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 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 5'5

Small

5.5 –6.5

Medium

6.5 –7.5

Large

>7.5

Data from reference 6.

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

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

P.10

Table 1.8 Estimating Frame Size Using Elbow Breadth

Female Elbow Measurements

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

Height

Elbow Breadth

4'10 –4'11

2 1/4 –2 1/2

5'0 –5'3

2 1/4 –2 1/2

5'4 –5'7

2 3/8 –2 5/8

5'8 –5'11

2 3/8 –2 5/8

6'0 –6'4

2 1/2 –2 3/4

Male Elbow Measurements

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

Height

Elbow Breadth

5'2 –5'3

2 1/2 –2 7/8

5'4 –5'7

2 5/8 –2 7/8

5'8 –5'11

2 3/4 –3

6'0 –6'3

2 3/4 –3 1/8

6'4 –6'7

2 7/8 –3 1/4

Data from reference 5.

Table 1.9 Amputation Adjustments for Estimating Ideal Body Weight

Percentage Body Weight Contributed by Body Part

Hand

0.7%

Forearm and hand

2.3%

Entire arm

5.0%

Foot

1.5%

Lower leg and foot (below knee)

5.9%

Entire leg

16.0%

Data from reference 7.

P.11

Spinal Cord Injury Adjustment For patients with spinal cord injuries, estimation of IBW should be adjusted as follows:

Paraplegia: Subtract 5% to 10% from IBW Quadriplegia: Subtract 10% to 15% from IBW

Interpretation of Body Weight Data Percentage of Ideal Body Weight

Percentage of Usual Body Weight (UBW)

Table 1.10 shows how to evaluate % IBW and % UBW data.

Percentage of Weight Change This calculation is useful in assessing variations from the patient's usual weight, especially in the elderly population where unintentional weight loss is associated with increased morbidity and mortality (8). Once percentage of weight change has been calculated, use Table 1.11 to assess the significance of any weight changes.

Table 1.10 Interpreting % IBW and % UBW

% IBW

% UBW

Nutritional Risk

>120

__

Obesity

110–120

__

Overweight

90–109

__

Not at risk

80–89

85–95

Mild

70–79

75–84

Moderate

5%

3 months

7.5%

>7.5%

6 months

10%

>10%

Data from reference 9.

Assessment of Overweight and Obesity Body Mass Index BMI, or Quetelet's index, is a direct calculation based on height and weight, regardless of gender, and can be used to assess the severity of obesity. BMI does have limitations as a measure of total body fat, which must be considered when interpreting the data, particularly in the presence of edema, high muscularity, muscle wasting, or for very short people (under 5 ft) (10). See Table 1.12 for classifications of overweight and obesity based on BMI.

Waist Circumference and Waist-to-Hip Ratio The presence of excess fat in the abdomen, out of proportion to total body fat, is an independent predictor of risk factors and morbidity (10). Two methods for measuring abdominal fat are waist circumference and the waist-to-hip ratio (WHR). Both methods have been used to show increased risk for diabetes, coronary artery disease, and hypertension for those individuals with excess abdominal fat. Some studies suggest that waist circumference is a better predictor of disease risk than WHR, whereas other studies suggest WHR is the stronger indicator (10,11). Regardless of which method the clinician uses, measuring abdominal fat can help identify risk level for several chronic diseases (Tables 1.12 and 1.13). P.13

Table 1.12 Classification of Overweight and Obesity by Body Max Index, Waist Circumference, and Associated Disease Risk

BMI

(kg/m2)

Obesity

Disease Riska Relative to Normal Weight & Waist

Class

Circumference

Weight Status

Men =40 in.

Men >40 in.

Women =35 in.

Women >35 in.

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

Data from reference 11.

Table 1.14 Activity and Stress Factors for Determining Total Energy Expenditure

Condition

Factor

Activity Factors

Confined to bed

1.2

Ambulatory

1.3

Stress Factors Burns

=20% BSA

1.5

20%–40% BSA

1.8

>40% BSA

1.8–2.0

Infection

Mild

1.2

Moderate

1.4

Severe

1.8

Starvation

0.85

Surgery

Minor

1.1

Major

1.2

Trauma

Skeletal

1.2

Blunt

1.35

Closed head injury

1.4

BSA, body surface area.

Following is the Harris–Benedict Equation: Females: BEE = 655.1 + 9.6W + 1.9H - 4.7A Males: BEE = 66.5 + 13.8W + 5.0H - 6.8A W = weight in kilograms (use of actual vs. ideal weight is determined by the clinician); H = height in centimeters; A = age in years. P.15 Following is the Mifflin–St. Jeor Equation: Females: REE = 10W + 6.25H - 5A - 161 Males: REE = 10W + 6.25H - 5A + 5

W = actual weight in kilograms; H=height in centimeters; A = age in years.

Ireton–Jones Equations The Ireton–Jones equations for estimating energy expenditure have been found to be particularly useful for the obese population and for ill or injured patients in the intensive care unit (ICU) (12). Following are the Ireton–Jones equations: Spontaneously breathing patients: EEE = 629 - 11(A) 25(W) - 609(O) Ventilator-dependent patients: EEE = 1784 - 11(A) + 5(W) + 244(S) + 239(T) + 804(B) EEE = estimated energy expenditure (kcal/day); A = age (years); W = actual body weight (kg); O = obesity >30% above IBW or BMI >27 (present =1, absent = 0); S = sex (male=1, female=0); T=diagnosis of trauma (present =1, absent=0); B= diagnosis of burn (present=1, absent = 0).

Kilocalories per Kilogram A fast and easy method for estimating energy needs is using kilocalories per kilogram of body weight, with the reference weight as actual or ideal body weight, based on the clinician's judgment (Table 1.15).

Protein Requirements Table 1.16 contains protein recommendations for patients with several general conditions. Disease-specific protein requirements can be found in their respective chapters.

Fluid Requirements Methods for estimating fluid requirements for the normal person are typically based on body weight, kilocalorie P.16 intake, or body surface area (BSA). The caloric intake method uses 1 mL/kcal for adults and 1.5 mL/kg for infants. The BSA method uses 1,500 mL/m2/day (see Table 3.12 for calculating BSA). Table 1.17 shows two methods for estimating fluid requirements based on body weight.

Table 1.15 Energy Requirements Based on Kilocalories per Kilogram of Body Weight

Condition

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

Data from references 5 and 14.

Basic concepts in the interpretation of laboratory data include: No single test is diagnostic on its own; repeated draws are more valid; there can be diurnal variation for some tests; and some constituents can be affected by other superimposed conditions, diseases, and medications. Table 1.18 provides an overview of laboratory parameters (with 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

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

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.

Data from reference 9.

Table 2.5 Energy Needs in Pregnancy

Prepregnancy Body Weight

Energy Needs (kcal/kg body weight)

100%–120% desirable weight

30

>120% above desirable weight

24

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 90%

>95%

Stage 1 (mild)

81%–90%

90%–95%

Stage 2 (moderate)

70%–80%

85%–89%

Stage 3 (severe)

20 kg

1,500 mL + 20 mL/kg for each kg >20 kg

Data from reference 9.

Table 3.12 Calculating Body Surface Area (m2)

Body Surface Area (m2)

Weight in Kilograms

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 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

Data from references 4 and 5.

Summary Staging This simple staging system is often used by cancer registries and can be used for all types of cancer (5).

In Situ: Cancer cells are present only in the layer of cells where they developed and have not spread. Invasive: Cancer cells have spread beyond the original layer of tissue. Localized: An invasive malignant cancer is confined entirely to the organ of origin.

Table 6.2 Overall Stage Grouping

Stage

Definition

Stage 0

Carcinoma in situ (early cancer that is present only in the layer of cells in which it began)

Stages I, II, and III

Higher numbers indicate more extensive disease with greater tumor size, and/or spread of the cancer to nearby lymph nodes and/or organs adjacent to the primary tumor

Stage IV

The cancer has metastasized.

Data from references 4 and 5.

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

Medication Generic (Trade Name)

Dose

Action

Special Considerations

Dolasetron mesylate (Anzemet)

Oral: 100 mg IV: 1.8 mg/kg over 30 sec

Decreases N&V

Give 30–60 min before chemo

Granisetron HCl (Kytril)

Oral: 1 mg tablet or 5 mL suspension BID IV: 10 µg/kg

Decreases N&V

Oral: 1st dose 1 hour before chemo & 2nd 12 hr later. IV: 30 min before chemo

Lorazepam (Ativan)

Oral: 1–6 mg/day IV: 1.4 mg/m2

Decreases anxiety, relaxes muscles,

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

Data from references 6 and 7 and medication product labeling.

P.151

Table 6.7 Medications to Treat Diarrhea

Medication Generic (Trade Name)

Dose

Action

Special Considerations

Diphenoxylate HCl & atropine (Lomotil)

Oral: 5 mg QID

Slows peristalsis

Can cause nausea and dry mouth.

Loperamide HCl (Imodium)

Oral: 4 mg, followed by 2 mg after each unformed stool

Inhibits peristalsis

Shown to be 2–3 times more potent than Lomotil.

Data from references 6 and 7 and medication product labeling.

Patient Education The dietitian can play a vital role in helping cancer patients manage the symptoms associated with cancer and its treatments. Providing highly individualized meal plans and patient education can help minimize the toll that cancer can take on a patient's nutritional status. The following lists provide tips and techniques that the cancer patient and their families may find useful (8).

Managing Taste Changes Eliminate unpleasant odors and food from sight Drink fluids with meals and frequently throughout the day to moisten oral mucosa Increase taste by adding spices and flavorings such as sugar, lemon, herbs, wine Serve foods attractively, balancing colors and textures Use plastic utensils if metallic taste is a problem Use temperature extremes (hot and cold) to stimulate taste Use cold pineapple chunks between foods to change and stimulate taste sensation If foods are too sweet:

Gymnema Sylvestra, an herbal tea that is often used by professional wine tasters, will deaden the taste 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 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

20% = CHD Risk Equivalent 10%–20% 20%

9 lbs or have been diagnosed with GDM Hypertensive (=140/90 mm Hg) HDL cholesterol 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 85th percentile for age & sex, weight for height >85th percentile, or weight >120% of ideal for height Plus any two of the following risk factors: Family history of type 2 diabetes in first- or second-degree relative Race/ethnicity (African American, Asian American Latino, Native American, Pacific Islander) Signs of, or conditions associated with, insulin resistance (acanthosis nigricans, dyslipidemia, hypertension, or PCOS) Maternal history of diabetes or GDM

Data from references 3 and 4.

Children Due to the dramatic increase of type 2 diabetes in children, the ADA recommends screening for children at increased risk for the presence or development of type 2 diabetes (4). Table 8.3 shows the testing criteria for type 2 diabetes in children.

Pregnant Women It was previously recommended that all pregnant women be screened for gestational diabetes mellitus (GDM); however, there are certain factors that place women at either higher or lower risk for developing glucose intolerance during pregnancy. Table 8.4 summarizes the screening recommendations for GDM. 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

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

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

Adapted from reference 4.

Table 10.3 Treatment and Dietary Recommendations for Hepatitis

Diet

Other

High energy (30–35 kcal/kg body weight)

Bed rest

High protein (1.0–1.2 g/kg body weight)

Isolation to prevent spread

Carbohydrate (50%–55% energy)

Interferon a-2b for HBV, HBC

Supplement: B-complex, vitamins C, K, and zinc

Steroids (may cause sodium retention)

Adequate fluids Progress as tolerated from liquid to small, frequent feedings (soft or regular as tolerated)

Adapted from reference 6.

Fatty Liver (Hepatic Steatosis) Disease Process Fatty liver consists of a buildup of triglycerides in hepatic tissue. The reason for the accumulation is unclear, although the root cause is an imbalance between endogenous triglyceride synthesis and export via very-low-density lipoprotein (VLDL). The condition is reversible, but it may progress to chronic and irreversible damage. Several toxins can cause fatty liver, including alcohol, drugs, and environmental toxins. If related to toxins, eliminating the underlying cause is the most important treatment component. Dietary treatment is similar to that for hepatitis (6). Disease and other conditions that can also cause fatty liver include:

Diabetes Malnutrition Gastrointestinal bypass surgery Long-term parenteral nutrition

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

Adapted from references 6 and 10.

Table 10.6 Dietary Recommendations for Chronic Pancreatitis

Protein: 1.0 g/kg body weight, up to 2.0 g/kg for repletion Low fiber Small, frequent meals Pancreatic enzyme replacements Fat restriction, if enzyme replacement insufficient MCT, if steatorrhea severe Adequate diet or supplement: calcium, magnesium, fat-soluble vitamins, B-complex vitamins, vitamin C, zinc No caffeine or other gastric stimulants No alcohol

Adapted from references 6 and 10.

Patient Education In chronic pancreatitis, eating exacerbates the chronic abdominal pain, which frequently reduces food intake and leads to weight loss. In addition, the loss of acinar cells reduces lipases and bicarbonate, causing steatorrhea. Goals for nutritional intervention include repletion of nutritional status and reduction of malabsorption. Pancreatic replacement enzymes are important therapeutic agents to achieve these goals. Fat restriction is needed if malabsorption persists with replacement enzymes, and medium-chain triglycerides (MCT) are useful in these cases.

References 1. Mahan LK, Escott-Stump S. Krause's Food, Nutrition, and Diet Therapy, 11th ed. Philadephia: Saunders; 2004, 740–743.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Acute Renal Failure: Disease Process The causes are varied and are categorized by their relationship to prior kidney function (prerenal, intrarenal [also intrinsic], and postrenal). Most causes of ARF are prerenal, representing up to 70% of cases and include: 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

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

Data from references 9 and 10.

Table 12.2 Respiratory Acidosis

Common Causes

Asphyxia, respiratory depression (drugs, central nervous system trauma), pulmonary disease (pneumonia, COPD, respiratory underventilation).

Mechanism of Compensation

Kidneys will retain HCO3 and excrete H+ to increase pH.

pH

Uncompensated

Compensated

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: 7.55) PCO2: 35–45 mm Hg (critical values: 60 mm Hg)

HCO3: 21–28 mEq/L (critical values: 40) PO2: 80–100 mm Hg (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: 13 mg/dL or 3.25 mmol/L) Ionized Ca: 4.5–5.6 mg/dl or 1.05–1.30 mmol/L (Critical values: 7 mg/dL 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: 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