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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

(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.




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

DISCLAIMER

Care has been taken to confirm the accuracy of the information presented and to describe generally

accepted practices. However, the authors, editors, and publisher are not responsible for errors or omissions

or for any consequences from application of the information in this book and make no warranty, expressed

or implied, with respect to the currency, completeness, or accuracy of the contents of the publication.

Application of this information in a particular situation remains the professional responsibility of the

practitioner; the clinical treatments described and recommended may not be considered absolute and

universal recommendations.

The authors, editors, and publisher have exerted every effort to ensure that drug selection and dosage set

forth in this text are in accordance with the current recommendations and practice at the time of

publication. However, in view of ongoing research, changes in government regulations, and the constant

flow of information relating to drug therapy and drug reactions, the reader is urged to check the package

insert for each drug for any change in indications and dosage and for added warnings and precautions. This

is particularly important when the recommended agent is a new or infrequently employed drug.

Some drugs and medical devices presented in this publication have Food and Drug Administration (FDA)

clearance for limited use in restricted research settings. It is the responsibility of health care providers to

ascertain the FDA status of each drug or device planned for use in their clinical practice.

To purchase additional copies of this book, call our customer service department at (800) 639-3030 or fax

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10 9 8 7 6 5 4 3 2 1




> 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




> 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




> 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




> 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.

http://www.shorrproductions.com).

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


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


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


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%


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%


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.


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


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


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

P.18

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


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.


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


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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


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


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


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


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


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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outcomes management. J Am Diet Assoc 2003;103(8):1061–1072.

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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8. Huffman GB. Evaluating and treating unintentional weight loss in the elderly. Am Fam Phys

2002;65(4):640–650.

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1998;47(1):19–25.

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overweight and obesity in adults: The Evidence Report. 1998. Available at:

http://www.ncbi.nlm.nih.gov/books/bv.fcgi?rid=obesity. Accessed February 15, 2007.

11. Yusuf S, Hawken S, Ounpuu S, et al. Obesity and the risk of myocardial infarction in 27,000

participants from 52 countries: A case-control study. Lancet 2005;366:1640–1650.

12. Ireton-Jones C, Jones J. Improved equations for estimating energy expenditure in patients: The

Ireton-Jones equations. Nutr Clin Pract 2002;17(4):236–239.

13. Escott-Stump S. Nutrition and Diagnosis-Related Care, 5th ed. Baltimore, MD: Lippincott Williams

& Wilkins; 2002.

14. Mahan LK, Escott-Stump S. Krause's Food, Nutrition, and Diet Therapy, 11th ed. Philadephia:

Saunders; 2004.

15. Bergstrom N, Bennett MA, Carlson CE, et al. Treatment of Pressure Ulcers: Clinical Practice

Guideline, No. 15. Rockville, MD: U.S. Department of Health and Human Services, Public Health

Service, Agency for Health Care Policy and Research; 1994. AHCPR Publication No. 95–0652. Available

at: http://www.ncbi.nlm.nih.gov/books/bv.fcgi?rid=hstat2.chapter.5124. Accessed February 19, 2006.

16. Fuhrman MP, Charney P, Mueller CM. Hepatic proteins and nutrition assessment. J Am Diet Assoc

2004;104(8):1258–1264.

17. Kuzuya M, Kanda S, Koike T, et al. Lack of correlation between total lymphocyte count and

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> 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.


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.


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.

http://www.emedicine.com/med/topic1075.htm. Accessed August 26, 2006.


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.

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http://www.fda.gov/ fdac/features/2001/301-preg.html#categories.




> 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


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


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

http://www.cdc.gov/growthcharts.

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


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:

http://www.kennedykrieger.org/kki_miscjsp?pid2694.

http://www.ndss.org/index.php?option=com_content&task=view&id=603&Itemid=119

>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%


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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


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


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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


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


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


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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)


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)


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


be =1.6 <1.9 (active)


be =1.9 <2.5 (very active)


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


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


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?



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


Diagnosis

Weight status/change

Albumin level

Degree of metabolic stress

Presence of decubitus ulcers

Need for nutrition support


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 ).


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


Dysphagia

Severity Swallowing Stage Affected Food Characteristics

Level of Supervision During Meals/Assessment

Needed

Table 4.9 Overview of the National Dysphagia Diet


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.




> 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


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


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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


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


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)


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


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


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


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


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.

http://www.hormelhealthlabs.com/home.asp

http://www.meadjohnson.com/professional/index.html

http://www.nestle-nutrition.com

http://www.novartisnutrition.com/us/home

http://www.ross.com

http://www.espen.org/Education/documents/ ENICU.pdf. Accessed February 5, 2008.

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.




> 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


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.


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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


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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.


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


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)


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)


(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.

http://www.cancer.gov/cancertopics/ factsheet/Detection/staging. Accessed August 10, 2007.

http://www.cancer.gov/cancertopics/pdq/supportivecare/nutrition/HealthProfessional/




> 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


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


=240 High

HDL Cholesterol

<40 mg/dL Low

=60 mg/dL High


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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%


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)


>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


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.


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


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


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).


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


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


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).


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


Table 7.15 Nutritional Problems After CVA

Dysphagia Physical Disability

Choking Physical activity

Dehydration Self-feeding

Weight loss Weight gain


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.


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).


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.


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


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.


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,

http://en.wikipedia.org/wiki/List_of_medical_abbreviations.

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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http://www.americanheart.org/presenter.jhtml?identifier=4764. Accessed March 17, 2007.

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.

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.

http://www.nhlbi.nih.gov/health/public/heart/hbp/dash/new_dash.pdf. Accessed March 20, 2007.




> 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


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.


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.


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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.


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.


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


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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.


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.


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


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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


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.


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.


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


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.

http://www.diabetes.org/type-1-diabetes/insulin-pumps.jsp. Accessed September 25, 2006.

http://pi.lilly.com/us/byetta-pi.pdf. Accessed September 20, 2006.

http://www.symlin.com/pdf/SYMLIN-pi-combined.pdf. Accessed September 20, 2006.

16. Haire-Joshu, D. Management of Diabetes Mellitus: Perspectives of Care Across the Life Span. St.

Louis: Mosby-Year Book, Inc.; 1992.




> 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 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.


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


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


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


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.


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.


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.


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 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


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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 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)


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


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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 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


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.


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.


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.


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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


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 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.


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.

P.238

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.




> 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).


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


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)


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).


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.



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

P.250

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


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


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


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.

http://labtestsonline.org/understanding/analytes/liver_panel/glance.html. Accessed on March 6,

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.




> 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


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


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].


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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.


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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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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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


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


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


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


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.




> 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).


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).


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.


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


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.


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.


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.


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.




> 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)


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)


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)


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


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


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


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


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)


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


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


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%


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


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)


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


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


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)


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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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)


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)


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)


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)


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


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)


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


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


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.

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Transferrin Saturation

Reference Range

Male: 20%–50%

Female:15%–50%


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


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)

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Lymphocytes: 1,000–4,000/mm3 (comprise 20%–40% of the total WBC; and in malnutrition, lymphocyte

count is reduced).


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).

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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.

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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.


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



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



Ery-Tab See erythromycinErythromycinEry-Tab



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


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



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


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


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


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


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


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


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




> 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

P.328

P.329

P.330

P.331

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%

P.332

P.333

P.334

P.335

P.336

P.337

P.338

P.339

P.340

P.341

P.342

P.343

P.344

P.345

P.346

P.347

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%


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%


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%




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%


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%


Buttermilk 8 oz, cultured 0.54 23%

Egg 1 whole fresh 0.5 21%


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%


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%


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%


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%


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%


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%


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%


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%


Lamb chop 3.5 oz braised 5.5 39% 34%

Turkey 3.5 oz w/o skin 5.4 39% 34%


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%


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%



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%


Lentils 1 cup boiled 1.3 25%

Split peas 1 cup boiled 1.2 23%

Potato 1 whole baked 1.1 22%


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%



Broccoli 1 cup cooked 0.5 10%

Ham 3.5 oz cooked 0.47 9%


Kidney beans 1 cup canned 0.38 8%


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%


Macaroni 1 cup cooked, enriched 0.16 3%



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%


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%


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%


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%


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%


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


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%


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%


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%



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%


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%


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%


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%


Potato 1 whole baked 6 8%

Cucumber 1 cup raw 6 8%


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.

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