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Authors: Width, Mary; Reinhard, Tonia
Title: Clinical Dietitian's Essential Pocket Guide,The: Essential Pocket Guide, 1st Edition
Copyright ©2009 Lippincott Williams & Wilkins
2009
Lippincott Williams & Wilkins
Philadelphia
351 West Camden Street, Baltimore, Maryland 21201-2436 USA; 530 Walnut Street, Philadelphia,
Pennsylvania 19106 USA
978-0-7817-8829-8
0-7817-8829-3
Copyright © 2009 Lippincott Williams & Wilkins
351 West Camden Street, Baltimore, Maryland 21201-2436 USA
530 Walnut Street, Philadelphia, Pennsylvania 19106 USA
All rights reserved. This book is protected by copyright. No part of this book may be reproduced or
transmitted in any form or by any means, including as photocopies or scanned-in or other electronic copies,
or utilized by any information storage and retrieval system without written permission from the copyright
owner, except for brief quotations embodied in critical articles and reviews. Materials appearing in this
book prepared by individuals as part of their official duties as U.S. government employees are not covered
by the above-mentioned copyright. To request permission, please contact Lippincott Williams & Wilkins at
530 Walnut Street, Philadelphia, PA 19106, via email at [email protected], or via website at lww.com
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Printed in China
Acquisitions Editor: David Troy
Managing Editor: Linda G. Francis
Marketing Manager: Katie Schauer
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Creative Director: Doug Smock
Compositor: Aptara, Inc.
Library of Congress Cataloging-in-Publication Data
Width, Mary.
The clinical dietitian's essential pocket guide / Mary Width and Tonia Reinhard. — 1st ed.
p.; cm.
Includes bibliographical references and index.
ISBN 978-0-7817-8829-8
1. Dietetics—Handbooks, manuals, etc. 2. Diet therapy—Handbooks, manuals, etc. I. Reinhard, Tonia. II.
Authors: Width, Mary; Reinhard, Tonia
Title: Clinical Dietitian's Essential Pocket Guide,The: Essential Pocket Guide, 1st Edition
Copyright ©2009 Lippincott Williams & Wilkins
2009
Lippincott Williams & Wilkins
Philadelphia
351 West Camden Street, Baltimore, Maryland 21201-2436 USA; 530 Walnut Street, Philadelphia,
Pennsylvania 19106 USA
978-0-7817-8829-8
0-7817-8829-3
Copyright © 2009 Lippincott Williams & Wilkins
351 West Camden Street, Baltimore, Maryland 21201-2436 USA
530 Walnut Street, Philadelphia, Pennsylvania 19106 USA
All rights reserved. This book is protected by copyright. No part of this book may be reproduced or
transmitted in any form or by any means, including as photocopies or scanned-in or other electronic copies,
or utilized by any information storage and retrieval system without written permission from the copyright
owner, except for brief quotations embodied in critical articles and reviews. Materials appearing in this
book prepared by individuals as part of their official duties as U.S. government employees are not covered
by the above-mentioned copyright. To request permission, please contact Lippincott Williams & Wilkins at
530 Walnut Street, Philadelphia, PA 19106, via email at [email protected], or via website at lww.com
(products and services).
Printed in China
Acquisitions Editor: David Troy
Managing Editor: Linda G. Francis
Marketing Manager: Katie Schauer
Associate Production Manager: Kevin P. Johnson
Creative Director: Doug Smock
Compositor: Aptara, Inc.
Library of Congress Cataloging-in-Publication Data
Width, Mary.
The clinical dietitian's essential pocket guide / Mary Width and Tonia Reinhard. — 1st ed.
p.; cm.
Includes bibliographical references and index.
ISBN 978-0-7817-8829-8
1. Dietetics—Handbooks, manuals, etc. 2. Diet therapy—Handbooks, manuals, etc. I. Reinhard, Tonia. II.
Title.
[DNLM: 1. Dietetics—methods—Handbooks. 2. Nutrition Assessment—Handbooks. 3. Nutrition
Therapy—methods—Handbooks. QU 39 W642c 2009]
RM217.2.W53 2009
615.8'54—dc22
2008006120
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Application of this information in a particular situation remains the professional responsibility of the
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10 9 8 7 6 5 4 3 2 1
Authors: Width, Mary; Reinhard, Tonia
Title: Clinical Dietitian's Essential Pocket Guide,The: Essential Pocket Guide, 1st Edition
Copyright ©2009 Lippincott Williams & Wilkins
> Front of Book > Authors
Authors
Mary Width MS, RD
Lecturer
Coordinated Program in Dietetics, Department of Nutrition and Food Science, Wayne State University,
Detroit, Michigan
Tonia Reinhard MS, RD
Director
Coordinated Program in Dietetics, Department of Nutrition and Food Science, Wayne State University,
Detroit, Michigan
Contributors
Sheri Betz RD
St. John Hospital and Medical Center, Detroit, Michigan
Monica L. Griffin RD
DaVita Dialysis, Southgate, Michigan
Brenda Howell RD, CNSD
Genesys Regional Medical Center, Grand, Michigan
Angela M. Lada RD, RN
Detroit, Michigan
Lisa Ventrella Lucente RD
Department of Nutrition and Food Science, Wayne State University, Detroit, Michigan
Reviewers
Judi Brooks
Coordinated Program in Dietetics, Eastern Michigan University, Ypsilanti, Michigan
Christine Haar
Family and Consumer Sciences, Bowling Green State University, Bowling Green, Ohio
Emily Hoffman
Nutrition and Food Science, Utah State University, Logan, Utah
Kelly Sanna-Gouin
Food and Nutrition Services, Detroit Receiving Hospital, Detroit, Michigan
Zara Shah-Rowlands
Department of Human Ecology, Coordinated Program in Dietetics, Youngstown State University,
Youngstown, Ohio
Authors: Width, Mary; Reinhard, Tonia
Title: Clinical Dietitian's Essential Pocket Guide,The: Essential Pocket Guide, 1st Edition
Copyright ©2009 Lippincott Williams & Wilkins
> Front of Book > Dedication
Dedication
“I dedicate this book to my husband, Curt, for his love, support, and most of all, his endless supply of
patience; and to the memory of my parents, Marian and Walter Thiede.”
Mary Width
“This book is dedicated to Brendan Reinhard and Faye Reinhard for their technical support, John Reinhard
for life support, and to the memory of Gea DeRubeis Pacifico and Antonietta Pacifico.”
Tonia Reinhard
Authors: Width, Mary; Reinhard, Tonia
Title: Clinical Dietitian's Essential Pocket Guide,The: Essential Pocket Guide, 1st Edition
Copyright ©2009 Lippincott Williams & Wilkins
> Front of Book > Preface
Preface
The Clinical Dietitian's Essential Pocket Guide is an up-to-date and concise pocket-sized reference that
clinical dietitians can tailor to their own practice. Like most dietitians, we both had our own pocket clinical
books—tabbed little binders jammed with snippets of information culled from years of collecting. We have
seen many personalized clinical books in all different shapes and sizes through our contact with countless
wonderful dietitians who bravely serve as preceptors for our students. We think a clinical guide is so
integral to the practice of dietetics that we have required every student who has come to Wayne State
University's Coordinated Program in Dietetics to prepare their own. We have continually searched over the
years to find a published book that would take the place of these homemade resource books, but we have
been unable to find a comprehensive, concise guide that could both fit in a lab coat pocket and also be
customized to the user's needs. The inability to find such a guide is what gave us the inspiration to develop
one for our own students. When talking with other dietetic educators, we were encouraged to publish our
book and share it with fellow dietitians and dietetic students from other programs. We believe our book
will become an indispensable guide for students, interns, and practicing dietitians for the following reasons:
The compact size will easily fit into any lab coat pocket.
The colored tabs enable quick, easy searching of contents.
The latest research is incorporated into all chapters, so the busy clinician doesn't have to spend
valuable time searching textbooks or the Internet for the most updated information.
Blank pages in each chapter allow the clinician to customize their book by adding their own
resources and references. Writing in a formula, cutting and pasting an article, or stapling a
hospital formulary card can be done with ease.
Concise, in-depth coverage of all major practice areas makes it easy to cover a colleague's units
or patients by providing the correct resources to do so.
The primary audience for this book is dietitians, dietetic technicians, and students and interns working in
hospitals, nursing homes, and clinics, but it will also be useful for other health professionals in community
and wellness programs who need a quick reference for nutrition screening and assessment. Part I contains
chapters covering nutritional assessment, life stage assessment, and nutrition support. Part II includes
seven chapters on the major nutritionally relevant diseases. Appendices on food and drug interactions,
laboratory assessment, and a miscellaneous appendix of useful reference materials, such as conversion
tables, and food sources of vitamins, round out the book.
This book could not have been developed without the help of our expert contributors. We would like to
express our gratitude and appreciation to Sheri Betz, Brenda Howell, Angela Lada, Monica Lowe, and Lisa
Ventrella Lucente for their hard work and valuable contributions to our book. In addition, we would like to
thank all the countless colleagues and preceptors who offered constant encouragement and excellent
suggestions during the writing process.
Today's fast-paced health care environment makes it crucial to have the information you need when you
need it. We struggled with decisions on what content to include, trying to avoid long chunks of text to keep
the content easy to find. We hope that you find this book to be the quick and useful reference we intend it
to be.
Mary Width MS, RD
Tonia Reinhard MS, RD
Authors: Width, Mary; Reinhard, Tonia
Title: Clinical Dietitian's Essential Pocket Guide,The: Essential Pocket Guide, 1st Edition
Copyright ©2009 Lippincott Williams & Wilkins
> Table of Contents > Part I - Nutrition Assessment and Support > Chapter 1 - Nutrition Assessment
Chapter 1
Nutrition Assessment
The Nutrition Care Process
The Nutrition Care Process (NCP), as defined by the American Dietetic Association (ADA), is “a systematic
problem-solving method that dietetics professionals use to critically think and make decisions to address
nutrition-related problems and provide safe and effective quality nutrition care” (1). Dietetics professionals
use the NCP mainly in acute care, extended care, and outpatient settings; however, the process is also
useful in a variety of community venues.
The NCP consists of four steps: Nutrition assessment, nutrition diagnosis, nutrition intervention, and
nutrition monitoring and evaluation. Nutrition assessment of the hospitalized patient is the first step in
effective patient care to identify and diagnose nutrition risks and plan appropriate interventions. It consists
of a comprehensive assessment of nutrition status and risks and includes the following major categories of
data collection and typical types of data included:
Anthropometric measurements: Height, weight, body mass index (BMI), weight change, body
frame measurement and adjustment, knee height
Biochemical data: Laboratory data
P.4
Nutrition-focused physical examination: Review of systems, including general conditions and
physical appearance, gastrointestinal, musculoskeletal, skin, extremities, and other systems
Patient history: Medication and supplement history, personal history, medical and health history,
and food and nutrition history (diet history), which includes food consumption, nutrition and
health awareness, physical activity and exercise, and food availability
Nutrition diagnosis is the second step in the NCP. After assessment, the registered dietitian (RD) determines
the patient's nutrition-related problems and needs, which form the nutrition diagnosis. The nutrition
diagnosis, in turn, is expressed and documented in a specific format: Problem, etiology, signs and
symptoms (PES). Tables 1.1 and 1.2 illustrate and provide an example for the PES format.
The nutrition diagnostic terms are classified according to the following three domains and subclasses (2):
Intake: Caloric energy balance; oral or nutrition support intake; fluid intake; bioactive
substances; essential nutrients
Clinical: Functional; biochemical; weight (anthropometric and other measures)
Behavior/environment: Knowledge and beliefs; physical activity and function; food safety and
access
Table 1.1 Nutrition Diagnosis: Problem/Etiology/Signs
The problem (P) describes alterations in patient nutritional status:
A diagnostic label (qualifier) is an adjective that describes the physiologic response,
e.g., altered, impaired, risk of
The etiology (E) refers to cause(s) or contributor(s) to the problem:
It is linked to the problem by the words, “related to”
The signs/symptoms (S) are clusters of subjective and objective factors that provide evidence
that a problem exists:
They also quantify the problem and describe severity
Linked to (E) by the words, “as evidenced by” (AEB)
P.5
Table 1.2 Writing the Nutrition Diagnosis (ND) Statement
Example for the ND statement format
(P)roblem/(E)tiology/(S)igns/symptoms:
Excessive caloric intake (P) related to frequent consumption of large portions of high fat meals
(E), as evidenced by:
Daily caloric intake exceeding DRIa by 500 kcal (S)1.
2 lb weight gain during past 18 months (S)2.
aDaily recommended intake.
Step 3 of the NCP is nutrition intervention. The RD plans interventions to solve the problems identified in
nutrition assessment and formulated as the nutrition diagnosis; the intervention step includes both planning
and implementation. The nutrition diagnoses direct the interventions, which are derived from the scientific
literature and established practice standards and protocols (evidence-based interventions). Nutrition
intervention components include:
Prioritization of the nutrition diagnoses as to each problem's severity or importance: To
prioritize, the RD assesses the impact of the problem on patient safety and need, patient
awareness and prioritization of the problem, and potential that the planned intervention will
positively affect the problem.
Use of evidenced-based interventions: RDs can access the ADA's Evidence Analysis Library at
www.adaevidencelibrary.com.
Establish patient-focused expected outcomes for each nutrition diagnosis: Outcomes must be
specific and measurable and are patient-focused (see example in Table 1.3). This component of
planning the nutrition intervention assumes collaboration with the patient, caregivers, and other
members of the health care team.
P.6
Implementation of the nutrition intervention: A key aspect of implementation is communication
of the plan to the patient, caregivers, and other members of the health care team.
Table 1.3 Example of Planning the Intervention
Nutrition
Diagnosis
Excessive fat intake related to frequent consumption of high-fat
meals as evidenced by fat kilocalories >55% of total kilocalories
per day
Expected
OutcomesLimit foods high in cholesterol, saturated fat1.
Use food sources of monounsaturated fat as preferred
fat
2.
Evidence-
Based
Ideal Goals
Consume 25%–35% of total kcal from fat1.
Consume <7% saturated fat2.
Isocaloric replacement of saturated with
monosaturated and polyunsaturated
3.
The final step in the NCP is monitoring and evaluation. In this last phase, the RD continues to re-examine
the patient's status by gathering new data (monitoring) and assessing patient status by comparison to
previous status, expected outcomes, and established standards (evaluation). The RD schedules follow-up
time points for monitoring and evaluation, based on the clinical protocols of the facility. This fourth step
helps the RD to determine whether the expected outcomes are being achieved. After discharge, the RD can
use phone, electronic communication, and mailings to gather data for monitoring and evaluation.
Anthropometric Assessment
There are several anthropometric measurements that are useful in the clinical setting. Measurements of
body weight, height, and composition can be used by the clinician when evaluating nutritional status.
Estimating Height
An estimation of height is necessary for patients that are confined to bed or a wheelchair, have curvature
of the
P.7
spine or contractures, or are otherwise unable to stand for an actual height measurement.
Knee Height
Knee height is measured using a sliding broad-blade caliper (available at
http://www.shorrproductions.com).
Patient should be in the supine position, and the left leg is preferable for measurement.
With both the knee and ankle at 90-degree angles, place one blade of the caliper under the heel
of the foot and the other on the anterior surface of the thigh.
The shaft of the caliper is held parallel to the long axis of the lower leg, and pressure is applied
to compress the tissue.
Height (in cm) is calculated using the formulas in Table 1.4.
Demi-span
The measurement is useful in the clinical setting because it requires no special equipment and is
particularly useful for patients with lower limb dysfunction.
Using the left arm if possible, measure the distance from the notch between the middle and the
ring fingers to the middle of the sternal notch.
Make sure the patient's arm is horizontal and in line with the shoulders.
Height (in cm) is calculated using the formulas in Table 1.5.
Table 1.4 Knee Height
Females
Height in cm = 84.88 - (0.24 × age in years) + (1.83 × knee height in cm)
Males Height in cm = 64.19 - (0.04 × age in years) + (2.02 × knee height in cm)
Data from reference 3.
P.8
Table 1.5 Demi-Span
Females
Height in cm = (1.35 × demi-span in cm) + 60.1
Males
Height in cm = (1.40 × demi-span in cm) + 57.8
Data from reference 4.
Evaluating Body Weight
Ideal Body Weight
A quick and easy method to calculate ideal body weight (IBW) is the Hamwi Method, shown in Table 1.6.
Frame Size Adjustment
In order to adjust for differences in body build (muscularity, bone thickness, and body proportions), it is
necessary to determine an individual's frame size when calculating IBW (5). Frame size can be estimated by
two methods. Measuring wrist circumference is easy and straightforward. Measuring elbow breadth is more
complex, but tends to provide a more accurate estimate of frame size. Both methods use the
measurements in relation to the patient's height.
Wrist Circumference
Measure the wrist circumference just distal to the styloid process at the wrist crease of the left
hand, in
P.9
inches. Compare the measurement to the values in Table 1.7.
Table 1.6 Ideal Body Weight
Females
IBW = 100 lb for 5 ft + 5 lb for each inch >60 in.
Males
IBW = 106 lb for 5 ft + 6 lb for each inch >60 in.
Table 1.7 Estimating Frame Size Using Wrist Circumference
Female Wrist Measurements
Height <5'2 Height 5'2 –5'5 Height >5'5
Small <5.5 <6.0 <6.25
Medium 5.5 –5.75 6.0 –6.25 6.25 –6.5
Large >5.75 >6.25 >6.5
Male Wrist Measurements
Height >5'5
Small 5.5 –6.5
Medium 6.5 –7.5
Large >7.5
Data from reference 6.
Elbow Breadth
Subject should stand, if possible, and extend the arm forward so that it is horizontal and parallel
to the ground.
Turn palm so that it is facing up and bend elbow so that the forearm is at a 90-degree angle to
the ground.
Measure the distance between the two prominent bones on either side of the elbow (the
epicondyles of the humerus). This measurement can be taken with a ruler or tape measure, but
using calipers is preferable.
Compare the measurement to the values in Table 1.8.
Amputation Adjustment
For patients with amputations, estimation of IBW should be adjusted with the following equation using the
factors in Table 1.9.
P.10
Table 1.8 Estimating Frame Size Using Elbow Breadth
Female Elbow Measurements
Medium Frame
If elbow breadth is less than those in the table for a specific height, subject is small
framed, and if elbow breadth is greater, subject is large framed.
Height Elbow Breadth
4'10 –4'11 2 1/4 –2 1/2
5'0 –5'3 2 1/4 –2 1/2
5'4 –5'7 2 3/8 –2 5/8
5'8 –5'11 2 3/8 –2 5/8
6'0 –6'4 2 1/2 –2 3/4
Male Elbow Measurements
Medium Frame
If elbow breadth is less than those in the table for a specific height, subject is small
framed, and if elbow breadth is greater, subject is large framed.
Height Elbow Breadth
5'2 –5'3 2 1/2 –2 7/8
5'4 –5'7 2 5/8 –2 7/8
5'8 –5'11 2 3/4 –3
6'0 –6'3 2 3/4 –3 1/8
6'4 –6'7 2 7/8 –3 1/4
Data from reference 5.
Table 1.9 Amputation Adjustments for Estimating Ideal Body Weight
Percentage Body Weight Contributed by Body Part
Hand 0.7%
Forearm and hand 2.3%
Entire arm 5.0%
Foot 1.5%
Lower leg and foot (below knee) 5.9%
Entire leg 16.0%
Data from reference 7.
P.11
Spinal Cord Injury Adjustment
For patients with spinal cord injuries, estimation of IBW should be adjusted as follows:
Paraplegia: Subtract 5% to 10% from IBW
Quadriplegia: Subtract 10% to 15% from IBW
Interpretation of Body Weight Data
Percentage of Ideal Body Weight
Percentage of Usual Body Weight (UBW)
Table 1.10 shows how to evaluate % IBW and % UBW data.
Percentage of Weight Change
This calculation is useful in assessing variations from the patient's usual weight, especially in the elderly
population where unintentional weight loss is associated with increased morbidity and mortality (8). Once
percentage of weight change has been calculated, use Table 1.11 to assess the significance of any weight
changes.
Table 1.10 Interpreting % IBW and % UBW
% IBW % UBW Nutritional Risk
>120 __ Obesity
110–120 __ Overweight
90–109 __ Not at risk
80–89 85–95 Mild
70–79 75–84 Moderate
<70 <75 Severe
P.12
Table 1.11 Interpreting Unintentional Weight Changes
Time Frame Significant Weight Loss Severe Weight Loss
1 week 1%–2% >2%
1 month 5% >5%
3 months 7.5% >7.5%
6 months 10% >10%
Data from reference 9.
Assessment of Overweight and Obesity
Body Mass Index
BMI, or Quetelet's index, is a direct calculation based on height and weight, regardless of gender, and can
be used to assess the severity of obesity. BMI does have limitations as a measure of total body fat, which
must be considered when interpreting the data, particularly in the presence of edema, high muscularity,
muscle wasting, or for very short people (under 5 ft) (10). See Table 1.12 for classifications of overweight
and obesity based on BMI.
Waist Circumference and Waist-to-Hip Ratio
The presence of excess fat in the abdomen, out of proportion to total body fat, is an independent predictor
of risk factors and morbidity (10). Two methods for measuring abdominal fat are waist circumference and
the waist-to-hip ratio (WHR). Both methods have been used to show increased risk for diabetes, coronary
artery disease, and hypertension for those individuals with excess abdominal fat. Some studies suggest that
waist circumference is a better predictor of disease risk than WHR, whereas other studies suggest WHR is
the stronger indicator (10,11). Regardless of which method the clinician uses, measuring abdominal fat can
help identify risk level for several chronic diseases (Tables 1.12 and 1.13).
P.13
Table 1.12 Classification of Overweight and Obesity by Body Max Index, Waist
Circumference, and Associated Disease Risk
BMI (kg/m2) Weight Status
Obesity
Class
Disease Riska Relative to Normal Weight & Waist
Circumference
Men =40 in. Men >40 in.
Women =35 in. Women >35 in.
<18.5 Underweight __ __
18.5–24.9 Normal __ __
25.0–29.9 Overweight Increased High
30.0–34.9 Obesity I High Very high
35.0–39.9 Obesity II Very high Very high
>40.0 Extreme
obesity
III Extremely high Extremely high
BMI, body mass index.aDisease risk for type 2 diabetes, hypertension, and CVD.
Data from reference 10.
Estimating Nutrient Requirements
Energy Requirements
Harris–Benedict and Mifflin–St. Jeor Equations
The Harris–Benedict and Mifflin–St. Jeor equations are two widely used predictive equations for estimating
basal (BEE) or resting energy expenditure (REE). Once BEE or REE have been calculated, the total energy
expenditure (TEE) would need to be estimated using a combination of activity and stress factors. Stress
factors are used
P.14
for hospitalized patients in a hypermetabolic state due to disease, infection, or trauma. The clinician's
judgment should be used to determine the appropriate activity and/or stress factor to use to estimate TEE.
See Table 1.14 for activity and stress factors.
Table 1.13 Waist-to-Hip Ratio
Male Female Health Risk
=0.95 =0.80 Low risk
0.96–1.0 0.81–0.85 Moderate risk
=1.0 =0.85 High risk
Data from reference 11.
Table 1.14 Activity and Stress Factors for Determining Total Energy Expenditure
Condition Factor
Activity Factors
Confined to bed 1.2
Ambulatory 1.3
Stress Factors
Burns
=20% BSA 1.5
20%–40% BSA 1.8
>40% BSA 1.8–2.0
Infection
Mild 1.2
Moderate 1.4
Severe 1.8
Starvation 0.85
Surgery
Minor 1.1
Major 1.2
Trauma
Skeletal 1.2
Blunt 1.35
Closed head injury 1.4
BSA, body surface area.
Following is the Harris–Benedict Equation:
Females: BEE = 655.1 + 9.6W + 1.9H - 4.7A
Males: BEE = 66.5 + 13.8W + 5.0H - 6.8A
W = weight in kilograms (use of actual vs. ideal weight is determined by the clinician); H = height in
centimeters; A = age in years.
P.15
Following is the Mifflin–St. Jeor Equation:
Females: REE = 10W + 6.25H - 5A - 161
Males: REE = 10W + 6.25H - 5A + 5
W = actual weight in kilograms; H=height in centimeters; A = age in years.
Ireton–Jones Equations
The Ireton–Jones equations for estimating energy expenditure have been found to be particularly useful for
the obese population and for ill or injured patients in the intensive care unit (ICU) (12).
Following are the Ireton–Jones equations:
Spontaneously breathing patients: EEE = 629 - 11(A)
25(W) - 609(O)
Ventilator-dependent patients: EEE = 1784 - 11(A)
+ 5(W) + 244(S) + 239(T) + 804(B)
EEE = estimated energy expenditure (kcal/day); A = age (years); W = actual body weight (kg); O = obesity
>30% above IBW or BMI >27 (present =1, absent = 0); S = sex (male=1, female=0); T=diagnosis of trauma
(present =1, absent=0); B= diagnosis of burn (present=1, absent = 0).
Kilocalories per Kilogram
A fast and easy method for estimating energy needs is using kilocalories per kilogram of body weight, with
the reference weight as actual or ideal body weight, based on the clinician's judgment (Table 1.15).
Protein Requirements
Table 1.16 contains protein recommendations for patients with several general conditions. Disease-specific
protein requirements can be found in their respective chapters.
Fluid Requirements
Methods for estimating fluid requirements for the normal person are typically based on body weight,
kilocalorie
P.16
intake, or body surface area (BSA). The caloric intake method uses 1 mL/kcal for adults and 1.5 mL/kg for
infants. The BSA method uses 1,500 mL/m2/day (see Table 3.12 for calculating BSA). Table 1.17 shows two
methods for estimating fluid requirements based on body weight.
Table 1.15 Energy Requirements Based on Kilocalories per Kilogram of Body Weight
Condition Energy Requirement (kcal/kg)
Normal 25–30
Stress
Mild 30–35
Moderate to severe 35–45
Data from references 5 and 13.
Biochemical Data
The purpose of collecting laboratory data for nutrition assessment is to determine status inside the body.
Blood and urine samples can be used to directly measure a nutrient or metabolite that is affected by the
nutrient. Each test is associated with a distinctive sensitivity and specificity. Sensitivity indicates the
degree to which the assay
P.17
for a particular constituent is accurate in determining the amount of that constituent in a sample.
Specificity refers to how specific the test is in reflecting a particular function or diagnosis, for example,
how specific blood urea nitrogen is for assessing renal function.
Table 1.16 Daily Protein Requirements for Hospitalized Patients
Condition Protein Requirement (g/kg)
Normal–maintenance 0.8–1.0
Metabolic stress
Mild 1.2–1.5
Moderate to severe 1.5–2.0
Pressure ulcers 1.25–1.5
Protein depletion
Mild (albumin 2.8–3.5 g/dL) 1.0–1.2
Moderate (albumin 2.1–2.7 g/dL) 1.2–1.5
Severe (albumin =2.0 g/dL) 1.5–2.0
Data from references 5, 13, 14, and 15.
Table 1.17 Estimating Fluid Requirements Based on Body Weight
Method 1
Body Weight Fluid Requirement
Young: 15–30 years 40 mL/kg
Average: 25–55 years 35 mL/kg
Older: 55–65 years 30 mL/kg
Elderly: >65 years 25 mL/kg
Method 2
Body Weight Fluid Requirement
1–10 kg 100 mL/kg
11–20 kg 1,000 mL + 50 mL/kg each kg >10 kg
>20 kg 1,500 mL + 20 mL/kg each kg >20 kg
Data from references 5 and 14.
Basic concepts in the interpretation of laboratory data include: No single test is diagnostic on its own;
repeated draws are more valid; there can be diurnal variation for some tests; and some constituents can be
affected by other superimposed conditions, diseases, and medications. Table 1.18 provides an overview of
laboratory parameters (with
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the associated values) correlated with nutritional risk. Laboratory parameters may also be used in various
formulas (Table 1.19) to predict the level of nutritional risk.
Table 1.18 General Biochemical Nutrition Risk Parameters
Parameter Level Associated with Risk
Albumin <3.5 g/dL
Cholesterol <160 mg/dL
Hemoglobin, hematocrit Male: <14 g/dL, 42%
Female: <12 g/dL, < 37%
Prealbumin <17 mg/dL
Total lymphocyte count <1,500 cells/mm3
Transferrin <150 mg/dL
Table 1.19 Formulas for Assessment of Nutrition Risk
Risk Assessment Formula Interpretation
Nutrition Risk
Index
(1.519 × albumin) + (41.7 × % IBW) >100, no risk
97.5–100, mild
risk
83.5–97.5,
moderate risk
<83.5, severe
risk
Prognostic
Nutrition
Index
158–16.6 (albumin)–0.78 (triceps skin fold in
mm)–0.2 (transferrin)–5.8 (delayed skin
hypersensitivity)
<40, normal
=40,
compromised
Prognostic
Inflammatory
and
Nutritional
=1, no risk
1–10, low risk
11–20,
moderate risk
21–30 severe
risk
Protein Status
Protein status, both visceral protein and somatic protein compartments, is a crucial aspect of nutrition
assessment. The three major hepatic proteins which RDs use to assess visceral protein are albumin,
transferrin, and prealbumin (Table 1.20). However, these hepatic proteins also reflect the physiologic
response to injury, stress, infection, surgery, and trauma (16). They are negative acute-phase proteins, in
that the level decreases in response to the acute phase of the stress response, which attends illness and
trauma, and in which inflammation figures prominently.
Total lymphocyte count (TLC) reflects visceral protein status, although because of its association with
immune system function, it will not be accurate in some circumstances (Table 1.21) (17). Another
parameter for assessment of visceral protein status is nitrogen balance, although it more properly reflects
total body
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protein (Table 1.22). Adults are normally in nitrogen balance, in that dietary protein (source of nitrogen) is
used for protein synthesis. When protein degradation exceeds synthesis, a person is in negative nitrogen
balance, which occurs in malnutrition. Children and pregnant women are in positive nitrogen balance,
because protein synthesis exceeds degradation during phases of growth.
Table 1.20 Visceral Protein Parameters
Protein Normal Range Implications & Considerations
Albumin 3.5–5.0
g/dL
Low when visceral protein is depleted; 17–20 days; low in
liver disease, malabsorption syndromes, protein-losing
nephropathies, ascites, burns, overhydration, inflammation;
elevated in dehydration
Fibronectin 220–400
mg/dL
Low when visceral protein is depleted; half-life 15 hr; low
in inflammation, injury; affected by coagulation factors
Prealbumin 15–36
mg/dL
Low when visceral protein is depleted; half-life 1.9 days;
low in liver disease, burns, inflammation; elevated in
nephrotic syndrome, chronic kidney disease, pregnancy,
Hodgkin's lymphoma
Retinol
binding
protein
3–6
mg/dL
Low when visceral protein is depleted; half-life 12 hr; low
in chronic pancreatitis or carcinoma, cystic fibrosis,
intestinal malabsorption, chronic liver diseases, vitamin A
deficiency; elevated in renal failure
Transferrin 188–341
mg/dL
Low when visceral protein is depleted (only if iron status is
normal); half-life 8–10 days; low in chronic infection,
malignancy; elevated in late pregnancy, use of oral
contraceptives, viral hepatitis
Data from references 18 and 19.
The somatic protein compartment is assessed using both anthropometric and biochemical measurements,
the
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latter through the use of creatinine excretion and nitrogen balance. Creatinine is a catabolic product of
creatine phosphate, a compound needed in muscular contraction. It is excreted at a constant daily rate
proportional to muscle mass. Kidney disorders and high intake of meat products can raise levels. Table 1.23
provides the formula for calculating creatinine height index and lists expected excretion rates.
Table 1.21 Total Lymphocyte Count and Visceral Protein Status
Formula: TLC = % of lymphocytes × No. of WBCs (103)
Interpretation
Normal: 2,000–3,500
Mild: 1,500–1,800
Moderate: 900–1,500
Severe: <900
Affected by:
Injury; viral infection; radiation therapy; surgery; chemotherapy, and other immunosuppressive
medications
Note: TLC may not be reliable indicator of malnutrition in the elderly.
TLC, total lymphocyte count; WBC, white blood cells.
Table 1.22 The Use of Nitrogen Balance in Assessment of Total Body Protein
Monitor dietary intake of protein (PRO) for 24 hr1.
Convert dietary protein intake to nitrogen intake:2.
Collect 24-hr urine; obtain urinary urea nitrogen (UUN)3.
Nitrogen Balance = Nitrogen intake - (UUN + 3a)4.
Interpretation: Adults are normally in nitrogen balance (0); pregnant women and
children (growth states) are in positive balance; negative balance may suggest
malnutrition
5.
a Insensible losses.
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Table 1.23 Calculation and Interpretation of Creatinine Height Index
24-hr Urine Collection; Meat-Free Diet (Ideally); Compare Creatinine to Standard for
Height/Gender
% CHI=
Interpret: 60%–80%, mild depletion
40%–59%, moderate depletion
<40%, severe depletion
Affected
by:
Renal dysfunction; advanced age; stress; trauma; sepsis; strenuous exercise;
use of corticosteroids
24-hr Urinary Creatinine Excretion in Adults
Males: 23 mg/kg/IBW Females: 18 mg/kg/IBW
Height
(cm)
Creatinine (mg) Height (cm) Creatinine (mg)
157.5 1,288 147.3 830
160.0 1,325 149.9 851
162.6 1,359 152.4 875
165.1 1,386 154.9 900
167.6 1,426 157.5 925
170.2 1,467 160.0 949
172.7 1,513 162.6 977
175.3 1,555 165.1 1,006
177.8 1,596 167.6 1,044
180.3 1,642 170.2 1,076
182.9 1,691 172.7 1,109
185.4 1,739 175.3 1,141
188.0 1,785 177.8 1,174
190.5 1,831 180.3 1,206
193.0 1,891 182.9 1,240
CHI, creatine height index; IBW, ideal body weight.
Data from reference 20.
Biochemical assessment also includes review of hematologic parameters, as they may be indicators of
nutritionally related anemia (Table 1.24). Several of these parameters can also be expected to be affected
by compromised visceral protein status.
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Table 1.24 Hematologic Parameters Related to Anemia
Constituent Normal Range Implications & Considerations
Erythrocyte
protoporphyrin
<5 µg/dL RBCs High in later stages of iron deficiency anemia
Ferritin Males:
18.0–350
ng/mL
Females:
15–49 yr:
12.0–156
ng/mL
>49 yr:
18.0–204
ng/mL
Low in early deficiency state in the presence of
depleted iron stores
Folate, red blood
cell content
95 ng/mL Low in later stages of folate deficiency anemia
Folate, serum 1.9 ng/mL Low as folate deficiency progresses
Hematocrit Males:
41%–50%
Females:
35%–46%
Low in anemia; represents percentage of red
blood cells in total blood volume
Hemoglobin Males:
13.8–17.2
g/dL
Females:
12.0–15.6
g/dL
Low in anemia; represents total amount of
hemoglobin in red blood cells
Mean corpuscular
hemoglobin
32–36 g/dL Low in iron deficiency anemia hypochromic);
normal in B12 and folate deficiency
concentration (normochromic); represents hemoglobin
(pigmentation) contained in an average red
blood cell
Red blood cell count Male: 4.4 –5.8
× 106 µL
Female: 3.9
–5.2 × 106 µL
Low in anemia; the number of red blood cells in
sample
Transferrin 188–341
mg/dL
High in iron-deficiency anemia as transport of
iron increases
Vitamin B12 200–800
pg/mL
Low in B12 deficiency
Data from references 18 and 19.
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Nutrition-Focused Physical Examination
Dietitians use data from the physical examination assessments conducted by other health care
practitioners, but they also conduct a nutrition-focused physical examination (21). The goal is to identify
signs and symptoms, which may be associated with specific nutrient deficiencies and compromised
nutritional status or malnutrition (Table 1.25). In this assessment, the RD uses visual inspection, palpation,
percussion, and auscultation. The Subjective Global Assessment (SGA) is another method of assessing
physical attributes and functional abilities, but it also combines other assessment parameters (Table 1.26).
Patient History
A comprehensive nutrition assessment includes many aspects of the patient's history. The main types of
history include health or medical, medications, personal, and food and nutrition. Sources for the historical
information include the medical record, the patient, and significant others.
The health or medical history identifies factors that affect nutrient needs or nutrition education needs or
that place the client at risk for poor nutrition status. One important component is the nutritional relevance
of the current diagnosis (Table 1.27). The diagnosis may present a specific level of risk based on the
potential to adversely affect nutritional status. In addition to the disease's potential to alter nutritional
status, the degree of risk posed to an individual patient depends on several factors, including its duration
and severity, the presence of other physiologic stressors, and the individual (genetics, age, and nutritional
status). Some diseases are nutritionally relevant because of the likelihood of the need for nutrition
intervention.
The medication history identifies substances that can affect nutrient needs or alter nutritional status. This
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includes prescribed medications, over-the-counter (OTC) medications, and dietary supplements (see
Appendix B). Personal history includes several aspects of psychosocial and lifestyle patterns that may affect
nutrient needs, influence food choices, or limit therapy options. The food and nutrition history identifies
food consumption patterns, specific nutrient intake and imbalances, reasons for potential nutrition
problems, and dietary factors important to shaping the nutrition care plan. Table 1.28 lists general
information for all categories of history in addition to specific information to collect from the patient or the
medical record.
Table 1.25 Nutrition-Focused Physical Examination
Observed Conditions
Body System Healthy Abnormal Implications
Hair Normal
distribution,
shiny
Thin, dull, dry, brittle,
corkscrew hairs
Chemotherapy,
protein or biotin
deficit, vitamin C
deficiency
Eyes Bright, clear,
pink conjunctiva
Sunken, dull, pale, dry
conjunctiva,
photophobia, xerosis
Deficiency of: Vitamin
A, zinc, riboflavin
Lips Moist, good
color
Swollen, dry, red,
cracked
Deficiency of:
riboflavin, pyridoxine,
niacin
Gums Pink, firm Sore, spongy, red,
swollen, bleed easily
Vitamin C deficiency
Tongue Pink, presence
of papillae
Purple, white or gray
coating, smooth, slick
Deficiency of:
riboflavin, pyridoxine,
folic acid, niacin,
vitamin B12, iron
Teeth Clean, intact, all
present
Dentures, missing teeth,
loss of tooth enamel
Calcium deficiency,
poor diet
Neck No swelling Presence of nodule(s),
goiter
Excess or deficiency of
iodine
Skin Smooth, slightly
moist, good
color
Pale, dry, scaly, bruises
easily, pressure ulcers,
dermatitis
Deficiency of: iron,
vitamins A or C, zinc,
essential fatty acid,
protein; excess of
niacin
Legs Well developed,
firm
musculature, no
joint or bone
pain
Calf tenderness, flaccid
muscles, pain, edema,
rickets, bone or joint
pain
Deficiency of: protein;
vitamins A, C, or D;
calcium
Abdomen No swelling or
pain
Mildly edematous,
diarrhea, ascites
Deficiency of: protein,
niacin, zinc
Hands/nails Smooth Brittle nails, atrophied
fine muscles, spoon-
shaped nails
Deficiency of: protein,
iron
Musculo-
skeletal,
adipose
Normal bone,
muscle, and fat
development
Calf tenderness, loss of
subcutaneous fat,
emaciated appearance,
pain, decreased grip
strength, hollow cheeks,
fractures, osteoporosis
Deficiency of: protein,
thiamin, vitamin C;
energy or fluid deficit
Neurologic Normal reflexes CVA, limited reflexes,
disorientation, paralysis,
convulsions, dementia
Deficiency of: thiamin,
niacin, vitamins B6 or
B12, folic acid, iodine,
phosphorus, calcium,
magnesium
Data from reference 13.
Table 1.26 Subjective Global Assessment
Category Criteria Points
1. Weight
Weight ______ Height _______
Weight loss:
6 mos _____% loss; 20% 4 pts; 10%-19.9% 3 pts; 6%–9.9% 2 pts;
2%–5.9% 1 pt
1 mo_____% loss; 10% +4 pts; 5%–9.9% 3 pts; 3%–4.9% 2 pts;
2%–2.9% 1 pt
2 wks _____ increased or no change 0 pts; decreased 1 pt
2. Food Intake
Previous month Change, less than usual intake; 1 pt
Normal foods, intake less than usual; 1pt
Little solid food; 2 pts
Only liquids or nutritional supplements; 3 pts
Very little of anything; 4 pts
3. Gastroin-testinal
Symptom
Previous
2 weeks
Vomiting or diarrhea or anorexia; 3 pts
Pain; 3 pts (specify location ______)
Mouth sores; 2 pts
Dry mouth; 1 pt
Nausea or constipation; 1 pt
Changes in taste/aversions; 1 pt
4. Functional
Capacity
Previous month
Not usual but normal activity; 1 pt
In bed less than half the day; 2 pts
Able to do little activity, mostly in bed or chair; 3 pts
Bedridden; 4 pts
5. Diagnosis/disease
Related to nutritional
requirements
Primary Diagnosis: ______ Stage______
1 pt: Cancer, AIDS, pulmonary or cardiac cachexia, pressure ulcer,
fistula, wound, trauma, age >65 yr
Metabolic Stress Level:
Low; 1 pt: temp 99–101°F <72 hr; low dose steroid
Moderate; 2 pts: temp 101–102°F of 72 hr; moderate steroid dose
High; 3 pts: temp >102°F over 72 hr; >30 mg prednisone/day
6. Physical
Examination
For each trait, rate: normal (0); mild (1); moderate (2); severe (3)
Loss of subcutaneous fat ____
Muscle wasting (quadriceps, deltoids) ____
Ankle edema ____ Sacral edema ____ Ascites ____
Mucosal lesions __ Cutaneous lesions __ Hair change __
SGA rating:
A____ Well-nourished: no weight loss, intake normal, no
functional deficits
B____ Moderately malnourished: >3 pts weight loss; change in
intake; GI symptoms; functional deficit; loss of fat or muscle mass
C____Severely malnourished: >3 pts weight loss; severe intake
deficit; GI symptoms; severe functional deficit; signs of
malnutrition, i.e., severe loss of subcutaneous fat, muscle mass,
and edema
Data from reference 22.
Food and Nutrition History
A comprehensive food and nutrition history (diet history) is generally not possible with most patients in the
acute care setting, although components of the history are vital in nutrition assessment. In other practice
settings, it is both possible and desirable to collect detailed information of this type. The goal of a food and
nutrition history is to identify nutrient intake and imbalances, the reasons for potential food and nutrition
problems, and all dietary factors important in generating the nutrition diagnosis and
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subsequent intervention. The RD needs the following types of data: Food intake, eating habits and patterns,
and lifestyle patterns related to nutrition and health. If it is likely the patient will require bedside
instruction, and depending on the diagnosis, the RD will need to collect more detailed information about
the patient's food intake.
Table 1.27 Nutritionally Relevant Diagnoses/Diseases
AIDS-HIV Dehydration Multiple sclerosis
Alcohol and/or drug abuse Diabetes Nephrotic
syndrome
Cachexia Dysphagia Neutropenia
Cancer Eating disorders Obesity
Celiac disease Gastrointestinal bleeding Pancreatitis
Cerebrovascular accident Hepatic encephalopathy Parkinson disease
Chronic obstructive pulmonary
disease
Hepatitis Peritonitis
Hypertension Pressure ulcers
Cirrhosis Inflammatory bowel
disease
Renal failure
Coronary artery disease Malabsorption Sepsis
Crohn disease Malnutrition Tuberculosis
Data from reference 13.
Table 1.28 Patient History Categories
History Category Specific Information
Health/Medical
Current health status and diagnoses
Previous medical history and health
status
Family history
Surgical history
Date of first diagnosis
Previous education on diagnosis
Specific family members affected by
nutritionally relevant disease and onset age
Recent diagnostic procedures requiring NPO
status
Difficulty chewing (state of dentition) or
swallowing
Chronic gastrointestinal problems (diarrhea,
constipation, nausea, vomiting)
Medications
Prescription medications
OTC meds
Dietary supplements (nutrient, herbal,
essential nutrients)
Illegal drugs
Use of multiple medications
Duration of medication use
Frequency of use (chronic or as needed)
Changes in sense of smell or taste related to
medications
Previous education on potential interactions
Personal
Age
Gender
Cultural/ethnic identity
Occupation/economic status
Role in family
Educational level
Motivational level
Income
Use of or eligibility for government programs
Communication barriers
Cognitive function
Smoking
Ability to perform daily functions
Person responsible for grocery shopping, meal
preparation
Access to transportation
Recent loss of spouse
Food and Nutrition/Diet
Food intake
Eating habits and patterns
Lifestyle patterns
Food intolerances or allergies
Appetite (current and prior to admission)
Weight history (recent weight loss in particular)
Physical handicaps affecting food preparation or
intake
Typical daily intake (types and amounts of foods
and beverages consumed
Meal pattern
Religious dietary restrictions
Ethnic dietary habits
Alcohol consumption
Frequency of dining out; types
Exercise, physical activity (type and frequency)
Attitude regarding diet and health
Previous diet instruction (location, year, topic)
Interest in diet instruction or outpatient
counseling
Stage of change/readiness to learn
Of the various methods for obtaining a patient's food intake, the most practical in the acute or extended
care settings are the typical daily intake (TDI) (Table 1.29) and simplified food frequency (FF) (Table 1.30).
In the TDI, the RD asks the patient what he or she typically eats on a daily basis. In contrast to a 24-hour
food recall, in which the patient recounts his intake beginning with the last meal eaten, the TDI begins with
the first meal of the day.
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To avoid a judgmental approach, it is best not to label meals as breakfast, lunch, and dinner, but rather
based on time of day. For example, the RD would ask, “What is the first thing you would eat or drink when
you get up in the morning?”
Table 1.29 Typical Daily Intake Form
Meal Timing Food Item Amount Where Eaten
Sample Form
Table 1.30 Food Frequency Form
Food Item/Group Amount/Day Amount/Week
Milk or other dairy products (yogurt, cheese)
Meat, poultry, eggs
Fish
Nuts, legumes, and legume products
Fruits
Vegetables
Starches (breads, cereals, grains)
Fats, added (oils, margarine, salad dressing)
Snack foods (chips, pretzels, crackers)
Desserts/sweets
Dining out:
Fast food
Restaurant dining
Beverages:
Alcohol
Coffee, tea
Carbonated beverages
Fruit juices
A simplified FF is not as detailed as a comprehensive FF questionnaire, but is advantageous for two reasons.
The first advantage is that the simplified FF is a quick method for determining whether the patient avoids
any major category of food, and the second is that it will provide a crosscheck of the TDI. After collecting
the food intake information, the RD compares it to an appropriate standard, such as the Dietary Guidelines
for Americans (Appendix C) or the Dietary Reference Intakes (Appendix C). The dietitian can also use a
simplified evaluation form of general aspects of diet (Table 1.31).
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Table 1.31 Evaluation of Dietary Intake
Group Servings/Day Recommended Adequate/Excess
Dairy
Protein
Fruit
Vegetable
Starch
Fat/sweets
Overall Diet Adequacy: ___yes___no
Specific Nutrients:
Deficit of:____kcals____PROa ____fiber ____Vit A ____Vit C ____Fe____Ca ____Other
Excess of:____kcals____Fat ____SFA ____Chol____Sugar ____Alcohol ____Na
Other: ______________
Summary: ______________________________________________
______________________________________________
aPRO, protein; Fe, iron; Ca, calcium, SFA, saturated fatty acid; Chol, cholesterol; NA, Sodium.
References
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2. American Dietetic Association. Nutrition Diagnosis: A Critical Step in the Nutrition Care Process.
Chicago, IL: American Dietetic Association; 2006.
3. Chumlea WC, Steinbaugh ML, Roche AF, et al. Nutritional anthropometric assessment in elderly
persons 65 to 90 years of age. J Nutr Elder 1985;4:39–51.
4. Bassey EJ. Demi-span as a measure of skeletal size. Ann Hum Biol 1986;13(5):499–502.
5. Zeman FJ, Ney DM. Applications in Medical Nutrition Therapy, 2nd ed. Upper Saddle River, NJ:
Merrill-Prentice Hall; 1996.
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7. Osterkamp LK. Current perspective on assessment of human body proportions of relevance to
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overweight and obesity in adults: The Evidence Report. 1998. Available at:
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participants from 52 countries: A case-control study. Lancet 2005;366:1640–1650.
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& Wilkins; 2002.
14. Mahan LK, Escott-Stump S. Krause's Food, Nutrition, and Diet Therapy, 11th ed. Philadephia:
Saunders; 2004.
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Guideline, No. 15. Rockville, MD: U.S. Department of Health and Human Services, Public Health
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Authors: Width, Mary; Reinhard, Tonia
Title: Clinical Dietitian's Essential Pocket Guide,The: Essential Pocket Guide, 1st Edition
Copyright ©2009 Lippincott Williams & Wilkins
> Table of Contents > Part I - Nutrition Assessment and Support > Chapter 2 - Pregnancy
Chapter 2
Pregnancy
Pregnancy represents a vulnerable life stage relative to a woman's nutritional status. In addition, both the
dietary intake and the nutritional status of the woman prior to and during pregnancy greatly influence fetal
development and, in turn, pregnancy outcome. The Update on Nutrition During Pregnancy and Lactation
report issued special recommendations for women before pregnancy (Table 2.1) (1). Recent research has
also shown the profound impact of maternal nutrition status and intake on the infant's risk in adulthood for
several chronic diseases such as hypertension and diabetes, largely via birth weight (2). Several of the
complications of pregnancy can also adversely affect nutritional status. For these reasons, nutritional
assessment is imperative to help ensure optimal pregnancy outcome.
One of the most important aspects of pregnancy is body weight, both prepregnancy weight and weight gain
during gestation, which significantly influence pregnancy outcome (3). A woman with either excess or low
body weight prior to pregnancy has a higher risk for poor outcome. However, weight gain during pregnancy,
specifically total amount and rate, are most correlated with infant birth weight, which in turn is associated
with infant mortality (4).
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Table 2.1 Special Recommendations for Women Before Pregnancy
Maintain a healthy weight.1.
Engage in physical activity regularly.2.
If you need to gain or lose weight, do so gradually (no more than 1–2 lbs/week).3.
If you are trying to become pregnant and you ordinarily drink alcoholic beverages,
stop drinking or cut back on the amount you drink.
4.
If you smoke, quit or cut back to improve your health.5.
To minimize your risk of having an infant with a neural tube defect, eat a highly
fortified breakfast cereal that provides 100% of the Daily Value (DV) for folate (read
the food label to find out) or take a vitamin supplement that provides 400 µg/day of
folic acid. Folic acid, the synthetic form of folate, is obtained only from fortified
foods or vitamin supplements. It is not yet known whether naturally occurring folate
is as effective as folic acid in the prevention of neural tube defects.
6.
From reference 1.
Guidelines for Pregnancy Weight Gain
The Institute of Medicine (IOM) issued pregnancy weight gain recommendations based on current body
weight for both total weight and rate of weight gain, which were reviewed again in 1998 (Table 2.2) (5,6).
The Maternal Weight Gain Expert Work Group convened by the Maternal and Child Health Bureau (MCHB)
made recommendations for weight gain during pregnancy for special
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groups. They suggested that adolescents “less than 2 years postmenarche and African-American women with
single pregnancies be advised to stay within the body mass index–specific weight range recommended by
the IOM, without either restricting weight gain or encouraging weight gain at the upper end of the range.”
Table 2.2 Guidelines for Pregnancy Weight Gain
Category BMI Weight Gain (lbs) Rate of Weight Gain for 2nd and 3rd Trimesters
Underweight <19.8 27.5–39.6 Slightly >1 lb/wk
Normal weight 19.8–25 25.3–35.2 1 lb/wk
Overweight 25–29 15.4–25.3 2/3 lb/wk
Obese >29 >12.9 Aim for steady rate of gain
From references 5 and 6.
Table 2.3 Weight Gain Recommendations for Multifetal Pregnancy
Twin gestation, any BMI 35–45 lbs
Triplet gestation, any BMI 50 lbs
From reference 8.
Internationally, multifetal pregnancies have increased significantly in the past several decades (7). This has
also resulted in a higher rate of low birth weight, so it is crucial to ensure adequate weight gain in these
pregnancies. The recommendation for multifetal pregnancy weight gain is 1.5 lbs/week for normal-weight
women during the second half of a twin pregnancy, and further recommendations for triplet gestation are
included in Table 2.3, based on recent research (8).
Nutrient Recommendations for Pregnancy
Requirements for most essential nutrients increase during pregnancy over nonpregnant status (Table 2.4)
(9). Meeting energy needs during pregnancy is crucial, because of the importance of adequate maternal
weight gain to prevent low birth weight (Table 2.5). Although the dietary reference intakes (DRIs) consider
only single-fetus pregnancy, data from research have generated an energy recommendation for multifetal
pregnancy of an additional 500 kcal to the single-fetus pregnancy level, based on prepregnancy weight (10).
Specific nutrients become “nutrients of concern,” as described by the U.S. Department of Agriculture (11),
because of their role in gestation and/or low intake by the
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American population (Table 2.6). Pregnant women are routinely prescribed a vitamin and mineral
supplement, but a healthful daily eating pattern is important. The Food Guide Pyramid can serve as the
basis for such a pattern (Table 2.7) (11).
Table 2.4 Percentage of Increase over Nonpregnant Women for Recommended
Nutrient Intakes
Macronutrients Vitamins Minerals
Energy, 19%a Vitamin A, 10%b Calcium, 0%
Carbohydrate, 35% Vitamin D, 0% Fluoride, 0%
Fiber, 12% Vitamin C, 13%c Iodine, 47%
Protein, 54% Vitamin E, 0% Iron, 50%c
Vitamin K, 0% Magnesium, 9%d
Thiamin, 27%c Phosphorus, 0%
Riboflavin, 27%c Selenium, 9%
Niacin, 28%
Vitamin B6, 46%c
Folate, 50%
Vitamin B12, 8%
Pantothenic acid, 20%
Biotin, 0%c
Choline, 6%c
Zinc, 38%b
aIncrease is only for the 3rd trimester of pregnancy.bAge 18 and under is somewhat lower.cAge 18 and under is somewhat higher.dAge 18 and under and for women 31 to 50 years is higher.
Data from reference 9.
Table 2.5 Energy Needs in Pregnancy
Prepregnancy Body Weight Energy Needs (kcal/kg body weight)
100%–120% desirable weight 30
>120% above desirable weight 24
<90% below desirable weight 36–40
From reference 10.
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Table 2.6 Recommendations for Nutrients of Concern in Pregnancy
Nutrient Age (years) Amount
Calcium Adolescent to 18 19 and older 1,300 mg
1,000 mg
Folate All ages 600 µg
Iron All ages 30 mg
Protein All ages 60 mg
From reference 5.
Table 2.7 The Food Guide Pyramid: Daily Food Choices for Pregnant Women
Food Group Servings Serving Size/Types
Breads, cereal, rice, and pasta 6–11 1 slice of bread
3 to 4 crackers
½ English muffin or bagel
½ cup cooked cereal
1 cup ready-to-eat cereal
½ cup cooked pasta, rice, or
other grain
Fruits 2–4 1 medium item (apple,
orange, banana)
1 cup fresh berries
½ cup canned fruit
Vegetables 3–5 ½ cup cooked
1 cup raw leafy greens
Protein foods: meat, poultry, fish, dry
beans, eggs, and nuts
3–4 2–3 oz cooked meat, poultry,
fish
½ cup cooked dry beans
1/3 cup nuts or 2 Tbsp
peanut butter
Milk and dairy products 3–4 1 cup skim or low-fat milk 8
oz yogurt
1½ oz cheese
Fats and sweets Use
sparingly
Limit fats and sweets
Alcohol Avoid Avoid all alcoholic beverages
From reference 11.
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Problems During Pregnancy
The most common problems during pregnancy include pre-existing diabetes, gestational diabetes,
hyperemesis gravidarum, morning sickness, and pregnancy-induced hypertension. Such problems, either
pre-existing or arising during pregnancy, pose varying degrees of risk to maternal and fetal status, and
ultimately pregnancy outcome. In addition, other factors such as adolescent pregnancy also influence the
risk of poor pregnancy outcome. This points to the importance of nutritional assessment with regard to
specific conditions to help ensure a positive pregnancy outcome.
Nausea and Vomiting of Pregnancy
Nausea and vomiting of pregnancy (NVP), also known as morning sickness, occurs in 50% to 90% of all
pregnancies and is not confined to only morning hours (12). It generally begins at the 9th gestational week,
with the symptomatic acme at weeks 11 to 13, and resolution for most pregnancies between weeks 12 and
14. A small number of women, 1% to 10%, experience continued symptoms to the 22nd week of gestation.
When symptoms are severe, sometimes requiring hospitalization, hyperemesis gravidarum (HEG) is
diagnosed. Parenteral nutrition may become necessary. Strategies to combat NVP are varied, and
sometimes contradictory, so a highly individualized approach is necessary (Table 2.8) (13,14,15).
Diabetes Mellitus
Diabetes affects up to 7% of all pregnancies, and women may enter pregnancy with pre-existing diabetes
(2%), or develop diabetes generally in the second trimester, termed gestational diabetes (GDM; 2% to 5%)
(16). The latter is one of the most common complications of pregnancy (17). All forms of diabetes during
pregnancy, both pre-existing (or pregestational) as type 1 or type 2 and gestational,
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increase the risk for adverse outcomes for the mother and infant. These risks include congenital anomalies,
macrosomia (birth of an infant at 9 lbs or more), delivery complications, and metabolic aberrations in the
(18). However, strict management of blood glucose level significantly reduces the risk, and daily self-
monitoring of blood glucose (SMBG) even in GDM is important. Individualized nutritional care is critical.
Table 2.8 Strategies for Nausea and Vomiting of Pregnancy
Eat smaller, more frequent meals and snacks (in addition to large meals, hunger/empty
stomach can cause nausea).
Avoid liquids 1 to 2 hr before and after eating.
Consume adequate liquids throughout the day.
Avoid odors that cause aversions and nausea.
Eat higher amount of protein (vs. carbohydrate and fat); although higher carbohydrate may be
helpful for some women.
Avoid high fat and fried foods, as this delays gastric emptying.
Eat crackers before rising from bed, if nausea occurs early.
Try salty or sour foods, as this is helpful to some women with nausea.
Avoid highly spiced foods, if this exacerbates nausea.
Vitamin B6 may be helpful for some women (25 mg three times daily).
From references 10 and 13, 14, 15.
Gestational Diabetes
Many women who develop GDM are overweight or obese, in addition to other risk factors (Table 2.9), and
benefit from following the Institute of Medicine weight gain and energy intake guidelines for their weight
category (5,6,10,19). Although adequate energy intake is crucial for appropriate fetal weight gain, a modest
reduction of 30% is associated with improved glycemic control, as is aerobic exercise (20). However, energy
restriction must be approached cautiously, with some evidence that 1,700 to 1,800 kcal/day should be the
minimum (21). In an effort to standardize nutrition therapy for GDM, the Diabetes Care and Education and
the Women and Reproductive
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Nutrition practice groups of the American Dietetic Association developed practice guidelines (21). Three
key components include: (a) SMBG with medical nutrition therapy (MNT), (b) adjustment of carbohydrate
intake, and (c) timing of nutrition office visits (Table 2.10) (21). In addition, they developed clinical
outcomes for MNT (Table 2.11).
Table 2.9 Questionnaire for Gestational Diabetes Riska
Question Yes No
Are you a member of a high-risk ethnic group (African American, Native American,
Hispanic, Pacific Islander)?
1.
Are you overweight or very overweight?2.
Are you related to anyone who has diabetes now or had diabetes in their lifetime?3.
Are you older than 25?4.
Did you have gestational diabetes with a past pregnancy?5.
Have you had a stillbirth or a very large baby with a past?6.
Do you have a history of abnormal glucose tolerance?7.
aHigh Risk: Yes to two or more questions; Average Risk: Yes to only one question.
Low Risk: No to all questions.
From reference 19.
Specific dietary measures are outlined in Table 2.12, and if this fails to control blood glucose levels,
exogenous
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insulin will be necessary as is the case in up to 25% of women with GDM (22). Oral hypoglycemic agents are
not currently recommended in pregnancy, although glyburide does not cross the placenta. Studies of the
drug's effectiveness and potential risk for pregnancy complications have yielded mixed results (23).
Table 2.10 Clinical Outcomes for MNT in GDM
Achieve and maintain normoglycemia.
Consume adequate calories to promote appropriate gestational weight gain and avoid maternal
ketosis.
Consume food providing nutrients necessary for maternal and fetal health.
Decrease pregnancy-related discomforts, such as hypoglycemia, nausea, vomiting,
constipation, and heartburn.
Ensure that GDM pregnancies result in the delivery of healthy babies without complications
From reference 21.
Table 2.11 Recommended MNT Schedule for GDM
Reason for Visit Timing
Referral contact Within 48 hr of referral
First visit Within 1 week of referral
Second visit 1 week after first visit
Third visit 1 to 3 weeks after second visit
Follow-up visits Every 2 to 3 weeks until delivery
Postpartum visits 6 to 12 weeks postpartum
From reference 21.
Pre-existing Diabetes
Pregnancy requires heightened vigilance with regard to glycemic control, so women who enter pregnancy
with diabetes may need to increase the frequency of SMBG and adjust insulin dose. In addition, insulin
requirements decrease in the first 20 weeks of gestation as the fetus uses a portion of maternal glucose.
This may necessitate an insulin dose reduction of up to 30%. However, typically
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during the 28th to 32nd week of gestation the insulin requirement increases up to 100% above the
prepregnancy level as a result of hormonal changes (24). A woman with pre-existing type 2 diabetes, who
previously managed glycemic control without insulin, may require insulin. Those using oral hypoglycemic
agents to control diabetes before pregnancy will also require insulin, because of a lack of consensus on
their use and potential complications.
Table 2.12 Specific Dietary Measures for GDM
Reduce energy intake by 30% (consider additional energy for pregnancy needs); no lower than
1,700 kcal/day for most women
Restrict carbohydrate intake to 40%–45% of total energy
Reduce carbohydrate intake in morning meals
Space carbohydrate evenly throughout the day (other than morning meals)
Eat several small meals and snacks versus large meals without snacks
From references 21 and 22.
Preeclampsia (Pregnancy-Induced Hypertension)
Preeclampsia, also termed pregnancy-induced hypertension (PIH), is a form of hypertension that arises
during pregnancy, typically in the third trimester (25). The term is derived from the potential culminating
event of eclampsia, or convulsions, which represents an obstetric emergency. Preeclampsia poses
significant risks for the mother and infant. In addition to a spike in blood pressure, a woman with PIH will
also exhibit proteinuria and significant edema. The cause is not known, although recent research has
focused on a two-stage mechanism (26). Stage one is characterized by reduced placental perfusion, which
is the physiologic cause that leads to stage two, the preeclamptic signs and symptoms.
Early identification of preeclampsia and careful management is essential to prevent adverse outcomes for
mother and fetus. There are several risk factors for preeclampsia to consider early in pregnancy, several of
which are moderated by parity status (Table 2.13) (27). African American women have a higher risk for
preeclampsia, and a recent study suggests that a lower dietary intake of folic acid, leading to elevated
plasma homocysteine, may add additional risk (28). Other nutrients that have been implicated in the
development of preeclampsia include sodium, calcium, magnesium, and protein.
In the past, sodium restrictions were standard practice, but the current recommendation is only a moderate
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restriction of 2 to 3 g/day. The Dietary Approaches to Stop Hypertension, or DASH Diet, may be useful
(Table 2.14) (29). Medical management involves bed rest and antihypertensive medications.
Table 2.13 Risk Factors for Preeclampsia
Nulliparity
Previous pregnancy with preeclampsia
High body mass index
Working during pregnancy
Family history of hypertension
African American, only for nulliparous women
Low socioeconomic status; less developed countries
Elevated plasma homocysteine
From references 25, 27, and 28.
Nutrition Assessment
An early nutrition assessment is crucial in pregnancy, given the relationship between nutritional status of
the mother
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and pregnancy outcome. In addition to the standard nutrition assessment categories, it is important to
consider key risk factors, which may be present prior to pregnancy or arise during prenatal care (Table
2.15).
Table 2.14 The DASH Diet in Pregnancy
Nutrient Dietary Amount
Carbohydrate 55% total energy
Protein 18% total energy
Fat 27% total energy
Unsaturated fat:saturated fat 1:3 (ratio)
Potassium 250% DRI
Calcium 250% DRI
Magnesium 250% DRI
Sodium (per preeclampsia) 2–3 g
Food Item Servings/day
Fruits and vegetables 10
Dairy (low or nonfat; per pregnancy) 3 or more
From reference 29.
Table 2.15 Nutrition Assessment Risk Factors in Pregnancy
Age: Younger than 17
Prepregnancy weight lower or higher than normal range BMI of 19.8–25
Chronic disease (e.g., diabetes, cardiovascular disease, gastrointestinal diseases)
Use of prescription drugs chronic disease management
Use of alcohol, illegal drugs
History of adverse gynecologic or obstetrical conditions
High parity; close birth spacing
Previous low-birth-weight pregnancy
Member of high-risk race or ethnic group (for low-birth-weight infant)
Late initiation of prenatal care
Smoking
Socioeconomic difficulties (low income, lack of family or social support)
Prenatal Care Nutrition Risk Factors
Multifetal pregnancy
Inappropriate weight gain:
Inadequate weight gain (below guidelines based on prepregnancy weight)
Excess weight gain (above guidelines)
Anemia
Anthropometric Measurement
As an assessment category, anthropometric measure is perhaps the most important because of the
relationship between prenatal weight gain and pregnancy outcome. Using the weight gain guidelines in
Tables 3.2 and 3.3, based on prepregnancy weight and multifetal pregnancy, allows the establishment of
weight gain goals. Recording prenatal weight gain on a growth grid to monitor weight gain is important in
assuring both adequate total weight gain and appropriate rate of gain (30).
Variations in weight gain goals (amount or rate) require further scrutiny to determine whether the cause is
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pathophysiologic or related to inadequate dietary intake. Fluid retention may cause a sudden surge in
weight after the 20th gestational week, and this may indicate development of preeclampsia.
Biochemical Data: Laboratory Data
Increasing maternal blood volume affects the assessment of laboratory data, with estimates ranging from
an onset at 6 weeks to 20 weeks of 20% (31). In addition, compared to the nonpregnant state, pregnancy
also causes changes in specific laboratory constituents (Table 2.16) (32).
Patient History
The history component of nutrition assessment in pregnancy is vital in identifying problems and risk factors
related to dietary intake and lifestyle, many factors of which will greatly influence pregnancy outcome. The
following relevant historical components provide detailed descriptions of such factors.
Food and Nutrition History
The importance of nutritional intake during pregnancy, in particular for specific nutrients, necessitates a
thorough food and nutrition history as part of nutrition assessment. Potential nutrients of concern, because
of their importance or increased need in pregnancy include calcium, iron, zinc, magnesium, folate, vitamin
B6, and protein. Table 2.17 provides dietary intake details and lifestyle factors, which are a critical
component of a complete food and nutrition history. Pregnant women are routinely prescribed a prenatal
vitamin and mineral supplement containing key nutrients (Table 2.18).
Medication and Supplement History
Many common medications, both prescription and over-the-counter, and dietary supplements can exert
adverse
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effects during pregnancy. In some cases, timing of the medication determines the potential for an adverse
effect (33). However, many women must take medications for a chronic disease or condition, and the
physician weighs the risks and benefits in those instances. For such determinations, the Food and Drug
Administration has developed a rating system for drug use during pregnancy (Table 2.19) (34).
Table 2.16 Laboratory Values in Pregnancy
Constituent (seruma) Normal Level/Range (common units)
Creatinine (s/p) 0.5–0.6
Creatinine clearance (s/p) Increases 50% (from prepregnant level, 87–107
mL/min)
Glucose (OGGT, 100 g test load to
diagnose GDM) (s/p) –GDM diagnosed: 2
abnormal values
Time (hr) mg/dL
0 >105
1 190
2 165
3 145
Hematocrit Decreases to 32.5%–41% in 2nd and early 3rd
trimester; return to prepregnant value at term
(37%–48%)
Hemoglobin (whole blood) Decreases to 10–13 g/dL in 2nd and early 3rd
trimester; return to prepregnant value at term
(13–15 g/dL)
Insulin (radioimmunoassay [RIA]) (p) 23 +/- 9 uIU/mL
Leukocyte count (trimesters 2 and 3) 6,000–16,000 mm3; 2nd and 3rd trimesters:
10,500
Lipids: Cholesterol 2nd trimester: 251 +/- 8 mg/dL
3rd trimester: 259 +/- 13 mg/dL
3 mos postpartum: 204 +/- 10 mg/dL
Lipids: Triglyceride 2nd trimester: 185 +/- 22
3rd trimester: 224 +/- 24
3 mos postpartum: 82 +/-
Osmolality 270–280 mOsm/kg
Thyroid hormones:
T4 (RIA) 8.0–14.5 µg/dL
T3 (RIA) 150–220 ng/dL
Free T4 (total) 0.9–2.3 ng/dL
T3 resin uptake (%) 15–25
Thyroxin binding globulin Increases up to 100% (from prepregnant level
16–26 µg/dL)
Urea nitrogen 8–9 mg/dL
Uric acid 2.0–3.0 mg/dL (to 24 weeks)
a Serum values, unless denoted as (p), plasma, or s/p, serum or plasma, or as noted.
Adapted from reference 32. Adapted from reference 32.
Table 2.17 Food and Nutrition History
I. Socioeconomic, Lifestyle, and Health Beliefs/Attitudes Y N
Body image problems/attempts at weight loss or restriction1.
Follows a special diet (e.g., vegan, strict vegetarian)2.
Food secure: adequate resources/availability of food3.
Poverty: adequate housing, transportation4.
Adequate social support5.
Appropriate physical activity (moderate, not excessive)6.
II. Physiologic Problems
Nausea, vomiting, diarrhea1.
Constipation2.
Gastroesophageal reflux3.
III. Nutritional Adequacy: Food Groups
Dairy products1.
Fruits and vegetables2.
Whole grains/fiber-containing breads and cereals3.
Protein foods4.
IV. Nutritional Adequacy: Specific Nutrients/Foods
Minerals: calcium, iron, zinc1.
Vitamins: B6, folate, B12, D2.
Protein: high biologic value3.
V. Contaminants/Other Substances
Fish (mercury/contaminants: check health department for advisories)1.
Pica2.
Excessive caffeine (>2 cups coffee/day)3.
Alcohol4.
Smoking5.
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Table 2.18 Nutrients in Prenatal Supplement
Vitamins Amount % DVa
A 4,000 IU 156
B1 1.8 mg 129
B2 1.7 mg 121
B6 2.6 mg 137
B12 8 µg 308
Folic Acid 800 µg 137
Niacin 20 mg 111
C 120 mg 141
D 400 IU 200
E 30 mg 90
Minerals Amount
Calcium 200 mg 20
Iron 28 mg 104
Zinc 25 mg 227
aDaily values for pregnant and lactating women.
Table 2.19 U.S. Food and Drug Administration Drug Categories for Pregnancy
Category Description
A These drugs have been demonstrated not to pose any risks to human fetuses.
B These drugs are believed not to pose any significant risk to human fetuses, based on
what has been learned from animal or human studies.
C These drugs may or may not be harmful to human fetuses. The data are
inconclusive; either because no studies have been done or because any adverse
effects that have been demonstrated have shown up in animal rather than human
studies.
D These drugs are known to pose a threat to human fetuses, but they may be
commonly found in cases where the benefits of using the drug outweigh these risks.
X These drugs have been proven to cause fetal abnormalities in humans and should not
be used by under any circumstances during pregnancy. (In other words, category X
drugs are FDA approved, but they are not to be used by pregnant women.)
From reference 34.
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Table 2.20 Medications and Dietary Supplements to Avoid During Pregnancy
Prescription Drugs
Ace inhibitors Captopril, Enalapril
Acne medications Accutane (isotretinoin, Amnesteem and Claravis)
Anticonvulsants Clonazepam, Diazepam, Lorazepam
MAO inhibitors Isocarboxazid (Phenelzine)
Tranquilizers Librium, Miltown, Valium
Others Soriatane (acitretin), Tegison (etretinate), Thalomid (thalidomide)
Drugs that
interfere with
folic acid
Phenobarbital, phenytoin (Dilantin), carbamazepine (Tegretol),
primidone (Mysoline), trimethoprim and sulfonamide (Bactrim, Septra),
triamterene (Dyrenium), sulfasalazine (Azulfidine), oral contraceptives,
tetracycline, valproic acid (Depakene); cimetidine (Tagamet), beta-
blockers, calcium-channel blockers, cholestyramine (LoCholest,
Questran)
Over-the-Counter Drugs
Aspirin Acetaminophen (Tylenol), Ibuprofen (Advil, Nuprin)
Cold preparations Antihistamines, decongestants
Dietary Supplements
Herbs and other
substances
Aloe vera, angelica, arnica, black cohosh, bladderwrack, bloodroot,
blue cohosh, celery seed, chaste berry, cinchona, cinnamon, coltsfoot,
comfrey, curcumin, ephedra, fenugreek, feverfew, ginger, ginseng,
goldenseal, gugul, horsetail, Indian tobacco, iris, kava, licorice root,
male fern, motherwort, nutmeg, parsley, pennyroyal, poke root,
rosemary, rue, sage, saw palmetto, senna, St. John's wort, thuja,
turmeric root, uva ursi, vervain, wormwood, wild carrot, wild indigo,
yarrow
Herbal teas Peppermint leaf, red raspberry leaf
From reference 33.
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Dietary supplements, including herbs, botanicals, and herbal teas, should be avoided. Table 2.20 provides a
listing, although not comprehensive, of common medications and supplements, which should be avoided
during pregnancy.
References
1. Nutrition National Center for Education in Maternal and Child Health under its cooperative
agreement (MCU-119301) with the Maternal and Child Heath Bureau, Health Resources and Services
Administration, Public Health Service, U.S. Department of Health and Human Services. Update for
Nutrition During Pregnancy and Lactation. Washington, DC: National Academy Press; 1998.
2. Barker DJ. Birth weight and hypertension. Hypertension 2006;48(3):357–358.
3. Carmichael SL, Abrams B. A critical review of the relationship between gestational weight gain and
preterm delivery. Obstet Gynecol 1997;89(5):865–873.
4. Ricketts SA, Murray EK, Schwalberg R. Reducing low birthweight by resolving risks: Results from
Colorado's prenatal plus program. Am J Publ Health 2005;95(11):1952–1957.
5. National Academy of Sciences, Institute of Medicine, Food and Nutrition Board, Committee on
Nutritional Status During Pregnancy and Lactation, Subcommittee for a Clinical Application Guide.
Nutrition During Pregnancy and Lactation: An Implementation Guide. Washington, DC: National
Academy Press; 1992.
6. Suitor CW. Maternal Weight Gain: A Report of an Expert Work Group. Arlington, VA: National Center
for Education in Maternal and Child Health; 1997.
7. Marcason W. What are the calorie requirements for women having twins? J Am Diet Assoc
2006;106(8):1292.
8. Brown JE, Carlson M. Nutrition and multifetal pregnancy. J Am Diet Assoc 2000;100:343–348.
9. Dietary Reference Intakes: Recommended Intakes for Individuals, National Research Council,
National Academy of Sciences, 1999, 2000, 2001, 2002.
10. American Dietetic Association. Nutrition Care Manual. Chicago, IL: American Dietetic Association;
2006.
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11. Dietary Guidelines for Americans, 2005, U.S. Department of Agriculture and the U.S. Department
of Health and Human Services.
12. Ogunyemi DO, Michelini GA. Hyperemesis gravidarum. Available at:
http://www.emedicine.com/med/topic1075.htm. Accessed August 26, 2006.
13. Escott-Stump S. Nutrition and Diagnosis-Related Care, 5th ed. Baltimore: Lippincott Williams &
Wilkins; 2002.
14. Mahan LK, Escott-Stump S. Krause's Food, Nutrition, and Diet Therapy, 11th ed. Philadephia:
Saunders; 2004.
15. Shils ME, Shike M, Ross AC, et al. Modern Nutrition in Health and Disease, 10th ed. Baltimore:
Lippincott Williams & Wilkins; 2006.
16. CDC MMNR Weekly. May 29, 1998;47(20):408–414.
17. American Diabetes Association. Gestational diabetes mellitus. Diabetes Care 2004;27:S88–S90.
18. Silverman BL, Purdy LP, Metzger BE. The intrauterine environment: Implications for the offspring
of diabetic mothers. Diabetes Rev 1996;4:21–35.
19. National Institutes of Health Publication No. 00-4818, June 2005.
20. American Diabetes Association. Evidence-based nutrition principles and recommendations for the
treatment and prevention diabetes and related complications. Diabetes Care 2002;25:148–198.
21. Reader D, Sipe M. Key components of care for women with gestational diabetes. Diabetes
Spectrum 2001;14(4):188–191.
22. Rolfes SR, Pinna K, Whitney E. Understanding Normal and Clinical Nutrition, 7th Ed. Belmont, NY:
Thomson Wadsworth; 2006.
23. Jacobson G, Ramos G, Ching J, et al. Comparison of glyburide and insulin for the management of
gestational diabetes in a large managed care organization. Am J Obstet Gynecol 2005;193(1):118–124.
24. Steele JM, Johnstone FD, Hume R, et al. Insulin requirements during pregnancy in women with
type 1 diabetes. Obstet Gynecol 1994;83:253–258.
25. Moodley J, Kalane G. A review of the management of eclampsia: practical issues. Hypertens
Pregnancy 2006;25(2):47–62.
26. Roberts JM, Gammill HS. Preeclampsia, recent insights. Hypertension 2005;46(6):1243–1249.
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27. Eskenazi B, Fenster L, Sidney S. A multivariate analysis of risk factors for preeclampsia. J Am Med
Assoc 1991;266 (2):237–241.
28. Patrick TE, Powers RW, Daftary AR, et al. Homocysteine and folic acid are inversely related in
black women with preeclampsia. Hypertension 2004;43(6):1279–1282.
29. Harsha DW, Lin PH, Obarzanek E, et al. Dietary approaches to stop hypertension: a summary of
study results. Dash collaborative research group. J Am Diet Assoc 1999;99(8 Suppl):S35–S39.
30. California Department of Health Services, Maternal and Child Health, Women, Infants and
Children. Nutrition During Pregnancy and the Postpartum Period. June 1990. Available at:
http://www.perinatology.com/Archive/Weightgrid.pdf.
31. Bernstein IM, Ziegler W, Badger GJ. Plasma volume expansion in early pregnancy Obstet Gynecol
2001;97(5):669–672.
32. Zeman FJ, Ney DM. Applications in Medical Nutrition Therapy, 2nd ed. Upper Saddle River, NJ:
Merrill/Prentice Hall; 1996.
33. March of Dimes. Drugs and herbs. Available at:
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Authors: Width, Mary; Reinhard, Tonia
Title: Clinical Dietitian's Essential Pocket Guide,The: Essential Pocket Guide, 1st Edition
Copyright ©2009 Lippincott Williams & Wilkins
> Table of Contents > Part I - Nutrition Assessment and Support > Chapter 3 - Assessing Pediatric Patients
Chapter 3
Assessing Pediatric Patients
Angela M. Lada RD
Nutrition assessment of the pediatric patient is unique in many ways. Nutrition screening is most useful in
identifying high-risk infants, children, and adolescents in all settings of health care. Table 3.1 lists some
“red flags” that warrant nutrition intervention in inpatient units, outpatient clinics, or in the community
setting. Table 3.2 lists some common classifications used when assessing infants.
Anthropometric Assessment
Measurement of growth is essential for assessing the health and nutritional status of the pediatric patient.
Serial measurements are best measures of growth and are more conclusive than isolated measurements.
Below are the recommended anthropometric measurements to use based on age:
0–36 months
Body weight
Recumbent length
Head circumference
Weight for length
36 months–18 years
Body weight
Height
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Waist circumference
Table 3.1 Indicators of Need for Nutrition Assessment
Infants/NICU Toddler/Child/Adolescent
Failure to Thrive Failure to Thrive
=37 weeks gestational age Weight for length <10th %tile or
BMI <10th %tile
Very low birth weight Weight for length >95% %tile or
BMI >95th %tile
Insufficient weight gain Significant weight loss or gain
Nonstandard formula Enteral or parenteral feeding
Formula concentrated to
nonstandard dilution
Special diet
Food allergies/intolerances
Food allergies/intolerances Eating disorder
Poor/inappropriate intake Malnutrition or at risk for
malnutrition due to diagnosis,
comorbidities, social or economic
status, etc.
Malnutrition or at risk for
malnutrition due to diagnosis,
comorbidities, social or economic
status, etc.
Omitting foods for religious
reasoning
Adolescent pregnancy
Inborn errors of metabolism
Table 3.2 Infant Classification and Associated Terms
Classification Parameters
Chronological or birth
age
Time since birth (days, weeks, months)
Gestational age Estimated time since conception or
postconceptional age
Corrected age Age adjusted for prematurity
Preterm infant <37 weeks gestation
Full-term infant 37–42 weeks gestation
Postterm infant >42 weeks gestation
Low birth weight <2,500 g
Very low birth weight <1,500 g
Extremely low birth
weight
<1,000 g
Small for gestational age Weight <10th %tile
Appropriate for
gestational age
Weight =10th %tile and =90th %tile
Large for gestational age Weight >90th %tile
Data from references 1 and 17.
Body mass index
Weight
Weight should be obtained using consistency in technique and scales. Infants should be nude and without
diaper. Children and adolescent patients should wear minimal clothing. Weight should be obtained to
nearest 0.1 kg.
Length
Length is measured crown to heel. Recumbent length should be measured by use of a length board in
infants ages birth to 24 months. Two people may be needed for this process. Standing height or stature,
using a perpendicular stadiometer, should be measured in children ages 24 months and older who are able
to stand. Measurement should be taken to nearest 0.5 cm. Knee/heel measurement may be used for older
patients who are unable to stand (Table 3.3).
Head Circumference
Head circumference is measured at the largest frontal–occipital plate. Head circumference is a useful tool
until about 3 years of age when head growth slows dramatically. Measurement should be taken to nearest
0.5 cm.
Body Mass Index 5 kg/m2
The body mass index (BMI) for children and adolescents is unique, and it is not appropriate to use the adult
BMI
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categories to interpret the value. BMI-for-age must be interpreted using the growth charts in order to
compare age- and sex-specific percentile (see “Relevant Web Sites Relating to Growth Charts”).
Table 3.3 Knee/Heel Measurement Equations
Males 6–18 years old Stature (cm) = (knee to heel length (cm) ÷ 2.22) + 40.54
Females 6–18 years old Stature (cm) = (knee to heel length (cm) ÷ 2.15) + 43.21
Data from reference 2.
Waist Circumference
Waist circumference is measured midway between the top of the iliac crest and the lowermost portion of
the rib cage. A nonstretchable measuring tape should be used. This measurement is most accurate if the
patient has not recently consumed a large meal and is demonstrating normal expiration (not “sucking in”).
Evaluation of Growth
Measurements should be plotted on growth charts and trends monitored. The appropriate standard Centers
for Disease Control (CDC) growth chart for age and gender should be used. In addition to standard growth
charts, there are specialty growth charts for some select conditions. When length is obtained, the 0- to 36-
month-old growth chart should be used. When height is obtained, the 2- to 20-year-old growth chart should
be used (see tables 3.5 and 3.6 for growth chart interpretations).
If using a standard growth chart for a preterm infant, postnatal age (age of infant calculated, in weeks,
from the date of birth) needs to be corrected for gestational age (age of infant calculated, in weeks, from
the date of conception, determined by ultrasound examination) until at least 24 months of age (3). Table
3.4 gives an example of calculating gestation-adjusted age.
Exclusively breast-fed infants and formula-fed infants are both represented by the standard growth curve. It
should be considered that the mode of feeding would influence growth trends. For the first few months of
life, both exclusively breast-fed infants and formula-fed infants grow at the same rate. Between 4 and 6
months, formula-fed infants tend to gain weight more rapidly than breast-fed
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infants. There is generally little difference in length and head circumference between the two groups (3).
Table 3.4 Gestation-Adjusted Age for Preterm Infants
Adjustment for Prematurity = 40 weeks (full term) - gestational age at birth (in weeks)
Gestation-Adjusted Age = postnatal age - adjustment for prematurity
Example: Michael was born March 1, 2006. His gestational age at birth was determined to be 30
weeks based on ultrasound examination. At the time of his admission into the hospital on May
24, 2006, his postnatal age was 12 weeks. Based on the previous equations, what is his
gestation-adjusted age?
Adjustment for Prematurity = 40 weeks - 30 weeks = 10 weeks
Gestation-Adjusted Age = 12 weeks - 10 weeks = 2 weeks
If this were plotted on a standard CDC growth chart, anthropometric measurements would be
plotted for a 2-week-old infant.
Relevant Web Sites Relating to Growth Charts
Standard CDC growth charts (including BMI-for-age) can be accessed at
http://www.cdc.gov/growthcharts.
The World Health Organization (WHO) multicultural growth charts for ages 0 to 5 years can be
accessed at: http://www.who.int/childgrowth/standards/en/
Table 3.5 Interpretation of Height-for-Age and Weight-for-Age Plotted on
Standard CDC Growth Charts
Percentile Interpretationa
50th Average for age
10th–90th Healthy for most pediatric patients
3rd–10th or 90th-97th Further investigation needed
<3rd or >97th Unhealthy until proven otherwise
aIf the patient plots higher or lower than expected potential, or if there are large
changes in measurements, pathological or nutritional factors should be considered.
Further assessment may include consideration of parental height, growth velocity,
bone age, pubertal status, and development.
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Premature infant growth charts can be found in the following publication: Fenton Tanis R. A new
growth chart for preterm babies: Babson and Benda's chart updated with recent date and a new
format. BMC Pediatrics 2003;3:13. Available at: http://www.pubmedcentral.
nih.gov/articlerender.fcgi?artid=324406
Table 3.6 Interpretation of BMI-for-Age Plotted on Standard CDC Growth
Charts
Percentile Interpretation
<5th Underweight
=5th and <85th Normal weight
=85 and <95th At risk of overweight
=95th Overweight
Data from reference 4.
Growth chart for children with cerebral palsy can be accessed at:
http://www.kennedykrieger.org/kki_miscjsp?pid2694.
Growth chart for children with Down syndrome can be accessed at:
http://www.ndss.org/index.php?option=com_content&task=view&id=603&Itemid=119
Assessment of Weight Changes
Newborn weight loss is expected after birth secondary to body composition shifts and total body water
decrease. Normal weight loss is 7% to 10% of birth weight in term infants. A preterm infant may lose =15%
of birth weight. An infant born at extremely low birth weight may lose =20% of birth weight. Birth weight
should be regained by the second week of life (1). Weight typically doubles by 5 to 6 months of age and
triples by 12 months old.
Usual Body Weight
Usual body weight (UBW) is useful in assessing weight status:
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% UBW = (actual weight/usual weight) ÷ 100
% Weight change = [(actual-usual weight)/usual weight] ÷ 100
Significant weight loss:
>2% in 1 week
>5% in 1 month
>7.5% in 3 months
>10% in 6 months
Waterlow Criteria
Waterlow criteria are for distinguishing malnutrition as acute (wasting) versus chronic (stunting) in children
1 to 3 years old (Table 3.7) (5):
McClaren Criteria
McClaren criteria are used for distinguishing the degree of malnutrition in children <4 years old (Table 3.8)
(6):
Table 3.7 Waterlow Criteria for Distinguishing Severity of Malnutrition
Nutritional Status Acute Chronic
Stage 0 (normal) >90% >95%
Stage 1 (mild) 81%–90% 90%–95%
Stage 2 (moderate) 70%–80% 85%–89%
Stage 3 (severe) <70% <85%
Data from reference 5.
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Table 3.8 McClaren Criteria
Normal >0.31
1st degree 0.28–0.30
2nd degree 0.25–0.27
3rd degree <0.25
Data from reference 6.
Gomez Criteria
Gomez criteria are used for assessing the degree of malnutrition in children (Table 3.9) (7). This may be
used when height is not available. However, it should be noted that this does not account for proportion of
weight in relation to height.
Determine the weight for age at the 50th percentile or ideal body weight (IBW; obtain from
growth chart)
% of IBW = (actual weight/IBW at 50th %tile for age) ÷ 100
Determine the degree of malnutrition present
Table 3.9 Gomez Criteria
Degree of Malnutrition Percentage of Ideal Body Weight
Normal 91–100
1st degree 76–90
2nd degree 61–75
3rd degree =60
Data from reference 7.
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Growth Velocity
Height or weight velocity measures the change in measurement over time. Alterations in normal growth
velocity indicate need for further investigation.
Example: At her 3-month well-baby visit, Stephanie weighed 5.2 kg and was 58 cm long. At her 6-month
well-baby visit, she weighed 6.8 kg and was 64 cm long. Based on the equation, what is Stephanie's height
and weight growth velocity?
Note: It is best to use actual days old for the weight velocity calculation, but if those data are not readily
available, it is acceptable to estimate how old the child is, in days, by using 30 days/month.
Height velocity in centimeters per month
According to Table 3.10, both weight and height growth velocity are within the ideal range of average
growth between 3 and 6 months age.
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Table 3.10 Average Normal Growth Velocity for Children Age 0 Months to 10 Years
Age Weight (g/day) Length (cm/month)
<3 months 25–35 2.6–3.5
3–6 months 15–21 1.6–2.5
6–12 months 10–13 1.2–1.7
1–3 years 4–10 0.7–1.1
4–6 years 5–8 0.5–0.8
7–10 years 5–12 0.4–0.6
Data from reference 8.
Estimating Nutrient Needs
Fluid needs
Fluid needs may be estimated using the formula in Table 3.11, or by using body surface area (9):
Fluid needs = 1,500 mL fluid/m2/day
Example: John weighs 15 kg. Using the equation in Table 3.12, what is his body surface area in m2?
Body surface area (m2) = (15 kg ÷ 0.03) + 0.2
= 0.45 + 0.2 = 0.65 m2
Based on the calculated body surface area, what are John's fluid requirements?
Fluid needs = 1,500 mL ÷ .65 m2 = 975 mL/day
Energy and Protein Needs
In the pediatric population, as in the adult, a variety of methods are used to estimate energy and protein
needs.
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Tables 3.13 and 3.14 provide commonly used methods. These methods are based on values determined for
the pediatric population who display normal body composition, metabolism, and activity level.
Table 3.11 Baseline Fluid Requirements
Weight in Kilograms Fluid Needs
1–10 kg 100 mL/kg
11–20 kg 1,000 mL + 50 mL/kg for each kg >10 kg
>20 kg 1,500 mL + 20 mL/kg for each kg >20 kg
Data from reference 9.
Table 3.12 Calculating Body Surface Area (m2)
Weight in Kilograms Body Surface Area (m2)
<5 kg kg × 0.05 + 0.05
5–10 kg kg × 0.04 + 0.1
10–20 kg kg × 0.03 + 0.2
20–40 kg kg × 0.02 + 0.4
>40 kg kg × 0.01 + 0.8
The use of basal energy metabolism is useful in estimating the energy needs of compromised infants and
children:
kcal/day = Basal Metabolic Rate ÷ Activity Factor ÷ Stress Factor
(see Tables 3.15,3.16,3.17)
Table 3.13 Estimated Energy and Protein Requirements
Reference RDAa RDA
Category Age (yrs) Reference Weight (kg) kcal/kg kcal/cm Pro g/kg Pro g/cm
Infants 0–0.5 6 108 n/a 2.2 N/A
0.5–1.0 9 98 n/a 1.6 N/A
Children 1–3 13 102 n/a 1.2 N/A
4–6 20 90 n/a 1.1 N/A
7–10 28 70 n/a 1.0 N/A
Males 11–14 45 55 15.9 1.0 0.29
15–18 66 45 17 0.9 0.34
19–24 72 40 16.4 0.8 0.33
Females 11–14 46 47 14 1.0 0.29
15–18 55 40 13.5 0.8 0.27
19–24 58 38 13.4 0.8 0.28
a Recommended Dietary Allowance
Data from references 2 and 10.
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Table 3.14 Dietary Reference Intakes of Estimated Energy Requirement (EER)
Sex and Age Calculation of Estimated Energy Requirements
Physical Activity (PA) Coefficient Based on
Physical Activity Level (PAL)
All infants and toddlers
0–3 months (89 ÷ wt [kg] - 100) + 175 N/A
4–6 months (89 ÷ wt [kg] - 100) + 56 N/A
7–12 months (89 ÷ wt [kg] - 100) + 22 N/A
13–35
months
(89 ÷ wt [kg] - 100) + 20 N/A
Boys 3–8
years old
EER = 88.5 - 61.9 ÷ age [y] + PA ×
(26.7 ×wt [kg] + 903 × ht [m]) + 20
PA = 1.0 if PAL is estimated to be
=1 <1.4 (sedentary)
PA = 1.13 if PAL is estimated to
be = 1.4 <1.6 (low active)
Boys 9–18 EER = 88.5 - 61.9 ÷ age [y] + PA ÷ PA = 1.26 if PAL is estimated to
years old (26.7 ÷ wt [kg] + 903 ÷ ht [m]) + 25 be =1.6 <1.9 (active)
PA = 1.42 if PAL is estimated to
be =1.9 <2.5 (very active)
Girls 3–8
years old
EER = 135.3 - 30.8 ÷ age [y]+ PA ÷ (10
÷ wt [kg] +934 ÷ ht [m]) + 20
PA = 1.0 if PAL is estimated to be
=1 <1.4 (sedentary)
PA = 1.16 if PAL is estimated to
be =1.4 <1.6 (low active)
Girls 9–18
years old
EER = 135.3 - 30.8 ÷ age [y] + PA ÷
(10 ÷ wt [kg] +934 ÷ ht [m]) + 25
PA = 1.31 if PAL is estimated to
be =1.6 <1.9 (active)
PA = 1.56 if PAL is estimated to
be =1.9 <2.5 (very active)
Data from reference 11.
Estimating Energy Needs for Catch-up Growth
For patients who are malnourished or for those whose growth is compromised, the nutritional goal is to
accelerate growth. This increase in normal weight and height velocity is referred to as “catch-up growth.”
Catch-up growth is optimal to facilitate normalized weight and height. Total energy needs for catch-up
growth may be as high as 150% of expected needs.
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Table 3.15 Metabolic Rates of Infants and Children
Age 1 Week–10 Months Age 11 Months–36 Months Age 3–18 years
Weight
(kg)
Male Females
(kcal/hr)
Weight
(kg)
Male
(kcal/hr)
Female
(kcal/hr)
Weight
(kg)
Male
(kcal/hr)
Female
(kcal/hr)
3.5 8.4 9.0 22.0 21.2 15 35.8 33.3
4.0 9.5 9.5 22.8 22.0 20 39.7 37.4
4.5 10.5 10.0 23.6 22.8 25 43.6 41.5
5.0 11.6 10.5 24.4 23.6 30 47.5 45.5
5.5 12.7 11.0 25.2 25.2 35 51.3 49.6
6.0 13.8 11.5 26.0 26.0 40 55.2 53.7
6.5 14.9 12.0 26.8 26.9 45 59.1 57.8
7.0 15.0 12.5 27.6 27.7 50 63.0 61.9
7.5 17.1 13.0 28.4 28.5 55 66.9 66.0
8.0 18.2 13.5 29.2 28.5 60 70.8 70.0
8.5 19.3 14.0 30.0 29.3 65 74.7 74.0
9.0 20.4 14.5 30.8 30.1 70 78.6 78.1
9.5 21.4 15.0 31.6 30.9 75 82.5 82.2
10.0 22.5 15.5 32.4 31.7
10.5 23.6 16.0 33.2 32.6
11.0 24.7 16.5 34.0 33.4
Data from reference 12.
General Method of Estimating Energy Needs for Catch-up Growth (14):
Example: Andrea is 5 years and 6 months old. She weighs 13 kg (<3rd %tile) and is 106 cm tall (between the
10th
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and 25th %tiles). Using the standard CDC growth chart, what is Andrea's ideal body weight for her height?
Table 3.16 Activity Factors
Condition Factor
Ambulatory 1.2–1.3
Confined to bed 1.1
Paralyzed 1.0
Table 3.17 Stress Factors
Condition Factor
Burn 1.5–2.5
Growth failure 1.5–2.0
Infection 1.2–1.6
Starvation 0.70
Surgery 1.2–1.5
Trauma 1.1–1.8
Data from reference 13.
IBW in kg = weight at the 50th %tile weight-for-height
= 17.2 kg
Using the general equation for catch-up growth, how many kilocalories per kilogram per day does Andrea
require?
Authors: Width, Mary; Reinhard, Tonia
Title: Clinical Dietitian's Essential Pocket Guide,The: Essential Pocket Guide, 1st Edition
Copyright 2009 Lippincott Williams & Wilkins
> Table of Contents > Part I - Nutrition Assessment and Support > Chapter 4 - Older Adults
Chapter 4
Older Adults
Aging produces numerous physical and physiologic changes, which in turn alter nutritional requirements and
affect nutritional status (Table 4.1 ). The presence of chronic disease, and/or medications can enhance
potential disparities between nutrient needs and dietary intake, leading to malnutrition. Indeed, research
suggests that malnutrition is a common condition among the elderly, with a prevalence of 12% to 50% of
those hospitalized, and 23% to 60% of elderly in extended care facilities (1 ,2 ).
Nutrient Recommendations
The physiologic changes associated with aging affect requirement for several essential nutrients. In general,
the requirement for many nutrients decreases, concomitant with the decrease in energy needs. However,
some nutrients are needed in higher amounts. Additionally, various psychosocial and socioeconomic changes
that often attend aging may also alter dietary intake (Table 4.2 ) (3 ).
The age category for adults was divided into two separate categories with the most recent Dietary
Reference Intakes (DRI) revision (Tables 4.3 ,4.4 ,4.5 ) (4 ). The adult age groups are 51 to 70 years and 70
and above, although the nutrient levels are the same for both adult categories for
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essential nutrients. One exception is the tolerable upper intake level (UL) for phosphorus, which decreases
from 4,000 to 3,000 mg for both males and females at the higher age group, and this is not a recommended
level but rather an upper limit to avoid toxicity.
Body composition
Increase in body fat, especially intraabdominal; Decrease in muscle (sarcopenia); bone loss (including
tooth)
Increased risk for obesity, cardiovascular disease, diabetes
Cardiovascular function
Reduced blood vessel elasticity, higher peripheral resistance, and blood flow to heart
Higher risk for hypertension and other cardiovascular disease
Gastrointestinal function
Reduction in secretions (especially acid, achlorhydria or hypochlorhydria (a consequence of atrophic
gastritis (AG), which occurs in 33% of elderly)
Impairment of digestion and absorption (iron, B12, zinc, folate, biotin, calcium); AG causes inflammation
and reduction in intrinsic factor which can cause B12 deficiency; AG can also cause B6 deficiency;
dysphagia; constipation
Immunocompetence
Reduced function, especially T-cell component
In combination with poor nutritional status, higher susceptibility to infection
Oral health
Reduction in saliva, leading to dry mouth (xerostomia); tooth loss
Problems chewing and swallowing
Neurologic function
Reduction in neurotransmitter synthesis; Less efficient nerve conduction; central nervous system (CNS)
changes cause problems in balance/coordination; depression; dementia
Depression can cause loss of appetite and food intake, leading to malnutrition
Nutrient metabolism
Lower synthesis of cholecalciferol in skin and renal activation; increased retention of vitamin A due to
reduced clearance
Vitamin D deficiency; Vitamin A retention could be toxic if high-dose supplement used
Renal function
Reduction in number of nephrons (therefore, lower glomerular filtration rate (GFR) and total renal function)
Fluid balance aberrations; Acid–base balance problems; metabolism of nutrients medication may be altered
Sensory losses
Decreased sensitivity in taste (dysgeusia), smell (hyposmia), sight, hearing, tactile
Dysgeusia and hyposmia cause loss of appetite and intake, and also increase risk for foodborne illness
Body System or Function Changes in Aging Nutrition Implications
Table 4.1 Physiologic Changes in Aging and Nutrition Implications
Common Problems in Aging
Several problems common in aging affect key aspects of either dietary intake or nutritional needs and may
adversely affect nutritional status. The most notable of these include dysphagia and pressure ulcers, which
although not unique to the elderly, are highest in this population. The profound and negative effects on the
nutritional status of these conditions make nutritional assessment of the elderly for their presence and or
severity imperative.
Dysphagia
Disease Process
Dysphagia represents both a symptom and a disorder, which affects one or all stages of the swallowing
mechanism
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making swallowing difficult (5 ). The possible causes are varied, although the specific cause may also be
indeterminate (Table 4.6 ). Depending on the cause, dysphagia may be an acute condition which resolves,
or it may be chronic. Early identification and intervention is critical, as potential risks include aspiration
and pneumonia (6 ). In addition, anorexia and weight loss are common outcomes, which can adversely
affect nutrition status.
Limited income
Buy low-cost food, such as dried beans/peas, rice, and pasta1.
2.
3.
4.
1.
Use coupons for money off on foods used and check store weekly circular to buy foods on sale2.
Buy store-brand foods3.
Check with local place of worship for free or low-cost meals4.
Participate in local senior nutrition programs,a offered at senior congregate feeding sites or
home-delivered meals
5.
Check for eligibility for the Food Stamp Programa6.
Contact local food banks or emergency food programa7.
Inability to grocery shop
Ask a friend or relative to grocery shop1.
Contact local grocery store to bring groceries to your home2.
Contact food delivery companies3.
Check with local place of worship or senior center for volunteers who will shop4.
Hire a home health worker (listed under “Home Health Services” in phone book)5.
Inability to prepare food
Use a microwave oven to cook frozen meals and foods1.
Buy easily prepared nutritious foods (fresh fruits, whole grain breads, peanut butter, tuna in foil
pouch)
2.
Participate in local senior nutrition programs.a offered at senior congregate feeding sites or
home-delivered meals
3.
Hire a home health worker (listed under “Home Health Services” in phone book) to cook meals
(also make-ahead meals that can be frozen)
4.
Psychological changes that cause poor appetite
The following can cause loss of appetite: living alone, having lost a spouse, feeling
depressed—participate in senior meal programs; invite family or friends to share a meal; check
with a doctor if depression continues
1.
If cooking for just one, you may not feel like making meals; invite family or friends for a meal2.
Food may not have much taste, which could be psychological, physiological, or due to
medications; it may help to:
(a) Eat with family and friends or participate in senior meal programs
(b) Ask the doctor if drugs could be affecting appetite or taste changes
(c) Increase the flavor of food by adding spices and herbs
3.
a Programs are listed under “County Government” in blue pages of phone book; elder care locator: (800)
677–1116.
Adapted from reference 3.
Problem Approach
Table 4.2 Psychosocial and Socioeconomic Problems Affecting Dietary Intake with
Aging
Energy, kcal
2204; 1989 RDA
1978; 1989 RDA
Carbohydrate, g
130
130
Protein, g
56
46
Total fat, g
NDa ; 1989 Recommended Dietary Allowance (RDA): 20%–35%
ND; 1989 RDA: 20%–35%
Linoleic acid, g
14
11
a-linolenic acid, g
1.6
1.1
Saturated fat, g
As low as possible while consuming a nutritionally adequate diet; 1989 RDA: <10%
As low as possible while consuming a nutritionally adequate diet; 1989 RDA: <10%
Cholesterol, mg
As low as possible while consuming a nutritionally adequate diet; 1989 RDA: <300
As low as possible while consuming a nutritionally adequate diet; 1989 RDA: <300
Fiber, g
30
21a ND, not determined.
Nutrient/Units Males, 51+ years Females, 51+ years
Table 4.3 Dietary Reference Intakes (DRI) for Older Adults for Macronutrients
Treatment and Nutritional Intervention
The team approach is important in both assessment and intervention, and this consists of physician,
registered dietitian, speech pathologist, and occupational therapist (7 ). Dysphagia symptoms (Table 4.7 )
often result in early identification; however, dietitians should also note screening
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parameters, both for identification and for nutrition risk assessment (Table 4.8 ).
51–70 Years
70+ Years
51–70 Years
70+ Years
51–70 Years
70+Years
51–70 Years
70+ Years
Vitamin A, g
900
900
3,000
3,000
700
700
3,000
3,000
Vitamin D, g
15
15
50
50
10
10
50
50
Vitamin E, mg
15
15
1,000
1,000
15
15
1,000
1,000
Vitamin K, g
190
190
ND
ND
120
120
ND
ND
Vitamin B6, mg
1.7
1.7
100
100
1.5
1.5
100
100
Vitamin B12, g
2.4
2.4
ND
ND
2.4
2.4
ND
ND
Biotin, g
30
30
ND
ND
30
30
ND
ND
Choline, mg
550
550
3,500
3,500
425
425
3,500
3,500
Folate, g
400
400
1,000
1,000
400
400
1,000
1,000
Niacin, mg
16
16
35
35
14
14
35
35
Pantothenic acid, mg
5
5
ND
ND
5
5
ND
ND
Riboflavin, mg
1.3
1.3
ND
ND
1.1
1.1
ND
ND
Thiamin, mg
1.2
1.2
ND
ND
1.1
1.1
ND
NDa DRIs represent RDAs except for vitamins D, K, biotin, choline, pantothenic acid (AI values).
Nutrient/Units Males Females
DRIa Tolerable Upper Intake Level (UL) DRI UL
Table 4.4 Dietary Reference Intakes for Older Adults for Vitamins
51–70 years
70+years
51–70 years
70+years
51–70 years
70+years
51–70 years
70+years
Chromium, g
30
30
ND
ND
20
20
ND
ND
Copper, g
900
900
10,000
10,000
900
900
10,000
10,000
Fluoride, mg
4
4
10
10
3
3
10
10
Iodine, g
150
150
1,100
1,100
150
150
1,100
1,100
Iron, mg
8
8
45
45
8
8
45
45
Magnesium, mg
420
420
350
350
320
320
350
350
Manganese, mg
2.3
2.3
11
11
1.8
1.8
11
11
Molybdenum, mg
45
45
2,000
2,000
45
45
2,000
2,000
Nickel, mg
ND
ND
1
1
ND
ND
1
1
Phosphorus, mg
700
700
4,000
3,000
700
700
4,000
3,000
Selenium, g
55
55
400
400
55
55
400
400
Sodium, mg; 1989 RDA
<2,400
<2,400
ND
ND
<2,400
<2,400
ND
ND
Vanadium, mg
ND
ND
1.8
1.8
ND
ND
1.8
1.8
Zinc, mg
11
11
40
40
8
8
40
40a DRIs represent RDAs except for calcium, chromium, fluoride, manganese (AI values).
Nutrient/Units Males Females
DRIa (UL) DRI UL
Table 4.5 Dietary Reference Intakes for Older Adults for Minerals
Aging
Alzheimer disease
Cancer, chemotherapy, radiation
Dementia
Head and neck surgery
Intubation
Multiple sclerosis
Neurologic disorders
Parkinson disease
Stroke
Trauma to the esophagus
Table 4.6 Causes of Dysphagia
The National Dysphagia Diet (NDD) is the current medical nutrition therapy for the disorder (8 ). It consists
of three stages, each of which modify the texture, consistency, and other attributes of foods and liquids
that affect the various stages of swallowing. The stage appropriate for an individual patient depends
primarily on the severity of the dysphagia and the stage of swallowing affected (i.e., oral, pharyngeal, or
esophageal) (Table 4.9 ).
Absence of gag reflex
Anorexia
Change in vocal quality (gurgling sound)
Choking
Coughing
Chronic upper respiratory infections
Dehydration
Drooling
Holding pockets of food in cheek
Inability to suck liquid via a straw
“Stuck” feeling in throat
Weight loss
Table 4.7 Symptoms of Dysphagia
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Common Diagnoses
Cerebral vascular accident
Intracerebral bleeding
Transient ischemic attack
Traumatic brain injury
Brain tumor
Diet Prescriptions
Puree
Fluid restriction
Transitional feedings
Nutrition Assessment
Diagnosis
Weight status/change
Albumin level
Degree of metabolic stress
Presence of decubitus ulcers
Need for nutrition support
Adapted from reference 7.
Table 4.8 Dysphagia Screening: Risk Factors
Pressure Ulcers
Disease Process
Pressure ulcers, also known as decubitus ulcers or bedsores, represent a point of skin breakdown from
continual contact with a surface, such as a bed or wheelchair. Pressure ulcers, or more precisely the
complications from them, account for approximately 60,000 deaths every year in the United States and a
cost of $1 billion to $5 billion (9 ). Of significance to health care practitioners is the statistic that 9% of
patients admitted to the hospital will develop a pressure ulcer. And of particular significance to the
registered dietitian (RD) is the fact that malnutrition is second only to pressure as a cause of pressure
ulcers (10 ).
Treatment and Nutritional Intervention
Pressure ulcers are assessed as being at one of four stages, relative to depth of tissue involvement and
therefore severity (9 ). Several nutrients are important in the nutrition care of patients with pressure
ulcers, but the most important of these is protein. Protein needs in the patient
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with pressure ulcers are based primarily on the stage (see Chapter 1 , Table 1.16 ). Table 4.9 lists
nutrients, which have been shown to be important in treating pressure ulcers (7 ). However, doses of single
nutrients needed for healing pressure ulcers have not been determined, as nutrients work in synergy.
Level 1
Moderate to severe
Poor oral phase ability; reduced ability to protect airway
Pureed, homogenous, cohesive foods; no course texture; no raw foods (fruits, vegetables, nuts); any foods
requiring chewing or bolus formation are excluded
Close or complete supervision
Level 2
Mild to moderate
Oral and or pharyngeal
Moist, soft-textured foods with some cohesion, which are easily formed into a bolus; meats are ground or
minced with pieces no larger than one quarter inch; transition to more solid texture from pureed; chewing
ability is required
Assess patient for tolerance to mixed textures; it is expected that some mixed texture foods are tolerated
Level 3
Mild
Oral and or pharyngeal (to a lesser degree than in level 2)
Nearly regular texture with exception of very hard, sticky or crunchy foods; foods still need to be moist in
bite-sized pieces; adequate dentition and mastication needed
Assess patient for tolerance to mixed textures; it is expected that some mixed texture foods are tolerated
Adapted from reference 7.
Dysphagia
Severity Swallowing Stage Affected Food Characteristics
Level of Supervision During Meals/Assessment
Needed
Table 4.9 Overview of the National Dysphagia Diet
Nutrition Assessment
Screening for Nutrition Risks in the Elderly
Nutrition assessment in elderly patients consists of the typical nutrition assessment parameters (refer to
Chapter 1 ); however, special considerations are important and are highlighted. The Nutrition Screening
Initiative was a collaborative effort of several lead agencies whose goal was to identify and treat nutritional
problems in the elderly (11 ). A simple screening tool focusing on all aspects of elderly health, including
psychosocial and environmental factors (DETERMINE), was developed and continues to be used by health
care providers working with the elderly (Table 4.10 ).
Anthropometric Measurements
In the elderly, mortality is not correlated with a body mass index (BMI) above the established norms as in
younger populations (12 ). Rather, the most significant anthropometric risk factor is unintentional weight
loss (13 ). For this reason, the use of ideal body weight is not necessarily appropriate, although it is widely
used. A more important parameter,
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then, is usual body weight and percentage of body weight loss. Related to body weight is the use of specific
energy expenditure formulas, and the preference would be to use the Mifflin–St. Jeor equation, which uses
actual body weight rather than ideal body weight, and has been shown to be more accurate than the
Harris–Benedict equation (14 ).
Fluid
Protein
Amino acids:
Arginine
Glutamine-n -acetyl cysteine
Carnitine
Vitamin A
Vitamin B complex
Vitamin C
Vitamin E
Zinc
Macronutrients Vitamins Minerals
Table 4.10 Nutrients Needed to Heal Pressure Ulcers
D
Presence of chronic disease or condition
E
Eating poorly; too little or poor quality of diet
T
Tooth loss or mouth pain
E
Economic hardship
R
Reduced social contact
M
Multiple medicines
I
Involuntary weight loss or gain
N
Needing assistance in self-care
E
Elder years; older than age 80
Table 4.11 Determine Your Nutrition Health Checklist
Patient History
Patient history is a significant area of assessment in the elderly, as a change in various functional abilities is
correlated with morbidity and mortality. The typical daily functions are described as activities of daily
living (ADL) and instrumental activities of daily living (IADL) (Table 4.11 ). Health care practitioners should
ask questions regarding any change in the patient's ADLs and IADLs of both the patient and the significant
others.
Bathing
Doing light housework
Dressing
Preparing meals
Eating
Using the telephone
Maintaining continence
Managing money
Mobility indoors and outdoors
Shopping
Moving into and out of bed and chairs
Traveling
Toileting
Taking medications
ADL IADL
Table 4.12 Activities of Daily Living (ADL) and Instrumental Activities of Daily Living
(IADL)
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References
1. Wallace JI. Malnutrition and enteral/parenteral alimentation. In: Hazzard WR, Blass JP, Ettinger
WH, Jr, Halter JB, Ouslander JG, Eds. Principles of Geriatric Medicine and Gerontology , 4th ed. New
York: McGraw-Hill, 1999; 1455–1469.
2. Ennis BW, Saffel-Shrier S, Verson H. Diagnosing malnutrition in the elderly. Nurse Pract
2001;26(3):52–65.
3. FDA: Eating Well As We Age. Available at: http://www.fda.gov/ opacom/lowlit/eatage.html.
Accessed February 13, 2007.
4. DRIs: USDA Food and Nutrition Information Center. Available
at:http://www.iom.edu/Object.File/Master/21/372/0.pdf. Accessed February 13, 2007.
5. Niedert KC, ed. Nutrition Care of the Older Adult, Second Edition: A Handbook for Dietetics
Professionals Working Throughout the Continuum of Care. Chicago, IL: American Dietetic Association,
2004:211.
6. Bales CW, Ritchie CS, eds. Handbook of Clinical Nutrition and Aging. 2004:547–568.
7. American Dietetic Association. Nutrition Care Manual. Online subscription. Accessed February 13,
2007.
8. National Dysphagia Diet Task Force. National Dysphagia Diet––Standardization for Optimal Care.
Chicago, IL: American Dietetic Association; 2002:17–19.
9. Lyder GH. Pressure ulcer prevention and management. J Am Med Assoc 2003;289(2):223–226.
10. Straus E, Margolis D. Malnutrition in patients with pressure ulcers: Morbidity, mortality, and
clinically practical assessments. Adv Wound Care 1996;9(5):37–40.
11. Editorial: Evaluating the nutrition screening initiative. Am J Publ Health 1993;83(7):944.
12. Stevens, J, Cai, J, Pamuk, ER, et al. The effect of age on the association between Body-mass
index and mortality. N Engl J Med 1998;338(1):1–7.
13. Diehr P, Bild DE, Harris TB, et al. Body mass index and mortality in nonsmoking older adults: the
cardiovascular health study. Am J Public Health 1998;88(6):623.
14. Validation of several established equations for resting metabolic rate in obese and nonobese
people. J Am Dietetic Assoc 2003;103(9):1152–1159.
Authors: Width, Mary; Reinhard, Tonia
Title: Clinical Dietitian's Essential Pocket Guide,The: Essential Pocket Guide, 1st Edition
Copyright ©2009 Lippincott Williams & Wilkins
> Table of Contents > Part I - Nutrition Assessment and Support > Chapter 5 - Nutrition Support
Chapter 5
Nutrition Support
Brenda Howell RD, CNSD
Patients who are unable to meet nutrition requirements by a conventional oral diet need alternative means of
nutrition, unless aggressive therapies are not warranted. Alternative means of nutrition are enteral nutrition
and parenteral nutrition.
Enteral Nutrition
Indications and Patient Selection
Enteral nutrition is the preferred route if the gut is functional due to fewer complications, fewer costs, and
improved outcomes. Benefits of enteral nutrition (EN) include increased nutrient utilization, maintenance of
normal gut pH and flora inhibiting opportunistic bacterial overgrowth, and support of gut mucosa's
immunologic barrier function, which may decrease risk of gut-related sepsis. Examples of patients who are not
able to orally meet nutrition needs are patients with altered mentation, severe dysphagia, poor appetite, and
respiratory failure requiring vent via endotracheal tube (1,2). Indications and contraindications for EN can be
found in Table 5.1.
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Table 5.1 Indications and Contraindications for Enteral Nutrition Support
Indications
Malnourished patient expected to be unable to eat for >5–7 days
Normally nourished patient expected to be unable to eat for >7–9 days
Functional or partially functionally gut
Adaptive phase of short bowel syndrome
Following severe trauma or burns
Contraindications
Terminal illness in which benefits would not outweigh risks
Short bowel syndrome
Bowel obstruction
Intractable vomiting and diarrhea
High-output fistula
GI ischemia
Ileus
GI inflammation
Malnourished patient expected to eat within 5–7 days with anticipated need <5–7 days
Severe acute pancreatitis
No tube access
Data from references 1 and 2.
Enteral Feeding Route
Route of EN is the next step after determining the patient would benefit from nutrition support (Table 5.2).
Long-term access should be considered if anticipated need will be >4 to 6 weeks.
Enteral Formula Selection
Due to the large number of enteral formulas that are available commercially, a comprehensive list is not
appropriate for a resource book of this size. A listing of contact information for enteral formula manufacturers
is available at the end of this chapter.
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Table 5.2 Enteral Access Devices
Description Pros Cons and Complications
Short Term (<4 weeks)
Nasogastric
tube (NGT):
prepyloric
tube
Used for
feeding,
decompression
of stomach,
administration
of medications,
measurement
of gastric pH &
residuals. At
least 10F
needed to
avoid clogging
from enteral
formulas
Variety of
sizes
available
(5F–18F)
Generally
easy
placement
Larger bore
tube makes
it easier to
bolus
enteral
formulas or
medications
Contraindicated if
nasal/facial
fractures, severe
coagulopathy,
severe
thrombocytopenia,
esophageal
obstruction
Complications
include clogging,
esophageal or sinus
perforation, nasal
mucosal ulceration,
pneumothorax,
epistaxis,
pulmonary
aspiration
Orogastric
tube:
prepyloric
tube
Optional route
when tube can
not be placed
nasally (facial
fracture or
head injury)
Lower
incidence of
sinusitis
Tolerated for short
periods of time
Complications are
the same as with
NGT, with
exception of nasal-
related events
Nasoenteric
tube:
postpyloric
tube
Tip of tube
placed past the
pyloric
sphincter.
Radiologic
verification of
placement
needed before
use. Tubes
available with
a separate
gastric port to
simultaneously
feed into the
small bowel &
suction gastric
secretions. Not
appropriate to
check residuals
Smaller
bore tubes
are more
flexible &
more
comfortable
Less risk of
aspiration,
esophageal
reflux,
delayed
gastric
emptying if
placement
past distal
third of
duodenum.
Infusion pumps
necessary
Difficulty of
postligament of
Treitz placement
Difficulty of
administering some
medications
Long-Term Devices (>4 weeks)
Gastrostomy
tube:
prepyloric
Placed
surgically,
endoscopically
(PEG), or
radiologically
into the
stomach.
Available sizes
from 10F to
28F
Allows bolus
feeding
Low-profile
tubes
available
Complications may
include aspiration,
dislodgment,
bleeding, wound
infection, tube
occlusion,
pneumoperitoneum,
wound infection,
stomal leakage
Jejunostomy
tube:
postpyloric
Placed
surgically,
endoscopically
(PEJ), or
radiologically
into the
jejunum. Size
of 9F to 12F
tube. Not able
to check
residuals to
assess
tolerance.
Requires
infusion via a
pump
Reduces
aspiration
risk
Low-profile
tubes
available
Not able to bolus
enteral feeding
Complications may
include wound
dehiscence or
infection, bowel
obstruction,
occlusion, bleeding,
dislodgment,
volvulus
Transgastric
jejunostomy
Placed
surgically,
endoscopically,
or
radiologically.
A jejunal port
is placed
through
gastrostomy
tube allowing
to feed into
the small
bowel while
suctioning of
gastric
contents
Can be
converted
to
gastrostomy
feeding as
tolerated
Reduces
aspiration
risk
Not able to bolus
enteral feeding
Complications of
both jejunostomy
and gastrostomy
tubes
Data from references 1 and 2.
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Enteral Nutrition Delivery Methods
Once the route of access for EN has been established, the method of delivery can be determined. Gravity
controlled and pump methods are available. Enteral formulas are provided at full strength due to
contamination risk. In critical care patients, EN should be initiated within 24 hours of admission if it is not
anticipated they will be taking a full oral diet within 3 days (3).
Bowel sounds do not need to be heard before initial feeding. Fluid and air must be present in the intestinal
lumen to hear bowel sounds, which may not be heard if there is a nasogastric or percutaneous endoscopic
gastrostomy (PEG) tube for suction or decompression (1). Water flushes should also be added to the EN
prescription to provide adequate hydration and decrease constipation. Water flushes can be provided by bolus
method, although some infusion pumps provide an “automatic” flush in which the pump automatically
administers 25 mL/hr of free water. If refeeding syndrome is a risk, EN should be initiated at 25% goal rate
and slowly advanced to the goal over 3 to 4 days with daily monitoring of potassium, magnesium, and
phosphorus. Refeeding syndrome is further discussed in the Parenteral Nutrition area of this book.
Bolus or Intermittent
Gravity controlled delivery
Best suited for gastric feeding
Appropriate for patients who can protect their airway and are neurologically intact
Most often used in the nonacute care or home care setting
Advantages include: No pump required so more economical; more physiologic because the regimen
closely mimic's normal meals; allows for increased patient mobility
Disadvantages include: Patients are at higher risk of aspiration and volume intolerance; poorly
tolerated as a small bowel feeding.
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Administration:
Bolus feeding: Up to 240 mL formula provided by a gravity bag or syringe in 5 to 10
minutes, pending tolerance. Can be initially provided three to eight times per day with
advancement by 60 to 120 mL every 8 to 12 hours as tolerated, up to goal volume
Intermittent feeding: Maximum of 200 to 300 mL formula over 30 to 60 minutes, every 4
to 8 hours, depending on the patient's requirements
Cyclic
Pump-assisted delivery
Can be used in the acute care or home care setting, especially when transitioning to an oral diet.
Advantages include: allows for maximal nutrient absorption; decreased aspiration risk; allows for
gut rest; allows for increased mobility and time away form the pump
Disadvantages include: requires high infusion rates to meet full nutrition and fluid requirements,
which can be poorly tolerated by some patients.
Administration: Typically runs for 8 to 20 hours per day, which can be infused either during daytime
or nocturnally. Can be initiated at 10 to 40 mL/hr with advancement by 10 to 20 mL/hr every 8 to
12 hours as tolerated, until goal is reached.
Cyclic feedings via the jejunum may be limited to =90 to 100 mL/hr depending on tolerance.
Continuous
Pump-assisted delivery
Can be used for gastric and transpyloric feedings
Commonly used for patients who cannot tolerate bolus or intermittent feedings, those requiring
mechanical ventilation, and critically ill patients
Advantages include: possible decreased risk of distention as compared to bolus/intermittent
infusion.
Disadvantages include: requires a pump, so more costly; limits patient mobility.
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Administration: runs for 24 hours per day, commonly referred to as “around the clock,” or ATC. Can
be initiated at 10 to 40 mL/hr with advancement by 10 to 20 mL/hr every 8 to 12 hours as tolerated,
until goal is reached.
Monitoring of Enteral Feeding
Monitoring of gastrointestinal (GI) tolerance, hydration status, and nutritional status of patients receiving EN is
important. Protocol for monitoring EN may vary by institution however; Table 5.3 lists some common
guidelines for monitoring EN.
Gastric Residuals
Monitoring gastric residuals aids with assessing EN tolerance as well as aspiration risk. Gastric residuals are
checked by withdrawing and measuring fluid and formula with a syringe via nasogastric tube (NGT) or
gastrostomy tube. Normal gastric secretions range from 3,000 to
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4,000 mL/day and residuals of 400 to 500 mL have shown to be tolerated without aspiration, therefore
residuals of =200 mL should not be an indication to stop feedings (4). If residual trends significantly increase or
are >200 mL, feedings can be held for 1 to 2 hours and restarted at the last tolerated rate as appropriate.
Residual policies are often in place and vary among facilities. Delayed gastric emptying can be caused by
medications like narcotics or paralytics in which initiating a promotility agent like metoclopramide or
erythromycin may be beneficial. Maintaining the head of bed (HOB) >30 to 45 degrees may also aid with tube
feeding tolerance. If high residuals persist, verifying tube placement may be needed. Aspirating syringes must
be at least 50 mL for small-bore tubes of 12F or less due to pressure in which the tube may collapse. Residuals
should not be checked when feeding via the jejunum.
Table 5.3 Enteral Nutrition Monitoring Guidelines
Parameter Frequency
Weight Before initiation and at least twice a week
Intake and output (I/O) Daily
Stool output and consistency Daily
Signs/symptoms of edema Daily
Signs/symptoms of dehydration Daily
Gastric residuals q4–6h when feeding into stomach
Abdominal exam: if soft, firm, or distended Daily
Serum electrolytes, blood urea nitrogen
(BUN), creatinine
Daily until stable, then 2–3 times/week
Calcium, magnesium, phosphorus Daily until stable, then weekly
Glucose Patients with diabetes: q6h
Patients without diabetes: daily until stable,
then weekly.
Nitrogen balance Weekly, if appropriate
GI Complications
Tube feeding or GI intolerance may be indicated by abdominal distention, fullness, and pain or cramping.
Decreasing infusion rate, ensuring formula is at room temperature, verifying tube placement and assessing
formula osmolarity can aid with tolerance. If the patient has delayed gastric emptying or is on medications
that slow peristalsis, high fiber and/or high fat formulas may not be tolerated and should be adjusted. Nausea
and vomiting may indicate tube migration, such as a balloon gastrostomy causing a gastric outlet obstruction
(1). Diarrhea can be defined as >200 mL stool or >3 stools per day. Potential causes of diarrhea are
medications, impactions, pathogenic bacteria, pancreatic insufficiency, short bowel syndrome, gut atrophy,
and inflammatory bowel disease. If disease-related causes, medications, or pathogen-induced diarrhea have
been ruled out, soluble fiber or antimotility agents may be beneficial. Elemental EN formulas may also aid
with nutrient absorption.
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Transitioning to Discontinue Enteral Nutrition
Temporary EN support is often needed during the critical care process and should be discontinued as patients
can adequately tolerate an oral diet. As oral diets are started, enteral feedings should be infused nocturnally
via pump, infused between meals via bolus, or stopped more than 1 hour before meals to aid with appetite.
When the patient is able to consume 75% of nutrition needs by mouth, the tube feeding can be discontinued
(1). If there is long-term enteral access and suspect of future necessity, the feeding tube may be left in place.
Parenteral Nutrition
Indications and Patient Selection
Parenteral nutrition (PN) is a method of nutrition support in which provision of macronutrients,
micronutrients, and some medications are infused directly into the blood stream via a peripheral or central
vein. PN is indicated when patients cannot meet their nutrient needs enterally, via either oral intake or
enteral tube feedings, due to the gastrointestinal tract being compromised. Indications for PN are outlined in
Table 5.4.
Patient selection for who may benefit from PN relies on thorough nutrition assessment, determination of
nutrition status, and the overall clinical condition and prognosis of the patient (Table 5.4). Benefits of PN
should outweigh the risks. PN should be considered, in indicated patients, within 1 to 3 days if malnourished or
highly catabolic, and within 7 to 14 days for well-nourished individuals if anticipated need is =5 days (2). Many
risk factors related to PN have been identified. Intravenous dextrose, lipid, and amino acids provide an
optimal host for bacterial and/or fungal infections. Patients are also at risk for catheter-related infections and
complications. Macronutrient, electrolyte, and mineral and fluid abnormalities are a risk factor as well
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as hyperglycemia, hepatic steatosis, and compromised renal clearance.
Table 5.4 Indications and Contraindications for Parenteral Nutrition Support
Indications for PN
Ischemic bowel
Paralytic ileus
Short bowel syndrome with malabsorption
Bowel obstruction
High output enterocutaneous fistula with inability to place enteral nutrition tube distal
of the fistula
Intractable vomiting or diarrhea
Peritonitis
Chylous effusion in which very-low-fat diet/enteral nutrition not feasible or has failed
Persistent enteral nutrition intolerance or inability to gain enteral access
Contraindications for PN
Catabolic patients expected to have usable GI tract within 5–7 days
Well nourished patient expected to resume enteral nutrition/oral diet within 7–10 days
Duration of therapy expected <5 days
Aggressive nutrition support not desired by the patient
Patients prognosis does not warrant aggressive nutrition support
Functional GI tract
Anorexia or inability to ingest enough nutrients orally
Data from references 1, 2, and 5.
Parenteral Nutrition Access
Central Venous Access
Central venous access allows hypertonic, hyperosmolar medications and nutrition therapy infusion into a large
diameter central vein via a central venous catheter (CVC). Subclavian, cephalic, jugular, femoral, and basilic
veins are the most common sites for a CVC. Parenteral nutrition via CVC is indicated if anticipated need is >10
to 14 days and/or peripheral PN would not be adequate or medically feasible. Types of CVCs are outlined in
Table 5.5.
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Table 5.5 Central Venous Catheter Types
Type of Access Definition/Description
Length of
Therapy
Nontunneled CVC Single or multilumen catheter inserted preferable into the
subclavian vein. Ease of removal and exchange for short-
term therapy, in an acute care setting.
Weeks
Tunneled CVC Single or multilumen catheter inserted into the jugular,
subclavian, or cephalic vein, then is tunneled in the
subcutaneous tissue (i.e., Hickman/ Broviac/Groshong).
Secured CVC for long-term use, less infection risk than
nontunneled CVC, ease of care.
Months to
years
Peripherally
inserted central
catheter (PICC)
Single or multilumen catheter inserted from peripheral
vein into large central vein. Use in acute care or
outpatient settings. Routine heparin flushes and site care
needed, not ideal for long-term home care.
Several
weeks to
months
Port Single or dual lumen subcutaneous port with silicone
septum, most commonly placed in anterior chest wall.
Venous access via port with noncoring needle.
Months to
years
Data from reference 1.
Peripheral Venous Access
Peripheral parenteral nutrition (PPN) is administered into a peripheral vein and is indicated for short-term
therapy of up to 14 days. Standard peripheral cannulas require site rotation every 72 to 96 hours to decrease
catheter related complications (1). Adequate veins are necessary, as well as ensuring PPN solutions do not
exceed 900 mOsm/L due to risk of thrombophlebitis. Formulations for PPN require higher volume and lipid
tolerance than central PN, in order to lower osmolarity and more closely meet caloric and protein
requirements. See Table 5.6 for calculating osmolarity of PPN solutions.
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Table 5.6 Calculating Osmolarity of PPN Solutionsa
1 g amino acid/L = 10 mOsm
1 g dextrose/L = 5 mOsm
1 g lipid (20% stock solution)/L = 1.3 mOsm
1 mEq –Calcium gluconate/L = 1.4 mOsm
–Magnesium sulfate/L = 1.0 mOsm
–Potassium and sodium/L = 2 mOsm
Example calculation: PPN solution provides 1,790 kcal, 80 g lipid, 120 g amino acid, 150 g
dextrose, 200 mEq sodium chloride, 8 mEq magnesium sulfate, 40 mEq potassium chloride, 5 mEq
calcium gluconate for total volume of 3,000 mL daily.
120 g amino acid ÷ 3.0 L = 40 g/L × 10 = 400 mOsm/L1.
150 g dextrose÷ 3.0 L = 50 g/L × 5 = 250 mOsm/L2.
80 g lipid ÷ 3.0 L = 26.7 g/L × 1.3 = 35 mOsm/L3.
8 mEq magnesium sulfate÷ 3.0 L = 2.7 mEq/L × 1 = 2.7 mOsm/L4.
5 mEq calcium gluconate÷ 3.0 L = 1.67 mEq/L × 1.4 = 2.3 mOsm/L5.
240 mEq sodium chloride & potassium chloride × 3.0 L = 80 mEq/L × 2 = 160 mOsm/L6.
Total osmolarity = 850 mOsm/La
aOsmolarity of nutrients may vary slightly among institutions.
Nutrition Requirements: Indirect Calorimetry
Indirect calorimetry is one of several methods in which metabolic requirements of macronutrients are
determined in the critically ill. Predictive equations such as those of Ireton–Jones, Mifflin–St. Joer, and Harris
Benedict are useful but can have significant variance in results. Indirect calorimetry measures energy
expenditure and macronutrient utilization by measuring the ratio of CO2 produced to O2 consumed, also called
the respiratory quotient (RQ). An RQ of >1.0 suggests overfeeding with lipogenesis, in which provision of total
kilocalories needs to be decreased. An RQ of 0.85 to 0.95 suggests mixed substrate utilization in which current
nutrition regimen is appropriate. An RQ of =0.82 suggests underfeeding in which increased provision of
kilocalories is indicated.
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Table 5.7 provides the RQ of various substrates (6). Table 5.8 reviews technical aspects, which may alter
indirect calorimetry results (1).
Table 5.7 Interpretation of Respiratory Quotients and Substrate Utilization
Substrate Utilization Respiratory Quotient (physiologic range 0.67–1.3)
Ethanol 0.67
Fat 0.7
Protein 0.8
Mixed substrate 0.85
Carbohydrate 1.0
Lipogenesis 1.0–1.2
Data from reference 6.
Parenteral Formulations: Macronutrients
Carbohydrate
Carbohydrate (CHO) is the primary source of energy for the body, including the brain and central nervous
system. Minimum CHO requirements recommended per Dietary
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Reference Intakes (DRI) are 130 g/day for healthy adults and children (7). Carbohydrate should not exceed 4
mg/kg/min in critically ill patients, and 7 mg/kg/min in stable patients (Table 5.9). Risks of excessive CHO
infusion include hyerglycemia, glucosuria, lipogenesis, hepatic steatosis, and hyperinsulinemia.
Table 5.8 Aspects That May Alter Indirect Calorimetry Results
Mechanical ventilation with FiO2 =60% and/or positive end expiratory pressure (PEEP)
>12 cm H2O
Acute changes of ventilation (if vent changes, wait 90 min to complete study)
Leak in sampling system
Inability to collect all expiratory flow (example of air leak via chest tube or
bronchopleural fistula)
Hemodialysis in progress (wait 3–4 hr after dialysis to complete the study)
Error in calibration of indirect calorimeter
General anesthesia given within 6–8 hr prior to the study
Painful procedure recently completed (wait 1 hr after procedure to complete the study)
Data from reference 1.
Table 5.9 Calculating Maximum CHO (g) Oxidative Capacity
To calculate maximum dextrose (g):
4–7 mg × wt (kg) × 1,440 mina = mg/day1.
mg/day ÷ 1,000 = g dextrose/day2.
Example: A critically ill patient weighs 73 kg.
4 mg × 73 kg × 1,440 min = 420,480 mg/day1.
420,480 mg/day ÷ 1,000 = 420 g/day dextrose2.
a60 min/hr × 24 hr/day = 1440 min/day
Dextrose monohydrate is the CHO source used for PN, which provides 3.4 kcal/g. Stock or base solutions of
dextrose range from 5% to 70%. Percentage dextrose concentration is grams of solute per 100 mL of solution. A
10% dextrose solution contains 10 g of dextrose per 100 mL solution, thereby providing 100 g dextrose/L.
Protein
Protein in PN is provided in the form of a crystalline amino acid solution, in which standard solutions contain a
physiologic mixture of essential and nonessential amino acids. Disease-specific amino acid solutions are
available, but controlled trials have not concluded their benefit over standard amino acid solutions (8).
Example disease-specific solutions are NephrAmine for renal failure and HepatAmine for liver disease. Amino
acids are required in PN to minimize lean body mass losses, promote tissue repair, and maintain oncotic
pressure in blood plasma. Protein requirements range from 1.2 to 2.0 g/kg/day in critically ill patients, and
0.8 to 1.0 g/kg/day in stable patients. Protein needs may exceed >2.0 g/kg if there are extreme losses such as
in weeping wounds or large body
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surface area burns. Amino acids provide 4 kcal/g with stock or base solutions ranging from 3% to 20%.
Lipid
Intravenous fat emulsions (IVFE), specifically long-chain fatty acids (LCFA), are required to prevent essential
fatty acid deficiency which can occur within 1 to 3 weeks of lipid-free nutrition administration. Long-chain
fatty acids are currently the only commercially available form of IVFE in the United States and are available in
concentrations of 10%, 20%, and 30%. IVFE contain egg phosphatides as an emulsifier and glycerol for stability.
A 10% IVFE concentration provides 1.1 kcal/mL, whereas a 20% concentration provides 2.0 kcal/mL or 10
kcal/g. Europe has medium-chain fatty acid (MCFA) and LCFA mixtures, which are not available yet in the
United States. Minimum LCFA requirements are 3% to 4% total kcal with a DRI equating to about 10% total kcal.
Risks of excessive or too rapid infusion of IV lipids include impairment of clearance as well as compromised
reticuloendothelial or immune function. Limiting IV lipid to 1 g/kg/day or 30% of total kilocalorie requirements
is recommended. Intravenous lipids in PN can be increased and are tolerated if serum triglycerides are =400
mg/dL.
Fluid
Formulation of PN includes total volume required to meet estimated fluid needs of 25 to 40 mL/kg/day. Fluid
requirements in the critically ill are dependent on total fluid status and organ function. Minimum volume of PN
in the critically ill is often required, as there is usually a simultaneous mode of intravenous fluids that can be
adjusted pending the patient's fluid status. Fluids provided by separate IV fluids, medications, and drips should
be subtracted from total fluid requirements in determining total volume requirements for PN. Additional fluids
may be required if there are excessive losses via diarrhea, vomiting, or fistula drainage. Estimation of total
body water
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(TBW) and TBW deficit can assist with estimating fluids needs in PN formulation (Table 5.10) (9).
Table 5.10 Estimating Total Body Water and Total Body Water Deficit
Total Body Water (TBW) Estimation TBW = 0.6 × wt (kg) males; 0.5 × wt for males =80 years of
age
= 0.5 × wt (kg) for females; 0.4 × wt for females =80 years of age
Subtract 10% for obese, 20% for very obese
TBW Deficit Estimation
Water deficit (L) = TBW × [(Na1/Na2) - 1]
Na1 = actual serum sodium
Na2 = desired serum sodium
Data from reference 8.
Types of Parenteral Nutrition
PN solutions are comprised of protein, CHO, electrolytes, vitamins, minerals, medications, and sterile water.
IVFE infused separately, or “piggy-backed,” are referred to as “2-in-1” solutions. Intravenous fat emulsions
admixed with other nutrients and additives are “3-in-1” solutions, or total nutrient admixtures (TNA).
Advantages of TNAs are decreased contamination, decreased nursing time, decreased pharmacy preparation
time, overall decreased cost, and better fat utilization. Disadvantages of a TNAs include decreased stability of
the fat emulsion and compatibility with other components. Components of PN must be compounded in a
specific sequence for optimal stability (1). Sample calculations for macronutrients in both 2-in-1 and TNAs are
in Table 5.11. Specifying quantity of needed AA, dextrose, and lipid can be ordered in grams or percentage of
solution depending on the facility. Ordering nutrients and additives either per day or per liter also varies
between facilities, although safe practice guidelines are standardized PN formulations in which nutrients
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should be in amounts per day (10). An exception to ordering per day is if the facility has admixed PN solutions
in 1-L volumes in which using quantity per liter is supported. Table 5.12 may aid with calculating the PN
formulation, as it displays concentrations of dextrose, amino acids, and lipids, as well as what they provide.
Table 5.11 Sample Calculation for 2-in-1 and TNA PN Formulations
Patient daily requirements based on nutrition assessment are: 80 g protein, 2,000 kcal, 2,000 mL
fluid with maximum CHO oxidative capacity of 385 g dextrose/day.
2-in-1: Facility options are:
AA Solutions: 10% or 15%
Dextrose solutions: 20%, 30%, 40%, 50% or ____%
Lipid: 10% (500 mL) or 20% (500 mL) ___ daily or ____ × per week
Determine needed lipids/day and what the solution provides:
10% lipid/day would provide 500 mL volume, 50 g lipid and 550 kcala.
1.
Assess the best AA volume needed to meet AA (g) requirements:
80g AA ÷ 10% AA concentration = 800 mL volume and 320 kcala.
2.
Calculate needed dextrose (g) by subtracting kcal from daily lipids and AA solutions:
2,000 kcal - 550 kcal (lipid) × 320 kcal (AA) = 1,130 kcal from dextrose
needed
a.
1,130 kcal ÷ 3.4 = 332 g dextrose needed/dayb.
3.
Assess the best dextrose volume needed to meet dextrose (g) requirements:
332 g dextrose ÷ 50% dextrose concentration = 664 mL volumea.
Round to 700 mL volume to provide 350 g dextrose and 1,190 kcalb.
4.
Calculate infusion rate per hour per total volume:
500 mL (lipid) + 800 mL (AA) + 700 mL (dextrose) = 2,000 mL volumea.
2,000 mL ÷ 24-hr infusion = 83 mL/hrb.
5.
PN goal = 83 mL/hr of 10% lipid (500 mL), 800 mL of 10% AA, 700 mL of 50% dextrose
solution to provide 2,060 total kcal, 80 g AA, 350 g dextrose, 50 g lipid, 2,000 mL
volume daily
6.
TNA: Macronutrients are ordered in grams per day for this facility
Calculate kilocalories provided by goal AA
80 g AA × 4 = 320 kcala.
1.
Calculate kilocalories provided by desired lipid (g)
2,000 kcal × 30% = 600 kcal from lipida.
600 kcal ÷ 9 kcal/g = 66 g lipid (round to 65 g)b.
65 g lipid × 10 kcal/g = 650 kcal from lipidc.
2.
Determine dextrose (g) needed by subtracting kilocalories from AA and lipids.
2,000 kcal × 320 kcal (AA) - 650 kcal (lipid) = 1,030 kcal needed from
dextrose
a.
1,030 kcal ÷ 3.4 kcal/g = 303 g dextrose (round to 300 g)b.
3.
PN goal: 80 g AA, 300 g dextrose, 65 g lipid to provide 1,990 total kcal in 2,000 mL
volume
4.
Table 5.12 Macronutrient Composition of Solutions
Macronutrient Concentrations (%) Grams per Liter Kilocalories per Liter
Dextrose 5 50 170
10 100 340
20 200 680
30 300 1,020
40 400 1,360
50 500 1,700
70 700 2,380
Amino acids 8.5 85 340
10 100 400
15 150 600
20 200 800
Concentration Kilocalories per Milliliter Kilocalories per Liter
Lipid emulsions 10 1.1 1,100
20 2 2,000
30 3 3,000
Parenteral Formulation: Micronutrients and Additives
Electrolytes
Altered serum electrolyte values are common in the acutely ill, and PN formulations can aid with correcting
these abnormalities. Assessing current intravenous electrolyte administration is needed before developing the
PN formulation. Table 5.13 shows the composition of intravenous solutions. Table 5.14 reviews daily
electrolyte requirements, what factors may alter electrolyte values,
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and dosage form (1,2). Formulation of PN is to maintain electrolyte balance; therefore repletion of an
electrolyte deficiency should be treated with a separate intravenous bolus. Acetate forms of potassium and
sodium are useful when serum CO2 is low and/or serum Cl- is elevated in which NaCl or KCl would not be
beneficial. Acetate is the precursor to bicarbonate, which is then converted to CO2 by the liver. Precipitation
of calcium or phosphorus may occur if high quantities are in the PN admixture. The precipitation factor of
calcium/phosphorus should be 30 or less.
Table 5.13 Standard Intravenous Solutions
IV Solution
Glucose
(g/dL)
Na+
(mEq/L)
Cl-
(mEq/L)
K+
(mEq/L)
Ca2+
(mEq/L)
Lactate
(mEq/L)
Osmolarity
(mOsm/L)
5% Dextrose in
water
5 — — — — — 252
10% Dextrose
in water
10 — — — — — 505
0.45% NaCl — 77 77 — — — 154
0.9% NaCl
(normal saline)
— 154 154 — — — 308
5% Dextrose in
0.45% NaCl
5 77 77 — — — 406
10% Dextrose
in 0.9% NaCl
5 154 154 — — — 560
Lactated
Ringer's
— 130 109 4 3 28 273
Data from reference 2.
Ca/Phos precipitation = [(Ca mEq/L + Phos mM/L)] ÷ 1,000 ÷ total volume
Vitamins, Minerals, and Trace Elements
Standard parenteral multivitamin and multiple-trace element supplements are included in the PN admixture.
Multivitamin solutions are based on the U.S. Food and
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Drug Administration daily requirements. Multivitamin formulations are available with or without vitamin K.
Once the multivitamins are added, the solution is stable for 24 hours. Trace elements contain a minimum of
chromium, copper, manganese, and zinc. Some trace element additives also contain iodine, molybdenum, and
selenium. Trace elements should be held if conjugated bilirubin exceeds >2.0, as copper and manganese
toxicity can result. Iron dextran is incompatible with IVFE and can only be added to 2-in-1 PN solutions with
caution. Separate intravenous infusion of iron dextran is a preferred method of administration if needed.
Table 5.14 Daily Electrolyte Requirements in Formulation of Parenteral Nutrition
Electrolyte
Daily
Requirement
(Adult) Causes of Elevated Levels Causes of Decreased levels Dosage form
Calcium 10–15
mEq
Vitamin D excess,
renal failure, tumor
lysis syndrome,
hyperparathyroidism,
prolonged
immobilization and
stress, bone cancer
Decreased vitamin D
intake,
hypoparathyroidism,
hypoalbuminemia,
hypomagnesemia,
citrate binding of
calcium with blood
product
administration
Ca
Gluconate
Magnesium 8–20
mEq
Excessive Mg intake in
renal insufficiency
Refeeding syndrome,
alcoholism, diuretic
use, nasogastric
suction, diabetic
ketoacidosis, elevated
stool output, Mg
wasting medications
Mg
Sulfate
Phosphorus 20–40
mmol
Excessive phosphate
administration, renal
Refeeding syndrome,
alcoholism,
Na
phosphate
failure inadequate intake K
phosphate
Sodium 1–2
mEq/kg
Inadequate free
water, excessive
water loss, excessive
sodium intake,
hyperaldosterism
Excessive hypotonic
fluid, nephritis,
adrenal insufficiency,
congestive heart
failure, syndrome of
inappropriate
antidiuretic hormones
(SIADH), cirrhosis with
ascites
Na
Chloride
Na
Acetate
Na
lactate
Potassium 1–2
mEq/kg
Renal dysfunction,
excessive K+ intake,
metabolic acidosis, K+-
sparing medications
Refeeding syndrome,
inadequate K+ intake,
excessive losses with
diarrhea or intestinal
fluids, diuretic
medications,
hypomagnesemia,
metabolic alkalosis
K
phosphate
K acetate
K chloride
Data from references 1 and 2.
Other Additives
Additional additives in PN formulation also can include insulin, gastrointestinal prophylaxis such as
Famotadine, and heparin. Regular insulin can be added starting at 0.1 units (U) per gram of dextrose per liter
of PN solution. Increasing insulin by 0.05 U per gram of dextrose per day may be needed if hyperglycemia
continues, until 0.2 U per gram of dextrose is reached (1). Not all insulin provided in PN is utilized, as some
will adhere to the plastic bag and tubing. Heparin is often added to PPN in 1 unit per mL dose as prophylaxis
against peripheral vein thrombophlebitis.
Initiation, Monitoring, and Discontinuation of PN
Initiation
Parenteral nutrition can be initiated in adult patients when they are hemodynamically stable and ideally if
they have satisfactory hydration, electrolyte, and acid–base status (1). Macronutrients of PN can be advanced
to goal by day 2 or 3 if serum glucose is consistently =180 mg/dL and electrolytes are satisfactory (Table 5.15).
Monitoring
Monitoring PN tolerance is necessary for achieving caloric and protein goals as well as prevention of metabolic
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complications. Table 5.16 provides appropriate frequency of lab monitoring (2). Hypertriglyceridemia >400
mg/dL or a rise of =50 mg/dL indicates compromised clearance in which temporary discontinuation or
decreased infusion rate of IVFE is warranted. Withholding IVFE is appropriate if triglycerides are >500 mg/dL.
Topical linoleic acid via soybean or safflower oil can be an alternative method of preventing essential fatty
acid deficiency without exacerbating hypertriglyceridemia.
Table 5.15 Initiation of Parenteral Nutrition
Macronutrient Initiation Amount Precautions
Amino
acid60–70 g/L Infusion of PN should be
completed within 24 hours
of initiation.
Dextrose 100–150 g/L or 10%–15%
final concentration with
glucose intolerance, risk for
hyperglycemia as with
steroid therapy, or diabetes
200 g/L or 15%–20% final
concentration as maximum
initial amount
Initiate with caution due to
metabolic side effects
including reactive
hyperglycemia,
hyponatremia, hyper-
insulinemia, glucosuria
Infusion of PN should be
completed within 24 hours
of initiation.
Lipid
(IVFE)Can initiate full
concentration as long as
precautions are met
Administer if baseline serum
triglycerides are <200 mg/dL
When infused separately as
in a 2-in-1, infusion should
be completed within 12
hours.
Elevated or increasing liver function tests (LFTs) from baseline can indicate hepatic steatosis in which
provision of dextrose should be reevaluated. Excessive or continuous infusion of dextrose can compromise
hepatic function. Decrease of dextrose infusion can ensure the maximum CHO utilization rate is not being
exceeded. Cycling PN is also recommended to provide hepatic rest. Cycling of PN requires infusion at 50% goal
for the first and last hour of infusion. PN can be initially decreased to an 18- to 20-hour
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infusion, and further decreased to 12-hour infusion if there is good glycemic control. Glucose should be
monitored before, during, and after PN cycle until glucose tolerance is established.
Table 5.16 Monitoring for Adult Patients on Parenteral Nutrition
Parameter Baseline Critically III Patients Stable Patients
Chemistry screen (Ca, Mg,
LFTs, P)
Yes 2–3×/week Weekly
Electrolytes, BUN,
creatinine
Yes Daily 1–2×/week
Serum triglycerides Yes Weekly Weekly
Complete blood count with
differential
Yes Weekly Weekly
Prothrombin time (PT),
partial thromboplastin time
(PTT)
Yes Weekly Weekly
Capillary glucose 3×/day 3×/day (until
consistently <200
mg/dL)
3×/day (until
consistently <200
mg/dL)
Weight If
possible
Daily 2–3×/week
Intake and output Daily Daily Daily unless fluid status
is assessed by physical
exam
Nitrogen balance As
needed
As needed As needed
Indirect calorimetry As
needed
As needed As needed
Prealbumin or transferrin Yes Weekly Weekly
Data from references 1 and 2.
Refeeding Syndrome
Metabolic side effects of PN can occur which may delay reaching nutrition goals. Refeeding syndrome can
occur with malnourished patients who have anorexia nervosa, have had extreme weight loss, or have been
without nutrition for 7 to 10 days. Refeeding syndrome occurs as the primary fuel source converts from stored
fat to carbohydrate as energy is provided
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after starvation. Carbohydrate as the fuel source causes insulin levels to rise and therefore intracellular shifts
of potassium, magnesium, and phosphorus. Rapid decrease of serum potassium, magnesium, and phosphorus
may lead to respiratory distress, tetany, cardiac arrhythmias, paresthesia, cardiac arrest, and sudden death.
Prevention of refeeding syndrome can be accomplished by correcting electrolyte abnormalities before PN
administration, initiating dextrose at =150 g/day and increasing PN to goal nutrients within 3 to 4 days. Caloric
and protein goals based on actual weight may also prevent initial overfeeding and refeeding syndrome.
Discontinuation of PN
Discontinuation of PN is the ultimate goal as patients are able to tolerate an oral diet or enteral nutrition
support. Well-nourished individuals prior to PN therapy, who are free of malignancy, not debilitated, or
without oral intake for <2 weeks, can have PN stopped as soon as diet tolerance is established (1). Transitional
weaning of PN is necessary in patients who are at higher risk of oral or enteral nutrition intolerance or
suboptimal nutrition intake. PN infusion can suppress appetite if providing >25% of caloric needs, therefore it
can start to be decreased as soon as patients are eating 500 kcal/day. Calorie counts can be beneficial to
more accurately estimate intake and therefore decrease PN in comparable amounts. Enteral nutrition support
should be considered if oral intake is inadequate in meeting nutrition requirements within a few days.
Transition of PN to enteral nutrition support should be done gradually. Decrease of PN by 50% as enteral
nutrition support is tolerated at 50% goal rate, then discontiuing of PN when enteral nutrition is tolerated at
75% goal rate is suggested. Rebound hypoglycemia can occur if PN is stopped abruptly, therefore decreasing
infusion rate by 50% for 1 to 2 hours before discontinuation is suggested. Blood glucose levels can be checked
30 to 60 minutes after central PN cessation if patient is at risk or has signs of hypoglycemia.
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Enteral Formula Manufacturers
Company Name Phone Number E-mail/Web Site
Hormel
Health Labs
800-866-7757 http://www.hormelhealthlabs.com/home.asp
Mead
Johnson
Nutritionals
812-429-6399 [email protected]
http://www.meadjohnson.com/professional/index.html
Nestle
Nutrition
800-422-2752
(for infant
products call
800-284-9488)
http://www.nestle-nutrition.com
Novartis
Medical
Nutrition
800-333-3785,
option 3
http://www.novartisnutrition.com/us/home
Ross
Products
Division
800-986-8510
(Medical and
Pediatric
Nutritional
Products)
http://www.ross.com
References
1. Merritt R. The A.S.P.E.N. Nutrition Support Practice Manual, 2nd ed. Silver Spring, MD: American
Society of Parenteral and Enteral Nutrition; 2005.
2. Gottschlich MM. The Science and Practice of Nutrition Support. A Case-Based Core Curriculum.
Dubuque, IA: Kendall/Hunt Publishing; 2001.
3. ESPEN Guidelines on Enteral Nutrition: Intensive Care. Available at:
http://www.espen.org/Education/documents/ ENICU.pdf. Accessed February 5, 2008.
4. McClave SA, Lukan JK, Stefater JA, et al. Poor validity of residual volumes as a marker for risk of
aspiration in critically ill patients. Crit Care Med 2005;33(2):324–330.
5. Cardillo K. Nutrition interventions for chylous effusions. Support Line 2001;23(6):18–23.
6. Wooley JA, Sax HC. Indirect calorimetry: Applications to practice. Nutrition Clin Pract
2003;18:434–439.
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7. Institute of Medicine, Food and Nutrition Board. Dietary Reference Intakes: Energy, Carbohydrate,
Fiber, Fat, Fatty Acids, Cholesterol, Protein and Amino Acids. Washington, DC: National Academy Press;
2002.
8. Gasser E, Parekh N. Parenteral nutrition: Macronutrient composition and requirements. Support Line
2005;27(6):6–12.
9. Kingley J. Fluid and electrolyte management in parenteral nutrition. Support Line 2005;27(6):13–22.
10. Task Force for the Revision of Safe Practices for Parenteral Nutrition. Safe practices for parenteral
nutrition. J Parenteral Enteral Nutr 2004;28:S39–S70.
Authors: Width, Mary; Reinhard, Tonia
Title: Clinical Dietitian's Essential Pocket Guide,The: Essential Pocket Guide, 1st Edition
Copyright ©2009 Lippincott Williams & Wilkins
> Table of Contents > Part II - Nutrition Considerations for Specific Diseases > Chapter 6 - Cancer
Chapter 6
Cancer
Sheri Betz RD
In the United States, the toll exacted by cancer is second only to that of heart disease, causing one of every
four deaths. Each year, more than 1.2 million Americans are diagnosed with cancer, and over 500,000 will
die of the disease (1). Cancer is not one disease; rather it represents over 100 diseases. The common
characteristics of all cancers are uncontrolled cellular proliferation and the ability of these cells to migrate
from the original site and spread to distant sites throughout the body.
Nutrition Implications of Cancer
One of the most severe and devastating aspects of cancer is cachexia. This condition of advanced calorie
protein malnutrition is characterized by anorexia, fat and muscle tissue wasting, involuntary weight loss,
weakness, psychological distress, and a lower quality of life. Often referred to as the “cancer anorexia-
cachexia syndrome,” this debilitating condition is present in 80% of patients with advanced-stage cancer,
and is estimated to be the immediate cause of death in 20% to 40% of cancer patients (2,3).
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The exact pathophysiologic processes of this complex syndrome are unknown. Cachexia should be suspected
in patients with cancer if an involuntary weight loss of >5% of premorbid weight occurs within a 6-month
period, especially when combined with muscle wasting. For obese patients, a weight loss of 10% or more,
which indicates severe depletion, is often used as a starting criterion for cachexia (3).
The dietitian's role in helping patients and families manage cachexia is to plan individualized treatment to
maximize oral intake and minimize the negative symptoms of nausea, vomiting, diarrhea, and changes in
taste or food preferences that influence appetite (see Management of Cancer Symptoms and Treatment
Side Effects later in this Chapter). It is essential to allow patients flexibility in the type, quantity, and
timing of their meals and snacks (3).
Cancer Staging
Staging is a system used by physicians and other medical professionals to describe the extent or severity of
an individual's cancer. Staging is based on the extent of the primary tumor, as well as on the extent of
metastasis. Staging is important when the diagnosis of cancer is made, because it helps the physician plan
the course of treatment, estimate the patient's prognosis, and identify any clinical trials that may be
suitable for that particular patient (4). Staging is also important for cancer registries and researchers, as it
provides a common language for cancer reporting and for evaluating and comparing the results of clinical
trials. Understanding of cancer staging is helpful to the dietitian working with oncology patients, as the
stage of the patient's cancer may correlate with nutritional status and provide insight into possible nutrition
interventions.
Staging systems for cancer are constantly evolving as scientists learn more about the disease. Many staging
systems are currently in use. Some cover many different
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types of cancer, whereas others are specific to a particular type of cancer (4). The common elements in
most staging systems include:
Location of the primary tumor
Tumor size and number of tumors
Lymph node involvement
Cell type and tumor grade
Presence or absence of metastasis
The Tumor, Node, Metastasis Staging System
The tumor, node, metastasis (TNM) staging system is one of the most commonly used staging systems. This
system has been accepted by the International Union Against Cancer (UICC) and the American Joint
Committee on Cancer (AJCC). The National Cancer Institute (NCI) uses this system in their comprehensive
cancer database, and most medical facilities use the TNM system as their main method for cancer reporting
(4).
The TNM system is based on the extent of the tumor (T), the extent of spread to the lymph nodes (N), and
the presence of metastasis (M). A number is added to each letter to indicate the size or extent of the tumor
and the extent of spread (see Table 6.1).
An example of the TNM system for staging colon cancer would be T3 N0 M0. This staging would mean a large
tumor, located only in the colon, without spread to lymph nodes or any other parts of the body.
Overall Stage Grouping
Overall Stage Grouping is also referred to as Roman Numeral Staging. This system uses numerals I, II, III,
and IV (plus the 0) to describe the progression of cancer. Once the TNM staging has been done, the result
can then be categorized into one of five stages (see Table 6.2). The criteria for stages differ for different
types of cancer, so a T3 N0 M0 bladder cancer may be a different overall stage than a T3 N0 M0 breast
cancer.
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Table 6.1 Tumor, Nodes, Metastasis Cancer Staging System
T = Primary Tumor
TX Primary tumor cannot be evaluated
T0 No evidence of primary tumor
Tis Carcinoma in situ (early cancer that has not spread to neighboring tissue)
T1–T4 Size and/or extent of primary tumor
N = Regional Lymph Nodes
NX Regional lymph nodes cannot be evaluated
N0 No regional lymph node involvement
N1–N3 Involvement of regional lymph nodes (number and/or extent of spread)
M = Distant Metastasis
MX Distant metastasis cannot be evaluated
M0 No distant metastasis
M1 Distant Metastasis
Data from references 4 and 5.
Summary Staging
This simple staging system is often used by cancer registries and can be used for all types of cancer (5).
In Situ: Cancer cells are present only in the layer of cells where they developed and have not
spread.
Invasive: Cancer cells have spread beyond the original layer of tissue.
Localized: An invasive malignant cancer is confined entirely to the organ of origin.
Table 6.2 Overall Stage Grouping
Stage Definition
Stage 0 Carcinoma in situ (early cancer that is present only in the layer of
cells in which it began)
Stages I,
II, and III
Higher numbers indicate more extensive disease with greater tumor
size, and/or spread of the cancer to nearby lymph nodes and/or
organs adjacent to the primary tumor
Stage IV The cancer has metastasized.
Data from references 4 and 5.
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Regional: Cancer that (a) has extended beyond the limits of the organ of origin directly into
surrounding organs or tissues and (b) involves regional lymph nodes by way of the lymphatic
system.
Distant Involvement: Cancer has spread to parts of the body remote from the primary tumor
either by direct extension or by discontinuous metastases.
Unknown: Used to describe cases in which there is not enough information to indicate a stage.
Cancer Treatments
Treatment of cancer with chemotherapy and radiation has significant nutritional consequences. Both types
of treatment contribute to nutrient alterations in the cancer patient by reducing food intake, decreasing
absorption, and/or altering metabolism.
Chemotherapy
Many chemotherapy medications are used in combination, often referred to as protocols or “cocktails,” for
treatment of specific cancers. Table 6.3 lists some common antineoplastic agents and their nutritional
implications.
Nutrition-Related Side Effects of Chemotherapy (effects depend on the
agents administered) (6):
Anorexia
Nausea, vomiting
Mucositis (stomatitis, esophagitis, gastritis, proctitis)
Diarrhea
Constipation
Weight loss
Taste alterations (hypogeusia-little taste, dysgeusia-distorted taste)
Metallic taste in mouth
Xerostomia (dry mouth)
Lactose intolerance
Thrush
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Table 6.3 Chemotherapy Medications
Chemotherapeutic Agent:
Generic Name (Trade
Name)
Nausea &
Vomiting Diarrhea Xerostomia
Stomatitis
&
Esophagitis Anorexia
Taste
Alterations
Bleomycin
(Blenoxane)
Mild to
moderate
No Yes Yes Yes No
Busulfan (Myleran) Mild No No No Yes No
Carboplatin
(Paraplatin)
Moderate Yes No No No No
Carmustine (BCNU) Moderate No No Yes Yes No
Cisplatin (CDDP) Severe Yes No No Yes Metallic
taste
Cyclophosphamide
(Cytoxan)
Severe No Yes Yes Yes No
Cyarabine (ARA-C) Severe Yes No Yes Yes No
Dacarbazine (DTIC-
Dome)
Severe Yes No Yes No Metallic
taste
Dactinomycin
(Actinomycin-D,
ACT)
Severe Yes Yes Yes No Yes
Daunorubicin
citrate
(Daunomycin)
Moderate Yes Yes Yes Yes Yes
Docetaxel
(Taxotere)
Mild No No No No No
Doxorubicin
(Adriamycin)
Moderate Yes Yes Yes Yes No
Epirubicin HCL
(Ellence)
Moderate Yes No Yes No No
Etoposide (VP-16-
23)
Mild to
moderate
Yes No Yes Yes No
Floxuridine (FUDR) Mild Yes No Yes Yes No
5-fluorouracil (5-
FU)
Moderate Yes No Yes No Yes
Hydroxyurea
(Hydrea)
Mild to
moderate
Yes No Yes Yes No
L-asparaginase
(Elspar)
Moderate No No Yes Yes No
Mechlorethamine
(Mustargen)
Severe Yes No No Yes Metallic
taste
Methotrexate
(MTX)
Mild to
moderate
Yes No Yes Yes Yes
Mitomycin
(Mutamycin)
Moderate Yes No Yes Yes No
Paclitaxel (Taxol) Mild No No Yes No No
Streptozocin
(Zanosar)
Severe Yes No No No No
Data from medication product labeling.
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Radiation Therapy
Side effects of radiation can be acute or chronic in nature and are dependent on area of the body that has
been irradiated. Changes in taste or saliva due to radiation to the head or neck can takes months to show
improvement and sometimes never return to baseline (6).
Nutrition-Related Side Effects of Radiation Therapy
General—anorexia, fatigue
Head and neck
Taste alterations (ageusia-no taste, hypogeusia, dysgeusia)
Mucositis (stomatitis, esophagitis)
Dysphagia, odynophagia (painful swallowing)
Xerostomia, thick saliva
Dental caries
Loss of teeth
Swollen, tender gums
Change or loss of smell
Esophagus/chest
Esophagitis
Dysphagia
Esophageal stricture
Abdomen/pelvsi
Nausea, vomiting
Diarrhea, steatorrhea
Acute colitis and enteritis
Fistulas
Maldigestion, malabsorption
Perforations
Management of Cancer Symptoms and Treatment Side Effects
The symptoms associated with cancer and the side effects of the treatments used to control cancer can
have devastating effects on the nutritional status of the cancer patient. Many of these symptoms and side
effects cannot
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be totally alleviated; however, they can be managed through the proper use of medications and through
patient education by the dietitian on tips and techniques used to control some of the most common
problems.
Table 6.4 Medications to Treat Anorexia
Medication Generic
(Trade Name) Dose Action Special Considerations
Dronabinol
(Marinol)
2.5 mg BID (up
to 20 mg/day)
Increases appetite,
decreases nausea
Drug may be habit
forming
Megestrol
Acetate
(Megace)
800 mg daily Increases appetite,
promotes weight
gain
May take 8–12 weeks to
reach maximal weight
gain
Data from references 6 and 7 and medication product labeling.
Pharmacologic Control
Many medications are available to manage the symptoms of cancer and the side effects of cancer
treatments. Tables 6.4,6.5,6.6 and 6.7 list the common medications used to help alleviate the anorexia,
oral problems, nausea and vomiting, and diarrhea associated with cancer and its treatments.
Table 6.5 Medications to Treat Oral Problems
Medication Uses
Benzocaine oral spray (hurricane spray) Relief of mouth pain, mouth sores
Artificial saliva (Xero-Lube, Salivart) Used for xerostomia
Nystatin oral suspension Antifungal used for treating thrush
Mix of Maalox, Benadryl, and lidocaine
(often called the “radiation cocktail”)
Used orally to swish and swallow for mouth
pain and esophagitis
Mix of Maalox, Benadryl, and Nystatin
(often called “cools solution”)
Used orally to swish and swallow for mouth
pain associated with and to treat thrush
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Table 6.6 Medications to Treat Nausea and Vomiting
Medication Generic (Trade
Name) Dose Action Special Considerations
Dolasetron
mesylate
(Anzemet)
Oral: 100 mg
IV: 1.8 mg/kg over
30 sec
Decreases N&V Give 30–60 min before
chemo
Granisetron HCl
(Kytril)
Oral: 1 mg tablet
or 5 mL suspension
BID
IV: 10 µg/kg
Decreases N&V Oral: 1st dose 1 hour
before chemo & 2nd
12 hr later.
IV: 30 min before
chemo
Lorazepam
(Ativan)
Oral: 1–6 mg/day
IV: 1.4 mg/m2
Decreases
anxiety, relaxes
muscles,
decreases N&V
Oral: in divided doses;
IV: 30 min before
chemo
Metoclopramide
(Reglan)
Oral: 10 mg QID
IV: 1–2 mg/kg q2h
Stimulates GI
motility &
gastric
emptying.
May cause diarrhea at
high doses
Ondansetron
(Zofran)
Oral: 8 mg q4h for
three doses; then
q8h for 1–2 days
IV: 32 mg bolus
Decreases N&V Start oral & IV 30 min
before chemo
Perphenazine
(Trilafon)
Oral: 4 mg q4–6h
IV/IM: 3–5 mg bolus
q4–6h
Decreases N&V May cause dry mouth
Prochlorperazine
(Compazine)
Oral: 5–10 mg QID
Rectal suppository:
25 mg BID
Decreases N&V Antacids decrease
absorption of oral
dose—separate by 2 hr
Data from references 6 and 7 and medication product labeling.
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Table 6.7 Medications to Treat Diarrhea
Medication Generic (Trade
Name) Dose Action Special Considerations
Diphenoxylate HCl &
atropine (Lomotil)
Oral: 5 mg QID Slows
peristalsis
Can cause nausea
and dry mouth.
Loperamide HCl
(Imodium)
Oral: 4 mg, followed
by 2 mg after each
unformed stool
Inhibits
peristalsis
Shown to be 2–3
times more potent
than Lomotil.
Data from references 6 and 7 and medication product labeling.
Patient Education
The dietitian can play a vital role in helping cancer patients manage the symptoms associated with cancer
and its treatments. Providing highly individualized meal plans and patient education can help minimize the
toll that cancer can take on a patient's nutritional status. The following lists provide tips and techniques
that the cancer patient and their families may find useful (8).
Managing Taste Changes
Eliminate unpleasant odors and food from sight
Drink fluids with meals and frequently throughout the day to moisten oral mucosa
Increase taste by adding spices and flavorings such as sugar, lemon, herbs, wine
Serve foods attractively, balancing colors and textures
Use plastic utensils if metallic taste is a problem
Use temperature extremes (hot and cold) to stimulate taste
Use cold pineapple chunks between foods to change and stimulate taste sensation
If foods are too sweet:
Gymnema Sylvestra, an herbal tea that is often used by professional wine tasters, will
deaden the taste
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buds to sweet tastes for about 20 minutes. This should be held in the mouth for about 5
minutes before eating.
Add a few drops of bitters (angostura bitters; found in grocery stores) to drinks to cut
the sweet taste (6).
Managing Xerostomia
Take several sips of water before swallowing
Cleanse mouth every 2 to 4 hours
Drink 2 to 3 L of fluid daily
Suck sugarless candy
Use Chapstick or Vaseline to keeps lips moist
Avoid citrus and dry foods
Use sauces and gravies with food to provide extra moisture
Use saliva substitute
Managing Stomatitis and Esophagitis
Avoid acidic foods and juices (orange, pineapple, tomato)
Avoid extreme temperatures and foods that are hard or irritating in texture
Eat food and fluids that are chilled
Drink nutritional supplements chilled
Rinse mouth with a warm saline solution after meals and at bedtime
Avoid alcohol-based mouthwashes
Managing Nausea
Eat small, frequent meals
Foods should be cold or room temperature, soft, salty, and not greasy or rich
Separate liquids and solid food by at least an hour
Liquids should be cold
Try ginger ale or other ginger foods
Stay upright 1 to 2 hours after eating, and keep head elevated
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Managing Diarrhea
Eat small, frequent meals that are warm or at room temperature.
Avoid fatty foods (bacon, cheese, oils) and food that causes gas (broccoli, beans).
Avoid citrus fruits and juices.
Eat foods high in soluble fiber (bran, granola, nuts, seeds, vegetables).
Avoid alcohol and caffeine.
Eat boiled white rice, tapioca, cream of rice cereal, bananas, and potatoes.
Use low-lactose dairy products such as yogurt and aged cheeses instead of milk and ice cream.
Increasing Kilocalorie and Protein Intake
The nutrition requirements of most cancer patients can be estimated using the following: protein: 1.2 to
2.0 g/kg body weight; energy: 25 to 35 kcal/kg body weight. It is important to note that a patient that has a
poor intake needs to consume nutritionally dense foods. Providing your patient with a high-kilocalorie, high-
protein diet will help prevent rapid weight loss. The following are some common tips for patients:
Eat small, frequent meals; keep snacks handy.
Use nutritional supplements such as Ensure, Boost, etc.
Add the following to foods to increase caloric and/or protein content: butter, margarine,
whipped cream, half and half, cream cheese, sour cream, salad dressings, mayonnaise, honey,
jam, sugar, granola, dried fruits, cottage or ricotta cheese, whole milk, powdered milk, ice
cream, yogurt, eggs, nuts, seeds, wheat germ, peanut butter.
Neutropenic Diet Guidelines
This diet is used for neutropenic patients to avoid the introduction of possible pathogens by way of foods.
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Doctors often recommend this diet before and after certain types of chemotherapy and radiation
treatments. A blood test called an absolute neutrophil count (ANC) can help determine the body's ability to
fight off infection. When the ANC is <1,000 cells/mm3, the patient is often instructed to follow a
neutropenic diet (9). Below are general guidelines for patients to follow. Table 6.8 lists foods allowed and
not allowed on the neutropenic diet.
General Guidelines
Check expiration dates on all products before buying. Be sure nothing is past its expiration date.
Wash the following with soap/cleanser and hot water before and after touching food. Air-dry or
use paper towels—do not use cloth towels (using a dishwasher is preferred if available):
counter tops
cutting boards
cooking utensils
silverware
pots and pans
dishes
Wash hands frequently with warm soapy water and dry with paper towels when preparing food.
This is especially important after touching raw meat, chicken, eggs, and fish.
Keep perishable food very hot or very cold. Do not leave perishable items at room temperature
for more than 10 to 15 minutes.
All perishable foods should be cooked thoroughly (no raw or rare meats).
Thaw frozen foods in the refrigerator overnight or quickly in the microwave. Do not thaw food on
the counter.
Refrigerate leftovers promptly in airtight containers.
Use leftovers only if they have been stored properly and have been around for no more than 24
hours.
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Table 6.8 Neutropenic Diet
Food Groups Allowed Not Allowed
Dairy All pasteurized, grade
‘A’ milk and milk
products
Commercially packaged
cheese and cheese
products made with
pasteurized milk (i.e.,
mild and medium
cheddar, mozzarella,
parmesan, Swiss)
Pasteurized yogurt
Dry, refrigerated, and
frozen pasteurized
whipped topping
Ice cream, frozen
Unpasteurized or raw
milk, cheese, yogurt,
and other milk products
Cheeses from
delicatessens
Cheeses containing chili
peppers or other
uncooked vegetables
Cheese with molds (i.e.,
blue, Stilton, Roquefort,
gorgonzola)
Sharp cheddar, brie,
camembert, feta
cheese, farmer's cheese
yogurt, sherbet, ice
cream bars, homemade
milkshakes
Commercial nutritional
supplements and baby
formulas, liquid and
powdered
Vegetables All cooked frozen or
canned vegetables.
All cooked herbs and
spices (add at least 5
min before end of
cooking)
Raw vegetables, salads
Caesar Salads with
Caesar dressing
Pepper
Garnishes
Uncooked herbs and
spices
Fruits &
NutsCanned and frozen fruit
and fruit juices
Thick skinned fruits
(oranges, bananas)
Melons cut up and used
immediately
Canned or bottled
roasted nuts
Nuts in baked products
Commercially packaged
peanut butter
Dried fruits
Raw fruit; foods
containing raw fruits
Unpasteurized fruit and
vegetable juices
Raw nuts
Roasted nuts in the shell
Precut fresh fruits
Bread, Grain
& Cereal
Products
All breads, bagels, rolls,
pancakes, sweet rolls,
waffles, French toast
Potato chips, corn chips,
tortilla chips, pretzels,
popcorn
Cooked pasta, rice, and
other grains
All cereals, cooked and
ready-to-eat
All well-cooked or
canned meats (beef,
pork, lamb, poultry,
fish, shellfish, game,
ham, bacon, sausage,
hot dogs)
Raw grain products
Bakery breads, cakes,
donuts, muffins
Potato/macaroni salad
Meat & Meat
ProductsWell-cooked eggs (white
cooked firm with
thickened yolk, such as
hard boiled, over hard)
Pasteurized egg
substitutes (i.e., Egg
Beaters)
Commercially packaged
salami, bologna, and
other luncheon meats
Canned and
commercially packaged
hard smoked fish,
refrigerated after
opening
Cooked tofu (must be
cut into 1-in. cubes or
smaller and boiled a
minimum of 5 min in
water or broth before
eating or using in
recipes)
Raw or undercooked
meat, poultry, fish,
game, tofu
Meats and cold cuts
from delicatessen
Hard cured salami in
natural wrap
Cold smoked salmon, lox
Pickled fish
Tempe (tempeh)
products
Sushi
Raw oysters/clams
Beverages Tap water
Commercial bottled
distilled and natural
waters
All canned, bottled,
powdered beverages
Instant and brewed
coffee, tea; cold,
brewed tea made with
boiling water
Brewed herbal teas using
commercially packaged
tea bags
Commercial nutritional
supplements, liquid and
powdered
Well water
Cold-brewed tea made
with warm or cold water
sun tea
Eggnog
Fresh apple cider
Homemade lemonade
Spring water
Fats Oil, shortening
Refrigerated lard,
margarine, butter
Commercial shelf-stable
mayonnaise and salad
dressings (including
cheese-based salad
Fresh salad dressings
containing aged cheese
(i.e., blue, Roquefort)
or raw eggs, stored in
refrigerated case
dressings, refrigerated
after opening)
Desserts Refrigerated commercial
and homemade cakes,
pies, pastries, and
pudding
Refrigerated cream-
filled pastries
Homemade and
commercial cookies
Shelf-stable cream-filled
cupcakes (i.e., Twinkies,
Ding Dong), fruit pies
(i.e., Pop tarts, Hostess
fruit pies), and canned
pudding
Unrefrigerated cream-
filled pastry products
(not shelf-stable)
Cream or custard-filled
donuts
Others Salt, granulated sugar,
brown sugar
Jam, jelly, syrups
(refrigerated after
opening)
Commercially packaged
(pasteurized) honey
Catsup, mustard, BBQ
sauce, soy sauce, other
condiments (refrigerated
after opening)
Pickles, pickle relish,
olives (refrigerated after
opening)
Raw or unpasteurized
honey
Herbal and
nontraditional (health
food store) nutritional
supplements, Chinese
herbs
Brewers yeast, if eaten
uncooked
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Table 6.9 Common Abbreviations Associated with Cancer
Abbreviations Term Associated with Cancer
ALL Acute lymphocytic leukemia
AML Acute myelocytic leukemia
CA Cancer
CLL Chronic lymphocytic leukemia
CML Chronic myelocytic leukemia
BMX Bone marrow biopsy
METS Metastases/metastatic
MDS Myelodysplastic syndrome
MP Mediport
NSCLC Non-small-cell lung cancer
ONC Oncology
RT Radiation therapy
References
1. Jemal A, Murray T, Ward E, et al. Cancer Statistics, 2005. CA Cancer J Clin 2005;55:10–30.
Available at: http://caonline.amcancersoc.org/cgi/content/full/55/1/10. Accessed August 10, 2007.
2. Nelson KA. Modern management of the cancer anorexia-cachexia syndrome. Curr Oncol Rep
2000;2(4):362–368.
3. Akio I. Cancer Anorexia-Cachexia Syndrome: Current issues in research and management. CA Cancer
J Clin 2002;52: 72–91.
4. Collaborative Staging Task Force of the American Joint Committee on Cancer. Collaborative Staging
Manual and Coding Instructions, version 01.03.00. U.S. Department of Health and Human Services,
National Institutes of Health, National Cancer Institute. NIH Publication Number 04-5496, Version
date: September 8, 2006. Available at http://www.cancerstaging.org/cstage/manuals.html. Accessed
August 8, 2007.
5. National Cancer Institute, U.S. National Institutes of Health. Cancer staging. Available at:
http://www.cancer.gov/cancertopics/ factsheet/Detection/staging. Accessed August 10, 2007.
6. McCallum PD, Polisena G. The Clinical Guide to Oncology Nutrition. United States: American
Dietetic Association, 2000; 45–47, 93, 127–131, 164–167.
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7. Wilkes GM. Cancer and HIV Clinical Nutrition Pocket Guide, 2nd ed. Sudbury, MA: Jones and
Bartlett Publishers; 1999.
8. Nutritional suggestions for symptom management. National Cancer Institute. Available at:
http://www.cancer.gov/cancertopics/pdq/supportivecare/nutrition/HealthProfessional/
page4#Section_117. Accessed February 21, 2007.
9. Neutropenic Diet? Available at: http://patienteducation.upmc.com/Pdf/NeutropenicDiet.pdf.
Accessed February 20, 2007.
Authors: Width, Mary; Reinhard, Tonia
Title: Clinical Dietitian's Essential Pocket Guide,The: Essential Pocket Guide, 1st Edition
Copyright ©2009 Lippincott Williams & Wilkins
> Table of Contents > Part II - Nutrition Considerations for Specific Diseases > Chapter 7 - Cardiovascular Diseases
Chapter 7
Cardiovascular Diseases
Cardiovascular disease (CVD) encompasses all diseases of the heart and blood vessels. Coronary heart
disease (CHD) and cerebrovascular accident (CVA) are the major forms of CVD and claim more lives in the
United States each year than any other disease (1).
Coronary Heart Disease
The underlying pathologic process of CHD, and of the major form of CVA, is atherosclerosis, in which fatty
plaques or atheromas develop in the intimal layer of the arterial wall. As plaques accumulate within a
blood vessel, the vessel becomes constricted, which is also a cause of congestive heart failure (CHF). If a
blood clot forms and cannot pass through the narrowed arterial opening, blood flow to the heart stops
causing myocardial infarction (MI) or heart attack. If the clot is in a vessel close to the brain, a CVA, or
stroke, ensues.
Myocardial Infarction
Disease Process
As the underlying process to CHD, of which MI is the culminating event, atherosclerosis represents a
response to
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arterial injury and an inflammatory process, often in response to infection (2,3,4). The causes of injury
appear to be diverse and include smoking, hypertension, oxidative damage, and the aging process. Even the
cumulative effects of normal physiologic stress that flowing blood exerts on arterial walls is a likely source.
Foods may be involved from both a protective and a detrimental standpoint by either promotion or
prevention of inflammation and oxidative damage (see Tables 7.1 and 7.2).
Table 7.1 Foods and Inflammation
Anti-inflammatory Pro-inflammatory
Alcohol Charred meats (advanced glycosylation end
products; AGEs)
Cocoa (polyphenols)
Fatty fish (n-3 fatty acids) Coffee (moderate to high consumption)
Fruits (containing vitamin C,
carotenoids)
High glycemic load foods (those raising blood
glucose)
Olive oil (oleocanthal)
Spices (curry, ginger)
Tea
Vegetables
Walnuts, (and others with alpha-
linoleic acid)
Whole grains
Various types of lipid oxidation products, particularly oxidized low-density lipoprotein (LDL)-cholesterol,
appear to cause arterial injury, with evidence that all vascular system cells can mediate LDL oxidation, and
transition metal ions catalyze the reaction (5). Oxidized LDL exerts many effects that promote
atherogenesis, and researchers now believe that oxidized LDL and
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lipid oxidation products are involved in all stages of CHD (6).
Table 7.2 Foods Containing Lipid Oxidation Products
Dehydrated foods (containing fat, such as meats)
Fried foods (cooked at high temperatures)
Powdered eggs
Rancid fats and oils
Treatment and Nutritional Intervention
In 2004, the National Heart, Lung, and Blood Institute's National Cholesterol Education Program (NCEP)
released revised guidelines for cholesterol management in its Third Report of the Expert Panel on
Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (ATP III) (7). The guidelines
established by ATP III place an emphasis on treatment based on risk stratification for the primary
prevention of CHD. The ATP III states, “A basic principle of prevention is that the intensity of risk-reduction
therapy should be adjusted to a person's absolute risk. Hence, the first step in selection of LDL-lowering
therapy is to assess a person's risk status.” Following are the ATP III guidelines for the diagnosis and
treatment of high cholesterol, approached in a stepwise fashion.
Step 1:
Determine lipoprotein levels-obtain complete lipoprotein profile after 9- to 12-hour fast.
Table 7.3 ATP III Classification of Cholesterol Levels
LDL Cholesterol—Primary Target of Therapy
<100 mg/dL Optimal
100–129 mg/dL Near optimal
130–159 mg/dL Borderline high
160–189 mg/dL High
=190 mg/dL Very high
Total Cholesterol
<200 mg/dL Optimal
200–239 mg/dL Borderline high
=240 High
HDL Cholesterol
<40 mg/dL Low
=60 mg/dL High
Data from reference 7.
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Table 7.4 CHD Risk Equivalents
Other clinical forms of atherosclerotic disease
Peripheral arterial disease
Abdominal aortic aneurysm
Symptomatic carotid artery disease
Diabetes (now regarded as a CHD risk equivalent)
10 year risk for CHD >20%
Data from reference 7.
Step 2:
Identify presence of clinical atherosclerotic disease that confers high risk for CHD events, called CHD risk
equivalents (RE).
CHD REs carry a risk for major coronary events equal to that of established CHD, which is 20% per 10 years
(i.e., more than 20 of 100 such individuals will develop CHD or have a recurrent CHD event within 10 years).
Diabetes counts as a CHD RE because it confers a high risk of new CHD within 10 years, in part because of
its frequent association with multiple risk factors (7).
Step 3:
Determine presence of major risk factors (other than LDL).
Step 4:
If 2+ non-LDL RFs (step 3) are present without CHD or CHD RE, assess 10-year (short-term) CHD risk.
Ten-year CHD risk is calculated using the Framingham Tables, and is a projection of 10-year absolute CHD
risk
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(i.e., the percentage probability of having a CHD event in 10 years). This helps to identify certain patients
with multiple (2+) risk factors for more intensive treatment. There are three levels of 10-year risk:
Table 7.5 Major Risk Factors That Modify LDL Goals
Age (men 45 years, women 55 years)
Cigarette smoking
Hypertension (BP 140/90 mm Hg or on antihypertensive medication)
Low HDL cholesterol (<40 mg/dL)
Family history of premature CHD (in first-degree male relative >44 years, or in first-degree
female relative >54 years)
Data from reference 7.
>20% = CHD Risk Equivalent
10%–20%
<10%
The Framingham Scoring Tables for calculating 10-year risk can be found in Appendix C.
Step 5:
Determine risk category, which helps to:
Establish LDL goal of therapy
Determine need for therapeutic lifestyle changes (TLC)
Determine level for drug consideration
Step 6:
If LDL is above goal, initiate Therapeutic Lifestyle Changes (TLC).
The terms “Step I” and “Step II” are no longer used in reference to heart-healthy diets for people at risk for
CHD. For those people with established CHD, CHD risk equivalents, or multiple (2+) non-LDL risk factors, the
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TLC diet approach is recommended (8). The TLC diet focuses on behavioral changes aimed at lowering LDL
cholesterol in the population whose LDL cholesterol is above the goal level for their category of risk for
heart disease.
Table 7.6 NCEP ATP III Treatment by Risk Category
Risk Category Risk Profile LDL Goal (mg/dL) Initiate TLC Consider Drug Therapy
High risk CHD or CHD RE
10-yr risk >20%
<100 =100 =100
Moderately high risk 2+ RF
10-yr risk =20%
<130 =130 =130
Moderate risk 2+ RF
10 yr risk <10%
<130 =130 =160
Lower risk 0–1 RF
10-yr risk <10%
<160 =160 =190
RF: risk factors; RE: risk equivalents
Data from reference 7.
Table 7.7 ATP III Nutritional Components of the TLC Diet
Nutrient Daily Recommended Intake
Total fat 25%–35% of total kilocalories
Saturateda fat <7% of total kilocalories
Polyunsaturated fat Up to 10% of total kilocalories
Monounsaturated fat Up to 20% of total kilocalories
Cholesterol <200 mg
Carbohydrate (esp. complex) 50%–60% of total kilocalories
Protein ~15% of total kilocalories
Therapeutic Options for LDL Lowering
Daily fiber intake 20–30 g, primarily soluble fiber
Plant stanols/sterols 2 g/day
a Trans-fatty acids are another LDL-raising fat that should be kept at a low intake.
Data from reference 7.
In addition to the TLC diet, nutrition education of the cardiac patient should focus on the following (9):
Changing modifiable risk factors
Importance of achieving a healthy weight, BMI, and waist circumference
Increasing physical activity
Appropriate macronutrient consumption (as outlined in TLC diet)
Increased intake of fruits and vegetables and high-fiber foods
Discussion of the values of the different types of fats in the diet
Food label reading
Selection and preparation of healthy foods
Importance of decreasing sodium intake
Addition of fish, nuts, and/or soy to the diet
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Table 7.8 Clinical Identification of Metabolic Syndrome—Any Three of the Following
Risk Factor Defining Level
Abdominal obesity Waist circumference
Men >102 cm (40 in.)
Women >88 cm (35 in.)
Triglycerides =150 mg/dL
HDL Cholesterol
Men <40 mg/dL
Women <50 mg/dL
Blood pressure =130/=85 mm Hg
Fasting glucose =110 mg/dL
Data from reference 7.
Step 7:
Consider drug therapy if LDL exceeds levels in step 5.
Step 8:
Identify and treat metabolic syndrome, if present after 3 months of TLC.
Treatment of Metabolic Syndrome
Treat underlying causes (overweight/obesity and physical inactivity)
Treat lipid and nonlipid risk factors if they persist despite these lifestyle therapies:
Treat HTN
Use aspirin for CHD patients to reduce prothrombotic state
Treat high TG and/or low HDL
Step 9:
Treat elevated triglyceride (TG) level.
Intensify weight management
Increase physical activity
If TG are >200 mg/dL after LDL goal is reached, set secondary goal for non-HDL cholesterol (total-
HDL) 30 mg/dL higher than LDL goal.
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Table 7.9 Classification of Triglyceride Levels
<150 mg/dL Normal
150–199 mg/dL Borderline high
200–499 mg/dL High
>500 mg/dL Very high
Note: Data from reference 7.
Congestive Heart Failure
Disease Process
Congestive heart failure (CHF) is a common disease among the elderly, affecting up to 10% of those over
age 65 (10). It develops when the heart fails to pump blood effectively, causing fluid congestion in blood
vessels and tissues leading to the heart. The consequences of CHF include a compensatory enlargement of
the heart, although the side of the heart affected (left or right) produces different symptoms. If affecting
the right side, blood backs up in peripheral and abdominal tissue. The symptoms include chest pain,
digestive problems, and peripheral edema. When CHF affects the left side, fluid accumulates in the lungs
and causes pulmonary edema, producing shortness of breath and often leading to respiratory failure.
Several conditions and other diseases may cause CHF (Table 7.10).
Treatment and Nutritional Intervention
Several nutritional concerns arise in CHF, including right-sided CHF leading to digestive problems and
hepatomegaly
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and left-sided leading to limb weakness and fatigue. Both types can lead to end-stage heart failure that
causes cardiac cachexia. The malnutrition is caused by symptoms, which affect ability or desire to eat, and
changes in oxygen consumption and altered metabolism. For these reasons, periodic and frequent
nutritional assessment is important.
Table 7.10 Causes of CHF
Cardiomyopathy
Congenital heart defects
Endocarditis and or myocarditis
Heart valve disease (due to rheumatic fever or other causes)
Hypertension
Narrowed arteries that supply blood to the heart muscle due to CHD
Previous MI with scar tissue
Data from reference 10.
Table 7.11 Treatment for CHF
Diet Drug Other
2–3 g sodium ACE
inhibitors
Modified daily
activities
Small frequent meals Beta-
blockers
Rest
Prevent, treat malnutrition (cardiac
cachexia)
Digitalis Smoking cessation
Diuretics Yearly flu vaccine
Vasodilators
Adapted from reference 10.
Drug therapy is key and consists of four main types, that is, diuretics, ACE inhibitors, beta-blockers, and
digitalis (Table 7.11). The edema that occurs and the types of drugs used necessitate a moderate sodium
restriction of 2,000 to 3,000 mg, with severe cases requiring the lower level. Small frequent meals may be
easier for a patient to consume, both the right-sided CHF because of abdominal bloating and left-sided
because of breathing difficulty. As a patient becomes depleted, oral supplements or possibly tube feeding
may be needed.
Cerebrovascular Accident (Stroke) and Hypertension
Stroke is the third leading cause of death in the United States and leading cause of disability (11). Although
a CVA can occur at any age, the risk doubles with each decade after the age of 55. The major risk factor for
CVA is hypertension (HTN), which is also a disease of the blood vessels.
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Cerebrovascular Accident
Disease Process
A CVA occurs from two situations: (a) a clot prevents blood flow (and oxygen) to a part of the brain
(ischemic stroke), or (b) a cerebral blood vessel ruptures (hemorrhagic stroke). Both types cause damage to
the brain resulting in a variety of disabilities, which may or may not be permanent. Risk factors vary as to
the type of stroke (Table 7.12). Evidence from epidemiological studies suggests that several nutrients may
either protect against or increase risk for CVA (Table 7.13).
Treatment and Nutritional Intervention
The most important aspect of treatment for CVA is immediate administration of thrombolytic drugs (11).
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These drugs, and others often used, may have diet or nutrient interactions, which will be important to
identify (Table 7.14) (19). In addition, several nutritionally relevant problems can arise after CVA (Table
7.15). Some of these problems will depend on the area of the brain that has been damaged. The nutrition
therapy objective is to maintain adequate nutritional status when nutritional problems occur. The most
common nutritional problem is dysphagia, which may be temporary or permanent (see Chapter 4). A
moderate sodium restriction of 2 to 3 g is typical, both for CVA prevention and to treat hypertension, which
is a major risk factor for both types of stroke.
Table 7.12 Risk Factors for CVA
Ischemic Stroke Hemorrhagic Stroke
Age
African American ethnicity
Body weight
White men: tricep to subscapular skinfold
thickness and CVA have U-shaped
relationship;
White men: never smokers: higher CVA risk
only at top BMI quartile;
African American women: higher CVA risk at
lower BMI (lowest quartile) (16)
Diabetes
Genetic factors
Heart disease
Hypertension
Smoking
Triglyceride, serum (>200 mg/dL)
Chlamydia pneumoniae (and other
infections) (15)
High blood cholesterol (14) (>280 has twice
the risk of 230)
Age
African American ethnicity
Body weight
White men: tricep to subscapular skinfold
thickness and CVA have U-shaped
relationship;
White men: never smokers: higher CVA risk
only at top BMI quartile;
African American women: higher CVA risk at
lower BMI (lowest quartile) (16)
Diabetes
Genetic factors
Heart disease
Hypertension
Smoking
Triglyceride, serum (>200 mg/dL)
Lower blood cholesterol (<180 has twice the
risk of 230)
Adapted from references 11,12,13,14.
Table 7.13 Dietary Components Associated with CVA Risk
Protective Factors Factors Associated with Risk
Alcohol (moderate intake) Alcohol (high intake)
B vitamins Sodium
Calcium Low fat and saturated fat (19,20)
Fish (17)
Fruits
Magnesium
Potassium
Vegetables
Whole grains (18)
Adapted from references 11 and 15,16,17,18.
Hypertension
Disease Process
The prevalence of hypertension (HTN) among Americans is close to 33% of the population (20). If untreated,
HTN increases the risk of stroke (CVA), peripheral vascular disease (PVD), CHD, CHF, atrial fibrillation, and
death. HTN is defined as having a sustained blood pressure (BP) >140 mm Hg (systolic) over 90 mm Hg
(diastolic). The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and
Treatment of High
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Blood Pressure, also known as the JNC 7 report, established categories of HTN (Table 7.16) (20).
Table 7.14 Nutrition Implications of Drugs Used in CVA
Drug Class Drug/Implications
Anticoagulants Aspirin:GI mucosal damage; reduced iron absorption
Herbs and supplements (danshen, dong quai, feverfew, garlic,
ginkgo, vitamin E, n-3 fatty acids, coenzyme Q): Interfere with
clotting times
Ticlopidine: GI distress
Warfarin: diarrhea
Antihypertensives ACE Inhibitors: Avoid potassium-containing salt substitutes; avoid
antacids containing calcium or magnesium or supplements if using
fosinopril
Beta-blockers:GI distress
Calcium channel blockers: Avoid grapefruit and its juice
Clonidine:Constipation
Antilipemics Cholestyramine:GI distress, constipation, reduced absorption of
vitamins A, D, E, K
Gemfibrozil:GI distress
Statins (lovastatin, pravastatin, simvastin): Avoid grapefruit products
and limit alcohol
Cardiac
Glycosides
Digitoxin, Digoxin, Digitalis: Anorexia and nausea; can be toxic in
hypercalcemia or hypokalemia; avoid antacids or supplements
containing magnesium; the herb hawthorn can increase the drug's
effects
Diuretics Potassium-sparing diuretics(amiloride, spironolactone, triamterene):
Can cause hyperkalemia; avoid potassium-containing salt substitutes
Thiazide and loop diuretics: Increased urinary potassium excretion;
oral aloe vera can further increase potassium excretion
Adapted from reference 19.
Table 7.15 Nutritional Problems After CVA
Dysphagia Physical Disability
Choking Physical activity
Dehydration Self-feeding
Weight loss Weight gain
Adapted from reference 11.
Table 7.16 Classification of Blood Pressure for Adults
Classificationa Blood Pressure Level (mm Hg)
Systolic Diastolic
Normal <120 and <80
Prehypertensionb 120–139 or 80–89
Stage 1 hypertension 140–159 or 90–99
Stage 2 hypertension =160 or =100
aClassification based on the average of two or more properly measured, seated BP readings on
each of two or more office visits.bPrehypertension is not a disease category, but rather a designation developed to identify
individuals at risk of developing HTN.
Data from reference 20.
Table 7.17 Lifestyle Modification Recommendations
Modification Recommendation
Approximate Systolic
BP Reduction Rangea
Weight reduction Maintain normal body weight (BMI 18.5–24.9) 5–20 mm Hg/10
kg
DASH eating plan Adopt a diet rich in fruits, vegetables, and low-
fat dairy products with reduced content of
saturated and total fat.
8–14 mm Hg
Dietary sodium
reduction
Reduce dietary sodium intake to =100
mmol/day (2.4 g sodium or 6 g sodium
chloride).
2–8 mm Hg
Aerobic physical
activity
Regular aerobic activity (e.g., brisk walking) at
least 30 min per day, most days of the week.
4–9 mm Hg
Moderation of
alcohol consumption
Men: limit to =2 drinksb per day
Women: limit to =1 drink per day.
2–4 mm Hg
aEffects are dose and time dependent.b1 drink = ½ oz or 15 mL ethanol (12 oz beer, 5 oz wine, 1.5 oz 80-proof whiskey).
Adapted from reference 20.
Table 7.18 Daily Nutrient Goals Used in the DASH Studiesa
Total fat 27% of kilocalories
Saturated fat 6% of kilocalories
Protein 18% of kilocalories
Carbohydrate 55% of kilocalories
Cholesterol 150 mg
Sodium 2,300b mg
Potassium 4,700 mg
Calcium 1,250 mg
Magnesium 500 mg
Fiber 30 g
aPlan is based on a 2,100-kcal diet.b1,500 mg was a lower goal tested and was found to be even more effective for lowering BP,
especially for middle-aged and older individuals, African Americans, and those who already had
high BP.
Data from references 21 and 22.
Table 7.19 DASH Eating Plan—Daily Number of Food Group Servings
Food Groups Servings per Day by Calorie Level
1,600
calories
2,000
calories
2,600
calories
3,100
calories
Grains 6 6–8 10–11 12–13
Vegetables 3–4 4–5 5–6 6
Fruits 4 4–5 5–6 6
FF or LF milk & milk products 2–3 2–3 3 3–4
Lean meats, poultry, fish 3–6 =6 6 6–9
Nuts, seeds, legumes 3/week 4-5/week 1 1
Fats, oils 2 2–3 3 4
Sweets, added sugar 0 =5/week =2 =2
Data from references 21 and 22.
Table 7.20 Common Cardiac Abbreviations
AAA Abdominal aortic aneurysm
ABG Arterial blood gases
ACLS Advanced cardiac life support
AF Atrial fibrillation
AI Aortic insufficiency
AICD Automatic implanted cardiac defibrillator
AMI Acute myocardial infarction
AR Aortic regurgitation
AS Aortic stenosis
ASHD Atherosclerotic heart disease
ASD Atrial septal defect
AVR Aortic valve replacement
CABG Coronary artery bypass graft
CAD Coronary artery disease
CHD Coronary heart disease
CHF Congestive heart failure
CO Cardiac output
CVA Cerebral vascular accident
CVC Central venous catheter
CVD Cardiovascular disease
CVP Central venous pressure
DCM Dilated cardiomyopathy
ECG/EKG Electrocardiogram
EF Ejection fraction
HCM Hypertrophic cardiomyopathy
HR Heart rate
IA Intra-arterial
IABP Intra-arterial balloon pump
ICD Implantable cardioverter-defibrillator
IHD Ischemic heart disease
MI Myocardial infarction
MR Mitral regurgitation
MVP Mitral valve prolapse
NSR Normal sinus rhythm
NTG Nitroglycerin
PVD Peripheral vascular disease
SSS Sick sinus syndrome
SVT Supraventricular tachycardia
TG Triglycerides
List of medical abbreviations, available at:
http://en.wikipedia.org/wiki/List_of_medical_abbreviations.
Treatment and Nutritional Intervention
The JNC7 report emphasizes the importance of lifestyle modification as prevention for the development of
HTN, as well as for the management of those with HTN (20).
Nutritional Recommendation
The Dietary Approaches to Stop Hypertension (DASH) diet, along with reducing sodium intake, can
significantly reduce BP (21). Patients should be educated on the appropriate number of servings to consume
from each food group, based on their recommended caloric intake. The diet is low in saturated fat,
cholesterol, and total fat; and emphasizes fruit, vegetables, and low-fat dairy products. Table 7.18 lists the
nutrient goals used in the DASH studies, and Table 7.19 lists the number of recommended servings, on the
DASH diet, for various kilocalorie levels.
References
1. American Heart Association. Available at: http://www.americanheart.org/presenter.jhtml?
identifier=4478. Accessed March 15, 2007.
2. Pearson TA, Mensah GA, Alexander RW, et al. Markers of inflammation and cardiovascular disease.
Circulation 2003; 107:499–511.
3. Mawhorter SD, Lauer MA. Is atherosclerosis an infection disease? Cleve Clin J Med 2001;68(5):449-
458.
4. Simoes C, Bianciardi G, Toti P, et al. Lipid and raised lesion distribution in the right coronary artery
of young people. Nutr Metab Cardiovasc Dis 1999;9(6):277–283.
5. Hulea SA, Wasowicz E, Kummerow FA. Inhibition of metal-catalyzed oxidation of low-density
lipoprotein by free and albumin-bound bilirubin. Biochim Biophys Acta 1995;1259(1):29–38.
6. Fuller CJ, Huet BA, Jialal I. Effects of increasing doses of alpha-tocopherol in providing protection
of low-density lipoprotein from oxidation. Am J Cardiol 1998;81(2):231–233.
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7. National Institutes of Health, National Heart, Lung, and Blood Institute. Third report of the National
Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, and Treatment of High
Blood Cholesterol in Adults (Adult Treatment Panel III). Final Report. NIH Publication No. 02-5215,
September 2002.
8. American Heart Association. Step 1, Step 2, and TLC Diets. Available at:
http://www.americanheart.org/presenter.jhtml?identifier=4764. Accessed March 17, 2007.
9. Burke Francis M, Carson Jo Ann S, Hark Lisa A. Cardiovascular nutrition disease management and
prevention, United States. Faulhaber 2004;32:237–253.
10. American Heart Association. Available at: http://www.americanheart.org/presenter.jhtml?
identifier=4585. Accessed March 15, 2007.
11. Centers for Disease Control and Prevention. Available at: http://www.cdc.gov/stroke/. Accessed
March 15, 2007.
12. American Heart Association, AHA Stroke Conference 1999. Available at:
http://stroke.ahajournals.org/cgi/content/full/30/11/2502#R21
http://stroke.ahajournals.org/cgi/content/full/30/4/905. Accessed March 14, 2007.
13. Joshipura KJ, Hung HC, Rimm EB, Willett WC, Ascherio A. Periodontal disease, tooth loss, and
incidence of ischemic stroke. Stroke 2003;34(1):47–52.
14. Gillum RF, Mussolino ME, Madans JH. Body fat distribution, obesity, overweight and stroke
incidence in women and men: the NHANES I Epidemiologic Follow-up Study. Int J Obes
2001;25(5):628–638.
15. Iso H, Rexrode KM, Stampfer MJ, et al. Intake of fish and omega-3 fatty acids and risk of stroke in
women. JAMA 2001;285:304–312.
16. Liu S, Manson JE, Stampfer MJ, et al. Whole grain consumption and risk of ischemic stroke in
women: A prospective study. JAMA 2000;284:1534–1540.
17. Iso H, Stampfer MJ, Manson JE, et al. Prospective study of fat and protein intake and risk of
intraparenchymal hemorrhage in women. Circulation 2001;103:856–863.
18. Sherwin R, Price TR. Fat chance: diet and ischemic stroke. JAMA 1997;278:2185–2186.
19. Rolfes SR, Pinna K, Whitney E. Understanding Normal and Clinical Nutrition, 7th ed. Belmont:
Thomson, Wadsworth; 2006.
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20. National Institutes of Health, National Heart, Lung, and Blood Institute. Seventh report of the
Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood
Pressure. Complete Report. NIH Publication No. 04-5230, August 2004.
21. Appel LJ, Moore TJ, Obarzanek E, et al. A clinical trial of the effects of dietary patterns on blood
pressure. N Engl J Med 1997;336:1117–1124.
22. National Institutes of Health, National Heart, Lung, and Blood Institute. Your guide to lowering
your blood pressure. NIH Publication No.06-4082. Revised April 2006. Available at:
http://www.nhlbi.nih.gov/health/public/heart/hbp/dash/new_dash.pdf. Accessed March 20, 2007.
Authors: Width, Mary; Reinhard, Tonia
Title: Clinical Dietitian's Essential Pocket Guide,The: Essential Pocket Guide, 1st Edition
Copyright ©2009 Lippincott Williams & Wilkins
> Table of Contents > Part II - Nutrition Considerations for Specific Diseases > Chapter 8 - Diabetes
Chapter 8
Diabetes
Diabetes mellitus is a disease known since ancient times, cited by both the Greeks and Egyptians in as early
as 1500 BC. In its various forms, it affects over 18 million Americans every year, and it is the sixth leading
cause of death and a major cause of complications, such as heart disease, kidney disease, blindness, and
amputations.
Diabetes: Classification, Screening, and Diagnosis
Classification of Diabetes
In order to provide comprehensive and effective medical and nutritional care for patients with diabetes, we
must first understand the precise definitions and classifications of diabetes. The American Diabetes
Association (ADA) issued new diagnostic and classification criteria for diabetes in 1997 (1). In 2003, revisions
were made regarding the diagnosis of impaired fasting glucose (IFG) (2). Table 8.1 includes the four clinical
classes of diabetes.
Screening for Diabetes
Adults
Dietitians and other health care providers should encourage regular screening for diabetes, especially for
individuals
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in high-risk groups. Table 8.2 shows the recommendations for screening for diabetes in asymptomatic
adults.
Table 8.1 Classification of Diabetes Mellitus
Type 1 Results from autoimmune destruction of pancreatic ß-cells, usually
leading to absolute insulin deficiency. Accounts for 5%–10% of diagnosed
diabetes in the United States.
Type 2 Results from a progressive insulin secretory defect on the background of
insulin resistance. Accounts for 90%–95% of diagnosed diabetes in the
United States.
Other specific
types of
diabetes
Genetic defects of the ß-cell; genetic defects in insulin action; diseases
of the exocrine pancreas; endocrinopathies; drug- or chemical-induced;
infections; uncommon forms of immune-mediated diabetes; other
genetic syndromes sometimes associated with diabetes.
Gestational
diabetes
mellitus (GDM)
Diagnosed during pregnancy
Data from references 1,2,3.
Table 8.2 Screening for Diabetes in Asymptomatic Adults
Testing for diabetes should be considered in all individuals at age 45 years and
above, particularly in those with a body mass index (BMI) =25 kg/m2. If normal,
repeat every 3 years.
1.
Testing should be considered before age 45 in individuals who are overweight (BMI
=25 kg/m2) and have additional risk factors:
Habitually sedentary
Have first-degree relative with diabetes
Members of a high-risk ethnic population (African American, Asian
American, Latino, Native American, Pacific Islander)
Have delivered a baby weighing >9 lbs or have been diagnosed with GDM
Hypertensive (=140/90 mm Hg)
HDL cholesterol level <35 mg/dL and/or triglyceride level >250 mg/dL
Had impaired glucose tolerance (IGT) or IFG on previous testing
History of vascular disease
Have other clinical symptoms associated with insulin resistance (PCOS,a
acanthosis nigricans)
2.
aPolycystic Ovarian Syndrome.
Table 8.3 Testing for Type 2 Diabetes in Children
Age of
Initiation
10 years of age or at onset of puberty, if puberty occurs at <10 years of age
Frequency Every 2 years
Test Fasting plasma glucose (FPG) preferred
Criteria Overweight: BMI >85th percentile for age & sex, weight for height >85th
percentile, or weight >120% of ideal for height
Plus any two of the following risk factors:
Family history of type 2 diabetes in first- or second-degree
relative
Race/ethnicity (African American, Asian American Latino, Native
American, Pacific Islander)
Signs of, or conditions associated with, insulin resistance
(acanthosis nigricans, dyslipidemia, hypertension, or PCOS)
Maternal history of diabetes or GDM
Data from references 3 and 4.
Children
Due to the dramatic increase of type 2 diabetes in children, the ADA recommends screening for children at
increased risk for the presence or development of type 2 diabetes (4). Table 8.3 shows the testing criteria
for type 2 diabetes in children.
Pregnant Women
It was previously recommended that all pregnant women be screened for gestational diabetes mellitus
(GDM); however, there are certain factors that place women at either higher or lower risk for developing
glucose intolerance during pregnancy. Table 8.4 summarizes the screening recommendations for GDM.
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Table 8.4 Testing Recommendations for GDM
Criteria for Group Level Testing Recommendation
Low-risk
group
Must meet all the following criteria:
<25 years of age
Normal body weight
before pregnancy
No known diabetes in a
first-degree relative
No history of abnormal
glucose tolerance
No history of poor
obstetric outcome
Not a member of an
ethnic/racial group with a
high prevalence of
diabetes
No glucose testing
required
High-risk
group
Women with any of the following:
Marked obesity
Personal history of GDM
Glycosuria
Strong family history of
diabetes
FPG or casual plasma
glucose as soon as
feasiblea
Retest between 24 and
28 weeks gestation if
initial screening is
negative for GDM
Average-
risk group
Any woman not meeting criteria for
the low-risk or high-risk groupsTest at 24–28 weeks
gestation
aFPG of >126 mg/dL or casual plasma glucose >200 mg/dL meets the threshold for the diagnosis
of diabetes. Diagnosis must be confirmed on a subsequent day in the absence of unequivocal
hyperglycemia.
Diagnosis of Diabetes
Children and Nonpregnant Adults
The fasting plasma glucose (FPG) is the preferred test for diagnosing diabetes in children and nonpregnant
adults due to its ease of use, acceptability to patients, and lower cost. It should be noted that many
individuals with impaired glucose tolerance display normal daily blood glucose levels and near normal
hemoglobin A1c (A1C) levels, and only manifest hyperglycemia when challenged with an oral glucose load
(3). These patients may need to be tested using the oral glucose tolerance test (OGTT), which is also the
preferred test for gestational diabetes. The use of A1C for the diagnosis of diabetes is not
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recommended at this time (3). Table 8.5 lists the diagnostic criteria for types 1 and 2 diabetes.
Table 8.5 Criteria for the Diagnosis of Diabetesa
Symptoms of Diabetes and a Casual Plasma Glucose 200 mg/dL
Casual is defined as any time of day without regard to time since last
meal.
Classic symptoms of diabetes include polyuria, polydipsia, and unexplained
weight loss.
OR
1.
Fasting Plasma Glucose (FPG) 126 mg/dL
Fasting is defined as no caloric intake for at least 8 hours.
OR
2.
2-hr Plasma Glucose 200 mg/dL During an Oral Glucose Tolerance Test (OGTT).
The test should be performed as described by the World Health
Organization, using a glucose load containing the equivalent of 75 g
anhydrous glucose dissolved in water.
3.
aEach criterion must be confirmed on a subsequent day unless unequivocal symptoms of
hyperglycemia are present.
Data from reference 3.
Gestational Diabetes
The ADA's 4th International Workshop Conference on GDM supports the use of the Carpenter and Coustan
diagnostic criteria for abnormal glucose tolerance (summarized in Table 8.6) (5).
Table 8.6 Detection and Diagnosis of Gestational Diabetes
Plasma Glucose 50-g Glucose Challenge Test 100-g Diagnostic OGTTa
Fasting — 95 mg/dL
1 hr 140 mg/dL 180 mg/dL
2 hr — 155 mg/dL
3 hr — 140 mg/dL
aTwo or more of the plasma glucose values must be met or exceeded for a positive diagnosis.
The test should be done in the morning after an overnight fast of 8–14 hours and after at least
3 days of unrestricted diet (>150 g carbohydrate per day) and unlimited physical activity. The
subject should remain seated and quiet during the test as activity can interfere with results.
Data from references 3 and 5.
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Table 8.7 Testing for Diabetes and Prediabetes
Fasting Plasma Glucose Test
<100 mg/dL 100–125 mg/dL =126 mg/dL
Normal Impaired Fasting Glucose (IFG)
Prediabetes
Diabetesa
Oral Glucose Tolerance Test
<140 mg/dL 140–199 mg/dL =200 mg/dL
Normal Impaired Glucose Tolerance (IGT)
Prediabetes
Diabetesa
aEach criterion must be confirmed on a subsequent day unless unequivocal symptoms of
hyperglycemia are present.
Data from reference 3.
The glucose testing at 24 to 28 weeks should follow one of two approaches:
One-step approach: Perform a diagnostic 100-g OGTT
Two-step approach: Perform an initial screening with a 50-g oral glucose load (glucose challenge
test or O'Sullivan test), and perform a diagnostic 100-g OGTT on the subset of women exceeding
the glucose threshold value on the glucose challenge test (see Table 8.6).
Prediabetes
An intermediate group of subjects has been recognized whose glucose levels do not meet the criteria for
diabetes, but are too high to be considered normal (1,2). Individuals that fall into this category are now
referred to as having “prediabetes,” and are considered at risk for future diabetes and cardiovascular
disease (3). Table 8.7 shows the categories for FPG and OGTT.
Medical Nutrition Therapy
MNT is an integral component of diabetes prevention, management, and self-management (3). The
recommendations by the ADA for medical nutrition therapy (MNT) in diabetes are based on the 2005 Dietary
Guidelines and the
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recommended daily allowances (RDAs) from the Institute of Medicine of the National Academy of Sciences.
Provide regular, individualized meal planning, advice, and guidelines.
Maintain a reasonable weight through therapeutic lifestyle change, including a reduction in
energy intake and an increase in physical activity. Weight loss diets should supply at least 1,000
to 1,200 kcal/day for women and 1,200 to 1,600 kcal/day for men.
10% to 20% of total kilocalories from protein. To reduce the risk of nephropathy, protein intake
should be limited to the RDA of 0.8 g/kg.
45% to 65% of total kilocalories from carbohydrate. Restricting carbohydrate to <130 g/day is not
recommended.
25% to 30% of total kilocalories from fat. Limit saturated fat to <7% and minimize the intake of
trans fats.
<300 mg cholesterol per day.
Carbohydrate Counting
Carbohydrate counting is a meal planning approach for people with diabetes that focuses on balancing
carbohydrate food choices throughout the day. It places emphasis on the total amount of carbohydrate
consumed, rather than on the source or type of carbohydrate consumed, and is based on two ideas:
Eating equal amounts of sugar, starch, or milk will raise blood sugar about the same amount.
Carbohydrate is the main nutrient that affects blood sugar. Within 1 to 2 hours after eating
carbohydrate, most of it is changed to blood sugar. Protein and fat have much less effect on
blood sugar.
One carbohydrate serving is equal to 15 g of carbohydrate and can be a starch, fruit, milk, or
sweet/dessert. Patients can use basic carbohydrate counting with type 1 or type 2 diabetes. For patients
with type 1 diabetes that use a basal-bolus insulin regimen or an insulin pump,
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advanced carbohydrate counting skills are needed. The ability to calculate a bolus insulin dose using the
insulin-to-carbohydrate ratio is helpful (Tables 8.8 and 8.9).
Table 8.8 Calculating the Insulin-to-Carbohydrate Ratio
Divide the number of grams of carbohydrate in the meal by the units of bolus insulin
given.
The correct ratio should return the blood glucose to baseline values.
Example: Patient had 3 servings of carbohydrate for a total of 45 g. The bolus insulin
dose was 3 units. 45 g divided by 3 units = 15 g of carbohydrate to one unit of insulin,
or a 1:15 insulin-to-carbohydrate ratio.
It should be noted that the insulin-to-carbohydrate ratio varies from person-to-
person, and can also vary for the same person during different times of the day,
based on their physical activity, insulin needs, and other variables.
The ratio may change with physical activity, body weight, hormonal changes, and
other factors. Daily blood glucose testing is imperative.
Data from reference 6.
Another method for calculating the insulin-to-carbohydrate ratio is the 450/500 Rule. This is a formula to
calculate how many grams of carbohydrate would be covered by 1 U of rapid-acting or short-acting insulin.
This allows flexibility in food choices because any number of carbohydrates can be covered with a matching
dose of insulin.
Table 8.9 The 450/500 Rule for Calculating the Insulin-to-Carbohydrate Ratio
If using rapid-acting insulin (i.e., Humalog or Novolog) use the 500 Rule. If short-
acting (regular) insulin is used (i.e., Humulin R or Novolin R), use 450.
Divide 500 by the total daily dose (TDD) of insulin. Example: 500 divided by 50 U
(TDD) of insulin = 10 g of carbohydrate covered by 1 U of insulin, or a 1:10 insulin-
to-carbohydrate ratio.
The TDD includes all basal plus bolus insulin.
It should be noted that the 450/500 Rule works best for those patients with no
insulin production, using the basal/bolus approach to insulin therapy.
As always, daily blood glucose testing is imperative
Data from reference 7.
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Table 8.10 Exchange Lists for Meal Planning
Food Groups Kilocalories Carbohydrate Protein Fat
Carbohydrates
Starch 80 15 3 0–1
Milk—skim & low-fat 90 12 8 0–3
2% 120 12 8 5
Whole 150 12 8 8
Fruit 60 15 — —
Vegetables 25 5 2 —
Meat & Meat Substitutes
Very Lean 35 — 7 1
Lean 55 — 7 2–3
Medium-Fat 75 — 7 5
High-Fat 100 — 7 8
Fat 45 — — 5
Exchange Lists
Some people with diabetes use the Exchange Lists for Meal Planning (Table 8.10). This system, established
by the American Dietetic and American Diabetes Associations, separates foods into six categories (or lists)
based on their macronutrient content. Depending on the energy level, an exchange pattern consists of a set
number of exchanges from each group. Within each list, foods can be exchanged, but the serving size may
vary. The Exchange Lists were one of the first meal planning systems used to help diabetic patients control
their blood sugar levels, and although many health professionals see the system as outdated and prefer to
use carbohydrate counting, many diabetic patients still rely on the Exchange system to help keep their
diabetes under control.
Pharmacological Management of Diabetes
Oral Hypoglycemic Medications
See Table 8.11 for a listing of oral medications for diabetes.
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Table 8.11 Oral Medications for Type 2 Diabetes
Mode of Action Class Brand Name (Generic Name)
Dosage Range (2nd
value is max. dose) When to Take
Insulin First-Generation
Sulfonylureas
Secretagogues Diabinese
(chlorpropamide)
100–750
mg/day
Stimulate insulin
secretion from the
pancreas
Second-Generation
Sulfonylureas:
Glucotrol (glipizide) 5–40 mg/daya 30 min
before meal
Glucotrol XL (glipizide) 2.5–20 mg/day Take with
first meal of
day
Micronase/DiaBeta
(glyburide)
1.25–20
mg/daya
Take with
first meal of
day
Amaryl (glimepiride) 1–8 mg/day Take with
first meal of
day
Meglitinide–Benzoic Acid
Derivative
Prandin (repaglinide) 0.5–16 mg/day Take with
meals
Meglitinide–D-
Phenylalanine Derivative
Starlix (nateglinide) 180–360
mg/day
1–30 min
before meals
Insulin Sensitizers Biguanides Take with
meals
Improve insulin
sensitivity via the liver
and peripheral tissue
Glucophage (metformin) 500–2,550
mg/day
Take with
meals
and peripheral tissue
Glucophage XR (extended
release)
500–2,000
mg/day
Thiazolidinediones
Avandia (rosiglitazone) 2–8 mg/day Take without
regard to
meals
Actos (pioglitazone) 15–45 mg/day Take without
regard to
meals
Delay Glucose Alpha-Glucosidase
Inhibitors
Absorption in GI Precose (acarbose) 75–300 mg/day Take with
first bite of
main meals
Glyset (miglitol) 75–300 mg/day Take with
first bite of
main meals
Combination Drugs Glucovance
(glyburide/metformin)
1.25 mg/250
mg–20
mg/2,000
mg/day
Take with
meals once
or twice per
day
Metaglip
(glipizide/metformin)
2.5 mg/250
mg–20
mg/2,000
mg/day
Take with
meals once
or twice per
day
AvandaMet
(Avandia/metformin)
1 mg/500 mg–8
mg/2,000 mg
Take with
meals once
or twice per
day
ACTOplus Met
(Actos/metformin)
15 mg/500
mg–45
Take with
meals once
mg/2,550 mg or twice per
day
Avandaryl
(Avandia/Amaryl)
4 mg/1 mg–8
mg/4 mg
Take with
first meal of
day
aOnce-a-day therapy is usually satisfactory, but higher doses may be divided.
Data from references 3 and 8, and medication product labeling.
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Insulin
Table 8.12 is a listing of insulin and insulin analogs and their action.
Insulin Sensitivity Factor
When a patient's blood sugar goes unexpectedly high, a correction bolus of insulin can be given to bring the
level back to baseline. The 1,500/1,800 Rule is a commonly accepted formula for estimating the drop in a
person's blood glucose per unit of rapid-acting or short-acting insulin (Table 8.13). This value is referred to
as an insulin sensitivity factor (ISF) or correction factor (CF). Knowing their ISF can help a person with type
1 diabetes to
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determine the correct dose of bolus insulin to take to correct an elevated blood sugar.
Table 8.12 Insulin and Insulin Analogs
Type of Insulin (Trade
Name) Onset (hr) Peak (hr)
Duration
(hr) When to Administer
Rapid Acting 0.25–0.5 0.5–4 4–6 0–15 min before meals
Lispro (Humalog) <0.5 1–3 3–5 0–15 min before meals
Aspart (NovoLog)
Glulisine (Apidra)
0.25 0.05–1.5 –5 0–15 min before meals
Short Acting
(Regular)
Humulin R, Novolin
R
0.5–1 2–3 6–8 30–45 min before meals
Intermediate
Acting
NPH, Humulin N,
Novolin N
2–4 6–10 14–18 Before am & pm meal or
before am meal and at
bedtime
Long Acting
Glargine (Lantus) 1 No peak Up to
24
In am or at bedtime
Detemir (Levemir) 1 No peak Up to
24
Once or twice daily
Combinations
Humulin 50/50 0.05-1 2.5–5 14–18 Before breakfast & dinner
Humulin 70/30 0.05–1 1.5–16 14–18 Before breakfast & dinner
Novolin 70/30 0.5 2–12 Up to
24
Before breakfast & dinner
Humalog Mix 75/25 <0.5 1–6.5 ~22 Before breakfast & dinner
NovoLog Mix 70/30 <0.5 1–4 Up to
24
Before breakfast & dinner
Data from references 3 and 8, and medication product labeling.
Table 8.13 1500/1800 Rule for Blood Sugar Correction
Use the 1500 Rule for patients using short-acting (Regular) insulin (i.e., Humulin R or
Novolin R) . Use the 1800 Rule for those using rapid-acting insulin (i.e., Humalog or
NovoLog).
Determine the total daily dose (TDD) of all basal and bolus insulin.
Divide 1,500 or 1,800 by the TDD to find the ISF. Example: 1,800 divided by 50 U
(TDD) of insulin = 36. So, it would be estimated that 1 U of rapid-acting insulin would
lower the blood sugar by 36 mg/dL.
This rule works best when basal insulin makes up about 50% of TDD.
Data from reference 9.
Adjunct Medications for Diabetes
Exenatide
Incretin mimetics are a new class of medication for the treatment of type 2 diabetes. In individuals with
type 2 diabetes, the naturally occurring incretin hormones are blunted. An incretin mimetic works to mimic
the antidiabetic or glucose-lowering actions of incretins by enhancing glucose-dependent insulin secretion
and several other glucoregulatory actions. These medications suppress inappropriately elevated glucagon
levels, promote satiety, reduce food intake, and slow the rate of gastric emptying (10).
BYETTA (exenatide) is the first FDA-approved agent of this new class of medications and exhibits many of
the same effects as the human incretin hormone glucagon-like peptide-1 (GLP-1). BYETTA was approved for
use by people with type 2 diabetes who are unsuccessful at controlling their blood sugar levels despite using
the commonly prescribed oral medications metformin, a sulfonylurea, or both. BYETTA should not be used
in patients with type 1 diabetes or for the treatment of diabetic ketoacidosis, nor is BYETTA a substitute for
insulin, in
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insulin-requiring individuals. BYETTA is formulated for self-administration as a fixed-dose subcutaneous
injection given prior to the morning and evening meals (10).
Table 8.14 Injectable (Noninsulin) Antihyperglycemic Medications
Type of Medication (Trade
Name) How Supplied
Initial
Recommended
Dose When to Inject
Exenatide
(Byetta)
-Used only in Type
2 patients
5 µg per dose, 60
doses, 1.2 mL prefilled
pen; 10 µg per dose,
60 doses, 2.4 mL
prefilled pen
5 mcg per
dose, BID
1–60 min prior to the
main morning and
evening meals (at least
6 hr apart). Do not take
after meals.
Pramlintide
Acetate (Symlin)
-Used only in type
1 or type 2
patients treated
with insulin
5 mL vials containing
0.6 mg/mL pramlintide
Type 2
diabetes:
60 µg
Type 1
diabetes:
15 µg
Immediately prior to
each major meala
aMajor meal is defined as containing at least 250 kcal or at least 30 g carbohydrate.
Data from references 10 and 11.
Pramlintide Acetate
SYMLIN (pramlintide acetate) is the first in a new class of injected antihyperglycemic medications for use in
patients with type 2 or type 1 diabetes treated with insulin. Pramlintide is a synthetic analog of human
amylin, a naturally occurring neuroendocrine hormone synthesized from pancreatic beta cells that
contributes to glucose control during the postprandial period. Amylin, similar to insulin, is absent or
deficient in patients with diabetes. When used with insulin, SYMLIN can help patients achieve improved
glycemic control (11).
SYMLIN is taken at mealtimes and is indicated for:
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Type 2 diabetes, as an adjunct treatment in patients who use mealtime insulin therapy and have
failed to achieve desired glucose control despite optimal insulin therapy, with or without a
concurrent sulfonylurea agent and/or metformin
Type 1 diabetes, as an adjunct treatment in patients who use mealtime insulin therapy and who
have failed to achieve desired glucose control despite optimal insulin therapy (11).
Blood Glucose, Blood Pressure, and Lipid Goals for Adults with
Diabetes
Blood Glucose and Hemoglobin A1c (A1C)
A1C is considered the primary target for glycemic control. The A1C test measures a patient's average
glycemia over the preceding 2 to 3 months and can help health providers to determine whether a patient's
metabolic control had been reached and maintained within a target range (3). Table 8.15 shows the
correlation between A1C and mean plasma glucose levels. The ADA recommends the following for A1C
testing (3):
Perform the A1C test at least two times per year in patients who are meeting treatment goals and
who have stable glycemic control.
Table 8.15 Correlation Between A1C Level and Mean Plasma Glucose Levels
A1C (%) Mean Plasma Glucose (mg/dL)
6 135
7 170
8 205
9 240
10 275
11 310
12 345
Data from reference 12.
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Table 8.16 Recommendations for Glycemic Control for Nonpregnant Adults
with Diabetes
Glycemic Control
ADA Goals AACEa Goals
A1C <7% 6.5% or less
Preprandial plasma glucose 90–130 mg/dL 110 mg/dL
Peak postprandial plasma glucose <180 mg/dLb 140 mg/dL
aAmerican Association of Clinical Endocrinologists.bPostprandial glucose measurements should be made 1–2 hr after the beginning of
the meal
Data from references 3 and 13.
Perform the A1C test every 3 months in patients whose therapy has changed or who are not
meeting glycemic goals.
The A1C goal for patients in general is <7%.
The A1C goal for the individual patient is as close to normal as possible (<6%) without significant
hypoglycemia.
Pre- and postprandial plasma glucose testing is an important part of diabetes management. Table 8.16 lists
current recommendation for glycemic control.
Blood Pressure and Lipids
Hypertension and dyslipidemia are common comorbid conditions for patients with diabetes, and evidence
indicates the control of these coexisting conditions is essential in the treatment of diabetes. Cardiovascular
disease accounts for 80% of mortality in patients with diabetes (13). The ADA recommendations for blood
pressure and lipids for patients with diabetes are included in Table 8.17.
Sick Day Management
Educating patients on sick day management is important. Illnesses such as viral colds or flu, infections,
injuries, fever, vomiting, and diarrhea all increase the need for
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insulin. Emotional stress or crises, physical injury, and surgery can also affect blood glucose levels.
Table 8.17 Lipid and Blood Pressure Goals for Nonpregnant Adults with Diabetes
Lipids
LDL <100 mg/dL
Triglycerides <150 mg/dL
HDL >40 mg/dLa
Blood Pressure
<130/80 mm Hg
aFor women, it has been suggested that the HDL be increased by 10 mg/dL.
Data from references 3 and 13.
Checking Blood Sugar and Ketones on Sick Days
Test blood glucose every 4 hours and record in logbook.
Test for urine ketones every 4 hours and record in log book (type 1 diabetes).
Insulin and Oral Medications on Sick Days
Continue taking insulin and diabetes medications.
Supplemental doses of rapid-acting or short-acting insulin may be needed due to elevated blood
glucose levels or the presence of large or persistent ketones (8).
Rapid- or short-acting insulin may be given every 1 to 4 hours, with the dose depending
on the severity of the illness.
During most illnesses, 10% of total daily insulin dose can be given as a supplemental
dose (i.e., if normal dose is 40 U/day, then give 10% or 4 U).
If blood glucose is >300 mg/dL with large ketones, 20% of total daily insulin dose can be
given as a supplemental dose (i.e., if normal dose is 40 U/day, then give 20% or 8 U).
Adjustments need to be individualized and based on tested blood glucose levels.
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Table 8.18 Foods for Sick Day Management (~15 g carbohydrate each)
½ cup (4 oz) fruit juice 1 cup (8 oz) milk (nonfat)a
1 cup (8 oz) Gatorade or sports drink 1/2 cup (4 oz) regular, nondiet soft drink
½ cup unsweetened applesauce 3 squares graham cracker
1 slice toast 1 cup soup
½ cup regular gelatin 6 saltine crackers
½ cup oatmeal 1 popsicle (single)
1/3 cup rice or pasta 1/2 cup ice cream
¼ cup sherbet 1/2 cup frozen yogurt
3 glucose tablets 8 Lifesavers
2 tablespoons raisins
aAvoid food high in fat content as it may slow gastric emptying and absorption of carbohydrate.
General Guidelines for Sick Days
Drink 8 oz of water or other caloriefree, caffeinefree fluids every hour when awake.
Eat at least 15 g of carbohydrate every hour or 45 to 50 g every 3 to 4 hours (Table 8.18).
Soft foods or liquids may be easier to consume.
When to Call the Doctor
Fever >100 degrees for 24 hours
Persistent hyperglycemia (blood glucose >300 mg/dL)
Persistent diarrhea (more than 8 hours)
Vomiting and unable to take fluids for over 4 hours
Sick for more than 24 hours
Severe abdominal pain, difficulty breathing or confusion
Moderate to large ketones
Acute Complications of Diabetes
Hypoglycemia
Hypoglycemia, or low blood sugar, occurs when the blood glucose level drops too low to provide enough
energy for the body's activities (Table 8.19). In adults or children
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older than 10 years, hypoglycemia is uncommon except as a side effect of diabetes treatment, but it can
result from other medications or diseases, hormone or enzyme deficiencies, or tumors (14).
Table 8.19 Hypoglycemia
Definition Plasma Glucose <70 mg/dL
Signs &
Symptoms
Mild: Hunger, sweating, shakiness, dizziness, lightheadedness, difficulty
concentrating, lack of coordination.
Severe: Frank mental confusion and disorientation, slurred or rambling
speech, extreme fatigue and lethargy, unconsciousness
Causes Excessive insulin or oral medications
Inappropriate timing of insulin in relation to food intake
Inadequate food intake (not eating enough or skipping
meals/snacks)
Prolonged duration or increased intensity of exercise
Alcohol intake without food
1.
Treatment Mild hypoglycemia: 15/15 Rule
Check blood glucose (BG)
If BG is 50–69 mg/dL give 15 ga carbohydrate.
If BG is <50 give 30 g carbohydrate.
1.
Wait 15 min and recheck BG
If BG <70, repeat step 1.
If BG >70, monitor for signs/symptoms of low BG.
Eat next meal or snack within 1 hr.
2.
Severe hypoglycemia:
If able to swallow without risk of aspiration, offer juice or
regular, nondiet soft drink or place glucose gel, honey, syrup, or
jelly inside the person's cheek.
1.
If unable to swallow without risk of aspiration, give glucagon
injection as recommended:
Older children and adults: 1 mg
Children under age 5: 0.5 mg
Infants: 0.25 mg
2.
aSee Table 8.18 for examples of food with 15 g of carbohydrate.
Data from references 3, 8, and 15.
Diabetic Ketoacidosis and Hyperosmolar Hyperglycemic State
Hyperglycemia can lead to diabetic ketoacidosis (DKA) or hyperosmolar hyperglycemic state (HHS), both
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of which are life-threatening conditions. DKA is a state of severe metabolic decompensation manifested by
the overproduction of ketone bodies and ketoacids, resulting in metabolic acidosis (16). DKA is
characterized by severe disturbances in carbohydrate, protein, and fat metabolism, and is most frequently
seen in those with type 1 diabetes (15). HHS is a metabolic derangement most frequently seen in type 2
diabetes and is usually precipitated by illness
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or infection. HHS is similar to DKA except that insulin deficiency is not as prevalent. Table 8.20 gives a
comparison of DKA and HHS.
Table 8.20 Comparison of DKA and HHS
DKA HHS
Age Under 40 years of age Over 60 years of age
Hallmark
Features
Ketosis, ketonuria, metabolic
acidosis, dehydration
Markedly elevated blood
glucose, hyperosmolality,
profound dehydration, no
significant ketosis
Signs &
Symptoms
Polyuria, polydipsia, hyper-
ventilation, dehydration, fruity odor
of ketones, fatigue, blurred vision,
weakness, abdominal pain, nausea,
vomiting
Fatigue, blurred vision, dry
mouth, mental status
changes, coma
Causes Absolute or relative insulin
deficiency
Illness, infection,
noncompliance, and
undiagnosed diabetes are
common precipitating
factors.
Plasma 250–600 mg/dL 600–2,000 mg/dL
Glucose Ketones 4+ <2+
Arterial pH Low Normal
Serum <320 mOsm/kg >320 mOsm/kg
Osmolality
Bicarbonate
Low Normal
Concentration
Treatment
Insulin administration, fluid
resuscitation, correction of
electrolyte imbalance, monitoring
for complications of treatment
Fluid and electrolyte
replacement and insulin
administration
Data from references 10, 15, and 16.
Table 8.21 Common Abbreviations Associated with Diabetes
Abbreviations Term Associated with Diabetes
A1C Hemoglobin A1c, HbA1c, glycohemoglobin, glycated hemoglobin, glycosylated
hemoglobin
ADA American Diabetes Association
DCCT Diabetes Control & Complications Trial
DKA Diabetic ketoacidosis
FPG Fasting plasma glucose
GDM Gestational diabetes mellitus
IFG Impaired fasting glucose
IGT Impaired glucose tolerance
OGGT Oral glucose tolerance test
PPG Postprandial plasma glucose
SMBG Self-monitoring of blood glucose
References
1. Expert Committee on the Diagnosis and Classification of Diabetes Mellitus. Report of the expert
committee on the diagnosis and classification of diabetes mellitus. Diabetes Care 1997;20:1183–1197.
2. Expert Committee on the Diagnosis and Classification of Diabetes Mellitus. Follow-up report on the
diagnosis of diabetes mellitus. Diabetes Care 2003;26:3160–3167.
3. American Diabetes Association. Clinical Practice Recommendations. Diabetes Care 2006;29(Suppl
1):S4–42.
4. American Diabetes Association. Type 2 diabetes in children and adolescents (Consensus Statement).
Diabetes Care 2000; 23:381–389.
5. Carpenter MW, Coustan DR. Criteria for screening test for gestational diabetes. Am J Obstet
Gynecol 1982;144: 768–773.
6. Kulkarni, KD. Carbohydrate counting: a practical meal-planning option for people with diabetes.
Clin Diabetes 2005; 23:120–122.
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7. The 450/500 Rule for determining insulin-to-carbohydrate ratio. Available at:
http://www.diabetes.org/type-1-diabetes/insulin-pumps.jsp. Accessed September 25, 2006.
8. Ackerman P, Williams R, Walters J, et al. Ouick reference guide to diabetes for health care
providers. Michigan Diabetes Outreach Network; 2006.
9. The 1800 Rule for determining your correction factor. Available at: http://www.diabetesnet.com/
diabetes_control_ tips/corr_factor.php. Accessed September 25, 2006.
10. Byetta (exenatide injection) product labeling information. Available at:
http://pi.lilly.com/us/byetta-pi.pdf. Accessed September 20, 2006.
11. Symlin (pramlintide acetate injection) product labeling information. Available at:
http://www.symlin.com/pdf/SYMLIN-pi-combined.pdf. Accessed September 20, 2006.
12. Rohlfing CL, Wiedmeyer H-M, Little RR, et al. Defining the relationship between plasma glucose
and HbA1c: analysis of glucose profiles and HbA1c in the Diabetes Control and Complications Trial.
Diabetes Care 2002;25:275–278.
13. American College of Endocrinology. Consensus statement on guidelines for glycemic control.
Endocrine Pract 2002; 8(Suppl 1)Jan/Feb.
14. Hypoglycemia. Available at: http://diabetes.niddk.nih.gov/ dm/pubs/hypoglycemia/ index.htm.
Accessed August 5, 2007.
15. Mahan LK, Escott-Stump, S. Krause's Food, Nutrition, & Diet Therapy, 11th ed. Philadelphia:
Saunders; 2004:792–833.
16. Haire-Joshu, D. Management of Diabetes Mellitus: Perspectives of Care Across the Life Span. St.
Louis: Mosby-Year Book, Inc.; 1992.
Authors: Width, Mary; Reinhard, Tonia
Title: Clinical Dietitian's Essential Pocket Guide,The: Essential Pocket Guide, 1st Edition
Copyright ©2009 Lippincott Williams & Wilkins
> Table of Contents > Part II - Nutrition Considerations for Specific Diseases > Chapter 9 - Gastrointestinal Disease
Chapter 9
Gastrointestinal Disease
Considering the importance of the gastrointestinal tract's (GI) key roles in maintaining life and health, it
becomes clear as to how profoundly GI diseases can affect nutritional status, and ultimately overall health.
Nutritional problems can arise from both upper gastrointestinal tract diseases (UGI), which includes the
esophagus and stomach, and lower gastrointestinal tract disease (LGI), which includes the small intestine
and the large intestine. These problems can be caused by the underlying disease process itself, or as a
consequence of prescribed dietary regimens, and or self-imposed restrictions. For these reasons, the
registered dietitian (RD) must conduct a comprehensive nutritional assessment, with particular focus on a
detailed diet history, and plan highly individualized interventions.
Diseases of the Upper Gastrointestinal Tract
Diseases of the UGI with nutritional relevance include ulcers and gastroesophageal reflux disease.
Medications have become increasingly important in both healing of damaged tissue and disease
management. Although diet does not cause either disease, it may require alteration to
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ameliorate symptoms of the disease process or as a result of surgical intervention.
Gastroesophageal Reflux Disease
Disease Process
Gastroesophageal reflux is the process in which acid from the stomach refluxes up into the esophagus, and
esophagitis is the resultant inflammation of the sensitive tissue of the esophagus. Acute esophagitis can be
caused by ingesting a caustic compound, often a medication, such as nonsteroidal anti-inflammatory drugs
(NSAIDs), and it can arise from repeated vomiting, especially when self-induced as in anorexia and bulimia.
Chronic reflux is termed gastroesophageal reflux disease (GERD) and increases risk for Barrett's esophagus,
a precancerous condition (1).
Many factors affect lower esophageal sphincter (LES) pressure and, therefore, its opening and closing,
including:
Hormones
Nutrients
Medications
High abdominal pressure, as with:
Chronic lung disease
Lying down after meals
Substances such as caffeine, mint, cigarettes, alcohol, and chocolate
Treatment and Nutritional Intervention
Treatment for GERD includes diet and lifestyle changes, medications, and, failing these, surgery. Physicians
often prescribe medications that reduce gastric acidity, which include antacids, H2 receptor antagonists,
and proton pump inhibitors. Reducing acidity of the gastric contents renders the reflux fluid less caustic.
Other types of drugs, such as metoclopramide and cisapride, increase gastric emptying rate.
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Table 9.1 Factors Affecting LES Pressure in GERD
Reduce Pressure (Open) Increase Pressure (Close)
Alcoholic Beverages Dietary Protein
Caffeine
Chocolate
Cigarettes Medications
Dietary fat Bethanechol
Mint oils Metoclopramide
High Pressure on Stomach
Overeating, drinking
Hormone level
Progesterone (pregnancy, late phase of menstrual cycle)
Medications
Anticholinergics: Atropine, Bentyl, Robinul, Scopolamine)
Bronchodilators: Albuterol (Proventil, Ventolin); Metaproterenol (Alupent);
Montelukast (Singulair); Terbutaline (Brethine) Theophyllin (Aerolate, Slo-Bid, Slo-
Phyllin, Theo-24, Theo-Dur, Theolair, Uniphyl); Zafirlukast (Accolate)
Table 9.2 Medications for GERD
Generic Names and Brand Names by Category
Antacids (see Table 9.6)
Aluminum hydroxide (Amphogel, Alternagel,a Dialume
Calcium carbonate (Tums)
Magnesium hydroxide (Mag-Ox 400, MOM (milk of magnesia)
Combinations of above (Gelusil,a Maalox, Mylanta/IIa)
Magaldrate (Riopan Plusa)
GI Stimulants
Metoclopramide (Reglan)
H2 Receptor Antagonists/Proton Pump Inhibitors
Cimetidine (Tagamet)
Famotidine (Pepcid)
Lansoprazole/Prevacid
Nizatidine (Axid)
Omeprazole (Prilosec)
Ranitidine (Zantac)
Roxatidine (Roxin)
aAlso contain simethicone.
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Table 9.3 Medications and Substances that Slow Gastric Emptying
Medications
Calcium Channel Blockers
Adalat, Calan, Cardene, Cardizem, DynaCirc, Isoptin, Nimotop, Norvasc, Plendil, Posicor,
Procardia, Sular, Vascor, Verelan
Opiates/Opioids
Alfenta, Buprenex, codeine, Dalgan, Darvon, Demerol, Dilaudid, Dolophine, Levo-dromoran,
Nubain, Roxicodone, Sublimaze, Sufenta, Talwin, Ultiva
Tricyclic Antidepressants
Anafranil, Adapin/Sinequan, Aventyl/Pamelor, Janimine/Tofranil, Vivactil,
Norpramin/Pertofrane
Other Substances
Alcohol
Marijuana
Tobacco
Patient Education
Dietary considerations for GERD focus on three objectives (2):
Prevent pain and irritation in the esophagus during a flare-up
Prevent reflux
Lower the acidity of the stomach's contents
Achievement of these objectives involves manipulating dietary aspects that affect LES pressure, reducing
gastric acid secretion, and avoiding tart or acidic foods and irritating spices in a flare-up. Smoking exerts a
wide range of GI effects, most of which worsen GI problems (3). Antacids are the most effective way to
reduce gastric acidity and should be taken about 1 to 3 hours after a meal for maximal acidity reduction.
Peptic Ulcer Disease
Disease Process
Peptic ulcer disease (PUD) is the collective term for ulcers, eroded areas of tissue in either the stomach or
the
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duodenum. The erosion arises from the stomach's own acid and protein-digesting enzyme pepsin. The stress
of severe illness or trauma can produce ulcers, termed stress ulcers. The past decade has witnessed the
advent of effective treatments for PUD, but the disease still causes life-threatening complications,
including perforation, bleeding, and obstruction. Of nutritional concern, PUD often results in unnecessary
dietary restriction and concomitant
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reduction in essential nutrients. In addition, pain and other GI symptoms may affect food intake and
compromise nutritional status. A breakthrough came in the 1990s with the discovery that the bacterium
Helicobacter pylori was responsible for half of all PUD cases (4).
Table 9.4 Dietary and Other Recommendations for GERD
Diet to Prevent Reflux Other Treatment Aspects Diet in Acute Esophagitis
Eat small frequent meals,
avoid large meals
Avoid single high-fat meals
Eat low-fat, higher protein
meals
Limit alcohol
Avoid foods that lower LESa
pressure: chocolate, coffee,
mints, garlic, onions,
cinnamon
Avoid drinking liquids with
meals; drink between meals
Don't lie down
after eating
(wait 3 hrs)
Elevate the
head of the
bed, if needed
Limit or avoid
smoking
Use antacids to
lower gastric
acidity
Avoid acidic foods
(citrus fruits,
tomatoes)
Avoid spicy foods
(red, black
pepper)
Follow a bland,
soft diet
Eat small
frequent meals
aBase on individual experience.
Adapted from reference 2.
Table 9.5 Effects of Smoking on the GIT
Increases acid secretion
Reduces LES pressure (opens)
Inhibits bicarbonate secretion from pancreas
Increases gastric emptying of liquids
Increases acidity in duodenum
Interferes with the action of some GI drugs
Impairs healing of ulcers
Adapted from reference 3.
Table 9.6 Types and Effects of Antacids
Types of Antacids
Four Main Types, Containing a Mineral-based Compound
Aluminum; magnesium; sodium; calcium
Mechanism of Action
All antacids act in the stomach to lower the acidity level; factors that can affect the
amount of acid lowering include the antacid's dose and form and the presence of
food in the stomach.
Antacids prevent reflux and make stomach contents less irritating if reflux occurs
Potential Problems with Chronic Antacid Use
All antacids may interfere with other medications; always take antacids 2 hrs before
or after taking other medications
By lowering gastric acidity, they interfere with the absorption of nutrients (iron,
vitamin B12)
Calcium antacids may be useful for women in helping to increase calcium intake and
preventing osteoporosis, but they may cause kidney stones and lower blood levels of
magnesium and phosphorus
Magnesium antacids can cause severe diarrhea
Aluminum antacids can cause severe constipation, low blood levels of phosphorus,
and adult rickets
Sodium antacids can cause water retention, increase blood pressure in salt-sensitive
people, and lower iron absorption
Gastric Ulcers and Duodenal Ulcers
Gastric ulcers are often the result of chronic use of medications that irritate the mucosa, such as NSAIDs.
On discontinuation of the drug, the ulcers heal and usually do not reoccur. People with gastric ulcers tend
to have normal to low-acid levels, so the development probably involves weakened defenses (5). In
contrast, 66% of people with duodenal ulcers have a high level of acid secretion, even in a nonstimulated
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state, such as fasting or sleeping. Gastric ulcers are associated with an increased risk for stomach cancer
and mortality, and duodenal ulcers are not. Diagnostic tests for PUD can include endoscopy, x-rays with
contrast, analysis of stomach secretions, and blood tests.
Table 9.7 Nonsteroidal Anti-inflammatory Drugs
Aleve/Anaprox
Aspirin
Ansaid
Arthropan
Clinoril
Daypro
Dolobid
Duract
Feldene
Indocin
Lodine
Magan
Motrin
Meclomen
Motrin
Nalfon
Naprosyn
Orudis
Relafen
Sodium salicylate
Tolectin
Toradol
Voltaren
Treatment and Nutritional Intervention
The history of PUD treatment is replete with regimens that were logical but ineffective to the nutrient-
deficient and potentially dangerous (4). Current treatment for PUD centers on determining the cause of the
disease, and when it exists, eradicating H. pylori. The foods and substances to avoid are those that may
irritate the mucosa or increase acid secretion. Avoiding smoking is another important aspect of lifestyle
change for treating PUD (2,3).
Other aspects of treatment include a variety of medications to accomplish the objectives of eradicating H.
pylori if present, reducing acid secretion and gastric acidity, and
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promoting ulcer healing. Surgery is sometimes needed because of complications such as perforation,
obstruction, or cancer. After surgery, nutritional problems can arise, such as nutrient malabsorption, poor
food intake, and weight loss. Surgery can cause dumping syndrome, which often leads to all these
nutritional problems.
Table 9.8 Diagnostic Tests for Peptic Ulcer Disease
Endoscopy1.
Upper GI (barium swallow with x-ray)2.
Gastric analysis3.
Blood tests, to detect:
Anemia (hemoglobin, hematocrit, mean cell volume, and mean cell
hemoglobin)
H. pylori
4.
Table 9.9 Treatment Objectives and Diet for Peptic Ulcer Disease
Objectives
Eradicate H. pylori infection if present1.
Reduce gastric acidity and gastric secretion2.
Avoid gastric irritants3.
Promote ulcer healing4.
Diet/Nutritional and Other Recommendations
Individualize the diet, or follow bland diet if preferred1.
Check for anemia (from bleeding ulcer), correct if exists2.
Check for B12 deficiency; correct if exists3.
Avoid large meals (distend the stomach)4.
Avoid excessive alcohol, coffee/decaffeinated use5.
Avoid cigarette smoking6.
Include extra protein and vitamin C to promote healing7.
Dumping Syndrome
Disease Process
The major nutritional complication, dumping syndrome, is a group of symptoms that result from rapid
emptying of undigested food into the jejunum from the stomach. Some people experience two different
phases of dumping syndrome, early and late; others only have one phase, and some have both. The early
phase develops within 20 to 90 minutes
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after eating and consists of gastrointestinal and vasomotor symptoms. The cause of late dumping is
hypoglycemia.
Table 9.10 Gastric Irritants and Gastric Acid Stimulants
Possible Gastric Irritants Gastric Acid Stimulants
Pepper (all types; red, black,
white)
Chili powder, curry powder
Alcohol
Regular and decaffeinated coffee
Frequent meals (3 meals
preferred)
Table 9.11 Common Medications in Peptic Ulcer Disease
Antacids (see Table 9.6)
Antibiotics (if H. pylori present)
Ulcer Drugs
H2 antagonists (cimetidine/Tagamet, famotidine/Pepcid, ranitidine/Zantac,
Nizatidine/Axid)
Omeprazole/Prilosec, lansoprazole/Prevacid
Sucralfate/Carafate
Misoprostol/Cytotec
Treatment and Nutritional Intervention
The treatment for dumping syndrome is the postgastrectomy diet or antidumping diet and may include
drugs to slow gastric emptying (2). Functional lactose intolerance tends to be a common problem after
surgery.
Table 9.12 Surgery for Peptic Ulcer Disease
Truncal Vagotomy and Pyloroplasty
The truncal vagotomy cuts the main trunks of the vagus nerve on each side of the distal
esophagus; it eliminates nerve-induced secretion of acid; it also reduces contractions and
delays gastric emptying. To offset these effects, the pyloroplasty is also done. In the
pyloroplasty, the pylorus is surgically altered so that it can act as a barrier to contents of the
stomach as it empties. The result is that liquids empty more quickly, but solids take longer.
Truncal Vagotomy and Antrectomy
This procedure is more aggressive, because the antrectomy connects the antrum and pylorus.
When the antrum is altered, the portion of the stomach that secretes gastrin (hormone which
stimulates all gastric secretions) is removed. The two surgical procedures for attaching the
remaining stomach to the intestine, Billroth I and Billroth II.
Highly Selective Vagotomy (proximal gastric vagotomy)
This procedure reduces gastric acid secretion but doesn't interfere with motility (i.e., the
stomach's movement). This prevents problems related to gastric emptying (i.e., dumping
syndrome).
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Table 9.13 Postgastrectomy Dietary Recommendations
Foods to Avoid
Concentrated sweets (i.e., soft drinks, juices, pies, cakes, cookies, desserts made
with sugar)
Foods containing lactose (i.e., milk, milk products, cream soups, ice cream)a
Dietary Recommendations
Obtain 30%-40% of kilocalories from fat
Obtain 20% of kilocalories from protein
Obtain 50%-60% of kilocalories from carbohydrates.
Only 0%-15% of kilocalories should come from simple sugars.
Consume 3 g of sodium or less daily.
Increase intake of fiber, especially pectin (found in fruits and vegetables, especially
apples and citrus fruit).
Use artificial sweeteners for beverages and desserts.
Behavior Modifications
After surgery, avoid eating until the function of the GI tract returns.1.
Begin with sips of water at room temperature or allow ice chips to melt in mouth.2.
Proceed to a clear liquid diet.3.
When tolerated, begin a full liquid diet.4.
As solids are introduced, begin with small amounts of soft, starchy, low-fat, low-
protein foods.
5.
Eat small frequent meals.6.
Avoid large amounts of liquids with meals. Take fluids 1-2 hours before or after
meals.
7.
Avoid activity and lie down for 1 hr after meals.8.
Avoid extremes in food temperature.9.
Possible Diet and Surgery-Induced Deficiencies
Iron
Calcium
Vitamin D
Riboflavin
Folacin
Vitamin B12
aSome aged cheeses and unsweetened yogurt may be tolerated.
Adapted from reference 2.
Diseases of the Lower Gastrointestinal Tract (LGI)
Diseases of the LGI include diverticular disease, irritable bowel syndrome (IBS), inflammatory bowel disease
(IBD), and celiac disease. The LGI's role in digestion and
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absorption increase the potential for adversely affecting nutritional status with any disease, but particularly
with IBD and celiac disease.
Diverticular Disease: Diverticulosis and Diverticulitis
Disease Process
Diverticular disease is the presence of small herniations of the colon, most often the sigmoid colon, which
form pouches. The presence of the pouches is diverticulosis, and when the pouches become inflamed and or
infected, it is termed diverticulitis. Life-threatening complications can occur in diverticulitis, such as pouch
rupture, which causes bleeding and can lead to sepsis and obstruction.
Current theory of etiology suggests that diverticulosis is caused by a combination of high pressure inside the
colon and a weakening in the organ's musculature (6). Factors that may increase intracolonic pressure and
or weaken musculature include:
Emotional stress
Constipation, especially with straining
Reduced GI motility
Increased transit time
From a nutritional standpoint, the major dietary constituent that most likely affects several of these factors
is a low-fiber diet.
Treatment and Nutritional Intervention
If a person has had diverticulitis in the past, future flare-ups, if not too severe, can often be treated at
home; rest, fasting at first and then a clear liquid diet, and antibiotics. As the symptoms subside, usually
within a few days, nutrition therapy consists of a soft, low-fiber diet (2). After 4 to 6 weeks, a high-fiber
diet is the recommendation for diverticulosis.
In the hospital, severe diverticulitis warrants complete bowel rest and only small sips of water or ice chips.
As
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the inflammation subsides, the diet progresses to clear liquids. It may be necessary to provide nutrition
support, either parenteral or a basic enteral formula, if the person is acutely ill and nutritionally
compromised. For most patients, antibiotics and bowel rest alleviate symptoms within 2 to 5 days. After a
clear liquid, patients progress to a bland or GI soft diet, with no nuts, seeds, or fibrous vegetables. The diet
is low-fiber for up to one month, after which the patient should consume a high-fiber diet.
Table 9.14 Dietary Recommendations for Diverticulitis and Diverticulosis
During acute flare-ups of diverticulitis which require hospitalization
Follow a low-residue diet. Oral elemental diet (AlitraQ, Subdue) or total parenteral
nutrition may be required.
1.
Proceed to a clear liquid diet.2.
As food is tolerated, begin a bland diet.3.
In cases of acute diverticulitis at home, avoid nuts, seeds, fruit/vegetable, skins, fibrous
vegetables, excessive fiber, highly spiced foods
For diverticulosis (after diverticulitis has subsided)
Consume 6-11 servings of whole grain bread, cereals, flours, and other whole-grain
products daily.
1.
Consume 5-8 servings of fruits and vegetables daily, especially legumes, raw fruits
with skins, dried fruits, raw vegetables (carrots, celery), and vegetables with skins
(potato).
2.
Consume 25 g of fiber daily.3.
Consume 2 quarts of water daily (eight 8-oz glasses)4.
Reduce fat intake.5.
Adapted from reference 2.
Irritable Bowel Syndrome
Disease Process
Irritable bowel syndrome (IBS), also called spastic colitis, is one of the most common disorders of the colon,
accounting for up to 40% of visits to a gastroenterologist (7). Symptoms vary and include abdominal
cramping and pain, bloating, flatulence, alternating bouts of both
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constipation and diarrhea or only one of these. The cause of IBS is unknown, but one theory suggests that
people with IBS respond in an exaggerated way to certain stimuli that would only cause a mild response or
none at all in a person without the disorder. Possible stimuli include dietary overindulgences, emotional
stress or trauma, medications, hormones, and intolerance to specific substances in foods. Diagnosis is made
by ruling out other LGI diseases and on the basis of ongoing symptoms for a period of 3 months.
Table 9.15 Fiber Content of Foods
Food Serving Fiber (g)
Bread: whole wheat 1 slice 2
Cereal, bran 1oz 2
Cereal, cooked oatmeal ½ cup 2
Fruit: apple, banana, kiwi, pear 1 med. 2
Legumes: cooked baked beans, kidney beans, navy beans ½ cup 8
Legumes:garbanzo, lima beans, lentils, split peas ½ cup 5
Vegetables: cooked broccoli green beans, corn, winter squash
raw carrots, peppers
½ cup
½ cup
3
3
Treatment and Nutritional Intervention
Treatment of IBS Centers on Diet and Lifestyle
Lifestyle changes emphasize establishing regular eating patterns, regular bowel habits, and stress reduction
and management. Medications may include bulk-forming laxatives, antispasmodic drugs, and tranquilizers.
To determine if specific foods are provoking flare-ups, an elimination and reintroduction approach can be
helpful, even more so than probiotics (10). Up to 40% of IBS sufferers are lactose intolerant, and other
common problematic foods include caffeine, alcohol, gas-forming vegetables, and wheat or yeast (11).
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Table 9.16 Recommendations for Irritable Bowel Syndrome
In cases of acute irritable colon, an elemental diet may be necessary (Criticare,
Subdue, AlitraQ).
1.
Progress to a soft, bland diet when tolerated.2.
Progress to a high-fiber diet slowly to avoid discomforts such as bloating and
flatulence.
3.
Foods to avoid: alcohol; black pepper; caffeine; chili powder; cocoa/chocolate;
coffee; colas; garlic; red pepper; spicy foods; sugars (especially fructose and lactose)
and sorbitol
4.
Avoid gas-producing foods (apples, artichokes, asparagus, avocados, barley, beer,
bran, broccoli, brussels sprouts, cabbage, carbonated beverages, cauliflower, celery,
coconut, cream sauces, cucumbers, eggplant, eggs, figs, fish, fried foods, garlic,
gravy, high-fat meats, honey, kohlrabi, leeks, lentils, legumes, mannitol, melons,
milk, molasses, nuts, onions, pastries, peppers, pimentos, prunes, radishes, raisins,
rutabaga, sauerkraut, scallions, shallots, sorbitol, soybeans, turnips, wheat, and
yeast).
5.
Avoid lactose if not tolerated (see Table 9.13).6.
Avoid wheat or yeast if not tolerated.7.
Common food allergies include chocolate, dairy products, wheat, yeast, and eggs.8.
Avoid excess fat (see low-fat diet).9.
Drink 2–3 quarts of water daily; Consume 20–30 g of fiber daily.10.
1 Tablespoon of a bulking agent, such as Metamucil, daily may be helpful. Bran may
be irritating.
11.
Probiotics may be useful.12.
Supplement with B-complex vitamins, calcium, vitamin D, and riboflavin (if lactose is
not tolerated).
13.
Dietary/Behavior Modifications
Eat small, frequent meals.
Eat at a relaxed pace and at regular times.
Avoid constipation.
Exercise regularly.
Use of products such as Bean-O may be helpful.
Biofeedback, relaxation, and stress-reduction techniques may be helpful.
Identify food sensitivities and omit offending foods.
Possible Modified Diet-Induced Deficiencies
Calcium
Vitamin D
Riboflavin
B vitamins
Adapted from reference 2.
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Patient Education
Dietary changes focus on eating small frequent meals at regular and consistent times, gradually increasing
fiber intake, ensuring adequate fluid intake, and avoiding any foods that cause problems. In addition to an
elimination diet to find problem foods, a person with IBS can keep a food diary to record food and beverage
intake and see if flare-ups are associated with certain foods.
Inflammatory Bowel Diseases
Disease Process
Inflammatory bowel disease (IBD) consists of two chronic diseases: Crohn's disease (CD) and ulcerative
colitis (UC), which both produce inflammation of the intestine. Both diseases tend to cause nutrient
malabsorption leading to malnutrition, and both can cause life-threatening complications (2). Several
aspects of the diseases are similar, making differential diagnosis difficult, but each also has its own pattern
of attack.
One significant difference between the two diseases is that surgery, which is often a necessity, can cure
ulcerative colitis by removing the entire colon. In contrast, having a surgery for CD increases the risk for
more surgeries, and the disease has no cure (11). The cause of IBD is unknown, although studies have shown
links to genetics, environmental toxins, infections, and autoimmune disorders.
Crohn's Disease
CD is also known as regional enteritis, granulomatous ileitis, and ileocolitis. It can strike anywhere in the GI
tract, from mouth to anus; however, it demonstrates a predilection for the terminal ileum. Complications
include obstruction, fissures, and fistulas, which increase the risk for mortality. The nutritional problems in
CD are potentially more severe compared to UC, because the small intestine is more often involved.
Another nutritional concern is the severe diarrhea, often steatorrhea from fat malabsorption. In addition to
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direct nutrient malabsorption, people with CD experience abdominal pain and other GI symptoms, which
decrease appetite and worsen after eating. This may cause a person to be afraid to eat, reducing their
nutrient and energy intake and further worsening malnutrition.
Table 9.17 Differentiation Between Crohn's Disease and Ulcerative Colitis
Parameter Ulcerative Colitis Crohn's Disease
Age at onset 15–30 years 15–30 years
Organ involved Rectum, sigmoid colon, colon
only
Ileum, small intestine, entire
GIT
Tissue layers Surface membrane All layers
Distribution of
disease
In segments Continuous
Cancer risk Higher, after 10 years No increased risk
Rectal bleeding Common Occasional
Steatorrhea No Common
Diarrhea Yes, frequent Yes, frequent
Vomiting Yes Yes
Nutritional Problems
Protein Lost due to diarrhea,
inflammation, poor intake
Lost due to diarrhea,
inflammation, poor intake
Fat No problem Malabsorption
Vitamin B12 No problem Yes, if terminal ileum
Vitamins A, D, E,
K
Yes; medications interfere Yes; medications and
malabsorption
Copper, zinc,
selenium
Yes; losses from diarrhea Yes; losses from diarrhea plus
malabsorption
Treatment and Nutritional Intervention
Treatment for CD depends on phase of the disease, and if during a flare-up, its severity. Treatment during a
flare-up revolves around countering the inflammation, treating symptoms of pain and diarrhea, and
preventing stimulation and irritation of the GI tract. Corticosteroids are used to reduce inflammation in a
CD exacerbation, and when used, a low-sodium diet can be helpful to prevent fluid
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retention (2). Parenteral nutrition may be necessary in severe cases, although small monomeric/elemental
enteral feedings may be tolerated.
Table 9.18 Medications in the Treatment of Crohn's Disease
Problem Medications
Diarrhea,
cramping
Diphenoxylate, loperamide, deodorized opium tincture, or codeine;
psyllium laxatives help diarrhea and constipation by firming stool
Infection Broad-spectrum antibiotics; metronidazole (antibiotic which helps relieve
Crohn disease, especially fistulas and anal abscesses)
Inflammation Prednisone (corticosteroids) for flare-ups, sulfasalazine, mesalamine,
olsalazine (to help prevent flare-ups)
Patient Education
Between flare-ups in remission periods, an optimally nutritious diet is important. This can help prevent
nutrient deficiencies when a flare-up arises,
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with the significant nutrient malabsorption that attends it. Nutrients of concern include:
Table 9.19 Dietary Recommendations for Crohn's Disease
In acute flare-up, or with obstruction, fistulas
A low-residue diet, elemental diet, or total parenteral nutrition may be required.
During the acute phase of Crohn's (once an oral diet is tolerated)
Foods to avoid
High-fiber foods such as nuts, seeds, fruit/vegetable skins, and fibrous vegetables
Foods suspected of causing intolerance
Alcohol
Caffeine and caffeine-containing beverages (cocoa, coffee, cola, tea)
Decaffeinated coffee and tea
Pepper and spicy foods
Reduce lactose if not tolerated (see Table 9.13)
If fat malabsorption exists, limit high-fat foods (see low-fat diet)
Avoid wheat/gluten if not tolerated (see celiac disease diet)
If corticosteroids are used in treatment, avoid excessive salt (limit to 2 g of sodium
per day, see low-sodium diet)
Adapted from reference 2.
Protein
Vitamins C, A, D, E, K, folate, B6, and B12
Minerals iron, zinc, copper, calcium, potassium, and magnesium
Functional lactose intolerance is common. In summary, careful attention to nutritional status and ensuring
a nutritious diet, especially a high-protein diet, during periods of remission can help prevent nutrient
deficiencies after flare-ups.
Table 9.20 Dietary Recommendations for Crohn's Disease in Remission
1. Try to consume:
6–11 servings of whole grain bread, cereals, flours and other whole-grain products daily
5–8 servings of fruits and vegetables daily, especially legumes, raw fruits with skins, dried
fruits, raw vegetables (carrots, celery), and vegetables with skins (potato)
25 g (females), 38 g (males) fiber daily
2 quarts of water daily (eight 8-oz glasses)
1–1.5 g/kg protein daily
30–40 kcal/kg body weight for adults
80–100 kcal/kg body weight for children; 60-80 kcal/kg body weight for teens
80–100 kcal/kg body weight for children; 60-80 kcal/kg body weight for teens
Higher intake of omega-3 fatty acids from foods (fish, especially mackerel and tuna) or through
supplements
2. Choose a vitamin/mineral supplement that includes:
Vitamins A, D, E, K, B6, B12, iron, zinc, copper, calcium, potassium, folate, and magnesium.
Selenium supplementation may be needed with resections >200 cm
3. If corticosteroids are used in treatment:
Increase potassium intake (bananas, oranges, orange juice, potatoes, legumes, fruits, and
vegetables)
4. If antidiarrheals are used in treatment:
Increase fluid intake to 2 L (2 quarts) per day
5. Suggested nutritional therapies include:
Antioxidants, fermentable fibers, medium-chain triglycerides (MCT oil), omega-3 fatty acids,
short-chain fatty acids, and specific amino acids such as glutamine
6. Commonly noted exacerbating factors in Crohn's disease include:
Increased sucrose (sugar) intake; lack of fruits and vegetables; low-fiber intake; altered N-6: N-
3 fatty acid ratios
7. Dietary/Behavior Modifications:
Eat small, frequent meals.
Chew food well; avoid swallowing air.
Note food intolerance and eliminate only those foods known to consistentlycause distress.
For extra kilocalories, drink small amounts of isotonic liquid oral supplement (Osmolite, Isocal)
throughout the day.
Possible Modified Diet-Induced Deficiencies:
Fiber (in acute phase); calcium; vitamin D; riboflavin; fat-soluble vitamins (A, D, E, K)
B vitamins
Adapted from reference 2.
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Ulcerative Colitis
Disease Process
Although symptoms are similar to CD, UC typically strikes the sigmoid segment of the colon, with extensive
involvement of the rectum. It often spreads further up throughout the colon so that the entire organ may
be affected, but it never involves the small intestine. Complications in UC are as severe as those for CD,
including toxic colitis in which the organ begins to dilate. The dilation can happen in hours or days, and
when severe, it is termed toxic megacolon, which can lead to perforation. Rectal bleeding is a common
problem that often causes iron-deficiency anemia. Other nutritionally relevant problems include:
Protein losses
Electrolyte disturbances
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Dehydration
Anorexia
Weight loss
In contrast to CD, most of the nutritional problems are not directly due to malabsorption. The diagnosis is
made on the basis of a sigmoidoscopy, and this test also indicates the UC severity.
Treatment and Nutritional Intervention
Treatment for UC is similar to that for CD, with the goals of countering the inflammation, alleviating
symptoms, and correcting dehydration and nutrient deficiencies (2). And as with CD, when the disease is in
remission, a high-protein, nutrient-dense diet is the best approach to stave off nutritional problems
between flare-ups. If the disease affects the descending colon, enemas containing corticosteriods or
mesalamine help to reduce symptoms. Enemas containing short chain fatty acids (SCFA) are also useful by
promoting tissue healing (12,13).
Celiac Disease
Disease Process
Celiac disease has several other aliases, including nontropical sprue, gluten-induced sprue, gluten-induced
enteropathy, and gluten-sensitive enteropathy. It is characterized by
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malabsorption of nutrients, which is caused by genetic sensitivity of mucosal cells in the small intestine to
various compounds in grain proteins. In wheat, the compound is gliadin, one of two protein components of
the main protein gluten, which gives flour its elastic qualities. Similar compounds in other grains include
(14):
Table 9.21 Dietary Recommendations for Ulcerative Colitis
During acute phases of ulcerative colitis:
Total parenteral nutrition (when large portions of the colon are surgically removed).
Oral elemental diet of products such as Subdue, AlitraQ, or EleCare that include short chain
fatty acids, glutamine, vitamin E, and omega-3 fatty acids.
During the acute phase of ulcerative colitis (once an oral diet is tolerated):
Follow a low-fiber diet and avoid high-fiber foods such as nuts, seeds, coarse grains, legumes,
fruit/vegetable skins, and fibrous vegetables.
Table 9.22 Other Dietary and Behavioral Changes for Ulcerative Colitis
Avoid foods known to cause diarrhea.1.
Avoid extremes in food and beverage temperatures (avoid iced beverages).2.
Avoid carbonated beverages.3.
Eat small, frequent meals; stop eating 2–3 hr before bed.4.
Eat slowly; chew well.5.
If corticosteroids are used in treatment: follow low-sodium diet; increase potassium
intake (bananas, oranges, orange juice, potatoes, legumes, fruits, and vegetables).
6.
Consume 2 quarts of water daily (eight 8-oz glasses).7.
Consume 1-1.5 g/kg protein daily.8.
Increase intake of omega-3 fatty acids from foods (fish, especially mackerel and
tuna) or through supplements.
9.
Choose a vitamin/mineral supplement that includes thiamin, vitamin E, iron, zinc,
calcium, potassium, and folacin.
10.
The following foods are suspected of causing intolerance; avoid if they have an
adverse effect:
alcohol; caffeine and caffeine-containing beverages (cocoa, coffee, cola, tea);
decaffeinated coffee and tea; pepper and spicy foods; reduce lactose if not
tolerated (see Table 9.13). If fat malabsorption exists, limit high-fat foods (see low-
fat diet); avoid wheat/gluten if not tolerated.
11.
Possible deficiencies, if lactose is not tolerated: calcium, vitamin D, riboflavin
Adapted from reference 2.
Table 9.23 Short Chain Fatty Acids
Definition
Compounds consisting of 6 carbons or less; eating soluble fiber helps to generate them in the
colon.
Mechanism of Actions
Increase acidity of the colon.
Limit colon cell's absorption of ammonia.
Promote bacterial growth in the colon
Potential Therapeutic Effects
Higher acidity in the colon lowers the breakdown of bile acids (potential
carcinogens).
Protect colon cells from cancerous changes.
More bacteria can convert toxic compounds to harmless forms.
Enemas containing butyrate, a short chain fatty acid, may help prevent flare-ups in
ulcerative colitis.
Adapted from reference 12.
Hordein in barley
Secalin in rye
Avidin in oats
Risk factors include genetics, Down syndrome, type 1 diabetes, and chronic arthritis in childhood.
Lymphoma is a possible complication (15). Symptoms include abdominal bloating, pain, diarrhea, and the
disease can be diagnosed with a blood test for gliadin antibodies and biopsy. Nutritional problems are
numerous, with malabsorption of several nutrients, and the following problems often arise (16):
Weight loss
Low serum albumin
Anemia
Bone disease due to malabsorption of:
Calcium
Phosphorus
Magnesium
Vitamin D.
Treatment and Nutritional Intervention
The treatment for celiac disease is elimination of gliadin/ gluten from the diet, which must be done as soon
as possible to prevent extensive damage to the intestine (2). Some patients with either a more severe or
long-standing case may not respond to dietary intervention, and corticosteroids become necessary. As with
IBD, damage of the intestinal tissue may necessitate the removal of the affected sections of the small
intestine. And as with CD, this poses nutritional concerns because of the small intestine's role in
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nutrient digestion and absorption. In contrast to CD, however, removal of the toxin from the diet precludes
further need for surgery. If a sufficient amount of small intestine is removed, this may cause short bowel
syndrome.
Patient Education
The patient must avoid all sources of gluten in the diet, with the most obvious being foods that contain
wheat, oats, rye, and barley. However, the patient must also learn to read food labels for ingredients made
from parts of one the grains including cereal, starch, flour, thickening agents, emulsifiers, stabilizers,
hydrolyzed vegetable proteins, caramel coloring, and monosodium glutamate.
Table 9.24 Foods to Avoid in Celiac Disease
Breads, Cereals, and Grains
Gluten, wheat, whole wheat flour, enriched flour, soft wheat flour, high-gluten
flour, high-protein flour; all flour containing wheat, oat, rye, or barley, bran,
graham, wheat germ, malt, kasha, bulgur, spelt, kamut, triticale, couscous, farina,
seitan, semolina, durum, durum flour, groats, millet, whole wheat berries, and
wheat starch
Commercially prepared mixes for biscuits, cornbread, muffins, pancakes, and waffles
Pasta, regular noodles, spaghetti, macaroni, and most packaged rice dishes
Bread crumbs, cracker meal, pretzels, and matzo
Gelatinized starch, which may contain wheat protein
Milk/Dairy
Malted milk, Ovaltine; any cheese product containing oat gum, chocolate milk with
cereal additive
Some sour cream, some yogurt, some nondairy creamers
If lactose tolerance is altered (see Table 9.13)
Meat/Fish/Poultry
Meats prepared with wheat, oat, rye, or barley (bologna, chili, hot dogs, luncheon
meats, and sandwich spreads)
Creamed meats, breaded or bread-containing products (i.e., croquettes, Swiss steak,
and meat loaf)
Meats injected with hydrolyzed vegetable protein
Tuna in vegetable broth, meat, or meat alternatives containing gluten stabilizers
Eggs in sauces with gluten
Fruits and Vegetables
Breaded or creamed vegetables, or vegetables in sauce
Some canned, baked beans
Some commercially prepared vegetables and salads
Thickened or prepared fruits, some pie fillings
Fats/Oils and Sweets
Some commercially prepared salad dressings
Some commercial candies, chocolate-coated nuts
Commercial cakes, cookies, pies, and doughnuts made with wheat, rye, oat, or
barley
Prepared dessert mixes including cookies and cakes
Puddings thickened with wheat flour
Ice cream or sherbet with gluten stabilizers; ice cream containing cookies, crumbs,
or cheesecake; ice cream cones
Alcohol
Ale, beer, gin, whiskies, vodka distilled from grain
Miscellaneous
Herbal teas with malted barley or other grains with gliadin (see: Bread/Cereal/Grain
list)
Most canned soups, cream soups and soup mixes, bouillon
Some curry powder, dry seasoning mixes, gravy extracts, meat sauces, catsup,
mustard, horseradish, soy sauce, chip dips, chewing gum, distilled white vinegar,
cereal extract, cereal beverages (Postum), root beer, yeast extract, malt syrup, malt
vinegar, and commercial infant dinners with flour thickeners
Caramel color and MSG may not be tolerated.
Adapted from reference 2.
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Intestinal Surgery: Short Bowel Syndrome and Ostomies
Disease Process
Several of the diseases from the previous chapters, and intestinal cancer, may necessitate intestinal
surgery. Many nutritional problems may arise depending on how much intestine is lost: more than 40% of
the small intestine
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produces nutrient malabsorption termed short bowel syndrome (SBS) and more than 75% of the small
intestine is associated with a high mortality rate (17,18).
Table 9.25 Dietary Recommendations for Celiac Disease
Celiac disease requires total avoidance of gluten—wheat, oat, rye, and barley.1.
Allowable foods include corn flour, corn meal, cornstarch, rice, rice flour, potato
flour, soybean flour, tapioca, sago, arrowroot, glutenfree wheat starch, and lima
bean flour.
2.
Obtain 1–2 g of protein per kilogram of body weight daily (about 80–120 g for adults).3.
Obtain 35–40 kcal/kg of body weight daily.4.
During the first few weeks of diet introduction, a multivitamin/mineral supplement
should be taken (iron, folate, vitamin B12, calcium, vitamin A, vitamin D, vitamin K,
thiamin, and B-complex vitamins).
5.
Reduce lactose intake (slowly increase lactose intake to tolerance).6.
Reduce fiber intake (slowly increase fiber intake to tolerance).7.
Label Reading
Read labels carefully and frequently. Watch for ingredients such as “hydrolyzed vegetable
protein (HVP),” “vegetable gum,” “vegetable starch,” “vegetable protein,” “flour,” “cereal,”
“cereal products,” “malt,” “malt flavoring,” “starch,” “gelatinized starch,” “modified starch,”
“modified food starch,” “fillers,” “natural flavoring,” “soy sauce,” “soy sauce solids,”
“monoglycerides,” and “diglycerides.”
Be sure to identify specific “thickening agents,” “emulsifiers,” and “stabilizers.”
When dining out, inquire about “special” or “secret” ingredients and preparation methods.
Baking Tips
The following may be substituted for 1 cup of wheat flour in baking:
1 cup corn flour
¾ cup coarse cornmeal (mix with liquid in recipe and boil; cool, then add to other ingredients.)
1 cup fine cornmeal
5/8 cup potato flour
7/8 cup rice flour (mix with liquid in recipe and boil; cool, then add to other ingredients.)
When using soy flour, combine with another flour for best results.
The leavening used with nonwheat flours must be increased (i.e., use 21/2 tsp. of baking
powder for each cup).
Nonwheat flours require longer, slower cooking times.
Better texture may be obtained by baking foods such as biscuits and muffins in small sizes.
To prevent excessive dryness, store baked goods in an air-tight container.
For thickening, the following may be substituted for 1 tablespoon (Tbsp) flour:
½ Tbsp arrowroot starch
½ Tbsp cornstarch
½ Tbsp potato starch
½ Tbsp rice flour
2 tsp quick-cooking tapioca
The remaining bowel can adapt to recover intestinal function, and four determinants of intestinal
adaptability include:
Type and location of the resection
Patient age
Patient nutritional status
Content of the diet
After intestinal surgery to remove sections of the organ, it may be necessary to create a stoma for waste
elimination. In a colostomy, part of the colon, the rectum, and anus are removed and the remaining
segment of colon is brought out through the abdominal wall and to form the stoma. An ileostomy involves a
colectomy, removal of the entire colon, the rectum, and anus, and bringing the ileum through the opening.
Ileostomy causes more problems because of the digestive and absorptive role of this portion of the small
intestine (19). In addition to nutritional problems, diet can influence various aspects of bowel regularity
and stool consistency.
Ileostomy: Treatment and Nutritional Recommendations
An ileostomy produces a watery stool making postsurgical adjustment more of a challenge than with
colostomy. Also, ileostomy often causes fat malabsorption because bile is not reabsorbed, along with
malabsorption of fat-soluble vitamins, which necessitates supplementation. Deficiency of vitamin B12 is also
common. The risk for both kidney and gallstones increases with steatorrhea, so it is important to monitor
for and counter the development of these conditions, and prudent to avoid foods high in oxalate. Ileostomy
also causes excessive fluid losses, along with electrolytes, making dehydration a special concern.
Obstruction is a possible complication, so thorough mastication of foods is important.
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Table 9.26 Dietary Recommendations for Ileostomy
A clear liquid diet follows surgery.1.
Progress to a bland, low-fiber diet with extra kilocalories (35–45 kcal/kg/day) and
protein (1.5 g/kg/day) for healing.
2.
Continue with low-fiber diet. Use sources of pectin such as oatmeal and applesauce.3.
Choose a vitamin/mineral supplement with vitamin B12, folacin, calcium,
magnesium, iron, and vitamin C.
4.
Supplement sodium and potassium.5.
If prednisone is used in treatment, limit salt intake (see low-sodium diet).6.
Avoid eating before bedtime.7.
If gassiness is a problem, avoid cruciferous vegetables, legumes, and other potential
gas-forming fruits and vegetables.
8.
See additional guidelines (colostomy recommendations).
Possible Nutrient Deficiencies (depending on food tolerances): Vitamin C
Adapted from reference 2.
Colostomy: Treatment and Nutritional Recommendations
With a colostomy, the stool consistency is close to normal or normal, depending on how much of the colon
was removed. If the colostomy is on the right side, the stool will be mushy, whereas a left-sided colostomy
produces a firm stool. Odor is a significant problem for the person with a colostomy, and attention to
specific foods that cause more of a problem is important. Because potential odor-causing foods are nutrient
dense, it is better to focus on other approaches, such as deodorizers. Many of the same diet
recommendations for ileostomy apply to colostomy, although the possible nutritional problems are more
likely with ileostomy.
Table 9.27 Foods High in Oxalate
Beets
Celery
Chocolate/cocoa
Nuts
Peanut butter
Rhubarb
Soy
Spinach
Strawberries
Sweet potatoes
Tea
Vitamin C supplements
Whole wheat
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Short Bowel Syndrome
Disease Process
With removal of 40% or more of the small intestine in a resection, short bowel syndrome (SBS) is a prime
concern, especially if the terminal ileum and ileocecal valve were removed (17). The nutritional problems
associated with SBS arise from malabsorption. Although the survival rate declines as more of the intestine is
removed, if the ileum and ileocecal valve remain intact, even an 80% resection can prove to be tolerated
(20). Because of its importance in long-term survival and the fact that it's the only controllable variable,
enhancing the intestine's ability to adapt is the focus of much current research.
Nutrition is the key to recovery and enhancing the intestine's adaptive ability. The reason is that many of
the typical symptoms a patient with SBS will experience are nutritionally relevant:
Diarrhea
Steatorrhea
Weight loss
Muscle wasting
Bone disease
Malabsorption of several nutrients
Resections of the jejunum initially cause malabsorption, because most nutrients are digested and absorbed
within the first forty inches of the small intestine. However, after the adaptation period, the ileum takes
over this function, as the remaining intestine grows in length, diameter, and thickness.
Treatment and Nutritional Intervention
Treatment focuses on managing symptoms and enhancing intestinal adaptation. Several medications are
useful in managing the symptoms of diarrhea, steatorrhea, and bacterial overgrowth (19). Drugs that slow
gastric emptying and intestinal motility (see Tables 9.3 and 9.18) can help control diarrhea and thereby
increase nutrient digestion
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and absorption, as well as those reducing acid and other intestinal secretions (see Table 9.2).
Table 9.28 Dietary Recommendations for Colostomy
A clear liquid diet follows surgery.1.
Progress to a bland, low-fiber diet with extra kilocalories (35–45 kcal/kg/day) and
protein (1.5 g/kg/day) for healing.
2.
After approximately 2 weeks, gradually increase fiber intake. Fiber intake may be
adjusted if diarrhea results.
3.
The following foods should be avoided only if they consistently cause undesirable
effects:May cause obstructions:
Bamboo shoots, bean sprouts, celery, citrus fruit membranes, coconut, coleslaw,
corn, fruits with skins and seeds, green beans, lettuce, mushrooms, nuts, peas/pea
pods, popcorn, potato skins, raw carrots, raw/dried fruit, relishes, seeds, spinach,
tough meats, and vegetables.May cause odor or gas:
Antibiotics, asparagus, beer, broccoli, brussels sprouts, cabbage family vegetables,
carbonated beverages, cauliflower, corn, cucumbers, deep fried foods, dried
beans/peas, eggs, fish, melons, milk, mustard, nuts, onions, pastries, pickles,
radishes, some vitamin/mineral supplements, spicy foods, strong-flavored cheeses,
and turnips.May contribute to diarrhea:
Beans, beer/wine, broccoli, coffee, fresh fruits/vegetables and juices, green leafy
vegetables (esp. spinach), highly spiced foods, licorice, and prune juice.
4.
Avoid high-oxalate foods (Table 9.25)5.
Foods such as applesauce, bananas, boiled milk, cheese, milk, peanut butter, rice,
and tapioca may reduce diarrhea. Reducing fluid intake does not reduce diarrhea,
and it may cause dehydration.
6.
If Prednisone is used in treatment, reduce salt intake to 2–3 g daily (see low-sodium
diet).
7.
Consume 1-2 quarts of fluid daily, between meals.8.
Choose a vitamin/mineral supplement with vitamin E, folacin, calcium, magnesium,
iron, vitamin C, vitamin K, and vitamin B12.
9.
Dietary/Behavior Modifications
Establish regular meal times.
Eat slowly and chew thoroughly with mouth closed.
Avoid chewing gum or drinking from straws to prevent excess gas.
Use cranberry juice, yogurt, buttermilk, and fresh parsley (as tolerated, in limited
amounts) as natural deodorizers.
Use products such as Bean-O to reduce gas.
If a food has been eliminated from the diet due to diarrhea, constipation, odor, or
gas, retest tolerance after 2–3 weeks.
Adapted from reference 2.
Table 9.29 Malabsorption in Short Bowel Syndrome
Deficit or Problem Result
Bile acid Fat not digested, bacterial overgrowth
Absorptive surface Maldigestion, malabsorption
Fluid reabsorption Dehydration
Increased motility, short
GIT
Dumping syndrome
Loss of ileocecal valve Bacterial overgrowth
Oversecretion of gastric
acid
Damage to duodenum, pancreatic enzyme activity
altered
Pancreatic enzyme
activity
Maldigestion, malabsorption
Fat malabsorption Kidney stones, gallstones
Nutritional Recommendations
The goals of nutrition therapy are similar to the overall treatment plan, but an additional point is to
improve nutritional status, as this may prevent nutritional symptoms and enhance intestinal adaptation (2).
If 50% or less of intestine was removed, feeding can begin within a few days after surgery. For higher
resections, parenteral nutrition is the first method of feeding. If the patient has become nutritionally
compromised because of the disease state that necessitated the surgery, parenteral nutrition support is
vital and must provide adequate energy for repletion. As soon as is possible, enteral feedings should start,
as this stimulates adaptation.
Depending on the extent of the resection, parenteral nutrition may need to continue from 3 weeks to 6
months. The timing on the different dietary changes is variable, but may take months before a patient can
resume a regular diet. Limited studies have suggested that compounds such as glutamine, recombinant
human growth hormone, and glucagons, like peptide 2, may promote intestinal adaptation (21,22).
However, their use is still controversial.
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Table 9.30 Dietary Recommendations for Short Bowel Syndrome
Immediately following intestinal resection surgery:
Parental nutrition (TPN) is required. The extent of the resection and overall health
of the subject will determine the duration of TPN.
Enteral nutrition should begin as soon as possible after surgery.
Oral diet:
Should progress slowly over several weeks or months depending on the speed of the
intestinal adaptation process (which may take up to 1 year).
Supplemental tube feedings may be necessary during this time. Optimally, enteral
formulas should include nucleotides, glutamine, short chain fatty acids (butyrate,
propionate, acetate), and fiber. Feedings should begin at 1,500 mL/day over several
hours and be increased as tolerated.
Transitional diet from enteral formulas to oral diet should be high in fat (with use of
MCT oil) and low in carbohydrate.
As oral diet tolerance improves:
Reduce fat intake to 40–50 g/day with use of MCT oil. Fat intake may be increased
for weight gain as tolerated.
Increase protein intake to 1.5–2 g/kg/day.
Increase kilocalorie intake to 35–45 kcal/kg/day.
Foods to avoid (A bland diet may be preferred.); caffeine; concentrated sweets;
mannitol; sorbitol; xylitol; lactose (if it causes problems)
Fiber supplement
Avoid high oxalate foods (Table 9.27)
Choose chewable or liquid vitamin/mineral supplements that include calcium,
magnesium, zinc, iron, manganese, vitamin C, selenium, potassium, folic acid, B-
complex vitamins, and water miscible forms of vitamins A, D, E, and K.
Parenteral administration of vitamin B12is likely needed.
If supplemental MCT oil is used, divide it into doses of 1 Tbsp and take throughout
the day with meals.
Diet and Behavior Modifications:
Eat 6–10 small meals daily
Consume fluids between meals in small amounts
Possible Nutrient Deficiencies: calcium, vitamin D, riboflavin, vitamins A, D, E, and K
Adapted from references 2, 18, and 19.
References
1. Dickman R, Kim, JL, Camargo, L, et al. Correlation of gastroesophageal reflux disease symptoms
characteristics with long-segment Barrett's esophagus. Dis Esophagus 2006;19(5):360–365.
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2. American Dietetic Association. Nutrition Care Manual. Online subscription. Accessed March 1, 2007.
3. Endoh K, Leung FW. Effects of smoking and nicotine on gastric mucosa: A review of clinical and
experimental evidence. Gastroenterology 1994;107:864–878.
4. Centers for Disease Control and Prevention. Available at: www.cdc.gov/ulcer/history.htm. Accessed
March 1, 2007.
5. Peura DA. Helicobacter pylori and ulcerogenesis. Am J Med 1996;100(5A):19S–25S.
6. Kang JY, Melville D, Maxwell JD. Drugs aging. Epidemiology and management of diverticular disease
of the colon. Drugs Aging 2004;21(4):211–228.
7. Drossman DA. Irritable bowel syndrome and sexual/physical abuse history. Eur J Gastroenterol
Hepatol 1997;9(4):327–330.
8. Cremonini F, Talley NJ. Irritable bowel syndrome: epidemiology, natural history, health care
seeking and emerging risk factors. Gastroenterol Clin North Am 2005;34(2):189–204.
9. Drisko J, Bischoff B, Hall M, McCallum R. Treating irritable bowel syndrome with a food elimination
diet followed by food challenge and probiotics. J Am Coll Nutr 2006;25(6):514–522.
10. Spellet G. Nutritional management of common gastrointestinal problems. Nurse Pract Forum
1994;5:24.
11. Cottone M, Orlando A, Viscido A, et al. Prevention of postsurgical relapse and recurrence in
Crohn's disease. Alimentary Pharmacol Therapeutics 2003;17(s2):38–42.
12. Wong JM, de Souza R, Kendall CW, Emam A, Jenkins DJ. Colonic health: fermentation and short
chain fatty acids. J Clin Gastroenterol 2006;40(3):235–243.
13. Scheppach W, Christl SU, Bartram HP, Richter F, Kasper H. Effects of short-chain fatty acids on
the inflamed colonic mucosa. Scand J Gastroenterol Suppl 1997;222:53–57.
14. Murray JA. The widening spectrum of celiac disease. Am J Clin Nutr 1999;69:354–365.
15. Holmes GKT, Prior P, Lane MR, Pope D, Allan RN. Malignancy in celiac disease—effect of a gluten-
free diet. Gut 1989;30:333–338.
16. Farrell RJ, Kelly CP. Celiac sprue. N Engl J Med 2002;346:180–188.
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17. American Society for Parenteral and Enteral Nutrition Board of Directors and the Clinical
Guidelines Task Force. Guidelines for the use of parenteral and enteral nutrition in adult and pediatric
patients. J Parenteral Enteral Nutr 2002; 26(1s):1SA–138SA.
18. Matarese LE, O'Keefe SJD, Kandil HM, et al. Short bowel syndrome: Clinical guidelines for nutrition
management. Nutr Clin Pract 2005;20(5):493–502.
19. Rees Parrish C. The clinician's guide to short bowel syndrome. Practical Gastroenterol
2005:67–106.
20. Dieleman LA, Heizer WD. Nutritional issues in inflammatory bowel disease. Gastroenterol Clin
North Am 1998;27(2):435–435.
21. Parekh NR, Steiger, E. Criteria for the use of recombinant human growth hormone in short bowel
syndrome. Nutr Clin Pract 2005;20(5):503–508.
22. Matarese LE, Seidner DL, Steiger E. Growth hormone, glutamine, and modified diet for intestinal
adaptation. J Am Diet Assoc 2004;104(8):1265–1272.
Authors: Width, Mary; Reinhard, Tonia
Title: Clinical Dietitian's Essential Pocket Guide,The: Essential Pocket Guide, 1st Edition
Copyright ©2009 Lippincott Williams & Wilkins
> Table of Contents > Part II - Nutrition Considerations for Specific Diseases > Chapter 10 - Liver and Pancreatic Diseases
Chapter 10
Liver and Pancreatic Diseases
The liver, pancreas, and gall bladder constitute the accessory organs because of their participation in
digestion. Given the crucial role the liver plays in nutrient metabolism, diseases affecting the organ can
profoundly and adversely affect nutritional status. The pancreas, a dual organ of both endocrine and
exocrine function, critically participates in digestion and also in blood glucose regulation. Problems with
this organ affect both of these functions. The gall bladder's role is limited, with minimal potential effect on
nutrition status.
Liver Disease
Liver abnormalities are of two types: those caused by a malfunction of the cells in the liver itself, such as
cirrhosis or hepatitis, and those caused by bile obstruction, such as occurs with bile stones or cancer (1).
Liver diseases with potential nutritional impact include hepatitis, hepatic steatosis, and cirrhosis, with
excessive alcohol intake being a common trigger for all. Because of its importance, the liver has extensive
regenerative ability and reserve capacity, posing a challenge for diagnosis, as significant function must be
lost before disease is clinically evident.
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Liver function tests (LFTs), mainly blood tests, provide information on the presence and extent of liver
disease (2,3). LFTs indicate the functional status of the liver, as with the synthesis of proteins such as
serum albumin and prothrombin, and indication of liver injury, as with various enzymes. These enzymes
include:
Aspartate aminotransferase (AST)
Alanine aminotransferase (ALT)
Although not specific for liver disease, other frequently tested enzymes that indicate biliary tract
obstruction, whether in the liver or in the bile channels outside the liver, include:
Alkaline phosphatase (ALP)
Gamma-glutamyltranspeptidase (GGT)
Table 10.1 Liver Function Tests
Function Test Derangement
Bile synthesis Bilirubin (serum, urine, fecal);
direct (conjugated) and indirect
(unconjugated)
Bilirubin not excreted in feces
(clay-colored); indirect bilirubin
high in liver disease, direct
bilirubin high in biliary tract
disease
Detoxification Bromsulphalein Retention high and urinary
excretion low in liver disease
Carbohydrate
metabolism
Oral Glucose Tolerance Test, Blood
glucose
Normal until advanced disease;
low in acute disease; high in
chronic disease
Lipid
metabolism
Triglyceride,
lipoproteins/cholesterol, ketones
All low in severe disease
Protein
metabolism
Urea (BUN, NH3), BUN low, NH3 high in advanced
disease
Plasma proteins(albumin,
transferrin), amino acid ratios
(BCAA vs. AAA)
Low protein levels, AA ratio
skewed toward higher AAA
Enzymes: (ALT, AST, GGT, ALP,
LDH)
High
Adapted from references 2 and 3.
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Enzymes
Hepatitis
Disease Process
Hepatitis is inflammation of the liver induced by the presence of a toxin, such as alcohol, medications and
some dietary supplements, environmental toxins, or viral infection (4). The major viral forms of hepatitis
include hepatitis A virus (HAV), hepatitis B virus (HBV), and hepatitis C virus (HCV). HAV is spread by
contact with infected persons or consumption of infected foods. The symptoms for type A include:
Jaundice
Nausea
Anorexia
Fever
Hepatomegaly
Clay-colored stools
Types B and C are often asymptomatic, and in the case of type C only arise after extensive hepatic damage.
HBV is spread parenterally (infected blood or needles) and by sexual contact. HCV is also parenterally
transmitted, but less so by sexual contact. HAV generally resolves without permanent damage, whereas 20%
of patients with type B and up to 70% of those with type C develop chronic liver disease (5).
Treatment and Nutritional Intervention
In acute hepatitis, the goals are to promote liver regeneration and prevent further injury, if a toxin is the
cause.
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The nutritional therapy components include an adequate diet, repletion of energy reserves (anorexia and
gastrointestinal symptoms result in weight loss), high protein, high carbohydrate (to spare protein for tissue
synthesis) (6). Small frequent meals may be needed if gastrointestinal symptoms are persistent.
Table 10.2 Dietary Supplements Associated with Hepatitis
Chaparral
Germander
Ma Huang
Saw Palmetto
Jin Buhuan
Adapted from reference 4.
Table 10.3 Treatment and Dietary Recommendations for Hepatitis
Diet Other
High energy (30–35 kcal/kg body weight) Bed rest
High protein (1.0–1.2 g/kg body weight) Isolation to prevent spread
Carbohydrate (50%–55% energy) Interferon a-2b for HBV,
HBC
Supplement: B-complex, vitamins C, K, and zinc Steroids (may cause sodium
retention)
Adequate fluids
Progress as tolerated from liquid to small, frequent feedings
(soft or regular as tolerated)
Adapted from reference 6.
Fatty Liver (Hepatic Steatosis)
Disease Process
Fatty liver consists of a buildup of triglycerides in hepatic tissue. The reason for the accumulation is
unclear, although the root cause is an imbalance between endogenous triglyceride synthesis and export via
very-low-density lipoprotein (VLDL). The condition is reversible, but it may progress to chronic and
irreversible damage. Several toxins can cause fatty liver, including alcohol, drugs, and environmental
toxins. If related to toxins, eliminating the underlying cause is the most important treatment component.
Dietary treatment is similar to that for hepatitis (6). Disease and other conditions that can also cause fatty
liver include:
Diabetes
Malnutrition
Gastrointestinal bypass surgery
Long-term parenteral nutrition
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Cirrhosis
Disease Process
Cirrhosis is a chronic degenerative disease, in which hepatic tissue becomes fibrous, with impairment of
liver function and leading ultimately to liver failure. It is the final stage of many forms of chronic liver
disease. With progression, the fibrosis becomes increasingly extensive, with fewer remaining functional
hepatocytes. In the United States, the most common cause is HCV, with alcoholic liver disease being the
next leading cause (5,7). Complications include:
Esophageal varices
Ascites
Edema
Portal hypertension
Insulin resistance (IR)
Insulin resistance (IR) develops in 60% of cirrhosis pts and leads to diabetes in 20%. Studies show that a high-
fiber, low-glycemic-index diet normalizes IR, hyperglycemia, and hyperinsulinemia in patients (8,9).
Treatment and Nutritional Intervention
The goals of medical nutrition therapy include maintenance of adequate nutrition, prevention tissue
catabolism, and the control of edema and ascites (6,10). A major concern is the development of hepatic
encephalopathy (HE). Although the exact cause of HE is not known, the major theory relates to the altered
ratio of aromatic amino acids to branched-chain amino acids (BCAA). The BCAA are:
Leucine
Isoleucine
Valine
Although ammonia is not the primary causative agent in HE, its levels are always elevated with impending
HE, and
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therefore involved in some way. Results of studies regarding the use of BCAA-containing enteral formulas
have been inconclusive (11,12).
Table 10.4 Dietary Recommendations for Cirrhosis
Protein
1.2–1.5 g/kg (70–100 g), as tolerated;
Source: lower AAA in favor of more BCAA; cut food sources of preformed NH3
Sodium
Restrict 2 to 3 g; possible fluid restricted if ascites (1.0 to 1.5 L/day); may depend on use of
diuretic
Texture
If esophageal varices, use soft, low fiber
Energy
Indirect calorimetry is best to determine energy (may vary as to 25% to 70% above resting
energy needs); based on dry weight
General
High kcal, CHO
Small frequent meals
Vitamin supplement (B-complex; folic acid)
If steatorrhea, restrict fat (and MCT); if severe, add fat-soluble vitamins
No alcohol
Adapted from references 6, 10, and 12.
Pancreatic Disease
Disease of the pancreas can significantly impact nutrition status, given the dual role of the organ, that is,
exocrine and endocrine. The former role will affect digestion and absorption of nutrients, whereas the
latter may cause diabetes mellitus. Both of these problems will necessitate nutritional assessment and
intervention.
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Pancreatitis
Disease Process
Inflammation of the pancreas can be either chronic or acute. In the United States, alcoholism is the most
common cause of chronic pancreatitis, and this is also true for acute pancreatitis, with the other common
trigger of gallstones (6,13). Additional causes include a genetic predisposition and obstruction of the
pancreatic duct, which can arise from narrowing of the duct or pancreatic cancer, and
hypertriglyceridemia. Although rare, severe acute pancreatitis can narrow the duct and cause chronic
pancreatitis.
As chronic pancreatitis progresses, digestive enzyme-secreting acinar cells are slowly destroyed, and
eventually pain does not occur. However, as the number of cells decrease, malabsorption occurs, causing
steatorrhea. The malabsorption leads to weight loss and malnutrition. Eventually, the insulin-secreting beta
cells maybe be destroyed, resulting in diabetes.
Treatment and Nutritional Intervention
Nutritional Recommendations
Medical nutrition therapy for acute pancreatitis depends on the severity of the patient's condition and is
focused on progression from nothing-by-mouth (NPO) status on admission to an oral low-fat diet in mild
cases, but possibly elemental enteral jejunal feedings for severe cases (6,10). Although enteral feeding is
preferred in severe cases, ileus may develop and necessitate parenteral feeding. If inflammation is
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extensive, protein and energy needs are high due to catabolism.
Table 10.5 Dietary Recommendations for Acute Pancreatitis
NPO for 48 hr
If mild, can advance to small oral feedings; liquids, low fat
If more severe, elemental jejunal feedings
If ileus, parenteral nutrition
Adapted from references 6 and 10.
Table 10.6 Dietary Recommendations for Chronic Pancreatitis
Protein: 1.0 g/kg body weight, up to 2.0 g/kg for repletion
Low fiber
Small, frequent meals
Pancreatic enzyme replacements
Fat restriction, if enzyme replacement insufficient
MCT, if steatorrhea severe
Adequate diet or supplement: calcium, magnesium, fat-soluble vitamins, B-complex vitamins,
vitamin C, zinc
No caffeine or other gastric stimulants
No alcohol
Adapted from references 6 and 10.
Patient Education
In chronic pancreatitis, eating exacerbates the chronic abdominal pain, which frequently reduces food
intake and leads to weight loss. In addition, the loss of acinar cells reduces lipases and bicarbonate, causing
steatorrhea. Goals for nutritional intervention include repletion of nutritional status and reduction of
malabsorption. Pancreatic replacement enzymes are important therapeutic agents to achieve these goals.
Fat restriction is needed if malabsorption persists with replacement enzymes, and medium-chain
triglycerides (MCT) are useful in these cases.
References
1. Mahan LK, Escott-Stump S. Krause's Food, Nutrition, and Diet Therapy, 11th ed. Philadephia:
Saunders; 2004, 740–743.
2. Pagana KD, Pagana TJ. Mosby's Manual of Diagnostic and Laboratory Tests; St. Louis MO: Mosby
Inc.; 2006.
3. Lab Tests Online. Available at:
http://labtestsonline.org/understanding/analytes/liver_panel/glance.html. Accessed on March 6,
2007.
P.251
4. Farrell GC. Liver disease caused by drugs, anesthetics, and toxins. In Feldman M, Friedman LS,
Sleisenger MH, eds., Sleisenger and Fordtran's Gastrointestinal and Liver Disease: Pathophysiology,
Diagnosis, Management. Philadelphia: Saunders; 2002:1403–1447.
5. Centers for Disease Control and Prevention. Available at: www.
cdc.gov/ncidod/diseases/hepatitis/b/fact.htm, www.cdc.gov/ ncidod/diseases/hepatitis/c/fact.htm.
Accessed on March 1, 2007.
6. Escott-Stump S. Nutrition and Diagnosis-Related Care, 5th ed. Baltimore: Lippincott Williams &
Wilkins; 2002:339–361.
7. eMedicine. Available at: http://emedicine.com/med/topic3183. htm. Accessed on March 3, 2007.
8. Barkoukis H, Fiedler KM, Lerner E. A combined high-fiber, low-glycemic index diet normalizes
glucose tolerance and reduces hyperglycemia and hyperinsulinemia in adults with hepatic cirrhosis. J
Am Dietetic Assoc 2002;102:1503–1508.
9. Jenkins DJ, Shapira N, Greenberg G, et al. Low glycemic index foods and reduced glucose, amino
acid, and endocrine responses in cirrhosis. Am J Gastroenterol 1989;84:732–739.
10. American Dietetic Association. Nutrition Care Manual. Online subscription. Accessed March 6,
2007.
11. Mascarenhas R. New support for branched-chain amino acid supplementation in advanced hepatic
failure. Nutr Rev 2004;62(1):33–38.
12. Cordoba J, Lopez-Hellin J, Planas M, et al. Normal protein diet for episodic hepatic
encephalopathy: results of a randomized study. J Hepatology 2004;41(1):38–43.
13. Nagar AB, Gorelick FS. Acute Pancreatitis. Curr Opin Gastroenterol 2004;20(5):439–443.
Authors: Width, Mary; Reinhard, Tonia
Title: Clinical Dietitian's Essential Pocket Guide,The: Essential Pocket Guide, 1st Edition
Copyright ©2009 Lippincott Williams & Wilkins
> Table of Contents > Part II - Nutrition Considerations for Specific Diseases > Chapter 11 - Kidney Disease
Chapter 11
Kidney Disease
Monica L. Griffin RD
Kidney disease, which can be chronic or acute, affects over 40 million Americans every year (1). For
400,000 Americans, it progresses to end-stage kidney disease (ESKD) necessitating either dialysis or
transplant. Although dialysis has been a life-saving technique, it is a catabolic process leading to
malnutrition. For the dietitian, all stages of chronic kidney disease (CKD), also termed chronic renal failure
(CRF), and ESKD will require careful assessment, monitoring, and dietary modification.
Acute Renal Failure
Acute renal failure (ARF) has a sudden onset with rapid deterioration in kidney function and a mortality rate
of up to 65% (1). In contrast to CKD, ARF is often reversible, although ARF can become chronic, leading to
the need for long-term dialysis or transplant.
Acute Renal Failure: Disease Process
The causes are varied and are categorized by their relationship to prior kidney function (prerenal,
intrarenal [also intrinsic], and postrenal). Most causes of ARF are prerenal, representing up to 70% of cases
and include:
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Cardiac diseases: congestive heart failure, myocardial infarction, cardiac arrhythmia
Disorders of the renal blood vessels
Low blood volume or low blood pressure
Intrarenal causes include:
Disorders of the blood vessels: sickle-cell anemia, diabetes, adverse reaction to blood
transfusions
Renal injury: infections, toxins, drugs, Escherichia coli ingestion (food-borne illness)
Renal obstructions: kidney stones, tumors, scar tissue formation, and tissue inflammation
Postrenal causes include:
Bladder or ureter obstructions: strictures, stones, trauma
Bladder rupture
Neurological bladder disorder
Pregnancy
Prostate cancer or hyperplasia
Renal vein thrombosis
Treatment and Nutritional Intervention
Short-term dialysis may be necessary to treat ARF, with the goal of preventing renal damage and returning
the kidneys to baseline function. Medications may include diuretics, potassium-exchange resins to bind
potassium in the gut, insulin to rapidly correct hyperkalemia, and bicarbonate if acidosis is present. ARF is
often a catabolic condition, so the registered dietitian (RD) must carefully monitor nutrition status.
Nutritional intervention includes:
Protein metabolite is urea, which increases renal workload; however, ARF catabolism must be
countered to prevent loss of visceral and somatic protein. The protein needed depends on dialysis
status, kidney function, and protein status. If the patient is undergoing dialysis or if renal
function increases, daily protein intake should be 1.2 to 1.3 g/kg body weight. If not
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being dialyzed, protein should be restricted to 0.6 to 0.8 g/kg body weight.
Energy must be adequate to spare protein for synthesis. The use of indirect calorimetry to
determine needs is ideal, but when not possible, daily energy intake can begin at 35 kcal/kg body
weight and adjusted based on monitoring of assessment parameters.
Electrolytes may require restriction, although laboratory values are carefully monitored to assess
the need for restriction of any electrolyte. Daily sodium intake is typically restricted to 2 to 3 g to
prevent fluid retention and control hypertension. Potassium and phosphorus may also require
restriction. Patients being dialyzed usually do not require restriction of electrolytes.
Fluid balance will be carefully monitored by various assessment parameters (e.g., blood sodium
level, weight changes, mucous membrane status, blood pressure). However, fluid restriction is
generally necessary in the nondialyzed patient, with daily intake equaling the volume of urine
output plus 500 mL. With dialysis, daily fluid intake of 1.5 to 2.0 L is usually adequate.
Chronic Kidney Disease
CKD represents a gradual and progressive loss of kidney function, which is irreversible. The most common
causes of CKD are diabetes and hypertension, which together account for 69% of cases (1,2). Others include
infections, exposure to nephrotoxic substances, and immunological disorders.
Even at 75% loss of renal function, a patient may not experience symptoms. The glomerular filtration rate
(GFR) is used to assess renal function and failure and indicate the stage of CKD (Table 11.1). At stage 5,
dialysis or transplant becomes necessary. Prior to stage 5, the patient is referred to as predialysis or
nondialysis. This is
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important, as nutrition therapy differs based on CKD stage and dialysis status.
Table 11.1 Classification of Chronic Kidney Disease
Stage Description Glomerular Filtration Rate (mL/min/1.72 m2)
1 Kidney damage with normal or increased GFR =90
2 Kidney damage with mild decrease in GFR 60–89
3 Moderate decrease in GFR 30–59
4 Severe decrease in GFR 15–29
5 Kidney failure <15
Data from reference 2.
CKD: Nondialysis
In the nondialysis stage of CKD, preservation of kidney function for as long as possible becomes the main
goal. The reason for this is that dialysis, which is a catabolic process, becomes necessary at stage 5 and
leads to malnutrition. Protein restriction is important in this regard, as well as to control symptoms.
Restriction of electrolytes, particularly potassium, which is fatal at high blood levels, becomes another key
nutritional intervention. The nephrotic syndrome is not a disease per se, but refers to any renal disorder
that causes proteinuria above 3.5 g daily. It can result from the same etiologic factors as those causing
CKD.
Disease Process
As GFR falls, the kidneys lose the ability to maintain fluid, electrolyte, and acid–base balance. These are
potentially life-threatening complications, so laboratory values must be carefully monitored (Table 11.2). In
addition, CKD and the restrictive diet can often adversely affect nutritional status; therefore the RD must
monitor nutritional assessment parameters.
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Laboratory values are monitored at least monthly and reviewed with the patient to determine any
necessary therapeutic interventions. Some values may be monitored more frequently, such as hemoglobin,
hematocrit, calcium, and phosphorus. These lab values can be affected by medications or acute medical
conditions, and in both cases more frequent monitoring will significantly improve the patient's outcomes.
Some biochemical parameters, such as lipid profile, are tested less frequently, generally on a quarterly
basis. For a patient with acute renal failure, parameters such as blood urea nitrogen (BUN), creatinine,
potassium, CO2, and chloride may be tested more frequently to determine whether kidney function is
returning to baseline levels.
Table 11.2 Commonly Monitored Laboratory Values in Kidney Disease
Test Normal Chronic Kidney Disease Range
Albumin WNL for laboratory
>4.0 is ideal
Blood urea nitrogen 60–80 mg/dL
Based on well-dialyzed patient with good intake
Corrected calciuma <10.2 mg/dL
8.4–9.5mg/dL is ideal
Chloride WNL
CO2, total >22
Cholesterol WNL
Creatinine 2–15 mg/dL
Ferritin >100 mg/mL
Glucose WNL
Hematocrit 33%–36%
Hemoglobin 11–12 g/dL
Phosphorus 3.5–5.5
Potassium 3.5–5.5
Parathyroid hormone, intact 150–300
Sodium WNL
WNL, within normal limits.aCorCa = total calcium mg/dL + 0.8 [4 –serum albumin g/dL].
Data from references 2, 4, and 6.
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Treatment and Nutritional Intervention
The monthly lab results will have an impact on interventions, both medications and nutrition therapy. The
medications used in CKD target the primary kidney functions, which are declining in predialysis patients and
absent in dialysis patients (Table 11.3). Phosphorus binders, intravenous iron, and parathyroid hormone
(PTH)-suppressing
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medications will have dose titration based on the laboratory results. Dose titration is generally addressed
monthly in a chronic dialysis patient. As with monitoring of lab values, medication dosage may need to be
addressed more frequently in a patient with acute renal failure.
Table 11.3 Common Medications in CKD
Common Name Use Timing
Phoslo, Tums,
Oscal
Calcium-based
phosphorus
binder
Taken with each meal
and snack
Renagel,
Fosrenol,
aluminum
hydroxide
Non-calcium-
based
phosphorus
binder
(Use of aluminum should
be limited to <14 days)
Dose is titrated based
on serum phosphorus
level and diet intake
Dialyvite, Diatx, B-complex Taken daily, usually
Nephrocaps,
Nephrovite
with vitamin C
and biotin
in the evening to
accommodate dialysis
treatment days when
fluid is removed
NephPlex,
RenaPlex
B-complex
with vitamin C
and zinc
(Replace water-soluble
vitamin losses)
Ferrous sulfate,
ferrous
gluconate,
ferrous
fumarate
Oral iron Oral iron should not
be taken with binders
Venofer,
Ferrlecit, Infed
IV iron IV iron is
administered during
hemodialysis
treatments
Calcijexa IV vitamin D IV forms are
administered during
hemodialysis
Oral agents are to be
taken consistently as
ordered
Calcium levels should
be monitored closely
with use of Rocaltrol
and Sensipar
Hectorol,
ZemplaraOral and IV
vitamin D
Rocaltrola Oral vitamin D
Sensipara Oral
calcimimetic
agent
aAll agents used to manage PTH level.
Data from reference 2.
Primary goals in the treatment of CKD include the preservation of kidney function and maintaining
adequate nutritional status, thus delaying the need for dialysis as long as possible. The National Kidney
Foundation has issued national guidelines, Kidney Disease Outcomes Quality Initiative (KDOQI), which
provide evidence-based clinical practice guidelines for all stages of CKD (2).
The KDOQI guidelines recommend nutrition evaluation and monitoring as early as stage 2 or 3. To prevent
further decline of kidney function, the cornerstone of treatment is intensive control of diabetes and
hypertension, if present. Nutritional intervention can help to control uremic symptoms such as anorexia,
diarrhea, and vomiting that frequently accompany the decline in GFR (Table 11.4). Preventing malnutrition
in the predialysis patient is of critical importance to overall patient outcome (3).
Energy and protein calculations are based on standard body weight (SBW) or adjusted body
weight (ABW) and provide for maintenance only. Kilocalorie provision
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should be adequate to prevent protein catabolism for energy needs. Activity level and stress
factor should be taken into account when planning for caloric and protein requirements. High
biologic value (HBV) protein should provide at least 50% of the total protein consumed (4). There
is no clear consensus as to whether urinary losses of protein in nephrotic syndrome should be
replaced.
Table 11.4 Daily Nutrient Needs for Nondialyzed Patients
CKD (Nondialysis) Nephrotic Syndrome
Protein (g/kg) 0.6–0.75 0.8–1.0
Energy (kcal/kg) Age <60 years 35 Age <60 years 35
Age >60 years 30–35 Age >60 years 30–35
Potassium (g) 2–3 2–3
Sodium (g) 2–4 2–4
Phosphorus 800–1,000 mg 800–1,000 mg
10–12 mg/g protein 10–12 mg/g protein
Data from references 2,3,4.
Potassium may be liberalized if potassium-depleting diuretics are in use. Restrictions are
implemented as the serum levels rise out of the normal range. Once a potassium restriction is
needed, diabetic patients should use caution in selecting items for the treatment of
hypoglycemic reactions.
Sodium (1 g) diets are generally not palatable enough to sustain adequate kilocalorie and protein
intake for most patients. Initiation of dialysis should be considered when the dietary restrictions
are such that palatability of the diet prevents adequate intake (5).
Controlling phosphorus intake will automatically limit calcium intake due to many high-
phosphorus foods also containing rich calcium sources. Early control of phosphorus intake will
help control the serum phosphorus and PTH levels. The phosphorus level is also controlled with
the addition of phosphorus-binding medications. These medications, taken with each meal and
snack, bind phosphorus in the gastrointestinal tract and reduce the amount of phosphorus
absorbed into the blood.
Elemental calcium intake from both the diet, and the medications should be limited to 2,000 mg
daily. Patients should read labels to avoid products that are fortified with calcium, an
increasingly common food industry practice.
Fluid needs to be limited in predialysis patients only when congestive heart failure appears
imminent. Fluid restrictions for patients on diuretics may cause progression of renal failure due
to volume depletion.
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Nutritional Recommendations
Blood levels of electrolytes are carefully monitored in the CKD patient to assess the need for restrictions.
However, the typical CKD diet, in which all restrictions are necessary, includes a daily protein restriction to
just below the RDA/DRI at 0.6 g/kg body weight; sodium at 2 g; potassium at 2 to 3 g; calcium at 1.2 g
(Table 11.5).
Potassium is of the most immediate concern, because both hypokalemia and hyperkalemia can cause heart
failure. Fruits and vegetables are the highest sources of potassium, and within each group, there is
considerable variation in potassium content (Table 11.6). Processing and food preparation alter the amount
of potassium, with raw foods often containing less due to the cooking process concentrating the volume.
Canning tends to cause potassium to leach out, so some canned foods have less.
CKD: Dialysis
Dialysis serves as artificial filtration of blood when kidney failure has progressed to stage 5. The two main
types are
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hemodialysis and peritoneal dialysis. In hemodialysis, blood from an artery circulates through a mechanical
dialyzer, where it is filtered and returned to the parallel vein. In peritoneal dialysis, the patient's own
peritoneum serves as the filtration membrane. The dialysate, a hyperosmolar solution, enters via a catheter
penetrating the abdominal wall and causes fluid flow into the peritoneal cavity. In both cases, the diet is
more liberalized compared to that in the predialysis state.
Table 11.5 Common Foods to Be Avoided
Dairy Protein Starch Fruit/Vegetables Fat Beverages
Limit ½
cup or 1
oz/day:
Milk
Yogurt
Cheese
Ice Cream
Salted,
cured
meat or
fish
Deli meat
Bacon
Sausage
Dried
beans,
peas,
legumes
Canned
sausages
Fish with
bones
Peanut
butter
Salted
crackers
Potato
chips
Prepared
biscuits,
rolls
Baking mix
Whole grain
bread and
cereal
Brown rice
High-fiber
muffins
Banana
Orange
Juice
Honeydew
Cantaloupe
Dried fruits
Prune juice
Prunes
Potato
Tomato
Sweet
potato
Salted
pork
fat
Cola
Cream
Tropical
punch
Miscellaneous
Chocolate
Nuts, seeds
Beer
Molasses
Table 11.6 Potassium Content in Fruits and Vegetables
High Potassium: 201–350 mg/serving Lower Potassium: 0–200 mg/serving
Vegetables Asparagus; avocado; beets and beet
greens; brussels sprouts; celery; cooked
greens (most types); mushrooms; okra;
parsnips; chili pepper; potato; pumpkin;
spinach (cooked); sweet potato; tomato;
tomato juice; tomato sauce/paste/puree;
vegetable juice; winter squash
Low (0–100 mg)
Alfalfa sprouts; bamboo
shoots; beans (green or
wax); cabbage (raw);
cucumber; endive; lettuce;
green or red pepper
Medium (101–200 mg)
Artichoke; broccoli;
cabbage (cooked); carrots
(raw); cauliflower; celery
(raw); corn; eggplant;
mustard greens; onions;
green peas; sauerkraut;
spinach (raw); turnips
Fruits Apricots; cantaloupe; banana; dates; figs;
honeydew melon; kiwi fruit; nectarine;
oranges and orange juice; pear; prunes and
prune juice
Low (0–100 mg)
Applesauce; blueberries;
cranberries and juice; grape
juice; lemons; papaya
nectar; peach nectar;
canned pears
Medium (101–200 mg)
Apple and juice; apricot
nectar; blackberries;
cherries; grapefruit and
juice; grapes; mango;
papaya; peach; pineapple;
plums; raisins; raspberries;
strawberries; watermelon
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Treatment and Nutritional Intervention
Kilocalorie and protein needs are based on SBW or ABW and provide only for maintenance (Table
11.7). Stress needs should be planned into the estimation of kilocalorie and protein provision.
Protein losses are high due to loss to the artificial kidney membrane and blood loss in
hemodialysis; and the peritoneal membrane, in peritoneal dialysis. HBV protein should account
for at least 50% of the protein allowance (4).
In peritoneal dialysis, the dialysate contains dextrose to remove fluid, and it is absorbed to a significant
extent. The daily amount of dextrose absorbed depends on the concentration of dextrose used for each
exchange, and on the number of exchanges (Table 11.8). The dextrose concentration can be altered to
either increase or decrease the amount of fluid removed. Currently, three concentrations are available:
1.5%, 2.5%, and 4.25%.
Although increasing from the lower to higher amounts will generally increase the amount of fluid removed,
it will also increase the amount of dextrose kilocalories absorbed. The dextrose and kilocalorie absorption
should be taken into consideration when developing a kilocalorie plan for
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peritoneal patients. It is important to monitor diabetic patients closely for glucose control.
Table 11.7 Daily Nutrient Needs for Dialyzed Patients
Hemodialysis Peritoneal Dialysis
Protein (g/kg) 1.2–1.3 1.3–1.4
Energy
(kcal/kg)
Age <60 years: 35 Age <60 years: 35
Age >60 years:
30–35
Age >60 years: 30–35
Potassium (g) 2–3 3–4
Sodium (g) 2–3 2–4
Phosphorus 800–1,000 mg 800–1,000 mg
10–12 mg/g protein 10–12 mg/g protein
Fluid Output + 1,000 mL Unrestricted, unless needed to maintain fluid
balance
Data from references 3 and 4.
Table 11.8 Simple Estimation of Dextrose Kilocalories Absorbed from Peritoneal
Dialysis
Continuous cyclic peritoneal dialysis (CCPD) allows 40% dextrose absorption
Continuous ambulatory peritoneal dialysis (CAPD) allows 60% dextrose absorption
Each gram of dextrose = 3.4 kcal
Dialysate Dextrose
Concentration
Grams of
Dextrose/L
kcal/L from
Dextrose
kcal/L with
CCPD (40%)
kcal/L with
CAPD (60%)
1.5% 15 g 51 kcal 21 kcal 31 kcal
2.5 % 25 g 85 kcal 34 kcal 51 kcal
4.25% 42.5 g 144.5 kcal 57.8 kcal 86.7 kcal
Example: A CAPD patient uses 4 L of 1.5% dialysate and 4 L of 4.25% dialysate daily.
4 L 1.5% = 124 kcal (31 kcal/L ÷ 4 L)
4 L 4.25% = 346 kcal (86.7 kcal ÷ 4 L)
Total kcal absorbed from dextrose = 470
Data from reference 3.
Potassium levels are liberalized in peritoneal dialysis due to frequent dialysis exchanges that
consistently remove potassium. Potassium supplementation is needed at times to maintain serum
levels in normal range. Hemodialysis patients may have increased potassium needs when
potassium-depleting diuretics are used or increased losses are related to the etiology of the renal
failure, as in polycystic kidney disease or high residual kidney function. For diabetic patients
requiring the standard potassium restriction, care should be taken in selecting interventions for
hypoglycemic reactions (Table 11.9). Orange juice has high potassium content and should be
avoided.
Sodium intake is limited to help control thirst, thus maintaining limited fluid intake, and edema.
Phosphorus intake is limited to maintain serum phosphorus levels in goal range and reduce
stimulation of PTH secretion (5). The phosphorus level is also controlled
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with the inclusion of phosphorus binding medications. These medications taken with meals and
snacks bind phosphorus in the GI tract and reduce the amount of phosphorus absorbed into the
blood.
Table 11.9 Low Potassium Hypoglycemic Interventions (15 g CHO)
Food Item Portion Size
Regular gelatin ½ cup
Honey 1 tbsp.
Regular soda or apple juice ½ cup
Sherbet or sorbet ½ cup
Glucose 1 tube
Glucose tablets 3
Data from reference 3.
Elemental calcium intake should be limited to 2,000 mg daily from oral intake and medication
(5). Calcium-based phosphorus binders and calcium-fortified foods that are widespread in the
food supply must be given close attention in meeting this dietary limitation.
Fluid limitations are dictated by the amount of urine output and intradialytic weight gains. Goal
fluid gains between treatments should not exceed 5% of the estimated dry weight. Patients
should be free of shortness of breath, edema (peripheral, facial and ascites), and significant
elevation in blood pressure prior to treatment (3).
When a patient's appetite and intake are significantly inadequate for estimated macronutrient
needs, the RD should consider diet liberalization. Intake of higher potassium, sodium, and
phosphorus foods in limited amounts can help the patient consume more kilocalories and protein.
Additionally, the RD must give priority to the patient's food preferences in meal planning. If
intake remains inadequate, use of appetite stimulants, liquid supplements, protein, and
kilocalorie modulars, as well as more aggressive interventions (tube
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feedings and total parenteral nutrition [TPN]), should be considered.
Nutrition supplements designed specifically for predialysis or dialysis patients can be useful.
These products offer the best nutrient profile with limited fluid for a dialysis patient; however,
many patients can also tolerate the standard or basic supplements. Generally, the more limited
the patient's oral intake, the more likely they are to tolerate the basic supplements. When
utilizing products for tube feedings, the renal products are generally the best option. The
addition of protein modulars and phosphorus supplementation is frequently needed for long-term
use. Intradialytic parenteral nutrition/intraperitoneal parenteral nutrition (IDPN/IPN) is the
process of providing macronutrients parenterally during the hemodialysis treatment.
Intraperitoneal amino acid administration in peritoneal dialysate is an amino acid and dextrose
infusion. The use of these aggressive intradialytic nutrition interventions is controversial (4).
Pregnancy and Dialysis
Research on successful pregnancy outcomes in the dialysis population is lacking; however, some general
guidelines have been developed (6). Pregnant patients should be dialyzed daily to maintain fluid balance,
control blood pressure, and reduce uremic toxins (BUN is maintained below a range of 50 to 60). The daily
dialysis allows for more diet liberalization in all areas. Daily protein intake should increase by an additional
20 g above standard dialysis calculations, and energy intake should increase by 100 to 300 kcal. Magnesium
levels should be monitored to determine if supplementation is needed (3).
Because of the maternal and infant weight gain, determining appropriate fluid removal with each
treatment can be difficult; close monitoring for signs and symptoms of fluid overload or excess fluid
removal is necessary. The pregnant patient's need for synthetic erythropoietin, iron,
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and folate increases significantly to support increased blood volume. Folate should be supplemented at 1.8
mg daily (7). The pregnant dialysis patient is at high risk for pre-eclampsia, hypertensive crisis, and
premature delivery.
Table 11.10 Daily Nutrient Needs for Posttransplant Patients
Nutrients Transplant
Postop Chronic
Protein (g/kg) 1.3–2.0 0.8–1.0
Energy
(kcal/kg)
30–35, maintain SBW, limit fat to 30% kcal, <300 mg cholesterol/day
Potassium (g) Unrestricted unless serum level high; may need diet restriction with
cyclosporin
Sodium (g) 2–4 2–4
Phosphorus Recommended Dietary Allowance (RDA),
supplement as needed
RDA
Fluid Maintain balance Unrestricted, unless
overloaded
Data from reference 3.
Posttransplant Considerations
In the immediate postoperative period, protein needs are increased to allow for appropriate healing (Table
11.10)
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(3). In the posthealing, chronic posttransplant period, fluid restriction may be needed if the patient has
significant fluid overload, but this is generally not needed. Immunosuppressive treatment with cyclosporin
can cause hyperkalemia, and if it occurs, potassium restriction is indicated. In the chronic transplant
period, most patients should follow the general nutrition guidelines for any healthy individual.
Table 11.11 Common Renal Abbreviations
Abbreviation Term Associated with Renal Disease
ABW Adjusted body weight
CAPD Continuous ambulatory peritoneal dialysis
CCPD Continuous cyclic peritoneal dialysis
CKD Chronic kidney disease
GFR Glomerular filtration rate
IDPN/IPN Intradialytic parenteral nutrition
KDOQI Kidney Disease Outcomes Quality Initiative
PTH Parathyroid hormone
SBW Standard body weight
References
1. Rolfes SR, Pinna K, Whitney E. Understanding Normal and Clinical Nutrition, 7th ed. Belmont:
Thomson, Wadsworth; 2006:848–860.
2. National Kidney Foundation KDOQI. Clinical Practice Guidelines for Chronic Kidney Disease:
Evaluation, Classification, and Stratification. AMJ Kidney Dis 2003;39(2) Suppl.1:S1–246.
3. Council on Renal Nutrition of the National Kidney Foundation. Pocket Guide to Nutrition
Assessment of the Patient with Chronic Kidney Disease, 3rd ed. New York: National Kidney
Foundation; 2002.
4. National Kidney Foundation KDOQI. Clinical Practice Guidelines for Nutrition in Chronic Renal
Failure. New York: National Kidney Foundation; 2001.
5. National Kidney Foundation KDOQI. Clinical Practice Guidelines for Bone Metabolism and Disease in
Chronic Kidney Disease. New York: National Kidney Foundation; 2004.
6. Alpers DH, Clouse RE, Stenson WF. Manual of Nutritional Therapeutics, 2nd ed. Boston/Toronto:
Little, Brown and Company; 1988:347–355.
7. Daugirdas JT, Ing TS. Handbook of Dialysis, 2nd ed. Boston/New York/Toronto/London: Little,
Brown and Company; 1994:649–652.
Authors: Width, Mary; Reinhard, Tonia
Title: Clinical Dietitian's Essential Pocket Guide,The: Essential Pocket Guide, 1st Edition
Copyright ©2009 Lippincott Williams & Wilkins
> Table of Contents > Part II - Nutrition Considerations for Specific Diseases > Chapter 12 - Pulmonary Disease
Chapter 12
Pulmonary Disease
Pulmonary disease is the fourth leading cause of chronic morbidity and mortality in the United States.
Currently, more than 35 million Americans are living with chronic lung diseases such as asthma,
emphysema, and chronic bronchitis (1). Pulmonary diseases have a significant impact on nutritional status,
and the RD's role is crucial in nutrition assessment and patient education to prevent or correct malnutrition.
Chronic Obstructive Pulmonary Disease
Disease Process
Chronic obstructive pulmonary disease (COPD) is a group of diseases characterized by airflow limitation that
is not fully reversible. The airflow limitation is usually both progressive and associated with an abnormal
inflammatory response of the lungs to noxious particles or gases (2). The two main diseases that fall under
the COPD umbrella include chronic bronchitis and emphysema. COPD patients either have bronchitis or
emphysema, or a mixture of both. Common causes of COPD include cigarette smoking, pipe smoking, and
cigar smoking; passive exposure to cigarette smoking; occupational dust and chemicals;
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air pollution; and genetic factors. The nutritional interventions for emphysema and bronchitis are similar.
Chronic Bronchitis
Chronic bronchitis is characterized by a chronic, productive cough (occurring on most days for a minimum of
3 months, for 2 consecutive years), inflamed bronchial tubes, excess mucus production, and shortness of
breath (2). Patients with chronic bronchitis, often called “blue bloaters” because of cyanosis and edema in
the extremities, usually present with right-sided cardiac failure and little to no weight loss (3). Chronic
bronchitis becomes chronic obstructive bronchitis if spirometric evidence of airflow obstruction develops,
which happens in a minority of patients (4).
Emphysema
Emphysema involves the destruction of lung parenchyma leading to loss of elastic recoil and loss of alveolar
septa and radial airway traction, which increases the tendency for airway collapse. Lung hyperinflation,
airflow limitation, and air trapping follow (4). These patients, often called “pink puffers” because of
reddish complexion and hyperventilation, are typically thin and breathe with pursed lips. Wheezing,
shortness of breath, and chronic mild cough are common. Nutritional depletion is significantly greater in
patients with emphysema than in those who have chronic bronchitis (3).
Treatment and Nutritional Intervention
COPD patients are at risk of weight loss and nutritional deficiencies because of a 15% to 25% increase in
resting energy expenditure due to difficulty breathing, a larger postprandial increase in metabolism and
heat production, a higher energy cost of daily activities, reduced caloric intake relative to need, and the
catabolic effect of inflammatory cytokines (4). A high-kilocalorie, high-protein diet
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is necessary to correct malnutrition. Start with 30 to 35 kcal/ kg and 1.2 to 1.5 g protein/kg. For
overweight or obese patients, controlled weight loss can be initiated using 20 to 25 kcal/kg, with frequent
monitoring to prevent rapid weight loss (3). Fluid intake should be 1 mL/ kcal, as a general rule. If the
patient has hypercapnia (CO2 retention), a diet moderate in carbohydrate and higher in fat may be
beneficial.
Patient Education
Gas-forming foods can cause discomfort because they bloat the abdomen and make breathing
more difficult, so educate patients on which foods to avoid/use in moderation (onions,
cauliflower, broccoli, melons, peas, corn, cucumbers, cabbage, brussels sprouts, turnips, raw
apples, and beans—except green beans). Fried and greasy foods can also cause gas or bloating.
Use medications that make breathing easier and/or clear airways about 1 hour before eating.
If the patient is using oxygen, make sure it is worn while eating because digestion requires
oxygen.
Eat six small meals each day instead of three large ones so that the stomach is never extremely
full. A full stomach can interfere with breathing by pushing on the diaphragm. Drink beverages at
the end of the meal to avoid early satiety.
Eat and chew slowly to avoid becoming short of breath.
Provide patient with tips to increase the nutrient density of foods, such as adding the following to
foods to increase caloric and/or protein content: butter, margarine, whipped cream, half and
half, cream cheese, sour cream, salad dressings, mayonnaise, honey, jam, sugar, granola, dried
fruits, cottage or ricotta cheese, whole milk, powdered milk, ice cream, yogurt, eggs, nuts,
seeds, wheat germ, peanut butter.
Avoid excess sodium, as it may increase edema and make breathing more difficult. Provide
patient with list of high-sodium foods.
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Cystic Fibrosis
Disease Process
Cystic fibrosis (CF) is an autosomal recessive inherited disease of the mucus and sweat glands. CF is
characterized by the secretion of thick, tenacious mucus that obstructs the ducts and glands of the
respiratory tract, sweat and salivary glands, intestine, pancreas, liver, and reproductive tract.
Complications include bronchitis, pneumonia, glucose intolerance, and malabsorption due to decreased
availability of digestive enzymes, decreased bicarbonate secretion, decreased bile acid reabsorption, and
decreased nutrient absorption by intestinal microvilli (3).
CF is caused by a defect in the cystic fibrosis transmembrane conductance regulator (CFTR) gene, which
codes for a chloride transporter found on the surface of the epithelial cells that line the lungs and other
organs. There are channels in these lining cells through which ions can pass. Normally, the movement of
ions brings water to the surface of the airway and keeps the mucus moist. The defective gene acts to block
the channels, which causes the mucus to dry out. It is difficult for a person to shift the thick mucus, which
then becomes prone to infection by bacteria. This defect also accounts for the high levels of sodium and
chloride that are present in the saliva, tears, and sweat of patients with CF (5).
Treatment and Nutritional Intervention
The risk for malnutrition in CF patients is high due to increased needs, decreased intake, and
malabsorption. The goals of nutritional care include controlling malabsorption with pancreatic enzyme
replacement, providing adequate energy, protein, and other nutrients, and preventing nutritional
deficiencies.
Energy
Energy needs are 120% to 150% of the Dietary Reference Intake (DRI) on average, but can be as high as 200%
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(gender, age, basal metabolic rate [BMR], physical activity, severity of lung disease, and severity of
malabsorption must all be considered when determining appropriate energy levels). Kilocalorie intake
should be approximately 200 kcal/ kg for infants, 150 kcal/kg for children, and 35 to 55 kcal/ kg for adults
(6,7). Nocturnal tube-feedings may be used to prevent or treat growth failure (usually providing 30%–50% of
established nutritional needs).
Protein
Protein needs are 150% to 200% DRI or higher, not to exceed 4 g/kg/day, unless severe malabsorption is
present. This may translate into 4 g/kg for infants, 3 g/kg for children, 2 g/kg for teens, and 1.5 g/kg for
adults (6,7).
Patient Education
Encourage intake of omega-3 fatty acids to reduce inflammation.
Vitamin/mineral supplementation should include a daily multivitamin plus extra vitamin E, or
give either an “ADEK”- or “Vitamax”-brand chewable tablet. Vitamin K should also be given to all
patients who are taking antibiotics.
Pancreatic enzyme capsules are taken by mouth with all meals and snacks that contain fat and/or
protein. Instruct parents that for children, capsules can be opened and the microspheres put in
applesauce or other soft foods, but not in anything with pH >6.0, which will destroy the enteric
coating and expose the enzymes to stomach acid, where they will be inactivated. This includes
dairy products such as milk, custard, and ice cream (3).
The typical North American diet is usually adequate in sodium, but CF patients may need sodium
replacement, especially during exertion, hot weather, and with fever. Infants may need to be
supplemented with 1/8 to 1/4 tsp daily (which amounts to a small pinch of salt) due to the low
sodium content of infant formulas, breast milk, and infant foods (3).
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Respiratory Failure
Disease Process
Respiratory failure (RF) is a syndrome in which the respiratory system fails in one or both of its gas-
exchange functions: oxygenation and carbon dioxide elimination. RF is defined as either hypoxemic (drop in
blood oxygen levels) or hypercapnic (rise in arterial carbon dioxide levels). Hypoxemic respiratory failure
(type I) is characterized by a PaO2 of <60 mm Hg with a normal or low PaCO2. This is the most common
form of respiratory failure and some examples include cardiogenic or noncardiogenic pulmonary edema,
pneumonia, and pulmonary hemorrhage. Hypercapnic respiratory failure (type II) is characterized by a
PaCO2 of >50 mm Hg. Type II RF patients who are breathing room air often develop hypoxemia as well.
Common etiologies of type II RF include drug overdose, neuromuscular disease, chest wall abnormalities,
and severe airway disorders, such as asthma and COPD (3).
RF can be either acute or chronic. Acute hypercapnic RF develops quickly, over minutes to hours, and
usually results in a pH <7.3. Chronic respiratory failure develops over several days or longer, allowing time
for renal compensation and an increase in bicarbonate concentration. Therefore, the pH usually is only
slightly decreased (8).
Arterial Blood Gases
The confirmation of the diagnosis of RF is based on arterial blood gas (ABG) analysis. ABG measurement is a
blood test that is performed to determine the oxygen, carbon dioxide, and bicarbonate content, as well as
the pH (acidity), of the blood. Its main use is in pulmonology, as many lung diseases feature poor gas
exchange, but it is also used in nephrology and electrolyte disturbances. In pulmonology, the test is used to
evaluate respiratory diseases and conditions that affect the lungs, to measure the effectiveness of
ventilation and oxygen therapy, and to
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evaluate overall acid-base balance (9). See Table 12.1 for ABG components.
Acid–Base Balance
When the pulmonary system is compromised by diseases such as RF or COPD, the ability of the lungs to
regulate acid–base balance can be affected. Acid–base balance within the body is required in order to
provide an optimal environment for enzymatic and cellular activity. When normal physiology is altered,
acid–base imbalances may
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result. These can be defined as either acidosis or alkalosis. When the acid–base disturbance results from a
primary change in HCO3-, it is a metabolic disorder; when the primary disturbance alters blood PaCO2, it is
a respiratory disorder. Compensation for these disturbances can be respiratory or metabolic in nature and is
intended to minimize further pH changes (9). Tables 12.2,12.3,12.4 and 12.5 list acid–base disturbances and
the body's physiological response (3,9,10).
Table 12.1 Arterial Blood Gases
Analyte Normal Range Interpretation
pH 7.35–7.45 <7.35 = acidosis
>7.45 = alkalosis
<6.8 or >7.8 is usually fatal
PaCO2 35–45 mm
Hg
Partial pressure of carbon dioxide in arterial blood (reflects CO2
concentration). A high PaCO2 (respiratory acidosis) indicates
hypoventilation; a low PaCO2(respiratory alkalosis) indicates
hyperventilation.
PaO2 70–100
mm Hga
On room air. Values below 60 may require immediate action and
possibly mechanical ventilation.
SaO2 94%–100% Saturation of hemoglobin available for transporting oxygen in the
arteries.
HCO3 22–26
mEq/L
Bicarbonate-metabolic indicator of kidney's role in maintaining
normal pH values. A low HCO3indicates metabolic acidosis; a high
HCO3indicates metabolic alkalosis.
CO2 19–24
mEq/L
Dissolved carbon dioxide in the blood.
Base
excess
–2 to 2
mEq/L
Represents the amount of buffering anions in the blood, with
HCO3 being the largest. A negative-base excess (deficit) indicates
metabolic acidosis. A positive-base excess indicates metabolic
alkalosis or compensation to prolonged respiratory acidosis.
aIn a patient >60 years old, PaO2 is equal to 80 mm Hg - 1 mm Hg for every year over 60.
Data from references 9 and 10.
Table 12.2 Respiratory Acidosis
Common Causes Asphyxia, respiratory depression (drugs, central nervous system
trauma), pulmonary disease (pneumonia, COPD, respiratory
underventilation).
Mechanism of
Compensation
Kidneys will retain HCO3 and excrete H+ to increase pH.
Uncompensated Compensated
pH <7.35 Normal
PaCO2
HCO3 Normal
Treatment and Nutritional Intervention
Mechanical ventilation is used when a patient's spontaneous ventilation is inadequate to maintain life. In
addition, it is indicated as a measure to control ventilation in critically ill patients and as prophylaxis for
impending collapse of other physiologic functions. Physiologic indications include
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respiratory or mechanical insufficiency and ineffective gas exchange (11).
Table 12.3 Respiratory Alkalosis
Common Causes Hyperventilation (anxiety, pain, respiratory overventilation),
pulmonary emboli
Mechanism of
Compensation
Kidneys will excrete HCO3and retain H+to decrease pH.
Uncompensated Compensated
pH >7.45 Normal
PaCO2
HCO3 Normal
Table 12.4 Metabolic Acidosis
Common Causes Diabetic ketoacidosis, shock, renal failure, intestinal fistula,
diarrhea, starvation
Mechanism of
Compensation
Respiratory rate increases, so lungs “blow off” excess CO2 to
increase pH.
Uncompensated Compensated
pH <7.35 Normal
PaCO2 Normal
HCO3
It is important for the dietitian working in intensive care to be familiar with ventilator modes and settings.
This information is useful when conducting nutrition assessments and calculating nutritional requirements
for RF patients on mechanical ventilation. Table 12.6 describes common ventilator modes.
The use of predictive equations to estimate energy expenditure is a regular part of the nutrition assesment
completed by a dietitian. However, in a critically ill patient with pulmonary disease, normal predictive
equations may be of little value. The meaurement of resting energy expenditure (REE), through indirect
calorimetry, has been shown to be more accurate than published formulas used to predict REE (12). Indirect
calorimetry (IC) is the measurement of gas exchange used to indicate a patient's cellular metabolic activity.
IC measures oxygen consumption
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and carbon dioxide production to calculate REE and the respiratory quotient. This information can be used
by the dietitian to prevent over- and underfeeding of patients.
Table 12.5 Metabolic Alkalosis
Common Causes Excessive vomiting, diuretics, hypercalcemia, antacid
overdose
Mechanism of
Compensation
Respiratory rate decreases to retain CO2 and decrease pH.
Uncompensated Compensated
pH >7.35 Normal
PaCO2 Normal
HCO3
Table 12.6 Ventilator Modes
Mode Name Description
ACV Assist-control
ventilation
Triggered by patient breaths, but if patient fails to trigger
the threshold, a mechanically controlled breath is
delivered.
CMV Continuous
mandatory
ventilation
Ventilator delivers breaths at a set rate and volume or
pressure, regardless of patient effort.
CPAP Continuous positive
airway pressure
Positive pressure applied during spontaneous breathing
and maintained throughout the entire respiratory cycle,
without ventilator assistance.
IMV Intermittent
mandatory
ventilation
Combination of spontaneous and CMV—patient can
breathe spontaneously between ventilator breaths that
are delivered at a set rate and volume or pressure.
MMV Mandatory minute
ventilation
Patient breathes spontaneously, yet a minimum level of
minute ventilation is ensured.
PEEP Positive-end
expiratory pressure
Positive pressure applied during machine breathing and
maintained at end-expiration.
PSV Pressure support
ventilation
Provides a preset level of positive pressure during each
inspiratory effort by the patient.
SIMV Synchronized in
termittent
mandatory
ventilation
Combines spontaneous and IMV. Intermittent ventilator
breaths are synchronized to spontaneous breaths to
reduce competition between the ventilator and the
patient. If no inspiratory effort is sensed, the ventilator
delivers a breath.
The respiratory quotient (RQ) measures the ratio of the volume of carbon dioxide (VCO2) produced to the
volume of oxygen consumed (VO). This is represented by the following equation:
RQ=VCO2/VO2
The RQ is useful because the volumes of CO2 produced and O2 consumed depend on which fuel source is
being
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metabolized (fat, carbohydrate, or protein). Table 12.7 lists the RQs for the macronutrients. Dietitians can
use this information to design nutritional regimens to reduce the rate of carbon dioxide production in
patients with COPD and patients requiring mechanical ventilation (13).
Table 12.7 Respiratory Quotients
Substrate Respiratory Quotient
Fat 0.7
Protein 0.8
Carbohydrate (glucose) 1.0
Mixed fuel diet 0.85
Table 12.8 Common Respiratory Abbreviations
ABG Arterial blood gas
ARDS Adult respiratory distress syndrome
BP Blood pressure
CF Cystic fibrosis
CO2 Carbon dioxide
COPD Chronic obstructive pulmonary disease
CPAP Continuous positive airway pressure
CVP Central venous pressure
CWP Coal worker's pneumoconiosis
DOE Dyspnea on exertion
ET Endotracheal tube
FEV Forced expiratory volume
FEV1 Forced expiratory volume in 1 second
Fio2 Fraction of inspired oxygen
HCO3 Bicarbonate
IF Inspiratory force
PaCO2 Partial pressure of arterial carbon dioxide
PaO2 Partial pressure of arterial oxygen
PEEP Positive end-expiratory pressure
SaO2 Saturation of arterial hemoglobin with oxygen
SOB Shortness of breath
TLC Total lung capacity
VT Tidal volume
VC Vidal capacity
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References
1. Miniño AM, Heron MP, Smith BL. Deaths: preliminary data for 2004. National Vital Statistics Report;
vol. 54 no.19. Hyattsville, MD: National Center for Health Statistics; 2006.
2. National Heart, Lung, Blood Institute/World Health Organization. Global Initiative for Chronic Lung
Disease: Global Strategy for the diagnosis, management, and prevention of chronic obstructive
pulmonary disease, updated 2005, Executive summary, 8/23/2005. Available at:
www.goldcopd.com/Guidelineitem.asp?l1=2&l2=1&intId=996. Accessed April 4, 2007.
3. Mahan LK, Escott-Stump, S. Krause's Food, Nutrition, & Diet Therapy, 11th ed. Philadelphia:
Saunders; 2004:792–833.
4. Chronic Obstructive Pulmonary Disease. Available at:
www.merck.com/mrkshared/mmg/sec10/ch78/ch78a.jsp. Accessed April 2, 2007.
5. Cystic Fibrosis transmembrane conductance regulator, CFTR Online Mendelian Inheritance in Man,
John Hopkins University. Available at: www.ncbi.nlm.nih.gov/entrez/dispomim.cgi?id=602421.
Accessed August 10, 2007.
6. Texas Children's Hospital. Pediatric Nutrition Reference Guide, 7th ed. Houston: Texas Children's
Hospital; 2005.
7. Escott-Stump, S. Nutrition and Diagnosis-Related Care, 6th ed. Philadelphia: Wolters
Kluwer/Lippincott Williams & Wilkins; 2008:270–306.
8. Sharma, S. Respiratory failure. Available at: www.emedicine. com/med/topic2011.htm. Accessed
April 10, 2007.
9. Acid-base tutorial. Available at: www.acid-base.com/index.php. Accessed April 3, 2007.
10. Pagana KD, Pagan TJ. Mosby's Manual of Diagnostic and Laboratory Test, 3rd ed. St. Louis: Mosby
Elsevier; 2006: 115–120.
11. Byrd RP. Mechanical ventilation. Available at: www.emedicine. com/med/topic3370.htm. Accesses
August 10, 2007.
12. American Association for Respiratory Care. Metabolic measurement using indirect calorimetry
during mechanical ventilation, 2004 revision & update. Respir Care 2004;49(9):1073–1079.
13. Shils ME, Shike M, Ross AC, et al. Modern Nutrition in Health and Disease, 10th ed. Philadelphia:
Lippincott, Williams & Wilkins; 2005.
Authors: Width, Mary; Reinhard, Tonia
Title: Clinical Dietitian's Essential Pocket Guide,The: Essential Pocket Guide, 1st Edition
Copyright ©2009 Lippincott Williams & Wilkins
> Back of Book > Appendix A: Laboratory Assessment
Appendix A: Laboratory Assessment
Laboratory and other diagnostic tests are tools used by clinicians to gain valuable, objective information
about their patients. When used in conjunction with other patient information, such as anthropometric
data, a thorough history, and a physical examination, laboratory tests can provide valuable information
about a patient's nutritional status and their response to medical nutrition therapy.
This appendix contains an alphabetical list of common laboratory (lab) measurements that are relevant to
nutrition assessment. This list is not meant to be comprehensive; rather it is a quick reference to the lab
tests most commonly used by dietitians in the clinical setting.
Normal values are listed, but it must be noted that normal ranges of lab test results vary significantly,
depending on the lab and their methods of testing. It is important to always check the normal values at the
facility where the test is performed. This information is almost always given directly adjacent to the
patient specific lab result. In this book, Reference Ranges for blood tests are reported in the conventional
U.S. system first, then in the SI system (International System of Units or Système Internationale d'Unités), if
available. Critical values are also listed, if
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applicable. All values given are for adults. Conditions that may cause test results to be increased or
decreased are listed under the heading “Clinical Implications.”
Typical Lab Charting
Figure A-1. Complete blood count.
Figure A-2. Electrolytes.
Laboratory Values for Assessing Nutritional Status
Albumin
Reference Range
3.5–5.0 g/dL or 35–50 g/L
Clinical Implications
Increased Levels
Dehydration.
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Decreased Levels
Malnutrition; pregnancy; acute and chronic inflammation and infections; cirrhosis, liver disease, alcoholism;
nephrotic syndrome, renal disease; Burns; third-space losses; protein-losing enteropathies, such as Crohn's
disease; overhydration.
Arterial Blood Gases (Blood Gases, ABG)
Reference Range
pH: 7.35–7.45 (critical values: <7.25 or >7.55)
PCO2: 35–45 mm Hg (critical values: <20 or >60 mm Hg)
HCO3: 21–28 mEq/L (critical values: <15 or >40)
PO2: 80–100 mm Hg (critical values: <40)
O2 Saturation: 95%–100% (critical values: 75% or lower)
Clinical Implications: pH
Increased Levels (Alkalosis)
Metabolic: Hypokalemia; hypochloremia; chronic vomiting; aldosteronism; chronic and high-volume gastric
suctioning; sodium bicarbonate administration.
Respiratory: Hypoxemic states (e.g., congestive heart failure [CHF], cystic fibrosis [CF], carbon monoxide
poisoning, pulmonary emboli, shock, acute pulmonary diseases); anxiety, neuroses, psychoses; pain;
pregnancy.
Decreased Levels (Acidosis)
Metabolic: Ketoacidosis (diabetes and starvation); lactic acidosis; severe diarrhea; renal failure; strenuous
exercise.
Respiratory: Respiratory failure; neuromuscular depression; pulmonary edema.
Clinical Implications: PCO2
Increased Levels
Chronic obstructive pulmonary disease (COPD; bronchitis, emphysema); oversedation; head trauma; other
causes of hypoventilation (e.g., Pickwickian syndrome).
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Decreased Levels
Hypoxemia; pulmonary emboli; anxiety; pain; pregnancy; other causes of hyperventilation.
Clinical Implications: HCO3
Increased Levels
Chronic vomiting or high-volume gastric suction; aldosteronism; COPD; use of mercurial diuretics.
Decreased Levels
Chronic or severe diarrhea; chronic use of loop diuretics; starvation; acute renal failure; diabetic
ketoacidosis.
Clinical Implications: PO2
Increased Levels
Polycythemia; increased inspired O2; hyperventilation.
Decreased Levels
Anemias; mucous plug; bronchospasm; atelectasis
Blood Urea Nitrogen (BUN)
Reference Range
10–20 mg/dL or 3.6–7.1 mmol/L
(Critical values: >100 mg/dL indicates serious impairment of renal function)
Clinical Implications
Increased Levels
Prerenal (hypovolemia, shock, burns, dehydration, congestive heart failure (CHF), myocardial infarction
(MI), gastrointestinal bleeding (GI bleed), excessive protein ingestion, and/or catabolism, starvation,
sepsis); renal (renal disease or failure, nephrotoxic drugs); postrenal (urethral obstruction from
stones/tumors/congenital anomalies, bladder outlet obstruction from prostatic hypertrophy, cancer, or
congenital anomalies.
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Decreased Levels
Liver failure; acromegaly; malnutrition; overhydration; negative nitrogen balance; syndrome of
inappropriate secretion of antidiuretic hormone (SIADH); pregnancy; nephrotic syndrome.
Calcium (Ca)—Total and Ionized Calcium
Reference Range
Total Ca: 9.0–10.5 mg/dL or 2.25–2.75 mmol/L
(Critical values: <6 or >13 mg/dL or <1.5 or >3.25 mmol/L)
Ionized Ca: 4.5–5.6 mg/dl or 1.05–1.30 mmol/L
(Critical values: <2.2 or >7 mg/dL or <0.78 or >1.58 mmol/L)
Clinical Implications
Increased Levels (Hypercalcemia)
Hyperparathyroidism; cancer with parathyroid hormone (PTH)-producing tumors (metastatic bone cancers,
Hodgkin lymphoma, leukemia, and non-Hodgkin lymphoma); Paget disease of the bone; prolonged
immobilization; milk–alkali syndrome; excessive intake of vitamin D, milk, antacids; Addison disease;
granulomatous infections (e.g., sarcoidosis, tuberculosis).
Decreased Levels (Hypocalcemia)
Pseudohypocalcemia due to low albumin levels1; hypoparathyroidism; renal failure; hyperphosphatemia
secondary to renal failure; rickets; vitamin D deficiency; osteomalacia; malabsorption; pancreatitis;
malnutrition; alkalosis.
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Chloride (CL)
Reference Range
98–106 mEq/L or 98–106 mmol/L
(Critical values: <80 or >115 mEq/L)
Clinical Implications
Increased Levels (Hyperchloremia)
Dehydration; Cushing syndrome; hyperparathyroidism; renal tubular acidosis; metabolic acidosis;
eclampsia; hyperventilation, which causes respiratory alkalosis.
Decreased Levels
Overhydration; prolonged vomiting or gastric suctioning; CHF; chronic diarrhea or high-output GI fistula;
metabolic alkalosis; burns; Addison disease; salt-losing nephritis; SIADH.
Cholesterol2
Reference Range
Desirable: 140–199 mg/dL or 3.63–5.17 mmol/L
Borderline high: 200–239 mg/dL or 5.18–6.21 mmol/L
High: >240 mg/dL or >6.22 mmol/L
Clinical Implications
Increased Levels (Hypercholesterolemia)
Familial hypercholesterolemia and/or hyperlipidemia; hypothyroidism; poorly controlled diabetes mellitus;
nephrotic syndrome; cholestasis; pregnancy; obesity; high dietary intake; Werner syndrome.
Decreased Levels
Malabsorption; malnutrition; advanced cancer; hyperparathyroidism; chronic anemias; severe burns; sepsis/
stress; liver disease.
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Creatinine (Serum Creatinine)
Reference Range
Female: 0.5–1.1 mg/dL or 44–97 µmol/L
Male: 0.6–1.2 mg/dL or 53–106 µmol/L
(Critical values for female and male: >4 mg/dL)3
Clinical Implications
Increased Levels
Impaired renal function (e.g., glomeruloneprhitis, pyelonephritis, acute tubular necrosis, urinary tract
obstruction); muscle disease (gigantism, acromegaly); rhabdomyolysis.
Decreased Levels
Debilitation; decreased muscle mass (e.g., muscular dystrophy, myasthenia gravis); advanced and severe
liver disease.
Erythropoietin (EPO)
Reference Range
5–35 IU/L
Clinical Implications
Increased Levels
Anemia (iron deficiency, megaloblastic, hemolytic); myelodysplasia; chemotherapy; AIDS; renal cell
carcinoma; adrenal carcinoma; pregnancy.
Decreased Levels
Polycythemia vera; rheumatoid arthritis; multiple myeloma.
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Folic Acid (Folate)
Reference Range
5–25 mg/mL or 11–57 mmol/L
Clinical Implications
Increased Levels
Pernicious anemia, vitamin B12 deficiency; vegetarianism; recent massive blood transfusion; blind loop
syndrome.
Decreased Levels
Inadequate intake (malnutrition, chronic disease, alcoholism, anorexia, diet devoid of fresh vegetables);
malabsorption (e.g., small bowel disease); pregnancy; megaloblastic anemia; hemolytic anemia;
malignancy; chronic renal disease; drugs that are folic antagonists (phenytoin, aminopterin, methotrexate,
antimalarials, alcohol, oral contraceptives).
Glucose (Blood Sugar, Fasting Blood Sugar [FBS])
Reference Range
<110 mg/dL or <6.1 mmol/L
(Critical values: <40 and >400 mg/dL)
Clinical Implications
Increased Levels (Hyperglycemia)
Diabetes mellitus (DM); Cushing syndrome; acute stress response (MI, cerebrovascular accident [CVA],
burns, infection, surgery); pheochromocytoma, acromegaly, gigantism; chronic renal failure; glucagonoma;
acute pancreatitis; pregnancy; corticosteroid therapy.
Decreased Levels (Hypoglycemia)
Pancreatic islet cell carcinoma; Addison disease; hypothyroidism; hypopituitarism; liver disease; starvation;
insulin overdose.
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Glucose, Postprandial (2-Hour Postprandial Glucose [2-Hour PPG])4
Reference Range
0–50 years: 40 mg/dL or <7.8 mmol/L
50–60 years: <150 mg/dL
>60 years: <160 mg/dL
Clinical Implications
Increased Levels
DM; gestational diabetes mellitus (GDM); malnutrition; hyperthyroidism; acute stress response (MI, CVA,
burns, infection, surgery); Cushing syndrome; pheochromocytoma; chronic renal failure; glucagonoma;
diuretic therapy; corticosteroid
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therapy; liver disease.
Decreased Levels
Insulinoma; hypothyroidism; hypopituitarism; insulin overdose; Addison disease.
Glucose Tolerance (GT, Oral Glucose Tolerance Test [OGTT])
Reference Range
Fasting: <110 mg/dL or <6.1 mmol/L
30 minutes: <200 mg/dL or <11.1 mmol/L
1 hour: <200 mg/dL or <11.1 mmol/L
2 hours: <140 mg/dL or <7.8 mmol/L
3 hours: 70–115 mg/dL or <6.4 mmol/L
Clinical Implications
Increased Levels
DM; acute stress response (MI, CVA, burns, infection, surgery); Cushing syndrome; pheochromocytoma;
chronic renal failure; glucagonoma; diuretic therapy; corticosteroid therapy; liver disease; acute
pancreatitis; myxedema; Somogyi response to hypoglycemia.
Glycosylated Hemoglobin (GHB; Glycohemoglobin [GHb], Hemoglobin
A1C [HbA1C])
Reference Range
Nondiabetic adult: 2.2%–4.8%
Good diabetic control: 2.5%–5.9%
Fair diabetic control: 6%–8%
Poor diabetic control: >8%
Clinical Implications
Increased Levels
Newly diagnosed DM; pregnancy; nondiabetic hyperglycemia (acute stress response, Cushing syndrome,
pheochromocytoma, glucagonoma, corticosteroid therapy).
Decreased Levels
Hemolytic anemia; chronic blood loss; chronic renal failure.
Hematocrit (Hct; Packed Cell Volume [PCV])
Reference Range5
Male: 42%–52% or 0.42–0.52 volume fraction
Female: 37%–47% or 0.37–0.47 volume fraction
Clinical Implications
Increased Levels
Erythrocytosis; congenital heart disease; polycythemia vera; severe dehydration; severe COPD.
Decreased Levels
Anemia; hemoglobinopathy; cirrhosis; hemolytic anemia; hemorrhage; dietary deficiency; renal disease;
pregnancy; leukemias, lymphomas, Hodgkin lymphoma.
Hemoglobin (Hgb, Hb)
Reference Range6
Male: 14–18 g/dL or 8.7–11.2 mmol/L
Female: 12–16 g/dL or 7.4–9.9 mmol/L
(Critical values: <5 g/dL or >20 g/dL)
Clinical Implications
Increased Levels
Erythrocytosis; congenital heart disease; polycythemia vera; severe dehydration; severe COPD
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Decreased Levels
Anemia; hemoglobinopathy; cirrhosis; hemolytic anemia; hemorrhage; dietary deficiency; bone marrow
failure; renal disease; pregnancy; leukemias, lymphomas, Hodgkin lymphoma.
Homocysteine (HCY)
Reference Range
4–14 µmol/L
Clinical Implications
Increased Levels
Vascular diseases (cardiac, cerebral, peripheral); cystinuria; vitamin B6 or B12 deficiency; folate deficiency;
malnutrition.
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Iron Level (Fe)
Reference Range
Male: 80–100 µg/dL or 14–32 µmol/L
Female: 60–60 µg /dL or 11–29 µmol/L
Clinical Implications
Increased Levels
Hemosiderosis or hemochromatosis; iron poisoning; hemolytic anemia; multiple or massive blood
transfusions; hepatitis; lead poisoning; nephritis.
Decreased Levels
Iron-deficiency anemia; chronic blood loss; insufficient dietary iron intake; third-trimester pregnancy;
inadequate intestinal absorption of iron.
Magnesium (Mg)
Reference Range
1.3–2.1 mEq/L or 0.65–1.05 mmol/L
(Critical values: <0.5 or >3 mEq/L)
Clinical Implications
Increased Levels
Renal insufficiency; Addison's disease; hypothyroidism; dehydration; use of magnesium-containing antacids
or salts.
Decreased Levels
Malnutrition; malabsorption; hypoparathyroidism; alcoholism; chronic renal tubular disease; diabetic
acidosis; excessive loss of body fluids (sweating, lactation, diuretic abuse, chronic diarrhea).
Osmolality (Serum Osmolality)
Reference Range
285–295 mOsm/kg H2O or 285–295 mmol/kg
(Critical values: <265 mOsm/kg or >320 mOsm/kg)
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Clinical Implications
Increased Levels
Dehydration; hypernatremia; hypercalcemia; DM, hyperglycemia, diabetic ketoacidosis; azotemia; mannitol
therapy; alcohol ingestion (ethanol, methanol, ethylene glycol); uremia; diabetes insipidus.
Decreased Levels
Overhydration; SIADH.
Phosphate (PO4), Phosphorus (P)
Reference Range
3.0–4.5 mg/dL or 0.97–1.45 mmol/L
(Critical values: <1 mg/dL)
Clinical Implications
Increased Levels
Renal failure; hypoparathyroidism; acromegaly; bone metastasis; sarcoidosis; hypocalcemia; Addison
disease; rhabdomyolysis.
Decreased Levels
Hyperparathyroidism; hypercalcemia; rickets; malnutrition; gram-negative sepsis; hyperinsulinism;
alkalosis; IV glucose administration (phosphorus follows glucose into cells).
Potassium (K)
Reference Range
3.5–5.0 mEq/L or 3.5–5.0 mmol/L
(Critical values: <2.5 or >6.5 mEq/L)
Clinical Implications
Increased Levels (Hyperkalemia)
Excessive dietary or IV intake; acute or chronic renal failure; Addison's disease; hypoaldosteronism;
aldosterone-inhibiting
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diuretics (spironolactone, traimterene); crush or cell damaging injuries (accidents, burns, surgery,
chemotherapy); hemolysis; acidosis; dehydration
Decreased Levels (Hypokalemia)
Deficient dietary or IV intake; burns/trauma/surgery; diarrhea/vomiting/sweating; diuretics;
hyperaldosteronism; Cushing syndrome; licorice ingestion; alkalosis; glucose administration; cystic fibrosis.
Prealbumin (PAB; Thyroxine-Binding Prealbumin [TBPA], Thyretin,
Transthyretin)
Reference Range
15–36 mg/dL or 150–360 mg/L
(Critical values: <10.7 mg/dL indicates severe nutritional deficiency)
Clinical Implications
Increased Levels
Hodgkin's lymphoma; pregnancy
Decreased Levels
Malnutrition; liver damage; burns; inflammation.
Prothrombin Time (PT; Pro-Time, International Normalized Ratio
[INR])
Reference Range
11.0–13.0 seconds; 85%–100% of control
Full anticoagulant therapy: <1.5–2 times control value; 20%–30% of control
(Critical values: >20 seconds; full anticoagulant therapy: 3 times control values)
Clinical Implications
Increased Levels (Prolonged PT)
Liver disease (hepatitis, cirrhosis); hereditary factor deficiency (factors II, V, VII, X); vitamin K deficiency;
bile
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duct obstruction; coumarin ingestion; massive blood transfusion; salicylate intoxication.
Red Blood Cell Count (RBC Count; Erythrocyte Count)
Reference Range
RBC ÷ 106/µL or RBC ÷ 1012/L
Male: 4.7–6.1; Female: 4.2–5.4
Clinical Implications
Increased Levels
Erythrocytosis; congenital heart disease; severe COPD; polycythemia vera; severe dehydration;
hemoglobinopathies.
Decreased Levels
Anemia; cirrhosis; hemorrhage; Addison's disease; renal disease; bone marrow failure; pregnancy;
rheumatoid/collagen-vascular diseases (rheumatoid arthritis [RA], systemic lupus erythematosus [SLE],
sarcoidosis); lymphoma/leukemia/Hodgkin's lymphoma.
Sodium (Na)
Reference Range
136–145 mEq/L or 136–145 mmol/L
(Critical values: <120 or >160 mEq/L)
Clinical Implications
Increased Levels (Hypernatremia)
Increased sodium intake (dietary or IV); decreased sodium loss (Cushing's syndrome, hyperaldosteronism);
excessive free body water loss (GI, excessive sweating, extensive burns, diabetes insipidus, osmotic
diuresis).
Decreased Levels (Hyponatremia)
Decreased sodium intake (deficient dietary or IV sodium); increased sodium loss (Addison's disease,
diarrhea/vomiting,
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intraluminal bowel loss, diuretic administration, chronic renal insufficiency); increased free body water
(excessive oral or IV water intake, hyperglycemia, CHF, peripheral edema, pleural effusion, SIADH).
Total Iron-Binding Capacity (TIBC)
Reference Range
250–460 µg/dL or 45–82 µmol/L
Clinical Implications
Increased Levels
Estrogen therapy; polycythemia vera; pregnancy (late); iron-deficiency anemia; acute and chronic blood
loss; acute hepatitis.
Decreased Levels
Hypoproteinemia (malnutrition or burns); inflammatory diseases; cirrhosis; hemolytic, pernicious, and
sickle cell anemias; thalassemia.
Transferrin
Reference Range
Male: 215–365 mg/L or 2.15–3.65 g/L
Female: 250–380 mg/dL or 2.50–3.80 g/L
Clinical Implications
Increased Levels
Estrogen therapy; polycythemia vera; pregnancy (late); iron-deficiency anemia.
Decreased Levels
Hypoproteinemia (malnutrition or burns); inflammatory diseases; cirrhosis; hemolytic, pernicious, and
sickle cell anemias; renal disease; acute liver disease.
P.303
Transferrin Saturation
Reference Range
Male: 20%–50%
Female:15%–50%
Clinical Implications
Increased Levels
Hemochromatosis; increased iron intake; hemolytic anemia; thalassemia; acute liver disease.
Decreased Levels
Iron-deficiency anemia; anemia of infection and chronic diseases; malignancy.
Vitamin B12 (Cyanocobalamin)
Reference Range
160–950 pg/mL or 118–701 mmol/L
Clinical Implications
Increased Levels
Leukemia, polycythemia vera; severe liver dysfunction; CHF; diabetes; myeloproliferative disease.
Decreased Levels
Pernicious anemia; malabsorption syndromes and inflammatory bowel disease (IBD); intestinal worm
infestation; Zollinger–Ellison syndrome; folic acid deficiency; vitamin C deficiency; achlorydria; large
proximal gastrectomy.
White Blood Count and Differential Count (WBC with differential)
Reference Range
Total WBCs: 5,000–10,000/mm3 or 5–10 (109/L
(Critical values: <2,500 or >30,000/mm3)
P.304
Lymphocytes: 1,000–4,000/mm3 (comprise 20%–40% of the total WBC; and in malnutrition, lymphocyte
count is reduced).
Clinical Implications
Increased WBC Count (Leukocytosis)
Infection; leukemic neoplasia or other myeloproliferative disorders; trauma/stress/hemorrhage; tissue
necrosis; inflammation; thyroid storm; steroid use.
Decreased WBC Count (Leukopenia)
Drug toxicity; bone marrow failure; dietary deficiency of vitamin B12 or iron; autoimmune disease;
hypersplensim.
Laboratory Test Panels
Laboratory tests are often ordered as panels that are disease or organ specific. Next are some common test
panels that have significance to the registered dietitian (RD). Note that panels may be modified or
expanded at different clinical facilities.
Anemia Panel
CBC; RBC indices; reticulocyte count:
Microcytic: erythrocyte sedimentation rate (ESR); iron panel
Normocytic: ESR; hemolysis profile
Macrocytic: vitamin B12; folate; thyroid-stimulating hormone (TSH)
Basic Metabolic Panel (7 Channel/Chem 7/SMA-7)
Carbon dioxide content; chloride, blood; creatinine, blood; glucose, blood; potassium, blood; sodium,
blood; urea nitrogen, blood (BUN).
P.305
Complete Blood Cell Count (CBC) with Differential (Diff)
RBC; Hgb; Ht; red blood cell indices (mean corpuscular volume [MCV], mean corpuscular hemoglobin [MCH],
mean corpuscular hemoglobin concentration [MCHC], red blood cell distribution width [RDW]); WBC and Diff
count (neutrophils; lymphocytes; monocytes; eosinophils; basophils); blood smear; platelet count; mean
platelet volume (MPV).
Comprehensive Metabolic Panel (12 Channel/Chem 12)
Albumin; alkaline phosphatase; AST (SGOT); bilirubin- total; BUN; calcium; chloride; creatinine; glucose;
potassium; protein-total; sodium.
The old Comprehensive Metabolic Panel or “Chem 20” includes all the above labs plus:
ALT (SGPT); bilirubin-direct; carbon dioxide; cholesterol; GGT; LDH; phosphorus; uric acid.)
Diabetes Mellitus Management
Anion gap; basic metabolic panel; hemoglobin A1C; lipid profile.
Hepatic Function
ALT; albumin; alkaline phosphatase; AST; bilirubin-direct; bilirubin-total; GGT; protein, total; prothrombin
time (PT).
Lipid Panel
Cholesterol-total; high-density lipoprotein (HDL); triglyceride; low-density lipoprotein (LDL); very-low-
density lipoprotein (VLDL).
Pancreatic Panel
Amylase; calcium; glucose; lipase; triglyceride.
P.306
Renal Panel
Albumin; basic metabolic panel; calcium; CBC; creatinine clearance; magnesium; phosphorus; protein-total;
protein-urine; protein-24-hour urine.
References
Bakerman S, Bakerman P, Strausbauch P. Bakerman's ABC's of Interpretive Laboratory Data, 4th ed.
Scottsdale: Interpretive Laboratory Data, Inc.; 2002.
Fischbach FT, Marshall BC. A Manual of Laboratory and Diagnostic Tests, 7th ed. Philadelphia:
Lippincott Williams & Wilkins; 2004.
Mahan LK, Escott-Stump, S. Krause's Food, Nutrition, & Diet Therapy, 11th ed. Philadelphia: Saunders;
2004:792–833.
Pagana KD, Pagana TJ. Mosby's Manual of Diagnostic and Laboratory Test, 3rd ed. Missouri: Mosby
Elsevier; 2006.
Because about one-half of blood calcium is bound to albumin, when albumin levels are low, the serum
calcium will also be low. Calcium levels can be adjusted with the following equation, when serum albumin
is low: Corrected calcium = total calcium mg/dL + 0.8 [4 –serum albumin g/dL].
Authors: Width, Mary; Reinhard, ToniaTitle: Clinical Dietitian's Essential Pocket Guide,The: Essential Pocket Guide, 1st EditionCopyright ©2009 Lippincott Williams & Wilkins> Back of Book > Appendix B: Food–Drug InteractionsAppendix B: Food–Drug InteractionsLisa Ventrella Lucente RDThe following table of medications is not meant to be comprehensive, but instead lists commonmedications that have significant nutritional implications. The list is alphabetical by generic name (initalics), and cross-referenced by brand or trade name.P.308P.309P.310P.311P.312P.313P.314P.315P.316P.317P.318P.319P.320P.321P.322P.323P.324P.325P.326
Medication Class & Action Side EffectsNutritionalImplications
Adalat See nifedipineAldactone See spironolactoneApresoline See hydralazineAtenololTenormin
Beta-blocker,antiadrenergic,antiarrhythmic
Diarrhea,constipation, nausea,and vomiting.Possiblehypoglycemia.Signs of sympatheticresponse tohypoglycemia maybe masked. Mayhave a decreasedinsulin release in
Adherence necessaryfor those followingdiabetic diet.Monitor bloodglucose levels. Becautious ofnonsympatheticsigns ofhypoglycemia.Consider fluid andelectrolyte
response tohyperglycemia.
replacement fordiarrhea andvomiting.
AtorvastatinLipitor
Inhibitor ofHMG-CoAreductase
Constipation,diarrhea, gas, upsetstomach, and upperright stomach pain.Coenzyme Q10 maybe significantlyreduced.
Avoid intake largequantities ofgrapefruit juice for itincreases theabsorption of statins(>1 qt/day). Eat alow-cholesterol,low-fat diet for bestresults.Gastrointestinalproblems generallytransient.
AzithromycinZithromax
AntibioticBacteriostatic orbacteriocidal
Occasional nausea,vomiting, diarrhea,abdominal pain,anorexia, stomatitis,bad taste in mouth
Take with food toavoid GIdisturbances.Azithromycin oralsuspension should betaken 1 hr before or2 hr after meals. Eatsmall, frequentmeals to avoidanorexia. Considerfluid and electrolytereplacement fordiarrhea. Avoidalcohol.
Bactrim, Bactrim DS See sulfamethoxazoleBenazeprilLotensin
AntihypertensiveACE Inhibitor
May increase serumpotassium.May decrease serumsodium.Nausea, salty ormetallic taste, mouthsores.
Caution with foodshigh in potassium orpotassiumsupplements. Avoidsalt substitutes.Maintain adequatehydration.
Betaloc See metoprololBiaxin See clarithromycinBumetanideBumex
DiureticLoop diuretic
Ginkgo Biloba maycause increasedblood pressure.Licorice can increasethe risk ofhypokalemia. May
Consume foods highin potassium andmagnesium. Avoidconsumption ofnatural licorice.Monitor electrolyte
increase bloodglucose, uric acid,cholesterol, LDL,calcium, andtriglycerides. Maydecrease urinaryexcretion of calciumand increaseexcretion ofmagnesium, sodiumand potassium levels.
levels and considersupplementation.Caution withcalciumsupplements.
BupropionWellbutrin, Zyban
AntidepressantSerotonin &norepinephrinereuptakeinhibitor
Dry mouth, upsetstomach, vomiting,weight loss, andconstipation. Alcoholmay increase sideeffects.
Monitor weight. Useice chips or chewgum for dry mouth.Avoid alcohol.
Bumex See bumetanideCalan See verapamilCalcijex See calcitriolCalcium saltsPhosLo, Caltrate, Dicarbosil, OsCal,Titralac, Tums, Citracal, Calcitrate
Calcium-basedphosphorusbinder
Hypercalcemia,stomach pains,nausea, vomiting,constipation, drymouth, thirst, andfrequent urination.
Maintain adequatehydration, serummagnesium,phosphate,potassium levels,and urine calciumlevels.
Calcitrate See calcium saltsCalcitriolCalcijex, Rocaltrol
Vitamin D May increasealuminumconcentration,hypercalcemia,serum cholesterol,serum phosphorous,and magnesiumconcentration. Upsetstomach, vomiting,dry mouth,constipation, metallictaste in mouth,increased thirst,decreased appetite,weight loss and fattystools.
Avoid use ofantacids. Only worksin conjunction withappropriate intake ofcalcium. Considerlow phosphate diet ifon dialysis.
Caltrate See calcium salts
Capoten See captoprilCapozide See captoprilCaptopril Antihypertensive
ACE InhibitorMay increase serumpotassium.May decrease serumsodium.Nausea, salty ormetallic taste, mouthsores.
Caution with foodshigh in potassium orpotassiumsupplements. Avoidsalt substitutes.Maintain adequatehydration.
Catapres See clonidineCelexa See citalopramCholestyramineQuestran, Prevalite
Bile acidsequestrant
May decrease serumpotassium andcalcium. Binds fat-soluble vitamin A, D,E, and K, folic acid,and beta-carotene.Constipation, nausea,vomiting, abdominalpain, indigestion.Occasional diarrhea.
Mix with 3 to 6 oz ofliquid, such as juice,milk, or water forpowdered form.Irritating to GI tract.Take before meals.Take fat-solublevitamins in a watermiscible form ortake a supplementprior to initial dailydose of drug.Monitor nutrientlevels if long-termuse of drug isindicated. Considerhigh fiber diet forconstipation.
Cinacalcet Sensipar Calcimimetic High-fat intake mayincrease cinacalcetconcentration ofplasma. Nausea,vomiting, anddiarrhea
Avoid taking withgrapefruit juice.
Ciprofloxacin Antibacterial Upset stomach,vomiting, stomachpain, indigestion.Inflammation of thestomach leading topossible diarrhea.Aluminum,magnesium, calcium,ferrous sulfate, andzinc are thought to
Take with 8 oz ofwater. Ensureadequate fluidintake. Considerfluid and electrolytereplacement forvomiting anddiarrhea. Should notbe taken with dairyproducts or calcium
form chelationcomplexespreventing the drugsfrom being absorbed.
containing fluids. Donot need to avoidfoods containingthese products.
CisplatinPlatinol, Platinol-AQ
Alkylating agent Loss of appetite,weight loss, diarrhea,nausea, vomiting,and altered taste.
Drink plenty offluids for drug;irritates the kidney.Vomiting is severe.May consider anti-emetic therapy.Monitor weight.Encourage foodintake when patientfeels best, e.g.,morning.
CitalopramCelexa
AntidepressantSelectiveserotoninreuptakeinhibitor
Nausea, diarrhea,vomiting, anorexia,dry mouth, anddyspepsia. Maydecrease serumsodium.
Consider fluid andelectrolytereplacement fordiarrhea andvomiting. Use icechips or chew gumfor dry mouth.Avoid alcohol.
Citracal See calcium saltsClarithromycinBiaxin
AntibioticBacteriostatic orbacteriocidal
Occasional nausea,vomiting, diarrhea,abdominal pain,anorexia, stomatitis,bad taste in mouth
Take with food toavoid GIdisturbances. Eatsmall, frequentmeals to avoidanorexia. Considerfluid and electrolytereplacement fordiarrhea. Avoidalcohol.
ClonidineCatapres, Duraclon
Alpha-antiadrenergic
Constipation, nausea,vomiting, dry mouth,and drowsiness.
Avoid alcohol intakefor it can exacerbatedrowsiness. Use icechips or chew gumfor dry mouth.
ClopidogrelPlavix
Anti-platelet Upset stomach,stomach pain,diarrhea, andconstipation. Gingermay increase thepossibility of
Consider small,frequent meals foranorexia. Considerfluid and electrolytereplacement fordiarrhea.
bleeding. Consistency indietary andsupplemental intakemust be consistent toachieve steady levelof anticoagulation.Those on long-termuse should bemonitored for bonedensity.
Co-trimoxazole/trimethoprim/SulfamethoxazoleBactrim, Bactrim DS
Bactericidal May cause anorexia,nausea, vomiting,diarrhea, abdominalpain, or stomatitis.May hinder folatemetabolism.
Take with 8 oz ofwater on an emptystomach. Eat small,frequent meals toavoid anorexia. Takea folate supplement.Consider fluid andelectrolytereplacement fordiarrhea.
Coumadin See warfarinCovera-HS See verapamilCyclophosphamideCytoxan
Alkylating agent,nitrogen mustard
Nausea, vomiting,loss of appetite, andweight loss.
Drink plenty offluids for drug;irritates bladder andkidneys. Encouragefood intake whenpatient feels best,e.g., morning.
Cytoxan See cyclophosphamideDialyviteDiatx, Nephrocaps, Nephrovite
B-complex withvitamin C andBiotin
Abdominal pain,cramps, dyspepsia,and nausea.
Taken whenvitamins inadequate,usually after dialysiswhen fluid isremoved. Used toreplace water-soluble vitaminlosses.
Diatx See dialyviteDicarbosil See calcium saltsDigoxinLanoxin
Antiarrhythmic,cardiac glycoside
Occasional diarrhea,loss of appetite,lower stomach pain,nausea, and/orvomiting. May
Hypomagnesemia,hypokalemia, andhypercalcemiaelevate drug toxicity.Ensure consumption
reduce potassiumlevels and increaseurinary excretion ofmagnesium.
adequate potassiumand magnesium.Care should be takenwith calciumsupplements andantacids.
DoxercalciferolHectorol
See calcitriol
Duraclon See clonidineDyrenium See triamtereneEffexor, Effexor XR See venlafaxineEnalaprilVasotec
AntihypertensiveACE Inhibitor
May increase serumpotassium.May decrease serumsodium.Nausea, salty ormetallic taste, mouthsores.
Caution with foodshigh in potassium orpotassiumsupplements. Avoidsalt substitutes.Maintain adequatehydration.
Ery-Tab See erythromycinErythromycinEry-Tab
AntibioticBacteriostatic orbacteriocidal
Occasional nausea,vomiting, diarrhea,abdominal pain,anorexia, stomatitis,bad taste in mouth
Take with food toavoid GIdisturbances. Eatsmall, frequentmeals to avoidanorexia. Considerfluid and electrolytereplacement fordiarrhea. Avoidalcohol.
Effexor See venlafaxineEskalith, Eskalith CR See lithiumExtentabs See quinidineFeostat See ferrous fumarateFemiron See ferrous fumarateFenofibrate Tricor See gemfibrozilFeosol See ferrous sulfateFeratab See ferrous sulfateFergon See ferrous sulfateFerrex See ferrous sulfateFerrlecit See sodium ferric gluconateFerrous fumarateFemiron, Feostat
Iron supplement Constipation,diarrhea, andabdominaldiscomfort.
Emphasize iron-richfood in a well-balanced diet.
Ferrous sulfateFeosol, Feratab, Fergon, Ferrex, Hemocyte,Nephro-Fer, Niferex
Iron supplement Constipation andstomach upset.
Emphasize iron-richfood in a well-balanced diet.
Ferrous gluconate See ferrous sulfateFlagyl See metronidazoleFluoxetineProzac
AntidepressantSelectiveserotoninreuptakeinhibitor
Alcohol mayincrease depression.St. John's Wort mayincrease drug effect.Nausea, diarrhea,decreased appetite,dry mouth, vomiting,constipation, andabdominal pain.
Avoid alcohol.Consider fluid andelectrolytereplacement fordiarrhea andvomiting. Use icechips or chew gumfor dry mouth.Consider small,frequent meals fordecreased appetite.
Fluvastatin See atorvastatinLescolFurosemideLasix
DiureticLoop diuretic
Ginkgo Biloba maycause increasedblood pressure.Licorice can increasethe risk ofhypokalemia. Mayincrease bloodglucose, uric acid,cholesterol, LDL,calcium, andtriglycerides. Maydecrease urinaryexcretion of calciumand increaseexcretion ofmagnesium, sodium,and potassium levels.
Consume foods highin potassium andmagnesium. Avoidconsumption ofnatural licorice.Monitor electrolytelevels and considersupplementation.Caution withcalciumsupplements.
Gemfibrozil Lopid Fibric acidderivative
Stomach pain,diarrhea,constipation,vomiting, and gas.
Eat a low-cholesterol, low-fat,low-sucrose diet forbest results. Avoidalcohol.Consider fluid andelectrolytereplacement fordiarrhea andvomiting.
Hectorol See doxercalciferol
HydralazineApresoline
Antiarrhythmic,Antiprotozoal
Nausea, vomiting,diarrhea, fluidretention, and edema.Impedes metabolismof pyridoxine(vitamin B6).
Doctor mayprescribe a low-saltor low-sodium diet.Take with food.Monitor forpyridoxinedeficiency. Consumediet high inpyridoxine. Considersupplementation.
Hemocyte See ferrous sulfateImfed See iron dextranIron dextranImfed
IV iron,Hematinic
Nausea, vomiting,and metallic taste.
Avoid taking oraliron. Emphasizeiron-rich food in awell-balanced diet.
Iron sucrose Venofer IV iron,Hematinic
Diarrhea Avoid taking oraliron. Emphasizeiron-rich food in awell-balanced diet.
IsocarboxazidMarplan
AntidepressantMonoamineoxidase inhibitor(MAOI)
Sudden high bloodpressure may occurwith ingestion ofcertain foods.Alcohol mayincrease depressanteffect. Caffeine mayincrease bloodpressure and cardiacarrhythmias.
Avoid foods high intyramine: cheeses,fava, or broad beanpods; yeast or meatextracts, smoked orpickled meat,poultry, or fish;fermented sausagesuch as bologna,pepperoni, salami, orother fermentedmeat; avocados;bananas; beer; wine;and raisins. Avoidexcess amounts ofcaffeine, tea, orchocolate. Avoidalcohol.
Isoptin, Isoptin SR See verapamilKeflex See cephalexinKinidine See quinidineLanoxin See digoxinLasix See furosemideLescol See fluvastatinLipitor See atorvastatin
LisinoprilPrinivil, Zestril
AntihypertensiveACE inhibitor
May increase serumpotassium.May decrease serumsodium.Nausea, salty ormetallic taste, mouthsores.
Caution with foodshigh in potassium orpotassiumsupplements. Avoidsalt substitutes.Maintain adequatehydration.
Lithane See lithiumLithiumEskalith, Eskalith CR, Lithobid, Lithane,Lithonate, Lithotabs
Antimanic agent Drug interferes withthe regulation ofsodium and waterlevels in the bodyand may lead todehydration.Toxicity may resultfrom sodiumdepletion. Caffeineappears to reduceserum lithiumconcentrations andincrease side effects.Loss of appetite,stomach pain orbloating, gas,indigestion, weightgain or loss, drymouth, excessivesaliva in the mouth,tongue pain, changein the ability to tastefood, swollen lips,and constipation.
Maintain steady saltand fluid intake.Avoid salt-free dietor sodium depletion.Avoid caffeine.
Lithobid See lithiumLithonate See lithiumLithotabs See lithiumLopid See gemfibrozilLopressor See metoprololMarplan See isocarboxazidMethotrexate Antimetabolite,
folate antagonistNausea, vomiting,diarrhea, stomachpain, mouth sores,and loss of appetite.Inhibitor ofdihydrofolatereductase, thus
Consume highVitamin B12 diet.Consider fluid andelectrolytereplacement fordiarrhea andvomiting. Encourage
decreasingavailability of activefolate.
food intake whenpatient feels best,e.g., morning. Drinkextra fluids to passmore drug throughthe urine.Leucovorin shouldbe considered toreverse toxic effectof folic acidantagonists.
MetoprololBetaloc, Lopressor, Toprol XL
Beta-blocker,antiadrenergic,antiarrhythmic
Diarrhea,constipation, nausea,and vomiting.Possiblehypoglycemia. Signsof sympatheticresponse tohypoglycemia maybe masked. Mayhave a decreasedinsulin release inresponse tohyperglycemia.
Adherence necessaryfor those followingdiabetic diet.Monitor bloodglucose levels. Becautious ofnonsympatheticsigns ofhypoglycemia.Consider fluid andelectrolytereplacement fordiarrhea andvomiting.
MetronidazoleFlagyl
Antibacterial,antiprotozoal
Anorexia, nausea,dry mouth,stomatitis, diarrheaor constipation,vomiting, andmetallic taste.
Avoid alcohol andalcohol-containingproducts during andat least 5 days aftertreatment. Avoid hotand spicy foods.Consider fluid andelectrolytereplacement fordiarrhea. Take withfood to prevent GIdistress. Considersmall, frequentmeals for anorexia.Use ice chips orchew gum for drymouth.
Nardil See phenelzineNephrocaps See dialyviteNephro-Fer See ferrous sulfate
Nephrovite See dialyviteNiacinNiacor, Niaspan, Nicotinex, Slo-Niacin
Nicotinic acidderivative
Alcohol mayincrease side effectsof niacin. Occasionalgas, nausea,vomiting, anddiarrhea. Mayincrease blood uricacid and glucoselevels.
Caution withdiabetes. Ensureadherence to diabeticdiet if necessary.May consider low-purine diet ifnecessary. Considerfluid and electrolytereplacement fordiarrhea andvomiting.
Niacor See niacinNiaspan See niacinNicotinex See niacinNifedical See nifedipineNifedipineAdalat, Nifedical, Procardia
Calcium channelblocker
Upset stomach,heartburn, nausea,and constipation.
Avoid drinkinggrapefruit juice oreating grapefruit 1 hrbefore or for 2 hrafter takingnifedipine.
Niferex See ferrous sulfateOncovin See vincristineOrlistatXenical
Lipase inhibitor Flatulence, fattystools, nausea,diarrhea. Decreasedabsorption vitaminsA and E.
Side effects aretransient.Monitor nutrientlevels.
OsCal See calcium saltsParnate See tranylcypromineParoxetinePaxeva, Paxil, Paxil CR
AntidepressantSelectiveserotoninreuptakeinhibitor
St. John's Wort mayincrease drug effect.Nausea, dry mouth,constipation,diarrhea, anddecreased appetite.
Consider fluid andelectrolytereplacement fordiarrhea. Use icechips or chew gumfor dry mouth.Consider small,frequent meals fordecreased appetite.
Paxeva See paroxetinePaxil, Paxil CR See paroxetinePenicillin Antibiotic
Kill or preventgrowth of
GI disturbancesincluding milddiarrhea, nausea, or
Should be taken 1 hrbefore or 2 hr afterfood to facilitate
bacteria vomiting. Some maycontain high amountsof sodium orpotassium.
absorption. Considerfluid and electrolytereplacement fordiarrhea. Caution ifon low sodium diet.Some strengths ofamoxicillin maycontainphenylalanine.
Paricalcitol Zemplar See calcitriolPhenelzineNardil
AntidepressantMonoamineoxidase inhibitor(MAOI)
Sudden high bloodpressure may occurwith ingestion ofcertain foods.Alcohol mayincrease depressanteffect. Caffeine mayincrease bloodpressure and cardiacarrhythmias.
Avoid foods high intyramine: cheeses,fava, or broad beanpods; yeast or meatextracts, smoked orpickled meat,poultry, or fish;fermented sausagesuch as bologna,pepperoni, salami, orother fermentedmeat; avocados;bananas; beer; wine;and raisins. Avoidexcess amounts ofcaffeine, tea, orchocolate. Avoidalcohol.
PhosLo See calcium saltsPlatinol, Platinol-AQ See cisplatinPlavix See clopidogrelPravachol See pravastatinPravastatinPravachol
Inhibitor ofHMG-CoAreductase
Constipation,diarrhea, gas, upsetstomach, and upperright stomach pain.Coenzyme Q10 maybe significantlyreduced.
Avoid intake largequantities ofgrapefruit juice for itincreases theabsorption of statins(>1 quart/day). Eat alow -cholesterol,low-fat diet for bestresults.Gastrointestinalproblems generallytransient.
Prevalite See cholestyramine
Prinivil See lisinoprilProcardia See nifedipinePropanololInderal See atenololProzac See fluoxetineQuestran See cholestyramineQuinidex See quinidineQuinidineKinidine, Quinidex, Extentabs
Antiarrhythmic,antiprotozoal
Abdominal pain andcramps, diarrhea,nausea, andvomiting. May causehypokalemia,hypomagnesemia,and/or hypocalcemia.
Consider fluid andelectrolytereplacement fordiarrhea andvomiting. Consumediet adequate inpotassium,magnesium, andcalcium.Supplementationmaybe necessary.
Renagel See sevelamerRocaltrol See calcitriolSensipar See cinacalcetSertralineZoloft
AntidepressantSelectiveserotoninreuptakeinhibitor
May increase serumtriglyceride and totalcholesterol. Maydecrease uric acidlevels. St. John'sWort may increaseadverse side effects.Nausea, diarrhea, drymouth, constipation,altered taste, anddyspepsia.
Monitor blood lipidlevels. Considerfluid and electrolytereplacement fordiarrhea andvomiting. Use icechips or chew gumfor dry mouth.Avoid alcohol.
SevelamerRenagel
Non-calcium-basedphosphorusbinder
Diarrhea, dyspepsia,gas, constipation,nausea, andvomiting.
Take with food. Useof aluminum shouldbe limited to <14days. Monitorbicarbonate,chloride, calcium,and phosphorouslevels.
SimvastatinZocor
Inhibitor ofHMG-CoAreductase
Constipation,diarrhea, gas, upsetstomach, and upperright stomach pain.Coenzyme Q10 maybe significantly
Avoid intake largequantities ofgrapefruit juice for itincreases theabsorption of statins(>1 quart/day). Eat a
reduced. low-cholesterol,low-fat diet for bestresults.Gastrointestinalproblems generallytransient.
Slo-Niacin See niacinSodium ferric Gluconate complexFerrlecit
See iron sucrose
SpironolactoneAldactone
DiureticPotassiumsparing diuretic
Hyperkalemia,dehydration,hyponatremia,nausea, vomiting,anorexia, abdominalcramps, and diarrhea.
Avoid foods high inpotassium,potassiumsupplements, andsalt substitutes.
Tenormin See atenololTitralac See calcium saltsToprol XL See metoprololTranylcypromineParnate
AntidepressantMonoamineoxidase inhibitor(MAOI)
Sudden high bloodpressure may occurwith ingestion ofcertain foods.Alcohol mayincrease depressanteffect. Caffeine mayincrease bloodpressure and cardiacarrhythmias. GIupset
Avoid foods high intyramine: cheeses,fava or broad beanpods, yeast or meatextracts, smoked orpickled meat,poultry, or fish,fermented sausagesuch as bologna,pepperoni, salami, orother fermentedmeat, avocados,bananas, beer, wine,and raisins. Avoidexcess amounts ofcaffeine, tea, orchocolate. Avoidalcohol.
TriamtereneDyrenium
DiureticPotassiumsparing diuretic
Hyperkalemia,dehydration,hyponatremia,nausea, vomiting,anorexia, abdominalcramps, and diarrhea.
Avoid foods high inpotassium,potassiumsupplements, andsalt substitutes.
Tricor See fenofibrateTrovafloxacinTrovan
Quinolone Iron preparationsmay increase drug
Consider fluid andelectrolyte
absorption.Dandelion mayincrease drug effect.Fennel seed maydecrease drug effectresulting in treatmentfailure. Diarrhea.
replacement fordiarrhea.
Trovan See trovafloxacinTums See calcium saltsVasotec See enalaprilVelban See vinblastineVelsar See vinblastineVenlafaxineEffexor, Effexor XR
Antidepressant St. John's Wort mayincrease sedativeeffect. May increasecholesterol and uricacid levels. Maydecrease serumsodium and serumphosphate levels.May modify bloodglucose and serumpotassium levels.Nausea, dry mouth,anorexia, andconstipation.
Use ice chips orchew gum for drymouth. Monitorweight.
Venofer See iron sucroseVerapamilCalan, Verelan, Verelan PM, Isoptin,Isoptin SR, Covera-HS
Calcium ChannelBlocker
Constipation, upsetstomach, heartburn.
Avoid drinkinggrapefruit juice oreating grapefruit 1 hrbefore or for 2 hrafter takingnifedipine.
Verelan, Verelan PM See verapamilVinblastineVelban, Velsar, vinblastine sulfate, VBL
Plant alkaloid Nausea, vomiting,stomach pain,constipation, anddiarrhea.
Drink plenty offluids to decreaseconstipation.
VincristineOncovin
Plant alkaloid Nausea, vomiting,stomach pain,stomach cramps,constipation, anddiarrhea.
Consider fluid andelectrolytereplacement fordiarrhea andvomiting. Mayconsider laxativesfor constipation.
Mild vomitingremedied withantiemetic.
WarfarinCoumadin
Anticoagulant Anorexia, nausea,abdominal crampingand diarrhea.Prevents theconversion ofvitamin K to itsactive form. Garlicmay increase the riskof bleeding.Mineralization ofnewly formed bonemay be deterred.
Consider small,frequent meals foranorexia. Considerfluid and electrolytereplacement fordiarrhea. Dietary andsupplemental intakemust be consistent toachieve steady levelof anticoagulation.Those on long-termuse should bemonitored for bonedensity.
Wellbutrin See bupropionXenical See orlistatZemplar See paricalcitolZestril See lisinoprilZithromax See azithromycinZocor See simvastatinZoloft See sertralineZyban See bupropion
Authors: Width, Mary; Reinhard, Tonia
Title: Clinical Dietitian's Essential Pocket Guide,The: Essential Pocket Guide, 1st Edition
Copyright ©2009 Lippincott Williams & Wilkins
> Back of Book > Appendix C: Nutrition-Related Information
Appendix C: Nutrition-Related Information
Listing of Contents
Conversion tables
Framingham Risk Scoring for Serum Cholesterol
Vitamin Facts and Nutrient Lists
Vitamins (A)
Food Sources of Individual Vitamins
Water Soluble (B–K)
Fat Soluble (L–O)
Table C.1 Conversion Tables
A. Length
1 m = 39 in.
1 cm = 0.4 in.
1 in. = 2.5 cm
1 ft = 30 cm
B. Temperature
Celsius Fahrenheit
Steam 100°C 212°F
Body temp. 37°C 98.6°F
Ice 0°C 32°F
°C = (°F –32) * 5/9
°F = (°C * 9/5) + 32
C. Volume
1 L = 1,000 mL 0.26 gal 1.06 qt 2.1 pt
1 mL = 1/1,000 L 0.03 fluid oz
1 gal = 128 oz 8 cups 3.8 L
1 qt = 32 oz 4 cups 0.95 L
1 pt = 16 oz 2 cups 0.47 L
1 cup = 8 oz 16 Tbs ~250 mL 0.25 L
1 oz = 30 mL
1 tablespoon (Tbs) = 3 tsp 15 mL
1 teaspoon (tsp) = 5 mL
D. Weight
1 kg = 1,000 g 2.2 lb
1 g = 1/1,000 kg 1,000 mg 0.035 oz
1 mg = 1/1,000 g 1,000 µg
1 µg = 1/1,000 mg
1 lb = 16 oz 454 g 0.45 kg
1 oz = ~28 g
E. Energy
1 kJ = 0.24 kcal
1 mJ = 240 kcal
1 kcal = 4.2 kJ
1 g carbohydrate = 4 kcal 17 kJ
1 g fat = 9 kcal 17 kJ
1 g protein = 4 kcal 17 kJ
1 g alcohol = 7 kcal 29 kJ
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Table C.2 Framingham Risk Scoring for Serum Cholesterol
The Framingham 10-Year Risk Estimates for heart disease include two categories, one for men
and one for women. To determine the 10-year risk estimate, total the points from all the
following parameters (1 through 5) and compare to the 10-Year Risk by Total Framingham
Point Scores at the end of each category.
A. Estimate of 10-Year Risk for Men
Men: Framingham Point Scores by Age Group
Age Points
20–34 -9
35–39 -4
40–44 0
45–49 3
50–54 6
55–59 8
60–64 10
65–69 11
70–74 12
75–79 13
1.
Men: Framingham Point Scores by Age Group and Total Cholesterol2.
Total
Cholesterol
Age
20–39
Age
40–49
Age
50–59
Age
60–69
Age
70–79
<160 0 0 0 0 0
160–199 4 3 2 1 0
200–239 7 5 3 1 0
240–279 9 6 4 2 1
=280 11 8 5 3 1
2.
Men: Framingham Point Scores by Age and Smoking Status
Age
20–39
Age
40–49
Age
50–59
Age
60–69
Age
70–79
Nonsmoker 0 0 0 0 0
Smoker 8 5 3 1 1
3.
Men: Framingham Point Scores by High-Density Lipoprotein (HDL) Level
HDL Points
=60 -1
50–59 0
40–49 1
<40 2
4.
Men: Framingham Point Scores by Systolic Blood Pressure (BP) and Treatment
Status
5.
Systolic BP If Untreated If Treated
<120 0 0
120–129 0 1
130–139 1 2
140–159 1 2
=160 2 3
5.
10-Year Risk by Total Framingham Point Scores
Point Total 10-Year Risk
<0 <1%
0 1%
1 1%
2 1%
3 1%
4 1%
5 2%
6 2%
7 3%
8 4%
6.
9 5%
10 6%
11 8%
12 10%
13 12%
14 16%
15 20%
16 25%
=17 =30%
B. Estimate of 10-Year Risk for Women
Women: Framingham Point Scores by Age Group
Age Points
20–34 -7
35–39 -3
40–44 0
45–49 3
50–54 6
55–59 8
1.
60–64 10
65–69 12
70–74 14
75–79 16
Women: Framingham Point Scores by Age Group and Total Cholesterol
Total
Cholesterol
Age
20–39
Age
40–49
Age
50–59
Age
60–69
Age
70–79
<160 0 0 0 0 0
160–199 4 3 2 1 1
200–239 8 6 4 2 1
240–279 11 8 5 3 2
=280 13 10 7 4 2
2.
Women: Framingham Point Scores by Age and Smoking Status
Age
20–39
Age
40–49
Age
50–59
Age
60–69
Age
70–79
Nonsmoker 0 0 0 0 0
Smoker 9 7 4 2 1
3.
Women: Framingham Point Scores by HDL Level4.
HDL Points
=60 -1
50–59 0
40–49 1
<40 2
4.
Women: Framingham Point Scores by Systolic Blood Pressure and Treatment
Status
Systolic BP If Untreated If Treated
<120 0 0
120–129 0 1
130–139 1 2
140–159 1 2
=160 2 3
5.
Women: 10-Year Risk by Total Framingham Point Scores
Point Total 10-Year Risk
<9 <1%
9 1%
10 1%
11 1%
12 1%
6.
13 2%
14 2%
15 3%
16 4%
17 5%
18 6%
19 8%
20 11%
21 14%
22 17%
23 22%
24 27%
25 or more =30%
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Table C.3 Vitamin Facts and Nutrient Lists
A. Vitamins
Vitamin Functions Deficiency Toxicity
A Maintain integrity of
cornea, epithelial cells,
and mucous
membranes; skin and
bone and teeth growth;
regulate synthesis of
reproductive hormones
immune and cancer
protection
Anemia
Blindness, night
blindness
Bone growth deficit
Corneal breakdown
Diarrhea
Joint pain
Kidney stones
Infection
susceptibility
Amenorrhea
Anorexia
Bone pain
Fatigue
Headache
Nosebleeds
Skin rash
D Maintain bone tissue by
regulating the
absorption and
excretion of calcium
and phosphorus
Defective bone
growth (bowed legs,
joint pain)
Muscle spasms
Anorexia
Headaches
Excessive thirst
hypercalcemia
Kidney stones
Nausea
Weakness
E Maintain cell
membranes; acts as an
antioxidant in fighting
disease-causing free
radicals and in
protecting other
important compounds
from oxidation
Anemia
Breast cysts
Leg cramps
Weakness
Enhances action
of anticoagulants
Gastrointestinal
distress
K Synthesis of blood
clotting compounds;
Excessive bleeding Jaundice
Interference of
regulation of calcium
levels in blood
anticoag-ulant
drugs
B1 Thiamin Coenzyme in energy
metabolism;
maintenance of
appetite and nervous
system function
Abnormal heart beat
Cardiomegaly/heart
failure
Fluid retention
Mental confusion
Muscle pain,
weakness, wasting
paralysis
None docu-
mented
B2 Riboflavin Coenzyme in energy
metabolism;
maintenance of skin
and visual function
Corneal
abnormalities
Dry, cracking at
corners of mouth
Sensitivity to light
Skin rash
Tongue
abnormalities
None docu-
mented
B3 Niacin,
Nico-tinamide
Coenzyme in energy
metabolism;
maintenance of skin,
nervous and digestive
systems
Anorexia
Diarrhea
Skin rash
Tongue
abnormalities
Weakness and
dizziness
Diarrhea
Dizziness
Liver dysfunction
Low blood
pressure
Sweating,
flushing
B6 Pyridoxine Coenzyme in protein
and fat metabolism;
synthesis of red blood
cells; synthesis of
niacin
Anemia
Kidney stones
Dermatitis
Spastic muscles,
convulsions
Tongue
abnormalities
Fluid retention
Depression,
memory loss
Fatigue
Weakness
Folate Coenzyme in cellular
synthesis
Anemia
Depression, mental
confusion
Diarrhea,
constipation
Infection
susceptibility
Tongue
abnormalities
Mask B12
deficiency
B12
Cobalamine
Cellular synthesis;
maintenance of
nervous system
function
Anemia
Fatigue
Paralysis
Skin abnormalities
Tongue
abnormalities
None docu-
mented
Panto-thenic
Acid
Coenzyme in energy
metabolism
Fatigue
Insomnia
Vomiting, other
intestinal problems
Fluid retention
Biotin Coenzyme in energy
metabolism; synthesis
of fat and glycogen
Alopecia
Anorexia
Depression
Fatigue
Heartbeat
abnormalities
Nausea
Skin rash
None docu-
mented
Choline Coenzyme in energy
metabolism; synthesis
of phospholipids and
neurotransmitters
Growth failure
Kidney failure
Liver dysfunction
(fat accumulation)
Memory
abnormalities
Fishy body odor
Low blood
pressure
C Ascorbic Acid Collagen synthesis;
antioxidant; immune
function; enhancement
of iron absorption;
synthesis of thyroid
hormone; protein
metabolism
Anemia
Bleeding gums, loose
teeth
Bone fracture
susceptibility
Depression
Infection
susceptibility
Joint pain
Muscle pain and
wasting
Skin problems
Wound healing
delayed
Abdominal
cramps, diarrhea
Headache
Nausea
Skin rash
Interferes with
interpretation of
some laboratory
values
B. Vitamin C
Food Portion Size Vitamin C (mg) % Daily Value
(DV)
Papaya 1 whole fresh 188 313%
Orange juice 1 cup fresh 124 207%
Brussel sprouts 1 cup cooked 96 160%
Grapefruit
juice
1 cup fresh 94 157%
Green pepper 1 whole 90 150%
Strawberries 1 cup fresh 85 142%
Orange 1 fresh medium 80 133%
Broccoli 1 cup cooked 74 123%
Cauliflower 1 cup cooked 72 120%
Cantaloupe 1 cup fresh 68 113%
Mango 1 fresh 57 95%
Pink grapefruit ½ fresh 47 78%
Honeydew
melon
1 cup fresh 42 70%
Turnip greens 1 cup cooked 40 67%
Parsley ½ cup chopped 40 67%
Mustard greens 1 cup cooked 36 60%
Tomatoes 1 whole canned 36 60%
Cabbage 1 cup raw 34 57%
Sauerkraut 1 cup canned 34 57%
Tomato juice 6 oz canned 33 55%
Raspberries 1 cup fresh 31 52%
Butternut
squash
1 cup boiled 30 50%
Sweet potato 1 baked w/skin 28 47%
Baked potato 1 whole 26 43%
Pineapple
chunks
1 cup fresh 24 40%
Asparagus 1 cup cooked 20 33%
Watermelon 1 cup fresh 15 25%
Apple 1 medium fresh 8 13%
Milk, 2% 8 oz 2 3%
Quick Reference Diet Integration
Snacks: orange, tomato, and grapefruit juices.
Entree: fried broccoli, brussel sprouts, green pepper, and cauliflower.
Mashed, baked, or boiled potatoes.
Fruit salad of strawberries, papaya, mango, watermelon in places of sweets.
Kabob of green peppers, cherry tomatoes, strawberries, and pineapples.
C. Riboflavin
% Dietary Reference Intake
(DRI)
Food Portion Size Riboflavin Women Men
Brewer's yeast 1 Tbs 1.21 110% 93%
Yogurt 1 cup low fat 0.51 46% 39%
Mushrooms 1 cup cooked 0.46 42% 35%
Ricotta cheese 1 cup part skim 0.46 42% 35%
Corn flakes 1 cup 0.43 39% 33%
Cottage cheese 1 cup low fat 0.42 38% 32%
Milk, 2% 8 oz 0.4 36% 31%
Buttermilk 1 cup 0.38 35% 29%
Sirloin steak 3.5 oz broiled 0.29 26% 22%
Peach halves 10 dried 0.28 25% 22%
Pork chop 3.5 oz roasted 0.26 24% 20%
Ground beef 3.5 oz lean
baked
0.24 22% 18%
Black-eyed
peas
1 cup cooked 0.24 22% 18%
Kidney beans 1 cup canned 0.23 21% 18%
Asparagus 1 cup cooked 0.22 20% 17%
Almonds 1 oz whole
dried
0.22 20% 17%
Oysters 3 oz raw 0.2 18% 15%
Ham 3.5 oz cooked 0.19 17% 15%
Turkey 3.5 oz w/o skin 0.18 16% 14%
Broccoli 1 cup cooked 0.16 15% 12%
Green beans 1 cup cooked 0.14 13% 11%
Cheddar
cheese
1 oz 0.11 10% 8%
Spinach 1 cup cooked 0.1 9% 8%
Strawberries 1 cup fresh 0.1 9% 8%
Chicken breast 1/2 breast
roasted
0.1 9% 8%
Sole/flounder 3 oz baked 0.07 6% 5%
Orange 1 medium fresh 0.06 5% 5%
Bread Whole wheat 1
slice
0.05 5% 4%
Bean sprouts 1 cup stir fried 0.04 4% 3%
Cantaloupe 1 cup fresh 0.03 3% 2%
Apple 1 medium fresh 0.02 2% 2%
Quick Reference Diet Integration
A bowl of corn flakes with 8 oz milk provides 75% of DRI for women.
Yogurt as a snack and as a dip for fruits and vegetables.
Mushrooms in pizza, salads, or stir frys.
Low-fat cottage or ricotta cheeses in lasagna, ravioli, or other main dish.
D. Vitamin B6
Food Portion Size B6 (mg) % DRI
Beef liver 3.5 oz braised 0.91 70%
Baked potato 1 whole 0.7 54%
Salmon 3 oz cooked 0.7 54%
Banana 1 peeled 0.66 51%
Chicken breast ½ breast w/o skin 0.51 39%
Corn flakes 1 cup 0.5 38%
Avocado ½ average 0.48 37%
Trout 3 oz broiled 0.46 35%
Turkey 3.5 oz w/o skin 0.46 35%
Brewer's yeast 1 oz 0.45 35%
Sirloin steak 3.5 oz broiled 0.45 35%
Pork chop 3.5 oz roasted 0.45 35%
Spinach 1 cup cooked 0.44 34%
Soybeans 1 cup cooked 0.4 31%
Wheat germ ¼ cup 0.38 29%
Tuna, in water 3 oz canned 0.3 23%
Navy beans 1 cup cooked 0.3 23%
Sunflower
seeds
¼ cup dry 0.3 23%
Turnip greens 1 cup cooked 0.26 20%
Cauliflower 1 cup cooked 0.26 20%
Broccoli 1 cup cooked 0.24 18%
Green pepper 1 whole 0.24 18%
Watermelon 1 cup fresh 0.23 18%
Ground beef 3.5 oz lean baked 0.22 17%
Asparagus 1 cup cooked 0.22 17%
Figs 5 dried 0.21 16%
Cantaloupe 1 cup fresh 0.18 14%
Sole/flounder 3 oz cooked 0.18 14%
Mustard greens 1 cup cooked 0.16 12%
Zucchini 1 cup cooked 0.14 11%
Milk 2%, 8 oz 0.11 8%
Quick Reference Diet Integration
Baked potato for lunch with fat-free sour cream or dressing.
Banana with corn flakes for breakfast.
Poach, grill, or broil salmon for a quick meal.
E. Vitamin B12
Food Portion Size B12 (µg) % DRI
Clams 3 oz cooked 84.1 3,500%
Beef liver 3.5 oz braised 71 3,000%
Oysters 3 oz cooked 32.5 1,350%
Clam chowder 1 cup 10.3 427%
Rabbit 3.5 oz roasted 8.3 346%
Braunschweiger 1 oz, tube type 5.2 216%
Sirloin steak 3.5 oz broiled 2.9 119%
Salmon 3 oz cooked 2.7 113%
Tuna, in water 3 oz canned 2.5 106%
Lamb chop 3.5 oz braised 2.3 95%
Vegetarian
burger
½ cup 2 83%
Raisin bran ¾ cup 2 83%
Ground beef 3.5 oz lean baked 1.7 71%
Cottage cheese 1 cup 1% fat 1.4 58%
Sole/flounder 3 oz cooked 1.3 54%
Shrimp 3 oz cooked 1.3 54%
Halibut 3 oz broiled 1.2 50%
Milk 2% 8 oz 0.89 37%
Frankfurter 1 beef, 2 oz 0.88 37%
Ham 3.5 oz cooked 0.74 29%
Tempeh ½ cup 0.7 29%
Pork chop 3.5 oz roasted 0.6 25%
Buttermilk 8 oz, cultured 0.54 23%
Egg 1 whole fresh 0.5 21%
Turkey 3.5 oz w/o skin 0.37 15%
Canadian bacon 2 slices cooked 0.36 15%
Miso ½ cup 0.29 12%
Chicken breast ½ breast w/o skin 0.29 12%
Yogurt 8 oz low fat 0.24 10%
Cheddar cheese 1 oz 0.23 10%
Goat's milk 8 oz 0.16 7%
Quick Reference Diet Integration
Raisin Bran with low-fat milk for breakfast.
Low-fat cottage cheese with fruit as a snack.
3 oz of salmon, tuna, or rabbit provides 100% DRI of B12.
Oysters or clams served steamed or in stews and chowders.
F. Biotin
Food Portion Size Biotin (µg) % DRI
Egg 1 whole fresh 10 33%
Wheat germ 1/4 cup toasted 7 23%
Ry-Krisp ½ oz 6.8 23%
Granola ¼ cup w/raisins 5 17%
Egg noodles 1 cup cooked 4 13%
Almonds 1 oz whole natural 1 3%
Pistachios 1 oz, red 1 3%
Corn meal 1 oz yellow 1 3%
Quick Reference Diet Integration
Granola as a cereal or snack, or mixed into yogurt.
Wheat germ in casseroles and breads or on cereal.
Ry-Krisp with peanut butter and jelly for a snack.
Egg noodles with veggies, fat-free Italian dressing.
Scrambled, poached, or hardboiled eggs.
G. Choline
% DRI
Food Portion Size Choline (µg) Women Men
Beef liver 3.5 oz 583.1 137% 106%
Cauliflower 1 cup cooked 162 38% 29%
Peanuts 1 oz, dried 127.3 30% 23%
Peanut butter 2 Tbs 124.6 29% 23%
Grape juice 8 oz, canned 120 28% 22%
Potato 1 whole baked 103.2 24% 19%
Iceberg lettuce 1 leaf raw 58.6 14% 11%
Tomato 1 whole raw 52.9 12% 10%
Milk Whole 8 oz 36.6 9% 7%
Orange 1 fresh medium 28 7% 5%
Banana 1 whole peeled 27.4 6% 5%
Bread Whole wheat 1 slice 24.2 6% 4%
Cucumber ½ cup raw 11.3 3% 2%
Beef steak 3.5 oz 7.5 2% 1%
Apple 1 fresh medium 3.7 <1% <1%
Egg 1 fresh whole 2.1 <1% <1%
Ginger ale 12 oz 0.73 <1% <1%
Butter 1 tsp 0.21 <1% <1%
Margarine 1 tsp, tub type 0.15 <1% <1%
Corn oil 1 Tbs 0.04 <1% <1%
Quick Reference Diet Integration Guide
Dinner: 3.5 oz beef liver, 1 cup cauliflower, baked potato, 8 oz grape juice, banana.
Add iceberg lettuce to a sandwich.
Swap straight soda for a “Choline Cocktail”—8 oz grape juice, 12 oz ginger ale.
Snack: 1 oz peanuts and 8 oz milk.
Lunch: Peanut butter and jelly sandwich with 8 oz grape juice.
H. Folate
Food Portion Size Folate (µg) % DRI
Pinto beans 1 cup cooked 294 74%
Asparagus 1 cup cooked 264 66%
Spinach 1 cup cooked 262 66%
Navy beans 1 cup cooked 255 64%
Beef liver 3.5 oz braised 217 54%
Black-eyed
peas
1 cup cooked 209 52%
Great northern
beans
1 cup cooked 181 45%
Turnip greens 1 cup cooked 170 43%
Lima beans 1 cup cooked 156 39%
Kidney beans 1 cup canned 129 32%
Broccoli 1 cup cooked 104 26%
Corn flakes 1 cup 100 25%
Parsley 1 cup chopped 92 23%
Beets 1 cup cooked 90 23%
Wheat germ 1/4 cup 82 21%
Romaine
lettuce
1 cup chopped 76 19%
Cauliflower 1 cup cooked 64 16%
Pineapple juice 8 oz canned 58 15%
Orange 1 fresh medium 47 12%
Zucchini 1 cup cooked 30 8%
Peanuts 1 oz dried 29 7%
Cantaloupe 1 cup fresh 27 7%
Winter squash 1 cup cooked 26 7%
Strawberries 1 cup fresh 26 7%
Grapefruit
juice
1 cup canned 26 7%
Egg 1 whole fresh 23 6%
Green beans 1 cup cooked 22 6%
Tofu 1/2 cup raw 19 5%
Tomato 1 whole raw 18 5%
Bread, whole
wheat
1 slice 14 4%
Quick Reference Diet Integration
Use dry beans in soups or as a main dish salad.
Add spinach to lasagna or serve cooked with lemon juice.
Salad of spinach, romaine, tomato, broccoli, cauliflower, and beets.
Dinner: 3.5 oz beef liver, 1 cup asparagus, 1 cup lima beans.
Breakfast: cornflakes in milk; fruit salad of cantaloupe, strawberries, orange.
I. Niacin
% DRI
Food Portion Size Niacin (mg) Women Men
Chicken breast ½ roasted w/o skin 11.8 84% 74%
Tuna, in water 3 oz canned 11.3 81% 71%
Beef liver 3.5 oz braised 10.7 76% 67%
Brewer's yeast 1 oz 10.7 76% 67%
Salmon 3 oz broiled 8.6 61% 54%
Mushrooms 1 cup cooked 7 50% 44%
Halibut 3 oz broiled 6.1 44% 38%
Peach halves 10 dried 5.7 41% 36%
Pink salmon 3 oz canned 5.6 40% 35%
Pork chop 3.5 oz roasted 5.5 39% 34%
Lamb chop 3.5 oz braised 5.5 39% 34%
Turkey 3.5 oz w/o skin 5.4 39% 34%
Sirloin steak 3.5 oz broiled 4.3 31% 27%
Ground beef 3.5 oz lean baked 4.2 30% 26%
Peanuts 1 oz dried unsalted 4 29% 25%
Baked potato 1 whole 3.3 24% 21%
Sole/flounder 3 oz baked 2.5 18% 16%
Kidney beans 1 cup canned 2.4 17% 15%
Braunschweiger 1 oz tube-type 2.3 16% 14%
Shrimp 3 oz boiled 2.2 16% 14%
Wheat bran ¼ cup 2 14% 13%
Asparagus 1 cup cooked 2 14% 13%
Oysters 3 oz raw 1.7 12% 11%
Sardines 2 sardines in oil 1.3 9% 8%
Crab meat 3 oz canned 1.2 9% 8%
Bread, whole wheat 1 slice 1 8% 6%
Summer squash 1 cup cooked 1 8% 6%
Cantaloupe 1 cup fresh 0.9 6% 6%
Peach 1 fresh medium 0.9 6% 6%
Spinach 1 cup cooked 0.9 6% 6%
Broccoli 1 cup cooked 0.8 6% 5%
Quick Reference Diet Integration
Choose tuna, halibut, and salmon instead of red meat.
Add mushrooms to soups and salads, and stir fry.
Dinner: half chicken breast, baked potato, 1 cup asparagus.
Fortified breakfast cereals contain 25% of the DRI for niacin per serving.
J. Pantothenic Acid
Food Serving Size Pantothenic Acid
(mg)
% DRI
Beef liver 3.5 oz braised 4.6 91%
Mushrooms ½ cup boiled 1.7 34%
Avocado 1 medium 1.7 34%
Salmon 3 oz cooked 1.4 28%
Lentils 1 cup boiled 1.3 25%
Split peas 1 cup boiled 1.2 23%
Potato 1 whole baked 1.1 22%
Turkey 3.5 oz w/o skin 0.94 19%
Pomegranate 1 medium raw 0.92 18%
Chicken breast ½ roasted w/o skin 0.83 17%
Peanuts 1 oz dried 0.79 16%
Milk, 2% 8 oz 0.78 16%
Sweet potato 1 whole baked 0.74 15%
Chickpeas 1 cup canned 0.72 14%
Wheat germ ¼ cup 0.66 13%
Pork chop 3.5 oz roasted 0.65 13%
Egg 1 whole fresh 0.63 13%
Broccoli 1 cup cooked 0.5 10%
Ham 3.5 oz cooked 0.47 9%
Sole/flounder 3 oz cooked 0.43 9%
Kidney beans 1 cup canned 0.38 8%
Sirloin steak 3.5 oz broiled 0.37 7%
Corn 1 cup boiled 0.36 7%
Orange 1 fresh medium 0.35 7%
Watermelon 1 cup fresh 0.34 7%
Ground beef 3.5 oz baked lean 0.27 5%
Spinach 1 cup cooked 0.26 5%
Bread, whole
wheat
1 slice 0.18 4%
Tuna, in water 3 oz canned 0.18 4%
Macaroni 1 cup cooked, enriched 0.16 3%
Cheddar cheese 1 oz 0.12 2%
Quick Reference Diet Integration
Avocado sliced in a salad or in a dip (guacamole).
Dinner: 3 oz salmon, 1 baked potato, 8 oz milk, 1 cup broccoli.
Soups with lentils or split peas.
Salad: chicken breast, avocado, spinach, mushrooms, broccoli.
K. Thiamin
% DRI
Food Portion Size Thiamin (mg) Women Men
Brewers yeast 1 oz 4.43 403% 369%
Pork chop 3.5 oz roasted 0.91 83% 76%
Ham 3.5 oz cooked 0.78 71% 65%
Green peas 1 cup cooked 0.42 38% 35%
Canadian bacon 2 pieces cooked 0.38 35% 32%
Corn flakes 1 cup 0.38 35% 32%
Split peas 1 cup cooked 0.37 34% 31%
Macaroni, enriched 1 cup cooked 0.29 26% 24%
Kidney beans 1 cup canned 0.27 25% 23%
Oatmeal 1 cup cooked 0.26 24% 22%
Millet 1 cup cooked 0.25 23% 21%
Acorn squash 1 cup boiled 0.24 22% 20%
Baked potato 1 whole 0.22 20% 18%
Asparagus 1 cup cooked 0.22 20% 18%
Peanuts 1 oz dry, unsalted 0.19 17% 16%
Black eyed peas 1 cup cooked 0.17 15% 14%
Watermelon 1 cup fresh 0.13 12% 11%
Sirloin steak 3.5 oz broiled 0.13 12% 11%
Honeydew melon 1 cup fresh 0.13 12% 11%
Orange 1 fresh medium 0.12 11% 10%
Winter squash 1 cup baked 0.12 11% 10%
Tofu ½ cup 0.1 9% 8%
Milk, 2% 8 oz 0.1 9% 8%
Green beans 1 cup cooked 0.1 9% 8%
Broccoli 1 cup cooked 0.1 9% 8%
Bread, whole wheat 1 slice 0.09 8% 8%
Sole/flounder 3 oz cooked 0.08 7% 7%
Cauliflower 1 cup cooked 0.08 7% 7%
Tomato 1 whole raw 0.07 6% 6%
Quick Reference Diet Integration
Include lean pork in weekly menus.
Use green peas, split peas, black peas, black-eyed peas, kidney beans in soups.
Choose enriched pasta and bread products.
Breakfast: oatmeal or fortified cereal
Side dish: boiled or baked squash
L. Vitamin A
Food Portion size Vitamin A (RE) % DRI
Beef liver 3 oz fried 9,123 1,042
Pumpkin 1 cup canned 5,424 620
Sweet potato 1 whole baked 2,486 284
Carrot 1 whole fresh 2,024 231
Spinach 1 cup cooked 1,474 168
Butternut
squash
1 cup baked 1,435 164
Mango 1 medium fresh 806 92
Papaya 1 medium fresh 612 70
Cantaloupe 1 cup fresh 516 59
Turnip greens ½ cup chopped 396 45
Collard greens 1 cup chopped 349 40
Apricot halves 10 halves 253 29
Winter squash ½ cup cubes 235 27
Mustard greens ½ cup chopped 212 24
Broccoli ½ cup frozen 174 20
Parsley ½ cup chopped 156 18
Milk, 2% 8 oz 140 16
Egg 1 whole fresh 95 11
Cheddar cheese 1 oz 86 10
Watermelon 1 cup fresh 58 7
Margarine Tub-type 1 tsp 47 5
Sole/flounder 3 oz cooked 28 3
Orange 1 medium fresh 26 3
Green beans ½ cup canned 24 3
Corn ½ cup canned 13 2
Apple 1 medium fresh 7 1
Chicken breast ½ roasted w/o skin 5 0.5
Sirloin steak 3.5 oz broiled 0 0
Brewers yeast 1 oz 0 0
Bread, whole
wheat
1 slice 0 0
Quick Reference Diet Integration
Use fresh spinach, romaine lettuce, carrots, and tomatoes in salads.
Use canned pumpkin in cookies, pies, and desserts.
Serve baked sweet potatoes in place of baked potatoes.
Breakfast: fruit salad of mango, papaya, and cantaloupe.
Snack: dried peaches and apricots.
M. Vitamin D
Food Portion Size Vitamin D (µg) % DRI
Milk, 2% 8 oz 1.6 33%
Corn flakes 1 cup 0.81 16%
Cod liver oil 1 Tbs 0.55 11%
Egg 1 whole fresh 0.41 8%
Margarine 1 tsp, tub type 0.34 7%
Frankfurter 1 beef frank 0.18 4%
Braunschweiger 1 oz tube type 0.15 3%
Rice, wild 2/3 cup instant 0.07 1%
Rice, white 2/3 cup instant 0.03 <1%
Cheddar cheese 1 oz 0.02 <1%
Quick Reference Diet Integration
Drink 2 to 3 eight-oz glasses of milk per day.
10 to 15 minutes of sunlight exposure 3 times per week.
Breakfast: vitamin-D-fortified cereals with milk.
Snack: pudding made with low-fat milk.
Use vitamin-D-fortified margarine instead of butter.
N. Vitamin E
Food Portion Size Vitamin E (mg) % DRI
Wheat germ oil 1 tablespoon 20.3 102%
Sunflower
seeds
1 oz dry roasted 14.2 71%
Mayonnaise 1 Tbs 11 55%
Almonds 1 oz dried 6.7 34%
Dried filberts 1 oz 6.7 34%
Sunflower seed
oil
1 Tbs 6.3 32%
Sweet potato 1 medium raw 5.9 30%
Almond oil 1 Tbs 5.3 27%
Cottonseed oil 1 Tbs 4.8 24%
Safflower oil 1 Tbs 4.6 23%
Wheat germ ¼ cup toasted 4.1 20%
Peanut butter 2 Tbs 3 15%
Shrimp 3 oz boiled 3 15%
Canola oil 1 Tbs 2.5 13%
Asparagus 1 cup cooked 2.4 12%
Mango 1 raw medium 2.3 12%
Avocado ½ cup 2.3 12%
Peanuts 1 oz dry roasted 2.2 11%
Brazil nuts 1 oz dried 2.1 11%
Salmon 3 oz baked 2 10%
Corn oil 1 Tbs 1.9 10%
Olive oil 1 Tbs 1.7 8%
Peanut oil 1 Tbs 1.6 8%
Soybean oil 1 Tbs 1.5 8%
Apple 1 fresh medium 1.5 8%
Brussel sprouts 1 cup cooked 1.3 7%
Spinach 1 cup raw 1.1 5%
Macaroni 1 cup cooked 1 5%
Parsley 1 Tbs 1 5%
Pear 1 fresh medium 0.83 4%
Cheddar cheese 1 oz 0.5 3%
Quick Reference Diet Integration
Use wheat germ or sunflower oil in salad dressings or baked goods.
Serve sweet potato chips instead of regular chips––slice thin and bake.
Replace cream cheese with peanut butter on bagels.
Add wheat germ to cereal or yogurt.
Snack: sunflower seeds, peanuts, or almonds.
O. Vitamin K
Food Portion Size Vitamin K (µg) % DRI
Turnip greens 1 cup chopped raw 364 455%
Green tea 1 oz dry 199 249%
Spinach 1 cup raw 148 185%
Broccoli 1 cup cooked 126 158%
Beef liver 3.5 oz raw 104 104%
Cauliflower 1 cup raw 96 120%
Soybean oil 1 Tbs 76 95%
Chickpeas 1 oz dry 74 93%
Asparagus 1 cup cooked 69 86%
Lentils 1 oz dry 62 78%
Soybeans 1 oz 53 66%
Cabbage 1 cup raw shredded 52 65%
Mung beans 1 oz dry 48 60%
Green beans 1 cup boiled 44 55%
Wheat flour Whole wheat, 1 cup 36 45%
Tomato 1 whole fresh 28 35%
Egg 1 whole fresh 25 31%
Peas 1 oz dry 23 29%
Wheat bran 1 oz 23 29%
Lettuce 1 leaf iceberg 22 28%
Strawberries 1 cup raw 21 26%
Watercress 1 cup chopped 20 25%
Oats 1 oz dry 18 23%
Wheat germ 1 oz 10 13%
Carrot 1 medium raw 9 11%
Corn oil 1 Tbs 8 10%
Orange 1 fresh medium 7 9%
Potato 1 whole baked 6 8%
Cucumber 1 cup raw 6 8%
Quick Reference Diet Integration
Add turnip greens to soup or eat as a side dish.
Entree: stir fry of broccoli, cauliflower, spinach, carrots, and asparagus.
Add spinach, watercress, and tomatoes to sandwiches.
Use soybean oil to make salad dressing.
Salad: spinach and lettuce with tomatoes and chickpeas.
Appetizer: coleslaw with low-fat or fat-free dressing.