because of carni-
tine deficiency.
* Factors that can be altered or treated. (2) Total energy expenditures (TEE), the sum of REE and addi-
tional physical activity, are increased from the usual 160%
of REE to about 200% of REE (140 to 160 kcal/kg/d).17
e) Fat malabsorption is usually less important than decreased (a) Increased energy consumption from hepatospleno-
intake and mainly due to reduced intestinal bile acids. megaly and ascites contributes to increased energy
(1) Bile acid deficiency reduces net lipid absorption from 95% expenditure.
to 75%. (b) TEE also increases intermittently as a result of infec-
(a) Moderate steatorrhea (<12 g daily) is typical. tious and inflammatory stresses.
(b) Stool fat loss may exceed 30 g daily with severe 3. Prognosis—Malnutrition predicts reduced survival after liver
cholestasis. transplantation independent of other features of advanced liver
(2) Bile acid deficiency also contributes to fat-soluble vitamin disease.18
deficiency (Table 17-4) and essential fatty acid deficiency, a) Any chronic liver disease causes malnutrition; malnutrition,
symptoms of which include dry skin and hair loss.13 in turn, promotes further deterioration in liver function irre-
(3) Enteropathy may coexist with liver disease (eg, celiac sprue spective of the original cause.
is associated with primary biliary cirrhosis or autoimmune b) Because malnutrition reflects the severity of liver disease, cor-
disease, and inflammatory bowel disease with primary scle- rection of malnutrition does not always improve survival in
rosing cholangitis). the absence of transplantation.
(4) Patients with alcoholic liver disease may have exocrine
pancreatic insufficiency with defective lipase secretion.
IV. Nutrition Assessment
f ) Increased intestinal protein losses
(1) Prevalence—Occurs in up to 40% of patients. Enteral feed- A. An initial comprehensive nutritional assessment includes objective
ing may actually improve intestinal absorption.14 and subjective parameters (see Table 17-6).

© 2005 A.S.P.E.N. www.nutritioncare.org. A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. 237
S E C T I O N I I I Gastrointestinal Related Conditions

TABLE 17-4. Fat-Soluble Vitamin Supplements for Prophylaxis and Treatment for Children with Liver Disease

Vitamin Brand Typical Dose Route Deficiency Comments

Vitamin A ADEKs Pediatric Drops* 5,000–25,000 USP PO Xerophthalmia Normal plasma

(Axcan Pharma, Birmingham, AL) units daily (dry eye) level=300–400 mcg/L Symp-
Aquaso® A Parenteral 5,000–50,000 daily IM Hyperkeratosis toms develop at
(aaiPharma, Wilmington, DE) for 1–2 weeks Night blindness 100 mcg/L
Plasma levels correlate
poorly with stores—aim to
maintain low levels

Vitamin D Rocaltrol (Roche Laboratories, 0.025 –1.0 mcg/kg PO Rickets Monitor calcium, phosphorus,
(Calcitriol) Nutley, NJ) daily Osteomalacia intact PTH levels
-Solution (1 mcg/mL)
-Capsules (0.25 and 0.5 mcg/mL)

Vitamin E Nutr-E-Sol; 400 IU/15 mL 25 IU/kg/d PO Peripheral neuropathy Desired plasma level
(Tocopheryl-PEGS) (Advanced Nutritional Technol- Ataxia (5–15 mcg/mL) affected by
ogy, Inc, Dublin, CA) serum lipids
ADEKs Pediatric Drops
(Axcan Pharma, Birmingham, AL)

Vitamin K Mephyton 5 mg tabs 2.5–5 mg daily PO Coagulopathic Monitor with prothrombin

(phytonadione) (Merck & Co., Whitehouse Sta- hemorrhage time (PT)
tion, NJ) Use SQ if PO ineffective
ADEKs Pediatric Drops 5–10 mg every SQ
(Axcan Pharma, Birmingham, AL) 2 weeks
AquaMEPHYTON
(Merck & Co., Whitehouse Sta-
tion, NJ)

*ADEKs Pediatric Drops include 3,170 USP units of vitamin A, 40 IU of tocopheryl-PEGS, and 0.1 mg of phytonadione per mL.

B. If possible, REE should be measured with indirect calorimetry. 2. Calorie counts and/or dietary recalls are important tools to deter-
1. REE is highly variable in cirrhosis: 30% of patients are hypometa- mine the adequacy of oral intake.
bolic and 20% hypermetabolic.19
2. Prediction of energy requirements based on standard equations
is unreliable.20 V. Objectives of Nutrition Therapy
3. If indirect calorimetry is not available, estimate energy expen-
diture with consideration of existing deficits and increased or A. Prevent or slow catabolism to prevent or correct PCM.
decreased ongoing needs. General energy estimates are: adults B. Attain optimal glucose control.
∼25 to 30 kcal/kg/d, children receiving tube feeding ∼130 to C. Sustain energy balance and deliver sufficient calories in children to
160 kcal/kg/d, children receiving parenteral nutrition ∼100 to ensure that linear growth is not limited by nutrient supply.
130 kcal/kg/d. D. Correct or prevent vitamin deficiencies and trace element abnor-
a) Ascites increases REE by 10%.21 malities.
b) If ascites or edema is present, it is controversial whether actual, E. Improve hepatic function and promote hepatocellular regeneration,
ideal, or estimated “dry” weight should be used in calculation. benefits of which include:
C. Follow-up assessment 1. Reversal of existing encephalopathy and prevention of future
1. Standard monitoring can be useful in patients with chronic liver episodes.23
disease.5,22 Patients with chronic liver disease must be monitored 2. Reduction of ascites and edema and correction of electrolyte dis-
for signs of encephalopathy, fluid retention (peripheral edema and orders (hyponatremia, hypokalemia, hypocalcemia, hypocal-
abdominal distention secondary to ascites), and gastrointestinal cemia) related to PCM and renin-angiotensin activation in chronic
blood loss. Weight change can signal fluctuation in fluid retention liver disease.
with or without alterations in lean or fat mass. F. Preparation for transplantation (if indicated).

238 A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. © 2005 A.S.P.E.N. www.nutritioncare.org.
 S E C T I O N I I I Gastrointestinal Related Conditions

3. The fat oxidation-predominant metabolic profile of cirrhosis is

TABLE 17-5. Studies in Which Protein Calorie Malnutri- similar to the fasting profile of normal individuals. Patients with
tion was Determined to be cirrhosis should avoid fasting which rapidly leads to muscle
a Poor Prognostic Factor in Cirrhosis catabolism.24,25
4. Diet composition is based on the natural history of the liver disease.
Condition or Clinical Outcome Study Author a) In the absence of severe anorexia, patients with mildly decom-
Procedure Measured (year) pensated cirrhosis, PCM, ascites, and hyponatremia, may be
able to consume the desired high-calorie/protein and low-
Cirrhosis Survival Caregaro (1996)51 sodium/fluid diet. Carbohydrate-controlled diets are indicated
Merli (1996)52 for patients with diabetes mellitus.
Immunodeficiency Qiao (1988)53 b) Enteral feeding improves liver function and encephalopathy in
malnourished patients with cirrhosis or decompensated alco-
O’Keefe (1980)54
holic liver disease.26–29 Hirsch et al provided nutritional supple-
Lautz (1994)55
ments (1000 kcal and 34 g of casein protein) for 1 year to
patients with complicated alcoholic cirrhosis, reducing their
Cirrhosis patients Predicting bleeding, Müller (1994)56 need for hospitalization to treat infections30, but positive effects
with varices survival on long-term survival remain difficult to demonstrate.
B. Specific nutrient guidelines (guidelines for adults with end-stage
Cirrhosis patients Survival Garrison (1984)57 liver disease are summarized in Table 17-7)
having abdominal Postoperative Ouchi (1988)58 1. Electrolytes
surgery complications a) Sodium—Dietary restriction (1500 to 2000 mg) is the corner-
stone of treatment of ascites and edema, supplemented with
Hospitalized patients Survival Llach (1988)59 diuretic therapy when necessary.
b) Potassium—Potassium levels must be monitored closely,
with ascites/ Blendis (1986)60
because hypokalemia can result from diarrhea or vomiting
cirrhosis Franco (1987)61
and hyperkalemia may occur in the presence of hepatorenal
syndrome. Diuretics can be either potassium-wasting or
Alcoholic hepatitis Survival Mendenhall (1984, potassium-sparing.
Liver function 1986)62,63 2. Fluid—Restriction to approximately 1000 mL to 1500 mL per day
is indicated for hyponatremia. Conversely, patients with liver dis-
Liver transplantation Patient/graft Shaw (1985)64 ease associated with intestinal insufficiency, for example, Crohn’s
survival Lautz (1992)55 disease or short bowel syndrome, may be at risk of dehydration
Moukarzel (1990)18 and periodically require extra fluids.
Selberg (1997)65 3. Vitamins
Harrison (1997)66 a) Generally, a multi-vitamin preparation is recommended.
b) Recommendations for fat-soluble vitamin supplementation in
Pikul (1994)67
children are listed in Table 17-2.
Hasse (1998)68
4. Trace elements
Length of post- Pikul (1994)67 a) Zinc requirements are increased31; children with liver disease
transplant Figueirdeo (2000)69 may require up to 0.3 mg/kg/d.
hospitalization Stephenson b) In patients with cholestatic liver disease receiving PN, high
(2001)70 serum levels of copper and manganese and low levels of sele-
nium are typical.32 Copper and manganese should be withheld
Hepatectomy Postoperative Fan (1994)71 unless serum levels are low. Serum copper and manganese
complications levels should be followed intermittently.
c) Selenium should be given based on serum concentration (up
to 5 mcg/kg/d) as should chromium (up to 0.2–0.3 mcg/kg/d).
Adapted from McCullough AJ. Malnutrition in liver disease. Liver Transplant. 2000;6(4, d) Iron—Increased losses due to chronic occult or overt gastroin-
Suppl 1):S85–S96 with permission of Wiley-Liss, Inc., a subsidiary of John Wiley &
testinal hemorrhage and repeated diagnostic blood testing gen-
Sons, Inc.
erally indicate supplementation based on serum iron saturation.
Ferritin concentration usually rises in chronic liver disease and
does not reliably reflect body iron stores.
VI. Feeding Goals
C. Additional pediatric considerations for macronutrient intake15
A. Background 1. Protein—The usual goal is 3.5–4.0 g/kg/d in patients receiving
1. Nutrition support is usually less relevant to acute liver failure enteral nutrition and 1.5–2.5 g/kg/d in patients receiving par-
secondary to drugs (eg, acetaminophen) or toxins (eg, Amanita enteral nutrition.
mushroom) than to chronic liver disease, because recovery or 2. Energy—The usual goal for enteral intake is 130–160 kcal/kg/d,
death occurs quickly in the absence of liver transplantation. including 35% to 45% of total calories as lipid. Although medium
2. The gastrointestinal tract functions adequately in most adult and chain triglyceride (MCT) oil in the amount of 1⁄3 to 1⁄2 of lipid calo-
pediatric patients with chronic liver disease, allowing correction ries is often recommended, no prospective data have confirmed a
of most deficits by oral or enteral route. benefit compared with long-chain triglyceride (LCT)-predominant

© 2005 A.S.P.E.N. www.nutritioncare.org. A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. 239
S E C T I O N I I I Gastrointestinal Related Conditions

TABLE 17-6. Nutritional Assessment in Patients with Liver Disease

Component of Additional considerations

Assessment Parameters with children

Medical history • Etiology, duration, and severity of liver damage

• Prognosis of disease
• GI function – propensity for nausea, vomiting, diarrhea, and GI bleeding
• Concomitant damage to other organs (eg, chronic pancreatitis in alcoholics,
diabetes and cardiomyopathy in hemochromatosis, heart and/or lung disease
increasing energy expenditure, renal disease affecting fluid and electrolyte
balance, glucose intolerance and hyperlipidemias)

Nutrition history • Diet history to assess quality and quantity of intake • Consider route of feeding and
• Medication history to identify drug-nutrient interactions type of formula if bottle fed
• Use of nutrition supplements including vitamin, mineral, and herbal preparations
• Psychosocial and economic conditions to determine patient’s or caregiver’s ability
to obtain/prepare food and comply with diet

Physical examination • Mental status

• Muscle and fat stores
• Edema or ascites
• Skin — jaundice, bruising, excoriations (from pruritus), or xanthomas
• Oral/dental health
• Assessment of activity

Anthropometric • Height • Height/length and percentile

measurements • Weight history (to assess degree of fluid retention and weight loss) for age
• Tricep skinfold and mid-arm muscle circumference measurements may be helpful if • Head circumference and
measured serially over time percentile for age
• Hand grip strength may be an indirect measure of muscle stores • Weight and percentile for age
• Weight for length percentile
• Tricep skinfold and mid-arm
muscle area measurements
and percentiles for age

Laboratory tests • Tests to evaluate liver function such as bilirubin, AST, ALT, GGT, prothrombin time • Urine calcium to creatinine
(or INR) ratio
• Serum electrolytes • Serum zinc and urine zinc to
• Tests to evaluate renal function such as blood urea nitrogen and creatinine creatinine ratio
• Hepatic transport proteins are not especially helpful because concentrations are • Fatty acid profile, including
affected by fluid status, liver and kidney function, and vitamin status. C20:3w9
• Iron studies such as serum iron, ferritin, total iron binding capacity, and iron • ESR, C-reactive protein
saturation
• Serum lipid levels
• Fat-soluble vitamin levels (especially in patients with cholestatic liver disease)

Other tests • Subjective global assessment may be helpful as an initial assessment tool
• Bioelectrical impedance is probably an inaccurate measure of PCM in cirrhosis
patients with ascites or edema
• Creatinine-height index is influenced by renal function
• Dual-energy X-ray absorptiometry can be used to accurately measure bone density
and body fat
• Indirect calorimetry can accurately determine resting energy expenditure

AST, aspartate aminotransferase; ALT, alanine aminotransferase; GGT, gamma glutamyltransferase; INR, international normalized ratio (for prothrombin time); ESR, erythrocyte
sedimentation rate

240 A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. © 2005 A.S.P.E.N. www.nutritioncare.org.
 S E C T I O N I I I Gastrointestinal Related Conditions

TABLE 17-7. Dietary Considerations for Adult Patients with End-stage Liver Disease

Symptom Nutrition Recommendations

Cachexia • Provide at least 120% of estimated energy expenditure

• Provide increased calories if malabsorption or malnutrition is present
• Offer small, frequent meals of calorie-dense foods

Encephalopathy • Maximize medical therapy (eg, lactulose, neomycin)

• Identify and treat cause(s) of acute bouts of encephalopathy (eg, variceal bleed, infection, electrolyte imbalance,
sedatives, constipation, etc.)
• Restrict protein only if patient is protein sensitive (uncommon)
• If patient is protein sensitive, start with 0.5 to 0.7 g protein/kg/d and increase level to tolerance, aiming for up to
1.5 g/kg/d if patient is malnourished
• Consider nutritional supplements enriched with branched-chain amino acids and restricted in aromatic amino acids and
methionine if intolerant to standard proteins
• Supplement with zinc if deficiency is suspected
• Provide adequate calories to prevent catabolism of endogenous protein stores

Ascites and edema • Limit sodium (restriction below 2 g/d may result in inadequate calorie and protein intake)
• Supplement protein if patient is undergoing frequent paracenteses

Hyponatremia • Restrict fluid to 1000 to 1500 mL/d

Hyperglycemia • Institute carbohydrate-controlled meal plan

• Treat with insulin or oral hypoglycemic agent as needed

Hypoglycemia • Provide frequent meals or snacks containing carbohydrate and protein

• Infuse intravenous dextrose if needed

Steatorrhea • Restrict dietary fat; if diarrhea does not resolve, discontinue fat restriction
• Try medium-chain triglyceride supplementation
• Supplement with fat-soluble vitamins

Osteopenia • Maintain an appropriate weight

• Encourage intake of a well-balanced diet with a wide variety of food choices
• Provide enough protein to maintain muscle mass
• Provide 1500 mg of calcium per day via diet and/or supplements
• Provide enough vitamin D via diet and/or supplementation (may need water-miscible form)
• Monitor for the development of steatorrhea and adjust the diet as needed to minimize nutrient losses
• Avoid alcohol

Adapted with permission from Hasse J, Weseman B, Fuhrman MP, Loeffler M, Francisco-Ziller N, DiCecco SR. Nutrition therapy for end-stage liver disease: a practical approach.
Support Line. 1997;19(4):8–15.

diets. When nutrition is delivered predominantly by vein, the goal 2. Oral supplements may increase total intake and preclude the need
is 100 to 130 kcal/kg/d with lipid providing 20% to 25% of total for enteral tube feeding when anorexia of chronic liver disease is
calories, usually up to 3 g/kg/day.33 mild. Supplements can be standard products or modular nutrients
such as MCT oil (7.7 kcal/mL), modular protein powders, or glu-
cose polymers (8 to 10 kcal/teaspoon).
VII. Methods of Nutrient Delivery
B. Enteral feeding
A. Oral diet 1. Indication—Tube feeding is indicated when oral intake is con-
1. Dietary restrictions should be prescribed only as needed. Table sistently inadequate to support appropriate nutritional status.
17-7 outlines guidelines for adults. 2. Feeding routes

© 2005 A.S.P.E.N. www.nutritioncare.org. A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. 241
S E C T I O N I I I Gastrointestinal Related Conditions

a) Small-caliber nasogastric or nasojejunal tubes may be used. (2) Nasojejunal tubes are indicated for infants who vomit or
Esophageal and gastric varices are not, in and of themselves, develop respiratory tract symptoms with gastric feedings.
contraindications to feeding tube placement. However, tube Unfortunately, nasojejunal tubes clog and are easily dis-
feeding should be interrupted or postponed until hemorrhagic placed making these tubes impractical for long-term use.
varices have been effectively treated.34 (3) As in adults with chronic liver diseases and portal hyper-
b) Placement of a gastrostomy or a jejunostomy tube in cirrhotic tension, gastrostomy tubes are usually contraindicated.
patients with ascites is usually not recommended. Potential Possible exceptions include Alagille syndrome.35
complications include ascitic leakage, bleeding, wound dehis- c) Delivery
cence, and peritonitis. (1) Intermittent daytime gavage feeding may preserve appetite
3. Formula selection but is often limited by emesis and diarrhea.
a) Standard polymeric (intact protein) formulas are indicated (2) Continuous pump infusion is better tolerated with less diar-
when anorexia rather than impaired digestive function is the rhea and emesis but often suppresses appetite.
main indication for nutrition support. Casein-based products d) Formula selection
are usually well-tolerated in patients with chronic liver disease. (1) Formulas containing MCT oil may have 25% to 50% bet-
b) Hydrolyzed formulas may be tried when patients develop ter lipid absorption than those containing only LCT (see
indications of intolerance when given polymeric formulas. Table 17-8). However, no data demonstrate superior clini-
c) Nutrient-dense formulas (greater than 1 kcal/mL) are indicated cal efficacy.
when fluid restriction is required. (2) There is no advantage to peptide- or amino acid-based for-
d) Renal formulas are indicated when a patient has hyperkalemia mulas in the absence of coexisting enteropathy or protein
and hyperphosphatemia (usually from renal impairment). hypersensitivity.
e) Branched-chain amino acid-enriched formulas are indicated (3) Amino acid-based formulas are mainly indicated for
when encephalopathy is refractory to pharmaceutical therapy hydrolysate hypersensitivity (intolerance).
and recurs with use of standard formulas. (4) Infants usually tolerate formula density up to 1 kcal/mL if
4. Special considerations in infants and children mandated by need to restrict fluid, while older children
a) Indications for tube feeding include subnormal weight gain usually tolerate up to 2 kcal/mL.
for age or actual weight loss on standard diet. (5) Appropriate tube feeding formulas for infants include:
b) Route of feeding Alimentum (Ross Products, Abbott Laboratories, Colum-
(1) Nasogastric tubes are easiest to use and are generally well- bus, Ohio) and Pregestimil (Mead Johnson, Evansville,
tolerated. IN; diluted to 0.67 to 1.0 kcal/mL).

TABLE 17-8. Proprietary Enteral Formulas Containing MCT Oil for Children with Chronic Liver Disease

Standard Density Nitrogen Lipid cals

Brand (kcal/mL) (g/dL) (% of total) MCT;LCT

Elecare
(Ross Products, Abbott Laboratories, Columbus, OH) 1.0 Amino acid (3.0) 43 33:67

Neocate Advance
(SHS, Gaithersburg, MD) 1.0 Amino acid (2.5) 32 35:65

Alimentum
(Ross Products, Abbott Laboratories, Columbus, OH) 0.67 Hydrolysate (1.8) 48 33:67

Pregestimil
(Mead Johnson, Evansville, IN) 0.67 Hydrolysate (1.9) 48 55:45

Peptamen Junior
(Nestle Clinical Nutrition, Glendale, CA) 1.0 Hydrolysate (3.0) 33 60:40

Deliver 2.0
(Mead Johnson, Evansville, IN) 2.0 Casein (7.4) 45 30:70

TwoCal HN
(Ross Products, Abbott Laboratories, Columbus, OH) 2.0 Casein (8.4) 40 19:81

MCT, medium-chain triglyceride; LCT, long-chain triglyceride

242 A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. © 2005 A.S.P.E.N. www.nutritioncare.org.
 S E C T I O N I I I Gastrointestinal Related Conditions

(6) Appropriate tube feeding formulas for children include: C. Vitamin/mineral supplements
Pregestimil (Mead Johnson, Evansville, IN; diluted to 1.0 1. Which type to take and which to avoid
kcal/mL), Peptamen Junior (Nestle Clinical Nutrition, 2. Dosage
Glendale, CA), Deliver 2.0 (Mead Johnson, Evansville, D. Food safety issues
IN), and 2 Cal HN (Ross Products, Abbott Laboratories, 1. General food safety guidelines (eg, avoid raw eggs; unpasteurized
Columbus, Ohio; diluted to 1.0 to 2.0 kcal/mL). milk; and raw or undercooked meats, poultry, and seafood)
C. Parenteral nutrition support in liver disease 2. Safe handling of enteral and parenteral products
1. Indications: Severe acute and chronic liver diseases with demon- E. Complementary products (eg, milk thistle)
strated intolerance of enteral nutrition. 1. Counsel about safety and efficacy of products.
a) Fulminant liver failure—When consciousness in impaired 2. Milk thistle (silymarin) is most popular in the lay community.
and aspiration risk is heightened. a) Purported anti-hepatotoxic activity and anti-inflammatory
b) Chronic liver disease—Patients who develop intractable diar- activity
rhea, ileus, emesis, or fluid intolerance with EN are likely to b) Scientific evidence is mixed.46–50 A recent meta-analysis con-
benefit from PN. The advantage of PN is the ability to deliver cluded that there is not adequate data to exclude benefit or
a very high caloric load with easily varied macronutrient mix harm.50
(based on nitrogen, lipid, and glucose tolerance) with rela- 3. Avoid products that are potentially hepatotoxic
tively little fluid and sodium. a) Borage
2. Risks of PN initiation in patients with decompensated liver dis- b) Chaparral
ease include bleeding and infection due to placement of a central c) Coltsfoot
venous catheter, as coagulopathy and compromised immunity d) Comfrey
are invariably present. PN itself may also worsen liver function. e) DHEA
3. Route of delivery—Central PN is usually preferable to periph- f) Germander
eral PN because of the latter’s low caloric density. g) Jin bu Huan
4. Home parenteral nutrition—Indicated when long-term PN ther- h) Kava Kava
apy is needed and the patient is sufficiently stable to remain at i) Liferoot
home. This situation is especially likely in the patient with both j) Pennyroyal
liver and intestinal failure awaiting combined liver and intestinal k) Periwinkle
transplantation. l) Poke root
5. Amino Acids—Amino acid mixtures enriched with BCAAs (and m)Skullcap (American)
restricted in aromatic amino acids and methionine) such as Hepat- n) Shark cartilage
amine (B. Braun, Irvine, CA)
a) BCAA formulas are used if standard amounts of amino acid (Liver chapter from the 1st edition was contributed by Arthur J.
precipitate encephalopathy. McCullough, J. Carlos Teran, and Elizabetta Bugianesi)
b) Studies demonstrating benefit are conflicting: BCAA-enriched
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69. Figueiredo F, Dickson ER, Pasha T, et al. Impact of nutritional status on out- Musso G, Gambino R, DeMicheli F, et al. Dietary habits and their relations to
comes after liver transplantation. Transplantation. 2000;70(9):1347–1352. insulin resistance and postprandial lipemia in nonalcoholic steatosis. Hepa-
70. Stephenson GR, Moretti EW, El-Moalem H, Clavien PA, Tuttle-Newhall tology. 2003;37:909–916.
JE. Malnutrition in liver transplant patients. Transplantation. 2001;72(4): Pagano G, Pacini G, Musso G, et al. Nonalcoholic steatohepatitis, insulin resist-
666– 670. ance, and metabolic syndrome: further evidence for an etiologic associa-
71. Fan ST, Lo CM, Lai ECS, Chu KM, Liu CL, Wong J. Perioperative nutri- tion. Heptatology. 2002;35:367–372.
tional support in patients undergoing hepatectomy for hepatocellular carci- Petrides AS, Matthews DE, Esser U. Effect of moderate exercise on insulin sen-
noma. N Engl J Med. 1994;331:1547–1552. sitivity and substrate metabolism during post-exercise recovery in cirrho-
sis. Hepatology. 1997;26(4):972–979.
Plauth M, Merli M, Kondrup J, Weimann A, Ferenci P, Müller MJ. ESPEN
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guidelines for nutrition in liver disease and transplantation. Clin Nutr.
Abbott WJ, Thomson A, Steadman C, et al. Child-Pugh class, nutritional indi- 1997;16:43–55.
cators, and early liver transplant outcomes. Hepato-Gastroenterology. Riggio O, Angeloni S, Ciuffa L, Nicolini G, Attili AF, Albanese C, Merli M.
2001;48:823–827. Malnutrition is not related to alterations in energy balance in patients with
Achord JL. A prospective randomized controlled study of peripheral parenteral stable liver cirrhosis. Clin Nutr. 2003;22(6):553–559.
nutrition in moderate and severe alcoholic hepatitis. J Hepatol. 1988;7: Ukleja A, Scolapio JS, McConnell JP Dickson RC, Nguyen JH, O’Brien PC.
200 –207. Serum and hepatic vitamin E assessment in cirrhotics before transplanta-
Achord JL. Malnutrition and the role of nutritional support in alcoholic liver tion. J Parenter Enteral Nutr. 2003;27:71–73.
disease. Am J Gastroenterol. 1987;82:1–7. Ukleja A, Scolapio JS, McConnell JP, et al. Nutritional assessment of serum and
Angulo P. Nonalcoholic fatty liver disease. N Engl J Med. 2002;346:1221–1231. hepatic vitamin A levels in patients with cirrhosis. J Parenter Enteral Nutr.
Biel AT, Cordoba J. Hepatic encephalopathy. Liver Transplant. 2000;6:575–581. 2002;26:184–188.

© 2005 A.S.P.E.N. www.nutritioncare.org. A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. 245
 Elizabeth Gleghorn, MD;
Karen Amorde-Spalding MS, RD, CSP;
Mark H. DeLegge, MD, FACG 18
Neurologic Diseases

Introduction 5. The incidence of ventilator associated pneumonia (VAP) is high.

Studies have shown that VAP is multi-variable in etiology and
The spectrum of neurologic diseases is very diverse and decisions regard- dependent on a patient’s immune function, swallowing reflex,
ing nutritional intervention in cases of neurologic disease must be indi- oropharyngeal hygiene, and route of enteral feeding.
vidualized to the patient. Neurosurgical patients requiring major spinal 6. Mechanical ventilation is generally required. Hyperventilation
or intracranial interventions experience the same intense catabolism can be employed to reduce intracranial pressure.
characteristic of major surgery patients. Neurologic diseases may alter 7. Dehydration and the use of osmotic diuretics, such as mannitol, are
the patient’s ability to swallow, resulting in nutritional deterioration or employed to reduce intravascular volume in an attempt to reduce
death from repeated episodes of aspiration pneumonia.
increased cerebral pressures.
The risk of nutrition problems in pediatric neurologic disease varies
8. Impaired physical activity requires specialized attention.
with the type of impairment and with its extent. Children who have cog-
C. Nutrition assessment
nitive and motor impairment are at higher risk for malnutrition. A team
1. An estimate of energy needs is required to provide patient-specific
approach, with involvement of occupational and feeding therapists,
nutrition support. No single test is able to predict a patient’s nutri-
social workers, psychologists, registered dietitians, as well as physicians
tional status under all conditions.
and nurse/nurse practitioners, is required to meet the needs of these com-
2. The complicated physiologic response to HI makes even the
plicated patients and their families.
simplest determination of calorie and protein needs difficult.
I. Acute Brain Injury 3. After HI, many catabolic hormones, such as cortisol and glucagon,
II. Spinal Cord Injury rise significantly.3
III. Chronic Neurological Diseases 4. The most commonly used formula for energy needs is the Harris-
IV. Cerebral Palsy and Other Pediatric Conditions with Motor Disorders Benedict equation.
V. Children with Seizure Disorders 5. Resting energy expenditure (REE) can also be measured by indi-
VI. Conclusions rect calorimetry, and is known as measured resting energy expen-
References diture (MREE).4 Estimated energy expenditure is calculated by
multiplying the REE by an activity factor or a disease factor to
arrive at a true energy expenditure.
I. Acute Brain Injury 6. Estimation of nitrogen losses plays an important role in determin-
A. Background ing a patient’s protein needs. Trauma patients have both increased
1. Acute head injury (HI) accounts for approximately one fourth of protein synthesis and a much larger increase in protein catabolism.5
all trauma deaths. These numbers have been increasing coinci- 7. Nitrogen losses of up to 30 g/d have been documented in acutely
dent with the rise in automobile-related injuries and an explosive ill HI patients. No studies have demonstrated a direct correlation
increase in firearm-related injuries. between the severity of head injury and the amount of urinary
2. Patients with brain injury are the most recognized at-risk nutri- nitrogen losses.
tional population of the neurological injured patient. 8. Immobility may increase nitrogen losses.
B. Acute medical management 9. High levels of nitrogen intake can partially reverse net nitrogen
1. Severely head-injured patients are usually treated in an intensive losses. However, high nitrogen excretion is not reversed by
care unit (ICU), where immediate management focuses on stabi- increasing caloric intake alone.6
lizing vital signs, reducing intracerebral pressure (ICP), and pre- 10. Supplementation of branched-chain amino acids (BCAAs) may
venting further injury. also reduce net nitrogen losses. The effect of BCAAs on patient
2. Cerebral edema is believed to be the key factor leading to increased outcome has not been studied.2
ICP pressure. 11. Laboratory assessment of nutritional status remains imperfect,
a) Vasogenic edema results from damage to capillary endothelium but may provide a snapshot of the adequacy of nutrition support.
with resultant leakage of protein-rich material into interstitial a) Albumin production is reduced as other acute-phase reactants
spaces and a rise in osmolality in this tissue.1 are produced preferentially in response to stressful stimuli.7
b) Free fluid flows into these highly osmotic areas and leads to b) Serum retinol binding protein and prealbumin may be moni-
the development of cerebral edema. tored to follow the nutritional status of HI patients later in the
3. Hyperglycemia is common after brain injury.2 course of their recovery.8
4. Assessment of neurologic function is accomplished using the 12. Global assessments of the nutritional status of critically ill patients
Glasgow coma scale. are less accurate than for the general outpatient population.9

246 A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. © 2005 A.S.P.E.N. www.nutritioncare.org.
 S E C T I O N I I I Gastrointestinal Related Conditions

D. Nutrition goals gow coma scale < 8 regained sufficient cognitive function to return
1. It may be difficult to assess calorie needs accurately in the HI to oral food intake.22
patient. One common approach is to provide 1.4 to 1.5 × the esti- 8. In general, the more severe the brain injury, the less likely the
mated REE.10 patient was to return to normal swallowing function. Prolonged
2. In this population, setting a goal to achieve nitrogen balance may time on the ventilator also reduced the likelihood of a return to
be unrealistic. normal swallowing.
3. Many centers aim for a protein intake between 1.5 and 2.2 g/kg/d H. Techniques for enteral access
to minimize protein losses or even achieve positive nitrogen bal- 1. The type of enteral access a patient receives may be very depend-
ance for some patients.11 ent on the clinical expertise available at a given medical center.
4. In general, the peak in nitrogen losses occurs in the first few weeks 2. In the acute HI patient, a feeding jejunostomy may be the most
following HI. It is not uncommon for nitrogen losses to lead to a appropriate enteral access.23–26
loss of lean body mass of 10% in the first 7 days. 3. Bedside placement of nasojejunal or orojejunal feeding tubes is
E. Nutrition therapy technically difficult.
1. When the head injury is associated with other abdominal trauma, a) Oroenteric tubes are used if trauma to the facial area prevents
the use of the GI tract may be compromised, thus affecting the nasal tube passage. Oroenteric tubes are short-term feeding
nutritional therapy options. devices.
2. If it is unsafe to use the gut, then parenteral nutrition (PN) may b) A nasoenteric tube (NET) is one that passes through the nasal
be useful until safe enteral access can be achieved. passage into or beyond the stomach, and is another short-term
3. Some authors have shown no outcome difference in comparing feeding device.
parenteral versus enteral nutrition (EN).12 However, many other c) An NET may cause local nasal irritation, epistaxis, and sinusi-
authors have found PN to be associated with greater complications tis if used long-term.
than EN in other critically ill populations. 4. Percutaneously placed gastric tubes and gastrojejunostomy tubes
F. Gastric function and feeding may be inserted either endoscopically (PEG and PEG/J) at the bed-
1. Gastric function is often abnormal in the critically ill patient. This side or fluoroscopically in HI patients who may require long-term
may be secondary to cytokine influence and GI hypoxia.13 Gastric enteral access.
function is also altered after severe HI.
5. If endoscopic or fluoroscopic attempts are contraindicated or
2. Delayed gastric emptying has been noted in the acutely HI patient
unsuccessful, surgeons may place a gastrojejunostomy device
population to a degree similar to patients receiving a surgical
similar to the endoscopic PEG/J tube.
vagotomy.14
6. Comparative studies of PEG versus surgical G-tube placement
3. Up to a 50% regurgitation of the volume of gastric tube feeding
have shown similar morbidity. However, the cost of PEG place-
has been reported in some HI patients. This resulted in a marked
ment in HI patients was significantly lower than the cost of surgi-
reduction in the EN formula delivered to these patients.15
cally placed G-tubes.27
4. There is a significant reduction in lower esophageal sphincter
I. Parenteral nutrition
(LES) pressure in head-injured patients.16 This lower LES pres-
1. The absence of a functioning GI tract or the inability to obtain
sure, in combination with gastroparesis, increases the risk of gastro-
enteral access is an indication for the use of PN.
esophageal reflux and aspiration associated with gastric feedings.
2. Central venous access is required to meet calorie needs.
5. Elevation of the head of the bed and pro-motility agents increase
the tolerance of gastric feeding in HI patients.17 3. There were early concerns about the potential for increased intra-
6. A prospective trial using jejunal tube feeding in severely head- cranial pressure with PN use.28 However, a randomized study found
injured patients allowed full caloric delivery in approximately no increases in ICP with the use of either EN and PN.29
4 days.18 4. Hyperglycemia is most common within the first 24 hours fol-
G. Enteral nutrition lowing HI and correlates to its degree of injury.
1. Enteral nutrition (EN) should be used as early as possible in the 5. Prolonged hyperglycemia may lead to immunosuppression, plac-
hospital course of an HI patient. Although it is often easier to ing the HI patient at greater risk for infectious complications.30,31
use parenteral nutrition due to the availability of central venous J. Nutritional outcomes
access, many potential complications are associated with par- 1. Early prospective studies comparing PN to EN in HI patients
enteral nutrition. demonstrated a greater delivery of calories in the parenteral group,
2. Providing energy needs to HI patients by day 7 significantly probably secondary to ineffective enteral access techniques.
reduced mortality as compared to patients underfed for 2 weeks.19 2. Parenteral nutrition versus EN studies have not been repeated
3. Patients for whom EN was initiated rapidly had fewer infectious with today’s better jejunal enteral access devices and feeding
complications, earlier hospital discharge, and better neurological techniques.
outcomes at 3 months as compared to patients whose EN formula K. Immune function and nutrition
rate was slowly increased over time.20 1. The incidence of infectious complications following HI is near
4. Head-injured patients can obtain full caloric needs in less than 60%.
5 days of jejunal feedings compared to > 10 days of gastric 2. There is a cellular immunity alteration believed to be secondary to
feeding.21 increases in IL-1 and IL-2 with a decrease in IL-6.2 The degree of
5. Small bowel feedings are well tolerated during barbituate coma immune alteration is directly related to the degree of head injury.
therapy. 3. EN promotes an improvement in the overall CD4 counts and
6. A potential benefit of jejunal feeding is the reduction in GI aspi- lymphocyte function.
ration and its associated morbidity. L. Specialized nutrient needs
7. The ultimate goal of enteral feeding is to obtain a return to oral 1. Zinc facilitates enzyme processes vital to the metabolism of fats,
food intake. In one study, a majority of patients with HI and a Glas- carbohydrates, and protein.

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S E C T I O N I I I Gastrointestinal Related Conditions

a) Serum zinc levels in HI patients fall and urinary zinc excretion 7. Liquids present more difficulty with oropharyngeal dysphagia than
increases.32 with esophageal dysphagia. In esophageal dysphagia, liquids pass
b) Zinc supplemented HI patients have shown a reduction in easily unless the esophagus is almost totally obstructed.
mortality.33 8. For dysphagia evaluation, the most important test is the modified
2. Magnesium supplementation given 1 hour post HI has been barium swallow using video fluoroscopy, which is often done by a
reported to decrease brain edema and improve neurologic scores radiologist and speech therapist.41
48 hours post head injury.34 C. Gastrointestinal motility
1. Chronic HI patients may also have underlying diffuse gastro-
intestinal motility disorders.
II. Spinal Cord Injury
2. Table 18-1 lists other neurologic diseases associated with GI motil-
A. Nutritional assessment ity disorders.
1. Patients experiencing spinal cord injury (SCI) experience many D. Gastroparesis
of the same intense catabolic events as those with HI. 1. Delayed gastric emptying is more common in older patients and
2. In general, directly following SCI, patients are in significant neg- in patients with a lower Glasgow coma scale.42
ative nitrogen balance. 2. Tolerance to gastric feeding is often less than 50 percent in acutely
3. Overall caloric needs are approximately 1.4–1.5 × BEE. The HI patients.16,43–47 This improves in chronic HI patients.
higher on the spinal cord an injury occurs, the more catabolic the E. Gastrointestinal motility evaluation and treatment
patient. 1. Evaluation of gastroparesis should first exclude obstruction
4. Immobilization also leads to a rapid loss of protein muscle mass.35 caused by an ulcerative, inflammatory, or neoplastic process of
Later, these same patients may experience an increase in body fat. the stomach or duodenum. This can be accomplished by upper
B. Nutrition and immunity—A decrease in immune function and an GI endoscopy or an upper gastrointestinal barium study.
increase in infectious episodes also occurs, similar to the HI patient.36 2. The gold standard for quantitative evaluation of gastric empty-
C. Nutritional therapy and outcomes ing is radioscintigraphic measurement (gastric emptying scan).
(1) The negative nitrogen balance can be reduced, but not cor- 3. Currently available medications in the United States that can
rected, by the provision of energy and protein.37 improve gastric emptying include metoclopramide, tegaserod,
(2) The malnourished spinal cord surgery patient has a signifi- and erythromycin.
cant increase in infectious complications and an increase in 4. An evaluation of chronic HI patients with documented tube feed-
hospital length of stay as compared to the well nourished ing aspiration demonstrated that the addition of a pharmacologic
spinal cord surgery patient.38 promotility agent allowed gastric feedings to continue without
(3) Patients with high spinal cord transections (above T5) may subsequent difficulties.48,49
experience delayed gastric emptying.39 5. There are no reliable pharmacologic agents for small bowel motil-
ity disorders.
F. Enteral feeding considerations for chronic neurologic patients
III. Chronic Neurologic Diseases
1. Many patients with depressed levels of consciousness tolerate
A. Background intragastric feedings well.
1. Depressed levels of consciousness are associated with a decreased 2. Recent studies show that elevation of the head of the bed has been
ability to protect the upper airway from episodes of gastroesopha- found to markedly decrease, but not eliminate, reflux episodes in
geal reflux, vomiting, and even oropharyngeal secretions. patients on mechanical ventilation.50,51
2. Some diseases may affect the neural or muscular coordination 3. Monitoring of patients with depressed consciousness who are fed
required for successful swallowing, while others may alter gas- intragastrically should include examining for abdominal disten-
tric or intestinal motility. This puts patients at risk for aspiration. tion, checking for high gastric residuals, and maintaining elevation
3. Aspiration is the entry of material below the true vocal cords.40 of the head of the bed.
B. Dysphagia 4. The presence of gastroesophageal reflux should be investigated
1. A careful history is important in dividing dysphagia into 2 broad in patients who experience multiple episodes of aspiration
groups: esophageal dysphagia and oropharyngeal (transfer) dys- pneumonia.
phagia. 5. Jejunal feeding is recommended in patients deemed to be at risk
2. Esophageal dysphagia refers to difficulty with esophageal pas- for aspiration pneumonia.5 (Table 18-2)
sage of a food bolus after successful passage from the pharynx to
the esophagus.
3. Oropharyngeal dysphagia is difficulty swallowing due to a lesion
that affects swallowing function above or proximal to the esopha- TABLE 18-1. Neurologic Diseases Associated with
gus. The patient complains of difficulty moving a food bolus into Gastrointestinal Motility Disorders
the pharynx and esophagus to initiate the involuntary swallowing
reflex. Diabetic neuropathy and diabetic gastroparesis syndrome
4. Swallowing is a combination of integrated neural and muscular Intracranial lesions
actions coordinated in the brain stem.
5. Any process that alters the fifth, seventh, ninth, or twelfth cranial Intrinsic myopathies and neuropathies
nerves or the brain stem swallowing center can cause oropharyn- • Dystrophia myotonica
geal dysphagia. • Familial gut myopathies and neuropathies
6. The patient may describe nasal regurgitation, dysarthria, nasal • Progressive muscular dystrophy
speech, or coughing during swallowing.

248 A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. © 2005 A.S.P.E.N. www.nutritioncare.org.
 S E C T I O N I I I Gastrointestinal Related Conditions

5. Short stature may reflect a long-term energy deficit or relate to the

TABLE 18-2. Patient Risk Factors for Aspiration underlying disorder.62
in Adult Patients 6. Global assessment of the child’s nutritional fitness as a mechanism
to avoid complications (decubiti, depletion of nutritional reserve,
Previous episode of aspiration intertrigo, obesity-related obstructive sleep apnea) may be the most
Decreased level of consciousness useful measurement of all.
B. Medical history
Neuromuscular disorders interfering with swallowing 1. Certain underlying disorders may predict feeding disorders, dys-
Endotracheal intubation phagia, or gastroesophageal reflux.
2. A large number of hospitalizations, especially recent, may predict
Vomiting the need for catch-up nutrition or indicate a decline in feeding
Persistently elevated gastric residuals skills.
3. Pulmonary complications may result from poor swallowing func-
Need for prolonged supine positioning
tion, gastroesophageal reflux, or their combination.
Poor orotracheal hygiene 4. Dental problems may limit intake and may increase the risk of
aspiration.63
5. Level of activity helps predict energy needs.
C. Diet history
6. Some patients who have difficulty only with liquids may benefit 1. The three-day diet record gives an estimate of the amount of
from thickening agents. energy the child is using to achieve the current body habitus. How-
7. Neurologic diseases in which the decline in swallowing function ever, some studies show the caretaker’s reported intake estimate to
is progressive should be considered candidates for early, more be artifactually elevated by as much as 50% for orally fed, handi-
permanent enteral access options, such as PEG placement. capped children.64
G. Enteral access considerations for the chronic neurologic patient 2. The baseline nutritional intake should be compared to published
1. For use less than 30 days, nasoenteric or oroenteric options are standards and also to the child’s nutritional state. (Table 18-3)
generally preferred. 3. Nutritional requirements of these children are extremely vari-
2. For longer periods, gastrostomies or jejunostomies are preferred. able. If the standard recommendation does not seem to match the
3. Gastric feeding is very common due to its convenience. individual, it may be more clinically appropriate to increase or
4. Continuous jejunostomy feeding is very effective in patients with decrease energy from the reported baseline.
documented tube feeding aspiration.53,54 4. A child who needs to be bottle- or spoon-fed inappropriately for
H. Ethics of enteral feeding chronological age is more likely to have disorders of appetite or
1. Multiple criteria need to be evaluated including predicted clini- swallowing.
cal outcome, quality of patient life and attitudes and beliefs of 5. Reliance on one exclusive feeder stresses the role of that caretaker,
patients and their families regarding artificial nutrition support. limits feeding frequency, and may cause social and economic stress.
2. The use of PEG in patients with cerebrovascular accident (CVA) 6. Respiratory symptoms such as choking, vomiting, change in voice,
has been shown to provide a significant improvement in survival or difficulty breathing after feeding may predict dysphagia and/or
and rehabilitation potential.55,56 aspiration.63
3. In amyotrophic lateral sclerosis (ALS) patients, placement of a 7. Stool output—Constipated children often vomit or refuse to
PEG and initiation of enteral feeding resulted in a significant sta- eat. Diarrhea may result from infection, medication, dysmotil-
bilization of global function.57 ity, or lack of fiber in the diet and may interfere with nutrient
4. Patients with chronic neurologic diseases, including dementia, absorption
were found to have maintained or improved their quality of life 8. Urine output may be low in children who feed orally but with dif-
following PEG placement.58 ficulty, reflecting low volitional free water intake. Hot weather and
5. The use of invasive enteral access in patients with dementia is very exercise increases fluid needs.
controversial. Dementia remains a progressive and ultimately fatal D. Social history
disease. 1. Family finances may be severely strained by the needs of these
children. Tube-fed children incur even more costs.
IV. Cerebral Palsy (CP) and Other Pediatric 2. Cultural and religious factors influence decision-making by the
Conditions with Motor Disorders family.
A. General nutritional assessment E. Physical exam
1. In general, nutritional assessment of these patients, most com- 1. Height measurement may be inaccurate because of contractures.
monly children, conforms to the principles of assessment of the Use of upper or lower limb measurement allows estimation of
normal child, although it may be difficult to use and interpret height and comparison to the measured weight.64,65
anthropometric parameters.59 2. Weight should be obtained with the child sitting or standing unsup-
2. A greater degree of motor involvement in these children is pre- ported if possible. A wheelchair scale should be used rather than
dictive of greater feeding dysfunction and thus of increased having a parent hold the child and then subtracting the parental
malnutrition.60 weight.
3. Problems range from lack of dexterity with utensils to food spilling 3. Measurement of skin fold thickness allows assessment of appro-
from the mouth to complete dysphagia. priate fat reserves.
4. Greater spasticity correlates with greater energy expenditure at rest 4. Arm muscle area is reported to be positively associated with bet-
and during feeding.61 ter subjective health of children with CP.66

© 2005 A.S.P.E.N. www.nutritioncare.org. A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. 249
S E C T I O N I I I Gastrointestinal Related Conditions

5. Children who are significantly underweight and then refed should

TABLE 18-3. Recommended Energy Intake64,73,81 be monitored for hypokalemia, hypomagnesemia, and hypophos-
phatemia as part of the refeeding syndrome.
1.5–1.89 × Resting 6. Measured weight should be compared to the weight appropriate
Normal children Energy Expenditure (REE) for the calculated height. Because these children often have low
muscle mass, the tenth to thirtieth percentile weight-for-height
Spastic quadriparesis (SP), 1.3 x REE may be suitable.
well-nourished G. Swallowing dysfunction, aspiration, and gastroesophageal reflux
evaluation
SP, malnourished 1.5 x REE (a) 1. Evaluation and treatment for this problem requires a multidisci-
plinary team approach.
2. Certain neurological disease states are commonly associated with
Ambulatory developmental 13.9 kcal/cm height
a risk for aspiration. (Table 18-4)
delay (DD) 5–12 yo

Non-ambulatory DD 5–12 yo 11.1 kcal/cm height

TABLE 18-4. Clinical Clues to Dysphagia
Very low activity Cerebral 10 kcal/cm height and Aspiration in Neurologically
Palsy (CP) Impaired Children

Conditions associated Moebius syndrome

Mild to moderate activity CP 15 kcal/kg height
with dysphagia or Cornelia de Lange syndrome
aspiration Bulbar polio, other bulbar
Severe choreoathetosis Up to 6000 kcal/d
syndromes, stroke
Familial dysautonomia
Trisomy 21 male 5–12 yo 16.1 kcal/cm height
Trisomies 18 and 21
Rett syndrome
Trisomy 21 female 5–12 yo 14.3 kcal/cm height
Guillain-Barre syndrome
Arnold-Chiari malformation
Myelomeningocele 50% RDA for age, as little as
Muscular dystrophies and
7 kcal/cm height
myopathies, myotonia
Poliomyelitis, post-diphtheritic
Prader-Willi syndrome 8–9 kcal/cm height for
paralysis
weight loss,
Cranial nerve palsy
10–11 kcal/cm height for main-
Infant botulism
tenance
Brain stem glioma
Long-term feeding deprivation
Myelomeningocele
5. Assessment of skin, hair, and other manifestations of nutrient Myasthenia gravis
deficit.
6. Examination of feeding device if present, including skin condi-
Symptoms predictive of Coughing, change in voice, or
tion around the tube.
dysphagia or aspiration tachypnea after eating
7. Assessment of pulmonary status can help predict the need for fur-
ther investigation of swallowing and possible need for feeding Recurrent respiratory infections or
intervention. asthma
8. Assessment of development, activity level, tone, and posture will Weak cry
help the clinician estimate calorie needs. Higher activity and tone Nasopharyngeal regurgitation
increases energy needs. Snoring
F. Laboratory testing Vomiting or gagging during feeding
1. There is evidence that freely eating children with developmental Feeding refusal
disability may have deficiencies of Vitamin A, Vitamin C, Vita- Poor trunk/neck/head tone
min D, calcium, iron, thiamin, folate, and riboflavin.64 Long time to feed
2. Some children with developmental disability choose very idio-
syncratic diets, putting them at further risk for specific nutritional
Physical exam Tongue thrust
deficiencies.
3. Children who continue to grow along an appropriate curve prob- Drooling
ably should have an annual CBC and chemistry panel and indi- Opisthotonus
cated medication monitoring. Stridor
4. Children who continue to grow along a normal curve should not Wheezing, rales, or rhonchi
need more elaborate testing than non-handicapped children.

250 A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. © 2005 A.S.P.E.N. www.nutritioncare.org.
 S E C T I O N I I I Gastrointestinal Related Conditions

3. An upper gastrointestinal (UGI) series shows the anatomy and 10. Children who have GER clinically or on testing should be ini-
motor function of the esophagus and stomach. tially treated medically. Surgery should be reserved for medical
4. A video swallow study done with the participation of a feeding failures, or recurrent vomiting or aspiration.
therapist skilled in this evaluation. 11. Often, the family is more ready for a feeding tube or antireflux
a) This is a good indicator of aspiration of food or fluids with surgery than the health professional initially realizes.
swallowing. J. Tube feeding access and tube feeding
b) Textures varying from thin to solid are offered to the child. 1. Children sometimes lose all interest in oral feeding after a gas-
c) Techniques to increase the safety of the swallow can be iden- trostomy tube is introduced. This can be very disappointing to the
tified. family.
5. A pH probe study counts the number of reflux events in a test 2. Nasoenteric tubes are useful in the trial of enteral feeds. They can
period, usually overnight or up to 24 hours. This study is the most be used for short-term feeding in acute situations in which the
accurate test to assess for the presence of gastroesophageal reflux child is expected to regain the ability to eat, such as after surgery.
(GER) but also has day to day variability.67,68 The presence of a) Nasogastric (NG) tubes can be placed at the bedside and place-
GER can predict patients who are more likely to aspirate gastric ment confirmed by auscultation of insufflated air and by clin-
contents. ical examination of the child.
6. Gastric emptying should be measured by the use of a gastric b) NG feeding is a useful way to assess how a child will respond
emptying scan. Patients with delayed gastric emptying are at to gastrostomy feeding.
increased risk for reflux and aspiration of gastric contents. c) Nasoduodenal or nasojejunal (NJ) tubes can be placed at the
7. A neurologically handicapped child shown to aspirate with feed- bedside blindly, by pH evaluation, or in the fluoroscopy or
ing presents a clinical decision regarding 3 points: Should a feed- endoscopy suite under direct visualization. These tubes tend
ing tube be used? Should oral feeding be stopped? Should an to reduce aspiration from gastroesophageal reflux.
antireflux operation be performed? d) Nasally placed tubes can cause annoying problems such as
H. Specialized tests increased ear and sinus infections as well as nosebleeds.
1. Bone densitometry (dual energy X-ray absorptiometry, DEXA) 3. If the child requires permanent gastric enteral access, a percuta-
is likely to be abnormal in children who are mostly recumbent,
neous endoscopic gastrostomy (PEG) should be placed.
because weight bearing is significantly important in building bone.
a) Small bowel access is possible using a jejunal tube placed
a) Children with CP who have had fractures have less dense
through a preexisting gastrostomy tube or gastrostomy site.
bone (by X-ray or densitometry) than patients who have had
Gastrojejunal tubes are more prone to mechanical complica-
no fractures.69–71
tions such as tube migration and occlusion and the need for a
b) However, bone density has not been shown to predict future
continuous enteral formula infusion.
fractures in normal or CP children.72
b) The percutaneous enteral access techniques are usually per-
2. Resting energy expenditure can be measured by indirect calori-
formed by an interventional radiologist or an endoscopist.
metry.
c) No matter who actually places the tube, a team approach
I. Nutrition plan
(MD, nurse with feeding expertise, and registered dietitian)
1. Assess the child’s status as overweight, appropriate weight, or
is needed so that complications can be resolved expedi-
undernourished based on the history, physical, and laboratory
parameters. (Figure 18-1) tiously.
2. Add supplements or increase feeding volume as needed to 4. Tube feedings should be given in the most physiologic manner
change the child’s habitus, and supplement significant micro- that the child can tolerate. Bolus feeds in an amount appropriate
and macronutrient deficits caused by low energy intake and by to the child’s age are usually the best way to start.
medications that increase requirements for specific nutrients. 5. If the child is taking oral feeds, these should be given first. Addi-
3. Children who are unable to meet increased oral calorie goals tional formula to meet a predetermined total should be given
should be evaluated for unrecognized swallowing dysfunc- either as a “top off” at each feed, at the end of the day, or overnight
tion and GER. as a drip.
4. Behavioral modification and appetite-stimulating medicine 6. Overnight continuous drip feeds with very small boluses in the
should be used as in any child with failure to thrive. daytime may work for those intolerant of large volumes.
5. A feeding therapist may be able to make the feeding process K. Low bone density
safer by altering the consistency of food and changing the feed- 1. Children with CP have a high prevalence of low bone density for
ing position.73 age.74,75 Pathologic fractures affect up to 25% of children with CP
6. Antireflux surgery can decrease the risk of gastric content aspira- who are in residential care.
tion due to GER episode. Antireflux surgery cannot stop aspira- 2. Bedrest and lack of weight-bearing is an important contributor
tion of saliva or food during swallowing. that can be treated by physical therapy.32
7. Some families will choose to feed the aspirating child by mouth. 3. With their low calorie intake, children with CP may not get
They feel that the pleasure experienced by the child and the fam- enough Vitamin D and calcium. They may also have insufficient
ily in feeding is worth the potential shortening of life. sun exposure.
8. Orally fed children who persistently fail to improve their nutri- 4. Antiepileptic drugs interfere with vitamin D metabolism.76
tional status should be considered for the initiation of tube 5. It is reasonable to give optimal calcium, phosphorus, and vitamin
feedings. D to all children with CP.
9. Antireflux surgery and tube feeding may be chosen on clini- 6. Increases in vitamin D and calcium intake have been shown to
cal grounds to improve management of the child with GER increase bone density. There has been no reported toxicity of
and aspiration. these dietary measures.

© 2005 A.S.P.E.N. www.nutritioncare.org. A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. 251
S E C T I O N I I I Gastrointestinal Related Conditions

FIGURE 18-1. Nutrition Assessment and Plan for Neurologically Impaired Children

Initial assessment: height, weight, skinfold

thickness, laboratory testing

Well-nourished Under-nourished Over-nourished

Assess diet adequacy: calories Post- Pre- and Decrease by 7200 kcal
Increase by 7200
and micro- and macronutrients pubertal pubertal per kg desired loss or
kcal per kg desired
gain over the time decreased gain over
before reassessment the time before
reassessment

Supplement deficient
nutrients as indicated
by diet history,
underlying condition,
medications

Reassess in Reassess in
6 months 3 months

7. Intravenous and oral bisphosphonates have been successfully 8. This diet is designed to support near normal growth and devel-
used to treat symptomatic low bone density in children with and opment while maintaining seizure control.
without CP.69,77,78 Pill formulations of these medications are 9. This diet is effective in controlling seizures in over half of the
well known to be hazardous in people with dysphagia. There- children treated.80
fore, IV administration, preferably in a clinic or hospital setting 10. Like conventional drug therapy, the ketogenic diet has the poten-
with close observation, would be necessary for most children tial for both short- and long-term side effects.
with CP a) Side effects include acidosis, nausea, vomiting and dehydra-
tion, constipation, cholelithiasis, nephrolithiasis, pancreatitis,
and cardiomyopathy.
V. Children with Seizures Disorders
b) Protein-losing enteropathy has been observed in several
A. Ketogenic diet instances.
1. The ketogenic diet is an established therapy for children with 11. Labs are monitored per a specific schedule. (Table 18-5)
intractable epilepsy.79 12. In some cases, the need for tube feeding makes it easier to pre-
2. If conventional drug therapy fails or is accompanied by intoler- scribe this diet, as taste and preference do not matter.
able drug side effects, the ketogenic diet is an appropriate next 13. The ketogenic diet prescription usually limits calories and protein
step. to less than typical allowances. This may interfere with projected
3. Ketosis can be accomplished by either fasting or consuming a normal weight gain and linear growth.
high fat diet. 14. Once seizure control is attained, protein and calories can be
4. Epileptic children usually begin the ketogenic diet by fasting for titrated up to support more normal growth
a limited time (12–36 hours) to quickly establishing ketosis. a) Overall micronutrient intake might be limited by the diet and
5. In order to maintain the ketosis while nourishing the growing a vitamin and mineral supplement is usually needed.
child, a high fat diet is slowly introduced. The traditional keto- b) A sugar-free supplement must be used.
genic diet derives 80–90 % of calories from fat. c) A daily calcium supplement is necessary as well.
6. The long-term success of the diet requires a consistent level of 15. The child is usually hospitalized to initiate the diet.
ketosis which is accomplished by following a prescribed intake 16. In the early weeks of the diet, the family is often overwhelmed
of energy, protein, fat, and carbohydrate. by the dramatic change in routine.
7. A targeted ratio of total fat to protein and carbohydrate combined 17. Regularly scheduled follow-up appointments with the entire team
is routinely consumed to maintain the deep ketosis and seizure are essential to assess for normal growth, metabolic complica-
control. The most frequently used ratios are from 3:1 to 4:1. tions, seizure control, and family coping.

252 A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. © 2005 A.S.P.E.N. www.nutritioncare.org.
 S E C T I O N I I I Gastrointestinal Related Conditions

TABLE 18-5. Ketogenic Diet Laboratory Value Assessment

Annual f/u and q

Preadmission n Admission PRN 1 month f/u 6 months f/u 6 months

CBC ● ● ● ●

Electrolytes ● ● ● ●

Metabolic Panel ● ● ● ●

Liver Function ● ● ● ●

Uric Acid ● ● ● ●

Carnitine (Free + Total) ● ● ● ●

Urinalysis ● ● ● ●

Amylase ● ● ● ●

Lipid panel ● ● ● ●

Abdominal Ultrasound ● ●

Renal Ultrasound ● ●

EKG ● ● ●

VI. Conclusion (Neurologic chapter from the 1st edition was contributed by L. Glen
Lewis, Shirley M. Ekvall, and Valli K. Ekvall)
1. The past 3 decades have seen dramatic improvements in the
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 SECTION EDITOR
J u a n O c h o a , M D , FA C S
IV
Surgical and Critically Ill
Conditions

19 Perioperative

20 Nutrition in Critical Illness, Including Immunonutrition

21 Trauma

22 Indirect Calorimetry in Critically Ill Patients

23 Nutrition Support for Adult Patients with

Acute Renal Failure

24 Nutrition Support for Pediatric Patients with

Acute Renal Failure

25 Burns

26 Neonatal Intensive Care

 Stephen L. Barnes, MD;
Marjorie Swintosky, MS, RD;
Andrew C. Bernard, MD;
Paul A. Kearney, MD
19
Perioperative Nutritional
Support

Introduction 2. Mildly malnourished: <10% weight loss; preoperative serum albu-

min 3.2 to 3.5 g/dL
Malnutrition is a common problem among perioperative patients, as the 3. Moderately malnourished: 10% to 20% weight loss; preoperative
primary condition may induce variable gastrointestinal obstruction, serum albumin 2.5 to 3.2 g/dL
anorexia, or malabsorption. Nutrient requirements may be increased 4. Severely malnourished: >20% weight loss; preoperative serum
and intake diminished. This chapter will review perioperative nutrition albumin <2.5 g/dL
implications, assessment, and practices. B. Perioperative nutritional assessment parameters should include a
complete medical history, surgical history, social history, diet history,
I. Goals of Perioperative Nutritional Support physical examination, anthropometric and laboratory evaluations,
II. Perioperative Nutritional Assessment
and indirect calorimetry when appropriate. A thorough physical
III. Nutritional Alterations in the Perioperative Period
assessment may also help to identify specific nutrient deficiencies and
IV. Perioperative Nutritional Management
must be correlated with the patient’s history and laboratory data to
V. Practice Guidelines
establish a deficiency diagnosis.4
References
C. Energy needs. Nutritional assessment also includes estimation of
Suggested Readings
energy and protein requirements. While over 200 formulas exist,
the most commonly employed is the Harris-Benedict equation. An
I. Goals of Perioperative Nutritional Support. Perioperative adjusted body weight is used for patients who are at greater than
nutrition is an important component of perioperative care. In 1936, Stud- 125% of their ideal body weight. (See Chapter 28.)
ley first revealed the link in peptic ulcer patients undergoing gastrec- D. Visceral proteins. Visceral protein evaluation is helpful in assessing
tomy,1 demonstrating that those with preoperative weight loss of less an individual’s nutritional status. Visceral proteins are affected by
than 20% had a 3.5% mortality rate; in contrast, those with preoperative many factors related to surgical disease, such as hydration, systemic
weight loss greater than 20% had a 33% mortality rate. inflammation, and metabolic state. Albumin, transferrin, prealbumin,
A. The goals of perioperative nutritional support are as follows: and retinol binding protein are all indicators of nutritional status;
1. Decrease surgical mortality. however, albumin and prealbumin are the most clinically relevant and
2. Decrease surgical complications and infection. frequently used.
3. Reduce the catabolic state and restore anabolism. E. Stress factors. Stress factors must be incorporated into the estimation
4. Support the depleted patient throughout the catabolic phase of of energy needs during the perioperative period based on the opera-
recovery. tive procedure performed and the clinical condition of the patient.
5. Decrease the hospital length of stay. They help to estimate increased needs as a result of the effects of tis-
6. Speed the healing/recovery process. sue repair and systemic inflammation in the perioperative period.
7. Ensure the prompt return of gastrointestinal function to resume F. Protein requirements. An estimation of protein requirements must
standard oral intake as soon as possible. take into account the increased requirements postoperatively during
B. Perioperative nutritional support, however, is not without its own the period of wound healing and increased metabolic activity. Protein
complications and cost. Risk-benefit and cost-benefit analysis must requirements can be estimated based on the patient’s age, size, phys-
therefore be taken into account in the decision-making process ical findings, and clinical condition and the operation performed.
regarding perioperative nutritional support.
III. Nutritional Alterations in the Perioperative Period.
II. Perioperative Nutritional Assessment. Malnutrition is Nutrient depletion occurs in the perioperative patient due to decreased
the result of extended periods of inadequate nutritional intake and results intake, increased metabolic expenditure, and altered nutrient use.
in changes in body composition and function, with a negative impact on A. Metabolic response. Hormonal and inflammatory medications
all organ systems. Estimates of the prevalence of malnutrition and the increase the mobilization and turnover of fatty acids, amino acids,
incidence of associated complications vary because of the many differ- and their precursors from skeletal muscle and adipose tissue. This
ent attempts to objectively define malnutrition.2 redistribution of substrate ensures the functioning of essential organs,
A. Individuals are generally classified as well nourished or mildly, supplies building blocks for tissue repair, and supports immune
moderately, or severely malnourished.3 response. An elective, uncomplicated operation produces a transient,
1. Well nourished: no significant weight change; preoperative serum modest increase in nutritional requirements that is of no clinical con-
albumin >3.5 g/dL sequence. Greater metabolic responses occur in proportion to the

© 2005 A.S.P.E.N. www.nutritioncare.org. A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. 259
S E C T I O N I V Surgical and Critically Ill Conditions

severity of stressors and the degree of tissue destruction associated interruption of gastrointestinal function in the face of increases in
with the operation. Preoperative hypermetabolism may be present nutrient requirements secondary to metabolic response to injury may
due to long-term inflammatory or infectious conditions (eg, inflam- combine to produce significant nutritional alterations and risk of
matory bowel disease, diverticulitis).5 complications in the perioperative patient.
B. Reduced preoperative intake. Preoperative reduced nutrient intake
can be primary (related to the disease) or secondary to an associated
IV. Perioperative Nutritional Management. The beneficial
or unrelated disease process resulting in the inability to maintain
effects of nutritional interventions are modest in well-nourished
adequate preoperative nutrient consumption or use. Anorexia is a
patients. In uncomplicated cases, these patients tolerate up to 10 days
result of the worsening of symptoms with eating or the inability to
of starvation with no medical consequences. Moderately or severely
eat secondary to obstruction. Depression, psychosocial deprivation,
malnourished patients may require nutritional support earlier. Severely
and physical or neurologic impairment may result in the inability to
malnourished patients are more likely to experience sepsis, pneumonia,
maintain adequate preoperative nutrition.
wound infections, and other complications; they benefit from preoper-
C. Preoperative malabsorption. Preoperative malabsorption may occur
ative nutritional support. Perioperative nutritional support should be
as a result of primary conditions or may be secondary to associated
limited to those in whom the benefits outweigh the risks. When indi-
or unrelated diseases. Biliary obstruction, pancreatic insufficiency,
cated, preoperative nutritional support can be provided only to those in
inflammatory bowel disease, and enterocutaneous fistulas can all
whom the operation can be safely delayed, and nutrition should be con-
lead to preoperative malabsorption.
tinued into the postoperative period. Postoperative nutritional support
D. Reduced postoperative intake. Postoperative ileus plays an important
comprises the majority of perioperative nutrition support and can be
role in the resumption of intake following surgery. All abdominal
complicated by the site of operation, the available routes of access, and
operations, including laparoscopic cholecystectomy, and major pro-
the physiologic status of the patient. As a rule, if the gut works, it should
cedures outside of the peritoneal cavity are associated with impaired
be used.
gastrointestinal motility in the early postoperative period.6 The extent
of ileus is directly related to the extent of dissection and degree of A. Indications for preoperative nutritional support. Many studies have
local and systemic inflammation. As a result, nearly all patients identified the severely malnourished as benefiting from preoperative
undergoing abdominal operations and major procedures at other sites nutritional support with parenteral nutrition (PN).3,7 Results from
exhibit at least transient cessation of oral intake. multiple preoperative parenteral nutrition studies of surgical patients
E. Preoperative nutrient losses. Accelerated nutrient losses as a result have shown no overall reduction in perioperative mortality, but sig-
of gastrointestinal fluid losses (gastric, enteric, biliary, pancreatic) nificant reductions in perioperative complications are achieved in the
that are either iatrogenic (nasogastric tubes) or due to diarrhea or severely malnourished receiving more than 7 days of preoperative
fistulas can result in substantial protein loss and electrolyte distur- parenteral support. These benefits were not seen in those receiving
bances as well as loss of fluid, minerals, and trace elements. Replen- fewer than 7 days of preoperative support. In the mildly to moder-
ishment of lost fluid, electrolytes, minerals, and trace elements is ately malnourished groups, there was a trend toward increased
mandatory in preparing a patient for surgery. infectious/septic-related complications.7 Studies of preoperative
F. Postoperative nutrient losses. The postoperative patient experiences enteral support are not as numerous, but available clinical evidence
a stress-mediated increase in the requirements for sodium and water, generally indicates a trend toward reduction in perioperative com-
resulting in increases in total body water and associated hemodilu- plications in the moderately and severely malnourished, as seen
tion. Electrolyte disturbances may be significant and can be readily with preoperative PN.3 This benefit may be amplified by the use of
identified and corrected. immune-enhancing enteral diets. (See Chapter 20 for a complete dis-
G. Protein depletion. Serum albumin concentrations fall rapidly in the cussion of immunonutrition.)
postoperative period in proportion to the degree of stress. This is B. Special preoperative conditions. Mental status and the ability to pro-
due principally to decreased albumin synthesis and also secondary tect one’s airway, symptoms worsened by eating, obstruction and
to hemodilution. Albumin thus cannot be used as the sole indicator ___location of the obstruction of the gastrointestinal tract, and the time
of protein depletion postoperatively. Wound healing, tissue repair, frame to operation are all crucial in the preoperative nutritional sup-
immunologic response, and blood synthesis are all of high biologic port decision-making process.
priority in the postoperative period. Net positive protein synthesis C. Access. Preoperative access for preoperative nutritional support can
may occur in some tissues or organs despite total body negative be divided into enteral and intravenous access.
nitrogen balance. However, wound healing and immune responses 1. Nasogastric/nasoenteral tubes. In the awake, competent patient
to stress may fail in states of advanced protein depletion. The effect able to protect his or her airway, nasogastric or nasojejunal tube
of intermediate degrees of protein depletion is difficult to determine placement is the easiest form of access for preoperative enteral
clinically. Generalized protein depletion may ultimately occur, lead- nutrition. The tubes can be placed by hand, with the assistance of
ing to an increased postoperative complication rate and other mani- fluoroscopy, or endoscopically with or without fluoroscopy. Bolus
festations of severe protein loss. feeding may be used with nasogastric tubes. Continuous feeding
H. Energy-store depletion. The depletion of stored carbohydrate is is required with nasojejunal tubes. The major risk of nasoenteral
generally not a clinical issue because of the routine infusion of iso- feedings is aspiration.
tonic glucose solutions in the perioperative period. Depletion of 2. Percutaneous endoscopic gastrostomy/jejunostomy (PEG, PEJ)
stored fat is of clinical significance only in the most extreme cases, tubes. Endoscopically placed gastrostomy tubes are excellent
when resumption of adequate nutrient intake after recovery from routes of access to the gastrointestinal tract. They can be placed
the operation is significantly delayed. without general anesthesia. PEG tubes allow for near-immediate
I. Alterations in protein synthesis, energy stores, electrolytes, minerals, gastric feedings and are useful in patients who are unable protect
and trace elements in the perioperative period may become severe their airway. The traditional “pull” PEG cannot be used with car-
and impair recovery. Preoperative malnutrition and postoperative cinoma of the upper aerodigestive tract, as cancerous seeding of

260 A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. © 2005 A.S.P.E.N. www.nutritioncare.org.
 S E C T I O N I V Surgical and Critically Ill Conditions

the PEG tract has been reported. Newer PEG tubes can be placed or her airway, gastric feedings can proceed once the periopera-
percutaneously through the abdominal wall by sequential dilata- tive gastroparesis has resolved. Nasojejunal feeding tubes can be
tion under direct endoscopic or fluoroscopic guidance. PEG tubes placed during most operations. Tube feedings can be initiated
are not without risk during placement and can become dislodged, into the small bowel in the immediate postoperative period.
become infected, or migrate. For patients who do not tolerate gas- 2. Surgical gastrostomy/jejunostomy. Traditional gastrostomy and
tric feedings or those with gastroparesis, a gastrojejunal tube can jejunostomy tubes can be placed during surgery, allowing long-
be placed. A second lumen is placed through the PEG tube and is term enteral access. Selection is based on the operative procedure
directed past the pylorus either endoscopically or fluoroscopi- being performed, the preoperative nutritional state, and the pre-
cally. Single-piece gastrojejunal devices are available and can be sumed length of need for nutritional support. Surgical access is
placed through a mature PEG site either fluoroscopically or endo- not without complications, and the risks must be weighed against
scopically. Both systems allow for simultaneous gastric drainage the nutritional benefits.
and jejunal feeding. In more advanced endoscopic centers, PEJ 3. PEG, PEJ tubes. Endoscopically placed gastrostomy tubes can be
tubes can be placed. The procedure is more technically demand- inserted intraoperatively or in the postoperative period in most
ing than PEG tube placement but can be an effective, minimally cases. They can be placed without general anesthesia or during the
invasive approach to long-term enteral access of the small bowel. initial procedure. PEG tubes allow for near-immediate gastric
3. Laparoscopic gastrostomy/jejunostomy. Minimally invasive feedings and are effective in patients who are unable to protect
access to the abdominal cavity by way of laparoscopic surgery can their airway. PEG tubes are not without risk during placement and
allow for placement of more traditional surgical-type feeding tubes can become dislodged, become infected, or migrate. For patients
in either the stomach or the small bowel. Most procedures can be who do not tolerate gastric feedings or for those with gastro-
performed on an outpatient basis. Though minimal access is paresis, a gastrojejunal tube can be placed. A second lumen is
involved, the procedures carry risks similar to those associated placed through the PEG tube and is directed past the pylorus either
with traditional open surgery. endoscopically or fluoroscopically. Single-piece gastrojejunal
4. Central venous access. Temporary or more permanent tunneled devices are available and can be placed through mature PEG sites
central venous catheters can be placed either in the operating room either fluoroscopically or endoscopically. Both systems allow for
or at the bedside to provide central venous access for parenteral gastric drainage and jejunal feeding. In more advanced endoscopic
preoperative therapy. Central lines carry some risk of injury at the centers, PEJ tubes can be placed if desired, although they likely
time of placement and ongoing risk of infection and thrombosis. have no significant benefit over transgastric tubes.
D. Indications for postoperative nutritional support. Well-nourished and 4. Central venous access. Temporary or more permanent tunneled
mildly malnourished patients tolerate the stresses of surgery without central venous catheters can be placed either in the operating room
significant difficulty, and most will not need nutritional support. Well- or at the bedside to provide central venous access for PN therapy.
nourished and mildly malnourished patients who resume an appro- Central lines carry some risk of injury at the time of placement and
priate oral regimen within 10 to 14 days of surgery will not benefit ongoing risk of infection and thrombosis. Most high-risk surgical
from postoperative nutritional support and will only incur additional patients will require central venous access for other reasons during
cost and medical risk. Moderately malnourished and severely mal- the postoperative period.
nourished patients will, however, benefit from postoperative nutri-
tional support. Early postoperative nutritional support benefits the V. Practice Guidelines. The American Society for Parenteral
high-risk surgical patient by decreasing septic morbidity, maintain- and Enteral Nutrition has developed evidence-based practice guide-
ing immunocompetence, and improving wound healing and overall lines regarding perioperative nutrition support.13
recovery. Barium studies8 have shown that small-bowel motility con- 1. Preoperative specialized nutrition support (SNS) should be admin-
tinues in the postoperative period, even though gastroparesis may be istered for 7 to 14 days to moderately or severely malnourished
present for 24 to 48 hours and colonic paresis for 3 to 5 days. Given patients undergoing major gastrointestinal surgery if the operation
the benefits of postoperative nutritional support, early postoperative can be safely postponed.
feeding is now encouraged in the high-risk surgical patient who will 2. PN should not be routinely given in the immediate postoperative
not resume oral intake within 10 days of surgery. Patients who are period to patients undergoing major gastrointestinal procedures.
clinically and mechanically able to tolerate enteral feedings should 3. Postoperative SNS should be administered to patients who are
be fed enterally. Enteral nutrition is superior to PN, with fewer post- expected to be unable to meet their nutrient needs orally for 7 to
operative infections and shorter hospital stays.9–12 However, enteral 10 days.
nutrition may not be appropriate for all high-risk surgical patients.
Selecting patients who will not resume oral intake within 10 days can (Perioperative nutrition support chapter from the 1st edition was con-
be difficult. Preoperative nutritional status should be taken into tributed by Bruce M. Wolfe)
account during surgery, as the choice of route for nutritional support
can be influenced at the time of operation. REFERENCES
E. Special postoperative conditions. Mental status and the ability to 1. Studley HO. Percentage of weight loss: a basic indicator of surgical risk in
maintain one’s airway once again play a significant role in postopera- patients with chronic peptic ulcer. JAMA. 1936;106:458–460.
tive nutritional support. Location of resection, postoperative compli- 2. Zaloga GP. Nutrition in Critical Care. St Louis, MO: Mosby; 1994.
cations and the need for recurrent operations, and the return of bowel 3. Howard L, Ashley C. Nutrition in the perioperative patient. Annu Rev Nutr.
2003;23:263–282.
function all play significant roles in postoperative nutritional support.
4. A.S.P.E.N. Board of Directors. Guidelines for the use of parenteral and
F. Access. Postoperative access for nutritional support can be divided enteral nutrition in adult and pediatric patients: nutrition assessment—adults.
into enteral and intravenous access. J Parenter Enteral Nutr. 2002;26(S):9SA–12SA.
1. Nasogastric/enteral tubes. Nasogastric tubes are placed routinely 5. Wilmore DW. Metabolic response to severe surgical illness: overview. World
during major operations. In the awake patient able to protect his J Surg. 2000;24:705–711.

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S E C T I O N I V Surgical and Critically Ill Conditions

6. Livingston EH, Passaro EP Jr. Postoperative ileus. Dig Dis Sci. 1990;35: 12. Moore FA, Feleciano DV, Andrassy RJ, et al. Early enteral feeding, com-
121–132. pared with parenteral, reduces postoperative septic complications: the
7. The Veterans Affairs Total Parenteral Nutrition Cooperative Study Group. results of a meta-analysis. Ann Surg. 1992;216(2):172–183.
Perioperative total parenteral nutrition in surgical patients. N Engl J Med. 13. A.S.P.E.N. Board of Directors. Guidelines for the use of parenteral and
1991;325:525–532. enteral nutrition in adult and pediatric patients: perioperative nutrition
8. Nachlas MM, Younis MT, Roda CP, Wityk JJ. Gastrointestinal motility support. J Parenter Enteral Nutr. 2002;26(S):95SA–96SA.
studies as a guide to postoperative management. Ann Surg. 1972;175(4):
510–522.
9. Moore FA, Moore EE, Jones TN, McCroskey BL, Peterson VM. TEN vs SUGGESTED READINGS
TPN following major abdominal trauma-reduced septic morbidity. J Trauma. Bengmark S. Aggressive perioperative and intraoperative enteral nutrition. In:
1989;29(7):916–922. Shikora S, Martindale RD, Schwaitzberg SD, eds. Nutritional Considera-
10. Bozzetti F, Braga M, Gianotti C, Mariani L. Postoperative enteral versus tions in the Intensive Care Unit. Dubuque, IA: American Society for Par-
parenteral nutrition in malnourished patients with gastrointestinal cancer: enteral and Enteral Nutrition/Kendall-Hunt; 2002:365–380.
a randomized multicenter trial. Lancet. 2001;358:1487–1492. Gottschlich MM. Early and perioperative nutrition support. In: Matarese LE,
11. Kudsk DA, Minard G, Croce MA, et al. A randomized trial of isonitroge- Gottschlich MM, eds. Contemporary Nutrition Support Practice: A Clinical
nous enteral diets after severe trauma: an immune-enhancing diet reduces Guide. 2nd ed. Philadelphia, PA: Saunders/Elsevier Science; 2003:
septic complications. Ann Surg. 1996;223(4):531–540. 276–289.

262 A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. © 2005 A.S.P.E.N. www.nutritioncare.org.
 Imad F. Btaiche, PharmD, BCNSP; Paul E. Marik, MD,
FCCM, FCCP; Juan Ochoa, MD; Robert Martindale, MD,
PhD; Jeffrey E. Salon, MD, FACP, FCCP, FCCM 20
Nutrition in Critical Illness,
Including Immunonutrition

Introduction release of cytokines and counterregulatory hormones leads to a cas-

cade of events that affect various body systems and have a profound
Adequate nutrition is essential to the critically ill patient. It helps sup- impact on the patient’s metabolic and nutritional status.1 When phys-
port anabolism, ameliorate uncontrolled catabolism, maintain a compe- iologically controlled, this response can facilitate recovery. When
tent immune system, and ultimately improve patient outcome. Critically uncontrolled, it can impair host responses to critical illness.
ill patients usually present with multiple medical problems that are asso- C. When severe infection is the etiology of the critical illness, the meta-
ciated with significant metabolic and nutritional alterations. Severe bolic and physiologic responses to systemic infection are referred to
trauma, burns, sepsis, and head injury are associated with marked hyper- collectively as “sepsis” or “sepsis syndrome.” The most severe form,
metabolism and hypercatabolism, which lead to dramatic metabolic septic shock, is associated with the development of multiorgan dys-
alterations, including increased glycogenolysis, gluconeogenesis, and function and may ultimately cause death. Sepsis leads to significant
lipolysis. Balancing nutritional needs while avoiding metabolic and metabolic changes that result in increased energy expenditure. In
iatrogenic complications is a challenge. Evidence suggests that enteral nonsurgical, mechanically ventilated septic patients, energy require-
feedings should begin early to preserve gut integrity. The use of par- ments have been estimated by the Harris-Benedict (HB) equation at
enteral nutrition (PN) should be kept as low as possible, although con- 20% above the basal energy expenditure (BEE).2 Since sepsis may
comitant use of PN may be necessary while enteral feeding tolerance is occur in the setting of other concomitant organ dysfunction, energy
established. The pediatric intensive care patient population, with patients expenditure varies with the severity of illness.
from birth to adolescence, encompasses a wide variety of critically ill D. The metabolic response to severe head injury is even more dramatic,
patients, including postoperative patients and patients with trauma, con- exceeding the HB prediction of BEE by 40% to 50%. Urinary nitro-
genital heart disease, severe respiratory disorders, sepsis, liver or renal gen losses exceeding 25 g/day have been reported.3 It may take sev-
failure, or multiorgan dysfunction. The prevalence of malnutrition in eral weeks following injury to restore a neutral to positive nitrogen
patients admitted to the pediatric intensive care unit (PICU) ranges balance in these patients.
between 15% and 20%, with a higher prevalence in patients with
congenital heart disease. This chapter discusses the metabolic and
nutritional changes that occur in adult and pediatric critically ill patients
II. Nutritional Alterations in Critically Ill Patients.
and provides guidelines for providing safe and effective nutrition sup- The cascade of events following injury may affect multiple organ sys-
port, including immunonutrition, to these patients. tems, can last from hours to days, and may be accompanied by impaired
immune function and delayed wound healing. The magnitude of the
I. Metabolic Response to Stress response depends mainly on the severity of illness, with individual vari-
II. Nutritional Alterations in Critically Ill Patients ability resulting from patient-specific illness(s) and genetic variations.
III. Nutrition Support in Critically Ill Patients A. The rate of protein catabolism exceeds the rate of protein synthesis,
IV. Complications of Parenteral Nutrition resulting in negative nitrogen balance. There is loss of muscle mass
V. Monitoring and protein degradation in vital organs. The accelerated skeletal mus-
References cle proteolysis causes movement of amino acids (especially alanine
Suggested Readings and glutamine) from the periphery to the viscera for gluconeogene-
sis. Alanine is the major amino acid used for hepatic gluconeogene-
sis. Glutamine is the preferred energy source for enterocytes, cells of
I. Metabolic Response to Stress
the immune system, and cells involved in tissue repair. It serves as a
A. Critically ill patients exhibit a characteristic metabolic response to substrate for renal gluconeogenesis and for hepatic synthesis of the
severe illness or traumatic injury independent of cause. Both types intracellular antioxidant glutathione. Branched-chain amino acids
of inciting events activate the immune system and induce a coordi- such as leucine, isoleucine, and valine also become important oxida-
nated systemic inflammatory response syndrome aimed at limiting tive substrates during critical illness. Cytokines released from mono-
the extent of injury and restoring normal physiologic processes. The cytes and macrophages cause the liver to reprioritize its protein
specific nature and extent of this response can vary widely based on synthesis, reflected by increased production of the “positive” acute-
the causative insult. See Table 20-1. phase proteins (eg, C-reactive protein, α1-antitrypsin) and decreased
B. In critical illness, there is increased release of inflammatory media- synthesis of the constitutive “negative” acute-phase proteins (albu-
tors or cytokines (eg, interleukins 1 and 6, tumor necrosis factor) and min, prealbumin, retinol-binding protein, transferrin). There are
simultaneous increased production of counterregulatory hormones decreased blood levels of visceral proteins regardless of the patient’s
(eg, catecholamines, cortisol, glucagon, growth hormone). The nutritional status.

© 2005 A.S.P.E.N. www.nutritioncare.org. A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. 263
S E C T I O N I V Surgical and Critically Ill Conditions

B. Glucose metabolism
TABLE 20-1. Metabolic Response During Starvation and 1. During stress, increased endogenous glucose production is the
Injury result of increased counterregulatory hormones and cytokines that
stimulate glycogenolysis and gluconeogenesis. Major substrates for
Injury gluconeogenesis are glycerol (from adipose tissues), alanine (from
Characteristic Starvation (Protein-Energy skeletal muscles), and lactate (from peripheral tissues and skeletal
Finding (Marasmus) Malnutrition) muscles). This response is believed to satisfy the glucose needs of
the brain, leukocytes, and the cells involved in tissue repair.
Energy needs Decreased Increased 2. Hyperglycemia may exist even with normal or increased blood
insulin level, as insulin resistance is characteristic of generalized
Primary fuel (RQ) Lipids (0.75) Mixed (0.85) stress. Septic patients have a significant increase in glucagon,
the primary hormonal mediator of gluconeogenesis. Changes in
Insulin Decreased Increased whole-body glucose uptake and glucose oxidation in sepsis are
(resistance) complex. Whole-body glucose uptake and oxidation may be
increased in the early stages of sepsis and endotoxemia. This is
possibly the result of a cytokine-induced increase in non-insulin-
Ketones Present Absent
mediated glucose uptake by tissues rich in mononuclear phago-
cytes (eg, liver, spleen, ileum, lung).
Counterregulatory Basal Increased C. Lipolysis is accelerated with mobilization of glycerol and free fatty
hormones acids, and there is increased fatty acid oxidation. Overall, the patient’s
energy stores are reduced.
Total body water Decreased Increased D. Critical illness is also characterized by activation of the hypothalamic-
pituitary-adrenal axis with the release of cortisol from the adrenal
Proteolysis Decreased Accelerated gland. This essential response to illness and stress contributes to main-
tenance of cellular and organ homeostasis.
Glycogenolysis Increased Accelerated E. Significant fluid and electrolyte disturbances may occur in the criti-
cally ill patient, depending on the patient’s underlying medical prob-
lems, nutritional status, and drug or resuscitative therapy. A detailed
Lipolysis Increased Increased
review of fluid and electrolytes disturbances can be found elsewhere.4
F. The physiologic response to stress and injury and its effects on the
Body stores metabolic and nutritional status of pediatric critically ill patients
are similar to those for adults. Due to their limited tissue reserves,
Skeletal muscle Reduced Reduced pediatric patients may develop malnutrition faster than adults.

Fat Reduced Reduced

III. Nutrition Support in Critically Ill Patients
Visceral proteins Preserved Increased A. Assessment of nutritional status in adults
liver/immune 1. The assessment of nutritional status includes a medical, surgical,
and dietary history obtained from the patient or caregiver. In con-
trast to isolated trauma or burn patients, septic patients often have
Refeeding response Net anabolism None (unless
some degree of underlying malnutrition before the septic episode.
reversed)
This may be a predisposing factor to immune dysfunction that
compromises the patient’s ability to fight infection. Since no sin-
Weight Gradual Accelerated gle measure can provide an accurate assessment of nutritional sta-
(lean tissue loss) tus, combined subjective and objective data should be used (see
Chapter 1). A multitude of factors may limit the accuracy of nutri-
Typical setting Patient with Patient in tional assessment.
chronic diseases hospital/ICU a) A history of acute or chronic weight loss or gain before hospi-
(cardiac, COPD, tal admission is an essential indicator of the patient’s nutritional
etc) status. Because body weight fluctuates with large-volume fluid
resuscitation, preinjury weight in critically ill patients provides
useful information on nutritional status.
COPD, chronic obstructive pulmonary disease; ICU, intensive care unit; RQ, respiratory b) Anthropometric parameters including skinfold thickness and
quotient arm circumference measurements may be unreliable and are
Adapted from Daley BJ, Bistrian BR. Nutritional assessment. In: Zaloga GP, ed. Nutri-
seldom used in critically ill patients because the patient’s posi-
tion in Critical Care. St Louis, MO: Mosby-Year Book; 1994:9–33 with permission from
Elsevier.
tioning and fluid status affect their accuracy.
c) Visceral protein (eg, albumin, prealbumin) levels are affected
by stress, fluid shifts, and other factors that limit their speci-
ficity and sensitivity.
d) Delayed hypersensitivity skin testing that measures cell-
mediated immunity also has limitations in the critically ill

264 A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. © 2005 A.S.P.E.N. www.nutritioncare.org.
 S E C T I O N I V Surgical and Critically Ill Conditions

patient. Many nonnutritional factors such as tissue disruption, D. Protein requirements

acute hemorrhage, hypovolemic shock, anesthesia, surgery, and 1. Protein requirements for critically ill adult patients are approx-
the use of steroids and immunosuppressants depress immune imately 1.5 g/kg/day. Proteins are administered based on the
function, independent of nutritional status. patient’s premorbid body weight or the adjusted ideal body weight
B. Assessment of nutritional status in pediatric patients in obese patients. The magnitude of nitrogen loss varies with the
1. Surgical and medical problems that may affect the patient’s clinical condition (Figure 20-1) and parallels the energy expendi-
nutritional status should be identified. Examples in the pediatric ture and stress level. Requirements may be up to 2 g/kg/day in
patient include congenital defects, gastrointestinal surgeries, patients with trauma, severe burns, and head injury and as high as
impaired neurological status, chronic lung disease, history of 2.5 g/kg/day in adult patients treated with continuous renal
premature birth, and the presence of gastrointestinal symptoms replacement therapy (CRRT).11
that impair food intake or absorption, such as nausea, vomiting, 2. It is the underlying paradigm that nutrition intervention is designed
constipation, or diarrhea. Among patients admitted to the PICU to sustain the body’s nutritional stores until the increased energy
with a diagnosis of congenital heart disease, 15% to 20% are and protein requirements subside. Since the catabolic rate exceeds
malnourished.5,6 the anabolic rate in critical illness, nutritional support can only
2. Anthropometric measurements such as length or height, weight, limit the loss of the body’s protein and calorie stores. The goal is
and head circumference should be obtained upon admission to the to administer sufficient nitrogen to provide a positive or neutral
PICU and compared with existing standards (see Chapter 1). The nitrogen balance. This is best assessed by nitrogen balance studies,
measurements are compared against weight-for-age, length-for- which are discussed in Section V.
age, and weight-for-length or BMI standard tables to determine 3. Protein requirements for the PICU patient vary with age and
whether the patient is adequately nourished or is experiencing clinical status. Protein/amino acids requirements in PN support
moderate or severe malnutrition. Weight or length status and for term infants are 2.5 to 3 g/kg/day. In older children, amino
growth patterns are the primary parameters for nutritional assess- acid requirements are 2 to 2.5 g/kg/day, and critically ill ado-
ment. Body weight should be obtained daily in the PICU patient lescent patients require 1.5 to 2 g/kg/day. Higher protein/amino
using the same scale. Fluid shifts and imbalances are common in acid amounts are required for trauma patients and those treated
critically ill patients and may make weight changes an inaccurate with CRRT to make up for the amino acid losses via the hemodia-
indicator of nutritional status. filter.
C. Energy requirements E. Benefits of enteral feeding
1. Because either overfeeding or severely restricting energy can be 1. Enteral nutrition (EN) should be considered within the first 48 hours
detrimental to the outcome of critically ill patients, sound esti- of injury once the patient is resuscitated and stabilized. Early
mates of energy requirements are necessary. Many equations initiation of EN is crucial to minimize the effects of hypercatab-
have been derived to estimate energy requirements; the HB equa- olism and hypermetabolism.
tion is the most widely used. Stress factors for various disease
states have been empirically determined by the use of indirect
calorimetry and are added to the estimated energy expenditure
calculated using the HB equation. The stress and activity factors FIGURE 20-1. Change in nitrogen excretion in various
used to adjust for the severity of illness may be excessive and can disease states.
lead to overfeeding critically ill patients. In fact, experimental
studies suggest that matching nutritional intake to metabolic 32
expenditure may exacerbate inflammation and increase mortal-
Starvation vs Injury
ity.7 Although energy requirements at approximately 25 to 30 kcal/ 28 Nitrogen Dynamics
kg/day have been recommended for the critically ill patient,8
there is increasing evidence that lower caloric intake (not exceed- Major burn
ing 25 kcal/kg/day) may be safer in these patients. In obese 24
Nitrogen excretion gm/day

patients, nutrition should be provided based on adjusted body Skeletal trauma

weight (see Chapter 28). 20
2. The gold standard for measuring energy expenditure in the clin- Severe sepsis
ical setting is indirect calorimetry (see Chapter 22). This is prob- 16
lematic in pediatric patients because of low gas flow rates and the Infection
use of noncuffed endotracheal tubes, which create an air leak,
12
making gas collections incomplete.
3. Energy requirements of the critically ill pediatric patient change
8 Normal
with the patient’s clinical status. Aside from the severity of ill- range
ness and stress level, other factors that affect energy expenditure Elective Op
include crying, blood draws, physical therapy, and endotracheal 4 Partial
starvation
tube suctioning.
4. The recommended daily allowance (RDA) for age includes a 30% Total
0
to 40% factor for growth in young infants and for activity in chil- 0 10 20 30 40 50
dren and thus typically overestimates energy requirements for Days
PICU patients.9,10 Energy requirements can be estimated at 1 to Reprinted from Long Metabolic response to injury and illness: estimation of energy
1.2 times the resting energy expenditure, depending on the nutri- and protein needs from in calorimetry and nitrogen balance. J Parenter Enteral Nutr
tional status, stress level, and nutrient tolerance. 1979;3:452–56 with permission.

© 2005 A.S.P.E.N. www.nutritioncare.org. A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. 265
S E C T I O N I V Surgical and Critically Ill Conditions

2. Oral nutrition is the preferred route of nutrient intake. If the oxidants. These agents are included in various combinations in
patient cannot or should not be fed orally, then EN is the pre- selected enteral feeding formulas.
ferred feeding route. EN is more physiologic, cheaper, and safer 2. Immunomodulating agents have specific favorable biological and
than PN. clinical effects. Randomized clinical trials have evaluated the role
3. The gastrointestinal tract has a highly metabolically active mucosa. of different immunomodulating enteral formulas in critically ill
Lack of enteral feeding results in gastrointestinal mucosal atrophy, adult patients but not the individual components, and the results
bacterial overgrowth, increased intestinal permeability, depletion of these studies have been widely debated. A meta-analysis by
of the liver’s antioxidant enzymes, and possible translocation of Heyland et al demonstrated reductions in infectious complica-
bacteria and/or bacterial products. EN increases mucosal blood tions, particularly in elective surgery patients, and reductions in
flow, provides a direct source of nutrients, and maintains the meta- length of stay in the intensive care unit.15 However, the effect of
bolic activity and hormonal and enzymatic balance between the these formulas on organ failure and mortality is less clear. These
gastrointestinal tract and the liver. Even low rates of enteral feed- formulas have not yet been studied in the pediatric population.
ing (eg, 10 mL/hr in adults) will have protective effects on the gut 3. Glutamine, the most abundant amino acid in skeletal muscles, is a
mucosa and liver. Enteral feeding maintains gut integrity, prevents precursor of the antioxidant glutathione and a primary nutrient for
gut mucosal atrophy, may prevent bacterial translocation, and pre- enterocytes and the GALT. Lack of glutamine may have profound
serves gut-associated lymphoid tissue (GALT), which is the major effects on gut integrity and lymphoid tissue. Prophylactic admin-
source of gut mucosal immunity. EN has been shown to replete the istration of glutamine to critically ill patients has been attempted
GALT that may become depleted with PN use. While PN bypasses to improve patient outcome, but data remain inconclusive.
first-pass liver metabolism, EN allows most nutrients to go through 4. The long chain omega-3 fatty acids (eicosapentaenoic acid and
the portal circulation. This may have a protective effect on the docosahexaenoic acid) found in fish oil are commonly added to
liver.12 immunomodulating enteral formulas. Increased intake of omega-
4. Enteral feeding is also associated with lower rates of infectious 3 fatty acids instead of omega-6 fatty acids has numerous poten-
complications than PN. Kudsk et al demonstrated significantly tially positive biological effects. Eicosanoids derived from linoleic
fewer cases of pneumonia, intra-abdominal abscesses, and episodes and arachidonic acids are proinflammatory. Those derived from
of catheter sepsis with lower septic morbidity in trauma patients omega-3 fatty acids are less inflammatory and less immunosup-
who were enterally fed than in those who received PN. The most pressive than eicosanoids derived from omega-6 fatty acids.
significant differences were seen in the more severely injured 5. Arginine, a nonessential amino acid, may become conditionally
patients.13 essential in the critically ill patient. Biological actions include
5. EN is associated with improved wound healing, greater wound stimulation of growth hormone, prolactin, and insulin-like
strength, and more wound hydroxyproline and collagen accu- growth factor. Arginine is required for the synthesis of hydroxy-
mulation, which may explain the lower risk of anatomic leaks proline, is essential for lymphocyte function, and is the precur-
and fistulas in bowel surgery patients who receive EN instead of sor of nitric oxide. Arginine levels may fall in septic patients due
PN.12 to decreased intake, increased metabolism to nitric oxide, and
6. Although EN has many safety and metabolic advantages over PN catabolism of arginine in the urea cycle as a consequence of
and is associated with fewer complications, it does not seem to increased arginase expression. If sepsis is potentially an arginine-
affect patient mortality or the incidence of multiple organ fail- deficient state, then arginine supplementation should be benefi-
ure.14 cial in septic patients. In a meta-analysis, immunomodulating
F. Enteral feeding in pediatric patients enteral formulas with high arginine content resulted in a signifi-
1. Pediatric patients on an oral diet who stay longer than 5 days in the cant reduction of infectious complications15 but had no effect on
intensive care unit should have ongoing calorie count monitoring. mortality. At this point, the role and safety of arginine supple-
2. The patient’s fluid requirements should be the primary consider- mentation for critically ill patients are not fully elucidated and
ation when the enteral formula is being selected. Then the energy require further studies.16,17
and protein requirements should be considered. A 20 kcal/oz for- H. Parenteral nutrition
mula is equivalent to 0.67 kcal/mL, and a 24 kcal/oz formula is 1. PN is used in patients for whom oral nutrition or EN is not feasi-
equivalent to 0.8 kcal/mL. ble or is contraindicated and who are malnourished or at high risk
3. In infants with congenital heart disease, fluid restriction often dic- for malnutrition (eg, critically ill patients). In adult patients who
tates concentrating enteral formulas beyond 24 kcal/oz to meet are not malnourished or at high risk for malnutrition, PN can be
energy and protein requirements in small volumes. safely withheld for up to 5 to 7 days while the enteral route is pur-
4. Enteral feeding is usually initiated at full strength since all infant sued. PN should be used for the shortest duration possible.
and pediatric formulas are hypotonic or isotonic and there is min- 2. PN should not be used to correct acute fluid and electrolyte defi-
imal risk for hyperosmolar diarrhea with these formulas. ciencies; instead, a separate intravenous solution with electrolyte
5. Continuous gastric or small-bowel feeding should be attempted supplements should be used as needed. The assessment and man-
first. Enteral feeding in infants is usually initiated at 1 mL/kg/hr agement of electrolyte disturbances should take into consideration
and advanced to energy goal at a rate of 1 to 2 mL/kg/hr every 8 electrolyte sources and losses, acid-base status, clinical condi-
to 12 hours as tolerated. The initial volume should not exceed tions, and medications that affect electrolyte balance.
50 mL/hr regardless of the patient’s age or weight. 3. Dextrose tolerance is dependent on its rate of infusion and under-
G. Immunonutrition lying patient conditions. Dextrose use is reduced in stressed
1. A number of specific nutritional supplements are now recognized patients, patients with diabetes, patients with acute pancreatitis,
to modulate the biologic response to injury, inflammation, and and patients treated with medications that alter glucose metabo-
infection. Collectively referred to as immunomodulating agents, lism (eg, corticosteroids, tacrolimus, catecholamine vasopres-
they include glutamine, omega-3 fatty acids, arginine, and anti- sors). Critically ill patients have a lower tolerance to dextrose

266 A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. © 2005 A.S.P.E.N. www.nutritioncare.org.
 S E C T I O N I V Surgical and Critically Ill Conditions

infusion compared to nonstressed subjects. In hypermetabolic 5. Multivitamin and trace element requirements
burn patients, glucose oxidation reaches a plateau at a dextrose a) Typical standard adult multivitamins and trace element formu-
infusion rate of 5 mg/kg/min.18 However, lower dextrose infusion lations are added to the daily PN. However, no specific guide-
rates are even better tolerated, and rates should be kept at ≤4 mg/ lines for multivitamin and trace element supplementation are
kg/min in adult critically ill patients and should not exceed 60% available for critically ill patients. Modification of specific
of total daily energy.19 In critically ill diabetic patients and those micronutrients is rather based on the patient’s underlying dis-
requiring insulin, the dextrose infusion rate should be started at no eases (eg, liver failure, wounds, burns, fistulas).32
more than 2 mg/kg/min and advanced slowly over a few days to b) Blood trace element concentrations may not necessarily reflect
energy goal while glucose control is maintained with intensive their total body stores due to changes in tissue distribution,
insulin therapy. Uncontrolled hyperglycemia may cause fluid and metabolism, or elimination. For example, during stress, blood
electrolyte abnormalities, hyperglycemic hyperosmolar nonketotic zinc concentrations may fall due to sequestration in the liver,
syndrome, and increased susceptibility to infections. Hyper- increased use in metabolic pathways, and increased renal
glycemia is also an early sign of sepsis, so sepsis should be ruled elimination.
out in patients who are stable on PN and suddenly develop c) Supplementation of specific micronutrients is based on the
hyperglycemia or increased insulin requirements. patient’s underlying diseases (eg, liver failure, wounds, burns,
4. Lipid requirements short gut syndrome) when alterations in micronutrient metab-
a) Lipid clearance is reduced in stressed patients due to decreased olism and requirements are needed. The role of antioxidant
activity of lipoprotein lipase (LPL), the main enzyme released supplementation (eg, supplementation of vitamins C, E, and
in the bloodstream that hydrolyzes lipid particles into fatty A and selenium) in critically ill patients remains unknown.33
acids. Since critically ill patients have reduced tolerance to lipid d) Iron metabolism is also altered under stress, leading to
emulsion infusion, the lipid infusion rate should not exceed decreased plasma iron concentrations. However, this may not
0.12 g/kg/hr to avoid the development of elevated triglyceride necessarily indicate iron deficiency. Intravenous iron adminis-
levels.20 tration in the septic patient is discouraged since iron is essential
b) A dose of intravenous lipid emulsion at 0.5 to 1 g/kg/day pre- for bacterial growth and may theoretically worsen sepsis.
vents essential fatty acid deficiency. Lipid emulsions may need
to be withheld in pediatric patients when serum triglyceride
concentrations exceed 275 mg/dL. IV. Complications of Parenteral Nutrition
c) Although it has been suggested that lipid emulsions may have A. In a meta-analysis of studies that evaluated PN use in critically ill
immunosuppressive effects by helping to reduce phagocytosis adult patients, the benefits of PN were most noticed in malnourished
and cytokine secretion, these effects have not been clinically patients, who also had fewer complications with PN than nonmal-
proven.21 nourished patients given PN. Critically ill patients who received PN
d) There is a difference in the clearance of various lipid emulsion had almost twice the risk of mortality (relative risk 1.78; 95% con-
concentrations due to the differences in the phospholipid-to- fidence interval 1.11–2.85).34 Similarly, the Veterans Affairs coop-
triglyceride (PL/TG) ratio of each emulsion. The PL/TG ratios erative study showed that perioperative PN improved the outcome
of the 10%, 20%, and 30% lipid emulsions are 0.12, 0.06, and
only of high-risk severely malnourished patients.35
0.04, respectively. In critically ill patients, lower plasma triglyc-
B. The deleterious effects of PN may be most evident in critically ill
erides, phospholipids, and cholesterol concentrations have been
patients who are at a particularly high risk for nosocomial infections.
seen with the use of 30% lipid emulsions compared to 10% and
A number of studies reported an increased risk of infectious compli-
20% lipid emulsions.22–24
cation, longer hospital stay, and an increased risk of mortality in
e) Structured lipids made of medium-chain triglycerides (MCT)
patients receiving PN. The Veterans Affairs study evaluated the role
are currently available only in Europe. These mixtures con-
of perioperative PN (7–10 days before and 3 days after surgery) in
tain MCT and long-chain triglycerides (LCT) in 75/25 or
patients who required noncardiac surgery. There were significantly
50/50 MCT/LCT ratios. The inclusion of LCT in the
MCT/LCT mix provides the essential fatty acids that are not more infectious complications in the PN group than in the control
provided in MCT. MCT are oxidized faster than LCT, a pos- group that did not receive PN (14.1% vs 6.4%). Also, a trend toward
sible advantage in patients with reduced lipid clearance, such higher 90-day mortality was observed in the PN group compared to
as critically ill patients.25 Although some research data the control group (13.4% vs 10.5%). Only those with severe malnu-
showed that the MCT/LCT lipid emulsion may result in a bet- trition appeared to benefit from PN as administered in that study.35
ter blood lipid profile and improved nitrogen balance, these C. PN may also be associated with a more pronounced proinflamma-
results were not replicated in other studies.26 tory response than EN. Clinical and experimental data have shown
f) In patients with acute renal failure, the clearance of both LCT higher levels of local and systemic proinflammatory mediators with
and MCT was found to be equally reduced in comparison to PN than EN. Higher levels of interleukins (IL-6, IL-8) were found
healthy volunteers, with similar increases in serum triglyceride after colorectal and major abdominal surgeries in patients receiving
levels between the 2 groups. PN compared to patients who were fed enterally.36,37 PN may be par-
g) In patients with respiratory failure, variable effects have been ticularly harmful in patients with severe inflammation such as acute
seen in measures of respiratory function and pulmonary and pancreatitis; such patients were shown to have higher infective and
arterial hemodynamics.27–29 Hyperlipidemia during lipid emul- noninfective complications if they received PN compared to jeju-
sion infusion has been reported to affect pulmonary gas dif- nal feeding.
fusion and pulmonary vascular resistance in patients with D. A recent meta-analysis of six randomized controlled trials com-
preexisting pulmonary disease.30,31 More research is needed pared the safety and clinical outcomes of PN versus EN in patients
before routine use of the mixed MCT/LCT lipid emulsions can with acute pancreatitis. Results of the meta-analysis showed that EN
be recommended. was associated with a significantly lower incidence of infections,

© 2005 A.S.P.E.N. www.nutritioncare.org. A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. 267
S E C T I O N I V Surgical and Critically Ill Conditions

shorter length of stay, and reduced surgical interventions compared dosing. The most effective way to maintain serum glucose con-
to control pancreatitis patients. However, no statistically significant centrations between 80 and 110 mg/dL in hyperglycemic criti-
difference was found for mortality and noninfectious complications cally ill patients is the use of continuous insulin infusion that
between the PN and EN groups.38 allows flexible titration of the insulin dose based on frequent
E. Complications of excess dextrose infusion include hyperglycemia, serum glucose monitoring. A serum glucose threshold that is
hypertriglyceridemia, hepatic steatosis, respiratory decompensation, associated with increased morbidity and mortality has not been
and depression of immune function. Hyperglycemia is now thought determined.
to be a major driver of parenteral nutrition complications, which 4. Enteral feeding is associated with fewer complications than PN
are reduced when insulin is used to maintain euglycemia.39 (See and allows carbohydrate to pass through the liver with resultant
Chapter 27.) hormonal/metabolic responses before reaching the systemic cir-
1. Dextrose overfeeding resulting in hyperglycemia can depress the culation. This reduces the hyperglycemic effect of glucose. In
immune system and increase infection risk. Hyperglycemia may the Van den Berghe study,39 patients who received exclusive PN
impair cellular and humoral host defenses by reducing phagocyto- required 26% more insulin to maintain euglycemia than those
sis, impairing neutrophil chemotaxis and adhesion, and inhibiting who received partial enteral feeding.40
complement fixation. In vitro and animal data showed a reduction F. Hypertriglyceridemia in patients receiving PN denotes excess
in phagocytic activity of polymorphonuclear granulocytes and triglyceride synthesis or reduced fat clearance. Hypertriglyceridemia
inhibition of immunoglobulin function with hyperglycemia. In during PN infusion is primarily due to dextrose overfeeding or
humans, postsurgical diabetic and nondiabetic hyperglycemic excess lipid infusion. Stressed patients are at higher risk for hyper-
patients have increased nosocomial and wound infections. Con- triglyceridemia due to increased lipolysis and hepatic fatty acid re-
trolling hyperglycemia has resulted in improved phagocytic func- esterification, increased hepatic triglyceride synthesis from dextrose
tion as well as improved patient outcome. infusion, and decreased LPL enzyme activity that results in reduced
2. Hyperglycemia has traditionally been defined as a random serum clearance of intravenously administered lipids. Also, certain med-
glucose concentration >200 mg/dL. Serum glucose concentrations ications used in critically ill patients, such as corticosteroids and
of 150 to 200 mg/dL have long been considered acceptable in immunosuppressants (sirolimus, cyclosporine), alter fat metabolism
stressed patients because it is believed that modest hyperglycemia and increase serum triglyceride levels. Patients who are especially
may promote cellular glucose uptake by glucose-dependent tissues at risk for hypertriglyceridemia include those with sepsis, multi-
(brain, red blood cells, wounds). However, recent data show that organ failure, diabetes, liver disease, renal failure, or pancreatitis.
maintaining euglycemia between 80 and 110 mg/dL reduces com- G. Total energy and dextrose overfeeding may result in hypercapnia,
plications and improves patient outcome. Van den Berghe et al, in especially in patients with borderline respiratory function and limited
a prospective randomized controlled study, evaluated the effects of
pulmonary reserve. Excess carbon dioxide is produced relative to
intensive and conventional insulin therapies in 1548 adult surgical
oxygen (O2) consumption during excess carbohydrate administra-
intensive care unit patients. Surgical patients were randomized to
tion, resulting in an increased respiratory quotient (RQ = VCO2/VO2).
receive intensive insulin therapy to maintain serum glucose con-
The RQs for carbohydrate, protein, and fat oxidation are 1, 0.8, and
centrations between 80 and 110 mg/dL or to receive a conventional
0.7, respectively. Energy-mixed substrates from fat, protein, and car-
insulin regimen to maintain serum glucose concentrations between
bohydrates normally yield an RQ of 0.85. The RQ exceeds 1 during
180 and 200 mg/dL. Study results showed that intensive insulin
carbohydrate overfeeding. As a result, increased carbon dioxide gen-
therapy was associated with a 34% reduction in overall in-hospi-
eration causes increased respiratory workload and minute ventilation.
tal mortality and a 46% reduction in septicemia. Intensive insulin
Mechanically ventilated patients may have prolonged ventilator
therapy significantly reduced mortality in the intensive care unit
dependence. In critically ill patients, overfeeding should be ruled out
(from 8% to 4.6%) and in patients who remained more than 5 days
in the intensive care unit (from 20.2% to 10.6%) compared to con- when the RQ exceeds 1. When total energy intake is appropriate,
ventional insulin therapy. Intensive insulin therapy was also asso- reducing the carbohydrate load and substituting fat calories lowers
ciated with reduced morbidity factors such as acute renal failure, the RQ. However, the RQ may be an insensitive indicator of over-
ventilator dependency, and polyneuropathy.39 A follow-up multi- feeding in hypermetabolic patients. Only minor changes to the RQ
variate logistic regression analysis of the data by the same investi- may occur despite major increases in minute ventilation and oxygen
gators showed that the benefits of intensive insulin therapy were consumption.
the result of normalizing serum glucose rather than the result of the H. Liver complications associated with PN include steatosis (fatty liver),
insulin dose.40 The Van den Berghe study data are applicable to cholestasis, biliary sludge, and cholelithiasis. In the critically ill inten-
adult surgical intensive care patients; studies are under way to sive care unit patient, these complications are unlikely to occur, due to
determine the role of tight glucose control in other intensive care the short duration of PN, assuming overfeeding is avoided. Although
and hospitalized patients. PN-associated steatosis is more common in adults and cholestasis
3. In the absence of dextrose overfeeding, insulin therapy may be is more common in children, both conditions may coexist in either
necessary to control hyperglycemia while meeting the patient’s patient population.
caloric needs, as insulin resistance is characteristic of general- 1. Steatosis occurs when fat accumulation exceeds its transport from
ized stress. Insulin stimulates glucose uptake and reduces the liver. In patients receiving PN, high dextrose load is the pri-
hepatic glucose production. However, insulin does not increase mary cause of steatosis. However, lipid overfeeding and deficien-
glucose oxidation, and excess dextrose is largely converted to cies of certain nutrients such choline, carnitine, and essential fatty
fat instead of being oxidized to carbon dioxide (CO2). In adults, acids may also lead to steatosis. Patients with hepatic steatosis are
the use of a sliding scale subcutaneously administered insulin is usually asymptomatic, and liver enzymes are poorly sensitive to
not recommended due to variability of tissue perfusion that may the degree of fatty infiltration. Hepatic steatosis in patients receiv-
lead to inadequate glycemic control between intermittent insulin ing PN is usually reversible. The key to preventing hepatic steato-

268 A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. © 2005 A.S.P.E.N. www.nutritioncare.org.
 S E C T I O N I V Surgical and Critically Ill Conditions

sis is to avoid overfeeding and provide balanced PN with no more 9. Chwals WJ. Metabolism and nutritional frontiers in pediatric surgical
than 60% of total calories from dextrose, about 20% to 30% of patients. Surg Clin North Am. 1992;72:1237–1266.
total calories from fat, and the remaining calories from protein. 10. Shanbhogue RLK, Lloyd DA. Absence of hypermetabolism after operation
in the newborn infant. J Parenter Enteral Nutr. 1992;16:333–336.
2. PN-associated cholestasis is more common in long-term PN
11. Scheinkestel CD, Adams F, Mahony L, et al. Impact of increasing parenteral
patients. Factors that predispose such patients to cholestasis
protein loads on amino acid levels and balance in critically ill patients on
include PN dependence, bowel rest, overfeeding, short gut syn- continuous renal replacement therapy. Nutrition. 2003;19:733–740.
drome, sepsis, and premature birth in newborn babies. Elevated 12. Marik PE, Zaloga GP. Early enteral nutrition in acutely ill patients: a sys-
serum bilirubin concentrations, especially conjugated bilirubin, tematic review. Crit Care Med. 2001;29:2264–2270.
are the earliest clinical signs of cholestasis. Patients supported 13. Kudsk KA, Croce MA, Fabian TC, et al. Enteral vs parenteral feeding.
with the extracorporeal membrane oxygenation (ECMO) system Effects on septic morbidity after blunt and penetrating abdominal trauma.
may show hyperbilirubinemia because of hemolysis from the Ann Surg. 1992;215:503–511.
mechanical stress on red blood cells as they pass through the 14. Cerra FB, McPherson JP, Konstantinides FN, et al. Enteral nutrition does
not prevent multiple organ failure syndrome (MOFS) after sepsis. Surgery.
ECMO circuit.41 Jaundice may or may not be present depending
1988;104:727–733.
on the severity of cholestasis. Measures to prevent PN-associated
15. Heyland DK, Novak F, Drover JW, et al. Should immunonutrition become
cholestasis include initiating enteral or oral feeding, weaning off routine in critically ill patients? A systematic review of the evidence. JAMA.
PN, avoiding overfeeding, using balanced sources of calories, 2001;286:944–953.
and cycling PN. 16. Kudsk KA, Moore FA. Proceedings from summit on immune-enhancing
enteral therapy. J Parenter Enteral Nutr. 2001;25(2 suppl):1S–63S.
17. Stechmiller JK, Childress B, Porter T. Arginine immunonutrition in criti-
V. Monitoring cally ill patients: a clinical dilemma. Am J Crit Care. 2004;13:17–23.
A. Standard laboratory parameters are monitored in critically ill patients 18. Burke JF, Wolfe RR, Mullany CJ, et al. Glucose requirements following
burn injury. Ann Surg. 1979;190:274–285.
receiving EN and PN (see Chapters 5 and 8).
19. Rosmarin DK, Wardlaw GM, Mirtallo J. Hyperglycemia associated with
B. Nitrogen balance is a generally accepted method for evaluating the
high, continuous infusion rates of total parenteral nutrition dextrose. Nutr
adequacy of protein intake and retention. Its validity can be limited Clin Pract. 1996;11:151–156.
by many factors, such as adequacy of urine collection, unrecorded 20. Iriyama K, Miki C, Inoue T, et al. Constant infusion rates of lipid emulsions
nitrogen losses from large open wounds, severe burns, diarrhea, or to stabilize plasma triglyceride concentrations: medium-chain triglyceride/
renal failure or liver failure with nitrogen accumulating in the blood. long-chain triglyceride emulsions (MCT/LCT) versus LCT. Surg Today.
Ideally, nitrogen balance should be measured in a “steady state,” but 1998;28:289–292.
this may be impossible in critically ill patients. Values should be inter- 21. Waitzberg DL, Lotierzo PH, Logullo AF, et al. Parenteral lipid emulsions
preted in the context of the patient’s clinical status. Difficulty with and phagocytic systems. Br J Nutr. 2002;87(suppl 1):S49–57.
urine collection makes determining nitrogen balance very difficult in 22. Kalfarentzos F, Kokkinis K, Leukaditi K, Maroulis J, Onoufriou A,
Alexopoulos K. Comparison between two fat emulsions: intralipid 30 percent
young pediatric patients.
vs intralipid 10 percent in critically ill patients. Clin Nutr. 1998;17:31–34.
23. Nordenstrom J, Thorne A. Comparative studies on a new concentrated fat
(Critical care chapters in the 1st edition were contributed by Elaine B.
emulsion: intralipid 30% vs. 20%. Clin Nutr. 1993;12:160–167.
Trujillo, Malcolm K. Robinson, Danny O. Jacobs, Theresa L. Han- 24. Garcia-de-Lorenzo A, Lopez-Martinez J, Planas M, et al. Safety and meta-
Markey, and John R. Wesley) bolic tolerance of a concentrated long-chain triglyceride lipid emulsion in
critically ill septic and trauma patients. J Parenter Enteral Nutr. 2003;27:
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stress and alterations in nutrient metabolism. In: Shikora SA, Martindale medium-chain triglyceride (75%) and long-chain triglyceride (25%) fat
RG, Schwaitzberg SD, eds. Nutritional Consideration in the Intensive Care emulsions in the nutritional management of multiple-trauma patients.
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8. American Society for Parenteral and Enteral Nutrition Board of Directors 32. Mason JB. Vitamins and trace elements in the critically ill patient. In: Shikora
and the Clinical Guidelines Task Force. Specific guidelines for disease— SA, Martindale RG, Schwaitzberg SD, eds. Nutritional Consideration in the
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270 A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. © 2005 A.S.P.E.N. www.nutritioncare.org.
 Rosemary A. Kozar, MD, PhD;
Margaret M. McQuiggan, MS, RD, LD, CNSD;
Frederick A. Moore, MD 21
Trauma

Introduction currently feasible because the driving mechanisms are not under-
stood. Our best options are to control the initiating insult and to pro-
Nutrition support is an integral part of therapy for patients who have vide high risk patients exogenous substrates that support the
undergone major trauma. To determine the feasibility and need for nutri- metabolic environment.
tion support in trauma patients, it is necessary to understand the body’s B. The injury stress response increases resting energy expenditure
response to stress and injury. This chapter reviews the nutritional meta- (REE). The increase in REE depends on both the type and severity of
bolic alterations associated with trauma and provides guidelines for the the insult. For example, REE can increase as much as 100% after
assessment and management of nutrition for these patients. burns, 50% with sepsis, 40% after trauma, and 30% after major sur-
gery. To meet this increased metabolic demand, endogenous sub-
I. Background-Trauma strates are mobilized.
II. Metabolic Response to Stress 1. Glucose stores (approximately 2000–3000 kcal glycogen) are
III. Rationale for Nutrition Support quickly depleted and gluconeogenesis (principally in liver, but also
IV. Initiation of Nutrition Support in kidney) produces glucose that is shunted to glucose-dependent
V. Enteral Nutrition tissues such as brain, erythrocytes, inflammatory cells, and injured
VI. Parenteral Nutrition tissue.
References 2. Adipose tissue is stimulated to release free fatty acids (FFA) and
glycerol. The rate of lipolysis, however, exceeds lipid oxidation.
I. Background-Trauma As a result, plasma triglyceride levels increase and considerable
re-esterification occurs in the liver. This requires energy and cre-
A. Trauma statistics ates futile cycles.
1. Trauma is the leading cause of death in Americans between the 3. The increase in protein catabolism is the most dramatic effect.
ages of 1–38 years.1 Skeletal muscle protein, and later constitutive proteins such as
2. Ten percent of hospital admissions are related to trauma and range albumin, prealbumin, and transferrin are broken down. The
from minor abrasions and contusions to those severe cases involv- released amino acids become substrates for acute-phase protein
ing multiple organs and requiring prolonged ICU stays.2 synthesis (clotting factors, gamma globulins, and C-reactive pro-
3. Blunt trauma admissions are decreasing while penetrating trauma tein), gluconeogenesis, and energy production.
admissions are increasing, particularly in urban areas.3 a) Glutamine and alanine account for 70% of the amino acids
B. Types of traumatic injuries released from peripheral tissues. Glutamine is the preferred
1. Traumatic injuries are characterized as blunt versus penetrating, oxidative fuel of enterocytes and is an important energy source
with electrical and thermal classified separately. for the immune system and for cells involved in tissue repair. It
2. Fifty to sixty percent of blunt trauma requiring hospital admission also may be important for hepatic synthesis of the critical intra-
results from motor vehicle accidents with another 10–20 percent cellular antioxidant, glutathione.
from falls.3 b) Alanine is the major amino acid used in hepatic gluconeo-
3. The severity of penetrating trauma is dependent on the mecha- genesis.
nism of injury and the organ systems involved. These types of c) Other amino acids such as the branched-chain amino acids
injuries include stab and gun shot wounds. leucine, isoleucine, and valine become important oxidative
C. Trauma presentation and outcome is also dependent on the patient’s fuels. The overall consequence of these processes is net total
age, gender, anatomy, and pre-existing disease.4 body protein catabolism and rapid reduction in lean body mass
primarily by effects on skeletal muscle.
(This material was borrowed from Cresci, GA and Martindale RG, Nutrition Support in
Trauma. In: Gottschlich MM. The Science and Practice of Nutrition Support: A Case-Based C. Traumatic stress also results in alterations in trace elements and
Core Curriculum. Kendall/Hunt Publishing 2001 with permission from the American Soci- minerals.
ety for Parenteral and Enteral Nutrition) 1. Iron metabolism is altered under conditions of trauma, leading to
decreased concentrations in the blood. However, it may not be
II. Metabolic Response to Stress advisable to administer iron under such circumstances because it
is essential for the growth of many bacteria and iron supplemen-
A. A variety of conditions in the trauma patient can lead to a metabolic tation in the critically ill has been reported to increase risk of
response referred to as the “injury stress response.” The systemic systemic infection.5,6
inflammatory response syndrome (SIRS) and its associated media- 2. Plasma zinc concentrations may be decreased because zinc is
tors (eg, TNFα, IL-1, IL-2, IL-6) play an important role in this sequestered in the liver during stress and is consumed in several
response. Favorable modulation of the injury stress response is not essential metabolic pathways that are accelerated in the critically ill.

© 2005 A.S.P.E.N. www.nutritioncare.org. A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. 271
S E C T I O N I V Surgical and Critically Ill Conditions

3. There are now a number of clinical trials supporting the use of 5. The primary route of dissemination of pathogens that colonize the
antioxidants in the critically ill.7–9 A recent study by Nathens et gastrointestinal tract (ie, aspiration versus translocation) is not
al demonstrated a decreased incidence of pulmonary morbidity clear. Although there is good epidemiologic evidence for this
and multiple organ failure as well as a shorter duration of sequence of events, prospective randomized controlled trials of
mechanical ventilation and ICU stay when Vitamin E and C were gut-specific therapies, such as early enteral nutrition and, more
administered to critically ill surgical patients at risk for organ recently, immune-enhancing enteral formulas, have demonstrated
dysfunction.7 a reduction in nosocomial infections.10,15 These studies provide the
D. Nutritional support needs to be tailored to the metabolic environment. most convincing evidence of the importance of the gastrointesti-
The stressed trauma patient requires approximately 25–30 kcal/kg/d nal tract as a source. Thus, the provision of early enteral nutrition
and 1.5–1.75 gm/kg/d of protein. As metabolic stress increases, to promote gut function is believed to prevent this cascade of
patients become more catabolic and less tolerant to glucose. events.

III. Rationale for Nutrition Support IV. Initiation of Nutritional Support

A. Prevention of acute protein malnutrition A. Nutritional assessment—A nutritional assessment should be per-
1. Persistent hypercatabolism results in acute protein malnutrition formed as soon after injury as possible.
and is associated with cardiac, pulmonary, hepatic, gastrointesti- 1. Physical assessment of the patient includes evaluation of body
nal, and immunologic dysfunction. Delayed infections then extend composition, edema, wound healing, and nutrient composition of
hypercatabolism with the progression to full-blown multiple organ fluid losses through wounds or drains, as well as review of the
failure. laboratory and medication profile. A height and pre-admission
2. A number of clinical studies have clearly demonstrated that early weight are obtained and information on chronic disease, activity
enteral nutrition improves outcome, as measured by improved level, medications, previous dietary restrictions, psychosocial
nitrogen balance and constitutive protein levels, improved immune data, and drug and tobacco patterns is noted.
function, decreased infections, and decreased length of stay.10–13 2. A history of 10% weight loss over three months is considered
B. Modulation of immune response significant. However, weight loss combined with physiologic
1. Despite tremendous advances in ICU care, nosocomial infections impairment may be even more important, as this can be associ-
remain a common problem. In large part, these late infections ated with increased septic complications, pneumonia, and a pro-
occur due to failure of local and systemic host defenses. While longed hospital stay.16
exact causes of late immunosuppression are not clear, it is now 3. Functional impairment may be assessed by crude measures
believed nosocomial infections occur partly as a result of dys- such as physical assessment of triceps skinfold, decreased pre-
functional regulation of inflammation.14 hospital activity, perception of fatigue, strength of cough, and
2. An initial insult, whether secondary to sepsis, trauma/burns, or skin integrity.
major operation, can precipitate early systemic hyperinflamma- 4. Body protein stores, as assessed by muscle mass and serum pro-
tion (ie, systemic inflammatory response syndrome, SIRS), which teins, should be evaluated, as they correlate more closely with sur-
when intense can precipitate early multiple organ failure (MOF). vival. Body composition can be assessed by a variety of techniques
3. Certain components of the early SIRS response are endoge- including caliper measurements, bioelectrical impedance analysis,
nously down-regulated to prevent unnecessary, potentially auto- and dual-energy X-ray absorptiometry for bone mineral density.
destructive inflammation. This is referred to as the compensatory 5. Age-related loss of skeletal muscle should also be taken into con-
anti-inflammatory response syndrome (CARS). The resulting sideration. The malnourished, elderly patient undergoing a cata-
delayed immunosuppression, however, sets the stage for sec- bolic illness will reach a critical cardiac or respiratory threshold
ondary infection, which can either worsen early MOF or trig- much earlier than a young, previously healthy individual.
ger late MOF. B. Estimating energy requirements
4. While no strategy can prevent or eliminate the dysfunctional 1. The Harris Benedict Equation is a common method to estimate
inflammatory response, the delivery of specific immune-enhancing energy expenditure and thus determine caloric requirements. It
nutrients (generally via the gut) may prove beneficial. estimates basal energy expenditure (BEE) based on age, sex,
C. Promotion of gut function height, and weight. The BEE represents energy requirements in the
1. The dysfunctional gut is believed to be a reservoir for pathogens fasted, resting, non-stressed state, so that in the presence of meta-
that can then cause late MOF-associated infections. bolic stress such as trauma, the BEE must be multiplied by an
2. The initial insult (which could be ischemia/reperfusion, shock, or empirically derived stress factor to obtain an estimate of the caloric
sepsis) and emergency laparotomy (via anesthesia and bowel requirement. Typical stress multiplication factors for trauma
manipulation) can cause early ileus. patients range from 1.2 to 1.6.
3. Disuse of the gastrointestinal tract, through the use of parenteral 2. Estimates of caloric support can also be made. In general, most
rather than enteral nutrition, or through commonly employed trauma patients should receive approximately 25–30 kcal/kg/d
intensive care unit therapies (eg, H2-antagonists, narcotics, or and 1.5–1.75 gm/kg/d of protein. Needs may decrease as patients
broad-spectrum antibiotics) can promote further gut dysfunction. move farther from the initial injury.
4. Gut dysfunction is characterized by progressive ileus, coloniza- C. Monitoring response to therapy
tion of the upper gut, increased permeability, and decreased gut- 1. Assessment of body protein stores
associated lymphoid tissue function. Consequently, the upper gut a) Serum protein status is conducted upon admission and period-
becomes a reservoir for pathogens. In addition, local and systemic ically through the hospital stay. Acute phase proteins, such
defense mechanisms that prevent the spread of these organisms as C-reactive protein, rise markedly within 72–96 hours
become impaired. after injury, while the constitutive proteins, albumin, prealbu-

272 A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. © 2005 A.S.P.E.N. www.nutritioncare.org.
 S E C T I O N I V Surgical and Critically Ill Conditions

min, and transferrin, all decline. Measuring both categories of Aid (McGaw, Inc., Irvine, CA) and Impact (Novartis Corp., Min-
proteins concurrently helps to determine the degree of physio- neapolis, MN) have been shown in clinical studies to improve
logic stress and the return of anabolism. patient outcome, principally by reducing infections and improv-
b) Once C-reactive protein falls below 10–15 mg/dl, a prompt ing wound healing. Other formulas have not been prospectively
increase in prealbumin should occur (0.5–1.0 mg/dl daily). If studied and are dissimilar enough from the tested formulas that no
an appropriate increase does not occur, then the adequacy of conclusions can be made about their use in trauma patients.
the support should be re-assessed. 2. Five PRCTs have tested the efficacy and safety of IEDs specifi-
2. Nitrogen balance cally in trauma patients. The majority demonstrate improved
a) Nitrogen balance is the difference between nitrogen intake patient outcome with the use of IEDs.21–25 The first three studies
and nitrogen output. Nitrogen intake is determined from daily by Brown21, Moore22, and Kudsk23, all showed a reduction in
dietary intake while nitrogen output is determined by meas- infectious complications, particularly intra-abdominal abscesses.
uring urinary urea nitrogen (UUN) in a 24-hour urine collec- The fourth study by Mendez et al failed to demonstrate any out-
tion and adding 4 gm to approximate non-urea nitrogen loss come improvement and suggested that the IED may exacerbate
in the urine and other N2 losses. organ failure.24 This study had several methodologic flaws, most
b) The formula to calculate nitrogen balance is as follows: notably that patients receiving the immune-enhancing diets had a
Nitrogen balance = (gm protein intake/6.25) − (gm nitrogen higher incidence of acute respiratory distress syndrome (ARDS)
in UUN + 4) prior to beginning the diet (IED=31% versus SED=14%). The last
c) UUN reflects the protein catabolic rate (degree of stress) and study by Weimann et al demonstrated a decrease in the number of
represents the majority of nitrogen excreted in the urine. It is days of systemic inflammatory response syndrome and a decrease
therefore a rough approximation of total urinary nitrogen. As in multiple organ failure.25 Analysis of these individual studies
the stress level increases, the concomitant increase in protein offers convincing evidence that IEDs provide additional benefits
catabolism results in an increase in urinary nitrogen. UUN may compared to standard enteral diets in patients sustaining major
not be valid in certain patient populations, such as patients with torso trauma. As with studies supporting the use of early enteral
compromised renal function (creatinine clearance < 50 mL/ nutrition, a decrease in mortality has not been demonstrated.
min) or in patients with spinal cord injury. (This material was borrowed from Kozar RA, McQuiggan MM, and Moore FA. Trauma,
d) Ideally, patients should be in positive nitrogen balance In: Cresci G , Nutrition Support in the Critically Ill Patient. Taylor & Francis, 2005 with
(3–5 g/day). permission)
3. Metabolic gas analysis- Also known as indirect calorimetry, meta-
C. Specialized enteral formulas in patients with ARDS
bolic gas analysis is a tool that can measure resting energy expen-
One PRCT demonstrated improved outcome in patients with ARDS
diture (REE). See chapter on Indirect Calorimetry for further
who were provided an enteral diet supplemented with high omega-
information on this technique.
3 fatty acids, γ-linolenic acid, and antioxidants versus a high
omega-6 formula. The control diet, a marketed high fat formula,
V. Enteral Nutrition could have worsened ARDS by increasing inflammation and the
A. Benefits of early enteral nutrition production of lipid mediators.26
In the 1980s, three prospective randomized controlled trials demon- D. Indications and contraindications of enteral nutrition
strated that trauma patients receiving early enteral nutrition had sig- 1. Patients who cannot adequately meet their nutritional goals by
nificantly fewer infectious complications than patients receiving oral intake alone for a period of approximately seven days should
parenteral nutrition, though a decrease in mortality was not demon- be considered for enteral supplementation. Additionally, early
strated.10–12 A meta-analysis that included eight randomized con- enteral nutrition should be considered for all acutely ill patients,
trolled trials (six published, two unpublished) verified these findings. such as patients with major torso trauma, chronically malnour-
As in the single institutional trials, this analysis concluded that fewer ished patients, and patients with limited physiologic reserve.
infectious complications developed in patients receiving enteral Early enteral nutrition is generally defined as support instituted
nutrition.13 Even when patients with catheter-related sepsis were within 48 to 72 hours of injury.
removed from the analysis, a significant difference in infections 2. Contraindications to enteral nutrition can be divided into absolute
between groups remained. These studies provide convincing evi- and relative. Absolute contraindications include functional com-
dence that enteral nutrition is preferred to parenteral nutrition in plications such as bowel obstruction, peritonitis, progressive ileus,
patients sustaining major torso trauma. Data are less clear for patients massive gastrointestinal hemorrhage, and gastrointestinal
with traumatic brain injury. The most recent Cochrane Review ischemia associated with shock and vasopressors. Relative con-
reported a trend towards better outcome (survival and disability) with traindications include intolerance to enteral nutrition. A recent
the administration of early feeding.17 bowel anastomosis is not a contraindication. Healing, in fact, may
B. Role of immune enhancing agents in the trauma patient be hastened by early feeding.27
More recent trials indicate that additional benefits can be achieved by E. Obtaining enteral access
the use of immune-enhancing agents compared to standard enteral 1. Access can be divided into gastric (and duodenal) and jejunal
diets. Immune-enhancing diets (IEDs) include a variety of potential with push, endoscopic, radiologic, and available surgical options.
immune-enhancing agents, including arginine, glutamine, omega-3- Plans to obtain access should be formulated upon admission to
fatty acids, and nucleotides. However, the contributions of individual the hospital.
nutrients have not been well investigated. As a single supplement, 2. For patients to be fed into the stomach, a soft, nonsump nasogas-
only glutamine (added to standard enteral diets) has been shown to tric tube or dobhoff can be placed. For patients anticipated to
decrease infectious morbidity in trauma and burn patients in prospec- require long-term feeding access, a percutaneous endoscopic gas-
tive randomized controlled trials (PRCTs).18–20 trostomy (PEG) is an option. Prior to instituting gastric feeds,
1. There are currently a number of commercially available formulas patients should be assessed for aspiration risk including factors
that contain two or more of these agents. Two formulas, Immun- such as endotracheal intubation, decreased level of consciousness,

© 2005 A.S.P.E.N. www.nutritioncare.org. A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. 273
S E C T I O N I V Surgical and Critically Ill Conditions

underlying neuromuscular disease, history of aspiration, recent tric decompression and either stopping gastric feeds or decreasing
stroke, and recent major upper abdominal surgery. If two or more the tube feed infusion rate by half for jejunal feeds. Additionally,
risk factors are present, strong consideration for jejunal feeding high nasogastric output in patients fed into the small bowel can be
should be given. Additionally, patients should be assessed for managed by verifying postpyloric placement of the feeding tube and
delayed gastric emptying, which may be seen with diabetes, sep- checking the nasogastric aspirate for glucose. Any amount of glu-
sis, hyperglycemia, and traumatic brain injury. Because of a high cose is considered abnormal and enteral feeds should be withheld.
incidence of gastroparesis in brain-injured patients, gastric feed- Finally, enteral feeds should be discontinued if vasopressors are
ing can be difficult.28 Newer promotility agents may be helpful in instituted.
this patient population.29 I. Complications of enteral nutrition
3. For those patients identified as candidates for jejunal feeds, access 1. Technical complications that can occur with the administration
can be obtained at the time of initial laparotomy, or at subsequent of enteral nutrition include aspiration, bowel perforation,
laparotomy if damage control is initially performed, either as a clogged tubes, and tube malposition/dislodgement.
needle catheter jejunostomy or a standard Witzel jejunostomy. 2. Functional complications are gastrointestinal manifestations fre-
Patients not undergoing laparotomy may have a “push” nasojeju- quently associated with intolerance and include emesis, nausea/
nal tube placed by a bedside nurse trained in this technique. If this vomiting, cramping pain or distention, and diarrhea.
is unsuccessful, an endoscopically-placed nasojejunal tube can be 3. Jejunostomy-related complications—Complication rates in trauma
inserted. Nasojejunal feeding may be done indefinitely, but if the patients have been reported at four percent.33 However, the major-
need for long-term access becomes apparent, a PEG with a jeju- ity of these complications occurred in patients with a standard,
nal extension limb (PEG-J) is appropriate. open jejunostomy rather than with a needle catheter jejunos-
F. Formula selection tomy. Complications included volvulus with infarction, small
1. Enteral formulas can be categorized into polymeric formulas bowel perforation, intraperitoneal leaks, and nonocclusive small
(which contain nutrients in high molecular weight form and mod- bowel necrosis.
erate fat loads, and require normal digestive and absorptive abil- 4. Nonocclusive bowel necrosis
ity), elemental formulas (which contain one or more partially a) This is a rare but devastating complication of bowel necrosis
digested macronutrients or combinations of nutrients and can be with no associated large vessel occlusion. This is similar to
absorbed in patients with compromised gastrointestinal tracts), necrotizing enterocolitis observed in neonates. The consistent
and modular formulas (which are composed of individual nutri- association with enteral nutrition suggests that inappropriate
ents but are nutritionally incomplete and intended for use as sup- administration of nutrients into a dysfunctional gut plays a
plements or in combination with other products). Unfortunately, pathogenic role. The incidence is less than one percent but the
with the exception of the immune-enhancing formulas, very little mortality frequently exceeds 50%.34,35
comparative data exists to guide clinicians in selecting the most b) Most cases of nonocclusive bowel necrosis occur in a delayed
appropriate formula. fashion in critically injured patients with a complicated course
2. In general, high risk trauma patients (injury severity score ≥ 18 or (pneumonia, sepsis, renal failure) that requires progressively
abdominal trauma index ≥ 20) should be considered for an higher acuity care.
immune-enhancing diet.30 The majority of critically ill trauma c) Gastrointestinal signs and symptoms are nonspecific and are
patients should receive a polymeric formula. An elemental diet typically those of intolerance. Therefore, standard clinical
should be considered for patients with proven intolerance to poly- monitoring fails to detect this entity early in its course. Though
meric formulas and those high-risk patients who have received no most cases will require exploratory laparotomy, less advanced
oral or enteral nutrition for over seven days. presentations may be managed with cessation of feeds, broad
G. Administration of feeds—Enteral feeds should be started at 15 mL/hr spectrum antibiotics, and aggressive fluid resuscitation.
of full-strength formula and advanced by 15mL/hr every 12 hours to
a set goal of 60mL/hr. To assure tolerance, this rate should be main-
tained for 24 hours and then advanced by 15mL/hr every 12 hours to VI. Parenteral Nutrition
a patient-specific targeted goal.31 A. Indications
H. Identification and management of intolerance—Frequently identi- Whenever possible, the gastrointestinal track should be utilized for
fied indicators of intolerance include vomiting, abdominal distention nutritional support. However, the following conditions may repre-
or cramping/tenderness, diarrhea, and high nasogastric tube output.32 sent indications for parenteral nutrition: persistent or progressive
Symptoms can be graded as mild, moderate, or severe. Mild symp- ileus, bowel obstruction, massive bowel resection refractory to an
toms of intolerance, such as mild abdominal distention or diarrhea, enteral diet, high output fistula refractory to elemental diet, mal-
can be monitored by repeat physical exams with no change in the absorption, high risk for nonocclusive bowel necrosis if fed enter-
current rate of feeding. Moderate symptoms are managed based ally (shock resuscitation, α-agonists, persistent severe distention or
on the particular symptom. For distention, enteral feeds should be cramping), or documented intolerance to enteral nutrition. In gen-
stopped and the patient assessed for evidence of a mechanical eral, parenteral nutrition should not be started in critically injured
obstruction. If distention remains moderate, an elemental formula patients for at least six days post injury if the patient is well nour-
should be considered. Moderate diarrhea can be managed by main- ished at baseline. Unlike with enteral feeding, there is NO benefit to
taining but not increasing the current feeding rate, and repeat exams. early parenteral nutrition. The only exception may be patients severely
Finally, for severe distention, enteral feeds should be stopped, intra- malnourished at baseline.
venous hydration begun, and the possibility of nonocclusive bowel B. Administration
necrosis should considered. For severe diarrhea, tube feeds can be Calories are provided by a mixture of dextrose, amino acids, and fat.
reduced and the patient should be evaluated for possible Clostridium Although only 2–4% of total calories as linoleic and linolenic acids
difficile infection. Vomiting is managed by ensuring adequate gas- are required to prevent clinical essential fatty acid deficiency, most

274 A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. © 2005 A.S.P.E.N. www.nutritioncare.org.
 S E C T I O N I V Surgical and Critically Ill Conditions

trauma patients require the use of additional fat as an alternative 3. Shatz D, Kirton O, McKenney M, et al. Manual of Trauma and Emergency
calorie source. The acute stress response that follows trauma is asso- Surgery. Philadelphia, PA: WB Saunders; 1991.
ciated with glucose intolerance, which can be minimized by decreas- 4. Cresci GA, Martindale RG. Nutrition support in trauma. In: Gottschlich
ing glucose calories and increasing fat calories, as well as by MM (ed). The Science and Practice of Nutrition Support: A Case-Based
Core Curriculum. Dubuque, IO: A.S.P.E.N./Kendall-Hunt; 2001.
aggressive use of insulin.
5. Bullen J, Griffiths E, Rogers H, Ward G. Sepsis: the critical role of iron.
C. Complications of parenteral nutrition can be divided into technical,
Microbes Infect 2000;4:409–415.
infectious, and metabolic. 6. Robien M. Iron and microbial infection. Support Line 2000;22(4):23–27.
1. Technical complications associated with the placement of a cen- 7. Nathens A, Neff M, Jurkovich G, et al. Randomized, prospective trial of
tral line, required for the administration of parenteral nutrition, antioxidant supplementation in critically ill surgical patients. Ann Surg
include injury to major veins, arteries, or nerves, and violation of 2002;236(6):814–822.
the pleural space. 8. Bulger EM, Maier RV. An argument for Vitamin E supplementation in the
2. Infectious complications include both catheter-related and management of systemic inflammatory response syndrome. Shock 2003;
-unrelated infections. 19(2):99–103.
a) Catheter-related infections most commonly stem from colo- 9. Tanaka H, Matsuda T, Miyagantani Y, Yukioka T, Matsuda H, Shimazaki S.
Reduction of resuscitation fluid volumes in severely burned patients using
nization of the patient’s skin and the catheter hub. Less fre-
ascorbic acid administration: a randomized, prospective study. Arch Surg
quent sources of contamination include infusion of contam-
2000;135(3):326–331.
inated solutions or hematogenous seeding from a distal site of 10. Moore EE, Jones TN. Benefits of immediate jejunal feeding after major
infection. abdominal trauma—a prospective randomized study. J Trauma 1986;26:
b) Recent evidence suggests that glutamine-supplemented par- 874–881.
enteral nutrition may decrease infectious complications and 11.Moore FA, Moore EE, Jones TN. TEN versus TPN following major abdom-
mortality rates in critically ill patients, with the greatest benefit inal trauma-reduced septic morbidity. J Trauma 1989;29:916–922.
with high-dose parenteral glutamine (> 0.2 g/kg/d).36 12. Kudsk KA, Croce MA, Fabian TC, et al. Enteral versus parenteral feeding:
c) Metabolic complications can include hyper or hypoglycemia, effects on septic morbidity following blunt and penetrating abdominal
electrolyte abnormalities, acid/base abnormalities, liver trauma. Ann Surg 1992;215:503–511.
13. Moore FA, Feliciano DV, Andrassy RJ, et al. Early enteral feeding, com-
function abnormalities, and trace mineral deficiencies.
pared with parenteral, reduces postoperative septic complications—the
(1) Critical illness is frequently accompanied by hyperglycemia
results of a meta-analysis. Ann Surg 1992;216:172–183.
with resistance to insulin. Hyperglycemia can adversely 14. Moore FA, Sauaia A, Moore EE, Haenel JB, Burch JM, Lezotte DC. Postin-
affect outcome through several mechanisms, including gly- jury multiple organ failure: a bimodal phenomenon. J Trauma. 1996;40:
cosuria with inappropriate diuresis, increased risk of infec- 501–512.
tion by impairment of neutrophil and immunoglobulin 15. Moore FA. Effects of immune-enhancing diets on infectious morbidity and
function, and exacerbation of cerebral edema. A recent multiple organ failure. J Parenter Enteral Nutr. 2001;25:S36–S42.
prospective randomized clinical trial demonstrated a reduc- 16. Windsor JA, Hill GL. Weight loss with physiologic impairment: a basic
tion both in infectious complications and mortality in criti- indicator of surgical risk Ann Surg. 1988;207(3):290–296.
cally ill surgical patients when glucose levels were strictly 17. Yanagawa T, Bunn F, Roberts I, Wentz R, Pierro A. Nutritional support for
head-injured patients. Cochrane Database Syst Rev. 2002;(3):CD001530.
controlled between 80 and 110 mg/dL versus conventional
18. Houdijk APJ, Rijnsburger ER, Jansen J, et al. Randomized trial of gluta-
therapy (120 to 180 mg/dL).37,38
mine-enriched enteral nutrition on infectious morbidity in patients with mul-
(2) The refeeding syndrome is a dramatic example of a meta- tiple trauma. Lancet 1998;352:772–776.
bolic complication that can be associated with parenteral 19. Wischmeyer PE, Lynch J, Liedel J, et al. Glutamine administration reduces
nutrition administration. It occurs with rapid and excessive Gram-negative bacteremia in severely burned patients: a prospective, ran-
feeding of patients with severe malnutrition due to condi- domized, double-blind trial versus isonitrogenous control. Crit Care Med.
tions commonly seen in trauma patients such as starvation, 2001;29:2075–2080.
alcoholism, delayed nutritional support, or chronic malnu- 20. Garrel D, Patenaude J, Nedelec B, et al. Decreased mortality and infectious
trition. As a result of ion fluxes into the cell, serum phos- morbidity in adult burn patients given enteral glutamine supplements: a
phate, magnesium, potassium, and calcium levels can drop prospective, controlled, randomized clinical trial. Crit Care Med. 2003;31:
rapidly. Additionally, severe hyperglycemia is commonly 2444–2449.
21. Brown RO, Hunt H, Mowatt-Larssen CA, Wojtysiak SL, Henningfield MF,
seen. Symptoms include cardiac arrhythmias, confusion,
Kudsk KA. Comparison of specialized and standard enteral formulas in
respiratory failure, and even death. The refeeding syndrome trauma patients. Pharmacotherapy. 1994;14:314–320.
can be prevented by initiating parenteral nutrition at a rate 22. Moore FA, Moore EE, Kudsk KA, et al. Clinical benefits of an immune-
lower than the required goal, primarily by reducing dex- enhancing diet for early postinjury enteral feeding. J Trauma. 1994;37:
trose calories and adding supplemental phosphate, magne- 607–615.
sium, potassium, and calcium in the parenteral nutrition. 23. Kudsk KA, Minard G, Croce MA, et al. A randomized trial of isonitroge-
Exogenous insulin is also frequently required. nous diets following severe trauma: an immune-enhancing diet reduces sep-
tic complications. Ann Surg.1996;224:531–540.
(Trauma material from the 1st edition was contributed by Elaine B. 24. Mendez C, Jurkovich GJ, Garcia I, Davis D, Parker A, Maier RV. Effects
of an immune-enhancing diet in critically injured patients. J Trauma.
Trujillo, Malcolm K. Robinson, and Danny O. Jacobs)
1997;42:933–944.
25. Weimann A, Bastian L, Bischoff WE, et al. Influence of arginine, omega-3-
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injured patient: relationship to feeding intolerance. J Neurosurg. 1991; 35. Marvin RG, McKinley BA, McQuiggan M, Cocanour CS, Moore FA.
74:738. Nonocclusive bowel necrosis occurring in critically ill trauma patients
29. Bovin MA, Levy H. Gastric feeding with erythromycin is equivalent to receiving enteral nutrition manifests no reliable signs for early detection.
transpyloric feeding in the critically ill. Crit Care Med 2001;29(10):1916. Am J Surg. 2000;179:7–12.
30. Consensus recommendations from the US summit on immune-enhancing 36. Novak F, Heyland DK, Avenell A, Drover JW, Su X. Glutamine supplemen-
enteral therapy. J Parenter Enteral Nutr. 2001;25(2 Suppl):S61–63. tation in serious illness: a systematic review of the evidence. Crit Care Med.
31. McQuiggan MM, Marvin RG, McKinley BA, Moore FA. Enteral feeding 2002;30:2022–2029.
following major torso trauma: from theory to practice. New Horizons. 37. Van den Berghe G, Wouters P, Weekers F, et al. Intensive insulin therapy in
1999;7:131–140. critically ill patients. N Engl J Med. 2001;345:1359–1367.
32. Kozar RA, McQuiggan MM, Moore EE, Kudsk KA, Jurkovich GJ, Moore 38. Van den Berghe G, Wouters PJ, Boullion R, et al. Outcome benefit of inten-
FA. Postinjury enteral tolerance is reliably achieved by a standardized pro- sive insulin therapy in the critically ill: insulin dose versus glycemic control.
tocol. J Surg Res 2002;104:70–75. Crit Care Med. 2003;31:359–366.

276 A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. © 2005 A.S.P.E.N. www.nutritioncare.org.
 Jennifer A. Wooley, MS, RD, CNSD

22
Use of Indirect Calorimetry
in Critically Ill Patients

Introduction c) Low transport protein levels in the absence of infection or

inflammation
A major advantage of indirect calorimetry (IC) over predictive energy d) Poor wound healing
expenditure equations is that it allows the clinician to measure a patient’s D. Signs of overfeeding
actual energy expenditure and “match” the nutrition support regimen to 1. Hyperglycemia
the individual patient’s needs. This facilitates nutrition support without 2. Electrolyte imbalances
the negative effects of under- or overfeeding.1 3. Hyperlipidemia
4. Hypermetabolism
I. Indirect Calorimetry (IC) is Useful in Many ICU Clinical 5. Fluid overload
Scenarios 6. Organ dysfunction, such as fatty liver
II. Ideal Parameters for Conducting Indirect Calorimetry 7. Failure to wean from mechanical ventilation such as elevated
III. Technical Aspects that May Interfere with an Accurate Indirect minute ventilation
Calorimetry Study
IV. Interpretation of Data Obtained from Indirect Calorimetry
V. Nutrition Recommendations II. Ideal Parameters for Conducting
VI. Frequency of IC Studies Indirect Calorimetry
VII. New Technology A. Patients have rested in a supine position (in bed or a recliner) for
VIII. Summary more than 30 minutes before the study2,3,5
References B. Patients receiving intermittent feedings (bolus enteral feeding, or
cyclic enteral or parenteral nutrition or meals) are studied approx-
imately 1 hour after the feeding if thermogenesis is to be included
I. Indirect Calorimetry (IC) is Useful in Many ICU
in the measured resting energy expenditure (REE), or 4 hours after
Clinical Scenarios
the feeding if thermogenesis is to be excluded in the REE.2,5
A. Inability to estimate accurately caloric requirements2–5 C. The study is conducted in a quiet, thermoneutral environment.2–5
1. Multiple trauma D. The rate and composition of nutrients being infused on a continu-
2. Neurological trauma ous basis are stable from at least 12 hours prior to the study until
3. Multiple Organ Dysfunction Syndrome (MODS) the end of the study.2,5
4. Sepsis E. All sources of supplemental oxygen (nasal cannulas, masks or tra-
5. Systemic Inflammatory Response Syndrome (SIRS) cheostomy collars) are turned off during routine room air meas-
6. Respiratory distress syndrome urements, if medically feasible.2,3,5
7. Paralytic or barbiturate agents F. The fraction of inspired oxygen (FiO2) remains constant during the
8. Large or multiple wounds measurement.2,3
9. Malnutrition associated with altered body composition: G . The study should be delayed for 90 minutes if changes are required
a) Underweight in ventilatory settings.2–5
b) Overweight H. The patient engages in typical patterns of voluntary skeletal mus-
c) Paraplegia or quadriplegia cle activity (movement of the extremities) during the study.2–5
d) Limb amputation I. No leaks are present in the sampling system.2–5
e) Peripheral edema J. All data used to derive REE and respiratory quotient (RQ) are
10. Post-operative organ transplantation taken from a period of equilibrium or steady state that has been
B. Inadequate response to nutrition support based on predictive identified according to statistically defined guidelines.2–5
equations2–5 K. The patient should not have received general anesthesia within
1. Malnutrition 6–8 hours prior to the study.2
2. Failure to wean from mechanical ventilation L. If the patient is in pain or agitated, analgesics or sedatives should
3. Poor wound healing be given at least 30 minutes before the study when clinically pos-
C. Clinical signs of underfeeding or overfeeding6–10 sible. Analgesics and sedatives administered should be docu-
1. Signs of underfeeding mented and this information should be considered during the
a) Respiratory dysfunction interpretation of the study.2–4,11
b) Failure to wean from mechanical ventilation M. The study should be delayed for 3 to 4 hours after hemodialysis.2,3,12

© 2005 A.S.P.E.N. www.nutritioncare.org. A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. 277
S E C T I O N I V Surgical and Critically Ill Conditions

N. The study should be delayed 1 hour after painful procedures have

been performed.2 TABLE 22-1. Situations that Can Affect VCO2 and VO2
O. Routine nursing care or activities involving other health-care pro-
fessionals should be avoided during the study.2,4 Elevated VCO2 • Metabolic acidosis • Hyperventilation
• Hypermetabolism • Overfeeding
III. Technical Aspects that May Interfere with an Decreased VCO2 • Metabolic alkalosis • Hypoventilation
Accurate Indirect Calorimetry Study • Hypometabolism • Gluconeogenesis
A. Mechanical ventilation with FiO2 ≥ 602,3 • Starvation/ketosis • Underfeeding
B. Mechanical ventilation with Positive End Expiratory Pressure
(PEEP) >12 cm H2O2,3 Elevated VO2 • Sepsis • Hypermetabolism
C. Hyper/hypoventilation (acute changes altering body CO2 stores)2,3,5 • Hyperthermia • Blood transfusions
D. Leak in the sampling system2,3,5 • Shivering/agitation/excessive movement
E. Moisture in the system, which can affect the oxygen analyzer2,3 • Increased minute ventilation
F. Continuous flow in the ventilator circuit with flow > 0 L/min dur- • Inotropic infusions (dopamine, dobutamine)
ing exhalation3 • Hemodialysis (within 4 hours of treatment)
G. Inability to collect all expiratory flow3 • Overfeeding
H. Unstable inspiratory FiO2 (> ±0.01%)2,3
I. Chest tube demonstrating the presence of an air leak (inability to Decreased VO2 • Hypothermia • Fasting/starvation
collect all expired gases)2,3 • Hypothyroidism • Advanced age
J. Bronchopleural fistula (inability to collect all expired gases)2,3 • Paralysis • General anesthesia
K. Supplemental oxygen in spontaneously breathing patients2,3,5 • Heavy sedation • Coma or deep sleep
L. Hemodialysis in progress2,3,12
M. Errors in calibration of indirect calorimeter2,3
Adapted with permission from the American Society for Parenteral and Enteral Nutri-
tion (A.S.P.E.N) from the following: McClave S, Snider HL. Use of indirect calorimetry
IV. Interpretation of Data Obtained from in clinical nutrition. Nutr Clin Pract. 1992;7:207–221.
Indirect Calorimetry
A. Resting Energy Expenditure (based on the abbreviated Weir
equation) B. In critically ill patients, the RQ may vary significantly based on
inter-patient variability, the metabolic response to stress, underlying
REE = [( 3.94 × VO2 L min ) + (1.11× VCO 2 L min )]1440 minn day lung disease, acid/base disturbances as well as substrate use. Low
sensitivity and specificity, as a result of these variables, can limit the
B. Respiratory Quotient (RQ) efficacy of using RQ as an indicator of under- or overfeeding.13,14
However, an RQ within normal biological range (0.67–1.3) serves
VCO 2 ( carbon dioxide production ) as a valuable marker of test reliability and validity.2,3,13
RQ =
VO2 ( oxygenn consumption )

C. Measurement of urinary nitrogen excretion (UUN) is not necessary

to ensure accuracy in the determination of REE.2,3,6 Even a 100% TABLE 22-2. Traditional Interpretation
error in the measurement of UUN will only produce an error of of Respiratory Quotient
approximately 1–2% in the true energy expenditure.2,6
D. In complex patients or when steady state during an IC study is not Respiratory Quotient
achieved, it may be helpful to compare predicted VCO2 and VO2 Substrate Utilization (physiologic range 0.67–1.3)
levels using the formulas below with measured VCO2 and VO2 lev-
els obtained from IC.2 Clinical situations that can affect VCO2 and Ethanol 0.67
VO2 levels are outlined in Table 22-1.
Fat oxidation 0.71
Normal adult VCO2 level = 2 − 3 mL / min/kg
Normal adult VCO2 level = 2 − 3 mL / min/kg Protein oxidation 0.82

V. Nutrition Recommendations Mixed substrate oxidation 0.85

A. Traditional view of RQ (Table 22-2):
1. An RQ < 0.82 suggests underfeeding. Increase caloric delivery Carbohydrate oxidation 1.0
unless contraindicated by clinical status.5
2. An RQ 0.85–0.95 suggests mixed substrate utilization indicating Lipogenesis 1.0–1.2
that the nutrition regimen is appropriate.5
3. An RQ > 1 suggests overfeeding and potential lipogenesis. Modi- Reprinted with permission from the American Society for Parenteral and Enteral Nutri-
fication of the nutrition support regimen to provide less than 130% tion (A.S.P.E.N) from the following: Wooley JA, Sax HC. Indirect calorimetry: applica-
measured REE from total calories would be appropriate.5 tions to practice. Nutr Clin Pract. 2003;18:434–439.

278 A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. © 2005 A.S.P.E.N. www.nutritioncare.org.
 S E C T I O N I V Surgical and Critically Ill Conditions

C. Traditional method of determining Total Energy Expenditure (TEE):

TABLE 22-3. Designing Specialized Nutrition Support
TEE = Measured REE × Activity Factor × Stress Facttor Regimens Based on Indirect Calorimetry

1. Activity factor—add 5–10% to REE to account for typical phys- Carbohydrate Stressed patients should receive approximately 50%
ical activity of intensive care patients.11,15–17 of energy requirements as carbohydrate.
2. Stress factors Maximum glucose utilization rate is 3–5
a) Thermogenesis—add 5% to REE if patient was measured in
mg/kg/min.21
a fasting state or if feedings will be intermittent to account for
thermogenesis.4 Lipid Stressed patients should receive ≤30% of energy
b) Anabolism—If feasible from a metabolic standpoint, add up requirements as lipid.22,23
to 30% to measured REE to promote repletion.4
c) TEE beyond 130% measured REE may lead to overfeeding, Limit total fat intake to ≤1g /kg/d via continuous
which often leads to metabolic and respiratory abnormalities.6 infusion.23
3. Current research has shown that feeding critically ill patients at Monitor triglyceride levels.23
100% of measured REE is appropriate.18 The addition of activity
and stress factors may increase the likelihood of complications At least 4% of total calories per day should come
related to overfeeding.18 from linoleic acid (10% of calories as long chain
4. A specific population of critically ill patients may benefit from fatty acids) or at least 500 mL of 10% IV lipid per
hypocaloric feeding,19 (50–75% measured REE from total calo- week is necessary to prevent essential fatty acid
ries.24 Protein provision must be aggressive (1.5–2.0 gm/kg). deficiency.22,23
Some examples of appropriate candidates for hypocaloric feeding
include: Protein Stressed patients receive 15–20% of energy
a) Class III obesity (BMI > 40) requirements as protein.
b) Refeeding syndrome
Critically ill patients with signs of hypercatabolism
c) Severe malnutrition
d) Trauma patients following shock resuscitation require 1.5–2.0 g/kg of protein per day.24
e) Hemodynamic instability Trends in acute transport protein (PAB, CRP) levels
f) Acute respiratory distress syndrome or COPD and nitrogen balance studies provide insight into the
g ) MODS patient’s degree of hypercatabolism and assist with
h) SIRS or sepsis identification of the anabolic phase of recovery.6
D. Once the caloric goal has been determined based on the measured
REE, recommendations for distributing the three energy-yielding
macronutrients are provided in Table 22-3.

achieve steady state (maximum of 10 minutes) due to altered men-

VI. Frequency of IC Studies
tal acuity or respiratory insufficiency, studies cannot be conducted
A. There is lack of consensus in the literature on frequency of meas- on patients with nasal tubes or nasal cannulas and the nose clip can
urement. become uncomfortable for some patients. Furthermore, data is lack-
B. IC is a “snapshot,” at one point in time, of a patient’s energy expen- ing about the most appropriate activity factors to add to the RMR in
diture. Measurement of REE, at regular intervals such as weekly or order to determine total energy expenditure.
whenever there is a significant change in the patient’s clinical status
that could affect energy expenditure, will optimize the provision of
nutrition support while minimizing the likelihood of under- or over-
VIII. Summary
feeding.1,2,5,6 Indirect calorimetry can make a vital contribution to the develop-
ment of individualized nutrition support for critically ill patients.
IC provides the most accurate method for determining energy
VII. New Technology
requirements and protects the patient from extremes of under- or
Recently, a hand-held device (MedGem; Healthetech, Inc, Golden, overfeeding. Protocols addressing the methodology required for
CO) for measurement of VO2 and resting metabolic rate (RMR) in technical accuracy and clinically useful results are necessary. The
spontaneously breathing patients was introduced which may make measured REE should be the energy target for nutrition support in
the measurement of energy expenditure more routine in a variety the ICU. The addition of stress or activity factors to the measured
of patient care settings. Validation studies comparing the perform- REE is unnecessary and may increase the risk of overfeeding.
ance of this handheld device to IC (open-circuit, Douglas bags, Although the RQ can indicate the presence of under- and overfeed-
Sensormedics 2900 metabolic cart [VIASYS Healthcare, Yorba ing, it should primarily be used as a marker of test validity. Optimal
Linda, CA], Deltatrac [Datex-Ohmeda, Andover, MA] ventilator nutrition intervention requires continuous evaluation of all perti-
hood) have established that it is valid and reliable.25,26 nent clinical data and careful monitoring of each patient’s response
Advantages of this device include convenience, ease of use and to therapy. Therefore, the use of IC in the critically ill patient on a
the reduced expense compared to a metabolic cart. Limitations are routine basis or in the presence of any “clinically significant” event
that some patients may have difficulty breathing continuously, with- that could affect energy expenditure would appear to be a prudent
out interruption, into the device for the entire period necessary to approach.

© 2005 A.S.P.E.N. www.nutritioncare.org. A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. 279
S E C T I O N I V Surgical and Critically Ill Conditions

REFERENCES 15. Weissman C, Kemper, MS, Askanazi J, Hyman AI, Kinney JM. Day to day
1. Wooley JA, Sax HC. Indirect calorimetry: applications to practice. Nutr variation in the resting metabolic rate of mechanically ventilated critically
Clin Pract. 2003;18:434–438. ill patients. Crit Care Med. 1986;14:408.
2. McClave S, Snider HL. Use of indirect calorimetry in clinical nutrition. 16. White MS, Shepherd RW, McEniery JA. Energy expenditure measurements
Nutr Clin Pract. 1992;7:207–221. in ventilated critically ill children: within- and between-day variability.
3. Branson RD. The measurement of energy expenditure: instrumentation, prac- J Parenter Enteral Nutr. 1999;23:300–304.
tical considerations, and clinical application. Respiratory Care. 1990;35: 17. Weissman C, Kemper M, Elwyn DH, et al. The energy expenditure of the
640–659. mechanically ventilated critically ill patient: an analysis. Chest. 1986;89:
4. Porter C, Cohen NH. Indirect calorimetry in critically ill patients: role of the 254–259.
clinical dietitian in interpreting results. J Am Diet Assoc. 1996;96:49–54, 57. 18. McClave SA, Spain DA, Skolnick JL, et al. Achievement of steady state opti-
5. Matarese LE. Indirect calorimetry: technical aspects. J Am Diet Assoc. mizes results when performing indirect calorimetry. J Parenter Enteral Nutr.
1997;97(suppl 2):S154–S160. 2003;27:16–20.
6. Brandi LS, Bertolini R, Calafa M. Indirect calorimetry in critically ill patients: 19. Zaloga GD. Permissive underfeeding. New Horizons. 1994;2:257–263.
clinical applications and practical advice. Nutrition. 1997;13:349–358. 20. Wolfe RR, O’Dossell TF Jr, Stone MD, et al. Investigation of factors
7. McClave SA, Lowen CC, Kleber MJ, et al. Are patients fed appropriately determining the optimal glucose infusion rate in total parenteral nutrition.
according to their caloric requirements? J Parenter Enteral Nutr. 1998;22: Metabolism. 1980;29:892–900.
375–381. 21. Cerra FB, Benitez MR, Blackburn GL, et al. Applied nutrition in ICU
8. Klein CJ, Stanek GS, Wiles CE. Overfeeding macronutrients to critically patients: a consensus state of the American College of Chest Physicians.
ill adults: metabolic complications. J Am Diet Assoc. 1998;98:795–806. Chest 1997;111:769–778.
9. McClave SA. The consequences of overfeeding and underfeeding. J Resp 22. Fuhrman MP. Management of complications of parenteral nutrition. In:
Care Pract. 1997;10:57–64. Matarese LE, Gottschlich MM, eds. Contemporary Nutrition Support Prac-
10. Liposky JM, Nelson LD. Ventilatory response to high caloric loads in crit- tice A Clinical Guide. Philadelphia, PA: WB Saunders Company;1998:
ically ill patients. Crit Care Med. 1994;22:796–802. 243–263.
11. Swinamer DL, Phang PT, Jones RL, Grace M, King EG. Twenty-four hour 23. Goodgame JT, Lowry SF, Brennan MF. Essential fatty acid deficiency in
energy expenditure in critically injured patients. Crit Care Med. 1987;15: TPN: time course of development and suggestions for therapy. Surgery
637–643. 1978;84:271–277.
12. Blumberg A, Keller G. Oxygen consumption during maintenance hemodial- 24. Dickerson RN. Specialize nutrition support in the hospitalized obese
ysis. Nephron. 1979;23:276–281. patient. Nutr Clin Pract. 2004;19:245–254.
13. McClave SA, Lowen CC, Kleber MJ, McConnell JW, Jung LY, Goldsmith 25. Nieman DC, Trone GA, Austin MD. A new handheld device for measuring
LJ. Clinical use of the respiratory quotient obtained from indirect calorime- resting metabolic rate and oxygen consumption. J Am Diet Assoc. 2003;103:
try. J Parenter Enteral Nutr. 2003;27:21–26. 588–592.
14. McClave SA, Lowen CC, Kleber MJ, et al. Is the respiratory quotient a use- 26. Melanson EL, Coelho LB, Tran ZV, et al. Validation of the BodyGem™ hand-
ful indicator of over or under feeding? J Parenter Enteral Nutr.1997;21:S11. held indirect calorimeter. J Parenter Enteral Nutr. 2003;27(Suppl 1):S39.

280 A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. © 2005 A.S.P.E.N. www.nutritioncare.org.
 Kathleen D. Liu, MD, PhD;
Annette Stralovich-Romani, RD, CNSD;
Glenn M. Chertow, MD, MPH 23
Nutrition Support for
Adult Patients With
Acute Renal Failure
Introduction are decompressed. However, if the obstruction is long-standing,
permanent kidney failure may occur.
Acute renal failure (ARF) is a common condition in hospitalized 3. Intrarenal. Intrarenal (or intrinsic) ARF may be caused by damage
patients.1–3 ARF is characterized by a decrement in the glomerular fil- to any one of the four components of the renal parenchyma: vas-
tration rate (GFR), which leads to reduced filtration and elimination of culature, tubules, glomeruli, or interstitium. The syndrome of a
the by-products of metabolism. Changes in serum creatinine, a product sudden and severe decline in GFR, or ATN, is common among crit-
of muscle protein breakdown that is excreted by the kidney, indicate ically ill patients. Common correlates of ATN include ischemia due
alterations in kidney function. A rise in serum creatinine usually reflects to hypotension, sepsis, and nephrotoxic injury (eg, myoglobin in
decreased filtration by the kidney. In the clinical literature, ARF is often rhabdomyolysis, radiocontrast injury).
defined as a doubling of the serum creatinine or an increase to above C. The clinical course of ARF depends on the underlying disease but
0.5 mg/dL creatinine. Causes of ARF are broadly characterized as pre- typically can be divided into three clinical phases: initiation, main-
renal, intrarenal, or postrenal (obstructive). Hospital-acquired ARF tenance, and recovery.8
is associated with mortality in 30% to 70% of patients.4–6 Once the cause 1. Initiation. During this phase, damage to the kidney starts and is
is identified, interventions and nourishment necessary for recovery must reflected in a rapid reduction in GFR, which is commonly, but not
be prescribed. At increased risk for ARF are certain acutely ill patients, always, associated with oliguria.
including patients with chronic kidney disease (CKD), diabetes melli- a) This phase is typically recognized when the creatinine starts
tus, or liver disease; elderly patients; patients receiving certain nephritic to rise or the urine output starts to fall. Recognition of this
drugs; postoperative patients; and patients with sepsis or hemorrhage. phase may be delayed since time is required for creatinine or
The “phase” or duration of renal injury, the volume of diuresis (oliguric
other markers of kidney function to accumulate. It should be
vs non-oliguric), and the dialytic modality used to treat the renal failure
noted that small changes in serum creatinine can reflect large
determine the nutritional prescription.
changes in kidney function and that serum creatinine reflects
I. Overview of ARF muscle mass as well as kidney function.
II. Nutritional Aspects of ARF b) The kidney is responsible for volume regulation. As ARF
III. Nutritional Assessment in Patients with ARF progresses, patients may become oliguric—usually defined
IV. Nutritional Requirements and Goals of Therapy in ARF as < 400 mL of urine output per day—and rapidly become
V. Enteral Nutrition in ARF volume overloaded, especially if they receive a large amount
VI. Parenteral Nutrition in ARF of intravenous colloid or crystalloid.
References c) The kidney critically regulates blood electrolytes. Serum potas-
sium and phosphorus may rise acutely. Hyperkalemia may lead
to arrhythmias and/or cardiac arrest. Hyperphosphatemia may
I. Overview of ARF provoke symptoms associated with hypocalcemia.
A. There is no uniform definition of ARF, but it is usually character- d) The kidney regulates the excretion of organic acids. If the
ized by an abrupt cessation or decline in renal function that may be patient has an underlying disease that results in a large acid
associated with a decline in urine output. ARF may be transient or load (eg, rhabdomyolysis, sepsis), the patient may become
lead to permanent renal failure. In clinical practice, ARF may be profoundly acidemic.
defined as a doubling of serum creatinine, as a change in creatinine e) Patients with ARF may manifest systemic signs of uremia,
of 0.5 mg/dL from baseline in adults, or as a need for renal replace- including nausea, vomiting, and altered mental status (includ-
ment therapy. ing confusion and seizures).
B. ARF’s etiology can be broadly divided into prerenal, postrenal, or 2. Maintenance. During this phase, ARF is established and recovery
intrarenal.3,7 has not occurred. In cases due to reversible causes of ARF, such as
1. Prerenal. Impaired renal perfusion from volume depletion, con- pre- and postrenal ARF, patients may start to recover rapidly. Dur-
gestive heart failure, cirrhosis, renovascular disease, or other con- ing the maintenance phase of intrinsic ARF, there are fewer
ditions can lead to ARF. If the underlying condition can be quickly dynamic changes. The patient may require dialysis or hemodia-
reversed, this type of ARF may resolve rapidly. However, if the filtration to control acidosis, electrolytes, and/or volume status.
condition is long-standing or cannot be corrected, prerenal ARF These therapies have important implications for the provision of
may progress to ARF in the form of acute tubular necrosis (ATN). selected nutrients, including amino acids and water-soluble vita-
2. Postrenal. This type of ARF is due to obstruction of the urinary mins. Dialysis removes amino acids, typically in the range of 8 to
tract below the kidneys and usually resolves when the kidneys 10 g per intermittent hemodialysis (IHD) session—and potentially

© 2005 A.S.P.E.N. www.nutritioncare.org. A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. 281
S E C T I O N I V Surgical and Critically Ill Conditions

more with high-efficiency continuous renal replacement therapy II. Nutritional Aspects of ARF
(CRRT).9–10
3. Recovery. As the name implies, this phase is characterized by A. General effect on nutrition. The wide range of nutritional require-
improving kidney function. During this phase, patients frequently ments of patients with ARF reflects the broad spectrum of disease
“auto-diurese,” leading to a large and inappropriate loss of fluid severity. Metabolic derangements may be attributable to uremia as
and electrolytes, while tubular function remains impaired. Fluid well as to underlying disease processes. Critical illness typically pre-
and nutrition prescriptions may need significant modification dur- cipitates a hypercatabolic and hypermetabolic response and is fre-
ing this phase, particularly if dialysis or hemodiafiltration is quently associated with ARF.19 Patients with multiorgan dysfunction
reduced or discontinued. from sepsis, pancreatitis, trauma, burns, neurological injury, or other
D. The methods of estimating renal function are described below. causes may be profoundly catabolic and have very high protein and
1. Creatinine clearance rate and GFR are measures of kidney func- energy requirements. In contrast, some patients, such as those with
tion. The normal GFR of a young, healthy adult is approximately isolated ARF due to nephrotoxic injury such as aminoglycoside or
130 mL/min. GFR declines by about 1 mL/min per year after the radiocontrast-associated injury, may have energy requirements that
age of 40.11 It is not usually feasible to measure GFR (determined do not differ significantly from those associated with other diseases
by injection of inulin or iothalamate and measuring clearance over of modest severity. Moreover, nutritional requirements are affected
time) in a critically ill patient. In ARF, the GFR can be estimated by whether the patient is on dialysis.
by calculating a creatinine clearance only if (1) the patient is not B. Energy. While ARF alone does not lead to a significant rise in energy
receiving dialytic support and (2) the serum creatinine concentra- expenditure, it is frequently associated with an underlying disease
tion is stable on a day-to-day basis. state that leads to a large increase in energy expenditure (eg, sepsis,
2. Kidney function may be estimated using the Cockcroft-Gault neurological injury, burns, trauma).20,21 Thus, assessment of the
estimated creatinine clearance12 or the modification of diet in underlying medical condition must be part of the initial nutritional
renal disease (MDRD) estimated GFR equations,13 if the above evaluation.
two conditions are met. The Cockcroft-Gault equation is as fol- C. Carbohydrate. ARF is frequently associated with disease states char-
lows: ([140 − age] × weight [in kg])/(serum creatinine [in mg/dL]) acterized by high levels of counterregulatory hormones that lead to
× 72) × 0.85 for women. The simplified MDRD equation is GFR hyperglycemia. ARF is usually associated with insulin resistance,
= 186 × (plasma creatinine)−1.154 × (age)−0.203 × 0.742 if female × reduced renal gluconeogenesis, and accelerated hepatic gluconeoge-
1.210 if African American. nesis, which in sum typically result in increased serum glucose lev-
3. Alternatively, a timed urine collection can be obtained and crea- els. However, the kidney is also a major site of insulin degradation,
tinine clearance may be calculated using the following equation: so serum insulin levels tend to be higher in patients with ARF.22
Creatinine clearance = (urine volume × urine creatinine)/(plasma Hyperglycemia is common among patients with ARF. There is grow-
creatinine × number of minutes of timed collection). Again, to ing evidence that aggressive glycemic control reduces intensive care
obtain an accurate measurement, the serum creatinine needs to unit (ICU) mortality and complication rates in hospitalized patients.23
be stable and the patient cannot be receiving dialysis. Typically,
In adults, this possibility must be balanced against the risk of hypo-
timed urine collections are clinically useful only in the recovery
glycemia in ARF.
phase of ARF.
D. Lipid
E. Dialytic support may be provided as IHD or as CRRT.
ARF leads to an impairment of lipolysis that may be further exac-
1. Peritoneal dialysis is not commonly used to treat ARF due to
erbated by metabolic acidosis, a frequent complication of ARF.
issues with access and solute clearance and the inability to use
E. Protein
after abdominal surgery.3
1. ARF leads to an increase in protein catabolism. Increased protein
2. IHD compares with CRRT as follows:
catabolism is due to both accelerated breakdown of muscle pro-
a) Both IHD and CRRT require vascular access, in the form of
either an arteriovenous fistula or graft or a double-lumen tein and abnormal use of amino acids by skeletal muscle.24,25
catheter placed in a large vessel. Few patients with ARF have 2. Accelerated protein breakdown is due to several factors. These fac-
preexisting angioaccess; therefore, the majority require place- tors include stimulation of hepatic gluconeogenesis, which cannot
ment of a dialysis catheter. be fully suppressed even when an exogenous substrate (eg, glu-
b) IHD is generally performed at least 3 times a week for 3 to cose) is added, and insulin resistance and acidosis, both of which
4 hours per session. A recent study demonstrated that patients promote muscle protein breakdown.26 Levels of endogenous coun-
with ARF may benefit from more frequent IHD.14 terregulatory hormones (cortisol, glucagon, epinephrine, and nor-
c) CRRT generally causes less hemodynamic stress than IHD and epinephrine) are frequently elevated in states associated with ARF;
over time can provide for greater clearance and tighter control these elevated levels increase protein catabolism. Cytokine release
of electrolytes and acidosis. However, it is labor-intensive also contributes to the acceleration in muscle proteolysis seen with
and requires the patient to be connected continuously to the critical illness.
dialysis machine. 3. Metabolism of certain amino acids is affected by a lack of kidney
d) The decision to use IHD or CRRT is based on many factors, function. Thus, amino acid pools are often altered.27 Several
including the hemodynamic stability of the patient, physician amino acids that are usually considered nonessential (eg, gluta-
preference, and nursing/staff resources. Data regarding the rel- mine) may become required in ARF. Lack of supplementation
ative benefits of these two modalities to patient outcome are with these amino acids can lead to hyperammonemia, metabolic
limited.15–17 acidosis, and coma.
e) A hybrid dialysis modality has been used more frequently of F. Fluid administration and volume status. Patients with ARF are often
late: slow, low-efficiency dialysis (SLED).18 SLED is given large quantities of intravenous fluid in an attempt to augment
intended to combine the benefits of CRRT and IHD and is typ- urine output. In addition, many patients have reduced urine output.
ically performed over 6 to 12 hours, 6 or 7 days per week. These factors conspire to create volume overload. In particular, vol-

282 A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. © 2005 A.S.P.E.N. www.nutritioncare.org.
 S E C T I O N I V Surgical and Critically Ill Conditions

ume overload complicates the management of patients with ARF 2. If a serious acid-base disorder is suspected, arterial blood gas
who are not yet receiving dialysis. Volume overload may also influ- should be obtained with the initial assessment.
ence the recognition of ARF, since large increases in total body 3. For patients undergoing IHD, laboratory values should be obtained
water can dilute the concentrations of creatinine and urea nitrogen, at the start of or before the dialysis session.
the usual markers of renal failure early in the course of ARF. Clin- 4. Various serum proteins have been used in the assessment of
icians commonly use diuretics to try to reduce volume overload; nutritional status. Albumin and thyroxine-binding prealbumin
often, dialysis is required to control volume overload. are most commonly used clinically.9 The advantages of serum
G. Electrolytes albumin include wide availability and low cost of measurement.
1. Serum electrolytes will vary considerably depending on the under- However, due to the multiple factors that can reduce serum albu-
lying disease state and on whether the patient is receiving dialy- min, little credence should be given to albumin as a marker of
sis. Electrolyte abnormalities present at the recognition of ARF nutritional status or response to nutritional therapy during peri-
are corrected with dialysis in most patients. Meticulous elec- ods of metabolic stress, which are common in conditions asso-
trolyte and mineral management is critical to the successful man- ciated with ARF.
agement of ARF. 5. Like that of albumin, the synthesis of prealbumin decreases inde-
2. Hyperkalemia is frequent. Hyperkalemia may be due to impaired pendent of nutritional status during metabolic stress. In addition,
renal potassium excretion, as well as to changes in the extracel- prealbumin may be falsely elevated in ARF due to reduced renal
lular and intracellular distribution of potassium due to the meta- clearance.
bolic acidosis associated with ARF. Endogenous or iatrogenic 6. Hypertriglyceridemia is more common in patients with ARF than
hyperglycemia can also contribute to hyperkalemia. in patients without ARF. As is done for all patients on total par-
3. Over the course of therapy, some patients develop hypokalemia enteral nutrition (PN), baseline and serial triglyceride concentra-
(and hypophosphatemia). tions should be obtained for ARF patients.
H. Minerals 7. Nitrogen balance can be calculated for patients with ARF, but the
1. Hyperphosphatemia is frequently observed as a result of impaired usual technique must be modified (Table 23-1). Studies of nitro-
renal phosphate excretion as well as increased release from cells. gen balance in patients with CKD suggest that nonurinary losses
2. Patients with ARF frequently present with hypocalcemia. Hypo- can be estimated based on body weight.29,30
calcemia is a multifactorial process, due at least in part to hyper-
phosphatemia as well as reduced formation of 1,25(OH)2 vitamin
D3, leading to reduced calcium absorption from the gastrointesti-
nal tract. Hypercalcemia is rare in critically ill patients with ARF, TABLE 23-1. Calculation of Nitrogen Balance in Adult
except those with particular underlying disorders otherwise asso-
Patients Receiving Dialytic Support
ciated with hypercalcemia (eg, fungal or mycobacterial infection,
lymphoma, milk alkali syndrome). Immobilization can contribute Nitrogen balance in g/day = (protein intake in g/day/6.25) − nitrogen
to hypercalcemia, particularly in adolescent and young adult
loss/day
patients.
3. As noted for potassium, over the course of therapy some patients A. Patients receiving intermittent hemodialysis
develop hypophosphatemia. Hypophosphatemia may need to be
corrected to prevent weakness and rhabdomyolysis. Hypophos- Nitrogen loss in g/day = 0.97 × UNA + insensible losses (2–4 g of
phatemia may be a particular problem during the diuretic or nitrogen/day) + dialysis amino acid losses (approximately 1 g of nitro-
recovery phase of ARF, as well as during “refeeding.” gen/dialysis session)
UNA = UUN + [(BUN2 − BUN1) × (0.6 × BW1)] + (BW2 − BW1)
III. Nutritional Assessment in Patients with ARF × BUN2
A. The usual procedures for nutritional assessment are followed (see Where UNA = urinary nitrogen appearance in g/day; UUN = urine
Chapter 1).
urea nitrogen in g/day; BUN1 = initial blood urea nitrogen in g/L (eg,
B. The clinical assessment must include evaluation of the current whole
postdialysis); BUN2 = final BUN in g/L (eg, predialysis); BW1 = initial
body fluid status. Patients with ARF are often fluid overloaded. The
usual, or ideal, weight of the patient is used to determine nutritional body weight in kg; BW2 = final body weight in kg; 0.6 = estimated
status and nutrient requirements, and to monitor response to nutri- fraction of BW that is water.
tional therapy.
C. Ongoing assessment of volume status can be made by following B. Patients receiving continuous renal replacement therapy
daily weights and maintaining accurate records of intake and output, Nitrogen loss in g/day = dialysate urea nitrogen losses in g/day +
along with physical examination findings (eg, jugular venous pres- amino acid losses across continuous renal replacement therapy mem-
sure). Sometimes, invasive monitoring such as monitoring of cen- brane in g/day + UUN in g/day + insensible losses (2–4 g/day)
tral venous pressure is needed.
D. Caliper skinfold measurements are of limited utility in patients with Dialysate urea nitrogen losses in g/day = total dialysate ultrafiltrate
ARF because of edema. There are limited data on bioelectrical imped- volume in L × average ultrafiltrate urea nitrogen in g/L
ance in patients with ARF.28 Amino acid losses can be approximated as follows: 1.5 g nitrogen/day
E. Biochemical measurements include the following:
for 1 L/hour flow rate and 2.0 g nitrogen/day for
1. Serum sodium, potassium, chloride, bicarbonate, urea nitrogen,
2 L/hour flow rate
creatinine, calcium, magnesium, and phosphorus should be
obtained at the initial assessment and up to several times a week,
depending on the clinical stability of the patient. Adapted with permission from Dr. Thomas Baumgartner

© 2005 A.S.P.E.N. www.nutritioncare.org. A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. 283
S E C T I O N I V Surgical and Critically Ill Conditions

IV. Nutritional Requirements and Goals of avoided, given the impaired excretion of oxalate, a vitamin C
Therapy in ARF by-product, in ARF. Vitamin B12 losses may be less than losses
of other water-soluble vitamins, as this vitamin is protein bound.
A. Overall goals of therapy b) Vitamin A supplementation should be avoided, at least initially,
1. Maintain appropriate hydration. in light of observations that patients with CKD have elevated
2. Establish and maintain acid-base equilibrium. serum concentrations of vitamin A. Usual doses of vitamin A
3. Establish and maintain electrolyte balance. have been reported to cause toxicity.
4. Control uremia.
5. Maintain normal body composition during ARF and critical ill-
ness, which should improve immune function, wound healing, V. Enteral Nutrition in ARF
and host resistance. A. Choice of enteral nutrition
B. Nutritional support for patients with ARF 1. Enteral nutrition provides significant benefits to the patient with
1. General requirements. Nutritional requirements for patients with ARF,19 as it does for most other patients. PN requires a larger fluid
ARF will vary based on underlying nutritional status, degree of load than enteral nutrition, which can make it less appealing for
hypermetabolism and hypercatabolism, residual renal function, use in ARF patients.
and clinical condition. In addition, plans for dialysis or ultrafil- 2. Special enteral formulas (with reduced concentrations of sodium,
tration may strongly influence the prescription for enteral nutri- potassium, and phosphorus, and often with reduced protein con-
tion or parenteral nutrition (PN). Patients with ARF may differ tent) have been developed for patients with CKD and are often
from patients with CKD (discussed in Chapter 31) with regard to used in patients with ARF. These formulas are more concentrated
protein and energy requirements and, therefore, nutritional goals. than standard formulas, usually supplying 1.5 to 2.0 kcal/mL.
2. Energy requirements. Among patients with ARF, energy require- Since the patient may undergo dialysis regularly, providing ade-
ments can be estimated in several ways, including by the Harris- quate energy and protein, rather than providing a particular volume
Benedict equation with adjustment for illness severity or by of the formula, should be the primary focus, and it may be possi-
indirect calorimetry using a metabolic chart (see Chapter 22).31,32 ble to use a standard formula. Once dialysis is stopped, one of the
The resting energy expenditure should not be measured during low-electrolyte “renal” formulas may be preferable.
intermittent hemodialysis treatments, because of changes in organ 3. Essential amino acid enteral formulas are no longer commonly
perfusion and other factors that may influence energy use. used in ARF.
3. Protein requirements. Protein requirements will vary depending 4. The use of immune-enhancing formulas is discussed in Chapter 20.
on the underlying clinical state and on whether or not the patient B. Access. Most enteral formulas can be taken orally. In patients who
is receiving IHD or CRRT. Table 23-2 outlines recommendations are unable to meet their nutritional goals or who are intubated and
regarding protein intake in ARF, with or without dialysis. unable to eat, a feeding tube may be placed.
a) Some have advocated that a limited subset of patients with ARF C. Complications. Three major types of complications—mechanical,
who have little to no protein depletion, who have no clinical gastrointestinal, and metabolic—are associated with enteral nutri-
evidence of uremia, and who are likely to recover rapidly from tion in patients with ARF.
ARF can be treated with a restricted, essential amino acid reg- 1. A recent study compared the rate of complications of enteral
imen,24 but this is rarely done. In fact, at present it is virtually feeding in patients with ARF and those without ARF.36 The only
impossible to predict the time course of recovery from ARF. complication that was more frequent in ARF was delayed gastric
b) Most patients with ARF are catabolic. Therefore, protein intake emptying. However, this complication did not result in additional
should generally not be limited to forestall dialysis. Rather, ade- episodes of aspiration or aspiration pneumonia.
quate nutrition should be provided early in the course of illness, 2. For patients on tube feeds, phosphate binders (calcium carbonate,
and dialytic support should be used to allow provision of ade- calcium acetate, sevelamer hydrochloride) may be required to
quate nutrition. Indeed, when ARF accompanies sepsis or multi- reduce the amount of absorbable phosphorus in the feeding.
organ dysfunction or failure, the combination of underlying 3. Phosphate binders, particularly sevelamer hydrochloride, a hydro-
disease and the provision of nutrition nearly always makes ini- gel that expands upon contact with liquid, may clog feeding tubes.
tiation of dialysis necessary. Sevelamer hydrochloride should not be administered via this route
c) Patients receiving CRRT or “daily” dialysis in the form of IHD without extensive postadministration tube flushing.
or SLED may require higher doses of protein or amino acids. 4. Sodium polystyrene sulfonate (eg, Kayexalate, Sanofi Winthrop
Patients receiving continuous hemodiafiltration should receive Pharmaceuticals) and aluminum hydroxide (eg, Amphojel, Wyeth-
at least 1.0 g/kg/day of protein, and many patients will require Ayerst Laboratories) should not be co-administered, as these med-
at least 1.5 to 1.8 g/kg/day of protein or amino acids. A num- ications polymerize to form an insoluble compound.
ber of groups have recently used up to 2.5 g/kg/day of amino 5. Electrolyte disturbances are common, in particular hyper- and
acids in these patients and demonstrated no apparent com- hypokalemia, hyper- and hyponatremia, and hyper- and hypophos-
plications,33,34 assuming that adequate solute clearance can be phatemia.
achieved. Nutritional goals need to be serially reevaluated based a) Some medications may cause potassium loss, in particular
on net nitrogen balance on an ongoing basis. amphotericin, semisynthetic penicillins such as piperacillin,
4. Vitamin and trace mineral requirements. These are not well defined and potassium-wasting diuretics.
for ARF.24,35 b) Some of the penicillins are formulated as either potassium or
a) Vitamin and mineral status is affected by dialysis. Patients sodium salts and may lead to hyperkalemia or volume over-
undergoing IHD lose water-soluble vitamins into the dialysate. load, respectively.
Vitamin supplementation is needed to compensate for the c) If patients are receiving concentrated enteral formulas, they
losses. Excessive doses of vitamin C (>1 g/day) should be may require free water (which can be given enterally or intra-

284 A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. © 2005 A.S.P.E.N. www.nutritioncare.org.
 S E C T I O N I V Surgical and Critically Ill Conditions

venously) to prevent or correct hypernatremia. Hypernatremia phosphorus levels, which will usually rise with ARF. However, as
may be particularly common in the early recovery phase of dialytic support is initiated and anabolism returns, serum concentra-
ARF (perhaps in response to high concentrations of retained tions may fall abruptly, and appropriate amounts need to be provided.
osmotically active, noncharged, and nonmeasured solutes). F. The balance of acetate and chloride needs to be adjusted in the PN
D. Monitoring. The major goals of monitoring are to minimize the com- solution based on the patient’s acid-base status. While typically com-
plications of enteral therapy and to maintain the patency of the plicated by acidosis, ARF can be accompanied by a wide variety of
small-bore feeding tube. Basic monitoring in ARF patients on metabolic disturbances. The PN prescription will depend on whether
enteral tube feeds is similar to that of other patients on enteral tube the patient’s underlying disease is characterized by high levels of
feeds. The patient’s intake and output, as well as serum electrolytes, organic acid production and whether the patient is receiving dialysis.
should be strictly monitored (see Section II for commonly found bio- G. Means of access must be considered carefully.
chemical abnormalities). 1. Because of its high osmolality, PN needs to be administered
through a central line or peripherally inserted central catheter
VI. Parenteral Nutrition in ARF (PICC). Patients with ARF typically have a large-bore hemodial-
ysis catheter in a large central vessel (eg, internal jugular or
A. The fluid tolerance of a patient with ARF depends on many factors, femoral). Recently, new triple-lumen dialysis catheters, which
including the phase of ARF, whether the patient is receiving dialytic contain a third lumen for medication administration, have been
support, and whether the dialysis is continuous or intermittent. Atten- developed. While it is generally accepted that PN should not be
tion must be paid to the volume of solution infused on a daily basis. administered through the large ports of a double-lumen dialysis
B. Standard amino acid solutions should be used for patients with catheter, there are insufficient safety data regarding using the third
ARF. There is no clear advantage to administering essential amino lumen for nutrition infusion.
acids alone.35 2. PICC lines have been shown to have lower risks of infection than
C. The “dose” of protein in the form of amino acids that is appropriate other central lines and thus may be preferable for administering
to the patient’s age and stress level, plus an additional component for PN.38 A potential disadvantage to PICC lines in patients with
losses from dialysis or hemodiafiltration (see Table 23-2), should be ARF is scarring of the basilic and cephalic veins that might later
prescribed. The A.S.P.E.N. guidelines state that patients with ARF be used for permanent vascular access (in the form of either an
should receive both essential and nonessential amino acids. In addi- arteriovenous fistula or a synthetic graft) if ARF does not resolve
tion, the guidelines recommend that patients undergoing CRRT but the patient survives. In ARF, the obvious focus of care should
should receive at least 1 g/kg/day of protein and that patients with be on recovery from the acute illness rather than long-term dial-
ARF who are severely malnourished or hypercatabolic should ysis access. However, if the latter can be preserved while the nec-
receive 1.5 to 1.8 g/kg/day of protein. However, whenever possi- essary goals within the ICU are accomplished, there is additional
ble these decisions should be guided by nitrogen balance calcula- potential for long-term patient benefit.
tions. H. Monitoring patients with ARF on PN is similar to monitoring other
D. Patients with ARF receiving PN should receive fat emulsions. Intra- patients on PN, although the PN prescription and fluid balance need
venous fat emulsions are not cleared with dialysis.37 The optimal dose to be frequently reassessed.
or frequency of fat administration is unknown. While some clinicians I. A number of potential complications must be considered.
favor a high fat-to-carbohydrate formula and severe fluid restriction 1. Patients with ARF are prone to the mechanical, metabolic, and
to delay dialysis, it is generally preferable to base nutrition therapy infectious complications of TPN to which other PN patients are
on needs and side effect profiles, rather than pursuing the usually prone.
futile course of trying to delay or avoid initiation of dialysis. 2. Hyperglycemia is common among patients with ARF. In hospi-
E. The PN’s electrolyte composition should be assessed and adjusted talized patients, there is growing evidence that aggressive
daily according to changes in the patient’s clinical condition and serum glycemic control reduces ICU mortality and complication rates.23
chemistries. Special attention should be paid to serum potassium and However, patients with kidney disease are at increased risk for
hypoglycemia (see above).

Table 23-2. Approximate Protein Requirements REFERENCES

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286 A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. © 2005 A.S.P.E.N. www.nutritioncare.org.
 Carolyn L. Abitbol, MD;
Marie Rossique, PharmD;
Mirta Rios, RD 24
Nutritional Support of the
Pediatric Patient with
Acute Renal Failure
Introduction C. Response to bodily injury in a child is extremely variable and is pri-
marily dependent on age, degree of organ maturity, underlying nutri-
Children present a unique challenge in nutritional and metabolic support tional status and the severity of the traumatic insult.
during periods of acute renal failure (ARF). The challenge is to make an D. The acute metabolic response to injury or stress is catabolism. It
appropriate assessment and prescribe interventions that provide neces- involves the mobilization and utilization of endogenous substrates
sary replacement and sustenance for recovery. As in adults, causes of (protein, fat, and carbohydrates) rather than tissue deposition and
ARF in infants and children are broadly characterized, as pre-renal, growth.4
intra-renal and post-renal (or obstructive). The “phase” or duration of E. Respiratory quotients indicate that the proportion of macronutrient
renal injury, the volume of diuresis (oliguric versus non-oliguric) and the utilization/expenditure during childhood stress is approximately 33%
effects of any needed form of renal replacement therapy determine the from carbohydrate, 53% from fat and 14% from protein oxidation5,
nutritional prescription. in contrast to normal substrate utilization of approximately 55% car-
bohydrate and 30% fat.
I. Overview of Pediatric Acute Renal Failure F. Early “overnutrition” or “overfeeding,” particularly with excessive
II. Nutritional Aspects of Pediatric Acute Renal Failure concentrations of carbohydrate, may jeopardize the subsequent hos-
III. Nutritional Assessment in Pediatric Patients with Acute Renal pital course.4 Studies using indirect calorimetry in critically ill pedi-
Failure atric patients indicate that the percent of energy from carbohydrate is
IV. Nutritional Goals and Requirements lower than previously predicted.5,6
V. Enteral Nutritional Support G. Over-feeding with carbohydrate in the face of insulin resistance and
VI. Parenteral Nutritional Support compensatory gluconeogenesis may lead to hyperglycemia, hyper-
References triglyceridemia and hyperosmolality.4 Recent reports indicate that
critically ill infants and children who demonstrated early and sus-
tained hyperglycemia > 126 mg/dL (7 mM/L) had a 3 fold risk of
I. Overview of Pediatric Acute Renal Failure mortality over those with well controlled glycemia.7
A. The pathophysiology and principles of management of ARF are
described in Chapter 23. This chapter presents information specif- III. Nutritional Assessment in Pediatric Patients
ically related to managing pediatric patients with ARF. with ARF
B. Estimation of kidney function in the pediatric population is based on
A. Nutritional assessment in ARF patients uses standard approaches
the serum creatinine (Scr) and the child’s height using the formula
described in Chapter 1.
of Schwartz, et al.1 Estimation of the severity of deterioration in
B. Of particular importance is itemization of fluid intake and output
renal function in normovolemic pediatric patients, including preterm
with a relative “balance” estimate. This is used in conjunction with
neonates with small muscle mass, is a doubling of the baseline Scr,
the clinical assessment of current whole body fluid status.
especially when associated with a fall in urine flow to < 0.5 to 1 ml/ C. Laboratory data at initial assessment should include the BUN, Scr,
kg/hr.2,3 This applies equally to preterm neonates prone to vasomo- electrolytes, calcium and phosphorus, total protein and serum albu-
tor nephropathy.3 min, lactic acid and magnesium.
D. See Table 24-1 for the Pediatric Intensive Care Global Nutritional
II. Nutritional Aspects of Pediatric ARF Assessment

A. Nutritional requirements for macronutrients should be estimated

based on the patient’s needs and current intakes. Enteral and par- IV. Nutritional Goals and Requirements
enteral nutrition must be determined in coordination with the plans A. Maintain adequate hydration and avoid “over-hydration” or dehy-
for fluid allowance and required dialysis modalities including con- dration
tinuous renal replacement therapies (CRRT). B. Establish and maintain acid-base equilibrium
B. Infants and children are metabolically and hormonally primed for C. Establish and maintain electrolyte and bone-mineral balance
maintaining growth and positive nitrogen balance. Although their D. Assess and reverse the catabolic stress (negative nitrogen balance)
energy requirements are inversely proportional to their age and size, E. Provide “co-factors” of metabolism
their metabolic vulnerability to stress may be less than in adults who F. Avoid “toxic” overload of macro and/or micro-nutrients
begin in a state of nitrogen equilibrium. G. Meet energy needs.

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S E C T I O N I V Surgical and Critically Ill Conditions

TABLE 24-1. Pediatric Intensive Care Global Nutritional Assessment Used in ARF

Age Parameter Notations

Primary Diagnosis

Time in ICU Yes No

Co-Morbid Profile ARF

Anemia
Sepsis
Edema
Surgery/Trauma

Output Urine
Stool
Emesis/NG
Ostomy
Dialysis

Fluid Intake Enteral

Intravenous (PN+IV)
Crystalloid
Colloid

Fluid Balance

Nutritional Assessment General Physical Exam

Estimated Wt/Ht SDS
Albumin;Pre-Albumin
Na+, K+, Cl-, Ca++, P, Mg++
BUN, Scr
Serum Bicarbonate
Lactate:Pyruvate
mNB (Urea Kinetics)

Nutritional Intake Enteral

CHO
Protein
Fat
Parenteral
CHO
Protein
Fat

(Continued )

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 S E C T I O N I V Surgical and Critically Ill Conditions

TABLE 24-1. Pediatric Intensive Care Global Nutritional Assessment Used in ARF (Continued)

Assessment Summary

Dialysis Plans

Enteral Feedings

Parenteral Nutrition

______________________________
Signature

1. Formulas commonly used to predict resting energy expenditure 3. During ARF without dialysis, endogenous catabolic nitrogen is
(REE) with modifications for stress factors in critically ill pedi- estimated by urea kinetics (change in total body urea nitrogen plus
atric patients have been shown to be unreliable.4 Indirect calorime- total urinary urea nitrogen). This must be added to any urinary pro-
try, when available, gives valuable insight into individual patient tein or total nitrogen losses, which may be extreme if the nephrotic
requirements. syndrome, proteinuria (>1 g/m2/day) is present.
2. Carbohydrate-The utilization of carbohydrate (CHO) is unpre- 4. Impact of dialytic modality on nutrition
dictable in critically ill infants and children, making glucose mon- a) All dialytic modalities, including peritoneal (PD), hemodial-
itoring extremely important. Although hypoglycemia may occur, ysis (HD), and continuous renal replacement therapy (CRRT)
the pediatric patient more often exhibits intolerance to rapid glu- or continuous veno-venous hemofiltration (CVVH), result in
cose infusions resulting in potentially lethal hyperglycemia and increased nitrogen and micronutrient losses.9–13
hyperosmolality.7 Insulin infusions may be required to maintain b) Peritoneal Dialysis.
normoglycemia. (1) Advantages of PD include slower osmolar fluid shifts and
H. Protein avoidance of the dialysis disequilibrium syndrome.11 While
1. A dietary protein prescription at the higher end of the recom- PD imposes a greater loss of proteins through the dialysate
mendation for infants and toddlers is appropriate (Table 24-2) than HD, it is often the only feasible modality for small
with a goal of maintaining the serum albumin > 3 g/L and BUN infants with ARF. Protein loss is inversely related to body
> 50 and < 60 mg/dL. size. A general estimate is 10 grams per liter of ultrafiltrate
2. Nitrogen Balance-Adjusted Protein Catabolic Rate. In renal fail- per treatment.13 In infants and children, 1 to 4 grams/kg/day
ure, protein nitrogen requirements are typically estimated from of protein losses must be added to the total daily protein
urea nitrogen appearance.6 The recently published Kidney Disease intake.
Outcomes Quality Initiative (K/DOQI)2,8 now term this normal- (2) The energy from dialysate glucose should be included in
ized Protein Nitrogen Appearance (nPNA). the total carbohydrate intake in patients treated with PD.

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S E C T I O N I V Surgical and Critically Ill Conditions

TABLE 24-2. Recommended Protein Intake(s) and Estimated Losses During Dialysis Treatments

Age Est’d Est’d Est’d

(Weight Range) RDI PD Losses HD Losses CRRT Losses Daily PI Goal

Infant Size
Age <2 Yrs
(≤10 kg) 1.6–2.2 2.0-4.0 0.5–1.0 2.0–3.0 2.0–6.0

Small Child
Age 1–6 Yrs
(>10 ≤ 25 kg) 1.0–1.2 2.0-3.0 0.5–1.0 2.0–3.0 1.0–3.0

Older Child
Age 7-14 Yrs
(>25 ≤ 40 Kg) 0.8–1.2 1.0-2.0 0.5–1.0 2.0–3.0 1.0–2.0

Adolescent
Age 15-21 Yrs
(>40 ≤ 70 kg) 0.8–1.0 1.0-2.0 0.5–1.0 2.0–3.0 1.0–2.0

Values are expressed as grams of Protein / kilogram / day. RDI = Recommended dietary intake for normal children.20 Estimated losses by peritoneal dialysis (PD) vary widely and
are inversely related to size. Estimated losses by hemodialysis are per treatment and are relatively stable according to size. There are no definitive data regarding protein require-
ments for children on dialysis, especially small children. Individualized recommendations for protein intakes of children with renal failure are best determined by estimated losses
and modified nitrogen balance (mNB) studies. The broad "goal" is to maintain the blood urea nitrogen (BUN) >40 mg/dl < 80 mg/dl.

NB = NI −  ∆ Vurea + ( U + PD )urea + ( U + PD )protein 6.25 

Peritoneal dialysate glucose absorption increases total
energy intake by 7 to 10 kcal/kg/day. Too often, infants on
chronic PD accumulate excessive fat mass due to supple- where NI is nitrogen intake from parenteral or dietary intake,
mentation with non-protein calories and inadequate protein ∆V is change in total body urea in 24 hours. The V is calculated
intake relative to losses through the PD. as 60 to 70% of total body weight. U is 24 hour urine. If the
c) Hemodialysis and CRRT patient is being treated with PD, the 24 hour peritoneal dialysate
(1) When dialytic or ultrafiltration treatment is required, is assayed for total urea and protein nitrogen. Estimates of pro-
dialysate nitrogen losses must be estimated for dialysis teinuria are made from 24 hour urine protein determinations or
modality and added to the nitrogen requirements. Nitro- spot urine protein to creatinine ratios (Up/c). The Up/c esti-
gen loss during HD is primarily free amino acids during mates daily proteinuria in g/m2/day.14 This number, in turn, is
the 2 to 3 hours of treatment and accounts for 3 to 12% of adjusted to “nitrogen” by dividing by the factor 6.25. For the
the patient’s daily protein requirement.10,11 This is equiv- NB assessment, results are reported in grams per kilogram per
alent to as much as 0.1 to 0.3 g/kg/treatment of protein as day. These calculations are provided in Table 24-3.
amino acids.13 b) In summary, the calculation involves an estimate of nitrogen
(2) Continuous veno-venous hemofiltration and/or dialysis intake from dietary / nutritional intake minus the total nitrogen
(CVVHD) entails continuous loss of plasma free amino output which includes the urea nitrogen generation (urine urea
acids, as well as all unbound nutritional cofactors in nitrogen, total body urea nitrogen appearance, dialysate urea
plasma water. Because of the associated nitrogen losses, nitrogen clearances) plus total protein losses from urine and/or
when CVVHD is maintained for greater than 24 hours, it dialysate corrected for nitrogen content (i.e., total protein/
should be accompanied by continuous parenteral nutri- 6.25 g/gram nitrogen).
tion via a separate central venous or through a port beyond 6. Protein:energy ratio. Few studies are available that allow esti-
the replacement port to maintain a positive nutritional mation of optimal protein:energy ratio in critically ill children.
status.12 Standard maintenance diets provide a total energy (calories)-to-
5. Urea kinetics nitrogen (g) ratio of 250. In metabolic studies, the mean ratio
a) Following urea kinetics allows assessment of protein nitrogen achieving nitrogen balance is lower, averaging 193 ± 96 or
balance as well as dialysis efficiency (Table 24-3). Adjustment approximately 13% of calories from protein.4
of pediatric dialysis prescriptions, particularly in ARF, requires 7. Adjustment of protein dose based on Blood Urea Nitrogen
careful attention to avoiding the acute disequilibrium syndrome a) A rapid assessment of protein catabolic rate, especially in chil-
which is acute brain swelling following too rapid lowering of dren, can be made from blood urea nitrogen (BUN), not the
plasma osmolality by rapid hemodialysis solute removal. Urea BUN to creatinine ratio. Infants and children with unusual
kinetics are used to estimate nitrogen balance (NB) from the physical stress, such as those undergoing visceral transplants,
following equation: trauma or infection, for example with the Human Immuno-

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 S E C T I O N I V Surgical and Critically Ill Conditions

TABLE 24-3. Formulae for Calculating Nitrogen Parameters in Pediatric Patients With ARF

Formula Normal Values

Creatinine Clearance1 (Ccr) Ccr = Ht(cm)*k ÷ Scr 95–110 mL/min/1.73m2

k = 0.35 (infant); 0.55 (child); 0.75 (adolescent male)

Oliguria (Inadequate or low urine output) <0.5 to 1 mL/kg/hr 10kg > 500 mL/d (>2 mL/kg/hr)
20kg > 750 mL/d (>1.5 mL/kg/hr)
30kg > 875 mL/d (>1.2 mL/kg/hr)
50kg > 1000 mL/d (>1 mL/kg/hr)

Modified Nitrogen Balance (mNB) mNB = NI − [∆ Vurea + Uurea] + Uprotein/6.25

Pre-Dialysis or HD Zero to 0.3 gram N/kg/d (2 grams
Protein/kg/d) ; Never negative
Modified Nitrogen Balance (mNB) for PD mNB = NI − [∆ Vurea + (U + PD)urea + (U + PD)protein/6.25]

V = Est’d Total Body Water 60 to 70% of Body Weight (kg = liters) Higher estimate recommended in
ill patients.

Kt/Vurea

Hemodialysis (HD) Kt/V = 1.2 [−Ln R] Goal Kt/V > 1.3

Ln = Natural log
R = Post/Pre plasma BUN ratio

Peritoneal Dialysis (PD) K = PD urea × Dialysate Volume [Initial Drain + (Infusion Volume Wide Variation:
× Cycles) + Ultrafiltrate Volume] ÷ Plasma urea CAPD: Kt/V = 1.75 to 2.0
t = time (days) CPPD: Kt/V = 2.0 to 2.5 per week
V = Body Weight (kg) × 0.7

deficiency Virus (HIV), may be chronically malnourished hyponatremia. As with adults, limiting fluids or nutritional support
with wasted muscle mass and will have a low serum creati- in an effort to delay the need for dialysis is usually unsuccessful and
nine. These patients often have subclinical renal disease and is not recommended.
are sensitive to the effects of endogenous catabolism, as well
as excessive nitrogen administered either enterally or par-
V. Enteral Nutritional Support
enterally. A safe target is to limit the protein to energy ratio to
that which will maintain the BUN > 50 and < 60 mg/dL. This A. Enteral supplements and food feedings used in ARF are included in
is usually of 10–15% of total energy as protein. If the BUN the Table 24-4.
jumps quickly to > 100 mg/dL, the protein content of the PN B. Carbohydrate supplements, polymerized glucose, have traditionally
can be cut in half for a brief period, then increased as possible been added to oral and enteral feedings. They contribute to carbo-
to maintain SAlb > 3.0 g/dL. hydrate “overfeeding,” particularly in patients on PD who absorb
b) It is well established that a low pre-dialysis BUN (< 50 mg/dL) the glucose from the dialysate solutions. These supplements are dis-
reflects an increased risk of mortality associated with poor or couraged, particularly if dialysis therapy is to continue for longer
inadequate protein intake, regardless of dialysis modality. This than 2 weeks.
same premise seems applicable in children with ARF who are C. Fat supplementation to provide energy and essential fatty acids may
not on dialysis, even in those who seem to have a relatively include long-chain fats and medium chain triglycerides (MCT).
large fat mass (as in infants or obese adolescents). These preparations can contribute significantly to the overall energy
I. Fluid and Solute Requirements-Ongoing losses from naso-gastric content of the diet. Eicosapentanoic acid (EPA) and fish oils are
drainage or from diuresis that frequently occur in the recovery phase potentially therapeutic entities for renal injury and repair.15
should be replaced with solutions matching the concentrations of D. Protein supplementation should be closely monitored and adjusted on
sodium (Na+) to the total from chloride (Cl−), bicarbonate (HCO3−), a daily basis until the patient demonstrates some degree of stability.
or acetate. Anuric (no urine flow) or oliguric (< 0.5–1 mL/kg/hr) As nitrogen balance becomes positive, requirements for minerals
patients are likely to require restriction of fluids. If parenteral fluids increase, such as potassium and phosphate, which are used in protein
are required for resuscitation or as vehicles for medications, they and lean tissue synthesis. Protein supplements are usually required in
should contain at least 60 to 140 mEq/L of Na+ to prevent dilutional infants and children on PD.

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S E C T I O N I V Surgical and Critically Ill Conditions

b) Potassium. Potassium intake is essential for cell anabolism but

TABLE 24-4. Commercial Enteral Preparations can become lethal during periods of ARF and catabolic stress.
Used in ARF21–24 For this reason, potassium supplementation is withheld during
ARF until a stable anabolic process is confirmed. This is usu-
Indication(s) Description Examples ally simultaneous with a concurrent fall in serum phosphorus.
Transient falls in serum potassium to < 3.0 mEq/L are common
Infant Formulas following dialysis (with 0 to 2 mEq/L dialysate bath) and are
routinely followed by a “rebound” phenomenon. If these levels
Decreased Renal Whey: Casein Similac PM 60:40
are treated aggressively with “bolus” potassium, the conse-
Function (approximately 60;40) Premature Formula quences may be lethal. Therefore, we recommend not to treat
Ca:P (2;1) any potassium level ≥ 2.0 mEq/L, unless it is sustained and/or
associated with electrocardiographic (EKG) evidence of
Pediatric Enteral Formulas (1–10 Years) arrhythmia. Hyperkalemia (≥ 6.0 mEq/L) should be treated with
kayexalate resin as a retention enema or mixed with enteral
Decreased Kidney 2 Kcal/cc, lactose free, Magnacal Renal feedings if possible. The dose is 0.5 to 1 gram/kg as necessary
Function 7.5 g/dL Protein 1 to 3 times daily. When mixed with sorbitol, it causes diarrhea
and has been associated with bowel necrosis. The powdered
2 Kcal/cc, lactose free, Nepro; Nutrirenal form of kayexalate may thicken in the intestine and, in the pres-
7 g/dL Protein ence of other products, cause constipation and bezoars. This can
be avoided by mixing the resin with the liquid formula, allow-
2 Kcal/cc, lactose free, Suplena
ing it to settle, then decanting the formula from the residue.17
low Vit A,D, Phos,
c) Calcium and phosphorus. The serum Ca × P product in ARF is
3 g/dL Protein extremely labile, particularly in infants and during parenteral
alimentation. Too often, only the serum Ca is measured and
2 Kcal/cc, semi- Renalcal
both Ca and P are added to the PN solution. With small amounts
elemental, lactose free,
of intravenous P, the serum P will rise and cause the serum Ca
low electrolytes, to fall precipitously causing seizures or tetany. The rapid cor-
3.4 g/dL Protein rection of the serum Ca with IV calcium chloride (CaCl2) may
cause acute intravascular and intrapulmonary calcifications
when the serum P is ≥ 7 mg/dL. It is imperative to always mon-
itor the Ca × P product in ARF in children. Do not add phos-
E. Phosphate binders (calcium carbonate, calcium acetate, sevelamer) phorus to the PN solution until the serum P is ≤ 4 mg/dL. Never
may be added to the feedings to help maintain normal phosphate infuse CaCl2 solution with a serum P ≥ 7 mg/dL.
levels.16 d) Iron deficiency is a common complication of patients under-
going treatment for ARF and is multifactorial. Intravenous
supplementation is not recommended due to frequent hyper-
VI. Parenteral Nutritional Support in Pediatric ARF sensitivity reactions and its association with septicemia.
A. Hemofiltration (CVVH) offers an exceptional, effective modality for e) Magnesium (Mg). Although Mg is essential for intermediary
treatment of prolonged ARF with anuria/oliguria, intractable lactic metabolism, it accumulates rapidly with ARF. Supplementa-
acidosis, and/or hepato- renal syndrome. Once the patient becomes tion should be cautious and monitored by serum levels. Infants
metabolically stable, continuous parenteral nutrition can be admin- are especially prone to toxicity.
istered at physiologic rates of glucose administration through the f ) Trace Elements—These micronutrients are key elements in
post-filter port of the CVVH circuit. Although this avoids the need immune and antioxidant defenses and are rapidly depleted in
for a second central venous catheter, the risk of sudden loss of dex- critically ill patients, especially those undergoing dialysis or
trose infusion due to catheter clotting should be considered. CRRT.18 Please see Table 24-5 for age and size adjusted rec-
B. Micronutrient Requirements ommendations for parenteral nutritions solutions.
1. Electrolytes, Minerals and Trace elements. 2. Vitamins
a) Sodium, chloride, and bicarbonate. These three electrolytes a) Water soluble
are the main components of plasma electroneutrality and (1) Folate and B12 are frequently low and require supplementa-
tonicity. Narrow limits (within 5 mEq/L) should be main- tion. Oral supplementation 400 µg to 1 mg/day of folate in
tained for each of these according to the following ratios pediatric patients with ARF is recommended. B12 is poorly
(Na:Cl:HCO3<135:105:25) with no more than 5 mEq/L of absorbed in patients with ARF due to achlorhydria. Sup-
unmeasured anion. When preparing the prescription for PN or plementation is recommended. (See Tables 24-5 and 24-6).
CVVH replacement fluids, these ratios should always be main- (2) Vitamin B6 (pyridoxine) is lost during dialysis treatment
tained. Infants and stressed children do not metabolize lactate and is an important co-factor in protein metabolism. Its defi-
to bicarbonate in a predictable fashion. For this reason, we do ciency has been associated with seizures in infants and chil-
not recommend the use of Lactated Ringer’s solution for fluid dren. Supplementation is recommended. (See Tables 24-5
resuscitation or any parenteral solutions containing lactate as and 25-6).
the primary buffer. This includes CVVH replacement solutions (3) Thiamine (B1) and riboflavin (B2) are also lost in dialysis
and/or dialysate solutions. Only acetate and bicarbonate are and are important co-factors in carbohydrate and protein
used in such solutions. metabolism.

292 A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. © 2005 A.S.P.E.N. www.nutritioncare.org.
 S E C T I O N I V Surgical and Critically Ill Conditions

TABLE 24-5 Components of Pediatric Parenteral Nutrition Formulations18–22

Weight

Components ≤10 Kg 10–20 Kg >20 Kg

Fluid Maintenance 100–150 ml/kg 1000 ml + 50 ml/kg >10 Kg 1500 ml + 25 ml/Kg >20 Kg

Dextrose (3.4 kcal/gram)

Grams/Kg/day 10–25 8–20 5–20

Amino Acid (+Losses)

1 gram=0.16 gram nitrogen 1.6–2.2 1–1.2 0.8–1.2

Fat (Lipids)
(grams/Kg/day) 0.5–4 1–3 1–3

Total Calories
(Kcal/kg/day) 75–110 50–80 30–70

Sodium (mEq/Kg/day)
Not to exceed 152 mEq/L 2–4 2–3 2–3

Potassium (mEq/Kg/day)
Not to exceed 40 mEq/L 0–3 0–3 0–2

Bicarbonate or acetate
mEq/Kg/day 1–3 1–2 1–2

Vitamins and Trace Minerals

Pediatric MVI ( See Table 24-6) 2 ml/day 2-5 ml/day 5 ml/day

Zinc 0.2 mg/kg/day Adult Dose 5 mg

Copper 20 µg/kg/day Adult Dose 2 mg

Manganese 5 µg/kg/day Adult Dose 500 µg

Chromium 0.2 µg/kg/day Adult Dose 20 µg

Selenium 2 µg/kg 2 µg/kg/day (Maximum 30 µg/day)

(4) Vitamin C, a water soluble vitamin, is metabolized to (3) Vitamin D. 25(OH)D2 and 1,25(OH)2D2 are the hydroxy-
oxalate which accumulates in tissues of patients with lated derivatives of calciferol. The vitamin is actually a hor-
chronic kidney disease (CKD) but this is not documented mone that requires hydroxylation in the liver after sterol
in ARF patients. Dialysis patients may become deficient isomerization in the skin by the sun. The most active form
without minimal supplementation. Supplement at no more is 1,25(OH)2D, calcitriol, which has been hydroxylated in
than the recommended dietary intake (RDI) of 60 mg/day. the kidney. Any renal injury, acidosis, or fluctuation(s) in
(See Tables 24-5 and 24-6). the Ca × P product with parathyroid hormone (PTH) can
b) Fat soluble vitamins are potentially toxic since they are not dia- markedly alter the production of calcitriol. Supplementa-
lyzed and may accumulate in CKD. If ARF is not prolonged tion is not within the nutritional prescription. Dosing and
(i.e., > 2 weeks), supplementation is usually recommended. administration must be a component of the medical man-
(See Tables 24-5 and 24-6). agement of Ca × P and intact PTH (iPTH) levels.
(1) Vitamin A is decreased in ARF and requires supplemen- (4) Vitamin K, synthesized by intestinal bacteria, may be com-
tation. promised in children with renal failure, especially during
(2) Vitamin E in ARF is decreased and may require supple- antibiotic therapy. Supplementation is recommended.
mentation. It may improve leg cramping but may also 3. Other Micronutrients and supplements. Carnitine deficiency
increase blood clotting. Supplementation is recommended. occurs in all dialyzed patients. It is easily supplemented either

© 2005 A.S.P.E.N. www.nutritioncare.org. A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. 293
S E C T I O N I V Surgical and Critically Ill Conditions

TABLE 24-6 Oral Vitamin & Mineral Supplements for Pediatric Patients With ARF

Parenteral Pediatric
Supplement Recommendation Dose & Formulation20-24 MVI/ 5 ml

Vitamin A Caution Not to Exceed RDA* 0.7 mg (2300 IU)

Vitamin E Caution Not to Exceed RDA* 7 mg (7 IU)

Vitamin D Cholecalciferol 400 µg /day; calcitriol separate from 10 µg (400 IU)

nutritional prescription

Vitamin C Caution ≤60 mg/ day 80 mg

Thiamine (B1) Recommended 0.2 to 1.0 mg/day 1.2 mg

Riboflavin (B2) Recommended 0.3 to 1.0 mg/day 1.4 mg

Pyridoxine (B6) Recommended 6.25 to 50 mg/day 1 mg

Folate Recommended 0.4 to 1.0 mg/day 140 µg

Vitamin K Caution 5 to 60 µg/day 200 µg

Vitamin B12 Recommended 0.5 to 2.5 µg/day 1 µg

Carnitine 50–300 mg/kg/day Levocarnitine (Carnitor) 330 mg/cap Separate Additive

(or 1 gram/10 mL PO/IV)

RDA* Recommended Dietary Allowances for Age

orally or parenterally and is well tolerated.18 Supplementation is 6. Coss-Bu J, Jefferson L, Walding D, David Y, Smith O, Klish W. Resting
recommended. energy expenditure and nitrogen balance in critically ill pediatric patients
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 Michele M. Gottschlich, PhD, RD;
Theresa Mayes, RD
25
Burns

Introduction 3. Hypermetabolic responses continue throughout the course of burn

recovery. Patients are in a net whole-body protein catabolic state
Nutrition support following burns represents a unique challenge because
with protein anabolism increased approximately one-third above
of the complex interactions of injury, organ function, wound healing, and
normal and protein catabolism increased two-thirds above nor-
immunocompetence. Nutrition is an important effector of each of these
mal. Extensive nitrogen losses occur from burn wound exudate as
events, and in burn patients, inefficient diet therapy will exacerbate
well as in the urine, both of which can result in massive daily
pathophysiologic abnormalities and catabolic sequelae, such as erosion
nitrogen losses. In the first week postburn, protein losses are par-
of lean body mass, bone, and blood proteins. The clinician is therefore
ticularly high, and then slowly decrease over the course of con-
faced with important decisions regarding what and how to feed burn
valescence. Abnormal protein loss is not observed once wounds
patients. This chapter outlines the impact of acute thermal injury on
and donor sites have healed.
metabolism and nutritional needs. Options for nutrient delivery as well
4. The metabolic response to thermal injury results is increased glu-
as guidelines for nutrition assessment and monitoring are presented.
cose production from gluconeogenesis in response to the altered
I. Pathophysiology of Burns hormonal and inflammatory mediator environment. The burn
II. Energy and Nutrient Requirements of Burn Patients wound itself metabolizes large quantities of glucose via anaero-
III. Nutritional Therapy for Burn Patients bic glycolytic pathways, producing large amounts of lactic acid as
IV. Nutrition Assessment and Management of Burn Patients an end product. Support of gluconeogenesis requires accelerated
References net protein catabolism and movement of amino acids from the
periphery to the viscera.
I. Pathophysiology of Burns
II. Energy and Nutrient Requirements of Burn Patients
A. Physical destruction of the skin
1. The severity of a burn is measured by evaluating the surface A. Energy requirements are heightened postburn; therefore, adequate
area involved and the depth of the tissue destroyed. These two (but not excessive) calories should be provided. Nutrition inter-
parameters successfully predict outcome and determine meta- vention is designed to provide adequate amounts of protein and
bolic arrangements and therapeutic interventions. The size of a calories to burn patients. Inadequate interventions result in over-
burn injury is expressed as a percentage of the total body sur- or under-feeding, both of which can harm the patient. Metabolic
face area (TBSA). Burn size is classified using the rule of nines needs are difficult to predict; therefore, numerous formulas are
or, more accurately in children, using the Lund and Browder used to estimate energy needs in burn patients.6–10 Most take into
chart.1 account weight and percentage of total body surface area burned;
2. Burns are also classified by the depth of skin injury (Figure 25-1). formulas may also include factors such as patient age and activ-
First degree burns affect the epidermal layers of the skin. Second ity. Mathematical equations for estimating the energy require-
degree burns involve the epidermis and some of the dermis. Third ments of pediatric and adult burn patients are listed in Table 25-1.
degree (full thickness) burns destroy all layers of the skin. Whenever possible, indirect calorimetry should be used to better
B. Metabolic response2–5 assess caloric needs.2 A factor of 20–30% above the measured
1. The early phase of burn injury is characterized by a decrease in energy expenditure is commonly added to account for increased
cardiac output, oxygen consumption, and resting energy expendi- energy demands from physical therapy along with the stresses of
ture. This is similar to the response observed following other trau- wound care.5
matic injuries. After resuscitation, a hypermetabolic response is B. Immediately after thermal injury, fluid, electrolytes and protein
observed and includes increased oxygen consumption, cardiac escape from the vascular compartment to the interstitial area sur-
output, and metabolic rate. rounding the burn wound. As a consequence, prompt provision of
2. Large thermal injuries cause the greatest degree of hypermetabo- intravenous fluid resuscitation is required to restore tissue blood flow
lism of all stress states. This metabolic response is proportional to and to prevent shock. The most popular fluid replacement formula
the extent of the burn injury. Other factors that contribute to hyper- is the Parkland formula,11 which must be modified for children, who
metabolism include fever, sepsis, surgery, environmental temper- require more fluid per square meter of body surface area than adults
ature, physical activity, and medications. Metabolic rate increases with burns.12
and peaks approximately 5–12 days postburn. Catecholamines C. As protein is essential for wound healing, close attention should be
may be an important stimulus for increased oxygen consumption paid to protein status.2 Protein losses may be massive in burned
and increased energy needs. patients secondary to both increases in net whole body catabolism

296 A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. © 2005 A.S.P.E.N. www.nutritioncare.org.
 S E C T I O N I V Surgical and Critically Ill Conditions

FIGURE 25-1. Interpretation of burn classification based on damage to the integument.

Reprinted from Mayes T, Gottschlich MM. Burns. In: Contemporary Nutrition Support Practice. Matarese L, Gottschlich MM, eds. Philadelphia, PA: WB Saunders Co;
2003:595–615, with permission from Elsevier.

and protein loss from the burn wound itself. Protein needs are per day. In addition, burn patients may benefit from further supple-
higher in burn patients than in other stress states and should com- mentation with vitamins D, K and folic acid; however, specific intake
pose approximately 20 to 25% of total calorie needs.5,9,13 Most burn guidelines do not yet exist.14–17
patients require protein intake of 1.5 to 2 g/kg/d depending on the
size of the burn. Some practitioners use 1.5 g/kg/d for burn wounds III. Nutritional Therapy for Burn Patients
that cover <20% of body surface area and 2.0 g/kg/d for wounds
that cover >20% body surface area. A. Nutritional intervention should be initiated as soon as the patient is
D. Carbohydrates have a protein-sparing effect in the postburn patient stabilized from the initial burn and other associated injuries.
and therefore should comprise approximately 60% of the energy pro- B. Nutrition support of the burn patient has changed substantially over
vided. Over-feeding of carbohydrates, however, can lead to hepatic the past 30 years. It was routine in the 1970s to use parenteral nutri-
steatosis and increased carbon dioxide production. Therefore, in the tion (PN) as a means of providing the large calorie and protein loads
adult burn patient, it is recommended that glucose administration not that are required by burn patients. It is now clear that PN offers no
exceed 5 mg/kg/min. advantage. In addition, the high incidence of septic complications,
E. Although lipid is calorically dense, its administration in excessive mucosal atrophy, and expense associated with PN,2,18 has led many cli-
amounts can lead to side effects including immunosuppression. nicians to restrict its use to supporting those burn patients with severe
Modest use of fat is recommended in burn patients, and diets con- diarrhea, gastrointestinal dysfunction, or intra-abdominal pathology.
taining 15 to 20% of calories as fat may be optimal. C. Nutrient delivery is best accomplished enterally.2 A high calorie,
F. Burned individuals also have increased vitamin and mineral needs. high protein oral diet may be sufficient to meet needs in patients with
Current knowledge supports administration of daily multivitamins burns <20% surface area. However, patients with larger burns and
until wound healing has been achieved.5 Vitamin A, which is impor- those presenting with facial injury, inhalation injury, psychological
tant for maintaining the immunologic response and for epithelializa- difficulties, or preburn malnutrition generally require a feeding tube
tion of wounds, should approximate 5000 IU per 1000 kcal of enteral to ensure adequacy of intake. Gastric ileus, which limits use of the
nutrition. Vitamin C is a coenzyme that is important for collagen syn- stomach for enteral nutrition, is common and often resurfaces with
thesis and immune function and should be provided at a dose of surgery, sepsis, major dressing changes, or other complications. As
500 mg twice daily. Zinc is a cofactor in energy and protein metabo- such, transpyloric feedings are commonly used in an effort to avoid
lism and should be supplemented at a dose of 220 mg of zinc sulfate the necessity for tube feeding interruptions.19

© 2005 A.S.P.E.N. www.nutritioncare.org. A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. 297
S E C T I O N I V Surgical and Critically Ill Conditions

TABLE 25-1 Formulae for Calculating Energy Requirements of Pediatric and Adult Burn Patients

Reference Age (yr) % BSAB Calories per day

Curreri6 0–1 yr <50 Basal + (15 × % BSAB)

1–3 yr <50 Basal + (25 × % BSAB)
4–15 yr <50 Basal + (25 × % BSAB)
16–59 yr Any (25 × W) + (40 × % BSAB)
>60 yr Any Basal + (65 × % BSAB)
Adult Any 20/kg + 70% BSAB

Davies and Liljdahl21 >60 yr Any Basal + (65 × % BSAB)

Adult Any 20/kg + 35% BSAB
Child Any 60/kg + 35% BSAB

Long modification of the Male Any (66.47 + 13.7W + 5H − 6.76A) × (activity factor) × (injury factor)
Harris-Benedict equation20 Female Any (655.1 + 9.56W + 1.85 − 6.68A) × (activity factor) × (injury factor)

Hildreth7 <15 yr >30 (1800/m2 BSA) + (2200/m2 burn)

Hildreth7 <12 yr (1800/m2 BSA) + (1300/m2 burn)

Mayes8 <3 yr 10–50 108 + 68W + 3.9 × % BSAB

5–10 yr 10–50 818 + 37.4W + 9.3 × % BSAB

BMR, basal metabolic rate; BSA, body surface area; BSAB, body surface area burned; W, weight in kg; A, age in years; H, height in cm.
Activity factor: Injury factor:
(a) confined to bed, use 1.2 (a) severe burn, use 2.0
(b) out of bed, use 1.3

D. Provision of adequate nutrition can attenuate whole-body catabolism D. Gastrointestinal tolerance of enteral feedings is monitored daily. Peri-
but rarely prevents or reverses loss of lean body mass by conventional odic, non-infectious diarrhea is often successfully managed by the
management principles. This has led to the adjunctive use of anabolic use of scheduled constipating medications (consider a combination
agents such as growth hormone and oxandrolone in critically ill burn of an anti-motility and bulking agent) without compromising the
patients.20 Clinical benefits reportedly include increased healing rate patient’s infusion rate or concentration of tube feeding.
and decreased length of hospital stay and mortality. Clinical risks E. The clinical dynamics of the burn patient fluctuate daily. These alter-
include hyperglycemia and increased mortality (growth hormone) ations influence nutrition status and thus the appropriateness of the
and nausea and virilism (oxandralone). care plan. Daily monitoring of changes in medications, infectious
episodes, surgical needs, and respiratory status dictate adjustments in
IV. Nutrition Assessment and Management nutrition goals and methods of therapy.
of Burn Patients5,21 F. Burn patients commonly experience hypophosphatemia, hypomag-
nesemia, and hypocalcemia. Serum electrolytes and minerals should
A. Regular assessment of the appropriateness of nutrition interven- be routinely monitored in patients with burns in excess of 25%
tion should continue until achievement of 95% wound closure at TBSA. Intravenous supplementation via maintenance fluid adjust-
a minimum. ment is most effective in stabilizing levels.
B. Tables 25-2 and 25-3 summarize guidelines for initial, daily, weekly, G. Adequacy of protein intake in burn patients can be determined by
and discharge evaluation of nutrition status. The initial nutrition serial measurements of nitrogen balance using the following formula:
assessment (Table 25-2) determines the appropriate route of feeding,
formula selection, and nutrition goals. The purpose of nutrition Nitrogen balance = nitrogen intake − (total urinary nitrogen
reassessment (Table 25-3) is to track restoration and maintenance of + fecal nitrogen loss + burn wound nitrogen loss)
nutrition stores due to their importance for wound healing and
immunity. where all of the above parameters are measured in grams per 24 hours.
C. Energy and protein from enteral and parenteral sources should be cal- The collection of wound exudate, however, is not routinely practiced
culated daily. Cumulative caloric balance ([current 24-hour caloric and, therefore, many clinicians estimate wound nitrogen losses as
intake − measured energy expenditure × 1.3] + cumulative caloric follows:
balance from the previous day) should be evaluated daily. A cumula-
tive balance within +/− 7000 calories over a patient’s hospital course ≤10% open wound = 0.02 g of nitrogen per kg off body weight
is desirable. per day

298 A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. © 2005 A.S.P.E.N. www.nutritioncare.org.
 S E C T I O N I V Surgical and Critically Ill Conditions

TABLE 25-2. Acute Burns—Guidelines for Initial Nutrition Assessment

Determine
Collect Obtain appropriate Determine preburn appropriate route Initiate assessment
objective data histories nutritional status Calculate of feeding tools

Age Past medical history Usual food intake Calorie and protein Oral Obtain indirect calorimetry
protein needs needs measurement within 24 hours
Total percent body Social history Nasoenteral of admission
surface area burn Food preferences Vitamin/mineral
Concomitant injuries supplementation Parenteral Begin 24-hour urinary urea
Body areas burned Food restrictions/ recommendations collection for nitrogen balance
Routine medications allergies determination
Inhalation injury Weight percentage:
Diet history Dentition • Percent ideal Obtain nutrition labs
Ventilatory status body weight (transferrin and prealbumin)
Referring hospital Appetite • NCHS* percentile
Gastric decom- course, as applicable (≤18 years) Begin monitoring calorie and
pression initiated Vitamin/mineral protein intake
supplementation
Anthropometrics:
• Weight
• Height/length
• Head circum-
ference (≤3 yrs)

*NCHS, National Center for Health Statistics

Reprinted with permission from Mayes T, Gottschlich MM. Burns and Wound Healing. In: Gottschlich MM. The Science and Practice of Nutrition Support A Case-Based Core Cur-
riculum. Silver Spring, MD: A.S.P.E.N.; 2001:391–419 with permission from the American Society for Parenteral and Enteral Nutrition (A.S.P.E.N.).

TABLE 25-3. Acute Burns—Recommendations for Nutrition Reassessment

Daily Weekly Upon discharge

Calorie and protein intake Weight (once edema resolved) Percent preburn weight at discharge

Labs: Transferrin Adequacy of oral intake

• Albumin
• BUN/creatinine Prealbumin Nutrition supplementation requirements
• Glucose
• Electrolytes Nitrogen balance trend Need for nutrition follow-up in the outpatient setting
• Nitrogen balance
Wound healing (% open wound)
Tolerance (nausea, vomiting, distention,
diarrhea, constipation) Indirect calorimetry:
• Resting energy expenditure
Clinical course (sepsis, infection, surgeries, • Respiratory quotient
fluid status, medications, respiratory status)

Appropriateness of diet, enteral or

parenteral alimentation order

BUN, blood urea nitrogen

Reprinted with permission from Mayes T, Gottschlich MM. Burns and Wound Healing. In: Gottschlich MM. The Science and Practice of Nutrition Support A Case-Based Core Cur-
riculum. Silver Spring, MD: A.S.P.E.N.; 2001:391–419 with permission from the American Society for Parenteral and Enteral Nutrition (A.S.P.E.N.).

© 2005 A.S.P.E.N. www.nutritioncare.org. A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. 299
S E C T I O N I V Surgical and Critically Ill Conditions

11% to 30% open wound = 0.05 g of nitrogen per kg of body 3. Mayes T, Gottschlich MM. Burns and wound healing. In: Gottschlich MM,
weight per day ed. The Science and Practice of Nutrition Support: A Case-based Core Cur-
riculum. Dubuque, IA: Kendall/Hunt Publishing Co; 2001:391–419.
≥31% open wound = 0.12 g of nitrogen per kg of body weight 4. Gottschlich MM, Mayes T. Nutrition support in the burned pediatric patient.
per day In: Samour P, King K, Lang C, eds. Handbook of Pediatric Nutrition. 3rd
ed. Boston: Jones & Bartlet; in press.
Fecal nitrogen losses can be estimated to be approximately 2–4 g/d. 5. Mayes T, Gottschlich MM. Burns. In: Contemporary Nutrition Support Prac-
It should be noted that serial nitrogen balance measurements are more tice. L. Matarese L, Gottschlich MM, eds. Philadelphia, PA: WB Saunders
Co; 2003:276–289.
reliable, as individual 24-hour urine nitrogen contents may vary sig-
6. Gottschlich MM, Ireton-Jones CS. The Curreri Formula: A landmark
nificantly. In the first 3 days postburn, nitrogen loss is very high and
process for estimating the caloric needs of burn patients. Nutr Clin Prac.
then decreases 4 to 16 days postburn. It should be realized that it is 2001;16:172–173.
difficult, if not impossible, to achieve nitrogen equilibrium or a pos- 7. Hildreth MA, Herndon DN, Desai MH, Duke MA. Caloric needs of adoles-
itive nitrogen balance in burn victims initially despite aggressive cent patient with burns. J Burn Care Rehabil. 1989;10:523–526.
nutrition support. 8. Mayes T, Gottschlich MM, Khoury J, Warden GD. An evaluation of predicted
H. Burn patients usually exhibit some degree of fluid retention. This nor- and measured energy requirements in burned children. J Am Diet Assoc.
mal postburn response interferes with the use of weight to assess 1996;96:24–29.
nutritional or fluid status in the acute postburn phase. An admission 9. Long CL, Schaffel N, Geiger JW. Metabolic response to injury and illness:
weight, before the onset of edema, or reliable statement of preburn Estimations of energy and protein needs from indirect calorimetry and nitro-
weight from the patient or family member, provides important base- gen balance. J Parenter Enteral Nutr. 1979;3:452–456.
line weight data. Resolution of edema may take weeks. Once this 10. Davies JWL, Liljedahl SL. Metabolic consequences of an extensive burn.
In: Polk HC, Stone HH, eds. Contemporary Burn Management. Boston: L
occurs, however, biweekly weight measurement and comparison to
Little, Brown & Co; 1971:151–169.
dry/preburn weight is essential. Achievement of 90% to 110% of pre-
11. Baxter CR, Shires T. Physiologic response to crystalloid resuscitation in
burn weight indicates optimal energy provision. thermally injured children. Ann NY Acad Sci. 1968;150:874–894.
I. Assessment of visceral protein status should consist of weekly eval- 12. Merrell SW, Saffle JR, Sullivan JJ, Navar PD, Kravitz M, Warden GD. Fluid
uation of either transferrin or prealbumin. Weekly trends of these resuscitation in thermally injured children. Am J Surg. 1986;152:664–669.
biochemical indices provide insight as to the adequacy of protein 13. Alexander JW, MacMillan BG, Stinnett JD, et al. Beneficial effects of
provision. aggressive protein feeding in severely burned children. Ann Surg. 1980;192:
J. Wound healing should be assessed weekly. This includes monitor- 505–517.
ing the healing status of partial thickness wounds and donor sites, as 14. Gottschlich MM. Fat soluble vitamins in wound healing. In: Molnar JA, ed.
well as graft adherence. Nutrition in Wound Healing. CRC Press; in press.
K. Assessment of energy needs is guided by indirect calorimetry a min- 15. Gottschlich MM, Mayes T, Khoury J, Warden GD. Hypovitaminosis D in
imum of once per week. Respiratory quotient (RQ) is a component pediatric burn patients. J Am Diet Assoc. 2004;104:931–941.
16. Jenkins ME, Gottschlich MM, Kopcha R, Khoury J, Warden GD. A
of this test that further assists in determining the adequacy of nutri-
prospective analysis of serum vitamin K and dietary intake in severely
ent provision. An RQ between 0.80 and 0.95 is indicative of appro-
burned pediatric patients. J Burn Care Rehabil. 1998;19:75–81.
priate substrate utilization. 17. Klein GL, Herndon DN, Rutan TC, et al. Bone disease in burn patients. J
L. Recent evidence suggests loss of bone mass postburn.15,17 Dual Bone Miner Res. 1993;8:337–345.
energy X-ray densitometry (DEXA) can be used to monitor changes 18. Herndon DN, Stein MD, Rutan TC, Abston S, Linares H. Failure of TPN
in bone mineral content as well as lean body and fat mass. supplementation to improve liver function, immunity and mortality in
thermally injured patients. J Trauma. 1987;27:195–204.
(Burns material from the 1st edition was contributed by Elaine B. 19. Gottschlich MM, Jenkins ME, Mayes T, Khoury J, Warden GD. An evalua-
Trujillo, Malcolm K. Robinson, and Danny O. Jacobs) tion of the safety of early versus delayed enteral support and effects on clin-
ical, nutritional, and endocrine outcomes after severe burns. J Burn Care
Rehabil. 2002;23:401–415.
REFERENCES 20. Demling RH. Comparison of the anabolic effects and complications of
1. Lund CC, Browder NC. The estimate of area of burns. Surg Gynecol Obstet. human growth hormone and the testosterone analog, oxandrolone, after
1960;79:352–358. severe burn injury. Burns. 1999;25:215–221.
2. ASPEN Board of Directors. Burns. In: August D, ed. Guidelines for the 21. Mayes T, Gottschlich MM, Warden GD. Clinical nutrition protocols for con-
Use of Parenteral and Enteral Nutrition in Adult and Pediatric Patients. J tinuous quality improvements in the outcomes of patients with burns. J Burn
Parenteral Enteral Nutr. 2002;26:88SA–90SA. Care Rehabil. 1997;18:365–368.

300 A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. © 2005 A.S.P.E.N. www.nutritioncare.org.
 Winston W. K. Koo, MB, BS, FRACP;
Kathleen McLaughlin, MS, RNC, NNP; and
May Saba, PharmD, BCNSP 26
Neonatal Intensive Care

Introduction 2. Therapies for the illness may interfere with nutritional status.
a) Long-term diuretic therapy results in increased loss of minerals
Nutrition support by the parenteral and/or enteral route is freely avail- and trace metals, nephrocalcinosis, and metabolic bone disease.
able in any neonatal intensive care unit (NICU) and plays an important b) Corticosteroid therapy to shorten the duration of mechanical
role in the management of sick neonates and infants. It can reduce meta- ventilator support can result in negative nitrogen balance,
bolic complications and minimize the interruption to normal growth. delayed growth, glucose intolerance, and possibly bone dem-
However, nutrition support is frequently applied inappropriately—that ineralization and neurodevelopment impairment.
is, “too little too late” or “too much too quickly.” The former often c) Bowel resection decreases the mucosal area for digestion and
occurs when the infant is considered “too sick” or “too immature,” and absorption of nutrients and fluid.
the latter often occurs when there is an unreasonable expectation that 3. After resolution of the acute illness, catch-up growth needs to
the effects of prior prolonged periods of inadequate nutritional support occur.
can be dramatically reversed. This overview, therefore, aims to provide
D. Nutrition support has several phases (Table 26-2). Metabolic response
a practical basis upon which optimal nutrition support can be provided
in the critically ill infant is proportional to the degree of stress and
to patients in the NICU, taking into account the unique challenges posed
involves an increase in the turnover of proteins, fats, and carbohy-
by the sick infant.
drates. The resting energy expenditure is high, with protein degrada-
tion rates elevated out of proportion to synthetic rates, and resultant
I. Special Considerations
negative protein balance. Appropriately designed nutritional support
II. Parenteral Nutrition
that has a mixed fuel system and is replete in protein does not quell
III. Enteral Nutrition
this metabolic response. However, it can minimize the morbidity and
IV. Nutrition Support for Sick Infants With Specific Disorders
mortality associated with depletion of the limited body stores of nutri-
References
ents and may result in anabolism and continued growth at a rate
appropriate to the gender and gestational and postnatal age. There-
I. Special Considerations. Nutrition support of sick infants, fore, no infant is too sick to receive nutrition support. It is a matter of
especially preterm infants, in the NICU must take into consideration whether the nutrients are delivered parenterally or enterally and the
the following issues: composition of the formulation.
A. Tissue stores of nutrients are rapidly depleted if exogenous nutri-
ent intake is not begun immediately. The critical role of early com- II. Parenteral Nutrition
plete nutrition support in minimizing potential problems is shown
in Table 26-1. A. Indications. PN can be used as the sole source of complete nutrition
B. The capacity of enzyme and organ systems is limited. support for infants who cannot be fed enterally or as an adjunct to
1. Gastric capacity and intestinal motility may be limiting factors for enteral feeding. In sick infants, PN allows prompt resumption of
the delivery, digestion, and absorption of nutrients. growth and expedites the transition to full-volume enteral feeding by
2. The limited capacity of enzyme systems can result in diminished providing supplemental nutrition while enteral tolerance is reduced.
tolerance of nutrients such as glucose and lipids. Any infant unable to tolerate adequate enteral feeding for more than
3. Limited organ function, for example, decreased renal capacity is 2 or 3 days should receive PN support. However, to optimize nutri-
associated with lower renal tubular glucose absorption and con- tional support and minimize complications, PN and/or enteral nutri-
tributes to glucose intolerance. tion (EN) should begin within 24 hours after birth.1–4
4. Neurobehavioral and neuromotor immaturity can impede normal B. Preparation. Because of stability and sterility issues5 and the need
nipple feeding. for adjustments to various nutrient components during the initial
5. There is an increased risk for disease conditions associated with phase of nutrition support, PN solutions are usually prepared daily
premature birth (e.g., respiratory distress syndrome, necrotizing for infants in the NICU. See Table 26-3 for PN macronutrient rec-
enterocolitis). ommendations for neonates. Major groups of nutrients include the
C. Different problems are associated with underlying illnesses. following:
1. Nutrient delivery needs to be tailored to the clinical situation and 1. Protein
biochemical parameters. For example, if nipple feeding is unsuc- a) During the immediate newborn period, sick infants, especially
cessful, a different route of delivery for enteral nutrients or the use preterm infants, may not tolerate standard amounts of nutrients
of parenteral nutrition (PN) may be needed. Different amounts or normally delivered to clinically stable infants and may not tol-
combinations of nutrients may be needed in renal or hepatic failure. erate adequate energy intakes for optimal utilization of amino

© 2005 A.S.P.E.N. www.nutritioncare.org. A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. 301
S E C T I O N I V Surgical and Critically Ill Conditions

those of breast-fed infants. Like human milk, these “pediatric”

TABLE 26-1. Nutritional Issues in the NICU* amino acid formulations contain taurine, tyrosine, histidine,
aspartic acid, and glutamic acid. They contain lower concen-
Problem** Potential solutions trations of glycine, methionine, and phenylalanine than the
amino acid preparations intended for older patients. Prepara-
Low tissue energy store Multiple sources of energy
tions with other sources of nitrogen, including dipeptides, are
(carbohydrate, fat, protein) from under study.
PN or EN c) Cysteine (a conditional essential amino acid for infants that also
enhances calcium and phosphorus solubility), glutamine (a pri-
Obligatory tissue (protein) Adequate protein and energy mary fuel for enterocytes, lymphocytes, and macrophages as
catabolism ≥ 0.5 g/kg/d intake from PN or EN well as a precursor for nucleotides and glutathione), and carni-
tine (required for optimal metabolism of fatty acids) are not
Essential fatty acid deficiency Essential fatty acids and currently included in commercial pediatric amino acid formu-
adequate energy intake from lations because of problems with short shelf life and uncertain
PN or EN efficacy. Cysteine hydrochloride can be added to PN infusate
at a dose of 40 mg/g of amino acids.
d) Carnitine can be added to PN infusate in varying amounts
Disturbance to circulating PN or EN with some modifica-
depending on institutional practice (see Section II.B.2.b).
concentrations of electrolytes tions as necessary e) Glutamine supplement to PN is not recommended. Glutamine
(sodium, potassium, chloride) at a dose of 20% of total amino acids of PN had no effect on
and minerals (calcium, mag- decreasing mortality, late-onset sepsis or necrotizing entero-
nesium, phosphorus) and colitis, or improving tolerance of enteral feeds or growth in
hydrogen ion ELBW infants.7
2. Energy. Carbohydrate and lipid emulsion are the major sources of
Hyperbilirubinemia EN to decrease enterohepatic energy used in PN. Provision of adequate energy is essential for
circulation of bilirubin optimal use of other nutrients for tissue synthesis and growth.
Energy requirements are influenced by many factors. Factors that
increase energy requirements include prematurity (increased
Glucose intolerance Complete nutrition support,
absorptive loss and heat loss), preexisting nutritional status (small
including nutrients such as
for gestational age versus appropriately grown infants), physio-
thiamine and chromium from logic stress (fever, sepsis, respiratory failure, etc), type (enteral
PN or EN (versus parenteral) nutrients have absorptive loss) and method of
feeding (nipple versus gavage feeding), and rate of growth (tissue
Delayed tolerance to full PN plus trophic feeding synthesis).8 Preterm infants receiving an energy intake as low as
enteral feeding 70 kcal/kg/d can achieve positive nitrogen balance9 because there
is no absorptive or digestive loss of energy with PN. In the pres-
Incomplete catch-up growth Early complete nutrition support ence of adequate protein intake, adequate weight gain occurs at a
and development parenteral energy intake of 80 to 130 kcal/kg/day. Excessive
energy intake is associated with increased fat deposition and
greater carbon dioxide production, which further complicates any
EN, enteral nutrition; NICU, neonatal intensive care unit; PN, parenteral nutrition underlying respiratory illness.10,11
* For neonates unable to receive adequate enteral feeding, the use of parenteral dex- a) Carbohydrate
trose (+/– electrolytes) and water should be limited to the brief period pending the
(1) Dextrose, hydrated glucose solution, is the standard source
routine availability of PN.
** Pathogenesis begins at birth.
of carbohydrate used in PN. It may be initiated at a rate of
about 4 to 8 mg/kg/min. This is comparable to the range of
endogenous glucose production rate in clinically stable
acids. The administration of glucose alone may result in hyper- infants.12,13 Normally, dextrose can be started at 10% con-
glycemia and cannot fully prevent tissue catabolism. Early centration, which delivers a glucose load of ∼7 mg/kg/min
administration of protein as amino acids may decrease the risk at 100 mL/kg/d. However, immediately after birth or dur-
for hyperglycemia and promote nitrogen retention. The usual ing acute stress events such as sepsis or corticosteroid ther-
starting dose for amino acids is 1 to 2 g/kg/day. The dose is apy, the sick or preterm infant may tolerate <5% dextrose
increased by similar amounts each day to the desired goal, solution, which provides a much lower glucose infusion
depending on the weight of the infant. Generally, the extremely rate. Dextrose concentration can be increased gradually at
low birth weight (ELBW, birth weight up to 1 kg) infant may about 2.5g/100 mL per day to deliver a load of 12 to 14 mg/
require up to 3.5 to 4 g/kg/day, the very low birth weight kg/min. For infants who need PN after a period of adequate
(VLBW, birth weight up to 1.5 kg) infant may require up to 3 enteral feeding, a PN infusate containing 10% or 12.5%
to 3.5 g/kg/day, and the term infant may require up to 2–3 g/ dextrose can be used from the onset, provided the blood
kg/day.1–4,6 Once EN is started, the volume (and therefore the glucose is normal.
amount) of nutrients from PN is correspondingly decreased. (2) A trace amount of glucosuria is not uncommon in critically
b) Commercial amino acid solutions used for infants are formu- ill infants, although glucosuria of >1% is of concern and the
lated to result in plasma amino acid profiles comparable to rate of glucose infusion may need to be decreased. The use

302 A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. © 2005 A.S.P.E.N. www.nutritioncare.org.
 S E C T I O N I V Surgical and Critically Ill Conditions

TABLE 26-2 Phases of Nutrition Support for Critically Ill Infants

Primary Source
Phase Duration* of Nutrient Goal

Immediate newborn period Days to weeks Parenteral nutrition** Minimize catabolism. Begin nutrition support within
and during acute illness 24 hours after birth. Aim to maintain normal biochemi-
cal status and some somatic growth, if possible.

Later neonatal period and Weeks to Enteral nutrition*** “Catch-up” growth. Aim to reach normal centile chan-
during hospitalization months nel for gestation and postnatal age.

Post–hospital discharge Months to years Enteral nutrition**** Slower growth rate than phase 2 but still may require
additional nutrients. Aim to achieve growth rate com-
parable to postmenstrual age–matched infants born at
term.

* May vary somewhat depending on the extent of functional immaturity and the course of underlying illness.
** Most critically ill infants require a period of PN during the transition to full enteral feeding.
*** Term infants require human (own mother's) milk or standard infant formula. Preterm infants require human milk with fortifier or specifically designed preterm formulas.
**** Ad libitum breast-feeding or standard formula. Preterm infants may require additional supplementation or use of specific postdischarge infant formula.

TABLE 26-3. Recommendations for Parenteral Nutrition Macronutrients for Neonates

Source Initiation Advancement Goal Neonate Blood or plasma monitoring

Amino acids 1.5–2 g/kg/d 0.5–1 g/kg/d 2–3 g/kg/d Term BUN, ammonia, arterial pH
1.5–2 g/kg/d 0.5–1 g/kg/d 3.5–4 g/kg/d ELBW
1 g/kg/d 0.25–0.5 g/kg/d 3–4 g/kg/d Septic, hypoxic Lactate concentration

Dextrose 8 mg/kg/min 1–3 mg/kg/min 12–14 mg/kg/min* ≥1 kg Glucose <150 mg/dL

6 mg/kg/min 1–3 mg/kg/min 12–14 mg/kg/min <1 kg Glucose <125 mg/dL

Fat 1–2 g/kg/d 0.5–1 g/kg/d 3 g/kg/d** Term Triglycerides <200 mg/dL***
and ****
0.5–1 g/kg/d 0.25–1 g/kg/d 3 g/kg/d Preterm Bilirubin, glucose
0.5 g/kg/d***** 0–0.5 g/kg/d 1–2 g/kg/d Hyperbilirubinemic****** Bilirubin*******
Sepsis
Severe respiratory distress

Energy 90–108 kcal/kg/d Term

100–120 kcal/kg/d Preterm

Fluid 130–150 mL/kg/d Term

130–180 mL/kg/d Preterm

BUN, blood urea nitrogen; ELBW, extremely low birth weight; FFA, free fatty acids
* Maximum recommended upper limit for glucose intake.
** May consider slightly higher dose in growth failure.
*** Heparin 1 unit per milliliter parenteral nutrition solution improves lipid clearance.
**** IV fat emulsion infusion over 24 hours maximizes clearance.
***** Minimum fat needed to prevent essential fatty acid deficiency.
****** Bilirubin approaching exchange transfusion levels.
******* IV lipid dose can be increased to normal range when bilirubin is below 50% of exchange level and when sepsis and respiratory distress is under adequate control
Adapted from: 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. J Par-
enter Enteral Nutr. 2002;26(1 suppl):1SA–138SA with permission.
Nash MA. The management of fluid and electrolyte disorders in the neonate. Clin Perinatol. 1981;8:251–262 with permission.
Table 26-3 adapted from work contributed by Gordon Sacks, Susan Mayhew, and Debbie Johnson.

© 2005 A.S.P.E.N. www.nutritioncare.org. A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. 303
S E C T I O N I V Surgical and Critically Ill Conditions

of insulin to treat hyperglycemia and promote growth in since both breast milk and infant formulas contain carnitine,
infants is not well established. Insulin infusion at 0.05 unit/ infants who received PN without carnitine have very low tissue
kg/hr14 has been associated with the development of lactic levels of carnitine. Since fatty acid oxidation is impaired when
acidosis. However, bolus doses of crystalline insulin may the tissue carnitine levels fall below 10% of normal, it seems
be useful to treat persistent hyperglycemia (blood glucose reasonable to provide L-carnitine at 2 to 10 mg/kg/d. This
>200 mg/dL) after lowering the dextrose concentration. In approximates the amount provided in human milk and the in
our experience, 0.05 to 0.1 unit/kg of crystalline insulin as utero rates of tissue carnitine accretion. There is no evidence
an intravenous bolus may be effective as an initial dose. that pharmacological concentrations of carnitine provide
Repeated monitoring of blood glucose and acid-base status greater benefit in infants in the absence of (rare) metabolic
at 1- to 4-hour intervals is needed to determine whether defects of carnitine metabolism.
there is a further need for insulin. Insulin administration 3. Electrolytes and minerals
should be discontinued when the blood glucose is <100 mg/ a) Sodium and potassium are available as chloride, acetate, and
dL. It is important to monitor for and manage other condi- phosphate salts. During the first one to two days after birth,
tions (e.g., sepsis) that could contribute to hyperglycemia. parenteral nutrition for small preterm infants need not contain
b) Fat emulsions. Available commercial fat emulsions provide a potassium until regular urine output is assured; and sodium
source of concentrated calories and prevent essential fatty acid phosphate can be used as the only source of sodium. The lat-
deficiency (EFAD). Fat emulsions are isotonic. When fat and ter practice allows the flexibility to use small amounts of
amino acid–dextrose solutions are infused simultaneously into sodium bicarbonate as needed and minimizes the risk of hyper-
the same vessel, the patient receives a higher energy and lower natremia if there is high insensible loss of water. The normal
osmolar solution (which helps spare peripheral veins from range of maintenance intake for sodium and potassium is 2 to
thrombophlebitis) than with amino acid–dextrose alone. Com- 4 mEq/kg/d.
mercial fat emulsion is available as 10% (1.1 kcal/mL) and 20% b) Calcium is usually delivered as 10% calcium gluconate. Phos-
(2 kcal/mL) soy or soy-safflower oil. These preparations con- phorus is added as either a sodium or a potassium salt. During
tain >40% by weight linoleic acid and >4% by weight linolenic the first one to two days after birth, the parenteral nutrition for
acid. The use of 20% emulsion is preferred since it is more small preterm infants may contain about half the mainte-
energy-dense and contains the same amount of phospholipid nance phosphorus content to minimize the risk for hyper-
(1.2% by weight) and same osmolarity as the 10% emulsion. phosphatemia. Sodium phosphate is preferred unless there is a
Phospholipid is believed to inhibit lipoprotein lipase, the main risk for hypernatremia. Potassium phosphate can be used in the
enzyme for intravenous lipid clearance. Newer lipid prepara- presence of adequate urine output. Maintenance calcium and
tions not available in North America include those containing phosphorus are usually added at 500 to 600 mg of elemental
structured triglycerides (mixture of long- and medium-chain calcium per L and 350 to 500 mg of elemental phosphorus per
fatty acids on a glycerol backbone) and water-soluble short- L of PN at a weight ratio of ∼1.3 to 1.7:1 (or 1 to 1.3:1 by molar
chain triglycerides, which may have some metabolic advan- ratio). The ability to maintain calcium and phosphorus solubil-
tages compared with the available lipid emulsions with ity in PN solution depends on a number of factors, particularly
long-chain triglycerides. However, none of the fat preparations the type and amount of amino acid and the presence of cysteine.
appear to be able to support the normal rate of intrauterine accu- The amount of calcium and phosphorus delivered in PN is sev-
mulation of very long chain polyunsaturated fatty acids of the eral times greater than that absorbed from human milk.
n-3 and n-6 families in developing infant tissues. c) Magnesium is usually added to PN at 25 to 50 mg/L of ele-
Administration of fat emulsion in an energy-deficient state mental magnesium. The amount of magnesium may need to be
may not adequately prevent development of EFAD because decreased in sick infants with impaired renal function or tran-
EFAs can be oxidized to meet energy needs. However, in siently withheld or provided in a lower amount for infants whose
the presence of adequate energy intake, a minimum of 0.5 mothers received intrapartum magnesium sulfate infusion.
to 1 g/kg/d of commercial fat emulsion containing the C18 fatty d) Chloride and other anions are normally provided in sufficient
acids, linoleic acid, and linolenic acid is needed to prevent clin- quantities if the minerals or cations are given in the recom-
ical EFA deficiency. Fat emulsion can be started on the first mended amounts. Current commercial amino acid prepara-
day of PN at 0.5 to 1 g/kg/d and increased by a similar tions for infants contained minimal amount of chloride at 0.46
amount daily up to 3 g/kg/d. To maximize lipid clearance, the to 0.97 mEq per gram of amino acid. Some clinicians also use
daily amount of fat emulsion is generally infused over 18 to small amounts of acetate (10–20 mEq/L PN solution) as part
24 hours. Smaller increments and lower total dose may be of anion intake and as a source of base to lower the risk of
prudent for acutely ill or ELBW infants. metabolic acidosis.
Jaundice and sepsis are not absolute contraindications to the e) Supplemental iron usually is not provided with PN for
use of fat emulsions. The dose probably should be in the range patients in the NICU. However, if PN is provided exclusively
of 1 to 2 g/kg/d if serum bilirubin is near the exchange level15 for >2 months after birth or if iron deficiency develops, par-
and during the acute phase of sepsis. Parenteral fat can be enteral iron can be administered at 0.1 to 0.2 mg/kg/d, up to as
increased to the normal dose once the serum bilirubin or sep- high as 10 mg/kg/d.17 Three parenteral products are currently
sis is controlled. available in the United States: iron dextran, sodium ferric glu-
Carnitine plays an essential role in the metabolism of long- conate complex in sucrose, and iron sucrose. Except for iron
chain fatty acids. However, no convincing evidence of clinical dextran, the experience with use of iron products in children is
benefit has been demonstrated in infants receiving carnitine- extremely limited.
supplemented PN; specifically, there was no evidence of effect 4. Trace minerals. Trace mineral preparations are commercially
on weight gain, lipid utilization, or ketogenesis.16 Nevertheless, available as single agents or as combinations of various trace min-

304 A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. © 2005 A.S.P.E.N. www.nutritioncare.org.
 S E C T I O N I V Surgical and Critically Ill Conditions

erals. There is no compelling reason to avoid providing trace min-

erals for infants requiring short- term PN, and they probably TABLE 26-4. Factors Affecting Water Requirements19
should be provided from initiation of PN. Recommended normal
daily trace mineral intakes are the same for preterm and term Environmental Factors Infant Factors
infants, except for zinc. Recommended intakes are as follows:
Factors increasing water requirements
chromium 0.2 mcg/kg; copper 20 mcg/kg; iodide 1 mcg/kg; man-
ganese 1 mcg/kg; molybdenum 0.25 mcg/kg; and selenium 2 mcg/ Radiant warmers Physiologic
kg.4 Zinc dosing for preterm infants is 400 mcg/kg; for term infants Increased permeability of the skin
Conventional single-walled
<3 months, 250 mcg/kg; and at >3 months, 100 mcg/kg. The use Larger body surface area relative
isolette
of both single and combination trace mineral preparations is usu- to body weight
ally needed to provide the recommended doses. Most institutions Phototherapy Increased blood flow to the skin
provide PN solutions containing chromium, copper, manganese,
Ambient temperature above Pathologic
selenium, and zinc.
the neutral thermal range Increased respiratory distress
5. Multivitamins. Two commercial multivitamin products are avail-
able for use in infants. Both products have the same contents in the Elevated body temperature
same concentration. Neither provides the exact range of estimated Glycosuria with osmotic diuresis
needs for all vitamins,4 and none of the several recommended Gastric or intestinal losses
dosages has been demonstrated to be superior for sick infants. The
manufacturers recommended that for infants weighing <1 kg, 1 to Factors decreasing water requirements
3 kg, and >3 kg, the intake should be 30%, 65%, and 100% of a
Thermal blankets Physiologic
5-mL vial. The American Academy of Pediatrics4 recommends
Double-walled isolette Increasing gestation and post-
2 mL/kg/day up to one vial (5 mL) of multivitamins. The Ameri-
can Society of Clinical Nutrition18 recommends 40% of a 5-mL menstrual age
Above-ambient humidity Pathologic
vial (2 mL) to patients less than 2.5 kg, and one vial (5 mL) to
patients >2.5 kg up to 11 years. Renal oliguria
C. Delivery
1. Peripheral or central catheters Adapted from Doyle LW, Sinclair JC. Insensible water loss in newborn infants. Clin
a) Peripheral catheter. To minimize thrombophlebitis, only PN Perinatol. 1982;9:453–482, with permission from Elsevier.
solutions with amino acids and a <12.5% concentration of dex-
trose are delivered via a peripheral intravenous catheter.4 Coin-
fusion of fat emulsions reduces the degree of venous irritation. 4. A 2-in-1 versus a 3-in-1 solution. The amino acid–dextrose solu-
b) Central catheter. Higher dextrose concentrations (>12.5%) can tion and lipid emulsion can be provided separately as a 2-in-1 solu-
be delivered through the central catheter to a large vessel with tion and delivered together through a Y connector to the peripheral
high blood flow. Insertion of the catheter into the central venous or central venous catheter or through umbilical venous or arterial
system by cutdown, percutaneously, or through the umbilical catheters. In some institutions, PN is delivered as a total nutrient
artery or vein is widely used in neonates. Central catheter place- admixture (TNA) or 3-in-1 solution (i.e., mixing all nutrient com-
ment must be confirmed by x-ray before infusion of PN solution. ponents in the same container). The disadvantages of TNA in the
2. Volume. The delivery of adequate amounts of nutrients parenter- NICU are that the stability of each component of TNA is not com-
ally often is limited by the amount of fluid that the sick infant needs pletely defined, it is impossible to determine whether there is a pre-
or can tolerate. In situations of severe fluid restriction, the concen- cipitation of nutrients in the admixture, and a 1.2 micron filter
tration of all nutrients must be increased, resulting in extremely must be used instead of the standard 0.22 micron bacterial filter.
high osmolarity and possibly exceeding the limits of solubility of TNA also may be a better bacteria growth medium than amino
calcium and phosphorus salts. In contrast, in situations of high acid–dextrose solution.4
fluid requirements (>200 mL/kg/d) in preterm infants with low 5. Light exposure. Amino acid–dextrose solution containing vita-
renal thresholds for many nutrients, a diluted infusate must be pro- mins and other additives and lipid emulsion should be protected
vided to prevent delivery of excessive nutrients, particularly dex- from direct exposure to phototherapy light to avoid photodegra-
trose. Normally, adequate amounts of parenteral nutrients can be dation. Some NICUs routinely protect PN infusate from expo-
delivered in a total volume of 120 to 160 mL/kg/d. Some flexibil- sure to ambient light.
ity in the tolerance to the volume infused can be achieved by D. Monitoring (see Tables 26-3 and 26-5).
manipulating environmental factors. For example, caring for the E. Complications. The potential complications of PN are all seen in
neonate under a radiant warmer results in greater insensible fluid the NICU patient.
loss, thus allowing delivery of a larger volume of PN (Table 26-4). 1. Mechanical
3. Infusion rate. In the NICU, amino acid–dextrose solution is a) Kinking, compression, or tearing of the catheter can occur with
infused continuously over 24 hours to improve tolerance, particu- all central catheters, but the thin-walled percutaneously inserted
larly if higher concentrations of dextrose are used. Fat emulsion is Silastic catheters used in neonates appear to be more prone to
also better tolerated if infused over 18 to 24 hours each day. Infus- kinking and compression. Pneumothorax and brachial plexus
ing fat emulsion over about 18 hours allows the measurement of injury may complicate the percutaneous insertion of a subcla-
plasma triglyceride level immediately prior to the next day’s infu- vian catheter.
sion, which makes it possible to determine tolerance to fat emul- b) Catheter occlusions presumed to be associated with thromboses
sion without concern about interference from the triglyceride are treated with 0.25 to 2 mg (0.25–2 mL) of tissue plasmino-
content of the lipid emulsion. gen activator (tPA) or 5000 units (1 mL) of urokinase instilled

© 2005 A.S.P.E.N. www.nutritioncare.org. A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. 305
S E C T I O N I V Surgical and Critically Ill Conditions

in the catheter for 30 to 60 minutes; then the blood and tPA or

TABLE 26-5. Guidelines for Metabolic Monitoring Dur- urokinase is aspirated from the catheter. This may be repeated
ing Parenteral Nutrition once. For chemical (e.g., calcium phosphate) or medication pre-
cipitate, 0.1N hydrochloric acid (HCl) (1 mL) or 0.1N sodium
Variable to hydroxide (NaOH) (1 mL) may be used with the same tech-
Be Monitored Initial Period* Later Period** nique. For lipid-related occlusion in TNA, 70% ethanol (1 mL)
may be used with the same technique. Some clinicians flush
Growth*** tPA or urokinase through the catheter to gain patency of the
• Weight Daily Daily catheter. In infants, experience with the use of these agents as
• Head circumference Baseline Twice weekly therapy for catheter occlusion, particularly for the percutaneous
• Length Baseline Weekly Silastic catheter, is limited.
c) Extravasation of nutrient infusate into interstitial space result-
Intake and output Every shift Daily ing in skin slough is a frequent complication associated with the
use of peripheral intravenous catheters in infants. This compli-
cation can be reduced by meticulous observation of the catheter
Glucose reagent strips 1 to 3 times/day As indicated
insertion site and removal of the catheter at the first sign of
swelling or thrombophlebitis. Extravasation of nutrient infusate
Serum electrolytes, Baseline and every Every 1 to 2 weeks into the pleural or pericardial space occurs rarely but may be
urea nitrogen, 1 to 3 days associated with acute metabolic (decreased plasma glucose),
creatinine circulatory, or respiratory compromise requiring symptomatic
support, including drainage of the fluid.
Serum calcium, Baseline and every Every 1 to 2 weeks 2. Sepsis
magnesium, 2 to 3 days a) Source identification. Sources of infection can be catheter
phosphorus related, involving the catheter insertion site, the subcutaneous
tunnel, or line sepsis (see Chapter 8). Non-catheter-related
Serum Daily during dose Every 1 to 2 weeks sources of sepsis should also be considered.
b) Diagnosis. Cultures of blood drawn from the catheter, a non-
triglycerides**** increase
catheterized blood vessel, and obvious sites of septic foci are
needed.
Serum glucose As needed As needed c) Therapy. Empiric antibiotic therapy should be started whenever
sepsis is suspected (e.g., sudden, unexpected glucose intoler-
Total and direct Baseline, as needed Every 1 to 2 weeks ance or temperature instability). Initial therapy should be based
bilirubin clinically on the clinical status of the neonate and the antibiotic sensitiv-
ities of microbial organisms prevalent in the NICU. Antibiotics
Total protein and Baseline Every 2 to 3 weeks should be adjusted on the basis of culture results. Catheter
albumin removal is indicated if sepsis is not promptly resolved. Some
clinicians recommend immediate catheter removal if there is
Alanine Baseline Every 2 to 3 weeks evidence of a fungal infection or some gram- negative rods such
as Klebsiella. Antibiotic lock and antimicrobial- impregnated
aminotransferase,
central venous catheters are not routinely used in NICU
aspartate amino-
patients.
transferase, and 3. Metabolic. Most metabolic complications are related to excessive,
alkaline phosphatase imbalanced, or inadequate intake.1 A recent shortage of multivit-
amin preparations resulted in more than 30 cases of vitamin
Complete blood Baseline Every 2 to 3 weeks deficiency.20
cell count a) Glucose disturbances. Hyperglycemia from excessive glucose
load or during short-term stress such as sepsis may result in glu-
Vitamin and trace As indicated As indicated cosuria, osmotic diuresis, and dehydration. Treatment of the
mineral status and underlying cause, a decrease in glucose load, and even the use
other specific tests of insulin for brief periods may be needed to correct hyper-
glycemia. Hypoglycemia may occur with abrupt discontinua-
tion of lipid-free PN containing >12.5% dextrose.
*The period before reaching maximum doses of glucose, amino acids, and lipid emul- b) Hypertriglyceridemia. Plasma triglyceride >200 mg/dL may
sion, or during any period of metabolic instability. This period normally lasts 3 to 4 occur during lipid infusion. The infusion of lipids over 18 to
days.
24 hours and the use of heparin in a dose of 1 unit/mL may
**The period during which the patient is in a metabolic steady state. For clinically sta-
increase lipid clearance. The latter increases lipoprotein lipase
ble infants receiving the desired intake of nutrients, the interval between laboratory
measurements may be increased beyond the above recommendations. activity. The use of carnitine may be beneficial in clearing
***All measurements should be plotted on growth charts appropriate for sex, gesta- triglycerides.
tion62 and postnatal63 age. Growth charts based on postnatal growth of preterm c) Mineral (calcium, phosphorus, magnesium), blood urea nitro-
infants are biased for nutritional management regimens and should not be used. gen (BUN), and acid-base disturbances. Hyper- or hypocal-
****Target level <200 mg/dL. cemia and hyper- or hypophosphatemia can result from

306 A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. © 2005 A.S.P.E.N. www.nutritioncare.org.
 S E C T I O N I V Surgical and Critically Ill Conditions

excessive or inadequate infusion of these minerals. In addition, ally, this is well tolerated by many VLBW infants because of
phosphate deficiency with hypophosphatemia and secondary the greater sodium needs secondary to decreased renal tubu-
parathyroid hormone resistance can cause hypercalcemia even lar absorption of sodium or concurrent diuretic therapy. Glu-
in the presence of low calcium intake.21 Phosphorus must be cose in the flushing solution can cause swings of blood sugar
added to the PN if serum phosphorus is <4 mg/dL during in VLBW infants. Only preservative-free flush solutions
infancy. Hyperphosphatemia (and secondary hypocalcemia) should be used.
may occur in preterm infants receiving high phosphorus intake g) PN-associated cholestasis26–28
because of limited renal excretory capacity. Adjustments may (1) Risk factors. The incidence varies inversely with the degree
be needed for one or both minerals. Hyper- or hypomagnesemia of prematurity, the duration of PN (>2 weeks), excessive
can result from excessive intake or inadequate renal excretory intake of calories and nutrients (e.g., glucose, lipids, amount
capacity, or inadequate intake or replacement of gastrointesti- and type of amino acids, copper, manganese), sepsis, and
nal losses.22 impaired intestinal function, including dysmotility, bowel
d) The potential for metabolic acidosis is higher during the imme- rest, and lack of enteral feedings.
diate newborn period and during acute stress. Abnormal serum (2) Management. Enteral feedings should be initiated and con-
chloride levels from inappropriate intake or inadequate replace- tinued if feasible. However, PN should not be discontinued
ment of losses can be associated with metabolic acidosis or if the infant is unable to tolerate enteral feeding. Excessive
alkalosis. intake of nutrients, particularly the nutrients that require
e) Increased BUN or plasma ammonia has been reported only in normal metabolic or excretory function of the liver, should
infants who received >4 g protein/kg/d and from the use of ear- be avoided. For example, protein intake should be the min-
lier amino acid preparations.4 Starvation and tissue catabolism imum that allows adequate growth and good nutritional sta-
is a more likely cause of raised BUN in the absence of docu- tus, and copper and manganese supplements may need to
mented renal failure. Underlying disease processes also may be held or reduced and their status monitored. Use of pedi-
result in disturbances of acid-base status. Occasionally, symp- atric amino acids solutions and change from continuous
tomatic treatment of metabolic acidosis with sodium or potas- infusion to cyclic PN may improve the cholestasis. Med-
sium acetate and treatment of metabolic alkalosis with sodium ications such as cholecystokinin, ursodeoxycholic acid, and
or potassium chloride may be appropriate. phenobarbital have been used with varying success to stim-
f) Decreased nutrient availability. Decreased nutrient availability ulate bile flow and lower the bilirubin level.
may result from adsorption to delivery systems (e.g., insulin, h) Metabolic bone disease21,29–31
vitamin A), light (especially phototherapy) degradation (e.g., (1) Risk factors. Metabolic bone disease incidence varies
tryptophan, methionine, histidine, riboflavin, vitamin A), and directly with degree of prematurity, duration of PN
increased nutrient loss (e.g., electrolyte, mineral, or trace metal (>4 weeks), prolonged volume restriction, PN solutions
loss from loop diuretics and to a lesser extent from thiazide with low mineral (calcium and phosphorus) content, sec-
diuretics; potassium and magnesium loss with amphotericin B). ondary vitamin D deficiency from calcium and/or phos-
g) Toxic products. Toxic products in PN can be found as con- phorus deficiency,29,31 aluminum contamination of nutrients,
taminants of nutrients or from exposure to the environment delayed initiation and delay in achieving the full volume of
during preparation, storage, or delivery to the patient. appropriate enteral feeding, and prolonged excessive phar-
(1) Aluminum is the best-studied contaminant of parenteral macotherapy, in particular, with loop diuretics and corti-
nutrients. Aluminum has no known physiologic role, and costeroids. Excessive force (e.g., physical restraint during
preterm infants and infants with severe renal impairment surgery) or during physical therapy has occasionally caused
are at risk for aluminum toxicity. Many nutrient compo- fractures in osteopenic patients.
nents of PN are contaminated with aluminum, and the same (2) Management. Enteral feedings should be initiated and con-
nutrients from different manufacturers can have different tinued if feasible. However, PN should not be discontinued
degrees of aluminum contamination.23 Calcium salts alone if the patient is unable to tolerate enteral feeding. The rec-
accounted for >80% of the total aluminum load from PN.23 ommended minerals, vitamin D, and other nutrients should
The Food and Drug Administration has labeling require- be maintained in the PN solution. Pharmacotherapy and
ments concerning aluminum contents on all PN compo- physical therapy should be reassessed and modified if nec-
nents, and efforts should be made to use products with the essary. Supplementation with calcium and/or phosphorus
lowest aluminum contamination. alone is not recommended since a balanced intake of all
(2) Formation of toxic lipid peroxidation products is also of nutrients is necessary for normal bone growth.
potential concern. Ambient and especially phototherapy i) Oral aversion. Oral aversion may occur in chronically ill infants
light increase peroxidation of fatty acids lipid emulsion to who have not been fed for many months. Difficulty in achiev-
form lipid hydroperoxides24 and also increase hydrogen ing adequate nipple feeding is particularly notable in ELBW
peroxide generation from multivitamins, in particular the infants and those who have experienced hypoxic insults. Non-
riboflavin in amino acid–dextrose solutions.25 nutritive sucking during the course of illness does not appear to
f ) PN flush solutions and drug-nutrient interactions. All med- improve the ability to nipple-feed; actual oral feeding is neces-
ications not compatible with PN infusate should be adminis- sary for the development of sucking behavior.32
tered as close to the catheter entry site as possible or via a
separate catheter. Most, but not all, medications can be flushed
III. Enteral Nutrition
with normal saline before and after infusion of medication to
minimize any risk of drug-nutrient interaction. Normal saline A. Assessing readiness for enteral feeding. For the healthy neonate born
flush solutions can result in significant sodium intake. Gener- at term, transition from the placental source of nutrients to enteral

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S E C T I O N I V Surgical and Critically Ill Conditions

feeding usually occurs within a few hours after birth once physio- Encouragement and support of the mother may be needed to
logic adaptation to the extrauterine environment is achieved. For the maintain the milk supply. Routine use of oxytocin nasal spray
sick and/or premature neonate, indicators of readiness for enteral to promote a let-down response or metoclopramide to stimu-
feeding include the following: late prolactin secretion, and the use of herbal products to stim-
1. Absence of gastrointestinal anomalies that interfere with adequate ulate milk production, are not recommended.
delivery, digestion, or absorption of enteral nutrients c) Plastic containers are preferred to glass containers for storage of
2. Cardiorespiratory stability as indicated by the absence of respira- breast milk.36 Fresh breast milk can be refrigerated for 48 hours
tory distress and consistently normal vital signs. The prone or side- without significant microbial growth. During transport from
lying position with the head of the bed elevated generally improves the home to the hospital, fresh milk should be cooled or
respiratory gas exchange and decreases gastroesophageal reflux frozen by packing tightly in a cooler with freezer gel packs.
and aspiration. Frozen milk can be stored for about 3 months in a home freezer
3. Controversial issues. There are generally no contraindications to at −20 degrees Celsius (−4 degrees Fahrenheit).37 Frozen milk
enteral feeding under the following conditions, provided the infant should be thawed in the storage container in a refrigerator or
is clinically stable: under cool running water. Boiling or microwave heating can
a) Mechanical ventilation or continuous positive airway pressure affect the nutritional and immunologic properties of human
b) Indwelling umbilical vein or arterial catheters milk. Thawed or refrigerated milk is often warmed under hot
c) Perinatal asphyxia water and several drops of milk should be dripped onto the dor-
d) Inotropic, sedative, or indomethacin therapy sum of the hand to confirm that it is not too hot prior to feeding
B. Enteral preparations the baby.
1. Human milk. The advantages to the use of human milk include d) The use of donated human milk is controversial, and the
psychosocial benefits to the mother and easy digestibility, low for- practice remains regional.
mula and renal solute load, and potential benefits from immuno- 2. Commercial preparations
logic and trophic factors for the infant.33 Human milk contains a) Infant formulas are designed to substitute for human milk in
long-chain polyunsaturated fatty acids (LCPUFA) of the n-3 and the event that the mother decides not to breast-feed or in the
n-6 fatty acid families, and some data show possible neurological presence of contraindications to breast-feeding. For infants
or visual developmental advantages in preterm infants fed human born at term or small preterm infants beyond 6 to 12 months of
milk compared to those fed formulas without LCPUFA supple- postnatal age, standard cow milk–based infant formulas should
mentation.34 There are very few contradictions to feeding human be used. There are limited indications for soy formula38 or par-
milk.33 These include the presence of certain maternal systemic tially hydrolyzed protein formulas.39 Highly modified infant
infections such as tuberculosis and human immunodeficiency formulas based on extensive protein hydrolysates or amino
virus, and certain metabolic disorders affecting the infants, includ- acids are used in certain allergic or intestinal disorders (see
ing galactosemia. A number of drugs may be secreted into human Section IV).
milk, but not all are thought to be of concern to the infant.35 The For small preterm infants, only formulas designed specifically
mother should be encouraged to discuss any use of prescription to meet the nutrient requirements of VLBW infants should be
drugs, over-the-counter drugs, or herbal medications with the used.40 The two commercially available iron-fortified preterm
physician. Presence of jaundice (if determined to be breast infant formulas contain whole protein with a whey-casein
milk–associated jaundice) does not preclude continuation of weight ratio of 60:40, long-chain and medium-chain triglyc-
breast-feeding, although a 24- to 48-hour substitution with infant erides in an approximate weight ratio of 1:1, and lactose and
formula may be useful as a diagnostic test and for management. glucose polymers in an approximate weight ratio of 1:1. All
a) Human milk can be the exclusive source of nutrition for all other nutrients, including LCPUFA, are added in amounts
term infants for 4 to 6 months after birth.33 For small preterm designed to meet the nutrient requirements of preterm infants
infants, breast milk has insufficient amounts of protein, energy, when fed at about 150 mL/kg/d. Both commercial preterm
sodium, calcium, phosphorus, vitamin D, zinc, and probably infant formulas are available in 20 or 24 kcal/oz preparations
folic acid to for adequate growth. Commercial powder or liq- and all are isotonic. The higher nutrient density preparation can
uid human milk fortifier containing multiple nutrients should be used as the initial feeding and there is no advantage in the
be used to supplement all small preterm infants fed human use of the lower density preparation.
milk, at least until ad libitum breast-feeding begins. Soy protein–based formula should not be used because of
b) Critically ill infants are usually unable to nipple-feed and may uncertain mineral absorption and higher concentrations of some
not tolerate enteral feeding, and mother’s milk is collected for trace elements such as manganese and aluminum. Protein
delivery via gavage feeding or stored for later use. A lactation hydrolysate formulas with other highly modified macronutri-
specialist may be helpful in teaching and assisting in breast- ents, including a high proportion of medium-chain triglycerides
pumping techniques and for support in maintaining lactation with glucose polymers as the sole source of carbohydrate, the-
for the mother. Manual expression of breasts or mechanical oretically can improve absorption of these nutrients. However,
aids can be used depending on the mother’s preference. An VLBW infants who receive these formulas may have distor-
electric breast pump that allows simultaneous emptying of tions of the plasma aminogram, lower total nitrogen absorption
both breasts shortens the duration of milk expression and tends and retention, and lower phosphorus absorption compared with
to encourage the most milk production. Breast pumping should those fed formulas designed specifically for VLBW infants.
begin within 24 hours after delivery and should be done every Elemental formulas containing free amino acids are rarely
3 to 4 hours during the day and once or twice at night. A ster- needed and should be used only under the supervision of physi-
ile bottle or plastic bag should be used for each collection. cians with special knowledge of nutrition support in infants. It
Maternal stress and fatigue can decrease milk production. is important to note that commercial milk powder preparations

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 S E C T I O N I V Surgical and Critically Ill Conditions

are not sterile and are not recommended for in-hospital use for static activities and increase generation of free radicals and per-
small preterm infants unless there is no suitable alternative.41 oxidation products.44,45 Medicinal iron given as once or twice
Careful preparation and handling of all infant formulas, daily supplementation is a proven effective therapy and may be
particularly those prepared from powder, is warranted. All preferably to the continuous contact of human milk to the high
formulas should be fed immediately or refrigerated and fed iron containing fortifier. No fluoride supplementation is rec-
within 24 hours of preparation. For infants requiring contin- ommended for infants in the first 6 months of life. Thereafter,
uous infusion of milk feeding, the “hang time” of each feed daily supplementation of 0.25 mg of fluoride until 3 years of
type depends on institution practice. In any case, hang time of age is recommended if the drinking water contains <0.3 ppm of
>4 hours is not recommended for enteral feeding.42,43 For fluoride.50
human milk containing human milk fortifier, the maximum e) Commercial modular nutrient components are available to meet
suggested hang time is 4 hours. the increased or altered dietary needs of infants in the NICU.
b) Commercial human milk fortifiers are available from two man- These components include carbohydrate, fat, and protein mod-
ufacturers in North America. They provide additional energy ules. Modular protein products may be used to increase protein
and multiple nutrients when added to human milk. The contents density (but are only available in powder), and emulsified fat
of the two commercial fortifiers differ, and when the fortifiers products, medium-chain triglyceride, or glucose polymer may
are added to human milk in the recommended amounts, the be used to increase caloric density. The use of modular nutri-
final nutrient compositions tend to resemble the commercial ents may result in imbalanced intake of various nutrients. For
preterm infant formulas from the respective manufacturers. The example, increased protein density may result in an abnormal
optimal level of iron content in human milk fortifier is contro- plasma aminogram, and increased caloric density may result in
versial. In vitro studies indicated that a higher iron content may excessive fat deposition as adipose tissue and in various organs
adversely affect the bacteriostatic properties of human milk (including the liver), with adverse consequences. Thus, sick
against Escherichia coli, Staphylococcus, Enterobacter sakaza- infants without significant gastrointestinal problems can have
kii, and group B streptococcus,44 and results in greater genera- the infant formula concentrated. For those without the need for
tion of free radicals and lipid peroxidation products.45 Thus, use severe fluid restriction, the use of a greater volume of mother’s
of a low iron–containing human fortifier may be preferable. milk or infant formula is preferred since the intake of all
However, one report of short term (up to 28 days) use of human nutrients is proportionally increased. The experimental use
milk fortifier with 1.44 mg of iron added to 100 mL of human of recombinant human lactoferrin, oligosaccharides, prebiotics,
milk showed there was no increase in the incidence of sepsis or and probiotics in the diet holds promise to improve the gastro-
necrotizing enterocolitis.46 The low-iron, insoluble calcium intestinal function and growth of sick and healthy infants.
salt-containing human milk fortifier also resulted in better C. Feeding methods. Enteral feeding methods should be individualized
growth than the one with soluble calcium salts.47 In terms of on the basis of gestational age, clinical status, and expected tolerance
product sterility, there is no alternative to powdered human to feeding. Before about 32 weeks postmenstrual age (PMA), most
milk fortifier for in-hospital use. When mixed with human milk, preterm infants require gavage feeding because the integration of
the fortified milk should be used within 4 hours of preparation. sucking, swallowing, gastrointestinal motility, and breathing neces-
A sterile liquid human milk fortifier is available, but when used sary for successful oral feeding is generally inadequate. Between 32
according to the manufacturer’s directions, it reduces human and 36 weeks PMA, the preterm infant may need a combination of
milk intake by 50%. gavage and bottle (or breast) feedings. Once a coordinated suck and
c) Vitamin D supplementation is recommended for all infants swallow are present, the change to full oral feedings usually can be
receiving human milk as an exclusive source of nutrition.48 It is established within 1 to 2 weeks.51 Avoidance of hypoxemia is critical
often part of commercial infant multivitamin preparations. to successful enteral feeding. Use of a pulse oximeter should be part
Preterm infants, especially ELBW infants, are often given addi- of the management during the transition from gavage to oral feedings.
tional multivitamin supplementation containing 400 interna- Parameters that should be evaluated include heart rate, respiration,
tional units of vitamin D early in their course, whether they are and oxygenation relative to baseline through sucking and the post-
receiving fortified human milk or preterm infant formula. Anec- feed period. Illnesses, particularly those affecting the central nerv-
dotal reports exist for hypercalcemia with or without hypervit- ous system—whether congenital or secondary to severe asphyxia
aminosis D in VLBW infants receiving preterm formula or insult—can affect the normal maturation of the physiologic actions
fortified human milk with additional vitamin D or multivitamin needed for successful nipple feeding.
supplementation. In any case, vitamin supplementation is 1. Gastric gavage
unnecessary when these infants reach about 2 kg and are receiv- a) Indications include infants with a poor suck-and-swallow
ing adequate feedings of fortified human milk or preterm infant reflex, such as extremely premature infants and infants with
formula. congenital or acquired neuromuscular disorders. Gavage feed-
d) For term infants, adequate intake of iron during the first ing may be used during the transition from PN to EN or during
6 months is <0.3 mg/d and can be met by breast-feeding alone. the establishment of nipple feedings. Some infants with high
For the small preterm infant, the recommended daily iron intake respiratory rates may require gavage feeding, although enteral
is 1.7 to 2.5 mg elemental iron/100 kcal (2–4 mg/kg) during feeding probably should be withheld if the respiratory rate
early infancy. Iron supplementation can be started once the exceeds 80 breaths per minute to minimize the risk of aspiration.
infant achieves full enteral feeding and continues for the first b) The appropriate size gavage tube, which ranges from a 5F to
year up to a maximum of 11 mg of elemental iron per day.49 For an 8F catheter for intermittent gavage feeding, or an anchored
infants receiving erythropoietin therapy, the iron requirement is indwelling naso- or orogastric catheter, should be selected. For
substantially higher, and 10 mg/kg/d has been used.17 Pro- ELBW infants, the smaller catheter is preferred to minimize
longed contact of human milk with iron may impede bacterio- occlusion of the nares, although an anchored orogastric tube

© 2005 A.S.P.E.N. www.nutritioncare.org. A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. 309
S E C T I O N I V Surgical and Critically Ill Conditions

may result in less airway resistance and less impairment of b) Placement method. Gastrostomy tubes are percutaneously
minute ventilation than a nasogastric tube. placed by radiologists with skill in invasive procedures or by
c) Clinical verification of correct tube placement must be done surgeons as a specific surgical procedure. Tubes can be eas-
immediately after insertion, at regular intervals during each ily replaced 2 to 3 weeks after the initial operative procedure.
nursing shift, and prior to each bolus feeding. c) Potential complications
d) Polyvinyl chloride catheters should be changed every 24 to (1) Risk of surgical and anesthesia procedures
48 hours to prevent stiffening of the plastic and potential gut (2) Local skin breakdown
perforation. Silastic or polyurethane catheters are preferable if (3) Leakage of gastric contents around the gastrostomy tube
a feeding tube is to be left indwelling for more than 72 hours. insertion site
e) For continuous gavage feedings, the amount of breast milk (4) Accidental removal of tube or tube migration
or formula placed on the constant-rate infusion pump should (5) Gastroesophageal reflux worsening with gastrostomy with-
be only the amount that is to be delivered for a 3- to 4-hour out fundoplication
period. Possible advantages compared with bolus feeding 4. Nipple feeding
include less abdominal distention, improved intestinal absorp- a) Breast-feeding. General hygienic practice is essential. This
tion, better tolerance to feeding, and faster growth rates. Pos- includes hand washing and making sure the breast/nipple area
sible disadvantages may include increased risk of aspiration is clean before feeding. A lactation consultant or clinician can
from the potential for increased gastroesophageal reflux (com- teach and support the mother to help ensure effective breast-
mon in this population) or dislodgment of the feeding tube feeding. Postsurgical infants may need additional positioning
from the stomach to above the gastroesophageal junction. In supports to minimize stress on the surgical incision. The
addition, when breast milk is continuously infused, large infant should be assessed for respiratory and gastrointestinal
amounts of fat may be lost with separation and layering of tolerance, sucking strength, and coordination. The feeding
fat in the delivery system. This loss can be minimized by tilt- duration on each breast should start at 3 to 5 minutes, there-
ing the infusion pump so the fat is delivered before the water- after increasing daily by 1 to 2 minutes, up to a total of 10 to
soluble portion. 12 minutes per breast per feeding. For some infants, supple-
f) For bolus gavage feeding, most infants weighing >1500 g will mental gavage feedings after breast-feeding attempts may be
tolerate feedings every 3 hours. Each feeding can be delivered needed during the transition to complete breast-feeding. Con-
by gravity or infused over 15 to 20 minutes. Smaller infants tinued support and education helps promote a let-down reflex
may require delivery over 1 to 2 hours to improve tolerance to and a positive breast-feeding experience for both the mother
intermittent bolus feeding. Possible advantages compared with and the infant. Test weighing after breast-feeding to determine
continuous gavage feedings include more complete delivery of the volume of milk ingested is unnecessary. Observing the
nutrients. For example, there is less risk of mineral sedimenta- infant during breast-feeding, monitoring urine and stool pat-
tion from high-mineral preterm infant formula or separation of terns, and following daily and preferably weekly weight gains
human milk fat during delivery. In addition, bolus gavage feed- are better indicators of successful breast-feeding. If there is a
ing is simple to administer and requires minimal equipment. local breast infection, milk should be expressed from the
Possible disadvantages may include an increased risk of gastric breast and discarded.
residuals, abdominal distention, and gastroesophageal reflux. b) Bottle feeding. Appropriate flow from the nipple is important.
g) Potential complications of gavage feedings Too slow a flow requires excessive effort and may not allow
(1) Misplacement of the tube into the trachea adequate intake; excessive flow may result in choking or aspi-
(2) Irritation or perforation of the pharynx, esophagus, or ration. Typically, more time is required to complete a feeding in
stomach the preterm or sick infant compared to the healthy term infant.
(3) Vagal stimulation resulting in apnea and bradycardia The infant should be allowed to set the pace of bottle feeding
(4) Gastroesophageal reflux and aspiration with subsequent so less energy is expended for feeding. Force-feeding or over-
pneumonia stimulation of the infant may result in hypoxia or vomiting. It
h) Infants showed variable responses to non-nutritive sucking. is important that the infant be held comfortably and securely
Some studies reported benefits in weight gain, energy intake, during the feeding. The infant’s head should be higher than the
heart rate, oxygen saturation, and intestinal transit time, and rest of the body to minimize the risk of gastroesophageal reflux.
decreased time to full oral feeds.52 A pacifier may be offered to The bottle should be held so the infant sucks in only milk and
infants during gavage feedings, although actual oral feeding is not air through the nipple. The bottle should never be propped
necessary for the development of sucking behavior.32 in the bed for feeding.
2. Transpyloric feeding. The transpyloric feeding route is rarely used D. Transition from PN and initial feeding
because of multiple potential complications, including abdominal 1. Achieving adequate enteral intake may require considerable time
distention, diarrhea, fat malabsorption, bacterial overgrowth, depending on the infant’s gestational age and clinical status. PN
necrotizing enterocolitis, malposition or dislodgment of the tube, should be continued until about 70% of intended intake is provided
and perforation of the intestine. through the enteral route. However, in extremely small preterm
3. Gastrostomy tube infants weighing <1 kg, PN should be continued even at 1 mL/hr
a) Indications. Infants who have a functional stomach and intes- since this is equivalent to as much as 50 mL/kg/d for infants with
tine but a major impairment in swallowing or an esophageal birth weight of <500g, a substantial source of nutrition support.
obstruction are candidates for gastrostomy feeding. For exam- 2. Full-strength feedings can be attempted whenever the infant is
ple, a gastrostomy tube can be used as a long-term route for clinically stable. There is no advantage to the use of diluted milk
feeding infants with severe neurological deficits or as a tem- for initial feedings. Human milk should never be diluted. Some
porary measure in infants with congenital esophageal atresia. clinicians prefer that infants first tolerate some enteral feeding,

310 A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. © 2005 A.S.P.E.N. www.nutritioncare.org.
 S E C T I O N I V Surgical and Critically Ill Conditions

∼30 mL/kg/d, before adding human milk fortifier. Formula-fed All measurements should be plotted on appropriate growth charts.
preterm infants should start with 81 kcal/dL formulations since See Chapter 1.
they are isotonic and there is no advantage in the use of 67 kcal/dL 2. The type and frequency of laboratory monitoring should be based
formulations. Some clinicians use protein hydrolysate formula on the individual needs of the infant and his or her tolerance of
with the aim of maximizing macronutrient absorption. However, enteral feedings. Laboratory studies may be similar to those
this type of formulation was not designed to meet the nutrient needed for PN but are oriented toward determining hematologic
needs of the preterm infant, and specific indications for the term and biochemical homeostasis and improving nutritional status.
infant are limited. Their use in small preterm infants has been 3. If an infant has signs or symptoms such as lethargy, abdominal
associated with altered plasma amino acid patterns. distention, increased gastric residuals, vomiting, bilious aspirate,
E. Feeding volume and energy. In contrast to PN, in which the content diarrhea, or bloody stools, feedings should be stopped to allow for
of multiple nutrients and fluid volume can be adjusted, EN support assessment of the cause and appropriate management instituted.
is limited to the type of milk and the volume provided to the infant. 4. Apnea, bradycardia, and desaturation may result in or be caused
For the vast majority of infants in the NICU, the type of milk would by feeding intolerance. Care should be taken to define the origin of
be mother’s milk or standard infant formula for those born at term, these signs so the infant can be treated appropriately. Head up with
and mother’s milk with fortifier or preterm infant formulas for those prone or right lateral positions are best during gavage feeding to
born prematurely. The fortified human milk and the preterm infant maximize gastric emptying and minimize respiratory impairment.
formula provide a caloric density of 24 kcal/oz, with fixed content After hospital discharge, the head-up feeding position can be main-
of specific nutrients in the range to meet the estimated require- tained, but a supine sleep position is strongly recommended.55
ment.40 The practice in most NICUs is to start with small volumes Caution should be exercised with the prolonged use of antireflux
and advance slowly to allow for adaptation of the gastrointestinal medication.
tract (GIT) to avoid distention, emesis, and diarrhea. 5. Gastric residual is normally used as an indicator of feeding tol-
1. A typical starting volume is 10 to 30 mL/kg/d, advanced daily in erance. There is no specific cutoff for the amount of residual as
increments of similar amounts as tolerated until the fluid goal is a predictor of additional complications such as necrotizing ente-
reached. Smaller, sicker infants generally tolerate the smaller ini- rocolitis.56
tial volume of feeds and a slower rate of increase. a) With gavage feedings, check for aspirates before each feeding.
2. The volume of feedings needs to be adjusted daily or on alternate b) The aspirate volume should be less than the volume infused
days with increasing body weight to maintain the fluid and nutri- over the previous hour if fed by continuous infusion, or 10% to
ent goals for growth. Consistent weight gain usually occurs with 20% of the bolus volume. Refeed the aspirate, give the intended
an intake between 150 and 200 mL/kg/d. volume for the next feed, and continue with the same feeding
3. Sick infants, particularly preterm infants, even if they are not schedule.
expected to tolerate much milk feeding, may benefit from minimal c) If the aspirate is >20% of the volume fed, assess the infant for
enteral feeding (<10 mL/kg/d) soon after birth once clinically sta- other signs of intolerance such as abdominal distension. If no
ble. This minimal enteral feeding is intended as trophic stimulus other signs are noted, reduce the feeding volume to the previ-
for gut growth and function. Trophic feeding alters gastrointesti- ously tolerated volume and adjust the PN intake accordingly.
nal disaccharidase activity, hormone release, blood flow, motility, Continue to assess the infant for signs of intolerance.
and microbial flora. The clinical benefits appear to include d) If feeding intolerance continues or other signs of intolerance
improved milk tolerance, greater postnatal growth, reduced sys- develop, stop feedings immediately and assess the infant for
temic sepsis, and shorter hospital stay.53 There is no evidence of complications.
any adverse effects from trophic feeding.
4. Energy requirements for enterally fed infants are generally 10% to
IV. Nutrition Support for Sick Infants With
20% higher than for parenterally fed infants because of individual
Specific Disorders
variability in digestion and absorption. Generally, an enteral intake
of 110 to 130 kcal/kg/d (∼136 to 160 mL/kg/d of 24 kcal/oz milk) The key to maintaining optimal nutritional status in the critically ill
should allow adequate growth in most sick infants, even those born infant is to begin appropriate nutrition support via the enteral or par-
prematurely. enteral route within 24 hours of admission. Nutrition support should
F. Complementary feeding. Additional foods or fluids are rarely needed. include taking into account the influence of the underlying patho-
For patients in the NICU, the priority is to achieve adequate intake of physiology of the disease process and minimizing the use of thera-
mother’s milk (with or without fortification, depending on the infant’s peutic measures that might interfere with nutrient utilization and
weight, as discussed in Section III.B) or nutritionally complete infant tolerance. Nutrition support of all infants depends on a number of
formulas. There is no nutritional indication to add complementary factors. See Table 26-6.
foods before 4 to 6 months. Infants who are ready to receive com- A. Functional capacity of the GIT and cardiorespiratory stability. If the
plementary feeding for the purpose of adding variety in texture and GIT function is intact and the cardiorespiratory status is stable, then
taste to the diet normally would have been discharged from the the use of enteral feeding with standard enteral preparations (see
NICU. In a few infants being prepared for home ventilator support, Section III.B) is appropriate, except in patients with inborn errors
the use of complementary feeding should be similar to that for of metabolism. The route (see Section III.C) of feeding will vary
healthy infants, with one “single-ingredient” new food introduced at depending on the neurodevelopmental maturity of the patient.
a time and at the consistency or texture appropriate for oral motor GIT function is significantly impaired in primary or secondary
development.54 short-bowel syndrome or severe intractable diarrhea. The presence of
G. In-hospital monitoring enterostomy (especially at the upper small bowel), motility disorder,
1. Daily body weight in addition to intake and output, twice-weekly or bacterial overgrowth also may complicate the nutritional manage-
head circumference, and weekly body length should be measured. ment. To improve digestion and absorption of nutrients, protein

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S E C T I O N I V Surgical and Critically Ill Conditions

hydrolysate formula with modified fat and carbohydrate delivered

TABLE 26-6. Nutrition Support for Critically Ill Infants by continuous infusion is usually used as the initial feeding. The
amount can be increased slowly, depending on the volume of gastric
Nutrition concerns Nutritional management residual and the quality and quantity of stool. Gastric residuals may
be reduced by continuous gavage feeding, and the short-term use
Impaired function of • Modify protein (hydrolysate or
of a prokinetic agent may be helpful. There is no agreement on the
gastrointestinal tract amino acids), carbohydrate (glucose amount of stool or enterostomy output that is acceptable. A
from polymer), and fat (medium-chain decrease in enteral intake and supplemental PN is generally indi-
• Primary or secondary triglyceride) components of milk. cated if the volume of output is >20% to 30% of enteral intake and
shortening • Supplement other nutrients (eg, the infant fails to gain weight, head circumference, and length.
• Motility or mucosal electrolytes, vitamins) as needed. There are some differences in the contents of the two commercial
dysfunction • Give continuous infusion rather than protein hydrolysate formulations. The most convenient and impor-
bolus feeding. tant indicator of its adequacy would be clinical tolerance and ade-
• Use total or supplementary par- quate growth. An amino acid–based elemental formula containing
enteral nutrition. modified fat and carbohydrate source can be used57 if a protein
hydrolysate formula is not tolerated. Supplementation of fluid and
multiple nutrients such as electrolytes, minerals, trace minerals, and
Impaired function of • Modify fluid goal and components
vitamins such as B12 and fat-soluble vitamins are frequently needed.
other organ function of milk as needed. Pharmacotherapy to modulate intestinal motility, intestinal fluid loss,
• Limit nutrients that require the gastric acid production, and the use of growth hormone and other
metabolic or excretory capacity of intestinal growth–enhancing agents in short-bowel syndrome (see
the organ (eg, fluid and electrolyte Chapter 14) may be needed. Early provision of a central venous
restriction in renal impairment, cop- catheter is necessary in these infants to allow easy access for supple-
per and manganese restriction in mental or total PN, including home PN, as necessary.
hepatic impairment). To optimize nutrition support, it is better to provide the infant a
small volume of full-strength milk formula and employ supple-
Underlying disease • Modify route of delivery (eg, naso- mental PN rather than providing a high volume (but nutritionally
insufficient) of diluted milk formula alone. Maintaining even a min-
gastric or gastrostomy feeding in
imal amount of enteral feeding, if tolerated, may be helpful to intes-
patients with impairment of sucking
tinal growth and adaptation. The rate of intestinal adaptation to
and swallowing). EN varies with the gestation of the infant (preterm infants may
• Increase nutrient density of stan- have better potential than term infants for compensatory intestinal
dard milk preparations (eg, small growth), the site and length of residual bowel (upper or lower small
preterm infants, infants with poorly bowel with or without the presence of ileocecal valve, or colon), the
controlled cardiac failure). response to other medical and surgical therapy, and the ability to
• Adjust nutrient (glucose and/or maintain or improve the nutritional status throughout the course of
lipid) load in septic subjects. illness. In any case, meticulous attention to details of fluids and
• Replace abnormal losses (eg, gastric, electrolytes, and all aspects of macro- and micronutrient status, is
enterostomy, or diarrhea losses). essential. If a small preterm infant with impaired GIT function has
tolerated protein hydrolysate formula, cautious introduction of
• Provide specific formulation for cow
preterm formula with more appropriate nutrient composition for the
milk protein or soy protein allergy,
infant’s needs should be attempted. Ultimately, functional adapta-
and inborn errors of metabolism. tion of the intestine may allow gradual transition to a normal diet.
Management of these infants by a small group of multidisciplinary
Therapy for underlying • Adjust glucose load in patients professionals is strongly recommended.
illness receiving systemic steroid B. Functional capacity of organs other than the GIT system. This also
therapy. is important to the tolerance and type of nutrients delivered. For
• Minimize therapy that might example, with renal disorders, most infants can be fed human milk
increase nutrient losses or or “humanized” infant formulas, depending on the extent of renal
adversely affect nutrient digestion, impairment and the treatment for it. Close monitoring of serum elec-
absorption, metabolism, or excre- trolytes, minerals, urea nitrogen, and albumin status is needed.
Infants with biliary atresia often have reduced intake and impaired
tion (eg, proton pump inhibitor, cor-
digestion and absorption of nutrients, particularly long-chain fats
ticosteroids, phenobarbital, chronic
and fat-soluble vitamins. The use of protein hydrolysate formula rich
diuretics). in medium-chain triglycerides, supplementation of multivitamins,
• Use appropriate analgesia and and continuous enteral feedings may be needed to maximize diges-
anesthesia to minimize tissue tion and absorption of nutrients to promote growth until definitive
catabolism. treatment for the underlying disease can take place.
C. Constraints imposed by the underlying disease state. Fluid restric-
tion may limit the amount of nutrient that can be delivered in infants
with acute renal failure or the syndrome of inappropriate antidiuretic

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 S E C T I O N I V Surgical and Critically Ill Conditions

hormone secretion. However, an increase in fluid intake may be fea- other sick infants with non-GIT problems, and there is no indica-
sible with manipulation of environmental factors (Table 26-4). tion to use milks other than human milk or standard infant formula.
In other situations such as infants with poorly controlled cardiac fail- Infants with chronic disease states such as Bronchopulmonary Dys-
ure, can be fed with standard infant formula concentrated to 80 to plasia (BPD) may require relative fluid restriction but possibly have
100 kcal/dL as necessary. Infants receiving the highly concentrated increased energy needs because of increased respiratory effort.
formulas should be observed for gastrointestinal tolerance, and use Increased energy intake in this situation should be managed with
of the concentrated formula should be terminated if the infant is hav- the understanding that excessive carbohydrate load also may increase
ing other problems such as gastroenteritis. the work of respiration and that balanced macronutrient content is
With surgical operation and sepsis, the increased metabolic needed.
demands return to normal upon resolution of the primary conditions. All pharmacotherapy including but not limited to diuretics, corti-
After most elective operations in otherwise normal infants, the costeroids, proton pump inhibitors, and phenobarbital must be regu-
increase in metabolic demand often lasts only 4 to 6 hours58 and no larly reassessed to determine its continuing need. This could minimize
change to standard nutrition support is needed. Septic infants fre- the adversely effect on nutrient digestion, absorption, metabolism and
quently do not tolerate the increased amount of nutrients needed to excretion. Adequate analgesia and anesthesia are proven means of
compensate for their greater metabolic demands, and complications reducing the catabolism associated with sick and stressed infants and
such as hyperglycemia may develop while they are receiving the pre- are useful adjuncts to optimize the nutritional management.
viously tolerated PN infusate. Replacement of losses such as enteros-
tomy losses of electrolytes is needed. The clinician also must be REFERENCES
cognizant of the loss of minerals and trace minerals in addition to 1. Koo WWK, Cepeda E. Parenteral nutrition in neonates. In: Rombeau JL,
electrolytes, since the content of minerals such as magnesium22 or Rolandelli RH, eds. Clinical Nutrition: Parenteral Nutrition. 3rd ed.
trace minerals such as zinc59 and many other nutrients in the fecal or Philadelphia, PA: WB Saunders; 2000:463–475.
2. Ziegler EE, Thureen PJ, Carlson SJ. Aggressive nutrition of the very low
enterostomy fluid is rarely measured. Zinc status may be the limiting
birthweight infant. Clin Perinatol. 2002;29:225–244.
factor in immunologic and numerous other functions and growth. 3. A.S.P.E.N. Board of Directors and the Clinical Guidelines Task Force.
Infants with demonstrated allergy to cow milk or soy protein may Guidelines for the use of parenteral and enteral nutrition in adult and pedi-
require protein hydrolysate formula. The use of elemental amino atric patients. J Parenter Enteral Nutr. 2002;26(1 suppl):1SA–138SA.
acid infant formula and even PN also may be needed. Infants with 4. Committee on Nutrition. Parenteral nutrition. In: Kleinman RE, ed. Pediatric
inborn errors of metabolism such as phenylketonuria have specific Nutrition Handbook. 5th ed. Elk Grove Village, IL: American Academy of
needs and therapy regardless of gestational age or birth weight. Pediatrics; 2004:369–389.
These groups of patients should be comanaged by a physician and a 5. Ockerman AV. Compounded sterile preparations. An overview of the new
dietitian familiar with the management of these disorders. standards in USP <797>. U.S. Pharmacist. 2004;29:46–62.
6. Thureen PJ, Melara D, Fennessey PV, Hay WW Jr. Effect of low versus high
D. Alteration in the form of nutrients and adjunctive support. Changes
intravenous amino acid intake on very low birth weight infants in the early
in the form of nutrients are not necessary for many complications neonatal period. Pediatr Res. 2003;53:24–32.
commonly found in patients in the NICU. For example, some condi- 7. Poindexter BB, Ehrenkranz RA, Stoll BJ, et al. Parenteral glutamine sup-
tions such as feeding difficulties associated with central nervous plementation does not reduce the risk of mortality or late-onset sepsis in
system complications require a change in the route of delivery extremely low birth weight infants. Pediatrics. 2004;113:1209–1215.
rather than a change in the form of nutrients. Even gastrointestinal 8. O’Leary MJ. Nourishing the preterm and low birthweight infant. In: Pipes
complications normally do not require modification of standard PN PL, ed. Nutrition in Infancy and Childhood. St. Louis, MO: McGraw-Hill;
infusate or enteral feeding unless there is a significantly shortened 1985:145.
9. Zlotkin SH, Bryan MH, Anderson GH. Intravenous nitrogen and energy
intestinal tract or dysmotility problems. Infants requiring extracor-
intakes required to duplicate in utero nitrogen accretion in prematurely born
poreal membrane oxygenation (ECMO) therapy generally have human infants. J Pediatr. 1981;99:115–120.
severe respiratory failure. Protein catabolism in these infants is 10. Jones MO, Pierro A, Hammond P, Nunn A, Lloyd DA. Glucose utilization
markedly elevated, consistent with their severe illness. A surplus of in the surgical newborn infant receiving total parenteral nutrition. J Pediatr
dietary caloric intake does not improve protein catabolism and Surg. 1993;28:1121–1125.
merely increases carbon dioxide production in the highly stressed 11. Chwals WJ. Overfeeding the critically ill child: fact or fantasy? New Horiz.
neonates.60 Thus, excess nutrient intake, especially during the acute 1994;2:147–155.
phase of illness, including the period on ECMO, is not warranted and 12. Lafeber HN, Sulkers EJ, Chapman TE, Sauer PJ. Glucose production and
may be detrimental. Some infants on ECMO show intolerance to oxidation in preterm infants during total parenteral nutrition. Pediatr Res.
1990;28:153–157.
nutrients such as carbohydrate load, as other sick infants do, and
13. Sunehag A, Gustafsson J, Ewald U. Glycerol carbon contributes to hepatic
some develop hypercalcemia if they are receiving PN solutions high glucose production during the first eight hours in healthy term infants. Acta
in calcium. Hyperglycemia and hypercalcemia are transient and Paediatr. 1996;85:1339–1343.
resolved with temporary lowering of dextrose and calcium in PN. 14. Poindexter BB, Karn CA, Denne SC. Exogenous insulin reduces proteoly-
Occasionally, calcium may need to be withheld from PN for 2 or 3 sis and protein synthesis in extremely low birth weight infants. J Pediatr.
days. Many infants who received ECMO therapy suffer from vari- 1998;132:948–953.
able periods of hypoxia and are at risk for increased intestinal per- 15. American Academy of Pediatrics, Subcommittee on Hyperbilirubinemia.
meability with the potential for bacterial translocation and sepsis. Management of hyperbilirubinemia in the newborn infant 35 or more weeks
of gestation. Pediatrics. 2004;114:297–316.
However, neonates on ECMO have tolerated some enteral feeding
16. Cairns PA, Stalker DJ. Carnitine supplementation of parenterally fed
without further clinical deterioration.61 The major complication with neonates [Cochrane Review]. The Cochrane Library. 2004;issue 2.
feeding is the poor nipple-feeding effort of many infants after dis- 17. Ohls RK, Ehrenkranz RA, Wright LL, et al. Effects of early erythropoi-
continuation of ECMO therapy, and almost all infants require a etin therapy on the transfusion requirements of preterm infants below
period of gavage feeding. There are no data to indicate that the nutri- 1250 grams birth weight: a multicenter, randomized, controlled trial.
ent requirement for infants needing ECMO would differ from that of Pediatrics. 2001;108:934–942.

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18. Greene HL, Hambidge KM, Schanler R, Tsang RC. Guidelines for the use of 42. American Dietetic Association. Preparation of Formula for Infants: Guide-
vitamins, trace elements, calcium, magnesium, and phosphorus in infants and lines for Healthcare Facilities. Chicago, IL: American Dietetic Association;
children receiving total parenteral nutrition. Am J Clin Nutr. 1988;48: 2002:64.
1324–1342. 43. Food and Drug Administration, USA. Letter to health-care professionals.
19. Doyle LW, Sinclair JC. Insensible water loss in newborn infants. Clin October 2002. Available at: http://www.cfsan.fda.gov. Accessed August 15,
Perinatol. 1982;9:453–482. 2004.
20. Nelson RE, Biberdorf RI. Nationwide drug shortage: it’s time to take the lead. 44. Chan GM. Effects of powdered human milk fortifiers on the antibacterial
Nutr Clin Pract. 1998;13:295–297. actions of human milk. J Perinatol. 2003;23:620–623.
21. Koo WWK. Neonatal calcium and phosphorus disorders. In: Lifshitz F, ed. 45. Raghuveer TS, McGuire EM, Martin SM, et al. Lactoferrin in the preterm
Pediatric Endocrinology: A Clinical Guide. 4th ed. New York, NY: Marcel infant’s diet attenuates iron-induced oxidation products. Pediatr Res. 2002;
Dekker; 2003:481–515. 52:964–972.
22. Thoren L. Magnesium deficiency in gastrointestinal fluid loss. Acta Chir 46. Berseth CL, Van Aerde JE, Gross S et al. Growth, efficacy, and safety
Scand. 1963;306(suppl):1–65. of feeding an iron-fortified human milk fortifier. Pediatrics 2004;114:
23. Koo WWK, Kaplan LA, Horn J, Tsang RC, Steichen JJ. Aluminum in par- 699–706.
enteral nutrition solution—sources and possible alternatives. J Parenter 47. Reis BB, Hall RT, Schanler RJ, et al. Enhanced growth of preterm infants
Enteral Nutr. 1986;10:591–595. fed a new powdered human milk fortifier: a randomized, controlled trial.
24. Neuzil J, Darlow BA, Inder TE, et al. Oxidation of parenteral lipid emulsion Pediatrics. 2000;106:581–588.
by ambient and phototherapy lights: potential toxicity of routine parenteral 48. Gartner LM, Greer FR on behalf of Section on Breastfeeding and Commit-
feeding. J Pediatr. 1995;126:785–790. tee on Nutrition, American Academy of Pediatrics. Prevention of rickets and
25. Chessex P, Lavoie JC, Rouleau T, et al. Photooxidation of parenteral multi- vitamin D deficiency: new guidelines for vitamin D intake. Pediatrics.
vitamins induces hepatic steatosis in a neonatal guinea pig model of intra- 2003;111:908–910.
venous nutrition. Pediatr Res. 2002;52:958–963. 49. Food and Nutrition Board, Institute of Medicine. Dietary Reference Intake
26. Kaufman SS. Prevention of parenteral nutrition-associated liver disease in for Iron. Washington, DC: National Academy Press; 2001:290–393.
children. Pediatr Transplant. 2002;6:37–42. 50. Committee on Nutrition. Nutrition and oral health. In: Kleinman RE, ed.
27. Btaiche IF, Khalidi N. Parenteral nutrition-associated liver complications in Pediatric Nutrition Handbook. 5th ed. Elk Grove Village, IL: American
children. Pharmacotherapy. 2002;22:188–211. Academy of Pediatrics; 2004:789–800.
28. Forchielli ML, Walker WA. Nutritional factors contributing to the develop- 51. Lemons PK, Lemons JA. Transition to breast/bottle feedings: the premature
ment of cholestasis during total parenteral nutrition. Adv Pediatr. 2003;50: infant. J Am Coll Nutr. 1996;15:126–135.
245–267. 52. Pinelli J, Symington A. Non-nutritive sucking for promoting physiologic sta-
29. Koo WWK, Steichen JJ. Osteopenia and rickets of prematurity. In: Polin R, bility and nutrition in preterm infants. Cochrane Database Syst Rev. 2001;
Fox W, eds. Fetal and Neonatal Physiology. 2nd ed. Philadelphia, PA: W. B. 3:CD001071.
Saunders; 1998:2335–2349. 53. McClure RJ. Trophic feeding of the preterm infant. Acta Paediatr. 2001;
30. Koo WWK. Preterm infants with fractures. In: Kleerekoper M, Siris E, 90(suppl):19–21.
McClung M, eds. The Bone and Mineral Manual. A Practical Guide. 2nd ed. 54. Committee on Nutrition. Complementary feeding. In: Kleinman RE, ed.
San Diego, CA: Academic Press. In press. Pediatric Nutrition Handbook. 5th ed. Elk Grove Village, IL: American
31. Koo WWK, Warren L. Calcium and bone health in infants. Neonatal Netw. Academy of Pediatrics; 2004:103–118.
2003;22:23–37. 55. American Academy of Pediatrics, Task Force on Infant Sleep Position and
32. Mizuno K, Ueda A. Development of sucking behavior in infants who have Sudden Infant Death Syndrome. Changing concepts of sudden infant death
not been fed for 2 months after birth. Pediatr Int. 2001;43:251–255. syndrome: implications for infant sleeping environment and sleep position.
33. American Academy of Pediatrics, Committee on Nutrition. Breastfeeding Pediatrics. 2000;105:650–656.
and the use of human milk. Pediatrics. 2005;115:496–506. 56. Kenton AB, Fernandes CJ, Berseth CL. Gastric residuals in prediction of
34. Koo WWK. Efficacy and safety of docosahexaenoic acid and arachidonic necrotizing enterocolitis in very low birth weight infants. Pediatrics. 2004;
acid addition to infant formulas: can one buy better vision and intelligence? 113:1848–1849.
J Amer Coll Nutr. 2003;22:101–107. 57. Bines J, Francis D, Hill D. Reducing parenteral requirement in children
35. American Academy of Pediatrics, Committee on Drugs. The transfer with short bowel syndrome: impact of an amino acid–based complete infant
of drugs and other chemicals into human milk. Pediatrics. 2001;108:776–789. formula. J Pediatr Gastroenterol Nutr. 1998;26:123–128.
36. Committee on Nutrition. Breastfeeding. In: Kleinman RE, ed. Pediatric 58. Pierro A. Metabolism and nutritional support in the surgical neonate.
Nutrition Handbook. 5th ed. Elk Grove Village, IL: American Academy of J Pediatr Surg. 2002;37:811–822.
Pediatrics; 2004:55–85. 59. Wolman SL, Anderson GH, Marliss EB, Jeejeebhoy KN. Zinc in total par-
37. Robbins ST and Baker LT. Infant Feedings: Guidelines for Preparation of enteral nutrition. Requirement and metabolic effects. Gastroenterology.
Formula and Breastmilk in Health Care Facilities. Chicago, IL: American 1979;76:458–467.
Dietetic Association; 2004:71–75. 60. Shew SB, Keshen TH, Jahoor F, Jaksic T. The determinants of protein catab-
38. American Academy of Pediatrics, Committee on Nutrition. Soy protein- olism in neonates on extracorporeal membrane oxygenation. J Pediatr Surg.
based formulas: recommendations for use in infant feeding. Pediatrics. 1999;34:1086–1090.
1998;101:148–153. 61. Piena M, Albers MJ, Van Haard PM, et al. Introduction of enteral feeding in
39. American Academy of Pediatrics, Committee on Nutrition. Hypoallergenic neonates on extracorporeal membrane oxygenation after evaluation of intes-
infant formulas. Pediatrics. 2000;106:346–349. tinal permeability changes. J Pediatr Surg. 1998;33:30–34.
40. Klein CJ, ed. Nutrient requirements for preterm infant formulas: a report from 62. Alexander GR, Himes JH, Kaufman RB, Mor J, Kogan M. A United
the American Society for Nutritional Sciences, Life Sciences Research States national reference for fetal growth. Obstet Gynecol 1996;87:
Office. J Nutr. 2002;132:1395S–1577S. 163–168.
41. U.S. Food and Drug Administration. Recalls and safety alerts. FDA warns 63. Kuczmarski RJ, Ogden CL, Grummer-Strawn LM, et al. 2000 CDC growth
about possible Enterobacter Sakazakii infection in hospitalized newborns fed charts: United States. Advance data from vital and health statistics; no 314.
powdered infant formula. MMWR. 2002;51:298–300. Hyattsville, Marylands: National Center for Health Statistics.

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 SECTION EDITOR
W. Frederick Schwenk, MD
V
Metabolic Conditions

27 Diabetes Mellitus

28 Obesity

29 Inborn Errors of Metabolism

30 Chronic Kidney Disease

31 Pregnancy

32 Anorexia Nervosa
 M. Molly McMahon, MD

27
Diabetes Mellitus

Introduction The postprandial glucose concentration rarely exceeds

150 mg/dL.
In practice, most nutrition clinicians will manage the care of hospital- D. The homeostatic mechanisms that maintain euglycemia in the
ized patients with diabetes mellitus who require parenteral nutrition or postabsorptive state and blunt the postprandial glycemic response
enteral tube feeding. An important management goal in the care of the in nondiabetic subjects are impaired in patients with diabetes. These
hospitalized patient with diabetes is to avoid the extremes of hypo- patients have both preprandial and postprandial hyperglycemia
glycemia and hyperglycemia. This chapter provides an approach to because of excessive hepatic glucose production, impaired glucose
achieving glucose control in stressed hospitalized patients with diabetes uptake, and decreased insulin secretion or action.
who are receiving nutrition support. E. Under conditions of severe stress, patients without an antecedent
diagnosis of diabetes mellitus may develop hyperglycemia.3
I. Background Information 1. Severe stress is accompanied by marked increases in the plasma
II. Unique Nutrition Issues Associated with Diabetes Mellitus concentration of counterregulatory hormones (ie, glucagon, epi-
III. Glucose Goals and Rationale of Therapy nephrine, cortisol, and growth hormone) and cytokines.
IV. Management a) Hyperglycemia results from increased hepatic glucose produc-
References tion and decreased peripheral glucose uptake.
b) Stress causes a greater derangement in glucose metabolism in
I. Background Information diabetic patients because they cannot increase insulin secretion
as a compensatory response and this is one mechanism for the
A. Diabetes mellitus is a metabolic disorder caused by an absolute deterioration in glucose control often observed in sick diabetic
(Type 1; previously called insulin-dependent diabetes mellitus) or patients.4
a relative (Type 2; previously called non-insulin-dependent diabetes
mellitus or stress-induced hyperglycemia) lack of insulin.1
1. Type 1 diabetes is associated with onset at an earlier age, a ten-
II. Unique Nutritional Issues Associated with
dency toward ketosis, and an absolute dependency on insulin.
Diabetes Mellitus
2. Type 2 diabetes, by far the more common type, is associated with A. Although the nutrition assessment, indications for nutrition support,
adult onset, obesity, and need for larger doses of insulin. and estimate of nutritional needs for critically ill diabetic patients
B. Because of the increasing prevalence of diabetes, the co-morbidity are similar to those of nondiabetic patients, special attention should
of the disease, and the number of patients with stress-induced be focused on caloric requirements. Overfeeding should be avoided
hyperglycemia, many hospital clinicians will manage patients with because excessive calories can cause hyperglycemia.
hyperglycemia receiving nutrition support. A third of all patients 1. Studies using the Harris-Benedict equation have shown that the
admitted to an urban general hospital had fasting glucose levels measured energy expenditure of most hospitalized patients is
exceeding 126 mg/dL or two or more random glucose levels exceed- between 100% and 120% of predicted resting energy expenditure.5
ing 200 mg/dL, and a third of these patients did not have known 2. Many patients with diabetes are overweight, yet data are limited
diabetes.2 and there is no consensus about the nutritional requirements of
C. Carbohydrate metabolism is closely regulated in both the post- obese patients.
absorptive (overnight fasted state) and postprandial periods in healthy, 3. Certain groups recommend that, in obese patients, the weight used
nondiabetic subjects. to estimate caloric requirements should be the weight halfway
1. In the postabsorptive period, euglycemia is maintained because the between ideal and current weight. Others recommend feeding
rate of hepatic glucose production approximates the rate of glucose ∼75% of the Harris-Benedict estimate of energy requirements
uptake by the liver, brain, and peripheral tissues. These rates aver- based on the current weight. Outcome studies are needed.
age 2 mg/kg/min or approximately 200 g/d in a 70-kg person. B. Although the nutrition assessment, indications for nutrition support,
2. After a meal, the increase in plasma glucose and insulin decreases and estimate of nutritional needs for critically ill diabetic patients
hepatic glucose release and increases peripheral glucose uptake, are similar to those of nondiabetic patients, special attention should
thereby decreasing the amount of glucose that must be used by be focused on diabetes-related gastrointestinal complications.
extrahepatic tissues. 1. Diabetic gastroparesis denotes gastric atony and delayed gastric
As the plasma glucose and insulin concentrations decrease after emptying; however, symptoms are related to dysmotility not only
a meal, the rates of hepatic glucose production and peripheral glu- of the stomach but also of the small bowel.6
cose uptake are restored to basal levels, allowing glucose pro- Common manifestations of diabetic enteropathy include heart-
duction to increase and glucose uptake to decrease. burn, dysphagia, early satiety, postprandial vomiting (especially

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S E C T I O N V Metabolic Conditions

partially digested food retained from earlier meals), and epigas- 3. In addition, patients with long-standing diabetes may develop
tric pain. hypoglycemic unawareness, a loss of the ability to recognize
Although demonstration of delayed gastric emptying estab- warning symptoms of hypoglycemia.
lishes the diagnosis of gastroparesis, the diagnosis should be 4. To minimize subsequent hypoglycemia, clinicians should attempt
strongly suspected from the history. to identify the factor(s) responsible for hypoglycemia.
Peripheral neuropathy, retinopathy, and nephropathy are fre- 5. Potential causes include excess insulin dose, unanticipated dis-
quently found in patients with symptomatic diabetic gastroparesis. continuation of nutrition support in patients receiving insulin,
Delayed gastric emptying makes regulation of glucose control resolution of severe stress, discontinuation or decreased doses of
difficult. Hyperglycemia may further delay gastric emptying, corticosteroids or sympathomimetic agents, renal dysfunction,
whereas hypoglycemia may develop in patients treated with severe hepatitis, sepsis, or diabetic gastroparesis.
insulin or with oral diabetic agents who do not absorb ingested C. Avoidance or minimization of hyperglycemia is important during
food normally because of a delay in gastric emptying. short-term hospitalization to avoid adverse effects on fluid balance.
Glucose levels should be carefully monitored and appropri- 1. As the filtered load of glucose increases, it eventually exceeds
ately managed because gastric emptying can be slowed by hyper- tubular reabsorptive capacity.
glycemia. 2. As a result, glucose remains in the tubular lumen and acts as an
Accurate diagnosis of gastroparesis is important to avoid osmotic diuretic, increasing the urinary loss of electrolytes and
attributing the gastrointestinal symptoms to tube feeding alone or water.
to other factors capable of slowing gut motility. D. Avoidance or minimization of hyperglycemia is also important to
The patient’s medication profile should be reviewed for med- enhance immune function.
ications with potential to slow gastric emptying, such as anti- 1. Hyperglycemia is associated with abnormalities in granulocyte
cholinergics, antidepressants, α2-adrenergic agonists, calcium adhesion, chemotaxis, phagocytosis, respiratory burst function,
channel blockers, and opiates. and intracellular killing; significant improvement occurs with
Knowledge of the fat content of the tube feeding formula is control of blood glucose.7–12
important because enteral fat can decrease gut motility. 2. Hyperglycemia can impair complement function.9 Glucose can
If tube feeding is required, most patients tolerate jejunal tube
attach to complement, preventing its attachment to a microbe and
feeding, provided that iso-osmolar feedings are started at a low
impairing opsonization.
rate and are advanced slowly. Certain patients require a decom-
3. The association between hyperglycemia and infections with the
pression (venting) gastrostomy tube.
yeast Candida albicans is well known and a potential mechanism
Parenteral nutrition (PN) should be reserved for patients who
has been identified.7–8
have severe small bowel dysmotility and who have failed a rea-
a) The yeast expresses a surface protein that is homologous with
sonable trial of nasojejunal tube feeding.
the alpha chain of the neutrophil receptor for complement and
C. Constipation, diarrhea, or fecal incontinence may also develop with
its expression is increased with hyperglycemia.
long-standing diabetes.
b) This surface protein can impair phagocytosis by binding to
complement and mediate adhesion of the yeast to endothelial
III. Glucose Goals and Rationale of Therapy surfaces.
4. Clinical evidence has linked hyperglycemia to nosocomial infec-
A. There are limited data establishing “ideal” glucose goals in hospi-
talized patients. tion in stressed hospitalized patients.
1. In an effort to balance potential benefits derived by prevention of a) Hyperglycemia (plasma glucose concentration > 200 mg/dL)
hyperglycemia and risks due to hypoglycemia, aiming for a glu- within 3 days before the diagnosis was the most common risk
cose goal range of 80 to 120 mg/dL is recommended for critically factor for candida infection.7
ill patients in intensive care unit settings. b) A meta-analysis summarizing results from prospective ran-
2. Aiming for a range of 100 to 150 mg/dL is recommended for non- domized trials comparing parenteral with enteral nutrition in
critically ill patients in ward settings. Safe achievement of tighter critically ill patients reported that significantly fewer enterally
glucose goal ranges is difficult, as nurse to patient staffing ratios fed patients experienced septic complication (16% versus 35%,
are different in ward and intensive care unit settings and many respectively). Hyperglycemia may have been one variable
patients are managed with subcutaneously administered insulin responsible for the increased infection rate, as the mean glucose
regimens. Finally, studies showing an outcome advantage with concentration at the conclusion of the study was 230 mg/dL in
tight glucose control did not include non-critically ill patients on the parenterally fed patients compared with 130 mg/dL in the
ward settings. Additional studies are required to establish risks, enterally fed group.13
benefits, and goals for differing subsets of hospitalized patients. In c) Hyperglycemia itself may be an independent risk factor for
addition, to date studies have not included pediatric patients. development of infection.14 Investigators who monitored
3. Aggressive treatment of hyperglycemia is indicated regardless of perioperative glucose control in 100 previously uninfected
whether a previous diagnosis of diabetes has been established. patients with diabetes and followed the subsequent develop-
B. Avoidance or minimization of hypoglycemia is important as hypo- ment of postoperative infection found that hyperglycemia
glycemia can cause adrenergic or neuroglycopenic symptoms. (glucose level in excess of 220 mg/dL) on postoperative day 1
1. Adrenergic symptoms include sweating, palpitations, anxiety, was associated with a higher rate of infection.
tachycardia, and hunger; neuroglycopenic symptoms include 5. Observational studies indicate that hyperglycemia in patients
headache, visual changes, and alterations in behavior. without known diabetes is a risk factor for adverse outcome in
2. Identification of the neuroglycopenic or adrenergic symptoms of patients experiencing acute illnesses.
hypoglycemia is difficult in severely ill patients who are sedated a) A meta-analysis of observational studies quantified the impact
or ventilator-dependent. of hyperglycemia on the prognosis of patients without known

318 A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. © 2005 A.S.P.E.N. www.nutritioncare.org.
 S E C T I O N V Metabolic Conditions

diagnoses of diabetes following myocardial infarction. In b) Unexplained hyperglycemia may be a harbinger of infection
patients immediately following myocardial infarction, glucose so potential sources should be evaluated.
values in excess of 110 to 144 mg/dL were associated with a
3-fold increase in mortality and a higher risk of heart failure.15 IV. Management
b) In patients suffering ischemic strokes, glucose values in excess
of 108 to 144 mg/dL (range) were associated with a 3-fold A. Special aspects of diet and nutritional supplements
increase in mortality and appear related to the degree of per- 1. The American Diabetes Association position statement on nutri-
manent disability after stroke.16 tion states that although selected soluble fibers are capable of
6. Randomized trials of interventions in critically ill patients have delaying glucose absorption from the small intestine, the effect
documented association between hyperglycemia and adverse of dietary fiber on glycemic control is probably insignificant.22
outcomes. Therefore, the fiber intake recommendations for diabetics are
a) The Veteran Administration Cooperative Study was designed probably the same as for the general hospitalized population.
to test the hypothesis that perioperative parenteral nutrition 2. The availability of enteral formulas lower in carbohydrate and
would prevent serious complications following major surgery.17 higher in fat content than standard formulas has prompted stud-
While patients receiving parenteral nutrition had fewer non- ies examining their effects on glycemic control.
infectious complications, infections were twice as common as 3. Evidence from single meal and short-term studies report better
in control patients. This higher infection rate was associated glycemic control. However, no prospective randomized trials
with severe hyperglycemia and provision of excess calories. A have compared continuous or gravity feeding of these formulas
serum glucose concentration greater then 300 mg/dL occurred compared with standard formulas in hospitalized patients. Thus,
in 20% of patients receiving parenteral nutrition and in 1% of whether these products are helpful in these patients has yet to be
the control group. established.23 See Chapter 4 for further detail on formulas.
7. Control of hyperglycemia during acute illness has been associ- B. Special aspects of enteral and parenteral nutrition24
ated with improved outcomes. 1. Although many approaches can be used to achieve glucose con-
a) In an observational study, implementation of an insulin infu- trol, the following approach works effectively in an institution
sion to maintain glucose levels between 150 and 200 mg/dL where many clinicians prescribe nutrition.25
decreased by 58% the risk of sternal wound infections fol- 2. Although it is not recommended to initiate long-acting (eg, Ultra-
lowing coronary artery bypass grafting.18 lente or Glargine) insulin programs in hospitalized patients, it is
b) This same group of investigators compared insulin infusion recommended to continue basal doses of these insulins for patients
with subcutaneous insulin management in diabetic patients admitted to the hospital on established multiple daily insulin pro-
undergoing coronary artery bypass grafting procedures. Insulin grams (Table 27-1).
infusion resulted in improved glucose control, and decreased C. Enteral nutrition
mortality by 57%.19 1. Although subcutaneous (SQ) insulin administration aims to pre-
c) Malmberg et al conducted a randomized trial of intensive vent hyperglycemia in patients receiving enteral calories, glycemic
insulin therapy (from admission to 3 months after discharge) control can be difficult to achieve.
in patients with diabetes after myocardial infection.20 In this
study known as the DIGAMI Trial, the 1-year mortality was
29% lower in patients receiving insulin therapy compared TABLE 27-1. Insulin Preparation Pharmacokinetics
with the standard treatment group.
d) Van den Berghe et al conducted a randomized trial of intensive Effective
glycemic control (glycemic goal of 80 to 110 mg/dL) compared Insulin Route Onset Peak duration
with usual care in a surgical intensive care unit.21 Patients
received intravenous dextrose day one and then either par- Rapid-acting SQ
enteral nutrition, enteral nutrition, or combined parenteral
• Lispro 5–15 min 30–90 min 5 hr
and enteral nutrition. The mean caloric intake was ∼19 non-
protein calories per kilogram body weight. At the end of the • Aspart 5–15 min 30–90 min 5 hr
study period, patients with average blood glucose levels of
103 mg/dL (study group) experienced 44% lower mortality Short-acting
than patients with average blood glucose of 153 mg/dL. Inten- • Regular SQ 30–60 min 2–3 hr 5–8 hr
sive insulin treatment also reduced bloodstream infections,
acute renal failure requiring dialysis or hemofiltration, median IV 0.5 hr 3.5 hr
number of red cell transfusions, and critical illness polyneu-
ropathy. However, there was a 60% increase in the risk of hypo- Intermediate- SQ
glycemia (defined as glucose concentration below 40 mg/dL). acting
8. Benefits may be due to insulin, correction of hyperglycemia, or
a combination. NPH 2–4 hr 4–10 hr 10–16 hr
9. The cause or causes of hyperglycemia must be identified. Lente 2–4 hr 4–10 hr 10–16 hr
a) Potential causes include illness or infection, overfeeding (nutri-
tion support, dextrose-containing crystalloid, dextrose absorp- Long-acting SQ
tion during peritoneal dialysis, and medications formulated in Ultralente 6–10 hr 10–16 hr 18–24 hr
lipid emulsion, such as propofol), medications (eg, corticos-
teroids, sympathomimetic infusion, or immunosuppressants), Glargine 2–4 hr No peak 20–24 hr
insufficient insulin, and volume depletion

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S E C T I O N V Metabolic Conditions

a) Measurement of glucose by reflectance meter is recommended k) Increases in the tube feeding infusion rate should be avoided
because the results are rapidly obtained and the need for veni- until adequate glucose control has been achieved. Insulin doses
puncture is avoided. However, a control program including should be appropriately adjusted.
meter calibration, personnel training, comparison measure- Although gastroparesis may make tube-feeding tolerance
ments, and monitoring of results must be established to ensure more difficult, most patients tolerate jejunal feedings when iso-
accuracy of results. osmolar formulas are started at a low rate (eg, 20 mL/h) and
b) Oral diabetic agents may be administered by feeding tube in advanced slowly (eg, increased at increments of 10 to 20 mL/h
medically stable patients with well-controlled type 2 diabetes every 12 hours) to the goal infusion rate. Avoidance of higher
mellitus and normal renal and hepatic function. fat formulas is needed because enteral fat may decrease gastric
c) Use of metformin in hospitalized patients is not recommended emptying. In addition, review of the patient’s medication pro-
because a major (although very uncommon) risk of metformin file is important. Certain medications (eg, anticholinergics, anti-
use is lactic acidosis, which can occur in patients with hepatic depressants, α2-adrenergic agonists, calcium channel blockers,
or renal disease or in those with tissue ischemia. and opiates) may decrease gut motility and, if not needed,
d) When initiating tube feeding, use of short-acting insulin is rec- should be discontinued. Prokinetic agents remain the treatment
ommended to minimize the risk of hypoglycemia which could of choice. Selected patients require use of a venting decom-
result from continued absorption of insulin from NPH (insulin pression tube.
suspension, isophane) or Lente (insulin zinc suspension) prepa- Unexpected discontinuation of tube feeding may cause
rations after unexpected discontinuation of tube feeding. hypoglycemia in patients treated with subcutaneous injections
e) Once the tube feeding infusion rate has reached 30 to 40 mL/h,
of insulin. A protocol to treat hypoglycemia is shown in
the use of NPH or Lente insulin preparation (intermediate-
Table 27-3.
acting insulin) generally is safe.
f ) If tube feedings are administered during the day, begin by
providing one-half of the patient’s preadmission morning
insulin dose as intermediate-acting insulin, while adhering to
the SQ regular insulin algorithm (Table 27-2), and then TABLE 27-3. Treatment of Hypoglycemia in Hospital-
appropriately adjust the following day’s doses of intermediate- ized Adult Patients with Hyperglycemia
acting insulin. on Insulin or Oral Diabetic Agents
g) For some patients with type 2 diabetes receiving nocturnal tube
feeding, administration of intermediate-acting insulin prior to
the initiation of nocturnal feeds is adequate. I. Presumed symptomatic hypoglycemia should be treated without
h) Twice daily administration of intermediate-acting insulin may waiting to check plasma or blood glucose level.
be required if tube feedings are administered continuously A. If patient able to swallow safely, administer ~15 grams carbo-
over 24 hours. hydrate in one of the following forms:
i) If feedings are infused by gravity administration, the glucose
1. 5 sugar packets dissolved in 4 ounces ( 1⁄2 cup) of water
concentration should be checked immediately before the
feeding is initiated and no sooner than 4 hours after the end 2. 4 ounces (1⁄2 cup) of fruit juice
of the prior feeding. 3. Glucose Oral Gel 15 grams orally must be used for those on
j) Although some patients receiving gravity feeding can be Acarbose or Miglitol
managed with intermediate-acting insulin alone, others need B. If the patient has a functioning feeding tube, administer one
combined treatment with intermediate-acting and short-acting of the following by feeding tube:
insulin. 1. 4 ounces (1⁄2 cup) of fruit juice (not orange juice or other
pulp-containing juice)
2. 5 sugar packets dissolved in 4 ounces (1/2 cup) of water
C. If patient not able to take oral feeding safely or NPO:
TABLE 27-2. Guidelines for SQ Regular
1. If IV access available, administer D50W 25 mL (12.5 grams)
Insulin Supplementation
intravenously
Adjustment of algorithm may be required for differences in patient 2. If no IV access present, administer Glucagon 1 mg by SQ
weight, response to insulin, and treatment goals. Insulin should not injection. Following Glucagon treatment, for patients not
be administered more often than every four to six hours. Initiate sup- NPO, provide snack to prevent subsequent hypoglycemia.
plementation if two consecutive glucose values exceed D. Contact the service responsible for the patient’s diabetes
150 mg/dL. management
II. For treatment of asymptomatic hypoglycemia (glucose less than
Glucose, mg/dL SQ Regular Insulin Dose, Units or equal to 60 mg/dL) follow steps A through C above
III. Glycemic monitoring following treatment
150–200 1–2 A. Measure reflectance meter glucose level in 15 minutes. If glu-
201–250 2–4 cose not greater than 80 mg/dL, repeat treatment outlined
251–300 3–6 above. Recheck glucose value in 15 minutes. Repeat further
301–350 4–8 treatment (and glucose checks at 15 minutes intervals) until
>350 5–10 glucose level greater than 80 mg/dL.

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 S E C T I O N V Metabolic Conditions

An IV insulin infusion should be initiated (Tables 27-4 and patients with diabetes or significant hyperglycemia we initially
27-5) for severe hyperglycemia or if glucose goals cannot be measure glucose levels two to four times per day until glucose val-
achieved with subcutaneous insulin. We use different infusion ues are stable. Subsequently, glucose levels are checked twice daily.
algorithms in intensive care unit settings compared with ward 3. The majority of diabetic patients require supplemental insulin
settings. As discussed earlier, outcome studies testing degrees when glucose is infused.
of glucose control have not included patients on ward settings. a) For patients previously treated with insulin or oral diabetic
In addition, nursing staff to patient ratios are typically different agents or for patients with two more glucose values > 120 or
in intensive care unit and ward settings, and safe achievement 150 mg/dL (120 mg/dL for intensive care unit settings and
of tighter glucose goals is a challenge. Appropriate adjustment 150 mg/dL for ward settings), adding a basal amount of
of the insulin infusion is required for effective use of infusions. insulin to PN solutions is recommended.
Studies testing which insulin infusion achieves desired goals b) A common starting point is 0.1 units of insulin per g of dextrose
are limited. (eg, 10 units/L of 10% dextrose [100 g/L], 20 units/L of 20%
D. Special aspects of parenteral nutrition25 dextrose [200 g/L]).
1. A glucose level should be measured before initiation of PN. Avoid c) This ratio of insulin to dextrose is unlikely to cause hypo-
overfeeding and limit PN dextrose to ∼ 150–200 g on the first day glycemia and thus minimizes the need to discard a bag of PN
of nutrition. because it contains too much insulin.
2. Measuring glucose levels on the first and second morning follow- d) If needed, supplemental SQ regular insulin is administered
ing implementation of PN is recommended in all patients. The fre- according to an algorithm (Table 27-2) to supplement the PN
quency of subsequent monitoring should be individualized. For insulin.

TABLE 27-4. Intravenous Insulin Infusion Algorithm for ICU Use

Column 1 Column 2 Column 3 Column 4

Insulin Insulin Insulin Insulin

Bedside infusion Bedside infusion Bedside infusion Bedside infusion
glucose rate glucose rate glucose rate glucose rate
(mg/dL) (units/hr) (mg/dL) (units/hr) (mg/dL) (units/hr) (mg/dL) (units/hr)

>400 8 ≥360 12 ≥360 16 ≥270 20

351–400 6 330–359 8 330–359 14 240–269 16
301–350 4 300–329 7 300–329 12 210–239 12
251–300 3 270–299 6 270–299 10 180–209 8
200–250 2.5 240–269 5 240–269 8 150–179 4
150–199 2 210–239 4 210–239 6 120–149 2
120–149 1.5 180–209 3 180–209 4 100–119 1
100–119 1 150–179 2 150–179 3 <100 Off
<100 Off 120–149 1.5 120–149 2
100–119 1 100–119 1
<100 Off <100 Off

1. Glucose goals should be determined for each patient. In critically ill patients, a glucose goal range of 80 to120 mg/dL is appropriate. This infusion algorithm is designed for the
average 70-kg patient and may require modification for smaller or larger patients. This infusion is not appropriate for the treatment of diabetic ketoacidosis or hyperosmolar
states.
2. Choose appropriate columns for insulin infusion. Follow a column for two hours and if reflectance meter glucose (RMG) is still greater than 120 mg/dL or is not decreasing, pro-
ceed to next column. If patient treated by column 3 or 4 has RMG less than 120 mg/dL for 4 hours, then go to the next lowest column.
3. Instructions for use of columns: Use if any of the following criteria listed for each column are met. Column 1: RMG 120 to 200 mg/dL; not on corticosteroids or sympathomimetic
infusion.
Column 2: Initial RMG greater than 200 mg/dL; receiving oral or IV corticosteroids
(excludes inhaled or ophthalmic); on sympathomimetic infusion; has not reached RMG range of 80 to 120 mg/dL within two hours of using Column 1.
Column 3: Patient who has not reached RMG of 80 to 120 mg/dL within two hours using Column 2.
Column 4: Patient who has not reached RMG range of 80 to 120 mg/dL within two hours using Column 3.
4. Glucose level should be measured hourly until glucose concentration has stabilized in the desired goal range for four hours. Testing frequency may then be decreased to every
two hours. Return to hourly monitoring with any of the following: change in nutritional status, RMG is above goal for two consecutive readings or below 100 mg/dL, or change in
clinical status or column use.

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S E C T I O N V Metabolic Conditions

centration over a 24-hour period to values below the goal

TABLE 27-5. IV Insulin Infusion for Use range.
in Non-ICU Settings Symptomatic hypoglycemia after sudden discontinuation
of PN is uncommon provided that the patient has not received
IV infusion rate Insulin infusion rate excess calories.
Glucose mg/dL mL/hr units/hr If PN is discontinued it is important to remember that the
PN insulin also will be stopped.
>400 8 8 Subcutaneous insulin should be administered several hours
351–400 6 6 before discontinuation of intravenous insulin infusion to
avoid rebound hyperglycemia. For example, in patients
301–350 4 4 treated with combined intermediate and short-acting insulin
250–300 3 3 programs, administration of small amounts (eg, 4 to 5 units)
of short-acting insulin combined with a ‘basal’ insulin (eg,
200–249 2.5 2.5
glargine or ultralente insulin or small doses of NPH insulin)
150–199 2 2 is recommended.
While the technology to deliver tight glucose control in the
120–149 1.5 1.5
intensive care unit is widely available, implementing a safe
100–119 1 1 and effective program may present logistical challenges.26
70–99 0 0 One safety concern of tight glucose control is the potential
increase in the risk of hypoglycemia.
<70 0 0 E. Focused monitoring/goals assessment—In addition to the usual care-
ful monitoring required after initiation of nutrition support in a mal-
1. Guidelines are for the average 70-kg patient and modifications may be necessary nourished patient, special attention should be focused on glucose
for smaller or larger patients. Guidelines not appropriate for treatment of patients control (discussed above), fluid balance, sodium, potassium, magne-
with diabetic ketoacidosis or hyperosmolar states. sium, phosphorus, and triglyceride values.
2. Glucose should be measured hourly until glucose concentrations have stabilized in 1. A baseline glycated hemoglobin value is useful to establish
the patient's goal glucose range for 4 hours. Frequency of testing may then be recent glucose control and to determine the appropriate diabetic
decreased to every 2 hours, and once glucose control remains stable, frequency of treatment after dismissal from the hospital.
testing may be reduced to every 4 hours. 2. The presence of high urine output, negative fluid balance, weight
3. If glucose value is >200 mg/dL and does not decrease by at least 50 mg/dL by loss, or hypernatremia should prompt a review of recent glucose
2 hours, increase insulin infusion by 50% increment for each glucose range
trends to be certain hyperglycemia is not causing an osmotic
>150 mg/dL. Make the same adjustment if glucose <200 mg/dL (but >150 mg/dL)
and does not decrease by at least 25 mg/dL by 2 hours. Risk of hypoglycemia may
diuresis.
be greater if infusions are increased for glucose ranges <150 mg/dL. 3. Hyperglycemia may cause a pseudohyponatremia. In general,
4. When converting from an IV to SQ insulin program, continue infusion for 1 to each incremental increase in plasma glucose of ∼60 mg/dL
3 hours after administration of first SQ insulin dose. reduces the plasma sodium concentration by 1 mEq/L.
4. Hyperkalemia, if accompanied by hyperglycemia, if often effec-
tively treated by an increase in insulin supplementation.
If over a 24-hour period glucose values consistently exceed 5. Hyperinsulinemia due to refeeding or insulin administration may
the desired goal, the PN insulin is increased by 0.05 units of lead to a decrease in plasma levels of potassium, magnesium, and
insulin injection per g of dextrose each day to 0.2. phosphorus.27
Order forms to standardize use of insulin infusions are pre- 6. Hyperinsulinemia shifts potassium and magnesium into skele-
sented in Tables 27-4 and 27-5. tal muscle and hepatic cells.
If two consecutive glucose values exceed 120 mg/dL in 7. Glucose and insulin-stimulated glycolysis increases cellular
patients in intensive care units, it is reasonable to initiate an uptake and utilization of phosphorus for phosphorylation of glu-
insulin infusion. On wards, guidelines for when to initiate cose and fructose and for synthesis of adenosine triphosphate.
infusions are less clear as data is limited. It is recommended 8. Serum potassium and phosphorus concentrations should be mon-
to continue providing PN insulin for patients treated with an itored daily (and appropriately managed) until values are in the
insulin infusion. However the SQ insulin algorithm should be normal range.
discontinued. 9. For patients with known hypertriglyceridemia receiving PN,
In general, the dextrose content of the PN should not be triglycerides should be checked before initiation and during fat
increased until the glucose concentrations during the previous emulsion administration. Measuring a triglyceride level before
24-hour period are in goal range. initiation of PN is also recommended in patients with pancre-
Insulin in the PN should be proportionally increased or atitis or poorly controlled diabetes and in those receiving med-
decreased when the PN dextrose content is increased or ications formulated in fat emulsion.
decreased. 10. Although there are limited data regarding infusion of fat emulsion
If the patient develops hypoglycemia, parenteral dextrose in patients with hypertriglyceridemia, if the plasma triglyceride
should be administered (Table 27-3) and the PN insulin con- concentration exceeds 350 to 400 mg/dL reducing the amount of
tent should be reduced by approximately 50% to minimize fat or discontinuing fat altogether is recommended, as lipoprotein
recurrent hypoglycemia. lipase-mediated triglyceride uptake may be saturated above this
Similar reductions in the PN insulin should also be made level.28 Triglyceride-rich lipoproteins are removed from the cir-
if there is a significant decrease in the mean glucose con- culation by zero- and first-order kinetics and therefore, when sat-

322 A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. © 2005 A.S.P.E.N. www.nutritioncare.org.
 S E C T I O N V Metabolic Conditions

urated, plasma triglyceride concentrations will increase exponen- 12. Bistrian BR. Hyperglycemia and infection. Which is the chicken and which
tially with incremental changes in the rate of infusion of intra- the egg? J Parenter Enter Nutr. 2001;25:180–181.
venous fat emulsion. 13. Moore FA, Feliciano DV, Andrassy RJ, et al. Early enteral feeding, com-
pared with parenteral, reduces postoperative septic complications. The
F. System of care
results of a meta-analysis. Ann Surg. 1992;216(2):172–83.
1. Implementation of a safe and effective program for glucose con-
14. Pomposelli JJ, Baxter JK, Babineau TJ, et al. Early postoperative glucose
trol is required. control predicts nosocomial infection rate in diabetic patients. J Parenter
2. One safety concern relates to the potential increase in the occur- Enter Nutr. 1998;22:77–81.
rence of hypoglycemia in patients with a goal of tight glucose 15. Capes SE, Hunt D, Malmberg K, Gerstein HC. Stress hyperglycemia and
control. increased risk of death after myocardial infarction in patient with and with-
3. Well-defined algorithms to manage high and low glucose levels out diabetes. A systematic overview. Lancet. 2000;355:773–778.
are required as well as education of managing staff. 16. Capes SE, Hunt D, Malmberg K, et al. Stress hyperglycemia and progno-
sis of stroke in nondiabetic and diabetic patients: A systematic overview.
(Diabetes chapter from the 1st edition was contributed by Susan A. Stroke. 2001;32:2426–2432.
17. The Veterans Affairs Total Parenteral Nutrition Cooperative Study Group.
Romanski and M. Molly McMahon)
Perioperative total parenteral nutrition in surgical patients. N Engl J Med.
1993;325:525–532.
REFERENCES 18. Furnary AP, Zerr KJ, Grunkemeier GL, et al. Continuous intravenous
1. The Expert Committee on the Diagnosis and Classification of Diabetes insulin infusion reduces the incidence of deep sternal wound infection in
Mellitus. Report of the expert committee on the diagnosis and classifica- diabetic patients after cardiac surgical procedures. Ann Thorac Surg.
tion of diabetes mellitus. Diabetes Care. 1997; 20:1183–1197. 1999;67:352–362.
2. Umpierrez GE, Isaacs SD, Bazargan N, et al. Hyperglycemia: an inde- 19. Furnary AP, Guangqiang G, Grunkemeier GL, et al. Continuous insulin
pendent marker of in-hospital mortality in patients with undiagnosed dia- infusion reduces mortality in patients with diabetes undergoing coronary
betes. J Clin Endocrinol Metab. 2002;87:978–982. artery bypass grafting. J Thorac Cardiovasc Surg. 2003;1125:1007–1021.
3. Shamoon M, Hendler R, Sherwin R. Synergistic interactions among anti- 20. Malmberg K, for the DIGAMI Study Group. Prospective randomized study
insulin hormones in the pathogenesis of stress hyperglycemia in humans. J of intensive insulin treatment on long-term survival after acute myocardial
Clin Endocrinol Metab. 1981;52:1235–1241. infarction in patients with diabetes mellitus. Br Med J. 1997;314:1512–1515.
4. Shamoon M. Hendler R, Sherwin R. Altered responsiveness to cortisol, epi- 21. Van den Berghe G, Wouters P, Weekers F, et al. Intensive insulin therapy in
nephrine, and glucagon in insulin-infused juvenile-onset diabetes. Dia- critically ill patients. N Engl J Med. 2001;345:1359–1367.
betes. 1980;29:284–301. 22. American Diabetes Association. Nutrition recommendations and principles
5. McMahon MM, Farnell MB, Murray MJ. Nutritional support of critically for people with diabetes mellitus. Diabetes Care. 1995;18:16–19.
ill patients. Mayo Clin Proc. 1993;68:911–920. 23. Nutrition Subcommittee of the Diabetes Care Advisory Committee of Dia-
6. Camilleri M. Advances in diabetic gastroparesis. Rev Gastroenterol Disord. betes UK. The implementation of nutritional advice for people with dia-
2002;2:47–56. betes. Diabet Med. 2003;20:786–807.
7. Hostetter M. Perspectives in diabetes: Handicaps to host defense: effects of 24. A.S.P.E.N. Board of Directors. Clinical pathways and algorithms for deliv-
hyperglycemia on C3 and Candida albicans. Diabetes. 1990;39:271–275. ery of parenteral and enteral nutrition support in adults. Silver Spring, MD:
8. Gustafson KS, Vercellotti GM, Bendel CM, et al. Molecular mimicry in American Society for Parenteral and Enteral Nutrition; 1998:4–11.
Candida albicans: role of an integrin analogue in adhesion of the yeast to 25. McMahon M. Management of parenteral nutrition in acutely ill patients
human endothelium. J Clin Invest. 1991;87:1896–1902. with hyperglycemia. Nutr Clin Practice. 2004;19:120 –128.
9. Hostetter M. The third component of complement: new functions for an old 26. Montori VM, Bistrian BR, McMahon M. Hyperglycemia in acutely ill
friend. J Lab Clin Med. 1993;122:491– 496. patients. J Am Med Ass. 2002;288:2167–2169.
10. McCowen KC, Malhotra A, Bistrian BR. Stress-induced hyperglycemia. 27. Knochel JP. Complications of total parenteral nutrition. Kidney Int. 1985;27:
Crit Care Clin. 2001;17:107–124. 489– 496.
11.McMahon M, Bistrian BR. Host defenses and susceptibility to infection in 28. Carpentier YA. Intravascular metabolism of fat emulsions. Clin Nutr.
patients with diabetes mellitus. Infect Dis Clin N Am. 1995;9:1–9. 1989;8:115–1.

© 2005 A.S.P.E.N. www.nutritioncare.org. A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. 323
 Julie L. Roth, MD; Robert F. Kushner, MD;
Eden Bateman, MS, RD, LD
28
Obesity

Introduction II. Nutritional Alterations

One third of Americans and over 50% of minority women are consid- A. The nutritional alterations of obesity primarily include changes in
ered obese, while 15% of US children and adolescents are overweight. body composition and energy expenditure. These variables are
Obesity, defined as a body mass index (BMI) of greater than or equal to interrelated, since body weight (kg) is a function of energy balance
30 kg/m2, is associated with several chronic degenerative diseases that (calories).
often require medical and surgical attention. Nutritional care of obese 1. Body composition. A positive energy balance produced and sus-
individuals requires expertise in management of the associated comor- tained over time must result in the storage of excess calories and
bidities, assessment of energy and protein requirements, special tech- a gain in body weight. These excess calories are stored in adipose
niques of access, and delivery and monitoring of nutrition support. tissue (fat mass) and used to synthesize adipose tissue-free mass
(lean body mass [LBM]). Forbes et al found the increase in LBM
I. Background accounts for 29% (range 20%–40%) of the excess weight.4 This
II. Nutritional Alterations LBM/body weight relationship is not linear, however; the fatter
III. Focused Assessment the individual, the less will be the relative contribution of LBM
IV. Approach to the Patient to the total weight.
V. Management 2. Total energy expenditure (TEE). TEE increases with increasing
References body weight in both men and women. Interpersonal variability in
this relationship is due to genetic determinants, body composition,
I. Background and level of physical activity. TEE is composed of three distinct
factors: basal metabolic rate (BMR), thermogenic effect of food,
A. Prevalence. The 1999 National Health and Nutrition Examination and physical activity. The increased energy expenditure observed
Survey (NHANES 1999) found that 34% of the adults in the United in obesity is primarily attributed to an elevated BMR that results
States aged 20 and over are overweight, and 27% are obese.1 This from increased LBM. Differences in energy requirements within
represents a 100% increase in obesity prevalence from the 15% and between individuals are primarily due to differences in physi-
reported during NHANES II (1976–1980).2 For these population sur- cal activity. Since the energy cost of a given activity (workload) is
veys, adults were classified as overweight when their BMI (defined proportional to body weight, total absolute energy expended in
as the weight in kilograms divided by the height in meters squared physical activity is higher in healthy obese individuals than in their
[kg/m2]) was 25 to 29.9 kg/m2 and obese when their BMI was greater lean counterparts. However, when energy expenditure or physical
than or equal to 30 kg/m2.
activity is normalized for BMR (physical activity level index =
B. Etiology. Obesity is a heterogeneous disease involving genetic, envi-
TEE/BMR), the influence of body weight disappears. An average
ronmental, psychological, and other factors. The current view holds
physical activity level index (light to moderate activities) can be
that genetics determines vulnerability (penetrance) while environ-
assumed to be 1.55 to 1.65, whereas sedentary individuals (chair-
ment determines the presence in vulnerable individuals and the extent
bound or bed-bound) exhibit a physical activity level index of 1.2
of disease. Regardless of the etiology, however, obesity occurs when
energy intake exceeds the amount of energy expended over time. (an index that is commonly seen among hospitalized patients).5
1. Obesity is considered a disorder of energy balance. Persons become 3. Substrate metabolism. Studies by Jeevanandam et al6,7 suggest that
overweight when a positive energy balance is produced when- the sources of endogenous metabolic fuels differ significantly
ever (1) energy intake is increased, (2) energy output is lowered, in obese and nonobese patients in response to injury. Whereas
or (3) both occur. In contrast, maintenance of the obese state is nonobese patients displayed an increase in net fat oxidation, obese
sustained when the individual is once again in energy balance, patients derived a significantly lower percentage of their energy
produced when either (1) energy intake and output are both low requirements from mobilization of fat. Energy was produced
or (2) energy intake and output are both high. instead from oxidation of carbohydrates and protein. Thus, there is
2. The role of genetics in human obesity may involve appetite reg- concern that obese patients have both a reduced ability to mobilize
ulation, metabolic partitioning of nutrients, and thermogenesis. fat stores after acute injury and a limited capacity to oxidize fat.
3. Although genetics influences the tendency to become obese, the B. Health alterations
development and severity of obesity depend on the environment. 1. Endocrine system
Improving on the unhealthy eating and physical activity habits of a) Glucose intolerance. Increasing severity of obesity is associated
Americans forms the basis for several initiatives of the Public with the development of reduced insulin sensitivity, increased
Health Service’s Healthy People 2010 campaign.3 insulin secretion, glucose intolerance, and type 2 diabetes

324 A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. © 2005 A.S.P.E.N. www.nutritioncare.org.
 S E C T I O N V Metabolic Conditions

mellitus. Thus, the occurrence of acute illness, administration put. This is accomplished by increasing stroke volume; heart
of anti-insulin medications (eg, corticosteroids), or infusion of rate usually remains normal. Over time, an increased cardiac
intravenous dextrose often results in glucose intolerance and preload results in increased left ventricular end-diastolic vol-
uncontrolled hyperglycemia. ume, wall stress, and development of eccentric left ventricular
b) Dyslipidemia. Obesity is associated with a higher prevalence hypertrophy. Development of hypertension and increased car-
of hypertriglyceridemia, low levels of high-density lipoprotein diac afterload results in concentric left ventricular hypertrophy.
(HDL) cholesterol, and elevated total cholesterol. The admin- The consequences of increasing severity and duration of obe-
istration of intravenous fat may cause hypertriglyceridemia sity include coronary artery disease and congestive heart fail-
and requires close monitoring. ure. Hypoventilation and obstructive sleep apnea result in
2. Metabolic syndrome increased pulmonary artery pressure, right-sided hypertension,
a) The metabolic syndrome is a constellation of cardiovascular and cor pulmonale. The fluid-overloaded status and congestive
disease (CVD) risk factors that is present in approximately 24% changes of the severely obese patient require that fluid admin-
of US adults.8 According to the Adult Treatment Panel defini- istration be carefully monitored.
tion of the metabolic syndrome,9 three of the following five cri- b) Obesity is often associated with peripheral venous stasis and
teria must be present for diagnosis: increased abdominal girth risk for thromboembolism. This increased risk may be due to
(>35 inches for women or >40 inches for men), increased a deficiency in antithrombin III, a serum protein that inhibits
triglyceride levels (≥150 mg/dL), decreased HDL choles- thrombin activity, and other prothrombotic factors, including
terol levels (<50 mg/dL for women or <40 mg/dL for men), increased plasma PAI-1, fibrinogen, and factor VIII. The throm-
increased blood pressure (≥130/85 mm Hg), and increased botic tendency is of particular concern when an indwelling
fasting glucose (≥110 mg/dL). venous catheter is placed for intravenous fluids and nutritional
b) Lemieux et al10 have suggested that simultaneous measurement support. Thus, obese patients require primary prevention that
of waist circumference and fasting triglyceride levels could be often includes pneumatic compression of the lower extremi-
used to identify individuals who meet the metabolic syndrome ties combined with subcutaneous or intravenous unfraction-
criteria. Presence of the metabolic syndrome increases risk for ated heparin or low-molecular weight heparin.
development of type 2 diabetes and CVD.11 5. Gastrointestinal system. Obese patients’ increased risk for devel-
c) The syndrome is also associated with insulin resistance; small, oping gallbladder disease is proportional to their higher BMI,
dense low-density lipoprotein particles; increased biomarkers with a significant increase above 30 kg/m2.14 Obese patients are
of chronic inflammation (eg, C-reactive protein, tumor necro- also at increased risk for developing nonalcoholic fatty liver dis-
sis factor-α); a prothrombotic state; endothelial dysfunction; ease, gastroesophageal reflux disease, and colon cancer.
and hemodynamic changes (increased sympathetic nervous 6. Psychiatric issues. Obese patients often suffer from depression that
system activity and renal sodium retention)—although these may or may not be diagnosed. One study found higher depression
are not routinely measured.12 Recent studies have linked the scores in women, younger subjects, and those with body image
metabolic and inflammatory abnormalities seen in obesity to issues at baseline; these scores significantly decreased with surgi-
the secretion of adipocyte and adipose connective tissue prod- cally induced weight loss at 4-year follow-up.15
ucts, or adipokines. Peptides secreted by the adipocyte include 7. Nursing care issues. The heavy body weight and immobility of the
leptin, plasminogen activator inhibitor-1 (PAI-1), interleukin- obese patient increases the risk for skin breakdown, development
6, adiponectin, angiotensinogen, and tumor necrosis factor-α.13 of decubitus ulcers, and infection. Necrosis and infection may
3. Respiratory system quickly spread through the subcutaneous tissue with little warning.
a) Pulmonary function. The most frequently described alter- Intertriginous areas, such as under the breasts, on inguinal folds,
ations in pulmonary function of the obese patient are restric-
beneath the abdominal pannus, and on inner thighs, are often sites
tive defects: a decreased functional residual capacity (FRC)
for skin maceration and fungal infections. Care is needed to pre-
and a decreased expiratory reserve volume (ERV). These
vent skin breakdown by frequently rolling the bedridden patient,
changes result from reduced compliance of the chest wall and
closely examining all skin areas, and using beds specially designed
lung tissue, primarily due to the cephalad displacement of the
to facilitate care of the severely obese patient.
diaphragm and increased weight of fat tissue on the chest wall
during tidal breathing. The loss of FRC and ERV results in air-
way closure, alveolar dysfunction, and ventilation/perfusion III. Focused Assessment
abnormalities. Increased metabolic requirements for oxygen
consumption and carbon dioxide excretion may exceed pul- A. History
monary capacity. 1. Obesity is associated with the coexistence of multiple diseases.
b) Obesity hypoventilation syndrome (OHS) and obstructive Therefore, a detailed history of the obese patient should include a
sleep apnea (OSA). More severe degrees of obesity may result collection of medical information related to any comorbid condi-
in further impairment of pulmonary function and develop- tions, use of medications that may influence body weight (includ-
ment of hypoventilation, hypoxia, hypercarbia, and obstruc- ing a history of medications specifically related to the treatment of
tive sleep apnea. Patients with OHS and/or OSA should be obesity), a family history of obesity and related diseases, and a his-
closely monitored with pulse oximetry and capnography dur- tory of surgeries specifically related to the treatment of obesity. A
ing nutrition support. Use of continuous positive airway pres- thorough medication history should be obtained, looking for pos-
sure in both hospitalized and ambulatory patients should be sible drug-induced weight gain. Medications associated with
instituted if obstructive sleep apnea is detected. weight gain are listed in Table 28-1.16
4. Cardiovascular system 2. Dietary assessment is an important tool to identify premorbid
a) The increased metabolic demands of obesity with increased nutritional risk factors, to provide information about previous
VO2 , VCO2 , and blood volume require an increased cardiac out- attempts at weight reduction, and to document current intake.

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S E C T I O N V Metabolic Conditions

calculation can also be easily performed by dividing the weight

TABLE 28-1. Medications Associated With Body Fat by height twice, for example, kg/m/m. The BMI uses a ratio of
Weight Gain height to weight, thus eliminating the need to compare weight
to a reference value. Several classifications of obesity have
Psychiatric/neurological been proposed based on health outcomes. The Expert Panel on
• Antipsychotic agents: phenothiazines, olanzapine, clozapine, the Identification, Evaluation, and Treatment of Overweight
risperidone and Obesity in Adults recommends the classification shown in
• Mood stabilizers: lithium Table 28-2.18 BMI measurements should be used as a screening
• Antidepressants: tricyclics, MAOIs, SSRIs (paroxetine), tool in all hospitalized patients.
mirtazapine 2. Assessment of body composition/fat distribution
• Antiepileptic drugs: gabapentin, valproate, carbamazepine a) Waist measurements are commonly used to evaluate the dis-
tribution of body fat, especially in persons with a BMI less than
Steroid hormones 35 kg/m2. A waist circumference ≥35 inches (85 cm) in women
• Corticosteroids or ≥40 inches (100 cm) in men leads to an increased risk of
• Progestational steroids developing obesity-related comorbidities regardless of the
BMI classification. The presence of excess fat stores in the
Antidiabetes agents abdominal visceral depot has significant prognostic impor-
• Insulin, sulfonylureas, thiazolidinediones tance. Patients with greater upper body fat tend to have greater
visceral fat stores and increased risk for developing hyper-
Antihypertensive agents insulinemia, glucose intolerance, hypertriglyceridemia, hyper-
• Beta- and alpha-1 adrenergic receptor blockers tension, diabetes mellitus, and coronary artery disease than
individuals with lower body obesity.19 According to the Prac-
Antihistamines tical Guide,20 “To measure waist circumference, locate the
• Cyproheptadine upper hip bone and the top of the right iliac crest. Place a meas-
uring tape in a horizontal plane around the abdomen at the
HIV protease inhibitors: lipodystrophy level of the iliac crest. Before reading the tape measure, ensure
that the tape is snug, but does not compress the skin, and is par-
HIV, human immunodeficiency virus
allel to the floor. The measurement is made at the end of a nor-
Reprinted from Kushner RF, Roth JL. Assessment of the obese patient. Endocrinol mal expiration.”
Metab Clin N Am. 2003;32:915–933 with permission from Elsevier. b) Skinfold measurements are used to estimate the quantity of sub-
cutaneous fat. Measurements can be taken from various body
sites and then compared with standard reference values. These
estimates are most useful when serial measurements are taken
3. For long-term planning it is important to know which member of over time to assess changes in body composition. For this rea-
the household is primarily responsible for shopping and meal son, skinfold measurements are rarely used to assess nutritional
preparation. This person should be involved in discharge planning status in the acute care setting. The reliability of skinfold meas-
and education. urements decreases as body fat increases because there are large
4. Weight history is essential to gain an understanding of the patient’s fat folds that the caliper cannot accurately measure.21 In the
weight patterns and potential for successful, long-term weight
management. Patients who have made recent attempts to lose
weight and have suffered nutritional deficiencies may need a
period of refeeding or nutritional replenishment prior to a surgical
procedure. TABLE 28-2. Classification of Overweight
5. Habitual physical activity level and limitations should be assessed. and Obesity by BMI
Information regarding actual activities as well as the duration
and frequency of the activities prior to admission should be Obesity Class BMI (kg/m2)
documented.
B. Physical examination Underweight <18.5
1. Anthropometric measurements Normal 18.5–24.9
a) Measurement of an obese patient’s body weight is useful for
Overweight 25.0–29.9
nutrition calculations and medical management. The admission
weight is used for the calculation of nutrient requirements and Obesity I 30–34.9
medication dosing. However, several disease states can cause
Obesity II 35–39.9
physically undetectable increases in fluid retention or total body
water in the severely obese patient. Any calculations that Extreme obesity III ≥40.0
include excess fluid weight will introduce error into the final
estimate. Daily weights obtained with the same scale will assist BMI, body mass index
the clinician with monitoring alterations in fluid, as opposed to Reprinted from National Heart, Lung, and Blood Institute. Clinical Guidelines on the
indicating changes in nutritional status. Identification, Evaluation, and Treatment of Overweight and Obesity in Adults. The evi-
b) BMI (weight divided by height squared [kg/m2]) is the most dence report. Obes Res. 1998;6(suppl 2):51S–210S with permission from the North
useful and practical measure for assessing body fatness.17 The American Association for the Study of Obesity.

326 A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. © 2005 A.S.P.E.N. www.nutritioncare.org.
 S E C T I O N V Metabolic Conditions

acute care setting, skinfold measurements can be taken if the

patient intends to follow up for long-term weight management. TABLE 28-3. Predictive Equations to Estimate
C. Laboratory data Energy Expenditure
1. Abnormalities seen in obese patients may include hyperglycemia,
hyperinsulinemia, dyslipidemia, elevated uric acid levels, and Harris-Benedict
abnormal liver function tests. Patients with OHS may present with Men: 66.47 + 13.75(W) + 5.0(H) − 6.75(A)
hypoxemia and hypercarbia. Women: 655.1 + 9.56(W) + 1.85(H) − 4.68(A)
2. Laboratory abnormalities seen in patients who have previously W, weight (kg); H, height (cm); A, age (yr)
undergone malabsorptive procedures for obesity include iron defi-
ciency anemia, vitamin B12 and folate deficiency, and calcium Ireton-Jones
deficiency. Laboratory evaluation may demonstrate elevated EEE(V) = 1925 − 10(A) + 5(W) + 281(S) + 292(T) + 851(B)
parathyroid hormone levels with depressed 25-hydroxyvitamin D EEE(S) = 629 − 11(A) + 25(W) − 609(O)
and normal calcium levels.22 V, ventilator; S, spontaneous breather; A, age (yr); W, weight (kg);
S, sex (male = 1, female = 0); T, trauma (present = 1, absent = 0);
IV. Approach to the Patient B, burns (present = 1, absent = 0); O, obesity (present = 1,
absent = 0)
A. Objectives/goals of therapy. Traditional practice is to provide ade-
quate energy for weight maintenance or to provide enough calories Amato
to support anabolism. More recently, though, practitioners have EE = 21 kcal/kg (kg in actual weight)
started to implement nutrition care plans for obese patients that pro-
mote gradual loss of body fat while maintaining or replenishing Adjustment of body weight for obesity
LBM. This therapy is often referred to as a protein-sparing modified Adjusted body weight = [(actual weight − ideal weight) × 0.25)
fast (PSMF). The PSMF is designed to promote use of endogenous + ideal weight]
fat stores for energy while maintaining nitrogen balance, maintaining
LBM, and promoting anabolism. The PSMF has been used for years
to treat nonstressed obese people. More recently, the PSMF theory EE, energy expenditure; EEE, estimated energy expenditure
has been applied to metabolically stressed obese patients who require Reprinted from Amato P, Keating K, Quercia R, et al. Formulaic methods of estimating
enteral nutrition or parenteral nutrition (PN) support. Dickerson et al23 calorie requirements in mechanically ventilated obese patients: a reappraisal. Nutr
Clin Pract. 1995;10:229–232, with permission from the American Society for Par-
found that obese patients given hypocaloric PN achieved a beneficial
enteral and Enteral Nutrition (A.S.P.E.N.).
clinical outcome with complete wound healing, weight loss, and
improved plasma proteins. Using a randomized, prospective, double-
blind, controlled trial design, Choban et al24 demonstrated that obese
patients receiving hypoenergetic feedings achieved a nitrogen bal- estimate of energy requirements. The Ireton-Jones equation
ance comparable to that of patients given conventional PN regimens. was developed specifically for hospitalized patients and takes
B. Clinical considerations into account mechanical ventilation and obesity (Table 28-3).
1. Severity of obesity. Patients with mild obesity may benefit from Amato et al25 compared these formula estimates, as well as their
a weight maintenance feeding regimen until they are medically own estimate of 21 kcal/kg of actual weight/day for obese
stable. This is especially true if the patients are not motivated to patients, to actual measured energy expenditure (MEE) by
continue with weight loss after discharge from the hospital. Mod- indirect calorimetry. With a total of 188 measurements on 113
erately and severely obese patients may develop comorbidities obese mechanically ventilated patients, they found an overall
related to their excess weight. For these patients, hypocaloric precision of ± 400 kcal between the calculated requirements
feedings for gradual weight loss may be beneficial. and MEE, thus suggesting that the use of predictive equations
2. Comorbid considerations. Hypocaloric, protein-sparing therapy should be limited to situations in which actual measurement of
can be useful for patients with poor respiratory status, hyper- resting metabolic rate by indirect calorimetry is not available.
glycemia, and positive fluid balance. A reduction of total calorie One of the most controversial aspects of using predictive equa-
input reduces carbon dioxide production and enhances diuresis, tions to estimate energy requirements for obese patients is
which can improve ventilation and facilitate liberation from the choosing which weight to use in the calculation: actual, ideal,
ventilator. The low glucose load from the hypocaloric feeding or adjusted. It is thought that if the actual weight of an obese
reduces the risk of carbohydrate intolerance and can decrease patient is used, then the estimate will be significantly above the
insulin requirements. actual energy requirement, since adipose tissue is less meta-
3. Premorbid nutritional status. Patients assessed as having malnutri- bolically active than LBM. Obese people are known to have
tion may need a maintenance nutrition care plan during the critical higher LBM than nonobese people of equal stature.26 If ideal
phase of their illness or until nutritional replenishment/refeeding body weight (IBW) is used to calculate energy requirements,
has occurred. Hypocaloric feeding is most appropriate for obese the final estimate will fail to account for the increased metabolic
patients who are not malnourished upon admission. activity of the extra LBM and underestimate the total energy
C. Assessment of energy requirements requirement. The adjustment of body weight for an obese
1. Calculated patient is based on an average increase in LBM of approxi-
a) The Harris-Benedict equation was developed with the use of mately 25% (as discussed in Section II.A.1) to account for
healthy subjects and, therefore, requires the addition of stress metabolically active tissue (Table 28-3).
factors that involve subjective judgment of the patient’s stress b) A recent study evaluated four different equations (Harris-
level (Table 28-3). This introduces bias and error to the final Benedict, Harris-Benedict using adjusted body weight in

© 2005 A.S.P.E.N. www.nutritioncare.org. A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. 327
S E C T I O N V Metabolic Conditions

obese individuals, Owen, and Mifflin) in nonhospitalized obese this practice, the following guidelines should be used for calcu-
and nonobese subjects. The Mifflin calculation (men: kcal/ lating protein requirements:
day = 879 + 10.2 [weight in kg]; women: kcal/day = 795 + 7.2 1. Maintenance32: 1.0 g/kg IBW
[weight in kg]) provided a more accurate estimate of actual 2. Stress32,33: 1.5 to 2.0 g/kg IBW
resting metabolic rate in the largest percentage of obese and E. Vitamin and mineral requirements for obese patients are based on
nonobese subjects, with a low rate of overestimation.27 This dietary reference intakes. Any deficiencies should be corrected with
study confirmed the tendency to underestimate resting meta- supplements. Close attention must be paid to the vitamins and min-
bolic rate with the Harris-Benedict equation when using an erals provided by hypocaloric feedings. It is likely that patients who
adjusted body weight. receive hypocaloric feedings in an oral diet or via enteral nutrition
c) Another study assessed the use of bioelectrical impedance support will need daily vitamin and mineral supplements.
analysis to develop predictive equations for resting energy F. Periodic reassessment of the patient’s nutritional status and goals
expenditure (REE).28 This method provided an REE estimate should be conducted every 2 weeks, or earlier if there is a change
that was significantly more accurate than the Harris-Benedict in the patient’s medical condition. Calorie and protein requirements
equation in 75% of patients. In male subjects, the mean error of should be more frequently assessed for patients being treated with
the estimate using the Harris-Benedict equation was 372 kcal/d, hypocaloric feedings, as weight loss may alter energy expenditure.
whereas it was 242 kcal/d with the predictive equation. In
female subjects, the mean error of the estimate with the Harris-
Benedict equation was 343 kcal/d, whereas it was 158 kcal/d V. Management
using the predictive equation A. Special aspects of diet and nutritional supplements
1. Dietary modifications
Men: EE = [858 − 4.6 age + 12.1 FFM
a) A balanced-calorie weight maintenance diet is appropriate for
+ 15.0] (stress factor) obese patients who do not desire weight loss or for whom it is
not indicated. A macronutrient distribution of 45% to 65%
Women: EE = [812 − 5.57 age + 15.2 FFM carbohydrate, 10% to 35% protein, and 20% to 35% fat is rec-
+ 5.61FM] (stress factor) ommended by the Institute of Medicine,34 although guidelines
should be consistent with those for any comorbidities, for
where EE is energy expenditure, FFM is fat-free mass (in example, 2 g of sodium for renal dysfunction or 20% of calo-
kg), and FM is fat mass. ries from protein for wound healing. These patients should
2. MEE with use of indirect calorimetry is the most accurate, reli- have an adequate serum protein status and should be hemo-
able, and practical method of assessing energy requirements in dynamically stable. The total daily calorie deficit should not
critically ill patients. Continuous indirect calorimetry is ideal exceed 500 kcal/d for very gradual weight loss.
for measuring REE as well as the metabolic and mechanically b) In very low calorie diets (VLCD), usual food intake is replaced
induced rises in energy expenditure. Unfortunately, few hospitals
by specific liquid or food formulations containing 800 kcal/d or
have the resources to routinely conduct continuous indirectly
less.35 Patients are considered appropriate for VLCD when they
calorimetry. Commonly, intermittent indirect calorimetry is con-
have failed at more conventional approaches to weight loss, are
ducted over 30 to 60 minutes at various times during the hospi-
well motivated, and have a BMI of greater than 30 kg/m2.
talization to periodically determine average energy expenditures.
Patients should undergo a thorough history and physical
Indirect calorimetry is the ideal method for determining energy
examination before beginning VLCD. Initial laboratory test-
requirements in the obese patient population, since the measure-
ing should include complete blood cell count, serum elec-
ment eliminates the need to use judgment with regard to body
weight, alterations in body composition, and stress factors. trolytes, liver function tests, serum urea nitrogen and creatinine,
3. If weight loss is desired during an acute illness, the preferred mode a fasting or postprandial blood glucose, and uric acid. Patients
is to institute hypocaloric nutrition support. This type of regimen on VLCD must be closely monitored in clinic and generally
will induce weight loss while minimizing loss of LBM. The basic lose 1.5 to 2.5 kg/week, with total weight loss of 20 kg at 12 to
approach is to provide 50% to 60% of MEE or calculated energy 16 weeks. The risk for gallstone formation increases expo-
requirements,23,28 with adequate protein to preserve LBM, and min- nentially at rates of weight loss above 1.5 kg/week.36 Prophy-
imal or no fat. Shikora and Muskat29 favor the use of adjusted body laxis against gallstone formation with ursodeoxycholic acid,
weight, which accounts for the larger LBM, when calculating the 600 mg/day, is effective in reducing this risk.37 Usually within
energy requirements for a patient receiving hypocaloric feedings. 1 week, diabetic patients’glycemic control improves, with blood
Choban et al24 base their caloric requirements on a fixed total pressure improving at a slower rate.
energy-to-nitrogen ratio (kcal/g of nitrogen) of 75:1, where all c) Progression of diet in a hospitalized critically ill obese patient
patients receive 2 g of protein/kg of IBW. This form of nutrition is similar to that of a nonobese patient. Ideal dietary intake con-
support has been used for patients with weights 130% or greater sists of food taken orally. If patients are unable to take food
than ideal. The nutrients for hypocaloric nutrition support can be orally or if they are unable to meet their caloric needs in this
delivered enterally or parenterally. A more recent study30 cautions manner, then enteral nutrition is the next-best option. If patients
against the use of hypocaloric high-protein nutritional support in are unable to tolerate oral food or enteral nutrition (eg, owing
hospitalized stressed obese patients over the age of 60. In this study, to bowel obstruction, bowel ischemia, or severe pancreatitis),
5 of 12 patients over the age of 60 had negative nitrogen balance. then PN should be employed.
D. Protein requirements can be calculated after an assessment is 2. Dietary considerations after surgical treatment of obesity, which
made of serum protein status, renal function, and metabolic stress depend upon the procedure performed
level. A review of the literature indicates a general practice of a) Patients who have undergone a Roux-en-Y gastric bypass
using IBW when protein requirements are calculated.31 Based on (RYGB) procedure are at risk of developing dumping syndrome

328 A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. © 2005 A.S.P.E.N. www.nutritioncare.org.
 S E C T I O N V Metabolic Conditions

because of alterations of the intestinal anatomy that involve syndrome, and very light sedation with simple draping of the face
bypassing the pyloric valve. These patients should restrict and neck can significantly increase the PCO2. Therefore, with any
their intake of simple sugars to reduce the risk of dumping approach to enteral access in the severely obese, maintenance
hypertonic gastric contents into the small bowel, which can of an adequate airway and assurance of normal oxygenation and
cause abdominal cramping, osmotic diarrhea, and vasomotor ventilation are mandatory. An increase in morbidity and mortal-
changes. ity is associated with pickwickian syndrome (sleep apnea syndrome
b) The RYGB and laparoscopic adjustable silicone gastric band- and obstructive hypoventilation syndrome), benzodiazepine use,
ing procedures reduce the capacity of the stomach, so small, epidural use, and morphine administration.
frequent meals are required. Often the diet is initiated with a) Surgical gastrostomy. Surgical gastrostomy or gastrojejunos-
clear liquids and advanced slowly to pureed or soft foods. tomy can be performed primarily for enteral access in severely
The ideal dietary composition of the liquids is high protein obese patients. A midline incision is preferred. The severely
(usually 60–100 g protein/d), moderate carbohydrate, and obese can develop significant debilitating and serious wound
very low fat. Intake of carbonated beverages should be lim- infections from a simple gastrostomy. These techniques can
ited to avoid excess pressure on the remnant pouch and the also be performed laparoscopically with excellent results and
gastric outlet port. Beverages consumed by patients should be avoid the complications of a midline incision. The rate of inci-
no calorie or low calorie. sional hernia following midline incisions in severely obese
c) Post-bariatric surgery patients should consume a clear liquid patients approaches 30%, so laparoscopic techniques may be
diet for the first 1 to 2 days, progressing to a full liquid diet. advantageous.
At the time of discharge, patients are generally eating a b) Surgical jejunostomy. Jejunostomy in the severely obese is often
pureed/soft diet. At 4 to 6 weeks, patients should gradually associated with many complications: subcutaneous abscess for-
transition to a regular-consistency low-fat, controlled-energy mation, small-bowel obstruction, feeding into the subcutaneous
diet. Patients should be instructed to avoid consuming fluids space, and peritonitis. This option is best reserved for cases in
for at least 30 minutes before and after meals. Minimum daily which gastrostomy or gastrojejunostomy cannot be performed.
protein intake should be 60 to 75 grams divided into four to c) Percutaneous endoscopic gastrostomy (PEG) or gastrojejuno-
six small meals daily. Patients should also keep food logs, stomy. PEG or gastrojejunostomy is useful for the severely
including foods not tolerated, for discussion with the dieti- obese patient requiring enteral access. In patients greater than
tian at follow-up.38 300 lb, the technique can be difficult to perform if the endo-
3. Supplements scope is unable to transilluminate the abdominal wall.
a) Dietary supplements for obese patients can be used for calorie 2. Selecting an enteral formula
and protein supplementation. The supplements that are fat-free a) The nutrient composition of an enteral formula should be based
or low fat can help to meet the dietary goals without providing on the assessed calorie, protein, and volume requirements or
excess fat. Hospitalized obese patients who are eating food and restrictions. If hypocaloric feedings are instituted, then a very
taking supplements should be monitored with daily weights and high protein, low-fat formula should be used. This may require
calorie counts to help prevent overfeeding and weight gain. the addition of a modular protein supplement to the enteral for-
b) Vitamin and mineral supplements should be prescribed for all mula to ensure adequate protein input to spare LBM.
patients who are on a calorie-restricted, carbohydrate-restricted, b) The vitamin and mineral composition of the enteral formula
or specific nutrient-restricted diet. Specialized vitamin prepa- used for the hypocaloric feeding should be compared with the
rations may be required for patients who have had surgical recommended daily allowances (RDAs). Daily vitamin and
treatment of their obesity. Gastric bypass patients need calcium, mineral supplementation may be required.
iron, folate, and vitamin B12 supplements. A typical supplement C. Special aspects of PN
regimen includes a prenatal vitamin daily, 500 to 1000 mcg 1. Obtaining venous access. Securing central venous access for mon-
vitamin B12 daily (or monthly injections), and 1000 mg calcium itoring or PN administration is a formidable task in the severely
citrate with vitamin D daily in divided doses (the dosage may obese.40 Central venous access is defined as catheter placement in
be decreased if there is significant calcium intake in the diet). the superior vena cava–right atrial junction. Monitoring and posi-
B. Special aspects of enteral nutrition tioning are key elements in the successful and safe placement of
1. Obtaining enteral access. As with nonobese patients, in obese temporary and permanent central venous access. In the severely
patients, access to the gastrointestinal tract can be achieved obese patient with congestive heart failure or sleep apnea syn-
nasoenterically, surgically, endoscopically, or laparoscopically. drome, central venous access should be obtained only with an
These procedures can often be technically challenging when per- anesthesiologist or nurse anesthetist monitoring the airway and
formed in the severely obese.39 Often they cannot be performed with the administration of intravenous sedation. Studies have
because of difficulty with patient cooperation or lack of special demonstrated that Trendelenburg’s position or the head-down
instrumentation. In the case of endoscopic placement or naso- position can result in a 35% to 50% decrease in the functional
enteric placement, which often require fluoroscopy, patients whose residual capacity of the lung, significantly impairing gas exchange.
weight exceeds 300 lb (136 kg) will be unable to undergo this pro- Therefore, cardiac monitoring and pulse oximetry are recom-
cedure in certain institutions where damage to the operating, mended. Because the placement of central venous catheters can
movable roentgenogram table is likely. When patients undergo require extended operating time and because the airway is often
techniques that require light sedation without airway security or draped, capnography is also strongly recommended. It is very
general endotracheal intubation, extreme caution should be used, helpful in patients without well-defined landmarks to define the
and continuous arterial saturation monitoring with or without anatomy of the jugular and subclavian venous system with duplex
capnography is recommended. Patients who are severely obese imaging preoperatively. Indelible markings can be made and fol-
frequently have either congestive heart failure or sleep apnea lowed during placement.

© 2005 A.S.P.E.N. www.nutritioncare.org. A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. 329
S E C T I O N V Metabolic Conditions

a) Internal jugular vein. The internal jugular vein is the most high infusion rates needed to feed the total volume required.
accessible site for central line placement in the severely obese. The length of PN infusion should be gradually decreased by
If an assistant pulls the skin overlying the pectoralis muscle and 1 to 3 hours each day, as the patient can tolerate, to the goal of
the anesthetist provides countertraction, the anterior triangle 12 hours per day.
of the neck will be defined and internal jugular cannulation D. Focused monitoring/goals assessment
allowed without difficulty. The central venous catheter can then 1. Complications and postoperative considerations. While meticu-
be placed with use of fluoroscopic guidance. The internal jugu- lous attention to aseptic technique and intraoperative monitoring
lar vein is often the first choice for patients who weigh greater are key to reducing postoperative morbidity, being aware of the
than 300 lb. self-care limitations of some severely obese patients is important.
b) External jugular vein cutdown. An alternate site for central Some patients are unable to provide care and hygiene to feeding
venous catheterization in the severely obese is the external access sites and cannot recognize serious problems. Follow-up
jugular vein. This can often be identified and marked preoper- care is important. Soft-tissue infection can be insidious and viru-
atively by duplex imaging. Cutdown avoids the complications lent because of the depth of the subcutaneous fat and the number
of pneumothorax or local hematoma, which can contribute to of microbes that establish a niche in moist and excoriated skin
airway compromise. The severely obese may not clinically folds. Patients may fail to recognize and seek attention for these
manifest a neck hematoma; the first sign may be stridor. This problems. Patients with diabetes may harbor particularly hostile
approach is both safe and practical for many patients. microbes. Since severely obese patients do not tolerate surgical
c) Subclavian vein catheterization. While considered by many complications well, the best strategy is to avoid them.
the preferred site for venous cannulation, the subclavian vein 2. Special needs. An area of growing concern is the need for facili-
can be extremely difficult and dangerous to access in the ties equipped to care for the morbidly obese patient. Hospitals and
severely obese. Landmarks are ill-defined, which can make this physicians’offices are often not equipped with larger beds, gowns,
approach a formidable undertaking. Furthermore, even when and blood pressure cuffs. Many radiology tables cannot accom-
modate patients weighing greater than 300 or 350 pounds, leading
cannulation is successful, passage of the dilators and indwelling
to difficulty in obtaining tests in these patients.
catheters is often impossible because of the circuitous route of
E. Patient/caregiver education
entry into the vein from the skin puncture. If a pneumothorax
1. Obese patients and their family members should receive education
develops or bleeding occurs within the chest, both tube thora-
about the long-term effects of carrying excess body weight (as dis-
coscopy and thoracotomy are fraught with technical difficulty
cussed in Section II), the high rate of comorbid diseases related to
and high morbidity in this group of patients. However, if this
obesity, and the options for treatment. Information related to the
approach is necessary, in experienced hands it can be success-
health benefits of reducing weight and maintaining a lower body
fully accomplished and safe. For patients who are superobese weight should be provided during the education phase.
(greater than 400 lb [182 kg]), the posterior approach (supra- 2. Many weight management programs are available. If a patient is
clavicular and posterior to the subclavian vein) can be useful. motivated to lose weight, the various options should be discussed
Venous access with a peripherally inserted central catheter prior to discharge from the hospital. To date, most people who
obviates many of these problems. attempt weight loss are unable to maintain a significant weight loss
2. Selecting a formula for more than 5 years. However, this fact should not prevent an
a) The nutrient composition of PN support for obese patients obese patient from attempting to lose weight, since as little as a 5%
depends on the overall nutrition care plan. If weight mainte- to 10% decrease in weight can have health benefits. The ideal
nance is desired, then a mixed-nutrient formula that provides weight management program uses a multidisciplinary approach to
100% of the required nutrients is appropriate. To avoid essen- modify behavior and eating habits, provide emotional support,
tial fatty acid deficiencies, approximately 4% of total daily incorporate physical activity, and monitor the patient’s physical
energy should be provided as linoleic acid. This can be accom- well-being. Participation of obese family members or cohabitants
plished by using 500 cc of 10% intralipid solution twice can be motivational and supportive to the patient as well as pro-
weekly.41 vide health benefits to the other participants.
b) The infusion regimen depends on the patient’s hemodynamic 3. Patients who choose to undertake weight management after recov-
and metabolic stability, the anticipated length of support, and ery from an acute illness should modify their home environment
the desired outcome. Continuous infusions of PN are usually before attempting to lose weight. Modification of the types of
required when a patient is hemodynamically unstable (requir- foods procured, food preparation methods, and general eating
ing constant infusion rates) or when serum glucose control is habits of all cohabitants may be necessary to allow for successful
difficult to optimize. Cyclical PN should be considered for weight management of the obese patient.
patients who are hemodynamically and metabolically stable,
have increasing activity and mobility, need long-term support (Obesity chapter from the 1st edition was contributed by Robert F.
(months to years), or need mobilization of lipid stores. In a Kushner, Elizabeth Wall-Alonso, and John Alverdy)
review article by Matuchansky et al,42 the benefits of cyclic PN
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among US adults. JAMA. 2002;287:356–359. 28. Barak N, Wall-Alonso E, Cheng A, et al. Use of bioelectrical impedance
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Expert Panel on Detection, Evaluation, and Treatment of High Blood Cho- nutrition support. J Parenter Enteral Nutr. 2003;27:43–46.
lesterol in Adults (Adult Treatment Panel III) (Final Report). National 29. Shikora S, Muskat P. Protein-sparing modified fast total parenteral nutri-
Heart, Lung, and Blood Institute, National Institutes of Health, Publication tion formulation for a critically ill morbidly obese patient. Nutrition. 1994;
#NIH 02;5215. Bethesda, MD: National Heart, Lung, and Blood Institute, 10:155–158.
National Institutes of Health; 2002. 30. Liu KJ, Cho MJ, Atten MJ, et al. Hypocaloric parenteral nutrition support
10. Lemieux I, Pascot A, Couillard C, et al. Hypertriglyceridemic waist: a marker in elderly obese patients. Am Surg. 2000;66:394 – 400.
of the atherogenic metabolic triad in men? Circulation. 2000;102:179–184. 31. Hopkins B. Assessment of nutritional status. In: Gottschlich M, Matarese
11. Lakka HM, Laaksonen DE, Lakka TE, et al. The metabolic syndrome and L, Shronts E, eds. Nutrition Support Dietetics Core Curriculum. 2nd ed.
total and cardiovascular disease mortality in middle-aged men. JAMA. 2002; Silver Spring, MD: American Society for Parenteral and Enteral Nutri-
288:2709–2716.
tion; 1993.
12. Haffner S, Taegtmeyer H. Epidemic obesity and the metabolic syndrome.
32. Ireton-Jones C. Obesity. In: Gottschlich M, Matarese L, Shronts E, eds.
Circulation. 2003;108:1541–1545.
Nutrition Support Dietetics Core Curriculum. 2nd ed. Silver Spring, MD:
13. Mattison R, Jensen M. The adipocyte as an endocrine cell. Curr Opin
American Society for Parenteral and Enteral Nutrition; 1993.
Endocrin Diab. 2003;10:317–321.
33. Ireton-Jones C, Francis C. Obesity: nutrition support practice and applica-
14. Bray GA. Risks of obesity. Endocrinol Metab Clin N Am. 2003;32:787–804.
tion to critical care. Nutr Clin Pract. 1995;10:144 –149.
15. Dixon JB, Dixon ME, O’Brien PE. Depression in association with severe
34. Institute of Medicine. Dietary Reference Intakes for Energy, Carbohydrate,
obesity: changes with weight loss. Arch Intern Med. 2003;163:2058–2065.
Fiber, Fat, Fatty Acids, Cholesterol, Protein, and Amino Acids. Washing-
16. Kushner RF, Roth JL. Assessment of the obese patient. Endocrinol Metab
ton, DC: National Academy of Sciences; 2003.
Clin N Am. 2003;32:915–933.
17. Bray G. Pathophysiology of obesity. Am J Clin Nutr. 1992;55:488S– 494S. 35. National Task Force on the Prevention and Treatment of Obesity. Very low-
18. National Heart, Lung, and Blood Institute. Clinical Guidelines on the Iden- calorie diets. JAMA. 1993;270:967–974.
tification, Evaluation, and Treatment of Overweight and Obesity in Adults. 36. Weinsier RL, Wilson LJ, Lee J. Medically safe rate of weight loss for the
The evidence report. Obes Res. 1998;6(suppl 2):51S–210S. treatment of obesity: a guideline based on risk of gallstone formation. Am
19. Fujioka S, Matsuzawa Y, Tokunaga K, et al. Contribution of intra-abdominal J Med. 1995;98:115–117.
fat accumulation to the impairment of glucose and lipid metabolism in human 37. Shiffman ML, Kaplan GD, Brinkman-Kaplan V, Vickers FF. Prophylaxis
obesity. Metabolism. 1987;36:54–59. against gallstone formation with ursodeoxycholic acid in patients partici-
20. National Heart, Lung, and Blood Institute, and North American Associa- pating in a very-low-calorie diet program. Ann Intern Med. 1995;122:
tion for the Study of Obesity. Practical Guide to the Identification, Evalu- 899–905.
ation, and Treatment of Overweight and Obesity in Adults. Publication 38. Gastric bypass diet and bariatric surgery for obesity. In: Manual of Clinical
#NIH 00-4084. Bethesda, MD: National Institutes of Health; 2000. Nutrition Management. Atlanta, GA: Morrison Management Specialist;
21. Gray D, Bray G, Bauer M, et al. Skinfold thickness measurements in obese 2003:B-10 to B-20.
subjects. Am J Clin Nutr. 1990;51:571–577. 39. Shikora SA. Enteral feeding tube placement in obese patients: considera-
22. Kokkoris P, Pi-Sunyer FX. Obesity and endocrine disease. Endocrinol tions for nutrition support. Nutr Clin Pract. 1997;12(suppl):S9–S13.
Metab Clin N Am. 2003;32:895–914. 40. Jefferson P, Ball DR. Central venous access in morbidly obese patients.
23. Dickerson R, Rosato E, Mullen J. Net protein anabolism with hypocaloric par- Anesth Analg. 2002;95(3):782.
enteral nutrition in obese stressed patients. Am J Clin Nutr. 1986;44;747–755. 41. Nutrition management of obesity. In: Manual of Clinical Dietetics. 6th ed.
24. Choban PS, Burge JC, Scales D, Flancbaum L. Hypoenergetic nutrition Chicago, IL: American Dietetic Association; 2000:621.
support in hospitalized obese patients: a simplified method for clinical 42. Matuchansky C, Messing B, Jeejeebhoy K, et al. Cyclical parenteral nutri-
application. Am J Clin Nutr. 1997;66:546 –550. tion support. Lancet. 1992;340:588–592.

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 Margretta R. Seashore, MD, FAAP, FACMG;
Crystal A. Reil, RD, CD-N
29
Inborn Errors of
Metabolism

Introduction 2. In lysinuric protein intolerance, there is a defect in the transport

of dibasic amino acids (lysine, arginine, and ornithine) not only
Specialized nutrition support is frequently required for patients who in the intestine but also in the liver and kidney.2
have an inborn error of metabolism. These inherited disorders result in C. Utilization
abnormal concentrations of certain metabolites, which frequently cause 1. The problem in most inborn errors of metabolism is that there is
neurologic symptoms. Treatment goals include supporting normal an enzyme defect that either causes accumulation of a substrate or
growth and optimizing neurologic development in children, as well as a toxic metabolite, or prevents production of an essential end
minimizing neurologic compromise in patients of all ages. Nutritional product.1,3
therapy for these patients usually involves following a specific nutrition 2. Therapy in these disorders may be an attempt to increase enzyme
protocol. In some of these disorders, the intake of certain nutrients such activity (or even replace the enzyme by transplantation), and in
as specific amino acids needs to be limited or supplemented. In addi- most cases requires some sort of dietary prescription.1,3
tion, specific nutrients such as carnitine may be prescribed. Specialized D. Losses
enteral and parenteral nutrition products may also be necessary to opti- 1. In some inborn errors of metabolism, the metabolites whose con-
mize therapy. centrations become abnormally increased (such as amino acid
metabolites and other organic acids) bind to carnitine and glycine.
I. Nutritional Aspects of the Disorder
The resulting acylcarnitines and acylglycines are water soluble
II. Nutritional Alterations Seen With the Disorder
and are excreted in the urine without further metabolism.
III. Focused Assessment
2. Acylcarnitine lost in the urine frequently leads to a secondary
IV. Objectives/Goals of Therapy in Infants and Children
V. Management carnitine deficiency. Inborn errors of metabolism where carnitine
References supplementation is usually given are shown in Table 29-1.4

I. Nutrition Aspects of the Disorder II. Nutritional Alterations Seen with the Disorder
A. Intake A. Common
1. Treatment for many inborn errors of metabolism involves alter- 1. All inborn errors of metabolism result in abnormal concentra-
ations of dietary intake tions of certain metabolites; diagnosis of the specific enzyme
a) By substrate restriction (phenylalanine in phenylketonuria). defect in these conditions is usually made by measuring the con-
b) By vitamin/cofactor administration (biotin in biotinidase centrations of various metabolites in blood or urine, although in
deficiency) certain conditions specific enzyme analysis is required.
c) By end-product supplementation (arginine in argininosuccinic 2. Because of the wide range of inborn errors, there are no uniform
acidemia) nutritional alterations seen in these conditions; in those patients
2. Problems with intake with severe neurologic impairment, both under- and overnutrition
a) Infants and children with many of these diagnoses may have are possible.
severe neurologic impairment that limits their ability to con- B. Less common
sume food orally.1 1. As listed in Table 29-1, a number of these conditions result in a
b) Many inborn errors of metabolism are associated with abnor- secondary carnitine deficiency. Patients with carnitine deficiency
mal concentrations of metabolites, which often cause anorexia, can develop a Reye-like syndrome, including hypoglycemia with
nausea, and vomiting, resulting in limited oral nutrition intake. illness or stress.
c) Most of the specialized formulas that have been developed for 2. Several other conditions are associated with hypoglycemia,
patients with inborn errors of metabolism contain elemental including glycogen storage disease type I,5,6 and hereditary fruc-
amino acids and are not very palatable. Patients tend to demon- tose intolerance.7
strate improved acceptance with these formulas when they are
used on a consistent basis since infancy. III. Focused Assessment
3. Some older children with inborn errors of metabolism who are not
neurologically impaired may naturally self-restrict specific nutri- A. History
ents from their diets that are likely to cause metabolic aberrations. 1. Growth and development of the patient needs to be a major focus
B. Absorption of the nutrition history; in most cases, poor growth and delayed
1. In most inborn errors of metabolism, the normal absorption of neurologic development are the results of late treatment, poor
nutrients is not affected. intake, or poor metabolic control.1,3

332 A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. © 2005 A.S.P.E.N. www.nutritioncare.org.
 S E C T I O N V Metabolic Conditions

C. Prevent metabolic crises8

TABLE 29-1. Inborn Errors of Metabolism in 1. The primary goal is usually to correct the primary metabolic imbal-
Which Carnitine Supplementation ance, such as by restricting a particular amino acid in an amino
is Usually Given acidopathy. Often, medical foods are utilized for such therapy.
2. Occasionally, a substrate is given to provide an alternative meta-
3-Hydroxyisobutyric aciduria bolic pathway, such as giving glycine and carnitine to children with
Isovaleric acidemia isovaleric acidemia.
3. Occasionally, a particular substrate of a blocked pathway needs to
Glutaric aciduria type I be given, such as glucose to patients with type I glycogen storage
Methylmalonic acidemia disease.
4. In these patients, it is also possible for certain substances, such
Propionic acidemia as carnitine, to become “conditionally essential” (Table 29-1).
Carbamoyl-phosphate synthetase deficiency 5. Additional vitamins are often useful either to stabilize altered
enzymes (thiamine in maple syrup urine disease), to replace defi-
Ornithine transcarbamylase deficiency cient cofactors (vitamin B12 in methylmalonic aciduria), or to sup-
Citrullinemia plement nutrients not released from their apoenzyme (biotin in
biotinidase deficiency).
Argininosuccinic aciduria
Argininemia
V. Management
N-Acetylglutamate synthetase deficiency
A. Special aspects of diet and nutritional supplements
Long-, medium-, or short-chain fatty acid oxidation defects 1. In many of these patients, the intake of specific compounds or sub-
stances frequently must be limited to optimize metabolic control.1,7,9
a) In many inborn errors of amino acid metabolism, the intake of
specific amino acids must be restricted (Table 29-2).
b) In some inborn errors of carbohydrate metabolism, a particu-
2. In all patients, a detailed summary of nutritional intake needs to be lar kind of carbohydrate may need to be limited (Table 29-3).
completed. At a minimum, the history should document average
caloric and protein intake. For patients with errors in amino acid
metabolism, the specific intake of individual amino acids should
be calculated.
3. Tolerance of oral nutrition is also an important focus of the history, TABLE 29-2. Inborn Errors of Amino Acid Metabolism
particularly because some of these patients frequently experience that Require Limited Intake of Particular
anorexia, nausea, and vomiting.
Amino Acids
4. Symptoms suggestive of hypoglycemia should be noted.
B. Physical exam Amino acid that
1. Accurate documentation of the patient’s height (length), weight, Inborn error of metabolism must be limited
and head circumference (birth to age 3) is one of the most impor-
tant parts of the physical examination. Phenylketonuria Phenylalanine
2. Neurologic examination is particularly important in determining
not only whether the patient is developmentally normal but also Maple syrup urine disease Leucine, isoleucine, valine
whether there might be factors such as spasticity or chewing or (Branched-chain ketoaciduria)
swallowing difficulties that might affect dietary intake or nutri-
Tyrosinemia types I and II Phenylalanine, tyrosine
tional requirements, or interfere with the development of feeding
capabilities. Homocystinuria Methionine
C. Quality of life
Isovaleric acidemia Leucine
1. Quality of life varies considerably with each diagnosis and also
depends on whether the patient was treated early in life with proper 3-Methylcrotonylglycinuria Leucine
metabolic control. 3-Methylglutaconic aciduria Leucine
2. Inborn errors of metabolism do not resolve as the patient ages, so
dietary treatment should be considered lifelong unless effective 3-Hydroxy-3-methylglutaric Leucine
alternate therapies are discovered (enzyme replacement, organ aciduria
transplantation, or gene therapy). Glutaric aciduria type I Lycine, tryptophan
3. The level of care required is an important factor in planning nutri-
tion support for these patients. 2-Ketoadipic aciduria Lycine, tryptophan
Propionic acidemia Isoleucine, methionine,
IV. Objectives/Goals of Therapy in Infants and threonine,valine
Children Methylmalonic acidemia Isoleucine, methionine,
A. Support normal growth threonine,valine
B. Minimize neurologic impairment

© 2005 A.S.P.E.N. www.nutritioncare.org. A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. 333
S E C T I O N V Metabolic Conditions

c) Changes in the nutrition prescription are made at regular inter-

TABLE 29-3. Inborn Errors of Amino Acid Metabolism vals based on the infant’s or child’s growth and development
that Require Limited Intake of Particular and clinical symptoms as well as metabolic control and nutri-
Carbohydrates tional status as assessed by laboratory testing.
d) For many infants and children with inborn errors of metabo-
Carbohydrate that lism, the majority of their nutritional needs are met by medical
Inborn error of metabolism must be limited food(s), as only a small amount of normal foods are allowed in
accordance with their disease-specific dietary restriction(s).8
Galactosemia Galactose e) When preparing medical foods, care must be taken to prevent
Hereditary fructose intolerance Fructose, sorbitol, sucrose the Maillard reaction, which involves condensation of amino
acids and sugars into an undigestible complex. This reaction
Glycogen storage disease types I and II Lactose, fructose, sucrose is accelerated by heat and gives the formula a yellow to brown
color.7
3. In the special case of children with glycogen storage disease
type I, frequent feedings of carbohydrate are needed to prevent
c) In some inborn errors of metabolism, select nutrients (ie, car- hypoglycemia.5,6
bohydrate, fat, or protein) must be restricted in treating the a) During the day, some of the carbohydrate is often given orally
disorder (Table 29-4). as boluses of uncooked cornstarch.
2. For those conditions where specific amino acids need to be b) Overnight, hypoglycemia is prevented by either continuing oral
restricted (Table 29-2), chemically defined formulations (medical boluses of uncooked cornstarch or providing an enteral infusion
foods) have been developed. For each of these conditions, specific of glucose polymers at about 8 to 9 mg of carbohydrate per kilo-
protocols have been developed to optimize the nutrition support;4,9 gram per minute.5
these protocols are useful regardless of whether the nutrition is B. Special aspects of enteral nutrition
being given orally, enterally, or parenterally. 1. Patients who have severe neurologic impairment, frequent meta-
a) The basic approach in each of these protocols is to create a bolic crises, or intolerance of the medical foods often benefit from
nutrition prescription based on the need to limit or supplement enteral feedings; placement of a feeding gastrostomy is usually
a particular substrate or substrates, while meeting total protein, indicated.
energy, and fluid requirements. In cases where the intake of a 2. For those patients on enteral feedings, the nutrition prescription
particular amino acid is limited, the daily intake of that amino is similar to what is used for patients on oral nutrition. If a diet
acid may be given in the form of normal table foods. To pre- restricted in an amino acid(s) is being used, the restricted amino
vent the development of protein deficiency, additional protein acid(s) is usually supplied via a commercial formula.10
is given in the form of a medical food that does not contain the C. Special aspects of parenteral nutrition
restricted amino acid(s). Additional calories are provided with 1. In some patients with inborn errors of metabolism, aggressive
a protein-free formula or protein-free foods. nutritional intervention may be important at the time of initial
b) Usually, recommended dietary allowances for protein and diagnosis or at times of catabolic stress to prevent severe neuro-
energy are utilized in the prescription. However, when medical logic complications and even death.11
foods that contain free L-amino acids are used, the total protein 2. In many cases, all that is needed is to infuse glucose at high-
requirements frequently exceed the recommended dietary infusion rates; the concomitant hyperinsulinemia suppresses
allowances for protein. catabolism and improves metabolic control.
3. In selected circumstances involving inborn errors of amino acid
metabolism, specialized parenteral amino acid formulations defi-
cient in one or more amino acids may be useful to optimize the
TABLE 29-4. Inborn Errors of Metabolism plasma amino acid concentrations.11
that Require Limited Intake of 4. In patients with propionic and methylmalonic acidemia, long-
Carbohydrate, Fat, or Protein term parenteral nutrition with standard amino acid solutions has
also been reported to be effective.12,14
Type of nutrient that 5. Use of IV fat emulsion may need to be restricted in patients with
Inborn error of metabolism must be limited a disorder of long-chain fatty acid oxidation or glutaric aciduria
type II.15
Pyruvate dehydrogenase deficiency Carbohydrate D. Focused monitoring/goals assessment
1. To meet the goals of adequate growth and minimal neurologic
3-Hydroxy-3-methylglutaric aciduria Protein, Fat
impairment, children with inborn errors of metabolism need to
Fatty acid oxidation defects Long-,medium-, or short- have frequent monitoring of their condition; the metabolites that
are measured depend on the specific condition and are part of the
chain fatty acids
treatment protocol.
Urea cycle disorders Protein 2. Changes in the nutrition prescription need to be made frequently
(days to months) depending on the age of the patient, their rate of
Nonketotic hyperglycinemia Protein growth, the inborn error, and the degree of metabolic control.
E. Patient/caregiver education
Lysinuric protein intolerance Protein 1. The patient and/or caregiver needs to be fully educated in all
aspects of the nutrition prescription; in the case of inborn errors

334 A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. © 2005 A.S.P.E.N. www.nutritioncare.org.
 S E C T I O N V Metabolic Conditions

of amino acid metabolism, detailed lists of the amino acid con- 7. Bell L, Sherwood WG. Current practices and improved recommendations for
tent of foods are available to aid in meal planning.4,16 treating hereditary fructose intolerance. J Am Diet Assoc. 1987;87:721–728.
2. Specific instruction needs to be given about the signs and symp- 8. A.S.P.E.N. Board of Directors: Guidelines for the use of parenteral and
toms of metabolic crises, because early medical/nutritional inter- enteral nutrition in adult and pediatric patients. J Parenter Enteral Nutr.
1993:17:1SA–52SA.
vention is critical to prevent long-term sequelae.
9. Mead Johnson Nutritionals. Dietary Management of Metabolic Disorders.
Evansville, IN: Mead Johnson & Co; 1991.
REFERENCES 10. Parini R, Sereni LP. Bagozzi DC, et al. Nasogastric drip feeding as the only
1. Elsas LJ, Acosta PB. Nutrition support of inherited metabolic disease. In: treatment of neonatal maple syrup urine disease. Pediatrics. 1993;92:280–283.
Shils ME, Young VR, eds. Modern Nutrition in Health and Disease. 8th ed, 11. Morton DH, Strauss KA, Robinson DL, Puffenberger EG, Kelley RI. Diag-
Philadelphia, PA: Lea & Febiger; 1994:1147–1206. nosis and treatment of maple syrup disease: a study of 36 patients. Pediatrics.
2. Scriver C, Beaudet A, Sly W, Valle D. The Metabolic Basis of Inherited Dis- 2002;109(6):999–1008.
ease. 8th Edition ed: McGraw Hill; 2001. 12. Kahler SG, Millington DS, Cederbaum SD, et al. Parenteral nutrition in
3. Acosta PB. Nutrition support of inborn errors of metabolism. In: Queen PM, propionic and methylmalonic acidemia. J Pediatr. 1989;115:235–241.
Land CE, eds. Handbook of Pediatric Nutrition. Gaithersburg, MD: Aspen 13. Walter JH, Leonard JV, Thompson GN. Halliday D: Parenteral nutrition in
Publishers; 1993:315–364. propionic acidemia and methylmalonic acidemia. J Pediatr. 1990;117:339
4. Acosta PB, Yannicelli S. Nutrition Support Protocols. 4th ed. Columbus, 14. Kalloghlian A, Gleispach H, Ozand PT. A patient with propionic acidemia
OH: Ross Laboratories; 2001. managed with continuous insulin infusion and total parenteral nutrition. J
5. Schwenk WF, Haymond MW. Optimal rate of enteral glucose administra- Child Neurol. 1992;7:88–91.
tion in children with glycogen storage disease type I. N Engl J Med. 15. al-Essa MA, Rashed MS, Bakheet SM, Patay ZJ, Ozand PT. Glutaric
1986;314:682–685. aciduria type II: observations in seven patients with neonatal- and late-onset
6. Chou JY, Matern D, Mansfield BC, Chen YT. Type I glycogen storage dis- disease. J Perinatol. 2000;20(2):120–128.
eases: disorders of the glucose-6-phosphatase complex. Curr Mol Med. 16. Nelson JK, Moxness KE, Jensen MD, Gastineau CF, eds. Mayo Clinic Diet
2002;2(2):121–143. Manual. 7th ed. St. Louis, MO: Mosby; 1994:495–545.

© 2005 A.S.P.E.N. www.nutritioncare.org. A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. 335
 Charles J. Foulks, MD, FACP, FACN

30
Chronic Kidney Disease

Introduction The following formula can be used to calculate the adjusted

aBW: adjusted aBW (kg) = ((edema-free aBW- nBW) (0.25))
Patients with Chronic Kidney Disease have a wide spectrum of clinical + nBW, where edema-free aBW is the patient’s actual body
disorders that may affect the provision of adequate nutrition. This chap- weight minus any estimated excess or deficit in total body
ter focuses on the nutritional support of patients with Chronic Kidney water, and nBW is the normal or standard body weight for
Disease (Stages III–V) and patients who have undergone renal trans- the patient, as determined from the NHANES data.2 The
plantation and have superimposed illnesses. It is now widely accepted NHANES data are not used or referred to by busy clinicians
by the nephrology community that the term Chronic Kidney Disease and most use the patient’s usual weight (from the patient, the
(CKD) covers all gradations of renal dysfunction (Table 30-1). family, or from medical records) instead of the NHANES
nBW.
I. Nutritional Assessment of Patients with Chronic Kidney Disease e) Skinfold measurements (eg, biceps, triceps, or subscapular)
(CKD) may be used to estimate body fat; however, these assessments
II. Objectives and Goals for Nutrition Support for Patients with are not practical in a clinical setting, particularly in patients
Chronic Kidney Disease who may have an abnormal amount of total body water. They
III. Nutrition Support for Renal Transplant Patients are subject to marked inter-observer variability and are of lit-
IV. Intradialytic Parenteral Nutrition (IDPN) tle clinical utility.
V. Monitoring Patients Receiving Nutritional Support 2. Change in fluid status is determined by maintaining accurate
Vl. Complications of Nutrition Support intake and output records and especially by precisely measuring
References weight on a daily basis. The astute clinician will also use the
Appendix physical examination and interval history to help make the diag-
nosis of volume depletion, hypervolemia, or normovolemia.
I. Nutritional Assessment of Patients with Chronic 3. Subjective global nutritional assessment can give a rapid, repro-
Kidney Disease (CKD) ducible, overall assessment of the protein-calorie nutritional sta-
tus of the patient.3 Selective global nutrition assessment uses the
A. History—This assessment requires a detailed history and review of following six subjective measurements:
the medical records including past medical and surgical history, his- a) the patient’s history of weight loss
tory of renal disease and dialysis treatments, medications, and pre- b) incidence of anorexia
vious and current dietary intake. It is important to document the c) vomiting and diarrhea
types and amount of food eaten in the previous 2– 4 weeks and the d) the clinician’s estimate of muscle wasting
presence of anorexia, nausea, vomiting, diarrhea, or early satiety. e) edema
The patient’s ethnic background and cultural food should be noted. f) loss of subcutaneous fat
B. Physical examination These measures are graded as 1 = severe, 3 = moderate, and 5
1. Anthropometric measurements are affected by the fluid status of = none. A subjective nutrition assessment of the patient is then
the patient and are often of limited usefulness in patients with made as normal, mildly to moderately malnourished, or severely
renal failure and superimposed illnesses. malnourished. This method has been applied to the assessment of
a) Dry body weight (edema-free body weight) should be recorded CKD patients in a number of studies.4,5
if known. If not, one can substitute standard or normal body 4. Visual signs of micronutrient (eg, zinc or iron) or essential fatty
weight, defined as the median body weight of normal Ameri- acid deficiencies.
cans of the same age range, height, sex, and skeletal frame C. Biochemical assessment should include:
size as the patient as determined from the National Health and 1. Serum urea nitrogen (SUN; reflecting protein intake and catabolic
Nutrition Examination Survey (NHANES) data.1 In reality, state), creatinine (reflecting muscle mass), potassium and phos-
most clinicians either accept the weight given by the family phorus (reflecting the stage of CKD and starvation, especially if
or they estimate the weight. the potassium and phosphorus are normal or low), calcium, mag-
b) Height, skeletal frame size (estimated, rarely measured). nesium, glucose, sodium, chloride, bicarbonate, albumin, transfer-
c) Body mass index = body weight/(height)2, expressed in kg/m2. rin, and prothrombin time (INR; if elevated, reflecting starvation
d) For patients whose body weight is greater than 120% or less or the absence of intake of green and yellow vegetables).
than 90% of standard body weight, nutrients may be pre- 2. Blood pH, PCO2, and PO2, if a serious acid-base disorder is sus-
scribed according to the adjusted actual body weight (aBW). pected.

336 A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. © 2005 A.S.P.E.N. www.nutritioncare.org.
 S E C T I O N V Metabolic Conditions

ment. The Total Body Water is 0.60 × (body weight). This esti-
TABLE 30-1. Classification of mate should be adjusted in patients who are edematous or lean.
Chronic Kidney Disease (CKD) d) For patients who are undergoing hemodialysis, the UNA must
be calculated during the interdialytic interval and extrapolated
GFR to 24 hours, or it may be measured directly or through dialysis
Stage Description (mL/min/1.73m2) kinetic techniques.2,6 To assess UNA in people undergoing
Continuous Veno-Venous Hemofiltration or Hemodialysis
1 Kidney damage with ≥90 (CVVH/CVVHD), the urea in the ultrafiltrate or dialysate
normal or increased GFR must be collected and measured, and this value must be added
to urinary urea nitrogen and changes in body urea nitrogen.
2 Kidney damage with mild 60–89 Practically speaking, the UNA is rarely used clinically. Many
decrease in GFR nephrologists estimate the degree of catabolism by calculating
the rate of rise of the SUN from one day to the next. In general,
3 Moderate decrease in GFR 30–59 if the rate of rise of the SUN ≤ 30 mg/dL per day, the stress of
the illness is presumed to be mild.
5. Total nitrogen appearance in (g/d) = 1.19 UNA (g/d) + 1.27 g/d,
4 Severe decrease in GFR 15–29
where total nitrogen appearance is the sum of all outputs of nitro-
gen from the body, including dialysate, urine, and feces, plus the
5 Kidney Failure <15 (or dialysis) change in body urea nitrogen. This equation was derived from clin-
ically stable CKD patients who were not undergoing hemodialy-
Chronic kidney disease is defined as kidney damage or GFR < 60 mL/min/1.73 m2 ≥ 3 sis or peritoneal dialysis, and its applicability to unstable, stressed
months. Kidney damage is defined as pathologic abnormalities or markers of damage, CKD patients or acute renal failure (ARF) patients is unknown.6
including abnormalities in blood or urine tests or imaging studies. 6. Protein equivalent of total nitrogen appearance (PNA in g/d) = total
Reprinted from National Kidney Foundation, K/DOQI. Clinical practice guidelines for nitrogen appearance (g of nitrogen per day) × 6.25. PNA expresses
chronic kidney disease: evaluation, classification, and stratification. Am J Kidney Dis total nitrogen appearance in terms of the equivalent amount of pro-
2002;39 (suppl 1):S1-S000 with permission from National Kidney Foundation. tein that has been lost or has undergone net catabolism. In pre-
vious publications, PNA has been referred to as PCR (protein
catabolic rate).
3. Calculated Glomerular Filtration Rate (GFR)—Glomerular fil-
tration rate is a reflection of renal function as derived from clear-
ance tests that measure the rate at which substances are cleared II. Objectives and Goals for Nutrition Support for
from the plasma by the glomeruli. See Appendix 29-1 for for- Patients with Chronic Renal Disease
mulas and resources.
4. Urea nitrogen appearance (UNA)—This allows the clinician to A. Overall goals for nutritional treatment
estimate net protein degradation. Because urea is the major 1. To maintain, improve, and, if possible, restore normal body com-
nitrogenous product of protein metabolism, UNA correlates position of somatic proteins, visceral proteins, and other nutri-
closely with total nitrogen output. UNA indicates the net rate of ents as well as normal immune function, wound healing, and host
protein catabolism (ie, total body degradation minus total body resistance.
synthesis of proteins and amino acids). 2. To prevent or ameliorate uremic toxicity and other metabolic dis-
a) In clinically stable patients, who are in strongly positive or orders and to prevent or correct abnormal total body water and
negative protein balance, the UNA will indicate recent protein serum electrolyte and hydrogen ion disorders.
intake. If both nitrogen intake and total nitrogen appearance, B. Nutritional support for patients with CKD
as estimated from the UNA, are known, nitrogen balance can 1. The prescription for nutritional support varies according to the
be calculated from the difference between these values.6 patient’s nutritional status, degree of catabolism, GFR, and clin-
b) In patients who are receiving exogenous protein or amino ical condition. The patient’s tolerance for water, minerals, amino
acids by enteral or parenteral routes, the difference between acids and protein; the degree of uremic toxicity; and the plans
nitrogen intake and UNA provides a measure of the catabolic for dialysis or ultrafiltration therapy may heavily influence the
status of the patient. For patients who are in negative nitrogen prescription for oral, enteral, or parenteral nutrition. Often,
balance, the degree to which the total nitrogen appearance, patients undergoing long-term peritoneal dialysis are treated
estimated from the UNA, exceeds the nitrogen intake is often with hemodialysis therapy during an acute illness if it is of suf-
a measure of the severity of their underlying illnesses. ficient magnitude to require nutrition support.
c) UNA can be calculated as follows: a) A hospitalized patient with CKD who has little or no protein
depletion, a low UNA (eg, 4 to 5 g/d), and SUN < 90 mg/dL;
UNA ( g d ) = urinary urea nitrogen ( g d ) and in whom the health care team is trying to avoid dialysis
treatment (eg, awaiting vascular access maturation, accept-
+ change in SUN ( g d ) ance into a dialysis unit); may be treated with 0.5–0.6 g/kg/d
of protein (>75% high biologic value) with supplementation
Change in SUN = ( SUNf − SUNi ) × (( 0.60 )( BW )) of water soluble vitamins and minerals. This is a version of
+ ( BWf − BWi )(SUNf ) the low protein diet used in the management of the pre-
ESRD (end stage renal disease) patient, and as long as
where SUN = serum urea nitrogen (g/L), BW = body weight energy needs are met and the catabolic stress is modest, this
(kg), i and f = initial and final values for the period of measure- diet will suffice to prevent nutritional injury. If the patient

© 2005 A.S.P.E.N. www.nutritioncare.org. A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. 337
S E C T I O N V Metabolic Conditions

requires treatment with parenteral nutrition, 20–30 g/d of indicate that a higher energy intake is necessary to maintain
essential amino acids with appropriate caloric provision can nitrogen balance when a low nitrogen diet is given. In general,
be safely used until dialysis is begun, and can be used for energy intakes > 45 kcal/kg/d are not recommended because
2–3 weeks. No more than 30–40 g of the nine essential amino the high energy levels tend to promote hypercapnia, obesity,
acids per day should be given, because larger quantities may and fatty liver.12 In addition, greater energy intakes usually
cause hazardous amino acid imbalances and precipitate uremic increase the amount of fluid necessary to meet these higher
symptoms.7,8 Although histidine is not an essential amino acid calorie goals.
in normal patients, it is an essential amino acid in the CKD C. Specific guidelines for parenteral nutrition (PN) for patients with
patient. Modern essential amino acid formulations contain his- CKD
tidine. When dialysis is initiated, nutrition support with essen- 1. Because most patients with CKD do not tolerate large volumes of
tial amino acids is modified to provide larger amounts of both water, efforts are made to use more concentrated nutrient solu-
essential and nonessential amino acids at 1.2–1.3 g/kg nBW/d. tions. A 70% dextrose (d-glucose) solution is usually used. This
b) For hypercatabolic or severely wasted CKD patients or for solution provides 70 g/dL of d-glucose monohydrate (3.4 kcal/g)
patients who are expected to require dialysis in the near future, or about 63 g of anhydrous glucose so that 70% d-glucose mono-
a higher amino acid or protein intake may be prescribed; how- hydrate provides 2.38 kcal/mL of solution.
ever this will hasten the uremic state and will require dialysis to 2. Amino acids are usually supplied in 8.5%, 10%, or 15% solutions.
be started early. Generally about 1.2 g/kg/d should be prescribed To provide more concentrated PN solutions, 10% or 15% amino
for patients who will receive intermittent hemodialysis. This is acids are usually employed. However, the 15% amino acid solu-
the amount used for stable, ESRD patients although the clini- tion is more expensive. A mixture of essential and nonessential
cal circumstances may call for an increase in the protein intake amino acids generally provides 3.5 kcal/g. Specialized solutions
> 1.2 g/kg/d. If a CKD patient undergoing hemodialysis is given are available that provide the nine essential amino acids with or
greater than 1.2 g/kg/d protein, the dialysis schedule must be without arginine, a mixture of the nine essential amino acids and
intensified and daily dialysis should be strongly considered. For the nonessential amino acids in a 2:1 ratio, or a high concentra-
individuals receiving CVVH/CVVHD, 1.5 to 2.5 g of protein tion of branched-chain amino acids.
per kg per day is often prescribed.9,10 These increased nitrogen 3. Patients receiving PN should be given IV fat emulsions. Fat emul-
loads and the larger volumes of water necessary to provide these sions are necessary to prevent essential fatty acid deficiency, to
nutrients may increase the need for dialysis therapy unless the reduce the risk of hyperglycemia that is associated with large dex-
CVVH/CVVHD is performed efficiently. trose loads, and to provide a more normal mixture of fuel sub-
2. Energy requirements can be estimated in several ways for patients strates. Fat emulsions are available as 10% or 20% emulsions and
with renal failure. provide 1.1 and 2.0 kcal/mL, respectively. The 20% emulsion is
a) The Harris-Benedict equation,11 which estimates the basal recommended when fluid restriction is indicated. The phosphorus
energy expenditure (BEE) from the individual’s age, sex, content of fat emulsions is about 14.8 mmol/L in both the 10% and
weight, and height, can be calculated as follows: 20% emulsions. Therefore, using a 20% fat emulsion may be more
desirable when phosphorus intake needs to be restricted. Fat emul-
Female: BEE = 655 + ( 9.6 × aBW ) + (1.8 × height ) sions should be incorporated into the dextrose and amino acid solu-
+ ( 4.7 × age ) , tion and infused simultaneously as a “3-in-1” formulation.
4. Mineral and electrolyte composition of the nutritional prescrip-
Male: BEE = 66 + (13.7 × aBW ) + ( 5 × height ) tion must be adjusted according to the patient’s clinical condition
and serum chemistries.
+ ( 6.8 × age )
a) Sodium and water intake should be adjusted according to the
where aBW = edema-free actual body weight (kg) if it is fluid status of the patient and are often restricted to control
between 90% and 120% of normal (standard) body weight, edema or hypertension. Most non-edematous patients with
height = height (cm), and age = age (years). If aBW is <90% or CKD can tolerate a daily intake of 1000 to 2000 mg (43 to
>120% of normal body weight, the adjusted aBW is used (see 87 mEq) of sodium, particularly if they are receiving regular
above). dialysis therapy. Water intake may be limited to the urine out-
b) The estimated energy requirement should be increased as put plus 500 mL/d for insensible losses if the patient is nor-
needed for stress and then by 25% to adjust for individual vari- mothermic. However, to provide sufficient protein or amino
ability and physical activity, if any, and to ensure that energy acids and energy, patients receiving nutrition support, particu-
intake is sufficient. The higher energy intakes may increase larly those given PN, often are given quantities of water in
the efficiency of nitrogen utilization when small quantities of excess of what they need or can tolerate. Careful attention to
protein or amino acids are provided to the patient. The calcu- the sodium concentration (a measure of water status) or serum
lation of energy requirements for ill patients with CKD is osmolality should guide the amount of water that should be
energy requirement = estimated BEE + adjustment factor for administered. The nephrologist must be intimately involved
illness + 25%. with the development and use of PN.
c) As an approximate guide, acutely ill patients with CKD usually b) To prevent hyponatremia in patients receiving large water
require between 30 and 45 kcal/kg of normal or adjusted actual loads, the sodium concentration of the PN solution is usually
body weight per day. The lower end of this range is recom- maintained at about 40 to 50 mEq/L, although higher amounts
mended for the elderly individuals, non-hypercatabolic obese may be required to maintain a normal osmolality.
patients, and patients with higher nitrogen intake (ie, 1.5 to 2.5 c) Potassium intake is limited because of decreased excretion
g of protein or amino acids per kg per day). The higher end of and because hypercatabolism and acidemia may increase the
this range is used for patients who are severely catabolic or who movement of intracellular potassium out of the cell. Potas-
have low nitrogen intakes. Data in non-hypercatabolic animals sium intake is often limited to 30 to 50 mEq/d until it has

338 A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. © 2005 A.S.P.E.N. www.nutritioncare.org.
 S E C T I O N V Metabolic Conditions

been established that the patient tolerates or requires larger acid doses are administered.14 About 1.0 mg of folate is
doses of potassium. An alternate is to provide 10–20 mEq of given each day. The recommended daily allowances for the
potassium/1000 kcal. other water-soluble vitamins are given each day.15
d) Phosphorus intake is restricted to maintain normal or near- b) In general, vitamin A supplements should be avoided in CKD
normal serum levels. In general, such patients are given 200– patients because serum vitamin A levels are elevated, and small
300 mg of phosphorus per day. Alternatively, phosphorus can supplements of vitamin A have been reported to cause toxic-
be given as 10–20 mmol for every 1000 kcal delivered. ity.16 If patients are to receive PN for more than 1 to 2 weeks,
e) Special attention should be paid to serum potassium and phos- small doses of vitamin A may be given (ie, 800 retinol equiva-
phorus at the initiation of PN. The potassium and phosphorus lents, which is the recommended daily allowance).
in the PN are often withheld from patients who are hyper- c) Vitamin K (10 mg) should be given weekly to patients. It is gen-
kalemic or hyperphosphatemic at the onset of nutrition ther- erally given intramuscularly. It is particularly important to give
apy. Once nutrition support is inaugurated in these individuals, vitamin K to patients who are receiving antibiotics that may
serum potassium and phosphorus concentrations may fall pre- suppress the intestinal bacteria that produce vitamin K.
cipitously, particularly if the patient is receiving dialysis ther- d) Although vitamin D is a fat-soluble vitamin and stores should
apy. Some patients may present with severe protein-calorie not be depleted during the few days to weeks that most patients
malnutrition and these are the patients who are at the highest receive parenteral nutrition, the turnover of 1,25-dihydroxyc-
risk of the refeeding syndrome in which the patient has holecalciferol is much faster.17 Therefore, there may be a need
depleted potassium and phosphorus stores and the serum val- for supplementation with this vitamin D analog in patients with
ues may plummet when dextrose is provided. Patients who are CKD who are receiving nutrition support for a prolonged
severely malnourished and who are believed to have had poor period of time.
intake over 2–4 weeks should be considered to be thiamine D. Specific guidelines for enteral nutrition for patients with CKD.
deficient and thiamine 100 mg should be given intravenously 1. Generally, the guidelines listed for PN can be applied to enteral
before dextrose is given. nutrition support. Specific formulas are available to meet the
5. Calcium provision in parenteral solutions should provide 10– needs of patients during the different phases of renal failure.
15 mEq/d for the short term. If the PN is to be required for more Enteral products vary in the amount of electrolytes, vitamins,
than 3–4 weeks, the provision of more calcium (up to 20mEq/d) and minerals provided.
should be considered, as metabolic bone disease may begin during a) It is often difficult to meet the individual’s energy requirement
this time. The provision of calcium in patients with rhabdomyoly- or limited protein need and to restrict the necessary electrolytes
sis, multiple myeloma, or tumor-lysis syndrome should be min- at the same time. Because of these specific nutritional con-
imal and closely regulated. The serum concentration of total straints engendered by renal failure, specialized formulations
calcium should be maintained between 8.5 g/dL and 10 g/dL. for patients with CKD have been developed. For example, a
6. Magnesium is usually provided at 10–30 mEq/d. In CKD calorie-dense formula is necessary to meet the patient’s energy
patients who have undergone cardiac surgery and who require needs under the constraints of limited water tolerance. Most
PN, the magnesium level must be measured frequently and main- commercial formulas for patients with renal failure provide
tained in the normal range. appropriate vitamins and minerals and 1.5 to 2.0 kcal/mL, with
7. Trace minerals probably do not need to be added to PN solutions, generally about 6% to 20% of calories derived from protein or
with the exception of iron and possibly zinc, unless parenteral amino acids.
nutrition is the sole source of nutrition support for more than b) Protein sources in renal-specific formulas are variable. Some for-
2 weeks. Iron should be avoided in the infected or septic patient. mulas provide the nine essential amino acids (Amin-Aid,
The nutritional requirements for trace minerals have not been McGaw Laboratories). Others provide high-quality protein
established for uremic patients receiving PN. In general, the (Nepro, Suplena, Ross Products). Essential amino acid for-
following trace minerals can be given once weekly if the patient mulas may be used for short periods of time (no more than 2 to
is receiving PN for more than 2 weeks: chromium (10 mcg), cop- 3 weeks) to prevent or delay the use of dialysis therapy as
per (1 mg), iodide (75 mcg), manganese (500 mcg), selenium described above. These essential amino acid preparations
(60 mcg), and zinc (5 mg). However, the need for trace miner- are indicated only for short-term use because the total essen-
als is probably not great if the patient is receiving parenteral tial amino acid intake must be limited to marginal quantities,
blood products. ie, 0.30 to 0.50 g/kg/d and a total of no more than 30 to 40 g/d.
8. Vitamin requirements have not been well defined for patients with Also, Amin-Aid does not provide vitamins and essential miner-
CKD who are receiving nutritional support. Water-soluble vita- als; these must be added separately. Most enteral formulas pro-
mins are lost into the dialysate, except for B12, which is protein vide approximately 30% of calories from fat. Specialty formulas
bound in plasma. These losses as well as a number of drug- for renal disease such as Nepro and Suplena (Ross Products) pro-
nutrient interactions may alter the intestinal absorption, metab- vide approximately 40% of calories from fat, as they are limited
olism (eg, vitamin B6 or 1,25-dihydrocholecalciferol), or actions in carbohydrate and protein content, respectively. Formulas with
(eg, folate) of these vitamins. a lower fat content may be beneficial if malabsorption is present.
a) There appears to be an increased need for certain vitamins However, it may be difficult to meet the patient’s calorie and fluid
in patients undergoing dialysis. Patients receiving hemodial- prescription with these preparations.
ysis should receive 10 mg/d of pyridoxine hydrochloride c) Enteral formulas vary in sodium and potassium content. Stan-
(8.2 mg/d of pyridoxine) to prevent deficiency.13 No more dard 1.0-kcal/mL formulas generally supply 500 to 1000 mg/L
than 60 to 100 mg/d of ascorbic acid should be given because of sodium and 1000 to 2000 mg/L of potassium; 2.0-kcal/mL
of the risk of increasing serum oxalate concentrations and formulas provide similar amounts of sodium and potassium.
precipitating episodes of pseudo-gout when greater ascorbic However, patients generally require less of these formulas to

© 2005 A.S.P.E.N. www.nutritioncare.org. A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. 339
S E C T I O N V Metabolic Conditions

meet their energy needs; hence, their total sodium and potas- or liver failure; or is retaining sodium and water due to other
sium intake may be less. Most CKD patients can tolerate causes.
1000 to 2000 mg/d (43 to 87 mEq/d) of sodium and 1100 to 8. When catabolic stress supervenes, renal transplant recipients are
1950 mg/d (30 to 50 mEq/d) of potassium. Potassium may be given essentially the same nutrition support as acutely ill patients
increased to 2700 mg/d (about 70 mEq/d) if well tolerated, or who do not have renal failure and who are receiving glucocorticoid
reduced if the serum potassium increases. therapy. If acutely ill renal transplant recipients also have renal fail-
d) Phosphorus intake from enteral formulas should be limited to ure, their nutrition support is similar to that of non-transplanted
10–20 mEq per 1000 kcal or lower if the patient is hyper- CKD patients who have superimposed stress.
phosphatemic. Magnesium intake should be approximately
10 mEq/d and should be carefully monitored especially in car-
IV. Intradialytic Parenteral Nutrition (IDPN)
diac surgery patients or those with active or unstable ischemic
heart disease. A. Intradialytic parenteral nutrition is not commonly used in hospital-
ized ESRD patients with acute superimposed illnesses, because the
day-to-day nutritional needs rarely can be met by nutrients infused
III. Nutritional Support for Renal Transplant Patients
during the dialysis period alone. However, intradialytic parenteral
A. Nutritional therapy for renal transplant patients varies according to nutrition may be useful to provide extra nutrients during dialysis in
the different stages in the clinical course of the patient. patients in whom oral or enteral intake is sub-optimal, because
1. Patients who are immediately post-transplantation may require infused water and electrolytes can be easily removed during these
about 1.3 to 1.5 g/kg/d of protein because of the high doses of pred- times. These conditions rarely occur clinically. The one clinical set-
nisone administered and the catabolic stress of surgery. If patients ting in which IDPN might be helpful is in the patient with ischemic
have a very high UNA, they may receive protein up to 2.0 g/kg/d. bowel who cannot meet nutrient needs with oral intake. In this
For patients who develop ARF or who have delayed graft function instance the IDPN may provide the supplemental nutrition that the
in the transplanted kidney, these higher protein intakes increase the patient requires.
need for hemodialysis therapy. When the dose of prednisone is 1. Amino acids, glucose, and lipids may be delivered IV during hemo-
reduced to <30 mg/d, protein intake can be decreased. dialysis treatment. The mixture is infused into the venous drip
2. Later in the clinical course after renal transplantation, when a chamber. For patients receiving oral or enteral nutrition support,
rejection or an acute reaction supervenes and the prednisone dose intradialytic parenteral nutrition offers an opportunity to provide
is increased, protein or amino acid intake may again be increased. additional nutrients to augment the oral or enteral nutrition with-
3. Renal transplant recipients who have diminished GFR but do not out the need to catheterize a central vein.
have acute rejection and who are not on high doses of prednisone 2. Standard mixtures of essential and nonessential amino acids with-
may be prescribed 0.60 g of protein per kg per day. This intake out added electrolytes are generally used. Amino acid solutions of
should maintain good nutrition and may retard the rate of pro- 8.5% or 10% and dextrose monohydrate concentrations of 50% to
gression of renal failure.18 70% are generally mixed together; 10% or 20% lipid emulsions
4. Although renal transplant patients often increase their body fat may also be used. The nutrient concentrations of the solutions
after transplantation and hence may benefit from calorie restric- selected are determined by the patient’s requirements and tolerance
tion, during an acute rejection reaction their energy needs are sim- for water and sodium.
ilar to stressed ARF patients (30 to 45 kcal/kg). Although most 3. The nutrients are usually given in a 750- to 1000-mL solution that
transplant patients and many surgeons advocate an unlimited diet, is infused throughout the hemodialysis treatment.
it is prudent to recommend, at the least, an American Heart 4. On the other hand, nutrition support can be readily administered
Associate (AHA) Step 1 diet with the RDI for protein intake of during CVVH or CVVHD. Patients receive these renal replace-
0.75 g/kg/d. If the transplant patient has a GFR using the Mod- ment therapies virtually continuously and therefore are easily
ification of Diet in Renal Disease (MDRD) GFR formula (see able to handle the nutritional load. The PN prescription during
Appendix 29-1) that is less than 60 mL/min/1.73 m2 bsa, protein CVVH/CVVHD is described above. The PN solutions can be
restriction to 0.6 g/kg aBW should be prescribed. infused into the blood line that is post-dialyzer or CVVH/CVVHD
5. Plasma glucose levels may be elevated because of glucocorticoid filter to decrease the need for central line placement. However, a
therapy. Under these circumstances, carbohydrate intake should risk of this procedure is that if the CVVH/CVVHD is suddenly dis-
be limited to about 60% of calories and, to the extent possible, continued, the patient may have no central vein access to continue
should be complex. Patients who develop diabetes mellitus should receiving PN.
be placed on a diet appropriate for their weight and an exercise
program, and their blood glucose should be tightly controlled with
V. Monitoring Patients Receiving Nutritional Support
the goal for the Hemoglobin A1c in the normal range.
6. Renal transplant patients also tend to have increased serum triglyc- A. At the onset of nutritional support (ie, for about the first week)
eride and cholesterol concentrations.19 Lipids should be limited 1. Daily: complete blood count, serum sodium, potassium, chloride,
to <30% of calories and should be limited to 2 to 3 times per bicarbonate, urea, creatinine, glucose, phosphorus, calcium, mag-
week if triglyceride levels are markedly elevated. Again, the use nesium, and blood gases (measurement of blood gases is not always
of the AHA diets are recommended and if the LDL cholesterol indicated)
cannot be controlled < 100 mg/dL, use of an HMG co-A reductase 2. Daily: water intake and output, accurate body weights
inhibitor is indicated. The lipid levels should be controlled for sec- 3. Once or twice weekly: UNA
ondary, not primary, prevention guidelines. B. During weeks 2 to 4
7. Sodium and potassium generally do not need to be restricted after 1. Every other day or twice weekly: serum sodium, potassium, chlo-
the transplant unless the patient is hypertensive; has renal, heart, ride, bicarbonate, urea, creatinine, glucose, body weight

340 A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. © 2005 A.S.P.E.N. www.nutritioncare.org.
 S E C T I O N V Metabolic Conditions

2. Once or twice weekly: calcium, phosphorus, magnesium, com- 4. Cianciaruso B, Brunori G, Kopple JD, et al. Cross-sectional comparison of
plete blood count malnutrition in continuous ambulatory peritoneal dialysis and hemodialy-
3. Weekly: serum albumin, transferrin sis patients. Am J Kidney Dis. 1995;26:475–486.
5. Young GA, Kopple JD, Lindhom B, et al. Nutritional assessment of con-
tinuous ambulatory peritoneal dialysis patients: An international study. Am
J Kidney Dis. 1991;17:462–471.
VI. Complications of Nutrition Support 6. Goa XL, Kopple JD. Relationship between dietary protein, urea nitrogen
A. Complications of PN. (For a complete review of complications, see appearance (UNA) and total nitrogen appearance (TNA) in patients with
PN Management chapter). One of the most common complications chronic renal failure (CKD) [abstract]. J Am Soc Nephrol. 1995;5:491.
7. Najjar MF, Rowland M. Anthropometric Reference Data and Prevalence of
of PN in patients with CKD is hyperglycemia. This complication
Overweight, United States, 1976–1980. Hyattsville, Md: U.S. Dept. of
occurs because patients often receive large doses of dextrose to meet Health and Human Services, Public Health Service, National Center for
their calorie needs, and they frequently have glucose intolerance. Health Statistics; 1987.
Increased serum glucose concentrations have been implicated as a 8. Nakasaki H, Katayama T, Yokoyama S, et al. Complications of parenteral
cause of impaired leukocyte function, which can suppress wound nutrition composed of essential amino acids and histidine in adults with
healing. Serum glucose should be monitored closely; insulin should renal failure. J Parenter Enteral Nutr. 1993;17:86–90.
be provided in the PN solution to maintain serum glucose within the 9. Chima CS, Meyer L, Hummell AC, et al. Protein catabolic rate in patients
normal range. with acute renal failure on continuous arteriovenous hemofiltration and
total parenteral nutrition. J Am Soc Nephrol. 1993;3(8):1516–1521.
B. Complications of enteral nutritional support in patients with CKD.
10. Bellomo R, Mansfield D, Rumble S, et al. A comparison of conventional
(For a complete review of complications, see EN management dialytic therapy and acute continuous hemodiafiltration in the management
chapter.) of acute renal failure in the critically ill. Renal Failure. 1993;15:595–602.
1. Because the electrolyte composition of enteral formulas cannot be 11.Harris JA, Benedict FG. A Biometric Study of Basal Metabolism in Men.
manipulated as easily as with PN solutions, it may be difficult to Publication 279. Washington, DC: Carnegie Institute; 1919.
maintain serum electrolytes within the normal range with enteral 12. Askanazi J, Rosenbaum SH, Hyman AL, et al. Respiratory changes induced
formulas. by large glucose loads of total parenteral nutrition. J Am Med Assoc. 1980;
243:1444–1447.
2. It also is often difficult to maintain water balance with enteral for-
13. Kopple JD, Mercurio K, Blumenkrantz MJ, et al. Daily requirement for pyri-
mulas, because large volumes of formula are often required to doxine supplements in chronic renal failure. Kidney Int. 1981;19:694–704.
meet energy needs. At times, enteral formulas must be diluted 14. Pru C, Eaton J, Kjellstrand C. Vitamin C intoxication and hyperoxalemia
with water and occasionally fortified with salt. in chronic hemodialysis patients. Nephron. 1985;39:112–116.
3. The complications that are common to all patients receiving 15. National Research Council. Recommended Dietary Allowances. 10th ed.
enteral nutrition such as diarrhea, aspiration, and mechanical Washington, DC: National Academy Press; 1989.
problems with pumps and tubing are also common in patients 16. Gleghorn EE, Eisenberg LD, Hack S, et al. Observations of vitamin A tox-
with ARF and CKD. icity in three patients with renal failure receiving parenteral alimentation.
Am J Clin Nutr. 1986;44:107–112.
17. Audran M, Kumar R. The physiology and pathophysiology of vitamin D.
(Renal disease chapters in first edition contributed by Christie Amble, Mayo Clin Proc. 1985;60:851–866.
Joel Kopple, Robert Wolk, Rowena Stokowski, and Peter Yorgin) 18. Nelson J, Beauregard H, Gelinas M, et al. Lipoprotein abnormalities in
renal transplant recipients with chronic vascular rejection. Transplant Proc.
REFERENCES 1992;24:366.
19. Dimeny E, Fellstrom B, Larsson E, et al. Lipoprotein abnormalities in renal
1. National Center for Health Statistics. DHHS publication (PHS)87-1688.
transplant recipients. Clin Nephrol. 1982;18:306.
Washington, DC: National Center for Health Statistics, U.S. Public Health
Service; 1987.
2. Kopple JD, Jones MR, Keshaviah PR, et al. A proposed glossary for dialy- SUGGESTED WEB SITE REFERENCE
sis kinetics. Am J Kidney Dis. 1995;26:963–981. 1. National Kidney Foundation Kidney Disease Outcomes Quality Initiative.
3. Detsky AS, McLaughlin JR, Baker JP, et al. What is subjective global Available at: http://www.kidney.org/professionals/kdoqi/index.cfm. Accessed
assessment of nutrition status. J Parenter Enteral Nutr. 1987;11:8–13. October 2, 2004.

© 2005 A.S.P.E.N. www.nutritioncare.org. A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. 341
 APPENDIX

30-1
Calculated Glomerular
Filtration Rate (GFR)

The estimations of GFR from serum creatinine concentra-

tion or from formulas that rely on age, sex, weight, and
serum creatinine are imprecise and may over- or under-
estimate the actual GFR. Several formulas exist but they
are flawed because they were developed in normal,
healthy persons aged 18–65; they use too few variables;
and they ignore the influences of sex and ethnicity. The
National Kidney Disease Education Program, a joint pro-
gram between the NIH and the Kidney Disease Outcomes
Quality Initiative of the National Kidney Foundation, has
proposed using the estimation formula developed by the
Modification of Diet in Renal Disease study (MDRD).
This equation has been validated in a large cohort of
patients with kidney disease, has been proven superior to
other regression formulas, and does not rely upon weight.
The results from this formula are already normalized to a
1.73-m2 body surface area. The simple and extended for-
mulas have exponents that are in fractions and are nega-
tive. Therefore, because of the complicated math, it is
most practical to use a GFR calculator found on the web
such as: http://www.nkdep.nih.gov/GFR-cal-adult.html
(this site also has a calculator for children), http://med-
calc3000.com/GFREstimator.htm, or http://www.
nephron.com/cgi-bin/MDRD-GFR.cgi (this site has the
Cockcroft-Gault formula, the extended MDRD formula,
and a formula for pediatrics). These equations can be
downloaded into a PDA or placed on a computer desktop
as a shortcut to the web site.

342 A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. © 2005 A.S.P.E.N. www.nutritioncare.org.
 David Frankenfield, MS, RD

31
Pregnancy

Introduction nancy are somewhat higher than normal. Impediments to intake need
not be physical or disease related. Poor dietary habits exist in various
Nutrition support plays a role in almost every phase of the life cycle. For segments of the population because of a lack of resources or educa-
the pregnant woman and her fetus, nutrition support can be lifesaving. tion, or cultural or other pressures to avoid certain foods. The most
For the practitioner, nutrition support of the pregnant woman can be common condition that might seriously impair nutrient intake is
intimidating, partly because the need for nutrition support in pregnancy hyperemesis gravidarum.
is rare (limiting experience), and partly because few scientific data exist B. Absorption. Nutrient absorption is not adversely affected during nor-
on which to base provision of care. This chapter will outline the standard mal pregnancy, but preexisting conditions that impair absorption
for enteral and parenteral feeding during pregnancy. may remain and lead to malnutrition because increased demand for
nutrient intake is imposed upon an already limited ability to digest
I. Background and absorb nutrients. On the other hand, there is anecdotal evidence
II. Nutritional Aspects of Pregnancy for improved absorption during pregnancy among women with nor-
III. Nutritional Alterations in Pregnancy mally impaired absorption. One such case was described by Mont-
IV. Focused Assessment
gomery and Pincus in 1955.10 A woman with 3 feet of duodenum and
V. Objectives and Goals of Therapy
jejunum who passed two to four soft stools per day containing sig-
VI. Management
nificant undigested fat and meat fibers plus undigested vegetable
References
matter began to pass only one, more formed stool per day upon
Suggested Readings
becoming pregnant. Microscopic examination of the fecal material
appeared to show less undigested food than that found in pre-
I. Background. Optimal outcome in pregnancy is dependent upon pregnancy fecal material. The patient consumed 4000 to 5000 kcal/d
good maternal nutrition.1 Poor maternal nutrition can lead to intrauter- and gained 14 pounds during pregnancy, delivering a 6-pound infant.
ine growth retardation, low-birth-weight babies, and increased prenatal Two more successful pregnancies followed, and in each case the
morbidity and mortality.2,3 If the mother cannot maintain adequate oral patient’s postpartum bowel function returned to that occurring
nutritional intake because of disease or other conditions, intake can be before the first pregnancy.
ensured by use of tube feeding or parenteral nutrition. Nearly all of the C. Utilization. Pregnancy is an anabolic state. An average of 925 g of
literature regarding nutrition support during pregnancy is anecdotal, con- protein and 3825 g of fat accumulate in the mother and fetus.11 Oxy-
sisting of case reports.4–7 Thus, principles and practices for nutrition sup- gen consumption increases steadily through pregnancy, starting
port during pregnancy are very much experience based and extrapolated with a 5% increase in the first 10 weeks, then increasing by approx-
from normal diet in pregnancy and nutrition support practices in non- imately 7%, 11%, and 15% in each subsequent 10-week period.
pregnant people. These increases must be thought of as general values, as there is great
interindividual variability in actual measurements in oxygen con-
sumption, especially in the last 10 weeks.12 Eighty percent of the
II. Nutritional Aspects of Pregnancy increase in oxygen consumption is for maternal tissue metabolism
A. Intake. In normal pregnancy there are few conditions which seriously and work (cardiac output, respiration, uterus muscles, breast, and kid-
decrease nutrient intake. Nausea may occur because of gastric atony, ney).11 The remaining 20% is for the fetus.
which is consistent with generalized relaxation of smooth muscles Additional macronutrient intake is needed to meet increased
during pregnancy. Severe nausea or vomiting impairs nutrient intake, energy requirements and to provide substrate for tissue growth.
sometimes severely. However, the nausea of pregnancy is not usually The increase in oxygen consumption of pregnancy represents oxida-
a major impediment to nutrition intake. In one study, more than half tive macronutrient use and accounts for only about 40% of the
of pregnant women reported an obvious increase in appetite and increase in total macronutrient requirements. The remaining 60%
thirst8 beginning in the first trimester. However, nutrient intake gen- of macronutrient requirement increase is used for tissue growth.11
erally increases even without an increase in appetite.9 Greater intake D. Losses. Nutrient losses during pregnancy are not different from
and reduced ability to consume large meals (because of early full- those in nonpregnancy. In fact, certain nutrient losses are reduced.
ness) as pregnancy progresses may cause a change in dietary habits, For example, iron is normally absorbed from the gastrointestinal
with more frequent but smaller meals being consumed. tract in proportion to the level of deficiency in the body. Because iron
Obviously, preexisting impediments to nutrient intake would requirements during pregnancy are elevated, a greater percentage of
remain problems during pregnancy, and in fact the related nutrient dietary iron is absorbed (ie, less is lost).13 Furthermore, menstruation
deficits might be exacerbated, since nutrient requirements in preg- ceases, eliminating another source of iron loss.

© 2005 A.S.P.E.N. www.nutritioncare.org. A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. 343
S E C T I O N V Metabolic Conditions

III. Nutritional Alterations in Pregnancy ber of previous pregnancies, and maternal history of low-birth-weight
babies. Each of these factors, in addition to weight history, should be
A. Common. Calorie and protein requirements are elevated in preg- ascertained during the workup.14
nancy. As discussed Section II.C, calorie requirements are elevated B. Physical examination. Prepregnancy body weight and weight gain
for both increased fuel utilization (oxygen consumption) and tissue during pregnancy are critical determinants of fetal growth rate and
growth. The average increase in calorie requirement is 300 kcal/d, pregnancy outcome.2 Therefore, prepregnancy weight in relation to
although the caloric requirement through pregnancy increases from height (percentage of ideal body weight or body mass index) is an
the first to the third trimester.14 Calorie intake should be adjusted up important physical finding (Table 31-1).21 Consistency in methods
or down to achieve weight gain goals (Table 31-1).15 Protein intake and equipment is necessary in making these measurements, since the
should be increased by about 10 to 15 g/d above the recommended change over time is important to monitor, and alterations in methods
dietary allowance or should be sufficient to achieve positive nitro- or equipment may mask changes in true body weight. Certain overt
gen balance. As with calories, the increase in protein requirement is vitamin and protein deficiencies can be detected upon physical exam-
greater later in pregnancy. ination. The signs of such deficiencies are the same as in nonpregnant
Requirements for micronutrients, with some exceptions, are women.
elevated during pregnancy (Table 31-2).14,16 Both fetal growth and
development and growth of maternal tissues (placenta, uterus,
breast, blood tissue) must be supported. Hypoalbuminemia (mean V. Objectives and Goals of Therapy. The goal of nutrition sup-
total decline of 1 g/dL) is common in pregnancy and represents a port during pregnancy is the delivery of a normal-weight, healthy child.
dilution of blood volume.17 For similar reasons, hemoglobin falls in To that end, macronutrient and micronutrient intake must be adequate to
the first and second trimesters of pregnancy but then rises in the achieve weight gain goals24 and to ensure adequate substrate and cofac-
third trimester. tors for development of fetal organ systems. To meet the goal of a suc-
Alterations in glucose homeostasis can occur, with fasting hypo- cessful pregnancy, the nutrition plan should help the pregnant woman
glycemia and postprandial hyperglycemia. Serum triglycerides and consume enough energy and protein to gain the appropriate amount of
cholesterol levels are generally elevated during pregnancy.18 weight and to achieve a positive nitrogen balance. Adequate and safe
B. Less common. Disease states may add further demands for nutrients vitamin and mineral supplementation should be provided. If nonvoli-
and alter the efficiency of nutrient utilization during pregnancy.19 tional nutrition support (tube feeding or parenteral feeding) is necessary,
Accidental or surgical trauma, infection, sepsis, or other diseases the goal is to meet the calorie, protein, and micronutrient needs while
eliciting a systemic inflammatory response can increase body catab- avoiding complications associated with the nutrient delivery method
olism and metabolic rate. Fetal requirements must still be met dur- (mechanical, physiologic, or infectious complications).
ing times of metabolic stress. Nitrogen balance is difficult to achieve
in metabolically stressed patients on bed rest. Protein intake should
not exceed 2.0 g/kg.20 See disease-specific chapters in this volume VI. Management
for the requirements of each disease state. A. Special aspects of diet and nutritional supplements. In normal preg-
Malnutrition also alters nutritional needs above the alterations seen nancy, unless there are physiologic, economic, social, or cultural
with normal pregnancy. Underweight women are encouraged to gain restrictions on intake, the pregnant woman can normally regulate
slightly more weight than normal-weight women, and obese women nutrient intake without much conscious effort.9 If impinging factors
are encouraged to gain slightly less (Table 31-1).21 do exist, they must be identified and circumvented to ensure ade-
quate intake.
IV. Focused Assessment22,23 In underweight or obese women, women with concurrent disease
states, or women with impaired intake, more than usual care must be
A. History. Numerous factors can influence fetal growth rate.14 Fetal taken in diet planning and monitoring. Plans for increasing nutrient
growth rate is an important parameter, since birth weight is an intake (eg, use of calorie-dense foods, more frequent meals, vitamin
important indicator of pregnancy outcome.17 Factors predicting low and mineral supplements) should be individualized based on what is
fetal growth rates include maternal cigarette smoking, nutrient causing the impaired intake.19
intake and dietary habits, weight prior to becoming pregnant, num- Potential nutrition problems are most appropriately identified by
eliciting from the woman her dietary patterns (food history, food fre-
quency questionnaires, interview questions about special problems
TABLE 31-1. Weight Goals for Pregnant Women Based or conditions that might affect diet adequacy). This approach to iden-
on Prepregnancy Weight15 tifying nutrition problems and the need for intervention is preferable
to biochemical testing (except for hemoglobin and hematocrit lev-
Body mass Percentage of els).9 Multivitamins are recommended for women who do not nor-
index* ideal weight Weight gain (lbs) mally consume an adequate diet or who are in high-risk categories
(multiple fetuses, smoking, ethanol or other drug abuse, chronic
<19.8 <90 12.5–18.0 disease). If the diet is adequate and the woman does not fit into a
high-risk category, micronutrient supplementation is not considered
19.8–26 90–120 11.5–18.0 necessary by the Food and Nutrition Board of the National Academy
of Sciences (one exception is for iron, the requirements for which
>26 >120 7.0–11.5 the board believes cannot reasonably be met by diet alone).21 Folate
intake appears to be a critical factor during the development of the
*Body mass index calculated as weight/height2 with height in meters and weight in neural tube.25 The need for folate is most critical during the first
kilograms. month of fetal development, when many women are still unaware

344 A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. © 2005 A.S.P.E.N. www.nutritioncare.org.
 S E C T I O N V Metabolic Conditions

TABLE 31-2. Micronutrient Requirements in Pregnancy (Dietary Reference Intakes)14,16

Percentage of
Nonpregnancy Pregnancy nonpregnancy
Nutrient requirement requirement requirement

Vitamin A (mcg) 700 770 110

Vitamin D (mcg) 5 5 100
Vitamin E (mg alpha-TE) 15 15 100
Vitamin K (mcg) 90 90 100
Vitamin C (mg) 75 85 113
Pyridoxine (mg) 1.3 1.9 146
Thiamine (mg) 1.1 1.4 127
Riboflavin (mg) 1.1 1.4 127
Niacin (NE) 14 18 128
Folate (mcg) 400 600 150
Cobalamin (mcg) 2.4 2.6 108
Calcium (mg) 1000 1000 100
Phosphorus (mg) 700 700 100
Magnesium (mg) 320 350 109
Zinc (mg) 8 11 138
Iodine (mcg) 150 220 147
Selenium (mcg) 55 60 109
Iron (mg) 18 27 150

NE, niacin equivalents; TE = tocopherol equivalents

Adapted with permission from Food and Nutrition Board, Institute of Medicine, National Academy of Sciences. Dietary Reference Intakes: Recommended Intakes for Individuals.
www.nap.edu. 2004.
Accessed Aug. 21, 2004.

of their pregnancy. Routine, early use of folate supplements therefore ventions for patients with hyperemesis. If tube feedings are nec-
seems reasonable. Some medications, such as anticonvulsants, alter essary, continuous feeding offers the best chance for success.19 As
nutrition requirements. For that reason, the American College of always, both the benefits and risks of tube feeding should be con-
Gynecology recommends that pregnant women taking anticonvul- sidered. Tube feedings should be initiated slowly and advanced
sants supplement their diet with 4 mg per day of folic acid. Micro- slowly as tolerated. Oral intake should be eliminated until toler-
nutrient supplements, when prescribed, should be taken between ance to the tube feeding is established (so as not to confuse food
meals or at bedtime, to promote absorption.21 intolerance with tube feeding intolerance). Oral feeding should be
B. Special aspects of enteral nutrition reintroduced slowly, to tolerance.
1. Indications. Indications for tube feeding in pregnant women are the 2. Access. Nasogastric tubes are indicated if the stomach is func-
same as those for nonpregnant people. Women who are unable to tional, and nasojejunal tubes are indicated if the stomach is dys-
eat adequately but have a functional gastrointestinal tract are can- functional. For endoscopic nasojejunal tube placement, the woman
didates for tube feeding. Nutrient requirements will be based on should not be exposed to sedatives that might injure the fetus, and
needs during pregnancy plus needs for specific disease states if if radiation exposure is necessary for tube placement, special care
present. Use of tube feeding per se does not alter nutrient require- must be taken to avoid exposing the fetus.
ments or utilization. 3. Regimen. Certain conditions, such as hyperemesis gravidarum or
One special indication for tube feeding during pregnancy is diabetes, or use of small-bowel feeding tubes may require a con-
hyperemesis gravidarum. This condition often resolves after the tinuous rather than an intermittent feeding schedule to ensure
first trimester, and in previously well-nourished women it may not adequate tolerance. Often, 24-hour continuous feeding is best tol-
require intervention. An intermediate step before the use of tube erated; however, intermittent feedings (cyclic nocturnal; or for
feeding is oral supplementation and intensive nutrition counsel- gastric tubes, bolus or gravity drip) allow the woman greater free-
ing.19 Antiemetics and promotility agents are also important inter- dom of movement and independence. The feeding schedules

© 2005 A.S.P.E.N. www.nutritioncare.org. A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. 345
S E C T I O N V Metabolic Conditions

should not sacrifice intake for the sake of greater independence, ance, and to provide safe and adequate micronutrient therapy. In
however. addition, complications associated with tube feeding should be
4. Duration. Initiation and termination of tube feedings can occur at avoided by timely monitoring and intervention.
any time during pregnancy. A fair attempt at oral feeding should C. Special aspects of parenteral nutrition
first be made before tube feeding is initiated, and the cause of oral 1. Indications. Parenteral nutrition should be considered only if all
feeding failure should be resolved before the termination of tube attempts at oral and tube feeding have failed and the woman is or
feeding. is becoming malnourished. Parenteral nutrition is the most expen-
5. Formulas. In most cases, a polymeric tube feeding is sufficient. sive and risky form of nutrition support, but it can be lifesaving
In patients with a preexisting disease such as Crohn’s disease, when the gastrointestinal tract is dysfunctional. Higher rates of
digestion and/or absorption impairment may necessitate elemen- complications during the use of parenteral nutrition have been
tal or peptide-based feedings. Feedings containing dietary fiber reported in pregnant women.26,27 Women with hyperemesis gravi-
are desirable to minimize the chance of developing constipation. darum will often continue to have symptoms of nausea and retch-
The tube feeding should provide adequate calorie, protein, and ing even with parenteral nutrition. Parenteral nutrition is not a
micronutrient support for the stage of pregnancy (micronutrient treatment but can support the fetus and mother until enteral feed-
limitations may be overcome by use of supplements). Free water ing can be reinstituted.
can be added as flushes or boluses. 2. Access. For short-term use, either central venous or peripherally
6. Monitoring. Maternal weight gain and fetal growth are the most inserted central catheters are acceptable. Single- or multiple-
important factors in assessing the adequacy of tube feeding. It is lumen catheters can be used. For long-term use, surgically
important to differentiate weight gain due to fluid retention from inserted or implanted single- or multiple-lumen catheters are
other weight gain, especially with preeclampsia. Actual feeding available. Peripheral parenteral nutrition generally is not indi-
volume infused (to identify underfeeding or overfeeding) and the cated for greater than 2 weeks because it cannot provide enough
presence of an inflammatory response (to identify possible hyper- calories and there is a risk of phlebitis. If the gut is dysfunctional
metabolism) may be helpful in determining why weight gain or and all requirements must be met parenterally, peripheral solu-
nitrogen balance goals are not being achieved. Biochemical test- tions may not be adequate because of limitations on solution
ing for nutritional adequacy can be limited to nitrogen balance, osmolality, while if supplementation of oral intake is all that is
hemoglobin, and hematocrit checks. Nitrogen balance is not usu- required, tube feeding is more appropriate, since the gut is func-
ally monitored in this population; however, values should be pos- tional. Peripheral parenteral nutrition solutions usually are more
itive with provision of adequate protein. Table 31-3 provides dilute (higher volume), with a higher percentage of fat emulsion,
laboratory values used to assess anemia in pregnant women. than central parenteral nutrition. For these reasons, peripheral
Hyperglycemia is a risk factor for fetal macrosomia and death. solutions often are not ideal for pregnant women.
Therefore, women with glucose intolerance should be identified 3. Regimen. Parenteral nutrition must always be administered by
and their blood glucose concentration monitored, with insulin infusion pump. Parenteral nutrition can be infused continuously
coverage to maintain blood glucose levels below 120 mg/dL. over 12 to 24 hrs/d. One common infusion method is to infuse noc-
Metabolic monitoring (labs, fluid balance) and tolerance to feed- turnally over 12 hours to allow freedom of movement and inde-
ing should follow the guidelines set forth in Chapter 5. Indirect pendence from the pump during the day. Keeping mean blood
calorimetry is sometimes performed during pregnancy when glucose concentrations below 100 mg/dL during parenteral nutri-
nonvolitional feedings are used or if appropriate weight gain is tion has been reported to lead to good pregnancy outcome,
not being achieved. If indirect calorimetry is performed, it must including a decreased incidence of macrosomia and neonatal
be recognized that the results will reflect only the energy require- hypoglycemia.28 Women with glucose intolerance need longer
ment for fuel utilization, not the substrate requirement for tissue cycles (16 hours) with cautious taper down. Blood glucose con-
accumulation. centration should be monitored midcycle and 1 hour postinfusion.
7. Objectives. The goals of tube feeding during pregnancy are to 4. Duration. Parenteral nutrition is generally not indicated during
achieve appropriate weight gain, to achieve positive nitrogen bal- the first trimester for several reasons:
a) Nutrient requirements during the first trimester generally are
not much higher than normal requirements.
b) The woman can usually support the early phase of pregnancy
TABLE 31-3. Assessment of Anemia in Pregnancy from endogenous nutrients and minimal exogenous intake.
c) Many early feeding problems (eg, hyperemesis gravidarum)
First Second Third resolve by the end of the first trimester. If there is significant
trimester trimester trimester weight loss or malnutrition and gut dysfunction, then total par-
enteral nutrition may be considered during the first trimester.
Hemoglobin (g/dL) 11 10.5 11 During the second and third trimesters, parenteral nutrition
should not be used if duration of therapy is anticipated to be less
Hematocrit (%)* 33 32 33 than 1 week. Once initiated, parenteral nutrition can be main-
Iron deficiency <Ferritin 20 mcg/L with hemoglobin >10.5 g/dL tained indefinitely if proper access and care of the access device
is achieved.
Iron deficiency <Ferritin 12–20 mcg/L with low hemoglobin
5. Formulas. With parenteral nutrition, carbohydrate, lipid, protein,
anemia electrolytes, vitamins, and minerals are each added to the mixture
separately (ie, parenteral nutrition is completely modular). This
*CDC criteria for anemia in children and childbearing-aged women. MMWR. allows full flexibility in designing the regimen. Glucose intake
1980;38:400–404. generally is limited to 5 mg/kg/min (7 g/kg/d) or less.19 Standard

346 A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. © 2005 A.S.P.E.N. www.nutritioncare.org.
 S E C T I O N V Metabolic Conditions

amino acid solutions with a balance of essential and nonessential mended allowances for some micronutrients. Therefore, standard
amino acids should be used.19 Solutions high in branched-chain intravenous multivitamin and trace mineral preparations may pro-
amino acids, sometimes used in liver disease and sepsis, have not vide adequate micronutrient intake during pregnancy (Table 31-4),
been tested for possible teratogenic effects (per package insert). with the following exceptions:
Lipids should make up no more than 30% of total calories to limit a) Folate is sometimes supplemented (1 mg/d), even though the
possible hypertriglyceridemia and immune dysfunction. Minimal content in most standard parenteral multivitamin preparations
essential fatty acid intake should be 4.5% of total calories.29 Both meets the recommended dietary allowance for pregnancy.
linolenic and linoleic acids should be provided; all commercially b) Vitamin K is not contained in all multivitamin preparations and
available lipid emulsions contain both types of fatty acids. therefore must sometimes be supplemented (1 mg/d). It must
Micronutrients infused parenterally are not subject to the some- be kept in mind that there is Vitamin K activity in intravenous
times inefficient enteral absorption process and so have much fat emulsions, reducing or negating the need for supplementa-
greater bioavailability than micronutrients fed enterally. Therefore, tion of Vitamin K.30,31
the requirements for micronutrients in parenteral nutrition are c) For long-term parenteral nutrition, iron may be supplemented.
sometimes lower than in enteral nutrition. The composition of par- There are several methods of iron supplementation. A weekly
enteral micronutrient preparations may meet or exceed the recom- dose of 25 mg intramuscularly meets iron requirements but may

TABLE 31-4. Vitamin and Mineral Requirements in Pregnancy Compared With

Standard Multivitamin and Trace Element Parenteral Preparations*

Pregnancy Standard parenteral

Nutrient requirement** content***

Vitamin A 770 mcg 3300 international units

Vitamin D 5 mcg 200 international units

Vitamin E 15 mg alpha-TE 10 international units

Vitamin C (mg) 90 200

Vitamin K (mcg) 90 150

Thiamine (mg) 1.4 6

Riboflavin (mg) 1.4 3.6

Pyridoxine (mg) 1.9 6

Niacin (NE) 18 40

Pantothenic acid (mg) 6 15

Biotin (mcg) 30 60

Folate (mcg) 600 600

Cyanocobalamin (mcg) 2.6 5

Zinc (mg) 11 2.5–5****

Copper (mg) 1.0 0.3–0.3****

Manganese (mg) 2.0 0.6–1****

Selenium (mcg) 60 20–60****

NE, niacin equivalents; TE, tocopherol equivalents

* Check specific manufacturer’s labeling for parenteral vitamin, mineral, and trace element doses.
** Food and Nutrition Board, Institute of Medicine, National Academy of Sciences. Dietary Reference Intakes: Recommended Intakes for Individuals. www.nap.edu. 2004.
Accessed Aug. 21, 2004.
*** US Department of Health and Human Services. Parenteral multivitamin products. Fed Regist. 2000;65:21200–21201.
**** Task Force for the Revision of Safe Practices for Parenteral Nutrition. Safe practices for parenteral nutrition. J Parenter Enteral Nutr. 2004;28:S39–S70.

© 2005 A.S.P.E.N. www.nutritioncare.org. A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. 347
S E C T I O N V Metabolic Conditions

be uncomfortable for the patient. Some clinicians provide low- 12. Goldberg GR, Prentic AM, Coward WA, et al. Longitudinal assessment of
dose iron dextran in the parenteral solution when a fat emulsion energy expenditure in pregnancy by the doubly labeled water method. Am
free base solution is used and test doses are properly adminis- J Clin Nutr. 1993;57:494–505.
tered.32 It is always best to provide iron supplements orally if 13. Svanberg B. Absorption of iron in pregnancy. Acta Obstet Gynecol Scand.
1975;48(suppl):69.
possible.
14. Food and Nutrition Board, Institute of Medicine, National Academy of Sci-
d) Iodine may be supplemented if parenteral nutrition is required
ences. Dietary Reference Intakes: Recommended Intakes for Individuals.
for longer than 2 weeks, as currently available trace element www.nap.edu. Accessed Aug. 21, 2004.
preparations do not contain it. 15. Abrams B. Weight gain and energy intake during pregnancy. Clin Obstet
e) Calcium, phosphorus, and magnesium are not contained in Gynecol. 1994;37:515.
any multiple–trace element preparations and thus need to be 16. Wada L, King JC. Trace element nutrition during pregnancy. Clin Obstet
supplemented. Gynecol. 1994;37:574.
Unlike micronutrient requirements, dextrose, lipid, and amino 17. Robertson EG, Cheyne GA. Plasma biochemistry in relation to oedema of
acid requirements during parenteral nutrition are equivalent pregnancy. J Obstet Gynaecol Br Commonw. 1972;79:769–776.
to those provided by the enteral route, because enteral absorp- 18. MacBurney M, Wilmore DW. Parenteral nutrition in pregnancy. In:
tion of these macronutrients is approximately 98% (ie, there Rombeau J, Caldwell M, eds. Parenteral Nutrition. 2nd ed. Philadelphia,
PA: WB Saunders; 1992.
is very little difference in the bioavailability of macronutrients
19. Greig PD, Elwyn DH, Askanazi J, et al. Parenteral nutrition in septic
delivered parenterally versus enterally).
patients: effect of increasing intake. Am J Clin Nutr. 1987;46:1040–1047.
6. Monitoring. Monitoring of parenteral nutrition is similar to that for 20. National Academy of Sciences. Nutrition During Pregnancy. Washington,
tube feeding. See Chapter 8 for specific monitoring methods dur- DC: National Academy Press; 1990.
ing parenteral nutrition. Monitoring serum glucose and triglyceride 21. Hamaoui E, Hamaoui M. Nutritional assessment and support during preg-
levels is particularly important during pregnancy. nancy. Gastroenterol Clin North Am. 1998;27:89.
7. Objectives. The goals during parenteral nutrition are the same as 22. Suitor CW. Nutritional assessment of the pregnant woman. Clin Obstet
those in oral or tube feeding: appropriate weight gain, positive nitro- Gynecol. 1994;37:501.
gen balance, safe and adequate micronutrient intake, and avoidance 23. Dawes MG, Grudzinskas JG. Patterns of maternal weight gain in preg-
of complications associated with the therapy. nancy. Br J Obstet Gynaecol. 1991;98:195–201.
24.Czeizel AE, Dudas I. Prevention of the first occurrence of neural tube defects
REFERENCES by periconceptual vitamin supplementation. N Engl J Med. 1992;327:
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1. Kramer MS. Intrauterine growth and gestational duration determinants.
25. Russo-Stieglitz KE, Levine AB, Wagner BA, et al. Pregnancy outcome in
Pediatrics. 1987;80:502.
patients requiring parenteral nutrition. J Matern Fetal Med. 1999;8:164.
2. Van den Berg BJ. Maternal variables affecting fetal growth. Am J Clin Nutr.
26. Caruso A, DeCarolis S, Ferrazzani S, et al. Pregnancy outcome and total par-
1981;34:722–726.
enteral nutrition in malnourished women. Fetal Diagn Ther. 1998;13:136.
3. Naeve RL. Weight gain and the outcome of pregnancy. Am J Obstet Gynecol.
27. Kitzmiller JL. Intensified glucose monitoring in gestational diabetes. Clin
1979;135:3–9.
Diabetes. 1995;13:110.
4. Breen KJ, McDonald IA, Panelli D, et al. Planned pregnancy in a patient
28. Crawford MA. Estimation of essential fatty acid requirements in pregnancy
who was receiving home parenteral nutrition. Med J Aust. 1987;146:215.
and lactation. Prog Food Nutr Sci. 1980;4:75–80.
5. Mughal MM, Shaffer JL, Turner M, et al. Nutritional management of preg-
29. Camilo ME, Jatoi A, O’Brien M, et al. Bioavailability of phylloquinone from
nancy in patients on home parenteral nutrition. Br J Obstet Gynaecol.
an intravenous lipid emulsion. Am J Clin Nutr. 1998;67:716.
1987;94:44.
30. Duerksen DR, Papineau N. The prevalence of coagulation abnormalities in
6. Tresadern JC, Falconer GF, Turnberg LA, et al. Maintenance of pregnancy
hospitalized patients receiving lipid-based parenteral nutrition. J Parenter
in a home parenteral nutrition patient. J Parenter Enteral Nutr. 1984;8:199.
Enteral Nutr. 2004;28:30.
7. Badgett T, Feingold M. Total parenteral nutrition in pregnancy: case review
31. MacBurney M, Matarese LE. Pregnancy. In: Matarese LE, Gottschlich MM,
and guidelines for calculating requirements. J Matern Fetal Med. 1997;6:215.
eds. Contemporary Nutrition Support Practice. 2nd ed. Philadelphia, PA:
8. Taggart N. Food habits in pregnancy. Proc Nutr Soc. 1961;20:35.
9. Hytten FE. The alimentary system. In: Hytten FE, Chamberlain G, eds. Clin- Saunders; 2003:337–356.
ical Physiology in Obstetrics. Oxford, UK: Blackwell Scientific Publications;
1980:147–162. SUGGESTED READINGS
10. Montgomery TL, Pincus IJ. A nutritional problem in pregnancy resulting Gardner DK. Parenteral nutrition in pregnancy. Nutr Clin Pract. 2000;15:
from extensive resection of the small bowel: case report. Am J Obstet 63–64.
Gynecol. 1955;69(4):865–868. Wagner BA, Worthington P, Russo-Stieglitz KE, Levine AB, Armenti VT.
11. Hytten FE. Nutrition. In: Hytten FE, Chamberlain G, eds. Clinical Physiology Nutritional management of hyperemesis gravidarum. Nutr Clin Pract.
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348 A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. © 2005 A.S.P.E.N. www.nutritioncare.org.
 J. Scott Whittaker, BSc, MD;
Laura Sware, RD; Lori Hards, BSc, RD
32
Anorexia Nervosa

Introduction appreciable rise in plasma glucose, while intravenous glucose

results in the normal expected rise in plasma glucose.5 The pro-
Anorexia nervosa is a psychiatric condition that is observed predomi- posed explanation is that glucose absorption is delayed as a result
nantly, but not exclusively, in girls and young women and is charac- of decreased intestinal motility. The plasma glucose response to
terized by restriction of food intake in what has been termed the oral glucose returns to normal with renutrition.
“relentless pursuit of thinness.” Males represent about 5 to 10 percent 2. There have been isolated reports of an association between anorexia
of anorexia nervosa patients. Patients with anorexia nervosa are gen- and inflammatory bowel disease, including Crohn’s disease.6–8
erally subclassified into “restricting type” and “binge-eating/purging Crohn’s disease may be associated with nutrient malabsorption if
type.” Patients in the latter group, in addition to restricting food intake, there is extensive small-bowel disease or if small-bowel resec-
partake in bouts of bingeing and vomiting, and they tend to have a tions have resulted in a short bowel.
poorer prognosis. Unlike most other patients in developed countries C. Utilization. Most nutrients appear to be absorbed and metabolized
with wasting disorders, patients with anorexia have no underlying phys-
normally, but serum carotene levels are elevated, leading to sugges-
ical problem with food intake or absorption. Hence, the patients’ phys-
tions of decreased hepatic metabolism; however, studies have not
ical and biochemical abnormalities are almost entirely attributable to
found altered metabolism of carotene.9
starving or vomiting or to the use of emetics, laxatives, or diuretics.
D. Losses. Vomiting and the use of purgatives, laxatives, and diuretics
This chapter will discuss the nature of anorexia nervosa, with special
in some patients lead to losses of water and various electrolytes,
emphasis on nutritional consequences, nutritional assessment, and
including sodium, chloride, potassium, magnesium, hydrogen ion
approach to therapy.
(with vomiting), and bicarbonate (with diarrhea).
I. Nutritional Aspects of the Disorder E. Nutrient requirements
II. Nutritional Alterations Seen With the Disorder 1. Metabolic rates in malnourished phase of anorexia nervosa are
III. Focused Assessment lower than predicted by the Harris-Benedict equation,10,11 but no
IV. Objectives and Goals of Therapy single simple formula is available. A reasonable average resting
V. Management energy expenditure in a moderately malnourished patient is about
References 70% of the predicted value, but different studies have found a
wide range of values.12 This initial low resting rate is of limited
I. Nutritional Aspects of the Disorder importance, because refeeding quickly leads to increases in meta-
bolic rates to levels very similar to those predicted by the Harris-
A. Intake
Benedict equation.13
1. By definition, patients with anorexia nervosa have decreased food
2. Adipose tissue in the body contains about 8 kcal per gram of tis-
intake. There is a wide variation among these patients in quantity
sue; hence, restoration of body fat theoretically requires ingestion
and quality of food eaten as well as in the frequency of meals. Gen-
of about 3600 kcal per pound of fat (8000 kcal/kg) exclusive of the
eralizations from studies therefore must be tempered with knowl-
edge of the individual patient. thermic effect of food and energy required to produce the support-
2. Recent studies have shown that compared with controls, patients ing connective tissue. Lean body mass contains less stored energy
with restrictive anorexia nervosa eat proportionally fewer of their but needs relatively more energy to build. Studies have shown that
calories as fat.1 Proportionally more calories are eaten as carbohy- to increase the weight of patients with anorexia nervosa by 1 kg,
drate, with about the usual or a higher proportion of calories taken about 5000 to 7500 kcal above maintenance needs is required.13
as protein. Up to one half of patients with anorexia nervosa prac- Care must be taken in these patients to avoid rapid weight increases
tice vegetarianism.2,3 Furthermore, because total food intake is with large calorie loads because of the potential risk of “refeeding
decreased, there often are absolute decreases in micronutrient syndrome.”
intake.4 Many patients with anorexia nervosa supplement their diet 3. The term refeeding syndrome has been used to describe the meta-
with multivitamin preparations, and the tendency to relative bolic complications observed in malnourished patients when
increases in intake of vegetables usually allows vitamin require- nutrition support is initiated, including hypophosphatemia,14–19
ments to be met. Intake of trace elements, particularly zinc and hypokalemia,20 and hypomagnesia20,21 as well as cardiovascu-
copper, is more likely to be decreased.2 lar, pulmonary, and hepatic compromise.14
B. Absorption 4. Protein restitution in patients with anorexia nervosa is relatively
1. Nutrient absorption is expected to be normal in patients with easily accomplished when a complete diet is given, as would be
anorexia. However, in some patients, oral glucose results in no predicted with a protein-calorie malnourished state.22

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S E C T I O N V Metabolic Conditions

II. Nutritional Alterations Seen With the Disorder observed in female patients, including retarded bone maturation, low
estrogen status, and elevated levels of plasma cortisol.41,42 Although
A. Nutrition changes are listed in Table 32-1. For the most part, clini- there is no doubt that calcium intake is depressed in these patients,
cally detectable vitamin deficiencies are exceedingly rare, but abnor- calcium supplementation alone does not reverse the changes. There
malities in enzymatic function, indicating subclinical deficiency, have been rare reports of osteomalacia in anorexia nervosa.24,25
are not rare. The clinically notable changes that occur with anorexia
nervosa include protein-calorie malnutrition, which is universal,
increases in serum carotene concentrations, and possible zinc defi- III. Focused Assessment
ciency as well as osteoporosis. A. History
B. Zinc metabolism in patients with anorexia nervosa has been of con- 1. There are two aspects that need careful attention: psychiatric and
siderable interest because of the known effects of zinc deficiency in medical. This discussion focuses on the medical aspects, which
reducing or altering taste acuity and decreasing food intake. In some comprise malnutrition and its consequences as well as other behav-
studies, decreased quantities of zinc in plasma have been found, iors that influence the physical condition of the patient, particularly
although there is little correlation between plasma levels and total vomiting and the use of emetics, diuretics, and laxatives.
body zinc. Controlled trials of zinc supplementation have shown a) Weight. A detailed weight history should include current
inconsistent results, with one report showing improvement in the weight, premorbid weight (most useful in adults who had
rate of restoration of body mass index,40 whereas older reports acquired a stable height and weight), highest and lowest (adult)
found no difference in nutritional parameters. weights, and, in women, the weight at which amenorrhea or
C. Bone density consistently has been found to be depressed in patients oligomenorrhea occurred. The current weight is more properly
with anorexia nervosa; bone biopsies are consistent with osteo- part of the physical examination, because self-reported weights
porosis.41 There are several possible explanations for the changes are frequently inaccurate or unknown to the patient.
b) Weight control. The way the patient has lost weight is impor-
tant. This history, when accurately obtained, allows characteri-
TABLE 32-1. Nutritional Deficiencies in Anorexia Ner- zation of patients into “restricting” and “binge-eating/purging”
vosa classes. The diet history should be carefully obtained, with
attention to types and amounts of foods eaten, frequency of eat-
Prevalence ing, and duration of the dieting pattern. Involvement in organ-
Nutrient of deficiency ized groups of dieters as well as use of ancillary diet aids such
as liquid protein drinks and vitamin supplements should be
Macronutrients determined.
Muscle wasting Universal 2. Beliefs about food should be determined, including the patient’s
Adipose tissue depletion Universal feelings about food allergies and intolerances.
3. When bingeing has been a feature of the illness, the frequency and
Micronutrients duration of episodes as well as the food or foods usually consumed
Fat-soluble vitamins should be determined.
Vitamin A Levels tend to be high23 4. It is necessary to inquire about purging behaviors, including vom-
Vitamin D Rare; 2 case reports of iting and methods of inducing vomiting. Vomiting occurs in
approximately a third of patients, though it is less common in
osteomalacia24,25
restricting patients44 than in binge-eating/purging patients, up to
Vitamin E Biochemical23,26
80% of whom may vomit.45 Whether the patient uses emetics such
Vitamin K None (1 case in bulimia nervosa)27 as ipecac must be determined because these substances can lead
Water-soluble vitamins to cardiac myonecrosis and death.46,47 Laxative and diuretic use is
Thiamine Biochemical28 extremely common in patients with anorexia nervosa, especially
Riboflavin Biochemical29,30 those who also have bulimia. Often, in the case of laxatives, tens
Niacin Rare; 2 case reports of pellagra31–33 or even hundreds of tablets are taken. The laxatives used are most
frequently the stimulant type, such as phenolphthalein. These
Pyridoxine Biochemical29
substances may lead to profound fluid and electrolyte distur-
Folate Biochemical34
bances. It should be determined whether the patient has a history
Vitamin B12 Rare; 2 case reports35,36 of this behavior (ie, hospital admission for volume depletion or
Vitamin C Rare; 3 case reports of scurvy37–39 hypokalemia).
5. Exercise behavior, including type and duration, must be deter-
Trace elements
mined. Aerobics and running are frequently used as methods of
Zinc Serum levels usually normal but may weight loss.
be low; decreased urinary excretion is B. Physical examination
common; taste sensation is normal; 1. A detailed physical examination is clearly essential, because nutri-
supplementation may be helpful40 tion assessment is best done by looking at the patient. The impor-
tance of physical examination and careful, detailed history taking
Other nutrients as opposed to other measures is highlighted by the term “subjec-
Calcium Intake is decreased; serum levels are tive global assessment.”48 For example, patients with anorexia ner-
normal; osteoporosis is common41–43 vosa usually have normal concentrations of serum albumin; hence,
traditional objective measures may be misleading.

350 A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. © 2005 A.S.P.E.N. www.nutritioncare.org.
 S E C T I O N V Metabolic Conditions

a) Body measurements. All patients should have their height and The psychiatric portion of therapy is not addressed here but obvi-
weight checked, and body build should be estimated. Body ously is critical as well.
mass index and percentage of ideal body weight should be cal- B. Short-term intervention for fluid and electrolyte abnormalities, other
culated. Anthropometric measures such as skinfold thicknesses complications, profound malnutrition, or rapid weight loss necessi-
and midarm muscle circumference are sometimes used. tates hospital admission. There are no well-defined guidelines for
b) Physical findings. General examination includes attention to degree of weight loss requiring rapid intervention, but previous stud-
muscle mass and subcutaneous tissue stores as well as the pres- ies on starvation have suggested that a decrease of 30% in a previous
ence of edema, which is not common in patients with anorexia healthy weight should lead to consideration for hospitalization62,63; a
nervosa before refeeding. Thinning of scalp hair and the pres- decrease of 40% constitutes strong grounds for hospitalization. Many
ence of lanugo hair may be evident, and occasionally the yel- workers in the field are concerned that even a 25% reduction in body
low appearance of carotenemia may be noticed (with normal weight from a previous healthy weight may lead to cognitive impair-
sclerae).49 The skin is often dry, nails are brittle, and there may ment, with serious difficulties in intervention on an outpatient basis.
be acrocyanosis and cold extremities.49 Pulse rate and blood However, there appear to be no data to allow a firm recommendation.
pressure are often quite low.50 C. There is no other area of nutritional intervention in which a multi-
2. When vomiting is a feature of the illness, there may be parotid disciplinary approach to the patient is more important. Psychiatrists,
enlargement, thickening of the dorsal aspects of the fingers of the internists, pediatricians, nutritionists, pharmacists, and nurses are all
hand used to induce vomiting (Russell’s sign), and erosion of the critical parts of the treatment team because of the multifaceted prob-
enamel of the lingual aspects of the upper teeth. Petechiae are seen lems faced by the anorexia nervosa patient.
less often but may involve the sclerae, face, and palate. D. Two decisions must be made about the weight restoration program.
3. Medical complications, including volume depletion, may occur in 1. The actual target must be agreed upon, including which parameter
those who are vomiting or abusing laxatives or diuretics. Elec- will be taken as the measure. Often, this is body weight or body
trolyte disturbances may lead to weakness and dysrhythmias,51 but mass index, but some have suggested anthropometric measures
physical findings are usually absent. such as body fat.64 All these measures have confounding problems,
C. Laboratory tests including weight gain via edema and high inter- and intraobserver
1. Hematologic changes are common and include anemia, neutro- errors with measurements of skinfold thickness.
penia, and occasionally thrombocytopenia.52 Anemia, observed in 2. The actual goal weight or other value must be decided. In the case
up to 30% of patients, is usually normochromic and normocytic of target weight, the decision must take into account premorbid
and is only rarely due to iron deficiency.53 Neutropenia secondary weight, if a reliable number is determinable, as well as published
to bone marrow hypoplasia occurs in up to 50% of patients and “ideal weight,” which is a poor term to use in this field of medi-
appears to be attributable to the generalized malnutrition rather cine. The amount of recent weight loss has a bearing on target
than to a specific nutrient abnormality.52,54 In particular, folic acid weight. The target weight should include an acceptable weight for
and vitamin B12 levels are almost always normal. discharge from the hospital for inpatients as well as a long-term
2. Electrolyte disturbances include hyponatremia, hypochloremia, goal weight.
hypokalemia (severe [ie, <2.6] in about 5% of patients), and meta- E. Much of the approach taken by centers that focus on treatment of
bolic alkalosis.55 These changes almost inevitably result from patients with anorexia nervosa is based on local preferences and
vomiting or from laxative and diuretic use. Occasionally, water biases as well as past experience. There is a paucity of studies evalu-
intoxication may be the cause of hyponatremia.56,57 Urea concen- ating the different modes and nuances of therapy on outcome; there-
trations may be elevated in about one quarter of patients. fore, programmatic development has been largely anecdotal, often
3. Electrocardiographic abnormalities occur in most patients, perhaps borrowed from larger centers that have described their approaches in
60% to 70%.58,59 The changes include sinus bradycardia, low- a number of publications. There have also been changes in the rec-
amplitude QRS complexes, and nonspecific changes in ST and T ommendations for hospital admission.
waves. Hypokalemia may result in the presence of U waves. Pro- 1. In the classic treatise of Toronto-based Garfinkel and Garner65 pub-
longation of the QT interval (ie, QT interval greater than 0.44 sec- lished in 1982, there was an attitude that favored hospital admis-
onds) is a very worrisome finding and may be associated with sion. They believed that it was usually warranted to admit the
sudden death.60 anorexic patient to hospital. The Toronto Programme for Eating
Disorders has seen a steady decline in the percentage of patients
admitted as inpatients, however.
IV. Objectives and Goals of Therapy. The short-term and 2. In support of the outpatient approach is a study that showed no
long-term goals of therapy may be at odds with each other at times.
difference in outcome between inpatient and outpatient treatments
A. The short-term goals are readily apparent: treatment of complica- after 1 year, although there were methodological problems with
tions of the condition, some of which may be life-threatening, and randomization.66 Counter to this trend is the financial incentive for
restoration of nutritional status to the premorbid state. private facilities to favor hospital admission.
B. One of the long-term goals is to restore a normal body image so that F. Special aspects of diet and nutritional supplements
normal nutritional status can be maintained. 1. Outpatient treatment
a) Weight restoration in patients not requiring hospitalization is
generally believed to be optimally achieved by consumption of
V. Management a normal diet, with avoidance of “artificial” means of nutrition
A. Patients with anorexia nervosa have essentially a normal gastro- support such as liquid supplements or tube feeding. Because
intestinal tract, with perhaps the exception of some dysmotility with these patients tend to be initially better nourished than their
profound malnutrition.61 Hence, complete reversal of metabolic and inpatient counterparts, a slower rate of weight gain is generally
nutritional abnormalities can be anticipated with successful therapy. accepted.

© 2005 A.S.P.E.N. www.nutritioncare.org. A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. 351
S E C T I O N V Metabolic Conditions

b) There are two types of outpatients: those followed by a psychi-

atrist and his or her team in a private setting, and those admit- TABLE 32-2. Monitoring of Inpatients
ted to day-treatment programs.
c) In the total outpatient setting, as in the day care and inpatient Initial Follow-up
settings, a dietitian or nutritionist is frequently the person who
Hemoglobin, white blood cell, Weekly unless abnormal
prescribes the dietary education and counseling and recom-
mends caloric goals and other nutrient intake. In some centers, and platelet counts
an internist or pediatrician is actively involved in this aspect. Sodium, potassium, Daily for 3 days, then every 3 days
d) Discussion about the types and quantities of foods eaten is an chloride, HCO3 until stable
important part of dietary counseling. Patients should be per-
mitted to avoid only a limited number of foods; an important Calcium, magnesium, Daily for 3 days, then every 3 days
goal is to widen food choices. There can be no hard guidelines phosphorus
for caloric intake, but frequent follow-up (weekly, biweekly, or Creatinine Daily for 3 days, then every 3 days
monthly) is essential to determine whether goal intakes and
weights or other nutrition assessment goals are being met. It is Glucose Daily for 3 days, then every 3 days
necessary to intervene early if there are shortfalls. Because Prothrombin time or INR None if normal
these patients are usually consuming very little when initially
B12, folate levels None
assessed and because of the dangers of rapid weight gain and
edema, the initial recommended caloric intake generally should Electrocardiogram If abnormal (other than
be quite low—1000 to 1500 kcal/d. Weekly increments of about bradycardia)
250 to 500 kcal/d12 up to a level that results in a weekly weight
Bone density if depressed Annually
gain of 1 kg (2 lb) are recommended. The absolute number of
calories needed to accomplish this varies widely, depending on
basal needs and levels of exercise. INR, international normalized ratio
e) The downside to a total outpatient approach is that eating pat-
terns cannot be observed, and other activities such as bingeing
and purging cannot be monitored.
f) Day-treatment programs use approaches similar to the total d) There are no simple measures to determine subclinical defi-
outpatient approach but allow for closer monitoring of food ciencies of many vitamins. Multivitamin supplementation is
intake, provision and observation of one or two meals, and pro- prescribed as vitamins will be needed once anabolism is stim-
vision of a wider variety of food types. Group counseling is ulated. Trace element requirements during refeeding in most
usually a part of this process. The efficacy of each component cases should be no different from those recommended for the
of these programs has not been determined. general population, with the exception of zinc, which some
2. Inpatient treatment authors recommend should be supplemented at perhaps 15 mg
a) Inpatient medical and nutritional treatment often has different of elemental zinc per day.40
phases. Initially, stabilization of an ill patient involves bed e) Oral intake of a balanced diet is recommended, with some
rest, fluid and electrolyte (especially potassium and phospho- patients using liquid polymeric supplements. The use of these
rus and occasionally magnesium) repletion, and administra- supplements is controversial. In the severely malnourished
tion of micronutrients before formal nutritional repletion. patient, cognitive function may be impaired, or patient’s energy
b) Blood tests are done immediately on admission, as indicated level or desire to cooperate may be impaired, and enteral nutri-
in Table 32-2; an electrocardiogram should be done if there are tion may be recommended, starting at the same levels as one
electrolyte disturbances or signs or symptoms of possible car- would use for oral refeeding.
diac origin. Laboratory values that should be monitored over G. Special aspects of enteral nutrition
the first week include phosphorous, potassium, magnesium, 1. Enteral feeding remains a controversial topic in anorexia ner-
glucose, and urinary electrolytes. Phosphorus requirements vosa, with respect to both indications and the ethics of placing a
during repletion are greater than those provided in a standard tube in an uncooperative or unwilling patient.
diet or with enteral feeding. The need for extra phosphorus is 2. In very malnourished patients, tube feeding appears to be essential
determined by monitoring levels in serum. for restoring body mass because these patients may be incapable
c) Refeeding either is undertaken immediately or, occasionally, is of restoring body mass on their own. The unusual complication of
delayed for 24 hours, at which point monitoring becomes very gastric retention may occur; monitoring patient complaints and
important. Refeeding can lead to alterations in serum phospho- abdominal size and taking an abdominal film in selected patients
rus and potassium concentrations, peripheral edema, dysrhyth- should help avoid the very rare complication of gastric rupture.
mias, congestive heart failure, and gastric retention, the latter The other difference in this population is that the patient may waste
especially if tube feeding is instituted. To avoid refeeding syn- the formula by running the tube into the toilet, the sink, or a con-
drome, electrolyte abnormalities should be looked for and tainer. Whenever the weight response to the feeding appears to be
corrected before nutrition support is initiated, whether by the inappropriate, the possibility of wastage should be considered.
oral, enteral, or parenteral route. Circulatory volume should be H. Special aspects of parenteral nutrition
restored slowly; pulse rate and fluid intake and output should 1. Only very few patients require parenteral nutrition. Indications in
be monitored. Refeeding is begun slowly by providing ∼20 to this setting include severe gastric retention or some unrelated but
25 kcal per kg of body weight or ∼1000 to 1500 kcal/d to start, important gastrointestinal problems, such as bowel obstruction
and calorie increases should be modest during the first week.12 from adhesions or Crohn’s disease. In cases of gastric retention

352 A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. © 2005 A.S.P.E.N. www.nutritioncare.org.
 S E C T I O N V Metabolic Conditions

where vomiting is not an issue, a postpyloric nasoenteric tube 6. Bayle FJ, Bouvard MP. Anorexia nervosa and Crohn’s disease dual diag-
should be considered before parenteral nutrition is instituted. nosis: a case study. Eur Psychiatry. 2003;18(8):421–422.
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troenterol. 1993;88(2):293–296.
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8. Mallett P, Murch S. Anorexia nervosa complicating inflammatory bowel
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disease. Arch Dis Child. 1990;65(3):298–300.
patients tampering with the intravenous tubing, with the poten- 9. Rock CL, Swendseid ME. Plasma carotenoid levels in anorexia nervosa
tially lethal complications of infection or air embolus. and in obese patients. Methods Enzymol. 1993;214:116–123.
2. Furthermore, with parenteral nutrition there is a tendency to push 10. Schebendach J, Golden NH, Jacobson MS, et al. Indirect calorimetry in the
calories perhaps more than with tube feeding, with potentially dis- nutritional management of eating disorders. Int J Eat Disord. 1995;17(1):
astrous complications of cardiac or pulmonary decompensation or 59–66.
hypophosphatemia14 (although phosphorus levels in current regi- 11. de Zwaan M, Aslam Z, Mitchell JE. Research on energy expenditure in indi-
mens usually are adequate to prevent the latter). viduals with eating disorders: a review. Int J Eat Disord. 2002;32(2):
I. Focused monitoring and goals assessment 127–134.
12. Rock CL, Curran-Celentano J. Nutritional disorder of anorexia nervosa: a
1. Although nutritional replenishment is one of the main goals of
review. Int J Eat Disord. 1994;15(2):187–203.
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17. Cariem AK, Lemmer ER, Adams MG, Winter TA, O’Keefe SJ. Severe
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drome and anorexia nervosa. Int J Eat Disord. 1994;16(1):101–103. study. Q J Med. 1993;86(12):791–799.
36. Patchell RA, Fellows HA, Humphries LL. Neurologic complications of 53. Kennedy A, Kohn M, Lammi A, Clarke S. Iron status and haematological
anorexia nervosa. Acta Neurol Scand. 1994;89(2):111–116. changes in adolescent female inpatients with anorexia nervosa. J Paediatr
37. George GC, Zabow T, Beumont PJ. Letter: scurvy in anorexia nervosa. S Child Health. 2004;40(8):430–432.
Afr Med J. 1975;49(35):1420. 54. Abella E, Feliu E, Granada I, et al. Bone marrow changes in anorexia ner-
38. Woodruff PW, Morton J, Russell GF. Neuromyopathic complications in a vosa are correlated with the amount of weight loss and not with other clin-
patient with anorexia nervosa and vitamin C deficiency. Int J Eat Disord. ical findings. Am J Clin Pathol. 2002;118(4):582–588.
1994;16(2):205–209. 55. Schutte M, Mehler P. Metabolic abnormalities in eating disorders. In: Mehler
39. Christopher K, Tammaro D, Wing EJ. Early scurvy complicating anorexia P, Anderson A, eds. Eating Disorders: A Guide to Medical Care and Com-
nervosa. South Med J. 2002;95(9):1065–1066. plications. Baltimore, MD: Johns Hopkins University Press; 2000:76–85.
40. Birmingham CL, Goldner EM, Bakan R. Controlled trial of zinc supple- 56. Santonastaso P, Sala A, Favaro A. Water intoxication in anorexia nervosa:
mentation in anorexia nervosa. Int J Eat Disord. 1994;15(3):251–255. a case report. Int J Eat Disord. 1998;24(4):439–442.
41. Mehler PS. Osteoporosis in anorexia nervosa: prevention and treatment. Int 57. Cuesta MJ, Juan JA, Peralta V. Secondary seizures from water intoxication
J Eat Disord. 2003;33(2):113–126. in anorexia nervosa. Gen Hosp Psychiatry. 1992;14(3):212–213.
42. Rigotti NA, Nussbaum SR, Herzog DB, Neer RM. Osteoporosis in women 58. Panagiotopoulos C, McCrindle BW, Hick K, Katzman DK. Electrocardio-
with anorexia nervosa. New Engl J Med. 1984;311(25):1601–1606. graphic findings in adolescents with eating disorders. Pediatrics.
43. Golden NH. Osteopenia and osteoporosis in anorexia nervosa. Adolesc 2000;105(5):1100–1105.
Med. 2003;14(1):97–108. 59. Vanderdonckt O, Lambert M, Montero MC, Boland B, Brohet C. The 12-
44. Keel PK, Fichter M, Quadflieg N, et al. Application of a latent class analy- lead electrocardiogram in anorexia nervosa: a report of 2 cases followed by
sis to empirically define eating disorder phenotypes. Arch Gen Psychiatry. a retrospective study. J Electrocardiol. 2001;34(3):233–242.
2004;61(2):192–200. 60. Moss A, Schwartz P. Sudden death and the idiopathic long Q-T syndrome.
45. Mazzeo SE, Espelage DL, Sherman R, Thompson R. Trends in eating disor- Am J Med. 1979;66(1):6–7.
der symptomatology in an outpatient clinic: 1988–1998. Eat Behav. 2003; 61. Kamal N, Chami T, Andersen A, Rosell FA, Schuster MM, Whitehead WE.
4(2):211–220. Delayed gastrointestinal transit times in anorexia nervosa and bulimia ner-
46. Ho PC, Dweik R, Cohen MC. Rapidly reversible cardiomyopathy associ- vosa. Gastroenterology. 1991;101(5):1320–1324.
ated with chronic ipecac ingestion. Clin Cardiol. 1998;21(10):780–783. 62. Cahill GF Jr. Starvation in man. N Engl J Med. 1970;282(12):668–675.
47. Friedman AG, Seime RJ, Roberts T, Fremouw WJ. Ipecac abuse: a serious 63. Cahill GF Jr. Survival in starvation. Am J Clin Nutr. 1998;68(1):1–2.
complication in bulimia. Gen Hosp Psychiatry. 1987;9(3):225–228. 64. Goldner E, Birmingham C. Anorexia nervosa: methods of treatment. In:
48. Detsky AS, McLaughlin JR, Baker JP, et al. What is subjective global Alexander L, Lumsden B, eds. Understanding Eating Disorders. Washing-
assessment of nutritional status? J Parenter Enteral Nutr. 1987;11(1):8–13. ton, DC: Taylor & Francis International; 1994:135–158.
49. Strumia R, Varotti E, Manzato E, Gualandi M. Skin signs in anorexia ner- 65. Garfinkel P, Garner D. Anorexia Nervosa: A Multidimensional Perspective.
vosa. Dermatology. 2001;203(4):314–317. New York, NY: Brunner/Mazel; 1982.
50. Mont L, Castro J, Herreros B, et al. Reversibility of cardiac abnormalities 66. Crisp AH, Norton K, Gowers S, et al. A controlled study of the effect of
in adolescents with anorexia nervosa after weight recovery. J Am Acad therapies aimed at adolescent and family psychopathology in anorexia ner-
Child Adolesc Psychiatry. 2003;42(7):808–813. vosa. Br J Psychiatry. 1991;159:325–333.

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 SECTION EDITOR
Charles Mueller, PhD, RD, CNSD
VI
Site Related and
Ethical Issues

33 Acute Care Organizations

34 Long Term Care

35 Considerations for Home Nutrition Care

36 Ethics
 Denise Baird Schwartz, MS, RD, FADA, CNSD;
Caroline M. Apovian, MD, FACN
33
Acute Care Organizations

Introduction 1. Registered Dietetic Technician—Provides patient nutrition

screening and basic level assessments of patients at low risk for
Nutrition support in acute care organizations requires an understanding nutrition deficits2,3
of the processes, personnel, tools, communication systems, and regula- 2. Registered Dietitian—Provides nutrition assessment, develops
tory agencies that form the nutrition support care structure. Identifying medical nutrition therapy (MNT) care plan, and monitors goal
patients at risk and providing specialized nutrition therapy in a safe and achievement3,4
effective manner is the goal of nutrition and nutrition support depart- 3. Physician—Provides leadership, coordinating medical practice
ments and committees. The concept of the nutrition support team, an with nutrition support in conjunction with other team members5
interdisciplinary collaboration among nurses, pharmacists, physicians, 4. Registered Nurse—Intravenous site maintenance, parenteral and
and dietitians, is explained and reimbursement issues are outlined. enteral nutrient delivery, and nasogastric and small bowel feed-
ing tube placement6
I. Integrating Nutrition Support in Acute Care Organizations 5. Registered Pharmacist—Focuses on parenteral nutrition com-
II. Nutrition Support Organizational Structure pounding, preventing electrolyte derangements and drug-nutrient
III. Controlling Costs of Nutrition Support interaction7
IV. Reimbursement Issues 6. Registered Nurse Epidemiologist—Documents infection rate
References related to central line access and ventilator-associated pneumonia
rate
7. Respiratory Therapist—Participates in ventilator weaning and
I. Integrating Nutrition Support in Acute Care assaying metabolic rates to optimize nutrient delivery3
Organizations 8. Physical Therapist—Provides appropriate exercises as clinical
A. Process (first row in Table 33-1) status warrants to increase muscle mass in conjunction with nutri-
1. Identification of nutrition status tion support intervention3
a) Screening process to identify level of care, and high risk versus 9. Speech Pathologist—Assesses ability to resume safe swallow
low risk patients when transitioning from nutrition support and in recommenda-
b) Designates timing of initial nutrition assessment by dietitian/ tions for nutrient delivery options when dysphagia present
dietetic technician and follow-up frequency 10. Social Worker—Provides psychological support and addresses
c) Determination of a patient’s current nutrition status via diet social issues and financial concerns related to nutrition support3
therapy, anthropometric data, biochemical data, and clinical 11. Case Manager—Participates in evaluating situations where the
signs when available appropriate cost effectiveness of interventions for specialized
nutrition support might be enhanced and optimum patient place-
d) Determination of a patient’s nutrient requirements
ment based on medical needs
e) Goals to identify/apply early nutrition therapies for patients at
12. Ethics Committee Member—Assists in development of ethical
risk for malnutrition
guidelines when feeding may or may not be in patient’s best
2. Nutrition therapy implementation
interest
a) Appropriate patient selection, including nutrition support team
13. Patient Involvement in Healthcare—Patient/caregivers involved
consultation/evaluation for specialized nutrition support whenever appropriate and possible in discussions and decisions
b) Correct composition and route of nutrition delivery about their treatment; essential when long-term nutrition inter-
3. Nutrition therapy monitoring vention is likely
a) Monitoring done by nutrition support team or appropriate indi- C. Tools/equipment (third row in Table 33-1)
viduals as set forth in the institution’s policies and procedures 1. Computerized data management system
b) Management of treatment, and type and amount of nutrients 2. Patient’s chart
infused 3. Enteral and parenteral nutrition protocols
c) Achievement of documented goals 4. Enteral and parenteral equipment/pumps
d) Provide a pharmaceutical approach with achievement of tar- 5. Enteral formulas and parenteral solutions
geted nutrient goals1 6. Patient education forms and materials
e) Eliminate difference between prescribed versus actually 7. Parenteral nutrition compounding equipment
administered amounts of formula/solutions1 8. Metabolic cart
f) Goal-centered for improved patient outcome D. Information communication (fourth row in Table 33-1)
B. Health care team members (second row in Table 33-1) 1. Computer information system

© 2005 A.S.P.E.N. www.nutritioncare.org. A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. 357
S E C T I O N V I Site Related and Ethical Issues

TABLE 33-1. Nutrition Support—Who Owns the Process?

Identification nutrition status Nutrition therapy implementation Nutrition therapy monitoring

Nutrition Nutrition Enteral Parenteral Enteral and
Process screening assessment nutrition (EN) nutrition (PN) parenteral nutrition

Health Care DTR, RD RD MD order MD order MD orders changes to

Team Members MD referrals alimentation
RD determines nutrient RD determines RD recommendations to meet
adequacy nutrient adequacy nutrient needs to achieve
documented goals to improve
outcomes based on changing
parameters
RN triggers RN administers EN RN administers PN RN determines GI tolerance
to EN and PN IV site
management
PharmD compounds PN PharmD monitors PN com-
pounding and electrolytes
Epidemiologist monitors central
line infection rates
Respiratory Therapist performs
metabolic rates
Speech Pathologist monitors
transition to oral diet
Case Manager coordinates
transfer to home on nutrition
therapy

Tools/ Laboratory Feeding Tubes Protocol Parenteral Nutrition

Equipment Equipment—pumpsa Protocol
Enteral feeding bagsb Parenteral Nutrition
Enteral formulasc Orders
Education Form— Equipment—pumpsa
Enteral Nutrition Feeding bagsb
Parenteral bags, IV
tubingb
Education Form—
Parenteral Nutrition

Information Progress/notes/interdisciplinary Progress notes/ Progress notes/ Progress notes interdisciplinary

Communication documentation interdisciplinary interdisciplinary documentation
documentation documentation Weekly multidisciplinary rounds
edical Committeesd

Regulations/ JCAHO JCAHO JCAHO JCAHO

Recommendations State law A.S.P.E.N. A.S.P.E.N. A.S.P.E.N.
A.S.P.E.N. HACCP CDC

Assess/Improving Quarterly Level of Monthly RD peer Annual Parenteral Annual Parenteral Nutrition Uti-
Performance care evaluation reviews Nutrition Utilization lization Study
Monthly peer Study Nutrition Management of Ven-
reviews Monthly RD peer tialtor Dependent Patients
reviews IOP
Monthly RD peer reviews

a. Biomedical Engineering
b. Central Supply
c. Nutrition Services
d. Nutrition and Metabolic Committee, ICU Committee, Pharmacy and Therapeutic Committee
September 2003 Denise Schwartz, MS, RD, FADA, CNSD
Nutrition Support Coordinator, Providence Health System, San Fernando Valley Service Area, Burbank, CA

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 S E C T I O N V I Site Related and Ethical Issues

2. Progress notes/interdisciplinary charting (5) Monitoring and re-evaluating nutrition care plan includes
3. Multidisciplinary rounds defining parameters and frequency of monitoring, proce-
4. Medical committees dures and re-evaluation of nutrition care plan
5. Hospital-wide continuing medical education programs (6) Transition of therapy involves assuring adequacy of intake,
6. Department education programs continuity of care, and termination of nutrition therapy
E. Regulations/recommendations (fifth row in Table 33-1) b) Standards for Hospitalized Pediatric Patients10
1. Intent of regulations and recommendations—To provide clear (1) Criteria established for identification of pediatric patients
guidelines on what is supposed to be optimum nutrition support who are nutritionally-at-risk
2. Joint Commission on Accreditation of Healthcare Organizations (2) Use of subjective and/or objective criteria specific to pedi-
(JCAHO)8 atrics; appropriate growth charts shall be used
a) The hospital defines in writing the data and information (3) Nutrition assessment and reassessment shall be performed
gathered during assessment and reassessment. by or under supervision of a registered dietitian with pedi-
b) The hospital defines in writing the time frame(s) for conduct- atric experience or by a pediatric nutrition care specialist
ing the initial assessment(s). within a time frame specified by institutional policy
c) Patients are reassessed as needed. (4) Development of nutrition care plan using interdisciplinary
d) Development of a plan for care, treatment, and services is approach, with documentation of goals of nutrition therapy,
individualized and appropriate to the patient’s needs, strengths, discharge planning, route selection of nutrition therapy, and
limitations, and goals. patient/care giver education
e) Care, treatment, and services are provided in an interdiscipli- (5) Implementation of nutrition care should commence follow-
nary, collaborative manner. ing assessment and development of a nutrition care plan
f ) The hospital has a process for preparing and/or distributing with a defined ordering process minimizing risks to the
food and nutrition products as appropriate to the care, treat- patient
ment, and services provided. (6) Patient monitored for therapeutic and adverse effects and
g) The patient receives education and training specific to the clinical changes that may influence nutrition therapy using
protocols specific to pediatric patients involving physical
patient’s needs and as appropriate to the care, treatment, and
assessment, biochemical indices, and nutrition therapy
services provided.
tolerance
h) The hospital collects data to monitor its performance.
(7) Transitional and discontinuation of nutrition therapy shall
i) Data are systematically aggregated and analyzed.
be addressed
j) Undesirable patterns or trends in performance are analyzed.
5. Centers for Disease Control (CDC) guidelines pertaining to
k) Processes for identifying and managing sentinel events are
nutrition support11
defined and implemented.
a) Guidelines for the prevention of intravascular catheter-related
l) Information from data analysis is used to make changes that
infections
improve performance and patient safety and reduce the risk
b) Designates hang time for parenteral solutions
of sentinel events.
c) Indicates timeliness for replacement of administration sets
m) An ongoing, proactive program for identifying and reduc-
F. Assess/improving performance (sixth row in Table 33-1)
ing adverse events and safety risks to patients is defined and 1. Goal
implemented. a) Better define the patient populations requiring specialized
n) Competence to perform job responsibilities is assessed, demon- nutrition support
strated, and maintained. b) Focus on areas where improvement is required
3. State regulations9 c) Monitor and evaluate quality of care provided
a) Provides for licensing and certification of health facilities d) Pursue opportunities to improve patient care
b) Competency validation for patient care personnel e) Identify and correct problems to save costs
c) Designates nutrition care integration in patient care plan, doc- f ) Implement cost containment for product selection, standardi-
umentation in medical record, and transfer of information at zation, and management efforts
discharge to ensure continuity of nutrition care 2. Peer review—to enhance performance of each clinician based on
4. American Society for Parenteral and Enteral Nutrition (A.S.P.E.N.) identified standards agreed on by the group of clinicians
a) Standards for Specialized Nutrition Support: Adult Hospital- 3. Parenteral and enteral utilization analysis—to determine if appro-
ized Patients6 priate patient selection for nutrition therapy occurs and impact on
(1) Organization defines interdisciplinary nutrition support patient outcomes
process, requires policies and procedures and performance 4. Sterility testing of parenteral nutrition solutions—to maintain safe
improvement component compounding practice for parenteral solutions
(2) Nutrition care process includes nutrition screening and 5. Medication safety variance reports
nutrition assessment a) Identify frequency of occurrence of problems with enteral and
(3) Development of nutrition care plan includes defined objec- parenteral nutrition therapy and drug-nutrient interaction
tives, interdisciplinary approach, goals and expectations, b) Develop a mechanism to prevent problem reoccurrence
selection of nutrition therapy route, and formula selection 6. Sentinel event
(4) Implementation includes ordering process, nutrition sup- a) Unexpected occurrence involving death or serious physical or
port access, formulation preparation, additives, packaging psychological injury, or risk thereof
and labeling, administration of specialized nutrition support b) Conducts a timely, thorough, and credible root cause analysis;
formulations, and sentinel event management developing an action plan designed to implement improvements

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S E C T I O N V I Site Related and Ethical Issues

to reduce risk; implementing the improvements; and monitor- (8) Focuses on the anticipated medical and surgical plan and
ing the effectiveness of those improvements how nutrition support measures are beneficial
7. Improving organization performance applied to specific nutrition (9) May place central venous catheter
support processes12–14 (10) Participates in the administrative responsibilities to make
a) Important for identifying processes that need to be changed to certain the team has the appropriate multidisciplinary
improve the outcome15 focus, that policies and procedures are in place, and that
b) Provides an awareness of need and how to improve practice education programs are implemented
and assess performance15 (11) Participates in education of medical staff and students in
c) Used as a means of identifying success matters related to nutrition assessment, care plan, and
treatment of patients
II. Nutrition Support Organizational Structure (12) Ensures appropriate medical documentation related to
malnutrition, and enteral and parenteral nutrition
A. Nutrition support team b) Dietitian
1. Functions and goals (1) Acts as patient’s primary advocate for all aspects of nutri-
a) Defined as a group of healthcare professionals who in their tion care21
daily activities manage patients who require either enteral or (2) Acts as a liaison with other in-patient dietitians in mat-
parenteral nutrition13 ters related to specialized nutrition support
b) Provides optimum nutrition support practice to improve patient (3) Provides initial and periodic assessments of nutrient intake
outcomes, defined as decreased intensive care unit (ICU) and nutrition status, including the diagnostic recommen-
days, decreased hospital days, and decreased morbidity and dation for various classifications of malnutrition3,4,22,23
mortality3,16,17 (4) Anticipates the effect of procedures, treatments, therapies
c) Promotes cohesive patient management with a collaborative and psychosocial issues on the patient’s nutrition status21
approach to patient care18 (5) Advises colleagues of altered or potential nutrition
d) Achieves recognition and integration as a primary clinical deficiencies22
service
(6) Documents nutrition care plans for the application of med-
e) Acts as a consultation service
ical nutrition therapy for high nutrition risk or nutrition-
f ) Provides continuity of care for patients being discharged
ally compromised patients4
home on nutrition support
(7) Translates clinical nutrition concepts into simple language
g) Decreases both the variance in practice and cost of nutrition
for the patient with acceptable strategies for implementing
support18,19
nutritional change22
2. Key characteristics of a successful nutrition support team3,20
(8) Maintains current knowledge of developments in product
a) Motivated, committed, and persistent team members
specifications, technology, and clinical practice22
b) Attention to team welfare and high quality working relationships
(9) Participates in the design, implementation, and monitor-
c) Good communication both internally among team members
ing of nutrition therapies, including oral, enteral and par-
and with other professional patient care providers
enteral, and transition at discharge3,4,22,23
d) Shared team vision
e) Robust clinical audit program (10) Writes orders for enteral and parenteral nutrition as delin-
f ) Integrates the expertise of each individual team member eated by clinical privileges of the institution3
g) Awareness of each member’s particular knowledge, skills, and (11) May place enteral feeding tubes preceded by specialized
attitudes towards nutrition support practice training, demonstrated competency, and delineated insti-
h) Strategizes for sharing success tution clinical privileges3
i) Members keep abreast of the literature and current practice, (12) Oversees enteral nutrition compounding based on safety/
attend professional meetings, and network quality standards
3. Role of nutrition support team members (13) Provides appropriate nutrition education for healthcare
a) Physician professionals, students, and patients and their families
(1) Leadership role on the collaborative nutrition support and caregivers3,4,22
team5 (14) Participates in patient-focused quality assurance process
(2) Reviews the completed nutrition assessment and approves with well-controlled projects, highlights good practice,
the therapeutic plan as the decision-making leader and identifies where sub-optimal practice needs change
(3) Responsible for medical direction of team overseeing to improve clinical effectiveness Collaborates with team
patient care activities3 physician(s) in proper medical record documentation
(4) Familiar with all aspects of nutrition care from screening, related to both treatment and diagnosis allowing for
assessment, care plan development, implementation, mon- appropriate coding and reimbursement21
itoring, and reassessment, to therapy termination5 (15) Participates in ethical deliberations for withdrawing nutri-
(5) Effective collaborator, leading, working with, and accept- tion support and selecting palliative alternatives4,21,24
ing direction from team members representing other dis- (16) Participates in research studies and quality assurance
ciplines5 process4,21
(6) Evaluates the pathophysiology and expected clinical c) Nurse
course (1) Primary liaison with unit nursing staff, may provide direct
(7) Ensures that the nutrition support goals, route of deliv- patient care, consultation with nurses and other healthcare
ery, and formula selected are clinically appropriate5 professionals25,26

360 A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. © 2005 A.S.P.E.N. www.nutritioncare.org.
 S E C T I O N V I Site Related and Ethical Issues

(2) Educates patients and caregivers, students, colleagues, and (1) Pharmacist certified through the Board of Pharmaceutical
the public25,26 Specialties (BPS), designated as a Board Certified Nutri-
(3) Assesses ability of patient/caregiver to safely perform tasks tion Support Pharmacist (BCNSP)
related to nutrition therapy (2) Certification through BPS is a credential granted to phar-
(4) Principle resource on implementation of administration of macists who have demonstrated a level of competence in
feeding formulations and management of access devices, nutrition support that exceeds minimum requirements for
and vascular access expert3,25 licensure
(5) May place peripherally inserted central catheter lines (3) Certification is granted on the basis of successful completion
(PICC) preceded by specialized training, demonstrated of eligibility criteria and includes passing a written exami-
competency, and delineated institution clinical privileges27 nation, and in some cases, an experimental component
(6) Facilitates discharge planning, and educates patient and B. Nutrition support committee
family in techniques of home nutrition support prior to 1. Functions and goals
discharge3 a) Defined as a formalized committee of individuals to address
(7) Participates in research activities and administrative institutional issues for patients receiving enteral or parenteral
functions25,26 nutrition
(8) Conducts educational and quality assurance programs on b) To provide, facilitate, and disseminate information on opti-
administration of parenteral and enteral formulas and cen- mum nutrition support practice to improve patient outcomes
tral venous access or feeding tube care3 c) Standardizes ordering, preparation, and administration of
d) Pharmacist nutrition support so that infection rate, glucose tolerance,
(1) Oversees compounding of parenteral nutrition based on fluid and electrolyte imbalances, and acid-base disturbances
safety/quality standards28,29 are reduced30
(2) Uses acceptable standard ranges for parenteral nutrition d) Develops nutrition regimens and education and monitoring
solutions to prevent potential problems with compatibility protocols
and stability3,28,29 e) Ensures early recognition/documentation of malnutrition and
(3) Ensures that the nutrition care plan includes the route and high quality performance in nutrition therapy
composition of formulation, pharmacological adjuncts to f) Reinforces the importance of medical nutrition therapy in the
nutrition support, and nutrient delivery system7,29 overall treatment and achievement of positive outcomes for
(4) Uses expertise to evaluate nutrient-nutrient, drug-nutrient, patients
and drug-disease interactions; drug doses; and drug- g) Supports high quality, cost-effective patient care by overseeing
induced feeding intolerance3,30 product/device selection, standardization, and management as
(5) Helps teach home nutrition support techniques to patients this relates to enteral/parenteral and metabolic monitoring
and their families prior to discharge3,7 h) Develops policies and procedures for safe practice and effec-
(6) Participates in surveillance and management of therapy- tive risk management, and enhances quality of care as well
associated complications, and delivery of cost-effective as legal protection
care7 i) Develops clear guidelines for the instigation and selection of
4. Credentialing team members in nutrition support appropriate route of nutrition intervention
a) Physician j) Identifies compelling rationale for choosing enteral over par-
(1) Licensed physician or Doctor of Osteopathy certified enteral nutrition support with functional gastrointestinal tracts18
through the National Board of Nutrition Support Certifi- k) Promotes timeliness of nutrition intervention, so that severe
cation as a Certified Nutrition Support Physician (CNSP) nutrition depletion is avoided18
and/or American Board of Physician Nutrition Specialists l) Produces proof of effectiveness of nutrition therapies
certified5 Recommended that candidates taking the CNSP m) Provides mechanism for education, research, and quality
examination for certification have at least two years of management
experience beyond residency training in administration n) Provides documentation of practice and outcomes
and monitoring of patients receiving parenteral and enteral o) Develops effective methods to spread new practices widely
nutrition throughout the organization30
b) Dietitian3 2. Role of committee members
(1) Registered dietitian certified through National Board of a) Physician—effectively understands and manages the array of
Nutrition Support Certification as a Certified Nutrition policies and procedures, finance, and quality improvement
Support Dietitian (CNSD) issues confronted by nutrition support intervention5
(2) Recommended that candidates taking examination have at b) Dietitian
least two years of experience in parenteral and enteral (1) Develops policies and procedures and standards of prac-
nutrition tice to ensure optimal nutrition support through nutrition
c) Nurse screening, nutrition assessment, and development of a
(1) Registered nurse certified through National Board of medical nutrition therapy (MNT) care plan, its imple-
Nutrition Support Certification as a Certified Nutrition mentation, monitoring and reassessment, and transition
Support Nurse (CNSN) or termination of nutrition care as appropriate4
(2) Recommended that candidates taking examination have (2) Provides transitional elements to all modalities of alimen-
at least two years of experience in parenteral and enteral tation, oral to enteral to parenteral4
nutrition (3) Obtains institutional clinical privileges for order-writing in
d) Pharmacist31 the medical record with or without physician co-signature,

© 2005 A.S.P.E.N. www.nutritioncare.org. A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. 361
S E C T I O N V I Site Related and Ethical Issues

for nutrition support interventions and monitoring within 6. Objectives of hospital/conflicting priorities
institutional governance of medical policy and procedure. 7. Staff availability/changes/shortages
Clinical privileges may also encompass specific skills 8. Profit versus nonprofit
such as feeding tube insertion and metabolic rate meas- 9. Competition for scarce healthcare resources
urement.3,32,33 10. Local practice and comparison to published data
c) Nurse 11. Dynamic health care environment issues, affecting all patient
(1) Participates in the development and review of nutrition care and health care providers
organizational policies and procedures for specialized 12. Previously recognized clinical issues with the treatment of
support26 patients requiring enteral or parenteral nutrition
(2) Supports nursing in the development of policies related to
administration of enteral/parenteral nutrition and issues
related to patient care III. Controlling costs of nutrition support
(3) Develops protocols for central and peripheral line moni- A. Nutrition Support Team/Committee can result in improved cost
toring26 efficacy as documented by data in the literature3
(4) May obtain clinical privileges for placement of peripherally B. Reducing complications with optimum nutrition support delivery3
inserted central catheters preceded by specialized training, C. Accurately determining appropriate parenteral and enteral nutrition
demonstrated competency, and delineated institution clini- candidates3,35
cal privileges27 D. Reducing laboratory tests for monitoring parenteral and enteral
(5) Keeps database for line infections
nutrition3
d) Pharmacist
E. Preventing overfeeding3
(1) Develops policies and procedures for parenteral nutrition,
F. Decreasing duration of nutrition support3
addressing labeling, compounding, formulas, stability, and
G. Standardizing enteral and parenteral nutrition protocols
filtration28,29
H. Reducing use of expensive, non-standardized parenteral nutrition
(2) Maintains quality monitors regarding effectiveness of par-
formulations3
enteral nutrition
I. Preventing waste of formulas3
(3) Determines implications of Food and Drug Administra-
J. Formal infection control practices reducing catheter related sepsis35
tion’s amendment on regulations on aluminum in large
K. Encouraging appropriate use of enteral nutrition rather than par-
and small volume parenterals used in parenteral nutrition34
enteral nutrition35
(4) Develops policies on the safe use and guidelines for use of
L. Achieving economics of scale through standardization of solutions
extemporaneously prepared lipid emulsion syringes29,34
and devices
(5) Develops safe infusion dosing of macronutrients (protein,
M. Preventing inappropriate use of parenteral nutrition3
fat, and carbohydrate), as well as electrolytes and medica-
N. Performing cost analysis of supplies and solutions3
tions in enteral and parenteral nutrition with minimum and
O. Cost versus charges
maximum dosages29,34
P. Cost-effectiveness outcomes15
e) Administrator—focuses on financial aspects of nutrition sup-
port therapy in conjunction with other healthcare team mem-
bers to provide cost effective nutrition while improving patient IV. Reimbursement Issues
outcomes.
3. Committee reporting structure examples A. Reimbursement for nutrition support service consultation
a) Chair of Nutrition Support Committee reports to Pharmacy and 1. Physician nutrition support service billing
Therapeutics Committee or directly to Patient Care Committee 2. Initial consult
and then this committee reports to the Executive Committee. 3. Follow-up consults (concurrent care)
b) Sub-committee on Specialized Nutrition Support reports to 4. Institution coding for malnutrition diagnosis and for enteral/
the Nutrition Advisory Board, which reports to the Medical parenteral treatment in association with specified diagnosis
Board. Directors of Nutrition Support Services report to Med- 5. Billing for metabolic monitoring
ical Directors of various services and these Medical Directors B. Reimbursement for acute care nutrition support36
then report to the Chief Medical Officer. 1. Medicare—parenteral and enteral nutrition (PEN) covered under
4. Communicating committee actions and recommendations both parts of Medicare when “medically necessary”
a) Each committee member responsible for dissemination of poli- a) Part A—inpatient hospital care, skilled nursing care, home
cies and procedures and recommendations of Nutrition Support care nursing visits, hospice care
Committee to their respective disciplines b) Part B—nonhospital costs such as physician services, medical
b) Development of tools and education of hospital staff and other supplies, and equipment
health care providers on nutrition support policies and proce- 2. Diagnosis-Related Grouping (DRG) system—payments to hos-
dures coordinated by Nutrition Support Committee members pitals under Medicare Part A made pursuant to predetermined spe-
C. Factors influencing existence and structure of nutrition support cific rates according to patients’ primary diagnoses, PEN covered
team3 as part of the hospital stay
1. Institution size a) Malnutrition and other nutrition diagnoses qualify as co-
2. Age-specific needs: adults, pediatrics, and neonates morbidities or complications.
3. Internal structure/decision making process b) Co-morbidity—condition that existed at the time of hospital
4. University affiliation and academic role of institution admission that causes at least one extra day of hospitalization
5. Local case mix c) Complication—arises during the hospital stay

362 A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. © 2005 A.S.P.E.N. www.nutritioncare.org.
 S E C T I O N V I Site Related and Ethical Issues

d) Co-morbidity and complications result in higher reimburse- Support A Case-Based Core Curriculum. Dubuque, IA: Kendall/Hunt Pub-
ment through DRGs lishing Company; 2002:757–776.
3. Medicaid—administered and funded jointly by the states and the 15. August DA, Thorn D, Gannon J. Outcomes research. In: Gottschlich MM,
federal government. There is great diversity in programs, but Med- ed. The Science and Practice of Nutrition Support: A Case-Based Core Cur-
riculum. Dubuque, IA: Kendall/Hunt Publishing Company; 2002:777–792.
icaid programs for PEN coverage in general mimic the Medicare
16. Senkal M, Dormann A, Stehle P, Shang E, Suchner U. Survey on structure
coverage program. and performance of nutrition-support teams in Germany. Clinical Nutrition.
4. International Classification of Diseases (ICD)-9-CM classifies 2002;21(4):329–335.
morbidity and mortality information based on the official version 17. DeJonghe B, Appere-De-Vechi C, Fournier M, et al. A prospective survey
of the World Health Organization’s 9th Revision. The ICD-9-CM of nutritional support practices in intensive care units: what is prescribed?
is recommended for use in all clinical settings but is required for What is delivered: Crit Care Med. 2001;29:8–12.
reporting diagnoses and diseases to all U.S. Public Health Service 18. Bowman LC, Williams R, Sanders M, Ringwald-Smith K, Baker D, Gajjar
and Health Care Financing Administration programs. The ICD-9- A. Algorithm for nutritional support experience of the metabolic and infu-
CM is used for DRG coding of co-morbidities and conditions. The sion support service of St. Jude Children’s Research Hospital. Int J Cancer
following are relevant ICD-9-CM codes.37 Supplement. 1998;11:76–80.
19. Maurer J, Weinbaum F, Turner J, et al. Reducing the inappropriate use of par-
a) 99.15—Parenteral infusion of concentrated nutritional sub-
enteral nutrition in acute care teaching hospital. J Parent Ent Nutr. 1996;20:
stances 272–274.
b) 96.6—Enteral infusion of concentrated nutritional substances 20. Howard P. Organizational aspect of starting and running an effective nutri-
c) 260.0—Kwashiorkor tion support service. Clinical Nutrition. 2001;20(4):367–374.
d) 261.0—Marasmus 21. Mueller C, Shronts EP. Position of The American Dietetic Association: the
e) 262.0—Other severe protein-calorie malnutrition: nutritional role of registered dietitians in enteral and parenteral nutrition support. J Am
edema without dyspigmentation of skin and hair Diet Assoc. 1997;97(3):302–304.
f ) 263.0—Malnutrition of moderate degree 22. Howard P, Jonkers-Schuitema CF, Kyle U. The role of the nutritional sup-
g) 263.1—Malnutrition of mild degree port dietitian in Europe. Clinical Nutrition. 1999;18(6):379–383.
h) 263.8—Other protein-calorie malnutrition 23. Schwartz DB. History and evolution of a successful certification program in
nutrition support: the CNSD experience. J Am Diet Assoc. 2003;103(6):
i) 263.9—Unspecified protein-calorie malnutrition
736–741.
24. Maillet JO, Potter RL, Heller L. Position of the American Dietetic Associ-
REFERENCES ation: ethical and legal issues in nutrition, hydration, and feeding. J Am Diet
1. Jonkers CF, Prins F, Van Kempen A, Tepaske R, Sauerwein HP. Towards Assoc. 2002;102(5):716–726.
implementation of optimum and better clinical nutrition support. Clinical 25. Guenter P, Curtas S, Murphy L, Orr M. The impact of nursing practice on
Nutrition. 2001;20(4):361–366. the history and effectiveness of total parenteral nutrition. J Parent Ent Nutr.
2. Arena J, Walters P. Do you know what a dietetic technician can do? A focus 2004;28(1):54–59.
on clinical technicians. J Am Diet Assoc. 1997;97(suppl 2):S139–S141. 26. A.S.P.E.N. Board of Directors. Standards of practice for nutrition support
3. Colaizzo-Ana T. The evolution of nutrition support services. In: Matarese nurse. Nutr Clin Prac. 2001;16:56–62.
LE, Gottschlich mM, eds. Contemporary Nutrition Support Practice. 2nd 27. Vanek WV. The ins and outs of venous access: part II. Nutr Clin Prac. 2002;
ed. Philadelphia, Pa: Saunders; 2003:1–13. 17:142–155.
4. A.S.P.E.N. Board of Directors. Standards of practice for nutrition support 28. O’Neal BC, Schneider PJ, Pedersen CA, Mirtallo JM. Compliance with
dietitian. Nutr Clin Prac. 2000;15:53–59. safe practices for preparing parenteral nutrition formulations. Am J Health-
5. A.S.P.E.N. Board of Directors. Standards of practice for nutrition support Syst Pharm. 2002;59:264–269.
physician. Nutr Clin Prac. 2003;18:270–275. 29. National Advisory Group on Standards and Practice Guidelines for Par-
6. A.S.P.E.N. Board of Directors and Task Force. Standards for specialized nutri- enteral Nutrition. Safe practices for parenteral nutrition formulations. J Par-
tion support: adult hospitalized patients. Nutr Clin Prac. 2002;17:384–391. ent Enter Nutr. 1998;22(2):49–66.
7. A.S.P.E.N. Board of Directors. Standards of practice for nutrition support 30. Schneider PJ, Bothe A, Bisognago M. Improving the nutrition process:
pharmacist. Nutr Clin Prac. 1999;14:275–281. assuring that more patients receive optimal nutrition support. Nutr Clin
8. Joint Commission on Accreditation of Healthcare Organizations. Hospital Prac. 1999;14:221–226.
Accreditation Standards. Oakbrook Terrace; IL: Joint Commission on 31. Ebiasah RP, Schneider PJ, Pedersen CA, Mirtallo JM. Evaluation of board
Accreditation of Healthcare Organizations; 2004:333–384. certification in nutrition support pharmacy. J Parent Enter Nutr. 2002;
9. Barclays Official California Code of Regulations. Title 22. Social Security 26(4):230–247.
Division 5. Licensing and Certification of Health Facilities. Home Health 32. Silver HJ, Wellman NS. Nutrition diagnosing and order writing: value for
Agencies Clinics and Referral Agencies. San Francisco, CA: Barclays Law practitioners, quality for clients. J Am Diet Assoc. 2003;103(11):1470–1472.
Publishers; 1999:759–773. 33. Mueller CM, Colaizzo-Anas T, Shronts EP, Gaines JA. Order writing for par-
10. A.S.P.E.N. Board of Directors. Standards of practice for hospitalized pedi- enteral nutrition by registered dietitians. J Am Diet Assoc. 1996;96:764–768.
atric patients. Nutr Clin Prac 1996;11:217–228. 34. Driscoll DF. Compounding TPN admixtures: then and now. J Parent Ent
11.Centers for Disease Control. Guidelines for the prevention of intravascular Nutr. 2003;27(6):433– 438.
catheter-related infections. MMWR. 2002;51(RR10):1–26. 35. Payne-James J. Cost-effectiveness of nutrition support teams. Are they nec-
12. Schwartz DB. Enhanced enteral and parenteral nutrition practice and out- essary? Nutrition. 1997;13(10): 928–930.
comes in an intensive care unit with a hospital-wide performance improve- 36. Centers for Medicare & Medicaid Services. Chapter 3: Inpatient Hospital
ment process. J Am Diet Assoc. 1996;96:484 – 489. Billing. In: Medicare Claims Processing Manual. Rev. 221. Baltimore,
13. Winkler MF, Hedberg A. Quality and performance improvement. In: MD: Centers for Medicare & Medicaid Services; 2003.
Matarese LE, Gottschlich MM, eds. Contemporary Nutrition Support Prac- 37. International Classification of Disease-9-CM. Department of Health and
tice. 2nd ed. Philadelphia, PA: Saunders; 2003:616 – 624. Human Services, Centers for Disease Control and Prevention, Epidemiol-
14. Marian M, Stieber M. Quality performance improvement, indicators, and ogy Program Office, Division of Public Health Surveillance and Informat-
standards. In: Gottschlich MM, ed. The Science and Practice of Nutrition ics. June 5, 2003.

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 Mary Ellen Posthauer, RD, CD, LD;
Gretchen Robinson, MS, RD, LD, FADA
34
Long-Term Care Facilities

Introduction requirements independent of disease or rehabilitation.6 Nutritional

interventions include liberalizing therapeutic diets, using nutritional
Nutrition support practice in long-term care (LTC) facilities resembles supplements, using specialized feeding utensils and instruments to
nutrition support practice among other adult populations. This chapter facilitate oral intake, and providing nutrition support. The use of
focuses on special considerations for the mostly elderly residents in these
enteral nutrition in elderly residents has increased significantly
facilities. Notable among these differences are the mandated assessment
since 1990, with an estimated 10% of today’s LTC facility residents
and care plan systems set forth by the Centers for Medicare and Medic-
receiving enteral nutrition through percutaneous endoscopic gas-
aid Services (CMS). These systems not only direct care and monitor
trostomy devices.7 Approximately one third of residents in LTC
facility practice but also direct reimbursement for care, including nutri-
tion support. facilities who have advanced dementia have their nutritional require-
ments met by enteral nutrition.8 Most receive enteral nutrition
I. Background because of dementia related to chronic neurologic impairment or, to
II. Nutrition Care Process a lesser extent, cancer.9–11
III. Mandated Care and Regulation D. Residents’ rights: to feed or not to feed? Residents’ rights are para-
IV. Reimbursement mount in the decision to feed or not to feed. All professionals should
References be able to assist residents and their families in the decision about
whether to use nutrition support at the end of life or in conditions of
terminal disease, including end-stage dementia. Advance directives
I. Background. are the primary tools for documenting a resident’s preferences regard-
The provision of nutrition is a key component of the care provided to ing nutrition support. A resident can change these directives if the res-
residents in LTC facilities. The decision to provide enteral or parenteral ident is still competent at the time a decision is being made about tube
nutrition to residents requires careful consideration of the therapies’ feeding.12 In the absence of advance directives, professionals should
potential benefits and risks. Practitioners should understand mandated be prepared to provide expert guidance to families and accommodate
care guidelines for LTC facilities as well as professional good practice the resident’s known beliefs, including ethnic and cultural values, and
standards to achieve optimal outcomes for residents. best interests.6,13
A. Demographics of aging and malnutrition in aging. Health care trends 1. Advance directives. Advance directives enable residents to docu-
indicate that the number of US individuals 85 years and older will ment in advance preferences regarding treatment and care, includ-
increase to 18 million by 2050.1 During the same period, the num- ing end-of-life wishes. Two common forms of advance directives
ber of people over 85 with moderate or severe dementia will increase are a living will and a durable power of attorney for health care.
from 1.4 million to 6.3 million.2 The incidence of LTC placement a) A living will states a person’s choices regarding future med-
increases with age: 31% of those who are severely impaired and ical care decisions, including the use of artificial life support
between the ages of 65 and 70 reside in LTC facilities, compared to
and nutrition support.
61% of those age 85 and older. There were 1,465,000 people in LTC
b) A durable power of attorney for health care enables a resident
facilities in 1997 nationally, approximately 4% of the older popula-
to appoint another individual to make all decisions regarding
tion.3 In 1997, 46% of the LTC population was aged 85 or older,
compared to 33% aged 75 to 84, 13% aged 65 to 74, and 8.5% under health care, including choice of provider, medical treatment,
age 65.4 and end-of-life care.
B. Definition of LTC. The US Senate Special Committee on Aging E. Professional staff. The great majority of LTC facilities do not have
described LTC as follows: LTC “differs from other types of health formal nutrition support teams or services. An interdisciplinary team
care in that the goal of long-term care is not to cure an illness, but to of health professionals provides nutrition support. Residents and
allow an individual to attain and maintain an optimal level of func- their families are involved as much as possible in care and treatment
tioning. Long-term care encompasses a wide array of medical, social, decisions.14,15
personal and supportive and specialized housing services needed by 1. Physicians
individuals who have lost some capacity for self-care because of a a) Maintain overall responsibility for residents’ care.
chronic illness or disabling condition.”5 b) Diagnose disease conditions and alterations in metabolism;
C. Role of nutrition support in LTC. Available data indicate that confirm malnutrition.
advancing age brings physiological changes: reduction in lean body c) Evaluate the residents’ nutrition needs in relation to the clinical
mass, decline in bone density, increase in total body fat, and decrease profile.
in total body water. These changes affect an individual’s nutrition d) Prescribe all diets and nutrition support interventions.

364 A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. © 2005 A.S.P.E.N. www.nutritioncare.org.
 S E C T I O N V I Site Related and Ethical Issues

e) Prescribe, review, and modify medication regimes to adjust 7. Pharmacists

for possible side effects contributing to eating problems. a) Review medications for adverse effects on nutritional status.
f) Consult with family/caregivers to determine residents’ wishes b) Compound parenteral nutrition and monitor solution stability
regarding nutrition support. and safety.
2. Physician’s assistants c) Participate in surveillance and management of therapy, includ-
a) Evaluate the clinical status, including the nutritional status, of ing associated complications and delivery of cost-effective
residents in the absence of or in collaboration with the physician. care.
b) Collaborate with the other team members (ie, nurse, speech 8. Dietitians
pathologists, dietitian). a) Are the primary advocates for all aspects of residents’ nutri-
c) Prescribe diets and nutrition support regimens as needed. tional care.
3. Nurses b) Provide initial and periodic assessment of nutrient intake and
a) Provide direct resident care nutrition status.
b) Administer nutrition support and manage the care of nutrition c) Are the professionals primarily responsible for the design,
support access devices. implementation, and monitoring of nutritional interventions.
c) Serve as primary liaison with nursing staff, certified nursing d) Anticipate the effect of procedures, treatments, therapies, and
assistants, and other team members. psychosocial issues on the residents’ nutrition status.
d) Inform physician and family/caregivers of any condition e) Advise colleagues of altered nutritional status or potential
changes (ie, weight loss, falls, pressure ulcers, medication nutrition deficiencies.
change, mental status). f ) Document nutrition assessment and nutrition care plans.
4. Occupational and/or physical therapists 9. Others. A number of additional personnel (eg, certified nursing
a) Assess residents’ potential for eating rehabilitation. assistants, dietary technicians and assistants, and other food serv-
b) Introduce compensatory techniques to minimize the effects of ice personnel) also have a role in nutritional care, although the role
sensory-perceptual problems that affect eating performance. can vary from one facility to another. Their duties range from deliv-
c) Use specialized seating and orthoses to facilitate the postural ering trays and supplements to assisting with meals and feeding.
control and coordination necessary for eating.
d) Provide adaptive tableware and utensils to assist with self-
II. Nutrition Care Process.
feeding.
e) Devise adaptations and environmental controls to facilitate Wherever relevant, Standards for Nutrition Support for Adult Resi-
independent self-feeding. dents of Long-Term Care Facilities16 should be used in tandem with the
f) Recommend eating and feeding techniques to promote the following section on the nutrition care process.
residents’ abilities to self-feed. A. Nutrition assessment. In general, as the elderly age, their caloric intake
g) Provide or recommend active and passive range-of-motion declines17 and they become increasingly frail. Frailty is distinguished
exercises and coordination and strength-building exercises to by weakness, immobility, and weight loss caused or exacerbated by
facilitate functional self-feeding. inadequate nutrition. Frailty occurs frequently in older residents with
h) Evaluate the impact of cognitive impairments on eating and moderate to advanced dementia. It is not known whether it is a result
self-feeding ability and address cognitive issues to ensure that of the aging process, malnutrition, or both.
safe feeding practices are followed. 1. Residents usually have comorbid conditions such as dementia,
i) Recommend seating devices (eg, wheelchair arm supports Parkinson’s disease, cerebrovascular accident, congestive heart
and wedge cushions) to ensure the safety of clients during eat- failure and cardiovascular disease, chronic obstructive pulmonary
ing and transfer from wheelchair to dining chair. disease, diabetes, and rheumatoid arthritis and osteoarthritis. In
5. Speech pathologists many cases, these conditions lead to increased levels of circu-
a) Perform dysphagia/swallowing evaluations. lating cytokines, which can subtly alter normal metabolism and
b) Provide retraining in swallowing; design and supervise exer- immunity. One effect of increased systemic cytokines is decreased
cises to strengthen facial muscles, increase range of motion of serum albumin, which has long been used as an indicator of nutri-
the lips and control of the tongue, and facilitate safe oral and tional status. In fact, it is much more useful as an indicator of
pharyngeal phase swallowing. morbidity.18,19
c) Evaluate the resident’s ability to eat and drink by mouth and 2. Elements of assessment
ensure proper positioning and techniques necessary for safe a) Weight16
swallowing. (1) Determine whether resident is nutritionally at risk
d) Assess ability to resume safe swallowing when transitioning (a) Involuntary loss or gain of ≥10% of usual body weight
from nutrition support and recommend nutrient delivery options within 6 months
when dysphagia is present. (b) Or involuntary loss or gain of ≥5% of usual body
6. Social workers weight in 1 month
a) Function as the residents’ advocate in all aspects of care. (c) Or a weight 20% over or under ideal body weight
b) Assist residents and families in articulating wishes regarding (2) Determine possible causes of weight change
nutritional interventions. (a) Review for clinical signs, symptoms, and causes of
c) Educate families about residents’ conditions and prognoses. malnutrition.
d) Initiate advance directives at admission and review them with (b) Review for increased nutrient needs.
families and caregivers as conditions change. (c) Review lab tests indicating undernutrition.
e) Provide psychological support and address social and finan- (d) Review clinical conditions that may cause unintended
cial concerns. weight loss.

© 2005 A.S.P.E.N. www.nutritioncare.org. A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. 365
S E C T I O N V I Site Related and Ethical Issues

(e) Review medications that cause anorexia, altered taste, prescriptions such as those used for renal and cardiovascular
and psychosocial needs. abnormalities. The purpose of liberalizing restrictive diets is to
b) Food/fluid intake/adequacy promote intake and improve quality of life in anorexic residents
(1) The estimated adequate fluid requirement per 24 hours is who might otherwise be uninterested in therapeutic diets.27
1 mL fluid per kcal, 30 mL per kg, minimum 1500 mL per 2. Restorative dining.25 Restorative dining refers to improving or
day regardless of weight. Requirements are adjusted as maintaining a resident’s ability to eat independently, rehabilitat-
needed for cardiac, pulmonary, and renal restrictions.20 ing residents who cannot eat independently to a level where they
(2) The estimated adequate energy requirement per 24 hours require minimal assistance, or enabling the caregiver to provide
is basal metabolic rate (as estimated by the Harris- assistance to residents who cannot eat entirely independently.
Benedict equation21) × 1.3 (unspecified factor for activ- 3. Self-help devices/utensils.25 Utensils modified to compensate for
ity and/or stress22,23). residents’ inability to use standard utensils can facilitate adequate
(3) The estimated adequate protein requirement per 24 hours oral intake. Posture, food consistency, and table height should
is 1 g per kg, and up to 1.5 g per kg for healing pressure be addressed before adaptive equipment and utensils are con-
ulcers or surgical wounds.24 sidered. Two principal considerations in selecting modified uten-
(4) Elderly residents are more likely than younger adults to be sils are (1) the device should address the problem that interferes
deficient in vitamins D, B12, folate, and riboflavin. See with the resident’s eating ability; and (2) the device should be
Chapter 2 for the dietary reference intakes. acceptable to the resident. There are various utensils and devices
(5) Obtain diet history, food allergies/intolerances, food pref- to aid in eating:
erences, and cultural concerns. a) Lightweight utensils
(6) Observe intake during meals. b) Plate guard/scoop dish/inner-lip plate
(7) Determine possible causes of dehydration and identify c) Nonslip matting
appropriate interventions. d) Rocker knife/roller knife
(8) Review advance directives, verifying with residents and e) Utensil with built-up, angled, or bent handles
family their wishes regarding nutrition support. f) Wrist support/splint
c) Drug-nutrient interactions g) Wide handles on thermal mugs
(1) Review medical record for current medications. h) Suction-based tableware
(2) Evaluate nutritional implications of current medications. i) Long, bendable straw and holder
d) Serum laboratory concentrations. Laboratory assays can be j) Covered mug with lid
prudently used to confirm suspected nutrition-related problems k) Nosey cut-out tumbler
(organ dysfunction, nutrient deficiencies) identified by clinical l) Dysphagia cup
diagnosis, observation, history, and physical examination. The 4. Oral supplements. Nutritional supplements can be initiated when
use of hepatic proteins and total cholesterol to measure nutri- oral intake is determined to be inadequate. Most supplements are
tional status is controversial. In general, they are more useful commercially available liquid formulations. Evidence suggests
as prognostic indicators.18,19 that supplements can improve outcomes in elderly residents with
e) Physical and mental function relevant to oral intake25 hip fractures,28 pressure ulcers,29 or chest infections.30 One recent
(1) Evaluate functional abilities during meals. study indicated that providing supplements 60 minutes before a
(a) Identify need for use of adaptive devices. meal increases total caloric intake.31
(b) Identify need for special positioning devices. a) Standard liquid supplements (2 cal/mL), lactose-free
(c) Identify physical and/or verbal cues resident needs to b) Concentrated liquid supplements (2 cal/mL), lactose-free
initiate and continue with meal. c) Juice-based formulas with minimal fat
(2) Evaluate oral status. d) High-calorie puddings, cookies, and energy bars
(a) Perform complete oral cavity assessment. C. Nutrition support (enteral and parenteral nutrition)
(b) Review need for mechanically altered diet. 1. Enteral nutrition. See Chapter 5 for enteral nutrition management
(3) Evaluate for signs and symptoms of dysphagia. in general adult populations.
(4) Evaluate for communication barriers (vision, speech, hear- a) Candidates. Enteral nutrition (tube feeding) is used in residents
ing, cognition status). of LTC facilities for the same reasons it is used in adult popu-
f ) Pressure ulcers. Poor nutritional status is a risk factor for lations: inadequate oral intake. Most residents requiring enteral
development of pressure ulcers, but attempts to prevent the nutrition have sustained neurologic injury such as stroke or
occurrence of pressure ulcers by nutritional intervention have head trauma, or have degenerative neurologic conditions such
produced equivocal outcomes. This may be due to the difficulty as Alzheimer’s disease, end-stage dementia, or Parkinson’s
in meeting daily requirements as well as the lack of definitive disease.32–34 Residents’ wishes regarding enteral nutrition
data on the nutritional requirements of wound healing. Atten- should be factored into decisions about whether to use enteral
tion should focus on adequate nutrition up to 35 kcal/kg/day nutrition, as should specific achievable goals for an individual
and 1.5 g protein/kg/day. Adequate micronutrient provision resident.35
with special attention to vitamin A, B vitamins, vitamin C, zinc, b) Access. Enteral nutrition access is based on the physiology of
manganese, copper, and selenium may also be helpful.26 the gastrointestinal tract and the anticipated length of time
B. Oral diet interventions enteral support will be needed. Enterostomy devices placed
1. Liberalized diet for older adults in LTC. The American Dietetic either surgically or percutaneously are the most common access
Association maintains that the quality of life and nutritional status routes in LTC facility residents and are recommended when
of older residents in LTC facilities may be enhanced by a liberal- enteral nutrition is anticipated to be required for greater than
ized diet. This diet refers to the withholding of restrictive nutrition 30 days. Of these, percutaneous endoscopic gastrostomies pre-

366 A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. © 2005 A.S.P.E.N. www.nutritioncare.org.
 S E C T I O N V I Site Related and Ethical Issues

dominate.9 For short-term enteral nutrition (less than 4 weeks), (4) Consult the pharmacy for questions regarding drug/enteral
nasoenteric tubes are used.6 formula administration compatibility.
c) Administration. Enteral feeding is administered continuously, f ) Monitoring guidelines. Monitoring guidelines for stable resi-
intermittently, or by gravity. dents of LTC facilities are variable, depending on individual
(1) Continuous administration is given at a slow, continuous resident morbidity. For less stable residents or those requiring
rate via a pump over 16 to 24 hours per day. This is the pre- parenteral nutrition (see Section II.C.2), monitoring may be
ferred method when enteral nutrition is initiated; the resi- more frequent.38 The following are suggested monitoring
dent has not been fed for 3 or more days; or the resident is parameters for enteral nutrition37:
unstable and at risk for aspiration. (1) Serum albumin, electrolytes, blood urea nitrogen (BUN)/
(2) Cyclic administration is continuous feeding for a specified creatinine, magnesium, phosphorus, calcium, complete
period of time (ie, 8–16 hours) in amounts to meet esti- blood cell count, glucose—every 6 months
mated nutritional needs, usually via a pump. This method (2) Weight—monthly or as needed
is used when progressing to oral feedings and for residents (3) Intake and output—daily
unable to tolerate intermittent or bolus feedings. Cyclic (4) Bowel function—daily
feedings promote resident mobility, allowing participation (5) Patency of tube—daily
in rehabilitation and other activities. (6) Residual check—prior to each feeding
(3) Intermittent administration delivered via slow gravity drip, g) Common complications
pump, or intermittent bags. Usually, 250 to 500 mL of for- (1) Diarrhea
mula is delivered over 60 to 75 minutes 5 to 8 times per day (2) Constipation
as needed to meet estimated nutritional needs. The sched- (3) Nausea and vomiting
ule simulates the meal pattern and allows more freedom of (4) Abdominal distension, bloating, cramping, and gas
activity between meals. This type of feeding is contraindi- (5) Aspiration
cated in residents at high risk of aspiration. (6) Clogged tube
(4) Bolus administration of 200 to 400 mL over 20 to 30 min- h) Transition from enteral nutrition to oral intake39
utes 3 to 5 times per day, usually administrated by a 60-mL (1) The speech pathologist evaluates the resident’s readiness
syringe or gravity. for an oral diet.
d) Formulas (2) The dietitian and the speech pathologist consider modifi-
(1) Polymeric formulas are composed of isolated sources of cations in the oral diet to maximize intake.
protein, carbohydrate, and fat in high-molecular form. (3) Daily food/fluid intake is monitored.
These formulas usually have a low osmolality (300– (4) Adding a nighttime enteral nutrition cycle is considered.
500 mOsm/kg) and are lactose-free; some are supple- (5) Resident weight is monitored frequently.
mented with fiber. They usually contain 1 kcal/mL, (6) Enteral nutrition is stopped when oral intake is adequate.
although some are concentrated up to 2 kcal/kg for resi- 2. Parenteral nutrition. See Chapters 7 and 8 for parenteral nutrition
dents requiring fluid restriction. ordering and management. Anecdotally, parenteral nutrition is
(2) Monomeric or elemental formulas contain hydrolyzed rarely used in LTC settings, possibly because of risk (of sepsis and
macronutrients and are lactose-free. They are more expen- other complications), inability to prepare solutions at the facility,
sive than polymeric formulas and should be used for resi- lack expertise in management, and cost. Perhaps the decision to
dents with maldigestion or malabsorption. initiate parenteral nutrition in elderly residents is less likely to
(3) Modular nutrients are individually packaged macronutri- favor starting the therapy because clinicians, residents, and surro-
ents (protein, carbohydrate, fat) that are usually used to gates perceive (correctly) that the risks of parenteral nutrition can
supplement standard formulas in varying amounts to meet outweigh the potential benefits to residents at the end of their lives.
individual nutritional requirements. The use of peripheral parenteral nutrition as opposed to central par-
(4) Disease-specific formulas are modified in one or more enteral nutrition is discouraged in LTC because short-term nutri-
nutrients for certain disease states. Most of these formulas tion support is unlikely to benefit residents6 and the fragility of skin
are more expensive, so their potential benefit to residents in the elderly complicates venous access.24
should be evaluated before they are used. a) Parenteral nutrition should be considered for LTC facility res-
e) Drug-nutrient interactions. See Chapter 9. Medications may idents who have gastrointestinal dysfunction (similar to gen-
be administered via enterostomy tube.36,37 eral adult populations) such as occurs with diffuse peritonitis,
(1) Flush the feeding tube with water prior to medication intestinal obstruction, intractable vomiting, paralytic ileus,
administration, between medications, and after the last intractable diarrhea, gastrointestinal ischemia, and short-gut
medication to reduce clogging of the tube. syndrome.6
(2) Never add medications directly to enteral formulas or b) Access for LTC facility residents is provided by permanent
administer them through the same port of the feeding tube devices such as an implanted port or a subcutaneously tunneled
when the feeding is being infused. (Hickman) catheter.40 Peripherally inserted central catheters
(3) Use liquid forms of medications whenever possible. (PICCs) are also used for venous access greater than 1 month,
Check the dosage, since many liquid forms are intended although not usually more than several months. Appropriately
for pediatric use. trained nurses can place PICCs, although fragile peripheral ves-
(a) Dilute liquid medications with at least 30 mL of water. sels in the elderly may complicate the use of these devices.
(b) Many liquid medications have high osmolalities c) Parenteral nutrition monitoring is generally more frequent
(>1000 mOsm/kg). Administration of hyperosmolar than enteral nutrition monitoring. The following are suggested
products through the feeding tube may result in diar- general parameters16:
rhea, cramping, abdominal distention, and vomiting. (1) Physical assessment

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S E C T I O N V I Site Related and Ethical Issues

(2) Clinical status E. Data Assessment Verification Project (DAVE). DAVE is a program
(3) Actual nutrient intake funded by CMS to monitor and improve the care provided to resi-
(4) Fluid balance dents of LTC facilities. The MDS provides the data for the program
(5) Weight to monitor the quality of care, to report to the public on the quality
(6) Assessment of major organ function of care, and to determine Medicare payments. DAVE also evaluates
(7) Visual inspection of access devices and site the MDS in order to improve the accuracy of the data that the MDS
(8) Temperature and signs and symptoms of infection generates.42
(9) Serum chemistries, including complete blood cell count F. Joint Commission on Accreditation of Healthcare Organizations
d) Transitional Feeding-Total parenteral nutrition is discontin- (JCAHO).38 The 2004 JCAHO accreditation processes emphasize
ued when adequate oral intake or enteral nutrition has been continuous standards compliance, with a focus on encouraging health
established. See Section II.C.1.h for a discussion of the tran- care organizations to continuously use the standards to achieve and
sition to oral intake. maintain excellent operations systems.
1. Tracer methodology. The tracer system is an evaluation process
conducted by the JCAHO during on-site surveys that traces the
III. Mandated Care and Regulation
care residents receive in a facility. The surveyor randomly selects
A. Resident Assessment Instrument (RAI). RAI is an interdisciplinary active files and traces residents throughout the organization. The
care system mandated by the CMS that sets forth a program designed surveyor may pull closed charts if a standards compliance issue is
to assess all aspects of clinical status and to facilitate problem identi- identified to determine whether the problem is part of a pattern or
fication, clinical interventions, and care plans for LTC facility resi- an isolated case. Surveyors also interview staff members involved
dents. The components of RAI are the Minimum Data Set (MDS), in the care of residents.
Resident Assessment Protocols (RAPs), and triggers.41 2. JCAHO LTC standards relevant to enteral and parenteral nutrition
1. The MDS is a form containing a range of clinical and functional a) Residents are involved in decisions about care, treatment,
status attributes that provide the foundation for the comprehensive and services provided.
assessment of residents of LTC facilities. The oral/nutritional b) Residents have the right to refuse care, treatment, and serv-
status sections contain categories for oral problems; height and ices in accordance with laws and regulations.
weight; weight change; nutritional problems; nutritional attributes, c) The organization addresses the wishes of residents relating
including oral, parenteral, and enteral interventions; and parenteral to end-of-life decisions.
or enteral intake. d) Residents—and, when appropriate, their families—are
2. RAPs are problem-oriented frameworks for organizing MDS informed about the outcomes of care, treatment, and serv-
data; they form the basis for individualized care planning. There ices, including unanticipated outcomes.
are 18 RAPs focused on social, medical, and psychological prob- e) The organization defines in writing the time frame for con-
lems. Specific nutrition RAPs include nutritional status, feeding ducting initial (nutritional) assessments.
tubes, and dehydration and fluid maintenance. f ) Initial (nutritional) assessments are performed as defined by
3. Triggers are links between the MDS and RAPs. They identify the organization.
RAPs that can be applied from MDS data. Examples of nutrition g) Residents are reassessed as needed.
triggers are weight loss; taste alterations; parenteral/intravenous h) Development of a plan of care, treatment, and services is
feedings; tube feedings; mechanically altered diets; incomplete individualized and appropriate to the resident’s needs,
meal consumption (leaving 25% of food uneaten); pressure ulcers; strengths, limitations, and goals.
syringe feeding; and therapeutic diet. i) The organization provides care, treatment, and services for each
4. Utilization guidelines explain how to use the RAI care system. resident according to the plan for care, treatment, and services.
These guidelines are available on the Internet in the RAI User’s j) Care, treatment, and services are provided in an interdisci-
Manual.41 plinary, collaborative manner.
B. RAI timelines41 k) The organization coordinates the care, treatment, and services
1. Initially, upon admission to facility provided to a resident as part of the plan for care, treatment,
2. Quarterly, with each care plan review and services and makes sure that they are consistent with the
3. With each significant change in condition organization’s overall scope of care, treatment, and services.
4. Upon readmission l) Comfort and dignity are optimized during end-of life care.
5. Annually m) The effects of medication(s) on residents are monitored.
C. Care plan41 n) The organization designs infection control programs to
1. Care plans are to be completed within 7 days of completing the reduce the risks of acquired or transmitted infections.
RAI. o) The organization collects data to monitor its performance.
2. Care plans must include measurable objectives and time frames p) The organization provides staff and licensed independent
and describe services that are to be furnished. practitioners in an adequate number and mix that are consis-
3. Care plans are revised on an ongoing basis and reflect changes in tent with the organization’s staffing plan.
residents’ clinical status and care. q) The organization has a complete and accurate clinical record
D. CMS Quality Indicator. The MDS is also used to evaluate the qual- for every individual assessed or treated.
ity of care a facility provides. There are 24 quality indicators r) Clinical record documentation includes at least quarterly
among the numerous clinical assessment entities in the MDS. notations regarding the provision of and response to nutrition
These indicators compose the Facility Quality Indicator Profile. care services.
This profile helps identify possible areas for quality improvement G. State regulations
within a facility.41 1. License and certify LTC facilities.

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2. Validate competencies for personnel involved in resident care. c) Residents enrolled in Medicare Part B can collect allowable
3. Designate nutrition care integration in the patient care plan, docu- charges for parenteral and enteral nutrition.
mentation in the medical record, and transfer of information at dis- C. Medicare Part B reimbursement guidelines for nutrition support
charge to ensure the continuity of nutrition care. 1. Enteral
H. State licensure. All LTC facilities are governed by state licensure, a) Requirements
usually under the health department. State surveyors conduct (1) Permanence of condition (3 months is considered perma-
unannounced annual surveys. The state licensure boards are also nent)
responsible for investigating all complaints that are logged to their (2) Qualifying diagnosis and functional impairment precluding
department about any issue in an LTC facility that involves the oral intake
quality of care, the environment, or staffing issues. The majority of (3) Acceptable calorie, protein, and fluid requirements
state licensure laws are derived from federal regulations. (a) Residents who are stable, healthy, and sedentary should
I. Hazard Analysis Critical Control Points (HACCP).36,43 HACCP is a receive 25 kcal/kg/day. Active residents with comor-
program based on historical data about the causes of food spoilage bidities under active treatment should receive 30 to
and illness. It focuses on a systematic, thorough plan covering step- 35 kcal/kg/day.
by-step operations, procedures, and control measures designed to (b) Suggested protein requirements are 1.0 to 1.5 g/kg/day.
reduce the risk of food-borne disease. When problems are detected, (c) Suggested fluid requirements are 30 to 35 cc/kg/day.
prompt action should be taken to correct them. HACCP points of b) Product justification
concern relevant to enteral nutrition include improper handling, (1) Category 1 (semisynthetic intact protein or protein isolates)
holding, and administration of enteral formulas. or Category 2 (calorie-dense formulas) provides complete
nutrition and is considered appropriate for most residents
without metabolic stress or significant compromises in gas-
IV. Reimbursement trointestinal, pulmonary, renal, liver, or immune function.
A. Medicare. CMS is the federal agency responsible for the administra- Standard products provide 1.0 to 2.0 kcal/mL.
tion of Medicare and Medicaid. Medicare is the health care insurance (2) Specialty products and formulas (Categories 3–6) must be
program for people age 65 or older, some people under age 65 with justified with documentation supporting medical necessity
and evidence that a general-purpose product was used
disabilities, and people with end-stage renal disease. Medicare is
unsuccessfully in the past or the trial of a general-purpose
administered in two parts: Part A (hospitalization) and Part B (med-
product would put the resident’s well-being or survival at
ical insurance). Part B has provisions for parenteral and enteral nutri-
risk.
tion, but nutrition support in LTC facilities is nominally covered as a
(3) Blenderized foods given via an enteral tube are not covered
per diem charge under the prospective payment system using the
by Medicare.
resource utilization groups (RUGs) system. RUGs determines the
c) Equipment and supplies
amount of required care and thus determines (prospectively) the pay-
(1) Gravity or bolus feedings must be tried and cause a docu-
ment required to cover the care of LTC facility residents.
mented complication before a pump is considered med-
1. The MDS determines a resident’s RUG classification.
ically necessary.
2. Tube-fed residents fall into one of two RUGs categories: special
(2) Medicare will not pay for a pump to prevent complica-
care and clinically complex. Parenteral nutrition falls into the tions.
extensive service category. Categories are determined by activity (3) One feeding supply kit corresponding with the method of
of daily living scores and the specific mix of clinical conditions. administration may be issued daily.
3. LTC facilities are reimbursed at a higher rate if they are able to (4) Medicare allows for one gastrostomy or jejunostomy tube
classify residents in the enteral nutrition categories. This fact may or three nasogastric tubes every 90 days.
present a financial gain to facilities that is not entirely justified, 2. Parenteral nutrition
because published evidence on the effectiveness of enteral nutri- a) Permanence of the condition (3 months is considered perma-
tion in LTC populations is poor,44,45 and residents with advanced nent) is a requirement.
dementia receiving enteral nutrition may use less nursing time than b) Parenteral nutrition is covered for a resident with the ability
residents who are fed by hand.46 At least in theory, the DAVE proj- to obtain partial nutrition from oral intake or a combination of
ect monitors LTC facilities’ match between reimbursement and oral/enteral/parenteral intake as long as the following condi-
actual resident acuity. tions are met:
B. Medicaid. Medicaid comprises individual state insurance programs. (1) The resident’s gastrointestinal tract is permanently unre-
Most states include nutrition support reimbursement as part of per sponsive to standard medical management (ie, continuous
diem rates for nursing home care, although beneficiaries must be enteral nutrition via pump is not tolerated).
enrolled in Medicare Part B to receive coverage for nutrition support. (2) The resident is unable to maintain weight and strength (10%
1. The Medicaid per diem reimbursement rate varies among states. weight loss over 3 months and serum albumin <3.4 g/dL).
a) As with the Medicare system, residents are placed in the spe- c) Other requirements
cial care category, which provides higher reimbursement for (1) A range of 20 to 35 kcal/kg/day; a physician must docu-
enteral nutrition. ment caloric requirements outside this range.
b) Not all states use the RUGs classification system; some use (2) The physician must document a medical necessity for pro-
reimbursement schemes that lead to higher payment for enteral tein requirement outside the range of 0.8 to 1.5 g/kg/day;
nutrition (ie, Massachusetts uses “predetermined manage- dextrose concentration less than 10%; or fat emulsion use
ment,” assigning tube-fed residents 135 minutes and hand-fed greater than 15 units of a 20% solution or 30 units of a 10%
residents 45 minutes47). solution per month.

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S E C T I O N V I Site Related and Ethical Issues

(3) There must be documentation of medical necessity for spe- 22. Taffe DR, Thompson J, Butterfield G, Marcus R. Accuracy of equations to
cial parenteral solutions, for instance, essential amino acid predict basal metabolic rate in older women. J Am Diet Assoc. 1995;95:
solutions. 1389–1392.
d) Equipment and supplies 23. Henderson CT, Trumbore LS, Mobarhan S, Benya R, Miles TP. Prolonged
tube feeding in long-term care: nutritional status and clinical outcomes. J Am
(1) Infusion pumps are covered for parenteral nutrition.
Coll Nutr. 1992;11:309–325.
(2) One supply kit and one administration kit is covered each 24. Johnston RE, Chernoff R. Geriatrics. In: Matarese LE, Gottschlich MM,
day parenteral nutrition is administered. eds. Contemporary Nutrition Support Practice. 2nd ed. Philadelphia, PA:
Saunders; 2003:376–383.
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1. US Census Bureau. Statistical Abstract of the United States; 1999. Wash- Older Adults. Chicago, IL: Consultant Dietitians in Health Care Facili-
ington, DC: US Census Bureau; 1999. ties/American Dietetic Association; 2001:117–119.
2. US Department of Health and Human Services. The Characteristics of Long- 26. Mathus-Vliegen EM. Old age, malnutrition, and pressure sores: an ill-fated
Term Care Users. Rockville, MD: Agency for Healthcare Research and Qual- alliance. J Gerontol A Biol Sci Med Sci. 2004;59:355–360.
ity; 2000. 27. American Dietetic Association. Position statement: liberalized diets for
3. Gabrel CS. Characteristics of Elderly Nursing Home Current Residents older adults in long term care. J Am Diet Assoc. 2002;102:1316–1323.
and Discharges: Data from the 1997 National Nursing Home Survey. 28. Delmi M, Rapin CH, Bengoa JM, et al. Dietary supplementation in elderly
Advance Data from Vital and Health Statistics, No 312. Hyattsville, MD: patients with fractured neck of the femur. Lancet. 1990:335:1013–1016.
National Center for Health Statistics; 2000. 29. Breslow RA, Hallfrisch J, Guy DG, et al. The importance of dietary protein
4. National Center for Health Statistics. Health, United States, 2000. in healing pressure ulcers. J Am Geriatr Soc. 1993;41:357–362.
Hyattsville, MD; 2000. 30. Woo J, Ho SC, Mak YT, et al. Nutritional status of elderly patients during
5. Special Committee on Aging, United States Senate. Developments in recovery from chest infection and the role of nutritional supplementation
Aging; 1997 and 1998. Vol 1. Report 106-229. Washington, DC: 2000. assessed by a prospective randomized single blind trial. Age Ageing.
6. A.S.P.E.N. Board of Directors. Guidelines for the use of parenteral and 1994;23:40–48.
enteral nutrition in adults and pediatric patients. J Parenter Enteral Nutr. 31. Wilson MM, Purushothaman R, Morley JE. Effect of liquid dietary supple-
2002;26(suppl):15SA–59SA. ments on energy intake in the elderly. Am J Clin Nutr. 2002;75(5):944–947.
7. Mitchell SL, Kiely DK, Lipsitz LA. The risk factors and impact on survival 32. Morley JE, Silver AJ. Nutritional issues in nursing home care. Ann Intern
of feeding tube placement in nursing home residents with severe cognitive Med. 1995;123:850–858.
impairment. Arch Intern Med. 1997;157(3):327–332. 33. Posthauer ME, Russell C. Ensuring optimal nutrition in long-term care.
8. Mitchell SL, Teno JM, Roy J, et al. Clinical and organizational factors asso- Nutr Clin Pract. 1997;12:247–255.
ciated with feeding tube use among nursing home residents with advanced 34. Peck AP, Cohen CE, Mulvihill MN. Long-term feeding of aged demented
cognitive impairment. JAMA. 2003;290(1):73–80. nursing home patients. J Am Geriatr Soc. 1990;38:1195–1198.
9. Grant MD, Rudberg MA, Brody JA. Gastrostomy placement and mortality 35. Mueller C, Gilbride J, Nestle M. Enteral nutrition support in elderly resi-
among hospitalized Medicare beneficiaries. JAMA. 1998;279(24):1973–1976. dents of long-term care facilities. Controversies and practical solutions. Top
10. Light VL, Siezak FA, Porter JA, Gerson LW, McCord G. Predictive factors Clin Nutr. 2003;18:13–20.
for early mortality after percutaneous endoscopic gastrostomy. Gastrointest 36. Enteral Therapy Policy and Procedure Manual for Assisted Living, Home
Endosc. 1995;42(4):330–335. Care, Nursing Facilities. Alexandria, VA: American Society of Consultant
11. Taylor CA, Larson DE, Ballard DJ, et al. Predictors of outcome after percu- Pharmacists; 1999.
taneous endoscopic gastrostomy: a community-based study. Mayo Clin Proc. 37. Avoiding drug-nutrient interactions in enteral nutrition. Nutrition and the
1992;67(11):1042–1049. M.D. 2003;29:7–8.
12. Morrison RS, Olson E, Mertz K, Meier DE. The inaccessibility of advance 38. Comprehensive Accreditation Manual for Long Term Care. Oakbrook Ter-
directive on transfer from ambulatory to acute care settings. JAMA. 1995; race, IL: JCAHO; 2004.
274:478–482. 39. Dorner B. Diet Manual, A Comprehensive Resource and Guide. Akron,
13. Position of the American Dietetic Association. Ethical and legal issues in OH: Becky Dorner and Associates; 2002:210–217.
nutrition, hydration, and feeding. J Am Diet Assoc. 2002;102:716–726. 40. Ireton-Jones C. Enteral and parenteral nutrition. In: Robinson G, Leif BJ.
14. Consultant Dietitians in Health Care Facilities. Nutrition Management and Nutrition Management and Restorative Dining for Older Adults. Chicago,
Restorative Dining for Older Adults. Chicago, IL: American Dietetic Asso- IL: Consultant Dietitians in Health Care Facilities/American Dietetic Asso-
ciation; 2001:19–20. ciation; 2001:363–388.
15. A.S.P.E.N. Board of Directors. Standards of practice for nutrition support 41. MDS 2.0 RAI User’s Manual. Marblehead, MA: HCPro; 2003.
pharmacists. Nutr Clin Pract. 1999;14:275–281. 42. Data Assessment and Verification Project. June 20, 2003. Available at:
16. A.S.P.E.N. Board of Directors. Standards for nutrition support for adult res- http://www.cms.hss.gov/providers/psc/DAVE/background.asp. Accessed
idents of long-term care facilities. Nutr Clin Pract. 1997;12:284–293. August 26, 2004.
17. Anonymous. Daily dietary fat and total food energy intakes: Third National 43. Dentinger B, Faucher KJ, Ostrom SM, Schmidl MK. Controlling bacterial
Health and Nutrition Examination Survey, phase III: 1988–1991. MMWR. contamination of an enteral formula through use of a unique closed system:
1994;43:116–125. contamination, enteral formulas, system. Nutrition. 1995;11:747–750.
18. Reuban DB, Cheh Al, Harris TB, et al. Peripheral blood markers of inflam- 44. Finucane TE, Christmas C, Travis K. Tube feeding in patients with advanced
mation predict mortality and functional decline in high-functioning com- dementia. A review of the evidence. JAMA. 1999;282:1365–1370.
munity-dwelling older persons. J Am Geriatr Soc. 2002;50:638–644. 45. Gilluk MR. Rethinking the role of tube feeding in patients with advanced
19. Erchler WB, Keller ET. Age-associated increased interleukin-6 gene dementia. N Engl J Med. 2000;342:206–210.
expression, late-life diseases and frailty. Ann Rev Med. 2000;51:245–270. 46. Callahan CM, Buchanan NN, Slump TE. Health care costs associated with
20. Chernoff R. Thirst and fluid requirements. Nutr Rev. 1994;52:S3–S5. percutaneous endoscopic gastrostomy among older adults in a defined com-
21. Harris JA, Benedict FG. A Biometric Study of Basal Metabolism in Man. munity. J Am Geriatric Soc. 2001;49:1525–1529.
Publication No 279. Washington, DC: Carnegie Institute of Washington; 47. Mitchell SL. Financial incentives for placing feeding tubes in nursing home
1919. residents with advanced dementia. J Am Geriatr Soc. 2003;51:129–131.

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 Debra S. Kovacevich, RN, MPH;
Marsha E. Orr, RN, MS
35
Considerations for Home
Nutrition Support

Introduction
D. Adequate professional support must be available to implement ther-
Home nutrition support (HNS) is the provision of nutrients and any nec- apy, provide care, and monitor therapy.
essary adjuvant agents to patients by administration into the intestine or 1. An interdisciplinary approach by qualified health care profes-
stomach or by intravenous infusion for the purpose of improving or sionals is necessary to ensure that all aspects of care are addressed
maintaining a patient’s nutritional status in the home care environment.1 throughout the duration of therapy.
There are few differences between the indications for home and acute a) An interdisciplinary nutrition care plan must be developed.
care specialized nutrition; however, nutritional formulas and solutions, b) Only authorized individuals can prescribe or order nutrition
access devices, administration schedules, and the frequency and inten- therapies.
sity of laboratory and clinical monitoring can differ substantially. Addi- c) Responsibilities for nutrition support functions (preparation,
tionally, home care organizations and hospitals are accredited using storage, distribution, administration, monitoring) must be
distinct standards, so there are different standards of care for home care defined and assigned to appropriate individuals.
and hospital services. Ideally, the concept of the nutrition support team— 2. There must be appropriate involvement of patients, family mem-
interdisciplinary collaboration among nurses, pharmacists, physicians, bers, caregivers, clergy, and others in decisions about nutrition sup-
and dietitians—endures in both settings. The goal of care is to provide port, which may include initiating, continuing, withholding, or
individualized, compassionate, appropriate, cost-effective, safe, and withdrawing nutrition support.
effective HNS. 3. The home environment must allow for safe storage, preparation,
and administration of therapy.
I. Identification of Candidates for HNS a) Storage areas must be available to protect the equipment and
II. Formulating a Discharge Plan solutions from damage and contamination; they must be located
III. Coordination of the Referral for HNS out of the reach of children and pets.
IV. Educating and Training Patients and Caregivers b) A clean environment is required for preparing solutions and
V. Reimbursement for HNS equipment.
VI. HNS Outcomes 4. A home infusion provider for nutrition and medical products,
VII. Accreditation of Home Care and HNS services, and other necessary supplies must be available.2
References a) The provider must prepare, deliver, and store nutrient solutions
under proper conditions in a safe, accurate, and timely manner.
Suggested Readings
b) Changes in nutrition support must be accommodated in a timely
manner.
I. Identification of Candidates for HNS. c) Ongoing monitoring of the patient for is required safety, effec-
tiveness, and appropriateness of nutrition support.
Patients should be thoroughly evaluated prior to the initiation of HNS
therapy to ensure the best possible outcome.
A. Candidates include patients who are unable to maintain nutritional II. Formulation of a Discharge Plan.
status by oral intake alone. Prior to the initiation of home therapy, an interdisciplinary team should
B. The patient’s medical condition must be stable enough to allow for develop and document a comprehensive plan for nutrition support. A
safe discharge to an alternative care site (ie, nursing home, interme- thorough reassessment must be undertaken of the nutrition support plan,
diate care facility, infusion center, or home). because patients’needs and requirements will change as they move from
C. Patients and caregivers should understand and accept the risks and hospital to home. All the patients’ home care needs have to be addressed
responsibilities for home nutrition therapy. by including relevant health care professionals prior to hospital dis-
1. Patients and caregivers should understand the following: charge. Often, it is more difficult to initiate services once the patient is
a) The rationale for and the risks, benefits, and responsibilities home; this may result in delays of needed services such as physical ther-
of HNS apy and social work.
b) Therapeutic expectations, including immediate and long-term A. Definition of the individual’s nutrition goals
goals, and the anticipated length of therapy 1. Short- and long-term goals need to be developed with the patient,
c) The cost of therapy, insurance coverage, and the patients’ and the caregivers, and health care professionals involved in the care
caregivers’ financial responsibilities of the patient.
2. Patients and caregivers should be willing and able to perform HNS 2. The duration of therapy anticipated must be discussed with the
procedures and agree to the therapy. patient and caregivers.

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S E C T I O N V I Site Related and Ethical Issues

B. Development of a patient-specific nutrient prescription and nasopharyngeal ulcers. Additionally, they are uncomfort-
1. Calculate macronutrient requirements to meet nutritional goals. able and less stable, must be regularly replaced, and are prone
a) Determine the desired proportion of calories from carbohy- to clogging.
drates, protein, and fat. d) To the extent possible, patients should be involved in the deci-
b) Address the need for specialized formulas. sion about the type of enteral access device selected.
c) Adjust the nutrient prescription for impairments in organ func- (1) Nasally placed tubes add psychosocial stress but may be
tion (eg, reduced amount of protein for renal failure). needed initially to demonstrate tube feeding tolerance.
2. Determine the amounts of vitamins, trace elements, and minerals These types of feeding tubes should be replaced as soon as
to be added to the nutrition formulation. Patients who received possible.
less than daily infusions of parenteral or enteral solutions or who (2) Low-profile devices placed through a mature gastrostomy
are transitioning to an oral diet may need supplemental oral vita- are less obtrusive than gastrostomy tubes and should be
mins and minerals to meet recommended dietary reference considered.
intakes. (3) Preplacement markings for gastric and jejunostomy tubes
3. Calculate the patient’s total daily fluid needs, including losses allow for self-care and may decrease complications.4
from the gastrointestinal (GI) tract. 2. Parenteral access should be in a ___location that is visible and easy for
4. Order appropriate levels of electrolytes to maintain normal serum the patient and caregivers to reach to connect or disconnect intra-
concentrations. The prescription must be appropriate for organ venous tubing, change dressings, and observe for signs and symp-
dysfunction or large GI losses. toms of infection.
5. Evaluate serum glucose levels to determine the need for insulin or a) Standard long-term central venous access devices include
adjustment in the nutrients provided. Instruct patients and care- implanted and tunneled catheters.
givers on how to monitor glucose levels and adjust insulin dosages b) Peripherally inserted central catheters (PICCs) are generally
to maintain acceptable levels. used for intermediate-term therapy.
C. Selection of the appropriate route of administration for parenteral c) The tip of central venous access catheters should be located in
and enteral nutrition the superior vena cava adjacent to the right atrium.5
1. The parenteral route should be used only when the GI tract does d) Peripheral catheters <8 inches in length should not be used in
not allow adequate absorption or transport of sufficient nutrients to the home care setting for the administration of parenteral nutri-
maintain appropriate weight or growth and to support life. tion due to the increase risk of phlebitis and infiltration.
2. The enteral route is indicated in patients with a functional GI tract e) Peripheral catheters (midlines) are used for short-term therapy
who are malnourished or are at risk for malnutrition from not eat- (<7 days) and when the final dextrose concentration of the solu-
ing and in whom oral feedings are inadequate to maintain nutrition tion/emulsion is less than 10% and/or the final osmolarity is less
status. It is also indicated in patients who will not, should not, or than 900 mOsm.5
cannot eat adequately to maintain their nutrient stores.3 f ) To the extent possible, patients should be involved in the deci-
D. Selection of the appropriate access device to allow for safe adminis- sion about the type of central venous access device selected.
tration of specialized nutrition in the home setting. The patient should (1) The type of catheter required should be based on the length
be involved in selecting the type of access device, including its loca- of therapy, the frequency of infusions, and caregiver/patient
tion. If two access locations will provide equally acceptable access, ability.
the patient should be allowed to choose between them. (2) Central venous access devices are available with single,
1. Enteral access should be placed in a ___location accessible to the double, or triple lumens. Many patients may require mul-
patient and caregivers so that they can connect or disconnect tiple intravenous infusions for therapies such as antibiotics
tubing, change dressings, and observe for signs and symptoms or chemotherapy. Catheters with the smallest number of
of infection. The device should be properly secured to prevent lumens that can still meet all the intravenous therapy needs
inadvertent dislodgment. The site for the enteral route may be the of the patient and medication dosing intervals should be
stomach or the small intestine. Feeding into the stomach (eg, naso- used to minimize the risk of infection and decrease time
gastric, gastrostomy access) is the preferred route and is indi- and cost for catheter care.
cated when there is impairment in the ability to swallow or (3) Advantages and disadvantages of each type of catheter
obstruction between the mouth and stomach and the patient is not should be thoroughly discussed with the patient.
at increased risk for aspiration. Feeding into the small intestine (a) Implanted ports may be desirable for cosmetic rea-
(eg, nasointestinal, jejunostomy access) is indicated when there sons or for patients who are frequently on and off
is delayed gastric emptying, an obstructive upper-intestinal-tract therapy. Adolescents may prefer an implanted port,
tumor, other severe disease, or an increased risk of aspiration. as it is not visible to their peers once the needle is
a) Long-term enteral access devices include gastrostomy tubes, removed. The port is ideal for individuals who swim,
percutaneous endoscopic gastrostomy tubes, jejunostomy as the needle may be removed prior to going into the
tubes, low-profile gastrostomy and jejunostomy devices, and pool. Many individuals do not prefer an implanted
combined gastric decompression and jejunostomy feeding port due to the weekly or daily needle stick and risk
tubes. of extravasation. Some patients apply a topical anes-
b) Low-profile or skin-level enteral feeding devices are used more thetic 30 to 60 minutes prior to needle insertion to
frequently in home care for the very old (eg, a confused geri- decrease the pain.
atric patient) or the very young (eg, an active pediatric patient). (b) PICCs may not be suitable for patients who need to
c) Nasointestinal or nasojejunal tubes are not frequently used in change their own dressing due to a lack of visiting nurse
home care because they are irritating, leading to sinusitis, oti- services. An extension tube usually needs to be added
tis, hoarseness, vocal cord paralysis, nasal septum necrosis, so the patient can flush and connect parenteral nutrition

372 A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. © 2005 A.S.P.E.N. www.nutritioncare.org.
 S E C T I O N V I Site Related and Ethical Issues

solutions. Whenever possible, the patient’s nondomi- g) It is possible to do frequent laboratory monitoring during
nant arm should be used for catheter insertion. advancement of the home formula’s dextrose concentration
E. Development of a schedule for the infusion of parenteral and/or and total volume, and the laboratory monitoring includes elec-
enteral nutrition therapy that takes into account the patient’s nutri- trolytes, calcium, phosphorus, magnesium, and glucose.
tional and fluid needs and lifestyle h) The patient’s insurance provider covers visiting nurse services
1. The infusion schedule must be appropriate for the therapy and to assist with monitoring and education.
manageable for the patient and caregivers. i) The home care nurses and pharmacists carefully assess the
2. “Cycled” infusions are typically administered at night to allow patient for potential adverse reactions no less than daily during
for independence during the day. home initiation of parenteral nutrition.
3. Cycling of infusions should be started prior to discharge to assess F. Establishment of appropriate preparation and administration tech-
patient tolerance. It is preferable for the goal infusion rate to be niques for the patient and caregivers
achieved prior to discharge. Goal infusion rates are usually 10 to 1. Home parenteral nutrition is prepared in the infusion pharmacy
12 hours per night based on the amount of dextrose in the solu- under a laminar flow hood using appropriate sterile compound-
tion, glucose levels, and fluid tolerance. To avoid hyperglycemic ing processes (US Pharmacopeia).8 Home additives are limited
episodes and minimize the use of insulin, the dextrose infusion to pharmaceuticals, such as multivitamins, that lose potency once
rate should be calculated at the peak rate of infusion and not exposed to light or are unstable for the standard length of storage
exceed 14 mg/kg/min in pediatrics, 17 mg/kg/min in infants, and of home parenteral nutrition solutions/emulsions.
12 mg/kg/min in adults. a) Home additives to parenteral solutions typically include mul-
4. Infants, children, and adults with glucose intolerance may not be tivitamins, H2 blockers, and insulin. The compatibility of all
able to be cycled or off therapy for long periods. Cycle schedules additives must be verified by a pharmacist before the additive
should be decreased by 1 to 2 hours per day. is administered at home.
5. It may not be necessary to taper parenteral nutrition solutions up b) Commercially prepared home enteral solutions are preferable
and down based on the amount of dextrose in the solution. How- to powdered solutions that must be reconstituted in the home
ever, because ambulatory infusion devices can gradually increase setting.
and decrease the solution without the patient having to reprogram c) Home additives to enteral solutions may include modular nutri-
the pump on a nightly basis, it is prudent to use a tapering sched- ents, water, or selected medications. Clean technique must be
ule. Usual taper-up and taper-down times are 1 or 2 hours. Taper- used to prepare enteral solutions in the home.
ing may be particularly important for pediatric patients. d) Home parenteral solutions must be maintained at appropriate
6. The acceptable range for glucose levels has not been determined temperature during transport to the patient’s home. Patients
in the home care population. However, research in other settings and caregivers must be taught the proper storage and temper-
suggests that levels should be maintained at <110 mg/dL.6 For dia- ature conditions for keeping parenteral nutrition in the home.
betics, the goal should be attaining a glucose level between 100 e) Parenteral nutrition solutions should be labeled with instruc-
and 200 mg/dL while minimizing the incidence of hypoglycemia.7 tions for use and beyond-use dating (see Chapter 7 for specific
7. In some carefully selected circumstances, determined by the labeling recommendations).
physician, the patient and caregivers, and the home care organi- f ) Enteral nutrition formulas must be stored and maintained in
zation, parenteral nutrition may be initiated in the home (started, an area that does not exceed the manufacturer’s recommended
advanced, and cycled without being administered in the hospital temperature ranges for storage (avoiding excessive heat or
prior to discharge). This option should be considered only when freezing).
an assessment confirms that the benefits greatly outweigh the g) Once cans or containers of enteral nutrition formulas are opened
risks.1 General criteria for home initiation include but are not lim- in the home, the remaining formula should be used within 24 to
ited to the following: 48 hours according to manufacturer’s recommendations.
a) The patient is clinically stable. High-risk patients who may not h) Patients and caregivers should be taught to carefully examine
be candidates include patients at risk for refeeding syndrome; containers/bags of parenteral and enteral nutrition for evi-
infants; intravenous drug abusers; and patients with poorly con- dence of damage, leaks, discoloration, odor, separation, con-
trolled diabetes, fluid and electrolyte disorders, and major organ tamination, or beyond-use dating.
failure.1 Patients with these conditions may require more fre- 2. Techniques for administering enteral and parenteral therapy must
quent monitoring than can be accomplished in the home. be appropriate and safe.
b) The patient and caregivers have previous experience with par- a) An infusion pump must be used to administer parenteral nutri-
enteral nutrition or infusion therapy. tion solutions. Volumetric or peristaltic pumps with free flow
c) The patient and caregivers learn readily and are willing and protection are recommended for administration of parenteral
able to perform the additional monitoring to ensure the safety nutrition.
of home initiation. b) Enteral feeding into the small intestine is best tolerated when
d) The patient and caregivers are able to recognize complica- infused slowly via enteral pump. Pump-assisted feedings may
tions of therapy and how to troubleshoot or notify medical be administered continuously or cycled over a shorter time
personnel. according to patient tolerance. Gastric feedings may be deliv-
e) The patient is able to receive a home formula in which the ered by pump, by gravity drip, or by using a syringe and admin-
dextrose concentration is gradually increased over several istering each feeding over 30 to 60 minutes or according to
days (typically starting with 150–200 g/day and increasing by patient tolerance.
no more than 100 g/day to the final concentration). 3. The home care organization must have a process for routine main-
f ) The patient’s blood sugar is carefully monitored by capillary tenance and for emergency repair and replacement of infusion
blood testing or serum glucose levels drawn no less than daily. equipment. It may be necessary to have a replacement infusion

© 2005 A.S.P.E.N. www.nutritioncare.org. A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. 373
S E C T I O N V I Site Related and Ethical Issues

pump available in the home if the patient is unable to tolerate bleeding, or inability to administer solutions. The patient and care-
being off the infusion until a delivery can be made. givers should be taught parameters to report adverse effects to the
4. A plan for the care, repair, or replacement of the enteral or par- appropriate member of the health care team.
enteral access device should be developed as part of the home care H. The goals and progress toward them should be regularly evaluated.
plan or as part of the home care organization’s policies and proce- As feasible, the patient is transitioned from one feeding modality to
dures to address the following: another to promote progression toward an enteral or oral diet, with
a) Procedures for emergency repairs and replacement of the the goal to discontinue nutrition support if possible.
access device 1. Calorie counts should be obtained prior to tapering enteral or par-
b) Procedures for preventing and managing occlusion enteral therapy to an oral diet or when transitioning to enteral
c) Procedures for site care and dressing changes to prevent from parenteral nutrition.
infections 2. Nutrition infusions may be tapered in a variety of ways. Patients
G. An interdisciplinary plan for monitoring home nutrition therapy who are able to maintain their hydration status may wish to
should be established to ensure positive nutritional, psychological, decrease the number of infusions per week to give themselves a
and metabolic outcomes.9 Through monitoring, the incidence of com- “holiday.” Another method may be to begin decreasing the total
plications can be minimized and the nutritional status of the patient amount of calories provided per day by enteral or parenteral nutri-
can be optimized. tion. Patients should be instructed to take an oral multivitamin with
1. Specific monitoring parameters and the frequency of monitoring minerals during the transition phase.
depend on the therapy, the severity of illness, and the presence of 3. Enteral or parenteral nutrition should not be discontinued until at
diseases that require more frequent monitoring. least 75% of the patient’s nutritional requirements have been
2. In addition to monitoring nutritional parameters, mechanical, obtained via the alternate source, tolerance has been demonstrated,
infectious, metabolic, GI, hepatic, renal, bone, and growth indices and the patient is either gaining or maintaining weight according
in children should be followed at established intervals. to goals.
a) Vitamin and mineral studies should be obtained for patients 4. Children on parenteral and/or enteral nutrition may display an
on long-term therapy. oral aversion to food and may require behavioral interventions.
b) The use of long-term (home) parenteral nutrition has been asso- I. For patients who will receive lifetime therapy, goals and outcomes
ciated with the development of metabolic bone disease (MBD). may focus on maintaining an adequate nutritional status. For children,
Usually asymptomatic, bone pain and fracture may occur goals and outcomes may focus on adequate growth and development.
with minimal trauma. Elevated urinary calcium and increases
in serum concentrations of calcium, phosphorus, and alkaline
III. Coordination of the Referral for HNS.
phosphatase may be present. Osteoporosis and osteomalacia
have both been linked to parenteral nutrition-associated MBD. Safe and effective HNS requires a comprehensive, well-executed,
The causes of MBD are poorly understood and include MBD interdisciplinary discharge plan that includes the patient’s physician,
predating parenteral nutrition (such as can occur with inflam- the hospital health care team, the home care team, and the patient, and
matory bowel disease), excess dietary protein, aluminum family/caregivers. The plan should be developed before discharge.
contamination (of parenteral solutions), metabolic acidosis A. Selection of a home care provider may depend upon contractual
(associated with amino acid metabolism), and abnormalities in agreements between the patient’s insurance provider and home care
vitamin D metabolism (associated with parenteral nutrition).10 agencies. However, hospital staff that has the responsibility for dis-
Recently, a group of investigators noted that the current inci- charge planning must ensure that the home care provider is able to
dence of MBD in patients receiving long-term parenteral nutri- safely provide HNS services. Markers of high-quality agencies
tion is not significantly larger than the incidence in sex-matched include the following:
healthy subjects. Furthermore, MBD is probably related pri- 1. Accreditation by a national accreditation body, such as the Joint
marily to the underlying reason for which parenteral nutrition Commission for Accreditation of Healthcare Organizations
was indicated.11 (JCAHO), the Accreditation Commission for Healthcare (ACHC),
c) Laboratory monitoring for home enteral nutrition patients is or the Community Health Accreditation Program (CHAP)
poorly described and is not perceived to be as important as for 2. Staff who have expertise in specialized nutrition as evidenced by
home parenteral nutrition patients. However, laboratory tests national certification or documented experience, competency,
of electrolytes, renal function, glucose, calcium, magnesium, and continuing education about HNS
phosphorus, and albumin should be done, especially during 3. Specific protocols, pathways, or procedures for HNS
times of tube feeding intolerance. 4. Adherence to standards of practice developed by national and
3. The patient and caregivers should be included in the develop- state organizations
ment of the plan for monitoring, including frequency of nursing 5. Twenty-four-hour availability of services
visits, laboratory work, and office visits. Appropriate transporta- B. The hospital team and the home care provider must work collabora-
tion must be available (or arranged). tively to ensure that the patient is adequately prepared for discharge.
4. The patient and caregivers must be able and willing to take an Discharge planning includes
active role in monitoring the patient’s response to nutrition ther- 1. Supplies and equipment determined, ordered, and delivered to
apy. Monitoring may include intake (oral, tube, parenteral); out- the patient’s home
put, when indicated (urine, stool, and other body fluids); body 2. Development and documentation of an administration schedule,
weight; temperature; medication (type, amount, and timing); blood nutrient prescription, type of infusion pump, additional medica-
glucose (if needed); and changes in the appearance or function of tions, and materials for access site care
the access site, unusual sensations during or after administration of 3. Development and documentation of goals of care, frequency
the nutrition formula, pain (new, increased intensity, changed), of monitoring, methods of communication between the hospi-

374 A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. © 2005 A.S.P.E.N. www.nutritioncare.org.
 S E C T I O N V I Site Related and Ethical Issues

tal team and all members of the home care team, and physician 1. Intolerance to the therapy, such as GI or metabolic therapy, and
follow-up intolerance resulting from the disease process or from drug-
4. Definition of nursing services prior to discharge, including the fre- nutrient interactions
quency of visits, monitoring guidelines, and required blood work 2. Mechanical complications such as catheter or tube occlusion,
leakage, breakage, or dislodgment and equipment malfunction or
breakage
IV. Education and Training of Patients 3. Localized (access site) or systemic infection
and Caregivers 4. Relevant drug-drug, drug-nutrient, and nutrient-nutrient interac-
The goals of education are to provide the patient and caregivers with tions; side effects; infusion solution or formula stability issues; and
knowledge and skills that facilitate appropriate involvement in self-care, precipitation
decision making, and successful outcomes for nutrition support. Train- 5. Monitoring parameters should be given to the patient/caregiver so
ing should be well designed and individualized to meet learning needs. they know when and whom to contact should complications occur.
A. Education is individualized and provided by an interdisciplinary E. The patient and caregivers should receive education about the need
staff in a coordinated and consistent fashion. for medical services to evaluate the ongoing effectiveness of HNS.
1. Training should be individualized according to the patient’s and 1. In-home evaluation by home health professionals as needed.
caregivers’ assessed needs, abilities, and readiness to learn. 2. Routine (and nonroutine) physician evaluation.
2. Training should be provided by qualified interdisciplinary staff 3. The patient and caregivers(s) should receive periodic reassess-
who have appropriate education, specialized training, and expe- ment and retraining as needed.
rience in HNS. 4. The patient can be discharged when services are no longer required
3. There must be written policies and procedures coordinating the or when services can no longer be provided safely in the home or
education process so that information provided to the patient and by the home care provider.
caregivers is consistent.
4. Educational materials (written information or other educational V. Reimbursement for HNS
devices) should be provided.
5. Ongoing patient and caregiver training should be provided during A. HNS is covered by federal (Medicare) and state (Medicaid) health
care. care programs when specific criteria are met.15,16
a) Ongoing education has been shown to have a positive impact 1. Parenteral nutrition is covered under the prosthetic device act of
Medicare, which requires an “artificial gut” (intravenous deliv-
upon patient outcomes, specifically catheter-related infec-
ery) and “permanency” (at least 90 days of therapy). The patient
tion.12–14
must have documented evidence of inability to tolerate feeding
b) Patients and families often display deterioration of sterile
through the enteral route (malabsorption, obstruction, resection,
technique over time, and reeducation sessions help to improve
maldigestion).
compliance.
a) There is less than 5 feet of small bowel beyond the ligament
6. Education interventions ideally address the emotional response
of Treitz.
to specialized nutrition support.12
b) GI losses exceed 50% of an oral intake of 2.5 to 3 L/day, and
B. The patient and caregivers need to receive education and demon-
urine output is less than 1 L/day.
strate competence in preparing and administering nutrients.
c) Bowel rest is required for at least 90 days, and 20 to 35 kcal/
1. Parenteral nutrition patients and their caregivers must receive kg/day is prescribed for a patient with specified conditions.
training and demonstrate competence in storage and inspection d) Many other aspects of parenteral nutrition require specific jus-
of solutions and containers, response to beyond-use dating, asep- tification, such as calorie levels <20 kcal/day or >35 kcal/day,
tic procedures for solution admixing and administration, issues protein >1.5 g/day or <0.8 g/day, and lipids >15 units of 20%
of compatibility/stability of solutions, an infusion method/sched- or >30 units of 10% per month. When these criteria are not
ule, use and maintenance of equipment, and disposal of used adequately documented, payment is denied or delayed.
equipment. 2. Enteral nutrition is also covered under the prosthetic device act,
2. Enteral nutrition patients and their caregivers need to receive where the enteral feeding tube becomes the “artificial gut” and the
training and demonstrate competence in storage and inspection permanency requirement must still be met. The patient must have
of formula, response to expiration dates, clean technique for for- disease of the small intestine such that digestion or absorption of
mula preparation and administration, issues of stability, product an oral diet is insufficient to maintain weight and strength.
hang time, infusion method/schedule, cleaning and reuse of sup- 3. Documentation must include information about why the patient’s
plies, use and maintenance of equipment, and disposal of used needs cannot be met by oral nutrition. Enteral nutrition formulas
equipment and supplies. are divided into specific “categories.” Aside from the standard for-
C. The patient and caregivers must receive education and demonstrate mulas in Category I, formulas in all other categories require spe-
competence in access care. The patient and caregivers must receive cific documentation to support their use.
training and demonstrate competence in aseptic technique for par- a) B4150; Category I: semisynthetic intact protein/protein isolates
enteral access and clean technique for enteral access to maintain the b) B4151; Category I: natural intact protein/protein isolates
access device and its site, infection prevention, connecting and dis- c) B4152; Category II: intact protein/protein isolates (calorically
connecting to and from the access device, medication administration, dense)
and postinfusion flushing to prevent obstruction. d) B4153; Category III: hydrolyzed protein/amino acids
D. The patient and caregivers must receive education and demon- e) B4154; Category IV: defined formula for special metabolic need
strate competence in recognition of and appropriate response to f ) B4155; Category V: modular components
complications. g) B4156; Category VI: standardized nutrients

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S E C T I O N V I Site Related and Ethical Issues

B. State-funded programs (Medicaid, Medi-Cal, TennCare) develop 6. Quality of life tends to be poorer in patients who are elderly, sin-
state-specific criteria for coverage of specialized nutrition. Because gle, poor, or unemployed; those addicted to narcotics; and those
these plans vary widely, they are not covered in detail here. who are early in their therapy.
C. Managed care and private insurance coverage of specialized nutri- 7. Affiliation with a national support group significantly increases
tion also varies widely. Often, managed care plans “contract” with quality of life, lowers depression scores, and lowers the incidence
home care providers for therapy-specific or per diem rates that may of catheter-related infections.32,33 The major national support
include supplies, pharmacy services, and nursing services. Other organization for home nutrition patients is the Oley Foundation
plans use Medicare criteria for coverage. (www.oley.org). Local chapters are available in many regions of
D. A major concern with long-term HNS is exceeding the lifetime max- the United States. Its purpose is to enrich the quality of life and
imum for insurance coverage. This is a special concern for infants and functional status of persons requiring HNS therapies, build a
young children who are expected to require HNS for extended peri- “community” among those facing a lifetime of nutrition support,
ods of time or their lifetimes. improve the quality of life for families challenged with this ther-
apy, and promote the availability of information and opportunities
for home parenteral and enteral nutrition families.
VI. HNS Outcomes. F. The most common complications of home parenteral nutrition are
For patients, their caregivers, health care professionals, and health care 1. Catheter-related infection and sepsis
payers, it is critical to determine the outcomes and psychosocial impli- 2. Fluid and electrolyte disturbances
cations of such an expensive therapy. The study of health-related qual- 3. Liver or bone disease
ity of life in the fields of home enteral and parenteral nutrition is still G. Most deaths during home parenteral and enteral treatment are from
the underlying disease.34,35
in its infancy. Yet it is an important aspect of providing care to enhance
H. Outcome data on home enteral nutrition patients are very limited, and
patient experiences.
outcomes may be due to the patient’s underlying disease state. Com-
A. Currently, there is no national outcome reporting system specifically
mon disease groups include patients with neurological dysfunction,
for HNS. Most home care organizations incorporate outcome meas-
upper GI cancers, anorexia, failure to thrive, swallowing disorders,
ures into their quality improvement processes; however, these data
cerebrovascular accidents, and neuromuscular disorders.
are proprietary. Although Medicare has incorporated outcome meas-
1. At 1 year, between 45% and 60% of patients with varying dis-
urements for home care through its OASIS system, parenteral and eases had died. The actual number of patients who were able to
enteral nutrition has not been reported separately. transition to oral intake ranged between 19% and 30%.
B. Data compiled by the former Health Care Financing Administration 2. Quality of life scores are lower in home enteral nutrition patients
(now Centers for Medicare and Medicaid Services) and Blue Cross/ than the normal control group, which may be due to significant
Blue Shield of South Carolina during 1986 to 1993, and the North medical disabilities in the home enteral nutrition group.36
American HPEN Patient Registry (no longer active), was used to pro- 3. Children on home enteral nutrition are able to gain weight, increase
vide HNS outcome reports during the late 1990s.17–19 muscle strength, and increase overall muscle mass.37,38
C. Other outcome data have been reported from programs in large I. The most common complications of home enteral nutrition are
medical centers.20,21 1. GI complications
D. During the past decade, outcome reports from outside the United 2. Tube displacement, occlusions, or leaking
States have been published.22–25 3. Dehydration
E. Outcome reports for specific age-related or disease-related cohorts,
such as children, patients with AIDS, and patients with cancer, have VII. Accreditation of Home Care and HNS.
also been published.26–29 Factors influencing patient outcome on
home parenteral nutrition include the following: Accreditation by national organizations provides an organization with
1. Patients with Crohn’s disease, ischemic bowel, or a congenital dis- an objective performance evaluation of its customer care, measured
order have an 87%, 84%, and 80% 3-year survival, respectively. against national standards. It may also serve to meet certain Medicare
Patients with motility disorder (pseudo-obstruction), radiation certification requirements, expedite third-party payments, and favor-
enteritis, or chronic adhesive disease have a 62%, 58%, and 40% ably influence managed care contract decisions.
3-year survival, respectively. Patients with advanced cancer usu- A. Three organizations currently provide accreditation for home care
ally do not survive past 4 months, with only 20% surviving their organizations:
first year on home parenteral nutrition.30 1. JCAHO
2. Bowel anatomy may influence survival. Patients with bowel 2. ACHC
obstruction on home parenteral nutrition have a risk of death 2.5 3. CHAP
times higher than that of non obstructed patients.31 Permanent B. Each organization has developed standards against which the home
intestinal failure is likely if the small bowel is <100 cm in adults care agency is measured. Although the standards differ, all three
and <50 cm in children. The presence of in-continuity of terminal organizations examine areas such as staff education and compe-
ileum or colon enhances weaning off home parenteral nutrition and tency, patient safety, infection control, quality improvement, com-
survival. pliance with law and regulation, confidentiality and privacy, fiscal
3. The mortality rate of Crohn’s patients is significantly lower in management, equipment management, and quality of care.
large programs than in small programs. (Home care material from the 1st edition was contributed by Jennifer
4. Patients dependent on opiates and sedatives have increased sep- K. Nelson, Jay Mirtallo, and Nancy J. Evans-Stoner)
sis rates and require more hospital admissions.28
5. Quality of life tends to be higher in younger patients, long-term REFERENCES
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2001. Available at: http://www.cms.hhs.gov/suppliers/dmepos/default.asp J Pediatr. 1994;124:244–248.
Accessed August 19,2004. 38. Kang A, Zamera SA, Scott B, et al. Catch-up growth in children treated
16. DMERC Region D Supplier Manual, ENT (L11568) Enteral Nutrition, 2002. with home enteral nutrition. Pediatrics. 1998;102:951–955.
Available at http:www.cms.hhs.gov/manuals/14_car/3b3300.asp Accessed
December 28, 2004. SUGGESTED READINGS
17. Howard L, Ament M, Fleming CR, Shike M, Steiger E. Current use and Candusso M, Faraguna D, Sperli D, et al. Outcome and quality of life in paedi-
clinical outcome of home parenteral and enteral nutrition therapies in the atric home parenteral nutrition. Curr Opin Clin Nutr Metab Care. 2002;5:
United States. Gastroenterology. 1995;109:355–365. 309–314.
18. Williams DM. The current state of home nutrition support in the United Davis JH. Total parenteral nutrition (TPN) at home: prototype high-tech home
States. Nutrition. 1998;14:416–419. care nursing. Gastroenterol Nurs. 1996;19:207–209.
19. Howard L, Malone M. Clinical outcome of geriatric patients in the United Goff K. Cost and cost-benefit of enteral nutrition. Gastrointest Endosc Clin
States receiving home parenteral and enteral nutrition. Am J Clin Nutr. North Am. 1998;8:733–744.
1997;99:1364–1370. Jeppesen PB, Langholz E, Mortensen PB. Quality of life in patients receiving
20. Scolapio JS, Fleming CR, Kelly DG, et al. Survival of home parenteral nutri- home parenteral nutrition. Gut. 1999;44:844–852.
tion-treated patients: 20 years of experience at the Mayo Clinic. Mayo Clin Moreno Villares JM. The practice of home artificial nutrition in Europe. Nutr
Proc. 1999;74:217–222. Hosp. 2004;19:59–67.
21. Knafelz D, Bambarara M, Diamanit A, et al. Complications of home par- Pironi L, Paganelli F, Mosconi P, et al. The SF-36 instrument for the follow-up
enteral nutrition in a large pediatric series. Transplant Proc. 2003;35: of health-related quality-of-life assessment of patients undergoing home
3050–3051. parenteral nutrition for benign disease. Transplant Proc. 2004;3:255–258.
22. Ksiazyk J, Lyszkowska M, Kierkus J, et al. Home parenteral nutrition in Reimund JM, Duclos B, Cuby C, et al. Home parenteral nutrition: clinical and
children: the Polish experience. J Pediatr Gastroenterol Nutr. 1999;28: laboratory analysis of initial experience (1994–1997). Ann Nutr Metab.
152–156. 1999;43:329–338.

© 2005 A.S.P.E.N. www.nutritioncare.org. A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. 377
 Julie O’Sullivan Maillet, PhD, RD, FADA

36
Ethics

Introduction II. Ethical Issues in Patient Care

The purpose of this chapter is to provide guidance to clinicians in ethi- A. Within American bioethics, the patient’s right to self-determination
cal issues that are relevant to nutrition support. Ethics are defined and is the guiding principle.
placed in the context of patient care. Significant legal decisions are dis- 1. Patients and families face a difficult process when ethical issues
cussed, as are specific attributes of patients that influence their care, such supersede medical issues. The health care team should help the
as clinical status, stage of life, cultural tradition, and religion. Finally, patient and family understand their options.
practical considerations for ethical deliberations related to nutrition sup- 2. Food and fluids are essential for life. There are strong cultural and
port are offered. philosophical issues that distinguish feeding issues from other
medical care issues.
I. Background
B. Patients need to be informed and deemed competent when they make
II. Ethical Issues in Patient Care
their treatment choices. Competence is having an adequate decision-
III. Key Legal and Regulatory Decisions Influencing Patient Care and
making capacity. Generally, a patient is considered to be able to make
Feeding
an informed decision if he or she responds appropriately, the decision
IV. Ethical Issues Regarding Feeding Patients
is authentic, and the decision is voluntary.
V. Key Considerations to Frame Ethical Deliberations
1. Advance directives can aid in explaining the patients’wishes. The
References
two most common forms of advance directives are the living will
I. Background and durable power of attorney (see Section III.D).
2. Substitute decision makers may serve for the patient in some states
A. Ethics is the study of morals. when the patient cannot make a decision.
1. Ethics are standards of conduct or codes of conduct. C. Generally, the individual’s right takes precedence over the health
2. Ethics is the part of philosophy that deals with morals. care providers’ view, with the following exceptions:
3. Morality defines how people ought to behave toward one another. 1. Providers have the right to determine the medical futility of a treat-
4. The goal of moral behavior is to protect the values cherished by ment and need not offer or provide a futile treatment.
society. 2. When the individual’s view is unknown, a surrogate decision
5. The values include quality of life, liberty, and freedom. maker is consulted. When the surrogate decision maker disagrees
6. Ethical dilemmas occur when ethical principles conflict. with the provider, the court generally supports feeding.
7. Conflicts are often between two rights or between a right and a D. Distinguishing between obligatory and optional patient care involves
duty. For example, the individual has the right to choose, and examining the positive and negative consequences of the action.
society has the duty to protect individuals. 1. Will the action prolong life or prolong death?
B. Ethical principles of autonomy, beneficence, nonmaleficence, and 2. Will the action provide comfort or prolong suffering?
justice apply to all health professionals. 3. How will the action provide a benefit and/or burden to the patient?
1. Autonomy is the right of individuals to make their own decisions. E. The use of an ethics team for consultation is highly encouraged in
2. Beneficence is doing the right thing for the patient. complex decision-making situations.
3. Nonmaleficence is doing no harm ; it is balancing helping the
1. The complexity and irreversibly of stopping feeding mandates
patient through care as opposed to hurting them.
that the health care team, the patient, and the family participate in
4. Justice is acting fairly—providing similar treatment to patients
decisions.
in similar situations.
2. If disagreement occurs, ethics committees or consultants should
C. There are three major ethical theories represented by three philoso-
be contacted.
phers: the utilitarian view (Mills), the deontological view (Kant), and
the virtues view (Aristotle).
1. The utilitarian view is that ethical decisions are a balance of posi- III. Key Legal and Regulatory Decisions Influencing
tive values over negative values for all involved, so consequences Patient Care and Feeding
matter.
2. The deontological view is that acts can be inherently right or wrong A. In the case of In re Quinlan in 1976, the US Supreme Court ruled that
independent of consequences. patients have the right to terminate medical care, because the indi-
3. The virtues view involves the use of various virtues—integrity, vidual has the right of autonomy.1
respect, compassion, and the character of the patient—to guide B. In the case of Nancy Beth Cruzan in 1991, the US Supreme Court
care. ruled that nutrition and hydration are considered medical care and

378 A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. © 2005 A.S.P.E.N. www.nutritioncare.org.
 S E C T I O N V I Site Related and Ethical Issues

thereby can be terminated on the wishes of the patient. The ruling also tory to provide enteral nutrition to the elderly unless doing so will
dictated that states have the right to determine what constitutes “clear improve the medical outcome, with variation based on patient
and convincing evidence” of the patient’s wishes.2 preference.
C. In cases where a child has become incompetent or never was com- 4. There is no ethical distinction between withholding food and
petent and is permanently unconscious, the courts have honored the withholding fluids. Withdrawal of food and withdrawal of fluids
parental decision.3 should be considered equal unless the patient or family wishes to
D. The Patient Self-Determination Act, effective 1991,4 encourages the distinguish them.
use of advanced directives, including a living will and durable power 5. Although there is no ethical distinction between withholding and
of attorney, as evidence of the patient’s choice. withdrawing treatment, in practice is it more emotionally difficult
1. A living will is a written legal document that states the care a to withdraw. Because of this, there may be a temptation not to ini-
patient would want at a time when the patient is incapable of tiate a treatment that may ultimately require discontinuation. How-
making health care decisions. ever, it is ethically more appropriate to initiate a treatment with
2. A person with durable power of health care is appointed by the potential benefit and later discontinue it if the benefit is not real-
patient to make health care decisions when that patient is not capa- ized than to withhold it to avoid this difficult situation.
ble of making decisions. States vary in their acceptance of orally B. The route of feeding will influence the feeding choices.
identified durable powers of attorney. 1. Oral feeding should be encouraged whenever possible, with the
3. The Patient Self-Determination Act has been only somewhat effec- emphasis on patient wishes and the physical and emotional enjoy-
tive. The use of living wills and health care durable power of attor- ment of food. Therapeutic diets should be reevaluated for outcome
ney is still low and inconsistent.5 Health professionals need to and discontinued when a positive outcome cannot reasonably be
continue to advocate the use of these tools to improve patient care. expected.
E. Helga Wanglie was an elderly stroke patient who was unconscious. 2. If oral intake is decreasing, nutrition supplements may be encour-
Her physician wanted to discontinue her enteral nutrition, stating aged to increase intake and reduce symptoms of malnutrition or
that it was medically inappropriate. Her husband disagreed, and in prevent hunger. The emphasis is on patient comfort, both physio-
1991 the Minnesota court (In re Helga Wanglie) held that the spouse logical and emotional.
was the best decision maker.6 The patient remained on enteral nutri- 3. The potential benefits of intravenous hydration and enteral or
tion to the end of life. parenteral nutrition should be weighed against the burdens of arti-
F. Finn v the Commonwealth of Virginia, 19987, ruled that discontin- ficial feeding. Self-determination is the guiding principle; there-
fore, using the level of intervention preferred by the patient is
uing enteral nutrition for a severely brain-damaged individual upon
generally recommended. However, it is essential that the health
that individual’s previously stated wishes was permissible, because
professional provide the facts about risk, benefit, and expected out-
natural progress of dying rather than removal of feeding was the
come to promote an “informed” patient decision. If conflicts occur,
cause of death.
the use of an ethics committee or consultant is recommended.
G. In the 1992 Baby K case, a court ruled that an infant with anencephaly
4. Institutions should have protocols on the provision and termina-
should receive life support, including nutrition and hydration, if the
tion of enteral and parenteral nutrition.
parents requested. The issue of futility was not clearly addressed.8
C. Patients’ health status will influence feeding choices.
H. On October 21, 2003, the Florida legislature empowered the gov-
1. Acutely ill patients should be fed when medically stable based on
ernor of Florida to reinstate enteral nutrition to Terri Schiavo, a
the best feeding choices for each patient.
chronically disabled woman, despite a court order allowing the
2. Chronically ill patients should be fed based on best nutritional
discontinuation.9 Her husband states that she did not “want tubes,”
practices and patient willingness to follow that advice. If a patient
but her family disagrees. Terri has no advance directive. The case refuses the optimal diet after clear education, discussion should
continues. be documented, but in most cases patients’ right of determination
I. In 1993, Robert Wendland suffered brain damage in an accident, predominates.
but he is not permanently unconscious. In 1995, his wife tried to 3. Advance directives should guide feeding decisions for patients in
stop enteral nutrition, saying that her husband would not want to a persistent vegetative state (PVS). The Multi-Society Task Force
live under these circumstances. His mother disagreed. In 2001, the on PVS defines PVS as “a vegetative state present one month after
California Supreme Court ruled that the enteral nutrition could not traumatic or nontraumatic brain injury or lasting for at least one
be stopped because the patient’s wishes were not known.10,11 month in patients with degenerative or metabolic disorders or
developmental malformations.”12 Others define “persistent” as
IV. Ethical Issues Regarding Feeding Patients extending to 1 to 3 years. While society has agreed that care may
be stopped for patients in a PVS, the requirement to honor the
A. Food and fluids may be optional or obligatory, depending on the patient’s wishes in relation to the issue of futility is still in an early
situation. stage and is evolving.
1. Food and fluids are obligatory when they improve the patient’s 4. Patients with advanced dementia in the United States receive
health status or well-being. Thus, for acutely ill patients, feeding is enteral nutrition more frequently than those in other countries.
obligatory. Food and fluids are also obligatory in chronic care to Several authors have reviewed the literature and have not found
improve health status, such as in diabetes or wound healing. evidence that enteral nutrition prolongs survival, reduces pressure
2. Artificially provided food and fluids are optional and provided on sores, or improves function.13–16 Their recommendations are to
the basis of individual patient preference for terminally ill and have the least restrictive environment, to allow patients to select
permanently unconscious patients (see Section IV.C). their foods, and to encourage hand feeding rather than enteral
3. Withdrawal of food and fluids in other cases may be optional or nutrition. If enteral nutrition is initiated, goals for the intervention
obligatory depending on the situation and the intent. For exam- should be established and monitored. If the goals are not being met,
ple, it is obligatory to orally feed the elderly, but it is not obliga- the enteral nutrition may be stopped.

© 2005 A.S.P.E.N. www.nutritioncare.org. A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. 379
S E C T I O N V I Site Related and Ethical Issues

5. Terminally ill patients often lose their appetite and reduce their medical information, thus allowing the patient “informed refusal”
consumption of food and fluids. In a study of 31 terminally ill can- through a surrogate. This preference should be documented.
cer patients,17 the patients were given fluids and food as requested. Kagawa-Singer suggests that cultural influence be ascertained
Despite low intakes, hunger was low to nonexistent. Ice chips and through questions related to the mnemonic ABCDE:
lip moisturizer reduced thirst and dry mouth. There is growing evi- Attitudes of patients and families within their culture
dence that the patients do not suffer and may benefit from reduced Beliefs, such as religious beliefs and traditions
hydration. Feeding decisions18 should maximize enjoyment of Content, such as personal history, including economics,
food, minimize symptoms, and continually be reassessed to max- emigration, and role of food in the family
imize responses to patient needs when palliative care is the goal.19 Decision-making style within the family and culture
6. Feeding nonpermanently unconscious but disabled patients is cur- Environment, such as interpreters of culture or language23
rently being debated in the courts (see Sections III.H and III.I). Being aware of and sensitive to cultural differences—without
Both cases illustrate the importance of an advanced directive. stereotyping—is essential to providing good care.
D. Patient stage of life also influences feeding choices. 2. Health care providers must be comfortable discussing religious
1. For newborns and spiritual issues, particularly end-of-life issues, with patients.
a) The American Academy of Pediatrics says that the neonatol- Religious beliefs come up in many discussions of resuscitation or
ogist/pediatrician must advocate for the best for the infant; termination of feeding. Care must be given to elicit concerns but
this beneficence overrides parental autonomy. not impose beliefs or try to resolve spiritual issues that are beyond
b) Communication among practitioners, parents, and ethical serv- the health care provider’s expertise.24 The religious premises dis-
ices before delivery is encouraged. cussed below offer general frames of reference for ethical deliber-
c) Consent for treatment should be obtained before medical treat- ation on feeding issues.
ment of the infant; otherwise, a battery charge is possible. 3. The US Catholic Church25 stated in 1999 that the presumption
d) Parental decisions can be overruled by court order. should be to feed and provide fluids, but that there is a subjective
e) The initial “Baby Doe” law from the 1980s requiring that element that should be guided by the patient’s family and the health
aggressive treatment be provided with or without parental care professional. This guidance should include weighing the ben-
consent was invalidated in 1986, with the Supreme Court re- efit and burden to the patient. In early 2004, the Pope stated that
iterating the rule of consent. The Baby Doe law should not be feeding was required: “I should like particularly to underline how
viewed as requiring feeding, however. the administration of water and food, even when provided by arti-
f ) In most cases, informed parental decisions should be used.20 ficial means, always represents a natural means of preserving life,
2. For children not a medical act. Its use, furthermore, should be considered, in
a) The guidelines of the American Academy of Pediatrics consider principle, ordinary and proportionate, and as such morally oblig-
feeding the standard of care unless otherwise indicated by the atory, insofar as and until it is seen to have attained its proper final-
parents. ity, which in the present case consists in providing nourishment to
b) When parents disagree on feeding, the decision is generally to the patient and alleviation of his suffering.”26 He concluded by say-
support the parent maintaining feeding. ing that one should “guard jealously the principle according to
c) The assent (not consent) of minors who are old enough to par- which the true task of medicine is ‘to cure if possible, always to
ticipate in treatment decision making is strongly encouraged care.’ ” The interpretation of this statement will evolve within the
by the American Academy of Pediatrics.21 Church. It is substantively different from the 199227 and 199925
3. For geriatric patients American National Conference of Catholic Bishops statements
a) An alert elderly individual should be treated as any other adult that focused on moral obligation, stating that if medical care had
would be. no benefit, it could not be obligatory but should not be consid-
b) A cognitively impaired elder often has a substitute decision ered automatically indicated. The conferences recognized that
maker. Unfortunately, in a Boston/Ottawa study, these decision the patient, family, and health care professionals generally can best
makers often did not know whether the patient had an advance decide the benefits and burdens for each individual.25,27
directive or what the elder’s enteral nutrition wishes were.22 4. Many Protestant churches28 have rejected the concept of prolong-
c) When there is disagreement among surrogate decision mak- ing life at all costs, saying that artificial feeding that prolongs dying
ers, feeding should be favored. is different from artificial feeding that enhances quality of life.
E. Culture, religion, and values will influence feeding choices. 5. Within Judaism, the concept of continuing treatment (feeding)
1. Many environmental factors influence decisions, including cul- once it is initiated is prevalent. Orthodox groups are the most
tural and religious beliefs and personal and family experiences, insistent and Reform groups less insistent that feeding not be
philosophies, and values. Although within American bioethics, stopped once it is started. The question of the need to initiate
autonomy and self-determination are guiding principles (see Sec- treatment is controversial.29,30 Feeding decisions are often post-
tion II), diverse cultural differences exist, and good cross-cultural poned until making them becomes medically essential.
understanding and communication are important to quality care.23 6. Within Islam, sanctity of life is important, but “maintaining a ter-
Religion and culture are neither independent nor homoge- minal patient on artificial life support for a prolonged period in a
neous; there are wide variations in family and personal beliefs vegetative state is not encouraged,” and advanced directives are
within each. Much of what we discuss in bioethics is based on encouraged.31
a European-American model. Yet within many Asian communi-
ties, families insist that the patient, especially an elderly patient,
V. Key Considerations to Frame Ethical Deliberations
not be told the prognosis or be burdened with decisions. To com-
bine normal practice and respect cultural preferences, the health A. Know the ethical positions of professional associations as well as
care professional might ask the patient who should receive the state laws and institutional policies.

380 A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. © 2005 A.S.P.E.N. www.nutritioncare.org.
 S E C T I O N V I Site Related and Ethical Issues

1. Professional associations 4. White M, Fletcher J. The Patient Self-Determination Act. JAMA. 1991;266
a) The American Medical Association recommends that patient (3):410–412.
preferences prevail on forgoing “life-sustaining treatment,” 5. Kass-Bartelmes BL, Hughes R. Advance care planning: preferences for
defined as “any treatment that serves to prolong life without care at the end of life. Research in Action, Issue 12. Agency for Healthcare
Research and Quality. Available at: http://www.ahrq.gov/research/endliferia/
reversing the underlying medical condition.”32 This includes
endria.htm. Accessed August 9, 2004.
artificial nutrition and hydration.
6. In re Helga Wanglie, Fourth Judicial District (Dist. Ct. Div.) PX-91-283.
b) The American Nurses Association distinguishes between food Minnesota, Hennepin County.
and water orally administered and artificial nutrition and hydra- 7. James S. Gilmore II v Michele Finn; Michele P. Finn v James S. Gilmore III,
tion, stating that use of the latter should be justified. If artificial 259 Va 448; 527 SE2d 426; 200 Va Lexis 52 (2000).
nutrition is forgone, comfort care should continue.33 8. Annas G. Asking the courts to set the standard of emergency care—the case
c) The American Dietetic Association recommends that the of baby K. New Engl J Med. 1994;330(21):1542–1545.
patient be at the center of the issue and that the health care 9. Bandow D. How much is Terri Schiavo’s life worth? April 12, 2004. Avail-
team develop criteria for nutrition and hydration.19 able at: http://www.terrisfight.org/. Accessed May 1, 2004.
d) The American College of Physicians recommends honoring 10. Reynolds D. CA high court says wife can’t stop disabled husband’s food,
“voluntary refusal of hydration.”34 water. Inclusion Daily Express, August 9, 2001. Available at http://www.
ragged-edge-mag.com/drn/drn080901wendland.htm. Accessed May 1, 2004.
e) The American Academy of Pediatrics35 includes enteral nutri-
11. Lo B, Dornbrand L, Wolf L, Groman M. The Wendland case—withdrawing
tion and intravenous feeding as part of life support that may be
life support from incompetent patients who are not terminally ill. N Engl J
discontinued. More recently, in discussing palliative care states, Med. 2002;346(19):1489–1493.
the academy stated that the family opinion is key.36 12. The Multi-Society Task Force on PVS. Medical aspects of the persistent
2. State laws. The use of surrogate decision makers is dependent on vegetative state. New Engl J Med. 1994;330:1499–1506.
state law. The health care team should work closely with these 13. Finucane T, Christmas C, Travis K. Tube feeding in patients with advanced
decision makers to act based on patient preference. If patient dementia. JAMA. 1999;282:1365–1370.
preference is not known, the team should act based on the best 14. McCann R. Lack of evidence about tube feeding—food for thought. JAMA.
interests of the patient.32 1999;282:1380–1381.
3. Institutional policies 15. Gillick M. Rethinking the role of tube feeding in patients with advanced
a) Institutions should have policies on administering and remov- dementia. N Engl J Med. 2000;342:206–209.
16. Sheiman S. Tube feeding the demented nursing home resident. J Am Geri-
ing artificial nutrition and hydration.
atr Soc. 1996;44:1268–1270.
b) Staff and patients should be aware of these policies. 17. Winter SM. Terminal nutrition: framing the debate for the withdrawal of
B. When in doubt, consult with the ethics team. nutritional support in terminally ill patients. Am J Med. 2000;109:723–741.
C. Use several frameworks to assist in deliberations. 18. Emanuel LL, von Gunten CF, Ferris FD. The Education for Physicians End-
1. The wanted-warranted question of-Life Care. Chicago, IL:Institute of Ethics, American Medical Association;
a) If what is requested by the patient or family is also warranted 1999.
by evidence, there is no dilemma. Ethical dilemmas occur when 19. Maillet JD, Potter RL, Heller L. Position of the American Dietetic Associ-
there is a conflict between different principles and different ation: ethical and legal issues in nutrition, hydration and feeding. J Am Diet
value systems. Assoc. 2002;102:716–726.
b) The question of sustaining life versus prolonging dying is 20. Pinkerton JV, Finnerty JJ, Lombardo PA, Rorty MV, Chapple H, Boyle RJ.
Parental rights at the birth of a near-viable infant: conflicting perspectives.
important. Health care professionals are obligated to sustain
Am J Obstet Gynecol. 1997;177(2):283–290.
life but not to prolong dying. The concept of intent is impor-
21. American Academy of Pediatrics, Committee on Bioethics. Informed consent,
tant here. parental permission and assent in pediatric practice. Pediatrics. 1995;95:317.
2. A patient-centered focus 22. Mitchell S, Berkowitz R, Lawson F, Lipsitz L. A cross-national survey of
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b) Define the context of the situation. Soc. 2000;48:391–397.
c) Identify family/patient issues: values, living wills, and substi- 23. Kagawa-Singer M, Blackhall L. Negotiating cross-cultural issues at the end
tute decision making. of life. JAMA. 2001;286(23):2993–3001.
d) Review law and policies. 24. Lo B, Ruston D, Kates L. Discussing religious and spiritual issues at the
e) Search for options. end of life. JAMA. 2002;287(6):749–755.
f) Choose and explain options.19 25. National Conference of Catholic Bishops Committee for Pro-Life Activi-
ties. Nutrition and hydration: moral and pastoral reflections. J Contemp
3. Consideration of the goals of health care
Health Law Policy. 1999;15:455–477.
a) Maximize health by curing or minimizing conditions/disorders.
26. Pope John Paul. Address of John Paul II to the Participants in the Interna-
b) Minimize suffering by reducing symptoms. tional Congress on “Life-Sustaining Treatments and Vegetative State: Sci-
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1. In re Quinlan, 70 NJ 10,355, A2d 647, cert denied sub nom, Garger v New ties. Nutrition and hydration: moral and pastoral reflections. Catholic News.
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2. Nancy Beth Cruzan, by Her Parents and Co-Guardians, Lester L. Cruzan, 28. Frederick HD. On dying and dying well: spiritual and moral aspects. J Soc
et ux. Petitioners v Director, Missouri Department of Health, et al. Supreme Med. 1977;70:75–81.
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3. Nelson LJ, Rushton CH, Cranford RE, Nelson RM, Glover JJ, Truog RD. 30. Gillick M. Artificial nutrition and hydration in the patient with advanced
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31. Athar S. Information for health care providers when dealing with a Muslim 34. Quill T, Byock IR. Responding to intractable terminal suffering: the termi-
patient. Islamic Medical Association of North America. Available at: nal sedation and voluntary refusal of food and fluids: position paper. Intern
http://www.islam-usa.com/e40.html. Accessed May 1, 2004. Med. 2000;132:408–414.
32. American Medical Association. Withholding or withdrawing life-prolong- 35. American Academy of Pediatrics, Committee on Bioethics. Guidelines
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382 A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. © 2005 A.S.P.E.N. www.nutritioncare.org.
 Index

A nutrition support in postrenal causes of, 281

AAA. See Aromatic amino acids (AAA) cost control for, 362 prerenal causes of, 281
Abacavir (Ziagen), diet and nutrition interactions implementation of, 357, 358t risk factors for, 281
with, 141t monitoring of, 357, 358t Acute respiratory distress syndrome (ARDS), in
ABCDE mnemonic, 380 organizational structure for, 360–362 adults, enteral formulations for, 67–68
Abdominal cramping, drug-induced, 127 performance in, assessment/improvement of, Acyclovir, effects on clinical laboratory values,
Abdominal distention, with enteral nutrition, 79 358t, 359–360 128t
Abdominal girth process for, 357, 358t Acylcarnitine, excretion, in inborn errors of
clinical significance of, 16 recommendations for, 358t, 359 metabolism, 332
measurement of, 16 reimbursement for, 362–363 Acylglycines, excretion, in inborn errors of
Abdominal pain, drug-induced, 127 nutrition support team in, 360 metabolism, 332
Absolute neutrophil count, in pediatric cancer credentialing of members of, 361 Adequate intake (AI), 43
patients, 158 existence and structure of, factors affecting, Adipokines, 325
Absorption 362 Adipose tissue
of drugs, 118–119 members’ roles in, 360–361 distribution of, in obese patient, 326
factors affecting, 118–119 patients in, nutrition status of, identification of, Adipose tissue, depletion of, in anorexia nervosa,
gastrointestinal, impaired, enteral formulations 357, 358t 349, 350t
for, 67 regulation of, 358t, 359 Administration set(s)
nutrient tools/equipment in, 357, 358t for enteral nutrition, 61
in anorexia nervosa, 349 Acute lymphoblastic leukemia (ALL) hang times for, 73
in cancer patients, 152 nutritional effects of, 150 for parenteral nutrition, 111, 126
in inborn errors of metabolism, 332 prognosis for, nutritional status and, 160 Administrator(s), in acute care organizations, role
in pregnancy, 343
survivors, 150–151 on nutrition support committee, 362
ACD. See Automated compounding device (ACD)
long-term effects in, 165 Adrenal glands
Acetaminophen, effects on clinical laboratory val-
treatment of in critical illness, 264
ues, 128t
nutritional effects of, 150 in HIV-infected (AIDS) patients, 140
Acetate
nutritional status and, 160 in stem cell transplant recipient, 193
in parenteral formulations (admixtures), 98
Acute-phase proteins Adrenergic symptoms, of hypoglycemia, 318
for pediatric patients, 109t
functions of, 19, 22t Adults
for preterm infants, 109t
negative, 19, 22t, 263 cancer in. See Cancer, adults with
requirements for, in adults, 52t
positive, 19, 22t, 263 carbohydrate requirements in, 46t, 109t
Acid reflux, in neonates, 71
Acid suppression, protective effect, for skin, with in trauma, 272 electrolyte requirements in, 49t, 51, 52t
feeding tube, 60 Acute renal failure enteral nutrition for, trace element requirements
Activities of daily living, functional assessment of in adults, 281–285 in, 49t, 52
in adult cancer patient, 154–157 assessment in, 283 fiber intake by, 47t
in pediatric cancer patient, 157–158 enteral nutrition in, 284–285 fluid requirements in, 51, 80, 109t
Activity nitrogen balance in, 283, 283t nutritionally at risk, 3
energy expenditure in, in obesity, 324 nutritional aspects of, 282–283 organ transplant recipients. See Organ transplan-
and energy requirements, 39 nutritional requirements in, 284 tation
level of nutritional support in, 284 pancreatitis in. See Pancreatitis
classification of, 44 parenteral nutrition in, 285 parenteral nutrition for
and energy requirements, in children and ado- clinical course of, 281–282 hyperglycemia in, 115
lescents, 44, 44t definition of, 281 hypertriglyceridemia with, 115
Acute brain injury etiology of, 281 trace element intake in, 52, 110t
acute medical management of, 246 hospital-acquired, 281 vitamin requirements in, 51–52, 110t
assessment in, 246 intrarenal causes of, 281 PN-associated metabolic bone disease in, 114,
epidemiology of, 246 pediatric, 287 114t
nutrition support in, 247–248 enteral nutrition in, 291–292, 292t protein requirements in, 45t, 51, 109t
Acute care organizations nitrogen balance in, 289, 290, 291t refeeding syndrome in, 114
health care team members in, 357, 358t nutritional aspects of, 287 trace element requirements in, 49t, 52
information communication in, 357–359, 358t nutritional assessment in, 287, 288t–289t vitamin requirements for, 48t, 51
nutrition support committee in, 361–362 parenteral nutrition in, 292–294, 293t Advance directives, 364, 378, 379
reporting structure for, 362 urea kinetics in, 290, 291t Agenerase. See Amprenavir (Agenerase)

© 2005 A.S.P.E.N. www.nutritioncare.org. A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. 383
INDEX

Aging for neonates, 119 in obese patient, 326

demographics of, 364 for pediatric patients, 119, 293t in organ transplant recipient, 175t
malnutrition in, 364 in parenteral nutrition in pediatric cancer patient, 157–158
AI. See Adequate intake (AI) for pediatric patients, 45–46 in pediatric HIV-infected (AIDS) patients,
AIDS (acquired immune deficiency syndrome), for premature infants, 40–42 144–145
139. See also HIV infection Aminoglycosides, nephrotoxicity of, 189 in stem cell transplant recipient, 193
Airway Amiodarone, effects on clinical laboratory values, Antibiotics
complications in, with feeding tube, 81–82 128t for Crohn’s disease, 231
injury to, in feeding tube placement, 81 Amitriptyline diarrhea caused by, 204
Alagille’s syndrome, pancreatic insufficiency in, appetite stimulation by, 127 gastrointestinal effects of, 127
220 effects on clinical laboratory values, 128t hepatic effects of, 127
Alanine aminotransferase, parenteral nutrition and, Amphotericin B pancreatic effects of, 127
114 effects on clinical laboratory values, 128t taste alterations caused by, 127
Albumin hepatic effects of, 127 Anticholinergics
in HIV-infected (AIDS) patients, 140 nephrotoxicity of, 189 dry mouth caused by, 127
serum. See also Hypoalbuminemia for stem cell transplant recipient, nutritional gastrointestinal effects of, 127, 318
in cancer patient, 157 implications of, 194t in tube-fed patients, adverse effects of, 119
in chronic kidney disease, 336 Ampicillin, effects on clinical laboratory values, Anticonvulsants
in cystic fibrosis, 222 128t drug-nutrient interactions, 345
cytokines and, 365 Amprenavir (Agenerase), diet and nutrition inter- and folic acid requirements, in pregnancy, 345
evaluation of, during parenteral nutrition, 112 actions with, 141t pancreatic effects of, 127
in pediatric cancer patients, 158 Amyotrophic lateral sclerosis (ALS), nutrition Antidepressants, gastrointestinal effects of, 318
Alcohol. See also Ethanol abuse support in, 249 Antidiabetic agents, for HIV-infected (AIDS)
abstinence from, in chronic pancreatitis, 215 Anabolism, as goal, in adults, 39 patients, 147
hepatic effects of, 127 Anemia Antiemetics
intake, in HIV-infected (AIDS) patients, 144 in anorexia nervosa, 351 for cancer patients, 161
and liver disease, 235, 236 in inflammatory bowel disease, 232 for stem cell transplant recipient, 188
pancreatic effects of, 127
in pregnant women, assessment of, 346, 346t Antihistamines
Alimentum, 242, 242t
Anesthetics, hepatic effects of, 127 antiemetic therapy with, for cancer patients, 161
Alkaline phosphatase, parenteral nutrition and, 114
Anorexia dry mouth caused by, 127
Allergy(ies), diarrhea caused by, 205
in cancer patients, 151 hepatic effects of, 127
Allopurinol, hepatic effects of, 127
drug-induced, 127 Anti-inflammatory drugs, hepatic effects of, 127
Alpha-1-antitrypsin deficiency, 235
in stem cell transplant recipient, 188, 189t Antilymphocyte serum (ATGAM, Thymoglobulin)
Aluminum, as contaminant, in parenteral formula-
Anorexia nervosa in immunosuppression for organ transplant
tions (admixtures), 98–99, 307
binge-eating/purging type, 349, 350 recipients, 171, 173t
Aluminum antacids, effects on clinical laboratory
day-treatment programs for, 352 nutritional side effects and interventions, 173t
values, 128t
diet and nutritional supplements for, 351–352 Antioxidant(s). See also specific antioxidant
American Academy of Pediatrics, ethical position
dietary counseling in, 352 supplementation, in critical illness, 267
on artificial nutrition and hydration, 381
electrocardiographic abnormalities in, 351 therapy with
American Cancer Society, Internet address and
electrolyte imbalances in, 351 in chronic pancreatitis, 219–220
resources provided by, 165
American College of Physicians, ethical position enteral nutrition in, 352 in critical illness, 272
on artificial nutrition and hydration, 381 epidemiology of, 349 Antireflux surgery, in neurologically impaired chil-
American Dietetic Association, ethical position on focused assessment in, 350–351 dren, 251
artificial nutrition and hydration, 381 hematologic findings in, 351 Antiretroviral (ARV) therapy, 139
American Institute for Cancer Research, Internet history-taking in, 350 adverse effects and side effects of, 141t–142t
address and resources provided by, 165 and inflammatory bowel disease, 349 diet and nutrition interactions with, 140–143,
American Medical Association (AMA), ethical inpatient treatment of, 352 141t–142t
position on artificial nutrition and hydration, 381 in males, 349 gastrointestinal effects of, 143
American Nurses Association, ethical position on nutritional alterations in, 350, 350t Antithymocyte globulin, nutritional side effects
artificial nutrition and hydration, 381 nutritional aspects of, 349 and interventions, 192t
American Society for Parenteral and Enteral Nutri- nutritional therapy for APACHE II score, in acute pancreatitis, 213–214,
tion, standards for specialized nutrition support goals of, 351 215
for adult hospitalized patients, 359 assessment of, 353 Appetite
for pediatric hospitalized patients, 359 management of, 351–353 after discontinuation of PN, 116
Amin-Aid, 339 monitoring, 353 drugs affecting, 127
Amino acid(s) outpatient treatment of, diet and nutritional loss of, in cancer patients, 151
in enteral formulations, 64 supplements for, 351–352 nutritional therapy for, 162
for renal failure patients, 339 parenteral nutrition in, 352–353 Apple juice, in enteral formulations, for pediatric
and wound healing, 68 patient/caregiver education in, 353 patients, 69
essential, for premature infants, 40 restricting type, 349, 350 ARA. See Arachidonic acid (ARA)
intake, in chronic kidney disease, 337–338 Antacids, aluminum-containing, in tube-fed Arachidonic acid (ARA)
metabolism of patients, adverse effects of, 119 in enteral formulations, 63
in acute renal failure, in adults, 282 Anthropometry in enteral nutrition, for preterm infants, 42
inborn errors of, 333, 333t in anorexia nervosa, 351 ARDS. See Acute respiratory distress syndrome
in parenteral formulations (admixtures), 97 in cancer patients, 154, 157 (ARDS)
for chronic kidney disease, 338 in cystic fibrosis, 222 Area under the curve (AUC), 125
for neonatal intensive care, 302 in HIV-infected (AIDS) patients, 143 ARF. See Acute renal failure

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Arginine Automated compounding device (ACD), for par- Bioavailability, 118

in enteral formulations, 64 enteral formulations (admixtures), 102–103 of parenteral medications, entry point into
for burn patients, 68 Autonomic agents, gastrointestinal effects of, 127 bloodstream and, 119
for critically ill adults, 66 Autonomy, as ethical principle, 378 Biochemical monitoring/testing
and wound healing, 68 Azathioprine in cancer, 157
therapy with, in critical illness, 266 for Crohn’s disease, 231 in chronic kidney disease, 336
Aromatic amino acids (AAA), in enteral formula- nutritional side effects and interventions, 173t, during enteral nutrition, 81
tions, for liver disease, 64, 66 192t for organ transplant recipient, 175t
Arterial puncture, central venous catheter place- pancreatic effects of, 127 in pediatric cancer patients, 158
ment and, 90 Bioelectrical impedance analysis (BIA), 19, 328
ARV therapy. See Antiretroviral (ARV) therapy B in HIV-infected (AIDS) patients, 143
5-ASA products, for inflammatory bowel disease, Baby K case, 379 in pediatric cancer patients, 158
231 in pediatric HIV-infected (AIDS) patients, 145
Bacterial translocation
Ascites Biotherapy
GI disuse and, 114
in end-stage liver disease, 241t definition of, 151
in trauma patient, 272
evaluation of, in cancer patient, 154 nutritional effects of, 151
Barbiturates, hepatic effects of, 127
Ascorbic acid. See also Vitamin C Biotin
Bariatric surgery, dietary considerations after,
effects on clinical laboratory values, 128t dietary reference intakes for, by life stage group,
328–329
Asparaginase, pancreatic effects of, 127 48t
A.S.P.E.N. See American Society for Parenteral Barium, effects on clinical laboratory values, 128t
Basal energy expenditure (BEE), estimation of, in parenteral formulations (admixtures)
and Enteral Nutrition for adults, 110t
Aspiration 338
Basal metabolic rate (BMR), 39 for pregnant women, 347t
in neurologically impaired children, 250, 250t requirements for, in preterm infants, 41t
in neurologic disease, 248, 249t estimation of, 44, 44t
in obesity, 324 Biotinidase deficiency, biotin supplementation in,
tube feeding–related, 54, 56, 57, 58, 82–83 333
detection of, 80 in stress/illness, 45
Bisphosphonates
prevalence of, 82 Basiliximab (Simulect)
for cystic fibrosis patients, 226
prevention of, 79–80, 83 in immunosuppression for organ transplant
for neurologically impaired children, 252
risk factors for, 83 recipients, 171, 173t
Bisphosphonates, for stem cell transplant recipient,
Assessment nutritional side effects and interventions, 173t
192
in acute brain injury, 246 BCAA. See Branched-chain amino acids (BCAA)
Bleeding, gastrointestinal, enteral nutrition in, con-
in acute pancreatitis, 213–214 B cells (B lymphocytes), abnormalities of, in
traindications to, 77
in acute renal failure cancer patients, 152
Blood-borne pathogen exposure, prevention of, in
in adults, 283 BCM. See Body cell mass (BCM)
parenteral nutrition, 111
in pediatric patients, 287, 288t–289t Beclomethasone dipropionate, nutritional side
Blood pressure
algorithm for, 3, 4f effects and interventions, 192t
in adult organ transplant recipient, 176
of anorexia nervosa patient, 350–351 BEE. See Basal energy expenditure (BEE)
in pediatric organ transplant recipient, 178
anthropometric parameters for, 4–16 Beef, in enteral formulations, 64
Blood urea nitrogen
of burn patients, 298, 299t for pediatric patients, 68
in acute renal failure, in pediatric patients,
of cancer patients, 154–159 Behavioral development, nutritional support and, 290–291
in chronic kidney disease, 336–337 38
in chronic pancreatitis, 217 in critically ill infants, 307
Beneficence, as ethical principle, 378 BMI. See Body mass index (BMI)
in critical illness Benzodiazepines, antiemetic therapy with, for can-
in adults, 264–265 BMR. See Basal metabolic rate (BMR)
cer patients, 161 Body cell mass (BCM), in HIV-infected (AIDS)
in pediatric patients, 265 Beta-2 agonists, effects on clinical laboratory
in cystic fibrosis, 221–222 patients, 143, 145
values, 128t Body composition
of HIV-infected (AIDS) patients, 143–145
Beta blockers assessment of, in obese patient, 326
in liver disease, 237–238, 240t
effects on clinical laboratory values, 128t and drug distribution, 134
of obese patient, 325–327
gastrointestinal effects of, 127 in HIV-infected (AIDS) patients, 143
objective parameters for, 3–4
pancreatic effects of, 127 in obesity, 324
of organ transplant recipient, 174, 175t
Beta-carotene in pediatric cancer patients, 158
of patient in long-term care facility, 365–366
deficiency of, in cancer patients, 153 Body mass index (BMI)
of patients in acute care organizations, 357, 358t
depletion, in cystic fibrosis, 221 calculation of, 16, 326
perioperative, 259
of pregnant woman, 344 plasma, in chronic pancreatitis, 216 classification of, 326, 326t
of stem cell transplant recipient, 193–194 Beta-cryptoxanthine, plasma, in chronic pancreati- clinical significance of, 16
subjective parameters for, 3 tis, 216 in cystic fibrosis, 221–222
of trauma patient, 272 BIA. See Bioelectrical impedance analysis (BIA) Body mass index-for-age
Astemizole, hepatic effects of, 127 Bicarbonate in pediatric cancer patients, 157–158
Atazanavir (Reyataz), diet and nutrition interac- effects on clinical laboratory values, 128t percentiles
tions with, 141t pancreatic secretion of, 216 for boys, 2 to 20 years, 34
Atenolol, effects on clinical laboratory values, 128t in parenteral formulations (admixtures), for for girls, 2 to 20 years, 35
ATGAM. See Antilymphocyte serum (ATGAM, pediatric patients, 293t Body shape changes, in HIV-infected (AIDS)
Thymoglobulin) serum, in chronic kidney disease, 336 patients, 143
Atovaquone, drug-nutrient interactions, 125 Bicarbonate salts, contraindications to, in par- Body surface area, and fluid requirement estima-
AUC. See Area under the curve (AUC) enteral formulations (admixtures), 100 tion, for children, 50
Autoimmune disease, hematopoietic stem cell Bile acid(s), deficiency of, in liver disease, 237 Body weight. See Weight
transplantation in, 187 Bilirubin, serum, parenteral nutrition and, 114 Bone health, in cystic fibrosis, 221–222

© 2005 A.S.P.E.N. www.nutritioncare.org. A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. 385
INDEX

Bone mass dietary reference intakes for, by life stage group, nutritional interventions for
in anorexia nervosa, 350 49t criteria for, 160
loss of effects on clinical laboratory values, 128t goals of, 161
in burn patients, 300 in enteral nutrition, 84–87, 85t–86t indications for, 160–161
in organ transplant recipient, prevention/ imbalances, in tube-fed patients, 84–87, 85t–86t nutritional status in, factors affecting, 160
treatment of, 176 ionized oral supplements for, 164
in pediatric organ transplant recipient, clinical significance of, 158 parenteral nutrition for, 164
prevention/treatment of, 178 level of, calculation of, 84 and patient/caregiver education, 165
in stem cell transplant recipient, 191–192 in parenteral formulations (admixtures), 98 prognosis for, nutritional status and, 160
Bone mineral density for adults, 109t quality of life for, 158–159, 161
in chronic pancreatitis, 216–217 for chronic kidney disease, 339 relapse rate in, nutritional status and, 160
in cystic fibrosis, 221 for neonatal intensive care, 304 screening for, 157
in neurologically impaired children, 251–252 survivors, long-term effects in, 165
for pediatric patients, 109t
in pediatric cancer patients, 157 trace element deficiencies in, 153, 154
for preterm infants, 109t
in stem cell transplant recipient, 191–192 trends in, 150
physiologic functions of, 84, 85t
Bone tumor(s), malignant complementary and alternative medicine (CAM)
requirements for
micronutrient deficiencies with, 153 in, 162, 163
in acute renal failure, in pediatric patients,
trace element deficiencies with, 153 diagnosis of, copper-to-zinc ratio in, 154
292
Bottle feeding, in critically ill infants, 310 enteral nutrition in, for adults, 65
Bowel mediations, for cancer patients, 161–162 in adults, 52t
functional assessment in
Bowel necrosis, nonocclusive, in tube-fed trauma in cystic fibrosis, 225, 226
for adult patients, 154–157
patient, 274 in pregnancy, 345t for pediatric patients, 157–158
Bowel sounds, with enteral nutrition, 79 in preterm infants, 41t, 43 hematopoietic stem cell transplantation in, 187
Bowel stasis, in cancer patients, 152 in stem cell transplant recipient, 195 history-taking in, 154
BPD. See Bronchopulmonary dysplasia (BPD) serum. See also Hypercalcemia; Hypocalcemia home nutrition support in, outcome of, 376
Brain injury, acute. See Acute brain injury in chronic kidney disease, 336 and immunodeficiency, 152
Branched-chain amino acids (BCAA) in pediatric cancer patients, 158 laboratory testing in, 157
in enteral formulations, 64 supplementation metabolic alterations in, 153
for critically ill adults, 66 during parenteral nutrition in pregnancy, 348 mortality from, trends in, 150
for hepatic disease in adults, 66–67 for pediatric cancer patients, 157 nutritional assessment of patient with, 154–159
metabolism of, in critical illness, 263 for stem cell transplant recipient, 192, 195 nutritional interventions in
Breast cancer Calcium-channel blockers, gastrointestinal effects criteria for, 159–161
trace element deficiencies in, 153, 154 of, 318 goals of, 159–161
weight loss in, 150 Calcium phosphate precipitation, in parenteral nutritional management in, 161–165
Breast feeding, in critically ill infants, 310 formulations (admixtures), 100, 113 pain in, 157
Bronchopulmonary dysplasia (BPD), nutrition Calories. See Energy in pediatric patients, 158
support in, 313 CAM. See Complementary and alternative palliative nutrition support in
Budesonide, nutritional side effects and interven- medicine (CAM) for adults, 159
tions, 192t Cancer for children, 160
Buried bumper syndrome, 82 adults with patient/caregiver education in
Burn(s) cancer types most likely to have nutritional for adult patients, 163–164
classification of, 296, 297f effects in, 150 Internet resources for, 165
metabolic response to, 296 for pediatric patients, 165
diet and nutritional supplements for, 162
pathophysiology of, 296 Patient-Generated Subjective Global Assessment
enteral nutrition for, 163
Burn patients (PG-SGA) in, 154, 155f–156f
ethical considerations with, 163
assessment of, 298, 299t radiation therapy for
nutritional assessment of, 154–157
energy requirements of, 296, 298t malabsorption caused by, 152
nutritional interventions for
enteral formulations for, 68 nutritional effects of, 151
enteral nutrition for, 297–300 criteria for, 159
surgical therapy for
nutritional therapy for, 297–298 goals of, 159–160
malabsorption caused by, 152
Busulfan, for stem cell transplant recipient, nutri- nutrition counseling for, 163
nutritional considerations in, 159
tional implications of, 194t oral supplements for, 162–163
nutritional effects of, 151
parenteral nutrition for, 163
survival rates, trends in, 150
C and patient/caregiver education, 163–164
treatment of
Cachexia quality of life for, 157, 160
adverse effects and side effects of
in cancer patients, 151–153 screening in, 154 nutritional management of, 162
cytokines and, 152 biochemical testing in, 157 pharmacological management of, 161–162
evaluation of, 154 biotherapy for, nutritional effects of, 151 effect on food intake, 151
hormones and, 152 chemotherapy for, malabsorption caused by, 152 Cancer Centers, Internet address and resources
management of, polyunsaturated fatty acids children with provided by, 165
in, 163 assessment of, 157–159 Cancer Research and Prevention Foundation,
definition of, 151 cancer types most likely to have nutritional Internet address and resources provided by, 165
in end-stage liver disease, 241t effects in, 150–151 Candida albicans, growth of, in parenteral formu-
Calcium complementary and alternative medicine lations (admixtures), 102
deficiency of (CAM) for, 164–165 Cannabinoids, antiemetic therapy with, for cancer
in anorexia nervosa, 350t diet and nutritional supplements for, 164 patients, 161
in cancer patients, 153 enteral nutrition for, 164 Captopril, effects on clinical laboratory values,
in inflammatory bowel disease, 232 ethical considerations for, 165 128t

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Carbamazepine Celiac disease, 205–206, 206t cut down for, 90

drug-nutrient interactions, 125 CellCept. See Mycophenolate mofetil (CellCept) infection control in, 91, 113
effects on clinical laboratory values, 128t Centers for Disease Control and Prevention (CDC) introducers for, 90
pancreatic effects of, 127 growth charts published by, 16, 27–37 modified Seldinger technique for, 90
Carbidopa/levidopa, drug-nutrient interactions, 125 guidelines for nutrition support, 359 in obese patient, 329–330
Carbohydrate(s) Centers for Medicare and Medicaid Services patient evaluation before, 91
acceptable macronutrient distribution range for, (CMS), 364 patient preparation for, 90–91
by life stage group, 46t care mandated by, in long-term care, 364 peel-away introducer sheath and tissue dilator
adequate intake of, by life stage group, 46t Data Assessment Verification Project, for long- for, 90
in enteral formulations term care (LTC) facilities, 368 percutaneous approach for, 90
for critically ill adults, 66 home nutrition support outcome data of, 376 setting for, 90
for pediatric patients, 69 Quality Indicator, for long-term care, 364 sites for, 90
and wound healing, 68 Central nervous system (CNS), cancer of care of, 93, 94t
in enteral nutrition, 63 in children, 150 tunneled, 90
for adults, 51 micronutrient deficiencies in, 153
ultrasound guidance for, 90
modular products, 63 trace element deficiencies with, 153
polyethylene, 91
percentage of energy contributed by, 63 Central venous access. See also Central venous
polytetrafluoroethylene (Teflon), 91
estimated average requirement for, by life stage catheter; Peripherally inserted central catheter
polyurethane, 91
group, 46t (PICC)
polyvinyl chloride, 91
metabolism of complications of, 112–113
replacement/removal of, 113
in acute pancreatitis, 213 duration of, and catheter selection, 92–93, 93t
in acute renal failure, in adults, 282 for home nutrition support, 372 selection of, 92–93
inborn errors of, 333, 334t indications for, 90 silicone elastomer (Silastic), 91
regulation of, 317 infectious complications of. See Infection(s), site care with, 93, 94t
in nutritional support, for adults, 51 catheter-related tubing changes with, 93
for organ transplant recipient length of therapy with, and catheter selection, tunneled cuffed, 92
maintenance needs, 183 92–93, 93t maintenance of, 93, 94t
recommendations, 179t in obese patient, 329–330 types of, 92
overfeeding, in acute renal failure, in pediatric in patients in long-term care, 367 and length of therapy with, 92–93, 93t
patients, 287 ports for, 92 Cephalexin, effects on clinical laboratory values,
in parenteral formulations (admixtures), 97, 109t postoperative, 261 128t
for adults, 51, 109t in pregnancy, 346 Cerebral palsy
for neonatal intensive care, 302 preoperative, 261 nutrition support in, 249–252
recommended dietary allowances, by life stage principles and rationale for, 90 recommended energy intake in, 250t
group, 46t in stem cell transplant recipient, 197 Cerebrovascular accident. See Stroke
requirements for Central venous catheter Certican, 171
in burn patients, 297 breakage of, 93 Cervical cancer, trace element deficiencies in, 153,
pediatric, 46, 46t care of, 93 154
in premature infants, 41t, 42 coated/bonded, 91 CFRD (cystic fibrosis-related diabetes mellitus).
in stem cell transplant recipient, 194 complications of, 112–113 See Diabetes mellitus, in cystic fibrosis
Carbon dioxide (CO2) production, clinical factors long-term, 93 CFTR gene, 220
affecting, 278, 278t composition of, 91 Chemotherapy
Cardiovascular system, obesity and, 325 cuffs for, 91 electrolyte imbalances in, 154
Carnitine collagen, 91 gastrointestinal effects of, 127
deficiency of, in inborn errors of metabolism, polyethylene eterphthalate (Dacron), 91 immunological effects of, 152
332 diameter/circumference of, 92 malabsorption caused by, 152
in parenteral formulations (admixtures), for features of, 91–92 metabolic effects of, 127
neonatal intensive care, 302 flushing of, 93, 94t nephrotoxicity of, 189
in parenteral nutrition, for pediatric patients, 50 hub care for, 93
nutritional considerations in, 159
requirements for, in preterm infants, 41t, 43 in-line filters for, 110–111
nutritional effects of, 150
supplementation length of, 92
in preparative conditioning for hematopoietic
in acute renal failure, in pediatric patients, lumens, 91, 93, 372
stem cell transplantation, 187
293–294, 294t maintenance of, 93, 94t
CHI. See Creatinine height index (CHI)
for critically ill infants, 304 malposition of, 93
Children. See Pediatric patient(s)
in inborn errors of metabolism, 332, 333t nontunneled, 92
CARS. See Compensatory anti-inflammatory maintenance of, 93, 94t Chlorambucil, effects on clinical laboratory values,
response syndrome occlusion of, 113 128t
Caseinates, in enteral formulations, 64 mechanical, 113 Chloramphenicol
for pediatric patients, 68 nonthrombotic, 113 adverse effects and side effects of, 127
Case manager, in acute care organizations, 357, thrombotic, 113 effects on clinical laboratory values, 129t
358t patient assessment for, 92 hepatic effects of, 127
Catabolism for patients in long-term care, 367 Chlordiazepoxide, effects on clinical laboratory
in acute renal failure, in adults, 282 peripherally inserted. See Peripherally inserted values, 129t
in critical illness, 263 central catheter (PICC) Chlorfibrate, effects on clinical laboratory values,
in HIV-infected (AIDS) patients, 140 pinch-off syndrome with, 93, 113 129t
muscle, in cancer patients, 153 placement of, 90–91 Chloride
CDC. See Centers for Disease Control and Preven- complications of, 90 dietary reference intakes for, by life stage group,
tion (CDC) confirmation of, 90, 110, 112 49t

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INDEX

in parenteral formulations (admixtures), 98 Clostridium difficile, 77, 83 and growth, 178

for neonatal intensive care, 304 diarrhea caused by, 203, 204 in immunosuppression for organ transplant
for pediatric patients, 109t CMS. See Centers for Medicare and Medicaid recipients, 171, 173t
for preterm infants, 109t Services (CMS) for inflammatory bowel disease, 231
requirements for Cobalamin, requirements for, in pregnancy, 345t nutritional side effects and interventions, 173t,
in adults, 52t Cockcroft-Gault equation, 282 192t
in preterm infants, 41t Cognitive development, nutritional support and, 38 pancreatic effects of, 127
serum, in chronic kidney disease, 336 Colchicine, gastrointestinal effects of, 127 Corticotropin-releasing hormone (CRH), metabolic/
Chloroquine, effects on clinical laboratory values, Colon cancer, weight loss in, 150 nutritional effects of, in cancer patients, 152
129t Colorectal cancer, micronutrient deficiencies in, Costs
Chlorpromazine 153 of enteral nutrition, 76
effects on clinical laboratory values, 129t Coloring agents, in detection of tube nutritional interventions and, 38
gastrointestinal effects of, 127 feeding–related aspiration, 80 Cranberry juice, and warfarin metabolism, 120
Chlorpromethazine, antiemetic therapy with, for Compensatory anti-inflammatory response C-reactive protein (CRP), 19, 22t
cancer patients, 161 syndrome, 272 in trauma, 272–273
Chlorpropamide, effects on clinical laboratory val- Competence, 378 Creatinine, serum
ues, 129t Complementary and alternative medicine (CAM) in chronic kidney disease, 336
Cholestasis for cancer patients, 162, 163 in pediatric patients, 287
PN-associated in liver disease, 243 Creatinine height index (CHI), 16–19
in critical illness, 268–269 nutrient-based, for HIV-infected (AIDS) Credentialing, of nutrition support team members,
in neonatal intensive care, 307 patients, 146 in acute care organizations, 361
in pediatric patients, 114 for pediatric cancer patients, 164–165 Critical illness
in stem cell transplant recipient, 197 Constipation in adults
Cholesterol, serum, in pregnancy, 344 in cancer patients, nutritional therapy for, 162 assessment in, 264–265
Cholestyramine, effects on clinical laboratory val- in diabetic patients, 318 enteral formulations for, 65–66
ues, 129t in stem cell transplant recipient, 189t antioxidant therapy in, 272
Cholestyramine resin, administration of, via in tube-fed patients, 79, 84 immunonutrition in, 266
enteral tubes, 123 Continuous renal replacement therapy (CRRT), indirect calorimetry in, 277–280
Choline, dietary reference intakes for, by life stage 282 in infants. See Neonatal intensive care
group, 48t in acute renal failure, in pediatric patients, nutri- metabolic response to, 263, 264t
Choreoathetosis, children with, recommended tional considerations in, 290 nutritional alterations in, 263–264
energy intake for, 250t Continuous venovenous hemodialysis (CVVHD) nutrition support in, 264–267
Chromium and intradialytic parenteral nutrition, 340 enteral, 265–266
dietary reference intakes for, by life stage group, and nutrition support, 338 monitoring, 269
49t in pediatric patients, nutritional considerations parenteral, 266–269
in parenteral formulations (admixtures), 98 in, 290 parenteral nutrition in
for adults, 110t urea nitrogen appearance in, assessment of, 337 carbohydrate in, 109t
for chronic kidney disease, 339 Continuous venovenous hemofiltration (CVVH) fluid in, 109t
for neonatal intensive care, 305 and intradialytic parenteral nutrition, 340 lipids in, 109t
for pediatric patients, 110t, 293t and nutrition support, 338 protein in, 109t
requirements for in pediatric patients, 292 total calories in, 109t
in acute renal failure, in pediatric patients, 293t nutritional considerations in, 290 in pediatric patients
in elderly, 52 urea nitrogen appearance in, assessment of, 337 assessment in, 265
in preterm infants, 41t Copper enteral nutrition in, 266
Chronic Kidney Disease (CKD). See Kidney deficiency of metabolic response in, 264
disease, chronic in cancer patients, 154 Critic Care Skin Paste, 60
Chronic lymphocytic leukemia (CLL), immuno- in inflammatory bowel disease, 232 Crixivan. See Indinavir (Crixivan)
logical effects of, 152 dietary reference intakes for, by life stage group, Crohn’s disease (CD). See also Inflammatory
Cimetidine, hepatic effects of, 127 49t bowel disease (IBD)
Ciprofloxacin in parenteral formulations (admixtures), 98 anemia in, 232
absorption of, 118–119 for adults, 110t and anorexia nervosa, 349
for Crohn’s disease, 231 for chronic kidney disease, 339 diarrhea in, 232
drug-nutrient interactions, 125 for neonatal intensive care, 305 home nutrition support in, outcome of, 376
Cirrhosis, 235–236 for pediatric patients, 110t, 293t hypoalbuminemia in, 232
malnutrition in, 236–237, 236t, 237t for pregnant women, 347t nutrition support in, 232
prognosis for, 237, 239t physiologic functions of, 153, 154 pathophysiology of, 231
Cisapride, gastrointestinal effects of, 127 requirements for CRRT. See Continuous renal replacement therapy
Cisplatin in acute renal failure, in pediatric patients, (CRRT)
effects on clinical laboratory values, 129t 293t Cruzan, Nancy Beth, 378–379
metabolic effects of, 127 in parenteral nutrition for adults, 52 Culture, and feeding choices, 380
Citrates, effects on clinical laboratory values, 129t in preterm infants, 41t, 43 CVVH. See Continuous venovenous hemofiltration
CKD (Chronic Kidney Disease). See Kidney Copper-to-zinc ratio, in cancer diagnosis, 154 (CVVH)
disease, chronic Cornstarch, modified, in enteral nutrition, 63 CVVHD. See Continuous venovenous hemodialy-
Clarithromycin, drug-nutrient interactions, 125 Corn syrup, in enteral nutrition, 63 sis (CVVHD)
Clinitest, 203 Corticosteroids Cyanocobalamin. See also Vitamin B12
Clonidine, effects on clinical laboratory values, effects on clinical laboratory values, 129t in parenteral formulations (admixtures), for
129t gastrointestinal effects of, 127 pregnant women, 347t

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Cyclophosphamide Delayed hypersensitivity reaction (DHR), 20 in children, epidemiology of, 203

effects on clinical laboratory values, 129t Deliver 2.0, 242t, 243 chronic, 203, 205–209
hyponatremia caused by, 154 Dementia, nutrition support for patient with, 249 nonspecific, 206
for stem cell transplant recipient, nutritional ethical considerations with, 379 in chronic pancreatitis, 215
implications of, 194t Depression classification of, 203
Cyclosporine in cancer patient, 151 definition of, 203
and bone mineral density, 192 obesity and, 325 in diabetic patients, 318
effects on clinical laboratory values, 129t DEs. See Dextrose equivalents (DEs) diagnostic evaluation of, 203
hepatic effects of, 127 Development drug-induced, 77, 83, 127, 204
in immunosuppression for organ transplant cystic fibrosis and, 221 dysmotility-related, 203
recipients, 171, 173t in stem cell transplant recipient, 193 enteral nutrition with, contraindications to, 77
nephrotoxicity of, 189, 192 Developmental delay, children with, recommended epidemiology of, 203
nutritional side effects and interventions, 173t, energy intake for, 250t history-taking in, 203
192t Dexamethasone in HIV-infected (AIDS) patients, 146
pancreatic effects of, 127 antiemetic therapy with, for cancer patients, 161 hypersecretory, 203
Cyproheptadine, appetite stimulation by, 127 gastrointestinal effects of, 127 infectious, 203, 204
Cysteine, in parenteral formulations (admixtures), Dextrose inflammatory, 203
for neonatal intensive care, 302 overfeeding, in critical illness, 268 in inflammatory bowel disease, 232
Cystic fibrosis in parenteral formulations (admixtures) intractable/protracted, of infancy, 207
bone disease in, 226 for neonatal intensive care, 302 lactose intolerance and, 206–207
comorbidity in, 222 for pediatric patients, 109, 293t malabsorptive, 203
diet history in, 222 in parenteral nutrition, in critical illness, in organ transplant recipient, 181
focused assessment in, 221–222 266–267 osmotic, 203
genetics of, 220 Dextrose equivalents (DEs), in enteral nutrition, 63 in short-bowel syndrome, 207–209
and growth and development, 221 Dextrose monohydrate, in parenteral formulations in stem cell transplant recipient, 188, 189t
nutrient intake in, 220 (admixtures), 97 toddler’s, 206
nutrient losses in, 220 DHA. See Docosahexaenoic acid (DHA) in tube-fed patients, 79, 83, 83t, 119, 204–205
nutrient requirements in, 220–221 Diabetes mellitus causes of, 83, 83t
nutritional alterations in, 221 in adults, enteral formulations for, 66 management of, 83
nutrition support in chronic pancreatitis and, 217 in pediatric cancer, 163
enteral, 220, 224 in cystic fibrosis, 220, 222, 223, 224 types of, 77
goals of, 222–223 electrolyte imbalances in, 323 viral, 204
management of, 223–226 glucose levels in, 317–318 Diazepam, hepatic effects of, 127
parenteral, 220, 224 goals for, 318 Didanosine (Videx), diet and nutrition interactions
pancreatic enzyme replacement in, management rationale of therapy for, 318 with, 141t
of, 225–226 management of, 319–323. See also Insulin Diet(s)
pancreatic insufficiency in, 220–226 therapy for critically ill obese patients, 328
patient education in, 226 focused monitoring in, 322–323 ketogenic, 252, 253t
severity of, determinants of, 222 goals assessment in, 322–323 liberalized, for patients in long-term care, 366
Cystic Fibrosis Foundation, 226 in organ transplant recipient, 176 for obese patients, 328
Cystic fibrosis-related diabetes mellitus (CFRD). patient/caregiver education about, 183 very low calorie, for obese patients, 328
See Diabetes mellitus, in cystic fibrosis safety issues in, 323 Dietary reference intakes (DRI), in infancy to
Cytochrome P450 nutritional issues in, 317–318 adolescence, 43
CYP1A2, in drug metabolism, 119–120 plasma triglycerides in, 323–324 Dietary supplements, for obese patients, 329
CYP3A4, in drug metabolism, 119–120 posttransplant, treatment of, 178 Dietetic technician, in acute care organizations,
in drug metabolism, 119–120 prevalence of, 317 357, 358t
Cytokines type 1, 317 Diet Guidelines for Immunosuppressed Patients,
metabolic/nutritional effects of, in cancer type 2, 317 Internet address and resources provided by, 165
patients, 152 obesity and, 324–325 Diet history. See Nutritional history
in metabolic response to stress, 263 Diagnosis-Related Grouping (DRG), and reim- Di(2-ethylhexyl)phthalate (DEHP), contamination,
and serum albumin, 365 bursement for acute care nutrition support, in parenteral nutrition, 111
Cytotoxic agents 362–363 Diethylstilbestrol, effects on clinical laboratory
gastrointestinal effects of, 127 Dialysis values, 129t
hepatic effects of, 127 in acute renal failure, 281–282 Dietitian
in pediatric patients, nutritional considera- in acute care organizations, 357, 358t
D tions in, 287–291 credentialing of, 361
Daclizumab (Zenapax) slow, low-efficiency, 282 role in nutrition support, 360
for immunosuppression in organ transplant vitamin requirements in, 339 role on nutrition support committee, 361–362
recipients, 171, 173t Diarrhea in long-term care facility, 365
nutritional side effects and interventions, 173t acute, 204–205 Digestion, gastrointestinal, impaired, enteral
Data Assessment Verification Project, for long- in allergic disorders, 205 formulations for, 67
term care (LTC) facilities, 368 antibiotic-associated, 204 Digoxin
DEHP. See Di(2-ethylhexyl)phthalate (DEHP) bacterial, 203, 204 effects on clinical laboratory values, 129t
Dehydration in cancer patients gastrointestinal effects of, 127
in enteral nutrition, 80–81 nutritional therapy for, 162 Diltiazem, effects on clinical laboratory values,
in tube-fed patients, 87 pharmacotherapy for, 162 129t
Delavirdine (Rescriptor), diet and nutrition interac- causes of, 77 Diphenhydramine, antiemetic therapy with, for
tions with, 141t in celiac disease, 205–206, 206t cancer patients, 161

© 2005 A.S.P.E.N. www.nutritioncare.org. A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. 389
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Disaccharides, in enteral nutrition, 63 Durable power of attorney for health care, 364, for chronic kidney disease, 338–339
Disease 378, 379 for neonatal intensive care, 304
evolution of, nutrition and, 38 Dysgeusia, in stem cell transplant recipient, 188, requirements for
outcomes, in adults, nutritional support and, 39 189t in acute renal failure, in pediatric patients, 292
Diuresis, in preterm infants, 42 Dyslipidemia in adults, 49t, 51, 52t
Diuretics in obesity, 325 in burn patients, 296
abuse of, in anorexia nervosa, 350, 351 in organ transplant recipient, patient/caregiver in pediatric patients, 49t, 50, 109t
adverse effects and side effects of, 127 education about, 183 in stem cell transplant recipient, 195
anorexia caused by, 127 Dysphagia supplementation of, after discontinuation of PN,
dry mouth caused by, 127 in cancer patient, 151 116
pancreatic effects of, 127 esophageal, 248 Emetics, use of, in anorexia nervosa, 350
Docosahexaenoic acid (DHA) in neurologically impaired children, 250, 250t Emtricitabine (Emtriva), diet and nutrition interac-
in enteral formulations, 63 in neurologic disease, 248 tions with, 141t
in enteral nutrition, for preterm infants, 42 in organ transplant recipient, 183 EN. See Enteral nutrition
therapy with, in critical illness, 266 oropharyngeal, 248 Enalapril, effects on clinical laboratory values, 129t
Doxorubicin, metabolic effects of, 127 Endocrine system, in obesity, 324–325
DRI. See Dietary reference intakes (DRI) E Endoscopy. See also Percutaneous endoscopic gas-
Dronabinol, appetite stimulation by, 127 EAR. See Estimated average requirement (EAR) trostomy (PEG)
Drug(s). See also Medication(s) ECMO. See Extracorporeal membrane oxygena- for nasoenteric tube insertion, 56
absorption of, 118–119 tion (ECMO) Energy
enteral, 118–119 Edema in enteral formulations
factors affecting, 118–119 in burn patients, 300 for adult organ transplant recipient, 180
parenteral, 119 in end-stage liver disease, 241t for pediatric organ transplant recipient, 181
bioavailability of, 118 evaluation of, in cancer patient, 154 for pediatric patients, 68
diarrhea caused by, 204 in pediatric cancer patients, 158 imbalance, in obesity, 324
disintegration of, in digestive fluid, 118 EER. See Estimated energy requirement (EER) intake, in neurologically impaired children, rec-
disposition of, nutrition and, 134 EFAD. See Essential fatty acid deficiency (EFAD) ommendations for, 250t
dissolution of, in digestive fluid, 118 Efavirenz (Sustiva), diet and nutrition interactions losses of, 39
distribution of, 119 with, 141t in nutritional support, for adults, 51
enteral incompatibilities, 120 Eicosapentaenoic acid (EPA) for organ transplant recipient
pharmaceutical, 120 beneficial effects of, in cancer cachexia, 163 maintenance needs, 183
pharmacokinetic, 120 in enteral formulations, for adult cancer patients, recommendations, 179t
pharmacologic, 120 65 in parenteral formulations, for adults, 109t
physical, 120, 121t–122t therapy with, in critical illness, 266 in parenteral formulations (admixtures)
physiologic, 120 Elderly for neonatal intensive care, 302
excretion of, 120 energy requirements in, 51 for pediatric patients, 293t
gastrointestinal, 120 fiber intake by, 47t requirements for, 39
urinary, 120 fluid requirements in, 51 activity and, 39
with gastrointestinal effects, 127 nutrition screening for, 3 in acute renal failure, in adults, 284
hepatotoxicity of, 235 nutrition support for, ethical considerations in, of adult cancer patients, 159
metabolism of, 119–120 380 in adults, 50–51, 50t
by CYP1A2, 119–120 protein requirements in, 51 in anorexia nervosa, 349
by CYP3A4, 119–120 resting energy expenditure in, 51 basal metabolic rate and, 44, 44t
parenteral administration of trace element requirements in, 52 in burn patients, 296, 298t
entry point into bloodstream and, 119 vitamin requirements in, 52 in critical illness, 265
pharmacokinetics of, 119 Elecare, 242t in cystic fibrosis, 223–224, 223t, 226
routes for, 119 Electrocardiography, in anorexia nervosa, 351 in diabetic patients, 317
physical compatibilities with enteral feeding Electrolyte(s) in HIV-infected (AIDS) patients, 145
products, 120, 121t–122t in acute renal failure, in adults, 283 in hospitalized patients, 317
protein binding by, 119 dietary reference intakes for, by life stage group, maintenance, 39
volume of distribution of, 119 49t in obese patients, 317
Drug-nutrient interactions, 124–126, 127 in enteral formulations, for adult organ trans- assessment of, 327–328
in enteral nutrition, 367 plant recipient, 180 for organ transplant recipient, 176t
in immunosuppression for organ transplant imbalances pediatric, 43–45, 44t
recipients, 171, 173t–174t in anorexia nervosa, 351 activity level and, 44, 44t
in inflammatory bowel disease, 232 in cancer patients, 154 in pediatric liver disease, 239–241
in patients in long-term care, assessment for, in critical illness, 264 perioperative, 259
366 in inflammatory bowel disease, 232 in pregnancy, 343, 344
in tube-fed patients, 124–126 parenteral nutrition and, 115–116 in renal failure, 338
Dry mouth in pediatric cancer patients, 158 in stem cell transplant recipient, 194
in cancer patients, nutritional therapy for, 162 in tube-fed patients, 84, 85t–87t as total kcal versus nonprotein kcal, 50–51
drug-induced, 127 in liver disease, 239 in trauma, estimation of, 272
in stem cell transplant recipient, 188, 189t for organ transplant recipient supplements, for obese patients, 329
Dumping syndrome, 328–329 patient/caregiver education about, 183 Energy expenditure
Duodenal-gastric (DG) reflux, in tube-fed patients, recommendations, 180t in acute renal failure, in adults, 282
83 in parenteral formulations (admixtures), 97–98, calculation of, 327, 327t
DuoDERM, for skin protection, 60 109t, 110 in cancer patient, 151–152

390 A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. © 2005 A.S.P.E.N. www.nutritioncare.org.
 INDEX

in Crohn’s disease, 232 administration of, reducing contamination for renal disease in infants, 70
of hospitalized patients, 317 during, 73 in thickened products for infants, 71
measurement of, handheld device for, 279 for adults, 65–68 for wound healing, 68
Enfurvitide (Fuzeon), diet and nutrition interac- after organ transplantation, 180 for pancreatitis, in adults, 67
tions with, 141t for burn patients, 68 for patients in long-term care, 367
Enteral nutrition calorie-dense, for renal failure patients, 339 for pediatric patients, 68–69
abdominal distention with, 79 for cancer patients, adult, 65 after organ transplantation, 180–181
access for carbohydrate content of, 63 peptide based, 64
device features, selection of, 58–59 characteristics of, 63–65 polymeric, 367
postpyloric, 54 chemically defined for pregnant women, 346
prepyloric, 54 for infants, 70 preparation of, 73
in acute brain injury, 247 for pediatric patients, 69 and pressure ulcer prevention, 68
in acute pancreatitis, 214, 215 composition of, 63–65 for preterm infants, 71–73
early, safety of, 212 contamination of, reduction of, 73–74 protein in, 64
effect on pancreatic inflammation, 212 cow milk–based for pulmonary disease, in adults, 67–68
formulations for, 212 lactose-free, 69–70 for renal failure patients, 339
and gut integrity, 213 for term infants, 69 soy-based lactose-free, 70
in acute renal failure critical care/immunomodulating, for adults, storage of, 73
in adults, 284–285 65–66 thickened, for pediatric patients, 71
in pediatric patients, 291–292, 292t commercially prepared, 66 water in, 64
for adults for diabetes mellitus, in adults, 66 and wound healing, in adults, 68
in cancer, 159, 163 disease-specific, 367 gastrointestinal intolerances in, medications and,
fiber in, 64 elemental, 367 119
formulations for, 65–68 fat in, 63–64 gastrointestinal tolerance of, assessment of,
initiation of, 78 fiber in, 64 78–79
micronutrients in, 64–65 fish oils in, for adult cancer patients, 65 gravity-controlled feedings, 77–78
protein in, 64 general-purpose for adults, 78
after discontinuation of PN, 116 for adults, 65 for children, 78
in anorexia nervosa, 352 for pediatric patients, 68 continuous, 77–78
aspiration precautions with, 79–80 for glucose intolerance, in adults, 66 initiation of, 78
benefits of, 76 and glycemic control, 319 intermittent, 78
bolus feedings, 78 immune-enhancing, for adults, 65 hang times for, 73–74
for adults, 78 for impaired GI digestion or absorption, in for head and neck cancer patients, 160
for children, 78 adults, 67 head-of-bed elevation in, 80
initiation of, 78 for infants, 69–70 for HIV-infected (AIDS) patients, 146
bowel sounds with, 79 delivery guidelines for, 73–74 home, costs of, 38
for burn patients, 297–300 for kidney disease hydration status in, 80–81
in chronic kidney disease, 339–340 in adults, 68 implementation of, 77–78
complications of, 341 in pediatric patients, 70–71 in inborn errors of metabolism, 334
in chronic neurologic disease, 248–249 for liver disease, in adults, 66–67 indications for, 22, 76–77
complications of, 81–87 micronutrients in, 64–65 for infants
in critical illness, 267–269 modular, 367 cow milk protein allergy and, 70
gastrointestinal, 83–84 monomeric, 367 delivery guidelines for, 73–74
mechanical, 81–83 in neonatal intensive care, 308–309 formulations for, 69–70
metabolic, 84–87 nutrient-dense, for adults, 65 chemically defined, 70
in patients in long-term care, 367 for obese patient, 329 micronutrients in, 65
posttransplant, 181, 181t osmolality of soy protein allergy and, 70
in stem cell transplant recipient, 196 for adults, 65 thickened formulations, 71
in trauma patient, 274 for cancer patients, 65 infusion equipment for, selection of, 60–61
constipation with, 79, 84 in chemically defined products for infants, initiation of, 78
continuous feedings, transitioning from, 87 70 and insulin therapy, 319–321
contraindications to, 77 in chemically defined products for pediatric length of time required for, and selection of
cost of, 76 patients, 69 route, 54
in critical illness, 265–266 for critically ill adults, 66 long-term
in cystic fibrosis, 224 for diabetic adults, 66 candidates for, 54
delivery of, methods for, 77–78 for GI impairment in adults, 67 postpyloric access for, 57–58
device for, decision making about, 54 in high-MCT products, 69 pre-pyloric access for, 56–57
for diabetic patients, 318 for infants, 69–70 management of, 78–81
diarrhea with, 79, 83, 83t, 204–205 for liver disease in adults, 66 medication administration with, 120–126
discontinuation of, 87 in nutrient-dense products for preterm monitoring of, 78–81
drug-nutrient interactions in, 124–126, 367 infants, 72 in adult cancer patients, 163
effects on clinical laboratory values, 133t for pancreatitis, 67 in patients in long-term care, 367
ethical considerations with, 379 for pediatric patients, 68 in pediatric cancer patients, 164
formulations for for preterm discharge products, 72 nausea and vomiting with, 79
in acute pancreatitis, 212 for preterm infants, 71 in neonatal intensive care, 307–313
for acute renal failure, in pediatric patients, for pulmonary disease, 67 complementary feeding with, 311
291–292, 292t for renal disease in adults, 68 monitoring, 311

© 2005 A.S.P.E.N. www.nutritioncare.org. A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. 391
INDEX

for neurologically impaired children, 251 Esophagitis, in stem cell transplant recipient, for pediatric organ transplant recipient, 181
nutrient intake in, assessment of, 81 187–188 for pediatric patients, 69
nutritional requirements in, 39 Esophagus, complications in, with feeding tube, 82 pediatric requirements for, 46, 47t
for obese patient, 329 Essential fatty acid deficiency (EFAD), 224 percentage of energy contributed by, 63
for patients in long-term care, 366–367 in critically ill infants, 304 and wound healing, 68
JCAHO standards relevant to, 368 in cystic fibrosis, 221 metabolism of
reimbursement for, 369–370 in liver disease, 237 in acute pancreatitis, 213
for pediatric patients prevention of, 109 inborn errors of, 334t
with cancer, 151, 161, 164 in stem cell transplant recipient, 197 for organ transplant recipient
carbohydrate requirements in, 46, 46t treatment of, 225 maintenance needs, 183
chemically defined formulations for, 69 Estimated average requirement (EAR), 43 recommendations, 179t
in critical illness, 266 Estimated energy expenditure (EEE), 327, 327t in parenteral formulations (admixtures), 97
fiber in, 64 Estimated energy requirement (EER) for neonatal intensive care, 304
formulations for, 68–69 for healthy adults, 50, 50t for pediatric patients, 293t
high-MCT formulations for, 69 for sick adults, 50–51, 50t, 51t pediatric requirements for, 47, 47t
indications for, 76–77 Estrogens for preterm infants, 41t, 42
initiation of, 78 anorexia caused by, 127 requirements for
micronutrients in, 65 effects on clinical laboratory values, 129t pediatric, 46–47
oral stimulation with, 81 gastrointestinal effects of, 127 requirements for, in stem cell transplant recipient,
protein in, 45, 45t, 64, 109 pancreatic effects of, 127 194
postoperative, 261 Ethacrynic acid, effects on clinical laboratory
posttransplant Fat emulsion. See also Intravenous (IV) fat
values, 130t emulsions
in critically ill patients, 178, 182f Ethanol abuse
indications for, 178 effects on clinical laboratory values, 130t
and acute pancreatitis, 211–215 Fatigue, in cancer patients, nutritional therapy for,
route of, 178–180 and chronic pancreatitis, 215–220
in pregnancy, 345–346 162
micronutrient deficiencies in, 213 Fatty acid(s). See also Essential fatty acid defi-
for premature infants Ethical issues, 378
carbohydrate requirements in, 41t, 42 ciency (EFAD)
and adult cancer patients, 163
nutrient requirements in, 40, 41t in enteral formulations, 63
in chronic neurologic disease, 249
protein requirements in, 40, 41t metabolism of, inborn errors of, 334t
deliberations about, key considerations in,
preoperative, 260–261 omega-3, 40, 63, 66. See also Polyunsaturated
380–381
for preterm infants, formulations for, 71–73 fatty acids (PUFA)
in feeding patients, 379–380
for hospital discharge, 72 in enteral formulations, for burn patients, 68
goals of health care and, 381
nutrient-dense products, 72–73 supplementation of, in ulcerative colitis, 233
patient-centered focus and, 381
pump-assisted feedings, 78 therapy with, in critical illness, 266
and pediatric cancer patients, 165
for adults, 78 omega-6, 40, 63, 66. See also Polyunsaturated
wanted-warranted question and, 381
for children, 78 fatty acids (PUFA)
Ethical theory(ies), 378
initiation of, 78 Fatty acid oxidation defects, 334t
Ethics
and refeeding syndrome, 87 Fecal incontinence, in diabetic patients, 318
definition of, 378
residual volume in, 79 Fecal test(s), in diarrhea, 203
principles of, 378
in critically ill infants, 311 Feeding tube(s). See also specific tube
route for, selection of, 54, 55f of sustaining life versus prolonging dying, 381
Ethics committee, 378 care of, 59–60
safety of, 76 clogging of, 82
short-term in acute care organizations, 357, 358t
Ethics team, 378, 381 composition of, 58
candidates for, 54 declogger devices for, 82
nonsurgical postpyloric access for, 56 Ewing’s sarcoma, hematopoietic stem cell trans-
plantation for, 187 declogging
nonsurgical prepyloric access for, 54–55 catheter for, 82
surgical pre- and postpyloric access for, 56 Excretion, of drugs, 120
Exercise behavior, in anorexia nervosa, 350 endoscopy/cytology brushes for, 82
for stem cell transplant recipient, 196
Exercise therapy irrigants for, 82
stool pattern with, 79
for HIV-infected (AIDS) patients, 147 mechanical methods for, 82
transitioning from, 87
for stem cell transplant recipient, 193 methods for, 82
in patients in long-term care, 367
External jugular vein, cutdown. See also Central irrigant for, 81, 82
in trauma patient, 273–274
venous access irrigation of, 81, 82
tube features, 58–59. See also Feeding tube(s)
weight assessment during, 81 in obese patient, 330 latex, 58
Enteroglucagon, therapy with, in short-bowel syn- Extracorporeal membrane oxygenation (ECMO), length of, 58
drome, 209 for infants, 313 low-profile device, 58–59
Enteropathy, diabetic, 317–318 medication administration via, 82, 120–126
EPA. See Eicosapentaenoic acid (EPA) F patency of, maintenance of, 81
Epilepsy, ketogenic diet for, 252, 253t Failure to thrive, 38 placement of, complications of, 81
Epivir. See Lamivudine (Epivir) Fat(s). See also Intravenous (IV) fat emulsions; polyurethane, 58, 82
Erythromycin Lipid(s) polyvinyl chloride, 58
effects on clinical laboratory values, 129t body. See Adipose tissue presence of, complications of, 81–82
gastrointestinal effects of, 127 in enteral formulations, 63–64 red rubber catheter, 58
hepatic effects of, 127 for adults, 51 silicone, 58, 82
for nasoenteric tube placement, 56 for critically ill adults, 66 skin care with, 60
Esophageal cancer, micronutrient deficiencies in, for hepatic disease in adults, 66 stylet use with, 58
153 modular products, 63–64 weighted versus nonweighted, 58

392 A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. © 2005 A.S.P.E.N. www.nutritioncare.org.
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Female(s) in enteral nutrition, 80 G

basal energy expenditure (BEE) in, calculation in parenteral nutrition, 109t Galactosemia, 334t
of, 338 in pediatric patients, 50 Gallbladder cancer
basal metabolic rate in, 44, 44t in preterm infants, 41t, 42 diagnosis of, copper-to-zinc ratio in, 154
carbohydrate requirements in, 46t in stem cell transplant recipient, 194 micronutrient deficiencies in, 153
estimated energy requirements for, 50t restriction, in acute renal failure, in pediatric trace element deficiencies in, 154
fiber intake by, by life stage group, 47t patients, 291 Gallbladder sludge, in stem cell transplant recipient,
Harris-Benedict equation for, 50t withdrawal of, 379 197
ideal body weight of Fluoride Gastric banding, for obesity, dietary considerations
determination of, 5 dietary reference intakes for, by life stage group, after, 328–329
reference data for, 5, 17t 49t Gastric bypass, for obesity
mineral requirements in, 49t supplementation, in cystic fibrosis, 225 dietary considerations after, 328–329
protein requirements in, 45t Fluoroscopy, for nasoenteric tube insertion, 56 dietary supplements after, 329
resting energy expenditure in, estimation of, 44, Fluoxetine, anorexia caused by, 127 Gastric cancer
44t Folate. See Folic acid micronutrient deficiencies in, 153
vitamin requirements of, 48t Folic acid weight loss in, 150
Fetal growth rate, factors affecting, 344 deficiency of Gastric emptying, in diabetes, 317–318
Fiber(s) in acute pancreatitis, 213 Gastric gavage, for critically ill infants, 309–310
dietary in anorexia nervosa, 350t Gastritis, drug-induced, 127
adequate intake of, by life stage group, 47t in inflammatory bowel disease, 232 Gastroesophageal reflux
for diabetic patients, 319 in tube-fed patients, 87 in neonates, thickened enteral formulations for,
and glycemic control, 319 dietary reference intakes for, by life stage group, 71
requirements for, 40 48t in neurologically impaired children, 250
adult, 47, 47t intake, in pregnancy, 344–345 in tube-fed patients, 83
in elderly, 47, 47t in parenteral formulations (admixtures), 98 Gastrointestinal cancer. See also specific malig-
pediatric, 47, 47t for adults, 110t nancy
in enteral formulations, 64 for pregnant women, 347, 347t diagnosis of, copper-to-zinc ratio in, 154
requirements for Gastrointestinal injury, with feeding tube, 82
complications of, 64
in acute renal failure, in pediatric patients, Gastrointestinal motility
for pediatric patients, 69
292, 294t evaluation of, 248
functional, for preterm infants, 42
in burn patients, 297 in neurologic disease, 248, 248t
Finn v Commonwealth of Virginia, 379
in dialysis patients, 339 pharmacotherapy for, 248
First-pass effect, 119
in pregnancy, 345t Gastrointestinal obstruction, enteral nutrition in,
Fish oils, in enteral formulations, for adult cancer
in preterm infants, 41t contraindications to, 77
patients, 65
supplementation of, in ulcerative colitis, 233 Gastrointestinal pseudo-obstruction, enteral nutri-
Fistula(s)
Food(s) tion in, contraindications to, 77
enteral nutrition with, contraindications to, 77
intake, assessment of, in patients in long-term Gastrointestinal tract
enterocutaneous
care, 366 in diabetes, 317–318
in Crohn’s disease, 232
optional versus obligatory, 379 in HIV-infected (AIDS) patients, 140
with feeding tube, 82
safety precautions with obesity and, 325
FK506. See Tacrolimus
for immunosuppressed patients, 195–196, 196t obstruction of, in cancer patient, 151
Fluconazole, drug-nutrient interactions, 125–126 in liver disease, 243 Gastrojejunostomy
Fluid(s) for neutropenic patients, 162, 163 in obese patient, 329
in acute renal failure, in adults, 282–283 for organ transplant recipients, 183–184 percutaneous, 57–58
and body weight, 16 thermic effect of, 39 Gastroparesis
in children, 50 withdrawal of, 379 diabetic, 317–318
in neonates, 50 Food allergy, diarrhea caused by, 205 in neurologic disease, 248
in enteral formulations, for adult organ trans- Food aversions in organ transplant recipient, 181
plant recipient, 180 in critically ill infants, 307 in tube-fed patients, 83
extra, with enteral nutrition, 80–81 in pediatric intestinal transplant recipient, 178 Gastrostomy. See also Percutaneous endoscopic
imbalances Fortovase. See Saquinavir (Invirase, Fortovase) gastrostomy (PEG)
in critical illness, 264 FOS. See Fructooligosaccharides (FOS) complications of, 57, 57t
parenteral nutrition and, 115–116 Fosamprenavir (Lexiva), diet and nutrition interac- in pediatric cancer patients, 163
intake and output tions with, 141t in critically ill infants, 310
assessment of, in patients in long-term care, Foscarnet, for stem cell transplant recipient, nutri- for home nutrition support, 372
366 tional implications of, 194t laparoscopic, preoperative, 261
in enteral nutrition, 80 Fructooligosaccharides (FOS), in enteral formula- versus low-profile device, 58–59
in liver disease, 239 tions, 64 in obese patient, 329
for organ transplant recipient, recommendations, Fructose, in enteral formulations, for pediatric for organ transplant recipient, 180
179t–180t patients, 69 postoperative use of, 261
in parenteral formulations (admixtures) Functional assessment, of patients in long-term tube care in, 59
for chronic kidney disease, 338 care, 366 tube feeding via, 56
for pediatric patients, 293t Furosemide advantages and disadvantages of, 57
requirements for and bone mineral density, 192 long-term, 56–57
in acute renal failure, in pediatric patients, 291 effects on clinical laboratory values, 130t tube placement in
in adults, 51, 80, 109t Fusion inhibitor(s), diet and nutrition interactions radiologic, 57
in burn patients, 296 with, 141t surgical, 57
in elderly, 51 Fuzeon. See Enfurvitide (Fuzeon) tube replacement in, 59–60

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Gastrostomy tube(s), in children, 54 medications for, nutritional implications of, 192t Hazard Analysis Critical Control Point (HACCP),
Gatifloxacin, drug-nutrient interactions, 125 oral, in stem cell transplant recipient, 188 73, 369
Gentamicin, effects on clinical laboratory values, pancreatic, in stem cell transplant recipient, 193 Head circumference, for age, percentiles
130t skin, in stem cell transplant recipient, 188, 190t for boys, birth to 36 months, 30
GFR. See Glomerular filtration rate (GFR) in stem cell transplant recipient, 188–189 for girls, birth to 36 months, 31
Glomerular filtration rate (GFR) acute, 188, 190t Head injury
in acute renal failure, 281 chronic, 189 acute. See Acute brain injury
calculation of, 342 hyperacute, 188 metabolic response to, 263
cancer, 337 Granisetron, antiemetic therapy with, for cancer Health Care Financing Administration. See Centers
Glomerulonephritis, diffuse proliferating, in stem patients, 161 for Medicare and Medicaid Services (CMS)
cell transplant recipient, 190 Growth Heart transplantation
Glucagon-like peptide-2, therapy with, in short- abnormalities, in pediatric cancer patients, indications for, 172t
bowel syndrome, 209 157–158 outcome, malnutrition and, 171
Glucocorticoid(s) catch-up requirements, for pediatric organ trans- Height
and bone mineral density, 192 plant recipient, 176, 182t in cystic fibrosis, 221, 222
pancreatic effects of, 127 in cystic fibrosis, 222 evaluation of, in pediatric cancer patients,
Gluconeogenesis, in cancer patients, 153 cystic fibrosis and, 221 157–158
Glucose and energy requirements, 39 in stem cell transplant recipient, 193
in enteral nutrition, for pediatric patients, 46 inflammatory bowel disease and, 232 Height-for-age, in pediatric cancer patients,
homeostasis of pediatric patient 157–158
in adult cancer patients, 153 with cancer, nutritional support and, 164 Hematological monitoring, during enteral nutri-
in critically ill infants, 306 nutritional support and, 38 tion, 81
in pediatric cancer patients, 158 posttransplant, 176, 182t Hematopoietic stem cell transplantation
in pregnancy, 344 in stem cell transplant recipient, 193 allogeneic, 187
metabolism of, in critical illness, 264 Growth charts, 16 autologous, 187
in parenteral nutrition, for pediatric patients, 46 CDC, 16, 27–37 diseases and conditions treated by, 187
for children and adolescents, 16, 21t
for preterm infants, 42 food safety precautions with, 195–196, 196t
female, 33, 35, 37
serum. See also Hyperglycemia; Hypoglycemia indications for, 187
male, 32, 34, 36
in chronic kidney disease, 336 nutritional aspects of, 187–193
for infants
tracheal, measurement of, in detection of tube nutritional history in, 193
according to gestational age, 16, 20t
feeding–related aspiration, 80 nutrition management for, 195–197
female, 29, 31
Glucose intolerance nutrition support for
male, 28, 30
in adults, enteral formulations for, 66 enteral, 196
for premature infants, 16
in cancer patients, 153 monitoring of, 197
for toddlers, by birth weight group and sex, 16,
in obesity, 324–325 parenteral, 196–197
21t
Glucose polymers, for preterm infants, 42 nutrition therapy with, 194–195
Growth hormone (GH)
Glutamine goals of, 194
deficiency of
effects on clinical laboratory values, 130t nutrient requirements in, 194–195
in cystic fibrosis, 221
in enteral formulations, 64 in stem cell transplant recipient, 193 oral feedings and, 195–196, 196t
for burn patients, 68 effects on clinical laboratory values, 130t patient/caregiver education in, 197
for critically ill adults, 66 for HIV-infected (AIDS) patients, 147 pediatric patient, assessment of, 193
in parenteral formulations (admixtures), for in HIV-infected (AIDS) patients, 140 preparative conditioning for, 187
neonatal intensive care, 302 metabolic effects of, 127 renal complications of, 189–190
in parenteral nutrition, for pediatric patients, 46 pancreatic effects of, 127 sources of stem cells for, 187
therapy with therapy with syngeneic, 187
in critical illness, 266 in cystic fibrosis, 221, 224 Hemochromatosis, 235
in short-bowel syndrome, 208–209 in short-bowel syndrome, 208–209 Hemodialysis. See also Continuous venovenous
Glutaric aciduria type I, 333t Guar gum, in enteral formulations, 64 hemodialysis (CVVHD)
Glycemic control Gum arabic, in enteral formulations, 64 in acute renal failure, in pediatric patients, nutri-
in critical illness, 275 Gut integrity tional considerations in, 290
enteral formulations for, 66 in acute pancreatitis, 212 intermittent, 281–282
and outcomes of illness, 319 and disease outcome, 212 Hemofiltration. See Continuous venovenous
Glycerol, in parenteral formulations (admixtures), 97 enteral nutrition and, 213 hemofiltration (CVVH)
Glycogen storage disorder(s) promotion of, in trauma patient, 272 Hemoglobin, synthesis of, drugs affecting, 127
type I, 334t starvation and, 213 Hemolytic uremic syndrome (HUS), in stem cell
hypoglycemia in, prevention of, 334 Gynecologic malignancy, trace element deficiencies transplant recipient, 190
type II, 334t in, 153 Heparin
Glycolysis, in cancer patients, 153 and bone mineral density, 192
Goals, nutritional, 38–39 H effects on clinical laboratory values, 130t
in adults, 39 HACCP. See Hazard Analysis Critical Control Hepatic encephalopathy, 236, 236t, 241t
in HIV-infected (AIDS) patients, 145 Point (HACCP) Hepatic transport proteins, 19
pediatric, 38 Hamwi rule of thumb method, for determination of Hepatic veno-occlusive disease, in stem cell trans-
Gold products, taste alterations caused by, 127 ideal body weight, 5 plant recipient, 188
Graft-versus-host disease (GVHD) Harris-Benedict equations, 50, 50t, 272, 317, Hepatitis
gastrointestinal, in stem cell transplant recipient, 327–328, 327t, 338 toxic, 235
188, 190t, 191t using adjusted body weight in obese individuals, viral, 235
hepatic, in stem cell transplant recipient, 188, 190t 327–328, 327t in HIV-infected (AIDS) patients, 140

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Hepatitis A, 235 for organ transplant recipient, 181–182 and adverse outcomes in illness, 318–319
Hepatitis B, 235 preparation and administration of, 373 causes of, 318, 319
Hepatitis C, 235 reimbursement for, 375 in critical illness, 264, 275
Hepatitis D, 235 equipment maintenance and emergency in critically ill infants, 306
Hepatitis E, 235 repair/replacement, 373–374 in diabetic patient, 318–319
Hepatocellular carcinoma (HCC), trace element goals of, 371 osmotic diuresis caused by, 323
deficiencies in, 154 assessment of progress toward, 374 and pseudohyponatremia, 323
Herbal remedies, hepatotoxic, 243 and metabolic bone disease, 374 stress and, 317
Hereditary fructose intolerance, 334t monitoring of, 374 in organ transplant recipient, 181t
Histamine (H2) antagonists nutrient prescription in, 372 parenteral nutrition and, 114–115
adverse effects and side effects of, 127 outcomes of, 376 postprandial, in pregnancy, 344
drug-nutrient interactions, 127 parenteral in stem cell transplant recipient, 193, 197
History. See Medical history; Medication history; access for, 372 in tube-fed patients, 84
Nutritional history for cancer patients, 160 Hypergranulation, with feeding tube, 60
Hivid. See Zalcitabine (Hivid) complications of, 376 Hyperkalemia
HIV infection, 139 indications for, 372 in acute renal failure, in adults, 283
alcohol intake in, 144 infusion schedule for, 373 parenteral nutrition and, 115
anemia in, 146 for organ transplant recipient, 183 in tube-fed patients, 84, 85t
antioxidant therapy in, 145 preparation and administration of, 373 in tumor lysis syndrome, 154
appetite loss in, 146 reimbursement for, 375 Hyperlipidemia
body cell mass in, 143, 145 patient/caregiver education in, 371, 375 parenteral nutrition and, 115
bone loss in, 146–147 plan for, 374–375 posttransplant
chronic, nutritional effects of, 140 formulation of, 371–374 in adults, prevention/treatment of, 176
coinfections in, 144 professional support in, 371 in children, prevention/treatment of, 178
viral hepatitis, 140 provider of, selection of, 374 Hypermagnesemia
comorbidity in, 144 referral for, coordination of, 374–375 in critically ill infants, 307
diarrhea in, 146 reimbursement for, 375–376 parenteral nutrition and, 116
dyslipidemia in, 147 support organization for, 376
Hypermetabolism
energy needs in, 145 tapering of, 374
in burn patients, 296
enteral nutrition support in, 146 transitional feeding in, 374
in cancer patients, 151–152
hypogonadism in, 146 Homocystinuria, 333t
in chronic pancreatitis, 217
insulin resistance in, 147 Hormone(s), counterregulatory, in metabolic
Hypernatremia
medication side effects in, 144 response to stress, 263
parenteral nutrition and, 115
metabolic effects of, 140 Hormone replacement therapy (HRT), for stem cell
in tube-fed patients, 84, 85t
micronutrient interventions in, 145 transplant recipient, 192
Hyperphosphatemia
muscle wasting in, 146–147 Hormones, metabolic/nutritional effects of, in
in acute renal failure, in adults, 283
nonnutrient adjunctive therapies in, 146–147 cancer patients, 152
in critically ill infants, 306–307
nutritional aspects of, 139–143 HTN. See Hypertension
parenteral nutrition and, 116
nutritional management in, 145–147 Human immunodeficiency virus (HIV). See HIV
in tube-fed patients, 86t, 87
nutritional therapy in, goals of, 145 infection
in tumor lysis syndrome, 154
nutrition-related interventions in, 145 Human milk fortifiers (HMF), in enteral formula-
oral nutrient supplementation in, 146 tions, 309 Hypertension
organ and tissue function in, 140 for preterm infants, 71 in organ transplant recipient, patient/caregiver
parenteral nutrition support in, 146 Hydralazine education about, 183
patient counseling in, 145–146 adverse effects and side effects of, 127 post-transplant, 178
patient education in, 145 drug-nutrient interactions, 125, 127 Hypertriglyceridemia
pediatric Hydration status, in enteral nutrition, 80–81 in critical illness, 268
nutritional assessment in, 144–145 Hydrochlorothiazide, effects on clinical laboratory in critically ill infants, 306
nutritional compromise in, 143 values, 130t in obesity, 325
primary, metabolic effects of, 140 Hydrocolloids, for skin protection, with feeding parenteral nutrition and, 115
protein turnover in, 145 tube, 60 in stem cell transplant recipient, 197
smoking in, 144 Hydrocortisone, gastrointestinal effects of, 127 Hyperuricemia, in tumor lysis syndrome, 154
HNS. See Home nutrition support (HNS) 3-Hydroxy-3-methylglutaric aciduria, 333t, 334t Hypoalbuminemia
Holliday-Segar method, of fluid requirement Hydroxyzine, antiemetic therapy with, for cancer and drug disposition, 134
estimation, for children, 50 patients, 161 in inflammatory bowel disease, 232
Home care, accreditation for, 376 Hypercalcemia in pediatric cancer patients, 158
Home nutrition support (HNS) in critically ill infants, 306–307 Hypocalcemia
accreditation for, 376 parenteral nutrition and, 116 in acute pancreatitis, 213
administration route for, 372 in tube-fed patients, 85t–86t in acute renal failure, in adults, 283
candidates for, identification of, 371 in tumor lysis syndrome, 154 chemotherapy-induced, 154
components of, 371 Hypercapnia, in critical illness, 268 in critically ill infants, 306–307
costs of, 38 Hyperemesis gravidarum parenteral nutrition and, 115
death during, 376 enteral nutrition for, 345 in tube-fed patients, 85t
documentation of, 375 parenteral nutrition in, 346 in tumor lysis syndrome, 154
enteral Hyperglycemia Hypocaloric feeding
complications of, 376 in acute renal failure candidates for, 279
indications for, 372 in adults, 282 definition of, 279
infusion schedule for, 373 in pediatric patients, 287 in obesity, 328

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Hypochloremia, in anorexia nervosa, 351 Imipramine, appetite stimulation by, 127 Infant(s)
Hypogeusia, in stem cell transplant recipient, 188 Immune response, modulation of, in trauma critical illness in. See Neonatal intensive care
Hypoglycemia patient, 272 extracorporeal membrane oxygenation (ECMO)
adrenergic symptoms of, 318 Immune system, changes in, in cancer patients, for, 313
after discontinuation of tube feeding, in diabetic 152 nutrition support for
patient, 320, 320t Immunocompetence, evaluation of, 20 factors affecting, 311–313, 312t
in critically ill infants, 306 Immunodeficiency. See also HIV infection in specific disorders, 311–313, 312t
in diabetic patients, 318 in cancer patients, 152 oral stimulation for, with enteral nutrition, 81
in end-stage liver disease, 241t hematopoietic stem cell transplantation in, 187 Infant formula(s), for premature infants, compo-
fasting, in pregnancy, 344 Immunoglobulin A deficiency, in cancer patients, nents of, 40
in glycogen storage disorder type I, prevention 152 Infantile osteopetrosis, hematopoietic stem cell
of, 334 Immunomodulating agents, therapy with, in criti- transplantation in, 187
parenteral nutrition and, 115 cal illness, 266 Infection(s)
rebound Immunonutrition, in critical illness, 266 catheter-related, 113
after discontinuation of PN, 116, 322 Immunosuppression in critically ill infants, 306
after discontinuation of tube feeding, 320, in adults, enteral formulations for, 65–66 prevalence of, 113
320t diet guidelines for, Internet address and prevention of, 90, 91, 113
Hypoglycemic unawareness, in diabetic patients, resources for, 165 in trauma patient, 275
318 food safety precautions with, 195–196, 196t hyperglycemia and, 318
Hypokalemia for organ transplant recipients, 171 metabolic response to, 263
in acute renal failure, in adults, 283 agents for, 171, 173t–174t nosocomial, hyperglycemia and, 318
in anorexia nervosa, 351 antirejection regimens, 171 in organ transplant recipient, 181t
parenteral nutrition and, 115 drug-nutrient interactions in, 171, 173t–174t in stem cell transplant recipient, 190–191
in refeeding syndrome, 349 induction regimens, 171 parenteral nutrition and, 197
in tube-fed patients, 84, 85t maintenance regimens, 171 in tube-fed pediatric cancer patients, 163
Hypomagnesemia Immunotherapy, nutritional considerations in, 159 Inflammation
in acute pancreatitis, 213 Imuran. See Azathioprine acute-phase proteins in, 19, 22t
chemotherapy-induced, 154 Inborn errors of metabolism. See also specific dis- gastrointestinal, enteral nutrition with, con-
in critically ill infants, 307 order traindications to, 77
parenteral nutrition and, 116 and amino acid intake limitations, 333, 333t Inflammatory bowel disease (IBD). See also
in refeeding syndrome, 349 carbohydrate intake limitations in, 333, 334t Crohn’s disease (CD); Ulcerative colitis (UC)
Hypometabolism, in cancer patients, 151–152 carnitine supplementation in, 332, 333t and anorexia nervosa, 349
Hyponatremia chemically defined nutrient formulations for, definition of, 231
in anorexia nervosa, 351 334 malnutrition in, 231–232, 232t
chemotherapy-induced, 154 enteral nutrition in, 334 nutritional status in, 231–232
in end-stage liver disease, 241t focused assessment in, 332–333 pathophysiology of, 231
parenteral nutrition and, 115 hematopoietic stem cell transplantation in, 187 pharmacologic therapy for, 231
in tube-fed patients, 84, 85t history-taking in, 332–333 prevalence of, 231
Hypophosphatemia management of, 333–335 Infliximab, for Crohn’s disease, 231
in acute renal failure, in adults, 283 focused monitoring in, 334 Infusion pump(s)
chemotherapy-induced, 154 goals assessment in, 334 for enteral nutrition, 60
in critically ill infants, 306–307 patient/caregiver education in, 334–335 alarms for, 61
parenteral nutrition and, 116 nutrient intake limitations in, 333–334, 333t, automatic flush systems for, 61
in refeeding syndrome, 349 334t cassette devices, 60
in tube-fed patients, 86t, 87 nutritional alterations in, 332 cleaning of, 61
Hypoproteinemia, and drug disposition, 134 nutritional aspects of, 332 fluid delivery mechanisms, 60
Hypothalamic-pituitary-adrenocortical axis, in crit- parenteral nutrition in, 334 infusion rates, 60–61
ical illness, 264 and quality of life, 333 maintenance of, 61
Hypoventilation, in obesity, 325 treatment of, in infants and children, objec- mechanics of, 60
tives/goals of, 333 for outpatient, 60
I Indinavir (Crixivan), diet and nutrition interactions rotary peristaltic devices, 60
IBW. See Ideal body weight (IBW) with, 141t selection of, 60
Ideal body weight (IBW) Indirect calorimetry, 45, 50, 328 servicing of, 61
amputations and, 5–6, 19f accuracy of, technical factors affecting, 278 intravenous, 60
in cystic fibrosis, 221 advances in (future directions for), 279 for parenteral nutrition, 94, 94t, 111, 346
determination of, 5 conduction of, ideal parameters for, 277–278 ambulatory, 94, 94t
and energy requirements, 327 data interpretation in, 278 stationary, 94, 94t
percentages contributed by individual body frequency of measurement with, 279 Injury, metabolic response to, 263, 264t, 271–272
parts, 5–6, 19f in ICU, indications for, 277 Insulin
reference data for in liver disease, 238 effects on clinical laboratory values, 130t
for females, 5, 18t in neurologically impaired children, 251 pancreatic effects of, 127
for males, 5, 17t nutrition support regimens based on, 279, 279t preparations, pharmacokinetics of, 319t
and usual weight, comparison of, 6–16 in pregnancy, 346 Insulin resistance
IDPN. See Intradialytic parenteral nutrition (IDPN) in trauma patients, 273 in acute renal failure, in adults, 282
Ileus, enteral nutrition with, contraindications to, Indomethacin in cancer patients, 153
77 effects on clinical laboratory values, 130t in critical illness, 264
Illness, and energy requirements, 39 gastrointestinal effects of, 127 in stem cell transplant recipient, 193

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Insulin therapy supplementation, during parenteral nutrition in Jeune’s thoracic dystrophy, pancreatic insufficiency
in critical illness, 268 pregnancy, 348 in, 220
and enteral nutrition, 319–321 Ireton-Jones equations, 50, 51t, 327, 327t Johanson-Blizzard syndrome, pancreatic insuffi-
and hypoglycemia after discontinuation of tube Iron ciency in, 220
feeding, 320, 320t absorption, drugs affecting, 127 Joint Commission on Accreditation of Healthcare
intravenous deficiency of Organizations (JCAHO)
for ICU use, 321, 321t in acute renal failure, in pediatric patients, regulation of acute care organizations, 359
for non-ICU use, 321, 322t 292 regulation of long-term care (LTC) facilities, 368
and parenteral nutrition, 319, 321–322 in inflammatory bowel disease, 232 tracer methodology used by, 368
subcutaneous regular insulin supplementation, dietary reference intakes for, by life stage group, Justice, as ethical principle, 378
for tube-fed patient, 320, 320t 49t
Insurance coverage, for home nutrition support, 376 metabolism of, in trauma, 271 K
Interferon(s) (IFN), IFN-γ, metabolic/nutritional in parenteral formulations (admixtures), 98 Kaletra. See Lopinavir (Kaletra)
effects of, in cancer patients, 152 for critically ill infants, 304 Karnofsky Performance Status Scale, 157
Interleukin(s) (IL) requirements for 2-Ketoadipic aciduria, 333t
IL-1, metabolic/nutritional effects of, in cancer in critical illness, 267 Ketogenic diet, 252, 253t
patients, 152 in infancy, 49, 49t Ketorolac, gastrointestinal effects of, 127
IL-6, metabolic/nutritional effects of, in cancer in liver disease, 239 Kidney disease. See also Acute renal failure
patients, 152 in parenteral nutrition for adults, 52 in adults, enteral formulations for, 68
Internal jugular vein, catheterization. See also in postmenopausal women, 52 in children, and growth, 176
Central venous access in pregnancy, 343, 344, 345t chronic
in obese patient, 330 in preterm infants, 41t, 43 classification of, 337t
International Classification of Diseases (ICD)-9- storage, in HIV-infected (AIDS) patients, 140 enteral nutrition in, 339–340
CM, and reimbursement for acute care nutrition supplementation complications of, 341
support, 363 for critically ill infants, 309 nutritional assessment in, 336–337
Internet resources, for patient/caregiver education, in cystic fibrosis, 225 nutrition support in, 337–338
in cancer, 165 for HIV-infected (AIDS) patients, 146 complications of, 341
Intervention(s), nutritional. See also specific during parenteral nutrition in pregnancy, goals for, 337
intervention 347–348 monitoring during, 340–341
Iron dextran, in parenteral formulations (admix- parenteral nutrition in, 338–339
in adults, goals of, 39
tures), 98, 101 complications of, 341
mode of, 22
Irritable colon of childhood, 206 in organ transplant recipient, 181t
for pediatric patient, goals of, 38
in pediatric patients, enteral formulations for,
timing of, 22 Ischemia, gastrointestinal, enteral nutrition with,
70–71
Intestinal motility, drug-induced changes in, 127 contraindications to, 77
in stem cell transplant recipient, 189–190
Intestinal transplantation, in pediatric patient Isoleucine, in enteral formulations, 64
Kidney function, evaluation of
and growth, 178 Isoniazid
in adults, 282
oral aversions after, 178 effects on clinical laboratory values, 131t
in pediatric patients, 287
pretransplant nutritional considerations in, 177t hepatic effects of, 127
Kidney/pancreas transplantation, outcome, obesity
Intradialytic parenteral nutrition (IDPN), 340 Isovaleric acidemia, 333t
and, 171–174
Intravenous (IV) fat emulsions, 108 Itraconazole, absorption of, 118
Kidney transplantation
administration sets for, 111 IVFE. See Intravenous (IV) fat emulsions
indications for, 172t
for chronic kidney disease patients, 338 outcome
in critical illness, 267 J malnutrition and, 171
di(2-ethylhexyl)phthalate (DEHP) contamina- Jejunostomy. See also Needle catheter jejunostomy obesity and, 171–174
tion in, 111 (NCJ) in pediatric patient, pretransplant nutritional
inborn errors of metabolism and, 334 advantages and disadvantages of, 58 considerations in, 177t
infusion time for, 111 button, 58 recipient, nutritional support for, 340
iron dextran in, precautions with, 98 complications of, 56, 56t, 58 Kwashiorkor, 21–22
label templates for, 105, 106f in trauma patient, 274
microbial growth potential in, 102 for head and neck cancer patients, 160 L
for neonatal intensive care, 304 for home nutrition support, 372 Labetalol, gastrointestinal effects of, 127
in parenteral formulations (admixtures), 97 laparoscopic, 58 Laboratory monitoring
for preterm infants, 42 preoperative, 261 during enteral nutrition, 81
for pediatric patients, 109 in obese patient, 329 in home nutrition support, 374
Intravenous (IV) hyperalimentation. See Parenteral for organ transplant recipient, 178 during parenteral nutrition, 112
nutrition postoperative use of, 261 Laboratory test(s)
Invirase. See Saquinavir (Invirase, Fortovase) radiologic, 58 in anorexia nervosa, 351, 352, 352t
Iodide, in parenteral formulations (admixtures) roux-en-Y, 58 in cancer, 157
for chronic kidney disease, 339 serosal tunnel, 58 in cystic fibrosis, 222
for neonatal intensive care, 305 tube care in, 59 in HIV-infected (AIDS) patients, 143–144
Iodine tube feeding via, 56, 57–58 medications and, 127, 128t–134t
dietary reference intakes for, by life stage group, indications for, 57 in obese patient, 327
49t tube insertion in, 57–58 for organ transplant recipient, 175t
in parenteral formulations (admixtures), 98 surgical, 58 in patients in long-term care, 366
requirements for, 52 tube replacement in, 60 in pediatric cancer patients, 158
in pregnancy, 345t Witzel, 58 in pediatric HIV-infected (AIDS) patients, 145
in preterm infants, 41t Jejunum, medication administration in, 119 in stem cell transplant recipient, 193

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Lactalbumin, in enteral formulations, 64 structured in pediatric patient

Lactate, in cancer patients, 153 in enteral formulations, for critically ill adults, pretransplant nutritional considerations in, 177t
Lactation 66 prognosis for, 237
mineral requirements in, 49t MCFA/LCFA, in parenteral formulations vitamin recommendations for, 178t
vitamin requirements in, 48t (admixtures), 97 Living will, 364, 378, 379
Lactose in parenteral nutrition, in critical illness, 267 Long-chain fatty acids (LCFA)
in enteral nutrition, 63 types of, 39–40 emulsions, in parenteral formulations (admix-
for preterm infants, 42 Lipid-lowering therapy, for HIV-infected (AIDS) tures), 97
Lactose-free enteral formulations patients, 147 in enteral formulations, 63
cow milk–based, for infants, 69–70 Lipid-mobilizing factor, metabolic/nutritional in nutritional support, for adults, 51
soy-based, for infants, 70 effects of, in cancer patients, 152 in parenteral nutrition, for pediatric patients, 47
Lactose intolerance, diarrhea caused by, 206–207 Lipolysis Long-term care (LTC), definition of, 364
Lamivudine (Epivir), diet and nutrition interactions in cancer patients, 153 Long-term care (LTC) facility(ies)
with, 142t in critical illness, 264 care plans in, 368
Lanugo, in anorexia nervosa, 351 Lithium, effects on clinical laboratory values, 131t CMS Quality Indicator used in, 368
Latex allergy, 58 Liver Data Assessment Verification Project for, 368
Laxatives cancer of, trends in, 150 enteral nutrition in, 366–367
abuse of, in anorexia nervosa, 350, 351 drugs affecting, 127 JCAHO standards relevant to, 368
for cancer patients, 161–162 in HIV-infected (AIDS) patients, 140 reimbursement for, 369
effects on clinical laboratory values, 131t metabolic functions of, in cancer patients, 153 liberalized diet in, 366
LBM. See Lean body mass Liver disease mandated care in, 368
LCFA. See Long-chain fatty acids (LCFA) in adults nutrition care process in, 365–368
Lean body mass, 324 acute, 235 nutrition support in, 364
and energy requirements, 327 chronic, 235 professional staff and, 364–365
estimation of, 16 enteral formulations for, 66–67 reimbursement for, 369–370
loss of, 16 malnutrition in, 236–237, 236t, 237t residents’ rights and, 364
maintenance of types of, 235 role of, 364
in adults, 39 alcoholic, 235
oral diet interventions in, 366
in pediatric patient, 38 metabolic alterations in, 236
oral supplements in, 366
Legal aspects, of patient care and feeding, 378–379 assessment in, 237–238, 240t
parenteral nutrition in, 367–368
Length-for-age percentiles autoimmune, 235
JCAHO standards relevant to, 368
for boys, birth to 36 months, 28 cholestatic, 235
reimbursement for, 369–370
for girls, birth to 36 months, 29 chronic
regulation of, 368–369
Leptin, metabolic/nutritional effects of, in cancer malnutrition in, 236–237, 236t
Resident Assessment Instrument for, 368
patients, 152 metabolic alterations in, 235–236
residents
Leucine, in enteral formulations, 64 enteral nutrition in, 241–243
comorbidity in, 365
Leukemia. See also Acute lymphoblastic leukemia in infants
nutrition assessment for, 365–366
(ALL) enteral formulas for, 242
restorative dining in, 366
in children, 150 types of, 235
self-help devices/utensils in, 366
hematopoietic stem cell transplantation in, 187 infectious, 235
state licensure for, 369
pediatric nutrition support in, goals of, 238–241
micronutrient deficiencies in, 153 oral diet in, 241 state regulation of, 368–369
trace element deficiencies in, 153 parenteral nutrition in, 243 Long-term disability(ies), in pediatric patient,
weight loss in, 150 patient education in, 243 reduction of, 38
Leukemia inhibitory factor (LIF), 152 in pediatric patients Lopinavir (Kaletra), diet and nutrition interactions
Levofloxacin, drug-nutrient interactions, 125 chronic, 235 with, 142t
Levothyroxine, drug-nutrient interactions, 126 enteral formulas for, 242, 242t, 243 Lorazepam, antiemetic therapy with, for cancer
Lexiva. See Fosamprenavir (Lexiva) feeding goals in, 239–241 patients, 161
LIF. See Leukemia inhibitory factor (LIF) malnutrition in, 237, 237t Low-profile device (LPD)
Linoleic acid parenteral nutrition for, 243 for enteral nutrition, 58–59
in enteral formulations, 64 types of, 235 for home nutrition support, 372
requirements for, pediatric, 47t protein-calorie malnutrition in, 236–237 LPD. See Low-profile device (LPD)
Linolenic acid, requirements for, pediatric, 47t prognosis for, 237, 239t LTC. See Long-term care (LTC)
Lipid(s) Liver enzyme(s) Lung cancer
in acute renal failure, in adults, 282 in drug metabolism, 119–120 diagnosis of, copper-to-zinc ratio in, 154
hydroperoxides, as contaminants in parenteral drugs affecting, 127 energy expenditure in, 151
formulations, 307 parenteral nutrition and, 114 micronutrient deficiencies in, 153
metabolism of, in cancer patients, 153 Liver failure trace element deficiencies in, 153
in nutritional support, for adults, 51, 109t acute, 235 weight loss in, 150
in parenteral nutrition, in critical illness, 267 fulminant, 235 Lung transplantation
in pediatric cancer patients, 158 late-onset, 235 indications for, 172t
for preterm infants, 41t, 42 in pediatric patients, 235 outcome
requirements for, 39–40 subfulminant, 235 malnutrition and, 171
in burn patients, 297 Liver transplantation obesity and, 171
serum levels. See also Dyslipidemia; Hyperlipi- indications for, 172t in pediatric patient
demia outcome and growth, 178
in adult organ transplant recipient, 176 malnutrition and, 171 pretransplant nutritional considerations in, 177t
in pediatric organ transplant recipient, 178 obesity and, 174 Lycopene, plasma, in chronic pancreatitis, 216

398 A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. © 2005 A.S.P.E.N. www.nutritioncare.org.
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Lymphoma(s) fiber intake by, by life stage group, 47t Medicaid, reimbursement for nutrition support
in children, 150 Harris-Benedict equation for, 50t in acute care, 363
hematopoietic stem cell transplantation in, 187 ideal body weight of in long-term care, 369
pediatric determination of, 5 Medical history
micronutrient deficiencies in, 153 reference data for, 5, 17t in acute pancreatitis, 213
prognosis for, nutritional status and, 160 mineral requirements in, 49t in anorexia nervosa, 350
trace element deficiencies in, 153 protein requirements in, 45t of cancer patient, 154
Lysinuric protein intolerance, 332, 334t resting energy expenditure in, estimation of, 44, components of, 4, 6t
Lysosomal disorders, hematopoietic stem cell 44t of organ transplant recipient, 175t
transplantation in, 187 vitamin requirements of, 48t in pediatric cancer patient, 157
Malnutrition Medicare
M in aging, 364 prosthetic device act of, 375
MAC. See Mid-arm circumference (MAC) in cancer patients, 150 reimbursement for nutrition support
Macronutrients, requirements for, 39 in children, nutrition support for, initiation of, 22 in acute care, 362
in cystic fibrosis, 223–224 in chronic pancreatitis, 216–217 in home, 375
Magnesium in Crohn’s disease, 231–232, 232t in long-term care, 369–370
deficiency of, in inflammatory bowel disease, 232 diagnosis of, 21 Medication(s). See also Drug(s)
dietary reference intakes for, by life stage group, and disease outcomes, 38 absorption of
49t and drug distribution, 134 enteral, 118
excretion of, drugs affecting, 127 in HIV-infected (AIDS) patients, 140 factors affecting, 118–119
imbalances, in tube-fed patients, 86t, 87 immunosuppression in, detection of, 20 administration of
ionized, clinical significance of, 158 indicators of, in adults, 3 in jejunum, 119
in parenteral formulations (admixtures), 98, 110 and infection, 38 parenteral considerations, 126–127
micronutrient status in, 20 via enteral tubes, 120–126
for adults, 109t
mild, 19t, 21, 259 dosage forms not recommended for,
for chronic kidney disease, 339
moderate, 19t, 21, 259 123–124
for neonatal intensive care, 304
adverse effects and side effects of, in HIV-
for pediatric patients, 109t and morbidity and mortality, 38
infected (AIDS) patients, 144
for preterm infants, 109t in organ transplant recipient, and posttransplant
and bone mineral density, 192
physiologic functions of, 86t, 87 survival, 171
buccal, 123
requirements for in pediatric cancer patient, 157–158
compatibility with parenteral formulations,
in adults, 52t and outcomes, 160
126–127
in pregnancy, 345t in pediatric patient, effects of, 38
constipation caused by, 84
in preterm infants, 41t, 43 severe, 19t, 21, 259
diarrhea caused by, 77, 83
in stem cell transplant recipient, 195 in ulcerative colitis, 231–232, 232t
effects on clinical laboratory values, 127,
serum. See also Hypermagnesemia; Hypomag- uncomplicated, causes of, 3
128t–134t
nesemia weight data indicating, 6–16, 19t
enteric-coated, 123
in acute renal failure, in pediatric patients, 292 Maltodextrin
feeding tube clogging caused by, 82
in chronic kidney disease, 336 in enteral formulations, for pediatric patients, 69
gastrointestinal effects of, 318
in diabetic patient, 323 in enteral nutrition, 63
granular-type, administration of, via enteral
in pediatric cancer patients, 158 MAMC. See Mid-arm muscle circumference tubes, 123
supplementation (MAMC) immediate-release oral, administration of, via
in acute brain i jury, 248 Managed care, and home nutrition support, 376 enteral tubes, 120–122
during parenteral nutrition in pregnancy, 348 Manganese liquid
Magnesium hydroxide, effects on clinical laboratory as contaminant, in parenteral formulations absorption of, enteral, 118
values, 131t (admixtures), 99 administration of, via enteral tubes, 122–123
Magnesium salts, effects on clinical laboratory dietary reference intakes for, by life stage group, for enteral administration, 367
values, 131t 49t metabolic effects of, 127
Maintenance energy requirement, 39 in parenteral formulations (admixtures), 98 nephrotoxicity of, 189
Malabsorption. See also Diarrhea for adults, 110t in parenteral formulations (admixtures), 101
in cancer patients, 152 for chronic kidney disease, 339 secondary (Y site), 126
in chronic pancreatitis, 216–217 for neonatal intensive care, 305 solid-dose forms
diarrhea in, 203 for pediatric patients, 110t, 293t absorption of, enteral, 118
and disease outcomes, 38 for pregnant women, 347t that should not be crushed, 123
evaluation for, in cystic fibrosis, 222 physiologic functions of, 153 sorbitol in, 122–123
in HIV-infected (AIDS) patients, 140 requirements for for stem cell transplant recipient, nutritional
in inflammatory bowel disease, 232, 232t in acute renal failure, in pediatric patients, 293t implications of, 193, 194t
without diarrhea, in tube-fed patients, 84 in parenteral nutrition for adults, 52 sublingual, 123
Malassezia furfur, growth of, in parenteral formu- in preterm infants, 41t suspensions, administration of, via enteral tubes,
lations (admixtures), 102 Mannitol, effects on clinical laboratory values, 123
Maldigestion, in inflammatory bowel disease, 232, 131t sustained-release, 123
232t Maple syrup urine disease, 333t syrups, 123–124
Male(s) thiamine supplementation in, 333 weight gain caused by, 325, 326t
basal energy expenditure (BEE) in, calculation Marasmus, 21–22 Medication history
of, 338 MBD. See Metabolic bone disease (MBD) in cancer patients, 154
basal metabolic rate in, 44, 44t MCT. See Medium-chain triglycerides (MCT) in obesity, 325, 326t
carbohydrate requirements in, 46t Measured energy expenditure (MEE), 327, 328 in pediatric cancer patient, 157
estimated energy requirements for, 50t Meat protein, in enteral formulations, 64 in stem cell transplant recipient, 193

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INDEX

Medium-chain fatty acid (MCFA)/LCFA mixtures, Metoprolol, effects on clinical laboratory values, in acute renal failure, in pediatric patients, 292
in parenteral formulations (admixtures), 97 131t in females, 49t
Medium-chain triglycerides (MCT) Metronidazole in lactation, 49t
in enteral formulas, for children with liver for Crohn’s disease, 231 in males, 49t
disease, 242, 242t effects on clinical laboratory values, 131t in obese patients, 328
in enteral formulations, 63 taste alterations caused by, 127 pediatric, 47–49, 49t
for pediatric organ transplant recipient, 181 MIC. See Minimum inhibitory concentration in pregnancy, 49t
for pediatric patients, 69 (MIC) in preterm infants, 41t, 43
in nutritional support, for adults, 51 Microbe(s), growth of, in parenteral formulations in stem cell transplant recipient, 195
in parenteral nutrition (admixtures), 102 supplements
in critical illness, 267 Microlipid, 63–64 for cancer patients, 153
for pediatric patients, 47 Micronutrients for obese patients, 329
for preterm infants, 42 deficiencies of for organ transplant recipient, patient/care-
Melanoma, trace element deficiencies in, 153 in acute pancreatitis, 213 giver education about, 183
Melphalan, for stem cell transplant recipient, nutri- in anorexia nervosa, 350t Minimum inhibitory concentration (MIC), 125
tional implications of, 194t in cancer patients, 153 Molybdenum
Mental assessment, of patients in long-term care, in cystic fibrosis, 221 dietary reference intakes for, by life stage group,
366 in enteral formulations, 64–65 49t
Meperidine, effects on clinical laboratory values, in parenteral formulations (admixtures), for in parenteral formulations (admixtures), 98
131t pregnant women, 347, 347t for neonatal intensive care, 305
6-Mercaptopurine, for Crohn’s disease, 231 requirements for, 39, 40 in parenteral nutrition, for pediatric patients, 50
Mesalamine, for inflammatory bowel disease, 231 in acute renal failure, in pediatric patients, 292 requirements for, 52
Metabolic acidosis, in critically ill infants, 307 in HIV-infected (AIDS) patients, 145 in preterm infants, 41t
Metabolic bone disease (MBD), 374 in pregnancy, 344, 345t Monoclonal antibody(ies) (MAb), nutritional side
in neonatal intensive care, 307 supplementation effects and interventions, 192t
PN-associated, 114, 114t in cystic fibrosis, 224–225, 225t Monosaccharides, in enteral nutrition, 63
Metabolic response to burns, 296 for HIV-infected (AIDS) patients, 146 Morbidity and mortality, in pediatric patient,
reduction of, 38
Metabolic response to stress, 263, 264t, 271–272 and wound healing, 68
Morphine, effects on clinical laboratory values,
Metabolic stress state, in acute pancreatitis, 213 Mid-arm circumference (MAC), 16
131t
Metabolic syndrome in pediatric cancer patients, 158
Mucolipidoses, hematopoietic stem cell transplan-
clinical features of, 325 in stem cell transplant recipient, 193
tation in, 187
diagnostic criteria for, 325 Mid-arm muscle area, in pediatric cancer patients,
Mucopolysaccharidosis (MPS), hematopoietic
Metabolism. See also Inborn errors of metabolism 158
stem cell transplantation in, 187
in cancer patients, 153 Mid-arm muscle circumference (MAMC), 16
Mucosa, everted, with feeding tube, 60
in HIV-infected (AIDS) patients, 140 Mifflin equation, in estimation of metabolic rate,
Mucositis
substrate 328
in cancer patients, nutritional therapy for, 162
in acute pancreatitis, 213 Milk
cancer treatment–related, 151
in obesity, 324 cow’s
prevention/treatment of, for cancer patients, 161
Metamucil, administration of, via enteral tubes, 123 allergy to, in infants, 70
in stem cell transplant recipient, 187–188, 189t
Metformin, effects on clinical laboratory values, in enteral formulations, 64
Multiple myeloma (MM)
131t lactose-free products, 69–70 hematopoietic stem cell transplantation in, 187
Methionine, in enteral formulations, 64 for pediatric patients, 68 immunological effects of, 152
Methotrexate for term infants, 69 Multiple organ failure, 272
for Crohn’s disease, 231 human Multivitamin products
effects on clinical laboratory values, 131t components of, 40 for cancer patients, 153
metabolic effects of, 127 for critically ill infants, 308 for infants, 305
mucositis caused by, 187 fortifiers, 309 in liver disease, 239
nutritional side effects and interventions, 192t in enteral formulations for preterm infants, for parenteral formulations (admixtures), 98
Methoxsalen, nutritional side effects and interven- 71 for pediatric patients, daily dose recommenda-
tions, 192t protein in, 45t tions, 110t
3-Methylcrotonylglycinuria, 333t Milk protein, in enteral formulations, for pediatric for pregnant women, 344
Methyldopa patients, 68 Muromonab CD3 (OKT3)
dry mouth caused by, 127 Milk thistle, 243 in immunosuppression for organ transplant
effects on clinical laboratory values, 131t Minerals. See also Trace mineral status recipients, 171, 174t
3-Methylglutaconic aciduria, 333t in acute renal failure, in adults, 283 nutritional side effects and interventions, 174t
Methylmalonic acidemia, 333t deficiencies of, in inflammatory bowel disease, Muscle catabolism, in cancer patients, 153
Methylmalonic aciduria, vitamin B12 supplementa- 232 Muscle function, assessment of, in cancer patient,
tion in, 333 dietary reference intakes for, by life stage group, 157
Methylprednisolone 49t Muscle mass, estimation of, 16
gastrointestinal effects of, 127 imbalances Muscle wasting
nutritional side effects and interventions, 173t in pediatric cancer patients, 158 in anorexia nervosa, 350t
Methylprogesterone, appetite stimulation by, 127 in tube-fed patients, 84, 85t–87t evaluation of, in cancer patient, 154
Metoclopramide for organ transplant recipient, recommendations, Mycophenolate mofetil (CellCept)
effects on clinical laboratory values, 131t 180t in immunosuppression for organ transplant
gastrointestinal effects of, 127 in parenteral formulations (admixtures), for recipients, 171, 174t
for nasoenteric tube placement, 56 chronic kidney disease, 338 nutritional side effects and interventions, 174t,
in tube-fed patients, diarrhea caused by, 119 requirements for 192t

400 A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. © 2005 A.S.P.E.N. www.nutritioncare.org.
 INDEX

Myelodysplastic syndromes, hematopoietic stem parenteral nutrition for Nucleoside reverse transcriptase inhibitors, diet
cell transplantation in, 187 hyperglycemia with, 114–115 and nutrition interactions with, 141t–142t, 142
Myelomeningocele, children with, recommended initiation of, 109 Nucleotides, in enteral formulations, for critically
energy intake for, 250t protein in, 46t, 109 ill adults, 66
Myfortic, 171 regurgitation in, thickened enteral formulations Nurse(s)
for, 71 in acute care organizations, 357, 358t
N Neoral. See Cyclosporine credentialing of, 361
Narcotics, in tube-fed patients, adverse effects of, Nepro, 339 role in nutrition support, 360–361
119 Neuroblastoma role on nutrition support committee, 362
Nasoenteric tube(s). See also Feeding tube(s) hematopoietic stem cell transplantation for, 187 in long-term care facility, 365
advantages and disadvantages of, 56 prognosis for, nutritional status and, 160 Nutrient(s)
care of, 59 Neuroglycopenia, in diabetic patients, 318 absorption of
complications of, 56, 56t Neurologic disease, 246–253. See also Acute brain in anorexia nervosa, 349
contraindications to, in adult cancer patients, 163 injury; Spinal cord injury in cancer patients, 152
and home nutrition support, 372 aspiration in, 248, 249t in inborn errors of metabolism, 332
insertion of, 56 chronic, 248–249 in pregnancy, 343
for organ transplant recipient, 178 ethical issues in, 249 intake
for patients in long-term care, 367 gastrointestinal motility in, 248, 248t assessment of, in patients in long-term care,
postoperative use of, 261 Neuropeptide(s), metabolic/nutritional effects of, 366
in pregnancy, 345 in cancer patients, 152–153 in inflammatory bowel disease, 232, 232t
preoperative use of, 260 Neuropeptide Y, metabolic/nutritional effects of, in in pancreatic insufficiency, 220–221
in stem cell transplant recipient, 196 cancer patients, 152 intake of
surgical insertion of, 56 Neutropenia alterations of, in cancer patients, 151
Nasogastric tube(s), 54–55. See also Feeding tube(s) in anorexia nervosa, 351 in anorexia nervosa, 349
advantages and disadvantages of, 55 in cancer patients, nutritional therapy for, 162 in inborn errors of metabolism, 332
care of, 59 food safety precautions for patients with, 162, in pregnancy, 343
complications of, 55, 56t 163 losses of
in pediatric cancer patients, 163 Nevirapine (Viramune), diet and nutrition interac- in anorexia nervosa, 349
functions of, 54 tions with, 142t in inborn errors of metabolism, 332
insertion of, 55 Niacin in inflammatory bowel disease, 232
for organ transplant recipient, 178 deficiency of, in anorexia nervosa, 350t in pancreatic insufficiency, 220
placement of, documentation of, 55 dietary reference intakes for, by life stage group, in pregnancy, 343
postoperative use of, 261 48t requirements for, 39
in pregnancy, 345 effects on clinical laboratory values, 131t in anorexia nervosa, 349
preoperative use of, 260 in parenteral formulations (admixtures) in cystic fibrosis, 221
sizes of, 54–55 for adults, 110t in pancreatic insufficiency, 221
National Cancer institute, Internet address and for pregnant women, 347t utilization of
resources provided by, 165 requirements for in anorexia nervosa, 349
Nausea and vomiting in pregnancy, 345t in inborn errors of metabolism, 332
in cancer patients, nutritional therapy for, 162 in preterm infants, 41t in pregnancy, 343
cancer treatment–related, 151 NICU. See Neonatal intensive care Nutritional history
chemotherapy and, 127 Nipple feeding, in critically ill infants, 310 of cancer patient, 154
drug-induced, 127 Nitrofurantoin, effects on clinical laboratory val- components of, 4, 6t
with enteral nutrition, 79 ues, 131t in cystic fibrosis, 222
in stem cell transplant recipient, 188, 189t Nitrogen balance, 19–20, 39 of organ transplant recipient, 175t
in tube-fed patients, in pediatric cancer, 163 in acute renal failure in pediatric cancer patient, 157
NCJ. See Needle catheter jejunostomy (NCJ) in adults, 283, 283t of stem cell transplant recipient, 193
Needle catheter jejunostomy (NCJ), 54 in pediatric patients, 289, 290, 291t Nutritional status
enteral feeding via, 56, 56t in burn patients, 298–300 acute, 16
Needlestick injury, prevention of, in parenteral in cancer patients, 153 chronic, 16
nutrition, 111 in critical illness, 265, 265f Nutrition assessment. See Assessment
Nelfinavir (Viracept), diet and nutrition interac- monitoring, 269 Nutrition care, discharge from, 22
tions with, 142t evaluation of, during parenteral nutrition, 112 Nutrition care process, 3
Neocate Advance, 242t in pediatric patient, nutritional support and, 38 monitoring in, 22
Neonatal intensive care in pregnancy, 344 reassessment in, 22
enteral nutrition in, 307–313 in trauma patients, 273 Nutrition monitoring, 22
nutritional issues in, 301, 302t Non-Hodgkin’s lymphoma (NHL), weight loss in, Nutrition Risk Index, 21
nutrition support in 150 Nutrition support. See also Enteral nutrition;
parenteral, 301–307 Nonketotic hyperglycinemia, 334t Parenteral nutrition
phases of, 301, 303t Nonmaleficence, as ethical principle, 378 for adults
Neonate(s) Non-nucleoside reverse transcriptase inhibitors, decision making about, 21–22, 24f
acid reflux in, 71 diet and nutrition interactions with, 141t–142t initiation of, timing of, 22
gastroesophageal reflux in, thickened enteral Nonsteroidal anti-inflammatory drugs (NSAIDs) and disease outcomes, 38
formulations for, 71 effects on clinical laboratory values, 131t hypocaloric, 328
nutritionally at risk, 3 gastrointestinal effects of, 127 and morbidity and mortality, 38
nutrition support for, ethical considerations in, Norvir. See Ritonavir (Norvir) for pediatric patients, initiation of, timing of, 22
380 NPY. See Neuropeptide Y perioperative, 259–261

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specialized, 22 Opportunistic infection, in HIV-infected (AIDS) Osteoporosis

weaning from, for organ transplant recipient, 176 patients in chronic pancreatitis, 216–217
withdrawal of, 379 nutritional effects of, 140 in cystic fibrosis, 221
prophylaxis for, 139 in stem cell transplant recipient, 191–192
O Oral cancer, micronutrient deficiencies in, 153 Osteosarcoma, nutritional effects of, 150
Obesity Oral contraceptives, effects on clinical laboratory Ovarian cancer, hematopoietic stem cell transplan-
assessment in, 325–327 values, 131t tation for, 187
body mass index (BMI) in, 326, 326t Oral intake, for pediatric cancer patients, 160–161 Overhydration, in enteral nutrition, 80–81
cardiovascular effects of, 325 Oral nutrient supplementation Overweight
comorbidity in, 327 for HIV-infected (AIDS) patients, 146 body mass index (BMI) in, 326, 326t
dietary modifications in, 328 for organ transplant recipients, 183 in pediatric cancer patients, 158
dietary supplements in, 329 for patients in long-term care, 366 Oxazepam, effects on clinical laboratory values,
and drug disposition, 134 Oral nutrition 131t
dyslipidemia in, 325 after discontinuation of PN, 116 Oxygen consumption
and energy requirements, 317 in anorexia nervosa, 352 clinical factors affecting, 278, 278t
energy requirements in, assessment of, 327–328 in chronic pancreatitis, 217–218 measurement of, handheld device for, 279
enteral nutrition in, 329 ethical considerations with, 379 Oxytocin, effects on clinical laboratory values, 131t
etiology of, 324 in liver disease, 241
gastrointestinal effects of, 325 for organ transplant recipients, 183 P
genetics in, 324 for patients in long-term care, 366 Pain
health alterations of, 324–325 Oral rehydration solutions, in short-bowel in cancer patient, 157
history-taking in, 325–326 syndrome, 208 in chronic pancreatitis, 217, 219
hypocaloric nutrition support in, 328 Oral stimulation, for pediatric patients, with enteral Pamidronate, for stem cell transplant recipient,
laboratory findings in, 327 nutrition, 81 nutritional implications of, 194t
management of, 328–330 Organ transplantation. See also specific organ Pancreas
focused monitoring in, 330 diseases leading to, 171, 172t drugs affecting, 127
goals assessment in, 330 immunosuppression for, 171 in HIV-infected (AIDS) patients, 140
patient/caregiver education in, 330 agents for, 171, 173t–174t in stem cell transplant recipient, 193
metabolic effects of, 324 indications for, 171, 172t Pancreas transplantation, indications for, 172t
metabolic syndrome in, 325 postoperative outcomes in, nutritional factors Pancreatic cancer
mineral requirements in, 328 affecting, 171–174 cachexia in, management of, eicosapentaenoic
and nursing care, 325 posttransplant complications of, nutrient acid in, 163
nutritional alterations of, 324 requirements with, 174, 181t energy expenditure in, 151
nutritional interventions in, goals of, 327 recipient micronutrient deficiencies in, 153
in organ transplant recipient, and posttransplant adult weight loss in, 150
outcome, 171–174 oral nutrition for, 183 Pancreatic enzyme replacement, 218–219, 218t,
parenteral nutrition in, 329–330 posttransplant maintenance, nutritional 223, 224
in pediatric organ transplant recipient, prevention goals for, 174–176 in cystic fibrosis, management of, 225–226
of, 178 posttransplant nutrient requirements of, Pancreatic insufficiency
physical examination in, 326 174, 179t–180t causes of, 220
premorbid nutritional status in, 327 pretransplant nutrient requirements of, 174, in cystic fibrosis, 220–226
prevalence of, 324 177t pathophysiology of, 220
protein requirements in, 328 assessment of, 174, 175t definition of, 220
psychiatric issues in, 325 food safety for, 183–184 nutritional aspects of, 220–221
pulmonary function in, 325 nutrient requirements of pathophysiology of, 220
severity of, 327 posttransplant, 174, 179t–180t in Shwachman syndrome, 220
surgical treatment of, dietary considerations pretransplant, 174, 176t, 177t Pancreatic rest, 211–212
after, 328–329 patient education for, 183–184 Pancreatic secretion, stimulation of, 212
thrombotic tendency in, 325 pediatric Pancreatitis
vitamin requirements in, 328 oral nutrition for, 183 acute, 211
Obesity hypoventilation syndrome (OHS), 325 posttransplant maintenance, nutritional in adults, etiology of, 211
Obstructive sleep apnea (OSA), obesity and, 325 goals for, 176–178 in children, etiology of, 211
Occupational therapist, in long-term care facility, posttransplant nutrient requirements of, etiology of, 211
365 174, 179t–180t focused assessment in, 213–214
Octreotide pretransplant nutrient requirements of, 174, history-taking in, 213
pancreatic effects of, 127 177t, 178t metabolic stress state in, 213
in short-bowel syndrome, 208 Oroenteric tube(s), 56. See also Feeding tube(s) nutritional alterations in, 213
Ofloxacin, drug-nutrient interactions, 125 care of, 59 nutritional aspects of, 211–213
OHS. See Obesity hypoventilation syndrome (OHS) Orogastric tube(s). See also Feeding tube(s) nutritional support in
OKT3. See Muromonab CD3 (OKT3) advantages and disadvantages of, 55 enteral, 214, 215
Oley Foundation, 376 care of, 59 goals of, 214
OncoLink, Internet address and resources provided complications of, 55, 56t monitoring, 215
by, 165 indications for, 55 parenteral, 214–215
Oncology Nutrition Dietetic Practice Group, OSA. See Obstructive sleep apnea (OSA) pancreatic rest for, 211–212
Internet address and resources provided by, 165 Osteopenia in pediatric patients, treatment of, 215
Ondansetron, antiemetic therapy with, for cancer in cystic fibrosis, 221 recurrent, 211
patients, 161 in end-stage liver disease, 241t severity of, determination of, 213–214, 215
Opiates, gastrointestinal effects of, 127, 318 Osteopenia of prematurity, PN-associated, 114, 114t stress responses in, 213

402 A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. © 2005 A.S.P.E.N. www.nutritioncare.org.
 INDEX

in adults, enteral formulations for, 67 posttransplant, 181, 181t for pregnant women, 346–347
chronic in stem cell transplant recipient, 197 protein in, 97, 109t
antioxidant therapy in, 219–220 in trauma patient, 275 quantity per total volume, labeling and, 103
comorbidity in, 217 in critical illness, 266–269 stability issues with, 101–102
complications of, 215 in Crohn’s disease, 232 sterile compounding procedure for, 102
definition of, 215 in cystic fibrosis, 224 temperature of
epidemiology of, 215 for diabetic patients, 318 for infusion, 111
etiology of, 216 di(2-ethylhexyl)phthalate (DEHP) contamina- and microbial growth potential, 102
focused assessment in, 217 tion in, 111 and stability, 101
nutritional aspects of, 216–217 discontinuation of, 116 three-in-one (3-in-1). See Total nutrient
nutrition support in ethical considerations with, 379 admixture (TNA)
goals of, 217 fluid and electrolyte imbalances with, 115–116 types of, 99, 108
management of, 217–220 fluid requirements in, 109t vitamins in, stability of, 102
parenteral, 219 formulations (admixtures) for. See also Total water in, 97
pain control in, 217, 219 nutrient admixture (TNA) gravity infusion device for, 94
pathophysiology of, 216 all-in-one. See Total nutrient admixture (TNA) for HIV-infected (AIDS) patients, 146
in pediatric patients, management of, 215 amino acid composition of, 97 home, costs of, 38
definition of, 211 automated compounding of, 99, 102–103 hyperglycemia with, 114–115
drugs and, 127 auxiliary labels for, 105–106 hyperlipidemia with, 115
enteral nutrition in, contraindications to, 77 calcium and phosphorus in, compatibility hypertriglyceridemia with, 115
mild, 211 issues with, 100 hypoglycemia with, 115
pathophysiology of, 211 calcium phosphate precipitation in, 100, 113 in inborn errors of metabolism, 334
severe, 211 carbohydrates in, 97, 109t indications for, 22, 108
Pantothenic acid central vein infusion, osmolarity and, 100 infusion delivery devices for, 94–95
dietary reference intakes for, by life stage group, component compatibility issues, 100–101 ambulatory, 94, 94t
48t components of, 97–98 controllers for, 94
in parenteral formulations (admixtures) composition of cost-effectiveness of, factors affecting, 94
for adults, 110t and microbial growth potential, 102 patient characteristics and, 94
for pregnant women, 347t and stability, 101 reimbursement for, 94
requirements for, in preterm infants, 41t contaminants in, 98–99, 307 selection criteria for, 94
Parenteral nutrition. See also Intradialytic contraindications to bicarbonate salts in, 100 stationary, 94, 94t
parenteral nutrition (IDPN) design of, 97–100 infusion pumps for, 111
access for, 90. See also Central venous access; dextrose/amino acids (2-in-1), 99, 108 infusion time in, 111
Central venous catheter; Peripherally inserted medications in, compatibility issues with, initiation of, 108–110
central catheter (PICC) 101 in-line filters for, 110–111
peripheral, 93–94 and microbial growth potential, 102 and insulin therapy, 319, 321–322
in acute brain injury, 247 stability of, 102 in liver disease, 243
in acute pancreatitis, 214–215 electrolytes in, 97–98, 109t management of, 111–112
in acute renal failure evaluation of, prior to administration, 111 medication administration with, 126–127
in adults, 285 fat in, 97 monitoring of, 111–112
in pediatric patients, 292–294, 293t gravity transfer compounding of, 99–100 in neonatal intensive care, 305, 306t
administration of, 110–111 labeling of, 103–106 in patients in long-term care, 367–368
administration sets for, 111, 126 practice guidelines for, 105–106 in pediatric cancer patients, 164
for adults standardization of, 105–106 needlestick injury prevention in, 111
in cancer, 159, 163 label templates for, 103–105, 105f–106f for neonates
discontinuation of, 116 light exposure, and stability, 101 initiation of, 108–110
electrolytes in, 109t medications in, 101 labeling of formulations (admixtures) for,
energy in, 109t microbial growth potential in, 102 105, 105f
guidelines for, 108 mislabeling of, 103 monitoring of, 111–112, 111t
initiation of, 108–110 for neonatal intensive care, 305 nutritional requirements in, 39
labeling of formulations (admixtures) for, nutrient additives, compatibility issues with, for obese patient, 327, 329–330
103, 105f 100 for organ transplant recipients, indications for,
monitoring of, 111–112, 112t for obese patient, 330 182–183
trace element intake in, 52, 110t off-site compounding centers providing, 103 for patients in long-term care
vitamins in, 51–52, 98, 110t order form for, 103, 104f JCAHO standards relevant to, 368
in anorexia nervosa, 352–353 ordering, 103, 104f reimbursement for, 369–370
blood-borne pathogen exposure prevention in, 111 order of admixing in, 99–100 in patients in long-term care, 367–368
in chronic kidney disease, 338–339 for organ transplant recipients, 183 for pediatric patients
complications of, 341 osmolarity of, 100 with cancer, 151, 161, 164
in chronic pancreatitis, 219 and central vein infusion, 100 carbohydrate requirements in, 46, 46t
complications of, 112–116 estimation of, 100 discontinuation of, 116
in critical illness, 267–269 and peripheral vein infusion, 100 energy requirements in, 44–45, 45t
gastrointestinal, 114 oxygen exposure, and stability, 101 guidelines for, 108
hepatobiliary, 114 peripheral vein infusion, osmolarity and, 100 initiation of, 108–110
metabolic, 114–115 pH of labeling of formulations (admixtures) for,
in neonatal intensive care, 305–307 and microbial growth potential, 102 105, 105f
in organ transplant recipients, 183 and stability, 101 monitoring of, 111–112, 111t
in pediatric cancer patients, 163 precipitates in, 100, 113 protein requirements in, 45–46, 46t, 109

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vitamin requirements in, 49–50 nutritional goals for, 38 nutritional support in, 259–261
vitamins in, 98 nutritional history of, components of, 4 assessment for, 259
peripheral, 108. See also Peripheral parenteral nutritionally at risk, 3 goals of, 259
nutrition (PPN) nutritional requirements in, 43–50 management of, 260–261
postoperative, 261 nutrition screening for, 3 Peripherally inserted central catheter (PICC), 92
in pregnancy, 346–348 nutrition support for, ethical considerations in, in acute renal failure, in adults, 285
for premature infants 380 for home nutrition support, 372
carbohydrate requirements in, 41t, 42 organ transplant recipients. See Organ transplan- advantages and disadvantages of, 372–373
electrolytes in, 109t tation maintenance of, 93, 94t
initiation of, 108–110 pancreatitis in. See Pancreatitis for patients in long-term care, 367
nutrient requirements in, 40, 41t parental decision making for, 379 in pregnancy, 346
protein requirements in, 40–42, 41t parenteral nutrition for replacement/removal of, 113
trace element requirements in, 41t, 43 carbohydrate requirements in, 46, 46t Peripheral parenteral nutrition (PPN), 108
vitamin requirements in, 41t, 43 energy requirements in, 44–45, 45t administration of, 110
preoperative, 260–261 fat requirements in, 47, 47t electrolytes in, 110
prescription for, transfer of, 106 hyperglycemia in, 114–115 initiation of, 110
and refeeding syndrome, 114 hypertriglyceridemia with, 115 Peripheral venous access
for stem cell transplant recipient, 196–197 initiation of, 109 catheters for, 94
syringe infusion device for, 94–95 mineral requirements in, 49–50 complications of, 112
transitional, 116 protein requirements in, 45–46, 46t, 109 for parenteral nutrition, 93–94
in patients in long-term care, 368 trace elements in, 110t thrombophlebitis prophylaxis during, 94
in trauma patient, 274–275 vitamin requirements in, 49–50 Peritoneal dialysis, in pediatric patients, nutritional
tubing changes in, 93 PN-associated cholestasis (PNAC) in, 114 considerations in, 289–290
Patient(s) PN-associated metabolic bone disease in, 114, Peritonitis, in tube-fed pediatric cancer patients, 163
involvement in health care, in acute care organi- 114t Persistent vegetative state, 379
zations, 357, 358t refeeding syndrome in, 87 PG-SGA. See Patient-Generated Subjective Global
right to self-determination, 378, 379 with seizure disorders, 252 Assessment (PG-SGA)
sexual development of Pharmacist(s)
Patient-Generated Subjective Global Assessment
assessment of, 4, 16t in acute care organizations, 357, 358t
(PG-SGA), 154, 155f–156f
Tanner staging of, 4, 16t credentialing of, 361
pediatric application of, 157
vitamin requirements in, 47–49, 48t role in nutrition support, 361
Patient Self-Determination Act, 379
weight changes in, 16 role on nutrition support committee, 362
Pearson’s pancreas/marrow syndrome, pancreatic
Pediatric patients in long-term care facility, 365
insufficiency in, 220
enteral nutrition for, oral stimulation with, 81 Pharmacokinetics, of parenteral medications, 119
Pectin, in enteral formulations, 64
nutrition support for, initiation of, timing of, 22 Phenobarbital, effects on clinical laboratory values,
Pectin wafer, for skin protection, with feeding
oral stimulation for, with enteral nutrition, 81 132t
tube, 60
PEG. See Percutaneous endoscopic gastrostomy Phenothiazines
Pediatric Intensive Care Global Nutritional Assess-
(PEG) antiemetic therapy with, for cancer patients, 161
ment, 287, 288t–289t
PEJ. See Percutaneous endoscopic jejunostomy effects on clinical laboratory values, 132t
Pediatric patient(s)
(PEJ) gastrointestinal effects of, 127
body weight of, measurement of, 5
Penicillin Phenylketonuria, 333t
cancer in. See Cancer, children with absorption of, 119 Phenytoin
carbohydrate requirements of, 46, 46t effects on clinical laboratory values, 132t adverse effects and side effects of, 127
with cerebral palsy, nutrition support for, taste alterations caused by, 127 drug-nutrient interactions, 124–125, 127
249–252 Peptamen Junior, 242t, 243 effects on clinical laboratory values, 132t
cystic fibrosis in. See Cystic fibrosis Peptides, in enteral formulations, for GI impair- toxicity of, 124–125
electrolyte requirements in, 49t, 50, 109t ment in adults, 67 Phosphates, effects on clinical laboratory values,
enteral nutrition for Percutaneous endoscopic gastrostomy (PEG), 54, 132t
carbohydrate requirements in, 46, 46t 55f, 56 Phosphorus
energy requirements in, 44, 44t in chronic neurologic disease, 249 dietary reference intakes for, by life stage group,
fat requirements in, 46, 47t complications of, in pediatric cancer patients, 49t
formulations for, 68–69 163 in enteral formulations, for renal failure patients,
mineral requirements in, 47–49, 49t for head and neck cancer patients, 160 340
protein requirements in, 45, 45t for home nutrition support, 372 imbalances, in tube-fed patients, 86t, 87
route for, 54 in obese patient, 329 in parenteral formulations (admixtures), 98, 110
vitamin requirements in, 47–49, 48t for patients in long-term care, 366–367 for adults, 109t
fat requirements of, 46–47 postoperative use of, 261 for chronic kidney disease, 339
fiber intake by, 47, 47t preoperative use of, 260–261 for pediatric patients, 109t
fluid requirements in, 50 procedure for, 57 for preterm infants, 109t
growth of. See Growth in stem cell transplant recipient, 196 physiologic functions of, 86t, 87
height, measurement of, 6 Percutaneous endoscopic jejunostomy (PEJ), 57 requirements for
HIV-infected (AIDS) patients. See HIV infection, postoperative use of, 261 in acute renal failure, in pediatric patients, 292
pediatric preoperative use of, 260–261 in adults, 52t
length/head circumference, measurement of, 6 Percutaneous gastrojejunostomy, 57–58 in pregnancy, 345t
with motor disorders, nutrition support for, Pericardial tamponade, central venous catheter in preterm infants, 41t, 43
249–252 placement and, 90 in stem cell transplant recipient, 195
neurologically impaired, nutrition support for, Perioperative period serum. See also Hyperphosphatemia; Hypophos-
249–252 nutritional alterations in, 259–260 phatemia

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in chronic kidney disease, 336 excretion of, drugs affecting, 127 fluid requirements in, 41t, 42
in diabetic patient, 323 imbalances, in tube-fed patients, 84–87, 85t–86t lipid requirements of, 41t, 42
and parenteral nutrition, for chronic kidney in parenteral formulations (admixtures), 98, 110 nutritional requirements of, 40
disease, 339 for adults, 109t nutrition support for, initiation of, timing of, 22
in pediatric cancer patients, 158 for chronic kidney disease, 338–339 parenteral nutrition for
supplementation, during parenteral nutrition in for neonatal intensive care, 304 carbohydrate requirements in, 41t, 42
pregnancy, 348 for pediatric patients, 109t, 293t energy requirements in, 40, 41t
Photopheresis, extracorporeal, nutritional side for preterm infants, 109t fluid requirements in, 41t, 42
effects and interventions, 192t physiologic functions of, 84, 85t hyperglycemia with, 114–115
pH sensor(s), for nasoenteric tube insertion, 56 requirements for hypoglycemia with, 115
Physical activity level index, 324 in acute renal failure, in pediatric patients, lipid requirements in, 41t, 42
Physical examination 292 mineral requirements in, 41t, 43
in acute pancreatitis, 213 in adults, 52t nutrient requirements in, 40, 41t
of anorexia nervosa patient, 350–351 in preterm infants, 41t protein requirements in, 40–42, 41t
of cancer patient, 154–157 in stem cell transplant recipient, 195 trace element requirements in, 41t, 43
of HIV-infected (AIDS) patients, 143 serum. See also Hyperkalemia; Hypokalemia trace elements in, 110t
in inborn errors of metabolism, 333 in chronic kidney disease, 336 vitamin requirements in, 41t, 43
nutrition-focused, guidelines for, 4, 7t–15t in diabetic patient, 323 protein requirements of, 40–42, 41t
of obese patient, 326 in liver disease, 239 Preoperative period, nutritional support in, man-
of organ transplant recipient, 175t and parenteral nutrition, for chronic kidney agement of, 260–261
of pediatric cancer patients, 157–158 disease, 339 Pressure ulcer(s)
of pediatric HIV-infected (AIDS) patients, in pediatric cancer patients, 158 development of, 68
144–145 PPN. See Peripheral parenteral nutrition (PPN) in patients in long-term care, 366
of pregnant woman, 344 Prader-Willi syndrome, children with, recom- prevention of, 68
of stem cell transplant recipient, 193 mended energy intake for, 250t Primary biliary cirrhosis (PBC), 235
Physical therapist Prealbumin, serum Probenecid, effects on clinical laboratory values,
in acute care organizations, 357, 358t in cancer patient, 157 132t
in long-term care facility, 365
evaluation of, during parenteral nutrition, 112 Probiotics
Physician(s)
in pediatric cancer patients, 158 for antibiotic-associated diarrhea, 204
in acute care organizations, 357, 358t
Prebiotics, for preterm infants, 42 therapy with, in acute pancreatitis, 214
credentialing of, 361
Precipitates, insoluble, in parenteral formulations Procainamide, effects on clinical laboratory values,
role in nutrition support, 360
(admixtures), 100, 113 132t
role on nutrition support committee, 361
Prednisolone, nutritional side effects and interven- Prograf. See Tacrolimus
in long-term care facility, 364–365
tions, 173t Prokinetic agents, in tube-fed patients, diarrhea
Physician’s assistant(s), in long-term care facility,
Pregestimil, 242, 243 caused by, 119
365
Pregnancy Promethazine, antiemetic therapy with, for cancer
PICC. See Peripherally inserted central catheter
anemia in, assessment of, 346, 346t patients, 161
(PICC)
diet and nutritional supplements in, 344–345 Propionic acidemia, 333t
Pinch-off syndrome, with central venous catheter,
enteral nutrition in, 345–346 Propranolol
93, 113
focused assessment in, 344 effects on clinical laboratory values, 132t
PN. See Parenteral nutrition
PNAC. See PN-associated cholestasis (PNAC) history-taking in, 344 gastrointestinal effects of, 127
PN-associated cholestasis (PNAC), in pediatric mineral requirements in, 49t Prostate cancer
patients, 114 nutritional alterations in, 344 hematopoietic stem cell transplantation for, 187
Pneumothorax, central venous catheter placement nutritional aspects of, 343 micronutrient deficiencies in, 153
and, 90 nutrition support during trace element deficiencies in, 153
Polyunsaturated fatty acids (PUFA) goals of, 344 weight loss in, 150
beneficial effects of, in cancer cachexia, 163 management of, 344–348 Protease inhibitor(s), diet and nutrition interactions
in enteral formulations, 63 parenteral nutrition in, 346–348 with, 141t, 142
in enteral nutrition, for preterm infants, 42 vitamin requirements in, 48t Protein
functions of, 40 weight goals in, based on prepregnancy weight, adequate intake, by life stage group, 45t
for pediatric patient, 38 344, 344t catabolism
requirements for, 40 Premature infants in acute renal failure, in adults, 282
pediatric, 46–47, 47t carbohydrate requirements of, 41t, 42 in critical illness, 263
Port(s) carnitine requirements in, 41t, 43 deficiency of, 21–22
for central venous access, 92 energy requirements of, 40, 41t in enteral formulations, 64
care of, 93, 94t enteral nutrition for for adult organ transplant recipient, 180
infection control for, 113 carbohydrate requirements in, 41t, 42 for critically ill adults, 66
maintenance of, 93, 94t energy requirements in, 40, 41t for hepatic disease in adults, 66
in patients in long-term care, 367 fluid requirements in, 41t, 42 modular products, 64
for home nutrition support, advantages and dis- formulations for, 71–73 for pediatric organ transplant recipient, 181
advantages of, 372 lipid requirements in, 41t, 42 for pediatric patients, 68
Postoperative period, nutritional support in, 261 mineral requirements in, 41t, 43 for renal failure patients, 339
Potassium nutrient requirements in, 40, 41t sources of, 64
dietary reference intakes for, by life stage group, protein requirements in, 40, 41t and wound healing, 68
49t trace element requirements in, 41t, 43 estimated average requirement for, by life stage
in enteral formulations, for renal failure patients, vitamin requirements in, 41t, 42–43 group, 45t
339–340 essential amino acids for, 40 imbalance, in chronic liver disease, 236

© 2005 A.S.P.E.N. www.nutritioncare.org. A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. 405
INDEX

intake Pyridoxine. See also Vitamin B6 Renal solute load

in acute renal failure, in pediatric patients, deficiency of, in anorexia nervosa, 350t definition of, 72
289, 290t in parenteral formulations (admixtures) and enteral formulations for preterm infants, 72
in chronic kidney disease, 337–338 for adults, 110t Reproductive failure, in stem cell transplant
metabolism of for pregnant women, 347t recipient, 193
in cancer patients, 153 requirements for Requirements, nutritional, 39–40
inborn errors of, 334t in dialysis patients, 339 in enteral nutrition, 39
for organ transplant recipient in pregnancy, 345t for healthy people, 39
maintenance needs, 183 Pyruvate dehydrogenase deficiency, 334t from infancy to adolescence, 43–50
recommendations, 179t in parenteral nutrition, 39
in parenteral formulations (admixtures), 97, 109t Q in premature infants, 40–43, 41t
for neonatal intensive care, 301–302 QOL. See Quality of life Rescriptor. See Delavirdine (Rescriptor)
recommended dietary intake of, by life stage Quality of life Resident Assessment Instrument (RAI), 368
group, 45t in adult cancer patient Resource utilization groups, 369
requirements for, 39 assessment of, 157 Respiratory Quotient
in acute renal failure, in adults, 284 improvement of, 160 from indirect calorimetry, 278
of adult cancer patients, 159 assessment tools, for pediatric cancer patients, 159 traditional interpretation of, 278, 278t
in adults, 45t, 51 home nutrition support and, 376 Respiratory system, obesity and, 325
with normal renal function, 285, 285t inborn errors of metabolism and, 333 Respiratory therapist, in acute care organizations,
with renal failure, 285, 285t in pediatric cancer patient 357, 358t
in burn patients, 296–297 assessment of, 158–159 Resting energy expenditure (REE), 39, 50
in critical illness, 265 assessment tools for, 159 in anorexia nervosa, 349
in elderly, 51 improvement of, 161 in cancer patient, 151
in obese patients, 328 for pediatric patient, 38 in children, chronic liver disease and, 237
for organ transplant recipient, 176t for stem cell transplant recipient, 193–194 in elderly, 51
pediatric, 45–46, 45t, 46t Quinidine estimation of, 44, 44t, 328
in pediatric liver disease, 239 effects on clinical laboratory values, 132t from indirect calorimetry, 278
perioperative, 259 gastrointestinal effects of, 127 measurement of, in liver disease, 238
in pregnancy, 344 Quinlan, In re, 378 in metabolic response to stress, 271
in premature infants, 40–42, 41t Quinolones in neurologically impaired children, 251
in stem cell transplant recipient, 194 area under the curve (AUC) for, 125 in stress/illness, 45
restitution, in anorexia nervosa, 349 AUC/MIC ratio for, 125 Resting metabolic rate, measurement of, handheld
supplements, for obese patients, 329 drug-nutrient interactions, 125 device for, 279
turnover, requirements for, 145 efficacy of, evaluation of, 125 Restorative dining, for patients in long-term care,
visceral 366
in adult cancer patients, 160 R Reticuloendothelial neoplasms, in children, 150
in burn patients, 300 Radiation therapy. See also Total body irradiation Retrovir. See Zidovudine (Retrovir)
in cancer patient, 157 malabsorption caused by, 152 Reyataz. See Atazanavir (Reyataz)
evaluation of, during parenteral nutrition, 112 nutritional considerations in, 159 Riboflavin
in pediatric cancer patients, 158 nutritional effects of, 151 deficiency of, in anorexia nervosa, 350t
perioperative assessment of, 259 RAI. See Resident Assessment Instrument (RAI) dietary reference intakes for, by life stage group,
Protein binding, by drugs, 119 Ranson criteria, 213–214 48t
Protein-calorie malnutrition, in liver disease, Rapamune. See Sirolimus (Rapamycin, Rapamune) in parenteral formulations (admixtures), 98
236–237 Rapamycin. See Sirolimus (Rapamycin, Rapamune) for adults, 110t
prognosis for, 237, 239t RDA. See Recommended dietary allowances (RDA) for pregnant women, 347t
Protein nitrogen appearance, normalized, in acute Recommended dietary allowances (RDA), 43 stability of, 102
renal failure, in pediatric patients, 289 REE. See Resting energy expenditure (REE) requirements for
Protein-sparing modified fast (PSMF) Refeeding syndrome in acute renal failure, in pediatric patients,
definition of, 327 in adults, 114 292, 294t
for obese patient, 327 in anorexia nervosa, 349, 352 in pregnancy, 345t
Proteolysis, in critical illness, 263 metabolic manifestations of, 349 in preterm infants, 41t
Proteolysis-inducing factor, metabolic/nutritional prevention of, in pediatric cancer patients, 163 and wound healing, 68
effects of, in cancer patients, 152 in trauma patient, 275 Rifampin
Prothrombin time (PT), in chronic kidney disease, in tube-fed patients, 87 absorption of, 119
336 Registered nurse(s), in acute care organizations, effects on clinical laboratory values, 132t
Proton pump inhibitors 357, 358t Risperidone, effects on clinical laboratory values,
adverse effects and side effects of, 127 Registered nurse epidemiologist, in acute care 132t
drug-nutrient interactions, 124, 127 organizations, 357, 358t Ritonavir (Norvir), diet and nutrition interactions
protective effect, for skin, with feeding tube, 60 Regulatory aspects with, 142t
Pseudohyponatremia, in diabetic patient with of acute care, 358t, 359 Roux-en-Y gastric bypass (RYGB), for obesity,
hyperglycemia, 323 of long-term care, 368–369 dietary considerations after, 328–329
PSMF. See Protein-sparing modified fast (PSMF) of patient care and feeding, 378–379 RQ. See Respiratory Quotient
Psyllium hydrophilic mucilloid, administration of, Regurgitation, in neonates, thickened enteral Russell’s sign, 351
via enteral tubes, 123 formulations for, 71 RYGB. See Roux-en-Y gastric bypass (RYGB)
Puberty Rejection, in organ transplant recipient, 181t
in cystic fibrosis, 222 Religion, and feeding choices, 380 S
delayed, in cystic fibrosis, 221 Renal cell carcinoma, hematopoietic stem cell Saline infusions, effects on clinical laboratory val-
PUFA. See Polyunsaturated fatty acids (PUFA) transplantation for, 187 ues, 132t

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 INDEX

Salivation, altered. See also Dry mouth octreotide in, 208 Solid organ transplantation. See Organ transplanta-
in stem cell transplant recipient, 188, 189t oral rehydration solutions in, 208 tion; specific organ
Sandimmune. See Cyclosporine Shwachman syndrome Solu-Cortef, nutritional side effects and interven-
Saquinavir (Invirase, Fortovase), diet and nutrition clinical features of, 220 tions, 173t
interactions with, 142t pancreatic insufficiency in, 220 Solu-Medrol, nutritional side effects and interven-
Sarcoma, weight loss with, 150 Sildenafil, effects on clinical laboratory values, tions, 173t
Satiety, early, in cancer patients, 151 132t Sorbitol, in medications, 122–123
Schiavo, Terri, 379 Silymarin, 243 Soy polysaccharide, in enteral formulations, 64
Sclerosing cholangitis, 235 Simulect. See Basiliximab (Simulect) Soy protein
Screening, nutrition, 3 Sinusoidal obstructive syndrome, in stem cell allergy to, in infants, 70
of adult cancer patients, 154 transplant recipient, 188 in enteral formulations, 64
algorithm for, 3, 4f Sirolimus (Rapamycin, Rapamune) Spastic quadriparesis, children with, recommended
of elderly, 3 in immunosuppression for organ transplant energy intake for, 250t
of patients in acute care organizations, 357, 358t recipients, 171, 174t Speech pathologist
of pediatric cancer patients, 157 nutritional side effects and interventions, 174t, in acute care organizations, 357, 358t
of pediatric patients, 3 192t in long-term care facility, 365
tool for, 3, 5t SIRS. See Systemic inflammatory response syn- Spinal cord injury, 248
Seizure disorders, children with, 252 drome (SIRS) Spironolactone, effects on clinical laboratory
Selective serotonin reuptake inhibitors (SSRIs) Skin, breakdown, with feeding tube, 60 values, 132t
anorexia caused by, 127 Skin care Stadiometer, 6
antiemetic therapy with, for cancer patients, 161 for central venous access, 113 Staphylococci, coagulase-negative, growth of, in
gastrointestinal effects of, 127 with feeding tube, 60 parenteral formulations (admixtures), 102
Selenium Skinfold thickness (ST), 16 Staphylococcus saprophyticus, growth of, in
deficiency of in obese patient, 326–327 parenteral formulations (admixtures), 102
in cancer patients, 154 in pediatric cancer patients, 158 Starvation
in chronic pancreatitis, 216 in stem cell transplant recipient, 193 in chronic liver disease, 235–236
Small-bowel transplantation complications caused by, prevention of, 39
in inflammatory bowel disease, 232
enteral nutrition after, 178 and gut integrity, 213
dietary reference intakes for, by life stage group,
indications for, 172t metabolic response to, 263, 264t
49t
in pediatric patient State licensure, for long-term care (LTC) facilities,
in parenteral formulations (admixtures), 98, 110t
enteral formulations for, 181 369
for adults, 110t
and growth, 178 State regulations
for chronic kidney disease, 339
posttransplant feeding therapy with, 178 for acute care organizations, 359
for neonatal intensive care, 305
Small intestine, complications in, with feeding and artificial nutrition and hydration, 381
for pediatric patients, 293t
tube, 82 for long-term care (LTC) facilities, 368–369
for pregnant women, 347t
Smoking, in HIV-infected (AIDS) patients, 144 Stature-for-age percentiles
in parenteral nutrition, for pediatric patients, 50
Social worker(s) for boys, 2 to 20 years, 32
physiologic functions of, 153
in acute care organizations, 357, 358t for girls, 2 to 20 years, 33
requirements for
in long-term care facility, 365 Stavudine (Zerit), diet and nutrition interactions
in acute renal failure, in pediatric patients,
Sodium with, 142t
293t depletion, in cystic fibrosis, 221 Steatorrhea
in liver disease, 239 dietary reference intakes for, by life stage group, in children, 203
in parenteral nutrition for adults, 52 49t in chronic pancreatitis, 213, 216–217, 217, 219
in pregnancy, 345t in enteral formulations, for renal failure patients, definition of, 203
in preterm infants, 41t 339–340 in end-stage liver disease, 241t
supplementation, in chronic pancreatitis, 220 excretion of, drugs affecting, 127 in stem cell transplant recipient, 188
Self-determination, patient’s right to, 378, 379 imbalances, in tube-fed patients, 84, 85t Steatosis
Self-help devices/utensils, for patients in long-term in parenteral formulations (admixtures), 98 in critical illness, 268
care, 366 for adults, 109t PN-associated, 114
Sepsis, 263 for chronic kidney disease, 338 Steroid(s)
Sepsis syndrome, 263 for neonatal intensive care, 304 anabolic, for HIV-infected (AIDS) patients, 146
Sertraline, anorexia caused by, 127 for pediatric patients, 109t, 293t antiemetic therapy with, for cancer patients, 161
Serum urea nitrogen, in chronic kidney disease, for preterm infants, 109t hepatic effects of, 127
336 physiologic functions of, 84, 85t metabolic effects of, 127
Sex hormone(s), in HIV-infected (AIDS) patients, plasma levels. See also Hypernatremia; Stomach, complications in, with feeding tube, 82
140 Hyponatremia Stomadhesive, 60
SGA. See Subjective Global Assessment (SGA) in chronic kidney disease, 336 Stool
Short bowel, enteral nutrition in, contraindications in diabetic patient, 323 analysis, in diarrhea, 203
to, 77 requirements for osmolality of, 203–204
Short-bowel syndrome in acute renal failure, in pediatric patients, Stool pattern, with enteral nutrition, 79
definition of, 207 292 Stool softeners, for cancer patients, 161
diarrhea in, 207–209 in adults, 52t Storage disorders, hematopoietic stem cell trans-
enteroglucagon for, 209 in preterm infants, 41t, 43 plantation in, 187
glucagon-like peptide-2 for, 209 in stem cell transplant recipient, 195 Stress
management of restriction, in liver disease, 239 and energy requirements, 39
dietary, 207–208 supplementation, in cystic fibrosis, 224 hyperglycemia caused by, in diabetic patient,
glutamine in, 208–209 Sodium acetate, in parenteral formulations (admix- 317
growth hormone in, 208–209 tures), 98 metabolic response to, 263, 264t, 271–272

© 2005 A.S.P.E.N. www.nutritioncare.org. A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. 407
INDEX

Stroke Testicular cancer, hematopoietic stem cell trans- in preparative conditioning for hematopoietic
nutrition support after, 249 plantation for, 187 stem cell transplantation, 187
outcome after, hyperglycemia and, 319 Testosterone replacement, for HIV-infected Total energy expenditure (TEE), 39
Subclavian vein (AIDS) patients, 146 in children, chronic liver disease and, 237
catheterization. See also Central venous access Tetracycline determination of, 279
in obese patient, 330 absorption of, 119 in obesity, 324
thrombosis, 113 effects on clinical laboratory values, 133t Total lymphocyte count (TLC), 20
Subjective Global Assessment (SGA), 4, 6t. See Thalidomide, nutritional side effects and interven- Total nitrogen appearance
also Patient-Generated Subjective Global tions, 192t in chronic kidney disease, 337
Assessment (PG-SGA) Theophylline protein equivalent of, 337
in anorexia nervosa, 350 drug-nutrient interactions, 126 Total nutrient admixture (TNA), 108
in chronic kidney disease, 336 effects on clinical laboratory values, 133t administration sets for, 111
in chronic pancreatitis, 217 gastrointestinal effects of, 127 advantages and disadvantages of, 99
for organ transplant recipient, 175t hepatic effects of, 127 aggregation (flocculation) of, 101
Subscapular skinfold thickness, in pediatric cancer Thermal injury. See Burn(s) coalescence of, 101
patients, 158 Thermic effect of food (TEF), 39 component compatibility issues with, 100–101
Substitute decision maker(s), 378 Thiamine creaming of, 101
Substrate metabolism, in obesity, 324 deficiency of deterioration of, stages of, 101–102
Succinylcholine, effects on clinical laboratory in acute pancreatitis, 213 di(2-ethylhexyl)phthalate (DEHP) contamina-
values, 132t in anorexia nervosa, 350t tion in, 111
Sucking, non-nutritive, in critically ill infants, 310 in tube-fed patients, 87 iron dextran in, contraindications to, 98
Sucralfate dietary reference intakes for, by life stage group, medications in, compatibility issues with, 101
drug-nutrient interactions, 126 48t microbial growth potential in, 102
effects on clinical laboratory values, 132t for parenteral formulations (admixtures), 98 oiling out of, 102
Sucrose in parenteral formulations (admixtures), 98 stability of, 101–102
in enteral formulations, for pediatric patients, 69 Trace element(s). See also specific element
for adults, 110t
in enteral nutrition, 63 deficiencies of
for pregnant women, 347t
Sulfasalazine in anorexia nervosa, 350t
stability of, 102
drug-nutrient interactions, 232 in cancer patients, 153–154
physiologic function of, 87
for inflammatory bowel disease, 231 dietary reference intakes for, by life stage group,
requirements for
Sulfonylureas, effects on clinical laboratory values, 49t
in acute renal failure, in pediatric patients,
132t–133t in parenteral formulations (admixtures), 98
292, 294t
Suplena, 339 for adolescents, 110t
in pregnancy, 345t
Surgery, complications of, in organ transplant for adults, 52, 110t
in preterm infants, 41t
recipient, 181t for chronic kidney disease, 339
and wound healing, 68
Surrogate decision maker(s), 378, 381 for neonatal intensive care, 304–305
Thiazides
Sustiva. See Efavirenz (Sustiva) for pediatric patients, 110t
Sympathomimetics, anorexia caused by, 127 effects on clinical laboratory values, 133t
for preterm infants, 41t, 43, 110t
Systemic inflammatory response syndrome (SIRS), hepatic effects of, 127
requirements for, 40
271, 272 Thiotepa, for stem cell transplant recipient, nutri-
in acute renal failure
tional implications of, 194t
in adults, 284
Thrombocytopenia, in anorexia nervosa, 351
T in pediatric patients, 292
Thromboembolism, obesity and, 325 in adults, 49t, 52
Tacrolimus
Thrombophlebitis, peripheral venous, prophylaxis in anorexia nervosa, 352
and bone mineral density, 192
drug-nutrient interactions, 126 for, during peripheral venous access, 94 in liver disease, 239
in immunosuppression for organ transplant Thrombotic microangiopathy, in stem cell trans- in preterm infants, 41t, 43
recipients, 171, 174t plant recipient, 190 Trace mineral status, assessment of, 20, 24t
nephrotoxicity of, 189, 192 Thymoglobulin. See Antilymphocyte serum Transferrin, serum
nutritional side effects and interventions, 174t, (ATGAM, Thymoglobulin) in chronic kidney disease, 336
192t Thyroid cancer, micronutrient deficiencies in, 153 evaluation of, during parenteral nutrition, 112
Tanner stages, 4, 16t Thyroid function, in stem cell transplant recipient, Transferrin receptor status, in cystic fibrosis, 222
Taste 193 Transplantation. See Hematopoietic stem cell
changes in Thyroid hormone(s) transplantation; Organ transplantation
in cancer patients, nutritional therapy for, 162 effects on clinical laboratory values, 133t Transpyloric feeding, in critically ill infants, 310
in stem cell transplant recipient, 188, 189t in HIV-infected (AIDS) patients, 140 Trauma. See also Acute brain injury
drugs affecting, 127 metabolic effects of, 127 blunt, 271
TBI. See Total body irradiation TLC. See Total lymphocyte count (TLC) mechanism of injury in, 271
T cells (T lymphocytes), abnormalities of, in TLS. See Tumor lysis syndrome (TLS) metabolic response to, 271–272
cancer patients, 152 TNA. See Total nutrient admixture (TNA) nutritional assessment in, 272
TEE. See Total energy expenditure (TEE) Toddler’s diarrhea, 206 nutrition support in
TEF. See Thermic effect of food (TEF) Tolbutamide, effects on clinical laboratory values, enteral, 272, 273–274
Tenofovir (Viread), diet and nutrition interactions 133t initiation of, 272–273
with, 142t Tolerable upper level (UL), 43 monitoring, 272–273
Terfenadine, hepatic effects of, 127 Tools/equipment, in acute care organizations, 357, rationale for, 272
Terminal illness, enteral nutrition in, contraindica- 358t and refeeding syndrome, 275
tions to, 77 Total body irradiation penetrating, 271
Terminally ill patient(s), nutrition support for, endocrine effects of, 193 statistics for, 271
ethical considerations in, 380 nephrotoxicity of, 189 types of injury in, 271

408 A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. © 2005 A.S.P.E.N. www.nutritioncare.org.
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Treatment Vegetable oils, in enteral formulations, 63 dietary reference intakes for, by life stage group,
withdrawal of, 379 Vegetarianism, and anorexia nervosa, 349 48t
withholding of, 379 Ventilator-dependent patient(s), energy require- in enteral formulations
Triamterene, effects on clinical laboratory values, ments of, estimation of, 51t for burn patients, 68
133t Verapamil, effects on clinical laboratory values, and wound healing, 68
Triceps skinfold thickness, in pediatric cancer 133t in parenteral formulations (admixtures), 98
patients, 158 Very low calorie diet (VLCD), for obese patients, for adults, 110t
Tricyclic antidepressants 328 for chronic kidney disease, 339
appetite stimulation by, 127 Videx. See Didanosine (Videx) for pregnant women, 347t
hepatic effects of, 127 Villous atrophy, GI disuse and, 114 stability of, 102
Triglyceride levels. See also Hypertriglyceridemia Vincristine for pediatric liver transplant recipient, 178t
in diabetic patient, 323–324 effects on clinical laboratory values, 133t requirements for
in pregnancy, 344 hyponatremia caused by, 154 in acute renal failure, in pediatric patients,
Trimethoprim-sulfamethoxazole Viracept. See Nelfinavir (Viracept) 293, 294t
nephrotoxicity of, 189 Viramune. See Nevirapine (Viramune) in burn patients, 297
for stem cell transplant recipient, nutritional Viread. See Tenofovir (Viread) in pregnancy, 345t
implications of, 194t Vitamin(s) in preterm infants, 41t
Trisomy 21, children with, recommended energy deficiencies of supplementation
intake for, 250t in anorexia nervosa, 350t in cystic fibrosis, 224, 225t
Tube feeding. See Enteral nutrition in cancer patients, 153 for liver disease in children, 238t
Tumor lysis syndrome (TLS), electrolyte imbal- in chronic pancreatitis, 216–217 and wound healing, 68
ances in, 154 in cystic fibrosis, 221 Vitamin B1. See Thiamine
Tumor necrosis factor (TNF), metabolic/nutritional in inflammatory bowel disease, 232 Vitamin B2. See Riboflavin
effects of, in cancer patients, 152 in liver disease, 237, 238t Vitamin B6. See also Pyridoxine
Tumor necrosis factor (TNF) antibody in tube-fed patients, 87 deficiency of, in cystic fibrosis, 221
for Crohn’s disease, 231 dietary reference intakes for, by life stage group, dietary reference intakes for, by life stage group,
drug-nutrient interactions, 232 48t 48t
TwoCal HN, 242t, 243 for organ transplant recipient, recommendations, in parenteral formulations (admixtures), 98
Tyrosinemia, types I and II, 333t 180t requirements for
in parenteral formulations (admixtures), 98 in acute renal failure, in pediatric patients,
U for adults, 110t 292, 294t
Ulcer(s) for chronic kidney disease, 339 in elderly, 52
gastrointestinal, drug-induced, 127 for infants, 305 in preterm infants, 41t
pressure. See Pressure ulcer(s) for pediatric patients, 110t, 293t Vitamin B12
Ulcerative colitis (UC). See also Inflammatory stability of, 102 deficiency of
bowel disease (IBD) for pediatric liver transplant recipient, 178t in acute pancreatitis, 213
anemia in, 232 requirements for, 40 in anorexia nervosa, 350t
diarrhea in, 232 in acute renal failure in chronic pancreatitis, 216
hypoalbuminemia in, 232 in adults, 284 in cystic fibrosis, 221
nutrition support in, 232–233 in pediatric patients, 292–293 in inflammatory bowel disease, 232
pathophysiology of, 231 adult, 48t dietary reference intakes for, by life stage group,
UNA. See Urea nitrogen appearance in adults, 48t, 51 48t
Uncoupling protein(s), metabolic/nutritional in burn patients, 297 in parenteral formulations (admixtures), 98
effects of, in cancer patients, 152–153 in dialysis patients, 339 for adults, 110t
Urea cycle disorders, 334t in elderly, 52 requirements for
Urea nitrogen appearance in females, 48t in acute renal failure, in pediatric patients,
calculation of, 337 in lactation, 48t 292, 294t
in chronic kidney disease, 337 in males, 48t in preterm infants, 41t
Urinary urea nitrogen (UUN), in trauma patients, in obese patients, 328 Vitamin C. See also Ascorbic acid
273 pediatric, 47–49, 48t deficiency of
Ursodeoxycholic acid, nutritional side effects and in pregnancy, 48t in anorexia nervosa, 350t
interventions, 192t in preterm infants, 41t, 42–43 in cancer patients, 153
Usual body weight (UBW), in cystic fibrosis, 221 in stem cell transplant recipient, 195 in inflammatory bowel disease, 232
UUN. See Urinary urea nitrogen (UUN) supplements in tube-fed patients, 87
in liver disease, 239 dietary reference intakes for, by life stage group,
V for obese patients, 329 48t
Valine, in enteral formulations, 64 for organ transplant recipient, patient/care- in enteral formulations
Valproic acid, effects on clinical laboratory values, giver education about, 183 for burn patients, 68
133t and wound healing, 68 and wound healing, 68
Valsartan, effects on clinical laboratory values, 133t Vitamin A in parenteral formulations (admixtures), 98
Values, and feeding choices, 380 deficiency of for adults, 110t
Vancomycin in anorexia nervosa, 350t for pregnant women, 347t
effects on clinical laboratory values, 133t in cancer patients, 153 stability of, 102
nephrotoxicity of, 189 in chronic pancreatitis, 216 physiologic functions of, 153
Vasopressin, effects on clinical laboratory values, in cystic fibrosis, 221 requirements for
133t in inflammatory bowel disease, 232 in acute renal failure, in pediatric patients,
VCO2. See Carbon dioxide (CO2) production in liver disease, 238t 293, 294t
Vd. See Volume of distribution in tube-fed patients, 87 in burn patients, 297

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INDEX

in dialysis patients, 339 for chronic kidney disease patients, 339 assessment of
in pregnancy, 345t deficiency of during enteral nutrition, 81
in preterm infants, 41t in anorexia nervosa, 350t in patients in long-term care, 365–366
in stem cell transplant recipient, 195 in chronic pancreatitis, 216 and basal metabolic rate, 44, 44t
supplementation, in chronic pancreatitis, 220 in cystic fibrosis, 221, 222 bed or sling, measurement of, 5
and wound healing, 68 in inflammatory bowel disease, 232 control
Vitamin D in liver disease, 238t in anorexia nervosa, 350
for chronic kidney disease patients, 339 in tube-fed patients, 87 in organ transplant recipient, patient/caregiver
deficiency of effects on clinical laboratory values, 133t education about, 183
in anorexia nervosa, 350t for infants, 47, 48t, 50 data for, interpretation of, 6–16, 19t
in chronic pancreatitis, 216–217 in parenteral formulations (admixtures), 98 factors affecting, 16
in cystic fibrosis, 221 for adults, 110t and drug distribution, 134
in inflammatory bowel disease, 232 for pregnant women, 347, 347t evaluation of
in liver disease, 238t for pediatric liver transplant recipient, 178t in cancer patient, 154
in stem cell transplant recipient, 193 physiologic function of, 87 in pediatric cancer patients, 157–158
in tube-fed patients, 87 requirements for history, in obese patient, 326
dietary reference intakes for, by life stage group, in acute renal failure, in pediatric patients, maintenance of
48t 293, 294t in adults, 39
in parenteral formulations (admixtures), 98 in burn patients, 297 in pediatric patient, 38
for adults, 110t in pregnancy, 345t management of
for pregnant women, 347t in preterm infants, 41t in obese patient, 330
for pediatric liver transplant recipient, 178t in stem cell transplant recipient, 195 in organ transplant recipient, 174–176, 176t
physiologic function of, 87 supplementation measurement of, 4–5
requirements for in cystic fibrosis, 224 in obese patient, 326
in acute renal failure, in pediatric patients, for liver disease in children, 238t pediatric, measurement of, 5
293, 294t and wound healing, 68
and resting energy expenditure estimation, 44, 44t
in burn patients, 297 Vitamin status, assessment of, 20, 23t
standing, measurement of, 4–5
in cystic fibrosis, 224, 225t, 226 in adults receiving nutritional support, 52
in stem cell transplant recipient, 193
in elderly, 52 VLCD. See Very low calorie diet (VLCD)
usual
in pregnancy, 345t VO2. See Oxygen consumption
in cystic fibrosis, 221
in preterm infants, 41t Volume of distribution, 119
and ideal, comparison of, 6–16
supplementation Volume overload, in acute renal failure, in adults,
wheelchair, measurement of, 5
in chronic pancreatitis, 220 282–283
Weight-for-age percentiles
for critically ill infants, 309 Vomiting
for boys, birth to 36 months, 28
in cystic fibrosis, 224, 225t in anorexia nervosa, 350
for boys, 2 to 20 years, 32
for liver disease in children, 238t physical findings with, 351
for girls, birth to 36 months, 29
for pediatric cancer patients, 157 enteral nutrition with, contraindications to, 77
for girls, 2 to 20 years, 33
for pediatric patients, 48t, 49
Weight-for-height, in pediatric cancer patients,
for stem cell transplant recipient, 192, 195 W
157–158
Vitamin E Waist circumference
Weight-for-length percentiles
deficiency of clinical significance of, 16
in anorexia nervosa, 350t for boys, birth to 36 months, 30
measurement of, 16
in cancer patients, 153 for girls, birth to 36 months, 31
in obese patient, 326
in chronic pancreatitis, 216 Weight-for-stature percentiles
Wanglie, Helga, 379
in cystic fibrosis, 221 Wanted-warranted question, 381 for boys, 36
in inflammatory bowel disease, 232 Warfarin for girls, 37
in liver disease, 238t drug-nutrient interactions, 125 Weight gain
in tube-fed patients, 87 metabolism of, cranberry juice and, 120 drug-induced, 325, 326t
dietary reference intakes for, by life stage group, Wasting. See also Anorexia nervosa as goal, in adults, 39
48t in anorexia nervosa, 350t in pregnancy
in enteral formulations, and wound healing, 68 in cancer patients based on prepregnancy weight, 344, 344t
in parenteral formulations (admixtures) cytokines and, 152 monitoring, during tube feeding, 346
for adults, 110t hormones and, 152 Weight history, in anorexia nervosa, 350
for pregnant women, 347t in HIV-infected (AIDS) patients, 140 Weight loss
for pediatric liver transplant recipient, 178t indicators of, 143 in cancer patients, 150, 151–153, 154
physiologic functions of, 153 Water in children, clinical significance of, 16
requirements for in enteral formulations, 64, 80–81 in chronic pancreatitis, 215
in acute renal failure, in pediatric patients, intake, in chronic kidney disease, 338 in HIV-infected (AIDS) patients, 140
293, 294t in parenteral formulations (admixtures), 97 hypocaloric nutrition support and, 328
in pregnancy, 345t requirements for, in critically ill infants, 305, 305t in pediatric cancer patients, 160–161
in preterm infants, 41t Weight severe, 19t
supplementation actual, adjusted, calculation of, 336 significant, 19t
in chronic pancreatitis, 220 adjusted for children, 16
in cystic fibrosis, 224, 225t calculation of, 336 Well-nourished status, definition of, 259
for liver disease in children, 238t for obesity, 327, 327t Wendland, Robert, 379
and wound healing, 68 in anorexia nervosa Wheat, in enteral formulations, 64
Vitamin K measurement of, 351 Whey, in enteral formulations, 64
antibiotics and, 127 restoration of, 351 for pediatric patients, 68

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Wilms’ tumor, treatment of, nutritional status and, Zerit. See Stavudine (Zerit) for infants, 305
160 Ziagen. See Abacavir (Ziagen) for pediatric patients, 110t, 293t
Wilson’s disease, 235 Zidovudine (Retrovir), diet and nutrition interac- for pregnant women, 347t
Withdrawing treatment, 379 tions with, 142t physiologic functions of, 153, 247
Withholding treatment, 379 Zinc requirements for
Wound healing deficiency of in acute renal failure, in pediatric patients,
enteral formulations for, 68 in cancer patients, 153–154 293t
factors affecting, 68 in inflammatory bowel disease, 232 in burn patients, 297
in organ transplant recipient, 181t definition of, in anorexia nervosa, 350, 350t in liver disease, 239
dietary reference intakes for, by life stage group, in parenteral nutrition for adults, 52
49t in pregnancy, 345t
X
in enteral formulations, and wound healing, 68 in preterm infants, 41t, 43
Xanthine, plasma, in chronic pancreatitis, 216 excretion of, drugs affecting, 127 supplementation
Xerostomia. See Dry mouth metabolism of in acute brain i jury, 248
in anorexia nervosa, 350 in anorexia nervosa, 350, 352
Z in trauma, 271 in cystic fibrosis, 222, 225
Zalcitabine (Hivid), diet and nutrition interactions in parenteral formulations (admixtures), 98 for stem cell transplant recipient, 195
with, 142t for adults, 110t and wound healing, 68
Zenapax. See Daclizumab (Zenapax) for chronic kidney disease, 339 Z score, in evaluation of growth, 16

© 2005 A.S.P.E.N. www.nutritioncare.org. A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. 411