The Clinical Dietitian's Essential Pocket Guide

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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.

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 orders to (301) 824-7390. International customers should call (301) 714-2324. Visit Lippincott Williams & Wilkins on the Internet: http://www.lww.com. Lippincott Williams & Wilkins customer service representatives are available from 8:30 am to 6:00 pm, EST, Monday through Friday, for telephone access. 10 9 8 7 6 5 4 3 2 1

Authors: Width, Mary; Reinhard, Tonia Title: Clinical Dietitian's Essential Pocket Guide,The: Essential Pocket Guide, 1st Edition Copyright ©2009 Lippincott Williams & Wilkins > Front of Book > Authors

Authors Mary Width MS, RD Lecturer Coordinated Program in Dietetics, Department of Nutrition and Food Science, Wayne State University, Detroit, Michigan

Tonia Reinhard MS, RD Director Coordinated Program in Dietetics, Department of Nutrition and Food Science, Wayne State University, Detroit, Michigan

Contributors Sheri Betz RD St. John Hospital and Medical Center, Detroit, Michigan

Monica L. Griffin RD DaVita Dialysis, Southgate, Michigan

Brenda Howell RD, CNSD Genesys Regional Medical Center, Grand, Michigan

Angela M. Lada RD, RN Detroit, Michigan

Lisa Ventrella Lucente RD Department of Nutrition and Food Science, Wayne State University, Detroit, Michigan

Reviewers Judi Brooks Coordinated Program in Dietetics, Eastern Michigan University, Ypsilanti, Michigan

Christine Haar Family and Consumer Sciences, Bowling Green State University, Bowling Green, Ohio

Emily Hoffman Nutrition and Food Science, Utah State University, Logan, Utah

Kelly Sanna-Gouin Food and Nutrition Services, Detroit Receiving Hospital, Detroit, Michigan

Zara Shah-Rowlands Department of Human Ecology, Coordinated Program in Dietetics, Youngstown State University, Youngstown, Ohio

Authors: Width, Mary; Reinhard, Tonia Title: Clinical Dietitian's Essential Pocket Guide,The: Essential Pocket Guide, 1st Edition Copyright ©2009 Lippincott Williams & Wilkins > Front of Book > Dedication

Dedication “I dedicate this book to my husband, Curt, for his love, support, and most of all, his endless supply of patience; and to the memory of my parents, Marian and Walter Thiede.” Mary Width

“This book is dedicated to Brendan Reinhard and Faye Reinhard for their technical support, John Reinhard for life support, and to the memory of Gea DeRubeis Pacifico and Antonietta Pacifico.” Tonia Reinhard

Authors: Width, Mary; Reinhard, Tonia Title: Clinical Dietitian's Essential Pocket Guide,The: Essential Pocket Guide, 1st Edition Copyright ©2009 Lippincott Williams & Wilkins > Front of Book > Preface

Preface The Clinical Dietitian's Essential Pocket Guide is an up-to-date and concise pocket-sized reference that clinical dietitians can tailor to their own practice. Like most dietitians, we both had our own pocket clinical books—tabbed little binders jammed with snippets of information culled from years of collecting. We have seen many personalized clinical books in all different shapes and sizes through our contact with countless wonderful dietitians who bravely serve as preceptors for our students. We think a clinical guide is so integral to the practice of dietetics that we have required every student who has come to Wayne State University's Coordinated Program in Dietetics to prepare their own. We have continually searched over the years to find a published book that would take the place of these homemade resource books, but we have been unable to find a comprehensive, concise guide that could both fit in a lab coat pocket and also be customized to the user's needs. The inability to find such a guide is what gave us the inspiration to develop one for our own students. When talking with other dietetic educators, we were encouraged to publish our book and share it with fellow dietitians and dietetic students from other programs. We believe our book will become an indispensable guide for students, interns, and practicing dietitians for the following reasons:

The compact size will easily fit into any lab coat pocket. The colored tabs enable quick, easy searching of contents. The latest research is incorporated into all chapters, so the busy clinician doesn't have to spend valuable time searching textbooks or the Internet for the most updated information. Blank pages in each chapter allow the clinician to customize their book by adding their own resources and references. Writing in a formula, cutting and pasting an article, or stapling a hospital formulary card can be done with ease. Concise, in-depth coverage of all major practice areas makes it easy to cover a colleague's units or patients by providing the correct resources to do so.

The primary audience for this book is dietitians, dietetic technicians, and students and interns working in hospitals, nursing homes, and clinics, but it will also be useful for other health professionals in community and wellness programs who need a quick reference for nutrition screening and assessment. Part I contains chapters covering nutritional assessment, life stage assessment, and nutrition support. Part II includes seven chapters on the major nutritionally relevant diseases. Appendices on food and drug interactions, laboratory assessment, and a miscellaneous appendix of useful reference materials, such as conversion tables, and food sources of vitamins, round out the book. This book could not have been developed without the help of our expert contributors. We would like to express our gratitude and appreciation to Sheri Betz, Brenda Howell, Angela Lada, Monica Lowe, and Lisa Ventrella Lucente for their hard work and valuable contributions to our book. In addition, we would like to thank all the countless colleagues and preceptors who offered constant encouragement and excellent suggestions during the writing process.

Today's fast-paced health care environment makes it crucial to have the information you need when you need it. We struggled with decisions on what content to include, trying to avoid long chunks of text to keep the content easy to find. We hope that you find this book to be the quick and useful reference we intend it to be. Mary Width MS, RD Tonia Reinhard MS, RD

Authors: Width, Mary; Reinhard, Tonia Title: Clinical Dietitian's Essential Pocket Guide,The: Essential Pocket Guide, 1st Edition Copyright ©2009 Lippincott Williams & Wilkins > Table of Contents > Part I - Nutrition Assessment and Support > Chapter 1 - Nutrition Assessment

Chapter 1 Nutrition Assessment The Nutrition Care Process The Nutrition Care Process (NCP), as defined by the American Dietetic Association (ADA), is “a systematic problem-solving method that dietetics professionals use to critically think and make decisions to address nutrition-related problems and provide safe and effective quality nutrition care” (1). Dietetics professionals use the NCP mainly in acute care, extended care, and outpatient settings; however, the process is also useful in a variety of community venues. The NCP consists of four steps: Nutrition assessment, nutrition diagnosis, nutrition intervention, and nutrition monitoring and evaluation. Nutrition assessment of the hospitalized patient is the first step in effective patient care to identify and diagnose nutrition risks and plan appropriate interventions. It consists of a comprehensive assessment of nutrition status and risks and includes the following major categories of data collection and typical types of data included:

Anthropometric measurements: Height, weight, body mass index (BMI), weight change, body frame measurement and adjustment, knee height Biochemical data: Laboratory data P.4 Nutrition-focused physical examination: Review of systems, including general conditions and physical appearance, gastrointestinal, musculoskeletal, skin, extremities, and other systems Patient history: Medication and supplement history, personal history, medical and health history, and food and nutrition history (diet history), which includes food consumption, nutrition and health awareness, physical activity and exercise, and food availability

Nutrition diagnosis is the second step in the NCP. After assessment, the registered dietitian (RD) determines the patient's nutrition-related problems and needs, which form the nutrition diagnosis. The nutrition diagnosis, in turn, is expressed and documented in a specific format: Problem, etiology, signs and symptoms (PES). Tables 1.1 and 1.2 illustrate and provide an example for the PES format. The nutrition diagnostic terms are classified according to the following three domains and subclasses (2):

Intake: Caloric energy balance; oral or nutrition support intake; fluid intake; bioactive substances; essential nutrients Clinical: Functional; biochemical; weight (anthropometric and other measures)

Behavior/environment: Knowledge and beliefs; physical activity and function; food safety and access

Table 1.1 Nutrition Diagnosis: Problem/Etiology/Signs

The problem (P) describes alterations in patient nutritional status: A diagnostic label (qualifier) is an adjective that describes the physiologic response, e.g., altered, impaired, risk of

The etiology (E) refers to cause(s) or contributor(s) to the problem: It is linked to the problem by the words, “related to”

The signs/symptoms (S) are clusters of subjective and objective factors that provide evidence that a problem exists: They also quantify the problem and describe severity Linked to (E) by the words, “as evidenced by” (AEB)

P.5

Table 1.2 Writing the Nutrition Diagnosis (ND) Statement

Example for the ND statement format (P)roblem/(E)tiology/(S)igns/symptoms: Excessive caloric intake (P) related to frequent consumption of large portions of high fat meals (E), as evidenced by: 1. Daily caloric intake exceeding DRIa by 500 kcal (S) 2. 2 lb weight gain during past 18 months (S)

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

Excessive fat intake related to frequent consumption of high-fat

Diagnosis

meals as evidenced by fat kilocalories >55% of total kilocalories per day

Expected Outcomes

1. Limit foods high in cholesterol, saturated fat 2. Use food sources of monounsaturated fat as preferred fat

EvidenceBased Ideal Goals

1. Consume 25%–35% of total kcal from fat 2. Consume <7% saturated fat 3. Isocaloric replacement of saturated with monosaturated and polyunsaturated

The final step in the NCP is monitoring and evaluation. In this last phase, the RD continues to re-examine the patient's status by gathering new data (monitoring) and assessing patient status by comparison to previous status, expected outcomes, and established standards (evaluation). The RD schedules follow-up time points for monitoring and evaluation, based on the clinical protocols of the facility. This fourth step helps the RD to determine whether the expected outcomes are being achieved. After discharge, the RD can use phone, electronic communication, and mailings to gather data for monitoring and evaluation.

Anthropometric Assessment There are several anthropometric measurements that are useful in the clinical setting. Measurements of body weight, height, and composition can be used by the clinician when evaluating nutritional status.

Estimating Height An estimation of height is necessary for patients that are confined to bed or a wheelchair, have curvature of the P.7 spine or contractures, or are otherwise unable to stand for an actual height measurement.

Knee Height Knee height is measured using a sliding broad-blade caliper (available at http://www.shorrproductions.com). Patient should be in the supine position, and the left leg is preferable for measurement. With both the knee and ankle at 90-degree angles, place one blade of the caliper under the heel of the foot and the other on the anterior surface of the thigh. The shaft of the caliper is held parallel to the long axis of the lower leg, and pressure is applied to compress the tissue. Height (in cm) is calculated using the formulas in Table 1.4.

Demi-span The measurement is useful in the clinical setting because it requires no special equipment and is particularly useful for patients with lower limb dysfunction. Using the left arm if possible, measure the distance from the notch between the middle and the ring fingers to the middle of the sternal notch. Make sure the patient's arm is horizontal and in line with the shoulders. Height (in cm) is calculated using the formulas in Table 1.5.

Table 1.4 Knee Height

Females Height in cm = 84.88 - (0.24 × age in years) + (1.83 × knee height in cm) Males Height in cm = 64.19 - (0.04 × age in years) + (2.02 × knee height in cm) Data from reference 3.

P.8

Table 1.5 Demi-Span

Females Height in cm = (1.35 × demi-span in cm) + 60.1 Males Height in cm = (1.40 × demi-span in cm) + 57.8 Data from reference 4.

Evaluating Body Weight Ideal Body Weight A quick and easy method to calculate ideal body weight (IBW) is the Hamwi Method, shown in Table 1.6.

Frame Size Adjustment In order to adjust for differences in body build (muscularity, bone thickness, and body proportions), it is necessary to determine an individual's frame size when calculating IBW (5). Frame size can be estimated by two methods. Measuring wrist circumference is easy and straightforward. Measuring elbow breadth is more complex, but tends to provide a more accurate estimate of frame size. Both methods use the

measurements in relation to the patient's height.

Wrist Circumference Measure the wrist circumference just distal to the styloid process at the wrist crease of the left hand, in P.9 inches. Compare the measurement to the values in Table 1.7.

Table 1.6 Ideal Body Weight

Females IBW = 100 lb for 5 ft + 5 lb for each inch >60 in. Males IBW = 106 lb for 5 ft + 6 lb for each inch >60 in.

Table 1.7 Estimating Frame Size Using Wrist Circumference

Female Wrist Measurements

Height <5'2

Height 5'2 –5'5

Height >5'5

Small

<5.5

<6.0

<6.25

Medium

5.5 –5.75

6.0 –6.25

6.25 –6.5

Large

>5.75

>6.25

>6.5

Male Wrist Measurements

Height >5'5

Small

5.5 –6.5

Medium

6.5 –7.5

Large

>7.5

Data from reference 6.

Elbow Breadth Subject should stand, if possible, and extend the arm forward so that it is horizontal and parallel to the ground. Turn palm so that it is facing up and bend elbow so that the forearm is at a 90-degree angle to the ground. Measure the distance between the two prominent bones on either side of the elbow (the epicondyles of the humerus). This measurement can be taken with a ruler or tape measure, but using calipers is preferable. Compare the measurement to the values in Table 1.8.

Amputation Adjustment For patients with amputations, estimation of IBW should be adjusted with the following equation using the factors in Table 1.9.

P.10

Table 1.8 Estimating Frame Size Using Elbow Breadth

Female Elbow Measurements

Medium Frame If elbow breadth is less than those in the table for a specific height, subject is small framed, and if elbow breadth is greater, subject is large framed.

Height

Elbow Breadth

4'10 –4'11

2 1/4 –2 1/2

5'0 –5'3

2 1/4 –2 1/2

5'4 –5'7

2 3/8 –2 5/8

5'8 –5'11

2 3/8 –2 5/8

6'0 –6'4

2 1/2 –2 3/4

Male Elbow Measurements

Medium Frame If elbow breadth is less than those in the table for a specific height, subject is small framed, and if elbow breadth is greater, subject is large framed.

Height

Elbow Breadth

5'2 –5'3

2 1/2 –2 7/8

5'4 –5'7

2 5/8 –2 7/8

5'8 –5'11

2 3/4 –3

6'0 –6'3

2 3/4 –3 1/8

6'4 –6'7

2 7/8 –3 1/4


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)

Obesity

Disease Riska Relative to Normal Weight & Waist

Class

Circumference

Weight Status

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

30.0–34.9

Obesity

35.0–39.9

>40.0

Increased

High

I

High

Very high

Obesity

II

Very high

Very high

Extreme obesity

III

Extremely high

Extremely high

BMI, body mass index. aDisease risk for type 2 diabetes, hypertension, and CVD. Data from reference 10.

Estimating Nutrient Requirements Energy Requirements Harris–Benedict and Mifflin–St. Jeor Equations The Harris–Benedict and Mifflin–St. Jeor equations are two widely used predictive equations for estimating basal (BEE) or resting energy expenditure (REE). Once BEE or REE have been calculated, the total energy expenditure (TEE) would need to be estimated using a combination of activity and stress factors. Stress factors are used P.14

for hospitalized patients in a hypermetabolic state due to disease, infection, or trauma. The clinician's judgment should be used to determine the appropriate activity and/or stress factor to use to estimate TEE. See Table 1.14 for activity and stress factors.

Table 1.13 Waist-to-Hip Ratio

Male

Female

Health Risk

=0.95

=0.80

Low risk

0.96–1.0

0.81–0.85

Moderate risk

=1.0

=0.85

High risk


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

Normal

Energy Requirement (kcal/kg)

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 P.19 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 P.20 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

1. Monitor dietary intake of protein (PRO) for 24 hr 2. Convert dietary protein intake to nitrogen intake:

3. Collect 24-hr urine; obtain urinary urea nitrogen (UUN) 4. Nitrogen Balance = Nitrogen intake - (UUN + 3a) 5. Interpretation: Adults are normally in nitrogen balance (0); pregnant women and children (growth states) are in positive balance; negative balance may suggest malnutrition

a Insensible losses.

P.21

Table 1.23 Calculation and Interpretation of Creatinine Height Index

24-hr Urine Collection; Meat-Free Diet (Ideally); Compare Creatinine to Standard for Height/Gender

% CHI=

Interpret:

60%–80%, mild depletion 40%–59%, moderate depletion <40%, severe depletion

Affected by:

Renal dysfunction; advanced age; stress; trauma; sepsis; strenuous exercise; use of corticosteroids

24-hr Urinary Creatinine Excretion in Adults

Males: 23 mg/kg/IBW

Females: 18 mg/kg/IBW

Height (cm)

Creatinine (mg)

Height (cm)

Creatinine (mg)

157.5

1,288

147.3

830

160.0

1,325

149.9

851

162.6

1,359

152.4

875

165.1

1,386

154.9

900

167.6

1,426

157.5

925

170.2

1,467

160.0

949

172.7

1,513

162.6

977

175.3

1,555

165.1

1,006

177.8

1,596

167.6

1,044

180.3

1,642

170.2

1,076

182.9

1,691

172.7

1,109

185.4

1,739

175.3

1,141

188.0

1,785

177.8

1,174

190.5

1,831

180.3

1,206

193.0

1,891

182.9

1,240

CHI, creatine height index; IBW, ideal body weight. Data from reference 20.

Biochemical assessment also includes review of hematologic parameters, as they may be indicators of nutritionally related anemia (Table 1.24). Several of these parameters can also be expected to be affected by compromised visceral protein status. P.22

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

Low in early deficiency state in the presence of depleted iron stores

Females: 15–49 yr: 12.0–156 ng/mL >49 yr: 18.0–204 ng/mL

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


P.23

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 P.24 P.25

P.26 P.27 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

Hair

Eyes

Healthy

Abnormal

Implications

Normal

Thin, dull, dry, brittle,

Chemotherapy,

distribution, shiny

corkscrew hairs

protein or biotin deficit, vitamin C deficiency

Bright, clear, pink conjunctiva

Sunken, dull, pale, dry conjunctiva,

Deficiency of: Vitamin A, zinc, riboflavin

photophobia, xerosis

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-

Deficiency of: protein, iron

shaped nails

Musculoskeletal, adipose

Normal bone, muscle, and fat development

Calf tenderness, loss of subcutaneous fat, emaciated appearance, pain, decreased grip

Deficiency of: protein, thiamin, vitamin C; energy or fluid deficit

strength, hollow cheeks, fractures, osteoporosis

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

Vomiting or diarrhea or anorexia; 3 pts Pain; 3 pts (specify location ______)

2 weeks

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 P.28 P.29 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

Hepatitis

Peritonitis

Hypertension

Pressure ulcers

Inflammatory bowel

Renal failure

disease

Cirrhosis

disease

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,

Use of multiple medications Duration of medication use Frequency of use (chronic or as needed)

essential nutrients) Illegal drugs

Changes in sense of smell or taste related to medications Previous education on potential interactions

Personal

Age Gender

Income Use of or eligibility for government programs

Cultural/ethnic identity

Communication barriers

Occupation/economic status Role in family Educational level Motivational level

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. P.30 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

Sample Form

Where Eaten

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). P.31

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____PRO a ____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 1. Lacey K, Pritchett E. Nutrition Care Process and Model: ADA adopts roadmap to quality care and 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.

6. National Library of Medicine (NLM). Calculating body frame size. Available at: http://www.nlm.nih.gov/ medlineplus/ency/ imagepages/17182.htm. Accessed February 1, 2006. P.32 7. Osterkamp LK. Current perspective on assessment of human body proportions of relevance to amputees. J Am Dietetic Assoc 1995;95:215–218.

8. Huffman GB. Evaluating and treating unintentional weight loss in the elderly. Am Fam Phys 2002;65(4):640–650.

9. Gazewood JD, Mehr DR. Diagnosis and management of weight loss in the elderly. J Fam Pract 1998;47(1):19–25.

10. National Institutes of Health Clinical Guidelines on the identification, evaluation, and treatment of 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 nutritional status in the elderly. Clin Nutr 2005;24:427–432.

18. Labs: Merck Manual (http://www.merck.com/mmpe/sec22/ ch328d.html#sec22-ch328-ch328d-76).

19. Pagana KD, Pagana TJ. Mosby's Manual of Diagnostic and Laboratory Tests. St. Louis, MO: Mosby; 2006. P.33 20. Blackburn GL, Bistrain BR, Maini BS, et al. Nutritional and metabolic assessment of the hospitalized patient. J Parenteral Enteral Nutr 1977;1:11–12.

21. Mackle TJ, Touger-Decker R, O'Sullivan Maillet J, et al. Registered dietitians' use of physical assessment parameters in professional practice. J Am Diet Assoc 2003;103(12):1632–1638.

22. Detsky AS, McLaughlin JR, Baker JP, et al. What is subjective global assessment of nutritional status? J Parenteral Enteral Nutr 1987;11:8–13.

Authors: Width, Mary; Reinhard, Tonia Title: Clinical Dietitian's Essential Pocket Guide,The: Essential Pocket Guide, 1st Edition Copyright ©2009 Lippincott Williams & Wilkins > Table of Contents > Part I - Nutrition Assessment and Support > Chapter 2 - Pregnancy

Chapter 2 Pregnancy Pregnancy represents a vulnerable life stage relative to a woman's nutritional status. In addition, both the dietary intake and the nutritional status of the woman prior to and during pregnancy greatly influence fetal development and, in turn, pregnancy outcome. The Update on Nutrition During Pregnancy and Lactation report issued special recommendations for women before pregnancy (Table 2.1) (1). Recent research has also shown the profound impact of maternal nutrition status and intake on the infant's risk in adulthood for several chronic diseases such as hypertension and diabetes, largely via birth weight (2). Several of the complications of pregnancy can also adversely affect nutritional status. For these reasons, nutritional assessment is imperative to help ensure optimal pregnancy outcome. One of the most important aspects of pregnancy is body weight, both prepregnancy weight and weight gain during gestation, which significantly influence pregnancy outcome (3). A woman with either excess or low body weight prior to pregnancy has a higher risk for poor outcome. However, weight gain during pregnancy, specifically total amount and rate, are most correlated with infant birth weight, which in turn is associated with infant mortality (4). P.38

Table 2.1 Special Recommendations for Women Before Pregnancy

1. 2. 3. 4.

Maintain a healthy weight. Engage in physical activity regularly. If you need to gain or lose weight, do so gradually (no more than 1–2 lbs/week). If you are trying to become pregnant and you ordinarily drink alcoholic beverages, stop drinking or cut back on the amount you drink. 5. If you smoke, quit or cut back to improve your health. 6. 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.

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 P.39 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 P.40 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%

Zinc, 38%b

Pantothenic acid, 20% Biotin, 0%c Choline, 6%c

aIncrease is only for the 3rd trimester of pregnancy. b Age 18 and under is somewhat lower. c Age 18 and under is somewhat higher. d Age 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.

P.41

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.

P.42

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, P.43 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 selfmonitoring 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 P.44 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

1. Are you a member of a high-risk ethnic group (African American, Native American, Hispanic, Pacific Islander)? 2. Are you overweight or very overweight? 3. Are you related to anyone who has diabetes now or had diabetes in their lifetime? 4. Are you older than 25? 5. Did you have gestational diabetes with a past pregnancy? 6. Have you had a stillbirth or a very large baby with a past? 7. Do you have a history of abnormal glucose tolerance?

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 P.45 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 P.46 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 P.47 restriction of 2 to 3 g/day. The Dietary Approaches to Stop Hypertension, or DASH Diet, may be useful (Table 2.14) (29). Medical management involves bed rest and antihypertensive medications.

Table 2.13 Risk Factors for Preeclampsia

Nulliparity Previous pregnancy with preeclampsia High body mass index Working during pregnancy Family history of hypertension African American, only for nulliparous women Low socioeconomic status; less developed countries Elevated plasma homocysteine

From references 25, 27, and 28.

Nutrition Assessment An early nutrition assessment is crucial in pregnancy, given the relationship between nutritional status of the mother P.48 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 P.49 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 P.50 P.51 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

2nd trimester:

185 +/- 22

Lipids: Triglyceride

Osmolality

3rd trimester:

224 +/- 24

3 mos postpartum:

82 +/-

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

1. 2. 3. 4. 5. 6.

Y

N

Body image problems/attempts at weight loss or restriction Follows a special diet (e.g., vegan, strict vegetarian) Food secure: adequate resources/availability of food Poverty: adequate housing, transportation Adequate social support Appropriate physical activity (moderate, not excessive)

II. Physiologic Problems 1. Nausea, vomiting, diarrhea 2. Constipation 3. Gastroesophageal reflux

III. Nutritional Adequacy: Food Groups 1. 2. 3. 4.

Dairy products Fruits and vegetables Whole grains/fiber-containing breads and cereals Protein foods

IV. Nutritional Adequacy: Specific Nutrients/Foods 1. Minerals: calcium, iron, zinc 2. Vitamins: B6, folate, B12, D 3. Protein: high biologic value

V. Contaminants/Other Substances 1. 2. 3. 4. 5.

Fish (mercury/contaminants: check health department for advisories) Pica Excessive caffeine (>2 cups coffee/day) Alcohol Smoking

P.52

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.

P.53

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), betablockers, 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.

P.54 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. P.55 11. Dietary Guidelines for Americans, 2005, U.S. Department of Agriculture and the U.S. Department of Health and Human Services.

12. Ogunyemi DO, Michelini GA. Hyperemesis gravidarum. Available at: http://www.emedicine.com/med/topic1075.htm. Accessed August 26, 2006.

13. Escott-Stump S. Nutrition and Diagnosis-Related Care, 5th ed. Baltimore: Lippincott Williams & Wilkins; 2002.

14. Mahan LK, Escott-Stump S. Krause's Food, Nutrition, and Diet Therapy, 11th ed. Philadephia: Saunders; 2004.

15. Shils ME, Shike M, Ross AC, et al. Modern Nutrition in Health and Disease, 10th ed. Baltimore: Lippincott Williams & Wilkins; 2006.

16. CDC MMNR Weekly. May 29, 1998;47(20):408–414.

17. American Diabetes Association. Gestational diabetes mellitus. Diabetes Care 2004;27:S88–S90.

18. Silverman BL, Purdy LP, Metzger BE. The intrauterine environment: Implications for the offspring of diabetic mothers. Diabetes Rev 1996;4:21–35.

19. National Institutes of Health Publication No. 00-4818, June 2005.

20. American Diabetes Association. Evidence-based nutrition principles and recommendations for the treatment and prevention diabetes and related complications. Diabetes Care 2002;25:148–198.

21. Reader D, Sipe M. Key components of care for women with gestational diabetes. Diabetes Spectrum 2001;14(4):188–191.

22. Rolfes SR, Pinna K, Whitney E. Understanding Normal and Clinical Nutrition, 7th Ed. Belmont, NY: Thomson Wadsworth; 2006.

23. Jacobson G, Ramos G, Ching J, et al. Comparison of glyburide and insulin for the management of gestational diabetes in a large managed care organization. Am J Obstet Gynecol 2005;193(1):118–124.

24. Steele JM, Johnstone FD, Hume R, et al. Insulin requirements during pregnancy in women with type 1 diabetes. Obstet Gynecol 1994;83:253–258.

25. Moodley J, Kalane G. A review of the management of eclampsia: practical issues. Hypertens Pregnancy 2006;25(2):47–62.

26. Roberts JM, Gammill HS. Preeclampsia, recent insights. Hypertension 2005;46(6):1243–1249. P.56 27. Eskenazi B, Fenster L, Sidney S. A multivariate analysis of risk factors for preeclampsia. J Am Med Assoc 1991;266 (2):237–241.

28. Patrick TE, Powers RW, Daftary AR, et al. Homocysteine and folic acid are inversely related in black women with preeclampsia. Hypertension 2004;43(6):1279–1282.

29. Harsha DW, Lin PH, Obarzanek E, et al. Dietary approaches to stop hypertension: a summary of study results. Dash collaborative research group. J Am Diet Assoc 1999;99(8 Suppl):S35–S39.

30. California Department of Health Services, Maternal and Child Health, Women, Infants and Children. Nutrition During Pregnancy and the Postpartum Period. June 1990. Available at: http://www.perinatology.com/Archive/Weightgrid.pdf.

31. Bernstein IM, Ziegler W, Badger GJ. Plasma volume expansion in early pregnancy Obstet Gynecol 2001;97(5):669–672.

32. Zeman FJ, Ney DM. Applications in Medical Nutrition Therapy, 2nd ed. Upper Saddle River, NJ: Merrill/Prentice Hall; 1996.

33. March of Dimes. Drugs and herbs. Available at: http://www.marchofdimes.com/pnhec/159_529.asp. Accessed September 19, 2006.

34. U.S. Food and Drug Administration. Current Categories for Drug Use in Pregnancy. Available at: http://www.fda.gov/ fdac/features/2001/301-preg.html#categories.

Authors: Width, Mary; Reinhard, Tonia Title: Clinical Dietitian's Essential Pocket Guide,The: Essential Pocket Guide, 1st Edition Copyright ©2009 Lippincott Williams & Wilkins > Table of Contents > Part I - Nutrition Assessment and Support > Chapter 3 - Assessing Pediatric Patients

Chapter 3 Assessing Pediatric Patients Angela M. Lada RD Nutrition assessment of the pediatric patient is unique in many ways. Nutrition screening is most useful in identifying high-risk infants, children, and adolescents in all settings of health care. Table 3.1 lists some “red flags” that warrant nutrition intervention in inpatient units, outpatient clinics, or in the community setting. Table 3.2 lists some common classifications used when assessing infants.

Anthropometric Assessment Measurement of growth is essential for assessing the health and nutritional status of the pediatric patient. Serial measurements are best measures of growth and are more conclusive than isolated measurements. Below are the recommended anthropometric measurements to use based on age:

0–36 months

Body weight Recumbent length Head circumference Weight for length 36 months–18 years

Body weight Height P.60 P.61 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

<1,000 g

weight

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 P.62 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 36month-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 P.63 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

Interpretation a

Percentile

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.

P.64 Premature infant growth charts can be found in the following publication: Fenton Tanis R. A new growth chart for preterm babies: Babson and Benda's chart updated with recent date and a new format. BMC Pediatrics 2003;3:13. Available at: http://www.pubmedcentral. nih.gov/articlerender.fcgi?artid=324406

Table 3.6 Interpretation of BMI-for-Age Plotted on Standard CDC Growth Charts

Percentile

Interpretation

<5th

Underweight

=5th and <85th

Normal weight

=85 and <95th

At risk of overweight

=95th

Overweight


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: P.65 % UBW = (actual weight/usual weight) ÷ 100 % Weight change = [(actual-usual weight)/usual weight] ÷ 100

Significant weight loss:

>2% in 1 week >5% in 1 month >7.5% in 3 months >10% in 6 months

Waterlow Criteria Waterlow criteria are for distinguishing malnutrition as acute (wasting) versus chronic (stunting) in children 1 to 3 years old (Table 3.7) (5):

McClaren Criteria McClaren criteria are used for distinguishing the degree of malnutrition in children <4 years old (Table 3.8) (6):

Table 3.7 Waterlow Criteria for Distinguishing Severity of Malnutrition

Nutritional Status

Acute

Chronic

Stage 0 (normal)

>90%

>95%

Stage 1 (mild)

81%–90%

90%–95%

Stage 2 (moderate)

70%–80%

85%–89%

Stage 3 (severe)

<70%

<85%


P.66

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


P.67

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. P.68

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. P.69 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)

Body Surface Area (m2)

Weight in Kilograms

<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

RDAa

Reference

Category

Infants

Children

Males

Age (yrs)

Reference Weight (kg)

RDA

kcal/kg

kcal/cm

Pro g/kg

Pro g/cm

0–0.5

6

108

n/a

2.2

N/A

0.5–1.0

9

98

n/a

1.6

N/A

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

11–14

45

55

15.9

1.0

0.29

Females

15–18

66

45

17

0.9

0.34

19–24

72

40

16.4

0.8

0.33

11–14

46

47

14

1.0

0.29

15–18

55

40

13.5

0.8

0.27

19–24

58

38

13.4

0.8

0.28

a

Recommended Dietary Allowance Data from references 2 and 10.

P.70

Table 3.14 Dietary Reference Intakes of Estimated Energy Requirement (EER)

Physical Activity (PA) Coefficient Based on Sex and Age

Calculation of Estimated Energy Requirements

Physical Activity Level (PAL)

All infants and toddlers

0–3 months

(89 ÷ wt [kg] - 100) + 175

N/A

4–6 months

(89 ÷ wt [kg] - 100) + 56

N/A

7–12 months

(89 ÷ wt [kg] - 100) + 22

N/A

13–35 months

(89 ÷ wt [kg] - 100) + 20

N/A

Boys 3–8 years old

EER = 88.5 - 61.9 ÷ age [y] + PA × (26.7 ×wt [kg] + 903 × ht [m]) + 20

PA = 1.0 if PAL is estimated to be =1 <1.4 (sedentary) PA = 1.13 if PAL is estimated to be = 1.4 <1.6 (low active)

Boys 9–18

EER = 88.5 - 61.9 ÷ age [y] + PA ÷

PA = 1.26 if PAL is estimated to

years old

(26.7 ÷ wt [kg] + 903 ÷ ht [m]) + 25

be =1.6 <1.9 (active) PA = 1.42 if PAL is estimated to be =1.9 <2.5 (very active)

Girls 3–8 years old

EER = 135.3 - 30.8 ÷ age [y]+ PA ÷ (10 ÷ wt [kg] +934 ÷ ht [m]) + 20

PA = 1.0 if PAL is estimated to be =1 <1.4 (sedentary) PA = 1.16 if PAL is estimated to be =1.4 <1.6 (low active)

Girls 9–18 years old

EER = 135.3 - 30.8 ÷ age [y] + PA ÷ (10 ÷ wt [kg] +934 ÷ ht [m]) + 25

PA = 1.31 if PAL is estimated to be =1.6 <1.9 (active) PA = 1.56 if PAL is estimated to be =1.9 <2.5 (very active)


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. P.71

Table 3.15 Metabolic Rates of Infants and Children

Age 1 Week–10 Months

Age 11 Months–36 Months

Age 3–18 years

Weight

Male Females

Weight

Male

Female

Weight

Male

Female

(kg)

(kcal/hr)

(kg)

(kcal/hr)

(kcal/hr)

(kg)

(kcal/hr)

(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 P.72 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?

Authors: Width, Mary; Reinhard, Tonia Title: Clinical Dietitian's Essential Pocket Guide,The: Essential Pocket Guide, 1st Edition Copyright 2009 Lippincott Williams & Wilkins > Table of Contents > Part I - Nutrition Assessment and Support > Chapter 4 - Older Adults

Chapter 4 Older Adults Aging produces numerous physical and physiologic changes, which in turn alter nutritional requirements and affect nutritional status (Table 4.1 ). The presence of chronic disease, and/or medications can enhance potential disparities between nutrient needs and dietary intake, leading to malnutrition. Indeed, research suggests that malnutrition is a common condition among the elderly, with a prevalence of 12% to 50% of those hospitalized, and 23% to 60% of elderly in extended care facilities (1 ,2 ).

Nutrient Recommendations The physiologic changes associated with aging affect requirement for several essential nutrients. In general, the requirement for many nutrients decreases, concomitant with the decrease in energy needs. However, some nutrients are needed in higher amounts. Additionally, various psychosocial and socioeconomic changes that often attend aging may also alter dietary intake (Table 4.2 ) (3 ). The age category for adults was divided into two separate categories with the most recent Dietary Reference Intakes (DRI) revision (Tables 4.3 ,4.4 ,4.5 ) (4 ). The adult age groups are 51 to 70 years and 70 and above, although the nutrient levels are the same for both adult categories for P.96 P.97 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 P.98 P.99 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 1. Buy low-cost food, such as dried beans/peas, rice, and pasta 2. 3. 4.

1. 2. 3. 4. 5.

Use coupons for money off on foods used and check store weekly circular to buy foods on sale Buy store-brand foods Check with local place of worship for free or low-cost meals Participate in local senior nutrition programs,a offered at senior congregate feeding sites or home-delivered meals 6. Check for eligibility for the Food Stamp Programa 7. Contact local food banks or emergency food programa Inability to grocery shop 1. 2. 3. 4. 5.

Ask a friend or relative to grocery shop Contact local grocery store to bring groceries to your home Contact food delivery companies Check with local place of worship or senior center for volunteers who will shop Hire a home health worker (listed under “Home Health Services” in phone book)

Inability to prepare food 1. Use a microwave oven to cook frozen meals and foods 2. Buy easily prepared nutritious foods (fresh fruits, whole grain breads, peanut butter, tuna in foil pouch) 3. Participate in local senior nutrition programs.a offered at senior congregate feeding sites or home-delivered meals 4. Hire a home health worker (listed under “Home Health Services” in phone book) to cook meals (also make-ahead meals that can be frozen) Psychological changes that cause poor appetite 1. 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 2. If cooking for just one, you may not feel like making meals; invite family or friends for a meal 3. 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 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 21 a 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 P.100 P.101 P.102 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 ND a DRIs represent RDAs except for vitamins D, K, biotin, choline, pantothenic acid (AI values). Nutrient/Units

DRIa

Males

Tolerable Upper Intake Level (UL)

Females

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 40 a DRIs represent RDAs except for calcium, chromium, fluoride, manganese (AI values). Nutrient/Units

DRIa

Males

(UL)

Females

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 P.103 Common Diagnoses Cerebral vascular accident Intracerebral bleeding Transient ischemic attack Traumatic brain injury Brain tumor Diet Prescriptions Puree Fluid restriction Transitional feedings Nutrition Assessment Diagnosis Weight status/change Albumin level Degree of metabolic stress Presence of decubitus ulcers Need for nutrition support Adapted from reference 7.

Table 4.8 Dysphagia Screening: Risk Factors

Pressure Ulcers Disease Process Pressure ulcers, also known as decubitus ulcers or bedsores, represent a point of skin breakdown from continual contact with a surface, such as a bed or wheelchair. Pressure ulcers, or more precisely the complications from them, account for approximately 60,000 deaths every year in the United States and a cost of $1 billion to $5 billion (9 ). Of significance to health care practitioners is the statistic that 9% of patients admitted to the hospital will develop a pressure ulcer. And of particular significance to the registered dietitian (RD) is the fact that malnutrition is second only to pressure as a cause of pressure ulcers (10 ).

Treatment and Nutritional Intervention Pressure ulcers are assessed as being at one of four stages, relative to depth of tissue involvement and therefore severity (9 ). Several nutrients are important in the nutrition care of patients with pressure ulcers, but the most important of these is protein. Protein needs in the patient

P.104 P.105 with pressure ulcers are based primarily on the stage (see Chapter 1 , Table 1.16 ). Table 4.9 lists nutrients, which have been shown to be important in treating pressure ulcers (7 ). However, doses of single nutrients needed for healing pressure ulcers have not been determined, as nutrients work in synergy. Level 1 Moderate to severe Poor oral phase ability; reduced ability to protect airway Pureed, homogenous, cohesive foods; no course texture; no raw foods (fruits, vegetables, nuts); any foods requiring chewing or bolus formation are excluded Close or complete supervision Level 2 Mild to moderate Oral and or pharyngeal Moist, soft-textured foods with some cohesion, which are easily formed into a bolus; meats are ground or minced with pieces no larger than one quarter inch; transition to more solid texture from pureed; chewing ability is required Assess patient for tolerance to mixed textures; it is expected that some mixed texture foods are tolerated Level 3 Mild Oral and or pharyngeal (to a lesser degree than in level 2) Nearly regular texture with exception of very hard, sticky or crunchy foods; foods still need to be moist in bite-sized pieces; adequate dentition and mastication needed Assess patient for tolerance to mixed textures; it is expected that some mixed texture foods are tolerated Adapted from reference 7. Dysphagia Severity

Level of Supervision During Meals/Assessment Swallowing Stage Affected

Food Characteristics

Needed

Table 4.9 Overview of the National Dysphagia Diet

Nutrition Assessment Screening for Nutrition Risks in the Elderly Nutrition assessment in elderly patients consists of the typical nutrition assessment parameters (refer to Chapter 1 ); however, special considerations are important and are highlighted. The Nutrition Screening Initiative was a collaborative effort of several lead agencies whose goal was to identify and treat nutritional problems in the elderly (11 ). A simple screening tool focusing on all aspects of elderly health, including psychosocial and environmental factors (DETERMINE), was developed and continues to be used by health care providers working with the elderly (Table 4.10 ).

Anthropometric Measurements In the elderly, mortality is not correlated with a body mass index (BMI) above the established norms as in younger populations (12 ). Rather, the most significant anthropometric risk factor is unintentional weight loss (13 ). For this reason, the use of ideal body weight is not necessarily appropriate, although it is widely

used. A more important parameter, P.106 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 Vitamin Vitamin Vitamin

A B complex C 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) P.107

References 1. Wallace JI. Malnutrition and enteral/parenteral alimentation. In: Hazzard WR, Blass JP, Ettinger WH, Jr, Halter JB, Ouslander JG, Eds. Principles of Geriatric Medicine and Gerontology , 4th ed. New York: McGraw-Hill, 1999; 1455–1469.

2. Ennis BW, Saffel-Shrier S, Verson H. Diagnosing malnutrition in the elderly. Nurse Pract 2001;26(3):52–65.

3. FDA: Eating Well As We Age. Available at: http://www.fda.gov/ opacom/lowlit/eatage.html. Accessed February 13, 2007.

4. DRIs: USDA Food and Nutrition Information Center. Available at:http://www.iom.edu/Object.File/Master/21/372/0.pdf. Accessed February 13, 2007.

5. Niedert KC, ed. Nutrition Care of the Older Adult, Second Edition: A Handbook for Dietetics

Professionals Working Throughout the Continuum of Care. Chicago, IL: American Dietetic Association, 2004:211.

6. Bales CW, Ritchie CS, eds. Handbook of Clinical Nutrition and Aging. 2004:547–568.

7. American Dietetic Association. Nutrition Care Manual. Online subscription. Accessed February 13, 2007.

8. National Dysphagia Diet Task Force. National Dysphagia Diet––Standardization for Optimal Care. Chicago, IL: American Dietetic Association; 2002:17–19.

9. Lyder GH. Pressure ulcer prevention and management. J Am Med Assoc 2003;289(2):223–226.

10. Straus E, Margolis D. Malnutrition in patients with pressure ulcers: Morbidity, mortality, and clinically practical assessments. Adv Wound Care 1996;9(5):37–40.

11. Editorial: Evaluating the nutrition screening initiative. Am J Publ Health 1993;83(7):944.

12. Stevens, J, Cai, J, Pamuk, ER, et al. The effect of age on the association between Body-mass index and mortality. N Engl J Med 1998;338(1):1–7.

13. Diehr P, Bild DE, Harris TB, et al. Body mass index and mortality in nonsmoking older adults: the cardiovascular health study. Am J Public Health 1998;88(6):623.

14. Validation of several established equations for resting metabolic rate in obese and nonobese people. J Am Dietetic Assoc 2003;103(9):1152–1159.

Authors: Width, Mary; Reinhard, Tonia Title: Clinical Dietitian's Essential Pocket Guide,The: Essential Pocket Guide, 1st Edition Copyright ©2009 Lippincott Williams & Wilkins > Table of Contents > Part I - Nutrition Assessment and Support > Chapter 5 - Nutrition Support

Chapter 5 Nutrition Support Brenda Howell RD, CNSD Patients who are unable to meet nutrition requirements by a conventional oral diet need alternative means of nutrition, unless aggressive therapies are not warranted. Alternative means of nutrition are enteral nutrition and parenteral nutrition.

Enteral Nutrition Indications and Patient Selection Enteral nutrition is the preferred route if the gut is functional due to fewer complications, fewer costs, and improved outcomes. Benefits of enteral nutrition (EN) include increased nutrient utilization, maintenance of normal gut pH and flora inhibiting opportunistic bacterial overgrowth, and support of gut mucosa's immunologic barrier function, which may decrease risk of gut-related sepsis. Examples of patients who are not able to orally meet nutrition needs are patients with altered mentation, severe dysphagia, poor appetite, and respiratory failure requiring vent via endotracheal tube (1,2). Indications and contraindications for EN can be found in Table 5.1. P.112

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. P.113 P.114

Table 5.2 Enteral Access Devices

Description

Short Term (<4 weeks)

Pros

Cons and Complications

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

Orogastric

Optional route

tube: prepyloric tube

when tube can not be placed nasally (facial fracture or

Variety of sizes available (5F–18F) Generally easy placement Larger bore tube makes

Contraindicated if nasal/facial fractures, severe coagulopathy, severe thrombocytopenia, esophageal obstruction Complications

it easier to bolus enteral formulas or medications

include clogging, esophageal or sinus perforation, nasal mucosal ulceration, pneumothorax, epistaxis, pulmonary aspiration

Lower incidence of

Tolerated for short periods of time

sinusitis

Complications are the same as with NGT, with exception of nasal-

head injury)

related events

Nasoenteric tube: postpyloric

Tip of tube placed past the pyloric

tube

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:

Placed surgically,

postpyloric

endoscopically (PEJ), or radiologically into the

Reduces aspiration risk

Not able to bolus enteral feeding Complications may

Low-profile tubes available

include wound dehiscence or infection, bowel obstruction,

jejunum. Size of 9F to 12F tube. Not able to check

occlusion, bleeding, dislodgment, volvulus

residuals to assess tolerance. Requires infusion via a pump

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


P.115

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. P.116 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. P.117 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 P.118 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. P.119

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 P.120 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. P.121

Table 5.5 Central Venous Catheter Types

Length of Type of Access

Definition/Description

Therapy

Nontunneled CVC

Single or multilumen catheter inserted preferable into the subclavian vein. Ease of removal and exchange for shortterm 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

Single or multilumen catheter inserted from peripheral

Several

inserted central catheter (PICC)

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.

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. P.122

Table 5.6 Calculating Osmolarity of PPN Solutionsa

1 1 1 1

g amino acid/L = 10 mOsm g dextrose/L = 5 mOsm g lipid (20% stock solution)/L = 1.3 mOsm 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. 1. 120 g amino acid ÷ 3.0 L = 40 g/L × 10 = 400 mOsm/L 2. 150 g dextrose÷ 3.0 L = 50 g/L × 5 = 250 mOsm/L 3. 4. 5. 6.

80 g lipid ÷ 3.0 L = 26.7 g/L × 1.3 = 35 mOsm/L 8 mEq magnesium sulfate÷ 3.0 L = 2.7 mEq/L × 1 = 2.7 mOsm/L 5 mEq calcium gluconate÷ 3.0 L = 1.67 mEq/L × 1.4 = 2.3 mOsm/L 240 mEq sodium chloride & potassium chloride × 3.0 L = 80 mEq/L × 2 = 160 mOsm/L

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. P.123 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 P.124 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): 1. 4–7 mg × wt (kg) × 1,440 mina = mg/day 2. mg/day ÷ 1,000 = g dextrose/day Example: A critically ill patient weighs 73 kg. 1. 4 mg × 73 kg × 1,440 min = 420,480 mg/day 2. 420,480 mg/day ÷ 1,000 = 420 g/day dextrose

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 P.125 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 P.126 (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 × [(Na 1/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 P.127 P.128 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 1. Determine needed lipids/day and what the solution provides: a. 10% lipid/day would provide 500 mL volume, 50 g lipid and 550 kcal 2. Assess the best AA volume needed to meet AA (g) requirements: a. 80g AA ÷ 10% AA concentration = 800 mL volume and 320 kcal 3. Calculate needed dextrose (g) by subtracting kcal from daily lipids and AA solutions: a. 2,000 kcal - 550 kcal (lipid) × 320 kcal (AA) = 1,130 kcal from dextrose needed b. 1,130 kcal ÷ 3.4 = 332 g dextrose needed/day 4. Assess the best dextrose volume needed to meet dextrose (g) requirements: a. 332 g dextrose ÷ 50% dextrose concentration = 664 mL volume b. Round to 700 mL volume to provide 350 g dextrose and 1,190 kcal 5. Calculate infusion rate per hour per total volume: a. 500 mL (lipid) + 800 mL (AA) + 700 mL (dextrose) = 2,000 mL volume b. 2,000 mL ÷ 24-hr infusion = 83 mL/hr 6. 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 TNA: Macronutrients are ordered in grams per day for this facility 1. Calculate kilocalories provided by goal AA a. 80 g AA × 4 = 320 kcal 2. Calculate kilocalories provided by desired lipid (g) a. 2,000 kcal × 30% = 600 kcal from lipid b. 600 kcal ÷ 9 kcal/g = 66 g lipid (round to 65 g) c. 65 g lipid × 10 kcal/g = 650 kcal from lipid 3. Determine dextrose (g) needed by subtracting kilocalories from AA and lipids. a. 2,000 kcal × 320 kcal (AA) - 650 kcal (lipid) = 1,030 kcal needed from dextrose b. 1,030 kcal ÷ 3.4 kcal/g = 303 g dextrose (round to 300 g) 4. PN goal: 80 g AA, 300 g dextrose, 65 g lipid to provide 1,990 total kcal in 2,000 mL volume

Table 5.12 Macronutrient Composition of Solutions

Macronutrient

Dextrose

Amino acids

Concentrations (%)

Kilocalories per Liter

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

8.5

85

340

10

100

400

15

150

600

20

200

800

Concentration

Lipid emulsions

Grams per Liter

Kilocalories per Milliliter

Kilocalories per Liter

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, P.129 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 CO 2 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

Na+

Cl-

K+

Ca2+

Lactate

Osmolarity

(g/dL)

(mEq/L)

(mEq/L)

(mEq/L)

(mEq/L)

(mEq/L)

(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 P.130 P.131 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

Daily Requirement Electrolyte

Calcium

(Adult)

10–15 mEq

Causes of Elevated Levels

Causes of Decreased levels

Vitamin D excess, renal failure, tumor lysis syndrome, hyperparathyroidism,

Decreased vitamin D intake, hypoparathyroidism, hypoalbuminemia,

prolonged immobilization and stress, bone cancer

hypomagnesemia, citrate binding of calcium with blood product administration

Dosage form

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

Sodium

1–2 mEq/kg

failure

inadequate intake

K phosphate

Inadequate free water, excessive water loss, excessive sodium intake, hyperaldosterism

Excessive hypotonic fluid, nephritis, adrenal insufficiency, congestive heart failure, syndrome of inappropriate

Na Chloride Na Acetate Na lactate

antidiuretic hormones (SIADH), cirrhosis with ascites

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

K phosphate K acetate K chloride

fluids, diuretic medications, hypomagnesemia, metabolic alkalosis


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 P.132

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 acid

60–70 g/L

Infusion of PN should be completed within 24 hours of initiation.

Dextrose

100–150 g/L or 10%–15%

Initiate with caution due to

final concentration with glucose intolerance, risk for hyperglycemia as with steroid therapy, or diabetes

metabolic side effects including reactive hyperglycemia, hyponatremia, hyper-

200 g/L or 15%–20% final concentration as maximum initial amount

insulinemia, glucosuria Infusion of PN should be completed within 24 hours of initiation.

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.

Lipid (IVFE)

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 P.133 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

Yes

Weekly

Weekly

3×/day

3×/day (until

3×/day (until

consistently <200 mg/dL)

consistently <200 mg/dL)

(PTT)

Capillary glucose

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 P.134 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. P.135

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

http://www.nestle-nutrition.com

products call 800-284-9488)

Novartis Medical Nutrition

800-333-3785, option 3

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

Ross Products

800-986-8510 (Medical and

http://www.ross.com

Division

Pediatric Nutritional Products)

References 1. Merritt R. The A.S.P.E.N. Nutrition Support Practice Manual, 2nd ed. Silver Spring, MD: American Society of Parenteral and Enteral Nutrition; 2005.

2. Gottschlich MM. The Science and Practice of Nutrition Support. A Case-Based Core Curriculum. Dubuque, IA: Kendall/Hunt Publishing; 2001.

3. ESPEN Guidelines on Enteral Nutrition: Intensive Care. Available at: http://www.espen.org/Education/documents/ ENICU.pdf. Accessed February 5, 2008.

4. McClave SA, Lukan JK, Stefater JA, et al. Poor validity of residual volumes as a marker for risk of aspiration in critically ill patients. Crit Care Med 2005;33(2):324–330.

5. Cardillo K. Nutrition interventions for chylous effusions. Support Line 2001;23(6):18–23.

6. Wooley JA, Sax HC. Indirect calorimetry: Applications to practice. Nutrition Clin Pract 2003;18:434–439. P.136 7. Institute of Medicine, Food and Nutrition Board. Dietary Reference Intakes: Energy, Carbohydrate, Fiber, Fat, Fatty Acids, Cholesterol, Protein and Amino Acids. Washington, DC: National Academy Press; 2002.

8. Gasser E, Parekh N. Parenteral nutrition: Macronutrient composition and requirements. Support Line 2005;27(6):6–12.

9. Kingley J. Fluid and electrolyte management in parenteral nutrition. Support Line 2005;27(6):13–22.

10. Task Force for the Revision of Safe Practices for Parenteral Nutrition. Safe practices for parenteral nutrition. J Parenteral Enteral Nutr 2004;28:S39–S70.

Authors: Width, Mary; Reinhard, Tonia Title: Clinical Dietitian's Essential Pocket Guide,The: Essential Pocket Guide, 1st Edition Copyright ©2009 Lippincott Williams & Wilkins > Table of Contents > Part II - Nutrition Considerations for Specific Diseases > Chapter 6 - Cancer

Chapter 6 Cancer Sheri Betz RD In the United States, the toll exacted by cancer is second only to that of heart disease, causing one of every four deaths. Each year, more than 1.2 million Americans are diagnosed with cancer, and over 500,000 will die of the disease (1). Cancer is not one disease; rather it represents over 100 diseases. The common characteristics of all cancers are uncontrolled cellular proliferation and the ability of these cells to migrate from the original site and spread to distant sites throughout the body.

Nutrition Implications of Cancer One of the most severe and devastating aspects of cancer is cachexia. This condition of advanced calorie protein malnutrition is characterized by anorexia, fat and muscle tissue wasting, involuntary weight loss, weakness, psychological distress, and a lower quality of life. Often referred to as the “cancer anorexiacachexia 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). P.142 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 P.143 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. P.144

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.


P.145 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

P.146 P.147

Table 6.3 Chemotherapy Medications

Chemotherapeutic Agent:

Stomatitis

Generic Name (Trade

Nausea &

Name)

Vomiting

& Diarrhea

Xerostomia

Esophagitis

Taste Anorexia

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 (DTICDome)

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

Moderate

Yes

No

Yes

No

No

Etoposide (VP-1623)

Mild to moderate

Yes

No

Yes

Yes

No

Floxuridine (FUDR)

Mild

Yes

No

Yes

Yes

No

5-fluorouracil (5FU)

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

(Ellence)

Mechlorethamine (Mustargen)

Severe

Yes

No

No

Yes

Metallic taste

Methotrexate (MTX)

Mild to moderate

Yes

No

Yes

Yes

Yes

Mitomycin

Moderate

Yes

No

Yes

Yes

No

Paclitaxel (Taxol)

Mild

No

No

Yes

No

No

Streptozocin

Severe

Yes

No

No

No

No

(Mutamycin)

(Zanosar)

Data from medication product labeling.

P.148

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 P.149 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

P.150

Table 6.6 Medications to Treat Nausea and Vomiting


Dose

Action


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,

Oral: in divided doses; IV: 30 min before chemo

decreases N&V

Metoclopramide

Oral: 10 mg QID

Stimulates GI

May cause diarrhea at

(Reglan)

IV: 1–2 mg/kg q2h

motility & gastric emptying.

high doses

Ondansetron (Zofran)

Oral: 8 mg q4h for three doses; then

Decreases N&V

Start oral & IV 30 min before chemo

q8h for 1–2 days IV: 32 mg bolus

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


P.151

Table 6.7 Medications to Treat Diarrhea


Dose

Action


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 P.152 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

P.153

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, highprotein 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. P.154 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.

P.155 P.156 P.157

Table 6.8 Neutropenic Diet

Food Groups

Dairy

Allowed

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

Not Allowed

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 & Nuts

Canned and frozen fruit and fruit juices Thick skinned fruits

Dried fruits Raw fruit; foods containing raw fruits

(oranges, bananas) Melons cut up and used immediately Canned or bottled

Unpasteurized fruit and vegetable juices Raw nuts Roasted nuts in the shell

roasted nuts Nuts in baked products Commercially packaged peanut butter

Precut fresh fruits

All breads, bagels, rolls,

Raw grain products

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)

Bakery breads, cakes, donuts, muffins Potato/macaroni salad

Bread, Grain & Cereal Products

Meat & Meat Products

Well-cooked eggs (white cooked firm with thickened yolk, such as hard boiled, over hard) Pasteurized egg

Raw or undercooked meat, poultry, fish, game, tofu Meats and cold cuts from delicatessen

substitutes (i.e., Egg Beaters) Commercially packaged salami, bologna, and other luncheon meats Canned and commercially packaged hard smoked fish, refrigerated after opening Cooked tofu (must be

Hard cured salami in natural wrap Cold smoked salmon, lox Pickled fish Tempe (tempeh) products Sushi Raw oysters/clams

cut into 1-in. cubes or smaller and boiled a minimum of 5 min in water or broth before eating or using in recipes)

Beverages

Fats

Tap water Commercial bottled distilled and natural

Well water Cold-brewed tea made with warm or cold water

waters All canned, bottled, powdered beverages Instant and brewed

sun tea Eggnog Fresh apple cider Homemade lemonade

coffee, tea; cold, brewed tea made with boiling water Brewed herbal teas using commercially packaged tea bags Commercial nutritional supplements, liquid and powdered

Spring water

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

Others

Refrigerated commercial

Unrefrigerated cream-

and homemade cakes, pies, pastries, and pudding Refrigerated creamfilled 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

filled pastry products (not shelf-stable) Cream or custard-filled donuts

Salt, granulated sugar,

Raw or unpasteurized

brown sugar Jam, jelly, syrups (refrigerated after opening)

honey Herbal and nontraditional (health food store) nutritional

Commercially packaged (pasteurized) honey Catsup, mustard, BBQ sauce, soy sauce, other

supplements, Chinese herbs Brewers yeast, if eaten uncooked

condiments (refrigerated after opening) Pickles, pickle relish, olives (refrigerated after opening)

P.158

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. P.159 7. Wilkes GM. Cancer and HIV Clinical Nutrition Pocket Guide, 2nd ed. Sudbury, MA: Jones and Bartlett Publishers; 1999.

8. Nutritional suggestions for symptom management. National Cancer Institute. Available at: http://www.cancer.gov/cancertopics/pdq/supportivecare/nutrition/HealthProfessional/ page4#Section_117. Accessed February 21, 2007.

9. Neutropenic Diet? Available at: http://patienteducation.upmc.com/Pdf/NeutropenicDiet.pdf. Accessed February 20, 2007.

Authors: Width, Mary; Reinhard, Tonia Title: Clinical Dietitian's Essential Pocket Guide,The: Essential Pocket Guide, 1st Edition Copyright ©2009 Lippincott Williams & Wilkins > Table of Contents > Part II - Nutrition Considerations for Specific Diseases > Chapter 7 - Cardiovascular Diseases

Chapter 7 Cardiovascular Diseases Cardiovascular disease (CVD) encompasses all diseases of the heart and blood vessels. Coronary heart disease (CHD) and cerebrovascular accident (CVA) are the major forms of CVD and claim more lives in the United States each year than any other disease (1).

Coronary Heart Disease The underlying pathologic process of CHD, and of the major form of CVA, is atherosclerosis, in which fatty plaques or atheromas develop in the intimal layer of the arterial wall. As plaques accumulate within a blood vessel, the vessel becomes constricted, which is also a cause of congestive heart failure (CHF). If a blood clot forms and cannot pass through the narrowed arterial opening, blood flow to the heart stops causing myocardial infarction (MI) or heart attack. If the clot is in a vessel close to the brain, a CVA, or stroke, ensues.

Myocardial Infarction Disease Process As the underlying process to CHD, of which MI is the culminating event, atherosclerosis represents a response to P.164 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

Alcohol

Pro-inflammatory

Charred meats (advanced glycosylation end products; AGEs)

Cocoa (polyphenols)

Fatty fish (n-3 fatty acids)

Coffee (moderate to high consumption)

Fruits (containing vitamin C,

High glycemic load foods (those raising blood

carotenoids)

glucose)

Olive oil (oleocanthal)

Spices (curry, ginger)

Tea

Vegetables

Walnuts, (and others with alphalinoleic 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 P.165 lipid oxidation products are involved in all stages of CHD (6).

Table 7.2 Foods Containing Lipid Oxidation Products

Dehydrated foods (containing fat, such as meats) Fried foods (cooked at high temperatures) Powdered eggs Rancid fats and oils

Treatment and Nutritional Intervention In 2004, the National Heart, Lung, and Blood Institute's National Cholesterol Education Program (NCEP) released revised guidelines for cholesterol management in its Third Report of the Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (ATP III) (7). The guidelines established by ATP III place an emphasis on treatment based on risk stratification for the primary prevention of CHD. The ATP III states, “A basic principle of prevention is that the intensity of risk-reduction therapy should be adjusted to a person's absolute risk. Hence, the first step in selection of LDL-lowering therapy is to assess a person's risk status.” Following are the ATP III guidelines for the diagnosis and treatment of high cholesterol, approached in a stepwise fashion.

Step 1: Determine lipoprotein levels-obtain complete lipoprotein profile after 9- to 12-hour fast.

Table 7.3 ATP III Classification of Cholesterol Levels

LDL Cholesterol—Primary Target of Therapy

<100 mg/dL

Optimal

100–129 mg/dL

Near optimal

130–159 mg/dL

Borderline high

160–189 mg/dL

High

=190 mg/dL

Very high

Total Cholesterol

<200 mg/dL

Optimal

200–239 mg/dL

Borderline high

=240

High

HDL Cholesterol

<40 mg/dL

Low

=60 mg/dL

High


P.166

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 P.167 (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 P.168 TLC diet approach is recommended (8). The TLC diet focuses on behavioral changes aimed at lowering LDL cholesterol in the population whose LDL cholesterol is above the goal level for their category of risk for heart disease.

Table 7.6 NCEP ATP III Treatment by Risk Category

Risk Category

Risk Profile

LDL Goal (mg/dL)

Initiate TLC

Consider Drug Therapy

High risk

CHD or CHD RE 10-yr risk >20%

<100

=100

=100

Moderately high risk

2+ RF 10-yr risk =20%

<130

=130

=130

Moderate risk

2+ RF 10 yr risk <10%

<130

=130

=160

Lower risk

0–1 RF 10-yr risk <10%

<160

=160

=190

RF: risk factors; RE: risk equivalents Data from reference 7.

Table 7.7 ATP III Nutritional Components of the TLC Diet

Nutrient

Daily Recommended Intake

Total fat

25%–35% of total kilocalories

Saturateda fat

<7% of total kilocalories

Polyunsaturated fat

Up to 10% of total kilocalories

Monounsaturated fat

Up to 20% of total kilocalories

Cholesterol

<200 mg

Carbohydrate (esp. complex)

50%–60% of total kilocalories

Protein

~15% of total kilocalories

Therapeutic Options for LDL Lowering

Daily fiber intake

20–30 g, primarily soluble fiber

Plant stanols/sterols

2 g/day

a Trans-fatty acids are another LDL-raising fat that should be kept at a low intake.


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

P.169

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 (totalHDL) 30 mg/dL higher than LDL goal.

P.170

Table 7.9 Classification of Triglyceride Levels

<150 mg/dL

Normal

150–199 mg/dL

Borderline high

200–499 mg/dL

High

>500 mg/dL

Very high

Note: Data from reference 7.

Congestive Heart Failure Disease Process Congestive heart failure (CHF) is a common disease among the elderly, affecting up to 10% of those over age 65 (10). It develops when the heart fails to pump blood effectively, causing fluid congestion in blood vessels and tissues leading to the heart. The consequences of CHF include a compensatory enlargement of the heart, although the side of the heart affected (left or right) produces different symptoms. If affecting the right side, blood backs up in peripheral and abdominal tissue. The symptoms include chest pain,

digestive problems, and peripheral edema. When CHF affects the left side, fluid accumulates in the lungs and causes pulmonary edema, producing shortness of breath and often leading to respiratory failure. Several conditions and other diseases may cause CHF (Table 7.10).

Treatment and Nutritional Intervention Several nutritional concerns arise in CHF, including right-sided CHF leading to digestive problems and hepatomegaly P.171 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

Betablockers

Rest

Prevent, treat malnutrition (cardiac cachexia)

Digitalis

Smoking cessation

Diuretics

Yearly flu vaccine

Vasodilators

Adapted from reference 10.

Drug therapy is key and consists of four main types, that is, diuretics, ACE inhibitors, beta-blockers, and digitalis (Table 7.11). The edema that occurs and the types of drugs used necessitate a moderate sodium restriction of 2,000 to 3,000 mg, with severe cases requiring the lower level. Small frequent meals may be easier for a patient to consume, both the right-sided CHF because of abdominal bloating and left-sided because of breathing difficulty. As a patient becomes depleted, oral supplements or possibly tube feeding may be needed.

Cerebrovascular Accident (Stroke) and Hypertension Stroke is the third leading cause of death in the United States and leading cause of disability (11). Although a CVA can occur at any age, the risk doubles with each decade after the age of 55. The major risk factor for CVA is hypertension (HTN), which is also a disease of the blood vessels. P.172

Cerebrovascular Accident Disease Process A CVA occurs from two situations: (a) a clot prevents blood flow (and oxygen) to a part of the brain (ischemic stroke), or (b) a cerebral blood vessel ruptures (hemorrhagic stroke). Both types cause damage to the brain resulting in a variety of disabilities, which may or may not be permanent. Risk factors vary as to the type of stroke (Table 7.12). Evidence from epidemiological studies suggests that several nutrients may either protect against or increase risk for CVA (Table 7.13).

Treatment and Nutritional Intervention The most important aspect of treatment for CVA is immediate administration of thrombolytic drugs (11).

P.173 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

Age African American ethnicity

Body weight White men: tricep to subscapular skinfold thickness and CVA have U-shaped relationship;

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)

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

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)

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 P.174 P.175 P.176 P.177 P.178 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

Anticoagulants

Drug/Implications

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. b Prehypertension is not a disease category, but rather a designation developed to identify individuals at risk of developing HTN. Data from reference 20.

Table 7.17 Lifestyle Modification Recommendations

Approximate Systolic Modification

Recommendation

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 lowfat 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 drinks b per day Women: limit to =1 drink per day.

2–4 mm Hg

aEffects are dose and time dependent. b 1 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

2,300 b mg

Potassium

4,700 mg

Calcium

1,250 mg

Magnesium

500 mg

Fiber

30 g

a

Plan is based on a 2,100-kcal diet.

b 1,500 mg was a lower goal tested and was found to be even more effective for lowering BP,

especially for middle-aged and older individuals, African Americans, and those who already had high BP. Data from references 21 and 22.

Table 7.19 DASH Eating Plan—Daily Number of Food Group Servings

Food Groups

Servings per Day by Calorie Level

1,600 calories

2,000 calories

2,600 calories

3,100 calories

Grains

6

6–8

10–11

12–13

Vegetables

3–4

4–5

5–6

6

Fruits

4

4–5

5–6

6

FF or LF milk & milk products

2–3

2–3

3

3–4

Lean meats, poultry, fish

3–6

=6

6

6–9

Nuts, seeds, legumes

3/week

4-5/week

1

1

Fats, oils

2

2–3

3

4

Sweets, added sugar

0

=5/week

=2

=2


Table 7.20 Common Cardiac Abbreviations

AAA

Abdominal aortic aneurysm

ABG

Arterial blood gases

ACLS

Advanced cardiac life support

AF

Atrial fibrillation

AI

Aortic insufficiency

AICD

Automatic implanted cardiac defibrillator

AMI

Acute myocardial infarction

AR

Aortic regurgitation

AS

Aortic stenosis

ASHD

Atherosclerotic heart disease

ASD

Atrial septal defect

AVR

Aortic valve replacement

CABG

Coronary artery bypass graft

CAD

Coronary artery disease

CHD

Coronary heart disease

CHF

Congestive heart failure

CO

Cardiac output

CVA

Cerebral vascular accident

CVC

Central venous catheter

CVD

Cardiovascular disease

CVP

Central venous pressure

DCM

Dilated cardiomyopathy

ECG/EKG

Electrocardiogram

EF

Ejection fraction

HCM

Hypertrophic cardiomyopathy

HR

Heart rate

IA

Intra-arterial

IABP

Intra-arterial balloon pump

ICD

Implantable cardioverter-defibrillator

IHD

Ischemic heart disease

MI

Myocardial infarction

MR

Mitral regurgitation

MVP

Mitral valve prolapse

NSR

Normal sinus rhythm

NTG

Nitroglycerin

PVD

Peripheral vascular disease

SSS

Sick sinus syndrome

SVT

Supraventricular tachycardia

TG

Triglycerides

List of medical abbreviations, available at: http://en.wikipedia.org/wiki/List_of_medical_abbreviations.

Treatment and Nutritional Intervention The JNC7 report emphasizes the importance of lifestyle modification as prevention for the development of HTN, as well as for the management of those with HTN (20).

Nutritional Recommendation The Dietary Approaches to Stop Hypertension (DASH) diet, along with reducing sodium intake, can significantly reduce BP (21). Patients should be educated on the appropriate number of servings to consume from each food group, based on their recommended caloric intake. The diet is low in saturated fat, cholesterol, and total fat; and emphasizes fruit, vegetables, and low-fat dairy products. Table 7.18 lists the nutrient goals used in the DASH studies, and Table 7.19 lists the number of recommended servings, on the DASH diet, for various kilocalorie levels.

References 1. American Heart Association. Available at: http://www.americanheart.org/presenter.jhtml? identifier=4478. Accessed March 15, 2007.

2. Pearson TA, Mensah GA, Alexander RW, et al. Markers of inflammation and cardiovascular disease. Circulation 2003; 107:499–511.

3. Mawhorter SD, Lauer MA. Is atherosclerosis an infection disease? Cleve Clin J Med 2001;68(5):449458.

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. P.179 7. National Institutes of Health, National Heart, Lung, and Blood Institute. Third report of the National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III). Final Report. NIH Publication No. 02-5215,

September 2002.

8. American Heart Association. Step 1, Step 2, and TLC Diets. Available at: http://www.americanheart.org/presenter.jhtml?identifier=4764. Accessed March 17, 2007.

9. Burke Francis M, Carson Jo Ann S, Hark Lisa A. Cardiovascular nutrition disease management and prevention, United States. Faulhaber 2004;32:237–253.

10. American Heart Association. Available at: http://www.americanheart.org/presenter.jhtml? identifier=4585. Accessed March 15, 2007.

11. Centers for Disease Control and Prevention. Available at: http://www.cdc.gov/stroke/. Accessed March 15, 2007.

12. American Heart Association, AHA Stroke Conference 1999. Available at: http://stroke.ahajournals.org/cgi/content/full/30/11/2502#R21 http://stroke.ahajournals.org/cgi/content/full/30/4/905. Accessed March 14, 2007.

13. Joshipura KJ, Hung HC, Rimm EB, Willett WC, Ascherio A. Periodontal disease, tooth loss, and incidence of ischemic stroke. Stroke 2003;34(1):47–52.

14. Gillum RF, Mussolino ME, Madans JH. Body fat distribution, obesity, overweight and stroke incidence in women and men: the NHANES I Epidemiologic Follow-up Study. Int J Obes 2001;25(5):628–638.

15. Iso H, Rexrode KM, Stampfer MJ, et al. Intake of fish and omega-3 fatty acids and risk of stroke in women. JAMA 2001;285:304–312.

16. Liu S, Manson JE, Stampfer MJ, et al. Whole grain consumption and risk of ischemic stroke in women: A prospective study. JAMA 2000;284:1534–1540.

17. Iso H, Stampfer MJ, Manson JE, et al. Prospective study of fat and protein intake and risk of intraparenchymal hemorrhage in women. Circulation 2001;103:856–863.

18. Sherwin R, Price TR. Fat chance: diet and ischemic stroke. JAMA 1997;278:2185–2186.

19. Rolfes SR, Pinna K, Whitney E. Understanding Normal and Clinical Nutrition, 7th ed. Belmont: Thomson, Wadsworth; 2006. P.180

20. National Institutes of Health, National Heart, Lung, and Blood Institute. Seventh report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure. Complete Report. NIH Publication No. 04-5230, August 2004.

21. Appel LJ, Moore TJ, Obarzanek E, et al. A clinical trial of the effects of dietary patterns on blood pressure. N Engl J Med 1997;336:1117–1124.

22. National Institutes of Health, National Heart, Lung, and Blood Institute. Your guide to lowering your blood pressure. NIH Publication No.06-4082. Revised April 2006. Available at: http://www.nhlbi.nih.gov/health/public/heart/hbp/dash/new_dash.pdf. Accessed March 20, 2007.

Authors: Width, Mary; Reinhard, Tonia Title: Clinical Dietitian's Essential Pocket Guide,The: Essential Pocket Guide, 1st Edition Copyright ©2009 Lippincott Williams & Wilkins > Table of Contents > Part II - Nutrition Considerations for Specific Diseases > Chapter 8 - Diabetes

Chapter 8 Diabetes Diabetes mellitus is a disease known since ancient times, cited by both the Greeks and Egyptians in as early as 1500 BC. In its various forms, it affects over 18 million Americans every year, and it is the sixth leading cause of death and a major cause of complications, such as heart disease, kidney disease, blindness, and amputations.

Diabetes: Classification, Screening, and Diagnosis Classification of Diabetes In order to provide comprehensive and effective medical and nutritional care for patients with diabetes, we must first understand the precise definitions and classifications of diabetes. The American Diabetes Association (ADA) issued new diagnostic and classification criteria for diabetes in 1997 (1). In 2003, revisions were made regarding the diagnosis of impaired fasting glucose (IFG) (2). Table 8.1 includes the four clinical classes of diabetes.

Screening for Diabetes Adults Dietitians and other health care providers should encourage regular screening for diabetes, especially for individuals P.184 P.185 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

Genetic defects of the ß-cell; genetic defects in insulin action; diseases

types of diabetes

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

Diagnosed during pregnancy

mellitus (GDM)

Data from references 1,2,3.

Table 8.2 Screening for Diabetes in Asymptomatic Adults

1. 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. 2. 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)

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. P.186

Table 8.4 Testing Recommendations for GDM

Criteria for Group Level

Low-risk group

Must meet all the following criteria:

Testing Recommendation

No glucose testing required

<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

High-risk group

Women with any of the following: Marked obesity Personal history of GDM Glycosuria Strong family history of diabetes

Averagerisk group

Any woman not meeting criteria for the low-risk or high-risk groups

FPG or casual plasma glucose as soon as feasiblea Retest between 24 and 28 weeks gestation if initial screening is negative for GDM

Test 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 P.187 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

1. 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 2. Fasting Plasma Glucose (FPG) 126 mg/dL Fasting is defined as no caloric intake for at least 8 hours. OR 3. 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.

aEach criterion must be confirmed on a subsequent day unless unequivocal symptoms of

hyperglycemia are present. Data from reference 3.

Gestational Diabetes The ADA's 4th International Workshop Conference on GDM supports the use of the Carpenter and Coustan diagnostic criteria for abnormal glucose tolerance (summarized in Table 8.6) (5).

Table 8.6 Detection and Diagnosis of Gestational Diabetes

Plasma Glucose

50-g Glucose Challenge Test

100-g Diagnostic OGTTa

Fasting

—

95 mg/dL

1 hr

140 mg/dL

180 mg/dL

2 hr

—

155 mg/dL

3 hr

—

140 mg/dL

a

Two or more of the plasma glucose values must be met or exceeded for a positive diagnosis. The test should be done in the morning after an overnight fast of 8–14 hours and after at least 3 days of unrestricted diet (>150 g carbohydrate per day) and unlimited physical activity. The subject should remain seated and quiet during the test as activity can interfere with results. Data from references 3 and 5.

P.188

Table 8.7 Testing for Diabetes and Prediabetes

Fasting Plasma Glucose Test

<100 mg/dL

100–125 mg/dL

=126 mg/dL

Normal

Impaired Fasting Glucose (IFG) Prediabetes

Diabetesa

Oral Glucose Tolerance Test

<140 mg/dL

140–199 mg/dL

=200 mg/dL

Normal

Impaired Glucose Tolerance (IGT) Prediabetes

Diabetesa

aEach criterion must be confirmed on a subsequent day unless unequivocal symptoms of

hyperglycemia are present. Data from reference 3.

The glucose testing at 24 to 28 weeks should follow one of two approaches:

One-step approach: Perform a diagnostic 100-g OGTT Two-step approach: Perform an initial screening with a 50-g oral glucose load (glucose challenge test or O'Sullivan test), and perform a diagnostic 100-g OGTT on the subset of women exceeding the glucose threshold value on the glucose challenge test (see Table 8.6).

Prediabetes An intermediate group of subjects has been recognized whose glucose levels do not meet the criteria for diabetes, but are too high to be considered normal (1,2). Individuals that fall into this category are now referred to as having “prediabetes,” and are considered at risk for future diabetes and cardiovascular disease (3). Table 8.7 shows the categories for FPG and OGTT.

Medical Nutrition Therapy MNT is an integral component of diabetes prevention, management, and self-management (3). The recommendations by the ADA for medical nutrition therapy (MNT) in diabetes are based on the 2005 Dietary Guidelines and the P.189 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, P.190 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-toperson, 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 shortacting (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 insulinto-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


P.191

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

45

—

—

5

Fat

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. P.192 P.193

Table 8.11 Oral Medications for Type 2 Diabetes

Dosage Range (2nd Mode of Action

Insulin

Class Brand Name (Generic Name)

First-Generation Sulfonylureas

value is max. dose)

When to Take

Secretagogues

Diabinese (chlorpropamide)

Stimulate insulin secretion from the pancreas

Second-Generation Sulfonylureas:

Glucotrol (glipizide)

100–750 mg/day

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


Amaryl (glimepiride)

1–8 mg/day


Meglitinide–Benzoic Acid Derivative

Prandin (repaglinide)

0.5–16 mg/day

Take with meals

180–360 mg/day

1–30 min before meals

Meglitinide–DPhenylalanine Derivative

Starlix (nateglinide)

Insulin Sensitizers

Biguanides

Improve insulin sensitivity via the liver and peripheral tissue

Glucophage (metformin)

Take with meals

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)

Delay Glucose

Alpha-Glucosidase Inhibitors

Absorption in GI

Precose (acarbose)

15–45 mg/day

Take without regard to meals

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


AvandaMet (Avandia/metformin)

1 mg/500 mg–8 mg/2,000 mg


ACTOplus Met (Actos/metformin)

15 mg/500 mg–45

Take with meals once

Avandaryl (Avandia/Amaryl)

mg/2,550 mg

or twice per day

4 mg/1 mg–8 mg/4 mg


aOnce-a-day therapy is usually satisfactory, but higher doses may be divided.

Data from references 3 and 8, and medication product labeling.

P.194

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 P.195 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)

Duration Onset (hr)

Peak (hr)

Rapid Acting

0.25–0.5

0.5–4

4–6


Lispro (Humalog)

<0.5

1–3

3–5


Aspart (NovoLog) Glulisine (Apidra)

0.25

0.05–1.5

–5


Short Acting (Regular)

(hr)

When to Administer

Humulin R, Novolin R

0.5–1

2–3

6–8


2–4

6–10

14–18

Before am & pm meal or

Intermediate Acting

NPH, Humulin N, Novolin N

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

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


Novolin 70/30

0.5

2–12

Up to 24


Humalog Mix 75/25

<0.5

1–6.5

~22


NovoLog Mix 70/30

<0.5

1–4

Up to 24


Combinations

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 P.196 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

Initial Type of Medication (Trade

Recommended

Name)

How Supplied

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

5 mL vials containing

Type 2

Immediately prior to

Acetate (Symlin) -Used only in type 1 or type 2 patients treated

0.6 mg/mL pramlintide

diabetes: 60 µg Type 1 diabetes:

each major meala

with insulin

Dose

When to Inject

15 µg

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: P.197 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


P.198

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

a

American Association of Clinical Endocrinologists.

b Postprandial glucose measurements should be made 1–2 hr after the beginning of

the meal Data from references 3 and 13.

Perform the A1C test every 3 months in patients whose therapy has changed or who are not meeting glycemic goals. The A1C goal for patients in general is <7%. The A1C goal for the individual patient is as close to normal as possible (<6%) without significant hypoglycemia.

Pre- and postprandial plasma glucose testing is an important part of diabetes management. Table 8.16 lists current recommendation for glycemic control.

Blood Pressure and Lipids Hypertension and dyslipidemia are common comorbid conditions for patients with diabetes, and evidence indicates the control of these coexisting conditions is essential in the treatment of diabetes. Cardiovascular disease accounts for 80% of mortality in patients with diabetes (13). The ADA recommendations for blood pressure and lipids for patients with diabetes are included in Table 8.17.

Sick Day Management Educating patients on sick day management is important. Illnesses such as viral colds or flu, infections, injuries, fever, vomiting, and diarrhea all increase the need for P.199

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/dL a

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.

P.200

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/ cup (4 oz) regular, nondiet soft drink 2

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/ cup ice cream 2

¼ cup sherbet

1

3 glucose tablets

8 Lifesavers

/2 cup frozen yogurt

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 P.201 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

Signs & Symptoms

Plasma Glucose <70 mg/dL

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 1. Check blood glucose (BG) If BG is 50–69 mg/dL give 15 ga carbohydrate. If BG is <50 give 30 g carbohydrate. 2. 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. Severe hypoglycemia: 1. 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. 2. 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

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 P.202 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 P.203 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, hyperventilation, dehydration, fruity odor of ketones, fatigue, blurred vision, weakness, abdominal pain, nausea,

Fatigue, blurred vision, dry mouth, mental status changes, coma

vomiting

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. P.204 7. The 450/500 Rule for determining insulin-to-carbohydrate ratio. Available at: http://www.diabetes.org/type-1-diabetes/insulin-pumps.jsp. Accessed September 25, 2006.

8. Ackerman P, Williams R, Walters J, et al. Ouick reference guide to diabetes for health care providers. Michigan Diabetes Outreach Network; 2006.

9. The 1800 Rule for determining your correction factor. Available at: http://www.diabetesnet.com/ diabetes_control_ tips/corr_factor.php. Accessed September 25, 2006.

10. Byetta (exenatide injection) product labeling information. Available at: http://pi.lilly.com/us/byetta-pi.pdf. Accessed September 20, 2006.

11. Symlin (pramlintide acetate injection) product labeling information. Available at: http://www.symlin.com/pdf/SYMLIN-pi-combined.pdf. Accessed September 20, 2006.

12. Rohlfing CL, Wiedmeyer H-M, Little RR, et al. Defining the relationship between plasma glucose and HbA1c: analysis of glucose profiles and HbA1c in the Diabetes Control and Complications Trial. Diabetes Care 2002;25:275–278.

13. American College of Endocrinology. Consensus statement on guidelines for glycemic control. Endocrine Pract 2002; 8(Suppl 1)Jan/Feb.

14. Hypoglycemia. Available at: http://diabetes.niddk.nih.gov/ dm/pubs/hypoglycemia/ index.htm. Accessed August 5, 2007.

15. Mahan LK, Escott-Stump, S. Krause's Food, Nutrition, & Diet Therapy, 11th ed. Philadelphia: Saunders; 2004:792–833.

16. Haire-Joshu, D. Management of Diabetes Mellitus: Perspectives of Care Across the Life Span. St. Louis: Mosby-Year Book, Inc.; 1992.

Authors: Width, Mary; Reinhard, Tonia Title: Clinical Dietitian's Essential Pocket Guide,The: Essential Pocket Guide, 1st Edition Copyright ©2009 Lippincott Williams & Wilkins > Table of Contents > Part II - Nutrition Considerations for Specific Diseases > Chapter 9 - Gastrointestinal Disease

Chapter 9 Gastrointestinal Disease Considering the importance of the gastrointestinal tract's (GI) key roles in maintaining life and health, it becomes clear as to how profoundly GI diseases can affect nutritional status, and ultimately overall health. Nutritional problems can arise from both upper gastrointestinal tract diseases (UGI), which includes the esophagus and stomach, and lower gastrointestinal tract disease (LGI), which includes the small intestine and the large intestine. These problems can be caused by the underlying disease process itself, or as a consequence of prescribed dietary regimens, and or self-imposed restrictions. For these reasons, the registered dietitian (RD) must conduct a comprehensive nutritional assessment, with particular focus on a detailed diet history, and plan highly individualized interventions.

Diseases of the Upper Gastrointestinal Tract Diseases of the UGI with nutritional relevance include ulcers and gastroesophageal reflux disease. Medications have become increasingly important in both healing of damaged tissue and disease management. Although diet does not cause either disease, it may require alteration to P.208 ameliorate symptoms of the disease process or as a result of surgical intervention.

Gastroesophageal Reflux Disease Disease Process Gastroesophageal reflux is the process in which acid from the stomach refluxes up into the esophagus, and esophagitis is the resultant inflammation of the sensitive tissue of the esophagus. Acute esophagitis can be caused by ingesting a caustic compound, often a medication, such as nonsteroidal anti-inflammatory drugs (NSAIDs), and it can arise from repeated vomiting, especially when self-induced as in anorexia and bulimia. Chronic reflux is termed gastroesophageal reflux disease (GERD) and increases risk for Barrett's esophagus, a precancerous condition (1). Many factors affect lower esophageal sphincter (LES) pressure and, therefore, its opening and closing, including:

Hormones Nutrients Medications

High abdominal pressure, as with:

Chronic lung disease Lying down after meals Substances such as caffeine, mint, cigarettes, alcohol, and chocolate

Treatment and Nutritional Intervention Treatment for GERD includes diet and lifestyle changes, medications, and, failing these, surgery. Physicians often prescribe medications that reduce gastric acidity, which include antacids, H2 receptor antagonists, and proton pump inhibitors. Reducing acidity of the gastric contents renders the reflux fluid less caustic. Other types of drugs, such as metoclopramide and cisapride, increase gastric emptying rate. P.209

Table 9.1 Factors Affecting LES Pressure in GERD

Reduce Pressure (Open)

Alcoholic Beverages

Increase Pressure (Close)

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, SloPhyllin, 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/II a) 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.

P.210

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

P.211 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 P.212 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

Don't lie down after eating (wait 3 hrs) Elevate the

Avoid acidic foods (citrus fruits, tomatoes) Avoid spicy foods

meals Limit alcohol Avoid foods that lower LES a pressure: chocolate, coffee,

head of the bed, if needed Limit or avoid smoking Use antacids to

(red, black pepper) Follow a bland, soft diet Eat small

lower gastric acidity

frequent meals

mints, garlic, onions, cinnamon Avoid drinking liquids with meals; drink between 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 P.213 state, such as fasting or sleeping. Gastric ulcers are associated with an increased risk for stomach cancer and mortality, and duodenal ulcers are not. Diagnostic tests for PUD can include endoscopy, x-rays with contrast, analysis of stomach secretions, and blood tests.

Table 9.7 Nonsteroidal Anti-inflammatory Drugs

Aleve/Anaprox Aspirin Ansaid Arthropan Clinoril Daypro Dolobid Duract Feldene Indocin Lodine Magan Motrin Meclomen Motrin Nalfon Naprosyn Orudis Relafen Sodium salicylate Tolectin Toradol Voltaren

Treatment and Nutritional Intervention The history of PUD treatment is replete with regimens that were logical but ineffective to the nutrientdeficient 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 P.214 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

1. Endoscopy 2. Upper GI (barium swallow with x-ray) 3. Gastric analysis 4. Blood tests, to detect: Anemia (hemoglobin, hematocrit, mean cell volume, and mean cell hemoglobin) H. pylori

Table 9.9 Treatment Objectives and Diet for Peptic Ulcer Disease

Objectives

1. 2. 3. 4.

Eradicate H. pylori infection if present Reduce gastric acidity and gastric secretion Avoid gastric irritants Promote ulcer healing

Diet/Nutritional and Other Recommendations

1. Individualize the diet, or follow bland diet if preferred 2. Check for anemia (from bleeding ulcer), correct if exists 3. 4. 5. 6.

Check for B12 deficiency; correct if exists Avoid large meals (distend the stomach) Avoid excessive alcohol, coffee/decaffeinated use Avoid cigarette smoking

7. Include extra protein and vitamin C to promote healing

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 P.215 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

Pepper (all types; red, black, white) Chili powder, curry powder Alcohol

Gastric Acid Stimulants

Regular and decaffeinated coffee Frequent meals (3 meals preferred)

Table 9.11 Common Medications in Peptic Ulcer Disease

Antacids (see Table 9.6) Antibiotics (if H. pylori present) Ulcer Drugs H2 antagonists (cimetidine/Tagamet, famotidine/Pepcid, ranitidine/Zantac, Nizatidine/Axid) Omeprazole/Prilosec, lansoprazole/Prevacid Sucralfate/Carafate Misoprostol/Cytotec

Treatment and Nutritional Intervention The treatment for dumping syndrome is the postgastrectomy diet or antidumping diet and may include drugs to slow gastric emptying (2). Functional lactose intolerance tends to be a common problem after surgery.

Table 9.12 Surgery for Peptic Ulcer Disease

Truncal Vagotomy and Pyloroplasty

The truncal vagotomy cuts the main trunks of the vagus nerve on each side of the distal esophagus; it eliminates nerve-induced secretion of acid; it also reduces contractions and delays gastric emptying. To offset these effects, the pyloroplasty is also done. In the pyloroplasty, the pylorus is surgically altered so that it can act as a barrier to contents of the stomach as it empties. The result is that liquids empty more quickly, but solids take longer.

Truncal Vagotomy and Antrectomy

This procedure is more aggressive, because the antrectomy connects the antrum and pylorus. When the antrum is altered, the portion of the stomach that secretes gastrin (hormone which stimulates all gastric secretions) is removed. The two surgical procedures for attaching the remaining stomach to the intestine, Billroth I and Billroth II.

Highly Selective Vagotomy (proximal gastric vagotomy)

This procedure reduces gastric acid secretion but doesn't interfere with motility (i.e., the stomach's movement). This prevents problems related to gastric emptying (i.e., dumping syndrome).

P.216

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

1. 2. 3. 4. 5.

After surgery, avoid eating until the function of the GI tract returns. Begin with sips of water at room temperature or allow ice chips to melt in mouth. Proceed to a clear liquid diet. When tolerated, begin a full liquid diet. As solids are introduced, begin with small amounts of soft, starchy, low-fat, lowprotein foods.

6. Eat small frequent meals. 7. Avoid large amounts of liquids with meals. Take fluids 1-2 hours before or after meals. 8. Avoid activity and lie down for 1 hr after meals. 9. Avoid extremes in food temperature.

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 P.217 absorption increase the potential for adversely affecting nutritional status with any disease, but particularly with IBD and celiac disease.

Diverticular Disease: Diverticulosis and Diverticulitis Disease Process Diverticular disease is the presence of small herniations of the colon, most often the sigmoid colon, which form pouches. The presence of the pouches is diverticulosis, and when the pouches become inflamed and or infected, it is termed diverticulitis. Life-threatening complications can occur in diverticulitis, such as pouch rupture, which causes bleeding and can lead to sepsis and obstruction. Current theory of etiology suggests that diverticulosis is caused by a combination of high pressure inside the colon and a weakening in the organ's musculature (6). Factors that may increase intracolonic pressure and or weaken musculature include:

Emotional stress Constipation, especially with straining Reduced GI motility Increased transit time

From a nutritional standpoint, the major dietary constituent that most likely affects several of these factors is a low-fiber diet.

Treatment and Nutritional Intervention If a person has had diverticulitis in the past, future flare-ups, if not too severe, can often be treated at home; rest, fasting at first and then a clear liquid diet, and antibiotics. As the symptoms subside, usually within a few days, nutrition therapy consists of a soft, low-fiber diet (2). After 4 to 6 weeks, a high-fiber diet is the recommendation for diverticulosis. In the hospital, severe diverticulitis warrants complete bowel rest and only small sips of water or ice chips. As P.218 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

1. Follow a low-residue diet. Oral elemental diet (AlitraQ, Subdue) or total parenteral nutrition may be required. 2. Proceed to a clear liquid diet. 3. As food is tolerated, begin a bland diet.

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)

1. Consume 6-11 servings of whole grain bread, cereals, flours, and other whole-grain products daily. 2. 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). 3. Consume 25 g of fiber daily. 4. Consume 2 quarts of water daily (eight 8-oz glasses) 5. Reduce fat intake.


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 P.219 constipation and diarrhea or only one of these. The cause of IBS is unknown, but one theory suggests that people with IBS respond in an exaggerated way to certain stimuli that would only cause a mild response or none at all in a person without the disorder. Possible stimuli include dietary overindulgences, emotional stress or trauma, medications, hormones, and intolerance to specific substances in foods. Diagnosis is made by ruling out other LGI diseases and on the basis of ongoing symptoms for a period of 3 months.

Table 9.15 Fiber Content of Foods

Food

Serving

Fiber (g)

Bread: whole wheat

1 slice

2

Cereal, bran

1oz

2

Cereal, cooked oatmeal

½ cup

2

Fruit: apple, banana, kiwi, pear

1 med.

2

Legumes: cooked baked beans, kidney beans, navy beans

½ cup

8

Legumes:garbanzo, lima beans, lentils, split peas

½ cup

5

Vegetables: cooked broccoli green beans, corn, winter squash raw carrots, peppers

½ cup ½ cup

3 3

Treatment and Nutritional Intervention Treatment of IBS Centers on Diet and Lifestyle Lifestyle changes emphasize establishing regular eating patterns, regular bowel habits, and stress reduction and management. Medications may include bulk-forming laxatives, antispasmodic drugs, and tranquilizers. To determine if specific foods are provoking flare-ups, an elimination and reintroduction approach can be helpful, even more so than probiotics (10). Up to 40% of IBS sufferers are lactose intolerant, and other common problematic foods include caffeine, alcohol, gas-forming vegetables, and wheat or yeast (11). P.220

Table 9.16 Recommendations for Irritable Bowel Syndrome

1. In cases of acute irritable colon, an elemental diet may be necessary (Criticare, Subdue, AlitraQ). 2. Progress to a soft, bland diet when tolerated. 3. Progress to a high-fiber diet slowly to avoid discomforts such as bloating and flatulence. 4. 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 5. 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). 6. 7. 8. 9.

Avoid lactose if not tolerated (see Table 9.13). Avoid wheat or yeast if not tolerated. Common food allergies include chocolate, dairy products, wheat, yeast, and eggs. Avoid excess fat (see low-fat diet).

10. Drink 2–3 quarts of water daily; Consume 20–30 g of fiber daily. 11. 1 Tablespoon of a bulking agent, such as Metamucil, daily may be helpful. Bran may be irritating. 12. Probiotics may be useful. 13. Supplement with B-complex vitamins, calcium, vitamin D, and riboflavin (if lactose is not tolerated).

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


P.221

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 P.222 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

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

Nutritional Problems

Treatment and Nutritional Intervention Treatment for CD depends on phase of the disease, and if during a flare-up, its severity. Treatment during a flare-up revolves around countering the inflammation, treating symptoms of pain and diarrhea, and preventing stimulation and irritation of the GI tract. Corticosteroids are used to reduce inflammation in a CD exacerbation, and when used, a low-sodium diet can be helpful to prevent fluid P.223 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, P.224 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, B 6, 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: N3 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


P.225

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 P.226 Dehydration Anorexia Weight loss

In contrast to CD, most of the nutritional problems are not directly due to malabsorption. The diagnosis is made on the basis of a sigmoidoscopy, and this test also indicates the UC severity.

Treatment and Nutritional Intervention Treatment for UC is similar to that for CD, with the goals of countering the inflammation, alleviating symptoms, and correcting dehydration and nutrient deficiencies (2). And as with CD, when the disease is in remission, a high-protein, nutrient-dense diet is the best approach to stave off nutritional problems between flare-ups. If the disease affects the descending colon, enemas containing corticosteriods or mesalamine help to reduce symptoms. Enemas containing short chain fatty acids (SCFA) are also useful by promoting tissue healing (12,13).

Celiac Disease Disease Process Celiac disease has several other aliases, including nontropical sprue, gluten-induced sprue, gluten-induced enteropathy, and gluten-sensitive enteropathy. It is characterized by P.227 P.228 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

1. 2. 3. 4. 5. 6.

Avoid foods known to cause diarrhea. Avoid extremes in food and beverage temperatures (avoid iced beverages). Avoid carbonated beverages. Eat small, frequent meals; stop eating 2–3 hr before bed. Eat slowly; chew well. If corticosteroids are used in treatment: follow low-sodium diet; increase potassium intake (bananas, oranges, orange juice, potatoes, legumes, fruits, and vegetables). 7. Consume 2 quarts of water daily (eight 8-oz glasses). 8. Consume 1-1.5 g/kg protein daily. 9. Increase intake of omega-3 fatty acids from foods (fish, especially mackerel and tuna) or through supplements. 10. Choose a vitamin/mineral supplement that includes thiamin, vitamin E, iron, zinc, calcium, potassium, and folacin. 11. 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 lowfat diet); avoid wheat/gluten if not tolerated. 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.

Treatment and Nutritional Intervention The treatment for celiac disease is elimination of gliadin/ gluten from the diet, which must be done as soon as possible to prevent extensive damage to the intestine (2). Some patients with either a more severe or long-standing case may not respond to dietary intervention, and corticosteroids become necessary. As with IBD, damage of the intestinal tissue may necessitate the removal of the affected sections of the small intestine. And as with CD, this poses nutritional concerns because of the small intestine's role in P.229 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.


P.230

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 P.231 P.232 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

1. Celiac disease requires total avoidance of gluten—wheat, oat, rye, and barley. 2. Allowable foods include corn flour, corn meal, cornstarch, rice, rice flour, potato

3. 4. 5.

6. 7.

flour, soybean flour, tapioca, sago, arrowroot, glutenfree wheat starch, and lima bean flour. Obtain 1–2 g of protein per kilogram of body weight daily (about 80–120 g for adults). Obtain 35–40 kcal/kg of body weight daily. 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). Reduce lactose intake (slowly increase lactose intake to tolerance). Reduce fiber intake (slowly increase fiber intake to tolerance).

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. P.233

Table 9.26 Dietary Recommendations for Ileostomy

1. A clear liquid diet follows surgery. 2. Progress to a bland, low-fiber diet with extra kilocalories (35–45 kcal/kg/day) and protein (1.5 g/kg/day) for healing. 3. Continue with low-fiber diet. Use sources of pectin such as oatmeal and applesauce. 4. Choose a vitamin/mineral supplement with vitamin B12, folacin, calcium, magnesium, iron, and vitamin C. 5. Supplement sodium and potassium. 6. If prednisone is used in treatment, limit salt intake (see low-sodium diet). 7. Avoid eating before bedtime. 8. If gassiness is a problem, avoid cruciferous vegetables, legumes, and other potential gas-forming fruits and vegetables. 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

P.234

Short Bowel Syndrome Disease Process With removal of 40% or more of the small intestine in a resection, short bowel syndrome (SBS) is a prime concern, especially if the terminal ileum and ileocecal valve were removed (17). The nutritional problems associated with SBS arise from malabsorption. Although the survival rate declines as more of the intestine is removed, if the ileum and ileocecal valve remain intact, even an 80% resection can prove to be tolerated (20). Because of its importance in long-term survival and the fact that it's the only controllable variable, enhancing the intestine's ability to adapt is the focus of much current research. Nutrition is the key to recovery and enhancing the intestine's adaptive ability. The reason is that many of the typical symptoms a patient with SBS will experience are nutritionally relevant:

Diarrhea Steatorrhea Weight loss Muscle wasting Bone disease Malabsorption of several nutrients

Resections of the jejunum initially cause malabsorption, because most nutrients are digested and absorbed within the first forty inches of the small intestine. However, after the adaptation period, the ileum takes over this function, as the remaining intestine grows in length, diameter, and thickness.

Treatment and Nutritional Intervention Treatment focuses on managing symptoms and enhancing intestinal adaptation. Several medications are useful in managing the symptoms of diarrhea, steatorrhea, and bacterial overgrowth (19). Drugs that slow gastric emptying and intestinal motility (see Tables 9.3 and 9.18) can help control diarrhea and thereby increase nutrient digestion P.235 P.236 and absorption, as well as those reducing acid and other intestinal secretions (see Table 9.2).

Table 9.28 Dietary Recommendations for Colostomy

1. A clear liquid diet follows surgery. 2. Progress to a bland, low-fiber diet with extra kilocalories (35–45 kcal/kg/day) and protein (1.5 g/kg/day) for healing. 3. After approximately 2 weeks, gradually increase fiber intake. Fiber intake may be adjusted if diarrhea results. 4. 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,

5. 6.

7. 8. 9.

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. Avoid high-oxalate foods (Table 9.25) 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. If Prednisone is used in treatment, reduce salt intake to 2–3 g daily (see low-sodium diet). Consume 1-2 quarts of fluid daily, between meals. Choose a vitamin/mineral supplement with vitamin E, folacin, calcium, magnesium, iron, vitamin C, vitamin K, and vitamin B12.

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. P.237

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, Bcomplex 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 glutenfree diet. Gut 1989;30:333–338.

16. Farrell RJ, Kelly CP. Celiac sprue. N Engl J Med 2002;346:180–188. P.239 17. American Society for Parenteral and Enteral Nutrition Board of Directors and the Clinical Guidelines Task Force. Guidelines for the use of parenteral and enteral nutrition in adult and pediatric patients. J Parenteral Enteral Nutr 2002; 26(1s):1SA–138SA.

18. Matarese LE, O'Keefe SJD, Kandil HM, et al. Short bowel syndrome: Clinical guidelines for nutrition management. Nutr Clin Pract 2005;20(5):493–502.

19. Rees Parrish C. The clinician's guide to short bowel syndrome. Practical Gastroenterol 2005:67–106.

20. Dieleman LA, Heizer WD. Nutritional issues in inflammatory bowel disease. Gastroenterol Clin North Am 1998;27(2):435–435.

21. Parekh NR, Steiger, E. Criteria for the use of recombinant human growth hormone in short bowel syndrome. Nutr Clin Pract 2005;20(5):503–508.

22. Matarese LE, Seidner DL, Steiger E. Growth hormone, glutamine, and modified diet for intestinal adaptation. J Am Diet Assoc 2004;104(8):1265–1272.

Authors: Width, Mary; Reinhard, Tonia Title: Clinical Dietitian's Essential Pocket Guide,The: Essential Pocket Guide, 1st Edition Copyright ©2009 Lippincott Williams & Wilkins > Table of Contents > Part II - Nutrition Considerations for Specific Diseases > Chapter 10 - Liver and Pancreatic Diseases

Chapter 10 Liver and Pancreatic Diseases The liver, pancreas, and gall bladder constitute the accessory organs because of their participation in digestion. Given the crucial role the liver plays in nutrient metabolism, diseases affecting the organ can profoundly and adversely affect nutritional status. The pancreas, a dual organ of both endocrine and exocrine function, critically participates in digestion and also in blood glucose regulation. Problems with this organ affect both of these functions. The gall bladder's role is limited, with minimal potential effect on nutrition status.

Liver Disease Liver abnormalities are of two types: those caused by a malfunction of the cells in the liver itself, such as cirrhosis or hepatitis, and those caused by bile obstruction, such as occurs with bile stones or cancer (1). Liver diseases with potential nutritional impact include hepatitis, hepatic steatosis, and cirrhosis, with excessive alcohol intake being a common trigger for all. Because of its importance, the liver has extensive regenerative ability and reserve capacity, posing a challenge for diagnosis, as significant function must be lost before disease is clinically evident. P.244 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

Bile synthesis

Test

Bilirubin (serum, urine, fecal); direct (conjugated) and indirect (unconjugated)

Derangement

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,

Low protein levels, AA ratio

transferrin), amino acid ratios (BCAA vs. AAA)

skewed toward higher AAA

Enzymes: (ALT, AST, GGT, ALP, LDH)

High

Adapted from references 2 and 3.

P.245

Enzymes Hepatitis Disease Process

Hepatitis is inflammation of the liver induced by the presence of a toxin, such as alcohol, medications and some dietary supplements, environmental toxins, or viral infection (4). The major viral forms of hepatitis include hepatitis A virus (HAV), hepatitis B virus (HBV), and hepatitis C virus (HCV). HAV is spread by contact with infected persons or consumption of infected foods. The symptoms for type A include:

Jaundice Nausea Anorexia Fever Hepatomegaly Clay-colored stools

Types B and C are often asymptomatic, and in the case of type C only arise after extensive hepatic damage. HBV is spread parenterally (infected blood or needles) and by sexual contact. HCV is also parenterally transmitted, but less so by sexual contact. HAV generally resolves without permanent damage, whereas 20% of patients with type B and up to 70% of those with type C develop chronic liver disease (5).

Treatment and Nutritional Intervention In acute hepatitis, the goals are to promote liver regeneration and prevent further injury, if a toxin is the cause. P.246 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

P.247

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 highfiber, low-glycemic-index diet normalizes IR, hyperglycemia, and hyperinsulinemia in patients (8,9).

Treatment and Nutritional Intervention The goals of medical nutrition therapy include maintenance of adequate nutrition, prevention tissue catabolism, and the control of edema and ascites (6,10). A major concern is the development of hepatic encephalopathy (HE). Although the exact cause of HE is not known, the major theory relates to the altered ratio of aromatic amino acids to branched-chain amino acids (BCAA). The BCAA are:

Leucine Isoleucine Valine

Although ammonia is not the primary causative agent in HE, its levels are always elevated with impending HE, and P.248 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.

P.249

Pancreatitis Disease Process Inflammation of the pancreas can be either chronic or acute. In the United States, alcoholism is the most common cause of chronic pancreatitis, and this is also true for acute pancreatitis, with the other common trigger of gallstones (6,13). Additional causes include a genetic predisposition and obstruction of the pancreatic duct, which can arise from narrowing of the duct or pancreatic cancer, and hypertriglyceridemia. Although rare, severe acute pancreatitis can narrow the duct and cause chronic pancreatitis. As chronic pancreatitis progresses, digestive enzyme-secreting acinar cells are slowly destroyed, and eventually pain does not occur. However, as the number of cells decrease, malabsorption occurs, causing steatorrhea. The malabsorption leads to weight loss and malnutrition. Eventually, the insulin-secreting beta cells maybe be destroyed, resulting in diabetes.

Treatment and Nutritional Intervention Nutritional Recommendations Medical nutrition therapy for acute pancreatitis depends on the severity of the patient's condition and is focused on progression from nothing-by-mouth (NPO) status on admission to an oral low-fat diet in mild cases, but possibly elemental enteral jejunal feedings for severe cases (6,10). Although enteral feeding is preferred in severe cases, ileus may develop and necessitate parenteral feeding. If inflammation is 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 1. Mahan LK, Escott-Stump S. Krause's Food, Nutrition, and Diet Therapy, 11th ed. Philadephia: Saunders; 2004, 740–743.

2. Pagana KD, Pagana TJ. Mosby's Manual of Diagnostic and Laboratory Tests; St. Louis MO: Mosby Inc.; 2006.

3. Lab Tests Online. Available at: http://labtestsonline.org/understanding/analytes/liver_panel/glance.html. Accessed on March 6, 2007. P.251 4. Farrell GC. Liver disease caused by drugs, anesthetics, and toxins. In Feldman M, Friedman LS, Sleisenger MH, eds., Sleisenger and Fordtran's Gastrointestinal and Liver Disease: Pathophysiology, Diagnosis, Management. Philadelphia: Saunders; 2002:1403–1447.

5. Centers for Disease Control and Prevention. Available at: www. cdc.gov/ncidod/diseases/hepatitis/b/fact.htm, www.cdc.gov/ ncidod/diseases/hepatitis/c/fact.htm. Accessed on March 1, 2007.

6. Escott-Stump S. Nutrition and Diagnosis-Related Care, 5th ed. Baltimore: Lippincott Williams & Wilkins; 2002:339–361.

7. eMedicine. Available at: http://emedicine.com/med/topic3183. htm. Accessed on March 3, 2007.

8. Barkoukis H, Fiedler KM, Lerner E. A combined high-fiber, low-glycemic index diet normalizes glucose tolerance and reduces hyperglycemia and hyperinsulinemia in adults with hepatic cirrhosis. J Am Dietetic Assoc 2002;102:1503–1508.

9. Jenkins DJ, Shapira N, Greenberg G, et al. Low glycemic index foods and reduced glucose, amino acid, and endocrine responses in cirrhosis. Am J Gastroenterol 1989;84:732–739.

10. American Dietetic Association. Nutrition Care Manual. Online subscription. Accessed March 6, 2007.

11. Mascarenhas R. New support for branched-chain amino acid supplementation in advanced hepatic failure. Nutr Rev 2004;62(1):33–38.

12. Cordoba J, Lopez-Hellin J, Planas M, et al. Normal protein diet for episodic hepatic encephalopathy: results of a randomized study. J Hepatology 2004;41(1):38–43.

13. Nagar AB, Gorelick FS. Acute Pancreatitis. Curr Opin Gastroenterol 2004;20(5):439–443.

Authors: Width, Mary; Reinhard, Tonia Title: Clinical Dietitian's Essential Pocket Guide,The: Essential Pocket Guide, 1st Edition Copyright ©2009 Lippincott Williams & Wilkins > Table of Contents > Part II - Nutrition Considerations for Specific Diseases > Chapter 11 - Kidney Disease

Chapter 11 Kidney Disease Monica L. Griffin RD Kidney disease, which can be chronic or acute, affects over 40 million Americans every year (1). For 400,000 Americans, it progresses to end-stage kidney disease (ESKD) necessitating either dialysis or transplant. Although dialysis has been a life-saving technique, it is a catabolic process leading to malnutrition. For the dietitian, all stages of chronic kidney disease (CKD), also termed chronic renal failure (CRF), and ESKD will require careful assessment, monitoring, and dietary modification.

Acute Renal Failure Acute renal failure (ARF) has a sudden onset with rapid deterioration in kidney function and a mortality rate of up to 65% (1). In contrast to CKD, ARF is often reversible, although ARF can become chronic, leading to the need for long-term dialysis or transplant.

Acute Renal Failure: Disease Process The causes are varied and are categorized by their relationship to prior kidney function (prerenal, intrarenal [also intrinsic], and postrenal). Most causes of ARF are prerenal, representing up to 70% of cases and include: P.256 Cardiac diseases: congestive heart failure, myocardial infarction, cardiac arrhythmia Disorders of the renal blood vessels Low blood volume or low blood pressure

Intrarenal causes include:

Disorders of the blood vessels: sickle-cell anemia, diabetes, adverse reaction to blood transfusions Renal injury: infections, toxins, drugs, Escherichia coli ingestion (food-borne illness) Renal obstructions: kidney stones, tumors, scar tissue formation, and tissue inflammation

Postrenal causes include:

Bladder or ureter obstructions: strictures, stones, trauma Bladder rupture Neurological bladder disorder Pregnancy Prostate cancer or hyperplasia Renal vein thrombosis

Treatment and Nutritional Intervention Short-term dialysis may be necessary to treat ARF, with the goal of preventing renal damage and returning the kidneys to baseline function. Medications may include diuretics, potassium-exchange resins to bind potassium in the gut, insulin to rapidly correct hyperkalemia, and bicarbonate if acidosis is present. ARF is often a catabolic condition, so the registered dietitian (RD) must carefully monitor nutrition status. Nutritional intervention includes:

Protein metabolite is urea, which increases renal workload; however, ARF catabolism must be countered to prevent loss of visceral and somatic protein. The protein needed depends on dialysis status, kidney function, and protein status. If the patient is undergoing dialysis or if renal function increases, daily protein intake should be 1.2 to 1.3 g/kg body weight. If not P.257 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 P.258 important, as nutrition therapy differs based on CKD stage and dialysis status.

Table 11.1 Classification of Chronic Kidney Disease

Glomerular Filtration Rate (mL/min/1.72 m2)

Stage

Description

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. P.259 Laboratory values are monitored at least monthly and reviewed with the patient to determine any necessary therapeutic interventions. Some values may be monitored more frequently, such as hemoglobin, hematocrit, calcium, and phosphorus. These lab values can be affected by medications or acute medical

conditions, and in both cases more frequent monitoring will significantly improve the patient's outcomes. Some biochemical parameters, such as lipid profile, are tested less frequently, generally on a quarterly basis. For a patient with acute renal failure, parameters such as blood urea nitrogen (BUN), creatinine, potassium, CO2, and chloride may be tested more frequently to determine whether kidney function is returning to baseline levels.

Table 11.2 Commonly Monitored Laboratory Values in Kidney Disease

Test

Normal Chronic Kidney Disease Range

Albumin

WNL for laboratory >4.0 is ideal

Blood urea nitrogen

60–80 mg/dL Based on well-dialyzed patient with good intake

Corrected calciuma

<10.2 mg/dL 8.4–9.5mg/dL is ideal

Chloride

WNL

CO2, total

>22

Cholesterol

WNL

Creatinine

2–15 mg/dL

Ferritin

>100 mg/mL

Glucose

WNL

Hematocrit

33%–36%

Hemoglobin

11–12 g/dL

Phosphorus

3.5–5.5

Potassium

3.5–5.5

Parathyroid hormone, intact

150–300

Sodium

WNL

WNL, within normal limits. aCorCa = total calcium mg/dL + 0.8 [4 –serum albumin g/dL]. Data from references 2, 4, and 6.

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Treatment and Nutritional Intervention The monthly lab results will have an impact on interventions, both medications and nutrition therapy. The medications used in CKD target the primary kidney functions, which are declining in predialysis patients and absent in dialysis patients (Table 11.3). Phosphorus binders, intravenous iron, and parathyroid hormone (PTH)-suppressing P.261 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-calciumbased phosphorus binder

Dose is titrated based on serum phosphorus level and diet intake

(Use of aluminum should be limited to <14 days)

Dialyvite, Diatx,

B-complex

Taken daily, usually

Nephrocaps, Nephrovite

with vitamin C and biotin

NephPlex,

B-complex

RenaPlex

with vitamin C and zinc

in the evening to accommodate dialysis treatment days when fluid is removed

(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

Hectorol,

Oral and IV

Zemplara

vitamin D

Rocaltrol a

Oral vitamin D

Sensipara

Oral calcimimetic agent

administered during hemodialysis Oral agents are to be taken consistently as ordered Calcium levels should be monitored closely with use of Rocaltrol and Sensipar

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 P.262 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


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 highphosphorus foods also containing rich calcium sources. Early control of phosphorus intake will help control the serum phosphorus and PTH levels. The phosphorus level is also controlled with the addition of phosphorus-binding medications. These medications, taken with each meal and snack, bind phosphorus in the gastrointestinal tract and reduce the amount of phosphorus absorbed into the blood. Elemental calcium intake from both the diet, and the medications should be limited to 2,000 mg daily. Patients should read labels to avoid products that are fortified with calcium, an increasingly common food industry practice. Fluid needs to be limited in predialysis patients only when congestive heart failure appears imminent. Fluid restrictions for patients on diuretics may cause progression of renal failure due to volume depletion.

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Nutritional Recommendations Blood levels of electrolytes are carefully monitored in the CKD patient to assess the need for restrictions. However, the typical CKD diet, in which all restrictions are necessary, includes a daily protein restriction to just below the RDA/DRI at 0.6 g/kg body weight; sodium at 2 g; potassium at 2 to 3 g; calcium at 1.2 g (Table 11.5). Potassium is of the most immediate concern, because both hypokalemia and hyperkalemia can cause heart failure. Fruits and vegetables are the highest sources of potassium, and within each group, there is considerable variation in potassium content (Table 11.6). Processing and food preparation alter the amount of potassium, with raw foods often containing less due to the cooking process concentrating the volume. Canning tends to cause potassium to leach out, so some canned foods have less.

CKD: Dialysis Dialysis serves as artificial filtration of blood when kidney failure has progressed to stage 5. The two main types are P.264 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

Limit ½ cup or 1 oz/day:

Salted, cured meat or

Salted crackers Potato

Banana Orange Juice

Milk Yogurt Cheese Ice Cream

fish Deli meat Bacon Sausage Dried beans, peas, legumes Canned

chips Prepared biscuits, rolls Baking mix Whole grain bread and cereal Brown rice

Honeydew Cantaloupe Dried fruits Prune juice Prunes Potato Tomato Sweet potato

sausages Fish with bones Peanut

High-fiber muffins

Fat

Salted pork fat

Beverages

Cola Cream Tropical punch Miscellaneous Chocolate Nuts, seeds Beer Molasses

butter

Table 11.6 Potassium Content in Fruits and Vegetables

High Potassium: 201–350 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

Lower Potassium: 0–200 mg/serving

Low (0–100 mg) Alfalfa sprouts; bamboo shoots; beans (green or wax); cabbage (raw); cucumber; endive; lettuce; green or red pepper Medium (101–200 mg) Artichoke; broccoli; cabbage (cooked); carrots (raw); cauliflower; celery (raw); corn; eggplant; mustard greens; onions; green peas; sauerkraut; spinach (raw); turnips

Fruits

Apricots; cantaloupe; banana; dates; figs; honeydew melon; kiwi fruit; nectarine; oranges and orange juice; pear; prunes and prune juice

Low (0–100 mg) Applesauce; blueberries; cranberries and juice; grape juice; lemons; papaya nectar; peach nectar; canned pears Medium (101–200 mg) Apple and juice; apricot nectar; blackberries; cherries; grapefruit and juice; grapes; mango; papaya; peach; pineapple; plums; raisins; raspberries; strawberries; watermelon

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Treatment and Nutritional Intervention Kilocalorie and protein needs are based on SBW or ABW and provide only for maintenance (Table 11.7). Stress needs should be planned into the estimation of kilocalorie and protein provision. Protein losses are high due to loss to the artificial kidney membrane and blood loss in hemodialysis; and the peritoneal membrane, in peritoneal dialysis. HBV protein should account for at least 50% of the protein allowance (4).

In peritoneal dialysis, the dialysate contains dextrose to remove fluid, and it is absorbed to a significant extent. The daily amount of dextrose absorbed depends on the concentration of dextrose used for each exchange, and on the number of exchanges (Table 11.8). The dextrose concentration can be altered to either increase or decrease the amount of fluid removed. Currently, three concentrations are available: 1.5%, 2.5%, and 4.25%. Although increasing from the lower to higher amounts will generally increase the amount of fluid removed, it will also increase the amount of dextrose kilocalories absorbed. The dextrose and kilocalorie absorption should be taken into consideration when developing a kilocalorie plan for P.266 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



Output + 1,000 mL

Unrestricted, unless needed to maintain fluid balance

Fluid


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 P.267 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 P.268 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, P.269 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) P.270 (3). In the posthealing, chronic posttransplant period, fluid restriction may be needed if the patient has significant fluid overload, but this is generally not needed. Immunosuppressive treatment with cyclosporin can cause hyperkalemia, and if it occurs, potassium restriction is indicated. In the chronic transplant period, most patients should follow the general nutrition guidelines for any healthy individual.

Table 11.11 Common Renal Abbreviations

Abbreviation

Term Associated with Renal Disease

ABW

Adjusted body weight

CAPD

Continuous ambulatory peritoneal dialysis

CCPD

Continuous cyclic peritoneal dialysis

CKD

Chronic kidney disease

GFR

Glomerular filtration rate

IDPN/IPN

Intradialytic parenteral nutrition

KDOQI

Kidney Disease Outcomes Quality Initiative

PTH

Parathyroid hormone

SBW

Standard body weight

References 1. Rolfes SR, Pinna K, Whitney E. Understanding Normal and Clinical Nutrition, 7th ed. Belmont: Thomson, Wadsworth; 2006:848–860.

2. National Kidney Foundation KDOQI. Clinical Practice Guidelines for Chronic Kidney Disease: Evaluation, Classification, and Stratification. AMJ Kidney Dis 2003;39(2) Suppl.1:S1–246.

3. Council on Renal Nutrition of the National Kidney Foundation. Pocket Guide to Nutrition Assessment of the Patient with Chronic Kidney Disease, 3rd ed. New York: National Kidney Foundation; 2002.

4. National Kidney Foundation KDOQI. Clinical Practice Guidelines for Nutrition in Chronic Renal Failure. New York: National Kidney Foundation; 2001.

5. National Kidney Foundation KDOQI. Clinical Practice Guidelines for Bone Metabolism and Disease in Chronic Kidney Disease. New York: National Kidney Foundation; 2004.

6. Alpers DH, Clouse RE, Stenson WF. Manual of Nutritional Therapeutics, 2nd ed. Boston/Toronto: Little, Brown and Company; 1988:347–355.

7. Daugirdas JT, Ing TS. Handbook of Dialysis, 2nd ed. Boston/New York/Toronto/London: Little, Brown and Company; 1994:649–652.

Authors: Width, Mary; Reinhard, Tonia Title: Clinical Dietitian's Essential Pocket Guide,The: Essential Pocket Guide, 1st Edition Copyright ©2009 Lippincott Williams & Wilkins > Table of Contents > Part II - Nutrition Considerations for Specific Diseases > Chapter 12 - Pulmonary Disease

Chapter 12 Pulmonary Disease Pulmonary disease is the fourth leading cause of chronic morbidity and mortality in the United States. Currently, more than 35 million Americans are living with chronic lung diseases such as asthma, emphysema, and chronic bronchitis (1). Pulmonary diseases have a significant impact on nutritional status, and the RD's role is crucial in nutrition assessment and patient education to prevent or correct malnutrition.

Chronic Obstructive Pulmonary Disease Disease Process Chronic obstructive pulmonary disease (COPD) is a group of diseases characterized by airflow limitation that is not fully reversible. The airflow limitation is usually both progressive and associated with an abnormal inflammatory response of the lungs to noxious particles or gases (2). The two main diseases that fall under the COPD umbrella include chronic bronchitis and emphysema. COPD patients either have bronchitis or emphysema, or a mixture of both. Common causes of COPD include cigarette smoking, pipe smoking, and cigar smoking; passive exposure to cigarette smoking; occupational dust and chemicals; P.274 air pollution; and genetic factors. The nutritional interventions for emphysema and bronchitis are similar.

Chronic Bronchitis Chronic bronchitis is characterized by a chronic, productive cough (occurring on most days for a minimum of 3 months, for 2 consecutive years), inflamed bronchial tubes, excess mucus production, and shortness of breath (2). Patients with chronic bronchitis, often called “blue bloaters” because of cyanosis and edema in the extremities, usually present with right-sided cardiac failure and little to no weight loss (3). Chronic bronchitis becomes chronic obstructive bronchitis if spirometric evidence of airflow obstruction develops, which happens in a minority of patients (4).

Emphysema Emphysema involves the destruction of lung parenchyma leading to loss of elastic recoil and loss of alveolar septa and radial airway traction, which increases the tendency for airway collapse. Lung hyperinflation, airflow limitation, and air trapping follow (4). These patients, often called “pink puffers” because of reddish complexion and hyperventilation, are typically thin and breathe with pursed lips. Wheezing, shortness of breath, and chronic mild cough are common. Nutritional depletion is significantly greater in patients with emphysema than in those who have chronic bronchitis (3).

Treatment and Nutritional Intervention COPD patients are at risk of weight loss and nutritional deficiencies because of a 15% to 25% increase in resting energy expenditure due to difficulty breathing, a larger postprandial increase in metabolism and heat production, a higher energy cost of daily activities, reduced caloric intake relative to need, and the catabolic effect of inflammatory cytokines (4). A high-kilocalorie, high-protein diet P.275 is necessary to correct malnutrition. Start with 30 to 35 kcal/ kg and 1.2 to 1.5 g protein/kg. For overweight or obese patients, controlled weight loss can be initiated using 20 to 25 kcal/kg, with frequent monitoring to prevent rapid weight loss (3). Fluid intake should be 1 mL/ kcal, as a general rule. If the patient has hypercapnia (CO2 retention), a diet moderate in carbohydrate and higher in fat may be beneficial.

Patient Education Gas-forming foods can cause discomfort because they bloat the abdomen and make breathing more difficult, so educate patients on which foods to avoid/use in moderation (onions, cauliflower, broccoli, melons, peas, corn, cucumbers, cabbage, brussels sprouts, turnips, raw apples, and beans—except green beans). Fried and greasy foods can also cause gas or bloating. Use medications that make breathing easier and/or clear airways about 1 hour before eating. If the patient is using oxygen, make sure it is worn while eating because digestion requires oxygen. Eat six small meals each day instead of three large ones so that the stomach is never extremely full. A full stomach can interfere with breathing by pushing on the diaphragm. Drink beverages at the end of the meal to avoid early satiety. Eat and chew slowly to avoid becoming short of breath. Provide patient with tips to increase the nutrient density of foods, such as adding the following to foods to increase caloric and/or protein content: butter, margarine, whipped cream, half and half, cream cheese, sour cream, salad dressings, mayonnaise, honey, jam, sugar, granola, dried fruits, cottage or ricotta cheese, whole milk, powdered milk, ice cream, yogurt, eggs, nuts, seeds, wheat germ, peanut butter. Avoid excess sodium, as it may increase edema and make breathing more difficult. Provide patient with list of high-sodium foods.

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Cystic Fibrosis Disease Process Cystic fibrosis (CF) is an autosomal recessive inherited disease of the mucus and sweat glands. CF is characterized by the secretion of thick, tenacious mucus that obstructs the ducts and glands of the respiratory tract, sweat and salivary glands, intestine, pancreas, liver, and reproductive tract. Complications include bronchitis, pneumonia, glucose intolerance, and malabsorption due to decreased availability of digestive enzymes, decreased bicarbonate secretion, decreased bile acid reabsorption, and

decreased nutrient absorption by intestinal microvilli (3). CF is caused by a defect in the cystic fibrosis transmembrane conductance regulator (CFTR) gene, which codes for a chloride transporter found on the surface of the epithelial cells that line the lungs and other organs. There are channels in these lining cells through which ions can pass. Normally, the movement of ions brings water to the surface of the airway and keeps the mucus moist. The defective gene acts to block the channels, which causes the mucus to dry out. It is difficult for a person to shift the thick mucus, which then becomes prone to infection by bacteria. This defect also accounts for the high levels of sodium and chloride that are present in the saliva, tears, and sweat of patients with CF (5).

Treatment and Nutritional Intervention The risk for malnutrition in CF patients is high due to increased needs, decreased intake, and malabsorption. The goals of nutritional care include controlling malabsorption with pancreatic enzyme replacement, providing adequate energy, protein, and other nutrients, and preventing nutritional deficiencies.

Energy Energy needs are 120% to 150% of the Dietary Reference Intake (DRI) on average, but can be as high as 200% P.277 (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 gasexchange 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 P.279 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 P.280 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

Dissolved carbon dioxide in the blood.

mEq/L

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, PaO is equal to 80 mm Hg - 1 mm Hg for every year over 60. 2


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.

pH

Uncompensated

Compensated

<7.35

Normal

PaCO2

HCO3

Normal

Treatment and Nutritional Intervention Mechanical ventilation is used when a patient's spontaneous ventilation is inadequate to maintain life. In addition, it is indicated as a measure to control ventilation in critically ill patients and as prophylaxis for impending collapse of other physiologic functions. Physiologic indications include P.281 respiratory or mechanical insufficiency and ineffective gas exchange (11).

Table 12.3 Respiratory Alkalosis

Common Causes

Hyperventilation (anxiety, pain, respiratory overventilation), pulmonary emboli


Kidneys will excrete HCO3and retain H+to decrease pH.

pH

Uncompensated

Compensated

>7.45

Normal

PaCO2

HCO3

Normal

Table 12.4 Metabolic Acidosis

Common Causes

Diabetic ketoacidosis, shock, renal failure, intestinal fistula, diarrhea, starvation


Respiratory rate increases, so lungs “blow off” excess CO2 to increase pH.

Uncompensated

Compensated

pH

<7.35

Normal

PaCO2

Normal

HCO3

It is important for the dietitian working in intensive care to be familiar with ventilator modes and settings.

This information is useful when conducting nutrition assessments and calculating nutritional requirements for RF patients on mechanical ventilation. Table 12.6 describes common ventilator modes. The use of predictive equations to estimate energy expenditure is a regular part of the nutrition assesment completed by a dietitian. However, in a critically ill patient with pulmonary disease, normal predictive equations may be of little value. The meaurement of resting energy expenditure (REE), through indirect calorimetry, has been shown to be more accurate than published formulas used to predict REE (12). Indirect calorimetry (IC) is the measurement of gas exchange used to indicate a patient's cellular metabolic activity. IC measures oxygen consumption P.282 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


Respiratory rate decreases to retain CO2 and decrease pH.

Uncompensated

Compensated

pH

>7.35

Normal

PaCO2

Normal

HCO3

Table 12.6 Ventilator Modes

Mode

Name

Description

ACV

Assist-control ventilation

Triggered by patient breaths, but if patient fails to trigger the threshold, a mechanically controlled breath is delivered.

CMV

Continuous mandatory ventilation

Ventilator delivers breaths at a set rate and volume or pressure, regardless of patient effort.

CPAP

Continuous positive

Positive pressure applied during spontaneous breathing

airway pressure

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

Positive pressure applied during machine breathing and

expiratory pressure

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 P.283 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

P.284

References 1. Miniño AM, Heron MP, Smith BL. Deaths: preliminary data for 2004. National Vital Statistics Report; vol. 54 no.19. Hyattsville, MD: National Center for Health Statistics; 2006.

2. National Heart, Lung, Blood Institute/World Health Organization. Global Initiative for Chronic Lung Disease: Global Strategy for the diagnosis, management, and prevention of chronic obstructive pulmonary disease, updated 2005, Executive summary, 8/23/2005. Available at: www.goldcopd.com/Guidelineitem.asp?l1=2&l2=1&intId=996. Accessed April 4, 2007.

3. Mahan LK, Escott-Stump, S. Krause's Food, Nutrition, & Diet Therapy, 11th ed. Philadelphia: Saunders; 2004:792–833.

4. Chronic Obstructive Pulmonary Disease. Available at: www.merck.com/mrkshared/mmg/sec10/ch78/ch78a.jsp. Accessed April 2, 2007.

5. Cystic Fibrosis transmembrane conductance regulator, CFTR Online Mendelian Inheritance in Man, John Hopkins University. Available at: www.ncbi.nlm.nih.gov/entrez/dispomim.cgi?id=602421. Accessed August 10, 2007.

6. Texas Children's Hospital. Pediatric Nutrition Reference Guide, 7th ed. Houston: Texas Children's Hospital; 2005.

7. Escott-Stump, S. Nutrition and Diagnosis-Related Care, 6th ed. Philadelphia: Wolters Kluwer/Lippincott Williams & Wilkins; 2008:270–306.

8. Sharma, S. Respiratory failure. Available at: www.emedicine. com/med/topic2011.htm. Accessed April 10, 2007.

9. Acid-base tutorial. Available at: www.acid-base.com/index.php. Accessed April 3, 2007.

10. Pagana KD, Pagan TJ. Mosby's Manual of Diagnostic and Laboratory Test, 3rd ed. St. Louis: Mosby Elsevier; 2006: 115–120.

11. Byrd RP. Mechanical ventilation. Available at: www.emedicine. com/med/topic3370.htm. Accesses August 10, 2007.

12. American Association for Respiratory Care. Metabolic measurement using indirect calorimetry during mechanical ventilation, 2004 revision & update. Respir Care 2004;49(9):1073–1079.

13. Shils ME, Shike M, Ross AC, et al. Modern Nutrition in Health and Disease, 10th ed. Philadelphia: Lippincott, Williams & Wilkins; 2005.

Authors: Width, Mary; Reinhard, Tonia Title: Clinical Dietitian's Essential Pocket Guide,The: Essential Pocket Guide, 1st Edition Copyright ©2009 Lippincott Williams & Wilkins > Back of Book > Appendix A: Laboratory Assessment

Appendix A: Laboratory Assessment Laboratory and other diagnostic tests are tools used by clinicians to gain valuable, objective information about their patients. When used in conjunction with other patient information, such as anthropometric data, a thorough history, and a physical examination, laboratory tests can provide valuable information about a patient's nutritional status and their response to medical nutrition therapy. This appendix contains an alphabetical list of common laboratory (lab) measurements that are relevant to nutrition assessment. This list is not meant to be comprehensive; rather it is a quick reference to the lab tests most commonly used by dietitians in the clinical setting. Normal values are listed, but it must be noted that normal ranges of lab test results vary significantly, depending on the lab and their methods of testing. It is important to always check the normal values at the facility where the test is performed. This information is almost always given directly adjacent to the patient specific lab result. In this book, Reference Ranges for blood tests are reported in the conventional U.S. system first, then in the SI system (International System of Units or Système Internationale d'Unités), if available. Critical values are also listed, if P.288 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. P.289

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). P.290

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 O 2; hyperventilation.

Decreased Levels Anemias; mucous plug; bronchospasm; atelectasis

Blood Urea Nitrogen (BUN) Reference Range 10–20 mg/dL or 3.6–7.1 mmol/L (Critical values: >100 mg/dL indicates serious impairment of renal function)

Clinical Implications Increased Levels Prerenal (hypovolemia, shock, burns, dehydration, congestive heart failure (CHF), myocardial infarction (MI), gastrointestinal bleeding (GI bleed), excessive protein ingestion, and/or catabolism, starvation, sepsis); renal (renal disease or failure, nephrotoxic drugs); postrenal (urethral obstruction from stones/tumors/congenital anomalies, bladder outlet obstruction from prostatic hypertrophy, cancer, or congenital anomalies. P.291

Decreased Levels Liver failure; acromegaly; malnutrition; overhydration; negative nitrogen balance; syndrome of inappropriate secretion of antidiuretic hormone (SIADH); pregnancy; nephrotic syndrome.

Calcium (Ca)—Total and Ionized Calcium Reference Range Total Ca: 9.0–10.5 mg/dL or 2.25–2.75 mmol/L (Critical values: <6 or >13 mg/dL or <1.5 or >3.25 mmol/L) Ionized Ca: 4.5–5.6 mg/dl or 1.05–1.30 mmol/L (Critical values: <2.2 or >7 mg/dL or <0.78 or >1.58 mmol/L)

Clinical Implications Increased Levels (Hypercalcemia)

Hyperparathyroidism; cancer with parathyroid hormone (PTH)-producing tumors (metastatic bone cancers, Hodgkin lymphoma, leukemia, and non-Hodgkin lymphoma); Paget disease of the bone; prolonged immobilization; milk–alkali syndrome; excessive intake of vitamin D, milk, antacids; Addison disease; granulomatous infections (e.g., sarcoidosis, tuberculosis).

Decreased Levels (Hypocalcemia) Pseudohypocalcemia due to low albumin levels1; hypoparathyroidism; renal failure; hyperphosphatemia secondary to renal failure; rickets; vitamin D deficiency; osteomalacia; malabsorption; pancreatitis; malnutrition; alkalosis. P.292

Chloride (CL) Reference Range 98–106 mEq/L or 98–106 mmol/L (Critical values: <80 or >115 mEq/L)

Clinical Implications Increased Levels (Hyperchloremia) Dehydration; Cushing syndrome; hyperparathyroidism; renal tubular acidosis; metabolic acidosis; eclampsia; hyperventilation, which causes respiratory alkalosis.

Decreased Levels Overhydration; prolonged vomiting or gastric suctioning; CHF; chronic diarrhea or high-output GI fistula; metabolic alkalosis; burns; Addison disease; salt-losing nephritis; SIADH.

Cholesterol2 Reference Range Desirable: 140–199 mg/dL or 3.63–5.17 mmol/L Borderline high: 200–239 mg/dL or 5.18–6.21 mmol/L High: >240 mg/dL or >6.22 mmol/L

Clinical Implications Increased Levels (Hypercholesterolemia) Familial hypercholesterolemia and/or hyperlipidemia; hypothyroidism; poorly controlled diabetes mellitus; nephrotic syndrome; cholestasis; pregnancy; obesity; high dietary intake; Werner syndrome.

Decreased Levels Malabsorption; malnutrition; advanced cancer; hyperparathyroidism; chronic anemias; severe burns; sepsis/ stress; liver disease. P.293

Creatinine (Serum Creatinine) Reference Range Female: 0.5–1.1 mg/dL or 44–97 µmol/L Male: 0.6–1.2 mg/dL or 53–106 µmol/L (Critical values for female and male: >4 mg/dL)3

Clinical Implications Increased Levels Impaired renal function (e.g., glomeruloneprhitis, pyelonephritis, acute tubular necrosis, urinary tract obstruction); muscle disease (gigantism, acromegaly); rhabdomyolysis.

Decreased Levels Debilitation; decreased muscle mass (e.g., muscular dystrophy, myasthenia gravis); advanced and severe liver disease.

Erythropoietin (EPO) Reference Range 5–35 IU/L

Clinical Implications Increased Levels Anemia (iron deficiency, megaloblastic, hemolytic); myelodysplasia; chemotherapy; AIDS; renal cell carcinoma; adrenal carcinoma; pregnancy.

Decreased Levels Polycythemia vera; rheumatoid arthritis; multiple myeloma. P.294

Folic Acid (Folate) Reference Range 5–25 mg/mL or 11–57 mmol/L

Clinical Implications Increased Levels Pernicious anemia, vitamin B12 deficiency; vegetarianism; recent massive blood transfusion; blind loop syndrome.

Decreased Levels Inadequate intake (malnutrition, chronic disease, alcoholism, anorexia, diet devoid of fresh vegetables); malabsorption (e.g., small bowel disease); pregnancy; megaloblastic anemia; hemolytic anemia; malignancy; chronic renal disease; drugs that are folic antagonists (phenytoin, aminopterin, methotrexate, antimalarials, alcohol, oral contraceptives).

Glucose (Blood Sugar, Fasting Blood Sugar [FBS]) Reference Range <110 mg/dL or <6.1 mmol/L (Critical values: <40 and >400 mg/dL)

Clinical Implications Increased Levels (Hyperglycemia) Diabetes mellitus (DM); Cushing syndrome; acute stress response (MI, cerebrovascular accident [CVA], burns, infection, surgery); pheochromocytoma, acromegaly, gigantism; chronic renal failure; glucagonoma; acute pancreatitis; pregnancy; corticosteroid therapy.

Decreased Levels (Hypoglycemia) Pancreatic islet cell carcinoma; Addison disease; hypothyroidism; hypopituitarism; liver disease; starvation; insulin overdose. P.295

Glucose, Postprandial (2-Hour Postprandial Glucose [2-Hour PPG])4 Reference Range 0–50 years: 40 mg/dL or <7.8 mmol/L

50–60 years: <150 mg/dL >60 years: <160 mg/dL

Clinical Implications Increased Levels DM; gestational diabetes mellitus (GDM); malnutrition; hyperthyroidism; acute stress response (MI, CVA, burns, infection, surgery); Cushing syndrome; pheochromocytoma; chronic renal failure; glucagonoma; diuretic therapy; corticosteroid P.296 therapy; liver disease.

Decreased Levels Insulinoma; hypothyroidism; hypopituitarism; insulin overdose; Addison disease.

Glucose Tolerance (GT, Oral Glucose Tolerance Test [OGTT]) Reference Range Fasting: <110 mg/dL or <6.1 mmol/L 30 minutes: <200 mg/dL or <11.1 mmol/L 1 hour: <200 mg/dL or <11.1 mmol/L 2 hours: <140 mg/dL or <7.8 mmol/L 3 hours: 70–115 mg/dL or <6.4 mmol/L

Clinical Implications Increased Levels DM; acute stress response (MI, CVA, burns, infection, surgery); Cushing syndrome; pheochromocytoma; chronic renal failure; glucagonoma; diuretic therapy; corticosteroid therapy; liver disease; acute pancreatitis; myxedema; Somogyi response to hypoglycemia.

Glycosylated Hemoglobin (GHB; Glycohemoglobin [GHb], Hemoglobin A1C [HbA1C]) Reference Range Nondiabetic adult: 2.2%–4.8% Good diabetic control: 2.5%–5.9%

Fair diabetic control: 6%–8% Poor diabetic control: >8%

Clinical Implications Increased Levels Newly diagnosed DM; pregnancy; nondiabetic hyperglycemia (acute stress response, Cushing syndrome, pheochromocytoma, glucagonoma, corticosteroid therapy).

Decreased Levels Hemolytic anemia; chronic blood loss; chronic renal failure.

Hematocrit (Hct; Packed Cell Volume [PCV]) Reference Range5 Male: 42%–52% or 0.42–0.52 volume fraction Female: 37%–47% or 0.37–0.47 volume fraction

Clinical Implications Increased Levels Erythrocytosis; congenital heart disease; polycythemia vera; severe dehydration; severe COPD.

Decreased Levels Anemia; hemoglobinopathy; cirrhosis; hemolytic anemia; hemorrhage; dietary deficiency; renal disease; pregnancy; leukemias, lymphomas, Hodgkin lymphoma.

Hemoglobin (Hgb, Hb) Reference Range6 Male: 14–18 g/dL or 8.7–11.2 mmol/L Female: 12–16 g/dL or 7.4–9.9 mmol/L (Critical values: <5 g/dL or >20 g/dL)

Clinical Implications Increased Levels

Erythrocytosis; congenital heart disease; polycythemia vera; severe dehydration; severe COPD P.297

Decreased Levels Anemia; hemoglobinopathy; cirrhosis; hemolytic anemia; hemorrhage; dietary deficiency; bone marrow failure; renal disease; pregnancy; leukemias, lymphomas, Hodgkin lymphoma.

Homocysteine (HCY) Reference Range 4–14 µmol/L

Clinical Implications Increased Levels Vascular diseases (cardiac, cerebral, peripheral); cystinuria; vitamin B6 or B12 deficiency; folate deficiency; malnutrition. P.298

Iron Level (Fe) Reference Range Male: 80–100 µg/dL or 14–32 µmol/L Female: 60–60 µg /dL or 11–29 µmol/L

Clinical Implications Increased Levels Hemosiderosis or hemochromatosis; iron poisoning; hemolytic anemia; multiple or massive blood transfusions; hepatitis; lead poisoning; nephritis.

Decreased Levels Iron-deficiency anemia; chronic blood loss; insufficient dietary iron intake; third-trimester pregnancy; inadequate intestinal absorption of iron.

Magnesium (Mg) Reference Range

1.3–2.1 mEq/L or 0.65–1.05 mmol/L (Critical values: <0.5 or >3 mEq/L)

Clinical Implications Increased Levels Renal insufficiency; Addison's disease; hypothyroidism; dehydration; use of magnesium-containing antacids or salts.

Decreased Levels Malnutrition; malabsorption; hypoparathyroidism; alcoholism; chronic renal tubular disease; diabetic acidosis; excessive loss of body fluids (sweating, lactation, diuretic abuse, chronic diarrhea).

Osmolality (Serum Osmolality) Reference Range 285–295 mOsm/kg H2O or 285–295 mmol/kg (Critical values: <265 mOsm/kg or >320 mOsm/kg) P.299

Clinical Implications Increased Levels Dehydration; hypernatremia; hypercalcemia; DM, hyperglycemia, diabetic ketoacidosis; azotemia; mannitol therapy; alcohol ingestion (ethanol, methanol, ethylene glycol); uremia; diabetes insipidus.

Decreased Levels Overhydration; SIADH.

Phosphate (PO4), Phosphorus (P) Reference Range 3.0–4.5 mg/dL or 0.97–1.45 mmol/L (Critical values: <1 mg/dL)

Clinical Implications

Increased Levels Renal failure; hypoparathyroidism; acromegaly; bone metastasis; sarcoidosis; hypocalcemia; Addison disease; rhabdomyolysis.

Decreased Levels Hyperparathyroidism; hypercalcemia; rickets; malnutrition; gram-negative sepsis; hyperinsulinism; alkalosis; IV glucose administration (phosphorus follows glucose into cells).

Potassium (K) Reference Range 3.5–5.0 mEq/L or 3.5–5.0 mmol/L (Critical values: <2.5 or >6.5 mEq/L)

Clinical Implications Increased Levels (Hyperkalemia) Excessive dietary or IV intake; acute or chronic renal failure; Addison's disease; hypoaldosteronism; aldosterone-inhibiting P.300 diuretics (spironolactone, traimterene); crush or cell damaging injuries (accidents, burns, surgery, chemotherapy); hemolysis; acidosis; dehydration

Decreased Levels (Hypokalemia) Deficient dietary or IV intake; burns/trauma/surgery; diarrhea/vomiting/sweating; diuretics; hyperaldosteronism; Cushing syndrome; licorice ingestion; alkalosis; glucose administration; cystic fibrosis.

Prealbumin (PAB; Thyroxine-Binding Prealbumin [TBPA], Thyretin, Transthyretin) Reference Range 15–36 mg/dL or 150–360 mg/L (Critical values: <10.7 mg/dL indicates severe nutritional deficiency)

Clinical Implications Increased Levels Hodgkin's lymphoma; pregnancy

Decreased Levels Malnutrition; liver damage; burns; inflammation.

Prothrombin Time (PT; Pro-Time, International Normalized Ratio [INR]) Reference Range 11.0–13.0 seconds; 85%–100% of control Full anticoagulant therapy: <1.5–2 times control value; 20%–30% of control (Critical values: >20 seconds; full anticoagulant therapy: 3 times control values)

Clinical Implications Increased Levels (Prolonged PT) Liver disease (hepatitis, cirrhosis); hereditary factor deficiency (factors II, V, VII, X); vitamin K deficiency; bile P.301 duct obstruction; coumarin ingestion; massive blood transfusion; salicylate intoxication.

Red Blood Cell Count (RBC Count; Erythrocyte Count) Reference Range RBC ÷ 106/µL or RBC ÷ 101 2/L Male: 4.7–6.1; Female: 4.2–5.4

Clinical Implications Increased Levels Erythrocytosis; congenital heart disease; severe COPD; polycythemia vera; severe dehydration; hemoglobinopathies.

Decreased Levels Anemia; cirrhosis; hemorrhage; Addison's disease; renal disease; bone marrow failure; pregnancy; rheumatoid/collagen-vascular diseases (rheumatoid arthritis [RA], systemic lupus erythematosus [SLE], sarcoidosis); lymphoma/leukemia/Hodgkin's lymphoma.

Sodium (Na)

Reference Range 136–145 mEq/L or 136–145 mmol/L (Critical values: <120 or >160 mEq/L)

Clinical Implications Increased Levels (Hypernatremia) Increased sodium intake (dietary or IV); decreased sodium loss (Cushing's syndrome, hyperaldosteronism); excessive free body water loss (GI, excessive sweating, extensive burns, diabetes insipidus, osmotic diuresis).

Decreased Levels (Hyponatremia) Decreased sodium intake (deficient dietary or IV sodium); increased sodium loss (Addison's disease, diarrhea/vomiting, P.302 intraluminal bowel loss, diuretic administration, chronic renal insufficiency); increased free body water (excessive oral or IV water intake, hyperglycemia, CHF, peripheral edema, pleural effusion, SIADH).

Total Iron-Binding Capacity (TIBC) Reference Range 250–460 µg/dL or 45–82 µmol/L

Clinical Implications Increased Levels Estrogen therapy; polycythemia vera; pregnancy (late); iron-deficiency anemia; acute and chronic blood loss; acute hepatitis.

Decreased Levels Hypoproteinemia (malnutrition or burns); inflammatory diseases; cirrhosis; hemolytic, pernicious, and sickle cell anemias; thalassemia.

Transferrin Reference Range Male: 215–365 mg/L or 2.15–3.65 g/L Female: 250–380 mg/dL or 2.50–3.80 g/L

Clinical Implications Increased Levels Estrogen therapy; polycythemia vera; pregnancy (late); iron-deficiency anemia.

Decreased Levels Hypoproteinemia (malnutrition or burns); inflammatory diseases; cirrhosis; hemolytic, pernicious, and sickle cell anemias; renal disease; acute liver disease. P.303

Transferrin Saturation Reference Range Male: 20%–50% Female:15%–50%

Clinical Implications Increased Levels Hemochromatosis; increased iron intake; hemolytic anemia; thalassemia; acute liver disease.

Decreased Levels Iron-deficiency anemia; anemia of infection and chronic diseases; malignancy.

Vitamin B12 (Cyanocobalamin) Reference Range 160–950 pg/mL or 118–701 mmol/L

Clinical Implications Increased Levels Leukemia, polycythemia vera; severe liver dysfunction; CHF; diabetes; myeloproliferative disease.

Decreased Levels Pernicious anemia; malabsorption syndromes and inflammatory bowel disease (IBD); intestinal worm infestation; Zollinger–Ellison syndrome; folic acid deficiency; vitamin C deficiency; achlorydria; large

proximal gastrectomy.

White Blood Count and Differential Count (WBC with differential) Reference Range Total WBCs: 5,000–10,000/mm3 or 5–10 (109/L (Critical values: <2,500 or >30,000/mm3) P.304 Lymphocytes: 1,000–4,000/mm3 (comprise 20%–40% of the total WBC; and in malnutrition, lymphocyte count is reduced).

Clinical Implications Increased WBC Count (Leukocytosis) Infection; leukemic neoplasia or other myeloproliferative disorders; trauma/stress/hemorrhage; tissue necrosis; inflammation; thyroid storm; steroid use.

Decreased WBC Count (Leukopenia) Drug toxicity; bone marrow failure; dietary deficiency of vitamin B1 2 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 B 12; folate; thyroid-stimulating hormone (TSH)

Basic Metabolic Panel (7 Channel/Chem 7/SMA-7) Carbon dioxide content; chloride, blood; creatinine, blood; glucose, blood; potassium, blood; sodium, blood; urea nitrogen, blood (BUN). P.305

Complete Blood Cell Count (CBC) with Differential (Diff) RBC; Hgb; Ht; red blood cell indices (mean corpuscular volume [MCV], mean corpuscular hemoglobin [MCH], mean corpuscular hemoglobin concentration [MCHC], red blood cell distribution width [RDW]); WBC and Diff count (neutrophils; lymphocytes; monocytes; eosinophils; basophils); blood smear; platelet count; mean platelet volume (MPV).

Comprehensive Metabolic Panel (12 Channel/Chem 12) Albumin; alkaline phosphatase; AST (SGOT); bilirubin- total; BUN; calcium; chloride; creatinine; glucose; potassium; protein-total; sodium. The old Comprehensive Metabolic Panel or “Chem 20” includes all the above labs plus: ALT (SGPT); bilirubin-direct; carbon dioxide; cholesterol; GGT; LDH; phosphorus; uric acid.)

Diabetes Mellitus Management Anion gap; basic metabolic panel; hemoglobin A1C; lipid profile.

Hepatic Function ALT; albumin; alkaline phosphatase; AST; bilirubin-direct; bilirubin-total; GGT; protein, total; prothrombin time (PT).

Lipid Panel Cholesterol-total; high-density lipoprotein (HDL); triglyceride; low-density lipoprotein (LDL); very-lowdensity lipoprotein (VLDL).

Pancreatic Panel Amylase; calcium; glucose; lipase; triglyceride. P.306

Renal Panel Albumin; basic metabolic panel; calcium; CBC; creatinine clearance; magnesium; phosphorus; protein-total; protein-urine; protein-24-hour urine.

References Bakerman S, Bakerman P, Strausbauch P. Bakerman's ABC's of Interpretive Laboratory Data, 4th ed. Scottsdale: Interpretive Laboratory Data, Inc.; 2002.

Fischbach FT, Marshall BC. A Manual of Laboratory and Diagnostic Tests, 7th ed. Philadelphia: Lippincott Williams & Wilkins; 2004.

Mahan LK, Escott-Stump, S. Krause's Food, Nutrition, & Diet Therapy, 11th ed. Philadelphia: Saunders; 2004:792–833.

Pagana KD, Pagana TJ. Mosby's Manual of Diagnostic and Laboratory Test, 3rd ed. Missouri: Mosby Elsevier; 2006. Because about one-half of blood calcium is bound to albumin, when albumin levels are low, the serum calcium will also be low. Calcium levels can be adjusted with the following equation, when serum albumin is low: Corrected calcium = total calcium mg/dL + 0.8 [4 –serum albumin g/dL].

Authors: Width, Mary; Reinhard, Tonia Title: Clinical Dietitian's Essential Pocket Guide,The: Essential Pocket Guide, 1st Edition Copyright ©2009 Lippincott Williams & Wilkins > Back of Book > Appendix B: Food–Drug Interactions Appendix B: Food–Drug Interactions Lisa Ventrella Lucente RD The following table of medications is not meant to be comprehensive, but instead lists common medications that have significant nutritional implications. The list is alphabetical by generic name (in italics), and cross-referenced by brand or trade name. P.308 P.309 P.310 P.311 P.312 P.313 P.314 P.315 P.316 P.317 P.318 P.319 P.320 P.321 P.322 P.323 P.324 P.325 P.326 Nutritional Medication Class & Action Side Effects Implications Adalat See nifedipine Aldactone See spironolactone Apresoline See hydralazine Atenolol Beta-blocker, Diarrhea, Adherence necessary Tenormin antiadrenergic, constipation, nausea, for those following antiarrhythmic and vomiting. diabetic diet. Possible Monitor blood hypoglycemia. glucose levels. Be Signs of sympathetic cautious of response to nonsympathetic hypoglycemia may signs of be masked. May hypoglycemia. have a decreased Consider fluid and insulin release in electrolyte

response to hyperglycemia. Atorvastatin Lipitor

Inhibitor of HMG-CoA reductase

Azithromycin Zithromax

Antibiotic Occasional nausea, Bacteriostatic or vomiting, diarrhea, bacteriocidal abdominal pain, anorexia, stomatitis, bad taste in mouth

Bactrim, Bactrim DS Benazepril Lotensin

See sulfamethoxazole Antihypertensive May increase serum Caution with foods ACE Inhibitor potassium. high in potassium or May decrease serum potassium sodium. supplements. Avoid Nausea, salty or salt substitutes. metallic taste, mouth Maintain adequate sores. hydration. See metoprolol See clarithromycin Diuretic Ginkgo Biloba may Consume foods high Loop diuretic cause increased in potassium and blood pressure. magnesium. Avoid Licorice can increase consumption of the risk of natural licorice. hypokalemia. May Monitor electrolyte

Betaloc Biaxin Bumetanide Bumex

Constipation, diarrhea, gas, upset stomach, and upper right stomach pain. Coenzyme Q10 may be significantly reduced.

replacement for diarrhea and vomiting. Avoid intake large quantities of grapefruit juice for it increases the absorption of statins (>1 qt/day). Eat a low-cholesterol, low-fat diet for best results. Gastrointestinal problems generally transient. Take with food to avoid GI disturbances. Azithromycin oral suspension should be taken 1 hr before or 2 hr after meals. Eat small, frequent meals to avoid anorexia. Consider fluid and electrolyte replacement for diarrhea. Avoid alcohol.

Bupropion Wellbutrin, Zyban

Bumex Calan Calcijex Calcium salts PhosLo, Caltrate, Dicarbosil, OsCal, Titralac, Tums, Citracal, Calcitrate

Calcitrate Calcitriol Calcijex, Rocaltrol

Caltrate

increase blood levels and consider glucose, uric acid, supplementation. cholesterol, LDL, Caution withcalcium calcium, and supplements. triglycerides. May decrease urinary excretion of calcium and increase excretion of magnesium, sodium and potassium levels. Antidepressant Dry mouth, upset Monitor weight. Use Serotonin & stomach, vomiting, ice chips or chew norepinephrine weight loss, and gum for dry mouth. reuptake constipation. AlcoholAvoid alcohol. inhibitor may increase side effects. See bumetanide See verapamil See calcitriol Calcium-based Hypercalcemia, Maintain adequate phosphorus stomach pains, hydration, serum binder nausea, vomiting, magnesium, constipation, dry phosphate, mouth, thirst, and potassium levels, frequent urination. and urine calcium levels. See calcium salts Vitamin D May increase Avoid use of aluminum antacids. Only works concentration, in conjunction with hypercalcemia, appropriate intake of serum cholesterol, calcium. Consider serum phosphorous, low phosphate diet if and magnesium on dialysis. concentration. Upset stomach, vomiting, dry mouth, constipation, metallic taste in mouth, increased thirst, decreased appetite, weight loss and fatty stools. See calcium salts

Capoten Capozide Captopril

Catapres Celexa Cholestyramine Questran, Prevalite

Cinacalcet Sensipar

Ciprofloxacin

See captopril See captopril Antihypertensive May increase serum Caution with foods ACE Inhibitor potassium. high in potassium or May decrease serum potassium sodium. supplements. Avoid Nausea, salty or salt substitutes. metallic taste, mouth Maintain adequate sores. hydration. See clonidine See citalopram Bile acid May decrease serum Mix with 3 to 6 oz of sequestrant potassium and liquid, such as juice, calcium. Binds fat- milk, or water for soluble vitamin A, D,powdered form. E, and K, folic acid, Irritating to GI tract. and beta-carotene. Take before meals. Constipation, nausea,Take fat-soluble vomiting, abdominal vitamins in a water pain, indigestion. miscible form or Occasional diarrhea. take a supplement prior to initial daily dose of drug. Monitor nutrient levels if long-term use of drug is indicated. Consider high fiber diet for constipation. Calcimimetic High-fat intake may Avoid taking with increase cinacalcet grapefruit juice. concentration of plasma. Nausea, vomiting, and diarrhea Antibacterial Upset stomach, Take with 8 oz of vomiting, stomach water. Ensure pain, indigestion. adequate fluid Inflammation of the intake. Consider stomach leading to fluid and electrolyte possible diarrhea. replacement for Aluminum, vomiting and magnesium, calcium, diarrhea. Should not ferrous sulfate, and be taken with dairy zinc are thought to products or calcium

Cisplatin Platinol, Platinol-AQ

Citalopram Celexa

Citracal Clarithromycin Biaxin

Clonidine Catapres, Duraclon

Clopidogrel Plavix

form chelation containing fluids. Do complexes not need to avoid preventing the drugs foods containing from being absorbed. these products. Alkylating agent Loss of appetite, Drink plenty of weight loss, diarrhea, fluids for drug; nausea, vomiting, irritates the kidney. and altered taste. Vomiting is severe. May consider antiemetic therapy. Monitor weight. Encourage food intake when patient feels best, e.g., morning. Antidepressant Nausea, diarrhea, Consider fluid and Selective vomiting, anorexia, electrolyte serotonin dry mouth, and replacement for reuptake dyspepsia. May diarrhea and inhibitor decrease serum vomiting. Use ice sodium. chips or chew gum for dry mouth. Avoid alcohol. See calcium salts Antibiotic Occasional nausea, Take with food to Bacteriostatic or vomiting, diarrhea, avoid GI bacteriocidal abdominal pain, disturbances. Eat anorexia, stomatitis, small, frequent bad taste in mouth meals to avoid anorexia. Consider fluid and electrolyte replacement for diarrhea. Avoid alcohol. AlphaConstipation, nausea,Avoid alcohol intake antiadrenergic vomiting, dry mouth, for it can exacerbate and drowsiness. drowsiness. Use ice chips or chew gum for dry mouth. Anti-platelet Upset stomach, Consider small, stomach pain, frequent meals for diarrhea, and anorexia. Consider constipation. Ginger fluid and electrolyte may increase the replacement for possibility of diarrhea.

bleeding.

CoBactericidal trimoxazole/trimethoprim/Sulfamethoxazole Bactrim, Bactrim DS

Coumadin Covera-HS Cyclophosphamide Cytoxan

Cytoxan Dialyvite Diatx, Nephrocaps, Nephrovite

Diatx Dicarbosil Digoxin Lanoxin

Consistency in dietary and supplemental intake must be consistent to achieve steady level of anticoagulation. Those on long-term use should be monitored for bone density. May cause anorexia, Take with 8 oz of nausea, vomiting, water on an empty diarrhea, abdominal stomach. Eat small, pain, or stomatitis. frequent meals to May hinder folate avoid anorexia. Take metabolism. a folate supplement. Consider fluid and electrolyte replacement for diarrhea.

See warfarin See verapamil Alkylating agent, Nausea, vomiting, Drink plenty of nitrogen mustard loss of appetite, and fluids for drug; weight loss. irritates bladder and kidneys. Encourage food intake when patient feels best, e.g., morning. See cyclophosphamide B-complex with Abdominal pain, Taken when vitamin C and cramps, dyspepsia, vitamins inadequate, Biotin and nausea. usually after dialysis when fluid is removed. Used to replace watersoluble vitamin losses. See dialyvite See calcium salts Antiarrhythmic, Occasional diarrhea, Hypomagnesemia, cardiac glycoside loss of appetite, hypokalemia, and lower stomach pain, hypercalcemia nausea, and/or elevate drug toxicity. vomiting. May Ensure consumption

reduce potassium levels and increase urinary excretion of magnesium.

Doxercalciferol Hectorol Duraclon Dyrenium Effexor, Effexor XR Enalapril Vasotec

Ery-Tab Erythromycin Ery-Tab

Effexor Eskalith, Eskalith CR Extentabs Feostat Femiron Fenofibrate Tricor Feosol Feratab Fergon Ferrex Ferrlecit Ferrous fumarate Femiron, Feostat

adequate potassium and magnesium. Care should be taken with calcium supplements and antacids.

See calcitriol See clonidine See triamterene See venlafaxine Antihypertensive May increase serum Caution with foods ACE Inhibitor potassium. high in potassium or May decrease serum potassium sodium. supplements. Avoid Nausea, salty or salt substitutes. metallic taste, mouth Maintain adequate sores. hydration. See erythromycin Antibiotic Occasional nausea, Take with food to Bacteriostatic or vomiting, diarrhea, avoid GI bacteriocidal abdominal pain, disturbances. Eat anorexia, stomatitis, small, frequent bad taste in mouth meals to avoid anorexia. Consider fluid and electrolyte replacement for diarrhea. Avoid alcohol. See venlafaxine See lithium See quinidine See ferrous fumarate See ferrous fumarate See gemfibrozil See ferrous sulfate See ferrous sulfate See ferrous sulfate See ferrous sulfate See sodium ferric gluconate Iron supplement Constipation, Emphasize iron-rich diarrhea, and food in a wellabdominal balanced diet. discomfort.

Ferrous sulfate Iron supplement Constipation and Emphasize iron-rich Feosol, Feratab, Fergon, Ferrex, Hemocyte, stomach upset. food in a wellNephro-Fer, Niferex balanced diet. Ferrous gluconate See ferrous sulfate Flagyl See metronidazole Fluoxetine Antidepressant Alcohol may Avoid alcohol. Prozac Selective increase depression. Consider fluid and serotonin St. John's Wort may electrolyte reuptake increase drug effect. replacement for inhibitor Nausea, diarrhea, diarrhea and decreased appetite, vomiting. Use ice dry mouth, vomiting, chips or chew gum constipation, and for dry mouth. abdominal pain. Consider small, frequent meals for decreased appetite. Fluvastatin See atorvastatin Lescol Diuretic Ginkgo Biloba may Consume foods high Furosemide Loop diuretic cause increased in potassium and Lasix blood pressure. magnesium. Avoid Licorice can increase consumption of the risk of natural licorice. hypokalemia. May Monitor electrolyte increase blood levels and consider glucose, uric acid, supplementation. cholesterol, LDL, Caution with calcium, and calcium triglycerides. May supplements. decrease urinary excretion of calcium and increase excretion of magnesium, sodium, and potassium levels. Gemfibrozil Lopid Fibric acid Stomach pain, Eat a lowderivative diarrhea, cholesterol, low-fat, constipation, low-sucrose diet for vomiting, and gas. best results. Avoid alcohol. Consider fluid and electrolyte replacement for diarrhea and vomiting. Hectorol See doxercalciferol

Hydralazine Apresoline

Hemocyte Imfed Iron dextran Imfed

Iron sucrose Venofer

Isocarboxazid Marplan

Isoptin, Isoptin SR Keflex Kinidine Lanoxin Lasix Lescol Lipitor

Antiarrhythmic, Nausea, vomiting, Doctor may Antiprotozoal diarrhea, fluid prescribe a low-salt retention, and edema.or low-sodium diet. Impedes metabolism Take with food. of pyridoxine Monitor for (vitamin B6). pyridoxine deficiency. Consume diet high in pyridoxine. Consider supplementation. See ferrous sulfate See iron dextran IV iron, Nausea, vomiting, Avoid taking oral Hematinic and metallic taste. iron. Emphasize iron-rich food in a well-balanced diet. IV iron, Diarrhea Avoid taking oral Hematinic iron. Emphasize iron-rich food in a well-balanced diet. Antidepressant Sudden high blood Avoid foods high in Monoamine pressure may occur tyramine: cheeses, oxidase inhibitor with ingestion of fava, or broad bean (MAOI) certain foods. pods; yeast or meat Alcohol may extracts, smoked or increase depressant pickled meat, effect. Caffeine may poultry, or fish; increase blood fermented sausage pressure and cardiac such as bologna, arrhythmias. pepperoni, salami, or other fermented meat; avocados; bananas; beer; wine; and raisins. Avoid excess amounts of caffeine, tea, or chocolate. Avoid alcohol. See verapamil See cephalexin See quinidine See digoxin See furosemide See fluvastatin See atorvastatin

Lisinopril Prinivil, Zestril

Lithane Lithium Eskalith, Eskalith CR, Lithobid, Lithane, Lithonate, Lithotabs

Lithobid Lithonate Lithotabs Lopid Lopressor Marplan Methotrexate

Antihypertensive May increase serum Caution with foods ACE inhibitor potassium. high in potassium or May decrease serum potassium sodium. supplements. Avoid Nausea, salty or salt substitutes. metallic taste, mouth Maintain adequate sores. hydration. See lithium Antimanic agent Drug interferes with Maintain steady salt the regulation of and fluid intake. sodium and water Avoid salt-free diet levels in the body or sodium depletion. and may lead to Avoid caffeine. dehydration. Toxicity may result from sodium depletion. Caffeine appears to reduce serum lithium concentrations and increase side effects. Loss of appetite, stomach pain or bloating, gas, indigestion, weight gain or loss, dry mouth, excessive saliva in the mouth, tongue pain, change in the ability to taste food, swollen lips, and constipation. See lithium See lithium See lithium See gemfibrozil See metoprolol See isocarboxazid Antimetabolite, Nausea, vomiting, Consume high folate antagonist diarrhea, stomach Vitamin B12 diet. pain, mouth sores, Consider fluid and and loss of appetite. electrolyte Inhibitor of replacement for dihydrofolate diarrhea and reductase, thus vomiting. Encourage

decreasing food intake when availability of active patient feels best, folate. e.g., morning. Drink extra fluids to pass more drug through the urine. Leucovorin should be considered to reverse toxic effect of folic acid antagonists. Diarrhea, Adherence necessary constipation, nausea, for those following and vomiting. diabetic diet. Possible Monitor blood hypoglycemia. Signs glucose levels. Be of sympathetic cautious of response to nonsympathetic hypoglycemia may signs of be masked. May hypoglycemia. have a decreased Consider fluid and insulin release in electrolyte response to replacement for hyperglycemia. diarrhea and vomiting. Anorexia, nausea, Avoid alcohol and dry mouth, alcohol-containing stomatitis, diarrhea products during and or constipation, at least 5 days after vomiting, and treatment. Avoid hot metallic taste. and spicy foods. Consider fluid and electrolyte replacement for diarrhea. Take with food to prevent GI distress. Consider small, frequent meals for anorexia. Use ice chips or chew gum for dry mouth.

Metoprolol Betaloc, Lopressor, Toprol XL

Beta-blocker, antiadrenergic, antiarrhythmic

Metronidazole Flagyl

Antibacterial, antiprotozoal

Nardil Nephrocaps Nephro-Fer

See phenelzine See dialyvite See ferrous sulfate

Nephrovite Niacin Niacor, Niaspan, Nicotinex, Slo-Niacin

See dialyvite Nicotinic acid derivative

Niacor Niaspan Nicotinex Nifedical Nifedipine Adalat, Nifedical, Procardia

See niacin See niacin See niacin See nifedipine Calcium channel Upset stomach, blocker heartburn, nausea, and constipation.

Niferex Oncovin Orlistat Xenical

See ferrous sulfate See vincristine Lipase inhibitor Flatulence, fatty stools, nausea, diarrhea. Decreased absorption vitamins A and E. See calcium salts See tranylcypromine Antidepressant St. John's Wort may Selective increase drug effect. serotonin Nausea, dry mouth, reuptake constipation, inhibitor diarrhea, and decreased appetite.

OsCal Parnate Paroxetine Paxeva, Paxil, Paxil CR

Paxeva Paxil, Paxil CR Penicillin

See paroxetine See paroxetine Antibiotic Kill or prevent growth of

Alcohol may Caution with increase side effects diabetes. Ensure of niacin. Occasional adherence to diabetic gas, nausea, diet if necessary. vomiting, and May consider lowdiarrhea. May purine diet if increase blood uric necessary. Consider acid and glucose fluid and electrolyte levels. replacement for diarrhea and vomiting.

Avoid drinking grapefruit juice or eating grapefruit 1 hr before or for 2 hr after taking nifedipine.

Side effects are transient. Monitor nutrient levels.

Consider fluid and electrolyte replacement for diarrhea. Use ice chips or chew gum for dry mouth. Consider small, frequent meals for decreased appetite.

GI disturbances Should be taken 1 hr including mild before or 2 hr after diarrhea, nausea, or food to facilitate

bacteria

vomiting. Some may absorption. Consider contain high amountsfluid and electrolyte of sodium or replacement for potassium. diarrhea. Caution if on low sodium diet. Some strengths of amoxicillin may contain phenylalanine.

Paricalcitol Zemplar Phenelzine Nardil

See calcitriol Antidepressant Sudden high blood Monoamine pressure may occur oxidase inhibitor with ingestion of (MAOI) certain foods. Alcohol may increase depressant effect. Caffeine may increase blood pressure and cardiac arrhythmias.

PhosLo Platinol, Platinol-AQ Plavix Pravachol Pravastatin Pravachol

See calcium salts See cisplatin See clopidogrel See pravastatin Inhibitor of Constipation, HMG-CoA diarrhea, gas, upset reductase stomach, and upper right stomach pain. Coenzyme Q10 may be significantly reduced.

Prevalite

See cholestyramine

Avoid foods high in tyramine: cheeses, fava, or broad bean pods; yeast or meat extracts, smoked or pickled meat, poultry, or fish; fermented sausage such as bologna, pepperoni, salami, or other fermented meat; avocados; bananas; beer; wine; and raisins. Avoid excess amounts of caffeine, tea, or chocolate. Avoid alcohol.

Avoid intake large quantities of grapefruit juice for it increases the absorption of statins (>1 quart/day). Eat a low -cholesterol, low-fat diet for best results. Gastrointestinal problems generally transient.

Prinivil Procardia PropanololInderal Prozac Questran Quinidex Quinidine Kinidine, Quinidex, Extentabs

Renagel Rocaltrol Sensipar Sertraline Zoloft

Sevelamer Renagel

Simvastatin Zocor

See lisinopril See nifedipine See atenolol See fluoxetine See cholestyramine See quinidine Antiarrhythmic, Abdominal pain and Consider fluid and antiprotozoal cramps, diarrhea, electrolyte nausea, and replacement for vomiting. May cause diarrhea and hypokalemia, vomiting. Consume hypomagnesemia, diet adequate in and/or hypocalcemia.potassium, magnesium, and calcium. Supplementation maybe necessary. See sevelamer See calcitriol See cinacalcet Antidepressant May increase serum Monitor blood lipid Selective triglyceride and total levels. Consider serotonin cholesterol. May fluid and electrolyte reuptake decrease uric acid replacement for inhibitor levels. St. John's diarrhea and Wort may increase vomiting. Use ice adverse side effects. chips or chew gum Nausea, diarrhea, dry for dry mouth. mouth, constipation, Avoid alcohol. altered taste, and dyspepsia. Non-calcium- Diarrhea, dyspepsia, Take with food. Use based gas, constipation, of aluminum should phosphorus nausea, and be limited to <14 binder vomiting. days. Monitor bicarbonate, chloride, calcium, and phosphorous levels. Inhibitor of Constipation, Avoid intake large HMG-CoA diarrhea, gas, upset quantities of reductase stomach, and upper grapefruit juice for it right stomach pain. increases the Coenzyme Q10 may absorption of statins be significantly (>1 quart/day). Eat a

reduced.

Slo-Niacin Sodium ferric Gluconate complex Ferrlecit Spironolactone Aldactone

Tenormin Titralac Toprol XL Tranylcypromine Parnate

Triamterene Dyrenium

Tricor Trovafloxacin Trovan

low-cholesterol, low-fat diet for best results. Gastrointestinal problems generally transient.

See niacin See iron sucrose Diuretic Hyperkalemia, Avoid foods high in Potassium dehydration, potassium, sparing diuretic hyponatremia, potassium nausea, vomiting, supplements, and anorexia, abdominal salt substitutes. cramps, and diarrhea. See atenolol See calcium salts See metoprolol Antidepressant Sudden high blood Avoid foods high in Monoamine pressure may occur tyramine: cheeses, oxidase inhibitor with ingestion of fava or broad bean (MAOI) certain foods. pods, yeast or meat Alcohol may extracts, smoked or increase depressant pickled meat, effect. Caffeine may poultry, or fish, increase blood fermented sausage pressure and cardiac such as bologna, arrhythmias. GI pepperoni, salami, or upset other fermented meat, avocados, bananas, beer, wine, and raisins. Avoid excess amounts of caffeine, tea, or chocolate. Avoid alcohol. Diuretic Hyperkalemia, Avoid foods high in Potassium dehydration, potassium, sparing diuretic hyponatremia, potassium nausea, vomiting, supplements, and anorexia, abdominal salt substitutes. cramps, and diarrhea. See fenofibrate Quinolone Iron preparations Consider fluid and may increase drug electrolyte

Trovan Tums Vasotec Velban Velsar Venlafaxine Effexor, Effexor XR

Venofer Verapamil Calan, Verelan, Verelan PM, Isoptin, Isoptin SR, Covera-HS

Verelan, Verelan PM Vinblastine Velban, Velsar, vinblastine sulfate, VBL

Vincristine Oncovin

absorption. replacement for Dandelion may diarrhea. increase drug effect. Fennel seed may decrease drug effect resulting in treatment failure. Diarrhea. See trovafloxacin See calcium salts See enalapril See vinblastine See vinblastine Antidepressant St. John's Wort may Use ice chips or increase sedative chew gum for dry effect. May increase mouth. Monitor cholesterol and uric weight. acid levels. May decrease serum sodium and serum phosphate levels. May modify blood glucose and serum potassium levels. Nausea, dry mouth, anorexia, and constipation. See iron sucrose Calcium ChannelConstipation, upset Avoid drinking Blocker stomach, heartburn. grapefruit juice or eating grapefruit 1 hr before or for 2 hr after taking nifedipine. See verapamil Plant alkaloid Nausea, vomiting, Drink plenty of stomach pain, fluids to decrease constipation, and constipation. diarrhea. Plant alkaloid Nausea, vomiting, Consider fluid and stomach pain, electrolyte stomach cramps, replacement for constipation, and diarrhea and diarrhea. vomiting. May consider laxatives for constipation.

Warfarin Coumadin

Anticoagulant

Wellbutrin Xenical Zemplar Zestril Zithromax Zocor Zoloft Zyban

See bupropion See orlistat See paricalcitol See lisinopril See azithromycin See simvastatin See sertraline See bupropion

Mild vomiting remedied with antiemetic. Anorexia, nausea, Consider small, abdominal cramping frequent meals for and diarrhea. anorexia. Consider Prevents the fluid and electrolyte conversion of replacement for vitamin K to its diarrhea. Dietary and active form. Garlic supplemental intake may increase the risk must be consistent to of bleeding. achieve steady level Mineralization of of anticoagulation. newly formed bone Those on long-term may be deterred. use should be monitored for bone density.

Authors: Width, Mary; Reinhard, Tonia Title: Clinical Dietitian's Essential Pocket Guide,The: Essential Pocket Guide, 1st Edition Copyright ©2009 Lippincott Williams & Wilkins > Back of Book > Appendix C: Nutrition-Related Information

Appendix C: Nutrition-Related Information Listing of Contents Conversion tables Framingham Risk Scoring for Serum Cholesterol Vitamin Facts and Nutrient Lists

Vitamins (A) Food Sources of Individual Vitamins

Water Soluble (B–K) Fat Soluble (L–O)

Table C.1 Conversion Tables

A. Length 1m

=

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 1L

= 1,000 mL

0.26 gal

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

1 oz

= 30 mL

1 tablespoon (Tbs)

= 3 tsp

1 teaspoon (tsp)

= 5 mL

D. Weight

15 mL

1.06 qt

2.1 pt

0.25 L

1 kg

=

1,000 g

2.2 lb

1g

=

1/1,000 kg

1,000 mg

1 mg

=

1/1,000 g

1,000 µg

1 µg

=

1/1,000 mg

1 lb

=

16 oz

1 oz

=

~28 g

0.035 oz

454 g

0.45 kg

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 1. 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

2. Men: Framingham Point Scores by Age Group and Total Cholesterol

2. 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

3. 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

4. Men: Framingham Point Scores by High-Density Lipoprotein (HDL) Level HDL

Points

=60

-1

50–59

0

40–49

1

<40

2

5. 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

6. 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%

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 1. 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

60–64

10

65–69

12

70–74

14

75–79

16

2. 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

3. 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

4. Women: Framingham Point Scores by HDL Level

4. HDL

Points

=60

-1

50–59

0

40–49

1

<40

2

5. 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

6. Women: 10-Year Risk by Total Framingham Point Scores Point Total

10-Year Risk

<9

<1%

9

1%

10

1%

11

1%

12

1%

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

Anemia Blindness, night blindness Bone growth deficit

Amenorrhea Anorexia Bone pain Fatigue

bone and teeth growth; regulate synthesis of reproductive hormones immune and cancer

Corneal breakdown Diarrhea Joint pain Kidney stones

Headache Nosebleeds Skin rash

protection

Infection susceptibility

Maintain bone tissue by regulating the absorption and

Defective bone growth (bowed legs, joint pain)

Anorexia Headaches Excessive thirst

excretion of calcium and phosphorus

Muscle spasms

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

D

regulation of calcium levels in blood

B1 Thiamin

Coenzyme in energy metabolism; maintenance of appetite and nervous system function

anticoag-ulant drugs

Abnormal heart beat Cardiomegaly/heart failure Fluid retention Mental confusion Muscle pain,

None documented

weakness, wasting paralysis

B2 Riboflavin

Coenzyme in energy metabolism; maintenance of skin and visual function

Corneal abnormalities Dry, cracking at corners of mouth Sensitivity to light

None documented

Skin rash Tongue abnormalities

B3 Niacin, Nico-tinamide

Coenzyme in energy metabolism;

Anorexia Diarrhea

Diarrhea Dizziness

maintenance of skin, nervous and digestive systems

Skin rash Tongue abnormalities Weakness and

Liver dysfunction Low blood pressure Sweating,

dizziness

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 documented

Panto-thenic Acid

Coenzyme in energy metabolism

Fatigue Insomnia Vomiting, other intestinal problems

Fluid retention

Biotin

Coenzyme in energy

Alopecia

None docu-

metabolism; synthesis of fat and glycogen

Anorexia Depression Fatigue Heartbeat

mented

abnormalities Nausea Skin rash

Choline

C Ascorbic Acid

B. Vitamin C

Coenzyme in energy metabolism; synthesis

Growth failure Kidney failure

Fishy body odor Low blood

of phospholipids and neurotransmitters

Liver dysfunction (fat accumulation) Memory abnormalities

pressure

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

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 B 6

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%

Sirloin steak

3.5 oz broiled

2.9

119%

Salmon

3 oz cooked

2.7

113%

Tuna, in water

3 oz canned

2.5

106%

Lamb chop

3.5 oz braised

2.3

95%

Vegetarian burger

½ cup

2

83%

Raisin bran

¾ cup

2

83%

Ground beef

3.5 oz lean baked

1.7

71%

Cottage cheese

1 cup 1% fat

1.4

58%

Sole/flounder

3 oz cooked

1.3

54%

Shrimp

3 oz cooked

1.3

54%

Halibut

3 oz broiled

1.2

50%

Milk

2% 8 oz

0.89

37%

Frankfurter

1 beef, 2 oz

0.88

37%

Ham

3.5 oz cooked

0.74

29%

Tempeh

½ cup

0.7

29%

Pork chop

3.5 oz roasted

0.6

25%

Buttermilk

8 oz, cultured

0.54

23%

Egg

1 whole fresh

0.5

21%

Turkey

3.5 oz w/o skin

0.37

15%

Canadian bacon

2 slices cooked

0.36

15%

Miso

½ cup

0.29

12%

Chicken breast

½ breast w/o skin

0.29

12%

Yogurt

8 oz low fat

0.24

10%

Cheddar cheese

1 oz

0.23

10%

Goat's milk

8 oz

0.16

7%


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%

Asparagus

1 cup cooked

264

66%

Spinach

1 cup cooked

262

66%

Navy beans

1 cup cooked

255

64%

Beef liver

3.5 oz braised

217

54%

Black-eyed peas

1 cup cooked

209

52%

Great northern beans

1 cup cooked

181

45%

Turnip greens

1 cup cooked

170

43%

Lima beans

1 cup cooked

156

39%

Kidney beans

1 cup canned

129

32%

Broccoli

1 cup cooked

104

26%

Corn flakes

1 cup

100

25%

Parsley

1 cup chopped

92

23%

Beets

1 cup cooked

90

23%

Wheat germ

1/4 cup

82

21%

Romaine lettuce

1 cup chopped

76

19%

Cauliflower

1 cup cooked

64

16%

Pineapple juice

8 oz canned

58

15%

Orange

1 fresh medium

47

12%

Zucchini

1 cup cooked

30

8%

Peanuts

1 oz dried

29

7%

Cantaloupe

1 cup fresh

27

7%

Winter squash

1 cup cooked

26

7%

Strawberries

1 cup fresh

26

7%

Grapefruit juice

1 cup canned

26

7%

Egg

1 whole fresh

23

6%

Green beans

1 cup cooked

22

6%

Tofu

1/2 cup raw

19

5%

Tomato

1 whole raw

18

5%

Bread, whole

1 slice

14

4%

wheat


Use dry beans in soups or as a main dish salad. Add spinach to lasagna or serve cooked with lemon juice. Salad of spinach, romaine, tomato, broccoli, cauliflower, and beets. Dinner: 3.5 oz beef liver, 1 cup asparagus, 1 cup lima beans. Breakfast: cornflakes in milk; fruit salad of cantaloupe, strawberries, orange.

I. Niacin % DRI

Food

Portion Size

Niacin (mg)

Women

Men

Chicken breast

½ roasted w/o skin

11.8

84%

74%

Tuna, in water

3 oz canned

11.3

81%

71%

Beef liver

3.5 oz braised

10.7

76%

67%

Brewer's yeast

1 oz

10.7

76%

67%

Salmon

3 oz broiled

8.6

61%

54%

Mushrooms

1 cup cooked

7

50%

44%

Halibut

3 oz broiled

6.1

44%

38%

Peach halves

10 dried

5.7

41%

36%

Pink salmon

3 oz canned

5.6

40%

35%

Pork chop

3.5 oz roasted

5.5

39%

34%

Lamb chop

3.5 oz braised

5.5

39%

34%

Turkey

3.5 oz w/o skin

5.4

39%

34%

Sirloin steak

3.5 oz broiled

4.3

31%

27%

Ground beef

3.5 oz lean baked

4.2

30%

26%

Peanuts

1 oz dried unsalted

4

29%

25%

Baked potato

1 whole

3.3

24%

21%

Sole/flounder

3 oz baked

2.5

18%

16%

Kidney beans

1 cup canned

2.4

17%

15%

Braunschweiger

1 oz tube-type

2.3

16%

14%

Shrimp

3 oz boiled

2.2

16%

14%

Wheat bran

¼ cup

2

14%

13%

Asparagus

1 cup cooked

2

14%

13%

Oysters

3 oz raw

1.7

12%

11%

Sardines

2 sardines in oil

1.3

9%

8%

Crab meat

3 oz canned

1.2

9%

8%

Bread, whole wheat

1 slice

1

8%

6%

Summer squash

1 cup cooked

1

8%

6%

Cantaloupe

1 cup fresh

0.9

6%

6%

Peach

1 fresh medium

0.9

6%

6%

Spinach

1 cup cooked

0.9

6%

6%

Broccoli

1 cup cooked

0.8

6%

5%


Choose tuna, halibut, and salmon instead of red meat. Add mushrooms to soups and salads, and stir fry. Dinner: half chicken breast, baked potato, 1 cup asparagus. Fortified breakfast cereals contain 25% of the DRI for niacin per serving.

J. Pantothenic Acid

Food

Serving Size

Pantothenic Acid (mg)

% DRI

Beef liver

3.5 oz braised

4.6

91%

Mushrooms

½ cup boiled

1.7

34%

Avocado

1 medium

1.7

34%

Salmon

3 oz cooked

1.4

28%

Lentils

1 cup boiled

1.3

25%

Split peas

1 cup boiled

1.2

23%

Potato

1 whole baked

1.1

22%

Turkey

3.5 oz w/o skin

0.94

19%

Pomegranate

1 medium raw

0.92

18%

Chicken breast

½ roasted w/o skin

0.83

17%

Peanuts

1 oz dried

0.79

16%

Milk, 2%

8 oz

0.78

16%

Sweet potato

1 whole baked

0.74

15%

Chickpeas

1 cup canned

0.72

14%

Wheat germ

¼ cup

0.66

13%

Pork chop

3.5 oz roasted

0.65

13%

Egg

1 whole fresh

0.63

13%

Broccoli

1 cup cooked

0.5

10%

Ham

3.5 oz cooked

0.47

9%

Sole/flounder

3 oz cooked

0.43

9%

Kidney beans

1 cup canned

0.38

8%

Sirloin steak

3.5 oz broiled

0.37

7%

Corn

1 cup boiled

0.36

7%

Orange

1 fresh medium

0.35

7%

Watermelon

1 cup fresh

0.34

7%

Ground beef

3.5 oz baked lean

0.27

5%

Spinach

1 cup cooked

0.26

5%

Bread, whole wheat

1 slice

0.18

4%

Tuna, in water

3 oz canned

0.18

4%

Macaroni

1 cup cooked, enriched

0.16

3%

Cheddar cheese

1 oz

0.12

2%


Avocado sliced in a salad or in a dip (guacamole). Dinner: 3 oz salmon, 1 baked potato, 8 oz milk, 1 cup broccoli. Soups with lentils or split peas. Salad: chicken breast, avocado, spinach, mushrooms, broccoli.

K. Thiamin

% DRI

Food

Portion Size

Thiamin (mg)

Women

Men

Brewers yeast

1 oz

4.43

403%

369%

Pork chop

3.5 oz roasted

0.91

83%

76%

Ham

3.5 oz cooked

0.78

71%

65%

Green peas

1 cup cooked

0.42

38%

35%

Canadian bacon

2 pieces cooked

0.38

35%

32%

Corn flakes

1 cup

0.38

35%

32%

Split peas

1 cup cooked

0.37

34%

31%

Macaroni, enriched

1 cup cooked

0.29

26%

24%

Kidney beans

1 cup canned

0.27

25%

23%

Oatmeal

1 cup cooked

0.26

24%

22%

Millet

1 cup cooked

0.25

23%

21%

Acorn squash

1 cup boiled

0.24

22%

20%

Baked potato

1 whole

0.22

20%

18%

Asparagus

1 cup cooked

0.22

20%

18%

Peanuts

1 oz dry, unsalted

0.19

17%

16%

Black eyed peas

1 cup cooked

0.17

15%

14%

Watermelon

1 cup fresh

0.13

12%

11%

Sirloin steak

3.5 oz broiled

0.13

12%

11%

Honeydew melon

1 cup fresh

0.13

12%

11%

Orange

1 fresh medium

0.12

11%

10%

Winter squash

1 cup baked

0.12

11%

10%

Tofu

½ cup

0.1

9%

8%

Milk, 2%

8 oz

0.1

9%

8%

Green beans

1 cup cooked

0.1

9%

8%

Broccoli

1 cup cooked

0.1

9%

8%

Bread, whole wheat

1 slice

0.09

8%

8%

Sole/flounder

3 oz cooked

0.08

7%

7%

Cauliflower

1 cup cooked

0.08

7%

7%

Tomato

1 whole raw

0.07

6%

6%


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

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

squash

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%

Egg

1 whole fresh

0.41

8%

Margarine

1 tsp, tub type

0.34

7%

Frankfurter

1 beef frank

0.18

4%

Braunschweiger

1 oz tube type

0.15

3%

Rice, wild

2/3 cup instant

0.07

1%

Rice, white

2/3 cup instant

0.03

<1%

Cheddar cheese

1 oz

0.02

<1%


Drink 2 to 3 eight-oz glasses of milk per day. 10 to 15 minutes of sunlight exposure 3 times per week. Breakfast: vitamin-D-fortified cereals with milk. Snack: pudding made with low-fat milk. Use vitamin-D-fortified margarine instead of butter.

N. Vitamin E

Food

Portion Size

Vitamin E (mg)

% DRI

Wheat germ oil

1 tablespoon

20.3

102%

Sunflower seeds

1 oz dry roasted

14.2

71%

Mayonnaise

1 Tbs

11

55%

Almonds

1 oz dried

6.7

34%

Dried filberts

1 oz

6.7

34%

Sunflower seed oil

1 Tbs

6.3

32%

Sweet potato

1 medium raw

5.9

30%

Almond oil

1 Tbs

5.3

27%

Cottonseed oil

1 Tbs

4.8

24%

Safflower oil

1 Tbs

4.6

23%

Wheat germ

¼ cup toasted

4.1

20%

Peanut butter

2 Tbs

3

15%

Shrimp

3 oz boiled

3

15%

Canola oil

1 Tbs

2.5

13%

Asparagus

1 cup cooked

2.4

12%

Mango

1 raw medium

2.3

12%

Avocado

½ cup

2.3

12%

Peanuts

1 oz dry roasted

2.2

11%

Brazil nuts

1 oz dried

2.1

11%

Salmon

3 oz baked

2

10%

Corn oil

1 Tbs

1.9

10%

Olive oil

1 Tbs

1.7

8%

Peanut oil

1 Tbs

1.6

8%

Soybean oil

1 Tbs

1.5

8%

Apple

1 fresh medium

1.5

8%

Brussel sprouts

1 cup cooked

1.3

7%

Spinach

1 cup raw

1.1

5%

Macaroni

1 cup cooked

1

5%

Parsley

1 Tbs

1

5%

Pear

1 fresh medium

0.83

4%

Cheddar cheese

1 oz

0.5

3%


Use wheat germ or sunflower oil in salad dressings or baked goods. Serve sweet potato chips instead of regular chips––slice thin and bake. Replace cream cheese with peanut butter on bagels. Add wheat germ to cereal or yogurt. Snack: sunflower seeds, peanuts, or almonds.

O. Vitamin K

Food

Portion Size

Vitamin K (µg)

% DRI

Turnip greens

1 cup chopped raw

364

455%

Green tea

1 oz dry

199

249%

Spinach

1 cup raw

148

185%

Broccoli

1 cup cooked

126

158%

Beef liver

3.5 oz raw

104

104%

Cauliflower

1 cup raw

96

120%

Soybean oil

1 Tbs

76

95%

Chickpeas

1 oz dry

74

93%

Asparagus

1 cup cooked

69

86%

Lentils

1 oz dry

62

78%

Soybeans

1 oz

53

66%

Cabbage

1 cup raw shredded

52

65%

Mung beans

1 oz dry

48

60%

Green beans

1 cup boiled

44

55%

Wheat flour

Whole wheat, 1 cup

36

45%

Tomato

1 whole fresh

28

35%

Egg

1 whole fresh

25

31%

Peas

1 oz dry

23

29%

Wheat bran

1 oz

23

29%

Lettuce

1 leaf iceberg

22

28%

Strawberries

1 cup raw

21

26%

Watercress

1 cup chopped

20

25%

Oats

1 oz dry

18

23%

Wheat germ

1 oz

10

13%

Carrot

1 medium raw

9

11%

Corn oil

1 Tbs

8

10%

Orange

1 fresh medium

7

9%

Potato

1 whole baked

6

8%

Cucumber

1 cup raw

6

8%


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.

The Clinical Dietitian's Essential Pocket Guide

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